Jeffrey S.

Kreutzer
John DeLuca
Bruce Caplan
Editors

Encyclopedia of
Clinical
Neuropsychology
Second Edition
Encyclopedia of Clinical
Neuropsychology
Jeffrey S. Kreutzer • John DeLuca
Bruce Caplan
Editors

Encyclopedia of Clinical
Neuropsychology
Second Edition

With 230 Figures and 197 Tables

Editors
Jeffrey S. Kreutzer John DeLuca
Department of Physical Kessler Foundation
Medicine and Rehabilitation Pleasant Valley Way
Virginia Commonwealth University West Orange, NJ, USA
Richmond, VA, USA

Bruce Caplan
Independent Practice
Wynnewood, PA, USA

ISBN 978-3-319-57110-2 ISBN 978-3-319-57111-9 (eBook)

ISBN 978-3-319-57112-6 (print and electronic bundle)
https://doi.org/10.1007/978-3-319-57111-9
Library of Congress Control Number: 2018945469

# Springer Science+Business Media, LLC 2011

# Springer International Publishing AG, part of Springer Nature 2018
This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or
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Preface

Neuropsychology is a rapidly evolving field with inspiring advances in

neurotechnology, assessment, and intervention occurring regularly. An act of
labor and love, the conceptualization, compilation, and production of the
Encyclopedia of Clinical Neuropsychology (2nd ed.) spanned more than
4 years. Building on the foundation of the first edition, the editors-in-chief
sought to provide a current corpus of content of empirically based, relevant,
and practical information. To this end, we added three new topical sections:
neuroimaging, military neuropsychology, and DSM-5 and enlisted the help of
three superb new section editors: Erin Bigler, Ph.D., Risa Nakase-Richardson,
Ph.D., and Ana Mills, Psy.D, respectively, to orchestrate the new sections. An
immense project, the encyclopedia now contains more than 2,200 entries.
More than 1,600 first edition entries were updated and 230 new entries were
added. The newest edition of the encyclopedia now reflects the work of nearly
900 authors.
As with the first edition, we have aimed to create a comprehensive reference
for professionals involved in the evaluation, diagnosis, and rehabilitation of
children and adults with neurological disorders. We have also provided stu-
dents and researchers with the breadth of knowledge to facilitate success in
evaluating and treating these patients. Suggested readings and cross references
direct readers to additional information on the various topics. We anticipate
that the Encyclopedia of Clinical Neuropsychology will be the first place
readers turn for factual, relevant, and comprehensive information.

August 2018 Jeffrey S. Kreutzer

John DeLuca
Bruce Caplan

v
Acknowledgment

We are indebted to our cadre of esteemed Associate Editors for helping to

develop their sections, recruit contributors, and ensure the presence of consis-
tently high quality entries. We express our utmost appreciation to the brilliant
group of authors whose efforts form the core of our project. We are immensely
indebted to the superb Springer Major reference works team including Janice
Stern, Michael Hermann, and Sonja Peterson. They taught us, encouraged us,
kept us organized and on track, and helped us in every step of the way. We are
also grateful to our students, patients and their families from whom we learned
much about facing challenges and the value of being practical.

vii
 List of Topics

Cancer and Tumors–Bruce Caplan Hamartoma

Hemangioblastoma
Section Editor: Carol L. Armstrong
Hemangioma
Acoustic Neuroma Hemangiopericytoma
Acute Lymphoblastic Leukemia Hygroma
Acute Myelogenous Leukemia Hypothalamic Glioma
Acute Radiation Somnolence Intensity-Modulated Radiation Therapy
Adenoma Involved Field Radiotherapy
Angioma, Cavernous Angioma Late-Delayed Effects of Radiation Therapy
Astrocytoma Late Effects of Radiation Therapy
Atypical Teratoid/Rhabdoid Tumor (AT/RT) Leukemia
Biopsy Lymphoplasmacytic Tumor
Brachytherapy Meninges Type Tumors
Brain Tumor Meningioma
Brainstem Glioma Metastasis
Centigray Neoplasms
Cerebellar Mutism Neuroblastoma
Chemotherapy Neurocytoma
Cognitive Affective Syndrome Neurofibromatosis Type 1 (NF1)
Craniopharyngioma Neurofibromatosis Type 2 (NF2)
Craniospinal Radiotherapy Neuroma
Cyst Oligoastrocytoma
Desmoplastic Gangliocytoma Oligodendroglioma
Dysembryoplastic Neuroepithelial Tumor Optic Glioma, Optic Pathway Glioma
Early-Delayed Effects of Radiation Pilocytic Astrocytoma and Juvenile Pilocytic
Endothelial Proliferation Astrocytoma
Ependymoma Pineal Tumors
Ewing’s Sarcoma Pituitary Adenoma
Fibrillary Astrocytoma Pituitary Mass
Ganglioglioma Plasmacytoma
Germ Cell Tumors Pleomorphic, Pleomorphism
Glioblastoma Multiforme Plexiform Neurofibroma
Glioma Posterior Fossa
Gliomatosis Cerebri Posterior Fossa Syndrome

ix
x List of Topics

Primitive Neuroectodermal Tumor Competency

Proton Beam Therapy Confidentiality
Radiation Injury Criminal Forensics
Radiation Necrosis Criminal Litigation
Radiation Oncology Criminal Responsibility
Radiosurgery, Stereotactic Radiosurgery Cross-Examination
Retinoblastoma Daubert v. Merrell Dow Pharmaceuticals (1993)
Sarcoma Death Penalty
Schwannoma Deposition
Stereotactic Radiation Therapy Detroit Edison v. NLRB (1979)
Tectal Glioma Diminished Capacity
Teratoma Diminished Responsibility
Tuberous Sclerosis Direct Examination
Tumor Grade Discovery
Xanthoastrocytoma Dissimulation
Bacterial Ventriculitis Due Process
Chemo Brain Dusky v. United States (1960)
Dysmetria Estelle v. Smith (1981)
Epigenetics Ethical Principles in Forensics
Eyeblink Conditioning Expert v. Treater Role
Intraoperative fMRI Expert Witness
Neuroinformatics Fake Bad Scale
Pseudomeningocele Federal Rules of Civil Procedure 26 and 35
Teleneuropsychology Federal Rules of Criminal Procedures
Transcranial Electrical Stimulation (tES) Emphasizing 12.2
Federal Rules of Evidence
Financial Capacity
Forensics–Jeff Kreutzer Ford v. Wainwright
Forensic Neuropsychologist
Section Editor: Julie K. Lynch
Forensic Neuropsychology
AACN Practice Guidelines Forensic Psychology
Actus Reus FRE 104, 403, 702, and 704
Admissibility Frontal Lobe Defense
Aggravating Factors Furman v. Georgia (1972)
Americans with Disabilities Act of 1990 Guilty But Mentally III
Arbitration Hare Psychopathy Checklist
Atkins v. Virginia Hearsay Evidence
Attorney In Camera Review
Barefoot v. Estelle (1983) Independent Medical Evaluation
Baxter v. Temple (2005) Independent Neuropsychological Examination
Beyond a Reasonable Doubt Informed Consent
Bias Insanity
Burden of Proof Insanity Defense
Capacity Intent, General v. Specific
Chandler Exterminators v. Morris (1992) Irresistible Impulse
Chapple v. Ganger Jenkins v. U.S. (1962)
Civil Litigation Joiner v. General Electric (1997)
Clear and Convincing Evidence Kumho Tire v. Carmichael
List of Topics xi

Learned Treatise Assistive Technology

Legal Competency Attention Deficit Hyperactivity Disorder
Litigation Augmentative and Alternative Communication
Lockett v. Ohio (1978) (AAC)
M’Naghten Rule Autism Diagnostic Interview, Revised
Malingering Autism Diagnostic Observation Schedule
Mediation Autistic Disorder
Medical Malpractice Bayley Scales of Infant and Toddler Development
Mens Rea Beery Developmental Test of Visual-Motor
Mental State at Offense Integration (VMI), Sixth Edition
Miranda v. Arizona BASC-3
Mitigating Factors Rolandic Epilepsy
Motion for Summary Judgment California Verbal Learning Test – Children’s
Motion in Limine Version
Penry v. Lynaugh (1989) Central Auditory Processing Disorder
Personal Injury Cerebral Palsy
Preponderance of the Evidence Achenbach System of Empirically Based
Prima Facie Case Assessment (ASEBA)
Privilege Childhood Autism Rating Scales
Proximate Cause Children’s Category Test
Section 504 of the Rehabilitation Act of 1973 Children’s Memory Scale
Self-Incrimination Conners 3rd Edition (Conners 3; Conners 2008)
Specialty Guidelines for Forensic Psychology Conners Comprehensive Behavior Rating
Structured Interview of Reported Symptoms Scales™
(SIRS) Conners’ Continuous Performance Test Third
Subpoena Edition
Subpoena Duces Tecum Delis-Kaplan Executive Functioning System
Testamentary Capacity Developmental Gerstmann Syndrome
Testifying Expert Versus Fact Witness Differential Ability Scales (DAS and DAS-II)
Third Party Observer Down Syndrome
Trial Consulting Dyslexia
Voir Dire Expressive One-Word Picture Vocabulary Test
Workers’ Compensation Family-Centered Care
Febrile Seizures
Fetal Alcohol Spectrum Disorder
Pediatrics–Bruce Caplan Fragile X Syndrome
Functional Independence Measure for Children
Section Editor: Jennifer Ann Niskala Apps
General Language Composite
504 Plan Heterotopia
AAMD Adaptive Behavior Scales Human Figure Drawing Tests
Absence Epilepsy Hyperlexia
Accommodations Individuals with Disabilities Education Act
Adaptive Behavior Assessment System: Third Intellectual Disability
Edition Juvenile Huntington Disease
Anencephaly Juvenile Myoclonic Epilepsy
Angelman Syndrome Juvenile Parkinson’s Disease
Applied Behavior Analysis Landau-Kleffner Syndrome
Asperger’s Disorder Learning Disability
xii List of Topics

Leiter International Performance Scale, Third West Syndrome

Edition Williams Syndrome
Lennox-Gastaut Syndrome Continuous Auditory Test of Attention
Megalencephaly (CATA)
Microcephaly Duplication 7 Syndrome
Minimal Brain Dysfunction
Modified Checklist for Autism in Toddlers,
Revised, with Follow-Up (M-CHAT-R/F), also Movement–Jeff Kreutzer
M-CHAT
Section Editor: Douglas I. Katz
Mullen Scales of Early Learning
Myelomeningocele Abasia
Myoclonic Epilepsy in Infancy Action Tremor
National Dissemination Center for Children with Akathisia
Disabilities Akinesis
National Organization for Rare Disorders Allokinesia
(NORD) Apraxia
NEPSY-II Astasia-Abasia
No Child Left Behind Act of 2001 Ataxia
Nonverbal Learning Disabilities Automatism
Peabody Individual Achievement Test, Revised Balance Disorders
Peabody Picture Vocabulary Test Bell’s Palsy
Perceptual Reasoning Index Bradykinesia
Periventricular Leukomalacia Chorea
Personality Inventory for Children Circumduction
Pervasive Developmental Disorder NOS Dopamine-Related Dyskinesia
Phenylketonuria Dysdiadochokinesia
Plasticity Dystonia
Prader-Willi Syndrome Essential Tremor
Prematurity and Low Birth Weight Festination
Processing Speed Index (WPPSI-IV) Gait Disorders
Public Law 94-142 Headache
Semantic Pragmatic Disorder (SPD) Hemiparesis
Sensitive Periods Hemiplegia
Abusive Head Trauma Homunculus
Soft Signs Hypertrophy
Stanford-Binet Intelligence Scales and Revised Intention Tremors
Versions Internal Capsule
Stroop Color and Word Test, Children’s Version Internuclear Ophthalmoplegia
TEACCH Lateral Gaze Palsy
Tourette Syndrome Leukodystophy
Turner Syndrome Locked-In Syndrome
Vineland Adaptive Behavior Scales Magnetic Gait
Vineland Social Maturity Scales Masked Facies
Waisman Center, University of Wisconsin- Ménière’s Syndrome
Madison Micrographia
Wechsler Intelligence Scale for Children Motor Stereotypy
Wechsler Preschool and Primary Scale of Movement Disorders
Intelligence Myoclonus
List of Topics xiii

Orthostatic Tremor Fluorodeoxyglucose Positron Emission

Parkinson Plus Syndromes Tomography
Parkinsonism Fractional Anisotropy
Physiologic Tremor Frontal Lobotomy
Ptosis Functional Imaging
Restless Leg Syndrome Gamma Knife
Retropulsion Hemispherectomy
Rigidity Hemodynamic Response
Spastic Gait Hemoglobin
Tardive Dyskinesia International Classification of Diseases
Thalamus Intracarotid Sodium Amobarbital Test
Tic Leukotomy
Tremor Lobectomy
Wilson’s Disease Lumbar Puncture
Luxury Perfusion
Magnetic Resonance Angiography
Magnetic Resonance Imaging
Medical–Jeff Kreutzer Magnetic Resonance Spectroscopy
Magnetoencephalography
Section Editor: Nathan D. Zasler
Midline Shift
Abbreviated Injury Scale Neuroimaging
Ablation Neurologic Examination
Alpha Rhythm Nuclear Magnetic Resonance
Angiography, Cerebral Olfaction
Babinski Reflex P300
Blood Alcohol Level Pallidotomy
Blood Flow Studies PET
Blood Oxygen Level Dependent (BOLD) Physiatric Assessment
Brainstem Auditory Evoked Responses Pneumoencephalography
Carotid Angiography Polysomnography
Carotid Endarterectomy Post-traumatic Headache
Commissurotomy Posturography
Computed Tomography Prefrontal Lobotomy
Coronary Artery Bypass Graft Quantitative Encephalography
Cranioplasty Radiotherapy
Craniotomy Rancho Los Amigos Scale
Deep Brain Stimulator (Parkinson’s) Regional Cerebral Blood Flow
Diffusion Tensor Imaging Sensorimotor Assessment
Digital Subtraction Angiography Shunts
Doppler Ultrasound Signs
Dysconjugate Gaze Single Photon Emission Computed Tomography
Electrodiagnosis Somatosensory Evoked Potentials
Electroencephalography Stereotaxic Surgery
Endotracheal Tube Temporal Lobectomy
Event-Related Potentials Tesla
Evidence-Based Practice Transcranial Doppler
Evoked Potentials Transcranial Magnetic Stimulation
Fixed Pupils UBO
xiv List of Topics

Ventriculostomy Phonics
Visual Evoked Potentials Physical Disabilities
Voxel Praxis
Wada Test Primary Handicapping Conditions
Problem Solving
Proprioception
Academic Evaluation–John Deluca Rapid Automatic Naming
Reading
Section Editor: Rik Carl D’Amato
Reading Comprehension
Abstract Reasoning Reading Fluency
Academic Competency Reality Orientation
Academic Skills Reasoning
Acalculia Remedial Education Approach
Arithmetic Reasoning Response to Intervention
Auditory Discrimination Scholastic Aptitude Test
Auditory Processing Secondary Handicapping Condition
Social Awareness Self-Regulation
Basic Achievement Skills Inventory Sequential Processing
Bender Visual-Motor Gestalt Test II Simultaneous Processing
Cognitive Assessment System Social Competence
Compensatory Education Approach Special Education
Constructional Apraxia Speech/Communication Disabilities
Deaf/Hearing Impairment Stereognosis
Dean-Woodcock Neuropsychological Strength-Based Education
Assessment System Tests of General Educational Development
Developmental Milestones, Stages Vocabulary
Dyscalculia Wechsler Individual Achievement Test
Educational Testing Wechsler Test of Adult Reading
Emotional Disturbance Woodcock-Johnson IV
Emotional Intelligence Progress Monitoring
Emotionality Neuropsychologically Driven Interventions
Executive Functioning Evidence-Based Interventions
Finger Localization Single-Case Design Interventions
Individual Education Program Inclusive Education
Mainstreaming Homeschooling (Homeschool
Manual Dexterity Education)
Manual Strength Charter School
McCarthy Scales of Children’s Abilities Neurodiversity
Mental Tracking Neuroeducation
Metacognition Neuroleadership
Multitasking Neurotechnology
National Adult Reading Test and Orientation Neurosystems
(Left–Right) Immigrant Languages
Orientation Psychoeducation
Orientation (Left-Right) Education
Other Health Impairment Prevention
Otis-Lennon School Ability Test Family Education
Phonemic Awareness Neurotherapy
List of Topics xv

Neurofeedback Inspection Time

Mindfulness Interference
Infant/Toddler Preschool Assessment (0–6) Lethargy
N-Back Paradigm
Orienting Response
Attention and Concentration–John Deluca Paced Auditory Serial Attention Test
Parallel Processing
Section Editor: Ronald Cohen and Adam J.
Processing Speed Index
Woods
Searchlight Hypothesis
Action-Intentional Disorders Selective Attention Models
Anosognosia Serial Sevens
Anterior Cingulate Cortex Serial/Sequential Processing
Arousal Signal Detection Theory
Attention Span of Apprehension
Attention Network Test (ANT) Sustained Attention
Automaticity Symbol Search
California Computerized Assessment Package Test of Everyday Attention
Cancellation Tests Test of Everyday Attention for Children
Capacity Limitations Thalamic Gating
Catatonic Behavior Vigilance
Confabulation Working Memory
Conners Rating Scales Yerkes-Dodson Law
Consciousness Attentional Response Bias
Continuous Performance Tests Eye Tracking
Controlled Attention Flanker Task
Cue Dominance D2 Test of Attention
Default Network Digit Vigilance Test
Delirium Brief Test of Attention
Delusion Tests of Variables of Attention
Dichotic Listening Auditory Selective Attention Test
Digit Span Visual Search and Attention Test
Digit Symbol Substitution Test Attentional Blink
Directed Attention Vertical Neglect
Discriminability Useful Field of View (UFOV)
Disengagement of Attention Behavioral Inattention Test (BIT)
Disinhibition Visual Search
Divided Attention Troxler Fading
Effort Priming
Enhancement Pre-Pulse Inhibition
Extinction Inattentional Blindness
Facilitation
Filtering
Focused Attention Brain Injury–Jeff Kreutzer
Habituation
Section Editor: James F. Malec
Hemiinattention
Hemikinesis Acceleration Injury
Inferior Parietal Lobule Acute Respiratory Distress Syndrome
Information Processing Speed Appalic Syndrome
xvi List of Topics

Automated Neuropsychological Assessment Penetrating TBI

Metrics Pneumothorax
Battle’s Sign Polytrauma
Biomechanics of Injury Postacute Brain Injury Rehabilitation
Blast Injury Postconcussion Syndrome
Brain Swelling Post-traumatic Confusional State
Coma Pupillary Light Response, Pupillary Response
Concussion Raccoon Eyes
Contrecoup Injury Rotational Acceleration
Cortical Contusion Secondary Brain Injury
Craniectomy Severe Brain Injury
Deceleration Injury Shearing Injury, Shear Strain
Decerebrate Posturing Skull Fracture
Decorticate Posturing Sleep Apnea Syndrome
Depressed Skull Fracture Sleep Disturbance
Diffuse Axonal Injury Spinal Cord Injury
Distractibility Sport-Related Concussion
Edema Stupor
Electrical Brain Injury Subgaleal Hematoma
Embolism Time to Follow Commands
Epidemiology Toxic Exposure
Epidural Hematoma Trauma Center
Fatigue Traumatic Brain Injury (TBI)
Focal Lesion, Contusion Traumatic Brain Injury Model System
Head Injury Vegetative State (Persistent)
Heterotopic Ossification Whiplash
Holistic Brain Injury Rehabilitation Ohio State University Traumatic Brain Injury
Hypersomnia Identification Method
Hypoarousal Normal Pressure Hydrocephalus
Immediate Post-Concussion Assessment and
Cognitive Testing
Impaired Self-Awareness CNS–John Deluca
Initiation
Section Editor: Randall E. Merchant and John
Insomnia
DeLuca
Lead Exposure
Loss of Consciousness Afferent
Mass Effect Alzheimer’s Disease
Memory Impairment Amygdala
Mercury Exposure Arcuate Fasciculus
Mild Traumatic Brain Injury Associational Fibers
Minimally Conscious State Auditory Pathway
Minimally Responsive State Autonomic Nervous System
Moderate Brain Injury Basal Forebrain
Narcolepsy Basal Ganglia
Obstructive Sleep Apnea Syndrome Blood-Brain Barrier
Occult Head Injury Brain Death
Outcome, Outcome Measurement Brodmann’s Areas of the Cortex
Pediatric Traumatic Brain Injury Caudate Nucleus
List of Topics xvii

Cerebellum Pneumocephalus
Cerebral Cortex Pons
Cerebral Edema Postcentral Gyrus
Cerebral Perfusion Pressure Precentral Gyrus
Commissures, Cerebral Putamen
Corpus Callosum Pyramidal System
Cortical Motor Pathways Raphe Nucleus
Cortical-Subcortical Loop Reticular Activating System
Cranial Nerves Rostral
Dentate Gyrus Somatosensory System
Diencephalon Spinal Cord
Efferent Striate Cortex
Visual Fields Striatum
Forebrain Subfornical Organ
Fornix Subiculum
Frontal Lobe Substantia Nigra
Ganglion Superior Colliculus
Globus Pallidus Superior Longitudinal Fasciculus
Gray Matter Supramarginal Gyrus
Hemi-attention Syndrome Sylvian Fissure
Hindbrain Temporal Lobe
Hydrocephalus Uncus
Insular Lobe Ventral Tegmental Area of Midbrain
Intracranial Pressure Ventricles
Korsakoff’s Syndrome Ventricular Enlargement
Limbic System Vestibular Nuclei
Localization Visual Cortex
Locus Ceruleus White Matter
Mediodorsal Nucleus of Thalamus Caudal
Medulla Schizophrenia
Medulloblastoma
Meninges
Mesolimbic Dopaminergic Projections Cognitive Rehabilitation–John Deluca
Midbrain
Section Editor: Sarah A. Raskin
Midbrain Raphe
Multiple Sclerosis Active Limb Activation
Myelin Activities of Daily Living (ADL)
Neocortex Attention Training
Neuroglia Cognitive Correctors
Neuron Cognitive Functioning
Nucleus Accumbens Cognitive Rehabilitation
Nucleus Basalis of Meynert Compensatory Strategies
Occipital Lobe Concept Learning
Pallidum Constraint Induced Therapy
Papez Circuit Error Recognition and Correction
Parietal Lobe Errorless Learning
Parkinson’s Disease Insight: Effects on Rehabilitation
Periventricular White Matter Lighthouse Technique
xviii List of Topics

Memory Book Neurofibrillary Tangles

Method of Vanishing Cues Optic Neuropathy
Mnemonic Techniques Paralysis Agitans
Neuropsychological Rehabilitation Parkinson’s Dementia
Process Training Pick’s Disease
Prosthetic Memory Aids Primary Progressive Multiple Sclerosis
Quality of Life Progressive Aphasia
Strategy Substitution Progressive Supranuclear Palsy
Verbal Mediation Relapsing-Remitting Multiple Sclerosis
Computerized Treatment Secondary-Progressive Multiple Sclerosis
Goal Management Training Semantic Dementia
Academic Techniques Senile Dementia
Brain Training Senile Plaques
Small Vessel Ischemic Disease
Tauopathy
Dementia–John Deluca Vascular Cognitive Impairment
Vascular Dementia
Section Editor: Gordon Chelune
Alzheimer’s Dementia
Amyloid Plaques Frontal Lobe–John Deluca
Amyotrophic Lateral Sclerosis
Section Editor: Paul Malloy
Apoptosis
Atrophy Abulia
Beta-Interferons Adynamia
Binswanger’s Disease Akinetic Mutism
Blessed Dementia Scale Alien Hand Syndrome
CADASIL Anosmia
Cholinesterase Inhibitors Apathy
Clinical Dementia Rating Avolition
Consortium to Establish a Registry on Behavior Rating Inventory for Executive
Alzheimer’s Disease Function
Corticobasal Degeneration Category Test
Dementia Rating Scale-2 Central Executive
Dementia with Lewy Bodies Cingulate Gyrus
Demyelination Cingulum
Encephalopathy Delayed Response Tasks
Frontal Temporal Dementia Design Fluency Test
Frontotemporal Lobar Degenerations Dorsolateral Prefrontal Cortex
Gliosis Environmental Dependency
Huntington’s Disease Executive Abilities: Methods and Instruments for
Hypertensive Encephalopathy Neurobehavioral Evaluation and Research
Leukoaraiosis Executive Interview
Lewy Bodies Figural Fluency Test
Logopenic Aphasia Frontal Systems Behavior Scale
Metabolic Encephalopathy Gegenhalten
Mild Cognitive Impairment Glabellar Reflex
Modified Mini-Mental State Examination Grasp Reflex
Multi-infarct Dementia Klüver-Bucy Syndrome
List of Topics xix

Motor Impersistence Fugl-Meyer Assessment of Sensorimotor

Palmomental Reflex Impairment
Perseveration Functional Ambulation Classification
Prefrontal Cortex Functional Assessment
Reduplicative Paramnesia Functional Assessment Measure
Rooting Reflex Functional Assessment Multiple Sclerosis
Ruff 2 and 7 Selective Attention Test Functional Autonomy Measurement System
Ruff Neurobehavioral Inventory Functional Capacity Evaluations
Ruff-Light Trail Learning Test Functional Independence Measure
Sexual Disinhibition Functional Status
Snout Reflex Functional Status Questionnaire
Stroop Effect General Well-Being Schedule
Suck Reflex Glasgow Coma Scale
Utilization Behavior Glasgow Outcome Scale
Witzelsucht Glasgow Outcome Scale: Extended
Iowa Scales of Personality Change Health Assessment Questionnaire
High-Level Mobility Assessment Test
Impact on Participation and Autonomy
Functional Evaluation–Bruce Caplan Questionnaire
Independent Living Scales ®
Section Editor: Tamara Bushnik
Informant Questionnaire on Cognitive Decline in
Activities of Daily Living Questionnaire the Elderly
Alzheimer’s Disease Cooperative Study ADL Instrumental Activities of Daily Living
Scale Jebsen-Taylor Hand Function Test
Amyotrophic Lateral Sclerosis Functional Rating Katz Index of ADLs
Scale Kohlman Evaluation of Living Skills
Ashworth Spasticity Scale (and Modified Late Life Function and Disability Index
Version) Lawton-Brody Instrumental Activities of Daily
ASIA Impairment Scale Living Scale
Assessment of Life Habits (LIFE-H) Loewenstein Occupational Therapy Cognitive
Assessment of Motor Process Skills Assessment
Barthel Index Mayo-Portland Adaptability Inventory
Berg Balance Scale Mobility, Self-Care, and Domestic Life (MOSES)
Bristol Activities of Daily Living Scale Motor Activity Log
Brunel Balance Assessment Motor Assessment Scale
CHART Short Form Multiple Sclerosis Quality of Life-54
Cognitive Log Questionnaire
Community Integration Questionnaire National Institutes of Health Stroke Scale
Craig Handicap Assessment and Reporting Norwegian Function Assessment Scale
Technique Nottingham Health Profile
Direct Assessment of Functional Status Older Americans’ Resources and Services
Disability Assessment for Dementia Multidimensional Functional Assessment
Disability Rating Scale Questionnaire
Driving Assessment Participation Measure for Post-acute Care
EuroQol/EQ-5D Participation Objective, Participation Subjective
Expanded Disability Status Scale Patient Competency Rating Scale
Fibromyalgia Impact Questionnaire Patient Generated Index
Frenchay Activity Index Performance-Oriented Mobility Assessment
xx List of Topics

Physical Functional Performance American Psychological Association (APA)

PM-PAC Computerized Adaptive Testing American Psychological Association (APA),
Postural Assessment Scale for Stroke Division 22
Postural Control and Balance for Stroke American Psychological Association (APA),
Profile of Functional Impairment in Division 40
Communication Association for Postdoctoral Programs in
Psychological Health Assessment Questionnaire Clinical Neuropsychology (APPCN)
Rankin Scale Babcock, Harriet (1807–1952)
Raskin Rating Scale Balint, R. (Rezso (Rudolf) Balint) (1874–1929)
Reintegration to Normal Living Index Behaviorism
Rivermead Mobility Index Benton, Arthur (1909–2006)
Roland-Morris Questionnaire Ben-Yishay, Yehuda (1933–)
Severe Impairment Battery Brain Injury Association of America
SF-36/SF-12 Broca, Pierre Paul (1824–1880)
Short Physical Performance Battery Butters, Nelson (1937–1995)
Sickness Impact Profile Center for Outcome Measurement in Brain
6-Minute Walk Test Injury (COMBI)
Spinal Cord Independence Measure (SCIM) Centers for Medicare and Medicaid Service
Stroke Activity Scale Christensen, Anne-Lise (1926– )
Stroke Impact Scale Clinical Neuropsychology
Stroke-Adapted Sickness Impact Profile Commission on Accreditation of Rehabilitation
Supervision Rating Scale Facilities (CARF)
Timed Up and Go Test Cultural Diversity in Neuropsychology
UCSD Performance-Based Skills Assessment Damasio, Antonio R. (1944–)
Unified Parkinson’s Disease Rating Scale De Renzi, Ennio (1924–)
Visual Analog Scale Dejerine, Joseph Jules (1849–1917)
Wolf Motor Function Test Diller, Leonard (1924– )
PART-O Ethics in the Practice of Clinical
Neuropsychology: Foundations and
New Horizons
General/Historical–Bruce Caplan Gage, Phineas (1823–1860)
Gazzaniga, M. S. (1939–)
Section Editor: Anthony Y. Stringer
Gerstmann, Josef (1887–1969)
Akelaitis, Andrew John Edward (“A.J.”) Geschwind, Norman (1926–1984)
(1904–1955) Goldman-Rakic, Patricia (1937–2003)
Alzheimer, Alois (1864–1915) Goldstein, Kurt (1878–1965)
American Academy of Clinical Neuropsychology Goodglass, Harold (1920–2002)
(AACN) H.M.; Also the Case of H.M., Molaison,
American Academy of Neurology (AAN) Henry (1926–2008)
American Board of Pediatric Neuropsychology Halstead, Ward (1908–1968)
American Board of Professional Psychology Hebb, Donald (1904–1985)
(ABPP) Hécaen, Henry (1912–1983)
American Board of Professional Heilman, Kenneth M. (1938–)
Neuropsychology (ABN) International Neuropsychological Society
American Board of Rehabilitation Psychology International Neuropsychological
American College of Professional Symposium
Neuropsychology (ACPN) Jennett, Bryan (1926–2008)
American Congress of Rehabilitation Medicine Kaplan, Edith (1924–2009)
List of Topics xxi

Kinsbourne, Marcel (1931–) Genetics

Korsakoff (Korsakov), Sergei Sergeievich
Section Editor: John DeLuca
(1854–1900)
Lashley, Karl Spencer (1890–1958) Adoption Studies
Lezak, Muriel Allele
Liepmann, Hugo Karl (1863–1925) Chromosome
Luria, Alexander Romanovich (1902–1977) Cognitive Processing
Meier, Manfred John (1929–2006) Deoxyribonucleic Acid (DNA)
Milner, Brenda Atkinson (1918–) Frontal Lobe Syndrome
Mishkin, Mortimer (1926–) Gene
Monrad-Krohn, Georg H (1884–1964) Gene-Environment Interaction
National Academy of Neuropsychology (NAN) Genotype
National Center for the Dissemination of Heritability
Disability Research (NCDDR) Mesial Frontal System
National Institute of Neurological Disorders and Orbitofrontal System
Stroke Phenotype
National Institute on Disability Independent Polymorphism
Living and Rehabilitation Research Tower of London
(NIDILRR) Transgenic
National Institutes of Health (NIH) Twin Studies
National Rehabilitation Information Center
(NARIC)
Neuropsychiatry Illness or Disease–John Deluca
Neuropsychology
Section Editor: Susan K. Johnson
Occupational Therapy
Parsons, Oscar (1920–2000) Acquired Immunodeficiency Syndrome (AIDS)
Penfield, Wilder (1891–1976) Arachnoid Cyst
Physiatry Brain Abscesses
Pribram, Karl H. (1919–) Carbon Monoxide Poisoning
Rehabilitation Psychology Chelation
Reitan, Ralph (1922–) Chronic Fatigue Syndrome
Rosenthal, Mitchell (1949–2007) Chronic Obstructive Pulmonary Disease
Rourke, Byron (1939–) Circadian Rhythms
Sperry, Roger Wolcott (1913–1994) Creutzfeldt-Jakob Disease
Tan Cushing’s Syndrome
Teuber, Hans-Lukas (1916–1977) Developmental Delay
Warrington, Elizabeth Diabetes Mellitus
Wernicke, Karl (1848–1905) Encephalitis (Viral)
Zangwill, Oliver (1913–1987) Epstein-Barr Virus
American Board of Clinical Neuropsychology Fibromyalgia
(ABCN) Guillain-Barré Syndrome
Diagnostic and Statistical Manual of Mental Gulf War Syndrome
Disorders (DSM) Herniation Syndromes
Hispanic Neuropsychological Society Herpes Simplex Encephalitis
Hispanic/Latino Neuropsychology Hypoglycemia
Neuropsychology in Africa Hypothyroidism
Houston Conference Iatrogenic
Gerald Goldstein Inflammation
xxii List of Topics

Kuru Working Memory Index

Lyme Disease Fluid Reasoning
Meningitis Visual Spatial Index
Multiple Chemical Sensitivity
Myasthenia Gravis
Neurasthenia Interventions–Jeff Kreutzer
Neuropathy
Section Editor: Bruce Rybarczyk
Neurosyphilis
Neurotoxins Activity Restrictions, Limitations
Organic Brain Syndrome Advocacy
Prion Disease Assisted Living
Psychogenic Nonepileptic Seizures Attendant Care
Second Impact Syndrome Case Management
Sick Building Syndrome Circles of Support
Sjogren’s Syndrome Cognitive Behavioral Couples Therapy
Symptom Cognitive Behavioral Therapy
Syndrome Community Re-entry
Systemic Lupus Eythematosus Community-Based Rehabilitation
Temporomandibular Joint Dysfunction Crisis Intervention
Toxic-Metabolic Encephalopathy Customized Job Retention Services
Unexplained Illness Discharge Planning
Wallenberg’s Syndrome Employment Specialist
Environmental Modifications
Family Team Conference
Intelligence–John Deluca Family Therapy
Functional Compensation
Section Editor: Nancy D. Chiaravalloti
Group Therapy
Advanced Progressive Matrices Homework
Colored Progressive Matrices Independent Living Centers
Estimation Methods Interdisciplinary Team Rehabilitation
Flynn Effect Job Advocacy
Full Scale IQ Job Analysis
Intelligence Job Placement
Intelligence Quotient Job Retention
Kaufman Adult Intelligence Test Job Training
Kaufman Brief Intelligence Test Jobsite Training
Mental Age Life Care Planning
Perceptual Organization Index Managed Care
Performance IQ Motivational Interviewing
Porteus Maze Pastoral Counseling
Premorbid Intelligence Patient-Family Education
Raven’s Progressive Matrices Physical Therapy
Shipley Institute of Living Scale Problem-Solving Training
Standard Progressive Matrices Psychotherapy
Verbal Comprehension Index Recommendation
Verbal IQ Recreational Therapy
Wechsler Intelligence Tests for Adults and Rehabilitation Counseling
Children Relaxation Training
List of Topics xxiii

Sexual Surrogate Therapy Crossed Aphasia

Sheltered Employment Cue
Social and Occupational Functioning Assessment Discourse Assessment
Scale (SOFAS) Dysarthria
Stress Management Dysphagia
Supported Employment Dysphonia
Task Analysis F-A-S Test
Transitional Living Fluent Aphasia
Transitional Planning Global Aphasia
Vocational Rehabilitation Grammar
Cognitive Behavioral Therapy for Insomnia Grapheme
Jargon
Language
Language–Bruce Caplan Lexicon
Literal Paraphasia
Section Editor: Roberta DePompei and Aimee
Logorrhea
Dietz
Melodic Intonation Therapy
Agnosia Metacognitive Skills
Agrammatism Metalinguistic Skills
Agraphia Morpheme
Alexia Multilingual Aphasia Examination
American Speech-Language-Hearing Association Naming
(ASHA) Neologism
American Speech-Language-Hearing Association Nonfluent Aphasia
Functional Assessment of Communication Paragrammatism
Skills for Adults Paragraphia
Anarthria Paralexia
Anomia Paraphasia
Anomic Aphasia Phoneme
Aphasia Phonemic Cue
Aphasia Diagnostic Profiles Phonological Disorder
Aphasia Tests Phonology
Aphonia Phrase Length
Apraxia of Speech Pragmatic Communication
Aprosodia Primary Progressive Aphasia
Articulation Prosody
Articulation Disorders Pure Word Deafness
Automatic Language Repetition
Bilingual Aphasia Semantic Cue
Boston Diagnostic Aphasia Examination Semantic Paraphasia
Boston Naming Test Speech
Broca’s Aphasia Speech Sound Disorder
Circumlocution Speech-Language Pathology
Cognitive-Communication Disorder Speech-Language Therapy
Communication Ability Stereotypy
Conduction Aphasia Stuttering, Acquired
Confrontation Naming Stuttering, Developmental
Controlled Oral Word Association Test Subcortical Aphasia
xxiv List of Topics

Syntax Septum Pellucidum

Telegraphic Speech Splenium
Token Test Split-Brain
Transcortical Motor Aphasia Spontaneous Recovery
Transcortical Sensory Aphasia
Verbal Fluency
Wernicke’s Aphasia Memory–John Deluca
Wernicke–Lichtheim Model of Aphasia
Section Editor: Sarah A. Raskin
Western Aphasia Battery
Word Finding Amnesia
Writing Amnestic Disorder
Perseverative Speech Amnestic Syndromes
Gist Anterograde Amnesia
Strategic Learning Auditory Verbal Learning
Semantics Autobiographical Memory
AphasiaBank/TalkBank Benign Senescent Forgetfulness
Auditory Comprehension Benton Visual Retention Test
SFA California Verbal Learning Test (California
Conversational Treatments Verbal Learning Test-II)
Learned Non-use Cholinergic System
Right-Hemisphere Processing Cognitive Reserve
Social Communication Consolidation
Pediatric Test of Brain Injury (PTBI) Cued Recall
Reading Comprehension Battery for Declarative Memory
Aphasia-2 Dementia
Cognitive Linguistic Quick Test Disorientation
VNeST Dissociative Amnesia
ASHA Quality of Communication Echoic Memory
Life Scale Episodic Memory
False Memory
Forgetting
Laterality–Bruce Caplan Free Recall
Hippocampus
Section Editor: John E. Mendoza and Bruce
Hopkins Verbal Learning Test
Caplan
Hypothalamus
Agenesis of Corpus Callosum Implicit Memory
Ambidexterity Incidental Memory
Anomalous Dominance Intrusion Errors
Anterior Commissure Jamais Vu
Association Pathways Learning
Asymmetry Mammillary Bodies
Disconnection Syndrome Medial Temporal Lobe
Dominance (Cerebral) Memory
Edinburgh Handedness Inventory Memory for Intentions
Handedness N-Acetyl Aspartate
Hemispheric Specialization Paired-Associate Learning
Hemisphericity Post-traumatic Amnesia
Projection Pathways Practice Effects
List of Topics xxv

Presenile Dementia Dysphoria

Primacy Effect Frontal Behavioral Inventory
Proactive Interference Frontal Eye Fields
Procedural Memory Glucocorticoids
Prospective Memory Hormones
Pseudodementia Hyperbaric Therapy
Recency Effect Impersistence
Recent Memory Impulsivity
Recognition Memory Test Inhibition
Remote Memory Irritability
Retrieval Techniques Job Restructuring
Retroactive Interference Neuroleptic Malignant Syndrome
Retrograde Amnesia Neuroleptics
Rey Auditory Verbal Learning Test, Pharmacodynamics
Rey AVLT Pharmacokinetics
Rivermead Behavioral Memory Test Phenobarbital
Selective Reminding Test Projective Technique
Semantic Memory Psychopharmacology
Serial Recall Psychotropic
Short-Term Memory Qualitative Data
Source Memory Qualitative Neuropsychological Assessment
Subcortical Dementia Reuptake
Transient Global Amnesia Reuptake Inhibition
Warrington Recognition Memory Test Route Finding
Wechsler Memory Scale All Versions Sedative Hypnotic Drugs
Wernicke-Korsakoff Syndrome Social Skills Training
Wide Range Assessment of Memory and Steroids
Learning Stimulants
Serial Position Effect Stimulus-Bound Behavior
Memory for Intentions Screening Test Substance Abuse
Supplementary Motor Area (SMA)
Symmetril (Amantadine)
Miscellaneous–Jeff Kreutzer Tinkertoy Test
Tolerance
Section Editor: Stephanie A. Kolakowsky-
Vocational Counseling
Hayner
Wisconsin Card Sorting Test
Anticholinergic
Anticonvulsants
Antihistamines Neuropsychological Evaluation–Jeff Kreutzer
Antihypertensives
Section Editor: Yana Suchy
Antipsychotics
Anxiolytics Agitated Behavior Scale
Autoreceptor Behavioral Assessment of the Dysexecutive
Behavior Modification Syndrome
Compensation Neurosis Boston Process Approach
Corticotropin-Releasing Hormone Brief Cognitive Rating Scale
Dysexecutive Index (DEX) Cambridge Neuropsychological Testing
Dysexecutive Syndrome Automated Battery
xxvi List of Topics

Cognistat Symptom Validity Assessment

Coma Recovery Scale Tactile Form Recognition
Coma/Near Coma Scale Tactual Performance Test
Dot Counting Test Test of Memory Malingering
Double Simultaneous Stimulation Trail Making Test
Dynamic Assessment Wide Range Achievement Test-4
Finger Tapping Test Word Memory Test
Finger to Nose Test Barrow Neuropsychological Screen
Fingertip Number-Writing Perception
Fixed Battery
Flexible Battery Psychological Conditions–Bruce Caplan
Forced-Choice Test
Section Editor: Robert G. Frank
Galveston Orientation and Amnesia Test
Go/No-Go Testing Affect
Grooved Pegboard Test Affective Disorder
Halstead Impairment Index Agitation
Halstead-Reitan Neuropsychological Test Battery Alcohol Abuse
Hand Dynamometer Alcohol Dependence
Hypothesis Testing Approach to Evaluation Alcoholic Brain Syndrome
Katz Adjustment Scale Alcoholism
Kaufman Assessment Battery for Children Alertness
Line Bisection Alexithymia
Luria Nebraska Neuropsychological Battery Anxiety
Memory Assessment Scales Behavior Management
Mental Status Examination Behavioral Assessment
Meyers Neuropsychological Battery Behavioral Therapy
Mini-Mental State Exam Catastrophic Reaction
Neurobehavioral Assessment Circumstantiality
Neurobehavioral Functioning Inventory Clinical Practice Guidelines
Neurobehavioral Rating Scale Cogniform Disorder
Neuropsychological Assessment Battery Coping
Neurosensory Center Comprehensive De-escalation
Examination for Aphasia Denial
Orientation Log Depressive Disorder
Portland Digit Recognition Test Distributed Systems
Purdue Pegboard Emotional Lability
Reitan-Indiana Aphasia Screening Test Family Adjustment
Reitan-Klove Sensory Perceptual Examination Family Burden
Repeatable Battery for the Assessment of Flight of Ideas
Neuropsychological Status Frustration Tolerance
Rey 15 Item Test Grandiosity
Rivermead Behavioral Inattention Test Hallucination
Seashore Rhythm Test Hypersexuality/Hyposexuality
Serial Digit Learning Ideas of Reference
Serial Subtractions Irritable Bowel Syndrome
Stroop Color Word Test (Adult) La Belle Indifference
Stroop Neuropsychological Screening Test Major Depression
(Adult) Masked Depression
List of Topics xxvii

Medical Model Brief Symptom Inventory

Mental Flexibility CAGE Questionnaire
Minor Depressive Disorder Center for Epidemiological Studies: Depression
Mood Disorder Clinical Interview
Motivation Clinical Significance
Narcissism Computerized Assessment of Response Bias
Neurotic Disorder Confounding Variables
Neuroticism Eysenck Personality Inventory
Nonadherence F Minus K Index
Noncompliance with Treatment F Scale
Pain Faking Good, Bad
Paranoid Ideation Family Needs Questionnaire
Paranoid Psychosis Geriatric Depression Scale
Pica Hamilton Depression Rating Scale
Placebo Hiscock Forced-Choice Test
Positive Supports House-Tree-Person Test
Post-traumatic Stress Disorder K Scale
Premorbid Personality L Scale
Prescription Privilege MacArthur Competence Assessment Tools
Pressured Speech McGill Pain Questionnaire
Psychogenic Disorder McMaster Family Assessment Device
Psychogenic Pain Michigan Alcoholism Screen Test
Psychomotor Retardation Millon Adolescent Clinical Inventory
Psychosis Millon Behavioral Health Inventory
Psychotic Disorder Millon Clinical Multiaxial Inventory
Redirection Minnesota Multiphasic Personality Inventory
Schizotypal Personality Disorder Multiaxial Assessment
Sex Therapy Myers-Briggs Inventories
Somatization NEO Personality Inventory
Stages of Adjustment Patient Health Questionnaire
Stimulus Control Personality Assessment Inventory
Stimulus Generalization Projective Tests
Stress Psychometrician
Substance Use Disorders Rorschach
Suicidal Ideation Satisfaction with Life Scale
Tangentiality Sentence Completion
Therapeutic Community Structured Clinical Interview for DSM-IV
Therapist-Patient Relationship (SCID-I/SCID-II)
Third Party Administrator Symptom Checklist-90-Revised
Double Dissociation Thematic Apperception Test
True Response Inconsistency Scale (TRIN,
Psychological Evaluation–Bruce Caplan MMPI)
Validity Scales (MMPI)
Section Editor: Stephanie A. Reid-Arndt
Variable Response Inconsistency Scale (VRIN,
Beck Anxiety Inventory MMPI)
Beck Depression Inventory Victoria Symptom Validity Test
Bell Curve Vocational Assessment
Brief Psychiatric Rating Scale Zung Self-Rating Depression Scale
xxviii List of Topics

Positive and Negative Affect Schedule (PANAS) Intratest Scatter

Schedule for Nonadaptive and Adaptive Ipsative
Personality (SNAP) Item Analysis
Alcohol Use Disorders Indentification Test Item Difficulty
(AUDIT), The Item Response Theory
King-Devick Test Kappa Coefficient
Millon Behavioral Medicine Diagnostic Kennard Principle
Latent Variable
Mayo’s Older Americans Normative Studies
Psychometrics–Jeff Kreutzer (MOANS)
Measurement Theory
Section Editor: Michael Franzen
Meta-analysis
Age Decrements Modified Testing
Alternate Test Forms Multiple Comparisons
Analysis of Variance Multiple Regression
ANCOVA/MANCOVA Multivariate Analysis of Variance
Barona Index Negative Predictive Power
Base Rate (Population) Neuropsychological Deficit Scale
Battery Approach Neuropsychological Report
Best Performance Method Neuropsychological Screening Examination
Brain Reserve Capacity Nonparametric Statistics
Ceiling Effect Nonstandard Assessment
Chi-square Normal Aging
Classical Test Theory Normal Curve
Clustering Normative Data
Confirmatory Bias Observer Reports and Ratings
Contingency Table Parallel Forms
Correlation Coefficients Path Analysis
Cultural Sensitivity Pattern Analysis
Culture Fair Test Percentiles
Cutoff Scores, Cutting Scores Phrenology
Deficit Measurement Positive Predictive Power
Differential Diagnosis Premorbid Estimate
Disability Premorbid Functioning
Domain Referenced Test Interpretation Qualified Examiner
Dual Diagnosis Receiver-Operating Characteristics
Ecological Validity Referral Question
Error, Sources of Reliable Change Index
Factor Analysis Response Bias
False Negative Self-Report Measures
False Positive Sensitivity
Floor Effect Specificity
Generalizability Theory Speed-Accuracy Tradeoff
History (Medical, Social, Psychological) Standard Error of the Mean
Hold-Don’t Hold Tests Standard Scores
Individual Comparison Standards Standardized Tests
Inter-rater Reliability Statistical Significance
Intertest Scatter Structural Equation Modeling
List of Topics xxix

Subtest Scatter D-Amphetamine

T Scores Desipramine
Table of Specifications Dexamethasone
Task Load Dexmethylphenidate
Test Bias Diazepam
Test Construction Discontinuation Syndrome
Test Interpretations: Computer Based Donepezil
Test Reliability Dopamine
Test Validity Doxepin
Testing the Limits Duloxetine
Wonderlic Personnel Test Electro-Convulsive Therapy
Z Scores Enzyme
Basal and Ceiling Rules Epinephrine
Escitalopram
Extrapyramidal Symptoms
Psychopharmacology–John Deluca Fluoxetine
Fluphenazine
Section Editor: Efrain Antonio Gonzalez
GABA
Acetylcholine Gabapentin
Adrenocorticotropic Hormone Galantamine
Alprazolam Glutamate
Amitriptyline Half-Life
Amoxapine Haloperidol
Amphetamine Hydroxyzine
Anticholinesterase Inhibitors Imipramine
Antidepressants Lamotrigine
Apolipoprotein E Levetiracetam
Aripiprazole Levodopa
Atomoxetine Lithium
Barbiturates Lorazepam
Benzodiazepines L-Tryptophan
Bromocriptine Maprotiline
Bupropion Memantine
Buspirone Mesoridazine
Carbamazepine Methylphenidate
Catecholamines Midazolam
Chlordiazepoxide Mirtazapine
Chlorpromazine Moclobemide
Citalopram Modafinil
Clomipramine Molindone
Clonazepam Monoamine Oxidase
Clonidine Nefazodone
Clorazepate Neuropeptides
Clozapine Neurotransmitters
Cmax N-Methyl-D-Aspartate (NMDA) Receptors
Compartmentalization Norepinephrine
Contraindication Nortriptyline
Cytochrome P450 Olanzapine
xxx List of Topics

Oxazepam Valbenazine
Oxcarbazepine Vilazodone
Paroxetine Vortioxetine
Pentobarbital Paliperidone
Perphenazine Pimavanserin
pH Lisdexamfetamine Dimesylate
Phenelzine Desvenlafaxine
Phenytoin Cariprazine
Pimozide
Pregabalin
Seizure–John Deluca
Quazepam
Quetiapine Section Editor: Nancy D. Chiaravalloti
Receptor Spectrum
Absence Seizure
Reserpine
Aura
Risperidone
Complex Partial Seizure
Rivastigmine
Cortical Mapping
Selective Serotonin Reuptake Inhibitors
Epilepsy
Selegiline
Functional Magnetic Resonance Imaging
Serotonin
Grand Mal Seizure
Serotonin Syndrome
Ictal Phenomena
Sertraline
Interictal Behavior Syndrome
Tachyphylaxis
Ischemic Penumbra
Tacrine
Kindling
Temazepam
Paroxysmal Disorder
Thioridazine
Simple Partial Seizure
Thiothixene
Petit Mal Seizure
Tiagabine
Postictal Confusion
Tmax
Psychomotor Epilepsy
Topiramate
Seizure
Tranylcypromine
Status Epilepticus
Trazodone
Syncope
Triazolam
Temporal Lobe Epilepsy
Trifluoperazine
Trimipramine
Valproate Sensory–Bruce Caplan
Venlafaxine
Section Editor: John E. Mendoza and Bruce
Zaleplon
Caplan
Ziprasidone
Zolpidem Accessory Cuneate Nucleus
Zonisamide Afferent Paresis
Zopiclone Ageusia
Deutetrabenazine Ahylognosia
Asenapine Allesthesia
Brexipiprazole Amorphognosis
Eszopiclone Amusia
Iloperidone Anosodiaphoria
Fetzima (Levomilnacipran) Anterolateral System
Tetrabenazine Apperceptive Visual Agnosia
List of Topics xxxi

Asomatognosia Olfactory Bulb

Association Areas Olfactory Tract
Associative Visual Agnosia Optic Chiasm
Auditory Agnosia Optic Nerve
Auditory Cortex Optic Radiations
Auditory System Optic Tract
Autotopagnosia Pain Asymbolia
Body Schema Palinopsia
Brain Plasticity Pallanesthesia
Brown-Séquard Syndrome Pallesthesia
Calcarine Fissure Paresis
Chief Sensory Nucleus of V Paresthesia
Cochlea Peduncular Hallucinosis
Cochlear Nuclei (Dorsal and Ventral) Perception
Color Agnosia Peripheral Neuropathy
Color Anomia Posterior Columns
Color Imagery Primary Cortex
Dejerine-Roussy Syndrome Pronator Drift
Dermatome Protopathic Pain
Dorsal Nerve Roots Referred Pain
Dorsal Root Ganglia Right Left Disorientation
Epicritic Pain Romberg Test
Equipotentiality Secondary Cortex
Fasciculus Cuneatus Sensory Ataxia
Fasciculus Gracilis Somatosensory Cortex
Finger Agnosia Somatotopic Organization
Functional Neuroanatomy Somesthesia
Gerstmann’s Syndrome Spatial Dyscalculia
Global Versus Local Processing Spinal Nucleus of V
Graphesthesia Spinal Tract of V
Heschl’s Gyrus Spinocerebellar Tracts
Heteromodal Cortex Spinoreticular Tract
Homonymous Hemianopsia Spinothalamic Tract
Homonymous Quadrantanopsia Substantia Gelatinosa
Homotypic Cortex Superior Olivary Nucleus
Hyperesthesia Suppression
Idiotypic Cortex Synesthesia
Inferior Colliculi Tactile Agnosia
Kinesthesia Tactile Asymboly
Lateral Lemniscus Taste
Lingual Gyrus Temperature, Perception of
Medial Geniculate Nuclei Tertiary Cortex
Medial Lemniscus Thalamic Pain Syndrome
Metamorphopsia Thermoanesthesia
Meyer’s Loop Tinnitus
Nucleus Cuneatus Topographical Disorientation
Nucleus Gracilis Touch, Localization of
Nucleus Solitarius Trapezoid Body
xxxii List of Topics

Trigeminothalamic Tracts Infarction

Two-Point Discrimination Internal Carotid Artery
Unimodal Cortex Intracerebral Hemorrhage
Ventral Posterior Lateral Nucleus Intracranial Hemorrhage
Ventral Posterior Medial Nucleus Intraventricular Hemorrhage
Vertigo Ischemia
Vestibular Dysfunction Ischemic Stroke
Vestibular System L’etat Lacunaire
Vestibulocochlear Nerve Lacunar Infarction
Visual Object Agnosia Lobar Hemorrhage
Visual System Lupus Cerebritis
Weber Test Middle Cerebral Artery
Moyamoya Disease
Vascular–Bruce Caplan Myocardial Infarction
NIH Stroke Scale
Section Editor: Elliot Roth
Perfusion-Weighted Imaging
Aneurysm Peripheral Vascular Disease
Angioplasty Posterior Cerebral Artery
Anoxia Posterior Communicating Artery
Anterior Cerebral Artery Pure Motor Stroke
Anterior Communicating Artery Recombinant Tissue Plasminogen Activator
Anticoagulation Sickle-Cell Disease
Antiplatelet Therapy Stent
Arteriovenous Malformation (AVM) Stroke
Atherosclerosis Subarachnoid Hemorrhage
Basilar Artery Subdural Hematoma
Brainstem Strokes Thalamic Hemorrhage
Central Venous Thrombosis Thrombolysis
Cerebellar Hemorrhage Thrombosis
Cerebral Amyloid Angiopathy Transcranial Doppler Ultrasonography
Cerebral Angiitis Transient Ischemic Attack
Cerebral Blood Flow Vascular Malformations
Cerebral Embolism Vasculitis
Cerebrovascular Disease Vasospasm
Cholesterol Venous Thrombosis
Circle of Willis Vertebrobasilar System
Collagen Vascular Disease Warfarin (Coumadin)
Congestive Heart Failure Novel Oral Anticoagulants
Coronary Disease Thrombectomy
Diaschisis Endovascular Therapy
Diffusion-Weighted Imaging
Dissection Visual–John Deluca
Echocardiogram
Section Editor: Ronald Cohen and Adam J.
Hematoma
Woods
Hemorrhage
Hemorrhagic Stroke Achromatopsia
Heparin Astereognosis
Hypertension Balint’s Syndrome
List of Topics xxxiii

Bicycle Drawing Test Rey Complex Figure Test

Blindsight Saccadic Eye Movements
Block Design Scotoma
Calcarine Cortex Simultanagnosia
Capgras Syndrome Spatial Frequency Analysis
Charles Bonnet Syndrome Spatial Processing
Clock Drawing Tachistoscopic Presentation
Closure Temporal Inhibition
Conjugate Gaze Trochlear Nerve
Cortical Blindness Ventral Visual Pathway
Cortical Magnification Visual Agnosia
Cuneus Visual Angle
Diplopia Visual Field Deficit
Dorsal Visual Pathway Visual Form Discrimination
Dorsomedial Visual Area Visual Hallucinations
Edge Detection Visual Modularity
Embedded Figures Test Visual Neglect
Extrastriate Visual Tracking
Facial Recognition Test Visual-Motor Function
Feature Perception Visual-Spatial Ability
Figure-Ground Discrimination Visuoperceptual
Fourier Transforms Macular Degeneration
Fovea Distance Perception
Gollin Figures Binocular Disparity
Hemianopia Motion Parallax
Hemispatial Neglect Eye Dominance
Hooper Visual Organization Test Visual Convergence
Inferior Parietal Area Posterior Cortical Atrophy
Judgment of Line Orientation Motion Perception
Lateral Geniculate Nucleus of the Thalamus Visual Psychophysics
Lateral Inhibition Just Noticeable Difference
Macropsia Absolute Threshold
Magnocellular Neurons Appercetive Agnosia
Micropsia Retinotopic Mapping
Neglect Syndrome Spatial Sequence Synesthesia
Nystagmus Mach Bands
Object Recognition Backwards Masking
Ocular Dominance Post Trauma Vision Syndrome
Oculomotor Nerve Visual Assessment Battery (VAB)
Optic Ataxia
Optokinetic Reflex
Parvocellular Neurons Military Neuropsychology–Jeff Kreutzer
Prosopagnosia
Section Editor: Risa Nakase-Richardson
Pseudobulbar Palsy
Pulvinar Military Neuropsychology
Quadrantanopia Suicide
Receptive Fields Emerging Consciousness Program
Retinopathy Military Deployment
xxxiv List of Topics

Types of Military Discharge Graph Theory

Military Occupational Status Network Connectivity
Department of Defense (DoD) Network Edges
Post-concussive Syndrome Network Hubs
Post-deployment Syndrome Network Nodes
Pre-deployment Cognitive Testing Rich Club Networks
Blast Effects Ventricle-to-Brain (VBR) Ratio
Decompression Sickness Voxel-Based Morphometry
Cognitive Resilience Resting-State Functional Connectivity MRI
Slick Criteria (fcMRI)
Neurobehavioral Symptom Inventory Diffusion Kurtosis Mapping
PCL-C PET Imaging
VA TBI Model System Program Near-Infrared Spectroscopy
Polytrauma System of Care Tract-Based Spatial Statistics (TBSS)
Agent Orange
Arterial Gas Embolism
Noncredible Symptom History DSM-5–Jeff Kreutzer
Jennifer Vasterling
Section Editor: Ana Mills
Carrie Kennedy
Automated Neuropsychological Assessment Social (Pragmatic) Communication Disorder
Metrics (ANAM) Premenstrual Dysphoric Disorder
Battlefield Assessment Disruptive Mood Dysregulation Disorder
Fitness-for-Duty or Physical Evaluation Board Antidepressant Discontinuation Syndrome
Defense and Veterans Brain Injury Center Neurocognitive Disorders
Polytrauma Transitional Rehabilitation Program OCD
Chronic Effects of Neurotrauma Consortium Body Dysmorphic Disorder
Vietnam Head Injury Study Hoarding
Heat-Related Illness Excoriation
Military Acute Concussion Evaluation Reactive Attachment Disorder
National Intrepid Center of Excellence Acute Stress Disorder
Louis French, Ph.D. Adjustment Disorder
Disinhibited Social Engagement Disorder
Illness Anxiety Disorder
Neuroimaging–John Deluca Rumination Disorder
Anorexia Nervosa
Section Editor: Erin D. Bigler and Jo Ann
Bulimia Nervosa
Petrie
Avoidant/Restrictive Food Intake Disorder
False Discovery Rate Binge-Eating Disorder
Machine Learning Enuresis
Shape/Countour Analysis Encopresis
Quantitative Neuroimaging Analysis Gender Dysphoria
Lesion-Symptom Mapping Oppositional Defiant Disorder
Segmentation and Classification Intermittent Explosive Disorder
Cortical Thickness Conduct Disorder
FreeSurfer Pyromania
Lesion Burden Kleptomania
Surface Area Paranoid Personality Disorder
Susceptibility Weighted Imaging Schizoid Personality Disorder
List of Topics xxxv

Antisocial Personality Disorder Feeding and Eating Disorders

Borderline Personality Disorder Elimination Disorders
Histrionic Personality Disorder Disruptive, Impulse-Control, and Conduct
Narcissistic Personality Disorder Disorders
Dependent Personality Disorder Personality Disorders
Paraphilic Disorders Obsessive-Compulsive Personality Disorder
Sexual Dysfunctions Somatic Symptom Disorder
Obsessive-Compulsive and Related Disorders
Trauma- and Stressor-Related Disorders
Somatic Symptom and Related Disorders
About the Editors

Jeffrey S. Kreutzer Department of Physical Medicine and Rehabilitation,

Virginia Commonwealth University, Richmond, VA, USA

Dr. Jeffrey S. Kreutzer is the Rosa Schwarz Cifu Professor in the Department
of Physical Medicine and Rehabilitation (PM&R) at Virginia Commonwealth
University’s Medical College of Virginia Campus in Richmond. He first came
to VCU as a postdoctoral fellow in 1982 after completing an internship in
Neuropsychology and Family Therapy with Muriel Lezak at the Portland,
Oregon VA Medical Center. He joined Virginia Commonwealth University’s
medical school faculty in the Fall of 1983.
Board certified in rehabilitation psychology (ABPP), Dr. Kreutzer has
more than three decades of experience as a brain injury rehabilitation spe-
cialist. He was a founding member of the Virginia Head Injury Foundation,
now known as BIAV. Since 1987, he has served as the Director of VCU’s
federally designated Traumatic Brain Injury Model System (TBIMS). As a
clinician, Dr. Kreutzer provides neuropsychological and family support
services to persons with a wide variety of neurological disabilities. His
practice is holistic, emphasizing skills training, psychological support, and
patient education.
Throughout his career, Dr. Kreutzer has been involved in developing
empirically based intervention programs for persons with brain injury. For
example, in 1986 he and Dr. Paul Wehman received a federal grant to adapt

xxxvii
xxxviii About the Editors

supported employment methods for persons with brain injury. Their success-
ful program development along with very positive outcome data has helped
make supported employment the current “standard of care” for TBI employ-
ment services. More recently, Dr. Kreutzer is developing empirically based
programs to enhance resilience, couples’ relationships, and family
functioning.
Dr. Kreutzer has received numerous awards. In 1994, he received the Sheldon
Berrol Clinical Service Award from The National Head Injury Foundation. In
2002, he received the Robert L. Moody Prize for Distinguished Initiatives in
Brain Injury Research and Rehabilitation from the University of Texas. He has
received two awards from the American Psychological Association, the Roger
Barker Distinguished Research Contribution Award (2003) and the Diller
Award for Demonstrated Excellence in the Field of Neurorehabilitation
(2005). In 2010, he received the Distinguished Lifetime Contribution to Neuro-
psychology Award from the National Academy of Neuropsychology. In 2012, he
received the McCollom Research Award from the Foundation for Life Care
Planning Research, and in 2013 he received the Innovations in Treatment Award
from the North American Brain Injury Society. In 2017, he was presented with
the Jennett Plum Award for Clinical Achievement in the Field of Brain Injury
Medicine by the International Brain Injury Association.
A frequent speaker at national and international meetings, he has given
more than 500 invited presentations. A Fellow in the American Congress of
Rehabilitation Medicine (FACRM), National Academy of Neuropsychol-
ogy, and the American Psychological Association, Dr. Kreutzer has
co-authored more than 170 publications, mostly in the area of traumatic
brain injury and rehabilitation. Editor-in-Chief of two international journals,
Brain Injury and NeuroRehabilitation, he has also published more than
15 books covering topics such as family intervention, vocational rehabilita-
tion, community reintegration, behavior management, and cognitive
rehabilitation.

John DeLuca is the Senior Vice President for Research and Training at
Kessler Foundation, a Professor in the Department of Physical Medicine and
Rehabilitation, and the Department of Neurology at Rutgers, New Jersey
About the Editors xxxix

Medical School. He is a licensed Psychologist in New Jersey and New York

and is board certified in Rehabilitation Psychology by the American Board of
Professional Psychology. Dr. DeLuca has been involved in neuropsychology
and rehabilitation research for over 25 years. He is internationally known for
his research on disorders of memory and information processing in a variety of
clinical populations, including multiple sclerosis, traumatic brain injury, aneu-
rysmal subarachnoid hemorrhage, and chronic fatigue syndrome. Dr. DeLuca
has published over 300 articles and chapters in these areas; has edited 5 books
in neuropsychology, neuroimaging, and rehabilitation; and is a co-editor for
the Encyclopedia of Clinical Neuropsychology. He has received over 32
million dollars in grant support for his research. Dr. DeLuca’s most recent
research ventures include the cerebral mapping of human cognitive processes
using functional neuroimaging, as well as the development of research-based
techniques to improve cognitive impairment. He serves as an Associate Editor
of several journals and is on the editorial boards of many other journals. He is
the recipient of several awards in recognition of his work including the 2015
Arthur Benton Award from the International Neuropsychological Society and
2012 Rodger G. Barker Distinguished Research Contribution Award from
Division 22 (Rehabilitation Psychology) of the American Psychological Asso-
ciation. Dr. DeLuca has been very involved for many years in the training of
postdoctoral fellows in neuropsychology and rehabilitation and has directed
several advanced research and training programs sponsored by NIDRR, the
National MS Society, and NIH since 1990.

Bruce Caplan is board certified in clinical neuropsychology and rehabilita-

tion psychology by the American Board of Professional Psychology and is a
Fellow of the American Psychological Association (APA), National Academy
of Neuropsychology, and American Congress of Rehabilitation Medicine.
Dr. Caplan serves as Senior Editor of Journal of Head Trauma Rehabilitation,
is a member of the Editorial Board of Topics in Stroke Rehabilitation, and
previously served as Editor of Rehabilitation Psychology. In 1987, Dr. Caplan
published Rehabilitation Psychology Desk Reference, the first edited textbook
in the specialty. He is past President of the Philadelphia Neuropsychology
Society and of Division 22 (Rehabilitation Psychology) of the APA. He is the
recipient of two Distinguished Service Awards and the Lifetime Achievement
xl About the Editors

Award from Division 22. Dr. Caplan was a founding member of the American
Board of Rehabilitation Psychology. Currently in independent practice, he was
formerly Professor and Chief Psychologist in the Department of Rehabilitation
Medicine at Jefferson Medical College in Philadelphia.
Contributors

Galya Abdrakhmanova University of Richmond, Richmond, VA, USA

Thomas M. Achenbach Department of Psychiatry, University of Vermont,
Burlington, VT, USA
Russell Adams Department of Psychiatry and Behavioral Science, Univer-
sity of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
Adrienne Adler Department of Neurobiology and Anatomy, Wake Forest
School of Medicine, Winston-Salem, NC, USA
Adrienne Adler-Neal Department of Neurobiology and Anatomy, Wake
Forest School of Medicine, Winston-Salem, NC, USA
Amma A. Agyemang Department of Physical Medicine and Rehabilitation,
Virginia Commonwealth University Medical Center, Richmond, VA, USA
Cristy Akins Mercy Family Center, Metarie, LA, USA
Amy Alderson Department of Rehabilitation Medicine, Emory University,
Atlanta, GA, USA
Brittany J. Allen Cox Health System, Springfield, MO, USA
Daniel N. Allen Department of Psychology, University of Nevada, Las
Vegas, NV, USA
H. Allison Bender Department of Neurology, Icahn School of Medicine at
Mount Sinai, New York, NY, USA
Ahmad Alsemari Psychology, Edgewood College, Madison, WI, USA
Karin Alterescu Department of Psychology, Queens College of the City
University of New York (CUNY), Flushing, NY, USA
Robert A. Altmann A-PsychEd Publication Services, Minneapolis, MN,
USA
Akshay Amaraneni Department of Pharmacology, Virginia Commonwealth
University, Richmond, VA, USA

xli
xlii Contributors

Melissa Amick Department of Psychiatry and Human Behavior, Brown

University, Providence, RI, USA
Aaron Andersen Utah State University, Logan, UT, USA
Heather Anderson Department of Neurology, University of Kansas School
of Medicine, Kansas City, KS, USA
Steven W. Anderson University of Iowa Hospitals and Clinics, Iowa City,
Iowa, USA
Kevin M. Antshel Department of Psychology, Syracuse University,
Syracuse, NY, USA
Jennifer Ann Niskala Apps Department of Psychiatry and Behavioral
Medicine, Children’s Hospital of Wisconsin/Medical College of Wisconsin,
Milwaukee, WI, USA
Juan Carlos Arango-Lasprilla IKERBASQUE, Basque Foundation for
Science, Biocruces Research Institute, Bilbao, Spain
Amy J. Armstrong Department of Rehabilitation Counseling, Virginia
Commonwealth University, Richmond, VA, USA
Carol L. Armstrong Child and Adolescent Psychiatry and Behavioral Sci-
ences, The Children’s Hospital of Philadelphia, Philadelphia, PA, USA
Glenn S. Ashkanazi Department of Clinical and Health Psychology, Clinical
and Health Psychology Clinic, College of Public Health and Health Profes-
sions, University of Florida, Gainesville, FL, USA
Jane Austin Department of Psychology, William Paterson University,
Wayne, NJ, USA
Bradley N. Axelrod John D. Dingell VA Medical Center, Psychology Sec-
tion (11MHPS), Detroit, MI, USA
Lindsay E. Ayearst Multi-Health Systems Inc., Toronto, ON, Canada
Glen P. Aylward SIU School of Medicine- Developmental-Behavioral Pedi-
atrics, Springfield, IL, USA
Samantha Backhaus Department of Neuropsychology, Rehabilitation Hos-
pital of Indiana, Indianapolis, IN, USA
Erin Bailey Department of Psychology, Miami VA Healthcare System,
Miami, FL, USA
Maya Balamane Mount Sinai Brain Injury Research Center, San Francisco,
CA, USA
Angel Ball Department of Clinical Health Sciences, Texas A&M University –
Kingsville, Kingsville, TX, USA
Sandra Banks Department of Psychiatry, Allegheny General Hospital, Pitts-
burgh, PA, USA
Contributors xliii

James H. Baños Department of Medical Education, University of Alabama

School of Medicine, Birmingham, AL, USA
Russell A. Barkley Virginia Treatment Center for Children and Virginia
Commonwealth University Medical Center, Richmond, VA, USA
Ida Sue Baron Potomac, MD, USA
Erika M. Baron Pace University, New York, NY, USA
Mark S. Baron Department of Neurology, Virginia Commonwealth Univer-
sity Parkinson’s and Movement Disorders Center, Richmond, Virginia, USA
Walter Barr Department of Psychology, William Paterson University,
Wayne, NJ, USA
William B. Barr NYU Langone Medical Center, Comprehensive Epilepsy
Center, New York, NY, USA
Joseph Barrash Department of Neurology, University of Iowa, Iowa City,
IA, USA
Russell M. Bauer Department of Clinical and Health Psychology, University
of Florida, Gainesville, FL, USA
Allison Baylor Virginia Commonwealth University, Richmond, VA, USA
Jessica Bean Department of Psychology, University of Connecticut, Storrs,
CT, USA
Megan Becker Department of Psychology, University of Nevada, Las Vegas,
NV, USA
James T. Becker Department of Psychiatry, University of Pittsburgh School
of Medicine, WPIC, Pittsburgh, PA, USA
Pélagie M. Beeson Department of Speech, Language, and Hearing Sciences,
The University of Arizona, Tucson, AZ, USA
Jay Behel Department of Behavioral Sciences, Rush University Medical
Center, Chicago, IL, USA
Stephanie Behrens Department of Psychology, Utah State University,
Logan, UT, USA
Stacy Belkonen Salem VA Medical Center, Salem, VA, USA
Department of Psychiatry and Behavioral Medicine, Virginia Tech Carilion
School of Medicine, Roanoke, VA, USA
Andrew Bell Department of Anatomy and Neurobiology, Virginia Common-
wealth University, Richmond, VA, USA
Brian D. Bell Department of Neurology, University of Wisconsin, Madison,
WI, USA
Heidi A. Bender Department of Neurology, Icahn School of Medicine at
Mount Sinai, New York, NY, USA
xliv Contributors

Daniel B. Berch Curry School of Education, University of Virginia, Char-

lottesville, VA, USA
Brianne Magouirk Bettcher Department of Neurosurgery and Neurology,
University of Colorado School of Medicine, Denver, CO, USA
Rocky Mountain Alzheimer’s Disease Center, Aurora, CO, USA
Alyssa Beukema School Psychology, The Chicago School of Professional
Psychology, Chicago, IL, USA
John Bigbee Anatomy and Neurobiology, Virginia Commonwealth Univer-
sity, Richmond, VA, USA
Erin D. Bigler Department of Psychology and the Neuroscience Center,
Brigham Young University, Provo, UT, USA
Rebecca Bind Department of Neurology, Mount Sinai Medical Center, New
York, NY, USA
J. Audie Black Allegheny General Hospital, Pittsburgh, PA, USA
Department of Psychiatry; Neuropsychology Section, Allegheny Health Net-
work, Pittsburgh, PA, USA
Margaret Lehman Blake Communication Sciences and Disorders, Univer-
sity of Houston, Houston, TX, USA
Michelle L. Block Stark Neuroscience Research Institute, Indiana Univer-
sity, Indianapolis, IN, USA
Henrike K. Blumenfeld School of Speech, Language and Hearing Sciences,
San Diego State University, San Diego, CA, USA
Ty Bodily Psychology Department and the Neuroscience Center, Brigham
Young University, Provo, UT, USA
Doug Bodin Department of Pediatrics, Nationwide Children’s Hospital and
The Ohio State University, Columbus, OH, USA
Angela M. Bodling Center for Health Care Quality, University of Missouri—
Columbia, Columbia, MO, USA
Jennifer Bogner Department of Physical Medicine and Rehabilitation, Ohio
State University, Columbus, OH, USA
Robert J. Boland Department of Psychiatry, Brigham and Women’s Hospi-
tal/Harvard Medical School, Boston, MA, USA
Mark W. Bondi University of California San Diego School of Medicine, La
Jolla, CA, USA
Neuropsychological Assessment Unit, VA San Diego Healthcare System, San
Diego, CA, USA
Amanda D. Bono Department of Psychology, Queens College and The
Graduate Center of the City University of New York, Flushing, NY, USA
Contributors xlv

John G. Borkowski Department of Psychology, University of Notre Dame,

Notre Dame, IN, USA
Joan C. Borod Department of Psychology, Queens College and The Grad-
uate Center of the City University of New York (CUNY), New York, NY, USA
Department of Neurology, Icahn School of Medicine at Mount Sinai, New
York, NY, USA
Beth Borosh Cognitive/Behavioral Neurology Center Northwestern
Feinburg School of Medicine, Chicago, IL, USA
Carley Borza University of Alberta, Edmonton, AB, Canada
Dawn E. Bouman Neuropsychology and Medical Psychology, University of
Cincinnati, Department of Neurology and Rehabilitation Medicine, Cincin-
nati, OH, USA
Isabelle Bourdeau Division of Endocrinology, Department of Medicine,
Research Centre, Centre hospitalier de l’université de Montréal (CHUM),
Montreal, QC, Canada
Jessica Bove Emory University, Atlanta, GA, USA
Dawn Bowers Department of Clinical and Health Psychology, University of
Florida, Gainesville, FL, USA
Mary Boyle The College of Humanities and Social Sciences, Montclair State
University, Montclair, NJ, USA
Lauren E. Bradley Department of Behavioral Sciences, Rush University
Medical Center, Chicago, IL, USA
Natalie Brei Department of Psychology, University of Wisconsin-Milwau-
kee, Milwaukee, WI, USA
Lisa A. Brenner Rocky Mountain Mental Illness Research Education and
Clinical Center, Denver, CO, USA
University of Colorado, Anschutz Medical Campus, Aurora, CO, USA
Rachel M. Bridges Department of Psychology, University of South Caro-
lina, Columbia, SC, USA
Andrew Brodbelt The Walton Centre NHS Foundation Trust, Liverpool, UK
Justine S. Broecker The Westminster Schools, Atlanta, GA, USA
Alyssa M. Broomfield School of Psychology, The Chicago School of Pro-
fessional Psychology, Chicago, IL, USA
John Brown Medical College of Georgia, Augusta, GA, USA
Margaret Brown Mount Sinai School of Medicine, New York, NY, USA
Racine Brown Center of Innovation on Disability and Rehabilitation
Research, James A. Haley Veterans’ Hospital, Tampa, FL, USA
xlvi Contributors

Martha Brownlee-Duffeck Harry S. Truman Memorial, Columbia, MO,

USA
Kelly Broxterman School Psychology, The Chicago School of Professional
Psychology, Chicago, IL, USA
Hugh W. Buckingham Department of Communication Sciences and Disor-
ders, College of Allied Health Sciences, University of Oklahoma Health
Sciences Center, Oklahoma City, OK, USA
Ashley Bujalski Department of Psychology, William Paterson University,
Wayne, NJ, USA
Rebecca Burger-Caplan Yale Child Study Center, Yale University School of
Medicine, New Haven, CT, USA
Department of Pediatrics, Emory University School of Medicine, Atlanta, GA,
USA
Jeffrey M. Burns Department of Neurology, University of Kansas School of
Medicine, Kansas City, KS, USA
Thomas G. Burns Department of Neuropsychology, Children’s Healthcare
of Atlanta, Atlanta, GA, USA
Shane S. Bush Long Island Neuropsychology, P.C., Lake Ronkonkoma, NY,
USA
Tamara Bushnik Inter-Hospital Research and Knowledge Translation, Rusk
Rehabilitation, New York, NY, USA
Melissa Buttaro Department of Psychiatry, The Miriam Hospital, Provi-
dence, RI, USA
Meryl A. Butters Department of Psychiatry, University of Pittsburgh School
of Medicine, WPIC, Pittsburgh, PA, USA
Xavier E. Cagigas UCLA Semel Institute for Neuroscience and Human
Behavior, Los Angeles, CA, USA
Medical Psychology Assessment Center, Resnick Neuropsychiatric Hospital
at UCLA, Los Angeles, CA, USA
Department of Psychiatry and Biobehavioral Sciences, David Geffen School
of Medicine at UCLA, Los Angeles, CA, USA
Deborah A. Cahn-Weiner Department of Neurology, University of Califor-
nia, Davis, Davis, CA, USA
Rebecca M. Cain Fairfax Neonatal Associates, Fredericksburg, VA, USA
Charles D. Callahan Memorial Health System, Springfield, IL, USA
Jonathan Campbell Neurology, Virginia Commonwealth University, Rich-
mond, VA, USA
Bruce Caplan Independent Practice, Wynnewood, PA, USA
Contributors xlvii

Jessica A. Carboni Counseling and Psychological Services, Georgia State

University, Atlanta, GA, USA
Noelle E. Carlozzi Physical Medicine and Rehabilitation, University of
Michigan, Ann Arbor, MI, USA
Helen M. Carmine ReMed, Paoli, PA, USA
Dominic A. Carone University Hospital – Neuropsychology Assessment
Program, SUNY Upstate Medical University, Syracuse, NY, USA
Janessa O. Carvalho Department of Psychology, Bridgewater State Univer-
sity, Bridgewater, MA, USA
Jennifer Cass Department of Pediatrics, Nationwide Children’s Hospital and
The Ohio State University, Columbus, OH, USA
Adam Cassidy Harvard University, Cambridge, MA, USA
Eric Catlin Physical Medicine and Rehabilitation, University of South Flor-
ida, Tampa, FL, USA
Amiram Catz Department of Spinal Rehabilitation, Loewenstein Rehabili-
tation Hospital, Raanana, Israel
Tel-Aviv University, Tel-Aviv, Israel
Jessica Chaiken HeiTech Services, Inc., National Rehabilitation Information
Center, Landover, MD, USA
Grace-Anna Chaney Department of Psychology, Towson University,
Towson, MD, USA
Lanshin Chang University of Macau, Taipa, Macau SAR, China
Sandra Bond Chapman Center for BrainHealth, The University of Texas at
Dallas’ school of Behavioral and Brain Sciences, Dallas, TX, USA
Jesse Chasman Department of Psychology, University of Connecticut,
Storrs, CT, USA
Sandy Sut Ieng Cheang Department of Psychology, University of Macau,
Taipa, Macau, SAR, China
Colby Chlebowski Department of Psychiatry, University of California, San
Diego, USA
Woon N. Chow Department of Pathology, Microbiology, and Immunology,
Vanderbilt University Medical Center, Nashville, TN, USA
Shawn E. Christ University of Missouri, Columbia, MO, USA
Sarah S. Christman Buckingham Department of Communication Sciences
and Disorders, The University of Oklahoma Health Sciences Center, Okla-
homa City, OK, USA
Severn B. Churn Neurology, Virginia Commonwealth University, Rich-
mond, VA, USA
xlviii Contributors

Angela Hein Ciccia Department of Psychological Sciences, Program in

Communication Sciences, Case Western Reserve University, Cleveland, OH,
USA

Elaine Clark Department of Educational Psychology, The University of

Utah, Salt Lake City, UT, USA

Lee Anna Clark Department of Psychology, University of Notre Dame,

Notre Dame, IN, USA

Robert Clark School Psychology, The Chicago School of Professional Psy-

chology, Chicago, IL, USA

Uraina S. Clark Department of Neurology, Icahn School of Medicine at

Mount Sinai, New York, NY, USA

Dave Clarke Comprehensive Epilepsy Program, Dell Children’s Medical

Center of Central Texas, Austin, TX, USA
Department of Pediatrics, Dell Medical School, The University of Texas at
Austin, Austin, TX, USA

Lauren Clevenger University of Iowa, Iowa City, IA, USA

Derin Cobia Department of Psychology and Neuroscience Center, Brigham

Young University, Provo, UT, USA

Melanie M. Cochrane Department of Psychology, University of Victoria,

Victoria, BC, Canada

Ronald A. Cohen Department of Clinical and Health Psychology, College of

Public Health and Health Professions, University of Florida, Gainesville, FL,
USA
Center for Cognitive Aging and Memory, McKnight Brain Institute, Univer-
sity of Florida, Gainesville, FL, USA

Morris J. Cohen Neurology, Pediatrics and Psychiatry, Pediatric Neuropsy-

chology, Medical College of Georgia and BT-2601 Children’s Medical Center,
Augusta, GA, USA

Raymond J. Colello Anatomy and Neurobiology, Virginia Commonwealth

University, Richmond, VA, USA

G. Combs Legal Psychology (Psychology and Law), Neuropsychology,

Clinical Psychology, Chicago School of Professional Psychology, Chicago,
IL, USA

Brian Comly Magee Rehabilitation Hospital, Philadelphia, PA, USA

Adam Conley Virginia Commonwealth University Medical Center, Rich-

mond, VA, USA

Lori G. Cook Center for BrainHealth, The University of Texas at Dallas,

Dallas, TX, USA
Contributors xlix

Andrea Coppens Division of Neurology and Department of Psychology,

Sick Kids-Centre for Brain and Mental Health, Toronto, ON, Canada
Patrick Coppens Communication Sciences and Disorders, SUNY Platts-
burgh, Plattsburgh, NY, USA
Melinda A. Cornwell Department of Psychology, Queens College and The
Graduate Center of the City University of New York, Flushing, NY, USA
Stephen Correia Department of Psychiatry and Human Behavior, Alpert
Medical School, Brown University, Providence, USA
John D. Corrigan Department of Physical Medicine and Rehabilitation,
Ohio State University, Columbus, OH, USA
Joyce A. Corsica Department of Behavioral Sciences, Rush University
Medical Center, Chicago, IL, USA
H. Branch Coslett Department of Neurology, University of Pennsylvania,
HUP, Philadelphia, PA, USA
Kelly Coulehan Health Psychology, Neuropsychology, Clinical Psychology,
Fordham University, New York, NY, USA
John C. Courtney Socorro Mental Health, Presbyterian Medical Services,
Socorro, NM, USA
David R. Cox Neuropsychology and Rehabilitation Consultants, P.C.,
Chapel Hill, NC, USA
Laura Cramer-Berness Department of Psychology, William Paterson Uni-
versity, Wayne, NJ, USA
Chava Creque Department of Psychology and Neuroscience, University of
Colorado Boulder, Boulder, CO, USA
Savannah Crippen Department of Psychology, William Paterson Univer-
sity, Wayne, NJ, USA
Jessica Cruz School Psychology, The Chicago School of Professional Psy-
chology, Chicago, IL, USA
Yenisel Cruz-Almeida Pain Research and Intervention Center of Excellence
Clinical and Translational Science Institute, University of Florida, Gainesville,
FL, USA
Carter M. Cunningham Fairfax Neonatal Associates, Falls Church, VA,
USA
Jacqueline L. Cunningham Department of Psychology, Children’s Hospital
of Philadelphia, Philadelphia, PA, USA
Sean Cunningham Department of Educational Psychology, University of
Utah, Salt Lake City, UT, USA
Cody Curatolo Department of Psychology, William Paterson University,
Wayne, NJ, USA
l Contributors

Cherina Cyborski National Intrepid Center of Excellence, Walter Reed

National Military Medical Center, Bethesda, MD, USA
Rik Carl D’Amato School Psychology, Clinical Neuropsychology, Clinical
Psychology, The Chicago School of Professional Psychology, Chicago, IL,
USA
Kristen Dams-O’Connor Department of Rehabilitation Medicine, Mount
Sinai School of Medicine, New York, NY, USA
Natalie Dattilo Department of Psychiatry, Indiana University School of
Medicine, Indianapolis, IN, USA
Andrew S. Davis Department of Educational Psychology, Ball State Univer-
sity, Muncie, IN, USA
Marcus Ponce de Leon Madigan Army Medical Center, Tacoma, WA, USA
Ashley de Marchena Department of Psychology, University of Connecticut,
Storrs, CT, USA
Scott L. Decker Department of Psychology, University of South Carolina,
Columbia, SC, USA
Nathalie DeFabrique Cook County Department of Corrections, Chicago,
IL, USA
Nick A. DeFilippis Georgia School of Professional Psychology, Atlanta
Psychological Associates, Atlanta, GA, USA
Kathleen K. M. Deidrick Neuro- and Behavioral Psychology, St. Luke’s
Children’s Hospital, Boise, ID, USA
Lisa Delano-Wood Memory, Aging and Resilience Clinic (MARC), Depart-
ment of Psychiatry, University of California, San Diego, La Jolla, CA, USA
VA San Diego Healthcare System, San Diego, CA, USA
Dean C. Delis School of Medicine, University of California-San Diego, La
Jolla, CA, USA
John DeLuca Research Department, Kessler Foundation, West Orange, NJ,
USA
George J. Demakis Department of Psychology, University of North Carolina
at Charlotte, Charlotte, NC, USA
Theslee Joy DePiero Braintree Rehabilitation Hospital, Boston University
School of Medicine, Boston, MA, USA
Roberta DePompei School of Speech-Language Pathology and Audiology,
University of Akron, Akron, OH, USA
Emily Desbiens Department of Psychology, William Paterson University,
Wayne, NJ, USA
Contributors li

Krista Dettle Department of Psychology, William Paterson University,

Wayne, NJ, USA
Bruce J. Diamond Department of Psychology, William Paterson University,
Wayne, NJ, USA
Aimee Dietz Communication Sciences and Disorders, University of Cincin-
nati, Cincinnati, OH, USA
María Díez-Cirarda Department of Methods and Experimental Psychology,
Faculty of Psychology and Education, University of Deusto, Bilbao, Spain
Marcel P. J. M. Dijkers American Congress of Rehabilitation Medicine,
Reston, VA, USA
Department of Rehabilitation Medicine, Icahn School of Medicine at Mount
Sinai, New York, NY, USA
Ekaterina Dobryakova Traumatic Brain Injury Research, Kessler Founda-
tion, West Orange, NJ, USA
Carl B. Dodrill Department of Neurology, University of Washington School
of Medicine, Seattle, WA, USA
Ben Dodsworth PM&R, University of South Florida, Tampa, FL, USA
Peter Dodzik Fort Wayne Neurological Center, Fort Wayne, IN, USA
Christopher H. Domen School of Medicine, Department of Neurosurgery,
University of Colorado, Aurora, CO, USA
Jacobus Donders Mary Free Bed Rehabilitation Hospital, Grand Rapids,
MI, USA
Kerry Donnelly VA WNY Healthcare System, University of Buffalo
(SUNY) Behavioral Health Careline (116B), Buffalo, NY, USA
Jennifer M. Doran VA Connecticut Healthcare System, Yale School of
Medicine, Newington, CT, USA
Vonetta Dotson Department of Psychology, Georgia State University,
Atlanta, GA, USA
Department of Clinical and Health Psychology College of Public Health and
Health Professions, University of Florida, Gainesville, FL, USA
Lauren R. Dowell Laboratory for Neurocognitive and Imaging Research,
Kennedy Krieger Institute, Baltimore, MD, USA
Leah Drasher-Phillips Center of Innovation on Disability and Rehabilitation
Research, James A. Haley Veterans’ Hospital, Tampa, FL, USA
Elena Harlan Drewel Neuro- and Behavioral Psychology, St. Luke’s Chil-
dren’s Hospital, Boise, ID, USA
lii Contributors

Tina Drossos Departments of Psychiatry and Behavioral Neuroscience, and

Pediatrics, Section of Child and Adolescent Psychiatry, The University of
Chicago, Chicago, IL, USA
Lindsey Duca Department of Orthopedics and Rehabilitation, University of
Wisconsin School of Medicine and Public Health, Madison, WI, USA
Nicole M. Dudukovic Department of Psychology, University of Oregon,
Eugene, OR, USA
Mary Dunkle National Organization for Rare Disorders (NORD), Danbury,
CT, USA
Kari Dunning Department of Rehabilitation Sciences, University of Cincin-
nati, Cincinnati, OH, USA
Jeff Dupree Anatomy and Neurobiology, Virginia Commonwealth Univer-
sity, Richmond, VA, USA
Ana Durand Sanchez Physical Medicine and Rehabilitation, Baylor College
of Medicine, Houston, TX, USA
Moira C. Dux US Department of Veteran Affairs, Baltimore, MD, USA
Blessen C. Eapen Polytrauma Rehabilitation Center, South Texas Veterans
Health Care System, San Antonio, TX, USA
Department of Rehabilitation Medicine, UT Health San Antonio, San Antonio,
TX, USA
Angela Eastvold Department of Neurology, The University of Utah,
Salt Lake City, UT, USA
Natalie C. Ebner Department of Psychology, University of Florida, Gaines-
ville, FL, USA
Department of Aging and Geriatric Research, Institute on Aging, University of
Florida, Gainesville, FL, USA
Lisa Edmonds Communication Sciences and Disorders, Teachers College
Columbia University, New York, NY, USA
Dawn M. Ehde Department of Rehabilitation Medicine, University of Wash-
ington, Seattle, WA, USA
Alyssa Eidson Emory University/Rehabilitation Medicine, Atlanta, GA,
USA
Donovan Ellis Department of Psychology, University of Florida, Gaines-
ville, FL, USA
Erin E. Emery-Tiburcio Department of Behavioral Sciences, Rush Univer-
sity Medical Center, Chicago, IL, USA
Joel Eppig Joint Doctoral Program in Clinical Psychology, University of
California, San Diego State University, San Diego, CA, USA
Contributors liii

Jacqueline Estrada School of Psychology, The Chicago School of Profes-

sional Psychology, Chicago, IL, USA
Eleazar Eusebio School Psychology, The Chicago School of Professional
Psychology, Chicago, IL, USA
Allison S. Evans Concord Comprehensive Neuropsychological Services,
Concord, MA, USA
Daniel Erik Everhart Department of Psychology, Eastern Carolina Univer-
sity, Greenville, NC, USA
Nathan Ewigman Mental Health Service Line, San Francisco VA Health
Care System, San Francisco, CA, USA
Joseph E. Fair Brigham Young University, Provo, UT, USA
Jacob Faltin School Psychology, The Chicago School of Professional Psy-
chology, Chicago, IL, USA
Jaelyn R. Farris Department of Psychology, Youngstown State University,
Youngstown, OH, USA
Khan Fary Department of Medicine, University of Melbourne and the Royal
Melbourne Hospital, Parkville, VA, Australia
Deborah Fein Department of Psychological Sciences, University of Con-
necticut, Storrs, CT, USA
Leilani Feliciano Department of Psychology, University of Colorado at
Colorado Springs, Colorado Springs, CO, USA
Aaron Feliu James A Haley Veterans Hospital, Tampa, FL, USA
Warren L. Felton Department of Neurology, Virginia Commonwealth Uni-
versity Medical Center, Richmond, VA, USA
Kyle E. Ferguson University of British Columbia, Vancouver, BC, Canada
Robert Fieo Department of Aging and Geriatric Research, College of Med-
icine, Institute on Aging, University of Florida, Gainesville, FL, USA
Christina Figueroa Memory and Aging Program, Butler Hospital, Provi-
dence, RI, USA
Carole M. Filangieri Department of Behavioral Health, NYU Winthrop
Hospital, Mineola, NY, USA
Eric M. Fine Department of Neurology, University of California, San
Francisco, CA, USA
Jessica Fish Medical Research Council Cognition and Brain Sciences Unit,
Cambridge, UK
Julie Testa Flaada Rochester, MN, USA
Jennifer Fleming School of Health and Rehabilitation Sciences, The Uni-
versity of Queensland, Brisbane, QLD, Australia
liv Contributors

Kimberly Fleming Department of Psychiatry and Behavioral Sciences, The

University of Kansas KU Medical Center, Kansas City, KS, USA
James R. Flynn Department of Politics, The University of Otago, Dunedin,
New Zealand
Kristin Joan Flynn Peters Department of Health Sciences, University of
Missouri, Columbia, MO, USA
Nancy S. Foldi Department of Psychology, Queens College and The Grad-
uate Center, The City University of New York, New York, NY, USA
Department of Medicine, Winthrop University Hospital, Stony Brook School
of Medicine, Mineola, NY, USA
Samantha Foreman Immaculata University, Immaculata, PA, USA
Hélène Forget Département de psychoéducation et de psychologie,
Université du Québec en Outaouais, Gatineau, QC, Canada
Bonny J. Forrest Independent Practice, San Diego, CA, USA
Lisa M. Fox NYU Langone Medical Center, Department of Psychology,
Rusk Institute of Rehabilitation Medicine, New York, NY, USA
Michael A. Fox Anatomy and Neurobiology, Virginia Commonwealth Uni-
versity Medical Center, Richmond, VA, USA
Laura L. Frakey Memorial Hospital of Rhode Island and Alpert Medical
School of Brown University, Pawtucket, RI, USA
Robert G. Frank University of New Mexico, Albuquerque, NM, USA
Michael Franzen Allegheny General Hospital, Pittsburgh, PA, USA
Stacy Frauwirth Academic Therapy Publications, Novato, CA, USA
Ian Frazier Department of Psychology, University of Florida, Gainesville,
FL, USA
Kathleen L. Fuchs Department of Neurology, University of Virginia Health
System, Charlottesville, VA, USA
Shawn Gale Department of Psychology and Neuroscience Center, Brigham
Young University, Provo, UT, USA
Kristin Galetta Department of Neurology, Brigham and Women’s Hospital,
Boston, MA, USA
Steven Galetta Department of Neurology, New York University of Medi-
cine, New York, NY, USA
Sherri Gallagher Wellness PSI, LLC Private Practice, Flagstaff, AZ, USA
Frank J. Gallo Department of Psychology, University of Wisconsin-
Milwaukee, Milwaukee, WI, USA
Contributors lv

Emnet Gammada Department of Psychology, Queens College and The

Graduate Center, The City University of New York, New York, NY, USA
Sarah Garcia Department of Psychiatry- Neuropsychology, University of
Michigan Health System, Ann Arbor, MI, USA
Pamela Garn-Nunn Department of Pharmacology, Virginia Commonwealth
University, Richmond, VA, USA
Kelly Davis Garrett Intermountain Healthcare and University of Utah Cen-
ter on Aging, Salt Lake City, UT, USA
Kelli Williams Gary Department of Occupational Therapy, Virginia Com-
monwealth University, Richmond, VA, USA
Brandon E. Gavett Department of Psychology, University of Colorado
Colorado Springs, Colorado Springs, CO, USA
Helen M. Genova Neuropsychology and Neuroscience Laboratory, Kessler
Foundation Research Center, West Orange, NJ, USA
Savannah J. Geske Department of Psychiatry and Behavioral Sciences,
University of Kansas Medical Center, Kansas City, KS, USA
Glen E. Getz Department of Psychiatry, Allegheny General Hospital, Pitts-
burgh, PA, USA
Neuropsychology Specialty Care, LLC, Pittsburgh, PA, USA
Christine Ghilain Department of Neuropsychology, Children’s Healthcare
of Atlanta, Atlanta, Georgia, USA
Gerard A. Gioia Children’s National Medical Center, Rockville, MD, USA
Elizabeth Louise Glisky Department of Psychology, University of Arizona,
Tucson, AZ, USA
Emilie Godwin Virginia Commonwealth University, Richmond, VA, USA
Gary Goldberg Hunter Holmes McGuire Veterans Administration Medical
Center, Department of Physical Medicine and Rehabilitation, Virginia Com-
monwealth University School of Medicine/Medical College of Virginia, Rich-
mond, VA, USA
Myron Goldberg Department of Rehabilitation Medicine, University of
Washington Medical Center, Seattle, WA, USA
Diane Cordry Golden Association of Assistive Technology Act Programs,
Delmar, NY, USA
Charles J. Golden Center for Psychological Studies, Nova Southeastern
University, Fort Lauderdale, FL, USA
Amy S. Goldman Association of Assistive Technology Act Programs
(ATAP), Springfield, IL, USA
lvi Contributors

Bram Goldstein Department of Gynecologic Oncology, Hoag Hospital Can-

cer Center, Newport Beach, CA, USA
Assawin Gongvatana Department of Psychiatry, University of California,
San Diego, San Diego, CA, USA
Efrain Antonio Gonzalez College of Psychology, Nova Southeastern Uni-
versity, Fort Lauderdale, FL, USA
Utah State University, Logan, UT, USA
Matthew E. Goodwin Central Arkansas Veterans Healthcare System, Little
Rock, AR, USA
Robert M. Gordon Rusk Rehabilitation, New York University Langone
Medical Center, New York, NY, USA
Kimberly A. Gorgens Graduate School of Professional Psychology, Univer-
sity of Denver, Denver, CO, USA
Janet Grace Psychiatry and Human Behavior, Alpert Medical School of
Brown University, Providence, RI, USA
Martin R. Graf Department of Neurosurgery, Virginia Commonwealth Uni-
versity Medical Center, Richmond, VA, USA
Lori Grafton Carolinas Rehabilitation Carolinas HealthCare System, Char-
lotte, NC, USA
Kristin M. Graham Department of Physical Medicine and Rehabilitation,
Virginia Commonwealth University, Richmond, VA, USA
Michael R. Greher School of Medicine, Department of Neurosurgery, Uni-
versity of Colorado, Aurora, CO, USA
Sarah Griffin Virginia Commonwealth University, Richmond, VA, USA
Julie Griffith Department of Speech Pathology and Audiology, Ball State
University, Muncie, IN, USA
Stephanie Griffiths Simon Fraser University, Burnaby, BC, Canada
Elizabeth S. Gromisch Psychology Service, VA Connecticut, West Haven,
CT, USA
Benjamin Grover-Manthey Department of Physical Medicine and Rehabil-
itation, Indiana University, Indianapolis, IN, USA
William Guido Anatomy and Neurobiology, Virginia Commonwealth Uni-
versity Medical Center, Richmond, VA, USA
Desiree Gulliford Department of Psychology, University of Florida, Gaines-
ville, FL, USA
Carly Gundrum Legal Psychology (Psychology and Law), Neuropsychol-
ogy, Clinical Psychology, The Chicago School of Professional Psychology,
Chicago, IL, USA
Contributors lvii

Audrey H. Gutherie Rehabilitation Research and Development Center of

Excellence Atlanta Veterans Administration Medical Center, Decatur, GA,
USA
Karl Haberlandt Department of Psychology, Trinity College, Hartford, CT,
USA
Martin Hahn Department of Biology, William Paterson University, Wayne,
NJ, USA
Kathrine Hak Applied Psychology and Counselor Education, University of
Northern Colorado, Greeley, CO, USA
Katherine Hallahan University of Cincinnati, Cincinnati, OH, USA
John Halperin Overlook Medical Center, Atlantic Health System, Summit,
NJ, USA
Marla J. Hamberger Department of Neurology, Columbia University Med-
ical Center, New York, NY, USA
Flora M. Hammond Department of Physical Medicine and Rehabilitation,
Indiana University School of Medicine, Indianapolis, IN, USA
Benjamin Hampstead Department of Pharmacology, Virginia Common-
wealth University, Richmond, VA, USA
Department of Psychiatry, University of Michigan, Michigan Alzheimer’s
Disease Center, Ann Arbor, MI, USA
Sarah Hannigen Department of Psychology, Allegheny Health Network,
Pittsburgh, PA, USA
Stephanie L. Hanson College of Public Health and Health Professions,
University of Florida, Gainesville, FL, USA
Keith Happawana Department of Psychology, William Paterson University,
Wayne, NJ, USA
Janna L. Harris Department of Anatomy and Cell Biology, University of
Kansas Medical Center, Kansas City, KS, USA
Hoglund Brain Imaging Center, University of Kansas Medical Center, Kansas
City, KS, USA
Patti L. Harrison School Psychology, The University of Alabama, Tusca-
loosa, AL, USA
Eric S. Hart University of Missouri Center for Health Care Quality, Colum-
bia, MO, USA
Michael J. Hartman Department of Psychology, University of Wisconsin-
Milwaukee, Milwaukee, WI, USA
Kari Hawkins Neuropsychology Department, Addenbrooke’s Hospital,
Cambridge, UK
Amy Heffelfinger Medical College of Wisconsin, Milwaukee, WI, USA
lviii Contributors

Robert L. Heilbronner Chicago Neuropsychology Group, Chicago, IL, USA

Kenneth M. Heilman Department of Neurology, University of Florida Col-
lege of Medicine, Center for Neurological Studies and the Research Service of
the Malcom Randall Veterans Affairs Medical Center, Gainesville, FL, USA
Nancy Helm-Estabrooks Department of Communication Disorders and Sci-
ences, College of Health and Human Sciences, Western Carolina University,
Cullowhee, NC, USA
Nathan Henninger Department of Pediatrics, Nationwide Children’s Hospi-
tal College of Medicine, Ohio State University, Columbus, OH, USA
Mary Hibbard Department of Rehabilitation Medicine, New York School of
Medicine, New York, NY, USA
Ashley K. Hill Nationally Certified School Psychologist, Chicago, IL, USA
Tanisha G. Hill-Jarrett Division of Rehabilitation Neuropsychology,
Department of Rehabilitation Medicine, Emory University, Atlanta, GA, USA
Yvonne Hindes Division of Applied Psychology, Faculty of Education,
University of Calgary, Calgary, AB, Canada
Merrill Hiscock Department of Psychology, University of Houston, Hous-
ton, TX, USA
G. Alex Hishaw Neurology Section, Southern Arizona VA Healthcare Sys-
tem, Tucson, AZ, USA
Department of Neurology, University of Arizona, Tucson, AZ, USA
Elise K. Hodges Department of Psychiatry, Neuropsychology Division, Uni-
versity of Michigan Health System, Ann Arbor, MI, USA
Anna DePold Hohler Boston University Medical Center, Boston, MA, USA
Matthew H. Holcomb Department of Pharmacology, Virginia Common-
wealth University, Richmond, VA, USA
Tracey Hollingsworth Developmental Assessment Program, Nationwide
Children’s Hospital, Columbus, OH, USA
Stephanie Hooker Department of Behavioral Sciences, Rush University
Medical Center, Chicago, IL, USA
Kelly L. Hoover Department of Educational Psychology, Ball State Univer-
sity, Muncie, IN, USA
Crista A. Hopp Connected Pathways Coaching, Herndon, VA, USA
Karin F. Hoth Department of Medicine, University of Iowa, Iowa City, IA,
USA
Gillian Hotz Department of Neurosurgery/The Miami Project to Cure Paral-
ysis, University of Miami Miller School of Medicine, Miami, FL, USA
Contributors lix

Marianne Hrabok Department of Psychology, Addiction and Mental

Health, Alberta Health Services, Edmonton, AB, Canada
Gabrielle Hromas Department of Clinical and Health Psychology, Univer-
sity of Florida, Gainesville, FL, USA
Leesa V. Huang Department of Psychology, California State University,
Chico, CA, USA
Dawn H. Huber Department of Health Psychology, University of Missouri,
Columbia, MO, USA
Adam Hudepohl Georgia State University, Atlanta, GA, USA
Trevor Huff Department of Psychology and Neuroscience Center, Brigham
Young University, Provo, UT, USA
Bradley J. Hufford Neuropsychology, Rehabilitation Hospital of Indiana,
Indianapolis, IN, USA
Candace Hughes School of Psychology, The Chicago School of Profes-
sional Psychology, Chicago, IL, USA
Joel W. Hughes Department of Psychology, Kent State University, Kent,
OH, USA
David Hulac Department of School Psychology, College of Education and
Behavioral Sciences, University of Northern Colorado, Greeley, CO, USA
Faiza Humayun Inpatient Traumatic Brain Injury Unit, James Haley VA
Hospital, Tampa, FL, USA
Edward E. Hunter Department of Psychiatry and Behavioral Sciences,
University of Kansas Medical Center, Kansas City, KS, USA
Scott J. Hunter Departments of Psychiatry and Behavioral Neuroscience,
and Pediatrics, Pediatric Neuropsychology, Section of Child and Adolescent
Psychiatry, The University of Chicago, Chicago, IL, USA
Julia Hussey Department of Psychology, University of Nevada, Las Vegas,
Las Vegas, NV, USA
R. Matthew Hutchison Biogen Inc., Cambridge, MA, USA
Karen Hux Quality Living, Omaha, NE, USA
Summer Ibarra Rehabilitation Hospital of Indiana, Indianapolis, IN, USA
Naroa Ibarretxe-Bilbao Department of Methods and Experimental Psychol-
ogy, Faculty of Psychology and Education, University of Deusto, Bilbao,
Spain
Jean Ikanga Division of Rehabilitation Neuropsychology, Department of
Rehabilitation Medicine, Emory University, Atlanta, GA, USA
Matilde Inglese Department of Neurology, Radiology and Neuroscience,
Icahn School of Medicine at Mount Sinai, New York, NY, USA
lx Contributors

Farzin Irani Psychology Department, West Chester University of Pennsyl-

vania, West Chester, PA, USA
Rubyat Islam Department of Psychology, Queens College of the City Uni-
versity of New York, Flushing, NY, USA
Peter K. Isquith Dartmouth Medical School, Lebanon, NH, USA
Cindy B. Ivanhoe Neurorehabilitation Specialists Baylor College of Medi-
cine, The Institute for Rehabilitation and Research, Houston, TX, USA
Grant L. Iverson Department of Psychiatry, British Columbia Mental Health
and Addictions, University of British Columbia, Vancouver, BC, Canada
Colleen E. Jackson VA Boston Healthcare System, Boston, MA, USA
Kimberle M. Jacobs Department of Anatomy and Neurobiology, Virginia
Commonwealth University, Richmond, VA, USA
Mathew Jacobs Pennsylvania State University, University Park, PA, USA
Lisa A. Jacobson Department of Neuropsychology, Kennedy Krieger Insti-
tute, Baltimore, MD, USA
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University
School of Medicine, Baltimore, MD, USA
Kelly M. Janke Columbia University Medical Center, New York, NY, USA
Nicholas Jasinski Division of Neuropsychology, Henry Ford Health System,
Detroit, MI, USA
Beth A. Jerskey Department of Psychiatry and Human Behavior, Alpert
Medical School of Brown University, Providence, RI, USA
Amitabh Jha TBIMS National Data and Statistical Center, Craig Hospital,
Englewood, CO, USA
Mi-Yeoung Jo Sherman Oaks, CA, USA
Joshua Johnson Department of Psychiatry (MC-2103), UConn Health Cen-
ter, Farmington, CT, USA
Judy A. Johnson Special Education Department, Aldine Independent
School District, Houston, TX, USA
Julene K. Johnson Center for Aging in Diverse Communities, University of
California, San Francisco, San Francisco, CA, USA
Kristin L. Johnson Applied Psychology and Counselor Education, Univer-
sity of Northern Colorado, Greeley, CO, USA
Nancy Johnson Cognitive/Behavioral Neurology Center Northwestern
Feinburg School of Medicine, Chicago, IL, USA
Susan K. Johnson Department of Psychology, University of North Carolina
at Charlotte, Charlotte, NC, USA
Contributors lxi

Taylor Johnson School of Psychology, The Chicago School of Professional

Psychology, Chicago, IL, USA
Brick Johnstone Intrepid Spirit Center, Fort Belvoir, VA, USA
Robert D. Jones Department of Neurology, The University of Iowa, Iowa
City, USA
Aaron N. Juni Neuropsychology Center of Maryland, LLC, Owings Mills,
MD, USA
Solomon Kalkstein Psychiatry, University of Pennsylvania, Philadelphia,
PA, USA
Randy W. Kamphaus College of Education, The University of Oregon,
Eugene, OR, USA
Stephen M. Kanne Thompson Center for Autism and Neurodevelopmental
Disorders, University of Missouri, Columbia, MO, USA
Edith Kaplan Department of Psychology, Suffolk University, Boston, MA,
USA
Erica Kaplan Rehabilitation Medicine, Brain Injury Research Center, Icahn
School of Medicine at Mount Sinai, New York, NY, USA
Paul E. Kaplan Capitol Clinical Neuroscience, Folsom, CA, USA
Richard F. Kaplan Department of Psychiatry (MC-2103), UConn Health
Center, Farmington, CT, USA
Narinder Kapur Research Department of Clinical, Educational and Health
Psychology, University College London, London, UK
Ninad Karandikar RAC, Department of PM&R AND Physiatrist, Poly-
trauma Transitional Rehabilitation Program, VA Palo Alto, Palo Alto,
California, USA
Department of Orthoedics, Stanford University, Palo Alto, California, USA
Stella Karantzoulis Modern Brain Center, New York, NY, USA
Nadine J. Kaslow Department of Psychiatry and Behavioral Sciences,
Emory University School of Medicine, APA, Atlanta, GA, USA
Sheryl Katta-Charles Department of Physical Medicine and Rehabilitation,
Indiana University School of Medicine, Indianapolis, IN, USA
Douglas I. Katz Department of Neurology, Boston University School of
Medicine, Braintree, MA, USA
Michael Kaufman Department of Neurology, Carolinas Medical Center,
Charlotte, NC, USA

Edith Kaplan: deceased.

lxii Contributors

Margarita Kaushanskaya University of Wisconsin-Madison, Madison, WI,

USA
Jacqueline M. Kawa Psychiatry and Behavioral Medicine, Children’s Hos-
pital of Wisconsin, Milwaukee, WI, USA
Jaeson Kaylegian Departments of Psychiatry and Behavioral Neuroscience,
and Pediatrics, Pediatric Neuropsychology, Section of Child and Adolescent
Psychiatry, The University of Chicago, Chicago, IL, USA
Neuropsychology Technician III, University of Chicago Medicine, Chicago,
IL, USA
Jacob Kean Department of Physical Medicine and Rehabilitation, Indiana
University School of Medicine, Indianapolis, IN, USA
C. Keith Conners Duke University Medical School, Durham, NC, USA
Avril J. Keller Alberta Children’s Hospital, University of Calgary, Calgary,
AB, Canada
Kristy K. Kelly Educational Psychology, University of Wisconsin-Madison,
Madison, WI, USA
Sally L. Kemp University of Missouri, Columbia, MO, USA
Thomas R. Kerkhoff College of Public Health and Health Professions,
University of Florida, Gainesville, FL, USA
Kimberly A. Kerns Department of Psychology, University of Victoria, Vic-
toria, BC, Canada
So Hyun Kim Yale Child Study Center, Yale School of Medicine, New
Haven, CT, USA
Sangsun Kim Psychological Sciences, University of Missouri, Columbia,
MO, USA
Sun Mi Kim Department of Psychology, Queens College of the City Uni-
versity of New York, Flushing, NY, USA
Tricia Z. King Department of Psychology and the Neuroscience Institute,
Georgia State University, Atlanta, GA, USA
Brock Kirwan Psychology Department and the Neuroscience Center,
Brigham Young University, Provo, UT, USA
Bonita P. “Bonnie” Klein-Tasman Department of Psychology, University
of Wisconsin-Milwaukee, Milwaukee, WI, USA
Jennifer Sue Kleiner Department of Psychology, University of Arkansas for
Medical Sciences Blandford Physician Center, Little Rock, AR, USA
Daniel W. Klyce Virginia Commonwealth University – School of Medicine,
Richmond, VA, USA

C. Keith Conners: deceased.

Contributors lxiii

Samantha Knight Medicine, Royal College of Surgeons in Ireland, Dublin,

Ireland
Kelly Knollman-Porter Department of Speech Pathology and Audiology,
Miami University, Oxford, OH, USA
Tiffany Kodak Department of Psychology, University of Wisconsin-Mil-
waukee, Milwaukee, WI, USA
Julia Kolak Department of Psychology, William Paterson University,
Wayne, NJ, USA
Stephanie A. Kolakowsky-Hayner Department of Rehabilitation Medicine,
Icahn School of Medicine at Mount Sinai, New York, NY, USA
Dan Koonce The Chicago School of Psychology, Chicago, IL, USA
Paul T. Korte Harry S. Truman Memorial Veterans’ Hospital, Columbia,
MO, USA
Kathleen A. Koth Department of Psychiatry and Behavioral Medicine,
Medical College of Wisconsin, Milwaukee, WI, USA
Zhifeng Kou Biomedical Engineering and Radiology, Wayne State Univer-
sity, Detroit, MI, USA
Rothem Kovner Department of Psychiatry, University of Wisconsin-Madi-
son, Madison, WI, USA
Elizabeth Kozora Department of Medicine, National Jewish Medical and
Research Center, National Jewish Health, Denver, CO, USA
Joel H. Kramer UCSF Memory and Aging Center UCSF Med Ctr, 0984-
8AC, San Francisco, CA, USA
Matthew Kraybill Neuropsychology, Cottage Rehabilitation Hospital, Santa
Barbara, CA, USA
Denise Krch Kessler Foundation, East Hanover, NJ, USA
Kate Krival Speech Pathology, School of Health Sciences, Edinboro Uni-
versity of Pennsylvania, Edinboro, PA, USA
Lauren B. Krupp Department of Neuropsychology Research, Stony Brook
University SUNY Stony Brook, Stony Brook, NY, USA
Nuri Erkut Kucukboyaci Clinical Psychology, Rusk Institute – NYU
Langone Health, New York, NY, USA
Beth Kuczynski Imaging of Dementia and Aging (IDeA) Laboratory,
Department of Neurology and Center for Neuroscience, University of Cali-
fornia, Davis, CA, USA
Jeffrey G. Kuentzel Wayne State University, Detroit, MI, USA
Richard Kunz Department of Physical Medicine and Rehabilitation, Vir-
ginia Commonwealth University, Richmond, VA, USA
lxiv Contributors

Brad Kurowski Department of Physical Medicine and Rehabilitation,

Spaulding Rehabilitation Hospital, Massachusetts General Hospital, Brigham
and Women’s Hospital, Harvard Medical School, Cincinnati, OH, USA
Matthew M. Kurtz Department of Psychology, Wesleyan University, Mid-
dletown, CT, USA
Monica Kurylo Departments of Psychiatry and Rehabilitation Medicine,
University of Kansas Medical Center, Kansas City, KS, USA
Christina Kwasnica Barrow Neurological Institute, Phoenix, AZ, USA
David Lachar University of Texas Houston Health Science Center, Houston,
TX, USA
Susan Ladley Department of Physical Medicine and Rehabilitation, Univer-
sity of Colorado, Denver Health Medical Center, Denver, CO, USA
Ginette Lafleche Memory Disorders Research Center, VA Boston
Healthcare System and Boston University School of Medicine, Boston, MA,
USA
Audrey Lafrenaye Department of Anatomy and Neurobiology, Virginia
Commonwealth University, Richmond, VA, USA
Sarah K. Lageman Parkinson’s and Movement Disorders Center, Depart-
ment of Neurology, School Of Medicine, Virginia Commonwealth University,
Richmond, VA, USA
Melissa Lamar Rush Alzheimer’s Disease Center, Chicago, IL, USA
Damon G. Lamb Department of Clinical and Health Psychology, University
of Florida, Gainesville, FL, USA
Center for Cognitive Aging and Memory, McKnight Brain Institute, Univer-
sity of Florida, Gainesville, FL, USA
Department of Neurology, University of Florida, Gainesville, FL, USA
Brain Rehabilitation Research Center, Malcom Randall VAMC, Gainesville,
FL, USA
Gudrun Lange Pain and Fatigue Study Center, New York, NY, USA
Mount Sinai Beth Israel Medical Center, New York, NY, USA
Rael T. Lange Defense and Veterans Brain Injury Center, Walter Reed
National Military Medical Center, Bethesda, MD, USA
Karen G. Langer Department of Rehabilitation Medicine, Rusk Rehabilita-
tion, NYU Langone Medical Center, New York, NY, USA
Kayla LaRosa Educational and Psychological Studies/TBI Model Systems,
University of South Florida/J.A. Haley VA, Tampa, FL, USA
Michael J. Larson Brigham Young University, Provo, UT, USA
Jennifer C. G. Larson Department of Physical Medicine and Rehabilitation,
University of Michigan, Ann Arbor, MI, USA
Contributors lxv

Adele A. Larsson Department of Educational Psychology, Ball State Uni-

versity, Muncie, IN, USA
Javier Peña Lasa Department of Psychology, Deusto University, Bilbao,
Spain
Thomas M. Laudate Department of Adult Neurology, Tufts Medical Center,
Boston, MA, USA
Ronald M. Lazar Department of Neurology, University of Alabama at
Birmingham, Birmingham, AL, USA
Victoria M. Leavitt Cognitive Neuroscience Division, Columbia University
Medical School, New York, NY, USA
Sophie Lebrecht Visual Neuroscience Laboratory, Brown University, Prov-
idence, RI, USA
Kangmin D. Lee Department of Neurosurgery, Virginia Commonwealth
University, Richmond, VA, USA
Sing Lee Department of Psychiatry, The Chinese University of Hong Kong,
Shatin, Hong Kong SAR, China
Stacie A. Leffard Behavioral Medicine and Psychiatry, West Virginia Uni-
versity, Morgantown, WV, USA
George Leichnetz Virginia Commonwealth University, Richmond, VA, USA
Hoyle Leigh Department of Psychiatry, University of California, San
Francisco, CA, USA
Sarah J. Leinen Institute for Graduate Clinical Psychology, Widener Uni-
versity, Chester, PA, USA
Jeannie Lengenfelder Kessler Foundation Research Center, West Orange,
NJ, USA
José León-Carrión Human Neuropsychology Laboratory, School of Psy-
chology, Department of Experimental Psychology, University of Seville,
Seville, Spain
Center for Brain Injury Rehabilitation (CRECER), Seville, Spain
Umberto León-Domínguez Health Sciences Vice-Chancellor, Department
of Psychology, University of Monterrey, Monterrey, Mexico
Human Neuropsychology Laboratory, School of Psychology, Department of
Experimental Psychology, University of Seville, Seville, Spain
Pierre A. Leon Department of Psychology, William Paterson University,
Wayne, NJ, USA
Vanesa C. Lerma Department of Neurological Surgery, Weill Cornell Med-
icine, New York, NY, USA
Holly Levin-Aspenson Department of Psychology, University of Notre
Dame, Notre Dame, IN, USA
lxvi Contributors

Brian Levine Rotman Research Institute at Baycrest, Toronto, ON, Canada

Allen N. Lewis Jr. School of Health and Rehabilitation Science, University
of Pittsburgh, Pittsburgh, PA, USA
Pamela H. Lewis Department of Rehabilitation Counseling, School of Allied
Health Professions, Virginia Commonwealth University, Richmond, VA, USA
David J. Libon Departments of Geriatrics, Gerontology, and Psychology,
Rowan University, New Jersey Institute for Successful Aging, School of
Osteopathic Medicine, Stratford, NJ, USA
Edward Liebmann Department of Psychology, The University of Kansas,
Lawrence, KS, USA
Tanya P. Lin Neurology Section, Southern Arizona VA Healthcare System,
Tucson, AZ, USA
Department of Neurology, University of Arizona, Tucson, AZ, USA
Sara M. Lippa Defense and Veterans Brain Injury Center, Walter Reed
National Military Medical Center, Bethesda, MD, USA
Hayley Loblein Department of Educational Psychology, The University of
Texas at Austin, Austin, TX, USA
Dona Locke Psychiatry and Psychology, Mayo Clinic, Scottsdale, AZ, USA
Chris Loftis National Council for Community Behavioral Healthcare, Alex-
andria, VA, USA
Kenneth J. Logan Department of Speech, Language, and Hearing Sciences,
University of Florida, Gainesville, FL, USA
Michelle Loman Department of Neurology, Medical College of Wisconsin,
Milwaukee, WI, USA
Eduardo Lopez Rehabilitation Medicine, New York Medical College, Met-
ropolitan Hospital, New York, NY, USA
Catherine Lord Center for Autism and the Developing Brain, New York-
Presbyterian Hospital/Westchester Division, White Plains, NY, USA
Janis Lorman School of Speech–Language Pathology and Audiology, The
University of Akron, Akron, OH, USA
Rachel Losoff School Psychology, The Chicago School of Professional
Psychology, Chicago, IL, USA
John A. Lucas Department of Psychiatry and Psychology, Mayo Clinic,
Jacksonville, FL, USA
Stephen D. Luke National Dissemination Center for Children with Disabil-
ities (NICHCY), Washington, DC, USA
Jacob T. Lutz Department of Special Education, Ball State University,
Muncie, IN, USA
Contributors lxvii

Jon G. Lyon Mazomanie, WI, USA

Paige Lysne Department of Aging and Geriatric Research, Institute of Aging,
University of Florida – College of Medicine, Gainesville, FL, USA
Kelly Teresa Macdonald Department of Psychology, University of Houston,
Houston, TX, USA
Anna MacKay-Brandt Nathan S. Kline Institute for Psychiatric Research,
Orangeburg, NY, USA
Taub Institute for Research on Alzheimer’s Disease and the Aging Brain,
Columbia University, New York, NY, USA
Stephanie Magou Department of Psychology, William Paterson University,
Wayne, NJ, USA
E. Mark Mahone Department of Neuropsychology, Kennedy Krieger Insti-
tute, Baltimore, MD, USA
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University
School of Medicine, Baltimore, MD, USA
B. Makofske Legal Psychology (Psychology and Law), Neuropsychology,
Clinical Psychology, Chicago School of Professional Psychology, Chicago,
IL, USA
James F. Malec Department of Physical Medicine and Rehabilitation, Indi-
ana University School of Medicine and the Rehabilitation Hospital of Indiana,
Indianapolis, IN, USA
Amit X. Malhotra Department of Pediatric Specialty, Division of Neurol-
ogy, TPMG, Kaiser Permanente East Bay Medical Center, Oakland, CA, USA
Paul Malloy Department of Psychiatry and Human Behavior, Brown Uni-
versity, Providence, RI, USA
William Victor Maloy The Virginia Institute of Pastoral Care, Richmond,
VA, USA
Gail Malvestuto School of Psychology, The Chicago School of Professional
Psychology, Chicago, IL, USA
Carlye B. G. Manna Department of Psychology, Queens College of the City
University of New York (CUNY), Flushing, NY, USA
Bernice A. Marcopulos Department of Graduate Psychology, James Madi-
son University, Harrisonburg, VA, USA
Christina R. Marmarou Neurosurgery, Virginia Commonwealth Univer-
sity, Richmond, VA, USA
Patrick Marsh Department of Psychiatry and Behavioral Sciences, Univer-
sity of South Florida College of Medicine, Tampa, FL, USA
Matthew P. Martens University of Missouri, Columbia, MO, USA
lxviii Contributors

Thomas Martin Center for Health Care Quality, University of Missouri—

Columbia, Columbia, MO, USA
Jairo Enrique Martinez Columbia University, New York, NY, USA
Guido Mascialino Department of Rehab Medicine Brain Injury Research,
Mount Sinai School of Medicine, New York, NY, USA
Joshua M. Matyi Department of Psychology, Utah State University, Logan,
UT, USA
Micah O. Mazurek Curry School of Education, University of Virginia,
Charlottesville, VA, USA
Michèle M. M. Mazzocco Institute of Child Development, University of
Minnesota, Minneapolis, MN, USA
David L. McCabe Department of Psychology, Rusk Rehabilitation, NYU
Langone Medical Center, New York, NY, USA
Marissa McCarthy Department of Neurology, James A Haley Veterans
Hospital, University of South Florida, Tampa, FL, USA
Rebecca McCartney Department of Behavioral Health, Kaiser Permenante,
Atlanta, GA, USA
Rehabilitation Medicine, Emory University, Atlanta, GA, USA
Katherine S. McClellan Rehabilitation Research and Development Center,
Atlanta Veterans Affairs Medical Center, Decatur, GA, USA
Dalene McCloskey Centennial Board of Cooperative Educational Services,
Greeley, CO, USA
Erica McConnell Jefferson County Public Schools, School Psychologist,
Golden, CO, USA
Michael McCrea Departments of Neurosurgery and Neurology, Medical
College of Wisconsin, Milwaukee, WI, USA
Jacinta McElligott Rehabilitation Medicine, National Rehabilitation Hospi-
tal, Dun Laoghaire Co Dublin, Ireland
Melissa J. McGinn Anatomy and Neurobiology, Virginia Commonwealth
University School of Medicine, Richmond, VA, USA
Pip McGirl The Chicago School of Professional Psychology, School Psy-
chology Department, Chicago, IL, USA
Amanda McGovern Psychiatry, Columbia University Medical Center, New
York, NY, USA
David E. McIntosh Department of Special Education, Teachers College,
Bell State University, Muncie, IN, USA

Thomas Martin: deceased.

Contributors lxix

Miechelle McKelvey Department of Communication Disorders, COE B141,

University of Nebraska Kearney, Kearney, NE, USA
Tamara McKenzie-Hartman Defense and Veterans Brain Injury Center,
James A. Haley, VA Hospital, Tampa, FL, USA
Molly E. McLaren Center for Cognitive Aging and Memory, Department of
Clinical and Health Psychology, University of Florida, Gainesville, FL, USA
Nicole C. R. McLaughlin Butler Hospital Alpert Medical School of Brown
University, Providence, RI, USA
Brian T. McMahon Department of Rehabilitation Counseling, Virginia
Commonwealth University, Richmond, VA, USA
Lemmietta McNeilly Speech-Language Pathology, American Speech-Lan-
guage-Hearing Association, Rockville, MD, USA
Rory McQuiston Anatomy and Neurobiology, Virginia Commonwealth
University, Richmond, VA, USA
Linda McWhorter Department of Psychology, University of North Carolina
at Charlotte, Charlotte, NC, USA
Mary-Ellen Meadows Division of Cognitive and Behavioral Neurology,
Brigham and Women’s Hospital, Boston, MA, USA
Stephanie Mears MHS Inc, Toronto, ON, Canada
Michael S. Mega Center for Cognitive Health, Portland, OR, USA
Stephen S. Meharg Center for Memory and Learning, Longview, WA, USA
Erica P. Meltzer Department of Psychology, Queens College and The Grad-
uate Center of the City University of New York, Flushing, NY, USA
Patricia Melville Department of Neuropsychology Research, Stony Brook
University SUNY Stony Brook, Stony Brook, NY, USA
Andrew Menatti Neuropsychology, University of Missouri, Columbia, MO,
USA
John E. Mendoza Department of Psychiatry and Neuroscience, Tulane
Medical School and SE Louisiana Veterans Healthcare System, New Orleans,
LA, USA
Mark Mennemeier Neurobiology and Developmental Sciences, University
of Arkansas for Medical Sciences, Little Rock, AR, USA
Randall E. Merchant Department of Anatomy and Neurobiology, Virginia
Commonwealth University Medical Center, Richmond, VA, USA
Brad Merker Henry Ford Health Systems, Detroit, MI, USA
Carolyn B. Mervis Department of Psychological and Brain Sciences, Uni-
versity of Louisville, Louisville, KY, USA
lxx Contributors

Gary B. Mesibov University of North Carolina at Chapel Hill, Chapel Hill,

NC, USA
Linda A. Meyer Speech Therapy, Augusta Health, Waynesboro, VA, USA
John E. Meyers Department of Neuropsychology, Comprehensive
Medpsych Systems, Sarasota, FL, USA
David Michalec Division of Psychology Ohio State University Nationwide
Children’s Hospital, Developmental Assessment Program, Columbus, OH,
USA
Jackie L. Micklewright Georgia State University, Department of Psychol-
ogy and the Neuroscience Institute, Atlanta, GA, USA
Christine J. Mihaila Northeast Regional Epilepsy Group, New York, NY,
USA
Eric N. Miller Palm Springs, CA, USA
Ana Mills Department of Physical Medicine and Rehabilitation, Virginia
Commonwealth University, Richmond, VA, USA
Ginger Mills Graduate Institute of Professional Psychology, University of
Hartford, West Hartford, CT, USA
Brenda Atkinson Milner Montreal Neurological Institute and Hospital,
Montreal, QC, USA
Kristin Moffett Emory University, Atlanta, GA, USA
Ethan Moitra Department of Psychiatry and Human Behavior, Brown Uni-
versity, Providence, RI, USA
Doris S. Mok Department of Psychology, Faculty of Social Sciences and
Humanities University of Macau, Taipa, Macau SAR, China
Ashley Mondragon Department of Psychology, William Paterson Univer-
sity, Wayne, NJ, USA
Anna Bacon Moore Department of Rehabilitation Medicine, Division of
Neuropsychology, Emory University School of Medicine, Atlanta, GA, USA
Brittney Moore Department of Educational Psychology, Ball State Univer-
sity, Muncie, IN, USA
Lisa Moran Department of Psychology, Nationwide Children’s Hospital,
Columbus, OH, USA
Joseph E. Mosley Department of Psychology, William Paterson University,
Wayne, NJ, USA
Margaret Moult Olin Neuropsychiatry Research Center, Institute of Living,
Hartford, CT, USA
Martin Mrazik Department of Educational Psychology, University of
Alberta, Edmonton, AB, Canada
Contributors lxxi

Christine Mullen Emory Health Care, Atlanta, GA, USA

Courtney Murphy Belmont Behavioral Hospital, Philadelphia, PA, USA
Mary Pat Murphy MSN, CRRN, Paoli, PA, USA
Suzanne Musil Rush University Medical Center, Chicago, IL, USA
Charlsie Myers Department of Social Sciences, Coastal College of Georgia,
Brunswick, GA, USA
Sylvie Naar-King Detroit, MI, USA
Risa Nakase-Richardson Mental Health and Behavioral Sciences, Depart-
ment of Medicine, James A. Haley Veterans Hospital, University of South
Florida, Defense and Veterans Brain Injury Center, Center of Innovation in
Disability and Rehabilitation Research, Tampa, FL, USA
Luba Nakhutina Department of Neurology, SUNY Downstate Medical
Center, Brooklyn, NY, USA
Madison Neirmeyer Department of Psychology, The University of Utah,
Salt Lake City, UT, USA
Robi L. Nelson Department of Psychiatry and Behavioral Sciences, Univer-
sity of South Florida College of Medicine, Tampa, FL, USA
Department of Pharmacology, Virginia Commonwealth University, Rich-
mond, VA, USA
Aaron P. Nelson Center for Brain Mind Medicine, Brigham and Women’s
Hospital and Harvard Medical School, Boston, MA, USA
Christina Nessler VA Salt Lake City Health Care System, Salt Lake City,
UT, USA
Robert Newby Division of Neurology and Pediatrics, Medical College of
Wisconsin, Milwaukee, WI, USA
Paul Newman Department of Medical Psychology and Neuropsychology,
Drake Center, Cincinnati, OH, USA
Christine Maguth Nezu Department of Psychology, Drexel
University–Hahnemann Campus, Philadelphia, PA, USA
Louisa Ng Department of Rehabilitation Medicine, Royal Melbourne Hos-
pital, Parkville, VIC, Australia
Hien Nguyen Department of Pediatrics, Kaiser Permanente East Bay, Oak-
land, CA, USA
Jody S. Nicholson Department of Psychology, University of Notre Dame,
Notre Dame, IN, USA
Jared A. Nielsen Departments of Psychiatry and Psychology, Harvard Uni-
versity and Massachusetts General Hospital, Cambridge, MA, USA
lxxii Contributors

Janet P. Niemeier Carolinas Rehabilitation, Carolinas Healthcare System,

Charlotte, NC, USA

Madison Niermeyer Department of Psychology, Clinical Psychology, The

University of Utah, Salt Lake City, UT, USA

Christine Nieves Robert Wood Johnson Medical School, Rutgers University,

Piscataway, NJ, USA

C. Michael Nina Department of Psychology, William Paterson University,

Wayne, NJ, USA

Ignatius Nip School of Speech, Language, and Hearing Sciences, San Diego
State University, San Diego, CA, USA

Nicole R. Nissim Department of Clinical and Health Psychology College of

Public Health and Health Professions, Center for Cognitive Aging and Mem-
ory, McKnight Brain Institute (Primary), University of Florida, Gainesville,
FL, USA
Department of Neuroscience, University of Florida, Gainesville, FL, USA

Natalie O. Nordlund Legal Psychology (Psychology and Law), Neuropsy-

chology, Clinical Psychology, The Chicago School of Professional Psychol-
ogy, Chicago, IL, USA

David Nordstokke Werklund School of Education, University of Calgary,

Calgary, AB, Canada

Virginia A. Norris San Quentin State Prison, San Quentin, CA, USA

Olga Noskin Neurology Group of Bergen County, P.A, Ridgewood, NJ,

USA

Thomas A. Novack Department of Physical Medicine and Rehabilitation,

University of Alabama at Birmingham, Birmingham, AL, USA

Alicia Nuñez Department of Psychology, University of Nevada, Las Vegas,

NV, USA

Meena Nuthi University of Florida, Gainesville, FL, USA

Andrew O’Shea Department of Aging and Geriatric Research, College of

Medicine, Institute on Aging, University of Florida, Gainesville, FL, USA

Deirdre M. O’Shea Department of Clinical and Health Psychology, Center

for Cognitive Aging and Memory, University of Florida, Gainesville, FL, USA

Kathleen O’Toole Children’s Healthcare of Atlanta, Atlanta, GA, USA

Thomas Oakland Department of Educational Psychology, College of Edu-

cation University of Florida, Gainesville, FL, USA

Thomas Oakland: deceased.

Contributors lxxiii

Christa Ochoa Center for Cognitive Aging and Memory, Department of

Clinical and Health Psychology, University of Florida, Gainesville, Florida,
USA
Natalia Ojeda Department of Methods and Experimental Psychology, Fac-
ulty of Psychology and Education, University of Deusto, Bilbao, Spain
Jonathan A. Oler Department of Psychiatry, University of Wisconsin-Mad-
ison, Madison, WI, USA
Traci W. Olivier Neuropsychology Section, Department of Psychology, St.
Jude Children’s Research Hospital, Memphis, TN, USA
Katie Osborn Florida School of Professional Psychology at Argosy Univer-
sity, Tampa, FL, USA
Zachary H. Osborn Behavioural Health Service Line, Harry S. Truman
Memorial Veteran’s Hospital, Columbia, MO, USA
Celita J. Owens Immaculata University, Immaculata, PA, USA
Matthew J. L. Page Allegheny General Hospital, Pittsburgh, PA, USA
Psychology, Allegheny Health Network, Pittsburgh, PA, USA
Rohan Palmer Institute for Behavioral Genetics, University of Colorado at
Boulder, Boulder, CO, USA
Christina A. Palmese Department of Neurology, Mount Sinai Beth Israel,
New York, NY, USA
Teresa Palumbo Administration Communications Senior University Rela-
tions Specialist, University of Wisconsin-Madison Waisman Center, Madison,
WI, USA
Juhi Pandey Department of Psychology, University of Connecticut, Storrs,
CT, USA
Carlos Bo Pang Department of Psychology, Faculty of Social Sciences and
Humanities, University of Macau, Macao, Macau SAR, China
Aimilia Papazoglou Department of Psychology and the Neuroscience Insti-
tute, Georgia State University, Atlanta, GA, USA
Kathryn V. Papp Department of Psychology, The University of Connecticut,
Storrs, CT, USA
Rick Parente Department of Psychology, Towson University, Towson, MD,
USA
John Parkhurst Psychiatry and Behavioral Medicine, Children’s Hospital of
Wisconsin, Medical College of Wisconsin, Milwaukee, WI, USA
Matthew R. Parry Neurosurgery, Virginia Commonwealth University,
Richmond, VA, USA
Lisa A. Pass Department of Educational Psychology, Ball State University,
Muncie, IN, USA
lxxiv Contributors

Nicholas Pastorek Rehabilitation and Extended Care Line, Michael

E. DeBakey VA Medical Center, Houston, TX, USA
Janet P. Patterson Audiology and Speech-Language Pathology Service, VA
Northern California Health Care System, Martinez, CA, USA
Diane Paul Clinical Issues in Speech-Language Pathology, American
Speech-Language-Hearing Association, Rockville, MD, USA
Nina Paul Department of Psychology, University of Nevada-Las Vegas, Las
Vegas, Nevada, USA
Rebecca Pavlick Department of Psychology, William Paterson University,
Wayne, NJ, USA
Shelley Pelletier Board Certified in School Psychology, Shoreline Pediatric
Neuropsychology Services, LLC, Old Saybrook, CT, USA
Javier Peña Department of Methods and Experimental Psychology, Faculty
of Psychology and Education, University of Deusto, Bilbao, Spain
Suzanne Penna Department of Rehabilitation Medicine, Emory University
School of Medicine, Atlanta, GA, USA
Dana L. Penney Department of Neurology, The Lahey Clinic, Burlington,
MA, USA
Molly Penzenik Rocky Mountain Mental Illness Research Education and
Clinical Center, Denver, CO, USA
University of Colorado, Anschutz Medical Campus, Aurora, CO, USA
Alexandra Perrault University of Cincinnati, Cincinnati, OH, USA
Lexi Perrault University of Cincinnati, Cincinnati, OH, USA
Paul B. Perrin Department of Psychology, Virginia Commonwealth Univer-
sity, Richmond, VA, USA
Kenneth R. Perrine Neurological Surgery, Weill Cornell Medicine,
New York, NY, USA
Amy Peterman Department of Psychological Science, University of North
Carolina at Charlotte, Charlotte, NC, USA
Maria Petracca Department of Neurology, Icahn School of Medicine at
Mount Sinai, New York, NY, USA
Jo Ann Petrie Department of Psychology and the Neuroscience Center,
Brigham Young University, Provo, UT, USA
LeAdelle Phelps University at Buffalo, State University of New York, Buf-
falo, NY, USA
Angela M. Philippus Craig Hospital, Englewood, CO, USA
Linda L. Phillips Anatomy and Neurobiology, Virginia Commonwealth
University, Richmond, VA, USA
Contributors lxxv

Jesse J. Piehl Department of Pharmacology, Virginia Commonwealth Uni-

versity, Richmond, VA, USA
Elizabeth I. Pierpont Department of Pediatrics, Division of Clinical Behav-
ioral Neuroscience, University of Minnesota, Minneapolis, MN, USA
Eric E. Pierson Department of Educational Psychology, Ball State Univer-
sity, Muncie, IN, USA
Irene Piryatinsky Butler Hospital and Alpert Medical School of Brown
University, Providence, RI, USA
Jenni Pitkanen Product Development at MHS Inc., Toronto, ON, Canada
Kenneth Podell Houston Methodist Hospital, Houston, TX, USA
Henry Ford Health Systems, Detroit, MI, USA
Ben Polakoff Department of Educational Psychology, The University of
Utah, Salt Lake City, UT, USA
Elena Polejaeva Department of Clinical and Health Psychology, University
of Florida, Gainesville, FL, USA
Donna Polelle Communication Sciences and Disorders, College of Science
and Mathematics, University of South Florida Sarasota-Manatee, Sarasota,
FL, USA
Eric S. Porges Department of Clinical and Health Psychology, University of
Florida, Gainesville, FL, USA
Center for Cognitive Aging and Memory, McKnight Brain Institute, Univer-
sity of Florida, Gainesville, FL, USA
Department of Neurology, University of Florida, Gainesville, FL, USA
Matthew R. Powell Division of Neurocognitive Disorders, Department of
Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA
Tiffany L. Powell Department of Neurosurgery, Virginia Commonwealth
University, Richmond, VA, USA
Elizabeth Power Legal Psychology (Psychology and Law), Neuropsychol-
ogy, Clinical Psychology, Chicago School of Professional Psychology, Chi-
cago, IL, USA
The College of Saint Rose, Albany, NY, USA
Natalia Ojeda Del Pozo Fundamentals and Methods of Psychology, Univer-
sity of Deusto, Bilbao, Spain
Victor R. Preedy Faculty of Life Sciences and Medicine, King’s College
London, London, UK
Andrew Preston Department of Pediatrics, Chapel Hill Pediatric Psychol-
ogy, Chapel Hill, NC, USA
Catherine C. Price Department of Clinician and Health Psychology and
Dept of Anesthesiology, University of Florida, Florida, USA
lxxvi Contributors

George P. Prigatano Department of Clinical Neuropsychology, Barrow

Neurological Institute, St. Joseph’s Hospital and Medical Center, Phoenix,
AZ, USA
Michelle Ann Prosje NeuroBehavioral Specialists of Jacksonville, Inc.,
Jacksonville, FL, USA
Antonio E. Puente Depatment of Psychology, University of North Carolina
Wilmington, Wilmington, NC, USA
Anneliese Radke Department of Neurology, University of California, Davis,
CA, USA
Susie Engi Raiford Assessment and Instruction, Pearson, San Antonio, TX,
USA
Robert D. Rainer Department of Psychology, University of Florida, Gaines-
ville, FL, USA
Vanessa L. Ramos Scarborough Department of Neuropsychology, Ken-
nedy Krieger Institute, Baltimore, MD, USA
Kate D. Randall Department of Psychology, University of Victoria, Victoria,
BC, Canada
Steven Z. Rapcsak Neurology Section, Southern Arizona VA Healthcare
System, Tucson, AZ, USA
Department of Neurology, University of Arizona, Tucson, AZ, USA
Sarah A. Raskin Department of Psychology and Neuroscience Program,
Trinity College, Hartford, CT, USA
Joseph F. Rath NYU Langone Medical Center, Department of Psychology,
Rusk Institute of Rehabilitation Medicine, New York, NY, USA
Holly Rau Department of Psychology, The University of Utah, Salt Lake
City, UT, USA
Anastasia Raymer Communication Disorders and Special Education, Old
Dominion University, Norfolk, VA, USA
Jennifer Linton Reesman Kennedy Krieger Institute/Johns Hopkins Uni-
versity School of Medicine, Baltimore, MD, USA
Christine Reid Department of Rehabilitation Counseling, Virginia Com-
monwealth University, Richmond, VA, USA
Stephanie A. Reid-Arndt School of Health Professions – Health Psychol-
ogy, University of Missouri, Columbia, MO, USA
Sheryl Reminger Psychology Department, University of Illinois at Spring-
field, Springfield, IL, USA
Kathryn K. Reva University of Northern Colorado, New York, NY, USA
Jose A. Rey College of Pharmacy, Nova Southeastern University, Ft.
Lauderdale, FL, USA
Contributors lxxvii

Cecil R. Reynolds Texas A&M University, College Station, TX, USA

Jill B. Rich Department of Psychology, York University, Toronto, ON,
Canada
Lindsey Richards Department of Clinical and Health Psychology, Center for
Cognitive Aging and Memory, University of Florida, Gainesville, FL, USA
Robert Rider Department of Psychology, Drexel University, Philadelphia,
PA, USA
Giulia Righi Visual Neuroscience Laboratory, Brown University, Provi-
dence, RI, USA
Diana L. Robins AJ Drexel Autism Institute, Drexel University, Philadel-
phia, PA, USA
Tresa Roebuck-Spencer Jefferson Neurobehavioral Group, Metairie, LA,
USA
Daniel E. Rohe Mayo Clinic, Rochester, MN, USA
Cynthia Rolston Department of PM&R, Virginia Commonwealth Univer-
sity-Medical College of Virginia, Richmond, VA, USA
Maryellen Romero Department of Psychiatry and Behavioral Sciences,
Tulane University School of Medicine, New Orleans, LA, USA
Katherine A. Roof Department of Psychology, University of North Carolina
at Charlotte, Charlotte, NC, USA
Susan Ropacki VA Palo Alto, Polytrauma System of Care, Polytrauma
Transitional Rehabilitation Program, VA Palo Alto Health Care System, Palo
Alto, California, USA
Neurosurgery, Stanford University, Palo Alto, California, USA
Jon Rose Spinal Cord Injury Clinic, Veterans Affairs Palo Alto Healthcare
System, Palo Alto, CA, USA
Carole R. Roth Otolaryngology Clinic, Speech Division, Naval Medical
Center, San Diego, CA, USA
Elliot J. Roth Department of Physical Medicine and Rehabilitation, North-
western University, Feinberg School of Medicine, Chicago, IL, USA
Robert M. Roth Geisel School of Medicine at Dartmouth / DHMC, Leba-
non, NH, USA
Linda Rowley Waisman Center Family Village, University of Madison,
Madison, WI, USA
Donald R. Royall Deptartment of Psychiatry, The University of Texas Health
Center at San Antonio, San Antonio, TX, USA
Shahal Rozenblatt Advanced Psychological Assessment P. C., Smithtown,
NY, USA
lxxviii Contributors

Alexandra Rudd-Barnard One Neuro, West Los Angeles, California, USA

Ronald Ruff San Francisco Clinical Neurosciences, University of California,
San Francisco, CA, USA
Jessica Somerville Ruffolo Department of Psychology, University of Wash-
ington, Seattle, Washington, DC, USA
Ruba Rum College of Medicine Psychiatry and Behavioral Neurosciences,
University of South Florida, Tampa, FL, USA
Anthony C. Ruocco Department of Psychology, University of Toronto,
Toronto, ON, Canada
Beth Rush Psychiatry and Psychology, Mayo Clinic, Jacksonville, FL, USA
Michele Rusin Emory University/Rehabilitation Medicine, Atlanta, GA,
USA
Julia Rutenberg Rehabilitation Medicine, Emory University, Atlanta, GA,
USA
John P. Ryan Department of Psychiatry, University of Pittsburgh, Pittsburgh,
PA, USA
Bruce Rybarczyk Department of Psychology, Virginia Commonwealth Uni-
versity, Richmond, VA, USA
Catherine M. Rydell American Academy of Neurology, Minneapolis, MN,
USA
Sara R. Rzepa Clinical, Education, and Public Safety at MHS Inc, Toronto,
ON, Canada
Bonnie C. Sachs Parkinson’s and Movement Disorders Center, Virginia
Commonwealth University, Richmond, VA, USA
Amanda L. Sacks-Zimmerman Department of Neurological Surgery, Weill
Cornell Medicine, New York, NY, USA
Donald H. Saklofske Department of Psychology, University of Western
Ontario, London, ON, Canada
Christina Salama Kennedy Krieger Institute/Johns Hopkins University
School of Medicine, Baltimore, MD, USA
Christine M. Salinas Space Coast Neuropsychology Center, Melbourne, FL,
USA
Stephanie L. Salinas Department of Rehabilitation Medicine, The Georgia
School of Professional Psychology at Argosy University-Atlanta, Atlanta,
GA, USA
Stephen P. Salloway Butler Hospital Alpert Medical School of Brown Uni-
versity, Providence, RI, USA
Jeffery Samuels Inpatient Rehabilitation Unit, North Broward Medical Cen-
ter, Deerfield Beach, FL, USA
Contributors lxxix

Orlando Sánchez Minneapolis VA Health Care System, Minneapolis, MN,

USA
Mark A. Sandberg Neuropsychology, Northport VA Medical Center,
Smithtown, NY, USA
Chelsea Sanders Department of Psychology, Utah State University, Logan,
UT, USA
R. Sands Legal Psychology (Psychology and Law), Neuropsychology, Clin-
ical Psychology, The Chicago School of Professional Psychology, Chicago,
IL, USA
Marla Sanzone Independent Practice, Loyola College of Maryland, Annap-
olis, MD, USA
Celine A. Saulnier Department of Pediatrics, Emory University School of
Medicine, Atlanta, GA, USA
Lynn A. Schaefer Physical Medicine and Rehabilitation, Nassau University
Medical Center, East Meadow, NY, USA
Philip Schatz Department of Psychology, Saint Joseph’s University, Phila-
delphia, PA, USA
Mike R. Schoenberg Department of Psychiatry and Behavioral Sciences,
University of South Florida College of Medicine, Tampa, FL, USA
Aaron Schrader Applied Psychology and Counselor Education, University
of Northern Colorado, Greeley, CO, USA
William A. Schraegle Pediatric Neuropsychology, Dell Children’s Medical
Center of Central Texas, Austin, TX, USA
Department of Educational Psychology, The University of Texas at Austin,
Austin, TX, USA
Jillian Schuh Department of Psychology, University of Connecticut, Storrs,
CT, USA
Christian Schutte Henry Ford Allegiance, Jackson, MI, USA
John D. Dingell VA Medical Center, Psychology Section (11MHPS), Detroit,
MI, USA
Kerri A. Scorpio Department of Psychology, Queens College of the City
University of New York, Flushing, NY, USA
Paige Seegan Clinical Psychology Program, Texas Tech University, Lub-
bock, TX, USA
Peter W. Seely Department of Pharmacology, Virginia Commonwealth Uni-
versity, Richmond, VA, USA
Daniel L. Segal Department of Psychology, University of Colorado at Col-
orado Springs, Colorado Springs, CO, USA
lxxx Contributors

Talia R. Seider Department of Clinical and Health Psychology, College of

Public Health and Health Professions, University of Florida, Gainesville, FL,
USA
Center for Cognitive Aging and Memory, McKnight Brain Institute, Univer-
sity of Florida, Gainesville, FL, USA
Robin Sekerak Waikato District Health Board, Hamilton, New Zealand
Svetlana Serova Department of Rehabilitation Medicine, Mount Sinai
School of Medicine, New York, NY, USA
Laura Shank Rehabilitation Psychology and Neuropsychology, Physical
Medicine and Rehabilitation University of Michigan, Ann Arbor, MI, USA
Casey R. Shannon University of Northern Colorado, Greeley, CO, USA
Anuj Sharma Virginia Commonwealth University School of Medicine,
Richmond, VA, USA
Rhonna Shatz Department of Neurology and Rehabilitation, MED-Neurol-
ogy, University of Cincinnati, Cincinnati, OH, USA
Bennett A. Shaywitz Department of Pediatrics, Yale University School of
Medicine, New Haven, CT, USA
Sally E. Shaywitz Department of Pediatrics, Yale University School of
Medicine, New Haven, CT, USA
Victoria Shea University of North Carolina at Chapel Hill, Chapel Hill, NC,
USA
Judith A. Shechter Wynnewood, PA, USA
Tamara Goldman Sher Institute of Psychology, Illinois Institute of Tech-
nology, Chicago, IL, USA
Elisabeth M. S. Sherman Copeman Healthcare Centre, Calgary, AB,
Canada
Cynthia X. Shi Emory College at Emory University, Atlanta, GA, USA
Cheryl L. Shigaki Department of Health Psychology, University of Mis-
souri, Columbia, MO, USA
Lindsay C. Shima Department of Psychology, Neuropsychology Research
Group, West Chester University of Pennsylvania, West Chester, PA, USA
Gerald Showalter Department of Psychiatry and Neurobehavioral Sciences,
University of Virginia School of Medicine, Charlottesville, VA, USA
Seema Shroff Department of Anatomy and Neurobiology, Virginia Com-
monwealth University, Richmond, VA, USA
David Ho Keung Shum Griffith University, School of Psychology, Mt
Gravatt Campus Griffith University, Brisbane, QLD, Australia
Contributors lxxxi

Melissa Shuman-Paretsky Department of Rehabilitation Medicine, Mount

Sinai School of Medicine, New York, NY, USA

Linda Shuster Interdisciplinary Health Sciences Ph.D. Program and Depart-

ment of Speech, Language, and Hearing Sciences, Western Michigan Univer-
sity, Kalamazoo, MI, USA

Kevin Sickinger Chronic Effects of Neurotrauma Consortium (CENC), Vir-

ginia Commonwealth University, Richmond, VA, USA

Marc A. Silva Mental Health and Behavioral Sciences Service, James A.

Haley Veterans’ Hospital, Tampa, FL, USA

Preeti Sinha Department of Clinical and Health Psychology, University of

Florida, Gainesville, FL, USA

Sue Ann Sisto School of Health Technology and Management Stony Brook
University, Stony Brook, NY, USA

Gill Sitarenios Multi-Health Systems Inc., Toronto, ON, Canada

Ketharini Sivasegaran Whitby Vision Care, Whitby, ON, Canada

Amanda Skierkiewicz School Psychology, The Chicago School of Profes-

sional Psychology, Chicago, IL, USA

Beth Slomine Johns Hopkins University School of Medicine, Baltimore,

MD, USA

Audrey Smerbeck School and Educational Psychology, University at Buf-

falo, The State University of New York, Buffalo, NY, USA

Daniel Smith Department of Psychology, Drexel University, Philadelphia,

PA, USA
Winship Cancer Institute, Emory University, Atlanta, GA, USA

Kristen Smith Department of Psychology and the Neuroscience Institute,

Georgia State University, Atlanta, GA, USA

Marian L. Smith Via Christi Behavioral Health Crossroads Counseling

Center, Via Christi Hospital Pittsburg Mt. Carmel, Pittsburg, KS, USA

Nicholas David Smith Educational and Psychological Studies, University of

South Florida/TBI Model Systems, James A. Haley VA Hospital, Tampa, FL,
USA

Lucia Smith-Wexler Rusk Rehabilitation, New York University Langone

Health, New York, NY, USA

Kayle E. Sneed Department of Communication Sciences and Disorders, The

University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA

Jill Snyder Behavioral Health Services, Boston Public Schools, Roxbury,

MA, USA
lxxxii Contributors

McKay Moore Sohlberg Communication Disorders and Sciences, Univer-

sity of Oregon, Eugene, OR, USA
Carney Sotto College of Allied Health Sciences, University of Cincinnati,
Cincinnati, OH, USA
Barbara Spacca Anna Meyer Children’s Hospital, Florence, Italy
Sara S. Sparrow Yale University Child Study Center, New Haven, CT, USA
Ferrinne Spector Psychology, Edgewood College, Madison, WI, USA
April Spivack Department of Management and Human Resources, Univer-
sity of Wisconsin Oshkosh, Oshkosh, WI, USA
Beth Springate Department of Psychiatry, University of Connecticut Health
Center, Farmington, CT, USA
Maria St. Pierre Department of Psychology, Towson University, Towson,
MD, USA
Vess Stamenova Rotman Research Institute at Baycrest, Toronto, ON,
Canada
Amy J. Starosta Departments of Psychiatry and Physical Medicine and
Rehabilitation, University of Colorado Denver, Aurora, CO, USA
Susan Steffani CCC-SLP, Department of Communication Sciences and Dis-
orders, California State University, Chico, Chico, CA, USA
Taryn M. Stejskal Department of Physical Medicine and Rehabilitation,
Virginia Commonwealth University Medical Center, Virginia, VA, USA
Jeremy Stevenson Department of Family Medicine, University of Kansas
Medical Center, Kansas City, KS, USA
William Stiers Johns Hopkins University School of Medicine, Baltimore,
MD, USA
Jordan Stiver UCSF Memory and Aging Center, University California San
Francisco, San Francisco, CA, USA
Esther Strauss Department of Psychology, University of Victoria, Victoria,
BC, Canada
Anthony Y. Stringer Department of Rehabilitation Medicine, Emory Uni-
versity, Atlanta, GA, USA
Donald T. Stuss University of Toronto, Toronto, ON, Canada
Sunnybrook Health Sciences Centre, Toronto, ON, Canada
Rotman Research Institute of Baycrest, Toronto, ON, Canada
Lauren Stutts Department of Health and Human Values, Davidson College,
Davidson, NC, USA
Yana Suchy Department of Psychology, The University of Utah, Salt Lake
City, UT, USA
Contributors lxxxiii

Joyce Suh Kennedy Krieger Institute/Johns Hopkins University School of

Medicine, Baltimore, MD, USA
James F. Sumowski Teachers College Columbia University, New York, NY,
USA
Dong Sun Department of Aantomy and Neurobiology, School of Medicine,
Virginia Commonwealth University Medical Center, Richmond, VA, USA
Uma Suryadevara Department of Psychiatry, University of Florida, Gaines-
ville, FL, USA
Zoë N. Swaine Keele University, Keele, Newcastle ST5 5BG, UK
Joan Swearer Department of Neurology, University of Massachusetts Med-
ical School, Worcester, MA, USA
Lawrence H. Sweet Department of Psychology, University of Georgia,
Athens, GA, USA
Rod Swenson Department of Psychiatry and Behavioral Science, University
of North Dakota School of Medicine, Fargo, ND, USA
Russell H. Swerdlow University of Kansas School of Medicine, Landon
Center on Aging, Kansas City, KS, USA
Sarah M. Szymkowicz Department of Clinical and Health Psychology,
College of Public Health and Health Professions, University of Florida,
Gainesville, FL, USA
Jing Ee Tan Division of Neurology, University of British Columbia, Van-
couver, BC, Canada
Vancouver General Hospital, Vancouver, BC, Canada
Department of Psychology, University of Victoria, Victoria, BC, Canada
Michael J. Tarr Visual Neuroscience Laboratory, Brown University, Provi-
dence, RI, USA
David F. Tate Brain Imaging and Behavior Laboratory, Missouri Institute of
Mental Health (MIMH), University of Missouri, St. Louis (UMSL), Berkeley,
MO, USA
Ella B. Teague Department of Neurorehabilitation, Reykjalundur Rehabili-
tation Center, Mosfellsbær, Iceland
Richard Temple Clinical Operations, CORE Health Care, Dripping Springs,
TX, USA
Claire Thomas-Duckwitz University of Northern Colorado, Greeley, CO,
USA
Cynthia K. Thompson Northwestern University, Evanston, IL, USA

Esther Strauss: deceased.

lxxxiv Contributors

Jacob W. Tickle School of Psychology, The Chicago School of Professional

Psychology, Chicago, IL, USA
Jennifer Tinker Department of Neurology, Thomas Jefferson University,
Philadelphia, PA, USA
Michelle Marie Tipton-Burton Physical Medicine and Rehabilitation, Santa
Clara Valley Medical Center, San Jose, CA, USA
Jeffrey B. Titus Comprehensive Epilepsy Program, Dell Children’s Medical
Center of Central Texas, Austin, TX, USA
Department of Psychology, The University of Texas at Austin, Austin, TX,
USA
Teri A. Todd California State University, Northridge, Northridge, CA, USA
Nam Tran Neurosurgery, Virginia Commonwealth University Medical Cen-
ter, Richmond, VA, USA
Alexander I. Tröster Department of Clinical Neuropsychology and Center
for Neuromodulation, Barrow Neurological Institute, Phoenix, AZ, USA
Daniel Tranel Department of Neurology, The University of Iowa, Iowa City,
USA
Angela K. Troyer Neuropsychology and Cognitive Health Program,
Baycrest Centre for Geriatric Care, Toronto, ON, Canada
Tina Trudel Northeast Evaluation Specialists, PLLC, Dover, DE, USA
William Tsang Department of Psychology, William Paterson University,
Wayne, NJ, USA
Theodore Tsaousides Department of Rehab Medicine Brain Injury
Research, Mount Sinai School of Medicine, New York, NY, USA
JoAnn Tschanz Department of Psychology, Utah State University, Logan,
UT, USA
Center for Epidemiologic Studies, Utah State University, Logan, UT, USA
Jessica Tsou Department of Psychiatry, University of Kansas Medical Cen-
ter, Kansas City, KS, USA
Lyn S. Turkstra School of Rehabilitation Science, McMaster University,
Hamilton, ON, Canada
Margaret Tuttle Department of Psychiatry, Massachusetts General Hosptial,
Boston, MA, USA
Jamie T. Twaite Department of Psychology, Queens College and The Grad-
uate Center of the City University of New York, Flushing, NY, USA
Gary Tye Neurosurgery, Virginia Commonwealth University, Richmond,
VA, USA
Contributors lxxxv

Katherine Tyson Department of Psychology, University of Connecticut,

Storrs, CT, USA
Michelle Uher Marketing Communications, American Academy of Neurol-
ogy, Minneapolis, MN, USA
Jason Van Allen Clinical Psychology Program, Texas Tech University, Lub-
bock, TX, USA
Faye van der Fluit Department of Psychology, University of Wisconsin-
Milwaukee, Milwaukee, WI, USA
Timothy E. Van Meter Neurosurgery, Virginia Commonwealth University,
Richmond, VA, USA
Gertina J. van Schalkwyk Department of Psychology, University of Macau,
Taipa, Macao (SAR), China
Emily Vanderbleek Department of Psychology, University of Notre Dame,
Notre Dame, IN, USA
Susan Vandermorris Neuropsychology and Cognitive Health Program,
Baycrest, Toronto, ON, USA
Kimberly J. Vannest Department of Educational Psychology, Texas A&M
University, College Station, TX, USA
Jamie Vannice Applied Psychology and Counselor Education, University of
Northern Colorado, Greeley, CO, USA
Laura M. Vasel Department of Educational Psychology, Ball State Univer-
sity, Muncie, IN, USA
Rebecca Vaurio Kennedy Krieger Institute, Baltimore, MD, USA
Jennifer Venegas Department of Educational Psychology, The University of
Utah, Salt Lake City, UT, USA
Mieke Verfaellie Memory Disorders Research Center, VA Boston Healthcare
System and Boston University School of Medicine, Boston, MA, USA
Elizabeth K. Vernon Department of Psychology, Utah State University,
Logan, UT, USA
Jean Vettel US Army Research Laboratory, National Academy of the Sci-
ences, Washington, DC, USA
Clara Vila-Castelar Department of Psychology, Queens College and The
Graduate Center, The City University of New York, New York, NY, USA
Michael R. Villanueva Department of Psychology, University of North
Carolina at Charlotte, Charlotte, NC, USA
Martin A. Volker School and Educational Psychology, University at Buf-
falo, The State University of New York, Buffalo, NY, USA
lxxxvi Contributors

Fred R. Volkmar Child Study Center, Child Psychiatry, Pediatrics and

Psychology, Yale University School of Medicine, New Haven, CT, USA
Scott Vota Department of Neurology, Virginia Commonwealth University,
Richmond, VA, USA
Christopher Wagner Department of Rehabilitation Counseling, Virginia
Commonwealth University, Richmond, VA, USA
George C. Wagner Department of Psychology, Rutgers University, New
Brunswick, NJ, USA
Natalie Wahmhoff Department of Educational Psychology, The University
of Utah, Salt Lake City, UT, USA
Sarah E. Wallace John G. Rangos Sr. School of Health Sciences, Depart-
ment of Speech-Language Pathology, Duquesne University, Pittsburgh, PA,
USA
Erin Walsh Department of Pharmacology, Virginia Commonwealth Univer-
sity, Richmond, VA, USA
James Walsh School of Psychology, The Chicago School of Professional
Psychology, Chicago, IL, USA
Julie L. Wambaugh Veterans Affairs Salt Lake City Healthcare System,
University of Utah, Salt Lake City, UT, USA
Yuan Yuan Wang Faculty of Health Sciences, University of Macau, Macao,
China
Adam B. Warshowsky Clinical Neuropsychologist, Dual/SCI Unit, Mount
Sinai Medical Center, Shepherd Center, Atlanta, GA, USA
Seth Warschausky Department of Physical Medicine and Rehabilitation,
University of Michigan, Ann Arbor, MI, USA
David Watson Department of Psychology, 124B Haggar Hall, University of
Notre Dame, Notre Dame, IN, USA
Nadia Webb Children’s Hospital of New Orleans, New Orleans, LA, USA
Victoria L. Webb Department of Behavioral Sciences, Rush University
Medical Center, Chicago, IL, USA
Erica Weber Department of Physical Medicine and Rehabilitation, Kessler
Foundation, East Hanover, NJ, USA
Stephen T. Wegener Division of Rehabilitation Psychology and Neuropsy-
chology Department of Physical Medicine and Rehabilitation, The Johns
Hopkins School of Medicine, Baltimore, MD, USA
Alan Weintraub Craig Hospital, Rocky Mountain Regional Brain Injury
System, Englewood, CO, USA
Devon H. Weir Department of Psychology, University of Florida, Gaines-
ville, FL, USA
Contributors lxxxvii

Jonathan Wellman St. Luke’s Hospital, Kansas City, MO, USA

John D. Westbrook National Center for the Dissemination of Disability
Research (NCDDR), SEDL, Austin, TX, USA
Michael Westerveld Medical Psychology Associates, Florida Hospital,
Orlando, FL, USA
Holly James Westervelt Memory and Cognitive Assessment Program,
Department of Psychiatry, Rhode Island Hospital, Providence, RI, USA
Kristine B. Whigham Department of Neuropsychology, Children’s
Healthcare of Atlanta, Atlanta, GA, USA
Gale G. Whiteneck Craig Hospital, Englewood, CO, USA
John Whyte Moss Rehabilitation Research Institute, Albert Einstein
Healthcare Network, Elkins Park, PA, USA
Robert G. Will University of Edinburgh, Edinburgh, UK
Gavin Williams Epworth Rehabilitation Centre Epworth Hospital, Rich-
mond Melbourne, VIC, Australia
Travis Williams Department of Physical Medicine and Rehabilitation, Indi-
ana University, Indianapolis, IN, USA
Tricia S. Williams Division of Neurology and Department of Psychology,
Sick Kids-Centre for Brain and Mental Health, Toronto, ON, Canada
John B. Williamson Department of Neurology, University of Florida Col-
lege of Medicine, Center for Neurological Studies and the Research Service of
the Malcom Randall Veterans Affairs Medical Center, Gainesville, FL, USA
Meredith L. C. Williamson Department of Primary Care Medicine, College
of Medicine, Texas A&M Health Science Center, Bryan, TX, USA
Brenda Wilson Department of Communication Disorders and Sciences,
Eastern Illinois University, Charleston, IL, USA
Jill Winegardner Oliver Zangwill Centre, Ely, UK
Melissa Wingate Neuropsychology, The Chicago School of Professional
Psychology, Chicago, IL, USA
Deborah Witsken University of Minnesota Medical School, Minneapolis,
MN, USA
Ericka L. Wodka Center for Autism and Related Disorders, Kennedy
Krieger Institute and The Johns Hopkins University School of Medicine,
Baltimore, MD, USA
Thomas R. Wodushek School of Medicine, Department of Neurosurgery,
University of Colorado, Aurora, CO, USA
Edison Wong Center for Pain and Medical Rehabilitation, Fitchburg, MA,
USA
lxxxviii Contributors

Sarah Woodrow Oak Grove School District, San Jose, CA, USA
Adam J. Woods Department of Clinical and Health Psychology, College of
Public Health and Health Professions, University of Florida, Gainesville, FL,
USA
Center for Cognitive Aging and Memory, McKnight Brain Institute, Univer-
sity of Florida, Gainesville, FL, USA
Department of Neuroscience, University of Florida, Gainesville, FL, USA
Michael S. Worden Department of Neuroscience, Brown University, Prov-
idence, RI, USA
Jerry Wright Rehabilitation Research Center, Santa Clara Valley Medical
Center, San Jose, CA, USA
Fan Wu Outcomes Management, The Harris Center for Mental Health and
IDD, Houston, TX, USA
Glenn Wylie Neuropsychology and Neuroscience Laboratory, Kessler Med-
ical Rehabilitation Research and Education Center Kessler Foundation, West
Orange, NJ, USA
Naohide Yamamoto Queensland University of Technology, Brisbane,
Queensland, Australia
Keith Owen Yeates Department of Psychology, University of Calgary, Cal-
gary, AB, Canada
Angela Yi Department of Rehab Medicine, Mount Sinai School of Medicine,
New York, NY, USA
Brian Yochim Department of Psychology, University of Colorado at Colo-
rado Springs, Colorado Springs, CO, USA
Sevilay Yumusak Department of Psychology, University of Florida, Gaines-
ville, FL, USA
Michele L. Zaccario Department of Psychology, Pace University, Dyson
College of Arts and Sciences, New York, NY, USA
Christina Zafiris Applied Psychology and Counselor Education, University
of Northern Colorado, Greeley, CO, USA
Ross Zafonte Department of Physical Medicine and Rehabilitation,
Spaulding Rehabilitation Hospital, Massachusetts General Hospital, Brigham
and Women’s Hospital, Harvard Medical School, Boston, MA, USA
Nathan D. Zasler Concussion Care Centre of Virginia, Ltd., Richmond, VA,
USA
Islam Zaydan Neurology, Virginia Commonwealth University, Richmond,
VA, USA
Fadel Zeidan Department of Neurobiology and Anatomy, Wake Forest
School of Medicine, Winston-Salem, NC, USA
Contributors lxxxix

J. Zhou School Psychology, The Chicago School of Professional Psychol-

ogy, Chicago, IL, USA
Zheng Zhou Department of Psychology, St. John’s University, Queens, NY,
USA
Miriam Zichlin Health Economics and Outcomes Research, Analysis
Group, Inc., Boston, MA, USA
Rosemary Ziemnik Department of Psychology, The University of Utah, Salt
Lake City, UT, USA
Molly E. Zimmerman Department of Psychology, Fordham University,
Bronx, NY, USA
Davor Zink Neuropsychology Research Program, University of Nevada, Las
Vegas, Las Vegas, NV, USA
A

AACN Practice Guidelines Association’s focus on evidence-based practice,

the AACN established (AACN 2007) guidelines
Robert L. Heilbronner for the practice of neuropsychological assessment
Chicago Neuropsychology Group, Chicago, and consultation. The guidelines are intended to
IL, USA provide standards for competence and profes-
sional conduct within the practice of neuropsy-
chology by describing the “most desirable and
Synonyms highest level of professional conduct” for clinical
neuropsychologists providing clinical neuropsy-
Practice development; Practice guidelines chology services. It is important to note that the
guidelines are fully compatible with the current
APA (2002b) Ethical Principles of Psychologists
Historical Background and Code of Conduct (EPPCC) as well as the
Criteria for Practice Guideline Development and
The American Board of Clinical Neuropsychology Evaluation (2002a) and Determination and Docu-
(ABCN) is a specialty board within the American mentation of the Need for Practice Guidelines
Board of Professional Psychology (ABPP). For (2005). The AACN practice guidelines include
those seeking board certification in clinical neuro- recommendations for the practice of clinical neu-
psychology, ABCN is the board responsible for ropsychology, and they are not to be regarded as
overseeing the examination process. The American mandatory standards. The guidelines detail con-
Academy of Clinical Neuropsychology (AACN) is sideration of ethical and clinical issues as well as
the organization for those awarded board certifica- specific methods and procedures for the practice
tion by the ABCN. In 2007, AACN produced the of neuropsychology.
first set of practice guidelines, which were intended There are several major areas of emphasis in
to “. . .facilitate the continued systematic growth of the guidelines. They include (1) definitions,
the profession of clinical neuropsychology, and to (2) purpose and scope, (3) education and training,
help assure a high level of professional practice.” (4) work settings, (5) ethical and clinical issues
(e.g., informed consent, patient issues in third
party assessments, test security; underserved
Current Knowledge populations/cultural issues, and (6) methods and
procedures (e.g., review of records, measurement
Given the recent growth of clinical neuropsychol- procedures, test administration and scoring, and
ogy, coupled with the American Psychological interpretation).
# Springer International Publishing AG, part of Springer Nature 2018
J. S. Kreutzer et al. (eds.), Encyclopedia of Clinical Neuropsychology,
https://doi.org/10.1007/978-3-319-57111-9
2 AAMD Adaptive Behavior Scales

References and Readings of choice. The behavior scales have been

published in two versions, the Adaptive Behav-
American Psychological Association. (2002a). Criteria for ior Scales-Residential and Community, 2nd edi-
practice guideline development and evaluation. Amer-
tion (ABS-RC: 2) and the Adaptive Behavior
ican Psychologist, 57, 1048–1051.
American Psychological Association. (2002b). Ethical Scales-School, 2nd edition (ABS-S: 2). Current
principles of psychologists and code of conduct. Amer- versions are a comprehensive compilation of the
ican Psychologist, 57, 1060–1073. past versions. These assessments seek to
American Psychological Association. (2005). Determina-
develop an estimate of adaptive behaviors in
tion and documentation of the need for practice guide-
lines. American Psychologist, 60, 976–978. two scales defined with personal independence
Committee on Ethical Guidelines for Forensic Psycholo- and maladaptive behaviors in individuals with
gists. (1991). Specialty guidelines for forensic psychol- intellectual disabilities. Items are rated with a
ogists. Law and Human Behavior, 15, 655–665.
yes/no response, on a 0–3 scale, or by frequency.
The AACN practice guidelines can be found on the
AACN’s web site (www.theaacn.org) and are also Historically, the ABS-RC: 2 was used in insti-
published in the AACN’s journal: The Clinical Neuro- tutions, but it is now also used in community
psychologist, 21, 209–231. settings, whereas the ABS-S: 2 was designed for
school settings.
For both the ABS-RC: 2 and the ABS-S: 2,
the assessment can be administered by two
AAMD Adaptive Behavior approaches. The assessment can be completed
Scales by a professional or paraprofessional or by some-
one familiar with the individual. Interpretation of
Crista A. Hopp1 and Ida Sue Baron2 results should be completed by someone formally
1
Connected Pathways Coaching, Herndon, trained in psychometrics and these scales.
VA, USA The ABS-S: 2 evaluates an individual’s abil-
2
Potomac, MD, USA ity to cope with challenges they encounter
in their school, and aids in the diagnosis of
intellectual disabilities at ages 3–21. There
Synonyms are nine subscales in the first part of the assess-
ment, measuring personal independence and
AAMD ABS: 2; AAMR ABS-RC: 2; AAMR responsibility of daily living: independent func-
ABS-S: 2 tioning, physical development, economic activ-
ity, language development, numbers and time,
prevocational/vocational activity, self-direc-
Description tion, responsibility, and socialization. Part two
of the assessment addresses behavioral domains
The American Association for Mental Defi- and consists of seven subscales: social behavior,
ciency Adaptive Behavior Scales (AAMD conformity, trustworthiness, stereotyped and
ABS) is a revised edition (1993) of the original hyperactive behavior, self-abusive behavior,
assessments that were published in 1969. The social engagement, and disturbing interpersonal
American Association for Mental Retardation behavior.
(AAMR) (formerly known as the American The ABS-S: 2 was normed on 2,074 students
Association for Mental Deficiency) has changed with intellectual disabilities and 1,254 of
its name to American Association on Intellec- their peers without intellectual disabilities.
tual and Developmental Disabilities (AAIDD). Administration takes place in an interview for-
Therefore, intellectual disabilities have mat with parents or teachers and may vary from
replaced mental retardation as the terminology 20 min to 2 h. Scoring is completed by hand.
AAMD Adaptive Behavior Scales 3

Raw scores are converted into percentiles, stan- was also first published in 1969 by Nihira, Fos-
dard scores, and age equivalents for each sub- ter, Shellhaas, and Leland. It was revised in
domain. Five factors can be derived: personal 1974, and again in 1993. The goals of the revi- A
self-sufficiency, community self-sufficiency, sions were to improve the reliability of the inter-
personal social responsibility, social adjust- viewer in differentiating between individuals
ment, and personal adjustment. Percentiles, fac- with intellectual disabilities who are institution-
tor standard scores, and age equivalents are then alized and those living in the community. Previ-
reported based on factor scores. ously, these individuals had been classified at
The ABS-RC: 2 is also useful for the assess- different adaptive behavior levels according to
ment of personal development and social behav- the AAIDD.
ior in individuals with intellectual disabilities,
but it has been developed for individuals aged
18–79. Like the ABS-S: 2, the assessment has Psychometric Data
two parts, but there are more subscales in each
part. The first part has ten subscales: indepen- The authors of the ABS-S: 2 report three types of
dent functioning, physical development, eco- reliability: internal consistency, stability, and
nomic activity, language development, interscorer. Internal consistency is reported to
numbers and time, domestic activity, prevoca- range from 0.79 to 0.98, while measures of stabil-
tional/vocational activity, self-direction, respon- ity range from 0.82 to 0.97. For Part I, interscorer
sibility, and socialization. The second part reliability ranges from 0.95 to 0.98 whereas it is
contains eight subscales: social behavior, con- 0.96–0.99 for Part II. Authors report criterion
formity, trustworthiness, stereotyped and hyper- validity in Part 1 moderately correlated with the
active behavior, sexual behavior, self-abusive ABS and the Vineland Adaptive Behavior Scales,
behavior, social engagement, and disturbing although Part II was not significantly related to
interpersonal behavior. The ABS-RC: 2 was either (Lyman 2007).
normed on a sample of 4,000 adults with intel- The ABS-RC: 2 reports an internal consis-
lectual disabilities, and administration times tency ranging from 0.81 to 0.97. Concerning
vary between 15 and 40 min, depending on the discriminant validity, adaptive behavior as mea-
informant’s knowledge of the individual being sured in Part II was not related to the Vineland
assessed. Raw scores are recorded and then Adaptive Behavior Scale and Adaptive Behavior
converted to standard scores and percentiles. Inventory (ABI), other measures of maladaptive
The subscales yield the same five-factor scales behaviors.
as the ABS-S: 2.

Clinical Uses
Historical Background
The ABS: 2 assesses the status of individuals with
The AAMD first published the ABS in 1969 in intellectual disability, emotional maladjustment,
response to the definition of mental retardation autism, or developmental disability. It enables a
that was amended in 1959 to include adaptive professional to evaluate strengths and weaknesses
behavior. The ABS-S: 2, first published in 1969 of an individual in adaptive areas, document pro-
by Nihira, Foster, Shellhaas, and Leland, was gress, and measure the effectiveness of interven-
revised and standardized in 1974 by Lambert, tion/school programs. The manual cautions that
Windmiller, and Cole and again in 1981 by Lam- the examiner should interview a significant infor-
bert and Windmiller. The second and current mant or administer the instrument to that signifi-
edition was published in 1993. The ABS-RC:2 cant informant. If an informant is unable to
4 Abasia

provide needed information, then another informant

needs to be interviewed. Whereas the ABS is a Abasia
standard assessment used in determining adaptive
and maladaptive behavior, its psychometric proper- Douglas I. Katz
ties are limited, especially compared to other mea- Department of Neurology, Boston University
sures such as the Vineland Adaptive Behavior School of Medicine, Braintree, MA, USA
Scales.
Whereas a strength of the ABS-S: 2 is that it
was normed on students with and without intel- Definition
lectual disabilities, the ABS-RC: 2’s standard
scores and percentile ranks were not compared This refers to an inability to walk. Abasia may be
to individuals without intellectual disabilities. caused by a variety of conditions including weak-
Another weakness is that it has not been renormed ness, spasticity, cerebellar incoordination, and
in two decades. movement disorders of various types.
Therefore, assessment may not meet criteria
for a diagnosis of mental retardation according
to the AAMR requirements. Cross-References

▶ Ataxia
▶ Spastic Gait
Cross-References

▶ Adaptive Behavior Assessment System: Third

Edition
▶ Vineland Adaptive Behavior Scales
Abbreviated Injury Scale

Edison Wong1 and Richard Kunz2

References and Readings 1
Center for Pain and Medical Rehabilitation,
Aiken, L. (1996). Assessment of intellectual functioning. Fitchburg, MA, USA
2
Basel: Burkhauser. Department of Physical Medicine and
Balboni, G., Tasse, M., Schalock, R., Borthwick-Duffy, S., Rehabilitation, Virginia Commonwealth
Spreat, S., Thissen, D., Widaman, K., Zhang, D., &
University, Richmond, VA, USA
Navas, P. (2014). The diagnostic adaptive behavior
scale: Evaluating its diagnostic sensitivity and specific-
ity. Research in Developmental Disabilities, 35,
2884–2893. Synonyms
Bracken, B., & Nagle, R. (2007). Psychoeducational
assessment of preschool children. New York:
Routledge. Organ injury scale
Hogg, J., & Langa, A. (2005). Assessing adults with intel-
lectual disabilities. Malden: Blackwell.
Lyman, W. C. (2007). Test Review:Lambert, N., Nihira,
K., &Lel, H. (1993), AAMR Adaptive Behavior
Definition
Scales: School (ABS-S:2) Assessment for Effective
Intervention, 33(1), 55–57. The Abbreviated Injury Scale (AIS) is an anatom-
Reynolds, C., & Fletcher-Janzen, E. (2014). Encyclopedia ical scoring system first introduced in 1969. It has
of special education, a reference for the education of
been revised and updated against survival data so
children, adolescents, and adults with disabilities and
other exceptional individuals (Vol. 3, 4th ed.). Hobo- that it now provides a reasonably accurate way of
ken: Wiley. ranking the severity of injury.
Ablation 5

Abbreviated Injury Scale, Table 1 AIS scores and their Greenspan, L., McClellan, B. A., & Greig, H. (1985).
definition of injury severity Abbreviated injury scale and injury severity score:
A scoring chart. The Journal of Trauma, 25, 60–64.
AIS score Injury
Peitzman, A. B., Rhodes, M., Schwab, C. W., Yealy, D. M., A
1 Minor & Fabian, T. C. (2002). The trauma manual (pp. 29–30).
2 Moderate Hagerstown: Lippincott Williams & Wilkins.
3 Serious Yentis, S. M., Hirsch, N. P., & Smith, G. B. (2004). Anaes-
4 Severe thesia and intensive care A–Z. New York: Butterworth
& Heinemann.
5 Critical
6 Unsurvivable

Injuries are ranked on a scale of 1–6, with 1 being Ablation

minor, 5 severe, and 6 representing an unsurvivable
injury (Table 1). This represents the “threat to life” Edison Wong1 and Richard Kunz2
associated with an injury and is not meant to repre- 1
Center for Pain and Medical Rehabilitation,
sent a comprehensive measure of severity. An addi- Fitchburg, MA, USA
tional code of AIS9 is used to indicate an injury for 2
Department of Physical Medicine and
which more detailed coding is not possible due to Rehabilitation, Virginia Commonwealth
lack of information. The AIS is not a linear scale, in University, Richmond, VA, USA
that the difference between AIS1 and AIS2 is not
the same as that between AIS4 and AIS5. Organ
Injury Scales of the American Association for the Synonyms
Surgery of Trauma are mapped to the AIS score for
calculation of the Injury Severity Score. Resection

Current Knowledge Definition

The latest incarnation of the AIS score is the 2008 Ablation is the removal or destruction of an ana-
update. AIS is monitored by a scaling committee of tomical structure by means of surgery, disease, or
the Association for the Advancement of Automo- other physical or energetic process. Ablation can be
tive Medicine and has been adopted by the Amer- performed on any tissue (e.g., cardiac, neurologic,
ican Association for the Surgery of Trauma since or endometrium). Ablation is employed as a treat-
its publication in the Journal of Trauma in 1985. ment of various medical conditions and includes
recent advances in technology. Surgical ablation of
neuronal pathways to the globus pallidus or thala-
References and Readings mus has been used historically to treat Parkinson-
ism. Interventional pain experts use radiofrequency
Copes, W. S., Sacco, W. J., Champion, H. R., & Bain, L. W. ablation of nerves in the spine to treat chronic back
(1989). Progress in characterizing anatomic injury. In
Proceedings of the 33rd Annual Meeting of the Associ-
pain. Gamma radiation or “gamma knife surgery”
ation for the Advancement of Automotive Medicine is used to excise brain tumors when traditional
(pp. 205–218), Baltimore, 2–4 Oct 1989. surgical ablation is too destructive to neighboring
Gennarelli, T. A., Wodzin, E., & Association for the tissues. Even with sophisticated neurosurgical
Advancement of Automotive Medicine. (2008). The
abbreviated injury scale 2005. Update 2008. Des
techniques, ablation of any type in the central ner-
Plaines: American Association for Automotive Medi- vous system may still produce unwanted motor,
cine (AAAM). sensory, or cognitive-behavioral impairments.
6 Absence Epilepsy

Cross-References Definition

▶ Commissurotomy Childhood and juvenile absence epilepsy are

▶ Craniotomy forms of idiopathic (genetic) generalized epilepsy
▶ Gamma Knife that are characterized by seizures that involve
▶ Hemispherectomy sudden arrest in activity, awareness, and respon-
▶ Lobectomy siveness, and may include some mild motor fea-
▶ Pallidotomy tures. Typical absence seizures usually last less
▶ Prefrontal Lobotomy than 20 s and end as abruptly as they start. Patients
▶ Radiosurgery, Stereotactic Radiosurgery have no recollection of the event and often return
▶ Temporal Lobectomy immediately to their previous activity with little or
no postictal alterations in functioning. General-
ized 3 Hz spike-and-wave discharges on EEG
References and Readings are required for the diagnosis and are strongly
correlated with the clinical events.
Ansari, S. A., Nachanakian, A., & Biary, N. M. (2003).
Current surgical treatment of Parkinson’s disease. Neu-
roscience, 8(1), 3–7. Categorization
Lord, S. M., & Bogduk, N. (2002). Radiofrequency pro-
cedures in chronic pain. Best Practice & Research.
Clinical Anaesthesiology, 16, 597–617.
Childhood absence epilepsy (CAE)
Lunsford, L. D., Flickinger, J. C., & Steiner, L. (1988). The Juvenile absence epilepsy (JAE)
gamma knife. JAMA, 259, 2544.
Shah, R. V., Ericksen, J. J., & Lacerte, M. (2003). Inter-
ventions in chronic pain management. 2. New frontiers: Epidemiology
Invasive nonsurgical interventions. Archives of Physi-
cal Medicine and Rehabilitation, 84, S39–S44. The incidence of CAE is estimated at 6–8% per
100,000 in children younger than 15 years, and
the estimated prevalence is 10–12% in children
younger than 16 years with epilepsy. The inci-
Absence Epilepsy dence of JAE is less clear, but it is accepted as
being less common than CAE. Some estimates
Jeffrey B. Titus1,2, Hayley Loblein3 and suggest that JAE occurs in 10–15% of individuals
Dave Clarke1,4 with epilepsy, though there is likely a pattern of
1
Comprehensive Epilepsy Program, Dell under diagnosis in this condition due to less fre-
Children’s Medical Center of Central Texas, quent seizure and the higher rate of other seizure
Austin, TX, USA types. CAE is typically considered to be more
2
Department of Psychology, The University of common in females, but gender differences in
Texas at Austin, Austin, TX, USA JAE have not been reported.
3
Department of Educational Psychology, The CAE is strongly associated with a family his-
University of Texas at Austin, Austin, TX, USA tory of seizures, and there is robust concordance
4
Department of Pediatrics, Dell Medical School, among identical twins. Siblings of patients with
The University of Texas at Austin, Austin, CAE have about a 10% chance of having seizures,
TX, USA and about one third of patients with CAE have a
family member with epilepsy. Heritability of the
spike-and-wave trait has been found to peak at the
Synonyms age of 10 years and goes away almost completely
by the age of 40. Only about 20% of family
Childhood absence epilepsy; Juvenile absence members with the spike-and-wave trait develop
epilepsy; Petit mal epilepsy epilepsy. Multiple genes likely account for
Absence Epilepsy 7

transmission, but the causal influences are most heavily influenced by psychosocial factors,
believed to be multifactorial, depending on both such as family adjustment, support systems, edu-
genetic and nongenetic factors. Causal factors in cational attitudes, and stigma toward the condi- A
JAE have not been well-studied but may be sim- tion. Cognitive and/or behavioral side effects
ilar to what is found in CAE. from antiepileptic drug (AED) therapy may also
limit outcomes.

Natural History, Prognostic Factors, and

Outcomes Neuropsychology and Psychology of
Absence Epilepsy
Typical age of onset in CAE is between 3 and
10 years, with average age of onset of 6 years. Cognitive functioning in CAE is traditionally con-
Rare cases of onset prior to 3 years of age have sidered “benign” because children typically pre-
been reported. Most cases of JAE are believed to sent with normal intelligence and exhibit no
manifest between 10 and 17 years, and average significant impairments in functional outcomes.
age of onset is 12 or 13 years. Because of vari- However, more recent research has found evi-
ability in onset, there is diagnostic overlap dence that patients with CAE are more prone to
between CAE and JAE, potentially amounting to having cognitive deficits and psychosocial prob-
about 22% of cases with absence seizures. EEG lems, and they are more likely to receive special
and clinical findings are often useful in differenti- education services and display low academic
ating CAE from JAE in older children and youn- achievement. While patients with poor seizure
ger adolescents, and it is highly unusual for a child control exhibit the greatest difficulties, cognitive
with CAE to experience onset of seizures after and behavioral problems are also experienced by
11 years of age. patients with good seizure control. While limited
CAE and JAE are both associated with favor- information is known about cognitive and psy-
able outcomes. Most patients with CAE experi- chological functioning in JAE, some reports sug-
ence remission of seizures by mid-adolescence, gest that about one-third of patients have
with only a small proportion experiencing attention, concentration, or memory problems
absence seizures into adulthood. About 40% of before their diagnosis of JAE. These cognitive
patients with CAE also exhibit generalized tonic- concerns may improve with treatment.
clonic seizures that emerge around the time of Patients with CAE do not have a characteristic
puberty, are relatively easy to control, and more cognitive profile. Cognitive difficulties have been
commonly persist into adulthood than absence reported in multiple domains, including attention,
seizures. Generalized tonic-clonic seizures are executive functioning, memory, and visual-spatial
significantly more common in JAE and occur in processing. A study by Caplan et al. (2008)
about 80% of cases. Some patients with JAE also revealed the presence of subtle cognitive impair-
exhibit myoclonic seizures, but they are typically ments in children with CAE. When compared
mild and infrequent. While most patients with with controls, they found that children with CAE
CAE become seizure-free by adolescence, seizure (ages 6.7–11.2 years) had significantly lower
outcome in JAE is not well known. intelligence, as measured by the Wechsler Intelli-
CAE is considered a benign childhood epi- gence Scale for Children – Revised/Third Edition.
lepsy because of relatively good seizure and func- While, as a group, children with CAE performed
tional outcomes. Seizure control is less common in the average range, they were below the perfor-
in JAE, but functional outcomes may be similar. mance of a control group. Similar differences
Further research is needed to examine this. Tonic- were noted on verbally based and visually based
clonic seizures are believed to be a marker for intellectual tasks. The difference in performance
poorer seizure outcome in both CAE and JAE. IQ was less robust, but still significant, between
Functional outcomes in CAE are thought to be children with CAE and controls. Among their
8 Absence Epilepsy

sample of 69 children with CAE, 27% demon- that it is unclear whether psychological concerns
strated overall intelligence at least one standard in CAE are a consequence of disease related fac-
deviation below the mean. Similar rates were tors or are part of the epileptic syndrome; how-
found for VIQ and PIQ. Their spoken language ever, a recent report by Schwartz and Titus (2015)
quotient (SLQ), as measured by various versions with the BASC-2 suggested that children with
of the Test of Language Development, was aver- CAE may be more predisposed to depression
age, but it was also lower than controls. A high than other epilepsy syndromes.
percentage of children with CAE performed at
least one standard deviation below the mean on
language measures. Evaluation
In the double-blind, randomized controlled
clinical trial conducted by the Childhood Absence Children and adolescents with CAE and JAE typ-
Epilepsy Study Group, 36% of children with CAE ically present with no focal neurological abnor-
had pretreatment attention problems at a rate esti- malities on examination. The presence of absence
mated to be fourfold that of the general population seizures is a defining feature of absence epilepsy,
(Masur et al. 2013). This was despite average and hyperventilation or light stimulation can be
intelligence and otherwise normal neurocognitive highly effective at eliciting an event. In CAE,
functioning. Attention problems were dispropor- absence seizures occur multiple times per day,
tionately higher for children being treated with but, in JAE, seizures are less frequent.
valproic acid. Preferential cognitive deficits in Absence seizures can be either typical or atyp-
executive functioning have been found in multiple ical, and discrimination between the two types is
studies affecting problem solving, planning, and typically accomplished through EEG and clinical
fluency. presentation. While typical absence seizures are
Caplan et al. (2008) confirmed that children characterized by clearly delineated episodes of
with CAE are at higher risk for emotional and activity arrest and impaired consciousness for
behavioral problems. Among the 69 children less than 20 s, atypical absence seizures are asso-
with CAE in their sample, 30% had a diagnosis ciated with less abrupt onset and termination, and
of attention-deficit/hyperactivity disorder they may more commonly involve various semi-
(ADHD), with 52% of those children diagnosed ological phenomena. Atypical absence seizures
as ADHD-inattentive type. Moreover, about 29% are also frequently observed in epilepsy syn-
of their sample were diagnosed with a form of dromes that are characterized by more severely
internalizing psychopathology. Among those chil- impaired neurocognitive functioning, such as
dren, 75% had a diagnosis of anxiety, 20% had a Lennox-Gastaut syndrome. Tonic seizures are
diagnosis of depression, and 5% had both anxiety also frequently present in children with atypical
and depression. After controlling for IQ and absence seizures.
demographic variables, children with CAE were Typical absence seizures can be subdivided
found to have significantly higher ratings on into simple or complex. Simple typical absence
scales of the Child Behavior Checklist (CBCL) seizures constitute about 90% of cases and may
that assess attention problems, somatic problems, involve only minor motor mannerisms (e.g., mild
social problems, withdrawal, and thought prob- eyelid fluttering) and usually last less than 10 s.
lems. The authors discovered that children with Patients with complex typical absence seizures
lower intelligence had greater social problems, display more involvement of motor features,
and females in the CAE sample were almost six such as automatisms or decreased or increased
times more likely to be diagnosed with an anxiety muscle tone.
disorder. In addition, children with CAE were Complex partial seizures can often mimic
more likely to be diagnosed with ADHD or anx- absence seizures, particularly when their expres-
iety if they had more frequent seizures or a longer sion is limited. Typical absence seizures can be
duration of illness. Verrotti et al. (2015) proposed distinguished from complex partial seizures
Absence Epilepsy 9

because they are briefer, more frequent, and have period of 2 years is often recommended prior to
no postictal impairment. EEG characteristics and discontinuation of therapy; however, this should
the presence of various seizure types often distin- be determined on a case-by-case basis. About A
guish atypical absence seizures from complex 40% of children with CAE develop generalized
partial epilepsy. tonic-clonic seizures. Patients with JAE will
When evaluating for the presence of absence require longer treatment and may continue using
seizures, it is important to consider whether the AEDs indefinitely. In adolescent patients, it is
episodes can be accounted for by variations in important to educate about the increased risk of
attention. This is especially important when con- seizures with poor medication compliance, alco-
sidering the high rate of attention problems in hol consumption, or sleep deprivation.
children with epilepsy. Attempting to determine
the degree of responsiveness during the episodes
often helps with making the differential diagnosis; See Also
however, this can be difficult to determine when
episodes are very brief. Moreover, it is not uncom- ▶ Petit Mal Seizure
mon for patients to have both absence seizures and
attention problems. Therefore, a child’s ability to
respond during an episode cannot be used to rule- Absence Epilepsy – CAE and JAE
out the presence of absence seizures. Sometimes a
neuropsychological assessment can be helpful in
differentiating between absence seizures and epi-
sodes of inattention. If the examiner has experience EEG signature Characteristic generalized 3 Hz
spike and slow wave (may slow
with absence seizures, the neuropsychological
to 2.5 Hz during the absence and
assessment can provide multiple hours of one-on- may be faster in JAE).
one observation and interaction that might provide Activated by hyperventilation is
opportunities to observe the episodes and attempt more common than photic
stimulation.
to elicit responses. This can also be helpful if
Age of onset CAE: 3–10 years
mental fatigue tends to elicit more events. JAE: 10–17 years
On EEG, absence seizures are characterized by Clinical features Typical events last 4–20 s.
paroxysmal bursts of high amplitude 2.5–4 Hz Seizure semiology:
spike and slow waves that are superimposed on a (a) Frequent staring spells with
normal background. The bursts vary in length abrupt onset and offset without
aura (fewer seen in JAE).
(3–20 s), and the clinical absence is time-locked Occasional automatic mouth or
to the burst period. This activity (clinical and hand movements or subtle
electrographic) can be provoked during a routine myoclonus.
EEG recording using the hyperventilation activa- (b) Generalized tonic-clonic
seizures are more common in
tion procedure and, infrequently, from photic JAE.
stimulation. MRI is typically normal.
AED management Ethosuximide
Valproic acid or lamotrigine can
Treatment be helpful if generalized tonic-
clonic seizures manifest.
Response to Good
Response to AED therapy in CAE and JAE is treatment with
good, and ethosuximide is considered the drug AEDs
of first choice. Valproic acid or lamotrigine have Seizure freedom CAE: Expected by adolescence
also been recommended. In rare cases of more JAE: Less common
difficult to control seizures, polytherapy may be Functional CAE: Good
outcome JAE: Unknown
needed. In patients with CAE, a seizure-free
10 Absence Seizure

References and Readings generalized seizure caused by a large burst of elec-

trical discharges that begins in broad, bilaterally
Berkovic, S. F., & Benbadis, S. (2001). Childhood and distributed networks simultaneously as opposed to
juvenile absence epilepsy. In E. Wyllie (Ed.), The treat-
a complex partial seizure (focal seizure with altered
ment of epilepsy: Principles and practice (3rd ed., pp.
485–490). Philadelphia: Lippincott Williams & awareness/responsiveness).1 During an absence sei-
Wilkins. zure, the patient will lose interaction with the envi-
Caplan, R., Siddarth, P., Stahl, L., Lanphier, E., Vona, P., ronment, stare blankly (“zone out”), and perhaps
Gurbani, S., et al. (2008). Childhood absence epilepsy:
blink the eyes (eyelid myoclonia) or have sudden
Behavioral, cognitive, and linguistic comorbidities.
Epilepsia, 49(11), 1838–1846. jerks (myoclonic absence). There is no true loss of
Holtkamp, M. (2017). Genetic generalized epilepsies with consciousness or motor functions. The seizure is
adolescent onset. In J. M. Pellock, D. R. Nordli Jr., R. typically short in duration (only several seconds),
Sankar, & J. W. Wheless (Eds.), Pellock’s pediatric
and patients often resume their ongoing activity
epilepsy: Diagnosis and therapy (4th ed., pp.
337–346). without realizing even that they had a seizure (but
Masur, D., Shinnar, S., Cnaan, A., Shinnar, R. C., Clark, P., will be amnestic for anything occurring during the
Wang, J., Weiss, E. F., Hirtz, D. G., Glauser, T. A., & episode). There are no postictal problems after the
Childhood Absence Epilepsy Study Group. (2013).
end of the seizure. Although no first aid is required,
Pretreatment cognitive deficits and treatment effects
on attention in childhood absence epilepsy. Neurology, the patient should be protected from doing anything
81, 1572–1580. dangerous during the episode (e.g., cooking, cross-
Pearl, P. L., & Holmes, G. L. (2017). Childhood absence ing the street), but the episodes are often so brief
epilepsy. In J. M. Pellock, D. R. Nordli Jr., R. Sankar, &
that intervention is difficult.
J. W. Wheless (Eds.), Pellock’s pediatric epilepsy:
Diagnosis and therapy, (4th ed) pp. 309–336).
Schwartz, J. K., & Titus, J. B. (2015). Executive function-
ing and behavioral profiles in childhood absence epi- Current Knowledge
lepsy and juvenile myoclonic epilepsy [Abstract].
Journal of the International Neuropsychological Soci-
ety, 21(s1), 87–88. The cause of absence seizures is unknown.
Verrotti, A., Matricardi, S., Rinaldi, V. E., Prezioso, G., & Patients with typical absence seizures have no
Coppola, G. (2015). Neuropsychological impairment positive neuroimaging findings but usually have
in childhood absence epilepsy: Review of the literature.
bursts of 3-per-second bilaterally synchronous
Journal of the Neurological Sciences, 359(1–2), 59–66.
spike/wave epileptiform activity on a routine
EEG (even when not having a seizure). Atypical
absence seizures can have a slightly different fre-
quency or pattern. Absence seizures can be differ-
Absence Seizure entiated clinically from complex partial seizures
(focal seizures with altered awareness/responsive-
Kenneth R. Perrine ness), in which there is a similar disruption of
Neurological Surgery, Weill Cornell Medicine, consciousness and “zoning out,” by the duration
New York, NY, USA of the episode. Absence seizures last only a few
seconds, while complex partial seizures usually
last 1–1.5 min. Absence seizures typically begin
Synonyms in childhood, respond well to medication, and
often remit spontaneously by adulthood. Com-
Petit mal seizure; Psychomotor seizures mon medications for absence seizures include
divalproex/valproate sodium (Depakote),

Definition 1
The International League Against Epilepsy suggested new
terminology for seizure types (Berg et al. 2010). These new
An absence (usually pronounced with a French terms have not yet been fully adopted but are given in
accent as “ab-SAWNS”) seizure is a type of parentheses.
Abstract Reasoning 11

ethosuximide (Zarontin), and lamotrigine Definition

(Lamictal). Although the frequency of absence
seizures can approach dozens per day, only mild The absolute threshold is the smallest amount of A
(at worst) neuropsychological deficits are typi- stimulus energy necessary to produce a sensation
cally shown if the absence episodes occur without of the stimulus. The idea that a mental event has to
other seizure types. They do not have a dramatic exceed some critical amount is central to the con-
impact on academic performance. However, cept of a sensory threshold. The absolute thresh-
absence seizures may occur with other seizure old refers to the measurement of that critical
types in serious disorders such as Lennox-Gastaut amount.
syndrome, in which case there is considerable
cognitive dysfunction and a worse prognosis.
See Also

▶ Just Noticeable Difference

Cross-References

▶ Complex Partial Seizure

References and Readings
▶ Epilepsy
▶ Seizure Gescheider, G. A. (1997). Psychophysics: The fundamen-
tals (3rd ed.). London: Erlbaum, Chapter 1.

References and Readings

Berg, A. T., Berkovic, S. F., Brodie, M. J., Buchhalter, J., Abstract Reasoning
Cross, J. H., van Emde, B. W., Engel, J., French, J.,
Glauser, T. A., Mathern, G. W., Moshe, S. L., Nordli,
D., Plouin, P., & Scheffer, I. E. (2010). Revised termi- David Hulac
nology and concepts for organization of seizures and Department of School Psychology, College of
epilepsies: Report of the ILAE Commission on Classi- Education and Behavioral Sciences, University of
fication and Terminology, 2005–2009. Epilepsia,
51(4), 676–685.
Northern Colorado, Greeley, CO, USA
www.epilepsyfoundation.org
www.ilae.org
Wyllie, E. (Ed.). (2015). Wyllie’s treatment of epilepsy: Synonyms
Principles and practice (6th ed.). New York: Lippincott
Williams & Wilkins.
Logical reasoning

Definition
Absolute Threshold
The neuropsychological construct of abstract rea-
Mark Mennemeier soning refers to an individual’s ability to recog-
Neurobiology and Developmental Sciences, nize patterns and relationships of theoretical or
University of Arkansas for Medical Sciences, intangible ideas. Abstract reasoning is contrary
Little Rock, AR, USA to concrete reasoning whereby an individual rec-
ognizes patterns in information obtained through
the immediate senses. When thinking abstractly,
Synonyms an individual must be able to identify rules and
apply those rules to information without the aid of
Stimulus threshold empirical help or personal experience.
12 Abulia

Abstract reasoning is most closely related to

rational thought as opposed to empirical thought. Abulia
While using deductive reasoning, a purely rational
thinker does not look to determine the accuracy of Irene Piryatinsky
a premise, but seeks only to understand the rela- Butler Hospital and Alpert Medical School of
tionship between the premises. Brown University, Providence, RI, USA
An example of deductive reasoning, which
requires abstract reasoning, may go like this:
Synonyms
1. Premise 1: Egypt is located in South America.
2. Premise 2: The Sphinx lies in Egypt. Apathy; Athymia; Loss of psychic self-activation;
3. Conclusion: The Sphinx is located in South Psychic akinesia
America. Also spelled Aboulia

Empirically and concretely, it is obvious that

Egypt is not in South America, but in Africa. To Definition
complete the syllogism, however, the thinker must
ignore the concrete distortion and instead focus on The term is derived from the Greek “boul”
the two premises and understand if the conclusion (will). Abulia is manifested by lack of motiva-
logically flows. tion; lack of spontaneity in speech and action;
Common measures of abstract intelligence deficiency in initiation, inertia, mental, and
include the similarities, picture concepts, and motor slowness; poor attention; and easy dis-
matrix reasoning subtests of the Wechsler scales. tractibility. Inactivity comes from an inability
During a mental status exam, abstract reasoning to select a course of action, although a wish to
is measured by asking a subject to describe the participate may be present. Some research indi-
meanings of proverbs or to describe word cates that abulia occurs due to malfunction of
similarities. the brain’s dopamine-dependent circuitry. In
Abstract reasoning, most commonly under- neurologic diseases, it is associated with bilat-
stood as being a function of the frontal lobes of eral lesions in the medial or orbital frontal lobes.
the brain, is a precursor for using and under- The following criteria have been suggested for
standing language and mathematics. Individuals the diagnosis of abulia: (i) decreased spontane-
who struggle with abstract reasoning benefit ity in activity and speech; (ii) prolonged latency
when an instructor uses examples to make the in responding to queries, directions, and other
concept more concrete or observable. Fre- stimuli; and (iii) reduced ability to persist with
quently, children with learning disabilities have a task.
difficulty with these abstract concepts, but
achieve greater success in courses with more
concrete subject matter such as social studies Further Reading
and science.
Berrios, G. E., & Grli, M. (1995). Abulia and impulsive-
ness revisited: A conceptual history. Acta Psychiatrica
Scandinavica, 92(3), 161–167.
References and Readings Caplan, L. R., Schmahmann, J. D., Kase, C. S., Feldmann,
E., Baquis, G., Greenberg, J. P., et al. (1990). Caudate
Goldstein, G. (2004). Abstract reasoning and problem infarcts. Archives of Neurology, 47(2), 133–143.
solving in adults. In M. Hersen (Ed.), Comprehensive Drubach, D. A., Zeilig, G., Perez, J., Peralta, L., & Makley,
handbook of psychological assessment, Intellectual M. (1995). Treatment of abulia with carbidopa/
and neuropsychological assessment (Vol. 1, levadopa. Journal of Neuroengineering and Rehabili-
pp. 293–308). Hoboken: Wiley. tation, 9, 151–155.
Abusive Head Trauma 13

Egnelborghs, S., Marien, M. A., Pickut, B. A., Verstraeten, movement, acceleration and deceleration
M. A., & De Deyn, P. P. (2000). Loss of psychic self- changes, of the brain within the cranial vault of a
activation after paramedian bithalamic infarction.
Stroke, 31, 1762–1765. small child result in significant neural trauma. The A
Forstl, H., & Sahakian, B. A. (1991). A psychiatric presentation National Center for Injury Prevention and Control
of abulia: Three cases of frontal lobe ischaemia and atro- defines pediatric abusive head trauma as “an
phy. Journal of the Royal Society of Medicine, 84, 89–91. injury to the skull or intracranial contents of an
Kumral, E., Evyapan, D., & Balkir, K. (1999). Acute
caudate vascular lesions. Stroke, 30, 100–108. infant or young child (<5 years of age) due to
Laplande, D., Attal, N., Sauron, B., de Billy, A., & Dubois, inflicted blunt impact and/or violent shaking.”
B. (1992). Lesions of the basal ganglia due to disulfi- This definition excludes unintentional injuries
ram neurotoxicity. Journal of Neurology, Neurosur- and penetrating trauma (Parks et al. 2012).
gery, and Psychiatry, 55, 925–929.
Liddle, P. F. (1987). The symptoms of chronic schizophre-
nia. British Journal of Psychiatry, 151, 145–151.
Litvan, I., Paulsen, J. S., Mega, M. S., & Cummings, J. L. Categorization
(1998). Neuropsychiatric assessment of patients with
hyperkinetic and hypokinetic movement disorders.
Archives of Neurology, 55, 1313–1319. A form of child maltreatment or abuse, AHT
Powell, J. H., Al-Adawi, S., Morgan, J., & Greenwood, R. J. occurs as a result of a baby’s weak neck muscles
(1996). Motivation deficits after brain injury: Effects of in relation to its proportionally large head being
bromocriptine in 11 patients. Journal of Neurology, Neu- unable to compensate for rapid shaking, acceler-
rosurgery, and Psychiatry, 60, 416–421.
ating and decelerating velocity changes, and/or
impact to the head. While the injury itself can
present with a wide variety of clinical sequela,
the mechanism behind the injury is more exten-
Abusive Head Trauma sive force than noted in accidental or neglectful
events and different from penetrating injuries. The
Jennifer Ann Niskala Apps1 and most common injuries related to AHT include
Amy Heffelfinger2 subdural hematomas and retinal hemorrhage,
1
Department of Psychiatry and Behavioral with additional physical injuries such as fractures,
Medicine, Children’s Hospital of Wisconsin/ signs of impact, and spinal injuries noted
Medical College of Wisconsin, Milwaukee, (Nadarasa et al. 2014).
WI, USA
2
Medical College of Wisconsin, Milwaukee,
WI, USA Epidemiology

Determination of frequency, morbidity, and mor-

Synonyms tality is difficult because oftentimes no clear, vis-
ible injury occurs. In addition, given the abusive
Inflicted childhood neurotrauma; Nonaccidental nature of the injury, significant motives to avoid
or inflicted traumatic brain injury; Pediatric abu- detection often make investigating possible cases
sive head trauma; Shaken baby syndrome of AHT difficult. AHT likely occurs most often in
children under 2 years of age, but can occur
through 5 years of age. AHT can occur in the
Short Description or Definition context of additional abusive injuries, either cur-
rent or historical. Among cases of nonaccidental
Pediatric abusive head trauma (AHT) is a form of pediatric trauma, more than half of deaths are a
inflicted traumatic brain injury in an infant or result of AHT (Ross and Juarez 2014). Many
small child due to blunt trauma, being shaken, or children had prior additional abusive injuries or
a combination of both. Rapid rotation and nonspecific signs in the past of head trauma such
14 Abusive Head Trauma

that those nonfatal, non-life-threatening inci- to leave the baby in a safe place and walk away.
dences were not detected. Overall mortality is Unlike other forms of abuse, risk for AHT cuts
estimated to range up to almost 40%, with upward across all social classes, races, and gender
of 60% of infants who have been shaken dying or although recent studies indicate that it may be
experiencing profound long-term medical and more prevalent for babies in lower socioeconomic
cognitive consequences (www.dontshake.org). homes. Known risk factors of AHT include male
Incidence, according to research, is estimated to sex (Keenan et al. 2003), age under 1 year
be as many as 39.8 per 100,000 in children under (Keenan et al. 2003), having a young mother
1 year of age, with rates decreasing sharply as (Overpeck et al. 1998), having parents with low
children age (Niederkrotenthaler et al. 2013). socioeconomic status (Christian and Block 2009),
and some studies indicate a higher risk for racial/
ethnic minorities (Bennett et al. 2006; Drake et al.
Natural History, Prognostic Factors, and 2011). However, research on prevalence of risk
Outcomes factors related to race or socioeconomic status is
unclear and extremely variable, with possible
In the early 1970s, the term “whiplash shaken reporting issues related to these same factors.
baby syndrome” was used to describe symptoms Therefore, many authors urge caution when
consistent with AHT, which had been identified interpreting overall risk factors (Niederkro-
over two decades prior (Caffey 1974). Over the tenthaler et al. 2013).
last four decades, debate has centered on the Outcomes for children experiencing AHT are
methods for standardizing the diagnosis of extremely variable and relate to the amount of
AHT, as well as the implications of various damage inflicted and interventions received.
nomenclature to describe the trauma. Identifica- More subtle signs of neurotrauma after injury
tion of AHT generally includes neurological dys- can be mistaken for flu-like symptoms or other
function (i.e., apnea), subdural hemorrhage, and common presentations of childhood (i.e., colic),
retinal hemorrhage. As there are other possible and in some cases when a child is shaken into a
causes for this triad that does not include inflicted comatose state, the caretaker may believe that
trauma, it is difficult to correctly identify and to the child has gone to sleep or finally stopped
convict the suspected perpetrator of committing crying. Such complicating factors may result in
abuse. Formal definitions and nomenclature for significant delays before a child is brought for
AHT have been developed in order to drive diag- medical attention and lead to significant mortal-
nostic classifications. The CDC currently defines ity rates. Children who survive AHT may expe-
pediatric abusive head trauma “as an injury to the rience blindness if they have had retinal
skull or intracranial contents of an infant or young hemorrhaging, as well as significant long-term
child (<5 years of age) due to inflicted blunt neurological conditions such as mental retarda-
impact and/or violent shaking” (Parks et al. tion, seizure disorders, muscular spasticity or
2012). This definition excludes unintentional cerebral palsy, and structural abnormalities
injuries, such as from lack of supervision and such as microcephaly, hydrocephaly, cerebral
any penetrating trauma. Research has indicated atrophy, or encephalomalacia as a direct result
that medical signs such as the presence of intra- of neural trauma.
cranial injuries in coordination with a lack of
specific signs of impact assist in differentiating
between inflicted versus accidental trauma Neural System Damage and
(Vinchon et al. 2009). Neuropsychology Outcomes of AHT
Educational campaigns help new parents
expect intense crying, to recognize frustration Symptoms of AHT vary with the severity of
that is theorized to lead to abusive shaking, and the inflicted neural trauma. The neural injury
Abusive Head Trauma 15

typically includes acceleration injury during cardiorespiratory functioning or consciousness

shaking and deceleration when the shaking is and resulting in more frequent bilateral and ische-
stopped or the child is slammed or thrown into mic injuries and lower developmental scores post- A
an object. Recent research indicate differences injury (Hymel et al. 2007).
between AHT and accidental injury on retinal
hemorrhages, suggesting AHT causes diffuse,
multilayered hemorrhages, and additional Evaluation
research suggests AHT results in increased intra-
cranial pressure, brain swelling, as well as pos- Diagnosis of AHT requires extensive medical
sible rupture of bridging veins, often found in evaluations including radiology studies as well
coordination with spinal injuries (Nadarasa et al. as sociological evaluations of the caregivers.
2014). Subdural hemorrhage and subarachnoid Evidence of additional physical injuries indica-
hemorrhage are most often bilateral. Further, tive of abuse on the child should be documented.
neuronal injury occurs with resultant cerebral The presence or absence of retinal hemorrhages
edema. Additional pathology often includes should be evaluated by a pediatric ophthalmolo-
spine and neck injuries, rib fractures, and frac- gist or neurologist. Laboratory values can indi-
tures to the long bones of the infant (particularly, cate the presence of blood in the cerebral spinal
if they have been held by an appendage while fluid, coagulation changes following cerebral
shaken). As a result of neurological pathology, injury, and possible pancreas and liver damage.
immediate observable symptoms can include X-ray can reveal rib injuries. Most significantly,
lethargy, irritability, a high-pitched cry, poor CT scan is the primary method of evaluation for
sucking and feeding, problems breathing, a brain injury. Consecutive CT scans can reveal
blue or pale pallor, vomiting, and seizures. Lit- ongoing changes in a recently injured child as
erature suggests that apnea and severe retinal well as the evidence of older brain injuries. Uti-
hemorrhages are strongest indicators of AHT. lizing MRI as an adjunct in longer-term diagno-
Of those who survive, approximately two thirds sis can reveal more subtle white matter changes
are either moderately or severely impaired related to injury.
(Narang and Clarke 2014). Long-term outcomes
of these injuries are difficult to study and quan-
tify in a rigorous manner. Therefore, most Treatment
descriptions of AHT are based on the case stud-
ies, indicating that children who survive are Treatment of AHT most often involves life-saving
more severely impaired as they experience measures initially, including neurosurgery to
more severe injuries, including lacerations of address active bleeding and excessive intracranial
brain tissue, excessively elevated intracranial pressure. Medical life support may be required for
pressure, infarcts, and hemorrhage. A study of some time while swelling subsides. Long-term
a small number of children with inflicted head treatment of AHT involves addressing the most
trauma that were followed postinjury indicated salient of the resulting neurobiological symptoms.
over half experienced significant cognitive Children with more significant injuries often
impairments, as well as language delays (Barlow begin rehabilitation therapies immediately, much
et al. 2005). Limited research indicates that com- like other children who experience accidental
parisons to children experiencing nonabusive brain injuries. Neuropsychological evaluations
or accidental head trauma indicate far greater across development are often useful to detect
incidences of long-term cognitive impairments specific cognitive, functional, or educational
(Ewing-Cobbs et al. 1998). Those with AHT more impairments, with the most common believed to
likely experienced deeper, more extensive cortical be attention, executive, and visual perceptual
injury, more often resulting in impairments in deficits.
16 Academic Competency

Cross-References
Academic Competency
▶ Cerebral Edema
▶ Subarachnoid Hemorrhage Kristy K. Kelly
▶ Traumatic Brain Injury (TBI) Educational Psychology, University of
Wisconsin-Madison, Madison, WI, USA

References and Readings

Synonyms
Barlow, K. M., Thomson, E., Johnson, D., & Minns, R. A.
(2005). Late neurologic and cognitive sequelae of Academic ability; Academic performance; Edu-
inflicted traumatic brain injury in infancy. Pediatrics, cational productivity
116, 174–185.
Caffey, J. (1974). The whiplash-shaken infant syndrome:
Manual shaking by the extremities with whiplash- Definition
induced intra cranial and intra ocular bleeding, linked
with residual permanent damage and mental retarda-
tion. Pediatrics, 54(4), 396–403. Academic competency is the multidimensional
Ewing-Cobbs, L., Kramer, L., Prasad, M., Canales, D. N., characteristics of a learner – including skills, atti-
Louis, P. T., Fletcher, J. M., Vollero, H., Landry, S. H., tudes, and behaviors – that factor into their aca-
& Cheung, K. (1998). Neuroimaging, physical, and
developmental findings after inflicted and noninflicted
demic success. These characteristics can be
traumatic brain injury in young children. Pediatrics, separated and considered in one of two primary
102(2), 300–307. domains: academic skills or academic enablers
Hymel, K. P., Makoroff, K. L., Laskey, A. L., Conaway, M. (DiPerna and Elliot 2000; Elliot and DiPerna
R., & Blackman, J. A. (2007). Mechanisms, clinical
presentations, injuries, and outcomes from inflicted
2002). Academic skills are both the basic and
versus noninflicted head trauma during infancy: complex skills (e.g., reading, writing, calculating,
Results of a prospective, multicentered, comparative and critical thinking) needed to access and interact
study. Pediatrics, 119, 922–929. with content-specific knowledge. Academic
Lopes, N. R. L., Eisenstein, E., & Williams, L. C. A.
(2013). Abusive head trauma in children: A literature
enablers, however, are the attitudes and behaviors
review. Journal de Pediatria, 89, 426–433. (e.g., interpersonal skills, motivation, study skills,
Nadarasa, J., Deck, C., Meyer, F., Willinger, R., & Raul, J. and engagement) that a learner needs in order to
S. (2014). Update on injury mechanisms in abusive take advantage of education.
head trauma – Shaken baby syndrome. Pediatric Radi-
ology, 44(Suppl 4), S565–S570.
Research indicates that prior achievement and
Narang, S., & Clarke, J. (2014). Abusive head trauma: interpersonal skills influence motivation, thereby
Past, present, and future. Journal of Child Neurology, impacting study skills and engagement (e.g., time
29(12), 1747–1756. on task), which are skills positively associated
National Institutes of Health, National Institute of Neuro-
logical Disorder & Stroke NINDS Shaken Baby Syn-
with achievement (DiPerna et al. 2002, 2005).
drome Information page. www.ninds.nih.gov/
disorders/shakenbaby
Niederkrotenthaler, T., Xu, L., Parks, S. E., & Sugerman, Cross-References
D. E. (2013). Descriptive factors of abusive head
trauma in young children – United States, 2000–2009.
Child Abuse & Neglect, 37, 446–455. ▶ Academic Skills
Parks, S. E., Annest, J. L., Hill, H. A., & Karch, D. L. ▶ Learning
(2012). Pediatric abusive head trauma: Recommended
definitions for public health surveillance and research.
Atlanta: Centers for Disease Control and Prevention.
Ross, A. H., & Juarez, C. A. (2014). A brief history of fatal References and Readings
child maltreatment and neglect. Forensic Science, Med-
icine, and Pathology, 10, 413–422. DiPerna, J. C., & Elliot, S. N. (2000). The academic com-
Shaken Baby Association, Inc. www.shakenbaby.net petence evaluation scales (ACES college). San
The National Center on SBS. www.dontshake.org Antonio: The Psychological Association.
Academic Skills 17

DiPerna, J. C., Volpe, R. J., & Elliott, S. N. (2002). semantic maturity or vocabulary use, organization
A model of academic enablers and elementary read- of thought or content, and conventions (including
ing/language arts achievement. School Psychology
Review, 31(3), 298–312. grammar, spelling, and punctuation) (Howell and A
DiPerna, J. C., Volpe, R. J., & Elliott, S. N. (2005). Nolet 2000). Math skills include the general skills
A model of academic enablers and and mathematics of basic fact fluency (i.e., addition, subtraction,
achievement in the elementary grades. Journal of multiplication, division), math computation and
School Psychology, 43(5), 379–392.
Edl, H. M., Jones, M. H., & Estell, D. B. (2008). Ethnicity operations (e.g., multi-digit addition, fractions),
and english proficiency: Teacher perceptions of aca- and math application/problem-solving. Math skills
demic and interpersonal competence in European can further be categorized by the ten common core
American and Latino students. School Psychology math standards: counting and cardinality, opera-
Review, 37(1), 38–45.
Elliot, S. N., & DiPerna, J. C. (2002). Assessing the aca- tions and algebraic thinking, numbers and opera-
demic competence of college students: Validation of a tions in base 10, numbers and operations-fractions,
self-report measure of skills and enablers. Journal of measurement and data, geometry, ratios and propor-
Postsecondary Education and Disability, 15(2), 87–100. tional relationships, the number system, expression
Hutto, L. (2009). Measuring academic competence in col-
lege students: A review of research and instruments. and equations, functions, and statistics and proba-
Saarbrücken: VDM Verlag. bility (Common Core Standards Initiative 2016).
Ma, L., Phelps, E., Lerner, J. V., & Lerner, R. M. (2009). These three academic skills of reading, writing,
Academic competence for adolescents who bully and and math allow for the acquisition of other content
who are bullied. Journal of Early Adolescence, 29(6),
862–897. area school subjects. For example, social studies
Shapiro, E. S. (2008). From research to practice: Promot- and history require reading and writing, while sci-
ing academic competence for underserved students. ence and technology require math and reading (and
School Psychology Review, 37(1), 46–51. often writing). These academic skills are differenti-
ated from academic enabler skills, which enable the
acquisition of academic skills and include motiva-
Academic Skills tion, interpersonal skills, engagement, and study
skills (DiPerna et al. 2001).
Christina Zafiris1 and Rachel Losoff2
1
Applied Psychology and Counselor Education,
University of Northern Colorado, Greeley, CO, Cross-References
USA
2
School Psychology, The Chicago School of ▶ Academic Competency
Professional Psychology, Chicago, IL, USA ▶ Educational Testing
▶ Learning
▶ Reading
Definition

Academic skills refer to a student’s ability to per- References and Readings

form age-appropriate school activities related to
reading, writing, and mathematics. Reading skills Common Core State Standards Initiative. (2016). Common
include the five building blocks skills of phonemic core state standards for mathematics. Retrieved from
awareness, phonics, fluency, vocabulary, and com- http://www.corestandards.org/Math/
DiPerna, J. C., Volpe, R. J., & Elliot, S. N. (2001). A model of
prehension. These are listed in hierarchical order, as academic enablers and elementary reading/language art
the ultimate goal is comprehending whatever one achievement. School Psychology Review, 31(3), 298–312.
reads (National Reading Panel 2015). Writing Howell, K. W., & Nolet, V. (2000). Curriculum-based
skills begin with the basic skill of letter formation evaluation: Teaching and decision making (3rd ed.).
Belmont: Wadsworth.
and progress to the more advanced skills of fluency National Reading Panel. (2015, March 17). National Read-
(production of simple sentences), syntactic maturity ing Panel. Retrieved from https://www.nichd.nih.gov/
(production of increasingly complex sentences), research/supported/Pages/nrp.aspx
18 Academic Techniques

such as those with acquired brain injury, could

Academic Techniques benefit from strategies that are aimed at improving
encoding and retrieval (Wilson 2009). Thus,
Ginger Mills while academic techniques, and the models that
Graduate Institute of Professional Psychology, use them, are varied and diverse, they were devel-
University of Hartford, West Hartford, CT, USA oped to facilitate learning and in turn improve
functioning in individuals with cognitive
impairments.
Definition

Academic techniques are a set of rehabilitation Rationale or Underlying Theory

strategies that are aimed at facilitating learning.
While there are a myriad of techniques available Acquiring new information and skills is an
to aid in learning, evidence continues to grow for important part of recovery for individuals with
the effectiveness of specific instructional strate- cognitive impairment. It is through learning that
gies. These strategies assist individuals with cog- individuals are able to remediate and/or compen-
nitive impairments in learning new information sate for impairments and improve their daily
and skills. Various models for improving learning functioning. The underlying theory behind sev-
and memory have been developed, some of which eral rehabilitation strategies geared at improving
include TEACH-M (Task Analysis, Errorless learning and memory is to structure the input of
learning, Assessment, Cumulative review, High information in a way that aids learning, and in
rates of correct practice, Metacognitive strate- turn memory (Ehlhardt et al. 2008). For some
gies); PQRST (Preview, Question, Read, State, more extensive models, such as the PNI, hierar-
and Test); and the pediatric neurocognitive inter- chal levels are designed so that higher-level skills
vention (PNI) methods. are built on lower-level skills (Limond and
Adlam 2015).

Historical Background
Goals and Objectives
Much of the research for academic techniques and
strategies stems from the special education field, Specific goals vary from technique to technique
which utilizes such techniques to teach those with and within specific models of rehabilitation.
learning disabilities (Sohlberg et al. 2005). Generally, academic techniques are meant to
Researchers in the neuropsychology field have facilitate the learning process for individuals
continued to build upon such literature in order with cognitive impairments. General cognitive
to highlight and develop effective interventions rehabilitation objectives include changing target
for individuals with neuropsychological impair- behavior and/or restitution of cognitive abilities
ments. The various models developed from such (Raskin 2010). Academic techniques can be
research have their own unique origin and history, viewed as targeting both objectives, depending
but many have been developed in response to the on the technique and model, in that many strat-
needs of specific populations. For example, the egies seek to change the individual’s approach to
direct instruction method was developed by learning (e.g. PQRST) as well as restore certain
Engelmann and Carnine (Sohlberg et al. 2005) learning and memory capacities. Academic
as a model for teaching economically disadvan- strategies seek to structure the manner in which
taged children. Other approaches such as the information or procedures are taught and prac-
PQRST, stemmed from the notion that individuals ticed so as to facilitate learning (Ehlhardt
with partially intact explicit memory capabilities, et al. 2008).
Academic Techniques 19

Treatment Participants an acquired brain injury (Ehlhardt et al. 2005).

Techniques used include task analysis, errorless
Given their variety, academic techniques and strat- learning, assessment of skills, review of new and A
egies can be utilized across settings with different learned skills, frequent and distributed practice, as
individuals. Specific applications include cognitive well as encouragement of active processing and
rehabilitation and special education instruction. self-reflection (Sohlberg et al. 2005). The PQRST
Individuals with cognitive impairment due to model encourages individuals to develop ques-
developmental disabilities and neurological condi- tions about the information they are learning,
tions would benefit from academic techniques and read information carefully while thinking about
strategies. Additionally, various treatment their questions, summarize the information, and
approaches could be effective across populations test the knowledge acquired (Wilson 2009). This
with learning and memory impairments, including method allows for a systematic review of infor-
individuals with learning disabilities, psychiatric mation that encourages analysis and organization
disorders such as schizophrenia, and dementia of information, which is thought to later improve
(Sohlberg et al. 2005). retention. The PNI model consists of various
levels that build on previously learned skills.
The first level focuses on interventions and tech-
Treatment Procedures niques designed to aid in learning and memory in
addition to other cognitive skills (Limond and
Strategies for learning can be grouped into direc- Adlam 2015). This model is unique in that in
tion instruction, strategy-based instruction, a com- addition to the use of academic techniques and
bined strategy and direction instruction approach, strategies, it also utilizes strategies to increase
and nondirect/non-strategy techniques (Sohlberg metacognitive skills and encompasses both com-
et al. 2005). Direct instruction includes breaking pensatory and restorative strategies.
down instructions into smaller steps, modelling of While specific strategies and models can be used
a skill, and providing frequent feedback. Strategy- with a variety of patients, it is important that indi-
based instructions involve teaching individuals to viduals working to teach these strategies engage in
self-monitor, use prompts to foster self- careful and specific planning for their patients. Spe-
assessment, summarize and elaborate, and outline cifically for instructional strategies, Ehlhardt et al.
important themes. A combined approach utilizes (2008) recommend the following: clear specifica-
both a direct and strategy-based approach tion of intervention targets, constraining errors, suf-
(Sohlberg et al. 2005). Examples of techniques ficient and distributed practice, using multiple
include vanishing cues, a technique in which the examples, promoting effortful processing, and
amount of cuing is reduced over specific number selection of ecologically valid targets.
of trials. Errorless learning is another example of a
technique used for learning and involves reducing
errors during learning by breaking down tasks into Efficacy Information
discrete steps, providing sufficient examples
before the patient is asked to perform the task, Research on instructional methods suggests that
and correcting errors immediately (Raskin 2010; they are effective, although questions regarding
Sohlberg et al. 2005). what and how specific strategies are implemented
Several models utilize academic techniques for maximum benefit remain to be answered
and strategies in their protocols. TEACH-M is (Glang et al. 2008; Ehlhardt et al. 2008). Several
an instructional package designed to identify a models utilizing academic techniques have been
sequence of strategies that would be helpful in found to be effective in facilitating learning and
facilitating learning and memory in individuals the retention of information. The PQRST method
with memory impairments, specifically related to has been found to be effective for individuals with
20 Acalculia

memory impairments (Wilson 2009) and individ- Limond, J., & Adlam, A. L. (2015). Cognitive interven-
uals with memory impairments due to prefrontal tions for children with brain injury. In J. Reed,
K. Byard, & H. Fine(Eds.), Neuropsychological
cortex lesions (Ciaramelli et al. 2015). The rehabilitation of childhood brain injury (pp. 82–105).
TEACH-M method was also found to be effective London: Palgrave Macmillan.
in facilitating learning in a group of four individ- Raskin, S. A. (2010). Current approaches to cognitive
uals, as discussed by Ehlhardt et al. (2005). rehabilitation. In C. L. Armstrong, L. Morrow, C. L.
Armstrong, & L. Morrow (Eds.), Handbook of medical
neuropsychology: Applications of cognitive neurosci-
ence (pp. 505–517). New York: Springer Science þ
Qualifications of Treatment Providers Business Media. https://doi.org/10.1007/978-1-4419-
1364-7_28.
Sohlberg, M. M., Ehlhardt, L., & Kennedy, M. (2005).
Those individuals teaching academic strategies or Instructional techniques in cognitive rehabilitation:
rehabilitation techniques should be individuals A preliminary report. Seminars in Speech and Lan-
trained in special education and cognitive rehabil- guage, 26(4), 268–279. https://doi.org/10.1055/s-
itation. Some professions include special educa- 2005-922105.
Swanson, H. L. (1999). Instructional components that pre-
tion teachers, cognitive rehabilitation specialists, dict treatment outcomes for students with learning dis-
clinicians, and speech and language pathologists. abilities: Support for a combined strategy and direct
instruction model. Learning Disabilities Research &
Practice, 14(3), 129–140. https://doi.org/10.1207/
sldrp1403_1.
See Also Wilson, B. A. (2009). Memory rehabilitation: Integrat-
ing theory and practice. New York: The Guilford
Press.
▶ Cognitive Rehabilitation
▶ Errorless Learning
▶ Evidence-Based Practice
▶ Metacognitive Skills
▶ Method of Vanishing Cues Acalculia
▶ Mnemonic Techniques
Kelly Broxterman1, Natalie Wahmhoff2,
Elaine Clark2 and Alyssa Beukema1
1
References and Readings School Psychology, The Chicago School of
Professional Psychology, Chicago, IL, USA
Ciaramelli, E., Neri, F., Marini, L., & Braghittoni, D. 2
Department of Educational Psychology,
(2015). Improving memory following prefrontal cortex The University of Utah, Salt Lake City, UT, USA
damage with the PQRST method. Frontiers in Behav-
ioral Neuroscience, 9(211), 1–9. https://doi.org/
10.3389/fnbeh.2015.00211.
Ehlhardt, L. A., Sohlberg, M. M., Glang, A., & Albin, Synonyms
R. (2005). TEACH-M: A pilot study evaluating an
instructional sequence for persons with impaired memory
and executive functions. Brain Injury, 19(8), 569–583. Mathematics disability
https://doi.org/10.1080/002699050400013550.
Ehlhardt, L. A., Sohlberg, M. M., Kennedy, M., Coelho, C.,
Ylvisaker, M., Turkstra, L., & Yorkston, K. (2008).
Evidence-based practice guidelines for instructing indi- Definition
viduals with neurogenic memory impairments: What
have we learned in the past 20 years? Neuropsycholog-
ical Rehabilitation, 18(3), 300–342. https://doi.org/ Acalculia is an acquired impairment in which
10.1080/09602010701733190. people have difficulty performing mathematical
Glang, A., Ylvisaker, M., Stein, M., Ehlhardt, L., Todis, B., tasks, such as adding, subtracting, multiplying,
& Tyler, J. (2008). Validated instructional practices:
and dividing. Acalculia deficits can manifest in a
Application to students with traumatic brain injury. The
Journal of Head Trauma Rehabilitation, 23(4), 243–251. wide variety of number processing and calcula-
https://doi.org/10.1097/01.HTR.0000327256.46504.9f. tion abilities.
Acalculia 21

Categorization aphasia. In Broca’s aphasia, acalculia deficits

manifest as omissions, substitutions, and order
Generally, authors have agreed on two major dis- reversal. In Wernicke’s aphasia, difficulties are A
tinctions: primary and secondary acalculia especially evident when required to write quanti-
(Growth-Marnat 2000). These terms were first ties when they are orally dictated. Those with
described by Berger in 1926 (Boller and Grafman Wernicke’s aphasia also tend to make paralexias
1983). Primary acalculia refers to a basic defect in and paragraphias (Ardila and Rosselli 2002;
computational abilities, not resulting from separate Growth-Marnat 2000).
cognitive deficits. It is also known as anarithmetia. Frontal acalculia deficits occur in conjunction
Deficits in primary acalculia include poor estima- with attention difficulties, perseveration, and
tion, number comparison difficulties, and difficulty impairment of more complex math concepts
understanding procedural rules and numerical (Dehaene et al. 1998). Patients with frontal
signs. In primary acalculia, these deficits will exist acalculia often have significant damage to the pre-
regardless of whether tasks are presented in an oral frontal areas of their brain, which can cause trouble
or written format (Ardila and Rosselli 2002). with mental operations, operations that need to be
Secondary acalculia refers to calculation carried out successively, backward operations, and
defects due to primary deficits in other areas: numerical problems that require multiple steps. In
memory disorders, attention impairments, lan- these individuals, written mathematical problem-
guage defects, spatial deficits, etc. (Berger solving is easier to do than mental math operations.
1926). The secondary acalculias include aphasic While complex concepts are difficult for patients
acalculia, alexic acalculia, agraphic acalculia, with frontal acalculia, more basic math concepts
frontal acalculia, and spatial acalculia. are usually maintained (Ardila and Rosselli 2002).
Aphasic acalculia occurs in patients with Spatial acalculia impacts written mathematical
Broca’s and Wernicke’s aphasia. The deficits tasks more than mental math tasks. A difficulty
seen in patients with Broca’s aphasia are linguistic with writing numbers is quite apparent in these
in nature, and these individuals often have impair- cases and manifests in several ways. Writing on
ments in the syntax of calculation. This includes only one side of the page, inability to write num-
problems when translating word representations bers in a straight line, and general disorganization
of numbers (three hundred and forty-five) to their are some of the deficits that impact math perfor-
numeral form (345). They may also read numbers mance (Basso et al. 2000). Patients with spatial
with morphological errors (15 is read as 50) acalculia often forget where to place remainders
(Ardila and Rosselli 2002; Basso et al. 2000). and carried numbers, despite understanding the
When the secondary acalculia stems from basic division and multiplication functions. Math
Wernicke’s aphasia, deficits are more severe. procedure signs are often undetected or switched
Reading and writing of numbers often have (add instead of subtract).
semantic errors, and poor verbal memory often
impacts the calculation abilities of these patients
(Grafman and Rickart 2000). Epidemiology
Alexic acalculia is the inability to read number
and correlations with the inability to read text. Acalculia can result from stroke, tumors, and
People with this type of acalculia may focus trauma. It is also seen in patients with degenera-
only on beginning digits (538 is read as 53). For tive dementia (Ardila and Rosselli 2002).
those with alexic acalculia, mental calculation
abilities exceed written calculation abilities
(Ardila and Rosselli 2002). Prognostic Factors and Outcomes
Agraphic acalculia is the inability to write
numbers. Like aphasic acalculia, agraphic There is noted variability in prognosis for
acalculia correlates with Broca’s and Wernicke’s acalculia, ranging from no recovery to full
22 Acalculia

recovery. For primary acalculia, improvement is experimental batteries that target specific func-
limited. In the case of secondary acalculias, when tions and include error analysis. These batteries
recovery from the primary deficit, such as aphasia, often assess skills in the following areas: number
alexia, and agraphia, occur, the corresponding recognition, number writing, number transcoding,
acalculia deficits tend to improve as well. quantification, magnitude estimation, basic arith-
metic operations, calculation fact verification,
multicolumn calculations, magnitude compari-
Neuropsychology and Psychology of son, fractions, algebra, and numeric knowledge.
Acalculia When possible, these skills should be assessed in
both written and oral forms (Ardila and Rosselli
Primary acalculia is associated with left posterior 2002; Grafman and Rickart 2000).
parietal lesions. More specifically, damage to the
left angular and supramarginal gyri occurs with
primary acalculia (Grafman and Rickart 2000). It Treatment
is suggested that there are separate neuropathways
for rote number knowledge and semantic number Some authors have suggested beginning rehabilita-
knowledge. tion with an error analysis if it was not completed
Neuroimaging techniques reveal that several during the assessment. This will provide explicit
brain areas are active when performing calcula- areas to target during rehabilitation (Grafman and
tions and also that the pattern differs according to Rickart 2000). Long-term rehabilitation programs
what type of calculation is done (Dehaene et al. should begin simply and progressively work toward
1998). This occurs to the many abilities that cal- more complex tasks. With secondary acalculia,
culation often requires, including verbal, spatial, focusing rehabilitation on the primary deficit may
executive functioning, and memory. The areas significantly improve the secondary acalculia defi-
most associated with calculation are the upper cits (Ardila and Rosselli 2002).
cortical surface and anterior aspect of the left
middle frontal gyrus, the bilateral supramarginal
and angular gyrus, the left dorsolateral prefrontal Cross-References
and premotor cortices, Broca’s area, inferior pari-
etal and left parietal cortex, and the inferior ▶ Agraphia
occipitotemporal regions (Ardila and Rosselli ▶ Alexia
2002). ▶ Aphasia
It is important to keep in mind that damage to ▶ Gerstmann’s Syndrome
the right hemisphere and the frontal lobes also ▶ Spatial Dyscalculia
impact the occurrence of acalculia, especially
when it is a secondary acalculia.
References and Readings

Evaluation Ardila, A., Matute, E., & Inozemtseva, O. (2003). Progres-

sive agraphia, acalculia, and anomia: A single-case
report. Applied Neuropsychology, 10, 205–214.
The arithmetic section of the Wide Range
Ardila, A., & Rosselli, M. (2002). Acalculia and
Achievement Test (WRAT) has often been used dyscalculia. Neuropsychology Review, 12, 179–231.
to test operational skills. The Key Math, which is Basso, A., Burgio, F., & Caporali, A. (2000). Acalculia,
designed for children and adolescents, tests most aphasia, and spatial disorders in left and right brain-
damaged patient. Cortex, 36, 265–280.
targeted and specific abilities that are suggested
Berger, H. (1926). Uber Rechenstorunger bei
for an acalculia assessment (Grafman and Herderkraunkunger des Grosshirns. Arch Psychiatr
Rickart 2000). Many authors have suggested Nervenkr, 78, 236–263.
Acceleration Injury 23

Boller, F., & Grafman, J. (1983). Acalculia: Historical connections deep within the brain. Secondary injury
development and current significance. Brain and Cog- may occur hours or even days after the inciting
nition, 2(3), 205–223.
Dehaene, S., Cohen, L., & Changeux, J. P. (1998). Neuro- traumatic event. Secondary effects of injury can A
nal network models of acalculia and prefrontal deficits. include decreased cerebral blood flow, edema, hem-
In R. W. Parks, D. S. Levine, & D. L. Long (Eds.), orrhage, increased intracranial pressure, and bio-
Fundamentals of neural network modeling: Neuropsy- chemical changes that may cause excitotoxicity
chology and cognitive neuroscience (pp. 233–255).
Cambridge, MA: MIT. and more extensive damage to the surrounding
Grafman, J., & Rickart, T. (2000). Acalculia. In M. J. Farah brain structures and their associated connections.
& T. E. Fienberg (Eds.), Patient based approaches to Theoretical models of linear acceleration
cognitive neurosciences: Issues in clinical and cogni- injury now address the heterogeneity of effects
tive neuropsychology. Cambridge, MA: MIT.
Growth-Marnat, G. (Ed.). (2000). Neuropsychological that can result from such biomechanical injuries.
assessment in clinical practice. New York: Wiley. Although diffuse brain damage may result from
Scruggs, T. E., & Mastropieri, M. A. (2000). Acalculia. In this type of injury, a key factor that predicts the
Encyclopedia of special education (Vol. 1, 2nd ed., extent of damage following acceleration injury is
p. 27). New York: Wiley.
the area of initial impact. Given that the structure
and projection pathways of the brain have varying
densities and tensile strengths within different
regions of the brain, the point of impact is most
Acceleration Injury likely the key in determining the extent of damage
that takes place and the likelihood and course of
Beth Rush recovery that is possible following injury.
Psychiatry and Psychology, Mayo Clinic, Patients sustaining acceleration injury may
Jacksonville, FL, USA experience headache, photophobia, phonophobia,
nausea, and dizziness immediately following
injury onset. On neuropsychological evaluation,
Synonyms patients with acceleration injuries are more likely
to demonstrate a diffuse, rather than focal, profile
Acceleration-deceleration injury of cognitive impairment when cognitive impair-
ment is present. The lateralization of cognitive
impairment that is typically observed in focal
Definition brain injury is relatively uncommon following
acceleration injury. A diffuse profile of cognitive
Traumatic injury to the brain resulting from high- impairment in acceleration injury is due to the
speed acceleration of the brain within the skull disruption of white matter tracts that are responsi-
cavity in the direction of inertial force. ble for efficiency and coordination of communi-
cation between functional brain injuries. As such,
a patient with acceleration injury may demon-
Current Knowledge strate cognitive slowing, executive dysfunction,
and problems with simple and complex attention
During acceleration injury, movement of the head is as a consequence of his/her brain injury.
unrestricted. One of the most common scenarios
resulting in acceleration injury is a high-speed
motor vehicle accident. Primary brain injury results Cross-References
from brain tissue and brain structures compressing
against one another in the force of inertia. This may ▶ Biomechanics of Injury
result in bruising, hemorrhage, and shearing of the ▶ Deceleration Injury
underlying tensile strength of white matter ▶ Diffuse Axonal Injury
24 Accessory Cuneate Nucleus

References and Readings movement), but it is relatively small and isolated

lesions are likely to be extremely rare.
Bayly, P. V., Cohen, T. S., Leister, E. P., Ajo, D., Leuthardt,
E. C., & Genin, G. M. (2005). Acceleration-induced
deformation of the human brain. Journal of
Neurotrauma, 22(8), 845–856.
Li, Y., Zhang, L., Kallakuri, S., Zhou, R., & Cavanaugh, J. M. Accommodations
(2011). Quantitative relationship between axonal injury
and mechanical response in a rodent head impact acceler- Jacob T. Lutz1 and David E. McIntosh2
ation model. Journal of Neurotrauma, 28(9), 1767–1782. 1
Sabet, A. A., Christoforou, E., Zatlin, B., Genin, G. M., &
Department of Special Education, Ball State
Bayly, P. V. (2008). Deformation of the human brain University, Muncie, IN, USA
2
induced by mild angular head acceleration. Journal of Department of Special Education, Teachers
Biomechanics, 41, 307–315. College, Bell State University, Muncie, IN, USA

Synonyms
Accessory Cuneate Nucleus
Reasonable accommodations
John E. Mendoza
Department of Psychiatry and Neuroscience,
Tulane Medical School and SE Louisiana Definition
Veterans Healthcare System, New Orleans,
LA, USA In order to provide students with disabilities the
free, appropriate public education mandated by
IDEA 2004 and Section 504 of the Rehabilitation
Synonyms Act of 1973, changes typically must be made to a
child’s educational curriculum or environment.
Lateral cuneate nucleus These accommodations include changes in the
method of presentation of material, classroom
seating location, availability of an interpreter for
Definition those with hearing impairment, response format,
testing time allowed, setting, or other reasonable
Nucleus in the dorsolateral portion of the medulla steps that do not significantly alter the content of
that receives sensory information likely from educational material or the validity of tests. To be
touch, pressure, and stretch receptors in the eligible to receive accommodations, students
upper extremities. It gives rise to the must be identified as having a disability consistent
cuneocerebellar tract which enters the cerebellum with the guidelines presented in IDEA 2004 or
via the inferior cerebellar peduncle. The accessory Section 504 of the Rehabilitation Act of 1973.
cuneate nucleus is thought to be the equivalent of Accommodations may also be required in the
the dorsal nucleus of Clarke in the lumbar, tho- workplace under the Americans with Disabilities
racic, and lower cervical cord which is the source Act. These could include installation of a ramp to
of the dorsal spinocerebellar tract. These nuclei permit wheelchair access, flexible working hours,
and tracts provide unconscious (as opposed to or provision of TTY machines.
“conscious”) sensory feedback to the cerebellum
in its regulation of individual muscles. Lesions of
this nucleus might be expected to produce cere- Cross-References
bellar type symptoms of the ipsilateral upper
extremity (i.e., ataxia/incoordination of ▶ Americans with Disabilities Act of 1990
Acetylcholine 25

References and Readings enzymes known as cholinesterases. Acetylcholin-

esterase is the primary enzyme that breaks down
Education, 34 C.F.R. §104. acetylcholine in the synapse. Thus, to enhance
Individuals with Disabilities Education Improvement Act A
cholinergic function, a number of substances
of 2004, 20 U.S.C. § 1400 et seq.
Rehabilitation Act, 29 U.S.C. § 794. have been developed that inhibit the activity of
this enzyme (Iversen et al. 2008).
Based on differences in the agonists that stim-
ulate cholinergic receptors, two receptor sub-
Acetylcholine types have been identified, nicotinic and
muscarinic. Nicotinic receptors are stimulated by
JoAnn Tschanz1,2 and Elizabeth K. Vernon1 nicotine, are excitatory, and show a rapid response
1
Department of Psychology, Utah State to stimulation. Muscarinic receptors are stimu-
University, Logan, UT, USA lated by muscarine, have either excitatory or
2
Center for Epidemiologic Studies, Utah State inhibitory effects, and show a slower response to
University, Logan, UT, USA stimulation. Further subtypes exist within the nic-
otinic and muscarinic classes (Feldman et al.
1997; Iversen et al. 2008).
Synonyms Acetylcholine is involved in a number of
behavioral processes. As a neurotransmitter sub-
ACh; Cholinergic system stance at the neuromuscular junction, it acts on
motor neurons of the spinal cord and cranial motor
nerve nuclei, playing an important role in the
Definition contraction of skeletal muscles. Studies also sug-
gest a role in cortical arousal, REM sleep, and
Acetylcholine has been identified as a neurotrans- cognitive functions such as attention, learning,
mitter substance since the mid-1920s. It is the and memory. Its presence in cardiac and smooth
neurotransmitter substance present at the neuro- muscles, organs, and salivary, tear and sweat
muscular junction and also innervates structures glands affect autonomic functions (Feldman
of the parasympathetic and sympathetic nervous et al. 1997).
systems (Feldman et al. 1997; Iversen et al. 2008).
In the brain, cholinergic neurons have a wide
distribution. Projections emanate from the basal Current Knowledge
forebrain in the medial septal nucleus and termi-
nate in the hippocampus and limbic cortex. Applications
Among other areas receiving cholinergic input Dysfunction in the cholinergic system has been
are the neocortex, olfactory bulbs, amygdala, implicated in a number of clinical conditions
neostriatum (caudate nucleus and putamen), the including Alzheimer’s Disease (AD), Diffuse
hypothalamus, and various regions in the brain Lewy Body Dementia (Londos et al. 2003), and
stem (Feldman et al. 1997). Huntington’s Disease and Myasthenia Gravis
Acetylcholine is synthesized from the precur- (Iversen et al. 2008). Recent work also suggests
sors Acetyl CoA and choline in a chemical reac- a reduction in cholinergic activity in Parkinson’s
tion involving the catalytic enzyme, choline disease that may appear relatively early in the
acetyltransferase (ChAT). The presence of this course of the condition (Shimada et al. 2009).
enzyme has been used as a marker to locate Acetylcholinesterase inhibitors are used in the
cholinergic neurons. Acetylcholine degradation palliative treatment of AD and myasthenia gravis.
(the primary mode of removal from synapses) Cholinergic or anticholinergic compounds are
is accomplished by the activity of a group of also used as a muscle relaxant for surgery,
26 Achenbach System of Empirically Based Assessment (ASEBA)

treatment of parkinsonism, glaucoma, urinary Iversen, L. L., Iversen, S. D., Bloom, F. E., &
retention, and in nonclinical applications such as Roth, R. H. A. (2008). Introduction to neuropsycho-
pharmacology (pp. 128–149). New York: Oxford
insecticides in agriculture and neurotoxins (and University Press.
their antidotes) in warfare (Feldman et al. 1997; Londos, E., Brun, A., Gustafson, L., & Passant, U. (2003).
Iversen et al. 2008). Antagonism of brain cholin- Lewy body dementia. Clinical challenges in diagnosis
ergic function has been associated with worse and management. In K. Iqbal & B. Winblad (Eds.),
Alzheimer’s disease and related disorders: Research
cognitive performance, particularly in older advances (pp. 133–142). Bucharest: Ana Asian
adults. One longitudinal study reported that con- International Academy of Aging.
tinuous use of medications with anticholinergic Risacher, S. L., McDonald, B. C., Tallman, E. F.,
effects was associated with poorer reaction time, West, J. D., Farlow, M. R., Unverzagt, F. W., Gao, S.,
Boustani, M., Crane, P. K., Petersen, R. C., Jack, C. R.,
attention, delayed nonverbal memory, narrative Jr., Jagust, W. J., Aisen, P. S., Weiner, M. W.,
recall, visuospatial construction, and verbal flu- Saykin, A. J., & Alzheimer’s Disease Neuroimaging
ency, but no increase in conversion to dementia Initiative. (2016). Association between anticholinergic
after an 8-year follow-up (Ancelin et al. 2006). medication use and cognition, brain metabolism, and
brain atrophy in cognitively normal older adults. JAMA
However, a recent study reported that use of med- Neurology, 73, 721–732.
ications with medium or high anticholinergic Shimada, H., Hirano, S., Shinotoh, H., Aotsuka, A.,
effects was associated with worse performance Sato, K., Tanaka, N., Ota, T., Asahina, M.,
in delayed narrative recall and executive func- Fukushi, K., Kuwabara, S., Hattori, T., Suhara, T., &
Irie, T. (2009). Mapping of brain acetylcholinesterase
tions. Use of anticholinergic medications was alterations in Lewy body disease by PET. Neurology,
also associated with lower cortical volumes and 73, 273–278.
reduced cortical thickness of the temporal lobe as
well as greater ventricular volumes. Conversion to
Alzheimer’s disease was significantly greater in
users of anticholinergic medications, and espe-
cially among those with evidence of Amyloid Achenbach System of
Beta deposition on scans or inferred in cerebro- Empirically Based Assessment
spinal fluid (Risacher et al. 2016). (ASEBA)

Thomas M. Achenbach
Department of Psychiatry, University of Vermont,
See Also Burlington, VT, USA

▶ Alzheimer’s Disease
▶ Anticholinesterase Inhibitors Synonyms
▶ Cholinergic System
▶ Cholinesterase Inhibitors Achenbach System of Empirically Based Assess-
▶ Donepezil ment (ASEBA)

References and Readings Description

Ancelin, M. L., Artero, S., Portet, F., Dupuy, A. M.,
Touchon, J., & Ritchie, K. (2006). Non-degenerative
The Achenbach System of Empirically Based
mild cognitive impairment in elderly people and use of Assessment (ASEBA) comprises a family of
anticholinergic drugs: Longitudinal cohort study. forms for rating behavioral/emotional/social prob-
British Medical Journal, 332, 455–459. lems and adaptive characteristics. For ages 1½ to
Feldman, R. S., Meyer, J. S., & Quenzer, L. F. (1997).
Acetylcholine. In Principles of neuropsychoparh-
90þ years, developmentally appropriate forms are
macology (pp. 235–276). Sunderland: Sinauer designed to be completed by collaterals who know
Associates, Inc. the person who is being assessed. These forms
Achenbach System of Empirically Based Assessment (ASEBA) 27

Achenbach System of Empirically Based Assessment (ASEBA), Table 1 ASEBA assessment instruments
Instrument Ages Completed by Reference
CBCL/1½–5 1½–5 Parent figures Achenbach and Rescorla (2000) A
C-TRF 1½–5 Daycare providers, preschool teachers Achenbach and Rescorla (2000)
CBCL/6–18 6–18 Parent figures Achenbach and Rescorla (2001, 2007a)
TRF 6–18 Teachers Achenbach and Rescorla (2001, 2007a)
YSR 11–18 Youths Achenbach and Rescorla (2001, 2007a)
TOF 2–18 Psychological examiner McConaughy and Achenbach (2004)
DOF 6–11 Observer McConaughy and Achenbach (2009)
SCICA 6–18 Interviewer McConaughy and Achenbach (2001)
ASR 18–59 Adults Achenbach and Rescorla (2003)
ABCL 18–59 Collaterals Achenbach and Rescorla (2003)
OASR 60 Older adults Achenbach et al. (2004)
OABCL 60 Collaterals Achenbach et al. (2004)

include versions of the Child Behavior Checklist use to rate the behavior observed during the
(CBCL), completed by parent figures for 1½- to 5- administration of individual ability and achieve-
year-olds and for 6- to 18-year-olds; the Caregiver- ment tests to 2- to 18-year-olds. Table 1 summa-
Teacher Report Form (C-TRF) for ages 1½–5, com- rizes the ASEBA forms, ages covered, who
pleted by daycare providers and preschool teachers; completes the forms, and references to manuals
the Teacher’s Report Form (TRF) for ages 6–18, for each form.
completed by teachers and other school personnel;
the Adult Behavior Checklist (ABCL) for ages Normed Profiles
18–59, completed by spouses, partners, family Scores obtained from all ASEBA forms are
members, friends, therapists, and other collaterals; displayed on profiles in relation to norms that are
and the Older Adult Behavior Checklist (OABCL) based on distributions of scale scores obtained by
for ages 60 and older, completed by caregivers as large samples of peers. For the collateral and self-
well as by collaterals. report forms for ages 1½ to 90þ years, norms are
The ASEBA also includes parallel forms com- based on a US national probability sample of people
pleted by the people being assessed, including the who had not received mental health or substance
Youth Self-Report (YSR) for ages 11–18, the Adult abuse services in the preceding 12 months. For the
Self-Report (ASR) for ages 18–59, and the Older CBCL/6–18, TRF, and YSR, norms are provided
Adult Self-Report (OASR) for ages 60 and older. for many cultures in addition to the USA, as
The collateral and self-report forms assess function- detailed later (Achenbach and Rescorla 2007a, b).
ing in everyday contexts over periods of 2–6 months. Multicultural norms for the CBCL/1½–5 and C-
In addition to the collateral and self-report TRF were released in 2010 and for the ASR and
forms, other ASEBA forms are designed for rating ABCL in 2015 (Achenbach and Rescorla 2010,
behavior observed in specific situations. These 2015). For the DOF, SCICA, and TOF, norms are
forms include the Direct Observation Form based on ratings of children observed in the con-
(DOF), which is completed by observers who texts for which these instruments are designed.
rate two or more 10-min samples of children’s Each profile displays an individual’s scale
behavior observed in classrooms and other group scores in terms of standard scores (T scores) and
settings; the Semistructured Clinical Interview for percentiles based on the normative sample of that
Children and Adolescents (SCICA), which pro- individual’s peers, as rated by a particular type of
vides an interview protocol and a rating form informant (e.g., parent, teacher, self). The profiles
completed by the interviewer who administers also display demarcations between the normal
the SCICA to 6- to 18-year-olds, and the Test range, borderline clinical range, and clinical
Observation Form (TOF), which test examiners range on each scale. Figure 1 illustrates a profile
 28

YSR/11–18 - Syndrome scale scores for Boys (2001 version)

ID: 2301251405–003 Date filled: 01/08/2001 Informant: Self
Name: Wayne webster Gender: Male Birth date: 03/03/1986 Relationship: Self
Clinician: Dr.Barrett Age: 15 Agency: CMHC
Internalizing Verified: Scanned Externalizing
100
95 C
L
90 I
T 85 N
80 I
S C
C 75 A
O 70 L
R 65
E N
60 O
55 R
<50 M
Anxious/ Withdrawn/ Somatic Social Thought Attention Rule-breaking A
Aggressive
depressed depressed problems problems L
behavior
complaints problems behavior
Total score 12 12 6 14 14 9 5 14
T score 70-C 83-C 64 80-C 77-C 63 56 67-B
Percentile >97 >97 92 >97 >97 90 73 96
1 14.Cries 2 5.EnjoysLittle 2 47.Nightm ares 2 11.Dependent 2 9.MindOff 0 1.ActsYoung 1 2.Alcohol 2 3.Argues
0 29.Fears 2 42.PreferAlone 1 51.Dizzy 2 12.Lonely 0 18.HarmSelf 0 4.FallsToFinish 0 26.NoGuilt 1 16.Mcan
0 30.FearSchool 2 65.Won’tTalk 1 54.Tired 1 25.NotGetAlong 1 40.HearsThings 2 8.Concentrate 0 28.BreaksRules 0 19.DemAtten
0 31.FearDoBad 2 69.Secretive 0 56a.Aches 0 27.Jealous 2 46.Twitch 0 10.SitStill 0 39.BadFriends 1 20.DestroyOwn
0 32.Perfect 0 75.Shy 1 56b.Headaches 2 34.OutToGet 0 58.PicksSkin 2 13.Confused 0 43.LieCheat 0 21.DestroyOther
2 33.Unloved 0 102.LacksEnergy 0 56c.Nausea 2 36.GetsHurt 2 66.RepeatsActs 1 17.Daydream 0 63.PreferOlder 1 22.DisobeyHome
2 35.Worthless 2 103.Sad 0 56d.EyeProb 1 38.Teased 0 70.SeesThings 1 41.Impulsive 0 67.RunAway 1 23.DisobeySchl
2 45.Nervous 2 111.Withdrawn 1 56e.SkinProb 2 48.NotLiked 2 76.SleepsLess 1 61.PoorSchool 1 72.SetsFires 1 37.Fights
0 50.Fearful 0 56e.Stomach 1 62.Clumsy 0 83.StoresUp 2 78.Inattentive 0 81.StealsHome 0 57.Attacks
0 52.Guilty 0 56g.Vomit 1 64.PreferYoung 1 84.StrangeBehav 0 82.StealsOther 0 68.Screams
1 71.SelfConsc 0 79.SpeechProb 2 85.Strangeldeas 1 90.Swears 1 86.Stubborn
2 91.ThinkSuic 2 100.SleepProb 1 96.Think Sex 2 87.MoodChang
2 112.Worries 0 99.Tobacco 2 89.Suspicious
0 101.Truant 0 94.Teases
1 105.UsesDrugs 2 95.Temper
0 97.Threaten
0 104.Loud

Copyright 2001 T.M. Achenbach B = Borderline clinical range; C = Clinical range Broken lines = Borderline clinical range

Achenbach System of Empirically Based Assessment (ASEBA), Fig. 1 Syndrome profile scored from the Youth Self-Report completed by 15-year-old Wayne Webster
(Copyright Achenbach and Rescorla 2001, p. 33)
Achenbach System of Empirically Based Assessment (ASEBA)
Achenbach System of Empirically Based Assessment (ASEBA) 29

of syndrome scales scored from the YSR com- Cross-Informant Comparisons

pleted by 15-year-old Wayne Webster (not his real Meta-analyses have revealed that correlations
name). between parent, teacher, and self-reports of chil- A
dren’s problems are typically only low to moder-
Scales on Which ASEBA Instruments Are ate (Achenbach et al. 1987). Consequently,
Scored professionals who work with children recognize
ASEBA problem items are scored on scales for the need to obtain reports from multiple infor-
syndromes derived empirically via exploratory mants. Meta-analyses of correlations between col-
factor analyses (EFAs) and confirmatory factor lateral and self-reports of adult psychopathology
analyses (CFAs). These empirically derived syn- have also revealed only modest correlations that
dromes reflect patterns of problems found to co- argue for using multi-informant data to assess
occur in ratings by each kind of informant. adults (Achenbach et al. 2005).
In addition to the syndrome scales, each form is Because each informant may provide valid and
scored on DSM-oriented scales constructed by useful information that differs from what other
having experts from many cultures select informants provide, data from multiple infor-
ASEBA problem items that are very consistent mants should be compared. Software for scoring
with particular diagnostic categories of the Amer- ASEBA forms facilitates cross-informant com-
ican Psychiatric Association’s (2013) Diagnostic parisons by printing scores obtained from parallel
and Statistical Manual-Fifth Edition (DSM-5). forms on parallel profiles. In addition, it prints
Like the syndrome scales, the DSM-oriented side-by-side comparisons of ratings by up to ten
scales are displayed on profiles in terms of T informants on all problem items that have coun-
scores, percentiles, and normal, borderline clini- terparts on forms completed by different infor-
cal, and clinical ranges. Most forms are also mants. It also prints Q correlations that measure
scored on scales comprising critical items that the degree of agreement between each pair of
are of particular concern to clinicians. informants and compares them with Q correla-
The collateral and self-report forms are addi- tions between pairs of informants in large refer-
tionally scored on scales for favorable charac- ence samples.
teristics, such as competence, adaptive An especially useful kind of comparison
functioning, and personal strengths. The partic- between informants’ reports is illustrated in
ular items and scales are geared to the develop- Fig. 2. This is a comparison between syndromes
mental level of people being assessed and to the scored from the YSR completed by Wayne Web-
informants’ knowledge of people being ster, CBCLs completed by Wayne’s parents, and
assessed. For example, parents of 6- to 18- TRFs completed by three of Wayne’s teachers.
year-olds provide data regarding their children’s For each syndrome, such as the Anxious/
involvement in sports, nonsports activities, Depressed syndrome shown in the upper left-
organizations, jobs and chores, friendships, and hand corner, the bars reflect the magnitude of
relationships with parents, siblings, and peers. standard scores (T scores) obtained from ratings
Teachers provide data on children’s academic by each kind of informant. Because the T scores
performance and adaptive characteristics at are based on ratings by each kind of informant for
school. For adults, data are requested regarding a normative sample of children, the height of the
friendships, relations with spouse or partner, bar indicates the level of the problems reported by
children, job, and enrolment in educational pro- a particular kind of informant compared to prob-
grams. Only the items relevant to the adult being lems reported by that kind of informant for a
assessed are scored. For example, adults who normative sample of children. For example, the
lack a spouse or partner, children, job, or enrol- leftmost bars indicate that the Anxious/Depressed
ment in educational programs are not scored on syndrome scores obtained from CBCL ratings by
those items. Adult forms also have normed Wayne’s parents are above the top broken line
scales for substance use. compared to parents’ CBCL ratings of a
30 Achenbach System of Empirically Based Assessment (ASEBA)

Cross-informant comparison - CBCL/TRF/YSR Syndrome scale T Scores (2001 version)

ID: 2301251405 Name: Wayne webster Gender: Male Birth date: 03/03/1986 Comparison date: 04/13/2001
Form Eval ID Age Informant name Relationship Date Form Eval ID Age Informant name Relationship Date
CBC1 001 15 Alice N. Webster Biological mother 04/04/2001 TRF5 005 15 Carmen Hemandez Classroom teacher {F} 04/11/2001
CBC2 002 15 Ralph F. Webster Biological father 04/05/2001 TRF6 006 15 Charles Dwyer Classroom teacher {M} 04/12/2001
YSR3 003 15 Self Self 04/08/2001
TRF4 004 15 George jackson Classroom teacher {M} 04/10/2001

Anxious/depressed Wtihdrawn/depressed Somatic complaints

100

90

80

70

60

≤50
72–C 72–C 70–C 68–B 61 63 82–C 70–C 83–C 79–B 74–C 74–C 58 61 64 50 58 62
CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6

Social problems Thought problems Attention problems

100

90

80

70

60

≤50
69–B 69–B 80–C 70–C 65–B 69–B 69–B 66–B 77–C 70–C 60 66–B 71–C 76–C 63 68–B 65–B 64
CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6
Rule-breaking behavior Aggressive behavior
100
B= = Borderline clinical range; C = Clinical range
90 Broken lines = Borderline clinical range

80 {F} = Femal {M} = Male

70

60

≤50
57 62 56 63 53 53 73–C 73–C 67–B 82–C 65–B 67–B
CBC1 CBC2 YSR3 TRF4 TRF5 TRF6 CBC1 CBC2 YSR3 TRF4 TRF5 TRF6

Achenbach System of Empirically Based Assessment (ASEBA), Fig. 2 Cross-informant comparisons of syndrome
scores for Wayne Webster (Copyright Achenbach and Rescorla 2001, p. 39)

normative sample of adolescent boys. As scores However, some societies have substantially
above the top broken line are in the clinical range, lower or higher mean scores. To take account of
the CBCL bars indicate that Wayne’s parents societal differences in scale scores, separate sets
reported more problems of this syndrome than of norms have been constructed for the societies
were reported by parents of 97% of boys in the obtaining relatively low scores, societies
normative sample. obtaining intermediate scores, and societies
obtaining relatively high scores. Because parent,
Multicultural Norms teacher, and self-ratings often yield different
Norms obtained in one society may not be gener- scores, the multicultural CBCL, TRF, and YSR
alizable to other societies. To determine the norms were constructed separately. For some
degree of generalizability across societies, the societies, problem scores obtained from one kind
same assessment instruments must be adminis- of informant are relatively low, while scores
tered to large representative samples of people in obtained from another kind of informant are inter-
different societies. This has been done with mediate or high. For example, CBCL and TRF
ASEBA instruments in many societies. CFAs of problem scores obtained from Japanese parents
CBCL, TRF, and YSR data from many societies and teachers are in the low range, whereas YSR
support the generalizability of syndromes that scores obtained from self-ratings by Japanese
were initially derived from US samples. Compar- youths are in the intermediate range.
isons of scale scores show that the distributions of To enable practitioners and researchers to com-
CBCL, TRF, and YSR scores in many societies pare CBCL, TRF, and YSR scores with culturally
approximate those obtained in the USA. appropriate norms, the scoring software provides
Achenbach System of Empirically Based Assessment (ASEBA) 31

options for displaying problem scale scores in years. Achenbach (2009) documents the historical
relation to norms for low-scoring, intermediate- development of ASEBA research, instruments,
scoring, and high-scoring societies. For example, theory, and applications, as well as directions in A
CBCL and TRF scores for a Japanese youth which the ASEBA is now moving. Translations
would typically be displayed in relation to norms are available in 100 languages. Over 9500 publi-
for low-scoring societies. However, the youth’s cations by some 15,000 authors report use of the
YSR scores would be displayed in relation to ASEBA in 100 cultural groups and societies
norms for intermediate-scoring societies. If the (Bérubé and Achenbach 2017). ASEBA instru-
Japanese youth lived in the USA and attended an ments are available in paper and Internet-based
American school, the TRF scores would be electronic versions in many countries around the
displayed in relation to US norms for teachers’ world for practical assessment in clinical, educa-
ratings. If the youth’s parents were well accultur- tional, forensic, and other services, as well as for
ated to the USA, the CBCL scores could be research on countless topics, such as genetics,
displayed in relation to US norms and also in medical conditions, outcome evaluations,
relation to Japanese norms to see whether the epidemiology, development, diagnosis, and mul-
scores were clinically deviant according to either ticultural comparisons. Because the ASEBA’s
set of norms. conceptual framework is open ended and
generative, it continues to advance in multiple
directions.
Historical Background

The ASEBA stems from Achenbach’s (1966) Psychometric Data

factor-analytic derivation of syndromes of child
and adolescent psychopathology. Since then, five Table 2 summarizes psychometric data for all
decades of research and practical experience have ASEBA instruments in terms of mean alphas,
produced ASEBA instruments for ages 1½ to 90þ test-retest reliability, and the percentage of

Achenbach System of Empirically Based Assessment (ASEBA), Table 2 Summary of ASEBA psychometric data
Alphaa Reliabilityb Validityc
Instrument Narrow Broad Narrow Broad Narrow Broad
CBCL/1½–5 0.76 0.92 0.82 0.89 11 17
C-TRF 0.80 0.94 0.78 0.85 13 20
CBCL/6–18 0.83 0.94 0.88 0.92 24 32
TRF 0.86 0.94 0.84 0.90 15 20
YSR 0.78 0.92 0.78 0.85 10 14
TOF 0.82 0.90 0.76 0.84 9 14
DOF 0.68 0.79 0.51 0.72 7 20
SCICA 0.70 0.84 0.75 0.80 9 16
ASR 0.78 0.93 0.84 0.91 10 14
ABCL 0.80 0.94 0.84 0.88 6 8
OASR 0.80 0.96 0.86 0.95 13 20
OABCL 0.83 0.97 0.94 0.95 19 29
Narrow = mean for syndrome and DSM-oriented scales; broad = mean for internalizing, externalizing, and total
problems. Data are from manuals listed in the Further Reading
a
Cronbach’s coefficient alpha for the internal consistency of scales
b
Pearson rs for test-retest reliability over 8- to 16-day intervals. SCICA rs are between ratings by different interviewers
who interviewed children over intervals averaging 12 days
c
Percentage of variance accounted for by clinical referral status (referred vs. nonreferred) in multiple regressions of
referral status on ASEBA scale scores with demographic variables partialed out
32 Achenbach System of Empirically Based Assessment (ASEBA)

variance in ASEBA scale scores accounted for Achenbach, T. M., & Rescorla, L. A. (2000). Manual for
by clinical referral status, after partialing out the ASEBA preschool forms & profiles. Burlington:
University of Vermont, Research Center for Children,
demographic effects. Many additional psycho- Youth, and Families.
metric findings – including goodness of fit Achenbach, T. M., & Rescorla, L. A. (2001). Manual for
obtained from CFAs in diverse samples – are the ASEBA school-age forms & profiles. Burlington:
reported in ASEBA manuals and in refereed University of Vermont, Research Center for Children,
Youth, and Families.
publications listed by Bérubé and Achenbach Achenbach, T. M., & Rescorla, L. A. (2003). Manual for
(2017). the ASEBA adult forms & profiles. Burlington: Univer-
sity of Vermont, Research Center for Children, Youth,
and Families.
Clinical Uses Achenbach, T. M., & Rescorla, L. A. (2007a). Multicul-
tural supplement to the manual for the ASEBA school-
age forms & profiles. Burlington: University of Ver-
ASEBA instruments have numerous clinical uses. mont Research Center for Children, Youth, and
Bérubé and Achenbach (2017) list publications Families.
reporting use of the ASEBA in relation to over Achenbach, T. M., & Rescorla, L. A. (2007b). Multicul-
tural understanding of child and adolescent psychopa-
150 medical conditions. Over 1100 publications
thology: Implications for mental health assessment.
report use of the ASEBA for evaluating treat- New York: Guilford Press.
ments and outcomes for many kinds of psychopa- Achenbach, T. M., & Rescorla, L. A. (2010). Multicul-
thology and other problems. tural supplement to the manual for the ASEBA pre-
school forms & profiles. Burlington: University of
ASEBA instruments can be used at many stages
Vermont Research Center for Children, Youth, and
of clinical processes, including screening to identify Families.
needs for help, documentation of problems and Achenbach, T. M., & Rescorla, L. A. (2015). Multicultural
adaptive functioning for use in clinical referrals, supplement to the manual for the ASEBA adult forms &
profiles. Burlington: University of Vermont Research
and intake assessment on which to base treatment
Center for Children, Youth, and Families.
decisions. During the course of treatment, ASEBA Achenbach, T. M., McConaughy, S. H., & Howell, C. T.
instruments are useful for determining whether (1987). Child/adolescent behavioral and emotional
goals are being met. Following the treatment, problems: Implications of cross-informant correlations
for situational specificity. Psychological Bulletin, 101,
ASEBA instruments can be readministered to eval-
213–232.
uate outcomes and subsequent functioning. At any Achenbach, T. M., Newhouse, P. A., & Rescorla, L. A.
point, ASEBA instruments can be used to assess (2004). Manual for the ASEBA older adult forms &
behavioral/emotional/social concomitants of neuro- profiles. Burlington: University of Vermont, Research
Center for Children, Youth, and Families.
psychological and medical disorders. The availabil-
Achenbach, T. M., Krukowski, R. A., Dumenci, L., &
ity of similar ASEBA instruments for children and Ivanova, M. Y. (2005). Assessment of adult psychopa-
adults facilitates family assessment, as well as close thology: Meta-analyses and implications of cross-infor-
coordination between interventions for parents and mant correlations. Psychological Bulletin, 131,
361–382.
their children.
American Psychiatric Association. (2013). Diagnostic and
statistical manual of mental disorders (5th ed.). Wash-
ington, DC: Author.
References and Readings Bérubé, R. L., & Achenbach, T. M. (2017). Bibliography of
published studies using the Achenbach system of
Achenbach, T. M. (1966). The classification of children's empirically based assessment (ASEBA). Burlington:
psychiatric symptoms: A factor-analytic study. Psycho- University of Vermont, Research Center for Children,
logical Monographs, 80(7), 1–37. (No. 615). Youth, and Families.
Achenbach, T. M. (2009). The Achenbach system of empir- McConaughy, S. H., & Achenbach, T. M. (2001). Manual
ically based assessment (ASEBA): Development, find- for the semistructured clinical interview for children
ings, theory, and applications. Burlington: University and adolescents (2nd ed.). Burlington: University of
of Vermont, Research Center for Children, Youth, and Vermont, Research Center for Children, Youth, and
Families. Families.
Achromatopsia 33

McConaughy, S. H., & Achenbach, T. M. (2004). Manual half of their visual field. In less extreme cases,
for the test observation form for ages 2–18. Burlington: known as dyschromatopsia, patients lose the abil-
University of Vermont, Research Center for Children,
Youth, and Families. ity to perceive selective colors and/or color con- A
McConaughy, S. H., & Achenbach, T. M. (2009). Manual stancy. These neuropsychological disorders,
for the ASEBA direct observation form for ages 6–11. which are the result of damage to the cerebral
Burlington: University of Vermont, Research Center cortex, should not be confused with congenital
for Children, Youth, and Families.
achromatopsia, which occurs as a malfunction of
the cone photoreceptors.

Achromatopsia Epidemiology

Sophie Lebrecht and Michael J. Tarr Cerebral achromatopsia arises following brain dam-
Visual Neuroscience Laboratory, Brown age to V4/V4a located in the ventral medial region
University, Providence, RI, USA of the occipital lobe, typically caused by a tumor, a
hemorrhage, or some sort of brain trauma. Due to
the low incidence rate of cerebral achromatopsia, it
Synonyms is difficult to provide a reliable estimate of its prev-
alence. However, it seems safe to say that it is
Acquired achromatopsia; Color agnosia; Color extremely rare. A review of the documented cases
blindness; Cortical color blindness showed that of the 27 cases reported, 3 patients
recovered, 3 partially recovered, and 21 showed
no recovery (Bartels and Zeki 2000).
Short Description or Definition

Following damage to the ventral medial region Natural History, Prognostic Factors, and
of the occipital lobe, known as the “color center” Outcomes
of the brain (Bartels and Zeki 2000), patients
lose the ability to perceive color and therefore The first cases of cerebral achromatopsia were
experience the world as varying shades of gray. reported by Verrey (1888). In response to these
This disorder is termed cerebral achromatopsia. patients, Verrey introduced the concept of a “color
The loss of color vision in these patients cannot center” in the brain. Continued research con-
be explained by the photoreceptors typically firmed the existence of a cortical region devoted
damaged or absent in patients with other types to color processing. Almost a century later,
of color blindness. Meadows demonstrated a correlation between
the cortical regions sensitive to color and the
damaged cortical regions in achromatopsic
Categorization patients (Meadows 1974).

Cerebral achromatopsia results from bilateral

damage to the V4/V4a region of the color center. Neuropsychology and Psychology of
If patients experience complete ablation of V4, Achromatopsia
they lose color vision in their entire visual field.
However, if patients experience unilateral damage The region of damage in the visual field of
to V4, hemi-achromatopsia ensues, where achromotopsic patients, V4/V4a, is organized
patients only lose color vision in the contralateral retinotopically; therefore, damage to a particular
34 Achromatopsia

region of V4 results in a loss of color vision at the Treatment

corresponding location in the visual field. For
example, if damage to V4 occurs in the left hemi- There is a period of spontaneous recovery for
sphere, the patient will lose color vision in the neurovisual lesions, which typically lasts 3 months
right half of their visual field. Because V4 is post-lesion, but can occur for up to a year. With
located in the vicinity of the fusiform gyrus and regard to the treatment and diagnosis of cerebral
the lingual gyrus, known to process faces achromatopsia, experimenters report that some
(Kanwisher et al. 1997), the comorbidity between patients are not conscious of the absence of color
achromatopsia and prosopagnosia is extremely vision. This phenomenon has been explained by
high (Bouvier and Engel 2006). In addition, the ablation of a color module leaving patients
patients with achromatopsia also have a higher without even the concept of color post-lesion.
incidence of spatial and shape deficits. It has This symptom of achromatopsia should be noted
been noted that patients with complete when addressing patients, because pushing a
achromatopsia cannot even imagine color, which patient to describe a condition they are not aware
means they cannot dream in color or use color of could be distressing for the patient.
during mental imagery. This absence of color
vision often leaves patients with no appetite for
foods, which appear gray, and no desire for inti-
macy, as flesh appears gray. An insightful case Cross-References
study of a color-blind painter describes these
experiences in detail (Sacks 1995). ▶ Scotoma

Evaluation
References and Readings
Cerebral achromatopsia can be diagnosed using
a range of color vision tests. The simplest test is Bartels, A., & Zeki, S. (2000). The architecture of the color
centre in the human visual brain: New results and a
an explicit color-naming task that requires
review. The European Journal of Neuroscience, 12(1),
patients to name the color of individual flash 172–193.
cards. The most common test for color blindness Bouvier, S. E., & Engel, S. A. (2006). Behavioral deficits
is the Ishihara plate test. These plates contain and cortical damage loci in cerebral achromatopsia.
Cerebral Cortex (New York, N.Y.: 1991), 16(2),
isoluminant colored dots of varying sizes that
183–191.
together create the perception of a number Kanwisher, N., McDermott, J., & Chun, M. M. (1997). The
embedded in noise. In order to perceive the fusiform face area: A module in human extrastriate
number, patients must be able to distinguish cortex specialized for face perception. Journal of Neu-
roscience, 17(11), 4302–4311.
between the different colored dots. Another
Meadows, J. C. (1974). Disturbed perception of colors
widely used test is the Farnsworth-Munsell associated with localized cerebral lesions. Brain:
100-Hue test, in which patients are required to A Journal of Neurology, 97(4), 615–632.
order colored caps based on gradual shifts in hue Sacks, O. W. (1995). An anthropologist on mars: Seven
paradoxical tales. New York: Vintage Books.
from light to dark. Patients with color blindness
Verrey, D. (1888). Hémiachromatopsie Droite
are unable to perform this task. Rarely, a diag- Absolue. Conversation Partielle De La Perception
nosis is made using a Nagel anomaloscope. This Lumineuse Et Des Formes. Ancien Kyste
apparatus is typically used to determine whether Hémorrhagique De La Partie Inférieure Du Lobe
Occipital Gauche. Archives d’ophtalmologie, 8,
a patient is a monochromat or a dichromat; how-
289–300.
ever, some experimenters/practitioners use it in Werner, J. S., & Chalupa, L. M. (2004). The visual neuro-
the study of cerebral achromatopsia. sciences. Cambridge, MA: MIT Press.
Acoustic Neuroma 35

neurofibromatosis type 2 and often occurs bilater-

Acoustic Neuroma ally. Tumor growth is usually slow and may result
in some hearing loss or deafness, tinnitus, vertigo, A
Ethan Moitra and vestibular dysfunction. Most acoustic neuro-
Department of Psychiatry and Human Behavior, mas are diagnosed in patients between the ages
Brown University, Providence, RI, USA 30 and 60. Etiology is possibly related to gene
malfunction on chromosome 22. Treatment
options include radiosurgery and microsurgical
Synonyms removal (Figs. 1 and 2).

Neurolemmoma; Vestibular schwannoma

Cross-References

Definition ▶ Radiosurgery, Stereotactic Radiosurgery

▶ Radiotherapy
A benign tumor of the Schwann cells occurring
near the cerebellopontine angle of the brain stem.
Typically, it arises from the vestibulocochlear or References and Readings
eighth cranial nerve, which connects the brain to
the inner ear. It is commonly associated with Jørgensen, B. G., & Pedersen, C. B. (1994). Acoustic
neuroma. Follow-up of 78 patients. Clinical Otolaryn-
gology, 19, 478–484.

Acoustic Neuroma, Fig. 1 Example of acoustic Acoustic Neuroma, Fig. 2 Example of acoustic
neuroma neuroma
36 Acquired Immunodeficiency Syndrome (AIDS)

AIDS is the name given to the end stage of HIV

Acquired Immunodeficiency infection when the body’s ability to fight off
Syndrome (AIDS) microorganisms is compromised, resulting in
debilitating or fatal diseases, which are known as
Bruce J. Diamond, William Tsang, Cody “opportunistic infections.” An individual with
Curatolo, Savannah Crippen and C. Michael Nina HIV infection receives a formal diagnosis of
Department of Psychology, William Paterson AIDS when the individual has at least one oppor-
University, Wayne, NJ, USA tunistic infection or when the individual’s CD4+
T cell count is below 200 per mm3 of blood
(normal count is typically 500–1500 per mm3).
Short Description or Definition In the absence of anti-HIV or antiretroviral
drug therapy, progression to AIDS can take an
Acquired immunodeficiency syndrome (AIDS) is average of 8–12 years for adults and adolescents
a disease caused by infection with the human and 3 years from birth in prenatally infected chil-
immunodeficiency virus (HIV) (Portegies and dren. A quarter of a century after the first deaths
Berger 2007). HIV is a viral pathogen that targets from AIDS were identified, the AIDS pandemic
CD4+ T cells (also called T4 or T helper cells), has killed approximately 25 million people world-
which are lymphocyte cells with cluster determi- wide. UNAIDS, a joint program of the United
nant 4 + surface receptor sites, originating in the Nations and the World Health Organization, esti-
thymus of the human body’s immune system. HIV mates that globally, in 2014, 36.9 million people
is known to cause damage to the immune system lived with HIV, two million became newly
as well as the central nervous system. The exact infected, and 1.2 million died from AIDS. In
cause of this damage is unclear, but explanatory Western and Central Europe and North America
models have been proposed. For example, the alone, 2.4 million lived with HIV, 85,000 became
“Trojan horse” or neuroinflammation model is newly infected, and 26,000 died from AIDS
thought to involve immune system cells known (UNAIDS 2015).
as macrophages which conceal and convey HIV
into the brain, where they can disrupt supportive
brain cells such as astrocytes and microglia. In the Categorization
neuroinflammation model, the body’s over-
stimulated immune system causes an increased Differentiation between diagnoses of HIV or
production of CD14+ CD16+ monocytes which AIDS depends on CD4+ T cell count and the
flood the brain, causing inflammation and damage presence of opportunistic infections.
to brain cells and structures (Bartlett and
Finkbeiner 2006) (Table 1).
Etiology/Epidemiology

In 1981, the US Centers for Disease Control and

Acquired Immunodeficiency Syndrome (AIDS), Prevention (CDC) began receiving reports about
Table 1 Differentiation between human immunodefi-
unusual cases of Pneumocystis carinii pneumonia
ciency virus (HIV) infection and acquired immunodefi-
ciency syndrome (AIDS) in individuals infected with HIV (PCP) and Kaposi’s sarcoma in young men who
have sex with men (MSM) and PCP in injection
Symptom Diagnosis
drug users. These diseases were uncommon in
CD4+ T cell count of 200 or higher per HIV
mm3/blood infection individuals with healthy immune systems, and in
CD4+ T cell count below 200 per mm3/ AIDS early 1982, similar disease patterns were seen in
blood blood transfusion recipients, hemophiliacs, and
Presence of one or more opportunistic AIDS female partners of those already infected
infection (Portegies and Berger 2007). In late 1982, the
Acquired Immunodeficiency Syndrome (AIDS) 37

CDC officially named this disease pattern as infection among adults and adolescents. Black,
acquired immune deficiency syndrome (AIDS). Latino, younger White MSM bear the greatest
In 1984, a previously unknown human retrovirus burden of HIV infection, due to higher-risk sexual A
was discovered in the blood of individuals with behavior (CDC 2012).
AIDS by teams in the United States and France In Africa, transmission is primarily due to
and in 1986, the retrovirus was officially named male-to-female sexual contact. Asia has the sec-
human immunodeficiency virus (HIV) by ond greatest rates associated with IDU, paid sex,
the CDC. and MSM. In the Middle East, infection is thought
In 1985, a second strain of the virus was dis- to be associated with commercial sex work and
covered, which was designated as HIV-2. The IDU. In Latin America, transmission is primarily
original strain of the virus was designated as due to IDU, paid sex, and MSM. Females consti-
HIV-1. HIV-1 is much more common throughout tute a higher proportion of PLHIV (60%) in Latin
the world, while HIV-2 is more common in certain America and the Caribbean than in any other
parts of Africa. HIV-2 appears to be milder than region. In Eastern Europe, the major vectors are
HIV-1, with a slower progression to AIDS. Since IDU and heterosexual sexual contact. Western
its establishment in humans, HIV-1 has undergone Europe and Oceania are similar to North America
mutation of its genome, and there are now three in HIV transmission from MSM, IDU, and male-
groups of HIV-1. to-female sexual contact. The HIV epidemic is
Globally in 2014, there were approximately most severe in developing countries with inade-
36.9 (34.3–41.4) million people living with HIV quate medical and health education resources.
(PLHIV), with 2.0 [1.9–2.2] million new infec- Among high-income nations, racial and ethnic
tions. Sub-Saharan Africa has the highest global minority groups experience higher HIV preva-
HIV rates, with 25.8 [24.0–28.7] million PLHIV lence compared with the general population
in 2014 (WHO 2015). In recent years, there has (Fettig et al. 2014).
been a global increase in prevalence and decrease
in incidence attributable to a variety of factors
including reduced infectiousness of PLHIV indi- Natural History, Prognostic Factors, and
viduals on antiretroviral therapy medications Outcomes
(ART) and expansion of HIV prevention pro-
grams focusing on mother-to-child transmission, HIV is not transmitted through casual contact,
safer sex, and outreach to high-risk populations. such as touching. It can be transmitted when the
From 2000 to 2015, new HIV infections have bodily fluids of infected individuals – primarily
decreased by 35% and AIDS-related deaths by blood, semen, vaginal fluid, or breast milk –
24% (WHO 2015). comes into contact with the bloodstream or muco-
HIV transmission varies worldwide depending sal tissues of uninfected individuals. Transmission
upon the geographic region. In the United States, can occur through:
the estimated incidence is 50,000 new HIV infec-
tions per year. At the end of 2013, 70% of HIV 1. Unprotected sexual contact (anal, vaginal, or
infections were attributed to male-to-male sexual oral) with an individual infected with HIV
contact, 11% to injection drug use, 10% to hetero- 2. Sharing needles or syringes with HIV-infected
sexual contact, 7% to male-to-male sexual contact individuals
and injection drug use (IDU), and 1% to perinatal 3. Transfusion of infected blood or other bodily
transmission (CDC 2014). Transmission in incorporation of infected blood
women is primarily associated with heterosexual 4. A fetus or infant exposed to HIV before or
contact and IDU. The HIV incidence rate among during birth or through breastfeeding
women was 20% in 2010, and prevalence rate was
23% in 2011 (CDC 2015). In 2014, males The natural progression of HIV infection can
accounted for 81% of all diagnoses of HIV be divided into three stages: primary infection,
38 Acquired Immunodeficiency Syndrome (AIDS)

clinical latency, and symptomatic disease stage. of symptoms begin to manifest, including lymph-
The symptomatic disease stage is further divided adenopathy, lack of energy, diarrhea,
into early and late stages, with AIDS being unintentional weight loss, chronic low-grade
equated with the late-symptomatic disease stage. fever and sweats, frequent rashes or fungal infec-
After a person is initially infected with HIV, a tions, headaches, or short-term memory loss.
primary or acute infection stage commences, in Finally, individuals enter the late stage of the
which HIV replicates up to ten billion copies of symptomatic disease stage or AIDS when the
itself daily; high levels of HIV in the blood or person has at least one opportunistic infection or
viremia is evident. Approximately 2–4 weeks when the individual’s CD4+ T cell count is below
after exposure, nearly 70% of those newly infected 200 per mm3 of blood. The most common oppor-
will experience an acute illness, which has symp- tunistic infections are PCP, Kaposi’s sarcoma,
toms similar to influenza or mononucleosis, includ- HIV wasting syndrome, and HIV encephalopathy
ing fever, fatigue, muscle weakness, headache, (also known as dementia due to HIV disease or
ocular pain, sensitivity to light, sore throat, diar- AIDS dementia complex).
rhea, and lymphadenopathy. This illness is due to People who benefit from access to ART and
the temporary reduction of CD4+ T cells; it lasts for lifelong treatment no longer see AIDS-related ill-
approximately 2 weeks and then resolves sponta- nesses as primary threats. Instead, new HIV-
neously. It is during this stage that the individual related complications have emerged; serious
typically first begins to produce antibodies to HIV, non-AIDS events include cardiovascular disease,
which is designated as seroconversion. cancer, kidney disease, liver disease, osteopenia/
Serological testing of blood can reliably detect osteoporosis, and neurocognitive disease. Addi-
HIV antibodies 2–6 months after seroconversion. tional vulnerabilities include myocardial infarc-
Testing typically begins with an enzyme-linked tion, hypertension, hyperlipidemia, and diabetes
immunosorbent assay (ELISA) or test that looks mellitus. There can also be complications from
for antibodies to HIV. A second positive ELISA is opportunistic infections such as human papillo-
needed in order to confirm the result. This would mavirus, Epstein-Barr virus, and hepatitis B and
then be followed by the Western blot procedure to C (Deeks et al. 2013).
confirm the presence of at least two specific HIV
antigen groups. A diagnosis of HIV infection is
given after a positive Western blot test follows two
positive ELISA tests. If HIV is confirmed, addi- Psychological and Neuropsychological
tional tests for plasma viral RNA (viral load) and Correlates of HIV Infection
CD4+ T cell counts are then typically completed,
in order to assess the state of the immune system As HIV infection progresses, various psycholog-
and disease prognosis. Higher viral load counts ical and neuropsychological complications
are typically related to faster disease progression. involving both the central and peripheral nervous
Lower CD4+ T cell counts are typically related to systems can arise. During primary infection,
greater clinical vulnerabilities. reports of headaches and aseptic meningitis are
After the acute illness disappears, the individ- common. During the clinical latency stage, an
ual enters the clinical latency stage in which acute inflammatory demyelinating neuropathy
symptoms are typically absent, other than possible (similar to Guillain-Barre syndrome and charac-
chronic lymphadenopathy. This stage lasts an terized by progressive muscle weakness) can
average of 10 years. During the clinical latency occasionally develop. During the early symptom-
stage, HIV continues to replicate and attack CD4+ atic disease stage, peripheral neuropathy is com-
T cells, which in turn continue to counter attack. mon. This is characterized by spontaneous pain
As the immune system becomes progressively (dysesthesia), pain due to light touches or changes
compromised, individuals eventually enter the in temperature (hyperesthesia), and weakness and
early symptomatic disease stage, when a variety wasting in arms/legs (distal atrophy).
Acquired Immunodeficiency Syndrome (AIDS) 39

Several major neuropsychological complica- frequently occurring. This early stage is often
tions can develop during the late symptomatic labeled as HIV-associated minor cognitive motor
disease stage or AIDS, including: disorder. Later symptoms include partial paraly- A
sis, incontinence, and severe cognitive impair-
1. HIV encephalopathy (HIV dementia) ment. Death usually occurs within 1–6 months
2. Opportunistic infections after onset of severe symptoms. Individuals who
1. Viral (cytomegalovirus, herpes simplex are co-infected with hepatitis C or were intrave-
virus I and II, herpes zoster, and JC virus, nous drug users (IDU) typically display more
a polyomavirus or papovavirus which severe symptoms faster. As HIV-infected individ-
causes PML [progressive multifocal uals now live longer from ART, it is estimated that
leukoencephalopathy]) 47% experience HIV-associated neurocognitive
2. Fungal/protozoan (toxoplasmosis, Crypto- disorders (McGuire et al. 2013).
coccus, Candida, Mycobacterium) While HIV can be present in any region of the
3. Lymphomas brain, it is commonly observed in the basal ganglia
1. Primary central nervous system lymphomas and central white matter (and to a lesser extent in
2. Systemic (metastatic) lymphomas (The neocortical gray matter, the brainstem, and the cer-
most common systemic lymphomas are ebellum) in individuals not receiving highly active
Hodgkin’s, immunoblastic; Burkitt’s; and antiretroviral therapy (HAART) (see below). In
non-Hodgkin’s, which is particularly those receiving HAART, there is evidence of greater
prevalent.) inflammation in the hippocampus and surrounding
entorhinal and temporal cortex which would
HIV encephalopathy is the term used to account for associated memory difficulties.
describe the pathological features of encephalitis Peripheral mitochondrial DNA oxidative dam-
of the brain due to HIV, while HIV dementia (also age has been found to be associated with reduced
known as AIDS dementia complex) is used to hippocampal and subcortical gray matter volumes
describe the clinical syndrome. This syndrome is in chronic stable HIV disease. Oxidative stress-
characterized by behavioral, cognitive, and motor mediated neuroinflammation, caused by dysfunc-
declines and difficulties (Table 2). Initial symp- tional reactive oxygen species producing mitochon-
toms typically manifest as cognitive difficulties drial DNA, may contribute to neuronal loss in HIV.
(loss of concentration and mild deficits in mem- Findings have shown that volumes of multiple brain
ory) with motor and behavioral difficulties regions (e.g., enlarged lateral ventricles, reduced
hippocampal volume) are negatively correlated
with mitochondrial DNA in peripheral blood mono-
Acquired Immunodeficiency Syndrome (AIDS),
Table 2 HIV dementia symptoms
nuclear cells of HIV-infected individuals
(Kallianpur 2016). HIV infection may initiate sev-
Behavioral difficulties
eral potentially inflammatory cascades that cause
Depression
demyelinating lesions (Lescure et al. 2013).
Apathy, anhedonia, social withdrawal
Personality changes, including spontaneous, sudden, and
A therapeutic gap seems to exist between the
strong emotions salutary effects of antiretroviral regimens and the
Cognitive difficulties normalization of neurological function in HIV-
Confusion associated neurocognitive disorders. Despite the
Short-term memory lapses advances in antiretroviral therapy, CNS opportu-
Loss of concentration nistic infections remain a serious health burden
Motor difficulties worldwide (Tan et al. 2012). ART regimens differ
Lack of muscular coordination in their ability to penetrate CNS, and the problem
Tremors is that most of them do not. The current goal is to
Muscle weakness develop new medications that can penetrate the
Loss of balance CNS and eradicate HIV (Ene et al. 2011).
40 Acquired Immunodeficiency Syndrome (AIDS)

Treatment is significantly less effective if not taken consis-

tently. Lastly, PEP exists as a postexposure ART
While there is no cure or vaccine for HIVor AIDS regimen that must be taken within 72 h (Department
at this time, there are currently four different clas- of Health and Human Services 2016).
ses of antiretroviral drugs that interfere with the Current treatment investigations are seeking
ability of HIV to replicate: reverse transcriptase approaches that carry fewer side effects and do not
inhibitors (nucleoside and non-nucleoside types), require daily administration and thus increase com-
protease inhibitors, entry/fusion inhibitors, and pliance. Many vaccine trials have taken place with
integrase inhibitors. In 1987, the US Food and nonsignificant results, but the Thai RV144 trial
Drug Administration (FDA) approved azidothy- could lead to improved approaches in vaccines.
midine (AZT, also known as zidovudine), the first A major recent development involves the “Berlin
nucleoside-reverse transcriptase inhibitor patient” and a gene called CCR5. In this case, a
(NRTIs). Saquinavir, the first protease inhibitor, patient with HIV and leukemia no longer showed
was approved in 1995. Nevirapine, the first non- evidence of either disease, after stem cell transplan-
nucleoside-reverse transcriptase inhibitor, was tation from a donor with CCR5 (Levy et al. 2012).
approved in 1996. Enfuvirtide, the first fusion
inhibitor, was approved in 2003. Maraviroc, the
first entry inhibitor, and raltegravir, the first
Cross-References
integrase inhibitor, were approved in 2007.
In 1996, combination drug therapy began and
▶ Dementia
was called “highly active antiretroviral therapy”
▶ Encephalitis (Viral)
(HAART) (Portegies and Berger 2007). Three or ▶ Meningitis
more drugs are used in combination in order to
counter the development of drug resistance by
HIV. Strict adherence to medication intake sched- References and Readings
ules is required. Not only is this schedule difficult to
follow for many individuals, HAART often pro- Bartlett, J., & Finkbeiner, A. (2006). The guide to living
duces unpleasant and toxic side effects, including with HIV infection, developed at the John Hopkins
stomach problems and lipodystrophy. If followed AIDS clinic (6th ed.). Baltimore: Johns Hopkins Uni-
versity Press.
correctly, HAART typically and drastically reduces
CDC (2012). HIV surveillance supplemental report, Vol.
viral load, often to undetectable levels in the blood, 17, No. 4.
which allows the immune system to rebound. Anti- Centers for Disease Control and Prevention. (2014). HIV
retroviral drug therapy and treatments for opportu- surveillance report, vol. 26. http://www.cdc.gov/hiv/
library/reports/surveillance/. Published November
nistic infections have greatly increased life 2015. Accessed 13 April 2016.
expectancy of those with HIV infection, but due to Centers for Disease Control and Prevention. (2015). Prev-
the presence of HIV in cells that remain out of reach alence of diagnosed and undiagnosed HIV infection —
of antiretroviral drugs, eradication of HIV from the United States, 2008–2012. MMWR, 64, 657–662.
Deeks, S. G., Lewin, S. R., & Havlir, D. V. (2013). The end
human body is unattainable at this time.
of AIDS: HIV infection as a chronic disease. The Lan-
Several recent widespread interventions involve cet, 382(9903), 1525–1533.
treatment as prevention (TASP), preexposure pro- Ene, L., Duiculescu, D., & Ruta, S. (2011). How much do
phylaxis (PrEP), and postexposure prophylaxis antiretroviral drugs penetrate into the central nervous
system? Journal of Medicine and Life, 4(4), 432–439.
(PEP). In TASP, treatment through adherence to Fettig, J., Swaminathan, M., Murrill, C. S., & Kaplan, J. E.
ART reduces likelihood of transmission. In 2011, (2014). Global epidemiology of HIV. Infectious Dis-
the World Health Organization found a 96% trans- ease Clinics of North America, 28(3), 323–337.
mission risk reduction in PLHIV who used ART. Kallianpur, J. K. (2016). oxidative mitochondrial DNA
damage in peripheral blood mononuclear cells is asso-
PrEP is a preventative combination ART pill regi-
ciated with reduced volumes of hippocampus and sub-
men (tenofovir and emtricitabine) that has been cortical gray matter in chronically HIV-infected
shown to reduce HIV transmission up to 92% but patients. Mitochondrion, 28, 8–15.
Action-Intentional Disorders 41

Lescure, F., Moulignier, A., Savatovsky, J., Amiel, C., Definition

Carcelain, G., Molina, J., et al. (2013). CD8 encepha-
litis in HIV-infected patients receiving cART:
A treatable entity. Clinical Infectious Diseases, 57(1), Action tremor is a rhythmic, oscillatory, and A
101–108. involuntary movement of the limb that is seen
Levy, J. A., Autran, B., Coutinho, R. A., & Phair, J. P. with movement of an extremity. It may be seen
(2012). 25 years of AIDS: Recording progress and in isolation with a cerebellar lesion or associated
future challenges. AIDS, 26(10), 1187–1189.
McGuire, J. L., Goodkin, K., & Douglas, S. D. (2013). with other tremor types such as the postural
Neuropathogenesis of central nervous system HIV tremor of essential tremor or the rest tremor of
infection. Psychiatric Annals, 43(5), 212–216. Parkinson’s disease.
Panel on Antiretroviral Guidelines for Adults and Adoles-
cents. (2016). Guidelines for the use of antiretroviral
agents in HIV-1-infected adults and adolescents. Depart-
ment of Health and Human Services. Available at http:// Cross-References
www.aidsinfo.nih.gov/ContentFiles/AdultandAdolescent
GL.pdf. Accessed 03 April 2016. ▶ Essential Tremor
Portegies, P., & Berger, J. (Eds.). (2007). HIV/AIDS and
the nervous system: Handbook of clinical neurology. ▶ Parkinson’s Disease
Amsterdam: Elsevier.
Pratt, R. (2003). HIV & AIDS: A foundation for nursing
and healthcare practice. London: Arnold Publishers. References and Readings
Sande, M., & Volberding, P. (Eds.). (1999). The medical
management of AIDS (6th ed.). Philadelphia: Saunders.
Stine, G. (2005). AIDS update 2005. San Francisco: Pear- Fahn, S., & Jankovic, J. (Eds.). (2007). Tremors: Diagnosis
son/Benjamin Cummings. and treatment. In Movement disorders (pp. 451–479).
Tan, I. L., Smith, B. R., von Geldern, G., Mateen, F. J., & Philadelphia: Churchill Livingstone Elsevier.
McArthur, J. C. (2012). HIV-associated opportunistic
infections of the CNS. The Lancet Neurology, 11(7),
605–617.
UNAIDS. (2015). UNAIDS annual report 2015: Knowing
your epidemic. Retrieved 22 Mar 2016 from www. Action-Intentional Disorders
unaids.org/sites/default/files/media_assest/AIDS_by_
the_numbers_2015_en.pdf
Weeks, B. S., & Alcamo, I. E. (2006). AIDS: The biological Kenneth M. Heilman
basis (4th ed.). Sudbury: Jones and Bartlett Publishers. Department of Neurology, University of Florida
World Health Organization (2015, November). HIV/AIDS College of Medicine, Center for Neurological
fact sheet. Retrieved from http://www.who.int/
Studies and the Research Service of the Malcom
mediacentre/factsheets/fs360/en/
Randall Veterans Affairs Medical Center,
Gainesville, FL, USA

Action Tremor Synonyms

Anna DePold Hohler1 and Marcus Ponce de Abulia; Akinesis; Hypokinesis; Motor impersistence
Leon2 (These terms are not fully synonymous with action-
1
Boston University Medical Center, Boston, intentional disorders, but comprise important ele-
MA, USA ments of the syndrome and are often used when
2
Madigan Army Medical Center, Tacoma, describing specific these elements.)
WA, USA

Definition
Synonyms
In the absence of weakness, patients can have a
Intention tremors disability with initiating (akinesia, hypokinesia,
42 Action-Intentional Disorders

abulia) or sustaining actions (impersistence), motor disorders mentioned above, but these will
inhibiting irrelevant actions (defective response not be discussed here.
inhibition), and stopping an action when the task In the next section, we briefly describe each of
has been completed (motor perseveration). these intentional disorders, including subtypes of
each category, and in the final section, we briefly
discuss the possible pathophysiology.
Current Concepts

The motor system allows humans to interact with Clinical Manifestations

their environment and alter themselves as well as
others. The human corticospinal motor system Akinesia
together with the motor units and muscles can An organism might fail to initiate a movement for
mediate an almost infinite number of movements, many reasons, but comprehension, attentional,
and thus the human motor system needs to be perceptual, sensory, and motor disorders that
guided by at least two major types of programs: lead to a failure of movement initiation should
praxic and intentional. The praxic programs pro- not be termed akinesia. In contrast to these disor-
vide the corticospinal system with the knowledge ders, akinesia is caused by a failure of the systems
of how to make skilled movements (spatial and that are responsible for activating the motor
temporal aspects of movements), and the inten- system.
tional programs provide the corticospinal system There are three methods by which akinesia can
with information about when to move. In this be distinguished from extreme weakness. Certain
section, we will discuss disorders of the inten- forms of akinesia are present under certain sets of
tional, or “when,” systems. When interacting circumstances and absent in others. Thus, using
with environmental stimuli or the self, there are the behavioral method, if it can be demonstrated
four “when” questions that must be addressed: that a patient makes movements in one set of
these are (1) when to move, (2) when to persist circumstances (e.g., a motionless left hand is
at a movement or movements, (3) when to end a brought over to the right side of the body, and
movement or a series of movements, and (4) when the patient is able to now move this hand) and not
not to move. The inability to initiate a movement in the other, this failure to move is related to an
in the absence of a corticospinal or motor unit akinesia. If the akinesia is not limited to a set of
injury is called akinesia. Some patients are able circumstances then the clinician may have to
to move after a delay, and we call this hypokinesia. depend on brain imaging, or physiological tech-
Motor impersistence is when a patient cannot niques such as magnetic stimulation of the motor
sustain a movement or a series of movements cortex to demonstrate that the brain lesion did not
that are needed to complete a task. The inability involve the motor system and thus the failure to
to stop a movement or an action program when it move is not caused by weakness.
is no longer required is called motor perseveration There are at least three subtypes of akinesia:
and the inability to withhold a response to a sen- (1) body part: akinesia may involve the eyes, the
sory stimulus is called defective response neck and head, a limb, or the total body; (2) action
inhibition. space: akinesia of the limbs, eyes, or head may
These motor intentional disorders are parallel depend on where in space the body part is moved
to disorders of sensory attention, akinesia being or in what direction it is moved. The former is
akin to unawareness, impersistence being the called spatial akinesia (e.g., a hand that does not
motor parallel of decreased vigilance, motor per- move in left hemispace but does move in right
severation being parallel to failures of extinction body-centered hemispace), and the latter is called
or habituation, and defective response inhibition directional akinesia (e.g., a horizontal gaze palsy
being similar to distractibility. There are also cog- where patients cannot move their eyes to the left);
nitive defects that mirror four types of intentional (3) stimulus-response conditions: some patients,
Action-Intentional Disorders 43

such as those with Parkinson’s disease, are hemispatial (inability to maintain dorsiflexion of
impaired in spontaneously initiating a movement, the wrist in left space with the left arm but able to
but in response to a stimulus often have no trouble do so in right space). A
initiating a movement. We call this endogenously
evoked akinesia (endo-evoked). Patients who fail Defective Response Inhibition
to move to an imperative stimulus but will move Not all stimuli require a response, and sometimes
spontaneously, we call exogenously evoked a response might interfere with goal-oriented
akinesia. A patient may have both exo-evoked behavior. Defective response inhibition is defined
and endo-evoked akinesia, which we term mixed as responding when no response of that body part
or global akinesia. is required. It can be seen in a variety of body parts
and might also be directional and perhaps
Hypokinesia hemispatial.
A milder defect in the intentional motor (“when”) There are several forms of defective response
systems might not induce a total inability to initi- inhibition. One means of testing for this disorder
ate a response (i.e., akinesia), but rather these is to use the crossed response task. A blindfolded
patients’ intentional deficit might be manifested patient is instructed to raise the hand opposite to
by a delay in initiating a response. We call this that touched. Patients with defective response
delay hypokinesia. The hypokinesias may also be inhibition will often raise the touched hand first.
subtyped into body part (e.g., limb or eyes) and This type of defective response inhibition may be
action space (e.g., directional and hemispatial). termed motor (limb or eye directional) response
disinhibition. These can be either contralesional
Motor Extinction or bilateral. The eye directional defective
Patients with sensory extinction are able to detect response inhibition has also been called a visual
single stimuli on either side of their body, but grasp. There are some patients, however, who
when presented with two stimuli one on each have a perceptual disorder and when stimulated
side of their body, they remain unaware of on one side (e.g., left hand), feel that they were
contralesional stimuli. Motor extinction is a form stimulated on the other (e.g., right hand). This
of akinesia or hypokinesia where a patient who is phenomenon is called allesthesia, and it should
without sensory extinction is asked to respond by not be confused with defective crossed response
moving the hand (or hands) that was (were) inhibition.
touched. The examiner then delivers stimuli to Patients with defective response inhibition
the right, left, and both hands, and patients with may also fail on the types of go-no-go tasks
motor extinction are aware that both hands have described by Luria. For example, the patient may
been touched, but either fail to lift the be instructed to put up two fingers when the
contralesional hand to simultaneous stimuli or examiner puts up one finger and to put up no
lift it after a delay. fingers if the examiner puts up two fingers. If the
patient mimics the examiner such that when the
Motor Impersistence examiner puts up one finger, the patient puts up
The inability to sustain a motor act or a series of one finger and when the examiner puts up two
motor acts that are required to complete a goal is fingers, the patient puts up two fingers, the patient
called motor impersistence. Like akinesia, has echopraxia.
impersistence can be associated with various
body parts including the limbs, eyes, neck, eyelids Motor Perseveration
(e.g., keep your eyes closed for until I tell you to When a patient incorrectly repeats a prior
open them), jaw, and tongue. Patients can even response or when a patient continues to perform
demonstrate impersistence in activities such as the same act when the goal of the act has been
walking. Like akinesia, it may also be directional completed, it is called motor perseveration. In one
(e.g., inability to maintain leftward gaze) or type of motor perseveration, when the task
44 Action-Intentional Disorders

requirements have changed, the patient is unable the frontal lobe projects to the caudate. The
to switch to a different motor program and incor- premotor cortex projects to the putamen and
rectly repeats the movements. Luria (1965) calls the cingulate gyrus projects to the ventral stria-
this inertia of program action, and Sandson and tum. The striatum projects to the pars reticularis
Albert (1987) call this recurrent perseveration. In of the substantia nigra and the globus pallidus.
the second type, the patient continues to perform The globus pallidus projects to specific thalamic
movements even though the task is completed. nuclei, and these thalamic nuclei project back to
Luria (1965) called this efferent perseveration; the frontal cortex. Just as injury of the frontal
however, Sandson and Albert (1987) call this lobes can induce intentional deficits, injuries, or
continuous perseveration. diseases that injure the basal ganglia, the sub-
stantia nigra (e.g., Parkinson’s disease), por-
tions of the thalamus, as well as the white
Pathophysiology of Intentional matter connections can also induce intentional
Disorders deficits.

Intentional motor disorders are often associated

with bilateral hemispheric lesions, but when these Future Directions
disorders are caused by a unilateral hemispheric
lesion, they are more commonly associated with Disorders of intention have received considerably
right than left-hemisphere lesions. The intentional less neuroscientific study than have disorders of
disorders that have been reported to be induced by sensory selective attention. There is a need for
primarily right-hemisphere lesions include additional experimental and clinical neuropsycho-
akinesia (e.g., left-sided limbs, leftward arm logical studies of these disorders. Furthermore,
movements, and even left horizontal gaze), hypo- assessment batteries are needed that will facilitate
kinesia (slowed reaction times), motor the assessment of the subtypes of motor intention
impersistence of the left-sided limbs, left-sided disturbances and which may provide additional
gaze), and motor (continuous) perseveration. quantitative data for experimental analysis and
Many of the intentional defects associated with normative comparison between patient groups
right-hemisphere dysfunction, however, are not and healthy individuals.
just limited to the left limbs. For example, patients
with a right-hemisphere lesion are more often
abulic, have slowed reaction times of their right
hand, and have motor impersistence of eye clo- Cross-References
sure. These clinical studies suggest that the right
hemisphere may be dominant for intentional con- ▶ Attention
trol of the motor systems. Studies with normal ▶ Impersistence
subjects provide further evidence for right- ▶ Neglect Syndrome
hemisphere intentional dominance. The anatomic
and physiological basis for this dominance is not
entirely understood. References and Readings
Studies of patients with focal lesions and
Heilman, K. M. (2004). Intentional neglect. Frontiers in
studies of monkeys suggest that the frontal Bioscience, 9, 694–705.
lobes may play a critical role in mediating inten- Heilman, K. M., Valenstein, E., Rothi, L. J. G., & Watson,
tional activity. The most important areas of the R. T. (2004). Intentional motor disorders and apraxia.
In W. G. Bradley, R. B. Daroff, G. M. Fenichel, &
frontal lobes appear to be the medial and lateral
J. Jankovic (Eds.), Neurology in clinical practice: Prin-
frontal lobes. The frontal cortex has strong pro- ciples of diagnosis and management (pp. 117–130).
jections to the striatum. The lateral portion of Phila Penn: Butterworth Heineman.
Activities of Daily Living (ADL) 45

Heilman, K. M., Watson, R. T., & Valenstein, E. (2003). References and Readings
Neglect and related disorders. In K. M. Heilman &
E. Valenstein (Eds.), Clinical neuropsychology Brown, V., Walker, R., Gray, C., & Findlay, J. (1999). Limb
(4th ed., pp. 296–346). New York: Oxford University activation and the rehabilitation of unilateral neglect: A
Press. Evidence of task-specific effects. Neurocase, 5,
Luria, A. R. (1965). Two kinds of motor perseveration in 129–142.
massive injury to the frontal lobes. Brain, 88, 1–10. Mattingly, J., Robertson, I., & Driver, J. (1998). Modula-
Sandson, J., & Albert, M. L. (1987). Varieties of persever- tion of covert visual attention by hand movement:
ation. Neuropsychologia, 22, 715–732. Evidence from parietal extinction after right hemi-
sphere damage. Neurocase, 4, 245–253.
Priftis, K., Passarini, L., Pilosio, C., Meneghello, F., &
Pitteri, M. (2013). Visual scanning training, limb acti-
vation treatment, and prism adaptation for rehabilitat-
ing left neglect: Who is the winner? Frontiers in
Active Limb Activation Human Neuroscience, 7, 1–12.
Robertson, I., & North, N. (1992). Spatio-motor cueing in
Sarah A. Raskin unilateral left neglect: The role of hemispace, hand and
Department of Psychology and Neuroscience motor activation. Neuropsychologia, 30, 553–563.
Robertson, I., & North, N. (1993). Active and passive
Program, Trinity College, Hartford, CT, USA
activation of left limbs: Influence on visual and sensory
neglect. Neuropsychologia, 31, 293–300.
Robertson, I., & North, N. (1994). One hand is better than
Synonyms two: Motor extinction of left hand advantage in unilat-
eral neglect. Neuropsychologia, 32, 1–11.

Limb activation

Definition Activities of Daily Living (ADL)

Active limb activation is a rehabilitation technique Angela K. Troyer

for individuals with unilateral neglect. In a series of Neuropsychology and Cognitive Health program,
studies, Robertson and North (1992, 1993, 1994) Baycrest Centre for Geriatric Care, Toronto, ON,
and others (Mattingly et al. 1998) have demon- Canada
strated that moving the upper or lower extremity
on the affected side can reduce neglect symptoms.
The effect is seen only with active movement, as Synonyms
opposed to passive movement, and only when the
limb is moved in the effected hemispace. However, Adaptive functions; Functional abilities
the limb need not be observed visually. It should be
noted that the effect has not been demonstrated
universally (e.g., Brown et al. 1999), and treatment Definition
effects may be specific to movements in peri-
personal space (Priftis et al. 2013). Activities of daily living (ADLs) are self-care
activities that are important for health mainte-
nance and independent living. ADLs comprise a
Cross-References broad spectrum of activities, traditionally classi-
fied as basic and instrumental ADLs (BADLs and
▶ Attention Training IADLs, respectively). BADLs, also called physi-
▶ Behavioral Inattention Test (BIT) cal or self-maintenance ADLs, are life-sustaining
▶ Cognitive Rehabilitation self-care activities such as feeding, grooming,
▶ Neglect Syndrome bathing, dressing, toileting, and ambulation.
46 Activities of Daily Living (ADL)

IADLs are more complex activities that are nec- mental disorders requires an appraisal of the
essary for independent living, such as using the patient’s functional ability (American Psychiatric
telephone, preparing meals, shopping, managing Association 2013). For example, impairment in
finances, taking medications, arranging appoint- adaptive or functional ability is a diagnostic crite-
ments, and driving. These activities are important rion for intellectual disability and for schizophre-
for participating in one’s usual work, social, or nia. Impaired daily functioning is also required for
leisure roles. the diagnosis of dementia and is one of the defin-
ing differences between dementia (in which
IADLs are impaired) and mild cognitive impair-
Historical Background ment (in which IADLs are intact or minimally
affected).
The evolution of the concept of ADLs is reflected Increasingly, the evaluation of daily function-
in the development of instruments to measure ing is also used to identify appropriate treatments
these abilities. Measures of BADLs were first for cognitive and mental disorders. In particular,
developed in the 1940s and 1950s, primarily to an important part of determining the effectiveness
determine the required levels of care for institu- of behavioral or pharmacological interventions is
tionalized older adults and those with chronic measuring the impact of the intervention on the
illnesses. These early measures include the patient’s daily functional ability, in addition to
PULSES profile, the Barthel Index, and the Katz cognitive or affective outcomes.
Index of ADL, among others. Later, in the 1960s The ability to perform ADLs, and IADLs in
and 1970s, there was increased interest in caring particular, is related to sensory, motor, cognitive,
for older and disabled individuals in the commu- and behavioral functioning. Within cognition, the
nity, and this spawned the need for tools to mea- domain most consistently related to IADLs is
sure IADLs that are important for independent executive function, although memory, language,
living. Some of the first of these measures were visuospatial ability, and attention also play a role
Lawton and Brody’s IADL Scale and the Disabil- (Royall et al. 2007). Thus, neuropsychologists can
ity Interview Schedule. Recent work has focused expect that their clients with executive dysfunc-
on the development of disorder-specific measures tion are most likely to experience difficulties with
that take into account characteristics of the disor- daily functioning.
der that can systematically impact ADLs, such as
changes in motivation, behavior, vision, or motor Assessment of ADLs
functioning. Assessment of ADLs can be accomplished in a
number of ways. Real-world observation of the
patient in his or her own home provides relevant,
Current Knowledge objective information about daily function. How-
ever, this method is obviously time and labor
ADLs are of interest across various health disci- intensive, and there are practical limits to the
plines. Current knowledge in this area is based on number of behaviors that can be observed within
research conducted by psychologists, occupa- a given time period. An alternative is the use of
tional therapists, nurses, psychiatrists, neurolo- performance-based measures, which require the
gists, and social workers, among others. patient to complete functional tasks – such as
preparing a meal, using the telephone, or making
Relevance to Neuropsychology personal financial transactions – that are pre-
For the neuropsychologist, an understanding of sented in a standardized way in the laboratory or
the patient’s level of independence in ADLs, and clinic. A number of such instruments have been
in particular IADLs, is of interest for several rea- developed to measure single or multiple func-
sons. The diagnosis of a number of cognitive and tional domains. Tests include the Direct
Activities of Daily Living (ADL) 47

Assessment of Functional Status, the Indepen- what constitutes a meaningful change over time,
dent Living Scales, the Structured Assessment information about the relation between test
of Independent Living Skills, the Medication performance and actual real-world functioning, A
Management Abilities Assessment, and many and the development of comprehensive normative
others. data.
The use of questionnaires administered either
on paper or by interview allows the sampling of
a large number of behaviors in a short period of
time. Self-report questionnaires may be appro- Cross-References
priate for use with cognitively normal or mildly
impaired populations. In the evaluation of ▶ Functional Status
dementia and other cognitive disorders, how- ▶ Instrumental Activities of Daily Living
ever, self-reported abilities may be difficult to ▶ Lawton-Brody Instrumental Activities of Daily
interpret because of disease-related decreases in Living Scale
self-awareness. The use of informant-based ▶ Vineland Adaptive Behavior Scales
questionnaires avoids this limitation, although
informants can also be biased in their reports and
may not always be available. Nevertheless, this References and Readings
is one of the most common methods for measur-
ing IADLs, and a large number of informant- American Psychiatric Association. (2013). Diagnostic
and statistical manual of mental disorders
based questionnaires exist, such as the Lawton-
(5th ed.). Washington, DC: American Psychiatric
Brody IADL Scale, the Bristol ADL Scale, Association.
Vineland Adaptive Behavior Scales, and the Floyd, R. G., Shands, E. I., Alfonso, V. C., Phillips, J. F.,
ADL questionnaire. Autry, B. K., Mosteller, J. A., Skinner, M., & Irby, S.
(2015). A systematic review and psychometric evalua-
The choice of which particular method of
tion of adaptive behavior scales and recommendations
assessment to be used will depend, in addition to for practice. Journal of Applied School Psychology, 31,
practical considerations such as time, on the pur- 83–113.
pose of the assessment. Real-word observations Lawton, M. P., & Brody, E. M. (1969). Assessment of older
people: Self-maintaining and instrumental activities of
and performance-based measures provide infor-
daily living. Gerontologist, 9, 179–186.
mation about what the person is capable of McDowell, I. (2006). Measuring health: A guide to rating
doing. Questionnaires, on the other hand, measure scales and questionnaires (3rd ed.). New York:
what the individual is actually doing in his or her Oxford.
Moore, D. J., Palmer, B. W., Patterson, T. L., & Jeste, D. V.
day-to-day life.
(2007). A review of performance-based measures of
functional living skills. Journal of Psychiatric
Research, 41, 97–118.
Future Directions Pendleton, H. M., & Schultz-Krohn, W. (Eds.). (2011).
Pedretti’s occupational therapy: Practice skills for
physical dysfunction (7th ed.). St. Louis: Mosby.
Although there are a large number of relevant Royall, D. R., Lauterbach, E. C., Kaufer, D., Malloy, P.,
instruments that have been developed to assess Coburn, K. L., & Black, K. J. (2007). The cognitive
ADLs, they vary in terms of how well their psy- correlates of functional status: A review from the Com-
mittee on Research of the American Neuropsychiatric
chometric properties have been characterized.
Association. The Journal of Neuropsychiatry and Clin-
Systematic literature reviews (e.g., Floyd et al. ical Neurosciences, 19, 249–265.
2015; Moore et al. 2007; Sikkes et al. 2009) Sikkes, S. A. M., de Lange-de Klerk, E. S. M., Pijnenburg,
indicate that, for many of these measures, there Y. A. L., Scheltens, P., & Uitdehaag, B. M. J. (2009).
A systematic review of instrumental activities of daily
is a need for better theoretical justification of the
living scales in dementia: Room for improvement.
content of the instrument, additional information Journal of Neurology, Neurosurgery, and Psychiatry,
about test validity and reliability, indication of 80, 7–12.
48 Activities of Daily Living Questionnaire

performance and daily functioning in patients

Activities of Daily Living with Alzheimer’s disease (Locascio et al. 1995).
Questionnaire However, the development and psychometric
properties of the measure were first reported in
Jessica Fish Johnson et al. (2004). Since then, a Chinese ver-
Medical Research Council Cognition and Brain sion has been developed and evaluated (ADLQ-
Sciences Unit, Cambridge, UK CV; Chu and Chung 2008), and it has been used in
several studies involving people with non-
Alzheimer’s dementia.
Synonyms

ADLQ Psychometric Data

Johnson et al. (2004) collected ADLQ data from

Description the primary caregivers of 140 people with demen-
tia of various types (Alzheimer’s disease, vascu-
The activities of daily living questionnaire lar/mixed, and frontotemporal/primary
(ADLQ) was developed to measure the func- progressive aphasia). The scale was completed
tional abilities of people with dementia. It is an twice, with a 1 year interval between completions.
informant-rated questionnaire and should be Evidence of convergent validity was in the form
completed by the patient’s primary caregiver. of correlations with global severity ratings
It consists of 28 items covering both basic and (clinical dementia rating r = 0.5 and 0.55 for
instrumental activities of daily living, orga- first/second ratings, respectively; MMSE
nized into six subscales: self-care activities, r = 0.42 and 0.38 for first and second ratings,
household care, employment and recreation, respectively). Further evidence of its validity
shopping and money, travel, and communica- came from the finding that scores declined signif-
tion. The informant rates the subject’s compe- icantly over the year-long interval between test-
tence in each area according to a set of four ings, as would be expected in people with
descriptions of different competence levels; degenerative conditions. A subgroup of 28 partic-
scores range from 0 to 3 where higher scores ipants took part in a test-retest reliability study,
indicate greater impairment. A fifth response with a 2–8 week interval between testings (mean
option, “don’t know/has never done” is also 25.6 days, SD 12.2). Correlations between first
available, and if this option is selected, the and second ratings for the six subscales were
item is excluded from scoring. Scores from high, between 0.86 and 0.92, with the exception
individual items are summed (with adjustment of the employment subscale, which correlated at
for any items marked “don’t know/has never 0.65. Kappa scores for 25% of scale items were
done”) to form subscale scores and then trans- 0.42–0.60 (classified as “moderate”), for 54% of
formed to a percentage impairment total score. scale items were 0.61–0.80 (classified as “good”),
Scores of 0–33% are classified as no/mild and for 21% of scale items 0.81–1.0 (classified as
impairment, those of 34–66% as moderate “very good”). The validity of the ADLQ was
impairment, and those of 67–100% as severe investigated via correlations between 29 partici-
impairment. pants’ scores on the ADLQ and the record of
independent living (RIL), another ADL measure.
In line with Johnson et al.’s predictions, there
Historical Background were significant correlations between the ADLQ
and the “activities” and “communication” sub-
The first reported use of the ADLQ was in a scales of the RIL but not the “behavior” subscale
longitudinal study looking at cognitive test of the RIL.
Activity Restrictions, Limitations 49

Chu and Chung (2008) conducted a study exam-

ining the psychometric properties of a Chinese Activity Restrictions,
translation of the ADLQ (ADLQ-CV), with Limitations A
125 caregivers of people with moderate
Alzheimer’s disease. The ADLQ-CV was shown Brian Yochim
to have good internal consistency (a = 0.81), test- Department of Psychology, University of
retest reliability at a 2-week interval (intra-class Colorado at Colorado Springs, Colorado Springs,
correlation (ICC) = 0.998), and inter-rater reliability CO, USA
(ICC = 0.997, for primary and secondary caregiver
ratings). Correlations with the disability assessment
for dementia were strong (r = 0.92), suggesting that Definition
it is a valid measure. A factor analysis also con-
firmed that the ADLQ-CV has a six-factor structure, This idea refers to restrictions prescribed by clini-
following the six proposed subscales. cians who treat patients with recent strokes, head
injuries, or other neurological conditions, after a
neurological event has left the patient with deficits
in important areas of functioning. Patients are
Clinical Uses
often restricted from driving, cooking, managing
finances, or completing other instrumental activi-
The ADLQ may be used to assist in the diagnosis
ties of daily living after a neurological event. The
of dementia, in decision-making regarding neces-
activities of focus must be tailored to the patient
sary intervention and/or assistance, and in moni-
and can range from restrictions in playing profes-
toring change over time or in response to
sional sports to restrictions in managing small
treatment.
amounts of cash.

Cross-References
Current Knowledge
▶ Alzheimer’s Disease Cooperative Study ADL
Rehabilitation professionals encounter patients
Scale
whose injuries have left them with deficits both
▶ Bristol Activities of Daily Living Scale
in physical and cognitive realms. Strokes and
▶ Disability Assessment for Dementia
traumatic brain injuries can cause physical impair-
▶ Lawton-Brody Instrumental Activities of Daily
ments in walking, swallowing, use of an arm
Living Scale
and/or leg, communication, and other important
skills. Injuries can also lead to cognitive deficits in
memory, executive functioning, social function-
References and Readings
ing, language, visuospatial skills, attention, and/or
Chu, T. K. C., & Chung, J. C. C. (2008). Psychometric processing speed. These basic deficits in turn lead
evaluation of the Chinese version of the activities of to impaired functioning in everyday life. Rehabil-
daily living questionnaire (ADLQ-CV). International itation professionals must assess patients’ abilities
Psychogeriatrics, 20, 1251–1261. to complete these daily activities and often must
Johnson, N., Barion, A., Rademaker, A., Rehkemper, G., &
Weintraub, S. (2004). The activities of daily living place restrictions on what activities patients can
questionnaire: A validation study in patients with continue to complete. If patients are deemed to be
dementia. Alzheimer’s Disease and Associated Disor- unable to drive, for example, clinicians must fol-
ders, 18, 223–230. low appropriate legal and ethical channels to pro-
Locascio, J. J., Growdon, J. H., & Corkin, S. (1995). Cog-
nitive test performance in detecting, staging, and track- tect the patient and public.
ing Alzheimer’s disease. Archives of Neurology, These limitations in activities can lead to diffi-
52(11), 1087–1099. culties in adjustment for the patient, which can
50 Actus Reus

sometimes result in depressed mood and other established that the defendant also possessed
affective symptoms. This notion is related to the “mens rea,” which translates to “guilty mind,”
Activity Restriction Model of Depressed Affect referring to the mental element of the crime.
(Williamson and Shaffer 2000), which has been Thus, a conviction necessitates, beyond reason-
studied as one etiology of depressive symptoms able doubt, establishment of an illegal act
among older adults. coupled with a particular mental state (e.g.,
intent, knowledge, recklessness, or negligence).
Description of the actus reus is typically classi-
fied into one of three categories: commissions,
Cross-References
omissions, and/or commonwealth. Commission
refers to an affirmative act; omission refers to a
▶ Instrumental Activities of Daily Living
failure to act; and commonwealth refers to a state
▶ Recommendation
of affairs or circumstances. Commissions and
omissions necessitate causation; commonwealth
does not always require voluntariness; and
References and Readings
instead the actus reus is viewed in light of the
Greenwood, R. J., Barnes, M. P., McMillan, T. M., & Ward, severity of the offense.
C. D. (Eds.). (2003). Handbook of neurological reha-
bilitation (2nd ed.). New York: Psychology Press.
Mills, V. M., Cassidy, J. W., & Katz, D. I. (Eds.). (1997). Cross-References
Neurologic rehabilitation: A guide to diagnosis, prog-
nosis, and treatment planning. Malden: Blackwell. ▶ Insanity
Williamson, G. M., & Shaffer, D. R. (2000). The activity
restriction model of depressed affect: Antecedents and
▶ Insanity Defense
consequences of restricted normal activities. In G. M. ▶ Mens Rea
Williamson, D. R. Shaffer, & P. A. Parmelee (Eds.),
Physical illness and depression in older adults:
A handbook of theory, research, and practice.
New York: Kluwer/Plenum Publishers.
References and Readings

Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin,

C. (1997). Psychological evaluations for the courts:
A handbook for mental health professionals and law-
Actus Reus yers. New York: Guilford.

Moira C. Dux
US Department of Veteran Affairs, Baltimore, Acute Lymphoblastic
MD, USA Leukemia

Jacqueline L. Cunningham1 and

Definition Carol L. Armstrong2
1
Department of Psychology, Children’s Hospital
Actus reus is Latin for “guilty act.” Under most of Philadelphia, Philadelphia, PA, USA
circumstances, a crime consists of at least two 2
Child and Adolescent Psychiatry and Behavioral
factors. The first factor is the physical conduct or Sciences, The Children’s Hospital of
act associated with the crime, which is known as Philadelphia, Philadelphia, PA, USA
the “actus reus.” In order for an individual to be
convicted of a crime, it must be demonstrated
beyond a reasonable doubt that the defendant Synonyms
committed the physical act of the crime or the
“actus reus.” However, it must concurrently be ALL
Acute Lymphoblastic Leukemia 51

Definition survivors in both those who were not treated

with cranial irradiation and those who were.
Acute lymphoblastic leukemia (ALL) is a form of Whereas atrophy is associated with treatment- A
cancer of the white blood cells (leukocytes). ALL effects of cranial irradiation therapy and intra-
is the most common type of childhood leukemia thecal chemotherapy (usually methotrexate), it
and is distinguished from chronic lymphoblastic can also occur as a result of the condition, itself,
leukemia (CLL) and acute myeloid rather than as an outcome of treatment, as it
(or myelogenous) leukemia, which are more prev- appears to cause atrophy of the brain, which is
alent in adults. not specific to certain brain tissues (Lucy Rorke,
M.D., personal communication); however, few
children with ALL are naïve to chemotherapy
Current Knowledge and radiotherapy, and the effects of time are not
controlled in studies so that the developmental
Symptoms effects of damage from the disease and from the
ALL is characterized by the rapid proliferation treatments both magnify over time. A study to
of immature blood cells (lymphoblasts), which discriminate the effects of treatment versus dis-
crowd out mature, functional cells. It is associ- ease would require studies of children with ALL
ated with the enlargement of lymphoid tissue in at diagnosis and prior to treatments. Nonethe-
areas including the lymph nodes, spleen, bone less, the strongest detrimental impacts on cog-
marrow, and lungs and with increased lympho- nition are attributable to treatment effects and
cytic cells circulating in blood and in various their damaging influence on the biological sub-
tissues and organs. Persons afflicted will expe- strates of core neurocognitive abilities, includ-
rience weakness and fatigue, anemia, ing executive functions (self-regulation,
unexplained fever and infections, weight loss, inhibitory control, cognitive flexibility,
or loss of appetite. problem-solving), memory, verbal skills, and
information processing. Such impacts disrupt
Pathophysiology the secondary abilities, i.e., those that are
Cancer, including ALL, is caused by damage acquired and knowledge-based. The main
to DNA. approaches to alleviating neurocognitive effects
of treatment include cognitive remediation,
Treatment pharmacology, and ecological alterations in the
The earlier the ALL is detected, the more effective classroom.
is its treatment. The goal is to induce a lasting The presentation of survivors in adulthood is
remission, considered to be a prevalence of less highly variable in both IQ and neuropsychological
than 5% of lymphoblasts in bone marrow. tests, with clinical factors intermediating, includ-
Advances made in the ability to match the genetic ing polymorphisms that regulate inflammatory
properties of the blast cells to treatment options, in cytokine expression, cumulative dose, intensity
association with the availability of new drugs and of cancer therapy, age at diagnosis, years since
improvements made in bone marrow and stem cell diagnosis, and gender. Adult survivors are at
transplantation, have changed the prognosis for heightened risk of neurocognitive disorders.
ALL from a zero to a 75% survival rate over the
past 40 years.
Most (if not all) patients with a childhood
history of ALL have brain atrophy. MRI has Cross-References
also demonstrated white matter changes in a
minority of children. A large study identified ▶ Acute Myelogenous Leukemia
reduced cortical gray and white matter, caudate ▶ Leukemia
nucleus, amygdala, and hippocampus in adult ▶ Neoplasms
52 Acute Myelogenous Leukemia

References and Readings Definition

Butler, R. W., & Mulhern, R. K. (2005). Neurocognitive Acute myelogenous leukemia (AML) is a form of
interventions for children and adolescents surviving
cancer of the white blood cells (leukocytes). It is a
cancer. Journal of Pediatric Psychology, 30, 65–78.
Crosley, C. J., Rorke, L. B., Evans, A., & Nigro, M. (1978). relatively rare cancer that occurs more commonly
Central nervous system lesions in childhood leukemia. in adults than in children, with more men affected
Neurology, 28, 678–685. than women. The median age at diagnosis is
De Oliveira-Gomes, E. R., Leite, D. S., Garcia, D. F.,
63 years.
Maranhao, S., & Hazin, I. (2012). Neuropsychological
profile of patients with actue lymphoblastic leukemia.
Psychology & Neuroscience, 5(2), 175–182. https://
doi.org/10.3922/j.psns.2012.2.07. Current Knowledge
Edelmann, M. N., & Krull, K. R. (2013). Brain volume and
cognitive function in adult survivors of childhood acute
lymphoblastic leukemia. Translational Pediatrics, Symptoms
2(4), 143–147. Acute forms of leukemia are characterized by the
Lofstad, G. E., Reinfjell, T., Hestad, K., & Diseth, T. H. rapid proliferation of immature blood cells which
(2009). Cognitive outcome in children and adoles-
rapidly crowd out mature, functional cells. In
cents treated for acute lymphoblastic leukaemia
with chemotherapy alone. Acta Paediatrica, 98(1), AML, the cell type is granuloid, whose cancerous
180–186. change disrupts its normal ability to form red
Pääkkö, E., Harila-Saari, A., Vanionpää, L., Himanen, S., cells, some types of white cells, and platelets.
Pyhtinen, J., & Lanning, M. (2000). White matter
Resulting symptoms are anemia, easy bruising
changes on MRI during treatment in children with
acute lymphoblastic leukemia: Correlation with neuro- and bleeding, and disruption to the body’s ability
psychological findings. Pediatric Blood & Cancer, to resist infection. Impaired cognition and fatigue
35(5), 456–461. are also strongly associated with AML. Whereas
Prassopoulos, P., Carouras, D., Golfinopoulos, S.,
impairments in these areas have been attributed to
Evlogias, N., Theodoropoulos, V., & Panagiotou,
J. (1996). Quantitative assessment of cerebral atrophy effects of chemotherapy, recent research by
during and after treatment in children with acute lym- Meyers, Albitar, and Estey (2005) has identified
phoblastic leukemia. Investigational Radiology, 12, differing cytokine levels present prior to chemo-
749–754.
therapy as also contributing to these symptoms.
Pui, C.-H. (2003). Treatment of acute leukemias: New
directions for clinical research. New York: Humana
Press. Pathophysiology
Zeller, B., Tamnes, C. K., Kanellopoulos, A., Amlien, I. K., The malignant cell in AML is the myeloblast, a
Andersson, S., Due-Tønnessen, P., Fjell, A. M.,
mutated and immature cell in the granulocytic
Walhovd, K. B., Westlye, L. T., & Ruud, E. (2013).
Reduced neuroanatomic volumes in long-term survi- series, which undergoes combinations with other
vors of childhood acute lymphoblastic leukemia. Jour- mutations, to produce a leukemic clone of cells.
nal of Clinical Oncology, 31(17), 2078–2085. Because the process contributes to much diversity
and heterogeneity in cell differentiation, the diag-
nosis of AML can be challenging. It remains
important, however, since the chromosomal struc-
Acute Myelogenous Leukemia ture of the leukemic cells is the disease’s most
critical prognostic factor.
Jacqueline L. Cunningham
Department of Psychology, Children’s Hospital of Treatment
Philadelphia, Philadelphia, PA, USA Treatment in AML consists primarily of chemo-
therapy, with the goal of achieving remission.
Without postremission (consolidation) therapy,
Synonyms almost all patients eventually relapse. Neuro-
cognitive and neuropsychiatric symptoms are
Acute myeloid leukemia; AML highly prevalent in patients with cancer and
Acute Respiratory Distress Syndrome 53

cause significant impairments in their ability to common acute side effect during radiotherapy
function. Whereas such impairments are known than other complications that depend on the spe-
to be associated with aggressive cancer treatment, cific structures in the pathway of the target of the A
they are additionally attributed to biologic mech- radiation. Although it is self-limiting, and resolves
anisms underlying the cancer itself. Recent with medication and with the termination of irra-
research (Meyers et al. 2005) on AML has made diation, symptoms can be upsetting to patients.
linkages between cytokine-immunologic activa- Nursing intervention which focuses on prepara-
tion and factors including cognitive functioning, tion through counseling and education serves to
significant fatigue, and quality of life in AML alleviate distress. Acute radiation somnolence is
patients studied prior to the initiation of treatment. usually treated with steroids.

Cross-References Cross-References

▶ Acute Lymphoblastic Leukemia ▶ Radiation Oncology

▶ Leukemia ▶ Radiotherapy
▶ Neoplasms

References and Readings

References and Readings
Brady, L. W., Heilmann, H. P., Molls, M., & Schlegel,
W. (2006). New techniques in radiation oncology.
Meyers, C. A., Albitar, M., & Estey, E. (2005). Cognitive
New York: Springer.
impairment, fatigue, and cytokine levels in patients
Walker, A. J., Ruzevick, J., Malayeri, A. A., Rigamonti, D.,
with acute myelogenous leukemia or myelodysplastic
Lim, M., Redmond, K. J., & Kleinberg, L. (2014).
syndrome. Cancer, 104, 788–793.
Future Oncology, 10(7), 1277–1297.
Pui, C.-H. (2003). Treatment of acute leukemias: New
directions for clinical research. New York: Humana
Press.

Acute Respiratory Distress

Syndrome
Acute Radiation Somnolence
Dona Locke
Jacqueline L. Cunningham Psychiatry and Psychology, Mayo Clinic,
Department of Psychology, Children’s Hospital of Scottsdale, AZ, USA
Philadelphia, Philadelphia, PA, USA

Synonyms
Definition
Adult respiratory distress syndrome; Respiratory
Acute radiation somnolence is a relatively tran- distress syndrome
sient and benign effect of cranial irradiation. It is
manifested as sleepiness occurring during irradi-
ation used to treat brain tumors. Multiple variables Definition
are associated, including total dose, fraction size,
time between fractions, treatment volume, and Acute respiratory distress syndrome (ARDS) is
concurrent chemotherapy. It occurs in both the presence of pulmonary edema in the absence
children and adults and usually affects daily func- of volume overload or depressed left ventricular
tioning during the course of treatment and is a less function and is characterized by the development
54 Acute Respiratory Distress Syndrome

of sudden breathlessness within hours to days of Death usually results from multisystem organ fail-
an inciting event. ARDS is not a specific disease; ure rather than lung failure alone.
instead, it is a type of severe, acute lung dysfunc- Causes: A number of clinical conditions are
tion that is associated with a variety of diseases associated with the development of ARDS.
and trauma.
• Sepsis and the systemic inflammatory response
syndrome (SIRS) are the most common condi-
Historical Background tions associated with the development
of ARDS.
In the past, ARDS signified adult respiratory dis- • Severe traumatic injury (especially multiple
tress syndrome to separate this from infant respi- fractures), severe head injury, and pulmonary
ratory distress syndrome seen in premature contusion are strongly associated with the
infants. However, this type of pulmonary edema development of ARDS. In traumatic injury,
can also occur in children, so ARDS has gradually factures of the long bones can cause ARDS
evolved to mean acute rather than adult. through fat embolism. In severe brain injury,
ARDS is thought to develop owing to a sudden
discharge of the sympathetic nervous system,
Current Knowledge which then leads to acute pulmonary hyperten-
sion and injury to the pulmonary capillary bed.
ARDS typically develops within 12–48 h after the In pulmonary contusions, ARDS develops
inciting event, although, in rare instances, it may through direct trauma to the lung.
take up to a few days. Persons developing ARDS • Multiple blood transfusions are an independent
are critically ill, often with multisystem organ risk factor for ARDS. The risk is independent
failure. It is a life-threatening condition; therefore, of the reason for the transfusion or the coexis-
hospitalization is required for prompt tence of trauma. The incidence of ARDS
management. increases with the number of units of blood
ARDS is associated with severe and diffuse transfused. If the patient has preexisting abnor-
injury to the alveolar-capillary membrane (the air mal liver functioning or a coagulation abnor-
sacs and small blood vessels) of the lungs. Fluid mality, the risk is further increased.
accumulates in some alveoli of the lungs, while • Near drowning can be another cause of ARDS.
some other alveoli collapse. This alveolar damage Development of ARDS is slightly more com-
impedes the exchange of oxygen and carbon diox- mon with saltwater than with freshwater.
ide, which leads to a reduced concentration of Aspiration leads to an osmotic gradient that
oxygen in the blood. Low levels of oxygen in favors movement of water into air spaces of
the blood cause damage to other vital organs of the lung. Aspiration may be visible with chest
the body such as the kidneys. radiography, although the chest radiograph
The 1994 American-European Consensus may be normal early in the course of the
Committee defines ARDS as the acute onset of disease.
bilateral infiltrates on chest radiography, a partial • Smoke inhalation is another possible cause of
pressure of arterial oxygen (PaO2) to fraction of ARDS. Smoke inhalation causes lung tissue
inspired oxygen (FIO2) ratio of less than damage from direct heat, toxic chemicals, and
200 mmHg and a pulmonary artery occlusion particulate matter carried into the lung. Patients
pressure of less than 18, or the absence of clinical with smoke inhalation initially may be asymp-
evidence of left arterial hypertension. Revised tomatic, but patients with airway burns, expo-
definition in 2012 (JAMA) describes criteria for sure to toxic fumes, or exposure to carbon
mild, moderate, and severe ARDS based on PaO2 monoxide should be monitored closely for the
and FIO2. Mortality rate is approximately 27% for development of ARDS, even if the symptoms
mild, 32% for moderate, and 45% for severe. are initially absent.
Acute Stress Disorder 55

• Overdoses of narcotics, tricyclic antidepres- Cross-References

sants, and other sedatives have been associated
with the development of ARDS. Overdoses of ▶ Anoxia A
tricyclic antidepressants are the most common.
This risk is independent of the risk from con-
current aspiration. References and Readings

Acute Respiratory Distress Syndrome. (2012). The Berlin

Medical treatment for ARDS: definition. Journal of the American Medical Associa-
tion, 307(23), 2526–2533.
• People with ARDS require hospitalization and Bernard, G. R., Artigas, A., Brigham, K. L., Charlet, J.,
Falke, K., Hudson, L., Lamy, M., Legall, J. R., Morris,
treatment in an intensive care unit. A., & Spragg, R. (1994). Report of the American-
• There is no specific treatment for ARDS, but, European consensus conference on ARDS: Definitions,
rather, treatment is primarily supportive using mechanisms, relevant outcomes and clinical trial coor-
a mechanical respirator and supplemental dination. Intensive Care Medicine, 20, 225–232.
oxygen.
• Diuretics can be given to eliminate fluid from
the lungs. However, fluids are often given via
IV to provide nutrition and prevent dehydra-
Acute Stress Disorder
tion, but fluids must be carefully monitored to
avoid fluid accumulation in the lungs.
Daniel W. Klyce
• Antibiotic therapy may be administered to treat
Virginia Commonwealth University – School of
infection, which is often the underlying cause
Medicine, Richmond, VA, USA
of ARDS.
• Corticosteroids may sometimes be given late in
the process of ARDS or if the patient is in
Synonyms
shock. If the patient is in shock, drugs to coun-
teract low blood pressure caused by shock may
Acute stress response; Stress reaction
be administered.
• If the patient is experiencing anxiety, this can
be treated with antianxiety medications.
Short Description or Definition

Respiratory therapists may see these patients to Acute stress disorder (ASD) is defined in the
provide inhaled drugs to decrease inflammation Diagnostic and Statistical Manual of Mental Dis-
and provide respiratory comfort. orders (5th ed.; DSM-5; American Psychiatric
Because of the acute and medically serious Association 2013) by a pattern of symptoms asso-
nature of ARDS, it would be unlikely for neuro- ciated with exposure to an actual or threatened
psychological exam to be requested when a per- trauma or stressor. Exposure may involve (1)
son is acutely ill with ARDS. Mortality with direct experience of traumatic events, (2) person-
ARDS is 30–40%, and the person would typi- ally witnessing events, (3) learning of events that
cally be treated in an intensive care unit. If the occurred to others, and (4) repeated or extreme
person survives, outpatient neuropsychological exposure to details of traumatic events. Symptoms
evaluation could be requested, and results may associated with the exposure may include intru-
show memory deficits related to the hypoxia as sion symptoms (i.e., involuntary memories,
well as neuropsychological deficits related to the distressing dreams, flashbacks, intense responses
underlying medical cause for ARDS (e.g., to triggers), negative mood, dissociative symp-
severe TBI, near drowning, sepsis, medication toms, avoidance symptoms, and symptoms of
overdose). physiological arousal (i.e., sleep disturbance,
56 Acute Stress Disorder

irritability/anger, hypervigilance, poor concentra- individuals with a diagnosis of PTSD, it is esti-

tion, and exaggerated startle response). To be mated that 48% originally had symptoms of ASD.
diagnosed as ASD, symptoms must persist for at Acute stress disorder is a narrower form of an
least 3 days and not longer than a month (at which acute stress reaction with a prominent anxiety or
point they might be more representative of post- fear component. The diagnosis of adjustment dis-
traumatic stress disorder). order more appropriately captures the breadth of
disruptive psychological reactions to stress or
trauma that may be characterized by grief, anger,
Categorization depression, etc. Acute stress disorder may also be
difficult to distinguish from postconcussive symp-
The disorder is classified with the trauma- and toms following head trauma. These two disorders
stressor-related disorders in DSM-5. share many physiological, cognitive, emotional,
and behavioral sequelae (e.g., sensitivity to envi-
ronmental stimuli, difficulty concentrating, and
Current Knowledge irritability). Recent research has revealed that
individuals exposed to experimentally induced
Development and Course acute psychosocial stressors exhibit impairments
Prevalence rates for ASD tend to vary in associa- in attentional processes and spatial working mem-
tion with the nature or severity of the stressor and ory (e.g., Sänger et al., 2014; Olver et al., 2015).
situational factors following the onset of the
stressor (e.g., the persistence of the initial threat). Assessment and Treatment
Prevalence rates tend to be higher if the trauma A diagnosis of ASD should capture an individual’s
involves interpersonal violence, and these rates current distress and indicate the importance of facil-
have been reported to range from as much as itating treatment and resources. An essential feature
20% to 50% of such cases. Other common index of assessment involves the identification of an index
traumas include motor vehicle accidents, severe stressor or trauma. Assessment and treatment may
burns, work-related or industrial accidents, and be complicated in situations involving persistent
traumatic medical events. In a 2011 review of threat. Given the temporal proximity to traumatic
studies reporting incidence of ASD associated events associated with a diagnosis of ASD (i.e., as
with a variety of stressors, Bryant found rates of little as 3 days), it may be important to rule out
ASD ranging from 7% to 28%, with a mean inci- physical or medical conditions associated with
dence rate of 13%. By definition, ASD cannot be trauma or to facilitate medical stabilization and
diagnosed beyond 1 month from the onset of the treatment. Acute stress disorder may be assessed
stressor or trauma. During this period, symptoms with measures such as the Acute Stress Disorder
may worsen along with exacerbation of stress. Scale (Bryant et al., 2000) and the National Stress-
Women appear to be at higher risk for the devel- ful Events Survey Acute Stress Disorder Short
opment of ASD. The risk of ASD also appears to Scale (Kilpatric et al., 2013).
increase among individuals who have a history of Given the relatively brief course of symptoms
other psychological disorders and who perceive associated with ASD, it has been difficult to estab-
the index trauma as more severe. lish an evidence base for potential interventions.
Generally, once ASD has been diagnosed, it is
Associated Disorders and Current Research helpful to provide psychoeducation and normali-
Originally, ASD was developed to identify indi- zation regarding common psychological reactions
viduals who may eventually develop symptoms of to trauma, along with normative expectations for
posttraumatic stress disorder (PTSD). Acute stress recovery. Given the likelihood that individuals
disorder remains strongly associated with PTSD, with ASD may go on to develop PTSD, it may
with at least half of trauma survivors who have a be helpful to facilitate case management and refer-
diagnosis of ASD progressing to PTSD. Among rals for mental health treatment including
Adaptive Behavior Assessment System: Third Edition 57

psychopharmacological or psychotherapeutic
treatments for posttraumatic stress. Adaptive Behavior
During the acute phase of recovery from a Assessment System: Third A
stressor or trauma, it may also be possible to Edition
provide brief interventions for cognitive and
physiological symptoms of anxiety. These may Patti L. Harrison1 and Thomas Oakland2
1
include strengths-based coping strategies, behav- School Psychology, The University of Alabama,
ioral strategies for addressing symptoms of anx- Tuscaloosa, AL, USA
2
ious arousal (e.g., relaxation training), and Department of Educational Psychology, College
elements of trauma-focused cognitive-behavioral of Education University of Florida, Gainesville,
therapies to address common negative or cata- FL, USA
strophic thoughts associated with the trauma.

Synonyms
See Also
ABAS; ABAS-II; ABAS-3
▶ Adjustment Disorder
▶ Postconcussion Syndrome
Description
▶ Post-traumatic Stress Disorder
The Adaptive Behavior Assessment System – Third
Edition (ABAS-3; Harrison and Oakland 2015)
References provides an assessment of adaptive behavior and
skills for persons from birth through age 89. Five
American Psychiatric Association. (2013). Diagnostic and forms are available: parent/primary caregiver form
statistical manual of mental disorders (5th ed.). Arling-
ton: American Psychiatric Association Publishing.
(for ages 0–5), teacher/day-care provider form (for
Bryant, R. A. (2010). Acute stress disorder as a predictor of ages 2–5), parent form (for ages 5–21), teacher form
posttraumatic stress disorder: A systematic review. The (for ages 5–21), and adult form (for ages 16–89).
Journal of Clinical Psychiatry, 72(2), 233–239. The ABAS-3 standardization samples are large
Bryant, R. A., Moulds, M. L., & Guthrie, R. M. (2000). Acute
stress disorder scale: A self-report measure of acute stress
(4,500) and representative of 2010 US census data
disorder. Psychological Assessment, 12(1), 61–68. with respect to gender, race/ethnicity, and socioeco-
Bryant, R. A., Friedman, M. J., Spiegel, D., Ursano, R., & nomic status and included individuals with typical
Strain, J. (2011). A review of acute stress disorder in abilities as well as those with disabilities. Forms are
DSM-5. Depression and Anxiety, 28(9), 802–817.
Kilpatrick, D. G., Resnick, H. S., & Friedman, M. J.
available in Spanish in the USA and are being
(2013). National stressful events survey ASD short adapted for use in a number of other countries,
scale (NSESSS-ASD). Arlington: American Psychiatric including in Europe and Asia.
Association.
Olver, J. S., Pinney, M., Maruff, P., & Norman, T. R.
(2015). Impairments of spatial working memory and
attention following acute psychosocial stress. Stress Foundation and Structure
and Health, 31(2), 115–123.
Sänger, J., Bechtold, L., Schoofs, D., Blaszkewicz, M., Criteria for a diagnosis of intellectual disability
& Wascher, E. (2014). The influence of acute
stress on attention mechanisms and its electrophysi-
have been identified in policy and legislation for
ological correlates. Frontiers in Behavioral Neuro- community services and special education. A
science, 8, 353. diagnosis of intellectual disability requires docu-
Ursano, R. J., Bell, C., Eth, S., Friedman, M., Norwood, mentation of deficits in both intelligence and
A., Pfefferbaum, B., ... & Charles, S. C. (2004). Prac-
tice guideline for the treatment of patients with acute
stress disorder and posttraumatic stress disorder. The
American Journal of Psychiatry, 161(Suppl 11), 3–31. Thomas Oakland: deceased.
58 Adaptive Behavior Assessment System: Third Edition

adaptive behavior. Although supported by its caregivers, teachers, other relatives) familiar
foundation in assessment for intellectual disabil- with the daily functioning of an individual. All
ities, adaptive behavior assessment has broader items are scored on a four-point scale: 0 (cannot
uses for numerous individuals with a variety of perform the behavior), 1 (can perform the behav-
disabilities and challenges. Adaptive behavior ior yet does not), 2 (performs the behavior some-
assessment is conducted routinely to identify times), and 4 (performs the behavior most or
strengths and weaknesses and plan supports and all of the time). This feature is consistent with
services for children and adults with limitations the World Health Organization’s International
that may interfere with daily functioning. Classification of Functioning (Mpofu and Oak-
The ABAS (Harrison and Oakland 2000) and land 2010) effort to distinguish abilities and
ABAS-II (Harrison and Oakland 2003) preceded performance.
the development of the ABAS-3. As with previous Respondents may indicate that they guessed
editions, the ABAS-3 was developed to be a mea- item scores for behaviors that they have not
sure of adaptive behavior consistent with current observed but can estimate based on the person’s
definitions (e.g., most recently those promulgated performance of other skills. Data from adaptive
by the American Psychiatric Association’s (APA skill areas with four or more guesses should not be
2013) Diagnostic and Statistical Manual of Mental used. The ABAS-3’s scoring and reporting system
Disorders and the American Association on Intel- informs clinicians of interventions likely to pro-
lectual and Developmental Disabilities’ (AAIDD mote the development of selected behaviors asso-
2010) models of adaptive behavior) that ciated with critical items.
underscored the importance of three broad
domains of adaptive behavior: conceptual, social,
and practical. In addition, the three editions of the Psychometric Data
ABAS have included measurement of ten specific
adaptive skill areas commonly identified in defini- General Adaptive Composite and domain stan-
tions and measure of adaptive behavior: commu- dard scores generally range from 40 to 120. Con-
nication, community use, functional academics, sistent with all measures of adaptive behavior, the
health and safety, home or school living, leisure, ABAS-3 is more sensitive to the assessment of
self-care, self-direction, social, and work skills. adaptive behavior and skills at lower to average
Scaled scores (M = 10, SD = 3) for adaptive ranges than at higher ranges. Cut scores are not
skill areas are provided (Table 1). Ten skill area provided by disability category; instead, reliance
scores combine to produce standard scores is placed on diagnostic standards established by
(M = 100, SD = 15) in their respective domains: state and national authorities.
conceptual (communication, functional academics, The ABAS-3 demonstrates suitable psycho-
and self-direction), social (social skills and leisure), metric qualities. Internal consistency is high,
and practical (self-care, home or school living, com- with reliability coefficients of 0.85–0.99 for the
munity use, health and safety, and work for adults). General Adaptive Composite and three adaptive
Motor skill is an additional adaptive skill area behavior domains and somewhat lower coeffi-
assessed for young children but is not included in cients for the briefer adaptive skill areas. Test-
a broad domain. A General Adaptive Composite retest and interrater reliability coefficients gener-
standard score (M = 100, SD = 15) also is derived ally are in the 0.70s and 0.80s for the General
from the adaptive skill area scores. Adaptive Composite, three domains, and skill
areas. The ABAS-3 construct validity is strong
as displayed through factor analyses. Its concur-
Item Rating Data rent validity with the Vineland Adaptive Behavior
Scales – Second Edition – is generally high. The
ABAS-3 items are administered in rating scales validity of the ABAS-3 also is supported by evi-
completed by respondents (e.g., parents, dence that its scores distinguish between
Adaptive Behavior Assessment System: Third Edition 59

Adaptive Behavior Assessment System: Third Edition, Table 1 Adaptive skills and three adaptive domains
(Adapted from Harrison and Oakland 2015)
Adaptive skills
A
Communication Speech, language, and listening skills needed for communication with
others, including vocabulary, responding to questions, and participating
in conversations
Community use Skills needed for functioning in the community, including use of
community services, shopping, and getting around in the neighborhood
Functional academics (functional pre- Basic reading, writing, math, and other skills needed for daily
academics for young children) functioning, including telling time, measurement, writing, and counting
money
Home living (school living for teacher Skills needed for basic care of a home or school setting, including
forms) cleaning, straightening, cooking, and completing chores
Health and safety Skills needed to promote health and safety and respond to illness and
injury, including following safety rules, using medication, and staying
away from danger
Leisure Skills needed for participating in leisure and recreational activities,
including playing, attending community activities, and following game
rules
Self-care Skills needed for personal care including eating, dressing, bathing,
toileting, and grooming
Self-direction Skills needed for independence, responsibility, and self-control, including
completing tasks, keeping schedules, following directions, and making
choices
Social Skills needed to interact socially and get along with others, including
having friends, demonstrating emotions, and helping others
Work Skills needed for successful functioning in a part-time or full-time work
setting, including completing tasks, working with supervisors, and
following a schedule (completed only for individuals who have a job)
Motor skillsa Basic gross and fine motor skills needed for movement and manual
manipulation of objects, including sitting, standing, walking, and fine
motor control
Three domains and associated skill areas
Conceptual Includes communication, functional academics, self-direction,
Practical Includes social skills and leisure skills
Social Includes self-care, home/school living, community use, health and safety,
and work skills
General adaptive composite: Derived from all adaptive skill areas
a
Although fine and gross motor development is not included as one of the ten skills identified by the American Association
on Intellectual and Developmental Disabilities, it is included in some scales of adaptive behavior, including the ABAS-3
parent/primary caregiver form (for ages 0-5) and teacher/daycare provider form (for ages 2-5)

individuals with typical functioning and those in diagnosis as well as in intervention planning and
clinical groups, such as individuals with intellec- monitoring for this and other disorders. The
tual disabilities, autism, and attention disorders. ABAS-3 also may assist in promoting an under-
standing of the impact on daily life activities for
people with a number of other disorders and lim-
Clinical Uses itations, as described in resources about the
ABAS-II and applicable to the comparable
Measures of adaptive behavior have been most ABAS-3 (e.g., Ditterline et al. 2008; Harman et
important in the assessment of persons with intel- al. 2009; Oakland and Harrison 2008; Olley and
lectual disabilities The ABAS-3 is useful in this Cox 2008).
60 Adenoma

The ABAS-3 provides important information American Psychiatric Association. (2013). Diagnostic and
for the assessment and planning services for chil- statistical manual of mental disorders (5th ed.). Wash-
ington, DC: Author.
dren with limitations often diagnosed first during Ditterline, J., Banner, D., Oakland, T., & Becton, D.
infancy or early childhood including autism; dis- (2008). Adaptive behavior profiles of students with
orders of attention, communication, conduct, disabilities. Journal of Applied School Psychology,
elimination, feeding and eating, learning, and 24, 191–208.
Harman, J., Smith-Bonahue, T., & Oakland, T. (2009).
motor skills; and pervasive developmental disor- Assessment of adaptive behavior development in
ders. The ABAS-3 is useful with children and young children. In E. Mpofu & T. Oakland (Eds.),
adolescents who display disorders including Rehabilitation and health assessment: Applying ICF
attention deficit hyperactivity, acquired brain guidelines. New York: Springer.
Harrison, P., & Oakland, T. (2000). Adaptive behavior
injury, auditory or visual impairment, autism, assessment system. San Antonio: Psychological
developmental delays, emotional/behavioral dis- Corporation.
orders, learning disabilities, and physical Harrison, P., & Oakland, T. (2003). Adaptive behavior
impairments. assessment system (2nd ed.). San Antonio: Psycholog-
ical Corporation.
Adults diagnosed with such disorders as anxi- Harrison, P., & Oakland, T. (2015). Adaptive behavior
ety, acute stress, or adjustment disorder, bipolar assessment system (3rd ed.). Torrance: Western Psy-
disorder, depression, mood disorders, psychosis, chological Services.
Parkinson’s, postpartum depression, substance Mpofu, E., & Oakland, T. (2010). Assessment in rehabili-
tation and health. Upper Saddle River: Merrill.
abuse, schizophrenia, and sleep disturbance may Oakland, T., & Harrison, P. (2008). Adaptive behavior
display impairments in their functional daily liv- assessment system-II: Clinical use and interpretation.
ing skills. Older adults diagnosed with New York: Elsevier.
Alzheimer’s type dementia and other cognitive Olley, J. G., & Cox, A. (2008). Assessment of adaptive
behavior in adult forensic cases: The use of the ABAS-
and neuropsychological disorders with late-life II. In T. Oakland & P. Harrison (Eds.), Adaptive behav-
onset often display impairments in their functional ior assessment system-II: Clinical use and interpreta-
daily living skills. Although data from the ABAS- tion. Boston: Elsevier.
3 may not be crucial in the diagnosis of some of
these disorders, ABAS-3 data will promote an
understanding of their impact on daily living
skills. The ABAS-3 is used in the assessment of Adenoma
intellectual disabilities among death row inmates
in light of the 2002 US Supreme Court Atkins Ethan Moitra
decision. Department of Psychiatry and Human Behavior,
Brown University, Providence, RI, USA

Cross-References
Definition
▶ Activities of Daily Living (ADL)
A benign tumor of glandular origin. There are
▶ Activity Restrictions, Limitations
three types of adenomas: tubular (most common,
▶ Intellectual Disability
tubelike structure), villous (least common, most
likely to become cancerous, ruffled structure), and
tubulovillous (blend of tubular and villous struc-
References tures). Adenomas do not metastasize, though they
can develop into malignancies known as adeno-
American Association on Intellectual and Developmental
carcinomas. Most adenomas occur spontaneously.
Disabilities. (2010). Intellectual disability: Definition,
classification, and systems of support (11th ed.). Wash- The tumor may occur throughout the endocrine
ington, DC: Author. system, including the pituitary gland.
Adjustment Disorder 61

Pituitary adenomas occur at a much higher functioning, disproportionate to the intensity or

incidence in adults than in children. Because severity of the stressor, and must begin within
their invasiveness is local, they are almost always 3 months of the stressor’s onset. Symptoms do A
benign and can be difficult to detect. There is the not last for longer than 6 months from the time the
secreting and the nonsecreting type. Clinical stressor or its consequences have resolved. The
symptoms come from the endocrine dysfunction adjustment disorder may be characterized by
or from mass effect and include headaches, hypo- depressed mood, anxiety, mixed anxiety and
pituitarism, and visual loss (caused by compres- depressed mood, disturbance of conduct, mixed
sion in the optic chiasm). Treatment of pituitary disturbance of emotions and conduct, or other-
adenomas includes correction of electrolyte dys- wise unspecified. The adjustment disorder is spec-
function, replacement of pituitary hormones, sur- ified to be “acute” if the pattern of response lasts
gical resection, and radiotherapy. less than 6 months or “persistent” if longer than
6 months. Adjustment disorders are distinguished
from normal bereavement or the exacerbation of a
preexisting psychological disorder.
Cross-References

▶ Pituitary Adenoma
Categorization

The disorder is classified with the trauma- and

References and Readings
stressor-related disorders in DSM-5.
Mazzaferri, E. L., & Saaman, N. A. (Eds.). (1993). Endo-
crine tumors. Boston: Blackwell.
Current Knowledge

Development and Course

Adjustment Disorder An adjustment disorder may develop from a
variety of stressors, including single events,
Daniel W. Klyce recurrent events, ongoing or continuous
Virginia Commonwealth University – School of stressors, and developmental or social mile-
Medicine, Richmond, VA, USA stones (e.g., graduation, marriage, retirement,
etc.). The prevalence rate for adjustment disor-
ders as a primary diagnosis in outpatient mental
Synonyms health settings is estimated to range from 5% to
20% (Casey and Bailey 2011; American Psychi-
Stress reaction atric Association 2013). Adjustment disorders
are frequently diagnosed in medical settings
and associated with such conditions as cancers,
Short Description or Definition critical illness, traumatic injuries, childhood-
onset diabetes, etc. The disorder accounts for
Adjustment disorders are defined in the Diagnos- as much as 50% of diagnoses encountered by
tic and Statistical Manual of Mental Disorders psychiatric consult and liaison services in hos-
(5th ed.; DSM-5; American Psychiatric Associa- pital settings (American Psychiatric Associa-
tion 2013) by patterns of clinically significant tion, 2013). The expected course of an
behavioral or emotional symptoms related to a adjustment disorder is that symptoms will remit
distinct stressor. The behavioral or emotional within 6 months of the resolution of the initial
response is usually disruptive to everyday stressor.
62 Admissibility

Associated Disorders and Current Research ▶ Post-traumatic Stress Disorder

Adjustment disorders are often associated with ▶ Stress
symptoms of depressed mood, anxiety, grief, and ▶ Stress Management
acute or posttraumatic stress. Up to 25% of adoles- ▶ Trauma- and Stressor-Related Disorders
cents and 60% of adults with a diagnosis of an
adjustment disorder have been noted to engage in
suicidal behavior (Kryzhanovskaya and Canter- References
bury, 2001; Pelkonen et al., 2005; Casey and Bailey,
2011). Suicidal behavior associated with an adjust- American Psychiatric Association. (2013). Diagnostic and
statistical manual of mental disorders (5th ed.). Arling-
ment disorder tends to occur earlier in the course of
ton: American Psychiatric Association Publishing.
the disorder, whereas suicidal behaviors associated Arends, I., Bruinvels, D. J., Rebergen, D. S.,
with major depression tend to occur later. When Nieuwenhuijsen, K., Madan, I., Neumeyer-Gromen,
compared to major depressive disorder, adjustment A., Bültmann, U., & Verbeek, J. H. (2012). Interven-
tions to facilitate return to work in adults with adjust-
disorders tend to be associated with shorter time
ment disorders. Cochrane Database of Systematic
between communication of suicidal ideation to Reviews, 12, CD006389.
completion, lower hospital readmission rates, and Casey, P. (2014). Adjustment disorder: New developments.
shorter hospital stays. Common criticisms of the Current Psychiatry Reports, 16(6), 1–8.
Casey, P., & Bailey, S. (2011). Adjustment disorders: The
validity of adjustment disorder have been related
state of the art. World Psychiatry, 10(1), 11–18.
to the diagnosis being too broad, overused to justify Kryzhanovskaya, L., & Canterbury, R. (2001). Suicidal
reimbursement, and resulting in overpathologizing behavior in patients with adjustment disorders. Crisis:
reactions to everyday stressors. The Journal of Crisis Intervention and Suicide Preven-
tion, 22(3), 125.
Pelkonen, M., Marttunen, M., Henriksson, M., &
Assessment and Treatment Lönnqvist, J. (2005). Suicidality in adjustment disor-
Diagnosis of an adjustment disorder depends upon der. European Child & Adolescent Psychiatry, 14(3),
identifying a distinct stressor and distinguishing 174–180.
normal from pathological psychological responses
to the onset of a stressor in the context of factors
such as cultural normativity and relative personal
circumstances. It may also be challenging to diag- Admissibility
nose an adjustment disorder among individuals
with neurological injuries or illnesses due to factors Moira C. Dux
such as emotional lability or injury-related sequelae US Department of Veteran Affairs, Baltimore,
that impact social functioning. MD, USA
Given the expectation for a relatively brief
course of symptoms (i.e., less than 6 months
after resolution of the stressor), it is challenging Definition
to establish an evidence base for empirically
supported interventions. Treatment tends to Admissibility of evidence refers to any testimo-
involve brief interventions with emphasis on nial, documentary material, or other form of tan-
problem-solving skills, stress management strate- gible evidence that can be considered by the trier
gies, and medical management or behavioral of fact, most typically a judge or a jury, in the
health interventions for health-related stressors. context of a judicial or administrative proceeding.
In order for evidence to be admissible, it must be
relevant, non-prejudicial, and possess some indi-
See Also cia of reliability. For example, if evidence consists
of a witness testimonial, it must be established that
▶ Acute Stress Disorder the witness is credible and that he/she has knowl-
▶ Major Depression edge of that which he/she is declaring. For
Adoption Studies 63

neuropsychologists, a central issue is the admissi- References and Readings

bility of one’s data and opinions. Rules 401, 402,
and 702–705 from Article VII of the Federal A complete list of the federal rules of evidence. Available
at: http://judiciary.house.gov/media/pdfs/printers/ A
Rules of Evidence (FRE) relate to “Opinions and
108th/evid2004.pdf
Expert Testimony.” Perhaps of most relevance to Greiffenstein, M. F. (2009). Basics of forensic neuropsy-
psychologists is rule FRE 702 which states, “If chology. In J. Morgan & J. Ricker (Eds.), Textbook of
scientific, technical, or other specialized knowl- clinical neuropsychology. New York: Taylor & Francis.
Jenkins v. United States, 307 F. 2d 637 (1962).
edge will assist the trier of fact to understand the
Kaufmann, P. M. (2008). Admissibility of neuropsycho-
evidence or to determine a fact in issue, a witness logical evidence in criminal cases: Competency, insan-
qualified as an expert by knowledge, skill, expe- ity, culpability, and mitigation. In R. Denney &
rience, training or education, may testify thereto in J. Sullivan (Eds.), Clinical neuropsychology in the
criminal forensic setting. New York: Guilford.
the form of an opinion or otherwise.” In other
words, the expert should possess some form of
knowledge that a typical judge or juror would not
be expected to know or understand. Rule
703 states, “The facts or data in the particular Adoption Studies
case upon which an expert bases an opinion or
inference may be those perceived by or made Rohan Palmer1 and Martin Hahn2
1
known to the expert at or before the hearing. If Institute for Behavioral Genetics, University of
of a type reasonably relied upon by experts in the Colorado at Boulder, Boulder, CO, USA
particular field in forming opinions or inferences 2
Department of Biology, William Paterson
upon the subject, the facts or data need not be University, Wayne, NJ, USA
admissible in evidence in order for the opinion
or the inference to be admitted. Facts or data that
are otherwise inadmissible shall not be disclosed Definition
to the jury by the proponent of the opinion or
inference unless the court determines that their Adoption studies typically compare pairs of per-
probative value in assisting the jury to evaluate sons, e.g., adopted child and adoptive mother or
the expert’s opinion substantially outweighs their adopted child and biological mother to assess
prejudicial effect.” genetic and environmental influences on
Several important cases have addressed the behavior.
admissibility of scientific testimony. In the case
of Frye v. United States (1923), the Frye standard
was established which stated that only scientific Current Knowledge
methods and concepts with “general acceptance”
within a particular field are admissible. In the Design
more recent case of Daubert v. Merrell Dow Familial resemblance of behaviors is due to
(1993), it was determined that scientific testimony genetic and/or common familial environmental
has to abide by two criteria; the testimony must be influences. Adoption studies provide a direct test
(a) scientifically valid and (b) relevant to the case of the role of both factors. This is possible by
at hand. drawing comparisons between families that share
genetic and environmental influences and families
that share only genetic or environmental factors.
Adoption creates two types of families. The
Cross-References “genetic family” consists of pairs of genetically
related individuals who do not share a common
▶ Daubert v. Merrell Dow Pharmaceuticals family environment (e.g., biological parent and
(1993) adopted-away child). The similarity between
64 Adrenocorticotropic Hormone

these pairs of relatives provides a direct estimate References and Readings

of genetic effects on behaviors. The second type
family is the “environmental family,” which is Bricker, J. B., Stallings, M. C., Corley, R. P., Wadsworth,
S. J., Bryan, A., Timberlake, D. S., et al. (2006).
made up of pairs of individuals who are not genet-
Genetic and environmental influences on age at sexual
ically related but who share a common family initiation in the Colorado adoption project. Behavior
environment (e.g., adoptive parent and adopted Genetics, 36, 820–832.
child). The similarity between pairs of relatives Petrill, S. A., Plomin, R., DeFries, J. C., & Hewitt, J. K.
(2003). Nature, nurture, and the transition to early
from an “environmental family” indicates the
adolescence. Oxford: Oxford University Press.
presence of environmental influences on behavior. Plomin, R., Fulker, D. W., Corley, R., & DeFries, J. C.
Adoption studies utilize either parent-offspring (1997). Nature, nurture, and cognitive development
pairs or sibling pairs. Because data on biological from 1 to 16 years: A parent-offspring adoption study.
Psychological Science, 8, 442–447.
parents and siblings of adoptees are sometimes
Young, S. E., Rhee, S. H., Stallings, M. C., Corley, R. P., &
rare, comparison between “genetic-plus-environ- Hewitt, J. K. (2006). Genetic and environmental vul-
mental” families (i.e., intact families) and adop- nerabilities underlying adolescent substance use and
tive families also provides evidence of genetic and problem use: General or specific? Behavior Genetics,
36, 603–615.
environmental influences.

Relevance to Neuropsychology
The Colorado Adoption Project has been
collecting longitudinal data on biological and Adrenocorticotropic Hormone
adoptive parents and their biological or adopted
children for over 30 years (Petrill et al. 2003). In David J. Libon
one set of analyses from that project reported by Departments of Geriatrics, Gerontology, and
Plomin et al. (1997), parent-offspring correla- Psychology, Rowan University, New Jersey
tions were calculated for children aged Institute for Successful Aging, School of
3–16 years. The results of the analyses show Osteopathic Medicine, Stratford, NJ, USA
increasing correlations across those ages
between biological parents and their adopted-
away children on such special cognitive abilities Definition
as verbal skills and perceptual speed. Correla-
tions between adoptive parents and adopted chil- Adrenocorticotropic hormone (ACTH) is pro-
dren remained about zero across those ages. The duced by the anterior pituitary gland and is a
authors interpret the results to indicate that heri- component of the hypothalamic-pituitary-adrenal
tability increases for those special cognitive abil- axis. The release of ACTH is associated with the
ities with age and that the role of shared biological response to stress. The production of
environment is low or nonexistent. ACTH from the pituitary gland stimulates the
Today, adoption study data are used to adrenal glands to produce cortisol. The ACTH
assess the genetic and environmental influence stimulation test is a common procedure used to
on a variety of clinical outcomes that include assess the integrity of the adrenal glands. This test
drug addiction (Young et al. 2006) and age of is used to identify a number of medical conditions
sexual initiation (Bricker et al. 2006), to name including adrenal insufficiency, Addison’s dis-
a few. ease, and related medical conditions (Melmed
and Kleinberg 2008).

Cross-References Cross-References

▶ Twin Studies ▶ Hypothalamus

Advanced Progressive Matrices 65

References and Readings followed by Set II as a speed test. In this case,

40 min is the time limit most commonly given for
Melmed, S., & Kleinberg, D. (2008). Anterior pituitary. In Set II.
H. M. Kronenberg, S. Melmed, K. S. Polonsky, & P. R. A
Larsen (Eds.), Williams textbook of endocrinology
(11th ed.). Philadelphia: Saunders Elsevier.
Historical Background

The APM was designed in the 1940s to assess

nonverbal abstract conceptualization skills of
Advanced Progressive individuals for whom the standard version was
Matrices too easy, that is, those achieving a raw score of
50 or above on the SPM. For children over
Victoria M. Leavitt1 and Erica Weber2 10 years of age with high intellectual functioning,
1
Cognitive Neuroscience Division, Columbia the APM may be the appropriate version to ensure
University Medical School, New York, NY, USA an adequate ceiling (Mills et al. 1993). For addi-
2
Department of Physical Medicine and tional information about the historical back-
Rehabilitation, Kessler Foundation, East ground of the original test, please refer to the
Hanover, NJ, USA entry for Raven’s Progressive Matrices.

Synonyms Psychometric Data

APM Norms for adolescents (ages 12–16.5) and adults

(18–68+; Sets I and II) for untimed (ages 12–70+)
and timed (ages 17–28) versions are provided for
Description North America (Raven et al. 1998). The reliability
of the test is considered good, with high internal
First developed in the 1940s as an additional form consistency of APM Set II, and split-half reliabil-
of the Raven’s progressive matrices, the advanced ity coefficients varying between 0.83 and 0.87
progressive matrices (APM) were developed to (Strauss et al. 2006). Set I, as it has only
test intellectual efficiency in people with greater 12 items, yields lower figures. Reliability of the
than average intellectual ability and to differenti- original 48-item version was found to be high for
ate clearly between people of superior ability. adults and children aged 11.5 years + (>0.80); for
A nonverbal test of inductive reasoning, the younger children, it was only reasonably reliable
APM contains 48 items, presented as one set of (0.76). Overall, Set II scores increased by three
12 (Set I) and another of 36 (Set II). As in the points on retest (Raven et al. 1998).
standard version of the test (SPM), items are pre-
sented in black ink on a white background and
become increasingly difficult as progress is made Clinical Uses
through each set. Although it is an untimed task,
some clinicians administer the APM under time The SPM and CPM have been found to be sensi-
constraints. Set II can be used without a time limit tive to a variety of neurological and neuropsychi-
to assess the examinee’s total reasoning capacity. atric conditions (Raven’s Progressive Matrices).
In this case, the examinee would first be shown the The APM, designed for use with higher function-
problems of Set I as examples to explain the ing individuals, may be more appropriately
principles of the test and would then be given employed for assessing an individual’s capacity
approximately 1 h to complete the task. Alter- for decision-making or strategic planning at the
nately, Set I can be given as a short practice test management level in the workplace or in a higher
66 Advocacy

education setting. However, clinical utility for the Reading Test discrepancy as a measure of intellectual
APM has been more recently realized, in that decline in older adults. Applied Neuropsychology:
Adult, 20, 7–14.
discrepancy between expected (via regression-
based prediction models using NART scores;
Freeman and Godfrey 2000) and observed APM
scores has been used to detect intellectual decline
in older adults (van den Berg et al. 2013). Addi- Advocacy
tionally, the first set of items of the APM has been
validated for use as a short form of Raven’s SPM Amy J. Armstrong
to assess fluid intelligence (Chieri et al. 2012). Department of Rehabilitation Counseling,
Virginia Commonwealth University, Richmond,
VA, USA
Cross-References
The process of supporting or acting on behalf of a
▶ Colored Progressive Matrices
cause, facilitating equal community access and
▶ Raven’s Progressive Matrices
participation of individuals or groups that have
▶ Standard Progressive Matrices
typically been socially and/or economically mar-
ginalized. There are several types of advocacy to
include:
References and Readings
Systems advocacy: the process in which any system
Chiesi, F., Ciancaleoni, M., Galli, S., & Primi, C. (2012). (public, private, community based) is made more
Using the advanced progressive matrices (set I) to responsive to the needs of the individual served by
assess fluid ability in a short time frame: An item the system. This process may include increasing
response theory-based analysis. Psychological Assess- awareness of services and resources available
ment, 24, 892–900. within a community, identifying unmet needs of
Freeman, J., & Godfrey, H. (2000). The validity of the individuals, identifying existing barriers that
NART-RSPM index in detecting intellectual decline impede access to community services and
following traumatic brain injury: A controlled study. resources, and developing strategies to eliminate
British Journal of Clinical Psychology, 39, 95–103. legislative, regulatory, social and economic barriers
Mills, C. J., Ablard, K. E., & Brody, L. E. (1993). The that may impede access to one’s community sup-
Raven’s progressive matrices: Its usefulness for identi- ports and resources.
fying gifted/talented students. Roeper Review, 15, Individual advocacy: the process of increasing
183–186. awareness of unmet needs and procuring rights or
Raven, J. C. (1965, 1994). Advanced progressive matrices benefits on behalf of another individual or group of
sets I and II. Oxford: Oxford Psychologists Press. individuals.
Raven, J., Raven, J. C., & Court, J. H. (1996). Progressive Self-advocacy: the process of empowering an
matrices: A perceptual test of intelligence. Individual individual to rely upon him or herself to make
form. Oxford: Oxford Psychologists Press. (Original his/her own choices and decisions in order to direct
work published 1938). the course of his/her life.
Raven, J., Raven, J. C., & Court, J. H. (1998). Raven
manual: Section 4. Advanced progressive matrices. The People First movement of the 1970s was a
Oxford: Oxford Psychologists Press Ltd.. progenitor of self-advocacy as a civil rights move-
Raven, J., Raven, J. C., & Court, J. H. (2003). Manual for ment. The independent living movement engaged
Raven’s progressive matrices and vocabulary scales. in systems advocacy and also fostered self-
Section 1: General overview. San Antonio: Harcourt
Assessment. advocacy, providing a foundation for self-
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A advocacy activism in which people with signifi-
compendium of neuropsychological tests (3rd ed.). NY: cant disabilities had a right to live in an accessible
Oxford University Press. community of their choice. A core service of Cen-
van den Berg, E., Nys, G. M. S., Brands, A. M. A., Ruis,
C., van Zandvoort, M. J. E., & Kessels, R. P. C. (2013). ters of Independent Living is individual and sys-
Exploration of the Raven APM – National Adult tems advocacy, including providing opportunities
Affect 67

for skill development in self-advocacy. The Pro- observed after trauma to the frontal lobes, multi-
tection and Advocacy (P&A) System protects the ple sclerosis, and other conditions. In language,
rights of people with disabilities by providing legal verbal adynamia (lack of spontaneity of speech) is A
representation and other advocacy services associ- seen with lesions of the medial frontal lobes and
ated with state and federal laws. P&A Offices exist refers to difficulty in initiation and maintenance of
in each state. language output.

Cross-References Cross-References

▶ Americans with Disabilities Act of 1990 ▶ Abulia

▶ Independent Living Centers ▶ Apathy
▶ Transcortical Motor Aphasia

References and Readings

References and Readings
Dell Orto, A. E., & Marinelli, R. P. (Eds.). (1995). Ency-
clopedia of disability and rehabilitation. New York:
Berrios, G. E. (2008). Classic text no. 76: ‘Asthenia’ by
MacMillian Publishing.
A. Dechambre (1865). History of Psychiatry, 19(4),
Test, D., Fowler, C. H., Wood, W. M., Brewer, D. M., &
490–501.
Eddy, S. (2005). Conceptual framework of self-
Caplan, D. (1987). Neurolinguistics and linguistic
advocacy for students with disabilities. Remedial and
aphasiology: An introduction. New York: Cambridge
Special Education, 26, 43–54.
University Press.
Wehmeyer, M. L. (2004). Self-determination and the
empowerment of people with disabilities. American
Rehabilitation, 28, 22–29.

Affect

Adynamia Joel W. Hughes

Department of Psychology, Kent State University,
Irene Piryatinsky Kent, OH, USA
Butler Hospital and Alpert Medical School of
Brown University, Providence, RI, USA
Synonyms

Synonyms Affect display

Asthenia
Definition

Definition Affect is the displaying and experiencing of emo-

tion. It includes positive dimensions such as joy,
Adynamia refers to a general weakness and lack interest, and contentment, as well as negative
of energy evident through lack of verbal or overt dimensions of emotion such as disgust, fear, and
behavior due to a disease or neurological condi- anger. Affect is a very rapid response to internal
tions. It can manifest as lethargy, loss of strength, (e.g., thoughts, memory) or external stimuli (e.g.,
weakness in extremities, and difficulty initiating other people). It is different from mood, in that it is
activities or completing tasks. Adynamia can be more momentary and observable by others,
68 Affective Disorder

whereas mood is longer lasting and constitutes a major depressive disorder and dysthymia, as
symptom that patients may report (e.g., depres- well as manic disorders such as bipolar disorder
sion). Affect can be observed from facial expres- and cyclothymic disorder. Affective disorders
sion, gestures, posture, and speech (e.g., word may be primary or caused by medical conditions
choice, tone, rate). or substances.

Categorization
Cross-References
Mania and depression seem to anchor the ends
▶ Affective Disorder
of an emotional and behavioral continuum, an
▶ Emotionality
observation that dates from ancient times. In Hip-
▶ Mood Disorder
pocrates’ humoral theory, mania resulted from an
▶ Pseudobulbar Palsy
excess of yellow bile and depression to an excess
of black bile. In the early twentieth century, Ger-
man psychiatrist Emil Kraepelin described affec-
References and Readings
tive disorders as belonging to a manic-depressive
Batson, C. D., Shaw, L. L., & Oleson, K. C. (1992).
form of psychosis, which he differentiated from
Differentiating affect, mood and emotion: Toward dementia praecox. The term “manic depression”
functionally-based conceptual distinctions. Emotion. was replaced by more contemporary language,
Newbury Park: Sage. including major depressive disorder and bipolar
Blechman, E. A. (1990). Moods, affect, and emotions.
Hillsdale: Lawrence Erlbaum Associates.
disorder in the twentieth century, and for example,
Ekman, P. (1993). An argument for basic emotion. Cogni- major depressive disorder was first incorporated
tion and Emotion, 6, 169–200. into the third edition of the Diagnostic and Statis-
tical Manual (DSM-III).
Depressive disorders include major depressive
disorder and persistent depressive disorder. Diag-
Affective Disorder nosis of major depressive disorder is made by
symptoms, as there is no physiological test that
Joel W. Hughes reliably diagnoses depression. Major depressive
Department of Psychology, Kent State University, disorder requires at least 2 weeks of depressed
Kent, OH, USA mood and loss of interest in usually pleasurable
activities (anhedonia). In addition, at least four of
the following seven symptoms must also be pre-
Synonyms sent: significant weight gain or loss or appetite
changes, sleep disturbance (e.g., early morning
Emotional disorder; Mood disorder awakening with difficulty returning to sleep),
observable disturbances in psychomotor speed
(increased or diminished), loss of energy or exces-
Short Description or Definition sive fatigue, feelings of low self-worth or inap-
propriate guilt, cognitive changes such as the
An affective disorder is a mental disorder predom- subjective experience of difficulty concentrating,
inantly characterized by altered mood character- and thinking about or planning suicide.
ized by feelings of emptiness, irritability, or Persistent depressive disorder is similar to
sadness for a prolonged period that results in a major depressive disorder, although the depres-
significant impairment in social, occupational, or sion must be chronic (i.e., 2 or more years of
another important area of functioning. Affective depressed mood), and during the first 2 years of
disorders include depressive disorders such as dysthymia, there must not have been an episode
Affective Disorder 69

of major depression or a period of longer than typically 15–24 years of age. However, the
2 months with no symptoms. most likely ages for a first major depressive epi-
Bipolar disorder is diagnosed when there is a sode are 30–40 years of age. Depressive disor- A
“manic” mood disturbance characterized by ders often remit spontaneously, but recurrence is
markedly expansive, elevated, or irritable mood, common, and about 15% of individuals
lasting at least 1 week. The mood disturbance experiencing an initial major depressive episode
must be accompanied by additional symptoms will develop chronic recurrent depression. The
such as grandiosity, excessive risky behavior bipolar disorders are highly heritable, and
such as sexual behavior or irresponsible spending, research continues to determine genetic risk
and decreased need for sleep. A “mixed” episode markers for bipolar disorder. Brain imaging stud-
denotes mood disturbances that are characterized ies also suggest that a broad risk for unstable
by both manic and depressive symptoms. moods may underlie bipolar disorder, but more
A “hypomanic” episode is a less pronounced ele- research is warranted. The causes of depression
vation of mood that would not qualify as a true are not fully understood, but appear to involve
manic episode. Bipolar disorders follow a course the interaction of genetic and environmental fac-
in which periods of elevated mood alternate with tors such as stress and disruptions in interper-
periods of depression and are categorized sonal relationships. Thus, in addition to female
according to the nature of these episodes. For gender, risk factors for depression include severe
example, bipolar I involves alternating manic life stress such as traumatic events and loss of
and depressive episodes; in bipolar II, there are significant relationships. Depression is associ-
alternating hypomanic and depressive episodes; ated with shorter life expectancy from suicide
cyclothymic disorder involves alternating hypo- and other causes of death. For example, depres-
manic and depressive episodes that do not meet sion increases the risk of cardiac disease, as well
full criteria for major depression. as the risk of mortality among individuals with
cardiac disease.

Epidemiology
Neuropsychology and Psychology of
Affective disorders are very common. At any one Affective Disorder
time, approximately 10% of the adult population,
or nearly 20 million Americans, have a depressive Depression is common in neurological condi-
illness. Rates of depression are even higher in tions such as stroke and traumatic brain injury
patients with comorbid medical conditions, and (Robinson 2006; Rosenthal et al. 1998). Even
for example, about 30% of patients with cardiac without an obvious neurologic insult, individ-
disease have clinically significant depression. uals with alterations in executive control, mem-
Bipolar disorder is much less common than uni- ory, and emotion regulation are at increased risk
polar depression, occurring in between 2% and for depression. Furthermore, individuals with
4% of the population (including bipolar I, bipolar depression often show neuropsychological def-
II, and cyclothymic disorder). While depression is icits in the absence of neurological conditions.
twice as common among women as men, bipolar The neuropsychological deficits specified in the
is equally common in men and women. diagnostic criteria for depression include diffi-
culty concentrating and making decisions. Thus,
depressed patients often exhibit deficits in exec-
Natural History, Prognostic Factors, and utive control, memory, and processing speed.
Outcomes For bipolar disorder, distractibility is typically
present, as well as impaired decision-making
Affective disorders often start in adolescence. reflected in the criterion relating to distractibil-
For example, the onset of bipolar disorder is ity of excessive involvement in activities that
70 Afferent

present a significant risk of negative conse- References and Readings

quences. Current neuropsychological theories
of depression emphasize the frontal lobes and Allen, L. B., McHugh, R. K., & Barlow, D. H.
(2008). Emotional disorders: A unified protocol.
basal ganglia, including abnormalities in neural
In D. H. Barlow (Ed.), Clinical handbook of
circuitry involving the prefrontal cortex, psychological disorders: A step-by-step treatment
mesiotemporal cortex, striatum, amygdala, and manual (4th ed., pp. 216–249). New York: Guilford
thalamus (Chamberlain and Sahakain 2006). Press.
American Psychiatric Association. (2013). Diagnostic and
These areas may also be implicated in bipolar
statistical manual of mental disorders (DSM-5 ®).
disorder, as they appear to underlie mood symp- Arlington: American Psychiatric Association.
toms and treatment effects. Chamberlain, S. R., & Sahakain, B. J. (2006). The neuro-
psychology of mood disorders. Current Psychiatry
Reports, 8, 458–463.
Clark, L., Chamberlain, S. R., & Sahakian, B. J. (2009).
Evaluation Neurocognitive mechanisms in depression: Implica-
tions for treatment. Annual Review of Neuroscience,
Assessment of affective disorders focuses on 32, 57–74.
Robinson, R. (2006). The neuropsychiatry of stroke
self-report instruments and clinical interviews.
(2nd ed.). New York: Cambridge University Press.
Neuropsychological testing may reveal deficits Rosenthal, M., Christensen, B., & Ross, T. (1998).
in executive function, attention psychomotor Depression following traumatic brain injury.
slowing, and biases in the processing of emo- Archives of Physical Medicine and Rehabilitation,
79, 90–103.
tional stimuli. Specifically, depressed individuals
have exaggerated responses to negative feed-
back, including rumination. Neuropsychological
evaluations in depression and bipolar disorder
are frequently used in research, as tests with Afferent
broad clinical utility in the context of assessing
or treating affective disorders have not been John Bigbee
widely disseminated. Anatomy and Neurobiology, Virginia
Commonwealth University, Richmond, VA, USA

Treatment
Synonyms
Depression is often treated with medication and
psychotherapy. A large number of medications are Sensory
available to treat depression, including selective
serotonin reuptake inhibitors, which typically
have relatively milder side effects and lower Definition
risks than older drugs such as monoamine oxidase
inhibitors. Treatment of bipolar disorders requires Afferent is an anatomical term that indicates func-
pharmacotherapy. In contrast to major depressive tional directionality. In nervous tissue, afferent is
disorder, bipolar cannot be successfully treated by often used synonymously with sensory informa-
psychotherapy alone. tion when it refers to nerves carrying impulses
from peripheral receptors toward the central ner-
vous system. Afferent can also be used in general
Cross-References to refer to any connection coming into a structure
within the nervous system. The opposite direction
▶ Depressive Disorder of conduction is efferent.
Age Decrements 71

See Also
Age Decrements
▶ Efferent A
Michael Franzen
Allegheny General Hospital, Pittsburgh, PA, USA

Further Reading
Synonyms
Purves, D., et al. (Eds.). (2012). Neuroscience (5th ed.).
Sunderland: Sinauer Associates.
Age-associated cognitive decline

Definition
Afferent Paresis The concept of age decrements in neuropsychol-
ogy refers to a decline in cognitive performance
Maryellen Romero
due to normal aging rather than due to an extra-
Department of Psychiatry and Behavioral
neous or internal event that is known to negatively
Sciences, Tulane University School of Medicine,
affect cognitive performance, such as a traumatic
New Orleans, LA, USA
brain injury, stroke, psychiatric condition, or
extensive drug use history.

Definition Current Knowledge

A deficit in the ability to perform voluntary Variability in the performance of aging individuals
movements due to loss of kinesthetic feedback. adds complexity to the determination of specific age
The primary and secondary motor cortices have decrements on neuropsychological tests. It is gener-
extensive inputs from the somatosensory areas in ally thought that individuals are more likely to retain
the parietal lobes. Following lesions to this latter “crystallized” knowledge (e.g., that which is prac-
area, particularly the post-central gyrus or to the ticed, overlearned, and skill-based) than “fluid”
lemniscal system which provides proprioceptive knowledge (e.g., problem-solving). As there are fac-
information to it, motor difficulties may be tors that heighten the risk for age decrements, pro-
observed either in the limbs or in speech produc- tective factors may counteract the risk. For instance,
tion. Although the muscles involved in such higher levels of education and positive health status
activities are not weak per se, the loss of sensory may slow down the rate of cognitive decline that
information results in a disruption of motor con- would otherwise occur with increasing age.
trol and an imprecise excitation of muscle groups One concept that illustrates age decrements is
required to execute specific, voluntary fine-motor age-associated memory impairment (AAMI),
responses. which pertains to age-related decline in perfor-
mance specifically in terms of memory.

References and Readings Cross-References

Luria, A. L. (1976). The working brain: An introduction
to neuropsychology. New York: Perseus Books ▶ Cognitive Reserve
Group. ▶ Memory Impairment
72 Agenesis of Corpus Callosum

References and Readings H. L. Klawans (Eds.), Handbook of clinical neurology

(Vol. 50, pp. 149–173). New York: Elsevier.
Lezak, M., Howieson, D. B., Bigler, E. D., & Tranel, D. Marszal, E., Jamroz, E., Pilch, J., Kluczewska, E.,
(2012). Neuropsychological assessment (5th ed.). New Jablecka, H., & Krawczyk, R. (2000). Agenesis of the
York: Oxford University Press. corpus callosum: Clinical description and etiology.
Journal of Child Neurology, 15, 401–405.
Zaidel, E., & Iacoboni, M. (2003). The parallel brain: The
cognitive neuroscience of the corpus callosum. Cam-
bridge, MA: MIT Press.
Agenesis of Corpus Callosum

John E. Mendoza
Department of Psychiatry and Neuroscience,
Tulane Medical School and SE Louisiana Agent Orange
Veterans Healthcare System, New Orleans,
LA, USA Ben Dodsworth
PM&R, University of South Florida, Tampa,
FL, USA
Definition

A developmental defect in which either all or part Synonyms

of the corpus callosum fails to develop.
None

Current Knowledge
Definition
Agenesis can result from various etiologies,
including genetic predisposition, chromosomal A tactical herbicide and defoliant (chemical used
abnormalities, or intrauterine trauma, such as to remove leaves from trees and plants)
infection. When present, this condition is com- employed by the US military during the Vietnam
monly associated with other neuroanatomical War during “Operation Ranch Hand.” It was
anomalies, metabolic disturbances, and/or sprayed from aircraft with the purpose of depriv-
neurobehavioral deficits. The latter might include ing the enemies of food and removing dense
mental retardation, seizures, motor deficits, and tropical foliage that provided enemy cover. The
psychiatric disturbances. However, some patients name was derived from the orange stripe that
may be relatively asymptomatic, the callosal identified the large drums in which it was stored.
defect being discovered only serendipitously late It was composed of two active ingredients: 2,4-
in life. The latter is more likely to occur when the dichlorophenoxyacetic acid (2,4-D) and 2,4,5-tri-
agenesis is not accompanied by other neurological chlorophenoxyacetic acid (2,4,5-T). Studies
or metabolic defects. Whereas “disconnection involving US military personnel have linked expo-
syndromes” are routinely present following surgi- sure to these chemicals with higher incidence of
cal commissurotomy for intractable epilepsy, they various cancers, diabetes, heart disease,
are generally not present with agenesis. Parkinson’s disease, and other medical issues (US
Department of Veterans Affairs).

References and Readings

See Also
Aicardi, J., Chevrie, J.-J., & Baraton, J. (1987). Agenesis of
the corpus callosum. In P. J. Vinken, G. W. Bruyn, & ▶ Parkinson’s Disease
Aggravating Factors 73

References and Readings for cancer (radiation, chemotherapy), certain types

of influenza, diabetes, or certain medications.
US Department of Veterans Affairs. Facts About Herbicides. Taste acuity (hypogeusia) can decline with age
Retrieved January 24, 2017, from http://www. A
and may contribute to the anorexia and weight
publichealth.va.gov/exposures/agentorange/basics.asp.
loss often seen in elderly persons. The prognosis
in acquired ageusia is often correlated directly with
the expected course of the illness or injury causing
Ageusia the dysfunction.

Maryellen Romero
Department of Psychiatry and Behavioral
Sciences, Tulane University School of Medicine,
Cross-References
New Orleans, LA, USA
▶ Taste

Definition
References and Readings
Ageusia is the loss of the sense of taste. The Cerf-Ducastel, B., Van de Moortele, P. F., MacLeod, P., Le
disorder should be distinguished from a disruption Bihan, D., & Faurion, A. (2001). Interaction of gusta-
in the ability to perceive flavor, which requires a tory and lingual somatosensory perceptions at the cor-
combination of olfactory, gustatory, and somato- tical level in the human: A functional magnetic
resonance imaging study. Chemical Senses, 26(4),
sensory functions. Frequently, complaints of 371–383.
ageusia are often explained by olfactory dysfunc- Doty, R. L., & Kimmelman, C. P. (1992). Lesser20R.-
tion rather than a disruption in taste perception, P. Smell and taste and their disorders. In A. K. Asbury,
per se. The majority of taste receptors (buds) are G. M. McKhann, & W. I. McDonald (Eds.), Diseases of
the nervous system (2nd ed., pp. 390–403). Philadel-
located on the tongue and this information is phia: W.B. Saunders.
carried by the VIIth (anterior two thirds) and Wilson-Pauwek, L., Akesson, E., & Stewart, P. (1988).
IXth (posterior third) cranial nerves, with other Cranial nerves: Anatomy and clinical comments. Phil-
taste receptors (cranial nerve X) located in other adelphia: B.C. Decker.
regions of the mouth and throat. These taste fibers
enter the solitary nucleus (rostral portion) in the
upper medulla and from there second-order neu-
rons travel to the ventral posterior medial nuclei of Aggravating Factors
the thalamus. Thalamic projections carrying this
gustatory information then project to the post- Robert L. Heilbronner
central gyrus in the region of the parietal opercu- Chicago Neuropsychology Group, Chicago,
lum and to the underlying insular cortex where the IL, USA
sensation of taste is likely experienced.
Lesions of the VIIth nerve can result in loss of
taste in the ipsilateral anterior two thirds of the Definition
tongue which is more readily assessable to clinical
testing than lesions of the IXth or Xth nerve. Refers to any relevant circumstances in corre-
However, total loss of taste (ageusia) is seldom spondence with the evidence presented during
seen as a result of structural lesions because of the trial that, from the perspective of the jurors,
the multiple and bilateral pathways involved. makes the harshest penalty appropriate. By con-
Ageusia (or hypogeusia) is more likely to result trast, mitigating factors refer to evidence regard-
from more systemic problems such as treatments ing the defendant’s character or circumstances
74 Agitated Behavior Scale

related to the crime that would provide foundation References and Readings
for a juror to vote for a lesser sentence.
Denney, R. L. (2005). Criminal responsibility and other
criminal forensic issues. In G. Larrabee (Ed.), Forensic
neuropsychology: A scientific approach. New York:
Historical Background Oxford University Press.
Furman v. Georgia, 408 U.S. 238 (1972).
In 1972, the US Supreme Court considered the Gregg v. Georgia, 49 L.Ed.2d. 859 (1976).
Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin,
death penalty to be a cruel and an unusual pun-
C. (2007). Psychological evaluations for the courts:
ishment because the manner in which capital A handbook for mental health professionals and law-
sentences were decided in Georgia was capricious yers (3rd ed.). New York: Guilford Press.
(Furman v. Georgia 1972). This decision
discontinued death penalty litigation in the USA
at that time because none of the states had a
system that was substantially different. In 1976 Agitated Behavior Scale
(Gregg v. Georgia), the Court accepted as consti-
tutional Georgia’s rewrite of their statute which Megan Becker and Daniel N. Allen
included a capital sentencing process that required Department of Psychology, University of Nevada,
presentation before a judge or jury of aggravating Las Vegas, NV, USA
and mitigating factors. It required at least one or
ten specified aggravating circumstances to be
established beyond reasonable doubt to impose Synonyms
the death penalty. Some examples include
whether the crime (murder) was particularly ABS
cruel and atrocious, if more than one victim was
murdered, whether the murder occurred during
the commission of a felony, etc. Description

The agitated behavior scale (ABS) was designed to

Current Knowledge evaluate agitation and other problematic behaviors
that commonly occur during the acute recovery
Laws regarding how aggravating or mitigating fac- phase following traumatic brain injury (Corrigan
tors should be weighed by jurors vary based on 1989). The ABS is composed of 14 items that
state laws. Neuropsychological assessments in represent a number of commonly occurring prob-
death penalty cases typically focus on mitigating lematic behaviors such as short attention span,
factors, such as neuropsychological or impulsivity, uncooperativeness, violence, and
neurobehavioral impairments, as there is an angry outbursts. Information that assists in ABS
increased body of evidence demonstrating a pre- scoring is available from the author (Corrigan) and
ponderance of neurocognitive deficits in violent includes descriptions of item ratings and other
criminals. Neuropsychological assessment with examples. Each item on the ABS is rated on a
respect to aggravating factors is less common and 1–4-point scale based on the intensity or frequency
typically addresses increased risk of future of the behavior’s occurrence. Additionally, when
dangerousness. assigning ratings, the degree to which the behavior
interferes with functional behavior is also consid-
ered. If the behavior is absent, a rating of 1 is
Cross-References assigned. When the behavior is present, a rating of
2 or greater is assigned, with a rating of 4 indicating
▶ Mitigating Factors the presence of a behavior to an extreme degree.
Agitated Behavior Scale 75

A total score is derived through a summary of all Wolffbrandt et al. 2013). Thus, there is evidence
14 items (range 14–56) and interpreted as normal for the clinical utility of the ABS, a highly prac-
range (<22), mild agitation (22–28), moderate agi- tical measure with sound psychometric proper- A
tation (29–35), or severe agitation (35–56). Sub- ties that allow for assessment of agitation in
scale scores can also be calculated for populations with brain injury (Amato
disinhibition, aggression, and lability although it et al. 2012).
appears that ABS primarily measures a single con-
struct (Bogner et al. 2000), so interpretation of the
total score may be most appropriate. Cross-References

▶ Post-Traumatic Confusional State

Current Knowledge ▶ Traumatic Brain Injury (TBI)

The ABS is often used to perform serial assess-

ments and track changes in agitation that occur References and Readings
as a natural part of the recovery process and as a
Amato, S., Resan, M., & Mion, L. (2012). The feasibility,
result of treatment. Although designed for
reliability, and clinical utility of the agitated behavior
assessment of traumatic brain injury, the ABS scale in brain-injured rehabilitation patients. Rehabili-
has also been used to assess agitation in other tation Nursing, 37, 19–24.
populations, such as patients with progressive Bogner, J. A., Corrigan, J. D., Stange, M., & Rabold,
D. (1999). Reliability of the agitated behavior scale.
dementia (Corrigan et al. 1996; Tabloski et al.
The Journal of Head Trauma Rehabilitation, 14,
1995). No differences have been found between 91–96.
males and females with brain injury on the total Bogner, J. A., Corrigan, J. D., Bode, R. K., & Heinemann,
score or the subscale scores (Kadyan et al. A. W. (2000). Rating scale analysis of the agitated
behavior scale. The Journal of Head Trauma Rehabil-
2004). Internal consistency estimates range
itation, 15, 656–659.
from 0.74 to 0.92 (Bogner et al. 1999; Corrigan Corrigan, J. D. (1989). Development of a scale for assess-
1989), with interrater reliability of 0.92 for the ment of agitation following traumatic brain injury.
total score and with comparable reliabilities of Journal of Clinical and Experimental Neuropsychol-
ogy, 11, 261–277.
0.90, 0.91, and 0.73 for the disinhibition,
Corrigan, J. D., & Bogner, J. A. (1994). Factor structure of
aggression, and lability scores, respectively. the agitated behavior scale. Journal of Clinical and
Subscale to total score correlations range from Experimental Neuropsychology, 16, 386–392.
0.43 to 0.55. The construct validity of the ABS Corrigan, J. D., & Mysiw, W. J. (1988). Agitation fol-
lowing traumatic head injury: Equivocal evidence
has been supported by factor-analytic studies
for a discrete stage of cognitive recovery. Archives
that demonstrated the presence of three factors: of Physical Medicine and Rehabilitation, 69,
disinhibition, aggression, and lability (Corrigan 487–492.
and Bogner 1994). ABS scores account for a Hellweg, S., & Schuster-Amft, C. (2016). German ver-
sion, inter- and intrarater reliability and internal con-
substantial portion of the variance (from 36%
sistency of the “Agitated Behavior Scale” (ABS-G) in
to 62%) in independent observations of agitation patients with moderate to severe traumatic brain
(Corrigan 1989) and are able to predict changes injury. Health and Quality of Life Outcomes,
in cognition (Corrigan and Mysiw 1988), which 14(106), 1–8.
Kadyan, V., Mysiw, W. J., Bogner, J. A., Corrigan, J. D.,
provide additional support for its validity. The
Fugate, L. P., & Clinchot, D. M. (2004). Gender differ-
ABS was also translated into German (ABS-G) ences in agitation after traumatic brain injury. American
and Danish, and both translations demonstrated Journal of Physical Medicine & Rehabilitation, 83,
interrater reliability in individuals with trau- 747–752.
Wolffbrandt, M. M., Poulsen, I., Engberg, A. W., &
matic brain injury (0.85 and 0.75–0.91, respec-
Hornnes, N. (2013). Occurrence and severity of agi-
tively) with an internal consistency of 0.66 in the tated behavior after severe traumatic brain injury. Reha-
ABS-G (Hellweg and Schuster-Amft 2016; bilitation Nursing, 38, 133–141.
76 Agitation

as agitation can manifest in any setting in which an

Agitation individual experiences delirium and impaired cog-
nition (e.g., dementia).
Paul Newman The importance of the concept of agitation and its
Department of Medical Psychology and measurement was vital to the establishment of the
Neuropsychology, Drake Center, Cincinnati, now accepted viewpoint that recovery from agitation
OH, USA is preceded by improvement in cognition. Or con-
versely, interventions that decrease arousal and/or
cognition can lead to a worsening of agitation.
Synonyms

Posttraumatic agitation Cross-References

Definition ▶ Agitated Behavior Scale

▶ Behavior Management
Agitation is an excess of one or more behaviors ▶ De-escalation
that occur during the course of delirium when ▶ Dementia
cognition is impaired. The behaviors most often ▶ Frustration Tolerance
in excess during agitation include aggression, ▶ Post-traumatic Confusional State
akathisia, disinhibition, and/or emotional lability. ▶ Traumatic Brain Injury (TBI)
Specific examples of agitated behavior may
include pacing, hand wringing, pulling at tubes
or restraints, inappropriate verbalizations, exces- References and Readings
sive crying or laughter, etc.
Corrigan, J. D. (1989). Development of a scale for assess-
Agitation is often conceptualized to result from ment of agitation following traumatic brain injury.
an inability to cope with overstimulation. Stimula- Journal of Clinical and Experimental Neuropsychol-
tion may be internal (e.g., pain or hallucinations) or ogy, 69, 261–277.
external (e.g., noise, light, or conversation). One’s Sandel, M. E., & Bysiw, W. J. (1996). The agitated brain
injured patient. Part 1: Definitions, differential diagno-
ability to cope with stimulation may be viewed as a sis, and assessment. Archives of Physical Medicine and
threshold. Adverse changes to the brain’s typical Rehabilitation, 77, 617–623.
functioning have the potential to lower this thresh- Smith, M., Gardner, L. A., Hall, G. R., & Buckwalter, K. C.
old. Thus, individuals with traumatic brain injury or (2004). History, development, and future of the pro-
gressively lowered stress threshold: A conceptual
dementia may become agitated at lower levels of model for dementia care. Journal of the American
stimulation than noninjured individuals. Geriatric Society, 52, 1755–1760.

Current Knowledge
Agnosia
There was no consensus on the definition of agita-
tion within the greater health-care profession for Anastasia Raymer
many years. Clinicians in neuro-rehabilitation Communication Disorders and Special Education,
were using the term in the early 1980s to describe Old Dominion University, Norfolk, VA, USA
a pattern of behavior observed during recovery from
traumatic brain injury. The development of the Agi-
tated Behavior Scale by Corrigan and associates in Definition
the late 1980s to measure this brain-injury-related
behavior led to a more refined definition of the term. Agnosia is a failure to recognize a sensory stim-
The term is not limited to just traumatic brain injury ulus that is not attributable to dysfunction of
Agnosia 77

peripheral sensory mechanisms or to other cog- number does a peanut look like in its shell? 8).
nitive impairments associated with brain dam- In contrast, Lissauer’s associative agnosia refers
age (Bauer 2012). Agnosia is often described as to a pattern in which the person can perform A
a percept that is “stripped of its meaning” elementary perceptual tasks, such as copying or
(Teuber 1968). The individual can respond to matching, but is not able to conjure up informa-
the presence of the stimulus but has difficulty tion about perceptual characteristics of a stimu-
processing the perceptual information in suffi- lus from memory and also has difficulty
cient detail to make sense of and meaningfully interpreting the meaning of a percept, its cate-
recognize the stimulus. The difficulty is modal- gory, context, associated objects, and actions,
ity specific (e.g., visual), so the stimulus can be despite the ability to perform those interpreta-
recognized through other sensory modalities tions through alternative sensory modalities
(e.g., tactile or auditory). (e.g., failure to sort pictures by category and
retained ability to identify the category for the
same spoken words). Accurate diagnosis of
Current Knowledge agnosia depends upon careful examination
across modalities to rule out alternative cogni-
Different forms of agnosia have been described tive and linguistic bases for processing failure
that depend upon the detail with which the incom- (Bauer 2012).
ing stimulus is processed and the sensory modal-
ity and type of materials that pose difficulty.
Lissauer (1890) used the terms apperceptive and
associative, to classify the agnosias, terms that
Cross-References
continue to guide descriptions of agnosia (Farah
▶ Apperceptive Visual Agnosia
2004). Agnosia is also described with respect to
▶ Associative Visual Agnosia
the sensory modality affected (e.g., auditory agno-
▶ Auditory Agnosia
sia, tactile agnosia), although it is most commonly
▶ Prosopagnosia
reported to affect the visual modality (Farah
▶ Pure Word Deafness
2004). Rarely, multimodality forms of agnosia
▶ Tactile Agnosia
also have been described (Feinberg et al. 1986).
▶ Visual Object Agnosia
Finally, agnosia is discussed in the context of the
material to be perceived, for example, objects,
sounds, or faces (i.e., prosopagnosia, Gainotti
References and Readings
2014). Lesions that lead to agnosia vary across
sensory modalities, usually affecting bilateral Bauer, R. M. (2012). Agnosia. In K. M. Heilman &
post-Rolandic cortical sensory regions or E. Valenstein (Eds.), Clinical neuropsychology
disconnecting incoming pathways from one hemi- (5th ed., pp. 238–295). New York: Oxford University
sphere to the other (Bauer 2012). Press.
Farah, M. J. (2004). Visual agnosia (2nd ed.). Cambridge,
Apperceptive agnosia is associated with dis- MA: MIT Press.
ruption at early stages of perceptual processing Feinberg, T. E., Rothi, L. J. G., & Heilman, K. M. (1986).
beyond primary sensory appreciation of a stim- Multimodal agnosia after unilateral left hemisphere
ulus. For example, in the visual modality, the lesion. Neurology, 36, 864–867.
Gainotti, G. (2014). Familiar people recognition disorders:
person can see the percept but has difficulty An introductory review. Frontiers in Bioscience, S6,
copying or matching an incoming percept to a 58–64.
like stimulus and may make perceptual confu- Lissauer, H. (1890). Ein fall von seelenblindheit nebst
sions, yet when asked can conjure up some einem beitrage zur theorie derselben. Archiv für
Psychiatrie und Nervenkrankheiten, 21, 222–270.
visual information from memory or answer Teuber, H. L. (1968). Alteration of perception and memory
questions about visual attributes of a named in man. In L. Weiskrantz (Ed.), Analysis of behavioral
stimulus in visual imagery tasks (e.g., What change. New York: Harper & Row.
78 Agrammatism

conditions, and agrammatism is not attributable

Agrammatism to any single site of lesion.

Lyn S. Turkstra1 and Cynthia K. Thompson2

1
School of Rehabilitation Science, McMaster Current Knowledge
University, Hamilton, ON, Canada
2
Northwestern University, Evanston, IL, USA The underlying mechanisms of agrammatism
have been debated in the literature over the past
several decades. Some authors have argued that
Synonyms agrammatism reflects an underlying impairment
in language representation and/or processing
Agrammatic aphasia (Grodzinsky 1986, 1990, 1995; Zurif et al.
1993), while others contend that they represent
the speaker’s strategic adaptation to an underly-
Definition ing language processing impairment that is not
specific to grammar (Kolk and Heeschen 1990;
Agrammatism refers to language production that also see discussion in Beeke et al. 2007). Consis-
is lacking in grammatical structures. The basic tent with the processing deficit view, individuals
signs of agrammatism are short phrase length, with agrammatic aphasia show problems comput-
simplified syntax, errors and omissions of main ing syntactic structures in real time (Dickey et al.
verbs, and omission or substitution of grammat- 2007; Swinney et al. 2000; but see Blumstein et al.
ical morphemes such as plural markers or func- 1998); and may have deficits that impact both
tors (Saffran et al. 1989). There may also be production and comprehension, although not
errors in tense, number, and gender, and diffi- always the same structures (Dickey et al. 2008);
culty in producing sentences with movement of and their performance is influenced by contextual
grammatical elements, such as passive factors such as elicitation task (Faroqi-Shah and
sentences, Wh- questions, and complex Friedman 2015). Also, the structures that typically
sentences (Benedet et al. 1998; Caplan and are impaired in agrammatic aphasia are similar
Hanna 1998; Goodglass 1997; Faroqi-Shah and across many languages. In support of the adapta-
Thompson 2004). Spoken and written produc- tion view, there is evidence that the grammatical
tion typically shows similar error patterns. Typ- structures used by individuals with agrammatic
ically, individuals with agrammatic aphasia also aphasia vary as a function of the task. For exam-
show impaired comprehension of grammatical ple, individuals with agrammatic aphasia may
structures, particularly noncanonical semanti- produce more complex sentences on standardized
cally reversible sentences (e.g., “the boy was language tests, in which grammatical complete-
kicked by the horse”; Berndt et al. 1996; ness is the focus, than in conversational interac-
Caramazza and Zurif 1976). tions, in which the message and interaction are the
focus and the communication partners are
coconstructing a dialog (Beeke et al. 2008).
Historical Background There is evidence of treatment efficacy for
interventions aimed improvement of underlying
Historically, agrammatism was thought of as a representation/processing impairments and defi-
syndrome typically associated with nonfluent cits in adaptation. Verb as Core (Loverso et al.
aphasia (Goodglass 1997). More recent studies 1986), Mapping Therapy (Schwartz et al. 1994),
(e.g., Dick et al. 2001) have shown that features and Treatment of Underlying Forms (TUF;
of agrammatism are present in the production of Thompson et al. 2003; Thompson et al. 2010)
many individuals with various forms of aphasia, focus treatment on verbs and verb argument struc-
as well as in normal speakers under stressful ture, training patients to map form to meaning in
Agrammatism 79

both simple and complex sentences. Notably, model of language breakdown in aphasic patients and
TUF results in strong generalization from com- neurologically intact individuals. Psychological
Review, 108(4), 759–788.
plex to simple structures by controlling the lexical Dickey, M. W., Choy, J., & Thompson, C. K. (2007). Real- A
and syntactic variables of sentences trained (see time comprehension of wh-movement in apahsia: Evi-
Thompson and Shapiro 2007, for review). Various dence from eyetracking while listening. Brain and
approaches to treatment of grammatical morphol- Language, 100, 1–22.
Dickey, M. W., Milman, L. H., & Thompson, C. K. (2008).
ogy, such as deficits in verb tense and agreement, Judgment of functional morphology in agrammatic
also have been shown to be efficacious (Faroqi- aphasia. Journal of Neurolinguistics, 21(1), 35–65.
Shah 2008; Friedmann et al. 2000; Mitchum and Faroqi-Shah, Y., & Thompson, C. K. (2004). Semantic,
Berndt 1994; Weinrich et al. 1999). lexical, and phonological influences on the production
of verb inflections in agrammatic aphasia. Brain and
Language, 89(3), 484–498.
Faroqi-Shah, Y. (2008). A comparison of two theoretically-
Cross-References driven treatments of verb inflections in agrammatic
aphasia. Neuropsychologia, 46, 3088–3100.
Faroqi-Shah, Y., & Friedman, L. (2015). Production of
▶ Aphasia verb tense in agrammatic aphasia: A meta-analysis
▶ Grammar and further data. Behavioural Neurology, 2015,
▶ Nonfluent Aphasia 983870.
Friedmann, N., Wenkert-Olenik, D., & Gil, M. (2000).
▶ Paragrammatism From theory to practice: Treatment of agrammatic pro-
▶ Syntax duction in hebrew based on the tree pruning hypothesis.
▶ Telegraphic Speech Journal of Neurolinguistics, 13, 250–254.
Grodzinsky, Y. (1986). Language deficits and syntactic
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Grodzinsky, Y. (1990). Theoretical perspectives on lan-
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Grodzinsky, Y. (1995). A restrictive theory of agrammatic
Beeke, S., Maxim, J., & Wilkinson, R. (2008). Rethinking comprehension. Brain and Language, 50, 27–51.
agrammatism: Factors affecting the form of language Goodglass, H. (1997). Agrammatism in aphasiology. Clin-
elicited via clinical test procedures. Clinical Linguistics ical Neuroscience, 4(2), 51–56.
& Phonetics, 22(4-5), 317–323. Kolk, H. H. J., & Heeschen, C. (1990). Adaptation symp-
Beeke, S., Wilkinson, R., & Maxim, J. (2007). Individual toms and impairment symptoms in Broca’s aphasia.
variation in agrammatism: A single case study of the Aphasiology, 4, 221–231.
influence of interaction. International Journal of Lan- Loverso, F. L., Prescott, T. E., & Selinger, M. (1986).
guage and Communication Disorders, 42(6), 629–647. Cuing verbs: A treatment strategy for aphasic adults.
Benedet, M. J., Christiansen, J. A., & Goodglass, H. Journal of Rehabilitation Research, 25, 47–60.
(1998). A cross-linguistic study of grammatical mor- Mitchum, C., & Berndt, R. (1994). Verb retrieval and
phology in Spanish- and English-speaking agrammatic sentence construction: Effects of targeted intervention.
patients. Cortex, 34(3), 309–336. In M. J. Riddoch & G. Humphreys (Eds.), Cognitive
Berndt, R. S., Mitchum, C. C., & Haendiges, A. N. (1996). neuropsychology and cognitive rehabilitation. Hove:
Comprehension of reversible sentences in Erlbaum.
“agrammatism”: A meta-analysis. Cognition, 58(3), Saffran, E. M., Berndt, R. S., & Schwartz, M. F. (1989).
289–308. The quantitative analysis of agrammatic production:
Blumstein, S. E., Byma, G., Kurowski, K., Hourihan, J., Procedure and data. Brain and Language, 37(3),
Brown, T., & Hutchinson, A. (1998). On-line pro- 440–479.
cessing of filler-gap construction in aphasia. Brain Schwartz, M. F., Saffran, E. M., Fink, R. B., & Myers, J. L.
and Language, 61, 149–168. (1994). Mapping therapy: A treatment programme for
Caplan, D., & Hanna, J. E. (1998). Sentence production by agrammatism. Aphasiology, 8, 19–54.
aphasic patients in a constrained task. Brain and Lan- Swinney, D., Prather, P., & Love, T. (2000). The time
guage, 63(2), 184–218. course of lexical access and the role of context: Con-
Caramazza, A., & Zurif, E. B. (1976). Dissociation of verging evidence from normal and aphasic processing.
algorithmic and heuristic processes in language com- In Y. Grodzinsky, L. P. Shapiro, & D. Swinney (Eds.),
prehension: Evidence from aphasia. Brain and Lan- Language and the brain: Representation and pro-
guage, 3(4), 572–582. cessing. New York: Academic.
Dick, F., Bates, E., Wulfeck, B., Utman, J. A., Dronkers, Thompson, C. K., & Shapiro, L. P. (2007). Complexity in
N., & Gernsbacher, M. A. (2001). Language deficits, treatment of syntactic deficits. American Journal of
localization, and grammar: Evidence for a distributive Speech-Language Pathology, 16, 30–42.
80 Agraphia

Thompson, C. K., Shapiro, L. P., Kiran, S., & Sobecks, J. impairments of reading (alexia) and spoken lan-
(2003). The role of syntactic complexity in treatment of guage (aphasia).
sentence deficits in agrammatic aphasia: The complex-
ity account of treatment efficacy (CATE). Journal of
Speech, Language, and Hearing Research, 42,
690–707. Categorization
Thompson, C. K., Choy, J.J., Holland, A., Cole, R. (2010).
Sentactics1: Computer-Automated Treatment of
Underlying Forms. Aphasiology, 24(10), 1242–1266. Historically, the term agraphia was introduced in
Weinrich, M., Boser, K. I., & McCall, D. (1999). Repre- 1867 by Ogle with a description of two types:
sentation of linguistic rules in the brain: Evidence from amnemonic and atactic (Lorch 2013). As
training an aphasic patient to produce past tense verb researchers have developed models of writing
morphology. Brain and Language, 70, 144–158.
Zurif, E., Swinney, D., Prather, P., Solomon, J., & Bushell, processes, these types have become termed cen-
C. (1993). On-line analysis of syntactic processing in tral and peripheral syndromes, each with subcat-
Broca’s and Wernicke’s aphasia. Brain and Language, egories. Generally speaking, several distinct
45, 448-464. forms of acquired agraphia occur that reflect spe-
cific combinations of impaired and preserved
spelling and writing abilities following damage
to certain brain regions.
Agraphia Central agraphia produces one of five types
of word spelling difficulties, each associated
Pélagie M. Beeson1, Steven Z. Rapcsak2 and with damage to a part of the linguistic pro-
Angel Ball3 cessing model and having specific distinctive
1
Department of Speech, Language, and Hearing features and characteristic errors (Rapszak and
Sciences, The University of Arizona, Tucson, Beeson 2000). Agraphia may result from dam-
AZ, USA age to multiple areas of linguistic processing;
2
Neurology Section, Southern Arizona VA therefore, multiple subtypes may occur
Healthcare System, Tucson, AZ, USA concurrently.
3
Department of Clinical Health Sciences, Some central agraphia syndromes:
Texas A&M University – Kingsville, Kingsville,
TX, USA • Phonological agraphia refers to an impaired
ability to manipulate the sound system of the
language (phonology) which manifests as a
Synonyms disproportionate difficulty with the spelling of
nonwords (e.g., flig, merber) compared with
Dysgraphia; Written language disorders real words.
• Deep agraphia is characterized by a marked
impairment of spelling ability for nonwords, as
Short Description or Definition seen in phonological agraphia, but with the
additional hallmark feature of semantic errors
Agraphias are acquired disorders of spelling or (e.g., car for vehicle).
writing caused by neurological damage in indi- • Surface agraphia (also called lexical
viduals with normal premorbid literacy skills. agraphia) is characterized by relatively pre-
There are several different agraphia profiles served ability to spell nonwords and regularly
that variously result from impairments of spelled words in the face of marked impair-
spelling knowledge, sound-to-letter correspon- ment of spelling words with irregular sound-
dences, letter-shape information, or motor con- to-letter correspondences, such as choir.
trol for handwriting. Although agraphia can
occur in relative isolation (pure agraphia), Peripheral agraphias have been described as
more often agraphia co-occurs with acquired disorders of writing based on the final stage of
Agraphia 81

production; they often spare oral spelling. The cognitive operations necessary for normal spell-
disorder occurs in the peripheral processing com- ing and writing. One primary cause is a stroke
ponents that guide the selection and production of with the agraphia being worse immediately fol- A
appropriate letter shapes. Individuals can display lowing or in the acute stages post stroke. Agraphia
both central and peripheral type agraphias if, for post stroke often occurs concurrently with apha-
example, there is coexisting motor dysfunction. sia, motor apraxia, or dysarthria (when affecting
Some peripheral agraphia syndromes: the writing limb), but specific prevalence data are
not available. Agraphia is also observed in indi-
• Allographic agraphia is an impairment of writ- viduals with neurodegenerative disorders includ-
ten spelling due to errors in letter selection. ing (but not limited to) those with primary
• Apraxic agraphia is an impairment of the progressive aphasia, amyotrophic lateral sclero-
selection and implementation of graphic sis, multiple sclerosis, or Alzheimer’s disease.
motor programs necessary to move the hand Detection of deterioration in writing is easily
to form letter shapes. done when comparison is made to premorbid
• Nonapraxic disorders of motor execution, due samples. Sampling of written narratives over
to motor system control of movements. This time provides information about communicative
subcategory includes micrographia, which is and cognitive declines as seen in Alzheimer’s
the production of abnormally small letters due disease (Neils-Strunjas et al. 2006; Kemper
to defective control of the force, speed, and et al. 2001).
amplitude of handwriting movements.

Writing disorders also occur at the sentence Natural History, Prognostic Factors, and
and narrative levels. These are behaviors that Outcomes
occur when the left language dominant hemi-
sphere is affected. Disorders of syntax include The prognosis for recovery from agraphia
written agrammatism, with limited or misuse of depends on the etiology of the lesion and the
low content or function words (e.g., articles, prep- extent of the underlying brain damage. Agraphia
ositions), and decrease in clausal complexity, as in following stroke or traumatic brain injury tends to
fragmented clauses, restarts, and abandoned show some spontaneous recovery in the first
sentences (as seen in cases of dementia). Persev- months after damage occurs, but residual impair-
erative letters and words are also observed in ments often persist. Additional improvements
dementia-type written language, occurring along may be achieved with behavioral treatment
with decline in meaning. directed toward strengthening the weakened cog-
Individuals with both left and right hemisphere nitive processes that support spelling, syntax, and
damage can also demonstrate written disorders morphology, or motor control for writing. In indi-
related to visuoperceptual deficits (e.g., hemispatial viduals with neurodegenerative disorders, pro-
neglect), characterized by avoiding one side of the gressive worsening of the spelling impairment is
page, slanted writing, overwriting letters, etc. The observed along with the gradual deterioration of
reader is encouraged to seek entry on hemispatial other language and cognitive functions.
neglect.

Neuropsychology and Psychology of

Epidemiology Agraphia

Agraphia is commonly observed following dam- Neuroimaging of normal functioning individuals

age to the language-dominant hemisphere and can provides knowledge of brain pathways involved
follow any kind of focal damage to the brain in writing, which aids in describing the impaired
regions critical for implementing the various neurologic processing of writing. A recent meta-
82 Agraphia

Agraphia, Fig. 1 A
cognitive model indicating Semantics
the component processes
involved in spelling and
writing

Phonology Orthography

Lexical
Words Words
Spoken word Written word

Auditory Sublexical Visual

Phonemes Letters
analysis analysis

Motor speech Graphic motor

programs programs

Speech Writing

analysis of 18 neuroimaging studies during hand- basis of the knowledge of sound-to-letter corre-
writing provides a template for cortical and sub- spondences using a sublexical processing strat-
cortical involvement, with support for superior egy as depicted in Fig. 1. A sublexical approach
parietal involvement in the language dominant is often employed when one is unsure about the
hemisphere that could function to interface between spelling of a word, or when required to spell an
linguistic and motor systems (Planton et al. 2013). unfamiliar word or a nonword, such as glope.
Meanwhile, research that identifies regions of brain Spelling via sound-to-letter correspondences is
damage associated with various types of agraphia likely to yield correct responses for regularly
continues to help us understand the disorder and its spelled words, such as drive, but overreliance
subtypes. Nonetheless, researchers have not entirely on the sublexical route will result in phonologi-
unraveled specific brain regions for each step of the cally plausible errors for irregularly spelled
process (Lorch 2013). words, such as kwire for choir. Thus, according
Written words are typically produced in to a dual-route model as depicted in Fig. 1, only
response to activation of a concept in the seman- the lexical route can deliver correct spellings for
tic system. The motivation to write a word may irregularly spelled words. The final stages of
be driven by the desire to convey a message or in writing require translation of abstract spelling
response to an auditory stimulus, as in the con- knowledge into letter shapes and selection and
text of writing a word to dictation. As depicted in implementation of the graphic motor programs
the cognitive model of single-word processing for the appropriate handwriting movements. The
in Fig. 1, the word meaning (semantics) and various agraphia syndromes reflect specific
the phonological word form (phonology) impairments to these component processes nec-
both provide access to spelling knowledge essary for spelling and writing.
(orthography). In literate adults, the spellings
of familiar words are easily recalled as whole Phonological/Deep Agraphia
words from one’s spelling vocabulary (i.e., Phonological agraphia is characterized by diffi-
orthographic lexicon). In contrast to this lexical culty in the generation of spellings on the basis
approach, spellings can be assembled on the of sound-to-letter correspondences. This problem
Agraphia 83

is particularly evident during clinical evaluation includes all of the characteristic features of pho-
when an individual is asked to generate plausi- nological agraphia, but it is distinguished from
ble spellings for nonwords. The disproportion- the latter by the production of semantic errors A
ate difficulty in spelling nonwords compared to (e.g., husband written as wife). In essence, deep
familiar words gives rise to an exaggerated lex- agraphia can be considered a more severe form
icality effect (Henry et al. 2007; Rapcsak et al. of phonological agraphia.
2009). According to a dual-route model (Fig. 1), Like phonological/deep alexia, phonological/
poor nonword spelling in phonological agraphia deep agraphia is typically encountered in patients
is attributable to damage to the sublexical route, with aphasia syndromes characterized by phono-
while the better preserved real-word spelling by logical impairment including Broca’s, conduc-
these patients reflects the residual functional tion, and Wernicke’s aphasia. In such cases,
capacity of the lexical and semantic routes. there is damage to a network of perisylvian corti-
There is evidence to suggest that phonological cal regions involved in speech production/percep-
agraphia reflects a central impairment of phono- tion and phonological processing including
logical processing ability that is also apparent Broca’s area, precentral gyrus, insula, Wernicke’s
on reading tasks; however, the spelling impair- area, and supramarginal gyrus (Fig. 2). The con-
ment is typically of greater severity due to the tribution of these regions to phonological pro-
fact that spelling is a harder task than reading cessing skills is evident from both lesion studies
(Rapcsak et al. 2009). Although spelling accu- and also in functional imaging studies of healthy
racy for words (both regular and irregular) is individuals performing a variety of written and
better preserved than spelling of nonwords, per- spoken language tasks requiring phonological
formance is often degraded to some extent rela- processing (Jobard et al. 2003; Vigneau et al.
tive to premorbid performance. Due to the 2006; Rapcsak et al. 2009). In individuals with
reliance on lexical processing with limited sub- deep agraphia, the left hemisphere damage tends
lexical input, real-word spelling is typically to be more extensive than that associated with
influenced by lexical-semantic variables such phonological agraphia, and it has been hypothe-
as word frequency (high > low), imageability sized that the right hemisphere may be responsible
(concrete > abstract), and grammatical class for the characteristic deep agraphia profile
(nouns > verbs > functors). Deep agraphia (Rapcsak et al. 1991).

Agraphia, Fig. 2 Cortical

regions involved in spelling
and writing
84 Agraphia

Surface Agraphia spelling tasks (Beeson et al. 2003) and may rep-
Surface agraphia is characterized by difficulty in resent the neural substrate of the orthographic
spelling irregular words – i.e., those that contain lexicon. Surface agraphia has also been described
atypical sound-to-letter correspondences. Regular following focal damage to posterior middle/infe-
words are spelled with significantly better accu- rior temporal gyrus and angular gyrus (Rapcsak
racy, thus yielding a regularity effect. Nonword and Beeson 2004) and in patients with left anterior
spelling is relatively preserved. In a manner anal- temporal lobe atrophy (Graham et al. 2000). In
ogous to surface alexia, a dual-route theory attri- these cases, the spelling deficit may reflect dam-
butes surface agraphia to dysfunction of the age to a distributed extrasylvian cortical network
lexical spelling route (Fig. 1). Specifically, it has involved in semantic processing (Fig. 2).
been suggested that the spelling disorder results
from damage to the orthographic lexicon Allographic Agraphia
(Rapcsak and Beeson 2004). The loss of word- Allographic agraphia refers to a disturbance of the
specific orthographic knowledge prompts reliance ability to activate or select appropriate letter
on a sublexical phoneme-grapheme conversion shapes for the abstract orthographic representa-
strategy that produces phonologically plausible tions generated by central spelling routes. This
regularization errors on irregular words, a finding impairment of handwriting is characterized
that is most pronounced for low-frequency items by letter selection errors that often include the
(e.g., yot for yacht). A functional MRI study with substitution of physically similar letter forms
normal right-handed adults recently identified (e.g., b for h). The allographic difficulty may be
cluster of brain regions more activated with irreg- specific to letter case (upper vs. lower) or style
ular spelling: specifically involving the “left pos- (print vs. cursive). When allographic agraphia
terior IFG (pars, triangularis/opercularis) and occurs in isolation, oral spelling is preserved, as
adjacent insula, left mid-posterior superior tem- well as the ability to correctly arrange component
poral sulcus (STS) and the anterior cingulate/sup- letters that make up a word (i.e., anagram spelling)
plementary motor area (SMA)” and suggesting a and typing. Allographic agraphia is often associ-
network of cortical processing engaging ortho- ated with damage to left temporo-parieto-occipital
graphic and phonological systems (De Marco regions.
et al. 2017, p. 121).
Surface agraphia may also result from damage Apraxic Agraphia
to central semantic representations as observed in Apraxic agraphia is characterized by poor letter
individuals with semantic dementia (Graham et al. formation in handwriting that is not attributable
2000). The reduction in the ability to process to allographic disorder or sensorimotor, cerebel-
lexical-semantic information in such individuals lar, or basal ganglia dysfunction. The difficulty
results in overreliance on sublexical spelling pro- arises at the level of motor programming for the
cedures and regularization errors. As expected, it skilled movements of the hand so that the spa-
is not uncommon to observe co-occurrence of tiotemporal aspects of writing are disturbed.
surface alexia and agraphia in individuals with Individual letters are often difficult to recognize
semantic dementia (Graham et al. 2000). and may simply appear to be meaningless
Surface agraphia, like surface alexia, is typi- scrawls. Lesions associated with apraxic
cally associated with extrasylvian brain pathology agraphia have been noted in the hemisphere
(Fig. 2). Focal lesions that give rise to surface contralateral to the dominant hand. Thus, in
agraphia have been documented in the left inferior right-handed individuals, the damage typically
occipito-temporal cortex (Rapcsak and Beeson involves the left superior parietal lobe in the
2004). This region includes a portion of the fusi- region of the intraparietal sulcus, the dorsolat-
form gyrus known as the visual word form area eral premotor cortex just anterior to primary
that has been shown to be engaged in healthy motor cortex for the hand, or the supplementary
adults during reading (Cohen et al. 2002) and motor area. More recently, cases of thalamic
Agraphia 85

damage have also demonstrated disturbances premorbidly. In addition, access to premorbid

of the graphomotor process (Vandenborre handwriting samples is beneficial for identifica-
et al. 2015). tion of change in ability via comparisons A
(Papathanasiou and Cséfalvay (2013).
Nonapraxic Disorders of Motor Execution To evaluate word level spelling and determine
In addition to apraxic agraphia, there are several the agraphia subcategory type(s), several tasks
additional disorders of motor execution that affect should be included: spelling aloud, written spell-
the ability to form legible letter shapes. These ing of regular and irregular words, comparing
writing difficulties include disturbances of the word class (content vs functor), and word length.
regulation of movement force, speech, and ampli- Input stimuli to test routes of processing include
tude. Micrographia (the production of small let- written picture naming (pictorial visual), writing
ters with reduced legibility) is a common example to dictation (auditory), and manipulation of letters
that is associated with the basal ganglia pathology (graphemic visual). The Johns Hopkins Univer-
in Parkinson disease. Cerebellar pathology can sity Dyslexia and Dysgraphia Batteries (JHU Bat-
also result in poor handwriting due to irregular tery: Goodmann and Caramaaza 1986b, published
and disjointed hand movements. Handwriting dif- in Chapey 2008) is a word-only tool that includes
ficulty is also associated with damage to primary data on word frequency, word length, regular
sensorimotor cortex and/or associated corticospinal vs. irregular spelling, and nonwords, but is pri-
tracts that cause hemiparesis of the dominant hand. marily dictated task.
When the hemiparesis is marked, individuals typi- To evaluate sentence level writing acquired dis-
cally shift to writing with the nondominant hand. orders, the tasks of writing to dictated sentences or
Improvement in graphomotor control of the non- picture description are used in formal tests.
dominant hand is apparent with practice and often Researchers are also finding valuable diagnostic
provides a fully functional substitute; however, the information from narrative discourse samples,
automaticity of motor movements is rarely compa- using picture description, story retell, story scripts
rable to the premorbidly dominant hand. from sequential picture, or generated essays (e.g.,
Groves-Wright et al. 2004; Mitzner and Kemper
2003; Neils et al. 1989; Pennebaker and Stone
Evaluation 2003, Nippold et al. 2005). Discourse samples
will provide information on ability to express con-
The evaluation of writing in individuals with neu- tent (information units) and demonstrate syntactic
rological impairments is often part of a broader and morphological forms and clausal complexity
language and cognitive assessment. No current and measures of semantic usage (number of words,
modality-specific formal test tool is available for and type token ratio -TTR).
acquired agraphia. An evaluation of adult writing Standardized tests with writing subtests
must first include information regarding educa- include:
tional level, premorbid reading level, visual abil-
ity (e.g., access to glasses if needed), and • Boston Diagnostic Aphasia Examination-3
observations of any dominant hand paresis/paral- (Goodglass et al. 2001) – writing subtests
ysis/praxis. If the evaluation is proceeding with an include person’s name, dictated letters and
unimpaired dominant limb, then the focus can be numbers, abbreviations, one copied sentence,
primarily on linguistic features. However, if either the alphabet, dictated primer words, regular
an impaired dominant limb or use of unimpaired and irregular spelling words, nonsense words
nondominant limb is used, then consideration of irregular spelling, written picture naming of
must be given for slow productions, poor legibil- objects and actions, functor words, morpho-
ity, and possible apraxic-type errors. In some logical endings, functor loaded sentences, and
cases, keyboard writing can be assessed particu- picture description of the Cookie Theft line
larly if the individual used a keyboard drawing.
86 Agraphia

• Examining for Aphasia-4 (EFA-4; LaPointe visual shape of word, or provide letter ana-
and Eisenson 2008) – writing subtests include grams) (Murray and Clark 2015). To address
dictated letters, numbers, words, and short peripheral dysgraphia or visual perceptual diffi-
sentences (six to eight words in length) and a culties, clinicians can employ techniques such as
written narrative (either self-generated or using prompts (e.g., lined paper), encouraging
story-retell) based on a Beach scene line print or typing in lieu of handwriting, verbal
drawing. cues to attend to left visual field, or writing
• Multilingual Aphasia Examination 3rd Ed prosthesis. Facilitated writing with technology
(MAE-3; Benton et al. 1978) – writing subtest also provides functional abilities for use with
includes word level only for oral spelling, dic- computer or tablets. Software and apps with
tated words, and manipulation of tactile letters. word prediction and cued choices (auditory and
• Psycholinguistic Assessment of Language Pro- visual) are growing in use, but research is
cessing in Aphasia (PALPA: Kay et al. 1992) – needed to demonstrate efficacy in the adult
writing subtests include writing at word level populations (Dietz et al. Griffith 2011).
for word length, imageability and frequency of
words, grammatical class, morphological end-
Cross-References
ings, regularity, nonwords, and homophones
and option of written picture naming.
▶ Alexia
• Western Aphasia Battery-R (WAB-R; Kertesz
▶ Aphasia
2007) – writing subtests include dictated letters
▶ Hemispatial Neglect
and numbers, dictated words of increasing
▶ Phonological Disorder
length, irregular words and nonwords, one dic-
▶ Visual Neglect
tated sentence, name and address, and written
description of a Picnic scene line drawing.
References and Readings

Treatment Beeson, P. M., & Henry, M. L. (2008). Comprehension and

production of written language. In R. Chapey (Ed.),
Language intervention strategies in adult aphasia
Several behavioral treatment approaches have (5th ed., pp. 654–688). Baltimore: Wolters Kluwer/
shown positive outcomes in the rehabilitation of Lippincott, Williams & Wilkins.
agraphia (for reviews see Beeson and Henry 2008; Beeson, P. M., & Rapcsak, S. Z. (2002). Clinical diagnosis
and treatment of spelling disorders. In A. E. Hillis (Ed.),
Murray and Clark 2015; Papathanasiou and
Handbook on adult language disorders: Integrating cog-
Cséfalvay 2013; Peach and Shapiro 2012). In nitive neuropsychology, neurology, and rehabilitation
general, treatment is directed toward strengthen- (pp. 101–120). Philadelphia: Psychology Press.
ing impaired processes and training the use of Beeson, P. M., & Rapcsak, S. Z. (2006). Treatment of
alexia and agraphia. In J. H. Noseworthy (Ed.), Neuro-
compensatory strategies necessary to bypass the
logical therapeutics: Principles and practice (2nd ed.,
functional deficit. Most evidenced-based practice pp. 3045–3060). London: Martin Dunitz.
researches on clinical application of spelling inter- Beeson, P. M., Rapcsak, S. Z., Plante, E., Chargualaf, J.,
vention are case studies. For example, one Chung, A., Johnson, S. C., et al. (2003). The neural
substrates of writing: A functional magnetic resonance
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88 Ahylognosia

Vandenborre, D., van Dun, K., Engelborghs, S., & Mariën, differentiate structural components of objects,
P. (2015). Apraxic agraphia following thalamic dam- resulted from impairment of intensity analyzers.”
age: Three new cases. Brain and Language, 150,
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Vigneau, M., Beaucousin, V., Hervé, P. Y., Duffau, H., reflect “the loss of the capacity to differentiate
Crivello, F., Houdé, O., et al. (2006). Meta-analyzing forms, resulted from impairment of the analyzers
left hemisphere language areas: Phonology, seman- of extent.” Because determining any of these qual-
tics, and sentence processing. NeuroImage, 30,
1414–1432. ities requires discriminatory judgments, in the
absence of more elementary tactual defects, such
disturbances suggest pathology involving the
somatosensory areas of the parietal lobe.
Ahylognosia

John E. Mendoza Cross-References

Department of Psychiatry and Neuroscience,
Tulane Medical School and SE Louisiana ▶ Amorphognosis
Veterans Healthcare System, New Orleans, ▶ Astereognosis
LA, USA ▶ Tactile Agnosia

Definition References and Readings

Inability to determine by touch alone certain phys- Bauer, R. M., & Demery, J. A. (2003). Agnosia. In
K. Heilman & E. Valenstein (Eds.), Clinical Neuropsy-
ical properties of an object such as its texture, chology (4th ed., pp. 236–295). New York: Oxford Uni-
density (weight), or resistance to pressure, with versity Press.
difficulties in perceiving size or shape is referred Critchley, M. (1969). The parietal lobes. New York:
to as amorphognosia. While perhaps seeming a bit Hafner Publishing Co.
Delay, J. (1935). Les astereognosis. Pathologie due
artificial, according to Bauer and Demery (2003),
Toucher, Clinque, Physiologie, Topographie. Paris:
the distinction between ahylognosia and Masson.
amorphognosia apparently traces back to 1935 Hecaen, H., & Albert, M. L. (1978). Chapter 6, Disorders
when a French neurologist, Delay, divided of somesthesis and somatognosis. In Human neuropsy-
chology. New York: Wiley.
astereognosis into two subtypes of deficits:
amorphognosia, which was defined as a difficulty
in recognizing the size or shape of an object by
touch, and ahylognosia, which was described as a
failure to differentiate the “molecular qualities” of Akathisia
an object, such as its density, weight, thermal
conductivity, or roughness. Delay also defined a Anna DePold Hohler1 and Marcus Ponce de
third type of astereognosis, tactile asymboly, Leon2
1
which was characterized as the inability to iden- Boston University Medical Center, Boston,
tify an object by touch in the absence of MA, USA
2
amorphognosia and ahylognosia. These same dis- Madigan Army Medical Center, Tacoma,
tinctions were followed by Critchley (1969) and WA, USA
continue to be used by more recent authors (Bauer
and Demery 2003). Hecaen and Albert (1978) in
their book, Human Neuropsychology, attempted Synonyms
to explain these distinctions by suggesting that
ahylognosia was “the loss of the capacity to Restlessness
Akelaitis, Andrew John Edward (“A.J.”) (1904–1955) 89

Definition Rochester School of Medicine and Dentistry.

At the same time, he also held appointments at
Akathisia is a syndrome characterized by unpleasant the clinics of the Strong Memorial and Roch- A
sensations of inner restlessness that manifests itself ester Municipal Hospitals in Rochester,
with an inability to sit still or remain motionless. New York. He left these appointments to
serve in the Navy during World War II.
Following his service in the war, Dr. Akelaitis
Current Knowledge worked as an Assistant Professor of Neurology
at the New York Medical College and Assistant
It is most often seen as a side effect of medica- Professor of Clinical Medicine in Neurology at
tions, mainly neuroleptic antipsychotics. Patients Cornell University Medical College. He also
may have difficulty describing their symptoms, served as the attending neuropsychiatrist at
leading to a misdiagnosis of anxiety and worsen- Mount Vernon (New York) Hospital and on
ing of the condition upon treatment with neuro- the staff of the Bellevue Hospital and the
leptic antipsychotic agents. Several medications New York Hospital.
have been used to treat the condition, including
benztropine and beta-blocking agents. With-
Major Honors and Awards
drawal of the offending agent is often most effec-
tive. It may be seen with Parkinson’s disease.
• Dr. Akelaitis was a Fellow of the American
Psychiatric Association. He was specialty cer-
tified by the American Board of Psychiatry and
Cross-References
Neurology and held membership appointments
in the American Medical Association, the
▶ Parkinson’s Disease
New York State Medical Society, the
▶ Tardive Dyskinesia
New York Society for Clinical Psychiatry,
and the New York Neurological Society.
References and Readings

Kumar, A., & Calne, D. (2004). Approach to the patient with

a movement disorder and overview of movement disor- Landmark Clinical, Scientific, and
ders. In R. L. Watts & W. C. Koller (Eds.), Movement Professional Contributions
disorders (2nd ed., p. 9). New York: McGraw-Hill.
• Dr. A.J. Akelaitis is best known for his observa-
tions of patients who underwent sectioning of
the corpus callosum (i.e., “split-brain” patients).
Akelaitis, Andrew John Beginning in the late 1930s, the neurosurgeon
Edward (“A.J.”) (1904–1955) Dr. William P. van Wagenen pioneered surgical
sectioning of the corpus callosum for the treat-
Michael J. Larson and Joseph E. Fair ment of intractable epilepsy (Mathews et al.
Brigham Young University, Provo, UT, USA 2008). Dr. Akelaitis worked closely with
Dr. van Wagenen and performed pre and post-
operative tests of cognitive and neurological
Major Appointments functioning on many of these individuals.
According to Akelaitis’ reports, patients who
• Dr. A.J. Akelaitis began his career as an assis- underwent callosotomy surgery largely did not
tant professor in the Department of Medicine, show lasting changes in cognitive, intellectual,
Division of Psychiatry, at the University of or motor functioning, although their seizure
90 Akelaitis, Andrew John Edward (“A.J.”) (1904–1955)

activity was consistently alleviated. For nearly field. Such technology would possibly have
two decades, Akelaitis’ reports of largely normal given him insight into the specialization of
functioning after callosotomy perpetuated the the two hemispheres and interhemispheric
generally accepted belief that sectioning the cor- transfer of information via the corpus callosum
pus callosum did not impact cognitive or motor (Mathews et al. 2008).
functioning in humans. • Despite his contributions as one of the first indi-
• Despite his reports of few neurological changes viduals to study neurological functioning fol-
following callosotomy, Akelaitis noted periodic lowing callosotomy, Akelaitis has been
cases with hemiplegia and praxic disturbances. criticized for employing insensitive or inade-
He was slow, however, to include the sectioning quate testing procedures. However, reviews of
of the corpus callosum in his explanations for his cases have confirmed that his patients did
these changes; rather, he attributed the symp- exhibit what are now considered typical symp-
toms to unintended operative damage to adjacent toms, although his explanations for these mani-
cortical areas. In some cases, postoperative festations, while consistent with much of the
symptoms were seen as exacerbations of pre- research of the time, were often inadequate
callosotomy characteristics or were attributed (Sauerwein and Lassonde 1996). In the 1950s
to preexisting and/or postoperative psychologi- and 1960s, researchers including Roger Sperry,
cal or behavioral factors. Further, many of the Michael Gazzaniga, Norman Geschwind, Edith
symptoms observed by Akelaitis were transient Kaplan, and Joseph Bogen began to publish
and consequently not considered to be conclu- articles involving callosotomies in animals and
sively linked with callosal sectioning humans, which contradicted many of Akelaitis’
(Sauerwein and Lassonde 1996). findings. This sparked renewed interest in the
• Several factors most likely influenced function of the corpus callosum and eventually
Akelaitis’ reports of minimal neurological earned Sperry the Nobel Prize in 1981.
changes following callosotomy surgery. First, • Through the course of his short career,
the majority of patients Akelaitis observed did Dr. Akelaitis made significant contributions
not have complete callosotomies, nor were toward research on the corpus callosum and
neurosurgical procedures well standardized at advanced the treatment of intractable epilepsy.
the time. Of the 28 patients he studied, only He also published articles regarding the psy-
one third were reported to have undergone chiatric aspects of myxedema (severe hypo-
“complete” callosal sectioning, with the thyroidism), hereditary and vascular cerebral
remainder “nearly complete” or “partial” sec- atrophy, lead encephalopathy, acute demyelin-
tioning (Bogen 1995). The patients with only ating processes (multiple sclerosis), and Pick’s
partially sectioned callosal fibers undoubtedly disease.
continued to have interhemispheric transmis-
sion, thereby contributing to Akelaitis’ find-
ings of generally intact functioning. Next, Short Biography
emerging research at the time reported no cog-
nitive changes following sectioning of the cor- Andrew John (“A.J.”) Akelaitis was born in Balti-
pus callosum. For example, Walter Dandy more, Maryland, on July 11, 1904. He studied
stated in 1936 that when “the corpus callosum medicine at Johns Hopkins University and received
is split longitudinally. . . no symptoms follow his M.D. in 1929. In the early 1930s, he practiced
its division. This simple experiment at once clinical neurology in Rochester, New York. He
disposes of the extravagant claims to the func- subsequently became an Assistant Professor of
tions of the corpus callosum” (see Zaidel et al. Medicine at the University of Rochester School of
2003). Finally, Akelaitis lacked the technolo- Medicine and Dentistry. Dr. Akelaitis joined the
gies, such as the tachistoscope used by his Navy during World War II where he served with
successors, to present stimuli to one visual distinction at the rank of Commander. He married
Akinetic Mutism 91

the former Victoria Chesno. The couple had one

son, Andrew, and a daughter, Lillian. Akelaitis died Akinesis
at the New York Hospital on November 24, 1955 at A
the young age of 51. Douglas I. Katz
Department of Neurology, Boston University
School of Medicine, Braintree, MA, USA
Cross-References

▶ Corpus Callosum Synonyms

▶ Epilepsy
▶ Split-Brain Akinesia; Akinetic

References and Readings Definition

Akelaitis, A. J. (1941a). Psychobiological studies following Akinesis is an absence or paucity of movement,

section of the corpus callosum: A preliminary report. resulting from an abnormal motor control. It is a
American Journal of Psychiatry, 97, 1147–1157.
Akelaitis, A. J. (1941b). Studies on the corpus callosum.
problem that may occur in Parkinson’s disease
II. The higher visual functions in each homonymous when patients develop freezing or inability to
field following complete section of the corpus callosum. initiate movement. It may also occur as a result
Archives of Neurology and Psychiatry, 45, 788–796. of a paralyzed muscle, such as with an anesthetic
Akelaitis, A. J., Risteen, W. A., Herren, R. Y., & Van Wagenen,
W. P. (1942). Studies on the corpus callosum. III.
nerve block.
A contribution to the study of dyspraxia and apraxia fol-
lowing partial and complete section of the corpus callosum.
Archives of Neurology and Psychiatry, 47, 971–1008. Cross-References
Akelaitis, A. J. (1944a). Studies on the corpus callosum.
IV. Diagonistic dyspraxia in epileptics following partial
and complete section of the corpus callosum. American ▶ Action-Intentional Disorders
Journal of Psychiatry, 101, 594–599. ▶ Akinetic Mutism
Akelaitis, A. J. (1944b). Study on gnosis, praxis, and lan- ▶ Bradykinesia
guage following section of corpus callosum and anterior
commisure. Journal of Neurosurgery, 1, 94–102.
▶ Parkinson’s Disease
Bogen, J. (1995). Some historical aspects of callosotomy
for epilepsy. In A. G. Reeves & D. W. Roberts (Eds.),
Epilepsy and the corpus callosum 2 (pp. 107–121).
New York: Plenum Press.
Gazzaniga, M. S. (1995). Principles of human brain orga-
nization derived from split brain studies. Neuron, 14, Akinetic Mutism
217–228.
Gazzaniga, M. S. (2005). Forty-five years of split-brain Michael S. Mega
research and still going strong. Nature Reviews: Neu-
roscience, 6, 653–659.
Center for Cognitive Health, Portland, OR, USA
Mathews, S., Linskey, M., & Binder, D. (2008). William
P. van Wagenen and the first corpus callosotomies for
epilepsy. Journal of Neurosurgery, 108, 608–613. Synonyms
Sauerwein, H. C., & Lassonde, M. (1996). Akelaitis’
investigations of the first split-brain patients. In
C. Code, C.-W. Wallesh, Y. Joanette, & A. R. Lecours A spectrum of motivational impairment has abulia
(Eds.), Classic cases in neuropsychology at one end and akinetic mutism at the other. Coma
(pp. 305–317). Hove: Psychology Press. vigil is not akinetic mutism; it arises when a
Zaidel, E., Iacoboni, M., Zaidel, D., & Bogen, J. (2003).
The callosal syndromes. In K. M. Heilman &
comatose patient regains the sleep-wake cycle,
E. Valenstein (Eds.), Clinical neuropsychology eyes open during the day and closed during
(pp. 347–403). New York: Oxford University Press. sleep at night, usually after 2 weeks of a brain
92 Akinetic Mutism

lesion that produces irreversible coma. Coma vigil Categorization

is also referred to as a persistent vegetative state.
When brain lesions disconnect all descending When anterior cingulate lesions are bilateral, lim-
motor output but preserve conscious awareness bic, cognitive, and motor activation is disrupted
the patient is said to be locked in. In akinetic producing profound akinetic mutism. Loss of
mutism, patients still respond to their internal ascending input from the reticular core, due to
and external environment – and thus are not in bilateral lesions of the medial forebrain bundle,
coma, and they are not locked in since they can may also produce akinetic mutism. Rarely are
accomplish motor output, given sufficient complete bilateral lesions seen in humans, more
motivation. frequently partial circuit disruption results in a
graded loss in motivation depending upon which
circuit is damaged.
Five frontal-subcortical circuits have been
Short Description or Definition named according to their function or cortical site
of origin: the motor circuit, originating in the sup-
The fully formed akinetic mute state usually plementary motor area, and the oculomotor circuit,
results from bilateral anterior cingulate lesions originating in the frontal eye fields, are dedicated to
(Fig. 1). Patients are profoundly apathetic, motor function. The dorsolateral prefrontal, lateral
incontinent, and akinetic. They do not initiate orbitofrontal, and anterior cingulate circuits support
eating or drinking and if speech occurs, it is executive cognitive functions, personality, and
restricted to terse responses. They seem awake, motivation, respectively (Mega and Cummings
visually tracking objects, but displaying no emo- 1994). Each of the five circuits has the same mem-
tions – even during painful circumstances, they ber structures: the frontal lobe, striatum, globus
remain indifferent. The akinetic mute state also pallidus, substantia nigra, and thalamus. There is a
results from bilateral subcortical paramedian progressive spatial compaction of the circuits as
diencephalic and midbrain lesions possibly they travel through the basal ganglia. A lesion any-
affecting the ascending reticular core, medial where along the path of a circuit will produce the
forebrain bundles, and isolated bilateral globus same clinical result but only in the globus pallidus
pallidus lesions. interna are all the frontal-subcortical circuits in such

Akinetic Mutism,
Fig. 1 Arrows show the
left greater than right
anterior cingulate lesions
due to bilateral anterior
cerebral artery (ACA)
ischemic stroke. Bilateral
ACA lesions usually result
in death due to loss of all
limbic motivational input to
prefrontal cortex
Akinetic Mutism 93

a compact spatial volume that a relatively small Three anterior effector regions include a vis-
lesion can have profound effects. ceral effector region inferior to the genu of the
corpus callosum encompassing area 25, the ante- A
rior subcallosal portions of 24a-b, and 32; a cog-
Epidemiology nitive effector region that includes most of the
supracallosal area 24, and areas 24a0 -b0 and 320 ;
Akinetic mutism is exceedingly rare when perma- and a skeletomotor effector region within the
nent, since a bilateral lesion is necessary and depths of the cingulate sulcus, that includes
usually results in death. Unilateral anterior cere- areas 24c0 /23c on the ventral bank, with 24c0 g
bral artery (ACA) strokes are the usual cause of and 6c on the dorsal bank. These three cingulate
transient akinetic mutism, but ACA strokes only effector regions integrate ascending input
make up 1% of all cerebral vascular lesions. concerning the internal milieu of the organism
with visceral motor systems, cognitive-attentional
networks, and skeletomotor centers to produce the
Natural History, Prognostic Factors, and affective motivation necessary for the organism’s
Outcomes engagement in the environment.
Circumscribed lesions in humans are rarely
The natural history of akinetic mutism, when it confined to one region of the cingulate. With an
arises from a unilateral lesion, is usually a 2-week anterior lesion, the cognitive, skeletomotor, and
period of gradual improvement from the fully visceral effector regions are often affected. Bilat-
formed syndrome to near-complete recovery pre- eral lesions result in an akinetic mute state. The
sumably enabled by contralateral limbic activa- loss of spontaneous motor activity results when
tion gaining access to deafferented networks. The the lesion involves the supplementary motor area
outcome from bilateral lesions is usually death, and the skeletomotor effector region. When these
given no ability for cross-hemispheric motivation. two motor regions are spared, motor activity will
Thus, prognosis will rely upon neuroimaging be normal but the patient will demonstrate pro-
documenting the extent of the lesion. found indifference, docility, and the loss of moti-
vation to engage in a task. They can be led by the
examiner to engage in a task but will fail to self-
Neuropsychology and Psychology generate sustained directed attention. They lack
cognitive motivation.
Extracingulate connections support a segregation The role of the anterior cingulate as a cognitive
of the cingulate into functional subregions (for a effector is appreciated within the realm of lan-
complete discussion of these circuits, Cingulate guage. Language, a cognitive function, is distin-
Gyrus). Paralleling the general distinction guished from the motor function of speech.
between posterior granular sensory cortices and Transcortical motor aphasia (TCMA) is the usual
anterior agranular executive cortices, the anterior result of left anterior medial or anterior dorsolat-
cingulate can be considered an executive region eral prefrontal lesions. The classic syndrome of
for affective motivation and cognition, while the TCMA is initial mutism that resolves in days to
posterior cingulate, with its prominent granular weeks, yielding a syndrome featuring delayed
layer IV receiving sensory input, is engaged in initiation of brief utterances without impaired
visuospatial and memory processing. The inter- articulation, excellent repetition, inappropriate
connections between the anterior and posterior word selection, agrammatism, and poor compre-
cingulate allow for regulatory control by the ante- hension of complex syntax. Activation of dorso-
rior executive effector regions over posterior sen- lateral prefrontal cortices enabling language and
sory processing and reciprocal modulation of that speech arises from two sources: the anterior cin-
regulatory input by the posterior cingulate. gulate and the supplementary motor area (with the
94 Akinetic Mutism

cingulate skeletomotor region). When the execu- hippocampus, basal forebrain, amygdala, and all
tive prefrontal cortex (areas 9, 10, and 46) is cortical areas, as well as fibers of passage
disrupted, cognitive language deficits are promi- between hippocampus and prefrontal cortex,
nent (TCMA, type I); when motor neurons in area and from the median raphe to the dorsal hippo-
4, devoted to the speech apparatus, are discon- campus. Surgical ablation of the anterior portion
nected from their activation, speech hesitancy (sparing fibers relevant to memory function) is
and impoverished output ensues (TCMA, type most successful when treating aggression,
II). These two functional realms are separable extreme anxiety, obsessive-compulsive behav-
and can be disconnected anywhere along two iors, and severe pain. Psychotic symptoms
pathways. Direct damage to the supplementary show only a temporary response. The only pro-
motor area or its outflow to the motor cortex spective long-term follow-up of patients under-
traveling in the anterior superior paraventricular going supracallosal anterior cingulotomy for the
white matter will produce TCMA type II. Direct treatment of medically refractory obsessive-
damage to the anterior cingulate, its outflow to compulsive disorder revealed a clear response
areas 9, 10, and 46, or to the caudate – via the in 28% and a partial response in 17% (Baer et al.
subcallosal fasciculus, just inferior to the frontal 1995). Including the subcallosal anterior cingu-
horn of the lateral ventricle – will disrupt frontal- late/medial orbital cortex may provide the best
subcortical circuits involved in motivation and result in treating the refractory obsessive-com-
executive cognitive function. The initial muteness pulsive patient (Hay et al. 1993) due to the
has been described by a patient after recovery elimination of the visceromotor aspects of the
from an anterior cingulate/supplementary motor disorder. Postsurgical personality changes are
infarction as a loss of the “will” to reply to her subtle after the acute attentional disorder
examiners, because she had “nothing to say,” her resolves. Although formal cognitive testing is
“mind was empty,” and “nothing mattered” unaltered, affect is flattened. Motivation for pre-
(Damasio and Van Hoesen 1983). vious enjoyments, such as reading, hobbies, and
The loss of will to initiate a motor function even spectator sports, is lost (Tow and Whitty
results from supplementary motor or cingulate 1953) subtle changes that reflect the loss of
skeletomotor region damage, while poor initiation higher cognitive motivation. The three anterior
of a cognitive process results from lesions in cingulate regions, by virtue of the distinct func-
supracallosal cingulate areas. Loss of emotional tional systems they coordinate, are the conduits
vigilance ranging from flattened affect to neglect through which limbic motivation can activate
can be produced by surgery in this region. Ante- feeling, thought, and movement – partial lesions
rior cingulate lesions in monkeys – difficult sub- produce partial aspects of the akinetic mute state
jects in which to evaluate subtle behavioral depending upon their location.
changes – produce either no observable change Subcortical lesions can also produce the fully
or result in a transient stupor with ensuing leth- formed syndrome. Carbon monoxide poisoning
argy, tameness, disturbed intraspecies social with resultant apathy and placidity was described
behavior, and decreased pain sensitivity (Pribram in a patient with a ventral pallidal lesion who also
and Fulton 1954). Removal of the anterior cingu- had hypoperfusion on single photon emission
late (areas 24 and 32) in humans (cingulectomy) computed tomography (SPECT) predominately
has been employed as a treatment for epilepsy, in the cingulate bilaterally (Mori et al. 1996).
psychiatric, and pain disorders. Hypometabolism on 18F-fluorodeoxyglucose pos-
The cingulum bundle has also been the site of itron emission tomography (FDG-PET) in frontal
surgical lesions (cingulumotomy when only the cortex has also resulted from pallidal lesions
bundle is transected, or cingulotomy when cin- (Laplane et al. 1989) disconnecting their cortical
gulate cortex is also removed) to treat psychiat- targets. Yet, when pallidal lesions result from car-
ric and pain disorders. The cingulum contains bon monoxide poisoning, microscopic cortical
the efferents and afferents of the cingulate to the lesions may contribute to the functional imaging
Akinetic Mutism 95

abnormalities. Ventral extension of a pallidal Cross-References

lesion appears to disconnect the anterior cingulate
circuit, in nonhuman primates and humans (Mega ▶ Abulia A
and Cohenour 1997), from limbic drive. Bilateral ▶ Apathy
paramedian or anterior thalamic lesions ▶ Cingulate Gyrus
(Nagaratnam et al. 2004) caudate (Grunsfeld and ▶ Motivation
Login 2006) or putamen (Ure et al. 1998) lesions
will also disrupt the anterior cingulate frontal-
subcortical circuit.
References and Readings

Baer, L., Rauch, S. L., Ballantine, H. T., Martuza, R.,

Evaluation Cosgrove, R., Cassem, E., et al. (1995). Cingulotomy
for intractable obsessive-compulsive disorder: Pro-
spective long-term follow-up of 18 patients. Archives
Evaluation of the patient suspected of suffering
of General Psychiatry, 52, 384–392.
from akinetic mutism is to first rule out other Brefel-Courbon, C., Payoux, P., Ory, F., Sommet, A.,
causes of possible unresponsiveness. Slaoui, T., Raboyeau, G., et al. (2007). Clinical and
Documenting the response to first verbal stimuli, imaging evidence of zolpidem effect in hypoxic
encephalopathy. Annals of Neurology, 62(1), 102–105.
and then sensory stimuli, will provide evidence
Damasio, A. R., & Van Hoesen, G. W. (1983). Focal
for or against coma. Patients in coma will not lesions of the limbic frontal lobe. In K. M. Heilman &
respond to internal (e.g., hunger) or external (e. P. Satz (Eds.), Neuropsychology of human emotion (pp.
g., pain) stimuli. All patients who survive the 85–110). New York: Guilford.
Grunsfeld, A. A., & Login, I. S. (2006). Abulia following
myriad of insults producing coma will regain the
penetrating brain injury during endoscopic sinus sur-
sleep-wake cycle and will eventually open their gery with disruption of the anterior cingulate circuit:
eyes spontaneously. They are then described as Case report. BMC Neurology, 6, 4.
being in a persistent vegetative state. The locked- Hay, P., Sachdev, P., Cumming, S., Smith, J. S., Lee, T.,
Kitchener, P., et al. (1993). Treatment of obsessive-
in patient will blink to command and can be taught
compulsive disorder by psychosurgery. Acta
to use blinking as a form of communication. The Psychiatrica Scandinavica, 87, 197–207.
patient with akinetic mutism will respond to stim- Laplane, D., Levasseur, M., Pillon, B., Dubois, B., Baulac,
uli but will not initiate an unprovoked response. M., Mazoyer, B., et al. (1989). Obsessive-compulsive
and other behavioural changes with bilateral basal
When any patient with limited response is
ganglia lesions. Brain: A Journal of Neurology, 112,
encountered, a brain imaging study is required in 699–725.
their evaluation. Mega, M. S., & Cohenour, R. C. (1997). Akinetic mutism:
A disconnection of frontal-subcortical circuits. Neurol-
ogy, Neuropsychology, and Behavioral Neurology, 10,
254–259.
Treatment Mega, M. S., & Cummings, J. L. (1994). Frontal subcorti-
cal circuits and neuropsychiatric disorders. Journal of
Time is the best treatment for unilateral lesions Neuropsychiatry and Clinical Neurosciences, 6,
358–370.
producing akinetic mutism since after the acute
Mori, E., Yamashita, H., Takauchi, S., & Kondo, K. (1996).
phase of the lesion (4–6 weeks) the patients usu- Isolated athymhormia following hypoxic bilateral
ally recover limbic activation from unaffected pallidal lesions. Behavioral Neurology, 9, 17–23.
regions. When subcortical lesions destroy ascend- Nagaratnam, N., Nagaratnam, K., Ng, K., & Diu, P. (2004).
Akinetic mutism following stroke. Journal of Clinical
ing dopaminergic fibers in the medial forebrain
Neuroscience: Official Journal of the Neurosurgical
bundle, patients may respond to dopaminergic Society of Australasia, 11(1), 25–30.
agonist (Psarros et al. 2003), or paradoxically Pribram, K. H., & Fulton, J. F. (1954). An experimental
antagonists of the D2 receptor (Brefel-Courbon critique of the effects of anterior cingulate ablations in
monkey. Brain: A Journal of Neurology, 77, 34–44.
et al. 2007) and GABA activation (Spiegel et al.
Psarros, T., Zouros, A., & Coimbra, C. (2003). Bromocrip-
2008), perhaps due to blocking feedback-loop tine-responsive akinetic mutism following endoscopy
inhibition. for ventricular neurocysticercosis. Case report and
96 Alcohol Abuse

review of the literature. Journal of Neurosurgery, 99 • Craving or a strong desire to use alcohol
(2), 397–401. • Repeatedly unable to carry out major obli-
Spiegel, D. R., Casella, D. P., Callender, D. M., &
Dhadwal, N. (2008). Treatment of akinetic mutism gations at work, school, or home due to
with intramuscular olanzapine: A case series. Journal alcohol use
of Neuropsychiatry and Clinical Neurosciences, 20(1), • Continued use despite persistent or recur-
93–95. ring social or interpersonal problems caused
Tow, P. M., & Whitty, C. W. M. (1953). Personality
changes after operations of the cingulate gyrus in or made worse by alcohol use
man. Journal of Neurology, Neurosurgery, and Psychi- • Stopping or reducing important social,
atry, 16, 186–193. occupational, or recreational activities due
Ure, J., Faccio, E., Videla, H., Caccuri, R., Giudice, F., to alcohol use
Ollari, J., et al. (1998). Akinetic mutism: A report of
three cases. Acta Neurologica Scandinavica, 98(6), • Recurrent use of alcohol in physically haz-
439–444. ardous situations
• Consistent use of alcohol despite acknowl-
edgment of persistent or recurrent physical
or psychological difficulties from using
alcohol
Alcohol Abuse • Tolerance as defined by either a need for
markedly increased amounts to achieve
Nathan Ewigman intoxication or desired effect or markedly
Mental Health Service Line, San Francisco VA diminished effect with continued use of the
Health Care System, San Francisco, CA, USA same amount
• Withdrawal manifesting as either character-
istic syndrome or alcohol is used to avoid
Synonyms withdrawal

Alcoholism; Binge drinking; Excessive alcohol Although alcohol abuse is diagnosed primarily by
use observed or reported impairment and distress
related to alcohol use, the Dietary Guidelines for
Americans recommends no more than one drink
Short Description or Definition per day for women and two drinks per day for men
(USDA 2005).
Alcohol abuse refers to a “maladaptive pattern of
alcohol [use] leading to clinically significant
impairment or distress.” The DSM-5 criteria for Categorization
substance use disorders as applied to alcohol
abuse are presented below. In the DSM-5, alcohol abuse and dependence are
combined into alcohol use disorder (AUD) with a
severity specifier from mild to severe (DSM-5
DSM-5 Criteria for Alcohol Use Disorder 2013). Individuals with AUD may continue to
drink despite awareness of the potential negative
1. A minimum of 2–3 criteria is required for a physical, social, and legal consequences.
mild substance use disorder diagnosis, while
4–5 is moderate and 6–7 is severe (APA 2013):
• Taking alcohol in larger amounts and for Epidemiology
longer than intended
• Wanting to cut down or quit but not being Alcohol abuse is associated with diseases of the
able to do it liver, hypertension, neurological damage, and car-
• Spending a lot of time obtaining alcohol diac diseases such as heart failure. In 2000,
Alcohol Abuse 97

alcohol abuse was responsible for 85,000 deaths In Vaillant (1995) delinquent youth cohort, by
in the USA. National data suggest that the preva- age 70, 54% had already died, 32% were absti-
lence of DSM-IV-TR alcohol abuse (not including nent, 12% were still abusing alcohol, and 1% were A
alcohol dependence) was 4.65% in 2001–2002 controlled drinkers (i.e., drinking but not
(Grant et al. 2004). More recent data on 12- abusing).
month and lifetime prevalence on AUD (which In terms of prognostic factors, Vaillant (1995)
combines abuse and dependence diagnoses) was suggests that those who achieve “long-term sobri-
13.9% and 29.1%, respectively. Being male, ety usually [are characterized by] (1) a less harm-
white, Native American, younger, low income, ful, substitute dependency; (2) new relationships;
and having a disability has been associated with (3) sources of inspiration and hope; and (4)
AUD prevalence. Approximately one out of five experiencing negative consequences of drinking.”
individuals with AUD has ever been treated From a neurobiological perspective, a pattern of
(Grant et al. 2015). It appears that alcohol abuse long-term structural damage with region-specific
is generally more severe with earlier onset in age recovery is observable in alcoholics who have
of alcohol use (Grant et al. 2001). Results from a achieved long-term abstinence (O’Neill et al.
national survey suggest that close to one fifth of 2001). Neuropsychologically, early gains from
adolescents and adults engaged in binge drinking abstinence include improved short-term memory
one or more times within the last 30 days (US and visuospatial, attentional, and balance abilities
DHHS 2002). (Sullivan et al. 2000).

Natural History, Prognostic Factors, and Neuropsychology and Psychology of

Outcomes Alcohol Abuse

In The Natural History of Alcoholism Revisited, In a review of the literature of neuropsychological

George Vaillant (1995) described alcohol depen- deficits in chronic alcohol abusers, Chelune and
dence as a condition of gradual onset over Parker (1981) found patterns of neurological dam-
5–15 years of continuous alcohol abuse. He age such as cerebral atrophy, ventricular enlarge-
found that the average age of onset was 29 years ment, and decreased cerebral blood flow.
among a cohort of delinquent youth and 41 among Approximately 10% of chronic alcohol abusers
a higher-educated group. In the cohorts that have neurocognitive deficits commensurate with
Vaillant (1995) studied, the prevalence of alcohol- diagnoses of alcohol-related amnesia or dementia.
ism increased until age 40 and then declined at a A large portion of those without diagnosable
rate of 2–3% per year thereafter. neurocognitive deficits still evince disturbed neu-
Potential risk factors for alcohol abuse in ado- ropsychological performance (Rourke and Grant
lescence and early adulthood include being in 2009). Alcoholics generally function in the aver-
areas of high availability and accessibility, early age to above average range on IQ tests with con-
alcohol use (DeWit et al. 2014), sensation seeking sistently lower performance IQ (PIQ) scores
and low harm-avoidance in youth, family history relative to verbal IQ (VIQ). Their PIQ scores are
of alcohol abuse, liberal family attitude toward similar to those of persons with brain damage,
alcohol use, lack of family closeness, and early whereas VIQ scores are comparable with those
behavioral problems (Hawkins et al. 1992). of normal controls (Chelune and Parker 1981;
Another risk factor appears to be comorbid mental Rourke and Grant 2009). However, this discrep-
disorders. Epidemiological data suggest that 37% ancy is not diagnostic of alcoholism. Within the
of people who have an alcohol disorder also have Wechsler subtests, Block Design appears to be the
another mental disorder (Regier et al. 1990), most frequently impaired relative to normal con-
emphasizing the importance of mental and behav- trols in all studies reviewed. Block Design impair-
ior health screening. ment has been cited as an effective discriminator
98 Alcohol Abuse

between alcoholics and nonalcoholics. Object dendritic arbor (Rourke and Grant 2009). Grant
Assembly and Digit Symbol were also impaired and Adams (2009) note that molecular mechanisms
relative to normal controls in more than 3/4 of the of the influence of chronic alcohol abuse on neuro-
studies. Other tests that have revealed impairment psychological functioning are largely unknown.
in alcoholics include the Category Test, Wiscon-
sin Card Sorting Test, Raven’s Progressive Matri-
ces, Shipley-Hartford Abstract Age, and other Evaluation
tests of abstract thinking. Alcoholics also gener-
ally perform poorly on Part B of the Trail Making A common screening tool for alcohol abuse is the
Test relative to matched control groups (Chelune CAGE questionnaire (Ewing 1984; see An even
and Parker 1981). briefer CAGE Questionnaire, Table B).The
Overall, the most consistently impaired neuro- CAGE is highly effective at identifying problem
psychological domains include verbal and non- drinkers among adults (Bernadt 1982). Two “yes”
verbal learning and perceptual motor skills. responses on the CAGE indicate that the respon-
More broadly, most reviews conclude that dent should be investigated further. The question-
abstraction-executive abilities are impaired naire asks the following questions:
among alcohol abusers (Rourke and Grant
2009). Despite the consistency of these neuropsy- • Have you ever felt you needed to Cut down on
chological findings, many of the samples from your drinking?
these studies are recently detoxified adults. Grant • Have people Annoyed you by criticizing your
and Adams (2009) point out that neuropsycholog- drinking?
ical recovery typically occurs following the first • Have you ever felt Guilty about drinking?
year – and perhaps more – of detoxification. • Have you ever felt you needed a drink first
Although the exact mechanisms of these neu- thing in the morning (Eye-opener) to steady
ropsychological deficits are not known, some of your nerves or to get rid of a hangover?
the major hypotheses attempting to explain these
deficits have been (Chelune and Parker 1981): Other brief assessments for alcohol abuse
include the POSIT and CRAFFT for adolescents
(Knight et al. 2003), the Michigan Alcoholism
1. Chronic alcohol abuse results in premature
Screen Test (MAST) for adults (Magruder-Habib
aging of the brain.
et al. 1993), and the AUDIT-C for both adults and
2. Chronic alcohol abuse leads to global general-
adolescents (Bush et al. 1998). According to
ized CNS dysfunction.
Fiellin et al. (2000), the CAGE and the AUDIT
3. Chronic alcohol abuse differentially disrupts
are the superior screening instruments in primary
the right hemisphere of the brain.
care settings compared with other alcohol abuse
4. Chronic alcohol abuse exerts its detrimental
screeners and other clinical methods. The CAGE
effect on the anterior-basal regions of the brain.
is superior at detecting diagnosable abuse and
5. Chronic alcohol abuse produces a generalized
dependence, and the AUDIT is superior at
CNS impairment that is particularly disruptive
detecting at-risk and harmful drinking (Fiellin et
of the frontoparietal association areas of the
al. 2000). AUDIT-C has been shown to be effec-
brain.
tive in screening for alcohol use disorder in DSM-
5 (Dawson et al. 2012).
More recent neural hypotheses of the mecha-
nisms of neuropsychological deficits include
reduced regional blood flow to the frontal lobes, Treatment
reduction in metabolites (e.g., NAA) that indicate
lack of neuronal integrity, and frontal-striatal and Treatment ranges from support groups to rehabil-
cerebellar dysfunction manifesting as loss of itation centers. Treatments of alcohol abuse
Alcohol Abuse 99

appear to be largely psychosocial. In a systematic health approach to the management of substance

review, brief psychosocial interventions among abuse. Substance Abuse, 28(3), 7–30.
Bernadt, M. W. (1982). Comparison of questionnaire and
primary care patients were found to be effective laboratory tests in the detection of excessive drinking A
at reducing alcohol consumption (Kaner et al. and alcoholism. Lancet, 6, 325–328.
2007). Although well-known support groups Bommersbach, T. J., et al. (2015). Geriatric alcohol use
such as Alcoholics Anonymous (AA) have been disorder: A review for primary care physicians. Mayo
Clinic Proceedings, 90(5), 659–666. Elsevier.
helpful to many people and likely constitute the Bush, K., et al. (1998). The AUDIT alcohol consumption
most accessible form of treatment, evidence has questions (AUDIT-C): an effective brief screening test
not supported AA’s effectiveness at reducing alco- for problem drinking. Archives of internal medicine,
hol problems (Ferri et al. 2006). Medical treat- 158(16), 1789–1795.
Chelune, G. J., & Parker, J. B. (1981). Neuropsychological
ments of alcohol abuse focus on reducing deficits associated with chronic alcohol abuse. Clinical
craving. Naltrexone (Chick et al. 2000) and Psychology Review, 1, 181–195.
acamprosate (Garbutt et al. 1999) have been Chick, J., Anton, R., Checinski, K., Croop, R., Drummond,
found to be effective at reducing craving. How- D. C., Farmer, R., et al. (2000). A multicentre, random-
ized, double-blind, placebo-controlled trial of naltrex-
ever, most medications are aimed at dependence, one in the treatment of alcohol dependence or abuse.
not abuse symptoms. A common framework Alcohol, 35, 587–593.
called SBIRT (screening, brief intervention, and Dawson, D. A., et al. (2012). Comparative performance of
referral to treatment) has shown promising out- the AUDIT-C in screening for DSM-IV and DSM-5
alcohol use disorders. Drug and Alcohol Dependence,
comes toward a population-based management 126(3), 384–388.
approach of AUD (Babor et al. 2007). Secondary DeWit, D. J., et al. (2014). Age at first alcohol use: a risk
effects of alcohol abuse, such as Wernicke- factor for the development of alcohol disorders. Amer-
Korsakoff syndrome, can be treated through mon- ican Journal of Psychiatry, 157(5), 745–750.
Ewing, J. A. (1984). Detecting alcoholism: The CAGE
itoring and infusion to correct for vitamin defi- questionnaire. JAMA, 252, 1905–1907.
ciency (Isenberg-Grzeda et al. 2012); however, Ferri, M. M. F., Amato, L., & Davoli, M. (2006). Alco-
longer-term neurocognitive consequences can holics anonymous and other 12-step programmes for
only be managed and can lead to placement in alcohol dependence. Cochrane Database of Systematic
Reviews, 19(3), CD005032. https://doi.org/10.1002/
long-term care facilities (Bommersbach et al. 14651858.CD005032.pub2.
2015). Fiellin, D. A., Reid, M. C., & O’Connor, P. G. (2000).
Screening for alcohol problems in primary care: A
systematic review. Archives of Internal Medicine, 160
(13), 1977–1989.
Cross-References Garbutt, J. C., West, S. L., Carey, T. S., Lohr, K. N., &
Crews, F. T. (1999). Pharmacological treatment of alco-
hol dependence: A review of the evidence. JAMA, 281,
▶ Alcoholic Brain Syndrome 1318–1325.
▶ Alcohol Dependence Grant, I., & Adams, K. M. (Eds.). (2009). Neuropsycho-
▶ Blood Alcohol Level logical assessment of neuropsychiatric disorders (3rd
▶ Fetal Alcohol Spectrum Disorder ed.pp. 127–158). New York: Oxford University Press.
Grant, B. F., Stinson, F. S., & Harford, T. C. (2001). Age at
▶ Michigan Alcoholism Screen Test onset of alcohol use and DSM-IV alcohol abuse and
▶ Substance Abuse dependence: A 12-year follow-up. Journal of Sub-
▶ Wernicke-Korsakoff Syndrome stance Abuse, 13, 493–504.
Grant, B. F., Dawson, D. A., Stinson, F. S., Chou, S. P.,
Dufour, M. C., & Pickering, R. P. (2004). The 12-
month prevalence and trends in DSM-IV alcohol
References and Readings abuse and dependence: United States, 1991–1992 and
2001–2002. Drug and Alcohol Dependence, 74,
American Psychiatric Association. (2013). Diagnostic and 223–234.
statistical manual of mental disorders: DSM-5. Wash- Grant, B. F., et al. (2015). Epidemiology of DSM-5 alcohol
ington, DC: American Psychiatric Association. use disorder: Results from the national epidemiologic
Babor, T. F., et al. (2007). Screening, brief intervention, survey on alcohol and related conditions III. JAMA
and referral to treatment (SBIRT) toward a public Psychiatry, 72(8), 757–766.
100 Alcohol Dependence

Hasin, D. S., Van Rossem, R., McCloud, S., & Endicott, J. (2005). Dietary guidelines for Americans: Chap. 9 –
(1997). Alcohol dependence and abuse diagnoses: Alcoholic beverages (pp. 43–46). Washington, DC: US
Validity in a community sample of heavy drinkers. Government Printing Office.
Alcoholism, Clinical and Experimental Research, 21, Vaillant, G. E. (1995). The natural history of alcoholism
213–219. revisited. Cambridge, MA: Harvard University Press.
Hawkins, J. D., Catalano, R. F., & Miller, J. Y. (1992). Risk
and protective factors for alcohol and other drug prob-
lems in adolescence and early adulthood: Implications
for substance abuse prevention. Psychological Bulletin,
112, 64–105.
Alcohol Dependence
Isenberg-Grzeda, E., Kutner, H. E., & Nicolson, S. E.
(2012). Wernicke-Korsakoff-syndrome: Under-recog- Glenn S. Ashkanazi
nized and under-treated. Psychosomatics, 53(6), Department of Clinical and Health Psychology,
507–516.
Clinical and Health Psychology Clinic, College of
Kaner, Eileen F. S., et al. (2007). Effectiveness of brief
alcohol interventions in primary care populations. The Public Health and Health Professions, University
Cochrane Library. of Florida, Gainesville, FL, USA
Knight, J. R., Sherritt, L., Harris, S. K., Gates, E. C., &
Chang, G. (2003). Validity of brief alcohol screening
tests among adolescents: A comparison of the AUDIT,
POSIT, CAGE, and CRAFFT. Alcoholism, Clinical Synonyms
and Experimental Research, 27, 67–73.
Magruder-Habib, K., Stevens, H. A., & Alling, W. C. Alcoholism
(1993). Relative performance of the MAST, VAST,
and CAGE versus DSM-III-R criteria for alcohol
dependence. Journal of Clinical Epidemiology, 46, Definition
435–441.
O’Neill, J., Cardenas, V. A., & Meyerhoff, D. J. (2001).
Effects of abstinence on the brain: Quantitative mag- This diagnosis no longer exists and has been
netic resonance imaging and magnetic resonance spec- replaced by “Alcohol Use Disorder” in DSM-5
troscopic imaging in chronic alcohol abuse.
Alcoholism: Clinical and Experimental Research, 25 As described in DSM-IV, alcohol dependence is a
(11), 1673–1682. set of symptoms encompassing dysfunction in cog-
Regier, D. A., Farmer, M. E., Rae, D. S., Locke, B. Z.,
Keith, S. J., Judd, L. L., et al. (1990). Comorbidity of nitive, behavioral, and physiological domains
mental disorders with alcohol and other drug abuse. caused by continued alcohol use. A pattern of
Results from the epidemiologic catchment area (ECA) repeated alcohol ingestion exists, resulting in
study. JAMA, 264, 2511–2518. increasing amounts consumed in order to obtain
Rourke, S. B., & Grant, I. (2009). The neurobehavioral
correlates of alcoholism. In I. Grant & K. M. Adams the desired effect (i.e., tolerance) and characteristic
(Eds.), Neuropsychological assessment of neuropsychi- symptoms if use is suddenly suspended (i.e., with-
atric and neuromedical disorders (3rd ed., pp. drawal). There is a perceived loss of control over
398–454). New York: Oxford University Press. drinking, exhibited by repeated failed attempts to
Sullivan, E. V., et al. (2000). Longitudinal changes in
cognition, gait, and balance in abstinent and relapsed decrease or quit drinking. Individuals may spend
alcoholic men: Relationships to changes in brain struc- increasing amounts of time in drinking-related
ture. Neuropsychology, 14(2), 178. behaviors without being able to stop, despite being
U.S. Department of Health and Human Services. Sub- aware that drinking is causing, or exacerbating,
stance Abuse and Mental Health Services Administra-
tion(US DHHS). (2002). Results from the 2001 psychological or medical problems. Cognitive con-
national household survey on drug abuse: Volume I. sequences can include memory loss, difficulty
Summary of national findings (Office of Applied Stud- performing familiar tasks, poor or impaired judg-
ies, NHSDA Series H-17 ed.) (BKD461, SMA ment, and problems with language.
02–3758). Washington, DC: U.S. Government Printing
Office. Retrieved 14 Mar 2009, from the World Wide
Web: http://www.oas.samhsa.gov/nhsda/2k1nhsda/
vol1/Chapter3.htm. Cross-References
United States Department of Agriculture and United States
Department of Health and Human Services (USDA).
▶ Alcohol Abuse
Alcohol Use Disorders Indentification Test (AUDIT), The 101

▶ Alcoholic Brain Syndrome should be advised to consider cutting down

▶ Substance Abuse on their alcohol use and/or receive further in-
▶ Substance Use Disorders depth assessment (e.g., a structured diagnostic A
▶ Wernicke-Korsakoff Syndrome interview).
Researchers and clinicians sometimes use
a shortened measure of the AUDIT that assesses
References and Readings only alcohol consumption, the AUDIT-C (AUDIT
Alcohol Consumption Questions; Bush et al.
American Psychiatric Association. (1994). Diagnostic and 1998). The AUDIT-C consists of the first three
statistical manual of mental disorders (4th ed.).
items of the full measure, which assess frequency
Washington, DC: American Psychiatric Association.
of alcohol use, typical number of drinks con-
sumed on a drinking day, and number of days
engaging in heavy drinking (6þ drinks). The
brevity of the AUDIT-C makes it appealing as an
Alcohol Use Disorders
alcohol use screener in very busy clinical settings.
Indentification Test (AUDIT),
For example, the Veterans Administration uses the
The
AUDIT-C for annual routine alcohol screening
(Bradley et al. 2006), and those who exceed the
Matthew P. Martens
screening threshold (4þ for men, 3þ for women)
University of Missouri, Columbia, MO, USA
are required to receive a brief alcohol counseling
session from their provider.
Synonyms

AUDIT; AUDIT Alcohol Consumption Questions Historical Background

(AUDIT-C)
The Alcohol Use Disorders Identification Test
(AUDIT) is one of the most commonly used
Description measures to screen for at-risk alcohol use and is
available for public use. It was originally devel-
The Alcohol Use Disorders Identification Test oped as part of a World Health Organization
(AUDIT: Saunders et al. 1993) consists of ten initiative (Saunders et al. 1993), and has been
questions that assess quantity/frequency of alco- used extensively by researchers and clinicians
hol consumption (e.g., number of drinks typically throughout the world. The original article detail-
consumed when drinking alcohol), symptoms of a ing its development has been cited in the Web of
potential alcohol use disorder (e.g., frequency of Science Core Collection database over 3,000
not engaging in expected activities due to alcohol times and in Google Scholar over 5,000 times.
use), and specific problems associated with alco- The primary rationale for developing the AUDIT
hol use (e.g., injuring someone else). It is not a was the need for a screening measure that iden-
formal diagnostic measure but is used to identify tified problematic alcohol consumption at the
individuals who may be engaging in harmful alco- lower end of a severity continuum. Measures
hol use. Scores on each item range from 0 to 4, that existed at the time, such as the Michigan
with higher scores indicating more problematic Alcoholism Screening Test (MAST) or the
alcohol use. Scores of 8þ on the measure have CAGE, were reasonably effective at identifying
generally been used to identify individuals engag- individuals with the most severe alcohol-related
ing in potentially hazardous or harmful alcohol problems. However, they were considerably less
use. The developers of the measure recommend effective at identifying those experiencing
that those who exceed the screening threshold milder alcohol-related problems that might be
102 Alcohol Use Disorders Indentification Test (AUDIT), The

in an emerging phase. Without an effective be experiencing neuropsychological problems.

screening measure for less-severe alcohol- The AUDIT or AUDIT-C has been used as a
related problems, it would be impossible to pro- screening measure when neuropsychological
vide early intervention services that could inhibit researchers were interested in recruiting partici-
the development of a formal alcohol use disorder. pants experiencing alcohol-related problems
Researchers subsequently examined an even (e.g., Houben et al. 2011), or when researchers
shorter version of the AUDIT, the AUDIT-C, were interested in association between harmful
due in part to logistical concerns about the will- alcohol consumption and cognitive abilities
ingness of physicians and others in primary care (e.g., following a brain injury, see Ponsford
settings to administer a ten-item screening instru- et al. 2007, 2013). The full ten-item version
ment (Bush et al. 1998). can be used in research settings and in clinical
settings where patients have more time to com-
plete assessment measures, and the three-item
Psychometric Data AUDIT-C can be completed in less than a minute
and provide an accurate picture of an individ-
A vast array of research studies have examined ual’s drinking risk. Cutoff scores on the AUDIT
reliability and validity of scores on both the full can be easily adjusted to meet the needs of a
AUDIT and the AUDIT-C. Scores on the AUDIT specific setting (e.g., using a lower cutoff score
are consistently associated in the expected direc- to increase sensitivity and/or identify individ-
tion with other alcohol-related constructs, such as uals experiencing even mild alcohol-related
alcohol cravings and drinking motives. Consider- problems).
ing that the measure is designed to classify indi-
viduals into potential at-risk drinking categories,
it is particularly important to assess the accuracy See Also
of cutoff scores on the measures. In general,
research has shown that both the AUDIT and ▶ Alcohol Abuse
AUDIT-C have relatively high sensitivity (i.e., ▶ Alcohol Dependence
accurately identifying those with an alcohol use ▶ Michigan Alcoholism Screen Test
disorder and/or who are engaging in high-risk
drinking) and specificity (i.e., accurately identify-
ing those without an alcohol use disorder and/or References and Readings
who engage in low-risk drinking). For example, in
a national study of over 40,000 adults, a cutoff Bradley, K. A., Williams, E. C., Achtmeyer, C. E.,
Volpp, B., Collins, B. J., & Kivlahan, D. R. (2006).
score of 4þ on the AUDIT-C yielded sensitivity
Implementation of evidence-based alcohol screening in
values of 91.2 for alcohol dependence and 92.6 the Veterans Health Administration. American Journal
for at-risk drinking, with corresponding specific- of Managed Care, 12, 597–606.
ity values of 80.2 and 92.0 (Dawson et al. 2005). Bush, K., Kivlahan, D. R., McDonell, M. B., Fihn, S. D., &
Bradley, K. A. (1998). The AUDIT alcohol consump-
Similar findings have been reported for the full
tion questions (AUDIT-C): An effective brief screening
AUDIT with specific at-risk subgroups, such as test for problem drinking. Archives of Internal Medi-
young adults. cine, 158, 1789–1795.
Dawson, D. A., Grant, B. F., Stinson, F. S., & Zhou, Y.
(2005). Effectiveness of the derived Alcohol Use Dis-
orders Identification Test (AUDIT-C) in screening for
Clinical Uses alcohol use disorders and risk drinking in the US gen-
eral population. Alcoholism: Clinical and Experimental
The AUDIT and its shortened version are excel- Research, 29, 844–854.
Houben, K., Wiers, R. W., & Jansen, A. (2011). Getting a
lent measures to screen for at-risk alcohol con-
grip on drinking behavior: Training working memory
sumption and related problems in a variety of to reduce alcohol use. Psychological Science, 22,
settings, including those where individuals may 968–875.
Alcoholic Brain Syndrome 103

Ponsford, J., Whelan-Goodinson, R., & Bahar-Fuchs, A. cessation of chronic, extreme alcohol
(2007). Alcohol and drug use following traumatic brain intake. Symptoms include disturbed con-
injury: A prospective study. Brain Injury, 21,
1385–1392. sciousness (e.g., disruption in attention/ A
Ponsford, J., Tweedly, L., & Taffe, J. (2013). The relation- concentration) and disruption in memory,
ship between alcohol and cognitive functioning follow- orientation, and language beyond what
ing traumatic brain injury. Journal of Clinical and would be expected from typical alcohol
Experimental Neuropsychology, 35, 103–112.
Saunders, J. B., Aasland, O. G., Babor, T. F., withdrawal.
De La Fuente, J. R., & Grant, M. (1993). Development 2. Alcohol-induced persisting dementia (ICD-9):
of the Alcohol Use Disorders Identification Test A chronic condition that includes multiple cog-
(AUDIT): WHO collaborative project on early detec- nitive deficits as a result of prolonged alcohol
tion of persons with harmful alcohol consumption-II.
Addiction, 88, 791–804. abuse. Cognitive areas generally impaired
include memory, speech, motor/sensory func-
tions, and executive functions. Global impair-
ment in intellectual functioning evolves
Alcoholic Brain Syndrome gradually over time.
3. Alcohol-induced persisting amnestic disorder
Glenn S. Ashkanazi (ICD-10): A persistent disturbance in memory
Department of Clinical and Health Psychology, functioning caused by chronic alcohol abuse.
Clinical and Health Psychology Clinic, College of Memory impairment is severe enough to cause
Public Health and Health Professions, University significant disturbance in occupational or
of Florida, Gainesville, FL, USA social functioning.
4. Wernicke’s encephalopathy (WE) (ICD-10):
A syndrome resulting from chronic alcohol-
Synonyms ism leading to nutritional deficiency (i.e.,
vitamin B1 [thiamine]) and characterized by
Alcoholic dementia; Alcoholic hallucinosis; acute confusion, ataxia, sluggish pupillary
Delirium tremens; Korsakoff’s syndrome; reflexes, nystagmus, and memory deficits.
Wernicke-Korsakoff syndrome The syndrome can result in coma or death.
Lesions are centered in the midbrain, cerebel-
lum, and diencephalon.
Short Description or Definition
5. Korsakoff’s syndrome (ICD-10): This condi-
tion often follows episodes of WE. Thiamine
“Alcoholic brain syndrome” is a collection of
deficiency, as a result of chronic, severe alco-
several syndromes associated with the acute or
hol abuse, leads to a dense anterograde and
chronic use of alcohol, resulting in significant
retrograde amnesia. Patients with Korsakoff’s
impairment on normal brain functioning (APA
syndrome can store information for only a few
Dictionary of Psychology 2007), also referred to
seconds before they forget it. The resulting
as alcohol-related dementia (ARD).
amnesia is thought to be due to damage in the
mammillary bodies and anterior or
Categorization dorsomedial nuclei (or both) of the thalamus.
Another common feature is confabulation, in
As mentioned in the definition, alcoholic brain syn- which the patient recounts detailed and con-
drome encompasses several syndromes (newly vincing memories for events that have never
named “major neurocognitive disorder (NCD)-sub- happened.
stance/medication induced” in DSM-5): 6. Alcohol-induced psychotic disorder (ICD-10):
A condition involving the presence of delu-
1. Alcohol withdrawal delirium (ICD-9): sions and/or hallucinations due to the physio-
A reversible condition that develops after logical effects of alcohol.
104 Alcoholic Brain Syndrome

Epidemiology who survive, approximately 85% develop

Korsakoff’s syndrome. However, not every per-
Up to two million alcoholics have developed per- son who develops Korsakoff’s syndrome has a
manent and debilitating conditions that require previous episode of Wernicke’s. Some will
lifetime custodial care. A number of factors influ- develop Korsakoff’s gradually with either no
ence how and to what extent alcohol affects the known history or brief episodes of Wernicke’s.
brain. These include the age at which the person Some patients are initially comatose or semicon-
started drinking, duration of drinking, amount of scious and only when the acute disorder has
alcohol consumed, drinking style/pattern, resolved is the underlying Korsakoff’s syndrome
patient’s age, education, genetic background, manifests. These patients are still susceptible to
family history of alcoholism, neuropsychiatric developing Wernicke’s, especially if drinking
risk factors (e.g., prenatal alcohol exposure), and were to continue.
general health status. Studies comparing men and Loss of some cognitive functions including
women’s sensitivity to alcohol-induced brain memory in Korsakoff’s syndrome may be perma-
damage have not been conclusive. Of all cases nent. Once the patient has developed Korsakoff’s,
of dementia, ARD accounts between 4% and the treatment strategies are not clear. However, it
20%. is important for patients to remain abstinent from
Poor nutrition has been a major contributor to alcohol. Depending on the degree of memory and
the development of alcohol-induced brain dam- executive function impairment, and availability of
age. Up to 80% of alcoholics have a deficiency in family support, patients with Korsakoff’s may
thiamine (i.e., vitamin B1). This vitamin is an require long-term custodial care.
essential nutrient required by all tissues including
the brain. Some of these people will progress to
WE. Approximately 80–90% of alcoholics with Neuropsychology and Psychology of
Wernicke’s develop Korsakoff’s psychosis, which Alcoholic Brain Syndrome
is more prevalent in men aged 45–65. Women
who develop this condition tend to do so at a The classic symptom in Korsakoff’s syndrome is
younger age (i.e., 35–55). the inability to form new memories (i.e., antero-
grade amnesia). However, patients also demon-
strate significant deficits in their ability to recall
Natural History, Prognostic Factors, and incidents or events from their own past as well
Outcomes (i.e., episodic memory). Memory for facts, con-
cepts, and language (i.e., semantic memory) is
Wernicke ‘s encephalopathy is a medical emer- variable, while perceptual-motor memory is
gency and requires immediate treatment, as it can thought to be preserved.
lead to death in approximately 20% of untreated The inability to recall previously learned infor-
cases. Symptoms can develop within hours and mation (i.e., retrograde amnesia) can often extend
can be easily missed as many mimic intoxication. back 20–30 years in a person’s life with
If treatment is given in time, usually through the Korsakoff’s patients. Generally, a temporal gradi-
administration of thiamine, progression of symp- ent exists such that memories from the more dis-
toms can be slowed or stopped. Ocular abnormal- tant past are recalled better than the more recent
ities usually recover within a few days to a few ones. The basis of this extensive retrograde amne-
weeks, but ataxia takes 1–2 months longer to sia is still a matter of great controversy.
resolve. The acute confusion/delirium usually These patients are typically younger than most
improves within 1–2 days after the treatment but patients presenting to dementia services, and
may take 1–3 months to completely clear. because they often present as initially confused,
If treatment is not provided, then irreversible with concomitant frontal lobe pathology, they are
brain damage, or even death, is possible. Of those more likely to demonstrate aggressive, agitated
Alcoholic Brain Syndrome 105

behaviors and anxiety. Those with irreversible therefore, vitamin B1 supplementation is neces-
brain damage are unlikely to be able to live sary. Initially, the vitamins can be given intrave-
alone but also typically lack available social ser- nously or intramuscularly followed by oral A
vices. These patients often have a difficult time administration. Wernicke ‘s encephalopathy
maintaining social and familial relationships and responds well to high-dose vitamins, and such
live isolated lives. treatment can prevent the occurrence of severe,
The classic triad of symptoms for Wernicke’s chronic Korsakoff’s syndrome. Secondarily,
encephalopathy is: nutritional counseling to promote a vitamin-rich
and balanced diet is also part of this initial treat-
• Encephalopathy – demonstrative of damage to ment protocol, especially for longer-term recov-
the frontal lobes, mammillary bodies, thala- ery and prevention.
mus, and cerebellum
• Ataxic gait
• Some variant of oculomotor dysfunction
Cross-References

▶ Alcoholism
Evaluation ▶ Amnesia
▶ Anterograde Amnesia
For patients who meet the ICD-10 criteria for
▶ Dementia
Wernicke ‘s encephalopathy or Korsakoff’s syn-
▶ Encephalopathy
drome, neuropsychological assessment is useful
▶ Episodic Memory
for documenting functions that are impaired, the
▶ Korsakoff’s Syndrome
severity of impairment, and the prognostic factors
▶ Organic Brain Syndrome
involved in determining the patient’s ability to
▶ Retrograde Amnesia
manage daily life either independently or with
▶ Semantic Memory
assistance. However, it is preferable for the neu-
▶ Substance Abuse
ropsychological assessment to occur when the
patient has been abstinent from alcohol for a
long enough period of time to insure that the
References and Readings
acute symptoms of alcohol withdrawal have sub-
sided. Cognitive dysfunction includes aphasia, Horton, L., Duffy, T., & Martin, C. (2014). Comprehensive
apraxia, agnosia, memory impairment, and assessment of alcohol-related brain damage (ARBD):
decreased executive functions. Neuroimaging Gap or chasm in the evidence? Journal of Psychiatric
and Mental Health Nursing, 22(1), 3–14.
evidence of cerebellar atrophy/shrinkage also sup-
Kopelman, M., Thomson, A., Guerrini, I., & Marshall,
ports the diagnosis. E. (2009). The Korsakoff syndrome: Clinical aspects,
psychology and treatment. Alcohol & Alcoholism,
44(2), 148–154.
Martin, P., Singleton, C., & Hiller-Sturmhofel, S. (2003).
Treatment The role of thiamine deficiency in alcoholic brain dis-
ease. Alcohol Research & Health, 27(2), 134–142.
The primary treatment option for patients Moriyama, Y., Mimura, M., Kato, M., & Kashima,
H. (2006). Primary alcoholic dementia and alcohol-
experiencing alcoholic brain syndrome is to stop
related dementia. Psychogeriatrics, 6(3), 114–118.
drinking and remain abstinent. Without additional Oscar-Berman, M., & Marinkovic, K. (2003). Alcoholism
alcohol exposure, the recovery from the delirium and the brain: An overview. Alcohol Research &
caused by alcohol is usually good. This is obvi- Health, 27(2), 125–133.
Parsons, O. (1996). Alcohol abuse and alcoholism. In
ously the first treatment to be utilized. As men-
R. Adams, O. Parsons, J. Culbertson, & S. Nixon
tioned above, thiamine deficiency is an important (Eds.), Neuropsychology for clinical practice: Etiology,
contributor to alcohol-related brain damage; assessment, and treatment of common neurological
106 Alcoholism

disorders. Washington, DC: American Psychological must include the concepts of addiction and phys-
Association. iological withdrawal mechanisms, while for
Ridley, N., & Draper, B. (2015). Alcohol-related dementia
and brain damage. In J. Svanberg, A. Withall, others, these are consequences of drinking.
B. Draper, & S. Bowden (Eds.), Alcohol and the adult It is common for laypeople to equate any kind of
brain. New York: Psychology Press. excessive drinking with alcoholism. Those in the
Ridley, N., Draper, B., & Withall, A. (2013). Alcohol- mental health fields see that disorders related to
related dementia: An update of the evidence.
Alzheimer’s Research & Therapy, 5, 3. alcohol use lie along a continuum of severity that
Rourke, S., & Grant, I. (2009). The neurobehavioral cor- may include physical dependency/withdrawal (i.e.,
relates of alcoholism. In I. Grant & K. M. Adams alcohol dependence) or may involve impaired
(Eds.), Neuropsychological assessment of neuropsychi- drinking habits that lead to health or social prob-
atric and neuromedical disorders (3rd ed.). New York:
Oxford University Press. lems/consequences but without dependency/with-
Sachdev, P., Blacker, D., Blazer, D., Ganguli, M., Jeste, D., drawal (i.e., alcohol abuse). According to the APA
Paulsen, J., & Petersen, R. (2014). Classifying Dictionary of Psychology, alcoholism is the popular
neurocognitive disorders: The DSM-5 approach. term for “alcohol dependence.” “Alcoholism” is not
Nature, 10, 634–642.
White, A. (2003). What happened? Alcohol, memory an official diagnostic term. The DSM-5 term for
blackouts, and the brain. Alcohol Research & Health, alcohol-related problems is alcohol use disorder.
27(2), 186–196.

Historical Background

Alcoholism The term “alcoholism” was first used in 1849 by a

physician, Magus Haas, to describe the systematic
Glenn S. Ashkanazi adverse effects of alcohol overconsumption. In
Department of Clinical and Health Psychology, the USA, it became a popular term in the 1930s
Clinical and Health Psychology Clinic, College of as a result of the growth of Alcoholics Anony-
Public Health and Health Professions, University mous (AA). Previously, society viewed those who
of Florida, Gainesville, FL, USA drank to excess as immoral, weak of character,
and irresponsible. Society’s response was punish-
ment and removal of over-consumers from sober
Synonyms society to protect the community. With the rise of
AA, and their publication (i.e., the “Big Book”),
Alcohol abuse; Alcohol addiction; Alcohol the view of alcoholism changed from character
dependence; Problem drinking; Substance abuse flaw to medical disease. AA viewed alcoholism
as a physical allergy to alcohol accompanied by an
obsession with drinking. This organization began
Definition to dispel the previously held beliefs that alco-
holics were unemployable, destitute, and isolated
The term “alcoholism” has a variety of definitions. individuals by demonstrating that some highly
For some, it is a disease that makes a person respected people who had been alcohol dependent
dependent on alcohol and causes an obsession had eventually overcome their disorder and went
with alcohol and inability to control how much on to lead productive lives.
they drink even though their drinking causes seri-
ous problems in their relationships, health, work,
and finances. Others do not define it as a “disease” Epidemiology
per se but rather a “condition,” behavioral in
nature, which results in continued consumption The epidemiology of alcoholism can be confusing
of alcohol despite health problems and negative and contradictory, depending on the definition
social consequences. For some, the definition being utilized and the measurement tool. The
Alcoholism 107

generally accepted overall rate of occurrence of African-Americans. The risk for Hispanics is gen-
alcoholism in the USA is 10%. The US National erally the same as Whites.
Longitudinal Alcohol Epidemiologic Study con- Alcoholism is estimated to be the third leading A
cluded that alcoholism is prevalent in 20% of cause of preventable death in the USA (after
adult hospital inpatients and in 17% of smoking and obesity). In the USA, 85,000 deaths
community-based primary care practices. are attributable to alcohol each year at a cost of
A 1985 US National Hospital Survey found that $185 billion. The NIAAA estimates that intoxica-
528,000 patients were discharged from hospitals tion is present in 30–60% of homicides, 22% of
with a primary diagnosis of substance abuse, and suicides, 33–50% of automobile accidents, 67%
for 81% (428,000), alcohol was the abused of drownings, and 70–80% of fire-related deaths.
substance. More than 50% of American adults have a close
According to a 2001 survey conducted by the family member who has or has had alcoholism.
National Institute on Alcohol Abuse and Alco- Approximately one in four children younger than
holism (NIAAA) in the USA, approximately 18 in the USA is exposed to alcohol abuse or
48% of adults (aged 12 or older) are reported alcohol dependence in their family.
being current drinkers of alcohol (approximately Internationally, the World Health Organization
109 million). That number drops to 44% when estimates that there are 140 million people world-
the age is 18 or older. A 2014 survey found that wide that are alcohol dependent and they account
87.6% of people over age 18 reported they drank for 3.5% of the total cases of disease worldwide,
alcohol at some point in their lifetime and 56.9% which is a higher rate than tobacco or illicit drugs.
within the last month. Approximately 20% of They estimated that 5.9% of all global deaths were
persons aged 12 or older participated in binge attributable to alcohol consumption.
drinking at least once in 30 days prior to the
2001 survey. In the 2014 survey, that number
was 24.7%. Current Knowledge
“Heavy drinking” was reported by 5.7% of the
12 or older population (12.9 million). The highest Causes
prevalence for both binge and heavy drinking was There is no identifiable single cause of alcohol-
for those in the 18–25 age groups with the peak ism. Scientists believe that a myriad of factors
rate occurring at age 21. Studies have found those play a role in the development of alcoholism:
who begin drinking at an earlier age are at higher
risk to develop dependency. Those Americans 1. Genetics: Previous twin and adoption studies
who wait till age 21 are four times less likely to have demonstrated that genes play an impor-
become dependent than those who begin drinking tant role in the development of alcoholism.
before the age of 15 (i.e., 40% who start before Researchers found that identical twins (i.e.,
age 15 develop dependency on alcohol at some identical genes) have a higher concordance
point in their lives). The risk for developing rate for drinking behavior than fraternal
dependency declines with age, as the prevalence twins. Other studies have cast some doubt on
rate for alcoholism in those persons greater than these twin studies by suggesting the environ-
65 years old is 3%. ment of identical twins is more alike than fra-
There are other nonage risk factors as well. ternal twins, thus suggesting a weakening of
Those with lower education and lower socioeco- the argument in favor of genes. In the adoption
nomic status are also at higher risk. There are also studies, researchers found that whether reared
gender differences as men are at minimum 2.5 by biologic or adoptive parents, the sons of
times more likely to be defined as “alcoholic” as males with alcohol problems are four times
women; however, the proportion of female alco- more likely to have alcohol problems than
holics is increasing. White, non-Hispanic individ- sons of persons who are not. In either case,
uals are more likely to develop alcoholism than epidemiologic studies indicate that alcoholism
108 Alcoholism

tends to run in families. Alcoholics are six consumption, dependency, and alcohol-related
times more likely than nonalcoholics to have problems.
blood relatives who are alcohol dependent. In 3. Short Alcohol Dependence Data Questionnaire
summary, a person’s genetic makeup can pre- (SADD): More sensitive than the CAGE and
dispose them to alcoholism or not. can distinguish abuse versus dependence.
2. Peer influence: Social networks that include
heavy drinkers and alcohol abusers increase Diagnosis
an individual’s risk for alcoholism. Alcoholism is not a diagnosable term. The current
3. Cultural influence: Cultures that include well- term to describe “problem drinking” is alcohol use
established taboos against drunkenness and disorder found in the Diagnostic Statistical Man-
rules regarding drinking have lower alcohol- ual of the Mental Disorders, Fifth Edition
ism rates than those who do not. (DSM-V). The diagnosis requires:
4. Psychiatric conditions: Certain psychiatric
diagnoses increase the risk of alcoholism. 1. A problematic pattern of alcohol use leading to
These include ADHD, panic disorder, schizo- clinically significant impairment or distress as
phrenia, and antisocial personality disorder. manifested by at least two of the below occur-
ring in the same 12-month period.
Screening (a) Tolerance (as defined by either of the
There are a variety of measures for alcoholism following).
including the following: (i) A need for markedly increased
amounts of alcohol to achieve intoxi-
1. CAGE: The CAGE is named for the four ques- cation or desired effect
tions asked of a patient before any questions (ii) A markedly diminished effect with
regarding quantities drank are asked. continued use of the same amount of
1. Have you ever felt the need to Cut down on alcohol
your drinking? (b) Withdrawal (as manifested by either of the
2. Have people Annoyed you by criticizing following).
your drinking? (i) The characteristic withdrawal syn-
3. Have you ever felt Guilty about drinking? drome for alcohol.
4. Have you ever felt you needed a drink in the (ii) Alcohol (or benzodiazepines) is taken
morning to steady your nerves or get rid of a to relieve or avoid withdrawal
hangover? (Eye-opener) syndrome.
The CAGE has been extensively validated. (c) Alcohol is often taken over longer period
Those who answer “YES” to two or more of time or in larger amounts than intended.
questions are seven times more likely to be (d) Persistent desire to drink or unsuccessful
alcohol dependent. It is not an adequate mea- efforts to cut down or control use.
sure by itself but can alert a health-care pro- (e) Great deal of time spent in acquiring/using
vider to probe further. Another weakness is that alcohol or recovering from its effects.
it tends to be less reliable with populations with (f) Important social, occupational, or recrea-
lower alcoholism rates (e.g., elderly) and does tional activities given up or reduced
not identify “hazardous drinking.” because of alcohol.
2. Alcohol Use Disorders Identification Test (g) Drinking continues despite knowledge of
(AUDIT): The AUDIT can detect both hazard- persistent or recurrent physiological or
ous drinking and alcohol abuse. It does not psychological problems caused or exacer-
need to be administered face to face like the bated by drinking.
CAGE. It was developed by the World Health (h) Craving, or strong desire or urge to use
Organization and yields scores for alcohol.
Alcoholism 109

Treatment • Naltrexone (ReVia) – May work by

There are several well-accepted avenues of blocking the positive effects felt from drink-
treatment: ing by blocking opiate receptors in the brain A
thereby decreasing craving for alcohol.
1. Psychosocial: Studies have shown that simple, Clinical studies have found a modest
brief interventions can be effective in those not decrease in relapse (12–20%). This drug
severely alcohol dependent. One of those get- has an unknown cause of action.
ting an extensive trial has been “motivation • Acamprosate (Campral) – Used to maintain
interviewing” based on Prochaska’s five stages abstinence once alcoholics have stopped
of change model. A summary of the treatment drinking. Thought to work by stabilizing
approach is as follows: the chemical balance in the brain. In clinical
• Precontemplation – Patient expresses no trials, the 1-year abstinence rates have been
interest or need for change. The health- 18% and 12% at 2 years.
care professional’s options are limited. 3. Self-help groups: Perhaps the best-known orga-
They can point to discrepancies between nization involving alcoholism is AA. Until the
the patient’s goals and behavior and recom- mid-1930s in the USA, alcohol-dependent per-
mend 2 weeks of abstinence. sons who could not afford a private hospital or
• Contemplation – Patient expresses ambiva- private psychiatrist could only find help in state
lence or skepticism about change. The pro- hospitals, jails, or churches. AA was the first
vider should work to influence them in self-directed approach toward treatment. The
direction of change, provide information AA treatment model includes self-help groups,
about the dangers of alcohol abuse, and utilizing psychological principles organized in
recommend an abstinence trial. small local community groups. The “12 steps”
• Preparation – Patient accepts need for of AA encourage confrontation of denial and
change and makes plans to accomplish admission of powerlessness over alcohol and
changed drinking goal. strives for people to atone for harm caused by
• Action – Patient recognizes problem in their behavior while drinking. It encourages its
drinking behavior and takes observable members to live ethically with a reliance on a
steps to decrease alcohol use. Professional “higher power.” It is this sense of AA as a
reinforces decision for change and may “religion” that has led to nonreligious self-help
introduce self-help groups and/or groups including rational recovery, LifeRing,
medications. and SOS.
• Maintenance – Patient and professional
work together to maintain change and pre-
vent relapse. Future Directions
2. Medications: The most common medications
in the treatment of alcoholism are: The following are areas needing continued study:
• Disulfiram (Antabuse) – Prevents the elim-
ination of acetaldehyde, which is a 1. Genetic research – Current and future studies
by-product of alcohol metabolism. Results are looking at individuals with a family history
in unpleasant side effects in persons still of alcoholism to pinpoint the location of genes
drinking including nausea, dizziness, head- that influence vulnerability to alcoholism. This
ache, flushing, vomiting, heart palpitations, line of study will assist in the early identifica-
and sudden drop in blood pressure. Disulfi- tion of individuals at risk and of new, gene-
ram needs to be taken daily to be effective. based treatment approaches.
However, in at least one large clinical trial, 2. Treatment approaches – The NIAAA has been
it did not increase abstinence. funding a study called “Project MATCH”
110 Alertness

whose goal is to identify variables important in Reinert, D., & Allen, J. (2007). The alcohol use disorders
predicting outcome based on patient character- identification test: An update of research findings. Alco-
holism Clinical & Experimental Research, 31(2),
istics and treatment design. 185–199.
3. Medications – Naltrexone was the first drug Room, R., & Makela, K. (2000). Typologies of the cultural
approved by the FDA in 45 years to help alco- position of drinking. Journal of Studies on Alcohol and
holics stay sober following detoxification. Drugs, 61(3), 475–483.
Schuckit, M. (2000). Drug and alcohol abuse: A clinical
More research is needed. guide to diagnosis and treatment. New York: Kluwer/
Plenum Publishers.
U.S. Department of Health and Human Services and
Cross-References SAMHSAs National Clearinghouse for Alcohol and
Drug Information. http://ncadistore.samhsa.gov/cata
log/facts.aspx?topic=3.
▶ Alcoholic Brain Syndrome
▶ Fetal Alcohol Spectrum Disorder
▶ Korsakoff’s Syndrome
▶ Michigan Alcoholism Screen Test
▶ Motivational Interviewing Alertness
▶ Substance Use Disorders
▶ Twin Studies Chris Loftis
▶ Wernicke-Korsakoff Syndrome National Council for Community Behavioral
Healthcare, Alexandria, VA, USA

References and Readings

Synonyms
Borsari, B., & Carey, K. (2001). Peer influences on college
drinking: A review of the research. Journal of Sub-
Awareness; Consciousness; Vigilance;
stance Abuse, 13(4), 391–424.
Cavanaugh, S. (2014). Alcoholism and mental illness: Watchfulness
Overlapping diseases requiring a renewed focus. Men-
tal Health and Substance Abuse, 7(4), 487–496.
Davidson, R., & Raistrick, D. (1986). The validity of the
Short Alcohol Dependence Data Questionnaire
Definition
(SADD): A short self-report questionnaire for the
assessment of alcohol dependence. British Journal of A state of being mentally perceptive and respon-
Addiction, 81(2), 217–222. sive to external stimuli. A “readiness to respond”
Dhalla, S., & Kopec, J. (2007). The CAGE questionnaire
that can be detected by electroencephalography
for alcohol misuse: A review of reliability and validity
studies. Clinical and Investigative Medicine, 30(1), (EEG). Alertness is susceptible to fatigue;
33–41. maintaining a constant level of alertness is diffi-
Ducci, F., & Goldman, D. (2012). The genetic basis of cult, particularly for monotonous tasks demand-
addictive disorders. Psychiatric Clinics of North Amer-
ing continuous attention. Stimulants such as
ica, 35(2), 495–519.
National Institute on Alcohol Abuse and Alcoholism. nicotine, caffeine, and amphetamines can tempo-
(2005). Helping patients who drink too much: rally boost alertness. Diminished alertness is often
A clinician’s guide, updated 2005 edition. http://www. associated with the physiological response of
niaaa.nih.gov/Publications/EducationTrainingMaterials/
yawning, which may boost the alertness of the
guide.htm.
National Institute on Alcohol Abuse and Alcoholism. brain. Impaired alertness is a common symptom
Etiology and natural history of alcoholism. http://pubs. of a number of conditions, including narcolepsy,
niaaa.nih.gov/publications/social/module2etiology&nat attention deficit disorder, traumatic brain injury,
uralhistory/module2.html.
chronic fatigue syndrome, depression, Addison’s
Prochaska, J., DiClemente, C., & Norcross, J. (1992). In
search of how people change: Applications to addictive disease, and sleep deprivation. Although a broad
behaviors. American Psychologist, 47(9), 1102–1114. neurological network modulates alertness, the
Alexia 111

basal forebrain and a distinct group of neurons frequently encountered in the context of spoken
located in the periventricular areas of the mid- language dysfunction or aphasia. Most individ-
brain, pons, and medulla, referred to as the retic- uals with alexia have concomitant spelling impair- A
ular activating system (RAS), appear to be most ment, suggesting that reading and spelling rely on
directly responsible for modulating alertness and shared cognitive representations and neural
sleep. substrates.

Cross-References Categorization

▶ Attention Alexia is not a single clinical entity. Instead, there

▶ Attention Deficit Hyperactivity Disorder are several distinct forms of alexia characterized
▶ Basal Forebrain by specific combinations of impaired and pre-
▶ Coma served reading abilities and associated with
▶ Consciousness unique lesion profiles. The three most common
▶ Hindbrain alexia syndromes include pure alexia/letter-by-
▶ Reticular Activating System letter reading, phonological/deep alexia, and sur-
▶ Severe Brain Injury face alexia. Some individuals may also have a
▶ Vigilance coexisting visual field deficit, which causes errors
in reading. Clinicians should attempt to differen-
tiate the linguistic processing aspect from the
visual deficit. In order to understand the neuro-
psychological mechanisms underlying different
Alexia subtypes of alexia, it is important to briefly review
the cognitive processes involved in normal
Angel Ball reading.
Department of Clinical Health Sciences, Reading is a complex cognitive skill that
Texas A&M University-Kingsville, Kingsville, requires rapid visual discrimination of letters and
TX, USA words, as well as the ability to link information
about visual word forms (orthography) with
knowledge about word sounds (phonology) and
Synonyms word meanings (semantics). According to an
influential dual-route model of reading
Acquired reading disorder (Coltheart et al. 2001), perceptual processing of
written words begins with visual feature analysis
and letter shape detection (Fig. 1). Following the
Short Description or Definition letter identification stage, the model postulates
two distinct procedures or processing routes for
The term alexia is applied to acquired disorders of deriving phonology from print. The lexical route
reading produced by neurological injury in indi- requires the activation of memory representations
viduals with normal premorbid literacy skills. We of written word forms stored in the orthographic
differentiate here from developmental dyslexia lexicon, followed by the retrieval of the
which reflects a failure to attain normal reading corresponding spoken word forms from the pho-
skills. Clinically, patients with alexia have diffi- nological lexicon. The lexical route is normally
culty in recognizing, pronouncing, or used to read familiar words and can support the
comprehending written words. Although alexia processing of both regular words that have pre-
can occur in relative isolation, it is more dictable spelling-sound relationships (e.g., spring)
112 Alexia

Alexia, Fig. 1 A cognitive

model indicating the Semantics
component processes
involved in reading

Phonology Orthography

Lexical
Words Words
Spoken word Written word

Sublexical
Auditory Visual
Phonemes Letters
analysis analysis

Motor speech Graphic motor

programs programs

Speech Writing

and irregular words that contain atypical Woollams et al. 2007). In summary, skilled reading
letter-sound or grapheme-phoneme mappings depends on interactions among visual/orthographic
(e.g., choir). By contrast, the sublexical route processing, phonology, and semantics. Damage to
operates on units smaller than the whole word these functional domains or the disruption of the
and is thought to rely on the serial conversion of transfer of information between the cognitive/brain
individual graphemes to the corresponding pho- systems that support these operations results in
nemes. The sublexical route is essential for accu- alexia.
rate reading of unfamiliar words or nonwords (e.g.,
nace) because these novel items, by definition, do
not have preexisting representations in the ortho- Epidemiology
graphic or phonological lexicon. The sublexical
route can also be used to generate plausible pro- Alexia is commonly observed following damage
nunciations for regular words that strictly obey to the language-dominant hemisphere. Although
spelling-sound conversion rules. However, pro- it is most frequently caused by stroke, alexia can
cessing irregular words by the sublexical procedure follow any kind of focal injury (e.g., trauma,
results in regularization errors (e.g., have read to tumor) to the brain regions critical for
rhyme with save). Thus, according to dual-route implementing the various cognitive operations
theory, only the lexical reading route can deliver a necessary for normal reading. Data on stroke
correct response to irregular words. Note that the prevalence in the USA, Canada, and worldwide
model depicted in Fig. 1 also includes an indirect can be accessed via the Internet Stroke Center
route from orthography to phonology via the (n.d.); however, data on prevalence with alexia
semantic system. The activation of word meanings as an outcome is not well known. Alexia is also
by this semantic reading route is critical for written often seen in the setting of neurodegenerative
word comprehension. However, whether semantic disorders, especially in patients with primary pro-
mediation is also normally required for accurate gressive aphasia/semantic dementia or
oral reading of familiar words is a topic of contro- Alzheimer’s disease. In general, the specific
versy (Coltheart et al. 2001; Plaut et al. 1996; alexia profile is determined not so much by the
Alexia 113

etiology of the brain damage as by the location of processing deficit (Behrmann et al. 1998).
the responsible lesions. Within the framework of the cognitive model
depicted in Fig. 1, pure alexia is attributable to A
dysfunction at the visual feature analysis and/or
Natural History, Prognostic Factors, and letter identification stages of reading, or it may
Outcomes be produced by damage to the orthographic lex-
icon. Damage to any of these visual processing
The prognosis for recovery from alexia depends components would be expected to interfere with
both on the etiology of the lesion and the extent of the rapid perceptual identification of familiar
the underlying brain damage. Alexia following orthographic word forms and result in an abnor-
stroke tends to show some spontaneous recovery mal word length effect in oral reading.
over time, but patients with extensive brain dam- Pure alexia/letter-by-letter reading is most
age may never regain useful reading function and commonly seen following left inferior occipito-
typically stop reading for pleasure. In individuals temporal damage caused by posterior cerebral
with neurodegenerative disorders, progressive artery strokes. It has been proposed that the criti-
worsening of the reading impairment is observed cal lesions degrade or disrupt visual input to the
along with the gradual deterioration of other lan- visual word form area (VWFA) or directly dam-
guage and cognitive functions. age the VWFA itself (Cohen et al. 2003;
Epelbaum et al. 2008). The VWFA is consistently
activated in functional imaging studies of reading
Neuropsychology and Psychology of in normal individuals and has been localized to the
Alexia mid-lateral portions of the left fusiform gyrus
(BA37) (Cohen et al. 2002; Jobard et al. 2003)
Pure Alexia/Letter-by-Letter Reading (Fig. 2). The VWFA receives converging input
In pure alexia, the rapid visual identification of from bilateral posterior occipital areas (BA17,18/
familiar words that characterizes normal skilled 19) involved in visual feature analysis and letter
reading is disrupted. Reading is slow and labori- shape detection, and it integrates this information
ous, often relying on a serial letter-naming strat- into larger perceptual units corresponding to
egy known as “letter-by-letter” reading. Typically, whole words (Fig. 2). Activation of the VWFA
there is a monotonic increase in reading latencies is sensitive to the orthographic familiarity of the
as a function of the number of letters in the word, letter string, consistent with the notion that this
giving rise to an abnormal word length effect that cortical region may constitute the neural substrate
is considered the hallmark feature of the syn- of the orthographic lexicon. The orthographic
drome. Varying degrees of letter identification codes computed by the VWFA are subsequently
difficulty are present, and visual reading errors transmitted to cortical systems involved in the
are common (e.g., chain – charm). Collectively, phonological and semantic components of read-
these behavioral observations suggest that visual ing (Fig. 3). Importantly, it has been shown that
processing impairment plays a critical role in the spelling familiar words also activates the VWFA
pathogenesis of pure alexia (Behrmann et al. (Beeson et al. 2003). These observations confirm
1998). Although the reading disorder may be the central role for the VWFA in orthographic
unaccompanied by significant aphasia or processing and support the view that the same
agraphia, many patients with pure alexia dem- orthographic lexical representations mediate read-
onstrate concomitant anomia and spelling ing and spelling. Consistent with this hypothesis,
impairment (Rapcsak and Beeson 2004). Fur- patients with damage to the VWFA are likely to
thermore, patients often perform poorly on non- show evidence of reading and spelling impair-
reading tasks that require fine-grained visual ment attributable to the loss of word-specific
discrimination, suggesting that the reading orthographic representations (Rapcsak and
impairment is part of a more general visual Beeson 2004).
114 Alexia

Phonological/Deep Alexia Lambon Ralph 2006; Patterson and Lambon

Phonological alexia is characterized by a dispro- Ralph 1999; Rapcsak et al. 2009). Attempts to
portionate difficulty in processing nonwords read nonwords often result in real word responses
compared with familiar words, giving rise to an known as lexicalization errors (e.g., nace –
exaggerated lexicality effect in reading (Crisp and name). Although in phonological alexia reading
of familiar words (both regular and irregular) is
relatively preserved, performance is typically
influenced by lexical-semantic variables includ-
ing word frequency (high > low), imageability
(concrete > abstract), and grammatical class
(nouns > verbs > functors). Deep alexia includes
all the characteristic features of phonological
alexia, but it is distinguished from the latter by
the production of prominent semantic reading
errors (e.g., boy – son) (Coltheart et al. 1980).
Although phonological and deep alexia were
originally considered separate entities, there is
now much evidence to suggest that the difference
between these syndromes is quantitative rather
than qualitative. Thus, phonological and deep
alexia are more appropriately considered as
points along a continuum, with the latter
representing a more severe version of the former
(Crisp and Lambon Ralph 2006; Rapcsak
et al. 2009).
Phonological alexia is typically encountered in
Alexia, Fig. 2 Location of the visual word form area patients with aphasia syndromes characterized by
(VWFA) (indicated by green circle) as determined by func- phonological impairment (i.e., Broca’s, conduc-
tional neuroimaging studies of reading. This region
tion, Wernicke’s). Furthermore, it has been shown
receives input from bilateral posterior occipital visual
areas (shown in purple). Arrow indicates callosal transfer that most patients with phonological alexia dem-
of information initially processed by right visual cortex onstrate prominent deficits and increased

Alexia, Fig. 3 Cortical

regions involved in reading
Alexia 115

lexicality effects in spoken language tasks that phonological processing (Jobard et al. 2003;
require the manipulation and maintenance of sub- Rapcsak et al. 2009; Vigneau et al. 2006). As
lexical phonological information (e.g., repetition, predicted by the continuum model, there is con- A
rhyme judgments, phoneme segmentation, and siderable overlap between the perisylvian lesion
blending) and also that such non-orthographic profiles of patients with phonological and deep
measures of phonological ability correlate with alexia, although the damage in deep alexia tends
and are predictive of reading performance (Crisp to be more extensive. In fact, the massive destruc-
and Lambon Ralph 2006; Rapcsak et al. 2009). tion of left-hemisphere language areas in deep
These observations suggest that the written and alexia has led to the hypothesis that reading per-
spoken language impairments in phonological formance in these patients may be mediated by the
alexia have a common origin and are merely dif- intact right hemisphere (Coltheart et al. 1980).
ferent manifestations of a central or modality-
independent phonological deficit (Crisp and Surface Alexia
Lambon Ralph 2006; Patterson and Lambon In surface alexia, the main difficulty involves
Ralph 1999; Rapcsak et al. 2009). Consistent reading irregular words, especially when these
with this view, the reading disorder in phonolog- items are of low frequency. Regular words of
ical alexia is usually accompanied by a qualita- comparable frequency are processed more effi-
tively similar spelling impairment (phonological ciently, and the discrepancy in performance
agraphia) (Rapcsak et al. 2009). According to between words with predictable versus atypical
dual-route models (Fig. 1), poor nonword reading spelling-sound relationships is reflected by an
in phonological alexia is attributable to damage to increased regularity effect in reading. Nonword
the sublexical route, while the relatively preserved reading is typically preserved. According to
real word reading performance of these patients dual-route theory, surface alexia is attributable to
reflects the residual functional capacity of the dysfunction of the lexical reading route (Fig. 1).
lexical and semantic routes. The general phono- Specifically, it has been suggested that the reading
logical impairment observed in the vast majority disorder in some cases may result from damage to
of patients suggests that the most common site of the orthographic lexicon (Coltheart et al. 2001;
damage may be at the level of the phoneme units Patterson et al. 1985). Due to the loss of word-
(with additional damage to the phonological lex- specific orthographic knowledge, patients with this
icon in more severe cases), as these phonological type of deficit will be forced to rely on a sublexical
processing components are shared between writ- grapheme-phoneme conversion strategy that pro-
ten and spoken language tasks. duces phonologically plausible regularization
Phonological alexia is most often associated errors on irregular words. Low-frequency irregular
with damage to a network of perisylvian cortical words are especially vulnerable because the acti-
regions involved in speech production/perception vation of representations in the orthographic lexi-
and phonological processing in general. Compo- con is normally modulated by word frequency, and
nents of this distributed phonological system the relative refractoriness of low-frequency items
include posterior-inferior frontal gyrus/Broca’s may be further exaggerated by the brain damage.
area (BA44/45), precentral gyrus (BA4/6), insula, Consistent with the notion that reading and spell-
superior temporal gyrus/Wernicke’s area (BA22), ing rely on shared orthographic representations,
and supramarginal gyrus (BA40) (Rapcsak et al. patients with surface alexia following damage to
2009). Consistent with the phonological deficit the orthographic lexicon show similar difficulty in
hypothesis, there is an excellent neuroanatomical spelling irregular words (surface agraphia)
correspondence between the location of the (Patterson et al. 1985; Rapcsak and Beeson
lesions that produce phonological alexia and the 2004). Alternatively, surface alexia may result
location of the perisylvian cortical areas that show from damage to central semantic representations
activation in normal individuals during a variety (Woollams et al. 2007). Specifically, it has been
of written and spoken language tasks requiring proposed that accurate oral reading of low-
116 Alexia

frequency irregular words normally requires addi- (BA38,20/21) (Galton et al. 2001; Mummery
tional support from the semantic reading route and et al. 2000). Surface alexia has also been
cannot be mediated efficiently by pathways that described in patients with Alzheimer’s disease
rely on direct transcoding between orthographic (Patterson et al. 1994) and is likely to reflect the
and phonological representations (Plaut et al. frequent involvement of left temporoparietal cor-
1996). With the degradation of semantic knowl- tex by the disease process. Although distributed
edge, the relative inadequacy of non-semantic over a large anatomical area, the disparate extra-
reading routes is revealed and manifests itself sylvian lesion sites in surface alexia seem to have
as surface alexia. Consistent with the semantic in common the potential for disrupting either
deficit hypothesis, many patients with surface lexical orthographic or semantic processing.
alexia perform poorly on verbal and nonverbal Specifically, in patients with VWFA involve-
cognitive tasks requiring semantic processing ment, the reading disorder may reflect damage
(e.g., picture naming, verbal fluency, spoken to the orthographic lexicon resulting in the loss of
word, and picture comprehension). Furthermore, word-specific orthographic knowledge. By con-
the severity of the semantic impairment on these trast, in patients with anterior temporal lobe
nonreading tasks has been shown to correlate lesions, and possibly also in patients with poste-
with reading accuracy for low-frequency irregu- rior temporoparietal damage, surface alexia may
lar words (Woollams et al. 2007). The proposed be attributable to the degradation of central
central semantic deficit may also explain the semantic representations. The latter hypothesis
frequent co-occurrence of surface alexia and sur- is supported by functional imaging studies of
face agraphia (Graham et al. 2000). semantic processing in normal individuals that
In contrast to the strong association between have shown activation of a large-scale left-
perisylvian damage and phonological alexia, sur- hemisphere extrasylvian cortical network that
face alexia is typically encountered in the setting included both anterior temporal lobe and poste-
of extrasylvian brain pathology. Although rior temporoparietal sites (Vigneau et al. 2006;
uncommon in patients with stroke, surface alexia Binder et al. 2009) (Fig. 3).
has been described in individuals with left
temporoparietal lesions centered on posterior
middle/inferior temporal gyrus and angular Evaluation
gyrus (BA20/21,37/39), and also following infe-
rior occipitotemporal lesions that involved the In evaluating adults with alexia, it is important to
VWFA (Rapcsak and Beeson 2004; Vanier and assess the status of all the relevant component
Caplan 1985). As expected, patients with surface processes involved in reading (Fig. 1). A compre-
alexia following VWFA damage also showed hensive battery should include tests of letter and
evidence of visual processing impairment and word recognition, as well as measures of oral
features of pure alexia/letter-by-letter reading reading and reading comprehension. The evalua-
(Rapcsak and Beeson 2004). A particularly dra- tion should allow the clinician to identify the
matic and pure form of surface alexia is consis- nature of the functional impairment and to locate
tently observed in patients with semantic the level of breakdown with reference to a cogni-
dementia (SD) (Woollams et al. 2007). SD is a tive model of normal reading. It is equally impor-
subtype of primary progressive aphasia/ tant to document relatively spared reading abilities
frontotemporal dementia in which the neurode- and the use of compensatory strategies by the
generative process has a predilection for left patient, as this information may be helpful in
anterior and inferolateral temporal cortex, planning treatment.
including the temporal pole, middle/inferior tem- As reading inherently is a visual task, the
poral gyri, and anterior fusiform gyrus examiner must inquire as to any visual limitations
Alexia 117

with or without corrective lenses. One compensa- (including bound morphemes, derivational
tion may be to change font size or spacing, which morphemes(suffixes), word and sentence
if successful, will help distinguish a reading dis- (4–14 words) oral reading, and sentence and A
order from a visual limitation. In addition, the paragraph comprehension with word and
examiner should consider the age-level readabil- phrase choices.
ity of the material, in comparison to the premorbid • Examining for Aphasia-4 (EFA-4; LaPointe and
reading level of the client. Eisenson 2008) – reading subtests include silent
Silent reading is an internal event which may reading interrogative sentences (five to seven
be processed differently depending on the type of words) with semantic matching from set of
reading. Stories and books for pleasure are often four words, silent paragraph reading with inter-
read with a mental image of the story with no rogative sentence to test comprehension from
effort to memorize or learn material. Reading set of four sentence choices, and oral paragraph
texts or articles for learning requires acquisition reading with interrogative sentences to test com-
of knowledge, and readers vary in their style. prehension given set of four short phrases or
Most formal test does not prepare the examiner sentences.
for these differences. Test measurement has tra- • Multilingual Aphasia Examination 3rd Ed
ditionally required a technique to judge the inter- (MAE-3; Benton et al. 1978) – provides a
nal comprehension. Usually this is done by picture matching words and two to four word
asking questions on content information in a phrases to picture choices of four items.
series of yes/no questions or multiple choice • Psycholinguistic Assessment of Language
with visual choices or matching word or sentence Processing in Aphasia (PALPA English Ed:
to a picture. Kay et al. 1992) – reading subtests include
Oral reading accuracy can be monitored by the letter discrimination (mirror reversal, upper
examiner during the event. This task will help to and lower case matching), spoken letter to
reveal visual spatial or attention errors, such as written letters, recognition of non- and real
skipped words or lost place. Recording the oral words, homophones, oral reading tasks for
words per minute provides information on word letter and syllable length, word frequency
fluency. and grammatical class, regularity of spelling,
The only reading modality-specific commer- and sentence-level oral reading (five to seven
cially available reading test is the Reading Com- words), and defining with reading word
prehension Battery for Aphasia-2 (RCBA-2; tasks.
LaPointe and Horner 1998), which includes
oral and silent reading at word, sentence, para-
graph levels, and functional reading tasks (i.e., Treatment
calendar).
Standardized tests with reading subtests A variety of behavioral treatment approaches have
include: shown positive outcomes in the rehabilitation of
alexia. In general, treatment is directed toward
• Boston Diagnostic Aphasia Examination-3 strengthening the impaired reading procedure/
(Goodglass et al. 2001) – reading subtests route or it encourages the use of compensatory
include symbol letter and number recognition, strategies to bypass the functional deficit (for a
word identification given choice of 4 words review, see Beeson and Rapcsak 2006; Murray
with visually and semantically similar foils, and Clark 2015; Riley and Kendall 2013; Peach
lexical decision of real word from nonwords, and Shapiro 2012). Treatment approaches often
homophone matching, nonword to homophone align with the underlying problem, e.g., syntactic,
matching, matching written to spoken target visual-attention, memory.
118 Alexia

Material choices have extended beyond tradi- visual cortex? Functional properties of the visual word
tional text and into using supported technology form area. Brain, 125, 1054–1069.
Cohen, L., Martinaud, O., Lemer, C., Lehéricy, S., Sam-
such as highlighted text, read-aloud technology son, Y., Obadia, M., et al. (2003). Visual word recog-
(text to speech), and electronic access to dictionary nition in the left and right hemispheres: Anatomical and
(Deitz et al. 2011; Helm-Estabrooks et al. 2014). The functional correlates of peripheral alexias. Cerebral
number of software programs and apps designed for Cortex, 13, 1313–1333.
Coltheart, M., Patterson, K., & Marshall, J. C. (1980).
stimulation and practice are ever increasing (e.g., Deep dyslexia. London: Routledge & Kegan Paul.
Lingraphica TalkPath, Bungalow software). Readers Coltheart, M., Rastle, K., Perry, C., Langdon, R., &
are encouraged to view the online tables for evi- Ziegler, J. (2001). DRC: A dual route cascaded model
dence-based treatment for individuals with aphasia of visual word recognition and reading aloud. Psycho-
logical Review, 108, 204–256.
(Beeson, n.d.) for a list of reading treatments. Crisp, J., & Lambon Ralph, M. A. (2006). Unlocking the
nature of the phonological-deep dyslexia continuum:
The keys to reading aloud are in phonology ad seman-
tics. Journal of Cognitive Neuroscience, 18, 348–362.
See Also Epelbaum, S., Pinel, P., Gaillard, R., Delmaire, C., Perrin,
M., Dupont, S., et al. (2008). Pure alexia as a discon-
▶ Aphasia nection syndrome: New diffusion imaging evidence for
▶ Boston Diagnostic Aphasia Examination an old concept. Cortex, 44, 962–974.
Galton, C. J., Patterson, K., Graham, K., Lambon Ralph,
▶ Multilingual Aphasia Examination
M. A., Williams, G., Antoun, N., et al. (2001). Differ-
▶ Reading Comprehension Battery for Aphasia-2 ing patterns of temporal atrophy in Alzheimer's disease
▶ Western Aphasia Battery and semantic dementia. Neurology, 57, 216–225.
Goodglass, H., Kaplan, E., & Barresi, B. (2001). The
Boston diagnostic aphasia examination (3rd ed.). Bal-
timore: Lippincott Williams & Wilkins.
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neural substrates. Cortex, 45(5), 575–591.
Riley, E. A., & Kendall, D. L. (2013). The acquired disor- number of medical and psychiatric disorders.
ders of reading. In I. Papathanasiou, P. Coppens, & Alexithymia is associated with somatic com-
C. Potagas (Eds.), Aphasia and related neurogenic plaints such as headaches, lower back pain, irrita-
communication disorders (pp. 157–172). Burlington: ble bowel syndrome, and fibromyalgia. It is also
Jones & Bartlett Learning.
Sampson, G. (1985). Writing systems. Stanford: Stanford associated with psychiatric conditions such as
University Press. anorexia nervosa, autism spectrum disorders
Vanier, M., & Caplan, D. (1985). CT correlates of surface including Asperger’s, major depressive disorder,
dyslexia. In K. E. Patterson, J. C. Marshall, & panic disorder, post-traumatic stress disorder, and
M. Coltheart (Eds.), Surface dyslexia: Neuropsycho-
logical and cognitive studies of phonological reading substance abuse.
(pp. 511–525). London: Lawrence Erlbaum.
Vigneau, M., Beaucousin, V., Hervé, P. Y., Duffau, H.,
Crivello, F., Houdé, O., et al. (2006). Meta-analyzing See Also
left hemisphere language areas: Phonology, seman-
tics, and sentence processing. NeuroImage, 30,
1414–1432. ▶ Emotional Intelligence
120 Alien Hand Syndrome

Further Reading their hands as their own. The hand, effectively,

appears to manifest a “will of its own.” This unique
Sifneos, P. E. Alexithymia: Past and present. The American involuntary movement disorder is characterized by
Journal of Psychiatry, 153, 137–142.
coordinated, well-organized, and clearly goal-
Taylor, G. J., & Taylor, H. S. (1997). Alexithymia. In
M. McCallum & W. E. Piper (Eds.), Psychological directed limb movements that would otherwise be
mindedness: A contemporary understanding. Munich: indistinguishable from normal voluntary movement.
Lawrence Erlbaum Associates. This definition excludes disordered, non-purposeful,
Taylor, G. J., Bagby, R. M., & Parker, J. D. A. (1997).
and dyskinetic movements associated with other
Disorders of affect regulation: Alexithymia in medical
and psychiatric illness. Cambridge: Cambridge Uni- involuntary movement disorders such as chorea,
versity Press. ISBN 052145610X. athetosis, hemiballism, and myoclonus.
The alien hand can be engaged in performing a
specific goal-directed task or the purposeful use of an
external object. Distinguishing this condition from
Alien Hand Syndrome asomatognosia, there is typically normal awareness
and recognition of the limb reported by the patient.
Gary Goldberg1 and Matthew E. Goodwin2 However, the patient perceives a lack of self-agency
1
Hunter Holmes McGuire Veterans (“I am not doing that. . .”) with regard to the observed
Administration Medical Center, Department of behavior of the limb but displays an intact “sense of
Physical Medicine and Rehabilitation, Virginia ownership” (“. . .even though I know this is my
Commonwealth University School of Medicine/ hand”). While the original description of this condi-
Medical College of Virginia, Richmond, tion occurred in patients with well-defined focal
VA, USA lesions of cerebral cortex, with the majority of
2
Central Arkansas Veterans Healthcare System, cases due to cerebral infarction, it has since been
Little Rock, AR, USA described in a variety of different clinical conditions
including corticobasal syndrome, progressive supra-
nuclear palsy, Alzheimer’s disease, and Creutzfeldt-
Synonyms Jakob disease. Furthermore, while the alien limb is
typically and most often noted in an upper extremity,
Alien limb phenomenon; Anarchic hand; Callosal it has been described in the lower extremity as well.
apraxia; Diagnostic dyspraxia; Dr. Strangelove This suggests that the alien hand syndrome
syndrome; Intermanual conflict; Magnetic reflects a phenomenon that may result from
apraxia; Wayward hand impaired function at a variety of different points
in a widely distributed brain system involved in
the intentional preparation and generation of pur-
Short Description or Definition poseful voluntary movement. This system would
be expected to include both specifically defined
Alien hand syndrome (AHS) is a relatively rare motor and premotor regions of the cerebral cortex
manifestation of damage to specific brain regions as well as related interconnected subcortical
involved in purposive voluntary movement. It is regions such as the basal ganglia. The different
postulated to be an impairment of the “sense of clinical variants of AHS associated with
agency” or, alternatively, an impairment of intention- circumscribed cortical damage which will be
ality. The core observation is the patient report that reviewed below may reflect varying clusters of
one of his/her hands is displaying purposeful, coor- clinical manifestations resulting from disrupted
dinated, and goal-directed behavior over which the functions at different points and levels within
patient feels he/she has no direct voluntary control. this distributed brain system. As noted, this dis-
The patient fails to recognize the action of one of tributed brain system would be expected to
Alien Hand Syndrome 121

involve a variety of both cortical and associated injury extends posteriorly to involve the medial
subcortical regions engaged together in the aspect of the prefrontal gyrus associated with the
emerging brain process linked to voluntary move- primary motor cortex (PMC), the patient may A
ment generation, with the common pathophysio- present with crural hemiparesis, with greater
logic manifestation being a dissociation between weakness in the leg as compared to the arm. This
self-perceived will and action. presentation corresponds to the topographical
One of the significant difficulties in conceptual- organization of the PMC with control of lower
izing and studying AHS in the context of a conven- limb movement located more medially than the
tional scientific paradigm is that a mechanistic areas on the exterior lateral surface that control the
explanation alone cannot adequately account for upper limb and face. The frontal variant is seen
the process linked to intentionality and the teleolog- with involvement of the medial aspect of the pre-
ical aspect of goal-directed behavior. The emerging motor cortex anterior to PMC including the pre-
field of “biosemiotics” that recognizes the process supplementary (pre-SMA) and supplementary
of semiosis through which meaning and action- motor area (SMA), and anterior cingulate cortex
associated intentionality emerge in the behavior of (ACC), as well as connections to the posterior
living organisms promises to provide a new per- cingulate cortex (PCC). In functional activation
spective and, in the process, provide potential studies, the medial frontal cortex has also been
insights into this disorder. found to activate spontaneously with complex
purposeful movements and with internal imaging
of voluntary movement, suggesting that it may
Categorization serve as a higher-level system that modulates the
activation of PMC in accordance with volitional
Two major forms of AHS can be distinguished. features of the performance. The readiness poten-
One form is related to focal cortical and tial, or Bereitschaftspotential, a slowly developing
intercortical white matter damage and the other surface-negative shift that precedes an overt vol-
is associated with more diffusely distributed cor- untary movement by over 1200 ms, arises through
tical/subcortical damage (e.g., as seen in activation of the anteromedial frontal cortex,
corticobasal syndrome). Three variants of the suggesting that excitation of this system precedes
focal cortical form of AHS have been described, the appearance of the overt movement and activa-
each with unique behavioral manifestations and tion of the PMC. Activation of the ACC is
neuroanatomical correlations. These variants involved in intentional suppression of prepotent
include the frontal, callosal, and posterior forms. responses as tested with the Stroop test. These
areas may serve as a higher-level system modu-
Cortical Form lating the activation of PMC in accordance with
the volitional self-referenced aspects of the per-
Frontal Variant formance. Alternatively, they may be part of a
feed-forward system that generates an efference
Neuroanatomy The most common variant is the copy of the generated motor command that is
“frontal” form. It is typically associated with dam- transmitted to sensory cortex as a means of
age to the medial surface of the cerebral hemi- distinguishing active self-generated limb move-
sphere in the frontal region. This variant has been ment with its associated sensory re-afference,
described in cerebral infarction in the territory of from passive movement produced by external
the anterior cerebral artery, with tumors involving forces associated with sensory ex-afference.
the medial surface of the cerebral hemisphere, and
in other conditions affecting the function of the Clinical Presentation Behaviors seen frequently
medial frontal lobe region. When the region of with the frontal variant include involuntary,
122 Alien Hand Syndrome

visually driven reaching and grasping onto The voluntary motor systems of the two hemi-
objects, an inability to voluntarily release these spheres are isolated from each other due to lost
objects, and utilization behavior in which the interhemispheric communication resulting in
presence of a frequently encountered object used impaired intermanual coordination. This variant
in daily activities such as a comb or a toothbrush has been described most frequently as a transient
elicits behavior in which the object may be put to condition following callosotomy in the treatment
use independent of the general interpersonal con- of intractable seizures. It may also be seen follow-
text. A grasp reflex to tactile stimulation is often ing infarction or tumors selectively involving the
present in the affected hand. The patient may corpus callosum.
wake themselves up from sleep by grasping onto
and pulling at their own body parts. Patients may Clinical Presentation In the “callosal” variant of
show a prepotent tendency to be drawn toward AHS, the appearance of “intermanual conflict” or
external objects. They also may demonstrate “self-oppositional” behaviors is the predominant
alien-associated sexual self-stimulation or invol- feature. Grasping behaviors and externally driven
untary fondling of another’s body, a great source reaching movements seen in the frontal variant are
of public embarrassment (Ong Hai and Odderson notably less prominent. When there is a major
2000). Interestingly, while the patient clearly disconnection between the two hemispheres
manifests purposeful involuntary coordinated resulting from callosal injury, the language-linked
behaviors in the affected limb that appear to flow dominant hemispheric agent that maintains its
effortlessly, attempts to willfully move the limb primary control over the contralateral dominant
are effortful and arduous. Voluntary movement in limb effectively loses its direct and linked control
the affected limb is often hypokinetic and hypo- over the separate “agent” based in the non-
metric with greater activation of the axial and dominant hemisphere (and, thus, the nondominant
proximal limb muscles compared to the distal limb), which had been previously responsive and
muscles controlling the wrist and fingers, even “obedient” to the dominant agent. The possibility
though these muscles are fully and dexterously of purposeful action in the nondominant limb
activated in the alien movements. Generally, occurring outside of the realm of influence of the
these alien behaviors appear in the hand contra- dominant agent thus can occur. In the callosal
lateral to the damaged hemisphere regardless of variant, the problematic alien hand is consistently
hemispheric dominance. When the dominant the nondominant hand, while the dominant hand
hemisphere is damaged, in addition to alien is the identified “good” normally controlled hand.
hand behavior in the dominant hand, they may The patient may express frustration and bewil-
experience difficulty with the initiation of spon- derment at the conflicting and disruptive behav-
taneous speech while still being able to follow ior of the alien hand whose motivations remain
verbal commands and repeat phrases without dif- inaccessible to consciousness. There may be an
ficulty. These findings are consistent with a trans- attentional component that modulates the
cortical motor aphasia that affects spontaneous appearance of these episodes of self-oppositional
verbalization and production of propositional behavior since intermanual conflict is observed
speech more than repetition and generally respon- more frequently when the patient is fatigued,
sive language output. Alternatively, this has been stressed, or is engaged in effortful multitasking
interpreted as a partial mutism manifesting as an and divided-attention activity. Occasionally,
inability to initiate spontaneous propositional rather than acting in a contradictory manner, the
verbal output. two hands are observed to be engaged in two
different and entirely unrelated activities as if
Callosal Variant being guided by completely separate and inde-
pendent intentions.
Neuroanatomy The “callosal” variant is seen In a dramatic example of this behavior, one
with an isolated lesion of the corpus callosum. patient was observed to initiate smoking a
Alien Hand Syndrome 123

cigarette by pulling the cigarette out of the pack- avoid contact between the palmar surface of the
age and placing it in her mouth with the controlled affected hand and support surfaces. It may also be
dominant hand followed by the alien non- seen to withdraw from objects approaching the A
dominant hand, rather than beginning to light the hand in distinct contrast to the reaching and grasp-
cigarette, suddenly reaching up, pulling it out of ing behaviors that are seen in the frontal variant.
her mouth, and throwing it across the room. The alien hand may assume a characteristic posture
Astonished, the patient reasoned that perhaps the of fully extended digits with the palmar surface
alien hand was not in favor of her smoking! retreating from environmental objects, and support
The callosal and frontal variants are often seen surfaces an observation that has been labeled an
in combination with a corresponding overlap of “instinctive avoidance reaction” by Denny-Brown
observed behaviors. For example, following and has also been referred to as a “parietal hand.”
cerebral infarction in the territory of the anterior At times, grasping behaviors can also be observed
cerebral artery, there may be ischemic injury to with the posterior variant.
both the medial frontal lobe and the corpus Alien hand behavior has also been reported in
callosum. In this circumstance, there may be association with focal subcortical thalamic
both visually directed reaching and grasping infarction.
alien behaviors in the limb contralateral to
the area of injury as well as episodes of Distributed Cortical/Subcortical Form
intermanual conflict. However, a clear differen- In addition to having been observed in the context
tiation between apparent intermanual conflict of stroke, tumors, and callosotomy, alien hand
due to attempts to restrain alien behaviors asso- behavior has been described in a second general
ciated with the frontal variant (e.g., as in the case form linked to degenerative neurological condi-
of “self-grasping” described below), and true tions that tend to affect cortical and subcortical
intermanual conflict, in which the two hands are regions together. The progressive neurodegenera-
directed toward independently contradictory tive disorders associated with this form of AHS
purposes, may be difficult to differentiate. include corticobasal syndrome, progressive
supranuclear palsy, multiple sclerosis, spongiform
Posterior or “Sensory” Variant encephalopathy, and Alzheimer’s disease. When
AHS appears with these progressive encephalop-
Neuroanatomy The third identified variant of athies, it is usually accompanied by various forms
AHS is the “posterior” or “sensory” form, which of motor apraxia, along with multiple additional
appears most often with a parietal or parieto- cognitive and motor disturbances characteristic of
occipital focus of circumscribed damage. As in the particular condition.
the frontal variant, the alien behavior appears in
the hand contralateral to the damaged hemisphere.
Epidemiology
Clinical Presentation In the patient with the
posterior variant, the movement of the affected While there are no epidemiologic studies of the
alien limb is typically less organized and often occurrence of AHS variants in association with
has an ataxic instability particularly with visually acquired brain damage, it can be assumed that this
guided reaching. The limb also may show propri- is a relatively rare but striking manifestation of
oceptive sensory impairment with hypesthesia, so neurologic pathology.
that kinesthetic impairment limits the monitoring
of limb position. Visual field deficits as well as
hemi-inattention may be seen on the same side as Pathophysiology and Prognosis
the alien hand. In this variant, the limb may be
observed to lift up off of support surfaces invol- Adapting the concept developed by Derek Denny-
untarily and “levitate” in the air seemingly to Brown regarding positive and negative cortical
124 Alien Hand Syndrome

tropisms based in the parietal lobe and frontal systems, two in each hemisphere. The overall
lobes (Denny-Brown 1956, 1966), respectively, general configuration of this postulated heuristic
a heuristic model has been proposed. In this model is shown in Fig. 1.
model, there are two separable but interactive It is proposed that AHS, in its different variants
components of an intrahemispheric premotor described above, appears due to damage either to
intentional system that modulate the output of the corpus callosum in the callosal variant (Fig. 2),
the PMC of the hemisphere and its direct influence the AMPS of either hemisphere in the frontal
via the corticospinal tract over the spinal motor variant (Figs. 3 and 4), or to the PLPS of either
nuclei innervating the distal muscles of the con- hemisphere in the posterior variant (Figs. 5 and 6).
tralateral limbs (Goldberg and Bloom 1990). The common factor in these anomalous condi-
The first component is a posterolateral pre- tions is the relative sparing of the PMC region
motor system (PLPS) based in the posterior pari- controlling the contralesional alien hand, while
etal region that is involved in generating the premotor regions involved in the intentional
movements of the contralateral arm and hand, as selection of action and the inhibition of automatic
well as the lower limb, that are perceptually driven behaviors in response to external factors are
toward external objects and are responsive to impaired. A recent fMRI study of cortical activa-
externally sensed, contextually relevant, ecolog- tion patterns associated with alien and non-alien
ical contingencies. The second component is an movement has demonstrated that alien movement
anteromedial premotor system (AMPS) based in is in fact characterized by isolated activation of
the medial frontal region including medial pre- PMC without concomitant activation of
frontal, pre-SMA, SMA, and ACC that is intrahemispheric premotor regions, while volun-
involved in generating movements in the contra- tary behavior includes the activation of PMC in
lateral upper limb that are guided by an out- concert with activation of intrahemispheric pre-
wardly directed intentional action plan and motor regions (Assal et al. 2007).
driven by an anticipatory internally based
model of projected future contingencies. It pre-
sumably is also involved in activating with- Neuropsychology and Psychology
drawal movements that pull the limb back and of AHS
away from external stimuli. It also functions to
withhold action directly responsive to surround- The presence of AHS can cause the patient signif-
ing objects through inhibitory influence over icant psychological distress as the hand seems to
the PLPS. These two systems are proposed to possess the capability for acting autonomously,
be in a metastable balance through mutually independent of their conscious voluntary control.
inhibitory influence. Together, these two hemi- The patient may become fearful that they will be
spheric agency systems form an integrated held accountable for consequences of an action of
intrahemispheric agency system. Furthermore, the alien hand over which they do not feel control.
each intrahemispheric agency system has the The patient may display “autocriticism”
capability of acting autonomously in its control complaining that the alien hand is not doing
over the contralateral limb, although overall uni- what it has been “told to do” and is therefore
tary control by a singular conscious agent is characterized as disobedient, wayward, or “evil.”
maintained through interhemispheric communi- The hand is felt to be under the control of an
cation between these systems via the corpus external unknown agent to whose narrative and
callosum at the cortical level and other intentions the patient is not privy. They may even
interhemispheric commissures linking the two physically strike the alien hand with the controlled
cerebral hemispheres at the subcortical level. hand as a “punishment” intended to discourage its
Thus, conscious human agency can be thought wayward behavior, or restrain the movement of
of as emerging through the linked and coordi- the alien hand by grasping tightly onto it with the
nated action of at least four major premotor controlled hand (“self-grasping”). They may
Alien Hand Syndrome 125

LEFT RIGHT
HAND HAND
A

AMPS AMPS

PMC PMC

CC

PLPS PLPS

LH RH

Alien Hand Syndrome, Fig. 1 Heuristic Model for interactive inhibition creating a complementary metastable
Understanding Alien Hand Syndrome (AHS). Abbrevia- control of the contralateral hand. Solid arrows indicate
tions: RH right hemisphere, LH left hemisphere, CC corpus facilitatory connections or connections that maintain syn-
callosum, PMC primary motor cortex, AMPS anteromedial chrony and coherence between the connected structures.
premotor system, PLPS posterolateral premotor system. Output from PMC is directed primarily to the distal con-
This view is shown looking down from above the vertex tralateral limb with some less potent ipsilateral projections
with the face located at the top of the drawing and the back to primarily axial postural muscles illustrated by a dotted
of the head noted at the bottom of the drawing, the left side line. See text for further detail. Note that the left hemi-
to the left and the right side to the right of the diagram. The sphere is stippled in the diagram designating this as the
open bidirectional arrow between the AMPS and the PLPS dominant hemisphere for most individuals in correspon-
indicates an interaction characterized by mutually dence with a dominant right hand

verbally address and instruct the hand as if it were rational explanation for their concerns and that
an unruly child acting autonomously and in need there is evidence that these problems can be treated
of disciplinary intervention. Conversely, they may and are likely to gradually improve over time.
respond to these contrary actions with In AHS, different regions of the brain are able
amusement. to command purposeful limb movements, without
Given the predicament created, the patient may generating the conscious feeling of self-control
develop depersonalization and dissociate them- over these movements. There is thus a dissocia-
selves from the unintended actions of the hand. tion between the actual execution of the physical
They often choose to identify an external “alien” movements of the limb and the process that pro-
source for the voluntary control of the hand, or duces an internal sense of voluntary control over
assign a distinct personality to the hand as a way the movements. This latter process, impaired in
of seeking a satisfactory narrative to explain this AHS, normally produces the conscious sense of
perplexing and disturbing situation. agency that conveys that the movement is being
From a psychological perspective, it is helpful internally initiated and produced by an active self.
to counsel the patient regarding the organic basis of Presumably, this process differentiates reliably
their problem and provide assurance that there is a between “re-afference” (i.e., the return of
126 Alien Hand Syndrome

LEFT RIGHT
HAND HAND

AMPS AMPS

PMC PMC
CC

PLPS PLPS

LH RH

Alien Hand Syndrome, Fig. 2 The Callosal Variant of system in the dominant hemisphere is linked to the lan-
AHS. Theoretical explanatory model for the alien behav- guage system while that of the nondominant hemisphere is
iors observed in callosal damage. In this instance, there are separated from it. The dominant hand is understood as
findings consistent with callosal apraxia in addition to connected to the language-mediated narrative “self,”
intermanual conflict associated with the complete separa- while the nondominant hand is not directly accessible to
tion of the two intrahemispheric premotor intentional con- this narrative self. The alien hand in this variant is the
trol systems. The limbs appear to be operated by two nondominant hand that operates outside of the dominant
relatively autonomous hemispheric control systems that narrative. This is indicated by the stippled overlay in the
function as two distinct agents. The intentional premotor diagram on the left nondominant hand

kinesthetic sensation from the self-generated external forces. AHS may thus involve impaired
“active” limb movement) and “ex-afference” production and transmission of either an efference
(i.e., kinesthetic sensation generated from an copy or a corollary discharge signal.
externally produced “passive” limb movement).
It may do this by giving rise to a parallel output
signal from motor regions, a so-called efference Evaluation
copy. The efference copy is then translated into a
corollary discharge, which conveys the expected Evaluation of the patient with AHS involves care-
re-afferent sensory response from the commanded ful observation of limb movement in various natu-
movement. The corollary discharge can then be ralistic contexts, along with reports from the patient
used in somatosensory cortex as a referent to regarding their sense of control over these move-
distinguish re-afference from ex-afference and ments. The relative dependence of movement on
thus differentiate a self-produced active move- external context should be evaluated through
ment from a passive movement resulting from assessment for utilization behaviors elicited by the
Alien Hand Syndrome 127

Alien Hand Syndrome,

Fig. 3 The Non-dominant LEFT RIGHT
Frontal Variant of AHS. HAND HAND
Theoretical explanatory A
model for the alien
behaviors observed in the
frontal variant associated
with damage to the AMPS
of the nondominant AMPS
hemisphere. In this case, the
contralesional nondominant
hand develops alien hand
findings due to the release PMC PMC
by disinhibition of the
reaching and grasping CC
behaviors driven from the
nondominant PLPS

PLPS PLPS

LH RH

Alien Hand Syndrome,

Fig. 4 The Dominant LEFT RIGHT
Frontal Variant of AHS. HAND HAND
Theoretical explanatory
model for the alien
behaviors observed in the
frontal variant associated
with damage to the AMPS AMPS
of the dominant
hemisphere. In this case, the
contralesional dominant
hand develops alien hand
findings due to the release PMC PMC
by disinhibition of the
reaching and grasping CC
behaviors driven from the
dominant PLPS. In
addition, spontaneous
expressive language
PLPS PLPS
initiation is impaired due to
the role of the AMPS of the
dominant hemisphere in the
initiation of propositional
verbal output LH RH

presentation of external objects commonly encoun- Not only should the verbal reports of the patient be
tered in daily activities. A phenomenological noted but also the associated affect. The limb
approach to assessing and documenting the motor should be evaluated for evidence of a grasp reflex
behavior and linking it to introspective first-person with both tactile and visual stimulation. The ability
report of the patient’s own experience is essential. to release objects that have been grasped should
128 Alien Hand Syndrome

Alien Hand Syndrome,

Fig. 5 The Non-dominant LEFT RIGHT
Posterior Variant of AHS. HAND HAND
Theoretical explanatory
model for the alien
behaviors observed in the
posterior variant associated
with damage to the PLPS of AMPS AMPS
the nondominant
hemisphere. In this case, the
contralesional nondominant
hand develops alien hand
findings due to the release PMC PMC
by disinhibition of
behaviors driven from the CC
nondominant AMPS

PLPS

LH RH

Alien Hand Syndrome,

Fig. 6 The Dominant LEFT RIGHT
Posterior Variant of AHS. HAND HAND
Theoretical explanatory
model for the alien
behaviors observed in the
posterior variant associated
with damage to the PLPS of AMPS AMPS
the dominant hemisphere.
In this case, the
contralesional dominant
hand develops alien hand
findings due to the release PMC PMC
by disinhibition of
behaviors driven from the CC
dominant AMPS

PLPS

LH RH

also be assessed. Evaluation for callosal apraxia the affected limb should be completed as well as
and impairment of interhemispheric transfer of assessment for hemi-inattention. Evidence of an
information should be included. When the poste- avoidant tendency to withdraw the limb from tactile
rior variant of AHS is suspected, a visual field and visual stimulation should also be elicited and
assessment and careful sensory examination of noted when present.
Alien Hand Syndrome 129

Treatment possible to develop improved participation of

ipsilateral hemispheric premotor mechanisms by
There is no definitive specific treatment for AHS but engaging the patient in coordinated bimanual A
a number of different rehabilitative approaches have activities that necessitate cooperative coherent
been described. Furthermore, in the presence of coordinative mechanisms within residual intact
unilateral damage within a single cerebral hemi- components of the motor control systems in both
sphere, there is often a gradual reduction in the hemispheres.
frequency of alien behaviors observed over time
and a gradual restoration of normal voluntary con-
trol over the affected hand. This suggests that Cross-References
neuroplasticity in the bihemispheric and subcortical
brain systems involved in voluntary movement pro-
▶ Anterior Cingulate Cortex
duction can serve to reestablish functional connec- ▶ Apraxia
tion between the executive production process and
▶ Corpus Callosum
the internal self-generation and volitional registra-
▶ Environmental Dependency
tion process. Exactly how this may occur is not well ▶ Movement Disorders
understood but could involve a reorganization
▶ Utilization Behavior
within residual elements of the intrahemispheric
premotor systems both at the cortical and subcortical
levels. In addition, some degree of expanded partic-
References and Readings
ipation of the intact ipsilateral hemisphere may be
involved in the recovery process by extending ipsi- Assal, F., Schwartz, S., & Vuilleumier, P. (2007). Moving
lateral motor projections and influence. with or without will: Functional neural correlates of
Different strategies can be used to reduce the alien hand syndrome. Annals of Neurology, 62,
301–306.
interference of the alien hand behavior in the Bakheit, A. M., Brennan, A., Gan, P., Green, H., &
ongoing coherent controlled functional actions Roberts, S. (n.d.). Anarchic hand syndrome following
of everyday life being performed by the patient. resection of a frontal lobe tumor. Neurocase, 19,
In the frontal variant, an object such as a cane can 36–40.
Biran, I., & Chatterjee, A. (2004). Alien hand syndrome.
be placed in the grip of the alien hand so that it
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does not reach out to grasp onto other objects, thus Brugger, F., Galovic, M., Weder, B. J., & Kägi, G. (2015).
impeding the patient’s forward progress during Supplementary motor complex and disturbed motor
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patients after anterior cerebral artery syndrome. Fron-
of the limb is developed by training the patient to
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moving the alien hand to contact a specific object frontiersin.org/article/10.3389/fneur.2015.00209/full.
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130 Allele

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Neuropsychologia, 43, 75–88. tremorjournal.org/index.php/tremor/article/view/241
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masturbation as a manifestation of stroke-related alien
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Rehabilitation, 79, 395–398.
Pack, B. C., Stewart, K. J., Diamond, P. T., & Gate, S. D.
Allele is an alternate form of a gene, which is the
(2002). Posterior-variant alien hand syndrome: Clinical
features and response to rehabilitation. Disability and basic unit of inheritance. A gene is located at a
Rehabilitation, 24, 817–818. particular site on the chromosome and can have
Pynn, L. K., & DeSouza, J. E. X. (2013). The function of several alleles for that locus. For example, A, B,
efference copy signals: Implications for symptoms of
and O are different alleles for the ABO blood-type
schizophrenia. Vision Research, 76, 124–133.
Romano, D., Sedda, A., Dell’aquila, R., Dalla Costa, D., marker locus of a gene. Alleles greatly influence
Beretta, G., Maravita, A., & Bottini, G. (2014). Con- the expression of physical and behavioral pheno-
trolling the alien hand through the mirror box. types or traits such as eye color. For instance, the
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Other Hyperkinetic Movements, 4, 241. https://doi.org/ The APoE gene has three common alleles: epsilon
Allokinesia 131

2, epsilon 3, and epsilon 4. There is some evi- correctly but identify it as being applied to the
dence that carriers of the APoE epsilon 4 allele are comparable area on the opposite (unaffected) side
at a greater risk for the development of of the body. In some instances the stimulus may A
Alzheimer’s disease. In contrast, the APoE epsi- be perceived as being on the same side of the
lon 3 allele has been suggested as a “protective” body to which it was applied, but displaced sig-
factor in the development of Alzheimer’s disease nificantly from the point of the actual stimulation
(Plomin et al. 2003). (usually toward the midline). When present, this
phenomenon likely results from post-rolandic
(parietal) lesions of the right rather than the left
Cross-References hemisphere. More rarely it has been associated
with brainstem lesions.
▶ Alzheimer’s Disease
▶ Apolipoprotein E
▶ Chromosome Cross-References
▶ Deoxyribonucleic Acid (DNA)
▶ Gene ▶ Asomatognosia
▶ Phenotype

References and Readings Allokinesia

Plomin, R., Defries, J. C., Craig, W., & McGuffin, P. Douglas I. Katz
(2003). Behavioral genetics in the postgenomic era. Department of Neurology, Boston University
Washington, DC: American Psychological School of Medicine, Braintree, MA, USA
Association.

Definition

Allesthesia This phenomenon refers to a motor response in the

wrong limb, contralateral to the requested side,
John E. Mendoza sometimes opposite to the direction requested. It
Department of Psychiatry and Neuroscience, can include nonvoluntary, mirror movements.
Tulane Medical School and SE Louisiana
Veterans Healthcare System, New Orleans,
LA, USA Current Knowledge

Allokinesia is often associated with neglect syn-

Definition dromes, usually involving damage to the right hemi-
sphere. It is the motor counterpart of allesthesia.
Misperception of the location of a stimulus. Typically, a patient moves the right limb in response
Although it can occur in other modalities, it is to a request to move the left limb or moves toward
most commonly elicited by tactile stimulation the right, away from the neglected side, when asked
and is often seen in the presence of other symp- to move toward the neglected side. In animal models,
toms of unilateral asomatognosia. If a tactual the phenomena has been associated with frontal,
stimulus is applied to the side of the body contra- arcuate gyrus lesions (Heilman et al. 1995) and
lateral to a hemispheric lesion, the allesthetic disconnections of frontal and posterior parietal corti-
patient may perceive the nature of the stimulus ces (Burcham et al. 1997).
132 Alpha Rhythm

Cross-References visual cortex and are associated with feelings of

calmness and relaxation. Alpha waves increase
▶ Allesthesia when eyes are closed and during meditation and
▶ Neglect Syndrome are associated with creativity and mental
coordination.
After sustained wakefulness and during the
References and Readings transition from waking to sleeping when the
ability to respond to external stimuli ceases,
Burcham, K. J., Corwin, J. V., Stoll, M. L., & Reep, R. L. upper alpha power decreases, whereas theta
(1997). Disconnection of medial agranular and poste-
increases.
rior parietal cortex produces multimodal neglect in rats.
Behavioural Brain Research, 86(1), 41–47. It is suggested that the encoding of new infor-
Heilman, K. M., Valenstein, E., Day, A., & Watson, mation is reflected by theta oscillations in
R. (1995). Frontal lobe neglect in monkeys. Neurology, hippocampo-cortical feedback loops, whereas
45(6), 1205–1210.
search and retrieval processes in (semantic)
long-term memory are reflected by upper alpha
oscillations in thalamocortical feedback loops.
Alpha Rhythm The neuronal currents resulting from spontane-
ous alpha wave activity have been shown to gen-
Cindy B. Ivanhoe1 and Ana Durand Sanchez2 erate the largest extracranial magnetic fields. An
1
Neurorehabilitation Specialists Baylor College important application of this knowledge is the use
of Medicine, The Institute for Rehabilitation and of eye closure as a way to modulate alpha wave
Research, Houston, TX, USA reactivity. There is technology that allows para-
2
Physical Medicine and Rehabilitation, Baylor lyzed individuals to operate hand-free controls
College of Medicine, Houston, TX, USA with the use of eye closure.

Synonyms See Also

Alpha waves; Berger’s waves ▶ Electroencephalography

Definition
References and Readings
Normal electromagnetic oscillations produced by Bragatti, J. A., De Moura Cordova, N., Rossato, R., &
the brain when in a state of relaxation. They are in Bianchin, M. M. (2007). Alpha coma and locked-in
the frequency range of 8–12 Hz and arise from syndrome. Journal of Clinical Neurophysiology,
synchronous and coherent electrical activity of the 24(3), 308.
Craig, A., McIsaac, P., Tran, Y., Kirkup, L., & Searle,
thalamic pacemaker cells in the human brain. Also A. (1999). Alpha wave reactivity following eye closure:
called Berger’s waves. A potential method of remote hands free control for the
disabled. Technology and Disability, 10(3), 187–194.
Klimesch, W. (1999). EEG alpha and theta oscillations reflect
cognitive and memory performance: A review and anal-
Current Knowledge ysis. Brain Research Reviews, 29(2–3), 169–195.
Konn, D., Leach, S., Gowland, P., & Bowtell, R. (2004).
Alpha waves are believed to arise from the white Initial attempts at directly detecting alpha wave activity
in the brain using MRI. Magnetic Resonance Imaging,
matter of the occipital lobes. They increase during
22(10), 1413–1427.
periods of relaxation with eyes closed. Alpha Min, B. K., Busch, N. A., Debener, S., Kranczioch, C.,
waves are thought to represent activity in the Hansimayr, S., Engel, A. K., et al. (2007). The best of
Alternate Test Forms 133

both worlds: Phase reset of human EEG alpha Side Effects

activity and additive power contribute to ERP gener-
ation. International Journal of Psychophysiology,
65(1), 58–68. Serious A
Respiratory depression, hepatic dysfunction
(rare), renal dysfunction and blood dyscrasias,
grand mal seizures
Alprazolam
Common
1
John C. Courtney and Efrain Antonio Sedation, fatigue, depression, dizziness, memory
Gonzalez2,3 problems, disinhibition, confusion, ataxia, slurred
1
Socorro Mental Health, Presbyterian Medical speech
Services, Socorro, NM, USA
2
College of Psychology, Nova Southeastern
University, Fort Lauderdale, FL, USA References and Readings
3
Utah State University, Logan, UT, USA
Physicians’ Desk Reference (71st ed.). (2017). Montvale:
Thomson PDR.
Generic Name Stahl, S. M. (2007). Essential psychopharmacology: The
prescriber’s guide (2nd ed.). New York: Cambridge
University Press.
Alprazolam
Additional Information
Brand Name Drug Interaction Effects: http://www.drugs.com/drug_
Xanax, Xanax XR, Niravam interactions.html
Drug Molecule Images: http://www.worldofmolecules.
com/drugs/
Class Free Drug Online and PDA Software.: www.medscape.
Antianxiety agents, anxiolytics, benzodiazepines com
Free Drug Online and PDA Software: www.epocrates.com
Gene-Based Estimate of Drug interactions: http://mhc.dayt
ondcs.com:8080/cgibin/ddiD4?ver=4&task=getDrug
Proposed Mechanism(s) of Action List
Pill Identification.: http://www.drugs.com/pill_identifica
Binds to benzodiazepine receptors at the tion.html
GABA-A ligand-gated channel, thus allowing
for neuronal hyperpolarization. Benzodiazepines
enhance the inhibitory action of GABA via
boosted chloride conductance. Alternate Test Forms

Grant L. Iverson1 and Kyle E. Ferguson2

1
Indication Department of Psychiatry, British Columbia
Mental Health and Addictions, University of
Generalized anxiety and panic disorder British Columbia, Vancouver, BC, Canada
2
University of British Columbia,
Vancouver, BC, Canada
Off-Label Use

Other anxiety disorders, irritable bowel syn- Synonyms

drome, insomnia, adjunctive treatment in mania
and psychosis, premenstrual dysphoric disorder. Equivalent forms; Parallel forms
134 Alternate Test Forms

Definition correspondence between the two sets of scores

(Petersen 2008). Moreover, their means and
Alternate test forms are designed to avoid or variances would also be very similar. Therefore,
reduce content- or item-specific practice effects the coefficient of equivalence should be high
that are associated with repeated administrations (i.e., >0.80; Sattler 2001). Of course, though
of the same neuropsychological test(s) (Fastenau they appear similar, the two forms are often not
et al. 2002). Examination of the manuals for many of equivalent difficulty, or otherwise parallel.
intellectual and neuropsychological tests illus- Thus, in the absence of employing special
trates that practice effects are common, especially empirical procedures like test equating, which
over brief retest intervals (e.g., days or weeks). “fine-tune the test construction process”
Regarding test construction, alternate test forms (Petersen 2008, p. 99), the two forms cannot be
should include the same number of items, and used interchangeably.
the items should be of equivalent difficulty. More- Test equating refers to a class of statistical
over, the test instructions, time limits, examples, concepts and procedures that adjust for differ-
and format should be identical to the original ences in difficulty level on alternate test forms
instrument developed during standardization, (please note that these procedures adjust for
to reduce measurement error (Jackson 2009). differences in test difficulty, not differences in
Of course, measurement error can never be elim- content (see Kolen and Brennan 2004)), so that
inated. For example, content-sampling error and the forms can be used interchangeably (see Kolen
time-sampling error – inherent in all test-retest and Brennan 2004, pp. 2–3, for a discussion
paradigms – are always concerns in developing of this procedure; White and Stern 2003). Test
alternate test forms (Strauss et al. 2006). Addi- equating establishes, empirically, “a relationship
tionally, alternate test forms cannot control other between raw scores on two test forms that can then
factors such as positive carry-over effect (i.e., be used to express the scores on one form in terms
developing better test-taking strategies), familiar- of the scores on the other form” (Petersen et al.
ity with the testing context (i.e., novelty effects), 1989, p. 242; see also Dorans and Holland 2000;
performance anxiety, and regression to the mean, Petersen 2008). Common types of test equating
among others (Busch et al. 2006; Salinsky et al. are Item Response Theory (IRT), linear, and
2001). This might, to some extent, explain why equipercentile (Ormea et al. 2001).
some studies show that alternate test forms reduce The Neuropsychological Assessment Battery
or eliminate practice effects, whereas other studies (Stern and White 2003), Hopkins Verbal Learning
do not. Test-Revised (Brandt and Benedict 2001), Brief
Visuospatial Memory Test-Revised (Benedict
2001), and Wide Range Achievement Test-
Current Knowledge Fourth Edition (Wilkinson and Robertson
2006) are several examples of tests (or test
Alternate test forms are developed by administer- batteries) that provide alternate test forms.
ing an equivalent test – comprising items of sim- With the above caveats in mind, alternate test
ilar difficulty – to the same group of examinees forms can be useful in serial neuropsychological
or normative sample, shortly before or after being evaluations.
administered the original test form. Scores from
the two forms are then correlated (This is called
alternate form reliability, or equivalent or par- Cross-References
allel form reliability), which yields a reliability
coefficient – otherwise known as the coefficient ▶ Item Response Theory
of equivalence. If the original and alternate ▶ Reliable Change Index
test forms are truly equivalent, then there ▶ Test Construction
would be (theoretically) a one-to-one ▶ Test Reliability
Alzheimer, Alois (1864–1915) 135

References and Readings

Alzheimer, Alois (1864–1915)
Benedict, R. H. B. (2001). Brief visuospatial memory test – A
Revised. Odessa: Psychological Assessment Katherine S. McClellan1 and Anna Bacon Moore2
Resources. 1
Rehabilitation Research and Development
Brandt, J., & Benedict, R. H. B. (2001). Hopkins verbal
learning test-revised. Odessa: Psychological Center, Atlanta Veterans Affairs Medical Center,
Assessment Resources. Decatur, GA, USA
Busch, R. M., Chelune, G. J., & Suchy, Y. (2006). 2
Department of Rehabilitation Medicine, Division
Using norms in neuropsychological assessment. In
of Neuropsychology, Emory University School of
D. K. Attix & K. A. Welsh-Bohmer (Eds.), Geriatric
neuropsychology: Assessment and intervention Medicine, Atlanta, GA, USA
(pp. 133–157). New York: Guilford.
Dorans, N. J., & Holland, P. W. (2000). Population invari-
ance and equitability of tests: Basic theory and the
linear case. Journal of Educational Measurement, 37,
Major Appointments
281–306.
Fastenau, P. S., Hankins, W. T., McGinnis, C. M., Moy, T., • Intern – Mental Asylum at Frankfurt am Main,
& Richard, M. (2002). Effects of alternate forms on 1888–1895
retest effects in clinical testing. Journal of International
• Senior Physician – Mental Asylum at Frankfurt
Neuropsychological Society, 7(2), 151.
Jackson, S. L. (2009). Research methods and statistics: am Main, 1895–1903
A critical thinking approach (3rd ed.). Belmont: • Researcher – Royal Psychiatric Clinic and Dis-
Wadsworth Cengage Learning. trict Mental Asylum, Munich, 1903–1912
Kolen, M. J., & Brennan, R. L. (2004). Test equating,
• Assistant Professor – Ludwig-Maximilian
scaling, and linking: Methods and practices (2nd ed.).
New York: Springer. University, Munich, 1904–1912
Ormea, D., Reeb, M. J., & Riouxc, P. (2001). Premorbid • Chief Physician – Royal Psychiatric Clinic and
IQ estimates from a multiple aptitude test battery: District Mental Asylum, Munich, 1906–1909
Regression vs. equating. Archives of Clinical
• Professor of Psychiatry – Psychiatry Clinic of
Neuropsychology, 16, 679–688.
Petersen, N. S. (2008). A discussion of population invari- Silesian Friedrich-Wilhelm University,
ance of equating. Applied Psychological Measurement, Breslau, 1912–1915
32, 98–101.
Petersen, N. S., Kolen, M. J., & Hoover, H. D. (1989).
Scaling, norming, and equating. In R. L. Linn (Ed.), Major Honors and Awards
Educational measurement (3rd ed., pp. 221–262).
New York: Macmillan.
Salinsky, M. C., Storzbach, D., Dodrill, C. B., &
• Extraordinary Professor, Ludwig-Maximilian
Binder, L. M. (2001). Test-retest bias, reliability, University (1909)
and regression equations for neuropsychological mea- • Geheimer Ministerialrat (Cabinet Councillor)
sures repeated over a 12–16-week period. Journal (1915)
of the International Neuropsychological Society,
7(5), 597–605.
Sattler, J. M. (2001). Assessment of children: Cognitive
Landmark Clinical, Scientific, and
applications (4th ed.). San Diego: Jerome M. Sattler.
Stern, R. A., & White, T. (2003). Neuropsychological Professional Contributions
assessment battery. Lutz: Psychological Assessment
Resources. • Alois Alzheimer was both an excellent clini-
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A
cian and a notable researcher. He is best
compendium of neuropsychological tests: Administra-
tion, norms, and commentary (3rd ed.). New York: remembered for being the first to definitively
Oxford University Press. describe the symptoms and cerebral lesions of
White, T., & Stern, R. A. (2003). Neuropsychological the disease now known as Alzheimer’s disease.
assessment battery: Psychometric and technical
Nonetheless, his contributions to science and
manual. Lutz: Psychological Assessment Resources.
Wilkinson, G. S., & Robertson, G. J. (2006). Wide range medicine did not begin, nor do they end, there.
achievement test (4th ed.). Lutz: Psychological He was one of the leaders of the movement
Assessment Resources. to implement the nonrestraint principle
136 Alzheimer, Alois (1864–1915)

(explained more fully below) in asylums. His the fall of the following year, Alois left to
neurohistological work advanced the idea that spend his winter semester at the Eberhard Karls
psychiatric diseases were biological in origin. University of Tübingen. He returned in 1887 to
And, through his roles as both doctor and sci- the Würzburg Anatomical Institute’s department
entist, he contributed to our understanding of a of microscopy to write his doctoral thesis, “On
variety of conditions such as cerebral athero- the Earwax Glands.” The intricate figures he
sclerosis, alcoholism, and general paresis. presented in the paper, as in all his papers, were
proof of how scrupulously he conducted his
research and clinical work. With the completion
Short Biography of his thesis, Alois Alzheimer received his doctor
of medicine degree. He passed the state medical
In the German municipality Marktbreit, Alois examination and was awarded a license to prac-
Alzheimer was born on June 14, 1864, to Eduard tice medicine in 1888.
and Theresia Alzheimer. Eduard, a Royal Notary, Shortly thereafter, he became a personal phy-
provided his family with a comfortable upbring- sician to a mentally ill woman and traveled with
ing. Although Alois had only an older brother her for 5 months. Emil Sioli, the director of the
when he was born, six more siblings followed Municipal Asylum for the Insane and Epileptic in
him. Alois spent the first 4 years of his education Frankfurt am Main had advertized for an intern,
at Catholic school in Marktbreit, until his family specifically hoping for a competent doctor who
left the area to find a new home with superior was also adept with a microscope. Upon his
educational opportunities for the children. The return, the 24-year-old Dr. Alzheimer was hired
family’s chosen residence was in Aschaffenburg, immediately. Dr. Franz Nissl also was hired as
and in 1874, Alois moved there in order to study senior physician for the asylum. Nissl not only
at the Royal Humanistic Gymnasium. Alois became one of Alzheimer’s closest friends but
completed his high school degree in 1883 with also taught him a powerful staining technique for
excellent grades. He then decided to study med- highlighting neuronal cell bodies (the Nissl stain),
icine because of his aptitude and fondness for the which helped Alzheimer achieve success in his
natural sciences, as well as a sense of duty to histological studies. Sioli’s main goal for the asy-
mankind. lum was to fully employ the nonrestraint princi-
He enrolled at the Royal Friedrich-Wilhelm ple. Alzheimer was particularly skilled at gaining
University in Berlin for the 1883–1884 winter the trust of patients through conversation, and he
semester. In his psychiatry lecture there, he often documented these conversations. The dia-
learned of John Conolly’s nonrestraint principle. logues often were central to diagnosing a patient
Also called open treatment, the nonrestraint prin- and even more so to research. His talent in clinical
ciple proposed the novel view that the mentally ill interviewing was such that clinicians who later
should be treated with a minimal amount of phys- read his notes had sufficient information to eval-
ical constraint. Although Berlin was the medical uate his opinions and to make their own diagno-
capital of Germany, Alois disliked Berlin and its ses. Alzheimer drew on his microscopy and
distance from his family. Therefore, he was forensic psychiatry training, to do histological
transferred to the University of Würzburg investigations into the physical origins of psychi-
(Lower Franconia, Germany), where his older atric disorder. In Frankfurt, his topics of study
brother was studying. As an aside, due to the included epilepsy, senile dementia, criminal
influence of his older brother, Alois joined and minds, and a variety of psychoses. He established
later held several officer positions in the Franco- himself as a well-rounded physician by publishing
nian Corps. His histology professor, Alfred von papers on a wide variety of topics. Aside from his
Kölliker, gave him his first experience with duties as a physician and researcher, he also
microscopes and staining techniques, which appeared as an expert before courts and presented
lead to his passion for forensic psychiatry. In at many scientific meetings. While at Frankfurt,
Alzheimer, Alois (1864–1915) 137

Alzheimer became an expert on general paresis, was rejected, he joined Nissl in Heidelberg in
which later became the subject of his postdoctoral 1903 and went to work for Emil Kraepelin. The
thesis. group he joined there was an international team of A
In Algeria, a personal physician who had been researchers. Later that same year, Kraepelin was
traveling with a man suffering from general pare- named director of the Royal Psychiatric Clinic
sis sent a telegram to Alzheimer in 1892 to request and the District Mental Asylum in Munich.
that he treat the worsening patient. Alzheimer Alzheimer followed him, but was not paid in
obliged and went to North Africa. He intended Munich due to the lack of a position for him and
to bring the patient back to his hospital in Ger- also his desire to manage his own time. Despite
many, but the patient died before reaching Ger- his absence from Frankfurt, Alzheimer still
many, leaving his wife, Cecilie, a widow. received updates on Auguste D.
Alzheimer and Cecilie became close friends, and By this point, Alzheimer’s thesis on general
eventually the widow asked him to marry her. paresis was finished, but because he moved
They were married in April 1894 in the registry twice in such a short time, he had not yet turned
office of Frankfurt. Because Cecilie was Jewish, it in. Alzheimer submitted his postdoctoral thesis
she had to convert to Catholicism before the two to the Ludwig-Maximilian University in Munich
could be married by the church in February 1895. with the hopes of gaining associate professorship.
On March 10, 1895, their first child, Gertrud, was In it, he published not only his clinical dialogues
born, and Dr. Nissl was chosen to be her godfa- but also his postmortem histological findings.
ther. But Nissl soon moved to work with Emil With this paper, he asserted that histological
Kraepelin in Heidelberg. Nissl’s departure created examinations could definitively show the pres-
room for Alzheimer to be promoted to senior ence of general paresis. Until then, few doctors
physician within Sioli’s asylum. Also that year, suspected that syphilis was a cause of general
to lessen the overcrowding of the main hospital, a paresis, but shortly thereafter the link between
new branch asylum opened. With this addition, the two was found. His work was surpassed by
Sioli and Alzheimer furthered their goal of fully the discovery of a way to diagnose syphilis, with-
implementing the nonrestraint principle by insti- out resorting to autopsies. In August 1904, he
tuting duration baths rather than isolation. The joined the university’s medical faculty.
asylum became known as a revolutionary clinic, Because of his experience at remodeling the
and it elevated the reputations of all its doctors. Frankfurt clinic, Alzheimer was fundamental in
But above all, in 1901, Alzheimer met the patient finishing the plans for the new Munich clinic. He
who would immortalize his name: Auguste furnished his anatomic laboratory with the best
D. Auguste had been admitted to the asylum equipment and the brightest students – many of
because of delusional and excessively forgetful whom went on to make great contributions to
behavior. Although at admission she was science, including Ugo Cerletti, electrical shocks
disoriented, anxious, and suspicious, over time to generate convulsions; Hans Gerhard
she became unruly and disruptive. Alzheimer Creutzfeldt and Alfons Jakob, Creutzfeldt-Jakob
was particularly intrigued by her case for the disease; Frederic Lewy, Lewy bodies; and others.
duration of her stay in the hospital. Alzheimer was made chief physician in 1906, a
Alzheimer’s second child, Hans, was born in paid position, but also one that took away much of
1896, and his third, Maria, was born in 1900. his time in the laboratory.
However, the lavish lifestyle he had lived with Two topics that consumed Alzheimer in
Cecilie ended when she died in February 1901. Munich were psychiatric symptoms resulting
Alzheimer’s sister, Elisabeth, took over his house- from pathological anatomy and classification of
hold. Though she was strict, she became an inte- mental illnesses by etiology. The latter faced
gral part of the family. Without Cecilie, Alzheimer much opposition from the scientific community.
no longer had a reason to stay in Frankfurt. After Yet, the most opposition he ever faced was his
his application to be director of a regional asylum presentation of the Auguste D. case. Auguste
138 Alzheimer, Alois (1864–1915)

D. had always fascinated Alzheimer. He had paid notice of his kind, yet authoritative presence. In
special attention to her, taking copious notes about 1913, his health forced him to visit a private
their conversations. When he moved away, he still clinic. Though he returned to work, his health had
received updates about her condition, which not improved. This did not impede his ability to
worsened progressively until her death. When make significant contributions to science: in 1913
Auguste D. died in 1906, her files, brain, and he found the syphilis pathogen in the central ner-
spinal cord were sent to Munich. Alzheimer, vous system of a patient with general paresis.
along with his student Gaetano Perusini, immedi- After a long illness, Alois Alzheimer died on
ately began examining the case. In Tübingen, December 19, 1915, from a heart condition and
Alzheimer presented her case in a lecture entitled kidney failure. Though no one immediately took
“On a Peculiar Severe Disease Process of the over his pursuit of an understanding of Alzheimer’s
Cerebral Cortex,” in which he described the disease, people recommenced research on
lesions (now known to be neurofibullary tangles) Alzheimer’s disease cases in the 1950s. Studies of
that he believed caused Auguste’s symptoms. the disease began in earnest after Martin Roth’s
Based on records from the time, his peers did not assertion in the 1960s that Alzheimer’s disease
bother to ask questions, nor were there any com- was the most common cause of senile dementia.
ments about the lecture in the minutes. He later In the 1970s, Robert Katzman further propelled the
published the entire lecture, but still it received surge of interest in Alzheimer’s disease by stating
little attention. He then tasked Perusini to find that it was one of the most widespread diseases.
more patients, similar to Auguste D. in the Since then, the amount of research on Alzheimer’s
clinic. Perusini found four cases and published disease has increased exponentially, resulting in
an article entitled “On Clinically and Histologi- multiple foundations and centers devoted solely to
cally Peculiar Mental Illnesses in Advanced Age.” the disease that Alois Alzheimer’s colleagues con-
Another student of Alzheimer’s, Francesco sidered trivial.
Bonfiglio, found another case of presenile demen-
tia and also published on the disease. Spurred by
Bonfiglio’s paper, Kraepelin included a section on Cross-References
“Alzheimer’s Disease,” in the 1910 edition of his
textbook Clinical Psychiatry. This publication is ▶ Alzheimer’s Dementia
acknowledged as the origin of the term. ▶ Alzheimer’s Disease
Alzheimer himself never referred to it as ▶ Paresis
“Alzheimer’s disease,” though he had later publi-
cations on the disease. Alzheimer decided to
resign his post as chief physician in order to References and Readings
devote more time to research, specifically travel-
ing to study epilepsy. Although he was no longer Alzheimer, A. (1906). Über einen eigenartigen schweren
Erkrankungsprozeb der Hirnrincle. Neurol Central, 25,
employed by Kraepelin, Alzheimer undertook the
1134. (On a peculiarly difficult malady/pathology of
responsibilities of coeditor of Kraepelin’s Journal the cerebral cortex).
of Complete Neurology and Psychiatry. Engstrom, E. (2007). Researching dementia in imperial
Recognition for Alzheimer and the disease car- Germany: Alois Alzheimer and the economies of psy-
chiatric practice. Culture, Medicine and Psychiatry, 31,
rying his name began to spread. In 1912, the Sile-
405–413.
sian Friedrich-Wilhelm University in Breslau asked Graeber, M., Kösel, S., Egensperger, R., Banati, R., Müller,
him to join their faculty as a full professor of psy- U., Bise, K., et al. (1997). Rediscovery of the case
chiatry. During the move to Breslau, Alzheimer fell described by Alois Alzheimer in 1911: Historical and
molecular genetic analysis. Neurogenetics, 1(73), 80.
ill, but nevertheless assumed his duties with vivac- Lage, J. (2006). 100 years of Alzheimer’s disease
ity. His patients and coworkers, including Georg (1906–2006). Journal of Alzheimer’s Disease, 9,
Stertz, Ottfried Förster, and Ludwig Mann, took 15–26.
Alzheimer’s Dementia 139

Maurer, K., & Maurer, U. (1998). Alzheimer: The life of a of sufficient severity to cause impairment in social
physician and the career of a disease. New York: or occupational functioning. Recent changes to the
Columbia University Press.
Morris, R., & Salmon, D. (2007). The centennial of Diagnostic and Statistical Manual of Mental Dis- A
Alzheimer’s disease and the publication of “Über eine orders, Fifth Edition (DSM-V), allow a diagnosis of
eigenartige Erkankung der Hirnrinde” by Alöis AD under either major or mild neurocognitive dis-
Alzheimer. Cortex, 43, 821–825. order. The criteria for major neurocognitive disor-
Small, D., & Cappai, R. (2006). Alois Alzheimer and
Alzheimer’s disease: A centennial perspective. Journal der state that cognitive decline must be significant
of Neurochemistry, 99, 708–710. and interfere with daily activities (e.g., paying bills,
Snyder, P., & Pearn, A. (2007). Historical note on Darwin’s managing household chores, or shopping), whereas
consideration of early-onset dementia in older persons, mild neurocognitive disorder represents “modest”
thirty-six years before Alzheimer’s initial case report.
Alzheimer’s & Dementia, 3, 137–142. decline that does not necessarily interfere with
Zilka, N., & Novak, M. (2006). The tangled story of Alois accomplishing daily tasks. A diagnosis of mild
Alzheimer. Bratislavské Lekárske Listy, 107, 343–345. neurocognitive disorder due to Alzheimer’s disease
can be made if the condition has not yet progressed
to interfere with daily functioning (American Psy-
chiatric Association 2013). Diagnoses of AD are
Alzheimer’s Dementia based on the history and presentation of clinical
symptoms, evidence of cognitive impairment, and
Chelsea Sanders1, Joshua M. Matyi1, the exclusion of other causes of dementia such as
JoAnn Tschanz1,2 and Aaron Andersen3 stroke, metabolic disorders, or other conditions that
1
Department of Psychology, Utah State may account for the cognitive impairment. A diag-
University, Logan, UT, USA nosis of definite AD is based upon postmortem
2
Center for Epidemiologic Studies, Utah State neuropathological analysis and is made when
University, Logan, UT, USA there are sufficient numbers of senile plaques and
3
Utah State University, Logan, UT, USA neurofibrillary tangles in specific brain regions.

Synonyms Categorization

Alzheimer’s disease; Early-onset Alzheimer’s dis- AD may be categorized according to onset age,
ease; Familial Alzheimer’s disease; Late-onset family history, or presenting clinical features. Age
Alzheimer’s disease; Senile dementia of the categories distinguish between early (occurring
Alzheimer’s type before age 65) and late (occurring at age 65 and
older) onset. Classifications based on family his-
tory (familial AD vs. sporadic AD) distinguish
Short Description or Definition AD forms that show high heritability. Familial
AD is rare, generally of early onset, and has
One of the leading causes of dementia in late life, been associated with mutations in the APP gene
Alzheimer’s dementia (AD) is a progressive neuro- on chromosome 21, presenilin 1 gene on chromo-
degenerative disorder characterized by a gradual some 14, and presenilin 2 gene on chromosome 1
onset and progressive course, affecting memory (Hardy 2003). Its transmission resembles an auto-
and other cognitive domains. Traditionally, a diag- somal dominant pattern (Morris and Nagy 2004).
nosis of AD is made if the cognitive impairments do AD has also been classified according to the
not occur exclusively in the context of other condi- clinical presentation of symptoms. Its most com-
tions that affect cognitive status (e.g., delirium, mon presentation involves early and significant
depression, medication side effects, thyroid mal- memory impairment. Variants to this presentation
function, or certain vitamin deficiencies) and are have been reported in the literature and include a
140 Alzheimer’s Dementia

visual (posterior) form with significant impair- education (possibly due to less neural reserve),
ment in higher-level processing of visual stimuli, female sex (even after accounting for differential
an aphasic form with significant language survival), history of head trauma, and cardiovas-
involvement, and a frontal form with prominent cular factors (“2015 Alzheimer’s” 2015;
impairment of executive functions. At autopsy, Tschanz et al. 2013). Well-established vascular
these variants usually exhibit AD neuropathology risk factors include hypertension, high choles-
in brain regions typically involved in the specific terol, and diabetes (Tschanz et al. 2013). Some
neuropsychological domain (Grabowski and of these risk factors affect AD risk when occur-
Damasio 2004). ring earlier in the life span. For example, studies
suggest that high blood pressure, high serum
cholesterol, and obesity in midlife increase the
Epidemiology risk of AD later in life (“2015 Alzheimer’s”
2015; Kivipelto et al. 2005). Although inconsis-
AD is the most common cause of dementia in late tent, some studies report treatment with antihy-
life, accounting for 60–80% of all cases (“2015 pertensive medications or cholesterol-lowering
Alzheimer’s” 2015). Current estimates suggest agents reduces risk for AD (Soininen et al.
5.3 million individuals suffer from AD in the 2003). Among potential “protective” factors,
United States, and projections based on popula- data from epidemiological studies suggest a
tion trends suggest an increase to 13.8 million by lower risk of AD among women receiving hor-
2050, including approximately seven million mone replacement therapy (Zandi et al. 2002b;
individuals aged 85 and older (Hebert et al. Kawas et al. 1997). However, a large random-
2013). The overall prevalence of AD is about ized clinical trial of estrogen and estrogen-
11% in individuals age 65 years or older in Amer- þprogesterone in elderly women suggested an
ica and increases with age to include 32% of increase in all-cause dementia in those receiving
persons aged 85 and older (Hebert et al. 2013). the combination hormone treatment. Thus hor-
Incidence rates also exhibit an age-related mone therapy is not recommended for cognitive
increase. For example, of the 473,000 individuals health (Malaspina et al. 2008). Other modifiable
that are projected to develop AD in 2015, just risk factors that have shown potential benefits
61,000 new cases represent those aged 65 to 74, for cognitive health and reduced risk for demen-
while 172,000 new cases are among those age 75 tia include diet, nutrients, and nutrient supple-
to 84, and the final 240,000 cases are among ments such as antioxidant vitamins, omega-3
individuals aged 85 and older (the “oldest-old”) fatty acid, medications such as nonsteroidal
(“2015 Alzheimer’s” 2015; Hebert et al. 2013). anti-inflammatory agents, and lifestyle practices
Studies report differing patterns of AD prevalence such as physical activity and cognitive and
and incidence at the upper end of the life span, social engagement (Scarmeas et al. 2009; Zandi
with some reporting a plateau at very old ages (age et al. 2002a; Wengreen et al. 2009; Morris 2012;
90 or 100; Mendez and Cummings 2003). Addi- Engelhart et al. 2002; Norton et al. 2012; Wang
tionally, research demonstrates racial differences et al. 2012).
in the prevalence of dementia with higher rates
among Black and Latino populations. Some of
these differences are attributed to differences in Natural History, Prognostic Factors,
cardiovascular risk (“2015 Alzheimer’s” 2015). Outcomes

Risk Factors The clinical course of AD is usually one of the

Increasing age is among the strongest risk factor gradual onset of symptoms with progressive
for AD. Other risk factors include the e4 allele of decline. Many scientists believe the disease pro-
the apolipoprotein E (APOE) gene, positive cess starts in the brain decades before overt symp-
family history (also in sporadic AD), low toms emerge. A preclinical phase, characterized
Alzheimer’s Dementia 141

primarily by episodic memory deficits, heralds the sadness, progressing to delusions and, in some
onset of symptoms. This stage, also referred to as individuals, more severe psychiatric distur-
mild cognitive impairment (MCI), lasts approxi- bances such as hallucinations and agitation. In A
mately 1–3 years. Progression to dementia is end stages, there is severe deterioration of all
characterized by increasing severity of cognitive cognitive functions, speech is generally
impairment with severe memory deficits, visuo- unintelligible, and motor rigidity and urinary
spatial impairment, and other perceptual distur- and fecal incontinence are present. Death may
bances. Language impairment begins with mild occur as the result of other causes such as pneu-
naming difficulties and circumlocutory speech monia or infections (Mendez and Cummings
but progresses to include comprehension defi- 2003). On postmortem exam, the brain is char-
cits. Apraxia (difficulty performing learned acterized by generalized atrophy and sulcal and
motor tasks in the absence of impairment in ventricular enlargement. Figure 1a and b display
primary motor or sensory functions) and gross atrophy of an AD brain compared with a
impaired executive functions and computational brain from a cognitively normal elderly individ-
ability are also apparent. Behavioral changes are ual. Figure 2 displays a coronal section of an AD
common with indifference, irritability, and brain at the level of the hippocampus.

Alzheimer’s Dementia,
Fig. 1 (a and b) Displays
the brains from a
cognitively normal elderly
individual and an individual
who suffered from
advanced AD, respectively.
Note the severe atrophy
apparent in the AD brain
(Photo courtesy of Christine
Hulette, M.D., Bryan
Alzheimer Disease
Research Center, Duke
University. Used by
permission of Elsevier
Limited)
142 Alzheimer’s Dementia

Alzheimer’s Dementia,
Fig. 2 Displays atrophy in
AD in this coronal section
including the hippocampi.
Note dilated lateral
ventricles and loss of
inferior temporal mass are
present bilaterally (Photo
courtesy of Steven S. Chin,
M.D., Ph.D., University of
Utah Health Sciences
Center)

The duration of the entire disease course from unaffected. In early stages, standardized testing
MCI to death is highly variable. Mean survival with word lists may reveal relative preservation
estimates from symptom onset range from 4 to of immediate or working memory but impairment
8 years, but some studies have reported consider- in delayed (free) recall. There is usually some
ably longer duration of 20 years (“2015 benefit from cuing or recognition procedures.
Alzheimer’s” 2015). Regardless of duration, one With progression, cuing is no longer helpful, and
study suggests that individuals will spend the remote recall is affected. Implicit memory may be
majority of their total years with AD in the most relatively spared as patients show evidence of
severe stage (Arrighi et al. 2010). More rapid rate learning on priming or procedural motor tasks.
of disease progression has been associated with Orientation to time and place is also affected in
early, prominent language impairment, frontal AD (Knopman and Selnes 2003).
features, and extrapyramidal signs (Mendez and Language impairments progress from mild
Cummings 2003). Studies examining risk factors anomia and word finding difficulties in early
of progression after AD onset indicate more rapid stages to include impairment in comprehension
decline of cognitive and functional deficits for and writing. Errors in speech (paraphasias)
females, those with earlier onset ages, and those become more common, and word substitutions
with comorbid vascular risk factors. Alternatively, become progressively less related to the target
use of various vascular treatments and cholines- words. Repetition of speech may be relatively
terase inhibitors has been associated with slower unaffected until late in the disease course (Mendez
rates of decline (Tschanz et al. 2013). and Cummings 2003; Knopman and Selnes
2003). Sensitive to changes in language are tests
of verbal fluency and confrontation naming.
Neuropsychology and Psychology of Visuospatial disturbances may be subtle or non-
Alzheimer’s Dementia existent in the earliest stages of AD. In moderate
and severe stages, impairment may be evident
Neuropsychological Deficits on figure copying tasks or judgment of
The neuropsychology of AD follows the clinical line orientation (Knopman and Selnes 2003).
progression. In early stages, memory is almost Figure 3 displays characteristic examples of
always involved, with specific deficit in learning visuoconstructional impairment in four represen-
new information. Remote memory such as mem- tative patients with AD.
ory for autobiographical or other knowledge- Impaired abstract reasoning, sustained atten-
based systems (semantic memory) is relatively tion, planning, judgment, and problem-solving
Alzheimer’s Dementia 143

Alzheimer’s Dementia, Fig. 3 Displays visuocon- figure (Photographs courtesy of Norman L. Foster, M.D.,
structional impairments in the drawings of four individuals and Angela Y. Wang, Ph.D., Center for Alzheimer’s Care,
with possible or probable AD. The stimulus is the left-most Imaging and Research, University of Utah)

may characterize impairment in executive func- milder ones, raising questions about environmen-
tions. Deficits in executive functions may be dem- tal triggers. Noting the co-occurrence of several
onstrated on tests of verbal fluency, trailmaking, behaviors, some scientists believe these symp-
and set shifting. Tests such as the Rey complex toms are better conceptualized as behavioral syn-
figure and clock drawing may also elicit impair- dromes, with implications for underlying brain
ment in executive functions with poor planning pathology. Several questionnaires are available
and execution of the tasks. Deficits in working for assessing behavioral symptoms, ranging from
memory may be evident on tasks requiring mental a single symptom questionnaire to a large inven-
manipulation or divided attention (Knopman and tory of symptoms. Assessment of behavioral
Selnes 2003). symptoms is particularly important in an AD eval-
Other neurocognitive aspects of AD include uation as their presence may suggest other causes
apraxia and anosognosia. In mild AD, deficits in for dementia.
praxis are not common but emerge later in the
disease course. Assessment of apraxia may
involve pantomiming the execution of a task. Evaluation
Anosognosia or an unawareness of disability is
extremely common (Knopman and Selnes 2003). A thorough dementia work-up is important for
Standardized assessment approaches are few. diagnosing AD or determining the etiology of
Some approaches rely on clinical observation, dementia. Critical elements of an evaluation
noting a discrepancy between self-report of cog- include a detailed clinical history, mental status
nitive impairment and test performance or a dis- and physical exam, and, due to potential inaccu-
crepancy between caregiver and patient report of racies in patient reporting, an interview with a
impairment. reliable informant. Neuropsychological testing,
laboratory, and neuroimaging are important to
Behavioral Symptoms exclude other causes of dementia.
Behavioral changes are extremely common in Neuropsychological testing is especially
AD, with nearly all individuals exhibiting at important in determining severity of cognitive
least one symptom at some point over the disease decline and developing a differential diagnosis
course. Among the most common of these between dementia and cognitive deficits due to
changes is apathy, characterized by a lack of inter- other conditions. Neuropsychologists may admin-
est and indifference. Anxiety, irritability, and ister a battery of standardized assessments of
depression are also common, as are delusions. memory, visuospatial functioning, language, and
Some patients may exhibit hallucinations, and executive functions and estimate a discrepancy
particularly challenging for caregivers and family between current and premorbid functioning
are disruptive behaviors such as agitation and based on normative data associated with those
aggression. The course of behavioral symptoms tests. Alternatively, many neuropsychologists
is variable, with severe episodes alternating with may administer several follow-up examinations
144 Alzheimer’s Dementia

to identify patterns of cognitive change over time consistent pattern in early AD. Figures 4, 5, and 6
in establishing a diagnosis. Psychometric proper- display the pattern of glucose hypometabolism in
ties of these assessments as well as reliable change MCI and AD compared with a cognitively normal
methods should be considered when determining elderly individual. Additional examination of bio-
the validity and reliability of results. While prac- markers, such as sampling cerebrospinal fluid for
tice effects are generally considered problematic, tau and amyloid-B42 assays, may be helpful as
recent research has elucidated the utility of prac- supplemental procedures for complex cases
tice effects for prognosis and differential diagno- (Mendez and Cummings 2003).
sis (Chelune and Duff 2013). All acquired data are used in differential diag-
Laboratory testing may include a blood count, nosis under the DSM-V and National Institute of
routine chemistries, thyroid function, and B12 Neurological and Communicative Disorders and
levels. Neuroimaging with MRI or CT may reveal Stroke and the Alzheimer’s Disease and Related
generalized cerebral atrophy with associated Disorders Association (NINCDS-ADRDA)
sulcal widening and ventricular enlargement. In criteria (American Psychiatric Association 2013;
early stages of the disorder, the brain may appear McKhann et al. 1984). In 2011 the National Insti-
normal on MRI/CT. PET imaging is a more sen- tute on Aging (NIA) and Alzheimer’s Association
sitive technique for detecting changes in brain workgroup proposed updated criteria to increase
function in early stages. Reduced glucose metab- diagnostic range and specificity, including a pre-
olism, usually in the temporoparietal regions, is a clinical stage of AD before symptom onset and

Alzheimer’s Dementia, Fig. 4 These images are pro- significance, expressed as Z-scores, of the hypometabolism
cessed FDG-PET images obtained from elderly subjects. when compared to those of the normative sample. The
The images have been processed using Neurostat stereotactic brighter colors (red, white) represent areas of significant
surface projections to illustrate the changes of the brain in hypometabolism, and the cooler colors of blues and purples
Alzheimer’s disease. Subject scans are shown in two rows in represent relatively normal brain metabolism. 74-year-old
each figure, depicting projections onto six surfaces: R-lateral, control subject with normal cognition. The top row shows
L-lateral, R-medial, L-medial, superior, and inferior. The top normal brain metabolic activity, and the lower row shows
row in each figure displays regional glucose metabolism with very few regions of hypometabolism. The areas of significant
“cooler” colors (purple, blue) reflecting areas of hypo- hypometabolism indicated in the medial views are due to this
metabolism. The bottom row in each figure displays relative individual having enlarged lateral ventricles relative to nor-
glucose metabolism for each participant as compared with a mative subjects (Photographs courtesy of Norman L. Foster,
normative sample of 27 cognitively normal elderly individ- M.D., and Angela Y. Wang, Ph.D., Center for Alzheimer’s
uals. In this bottom series, the images display the statistical Care, Imaging and Research, University of Utah)
Alzheimer’s Dementia 145

Alzheimer’s Dementia, Fig. 5 These images are pro- brighter colors (red, white) represent areas of significant
cessed FDG-PET images obtained from elderly subjects. hypometabolism, and the cooler colors of blues and purples
The images have been processed using Neurostat stereotactic represent relatively normal brain metabolism. 60-year-old
surface projections to illustrate the changes of the brain in subject clinically diagnosed with MCI. The top row shows
Alzheimer’s disease. Subject scans are shown in two rows in symmetric decreases in metabolic activity in both hemi-
each figure, depicting projections onto six surfaces: R-lateral, spheres of the brain. Abnormalities are primarily in the pari-
L-lateral, R-medial, L-medial, superior, and inferior. The top etal lobe (shown in the R-lateral and L-lateral views) and the
row in each figure displays regional glucose metabolism with posterior cingulate cortex (shown in the R-medial and L-
“cooler” colors (purple, blue) reflecting areas of hypo- medial views), as seen in the green regions. The bottom row
metabolism. The bottom row in each figure displays relative confirms that these regions (green, yellow, and red areas) are
glucose metabolism for each participant as compared with a indeed significantly (Z-scores > = 2.5) hypometabolic. This
normative sample of 27 cognitively normal elderly individ- pattern is a distinguishing feature of AD seen in FDG-PET
uals. In this bottom series, the images display the statistical studies (Photographs courtesy of Norman L. Foster, M.D.,
significance, expressed as Z-scores, of the hypometabolism and Angela Y. Wang, Ph.D., Center for Alzheimer’s Care,
when compared to those of the normative sample. The Imaging and Research, University of Utah)

Alzheimer’s Dementia, Fig. 6 These images are pro- hypometabolism when compared to those of the normative
cessed FDG-PET images obtained from elderly subjects. sample. The brighter colors (red, white) represent areas of
The images have been processed using Neurostat stereotac- significant hypometabolism, and the cooler colors of blues
tic surface projections to illustrate the changes of the brain in and purples represent relatively normal brain metabolism.
Alzheimer’s disease. Subject scans are shown in two rows in 72-year-old subject clinically diagnosed with AD. This sub-
each figure, depicting projections onto six surfaces: R-lat- ject shows an even greater and more widely distributed
eral, L-lateral, R-medial, L-medial, superior, and inferior. decrease in glucose metabolism. Parietal and temporal
The top row in each figure displays regional glucose metab- lobes and posterior cingulate cortex (green and blue regions
olism with “cooler” colors (purple, blue) reflecting areas of in the top row) are affected. The statistically significant
hypometabolism. The bottom row in each figure displays changes in metabolic pattern (red and white regions in the
relative glucose metabolism for each participant as com- lower row) are much greater than the MCI case (Photo-
pared with a normative sample of 27 cognitively normal graphs courtesy of Norman L. Foster, M.D., and Angela Y.
elderly individuals. In this bottom series, the images display Wang, Ph.D., Center for Alzheimer’s Care, Imaging and
the statistical significance, expressed as Z-scores, of the Research, University of Utah)
146 Alzheimer’s Dementia

incorporation of diagnostic biomarkers See Also

(McKhann et al. 2011). These criteria are gaining
supporting scientific evidence toward their valid- ▶ Cholinesterase Inhibitors
ity although further evaluation is required before ▶ Neurofibrillary Tangles
they are adopted in clinical settings (“2015 ▶ Senile Dementia
Alzheimer’s” 2015). ▶ Senile Plaques

Treatment References and Readings

Treatment for AD is palliative, with medications 2015 Alzheimer’s. (2015). 2015 Alzheimer’s disease facts
and therapies for symptom management. Medica- and figures. Alzheimer’s & Dementia: The Journal of
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doi.org/10.1016/j.jalz.2015.02.003
itors that functionally address the cholinergic deficit American Psychiatric Association. (2013). Diagnostic and
of AD by blocking the activity of the acetylcholine- statistical manual of mental disorders: DSM-5. Wash-
degrading enzyme, acetylcholinesterase (see ington, DC: American Psychiatric Association.
Arrighi, H. M., Neumann, P. J., Lieberburg, I. M., &
▶ “Cholinesterase Inhibitors”). These medications
Townsend, R. J. (2010). Lethality of Alzheimer disease
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note an improvement in some cognitive and behav- Disease and Associated Disorders, 24(1), 90–95.
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Chelune, G. J., & Duff, K. (2013). The assessment of
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148 Alzheimer’s Disease

Historical Background changes), and histopathology (plaques and tan-

gles). By the 1970s, the number of demented
In 1902, a woman called Auguste D. came under elderly was growing fast as demographic shifts
the care of Dr. Alois Alzheimer and then at the in the aging population combined with increased
University of Frankfurt. The patient manifested recognition of the syndrome. At this point, the
changes in behavior and cognition. Her clinical original definition of Alzheimer’s disease
course was characterized by progressive paranoia, (as described by Alzheimer and named by
delusional thinking, disorientation, and poor Kraepelin) was expanded to account for all
memory. She was institutionalized for the last dementing individuals with plaques and tangles,
3 years of her life. Upon her death, Alzheimer although some separation of these groups was
analyzed her brain using a silver stain and envisioned. Those meeting the original criteria
described both extracellular and intracellular pro- of plaque and tangle dementia in presenile adults
tein accumulations. The extracellular protein were designated as having dementia of the
accumulations were termed plaques, and the Alzheimer type (DAT), while the previously
intraneuronal protein accumulations were called unconsidered elderly cases were designated as
tangles. Alzheimer presented the results of this having senile dementia of the Alzheimer type
autopsy in 1906. Several other similar cases of (SDAT). With increasing recognition of the prob-
relatively “presenile” (i.e., arbitrarily defined as lem, Alzheimer’s disease very quickly became
an onset prior to age 55–65) clinical dementia incredibly common, as well as a Western civiliza-
associated with plaques and tangles were noted tion health priority.
by Alzheimer and others over the next 4 years. In In the USA, the 1980s saw the establishment of
1910, Alzheimer’s departmental chair, Emil federally funded Alzheimer’s disease research
Kraepelin, published a textbook covering the centers, which began to systematically study the
fields of neurology and psychiatry and referred clinical course of this progressive dementia,
to patients with presenile dementia, plaques, and mostly in the common SDAT form. Academic
tangles as having “Alzheimer’s disease.” research began to unravel the chemical makeup
Concurrently, other investigators, such as of plaques and tangles. Investigations into pat-
Oscar Fischer, also reported plaque presence in terns and causes of neurodegeneration were
elderly demented individuals. These individuals performed. This advancing knowledge enhanced
were older than those with “presenile” dementia the ability of clinicians to diagnose Alzheimer’s
(i.e., generally older than age 55–65). As the com- disease at increasingly subtle stages, as well as the
monality of progressive dementia in the elderly ability to pharmacologically intervene to achieve
was well recognized, the presence of plaques in partial, temporary symptomatic benefits in at least
elderly demented individuals was felt to represent a some individuals.
normal phenomenon. Such individuals were not
diagnosed with Alzheimer’s disease. Instead, cog-
nitive decline in elderly adults was attributed to Current Knowledge
normal aging or other poorly described conditions,
such as “hardening of the arteries.” As a result, Scientific Perspective
Alzheimer’s disease remained relatively uncom- The plaques seen in persons with Alzheimer’s
mon for a number of subsequent decades. disease contain several aggregated proteins. The
In the 1960s, investigators began comparing major constituent is a protein called amyloid beta
elderly demented subjects to those diagnosed (Ab). “Beta” is a chemical term that specifies a
with “presenile” Alzheimer’s disease. Notable certain pattern of protein folding. “Amyloid” is a
similarities were observed regarding the clinical general term that refers to proteins that give a
course (chronic and progressive), the clinical fea- particular appearance when exposed to a particu-
tures (cognitive decline that featured evolution of lar type of stain, Congo red. The beta amyloid, or
an amnestic state, followed by behavioral Ab, found in the brains of Alzheimer’s disease
Alzheimer’s Disease 149

patients derives from a particular protein called consist of a protein called tau. Normally, tau is
the amyloid precursor protein (APP). found in association with microtubules, which act
In the human brain, the APP is 695 amino acids as a skeleton, or “cytoskeleton” supporting the A
long. It is a transmembrane protein. One end (the cellular structure. The function of tau appears to
carboxyl end) is found inside neurons, in the be the stabilization of these microtubules. Like
cytoplasm. The other end (the amino end) extends many proteins, after its production tau is modified
outside the cell. In between the cytoplasmic and by the addition and subtraction of phosphate
extracellular portions is a stretch that runs through groups on certain amino acids, especially serine
the membrane. The normal function of APP is not and threonine. During embryonic development, tau
well known. APP is digested by different is heavily phosphorylated, but during youth and
enzymes, which cut the protein at different points. early adulthood, this heavily phosphorylated pat-
An enzyme complex called the beta secretase tern is rare if at all seen. In Alzheimer’s disease,
(BACE) cuts APP in its extracellular portion. An though, tau again takes on a heavily phosphorylated
enzyme or group of enzymes referred to as the pattern, which is felt to reflect an abnormal physi-
alpha secretase cuts APP in its intramembrane ologic event and is referred to as tau “hyper-
segment. The gamma secretase cuts APP twice, phosphorylation.” Hyperphosphorylated tau
both times in its intramembrane segment. Both of molecules begin to pair off, a process called “dimer-
the gamma secretase cuts occur closer to the car- ization.” Hyperphosphorylated tau dimers, also
boxyl end of the APP than the alpha secretase cut. called “paired helical filaments,” are quite insoluble
Different cutting combinations generate vari- and begin to aggregate with each other. This aggre-
ous APP by-products. Cutting of an APP by beta gation, typically visible extending from cell bodies
and gamma secretases generates a 38–43 amino into axons, comprises the neurofibrillary tangle.
acid stretch, and this stretch tends to assume a beta As impressive as this advancing understanding
folding conformation and has the features of an of plaque and tangle composition is, recognizing
amyloid protein (i.e., birefringence under the what constitutes these aggregations does not
microscope when stained with Congo red). The address why they form. In this regard, genetic
40 and 42 amino acid-long variants of Ab pre- studies of DAT subjects who inherit the disorder
dominate in plaques and are often designated in an autosomal-dominant fashion have had a
Ab40 and Ab42. Ab42 seems to be particularly large impact. Several hundred such families have
important to the formation of the amyloid plaques been documented. In these families the disease
of Alzheimer’s disease, probably because this affects about 50% of each generation, with typical
version of the protein is quite insoluble. When onset occurring in the third, fourth, fifth, or sixth
Ab accumulations begin to form in brain, they decades. A small number of these families have
are not associated with disrupted cell elements demonstrable mutations in the gene that encodes
and are called “diffuse plaques.” Another type of the APP. This gene is located on chromosome
more evolved plaque can also be found in 21, the same chromosome that is present in excess
Alzheimer’s disease patients, in which Ab in Down’s syndrome. Down’s syndrome patients
becomes condensed at the center of the plaque, invariably accumulate Ab plaques in their fifth
and the vicinity of the plaque is associated with decade. A somewhat larger number of these fam-
disrupted cell elements such as degenerating ilies have mutations in the gene that encodes a
axons and dendrites. As axons and dendrites are protein called presenilin 1. This gene is found in
collectively called “neurites,” this type of plaque chromosome 14. Presenilin 1 protein constitutes
is called a “neuritic plaque.” part of the gamma secretase complex. A smaller
The tangles of Alzheimer’s disease are found number of families have mutation of a related
primarily in neurons. Under the microscope tan- gene on chromosome 1, which encodes a related
gles have a fibrous quality to them, and hence protein, presenilin 2. Presenilin 2 can also partic-
tangles in Alzheimer’s disease are referred to as ipate in formation of the gamma secretase. Muta-
“neurofibrillary tangles.” Neurofibrillary tangles tions in the genes that encode APP, presenilin 1,
150 Alzheimer’s Disease

and presenilin 2 all enhance the production of traditionally diagnosed at autopsy by the presence
Ab42. This has lent support to the “amyloid cas- of plaques and tangles (although in some older
cade hypothesis,” which posits as Ab42 is gener- schemas tangles are not requisite) in an individual
ated it begins to interfere with neuronal function, with a clinical history suggestive of dementia. The
kill neurons, and generate the other histologic presence of plaques and tangles in typical brain
features seen in Alzheimer’s disease. While the regions (mesial temporal, parietal, and inferior
logic underlying this hypothesis is obvious, it is frontal structures) is quite common in elderly per-
important to keep in mind it assumes the very sons with the clinical syndrome of Alzheimer’s
small subset of early-onset, autosomal-dominant disease. As a result of the high prevalence of
Alzheimer’s disease (which accounts for far less Alzheimer’s disease with advancing age (at least
than 1% of those affected) have a similar if not one commonly quoted study estimates approxi-
identical etiology to the common sporadic, late- mately half of those over the age of 85 have it), the
onset cases that constitute the vast majority. In specificity of the clinical diagnosis is high. Rec-
those subjects, what initiates Ab42 production ognition of how common Alzheimer’s disease is
remains an open area of debate. Conceivably, in later life has also served to enhance clinician
population diversity in genes that contribute to awareness, thus improving sensitivity of the diag-
APP production or processing could cause Ab42 nosis. In the hands of an experienced physician,
to appear. Environmental factors could lead to clinical diagnostic accuracy is excellent.
Ab42 formation. Also, a variety of age-related Criteria originally designed to facilitate identi-
factors promote Ab42 formation. fication of subjects for clinical trials have helped
Other factors are recognized to play a role in to standardize clinical diagnostic approaches.
Alzheimer’s disease, and where these factors fit These criteria, such as those proposed by the
into or what they tell us about the etiologic hier- National Institute of Neurologic, Communicative
archy of the disease is unclear. One factor relates Disorders, and Stroke (NINCDS) and the
to the APOE gene on chromosome 19. The APOE Alzheimer’s Disease and Related Disorders Asso-
gene shows population variability due to the pres- ciation (ADRDA) in the 1980s emphasize the
ence of two polymorphic positions. The common importance of establishing that a progressive
APOE variants are the e2, e3, and e4 forms. The dementia exists in a patient. Two basic approaches
APOE e4 form is over represented in those with are commonly used toward this end. One is to
Alzheimer’s disease, where it seems to move up demonstrate a pattern of cognitive domain strengths
the age of presentation in those destined to and weaknesses that reliably suggest decline from a
develop the disorder. Mitochondrial function is previous level of cognitive function has emerged.
also altered in Alzheimer’s disease, and these For example, defective memory retention in the
alterations are not limited to the brain. presence of another defective cognitive domain
(language, executive function, visuospatial func-
Diagnostic Perspective tion, and praxis) in an elderly patient with cognitive
Dementia is defined as a cognitive decline that has complaints and an otherwise unremarkable physi-
advanced to that point it interferes with activities cal exam is strongly suggestive of Alzheimer’s
of daily living. While dementia has many different disease. The other approach focuses more on defin-
etiologies, Alzheimer’s disease is the most com- ing the degree and nature of emerging declines in
mon cause of dementia, accounting for 50–60% of daily living activities. This latter technique focuses
dementia verified by neuropathological examina- extensively on collateral history obtained from fam-
tion of the brain at autopsy. The clinical diagnosis ily members or friends of the patient.
(i.e., diagnosis in life) of Alzheimer’s disease is The diagnosis is made primarily through clin-
made in patients who have progressive dementia ical impression, although that impression is
with no other systemic or brain diseases that could influenced by a small set of recommended labo-
account for the progressive cognitive decline. ratory and imaging tests. These tests are serologic
A diagnosis of “definite Alzheimer’s disease” is (vitamin B12 level, thyroid function tests,
Alzheimer’s Disease 151

electrolytes with renal and hepatic indices, and a Treatment Perspective

blood cell count) and structural (brain imaging by Although Alzheimer’s disease is currently neither
either computed tomography or magnetic reso- reversible nor curable, it is possible to treat its A
nance imaging) in nature. As currently used, symptoms. The first approved treatment for
they mostly serve to rule out the presence of Alzheimer’s disease was tacrine, a cholinesterase
concomitant pathologies that can interfere with inhibitor. This drug increased levels of brain ace-
cognition. Although this has contributed to the tylcholine by antagonizing its synaptic degrada-
view that the Alzheimer’s disease diagnosis is one tion. Increasing brain cholinergic tone was
of exclusion, it should be noted that certain patterns identified as a pharmacologic target because
of cognitive decline elicited by clinical history or Alzheimer’s disease patients show a profound
demonstrable by neuropsychological testing are so loss of acetylcholine due to degeneration of cho-
typical of Alzheimer’s disease they can be used to linergic neurons in the basal forebrain. Safer cho-
support a diagnosis of inclusion. It is important to linesterase inhibitors (donepezil, rivastigmine, and
note, though, that while fluorodeoxyglucose PET galantamine) have since superseded tacrine.
and APOE genotyping are occasionally used to In addition to inhibiting acetylcholinesterase,
address specific questions, such as whether the rivastigmine also inhibits butyrylcholinesterases
presence of Alzheimer’s disease versus a that also hydrolyze acetylcholine, and galantamine
frontotemporal dementia is more likely in a patient, is an allosteric modulator of acetylcholine nicotinic
these tests are not routinely used in the diagnosis of receptors. Each agent shows a similar overall
Alzheimer’s disease and cannot by themselves degree of efficacy, although the individual with
establish a diagnosis of Alzheimer’s disease. Alzheimer’s disease may respond to or tolerate
Another PET application is also now available, one drug better than the other. Treatment cohorts
which reveals the presence of brain fibrillary Ab followed for 12 weeks to 3 years indicate that as a
deposition (in essence, the presence of amyloid group, those started on cholinesterase inhibitors
plaques). At the time of this writing amyloid tend to perform and appear slightly improved com-
plaque scanning, which is expensive and not cov- pared to their immediate pretreatment baseline.
ered by third-party payers, is not routinely used to This improvement appears detectable for
diagnose Alzheimer’s disease although the utility 6–12 months. By 12 months, though, treatment
of this test is under study and this may change in groups return to their pretreatment performance as
the future. Spinal fluid measurements of Ab and ascertained by cognitive testing, clinical impres-
tau protein levels yield similar information to that sion, and caregiver impression. Beyond 12 months,
which is obtained through an amyloid scan, but patients continuously decline below their pre-
this test is currently used more in research settings treatment baseline, although for at least the next
than it is in the clinic setting. several years, patients appear to perform better on
An increasing emphasis on Alzheimer’s disease cognitive testing than would otherwise be expected.
biomarker measurements is apparent in new The clinical meaningfulness of this sustained bene-
Alzheimer’s disease diagnostic research criteria fit has fueled considerable debate. Benefits have
that were formulated in 2011. In addition to essen- been observed on measures of cognitive ability,
tially continuing recognition of existing Alzheimer’s functional ability, behavior, and caregiver stress.
disease criteria, two new largely biomarker-driven At the time of this writing, memantine is the
Alzheimer’s disease categories were proposed. only non-cholinesterase inhibitor specifically
One new category, “prodromal Alzheimer’s dis- approved for the treatment of Alzheimer’s dis-
ease,” captures individuals with a mild cognitive ease. Under in vitro conditions, memantine blocks
impairment (MCI) syndrome and evidence of a cation channel associated with the NMDA type
fibrillary brain amyloid plaque deposition. “Pre- of glutamate-activated ionotropic receptors.
clinical Alzheimer’s disease” is defined as intact Whether or not this is its primary mechanism of
cognitive function in an individual with evidence action in Alzheimer’s disease has been
of fibrillary brain amyloid plaque deposition. questioned. In any case, cohorts of patients with
152 Alzheimer’s Disease

moderate or severe Alzheimer’s disease, when amyloid), cellular mechanisms of Ab disposal, and
randomized to memantine, perform better on mea- tissue-level mechanisms of Ab disposal.
sures of cognitive and functional performance Research over the longer term will need to
than do concurrent placebo treatment groups. In address the fact that the predominant etiologic
severe Alzheimer’s disease, the magnitude of hypothesis, the amyloid cascade hypothesis, can-
observed benefit is similar to that obtained with not yet explain why Ab homeostasis changes in
donepezil. Memantine and donepezil have been most of those affected or how Ab might give rise to
studied in combination with each other. Subjects other aspects of Alzheimer’s disease pathology. It
with mini-mental state exam scores of 5–14, who is possible the amyloid cascade hypothesis will
were already on donepezil, did better as a group prove valid in those with early-onset, autosomal-
when memantine was added to their treatment dominant Alzheimer’s disease caused by mutations
regimen than when placebo was added. Demon- of the genes encoding APP, presenilin 1, and pre-
strable benefits in mild Alzheimer’s disease are senilin 2 proteins, but not the late-onset cases (the
lacking, and thus the role of memantine in the vast majority). Disproving the amyloid cascade
mild stages of Alzheimer’s disease is not clear. hypothesis in the late-onset cases will likely require
Two studies concluded high-dose vitamin two events. First, interventions that attempt to treat
E (2000 IU each day) might slightly slow decline Alzheimer’s disease by targeting Ab will need to
in Alzheimer’s disease patients. Other studies, show absent or limited efficacy. Second, other
though, suggest taking more than 400 IU of vitamin hypotheses better able to explain the overall
E on a daily basis increases overall mortality. The Alzheimer’s clinical, and pathological big picture
marginality of any vitamin E benefit, in conjunction will need to demonstrate viability and durability.
with safety concerns, has reduced enthusiasm for the
use of vitamin E in Alzheimer’s disease. Although a Diagnostic Perspective
variety of other prescription medications (estrogens, Because it may prove easier in the future to pre-
statins), nonprescription medications (nonsteroidal vent neurodegeneration rather than reverse it, the
anti-inflammatories), and nutraceuticals (gingko ability to render an early, accurate diagnosis is
biloba) have been considered for the treatment of crucial. Also, the ability to treat the disease (either
Alzheimer’s disease, published data to date on all symptomatically or disease modifying) increases
other treatment options has been at worst negative the importance of early diagnosis. This has led
and at best insufficient to earn regulatory approval. the field to recently define prodromal and preclin-
Other drug categories are commonly used ical Alzheimer’s disease categories. A key question
to treat targeted symptoms associated with is how these new categories, which were proposed
Alzheimer’s disease. For instance, antipsychotic for research purposes, should extrapolate to the
medications are often used to treat agitated behav- clinical setting. The use of biomarkers to define
ior. Some studies do show efficacy in this regard, how close an asymptomatic or very mildly
although other studies have argued the limited impaired individual is to clinical Alzheimer’s dis-
behavioral benefits antipsychotics may confer is ease outside of the research setting requires, and is
canceled out by increased morbidity. receiving, careful consideration.

Treatment Perspective
Future Directions None of the treatments approved for use in
Alzheimer’s disease are approved for use in
Scientific Perspective MCI/prodromal Alzheimer’s disease, although
In the short term, considerable effort will be available data argue cholinesterase inhibition
directed at additional studies of Ab dynamics and (at least with donepezil) may provide a marginal
homeostasis. Research will focus on the toxicities benefit. Such a benefit would not be surprising,
of different degrees of Ab aggregation (especially especially if MCI represents very early
oligomers, defined as short, soluble polymers of Alzheimer’s disease in most people.
Alzheimer’s Disease 153

Over a decade of experience with symptomatic Cross-References

treatment has made it abundantly clear that
disease-modifying treatments are required. Most ▶ Alzheimer’s Dementia A
current approaches toward disease modification ▶ Memory Impairment
are targeted to Ab homeostasis. Inhibition of its ▶ Mental Status Examination
production (gamma secretase inhibitors and mod- ▶ Mini-Mental State Exam
ifiers), its targeted removal (active and passive ▶ Senile Dementia
immunization approaches), prevention of its
aggregation, and enhancement of enzymatic deg-
radation are all under active pursuit. To date, a References and Readings
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compound-B. Annals of Neurology, 55, 306–319. Schneider, L. S., Tariot, P. N., Dagerman, K. S., Davis,
Mayeux, R., Saunders, A. M., Shea, S., Mirra, S., Evans, S. M., Hsiao, J. K., et al. (2006). Effectiveness of
D., Roses, A. D., et al. (1998). Utility of the apolipo- atypical antipsychotic drugs in patients with
protein E genotype in the diagnosis of Alzheimer’s Alzheimer’s disease. The New England Journal of
disease. Alzheimer’s Disease Centers Consortium on Medicine, 355, 1525–1538.
Apolipoprotein E and Alzheimer’s Disease. The New Snowdon, D. A., Kemper, S. J., Mortimer, J. A., Greiner,
England Journal of Medicine, 338, 506–511. L. H., Wekstein, D. R., & Markesbery, W. R. (1996).
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Linguistic ability in early life and cognitive function
Price, D., & Stadlan, E. M. (1984). Clinical diagnosis and Alzheimer’s disease in late life. Findings from the
of Alzheimer’s disease: Report of the NINCDS- Nun Study. JAMA, 275, 528–532.
ADRDA Work Group under the auspices of Depart- Sperling, R. A., Aisen, P. S., Beckett, L. A., Bennett,
ment of Health and Human Services Task Force on D. A., Craft, S., et al. (2011). Toward defining the
Alzheimer’s Disease. Neurology, 34, 939–944. preclinical stages of Alzheimer’s disease: Recommen-
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, dations from the National Institute on Aging-
B. T., Jack Jr., C. R., et al. (2011). The diagnosis of Alzheimer’s Association workgroups on diagnostic
dementia due to Alzheimer’s disease: Recommenda- guidelines for Alzheimer’s disease. Alzheimers
tions from the National Institute on Aging-Alzheimer’s Dement, 7, 280–292.
Association workgroups on diagnostic guidelines for Swerdlow, R. H. (2007). Is aging part of Alzheimer’s
Alzheimer’s disease. Alzheimers Dement, 7, 263–269. disease, or is Alzheimer’s disease part of aging? Neu-
Morris, J. C. (2006). Mild cognitive impairment is early- robiology of Aging, 28, 1465–1480.
stage Alzheimer disease: Time to revise diagnostic
criteria. Archives of Neurology, 63, 15–16.
Mosconi, L., De Santi, S., Li, J., Tsui, W. H., Li, Y.,
Boppana, M., et al. (2007). Hippocampal hypo-
metabolism predicts cognitive decline from normal
aging. Neurobiology of Aging. https://doi.org/ Alzheimer’s Disease
10.1016/j.neurobiolaging.2006.12.008. Cooperative Study ADL Scale
National Institute on Aging, and Reagan Institute Working
Group on Diagnostic Criteria for the Neuropathological Jessica Fish
Assessment of Alzheimer’s Disease. (1997). Consen-
sus recommendations for the postmortem diagnosis of Medical Research Council Cognition and Brain
Alzheimer’s disease. Neurobiology of Aging, 18 Sciences Unit, Cambridge, UK
(4 Suppl), S1–S2.
Petersen, R. C., Smith, G. E., Waring, S. C., Ivnik, R. J.,
Tangalos, E. G., & Kokmen, E. (1999). Mild cognitive
impairment: Clinical characterization and outcome. Synonyms
Archives of Neurology, 56, 303–308.
Petersen, R. C., Thomas, R. G., Grundman, M., Bennett, Alzheimer’s disease cooperative study ADL scale
D., Doody, R., Ferris, S., et al. (2005). Vitamin E and for mild cognitive impairment (ADCS-ADL-MCI);
donepezil for the treatment of mild cognitive impair-
ment. The New England Journal of Medicine, 352, Alzheimer’s disease cooperative study ADL scale
2379–2388. for severe impairment (ADCS-ADL-sev)
Alzheimer’s Disease Cooperative Study ADL Scale 155

Description be developed for use specifically in clinical trials

with people with AD across the range of severity.
The ADCS-ADL assesses the competence of The 24 items in the standard version were selected A
patients with Alzheimer’s disease (AD) in basic from a pool of 45 items based upon a stringent set
and instrumental activities of daily living of psychometric criteria (see section “Psychomet-
(ADLs). It can be completed by a caregiver in ric Data”). Using the same criteria, Galasko et al.
questionnaire format or administered by a clini- (2005) developed a version of the ADCS-ADL for
cian/researcher as a structured interview with a more severely impaired participants, which is
caregiver. All responses should relate to the known as the ADCS-ADL-sev, and a version for
4 weeks prior to the time of rating. The six basic people with MCI has also been developed
ADL items each take an ADL (e.g., eating) and (ADCS-MCI-ADL, Perneczky et al. 2006). The
provide descriptions of level of competence, with ADCS-ADL has been used in a variety of clinical
the rater selecting the most appropriate option trials.
(e.g., ate without physical help and used a knife,
used a fork or spoon but not a knife, used fingers
to eat, was usually fed by someone else). The Psychometric Data
16 instrumental ADL items follow the format
“In the past 4 weeks, did s/he use the telephone,” Galasko et al. (1997) selected the items for the
with the response options of yes/no/don’t know. ADCS-ADL from a pool of 45 items thought to be
If the response is “yes,” a rating is then made relevant to the target population on the basis of
regarding his/her competence according to a set existing scales and clinical experience. To deter-
of descriptions tailored to that activity (e.g., for mine which ADLs were most suitable for inclu-
the telephone item, whether the person looked up sion, the 45-item version was administered at
phone numbers and made calls, made calls only baseline, 6 months and 12 months later to
to well-known numbers without referring to a 64 elderly controls and 242 people with AD,
directory, made calls only to well-known num- stratified by MMSE score at baseline assessment.
bers using a telephone directory, answered the Half of participants were additionally assessed at
phone but did not make calls, or only spoke 1 and 2 months post-baseline. An item was
when put on the line). Adapted versions of the included in the final measure if it fits the criteria
scale suitable for people with MCI (ADCS-MCI- that it was performed either premorbidly or at
ADL) and moderate–severe AD (ADCS-ADL- baseline by >90% of participants (showing it
sev) have also been developed. Scores on the was applicable to the target group), had a kappa
24-item ADCS-ADL range from 0 to 78, those agreement statistic at 1–2 months of >0.4
on the 18-item ADCS-MCI-ADL range from 0 to (indicating good test-retest reliability), had a sig-
57, and on the 19-item ADCS-ADL-sev from 0 to nificant correlation with MMSE score (indicating
54, where higher scores reflect greater compe- appropriate scaling and validity), and showed
tence (see section “Psychometric Data” for fur- decline over 12 months in at least 20% of partic-
ther details). The entire instrument takes ipants (indicating validity and sensitivity to
15–30 min to administer. change).
Galasko et al. (2005) used the same criteria in
the development of the ADCS-ADL-sev, based on
Historical Background longitudinal data of 145 patients with Mini-
Mental State Examination (MMSE) scores
The ADCS is a US-based initiative that aims to between 0 and 15. Galasko et al. reported good
conduct research informing the prevention and test-retest reliability (baseline-1 month r = 0.94,
treatment of AD, as well as developing measures baseline-2 months r = 0.89, month1–month2
for use in people with AD, particularly in clinical r = 0.94), and there was evidence of convergent
trials. The ADCS-ADL was the first ADL scale to validity based upon the strong correlation
156 Ambidexterity

between ADCS-ADL-sev and other global ▶ Disability Assessment for Dementia

impairment measures (ADCS-ADL-sev – ▶ Lawton-Brody Instrumental Activities of Daily
MMSE r = 0.64; ADCS-ADL-sev – severe Living Scale
Impairment Battery r = 0.71). The mean score
on the first test was 25.4 (SD 12.7, maximum
obtainable 54), with a mean decline of 5.6 points References and Readings
(SD 7.5) over 6 months and 10.3 points (SD 10.3)
over 12 months. Galasko, D., Bennett, D., Sano, M., Ernesto, C., Thomas,
R., Grundman, M., et al. (1997). An inventory to assess
Perneczky et al. (2006) have found that the
activities of daily living for clinical trials in
ADCS-MCI-ADL scale can discriminate people Alzheimer’s disease. The Alzheimer’s disease cooper-
with MCI from control participants (a cutoff score ative study. Alzheimer’s Disease and Associated Disor-
of 52 gives sensitivity of 0.89 and specificity of ders, 11(S2), S33–S39.
Galasko, D., Schmitt, F., Thomas, R., Jin, S., Bennett, D.,
0.97). Further the scale has been shown to have
& Ferris, S. (2005). Detailed assessment of activities of
high discriminatory power to distinguish between daily living in moderate to severe Alzheimer’s disease.
MCI and AD (a cutoff score of 37/38 has a sensi- Journal of the International Neuropsychological Soci-
tivity of 85% and specificity of 87%) (Pedrosa ety, 11, 446–453.
Pedrosa, H., De Sa, A., Guerreiro, M., Maroco, J., Simoes,
et al. 2010).
M. R., Galasko, D., & de Mendonca, A. (2010). Func-
tional evaluation distinguishes MCI patients from
healthy elderly people – The ADCS/MCI/ADL scale.
The Journal of Nutrition, Health & Aging, 14,
703–709.
Clinical Uses
Perneczky, R., Pohl, C., Sorg, C., Hartmann, J., Komossa,
K., Alexopoulos, P., et al. (2006). Complex activities of
The ADCS-ADL and its variants are the only ADL daily living in mild cognitive impairment: Conceptual
scales designed with AD specifically in mind and and diagnostic issues. Age and Ageing, 35, 240–245.
can provide a fairly detailed assessment of compe-
tence in a variety of ADLs. Galasko et al. (2005)
state that the measure takes too long to administer
for it to be widely adopted in clinical practice, but Ambidexterity
it would be useful in intervention studies, and the
ADL-sev in particular where the severity of the John E. Mendoza
disorder may render measures such as the MMSE Department of Psychiatry and Neuroscience,
unsuitable due to floor effects. The careful selec- Tulane Medical School and SE Louisiana
tion of items for the ADCS-ADL suggests that Veterans Healthcare System, New Orleans,
they are eminently suitable for use in clinical trials. LA, USA
Perneczky et al. (2006) found that even patients
with a diagnosis of mild cognitive impairment
exhibit deficits in instrumental ADLs on the Definition
ADCS-ADL-MCI and that scores can successfully
discriminate patients with MCI from healthy con- Ambidexterity is the tendency for one to be more
trols; as such, results from this scale may be useful or less equally proficient in carrying out complex
in forming an MCI diagnosis. or skilled motor tasks with either the right or the
left hand. While complete ambidexterity is rela-
tively rare, mixed proficiencies or preferences are
not uncommon, with men more frequently dem-
Cross-References onstrating such mixed preferences than women.
Tan (1988) found that approximately 66% of the
▶ Activities of Daily Living Questionnaire population was noted to express a strong right-
▶ Bristol Activities of Daily Living Scale handed preference, while a little more than 3%
American Academy of Clinical Neuropsychology (AACN) 157

were predominately left handed. The remaining Pieniadz, J. M., Naeser, M. A., Koff, E., & Levine, H. L.
30% evidenced mixed hand preferences. As noted (1983). CT scan hemispheric asymmetry measurements
in stroke cases with global aphasia: Atypical
elsewhere in this volume, handedness is a com- asymmetries associated with improved recovery. Cor- A
mon, but not the only measure of what is referred tex, 19, 371–391.
to as “cerebral dominance.” Another of the more Pujol, J., Deus, J., Losilla, J. M., & Capdevila, A. (1999).
frequent indices of dominance is language, which Cerebral lateralization of language in normal left-
handed people studied by functional MRI. Neurology,
is typically organized primarily in the left hemi- 52, 1038–1043.
sphere. While in the majority of non-brain-injured Tan, Ü. (1988). The distribution of hand preference in
individuals, the control of both complex motor normal men and women. International Journal of Neu-
skills and language functions rest within the left roscience, 41, 35–55.
hemisphere, this may not always be the case, par-
ticularly for those who are either left handed or
ambidextrous. It has been shown that while right
hemisphere dominance for language is quite rare in American Academy of Clinical
right-handers, it could approach 30% in strong left- Neuropsychology (AACN)
handers. Individuals who are ambidextrous or
whose parents are left handed tend to fall some- Rebecca McCartney
where in between these two groups with regard to Department of Behavioral Health,
the hemispheric localization of language. Further- Kaiser Permenante, Atlanta, GA, USA
more, the localization of language may not be an
all-or-none phenomena. While one hemisphere
may be more predominant, language functions Membership
may be mediated to some extent by both hemi-
spheres. Individuals with mixed or anomalous American Academy of Clinical Neuropsychology
dominance, including those who were ambidex- (AACN) is an organization for psychologists who
trous, tend to have a greater incidence of at least have achieved board certification in the specialty
some degree of bilateral representation of language. of clinical neuropsychology, under the American
In the event of unilateral strokes, such individuals Board of Clinical Neuropsychology (ABCN).
may evidence less severe residual aphasic deficits Membership in the Academy consists of three
when compared to patients with strongly lateralized classes: active, senior, and affiliate. Active
language when that hemisphere is affected. members are elected from among psychologists
who have been certified in clinical neuropsy-
chology by the ABCN in affiliation with the
Cross-References American Board of Professional Psychology
(ABPP). Senior members are elected from
▶ Anomalous Dominance among active members who have been academy
▶ Dominance (Cerebral) members, for a period of no less than the five
preceding years, are age 65 or older or disabled,
and are fully retired from the active practice of
clinical neuropsychology. They continue to be
References and Readings listed in the membership directory of the acad-
emy, and they continue to receive any newslet-
Benson, D. F., & Geschwind, N. (1985). Aphasia and
related disorders: A clinical approach. In M. Mesulam ters distributed to academy members. Senior
(Ed.), Principles of behavioral neurology members have no financial obligations to the
(pp. 193–238). Philadelphia: F.A. Davis Co.. academy and are allowed to continue to sub-
Knecht, S., Drager, B., Deppe, M., Bode, L., Lohmann, H.,
Floel, A., et al. (2000). Handedness and hemispheric
scribe to any journal available through the acad-
language dominance in healthy humans. Brain, 123, emy. At the time of this publication, there were
2512–2518. 1045 members listed in the online directory.
158 American Academy of Clinical Neuropsychology (AACN)

Affiliate members are elected from among all Landmark Contributions

others who are intellectually interested in the AACN was founded in 1996. The first appointed
purposes of the academy and wish to participate president was Byron Rouke, Ph.D., and the first
in its nonvoting activities. All members are pro- elected president was Wilfred Van Gorp, Ph.D.
vided with a subscription to The Clinical Neu- AACN cosponsored the Houston Conference on
ropsychologist, access to the AACN Clinical Specialty Education and Training in Clinical Neu-
Discussion Email List, and discounted fees to ropsychology in 1997. This conference was a
meetings and workshops. national consensus conference of neuropsycho-
Presidents of the Academy include Byron logical organizations held with the purpose of
P. Rourke, (1995–1996), Wilfred van Gorp establishing training guidelines for clinical neuro-
(1996–2002), Catherine A. Mateer (2002–2004), psychology. The Houston Conference guidelines
Robert L. Mapou (2004–2006), Jerry J. Sweet have since become the model for most programs
(2006–2008), Gregory J. Lamberty (2008–2010), offering formal training in clinical neuropsychol-
Michael A. McCrea (2010–2012), Aaron Nelson ogy. AACN held its first annual conference in
(2012–2014), E. Mark Mahone, (2014–2016), and 2003. During that same year, The Clinical Neuro-
Karen Postal (2016–2018). psychologist became AACN’s official journal. In
2007, AACN began online continuing education
(CE) programs. In 2009, the American Academy
Major Areas or Mission Statement of Clinical Neuropsychology Foundation
(AACNF) was established to help fund outcome-
AACN’s stated mission is to advance the profes- oriented research for neuropsychological services.
sion of clinical neuropsychology through its advo- The first AACNF outcome grant was awarded in
cacy of outstanding educational and public policy 2011. During that same year, Child Neuropsychol-
initiatives. The academy holds the following ogy became the official journal of AACN’s Pedi-
objectives: atric Special Interest Group.

1. To promote board certification by the ABCN as Major Activities

the standard for competence in the practice of AACN hosts one conference each year. This con-
clinical neuropsychology ference is open to both members and nonmem-
2. Support for those principles, policies, and prac- bers. The official journal published by AACN is
tices that seek the attainment of the best in The Clinical Neuropsychologist.
clinical neuropsychological patient care
3. The pursuit of excellence in psychological
education, especially as it concerns the clinical Cross-References
neuropsychological sciences
4. The pursuit of high standards in the practice of ▶ American Board of Clinical Neuropsychology
clinical neuropsychology and support of the (ABCN)
credentialing activities of the ABCN ▶ International Neuropsychological Society
5. Support for the quest of scientific knowledge ▶ National Academy of Neuropsychology (NAN)
by support for research in neuropsychology
and related fields
6. The communication of scientific and scholarly References and Readings
information through continuing education, sci-
entific meetings, and publications Boake, C. (2008). Clinical neuropsychology. Professional
7. Provision for communication with other Psychology: Research and Practice, 39(2), 234–239.
Boake, C., & Bieliauskas, L. A. (2007). Development of
groups and representation for clinical neuro- clinical neuropsychology as a psychological specialty:
psychological opinion to best achieve and pre- A timeline of major events. The ABPP Specialist,
serve the purposes of the academy 26, 42–43.
American Academy of Neurology (AAN) 159

Lucas, J. A., Mahone, E. M., Westerveld, M., Bieliauskas, through education, information, policy develop-
L., & Baron, I. S. (2014). The American Board of Clin- ment, and advocacy for our members and their
ical Neuropsychology and American Academy of Clin-
ical Neuropsychology: Updated milestones 2005–2014. patients while maintaining the highest ethical and A
The Clinical Neuropsychologist, 28(6), 889–906. professional standards.
Yeates, K. O., & Bieliauskas, L. A. (2004). The American The mission of the AAN is to promote the
Board of Clinical Neuropsychology and American Acad- highest-quality patient-centered neurologic care
emy of Clinical Neuropsychology: Milestones past and
present. The Clinical Neuropsychologist, 18, 489–493. and enhance member career satisfaction.

Landmark Contributions
American Academy of
Neurology (AAN) The AAN was founded in 1948 by A. B. Baker, M.
D., chair of the neurology department of the Univer-
Catherine M. Rydell1 and Michelle Uher2 sity of Minnesota, in response to the difficulties of
1
American Academy of Neurology, Minneapolis, one of his residents, Joseph Resch, M.D., in finding a
MN, USA society that he could join to continue his education
2
Marketing Communications, American and network with fellow neurologists. Baker was
Academy of Neurology, Minneapolis, MN, USA aided by Adolph L. Sahs, M.D., of the University
of Iowa; Francis M. Forster, of Jefferson Medical
Hospital in Philadelphia; and Russell DeJong, M.D.,
Address (and URL) of the University of Michigan. Baker served as the
first academy president, and Forster and Sahs later
American Academy of Neurology had terms as president. DeJong was the founding
editor in chief of the journal Neurology®, which
201 Chicago Avenue began publication in 1951.
Minneapolis, Minnesota 55415 The AAN had 52 founding members. The
www.aan.com establishment of the academy, coupled with the
(800) 879–1960 (US) increased need for neurologists due to World War
(612) 928–6000 (International) II, helped elevate the status of neurology as a
(612) 454–2746 (fax) practice distinct from psychiatry. In 1947, there
were between 300 and 325 physicians in the USA
who designated themselves as primary neurolo-
Membership gists, and there were 32 residency positions avail-
able nationwide. By 1970, there were 2,727
The American Academy of Neurology (AAN) is primary neurologists and some 700 residents in
the world’s largest professional association of training. By the end of 2007, there were more than
neurologists and the leading online resource for 16,000 neurologists in the USA. In 2016, the
neurologists across the world. AAN has over 33,000 members worldwide.
Founded in 1948, the AAN now represents
33,000 members and is dedicated to promoting
the highest quality patient-centered care and Major Activities
enhancing member career satisfaction.
Physician Education and Lifelong Learning
The AAN Annual Meeting is one of the largest
Major Areas or Mission Statement gatherings of neurology professionals in the
world. Held each spring, the event attracts over
The vision of the AAN is to be indispensable to its 14,000 clinicians, academicians, researchers,
members by providing guidance and inspiration exhibitors, and media representatives to share
160 American Academy of Neurology (AAN)

the latest in neurology science and education. The Hill visits to the Capitol in Washington, DC. The
AAN also offers members a yearly 3-day regional Brain PAC political action committee also is
Educational Fall Conference, The Sports Concus- instrumental in representing neurology’s interests
sion Conference in the summer and a Break- on the federal level and supporting federal legis-
throughs in Neurology science conference in the lators who support the profession and patients
winter. Education activities and programs are with neurologic disorders.
structured to support the ongoing development
of neurology professionals from medical students Publishing
to accomplished clinicians and scientists. The AAN has several highly successful publications
published by Lippincott Williams and Wilkins.
Science and Research
The annual meeting is a leading forum for sharing • The weekly scientific journal Neurology ® is
the latest developments in science and research, as the most widely read peer-reviewed neurology
is the weekly peer-reviewed Neurology® journal journal in North America.
along with its spoke journals Neurology® • Neurology ® Clinical Practice, published
Neuroinflammation & Neuroimmunology and Neu- bimonthly, is the first “spoke” journal in the
rology® Genetics. AAN scientific awards, pre- Neurology family of publications.
sented at the annual meeting, honor outstanding • Neurology® Neuroinflammation &
achievements in neurology, from aspiring medical Neuroimmunology is the first open-access online
students to veteran researchers. The American journal in the Neurology portfolio of publications.
Academy of Neurology Institute provides support • Neurology® Genetics, launched in 2015, is the
to young researchers through clinical research train- academy’s latest open-access online journal.
ing fellowships, enabling them to pursue research • Neurology Today ®, published biweekly, leads
initiatives and helping them to secure academic all other neurology tabloids in readership.
appointments and future fundings. • Neurology Now ®, a bimonthly patient-oriented
magazine available to patients and caregivers
Clinical Practice currently, has a readership of 1.6 million.
The AAN develops evidence-based clinical prac- • Continuum: Lifelong Learning in Neurology ®,
tice guidelines to assist its members in clinical the AAN’s bimonthly continuing education
decision making related to the prevention, diag- monograph, is recognized by the American
nosis, treatment, and prognosis of neurologic dis- Board of Psychiatry and Neurology as a key
orders. Each guideline makes specific practice tool for maintenance of certification.
recommendations based upon a rigorous and com- • The AAN also publishes the monthly member
prehensive evaluation of all available scientific magazine AANnews ®, which focuses on AAN
data. The AAN develops position statements on activities, events, and services; a book series
a variety of ethical issues to help guide neurolo- for patient and their families on treating and
gists and others in decision making. Members also living with neurologic disorders; and text-
rely on the AAN for the latest information on books geared toward professionals.
coding, reimbursement, quality initiatives, patient
safety, and practice management issues.
Cross-References
Advocacy
To help foster changes in health care that will ▶ Neuropsychiatry
benefit patients and enhance the practice of
neurology, the AAN presents advocacy training
opportunities for members through the Donald M. References and Readings
Palatucci Advocacy Leadership Forum. Members
also participate in the annual Neurology on the Visit the AAN at American Academy of Neurology (AAN)
American Board of Clinical Neuropsychology (ABCN) 161

includes (1) review of training credentials, (2)

American Board of Clinical written examination, (3) review of case materials
Neuropsychology (ABCN) from the candidate’s clinical practice, and (4) oral A
examination.
John A. Lucas1 and Michael Westerveld2 Candidates who pass all stages of the ABCN
1
Department of Psychiatry and Psychology, Mayo examination process are awarded specialty certi-
Clinic, Jacksonville, FL, USA fication in clinical neuropsychology and are eligi-
2
Medical Psychology Associates, Florida ble for membership in the American Academy of
Hospital, Orlando, FL, USA Clinical Neuropsychology (AACN). All board-
certified specialists in good standing may vote in
elections for the ABCN Board of Directors
Address (and URL) (BOD), which is comprised of 15 members each
elected to 5-year terms. Officers of the ABCN
The American Board of Clinical Neuropsychol- BOD include the president, vice president, secre-
ogy (ABCN) is the specialty board of the Ameri- tary, treasurer, the ABCN representative to the
can Board of Professional Psychology (ABPP) ABPP board of trustees, and other agents as may
that is responsible for the development and be directed by the board.
administration of examinations of competence Neuropsychologists who possess subspecialty
for independent practice of Clinical Neuropsy- education, training, and clinical expertise in pedi-
chology. Information about ABCN can found at atric clinical neuropsychology may pursue sub-
the following websites: specialty certification after passing all stages of
the ABCN specialty examination process. Sub-
American Board of Clinical Neuropsychology specialty candidates must resubmit credentials
(www.theabcn.org) for review of education and training specific to
American Board of Professional Psychology the science and practice of pediatric neuropsy-
(www.abpp.org) chology. Once subspecialty credentials are
American Academy of Clinical Neuropsychology approved, candidates may take a subspecialty
(www.theaacn.org) written examination and, when passed, may sub-
mit a case sample from their pediatric neuropsy-
Mail correspondence can be directed to ABCN chology practice for peer review.
at the following street address:
Department of Psychiatry (F6248, MCHC-6)
University of Michigan Health System Mission Statement
1500 East Medical Center Drive, SPC 5295
Ann Arbor, MI 48109-5295 The mission of ABCN is to (1) develop and con-
duct examinations to determine the qualifications
of individuals who apply for board certifications,
Membership (2) award certification in clinical neuropsychol-
ogy and its subspecialties to candidates who pass
As of June 2017, ABCN/ABPP has awarded all stages of the examination process, and (3)
specialty certification in clinical neuropsychology evaluate compliance of certified specialists with
to 1201 specialists practicing across the United maintenance of certification requirements.
States and Canada. Of these, 91 have been
awarded subspecialty certification in the practice
of pediatric clinical neuropsychology. Neuropsy- Landmark Contributions
chologists certified through ABCN demonstrate
their scientific knowledge and clinical expertise Origins of ABCN. In June 1981, a joint task force
through a staged examination process that of the International Neuropsychological Society
162 American Board of Clinical Neuropsychology (ABCN)

and Division 40 of the American Psychological interest among clinical neuropsychologists in the
Association met to discuss education, credential- peer-review process. In 2014, ABCN awarded
ing, and accreditation in the specialty of clinical board certification to its 1000th specialist, dou-
neuropsychology. The task force concluded that bling the previous milestone in half the time
training as a neuropsychologist was poorly stan- (Lucas et al. 2014).
dardized and that many professionals claimed Enhancements to the Board Certification Pro-
expertise in clinical neuropsychology without cess. Bieliauskas and Matthews provided detailed
proper training or skill sets. During the meeting, facts and data regarding the development and
several members of the task force discussed the enhancement of ABCN policies and procedures
need to develop a formal credentialing process to in updates published in 1987, 1990, and 1996
assist the public in identifying professionals capa- (Bieliauskas and Matthews 1990, 1997, 1987).
ble of providing competent neuropsychological In 1997, representatives from each professional
services (Report of the Division 40/INS Joint neuropsychology organization were invited to
Task Force on Education, Accreditation, and meet in Houston to review current training models
Credentialing 1984; Reports of the INS – Division and propose universal standards for education and
40 Task Force on Education, Accreditation, and training in the specialty. The proceedings and
Credentialing 1987). A small planning group was consensus statement of the Houston Conference
subsequently formed to create a peer-review on Specialty Education and Training in Clinical
mechanism for this purpose, and in August Neuropsychology were published the following
1981, the American Board of Clinical Neuropsy- year (Hannay et al. 1998). Although largely aspi-
chology was incorporated in the state of Minne- rational at the time of publication, by 2002 the
sota as an independent credentialing body. ABCN Board determined that a sufficient number
The ABCN planning group included Linas of neuropsychology training programs had suc-
Bieliauskas, Louis Costa, Edith Kaplan, Muriel cessfully incorporated the Houston Conference
Lezak, Charles Matthews, Steven Mattis, (HC) model and voted to include HC training
Manfred Meier, and Paul Satz, who together and education guidelines as criteria for passing
developed a three-stage board certification pro- credential review. In recognition of earlier training
cess. At its inception, the ABCN examination models and to allow enough time for transition,
process included (1) review of training creden- the board allowed that only those applicants earn-
tials, (2) submission of case materials reflecting ing their doctoral degree on or after January 1,
the candidate’s practice of clinical neuropsychol- 2005, would be held to HC criteria. Others con-
ogy, and (3) an oral examination of, but not lim- tinued to be held to the eligibility criteria that were
ited to, clinical and scientific knowledge, in place at the time they earned their doctoral
assessment practices, and ethical/legal issues. degree (or completed respecialization in clinical
Prominent neuropsychologists of national reputa- neuropsychology). A survey conducted in 2012
tion were chosen by consensus of the planning by Sweet and colleagues (2012) indicated that HC
group to serve as the first board of directors of guidelines have become widely adopted by train-
ABCN. The inaugural board examined each other ing programs in clinical neuropsychology and that
and, in 1983, conducted the first formal set of professionals who complete training in HC-adher-
board examinations in clinical neuropsychology. ent programs report being well prepared to engage
Following the first formal exams, ABCN affiliated independently in key professional activities.
with ABPP, the unifying governing body for spe- In 1988, ABCN partnered with Psychological
cialty examining boards in psychology. The first Examination Services to develop a 100-item writ-
official ABPP/ABCN certifications in the spe- ten examination whereby candidates could objec-
cialty of clinical neuropsychology were awarded tively demonstrate the scientific knowledge
in 1984. Twenty years later, in 2004, ABCN acquired during their training and years of prac-
awarded its 500th certification (Yeates and tice. The written examination was implemented in
Bieliauskas 2004), demonstrating continued 1993 as the second stage of the certification
American Board of Clinical Neuropsychology (ABCN) 163

process and must be passed before a candidate subspecialty development begins with the aggre-
may submit practice samples. The content and gation of board-certified specialists into a “special
psychometric properties of the written examina- interest group” (SIG) representing shared exper- A
tion are reviewed and updated on an ongoing tise and interests in a component of the specialty.
basis. In 2012 ABCN transitioned the written This model was endorsed by the ABPP BOT in
examination from a paper-and-pencil test admin- December 2008 and incorporated into the formal
istered at national meetings to a computer-based policies and procedures of the ABPP Affiliations
test administered on an electronic platform during and Standards Committee.
2-week examination windows, four times per In 2009, a group of pediatric clinical neuropsy-
year. Candidates who are eligible to sit for the chologists formed the first official SIG within
written examination may do so locally at any of ABPP. The pediatric SIG (P-SIG) met over sub-
nearly 300 PSI testing sites across the United sequent years to vet the interest, feasibility, and
States and Canada. In 2015 a set of 25 beta-test viability of developing a subspecialty of pediatric
items were added to the core 100 test items to clinical neuropsychology within ABCN. Simulta-
provide psychometric data for informed item neously, the ABCN BOD tasked its committee on
selection of subsequent versions of the exam. subspecialization to consider and recommend a
Only the 100 core test items contribute to candi- model of requirements and procedures by which
date’s final exam score. In late 2015, the ABCN specialists might attain certification in a sub-
Board of Directors contracted with Alpine Testing specialty area of neuropsychology practice. The
Solutions, Inc. to develop and implement the next committee reasoned that subspecialty candidates
revision of the written exam. have already demonstrated competencies required
ABCN partnered with Thomson-Reuters in for neuropsychology practice by virtue of their
2012 to create an electronic portal in the board certification through ABCN. Thus, certifi-
ScholarOne online manuscript management sys- cation in a subspecialty of clinical neuropsychol-
tem to allow candidates to upload electronic cop- ogy should require only (1) clear demonstration of
ies of their practice sample case materials rather subspecialty-specific education, training, and
than mailing paper copies, as had been the prior practice requirements as determined by the
practice. Additionally, the ABCN Practice Sample ABCN Board in consultation with the sub-
Committee engaged in a multifaceted approach to specialty SIG, (2) a written examination of sub-
enhance both the standardization and turnaround specialty knowledge and clinical application, and
time of reviews. The committee recruited a cohort (3) demonstration of competent, evidence-based
of dedicated specialists and provided standardized clinical practice in the subspecialty as determined
guidelines and training for practice sample by review of a single representative assessment
reviews, thus allowing candidates to move more case. In October 2013 ABCN submitted this pro-
efficiently through the board certification posal to ABPP and in December 2013 pediatric
pipeline. clinical neuropsychology was approved as the
Subspecialty Certification. In 2006, the ABPP first official subspecialty within ABPP. In January
Board of Trustees requested that ABCN form a 2014, all ABCN specialists with expertise in pedi-
work group to consider issues regarding the atric clinical neuropsychology were invited to
emerging interest of subspecialty practices within submit applications for subspecialty credential
psychological specialties (Baron et al. 2011). review. Those who demonstrated the required
After careful deliberation, the work group pro- education and training were subsequently invited
posed a model whereby subspecialties reflect the to sit for a calibration administration of an objec-
normal evolution of psychological specialty prac- tive written examination. The data from the cali-
tice, emerging naturally as the core knowledge bration examination was used to create two
base of a specialty grows and begins to be applied parallel 30-item subspecialty written examina-
or tailored to unique populations, settings, or tions which were fielded in June 2015. The sub-
methods. The work group proposed that specialty written examination is currently
164 American Board of Clinical Neuropsychology (ABCN)

administered once per year. As of June 2017, 91 Although AACN began as an organization
ABCN specialists had passed the practice sample restricted only to board-certified neuropsychology
peer-review stage and successfully earned ABPP/ specialists, membership opportunities at this time
ABCN subspecialty certification in pediatric clin- also extend to students, individuals who are in the
ical neuropsychology. midst of the board certification process, and non-
Maintenance of Certification. ABCN has neuropsychology professionals (Table 1).
always recognized that competence in any field
of medical practice is dynamic and that specialists
must continuously maintain and update their com- Major Activities
petencies through ongoing professional education
and engagement. In 2010, the ABCN Board As noted above, ABCN focuses its primary activ-
endorsed a plan proposed by ABPP to require ities on developing, maintaining, reviewing,
specialists to formally document the ways in revising, and implementing the board certification
which they maintain the competencies required examinations in clinical neuropsychology and its
of ongoing specialty practice. In 2013, ABCN subspecialties. As of 2015, ABCN also conducts
created a maintenance of certification (MOC) reviews of documentation from specialists who
committee to develop and implement procedures, wish to demonstrate maintenance of certification.
materials, and criteria to allow neuropsychology The ABCN Specialty Certification Examina-
specialists and subspecialists the formal means of tion. A comprehensive overview of the ABCN
demonstrating MOC. This process adapts the core examination process was published in 2008 (Arm-
requirements expected across all ABPP special- strong et al. 2008) and can also be found within
ties in a way that is relevant to the functional the Candidate’s Manual on the ABCN website
competencies specific to ABCN. The MOC policy (www.theabcn.org). Briefly, the specialty exami-
and procedures developed by ABCN were nation process consists of four distinct and
approved by the ABPP Standards Committee in sequential steps. First, the education and training
2014 and implemented on January 1, 2015. experiences of the applicant are reviewed by
The American Academy of Clinical Neuropsy- ABPP for appropriate graduate training, intern-
chology (AACN). ABCN expanded its mission from ship, and licensure status in psychology. Applica-
being a board certification body to being a mem- tions that pass the ABPP general review are then
bership organization of board-certified specialists in forwarded to ABCN for review of advanced spe-
1983. The reason for this transition was to collect cialty credentials. Applicants who completed their
dues to fund the development of the written exam- doctoral training on or after January 1, 2005, must
ination. In 1996, ABPP legal counsel advised demonstrate training consistent with the Houston
examining boards against having a dual role of Conference on Specialty Education and Training
being both a certifying body and membership orga- in Clinical Neuropsychology, including required
nization. In response, the ABCN BOD voted to coursework and completion of a formal 2-year
incorporate its membership organization as a sepa- postdoctoral residency program in clinical neuro-
rate academy, with an independent board of direc- psychology. Policies and exceptions regarding
tors and separate mission statement. The AACN candidates who received their training before
took on the important task of promoting board implementation of the Houston Conference
certification, advocating for standards of training criteria respecialized in neuropsychology after
and education in clinical neuropsychology, and dis- obtaining a doctoral degree in another specialty
seminating information about the field of neuropsy- or received training in Canada are detailed on the
chology to the general public, forensic settings, ABCN website (www.theabcn.org).
schools, healthcare professionals, and clinical train- Once an applicant’s credentials are approved,
ing programs. The AACN provides mentorship and they may sit for the written examination. The
study support for candidates seeking board certifi- exam consists of 125 multiple-choice questions
cation through ABCN (Armstrong et al. 2008). that cover a range of topics in neuropsychology.
American Board of Clinical Neuropsychology (ABCN) 165

Only 100 items contribute to the candidate’s ability to demonstrate understanding of why the
final score. The other 25 items are included to issues are problematic. During this portion of the
gather psychometric data to determine the exercise, candidates are also invited to discuss A
item’s suitability as a future exam question. their own contributions to research, teaching,
The written examination tests the candidate’s practice administration, patient advocacy, or
breadth of knowledge and assures that they other activities that contribute to their professional
have the scientific foundation necessary for development. Currently, oral examinations are
competent practice in clinical neuropsychology. conducted twice annually in Chicago, Illinois,
Since 2012, the written examination has been hosted by the Neuropsychiatric Institute of the
administered electronically. It is currently University of Illinois at Chicago.
offered in 2-week windows, four times per The ABCN Subspecialty Examination in Pedi-
year through PSI testing centers across the atric Clinical Neuropsychology. ABCN special-
United States and Canada. ists who wish to become certified in the
Candidates who pass the written examination subspecialty of pediatric clinical neuropsychol-
may submit a practice sample consisting of two ogy may submit their credentials for review.
typical cases from their neuropsychology prac- Applicants who have been engaged in an active
tice. The practice samples are peer-reviewed by pediatric neuropsychology practice within the
at least three independent, board-certified neuro- 2 years prior to submission of their application
psychologists. Reviewers follow a standardized and document a minimum of 4000 h of postdoc-
rubric to determine whether the candidate’s clini- toral experience within pediatric neuropsychol-
cal practices, conclusions, and recommendations ogy meet criteria to pass subspecialty credential
as demonstrated in the sample would be defensi- review. Applicants who completed doctoral train-
ble upon oral examination. ing or respecialization in clinical neuropsychol-
If the practice sample is approved by at least ogy on or after January 1, 2005, must meet the
two reviewers, the candidate is invited to partici- additional requirement that at least 1000 of their
pate in an oral examination of their specialty com- 4000 h of postdoctoral clinical practice was
petencies. The oral examination consists of three obtained under the direct supervision of a pediat-
1-h exercises that cover (1) defense of the practice ric neuropsychologist. Two letters of reference
sample, (2) fact-finding, and (3) ethics and pro- must verify that the above criteria were met. Can-
fessional development. During the practice sam- didates who pass the credential review process
ple exercise, the candidate is given opportunities may take the 30-item subspecialty written exam-
to discuss their clinical practice as applied to the ination containing questions related to
specific cases they submitted. The cases also serve neurodevelopment, functional neuroanatomy,
as a starting point leading to more in-depth dis- pediatric clinical syndromes, specialized neuro-
cussion and evaluation of competencies such as psychological assessment techniques, develop-
assessment, intervention, consultation, and scien- mental psychology, and the ethical and legal
tific knowledge. The fact-finding exercise pre- issues of pediatric neuropsychological practice.
sents a brief description of a case that is new to Candidates who pass the written examination
the candidate. The candidate must then gather may submit a single pediatric neuropsychological
appropriate information from the clinical history, case evaluation of a patient age 16 or under that
test data, and medical record to generate an appro- clearly demonstrates independent practice at the
priate case conceptualization and differential subspecialist level of competence. The sub-
diagnosis. The ethics and professional develop- specialty review process differs in important
ment exercise allows candidates to demonstrate ways from that of the ABCN specialty review
knowledge of important ethical considerations as process because the specialty review is intended
presented in a brief vignette. Candidates are eval- to determine whether a candidate’s practice would
uated not only on their ability to identify the be defensible at oral examination. In contrast, the
ethical issues in the vignette but also on their subspecialty review process must determine if the
166 American Board of Clinical Neuropsychology (ABCN)

American Board of Clinical Neuropsychology (ABCN), Table 1 Timeline for major ABCN milestones
1981 ABCN incorporated in Minnesota
1983 Inaugural ABCN examinations completed and formal affiliation between ABCN and ABPP established
1984 First ABPP/ABCN certifications awarded
1988 Bylaws revised to create membership organization of board-certified neuropsychologists
1988 ABCN partners with professional examinations services to develop a specialty written examination
1993 Written examination implemented as the second stage of ABCN certification process
1996 The American Academy of Clinical Neuropsychology (AACN) becomes independently incorporated as the
membership organization of ABCN specialists
2002 ABCN endorses the Houston Conference on Specialty Education and Training in Clinical Neuropsychology
2004 500th ABCN certification awarded
2005 Houston Conference guidelines implemented as criteria for ABCN credential review process
2006 ABCN Committee on Innovations and Technology established to transition examination components to
electronic platforms
2007 Committee on subspecialization formed
2008 ABCN introduces fast-track credential review for applicants completing postdoctoral training in APPCN
member programs and APA-accredited specialty training programs
2009 First meeting of the ABCN Pediatric Special Interest Group (P-SIG)
2010 ABCN endorses the ABPP model for maintenance of certification
2011 P-SIG activities transfer from ABCN to AACN
2012 Written examination transitions to computer-based administration through Prometric
2012 Online ScholarOne portal implemented for electronic submission of practice sample materials
2013 Oral examinations move from Rush Presbyterian Hospital to University of Illinois, Chicago, Neuropsychiatric
Institute to accommodate growth of exams
2013 ABPP Board of Trustees approves ABCN subspecialty in pediatric clinical neuropsychology
2014 ABPP Standards Committee approves ABCN MOC procedures
2014 Specialty written examination expands from 100 to 125 items
2014 Implementation of the ABCN Practice Sample review cadre
2014 ABCN awards 1000th board certification.
2015 Credential reviews for the pediatric clinical neuropsychology subspecialty commence
2015 Written examination for the pediatric clinical neuropsychology subspecialty developed and implemented
2015 ABCN contracts with Alpine Testing Solutions and PSI Exams Online to manage and administer the specialty
written examination.
2016 Implementation of maintenance of certification policies

case sample on its own sufficiently demonstrates completed board certification prior to that date may
competent practice in the subspecialty. “opt in” to the process but are not required by ABPP
Maintenance of Certification. Maintenance of to do so.
certification (MOC) is a process of self-examination In the course of self-examination, specialists
of a specialist’s professional development since his survey their professional activities during the
or her initial board certification or last MOC review. 2 years prior to MOC submission and report/
The ABPP MOC model asserts that competence for describe the means by which those activities
independent specialty practice is established at the served to maintain the ABCN-defined competen-
time of initial board certification and can be contin- cies required for independent practice in clinical
uously maintained thereafter through lifelong learn- neuropsychology. Five broad categories of profes-
ing, ongoing participation in professional activities, sional activities support the maintenance of spe-
and self-evaluation related to core competencies. In cialty competencies. These include (1)
accordance with ABPP policy, MOC is required of collaborative clinical consultation; (2) teaching
all ABCN specialists awarded with board certifica- and training; (3) ongoing education; (4) research,
tion on or after January 1, 2015. Specialists who methodologies, and programs; and (5)
American Board of Pediatric Neuropsychology 167

professional leadership. Numerous activities fall Toward subspecialty designation. The Clinical Neuro-
within each of these categories and specialists psychologist, 25, 1075–1086. https://doi.org/10.1080/
13854046.2011.594455.
must indicate how the activities in which they Bieliauskas, L. A., & Matthews, C. G. (1987). American A
engaged served to support the competencies Board of Clinical Neuropsychology: Policies and pro-
defined by ABPP and ABCN as essential to neu- cedures. The Clinical Neuropsychologist, 1, 21–28.
ropsychological practice. Those with subspecialty Bieliauskas, L. A., & Matthews, C. G. (1990). American
Board of Clinical Neuropsychology update, 1990. The
certification must further ensure that MOC activ- Clinical Neuropsychologist, 4, 337–343.
ities support competencies required for sub- Bieliauskas, L. A., & Matthews, C. G. (1997). The Amer-
specialty practice. ican Board of Clinical Neuropsychology, 1996 update:
Beyond engagement in professional activities, Facts, data, and information for potential candidates.
The Clinical Neuropsychologist, 11, 222–225.
all ABCN specialists must also demonstrate Hannay, H. J., Bieliauskas, L., Crosson, B. A., Hammeke,
appropriate self-evaluation by describing their T. A., Hamsher K de, S., & Koffler, S. (1998). Pro-
practice, approaches to ethical or diversity issues, ceedings of the Houston Conference on specialty edu-
and the means by which they evaluate their clin- cation and training in clinical neuorpsychology.
Archives of Clinical Neuropsychology, 13, 157–250.
ical efficacy (e.g., ongoing peer review, perfor- Lucas, J. A., Mahone, M., Westerveld, M., Bieliauskas, L.,
mance evaluations, patient satisfaction data, & Baron, I. S. (2014). The American Board of Clinical
etc.). Members of the ABCN MOC Committee Neuropsychology and American Academy of Clinical
review all submissions against established ABCN Neuropsychology: Updated milestones 2005–2014.
The Clinical Neuropsychologist, 28, 889–906. https://
standards to determine if criteria for passing MOC doi.org/10.1080/13854046.2014.935484.
review have been met. Report of the Division 40/INS Joint Task Force on Educa-
tion, Accreditation, and Credentialing. (1984). Division
40 Newsletter, 2(2), 3–8.
Reports of the INS – Division 40 Task Force on Education,
Conclusion Accreditation, and Credentialing. (1987). The Clinical
Neuropsychologist, 1(1), 29–34.
With over 1200 certifications in clinical neuropsy- Sweet, J. J., Perry, W., Ruff, R. M., Shear, P. K., & Guidotti
Breting, L. M. (2012). The Inter-Organizational Summit
chology now awarded, ABCN specialists can be on Education and Training (ISET) 2010 survey on the
found across a multitude of practice settings, geo- influence of the Houston Conference training guidelines.
graphic locations, advocacy efforts, training pro- The Clinical Neuropsychologist, 26(7), 1055–1076.
grams, and research endeavors involving https://doi.org/10.1080/13854046.2012.705565.
Yeates, K. O., & Bieliauskas, L. A. (2004). The American
pediatric, adult, and older adult populations. Board of Clinical Neuropsychology and American Acad-
Board certification through ABCN reflects valida- emy of Clinical Neuropsychology: Milestones past and
tion of competence by one’s peers and assures the present. The Clinical Neuropsychologist, 18, 489–493.
public that the neuropsychologist has successfully
completed the education, training, and experience
requirements of the specialty, including examina-
tions designed to assess the competencies American Board of Pediatric
required to provide quality services in clinical Neuropsychology
neuropsychology.
Peter Dodzik
Fort Wayne Neurological Center, Fort Wayne,
References and Readings IN, USA

Armstrong, K., Beebe, D. W., Hilsabeck, R. C., & Kirk-

wood, M. W. (2008). Board certification in clinical Membership as of (January 2015)
neuropsychology: A guide to becoming ABPP/ABCN
certified without sacrificing your sanity. New York:
The American Board of Pediatric Neuropsychol-
Oxford Press.
Baron, I. S., Wills, K., Rey-Casserly, C., Armstrong, K., & ogy (ABPdN) was developed in 1996 by a coali-
Westerveld, M. (2011). Pediatric neuropsychology: tion of clinical practitioners representing
168 American Board of Pediatric Neuropsychology

institutions hiring pediatric neuropsychologists. general hospitals, hospital trauma centers, private
The original group conceived the board to practices, rehabilitation facilities, stroke centers,
advance their belief that a unique interplay exists memory disorders centers, group practices, and
between neurodevelopmental issues and neuro- child development centers. Current members
psychological assessment that requires special hold academic affiliations at over 40 colleges
sets of expertise not readily assessed by then and universities including Ivy League institutions
existing boarding entities. Following discussion and several university medical centers. Publica-
with colleagues who were members of medical tions from members of ABPdN include over 5000
practice and psychology boards, the coalition edited books, book chapters, and scholarly arti-
elected to establish an independent certifying cles. Several members have developed tests com-
authority. The examination process evolved into monly used in the practice of pediatric and general
a comprehensive and multi-level process that neuropsychology. Member accomplishments
includes a written application including clinical include:
case vignettes used to determine decision-making Professional Contributions
strategies of the applicant, scope of practice and a
thorough assessment of organized training in • Two past presidents of APA Division 40
pediatric neuropsychology (from graduate school • Past president of APA Division 2, 5 and 16
to continuing education), written examination, a • Current and past presidents of eight state psy-
practice sample submission, and an oral examina- chology boards
tion. The ABPdN does not have a “grand father- • Three past presidents of the National Academy
ing” policy and thus all existing board members of Neuropsychology
were required to complete all new phases of the • Two past editors of Archives of Clinical
examination process to ensure equality of stan- Neuropsychology
dards among boarded members. • Current editor of Archives of Clinical
As of early 2015, one hundred and eighty seven Neuropsychology
(187) neuropsychologists have submitted applica- • Current editor, Psychological Assessment
tions to ABPdN, and one hundred and thirty • Current editor, Journal of Attention Disorders
(130) members have passed the ABPdN examina- • Current editor, Journal of Pediatric
tion process. At present, there are ninety-three Neuropsychology
(93) active and five (5) emeritus members of the • Past editor, Journal of School Psychology
board from 28 states, Canada, and Puerto Rico. • Past editor, Applied Neuropsychology
• Eight prescribing psychologists

Major Areas or Mission Statement

Major Activities
Board certification in pediatric neuropsychology
serves to assist consumers by offering supportive The American Board of Pediatric Neuropsychol-
evidence of the competence of the pediatric ogy is the board-certifying arm of the American
neuropsychologists. The ABPdN is the only Academy of Pediatric Neuropsychology (AAPN),
board certification organization with the sole pur- which is devoted to training and promotion of the
pose of examining and certifying competence in field of pediatric neuropsychology. The AAPN
pediatric neuropsychology. holds an annual conference each spring with
topics related to the field of pediatric
neuropsychology.
Landmark Contributions The primary activity of ABPdN is conduct of
the Board certification process. Board examina-
Members of ABPdN practice in a variety of set- tion through the ABPdN involves several stages.
tings include universities, teaching hospitals, The format of the ABPdN’s examination
American Board of Pediatric Neuropsychology 169

processes has been constant since the examina- (VI) Detailed description of training in pedi-
tions held in 2004, but the procedures continue to atric neuropsychology (narrative)
be reviewed and amended. The purpose of the (B) Continuing Education A
ABPdN examination process is to ensure that the (I) Verification of CEUs in pediatric neuro-
examinee has demonstrated competency to prac- psychology for past 3 years
tice pediatric neuropsychology. The specific stages (C) Clinical Work
are discussed below and more detail can be (I) Clinical appointment verification con-
obtained from the ABPdN Web site (Beljan et al. tact information
2006). The overall pass rate for each stage of the (II) Breakdown of clinical practice by age,
examination process is between 73% and 81%. disorders, and ethnic background
(III) Completion of clinical vignettes
Credential Review (D) Educational Appointment (if applicable)
Minimum training and education standards (I) Academic institution verification contact
include completion of a doctoral degree from a information
regionally accredited program in applied psychol-
ogy that was, at the time the degree was granted, The application is first reviewed by
accredited by the APA and CPA or was listed in the examination chair for completion and accu-
the publication Doctoral Psychology Programs racy of documents and licensure status. The
Meeting Designation Criteria (“ASPPB National application is then reviewed by a panel of three
Register designation committee”, 2008). Mem- reviewers. A passing score by two of the three
bership in the National Register of Health Service reviewers is required to move to the next stage
Providers in Psychology, the Canadian Register of of the examination. Each reviewer evaluates the
Health Service Providers, or those holding the application for consistent and thorough training
Certificate of Professional Qualification qualify in pediatric neuropsychology at multiple levels
as meeting the doctoral requirements for member- of training.
ship. Licensure or certification at the independent
practice level as a psychologist in the state, prov- Practice Sample
ince, or territory in which the psychologist The purpose of the practice sample is determined
actively practices is also required. The applicant by the applicant’s clinical knowledge. While the
must be practicing as a pediatric neuropsycholo- written examination was designed to assess
gist and must have completed an APPIC or APA content-specific knowledge with regard to pediat-
accredited internship that included a documented ric neuropsychology, the practice sample allows
rotation or concentration in neuropsychology, and the board to evaluate the day-to-day skills of the
2 years of postdoctoral supervised experience in applicant. To that end, the sample should reflect a
neuropsychology, at least 50% of that being typical patient seen in the applicant’s clinical
pediatric-oriented. In addition, each applicant practice. Practice samples may include assess-
reviewed by the Board must provide the ment or intervention techniques. After an appli-
following: cation is reviewed and the candidate is
determined to be board-eligible, they will then
(A) Education be invited to provide a practice sample that
(I) Undergraduate degree transcript reflects their typical work in pediatric neuropsy-
(II) Graduate degree transcript chology. Prior to taking the objective and oral
(III) Internship verification contact examination, the candidate must prepare and
information tender one written sample of an original pediatric
(IV) Postdoctoral residency verification neuropsychological examination performed
contact information solely by the candidate. Appropriate samples
(V) Postdoctoral fellowship verification may include case analysis/interventions and
contact information (if applicable) supervision sessions.
170 American Board of Pediatric Neuropsychology

Written Examination and/or treatment) so that the fact-finding and prac-

The third step is the written exam, a 100-question, tice sample review can be conducted in the most
multiple-choice instrument designed and relevant fashion. This section is broken into two
constructed by other pediatric neuropsychologists parts:
whose purpose is to assess the candidate’s breadth
of knowledge in pediatric neuropsychology. The Part I: The examinee will explain their
questions were first assessed for face validity, background.
clustered for content area, rank ordered, deleted • The examinee will provide a history of their
or refined, reanalyzed, debated, approved, and educational and professional background.
then compiled into a larger item pool for random Special consideration should be given to
selection by domain each year. A passing score of their pediatric neuropsychological training
70% is required. Each exam includes the follow- and background.
ing basic core areas: • The examinee will explain their current role
as a pediatric neuropsychologist and the
• Psychometrics issues their typical clientele present.
• Pediatric Neurosciences Part II: The examinee will demonstrate
• Psychological and Neurological Development pertinent knowledge of practical pediatric
• Neuropsychological and Neurological neuropsychology.
Diagnostics Part III: Review of the practice sample.
• Ethics and Legal Issues This segment of the oral examination allows
• Research Design Review for Clinical the candidate to present the material in their
Application practice sample and to provide an overview of
• Intervention Techniques the history, evaluation process, and outcome of
• Consultation and Supervisory Practices the case. The examiners evaluate their ability
to articulate the major findings and their ratio-
Oral Examination nale. Candidates discuss their rationale in such
This part of the examination process is comprised areas as:
of a review of the candidate’s practice sample, the 1. Test selection (if applicable)
nature and application of neuropsychological Psychometric properties, test validity/
knowledge to their current practice, appreciation reliability, limitations for use, and exclusion
for ethical issues and obligations, and a review of of all competing diagnoses
the candidate’s views and philosophy on pediatric 2. Test interpretation (if applicable)
neuropsychology. The oral examination also Alternate interpretations of findings,
includes a mock case review, in which the candi- conflict resolution within the data, discus-
date is given information about a fictional case, sion of strengths and weaknesses, and envi-
and they develop and articulate their working ronmental and cultural factors
hypothesis. The oral examination is intended to 3. Diagnostic conclusions
be a collegial opportunity for the reviewers to Alternate diagnosis, ultimate under-
validate the candidate’s ability to “think on their standing of neuropathology, prognosis, pro-
feet” and discern their preparation and readiness gression, lateralizing/localizing effects,
for board certification. pathognomonic signs, causality, environ-
The first portion of the oral examination per- mental conditions, and effects on neural
mits the examination team to consider the scope of development
the candidate’s body of training and how they 4. Recommendations and treatment planning
practice pediatric neuropsychology (e.g., acute Best practices for treatment, availabil-
care, rehabilitation, outpatient, assessment, ity, prognosis, funding, delivery options,
American Board of Professional Neuropsychology (ABN) 171

cost/benefit analysis, iatrogenic outcomes,

parental compliance/agreement, and ethi- American Board of
cal issues Professional A
5. Consultation and supervision (if applicable) Neuropsychology (ABN)
Best practices for communication of
data, delivery options, supervisee needs/ John E. Meyers
relationships, and rapport/therapeutic Department of Neuropsychology, Comprehensive
relationship Medpsych Systems, Sarasota, FL, USA
This process is intended to be collegial
and the examiners endeavor to be sensitive
to the different and yet equally viable Address (and URL)
approaches within pediatric neuropsychol-
ogy. The purpose is to ascertain the candi- Geoffrey Kanter, Ph.D., ABN
date’s logic and thought processes and to Executive Director
allow them to demonstrate these skills. 1090 S Tamiami Trail
Part IV: Fact finding. Sarasota, FL 34236
The purpose of the fact finding portion of the (941) 363-0878
oral examination is to provide the candidate http://www.abn-board.com/
with the opportunity to review a clinical case
vignette including history, medical reports,
and test data and to generate diagnoses and
Membership
recommendations for treatment based on
that information. The candidate is expected
The American Board of Professional Neuropsy-
to use relevant information to generate
chology (ABN) is comprised of over 400 neuro-
hypotheses regarding the underlying pathol- psychologists who have doctoral degrees, are
ogy. Candidates will thoughtfully weigh eth-
licensed as psychologists, and have completed
ical and clinical considerations in the light of
the ABN diplomate examination process.
the APA ethics principles, professional prac- ABN was established in 1982 by a group of
tice standards, and relevant statutes.
clinical neuropsychologists, all of whom were
diplomates of the American Board of Professional
Psychology (ABPP), to provide peer regulation of
See Also the practice of professional neuropsychology. The
process of obtaining the ABN diplomate is a
▶ American Psychological Association (APA), dynamic one which has changed over the years
Division 40
and is expected to continue to evolve as the field
▶ National Academy of Neuropsychology (NAN)
of neuropsychology evolves. Initially, in addition
to obtaining a doctoral degree, acquiring licensure
as a psychologist, and completing a number of
References and Readings years of postdoctoral experience in neuropsychol-
ogy, early applicants were required to show evi-
ASPPB National Register Designation Committee. (2008).
Retrieved 1 Oct 2009 from http://www.nationalregister. dence of specialized training in neuropsychology
org/designate_stsearch.html and to provide supervisory evaluations of their
Beljan, P., Bos, J., Courtney, J., & Dodzik, P. (2006). competency in clinical neuropsychology.
Preparation guide for examination and certification
Between 1982 and 1985, following a review of
by the American board of pediatric neuropsychol-
ogy. Retrieved from http://abpdn.org/docs/ credentials and supervisory evaluations, work
studyguide.pdf samples were required. These were evaluated by
172 American Board of Professional Neuropsychology (ABN)

multiple examiners on a pass/fail basis. Individ- Maintenance of Certification requirement. ABN

uals who passed this final step were awarded a prefers an APA approved education program and
diplomate. Individuals who did not pass the eval- internship and for those who graduated after 2005
uation were allowed to apply for a “Certificate in requires a 2-year postdoctoral fellowship. ABN’s
Professional Neuropsychology,” indicating that application criteria are designed around the
they had some training in neuropsychology but Houston Conference Guidelines for postdoctoral
not sufficient enough to be awarded diplomate training in neuropsychology, though some flexi-
status. This was initially intended as an interim bility is allowed in meeting the internship and
credential as part of the process of obtaining a postdoctoral requirement, and graduated training
diplomate. After 1985, this process was aban- requirements are in place tied to era of gradua-
doned as increasing numbers of neuropsychology tion, to accommodate those who trained prior to
training programs became available. 2005. In 2008, the original acronym for ABN
In February of 1989, the ABN was reorganized was changed from ABPN to ABN to avoid con-
and the bylaws were modified. An annual dues fusion with the American Board of Psychiatry
structure was instituted and ABN became a mem- and Neurology. In January 2014 ABN created an
bership organization whose only credential is a affiliate organization the Academy of the Amer-
diplomate. This newly established organization ican Board of Professional Neuropsychology
mandated continuing education for active (AABN), which is a postdoctoral fellowship
membership. It was required that all those who organization.
had a “Certificate in Professional Neuropsychol- The current examination procedure includes:
ogy” complete the diplomate process to maintain
membership. At this time, an oral examination 1. Review of credentials and letters of
and essay examination were added to the case recommendation
study reviews, and all previous members were allo- 2. A 100-question multiple-choice examination
wed the opportunity to undergo the expanded 3. Case study/work samples review
examination process. Those who successfully com- 4. A 1 hour ethics oral examination and
pleted the process, including the new oral examina- 5. A 1 hour work style oral examination
tion, were given full diplomate status in ABN.
After 1991, those who did not successfully The multiple-choice written examination
complete the additional oral examination were no covers areas of general knowledge based on the
longer listed as diplomates through ABN. The recommended guidelines of the Houston Confer-
examination process included the essay examina- ence. The ethics examination addresses ethical
tion, and three 1 h oral examinations covering situations and current ethical dilemmas, and the
ethics, the work sample, and general knowledge. work style examination covers clinical vignettes
ABN no longer required letters of competency and clinical decision-making.
from supervisors but instead required letters of
recommendation from other neuropsychologists.
In 2004, the diplomate evaluation process was Major Areas or Mission Statement
again reevaluated and work began on substituting
a multiple-choice general knowledge examination ABN recognizes and encourages the pursuit of
for the oral examination on the same subject. This excellence in the practice of clinical neuropsy-
process took several years to complete, and as of chology. ABN’s primary objective is the estab-
January 1, 2009, all applicants were required to lishment of professional standards of expertise
complete the multiple-choice written examina- for the practice of clinical neuropsychology.
tion; the essay examination was dropped in favor Through its credentialing and examination pro-
of the multiple-choice exam. The continuing edu- cesses and its continuing education requirement,
cation requirement was expanded to a the ABN offers to the medical community, the
American Board of Professional Neuropsychology (ABN) 173

public, and to individuals who have a need for and interorganizational activities supporting the
applied neuropsychological services, a process development of neuropsychology.
whereby competent clinical neuropsychologists A
can be identified.
To achieve the standards set forth by the ABN Major Activities
for competent professional practice of neuropsy-
chology, the following outcome objectives have ABN holds an annual board of directors meeting
been developed: at the National Academy of Neuropsychology
(NAN) conference. Associated with ABN is the
• Validate the skills of clinical practitioners American College of Professional Neuropsychol-
• Identify competent practitioners ogy (ACPN) whose purpose is to provide continu-
• Provide public information about clinical ing education programs in neuropsychology.
neuropsychology ABN holds monthly meetings of the board of
• Document the maintenance of competence of directors and committee chairs to organize ABN’s
professional neuropsychology practitioners professional activities. ABN candidate examina-
with continuing education requirements tions and examiner training workshops are typi-
• Provide individuals, organizations, and agen- cally held a minimum of twice a year at locations
cies who use neuropsychology services with a throughout the country. A workshop on the ABN
referral directory of ABN diplomates examination process is held at least once a year.
Individual candidate mentoring is offered
Recognition by ABN signifies to the public throughout the year.
and to other health professionals a high level of ACPN is approved by the American Psycho-
competency in applied neuropsychology. The logical Association to sponsor continuing educa-
ABN does not ascribe to any specific theoretical tion for psychologists. ACPN typically holds at
framework. While recognizing the importance least one general meeting each year, covering
and contribution of a graduate education in neu- various subjects, offering continuing education
ropsychology and subsequent specialty training, credits to attendees.
the ABN believes that the critical element in the
practice of professional neuropsychology is the
application of that training to client issues and References and Readings
needs.
Bennett, T. L., Horton Jr., A. M., & Elliott, R. W. (1999).
American Board of Professional Neuropsychology
(ABPN). Bulletin of the National Academy of Neuro-
Landmark Contributions psychology, 14, 7–9.
Elliott, R. W., & Horton Jr., A. M. (1994). Philosophy of
Applied Neuropsychology: Adult, a peer-reviewed the American Board of Professional Neuropsychology.
Bulletin of the National Academy of Neuropsychology,
edited journal, is an official journal of the ABN.
11, 14–15.
Applied Neuropsychology: Child, a peer- Elliott, R. W., & Horton Jr., A. M. (1995). History and
reviewed edited journal, is an official journal of current status of the American Board of Professional
the ABN. Neuropsychology. The Independent Practitioner,
15, 175–177.
The Academy of ABN (AABN) is a postdoc-
Goldstein, G. (2001). Board certification in clinical neuro-
toral training site recognition organization. The psychology: Some history, facts and opinions. Journal
AABN uses a standard didactic curriculum to of Forensic Neuropsychology, 2, 57–65.
ensure that all sites can meet the Houston Confer- Horton Jr., A. M., Crown, B. M., & Reynolds, C. R. (2001).
American Board of Professional Neuropsychology: An
ence Training Guidelines. update-2001. Journal of Forensic Neuropsychology,
ABN actively participates in national and inter- 2, 67–78.
national neuropsychological specialty initiatives http://www.abn-board.org/
174 American Board of Professional Psychology (ABPP)

Psychology 2008). Moreover, ABPP board

American Board of certification is increasingly associated with
Professional Psychology greater opportunities for career growth, including
(ABPP) employment opportunities, practice mobility
between jurisdictions, and financial compensation
Christine Maguth Nezu (American Board of Professional Psychology;
Department of Psychology, Drexel Sweet et al. 2006).
University–Hahnemann Campus, Philadelphia, ABPP is currently a unique and unitary
PA, USA umbrella organization with multiple specialty
boards that include Clinical Child and Adolescent
Psychology, Clinical Health Psychology, Clinical
Membership Neuropsychology, Clinical Psychology, Cogni-
tive and Behavioral Psychology, Counseling
The American Board of Professional Psychology Psychology, Couple and Family Psychology,
(ABPP) has over 3100 currently active board- Forensic Psychology, Geropsychology, Group
certified specialists in membership. As a national- Psychology, Organizational and Business Con-
in-scope credentialing organization in profes- sulting Psychology, Police and Public Safety
sional psychology, its membership is comprised Psychology, Psychoanalysis in Psychology,
doctoral-level psychologists who provide profes- Rehabilitation Psychology, and School Psychol-
sional services and consultation and are licensed ogy. Many professional psychologists seek dual
to practice psychology in the jurisdiction in which certifications that reflect the full scope of their
they practice. Completion of a doctoral degree, specialties. Examples of these might include
completion of a qualified internship, relevant clinical and cognitive behavioral, clinical neuro-
postdoctoral experience, and relevant jurisdic- psychology and rehabilitation, or counseling and
tional licensure as a psychologist are the mini- group. Uniquely, the Clinical Neuropsychology
mum prerequisites for approval to take an ABPP board also offers a subspecialty in pediatric neu-
board certification exam. However, through its ropsychology, though, as of this writing, other
Early Entry Option, ABPP permits psychology subspecialties are being considered by other
graduate students, interns, and residents to begin ABPP boards.
the application process at a reduced fee, sub- For a licensed psychologist to be “board eligi-
mitting credentials as they are completed until ble,” each of the 15 boards requires that he or she
full eligibility criteria are met for the selected meets both generic and specialty eligibility
specialty area. criteria concerning education, professional
training, and licensure in the jurisdiction where
professional services are provided. Once an indi-
Major Areas or Mission Statement vidual’s credentials are reviewed and approved,
the individual seeking board certification moves
The American Board of Professional Psychology to the next phase of their candidacy process.
(ABPP) is a national-in-scope credentialing In clinical neuropsychology and forensic special-
organization that has been awarding board certifi- ties, this necessitates passing a written examina-
cation in professional psychology specialties for tion. In all other specialties, the candidates are not
over 60 years (Bent et al. 1999; Finch et al. 2006; required to take a written exam and may move
Packard and Reyes 2003). ABPP describes the directly to the final phases in the process. For all
value of its credential as one that “provides peer specialties, this includes first submitting a profes-
and public recognition of demonstrated compe- sional practice sample. After the practice sample
tence in an approved specialty area in professional is approved, the oral examination (final phase) is
psychology” (American Board of Professional typically scheduled. Specialty boards may also
American Board of Professional Psychology (ABPP) 175

provide a “senior option” regarding practice sam- process across specialty boards. Specialists certi-
ples submitted by candidates with at least 15 years fied after January 1, 2015, must successfully dem-
of experience post licensure who may submit onstrate maintenance of competency every A
samples of their professional work such as publi- 10 years to maintain their ABPP board-certified
cations, treatment manuals, program manuals, or a status. This requires detailed reporting of continu-
comprehensive summary of their professional ing education and other professional competency-
practice, to satisfy the requirements of a profes- related activities, appropriate for the certifying
sional practice sample. specialty board. Specialists certified before
With regard to both practice samples and oral January 1, 2015, may participate in formal MOC
exams, the candidate’s competency is assessed but also have the option of waiving this
across various domains. These competency requirement.
domains may be functional in nature and include
the day-to-day activities of specialty practice, such
as assessment, intervention, and/or consultation Landmark Contributions
that are informed by a scientific literature base.
They also include foundational competencies, The origins of ABPP can be traced back to its
such as ethics, individual and cultural diversity, establishment in 1947 as the American Board of
and interpersonal competence, which cut across Professional Examiners in Psychology (Bent et al.
all of a specialist’s other activities. The compe- 1999). The intention of the original board was to
tency model upon which ABPP board certification ensure that individuals were qualified to perform
is based draws from several important sources such the professional service activities associated with
as the APA-sponsored Competencies Conference clinical and counseling psychology. However,
in 2002 and resulting Task Force on Assessment as professional psychology expanded its scope
of Competence in Professional Psychology and depth, the organization changed its name to
(Kaslow et al. 2007), and a review of competency the American Board of Professional Psychology
assessment models developed both within (e.g., to reflect the expansion of specialization activities
Assessment of Competence Workgroup from that were emerging for professional psycholo-
Competencies Conference – Roberts et al. 2005; gists. As a result, the number of its affiliated
Leigh et al. 2007) and outside (e.g., American specialty boards and associated academies has
Council for Graduate Medical Education and grown from 3 to 13, reflecting this professional
American Board of Medical Specialties 2000) of expansion and the breadth of specialties that have
the profession of psychology. emerged in recent decades (Finch et al. 2006;
There is a strong consensus among many pro- Packard and Reyes 2003).
fessional psychologists that the American Board
of Professional Psychology represents a high
degree of integrity regarding specialty board cer- Major Activities
tification and serves as a gold standard for dem-
onstration of specialty competency in professional Each of the psychology specialty boards under the
psychology. In recent years, ABPP has turned its ABPP umbrella has an elected trustee who partic-
attention to maintenance of professional compe- ipates as a member of the ABPP Board of Trustees
tency over the specialist’s career. From 2006 to as the overall governance group of the ABPP.
2014, ABPP encouraged specialists to periodi- Each specialty board assumes the responsibility
cally review their performance to maintain quality for developing and carrying out the ABPP spe-
of professional care and to serve and protect con- cialty examinations. The ABPP central office,
sumers of psychological services. ABPP has under the management of a full-time executive
recently adopted formal Maintenance of Certifi- officer, executes important day-to-day functions
cation (MOC) procedures to standardize this for all of the 13 specialty boards. These include
176 American Board of Rehabilitation Psychology

generic candidacy verification of applicants, bud- Finch, A. J., Simon, N. P., & Nezu, C. M. (2006). The
get maintenance and accounting responsibilities, future of clinical psychology: Board certification. Clin-
ical Psychology: Science and Practice, 13, 254–257.
record keeping, development and maintenance of Kaslow, N. J., Rubin, N. J., Bebeau, M. J., Leigh, I. W.,
an ABPP Directory, development and editing Lichtenberg, J. W., Nelson, P. D., Portnoy, S. M., &
responsibility for the ABPP website, monitoring Smith, I. L. (2007). Guiding principles and recommen-
the organization relative to ethical/legal issues, dations for the assessment of competence. Professional
Psychology: Research and Practice, 38, 441–451.
planning of conference and governance activities, Leigh, I. W., Smith, I. L., Bebeau, M. J., Lichtenberg, J. W.,
and general administrative support. The primary Nelson, P. D., Portnoy, S., Rubin, N. J., & Kaslow, N. J.
publication of the organization, The Specialist, is (2007). Competency assessment models. Professional
published twice annually and available to all Psychology: Research and Practice, 38, 463–473.
Nezu, C. M., Finch, A. J., & Simon, N. P. (Eds.). (2009).
members in both electronic and printed format. Becoming board certified by the American board of
The organization website (www.ABPP.org) con- professional psychology (ABPP). New York: Oxford
tains important information regarding the mis- University Press.
sion, governance, and organizational documents. Packard, T., & Reyes, C. J. (2003). Specialty certification
in professional psychology. In M. J. Prinstein & M. D.
For the public, the website contains listings of Patterson (Eds.), The portable mentor: Expert guide to
board-certified specialists across specialties and a successful career in psychology (pp. 191–208).
practice jurisdictions. For interested applicants, it New York: Plenum.
contains application instructions as well as other Roberts, M. C., Borden, K. A., Christiansen, M. D., &
Lopez, S. J. (2005). Fostering a culture shift: Assess-
helpful information. The organization published ment of competence in the education and careers of
its first book, Becoming Board Certified by the professional psychologists. Professional Psychology:
American Board of Professional Psychology Research and Practice, 36, 355–361.
(ABPP), in 2009. This has been followed by pub- Sweet, J. J., Nelson, N. W., & Moberg, P. J. (2006). The
TCN/AACN 2005 “salary survey”: Professional prac-
lication of separate guides to become board certi- tices, beliefs, and incomes of U.S. neurophysiologists.
fied by many individual specialties. The Clinical Neuropsychologist, 20, 325–364.

Cross-References
American Board of
▶ American Academy of Clinical Neuropsychol- Rehabilitation Psychology
ogy (AACN)
▶ American Board of Clinical Neuropsychology Daniel E. Rohe
(ABCN) Mayo Clinic, Rochester, MN, USA
▶ American Board of Rehabilitation Psychology

Membership
References and Readings
The American Board of Rehabilitation Psychol-
American Board of Professional Psychology. (2008).
Retrieved June 25, 2008, from http://www.abpp.org ogy (ABRP) is 1 of 15-member boards of the
American Council for Graduate Medical Education and American Board of Professional Psychology
American Board of Medical Specialties. (2000). Tool- (ABPP). The ABRP has certified 186 (as of
box of assessment methods. Chicago: American Coun-
2017) doctoral-level psychologists who are
cil for Graduate Medical Education and American
Board of Medical Specialties. engaged in provision of rehabilitation psychology
Bent, R. J., Packard, R. E., & Goldberg, R. W. (1999). The services to individuals and their families affected
American board of professional psychology. Profes- by a wide range of disabilities and chronic health
sional Psychology: Research and Practice, 30, 65–73.
conditions including brain injury, spinal cord
Datillio, F. M. (2002). Board certification in psychology: Is
it really necessary? Professional Psychology: Research injury, amputations, chronic pain, multiple sclero-
and Practice, 33, 54–57. sis, cancer, and sensory impairment such as
American Board of Rehabilitation Psychology 177

blindness and deafness. In addition to clinical interpersonal interactions, individual and cultural
services, the majority of the board certified reha- diversity, ethical and legal foundations, and pro-
bilitation psychologists also engage in research, fessional identification. The functional competen- A
teaching, and administration of rehabilitation pro- cies encompass science base and application,
grams. Rehabilitation psychologists are also assessment, intervention, consultation, and con-
involved in interdisciplinary teamwork with sumer protection.
other medical and rehabilitation providers. Reha-
bilitation psychologists who are boarded in the
specialty reside in 30 states and 1 Canadian Landmark Contributions
province.
The primary contribution of ABRP is providing
the opportunity for psychologists, dedicated to the
Major Areas or Mission Statement health and psychological welfare of individuals
with a wide range of disabilities and chronic
The mission of the ABRP is to protect the public health conditions, to unite and be boarded in a
and enhance the quality of health care by certify- single specialty. The ABRP began as a credentials
ing rehabilitation psychologists who demonstrate committee within the Division of Rehabilitation
the knowledge, skills, and attitudes essential to Psychology of the American Psychological Asso-
maximize quality of life for individuals with dis- ciation in 1993. This committee incorporated as
abilities and chronic illness. The vision of the the American Board of Rehabilitation Psychology
ABRP is that all psychologists practicing in reha- in 1995. On December 4, 1994 they established
bilitation will be boarded in the specialty. Psy- bylaws and elected officers: Richard Cox (presi-
chologists who become board certified in dent, 1994–2000), Bernard Brucker (vice presi-
Rehabilitation Psychology must meet the generic dent), Mitchell Rosenthal (secretary), and Daniel
requirements for specialty certification by the Rohe (treasurer). The initial members at large
ABPP that include a doctoral degree in psychol- were Bruce Caplan, David Cox, Harry Parker,
ogy from an accredited degree program and licen- Anthony Ricci, James Whelan, and Mary
sure as a psychologist for independent practice in Willmuth. Subsequent board presidents have
the USA or Canada. The ABRP-specific eligibil- included Mitchell Rosenthal (2000–2003), Ber-
ity requirements include completion of a recog- nard Brucker (2004–2007), Daniel Rohe
nized internship program and 2 years of (2008–2011), Lester Butt (2012–2013), and
supervised practice in Rehabilitation Psychology. Michele Rusin (2014–present). The second
Given the diverse training experiences of rehabil- major contribution is crafting an organizational
itation psychologists, the credential review relies structure that reflects the values of Rehabilitation
on the ratings of supervisors (two required) and Psychologists. The ABRP designed an innovative
the endorsement of colleagues and peers (two examination process that is user-friendly, colle-
required). The candidate then submits a two-part gial, inclusive, competency-based, and affirming
practice sample (typically two case reports) that is of the candidate. The ABRP was the first ABPP
evaluated by three ABRP examiners. Finally, the board to devise a proactive mentoring program
candidate completes an oral examination on two that has a credentialed colleague guide the appli-
clinical vignettes, their clinical practice sample, cant through the process. The ABRP examination
and ethics. The entire examination process is and mentoring process has been emulated by other
designed to ensure that each candidate demon- ABPP boards. The third major contribution is
strates the foundational and the functional com- cosponsorship of the Rehabilitation Psychology
petencies required of a psychologist who is board Annual Conference with the Division of Rehabil-
certified in Rehabilitation Psychology. The foun- itation Psychology from 1999 to the present. The
dational competencies fall in four domains: annual meeting has become an institutionalized
178 American College of Professional Neuropsychology (ACPN)

opportunity for rehabilitation psychologists to

meet, present research, and promote the specialty American College of
to students. Professional
Neuropsychology (ACPN)
Major Activities John E. Meyers
Department of Neuropsychology, Comprehensive
The primary activity of ABRP is examination of Medpsych Systems, Sarasota, FL, USA
psychologists entering the field of Rehabilitation
Psychology. The second major activity is provid-
ing mentoring in the boarding process by the Membership
members of the board. The third major activity
of ABRP has been cosponsoring the Rehabilita- The American College of Professional Neuro-
tion Psychology Annual Conference. This confer- psychology (ACPN) is a membership organiza-
ence typically occurs the last weekend of tion formed on September 1, 1995, that is
February and provides the opportunity to earn composed of over 400 neuropsychologists who
continuing education credits specific to Rehabili- have doctoral degrees, are licensed as psycholo-
tation Psychology. The conference provides gists, and have completed the Diplomate exami-
ABRP sponsored educational sessions that nation process of the American Board of
explain the process of attaining board certification Professional Neuropsychology as well as 122
in Rehabilitation Psychology to interested candi- Affiliate members.
dates. The conference features nationally recog-
nized leaders in the field of Rehabilitation
Psychology. The ABRP board works in concert Major Areas or Mission Statement
with the newly created Academy of Rehabilitation
Psychology (ARP). The ARP is a separate orga- ACPN is the academic arm of the American Board
nization that is assuming the role of providing of Professional Neuropsychology (ABN). The
logistical support for the Rehabilitation Psychol- mission of the ACPN is to promote and provide
ogy Annual Conference. the highest levels of services related to profes-
sional neuropsychology for the benefit of the pub-
lic and the profession.
Cross-References

▶ American Board of Professional Psychology

Landmark Contributions
(ABPP)
▶ American Psychological Association (APA),
In addition to the continuing education benefit,
Division 22
ACPN also has two official quarterly journals –
▶ Rehabilitation Psychology
Applied Neuropsychology: Adult and Applied Neu-
ropsychology: Child, which are dedicated to the
presentation of practitioner-based scholarly research.
References and Readings Diplomates of the ABN who are in good stand-
Cox, D., Cox, R., & Caplan, B. (2013). Specialty compe-
ing are automatically Fellows of ACPN and may
tencies in rehabilitation psychology. New York: Oxford use the acronym FACPN on their signature line.
University Press. Members of other neuropsychological organiza-
Frank, R., Rosenthal, M., & Caplan, B. (Eds.). (2009). tions may also join the ACPN as Affiliate mem-
Handbook of rehabilitation psychology (2nd ed.). Wash-
bers and receive a subscription to the Applied
ington, DC: American Psychological Association.
Kennedy, P. (Ed.). (2012). Oxford handbook of rehabilita- Neuropsychology Journals and can participate in
tion psychology. New York: Oxford University Press. ACPN continuing education programs.
American Congress of Rehabilitation Medicine 179

Major Activities is an overlap in methods and sometimes clientele.

ACRM members share an interest in rehabilitation
ACPN is approved by the American Psychologi- research, and the translation of research-based A
cal Association to sponsor continuing education knowledge into formats that are of use to medical
for psychologists. ACPN typically holds at least rehabilitation clinicians. Within the organizations
one general meeting each year, covering various that employ them, ACRM members may play one
subjects, and offering continuing education or more roles: rehabilitation practitioner, rehabil-
credits to attendees. itation researcher, knowledge broker, research
funder staff, clinical administrator, teacher, etc.
About 550 members are located outside the
Cross-References United States in over 50 countries.

▶ American Board of Professional Neuropsy-

chology (ABN) Mission Statement

The slogan currently used by the organization

expresses its mission: “Improving lives through
interdisciplinary rehabilitation research.” This is
American Congress of further clarified by “We enhance the lives of peo-
Rehabilitation Medicine ple living with disabilities through a multi-
disciplinary approach to rehabilitation. As
Marcel P. J. M. Dijkers leaders in the physical medicine and rehabilitation
American Congress of Rehabilitation Medicine, field, we promote innovative research, new tech-
Reston, VA, USA nologies, and sharing information, and encourage
Department of Rehabilitation Medicine, Icahn evidence-based practices in clinical settings”
School of Medicine at Mount Sinai, New York, (About ACRM 2015). The interdisciplinary char-
NY, USA acter and research focus of the organization are
further expressed by another slogan: “Excellence
in the science of rehabilitation medicine through
Membership as of December 2016 interdisciplinary collaboration” (About ACRM
2015). ACRM supports research that promotes
Membership is about 2,300, consisting of clini- health, independence, productivity, and quality
cians and nonclinicians with an interest in medical of life and meets the needs of rehabilitation clini-
rehabilitation (rehabilitation medicine, physical cians and people with disabilities. In order to
medicine and rehabilitation) research, and training enhance current and future research and knowl-
in medicine, (neuro)psychology, occupational and edge translation, the organization:
physical therapy, nursing, speech and language
pathology, vocational counseling, rehabilitation • Assists researchers in improving their investi-
engineering, medical sociology, etc. Medical gations and dissemination of findings
rehabilitation concerns restoration of function for • Shares this information via education meetings
individuals who as a result of stroke, traumatic and its journal, Archives of Physical Medicine
brain injury, spinal cord injury, amputation, can- and Rehabilitation
cer, neurodegenerative diseases and other disor- • Encourages leaders in rehabilitation to identify
ders have impairments and activity limitations current best practices at all levels of care
that are primarily physical in nature but often • Serves as a forum for creating and discussing
also include cognitive and behavioral deficits; it new treatment paradigms to achieve optimal
is to be distinguished from psychiatric rehabilita- functional outcomes for people with chronic
tion, addiction rehabilitation, etc., although there disease and disabilities
180 American Congress of Rehabilitation Medicine

• Educates providers to deliver best practices professionals with a bachelor’s degree as mem-
• Advocates for funding of future rehabilitation bers starting in 1986. The first nonphysician to
research become president of the organization took office
in 1977; neuropsychologists who have served as
president include Leonard Diller, Mitchell
Landmark Contributions Rosenthal, and Wayne Gordon.
In recent years, ACRM has redefined itself as
The American Congress of Rehabilitation Medi- an organization focusing on rehabilitation sci-
cine was established in 1923 as the American ence, with strong interest in both generating
College of Radiology and Physiotherapy, a profes- knowledge through research and knowledge
sional organization of physicians who had a clini- translation to bring research results to clinical
cal interest in diagnostic and therapeutic radiology, practice in a format that practitioners can use
as well as the therapeutic application of electricity (Hart 1997; Heinemann 2006; Wilkerson 2004).
and other physical therapies (Dijkers 2009). It is now primarily a group of creators, transmit-
Reflecting the ongoing differentiation between ters, and users of research-based rehabilitation
radiologists and what (much later) would be called knowledge, both those with clinical training (phy-
physiatrists, the name was changed to American sicians, occupational and physical therapists, psy-
Congress of Physical Therapy in 1925. To empha- chologists, etc.) and those without (engineers,
size its link to medicine rather than allied health, social scientists, etc.), bound by the conviction
the organization renamed itself American Con- that the collaboration of disciplines is the best
gress of Physical Medicine in 1944. way to solve the problems inherent in disablement
While World War I had given rise to the devel- and the rehabilitation of persons with impairment,
opment of rehabilitation, the involvement of physi- activity limitations, and participation restrictions.
cians had been limited – rehabilitation was centered The seal of the organization until very recently
on the vocational rehabilitation of discharged ser- still reflected ACRM’s roots in physical medicine,
vicemen. During World War II, however, a number including the traditional symbols for medicine and
of military physicians became specialists in reha- for the four elements: water, earth, fire, and air. In
bilitation; after the war they started to apply the 2013 a new logo was unveiled, showing the over-
methods they had developed with injured service- lapping petals of a lotus flower, to visually commu-
men to the treatment of civilians with amputations, nicate the interdisciplinary culture of the
spinal cord injury, stroke, and developmental dis- organization.
abilities such as cerebral palsy. To avoid the crea-
tion of a separate organization involving physicians
with very similar interests and therapeutic regi- Major Activities
mens, a “shotgun marriage” between physiatrists
and these rehabilitation physicians was acknowl- ACRM communicates with its members through
edged in 1952 with the expansion of the name of its scientific journal (the Archives of Physical
the organization to American Congress of Physical Medicine and Rehabilitation – APM&R), a news-
Medicine and Rehabilitation (Zeiter 1954). letter (Rehabilitation Outlook), electronic news-
In the 1960s, the Congress opened its member- letters for various special interest groups, and the
ship to nonphysician rehabilitation professionals, weekly E-news, an electronic digest of time-sen-
first only those holding a doctoral degree (1965) sitive news. An annual scientific meeting of
and then also to nurses and therapists with a 3–4 days, often held jointly with other scientific
(earned) master’s degree (Anonymous 1998). To and professional organizations, brings together
acknowledge the diminishing emphasis on phys- members and nonmembers to discuss research
ical medicine, the Congress changed its name findings, research methods, and issues relevant
again, to American Congress of Rehabilitation to the funding, implementation, and dissemina-
Medicine, in 1966. ACRM accepted rehabilitation tion of rehabilitation research. A midyear meeting
American Congress of Rehabilitation Medicine 181

brings together members of task forces across the 40 (Clinical Neuropsychology) of the American
many special interest groups to further their mul- Psychological Association. Intense collaboration
tiple ongoing projects. in research and clinical care occurs among the BI- A
A number of standing committees offer mem- ISIG members, who have their own task forces;
bers an opportunity to work on issues of special communicate through the BI-ISIG newsletter,
interest. Current committees include the Interna- Moving Ahead; and come together at the ACRM
tional Committee (focusing on the communica- midyear meeting.
tions between US and foreign rehabilitation APM&R began in 1920 as the Journal of Radiol-
research specialists), the Evidence and Practice ogy and changed its name to the Archives of Physical
Committee (dealing with issues of evidence- Therapy, X-ray, Radium, in 1926. Later changes in
based rehabilitation and related matters), and the its name parallelled those in the name of its owner:
Health Policy Networking Group. The Early Archives of Physical Therapy in 1938 and the
Career Committee aims to assist individuals new Archives of Physical Medicine in 1945. In 1953,
to rehabilitation research in mastering the scien- the journal became the Archives of Physical Medi-
tific, administrative, and personal aspects of a cine and Rehabilitation, the name it still has (Nelson
career in rehabilitation research. 1969). However, the content has shifted gradually
Over the years, a number of interdisciplinary from emphasis on physical medicine, with a
special interest groups (ISIGs) have existed under fairly low research basis, to an accent on rehabil-
the aegis of ACRM; current groups include ISIGs itation as carried out by all disciplines that play a
focused on pain, spinal cord injury, stroke, mea- role in medical rehabilitation. It is now almost
surement, pediatric rehabilitation, geriatric reha- exclusively a research journal, with non-US con-
bilitation, cancer, and traumatic brain injury. tributions constituting over half the contents. It
The Brain Injury ISIG (BI-ISIG) grew out of has a respectable impact factor (3.3) ranking it
the ACRM Head Injury Task Force, first called fifth in the “rehabilitation” category, but because
together in 1979. The BI-ISIG, which attracts of the large number of papers published each
large numbers of psychologists and especially year, it has more influence than higher-ranked
neuropsychologists, has played a crucial role in journals. In fact, the annual number of citations
the development of services for individuals with is about is larger than those of the four higher-
traumatic brain injury (TBI) in the United States. ranked publications together.
A definition of mild TBI often used in the litera- The journal probably gives the best indication
ture emerged from the work of this group (ACRM of the role of neuropsychology in rehabilitation
Head Injury Interdisciplinary Special Interest settings and of neuropsychologists in ACRM. The
Group 1993). The Journal of Head Trauma Reha- first paper with neuropsychology in its title or
bilitation (JHTR) was founded by a physician abstract was distributed in 1975. About 300 have
(Sheldon Berrol) and a psychologist (Mitchell been published since, but they did not become an
Rosenthal) who were active in the BI-ISIG, as annual presence until 1984. The number now
well as involved with the fledgling National averages over 15 a year. In scanning the contribu-
Head Trauma Foundation, now the Brain Injury tions of neuropsychologists to APM&R, a number
Association of America. There is significant over- of characteristics of neuropsychology in rehabili-
lap between the BI-ISIG membership and both the tation stand out:
Editorial Board of JHTR and the leadership of the
TBI Model Systems of Care, demonstration, and • Many of these papers are coauthored with rep-
research grant programs supported by the resentatives of other disciplines, especially
National Institute on Disability, Independent Liv- physicians.
ing and Rehabilitation Research since 1987 • Several straddle neuropsychology and rehabil-
(Dijkers et al. 2010). There also is considerable itation psychology, reflecting the fact that in
overlap between the membership of the BI-ISIG many rehabilitation programs, psychologists
and Divisions 22 (Rehabilitation Psychology) and need to wear multiple hats.
182 American Psychological Association (APA)

• The focus, especially in recent years, is as Archives of Physical Medicine and Rehabilitation, 78
much on treatment as on diagnosis, with cog- (12), 1287–1289.
Heinemann, A. W. (2006). ACRM’s evolving mission:
nitive rehabilitation for TBI and other diagnos- Opportunities to promote rehabilitation research.
tic groups most prominent. Archives of Physical Medicine and Rehabilitation, 87
• A great variety of diagnostic groups have been (2), 157–159.
studied, including peripheral vascular disease Kottke, F. J., & Knapp, M. E. (1988). The development of
physiatry before 1950. Archives of Physical Medicine
amputations, post-polio fatigue, multiple scle- and Rehabilitation, 69. Spec No, 4–14.
rosis, sickle-cell disease, progressive supra- Krusen, F. H. (1969). Historical development in physical
nuclear palsy, myotonic muscular dystrophy, medicine and rehabilitation during the last forty years.
and spinal cord injury. Walter J. Zeiter lecture. Archives of Physical Medicine
and Rehabilitation, 50(1), 1–5.
• However, over the years and especially recently, Nelson, P. A. (1969). History of the archives – a journal of
stroke and TBI have been the etiologies of dis- ideas and ideals. Archives of Physical Medicine and
ability that rehabilitation neuropsychologists Rehabilitation, 50(7), 367–405. passim.
have most often been concerned with. Rusk, H. A. (1969). The growth and development of reha-
bilitation medicine. Archives of Physical Medicine and
Rehabilitation, 50(8), 463–466.
While the American Congress of Rehabilita- Wilkerson, D. L. (2004). Individual, science, and society:
tion Medicine is not an organization of psycholo- ACRM’s mission and the body politic. Archives of
gists, let alone neuropsychologists, it is safe to say Physical Medicine and Rehabilitation, 85(4), 527–530.
Zeiter, W. J. (1954). The history of the American Congress
that it has played a key role in the development of of Physical Medicine and Rehabilitation. Archives of
neuropsychology for medical rehabilitation Physical Medicine and Rehabilitation, 35(11),
patients in the United States. In the foreseeable 683–688.
future, it probably will continue to be the forum in
which these specialists, especially those who are
interested in research, interact with nurses,
speech/language pathologists, neuroscientists, American Psychological
and other specialists who contribute to rehabilita- Association (APA)
tion and its evidence base.
Nadine J. Kaslow1 and Jennifer M. Doran2
1
Department of Psychiatry and Behavioral
References and Readings Sciences, Emory University School of Medicine,
APA, Atlanta, GA, USA
2
About ACRM. (2015). Retrieved 4 Aug 2015, from http:// VA Connecticut Healthcare System, Yale School
www.acrm.org/about/ of Medicine, Newington, CT, USA
American-Congress-of-Rehabilitation-Medicine.-Head-
Injury-Interdisciplinary-Special-Interest-Group.
(1993). Definition of mild traumatic brain injury. The
Journal of Head Trauma Rehabilitation, 8(3), 86–87. Membership
Anonymous. (1998). Development of the American Con-
gress of Rehabilitation Medicine into a multi- As of 2017, the American Psychological Associ-
disciplinary professional society: Final report of the
Professional Development Committee, 1969–1972. ation (APA) had a total of 115,492 members
Archives of Physical Medicine and Rehabilitation, 79 (76,174 full members and 39,318 affiliate mem-
(12 Suppl. 2), 4–12. bers, including 31,560 students).
Dijkers, M. P. (2009). International collaboration and com-
munication in rehabilitation research. Archives of Phys-
ical Medicine and Rehabilitation, 90(5), 711–716.
Dijkers, M. P., Harrison-Felix, C., & Marwitz, J. H. (2010). Mission Statement
The traumatic brain injury model systems: History and
contributions to clinical service and research. The Jour- APA is the leading scientific and professional
nal of Head Trauma Rehabilitation, 25(2), 81–91.
Hart, K. A. (1997). Rehabilitation research: The new focus organization representing psychology in the
of the American Congress of Rehabilitation Medicine. United States. Its mission is to “advance the
American Psychological Association (APA) 183

creation, communication, and application of psy- initially created, with the two most populated
chological knowledge to benefit society and being clinical and personnel (now counseling).
improve people’s lives.” APA achieves this mis- Growth in the number of divisions was slow A
sion through four interrelated directorates, which until the 1960s in part because there was resis-
focus on education, science, practice, and the tance among APA leaders to increasing the num-
public interest. APA’s current strategic plan has ber of divisions. The trajectory with regard to the
three primary goals: (1) maximize organizational addition of divisions since the 1960s has been
effectiveness, (2) expand psychology’s role in slow but steady, with many of the newer divisions
advancing health, and (3) increase recognition of reflecting the growth of particular practice areas
psychology as a science. (e.g., addictions). Currently, there are 54 divisions,
with the most recent division being approved in
2006 (trauma psychology). This divisional struc-
History ture has resulted in a more broad-based and inclu-
sive organization. In conjunction with APA’s four
The APA was founded in 1892 at Clark University directorates, the organization’s scope includes
by a small group of scholars interested in the “new supporting professional practice, promoting
psychology” (Fernberger 1932). G. Stanley Hall human welfare, advancing psychological science,
was elected as the inaugural president. The orga- and fostering psychology education and training.
nization’s first meeting occurred in December Over the years, concerns mounted among
1892 at the University of Pennsylvania. APA’s some of the scientists in the organization that
founding at this time can best be understood in APA was no longer providing an adequate home
the context of myriad changes occurring in the for them and was drifting away from a primary
United States, including the emergence of the focus on scientific psychology. As a result, in the
modern university system; a broad reorganization 1950s, a group of experimental psychologists
of American knowledge production; the forma- formed the Psychonomic Society with the aim of
tion of several now-standard academic disci- fostering psychology as a science. A more serious
plines, including psychology; and mounting division occurred in the mid- to late 1980s, as
societal demands for individuals with advanced tensions escalated between those who wanted
degrees to serve in new professional niches. The APA to remain a primarily scientific organization
“new psychology” grew and prospered as it and those who sought a greater emphasis on pro-
responded to the changing needs of modern fessional practice issues. After a proposed reorga-
American society and contributed to the manage- nization plan was defeated by a vote of the
ment of an increasingly complex and diversified membership, a group of dissident psychological
world (Benjamin 2009). scientists, including several former APA presi-
Psychology expanded even further after World dents, left the APA to form what is now the Asso-
War II, and funding from various governmental ciation for Psychological Science (Evans et al.
offices began influencing psychology research, 1992). Today, all three of these organizations are
training, and practice (Pickren and Schneider strong, stable representatives of psychology, with
2005). This expansion was largely due to the many psychologists belonging to two or more of
increased prominence of the applied areas of psy- these associations.
chology. Realizing that the growth of applied psy- There are multiple smaller organizations that
chology represented a potential threat to its represent various areas of psychology, as well as a
preeminence, APA’s leaders responded via a reor- growing number of interdisciplinary and
ganization plan in which APA merged with other interprofessional organizations in which psychol-
psychological organizations. It was at this time ogy plays a major role. In addition, there are sepa-
that APA began creating divisions that rate organizations for psychologists with various
represented specialized fields of interest ethnic and racial identities, most notably the Asian
(Dewsbury 1997). Seventeen divisions were American Psychological Association, Association
184 American Psychological Association (APA)

of Black Psychologists, National Latina/o Psycho- members but also to inform the general public and
logical Association, and Society of Indian Psychol- the media about the breadth and depth of psychol-
ogists. These four ethnic minority psychological ogy and its relevance to societal issues. For exam-
associations have partnered with the APA to form ple, it hosts on its website the Psychology Help
the Alliance of National Psychological Associa- Center, which is an online resource for consumers
tions for Racial and Ethnic Equity. that offers information regarding psychological
The APA is a nonprofit 501 (c)(3) organization factors that impact emotional and physical well-
that has a companion 501 (c)(6) organization for being. Moreover, it continues to create, dissemi-
practitioners and educators of practitioners, the nate, and evaluate innovative and state-of-the-art
APA Practice Organization (APAPO). The programs designed to enhance psychology educa-
APAPO is tasked with advancing and protecting tion, science, public interest, and practice.
the profession of psychology and the economic
interests of practicing psychologists. The APAPO
focuses on legislative advocacy and mental health Organizational Structure
policy, as well as serving as a resource for mem-
bers’ professional needs. At the time the organization was founded, its basic
Over the past few years, APA has undergone governance structure consisted of a small council
periods of tension and conflict. These have been in that was overseen by an executive committee. This
response to myriad internal and external chal- structure remained in effect until the reorganization
lenges, such as those related to the organizational of APA during World War II. While the APA has
critiques launched in the Independent Review undergone a number of reorganizations since this
(IR) Relating to APA Ethics Guidelines, National time, its governance structure continues to include a
Security Interrogations, and Torture Board of Directors, which includes the Chair of the
(a.k.a. Hoffman Report); efforts at organizational American Psychological Association of Graduate
restructuring; concerns about the lack of prioriti- Students (APAGS), and a large Council of Repre-
zation of social justice in the organization’s stra- sentatives. Over the years this council has expanded
tegic plan; the alienation of marginalized groups; to include more diverse constituent-based represen-
the lack of clarity with regard to the functions of tation. For example, in 2017, this Council of Rep-
the 501 (c)(3) (i.e., APA) versus the 501(c)(6) resentatives has 177 members, with individual
(i.e., APAPO); the APA Assessment Fee Litiga- representing the 54 divisions of the APA, the
tion (i.e., class action settlement) that impacted State, Provincial, and Territorial Psychological
both the (c)(3) and (c)(6); and the sharp member- Associations, and APAGS.
ship decline of the APAPO. This large governing body creates an inherent
Despite these challenges, APA remains the tension between representation and a cumber-
largest scientific and professional organization some and somewhat unwieldy structure that has
representing psychology in the United States. Its been criticized. The most recent attempt at struc-
members are scientists, educators, practitioners, tural reorganization has occurred under the aus-
and psychologists working for the public interest, pices of the Good Governance Project (GGP),
as well as students in psychology. It is also the which had as its aim the enhancement of APA’s
most prominent national organization that advo- organizational effectiveness. Recommendations
cates at the federal level for psychology. Further, were made regarding distinguishing and clarify-
APA is a major publisher of professional books, ing the roles of the Board of Directors and the
children’s books, journals, magazines and news- Council of Representatives, increasing APA’s
letters, the Publication Manual of the American operational efficiency, and becoming a more
Psychological Association, reports and brochures, inclusive organization with a pipeline of diverse
videos, and data bases. It takes seriously its and well-trained leaders. While some of the
responsibility to not only communicate with its recommended changes have been instituted
American Psychological Association (APA) 185

already, many others have been challenging to dropped 11.6%. Membership has continued to
implement and/or require a vote of the member- decline at a slow but steady rate since this time,
ship. One of the most controversial sets of recom- which is consistent with broader trends in associ- A
mendations, tabled at the present time, is the ation management (Yohn 2016). This decline may
reduction of the overall size of the council also reflect specific sociopolitical factors within
along with a reconsideration of how membership the discipline, the profession, and the organiza-
in this body would be determined. The size of tion. To alter this membership trajectory, improve
the Council and the issues of representation the member value proposition and strengthen
and loss of voice continue to be debated among membership recruitment, retention, and engage-
governance members. A related challenge has ment, APA named its first executive director for
pertained to who should have a seat on the Coun- membership in 2015. Member benefits include,
cil, and there have been three failed votes by the but are not limited to, access to a directory of
members with regard to the inclusion of repre- members, an attendance discount at the annual
sentatives from the four major ethnic minority convention, a subscription to the American Psy-
psychological associations. Challenges related to chologist and the Monitor on Psychology, access
the inclusion of diverse psychologists within to continuing professional development pro-
psychology and APA have a long history grams, and discounts on both non-APA- and
(Guthrie 2004). APA-produced products (e.g., books, journals,
There also are a significant number of standing apps, videos).
boards and committees that help to advance APA’s
mission, support policy initiatives, and focus on
content specific to the discipline. In response to a Major Activities
recent vote by the Council of Representatives,
each of these boards and committees is now For detailed descriptions of APA’s major activi-
expected to include at least one Early Career Psy- ties, the reader is referred to the APA website. This
chologist (ECP) member in an effort to acknowl- section highlights some of the key activities across
edge their contributions and to expand the the organization and is meant to be illustrative
pipeline of emerging leaders. rather than inclusive.
APA’s Central Office includes the Executive
Office, which is responsible for overseeing and
Membership managing the association’s key functions and
implementing APA policies. Associated with the
Membership growth has fluctuated over time. Central Office is APA’s Center for Psychology
Growth was modest over the first 50 years of and Health, a cross-directorate center that collab-
APA’s existence; by 1940 there were only orates with the APAPO in order to provide coor-
664 members. In 1926, a new class of nonvoting dinated activities designed to secure and expand
membership was formed, deemed associate mem- psychology’s central role in improving health and
bers (now affiliate members). Membership healthcare in the United States. Another center
growth reflected the increased interest in the pro- that bridges APA’s component parts is the recently
fession following World War II, with rapid growth launched Center for Organizational Excellence,
occurring between 1945 and 1970. During this which aims to enhance employee well-being and
time, membership increased 630%. Membership strengthen organizational performance. Also
continued to boom through the early 2000s, with associated with the Executive Office is APA’s
the peak of membership occurring in 2010, when Ethics Office, which oversees the development
the association had a robust 155,138 full and and implementation of the APA’s Ethical Princi-
affiliate members. The upward trend began to ples of Psychologists and Code of Conduct (APA
reverse beginning in 2011, when membership 2002), educates members and the public about
186 American Psychological Association (APA)

ethics throughout the field of psychology, pro- The Science Directorate aims to advance psy-
vides ethics consultations, and supports the Ethics chological science, address the needs of psycholog-
Committee’s efforts to adjudicate ethics com- ical scientists, promote the integration of
plaints against APA members. psychological science with other core science dis-
The Central Office also includes the Office of ciplines, and advocate for psychological science at
the General Counsel, which is responsible for all the federal level (Science Government Relations
aspects of legal counsel and representation of Office). The Directorate offers a broad array of
APA. The Office of the General Counsel has services, including a Psychology: Science in Action
often spearheaded the development of amicus program that underscores how science benefits
briefs, documents used to educate courts on society and enhances people’s lives, guidelines on
issues relevant to legal cases that include pertinent topics (e.g., Ethical Conduct in the Care
supporting scientific research. These briefs have and Use of Nonhuman Animals in Research), and a
focused on diverse topics such as abortion, affir- toolkit for science advocacy. It shares with its con-
mative action, family law, the insanity defense, stituents information about research funding, ana-
scientific research, and sexual orientation lytic tools and methods, and publications. The
(discrimination). Directorate houses the Science Student Council to
Reflecting a life cycle perspective, the Educa- promote trainees in the leadership pipeline and
tion Directorate focuses on Pre-K to 12, under- offers fellowships for burgeoning and Early Career
graduate, graduate and postgraduate, and Psychologists (e.g., the Summer Science Fellow-
continuing education efforts. Through the Educa- ship, the APA Executive Branch Science Fellow-
tion Government Relations Office, it leads federal ship Program). The Science Directorate is also
advocacy efforts relevant to policies and funding committed to ensuring that psychological science
for psychology education and training. The Direc- is translated in meaningful ways to the public.
torate offers tools for teaching psychology, APA’s Public Interest Directorate aims to apply
engages in activities that enable APA to be a psychological science to the fundamental prob-
leader in ensuring that education and training are lems of human welfare and social justice and to
competency-based, provides information and pro- promote equitable and just treatment for all indi-
grams for trainers and trainees about the education viduals through education, training, and policy. It
and training pipeline and the range of employment supports offices, programs, governance activities,
opportunities, and collects and disseminates data and the creation of guidelines related to aging;
about the profession of psychology through its HIV/AIDS; children, youth, and families; disabil-
Center for Workforce Studies. To support the ities; ethnic minority affairs; lesbian, gay, bisex-
accreditation of doctoral, internship, and postdoc- ual, and transgender concerns; socioeconomic
toral programs, it houses the Office of Program status; violence prevention; women; and work,
Consultation and Accreditation and the APA stress, and health. It has a strong Government
Commission on Accreditation. Staff and gover- Relations Office that takes an active role in advo-
nance members collaboratively address critical cacy related to the aforementioned issues as well
issues facing the field and impacting high-quality as other human rights and social justice concerns,
education and training, such as the internship such as health disparities. The Directorate also
imbalance (i.e., more trainees seeking accredited houses APA’s Minority Fellowship Program,
internships than available positions). For exam- which provides funding support to racial and eth-
ple, they were instrumental in APA’s 2012 Intern- nic minority graduate students during their educa-
ship Stimulus Package, in which APA committed tion and training, as one mechanism for increasing
$3 million to increase the number of accredited the diversity of the profession.
internship positions. Finally, APA sponsors con- APA’s Practice Directorate has as its mission
tinuing education programs that support psychol- the promotion of the practice of psychology and
ogists’ professional development. the availability of behavioral health services
American Psychological Association (APA), Division 22 187

through advocacy, public education and outreach, moment appears to be a pivotal one in APA’s
and research. It participates actively in crafting history; how so, only time will tell.
policies and practice guidelines for specific areas A
of psychological practice and service delivery. It
oversees a major Public Education Campaign References and Readings
designed to educate the public about the value of
psychology. This campaign has addressed school American Psychological Association. (2002). Ethical prin-
violence, the mind/body health connection, and ciples of psychologists and code of conduct. Retrieved
from: http://www.apa.org/ethics/code/
the promotion of psychologically healthy work- American Psychological Association. (2016). About APA.
places. The Disaster Response Network also falls Retrieved from: http://www.apa.org/about/index.aspx
within the auspices of the Practice Directorate. In Benjamin, L. T., Jr. (2009). A history of psychology: Orig-
collaboration with the American Red Cross, this inal sources and contemporary research (3rd ed.). Mal-
den: Blackwell Publishing.
program involves licensed psychologist volun- Dewsbury, D. A. (1997). On the evolution of divisions.
teers who help individuals and communities American Psychologist, 52, 733–741. https://doi.org/
cope with and heal from disasters. The Directorate 10.1037/0003-066X.52.7.733.
creates and disseminates a range of resources for Evans, R. B., Sexton, V. S., & Cadwallader, T. C. (Eds.).
(1992). The American Psychological Association:
practitioners, such as information on transitioning A historical perspective. Washington, DC: American
to electronic medical records, evidence-based Psychological Association.
practice in psychology, and documents on self- Fernberger, S. W. (1932). The American Psychological
care and colleague assistance. Association: A historical summary, 1892–1930. Psy-
chological Bulletin, 29, 1–89. https://doi.org/10.1037/
Through its Office of International Affairs, h0075733.
APA is very invested in its relations with interna- Guthrie, R. V. (2004). Even the rat was white: A historical
tional psychology organizations. As one example view of psychology. Boston: Allyn and Bacon.
of this, APA engaged in an agreement with the Pickren, W. E., & Schneider, S. F. (Eds.). (2005). Psychol-
ogy and the National Institute of Mental Health:
International Union of Psychological Science to A historical analysis of science, practice, and policy.
provide technical assistance to the World Health Washington, DC: APA Books.
Organization (WHO) with regard to the revision World Health Organisation. (1992). International statisti-
of the WHO’s International Statistical Classifica- cal classification of diseases and related health prob-
lems, 10th revision (ICD-10). Geneva: WHO.
tion of Diseases and Related Health Problems Yohn, D. L. (January 2016). To stay relevant, professional
(ICD-10; World Health Organisation 1992) associations must rebrand. Harvard Business Review.
“Mental and Behavioural Disorders” chapter. Retrieved from: https://hbr.org/2016/01/to-stay-
relevant-professional-associations-must-rebrand

Concluding Comments

APA continues to adapt and redefine itself in light American Psychological

of a changing healthcare climate, the ongoing Association (APA), Division 22
implementation of the GGP’s recommended
structural reorganization, and declining member- William Stiers
ship trends and in the context of recent contro- Johns Hopkins University School of Medicine,
versies and conflict. APA remains the world’s Baltimore, MD, USA
largest membership organization of psycholo-
gists. It has a fascinating past, marked by growth,
conflict, and increasing diversification. Its Membership
response to current challenges will likely have
long-standing impacts on the association and pro- The American Psychological Association (APA)
fession of psychology as a whole. The present Division 22 – Rehabilitation Psychology is
188 American Psychological Association (APA), Division 22

composed of 1164 psychologists (as of December, Rehabilitation Psychology, the Academy of Reha-
2017) who provide health services, teach, manage bilitation Psychology, and the Council of Reha-
rehabilitation programs, conduct research, and bilitation Psychology Postdoctoral Training
perform other professional activities. They work Programs. The Rehabilitation Psychology Spe-
in hospitals and clinics, in independent practice, in cialty Council selects one of its members to
other human service settings, and in universities serve as the specialty’s representative to CoS,
and colleges. and this representative serves as a voting member
on CoS.

Major Areas or Mission Statement

Landmarks
The Division of Rehabilitation Psychology works
to unite psychologists and others interested in the
• Rehabilitation psychologists have worked in
prevention and rehabilitation of disability and
medical settings as part of teams of healthcare
chronic illness. Rehabilitation Psychology prac-
professionals for more than 70 years, long
tice is a specialty within the domain of profes-
before psychologists were regularly involved
sional healthcare psychology, which applies
in other healthcare settings.
psychological knowledge and skills on behalf of
• Division 22 was established in 1958, one of the
individuals with disabilities and chronic health
earlier divisions in APA.
conditions in order to maximize their health and
• Division 22 members conducted the initial
welfare, independence and choice, functional
research on individual, interpersonal, and
abilities, and social role participation. Such dis-
social changes related to changes in appear-
abilities include spinal cord injury, brain injury,
ance and physical capacity, as well as the social
stroke, amputations, burns, work-related injuries,
psychology of stereotyping and prejudice
multiple traumatic injuries, chronic pain, cancer,
faced by persons with disability.
heart disease, multiple sclerosis, neuromuscular
• Division 22 members were among the pioneers
disorders, AIDS, developmental disorders, psy-
helping psychology understand the world of
chiatric impairment, substance abuse, impair-
work, how work can be affected by impairment
ments in sensory functioning, and other physical,
and disability, and issues about vocational
mental, and/or emotional impairments. The broad
rehabilitation.
field of Rehabilitation Psychology also includes
• Rehabilitation psychologists have developed
rehabilitation program development and adminis-
the principles of cognitive rehabilitation and
tration, research, teaching, public education and
have served as leaders in the federal model
development of policies for injury prevention and
systems programs for traumatic brain injury,
health promotion, and advocacy for persons with
spinal cord injury, and burns.
disabilities and chronic health conditions.
• Board Certification in Rehabilitation Psychol-
APA Division 22 – Rehabilitation Psychology
ogy was established in 1997.
participates in the Rehabilitation Psychology Spe-
• Rehabilitation Psychology is recognized by the
cialty Council. In accordance with the policy of
Commission for the Recognition of Specialties
the Council of Specialties in Professional Psy-
and Proficiencies in Professional Psychology
chology (CoS – https://www.cospp.org/), this
since 2015.
Rehabilitation Psychology Specialty Council con-
sists of the professional groups and organizations
that represent the major educational, training, and Major Activities
professional constituencies and stakeholders rele-
vant to Rehabilitation Psychology, that is, APA • The journal Rehabilitation Psychology is
Division 22, the American Board of Rehabilita- published quarterly by the APA http://www.
tion Psychology, The Foundation for apa.org/pubs/journals/rep/.
American Psychological Association (APA), Division 40 189

• Division 22, in conjunction with the American

Board of Rehabilitation Psychology, holds an American Psychological
annual conference in the early spring of each Association (APA), Division 40 A
year.
William B. Barr
NYU Langone Medical Center, Comprehensive
Resources
Epilepsy Center, New York, NY, USA
• American Psychological Association (APA) –
http://www.apa.org
Membership
– General information about psychology and
about the divisions or sections within APA
The Society for Clinical Neuropsychology (SCN),
• Rehabilitation Psychology – http://www.
Division 40 of the American Psychological Asso-
div22.org/
ciation (APA) is one of 56 specialty divisions
– Specific information about the specialty of
recognized by the APA. Since its inception, it
Rehabilitation Psychology
has become one of APA’s most visible and active
divisions. In its nearly 40 years, membership has
grown from 433 psychologists to its current
Cross-References (based on 2016 statistics) membership of 3,423,
which currently makes it the largest of all APA
▶ American Board of Professional Psychology divisions. The division’s representation to the
(ABPP) APA council has grown over the years from its
▶ American Board of Rehabilitation Psychology initial one representative to the current allotment
▶ American Psychological Association (APA) of four seats. This trend coincides with SCN’s
▶ Rehabilitation Psychology increasing influence within APA and increasing
recognition of neuropsychology as a clinical
specialty.
References and Readings The division voted to change its name to SCN
in 2013 as part of a branding and public relations
American Psychological Association. (2008). A closer effort to enable greater flexibility in communica-
look at Division 22: A growing field meets the chal-
lenges of war. Monitor on Psychology, 38(8), 54–55.
tions and greater clarity for the public. Eligibility
Frank, R., Rosenthal, M., & Caplan, B. (Eds.). (2009). for division membership was previously based
Handbook of rehabilitation psychology (2nd ed.). on membership in APA. That criterion is no
Washington, DC: American Psychological longer required. Any psychologist, trainee, or
Association.
Larson, P., & Sachs, P. (2000). A history of Division 22. In
individual with an interest in clinical neuropsy-
D. A. Dewsbury (Ed.), Unification through division: chology is encouraged to join SCN. All members
Histories of the divisions of the American Psychologi- are provided access to SCN’s Internet LISTERVs
cal Association (Vol. 5, pp. 33–58). Washington, DC: and publications. All members of the division
American Psychological Association.
who are APA members have additional rights
and privileges to hold office and serve on divi-
Division Sections sion committees and vote in APA elections.
Pediatric Rehabilitation Information for joining SCN can be obtained on
Women in Rehabilitation Psychology
the division’s website at http://www.scn40.org/
mc.html.
Special Interest Groups APA statistics indicate that the majority of
Assistive Technology
SCN members are women by a slight majority
Psychologists with Disabilities
Deafness (49.9%). Ethnic minority members constitute 8%
Early Career Psychologists of the membership, consistent with larger APA
190 American Psychological Association (APA), Division 40

trends. Approximately, 80% of the division mem- Landmark Contributions

berships have a Ph.D. in clinical psychology or a
related field. Based on the previous statistics, Psychologists interested in the developing field of
nearly half of the members work in independent neuropsychology began participating on a regular
settings. Most other members work in medical basis at APA meetings during the 1960s. The ori-
schools, hospitals, and university settings. Many gins of SCN can be traced back to the development
combine their work in institutional and private of the International Neuropsychological Society
practice settings. Prior membership surveys have (INS), which is known as the field of neuropsy-
indicated that psychologists in SCN spend a sub- chology’s first formal organization. Informal meet-
stantially larger amount of time (>40%) in ings of psychologists interested in
assessment activities than other APA members neuropsychological issues were held at the annual
(<15%). Approximately, one third of the mem- APA meeting dating back to 1965. The INS was
bers are actively involved in research activities. formally organized in 1967 as an outgrowth of these
Approximately, 40% are involved in clinical meetings with the goal of serving as a scientific and
training. educational organization. The need for formal rep-
resentation in APA became increasingly apparent as
professional issues regarding practice, education,
Major Areas or Mission Statement and training in neuropsychology began to emerge.
Leaders in the field, including Arthur Benton, Louis
Division 40 was formed in 1980 with the mis- Costa, and Manfred Meier, saw the need for the
sion of enhancing the understanding of brain- development of an organization to promote the
behavior relationships and the application of growing specialty of clinical neuropsychology that
such knowledge to human problems. Activities was independent of INS and APA’s Division of
of the division encompass the areas of science Clinical Psychology (Division 12). The application
(e.g., presentations at the annual meeting of to establish a Division of Clinical Neuropsychology
APA, awards for outstanding scientific contri- was submitted to APA and approved by its Council
butions), practice (e.g., Current Procedural of Representatives in September 1979. The forma-
Terminology, “CPT,” billing codes, educa- tion of Division 40 was made effective in January
tional brochures for patients), education and 1980, consistent with APA procedures. The divi-
training (e.g., neuropsychology graduate stu- sion’s first President was Dr. Harold Goodglass
dent organization), and specialty public inter- with Dr. Gerald Goldstein serving as both the Sec-
est groups (e.g., women, minorities, geriatrics, retary and Treasurer. The presidents of the division
rural, etc.). include many of the most prominent names in the
The division upholds APA bylaws and field of neuropsychology (Table 1).
enacted its own divisional bylaws in 1980, One of the division’s earliest activities
which were subsequently revised to their included working with the INS Task Force on
current form in 2005. Over the years, SCN Education, Accreditation, and Credentialing
has provided published guidelines on many (TFEAC) in establishing guidelines for doctoral,
aspects of neuropsychological practice and internship, and postdoctoral training in clinical
training while also fostering continued develop- neuropsychology. Recommendations provided
ment of the science of neuropsychology through by that group, calling for a combination of train-
activity of its committees. The division ing experiences in psychology and the neurosci-
advances scientific knowledge in the field of ences, continue as the field’s dominant model of
neuropsychology through its support of publi- training. The INS Task Force was eventually
cation and presentation of scientific papers at discontinued as it became increasingly evident
professional conferences, including the APA’s that professional issues were becoming the
annual convention. domain of Division 40. A listing of early
American Psychological Association (APA), Division 40 191

American Psychological Association (APA), Division 40, Table 1 The Society for Clinical Neuropsychology
(SCN), Division 40 of the American Psychological Association (APA). Presidents of division, 1979–2017
1980s 1990s 2000s 2010s
1979–1980 Harold Goodglass 1989–1990 Charles G. Matthews 1999–2000 Gordon J. Chelune 2009–2010 Celiane M. Rey-Casserly A
1980–1981 Harold Goodglass 1990–1991 Raymond S. Dean 2000–2001 Jason Brandt 2010–2011 H. Gerry Taylor
1981–1982 Louis Costa 1991–1992 Steven Mattis 2001–2002 Allan F. Mirsky 2011–2012 William B. Barr
1982–1983 Nelson M. Butters 1992–1993 Oscar Parsons 2002–2003 Antonio Puente 2012–2013 Munro Cullum
1983–1984 Thomas J. Boll 1993–1994 Robert K. Heaton 2003–2004 Kathleen J. Haaland 2013–2014 Paula K. Shear
1984–1985 Lawrence C. Hartledge 1994–1995 Carl Dodrill 2004–2005 Robert J. Ivnik 2014–2015 Neil Pliskin
1985–1986 Manfred J. Meier 1995–1996 Kenneth M. Adams 2005–2006 Russell M. Bauer 2015–2016 Jennifer Vasterling
1986–1987 Edith F. Kaplan 1996–1997 Eileen B. Fennell 2006–2007 Keith O. Yeates 2016–2017 Mark Bondi
1987–1988 Byron P. Rourke 1997–1998 Linas A. Bieliauskas 2007–2008 Thomas A. Hammeke
1988–1989 Gerald Goldstein 1998–1999 Cecil R. Reynolds 2008–2009 Glenn E. Smith

American Psychological Association (APA), Division There has been a more recent trend to publish
40, Table 2 Published guidelines and online toolkits online WebKits and toolboxes with other APA
from Division 40 committees and task forces
divisions and neuropsychology organizations.
Year Activity The division has also continued to publish posi-
1987 Guidelines for Doctoral Training Programs in tion statements on a variety of topics in associa-
Clinical Neuropsychology
tion with other neuropsychological organizations,
1987 Task Force Report on Computer-Assisted
Neuropsychological Evaluation including the National Academy of Neuropsy-
1988 Guidelines of Continuing Education in Clinical chology (NAN) and the American Academy of
Neuropsychology Clinical Neuropsychology (AACN). The divi-
1989 Definition of a Clinical Neuropsychologist sion, in collaboration with these organizations,
1989 Guidelines Regarding the Use of Nondoctoral became a member of the Inter Organizational
Personnel in Clinical Neuropsychological Practice Committee (IOPC), which was devel-
Assessment
oped in 2013 to coordinate advocacy efforts and
1991 Recommendations for Education and Training
of Nondoctoral Personnel in Clinical improve the practice climate for neuropsychology
Neuropsychology as a profession.
1991 Guidelines for Computer-Assisted During the 1990s, a task force from SCN led by
Neuropsychological Rehabilitation and Manfred Meier successfully submitted a petition for
Cognitive Remediation
clinical neuropsychology to become the first psy-
2013 Webkit for Interdisciplinary Health Service
Psychology Trainees (www.wihpt.com)
chological specialty recognized by the APA’s Com-
2013 Health Care Reform and Neuropsychology mission on Recognition of Specialties and
Toolkit (https://iopc.online/practice-tools/) Proficiencies in Professional Psychology (CRSPP).
2015 The Concussion Toolkit for Psychologists Recognition of clinical neuropsychology as a spe-
(www.ucdenver.edu/academics/colleges/ cialty became official in 1997. This was followed by
medicalschool/departments/pmr/documents/ a set of activities, working in conjunction with
concussion_toolkit/index.htm)
NAN, AACN, American Board of Clinical Neuro-
psychology, and the Association of Postdoctoral
Programs in Clinical Neuropsychology (APPCN)
publications of other professional guidelines, in developing an integrated model for specialty
statements, and online toolkits developed by Divi- training in clinical neuropsychology. Representa-
sion 40 committees and task forces is provided in tives from these organizations and various training
Table 2. The purpose of these guidelines was to programs across the USA met in 1997 for what was
facilitate an adherence to standards for profes- termed the Houston Conference on Specialty Train-
sionals in the field of clinical neuropsychology ing in Clinical Neuropsychology. The conference
with the ultimate goal of ensuring the quality of led to the development and publication of a docu-
services provided to consumers. ment describing an integrated model of education
192 American Psychological Association (APA), Division 40

and training. Interactions between SCN and these reports are published biannually in Newsletter
other groups continued through an organization 40, the official division newsletter. Additional
called the Clinical Neuropsychology Synarchy communications are provided electronically
(CNS). In 2013, the division joined other organiza- through the SCN News, SCN NeuroBlog, and the
tions in forming the Inter Organizational Practice division’s five LISTERVs.
Committee (IOPC), with the goal of joining forces Continued commitments to training and entry
to increase the breadth and reach of grassroots’ level members have been demonstrated by the
advocacy for issues having local and national impli- formation of the Association for Neuropsychol-
cations. The group published its 360 Degree Advo- ogy Students in Training (ANST) and the estab-
cacy model in TCN and a Neuropsychology Toolkit lishment of an Early Career Psychologists
for Healthcare Reform on its website (http:// committee. Committees and mentoring programs
neuropsychologytoolkit.com). have been established for women entering the
field and for ethnic minority members. Bro-
chures describing an introduction to clinical neu-
Major Activities ropsychology are available through the
division’s Public Interest Advisory Committee
Officers of SCN include President, President- (PIAC). The Practice Advisory Committee
Elect, Past President, Secretary, and Treasurer. (PAC) provides monitoring of legislative activi-
These positions are elected by the general mem- ties and both local and national activities affect-
bership with the term of President lasting 1 year ing the practice of clinical neuropsychology.
and the roles of Secretary and Treasurer lasting This committee is also responsible for interac-
3 years. The officers serve on an Executive Com- tions with government agencies such as the Cen-
mittee (EC) joined by various Division Commit- ters for Medicare and Medicaid Services (CMS).
tee Chairs, Divisional Representatives to APA The PAC worked with other organizations in
Council, and three Members-at-Large. Meetings establishing a new set of CPT testing codes
of the EC are held twice yearly, with one of the aimed at optimizing reimbursement for neuro-
meetings held at the North American meeting of psychological services. These codes were offi-
the INS in midwinter and the other coinciding cially implemented in 2006.
with the APA convention in the summer. Presi- The division has maintained its goal of integrat-
dents of the division preside at meetings and serve ing science and practice. The Science Advisory
as the Chairperson of the EC. Terms of office Committee (SAC) continues in its role of produc-
begin and end at the completion of the annual ing scientific programs for the APA’s annual con-
business meeting held during the summer. vention. Studies on neurologic syndromes,
The division has four standing committees assessment, and developmental issues are among
including Membership, Fellowship, Elections, the topics most commonly presented in the SCN
and Program Committees and four continuing program at the annual APA meeting. The SAC also
committees consisting of the Science Advisory, provides a number of awards for students and early
Education Advisory, Practice Advisory, and Pub- career psychologists establishing careers in neuro-
lic Interest Advisory Committees. Special Com- psychological research. More recent SAC activities
mittees, including Task Force Committees, can include integration of neuropsychology’s scientific
also be established by vote of the Executive Com- activities with APA and government agencies such
mittee, when the need arises. The Committee on as the National Institutes of Health (NIH).
APA Relations and the Publications and Commu- SCN does not publish or provide an official
nications Committee are examples of these. The journal. However, over the years, the division
President, in consultation with the EC, appoints has maintained a close relationship with The
chairs of all divisional committees and task forces. Clinical Neuropsychologist (TCN), a journal
Summaries of divisional activities, minutes of focusing on clinical issues relevant to neuropsy-
executive committee meetings, and committee chologists. The journal has published a number
American Speech-Language-Hearing Association (ASHA) 193

of statements and guidelines prepared by SCN

task forces relevant to the practice of neuropsy- American Speech-Language-
chology and abstracts from SCN’s scientific pro- Hearing Association (ASHA) A
gram at APA. In 1989, TCN also began to publish
regular listings of training programs in neuropsy- Lemmietta McNeilly
chology. In 2006, a user-interactive revision of Speech-Language Pathology, American Speech-
the list was developed by the Education Advi- Language-Hearing Association, Rockville, MD,
sory Committee (EAC) and transferred to the USA
SCN website. The listing currently includes
40 doctoral training programs, 59 internships,
and 114 sites offering postdoctoral residencies Membership
for specialty training in clinical neuropsychol-
ogy. The website also includes descriptions of The American Speech-Language-Hearing Asso-
other divisional activities and links to the divi- ciation is the national professional, scientific,
sion’s archival material. and credentialing association for 191,500 mem-
bers and affiliates who are audiologists, speech-
language pathologists, and speech, language,
Cross-References and hearing scientists, audiology and speech-
language pathology support personnel, and
▶ American Academy of Clinical Neuropsychol- students.
ogy (AACN)
▶ American Board of Clinical Neuropsychology
(ABCN)
Vision
▶ American Psychological Association (APA)
▶ Association for Postdoctoral Programs in Clin-
Vision: Making effective communication, a
ical Neuropsychology (APPCN)
human right, accessible and achievable
▶ Houston Conference
for all.
▶ International Neuropsychological Society
▶ National Academy of Neuropsychology (NAN)

Mission
References and Readings
Empowering and supporting audiologists, speech-
Adams, K. M., & Rourke, B. P. (Eds.). (1992). The TCN language pathologists, and speech, language, and
guide to professional practice in clinical neuropsychol- hearing scientists through:
ogy. Berwyn: Swets & Zeitlinger.
Costa, L. (1998). Professionalization in neuropsychology:
The early years. The Clinical Neuropsychologist, 12, 1–7. • Advancing science
Meier, M. J. (1992). Modern clinical neuropsychology in • Setting standards
historical perspective. American Psychologist, 47, • Fostering excellence in professional practice
550–558. • Advocating for members and those they serve
Meier, M. J. (2002). In search of knowledge and compe-
tence. In A. Y. Stringer, E. L. Cooley, & A.-L.
Christensen (Eds.), Pathways to prominence in neuro-
psychology: Reflections of twentieth century pioneers.
Landmark Contributions
New York: Psychology Press.
Puente, A. E., & Marcotte, A. C. (2000). A history of ASHA has had several names during its more than
Division 40 (clinical neuropsychology). In D. A. Dews- 90-year history. The first was the American Acad-
bury (Ed.), Unification through division: Histories of
emy of Speech Correction (1925). The current
the divisions of the American Psychological Associa-
tion (Vol. V). Washington, DC: American Psychologi- name, the American Speech-Language-Hearing
cal Association Press. Association (ASHA), was adopted in 1978.
194 American Speech-Language-Hearing Association Functional Assessment

ASHA is the nation’s leading professional, References and Readings

credentialing, and scientific organization for
speech-language pathologists, audiologists, and American Speech-Language-Hearing Association. (2016).
Scope of practice in speech-language pathology
speech/language/hearing scientists. ASHA has
[Scope of practice]. Available from www.asha.org/
been the guardian of these professions for over policy/
85 years, initiating the development of national American Speech-Language-Hearing Association. www.
standards for each discipline and certifying pro- asha.org
fessionals since 1952.
ASHA began in 1925 at an informal meeting of
the National Association of Teachers of Speech
(NATS) in Iowa City, IA, an organization of peo- American Speech-Language-
ple working in the areas of rhetoric, debate, and Hearing Association
theater. Robert W. West was the first president of Functional Assessment of
the association from 1925 to 1928. Its members Communication Skills for
were becoming increasingly interested in speech Adults
correction and wanted to establish an organization
to promote “scientific, organized work in the field Diane Paul
of speech correction.” Accordingly, in December Clinical Issues in Speech-Language Pathology,
of that year, the American Academy of Speech American Speech-Language-Hearing
Correction – ASHA’s original predecessor – Association, Rockville, MD, USA
was born.
ASHA has grown exponentially since its
inception – from 25 members in 1925 to Synonyms
191,500 in 2016. ASHA opened its first national
office on January 1, 1958, in Washington, ASHA FACS
DC. The association subsequently moved four
times, most recently settling in its current location
in Rockville, MD, in 2008. ASHA’s new national Description
office is a LEED certified green building – the first
nonprofit company’s building of that distinction in The American Speech-Language-Hearing Asso-
Maryland. ciation Functional Assessment of Communica-
tion Skills for Adults (ASHA FACS) was
designed as a quick and easily administered
Major Activities measure of functional communication behaviors
at the level of disability in adults with speech,
Publications: The ASHA Leader; American language, and cognitive-communication impair-
Journal of Audiology; American ments (Frattali et al. 1995; Frattali et al. 2017).
Journal of Speech-Language The ASHA FACS uses the following definition
Pathology; Journal of Speech, of functional communication: “the ability to
Language, and Hearing receive or to convey a message, regardless of
Research; Language, Speech, the mode, to communicate effectively and inde-
and Hearing Services in Schools; pendently in a given [natural] environment”
and SIG Perspectives. (ASHA 1990, p. 2). The World Health Organi-
Conferences: Annual convention and niche zation (WHO 2001) International Classification
conferences addressing topics of Functioning, Disability and Health (ICF) pro-
in healthcare and schools, as vides the framework for functional assessment.
well as several web events The ICF consists of two components: function-
annually. ing and disability (body functions/structures and
American Speech-Language-Hearing Association Functional Assessment 195

activity/participation) and contextual factors Independence, which ranges from “does” the
(environmental and personal). The ASHA activity independently, through five levels of
FACS assesses communication in the context “does with” varying degrees of assistance, to A
of daily life activities. The ASHA FACS is “does not” perform the activity. A second scor-
based on direct observations by speech-lan- ing system, the Scale of Qualitative Dimensions
guage pathologists or significant others who of Communication, uses a five-point scale to rate
are familiar with the client’s typical communi- adequacy, appropriateness, promptness, and
cation performance across four assessment communication sharing.
domains: social communication; communica-
tion of basic needs; reading, writing, and num- Assessment Domains
ber concepts; and daily planning. Within each Table 1 shows the behaviors that are included
domain, specific functional behaviors are rated within the four assessment domains. The measure
on a seven-point Scale of Communication yields domain and dimension mean scores,

American Speech-Language-Hearing Association Functional Assessment of Communication Skills for Adults,

Table 1 ASHA FACS conceptual framework
Qualitative dimensions
Adequacy Appropriateness Promptness Communication sharing
Definitions
Frequency with which Frequency with which client’s Frequency with which Extent to which a client’s
client understands gist of communication is relevant and client responds without communication poses a
message and gets point done under the right delay and in an efficient burden to the
across circumstances manner communication partner
Assessment domains
Social communication Communication of basic Readings/writing/ Daily planning
needs number concepts
Behaviors
Uses names of familiar Recognizes familiar faces/ Understands simple Tells time
people voices signs Dials telephone numbers
Expresses agreement/ Makes strong likes/dislikes Uses references Keeps scheduled
disagreement known materials appointments
Explains how to do Expresses feelings Follows written Uses a calendar
something Requests help directions Follows a map
Requests information Makes needs/wants known Understands printed
Exchanges information Responds in an emergency material
on the telephone Prints/writes/types name
Answers yes/no Completes forms
questions Writes messages
Follows directions Understands signs with
Understands facial numbers
expressions/tone of Makes money
voice transactions
Understands nonliteral Understands units of
meaning and intent measurement
Understands
conversations in noisy
surroundings
Understands TV/radio
Participates in
conversations
Recognizes/corrects
communication errors
196 American Speech-Language-Hearing Association Functional Assessment

overall scores, and profiles of both communica- Psychometric Data

tion independence and qualitative dimensions.
The ASHA FACS includes: The usability, sensitivity, reliability, and validity
of the ASHA FACS were demonstrated through
A revised manual (Frattali et al. 2017) detailing two separate pilot tests and one field test. The first
the project rationale, review of functional com- version was piloted to determine the measure’s
munication measures, description and valida- usability, resulting in the development of a
tion data, and administration and scoring seven-point observational rating scale. A second
procedures pilot test confirmed the usability of the revised
A score summary and profile forms version, and acceptable levels of reliability and
A case example validity were found. A more sensitive scoring
A pull-out rating key with the Scale of Commu- system for capturing qualitative information
nication Independence and the Scale of Quali- about the nature of a client’s functional commu-
tative Dimensions of Communication nication led to the addition of a second scoring
feature, a five-point rating scale of qualitative
dimensions.
Historical Background To establish interrater reliability during the
field test, the ASHA FACS was completed inde-
The ASHA FACS evolved from the wave of pendently for 35 subjects by two examiners within
healthcare accountability and the widespread a 48-h period after a minimum of three subject-
need for an effective instrument to measure the examiner contacts. Interrater reliability correla-
functional communication of adults who have tions on the four assessment domain scores ranged
speech, language, or cognitive impairments for from 0.88 to 0.92. Overall communication inde-
purposes of justifying payment, defining service pendence scores had high interrater agreement
eligibility, and judging the value of care. Devel- (mean correlation = 0.95). Interrater consisten-
oped in 1995 by ASHA, it reflects the collabora- cies of the four qualitative dimension mean scores
tive effort of more than 70 individuals, both ranged from 0.72 to 0.84. The interrater reliability
ASHA members and related professionals. The of overall qualitative dimension mean scores was
ASHA FACS was supported in part by the U.S. 0.88. Intrarater reliability (38 subjects) for com-
Department of Education/National Institute on munication independence mean scores by assess-
Disability and Rehabilitation Research (NIDRR) ment domain ranged from 0.95 to 0.99 and
and the U.S. Department of Veterans Affairs. The intrarater reliability of overall communication
Psychological Corporation provided expert independence scores was 0.99. Intrarater reliabil-
advice and data analysis. ity of qualitative dimension mean scores ranged
The ASHA FACS originally was validated from 0.94 to 0.99 and 0.99 for the overall quali-
on adults with aphasia following left hemi- tative dimension scores.
sphere stroke and adults with traumatic brain The ASHA FACS was moderately correlated
injury (TBI). The original validation study with other measures of language and cognitive
was conducted primarily with African Ameri- function as demonstrated by external criterion
can and White adults with these communication measures used with subjects with aphasia and
impairments. ASHA conducted further valida- cognitive-communication impairments from
tion testing from 1998 to 2003 with other racial/ TBI. For subjects with aphasia, a correlation of
ethnic groups and patient populations and cre- 0.73 was obtained between the Western Aphasia
ated an addendum to the ASHA FACS (Paul et Battery (WAB) Aphasia Quotient (AQ) (Kertesz
al. 2004a). The research was supported in part 1982), and the ASHA FACS overall communi-
by NIDRR. A revised manual includes the val- cation independence score. Correlations were
idation data from the addendum (Frattali et al. obtained between ASHA FACS domain scores
2017). and WAB subtest scores, with a range of .038 to
American Speech-Language-Hearing Association Functional Assessment 197

0.81. Correlations between the ASHA FACS scores did not correlate well with family mem-
domain score and overall score and each of the bers’ or friends’ ratings of overall communication
Functional Independence Measure (FIM) scales effectiveness or CETI scores. CETI ratings were A
(FIM 4.0; SUNY at Buffalo Research Foundation consistently higher than those measured using the
1993) ranged from 0.61 to 0.83. For the subjects ASHA FACS.
with aphasia, correlations also were computed
between ASHA FACS qualitative ratings and
external criterion measures, the WAB and the Clinical Uses
FIM. These results indicated moderate correla-
tions. External validation data for the subjects The ASHA FACS was designed for clinicians to
with cognitive-communication impairments rate functional communication behaviors of adults
ranged from 0.66 to 0.78 between the Scales of with speech, language, and cognitive-communi-
Cognitive Ability for Traumatic Brain Injury cation impairments resulting from left hemisphere
(SCATBI) (Adamovich and Henderson 1992) stroke and from TBI. In a review of the evidence
severity scores and the ASHA FACS domain leading to recommended best practices for assess-
scores and a 0.78 correlation between the ment of individuals with cognitive-communica-
ASHA FACS overall domain score with the tion impairments after TBI, the ASHA FACS
SCATBI severity scores. Correlations ranging was one of a few standardized, norm-referenced
from 0.72 to 0.86 were found between ASHA tests that met most established criteria for validity
FACS overall mean communication indepen- and reliability for use with this clinical population
dence scores and FIM scores for subjects with (Turkstra et al. 2005). It was one of only four of
cognitive-communication impairments. Moder- the 31 tests reviewed that evaluated performance
ate correlations also were found between ASHA outside clinical settings. It was unique in that it
FACS qualitative ratings and the SCATBI and was based on research about daily communication
the FIM for this subject group. needs in the target population and incorporated
High internal consistency and social validity consumer feedback about ecological validity into
were reported. Internal consistency indicated that the design. The research is rich in the many clin-
most item scores covered the full seven-point ical benefits of the ASHA FACS. For example,
communication independence rating scale, this instrument has been used to measure commu-
showed high inter-item correlations between nication disability relative to quality of life in
items within assessment domains, were internally adults with chronic aphasia (Ross and Wertz
consistent with respect to assessment domain, and 2002; Davidson et al. 2003), to evaluate the effec-
that all items were measuring the same underlying tiveness of functionally based communication
construct. The data indicated that all domain therapy (Worrall and Yiu 2000), and to evaluate
scores correlated with overall ASHA FACS real-life outcomes of aphasia interventions
scores. Evaluation of social validity was accom- (Kagan et al. 2008). Using Rasch analysis of the
plished by correlating overall ASHA FACS ASHA FACS Social Communication Subtest
scores with measures scored by family members (SCS), Donovan et al. (2006) demonstrated that
or friends of subjects. These measures included caregivers were reliable respondents who could
the Communicative Effectiveness Index (CETI; use the SCS to rate therapy progress and func-
Lomas et al. 1989) and a rating of overall com- tional outcomes.
munication effectiveness, a single overall index Additional research (Paul et al. 2004a) demon-
of each subjects’ communication effectiveness strated that the ASHA FACS is a reliable and valid
rated on a scale from 1 (lowest) to 7 (highest). measure of functional communication for African
These data indicated high positive correlations American, Hispanic, and White adults with cog-
between ASHA FACS overall scores and ratings nitive-communication impairments resulting from
of overall communication effectiveness by clini- right hemisphere stroke or dementia. Validity
cians (i.e., r = 0.81). The ASHA FACS overall could not be determined for Asian Americans
198 American Speech-Language-Hearing Association Functional Assessment

and Native Americans due to the small sample Donovan, N. J., Rosenbek, J. C., Ketterson, T. U., &
size. Further research is needed to determine the Velozo, C. A. (2006). Adding meaning to measure-
ment: Initial Rasch analysis of the ASHA FACS social
validity of the ASHA FACS for adults with communication subtest. Aphasiology, 20(2–4),
dysarthria. 362–373.
ASHA established an international advisory Frattali, C. M., Thompson, C. K., Holland, A. L., Wohl, C.
group to determine the validity, reliability, and B., & Ferketic, M. M. (1995). American Speech-Lan-
guage-Hearing Association Functional Assessment of
usability of the ASHA FACS in other English- Communication Skills for adults (ASHA FACS). Rock-
speaking countries (Australia, Canada, Ireland, ville: ASHA.
New Zealand, South Africa, England, and Scot- Frattali, C. M., Thompson, C. K., Holland, A. L., Wohl, C.
land). Generally, the ASHA FACS was consid- B., Wenck, C. J., Slater, S. C., & Paul, D. (2017).
American Speech-Language-Hearing Association
ered to be appropriate for use in these other Functional Assessment of Communication Skills for
countries with adults with aphasia or TBI. Cer- adults (ASHA FACS). Rockville: ASHA.
tain test items were not relevant across groups, Kagan, A., Simmons-Mackie, N., Rowland, A.,
and there were difficulties in administration in Huijbregts, M., Shumway, E., McEwen, S., Threats,
T., & Sharp, S. (2008). Counting what counts: A frame-
countries where multiple primary languages are work for capturing real-life outcomes of aphasia inter-
used. A Portuguese version was found to be vention. Aphasiology, 22(3), 258–280.
valid and reliable for adults with mild or moder- Kertesz, A. (1982). Western aphasia battery. New York:
ate Alzheimer’s disease (de Carvalho and Grune & Stratton.
Lomas, J., Pickard, L., Bester, S., Elbard, H., Finlayson,
Mansur 2008). There continues to be broad A., & Zoghaib, C. (1989). The communicative effec-
interest in functional communication assess- tiveness index: Development and psychometric evalu-
ment for populations with communication ation of a functional communication measure for
impairments. adults. Journal of Speech and Hearing Disorders, 54,
113–124.
The ASHA FACS should be used as part of a Paul, D., Frattali, C. M., Holland, A. L., Thompson, C. K.,
comprehensive communication assessment, in & Slater, S. C. (2004a). American Speech-Language-
conjunction with measures of impairment and Hearing Association Functional Assessment of Com-
quality of life. Treatment decisions should not be munication Skills for adults: Addendum. Rockville:
ASHA.
made on the basis of a single instrument. The Paul, D., Frattali, C. M., Holland, A. L., Thompson, C. K.,
ASHA Quality of Communication Life Scale Caperton, C. J., & Slater, S. C. (2004b). Quality of
(QCL) may be used to assess the impact of com- communication life scale. Rockville: ASHA.
munication impairment on an adult’s participation Ross, K. B., & Wertz, R. T. (2002). Relationships between
language-based disability and quality of life in chroni-
in social, leisure, work, and education activities cally aphasic adults. Aphasiology, 16(8), 791–800.
(Paul et al. 2004b). State University of New York at Buffalo Research Foun-
dation. (1993). Guide for use of the uniform data set for
medical rehabilitation: Functional Independence Mea-
References sure. Buffalo: Author.
Turkstra, L. S., Coelho, C., & Ylvisaker, M. (2005). The
use of standardized tests for individuals with cognitive-
Adamovich, B., & Henderson, J. (1992). Scales of cogni-
communication disorders. Seminars in Speech and
tive ability for traumatic brain injury. Chicago:
Language, 26(4), 215–222.
Riverside.
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American Speech-Language-Hearing Association. (1990).
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Advisory report, functional communication measures
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project. Rockville: Author.
Worrall, L., & Yiu, E. (2000). Effectiveness of functional
de Carvalho, I. A. M., & Mansur, L. L. (2008). Validation
communication therapy by volunteers for people with
of ASHA FACS-functional assessment of communica-
aphasia following stroke. Aphasiology, 14(9), 911–924.
tion skills for Alzheimer disease population. Alzheimer
Disease & Associated Disorders, 22(4), 375–381.
Davidson, B., Worrall, L., & Hickson, L. (2003). Identify- Readings
ing the communication activities of older people with American Speech-Language-Hearing Association. (n.d.).
aphasia: Evidence from naturalistic observation. National outcomes measurement system (NOMS).
Aphasiology, 17(3), 243–264. Available from www.asha.org/NOMS
Americans with Disabilities Act of 1990 199

Davidson, B., & Worrall, L. (2000). The assessment of involvement in a particular endeavor. It was
activity limitation in functional communication: Chal- established due to Congress’s recognition of a
lenges and choices. In L. E. Worrall & C. M. Frattali
(Eds.), Neurogenic communication disorders: A func- large number of Americans with one or more A
tional approach (pp. 19–34). New York: Thieme. disabilities and the discrimination experienced
Golper, L. C., & Frattali, C. M. (2012). Outcomes in by such individuals with respect to employment
speech-language pathology: Contemporary theories, and access to services.
models, and practices (2nd ed.). New York: Thieme.
Worrall, L., McCooey, R., Davidson, B., Larkins, B., &
Hickson, L. (2002). The validity of functional assess-
ments of communication and the activity/participation
components of the ICIDH-2: Do they reflect what really Current Knowledge
happens in real-life? Journal of Communication Disor-
ders, 35(2), 107–137.
The ADA includes several sections that cover
different types of activities, most notably, employ-
ment (Title I), public services (Title II), public
accommodations and services operated by private
Americans with Disabilities entities (Title III), access to telecommunications
Act of 1990 (Title IV), and miscellaneous provisions (Title V).
Psychologists often conduct evaluations of dis-
Robert L. Heilbronner abled individuals to determine “reasonable
Chicago Neuropsychology Group, Chicago,
accommodations” in accordance with the ADA.
IL, USA
The most common referral involves Title 1,
employment issues. The ADA requires that an
evaluator assesses four distinct areas:
Historical Background (a) disability, (b) qualifications to perform an
essential function of the job, (c) reasonable
The Americans with Disabilities Act (ADA) was accommodations, and (d) threats to others. The
signed by President George Bush in 1990 and “reasonable accommodations” are typically bro-
went into effect in 1992. It is regarded by many ken down by short-term accommodations as well
as the most sweeping civil rights legislation since as long-term accommodations.
the Civil Rights Act of 1964, with its intent to
assist people with disabilities to obtain jobs and
achieve the goal of full functioning in the work-
place. The ADA contains provisions that outlaw References and Readings
discrimination against people with disabilities
(including those with learning disabilities and Americans with Disabilities Act of 1990,
mental disorders) in hiring, training, compensa- 42 U.S.C. 12101–12213 et seq.
Bell, C. (1997). The Americans with Disabilities Act,
tion, and benefits (Bell 1997) and mandates that mental disability and work. In R. Bonnie &
employers provide “reasonable accommodations” J. Monahan (Eds.), Mental disorder, mental disability
for disabled workers who could qualify for jobs if and the law. Chicago: University of Chicago Press.
such assistance is provided. It also protects indi- Foote, W. M. (2003). Forensic evaluation in Americans
with disabilities act cases. In A. Goldstein (Ed.), Hand-
viduals against retaliation for filing charges or book of psychology (Vol. 11). Forensic psychology.
otherwise being involved in an Equal Employ- Hoboken: Wiley.
ment Opportunity Commission (EEOC)-related Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin,
action. The act requires that people with disabil- C. (1997). Psychological evaluations for the courts:
A handbook for mental health professionals and law-
ities be treated like nondisabled persons, unless it
yers. New York: Guilford.
is determined that a certain individual’s disability More detailed information regarding the Americans with
produces significant hindrances to one’s Disabilities Act of 1990 can be found at www.ada.gov
200 Amitriptyline

tachycardia, QTc prolongation, hepatic failure,

Amitriptyline mania, and potential for activation of suicidal
ideation.
Efrain Antonio Gonzalez
College of Psychology, Nova Southeastern Common
University, Fort Lauderdale, FL, USA Blurred vision, constipation, urinary retention,
Utah State University, Logan, UT, USA increased appetite, dry mouth, diarrhea, heart-
burn, weight gain, fatigue, weakness, dizziness,
anxiety, sexual dysfunction, sweating, rash, and
Generic Name itching.
Amitriptyline

References and Readings

Brand Name
Physicians’ Desk Reference, (71st ed.). (2017). Montvale:
Thomson PDR.
Elavil, Levate Stahl, S. M. (2007). Essential psychopharmacology: The
prescriber’s guide (2nd ed.). New York: Cambridge
University Press.
Class
Additional Information
Tricyclic antidepressant Drug Interaction Effects. http://www.drugs.com/drug_
interactions.html.
Drug Molecule Images. http://www.worldofmolecules.
com/drugs/.
Proposed Mechanism(s) of Action Free Drug Online and PDA Software. www.epocrates.com.
Free Drug Online and PDA Software. www.medscape.
Increases available norepinephrine and serotonin, com.
blocks serotonin reuptake, and may desensitize Gene-Based Estimate of Drug interactions. http://mhc.
daytondcs.com:8080/cgi bin/ddiD4?ver=4&task=
both serotonins 1A and beta adrenergic receptors. getDrugList.
Pill Identification. http://www.drugs.com/pill_identifica
tion.html.
Indication

Depression
Amnesia

Off-Label Use Ginette Lafleche and Mieke Verfaellie

VA Boston Healthcare System, Memory
Postherpetic neuralgia, neuropathic pain, fibro- Disorders Research Center, Boston University
myalgia, headache, eating disorder, and insomnia. School of Medicine, Boston, MA, USA

Side Effects Definition

Serious Amnesia refers to the loss of ability to recall

Paralytic ileus, hyperthermia, lowered seizure facts, events, or concepts encountered prior to
threshold, sudden death, cardiac arrhythmias, the onset of illness (retrograde amnesia) or to
Amnestic Disorder 201

the loss of the ability to form new memories temporal gradient with recent memories affected
(anterograde amnesia), or both. Although anter- more than earlier ones. This entry focuses on
ograde and retrograde amnesia can each occur in persistent, nonprogressive etiologies of amnestic A
isolation, they frequently appear together follow- disorders, excluding etiologies such as transient
ing a single cause. The cause is commonly an global amnesia, neurodegenerative conditions
organic neurologic insult or illness, but it can (e.g., Alzheimer’s disease), and psychogenic
also be psychogenic. Although in most organic amnesias.
cases the memory loss is permanent, it can also
be temporary, as for example in transient global
amnesia. Categorization

Amnestic disorders can result from a variety of

Cross-References causes, including hypoxic/anoxic events, infec-
tions, nutritional deficiencies, and lesions such
▶ Anterograde Amnesia as those occurring following stroke or surgical
▶ Memory Impairment ablation, and are associated with damage to sev-
▶ Retrograde Amnesia eral brain regions. Two subtypes of amnestic dis-
▶ Transient Global Amnesia orders have received the most attention:
bitemporal amnesia and diencephalic amnesia
(e.g., Korsakoff’s syndrome and patients with dis-
References and Readings crete thalamic or mammillary body lesions).
A third subtype, basal forebrain amnesia, is
Baddeley, A. D., Kopelman, M. D., & Wilson, A. W. viewed as clinically distinctive (Bauer
(2002). The handbook of memory disorders. Chiches- et al. 2003).
ter: Wiley.

Epidemiology

Amnestic Disorder Amnestic disorders can be observed in several

classes of patients, including following viral
Beth Springate infections (e.g., herpes encephalitis), anoxic/hyp-
Department of Psychiatry, University of oxic events (e.g., after heart attack or near-
Connecticut Health Center, Farmington, CT, USA drowning, carbon monoxide exposure), nutri-
tional impairments (e.g., Korsakoff’s syndrome),
bilateral temporal lobectomies, traumatic brain
Short Description or Definition injury, and cerebrovascular events; epidemiolog-
ical data are available by specific etiology,
Amnestic disorders are defined by a decline in although pure global amnestic syndromes them-
explicit memory in the absence of other signifi- selves are relatively rare. For example, herpes
cant cognitive impairments and represent a dete- simplex encephalitis carries a 70% mortality
rioration from previous levels of function. The rate without treatment. The cognitive impair-
hallmark feature of classic amnestic disorders is ments in survivors are ranging, and in one study
anterograde amnesia (impairment in the ability to of long-term survivors, 19 of 22 participants
form new explicit memories), although retrograde experienced some form of memory impairment,
amnesia (inability to remember previously although only five subjects had memory difficul-
learned information) can be seen, usually in a ties that were categorized as severe (Utley et al.
202 Amnestic Disorder

1997). In a review of studies of cerebral anoxia, implicit learning, and general cognition remain
Caine and Watson (2000) concluded that while largely intact.
54% of case studies describe memory impair- Amnestic disorders resulting from bitemporal
ments, only 19% report memory deficits in or diencephalic insults are the most frequently
isolation. studied and similar in their neuropsychological
profiles. Although early studies suggested that
individuals with bitemporal amnesias have a
Natural History, Prognostic Factors, and more rapid forgetting rate, McKee and Squire
Outcomes (1992) found equivalent forgetting curves for pic-
tures when severity of amnesia was controlled.
The amnestic disorder is exemplified by the case Both subtypes of amnesia display a degree of
study of H.M., a patient who underwent a radical, retrograde amnesia (Kopelman et al. 1999).
experimental surgery in which the medial tempo- Bauer et al. (2003) argue that despite these simi-
ral lobes were removed bilaterally in an attempt to larities, some deficits are unique to patients with
treat intractable epilepsy. His resection included diencephalic amnestic disorders; although some
the hippocampal formation and adjacent struc- studies suggest patients with Korsakoff’s syn-
tures including most of the amygdala and para- drome display a unique deficit in memory for
hippocampal gyrus, including the entorhinal temporal order (e.g., Squire 1982; Kopelman
cortex. Following surgery, H.M. developed severe et al. 1999), others fail to support this finding
anterograde amnesia which manifested as (Downes et al. 2002).
impaired episodic memory. In addition, he devel- Basal forebrain amnesia typically results from
oped partial retrograde amnesia for events within vascular lesions or aneurysm surgery in the region
19 months before his surgery. However, earlier of the anterior communicating artery. After basal
memories were unaffected, and his working mem- forebrain damage, patients may demonstrate
ory and procedural memory (skill learning) also extensive anterograde amnesia (Bottger et al.
remained intact (Corkin 2002; Scoville and 1998; Tidswell et al. 1995). Confabulation is com-
Milner 1957). mon and may relate to the extent of orbitofrontal
Course: Onset is often acute due to the nature involvement (Hashimoto et al. 2000), but it often
of the pathological processes that cause amnestic subsides following the acute phase, while the
disorders (e.g., cerebrovascular events, anoxic/ amnestic state remains. There is evidence that
hypoxic events, surgical ablation, and infections patients with basal forebrain amnesia benefit
such as herpes encephalitis). Although some from the presentation of cues to enhance recall
degree of improvement may occur in some (Osimani et al. 2006).
patients, for example during the immediate period
of natural recovery which occurs following cere-
brovascular infarcts or traumatic injuries, deficits Evaluation
typically are persistent. Barring any additional
injury, worsening of memory over time would As amnestic disorders are defined by deficits in
not be anticipated. new learning, memory is the cognitive domain
General neuropsychological profile: Patients that should be emphasized within a comprehen-
exhibit deficits in explicit memory marked by sive neuropsychological evaluation that also
significant anterograde amnesia. They may also includes assessment of other areas of cognitive
exhibit retrograde amnesia, although this is typi- function such as orientation, attention, language,
cally less severe and exhibits a temporal gradient executive functions, visuospatial skills, and psy-
with older memories less likely to be disturbed. chological functioning. Patients fitting the classic
Attention, working memory, procedural memory, amnestic disorder profile will exhibit deficits in
Amnestic Disorder 203

memory with generally intact cognition within Treatment

other domains.
It is important to establish the specific nature of Treatment of amnestic disorders is nonspecific A
patients’ memory impairments. Immediate mem- and focused primarily on compensation for mem-
ory span (typically assessed through tests such as ory impairments. Cognitive rehabilitation and
Digit and Spatial Span from the Wechsler Mem- memory training programs often emphasize the
ory Scales) should be within the normal range. teaching of mnemonic strategies or the use of
Anterograde learning may be assessed with mea- external memory aids such as note-taking or
sures such as list learning, story learning, or figure audiotaping in order to enhance patients’ func-
memory. While patients will be able to retain tioning in daily life, although patients would con-
items and repeat them back as long as they can sciously need to recall learning these strategies
keep them in memory, learning curves are typi- and to utilize them. Implicit training procedures,
cally flat, and an intervening distractor task will such as those involving errorless learning strate-
typically cause items to be lost completely. It is gies, can be helpful, as are environmental supports
important to examine free recall vs. cued/recogni- (e.g., electronic reminders) and assistance from
tion formats, as patients with frontally medicated family, friends, and/or caregivers.
amnestic disorders may show some benefit (typi- The use of pharmacologic agents to treat
cally no benefit seen for patients with bitemporal amnestic disorders is not well studied, and large
or diencephalic etiologies). Some degree of randomized controlled trials are lacking. In an
laterality to memory profiles may be expected open-label pilot study, Benke et al. (2005) admin-
depending on the nature of injury (e.g., left hemi- istered donepezil, a cholinesterase inhibitor, to
sphere damage leading to verbal memory impair- patients with a chronic amnestic syndrome from
ments, right hemisphere damage impacting visual a ruptured and repaired aneurysm of the anterior
memory). communicating, anterior cerebral, or pericallosal
In addition, retrograde amnesia and memory artery. Some measures of performance on a list-
for remote events can be examined in a qualitative learning task improved significantly during the
manner by inquiring about autobiographical 12-week medication administration period,
events or memories that one can assume to be suggesting future double-blind controlled studies
present in most people from a given society would be useful to more thoroughly examine the
(e.g., pictures of famous individuals, questions potential utility of cholinergic medications. Stud-
regarding salient historical events). The aspects ies have also examined the use of cholinesterase
of memory that remain intact in classic amnestic inhibitors following traumatic brain injury; a
disorder patients (such as semantic memory and recent review (Bengtsson and Godbolt 2016)
motor skill learning) could also be assessed. found only three studies meeting somewhat
The main differential diagnoses to consider relaxed inclusion criteria (no studies located
include delirium and neurodegenerative demen- using their initial inclusion criteria). One study
tias (e.g., Alzheimer’s disease). Delirium is found no effect of treatment, and two studies
defined by a disturbance in attention and con- showed limited effects. Given that included stud-
sciousness, both of which are intact in amnestic ies had several methodological limitations, further
disorders. Although neurodegenerative demen- studies are needed to examine whether acetylcho-
tias present similarly to amnestic disorders in linesterase inhibitors may be beneficial in this
that patients often present with memory impair- population.
ments, cognitive decline (rather than stability) In addition, due to their memory impairment,
occurs and impairments in other cognitive patients are likely to experience impairments in
domains such as language or executive functions their social and vocational activities and may also
are present. require supervision and/or support in their living
204 Amnestic Syndromes

environment and a guardian or conservator to for complex visual material. Journal of Clinical and
assist with legal and medical concerns in more Experimental Neuropsychology, 14, 103.
Osimani, A., Vakil, E., Blinder, G., Sobel, R., & Abarbanel,
severe cases. J. M. (2006). Basal forebrain amnesia: A case study.
Cognitive and Behavioral Neurology, 19, 65–70.
Scoville, W. B., & Milner, B. (1957). Loss of recent
memory after bilateral hippocampal lesions. Journal
Cross-References of Neurology, Neurosurgery, and Psychiatry,
20, 11–21.
▶ Amnesia Squire, L. R. (1982). Comparisons between forms of amne-
sia: Some deficits are unique to Korsakoff’s syndrome.
▶ Amnestic Syndromes
Journal of Experimental Psychology: Learning, Mem-
▶ Dissociative Amnesia ory, and Cogntion, 8, 560–571.
▶ Korsakoff’s Syndrome Tidswell, P., Dias, P. S., Sagar, H. J., Mayes, A. R., &
▶ Temporal Lobectomy Battersby, R. D. E. (1995). Cognitive outcome
after aneurysm rupture: Relationship to aneurysm
site and perioperative complications. Neurology,
45, 875–882.
Utley, T. F. M., Ogden, J. A., Gibb, A., McGrath, N., &
References and Readings Anderson, N. E. (1997). The long-term neuropsycholog-
ical outcome of herpes simplex encephalitis in a series of
Bauer, R. M., Grande, L., & Valenstein, E. (2003). Amne- unselected survivors. Neuropsychiatry, Neuropsychol-
sic disorders. In K. M. Heilman & E. Valenstein (Eds.), ogy, and Behavioral Neurology, 10, 180–189.
Clinical neuropsychology (pp. 495–573). New York:
Oxford University Press.
Bengtsson, M., & Godbolt, A. K. (2016). Effects of ace-
tylcholinesterase inhibitors on cognitive function in
patients with chronic traumatic brain injury:
A systematic review. Journal of Rehabilitation Medi- Amnestic Syndromes
cine, 5, 1–5.
Benke, T., Köylü, B., Delazer, M., Trinka, E., & Kemmler, Ginette Lafleche and Mieke Verfaellie
G. (2005). Cholinergic treatment of amnesia following
Memory Disorders Research Center, VA Boston
basal forebrain lesion due to aneurysm rupture – An
open-label pilot study. European Journal of Neurology, Healthcare System and Boston University School
12, 791–796. of Medicine, Boston, MA, USA
Bottger, S., Prosiegel, M., Steiger, H., & Yassouridis,
A. (1998). Neurobehavioral disturbances, rehabilita-
tion outcome, and lesion site in patients after rupture
and repair of anterior communicating artery aneurysm. Short Description or Definition
Journal of Neurology, Neurosurgery, and Psychiatry,
65, 93–102. The amnestic syndromes are a group of neuro-
Caine, D., & Watson, J. D. G. (2000). Neuropsychological
and neuropathological sequelae of cerebral anoxia:
logic disorders characterized by a dense global
A critical review. Journal of the International Neuro- amnesia. This amnesia is comprised of an inability
psychological Society, 6, 86–99. to form new memories (anterograde amnesia) and
Corkin, S. (2002). What’s new with the amnesic patient H. an inability to retrieve old memories (retrograde
M.? Nature Reviews: Neuroscience, 3, 153–160.
amnesia) (Anterograde Amnesia and Retrograde
Downes, J. J., Mayes, A. R., MacDonald, C., & Hunkin,
N. M. (2002). Temporal order memory in patients with Amnesia). A unique feature of these disorders is
Korsakoff’s syndrome and medial temporal amnesia. that the dense memory loss occurs within the
Neuropsychologia, 40, 853–861. context of relatively preserved intelligence, lan-
Hashimoto, R., Tanaka, Y., & Nakano, I. (2000). Amnesic
guage, attention, and perceptual abilities.
confabulatory syndrome after focal basal forebrain
damage. Neurology, 54, 978–980.
Kopelman, M. D., Stanhope, N., & Kingsley, D. (1999).
Retrograde amnesia in patients with diencephalic, tem- Categorization
poral lobe or frontal lesions. Neuropsychologia, 37,
939–958.
McKee, R. D., & Squire, L. R. (1992). Both hippocampal The amnestic syndromes can be classified
and diencephalic amnesia result in normal forgetting according to cause or site of damage. Possible
Amnestic Syndromes 205

etiologies include herpes simplex encephalitis, The severity of memory impairment following
anoxia, Wernicke-Korsakoff syndrome, cerebro- HSE shows substantial variation that is directly
vascular accidents, anterior communicating artery proportional to the extent of medial temporal lobe A
aneurysm (ACoA), and tumors. These disorders damage (Stefanacci et al. 2000). Lesions are often
can give rise to amnesia by damaging any of an asymmetrical, and this will define the clinical
array of structures, such as the medial temporal presentation. If damage to the left medial temporal
lobes (including the hippocampus), the midline region is greater, verbal memory problems domi-
diencephalic nuclei, and the basal forebrain, or by nate, whereas if right medial temporal damage is
disrupting some of their interconnections such as greater, nonverbal aspects of memory, such as
the fornix. In such cases, the resulting amnestic memory for faces and designs, are predominantly
syndrome tends to be permanent because the struc- impaired.
tural damage to the brain is irreversible. However, In addition to an inability to acquire new infor-
amnesia can also be transient when it is due to a mation (anterograde amnesia), patients also have
functional disruption of these brain structures (see difficulty remembering events that occurred prior
Transient Global Amnesia) or psychogenic causes. to their illness (retrograde amnesia). Retrograde
amnesia can vary considerably in severity but is
particularly marked when lesions extend into lat-
Neuropsychology of the Amnestic eral temporal regions. Impairments in episodic
Syndromes memory, which is memory for specific events of
your life, for example, remembering your college
Herpes Simplex Encephalitis (HSE) graduation, are the primary complaint. Semantic
HSE is a viral infection of the brain that begins as memory, which is memory for non-personal facts,
a flu-like illness with headaches and fever, such as remembering that Paris is the capital of
followed by lethargy, confusion, and disorienta- France, may be more or less affected depending
tion. If treatment is delayed, severe neurological on the damage. Damage primarily to right anterior
deficits, including amnesia, agnosia (loss of the temporal regions is more likely to result in exten-
ability to recognize sensory impressions such as sive loss of personal (i.e., episodic) memories
objects, people, and sounds), and aphasia (loss of (O’Connor et al. 1992) while damage to the left
aspects of speech production or reception) can temporal cortex is associated with the loss of
develop. Recovery varies even with treatment, general world knowledge (i.e., semantic memory)
and many are left with a broad range of cognitive (DeRenzi et al. 1987). Unusual selective impair-
deficits. For a few, an isolated amnestic syndrome ments can also occur, such as the ability to identify
persists. Their presentation is similar to that of the inanimate objects but not living things or foods
well-known amnesic patient HM who became and the ability to comprehend concrete but not
unable to form new memories after undergoing a abstract words (Warrington and Shallice 1984).
neurosurgical operation in which a large portion
of the medial temporal lobe of his brain was Anoxia
removed bilaterally. Anoxic brain injury can result from any of a
Neuropathologically, the virus preferentially number of diverse etiologies including cardiac
affects limbic regions in the temporal lobe, includ- arrest, respiratory distress, carbon monoxide poi-
ing the hippocampus and adjacent medial tempo- soning, and drug overdose. These conditions all
ral lobe regions, as well as the amygdala and polar diminish or cut off the supply of oxygen to the
limbic cortices. Damage often extends to the lat- brain, either through reduced blood flow or
eral aspect of the temporal lobe, affecting the reduced blood oxygen saturation. The physio-
anterolateral aspect, the inferior aspect, or both. logical consequences of such anoxic events are
Anterior extension of damage into ventromedial complex. Brain areas particularly vulnerable to
areas of the brain, such as the insular cortex and anoxic injury include the hippocampus, the basal
the basal forebrain, has also been documented. ganglia, and other areas where the distributions
206 Amnestic Syndromes

of the cerebral arteries overlap in the cerebral hippocampus itself is critical for episodic memory
cortex. The clinical manifestations of anoxia are but not semantic memory.
highly variable, but memory impairment is a
common symptom. A review of 58 studies of Wernicke-Korsakoff Syndrome
cerebral anoxia showed that while damage to See ▶ Wernicke-Korsakoff Syndrome entry.
hippocampal structures was common, damage
restricted to the hippocampus was seen in only Cerebrovascular Accidents
18% of patients (Caine and Watson 2000). Bilateral posterior cerebral artery (PCA) infarc-
Accordingly, in a majority of patients, memory tion is a well-recognized cause of amnesia.
impairment occurs in the context of more diffuse Because the left and right PCA arise from the
cognitive deficits with executive problems and bifurcation of a common source, strokes that
motor dysfunction being particularly common occur upstream from the bifurcation can affect
(Alexander et al. 2011). In a minority of patients, the medial temporal lobes bilaterally, causing a
the anoxic injury leads to an isolated amnesia, dense amnesia with dysfunction in both antero-
that is, a memory disorder in the absence of other grade and retrograde memory. Neuroanatomical
neuropsychological impairments. In these cases, studies of patients with PCA infarction have
bilateral hippocampal damage is thought to revealed that lesions in the posterior para-
underlie the amnesic syndrome (Di Paola et al. hippocampus or the collateral isthmus (a pathway
2008). As with other forms of amnesia, the sever- connecting the posterior parahippocampus to
ity of the amnesia is proportional to the damage association cortex) are critical for the develop-
to the hippocampal formation (Zola-Morgan et ment of memory impairment (Von Cramon et al.
al. 1986; Rempel-Clower et al. 1996). While 1988). When damage extends posteriorly to
anterograde memory impairment is typically include occipitotemporal cortices, deficits beyond
accompanied by some degree of retrograde amnesia are often seen.
impairment, anterograde amnesia can occur in Early in their clinical course, patients with
the absence of retrograde amnesia as evidenced PCA infarction exhibit a confusional state that
by patient R.B. who exhibited bilateral damage eventually resolves into an amnestic syndrome
that was limited to the hippocampus (Zola-Mor- with or without additional neuropsychological
gan et al. 1986). symptoms involving primarily the processing of
Relatively selective amnesia has been visual information. The memory disturbance is
documented in children and adolescents who characterized by a classic profile of consolidation
experienced a hypoxic-ischemic event at birth or deficits in the context of normal short-term mem-
shortly after birth (i.e., developmental amnesia: ory and normal intelligence. There may or may
Vargha-Khadem et al. 1997). Gadian et al. not be associated retrograde amnesia. Memory
(2000) reported on five cases, all of whom problems have also been described with unilat-
exhibited bilateral damage that was limited to eral, usually left, PCA infarction. In such cases,
the hippocampus. All had a profound inability to the memory impairment can be transient or per-
form new episodic memories, but strikingly, they manent and is typically limited to verbal material.
were able to acquire a considerable amount of new Memory deficits in patients with right PCA infarc-
factual knowledge, which allowed them to attend tion have been less well studied, in part because
mainstream schools and maintain a relatively such examination is complicated by the percep-
higher level of functioning compared to adult tual problems that frequently accompany right
onset cases of amnesia described above. The rel- PCA infarction.
ative preservation of semantic learning in these Thalamic strokes can also lead to significant
children has been ascribed to the integrity of memory problems. Because the relevant thalamic
medial temporal areas outside of the hippocam- centers are small and adjacent to one another, it is
pus. Research on developmental amnesia has pro- difficult to establish associations between site of
vided additional support for the notion that the damage and clinical deficits. A review by Van der
Amnestic Syndromes 207

Werf et al. (2000) led to the conclusion that dam- often better preserved than performance on recall
age to the mammillothalamic tract (MTT) tests, particularly following a delay with interfer-
invariably causes anterograde amnesia and that ence. This reflects a disruption of strategic A
no amnesia occurs in the absence of damage retrieval processes that allow access to informa-
to the MTT. Medial dorsal thalamic lesions tion stored in memory. Deficient strategic memory
cause a memory disturbance that is mild in com- processes also contribute to poor encoding, and
parison to the severe amnesia that arises when the use of organizational strategies during the
the lesion extends to the MTT. Patients with learning phase can enhance patients’ perfor-
thalamic amnesia exhibit executive dysfunc- mance. A failure to monitor whether the outcome
tion, increased sensitivity to interference, and of a memory search led to the sought after infor-
variability in the persistence and extent of ret- mation can lead to a high number of false alarms
rograde amnesia. in recognition tests. In extreme cases, this can lead
to impairment in recognition memory that
ACoA Aneurysm exceeds that seen in recall. Other features linked
Rupture of the ACoA can result in a memory to frontal dysfunction include impaired source
disorder that ranges from mild to severe. The memory, which refers to when, where, and how
ACoA provides blood supply to the basal forebrain, information was learned.
the anterior cingulate, the anterior hypothalamus,
the anterior columns of the fornix (an important
neural pathway leading to and from the hippocam- Evaluation
pus), the anterior commissure, and the genu of the
corpus callosum. The pathological consequences of Although a primary focus of the assessment in
a ruptured aneurysm may be a result of infarction amnesia is on memory function, it is important
directly, or secondary to subarachnoid hemorrhage, to assess other cognitive domains as well, includ-
vasospasm, or hematoma formation. Because of the ing general intelligence, attention, executive func-
various neuropathological consequences, the clini- tions, language, and visuospatial skills. This
cal profiles associated with ACoA aneurysm are comprehensive approach is required to establish
more variable than those seen with diencephalic whether a patient presents with a pure amnestic
or medial temporal lobe injuries, and the impair- syndrome or with memory impairment in the con-
ments are often more diffuse in nature (see DeLuca text of more pervasive cognitive difficulty. New
and Diamond 1995 for review). learning abilities should be assessed using mea-
The acute phase of recovery following rupture sures that include free recall (unassisted by the
and repair of ACoA aneurysm is characterized by a examiner), cued recall (with some guidance from
severe confusional state and a marked attentional the examiner), and recognition (deciding whether
disorder. As the confusion resolves, memory prob- an item was or was not part of a learned list of
lems become more apparent. These can vary from items). Assessments should examine both imme-
mild impairments to severe amnesia and can diate and delayed retention. Information derived
include a retrograde amnesia. Other symptoms, from specific aspects of performance, such as the
including executive dysfunction, confabulation, shape of the learning curve, the comparison of
and poor insight, are likely to be part of the recall and recognition performance, and the
resulting clinical syndrome if the lesion extends impact of delay, all provide important pointers to
to the medial frontal lobes. The clinical outcome the nature of the memory breakdown and will
of patients with more extensive lesions is typically serve to inform remediation.
worse than that of patients with lesions limited to A variety of standardized tests are available to
the basal forebrain (Alexander et al. 1984). assess memory function, and the reader is referred
The amnesia associated with ACoA aneurysm to Lezak et al. (2004) for specific examples. The
has a marked frontal dysexecutive component. most commonly used standardized memory test is
Performance on recognition tests of memory is the Wechsler Memory Scale-III or IV, which
208 Amnestic Syndromes

consists of a series of subtests that probe various perceptual cues, through the use of implicit mem-
aspects of verbal and nonverbal memory in differ- ory. Once successful, cues are gradually reduced,
ent formats. The assessment of retrograde mem- eventually leading to the spontaneous generation
ory should cover knowledge of public events and of the to-be-learned information. This technique
people, personal facts, and autobiographical has proven successful for learning new vocabu-
events. With respect to public knowledge, areas lary and concepts. A caveat, however, is that such
of assessment include the knowledge of famous learning is a slow and laborious, and the informa-
names and faces, public news events, and new tion learned is typically inflexible and only acces-
vocabulary that has recently entered the language. sible in the exact form in which it was learned. An
The assessment of personal facts and events can important consideration in the use of implicit
be challenging, because there are few standard- memory techniques is the avoidance of errors, as
ized measures available, and corroboration from a patients have no recollection of their mistakes,
caregiver may be needed to establish the accuracy and consequently, errors, just like correct
of reported personal memories. responses, can be strengthened. Other methods
capitalize on preserved procedural learning and
use repetition to teach skills and habits that support
Treatment activities of daily living. Examples of external
compensatory aids that rely on procedural memory
There is no pharmacological or cognitive treatment are the use of notebooks, diaries, and alarm clocks.
that can restore memory in organic amnesia. How- Electronic devices such as computers,
ever, cognitive rehabilitation approaches have been smartphones, and paging systems have great flex-
developed that aim to foster routines and habits that ibility as compensatory aids, but training in the use
will increase independence, productivity, and qual- of such technology requires very lengthy practice
ity of life. The choice of rehabilitation approach sessions, and transfer of learning outside of the
should be informed by both cognitive and psycho- training sessions can be difficult. Such training is
social/emotional factors. Cognitive factors include therefore more appropriate for individuals who
premorbid skills and abilities and current neuro- have had premorbid experience with such devices
psychological functioning. A clear delineation of and are highly motivated to use them.
impaired and preserved aspects of memory is crit- For individuals with milder memory impair-
ical to guide rehabilitation efforts, as is the identi- ments, it may also be possible to directly focus
fication of other areas of cognitive impairment that on enhancing impaired forms of memory through
might hamper therapeutic efforts. Of the psychoso- the use of internal strategies. The choice of strat-
cial/emotional factors, insight and motivation are egy will be dependent on the nature of the mem-
perhaps the two most influential predictors of reha- ory process that appears defective. Examples of
bilitation success. Patients need to have some such techniques include enhanced organization of
awareness of their deficits and have some degree the to-be-learned information through chunking
of internal drive to understand the value of, and (i.e., breaking down or grouping information in
engage in, the rehabilitation process. short-term memory to make it more manageable)
Several approaches have been developed to or through categorization and elaboration of the
help patients with severe memory impairment material, whether through verbal associations or
learn new information. These approaches take the creation of visual images. Such strategies fall
advantage of preserved non-declarative (i.e., under the category of internal memory aids.
implicit) memory abilities to help amnesic There are no specific methods of treatment
patients acquire new information or skills. One available to restore memories from the past. Infor-
approach that capitalizes on preserved implicit mation and pictures about one’s life, such as
perceptual memory is the vanishing cues tech- places where one has resided, can be reintroduced
nique (Glisky et al. 1986). Patients are guided to and incorporated into the selected treatment
provide the correct information in response to approach. However, emotionally laden facts,
Amorphognosis 209

such as the death of a family member, can trigger and retrograde amnesia in a patient with herpes simplex
repeated emotional responses that can interfere encephalitis. Journal of Clinical and Experimental
Neuropsychology, 14, 159–178.
with adjustment and are best avoided in the early Rempel-Clower, N. L., Zola, S. M., Squire, L. R., & Amaral, A
stage of treatment. By nature, relearned personal D. (1996). Three cases of enduring memory impairment
information about one’s life will be recalled with- after damage limited to the hippocampal formation. The
out the emotional texture of the original event; Journal of Neuroscience, 16(16), 5233–5255.
Stefanacci, L., Buffalo, E. A., Schmolck, H., & Squire, L.
however, it can play an important role in helping R. (2000). Profound amnesia after damage to the
patients fill in the narrative of their own life. medial temporal lobe: A neuroanatomical and neuro-
psychological profile of patient EP. The Journal of
Neuroscience, 20, 7024–7036.
Van der Werf, Y. D., Witter, M. P., Uylings, H. B., & Jolles,
Cross-References J. (2000). Neuropsychology of infarctions in the thala-
mus: A review. Neuropsychologia, 38, 613–627.
▶ Anterograde Amnesia Vargha-Khadem, F., Gadian, D. G., & Mishkin, M. (2001).
Dissociations in cognitive memory: The syndrome of
▶ Retrograde Amnesia developmental amnesia. Philosophical Transactions of
▶ Transient Global Amnesia the Royal Society of London B, 356, 1435–1440.
Von Cramon, D., Hebel, N., & Schuri, U. (1988). Verbal
memory and learning in unilateral posterior cerebral
infarction. Brain, 111, 1061–1077.
References and Readings Warrington, E. K., & Shallice, T. (1984). Category specific
semantic impairments. Brain, 107, 829–854.
Alexander, M. P., & Freedman, M. (1984). Amnesia after Zola-Morgan, S., Squire, L. R., & Amaral, D. G. (1986).
anterior communicating artery aneurysm rupture. Neu- Human amnesia and the medial temporal region:
rology, 34(6), 5–11. Enduring memory impairment following a bilateral
Alexander, M. P., Lafleche, G., Schnyer, D., Lim, C., & lesion limited to field CA 1 of the hippocampus. The
Verfaellie, M. (2011). Cognitive and functional recov- Journal of Neuroscience, 6(10), 2950–2967.
ery after out of hospital cardiac arrest. Journal of the
International Neuropsychological Society, 17, 1–5.
Caine, D., & Watson, J. D. G. (2000). Neurospsychological
and neuropathological sequelae of cerebral anoxia: A
critical review. Journal of the International Neuropsy-
chological Society, 6, 86–99. Amorphognosis
DeLuca, J., & Diamond, B. J. (1995). Aneurysm of the
anterior communicating artery: A review of neuroanatom-
John E. Mendoza
ical and neuropsychological sequelae. Journal of Clinical
and Experimental Neuropsychology, 17, 100–121. Department of Psychiatry and Neuroscience,
DeRenzi, E., Liotti, M., & Nichelli, P. (1987). Semantic Tulane Medical School and SE Louisiana
amnesia with preservation of autobiographical mem- Veterans Healthcare System, New Orleans,
ory: A case report. Cortex, 23, 578–597.
Di Paola, M., Caltagirone, C., Fadda, L., Sabatini, U.,
LA, USA
Serra, L., & Carlesimo, G. A. (2008). Hippocampal
atrophy is the critical brain change in patients with
hypoxic amnesia. Hippocampus, 18(7), 719–728. Definition
Gadian, D. G., Aiardi, J., Watkins, K. E., Porter, D. A.,
Mishkin, M., & Vargha-Khadem, F. (2000). Develop-
mental amnesia associated with early hypoxic- Amorphognosis is that aspect of tactile agnosia
ischaemic injury. Brain, 123, 499–507. which refers specifically to deficits in the ability to
Glisky, E. L., Schacter, D. L., & Tulving, E. (1986). Learn- appreciate (identify) the external form of an object
ing and retention of computer-related vocabulary in
such as its shape, size, or other contour features by
memory-induced patients: Method of vanishing cues.
Journal of Clinic Journal of Clinical and Experimental tactual manipulation alone. In the absence of more
Neuropsychology, 8, 292–312. elementary somatosensory disturbances resulting
Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). from either peripheral nerve or the dorsal column
Neuropsychological assessment. New York: Oxford
University Press.
system, such deficits suggest lesions in the con-
O’Connor, M. G., Butters, N., Miliotis, P., Eslinger, P., & tralateral postcentral gyrus of the parietal lobe or
Cermak, L. S. (1992). The dissociation of anterograde in its adjacent association cortices.
210 Amoxapine

Cross-References Indication

▶ Ahylognosia Depression, reactive depressive disorder, psy-

▶ Astereognosis chotic depression, and depression accompanied
▶ Tactile Agnosia by anxiety or agitation.

Off-Label Use
References and Readings

Bauer, R. M., & Demery, J. A. (2003). Agnosia. In

Depressive phase of a bipolar disorder, anxiety,
K. Heilman & E. Valenstein (Eds.), Clinical neuropsy- insomnia, neuropathic pain, and treatment-
chology (4th ed., pp. 236–295). New York: Oxford resistant depression.
University Press.
Hecaen, H., & Albert, M. L. (1978). Chapter 6. Disorders
of somesthesis and somatognosis. In Human neuropsy-
chology. New York: Wiley. Side Effects

Serious
Paralytic ileus, hyperthermia, lowered seizure
Amoxapine threshold, sudden death, cardiac arrhythmias,
tachycardia, QTc prolongation, hepatic failure,
Efrain Antonio Gonzalez intraocular pressure, mania, and potential for acti-
College of Psychology, Nova Southeastern vation of suicidal ideation.
University, Fort Lauderdale, FL, USA
Common
Utah State University, Logan, UT, USA
Blurred vision, constipation, urinary retention,
increased appetite, dry mouth, diarrhea, heart-
burn, weight gain, fatigue, weakness, dizziness,
Generic Name
anxiety, sexual dysfunction, sweating, rash, and
itching. Can cause extrapyramidal symptoms such
Amoxapine
as akathisia and potentially tardive dyskinesia.

Brand Name References and Readings

Ascendin Physicians’ Desk Reference (71st ed.). (2017). Montvale:
Thomson PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The
prescriber’s guide (2nd ed.). New York: Cambridge
Class University Press.

Tetracyclic antidepressant Additional Information

Drug Interaction Effects. http://www.drugs.com/drug_
interactions.html.
Drug Molecule Images. http://www.worldofmolecules.
Proposed Mechanism(s) of Action com/drugs/.
Free Drug Online and PDA Software. www.epocrates.com.
Amoxapine inhibits reuptake of norepinephrine Free Drug Online and PDA Software. www.medscape.com.
and noradrenaline. It is also known to antago- Gene-Based Estimate of Drug interactions. http://mhc.
daytondcs.com: 8080/cgi bin/ddiD4?ver=4&task=
nize serotonin 2A receptors, thus increasing pre-
getDrugList.
synaptic release of amines. Mild dopamine Pill Identification. http://www.drugs.com/pill_identifica
2 blockade. tion.html.
Amphetamine 211

increasing attention and working memory. How-

Amphetamine ever, cognition is reportedly enhanced only
among those with poor baseline working memory A
Elizabeth K. Vernon1 and JoAnn Tschanz1,2 ability, and even detrimental to those with high
1
Department of Psychology, Utah State baseline ability (Iversen et al. 2009). At higher
University, Logan, UT, USA doses, the drugs produce symptoms similar to
2
Center for Epidemiologic Studies, Utah State schizophrenia (hallucinations, thought disorder,
University, Logan, UT, USA flat affect, and anhedonia) (Freberg 2014). In ani-
mals, there is a dose-dependent effect of increas-
ing activity such as locomotion or at higher doses,
Synonyms stereotyped motor behaviors. Amphetamine’s
reinforcing properties have been demonstrated in
Dexedrine; Dextro-amphetamine; d-amphetamine operant conditioning studies. The drug also
increases both systolic and diastolic blood pres-
sure and increases respiration and heart rate,
Definition among other sympathetic effects (Feldman et al.
1997). Amphetamine or its derivatives have been
Amphetamine refers to a group of synthetic used for clinical purposes (see “Historical Back-
chemicals with psychoactive stimulant effects. ground and Clinical Relevance”). However, its
Amphetamines are similar in molecular structure clinical use has been limited due to its abuse
to the catecholamine neurotransmitters, norepi- potential and dangerous sympathetic effects
nephrine and dopamine. They compete with the (Iversen et al. 2009).
endogenous monoamine (norepinephrine, dopa- At high doses, the drug also inhibits the metab-
mine, and serotonin) transporters to be transported olism of catecholamines by the enzyme mono-
into the nerve. Once inside the presynaptic termi- amine oxidase. Chronic use has been associated
nal, amphetamine displaces the monoamines from with damage to selective dopamine neurons and
the cytosolic pool, which reverses the direction of receptors (Feldman et al. 1997). The derivative
the reuptake transporter and thereby increases methamphetamine is also a potent neurotoxin,
synaptic concentrations of monoamine neuro- although unlike amphetamine, this drug predom-
transmitters (Heal et al. 2014). There are two inantly affects the serotonergic system (Feldman
forms, dextro-amphetamine (d-amphetamine) et al. 1997). The reinforcing properties of amphet-
and levo-amphetamine (l-amphetamine), of amine are hypothesized to reflect increased dopa-
which d-amphetamine is the more active form. mine neurotransmission in the subcortical
Chemical modifications to the basic structure structure, the nucleus accumbens.
have led to derivatives with even more potent
psychoactive properties. For example, addition
of a second methyl group to the chemical structure Historical Background and Clinical
creates methamphetamine, a highly addictive Relevance
drug. Modification of the benzene ring of the
amphetamine structure creates methylenedioxy- First commercially introduced in 1930s as a
methamphetamine (MDMA) or ecstacy, another nasal or bronchial decongestant, amphetamine
drug with high addiction and abuse potential was sought after for its psychoactive effects and
(Iversen et al. 2009). as an appetite suppressant. One of amphet-
The behavioral effects of lower doses of amines’ first clinical uses was for the treatment
amphetamine include increased alertness, confi- of narcolepsy. By 1946 there were more than
dence, euphoria, and well-being (Freberg 2014). 30 uses for amphetamine, including schizophre-
The drug also reduces fatigue and enhances per- nia, opiate addiction, infantile cerebral palsy,
formance on cognitive tasks, possibly by seasickness, radiation sickness, and persistent
212 Amphetamine

hiccups. At the beginning of the Spanish Civil vs. schizophrenia; Iversen et al. 2009). Other neg-
War, amphetamine was used to promote military ative effects of chronic amphetamine abuse
alertness (Sulzer et al. 2005). Amphetamine was include possible neurotoxic damage to the dopa-
then used in subsequent wars to enhance atten- mine system with reduced numbers of transporters
tion and fight the effects of sleep deprivation and receptors. Impairments in attention and mem-
(Iversen et al. 2009; Meyer and Quenzer ory have been reported with abuse, but their long-
2005). Early efforts to synthesize amphetamine term persistence, particularly with abstinence, is
on the basis of structure and function have unknown (Iversen et al. 2009).
resulted in trimethoxyamphetamine (TMA),
which led to nearly 200 potentially hallucino-
genic substituted amphetamines (Sulzer et al.
Future Directions
2005). Amphetamine and its derivatives have
been used for the treatment of narcolepsy, atten-
Research into the psychoactive and behavioral
tional problems, and as a stimulant to combat
effects of amphetamine has helped advance
fatigue and the need for sleep (Meyer and
knowledge of the psychological role of several
Quenzer 2005). In the 1930s, amphetamine
monoamine neurotransmitters and their relevance
was discovered to have beneficial effects for
to several clinical conditions such as addiction
treating children with attention deficit/hyperac-
and schizophrenia and the neurochemistry under-
tivity disorder (ADHD). Stimulants (e.g., meth-
lying some cognitive processes such as attention
ylphenidate) persist to this day as one of the
and working memory. Future research will
most effective drugs available for treating the
undoubtedly utilize advances in technology to
condition (Heal et al. 2013).
build on past research such as elucidating the
Over time, the addictive properties of amphet-
neural structures and pathways associated with
amine were realized, particularly of its potent
reward circuits, examining the neuroplasticity of
derivatives. The acute effects of the drug could
the nervous system after chronic substance abuse,
be enhanced by using a rapid route of administra-
and clarifying the moderating role of genetics in
tion such as an intravenous injection. Following
the behavioral response to amphetamine and other
the short-term “rush,” however, is a period of
compounds (Iversen et al. 2009).
restless agitation, depression, irritability, and
other symptoms. Repeated, continuous adminis-
trations will ultimately lead to a let down, with a
prolonged period of sleep. This alternating cycle is References and Readings
often repeated, resulting in a physical toll on the
Feldman, R. S., Meyer, J. S., & Quenzer, L. F. (1997).
body. As with other drugs of abuse, dependence
Stimulants: Amphetamine and Cocaine. In Principles
and tolerance can develop with chronic use, of neuropsychoparhmacology (pp. 549–568). Sunder-
resulting in the administration of increasing doses land: Sinauer Associates, Inc.
to achieve the desired effects. With sustained Freberg, L. (2014). Discovering behavioral neuroscience
(pp. 107–108). Boston: Cenage Learning.
chronic use, negative effects may emerge
Heal, D. J., Smith, S. L., Gosden, J., & Nutt, D. J. (2013).
consisting of repetitive, stereotyped behaviors as Amphetamine, past and present – A pharmacological
well as a psychotic syndrome consisting of hallu- and clinical perspective. Journal of Psychopharmacol-
cinations and paranoid delusions. This syndrome, ogy (Oxford, England), 27(6), 479–496. https://doi.org/
10.1177/0269881113482532.
referred to as “amphetamine psychosis,” was nota- Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H.
bly similar to the symptoms of paranoid schizo- (2009). Psychostimulants. In Introduction to Neuropsy-
phrenia and provided some support for the chopharmacology (pp. 447–472). New York: Oxford
dopamine hypothesis of schizophrenia. However, University Press.
Meyer, J. S., & Quenzer, L. F. (2005). Psychomotor stim-
qualitative differences between the two conditions
ulants: Cocaine and the amphetamines. In
were also noted (e.g., greater tendency for visual Psychopharmacoogy. Drugs, the brain and behavior
hallucinations in amphetamine psychosis (pp. 292–300). Sunderland: Sinauer Associates, Inc.
Amygdala 213

Sulzer, D., Sonders, M. S., Poulsen, N. W., & Galli,

A. (2005). Mechanisms of neurotransmitter release by Amygdala
amphetamines: A review. Progress in Neurobiology,
75(6), 406–433. https://doi.org/10.1016/j. A
pneurobio.2005.04.003. Rory McQuiston
Anatomy and Neurobiology, Virginia
Commonwealth University, Richmond, VA, USA

Amusia
Synonyms
John E. Mendoza
Department of Psychiatry and Neuroscience, Amygdaloid body; Amygdaloid nucleus
Tulane Medical School and SE Louisiana
Veterans Healthcare System, New Orleans,
LA, USA Historical Background

The amygdala was originally described by

Current Knowledge Burdach in the late nineteenth century as an
almond-shaped structure situated deep in the ante-
“Music” involves both complex qualities such as rior temporal lobe of the central nervous system.
familiar melodies, rhythm, or tempo, and more ele- The amygdala was subsequently shown to be
mentary aspects such as discrimination of timbre, important for the appropriate processing of emo-
pitch, or tone. While lesions of the temporal lobes tional information in nonhuman primates by
are fairly consistently implicated, the hemispheric Kluver and Bucy in the 1930s. This permitted
localization of lesions responsible for specific defi- McLean to include the amygdala in the group of
cits has been more controversial. Music, like lan- brain structures that make up the limbic system
guage, is composed of individual, temporally thought to be involved in processing of emotional
sequenced stimuli (musical notes, melodies, tunes), information. Since then, progress has continued
each capable of being analyzed with regard to par- toward understanding the role that the amygdala
ticular features such as pitch and timbre, functions plays in processing and encoding emotional infor-
that would appear to be more in keeping with the mation in the mammalian central nervous system.
suspected operations of the left hemisphere. By
contrast, melodies may also be perceived as a
gestalt, which is more characteristic of right hemi- Current Knowledge
sphere functions. There is evidence that well-trained
musicians come to rely more heavily on the left The amygdala is an almond-shaped structure
hemisphere for processing certain aspects of music located in the medial temporal lobe of mammals.
when compared with non-musicians. However, the However, the first description of this almond-
right hemisphere evidences superiority for both the shaped structure only referred to a portion of the
perception and expression of music in studies of amygdala called the basal nucleus. Currently, the
non-musicians. Thus, the strategies by which vari- amygdala is described as a collection of different
ous musical elements are approached, as well as the subnuclei or subareas, one of which is the basal
leading hemisphere in appreciating those elements, nucleus. The nuclei have been grouped together
are most likely determined in part by one’s prior based on their phylogenetic similarities or simi-
musical experience or training. In summary, while larities in their neuronal elements. Older phyloge-
both the right and left hemispheres are apparently netic nuclei include the olfactory areas (i.e.,
involved in the expression and perception or appre- cortical nucleus and nucleus of the olfactory
ciation of music, the specific contributions of each tract) and the central and medial nuclei. More
are still somewhat of a mystery. recent phylogenetic structures include areas
214 Amygdala

similar to the neocortex such as the lateral, basal, the effect of the amygdala on its targets that
and accessory basal nuclei, which are collectively contribute to the emotional assessment of
referred to as the basolateral region or complex. incoming sensory information and coordinated
Based on similarities in their neuronal compo- behavioral responses.
nents, various nuclei of the amygdala have been Most of what is known about human amyg-
defined as neocortical-like nuclei (such as the dala function comes from studies of patients
basolateral complex) that consist of glutamatergic with damage to the amygdala. However, most
pyramidal-like neurons or striatal-like nuclei damage in humans is not restricted to the amyg-
(such as the central and medial nuclei) that consist dala alone, and patients with damage to larger
of GABAergic medium spiny neurons. areas of the medial temporal lobe have more
In humans, the amygdala is located under the profound deficits. Nonetheless, patients with
uncus of the limbic lobe at the anterior end of the temporal lobe damage including the amygdala
hippocampus. It also merges with the peri- display a number of emotional and inappropriate
amygdaloid cortex and abuts the putamen and behavioral deficits. These include impaired fear
tail of caudate nucleus. As a whole, the amyg- responses, hypersexuality, hyperorality, and
dala receives diverse inputs from throughout the hyperattention. These behaviors were originally
central nervous system. The basolateral complex described by Kluver and Bucy in nonhuman
receives inputs encoding somatosensory, visual, primates.
auditory, gustatory, olfactory, and visceral infor- Much of what is known about functional cir-
mation from the dorsal thalamus, prefrontal cor- cuitry within the amygdala and how it relates to
tex, cingulate, parahippocampal gyrus, insular encoding of emotion has been gleaned from stud-
cortex, and sensory associational areas. The cen- ies in rodents. The amygdala can be divided into
tral and medial nuclei receive inputs from olfac- many subareas based on functional circuitry. Lat-
tory centers, hypothalamus (ventromedial and eral to the amygdala is the piriform cortex, which
lateral), dorsomedial and medial nuclei of the encodes olfactory information. Olfactory infor-
thalamus, and visceral inputs from the para- mation from the piriform cortex, and other olfac-
brachial nuclei, solitary nucleus, and peri- tory structures, projects to the most ventral and
aqueductal gray of the brainstem. Outputs from lateral portion of the amygdala, the cortical nuclei.
the amygdala are equally diverse. They leave via The cortical nuclei in turn project medially to the
two predominant pathways. The central nucleus ventrally located medial nuclei, which is a major
contributes to the stria terminalis where its effer- output for olfactory information from the amyg-
ents make connections with the hypothalamus dala. However, less is known about the ventrally
(preoptic nuclei, ventromedial nucleus, anterior located olfactory-associated amygdala nuclei
nucleus, and lateral hypothalamic areas), compared to the more dorsal multisensory nuclei.
nucleus accumbens, septal nuclei, and rostral The more dorsal nuclei receive information from
portions of the caudate and putamen. However, all sensory modalities. The major inputs to the
the primary output of the amygdala is the ventral amygdala innervate the lateral nuclei. The lateral
amygdalofugal pathway. Through this pathway, nuclei are the most dorsally located within the
the basolateral complex sends inputs to the amygdala, medial to the piriform cortex, and
hypothalamus, septal nuclei, substantia underneath the striatum. The lateral nuclei receive
innominata, prefrontal, cingulate, insular, and associational inputs encoding a single sensation
inferior temporal cortices. Through the same (somatosensory, visual, auditory, gustatory, olfac-
pathway, the central nucleus projects diffusely tory, or visceral). This is the first stage where
in the brainstem innervating the dorsal vagus, sensory input is assigned emotional value and
raphe, locus coeruleus, parabrachial nuclei, and also where some emotional memories may be
the periaqueductal gray. It is the interplay stored (however, the amygdala as a site for storing
between the diverse afferents projecting to the emotional memories remains a contentious issue).
amygdala, processing within the amygdala, and Although the lateral nuclei project to multiple
Amygdala 215

areas within and outside the amygdala, a major Future Directions

output is the basal nuclei (located ventral to the
lateral nuclei) where the initial sensory processing Most of what is known about emotional informa- A
of the lateral nuclei is integrated with inputs from tion processing performed by the amygdala has
highly processed areas including polymodal sen- been gleaned from studies of fear conditioning.
sory areas and areas involved in memory forma- However, the amygdala also likely plays a role in
tion like the hippocampus. The lateral and basal the encoding of positive emotions associated with
nuclei project medially to the central nucleus rewarding stimuli. Currently, efforts are being
either directly or indirectly through intercalated made toward understanding the different types of
cells (intercalated cells separate the basolateral emotional values encoded in the amygdala. Also, it
complex from the central and medial nuclei). remains somewhat contentious whether emotional
The central nuclei send much of the processed memory is actually stored by the amygdala. It is of
emotional content from the amygdala to the rest great interest to determine where emotional mem-
of the brain. Thus, the central nucleus is seen as ories are stored in the amygdala (possibly the lat-
the output region of the amygdala. The central eral nuclei) and precisely what types of memories
nucleus produces emotional responses through are being stored by the amygdala, that is, whether
its effects on its various targets throughout the these memories are of conscious declarative forms
central nervous system. For example, the central or more procedural reflexive forms. Understanding
nucleus produces arousal through its innervation how the amygdala contributes to the formation of
of modulatory systems in the brain stem that different forms of emotional memory will likely
release norepinephrine, dopamine, serotonin, and provide insights for the treatment of several psy-
acetylcholine. Its input to the periaqueductal gray chiatric illnesses such as posttraumatic stress dis-
produces freezing, startle, analgesia, and cardio- order, phobias, anxiety, and depression.
vascular changes associated with fear. It also
innervates the parabrachial nucleus where it
affects pain processing. Its inputs to the dorsal
motor vagal nucleus controls parasympathetic Cross-References
nervous system function, and it also affects vagal
nerve function through its projection to the soli- ▶ Efferent
tary nucleus. Finally, the central nuclei projects to ▶ Insular Lobe
the hypothalamus where it controls the release of ▶ Limbic System
hormones and activates the sympathetic nervous ▶ Locus Ceruleus
system. ▶ Midbrain Raphe
In summary, the amygdala is a complex group ▶ Neocortex
of nuclei that receive diverse inputs from various ▶ Striatum
regions of the central nervous system to assess ▶ Temporal Lobe
emotional value. Similarly, after extensive pro-
cessing, its outputs innervate a diverse group of
regions in the central nervous system to exert its References and Readings
effect. The result is that the amygdala is involved
in encoding fear, reward, aggression, and sexual, Ledoux, J. E. (2000). Emotion circuits in the brain. Annual
Review of Neuroscience, 23, 155–184.
maternal, and ingestive behaviors. This results in Ledoux, J. (2007). The amygdala. Current Biology, 17,
effects on cognition, attention, perception, and 868–874.
memory formation. Therefore, it is not surprising Phelps, E. A., & Ledoux, J. E. (2005). Contributions of the
that amygdala dysfunction has been associated amygdala to emotion processing: From animal models
to human behavior. Neuron, 48, 175–187.
with anxiety disorders such as posttraumatic stress Sah, P., Faber, E. S., Lopez De Armentia, M., & Power,
disorder, phobias and panic attacks, depression, J. (2003). The Amygdaloid complex: Anatomy and
and schizophrenia. physiology. Physiological Reviews, 83, 803–834.
216 Amyloid Plaques

and lack the surrounding neurites (Serrano-Pozo

Amyloid Plaques et al. 2011).

Elizabeth K. Vernon1 and JoAnn Tschanz1,2

1
Department of Psychology, Utah State Current Knowledge
University, Logan, UT, USA
2
Center for Epidemiologic Studies, Utah State It is unknown if the diffuse plaques later form into
University, Logan, UT, USA senile plaques. Both plaque types contain the
amyloid b protein (Ab), a portion of a larger
neuronal transmembrane protein of unknown
function. Other differences between senile and
Synonyms
diffuse plaques include the constituent Ab protein
and their regional distribution in the brain. Diffuse
Diffuse plaques; Neuritic plaques; Senile
plaques are common in the basal ganglia struc-
plaques
tures of the caudate nucleus and putamen as well
as the cerebellum, where neuritic plaques are rare.
In AD, neuritic plaques are more commonly
Definition found in the neocortex (Morris and Nagy 2004).
Distribution of amyloid plaques over the
An aggregation of beta-amyloid protein found in course of AD. In AD, amyloid plaque deposition
the extracellular space between neurons in the is less predictive than neurofibrillary tangles but
brain. Amyloid plaques may be of diffuse, pre- can be characterized by using staging system of
amyloid type or neuritic, mature senile type. The Braak and Braak. Braak and Braak suggest three
latter is recognized as one of the neuropatholog- stages of progression of amyloid deposition:
ical hallmarks of Alzheimer’s disease (AD). Stage A is characterized by amyloid deposition
Mature amyloid plaques are spherical in shape in the basal regions of the temporal, frontal, and
and consist of a central beta-amyloid core, occipital lobes; Stage B is characterized by
fibrillary outward extensions, and surrounding involvement of isocortical areas with mild depo-
dystrophic neurites (elements of degenerating sition in the hippocampus; and Stage C is char-
neurons). Unlike the mature, senile plaques, dif- acterized by deposition in primary isocortical
fuse plaques have an amorphous, irregular shape areas (sensory and motor regions) and less

Amyloid Plaques,
Fig. 1 Amyloid plaques
stained with a modified
Bielschowsky silver stain
(Photo courtesy of Steven S.
Chin, M.D., Ph.D.,
University of Utah Health
Sciences Center)
Amyotrophic Lateral Sclerosis 217

commonly, but in some cases, involving the cer-

ebellum and the striatum, thalamus, hypothala- Amyotrophic Lateral Sclerosis
mus, and other subcortical nuclei (Braak & A
Braak 1991). Other researchers have posited Alexander I. Tröster
five proposed stages in the progression of amy- Department of Clinical Neuropsychology and
loid deposition in AD: Stage I, isocortical; Stage Center for Neuromodulation, Barrow
II, allocortical deposition (e.g., entorhinal cortex, Neurological Institute, Phoenix, AZ, USA
hippocampal formation, amygdala, insula, and
cingulate cortex); Stage III, subcortical nuclei
(e.g., striatum, cholinergic nuclei in the basal Synonyms
forebrain, thalamus, and hypothalamus) and
white matter; Stage IV, involvement of brainstem Lou Gehrig’s disease
structures (e.g., red nucleus, substantia nigra,
portions of the medulla oblongata, and superior
and inferior colliculi); and Stage V, additional Short Description or Definition
deposition in pontine structures (reticular forma-
tion, raphe nuclei, locus ceruleus) (Thal et al. The features of amyotrophic lateral sclerosis (ALS)
2002). Recent studies have reported that amyloid were first described by Charcot in the nineteenth
burden does not correlate with the severity or century. ALS is a progressive, fatal neurodegener-
duration of dementia, but early amyloid deposi- ative disease affecting upper and lower motor neu-
tion has been correlated with the preclinical stage rons, although increasingly ALS is recognized as a
of AD, where there is Ab accumulation but no multisystem disorder whose manifestations may
apparent clinical symptoms of the disorder (Ser- also include cognitive and behavioral changes.
rano-Pozo et al. 2011) (see also Alzheimer’s Most patients present with motor neuron symp-
Disease) (Fig. 1). toms at disease onset, and as the disease progresses,
persons with ALS demonstrate impairments in
speech, swallowing, breathing, and use of upper
See Also and lower limbs, with eventual paralysis. The prev-
alence of cognitive changes, which is not well
studied, is estimated to range from about 20% to
▶ Senile Plaques
50% and most often involve executive dysfunction.
Deficits in visuospatial, language, and memory
functions are more inconsistently observed. When
References and Readings
dementia is seen, it resembles a frontotemporal
Braak, H., & Braak, E. (1991). Acta H ’ pathologica lobar degeneration or frontotemporal dementia
Neuropathological stageing of Alzheimer-related characterized by personality change, irritability,
changes, 239–259. diminution of insight, poverty of planning, abstrac-
Morris, J. H., & Nagy, Z. (2004). Alzheimer’s disease. In
tion and initiation, and obsessiveness.
M. M. Esiri, V. M.-Y. Lee, & J. Q. Trojanowski (Eds.),
The neuropathology of dementia (2nd ed., pp.
161–206). Cambridge: Cambridge University Press.
Serrano-Pozo, A., Frosch, M. P., Masliah, E., & Hyman, B. Categorization
T. (2011). Neuropathological alterations in Alzheimer
disease. Cold Spring Harbor Perspectives in Medicine,
1(1), a006189. https://doi.org/10.1101/cshperspect. Categorizations can be based on genetics, neuro-
a006189 logical levels inferred from symptoms, severity
Thal, D. R., Rüb, U., Orantes, M., & Braak, H. (2002). defined by number of neurological levels
Phases of Ab-deposition in the human brain and its
involved, and need for gastrostomy or noninva-
relevance for the development of AD. Neurology, 58
(12), 1791 LP – 1800. Retrieved from http://n.neurol- sive ventilation (King’s stages) and diagnostic
ogy.org/content/58/12/1791 probability (El Escorial criteria). At least eight
218 Amyotrophic Lateral Sclerosis

familial variants of ALS (ALS 1–8) have been involvement of either one, two, or three neurolog-
identified, though the vast number of cases ical levels. The fourth stage is identified by the
(about 90%) is sporadic. Of these eight, six need for either noninvasive ventilation or
forms are inherited in autosomal dominant man- gastrostomy.
ner and two in autosomal recessive manner. A The notion that FTD and ALS may be part of
large expansion of a hexanucleotide repeat in an the same spectrum of disorders has become less
intron of the gene C9orf72 (a gene also implicated controversial with the implication of the C9orf72
in frontotemporal dementia) is responsible for gene in both conditions and the observations that
about 30–60% of familial ALS cases. Mutations persons with ALS may develop FTD and persons
in the superoxide dismutase 1 gene (SOD1) with FTD or primary progressive aphasia (PPA)
account for about another 20% of familial cases. may develop ALS as well as by pathologic
Three neurological levels are most often iden- (ubiquitin-positive, tau-negative, and synuclein-
tified in the expression of ALS symptoms: bulbar, negative neuronal inclusions in some forms of
cervical, and lumbar. A fourth (thoracic) level ALS and FTD). Nonetheless, some propose a
is rarely encountered clinically. Persons with bul- categorization of ALS dependent upon the pres-
bar onset demonstrate problems with speech (dys- ence or absence of cognitive and behavioral fea-
arthria) and/or swallowing (dysphagia), and may tures, namely, ALS, ALS with cognitive
have disease that affects lower or upper motor impairment, ALS with behavioral impairment,
neurons (or both), showing features of bulbar and ALS with FTD. This categorization appar-
palsy (facial weakness, limited palatal movement ently failed to consider that about 25% of patients
and lingual atrophy, weakness, and fasciculation) may have both cognitive and behavioral abnor-
and/or pseudobulbar palsy (emotional lability, malities. Revised consensus criteria for the diag-
dysarthria, and brisk jaw jerk). Persons with cer- nosis of frontotemporal spectrum disorders in
vical onset can also show upper and or lower ALS were published in 2017 and these criteria
motor neuron involvement and have upper limb do recognize a group of persons with ALS having
signs. Such signs may include proximal weakness both cognitive and behavioral impairment. Addi-
(shoulder abduction as required in toothbrushing tionally, the criteria list both ALS-Frontotemporal
or combing) or distal weakness (carrying out pin- dementia and ALS-Parkinsonism-dementia com-
cer grip movements). Lumbar onset patients have plex, thus highlighting further the neuropsycho-
involvement of lower motor neurons and proxi- logical heterogeneity of ALS.
mal weakness (e.g., difficulty in climbing stairs)
or foot drop (resulting in tripping).
The most widely accepted clinical diagnostic Epidemiology
criteria (the El Escorial criteria) define definite
ALS by the presence of both upper and lower The incidence of ALS is about 1.5–2.5 per
motor neuron signs in three regions, probable 100,000 per year and a prevalence of about 6
ALS by signs in two regions, possible ALS by per 100,000. Prevalence and incidence of cogni-
signs in one region, and suspected ALS by only tive impairment are not well studied in ALS.
lower or upper motor neuron signs in one or more Although one study in a specialty clinic indicated
regions. The suspected ALS category may be the a prevalence of FTD features in about 40% of
most controversial, and some consider the pres- patients with ALS, this might represent an over-
ence of only upper motor neuron signs to repre- estimate, given sampling bias, and the figure may
sent primary lateral sclerosis, while the presence be as low as 5%. Generally it has been estimated
of only lower motor neuron signs represents spi- that dementia may occur at rates of 6–15% and
nal muscular atrophy. The King’s stages of sever- milder cognitive impairment in 20–51% of
ity are related to the El Escorial criteria. There are patients. Other behavioral abnormalities (e.g.,
four clinical stages (the fifth stage is death), and disinhibition, apathy) may occur in 14–40% of
the first three stages are identified by the patients.
Amyotrophic Lateral Sclerosis 219

Natural History, Prognostic Factors, and most susceptible to ALS. Verbal fluency decre-
Outcomes ments are observed even if one controls for
motor and speech impairments. Another task A
Incidence of ALS peaks in the 1960s and drops sensitive to deficits in ALS, and particularly to
rapidly thereafter. A broad estimate of mortality pseudobulbar ALS, are Tower tasks that place a
is that 50% of patients do not survive beyond premium on spatial working memory and plan-
3 years from symptom onset but that some may ning. Similarly, another test of working memory
survive 10 years or more. Three epidemiologic (digit span backward, requiring examinees to
studies provide fairly consistent survival data repeat increasingly long series of digits in
using time of diagnosis as the reference point reverse order of presentation) has also been
(though diagnostic confirmation may lag onset shown to be sensitive to ALS.
by 13–18 months): 78% at 1 year, 56% at Language (unlike motor speech) is less likely
2 years, and 32% at 4 years. Several factors are disrupted by ALS, although language task impair-
associated with poorer prognosis: low-forced vital ments are observed in patients with ALS and
capacity, bulbar onset (often less tolerant of forced dementia. Despite performing well on nonverbal
ventilation), older age at onset, and shorter inter- semantic knowledge and grammar tasks, patients
val between first symptom and presentation. with ALS and dementia perform poorly on verbal
Patients attending tertiary and specialized ALS tasks, making semantic paraphasic errors on nam-
clinics tend to show longer survival, and treatment ing tests. Some studies have observed tendencies
with riluzole, on average, extends life by toward echolalia, stereotypy of expression, and
3 months. Longer survival is seen in persons perseveration in ALS.
with only upper or lower motor neuron disease, When deficits in memory are observed in ALS,
though as noted, it is controversial whether vari- they are more likely to be evident on immediate
ants such as primary lateral sclerosis are ALS. than delayed recall tasks. Some take this to impli-
cate poorer executive control over encoding
processes, whereas others might invoke slowed
Neuropsychology and Psychology of information processing as an explanation. The
Amyotrophic Lateral Sclerosis finding that patients can benefit disproportion-
ately from the provision of recognition cues rela-
Most common among cognitive declines in ALS tive to free recall formats suggests that retrieval
is executive dysfunction. A recent meta-analysis deficits might also be implicated or that shallow
has revealed that ALS produces impairments in levels of encoding are sufficient to support recog-
cognitive domains (without bias due to motor nition but not recall.
impairment) of medium effect size in verbal Recent interest has focused on social cognition
fluency, language, and social cognition and of and especially on theory of mind (the ability to
small effect sizes in verbal memory and execu- infer another’s thoughts, beliefs, intentions, and
tive functions. Individual tests, within a domain emotions). Patients with ALS seem to show sig-
do, however, reveal impairments of varying nificant impairments in both the cognitive and
magnitude. Card-sorting tasks demanding of affective components of theory of mind.
conceptualization and cognitive flexibility are Concerning behavioral changes, rating scales
less sensitive to executive deficits in ALS than have revealed that as many as two thirds of per-
are verbal fluency tasks demanding initiation sons with ALS show one or more of irritability,
and deployment of efficient word retrieval strat- disinhibition, inflexibility, restlessness, and apa-
egies. Retrieval of verbs, putatively more depen- thy. Apathy and questionable or poor social judg-
dent upon frontal lobe integrity than upon ment are more likely to be observed in patients
phonemic or semantic fluency tasks (requiring with bulbar onset ALS. Surprisingly, although
word retrieval by initial sound or membership in reactive depressive reactions may occur after
semantic categories, respectively), may be the diagnosis, major depression is quite rare among
220 Amyotrophic Lateral Sclerosis

ALS patients (about 10%). Symptoms of depres- ameliorative therapies, often multidisciplinary,
sion are common, occurring in about half of are available. Cramps and spasticity can be
patients. Persons with ALS may in particular treated with a variety of medications including,
experience hopelessness and end-of-life concerns. for example, carbamazepine, quinine, baclofen,
Pathological laughing or crying, as seen in and tizanidine. Drooling can be treated with
pseudobulbar syndromes, should not be confused anticholinergics such as scopolamine, although
with depression. there is a risk of confusion and memory prob-
lems in older patients, and amitriptyline, which
may also alleviate depression and pathological
Evaluation
laughing and crying, may be preferable. Speech
therapy is helpful both for swallowing problems
Although consensus guidelines for assessment of
and dysarthria, although ultimately, severe
cognition in ALS are expected in the future, cur-
swallowing problems necessitate change in diet
rently only older suggestions are available. Experi-
and choking may necessitate percutaneous
mental modifications of tests to eliminate timing
endoscopic gastrostomy (PEG) placement.
and minimize motor requirements, while facilitat-
When communication becomes too difficult
ing patient performance, have unknown sensitivity.
due to speech problems or difficulty breathing,
Persons with hypophonic speech might be provided
computers can be used to facilitate communica-
an amplifier. Computers as augmentative commu-
tion, in some cases even when paralysis is pre-
nication devices, while not practical in traditional
sent. Because breathing difficulty and shortness
neuropsychological assessment, can be helpful in
of breath can be distressing to the patient, a
interviewing the patient. Yes-no or forced-choice
benzodiazepine or morphine use is
recognition paradigms might allow patients to dem-
recommended. Respiratory insufficiency can be
onstrate knowledge of memoranda.
alleviated with noninvasive ventilation and later
Verbal fluency tests are likely to be helpful in
invasive ventilation. Mood disturbances and
determining which patients might require fuller
family bereavement issues can be dealt with by
evaluations because traditional screening instru-
counseling and social work intervention. Physi-
ments, such as the Mini-Mental State Exam, are not
cal and occupational therapy may also be helpful
sensitive to cognitive impairment in ALS.
to facilitate mobility and, perhaps to lesser
In addition to measures of executive function, nam-
extent, strength and range of motion.
ing, and memory, it is important to include in
assessments self- or informant rating scales captur-
ing behavioral changes such as apathy, irritability, Cross-References
depression, disinhibition, etc. Such measures are
helpful in identifying those persons with behav- ▶ Assistive Technology
ioral changes or the behavioral variant of FTD. ▶ Cortical Motor Pathways
▶ Frontal Lobe
▶ Frontal Temporal Dementia
Treatment
▶ Frontotemporal Lobar Degenerations
▶ Speech
There are no curative treatments for ALS. The
only drug approved for ALS is riluzole, a gluta-
mate release inhibitor that shows moderate ben-
References and Readings
efit and extends life on an average of 3 months.
Palliative care (symptomatic control and qual- Averill, A. J., Kasarskis, E. J., & Segerstrom, S. C. (2007).
ity-of-life optimization in the absence of a cure) Psychological health in patients with amyotrophic lateral
is recommended from the outset, and numerous sclerosis. Amyotrophic Lateral Sclerosis, 8, 243–254.
Amyotrophic Lateral Sclerosis Functional Rating Scale 221

Beeldman, E., Raaphorst, J., Twennaar, M. K.,

de Visser, M., Schmand, B. A., & de Haan, R. J. Amyotrophic Lateral Sclerosis
(2015). The cognitive profile of ALS: A systematic
review and meta-analysis update. Journal of Neurol- Functional Rating Scale A
ogy, Neurosurgery, and Psychiatry. https://doi.org/
10.1136/jnnp-2015-310734. online first, 17 Aug Michelle Marie Tipton-Burton
2015. Physical Medicine and Rehabilitation, Santa
Brownlee, A., & Palovcak, M. (2007). The role
of augmentative communication devices in the Clara Valley Medical Center, San Jose, CA, USA
medical management of ALS. NeuroRehabilitation,
22, 445–450.
Kiernan, M. C. (2015). Palliative care in amyo-
trophic lateral sclerosis. Lancet Neurology, 14,
Synonyms
347–348.
Lewis, M., & Rushanan, S. (2007). The role of physical ALSFRS; ALSFRS-R
therapy and occupational therapy in the treatment
of amyotrophic lateral sclerosis. NeuroRehabilitation,
22, 451–461.
Logroscino, G., Traynor, B. J., Hardiman, O., Chio, A., Description
Couratier, P., Mitchell, J. D., et al. (2008).
Descriptive epidemiology of amyotrophic lateral
sclerosis: New evidence and unsolved issues. The Amyotrophic Lateral Sclerosis Functional
Journal of Neurology, Neurosurgery and Psychiatry, Rating Scale (ALSFRS) is a validated instru-
79, 6–11. ment designed to assess the functional status
McCluskey, L. (2007). Palliative rehabilitation and
and the disease progression in patients with
amyotrophic lateral sclerosis: A perfect match.
NeuroRehabilitation, 22, 407–408. amyotrophic lateral sclerosis (ALS). It is a
Murphy, J., et al. (2016). Cognitive-behavioral screening tool that can be used to monitor functional
reveals prevalent impairment in a large multicenter change in a patient over time. The ALSFRS is
ALS cohort. Neurology, 86, 813–820.
a ten-item functional inventory which was
Phukan, J., Pender, N. P., & Hardiman, O. (2007).
Cognitive impairment in amyotrophic lateral sclerosis. devised for use in therapeutic trials in ALS.
Lancet Neurology, 6, 994–1003. Each item is rated on a 0–4 scale, (with
Radunovic, A., Mitsumoto, H., & Leigh, P. N. (2007). 0 being severely impaired and 4 being normal)
Clinical care of patients with amyotrophic lateral
by the patient and/or caregiver, yielding a max-
sclerosis. Lancet Neurology, 6, 913–925.
Strong, M. J., Grace, G. M., Orange, J. B., & Leeper, H. A. imum score of 40 points. The ALSFRS assesses
(1996). Cognition, language, and speech in the patients’ levels of self-sufficiency in areas
amyotrophic lateral sclerosis: A review. Journal of self-feeding, grooming, ambulation, and
of Clinical and Experimental Neuropsychology,
communication and swallowing. Versions are
18, 291–303.
Trojsi, F., Santangelo, G., Caiazzo, G., Siciliano, M., available in Spanish, Dutch, and German.
Ferrantino, T., Piccirillo, G., Femiano, C.,
Cristillo, V., Monsurro, M., Espositio, F., &
Tedeschi, G. (2016). Neuropsychological assessment
at different King’s clinical stages of amyotrophic Historical Background
lateral sclerosis. Amyotrophic Lateral Sclerosis and
Frontotemporal Degeneration, 17, 1–7. The ALSFRS was developed because clinimetric
Van der Hulst, E.-J., Bak, T. H., & Abrahams, S. (2015).
scales being utilized at the time were contami-
Impaired affective and cognitive theory of mind and
behavioural change in amyotrophic lateral sclerosis. nated with impairment measurements, did not
Journal of Neurology, Neurosurgery, and Psychiatry, measure the broad range of disabilities that result
86, 1208–1215. from ALS, and did not lend themselves to sub-
Woolley, S. C., & Rush, B. K. (2017). Considerations for
score analysis that was based entirely on disability
clinical neuropsychoplogical evaluation in
amyotrophic lateral sclerosis. Archives of Clinical Neu- components (Feinstein 1987; Streiner and
ropsychology, 32, 906–916. Norman 1989).
222 Amyotrophic Lateral Sclerosis Functional Rating Scale

The ALSFRS is a validated rating instrument ALS. The tool has also been utilized to evaluate
for monitoring the progression of disability in the disease progression and predict hospital length
patients with ALS. One weakness of the of stay and survival time in ALS patients treated
ALSFRS, as it was originally designed, was that with tracheostomy-intermittent positive-pressure
it granted disproportionate weighting to the limb ventilation. Through observation and interview,
and bulbar, as compared to respiratory dysfunc- the evaluator assesses the following measures:
tion. Some patients with ALS are able to live for speech, salivation, swallowing, handwriting, cut-
several years past the lowest measurable level of ting food/handling utensils, turning in bed and
function on the Amyotrophic Lateral Sclerosis adjusting bed clothes, walking, climbing stairs,
Functional Rating Scale-Revised (ALSFRS-R), a and breathing.
widely used end point in ALS assessment. The
ALSFRS-R is also validated and incorporates addi-
tional assessments of dyspnea, orthopnea, and the
need for ventilator support. The ALSFRS-R retains Cross-References
the properties of the original scale and shows
strong internal consistency and construct validity. ▶ Amyotrophic Lateral Sclerosis
The ALSFRS extension offers improved sensitiv-
ity at lower levels of physical function.
Further Reading

Psychometric Data ALS CNTF Treatment Study (ACTS) Phase 1-11 Study
Group. (1996). The amyotrophic lateral sclerosis func-
tional rating scale. Assessment of activities of daily
The ALSFRS was developed as an internally con- living in patients with amyotrophic lateral sclerosis.
sistent, reliable, and valid measure of disability in Archives of Neurology, 53, 141–147.
ALS patients as part of the Amyotrophic Lateral Campos, T. S., Rodriquez-Santos, F., Esteban, J., Vasquez,
P. C., Mora Paradivia, J. S., & Carmona, A. C. (2010).
Sclerosis Ciliary Neurotrophic Factor (ALS Spanish adaption of the revised amyotrophic lateral
CNTF) Treatment Study (ACTS Phase 1–11 sclerosis functional rating scale (ALSFRS-R).
Study Group 1996). The ability of the ALSFRS Amyotrophic Lateral Sclerosis, 11(5), 475–477.
to be responsive to change in the clinical status of Cedarbaum, J. M., & Stambler, N. (1997). Performance of
the amyotrophic lateral sclerosis functional rating scale
ALS patients was evaluated cross sectionally and (ALSFRS) in multicenter clinical trials. Journal of the
prospectively over time in phase 1 and phase Neurological Sciences, 152(Suppl 1), S1–S9.
2 studies of CNTF in ALS. Feinstein, A. R. (1987) Clinimetric perspectives. Journal
The ALSFRS has been validated both cross of Chronic Diseases, 40(6), 635–40.
Herndon, R. M. (2006). Handbook of neurologic rating
sectionally and longitudinally against muscle scales (p. 96). New York: Demos Medical Publishing,
strength, the Schwab and England ADL rating LLC.
scale, the Clinical Global Impression of Change Lo Coco, D., Marchese, S., La Bella, V., Piccoli, T., & Lo
(CGIC) scale, and independent assessments of Coco, A. (2007). The amyotrophic lateral sclerosis
functional rating scale predicts survival time in
patient’s functional status (Cedarbaum and amyotrophic lateral sclerosis patients on invasive
Stambler 1997). mechanical ventilation. Chest, 132(1), 64–69.
Streiner, D. L. & Norman, G. R. (1989). A Review of:
“Health Measurement Scales: A Practical Guide to
Their Development and Use, Fourth Edition” New
York: Oxford University Press, 2008, ISBM 978-0-
Clinical Uses 19-923188-1, xvii + 431 pp
Wicks, P., Massagli, M. P., Wolf, C., & Heywood,
The ALSFRS is a straightforward instrument that J. (2009). Measuring function in Advaced ALS: Vali-
dation of ALSFRS-Ex extension items. European Jour-
can be utilized across disciplines to assess the
nal of Neurology, 16(3), 353–359. https://doi.org/
functional status of an individual diagnosed with 10.1111/j.1468-1331.2008.02434.x.
Analysis of Variance 223

means. Doing so is problematic because

Analysis of Variance conducting an increasing number of tests increases
the probability of making a type I error. ANOVA
Matthew J. L. Page can identify the presence of a significant difference
Allegheny General Hospital, Pittsburgh, PA, USA between any pair of means using a single test. If
Psychology, Allegheny Health Network, the F-test produces a significant result, the next
Pittsburgh, PA, USA step is to identify which pairs of means are statis-
tically significantly different using post-hoc ana-
lyses, such as Tukey’s honest significant
difference test.
Synonyms

ANOVA, F-test
Current Knowledge

When using ANOVA, observations must be ran-

Definition domly sampled and independent of each other.
Additionally, the use of ANOVA requires that the
Analysis of variance (ANOVA) is a statistical populations under examination are normally dis-
test that identifies whether two or more group tributed, although the F-test is fairly robust against
means are statistically different. ANOVA eval- violations of this rule with large sample sizes and
uates the null hypothesis that the means of each symmetrical population distributions. Another
group are equal, and, by implication, that each assumption of ANOVA is that the variances of
group represents the same population. The alter- the group populations are equal, and hence an
native hypothesis is that at least one pair of important step in ANOVA is to test this assump-
group means is different, suggesting that these tion using the group sample variances (for exam-
groups reflect different populations and that the ple, using Levene’s test or Bartlett’s test).
independent variable (IV) has a significant
effect on the dependent variable (DV).
ANOVA uses a statistic referred to as F, which See Also
is defined as the ratio between the between-
group (explained) variance and the within- ▶ False Positive
group (unexplained) variance. A one-way ▶ Multivariate Analysis of Variance
ANOVA analyzes the difference between the ▶ Statistical Significance
means of multiple levels of one independent
variable. A factorial ANOVA incorporates mul-
tiple independent variables (factors). For exam- Further Reading
ple, in a two-way ANOVA, the main effect of
both IVs is examined. The interaction effect is Gueorguieva, R., & Krystal, J. H. (2004). Move over
also analyzed, which examines whether the ANOVA: Progress in analyzing repeated-measures
effect of one variable changes at different levels data and its reflection in papers published in the
Archives of General Psychiatry. Archives of General
of the other variable. Psychiatry, 61, 310–317. https://doi.org/10.1001/
Like a t-test, ANOVA is appropriate for cate- archpsyc.61.3.310.
gorical IVs and continuous DVs with interval or Iverson, G. R., & Norpoth, H. (1987). Analysis of variance.
ratio data. However, t-tests are limited in that they Newbury Park: Sage.
Watson, P. (2009). Review of analysis of variance and
can evaluate the significance of the difference covariance: How to choose and construct models for
between only two group means; thus, multiple the life sciences. Psychological Medicine, 39,
t-tests are required to examine more than two 695–696.
224 Anarthria

Anarthria ANCOVA/MANCOVA

Ignatius Nip1 and Carole R. Roth2 Michael Franzen

1
School of Speech, Language, and Hearing Allegheny General Hospital, Pittsburgh, PA, USA
Sciences, San Diego State University, San Diego,
CA, USA
2
Otolaryngology Clinic, Speech Division, Naval Synonyms
Medical Center, San Diego, CA, USA
Analysis of covariance

Synonyms
Definition
Speechlessness
ANCOVA or analysis of covariance is a variant
of the ANOVA model in which the statistical
Definition effect of a nuisance variable is removed mathe-
matically from the analysis in order to clarify the
Anarthria is speechlessness due to a severe loss of relations between the independent and the
neuromuscular control over the speech muscula- dependent variables (Belin and Normand
ture and is the most severe form of dysarthria. 2009). The optimal situation would be if the
Language and cognition may be intact, but the independent variable levels or groups were not
neuromuscular disorder prevents speech. related to the nuisance variable. However, if the
Anarthric patients are motivated to speak but are nuisance variable is related to the dependent
unable. variable and if the nuisance variable is system-
Some patients with anarthria can produce some atically represented among the independent var-
oral movements and/or undifferentiated vocaliza- iables, ANCOVA may be used to partial out the
tions when attempting to speak. Occasionally, statistical effect of the nuisance variable or
there is no concomitant limb movement disorder, covariate. This is not a substitute for removing
but there is almost always a nonspeech oromotor the effect through experimental design. For
impairment. Frequent causes include brainstem example, level of education may be statistically
stroke, multiple strokes, closed head injury, and related to performance on a memory test. If two
degenerative diseases, including amyotrophic lat- groups of depressed and nondepressed individ-
eral sclerosis (ALS). uals differ systematically on the basis of their
level of education, any difference found with
regard to performance on a memory test might
be due to the different level of education. By
Cross-References
employing ANCOVA and using education level
as the covariate, the researcher may have a
▶ Dysarthria
clearer understanding of the relation between
the presence of depression and performance on
the memory test by statistically partialling out or
References and Readings removing the variance associated with the nui-
Duffy, J. R. (2013). Motor speech disorders: Substrates,
sance variable of education.
differential diagnosis, and management (3rd ed.). For example, Airaksinen et al. (2005) were
St. Louis: Elsevier Mosby. interested in differences on neuropsychological
Anencephaly 225

tests among groups of individuals with different

anxiety disorders. Unfortunately, their experimen- Anencephaly
tal groups differed in age, a variable which is A
known to influence neuropsychological test per- Erin D. Bigler and Jo Ann Petrie
formance. Therefore age was used as a covariate Department of Psychology and the Neuroscience
in their analysis. Center, Brigham Young University, Provo, UT,
Although there are different mathematical USA
methods for conducting an ANCOVA including
the use of multiple regression (which see),
ANCOVA under the general linear model pro- Synonyms
vides a useful conceptualization of the underly-
ing idea. We can think of calculating the Amnion rupture; Brain stem; Congenital defects;
regression between the covariate and the depen- Exencephaly; Forebrain; Lack of neural tube clo-
dent variable and then residualizing the influence sure; Magnetic resonance imaging; MRI; Neural
of the covariate. Then an ANOVA can be tube defects; NTD
conducted on the residual values. In order to
use ANCOVA, the data must satisfy a few basic
assumptions. There must be a linear relation Definition
between the covariate and the dependent vari-
able. The slope of the regression for each group Using “an” in front of an anatomical descriptor
or level of the independent variable must be the signifies absence. Cephalic is Greek for head with
same. The error term should be normally distrib- encephalon specifically referring to the brain.
uted with a mean of zero. The covariate should Therefore, the term anencephaly is used to denote
not be affected by the independent variable a congenital defect in the development of the
(Wildt and Ahtola 1978). head, including the meninges, the cranium, and
the scalp and, in particular, abnormal brain
growth, with an almost completely diminished
prosencephalon (telencephalon + diencephalon)
Cross-References or forebrain and only rudimentary development
of the brain stem.
▶ Analysis of Variance

Categorization
References
Anencephaly neural tube defects (NTD) result
Airaksinen, E., Larsson, M., & Fosell, Y. (2005). Neuro-
psychological functions in anxiety disorders in popula-
from the failure of closure of the headend of the
tion-based samples: Evidence of episodic memory neural tube in early fetal/embryolic development
dysfunction. Journal of Psychiatry Research, 39, (first 3–4 weeks); including lack of formation of
207–214. the brain, skull, and scalp (Greene and Copp
Belin, T. R., & Normand, S.-L. T. (2009). The role of
2014; Puvirajesinghe and Borg 2015; Yamaguchi
ANCOVA in analyzing experimental data. Psychiatric
Annals, 39, 753–759. and Miura 2013). Loss of the forebrain includes
Watson, P. (2009). Review of analysis of variance and loss of the two cerebral hemispheres, the
covariance: How to choose and construct models for connecting corpus callosum, neocortex, thalamus,
the life sciences. Psychological Medicine, 39,
hypothalamus, and other structures of the limbic
695–696.
Wildt, A. R., & Ahtola, O. T. (1978). Analysis of covari- system – the amygdala, hippocampus, caudate
ance. Beverly Hills: Sage. nucleus, ventricles, etc., and all of their
226 Anencephaly

connections (Kandel et al. 2013; Kolb and Rampersaud et al. 2016; Wang et al. 2016;
Whishaw 2008). These structures comprise the Zaganjor et al. 2016). However, since natural
majority of human brain tissue and are required folate is also readily available in other staple
for almost all sensation perception and basic phys- foods (e.g., dried beans, lentils, and leafy green
iological functions including body temperature vegetables) recent research also raises concerns
control, eating, sleeping, and motor function, for those areas with folic acid supplementation
and cognition, language, memory, emotion, to watch for excess folate consumption which
thought processing, inhibition, decision making, may also adversely increase growth in
and/or reasoning (see also Lezack et al. 2012). undetected cancer cells (see Castillo-Lancellotti
et al. 2013; Herrmann and Obeid 2011;
Strickland et al. 2013) or increased malaria
Epidemiology infection in those areas at high risk for the dis-
ease (Nzila et al. 2016).
Anencephaly results from NTD (Cohen 2002;
Detrait et al. 2005; Mitchell 2005; Yamaguchi
and Miura 2013) in approximately three pregnan- Natural History, Prognostic Factors, and
cies for every10,000 births in the USA and Outcomes
300,000 births per year worldwide (Flores et al.
2014). Such severe NTDs may be associated with With the major portion of an infant’s brain being
genetics, nutrition, environment, or a combination undeveloped, particularly the cerebrum, and
of all three (Centers for Disease Control and Pre- coupled with the brain often being exposed in
vention (CDC) 2015). There is a known higher utero, the anencephalic infant is frequently still-
prevalence of females born with anencephaly born (Creasy et al. 2014). An infant born alive
NTD as compared to males (James 1980). Over with anencephaly is, as a rule, blind, deaf, uncon-
the past several decades, worldwide research has scious, and may only reflexively respond. With
found an association between prenatal folic acid only a basic brain stem and a nonfunctioning
(synthetic vitamin B) deficits leading to folate cerebrum, prognosis is poor; anencephalic infants
(natural vitamin B) deficiencies (National Insti- will never gain consciousness and will only have
tute of Neurological Disorders and Stroke minimal reflex actions such as breathing. There
(NINDS) 2015; National Institutes of Health may be intermittent sound or touch responses;
(NIH): Office of Dietary Supplements 2016) and however, no further progress can be expected
NTD (Calvo and Biglieri 2008; Kondo et al. 2009; (see National Institute of Neurological Disorders
Wolff et al. 2009; Yila et al. 2016). While all the and Stroke 2015).
causes of open NTD are not known, research
indicates that daily consumption of 4 mg/day of
folic acid by women before and during pregnancy Neuropsychology and Psychology of
brings about a 70% reduction in NTD (Centers for Anencephaly
Disease Control and Prevention (CDC) 2015;
Cornel and Erickson 1997; MRC Vitamin Study There is essentially no assessment that neuropsy-
Research Group 1991; National Institutes of chological testing can offer given the absence of
Health (NIH): Office of Dietary Supplements cortical development in the anencephalic infant
2016). Since 1996 more than 50 countries world- who does survive. Such children have reflexive
wide have taken the critical step to mandate forti- function only (i.e., breathing and some responses
fication of staple grain food products with folic to sound or touch can manifest) and will rarely
acid to prevent NTD such as anencephaly and survive longer than a few hours or days. Neuro-
spina bifida and have been highly successful – psychologists should have an empathetic aware-
especially those with low and middle income ness of this condition and be prepared to consult
populations (Castillo-Lancellotti et al. 2013; with parents and families about the nature of the
Anencephaly 227

Anencephaly, Fig. 1 Magnetic resonance imaging skull defect the skin seems to be in continuity with the
(MRI) findings of the head and neck 8 h after birth. (a) superficial layer of the area cerebrovasculosa, probably the
Sagittal T1-weighted, (b) sagittal T2-weighted, and (c) pia mater (curved white arrow). The posterior fossa is
coronal T1-weighted images show cranial schisis. The funnel-shaped. A rudimentary brain stem (curved black
normal skin stops at the skull base and encircles abnor- arrows) and primordium of cerebellum (small black
mally developed cerebral structures, the so-called area arrows) are present. The cervical spine is normal (From
cerebrovasculosa (white arrows). Along the border of the Calzolari et al. 2004, with permission).

infants’ deficits and the poor prognosis (Ashwal et al. 2016), including the importance of continued
2005; Creasy et al. 2014). research to guide worldwide policy making for
better ways to prevent and treat neurological
birth defects.
Evaluation

Although the pathogenesis of anencephaly is still

References and Readings
not fully understood, several studies suggest that
exencephaly or the lack of skull growth or sepa- Ashwal, S. (2005). Recovery of consciousness and life
ration following NTD allows the cerebral tissue to expectancy of children in a vegetative state. Neuropsy-
be exposed in utero causing damage from the chological Rehabilitation, 15(3–4), 190–197.
Batavia, A. I. (2002). Disability versus futility in rationing
amniotic fluid (Calzolari et al. 2004; Sharif and health care services: Defining medical futility based on
Zhou 2016). As can be seen in Fig. 1, even though permanent unconsciousness – PVS, coma, and anen-
there are other anomalies of physical development cephaly. Behavioral Sciences & the Law, 20(3),
associated with the presence of anencephaly, the 219–233. https://doi.org/10.1002/bsl.483.
Calvo, E. B., & Biglieri, A. (2008). Impact of folic acid
most dramatic is a failure of brain development.
fortification on women’s nutritional status and on the prev-
alence of neural tube defects. Archives of Argentina Pedi-
atrics, 106(6), 492–498. https://doi.org/10.1590/S0325-
Treatment 00752008000600004. S0325-00752008000600004 [pii].
Calzolari, F., Gambi, B., Garani, G., & Tamisari, L. (2004).
Anencephaly: MRI findings and pathogenetic theories.
Ultimately, mortality rate is 100% with anencephaly. Pediatric Radiology, 34(12), 1012–1016. https://doi.
Some anencephalic children do survive from org/10.1007/s00247-004-1259-8.
hours to days but rarely longer and in a persistent Castillo-Lancellotti, C., Tur, J. A., & Uauy, R. (2013).
Impact of folic acid fortification of flour on neural tube
vegetative state (Payne and Taylor 1997); thus, defects: A systematic review. Public Health Nutrition,
treatment is purely supportive. The presence of a 16(5), 901–911. 10.1017/S1368980012003576.
surviving infant with anencephaly raises numer- Centers for Disease Control and Prevention (CDC). (2015).
ous ethical questions about care, treatment, and Facts about anencephaly. Retrieved from http://www.
cdc.gov/ncbddd/birthdefects/anencephaly.html
maintenance (Batavia 2002; Castillo-Lancellotti
Cohen, M. M., Jr. (2002). Malformations of the craniofa-
et al. 2013; Cook et al. 2008; Obeidi et al. 2010; cial region: Evolutionary, embryonic, genetic, and clin-
Rampersaud et al. 2016; Yila et al. 2016; Zhang ical perspectives. American Journal of Medical
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Genetics, 115(4), 245–268. https://doi.org/10.1002/ National Institute of Neurological Disorders and Stroke.
ajmg.10982. (2015). NINDS Anencephaly Information Page.
Cook, R. J., Erdman, J. N., Hevia, M., & Dickens, B. M. National institutes of health: Reducing the burden of
(2008). Prenatal management of anencephaly. Interna- neurological disease. Retrieved from http://www.
tional Journal of Obstetrics & Gynaecology, 102(3), ninds.nih.gov/disorders/anencephaly/anencephaly.htm
304–308. https://doi.org/10.1016/j.ijgo.2008.05.002. National Institutes of Health (NIH): Office of Dietary Sup-
S0020-7292(08)00210-5 [pii]. plements. (2016). Health information: Folate, dietary
Cornel, M. C., & Erickson, J. D. (1997). Comparison supplement fact sheet: Strengthening knowledge and
of national policies on periconceptional use of understanding of dietary supplements. Retrieved from
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(SBA). Teratology, 55(2), 134–137. https://doi.org/ nal/#h2
10.1002/(SICI)1096-9926(199702)55:2<134::AID- Nzila, A., Okombo, J., & Hyde, J. (2016). Malaria in the
TERA3>3.0.CO;2-3. era of food fortification with folic acid. Food and
Creasy, R. K., Resnik, R., Iams, J. D., Lockwood, C. J., Nutrition Bulletin, 1–11. https://doi.org/10.1177/
Moore, T. R., & Greene, M. F. (Eds.). (2014). Creasy 0379572116634511.
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Flores, A. L., Vellozzi, C., Valencia, D., & Sniezek, J. defects: From a proteomic standpoint. Metabolites, 5(1),
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Health, 26(Suppl 1), 3–5. Kauwell, G. P. (2016). Folate/folic acid knowledge, intake,
Greene, N. D., & Copp, A. J. (2014). Neural tube defects. and self-efficacy of college-age women: Impact of text
Annual Review of Neuroscience, 37, 221–242. https:// messaging and availability of a folic acid-containing sup-
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Herrmann, W., & Obeid, R. (2011). The mandatory org/10.1080/07448481.2016.1179196.
fortification of staple foods with folic acid: A current Sharif, A., & Zhou, Y. (2016). Fetal MRI characteristics of
controversy in Germany. Deutsches Arzteblatt Interna- exencephaly: A case report and literature review. Case
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arztebl.2011.0249. 10.1155/2016/9801267.
James, W. H. (1980). The sex ratios of anencephalics born Strickland, K. C., Krupenko, N. I., & Krupenko, S. A.
to anencephalic-prone women. Developmental Medi- (2013). Molecular mechanisms underlying the poten-
cine and Child Neurology, 22, 618–622. tially adverse effects of folate. Clinical Chemistry and
Kandel, E. R., Schwartz, J. H., Jessell, T. M., Siegelbaum, Laboratory Medicine, 51(3), 607–616. https://doi.org/
S. A., & Hudspeth, A. J. (Eds.). (2013). Principles of 10.1515/cclm-2012-0561.
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Companies. Gellynck, X., & Zheng, X. (2016). Effectiveness of
Kolb, B., & Whishaw, I. Q. (2008). Fundamentals of folic acid fortified flour for prevention of neural tubed
human neuropsychology (6th ed.). New York: Worth in a high risk region. Nutrients, 8(3). https://doi.org/
Publishers. 10.3390/nu8030152.
Kondo, A., Kamihira, O., & Ozawa, H. (2009). Neural tube Wolff, T., Witkop, C. T., Miller, T., & Syed, S. B. (2009).
defects: Prevalence, etiology and prevention. Interna- Folic acid supplementation for the prevention of neural
tional Journal of Urology, 16(1), 49–57. https://doi. tube defects: An update of the evidence for the U.S.
org/10.1111/j.1442-2042.2008.02163.x. preventive services task force. Annals of Internal Med-
Lezack, M. D., Howieson, D. B., Bigler, E. D., & Tranel, icine, 150(9), 632–639. https://doi.org/150/9/632 [pii].
D. (2012). Neuropsychological assessment (5th ed.). Yamaguchi, Y., & Miura, M. (2013). How to form and
New York: Oxford University Press. close the brain: Insight into the mechanism of cranial
Mitchell, L. E. (2005). Epidemiology of neural tube neural tube closure in mammals. Cellular and Molecu-
defects. American Journal of Medical Genetics. Part lar Life Sciences, 70(17), 3171–3186. https://doi.org/
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https://doi.org/10.1002/ajmg.c.30057. Yila, T. A., Araki, A., Sasaki, S., Miyashita, C., Itoh, K.,
MRC Vitamin Study Research Group. (1991). Prevention Ikeno, T., et al. (2016). Predictors of folate status
of neural tube defects: Results of the Medical Research among pregnant Japanese women: The Hokkaido
Council vitamin study. Lancet, 338(8760), 131–137. study on environment and Children’s health,
Aneurysm 229

2002–2012. British Journal of Nutrition, 1–9. https:// and symptoms, and, therefore, a patient with a
doi.org/10.1017/S0007114516001628. static aneurysm may be asymptomatic. How-
Zaganjor, I., Sekkarie, A., Tsang, B. L., Williams, J.,
Razzaghi, H., Mulinare, J.,


& Rosenthal, J. (2016). ever, a larger aneurysm with a steady growth A
Describing the prevalence of neural tube defects world- pattern may produce a variety of symptoms
wide: A systematic literature review. PloS One, 11(4), (e.g., headache, numbness, loss of feeling in
e0151586. https://doi.org/10.1371/journal.pone.0151586. the face, or problems with the eyes) (NINDS
Zhang, R., Wu, K., Zhan, C., Liu, X., & Gong, Z. (2016).
Folic acid supplementation reduces the mutagenicity 2015).
and genotoxicity caused by benzo(a)pyrene.
Journal of Nutritional Science and Vitaminology
(Tokyo), 62(1), 26–31. https://doi.org/10.3177/ Categorization
jnsv.62.26.
Intracranial aneurysms are commonly classified
as saccular, mycotic, traumatic, arteriosclerotic,
Aneurysm dissecting, or neoplasmic. Giant aneurysms
greater than 2.5 cm in diameter are believed
Bruce J. Diamond to be congenital anomalies. They are generally
Department of Psychology, William Paterson located on the anterior and middle cerebral,
University, Wayne, NJ, USA carotid and basilar arteries (Ropper et al. 2005).

Synonyms Etiology

Blood-filled dilatation The combination of high wall shear stress (WSS)

and high positive spatial wall shear stress gradient
(SWSSG) focused on a small segment of the arterial
Short Description or Definition wall may mediate aneurysm formation (Kulcsár
et al. 2011). Additionally, the proximity of the distal
An aneurysm is an abnormal blood-filled dilata- anterior cerebral artery (dACA) to the falx has been
tion of a blood vessel that can occur in vascular recently implicated in the pathogenesis of dACA
innervated areas (Webster 2006). Cerebral aneu- aneurysms with fibrous adhesions between the falx
rysms are generally located at arterial curvatures and the dACA observed in patients with this type of
and bifurcations that are exposed to major aneurysm (Scholtes et al. 2015).
hemodynamic forces (Kulcsár et al. 2011).
Aneurysms generally develop due to trauma, Epidemiological Factors
infections, congenital defects, or degenerative
diseases (Parkin and Leng 1993). Blood from a Ruptured aneurysms, specifically the saccular
ruptured brain aneurysm can leak into the brain type, are the most common cause of subarach-
(i.e., hemorrhagic stroke). If blood leaks into the noid hemorrhage (SAH) after 20 years of age.
space between the brain and the thin tissues This type of aneurysm accounts for about 80% of
covering the brain, this type of hemorrhagic nontraumatic aneurysms. Cerebral aneurysms
stroke is classified as a subarachnoid hemor- can occur throughout the lifespan but tend to be
rhage (Mayo Clinic Staff 2015). An aneurysm more common in adults than in children. They
can also dissect, which is a split in one or more are also slightly more common in women than in
layers of the artery wall that causes bleeding into men (NINDS 2015). It has been hypothesized
and along the layers of the artery wall (NIH that women may experience more ruptured aneu-
2011). The size and rate of growth of an rysms due to their higher proportion of superthin
unruptured cerebral aneurysm will affect signs tissue at the dome of their aneurysm in
230 Aneurysm

comparison to men. This superthin tissue is more Aneurysm, Table 1 Symptoms that may be associated
vulnerable to external forces and consequently with ruptured and unruptured cerebral aneurysms (From
Bonner and Bonner 1991; NINDS 2015; Walsh 2014)
more susceptible to rupture (Kadasi et al. 2013).
Inflammation accompanying cigarette smoke Ruptured aneurysms Unruptured aneurysms
exposure may also be an important pathway Parenchymal dissection Headache, neck rigidity
underlying the development, progression, and Hyperfusion Neurologic deficit
Cerebral edema Drowsiness, confusion,
rupture of cerebral aneurysms (Chalouhi
focal neurologic deficit
et al. 2012). Cognitive impairments, Decerebrate rigidity/
confusion vegetative disturbance
possible
Natural History, Prognostic Factors, and Disturbances in personality Deep coma
Outcomes Eye changes (drooping, Dilated pupil
blurred vision, light
sensitivity)
Unruptured aneurysms may be symptomatic and
Seizure Pain above/behind eye,
manifested as cranial nerve palsies. Moreover, drooping eyelid
unruptured aneurysms of sufficient size can com- Severe headache Double vision
press cerebral tissue and manifest as various neu-
rological signs (Ko and Kim 2011; Penn et al.
2011). Ruptured cerebral aneurysms can be asso-
ciated with states of consciousness ranging from Assessment and Treatment
lethargy to coma with outcome based on location
and severity of bleeding. A sudden loss of con- The Hunt-Hess grading scale is used for progno-
sciousness is a presenting feature in about 20% of sis and for timing of surgical interventions. Diag-
cases. Commonly observed systemic complica- nostic evaluations commonly include CT scans,
tions and sequelae are vasospasms, rebleeding, angiography, and MR angiography. Surgical
hydrocephalus, herniation, seizures, cardiac dys- treatment consists of clipping and endovascular
rhythmias, and respiratory depression (Bonner embolization of the aneurysm or implanting a
and Bonner 1991). Woven endobridge device to provide flow dis-
ruption at the aneurysm neck–parent artery inter-
face (Klisch et al. 2011). Pharmacologic
Neuropsychological and Medical interventions may include calcium channel
Outcomes blockers (e.g., nimodipine) in order to reduce
the severity of vasospasm (Bonner and Bonner
Symptoms and signs can include retinal hemor- 1991). Patients taking Aspirin three times
rhage, papilledema, and meningeal signs with sei- weekly to daily had significantly lower odds of
zure activity commonly observed. Focal signs are hemorrhage compared with controls, and thus,
prominent within the first 24 h (e.g., parenchymal Aspirin may reduce the risk of intracranial aneu-
dissection, hyperfusion distal to the aneurysm rysm rupture. However, additional research is
site, cerebral edema). Vasospasm may be the needed using both animal and clinical models
cause of focal signs within the 48–72 h window. in order to verify safety, dosage, and efficacy
Cognitive, psychiatric, and behavioral impair- (Hasan et al. 2011). The putative linkage
ments associated with ruptured and unruptured between cigarette smoke, inflammation and
aneurysms depend on the site and extent of dam- aneurysm formation, progression, and rupture
age, secondary sequelae, complications, and pre- may suggest new targeted interventions to treat
morbid health (see Table 1). aneurysms.
Aneurysm 231

Current research is examining DNA sequences Klisch, J., Sychra, V., Strasilla, C., Liebig, T., & Fiorella, D.
in order to identify families at increased risk for (2011). The Woven EndoBridge cerebral aneurysm
embolization device (WEB II): Initial clinical experi-
certain types of aneurysm and possibly identify ence. Neuroradiology, 53(8), 599–607. A
aneurysm-related genetic markers (NINDS 2015). Ko, J. H., & Kim, Y. J. (2011). Oculomotor nerve palsy
Research on the advantages and disadvantages of caused by posterior communicating artery aneurysm:
microsurgical clipping and endovascular surgery Evaluation of symptoms after endovascular treatment.
Interventional Neuroradiology, 17(4), 415–419.
for the treatment of both ruptured and unruptured Kohyama, S., Kakehi, Y., Yamane, F., Ooigawa, H., Kurita,
aneurysms is also underway (Kohyama et al. H., & Ishihara, S. (2014). Subdural and intracerebral
2014; Furuichi et al. 2015; Kamensky 2015; hemorrhage caused by spontaneous bleeding in the
NINDS 2015; Suzuki et al. 2015). middle meningeal artery after coil embolization of a
cerebral aneurysm. Journal of Stroke and Cerebrovas-
cular Diseases, 23(9), e433–e435.
Kulcsár, Z., Ugron, A., Marosfőia, M., Berenteia, Z., Paálc,
Cross-References G., & Szikoraa, I. (2011). Hemodynamics of cerebral
aneurysm initiation: The role of wall shear stress and
spatial wall shear stress gradient. American Journal of
▶ Anterior Cerebral Artery
Neuroradiology, 32, 587–594.
▶ Anterior Communicating Artery Mayo Clinic Staff. (2015). Brain aneurysm information
▶ Herniation Syndromes page. Rochester: Mayo Clinic. http://www.
▶ Hydrocephalus mayoclinic.org/diseases-conditions/brain-aneurysm/
basics/definition/con-20028457. Updated 1 Sept 2015.
NIH. (2011). National Heart Lung and Blood Institute aneurysm
information page. Bethesda: NIH. https://www.nhlbi.nih.
References and Readings gov/health/health-topics/topics/arm. Updated Oct 2015.
NINDS. (2015). NINDS cerebral aneurysm information
Bonner, J. S., & Bonner, J. J. (1991). The little black book page. National Institute of Neurologic Disorders and
of neurology: A manual for neurologic house officers Stroke website. http://www.ninds.nih.gov/disorders/
(2nd ed.). St Louis: Mosby-Year Book. aneurysm/aneurysm.htm. Updated 23 Feb 2015;
Chalouhi, N., Ali, M. S., Starke, R. M., Jabbour, P. M., accessed 5 Mar 2016.
Tjoumakaris, S. I., Gonzalez, L. F., . . ., & Dumont, Parkin, A., & Leng, R. C. (1993). Neuropsychology of the
A. S. (2012). Cigarette smoke and inflammation: Role amnestic syndrome. Hove: Lawrence Erlbaum.
in cerebral aneurysm formation and rupture. Mediators Penn, D. L., Komotar, R. J., & Connolly, E. S. (2011).
of Inflammation, 2012, 271582. Hemodynamic mechanisms underlying cerebral aneu-
Furuichi, M., Shimoda, K., Kano, T., Satoh, S., & Yoshino, A. rysm pathogenesis. Journal of Clinical Neuroscience,
(2015). A case of brainstem hemorrhage following 18(11), 1435–1438.
embolization of a large basilar aneurysm with hydrogel- Ropper, A. H., Brown, R. H., Adams, R. D., & Victor, M.
coated coils. No Shinkei Geka. Neurological Surgery, (2005). Adams & Victor’s principles of neurology.
43(9), 835–842. New York: McGraw-Hill.
Hasan, D. M., Mahaney, K. B., Brown, R. D., Meissner, I., Scholtes, F., Henroteaux, A., Otto, B., & Martin, D. (2015).
Piepgras, D. G., Huston, J., . . ., & International Study Head trauma and distal anterior cerebral artery aneu-
of Unruptured Intracranial Aneurysms Investigators. rysm: Potential role of an adhesion to the falx. Journal
(2011). Aspirin as a promising agent for decreasing of Neurological Surgery. Part A, Central European
incidence of cerebral aneurysm rupture. Stroke, Neurosurgery, 76(1), 72–75.
42(11), 3156–3162. Suzuki, M., Yoneda, H., Ishihara, H., Shirao, S., Nomura,
Kadasi, L. M., Dent, W. C., & Malek, A. M. (2013). S., Koizumi, H., . . ., & Inoue, T. (2015). Adverse
Cerebral aneurysm wall thickness analysis using events after unruptured cerebral aneurysm treatment:
intraoperative microscopy: Effect of size and gender A single-center experience with clipping/coil emboli-
on thin translucent regions. Journal of Neurointer- zation combined units. Journal of Stroke and Cerebro-
ventional Surgery, 5(3), 201–206. vascular Diseases, 24(1), 223–231.
Kamensky, J. (2015). Neurosurgical versus endovascular Walsh, M. E. (2014). The nose knows: An unusual presen-
treatment of subarachnoid haemorrhage caused by rup- tation of a cerebral aneurysm. Journal of Emergency
tured cerebral aneurysm: Comparison of patient out- Medicine, 47(5), e113–e115.
comes. Journal of Perioperative Practice, 25(3), Webster. (2006). Webster’s new explorer medical dictio-
53–57. nary (2nd ed.). Springfield: Merriam-Webster.
232 Angelman Syndrome

There are four main classes of Angelman syn-

Angelman Syndrome drome, based upon four primary genetic mecha-
nisms by which it occurs (Clayton-Smith and
Kristen Smith1 and Bonita P. “Bonnie” Laan 2003). In the general population, UBE3A
Klein-Tasman2 is expressed only from the maternal chromosome
1
Department of Psychology and the Neuroscience in particular regions of the brain, and the UBE3A
Institute, Georgia State University, Atlanta, gene on the paternal chromosome is inactive. In
GA, USA Angelman syndrome, as a result of the deletion,
2
Department of Psychology, University of only about 10% of UBE3A is expressed (Williams
Wisconsin-Milwaukee, Milwaukee, WI, USA 2005).

Definition Epidemiology

Angelman syndrome is a neurodevelopmental Exact prevalence rates of Angelman syndrome are

disorder caused by one of several genetic mech- unknown but have been estimated between
anisms involving maternal chromosome 15, spe- 1/12,000 and 1/24,000 (Dagli et al. 2015). See
cifically the region 15q11.2-13 (Dagli et al. Table 1 for estimates by subtype.
2015). Common features include microcephaly,
seizure disorder, impaired motor skills, and
developmental delays. Absent or extremely lim- Natural History, Prognostic Factors, and
ited expressive language skills are also com- Outcomes
monly observed. Behaviorally, individuals with
Angelman syndrome are known for a happy tem- Angelman syndrome was first described by
perament, frequent laughter, inattention/hyper- Dr. Harry Angelman in 1965. He observed several
activity, and stereotyped behaviors; these pediatric patients whom he referred to as “puppet
features have been identified as the most consis- children,” in light of their happy expressions and
tent features within this population (Clayton- “jerky” movements (Angelman 1965). This term
Smith and Laan 2003). was later abandoned, and the disorder instead came

Angelman Syndrome, Table 1 Sample caption

Categorization
Genetic
mechanism Incidence Definition
Deletion or mutation of genetic material on chro- De novo 75% Deletion on maternal
mosome 15q11-13 can result in one of two distinct deletion chromosome region
neurodevelopmental disorders, depending upon 15q11-13
whether the genetic material is from the maternal Uniparental 1–2% Both copies of
or paternal chromosome. This parent of origin disomy chromosome 15 are
inherited from the father,
effect is known as “imprinting.” Note that the rather than one from each
15q11-13 region is differently imprinted in mater- parent
nal and paternal chromosomes, and both imprint- Imprinting 3% Genes become inactivated
ings are needed for normal development. If a defect as a result of a disruption in
genes controlling the
maternal deletion occurs, the result is Angelman
imprinting process itself, or
syndrome; if a paternal deletion occurs, then the the imprinting center
result is Prader-Willi syndrome. Therefore, UBE3A 11%
Angelman and Prader-Willi have been termed mutation
“sister syndromes” or “sister disorders” (e.g., Unknown 10%
Cassidy et al. 2000). Buiting et al. (2015); Dagli et al. (2015)
Angelman Syndrome 233

to be known as Angelman syndrome. Diagnostic has been reported, including both generalized and
clinical criteria were developed by Williams and complex-partial types (Thibert et al. 2009). Sei-
colleagues in 1995 and revised in 2006. These zures usually appear in early childhood, with A
criteria include severe developmental delay, move- some indication of improvement during late child-
ment or balance disorder, unique behavior, and hood/adolescence, followed by recurrence in
severe speech impairment (Williams et al. 2006). some adults with Angelman syndrome (Clayton-
The prenatal and perinatal history of children Smith 2001). EEGs are typically abnormal and
with Angelman syndrome is typically unremark- often include large-amplitude spike-and-slow
able, and developmental delays first become evi- wave discharges (Dagli et al. 2015).
dent around 6–12 months of age (Cassidy et al. Variability is evident in the phenotypic expres-
2000). Head circumference is typically normal at sion of Angelman syndrome depending upon the
birth but growth is then delayed, resulting in specific genetic mechanism by which it occurs.
microcephaly by age 2 years (Dagli et al. 2015). Those with Angelman syndrome due to a de novo
Puberty usually occurs on time. There is generally deletion appear have the most severe medical/
no evidence of reduced life span, although the neurological effects, as well as greater motor and
severity of associated medical conditions (e.g., language deficits (e.g., Clayton-Smith and Laan
seizures) certainly impacts health and the overall 2003; Levitas et al. 2007). In contrast, those with
quality of life. Additionally, the long-standing uniparental disomy have lower rates of seizures
motor difficulties in this population often translate and less severe language impairments, as well as
into mobility issues later in life (Clayton-Smith fewer dysmorphic facial features. Individuals with
and Laan 2003) (Fig. 1). an imprinting center defect also appear to have
Epilepsy is common in Angelman syndrome, milder clinical presentations. Finally, those with
reported in at least 80% of cases (Dagli et al. 2015; UBE3A mutations have been found to have the
Williams et al. 2006). A variety of seizure types more severe medical and physical problems seen
in individuals with de novo deletions but fewer
difficulties with motor and language skills than
these individuals (Clayton-Smith and Laan 2003)
(Fig. 2).

Neuropsychology and Psychology of

Angelman Syndrome

Findings from neuroimaging studies have included

smaller gray matter volume in several cortical and
subcortical brain regions, as well as abnormal pat-
terns of myelination and white matter abnormali-
ties (Aghakhanyan et al. 2016; Harting et al. 2009;
Peters et al. 2011). Cognitive development is
severely delayed (Gentile et al. 2010). Adaptive
functioning is also delayed, with a relative strength
evident in social skills (Peters et al. 2004). As
mentioned above, a primary feature of Angelman
syndrome is limited expressive language, which
typically ranges from no language to very few
single words. There are relative strengths in recep-
tive language (Gentile et al. 2010). Marked deficits
Angelman Syndrome, Fig. 1 occur in fine motor skills.
234 Angelman Syndrome

social interactions has been described, although

the nature of these interactions differs depending
upon overall intellectual abilities (Williams
2010). Those with larger deletions have been
demonstrated to show more impaired social affect
and more repetitive behaviors than those with
smaller deletions, when controlling for cognitive
and adaptive abilities (Peters et al. 2012). Inci-
dence of parental stress is high and differs by
subtype, with those parents of children with
imprinting defects reporting the highest stress
levels (Miodrag and Peters 2015). Sleep and feed-
ing problems have been identified as associated
features of Angelman syndrome (Williams
et al. 2006).

Evaluation

Angelman syndrome is confirmed through genetic

testing (Dagli et al. 2015). Fluorescence in situ
hybridization (FISH) testing is typically employed
to identify genetic deletions; chromosomal microar-
ray is utilized in some specific instances. DNA-
Angelman Syndrome, Fig. 2
methylation testing can be used to detect uniparental
disomy or imprinting defects.
A “happy” temperament has been reported
among individuals with Angelman syndrome,
characterized by frequent smiling and laughter, Treatment
which persists across the life span (e.g., Clayton-
Smith and Laan 2003). A variety of other behav- There is no “cure” for Angelman syndrome itself.
ioral concerns have also been reported, most Given the high incidence of seizure disorder, man-
commonly inattention and hyperactivity (Clarke agement and follow-up by a neurologist is usually
and Marston 2000; Summers et al. 1995). How- necessary. Anticonvulsant medications have been
ever, there is some indication that these behav- used to manage seizures in this population, most
ioral difficulties improve with age (Clayton- often clonazepam, valproic acid, topiramate,
Smith and Laan 2003). Stereotyped motor behav- lamotrigine, and ethosuximide (Thibert et al. 2009).
iors, such as hand flapping, have frequently been Sleep difficulties have successfully been addressed
observed (Williams et al. 2006). Elevated risk of through behavioral intervention and with melatonin
autism spectrum disorder has often been (Allen et al. 2013; Braam et al. 2008).
suggested; however, this may be overdiagnosed Involvement in interventions such as occupa-
due to the severity of intellectual disability and tional, physical, and speech/language therapy is
especially communication problems and motor typically recommended to address language and
abnormalities, whereas social reciprocity is typi- motor deficits. In addition to speech/language ther-
cally relatively intact (Moss and Howlin 2009). apy, alternative communication methods typically
Social smiling may appear as early as 1 to need to be explored. Special education program-
3 months of age, and a strong preference for ming is indicated in light of cognitive deficits. Very
Angelman Syndrome 235

few behavioral intervention studies have been Clayton-Smith, J., & Laan, L. (2003). Angelman syn-
conducted for individuals with Angelman syn- drome: A review of the clinical and genetic aspects.
Journal of Medical Genetics, 40, 87–95.
drome. Behavioral training has been used in an Dagli, A. I., Mueller, J., & Williams, C. A. (2015). A
effort to address problematic social behaviors Angelman Syndrome. In: Pagon R. A., Adam, M. P.,
(Fichtner and Tiger 2015; Heald et al. 2013). Ardinger, H. H., Wallace, S. E., Amemiya, A., Bean,
L. J. H., . . . & Stephens, K. (Eds.). GeneReviews ®
[Internet]. Seattle: University of Washington, Seattle;
1993–2015. Available from: https://www.ncbi.nlm.nih.
Cross-References gov/books/NBK1144/
Fichtner, C. S., & Tiger, J. H. (2015). Teaching discrimi-
▶ Ataxia nated social approaches to individuals with Angelman
syndrome. Journal of Applied Behavior Analysis, 48,
▶ Developmental Delay 734–748.
▶ Epilepsy Gentile, J. K., Tan, W.-H., Horowitz, L. T., Bacino, C. A.,
▶ Intellectual Disability Skinner, S. A., Barbieri-Welge, R., et al. (2010).
▶ Microcephaly A neurodevelopmental survey of Angelman syndrome
with genotype-phenotype correlations. Journal of
▶ Prader-Willi Syndrome Developmental and Behavioral Pediatrics, 31(7),
▶ Seizure 592–601.
▶ Syndrome Harting, I., Seitz, A., Rating, D., Sartor, K., Zschocke, J.,
Janssen, B., et al. (2009). Abnormal myelination in
Angelman syndrome. European Journal of Pediatric
Neurology, 13(3), 271–275.
References and Readings Heald, M., Allen, D., Villa, D., & Oliver, C. (2013). Dis-
crimination training reduces high rate social approach
Aghakhanyan, G., Bonanni, P., Randazzo, G., Nappi, S., behaviors in Angelman syndrome: Proof of principle.
Tessarotto, F., De Martin, L., et al. (2016). From cortical Research in Developmental Disabilities, 34, 1794–1803.
and subcortical Grey matter abnormalities to Levitas, A., Dykens, E., Finucane, B., & Kates, W. (2007).
neurobehavioral phenotype of Angelman syndrome: Behavioral phenotype of genetic disorders. In
A voxel-based Morphometry study. PloS One, 11(9), R. Fletcher, E. Loschen, C. Stavrakaki, & M. First
e0162817. https://doi.org/10.1371/journal.pone.0162817. (Eds.), Diagnostic manual - intellectual disability:
Allen, K. D., Kuhn, B. R., DeHaai, K. A., & Wallace, D. P. A textbook of diagnoses of mental disorders in persons
(2013). Evaluation of a behavioral treatment package to with intellectual disability. Kingston: NADD Press.
reduce sleep problems in children with Angelman syn- Miodrag, N., & Peters, S. (2015). Parent stress across molec-
drome. Research in Developmental Disabilities, 34(1), ular subtypes of children with Angelman syndrome.
676–686. Journal of Intellectual Disability Research, 59, 816–826.
Angelman, H. (1965). ‘Puppet’ children: A report on three Moss, J., & Howlin, P. (2009). Autism spectrum disorders
cases. Developmental Medicine & Child Neurology, 7, in genetic syndromes: Implications for diagnosis, inter-
681–688. vention and understanding the wider autism spectrum
Braam, W., Didden, R., Smits, M. G., & Curfs, L. M. disorder population. Journal of Intellectual Disabilities
(2008). Melatonin for chronic insomnia in Angelman Research, 53, 852–873.
syndrome: A randomized placebo-controlled trial. Peters, S. U., Goddard-Finegold, J., Beaudet, A. L.,
Journal of Child Neurology, 23, 649–654. Madduri, N., Turcich, M., & Bacino, C. A. (2004).
Buiting, K., Clayton-Smith, J., Driscol, D. J., Gillessen- Cognitive and adaptive behavior profiles of children
Kaesbach, G., Kanber, D., Schwinger, E., et al. (2015). with Angelman syndrome. American Journal of Med-
Clinical utility card for: Angelman syndrome. ical Genetics, 128, 110–113.
European journal of human genetics, 23, online. Peters, S. U., Horowitz, L., Barbieri-Welge, R., Lounds
Cassidy, S. B., Dykens, E., & Williams, C. A. (2000). Taylor, J., & Hundley, R. J. (2012). Longitudinal
Prader-Willi and Angelman syndromes: Sister follow-up of autism spectrum features and sensory
imprinted disorders. American Journal of Medical behaviors in Angelman syndrome by deletion class.
Genetics, 97, 136–146. Journal of Child Psychology and Psychiatry, 53(2),
Clarke, D. J., & Marston, G. (2000). Problem behaviors 152–159.
associated with 15q- Angelman syndrome. American Peters, S. U., Kaufmann, W. E., Bacino, C. A., Angerson,
Journal on Mental Retardation, 105, 25–31. A. W., Adapa, P., Chu, Z., . . . & Wilde, E. A., (2011).
Clayton-Smith, J. (2001). Angelman syndrome: Evolution Alterations in white matter pathways in Angelman
of the phenotype in adolescents and adults. Develop- syndrome. Developmental Medicine & Child Neurol-
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236 Angiography, Cerebral

Summers, J. A., Allison, D. B., Lynch, P. S., & Sandler, L. aortic arch or selective means employed to cathe-
(1995). Behaviour problems in Angelman terize the carotid artery. Digital subtraction, com-
syndrome. Journal of Intellectual Disability Research,
39, 97–106. puted tomography (CT) scanning, and MRI
Summers, J. A., & Feldman, M. A. (1999). Distinctive pat- techniques can be applied as adjutant imaging tech-
tern of behavioral functioning in Angelman syndrome. niques once contrast is injected. Obstructions, ste-
American Journal on Mental Retardation, 104, 376–384. nosis, aneurysms, and A-V malformations can be
Thibert, R. L., Conant, K. D., Braun, E. K., Bruno, P., Said,
R. R., Nespeca, M. P., & Thiele, E. A. (2009). Epilepsy identified through this technique. Finer and more
in Angelman syndrome: A questionnaire-based assess- selective views are accomplished by using micro-
ment of the natural history and current treatment catheters. Some of the disease entities studied
options. Epilepsia, 50, 2369–2376. include ischemic cerebrovascular disease, aneu-
Williams, C. A. (2005). Neurological aspects of the
Angelman syndrome. Brain & Development, 27, 88–94. rysms, vascular malformations, neoplasms, and
Williams, C. A. (2010). The behavioral phenotype of the brain injuries. Angiography is the test of choice
Angelman syndrome. American Journal of Medical for arterial dissections and pseudoaneurysms
Genetics, 154C, 432–437. which may be associated with classic signs of
Williams, C. A., Beaudet, A. L., Clayton-Smith, J., Knoll,
J. H., Kyllerman, M., Laan, L. A., et al. (2006). pain, bruits, and/or cranial nerve palsies. Carotid
Angelman syndrome 2005: Updated consensus for angiography is also useful for imaging of carotid-
diagnostic criteria. American Journal of Medical cavernous fistulas which if not found early can
Genetics, 140, 413–418. cause blindness and may present with an ocular
Williams, C. A., Driscoll, D. J., & Dagli, A. I. (2010).
Clinical and genetic aspects of Angelman syndrome. bruit, scleral injection, and ocular proptosis.
Genetics in Medicine, 12(7), 385–395.

Current Knowledge

Angiography, Cerebral Can be part of the evaluation process of patients with

cerebrovascular disease or traumatic vascular insult.
Nathan D. Zasler1 and Richard Kunz2
1
Concussion Care Centre of Virginia, Ltd.,
Richmond, VA, USA
2
Department of Physical Medicine and
Rehabilitation, Virginia Commonwealth
University, Richmond, VA, USA

Synonyms

Angio

Definition

Angiography is the evaluation of the blood vessels

of the central nervous system and associated
cervicocerebral vasculature via radiographic imag-
ing of intravascular contrast media injected prior to
the imaging procedure. Femoral or axillary non-
selective approaches can be used to catheterize the
Angioma, Cavernous Angioma 237

Cross-References Three genetic loci responsible for familial

cavernous angioma (CCM1, CCM2, and
▶ Angioma, Cavernous Angioma CCM3) have been identified. Cavernomas are A
▶ Glioma typically found supratentorially (approximately
▶ Hemangioma 80%), predominantly in the subcortical rolandic
▶ Hemiplegia and temporal areas. Infratentorially, cavernous
angiomas are most commonly found in the pons
and cerebellar hemispheres (Sage and Blumbergs
References and Readings 2001). Originally thought to be relatively rare
and most commonly detected during autopsy,
Ahn, S. O., Prince, E. A., & Dubel, G. J. (2013). Basic the advent of MRI has led to an increased detec-
neuroangiography: Review of technique and perioper-
tion, with incidence rates now estimated between
ative patient care. Seminars in Interventional Radiol-
ogy, 30(3), 225–233. 0.02% and 0.8% of the general population. The
http://www.radiologyinfo.org/en/info.cfm?pg=angiocereb size of the well-circumscribed, “mulberry-like”
ral. Accessed 10/4/16. mass can range from less than 1 cm to greater
Kaufmann, T. J., & Kallmes, D. F. (2008). Diagnostic
than 4 cm. Prevalence rates are relatively equiv-
cerebral angiography: Archaic and complication-
prone or here to stay for another 80 years? AJR: Amer- alent among males and females. While it can
ican Journal of Roentgenology, 190(6), 1435–1437. remain asymptomatic lifelong, symptomatic pre-
sentation is most commonly seen in the third and
fourth decades of life. However, newly symp-
tomatic cases have been well reported through-
Angioma, Cavernous out the life span. Women are more likely to
Angioma present with hemorrhage and neurologic deficits
(Del Curling et al. 1991).
Jennifer Tinker Clinical manifestations, when present, vary
Department of Neurology, Thomas Jefferson significantly and generally correlate to location
University, Philadelphia, PA, USA of the lesion. Most commonly reported symp-
toms include headache (6–65%), seizure
(23–52%), focal neurological deficit (20–45%),
and intracranial hemorrhage (13–25%) (Conway
Synonyms
and Rigamonti 2006). Despite the regional affin-
ity for frontal and temporal regions, no studies
Cavernoma; Cavernous hemangioma; Cavernous
have specifically examined for selective neuro-
venous malformation; Cerebral cavernous malfor-
psychological deficits. Treatment can include
mation (CCM)
observation, surgical resection, or stereotactic
radiosurgery.

Definition
References and Readings
Cavernous angiomas are benign vascular
malformations found within the CNS that may Conway, J. E., & Rigamonti, D. (2006). Cavernous
occur sporadically or in a familial pattern. Cav- malformations: A review and current controversies.
Neurosurgery Quarterly, 16(1), 15–23.
ernous angiomas are also a complication of radi- Del Curling, O., Kelly, D. L., Elster, A. D., & Craven, T. E.
ation therapy, especially in children. These (1991). An analysis of the natural history of cavernous
angiomas can remain stable, enlarge over time, angiomas. Journal of Neurosurgery, 75(5), 702.
or bleed, and there are no factors that predict Sage, M. R., & Blumbergs, P. C. (2001). Cavernous
haemangiomas (angiomas) of the brain. Pathological-
their occurrence or behavior. Radiological Correlation, 45, 247–256.
238 Angioplasty

the tip of the catheter reaches the target blood

Angioplasty vessel, a previously folded balloon at the end of
the catheter is inflated to flatten the plaque in the
Elliot J. Roth vessel wall, thereby reducing the blockage and
Department of Physical Medicine and expanding the diameter of the artery. Usually, a
Rehabilitation, Northwestern University, stent, a metal mesh tube of small diameter which
Feinberg School of Medicine, Chicago, IL, USA also was on the end of the catheter, is then
placed inside the vessel and expanded by
manipulating the catheter tip. Many of these
Synonyms stents, called “drug-eluting stents,” contain and
secrete antiplatelet medications that assist in
Coronary angioplasty; Percutaneous coronary preventing arterial stenosis in the future. The
intervention (PCI); Percutaneous transluminal result of the angioplasty is a dilated artery and
angioplasty (PTA); Percutaneous transluminal improved blood flow through the vessel.
coronary angioplasty (PTCA) This procedure is done to prevent the vessel from
developing narrowing or becoming blocked again.
It is a relatively safe procedure, and complications
Definition are rare, but they include allergy, bleeding, clotting,
stroke, kidney failure, and re-blockage of the newly
Angioplasty is a minimally invasive (nonsurgical) opened artery. After the procedure, patients usually
percutaneously performed clinical procedure used remain on bedrest for a short time and are instructed
to dilate blood vessels narrowed or blocked by to use antiplatelet medications.
atherosclerosis. Historically, angioplasty was
performed most commonly on the coronary arter-
ies that supply blood to the heart muscle. How- See Also
ever, recent evidence indicates its effectiveness in
improving cerebral circulation in patients with
▶ Angiography, Cerebral
acute stroke. Angioplasty may be used to treat ▶ Atherosclerosis
coronary artery disease, which often presents
▶ Cerebrovascular Disease
with persistent angina (chest pain) or a myocardial
▶ Coronary Disease
infarction (heart attack), cerebrovascular disease
▶ Myocardial Infarction
causing stroke or transient ischemic attacks, renal
▶ Peripheral Vascular Disease
artery stenosis causing kidney dysfunction, and ▶ Stent
peripheral artery disease, usually in the blood
▶ Thrombectomy
vessel of the leg. During angioplasty, a stent is
placed in the vessel to keep the vessel patent.
References
Current Knowledge Levine, G. N., Bates, E. R., Blankenship, J. C.,
Bailey, S. R., Bittl, J. A., Cercek, B., Chambers,
In this procedure, a small incision is made over the C. E., Ellis, S. G., Guyton, R. A., Hollenberg,
S. M., Khot, U. N., Lange, R. A., Mauri, L., Mehran,
skin of a peripheral artery (usually the femoral R., Moussa, I. D., Mukherjee, D., Nallamothu, B. K.,
artery in the thigh), and the artery is punctured to & Ting, H. H. (2011). ACCF/AHA/SCAI guideline
gain access into the blood vessel. A thin catheter is for percutaneous coronary intervention: A report of
then inserted into the blood vessel, and both blood the American College of Cardiology Foundation/
American Heart Association Task Force on Practice
vessels and catheter are visualized by radiographic
Guidelines and the Society for Cardiovascular
fluoroscopy. The catheter is then pushed further into Angiography and Interventions. Circulation, 124,
the vessel (guided by fluoroscopic images). When 2574–2609.
Anomia 239

males when compared with females to have

Anomalous Dominance greater anatomical asymmetry in the region of
the frontal operculum (Broca’s area) and in the A
John E. Mendoza temporal operculum (planum temporale), both
Department of Psychiatry and Neuroscience, key language areas. This apparent tendency for
Tulane Medical School and SE Louisiana greater bilateral representation of language has
Veterans Healthcare System, New Orleans, LA, been suggested as a possible explanation for
USA (1) the earlier development (on average) of lan-
guage in females than in males, and (2) the supe-
rior recovery of language functions following
Synonyms strokes seen in some left-handers.

Mixed dominance
Cross-References
Definition ▶ Dominance (Cerebral)

Anomalous dominance describes any pattern of

cerebral organization of function in which the left References and Readings
hemisphere is not primarily responsible for initi-
ating propositional speech and processing written Geschwind, N., & Galaburda, A. (1985). Cerebral lateral-
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Geschwind, N., & Galaburda, A. M. (1987). Cerebral
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Current Knowledge and pathology. Cambridge, MA: MIT Press.
Herron, J. (Ed.). (1980). Neuropsychology of left-
Since the left hemisphere primacy for language is handedness. New York: Academic.
typical of most right-handers (who represent the vast
majority of the population), it is considered to be the
“dominant” pattern of brain organization. Hence, any
pattern that differs from this is considered to be Anomia
anomalous. Most deviations occur in left-handers,
approximately 30% of whom exhibit some form of Anastasia Raymer
anomalous dominance for language where these Communication Disorders and Special Education,
functions are organized either primarily in the right Old Dominion University, Norfolk, VA, USA
hemisphere (“reversed dominance”) or are more
bilaterally represented. Although anomalous domi-
nance can occur in right-handers, this is rare and, Synonyms
when present, is often a consequence of some early
developmental defect or brain trauma. Other associ- Naming impairments; Word-finding difficulties
ations that have been reported to be related to anom-
alous patterns of hemispheric organization of
language are female gender, mixed hand preference Definition
(ambidexterity), and family history of sinistrality. In
these situations, there is an increased tendency for Anomia generally refers to instances of word-
language functions to be organized in both hemi- finding difficulty that occur during the course of
spheres. Support for this hypothesis comes in part conversational discourse. It is often documented
from radiographic studies which show a tendency for clinically in confrontation picture-naming tasks.
240 Anomic Aphasia

Current Knowledge of anomia, neologisms may occur in which the

uttered word may not be recognizable at all (e.g.,
Anomia can occur in healthy individuals who occa- saying “bilan” for cat).
sionally experience difficulty retrieving an intended
word during a conversation, also known as the
tip-of-the-tongue state (Biedermann et al. 2008). It Cross-References
is a frequent occurrence in individuals with left
hemisphere brain damage and aphasia (Raymer ▶ Circumlocution
2011). Typically associated with difficulties for ▶ Confrontation Naming
nouns, anomia also can refer to difficulties in ▶ Paraphasia
retrieving other classes of words, such as verbs ▶ Semantic Paraphasia
and adjectives. Anomia arises from failure at any ▶ Word Finding
stage in the complex series of lexical processes
engaged in word retrieval, including activation of
semantic representations for the meaning to be con- References and Readings
veyed and phonological representations for the
form of the word to express that meaning (Tippett Biedermann, B., Ruh, N., Nickels, L., & Coltheart, M.
and Hillis 2015). These distinct processes in word (2008). Information retrieval in tip of the tongue states:
New data and methodological advances. Journal of
retrieval engage different parts of the brain distrib- Psycholinguistic Research, 37, 171–198.
uted throughout the left cerebral hemisphere (Race Laine, M., & Martin, N. (2006). Anomia: Theoretical and
and Hillis 2015). Therefore, when brain damage clinical aspects. New York: Psychology Press.
occurs, anomia may take somewhat different pat- Race, D. C., & Hillis, A. E. (2015). The neural mechanisms
underlying naming. In A. E. Hillis (Ed.), The handbook
terns (Laine and Martin 2006). For example, in of adult language disorders (pp. 151–160). New York:
semantic anomia, failure to retrieve words is accom- Psychology Press.
panied by difficulty in recognition of the same Raymer, A. M. (2011). Naming and word retrieval prob-
words. In contrast, phonologic anomia occurs lems. In L. L. LaPointe (Ed.), Aphasia and related
neurogenic language disorders (4th ed., pp. 95–110).
when a word is recognized but cannot be retrieved. New York: Thieme Medical Publishers.
It is important to note that anomia and anomic Tippett, D. C., & Hillis, A. E. (2015). The cognitive pro-
aphasia are not synonymous. Anomia is the primary cesses underlying naming. In A. E. Hillis (Ed.), The
symptom of anomic aphasia and also can be handbook of adult language disorders (pp. 141–150).
New York: Psychology Press.
observed in virtually all other forms of aphasia
(e.g., Broca’s aphasia, Wernicke’s aphasia), both
as initial and residual signs when other signs and
symptoms of aphasia have resolved.
When anomia occurs across different forms of Anomic Aphasia
aphasia, a number of errors can be seen (Laine and
Martin 2006). At times, the moment of anomia Anastasia Raymer
leads to complete inability to retrieve a word. Communication Disorders and Special Education,
Other times, an inappropriate word is retrieved, Old Dominion University, Norfolk, VA, USA
also known as a paraphasia. Sometimes, the error
word is somehow related to the intended word in
meaning (semantic paraphasia, e.g., saying “dog” Definition
for cat) or sound characteristics (phonologic para-
phasia, e.g., saying “crat” for cat). Sometimes, the Anomic aphasia is the language impairment that
moment of word-finding difficulty is filled with a involves only word-finding difficulties or pure
circumlocution or description of the intended anomia in contrast to other forms of aphasia
word (e.g., “That thing that meows and has whis- (Harnish 2015). Other language modalities typi-
kers. I can’t think of the name.”). In severe forms cally are intact in anomic aphasia, including
Anorexia Nervosa 241

auditory comprehension of language, repetition of ▶ Confrontation Naming

words and sentences, and spontaneous generation ▶ Paraphasia
of sentences, yet struggle may be noted to retrieve ▶ Semantic Paraphasia A
words during sentence generation. ▶ Word Finding

Current Knowledge References and Readings

Anomic aphasia is a form of language disorder Goodglass, H., Kaplan, E., & Barresi, B. (2001). The
assessment of aphasia and related disorders (3rd
associated with acquired brain damage typically
ed.). Philadelphia: Lippincott, Williams, &
affecting the left cerebral hemisphere (Raymer Wilkins.
2011). Anomic aphasia can be manifest as a Harnish, S. M. (2015). Anomia and anomic aphasia: Impli-
difficulty in retrieving specific intended words, cations for lexical processing. In A. M. Raymer & L. G.
Rothi (Eds.), The Oxford handbook of aphasia and
often nouns, but sometimes verbs, during the
language disorders. New York: Oxford Handbooks
course of sentence generation. The grammatical Online.
characteristics of the sentence remain intact. The Hoffmann, M., & Chen, R. (2013). The spectrum of
moments of word retrieval difficulty lead to long aphasia subtypes and etiology in subacute stroke.
Journal of Stroke and Cerebrovascular Disease, 22,
pauses, insertion of filler words, or selection of
1385–1392.
wrong words (paraphasias) during conversation Laine, M., & Martin, N. (2006). Anomia: Theoretical and
or other word retrieval activities, most com- clinical aspects. New York: Psychology Press.
monly in tasks requiring individuals to name Race, D. C., & Hillis, A. E. (2015). The neural mechanisms
underlying naming. In A. E. Hillis (Ed.), The handbook
pictures. Also common in anomic aphasia is cir-
of adult language disorders (pp. 151–160). New York:
cumlocution, in which the speaker cannot think Psychology Press.
of the intended word and instead describes or Raymer, A. M. (2011). Naming and word retrieval prob-
provides associated information about the word. lems. In L. L. LaPointe (Ed.), Aphasia and related
neurogenic language disorders (4th ed., pp. 72–86).
When anomic aphasia occurs as a result of an
New York: Thieme.
acute neurologic event (e.g., stroke), it can be
accompanied by pure alexia and difficulties with
color identification (Goodglass et al. 2001).
Acutely, anomic aphasia has been described follow-
ing left temporal/occipital lesions (e.g., area 37) and Anorexia Nervosa
left thalamic lesions (Race and Hillis 2015). Ano-
mic aphasia often can be seen chronically as indi- Kristin M. Graham
viduals recover from other forms of aphasia Department of Physical Medicine and
(Hoffmann and Chen 2013). In that case, the accom- Rehabilitation, Virginia Commonwealth
panying symptoms and neural correlates of anomic University, Richmond, VA, USA
aphasia vary. Treatment approaches for anomic
aphasia vary, including restorative approaches that
attempt to facilitate recovery using typical semantic Synonyms
and phonologic processes engaged in word retrieval
and compensatory approaches that circumvent Anorexia
word retrieval difficulties (Raymer 2011).

Definition
Cross-References
Anorexia nervosa is defined in the Diagnostic and
▶ Anomia Statistical Manual of Mental Disorders (5th ed.;
▶ Circumlocution DSM-5; American Psychiatric Association 2013)
242 Anorexia Nervosa

as a feeding and eating disorder characterized by bone mineral density), co-occurring psychologi-
restrictions on eating and significantly low cal disorders (e.g., bipolar, depressive, and anxi-
weight. This disorder is manifested through feel- ety disorders), and obsessive-compulsive features
ings of intense fear of gaining weight that lead to (e.g., preoccupied thoughts of food, food hoarding)
behaviors to stimulate weight loss (e.g., restricted are common. There is some evidence for brain
food intake). The fear is not alleviated by weight structural changes, such as increased ventricular
loss. Self-perception of body weight and shape is width and cortical sulci (Uher et al. 2003). Neuro-
often distorted. There are two subtypes: (1) psychological functioning deficits in the areas of
restricting type in which weight loss is accom- sustained and divided attention, working memory,
plished through dieting, caloric restriction, or inhibition, and mental flexibility have been identi-
excessive exercise and there is no binging/purging fied in individuals with anorexia nervosa.
behavior and (2) binge-eating/purging type in
which there are recurrent episodes of binging or Assessment and Treatment
purging behaviors. A comprehensive assessment interview for
anorexia nervosa should include clinical inter-
view, standardized self-report, interview-based
Categorization measures (e.g., Eating Attitudes Test (EAT-12),
Eating Disorder Inventory (EDI-3), Structured
The disorder is classified with the Feeding and Clinical Interview for DSM-5 (SCID-5), Eating
Eating Disorders in DSM-5. Disorder Examination (EDE)), and medical
assessment (e.g., assessing for laboratory abnor-
malities, amenorrhea, emaciation, hypotension,
Current Knowledge and bradycardia). Additionally, information
should be gathered from other sources (e.g., fam-
Development and Course ily members). Treatment of anorexia nervosa
The development of anorexia nervosa is common should include restoring healthy weight, medical
during adolescence and young adulthood and is treatment of physical complications, and evidence
often associated with a stressful life event. Course based psychotherapy (Watson & Bulik 2013).
and outcome is highly variable (e.g., recovery While no specific psychotherapy approach has
after one episode, fluctuating pattern of weight shown superiority, treatment modalities com-
gain leading to relapse). Likewise, functional con- monly utilized and recommended include cogni-
sequences (e.g., social and professional function- tive analytic therapy, cognitive behavioral
ing) vary between individuals, with some therapy, and interpersonal psychotherapy.
experiencing few functional consequences. Anorexia nervosa should be differentiated from
Anorexia nervosa is more common in females as other causes of significantly low body weight or
compared to males (female-to-male ratio, 10:1), significant weight loss, such as gastrointestinal
and the prevalence rate for young females is 0.4% disease, substance use disorders, or other feeding
(APA 2013). Risk of suicidal ideation or behav- and eating disorders. Additional differential diag-
iors is greater in individuals with this disorder. noses include major depressive disorder, schizo-
phrenia, social anxiety disorder, obsessive-
Associated Features and Current Research compulsive disorder, and body dysmorphic
Individuals with anorexia nervosa often lack disorder.
insight or deny it as being a problem. As such,
professional intervention is often sought by fam-
ily members or the individual when distressed See Also
over somatic or psychological sequelae. Signifi-
cant and life-threatening medical conditions (e.g., ▶ Avoidant/Restrictive Food Intake Disorder
amenorrhea, vital sign abnormalities, decreased ▶ Body Dysmorphic Disorder
Anosmia 243

▶ Bulimia Nervosa the strictest sense, “anosmia” refers to a total

▶ Feeding and Eating Disorders lack of olfactory ability, though the term is
often used more loosely to refer also to partial A
or diminished sense of smell. There are multiple
References and Readings additional terms describing olfactory abilities.
Normosmia is the intact ability to perceive
American Psychiatric Association. (2013). Diagnostic and odors. Hyposmia is a more precise term to
statistical manual of mental disorders (DSM-5 ®).
describe decreased ability to perceive smells,
Washington, DC: American Psychiatric Association.
Kidd, A., & Steinglass, J. (2012). What can cognitive whereas hyperosmia is the increased ability to
neuroscience teach us about anorexia nervosa? Current perceive odors. Dysosmia (a.k.a. parosmia)
Psychiatry Reports, 14(4), 415–420. refers to distortions in the sense of smell, includ-
Mustelin, L., Silén, Y., Raevuori, A., Hoek, H. W., Kaprio,
ing cacosmia (distortion of a smell as particularly
J., & Keski-Rahkonen, A. (2016). The DSM-5 diag-
nostic criteria for anorexia nervosa may change its unpleasant) and phantosmia (an olfactory hallu-
population prevalence and prognostic value. Journal cination, or the sensation of a smell in the
of Psychiatric Research, 77, 85–91. absence of a stimulus).
Reville, M. C., O’Connor, L., & Frampton, I. (2016). Liter-
ature review of cognitive neuroscience and anorexia
nervosa. Current Psychiatry Reports, 18(2), 1–8.
Surgenor, L. J., & Maguire, S. (2013). Assessment of anorexia Epidemiology
nervosa: An overview of universal issues and contextual
challenges. Journal of Eating Disorders, 1(1), 29.
Olfactory dysfunction is present in at least 1%
Uher, R., Brammer, M. J., Murphy, T., Campbell, I. C., Ng,
V. W., Williams, S. C. R., & Treasure, J. (2003) Recov- of individuals under the age of 65, with some
ery and chronicity in anorexia nervosa: brain activity estimates suggesting total anosmia in as much
associated with differential outcomes. Biological Psy- as 5% of the population. Rates of impairment
chiatry, 54(9), 934–942.
increase dramatically with age, with approxi-
Watson, H. J., & Bulik, C. M. (2013). Update on the
treatment of anorexia nervosa: review of clinical trials, mately 25% of older adults showing deficits in
practice guidelines and emerging interventions. Psy- olfaction (Murphy et al. 2002). In patients pre-
chological Medicine, 43(12), 2477–2500. senting to chemosensory clinics, olfactory def-
icits are reported to be related to disability and
quality of life, though most individuals with
Anosmia olfactory deficits are unaware of them. It is
well established that throughout the lifespan,
Holly James Westervelt1 and women show more acute olfactory abilities
Nicole C. R. McLaughlin2 than men.
1
Memory and Cognitive Assessment Program,
Department of Psychiatry, Rhode Island Hospital,
Providence, RI, USA Causes
2
Butler Hospital Alpert Medical School of Brown
University, Providence, RI, USA The causes of olfactory impairments are typi-
cally categorized as: (1) conductive/transport
Synonyms impairments, (2) sensory/sensorineural deficits,
or (3) central olfactory neural impairment,
Anosphrasia though these categories are not mutually exclu-
sive. The understanding of the potential causes of
olfactory deficits will be enhanced by a brief
Definition review of the olfactory system, though it is
noted that the olfactory pathways within the cen-
Anosmia is defined as a lack of the sense of smell tral nervous system (CNS) are not entirely
or an inability to detect odors of any kind. In agreed upon.
244 Anosmia

Anatomy of the Olfactory System smell loss, and is often transient. Permanent smell
The sensation of smell is the brain’s perception of loss due to URI can occur, presumably reflecting
odor in response to odorants activating olfactory direct insult to the neuroepithelium, and becomes
receptors. Odors enter the nose, where they come more likely in older age.
in contact with the olfactory epithelium, made up
of olfactory receptors. Olfactory receptor cells Sensorineural/Central Olfactory Neural
(first order neurons) send signals along the olfac- Impairment
tory nerve (first cranial nerve) to the mitral cells of Olfactory deficits within these categories arise
the olfactory bulb, where olfactory axons synapse from damage to the neuroepithelium and/or
with second-order neurons in the olfactory bulb. impairment or impingement of central olfactory
Each olfactory receptor type sends a signal to a structures from CNS disease. There are numerous
particular region of the olfactory bulb. Mitral cell congenital, endocrine, neurological/neurodegen-
axons project through the olfactory tract and lat- erative, nutritional/metabolic, and psychiatric dis-
eral olfactory stria to the primary olfactory cortex, orders that have been shown to be associated with
which is primarily made up of the piriform cortex. olfactory deficits (for a review of these causes, see
Other structures receiving direct input include the Murphy et al. 2003). In addition, injury, medica-
anterior olfactory nucleus, olfactory tubercle, tions (for review see Doty and Bromley 2004),
amygdala, and rostral entorhinal cortex (Gotfried environmental toxins (for review see Upadhyay
and Zald 2005). Projections from these primary and Holbrook 2004), structural lesions, and med-
areas extend to secondary olfactory regions in the ical/surgical interventions (for review see
hippocampus, hypothalamus, thalamus, amyg- Murphy et al. 2003) can affect neural function-
dala, and agranular insula, enabling encoding of ing. The Table 1 provides a small sampling of
odors into memory as well as emotional pro- disorders that can be associated with olfactory
cessing of specific odors (Gotfried and Zald loss. Given the vast number of disorders that
2005). There are also projections to the have shown olfactory deficits, theories have
orbitofrontal cortex (OFC), and it is believed that been postulated that olfactory impairment may
the OFC mediates conscious perception of odors;
lesions to this area often lead to impaired olfactory
abilities (Gotfried and Zald 2005). In addition to Anosmia, Table 1 Sampling of disorders associated with
the activation of the first cranial nerve, certain olfactory deficits
smells may also activate the trigeminal nerve Alcoholism/Korsakoff’s
(CNV), which mediates sensations associated syndrome Multiple sclerosis
Alzheimer’s disease Multiple system atrophy
with certain odorants, including burning, cooling,
Amyotrophic lateral Parkinson dementia
irritation, or tickling sensations. Activation of the
sclerosis complex of Guam
trigeminal nerve may allow the “detection” of Corticobasal Parkinson’s disease
some odors, even in the presence of primary olfac- degeneration
tory impairments. Cranial nerve zero (nervus Dementia with Lewy Progressive supranuclear
terminalis) may also play some role in olfaction, bodies palsy
though its function is poorly understood in Diabetes mellitus REM sleep behavior
disorder
humans.
Down’s syndrome Restless leg syndrome
Frontotemporal Schizophrenia
Conductive/Transport Impairment dementia
Olfactory impairment within this category arises Head injury Sjögren’s syndrome
from obstruction of nasal passages. Typical causes Human Syphilis
of obstruction include nasal inflammation, such as immunodeficiency virus
from allergies or upper respiratory infection Huntington’s disease Temporal lobe epilepsy
(URI), or other structural interference, such as Mild cognitive Vascular dementia
nasal polyps. URI is the most common cause of impairment
Anosmia 245

be a nonspecific marker of CNS dysfunction. be present before the motor symptoms become
This is likely not the case, given that the degree evident, and are apparent with both threshold
of deficit can differ widely among disorders, and identification tasks. The size of the effect is A
there exists significant range of deficits among astounding (ranging from 1.17 to 12.15 in a meta-
patients within disorders, and the deficits can be analysis; Mesholam et al. 1998), though the
unrelated to disease stage or magnitude of dis- majority of patients are not completely
ease symptoms in some diseases but not others. anosmic. Deficits do not appear to correlate with
Rather, it is probable that the presence and the extent of cognitive or motor involvement, do
degree of olfactory involvement is related to the not respond to treatment, and do not appear to be
relative degree of structural or biochemical dam- progressive over time.
age to the specific regions of the brain involved
in olfactory transduction. Other Parkinsonian Spectrum Disorders Other
Parkinsonian disorders, such as corticobasal
Neurodegenerative Diseases Interest in olfac- degeneration (CBD), multiple system atrophy,
tion in neurodegenerative disorders began most and progressive supranuclear palsy, are also asso-
intensely in the 1980s, with a focus on ciated with olfactory deficits, though the impair-
Alzheimer’s disease (AD) and Parkinson’s dis- ments tend to be more mild than is seen in PD
ease (PD). It was initially thought that these two (Doty 2003a, b). These findings suggest that
disorders, which were often thought of as the olfactory functioning may be useful in
prototypical examples of cortical and subcortical distinguishing PD from other parkinsonian disor-
diseases, would share an early and notable deficit. ders, though a more recent study of olfaction in
Olfactory deficits were then identified in a variety CBD raises some question of potentially more
of neurodegenerative disorders, making olfactory notable deficit in this disorder than was previously
loss a nonspecific finding, though the degree of described (Pardini et al. 2009).
impairment may be useful in distinguishing some
disorders. The cause of olfactory deficits in neu- Alzheimer’s Disease and Mild Cognitive
rodegenerative diseases is unknown (for a review Impairment There has been fairly good consis-
of potential causes, see Smutzer et al. 2003). The tency in the literature for most of the studies
deficits may be due at least in part to neurotrans- examining olfaction in Alzheimer’s disease (AD;
mitter system alterations, especially dopamine see Doty 2003a, b, for a review). The size of the
and acetylcholine. Damage to central processing effect is extremely large, ranging from 0.98 to
areas is also a likely explanation, particularly 8.55 in a meta-analysis (Mesholam et al. 1998),
involvement of the olfactory bulb and tracts, as though, as in PD, patients are typically not
relevant neuropathologic changes (e.g., neurofi- completely anosmic. Odor identification deficits
brillary tangles, amyloid plaques, dystrophic are always found; odor detection deficits are more
neurites, Lewy bodies, and disproportionate neu- inconsistently demonstrated and may be a later
ronal loss) are often seen in these areas. Other symptom. The odor identification deficit does
relevant central processing areas (e.g., entorhinal not seem to be primarily due to a general cognitive
cortex), however, also show neuropathologic deficit and deficits worsen with disease progres-
changes, as may peripheral structures (e.g., olfac- sion. Although group studies have shown consis-
tory epithelium). tent deficits in odor identification, it should be
noted that the presence of deficits is not a univer-
Parkinson’s Disease Olfactory impairment is a sal finding among patients with AD, making odor
prominent, common, and early feature of identification tests imperfect screening instru-
Parkinson’s disease (PD; see Doty 2003a, b, for ments for the disorder.
a review). The deficits tend to be bilateral, and are Odor identification has also been studied
more common than some of the hallmark symp- recently in patients with mild cognitive impair-
toms of PD, such as tremor. Olfactory deficits may ment (MCI) and cognitively intact older adults
246 Anosmia

with and without genetic risk for future cognitive possibility that olfactory measures may be useful
decline. Several longitudinal studies have demon- in distinguishing AD from DLB.
strated that odor identification has a strong rela-
tionship with memory performance, even in Other Dementias Olfactory deficits have also
healthy older adults performing within normal been described in other dementias, including
limits on cognitive measures (Devanand et al. recent, consistent findings of smell deficits in
2000; Wilson et al. 2007). These studies also frontotemporal dementia that are generally of the
show that odor identification is a unique and sig- magnitude of deficits seen in AD (Luzzi et al.
nificant predictor of future cognitive decline 2007; McLaughlin and Westervelt 2008; Pardini
above and beyond baseline memory performance, et al. 2009), and, in vascular dementia to a similar
as well as a good predictor of conversion to or lesser extent to that seen in AD (Gray et al.
dementia in patients with MCI. In cross-sectional 2001; Knupfer and Spiegel 1986).
studies of MCI subtypes, patients with both
amnestic and non-amnestic subtypes perform Head Injury Olfactory loss is fairly common
modestly worse than healthy older adults but following head injury (for review, see Costanza
better than patients with dementia (Devanand et al. 2003), with the incidence of anosmia ranging
et al. in press; Westervelt et al. 2008). In using from approximately 5 to 60%. These latter esti-
olfactory performance to distinguish MCI sub- mates represent the incidence among patients with
types, results are mixed, though when significant severe head injury, though total anosmia can
differences have been found between subtypes, occur even after very mild injury. Partial or uni-
the magnitude of the difference is of questionable lateral loss may be less likely to be detected than
clinical significance. Together, these studies sug- total anosmia. Deficits may be caused by a variety
gest that when a notable olfactory deficit is of mechanisms, including sinus/nasal injury,
observed in patients with MCI, there is substantial shearing of the olfactory nerve, or contusion/hem-
risk of future decline. However, odor identifica- orrhage in central processing regions. In regard to
tion measures may not be particularly clinically shear injuries, the axons of the olfactory receptor
useful in early detection or early differential diag- cells are particularly susceptible to injury as they
nosis for the modal patient. pass through the body ridges of the cribiform
plate. Coup and contra-coup forces are likely to
Dementia with Lewy Bodies Olfaction in result in anosmia, with occipital blows most fre-
dementia with Lewy bodies (DLB) was first quently causing smell loss.
described in a study that crudely measured anos-
mia with a brief detection task (McShane et al. Schizophrenia Olfactory deficits have been
2001). Forty percent of patients with DLB were well-studied in schizophrenia (for review, see
found to be anosmic, in contrast with 16% of Doty 2003a, b). Deficits have been shown to be
patients with AD, and 6% of the healthy controls. of lesser magnitude than typically seen in AD and
The presence of smell loss was not found to be PD, progress with disease duration, and are most
associated with concurrent AD and DLB pathol- associated with negative symptoms of the disease.
ogy on autopsy. Subsequent studies confirmed In patients showing olfactory deficits, the impair-
anosmia to be more common in DLB than in ments appear early in the disease, perhaps in pro-
AD, with anosmia present in 56–65% of patients dromal stages. There does not appear to be any
with DLB (and some degree of smell loss in notable relationship with antipsychotic medication
nearly 90%), but in only 11–23% of AD patients use or cigarette smoking. Odor identification deficits
(Olichney et al. 2005; Westervelt et al. 2003). correlate most strongly with measures of executive
Assessment of anosmia has been shown to functioning in this population, rather than those of
improve the sensitivity of diagnostic criteria for medial temporal lobe functioning. All aspects of
DLB, with minimal loss of specificity (Olichney olfaction appear to be impaired (i.e., identification,
et al. 2005). Combined, these few studies raise the threshold, discrimination, and memory).
Anosmia 247

Evaluation (somatosensory ERPs). Absence of olfactory

ERPs in presence of somatosensory ERPs sug-
Clinical History gests olfactory deficits. These measures are sensi- A
Obtaining a detailed clinical history is critical in tive to age and gender effects. Chemosensory
assessing olfactory deficits. Symptoms should be evoked potentials are unable to discern where
clearly defined, and the clinician should attempt to the impairment is within the olfactory pathway,
determine the extent and duration of the perceived but are considered among the only objective ways
loss, as well as the occurrence of any event asso- of establishing smell loss.
ciated with the deficit (e.g., head injury, illness).
Fluctuations in symptoms may be most suggestive Psychophysical
of obstructive causes, but need to be distinguished Psychophysical methods are the most commonly
from paroxysmal events. Medical history should used assessment practices in both clinical and
be carefully assessed, as multiple medical condi- research settings. In these techniques, stimuli are
tions and medications may be associated with presented, and the patient or participant reports
olfactory alterations. Referral for an ENT evalua- their perception (detection, discrimination, identi-
tion may be warranted. Olfactory hallucinations, fication); this category can be further sub-divided
in particular, require careful work-up as they may into threshold and suprathreshold tasks.
be indicative of seizure or tumor, and are less
likely of primary psychiatric origin. Threshold Testing Threshold testing is used to
determine at what concentration a patient or par-
Classes of Assessment ticipant can accurately detect the presence of an
There are three classes of olfactory assessment odor. Two methods have been developed to deter-
methods: psychophysical, electrophysiological, mine this threshold: the method of limits proce-
and psychophysiological, with psychophysical dure and the single staircase procedure. In the
assessment being the most common and most method of limits procedure, a low concentration
clinically relevant. of a specific odor is presented, and the concentra-
tion is increased until it can be detected. In the
Psychophysiological single staircase procedure, the concentration is
Psychophysiological assessment of olfactory abil- increased following trials in which the participant
ities relies on the measurement of changes in the cannot detect the odor, and decreased following
autonomic nervous system after presentation of an correct detection. There are commercially avail-
odorous stimuli, through such methods as heart able smell threshold tests, for example, using felt-
rate and blood pressure. These methods are tipped pens and squeeze bottles. Olfactometers
rarely used. can be used to present precise amounts of odorants
through constant airflow. However, many of these
Electrophysiological techniques can be cumbersome for clinical use.
Electrophysiological assessments examine elec-
trical activity generated in response to an odorant Suprathreshold Tasks Suprathreshold tasks
and are primarily research tools. Electro- include rating scales/magnitude estimation scales,
olfactograms (EOG) use electrodes placed on the odor identification tasks, and odor memory/rec-
human olfactory epithelium to directly assess ognition tasks. When using rating scales, the par-
olfactory abilities. Olfactory event-related poten- ticipant rates the amount of the attribute perceived
tials (ERP) are recorded from the scalp surface, (e.g., pleasantness); these may include category
measuring electroencephalographic activity after scales (which category describes sensation) and
presentation of brief, precisely defined odorous line scales (placement of mark on line with
stimuli. For example, chemosensory ERP’s can descriptors). When using a magnitude estimation
be obtained after stimulation of olfactory nerve scales, a participant will assign a number to stim-
(olfactory ERPs) or the trigeminal nerve uli in relation to relative intensity.
248 Anosmia

Odor Identification Tasks Odor identification or an odor, while wearing a nasal cannula
tasks also suprathreshold tasks, require partici- connected to a device to measure the negative
pants to identify odors, often by presenting pressure created by the sniff. The test is quick to
scratch-and-sniff items, tinctures in jars, or administer (about 5 min) and has minimal, if any,
odorant-soaked tampons. These tasks almost reliance on cognition, linguistic ability, and famil-
invariably include multiple choice options, as iarity of odors.
odor identification is otherwise extremely chal-
lenging even for individuals with intact olfactory Neuroimaging Imaging, particularly MRI, is
abilities. These tasks are easy to administer and clearly important for identification of structural
the most frequent type of task used in clinical lesions that may be impinging on the olfactory
settings, but can be somewhat costly depending system, or in assisting in diagnosis of other neu-
on the task. The most widely used odor identifica- rologic disorders that may account for smell loss.
tion task is the University of Pennsylvania Smell CT is frequently used in identifying sinonasal
Identification Task (UPSIT), which consists disease. MRI can also be useful in evaluating
40 micro-encapsulated odorants presented in a changes in olfactory bulb volume due to viral,
4-option, multiple choice format. Other, briefer traumatic, or idiopathic olfactory dysfunction,
measures include 12-item versions (e.g., Cross- with good relationship demonstrated between
Cultural Smell Identification Test/Brief Smell Iden- objective olfactometry (with chemosensory
tification Test (BSIT), the BSIT-A designed espe- evoked potentials) and bulb volume. Functional
cially for AD, the BSIT-B designed especially for scans, in particular fMRI and PET, are also often
PD) and a 3-item screen (Pocket Smell Test). The used as research tools in studying the functional
UPSIT and BSIT both have associated norms. organization of olfaction. These studies have
Sniffin’ Sticks includes both a threshold task and shown involvement in the amygdala, piriform cor-
an odor identification task, and is extensively tex, OFC, insula, anterior cingulate, thalamus, cau-
normed in European samples (Hummell et al. 2007). date, subiculum, upper pons, and cerebellar vermis,
with different activation patterns depending on the
Odor Memory Test Odor memory test involve nature of the task (e.g., sniffing, smelling single
having the individual smell an odor (or group of odors, discrimination, identification, etc.).
odors), and after a specified period of time, rec-
ognize the odor from a set of distracters. Often,
novel, non-descript odors are utilized to minimize Treatment
the ability to label, and interference tasks are
introduced during delays to minimize rehearsal Treatment is most promising in patients with
of the odor labels/qualifiers. smell loss associated with conduction problems.
For example, antibiotic treatment, steroids, and
Other Olfactory Assessment Tools allergy management may be helpful in reducing
deficits associated with inflammatory disease.
The Sniff Magnitude Test Surgical removal of other obstructions, such as
The sniff magnitude test is a recently developed nasal polyps, can also be effective in restoring
clinical measure of olfaction based on the reflex- olfactory ability. In contrast, treatment of sensori-
like reduction in sniffing that occurs in response to neural/central neural problems is often less effec-
detection of odors (especially unpleasant odors), tive. Exceptions may include resection of tumors
but does not occur when sniffing non-odorized air impinging on the olfactory system and, in some
(Frank et al. 2003). This response is observed in cases, resection of epileptogenic foci associated
people with normal sense of smell, but is absent in with olfactory seizures. Iatrogenic effects of med-
those with anosmia. The task involves having the ications are typically reversible with discontinua-
patient sniff a canister that releases either a blank tion of the medication and eventual improvement
Anosmia 249

in smell is expected after cessation of smoking. Frank, R. A., Dulay, M. F., & Gestland, R. C. (2003). Assess-
Recent work also suggests that olfactory training ment of the sniff magnitude test as a clinical test of
olfactory function. Physiology & Behavior, 78, 195–204.
may improve olfaction in some patients (Hummel Gotfried, J. A., & Zald, D. H. (2005). On the scent of A
et al. 2009). Zinc or vitamin therapies are at times human olfactory orbitofrontal cortex: Meta-analysis
prescribed to treat olfactory loss, but there is little and comparison to non-human primates. Brain
evidence of benefit in the absence of associated Research Brain Research Reviews, 50, 287–304.
Gray, A. J., Staples, V., Murren, K., Dhariwal, A., &
deficiencies. Typically, the more severe and long- Bentham, P. (2001). Olfactory identification is impaired
standing the smell loss, the less likely recovery is in clinic-based patients with vascular dementia and
in sensorineural/central neural disorders. Espe- senile dementia of the Alzheimer type. International
cially for individuals who do not respond to treat- Journal of Geriatric Psychiatry, 16, 513–517.
Hummel, T., Rissom, K., Reden, J., Hähner, A.,
ment, education about the safety implications of Weidenbecher, M., & Hüttenbrink, K. B. (2009).
smell loss is important, given concerns of the Effects of olfactory training in patients with olfactory
patient’s failure to detect hazardous odors (e.g., loss. Laryngoscope, 119, 496–499.
smoke) or spoiled food. Nutritional status may Hummell, T., Kobal, G., Gudziol, H., & Mackay-Sim, A.
(2007). Normative data for the “sniffin’sticks” includ-
also be compromised in patients with olfactory ing tests of odor identification, odor discrimination, and
deficits, and use of flavor enhancements in foods olfactory thresholds: An upgrade based on a group of
can be helpful in improving food intake more than 3000 subjects. European Archives of Otorhi-
(Schiffman 2000). nolaryngology, 264, 237–243.
Knupfer, L., & Spiegel, R. (1986). Differences in olfactory
test performance between normal aged, Alzheimer and
vascular type dementia individuals. International
Cross-References Journal of Geriatric Psychiatry, 1, 3–14.
Luzzi, S., Snowden, J. S., Neary, D., Coccia, M., Provinciali,
▶ Cranial Nerves L., & Lambon Ralph, M. A. (2007). Distinct patterns of
olfactory impairment in Alzheimer’s disease, semantic
▶ Olfaction
dementia, frontotemporal dementia, and corticobasal
▶ Olfactory Bulb degeneration. Neuropsychologia, 45, 1823–1831.
▶ Olfactory Tract McLaughlin, N., & Westervelt, H. J. (2008). Odor identi-
fication deficits in frontotemporal dementia:
A preliminary study. Archives of Clinical
Neuropsychology, 23, 119–123.
References and Readings McShane, R. H., Nagy, Z., Esiri, M. M., King, E.,
Joachim, C., Sullivan, N., et al. (2001). Anosmia in
Costanza, R. M., DiNardo, L. J., & Reiter, E. R. (2003). dementia is associated with Lewy bodies rather than
Head injury and olfaction. In R. L. Doty (Ed.), Hand- Alzheimer’s pathology. Journal of Neurology,
book of olfaction and gustation (2nd ed.). New York: Neurosurgery, and Psychiatry, 70, 739–743.
Marcel Dekker. Mesholam, R. I., Moberg, P. H., Mahr, R. N., & Doty, R. L.
Devanand, D. P., Michaels-Marston, K. S., Liu, X., Pelton, (1998). Olfaction in neurodegenerative disease. A meta-
G. H., Padilla, M., Marder, K., et al. (2000). Olfactory analysis of olfactory functioning in Alzheimer’s and
deficits in patients with mild cognitive impairment pre- Parkinson’s diseases. Archives of Neurology, 55, 84–90.
dict Alzheimer’s disease at follow-up. American Murphy, C., Schubert, C. R., Cruickshanks, K. J.,
Journal of Psychiatry, 157, 1344–1405. Klein, B. E., Klein, R., & Nondahl, D. M. (2002).
Devanand, D. P., Tabert, M. H., Cuasay, K., Manly, J. J., Prevalence of olfactory impairment in older adults.
Schupf, N., Brickman, A. M., et al. (in press). Olfactory Journal of the American Medical Association,
identification deficits and MCI in a multi-ethnic elderly 288, 2307–2312.
community sample. Neurobiology of Aging. Murphy, C., Doty, R. L., & Duncan, H. J. (2003). Clinical
Doty, R. L. (2003a). Odor perception in neurodegenerative disorders of olfaction. In R. L. Doty (Ed.), Handbook of
diseases. In R. L. Doty (Ed.), Handbook of olfaction olfaction and gustation (2nd ed.). New York: Marcel
and gustation (2nd ed.). New York: Marcel Dekker. Dekker.
Doty, R. L. (Ed.). (2003b). Handbook of olfaction and Olichney, J. M., Murphy, C., Hofstetter, C. R., Foster, K.,
gustation (2nd ed.). New York: Marcel Dekker. Hansen, L. A., Thal, L. J., et al. (2005). Anosmia is very
Doty, R. L., & Bromley, S. M. (2004). Effects of drugs on common in the Lewy body variant of Alzheimer’s
olfaction and taste. Otolaryngologic Clinics of North disease. Journal of Neurology, Neurosurgery, and
America, 37, 1229–1254. Psychiatry, 76, 1342–1347.
250 Anosodiaphoria

Pardini, M., Huey, E. D., Cavanagh, A. L., & condition is known as anosognosia. With time,
Grafman, J. (2009). Olfactory function in corticobasal patients typically show increased awareness of
syndrome and frontotemporal dementia. Archives of
Neurology, 66, 92–96. the deficit. For example, if asked, they might
Schiffman, S. S. (2000). Intensification of sensory proper- acknowledge that a stroke has occurred and that
ties of food for the elderly. Journal of Nutrition, their ability to use their arm or leg has been
130, 9275–9305. affected. However, the patient might fail to fully
Smutzer, G. S., Doty, R. L., Arnold, S. E., &
Trojanowski, J. Q. (2003). Olfactory system neuropa- appreciate the extent or functional implications of
thology in Alzheimer’s disease Parkinson’s disease, the deficit, attribute it to another more benign
and schizophrenia. In R. L. Doty (Ed.), Handbook of factor (such as being right-handed), or otherwise
olfaction and gustation (2nd ed.). New York: Marcel appear relatively unconcerned about it. This latter
Dekker.
Upadhyay, U. D., & Holbrook, E. H. (2004). Olfactory loss condition has been termed anosodiaphoria (Adair
as a result of toxic exposure. Otolaryngologic Clinics of et al. 2003; Critchley 1969). Thus, while acknowl-
North America, 37, 1185–1207. edging that his arm and/or leg are/is “weak,” a
Westervelt, H. J., Stern, R. A., & Tremont, G. (2003). Odor patient may talk about his plans to return to work
identification deficits in diffuse Lewy body disease.
Cognitive and Behavioral Neurology, 16, 93–99. in the near future, although that may be totally
Westervelt, H. J., Bruce, J. M., Coon, W. G., & unrealistic, given the severity of his condition and
Tremont, G. (2008). Odor identification in mild cogni- the nature of his work. There does not appear to be
tive impairment subtypes. Journal of Clinical and any clear consensus as to the etiology of this
Experimental Neuropsychology, 30, 151–156.
Wilson, R. S., Schneider, J. A., Arnold, S. E., Tang, Y., condition, the level of denial of which might be
Boyle, P. A., & Bennett, D. A. (2007). Olfactory iden- seen to vary from one day to the next. The more
tification and incidence of mild cognitive impairment in common hypotheses are that the anosodiaphoria
older age. Archives of General Psychiatry, likely reflects the same type of neglect or inatten-
64, 802–808.
tion that results in the original anosognosia, only
less severe, is a result of a general emotional
flattening or indifference that can follow right
hemispheric lesions, or a combination of the two
Anosodiaphoria (Heilman et al. 2003).

John E. Mendoza
Department of Psychiatry and Neuroscience,
Tulane Medical School and SE Louisiana Cross-References
Veterans Healthcare System, New Orleans, LA,
USA ▶ Anosognosia
▶ Denial

Definition
References and Readings
Anosodiaphoria is defined as the failure to fully
appreciate the significance of a neurological def- Adair, J. C., Schwartz, R. L., & Barrett, A. M. (2003).
Anosognosia. In K. Heilman & E. Valenstein (Eds.),
icit as a result of a brain lesion. Clinical neuropsychology (4th ed., pp. 185–214).
New York: Oxford University Press.
Critchley, M. (1969). The parietal lobes. New York:
Current Knowledge Hafner.
Heilman, K. M., Blonder, L. X., Bowers, D., & Valenstein, E.
(2003). Emotional disorders associated with neurological
Following certain injuries to the brain, most com- diseases. In K. M. Heilman & E. Valenstein (Eds.),
monly strokes in the right hemisphere, a patient Clinical neuropsychology (4th ed., pp. 447–478).
may fail to recognize (deny) the resulting neuro- New York: Oxford University Press.
Prigatano, G. P., & Schacter, D. L. (Eds.). (1991). Aware-
logical deficit(s), such as paralysis. This latter ness of deficit after brain injury. Oxford: New York.
Anosognosia 251

with Korsakoff’s amnesic disorder are unaware of

Anosognosia their memory loss, and aphasic patients such as
those with Wernicke’s aphasia appear to be A
Kenneth M. Heilman unaware of their jargon speech.
Department of Neurology, University of Florida
College of Medicine, Center for Neurological
Studies and the Research Service of the Malcom Current Knowledge
Randall Veterans Affairs Medical Center,
Gainesville, FL, USA Although of great academic interest, the presence
of anosognosia or anosodiaphoria has important
medical implications. For example, there are now
Synonyms treatments for stroke that must be given within
hours of the onset of symptoms. The patients who
Self-awareness are unaware of their disabilities or undervalue
their importance might not seek immediate med-
ical attention. In addition, people who have dis-
Definition abilities but are not aware of these disabilities
might inadvertently injure themselves and/or
Anosognosia is a disorder characterized by denial others. Rehabilitation works best, when patients
of illness or lack of awareness of disability. are strongly motivated to get well. When a person
is either unconcerned or unaware of their disabil-
ities, they are not motivated, and unmotivated
Historical Background patients are less likely to benefit from these treat-
ments. They might even refuse to undergo reha-
In the clinic, it is very common to see patients who bilitation, and they might not take their
suffer with a neurological disease, such as stroke, medications that can reduce their disability or
but who appear to deny illness or be unaware of possibly prevent further possible brain damage.
their disabilities. Seneca, the Stoic philosopher,
noted this about 2000 years ago, but the first mod- Possible Mechanisms of Anosognosia for
ern description of a patient with unawareness- Hemiplegia
denial was by von Monakow (1885). Although Patients with hemispheric strokes often develop
there were other investigators who wrote about an inability to use the arm-hand on the
this striking disorder, it was Babinski (1914), who contralesional side of their body (hemiparesis).
coined the term anosognosia. This word comes Many of these patients will be unaware of their
from three roots: a = without, noso = disease, weakness and when asked about the presence of
and gnosis = knowledge. In addition to describing weakness, they will deny this disability. Several,
patients who were unaware of their illness or dis- not mutually exclusive, mechanisms have been
ability, Babinski described other patients who used to explain this phenomenon.
appeared to be aware but remained unconcerned.
He called this disorder, anosodiaphoria. Psychological Denial Weinstein and Kahn
There are many forms of anosognosia and (1955) who brought modern attention to this syn-
these forms are related to the nature of a patient’s drome posited that for many people having a
disability. When Babinski first used this term, the stroke with weakness was a psychologically
patients he described denied or were unaware of traumatic event, and the means by which some
their hemiparesis. Anton (1898) described people deal with this trauma is to use psycho-
patients who were unable to see because they logical denial. To test this hypothesis, Weinstein
had destroyed their primary visual cortex but and Kahn studied patients who had anosognosia
were unaware or denied their blindness. Patients and found that even before their stroke, these
252 Anosognosia

patients frequently used this denial defense these strategies many, but not all, patients still
mechanism. denied weakness of that hand. Thus, a failure of
Some investigators have noted that anosognosia feedback can only explain anosognosia in some
for hemiplegia is more often associated with a left patients. In support of this postulate, several inves-
than right hemiparesis. The psychological denial tigators have reported dissociations between the
theory of anosognosia cannot explain this asym- presence of spatial neglect and anosognosia.
metry. Many patients with left hemisphere injury,
however, are aphasic and have problems with both Asomatognosia Hypothesis While patients with
the comprehension of questions (What is wrong personal neglect might be unaware of the parts of
with you? Are you weak?) as well as speaking- their body, patients with asomatognosia do not
answering questions. Thus, Weinstein and Kahn feel or claim that certain body parts belong to
thought what appeared to be a hemispheric asym- them. It has been posited that asomatognosia is
metry was induced by a sampling bias. caused by the alteration of the brain’s representa-
Using selective hemispheric anesthesia (the Wada tion of the body, a body schema. Like spatial and
study) and questioning the patient after they recover personal neglect, asomatognosia is more com-
from anesthesia revealed that unawareness of the monly associated with right than left hemisphere
hemiplegia (anosognosia) was more common with lesions. If patients with right hemisphere injury do
the right than left hemisphere anesthesia (Gilmore not believe their left arm-hand belongs to them,
et al. 1992). After the selective hemispheric anesthe- they will not recognize their own weakness. Dur-
sia has worn off, there is no aphasia or a need for ing right hemispheric anesthesia, the patients with
psychological denial. The right-left hemisphere left hemiplegia were shown their left hand or
asymmetries found were within subjects, and thus someone else’s left hand in a restricted view box
premorbid personality can also not account for this that projected to their right visual field. The
asymmetry. Although this study suggests that denial patients were asked if the hand they were viewing
cannot entirely explain anosognosia for hemiplegia, was their own or another person’s hand. We found
denial might be used by many people to help deal that there were some patients who had
with diseases and disabilities. anosognosia who also had asomatognosia, but
only a small proportion. Thus, asomatognosia
Failure of Feedback To know something is can also not fully account for this disorder.
impaired, a person requires feedback. Many
investigators have suggested that it is a failure of Disconnection Hypothesis When a patient with a
feedback, induced by either sensory loss (e.g., complete callosal disconnection receives a stimu-
proprioception and hemianopia) or inattention lus to the left visual field or on the left side of the
neglect, spatial or personal, that accounts for body and is asked to tell the examiner the nature of
anosognosia of hemiplegia. That inattention the stimulus, the left language-speech hemisphere
neglect that is more commonly associated with often confabulates a response. Geschwind (1965)
right hemisphere injury might also account for noted that large right hemisphere lesions can both
the asymmetries of anosognosia. injure the right hemisphere’s cortex and
Studies from our laboratory have revealed when intrahemispheric networks, as well as induce an
undergoing selective right hemisphere anesthesia, interhemispheric disconnection. Thus, when
during the time these patients demonstrate shoulder asked about weakness, the left hemisphere which
weakness, their shoulder proprioception is intact. is disconnected from the right will confabulate a
To learn if this disorder could be related to neglect, response – “I am not weak.” The observation
spatial or personal, we brought their hemiplegic left mentioned above, where during the right hemi-
forelimb over to the right side of their body and to sphere anesthesia the patient’s left hand is brought
their right visual field. To make certain subjects see over to the right visual field and thus has access to
their hand, we wrote a number on their hand, and the left language-speech-dominant hemisphere,
subjects were able to read these numbers. Despite also tests this disconnection hypothesis. As
Anosognosia 253

mentioned, in few patients when their arm could weakness. Electromyographic studies have also
be visualized in the right visual field, they did provided evidence in support of this akinesia
recognize their weakness. In these cases, we can- hypothesis. A
not be sure if their anosognosia was induced by a
failure in feedback or a disconnection. Future Summary Based on the above discussion, it
research will have to learn if these mechanisms appears that several mechanisms might contribute
can be dissociated. However, as mentioned above, to the presence of anosognosia for hemiplegia.
this procedure only helps a small minority of
patients. Possible Mechanisms of Anosognosia for
Amnesia and Cortical Blindness
Phantom Movements Limb amputation is often Damage to three interconnected brain networks can
associated with a perception that the limb is still produce amnesia, an impairment in the episodic
present, and this perception is thought to be memory system: (1) the medial temporal lobe –
related to the continued presence of a brain repre- Papez circuit (e.g., hippocampus, entorhinal and
sentation of that missing phantom limb. When perirhinal cortex, fornix, the mammillary bodies,
patients with a hemiparesis are asked to move a the mammillothalamic tract, the anterior thalamus,
limb, many often perceive that the paretic limb is and the retrosplenial cortex); (2) the dorsomedial
moving, and this phantom movement in combina- thalamus; and (3) the basal forebrain (medial septal
tion with impaired feedback might account for nucleus and the diagonal band of Broca), which
anosognosia. During selective hemispheric anes- provide acetylcholine to the hippocampus. Amnesic
thesia (Wada test), we had blindfolded subjects patients with medial temporal lesions are often
with left hemiplegia attempt to raise their paretic aware of their disability, and patients with damage
left arm, and we then asked them to raise their to the basal forebrain and to the medial thalamus are
right (non-paretic) arm to the same level as they often unaware of their memory deficit.
perceived the left arm. Some of the patients we The reason for this dichotomy is not fully
tested did raise their right arm, suggesting that known, but the dorsomedial thalamic nucleus is
they had phantom movements, but we found no heavily connected with the frontal lobes, and
significant relationship between phantom move- damage to this dorsomedial nucleus induces fron-
ments and anosognosia. tal dysfunction. Damage to the basal forebrain is
also often associated with frontal dysfunction.
Intentional Motor Disorder Patients with right Frontal lobe dysfunction is often associated with
hemisphere lesions often demonstrate contralesional impaired recall but not recognition, suggesting
limb akinesia also called motor neglect. Many of that the problem is not with the consolidation of
these patients do not attempt to spontaneously move memories but rather retrieval. The patients with
their akinetic arm, and while less common some amnesia from a thalamic or basal forebrain injury
do not even attempt to move this arm to com- more often confabulate memories than do those
mand. Limb akinesia can occur both with and with medial temporal lobe damage. Since these
without a hemiplegia. Patients with limb patients retrieve memories and have no means of
akinesia might not discover that they are weak testing these memories’ veracity, they might be
because they do not attempt to move this left unaware that their recall is incorrect, and therefore
arm. If they do not attempt to move this arm, they might be unaware of their memory disorder.
they will not experience a dissociation between
their expectations and performance, and it is this Blindness Patients with Anton’s syndrome have
dissociation that alerts people that there is a blindness from damage to their primary visual
problem. Providing external motivation such as cortex, usually from stroke. These patients often
suggestions or commands might entice patients deny their blindness, confabulate responses, and
to attempt a movement, and with these com- are unaware they are blind, anosognosic. The rea-
mands some patients do discover their son why these patients are not aware of their
254 Anoxia

blindness is not known. We examined a patient and to initiate behaviors. Future research is
with Anton’s syndrome who had intact visual needed. In addition to continuing to define and
imagery. Perhaps since these patients have intact test possible mechanisms, effective treatments for
visual imagery and cannot receive visual input, these disorders are needed.
this imagery is mistaken for online input.

Possible Mechanisms for Unawareness of Cross-References

Aphasia
Patients with Wernicke’s aphasia speak in jargon, ▶ Attention
cannot comprehend, name, or repeat. Many are not ▶ Consciousness
aware that they are aphasic and that they are speak- ▶ Impaired Self-Awareness
ing in jargon. For example, we saw a patient, who,
when speaking jargon, became angry when he was
not understood. It has been posited that Wernicke’s References and Readings
aphasia is induced by injury to the phonological
lexicon – a store of learned word sounds. To be Anton, G. (1898). Blindheit nach beiderseitiger
Gehirnerkrankung mit Verlust der Orienterung in
aware that an error has been made, a person needs to
Raume. Mitt. Ver. Arzte Steirmark, 33, 41–46.
have a normal representation of the targeted behav- Babinski, J. (1914). Contribution à l’etude des troubles
ior. Since patients with Wernicke’s aphasia have mentaux dans l’hémiplégie organique cérébrale
destroyed their representations of word sounds (anosognosie). Revue Neurologique, 27, 845–847.
Clare, L., & Halligan, P. (Eds.). (2006). Pathologies of
when they speak jargon, they have no representa-
awareness: Bridging the gap between theory and prac-
tions with which to compare their speech and are tice. New York: Psychology Press.
thus unaware of their errors. Geschwind, N. (1965). Disconnexion syndromes in ani-
We have also reported patients who appear to mals and man. Brain, 88(237–294), 585–644.
Gilmore, R. L., Heilman, K. M., Schmidt, R. P., Fennell,
have an intact input lexicon (e.g., can understand E. M., & Quisling, R. (1992). Anosognosia during
speech) but who make phonological errors and are Wada testing. Neurology, 42, 925–927.
not aware that they made these errors. If these Prigatano, G. P., & Schacter, D. L. (1991). Awareness of
patients’ speech is recorded and played back to deficit after brain injury: Clinical and theoretical
issues. New York: Oxford University Press.
them, they do detect their errors, suggesting that
von Monakow, C. (1885). Experimentelle und pathologisch-
their unawareness might have been related to not anatomische Untersuchungen über die Beziehungen der
being able to closely attend to their output. These sogenannten Sehphäre zu den infrakorticalen
aphasic patients might have focused their atten- Opticuscentren und zum N. opticus. Archiv für
Psychiatrie und Nervenkrankheiten, 16, 151–199.
tion on what they were attempting to say rather
Weinstein, E. A., & Kahn, R. L. (1955). Denial of illness:
than how they said it. Symbolic and physiological aspects. Springfield:
Charles C. Thomas.

Future Directions

Anosognosia, the failure to recognize a disease or Anoxia

a disability, might delay treatment, interfere with
rehabilitation, and put people in danger. Patients Bruce J. Diamond
might be anosognosic for a variety of neurological Department of Psychology, William Paterson
disorders such as weakness, sensory loss, personal University, Wayne, NJ, USA
and spatial neglect, memory loss, and aphasia.
There appears to be a variety of mechanism that
might account for anosognosia including psycho- Synonyms
logical denial, impaired and false feedback, alter-
ations of the body schema, failures to test systems, Severe hypoxia; Severe oxygen deficiency
Anoxia 255

Definition Neuropsychological and Psychological

Outcomes
Hypoxia refers to a decrease in oxygen supply A
rather than a complete loss of oxygenation Anoxia can result in impairments in anterograde
(Jones 2015). Anoxia refers to an extreme hyp- memory which in its most severe form may man-
oxia or deficiency in the oxygenation of the ifest as an amnestic disorder. Presenting symp-
arterial blood of sufficient severity to result in toms may also include impairments in awareness
permanent neurologic damage (Webster 2006). and affect as well as confabulatory behavior.
This vulnerability to severely reduced oxygen- Anoxia associated with cardiac arrest may include
ation is based on the fact that the brain has little amnesia, in addition to bibrachial paresis, cortical
to no reserve of oxygen or glucose, conse- blindness, and visual agnosia. Carbon monoxide
quently an anoxic episode of 4–6 min can result poisoning may be associated with affective and
in neuronal cell death or necrosis because of cognitive disturbances associated with anoxia-
impairment in cellular metabolism (Zillmer induced dysfunction (Aminoff et al. 2005). Vul-
and Spiers 2001). nerability to cognitive impairments in response to
decreased arterial oxygenation is supported by the
finding that experimental induction of hypoxia in
Etiology healthy subjects showed decrements of 10–36%
in neurocognitive processes that are vulnerable to
Anoxia can result from a number of conditions oxygen deprivation including verbal and visual
including cardiac arrest, carbon monoxide poi- memory, processing speed, executive function
soning, stroke, brain injury, and complications psychomotor speed, reaction time, complex atten-
due to anesthesia. It is thought that cells exposed tion, and cognitive flexibility (Turner et al. 2015).
to anoxia release glutamate. The CA1 cells of the
hippocampus contain high concentrations of glu-
tamate and are particularly vulnerable to subnor-
Cross-References
mal oxygenation levels. Therefore, it appears
that the action of glutamate on these cells is the ▶ Carbon Monoxide Poisoning
putative mechanism mediating cell death in this
▶ Glutamate
region of the hippocampus and helps explain
▶ Hippocampus
many of the signs and symptoms associated
with anoxia (Bonner and Bonner 1991). The
decreased oxygenation seen in hypoxia may be
References and Readings
caused by airway obstruction, apnea, lung col-
lapse, medication side effects, anemia, and heart Aminoff, M. J., Simon, R. P., & Greenberg, D. A. (2005).
failure (Auday et al. 2014). Clinical neurology. New York: McGraw-Hill.
Auday, B. C., Buratovich, M. A., Marrocco, G. F., &
Moglia, P. (Eds.). (2014) Salem health Magill’s medical
guide (7th ed., p. 1188). Ipswich: Grey House
Signs and Symptoms Publishing
Bonner, J. S., & Bonner, J. J. (1991). The little black book
Mild cerebral hypoxia may include the symptoms of of neurology: A manual for neurologic house officers
(2nd ed.). St Louis: Mosby-Year Book.
inattentiveness, poor judgment, memory loss, and a
Cavendish, M., Bernabeo, P., Esposito, M. (2008). Dis-
decrease in motor coordination (NINDS 2015), eases and disorders (1st ed., pp. 121-122). Tarrytown:
while anoxia often results in impairments in memory, Marshall Cavendish Corporation.
executive, and motor function. Signs and symptoms Golden, C. J., Zillmer, E. A., & Spiers, M. V. (1992).
Neuropsychological assessment and intervention.
are likely attributable to damage to limbic and sub-
Springfield: Charles C. Thomas.
cortical regions, in addition to the frontal lobes and Jones, K. (Ed.) (2015). Brain disorders sourcebook
the cerebellum (Golden et al. 1992). (4th ed., pp. 3306-3307). Detroit: Omnigraphics Inc.
256 Anterior Cerebral Artery

NINDS. (2015). NINDS cerebral hypoxia information ACA is also part of the vasculature of the Circle of
page. National Institute of Neurologic Disorders and Willis, arising from trifurcations implicated by an
Stroke website. http://www.ninds.nih.gov/disorders/
anoxia/anoxia.htm. Updated 14 Feb 2014; Accessed anastomosis created by the ICAs (Vrselja et al.
29 May 2014. 2014). Thus, when blood supply from the ACA is
Turner, C. E., Barker-Collo, S. L., Connell, C. J., & Gant, N. impeded (anterior cerebral artery syndrome), symp-
(2015). Acute hypoxic gas breathing severely impairs tomatology varies with the degree and location of
cognition and task learning in humans. Physiology &
Behavior, 142, 104–110. restriction within the ACA (Vrselja et al. 2014).
Webster. (2006). Webster’s new explorer medical dictio-
nary (new edition). Springfield: Merriam-Webster.
Zillmer, E. A., & Spiers, M. V. (2001). Principles of neuro- Categories
psychology. Belmont: Wadsworth/Thomson Learning.

The ACA is structurally delineated by five distinct

segments, commonly referred to as segments
A1–A5. A1 branches from the ICA bifurcation
Anterior Cerebral Artery and extends to also entail the anterior communi-
cating artery (ACoA). The A2 segment extends
Bruce J. Diamond and Keith Happawana from the ACoA to the bifurcation forming the
Department of Psychology, William Paterson pericallosal and callosomarginal arteries.
University, Wayne, NJ, USA Heubner’s artery (which supplies the internal cap-
sule) usually arises at the beginning of A2 near the
ACoA. Branching from Heubner’s artery are the
Synonyms orbitofrontal artery (medial frontal basal) and the
frontopolar artery (polar frontal) (which rises after
ACA; Cerebral artery the orbitofrontal artery and is close to A2’s span
over the corpus callosum). A2 mimics the length
and contours of the genu and rostrum in the corpus
Definition callosum. A3, known as the pericallosal artery,
extends posteriorly in the pericallosal sulcus to
The anterior cerebral artery (ACA) arises as the form the internal superior and inferior parietal
medial branch of an anterior bifurcation of the arteries, as well as the precuneal artery (Lawton
internal carotid artery (ICA) at later embryonic and Mirzadeh 2012). The callosal marginal artery
stages of development (Menshawi et al. 2015). branches out from the pericallosal artery. A3 is
The ACA supplies the anterior four-fifths of the also known to form anastomoses with neighbor-
medial surface of the cerebral hemisphere, frontal ing arteries. A4 and A5 segments are also known
and parietal lobes, the anterior four-fifths of the as the supracallosal and postcallosal segments
corpus callosum, and a narrow strip of the superior, (respectively) and outline the body of the corpus
lateral surface of the cerebral hemisphere (Zhou callosum, the division between them being
et al. 2013), as well as the front portion of the located at the plane of the coronal suture
diencephalon (Rea 2015). Three major vascular (Lawton and Mirzadeh 2012).
areas supply the head of the caudate nucleus, i.e.,
Heubner’s artery, the anterior lenticulostriate arter-
ies (from the proximal section of the anterior cere- Medical, Neuropsychological, and
bral artery), and the lateral lenticulostriate arteries Psychological Symptoms
(from the middle cerebral artery) (Mizuta and
Motomura 2006). Various motor areas are supplied Infarctions in the territory of this artery are asso-
by the ACA including the supplementary motor ciated with a variety of clinical signs and symp-
complex, the anterior and middle cingulate cortex, toms including gait, limb sensation, abulia, lack of
and the rostral section of the corpus callosum. The spontaneous activity, urinary incontinence, and
Anterior Cingulate Cortex 257

frontal and memory impairments, in addition to (Eds.), Operative neurosurgical techniques, indica-
emotional dysregulation (apathy) (Brust 1995). tions, methods, and results (5th ed., pp. 882–896).
Philadelphia: Saunders/Elsevier.
Associated aneurysms are found relatively fre- Menshawi, K., Mohr, J. P., & Gutierrez, J. (2015). A
quently in patients with ACA variations (Uchino A functional perspective on the embryology and anat-
et al. 2006). The effects of ACA occlusion vary in omy of the cerebral blood supply. Journal of Stroke,
severity depending on if the recurrent artery of 17(2), 144.
Mizuta, H., & Motomura, N. (2006). Memory dysfunc-
Heubner is present. Spastic arms, flaccid legs, and tion in caudate infarction caused by Heubner’s recur-
brisk reflexes may occur if the Heubner artery is ring artery occlusion. Brain and Cognition, 61(2),
present. Blockage in the proximal segment can 133–138.
result in upper motor neuron pathology of the Rea, P. (2015). Blood supply of the brain and clinical
issues. In B. V. Elsevier (Ed.), Essential clinical anat-
face. If branches to the olfactory bulb and tract omy of the nervous system (pp. 99–119). London: Aca-
are affected, anosmia may result. Extensive ante- demic Press.
rior cerebral artery occlusion can affect micturi- Uchino, A., Nomiyama, K., Takase, Y., & Kudo, S. (2006).
tion. If occlusion affects blood flow to the frontal Anterior cerebral artery variations detected by MR
angiography. Neuroradiology, 48(9), 647–652.
lobe or corpus callosum, apathy may result. Less Vrselja, Z., Brkic, H., Mrdenovic, S., Radic, R., & Curic,
severe occlusions may only affect the lower limbs G. (2014). Function of circle of Willis. Journal of
with signs such as reduced sensation, lack of Cerebral Blood Flow and Metabolism, 34(4), 578–584.
power, up-going plantar reflexes, and brisk Vrselja, Z., Brkic, H., & Curic, G. (2016). Penetrating
arteries of the cerebral white matter: The importance
reflexes (Rea 2015). In ACA stroke cases, patients of vascular territories of delivering arteries and com-
may present with difficulties in performing voli- pleteness of circle of Willis. International Journal of
tional hand movements, while movements in Stroke, 11(3), NP36–NP37.
response to external stimuli are preserved. In the Zhou, X. Y., Chen, L., & Zhang, S. Q. (2013). Nonfluent
aphasia and cognitive impairment caused by anterior
chronic stage (median follow-up of 83.5 days), cerebral artery infarction. CNS Neuroscience & Thera-
improvements in the initiation of voluntary move- peutics, 19(12), 987–989.
ments may occur, although signs of disturbed
motor control may persist (Brugger et al. 2015).

Anterior Cingulate Cortex

Cross-References Ronald A. Cohen1,2 and
Anna MacKay-Brandt3,4
▶ Anterior Communicating Artery 1
Department of Clinical and Health Psychology,
College of Public Health and Health Professions,
University of Florida, Gainesville, FL, USA
References and Readings 2
Center for Cognitive Aging and Memory,
McKnight Brain Institute, University of Florida,
Arboix, A., García-Eroles, L., Sellarés, N., Raga, A.,
Gainesville, FL, USA
Oliveres, M., & Massons, J. (2009). Infarction in the 3
territory of the anterior cerebral artery: Clinical study of Nathan S. Kline Institute for Psychiatric
51 patients. BMC Neurology, 9(1), 30. Research, Orangeburg, NY, USA
Brugger, F., Galovic, M., Weder, B. J., & Kägi, G. (2015). 4
Taub Institute for Research on Alzheimer’s
Supplementary motor complex and disturbed motor
Disease and the Aging Brain, Columbia
control – A retrospective clinical and lesion analysis
of patients after anterior cerebral artery stroke. Fron- University, New York, NY, USA
tiers in Neurology, 6, 209.
Brust, J. C. M. (1995). Agitation and delirium. In
J. Bogousslavsky & L. Caplan (Eds.), Stroke syndromes
(pp. 134–139). Cambridge: Cambridge University Press. Synonyms
Lawton, M. T., & Mirzadeh, Z. (2012). Surgical manage-
ment of anterior communicating and anterior cerebral
artery aneurysms. In H. H. Schmidek & W. H. Sweet
ACC
258 Anterior Cingulate Cortex

Structure Connections between the ACC and the mesial,

ventral, and orbital frontal areas appear to be
The anterior cingulate cortex (ACC) is a meso- particularly important for emotional and behav-
cortical paralimbic area located anterior to the ioral regulation.
corpus callosum and posterior to the prefrontal
cortex. The ACC was once viewed as a single
limbic structure, forming an important part of the Function
“Papez” circuit, though in reality analysis of its
cytoarchitecture indicates that it consists of Current knowledge regarding the functions of
regions with different cell types. Its cell charac- the ACC has its origins in the psychosurgical
teristics are agranular and therefore are distinct efforts of the mid-twentieth century. At that
from the cortex. time, the role of the frontal lobes in emotion
The ACC encompasses several Brodmann and behavioral control were recognized, and
areas, including areas 24, 25, 32, and 33. The frontal lobotomy was experimented with as a
ACC wraps around the corpus callosum, having means of treating a variety of psychiatric condi-
the appearance of a collar or belt. In fact, the term tions, including severe depression and schizo-
cingulum means belt in Latin. A large volume of phrenia. While frontal lobotomy resulted in a
the ventral ACC consists of Area 24, which reduction in agitation and other severe psychiat-
merges with the posterior cingulate cortex (Area ric symptoms, surgical removal of the frontal
23) along the posterior half of the corpus lobe caused severe cognitive dysfunction.
callosum. The division between the ACC and Given that the orbital frontal region was consid-
posterior cingulate is undifferentiated to a large ered to be particularly important for the control
extent, though these areas can be separated based of impulses and emotional regulation, subse-
on the cortical layer IV in the posterior cingulate. quent psychosurgical approaches typically
Anterior to Area 24 is the subgenual cortex (Area restricted ablation to these areas, often through
25), which may be considered to be distinct from leukotomy. Unfortunately, patients undergoing
other ACC areas. Anterior to this region is the this procedure often exhibited marked personal-
dorsal ACC, including areas 32 and 33. The mid- ity change, with flattening of affect, apathy, and
anterior section of the ACC is often termed mid- other undesirable effects. A third generation of
cingulate (mACC), while the more posterior psychosurgical procedures ensued with efforts
section is termed perigenual cingulate (pACC). to target brain areas more selectively. The ACC
These areas have distinct cell characteristics, and was a point of focus because of its association
there is strong evidence of functional differences with both limbic areas as well as the frontal
across subareas of the ACC. cortex. Beginning in the late 1950s,
Primary afferent input to the ACC is received cingulotomy was developed as an alternative to
via axons from the midline and intralaminar frontal ablation. Early studies suggested that it
thalamic nuclei, with the anterior nucleus had few adverse cognitive effects and that it
receiving input from mamillary neurons, which seemed helpful for certain patients, particularly
in turn has projections from the subiculum. The those with intractable obsessive-compulsive
ACC is associated with a large white-matter symptoms, chronic pain, and opiate dependence.
bundle, the cingulum, through which signals There was also some evidence that it was helpful
are transmitted to other limbic areas. As a para- for patients with severe chronic depression,
limbic area, the ACC is a transition area between though the basis for these effects may relate to
subcortical and limbic structures, such as the reductions in emotional tension, obsessive
amygdala and cortical areas, most notably in thought processes, and other depression-
the frontal lobes. The posterior ACC has heavy associated problems.
input from the amygdala, whereas the mid-ACC Literature on the psychosurgical effects of
receives greater input from parietal areas. cingulotomy provided compelling evidence that
Anterior Cingulate Cortex 259

the ACC plays a role in human emotional experi- et al. 1999). Some cognitive neuroscientists
ence and regulation. Furthermore, there is also argue that conflict monitoring is the primary
evidence that the ACC influences autonomic ner- function of the ACC, though it seems likely that A
vous system response, including heart rate, blood this capacity is closely associated with the
pressure, and galvanic skin response, with these broader functions of regulation of drive, emotion,
responses showing alterations in the rate of habit- attention, and response intention; and selection,
uation following cingulotomy (Cohen et al. initiation, and persistence relative to situational
1994). Yet, most early studies of the effects of demands.
cingulotomy suggested that the ACC had little
impact on intellectual ability or most neuropsy-
chological functions. Postsurgery patients tended Illness
not to experience significant memory, language,
or visual change. Subsequent controlled studies Focal brain diseases affecting only the ACC are
indicated that while these functions are largely rare. However, the ACC is vulnerable to the
spared following cingulotomy, there are alter- effects of tumor, stroke, and other neurological
ations in some attention-related functions, most conditions involving anterior cortical infarction
notably attentional focus, intention, and response or mass action. Unilateral ablation of the ACC in
selection and control (Cohen et al. 2001). These laboratory studies of primates, and also secondary
changes correspond with reductions in emotional to stroke, has been shown to produce hemineglect
tension and distress and also a tendency for syndrome, providing further evidence that the
reduced self-initiation of behavior (Cohen ACC plays an important role in attention. There
et al. 2001). is evidence of ACC dysfunction secondary to
Recent experimental evidence suggests a atrophy associated with neurodegenerative condi-
functional dissociation between the posterior tions, such as Alzheimer’s disease, which may
and middle ACC. The mid-ACC plays a role in contribute to symptoms of apathy and behavioral
response selection and control, including inten- inertia in certain patients. However, these changes
tion and planning to act or to engage in cognitive are usually part of a much more global pattern of
operations. It has also been implicated in pro- brain abnormality.
cessing new motor programs, working memory, The ACC plays a more obvious role in psychi-
and mismatch detection. In contrast, the poste- atric illness and also the range of normal behavior.
rior ACC appears to play a more direct role in Activation of the ACC occurs in association with
emotional processing, though these areas are increased levels of distress and emotional tension
likely highly interconnected, enabling the inte- and anxiety. It also tends to be associated with
gration of emotional and attentional processes obsessive rumination and preoccupation with
(Bush et al. 2000). internal states and signals, such as pain and
Interest in the functional significance of ACC impulses to seek reward. Accordingly, the ACC
increased dramatically with the advent of func- has been implicated in substance abuse, including
tional neuroimaging methods. Activation of the opiate addiction and nicotine dependence.
ACC is evident across a wide range of tasks. In Citalopram binds to the serotonin transporter at
fact, it is among the most responsive areas of the very high levels in the posterior ACC, which may
brain on fMRI. This probably reflects the fact that account for the effects of this type of drug on
it plays an increased role when tasks require moti- reducing mood, anxiety, and pain symptoms.
vation and drive to complete and where there is There is also evidence that functional response
demand for attentional effort and focus. of the ACC varies as a function of risk-reward
The ACC plays a significant role in response dynamics, appetitive state, and motivation. Neu-
to the conflict during cognitive tasks associated roimaging studies have begun to point to its role in
with decision making and the need to resolve a variety of behavior problems, such as obesity
competing or discrepant information (Botvinick and inactivity.
260 Anterior Commissure

Cross-References

▶ Apathy
▶ Executive Functioning
▶ Psychotherapy

References and Readings

Ballentine Jr., H. T., Levey, B. A., Dagi, T. F., & Diriunas,

I. B. (1977). Neurosurgical treatment in psychiatry,
pain, and epilepsy. In W. H. Sweet, S. Obrador, &
J. G. Martin-Rodriques (Eds.), Cingulotomy for psychi-
atric illness: Report of 13 years experience
(pp. 333–353). Baltimore: University Park Press.
Botvinick, M., Nystrom, L. E., Fissell, K., Carter, C. S., &
Cohen, J. D. (1999). Conflict monitoring versus
selection-for-action in anterior cingulate cortex.
Nature, 402(6758), 179–181.
Bush, G., Luu, P., & Posner, M. I. (2000). Cognitive and
emotional influences in anterior cingulate cortex.
Trends in Cognitive Sciences, 4(6), 215–222.
Cohen, R. A., Kaplan, R. F., Meadows, M. E., & Wilkin-
son, H. (1994). Habituation and sensitization of the
orienting response following bilateral anterior
cingulotomy. Neuropsychologia, 32(5), 609–617. Anterior Commissure, Fig. 1
Cohen, R. A., Kaplan, R. F., Zuffante, P., Moser, D. J.,
Jenkins, M. A., Salloway, S., et al. (1999). Alteration of
intention and self-initiated action associated with bilat-
eral anterior cingulotomy. Journal of Neuropsychiatry Definition
and Clinical Neurosciences, 11(4), 444–453.
Cohen, R. A., Paul, R., Zawacki, T. M., Moser, D. J., A relatively small commissure in the basal fore-
Sweet, L., & Wilkinson, H. (2001). Emotional and
personality changes following cingulotomy. Emotion, brain lying above the optic chiasm and anterior to
1(1), 38–50. the main columns of the fornix that connects
Devinsky, O., Morrell, M. J., & Vogt, B. A. (1995). Con- homologous areas of the middle and inferior tem-
tributions of anterior cingulate cortex to behaviour. poral gyri, including parts of the olfactory cortices
Brain, 118(Pt. 1), 279–306.
(Fig. 1).

Anterior Commissure
Anterior Communicating
John E. Mendoza Artery
Department of Psychiatry and Neuroscience,
Tulane Medical School and SE Louisiana Bruce J. Diamond
Veterans Healthcare System, New Orleans, LA, Department of Psychology, William Paterson
USA University, Wayne, NJ, USA

Synonyms Synonyms

Interhemispheric commissure ACoA; Communicating artery

Anterior Communicating Artery 261

Description the basal forebrain region contains cholinergic

neurons that project to the hippocampus and
The anterior communicating artery (ACoA) inter- amygdala, via the medial forebrain bundle to the A
connects the two anterior cerebral arteries just entire cerebral cortex. Damage to this area would
rostral to the optic chiasm and resides at the ante- potentially interfere with cholinergic activation of
rior portion of the Circle of Willis. structures and circuits implicated in memory
Ruptured ACoA aneurysms may impact a vari- within the medial temporal lobe (Schnider and
ety of neurologic, neuropsychological, and psy- Landis 1995). Moreover, vascular compromise
chological functions. This may, in part, be due to of the perforating branches of the ACoA are
the fact that the perforating branches of the ACoA believed to adversely impact a variety of cognitive
supply the anterior hypothalamus, mesial anterior domains (e.g., executive function, memory, and
commissure, lamina termininalis, and areas impli- affect) that are innervated by these vascular
cated in executive function, memory, and affect branches. Personality changes following ACoA
(e.g., fornix and basal forebrain, septal nuclei, aneurysm are thought to result from frontal lobe
nucleus accumbens, diagonal band, and the dysfunction in the medio-basal zones along the
medial substantia innominata) (DeLuca and distribution of the anterior cerebral artery. The
Diamond 1995; Sawada and Kazui 1995). The subcallosal perforating artery (ScA) has been
profound memory disorders that can be associated implicated in personality changes and short-term
with ACoA aneurysm rupture do not appear to memory impairments with stroke in the vascular
directly involve neuroanatomic areas traditionally territory of the ScA associated with ischemia
implicated in amnesia, which makes the ACoA involving the anterior columns of the fornix and
artery of both clinical and theoretical interest. the genu of the corpus callosum (Meila et al.
2015). Neurocomputational models of hippocam-
pal function may also provide insight into possible
Etiology mechanisms of action mediating learning impair-
ments in ACoA aneurysm. One such model shows
ACoA aneurysms may develop as a result of that simulating the loss of acetylcholine in the
trauma, infections, degenerative diseases, or a hippocampal region (as in ACoA aneurysm)
congenital defect (Parkin and Leng 1993). Aneu- results in slower acquisition learning (Moustafa
rysms often become symptomatic as a result of et al. 2012).
subarachnoid hemorrhage (SAH) following rup-
ture (Riina et al. 2002). SAH has an overall inci-
dence of 10 to 16 per 100,000 and is a major cause Epidemiological Factors
of mortality and morbidity (Clinchot et al. 1994).
Rupture of cerebral aneurysms strikes at a mean
age of 50 years and accounts for 5–10% of all
Mechanisms strokes (Dombovy et al. 1998), and approximately
85–95% of all aneurysms develop at the anterior
Ruptured ACoA aneurysms alter the hemody- portion of the cerebral arterial supply, primarily at
namic circulation of the anterior portion of the the Circle of Willis (Adams and Biller 1992;
Circle of Willis, often resulting in cerebral infarc- Ropper et al. 2005). The ACoA is one of the
tion and impairments in cognition, personality, most common sites of cerebral aneurysm and is
and activities of daily living (ADL’s) (DeLuca the most frequent site of cerebral infarct following
and Diamond 1995; McCormick 1984). Damage aneurysm rupture (DeLuca and Diamond 1995;
to the basal forebrain region may account for McCormick 1984). About 30–40% of cerebral
many of the cognitive impairments that are aneurysms affect the ACoA artery and 90% of
observed in ACoA aneurysm due to the fact that cases are asymptomatic (Beeckmans et al. 1998;
262 Anterior Communicating Artery

Manconi et al. 2001). Various reports suggest that and the morphological characteristics of the
the incidence of rupture is highest between 40 and aneurysm). Comparisons of clipping versus endo-
70 years of age (McCormick 1984; Sethi et al. vascular embolization procedures have shown
2000) and that rupture occurs more frequently in that, in a number of studies, clipped patients
females (i.e., 60% of cases) (Adams and Biller have more severe cognitive impairments than
1992). Some work suggests that risk factors such embolization patients and that 33% of clipped
as age, gender, and no alcohol consumption influ- patients had impairments in memory and execu-
ence the site of the aneurysm. For example, men tive functioning (Chan et al. 2002). There is a
have ruptured aneurysms more often at the ACoA report of a complete third nerve palsy following
compared to the PCoA (Lindner et al. 2010). a ruptured ACoA aneurysm resulting from an
interpeduncular hematoma. The patient did, how-
ever, fully recover 3 months after the coiling pro-
Natural History, Prognostic Factors, and cedure (Balossier et al. 2012).
Outcomes Generally, the severity of cognitive impairment
has predictive value for functional status particu-
The risk of ACoA aneurysm formation appears to larly with respect to levels of required supervision
be determined by a number of independent risk at discharge (Saciri and Kos 2002). Some work
factors, including clinical, morphological, and suggests that recovery of executive function and
hemodynamic. That is, smoking, asymmetry of not short- and long-term memory may, in fact, be
A1 segments >40%, low blood flow pulsatility, the best predictor of the ability to return to work
and the angle between A1 and A2 segments  100 (DeLuca and Diamond 1995).
have been identified as the strongest independent
risk factors (Kaspera et al. 2014). Surgical and/or
endovascular procedures should pay special atten- Neuropsychological and Psychological
tion to the subcallosal perforating artery given its Outcomes
putative role in disturbances in cognition and per-
sonality.With respect to impairment and chronic- Neuropsychological
ity, acute ACoA patients are more impaired than It is generally concluded that verbal intellectual
chronic ones with differences most notable on skills, language functions, visuo-spatial skills, and
tests of executive and memory function. attention/concentration are within normal limits
Relationships between recovery of executive or only mildly impaired, although complex con-
function and temporal gradients in retrograde centration appears to be reduced in ACoA aneu-
amnesia have been reported, with improvements rysm. An increased sensitivity to interference may
in executive function accompanied by parallel be a defining feature among ACoA amnesics and
improvements in the severity of retrograde amne- between ACoA amnesics and diencephalic-mesial
sia. Improvement in the recall of complex visual- and temporal amnesics. More severe impairments
spatial information and an enhanced ability to are seen in delayed versus immediate memory and
benefit from an executive learning strategy have in executive function (DeLuca and Diamond
also been reported in the absence of improvement 1995). Impairments in spatio-temporal discrimi-
on traditional measures of memory or executive nation appear similar to other populations with
function (Diamond et al. 1997a). Recovery from frontal lobe dysfunction (Schacter 1987). Implicit
neuropsychological disturbances is generally memory involving data- and concept-driven
poorer in patients with ventral frontal lesion com- retrieval processes and behavioral and physiolog-
pared to those with basal forebrain and striate ical indices (Diamond et al. 1996) appear to be
lesions. relatively intact, although the evidence is sparse.
Surgical outcome and prognosis following Procedural memory on serial reaction time and
aneurysms depend on multiple factors (e.g., initial mirror-reading tasks also appears to be preserved.
clinical status, localization of aneurysm, age, Spatial working memory in ACoA patients has
Anterior Communicating Artery 263

been reported to be impaired, and the impairment impairment in source monitoring (Turner
profile is similar to patients with temporal lobe et al. 2010).
excisions. ACoA patients have displayed impair- Two distinct types of confabulation are gener- A
ments in semantic memory, and difficulties in both ally recognized in the literature, spontaneous and
the acquisition and recall of verbal information provoked (Kopelman 1987), and the key differ-
showing little initial learning, a passive learning ence between them is that in spontaneous confab-
style, a flat learning slope, and impaired recogni- ulation the confabulation guides actions.
tion discrimination, in addition to emitting a high Recovery from confabulation appears to parallel
number of intrusions and false positives improvement in temporal context confusion, and
(Diamond et al. 1997b). recovery can occur in the absence of significant
ACoA amnesics (i.e., with putative basal fore- improvement on traditional tests of memory and
brain damage) have exhibited impairments in executive function. Interestingly, while confabu-
delay eyeblink classical conditioning (Myers lation associated with ACoA aneurysm is well
et al. 2001), event-related potentials (ERPs), and known, a clinical condition known as
in prospective remembering. Discrimination, in “Phantabulation” was recently reported. It is char-
addition to emitting a high number of intrusions acterized by the purposeful interaction with con-
and false positives (Diamond et al. 1997b). While textually appropriate imagined objects. It was
semantic memory impairment is generally associ- hypothesized that that these episodes depended
ated with lesion of the anterior temporal lobe, on a combination of phenomena, including a
there is a recent case of a patient with severely top-down mechanism involving florid visual-
impaired semantic knowledge and anterograde imagery, facilitated by cortical release secondary
amnesia after bilateral ischemic lesion of the for- to frontal damage and enhanced by an associated
nix and of the basal forebrain following clipping malfunction of the fronto-parietal pathway
of an ACoA aneurysm. This appears to have been resulting in real and functionally appropriate
mediated by functional disconnection of the tem- imagined objects being confused (Cocchini
poral lobe and associated temporal hypo- et al. 2014).
metabolism as verified by PET imaging (Solcà With respect to psychosocial outcomes, a sig-
et al. 2015). ACoA patients have shown impair- nificant percentage of SAH survivors are left with
ments in information processing and autobio- cognitive, emotional, and behavioral changes that
graphical memory (especially for events can profoundly impact their daily lives. Compared
associated with context). ACoA amnesics (i.e., with controls, SAH patients display an increased
with putative basal forebrain damage) have incidence of mood disturbance, cognitive impair-
exhibited impairments in delay eyeblink classical ment, and lower levels of independence, and par-
conditioning (Myers et al. 2001), event-related ticipation on measures that reflect social
potentials (ERPs), and in prospective remember- functioning. Levels of productive employment
ing. In addition, patients with subarachnoid hem- are generally reduced and many patients show
orrhage secondary to ruptured ACoA aneurysms clinically significant posttraumatic stress symp-
have exhibited deficits in decision-making under tomatology (see Table 1 for a list of neuropsycho-
ambiguity, with clipped patients, but not coiled logical and psychological impairments).
patients, showing deficits in making decisions in
comparison with controls (Escartin et al. 2012).
Assessment and Treatment
Psychological
Confabulation is observed in a subset of ACoA Given the wide range of impairments associated
aneurysm patients and is manifested by state- with ACoA aneurysm, it may be advisable for
ments or actions that involve unintentionally clinicians to use assessments that focus on those
false or distorted memories (Moscovitch and impairments that are most salient and have the
Melo 1997). This may be due to a generalized greatest impact on activities of daily living
264 Anterior Communicating Artery

Anterior Communicating Artery, Table 1 Neurop- Complex Figure Test (ROCFT)), sustained atten-
sychological and psychological impairments associated tion (e.g., Cancellation Test), information pro-
with ACoA aneurysm
cessing speed (e.g., n-back tasks), and impaired
Awareness, self- abstraction (e.g., Cognitive Estimation Test
monitoring, Cognitive/
mood, Memory/ executive, (CET)).
personality learning electrophysiological In some cases, modification of existing assess-
Disorders of Semantic Complex attention ment tools can be an effective way to enhance the
awareness memory assessment process. For example, the Rey-
Spontaneous Prospective Cognitive Osterrieth Organizational and Extended Memory
confabulation memory estimation (ROEM) test, which is a modification of the
Provoked Visuo- Decision-making
ROCFT, was reported to help identify mecha-
confabulation spatial under ambiguity
Phantabulation Working Dual task
nisms underlying the nature of the impaired mem-
memory performance ory in ACoA amnesics by using measures of recall
Anosognosia Recall Concentration and recognition (e.g., subunit recognition, spatial
Intrusions Spatial Proactive arrangement, and whole figure recognition).
working interference/ Moreover, encoding and recall were improved
memory vulnerability to
by using an executive organizational strategy, in
interference
addition to identifying patients who were more
Source Delayed Verbal fluency
monitoring memory likely to benefit from such an intervention
Mood Impaired Executive (Diamond et al. 1997a; Prigatano and DeLuca
initial dysfunction 1999).
learning Some work suggests that cognitive rehabilita-
Motor/sensory Passive Autonomic and tion can help increase compensatory strategies for
learning event-related
style potentials (ERP) attention and memory dysfunction and that reha-
Paraparesis Flat learning Electrocardiogram bilitation can help improve professional activities
syndrome slope (ECG) as well as ADLs with positive rehabilitation out-
Visuomotor Delay Delayed ERP comes primarily associated with changes in mem-
skill learning eyeblink (P300): Auditory ory and attention. In a mixed sample of SAH
conditioning
patients, a majority of survivors who receive inpa-
Alien hand Acquisition Delayed ERP
syndrome (P300): Visual
tient rehabilitation attain physical independence
Visual-sensory Recognition Prolonged QTc but impairments in cognition and ADLs persist in
function intervals upwards of 40% of the patients (Dombovy et al.
(unruptured 1998). Patients have generally shown impair-
aneurysms) ments 1–5 years post-stroke, in visual short-term
Third cranial Language Dichotic listening
memory, reaction-time, verbal long-term memory,
nerve palsy
concentration, and language and information pro-
cessing. Evaluation several years after SAH asso-
(ADLs). Impairments in memory, executive func- ciated with ACoA aneurysm rupture has shown
tion, and attention/concentration as well as mood that cognitive problems negatively correlate with
figure prominently following ACoA aneurysm the level of community integration and that
rupture and should be part of routine assessment. impairments in visual memory, verbal memory,
For example, assessments should examine set- and executive function are most frequently
shifting (e.g., Wisconsin Card Sort Test (WCST) observed. Therefore, while being characterized
and Trails B), verbal and visual fluency (e.g., as having a good outcome, many ACoA patients
CFT/FAS and Design Fluency Test), verbal recall continue to exhibit persistent cognitive impair-
and recognition (e.g., California Verbal Learning ments that negatively impact psychosocial func-
Test (CVLT)), visual recall (e.g., Rey-Osterreith tioning (Ravnik et al. 2006).
Anterior Communicating Artery 265

Cross-References Diamond, B. J., DeLuca, J., & Kelley, S. M. (1997b).

Verbal learning in anterior communicating artery aneu-
rysm and multiple sclerosis patients: Performance on
▶ Activities of Daily Living (ADL) the California verbal learning test. Applied Neuropsy- A
▶ Amnesia chology, 4, 89–98.
▶ Aneurysm Dombovy, M. L., Drew-Cates, J., & Serdans, R. (1998).
▶ Anterior Cerebral Artery Recovery and rehabilitation following subarachnoid
haemorrhage: Part II. Long-term follow-up. Brain
▶ Confabulation Injury, 12(10), 887–894.
▶ Executive Functioning Escartin, J., Juncadella, G., & de Miquel, R. (2012).
▶ Rey Complex Figure Test Decision-making impairment on the Iowa gambling
task after endovascular coiling or neurosurgical clip-
ping for ruptured anterior communicating artery aneu-
rysm. Neuropsychology, 26(2), 172–180.
Kaspera, W., Ładziński, P., Larysz, P., Hebda, A.,
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Morphological, hemodynamic, and clinical indepen-
Adams, H. P., & Biller, J. (1992). Hemorrhagic intracranial dent risk factors for anterior communicating artery
vascular disease. In A. B. Baker & R. J. Joynt (Eds.), aneurysms. Stroke; a Journal of Cerebral Circulation,
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Balossier, A., Postelnicu, A., Khouri, S., Emery, E., & Kopelman, M. D. (1987). Two types of confabulation.
Derlon, J. M. (2012). Third nerve palsy induced by a Journal of Neurology, Neurosurgery and Psychiatry,
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British Journal of Neurosurgery, 26(5), 770–772. Lindner, S. H., Bor, A. S. E., & Rinkel, G. J. E. (2010).
Beeckmans, K., Vancoillie, P., & Michiels, K. (1998). Differences in risk factors according to the site of
Neuropsychological deficits in patients with an anterior intracranial aneurysms. Journal of Neurology, Neuro-
communicating artery syndrome: A multiple case surgery & Psychiatry, 81(1), 116–118.
study. Acta Neurologica Belgica, 98(3), 266–278. Manconi, M., Paolino, E., Casetta, I., & Granieri, E.
Chan, A., Ho, S., & Poon, W. S. (2002). Neuropsycholog- (2001). Anosmia in a giant anterior communicating
ical sequelae of patients treated with microsurgical artery aneurysm. Archives of Neurology, 58(9),
clipping or endovascular embolization for anterior 1474–1475.
communicating artery aneurysm. European Neurology, McCormick, W. F. (1984). Pathology and pathogenesis of
47, 37–44. intracranial saccular aneurysms. Seminars in Neurol-
Clinchot, D. M., Kaplan, P., Murray, D. M., & Pease, W. S. ogy, 4(3), 291–303.
(1994). Cerebral aneurysms and arteriovenous Meila, D., Saliou, G., & Krings, T. (2015). Subcallosal
malformations: Implications for rehabilitation. artery stroke: Infarction of the fornix and the genu of
Archives of Physical Medicine and Rehabilitation, the corpus callosum. The importance of the anterior
75(12), 1342–1351. communicating artery complex. Case series and review
Cocchini, G., Lello, O., McIntosh, R. D., & Della Sala, of the literature. Neuroradiology, 57(1), 41–47. https://
S. (2014). Phantabulation: A case of visual imagery doi.org/10.1007/s00234-014-1438-8.
interference on visual perception. Neurocase, 20(5), Moscovitch, M., & Melo, B. (1997). Strategic retrieval and
581–590. the frontal lobes: Evidence from confabulation and
Cummings, J. L., & Trimble, M. R. (1995). A concise guide amnesia. Neuropsychologia, 35(7), 1017–1034.
to neuropsychiatry and behavioral neurology. Myers, C. E., DeLuca, J., Schultheis, M. T., Schnirman,
Washington, DC: American Psychiatric Press. G. M., Ermita, B. R., Diamond, B. J., Warren, S. G., &
DeLuca, J., & Diamond, B. J. (1995). Aneurysm of the Gluck, M. (2001). Impaired delay eyeblink classical
anterior communicating artery: A review of neuroana- conditioning in individuals with anterograde amnesia
tomical and neuropsychological sequelae. Journal of resulting from anterior communicating artery aneu-
Clinical and Experimental Neuropsychology, 17(1), rysm. Behavioral Neuroscience, 115(3), 560–570.
100–121. Parkin, A., & Leng, R. C. (1993). Neuropsychology of the
Diamond, B. J., Mayes, A. R., & Meudell, P. (1996). amnestic syndrome. Hove: Lawrence Erlbaum.
Autonomic and recognition indices of aware and Prigatano, G., & DeLuca, J. (1999). Methodological issues in
unaware memory in amnesics and healthy subjects. research on neuropsychological and intellectual assess-
Cortex, 32, 439–459. ment. In P. C. Kendall, J. Butcher, & G. Holmbeck (Eds.),
Diamond, B. J., DeLuca, J., & Kelley, S. M. (1997a). Handbook of research methods in clinical psychology
Executive and memory impairment in patients with (pp. 241–250). New York: Wiley.
anterior communicating artery aneurysm. Brain and Ravnik, J., Starovasnik, B., Šešok, S., Pirtošek, Z., Švigelj,
Cognition, 35, 340–341. V., Bunc, G., et al. (2006). Long-term cognitive deficits
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in patients with good outcomes after aneurysmal sub- ongoing events of one’s life (i.e., autobiograph-
arachnoid hemorrhage from anterior communicating ical information) or factual (semantic) informa-
artery. Croatian Medical Journal, 47, 253–263.
Riina, H. A., Lemole, G. M., Jr., & Spetzler, R. F. (2002). tion to which one was exposed following the
Anterior communicating artery aneurysms. Neurosur- onset of amnesia. In contrast to this, implicit
gery, 51(4), 993–996. memory (such as the acquisition of simple habits
Ropper, A. H., Brown, R. H., Adams, R. D., & Victor, or skills like riding a bicycle) is preserved in
M. (2005). Adams & Victor’s principles of neurology.
New York: McGraw-Hill. amnesia.
Saciri, B. M., & Kos, N. (2002). Aneurysmal subarachnoid
haemorrhage: Outcomes of early rehabilitation after
surgical repair of ruptured intracranial aneurysms. Brief Historical Background
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72(3), 334–337.
Sawada, T., & Kazui, S. (1995). Anterior cerebral artery. In Current scientific understanding of anterograde
J. Bogousslavsky & L. Caplan (Eds.), Stroke Syn- amnesia originated with the study of patient
dromes (pp. 235–246). Cambridge: Cambridge Univer- HM. In 1953, at age 27, HM underwent bilateral
sity Press.
Schacter, D. L. (1987). Implicit memory: History and cur- resection of the medial temporal lobes for alle-
rent status. Journal of Experimental Psychology. viation of refractory seizures, which had wors-
Learning, Memory, and Cognition, 13, 501–518. ened following a head injury he had suffered at
Schnider, A., & Landis, T. (1995). Memory loss. In age 9. The resection was successful in reducing
J. Bogousslavsky & L. Caplan (Eds.), Stroke syn-
dromes (pp. 145–150). Cambridge, MA: Cambridge his seizures, but, unexpectedly, following the
University Press. treatment, he was unable to remember his nor-
Sethi, H., Moore, A., Dervin, J., Clifton, A., & mal daily activities. For example, he could not
MacSweeney, J. E. (2000). Hydrocephalus: Compari- remember the content of a conversation or even
son of clipping and embolization in aneurysm treat-
ment. Journal of Neurosurgery, 92(6), 991–994. having had a conversation, minutes after it
Solcà, M., Di Pietro, M., Schnider, A., & Leemann, B. ended. He was unable to remember his regular
(2015). Impairment of semantic memory after basal caregivers, even though he could converse
forebrain and fornix lesion. Neurocase, 21(2), and interact normally with them when they
198–205.
Turner, M., Cipolotti, L., & Shallice, T. (2010). Spontane- were present. These findings established that
ous confabulation, temporal context confusion and intact medial temporal lobes are critical for
reality monitoring: A study of three patients with ante- establishing new memories: HM’s medial tem-
rior communicating artery aneurysms. Journal of the poral lobe resection had left him with a dense
International Neuropsychological Society, 16(6),
984–994. anterograde amnesia. In addition to his antero-
grade amnesia, HM also had difficulties remem-
bering information acquired prior to his surgery
(▶ Retrograde Amnesia). Initial observations
suggested that his retrograde amnesia was lim-
Anterograde Amnesia ited to approximately 2 years prior to the oper-
ation. However, more recent findings indicate
Ginette Lafleche and Mieke Verfaellie that he had a more lengthy retrograde amnesia
Memory Disorders Research Center, VA Boston that extended into the distant past (Steinvorth
Healthcare System and Boston University School et al. 2005). Yet, in spite of his memory difficul-
of Medicine, Boston, MA, USA ties, HM showed preservation of intelligence,
attention, language function, and social skills.
Subsequent neuropsychological studies of HM
Short Description or Definition and other amnesic individuals have further
informed our current understanding of both
The term “anterograde amnesia” refers to an impaired and preserved memory function in
inability to acquire or retain memories of the amnesia (Corkin 1984).
Anterograde Amnesia 267

Neuropsychology of Anterograde Failure of declarative memory in amnesia can

Amnesia arise from a number of different etiologies. These
include anoxia, herpes simplex encephalitis A
Patients suffering from anterograde amnesia have (HSE), anterior communicating artery aneurysm
great difficulty in bringing to mind new informa- (ACoA), Wernicke-Korsakoff syndrome (WKS),
tion that they were exposed to after the onset of and stroke. The amnesia is a direct consequence of
their amnesia. Although these patients have pre- damage to the medial temporal lobes, (i.e., HSE,
served short-term memory, in that they can hold in anoxia), the midline diencephalon (WKS, stroke),
mind a current topic of conversation and can basal forebrain structures (ACoA), or some of the
repeat a string of digits with no delay, if there is fiber tracts that link these regions. These amnesias
a distraction or delay, memory for the information are usually permanent. In contrast, in transient
is lost. Episodic memory (i.e., memory for per- global amnesia (TGA), there is temporary dysfunc-
sonal events) is severely impaired, and, as a result, tion of memory-related brain structures including
patients no longer form an ongoing record of their the hippocampal formation and thalamus. Episodes
lives. For example, it is common for patients to of TGA typically last no more than 24 h, after
forget what they ate for lunch only minutes after which the patient’s new learning returns to normal,
they finished eating. In the same vein, in the but a permanent amnesic gap remains for the period
laboratory, patients will typically forget material of the attack (see entry ▶ “Litigation”).
they learned minutes earlier in a session, such as The ability to remember newly encountered
images presented on a computer or the details of a information depends on a number of stages,
story. The precise nature of this memory loss including the processing and representation of
depends on the site and extent of damage. For immediate experience (encoding), the transfer of
example, impaired verbal recall results from dam- that encoded information to long-term storage
age to the left medial temporal lobe whereas (consolidation), and its re-manifestation in con-
impaired nonverbal recall results from right- sciousness upon deliberate recall (retrieval) at a
sided damage. With bilateral damage, both verbal later time. Disruption of any one of these stages
and nonverbal memory problems will ensue. In could lead to anterograde amnesia. In patients
addition to loss of episodic memory, patients also with medial temporal or diencephalic lesions,
experience difficulty learning and remembering encoding and retrieval are thought to be relatively
new facts or concepts (semantic memory). The intact. Such patients perform normally on intelli-
degree of impairment in new semantic learning gence tests and on short-term memory tests,
is also a function of the extent of the medial suggesting adequate encoding (Baddeley 1995).
temporal lobe lesion. Patients with injury limited Furthermore, impaired retrieval is unlikely to be
to the hippocampus are able to acquire some new the cause of their failed explicit memory, because
facts and concepts post-morbidly, even if ineffi- memories from many years ago can still be
ciently, but patients with more extensive medial retrieved. Therefore, it is assumed that their
temporal lobe damage show minimal ability to do impairments reflect deficient consolidation. The
so (Verfaellie 2000). Together, episodic and medial temporal lobes, through interactions with
semantic memory comprise declarative neocortical regions, are thought to be critical for
(or explicit) memory and are what the plain term consolidation. They bind together into a coherent
“memory” refers to in common usage. An impor- representation the different aspects of an event
tant insight to arise from the study of patients with that are neocortically represented (Eichenbaum
anterograde amnesia is that not all forms of long- 2006).
term memory are impaired. Forms of memory that Generally, the size of the causative brain lesion
do not require deliberate reference to a prior expe- is directly proportional to the density of the amne-
rience, often referred to as nondeclarative sia, but the specific location of the lesion will also
(or implicit) memory, remain intact. impact on the nature of the memory impairment.
268 Anterograde Amnesia

For example, if the damage is limited to the hip- deliberate encoding and will also disrupt initiation
pocampal formation, performance on recall tasks and evaluation of memory search during effortful
is impaired, but performance on recognition tasks retrieval. The latter can lead to unusually high
can remain intact (Mayes et al. 2002). To account levels of intrusions in recall or false alarms in
for these findings, it has been suggested that two recognition, and this is referred to as enhanced
distinct processes contribute to explicit memory: susceptibility to false memory.
recollection and familiarity. Recollection is Despite such pervasive impairments in declar-
thought to enable the conscious recovery of con- ative memory, patients with anterograde amnesia
textually specific information about an event (e.g., show intact performance in a variety of forms of
recalling the full context of how you met someone nondeclarative (implicit) memory. These include
for the first time on a particular street last Decem- procedural learning (the acquisition of new skills
ber in New York). Familiarity enables retrieval of or habits), eyeblink conditioning (learning to
context-free information through a feeling of blink the eyes in response to a tone because of
“knowing” (e.g., having the feeling that you the repeated association of the tone with an air
have met someone previously without remember- puff to the eye), and repetition priming (improved
ing where or when you met them). Whereas per- accuracy or speed of performance for stimuli to
formance on recall tasks depends on the ability to which an individual was recently exposed)
retrieve contextually relevant information (Verfaellie and Keane 2002). These forms of non-
(recollection), performance on recognition tasks declarative memory depend on neural circuits in
can be supported by either recollection or famil- the basal ganglia, cerebellum, or neocortex that
iarity. Thus, the preserved recognition perfor- remain spared in amnestic syndromes (Squire
mance observed in patients with limited 1994).
hippocampal lesions is thought to reflect pre-
served familiarity, despite impaired recollection.
The dissociation between recollection and famil- Evaluation
iarity is supported by findings from neuroimaging
(Diana et al. 2007) and neuropsychological stud- Anterograde amnesia refers to a severe and per-
ies (Zita-Patai et al. 2015) that suggest that the manent inability to learn new information in the
hippocampus is critical for recollection whereas presence of otherwise normal intelligence, atten-
familiarity is supported by the perirhinal cortex. If tion span, perception, reasoning, and language
the damage extends beyond the hippocampus to ability. The evaluation of anterograde amnesia
include other medial temporal lobe structures such must therefore, as a first step, include a compre-
as the perirhinal cortex, then both recollection and hensive neuropsychological work-up to deter-
familiarity are affected, leading to striking impair- mine whether other areas of cognitive
ments on tests of recognition as well as recall. functioning are intact and, if not, whether any
In some cases, for example, in patients with deficits found contribute to the memory disorder.
amnesia due to anoxia or rupture of an aneurysm With regard to assessment of memory functioning
of the anterior communicating artery, frontal lobe itself, there are a variety of standardized tests
impairments may be superimposed on the core available. Lezak et al. (2004) provide a compre-
amnesia (▶ Amnestic Syndromes). This can lead hensive review of the most commonly used ones.
to exacerbation of the anterograde amnesia by Assessing performance on recall and recognition
additional impairments in encoding and retrieval. tests is an essential component of the evaluation,
Executive functions such as planning, organizing, because their comparison can reveal the nature of
monitoring, and control of attention, all depend on the memory processes that are affected. Both ver-
the integrity of the frontal lobes. Executive bal and nonverbal memory should be examined,
impairments will interfere with the ability to men- and memory should be tested both shortly after
tally manipulate and organize information during learning and following a longer delay, to assess
Anterograde Amnesia 269

the rate of forgetting. Other factors of diagnostic appointment book, or written reminders. The
importance are a patient’s sensitivity to interfer- memory notebook is a preferred compensatory
ence and his or her ability to use organizational instrument for amnesics because it is divided A
strategies at encoding and retrieval. While a com- into sections that are personally tailored to a
prehensive assessment of anterograde memory patient’s life (i.e., daily tasks, future plans, notes
typically includes a variety of different tests, section, and so on). More sophisticated technol-
each developed for a specific purpose, the use of ogy, in the form of computerized paging systems,
a single standardized memory battery that evalu- electronic assistants, alarms, and timers, is most
ates all major aspects of new learning can provide useful for individuals who had some proficiency
a good overview of memory functioning. The in the use of such devices premorbidly.
Wechsler Memory Scale-III and Wechsler Mem- Other methods promote the use of strategies
ory Scale-IV (Wechsler 1997, 2009) are probably that make use of preserved priming abilities.
the most widely used instruments for this purpose. These approaches typically use structured presen-
In addition to indices of immediate and delayed tation of the to-be-learned material whereby
memory, they provide an index of short-term patients are encouraged to guess the correct
memory, and, in patients with anterograde amne- answer based on cues. One such approach uses
sia, a significant discrepancy in performance is to trial and error learning, and once a correct answer
be expected between the short-term and long-term is generated, cues are gradually reduced until the
memory measures. correct answer can be spontaneously generated.
A drawback of a trial and error approach, how-
ever, is that it allows for the generation of incor-
Treatment rect responses during the learning phase. There is
now considerable evidence that the generation of
Rehabilitation interventions in amnesia aim at errors may interfere with subsequent learning of
increasing day-to-day functional adaptation and the correct response. Therefore, the use of error-
independence. A wide array of intervention tech- less learning techniques is preferable, in which
niques is available, and the choice among them cues are used that prevent the occurrence of errors
should be informed by cognitive factors such as (Kessels and Haan 2003).
premorbid abilities and skills as well as post- For patients with milder memory impairments,
morbid neuropsychological strengths and weak- strategies aimed at strengthening the impaired form
nesses, including the severity of amnesia. Rele- of memory are more appropriate. Such patients
vant non-cognitive factors include premorbid may benefit from rehearsal and relearning of the
lifestyle and habits and educational background. material. Spaced repetitions across different time
Other contributing factors include insight and intervals and different spatial locations are espe-
motivation, which are essential for any treatment cially beneficial as they enhance the likelihood
choice, because the absence of either will under- that information will be richly encoded, thus
mine rehabilitation efforts. enhancing the chances that a freestanding mem-
Remediation of patients with severe amnesia ory will be integrated with preexisting memo-
relies largely on those aspects of memory that are ries. For patients whose memory impairment
preserved, such as procedural learning and prim- reflects impairment in effortful encoding and
ing. Techniques that capitalize on procedural retrieval, techniques that promote enhanced
learning use repetition to drill skills and habits organization (e.g., chunking, thematic organiza-
that range from essential activities of daily living tion) and elaboration (e.g., verbal mnemonics,
to simple assembly tasks and cognitive skills. visual imagery) at the time of learning may be
Such skill learning is frequently involved when useful. In a sense, elaboration provides the
teaching a patient to use an external memory aid, learner with alternative retrieval routes that
such as a memory notebook, calendar, diary, may enhance recall.
270 Anterolateral System

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Steinvorth, S., Levine, B., & Corkin, S. (2005). Medial
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Anticholinergic 271

cord, the peripheral nerves bifurcate into the dorsal Definition

and ventral nerve roots. The dorsal roots, which carry
sensory information, then synapse in the gray matter Anticholinergic agents alter the balance of neuro- A
of the cord (dorsal horns) on the same side in which transmitters in the central and peripheral nervous
they enter. Secondary fibers then cross the midline of system inhibiting parasympathetic nerve
the cord in the ventral white commissure and ascend impulses. Specifically, the agents diminish acetyl-
in the ventral-lateral portion of the spinal cord as the choline and allow for the increase of dopamine.
ventral and lateral spinothalamic tracts. While these Anticholinergic medications are divided into three
two tracts were once described as carrying different categories based on their specific receptor targets
and distinct types of sensory information, the current in the nervous system and in other sites in the
thinking is that they have extensive functional over- body: antimuscarinic, ganglionic blockers, and
lap and hence should be considered as a single neuromuscular blockers. The receptor subtypes
anterolateral system. These second-order fibers of affect the brain, salivary glands, smooth muscle,
the ALS ascend in the ventral lateral portion of the and ciliary muscles of the eye. Categories of med-
cord and then in the lateral and later in the dorsolat- ications are clinically used for the antimuscarinic
eral portions of the brainstem. These ascending path- effects and include medications for urinary spas-
ways continue to ventral posterior lateral nucleus of modics and overactive bladder, anticholinergic
the thalamus. From the thalamus, third-order neurons antiparkinson’s agents, antivertigo medications,
project to the somatosensory cortices in the parietal gastrointestinal antispasmodics, mydriatic medi-
lobes of the brain. Because the nerve fibers making cations, and medications for bronchospasm.
up the ALS cross the midline within a few vertebral Another group of medications not primarily
segments of where they enter the cord, lesions affect- targeting the cholinergic receptors include sedat-
ing the ALS will result in contralateral deficits. ing antihistamines, tricyclic antidepressants,
muscle relaxants, some antipsychotics, antiar-
rhythmics, and antiemetics. Neuropsychologists
Cross-References should be aware of the medications their patients
are taking and the potential impact on neuropsy-
▶ Medial Lemniscus chological test results. It is necessary to differen-
tiate between medication side effects and true
consequences or neurologic disorder.
References and Readings

Mendoza, J. E., & Foundas, A. L. (2008). The somatosen- Current Knowledge

sory systems. In J. E. Mendoza & A. L. Foundas (Eds.),
Clinical neuroanatomy – A neurobehavioral approach Anticholinergic medications are used in treating a
(pp. 23–47). New York: Springer.
variety of medical conditions. Anticholinergic
drugs are used in treating a variety of conditions
including Parkinson’s disease and other
Parkinsonian-like disorders, gastrointestinal dis-
Anticholinergic orders such as diverticulitis, respiratory disorders
such as asthma, and genitourinary disorders such
Mary Pat Murphy as prostatitis (Tables 1 and 2).
MSN, CRRN, Paoli, PA, USA

Side Effects
Synonyms
Anticholinergic side effects can be caused by a
Anticholinergic medications wide range of medications. Anticholinergic
272 Anticholinesterase Inhibitors

Anticholinergic, Table 1 Anticholinergic medications properties to address medical issues for bladder
clinically used for the antimuscarinic effects management, increased muscle tone, and behavior
Medications for Oxybutynin (Ditropan), (atypical antipsychotics). There may be a cumula-
neurogenic bladder tolterodine (Detrol), tive effect of taking multiple medications which act
including urge trospium (Sanctura),
incontinence, for solifenacin (VESIcare), on the cholinergic system. Anticholinergic side
overactive bladder darifenacin (Enablex) effects in older adults include an increase in delir-
Anticholinergic Benztropine (Cogentin), ium, diminished ADLs, and decrease in cognition
antiparkinson’s trihexyphenidyl (Artane) (Fick et al. 2003; Han et al. 2001).
medication
Antivertigo medication Meclizine (Antivert),
scopolamine (Transderm
Scop) Cross-References
Gastrointestinal Diphenoxylate/atropine
antispasmodics (Lomotil), belladonna
▶ Acetylcholine
medications (Donnatal)
▶ Dopamine
Medications for Tiotropium (Spiriva),
bronchospasm ipratropium (Atrovent) ▶ Neurotransmitters

Anticholinergic, Table 2 Anticholinergic medications References and Readings

not primarily targeting the cholinergic receptors
Sedating Diphenhydramine (Benadryl), Fick, D. M., Cooper, J. W., Wade, W. E., Waller, J. L.,
antihistamines hydroxyzine (Vistaril), Maclean, J. R., & Beers, M. H. (2003). Updating the
cyproheptadine (Periactin) beers criteria for potentially inappropriate medication
Tricyclic Amoxapine (Asendin), amitriptyline use in older adults: Results of a US consensus panel of
antidepressants (Elavil), desipramine (Norpramin), experts. Archives of Internal Medicine, 163(22),
imipramine (Tofranil), nortriptyline 2716–2724.
(Pamelor) Han, L., McCusker, J., Cole, M., Abrahamowicz, M.,
Certain Clozapine (Clozaril), olanzapine Primeau, F., & Élie, M. (2001). Use of medications
antipsychotics (Zyprexa), risperidone (Risperdal) with anticholinergic effect predicts clinical severity of
delirium symptoms in older medical inpatients.
Muscle Dantrolene (Dantrium),
Archives of Internal Medicine, 161(8), 1099–1105.
relaxants cyclobenzaprine (Flexeril)
Lieberman, J. A. (2004). Managing anticholinergic side
effects. Journal of Clinical Psychiatry, 6(Suppl. 2),
20–23.
medications have peripheral and central side
effects including dry mouth, blurred vision, uri-
nary retention or difficulty initiating voiding, con-
stipation or bowel obstruction, decreased
sweating, increased heart rate, ataxia, increased Anticholinesterase Inhibitors
body temperature, agitation, confusion, delirium,
memory impairment, decreased attention, dizzi- JoAnn Tschanz1,2 and Elizabeth K. Vernon1
1
ness, and drowsiness. Department of Psychology, Utah State
Certain populations are at greater risk for University, Logan, UT, USA
2
adverse events related to anticholinergic medica- Center for Epidemiologic Studies, Utah State
tions. They include older adults who already expe- University, Logan, UT, USA
rience a decrease in acetylcholine production, men
with benign prostatic hypertrophy, patients with
glaucoma, and individuals with dementia who are Synonyms
already taking cholinesterase inhibitors.
The elderly and patients with brain injury are Acetylcholinesterase inhibitors; ACHE inhibi-
often prescribed medications with anticholinergic tors; AchEIs; CHEIs; Cholinesterase inhibitors
Anticholinesterase Inhibitors 273

Definition Formulation and Side Effects

Several cholinesterase inhibitors are available.
A class of substances that target the cholinergic The primary mode of intake is oral, although a A
neurotransmitter system and are often used in cutaneous route through a dermal patch has been
the treatment of memory disorders such as developed. Common side effects of cholinesterase
Alzheimer’s disease (AD). Nonclinical uses inhibitors include nausea, vomiting, diarrhea,
include agricultural applications such as pesti- and anorexia. Less common are insomnia and
cides and military applications such as the cardiovascular symptoms such as bradycardia.
development of neurotoxins. Acetylcholine is Drug tolerability may be enhanced by varying
normally released by the presynpatic neuron dosing and titration rates to achieve therapeutic
and activates receptors on the postsynaptic levels (Orgogozo 2003).
cell. Acetylcholinesterase is the primary
enzyme that breaks down acetylcholine in the Other Applications
synaptic cleft. Agents such as cholinesterase In addition to its distribution in the brain, acetyl-
inhibitors block the activity of this enzyme, choline is also the neurotransmitter substance at
allowing the neurotransmitter substance to the neuromuscular junction and sympathetic and
remain in the synaptic cleft longer to stimulate parasympathetic nervous systems. Thus, acetyl-
postsynaptic receptors (see Cholinesterase choline plays an important role in the body’s
Inhibitors). motor and autonomic functions. Anticholinester-
ase inhibitors developed for agricultural or mili-
tary applications affect these systems by causing
Current Knowledge an accumulation of acetylcholine at synapses,
leading to excessive excitation of muscles, cessa-
Clinical Indications tion of muscle contraction (due to overexcitation),
Cholinesterase inhibitors (CHEI) are often and autonomic symptoms such as sweating and
used in the treatment of memory and other cog- bronchial constriction and congestion. Therefore,
nitive disorders. In AD, degeneration of brain anticholinesterase inhibitors may also be potent
cholinergic neurons has been associated with neurotoxins for use as insecticides or in warfare
progressive cognitive deterioration. Since cho- (Feldman et al. 1997; Iversen et al. 2008).
linesterase inhibitors do not reverse or stop the
progressive degeneration of cholinergic neu-
rons, their effectiveness is greatest early in the
See Also
course of AD while existing neurons are able to
continue to produce and release acetylcholine
▶ Acetylcholine
(Orgogozo 2003). The newest addition to the
▶ Alzheimer’s Disease
CHEI class, Namzaric is a combination of
▶ Cholinesterase Inhibitors
donepezil and memantine. CHEIs are moder-
ately effective on improvement of cognitive
processes, functional abilities, and possibly
References and Readings
neuropsychiatric symptoms. Other compounds
such as memantine (which acts on the Feldman, R. S., Meyer, J. S., & Quenzer, L. F. (1997).
glutamatergic system) have been approved for Acetylcholine. In Principles of Neuropsychoparh-
use in moderate to severe dementia. These macology (pp. 246–249). Sunderland: Sinauer Associ-
drugs do not stop the progression of AD or ates, Inc.
Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H.
stop the degeneration of cholinergic neurons, (2008). Acetylcholine. In Introduction to Neuropsycho-
but can temporarily reduce the degree of cogni- pharmacology (pp. 128–149). New York: Oxford
tive impairment. University Press.
274 Anticoagulation

Orgogozo, J.-M. (2003). Treatment of Alzheimer’s disease functions which can be used to monitor the effec-
with cholinesterase inhibitors. An update on currently tiveness of the medication regimen. Optimum
used drugs. In K. Iqbal & B. Winblad (Eds.), Alzheimer’s
disease and related disorders: Research advances (pp. ranges for the results of these tests are available
663–675). Bucharest: Ana Asian Intl. Acad. of Aging. for specific conditions and clinical situations.
The newer anticoagulants offer the advantages
of fixed dosing, minimal food and drug interac-
tions, and lack of requirement for blood test
Anticoagulation monitoring.
Predictably, adverse effects of all anticoagu-
Elliot J. Roth lants are largely hemorrhagic in nature. Pro-
Department of Physical Medicine and longed bleeding from simple superficial
Rehabilitation, Northwestern University, lacerations, and more serious internal hemor-
Feinberg School of Medicine, Chicago, IL, USA rhage into gastrointestinal system, brain, or mus-
cles in the pelvis or leg, occurs with greater
frequency depending on the type and level of
Synonyms anticoagulation. Rarely, a paradoxical throm-
botic disorder might occur as a result of using
Antithrombotic therapy one of these medications. On balance, the bene-
fits of using certain anticoagulants in selected
situations outweigh the risks of the medications
Definition but primarily in controlled circumstances when
clinical monitoring is feasible and when the
Anticoagulation refers to the prevention of blood patient does not have risk of falls, injuries, or
from clotting. An anticoagulant is a chemical that other contraindications.
prevents coagulation. The body contains a number
of naturally occurring physiological anticoagulants,
but other anticoagulants are used as pharmacologi-
See Also
cal agents to prevent and treat thrombotic disorders
such as coronary artery disease causing ischemic
▶ Atherosclerosis
heart disease, cerebrovascular disease causing
▶ Central Venous Thrombosis
stroke, peripheral arterial disease causing limb
▶ Cerebral Embolism
ischemia, and venous thromboembolic disease.
▶ Novel Oral Anticoagulants
Commonly used anticoagulation medications
▶ Thrombosis
include warfarin (Coumadin ®), heparin and low
▶ Venous Thrombosis
molecular weight heparin compounds such as
▶ Warfarin (Coumadin)
enoxaparin (Lovenox ®), tinzaparin (Innohep ®),
and dalteparin (Fragmin ®). New oral anticoagu-
lants, which use a different mechanism of action,
References
have recently gained widespread use. These med-
ications include apixaban (Eliquis ®), dabigatran Dentali, F., Douketis, J. D., Gianni, M., Lim, W., &
(Pradaxa ®), edoxaban (Savaysa ®), and Crowther, M. A. (2007). Meta-analysis: Anticoagulant
® prophylaxis to prevent symptomatic venous thrombo-
rivaroxaban (Xarelto ).
embolism in hospitalized medical patients. Annals of
Internal Medicine, 146, 278–288.
Kearon, C., Akl, E. A., Ornelas, J., Blaivas, A., Jimenez,
Current Knowledge D., et al. (2016). Antithrombotic therapy for VTE dis-
ease: CHEST guideline and expert panel report. Chest,
149, 315–352.
Dosages of warfarin can be adjusted using blood
van der Hulle, T., Kooiman, J., den Exter, P. L., Dekkers,
tests that measure the levels of certain clotting O. M., Klok, F. A., & Huisman, M. V. (2014).
Anticonvulsants 275

Effectiveness and safety of novel oral anticoagulants side effects. Usually, if one drug fails, another
as compared with vitamin K antagonists in the medication is trialed. If the initial AED fails, the
treatment of acute symptomatic venous thromboem-
bolism: A systematic review and meta-analysis. physician typically will wean this medication A
Journal of Thrombosis and Haemostasis, 12, and try another first-line drug. If monotherapy
320–328. fails, polytherapy may be tried. The physician
will maximize the first-line dose and then add a
second-line medication. General monitoring for
AEDs includes the frequency and severity of
Anticonvulsants seizures, adverse events and side effects, and
monitoring of plasma. The chart below identifies
Mary Pat Murphy FDA indications for commonly used AEDs
MSN, CRRN, Paoli, PA, USA (Table 1).

Synonyms Mechanism of Action for AEDs

Antiepileptic drugs (AED) Phenytoin, carbamazepine, lamotrigine, gabapentin,
topiramate, and valproate block sodium channel
and impede generation of high-frequency action
Definition potentials. Some of the drugs may also reduce
high-threshold calcium currents, resulting in a
A group of medications used in the management decrease in excitatory transmitter release. In ther-
of epilepsy. apeutic ranges, barbiturates and diazepam deriv-
atives enhance GABA responses. Topiramate
may enhance GABAergic inhibition. Gabapentin
Current Knowledge may promote nonsynaptic GABA release. Phe-
nobarbital is a long-acting barbiturate with seda-
The selection of an AED depends on the type of tive, hypnotic, and anticonvulsant properties. It
seizure, age of patient, and gender. According to acts on the GABA receptors, increasing synaptic
the literature, monotherapy is the goal for the inhibition. This has the effect of elevating the
treatment of epilepsy, choosing medications seizure threshold and reducing the spread of sei-
targeting seizure control with fewest side effects. zure activity in the brain. Phenobarbital may also
Monotherapy also makes it easier to monitor inhibit calcium channels.

Anticonvulsants, Table 1 Commonly used AED

Partial seizures Tonic-clonic Absence
First-line drugs Carbamazepine Valproate Ethosuximide
Phenytoin Phenytoin Valproate
Valproate Carbamazepine
Topiramate Topiramate
Second-line drugs Primidone Lamotrigine
(alternative therapy) Gabapentin Gabapentin
Phenobarbital Primidone Clonazepam
Primidone Phenobarbital Primidone
Valproate Topiramate
Felbamate (use when other Felbamate (use when other
alternative medications have alternative medications have
failed) failed)
276 Anticonvulsants

First-Line Medications Adverse Events/Side Effects

Phenytoin can be administered intravenously. As
Valproate (Depakote) a result, specific adverse events/side effects can
include hypotension, bradycardia, dysrhythmias,
Indication and cardiac changes, as well as venous irritation
Labeled indications include control of epilepsy and thrombophlebitis.
(seizure disorders). As an AED, it can be used as Other adverse events/side effects include gin-
monotherapy and adjunctive treatment of tonic- gival hyperplasia, hirsutism, rash, hepatitis, mega-
clonic, partial complex seizures, and simple and loblastic anemia, thrombocytopenia, Stevens-
complex absence seizures. It can be used as an Johnson syndrome, systemic lupus erythematosus,
adjunctive treatment in patients who have multi- and folic acid deficiency.
ple types of seizures.
Drug Interactions
Contraindications Drug interactions are many and include (but
The medication should be prescribed cautiously are not limited to) chloramphenicol, dexameth-
for individuals with liver disease and urea cycle asone, doxycycline, furosemide, haloperidol,
disorders and for pregnant women. meperidine, methadone, oral contraceptives,
theophylline, and warfarin. Non-AEDs that
Adverse Events/Side Effects affect phenytoin levels include alcohol, ant-
Weight gain, thrombocytopenia, and elevated acids, folic acid, rifampin, tube feedings, alco-
liver enzymes may be dose related. When initially hol, cimetidine, fluoxetine, imipramine, INH,
starting the medication, patients may complain of omeprazole, propoxyphene, sulfonamides, and
nausea and diarrhea. Hyperammonemia has been trazadone.
reported and may be present despite normal liver
function testing. In the elderly, there is a possible Carbamazepine (Tegretol)
increase in somnolence.
Indication
Drug Interactions Carbamazepine is indicated as a first-line drug for
Medications that may increase valproate levels use as an anticonvulsant for partial seizures, gen-
include felbamate, rifampin, and chlorpromazine; eralized tonic-clonic, and mixed seizures, but not
medications that valproate may affect include car- absence seizures. It is generally nonsedating
bamazepine, amitriptyline, nortriptyline, clonaze- within therapeutic range. It is also indicated in
pam, ethosuximide, lamotrigine, phenobarbital, the treatment of trigeminal neuralgia.
phenytoin, tolbutamide, and lorazepam.
Adverse Events/Side Effects
Phenytoin (Dilantin) Adverse events associated with carbamazepine
include aplastic anemia and agranulocytosis. Pre-
Indication treatment hematology testing should be com-
Phenytoin is the oldest and one of the most pleted to obtain a baseline. The patient should be
effective medications in the treatment of a monitored and treatment should be discontinued
wide range of seizure types. The labeled use is with hematology changes. Stevens-Johnson syn-
for tonic-clonic and partial complex seizures. drome (an exfoliating dermatitis) has been
It is often used as a first-line drug choice for reported. Carbamazepine has mild anticholinergic
monotherapy. The usual dose is 300 to 400 properties, so patients with intraocular eye pres-
mg/day. An extended-release capsule allows sure should be monitored. Carbamazepine should
for one-time-a-day dosing. The therapeutic not be used in pregnant women. Patients should
range is 10–20. be cautioned against drinking alcohol.
Anticonvulsants 277

In the beginning of treatment, patients report cognition including drowsiness, dizziness, irrita-
side effects including dizziness, drowsiness, nau- bility, hyperactivity, and fatigue; and ataxia. There
sea, and vomiting. have been reports of increased tonic-clonic A
seizures.
Medications that Affect Carbamazepine
Plasma Levels
Drugs that increase plasma levels include Second-Line Medications
cimetidine, danazol, macrolides, erythromycin,
troleandomycin, fluoxetine, nefazodone, loratadine, Gabapentin (Neurontin)
terfenadine, INH, propoxyphene, verapamil, Gabapentin is effective as an adjunctive therapy in
grapefruit juice, protease inhibitors, and valproate. the treatment of partial seizures with and without
Medications that decrease carbamazepine plasma generalization.
levels include cisplatin, felbamate, rifampin, phe-
nobarbital, phenytoin, primidone, methsuximide, Adverse Events/Side Effects
and theophylline. Adverse events/side effects include dizziness,
ataxia, weight gain, GI upset, somnolence, and
Topamax (Topiramate) other symptoms of CNS depression.
Topiramate is considered effective as a mono-
therapy for individuals with partial complex or Drug Interactions
generalized tonic-clonic seizures. It is also effec- Antacids decrease their bioavailability.
tive as an adjunctive treatment for partial complex
and generalized tonic-clonic seizures. Lamotrigine (Lamictal)
Lamotrigine is effective as monotherapy for
Adverse Events/Side Effects individuals with partial complex seizures; it is
Metabolic acidosis is an adverse event associ- also considered effective as an adjunctive ther-
ated with topiramate. Conditions that predis- apy for partial complex seizures and generalized
pose individuals include renal disease, severe tonic-clonic seizures. It is thought to inhibit
respiratory disorders, status epilepticus, and voltage-sensitive sodium channel mechanisms.
diarrhea. Measurement of baseline and periodic It is well tolerated and does not seem to have
sodium bicarbonate is recommended. Other side cognitive altering side effects. A therapeutic
effects/adverse events include kidney stones, plasma concentration has not been established
paresthesia of the extremities, acute myopia for lamotrigine.
and glaucoma, decreased sweating and hyper-
thermia, cognitive-related dysfunction, psychi- Side Effects/Adverse Events
atric/behavioral disturbances, and somnolence Side effects/adverse events include rash, fatigue,
or fatigue. dizziness, diplopia, and ataxia. Angioedema, nys-
tagmus, and hematuria also may occur.
Drug Interactions
Concomitant administration of topiramate and Drug Interactions
valproate has been associated with hyper- Medications that decrease lamotrigine’s effec-
ammonemia. Topiramate concentrations affect tiveness include carbamazepine, valproate, phe-
phenytoin and valproate. Topiramate concentra- nobarbital, primidone, and acetaminophen.
tions are affected by phenytoin, carbamazepine, Felbamate (Felbatol) has been approved for
valproate, and lamotrigine. adjunctive therapy or monotherapy for individ-
Ethosuximide (Zarontin) has been approved uals with partial complex or tonic-clonic seizures.
for absence (petit mal) seizures. Adverse events/ This medication is recommended when other ther-
side effects include blood dyscrasias; decreased apies have been tried and have failed.
278 Anticonvulsants

Adverse Events/Side Effects Adverse Events/Side Effects

This medication potentially causes aplastic ane- Adverse effects include sedation, ataxia, and cog-
mia or hepatotoxicity and should be used with nitive impairment and may cause a paradoxical
extreme care by a knowledgeable physician effect including hyperactivity and problems with
when other therapies have been tried. Other side sleep, megaloblastic anemia (responds to folic
effects/adverse events include anorexia, vomiting, acid) and rash, exfoliative dermatitis, and
and insomnia. Stevens-Johnson syndrome.

Drug Interactions Non-AEDs Affected by Phenobarbital

Felbatol affects phenytoin, valproate, and carba- Phenobarbital may interfere with the effective-
mazepine concentrations. ness of acetaminophen and increase liver dam-
age. The effectiveness of beta-blockers except
atenolol, levobunolol, metipranolol, and nadolol,
oral contraceptives, chloramphenicol, chlor-
Barbiturates (Second Line) promazine, cimetidine, corticosteroids, cyclo-
sporine, desipramine, doxycycline, folic acid,
Phenobarbital griseofulvin, haloperidol, meperidine, metha-
done, nortriptyline, quinidine, theophylline, and
Indication warfarin may be compromised when taking
Labeled indications include control of epilepsy phenobarbital.
(seizures disorders) and as a sedative/hypnotic
medication for short-term treatment of insomnia. Non-AEDs Affecting Phenobarbital Levels
As an AED, it can be used as monotherapy in the Chloramphenicol, propoxyphene, and quinine
treatment of generalized (tonic-clonic), simple, or may increase phenobarbital levels. Chlorproma-
partial complex seizures, for myoclonic epilepsy, zine, folic acid, and prochlorperazine may
and for neonatal and febrile seizures in children. It decrease phenobarbital levels. There may be
has also been prescribed for eclamptic seizures increased toxicity with benzodiazepines, CNS
during pregnancy. depressants, and methylphenidate.
Primidone (Mysoline) is related in structure to
Contraindications barbiturates. It is used in the management of tonic-
The medication should be prescribed cautiously clonic, partial complex, and focal seizures. The
for individuals with liver disease, CHF, and adverse events/side effects and drug interactions
hypovolemic shock and for pregnant women. are similar to phenobarbital.
The medication does cause both physical and
psychological drug dependence; for this reason, Benzodiazepines
it is not a first-line medication of choice for This class of medication is not typically used as
individuals with drug dependence. If prescribed first-line medications. As a class, they can pro-
for sleep, it should not be used longer than duce CNS depression and behavioral changes.
2 weeks and prescribed for the elderly because Other adverse reactions include tachycardia,
of its long half-life. Patients should avoid chest pain, headache, constipation, nausea, and
alcohol and other CNS depressants while taking ataxia.
phenobarbital. Other contraindications include Medications include the following:
preexisting CNS depression, severe uncontrolled Clonazepam (Klonopin) is effective as an
pain (may mask symptoms), porphyria, and adjunctive medication for individuals with
severe respiratory disease with obstruction or absence, tonic-clonic, and myoclonic seizures.
dyspnea. Abrupt discontinuation may cause Diazepam (Valium) and Lorazepam (Ativan) can
seizures. be used to treat status epilepticus.
Antidepressant Discontinuation Syndrome 279

Cross-References norepinephrine reuptake inhibitors), and others

(including noradrenergic and specific serotoner-
▶ Epilepsy gic antidepressant). A
▶ GABA
▶ Seizure
Categorization

References and Readings ADS is classified under medication-induced move-

ment disorders in the Diagnostic and Statistical
Lanctôt, K., Herrmann, N., Mazzotta, P., Khan, L., & Manual of Mental Disorders (5th ed.; DSM-5;
Ingber, N. (2004). GABAergic function in Alzheimer's
American Psychiatric Association 2013).
disease: Evidence for dysfunction and potential as a
therapeutic target for the treatment of behavioural and
psychological symptoms of Dementia. Canadian Jour-
nal of Psychiatry, 49(7), 439–453. Current Knowledge
MacQueen, G., & Young, T. (2003). Cognitive effects of
atypical antipsychotics: focus on bipolar spectrum dis-
orders. Bipolar Disorders, 5, 53–61. Clinical Presentation and Diagnosis
Yasseen, B., Colantonio, A., & Ratcliff, G. (2008). Prescrip- Consensus does not yet exist on diagnostic
tion medication use in persons many years following criteria for ADS. Symptoms begin abruptly
traumatic brain injury. Brain Injury, 22(10), 752–757.
(within days), continue only briefly even if
untreated (24 h–3 days), and rapidly resolve
(within 48 h) when antidepressant medication is
reintroduced. Common symptoms include dizzi-
Antidepressant ness, headache, nausea, gastrointestinal upset,
Discontinuation Syndrome lethargy, anxiety, agitation, dysphoria, irritabil-
ity, poor concentration, and sleep problems.
Cynthia Rolston Ataxia, electrical shock-like sensations, extrapy-
Department of PM&R, Virginia Commonwealth ramidal symptoms, and overt manic or hypo-
University-Medical College of Virginia, manic symptoms have also been reported. ADS
Richmond, VA, USA is differentiated from depression resurgence by
certain unique symptoms (e.g., “electric shock”
sensations, nausea, nightmares) and by occur-
Synonyms rence when treatment is ongoing, but when the
composition of treating agent is changed (i.e.,
Antidepressant discontinuation symptoms; Anti- generic or different brand). Risk of ADS is min-
depressant withdrawal syndrome (not preferred) imal if treatment has lasted less than 6 weeks
(Harvey and Slabbert 2014) and there is no evi-
dence to suggest that a longer course of antide-
Definition pressant treatment is associated with increased
risk of ADS (Baldwin et al. 2007).
Antidepressant discontinuation syndrome (ADS) Little is known how ASD events impact the
is cluster of physical and psychological symp- long-term management of depression. Under-
toms that may arise after sudden discontinuation standing ADS is essential, given widespread anti-
(either end of use or change in formulation) of depressant use paired with high rates of
antidepressant medication of any class, including nonadherence. Implications of misdiagnosis may
tricyclic antidepressants (TCAs), monoamine include physical discomfort, psychosocial prob-
oxidase inhibitors (MAOIs), serotonin-specific lems, inappropriate interventions, and reluctance
reuptake inhibitors (SSRIs), SNRIs (serotonin to use psychotropic medications.
280 Antidepressants

Incidence References and Readings

The likelihood of ADS is impacted by an agent’s
half-life: the shorter half-life, the greater the risk American Psychiatric Association. (2013). Diagnostic and
statistical manual of mental disorders (5th ed.). Arling-
of ADS (Warner et al. 2006). The highest inci-
ton: American Psychiatric Association Publishing.
dence of ASD is reported for TCA clomipramine Baldwin, D. S., Montgomery, S. A., Nil, R., & Lader, M.
(21.5–100%; Leujoyeux and Ades 1997), and the (2007). Discontinuation symptoms in depression and
lowest for fluoxetine (almost 0%; Wilson and anxiety disorders. International Journal of Neurophar-
macology, 10(1), 73–84.
Lader 2015). Further research is needed on how
Cleare, A., Pariante, C. M., Young, A. H., Anderson, I. M.,
patient factors such as age and sex impact the Christmas, D., Cowen, P. J., et al. (2015). Evidence-
course of ASD. based guidelines for treating depressive disorders with
antidepressants: A revision of the 2008 British Associ-
ation for Psychopharmacology guidelines. Journal of
Underlying Mechanism Psychopharmcaology, 29(5), 459–525.
The mechanisms of ASD are unclear, but symp- Cromarty, P., Jonsson, J., Moorhead, S., & Freeston, M. H.
toms clusters covary with specific antidepressant (2011). Cognitive behaviour therapy for withdrawal from
antidepressant medication: A single case series. Behav-
classes. TCAs, impacting serotonergic and cho- ioral and Cognitive Psychotherapy, 39(1), 77–97.
linergic pathways, may result in gait or balance Harvey, B. H., & Slabbert, F. N. (2014). New insights on
problems, or tremors (Shelton 2006). MAOIs the antidepressant discontinuation syndrome. Human
affect the alpha2-adrenergic and dopaminergic Psychopharmacology, 29(6), 503–516.
Lejoyeux, M., & Ades, J. (1997). Antidepressant discon-
receptors, causing risk for agitation and psycho- tinuation: A review of the literature. Journal of Clinical
sis (Warner et al. 2006). A novel agent called Psychiatry, 58(Suppl. 7), 11–15.
agomelatine does not seem to cause ADS; its Schatzberg, A. F., Haddad, P., Kaplan, E. M., Lejoyeux, M.,
unique profile may allow for further clarification Rosenbaum, J. F., Young, A. H., & Zajecka, J. (1997).
Serotonin reuptake inhibitor discontinuation syndrome:
of the mechanism underlying ADS (Harvey and A hypothetical definition. Discontinuation consensus
Slabbert 2014). panel. Journal of Clinical Psychiatry, 58(Suppl. 7), 5–10.
Shelton, R. C. (2006). The nature of the discontinuation
syndrome associated with antidepressant drugs. The
Treatment Recommendations Journal of Clinical Psychiatry, 67(Suppl. 4), 3–7.
Expert guidelines advise psychoeducation regard- Warner, C. H., Bobo, W., Warner, C., Reid, S., & Rachal,
ing ADS prior to prescribing and discontinuing J. (2006). Antidepressant discontinuation syndrome.
American Family Physician, 74(3), 449–456.
antidepressant medication, with close monitor- Wilson, E., & Lader, M. (2015). A review of the management
ing during a gradual taper (Cleare et al. 2015; of antidepressant discontinuation symptoms. Therapeutic
Schatzberg et al. 1997). At a minimum, a 4-week Advances in Psychopharmacology, 5(6), 357–368.
taper is suggested, with more rapid tapering
for lower doses and longer half-life agents like
fluoxetine. Sparse research exists on the role
psychotherapy may play, but a small study sug- Antidepressants
gests that cognitive-behavioral therapy may pro-
vide patients with useful support and skills Joshua M. Matyi1 and JoAnn Tschanz1,2
1
through the discontinuation process (Cromarty Department of Psychology, Utah State
et al. 2011). University, Logan, UT, USA
2
Center for Epidemiologic Studies, Utah State
University, Logan, UT, USA
See Also

▶ Antidepressants Definition
▶ Depressive Disorder
▶ Major Depression Antidepressants are a class of medications that
▶ Minor Depressive Disorder are used primarily in the treatment of clinically
Antidepressants 281

severe mood and anxiety disorders. The majority which inhibit the activity of both MAO-A and
of effective antidepressants currently in use MAO-B, were known for potentially serious side
enhance neurotransmission of serotonin and/or effects if patients also consumed foods containing A
norepinephrine. Generally, this is achieved by tyramine (fermented products such as wine or
blocking the reuptake of the neurotransmitter cheese). Potential effects included headache,
substance(s), inhibiting the enzymes responsible hypertension, cerebral hemorrhage, and death.
for its metabolism, or directly stimulating the Newer generation MAOIs that act more selec-
postsynaptic receptors (Iversen et al. 2009). Sev- tively on MAO-A do not require the dietary
eral antidepressants are also used in treating gen- restriction from tyramine-containing foods. Side
eralized anxiety disorder, panic disorder, and effects associated with TCAs include dry mouth,
obsessive-compulsive disorder (Bourin and urinary retention, sedation, orthostatic hypoten-
Lambert 2002). Other conditions for which anti- sion, constipation, blurred vision, and weight
depressants have demonstrated efficacy include gain. Additionally, a concern regarding TCAs is
eating disorders (Powers and Bruty 2009), neu- the narrow therapeutic index, thus raising the risk
ropathic pain (O’Connor and Dworkin 2009), of death with overdose due to Q-T prolongation.
stress incontinence, nocturnal enuresis, ejaculatory By contrast, SSRIs do not carry the same health
disorders (Michel et al. 2006), migraine headaches, concerns as those of the TCAs or MAOIs. Com-
fibromyalgia (Stone et al. 2003), attention deficit mon side effects of SSRIs include nausea, head-
hyperactivity disorder (Chung et al. 2002), ache, anxiety, sexual dysfunction, and, the topic of
smoking cessation, insomnia, and possibly patho- much controversy, a possible increase in suicidal
logical gambling (Grant and Grosz 2004). ideation and behavior (see “Current Knowl-
There are several classes of antidepressant edge”). Side effects reported with the mixed
medications. Tricyclic antidepressants (TCAs) SSRI-NRI compound venlafaxine include head-
block the reuptake of monoaminergic neurotrans- ache, dry mouth, sedation, hypertension, and con-
mitters in the synaptic cleft, and monoamine oxi- stipation (Iversen et al. 2009).
dase inhibitors (MAOIs) inhibit their metabolism
in the presynaptic cell. Other compounds are more
selective in blocking the reuptake of specific Current Knowledge
neurotransmitters [selective serotonin reuptake
inhibitors (SSRIs) and noradrenergic reuptake Approximately 60–70% of persons treated with
inhibitors (NRIs)]. Compounds with dual seroto- antidepressants show a positive response. The
nergic and noradrenergic actions that have better lack of response in 30–40% of depressed individ-
tolerability have also been developed (Iversen uals (at least to SSRIs) may, in part, reflect the
et al. 2009). effects of genes. Variations in the serotonin trans-
Regardless of the type of antidepressant, the porter gene (often referred to as 5-HTTLPR) mod-
compounds are similar in their effectiveness and ify the response of depressed persons to SSRIs.
the time course of their effects. Generally, the lag Compared to those with a long (L) allele of this
between the initiation of antidepressant treatment gene, persons with a short allele exhibit poorer
and alleviation of symptoms generally takes two response to SSRI treatment. Variations in
to six weeks for the maximal response. The delay 5-HTTLPR may also influence the experience of
in treatment response suggests that the therapeutic side effects (Horstmann and Binder 2009).
effects may result from “downstream” events that The response rate to placebo in clinical trials of
reflect the brain’s adaptation to treatment (Iversen antidepressants is relatively high, ranging from
et al. 2009). Alternative treatments with a shorter 30% to 50%. The placebo response is greater
treatment lag are under active investigation (see among individuals with mild depressive symp-
“Future Directions”). toms, and recent meta-analyses of clinical trials
Antidepressant medications differ in their pro- of second-generation antidepressants indicate sig-
file of side effects. First-generation MAOIs, nificant treatment effects only among those with
282 Antidepressants

severe symptoms (Kirsch et al. 2008; Fournier and the hypothalamic-pituitary axis (HPA) (Dale
et al. 2010). et al. 2015). Furthermore, there is increasing evi-
Significant concerns of an increased risk of dence regarding the relationship between depres-
suicidal ideation and behavior (suicidality) have sion and processes such as neuronal plasticity and
arisen over the use of new-generation antidepres- neuroinflammation; future research is directed
sants. In 2006, the US Food and Drug Adminis- toward expanding potential therapeutic targets.
tration (FDA) issued a standing “black box”
advisory on SSRIs and other antidepressants
regarding an increased risk for suicidality in the
References and Readings
first few months of treatment among pediatric
through young adult patients (FDA 2007). How- Bourin, M., & Lambert, O. (2002). Pharmacotherapy of
ever, the research surrounding the FDA advisory anxious disorders. Human Psychopharmacol clin Exp,
has received substantial criticism (Isacsson and 17, 383–400.
Chung, B., Suzuki, A. R., & McGough, J. J. (2002). New
Rich 2014). The observed increase in suicidal
drugs for treatment of attention-deficit/hyperactivity
behavior is in contrast to epidemiological data disorder. Expert Opinion Emerging Drugs, 7, 269–276.
that indicate reduced rates of completed suicides. Dale, E., Bang-Andersen, B., & Sánchez, C. (2015).
Additionally, subsequent studies have shown no Emerging mechanisms and treatments for depression
beyond SSRIs and SNRIs. Biochemical pharmacology,
association between SSRI treatment and suicide
95(2), 81–97.
risk in youths (Gibbons et al. 2012; Strawn et al. Fournier, J. C., DeRubeis, R. J., Hollon, S. D., Dimidjian,
2015). Some have hypothesized that the higher S., Amsterdam, J. D., Shelton, R. C., & Fawcett, J.
risk of suicidality with antidepressant treatment (2010). Antidepressant drug effects and depression
severity: A patient-level meta-analysis. JAMA, 303,
likely occurs in a subset of high-risk patients with
47–53.
agitated major depression or unrecognized bipolar Gibbons, R. D., Brown, C. H., Hur, K., Davis, J. M., &
disorder (Rihmer and Akiskal 2006). Mann, J. J. (2012). Suicidal thoughts and behavior with
antidepressant treatment: Reanalysis of the randomized
placebo-controlled studies of fluoxetine and
venlafaxine. Archives of General Psychiatry, 69(6),
Future Directions 580–587.
Grant, J. E., & Grosz, R. (2004). Pharmacotherapy out-
More research is needed to examine the safety of come in older pathological gamblers: A preliminary
investigation. Journal of Geriatric Psychiatry and Neu-
antidepressant treatment in pediatric and young
rology, 17, 9–12.
adult populations. Thorough characterization of Horstmann, S., & Binder, E. B. (2009). Pharmacogenomics
patients may help clarify whether certain sub- of antidepressant drugs. Pharmacology and Therapeu-
groups are more vulnerable to develop suicidal tics, 124, 57–73.
Isacsson, G., & Rich, C. L. (2014). Antidepressant drugs
behaviors while receiving antidepressants. Addi-
and the risk of suicide in children and adolescents.
tionally, antidepressants are not effective for Pediatric Drugs, 16(2), 115–122.
30–40% of depressed patients. Current work is Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H.
exploring alternative treatments, for example, (2009). Antidepressants and anxiolytics. Introduction
to neuropsychopharmacology (pp. 306–335).
testing antagonists of NMDA glutamate receptors
New York: Oxford University Press.
for an antidepressant effect (Dale et al. 2015). Kirsch, I., Deacon, B. J., Huedo-Medina, T. B., Scoboria,
Initial studies with ketamine, an NMDA antago- A., Moore, T. J., & Johnson, B. T. (2008). Initial sever-
nist, show a significant antidepressant effect ity and antidepressant benefits: A meta-analysis of data
submitted to the food and drug administration. PlOS
within two hours (Skolnick et al. 2009). In addi-
Medicine, 5, e45.
tion to a more rapid treatment effect, it is hoped Michel, M. C., Ruhe, H. G., de Groot, A. A., Castro, R., &
that glutamate-based therapies will alleviate Oelke, M. (2006). Tolerability of amine uptake inhibi-
depressive symptoms among those unresponsive tors in urologic diseases. Current Drug Safety, 1,
73–85.
to current treatments. Other neurobiological sys-
O’Connor, A. B., & Dworkin, R. H. (2009). Treatment of
tems have also been implicated in antidepressant neuropathic pain: An overview of recent guidelines.
studies, such as GABAergic, cholinergic, opioid, Am Journal of Medicine, 122, S22–S32.
Antihistamines 283

Powers, P. S., & Bruty, H. (2009). Pharmacotherapy for insomnia. Antihistamines are most commonly
eating disorders and obesity. Child Adolescent Psychi- used to treat allergies; H1 receptor inverse ago-
atric Clinics of North America, 18, 175–187.
Rihmer, Z., & Akiskal, H. (2006). Do antidepressants t(h) nists typically reduce swelling and vasodilation A
reat(en) depressives? Toward a clinical judicious for- within the nasal area. H1 receptor antagonists
mulation of the antidepressant-suicidality FDA advi- include cetirizine, diphenhydramine also known as
sory in light of declining national suicide statistics from Benadryl, desloratadine, doxylamine, ebastine,
many countries. Journal of Affective Disorders, 94,
3–13. fexofenadine, loratadine, pheniramine, and pro-
Skolnick, P., Popik, P., & Trullas, R. (2009). Glutamate- methazine. H2 inverse agonists reduce gastric acid
based antidepressants: 20 years on. Trends in Pharma- and are used to treat ulcers and reflux. H2 receptor
cological Sciences, 30, 563–569. antagonists include cimetidine, famotidine,
Stone, K. J., Viera, A. J., & Parman, C. L. (2003). Off-label
applications for SSRIs. American Family Physician, lafutidine, nizatidine, ranitidine, and roxatidine. H3
68, 498–504. and H4 receptor antagonists are experimental in
Strawn, J. R., Welge, J. A., Wehry, A. M., Keeshin, B., & nature and are being investigated for their cognitive
Rynn, M. A. (2015). Efficacy and tolerability of anti- enhancing and immunomodulation abilities. H3
depressants in pediatric anxiety disorders: A systematic
review and meta-analysis. Depression and Anxiety, receptors reside mostly on neurons, so antagonists
32(3), 149–157. to these receptors could treat cognitive impair-
U.S. Food and Drug Administration. (2007). FDA proposes ment, schizophrenia, sleep disorders, epilepsy,
new warnings about suicidal thinking, behaviour in and neuropathic pain. H4 receptors reside mostly
young adults who take antidepressant medications.
Retrieved from: http://www.fda.gov/NewsEvents/News on hemopoietic cells, so their antagonists might
room/PressAnnouncements/2007/ucm108905.htm treat inflammatory diseases, pruritus, dermatitis,
asthma, and arthritis. Additionally, antihistamines
may be used to treat off-label issues such as
motion sickness, anxiety, and insomnia. Neuro-
psychologists must be aware of the potential
Antihistamines
effects of antihistamines on the physical, emo-
tional, and cognitive functioning of their patients.
Maya Balamane1 and
Side effects of antihistamine use may include dry
Stephanie A. Kolakowsky-Hayner2
1 nose and mouth, drowsiness, dizziness, headache,
Mount Sinai Brain Injury Research Center, San
upset stomach, loss of appetite, irritability, motor
Francisco, CA, USA
2 slowness, diminished processing speed, and
Department of Rehabilitation Medicine, Icahn
impaired visual skills. Antihistamine effects are
School of Medicine at Mount Sinai, New York,
exacerbated by the use of alcohol and other sub-
NY, USA
stances, which in turn will be of further detriment
to neuropsychological testing.
Synonyms
Cross-References
Histamine antagonist; Inverse histamine agonists
▶ Pharmacodynamics
▶ Pharmacokinetics
Definition ▶ Psychopharmacology

Antihistamines have multiple clinical indications

including allergic conditions (rhinitis, dermato- References and Readings
ses, atopic dermatitis, contact dermatitis, allergic
conjunctivitis, hypersensitivity reactions to drugs, Hindmarch, I., & Shamsi, Z. (1999). Antihistamines:
mild transfusion reactions, and urticaria), chronic Models to assess sedative properties, assessment of
sedation, safety and other side-effects. Clinical &
idiopathic urticaria, motion sickness, vertigo, and Experimental Allergy, 29, 133–142.
284 Antihypertensives

Matsushita, A., Seike, M., Okawa, H., Kadawaki, Y., & disease, retinopathy) or cardiovascular disease.
Ohtsu, H. (2012). Advantages of histamine H4 receptor Cardiovascular risks decrease when the blood
antagonist usage with H1 receptor antagonist for the
treatment of murine allergic contact dermatitis. Exper- pressure is below 139/89. Typical agents for
imental Dermatology, 21(9), 714–7155. treating hypertension include diuretics, beta-
Parsons, M., & Ganellin, C. (2006). Histamine and its blockers, ACE (angiotensin-converting enzyme)
receptors. British Journal of Pharmacology, 147, inhibitors, calcium channel blockers, peripheral
S127–S135.
Theunissen, E., Vermeeren, A., van Oers, A., van Maris, I., alpha selective blockers, central alpha2 agonists,
& Ramaekers, J. (2004). A dose-ranging study of the direct vasodilators, and adrenergic antagonists.
effects of mequitazine on actual driving, memory and
psychomotor performance as compared to
dexchlorpheniramine, cetirizine and placebo. Clinical
& Experimental Allergy, 34(2), 250–258. Current Knowledge
Thurmond, R. L. (2015). The histamine H4 receptor:
From orphan to the clinic. Frontiers in Pharmacology, Hypertension is a risk factor for stroke, myocardial
6, 65. infarction, renal failure, congestive heart failure,
van Ruitenbeek, P., Vermeeren, A., Smulders, F., Sambeth,
A., & Riedel, W. (2009). Histamine H1 receptor block- progressive atherosclerosis, and dementia. Treat-
ade predominantly impairs sensory processes in human ment reduces the risks of heart disease as well as
sensorimotor performance. British Journal of Pharma- cardiovascular morbidity. For stage I hypertension,
cology, 157(1), 76–85. the blood pressure ranges from 140/90 to 159/99;
Vuurman, E., Rikken, G., Muntjewerff, N., de Halleux, F.,
& Ramaekers, J. (2004). Effects of desloratadine, for stage II and stage III blood pressure, the systolic
diphenhydramine, and placebo on driving performance number is greater than 160 and diastolic is greater
and psychomotor performance measurements. than 100.
European Journal of Clinical Pharmacology, 60(5), Monotherapy is preferred initially. The first
307–313.
Zlomuzica, A., Ruocco, L., Sadile, A., Huston, J., & Dere, line of treatment is beta-blockers and diuretics
E. (2009). Histamine H1 receptor knockout mice for uncomplicated hypertension individuals who
exhibit impaired spatial memory in the eight-arm do not have preexisting coronary disease, diabe-
radial maze. British Journal of Pharmacology, tes, or proteinuria. In patients with diabetes
157(1), 86–91.
mellitus, renal disease, or CHF, ACE inhibitors
and angiotensin receptor antagonists are the
appropriate initial therapy. Typically, the patient
is started on a low dose of long-acting, once-daily
Antihypertensives drug, and the dose is titrated until the blood pres-
sure is lowered. If blood pressure is not controlled
Mary Pat Murphy with the dose of a single drug, a second agent from
MSN, CRRN, Paoli, PA, USA a different class is recommended. Combination
therapy provides more rapid control of hyperten-
sion and is recommended for patients with stages
Definition II and III hypertension. Triple-drug therapy may
be required if the blood pressure control is not
Antihypertensives are pharmacologic agents used achieved. Some patients have resistant hyperten-
to lower blood pressure to normal levels or near sion. A fourth line of medications may be
normal levels. The initiation and intensity of drug required.
treatment depends on blood pressure level, the
individual’s risk factors (smoking, dyslipidemia,
diabetes mellitus, older than 60, male, postmeno- Classes of Antihypertensives
pausal women, and family history of cardiovascu-
lar disease for women under 65 and men under Diuretics
55 years of age), and target organ damage (e.g., Diuretics decrease blood pressure by causing
strokeor TIA, nephropathy, peripheral artery diuresis, which results in decreased blood volume,
Antihypertensives 285

cardiac output, and stroke volume. They fall into over 14 days to prevent withdrawal which
three categories: thiazides, loop diuretics, and includes unstable angina, myocardial infarction,
potassium-sparing diuretics. Thiazide’s onset of and death. A
action occurs within 2–3 h. Their half-life is
8–12 h allowing for once-daily dosing. Trade ACE Inhibitors
names include Hygroton, Hydrodiuril, Lozol, This class of antihypertensives inhibits ACE
and Zaroxolyn. which converts angiotensin I to II – a potent
Loop diuretics act in the loop of Henle in vasoconstrictor. This is a first-line therapy for
the kidney and are less effective in the long patients with diabetes and proteinuria. Medica-
term. Their duration is 6 h. These agents are tions include Lotensin, Capoten, Vasotec, Mono-
indicated with CHF or nephrotic syndrome. pril, Zestril, Univasc, Accupril, Altace, and
Bumex, Edecrin, Lasix, and Demadex are trade Mavik.
names. Side effects include cough, hypotension,
Potassium-sparing agents cause minimal hyperkalemia, rash, loss of taste, leukopenia, and
diuresis and are relatively ineffective in lowering neutropenia. They are contraindicated in preg-
the blood pressure. The medications correct nancy and for patients with bilateral real artery
thiazide-induced potassium and magnesium stenosis.
losses. Medication trade names include Midamor,
Aldactone, and Dyrenium. Calcium Channel Blockers
Calcium channel blockers relax the cardiac and
Adverse Events smooth muscle by blocking calcium channels that
Most complications occur related to dose and allow calcium into the cells. The result is vasodi-
duration of use. Hypokalemia is a side effect, but lation. They also decrease the heart rate and slow
can be managed with potassium chloride or use of cardiac conduction. Medications include Calan,
potassium-sparing agents. Cardizem, Norvasc, Plendil, Procardia Cardene,
Acute gouty arthritis, muscle cramps, develop- Sular, and DynaCirc.
ment of diabetes, nocturia or incontinence, and
sun sensitivity have been noted as clinical side Side Effects
effects. Side effects include GI upset, edema, and hypo-
tension. Rare side effects include bradycardia,
Beta-Blocking Agents CHF, and AV block. Other adverse effects include
Beta1-receptors are located in the heart and kid- dizziness, headache, shortness of breath, gingival
neys and regulate heart rate and cardiac contrac- hyperplasia, and edema.
tility. Beta2-receptors regulate bronchodilation
and vasodilation. Beta-blockers decrease blood Contraindications
pressure by blocking the beta-receptors. Some Calcium channel blockers should not be pre-
beta-blockers are cardioselective, that is, they scribed for individuals with second- and third-
do not block the beta2-receptors and, therefore, degree heart block or left ventricular dysfunction.
do not cause bronchoconstriction. These medi-
cations include Lopressor, Kerlone, Tenormin, Other Classes of Antihypertensives
Sectral and Zebeta, Corgard, Inderal, and Peripheral alpha1-receptors (Cardura, Minipress,
Cartrol. and Hytrin), central alpha2 (Clonidine, Aldomet,
Tenex, and Wytension), direct vasodilators
Side Effects (Apresoline and Loniten), and adrenergic antago-
The most common side effects of beta-blockers nists (Serpasil, Ismelin and Hylorel) are the
are fatigue, dizziness, bronchospasm, nausea, remaining categories of antihypertensives. They
and vomiting. Beta-blockers should not be are mainly used as second- and third-line
discontinued abruptly but should be tapered medications.
286 Antiplatelet Therapy

Cross-References together by the protein, fibrin. Together, the fibrin

and the platelet clump comprise the thrombus or
▶ Psychopharmacology blood clot. Thrombi are useful in that they stop
▶ Stroke bleeding in normal circumstances. When there is a
▶ Transient Ischemic Attack break in an artery, allowing blood to leave the
vessel, platelets become activated by attaching to
the wall of the blood vessel at the site of the bleeding
References and Readings and by attracting fibrin and other coagulation factors
to the area to stop the bleeding. However, if the
August, P. (2003). Initial treatment of hypertension. New blood clot forms inside the artery, it can block the
England Journal of Medicine, 348, 610–617.
flow of blood to the tissue that is supplied by the
Cranwell-Bruce, L. (2008). Antihypertensives. Medsurg
Nursing, 17(5), 337–341. artery, which can result in tissue damage. A clot
Ernst, M., & Moser, M. (2009). Use of diuretics in patients forming in the coronary artery causes ischemic heart
with hypertension. New England Journal of Medicine, disease (which may present as angina or myocardial
361, 2153–2164.
infarction), and when the blood clot forms in the
Houston, M. C., Pulliam Meador, B., & Moore Schipani, L.
(2000). Handbook of antihypertensive therapy carotid or cerebral arteries, it may cause a stroke.
(10th ed.). Philadelphia: Hanley & Belfus.
Staessen, J., & Birkenhager, W. (2005). Evidence that new
antihypertensives are superior to older drugs. Lancet,
366(9489), 869–871.
Current Knowledge

Many studies have demonstrated the effectiveness

of aspirin and other antiplatelet agents in pre-
venting heart attack and stroke. This favorable
Antiplatelet Therapy effect is based on the ability of these agents to
inhibit the chemicals that cause platelets to clump
Elliot J. Roth together initiating blood clot formation.
Department of Physical Medicine and Aspirin is the prototypical antiplatelet agent.
Rehabilitation, Northwestern University, Other currently available antiplatelet agents
Feinberg School of Medicine, Chicago, IL, USA include ticlopidine (Ticlid ®), clopidogrel
(Plavix ®), and dipyridamole (Persantine ®).
Recently, a newer antiplatelet drug, ticagrelor
Synonyms (BRILINTA ®), became available. Occasionally,
the drugs are used in combination with each
Platelet anti-aggregant drugs other or with anticoagulants. The most common
side effect of all of these medications is bleeding.

Definition
See Also
Antiplatelet therapy uses specific pharmacological
agents (antiplatelet drugs) to inhibit the ability of ▶ Anticoagulation
platelets to clump together to form blood clots or ▶ Atherosclerosis
thromboses, primarily in arteries. Antiplatelet ther- ▶ Cerebrovascular Disease
apy is commonly used in people with atherosclero- ▶ Coronary Disease
sis (narrowing of the arteries). Platelets are naturally ▶ Ischemic Stroke
occurring cells (actually, portions of cells) that cir- ▶ Myocardial Infarction
culate in the blood. They clump, or aggregate, under ▶ Novel Oral Anticoagulants
certain conditions to initiate the formation of blood ▶ Peripheral Vascular Disease
clots. These platelet clumps are then further bound ▶ Stent
Antipsychotics 287

References population and may require treatment with atyp-

ical antipsychotics to help restore behavioral
Jhansi, K., & Vanita, P. (2014). A review on antiplatelet and cognitive stability.
drugs and anticoagulants. Advance Pharmacoepi- A
demiology Drug Safety, 3, R003.
Tran, H., & Anand, S. S. (2004). Oral antiplatelet therapy
in cerebrovascular disease, coronary artery disease, and Historical Background
peripheral arterial disease. Journal of the American
Medical Association, 292, 1867–1874.
Antipsychotic medications according to Preston
White, H. D. (2011). Oral anti-platelet therapy for
atherothrombotic disease: Current evidence and new et al. (2006) have “truly revolutionized” the treat-
directions. American Heart Journal, 161, 450–461. ment of psychotic disorders. Conventional/typical
antipsychotics act primarily through blockade of
dopamine D2 receptors. Chlorpromazine(Thora-
zine), a phenothiazine, was first used in 1952 as a
Antipsychotics postoperative agent, but quickly became a stan-
dard treatment for sedation, reducing psychotic
Helen M. Carmine symptoms of psychiatric patients, and soon
ReMed, Paoli, PA, USA many other “phenothiazines” were developed
(Preston et al. 2006). The role of dopamine 2 post-
synaptic receptor blockade led to the development
Synonyms of future dopamine blockers that are chemically
targeted to reduce and selectively block/weakly
Antipsychotic medications; Atypicals block dopamine to minimize side effects. Since
(antipsychotics); Conventional antipsychotics; that time, off-label use of these agents has
High-potency/low-potency groups of antipsy- benefited other populations. These agents were
chotics; Neuroleptics; Standard antipsychotics called “neuroleptics” because as a result of their
dopamine blockade, they also lead to other neu-
rological side effects/undesired effects. The newer
Definition antipsychotics, known as “atypicals,” are strong
serotonin blockers (5-HT2A and 5-HT2C) and
Antipsychotic agents are used for the treatment of produce varying degrees of dopamine blockade,
psychotic disorders, severe mental illnesses, and weakly blocking D2 receptors and D1 receptors,
mood/behavior disorders not responsive to other and also act on the serotonin, dopamine, and
medication/behavioral interventions. Broader GABA neurotransmitter systems. This multiple
application/often “off-label” are used to address pathway approach may help with the individuali-
thought/behavior disorders in various populations zation and selection of the best agent based on the
including adults with dementia, traumatic brain individual’s response.
injury, developmental disorders with behavioral
symptoms unresponsive to other treatments, and
individuals with depression who are not respon- Current Knowledge
sive to antidepressant therapy alone. Specifically
in TBI populations, according to B.C. McDonald Standard antipsychotics have been used since the
et al. (2002), neuroleptics agents may have a 1950s for their sedating effects on individuals
role in individuals whose cognition and behav- with psychosis/psychotic symptoms. As pheno-
iors are disorganized and who are agitated. thiazines were known to produce these effects as
Another study by Ahmed and Fuiji (1998) iden- postoperative sedation agents, the sedating effect
tified that individuals who have a brain injury led to the development of additional standard
experience a two- to fivefold greater risk of antipsychotic agents produced and utilized
developing psychosis than the general through the 1980s, including, but not limited to,
288 Antipsychotics

agents such as Thorazine, Mellaril, Stelazine, Pro- However, with these newer “atypical antipsy-
lixin, Navane, and Trilafon. These standard anti- chotics,” other concerning side effects have been
psychotic agents were divided into high- and low- exposed including metabolic changes leading to
potency groups based on their profiles indicating alterations in carbohydrate and lipid metabolism,
desirable/undesirable effects including sedation, possible diabetes, and excessive weight gain. All
anticholinergic/parasympathetic side effects of these newer agents require routine monitoring
including urinary and bowel retention, dry of weight, blood sugar, and lipid profile studies to
mouth and cardiovascular effects, and extrapyra- control the potential adverse effects while achiev-
midal symptoms as a result of their dopamine ing improvement in both positive and negative
blockade, their effects on sympathetic blockade/ symptoms of psychosis. Treatment duration with
alpha adrenergic blockade leading to hypotension these agents is individually maximized based on
and dizziness, and the effects of neurotransmis- response to reduction in positive symptoms of
sion leading to involuntary movements (tardive chronic thought disorders/psychosis. Shorter
dyskinesias) and extrapyramidal symptoms. treatment durations may be possible in acute
Other adverse effects noted with typical antipsy- onset of delirium, acute psychoses, or brief reac-
chotics include lowering seizure threshold, ther- tive psychosis.
mal dysregulation, hormonal dysregulation
including hyperprolactinemia, and a fatal but
rare side effect known as neuroleptic malignant Future Directions
syndrome characterized by fever, rigidity, and
confusion. Obviously, all medication agents The use of the newer atypical agents has been
require close monitoring and may also require shown to produce a reduction in hostility and
other agents to address undesired effects, or low- aggression in schizophrenic patients, elderly
ering of the antipsychotic agent or change in patients with dementia, and empirically with indi-
administration time to minimize untoward effects. viduals experiencing aggression and agitation in
Newer “atypical” or “novel” agents with TBI. The next generation of agents will be directed
Clozaril (Clozapine) as the first agent in this cat- at further reducing overall side effects while max-
egory have been noted to be effective in signifi- imizing treatment response and symptom reduction
cantly reducing the symptoms of psychosis, while returning to optimal daily functioning and
particularly when other agents are unsuccessful, cognitive, mood, and behavioral stability.
by targeting specific dopamine receptors or
blocking/inhibiting reuptake of serotonin. The
most significant difference is in the reduction of Cross-References
the negative symptoms and the lower risk of
developing tardive dyskinesias. However, ▶ Neuroleptics
Clozaril’s effects on the bone marrow may lead ▶ Psychopharmacology
to a severe blood disorder, agranulocytosis. ▶ Psychotic Disorder
Clozaril requires adherence to an FDA protocol
for complete blood count/ANC monitoring based
on threshold values. Newer atypical agents were References and Readings
developed to improve the reduction of negative
Ahmed, I. I., & Fuiji, D. (1998). Posttraumatic Psychosis.
symptoms, improve cognition, and decrease risk Seminars in. Clinical Neuropsychology, 3(1), 23–33.
of tardive dyskinesias and other neurological McDonald, B. C., Flashman, L. A., & Saykin, A. J. (2002).
changes resulting from these agents. Executive dysfunction following traumatic brain
injury: neural substrates and treatment strategies.
Newer “atypical/novel” antipsychotic agents NeuroRehabilitation, 17(4), 333–344.
have included Risperidone, Zyprexa, Seroquel, Meredith, C., Jaffe, C., Ang-Lee, K., & Saxon, A. (2005).
Geodon, Abilify, and, most recently, Saphris. Implications of chronic methamphetamine use:
Antisocial Personality Disorder 289

A literature review. Harvard Review of Psychiatry, • Irritability and aggressiveness, with no

13(3), 141–154. remorse.
Preston, J., O’Neal, J. H., & Talaga, M. C. (2006). Child
and adolescent clinical psychopharmacology made A
simple. Oakland: New Harbinger Publications. The symptoms must not present exclusively in
Savitz, J., van der Merwe, L., Stein, D., Solms, M., & the course of schizophrenic or bipolar disorders.
Ramesar, R. (2008). Neuropsychological task perfor- Individuals with ASPD often display superficial
mance in bipolar spectrum illness: genetics, alcohol
abuse, medication and childhood trauma. Bipolar Dis- charm initially but then treat others with disdain
orders, 10(4), 479–494. and contempt.
Voruganti, L., & Awad, A. (2004). Neuroleptic dysphoria:
Towards a new synthesis neuroleptic dysphoria. Psy-
chopharmacology, 171(2), 121–132.
Wozniak, J., Block, E., White, T., Jensen, J., & Schulz, Categorization
S. (2008). Clinical and neurocognitive course in early-
onset psychosis: a longitudinal study of adolescents ASPD is classified with the Cluster B Personality
with schizophrenia-spectrum disorders. Early Interven- Disorders in DSM-5.
tion in Psychiatry, 2(3), 169–177.

Current Knowledge
Antisocial Personality
Prevalence
Disorder Prevalence estimates range from 0.2% to 3.3%,
with men outnumbering women 3:1 (APA 2013).
Cynthia Rolston
Higher rates of ASPD occur in males with alcohol
Department of PM&R, Virginia Commonwealth
abuse, individuals in substance abuse clinics and
University-Medical College of Virginia,
prisons, and people in adverse socioeconomic
Richmond, VA, USA
conditions.

Clinical Correlates
Synonyms Adolescent conduct disorder (CD) often predates
ASPD, with earlier onset predictive of poor prog-
Dyssocial personality disorder; Psychopathy; nosis (Black 2015). ASPD symptoms may be less
Sociopathy evident with age. Substance Abuse (SA) is com-
mon in ASPD. Men with SA and ASPD may
report more antisocial behaviors if they have a
Definition history of childhood trauma (Sher et al. 2015).
Women with SA and ASPD may be at risk for
Antisocial personality disorder (ASPD) is charac- committing violent acts in intimate relationships
terized by gross and guiltless disregard for and (Dykstra et al. 2015). Women have higher rates of
violation of others’ rights, present since age 15 aggressiveness and irritability (versus violence),
and persisting in adulthood. Diagnostic and Sta- greater overall impairment, lower social support,
tistical Manual of Mental Disorders (5th ed.; more emotional neglect in childhood, sexual
DSM-5; American Psychiatric Association 2013) abuse, and other victimization (Alegria et al.
criteria include: 2013). Cognitive performance and criminal
behavior patterns differed in inmates with ASPD
• Nonconformity to social norms, unlawful and psychopathy compared to those with only
behavior. ASPD, suggesting ASPD and psychopathy are
• Deceitful, impulsive, irresponsible, and reck- distinct, although frequently co-occurring (Riser
less behavior. and Kosson 2013).
290 Antisocial Personality Disorder

Physiology and Neuropsychology References and Readings

A “highly heritable common factor” may account
for ASPD criteria interrelations (Rosenström et al. Alegria, A. A., Blanco, C., Petry, N. M., Skodol, A. E., Liu,
2017). In one study, genetics accounted for 71% S. M., Grant, B., & Hasin, D. (2013). Sex differences in
antisocial personality disorder: Results from the
of the stability of ASPD, whereas environmental
national epidemiological survey on alcohol and related
factors impacted phenotypic expression of the conditions. Personality Disorders, 4(3), 214–222.
condition (Reichborn-Kjennerud et al. 2015). https://doi.org/10.1037/a0031681.
Monoamine oxidase A (MAO-A) has been linked American Psychiatric Association. (2013). Diagnostic and
statistical manual of mental disorders (5th ed.). Arling-
to deregulation of prefrontal regions and seroto-
ton: American Psychiatric Association Publishing.
nergic systems in this population (Kolla et al. Bateman, A., O’Connell, J., Lorenzini, N., Gardner, T., &
2016). ASPD has also been associated with Fonagy, P. (2016). A randomised controlled trial of
reduced grey matter volume in the frontal cortex mentalization-based treatment versus structured clini-
cal management for patients with comorbid borderline
(Rautiainen et al. 2016), reduced cortical thick-
personality disorder and antisocial personality disorder.
ness, increased surface area, and diminished BMC Psychiatry, 16, 304-016-1000-9. https://doi.org/
frontotemporal network activity (Jiang et al. 10.1186/s12888-016-1000-9.
2016; Liu et al. 2014). Black, D. W. (2015). The natural history of antisocial
personality disorder. Canadian Journal of Psychiatry
Revue Canadienne De Psychiatrie, 60(7), 309–314.
Assessment and Treatment Black, D. W., Simsek-Duran, F., Blum, N., McCormick,
B., & Allen, J. (2016). Do people with borderline
ASPD may be assessed through clinical inter- personality disorder complicated by antisocial person-
view, records review, self-report measures, and ality disorder benefit from the STEPPS treatment pro-
objective personality measures such as the Min- gram? Personality and Mental Health, 10(3), 205–215.
nesota Multiphasic Personality Inventory https://doi.org/10.1002/pmh.1326.
Dykstra, R. E., Schumacher, J. A., Mota, N., & Coffey, S.
(MMPI) or the Millon Clinical Multiaxial Inven- F. (2015). Examining the role of antisocial personality
tory (MCMI). Most individuals with ASPD do disorder in intimate partner violence among substance
not seek help for characterological concerns, but use disorder treatment seekers with clinically signifi-
they may seek treatment for depression, anxiety, cant trauma histories. Violence Against Women, 21(8),
958–974. https://doi.org/10.1177/1077801215589377.
or SA. ASPD treatment typically focuses on Jiang, W., Li, G., Liu, H., Shi, F., Wang, T., Shen, C., . . . Shen,
reducing negative and destructive behaviors. D. (2016). Reduced cortical thickness and increased sur-
Empirical supported psychotherapeutic interven- face area in antisocial personality disorder. Neuroscience,
tions include impulsive lifestyle counseling 337, 143–152. https://doi.org/S0306-4522(16)30434-1.
Kolla, N. J., Dunlop, K., Downar, J., Links, P., Bagby, R. M.,
(Thylstrup and Hesse 2016), affect management Wilson, A. A., et al. (2016). Association of ventral striatum
and problem solving (Black et al. 2016), monoamine oxidase-A binding and functional connectiv-
mentalization-based treatment emphasizing ity in antisocial personality disorder with high impulsivity:
appreciation of others’ mental states (Bateman A positron emission tomography and functional magnetic
resonance imaging study. European Neuropsychophar-
et al. 2016), and mindfulness-based treatment to macology: The Journal of the European College of
reduce aggression (Velotti et al. 2016). Pharma- Neuropsychopharmacology, 26(4), 777–786. https://doi.
cological treatments may include clozapine, org/10.1016/j.euroneuro.2015.12.030.
ACE inhibitors, and opioid antagonists for treat- Liu, H., Liao, J., Jiang, W., & Wang, W. (2014). Changes in
low-frequency fluctuations in patients with antisocial
ment of endogenous opioid system dysfunction. personality disorder revealed by resting-state func-
tional MRI. PloS One, 9(3), e89790. https://doi.org/
10.1371/journal.pone.0089790.
Rautiainen, M. R., Paunio, T., Repo-Tiihonen, E.,
See Also Virkkunen, M., Ollila, H. M., Sulkava, S., et al.
(2016). Genome-wide association study of antisocial
▶ Conduct Disorder personality disorder. Translational Psychiatry, 6(9),
e883. https://doi.org/10.1038/tp.2016.155.
▶ Hare Psychopathy Checklist Reichborn-Kjennerud, T., Czajkowski, N., Ystrom, E.,
▶ Personality Disorders Orstavik, R., Aggen, S. H., Tambs, K., et al. (2015).
▶ Substance Abuse A longitudinal twin study of borderline and antisocial
Anxiety 291

personality disorder traits in early to middle adulthood. Anxiety is similar to the emotion of fear,
Psychological Medicine, 45(14), 3121–3131. https:// although the function of chronic anxiety is
doi.org/10.1017/S0033291715001117.
Riser, R. E., & Kosson, D. S. (2013). Criminal behavior often to avoid or mask true fear through mecha- A
and cognitive processing in male offenders with anti- nisms of anxiety such as worry and anticipation
social personality disorder with and without comorbid of negative future outcomes. The physiological
psychopathy. Personality Disorders, 4(4), 332–340. manifestations of anxiety include increased
https://doi.org/10.1037/a0033303.
Rosenström, T., Ystrom, E., Torvik, F. A., Czajkowski, N. blood pressure; increased breathing rate (often
O., Gillespie, N. A., Aggen, S. H., . . . Reichborn- shallow); increased heart rate; other cardiac
Kjennerud, T. (2017). Genetic and environmental struc- symptoms (e.g., pain, “skipped” beats); gastro-
ture of DSM-IV criteria for antisocial personality dis- intestinal distress including nausea, stomach
order: A twin study. Behavior Genetics. https://doi.org/
10.1007/s10519-016-9833-z. aches, increased motility of the gut, and diarrhea;
Sher, L., Siever, L. J., Goodman, M., McNamara, M., and generalized bodily distress such as fatigue
Hazlett, E. A., Koenigsberg, H. W., & New, A. S. and pain. Cognitively, anxiety is frequently char-
(2015). Gender differences in the clinical character- acterized by an overestimation of the probability
istics and psychiatric comorbidity in patients
with antisocial personality disorder. Psychiatry of a negative future outcome and an exaggeration
Research, 229(3), 685–689. https://doi.org/10.1016/ of the consequences of the negative outcome. For
j.psychres.2015.08.022. example, an anxious person may believe that it is
Thylstrup, B., & Hesse, M. (2016). Impulsive lifestyle likely that they will fail a test with catastrophic
counseling to prevent dropout from treatment for
substance use disorders in people with antisocial consequences.
personality disorder: A randomized study. Addictive Anxiety often occurs in response to external
Behaviors, 57, 48–54. https://doi.org/10.1016/ stressors. It can be a normal reaction to stress,
j.addbeh.2016.02.001. in which case anxiety can help coping behavior
Velotti, P., Garofalo, C., D’Aguanno, M., Petrocchi, C.,
Popolo, R., Salvatore, G., & Dimaggio, G. (2016). by focusing attention, mobilizing energy,
Mindfulness moderates the relationship between and increasing goal-directed behavior. How-
aggression and antisocial personality disorder traits: ever, anxiety can also be a reaction to internal
Preliminary investigation with an offender sample. (physiological) cues or a generalized and
Comprehensive Psychiatry, 64, 38–45. https://doi.org/
10.1016/j.comppsych.2015.08.004. pervasive mood without identifiable precipi-
tants. When anxiety is an excessive reaction,
or present in the absence of any true challenges
or dangers, it is considered pathological. Indi-
viduals with pathological levels of anxiety are
Anxiety typically high in “trait” anxiety, which is a sta-
ble and enduring tendency to respond with anx-
Joel W. Hughes
iety to a wide variety of situations. Individuals
Department of Psychology, Kent State University,
high in trait anxiety are often also high in
Kent, OH, USA
neuroticism.

Synonyms
Historical Background
Fear
Anxiety is basic to human experience and has
been documented and treated since the beginning
of recorded history. The relation between anxiety
Definition and health complaints has been recognized since
the seventeenth century, although psychiatric
Anxiety is an unpleasant state characterized by nosology did not become well developed until
affective, cognitive, and physiological elements the last century. A number of anxiety disorders
such as fear, worry, apprehension, and tension. have been delineated in contemporary psychiatric
292 Anxiolytics

writings and are described in the most recent anxiety-generating cognitions. Anxiolytic medi-
edition of the Diagnostic and Statistical Manual cation is also often prescribed.
of Mental Disorders published by the American
Psychiatric Association.
Cross-References
Current Knowledge ▶ Anxiolytics
▶ Beck Anxiety Inventory
Although anxiety can be learned, it is thought to
have a biological basis in the amygdala and hip-
pocampus. When individuals are exposed to
potentially dangerous or harmful stimuli, brain References and Readings
imaging often shows increased activity in the
amygdala accompanied by participant reports of Allen, L. B., McHugh, R. K., & Barlow, D. H. (2008).
Emotional disorders: A unified protocol. In D. H. Bar-
increased anxiety. Excessive anxiety can also low (Ed.), Clinical handbook of psychological disor-
compromise performance on neuropsychological ders: A step-by-step treatment manual (4th ed.,
tests, especially by interfering with attention and pp. 216–249). New York: Guilford Press.
cognitive efficiency. American Psychiatric Association. (2000). Diagnostic and
statistical manual of mental disorders (4th ed.), Text
When suspected, the level of anxiety should be Revision. Washington, DC: American Psychiatric
assessed. Anxiety is often measured using the Association.
Beck Anxiety Inventory or Hamilton Anxiety American Psychiatric Association. (2013). Diagnostic and
Scale. They do not diagnose anxiety disorders statistical manual of mental disorders (DSM-5 ®).
Arlington: American Psychiatric Publishing.
but give a dimensional measure of anxiety. Beck, A. T., & Steer, R. A. (1990). Manual for the Beck
There are a number of recognized anxiety dis- anxiety inventory. San Antonio, TX: Psychological
orders in the contemporary psychiatric nosology Corporation.
(i.e., DSM 5). They are (alphabetically): Maier, W., Buller, R., Philipp, M., & Heuser, I. (1988). The
Hamilton anxiety scale: Reliability, validity and sensi-
tivity to change in anxiety and depressive disorders.
Agoraphobia Journal of Affective Disorders, 14(1), 61–68.
Generalized anxiety disorder
Panic disorder
Selective mutism
Separation anxiety disorder
Social anxiety disorder Anxiolytics
Specific phobia
Chava Creque1 and
Additional anxiety-related disorders in the cur- Stephanie A. Kolakowsky-Hayner2
1
rent diagnostic system such as obsessive compul- Department of Psychology and Neuroscience,
sive disorder and posttraumatic stress disorder University of Colorado Boulder, Boulder,
have been reclassified into new sections of the CO, USA
2
diagnostic and statistical manual of mental disor- Department of Rehabilitation Medicine, Icahn
ders (DSM-5 ®). School of Medicine at Mount Sinai, New York,
Effective treatment of anxiety almost always NY, USA
involves exposure to the feared stimulus. Treat-
ments are based on the principles of classical
conditioning, and the goal is to extinguish the
fear response through exposure and habituation. Synonyms
Exposure can be in vivo or imaginal, and therapy
frequently uses cognitive techniques to modify Anti-anxiety drugs; Anti-anxiety medications
Apathy 293

Definition References and Readings

Anxiolytics are prescription drugs used to reduce the Cosci, F., Schruers, K., Faravelli, C., & Griez, E. (2004).
The influence of alcohol oral intake on the effects of A
severity and extent of symptoms due to anxiety-
35% CO2 challenge: A study in healthy volunteers.
related disorders. The most commonly prescribed Acta Neuropsychiatrica, 16(2), 107–109.
anxiolytic drugs are benzodiazepines, drugs used to Deacon, R., Bannerman, D., & Rawlins, J. (2002). Anxio-
treat generalized anxiety disorder, panic attacks, pho- lytic effects of cytotoxic hippocampal lesions in rats.
Behavioral Neuroscience, 116(3), 494–497.
bias, and other ongoing issues of excessive fear and
Harmer, C. J. (2012). Have no fear: The neural basis of
dread. Medical illness often associated with high anxiolytic drug action in generalized social phobia.
levels of anxiety also includes brain injury, heart Biological Psychiatry Journal, 73(4), 300–301.
disease, and COPD. There are six approved benzo- Karl, T., Duffy, L., Scimone, A., Harvey, R., & Schofield, P.
(2007). Altered motor activity, exploration and anxiety
diazepines in the USA today including the popular
in heterozygous neuregulin 1 mutant mice: Implications
diazepam (Valium), lorazepam (Ativan), and alpraz- for understanding schizophrenia. Genes, Brain, and
olam (Xanax). Anxiolytics are designed to impact Behavior, 6(7), 677–687.
neurotransmitters in the amygdala by increasing Lanctôt, K., Herrmann, N., Mazzotta, P., Khan, L., &
Ingber, N. (2004). GABAergic function in Alzheimer’s
gamma-aminobutyric acid (GABA), an inhibitory
disease: Evidence for dysfunction and potential as a
neurotransmitter that diminishes the fear response. therapeutic target for the treatment of behavioural and
Other drugs with anxiolytic effects include selective psychological symptoms of dementia. Canadian Jour-
serotonin reuptake inhibitors (SSRIs). nal of Psychiatry, 49(7), 439–453.
McHugh, S., Deacon, R., Rawlins, J., & Bannerman, D.
Neuropsychologists must be aware of the poten-
(2004). Amygdala and ventral hippocampus contribute
tial effects of anxiolytics on the physical, emotional, differentially to mechanisms of fear and anxiety.
and cognitive functioning of their patients. Anxio- Behavioral Neuroscience, 118(1), 63–78.
lytics are highly addictive and are often abused Stein, R. A., & Strickland, T. L. (1998). A review of the
neuropsychological effects of commonly used prescrip-
when used as a recreational drug. Patients may
tion medications. Archives of Clinical Neuropsychol-
also become dependent on their medication if on ogy, 13(3), 259–284.
increased doses for long periods of time. Side Treit, D., & Menard, J. (1997). Dissociations among the
effects of anxiolytics may include excessive drows- anxiolytic effects of septal, hippocampal, and amygda-
loid lesions. Behavioral Neuroscience, 111(3), 653–658.
iness to the point of sedation; suicidal thoughts;
unexplained excitement, rage, anger, or hostility;
confusion and cognitive slowing; balance and diz-
ziness issues; diminished motor and visual skills; Apathy
breathing issues; and memory impairment. Nega-
tive side effects may impact neuropsychological Laura L. Frakey
testing and treatment, and these effects should be Memorial Hospital of Rhode Island and Alpert
considered in treatment planning and recommenda- Medical School of Brown University, Pawtucket,
tions. Clinicians should also take into account RI, USA
patient age, medication dose, and concurrent med-
ications, all of which can have an impact on neuro-
psychological performance of someone under the Synonyms
influence of anxiolytic medication.
Abulia; Amotivational; Anhedonia; Negative
symptom
Cross-References

▶ Benzodiazepines Short Description or Definition

▶ Diazepam
▶ GABA In the vernacular, the word apathy generally refers
▶ Psychopharmacology to indifference or a lack of feeling or concern. In
294 Apathy

clinical settings, “apathy” is often conceptualized While the above-described findings relate to
as a lack of drive or motivation, a lack of respon- clinic-based samples, apathy has also been reported
siveness (behavioral or emotional) to stimuli or a in a community-based sample of older adults with
lack of initiation, or a reduction in self-generated, prevalence rates of 1.4% in cognitively normal
purposeful behavior. elderly, 3.1% in mild cognitive syndrome, and
17.3% in dementia (Onyike et al. 2007). Apathy
also appears to be quite common in nursing home
Epidemiology settings, with one study reporting a prevalence rate
of 84.1% (Wood et al. 2000). Apathy may also
Apathy has been described in a variety of psychi- appear as an adverse effect of some prescription
atric, neurological, and medical conditions includ- drugs, including selective serotonin reuptake inhib-
ing depression, schizophrenia, Alzheimer’s itors (SSRIs) (Hoehn-Saric et al. 1990).
disease, frontotemporal dementia, mild cognitive
impairment (MCI), Parkinson’s disease, progres-
sive supranuclear palsy, Huntington’s disease, Natural History, Prognostic Factors, and
cortical basal degeneration, dementia with Lewy Outcomes
bodies, stroke, vascular dementia, cerebral auto-
somal dominant arteriopathy with subcortical The word apathy comes from the Greek word
infarcts and leukoencephalopathy (CADASIL), “apatheia” meaning an “absence of feeling.” The
traumatic brain injury (TBI), anoxic encephalop- Stoic philosophers used this term to connote the
athy, Wernicke-Korsakoff syndrome, hydroceph- total freedom from emotions and passions which
alus, human immunodeficiency virus (HIV), were thought to compromise rationality and the
multiple sclerosis, apathetic hyperthyroidism, desired state of mental tranquility. However, over
chronic fatigue syndrome, vitamin B12 defi- the centuries, the term apathy came to refer to a
ciency, Lyme disease, and drug intoxication and lack of reactivity and became viewed as patholog-
withdrawal. ical rather than desirable.
Following an extensive review of the literature, While apathy can be observed as a symptom
van Reekum et al. (2005) summarized the preva- associated with a variety of psychiatric, neurolog-
lence rates of apathy in many of the above-named ical, and medical conditions, some authors have
conditions derived from studies which employed argued that apathy, in some circumstances, may
a variety of assessment measures (see below). represent a neuropsychiatric syndrome as well.
Combining data from multiple studies, these Marin (1990) defined an apathy syndrome as a
authors report point prevalence rates of 60.3% in loss of motivation which could not be attributed to
Alzheimer’s disease, 46.7% in TBI, 60.3% in emotional distress, intellectual impairment, or a
persons with focal frontal lesions, 33.8% in vas- diminished level of consciousness. In contrast,
cular dementia, 34.7% post-stroke, 22.2% in apathy as a symptom was defined as a loss of
dementia with Lewy bodies, 29.8% in HIV, motivation due to a disturbance of intellect, emo-
20.5% in multiple sclerosis, and 53.3% in patients tion, or level of consciousness (Marin 1990). Apa-
with major depression. Studies examining apathy thy is not considered an independent syndrome in
in other neurological conditions have found prev- the current DSM-V, though it does appear as a
alence rates of 41% in CADASIL (Reyes et al. nonspecific symptom for several other disorders.
2009), 90% in frontotemporal dementia, 91% in Prognostically, there is evidence to suggest that
progressive supranuclear palsy, 59% in apathy may be associated with more severe
Huntington’s disease (Levy et al. 1998), and impairment and negative outcomes. For example,
54% in Parkinson’s disease (Aarsland et al. a longitudinal study examining apathy in persons
2007). Apathy is also one of the most commonly with Alzheimer’s disease found apathy at baseline
observed neuropsychiatric symptoms in MCI was associated with faster cognitive and func-
(Apostolova and Cummings 2008). tional decline at follow-up (Starkstein et al.
Apathy 295

2006) There is also some evidence that apathy to neuropsychiatric symptoms, including apathy,
may precede the development of Alzheimer’s dis- has been implicated in the eventual institutionali-
ease. One longitudinal study of patients with MCI zation of many patients with Alzheimer’s disease A
found that those patients who converted to (Scott et al. 1997; Steele et al. 1990).
Alzheimer’s disease had higher rates of apathetic
symptomatology (91.7%) than those patients who
did not convert (26.9%) (Robert et al. 2006). Neuropsychology and Psychology of
Apathy has also been found to be significantly Apathy
associated with lower cognitive functioning and
more severe motor symptoms in persons with In clinical practice and research, apathy is often
Parkinson’s disease (Pedersen et al. 2009). Apa- mistaken for depression, though it is a distinct
thetic symptomatology has also been found to be syndrome that can be distinguished from depres-
negatively associated with functional improve- sion (Levy et al. 1998; Marin 1991; Starkstein
ment in rehabilitation settings after strokes et al. 2001). The syndromes of depression and
(Hama et al. 2007) and increased risk for mortality apathy share some symptoms (Table 1) and may
in nursing home residents with dementia (van co-occur in that same individual making diagnosis
Dijk et al. 1994). challenging (Damsio and Van Hosen 1983). For
Studies have also found that apathy is asso- example, an apathetic demented patient who pre-
ciated with decreased performance of activities sents with fatigue, sleep disturbance, poor appe-
of daily living (ADLs) in persons with stroke tite and weight loss, poor concentration, and
(Mayo et al. 2009; Starkstein et al. 1993), vas- anhedonia may be diagnosed with major depres-
cular dementia (Zawacki et al. 2002), sive disorder even in the absence of dysphoria
frontotemporal dementia (Kipps et al. 2009), (Ishii et al. 2009). A number of studies have
dementia with Lewy bodies (Ricci et al. 2009), found apathy to be correlated with high scores
and major depression (Steffens et al. 1999). on various depression measures (Rabkin et al.
Alzheimer’s disease patients with apathy are 2000; Ready et al. 2003; Starkstein et al. 2006).
more likely to be impaired on basic activities of However, this correlation may be due to the fact
daily living (dressing, bathing, toileting, trans- that many clinical measures of depression include
ferring, walking, and eating) than nonapathetic questions assessing symptoms of both apathy and
Alzheimer’s disease patients, even when depression, which may lead to misdiagnosis.
matched on degree of cognitive impairment
(Albert et al. 1996; Stout et al. 2003). In addi-
Apathy, Table 1 Apathy vs. Depression
tion, apathy has been found to account for 27%
of the variance in instrumental activities of daily Symptoms of Overlapping Symptoms of
living scores (medication management, shop- apathy symptoms depression
Loss of Lack of interest in Dysphoria
ping, finances) in patients with Alzheimer’s dis-
motivation and events or activities
ease (Boyle et al. 2003). initiation
Finally, apathy does not only impact the Lack of Lack of energy Hopelessness
patient. Due to impairments in motivation, indi- persistence
viduals with apathy can require more support and Diminished Psychomotor Guilt
management, which can in turn result in increased emotional slowing
reactivity
caregiver burden and stress. The caregivers of
Reduced social Fatigue Pessimism
patients with Alzheimer’s disease-related apathy engagement Poor insight Suicidal
have been shown to report significantly elevated ideation
levels of distress and perceived burden compared Loss of
to those who are caring for less apathetic patients appetite
with a similar level of cognitive impairment Sleep
(Kaufer et al. 1998). Caregiver distress secondary problems
296 Apathy

Apathy may be distinguished from depression been observed with lesions to right hemisphere
by the absence of dysphoric mood symptoms such subcortical structures following TBI (Finset and
as sadness, guilt, hopelessness, and helplessness. Andersson 2000).
The difference in mood states, dysphoric vs. emo- Evidence from neuropsychological studies
tionally indifferent, is the most useful characteris- suggests apathy may be associated with cognitive
tic in making a differential diagnosis between impairment, in particular executive dysfunction.
apathy and depression. Apathy can be thought of Apathetic patients with Alzheimer’s disease have
as a syndrome of primary motivational loss and been shown to have greater executive functioning
diminished emotional reactivity, while depression deficits, abilities thought to be mediated by the
reflects a syndrome of mood disturbance. frontal lobes, than depressed patients with
The mechanisms of apathy are not fully under- Alzheimer’s disease (Kuzis et al. 1999). Another
stood, though most theories suggest it involves study found apathetic patients with Alzheimer’s
disruption of the frontal-subcortical neural circuit. disease showed significantly greater deficits on
This circuit begins with the anterior cingulate measures of executive functioning but performed
cortex, and continues to the ventral striatum, the similarly on other neuropsychological measures
globus pallidus, and the thalamus, before loping not dependent on executive function (McPherson
back to the anterior cingulate cortex. It has been et al. 2002). Apathy has also been associated with
hypothesized that neuropathological changes and executive dysfunction in other clinical populations,
alterations in regional chemistry, especially ace- including TBI (Andersson and Bergedalen 2002),
tylcholine, dopamine, and serotonin, in this circuit Parkinson’s disease (Starkstein et al. 1992), pro-
are responsible for the clinical manifestation of gressive supranuclear palsy (Litvan et al. 1998),
apathy (David et al. 2008; Franceschi et al. 2005; and HIV (Castellon et al. 2000).
Landes et al. 2001; Mega and Cummings 1994).
Apathy with impaired motivation and indifference
has most strongly been associated with damage to Evaluation
anterior cingulate cortex (ACC) (Damsio and Van
Hosen 1983). In the most extreme cases, damage Formal assessment measures for apathy focus on
to the ACC results in akinetic mutism and a com- those symptoms of apathy that are distinct from
plete loss of initiation and motivation. Single pho- depression. The most commonly employed
ton emission computed tomography (SPECT) assessment instruments for apathy in clinical and
studies of patients with Alzheimer’s disease research settings include the Apathy Evaluation
found that apathy was strongly and inversely cor- Scale (AES), the Neuropsychiatric Inventory
related with right anterior cingulate activity (NPI), and the Frontal Systems Behavior Scale
(Benoit et al. 1999) or with a bilateral reduction (FrSBe). Less commonly used but validated mea-
in cingulate activity (Migneco et al. 2001). sures include the Dementia Apathy Interview and
Frontal regions have also been implicated in Rating, the Lille Apathy Rating Scale, the Apathy
the manifestation of apathy. Neuroimaging stud- Inventory, the Behavior Rating Scale for Demen-
ies have found apathy in AD patients to be corre- tia, and the Scale for the Assessment of Negative
lated with hypoperfusion in frontotemporal Symptoms in Alzheimer’s Disease. Of note, while
regions (Benoit et al. 1999; Craig et al. 1996). In several of these measures include self-report ver-
one study, apathetic stroke patients showed sions, these may fail to identify apathy in patients
reduced regional cerebral blood flow in right dor- with reduced insight, and therefore informant
solateral prefrontal cortex and left frontotemporal measures may be more helpful in assessing for
regions (Okada et al. 1997). Subcortical regions apathy.
may also be implicated in the presence of apathy. The AES comes in a clinician-administered
In one study, apathy was seen in 80 stroke patients version, an informant version, and a self-report
with lesions to the posterior limb of the internal version, all of which have been shown to have
capsule (Starkstein et al. 1993). Apathy has also satisfactory reliability (Marin et al. 1991). The
Apathy 297

clinician-administered version of this measure caregiver distress using the same rating scale as
(AES-C) is a semi-structured interview which the NPI interview. Importantly, both of these ver-
includes 18 items and is focused on behavior sions of the NPI include separate questions for A
that has been present during the past month. depression and apathy. The NPI asks caregivers
Each item falls into one of four categories (cogni- to consider whether the behavior has been present
tive, behavior, emotional, or others) and is rated for the past month. The NPI has been shown to
on a four-point Likert scale with higher scores have good reliability and validity; however,
representing a greater degree of apathy. A recent unlike the other measures discussed, there is no
study examined the clinician-administered ver- recommended cutoff score for clinical signifi-
sion (AES-C) and found it to be valid and reliable cance. Of note, while the AES and FrSBe provide
for identifying and quantifying apathy and found more nuanced assessments of apathy, the NPI is
that using a cutoff score of 40.5 resulted in good the most widely reported measure of apathy
sensitivity and moderate specificity (Clarke et al. reported in the literature. This is likely due to the
2007a, b). fact that the NPI assesses for a wide array of
The FrSBe (Grace and Malloy 2001) was spe- neuropsychiatric symptomatology, and is often
cifically designed to assess for behavioral changes used in intervention studies for a variety of con-
associated with frontal lobe dysfunction and ditions of which apathy may be one symptom, but
comes in a self-report and informant version. not a cardinal feature, of a disorder.
These questionnaires consist of 46 items and ask
the respondent to rate the patient’s behavior on
each item using a five-point Likert scale. Respon- Treatment
dents are asked to rate the patient’s behavior both
before and after the onset of illness or injury. Nonpharmacologic interventions for apathy tend
Subscales assess apathy, disinhibition, and exec- to focus on introducing new sources of interest
utive dysfunction. This allows for an estimation of and stimulation. Pet therapy, art therapy, and
the extent to which current problem behaviors physical therapies may be useful in decreasing
represent a change from premorbid functioning. apathy, though the efficacies of these interven-
T-scores greater than 65 are clinically significant. tions have not been examined in a systematic
The FrSBe has been shown to be reliable, valid, fashion with apathetic patients. Increasing oppor-
and sensitive to behavior change due to frontal tunities for socialization and encouraging partici-
lobe damage (Grace et al. 1999), Alzheimer’s pation in social activities may also be helpful.
disease (Stout et al. 2003), TBI (Lane-Brown Patients should be encouraged to be as function-
and Tate 2009), and a variety of other neurological ally autonomous as possible. Sensory deficits and
conditions. pain should be managed so these do not interfere
The NPI is a structured interview conducted with activities. Implementing exercise programs
with an informant designed to assess for the pres- and scheduled activities may also be beneficial in
ence of 12 neuropsychiatric symptoms, including enhancing initiation and motivation. While there
apathy (Cummings 1997). A positive response to have been few studies on behavioral interventions
a screening question indicates the presence of the specifically for apathy, there is some evidence that
symptom and leads to further questions about the behavioral therapy may be helpful in reducing
behavior and eventual ratings of the symptom apathetic symptomatology. One randomized con-
severity (mild, moderate, or severe) and the trolled study comparing “reminiscence therapy”
amount of caregiver distress it causes. The Neu- (a treatment modality designed to facilitate recall
ropsychiatric Inventory Questionnaire (NPI-Q) of experiences from the past to promote intraper-
(Kaufer et al. 2000) is a self-administered ques- sonal and interpersonal functioning) to a time and
tionnaire completed by a caregiver or informant attention control group (one-on-one time with an
that assesses for the presence of the same 12 activity therapist) found that apathy was reduced
symptoms and asks for ratings of severity and for both groups of patients with dementia (Politis
298 Apathy

et al. 2004). Another study showed that individu- Alzheimer’s disease, normal pressure hydro-
alized functional and occupational training cephalus, Parkinson’s disease, cerebrovascular
reduced apathy in patients with mild-to-moderate accidents, and depression (Chatterjee and Fahn
stage dementia (Lam et al. 2009). Behavioral acti- 2002; Jansen et al. 2001; Keenan et al. 2005;
vation (BA) therapy is an intervention which Padala et al. 2007b; Spiegel et al. 2009). How-
focuses on alleviating depression by increasing ever, most of the evidence for the efficacy of
the individual’s exposure to rewarding and these medications in apathy comes from case
reinforcing stimuli by increasing activation and report or case series. These medications can
decreasing barriers and avoidance of activation also have negative side effects, including insom-
(Dimidjian and Davis 2009). This behavioral nia, loss of appetite, anxiety, and higher blood
approach includes goal-setting, activity schedul- pressure, which may deter their use with vulner-
ing, problem solving, and self-monitoring to get able populations (Ishii et al. 2009). Other “stim-
patients to become more active and thus increase ulating” medications such as modafinil (Padala et
exposure to reward and positive reinforcement to al. 2007a) and selegiline (Newburn and Newburn
combat depressive symptomatology. It has been 2005) have been reported to reduce apathy in
shown to be comparable to cognitive behavior case studies. A small double-blind placebo-con-
therapy and pharmacotherapy (paroxetine) in trolled study assessing for the effects of
reducing depressive symptomatology in pla- modafinil used in conjunction with a cholinester-
cebo-controlled studies (Dimidjian et al. 2006; ase inhibitor medication on apathy in a sample of
Sturmey 2009). While this intervention has not individuals with mild-to-moderate stage
been examined in the treatment of apathy, its Alzheimer’s disease failed to find significant
focus on increased activity and exposure to group differences. Indeed, both groups (treat-
pleasant, rewarding experiences would appear ment and control) showed small reductions in
to be particularly well-suited to address the lack caregiver-reported symptoms of apathy follow-
of interest, motivation, and anhedonia that char- ing this 8-week trial suggesting that a “placebo
acterize apathy. Future research may show this to effect” was observed (Frakey et al. 2012).
be a promising intervention for both depression Reductions in apathy with the use of dopami-
and apathy. nergic agents such as bromocriptine (Powell et al.
Psychoeducation for families and caregivers 1996) and amantadine (Swanberg 2007; Van
can also be beneficial. Oftentimes, apathy is mis- Reekum et al. 1995) have been reported in a few
characterized as a “willful behavior” (e.g., stub- case studies, but no randomized clinical trials
bornness or laziness) by caregivers who do not have been conducted to date. Apathetic-type
recognize that these behaviors are related to neu- symptoms and behavior may be seen in schizo-
rological, psychiatric, and medical comorbidities. phrenic patients with negative symptoms. Atypi-
Educating families on the underlying causes for a cal antipsychotic medications such as risperidone,
patient’s low initiation and motivation may help olanzapine, and clozapine have been shown to be
lessen perceived caregiver burden and stress. helpful in reducing negative symptoms in schizo-
Currently, there is no FDA-approved pharma- phrenia (van Reekum et al. 2005); however, none
cological intervention for apathy; however, many of the studies to date have specifically examined
different medications, including acetylcholines- apathy, and these medications can be associated
terase inhibitors, psychostimulants, dopaminergic with serious negative side effects such as tardive
drugs, and atypical antipsychotics, have been used dyskinesia, akathisia, extrapyramidal symptoms,
“off-label” to treat apathetic symptomatology. and orthostatic hypotension.
Methylphenidate and dextroamphetamine are As previously noted, apathy is the most com-
psychostimulant medications that are commonly mon neuropsychiatric symptom associated with
used to treat attention deficit/hyperactivity disor- Alzheimer’s disease, and modest improvements
der (AD/HD) and narcolepsy. These medications in apathy have been seen in patients with
have also been used to treat apathy in Alzheimer’s disease who are treated with
Apathy 299

acetylcholinesterase inhibitor medications (Cum- There does appear to be increasing recognition

mings 2000; Mega et al. 1999). Currently, there of the prevalence of apathy, its impact on patients
are three acetylcholine inhibitor medications and their families, and its importance in neuropsy- A
approved for use in the United States: donepezil, chiatric research. This recognition appears to be
galantamine, and rivastigmine. A meta-analysis fueling an interest in developing a more rigorous
identified 14 randomized, placebo-controlled tri- approach to clinical research on apathy. Recog-
als of monotherapy with these medications in nizing the need for reliable identification of apa-
patients with Alzheimer’s disease that reported a thy and seeking ways to improve communication
behavioral outcome (Rodda et al. 2009). Of these, in both research and treatment of apathy, the Cen-
only four were specifically designed to assess tre Memoire de Ressources et de Recherche orga-
behavioral outcomes, and the rest used behavioral nized a task force to develop a formal diagnostic
outcomes as secondary measures. Overall, 3 of the criteria for apathy which they hoped would be
14 studies reviewed reported a statistically signif- used to facilitate research in apathy (Robert et al.
icant improvement in overall score on the Neuro- 2009). Along those lines, Radakovic et al. (2015)
psychiatric Inventory, and only one found a recently conducted a systematic review of the
significant reduction in apathy, specifically literature to provide an overview of apathy scales
(Gauthier et al. 2002). which had been validated in generic and specific
A recent study investigated whether a neurodegenerative disorders and to compare that
sustained cholinergic challenge, such as treatment methodological quality and psychometric proper-
with a cholinergic precursor choline alphoscerate ties of these scales to provide recommendations
and the cholinesterase inhibitor medication for the use of several instruments with some spe-
donepezil, could improve apathy symptoms in cific neurodegenerative disorders. Finally, Cum-
patients with Alzheimer’s disease (Rea et al. mings et al. (2015), citing increased interest in
2015). The researchers examined changes in apa- new therapeutic options for apathy, recently
thy ratings on the NPI in participants in the ran- published a position paper offering recommenda-
domized double-blind ASCOMALVA study tions for the design and development of clinical
(Association Between the Cholinesterase Inhibi- studies investigating treatment of apathy in
tor Donepezil and the Cholinergic Precursor Cho- Alzheimer’s disease and Parkinson’s disease as
line Alphoscerate in Alzheimer’s Disease). well as a wider range of disorders.
Results indicated that subjects treated with the
combination of drugs had lower apathy scores
after 12 and 24 months as compared to the control See Also
group. A similar trend was observed for caregiver
ratings of distress with reductions noted in the ▶ Abulia
stress level of the caregivers of participants ▶ Akinetic Mutism
receiving the combination of medications as com- ▶ Anterior Cingulate Cortex
pared to their control counterparts. Interestingly, ▶ Avolition
the effects on apathy symptoms were unrelated to ▶ Major Depression
the level of cognitive impairment, as measured by ▶ Motivation
the Mini-Mental Status Exam (MMSE) and
Alzheimer’s Disease Assessment Scale Cognitive
Subscale (ADAS-cog), but may have been related Further Reading
to pretreatment level of executive dysfunction.
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treatment. Psychiatry, 78, 36–42.
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Aphasia 303

can be dichotomous (e.g., fluent vs. nonfluent or

Aphasia comprehension deficit vs. production deficit),
anatomically based (e.g., Boston classification A
Janet P. Patterson system of aphasia types, such as Broca’s aphasia),
Audiology and Speech-Language Pathology and behaviorally based (e.g., Schuell’s system of
Service, VA Northern California Health Care multimodality, unidimensional impairment, such
System, Martinez, CA, USA as aphasia with visual involvement), can be based
on severity (e.g., mild, moderate, or severe), or
can follow a processing model (e.g., cognitive
Short Description or Definition neuropsychological model of naming; Kay et al.
1996). Classification systems are useful for a gen-
“Aphasia is an acquired communication disorder eral understanding of an individual’s communica-
caused by brain damage, characterized by impair- tion ability; however, controversy exists regarding
ments of language modalities; speaking, listening, their clinical utility. Some individuals with apha-
reading and writing; it is not the result of a sensory sia show symptoms that match more than one type
or motor deficit, a general intellectual deficit, con- of aphasia, and others show symptoms that do not
fusion or a psychiatric disorder” (Hallowell and fit into any of the classification categories. Studies
Chapey 2008, p. 3). Aphasia is typically acquired examining classification report 35–70% success
suddenly as a result of a stroke or traumatic brain in classifying participants as one aphasia type
injury but can appear more slowly accompanying (Caramazza 1984; Crary et al. 1992). Table 1
other neurological events such as tumor or dis- shows three classification systems, with general
ease. When aphasia develops slowly over time characteristics of each aphasia type.
and is the only behavioral symptom present, the
diagnosis is primary progressive aphasia (PPA).
Aphasia is often classified according to the Epidemiology
appearance of a constellation of behavioral symp-
toms including impairment in auditory compre- Aphasia resulting from stroke occurs in approxi-
hension, reading comprehension, naming, mately 30% of the 15 million people worldwide
production of grammatically correct sentences, who experience a stroke each year. In the United
repetition, writing, and presence of paraphasic States alone, 80,000 new occurrences of aphasia
(substitution) sound or word errors (e.g., saying appear each year, and at any point in time, approx-
table for chair or pork for fork). Aphasia disrupts imately one million people are living with aphasia
communication ability, sometimes so severely following stroke. Aphasia resulting from trau-
that a person with aphasia withdraws from social matic brain injury and other causes is difficult to
interaction and other times only minimally so that estimate.
the person with aphasia continues his or her life
activities.
Natural History, Prognostic Factors, and
Outcomes
Aphasia Classification
Reports of language disorder following brain
Many systems have been proposed to classify injury have existed for hundreds of years, initially
aphasia types (Kertesz 1979). Each system repre- as case reports. Paul Broca and Carl Wernicke in
sents a theoretical perspective of aphasia and iden- the late 1800s presented clinical data relating
tifies aphasia types according to a constellation of behavioral and anatomical information, localizing
behavioral characteristics. Classification systems language ability to the left hemisphere, and
304 Aphasia

Aphasia, Table 1 Three examples of aphasia classification systems showing aphasia types and general characteristics of
each type
Dichotomous classification
Type Characteristics
Nonfluent aphasia Limited speech output
Effortful speech output
Content words retained; function words omitted
May or may not have articulation difficulties
Melodic contour altered
Fluent aphasia Approximates normal rate and sentence length
Content words omitted in severe fluent aphasia
Circumlocution present in mild fluent aphasia
Melodic contour preserved
Anatomical and behavioral classification
Type Characteristics
Broca’s aphasia Nonfluent aphasia; expressive aphasia
Effortful output
Reduced phrase length and syntactic complexity; content words usually
preserved
Auditory comprehension may or may not be impaired
Impairments in reading, writing, naming, and repetition
Right hemiplegia often present
Wernicke’s aphasia Fluent aphasia; receptive aphasia
Auditory comprehension often impaired
Impairments also may appear in reading, writing, naming, and repetition
Paraphasic errors
Melodic contour retained
Conduction aphasia Fluent aphasia
Auditory comprehension preserved
Impairment in repetition
Naming may be impaired
Error recognition typically preserved
Global aphasia Nonfluent aphasia
Impairments in auditory comprehension, reading, writing, naming, and
repetition
Limited functional communication often preserved
Anomic aphasia Fluent aphasia
Auditory and reading comprehension and repetition typically preserved
Word retrieval deficit
Transcortical motor aphasia Nonfluent aphasia
Auditory comprehension and naming may be impaired
Repetition preserved
Paraphasic errors and perseveration present
Transcortical sensory aphasia Fluent aphasia
Auditory comprehension impaired
Paraphasic errors
Repetition preserved
Naming may be impaired
(continued)
Aphasia 305

Aphasia, Table 1 (continued)

Behavioral classification
Type Characteristics A
Simple aphasia Mild impairment
Multimodality impairment (spoken language; speech; reading; writing)
No specific perceptual, sensorimotor, or dysarthric components
Aphasia with visual involvement Mild aphasia
Central impairment of visual modality
Aphasia with persisting dysfluency Mild aphasia
Verbal dysfluency
Aphasia with scattered findings Moderate aphasia
Impairments in one or more modalities
Functional communication preserved
Aphasia with sensorimotor Severe aphasia
involvement Impaired output
Aphasia with intermittent auditory Severe aphasia
imperception Impaired auditory comprehension
Irreversible aphasia syndrome Severe aphasia
Impairments in all modalities (comprehension of spoken language; speech;
reading; writing)

ultimately having their names adopted to identify impairment based (e.g., change in naming ability)
anatomical areas in the brain related to patterns of or activity/participation based (e.g., increased par-
language deficit. Current studies of persons with ticipation in social activities), following the World
aphasia use neuroimaging techniques to further elu- Health Organization’s International Classification
cidate the behavioral and anatomical relationship. of Functioning, Disability and Health (ICF;
Aphasia in the first few months after a stroke is WHO 2001). In addition to measuring functional
the acute stage and is often characterized by spon- communication outcomes, patient-reported out-
taneous recovery of language and communication comes (PRO) are gaining importance as a compo-
deficits. In the chronic stage, an individual learns nent of patient-oriented treatment (Hula et al.
to live with aphasia and returns to life activities. 2015). Some persons with aphasia recover to near-
Prognosis for recovery is variable and dependent normal premorbid language and communication
upon both internal patient factors (e.g., severity of performance, while others remain severely aphasic.
aphasia, type and extent of lesion, or concomitant Almost every person has the potential for some
medical problems), external factors (e.g., family level of functional communication, from being an
support or communication interaction opportuni- independent communicator in a variety of commu-
ties), and other ambient experiences (McClung nication interactions to being dependent upon an
et al. 2010). Personal variables such as age, edu- alternative or augmentative communication system
cation, and gender do not systematically influence or a conversational partner (Hachioui et al. 2013).
prognosis (Basso 1992; Pedersen et al. 2004;
Plowman et al. 2012).
Aphasia recovery occurs most rapidly imme- Models of Language, Communication,
diately following the brain injury as the brain and Aphasia
begins to heal itself. Studies have shown that
recovery also continues for years post-stroke and Numerous models serve to guide assessment and
following treatment (Moss and Nicholas 2006). treatment of persons with aphasia and foster
Outcome measures documenting change are understanding of how aphasia affects persons
306 Aphasia

with aphasia and their family members. Theoret- characteristics, their ability to adjust to change,
ical influences underpinning these models range and their external support network as they
from impairment-based models, such as cogni- and their family learn to live with aphasia. Sev-
tive neuropsychological models of language pro- eral models and tools exist to guide assessment
cessing, to models based on psychosocial theory, and treatment in these areas. For example,
such as the A-FROM (Kagan et al. 2008). Cog- quality-of-life scales ask questions about topics
nitive neuropsychology brought to aphasia eval- such as family support and general outlook on
uation and treatment a set of models of human life (e.g., communication-related quality-of-life
cognitive mechanisms and processes thought to scale; Cruice et al. 2003). An important model,
underlie language performance. An individual’s the A-FROM (Living with Aphasia: Framework
performance on several linguistic tasks is exam- for Outcome Measurement; Kagan et al. 2008)
ined for patterns of impaired and spared cogni- espouses an integrated approach to aphasia
tive processes in order to infer the cognitive assessment. The A-FROM clarifies outcomes
architecture that underlies the performance. For in five domains: participation, aphasia severity,
example, in a model of lexical processing, the language and communication environment,
linguistic tasks might be lexical recognition personal factors/identity, and life with aphasia.
(word/nonword identification), auditory compre- Social network diagrams illustrate the breadth
hension (pointing to a named word), and naming and depth of an individual’s support and
a picture (confrontation naming). An individual communication networks (e.g., Blackstone and
who scores high on auditory comprehension and Berg 2003).
reading words tasks but low on confrontation While aphasia tests are founded on specific
naming may be inferred to show a deficit in models of language, communication, or cogni-
phonological output lexicon but have an intact tion, assessment and treatment activities often
semantic system and ability to use phonic skills reflect a combination of impairment-based and
to read a word. That is, the individual may have activity/participation-based models.
intact semantic knowledge and be aware of the
phonological form of a word and be able to read
it but lack the phonological skills to generate the Evaluation
verbal label. The pattern of performance is
important to note and serves to direct treatment Approaches to evaluation of aphasia vary with the
to the impaired processes, using the spared pro- conceptualization of aphasia.
cesses as strengths. Cognitive neuropsychologi- Some approaches take an impairment-based
cal models of language processing frequently approach, viewing aphasia as a disorder of
used in aphasia assessment and treatment, how- selected abilities, while others, such as the Life
ever, are not without criticism as being descrip- Participation Approach to Aphasia (LPAA 2000)
tive and not prescriptive and requiring time- take an activity/participation approach, viewing
consuming assessment. aphasia as a disruption to communication and
In contrast to the deficit-specific models placing the person with aphasia and his or her
of cognitive neuropsychology, other models family at the center of clinical decision-making
recognize the importance of an individual’s activities. Schuell et al. (1964) proposed assess-
psychosocial state, quality of life, functional ment based on the definition of aphasia as lan-
communication abilities, and communication guage deficit that crosses all modalities, all of
network. Tanner (2003) proposed an eclectic which are examined in the Minnesota Test for
approach to examine the psychology of aphasia the Differential Diagnosis of Aphasia (Schuell
from three perspectives: effects of brain injury, 1965). Chapey (2008) suggested that evaluation
psychological defenses and coping styles, and stem from a cognitive stimulation model, which
responses to loss. This view speaks to the impor- views communication as a problem-solving and
tance of an individual’s premorbid personal decision-making task. Following the World
Aphasia 307

Health Organization ICF (2001), models of individual and family. Sometimes only some of
assessment and treatment typically incorporate these goals can be achieved. Examples of disor-
information at levels of impairment and activity/ ders that may accompany aphasia but that are not A
participation. aphasia are apraxia of speech, dysarthria, demen-
In contrast to language-based evaluation tia, memory impairment, or psychiatric problems.
tools, some approaches to evaluation consider These concomitant disorders will affect treatment
the circumstances in which treatment will be planning and task selection. Medical conditions,
conducted. Group treatment has gained popular- such as diabetes, cardiovascular disease, and any
ity in recent years, recognizing the value of social medications the patient takes, may affect perfor-
connectedness, and some assessment tools mance and should also be noted in the assessment
examine the social desires and needs of a person report.
with aphasia (Avent 1997; Kearns and Elman Sometimes people with aphasia experience
2008). Lubinski (2008) discussed an environ- depression, and several scales have been devel-
mental model, suggesting that clinicians con- oped to screen for depression. Some have a lin-
sider physical and social environments of a guistic bias or rely on caregiver report, while
person with aphasia to enhance treatment effects. others have been adapted to be “aphasia friendly”
Finally, psychosocial models of intervention and not depend exclusively on complex written
focus on integrating an individual into a commu- sentences. Three examples of instruments to
nicating society and promoting their participa- examine depression are the Stroke Aphasia
tion in personally relevant activities (Simmons- Depression Questionnaire (SADQ) (Lincoln
Mackie 2008). Regardless of the approach, in et al. 2000), the Aphasia Depression Question-
order to understand the linguistic and communi- naire (Benaim et al. 2004), and the Visual Analog
cative abilities and needs of an individual, it is Mood Scale (Stern et al. 1997). The SADQ while
important to conduct evaluation within a cultur- designed for persons with aphasia has a linguistic
ally sensitive framework. bias and is intended to rely on caregiver report.
Three types of aphasia tests are commonly The ADQ is a nine-item tool used to assess post-
used to assess language and communication abil- stroke depression in persons who are hospitalized
ities in persons who have aphasia: screening tests after a stroke. The VAMS is an example of a
(short assessments that may be administered at nonlinguistic mood scale used for self-report of
bedside), comprehensive aphasia tests (batteries depressive symptoms.
containing several subtests to examine language The goals of evaluation will vary depending
behavior such as naming, reading, and writing), upon factors such as severity of aphasia, age,
and tests of specific linguistic or communicative and time post-onset. For example, an individual
function (e.g., syntactic function or naming) with mild aphasia who anticipates returning to
(Patterson 2008). In addition, assessment of work should have an assessment that includes
aphasia and its impact on a person’s life include detailed information on linguistic processing
testing cognitive abilities (e.g., memory), testing and a job task analysis to determine the linguis-
executive functioning (e.g., divided attention), tic requirements of the position. This informa-
observing a person in activities of daily commu- tion may be used to determine the individual’s
nication, and interviewing the person with apha- ability to return to a job, to identify communica-
sia and family members about the impact of tion requirements of the job, and to guide
aphasia on life participation and functional employment-related treatment. In contrast, eval-
communication. uation for an individual with severe aphasia and
In aphasia assessment, it is as important to concomitant severe apraxia of speech may
determine the presence or absence of aphasia require an evaluation focused on functional
and the presence of concomitant disorders, as it communication strategies to use with familiar
is to classify aphasia type, describe aphasia symp- communication partners within a contained
toms, and understand how the aphasia affects the environment.
308 Aphasia

Treatment aphasia friendly), reciprocal scaffolding (e.g.,

Avent et al. 2009), and supported conversation
The acute stage of aphasia is the first few months (e.g., Kagan et al. 2001).
after a stroke as the brain recovers from injury Recently intensive treatment has become a
and is often characterized by spontaneous recov- focus for aphasia rehabilitation. Intensive treat-
ery of language and communication deficits, ment can be measured by the amount and fre-
while in the chronic stage of aphasia, an individ- quency of delivery of a treatment protocol.
ual learns to live with aphasia and returns to life Warren et al. (2007) suggest using cumulative
activities. There are many well-validated, effec- intervention intensity (a produce of dose of treat-
tive techniques for aphasia rehabilitation, partic- ment, frequency, and total duration) to equate
ularly for chronic aphasia. These range from intensity across various treatments. Evidence sup-
general stimulation approaches to treatments ports intensive treatment for aphasia under careful
aimed at specific signs of aphasia and are chosen considerations of treatment protocol and patient
according to the patient’s individual needs, characteristics. Intensive treatment can be effec-
goals, aphasia characteristics, and etiology. For tive at all stages of recovery from aphasia.
aphasia due to acute-onset causes (e.g., vascular Another form of intensive treatment is the Inten-
etiologies or trauma), therapy has been demon- sive Comprehensive Aphasia Program (ICAP;
strated to be effective both early after onset Babbitt et al. 2015) where individuals with apha-
(Carpenter and Cherney 2016) and in the chronic sia spend several hours each day for a few weeks
stage. For aphasia due to progressive etiologies, completing multiple treatment activities.
therapy has been shown to be effective in The four principles of evidence-based prac-
maintaining functional communication and max- tice, current best practices, clinical expertise,
imizing quality of communication life to the client/patient values, and context of treatment,
extent possible given the medical diagnosis guide treatment planning. Clinical practice
(Beeson et al. 2011). research and clinical trials support the efficacy
Pharmacological intervention for aphasia may and effectiveness of aphasia therapy. Systematic
be undertaken for direct treatment of the language reviews, such as the one for constraint-induced
deficit or administered to address a concomitant language therapy (Cherney et al. 2008), and
disorder, such as depression. Although research in meta-analyses (e.g., Robey 1998) report the evi-
this area is encouraging, to date, no pharmaco- dence from group studies and single-subject
logic treatment has emerged as consistently research studies for a specific treatment or aphasia
improving linguistic function without adverse therapy in general. Cherney and Robey (2008)
side effects (Greener et al. 2001; Murray and and the Academy of Neurological Communica-
Clark 2006; Troisi et al. 2002). tion Disorders and Sciences (ANCDS 2016) pre-
Treatment for aphasia historically focused pri- sent analyses of treatment effect sizes of aphasia
marily on restitution of function using impairment- treatment for specific treatment areas such as syn-
based treatment techniques, with treatment targets tax and language comprehension.
such as word or sentence production or writing.
Examples of these treatment techniques are
Melodic Intonation Therapy, a semantic or phono- Cross-References
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260, 166–171. Raaschou, H. O., & Olsen, T. S. (2004). Aphasia in
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(Ed.), Language intervention strategies in aphasia and Plowman, E., Hentz, B., & Ellis Jr., C. (2012). Post-stroke
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sational partners using “Supported Conversation for treatment of aphasia. Journal of Speech-Language-
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Kagan, A., Simmons Mackie, N., Rowland, A., Huijbregts, nosis of aphasia. Minneapolis: University of Minne-
M., Shumway, E., McEwen, S., et al. (2008). Counting sota Press.
what counts: A framework for capturing real-life out- Schuell, H., Jenkins, J., & Jimenez-Pabon, E. (1964).
comes of aphasia intervention. Aphasiology, 22(3), Aphasia in adults. New York: Harper medical
258–280. Division.
Kay, J., Lesser, R., & Coltheart, M. (1996). Psycholin- Simmons-Mackie, N. (2008). Social approaches to aphasia
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Kearns, K., & Elman, R. (2008). Group therapy for apha- Philadelphia: Wolters Kluwer.
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nication disorders (5th ed., pp. 319–349). Philadelphia: World Health Organization. (2001). International classifica-
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(2010). Ambient experience in restitutive treatment of Accessed 30 Mar 2010.
Aphasia Diagnostic Profiles 311

Aphasia Diagnostic Profiles, Table 1 Aphasia diag-

Aphasia Diagnostic Profiles nostic profiles: nine subtests and five profiles
ADP subtests
A
Janet P. Patterson Subtest Description
Audiology and Speech-Language Pathology Personal Verbal response to questions
information
Service, VA Northern California Health Care
Writing Complete patient information
System, Martinez, CA, USA sheet
Reading Read items on patient
information sheet
Description Fluency Produce connected speech in
three contexts
The Aphasia Diagnostic Profiles (ADP; Helm- Naming Name familiar pictured items
Estabrooks 1992) is an impairment-based mea- Auditory language Answer questions – word,
comprehension sentence, and story levels
sure (World Health Organization 2001) designed
Repetition Repeat words and phrases
to assess language and communication skills in
Elicited gestures Pretend to complete action
persons with aphasia, primarily following stroke.
Singing Sing three familiar songs
The ADP consists of nine subtests, each of which ADP profiles
yields a standard score and percentiles. The sub- Profile Description
tests assess speech, language, and communication Aphasia Identifies aphasia type (based on
in all modalities (verbal and written), and the test classification the Boston classification system)
emphasizes conversational interaction; verbal profile
instructions to the patient are written in an infor- Aphasia severity Indicates specific strengths and
profile weaknesses
mal style in the manner of conversation (e.g.,
Alternative Identifies patient’s strongest
“Well now that’s out of the way, I’m going to communication response modalities and guides
turn on the tape recorder”). profile therapy
Responses are typically scored on a five-point Error profiles Identifies the communicative
scale: immediately correct, mostly correct, some value of a patient’s responses
correct, fully incorrect, and no response. Scores Behavioral profile Indexes the patient’s overall
emotional state during testing
from the subtests are combined to produce five
profiles describing the level of impairment of apha-
sia. The profiles are the Aphasia Classification transcortical sensory, conduction, or anomic apha-
Profile, the Aphasia Severity Profile, the Alterna- sia, following the conventions of the Boston apha-
tive Communication Profile, the Error Profiles, and sia classification system.
the Behavioral Profile. Other scores of interest are The ADP was created in part to address the need
the ADP Phrase length (average length of longest for a comprehensive aphasia battery that could be
three phrases), Information Units (new pieces of administered in a relatively brief time (40–50 min)
information), and Index of Wordiness (Correct in a medical setting. The manual is clearly written
Information Units relative to total number of with explicit administration and scoring instruc-
words). Table 1 shows the titles and a brief descrip- tions. The record form is easy to use and facilitates
tion of the nine subtests and five profiles. the completion of the profile scores.
The ADP is used to classify an individual’s
aphasia type as nonfluent, borderline fluent, or
fluent. Using the lexical retrieval score, ADP Historical Background
phrase length, auditory comprehension score,
and repetition score, the ADP further classifies The ADP was first published in 1992 and since
the aphasia type as global, mixed nonfluent, then has been frequently used in clinical and
Broca’s, transcortical motor, Wernicke’s, research activities. Numerous studies of aphasia
312 Aphasia Tests

treatment use the ADP as a measure of behavior ▶ Aphasia Tests

change following intervention. ▶ Boston Diagnostic Aphasia Examination
▶ Broca’s Aphasia
▶ Conduction Aphasia
Psychometric Data ▶ Global Aphasia
▶ Goodglass, Harold (1920–2002)
The ADP manual reported that it was standardized ▶ Kaplan, Edith (1924–2009)
on 290 adults with neurological impairments ▶ Repetition
(222 potentially aphasic adults) and 40 nonaphasic ▶ Speech/Communication Disabilities
adults. The median age of these individuals was ▶ Speech-Language Therapy
70 years. The manual further reported reliability ▶ Transcortical Motor Aphasia
coefficients (inter-item consistency) for subtest ▶ Transcortical Sensory Aphasia
raw scores that ranged from 0.73 (behavioral ▶ Wernicke, Karl (1848–1905)
score) to 0.96 (repetition), with most of the coef- ▶ Wernicke’s Aphasia
ficients in the 0.90 s. Test-retest coefficients
ranged from 0.64 (elicited gestures) to 0.91
(information units). The ADP has a strong theo- References and Readings
retical and psychometric foundation but has not
Helm-Estabrooks, N. (1992). Aphasia diagnostic profiles.
been subjected to additional psychometric Austin: Pro Ed.
evaluation. World Health Organization. (2001). International classifi-
cation of functioning, disability and health.. http://
www.who.int/classifications/icfbrowser/.

Clinical Uses

Three characteristics make the ADP a valuable Aphasia Tests

clinical assessment tool: the theoretical founda-
tion and close relationship to the Boston aphasia Janet P. Patterson
classification system, the structure of the test and Audiology and Speech-Language Pathology
clarity of the administration manual, and the Service, VA Northern California Health Care
amount of administration and scoring time System, Martinez, CA, USA
required. It is also notable that both verbal and
nonverbal modalities of communication are
included in the assessment. One limitation of Synonyms
the ADP is that it does not examine any linguis-
tic, psycholinguistic, or neuropsychological Aphasia assessment; Aphasia diagnosis; Aphasia
behavior in detail; additional tests in specific evaluation
areas would be required to obtain in-depth infor-
mation as part of an extensive diagnostic
evaluation. Description

Tests of aphasia are used to diagnose the type and

Cross-References severity of aphasia and related disorders and to
plan intervention for the speech, language, and
▶ Anomia communication deficits demonstrated by persons
▶ Anomic Aphasia who have aphasia following brain injury (PWA).
▶ Aphasia Three types of aphasia tests are commonly used to
Aphasia Tests 313

assess language and communication abilities in In recent years, several tests have emerged to
PWA: screening tests, comprehensive aphasia assess specific language or communication func-
batteries, and tests of specific linguistic or tions in PWA, or to complete testing in a shorter A
communicative function (Patterson 2008, 2015). period of time. For example, the ASHA-FACS
In addition, assessment of aphasia and its impact (Frattali et al. 1995) assesses functional commu-
on a person’s life includes testing cognitive abil- nication skills such as participating in conversa-
ities and related disorders (e.g., memory), testing tion, while the Reading Comprehension Battery
executive functioning (e.g., attention and plan- for Aphasia – 2 (LaPointe and Horner 1998) eval-
ning), observing a person in activities of daily uates reading performance in several contexts,
communication (e.g., social functional communi- such as single words and paragraphs. The Aphasia
cation or work-related communication), Rapid Test (Azur et al. 2013) is a bedside scale
interviewing the person with aphasia and family developed for administration in acute stroke
members, assessing quality of communication life settings.
and communication participation, and determin-
ing an individual’s candidacy for use of alterna-
tive and augmentative communicative systems Psychometric Data
(e.g., an alphabet board to spell words, drawing,
or a commercially available device). The availability of psychometric data for apha-
sia tests ranges from prolific and well
documented for some tests to minimal or non-
Historical Background existent for others, and the data appear in schol-
arly journals as well as in the test manuals.
Aphasia has been assessed more or less systemat- Spreen and Risser (2003) and Strauss et al.
ically for many years. Clinical observation was (2006) provide overviews of psychometric data
the earliest method of assessment, and the first for many general aphasia tests and supplemental
standardized test was published in 1926 by language tests. Few studies, and none recently,
Henry Head. In the ensuing years, several com- compare psychometric data across tests. In eval-
prehensive aphasia tests and specific linguistic uating a general or supplemental test for apha-
tests appeared. Each comprehensive test is based sia, several factors should be considered,
upon a theoretical model of aphasia, and although including size and definition of the standardiza-
the tests contain common subtests (e.g., sentence tion sample; reports of item, concurrent and
repetition), the test results and aphasia diagnoses predictive validity; test-retest, interrater and
vary. For example, the Minnesota Test for Differ- intrarater reliability; report of raw score means,
ential Diagnosis of Aphasia (Schuell 1965) standard deviations, ranges, and standard error
assesses language performance across several of measurement; information about test devel-
modalities and rests upon Schuell’s theory of opment, examiner qualifications, administration
aphasia as a unitary reduction in language across instructions, scoring, and interpretation; and
modalities with or without accompanying percep- normative data.
tual or motor deficits. In contrast, the Boston Although it is difficult to judge which of the
Diagnostic Aphasia Examination (Goodglass many aphasia tests best meets all the factors men-
et al. 2001) relates speech and language behav- tioned above, five tests are frequently used in
ioral deficits to neurological lesions. With yet a clinical settings and have the most psychometric
different perspective, Luria (1966) proposed a data published about them: Boston Diagnostic
comprehensive examination for aphasia through Aphasia Examination, Boston Naming Test,
nonstandardized observation of language perfor- Token Test (and Revised Token Test), the Compre-
mance in several modalities, but without specific hensive Aphasia Test, and Western Aphasia
subtests. Battery.
314 Aphasia Tests

Clinical Uses of Language Processing in Aphasia (Kay et al.

1992) The PALPA uses a cognitive neuropsy-
Screening Tests for Aphasia chological model of language to understand the
Screening tests for aphasia are brief and may be deficit at the various stages of language
administered at bedside. Their purpose is to rap- processing.
idly determine the presence of aphasia or the
need for further assessment. A screening test Tests of Cognitive-Communication Abilities
may be independent (e.g., Quick Assessment for and Related Functions
Aphasia; Tanner and Culbertson 1999) or a Tests of cognitive-communicative abilities related
shortened form of a comprehensive aphasia bat- to language functions have been included as part
tery, such as the Western Aphasia Battery (WAB; of comprehensive aphasia batteries (e.g., the
Kertesz 2006). Raven’s Progressive Matrices (Raven et al.
1995) as part of the Cortical Quotient in the
Comprehensive Aphasia Batteries WAB) or administered independently (e.g.,
A comprehensive aphasia battery is based on a Wechsler Memory Scale; Wechsler 2009).
theoretical model of aphasia and contains several
subtests. For example, the Boston Diagnostic Tests of Functional Communication
Aphasia Examination (Goodglass et al. 2001a, b) Functional communication abilities in PWA are
has 34 subtests, and the performance pattern is assessed through observation or the use of specific
used to classify an individual with an aphasia type tests. Functional communication includes verbal
(e.g., Broca’s aphasia). Although some subtests of and nonverbal methods of conveying information
comprehensive aphasia batteries may appear sim- in activities of daily living, such as reading signs,
ilar, the data obtained from each of the subtests greeting individuals, and participating in conver-
and the resulting aphasia diagnosis will vary sation. Functional communication assessed
according to the theoretical model of aphasia through observation can be contextually bound,
which underlies the test. Other comprehensive such as assessing conversation with familiar or
aphasia batteries are the Comprehensive Aphasia unfamiliar partners. Tests of functional commu-
Test (Swinburn et al. 2004; the Western Aphasia nication are intended to simulate activities of
Battery (Kertesz 2006), the Multilingual Aphasia daily living but typically are acontextual. Two
Examination (Benton et al. 1994), and the Neuro- examples of tests of functional communication
sensory Center Comprehensive Examination for are the Communicative Activities of Daily Living
Aphasia (Spreen and Benton 1977). – 2 (Holland et al. 1999) and the Assessment of
Language-Related Functional Activities (Baines
Tests of Specific Linguistic or Communication et al. 1999).
Function Functional communication can also be
Tests of specific functions provide detailed infor- assessed in a contextually sensitive manner
mation about a person’s abilities in one area of through checklists or scales, as observed by clini-
linguistic or communication ability and are par- cians or reported by persons with aphasia or their
ticularly useful for persons who have severe or family members. Prutting and Kirchner (1987)
minimal aphasia and for whom comprehensive published the pragmatic protocol which is a list
aphasia batteries would understate communica- of communicative acts that are rated as appro-
tion strengths and weaknesses. Three examples priate, inappropriate, or no opportunity to
are the Revised Token Test (McNeil and Prescott observe. The third rating type is important in
1978) for auditory comprehension, the Boston assessing functional communication because
Naming Test (Goodglass et al. 2001b) for oral not all communicative acts can be observed
naming, and the Psycholinguistic Assessments within an interaction. Other examples of
Aphasia Tests 315

checklists or scales are the Functional Assess- ▶ Luria, Alexander Romanovich (1902–1977)
ment of Communication Skills for Adults (ASHA ▶ Multilingual Aphasia Examination
FACS; Frattali et al. 1995), the Functional Com- ▶ Neurosensory Center Comprehensive Exami- A
munication Profile (FCP; Sarno 1969), the Com- nation for Aphasia
municative Confidence Rating Scale for Aphasia ▶ Wechsler Memory Scale All Versions
(CCRSA; Babbitt and Cherney 2010), and the ▶ Western Aphasia Battery
Communicative Effectiveness Index (CETI;
Lomas et al. 1989).
Related to but non-synonymous with func- References and Readings
tional communication is quality of life, or more
specific to aphasia, quality of communication life Azur, C., Leger, A., Arbizu, C., Henry-Amar, F., Chomel-
Guillame, S., & Samson, Y. (2013). The aphasia rapid
(QCL). QCL examines the impact of a communi-
test: An NIHSS-like aphasia test. Journal of Neurology,
cation disorder on life aspects of a person with 260(8), 2110–2117.
aphasia, for example, participation in social, voca- Babbitt, E. M., & Cherney, L. R. (2010). Communication
tional, or educational activities, communication confidence in persons with aphasia. Topics in Stroke
Rehabilitation, 17(3), 197–206.
with friends and family, and development of sat-
Baines, K. A., Martin, K. W., & Heeringa, H. M. (1999).
isfying relationships. Examples of tools to mea- ALFA: Assessment of Language Related Functional
sure QCL are the Quality of Communication Life Activities. Austin: Pro-Ed.
Scale (ASHA QCL; Paul et al. 2004), the Stroke Benton, A. L., Hamsher, K., Rey, G. J., & Sivan, A. B.
(1994). Multilingual Aphasia Examination (MAE-3).
and Aphasia Quality of Life Scale-39 (SAQOL-
Lutz: Psychological Assessment Resources Inc
39; Hilari et al. 2003), and the Assessment for (PAR).
Living with Aphasia (ALA; Simmons-Mackie Davis, G. A. (2007). Aphasiology: Disorders and clinical
et al. 2014). practice (2nd ed.). Boston: Pearson Allyn & Bacon.
Doyle, P. J., McNeil, M. R., Mikolic, J. M., Prieto, L.,
Hula, W. D., Lustig, A. P., Ross, K. B., Wambaugh, J.
Patient-Reported Outcomes L., Gonzalez-Rothi, L. J., & Elman, R. J. (2004). The
Patient-reported outcomes (PRO) as a status report Burden of Stroke Scale (BOSS) provides valid and
on a health condition have gained importance in reliable score estimates of functioning and well-being
in stroke survivors with and without communication
understanding assessment and treatment. In addi-
disorders. Journal of Clinical Epidemiology, 57,
tion to measuring patient reports of communica- 997–1007.
tion, a PRO in aphasia testing also measures the Frattali, C. M., Thompson, C. K., Holland, A. L., Wohl, C.
physical, cognitive, and psychological burdens of B., & Ferketic, M. M. (1995). The American Speech-
Language-Hearing Association Functional Assessment
stroke on the person with aphasia and family mem-
of Communication Skills in Adults. Rockville: The
bers. Two examples of aphasia assessment PRO American Speech-Language-Hearing Association.
tools are the Aphasia Communication Outcome Goodglass, H., Kaplan, E., & Weintraub, S. (2001a). Bos-
Measure (ACOM; Hula et al. 2015) and the Burden ton Naming Test (2nd ed.). Austin: Pro-Ed.
Goodglass, H., Kaplan, E., & Baressi, B. (2001b). Boston
of Stroke Scale (BOSS; Doyle et al. 2004).
Diagnostic Aphasia Examination (3rd ed.). San
Antonio: Psychological Corporation.
Head, H. (1926). Aphasia and kindred disorders of speech.
Cross-References New York: MacMillan.
Hilari, K., Byng, S., Lamping, D. L., & Smith, S. C.
(2003). Stroke and Aphasia Quality of Life Scale-39
▶ Activities of Daily Living (ADL) (SAQOL-39): Evaluation of acceptability, reliability,
▶ Aphasia and validity. Stroke, 34(8), 1944–1950.
▶ Augmentative and Alternative Communication Holland, A. L., Frattali, C. M., & Fromm, D. (1999).
Communicative Activities of Daily Living (2nd ed.).
(AAC)
San Antonino: Psychological Corporation.
▶ Boston Diagnostic Aphasia Examination Hula, W. D., Doyle, P. J., Stone, C. A., Hula, S. N. A.,
▶ Boston Naming Test Kellough, S., Wambaugh, J. L., Ross, K. B.,
316 AphasiaBank/TalkBank

Schumacher, J. G., & St. Jacque, A. (2015). The Apha- Tanner, D.C. & Culbertson, W. (1999). Quick Assessment
sia Communication Outcome Measure (ACOM): for Aphasia. Oceanside CA: Academic Communica-
Dimensionality, item bank calibration, and initial vali- tion Associates, Inc.
dation. Journal of Speech, Language, and Hearing Wechsler, D. M. (2009). Wechsler Memory Scale (4th ed.).
Research, 58, 906–919. San Antonio: Psychological Corporation.
Kay, J., Lesser, R., & Coltheart, M. (1992). Psycholinguis-
tic Assessments of Language Processing in Aphasia.
London: Taylor & Francis Group.
Kertesz, A. (2006). Western Aphasia Battery. New York:
Grune & Stratton.
LaPointe, L. L., & Horner, J. (1998). Reading Comprehen-
AphasiaBank/TalkBank
sion Battery for Aphasia (RCBA-2). San Antonio:
Pearson. Roberta DePompei
Lomas, J., Pickard, L., Bester, S., Elbard, H., Finlayson, School of Speech-Language Pathology and
A., & Zoghaib, C. (1989). The Communicative Effec-
Audiology, University of Akron, Akron, OH,
tiveness Index: Development and psychometric evalu-
ation of a functional communication measure for adult USA
aphasia. Journal of Speech and Hearing Disorders, 54,
113–124.
Luria, A. R. (1966). Higher cortical functions in man. New
York: Basic Books.
Definition
McNeil, M. R., & Prescott, T. E. (1978). Revised Token
Test. Austin: Pro-Ed. The AphasiaBank/TalkBank is a federally funded
Patterson, J. P. (2008). Assessment of language disorders in project that supplies interested professionals with
adults. In R. Chapey (Ed.), Language intervention
information about aphasia from both a practical
strategies in aphasia and related neurogenic commu-
nication disorders (5th ed., pp. 64–160). Baltimore: and research (data based) perspective.
Wolters Kluwer. It is a shared database of multimedia interac-
Patterson, J. P. (2015). Aphasia assessment. In A.M. tions for the study of communication in aphasia.
Raymer & L. Gonzalez-Rothi (Eds.). The Oxford hand-
Access to AphasiaBank is through www.
book of aphasia and language disorders. New York:
Oxford University Press. AphasiaBank.com. While some information can
Paul, D., Fratalli, C. M., Holland, A. L., Thompson, C. K., be seen immediately, access to the data in
Caperton, C. J., & Slater, S. C. (2004). Quality of AphasiaBank is password protected and restricted
Communication Life Scale. Rockville: American
to members of the AphasiaBank consortium
Speech-Language-Hearing Association (ASHA).
Prutting, C., & Kirchner, D. (1987). A clinical appraisal of group.
the pragmatic aspects of language. Journal of Speech Researchers and clinicians working with apha-
and Hearing Disorders, 52, 105–119. sia who are interested in joining the consortium
Raven, J., Court, J., & Raven, J. C. (1995). Raven’s Pro-
should read the Ground Rules and then send email
gressive Matrices. San Antonio: The Psychological
Corporation. to [email protected] with contact information and
Sarno, M. T. (1969). The Functional Communication Pro- affiliation.
file. New York: Institute of Rehabilitation Medicine,
New York University Medical Center.
Schuell, H. (1965). Minnesota Test for Differential Diag-
nosis of Aphasia. Minneapolis: University of Minne-
sota Press. Aphonia
Spreen, O., & Benton, A. L. (1977). Neurosensory
Center Comprehensive Examination for Aphasia.
Lyn S. Turkstra
Victoria: University of Victoria Neuropsychology
Laboratory. School of Rehabilitation Science, McMaster
Spreen, O., & Risser, A. H. (2003). Assessment of aphasia. University, Hamilton, ON, Canada
Oxford: Oxford University Press.
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A
compendium of neuropsychological tests: Administra-
tion, norms and commentary (3rd ed.). Oxford: Oxford Synonyms
University Press.
Swinburn, K., Porter, G., & Howard, D. (2004). Compre- Mutism
hensive Aphasia Test. Hove: Psychology Press, Inc.
Apolipoprotein E 317

Definition
Apolipoprotein E
Aphonia is the complete absence of voice, i.e., A
adduction and vibration of the vocal folds are John DeLuca
insufficient for vocal production. Aphonia may Research Department, Kessler Foundation,
be associated with vocal fold paralysis; trauma; West Orange, NJ, USA
severe cases of inflammation, edema, or scarring
of the vocal folds; benign or malignant diseases of
the vocal folds that interfere with vocal fold clo- Definition
sure; neurologically based movement disorders
(e.g., spasmodic dysphonia); overuse of the Apolipoprotein E (ApoE) is a polymorphic
voice; or somatoform disorders (e.g., in forms of plasma glycoprotein that transports cholesterol
elective mutism). Aphonia may be intermittent or and other lipids and has been shown to be
episodic. For example, individuals with spas- involved in the growth and repair of neurons.
modic dysphonia may have periodic, abnormal There is also some evidence to suggest that
abduction or adduction of the vocal folds that ApoE is involved in lipid redistribution after
may be perceived as voice breaks. Individuals demyelination. The ApoE protein is mapped to
who stutter also may have periodic voice breaks, chromosome 19 and is polymorphic with three
in this case associated with tight adduction of the major isoforms, each of which translates into
vocal folds. three alleles of the gene: ApoE-2, ApoE-3, and
When voice loss is incomplete, or when vocal ApoE-4. ApoE-2 is associated with the genetic
quality is affected without complete loss of voice disorder type III hyperlipoproteinemia. There is
(e.g., if the voice is hoarse), it is referred to as also some evidence that this allele may serve as
dysphonia. Aphonia and dysphonia refer specifi- a protective role in the development of
cally to abnormal sound output from the Alzheimer’s disease (AD). ApoE-3 is found in
phonatory sound source (i.e., the larynx) and approximately 64% of the population and is
should be distinguished from anarthria or dysar- considered as the “neutral” ApoE genotype.
thria, which are disorders of articulation, i.e., ApoE-4 has been implicated in atherosclerosis
related to the movements of the tongue, lips, jaw, and AD and impaired cognitive functioning.
and soft palate. Accordingly, dysphonia or apho- More specifically, ApoE-4 has been shown to
nia can occur independently from anarthria or be a major risk factor for development of AD
dysarthria. and has been associated with subtle neuropsy-
chological deficits in preclinical AD. Brain
changes associated with ApoE-4 in AD include
increased counts of amyloid plaques and neuro-
Cross-References fibrillary tangles, smaller medial temporal lobe
structures, reduced glucose metabolism, and
▶ Dysphonia depletion of cholinergic markers in the hippo-
campus, frontal, and temporal cortices. ApoE-4
has also been associated with adverse recovery
after traumatic brain injury (TBI). Persons with
References and Readings TBI with the ApoE-4 allele are ten times more
likely to develop AD than those without the
Merati, A., & Bielamowicz, S. (Eds.). (2007). Textbook of ApoE-4 allele. In multiple sclerosis, ApoE-4
voice disorders. San Diego: Plural Publishing. has been found to be associated with rapid dis-
Stemple, J. C., Glaze, L. E., & Klaben, B. G. (2000).
Clinical voice pathology, theory & management
ease progression and increased cognitive
(3rd ed.). Thompson Learning (now Florence: Cengage impairment, although the findings for cognitive
Learning). impairment have been inconsistent.
318 Apoptosis

Cross-References References and Readings

▶ Alzheimer’s Disease Hengartner, M. O. (2000). The biochemistry of apoptosis.

Nature, 407, 770–776.
Yuan, J., & Yankner, B. A. (2000). Apoptosis in the ner-
vous system. Nature, 407, 802–809.
References and Readings

Plomin, R., Defries, J. C., Craig, I. W., & McGuffin, P.

(2003). Behavioral genetics in the postgenomic era.
Washington, DC: American Psychological Appalic Syndrome
Association.
Dona Locke
Psychiatry and Psychology, Mayo Clinic,
Scottsdale, AZ, USA
Apoptosis

Kathleen L. Fuchs Synonyms

Department of Neurology, University of Virginia
Health System, Charlottesville, VA, USA Persistent vegetative state; Unresponsiveness
wakefulness syndrome

Synonyms

Programmed cell death Definition

Apallic syndrome is an older term that was first

Definition replaced by persistent vegetative state. More
recently, unresponsive wakefulness syndrome
Apoptosis is both a normal developmental pro- (UWS) is the proposed nomenclature. The syn-
cess to rid the body of overproduced cells as drome is a clinical condition describing patients
well as a sign of pathology in mature neural who fail to show voluntary motor responsiveness
systems. Apoptosis involves activation of in the presence of eyes-open wakefulness.
caspases - proteins that cleave other proteins Patients show reflexive behavior such as sponta-
in order to inactivate or modulate them to trig- neous breathing, but no signs of awareness of the
ger “pro-death” molecular pathways. The self or the environment. A thorough clinical eval-
resulting cellular debris is then removed by uation may be required to distinguish between
microglia in the central nervous system. Abnor- UWS and other conditions, including coma,
mal protein cleavage and cell death has been brain death, and locked-in syndrome.
implicated in neurodegenerative disorders such
as Alzheimer’s disease as well as autoimmune
disorders such as multiple sclerosis. Cross-References

▶ Brain Death
Cross-References ▶ Coma
▶ Locked-in Syndrome
▶ Alzheimer’s Disease ▶ Minimally Conscious State
▶ Multiple Sclerosis ▶ Minimally Responsive State
Appercetive Agnosia 319

References and Readings Cross-References

(1994). Medical aspects of the persistent vegetative state- ▶ Associative Visual Agnosia A
first of two parts. NEJM, 330, 1499–1508.
Multi-society task force on PVS (1994). Medical aspects of
the persistent vegetative state-second of two parts.
NEJM, 330, 1572–1579. References and Readings
Laureys, S., Celesia, G. G., Cohadon, F., Lavrijsen, J., et al.
(2010). Unresponsive wakefulness syndrome: A new Bauer, R. M., & Demery, J. A. (2003). Agnosia. In
name for the vegetative state or apallic syndrome. BMC K. Heilman & E. Valenstein (Eds.), Clinical neuropsy-
Medicine, 8, 68. chology (4th ed., pp. 236–295). New York: Oxford
van Erp, W., Lavrijsen, J. C. M., van de Laar, F. A, University Press.
Vos, P . E., Laureys S., Koopmans, R. T. C. M. DeRenzi, E., & Spinnler, H. (1966). Visual recognition in
(2014). The vegetative state/unresponsiveness patients with unilateral cerebral disease. Journal of
wakefulness syndrome: A systematic review of prev- Nervous and Mental Disease, 142, 513–525.
alence studies. European Journal of Neurology, DeRenzi, E., Scotti, G., & Spinnler, H. (1969). Perceptual
21, 1361–1368. and associative disorders of visual recognition. Rela-
tionship to the side of the cerebral lesion. Neurology,
19, 634–642.

Apperceptive Visual Agnosia

Appercetive Agnosia
John E. Mendoza
Department of Psychiatry and Neuroscience,
Talia R. Seider1,2, Ronald A. Cohen1,2 and
Tulane Medical School and SE Louisiana
Adam J. Woods1,2,3
Veterans Healthcare System, New Orleans, LA, 1
Department of Clinical and Health Psychology,
USA
College of Public Health and Health Professions,
University of Florida, Gainesville, FL, USA
2
Center for Cognitive Aging and Memory,
Definition McKnight Brain Institute, University of Florida,
Gainesville, FL, USA
3
Inability or marked difficulty in visually identify- Department of Neuroscience, University of
ing an object or picture of an object as a result of Florida, Gainesville, FL, USA
impaired perceptual abilities. In apperceptive
agnosia, in addition to problems in the visual
identification of an object, patients show impair- A failure to recognize a stimulus due to impaired
ment in reproducing (e.g., by drawing) the object perceptual abilities, although elementary sen-
or image and even matching the item to a similar sory functions (acuity, color vision, etc.) are
one within a visual array. This contrasts with intact. Though most cases of apperceptive agno-
associative visual agnosia in which identification sia are visual, auditory and tactile cases have
may also be impaired but the patient can usually also been reported. Patients with visual apper-
render a reasonable representation (e.g., a drawing ceptive agnosia are a heterogeneous group who
or graphomotor copy) of the object that cannot be typically have damage in visual association cor-
visually identified and can visually match it to a tices and appear to have a profound visual defi-
sample. Apperceptive visual agnosia likely results cit. While both apperceptive and associative
from a defect in the secondary association areas of agnosics have difficulty with object naming,
the visual cortex and is usually found in patients they can be differentiated in that the associative
who complain of general loss or reduction in agnosic will be able to copy a drawing of the
visual acuity. object, while the apperceptive agnosic will have
320 Applied Behavior Analysis

difficulty drawing it or matching it to a visually result in an aversive state and will be less likely
similar stimulus. to occur in the future; Fisher et al. 2011). With
insight into the environmental variables sur-
rounding the behavior of interest, behavior ana-
References and Readings lysts can predict behavior and alter responding
based on manipulations of one or more of these
Bauer, R. M. (2012). Agnosia. In K. M. Heilman & E. variables.
Valenstein (Eds.), Clinical neuropsychology (5th ed., Whereas some scientists in other fields of
pp. 238–295). New York: Oxford University Press.
psychology assume that human behavior is
DeRenzi, E., Scotti, G., & Spinnler, H. (1969). Perceptual
and associative disorders of visual recognition. Rela- indicative of underlying cognitive mechanisms,
tionship to the side of the cerebral lesion. Neurology, behavior analysts do not. That is, behavior is
19, 634–642. studied as a subject matter in its own right.
Shelton, P. A., Bowers, D., Duara, R., & Heilman, K. M.
Nevertheless, a common misconception in
(1994). Apperceptive visual agnosia: a case study.
Brain and Cognition, 25(1), 1–23. other fields is that behavior analysts deny the
existence of covert (unobservable) behavior
such as thinking. However, behavior analysts
affirm the existence of covert behavior under
the premise that these events are governed by
Applied Behavior Analysis
the same laws that govern overt (observable)
behavior (Moore 2009).
Michael J. Hartman and Tiffany Kodak
Several dimensions define the field of ABA
Department of Psychology, University of
and were described in a seminal article by Baer
Wisconsin-Milwaukee, Milwaukee, WI, USA
et al. (1968). These dimensions stipulate that
applied behavior analytic research is (a) applied,
defined as addressing socially significant prob-
Introduction to Applied Behavior lems; (b) behavioral, defined as using the behavior
Analysis of the organism as the subject matter; (c), analytic,
defined as using objective and controlled designs
Applied behavior analysis (ABA) is a science in that engender clear demonstrations of a functional
which principles of behavior are applied to prob- relation between an independent variable (e.g., a
lems of social importance (Cooper et al. 2007). behavioral intervention) and target behavior;
Behavior analysts seek to predict and control (d) technological, defined as providing precise
behavior, and they are interested in analyzing descriptions of experimental methods in sufficient
and identifying environmental events surround- detail so that the procedure can be replicated by
ing behavior. Several categories of environmen- other behavior analysts; (e) conceptually system-
tal events are important in the prediction and atic, defined as linking the results of the study to
control of a given behavior. These include: behavioral principles in order to produce a body of
(a) the broader environmental context in which science; (f) effective, defined as showing changes
behavior occurs (e.g., employees behave differ- in behavior that are observable via visual inspec-
ently while in the workplace than at a holiday tion of graphical displays and are clinically sig-
party), (b) motivational variables (e.g., asking for nificant, and contrasts other areas in psychology
a glass of water is more likely to occur following in which statistical significance is used to deter-
a strenuous workout), (c) events that correlate mine intervention efficacy; and (g) generalizable,
with the availability of consequences for a defined as behavior that occurs across settings and
response (e.g., turning the handle on a doorknob people, is durable over time, and when the effects
and pulling the door open will be successful if the of intervention spread across behavior. Studies
deadbolt is unlocked), and (d) the consequence which meet these criteria are described as consis-
(s) of a response (e.g., touching a hot stove may tent with an applied behavior analysis.
Applied Behavior Analysis 321

Operant and Classical Conditioning described so that it can be reliably measured by

multiple observers. Further, behavior analysts uti-
The science of ABA is based on the fact that lize direct measurement systems (e.g., observing A
behaviors are learned (Fisher et al. 2011). There an individual during specified intervals) rather
exist two mechanisms through which organisms than indirect measurement systems (e.g., self-
learn: operant conditioning and classical condi- reports, personality inventories) to collect data
tioning. Both learning processes describe changes on the behavior of interest. A common direct
in the probability of a response given specific measurement method is to record the frequency
environmental events and learning histories. of a target behavior during which observers record
Classical conditioning is the process by each occurrence of a response. For example, head-
which responses occur because of learned asso- hitting is often recorded using a frequency
ciations between neutral stimuli and stimuli that method, as it is readily discernable when this
automatically elicit a response (Chance 2014). target behavior is and is not occurring. Behavior
For example, a puff of air in the eye (i.e., an analysts also measure the duration of behavior to
unconditioned stimulus) elicits the reflex of record the amount of time an individual engages
blinking (i.e., an unconditioned response). in a target response. This method is best for
A neutral stimulus (e.g., a clicking sound) can recording behavior that may occur less often but
become a conditioned stimulus and elicit an is problematic due to the duration of time spent
eyeblink if the sound consistently precedes a engaging in the behavior (e.g., crying). To ensure
puff of air into the eye. Though this chapter that measurement systems are reliable, behavior
focuses on operant conditioning, classical con- analysts assess interobserver agreement which
ditioning has been used successfully to address provides an estimate of agreement on the occur-
socially significant issues (e.g., Whitehead rence of behavior across multiple observers. This
et al. 1976). type of reliability provides verification of the level
Operant conditioning involves changes in the of accuracy in the data collected on the target
probability of a behavior as a function of conse- behavior.
quences that follow the behavior (Miltenberger Once behavior is precisely defined and can be
2012). Thus, operant behavior is selected, altered, reliably measured, the goal of most behavioral
and maintained by consequences. The effects that assessments is to identify the variables responsi-
consequences have on behavior are either ble for operant behavior (discussed above). To
reinforcing or punishing. That is, a specific behav- guide these investigations, researcher use a
ior is more likely to occur in the future if a rein- model of operant behavior referred to as the
forcer tends to follow the behavior, and a specific three-term contingency. This model asserts that
behavior is less likely to occur in the future if an behavior is controlled by both (a) antecedent
aversive consequence tends to follow the behav- events, which set the occasion for behavior to
ior, respectively. Importantly, consequences are occur (e.g., the removal of a preferred activity or
defined as reinforcers or punishers based on their the introduction of a demand) and (b) conse-
effects on behavior. quence events, which follow behavior.
Michael (1982) further refined the field’s
understanding of the three-term contingency
Components of Applied Behavior with the addition of a second antecedent variable,
Analysis referred to as motivating operations (MOs). Moti-
vating operations are events that alter the proba-
An early step in the analysis of behavior is to bility of a response (i.e., behavior-altering effect)
develop definitions of the behavior of interest, and the value of a consequence that typically
which are referred to as operational definitions. follows the behavior (i.e., the value-altering
Subjective terms (e.g., anxiety) to define behavior effect). For example, MOs that increase the prob-
are avoided; rather, behavior is objectively ability of a response and value of a consequence
322 Applied Behavior Analysis

are referred to as establishing operations (EOs), Strategies for Behavior Change

and MOs that decrease the probability of a
response and value of a consequence are referred As discussed previously, the main goal of applied
to as abolishing operations (AOs). Consistent behavior analysis is to solve problems of social
with the conceptual framework of behavior anal- significance using behavioral principles.
ysis, MOs fluctuate based on changes in an organ- Researchers and clinicians alike have identified
ism’s environment. For example, lengthy periods three categories for tactics to modify behavior.
of sleep deprivation increase the probability of Broadly, and with some overlap, these tactics
behavior that typically produces sleep (e.g., serve the purpose to (a) increase the prevalence
lying in bed) and the value of sleep. of a desired behavior, (b) decrease the prevalence
Functional relationships between environmen- of problem behavior, and/or (c) bring a target
tal variables and behavior are analyzed using behavior under contextual control so that it occurs
single-subject experimental designs, which are in some contexts but not others (referred to as
carefully designed to aid in the identification of stimulus control).
such relationships (Fisher et al. 2011). Further, Increasing Behavior. Behavioral treatment
single-subject designs help to ensure that ABA packages often identify responses that are desir-
research continually abides to the tenets discussed able or appropriate. For example, a child with an
in Baer et al. (1968). That is, single-subject intellectual disability may have limited commu-
designs permit an evaluation of the extent to nication. In such a scenario, it is beneficial to
which observed differences in behavior following teach functional communication skills that the
the introduction of intervention reflect clinically individual can emit to interact effectively in his
significant differences for all individuals in an or her environment (e.g., ask for a snack, have a
experimental group. The single-subject design is conversation). Common strategies that are used
preferable to the group design because an empha- to increase behavior include prompts and differ-
sis is placed on the importance of a beneficial ential reinforcement. A prompt is any stimulus
intervention outcome for each individual, not a that produces the target response (Miltenberger
statistically significant outcome for group means. 2012). A prompt is provided by an instructor
Participants who do not demonstrate a clinically to help the learner perform the appropriate
significant treatment effect may receive additional behavior so that the behavior can produce a
interventions that are tailored to the individual. reinforcing consequence, which will increase
Furthermore, individuals serve as their own con- the probability of the occurrence of the appro-
trol from which repeated measures of behavior are priate behavior in the future. For example, an
compared. The purpose of a single-subject design adult uses a model prompt with a child by show-
is to permit a valid demonstration of the prediction ing (modeling) how to zip up her coat, and the
and control over behavior. child has the opportunity to imitate the adult’s
A common experimental design that behavior model thereafter.
analysts use to demonstrate a functional relation- Differential reinforcement occurs when one
ship is a reversal design (Bailey and Burch behavior produces the reinforcing consequence
2002). In this design, the independent variable and another behavior does not produce the
is introduced and removed systematically to reinforcing consequence (Vladescu and Kodak
demonstrate its effect on the dependent variable. 2010). For example, during early instruction for
The strength of the relationship between vari- a novel skill, an instructor may provide a rein-
ables can be determined by the magnitude of forcer following a prompted correct response
change in behavior. Experimental control is (e.g., asking for help with a task after the adult
shown within the reversal design when behavior provides a prompt to demonstrate how to ask for
“turns on” with the introduction of independent help). However, as the learner begins to acquire
variable and “turns off” when the independent the skill, the instructor uses differential reinforce-
variable is removed. ment and only independent correct responses
Applied Behavior Analysis 323

(e.g., asking for help without the instructor’s pro- own home, whereas reading out loud during a
mpt) produce the reinforcer. standardized achievement test at school may be
Decreasing Behavior. Behavior analysts fre- considered problematic. Stimulus control refers to A
quently provide intervention to individuals who the extent to which behavior is controlled by
are referred for services due to problem behavior antecedent stimuli (Balsam 1993). Stimulus con-
that is of concern to the people in the person’s life trol exists along a continuum from strong (i.e.,
(e.g., parents, school staff). For example, individ- behavior is only emitted in the presence of a
uals may engage in self-injurious behavior that specific antecedent stimulus) to weak (i.e., behav-
produces bodily harm (Toussaint and Tiger 2012). ior is emitted in the presence of many antecedent
Other, frequently treated topographies of problem stimuli). Stimulus control is typically established
behavior include aggression, disruption, pica through differential reinforcement of behavior;
(eating of inedible substances), tantrums, among that is, behavior in the presence of a stimulus is
others. To effectively treat problem behavior, it is reinforced, and behavior in the absence of the
critical to identify the function of the problem stimulus is not reinforced. For example, we learn
behavior (i.e., the cause of the behavior). The func- to pick up the telephone and say hello when it
tion of problem behavior is commonly identified rings (i.e., when answering the telephone is likely
by an assessment called a functional analysis to be reinforced by talking to the person calling)
(Iwata et al. 1982/1994). The functional analysis and not when it is silent (which is unlikely to
includes test conditions that manipulate one ante- result in a conversation with another person).
cedent and consequence for behavior, such as the
availability of attention or brief breaks from com-
pleting difficult tasks. The rate of behavior in these Maintenance and Generalization
test conditions is compared to a control condition in
which no consequences are provided for problem A critical component of behavioral intervention
behavior and antecedents are arranged to decrease is strategies to promote the maintenance and
the likelihood of problem behavior (e.g., the indi- generalization of behavior change. Applied
vidual has preferred items, attention, and no behavior analysts have developed several tech-
demands are given). The test condition(s) that pro- niques to enhance the maintenance of target
duces high rates of behavior is identified as the responses and have further refined an under-
function (i.e., cause) of problem behavior. standing of generalization from one of passive
Once the function of problem behavior is iden- measurement to one of active programing
tified, behavior analysts provide function-based (Stokes and Baer 1997).
treatment (Iwata et al. 1994). That is, treatment Maintenance. When skills are first taught,
is arranged to ensure that problem behavior no responses are typically acquired under a dense
longer produces reinforcement. Extinction is the schedule of reinforcement. A schedule of rein-
process by which a previously reinforced forcement refers to when reinforcement is avail-
response no longer contacts reinforcement (i.e., able for a target response. This schedule can
the contingency between response and reinforce- fluctuate from continuous (reinforcement is pro-
ment is removed). Other interventions, such as vided following every response) to intermittent
differential reinforcement, are combined with (reinforcement is provided following some
extinction to teach an individual to engage in an responses). Following the acquisition of a target
alternative, appropriate behavior to produce rein- response, maintenance involves thinning of the
forcement rather than engaging in problem behav- reinforcement schedule (i.e., responding does not
ior (Cooper et al. 2007). produce reinforcement as often) and removing
Stimulus Control. Some behaviors may only some or all components of the intervention. This
present as inappropriate because of the context in transition in schedule density and intervention
which they occur. For example, reading out loud components is important as it helps to promote
may be acceptable while in the privacy of one’s lasting behavior change.
324 Applied Behavior Analysis

Generalization. Generalization occurs when of Mental Health), state committees (e.g.,

behavior is emitted in contexts similar in some New York State Department of Health), and pro-
ways to the context(s) present during training fessional organizations (e.g., American Academy
(Miltenberger 2012). Behavior analysts are inter- of Child and Adolescent Psychiatry, American
ested in stimulus generalization and response gen- Association on Intellectual and Developmental
eralization. Stimulus generalization occurs when Disabilities, and the Association for Science in
a newly acquired behavior occurs in a novel Autism Treatment).
setting, with people who did not participate in
intervention, and in the presence of other novel
stimuli. For example, if a child learns to ask her
Resources on Applied Behavior Analysis
teacher to go to the bathroom, the skill has gen-
eralized if the child asks her parents if she can go
To learn more about the evidence for ABA,
to the bathroom at a restaurant and successfully
readers should refer to several websites and
uses the toilet despite differences in aspects of
reports, including the National Autism Center’s
the toilet and toilet-paper dispenser. Response
website (http://www.nationalautismcenter.org/
generalization occurs when novel responses
reports/), the National Professional Development
occur under conditions that are similar to the
Center (NCPD) on Autism Spectrum Disorder
training context. For example, an individual
(http://autismpdc.fpg.unc.edu/), the What Works
may be taught the response, “hello” when
Clearinghouse (http://ies.ed.gov/ncee/wwc/), and
encountering a peer and, following the acquisi-
Overview and Summary of Scientific Support for
tion of the response, may then emit the response,
Applied Behavior Analysis (Hagopian et al. 2015;
“hi” without any direct training. There are
https://www.kennedykrieger.org/patient-care/pati
numerous strategies that behavior analysts use
ent-care-programs/inpatient-programs/neurobehavi
to increase the likelihood that skills generalize
oral-unit-nbu/applied-behavior-analysis/positions).
following training, as described by Stokes and
Baer (1977).

References
Applications of Applied Behavior
Baer, D. M., Wolf, M. M., & Risley, T. R. (1968). Some
Analysis current dimensions of applied behavior analysis. Jour-
nal of Applied Behavior Analysis, 1, 91–97. https://doi.
Applied behavior analysis has proliferated as an org/10.1901/jaba.1968.1-91.
effective field in addressing socially significant Bailey, J. S., & Burch, M. R. (2002). Research methods in
applied behavior analysis. Thousand Oaks: Sage.
problems in a variety of contexts. Behavior ana-
Balsam, P. B. (1988). Selection, representation, and equiv-
lytic practices have been successfully applied to alence of controlling stimuli. In R. C. Atkinson, R. J.
address problems of social importance for indi- Herrnstein, G. Lindzey, & R. D. Luce (Eds.), Stevens’
viduals with developmental and intellectual dis- handbook of experimental psychology (2. ed.,
pp. 111–166). New York: Wiley.
abilities, mental illness, traumatic brain injury,
Chance, P. (2014). Learning and behavior (7th ed.). Bel-
drug and alcohol addictions, gambling, feeding mont: Wadsworth Cengage Learning.
disorders, severe problem behavior, among Cooper, J. O., Heron, T. E., & Heward, W. L. (2007).
others. ABA-based practices have also been Applied behavior analysis (2nd ed.). Upper Saddle
River: Pearson.
incorporated into many other fields including edu- Fisher, W. W., Piazza, C. C., & Roane, H. S. (2011).
cation, medicine, occupational, physical, and Handbook of applied behavior analysis. New York:
speech therapy, counseling, business, govern- Guilford Press.
ment, rehabilitation, and gerontology, to name a Hagopian, L. P., Hardesty, S. L., & Gregory, M. K. (2015).
Overview and summary of scientific support for applied
few. ABA-based treatment has also gleaned con-
behavior analysis. Retrieved from https://www.
siderable support from federal agencies (e.g., kennedykrieger.org/sites/default/files/patient-care-files/
Centers for Disease Control, National Institutes aba-scientific-support-9-2015.pdf
Apraxia 325

Iwata, B. A., Pace, G. M., Cowdery, G. E., & Miltenberger, Current Knowledge
R. G. (1994). What makes extinction work: An analysis
of procedural form and function. Journal of Applied
Behavior Analysis, 27, 131–144. https://doi.org/ Apraxia is thought to involve a loss of represen- A
10.1901/jaba.1994.27-131. tations or the inability to adequately access rep-
Iwata, B. A., Dorsey, M. F., Sliffer, K. J., Bauman, K. E., & resentations of learned movements and motor
Richman, G. S. (1994/1982). Toward a functional anal- skills in the damaged brain. This may lead to a
ysis of self-injury. Journal of Applied Behavior Analy-
sis, 27, 19–209. https://doi.org/10.1901/jaba.1994.27- loss of recall of the concept or configuration of
197. the movement or the inability to transform or
Michael, J. (1982). Distinguishing between discriminative implement the representational knowledge of
and motivational functions of stimuli. Journal of the the movement into a well-coordinated, properly
Experimental Analysis of Behavior, 37, 149–155.
https://doi.org/10.1901/jeab.1982.37-149. configured, and sequenced gesture. The diagno-
Miltenberger, R. G. (2012). Behavior modification: Prin- sis of apraxia requires the exclusion of cognitive
ciples and procedures (5th ed.). Belmont, CA: Thom- and sensorimotor impairments that may affect
son Wadsworth. the ability to carry out the motor skill, such as
Moore, J. (2009). Why the radical behaviorist conception
of private events is interesting, relevant, and important. arousal, attention, intention, language deficits or
Behavior and Philosophy, 37, 21–37. weakness, discoordination, movement disor-
Stokes, T. F., & Baer, D. M. (1997). An implicit technology ders, and sensory loss.
of generalization. Journal of Applied Behavior Assessment: Assessment for apraxia involves
Analysis, 10, 349–367. https://doi.org/10.1901/
jaba.1977.10-349. asking a patient to carry out pantomimes of
Toussaint, K. A., & Tiger, J. H. (2012). Reducing covert movements (e.g., “show me how you would
self-injurious behavior maintained by automatic salute . . . brush your teeth with a toothbrush. . .
reinforcement through a variable momentary blow out a candle”). If the response in not cor-
DRO procedure. Journal of Applied Behavior Anal-
ysis, 45, 179–184. https://doi.org/10.1901/jaba. rect, the examiner may evaluate the patient’s
2012.45-179. response to imitation of the movement or ability
Vladescu, J. C., & Kodak, T. (2010). A review of recent to produce the movement using actual objects or
studies on differential reinforcement during skill acqui- tools. The patient may also be tested for recog-
sition in early intervention. Journal of Applied Behav-
ior Analysis, 43, 351–355. https://doi.org/10.1901/ nition of skilled movements produced by the
jaba.2010.43-351. examiner.
Whitehead, W. E., Lurie, E., & Blackwell, B. (1976). Clas- Classification of apraxia: Apraxias may be
sical conditioning of decreases in human systolic blood differentiated by the body elements involved in
pressure. Journal of Applied Behavior Analysis, 9,
153–157. https://doi.org/10.1901/jaba.1976.9-153. the impaired movement, using the terms limb
apraxia, oral or buccofacial apraxia, trunk or
axial apraxia. These disorders have different
neuroanatomical underpinnings and may occur
separately in different individuals. For instance,
Apraxia
patients with oral apraxia may demonstrate nor-
mal function on tests of limb praxis.
Douglas I. Katz
Apraxia has been subclassifed into ideational
Department of Neurology, Boston University
apraxia, ideomotor apraxia, and limb-kinetic
School of Medicine, Braintree, MA, USA
apraxia (Liepmann 1900). Ideational apraxia
is a loss of the conception of a gesture or skilled
movement. In this form, the patient does not
Definition seem to know what to do, and the motor activity
is not facilitated by the use of actual objects.
The inability to correctly carry out a learned, Ideomotor apraxia affects the implementation
skilled motor act despite the preserved capability of the movement, producing spatial and timing
of the sensorimotor system to produce the errors. The patient seems to know what to do
intended movement. but cannot carry the movement out properly.
326 Apraxia of Speech

Limb-kinetic apraxia is the inability to make Cross-References

finely graded, precise limb movements. It has
been difficult to separate this form of apraxia ▶ Balint’s Syndrome
from motor dysfunction related to elemental ▶ Broca’s Aphasia
motor disturbance, and it remains controversial ▶ Frontal Lobe
that this is actually an apraxic disorder of learned ▶ Movement Disorders
skilled movement. ▶ Supplementary Motor Area (SMA)
Neuropathological localization: Apraxias
are almost always associated with lesions in
the dominant hemisphere. The left parietal lobe References and Readings
is most often implicated in limb apraxia in right-
handers. Portions of the frontal lobes, including De Renzi, E. (1990). Apraxia. In F. Boller & J. Grafman
(Eds.), Handbook of neuropsychology (Vol. 2,
the supplementary motor area, have been impli-
pp. 245–263). New York: Elsevier.
cated in some forms of apraxia. Lesions in and Heilman, K. M. (1997). Disorders of skilled movements:
around Broca’s area are most often implicated in Limb apraxia. In T. E. Feinberg & M. J. Farah (Eds.),
cases of oral apraxia. Lesions affecting trans- Behavioral neurology and neuropsychology
(pp. 227–235). New York: McGraw Hill.
mission of information between the cerebral
Liepmann, H. (1900). Das Krankheitsbild der Apraxie
hemispheres, including lesions of the corpus (motorische Asymbolie) auf Grund eines Falles von
callosum, may lead to apraxia of just the left einseitiger Apraxie. Monatschrift Psychiatrie und Neu-
limbs because of disconnection of movement rologic, 8, 15–44, 102–132, 182–197.
Rothi, L. J. G., & Heilman, K. M. (1997). Apraxia: The
engrams in the left hemisphere from motor con-
neuropsychology of action. East Sussex: Psychology
trol areas in the right hemisphere (callosal Press.
apraxia).
Other disorders: A number of disorders have
labels that include the term “apraxia” but have no
relationship with apraxia according to the usual Apraxia of Speech
definition. These include dressing apraxia, diffi-
culty orienting clothes to the body, often asso- Julie L. Wambaugh
ciated with left neglect, and usually occurring Veterans Affairs Salt Lake City Healthcare
with superior parietal right hemisphere lesions; System, University of Utah, Salt Lake City,
constructional apraxia, difficulty drawing or UT, USA
copying pictures or designs; gait apraxia, diffi-
culty initiating or maintaining a normal gait
pattern as can be seen in normal pressure hydro- Synonyms
cephalus; and apraxia of gaze, difficulty
directing eye movements as seen in Balint’s Historically, acquired apraxia of speech (AOS)
syndrome. Apraxia of speech is a disorder that has been known under a variety of terminologi-
affects the sequencing of sounds in words and cal designations (e.g., aphemia, phonemic disin-
syllables. It can be developmental or acquired, tegration, cortical dysarthria, dyspraxia of
and people with this disorder have difficulty speech). Currently, there are no acceptable syn-
coordinating articulatory motor activities neces- onyms in use. The descriptor, “stroke induced”
sary for speech. It is controversial whether this (SI), has occasionally been used to specify AOS
represents an apraxia consistent with the defini- resulting from stroke (e.g., SI-AOS). Primary
tions described above or a subtype of language progressive apraxia of speech (PPAOS) is used
or elemental motor disorders affecting articula- to designate AOS associated with neurodegen-
tory sequencing. erative disease.
Apraxia of Speech 327

Definition injury, neoplasm resection) may also result in

AOS. Areas of injury that have been most often
AOS is a neurologic, motoric disorder of speech associated with AOS include regions in the pre- A
production that is characterized by slowed rate of motor cortex (notably, the left posterior, inferior
speech, difficulties in sound production, and frontal gyrus), supplementary motor area, pari-
disrupted prosody. AOS is not a disorder of lan- etal lobe, and insula (see Wambaugh and
guage, although it rarely occurs without aphasia. Shuster (2008) for a review). PPAOS has been
Consequently, there is no impairment of compre- associated with tauopathies such as corticobasal
hension or production of language in pure AOS. degeneration, progressive supranuclear palsy,
and amyotrophic lateral sclerosis (Duffy 2013).
Little objective evidence exists concerning the
Categorization natural course of AOS, including the factors
affecting prognosis. Duffy (2013) indicates that
AOS currently does not have subcategories but is mutism associated with AOS rarely lasts beyond a
differentiated relative to onset and progression: few days or weeks unless other speech, language,
PPAOS (primary progressive) or AOS/SI-AOS or cognitive deficits are also present.
(sudden onset with improving or stable course). Treatment can be expected to result in the
Childhood apraxia of speech (CAS) is a related improvement in symptoms of AOS, even when
disorder, but not a category of AOS. AOS is chronic. Treatment guidelines for AOS
have been developed, which provide effectiveness
ratings for different types of treatment based on
Epidemiology the existing published evidence (see below;
Wambaugh et al. 2006a, b).
Duffy (2013) reported that AOS was the primary
communication disorder in 6.9% of 8101 cases of
neurologic motor speech disorders. As a second- Neuropsychology and Psychology
ary diagnosis (e.g., accompanying aphasia), AOS of AOS
can be expected to occur more frequently.
AOS is a neurogenic, motoric speech disorder that
is characterized by reduced rate of speech,
Natural History, Prognostic Factors, and disrupted production of speech sounds, and disor-
Outcomes dered prosody. These symptoms may be accom-
panied by behaviors such as articulatory groping
The establishment of AOS as a distinct clinical (silent and/or audible), speech initiation difficul-
entity is typically credited to Dr. Fredrick Darley, ties, increasing number of sound errors with
who in the late 1960s stimulated much of the early increasing word length or phonetic complexity,
discussion and research concerning the nature and awareness of speech errors, and motoric persev-
characteristics of this disorder. Since that time, the erations. Its severity ranges from a total inability
definition and descriptors of AOS have continued to speak to negligible speech disruptions (McNeil
to evolve, with continuing research efforts being et al. 2009; Wambaugh et al. 2006a).
likely to result in further refinement of our knowl- AOS is thought to be caused by difficulties in the
edge concerning this disorder. process of translating correctly selected and ordered
The most frequent cause of AOS is cerebral sounds into previously learned movement informa-
vascular accident involving the language- tion necessary for the implementation of intended
dominant hemisphere of the brain. Other causes speech movements. That is, it is assumed that pho-
of focal brain damage (e.g., penetrating head nology is intact at the linguistic level of processing.
328 Apraxia of Speech

However, there is difficulty in accessing stored symptoms. For example, Duffy (2013) provides a
movement plans/programs needed to articulate tool that may be used to evaluate speech produc-
correctly chosen sounds. These difficulties cause tion across tasks such as sound, monosyllabic
disruptions in the selection, positioning, and word, multisyllabic word, and sentence repetition,
movement timing of the articulators (e.g., tongue, repeated word productions, alternate and sequen-
lips, etc.). Consequently, sound productions may tial motion rates, reading aloud, and connected
be inaccurate, transitions between sounds may be speech production. The Apraxia Battery for
disrupted, and prosody may be abnormal. Sound Adults-second edition (Dabul 2000) also provides
durations as well as the intervals between sounds, tasks that may be used for examining speech
syllables, and words tend to be prolonged. production in adults with suspected AOS. How-
Controversy continues to exist concerning ever, the criteria for diagnosis of AOS provided by
error variability in AOS. Early diagnostic this test will not differentiate AOS from aphasia
criteria included highly variable error patterns. with phonemic paraphasia.
Over the period of several decades, relative con-
sistency in the location and type of errors
replaced high variability as a diagnostic charac- Treatment
teristic (following findings by McNeil et al.
1995). However, more recent investigations Behavioral treatment has been demonstrated to
have called into question the use of relative have positive outcomes for persons with AOS.
error consistency as diagnostic criteria (e.g., The AOS practice guidelines report revealed
Staiger et al. 2012). Currently, observations of four general approaches to AOS treatment:
error variability (or consistency) in AOS appear (1) articulatory-kinematic treatments (techniques
to be influenced by numerous factors such type focused on improving articulation of sounds),
of stimuli, method of stimulus presentation, (2) rate/rhythm control treatments (therapies in-
method of variability measurement, AOS sever- volving manipulating rate of speech production or
ity, and the presence or absence of aphasia. imposing an external rhythm on speech),
AOS typically occurs with aphasia and rarely (3) alternative/augmentative communication
occurs without it. The symptoms of AOS, how- approaches (therapies involving training the
ever, are not attributable to disruptions in lan- use of methods/devices for supplementing or
guage. AOS may also occur with another motor replacing speech), and (4) intersystemic facilita-
speech disorder, dysarthria. Unlike the dysar- tion/reorganization treatments (therapies utiliz-
thrias, AOS is not associated with problems with ing a relatively intact system/modality such as
muscle tone, weakness, reflexes, or sensory singing or gesturing to facilitate speech produc-
processing. tion) (Wambaugh et al. 2006b). On the basis of
objective evaluation of the existing evidence,
the AOS guideline developers determined that
Evaluation articulatory-kinematic approaches were “proba-
bly effective” rate/rhythm control approaches
Diagnosis of AOS requires that the primary symp- and intersystemic approaches were “possibly
toms of reduced rate of speech, distorted sound effective”; and AAC approaches had insufficient
production, and disrupted prosody be present. support to warrant a rating. A systematic review
Behaviors such as difficulties with speech initia- of AOS treatment reports published from 2004
tion or articulatory groping (see above) may also through 2012 serves as an update to the guide-
be observed but should not be used alone for lines (Ballard et al. 2015). The systematic
purposes of differential diagnosis (Wambaugh review revealed that the majority of treatment
et al. 2006a). Screening for AOS typically investigations covering the 9-year period
involves eliciting a variety of speech samples reviewed provided evidence concerning articula-
and determining the presence or absence of AOS tory-kinematic treatments.
Aprosodia 329

Findings from a few reports of transcranial A matter of controversy. Journal of Speech, Language,
direct current stimulation (tDCS) paired with and Hearing Research, 55, S1544–S1561.
Wambaugh, J. L., & Shuster, L. I. (2008). The nature and
behavioral therapy suggest that neuromodulary management of neuromotor speech disorders accompa- A
treatments may have promise in the treatment nying aphasia. In R. Chapey (Ed.), Language interven-
of AOS. tion strategies in aphasia and related neurogenic
communication disorders (5th ed., pp. 1009–1042).
Philadelphia: Lippincott Williams & Wilkins.
Wambaugh, J. L., Duffy, J. R., McNeil, M. R.,
Cross-References Robin, D. A., & Rogers, M. (2006a). Treatment guide-
lines for acquired apraxia of speech: A synthesis and
▶ Aphasia evaluation of the evidence. Journal of Medical Speech
Language Pathology, 14(2), xv–xxxiii.
▶ Dysarthria Wambaugh, J. L., Duffy, J. R., McNeil, M. R.,
▶ Paraphasia Robin, D. A., & Rogers, M. (2006b). Treatment guide-
lines for acquired apraxia of speech: Treatment descrip-
tions and recommendations. Journal of Medical Speech
Language Pathology, 14(2), xxxv–ixvii.
References and Readings

Ballard, K., Wambaugh, J., Duffy, J., Layfield, C.,

Maas, E., Mauszycki, S., & McNeil, M. (2015).
Updated treatment guidelines for acquired apraxia of Aprosodia
speech: A systematic review of intervention research
between 2004 and 2012. American Journal of Speech-
Language Pathology, 24, 316–337. https://doi.org/ Kate Krival
10.1044/2015_AJSLP-14-0118. Speech Pathology, School of Health Sciences,
Dabul, B. (2000). Apraxia battery for adults (2nd ed.). Edinboro University of Pennsylvania,
Austin: Pro-ed.
Duffy, J. R. (2013). Motor speech disorders: Substrates, Edinboro, PA, USA
differential diagnosis, and management (3rd ed.).
St. Louis: Elsevier Mosby.
Marangolo, P., Marinelli, C. V., Bonifazi, S., Fiori, V., Definition
Ceravolo, M. G., Proviniali, L., & Tomaiuolo, F.
(2011). Electrical stimulation over the left inferior
frontal gyrus (IFG) determines long-term effects Aprosodia is a deficit in comprehending or
in the recovery of speech apraxia in three chronic expressing prosody, i.e., variations in pitch, loud-
aphasics. Behavioural Brain Research, 225(2), ness, or rhythm of speech used in addition to
498–504.
Marangolo, P., Fiori, V., Cipollari, S., Campana, S., words to convey specific meaning and emotional
Razzano, C., DiPaola, M., Koch, G., & Caltagirone, C. information (Monrad-Krohn 1948; Leon and
(2013). Bihemispheric stimulation over left and right Rodriguez 2008; Wymer et al. 2002). Aprosodia
inferior frontal region enhances recovery from apraxia is traditionally characterized as linguistic or affec-
of speech in chronic aphasia. European Journal of
Neuroscience, 38(9), 3370–3377. tive (Wymer et al. 2002). Linguistic prosody aids
McNeil, M. (2002). Apraxia of speech: From concept to meaning, e.g., convict vs. convict or the dog and
clinic. Seminars in Speech and Language, 23(4), the cat in the cage are mine vs. the dog, and the
221–222. cat in the cage, are mine allow unambiguous
McNeil, M. R., Odell, K. H., Miller, S. B., & Hunter, L.
(1995). Consistency, variability, and target approxima- discrimination of the semantic target. Affective
tion for successive speech repetitions among apraxic, prosody conveys attitude, e.g., incredulity, sad-
conduction aphasic, apraxic dysarthric speakers. Clin- ness, or anger, e.g., depending on the prosodic
ical Aphasiology, 23, 39–55. intonation, oh, yeah, I’m just great may be a
McNeil, M. R., Robin, D. A., & Schmidt, R. A. (2009).
Apraxia of speech: Definition and differential diagno- sincere expression of a good feeling or an equally
sis. In M. R. McNeil (Ed.), Clinical management of sincere communication that the speaker is angry
sensorimotor speech disorders (2nd ed., pp. 249–268). or frustrated. Linguistic aprosodia is associated
New York: Thieme. with both left and right hemisphere lesions; affec-
Staiger, A., Finger-Berg, W., Aichert, I., & Ziegler, W.
(2012). Error variability in apraxia of speech: tive aprosodia is more consistently associated
330 Aprosodia

with lesions of the right hemisphere (Baum and and suggested future directions in research, see
Pell 1999; Pell 2006; Ross and Monnot 2008). Hargrove (2013).
Additionally, the basal ganglia appear to play a
key role in processing and further distributing the
meaning associated with the prosodic characteris- Cross-References
tics (Cancelliere and Kertesz 1990; Pell and
Leonard 2003). ▶ Apraxia of Speech
Clinically, aprosodia is most often consid- ▶ Dysarthria
ered in terms of whether receptive, expressive, ▶ Prosody
or both aspects of prosodic ability are dimin-
ished in an individual. However, Ross and var-
ious colleagues have proposed a categorization
system for the aprosodias, which is similar to
References
that used to categorize aphasia types. The sys- Baum, S. R., & Pell, M. D. (1999). The neural bases of
tem is based on a combination of deficit profile prosody: Insights from lesion studies and neuroimag-
and site-of-lesion information: motor (in the ing. Aphasiology, 13, 581–608.
area of the frontal operculum), sensory (poste- Ballard, K. J., Robin, D. A., McCabe, P., & McDonald, J.
(2010). A treatment for dysprosody in childhood
rior temporal operculum), conduction (arcuate apraxia of speech. Journal of Speech, Language, and
fasciculus), transcortical (anterior or posterior Hearing Research, 53, 1227–1245.
watershed), or global deficits (Ross 1981, 2000; Bellon-Harn, M. (2011). Targeting prosody: A case study
Ross and Monnot 2008). For example, an indi- of an adolescent. Communication Disorders Quarterly,
2, 109–117.
vidual with motor aprosodia might not express Bellon-Harn, M., Harn, W. E., & Watson, G. D. (2007).
affective or emotional prosody when speaking; Targeting prosody in an eight-year-old child with high-
one with sensory aprosodia might not recognize functioning autism during an interactive approach to
the affective meaning of prosodic signals in therapy. Child Language Teaching and Therapy, 23,
157–179.
another’s speech. These nondominant hemi- Bornhofen, C., & McDonald, S. (2008). Comparing strat-
sphere anatomic correlates of prosodic deficits egies for treating emotion perception deficits in trau-
do have modest empirical support (see Ross and matic brain injury. Journal of Head Trauma
Monnot 2008 for a summary of related investi- Rehabilitation, 23(2), 103–115.
Bowers, D., Blonder, L., & Heilman, K. M. (1998). The
gations). Ross’ motor aprosodia should not be Florida Affect Battery. Gainesville: University of Florida
confused with prosodic production impairments Brain Institute.
that arise from deficits in speech production due Cancelliere, A. E. B., & Kertesz, A. (1990). Lesion local-
to dysarthria (Duffy 2005). ization in acquired deficits of emotional expression and
comprehension. Brain and Cognition, 13(2), 133–147.
Assessment of aprosodia is generally accom- Duffy, J. R. (2005). Motor speech disorders: Substrates,
plished through careful observation; however, the differential diagnosis, and management. St. Louis:
Florida Affect Battery (Bowers et al. 1998) and Mosby.
the Aprosodia Battery (Ross et al. 1997) may be Hargrove, P. M. (2013). Pursuing prosody interventions.
Clinical Linguistics & Phonetics, 27(8), 647–660.
useful additions to standard testing regimes. Jones, H. N., Plowman-Prine, E. K., Rosenbek, J. C.,
Until recently, management of aprosodic Shrivastay, R., & Wu, S. S. (2009). Fundamental fre-
impairments has received little attention in the quency and intensity mean and variability before and
literature. However, emerging evidence suggests after two behavioral treatments for aprosdia. Journal of
Medical Speech-Language Pathology, 17, 45–52.
that behavioral therapies may have some effect Leon, S. A., & Rodriguez, A. D. (2008). Aprosodia and its
(Ballard et al. 2010; Bellon-Harn et al. 2007; treatment. Perspectives on Neurophysiology and Neu-
Bellon-Harn 2011; Bornhofen and McDonald rogenic Speech and Language Disorders, 18, 66–72.
2008; Jones et al. 2009; Leon et al. 2005; Leon, S. A., Rosenbek, J. C., Crucian, G. P., Heiber, B.,
Holiway, B., Rodriguez, A. D., et al. (2005). Active
Rosenbek et al. 2004; Rosenbek et al. 2006; treatments for aprosodia secondary to right hemisphere
Russell et al. 2010). For recent analysis of this stroke. Journal of Rehabilitation Research and Devel-
literature, descriptions of selected approaches, opment, 42(1), 93–102.
Arachnoid Cyst 331

Monrad-Krohn, G. H. (1948). Dysprosody or altered ‘mel- Short Description or Definition

ody of language’. Brain, 70, 405–415.
Pell, M. D. (2006). Cerebral mechanisms for understand-
ing emotional prosody in speech. Brain and Language, Arachnoid cysts are benign intracranial space A
96(2), 221. occupying lesions. An arachnoid membrane sur-
Pell, M. D., & Leonard, C. L. (2003). Processing emotional rounds a collection of clear fluid, identical to
tone from speech in Parkinson’s disease: a role for the cerebrospinal fluid (CSF). Arachnoid cysts pre-
basal ganglia. Cognitive, Affective, & Behavioral Neu-
roscience, 3(4), 275–288. sent due to mass effect, sudden hemorrhage, or
Rosenbek, J. C., Crucian, G. P., Leon, S. A., Hieber, B., incidentally.
Rodriguez, A. D., Holiway, B., et al. (2004). Novel
treatments for expressive aprosodia: A phase I investi-
gation of cognitive linguistic and imitative interven-
tions. Journal of the International Categorization
Neuropsychological Society: JINS, 10(5), 786–793.
Rosenbek, J. C., Rodriguez, A. D., Hieber, B., Leon, S. A., Arachnoid cysts are classified according to their
Crucian, G. P., Ketterson, T. U., Ciampitti, M., location as intracranial or spinal. Intracranial
Singletary, F., Heilman, K. M., & Gonzalez-Rothi,
L. J. (2006). Effect of two treatments for aprosodia arachnoid cysts can be further subclassified
secondary to acquired brain injury. Journal of Rehabil- (Table 1). Middle fossa cysts (MFAC) can also
itation Research and Development, 43, 379–390. be classified according to their size and distortion
Ross, E. D. (1981). The aprosodias: Functional-anatomical of surrounding structures based on Galassi classi-
organization of the affective components of language in
the right hemisphere. Archives of Neurology, 38, fication (Galassi et al. 1982). Type I cysts are
561–569. small, biconvex, and have no mass effect
Ross, E. D. (2000). Affective prosody and the aprosodias. In (Fig. 1a); type II cysts have a rectangular shape
M. M. Mesulam (Ed.), Principles of behavioral and and involve proximal and intermediate segments
cognitive neurology. New York: Oxford University Press.
Ross, E. D., & Monnot, M. (2008). Neurology of affective of the Sylvian fissure (Fig. 1b); type III cysts
prosody and its functional-anatomic organization in entirely involve the Sylvian fissure and can pro-
right hemisphere. Brain and Language, 104(1), 51–74. duce midline shift (Fig. 1c). Arachnoid cysts may
Ross, E. D., Thompson, R. D., & Yenkosky, J. P. (1997). also be classified as primary congenital or
Lateralization of affective prosody in brain and the
callosal integration of hemispheric language functions. acquired (Di Rocco 1990; Oberbauer 1999). Mid-
Brain and Language, 56, 27–54. line posterior fossa arachnoid cysts must not be
Russell, S., Laures-Gore, J., & Patel, R. (2010). Treating confused with the Dandy-Walker complex. The
expressive aprosodia: A case study. Journal of Medical Dandy-Walker complex describes hypoplasia or
Speech-Language Pathology, 18, 115–120.
Wymer, J. H., Lindman, L. S., & Booksh, R. L. (2002). A agenesis of the cerebellar vermis, associated
neuropsychological perspective of aprosody: Features, hydrocephalus, structural anomalies such as agen-
function, assessment and treatment. Applied Neuropsy- esis of the corpus callosum (occurring in 68% of
chology, 9(1), 37–47. patients), and a post fossa arachnoid cyst-like
structure that is not a true arachnoid cyst
(Wilkinson and Winston 2008).

Arachnoid Cyst
Epidemiology
Barbara Spacca1 and Andrew Brodbelt2
1
Anna Meyer Children’s Hospital, Florence, Italy Arachnoid cysts are estimated to account for 1%
2
The Walton Centre NHS Foundation Trust, of all nontraumatic intracranial lesions and are
Liverpool, UK incidentally found in 1 per 1,000 autopsies
(Boop and Teo 2000; Di Rocco 1990; Oberbauer
1999; Wilkinson and Winston 2008). They pre-
Synonyms sent in the first two decades of life, with a mean
age at diagnosis of 6 years. There is a male pre-
Temporal lobe agenesis dominance (2–3:1). Arachnoid cysts are mainly
332 Arachnoid Cyst

Arachnoid Cyst, Table 1 Frequency and distribution of intracranial arachnoid cysts (Rengachary et al. 1978)
Position Incidence (%) Position Incidence (%)
Supratentorial 76.8 Infratentorial 23.2
Middle cranial fossa 38.6 Cerebellopontine angle 15.7
Sellar, intrasellar, suprasellar 13.3 Vermal 6.3
Convexity 11.5 Clival 1.2
Interhemispheric fissure 8.3
Quadrigeminal plate 5.1

Arachnoid Cyst, Fig. 1 Classification of middle fossa absence of mass effect; (b) type II middle fossa arachnoid
arachnoid cysts. (a) Bilateral type I middle fossa arachnoid cysts are rectangular; (c) type III middle fossa arachnoid
cyst demonstrating small size, biconvex appearance, and cyst are large and often have significant mass effect

localized to one side, but case reports of bilateral imaging confirms that the brain expands after cyst
cysts have been described (Ziaka et al. 2008). decompression (Fig. 2). Most arachnoid cysts are
Familial presentations occur (glutaric aciduria now considered to be the result of a defect in early
type I) (Jamjoom et al. 1995). fetal development. Between the sixth and the eight
week of gestation, the meninx primitiva differenti-
ates into the pia and arachnoid mater. Congenital
Etiology/Pathology duplication or splitting of the arachnoid layer at this
time is thought to lead to the formation of primary
Microscopic examination demonstrates splitting congenital arachnoid cysts (Bright 1831;
of the arachnoid membrane at the margin of the Gosalakkal 2002; Miyajima et al. 2000;
cyst, a thick layer of collagen, hyperplastic arach- Rengachary and Watanabe 1981; Schachenmayr
noid cells, and numerous blood vessels in the cyst and Friede 1978, 1979) (Fig. 3).
wall, and an absence of traversing trabeculae Imaging and endoscopic evidence exists
although fine blood vessels may be present demonstrating that at least in some arachnoid
(Miyajima et al. 2000; Rengachary and Watanabe cysts, enlargement is due to a unidirectional
1981). Arachnoid cysts can communicate or be valve-type mechanism (Gosalakkal 2002;
separated from the subarachnoid space (SAS) but Miyajima et al. 2000; Santamarta et al. 1995;
appear to contain fluid similar in composition to Schroeder and Gaab 1997). A secretory mecha-
CSF (Miyajima et al. 2000; Rengachary and nism from the cyst wall has been suggested,
Watanabe 1981; Yildiz et al. 2005). although others have disputed this because of
Originally thought to be due to congenital hypo- a lack of microscopic evidence of secretion
plasia of the brain (e.g., temporal lobe agenesis), including pinocytosis (Go et al. 1984;
this concept has been questioned, as postoperative Gosalakkal 2002; Schachenmayr and Friede
Arachnoid Cyst 333

Arachnoid Cyst,
Fig. 2 Middle fossa
arachnoid cyst both before
(a) and after (b) surgery. A
Note the significant brain
re-expansion, an
observation used to refute
the suggestion of a
congenital hypoplastic
origin

stable, rarely reduce, or disappear completely.

Spontaneous hemorrhage or hemorrhage occur-
ring after minor head injury have been
described. In patients with middle fossa arach-
noid cysts, the annual risk of symptomatic hem-
orrhage is less than 0.1% (Parsch et al. 1997).
Hemorrhage can be asymptomatic, or, at worst,
present as a life-threatening acute subdural
hematoma. Subdural hygromas can also develop
due to the rupture of the cyst wall. Symptomatic
patients may complain of symptoms related to
raised ICP or specific to the cyst location.
Described symptoms and signs include irritabil-
ity, lethargy, headache, nausea, vomiting, diplo-
pia, papilledema, cranial nerve dysfunction, and,
in infants, macrocrania, a tense fontanelle,
displayed sutures, failure to thrive, or to reach
Arachnoid Cyst, Fig. 3 Fetal magnetic resonance image developmental milestones.
demonstrating an interhemispheric arachnoid cyst In MFAC, bone deformities are common with
large cysts and usually consist of macrocrania,
temporal bone thinning, and bossing. Less com-
1979). Water movement along an osmotic pres-
monly, downward displacement of the temporal
sure gradient due to repeated small intracystal
floor and upward and forward displacement of the
hemorrhage has also been suggested (Di Rocco
lesser wing of the sphenoid may lead to proptosis
1990). Arachnoid cysts can also be acquired
and in extreme cases visual loss, facial numbness,
following hemorrhage, head injury, or surgery
and ocular palsies. Long tract compression can
(Kutlay et al. 1998).
lead to sensory and motor limb signs. Seizures
are common, occurring in up to 40% of patients.
Natural History, Prognostic Factors, Developmental delays, behavioral disorders,
Outcomes, Symptoms, and Signs memory, and attention dysfunction have also
been described (Boop and Teo 2000; Di Rocco
The natural history of arachnoid cysts is 1990; Oberbauer 1999; Wilkinson and Winston
unpredictable. Cysts can grow in size, remain 2008).
334 Arachnoid Cyst

Patients with sellar and suprasellar cysts typ- Neuropsychology and Psychology of
ically present with endocrine dysfunction, Arachnoid Cysts
manifesting as failure to thrive or precocious
puberty. Optic pathway compression can result Large arachnoid cysts may present with failure to
in the loss of visual fields or acuity, while hypo- reach developmental milestones and psychomotor
thalamic pressure can produce eating and behav- delay. Cases of dementia in adults have been reported
ioral disorders. Thinning and displacement of the (Harsh et al. 1986). Cerebellar signs may be mis-
floor of the sella turcica and an empty sella can be diagnosed as motor delay. MFAC and convexity
observed with intrasellar cysts. Rarely, Supra- cysts can be associated with cognitive problems,
sellar cysts compressing the third ventricle pre- developmental delay, behavioral disorders, and
sent with “bobblehead doll” syndrome, whose memory and attention deficits in up to 7.8% of
pathogenesis is unknown, consisting in involun- patients (Arai et al. 1996). Symptoms can be poten-
tary movement of the head forward and back- tiated with antiepileptic drugs and sedatives. The
ward at a rate of two to three times/s (Hagebeuk relationship between arachnoid cysts and develop-
et al. 2005). Cerebral convexity cysts often pre- mental and behavior problems is poorly understood.
sent with cranial deformity and asymmetry Functional magnetic resonance imaging demon-
alone. Quadrigeminal plate cysts (Fig. 4) can strates no alterations in blood-oxygen-level-
present with obstructive hydrocephalus or dependent responses (BOLD) yet single-photon
upward gaze palsies. Spinal arachnoid cysts usu- emission computed tomography (SPECT) images
ally present with myelopathy or nerve root com- can demonstrate reduced cerebral blood flow and
pression (Di Rocco 1990). glucose metabolism even in the contralateral hemi-
sphere (Wilkinson and Winston 2008). Pre- and
postoperative cognitive testing, in small series, dem-
onstrate improved performance in specific tasks after
treatment, suggesting that arachnoid cysts may sup-
press cognitive and cortical function (Baroey Raeder
et al. 2005; Wester and Hugdahl 2003). However,
larger series do not support significant clinical
improvement after surgery in patients with severe
developmental and behavior problems (Arai et al.
1996; Levy et al. 2003). In patients with develop-
mental delay, behavioral disorders, and an arachnoid
cyst, or in very young patients with large cysts,
preoperative neuropsychological testing, EEG,
and/or SPECT may have a role in supporting surgical
intervention (Wilkinson and Winston 2008).

Evaluation

Diagnosis and follow-up are based on clinical

evaluation and imaging. Arachnoid cysts appear
as cavities filled with fluid with the same charac-
teristics as CSF, surrounded by a thin wall that is
not calcified and does not enhance after contrast.
Arachnoid Cyst, Fig. 4 Quadrigeminal plate arachnoid Magnetic resonance imaging (MRI) is the diag-
cyst nostic tool of choice because of image resolution
Arachnoid Cyst 335

for the cyst and surrounding anatomy (Wilkinson Asymptomatic cysts without mass effect may
and Winston 2008). have a lower risk of bleeding if treated (Wilkinson
and Winston 2008; Parsch et al. 1997). Seizure A
control may be improved, but a causal link is not
Treatment always apparent. Currently, treatment in patients
with severe developmental delay does not appear
Indications to confer a significant functional improvement
Arachnoid cysts causing a focal neurological (Arai et al. 1996; Levy et al. 2003).
deficit, raised ICP, or enlarging should be treated.
The management of asymptomatic patients or Surgical Options
patients with functional symptoms, such as sei- Three surgical options exist. These include shunt
zures and developmental delay, is controversial. insertion, open exploration, or endoscopic fenestra-
tion (Lena et al. 1996; Kaufman and Park 2000).
Commonly, a cystoperitoneal shunt is placed,
although revision rates due to infection or system
failure remain at 20–40% at 8 years (Arai et al.
1996; Oberbauer et al. 1992). Cyst fenestration
consists of opening a window in both the superficial
and deep walls of the cyst to allow communication
between the cyst and the subarachnoid space
(Figs. 5 and 6). Both microsurgical and endoscopic
approaches demonstrate improvement in up to 90%
of patients (Karabatsou et al. 2007; Levy et al.
2003; Spacca et al. 2009). Endoscopic fenestration
is less invasive, and series suggest reduced morbid-
ity (Karabatsou et al. 2003; Spacca et al. 2009).
Treatment of an associated subdural hemorrhage
Arachnoid Cyst, Fig. 5 Intraoperative photograph dem- or hygroma may lead to the resolution of the arach-
onstrating microsurgical fenestration of an arachnoid cyst noid cyst (Parsch et al. 1997).

Arachnoid Cyst, Fig. 6 Appearance before (a) and during (b) endoscopic fenestration of a middle fossa arachnoid cyst
336 Arachnoid Cyst

References and Readings Lena, G., Erdincler, P., Van Calenberg, F., Genitori, L., &
Choux, M. (1996). Arachnoid cysts of the middle cra-
nial fossa in children. A review of 75 cases, 47 of which
Arai, H., Sato, K., Wachi, A., Okuda, O., & Takeda, N. have been operated in a comparative study between
(1996). Arachnoid cysts of the middle cranial fossa: membranectomy with opening of cisterns and
Experience with 77 patients who were treated with cystoperitoneal shunt. Neurochirurgie, 42(1), 29–34.
cystoperitoneal shunting. Neurosurgery, 39(6), Levy, M. L., Wang, M., Aryan, H. E., Yoo, K., & Meltzer,
1108–1113. H. (2003). Microsurgical keyhole approach for middle
Baroey Raeder, M., Helland, C. A., Hugdahl, K., & fossa arachnoid cyst fenestration. Neurosurgery, 53(5),
Wester, K. (2005). Arachnoid cysts cause cognitive 1138–1145.
deficits that improve after surgery. Neurology, 64, Miyajima, M., Arai, H., Okuda, O., Hishii, M., Nakanishi, H.,
160–162. & Sato, K. (2000). Possible origin of suprasellar arach-
Boop, F. A., & Teo, C. (2000). Congenital intracranial noid cysts: Neuroimaging and neurosurgical observations
cysts. In D. G. McLane (Ed.), Pediatric neurosurgery in nine cases. Journal of Neurosurgery, 93(1), 62–67.
(pp. 489–498). Philadelphia: W.B. Saunders. Oberbauer, R. W. (1999). Intracranial and intraspinal cysts.
Bright, R. (1831). Reports of medical cases selected with a In M. Choux, C. Di Rocco, A. D. Hockley, & M. L.
view of illustrating the symptoms and cure of diseases by Walker (Eds.), Pediatric neurosurgery (pp. 137–149).
a reference to morbid anatomy. In R. Longman, B. Orme, London: Churchill Livingstone.
P.-R. Green, et al. (Eds.), Diseases of the brain and Oberbauer, R. W., Haasa, J., & Pucher, R. (1992). Arach-
nervous system (pp. 437–439). London: W.B. Saunders. noid cysts in children: A European co-operative study.
Di Rocco, C. (1990). Arachnoid cysts. In Youmans: Neu- Child’s Nervous System, 8, 281–286.
rological surgery (1299–1323). Philadelphia: WB Parsch, C. S., Krauss, J., Hofmann, E., Meixensberger, J.,
Saunders Company. & Roosen, K. (1997). Arachnoid cysts associated with
Galassi, E., Tognetti, F., Gaist, G., Fagioli, L., Frank, F., & subdural hematomas and hygromas: Analysis of
Frank, G. (1982). CT scan and metrizamide CT cis- 16 cases, long-term follow-up and review of the litera-
ternography in arachnoid cysts of the middle cranial ture. Neurosurgery, 40(3), 483–490.
fossa: Classification and pathophysiological aspects. Rengachary, S. S., & Watanabe, I. (1981). Ultrastructure
Surgical Neurology, 17(5), 363–369. and pathogenesis of intracranial arachnoid cysts. Jour-
Go, K. G., Houthoff, H. J., Blaauw, E. H., Havinga, P., & nal of Neuropathology and Experimental Neurology,
Hartsuiker, J. (1984). Arachnoid cysts of the sylvian 40(1), 61–83.
fissure. Evidence of fluid secretion. Journal of Neuro- Rengachary, S., Watanabe, I., & Brackett, C. (1978). Path-
surgery, 60(4), 803–813. ogenesis of intracranial arachnoid cysts. Surgical Neu-
Gosalakkal, J. A. (2002). Intracranial arachnoid cysts in rology, 9, 139–144.
children: A review of pathogenesis, clinical features, Santamarta, D., Aguas, J., & Ferrer, E. (1995). The natural
and management. Pediatric Neurology, 26(2), 93–98. history of arachnoid cysts: Endoscopic and cine-mode
Hagebeuk, E. E., Kloet, A., Grotenhuis, J. A., & MRI evidence of a slit-valve mechanism. Minimally
Peeters, E. A. (2005). Bobble-head doll syndrome Invasive Neurosurgery, 38(4), 133–137.
successfully treated with an endoscopic ventriculo- Schachenmayr, W., & Friede, R. L. (1978). Fine structure
cystocisternostomy. Case report and review of the of arachnoid cysts. Journal of Neuropathology and
literature. Journal of Neurosurgery, 103(3 Suppl), Experimental Neurology, 38, 434–446.
253–259. Schachenmayr, W., & Friede, R. L. (1979). Fine structure
Harsh, G. R., Edwards, M. S. B., & Wilson, C. B. (1986). of arachnoid cysts. Journal of Neuropathology and
Intracranial arachnoid cysts in children. Journal of Experimental Neurology, 38(4), 434–446.
Neurosurgery, 64, 835–842. Schroeder, H. W., & Gaab, M. R. (1997). Endoscopic
Jamjoom, Z. A., Okamoto, E., Jamjoom, A. H., Al-Hajery, observation of a slit-valve mechanism in a suprasellar
O., & Abu-Melha, A. (1995). Bilateral arachnoid cysts in prepontine arachnoid cyst: Case report. Neurosurgery,
the Sylvian region in female siblings with glutaric 40(1), 198–200.
aciduria type I. Journal of Neurosurgery, 82, 1078–1081. Spacca, B., Kandasamy, J., Mallucci, C. L., &
Karabatsou, K., Hayhurst, C., Buxton, N., O’Brien, Genitori, L. (2010). Endoscopic treatment of mid-
D. F., & Mallucci, C. L. (2007). Endoscopic man- dle fossa arachnoid cysts: A series of forty patients
agement of arachnoid cysts: An advancing tech- treated in two centres. Childs Nerv Syst, 26(2),
nique. Journal of Neurosurgery, 106(6 Suppl 163–72.
pediatrics), 455–462. Wester, K., & Hugdahl, K. (2003). Verbal laterality and
Kaufman, B. A., & Park, T. S. (2000). Treatment of arach- handedness in patients with intracranial arachnoid
noid cysts. In D. G. McLane (Ed.), Pediatric neurosur- cysts. Journal of Neurology, 250, 36–41.
gery (pp. 499–504). Philadelphia: WB Saunders. Wilkinson, C. C., & Winston, K. R. (2008). Congenital
Kutlay, M., Colak, A., Demircan, N., & Akin, O. N. (1998). arachnoid cysts and the Dandy-Walker complex. In
Iatrogenic arachnoid cyst with distinct clinical picture as A. L. Albright, I. F. Pollack, & P. D. Adelson (Eds.),
a result of bone defect in the floor of the middle cranial Principles and practice of pediatric neurosurgery
fossa: Case report. Neurosurgery, 43(5), 1215–1218. (pp. 162–186). New York: Thieme.
Arcuate Fasciculus 337

Yildiz, H., Erdogan, C., Yalcin, R., Yazici, Z., Hakyemez, References and Readings
B., Parlak, M., et al. (2005). Evaluation of communi-
cation between intracranial arachnoid cysts and cisterns The Federal Arbitration Act 9 U.S.C. Section 1 et seq.,
with phase-contrast cine MR imaging. AJNR – Ameri- (1925). A
can Journal of Neuroradiology, 26(1), 145–151.
Ziaka, D. S., Kouyalis, A. T., Boviatsis, E. J., & Sakas,
D. E. (2008). Asymptomatic massive subdural hema-
toma in a patient with bitemporal agenesis and bilateral
temporal arachnoid cysts. The Southern Medical Jour-
nal, 101(3), 324–326. Arcuate Fasciculus

Martin R. Graf
Department of Neurosurgery, Virginia
Commonwealth University Medical Center,
Arbitration
Richmond, VA, USA
Robert L. Heilbronner
Chicago Neuropsychology Group, Chicago, IL,
USA Definition

The arcuate fasciculus is a large bundle of nerve

Definition fibers that curves around the lateral sulcus to con-
nect Broca’s area in the frontal cortex to
Arbitration is an alternative means of settling a Wernicke’s area located in the posterior portion
dispute by impartial person(s) without proceed- of the temporal lobe. This white matter pathway is
ing to a court trial. It is sometimes preferred as a essential for language processing in which the
means of settling a matter in order to avoid the arcuate fasciculus connects the region associated
expense, delay, and acrimony of litigation. There with the ability to produce spoken language,
is no discovery, and there are simplified rules of Broca’s area, to that of the ability to process spo-
evidence in arbitration. The arbitrator(s) are ken words that are heard which is associated with
selected directly by the parties or are chosen in Wernicke’s area. This language loop is located in
accordance with the terms of the contract in the left hemisphere in approximately 90% of the
which the parties have agreed to use a court- population. Lesions disrupting the arcuate fascic-
ordered arbitrator(s) or an arbitrator(s) from the ulus result in conduction aphasia, which is char-
American Arbitration Association. If there is no acterized by paraphasic errors in which incorrect
contract, usually each party chooses an arbitra- words or sounds are substituted and word repeti-
tor, and the two arbitrators select a third to com- tion is impaired, although these individuals gen-
prise the panel. When parties submit to erally show reasonably normal speech and
arbitration, they agree to be bound by and com- comprehension.
ply with the arbitrators’ decision. The arbitrators’
decision is given after an informal proceeding
where each party presents evidence and wit- Cross-References
nesses. Arbitration has long been used in labor,
construction, and securities regulation but is ▶ Superior Longitudinal Fasciculus
gaining popularity in other disputes.

References and Readings

Cross-References
LaPointe, L. L. (2005). Aphasia and related neurogenic
▶ Mediation language disorders. New York: Thieme.
338 Aripiprazole

Side Effects
Aripiprazole
Serious
Cristy Akins1 and Efrain Antonio Gonzalez2,3 Neuroleptic malignant syndrome and seizures.
1
Mercy Family Center, Metarie, LA, USA
2
College of Psychology, Nova Southeastern Common
University, Fort Lauderdale, FL, USA Insomnia, dizziness, activation, akathisia, nausea,
3
Utah State University, Logan, UT, USA and vomiting.

Generic Name References and Readings

Aripiprazole, Aripiprazole lauroxil Centerwatch: https://www.centerwatch.com/drug-

information/fda-approved-drugs/therapeutic-area/17/
psychiatry-psychology.
Physicians’ Desk Reference (71st ed.). (2017). Montvale:
Brand Name Thomson PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The
prescriber’s guide (2nd ed.). New York: Cambridge
Abilify, Abilify Maintena, Aristada (extended
University Press.
release, injectable)
Additional Information
Drug Interaction Effects: http://www.drugs.com/drug_
Class interactions.html.
Drug Molecule Images: http://www.worldofmolecules.
com/drugs/.
Atypical neuroleptic
Free Drug Online and PDA Software: www.epocrates.com.
Free Drug Online and PDA Software: www.medscape.
com.
Proposed Mechanism(s) of Action Gene-Based Estimate of Drug interactions: http://
mhc.daytondcs.com:8080/cgibin/ddiD4?ver=4&task=
getDrugList.
Partial agonism at dopamine 2 receptors. Also Pill Identification: http://www.drugs.com/pill_identifica
inhibits 5HT2a receptors, thus increasing presyn- tion.html.
aptic release of related catecholamines.

Indication Arithmetic Reasoning

Schizophrenia, bipolar (mixed/manic), adjunctive J. Zhou1 and R. Sands2

1
for major depressive disorder, and autistic irrita- School Psychology, The Chicago School of
bility in children and teens. Professional Psychology, Chicago, IL, USA
2
Legal Psychology (Psychology and Law),
Neuropsychology, Clinical Psychology,
Off-Label Use The Chicago School of Professional Psychology,
Chicago, IL, USA
Other psychotic disorders, acute mania, bipolar
maintenance, bipolar depression, behavioral dis-
turbances associated with dementias, behavioral Synonyms
disturbances in children and adolescents, and
impulse control disorders. Numerical reasoning; Quantitative reasoning
Arousal 339

Definition References and Readings

Mathematical reasoning is the mathematical Geary, D. C. (1995). Reflections on evolution and culture
in children’s cognition: Implications for mathematical A
methodology of axiomatic reasoning, logical
development and instruction. American Psychologist,
deduction, and formal inference. 50(1), 24–37.
Spelke, E. (2005). Sex differences in intrinsic aptitude for
mathematics and science? American Psychologist,
60(9), 950–958.
Varley, R. A., Klessinger, N. J. C., Romanowski, C. A. J.,
Current Knowledge & Siegal, M. (2005). Agrammatic but numerate. Pro-
ceedings of the National Academy of Science of the
Research in evolutionary genetics and neurosci- United States of America, 102, 3519–3524.
Zhou, Z. (2011). Mathematical reasoning. In J. S. Kreutzer,
ence suggests important neurological differ-
J. Deluca, & B. Caplan (Eds.), Encyclopedia of clinical
ences between mathematical capacities that are neuropsychology. New York: Springer.
evolutionary primitive (e.g., counting) and
those (e.g., arithmetic) that are more culturally
taught (Geary 1995). Empirical data demon-
strate that mathematical reasoning and language
are functionally and neuroanatomically inde-
Arousal
pendent, suggesting (a) there is a common and
Ronald A. Cohen
domain-general syntactic mechanism that
Department of Clinical and Health Psychology,
underpins both language and mathematics, but
College of Public Health and Health Professions,
that mathematical expressions can gain direct
University of Florida, Gainesville, FL, USA
access to this system without translation into a
Center for Cognitive Aging and Memory,
language format, and (b) autonomous, domain-
McKnight Brain Institute, University of Florida,
specific syntactic mechanisms exist for lan-
Gainesville, FL, USA
guage and mathematics (Varley et al. 2005).
Studies on sex differences provide evidence
that mathematical reasoning develops from a
set of biologically based cognitive capacities
Synonyms
that males and females share (Spelke 2005).
Cortical activation; Cortical arousal; Delirium;
Male infants show no advantage over females
Wakefulness
in the processing of objects, space, or numbers.
Highly selected male and female students show
equal ability to learn mathematics. However,
other studies found male advantage in arithmet- Definition
ical reasoning mediated by male advantages in
both computational fluency and spatial The psychological and physiological state of
cognition. wakefulness, excitement, and/or activation
enables readiness for action, increased sexual
desire, and readiness. From a neuropsychological
perspective, arousal refers to the tonic state of
Cross-References cortical activity elicited by the subcortical reticu-
lar formation that results in increased wakeful-
▶ Abstract Reasoning ness, alertness, muscle tone, and autonomic
▶ Academic Competency response (e.g., heart rate and respiration). Mobili-
▶ Academic Skills zation of arousal including autonomic resources is
▶ Problem Solving necessary for the performance of both volitional
340 Arousal

and non-volitional tasks. Further, arousal varies control of attention, an important theoretical neu-
across sleep stages, emotional states, and cogni- ropsychological work that tied these processes to
tive tasks. It is a broad construct encompassing underlying brain mechanisms. Heilman and
many physiological processes and meaning Valenstein’s (1979) attention-arousal hypothesis
requires context. proposed that the arousal associated with reticular
activation interacted with a number of distinct
cortical and subcortical systems involved in the
Historical Background control of attention and that unilateral brain
lesions across these brain systems occur in
The concept of arousal played a key role in many patients with hemineglect syndrome.
of the earliest psychological theories. Physiolo-
gists of the nineteenth century, such as Brücke,
focused on the basis of bioenergetics as they Current Knowledge
attempted to understand the basis of cell function.
This influenced Freud who posited that bioener- The concept of arousal has evolved substantially
getics were the driving forces underlying psycho- from its original conception. Some neuroscientists
logical experience and behavior and accounted for argue that the concept has outlived its usefulness
his construct of “Id.” William James proposed that because the term arousal is used to refer to a broad
emotional experience involved the labeling of range of different behavioral and physiological
arousal and behavioral response associated with phenomena with very different underlying mech-
affective stimuli. Later, Walter Cannon coined the anisms. This has led to overgeneralization of the
term fight or flight response, describing mobiliza- construct. Yet, arousal continues to have an
tion of arousal systems to threat. Classical condi- important role in neuropsychological theories.
tioning theory was also routed in Pavlov’s There is compelling evidence that brain stem and
observations of autonomic and behavioral uncon- subcortical activity influences cortical activity and
ditioned response to stimuli, such as foods that also autonomic response and that visceral activity
have appetitive value (i.e., unconditioned stim- influences these brain systems. At a behavioral
uli). His concept of the orienting response was and phenomenological level, arousal provides a
one of the first constructs that directly linked construct that links the more primitive bioener-
arousal and learning to an attentional response. getic responses of the brain with higher cortical
Subsequently, arousal became a key construct in functions. This is most obvious when considering
the development of the field of psychophysiology levels of consciousness that can range from deep
in its efforts to characterize the relationship sleep or coma to normal wakefulness to states of
between psychological experience and physiolog- extreme excitement, hyperactivity, or agitation.
ical response. The demonstration by Moruzzi and Altered arousal is a key feature of delirium that
Magoun (1949) shows that the brain-stem reticu- can occur due to transient disruptions in brain
lar formation plays a key role in generating brain function due to metabolic or drug influences.
activation as evident by electroencephalography. Stimulation of the sympathetic nervous system
This spurred subsequent neurophysiological and an increase in the secretion of epinephrine and
inquiry into the factors underlying arousal and norepinephrine increase the brain activity as
their mediation of higher-order cognitive func- evidenced by EEG recordings, along with behav-
tions. Early efforts to understand the actions of ioral response toward greater wakefulness, where
neurotransmitters in the brain were closely linked drugs like barbiturates and alcohol have the oppo-
to the concept of arousal, based on the effects of site effect. Tasks that require intense focused
norepinephrine on the sympathetic nervous sys- attention to perform, that are stressful, or that
tem response and wakefulness. Pribram and require rapid response for adequate performance
McGuinness (1975) posited dissociations tend to result in increased fast wave EEG activity
between arousal, activation, and effort in the as well as autonomic nervous system responses
Arousal 341

such as increased heart rate and respiration, met- wide range of cognitive, behavioral, and neuro-
abolic activity, and a diversion of blood from the psychological studies supporting the principle
gastrointestinal system to skeletal muscle. These that task performance varies as a function of A
responses are associated with a readiness to arousal, with optimal performance occurring at
respond, a key element of attention; the specific some intermediate level. Pathological states that
nature of this attention response depends on cause lethargy usually reduce attentional perfor-
whether the task demands involve passive vigi- mance. Similarly, drugs, anxiety, or other factors
lance or more effortful directed attention. that lead to excessive arousal also have detrimen-
There is now strong evidence that multiple tal consequences on performance. Disturbances of
neural systems are involved in the maintenance, arousal are commonly associated with both intox-
control, and allocation of arousal throughout the ication and withdrawal from drugs like alcohol
cortex. At least four neurotransmitter systems and barbiturates, electrolyte imbalances, trauma
(acetylcholine, norepinephrine, dopamine, and to brain from closed head injury, and various
serotonin) mediate the energetic state of the neurological disorders including encephalitis,
brain, though a variety of peptides influence the tumors, advanced Alzheimer’s disease, and
neural response across specific brain systems. stroke. Conditions that affect the brain stem,
While, hierarchically, the arousal originates in hypothalamus, thalamus, limbic areas (e.g.,
the brainstem, the nuclei of the hypothalamus amygdala), and frontal and temporal lobes are
play a critical role in the specificity of arousal most likely to alter arousal and thereby affect
relative to specific appetitive behaviors. For attention too.
example, while damage to the reticular system of From a neuropsychological perspective,
the brain stem often results in coma, hypothalamic arousal is an important factor influencing the
nuclei such as the suprachiasmatic nucleus exert intensity of attentional focus and also the ability
control over wakefulness, by maintaining circa- of people to sustain attention. Kahneman (1973)
dian rhythm. Furthermore, the arousal associated proposed that arousal is a governing factor under-
with drives such as eating and sexual response are lying attentional capacity. Cohen’s (2014) four-
directly governed by hypothalamic functions, factor attention framework and other neuropsy-
with higher level limbic (e.g., amygdala) and cor- chological theories of attention posit that capacity
tical control. And, further, vagal inputs, both limitations associated with the overall level of
efferent and afferent fibers, are important conduits behavioral and physiological arousal constrain
for the communication of visceral system activity attention by influencing the intensity of focus
as well as motor activation associated with that is possible, which in turn affects other aspects
brainstem, hypothalamic, and higher cortical sys- of attention, most notably sustained performance.
tems. These complex interactions have been
implicated in a number of cognitive and emotional
processes. Peripheral and central interactions in Future Directions
the process of social engagement have been
described by the Polyvagal Theory (Porges Arousal appears to be a necessary and durable
1995). The central autonomic network interacts construct within neuropsychology. Yet, some of
with these systems to manage and interpret the concerns of neuroscientists regarding the over-
arousal components to support behavioral use and overgeneralization of the term have merit.
requirements (Benarroch 1993). As knowledge increases regarding the functional
The most obvious clinical manifestations of neuroanatomy of specific white-matter pathways
disordered arousal occur in conjunction with projecting from subcortical to cortical regions,
delirium. However, factors that influence the there will be a need for further refinement of the
level of arousal have direct effects on perfor- arousal construct. Efforts to more clearly demon-
mance, as described at the turn of the last century strate the linkage between behavioral and physio-
in the Yerkes-Dodson law. There are data from a logical arousal in the clinical context are needed,
342 Arterial Gas Embolism

given that they are not always obviously coupled.

The example of decreased frontal lobe activation Arterial Gas Embolism
associated with hyperactivity and impulsivity in
attention deficit disorder illustrates that this is Ben Dodsworth
complex system and construct. At this point in PM&R, University of South Florida, Tampa,
time, arousal is typically not directly assessed as FL, USA
part of neuropsychological evaluations, except
through behavioral observation. However, with
advances in the functional neuroimaging, it is Synonyms
possible to demonstrate both activation and deac-
tivation of particular brain regions and to observe Arterial air embolism
how these responses change in association with
not only momentary task demands but also tonic
state of arousal. Accordingly, in the future physi- Definition
ological measurement of arousal and activation
across brain systems, it is likely to be a more Arterial gas embolism refers to the obstruction
common element of standard neuropsychological of an arterial (oxygen-rich) blood vessel
assessment. caused by gas bubbles forming within or enter-
ing into the blood vessel. The effect can be
devastating in cases where the gas bubbles
Cross-References are sufficient to cause ischemia (lack of blood
flow) to a vital organ such as the heart or brain.
▶ Attention Common causes include lung trauma and severe
▶ Consciousness decompression sickness as a result of ascending
▶ Orienting Response rapidly from a dive or to a high altitude. Symp-
▶ Reticular Activating System toms may consist of loss of consciousness,
▶ Yerkes-Dodson Law altered mental status, seizures, and extremity
weakness, with the risk of complications such
as kidney failure, cardiac arrest, brain injury
References and Readings secondary to oxygen deprivation, and death.
Treatment begins with immediate administra-
Benarroch, E. E. (1993). The central autonomic network:
Functional organization, dysfunction, and perspective. tion of 100% oxygen, followed by the use of a
Mayo Clinic Proceedings, 68(10), 988–1001. recompression chamber (Bove 2015).
Cohen, R. A. (2014). Neuropsychology of attention
(2nd ed.). New York: Springer.
Heilman, K. M., & Valenstein, E. (1979). Mechanisms
underlying hemispatial neglect. Annals of Neurology, See Also
5(2), 166–170.
Kahneman, D. (1973). Attention and effort. Englewood
▶ Decompression Sickness
Cliffs: Prentice-Hall.
Moruzzi, G., & Magoun, H. W. (1949). Brain stem reticular
formation and activation of the EEG. Electroencepha-
lography and Clinical Neurophysiology, 1(4),
455–473. References and Readings
Porges, S. W. (1995). Orienting in a defensive world:
Mammalian modifications of our evolutionary heritage. Bove, A. A., MD, PhD. (2015, Oct). Arterial gas embo-
A polyvagal theory. Psychophysiology, 32, 301–318. lism. Retrieved January 24, 2017. From http://www.
Pribram, K., & McGuinness, D. (1975). Arousal, activa- merckmanuals.com/professional/injuries-poisoning/injur
tion, and effort in the control of attention. Psychologi- y-during-diving-or-work-in-compressed-air/arterial-gas-
cal Review, 82(2), 116–149. embolism
Arteriovenous Malformation (AVM) 343

centimeters (Warlow 2001), with males being

Arteriovenous Malformation affected twice as frequently as females. Epidemi-
(AVM) ological and imaging research report that about A
50% of patients with AMB present with hemor-
Bruce J. Diamond and Joseph E. Mosley rhage and the other 50% either present with non-
Department of Psychology, William Paterson focal symptoms or display no symptoms (Choi
University, Wayne, NJ, USA and Mohr 2005). A multicenter study examining
the incidence of newly diagnosed brain AVM’s
reported 1.12–1.42 cases per 100,000 person-
Synonyms years (Abecassis et al. 2014).

Brain arteriovenous malformation; Cerebral mal-

formation; Vascular malformation Mechanisms

Due to chronic hypoperfusion associated with

Short Description or Definition cerebral AVM, translocation of eloquent neuro-
logical functions to other brain areas (i.e., cortical
Arteriovenous malformations (AVMs) are irregu- plasticity) can occur. Cortical plasticity appears to
lar, anomalous, abnormal, or faulty formations or be influenced by both AVM pathogenesis and the
structures connecting the arteries and veins nature of the intervention (Ding et al. 2015). Cog-
(Webster 2006). Intracranial hemorrhage is a nitive improvements have been attributed to
potential complication in patients with arteriove- improved cerebral blood flow and reduction of
nous malformations of the brain (AMB) (Stapf hypoperfusion (Lantz and Meyers 2008).
et al. 2006).

Neuropsychological and Psychological

Etiology Outcomes

AVMs arise about 3 weeks after conception, at the The occurrence of cognitive impairments in AVM
time when blood vessels are dividing into veins and is difficult to determine (Lantz and Meyers 2008)
arteries (Stein and Wolpertson 1980). It has been because much of the data have been pooled from
suggested that AVMs are dynamic and have the patients with ruptured and unruptured AVMs.
ability to grow, regress, and regenerate following Patients with AVM may exhibit below normal
obliteration by surgery or radiosurgery (Moftakhar performance on tests of intelligence, attention,
et al. 2009). It is hypothesized that the altered and memory (Lantz and Meyers 2008). Patients
expression of more than 900 genes is involved in with AVMs are more likely to report developmen-
the pathogenesis of AVMs (Moftakhar et al. 2009). tal learning disorders than patients with tumors or
aneurysms, with AVM patients reporting four
times the rate of learning disability compared to
Epidemiology the normal population (Lantz and Meyers 2008;
Lazar et al. 1999). This finding may suggest that
AVMs are the most common type of clinically disorders of learning and intellectual function may
significant vascular malformation, occurring serve as a marker for early cerebral dysfunction in
almost exclusively in the brain and can involve patients with AVMs (Lazar et al. 1999). With
extension of vessels from the subarachnoid space respect to outcomes, some research has demon-
into brain parenchyma (Frosch et al. 2005). AVM strated postsurgical improvement in patients’ neu-
sizes may vary from a few millimeters to several ropsychological functioning, including better
344 Arteriovenous Malformation (AVM)

performance on tasks requiring executive function xylocaine procedure), magnetic resonance imag-
(Lantz and Meyers 2008). Researchers have also ing, and functional magnetic resonance imaging
demonstrated brain reorganization of language (Lantz and Meyers 2008). Other research has dem-
function in patients with AVMs by using Wada onstrated structural reorganization involving the
testing (intracarotid amobarbital sodium and motor cortex (Lantz and Meyers 2008) (Fig. 1).

Arteriovenous Malformation (AVM), Fig. 1

Arteriovenous Malformation (AVM) 345

Assessment and Treatment ▶ Radiosurgery, Stereotactic Radiosurgery

▶ Shunts
The AVM is often recognized clinically between the ▶ Wada Test A
ages of 10 and 30, presenting as a seizure disorder,
an intracerebral hemorrhage, a subarachnoid hem-
orrhage, a nonspecific or migraine headache, and References and Readings
less frequently, as pulsatile tinnitus (Al-Shahi and
Warlow 2001; Frosch et al. 2005; Warlow 2001). Abecassis, I., Xu, D., Batjer, H., & Bendok, B. (2014).
Natural history of brain arteriovenous malformations:
The most commonly affected site is the middle
A systematic review. Neurosurgical Focus, 37(3),
cerebral artery, particularly its posterior branches; 1–11.
however, AVMs may occur anywhere along the Al-Shahi, R., & Warlow, C. (2001). A systematic review of
midbrain, cerebellum, or spinal cord (Frosch et al. the frequency and prognosis of arteriovenous
malformations of the brain in adults. Brain, 124,
2005). Because AVMs expose patients to the risk of
1900–1926.
permanent neurological deficits or death, surgical Aminoff, M. J., Greenberg, D. A., & Simon, R. P. (2005).
intervention may be necessary (Zhao et al. 2005). Clinical neurology. New York: McGraw-Hill.
Clinicians must consider a variety of factors, includ- Ding, D., Starke, R. M., Liu, K. C., & Crowley, R. W.
(2015). Cortical plasticity in patients with cerebral arte-
ing lesion size, location, and angioarchitecture in
riovenous malformations. Journal of Clinical Neuro-
determining the appropriate approach to treatment science, 22(12), 1857–1861.
(Abecassis et al. 2014). The decision to treat Frosch, M. P., Anthony, D. C., & De Girolami, U. (2005).
involves evaluating the risks of subsequent intra- The central nervous system. In V. Kumar, A. K. Abbas,
& N. Fausto (Eds.), Pathologic basis of disease
cranial hemorrhage versus the immediate risks
(pp. 1347–1420). Philadelphia: Elsevier.
resulting from intervention (Abecassis et al. 2014). Lantz, E. R., & Meyers, P. M. (2008). Neuropsychological
A randomized trial of unruptured brain AVMs effects of brain arteriovenous malformations. Neuro-
(ARUBA 2014) concluded that pharmacological psychology Review, 18, 167–177.
Lazar, R. M., Connaire, K., Marshall, R. S., Pile-Spellman,
therapy for neurological symptoms alone may be
J., Hacein-Bey, L., Solomon, R. A., et al. (1999).
superior to surgical intervention for prevention of Developmental deficits in adult patients with arteriove-
stroke, neurological disability, or death (Mohr et al. nous malformations. Archives of Neurology, 56,
2014). Surgery may result in severe neuropsycho- 103–106.
Moftakhar, P., Hauptman, J. S., Malkasian, D., & Martin,
logical complications for some patients, including
N. A. (2009). Cerebral arteriovenous malformations.
executive dysfunction and aphasia (Lantz and Part 1: Cellular and molecular biology. Neurosurgical
Meyers 2008; Zhao et al. 2005). However, Focus, 26(5), 1–15.
advances in interventional neuroradiology and ste- Mohr, J., Parides, M., Stapf, C., Moquete, E., Moy, C.,
Overbey, J., Al-Shahi Salman, R., Vicaut, E., Young,
reotactic radiosurgery (SRS) have provided alterna-
W., Houdart, E., Cordonnier, C., Stefani, M.,
tives to traditional microsurgery, such as gamma Hartmann, A., von Kummer, R., Biondi, A., Berkefeld,
knife SRS and proton beam radiosurgery (Ropper J., Klijn, C., Harkness, K., Libman, R., Barreau, X., &
et al. 2005; Zhao et al. 2005). It should be noted that Moskowitz, A. (2014). Medical management with or
without interventional therapy for unruptured arterio-
the treatment of giant cerebral AVMs (>6 cm in
venous malformations (ARUBA): A multicenter, non-
diameter) may require endovascular embolization blinded, randomized trial. Lancet, 15(383), 614–621.
as an adjunct to surgical intervention (Zhao Ropper, A. H., Brown, R. H., Adams, R. D., & Victor,
et al. 2005). M. (2005). Adams & Victor’s principles of neurology.
New York: McGraw-Hill.
Stapf, C., Mast, H., Sciacca, R. R., Choi, J. H., Khaw,
A. V., Connolly, E. S., Pile-Spellman, J., & Mohr,
Cross-References J. P. (2006). Predictors of hemorrhage in patients with
untreated brain arteriovenous malformation. Neurol-
ogy, 66(9), 1350–1355.
▶ Anterior Communicating Artery
Stein, B. M., & Wolpertson, S. M. (1980). Arteriovenous
▶ Gamma Knife malformations of the brain. I: Current concepts and
▶ Intracarotid Sodium Amobarbital Test treatments. Archives of Neurology, 37, 69–75.
346 Articulation

Warlow, C. (2001). Stroke, transient ischemic attacks, and ▶ Phoneme

intracranial venous thrombosis. In M. Donaghy (Ed.), ▶ Phonics
Brain’s diseases of the nervous system (pp. 775–896).
New York: Oxford University Press. ▶ Phonology
Webster. (2006). Webster’s new explorer medical dictio- ▶ Speech-Language Pathology
nary (new edition). Springfield: Merriam-Webster.
Zhao, J., Wang, S., Li, J., Qi, W., Sui, D., & Zhao,
Y. (2005). Clinical characteristics and surgical results
of patients with cerebral arteriovenous malformations. References and Readings
Surgical Neurology, 63, 156–161.
http://www.asha.org/public/speech/disorders/SpeechSound
Disorders/
Hulit, L. M., & Howard, M. R. (2005). Born to talk:
An introduction to speech and language development
(4th ed.). Boston: Pearson A & B.
Articulation Plante, E., & Beeson, P. M. (2013). Communication and
communication disorders: A clinical introduction (4th
Janet P. Patterson ed.). Boston: Pearson A&B.
Audiology and Speech-Language Pathology
Service, VA Northern California Health Care
System, Martinez, CA, USA
Articulation Disorders
Definition Pamela Garn-Nunn1 and Carney Sotto2
1
Department of Pharmacology, Virginia
Articulation is (1) the juncture between bones or Commonwealth University, Richmond, VA, USA
cartilages in the skeleton of a vertebrate and (2) the 2
College of Allied Health Sciences, University of
movement pattern and relationship of oral structures Cincinnati, Cincinnati, OH, USA
such as the tongue and lips, to produce the sounds of
speech. Speech sound articulation develops gradu-
ally and consistently across children of all cultures, Short Description or Definition
and the earliest sounds made by infants are
undifferentiated. As a child matures and motor An articulation disorder is a failure to acquire or
control becomes increasingly well-coordinated, the difficulty producing a speech sound or sounds of a
child’s speech becomes intelligible within the lin- particular language by the expected normative age
guistic community. due to some type of motoric production problem.
Speech sound articulation is evaluated through Speech sound errors in articulation disorders
tests of single sounds and words, and in contexts include:
such as oral reading and conversation. Speech Substitutions: replacing a standard speech
sound articulation disorders can disrupt speech sound with a different standard speech sound,
intelligibility temporarily or for extended periods e.g., w abbit for r abbit, thpoon for spoon, or
of time. bery for very.
Omissions/Deletions: a standard speech sound
is not produced and is deleted or omitted, e.g., ba
Cross-References for bat, gin for green. (Widespread omissions
often indicate a phonological disorder.)
▶ Apraxia of Speech Distortions: the replacement of a standard
▶ Articulation Disorders speech sound by a nonstandard sound. The
▶ Ataxia sound may be slightly changed, e.g., s in soup
▶ Dysarthria sounds “slushy” or “lateralized.” A, lisp is a
▶ Dystonia distortion.
Articulation Disorders 347

Additions: insertion of a sound or syllable into • Orofacial anomalies such as cleft palate
a word, e.g., cart for car or bə lack for black. • Myofunctional disorders (sometimes referred
Additions are the least commonly occurring type to as tongue thrust disorders) A
of articulation error.
While some of these sound changes are com- In some cases, no definitive etiological factor
mon for toddlers and early preschoolers, children will be found.
should master the speech sounds of English by the For school-aged children, articulation disor-
age of 8. ders can be a continuation of an earlier phonolog-
NOTE: Individuals whose sound substitu- ical or articulation problem or the result of some
tions or omissions reflect a dialectic variation type of neurological injury. Similarly, in adults, a
or acquisition of English as a second language speech sound disorder can consist of residual
are not considered to have an articulation errors of an earlier disorder or a new disorder
disorder. due to a variety of neurological causes. Please
refer ▶ “Dysarthria” and ▶ “Apraxia” for further
information on these adult causes of speech sound
Categorization disorders.

An articulation disorder is a type of speech

sound disorder. It is associated with a motoric Natural History, Prognostic Factors, and
inability to produce a speech sound or sounds Outcomes
(rather than a failure to acquire the speech sound
rules of a particular language) by the expected A child’s acquisition of the speech sounds is a
normative age (see ▶ “Phonological Disorder”). gradual process. Correct articulation can depend
Articulation and phonological disorders can not only on motor skills and perceptual develop-
co-occur. ment but also the sound makeup and length of a
word. Nevertheless, research indicates that the
following sounds should be mastered by the ages
Epidemiology indicated (Table 1):

Incidence figures are available for speech sound • Vowels: should all be acquired by age 3 with
disorders, of which articulation disorders are one the exception of the er sound in words like b ir
type. Figures cited for preschoolers are 8–9% with d and hamm er.
approximately 5% still demonstrating a speech • Consonants: these represent ages of mastery;
sound disorder by first grade. Incidence of speech prior to these ages, correct production
sound disorders in children is higher than in will vary.
adults. Some children will outgrow their errors,
while others will require treatment from a speech-
language pathologist to develop understandable Articulation Disorders, Table 1 Ages by which chil-
speech (see “Evaluation”). dren have mastered sounds
During the process of speech development, By age 3: p m h w b (emerging between ages 1½ and 3)
articulation disorders occur more often in children By age 3½: k g d t f y (girls only) (emerging between
with ages 2 and 3½)
By age 4: y (boys)
• Genetic syndromes such as Down syndrome or By age 5: s-blends (emerging between ages 3½ and 5)
other syndromes associated with cognitive By age 5½: v
delays By age 6: sh ch j (girls)
• Childhood apraxia of speech By age 7: sh ch j (boys) th (as in that)
• Neurological disorders such as cerebral palsy By age 8: r s ng l z th (as in thumb) zh (as in measure)
348 Articulation Disorders

For children who do not meet these milestones, 3. Possible etiology(ies) of the problem, e.g.,
testing and possible treatment by a certified structural problem or neurological disorder
speech–language pathologist is highly 4. Probable course of treatment
recommended. A person who continues to exhibit 5. Prognosis
articulation errors past age 8 should also be eval-
uated unless their sound usage is characteristic of To meet these goals, the following components
a dialect or first language. should be included in an evaluation for speech
sound disorders:

1. Case history
Neuropsychology and Psychology of 2. Hearing screening
Disorder 3. Oral mechanism evaluation
4. Phonemic sound-by-position articulation tests
In some cases, an articulation disorder may be 5. Conversational speech sample
associated with damage to the central or periph- 6. Statement of intelligibility
eral nervous system. Specific neurological cor- 7. Language testing
relates usually are not found except in cases of 8. Other tests as appropriate
dysarthria or apraxia. When misunderstood,
some children may react by refusing to speak
or withdrawing from others. Children who are Treatment
unable to communicate due to an articulation
disorder can become frustrated and act out For patients with simple articulation disorders, a
because they cannot make basic needs and traditional, phonetic approach can be successful.
wants known. The child’s family can also Please refer ▶ “Phonological Disorder” and
become frustrated at their inability to commu- ▶ “Articulation Disorders” for more information
nicate with their child. However, this type of on treatment.
behavior is much more likely to occur in con-
junction with phonological disorders rather
than articulation disorders. For adults with
speech sound disorders due to apraxia or dys-
Cross-References
arthria, the effect on communication will
depend on the number of sounds affected, the ▶ Apraxia
▶ Dysarthria
degree of speech understandability, and the
▶ Phonological Disorder
patient’s reaction to the communication
problem. ▶ Phonology
▶ Speech Sound Disorder

Evaluation References and Readings

American Speech-Language-Hearing Association. (2007).

Evaluation of articulation disorders is designed to Speech sound disorders: Articulation and phonological
determine: disorders. www.asha.org/public/speech/disorders/
SpeechSoundDisorders.
American Speech-Language-Hearing Association. (2008).
1. Existence of a problem
Incidence and prevalence of communication disorders
2. Nature of the problem (sounds in error, patterns and hearing loss in children (2008 edition). www.asha.
intelligibility) org/members/research/reports/children.
Asenapine 349

symptoms, prolongation of QT interval, and

Asenapine agranulocytosis.
A
Efrain Antonio Gonzalez
College of Psychology, Nova Southeastern Common
University, Fort Lauderdale, FL, USA • Headache, dizziness, somnolence, dry mouth,
Utah State University, Logan, UT, USA nausea, tachycardia, diarrhea, orthostatic
hypotension, and weight gain

Generic Name
References and Readings
Asenapine
Cutler, A. J., Kalali, A. H., Weiden, P. J., Hamilton, J., &
Brand Name Wolfgang, C. D. (2008). Four-week, double-blind, pla-
Saphris cebo- and ziprasidone-controlled trial of iloperidone in
patients with acute exacerbations of schizophrenia. Jour-
nal of Clinical Psychopharmacology, 28(2 Suppl 1),
Class S20–S28.
Antipsychotics, second generation, and mood Kane, J. M., Lauriello, J., Laska, E., Di Marino, M., &
stabilizer Wolfgang, C. D. (2008). Long-term efficacy and
safety of iloperidone: Results from 3 clinical trials
for the treatment of schizophrenia. Journal of Clinical
Psychopharmacology, 28(2 Suppl 1), S29–S35.
Proposed Mechanism(s) of Action Kongsamut, S., Roehr, J. E., Cai, J., Hartman, H. B.,
Weissensee, P., Kerman, L. L., Tang, L., &
Sandrasagra, A. (1996). Iloperidone binding to human
Combination of central dopamine D2 and seroto- and rat dopamine and 5-HT receptors. European Jour-
nin 5-HT2A receptor antagonism (sublingual) nal of Pharmacology, 317(2–3), 417–423.
Physicians’ desk reference (71st ed.) (2017). Montvale:
Thomson PDR.
Potkin, S. G., Litman, R. E., Torres, R., & Wolfgang, C. D.
Indication (2008). Efficacy of iloperidone in the treatment of
schizophrenia: Initial phase 3 studies. Journal of Clin-
For the treatment of schizophrenia and manic or ical Psycopharmacology, 28(2 Suppl 1), S4–11.
mixed bipolar 1 episodes. Sainati, S. M., Hubbard, J. W., Chi, E., Grasing, K., &
Brecher, M. B. (1995). Safety, tolerability, and effect of
food on the pharmacokinetics of iloperidone (HP 873),
a potential atypical antipsychotic. Journal of Clinical
Off-Label Use Pharmacology, 35(7), 713–720.
Stahl, S. M. (2007). Essential psychopharmacology: The
prescriber’s guide (2nd ed.). New York: Cambridge
Agitation associated with a myriad of psychiatric University Press.
conditions and dementia. Borderline personality Szczepanik, A. M., Brougham, L. R., Roehr, J. E., Con-
disorder. Disruptive behavioral disorders associ- way, P. G., Ellis, D. B., & Wilmot, C. A. (1996). Ex
ated with childhood. vivo studies with iloperidone (HP 873), a potential
atypical antipsychotic with dopamine D2/5-hydroxy-
tryptamine2 receptor antagonist activity. The Journal
of Pharmacology and Experimental Therapeutics,
Side Effects 278(2), 913–920.
Weiden, P. J., Cutler, A. J., Polymeropoulos, M. H., &
Wolfgang, C. D. (2008). Safety profile of iloperidone:
Serious A pooled analysis of 6-week acute-phase pivotal trials.
Increased risk of mortality in elderly patients with Journal of Clinical Psychopharmacology, 28(2 Suppl 1),
dementia-related psychosis, mania. Extrapyramidal S12–S19.
350 ASHA Quality of Communication Life Scale

Additional Information through this person’s perspective, allow meaning-

Drug Interaction Effects. http://www.drugs.com/drug_ ful participation in life situations” (Paul et al.
interactions.html.
2004). The QCL is intended to be used as part of
Drug Molecule Images. http://www.worldofmolecules.
com/drugs/. a comprehensive communication assessment in
Free Drug Online. www.medscape.com. conjunction with measures of impairment and
Free Drug Online and PDA Software. www.epocrates.com. functional communication skills, such as the
Free Drug Online Centerwatch. https://www.centerwatch.
ASHA Functional Assessment of Communication
com/drug-information/fda-approved-drugs/therapeu
tic-area/17/psychiatry-psychology. Skills for Adults (ASHA FACS; Frattali et al. 1995;
Gene-Based Estimate of Drug interactions. http:// Frattali et al. 2017).
mhc.daytondcs.com:8080/cgibin/ddiD4?ver=4&task=
getDrugList.
Pill Identification. http://www.drugs.com/pill_identifica
tion.html. Rationale

The QCL emerged from the widespread need by

speech–language pathologists for a reliable and
valid instrument to determine the quality of life
ASHA Quality of
and participation in daily life activities as a
Communication Life Scale
result of a communication disorder. Other mea-
sures of quality of life were available (see
Diane Paul
Frattali 1998; Hirsch and Holland 2000 for a
Clinical Issues in Speech-Language Pathology,
summary) and a few measures assessed a single
American Speech-Language-Hearing
aspect of communication, such as voice (Voice
Association, Rockville, MD, USA
Handicap Index; Jacobson et al. 1997) or hear-
ing (Hearing Handicap Inventory for the
Elderly; Ventry and Weinstein 1982). However,
Synonyms
no other measures were designed specifically
for evaluating communication-related quality
ASHA QCL; QCL
of life for adults with communication disorders.
The development of the QCL was supported, in
part, from a grant awarded to ASHA from the
Description US Department of Education, National Institute
on Disability and Rehabilitation Research (No.
The American Speech–Language–Hearing Asso- H133G970055).
ciation (ASHA) Quality of Communication Life
Scale (QCL) was designed to assess the impact of
a communication disorder on an adult’s relation- Development and Testing
ships and interactions with communication partners
and on participation in social, leisure, work, and Pilot Test
educational activities. The World Health Organiza- A pilot test was conducted to determine the appro-
tion (WHO) defines quality of life as individuals’ priateness of the QCL items for adults with neuro-
“perception of their position in life in the context of genic communication disorders. The pilot test
the culture and value systems in which they live included healthcare settings from different areas of
and in relation to their goals, expectations, stan- the country and with a diverse caseload mix, includ-
dards and concerns” (WHOQCL Group 1995). ing patients with aphasia, cognitive–communication
ASHA defines Quality of Communication Life as disorder, and dysarthria. The subjects, 31 male and
“. . .the extent to which a person’s communication 26 female, had a mean age of 58.1 years and showed
acts, as constrained within the boundaries drawn by a range in severity of communication disorder, edu-
personal and environmental factors, and as filtered cation, and employment. The 35 pilot test items
ASHA Quality of Communication Life Scale 351

were grouped into the following domains: (1) rela- with the item score for general well-being. The
tionships/social life, (2) interests and leisure, (3) correlation between the total score and the item
vocational and school life, and (4) autonomy and score for general well-being score was significant A
well-being. There also was an item related to overall at 0.59. The correlation between domain mean
quality of life. Subjects marked their responses on a scores and the item score for general well-being
vertical 10-cm scale. The scale was a vertical line was significant for socialization/activities (0.49)
because of a concern that patients with neurogenic and confidence/self-concept (0.54). Intra-rater
communication disorders might experience visual reliability was moderate to high and consistency
field neglect. A factor analysis showed that the of response was considered to be acceptable. The
domains did not reflect how the items were related. correlation between the total score for the ABS
Results also showed that using a ruler to measure the and the QCL was low (0.09) and was not statisti-
placement of the client rating added 25 min per cally significant, suggesting that the ABS and
subject. Modifications based on the pilot tests results QCL measure different constructs. A factor anal-
included developing a new scoring system that did ysis showed a strong relationship among most of
not necessitate the use of a ruler, omitting items that the test items; 16 of the 19 items loaded under one
could not be scored reliably, and changing the factor. The data did not support categorization into
domains. A question was added to ask about the three distinct domains. The field test results indi-
subject’s affect or mood at the time of cated that the QCL is a valid measure of quality of
administration. communication life for adults with neurogenic
communication disorders. All items were
Field Test included in the final version of the QCL, except
The field test was designed to determine test valid- the two duplicate items.
ity, intra-rater reliability, consistency of
responses, and usability. The field test had 19
items in three domains: (1) socialization/activi- Clinical Use
ties, (2) confidence/self-concept, and (3) roles
and responsibilities. The item to assess general The target population for the QCL is adults with
well-being remained on the field test version of neurologically based communication disorders,
the QCL. Two items were repeated to provide a including aphasia, cognitive–communication dis-
measure of response consistency. Field test sites order, and dysarthria.
included a range of healthcare settings from dif- The following materials are included with the
ferent geographic areas in the United States. QCL:
Eighty-six subjects (61% male and 39% female)
with a mean age of 57.2 years participated in the • Manual detailing the rationale, development,
field test. Most of the subjects had a primary and testing of the QCL and administration and
diagnosis of left hemisphere stroke (70.9%) or scoring instructions
traumatic brain injury (16.3%) with a primary • Case example with completed demographics
communication disorder of aphasia (70.9%), form and score sheet
cognitive–communication disorder (16.3%), or • Demographics form
dysarthria (12.8%) across severity levels. Each • Test items with rating scale
subject completed the QCL, with assistance if • Score sheet
needed, and also completed a measure of well- • Administration form
being, the Affect Balance Scale (ABS; Bradburn
1969). Examiners also had the option to complete The QCL consists of a sample item, practice
a posttest interview asking subjects to rate the item, and the following 18 test items:
importance of selected test items. Data analyses
consisted of correlation coefficients for each test 1. I like to talk with people.
item, each domain mean score, and total score 2. It’s easy for me to communicate.
352 ASHA Quality of Communication Life Scale

3. My role in the family is the same. tional assessment of communication skills for adults.
4. I like myself. Rockville, MD: American Speech-Language-Hearing
Association.
5. I meet the communication needs of my job or Hirsch, F. M., & Holland, A. L. (2000). Beyond activity:
school. Measuring participation in society and quality of life. In
6. I stay in touch with family and friends. L. E. Worrall & C. M. Frattali (Eds.), Neurogenic
7. People include me in conversations. communication disorders: A functional approach (pp.
35–54). New York: Thieme.
8. I follow news, sports, and stories on TV/ Jacobson, B. H., Johnson, A., Grywalski, C., Silbergliet,
movies. A., Jacobson, G., & Benninger, M. S. (1997). Voice
9. I use the telephone. handicap index (VHI): Development and validation.
10. I see the funny things in life. American Journal of Speech-Language Pathology, 6,
66–70.
11. People understand me when I talk. Paul, D. R., Frattali, C. M., Holland, A. L., Thompson, C.
12. I keep trying when people don’t understand me. K., Caperton, C. J., & Slater, S. C. (2004). Quality of
13. I make my own decisions. communication life scale. Rockville, MD: American
14. I am confident that I can communicate. Speech-Language-Hearing Association.
The WHOQOL Group. (1995). The World Health Organi-
15. I get out of the house and do things. zation quality of life assessment (WHOQOL): Position
16. I have household responsibilities. paper from the World Health Organization. Social Sci-
17. I speak for myself. ence and Medicine, 41(10), 1403–1409.
18. In general, my quality of life is good. Ventry, I. M., & Weinstein, B. E. (1982). The Hearing
Handicap Inventory for the Elderly: A new tool. Ear
and Hearing, 3, 128–134.
The QCL takes approximately 15 min to
administer. It was designed to be completed in a
Readings
short time, recognizing the time constraints on American Speech-Language-Hearing Association. (n.d.).
clinicians. Patients with more severe communica- National outcomes measurement system (NOMS).
tion impairments may take longer to complete the Available from www.asha.org/NOMS.
QCL and may need more assistance. The clinician Aphasia Institute. (2013). Assessment for living with apha-
sia toolkit (ALA)—second edition. Toronto, Ontario,
may assist by reading the test items and making Canada: Author. Retrieved from http://www.aphasia.
the mark on the rating scale to help the patient. ca/shop/assessment-for-living-with-aphasia-toolkit/
The information derived from the QCL about the Bose, A., McHugh, T., Schollenberger, H., & Buchanan, L.
psychosocial, vocational, and educational effects (2009). Measuring quality of life in aphasia: Results
from two scales. Aphasiology, 23(7–8), 797–808.
of a communication impairment can assist with Dalemans, R., de Witte, L. P., Lemmens, J., van den
treatment planning, goal setting, counseling, pro- Heuvel, W. J. A., & Wade, D. T. (2008). Measures for
gress monitoring, and documentation of treatment rating social participation in people with aphasia: A
outcomes. systematic review. Clinical Rehabilitation, 22(6),
542–555.
Golper, L. C., & Frattali, C. M. (2012). Outcomes in
speech-language pathology: Contemporary theories,
References models, and practices (2nd ed.). New York: Thieme.
Hilari, K., Byng, S., Lamping, D. L., & Smith, S. C.
Bradburn, N. M. (1969). The structure of psychological (2003). Stroke and Aphasia Quality of Life Scale-39
well-being. Chicago: Aldine. (SAQOL-39): Evaluation and acceptability, reliability,
Frattali, C. M. (1998). Measuring modality-specific behav- and validity. Stroke, 34(8), 1944–1950.
iors, functional abilities, and quality of life. In C. M. Kagan, A., Simmons-Mackie, N., Rowland, A., Huijbregts,
Frattali (Ed.), Measuring outcomes in speech-language M., Shumway, E., McEwen, S., . . . Sharp, S.
pathology (pp. 55–88). New York: Thieme. (2008). Counting what counts: A framework for cap-
Frattali, C. M., Thompson, C. K., Holland, A. L., Wohl, C. turing real-life outcomes of aphasia intervention.
B., & Ferketic, M. M. (1995). American speech-lan- Aphasiology, 22, 258–280.
guage-hearing association functional assessment of Post, M. W. M., Boosman, H., van Zandvoort, M. M.,
communication skills for adults. Rockville, MD: Amer- Passier, P. E. C. A., Rinkel, G. J. E., & Visser-Meily,
ican Speech-Language-Hearing Association. J. M. A. (2011). Development and validation of a short
Frattali, C. M., Thompson, C. K., Holland, A. L., Wohl, C. version of the Stroke Specific Quality of Life Scale.
B., Wenck, C. J., Slater, S. C., & Paul, D. (2017). Journal of Neurology, Neurosurgery & Psychiatry, 82
Americn speech-language-hearing association func- (3), 283–286.
Ashworth Spasticity Scale (and Modified Version) 353

Platz et al. 2005), which cannot be attributed to

Ashworth Spasticity Scale any one factor (Platz et al. 2005), although some
(and Modified Version) evidence suggests that the inter-rater reliability of A
the MAS is lower for heavier limbs (Ansari et al.
Kari Dunning 2008; Pandyan et al. 1999; Platz et al. 2005). Both
Department of Rehabilitation Sciences, scales have demonstrated responsiveness to treat-
University of Cincinnati, Cincinnati, OH, USA ment (Platz et al. 2005).
Spasticity is characterized by an involuntary
muscle activity (Pandyan et al. 2005) and has
Synonyms been traditionally defined as a velocity-dependent
increase in muscle tone due to a hyperactive
AS; MAS stretch reflex (Lance 1980). The construct validity
of the AS and MAS as spasticity assessments is
inadequate because they do not address velocity
Description dependence. Rather, these scales measure passive
resistance to movement (hypertonia), which is
The Ashworth Scale (AS) and Modified Ashworth influenced by spasticity but also altered by biome-
Scale (MAS) measure spasticity. During the chanical factors unrelated to involuntary muscle
administration of both AS (Ashworth 1964) and activation (Fleuren et al. 2009; Pandyan et al.
MAS (Bohannon and Smith 1987), the examiner 1999; Platz et al. 2005). Thus, AS and MAS scores
passively moves the joint being tested and rates are only moderately associated with reflexes (Platz
the perceived level of resistance in the muscle et al. 2005) and electromyographic assessments
groups opposing the movement. Both scales are (Fleuren et al. 2009; Pandyan et al. 1999; Platz
single-item measures ranging from 0 to 4, where et al. 2005) and more strongly associated with
0 indicates no increase in muscle tone and 4 indi- objective measures of resistance (Fleuren et al.
cates that the affected part is rigid in flexion or 2009; Pandyan et al. 1999; Platz et al. 2005).
extension. The AS is considered an ordinal scale,
whereas the MAS is considered a nominal scale
due to ambiguity created by the addition of the 1+ Clinical Uses
grade between 1 and 2 (Pandyan et al. 1999).
Despite the fact that the AS and MAS are actu-
ally only valid assessments of hypertonia
Historical Background (Fleuren et al. 2009; Pandyan et al. 1999;
Platz et al. 2005), these scales are the most
The AS was first described by Ashworth in 1964 commonly used clinical tools to assess spastic-
(Ashworth 1964) and was subsequently modified ity (Pandyan et al. 1999; Platz et al. 2005). Both
with the addition of a 1+ grade by Bohannon in scales have been used to describe treatment
1987 with the intent to increase sensitivity response for persons with a wide range of
(Bohannon and Smith 1987). However, this addi- upper motor neuron disorders, including trau-
tion may have decreased the reliability of the matic brain injury, stroke, multiple sclerosis,
MAS for heavier limbs (see below) (Ansari et al. cerebral palsy, and spinal cord injury (Platz
2008; Pandyan et al. 1999; Platz et al. 2005). et al. 2005).

Psychometric Data Cross-References

Inter- and intra-rater reliability of the AS and ▶ Severe Brain Injury

MAS show wide variation (Pandyan et al. 1999; ▶ Spinal Cord Injury
354 ASIA Impairment Scale

References and Readings accepted and readily administered guide to docu-

ment neurological function after spinal cord injury
Ansari, N. N., Naghdi, S., Arab, T. K., & Jalaie, S. (2008). (SCI) and is intended to be a standard for measur-
The interrater and intrarater reliability of the modified
ing neurological outcomes in both clinical and
Ashworth scale in the assessment of muscle spasticity:
Limb and muscle group effect. NeuroRehabilitation, research settings. Briefly, these standards utilize
23(3), 231–237. a two-step process consisting of a specific neuro-
Ashworth, B. (1964). Preliminary trial of carisoprodol in logical examination followed by a classification
multiple sclerosis. Practitioner, 192, 540–542.
procedure based on the results of the exam. The
Bohannon, R. W., & Smith, M. B. (1987). Interrater reli-
ability of a modified Ashworth scale of muscle spastic- systematic neurological examination assesses
ity. Physical Therapy, 67(2), 206–207. sensory and motor function of each spinal seg-
Fleuren, J. F., Voerman, G. E., Erren-Wolters, C. V., et al. mental level. Sensation of light touch and pinprick
(2009). Stop using the Ashworth scale for the assess-
(PP) stimuli is scored as 0 for absent, 1 for
ment of spasticity. Journal of Neurology, Neurosur-
gery, and Psychiatry, 81(2), 46–52. impaired, and 2 for normal. Motor function is
Lance, J. W. (1980). Symposium synopsis. In R. G. scored on a scale of 0 for total paralysis to 5 for
Feldman, R. R. Young, & W. P. Koella (Eds.), Spastic- normal strength. All 28 dermatomes are tested
ity: Disordered motor control (pp. 485–494). Chicago:
bilaterally for sensory function, and ten key mus-
Year Book Medical Publishers.
Pandyan, A., Johnson, G., Price, C., Curless, R., Barnes, cles are tested bilaterally for motor function,
M., & Rodgers, H. (1999). A review of the properties yielding sensory/light touch (LT) and sensory/pin-
and limitations of the Ashworth and modified prick (PP) summed scores ranging from 0 to
Ashworth scales as measures of spasticity. Clinical
112 and motor summed scores ranging from 0 to
Rehabilitation, 13(5), 373–383.
Pandyan, A. D., Gregoric, M., Barnes, M. P., et al. (2005). 100. The neurological level is assigned as the
Spasticity: Clinical perceptions, neurological realities lowest level with normal neurological function.
and meaningful measurement. Disability and Rehabil- In addition, the ASIA Impairment Scale (AIS)
itation, 27(1–2), 2–6.
grade classification, an indicator of injury “com-
Platz, T., Eickhof, C., Nuyens, G., & Vuadens, P. (2005).
Clinical scales for the assessment of spasticity, associated pleteness” similar to the Frankel scale, is assigned
phenomena, and function: A systematic review of the based on this information. AIS A denotes a com-
literature. Disability and Rehabilitation, 27(1–2), 7–18. plete injury with no sensory or motor function
below the level of injury. Incomplete injuries are
graded as AIS B if there is sensory but no motor
function below the injury level, AIS C if there is
ASIA Impairment Scale some motor sparing, AIS D for substantial motor
sparing, and AIS E for normal neurological exam-
Amitabh Jha ination (Fig. 1).
TBIMS National Data and Statistical Center,
Craig Hospital, Englewood, CO, USA
Historical Background
Synonyms ISNCSCI has been used extensively in clinical
practice and research since 1982. The standards
ASIA (American Spinal Injury Association) and accompanying reference manual have under-
exam; Frankel scale; International Standards for gone sequential revisions, most recently in 2000
Neurological Classification of Spinal Cord Injury and 2003, respectively.

Description Psychometric Data

The International Standards for Neurological Published studies have found total motor score
Classification of SCI (ISNCSCI) is a widely ICCs from 0.98 to 0.99 for intra-rater reliability
 ASIA Impairment Scale
355

ASIA Impairment Scale, Fig. 1 International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI)
A
356 Asomatognosia

and 0.97 for inter-rater reliability. Total sensory standards with the 1996 guidelines. American journal
intra-rater reliability score has ranged from 0.76 to of Physical Medicine & Rehabilitation, 81(7),
502–505.
0.98 and 0.88 to 0.96 for inter-rater. One study Mulcahey, M. J., Gaughan, J., Betz, R. R., & Johansen,
reported agreement on individual muscles with K. J. (2007). The international standards for neurolog-
Kappas ranging from 0.46 to 0.89 for each myo- ical classification of spinal cord injury: Reliability of
tome (elbow extensors had the worst agreement), data when applied to children and youths. Spinal Cord,
45(6), 452–459.
0.06 to 0.83 for dermatome assessment using pin-
prick (wrist extensors with worst agreement), and
0.23 to 1 when assessed using light touch (wrist
extensors with worst agreement).
Asomatognosia

John E. Mendoza
Clinical Uses Department of Psychiatry and Neuroscience,
Tulane Medical School and SE Louisiana
The exam is used to document sensory and motor Veterans Healthcare System,
function after SCI. It has been used to diagnose New Orleans, LA, USA
SCI, as an outcome measure in studies to treat
spinal cord pathology, as well as a tool to predict
outcomes such as independence with activities of Synonyms
daily living, employment, life satisfaction, and
life expectancy. Disturbance of body schema

Cross-References Definition
▶ Sensorimotor Assessment Disturbance in the normal awareness of one’s
▶ Spinal Cord Injury own body, typically characterized by one or
more of the following symptoms: (1) a tendency
to ignore or neglect one side of the body, (2) a
References and Readings failure to recognize or difficulty in identifying a
specific part of the body (usually a limb or part
American Spinal Injury Association. (2002). International
standards for neurological classification of spinal cord of a limb), (3) difficulty in differentiating the
injury (revised 2002). Chicago: American Spinal Injury right from the left side of the body, or (4) recog-
Association. nizing an impairment in a part of the body
American Spinal Injury Association. (2003). Reference
(anosognosia).
manual for the international standards for neurologi-
cal classification of spinal cord injury (revised 2003).
Chicago: American spinal injury association.
Furlan, J. C., Fehlings, M. G., Tator, C. H., & Davis, A. M. Current Knowledge
(2008). Motor and sensory assessment of patients in
clinical trials for pharmacological therapy of acute
spinal cord injury: Psychometric properties of the Asomatognosia most commonly results from
ASIA standards. Journal of Neurotrauma, 25(11), acute or subacute brain lesions and may affect
1273–1301. one or both sides of the body. Unilateral neglect
Jonsson, M., Tollback, A., Gonzales, H., & Borg, J. (2000).
Inter-rater reliability of the 1992 international standards generally involves an entire side of the body,
for neurological and functional classification of incom- more commonly the left. This might be reflected
plete spinal cord injury. Spinal cord, 38, 675–679. in a failure to shave the affected side of the face,
Kirshblum, S. C., Memmo, P., Kim, N., Campagnolo, D., putting a glove only on one hand, or reduced use
& Millis, S. (2002). Comparison of the revised 2000
American spinal injury association classification of the involved limb for certain activities, even
Asperger’s Disorder 357

though it is physically capable of doing so. If a References and Readings

limb is paralyzed, the patient may either deny or
minimize the impairment (anosognosia), or may Feinberg, T., Venneri, A., Simone, A., Fan, Y., &
Northoff, G. (2010). The neuroanatomy of A
even deny ownership of the affected limb. If
asomatognosia and somatoparaphrenia. Journal of
the affected side or a part of the body is stimu- Neurology, Neurosurgery, and Psychiatry, 81(3),
lated, the individual may report that the homo- 276–281.
logous area on the intact side was touched Hecaen, H., & Albert, M. L. (1978). Human neuropsychol-
ogy (pp. 303–330). New York: Wiley.
(allesthesia). Patients may also have difficulty
Heilman, K. M., Watson, R. T., & Valenstein, E. (2003).
localizing or identifying parts of their own Neglect and related disorders. In K. Heilman &
body (autotopagnosia). This is most commonly E. Valenstein (Eds.), Clinical neuropsychology
expressed as difficulty naming or identifying (pp. 296–346). New York: Oxford University Press.
Kortte, K. B., & Wegener, S. T. (2004). Denial of
individual fingers (especially the three middle
illness in medical rehabilitation populations: Theory,
digits) either of their own hands or those of others research and definitions. Rehabilitation Psychology,
(finger agnosia). This deficit is usually expressed 49, 187–199.
bilaterally. Right-left disorientation is generally Prigatano, G. P., & Schacter, D. L. (1991). Awareness of
deficit after brain injury: Clinical and theoretical
also considered a form of asomatognosia. Here,
issues. New York: Oxford University Press.
the individual has difficulty reliably identifying
the right and left sides of his or her own body or
those of the examiner.
Although asomatognosia strictly refers to im-
paired awareness or attention to parts of one’s
Asperger’s Disorder
own body, personal neglect often extends into
Micah O. Mazurek1 and Stephen M. Kanne2
extrapersonal space. Thus, a patient may fail to 1
Curry School of Education, University of
attend to visual or auditory stimuli on the affected
Virginia, Charlottesville, VA, USA
side, despite intact visual fields or the fact that 2
Thompson Center for Autism and
auditory stimuli enter both ears. This can be very
Neurodevelopmental Disorders, University of
disconcerting for family members if they are
Missouri, Columbia, MO, USA
not made aware of these phenomena, perhaps
believing the patient is purposely ignoring their
presence.
Unilateral neglect or anosognosia-type disor-
Synonyms
ders are most commonly found, following acute
Asperger syndrome
lesions (such as strokes) of the right hemisphere.
Although improvement is typically seen over
time, subtle degrees of deficit may persist indefi-
nitely. By contrast, those deficits that present bilat- Definition
erally (such as finger agnosia and right-left
disorientation) are usually the result of posterior Asperger’s disorder refers to a neurodeve-
left-hemispheric lesions. lopmental disorder, defined in the DSM-IV and
more recently removed in the DSM-5, associated
with impairment in social relatedness and repeti-
Cross-References tive or restricted behaviors and interests. Social
difficulties characteristic of Asperger’s disorder
▶ Allesthesia include nonverbal aspects of social interaction
▶ Anosognosia (e.g., eye contact, gestures, and facial expres-
▶ Autotopagnosia sions) as well as social and emotional reciprocity
▶ Finger Agnosia (e.g., sharing interests, taking turns, and demon-
▶ Right Left Disorientation strating empathy). Behaviorally, individuals with
358 Asperger’s Disorder

Asperger’s disorder often exhibit intense and nar- The DSM-IV criteria for Asperger’s disorder
row circumscribed interests, insistence on same- gave rise to a number of difficulties that reduced
ness or routine, and behavioral rigidity (American its clinical utility and made it difficult to demon-
Psychiatric Association 1994). While overall strate its etiological independence. For example,
level of intellectual functioning (i.e., IQ) is not individuals meeting criteria for Asperger’s disor-
impaired in individuals with Asperger’s disorder, der almost always demonstrated difficulties with
their cognition is often compromised in other reciprocal conversation, meaning that they would
areas such as executive functioning (see Neuro- have also met criteria for autistic disorder. As a
psychology and Psychology of Asperger’s result, the diagnosis demonstrated poor specificity
Disorder). and poor reliability across clinicians. Addition-
ally, individuals with Asperger’s disorder were
not distinguishable from individuals with high
Categorization functioning autism across a number of studies.
For these reasons, Asperger’s disorder was
Asperger’s disorder first appeared in DSM-IV removed as a distinct diagnostic category in
(1994) as a separate diagnostic category but has DSM-5 (see Ozonoff 2012 for review).
since been removed in the most recent version This decision to remove Asperger’s disorder
(DSM-5; American Psychiatric Association was met with controversy among some
2013). Asperger’s disorder was previously clas- researchers, clinicians, and community members.
sified in the DSM-IV as one of five separate A primary concern was that individuals previ-
pervasive developmental disorders (which also ously diagnosed with Asperger’s disorder may
included autistic disorder, Rett’s disorder, child- no longer meet criteria for autism spectrum disor-
hood disintegrative disorder, and pervasive der (ASD) under the new DSM-5. However, stud-
developmental disorder not otherwise specified, ies have found that most individuals meeting
PDD NOS). To meet DSM-IV criteria for DSM-IV criteria for Asperger’s disorder also
Asperger’s disorder, an individual needed to meet DSM-5 criteria for ASD (Huerta et al.
demonstrate impairment in social interaction 2014). To further allay these concerns, DSM-5
(exhibiting at least two out of four possible criteria specify that “individuals with a well-
symptoms) and restricted and repetitive patterns established DSM-IV diagnosis of autistic disor-
of behaviors or interests (exhibiting at least one der, Asperger’s disorder, or pervasive develop-
out of four possible symptoms). In addition, an mental disorder not otherwise specified should
individual must not have had a history of devel- be given the diagnosis of autism spectrum disor-
opmental delays in language, cognition, or der” (American Psychiatric Association 2013, p.
adaptive functioning. Of note, the criteria for 51). Although no longer recognized as a distinct
Asperger’s disorder were identical to those category, the term “Asperger’s disorder” will be
for autistic disorder (i.e., autism) in the areas used for simplicity in the sections that follow to
of social impairment and restricted and repeti- describe individuals who met previous criteria for
tive behavior. However, autistic disorder the disorder.
required an additional criterion of impairment
in communication (i.e., delays in language
development, impairment in conversation, ste- Epidemiology
reotyped language, or lack of pretend play).
Additionally, there was not a requirement in Prevalence estimates have varied widely from 0.3/
the criteria for autistic disorder that cognitive, 1000 to 6/1000 (see Mattila et al. 2007 for
language, and adaptive development fall within review). Based on a review of the literature,
the normal range in childhood as was the case in Fombonne (Fombonne and Tidmash 2003, 2005)
Asperger’s disorder (American Psychiatric estimated the prevalence rate for Asperger’s dis-
Association 1994). order to be approximately 2/10,000. Such wide
Asperger’s Disorder 359

variations in prevalence rates are likely due to spectrum. As a result, Asperger’s disorder is often
differences in diagnostic procedures and opera- used synonymously with the term “high-function-
tional definitions used in each study. In fact, ing autism” (which typically refers to individuals A
rates from the same study varied from 1.6/1000 meeting criteria for Autistic Disorder whose IQ
to 2.9/1000 depending on the specific criteria used levels are above 70). Ultimately, these issues
for diagnosis (Mattila et al. 2007). In terms of sex resulted in the decision by the DSM-5 Neurodeve-
differences, males are overrepresented in lopmental Disorders Workgroup to remove
Asperger’s disorder, with an estimated sex ratio Asperger’s disorder as a separate diagnosis, and
of 4:1 (see Schopler et al. 1998 for review). to consolidate previous PDD subgroups into a
single category. The intention of this change was
to retain a single diagnostic category (i.e., ASD),
Natural History, Prognostic Factors, and while allowing for characterization of variability
Outcomes in severity and symptom presentation within both
social-communication and restricted and repeti-
Asperger’s disorder took its name from the Aus- tive behavior domains.
trian physician, Hans Asperger, whose 1944 paper With regard to developmental course,
on “autistic psychopathy” described a group of Asperger’s disorder was generally diagnosed
children who showed deficits in social behaviors, much later than autistic disorder, with an average
insistence on sameness, a lack of nonverbal com- age of diagnosis being 11 years (possibly due to
munication, repetitive movements, and average the lack of early developmental delays). Individ-
intelligence. Asperger (in 1944) and Leo Kanner uals diagnosed with Asperger’s disorder exhibited
(in 1943), although unaware of one another’s a continuous course of symptoms throughout the
work, were the first to describe this cluster of life span, although for some individuals symp-
symptoms. While Leo Kanner’s seminal work toms improved substantially as a result of early
describing autistic behaviors was the subject of intervention (see Frith 2004 for review). Research
much discussion and resulted in the eventual into prognostic factors and outcome in Asperger’s
inclusion of autism in the DSM (in 1980), disorder is sparse, particularly since it was only
Asperger’s paper did not receive wide attention recognized as an official diagnosis for a brief
after publication and was not translated into period of time; however, IQ and language ability
English until 1991 (see Frith 1991). After the have been found to be strong predictors of out-
appearance of autism in the DSM-III, it became comes in autism spectrum disorders in general
apparent that there was a group of individuals who (see Magiati et al. 2014 for review).
did not meet the criteria for the narrowly defined
definition of infantile autism, but who demon-
strated deficits in social interaction and repetitive Neuropsychology and Psychology of
behaviors. As a result, Wing (1981) published an Asperger’s Disorder
influential paper reintroducing Asperger’s origi-
nal ideas and arguing for broadening the definition By definition, social interactions are impaired in
of autism to include Asperger’s disorder on the individuals with Asperger’s disorder. However,
autism continuum. Eventually, a separate diagno- the underlying processes by which social interac-
sis of Asperger’s disorder was added to the fourth tions are disrupted have been the source of recent
edition of the DSM (1994). Since that time, debate attention. First, there is clear evidence that indi-
continued as to whether or not Asperger’s disorder viduals with Asperger’s disorder have impair-
should remain a separate diagnosis from autism. ments in their ability to understand complex
The prevailing current view is that Asperger’s emotions and a resulting inability to recognize
disorder and autism are not distinctly different and empathize with others’ feelings. Individuals
and that Asperger’s disorder may simply represent with Asperger’s disorder also have impairments in
a specific phenotype or subgroup of the autism what is known as “theory of mind.” As such, they
360 Asperger’s Disorder

have difficulty automatically attributing mental These profiles are marked by relative strengths at
states to others. Although there were no formal rote verbal skills, with deficits in social under-
criteria concerning communication skills for standing and motor coordination. While there is
Asperger’s disorder according to DSM-IV, clini- a great deal of overlap among these conditions,
cal and research accounts highlight the presence empirical findings have been equivocal. Some
of social communication difficulties. Specifically, studies have found visual-spatial impairments
difficulties with pragmatic language and difficul- (with strengths in Verbal IQ) in Asperger’s disor-
ties with turn-taking in conversation are common der, while others have not demonstrated this pat-
(see Klin et al. 2000 for review). tern (see Klin et al. 2000). Given recent diagnostic
Asperger’s disorder is also associated with changes, further work with more specific sub-
cognitive features that affect functioning outside typing criteria is needed to continue to understand
the social domain. Studies have shown that indi- potential phenotypic and neuropsychological dif-
viduals with Asperger’s disorder have very ferences within the ASD population.
uneven cognitive profiles. One explanation for
this common finding is that these individuals
have “weak central coherence.” That is, they are Coexisting Conditions
more likely to process information as discrete
units rather than processing them as a unified In addition to the core symptoms, Asperger’s dis-
whole. There is some evidence that bottom-up order may also be accompanied by co-occurring
processing occurs without accompanying top- disorders. Studies have shown that a large per-
down control. As a result, high levels of details centage of children with Asperger’s disorder also
are perceived, while global information may be exhibit problems with attention and impulse con-
missed (see Frith 2004). Studies have also shown trol (similar to those found in ADHD). In adoles-
consistent deficits in overall executive function cence and adulthood, case studies indicate
among individuals with Asperger’s disorder. Spe- relatively high rates of depression, anxiety, and
cifically, poor performance has been shown on bipolar disorder among individuals with
both the Wisconsin Card Sorting Test and the Asperger’s disorder (see Ghaziuddin 2002 for
Tower of Hanoi. Particular deficits have been review). Individuals with Asperger’s disorder
noted in the ability to shift response set and in also have significant adaptive impairments (see
overall planning. Consistent with this, individuals Saulnier and Klin 2007).
with Asperger’s disorder are often described as
having difficulty adjusting to changes in routine or
task demands and as having a strong need for Evaluation
sameness (see Klin et al. 2000).
Some studies, including Wing’s (1981) origi- Diagnostic assessment of high functioning ASD
nal description, have found significantly higher (previously Asperger’s disorder) is best
verbal IQ scores than performance IQ scores conducted using multiple methods and observers.
among individuals with Asperger’s disorder (the Due to the complexity of the disorder, and its
reverse of which was often found in individuals effects on broad areas of functioning, interdisci-
who met DSM-IV criteria for autistic disorder). plinary assessment is recommended. First,
Motor clumsiness has also been observed among because ASD is a neurodevelopmental disorder,
children with Asperger’s disorder since Hans parent report of early history and development, as
Asperger’s original paper, although it has never well as structured observations of current behav-
been a part of the formal diagnostic criteria (see ior, are essential. Currently, the two “gold-stan-
Frith 1991). As a result, researchers have been dard” tools for diagnosis of ASD are the Autism
interested in potential similarities between Diagnostic Interview-Revised (ADI-R) and the
Asperger’s disorder and nonverbal learning disor- Autism Directed Observation Schedule – 2nd Edi-
ders (NVLD) or right hemispheric dysfunction. tion (ADOS-2). These are the most widely studied
Asperger’s Disorder 361

measures in the field, and reliability and validity include cognitive and behavioral components
have been well established. The ADI-R is a com- (including direct instruction, modeling skills,
prehensive interview that assesses past and cur- and skills practice) (see Klin et al. 2000). A
rent functioning in the areas of communication, Educationally, students with Asperger’s dis-
social interaction, and restricted or repetitive order often benefit from modifications and sup-
behavior. The ADOS-2 is another diagnostic tool ports provided through special education.
that allows for clinic-based observations across Although services vary widely based on the
various structured activity- and conversation- region, they may range from specialized schools
based interactions. A number of other scales designed to serve students with Asperger’s dis-
were previously developed to specifically assess order to modifications within general education
Asperger’s disorder, but systematic research is classrooms. Some students may get benefit and
lacking (see Matson & Boisjoli 2008; Mesibov support from paraprofessional aides in the class-
et al. 2001 for review). The removal of Asperger’s room, while others may require only slight aca-
disorder as a distinct diagnostic category in demic modifications. Most students with
DSM-5 may further limit their utility. Asperger’s disorder benefit greatly from commu-
In addition to assessing the core symptoms of nication interventions aimed at improving prag-
ASD, assessment should focus on cognitive, matic and social skills (see Klin et al. 2000;
adaptive, and communication skills. General Mesibov et al. 2001 for review).
measures of intelligence, such as the Wechsler Family support, parent training, and instruction
Scales and the Stanford Binet Intelligence Scales on behavior management strategies can also be
are useful in assessing overall functioning as well helpful when disruptive behaviors accompany the
as particular strengths and weaknesses. Addi- clinical picture. Recent research has also shown
tionally, it is helpful to include measures of that both individual and group-based cognitive
visual-spatial and visual-motor processing, par- behavioral therapy is effective in the treatment of
ticularly since skills in these areas were typically co-occurring symptoms of anxiety in individuals
weaker in prior studies of individuals with with Asperger’s disorder and high functioning
Asperger’s disorder. Given common deficits in ASD (Danial and Wood 2013; Sukhodolsky
executive function and attention, neuropsycho- et al. 2013). Individual work with counselors or
logical assessment of these functions is mental health professionals could also focus on
recommended. Measures of social communica- social and communication skills training as well
tion and pragmatic language, and adaptive skills, as bolstering adaptive functioning. In addition,
also add information to the clinical picture and medications may be prescribed to treat associated
help inform intervention recommendations (see symptoms (particularly inattention, depression,
Klin et al. 2000 for review). and anxiety).

Treatment Cross-References

There is, as of yet, no available treatment that ▶ Nonverbal Learning Disabilities

provides a “cure” for the core impairments of
ASD. However, there are a number of interven-
tions that target specific symptoms. For References and Readings
addressing social deficits, there have been several
promising studies of social competence interven- American Psychiatric Association. (1994). Diagnostic and
tions among children and adolescents with statistical manual of mental disorders (4th ed.). Wash-
ington, DC: American Psychiatric Publishing.
Asperger’s disorder and high functioning ASD. American Psychiatric Association. (2013). Diagnostic and
Such interventions can be delivered in educational statistical manual of mental disorders (5th ed.). Wash-
or outpatient clinic-based settings, and typically ington, DC: American Psychiatric Publishing.
362 Assessment of Life Habits (LIFE-H)

Danial, J. T., & Wood, J. J. (2013). Cognitive behavioral Schopler, E., Mesibov, G. B., & Kunce, L. J. (Eds.). (1998).
therapy for children with autism: Review and consid- Asperger syndrome or high-functioning autism? New
erations for future research. Journal of Developmental York: Plenum Press.
& Behavioral Pediatrics, 34(9), 702–715. Sukhodolsky, D. G., Bloch, M. H., Panza, K. E., et al.
Fombonne, E. (2005). The changing epidemiology of (2013). Cognitive-behavioral therapy for anxiety in
autism. Journal of Applied Research in Intellectual children with high-functioning autism: A meta-analy-
Disabilities, 18, 281–294. sis. Pediatrics, 132(5), e1341–e1350.
Fombonne, E., & Tidmarsh, L. (2003). Epidemiologic data Wing, L. (1981). Asperger’s syndrome: A clinical account.
on Asperger disorder. Child and Adolescent Psychiat- Psychological Medicine, 11, 115–130.
ric Clinics of North America, 12, 15–21.
Frith, U. (Ed.). (1991). Autism and Asperger syndrome.
Cambridge: Cambridge University Press.
Frith, U. (2004). Emanuel miller lecture: Confusions and
controversies about Asperger syndrome. Journal of Assessment of Life Habits
Child Psychology and Psychiatry, 45, 672–686. (LIFE-H)
Ghaziuddin, M. (2002). Asperger syndrome: Associated
psychiatric and medical conditions. Focus on Autism
and Other Developmental Disabilities, 17, 138–144. Jessica Fish
Huerta, M., Bishop, S. L., Duncan, A., et al. (2014). Medical Research Council Cognition and Brain
Application of DSM-5 criteria for autism spectrum Sciences Unit, Cambridge, UK
disorder to three samples of children with DSM-IV
diagnoses of pervasive developmental disorders.
American Journal of Psychiatry. https://doi.org/
10.1176/appi.ajp.2012.12020276. Synonyms
Klin, A., Volkmar, F. R., & Sparrow, S. (Eds.). (2000).
Asperger syndrome. New York: The Guilford Press. The abbreviation LIFE-H is consistent, but ver-
Magiati, I., Tay, X. W., & Howlin, P. (2014). Cognitive,
language, social and behavioural outcomes in adults sion numbers are often appended (e.g., LIFE-H
with autism spectrum disorders: A systematic review 1.0, 2.0, 3.0, 3.1)
of longitudinal follow-up studies in adulthood. Clinical
psychology review, 34(1), 73–86.
Matson, J. L., & Boisjoli, J. A. (2008). Strategies for
assessing Asperger’s syndrome: A critical review of Description
data based methods. Research in Autism Spectrum Dis-
orders, 2, 237–248. The Assessment of Life Habits (LIFE-H) is a
Mattila, M., Kielinen, M., Jussila, K., Linna, S., Bloigu, R., self-report measure of social participation of
Ebeling, H., et al. (2007). An epidemiological and
diagnostic study of Asperger syndrome according to people with disabilities. The original version of
four sets of diagnostic criteria. Journal of the American the scale consisted of 298 items; later versions
Academy of Child & Adolescent Psychiatry, 46, have reduced the number of items to 240 (version
636–646. 3.0). Various short forms are also available
McLaughlin-Cheng, E. (1998). Asperger syndrome and
autism: A literature review and meta-analysis. Focus (55–77 items), with the most recent being the
on Autism and Other Developmental Disabilities, 13, 77-item version 3.1. The long form is said to
234–245. take between 20 and 120 min to complete and
Mesibov, G. B., Shea, V., & Adams, L. W. (2001). Under- the short form, 20–60 min. In the short form
standing Asperger syndrome and high-functioning
autism. New York: Kluwer Academic/Plenum (version 3.1), items are organized into 12 catego-
Publishers. ries: nutrition, fitness, personal care, communi-
Ozonoff, S. (2012). Editorial perspective: Autism Spec- cation, housing, mobility (classified as activities
trum disorders in DSM-5 – An historical perspective of regular living) and responsibilities, interper-
and the need for change. Journal of Child Psychology
and Psychiatry, 53(10), 1092–1094. sonal relationships, community life, education,
Saulnier, C. A., & Klin, A. (2007). Brief report: Social and employment, and recreation (classified as social
communication abilities and disabilities in higher func- roles). The long form includes 31 subsections,
tioning individuals with autism and Asperger syn- essentially covering the listed domains with a
drome. Journal of Autism and Developmental
Disorders, 37(4), 788–793. greater degree of specificity. Each item is rated
Assessment of Life Habits (LIFE-H) 363

on a 4-point “level of accomplishment” scale Psychometric Data

(with an additional option to state “not applica-
ble,”) a 5-point “level of satisfaction” scale, as Fougeyrollas et al. (1998) reported that the A
well as a rating regarding the type and level of LIFE-H v1.0 demonstrated acceptable internal
assistance required (i.e., no assistance, assistive consistency in adults and children (intra-class cor-
device, adaptation, human assistance). A score relation (ICCs) > 0.5 for each life habit) and good
for each item is obtained with reference to a test-retest reliability in children and adults with
scoring template included in the manual, grad- spinal cord injury (ICC children r = 0.73 and
ing according to the level of difficulty and level adults r = 0.74). Inter-rater reliability was exam-
of assistance. Item scores range from 0 (not ined in a group of 20 stroke patients (Beaulieu
accomplished) to 9 (performed with no diffi- et al. 1996; Cited in Noreau et al. 2002), with
culty and no assistance), with mid-scale exam- ICCs for 6/12 “accomplishment” ratings of life
ples being 3 (performed with difficulty and habits above 0.6 and 10/12 “satisfaction” ratings
human assistance) and 6 (performed with diffi- for life habits above 0.6. Similar findings have
culty and technical aid or adaptation). Scores been reported for inter-rater reliability of LIFE-H
can then be weighted by the number of applica- scores for people with physical disabilities, with
ble activities to obtain domain-level scores, or ICCs of r > 0.75 for 7/10 categories and r = 0.89
a simple formula can be used to obtain an over- for the whole scale (Noreau et al. 2004).
all score. Several studies have examined the predictive
validity of the LIFE-H. Desrosiers et al. (2003)
presented evidence of the convergent validity of
the LIFE-H in the form of high correlations with
Historical Background
the Functional Autonomy Measurement System
(SMAF) and moderate correlations with the Func-
Noreau, Fougeyrollas, and Tremblay (2005)
tional Independence Measure (FIM). Further,
stated that the LIFE-H was developed to assess
LIFE-H scores were lower in stroke patients than
social participation in people with disabilities,
neurologically healthy controls. A comprehensive
regardless of the nature of those disabilities,
review of the psychometric properties of the
and based upon the Disability Creation Process
LIFE-H was performed by Figueiredo et al. (2010).
model, which views handicap as “the situational
result of the interaction of two causal dimen-
sions: the characteristics of the individual Clinical Uses
and those of the environment.” Version 2.0 of
the scale was developed following a content The LIFE-H is available in Dutch, English, and
validity study that involved 12 experts in reha- French versions. Adapted forms suitable for use
bilitation medicine evaluating the scale (in with children aged 0–4 and 5–13 are available (for
terms of clarity and pertinence of content, clas- which a proxy respondent is required). The
sifications used in the measurement scales, etc.); LIFE-H has been used to evaluate social partici-
modifications included reversing the scoring of pation in many patient groups, including children
the accomplishment section such that higher with cerebral palsy, adults with spinal cord injury,
scores reflected the competence in the activity. traumatic brain injury, and stroke.
Version 3.0 incorporated a greater number
of items within particular domains and added
additional filter questions to some sections (e.g., Cross-References
if you are not currently employed, skip to sec-
tion x). Version 3.1 is a short form based upon ▶ Functional Autonomy Measurement System
version 3.0. ▶ Functional Independence Measure
364 Assessment of Motor Process Skills

References and Readings Description

Desrosiers, J., Rochette, A., Noreau, L., Bravo, G., Hébert, The Assessment of Motor Process Skills (AMPS)
R., & Boutin, C. (2003). Comparison of two functional
is a standardized observational assessment widely
independence scales with a participation measure in
post-stroke rehabilitation. Archives of Gerontology used by occupational therapists to measure the
and Geriatrics, 37(2), 157–172. quality of performance in activities of daily living
Desrosiers, J., Noreau, L., Rochette, A., Bravo, G., & (ADL) of persons across the age spectrum begin-
Boutin, C. (2002). Predictors of handicap situations
ning at 2 years. Specifically, the AMPS tests func-
following post-stroke rehabilitation. Disability and
Rehabilitation, 24(15), 774–785. tions that relate to purposeful, goal-oriented daily
Figueiiredo, S., Korner-Bitensky, N., Rochette, A., & life tasks that a person wants, needs, and is
Desrosiers, J. (2010). Use of the LIFE-H in stroke expected to perform; it does not evaluate neuro-
rehabilitation: A structured review of its psychomet-
muscular, biomechanical, cognitive, and psycho-
ric properties. Disability and Rehabilitation, 32,
705–712. social impairments (Fisher and Jones 2011). The
Fougeyrollas, P., Noreau, L., Bergeron, H., Cloutier, R., current version of the assessment contains 110 cal-
Dion, S. A., & St-Michel, G. (1998). Social conse- ibrated ADL tasks that permit evaluation of
quences of long term impairments and disabilities:
36 skills (16 motor, 20 process); AMPS-trained
Conceptual approach and assessment of handicap.
International Journal of Rehabilitation Research, raters must observe two or more specific tasks in
21(2), 127–141. 10–20 min increments.
More information is available on http://ripph.qc.ca/en/ A multi-perspective approach is used to rate
assessment-tools/introduction/life-h. Accessed 25 Feb
each task by observing various motor and process
2017.
Noreau, L., Fougeyrollas, P., & Vincent, C. (2002). The skills in terms of physical effort, efficiency, safety,
LIFE-H: Assessment of the quality of social participa- and independence. The 16 motor skills reflect
tion. Technology and Disability, 14(3), 113–118. ability to use body positions, obtain and hold
Noreau, L., Desrosiers, J., Robichaud, L., Fougeyrollas, P.,
objects, move self and objects, and sustain perfor-
Rochette, A., & Viscogliosi, C. (2004). Measuring
social participation: Reliability of the LIFE-H in older mance during ADL task performance. The 20 pro-
adults with disabilities. Disability and Rehabilitation, cess skills are used to assess ability to sustain
26(6), 346–352. performance, apply knowledge, temporal organi-
Rochette, A., Desrosiers, J., & Noreau, L. (2001). Asso-
zation, organize space and objects, and adapt per-
ciation between personal and environmental factors
and the occurrence of handicap situations following a formance. Scores are based on observation of the
stroke. Disability and Rehabilitation, 23(13), client from certified raters (Fisher and Jones
559–569. 2011). Motor and process skills are rated simulta-
neously utilizing a 4-point ordinal criterion
referenced rating scale with the highest score
denoting competent performance, followed by
questionable, inefficient, and markedly inefficient
Assessment of Motor Process
performance. AMPS computer scoring software
Skills
converts ordinal raw scores of easy skill items for
persons of low ability and hard skill items for
Kelli Williams Gary
persons of high ability along a single common
Department of Occupational Therapy,
equal-interval linear scale (Fisher 2006).
Virginia Commonwealth University, Richmond,
VA, USA
Historical Background

Synonyms The genesis of the AMPS is found in the psychi-

atric assessment of clients with schizophrenia and
AMPS depression in Halifax, Canada (Fisher and
Assessment of Motor Process Skills 365

Bernspång 2007). In 1994, Anne G. Fisher, ScD, and can include fully equipped clinic kitchens,
OTR, and colleagues from the Division of Occu- laundry rooms, outdoor, and the client’s own
pational Therapy, Umeå University in Umeå, room in the hospital or nursing home. A
Sweden, further developed the idea of this assess- The primary advantage of the AMPS is that it
ment into a specific more standardized tool. At can be used with persons of virtually any age,
least 20 countries use the AMPS, and the use in diagnosis, or disability. However, the scope and
these countries have increased applicability breadth of evidence for AMPS use is limited in
across populations, diagnoses, disabilities, cul- psychiatric, neurologic, and pediatric settings.
tural background, nationality, and age groups by Geriatric settings have offered the most research
adding additional tasks (Fisher 2006). The sev- evidence for those with cognitive impairments
enth version was published in 2011 along with and dementias, followed by a sizable proportion
updated software to facilitate occupation-based of research for people with learning disabilities
documentation and intervention planning (Fisher (Hitch 2007).
and Jones 2011).

Cross-References
Psychometric Data
▶ Activities of Daily Living (ADL)
The AMPS has robust psychometric properties. ▶ Instrumental Activities of Daily Living
Interrater and intrarater reliability are high with ▶ Occupational Therapy
95% of calibrator raters demonstrating goodness
of fit to the many faceted Rasch model. Test-retest
reliability is high on a diagnostically heteroge- References and Readings
neous sample of older adults with r = 0.90 – 0.91
Doble, S. E., Fisk, J. D., Lewis, N., & Rockwood, K.
for AMPS process scale and motor scale, respec-
(1999). Test-retest reliability of the assessment of
tively (Doble et al. 1999). Internal studies have motor and process skills. Occupational Therapy Jour-
found good validity of the AMPS when applied nal of Research, 19, 203–215.
to groups of different racial, ethnic, and cultural Fisher, A. G. (2006). Assessment of motor and process
skills. Vol. 1: Development, standardization, and
backgrounds, across gender, and with multiple
administration manual (6th ed.). Fort Collins: Three
diagnoses (Stauffer et al. 2000; Fisher 2006; Star Press.
Wæhrens and Fisher 2007). Fisher, A. G., & Bernspång, B. (2007). Response to:
A critique of the Assessment of Motor and Process
Skills (AMPS) in mental health practice. Mental Health
Occupational Therapy, 12, 10–11.
Clinical Uses Fisher, A. G., & Jones, B. J. (2011). The assessment of
motor and process skills (AMPS) (7th ed., rev., Vols.
(Fisher 2006) states, “the AMPS provides occu- 1 & 2). Fort Collins: Three Star Press.
Hitch, D. (2007). A reply from Danielle Hitch to the Fisher
pational therapy practitioners with a powerful and
and Bernspång response to: A critique of the assess-
sensitive tool that can assist with planning effec- ment of motor and process skills (AMPS) in mental
tive ADL interventions and documenting health practice. Mental Health Occupational Therapy,
change.” Because of the AMPS’ unique and inno- 12, 14.
Stauffer, L. M., Fisher, A. G., & Duran, L. (2000). ADL
vative design, occupational performance is evalu-
performance of black Americans and white Ameri-
ated based on the familiarity and relevance of the cans on the assessment of motor and process skills.
tasks to the client’s daily life needs. Therefore, the American Journal of Occupational Therapy, 54,
environment should be naturalistic and approxi- 607–613.
Wæhrens, E. E., & Fisher, A. G. (2007). Improving quality
mate the conditions in which the client can com-
of ADL performance after rehabilitation among per-
fortably perform tasks. Settings for AMPS sons with acquired brain injury. Scandinavian Journal
observation can vary based on the space available of Occupational Therapy, 14, 250–257.
366 Assisted Living

part of an assisted living arrangement as the con-

Assisted Living sistent need for such basic care is often seen as an
indication that a traditional nursing facility or a
Jay Behel home-based parallel thereof is the more appropri-
Department of Behavioral Sciences, Rush ate level of care. Assisted living typically is not
University Medical Center, Chicago, IL, USA covered by private health insurance or Medicare,
and access to such care may be limited by an
individual’s finances.
Synonyms Although there has been increased scholarly
attention to assisted living in recent years, this
Domiciliary care; Residential care work includes topics as disparate as end-of-life
care and social networking in assisted living set-
tings speaks to the continued need for well-
Definition articulated, shared definitions for discussing
these care arrangements.
Assisted living is a care arrangement that provides
intermittent supervision and instrumental support
to individuals unable to live independently but not See Also
requiring the level of care provided in conven-
tional nursing facilities. ▶ Life Care Planning

Current Knowledge References and Readings

Assisted living arrangements may take place in Stone, R. I., & Reinhard, S. C. (2007). The place of assisted
structured assisted living facilities, small group living in long-term care and related service systems.
homes, or an individual’s own home or the home Gerontologist, 47(Spec No. 3), 23–32.
of a family member. These arrangements have as
their goal the preservation of a degree of auton-
omy and privacy at home or in a home-like set-
ting. When sited in one’s home, assistance may be Assistive Technology
provided by a combination of paid caregivers,
family members, and other paid or unpaid assis- Diane Cordry Golden1 and Amy S. Goldman2
1
tants to help with housekeeping, laundry, cooking, Association of Assistive Technology Act
and transportation. Assistance provided may Programs, Delmar, NY, USA
2
include supervision for safety, medication man- Association of Assistive Technology Act
agement, meal preparation, and accompaniment Programs (ATAP), Springfield, IL, USA
and assistance during community-based activi-
ties. Assisted living facilities may also offer social
activities and specialized services for individuals Definition
with cognitive impairment. There is a growing
interest in using technology to cost-effectively Assistive technology (AT) is a term used to refer
provide “ambient” assistance to older adults and to both AT devices and AT services. A formal,
people with disabilities both in formal assisted legal definition of AT devices and services was
living settings and in homes. Basic Activities of first published in the Technology-Related Assis-
Daily Living (BADL) such as hands-on bathing, tance for Individuals with Disabilities Act of 1988
dressing, and feeding usually are not considered a as follows:
Assistive Technology 367

assistive technology device means any item, piece patterned after the first folding, tubular steel
of equipment, or product system, whether wheelchair developed in the 1930s; while the
acquired commercially, modified, or custom- first dedicated wheelchair (called an invalids A
ized, that is used to increase, maintain, or chair) is thought to have been invented four cen-
improve functional capabilities of individuals turies ago for Phillip II of Spain. Some devices
with disabilities were developed as AT and evolved into main-
assistive technology service means any service stream technology. For example, in 1948 the
that directly assists an individual with a dis- National Bureau of Standards developed specifi-
ability in the selection, acquisition, or use of an cations for a low-cost reliable talking-book
assistive technology device machine for the blind that became the tape
recorder. Conversely, some items developed as
AT devices include a vast array of items mainstream technology became AT such as voice
such as wheelchairs, eyeglasses, hearing aids, recognition software originally developed for dic-
Braille printers, electronic note-takers and orga- tation that is used by individuals with motor dis-
nizers, augmentative communication systems, abilities who are unable to use a keyboard for
text-to-speech software, speech synthesizers, computer access.
adaptive keyboards, alternative pointing devices, In recent years, technology use has become
voice recognition software, aids for daily more commonplace for everyone. Similarly, AT
living, etc. AT services include evaluation/assess- use is now more frequent across the disability
ment services, selecting, fitting, customizing, and spectrum, addressing deficits in hearing, vision,
repairing devices, delivering training and techni- motor, social, organizational, cognitive, speech,
cal assistance supports, and coordinating funding language, information processing, etc. Especially
and other necessary interventions to support critical today is the use of information technology
device acquisition and use. (IT), including telecommunications. IT use is now
The definition of AT devices and services critical to success in education, employment,
has remained unchanged through numerous re- independent living, and community integration
authorizations of the Assistive Technology Act and AT is the interface that makes IT accessible.
and has been adopted in other statutes, such as
the Individuals with Disabilities Education Act.
The same definition has also been used in pro- Rationale or Underlying Theory
mulgating federal rules, such as the Electronic
and Information Technology Accessibility Stan- Today, AT intervention is rooted in the disability
dards developed pursuant to Section 508 of the rights movement and self-determination efforts of
Rehabilitation Act (https://www.access-board. individuals with disabilities and their advocates.
gov/guidelines-and-standards/communications-and- These initiatives helped to delineate the difference
it/about-the-section-508-standards/section-508- between the medical/rehabilitation and indepen-
standards). dent living models of intervention for individuals
with disabilities. The medical model identifies a
physical or mental impairment or lack of certain
Historical Background skills and treatment is delivered to remediate the
deficit(s). With the medical model, the locus of
A precise history of AT is difficult to depict the problem lies with the individual and the goal
because of the diversity of devices and services is to “fix” the individual in some way through
included in the definition of AT. The history of professional treatment. Under the independent
hearing aids can be traced back to Alexander living model, the problem is defined as a lack of
Graham Bell’s pioneering work on development supports and accommodations, inaccessibility,
of the telephone. Modern wheelchairs are and/or autonomy – the problem lies with the
368 Assistive Technology

environment or the interaction with the environ- of AT intervention that can be considered as a
ment, rather than within the person. In this model, treatment option (Cook and Hussey 2001).
AT plays a major role in addressing/ameliorating
interaction difficulties, typically without overtly
attempting to “fix” the disability itself (DeJong Treatment Procedures
1979; Pelka 1997).
Consideration for AT begins with assessment by a
qualified team of individuals who are knowledge-
Goals and Objectives able about the individual, their strengths and lim-
itations and the range of potential AT options
AT goals and objectives begin with a primary focus available to address the individual’s functional
on ameliorating and/or compensating for a specific needs. Best practice includes conducting struc-
functional deficit. For example, electronic orga- tured device trials with various AT devices in the
nizers can be used to address memory or informa- environment(s) in which the individual will be
tion processing problems; text-to-speech software using the technology (e.g., home, school, work,
can be used to address reading deficits; augmenta- community, etc.). This allows for comparative
tive communication systems can be used to address analysis of different device features and functions
communication limitations, etc. In most cases, sec- to determine which best addresses the individual’s
ondary goals are also targeted for outcomes includ- needs.
ing increasing academic success, fostering gainful Once AT has been acquired for an individual,
employment, supporting independent community training and support must be provided for the user,
living, decreasing inappropriate behaviors, etc. their family, and other critical individuals such
With expanding legal mandates for integration of as teachers, therapists, etc. More complex AT
individuals with disabilities into all societal set- (computer-based software applications, assistive
tings (Individuals with Disabilities Education Act, listening systems, augmentative communication
Section 504 of the Rehabilitation Act, and the devices, etc.) frequently requires significant
Americans with Disabilities Act), AT goals and investment of time and resources in initial pro-
objectives continue to expand into new outcome gramming, fitting, and set-up, in addition to train-
areas. ing on device use (Galvin and Scherer 1996).

Treatment Participants Efficacy Information

AT is an appropriate intervention option to con- Efficacy research on AT includes basic documen-

sider when functional limitations are encountered. tation of changes in functional skill areas (those
Candidacy for AT is not limited by age, disability the AT is intended to address) and potential sec-
diagnosis, or severity/combination of deficits. ondary improvements in academic, social, behav-
There are no prerequisites for AT consideration ioral, and other areas. Much of this efficacy is self-
and AT should not be relegated to a “last resort” evident and is reported by the AT users themselves
intervention after all other interventions have been (Scherer 1993).
tried and abandoned. No discussion of AT efficacy would be com-
AT can address a variety of human functions plete without addressing the issues of device
and is frequently grouped into areas such as abandonment and cost/benefit. For many types
vision, hearing, communication, daily living, of AT, consumer discontinuing use of the device
computer access, learning/cognition, environ- after acquisition has been a historic problem
mental adaptations, mobility/seating/positioning, (Wessels et al. 2003). Factors shown to mitigate
vehicle modifications, and recreation/leisure. For abandonment include active consumer and
almost all functional limitations, there is a range family involvement in the selection and
Assistive Technology 369

implementation of AT and the relative advantage assessments in the aided condition (using AT)
of AT within the array of intervention options can be useful in measuring outcomes in discreet
available (Alper and Raharinirina 2006; Riemer- skill areas (e.g., auditory discrimination, mem- A
Reiss and Wacker 2000). ory, expressive communication, etc.). In addi-
As technology continues to improve, the prob- tion, some global assessment of AT outcomes
lem of device abandonment steadily abates. can be helpful such as the Psychosocial Impact
Today, the greater challenge is in justifying the of Assistive Devices Scales (PIADS) (Jutai and
cost/benefit of AT to secure funding from private Day 2002), the Quebec User Evaluation of Sat-
insurance, local, state, federal, and other funding isfaction with Assistive Technology (QUEST)
sources. Some types of AT, such as durable med- (Demers et al. 1996), and similar instruments.
ical equipment, have a longer history of cost/ben- A number of online resources are also available
efit data including prevention of secondary with extensive data on AT outcome tools and
disabilities making funding more readily avail- research such as the Adaptive Technology
able. Other types of AT, such as electronic orga- Resource Center (http://www.adaptech.org/
nizers used to remediate/compensate for cognitive en), the Assistive Technology Outcomes Mea-
limitations, are relatively new with little cost/ben- surement System (ATOMS) Project (www.
efit data making funding difficult to secure uwm.edu/CHS/atoms), the Consortium for
(Gillette and DePompei 2004; Hart et al. 2004). Assistive Technology Outcomes Research,
and the Quality Indicators for Assistive Tech-
nology Services (www.qiat.org).
Outcome Measurement

The field of AT outcomes is quite young with Qualifications of Treatment Providers

most published work emerging in the 1990s.
Two of the first focused articles on evaluating AT intervention can be provided by an extensive
AT outcomes posed the questions “Are we ready list of professionals, usually specialists in the type
to answer the tough questions?” and “Do we of the AT provided. For example, hearing aids are
understand the commitment?” (DeRuyter 1995; typically provided by audiologists or hearing
Trachtmann 1994). In these articles, the authors instrument dispensers, eyeglasses by optometrists
postulated that stakeholders and AT providers and ophthalmologists, etc. However, as the AT
must be prepared to show how their devices/ser- becomes less “prescriptive” in nature, the range
vices make a difference in the lives of individuals of providers expands. Electronic note-takers and
who receive an AT intervention. organizers can be provided by a whole host of
Today, outcome measurement is occurring in all providers, special educators, rehabilitation coun-
AT service areas (medicine, education, employ- selors, behavior therapists, occupational thera-
ment/vocational rehabilitation, and independent pists, AT practitioners, etc. The Rehabilitation
living) through a variety of interdisciplinary activ- Engineering and Assistive Technology Associa-
ities. Some are driven by policy needs, in particu- tion of North America (RESNA) administers a
lar, accountability for public dollars spent on AT certification program for Assistive Technology
(e.g., Medicare, Medicaid, special education, voca- Professionals (ATPs) with associated standards
tional rehabilitation, etc.) and justification for pri- of practice (www.resna.org/certification).
vate insurance expenditures on AT. Others are
driven by an overarching goal of quality service
delivery and continuous program improvement. Cross-References
The most direct outcome measure for AT
intervention is demonstration of functional ▶ Americans with Disabilities Act of 1990
skills, independence, well-being, and quality ▶ Augmentative and Alternative Communication
of life. Administration of standardized (AAC)
370 Association Areas

▶ Independent Living Centers

▶ Individuals with Disabilities Education Act Association Areas
▶ Section 504 of the Rehabilitation Act of 1973
Maryellen Romero
Department of Psychiatry and Behavioral
Sciences, Tulane University School of Medicine,
References and Readings New Orleans, LA, USA
Alper, S., & Raharinirina, S. (2006). Assistive technology
for individuals with disabilities: A review and synthesis
of literature. Journal of Special Education Technology, Synonyms
21(2), 47–64.
Cook, A., & Hussey, S. (2001). Assistive technologies:
Association cortex
Principles and practice (2nd ed.). California: Mosby
Year-Book, Inc.
DeJong, G. (1979). Independent living: From social move-
ment to analytic paradigm. Archives of Physical Med- Definition
icine and Rehabilitation, 60, 435–446.
Demers, L., Weiss-Lambrou, R., & Ska, B. (1996). Devel-
opment of the Quebec user evaluation of satisfaction It is recognized that the brain is neither holistic nor
with assistive technology (QUEST). Assistive Technol- rigidly localized with respect to cognitive func-
ogy, 8, 3–13. tions. However, higher-order cognitive capabili-
DeRuyter, F. (1995). Evaluating outcomes in assistive
ties depend on specialized regions within the brain
technology: Do we understand the commitment? Assis-
tive Technology, 7(1), 3–16. that process, link or integrate elementary or new,
Galvin, J. C., & Scherer, M. J. (1996). Evaluating, as well as stored, information into increasingly
selecting and using appropriate assistive technology. complex wholes. Such regions are termed associ-
Gaithersburg: Aspen Publishers, Inc.
ation areas and are thought to be the neuroana-
Gillette, Y., & DePompei, R. (2004). The potential of
electronic organizers as a tool in the cognitive rehabil- tomical substrate for such higher functions as
itation of young people. NeuroRehabilitation, 19(3), memory, emotion, perception, language, spatial
233–243. and problem-solving skills, as well as the plan-
Hart, T., Buchhofer, R., & Vaccaro, M. (2004). Portable
ning and execution of behavioral responses.
electronic devices as memory and organizational
aids after traumatic brain injury: A consumer survey Three major association areas are recognized:
study. Journal of Head Trauma Rehabilitation, 19(5),
351–365. 1. Frontal association cortices, as the name
Jutai, J., & Day, H. (2002). Psychosocial impact of assis-
implies, are located in the more anterior aspects
tive devices scale (PIADS). Technology and Disability,
14(3), 107–111. of the frontal lobes and include dorsolateral,
Pelka, F. (1997). ABC-CLIO companion to the disability orbitofrontal, and premotor areas. While vari-
rights movement. Santa Barbara: ABC-CLIO, Inc. ous feedback loops are likely involved includ-
Riemer-Reiss, M. L., & Wacker, R. R. (2000). Factors
ing those from the posterior and limbic
associated with assistive technology discontinuance
among individuals with disabilities. Journal of Reha- association areas, conceptually, the initial deci-
bilitation, 66(3), 44–50. sions and planning regarding executive or
Scherer, M. J. (1993). Living in the state of stuck: How motor responses to a given situation are gener-
technology impacts the lives of people with disabilities.
ally thought to flow from the prefrontal (most
Cambridge, MA: Brookline Books.
Trachtmann, L. (1994). Outcome measures: Are we ready anterior) cortices to the premotor cortex that
to answer the tough questions? Assistive Technology, organizes, coordinates, and sequences the
6, 91–92. actions essential to the successful completion
Wessels, R., Dijcks, B., Soede, M., Gelderblom, G. J., &
of the response. From there, commands are
De Witte, L. (2003). Non-use of provided assistive
technology devices, a literature overview. Technology believed to be forwarded to the primary
and Disability, 15(4), 231–238. motor area (precentral gyrus) that then actually
Association for Postdoctoral Programs in Clinical Neuropsychology (APPCN) 371

executes the motor response. The orbitofrontal cal problem solving, any or all of which can
cortex is shared with limbic association cortex be adversely affected by lesions to these
(see below) that underscores the importance of areas. A
the integration of emotion, memory, and
behavior. Lesions to prefrontal association cor-
tices often affect self-monitoring, planning, Cross-References
and executive functions, including behavioral
inhibition. ▶ Association Pathways
2. The limbic association cortex includes ventro- ▶ Heteromodal Cortex
medial frontal lobe, medial parietal lobe, tem- ▶ Secondary Cortex
poral pole, and cingulate and parahippocampal ▶ Unimodal Cortex
areas. Integration of information from the
hypothalamus, other limbic or paralimbic
structures, and secondary sensory association References and Readings
areas is received and projected to other areas of
the cortex, including the prefrontal cortex Kupermann, I. (1991). Localization of higher cognitive and
affective functions: The association cortices. In E. R.
discussed above, again permitting the integra-
Kandel, J. H. Schwartz, & T. M. Jessel (Eds.), Princi-
tion of emotions, cognition and perceptions, ples of neural science (3rd ed., pp. 823–838). East
and memory. Dysfunction is often expressed Norwalk: Appleton & Lange.
as emotional/behavioral dysregulation and Mendoza, J. E., & Foundas, A. F. (2008). Clinical neuro-
anatomy: A behavioral approach. New York: Springer.
memory impairment.
Mesulam, M.-M. (2000). Principles of behavioral and cog-
3. The locations of the parieto-temporal-occip- nitive neurology. New York: Oxford University Press.
ital association cortices are described by Pandya, D. N., & Seltzer, B. (1982). Association areas of
their names and are typically divided into the cerebral cortex. Trends in Neurosciences, 5,
385–390.
secondary and tertiary areas. The former are
Pandya, D. N., & Yeterian, E. H. (2003). Cerebral cortex:
unimodal in nature (respond more or less Architecture and connections. In Encyclopedia of the
exclusively to a single sensory modality) neurological sciences (pp. 594–604). Amsterdam:
and lie adjacent to their respective primary Elsevier Science.
cortical sensory projection areas. They are
thought to be responsible for further integrat-
ing and processing sensory input into poten-
tially meaningful percepts. Hence, lesions of Association for Postdoctoral
these secondary association areas will com- Programs in Clinical
monly result in modality-specific perceptual Neuropsychology (APPCN)
disturbances or agnosias. By contrast, the
tertiary or heteromodal association areas Jacobus Donders
receive input from all sensory modalities. Mary Free Bed Rehabilitation Hospital, Grand
Because of this and their central location, Rapids, MI, USA
they are sometimes referred to as the PTO
(parietal-temporal-occipital) cortex. Because
of their crossed or multimodal inputs, these Membership
latter areas, which are very highly developed
in man, are thought to represent the founda- The Association of Postdoctoral Programs in Clin-
tions for higher-order conceptual and intel- ical Neuropsychology (APPCN) is an organization
lectual abilities, including abstraction, of over 75 member programs that offer compre-
language, and visual-spatial and mathemati- hensive, integrated postdoctoral residencies.
372 Association for Postdoctoral Programs in Clinical Neuropsychology (APPCN)

Major Areas or Mission Statement duration of training is for a minimum of 2 years,

or for an equivalent time on no less than a half-
The mission of APPCN is to foster the provision time basis, at a fixed site with regular, on-site
of advanced specialty education and training to supervision; (2) the program includes an orga-
promote the competencies that are necessary for nized and integrated combination of at least 50%
practice in the specialty of clinical neuropsychol- clinical service, at least 10% didactic/educa-
ogy (Boake et al. 2002). APPCN programs pre- tional activities, and at least 10% research or
pare residents for certification by the American other scholarly activities; and (3) the program
Board of Clinical Neuropsychology (ABCN). director is board-certified in clinical neuropsy-
Successful completion of an APPCN residency chology through the American Board of Profes-
is sufficient to demonstrate that one has met the sional Psychology (ABBP-CN). One of the
ABCN didactic requirements for board major accomplishments of APPCN is the devel-
certification. opment and implementation, in collaboration
with National Matching Services, of a comput-
erized system for matching of applicants for
Landmark Contributions postdoctoral residency training in clinical neu-
ropsychology to programs that offer such train-
Formally incorporated in 1992, APPCN contrib- ing. This electronic system, instituted in 2001, is
uted to the Houston Conference, which the most fair to applicants, and the most efficient
established that completion of 2 years of formal for programs, with all APPCN programs that
postdoctoral residency training is a uniform have open positions in any given year taking
requirement for entry into the professional prac- part in this electronic match. Postdoctoral pro-
tice of clinical neuropsychology (Hannay et al. grams that are not members of APPCN are also
1998). In more recent years, APPCN has been a allowed to participate as long as they meet
key representative to interorganizational groups APPCN standards #1 and #2 above, and if they
like the Clinical Neuropsychology Synarchy and agree to respect all other conditions of the
the Inter-organizational Summit on Education and match, including prohibition of preemptive
Training. offers, and adherence to the binding nature of
the match outcomes. Further details are avail-
able at http://www.natmatch.com/appcnmat/.
Major Activities APPCN is dedicated to education of aspiring
neuropsychologists about what it takes to become
APPCN is not an accrediting organization, a role a competitive candidate for postdoctoral resi-
which is left to the Commission on Accreditation dency training. For this purpose, several educa-
of the American Psychological Association tional seminars are offered on a regular basis,
(APA). However, a growing number of the some in collaboration with other organizations,
APPCN members are currently accredited by such as Division 40 (▶ “Clinical Neuropsychol-
APA as a postdoctoral specialty program in clin- ogy”) of the APA and the Association of Neuro-
ical neuropsychology. Details about individual psychology Students in Training (ANST). Over
APPCN member programs, including focus on the past several years, APPCN program directors
adult v. pediatric neuropsychology, accreditation have also consistently provided a “special topic
status, primary diagnostic groups served, and presentation” about postdoctoral residency train-
other characteristics, are available on the ing at the annual meeting of the National Acad-
APPCN website. emy of Neuropsychology (NAN).
The major standards for program member- APPCN has also strived to make the process
ship in APPCN include the following: (1) the of education and evaluation as part of
Association Pathways 373

postdoctoral residency training in clinical neu- ▶ American Board of Professional Psychology

ropsychology more standardized. For this pur- (ABPP)
pose, a 50-item written examination has been ▶ American Psychological Association (APA) A
developed by APPCN to be used with residents
who are near completion of their first postdoc-
toral training year, to evaluate their knowledge
of major content areas like functional neuroanat- References and Readings
omy, adult and pediatric syndromes, psychomet-
rics, etc. This exam is not intended to give Boake, C., Yeates, K. O., & Donders, J. (2002). Associa-
residents a “grade”; rather, it is to be used as an tion of Postdoctoral Programs in clinical neuropsychol-
ogy: Update and new directions. The Clinical
educational tool, to identify relative strengths
Neuropsychologist, 16, 1–6.
and weaknesses in the residents’ working Hannay, H. J., Bieliauskas, L., Crosson, B. A., Hammeke,
knowledge base, so that the relative lacunae T. A., Hamsher, K., & Koffler, S. P. (1998). The Hous-
can be addressed during the subsequent training ton conference on specialty education and training in
clinical neuropsychology. Archives of Clinical Neuro-
year. During that second year, APPCN member
psychology, 13, 157–250.
programs also have the opportunity to start pre-
paring residents for board certification, by
means of ethics vignettes and mock oral “fact
finding” case materials that are very similar in
format and level of difficulty to those used by Association Pathways
ABPP-CN.
Finally, the most recent initiative of APPCN John E. Mendoza
has involved advocacy with the United States Department of Psychiatry and Neuroscience,
Department of Veterans Affairs for the develop- Tulane Medical School and SE Louisiana
ment of more postdoctoral training programs in Veterans Healthcare System, New Orleans,
clinical neuropsychology, primarily because of LA, USA
the high number of traumatic brain injuries
among US service personnel involved in the
combat in Iraq. When more than a dozen of Definition
these training programs became available in the
Fall of 2007, APPCN contacted the programs, Fiber pathways that lie within the cerebrum that
provided mentoring as needed, and waived their connect one part of the cerebral cortex with
first-time participation fee in the electronic another within the same hemisphere. Association
match. APPCN has also continued to offer assis- pathways are thus contrasted with commissures
tance to new programs as they seek specialty that generally interconnect homologous areas of
accreditation through the APA. APPCN will the two halves of the brain, and projection path-
continue to embrace additional organized and ways that are fiber tracts interconnecting cortical
integrated postdoctoral training programs in and subcortical structures. They may be very long
clinical neuropsychology. (typically termed fasciculi) or very short. The
latter may consist of “U”-shaped fibers
connecting one gyrus with an adjacent one or
horizontal connections within a gyrus itself (e.g.,
Cross-References bands of Baillarger). These various pathways
allow different areas of the brain to communicate
▶ American Board of Clinical Neuropsychology with one another. Some of the major association
(ABCN) pathways are shown in Fig. 1.
374 Associational Fibers

Association Pathways,
Fig. 1

U
SLF
AF arcuate fasciculus
IOF inf. occiptofrontal fasc. AF
SLF sup. longitudinal fasc. IOF
U U-fibers UF
UF uncinate fasciculus

Cross-References same cerebral hemisphere. The most prevalent

type of white matter tract found in the cortex,
▶ Commissures, Cerebral associational fibers permit bidirectional commu-
▶ Projection Pathways nication between different cortical areas, thus
allowing the cortex to function as a coordinated
whole. Associational fibers predominantly arise
from cortical layer III pyramidal neurons and
can be classified as either short associational
Associational Fibers fibers, which connect adjacent gyri within the
same lobe, or long associational fibers,
Melissa J. McGinn interconnecting more distant regions located in
Anatomy and Neurobiology, Virginia different lobes. The major long associational
Commonwealth University School of Medicine, fibers tracts in the brain include the superior
Richmond, VA, USA longitudinal fasciculus, arcuate fasciculus, unci-
nate fasciculus, and cingulum.

Synonyms
Cross-References
Arcuate fibers
▶ Arcuate Fasciculus
▶ Association Pathways
Definition ▶ Cerebral Cortex
▶ Cingulum
Associational fibers are bundles of white matter ▶ Superior Longitudinal Fasciculus
that connect various cortical regions within the ▶ White Matter
Associative Visual Agnosia 375

match colors, but neither name them nor identify

Associative Visual Agnosia objects with which they might be associated (such
as cherries or apples for the color red). Facial A
John E. Mendoza agnosia (prosopagnosia) is a bit complex in that
Department of Psychiatry and Neuroscience, one may differentiate the inability to make discrim-
Tulane Medical School and SE Louisiana inations among unfamiliar faces (thought to be
Veterans Healthcare System, New Orleans, LA, more of a perceptual problem) from an inability to
USA recognize familiar faces (generally considered an
associative problem). Thus, in the latter instance,
while the patient might be able to match the face or
Definition picture of a familiar person to one within an array of
pictures, he would not be able to identify the face or
Regardless of modality, an associative agnosia the picture as that of his wife, his daughter, or other
implies that although perception is intact, the partic- famous person with whom he might be familiar.
ular stimulus has no meaning (“associative” value) While the specific lesions causing specific
to the individual. The stimulus can neither be named associative visual agnosias are not well defined,
nor linked to other personal or sensory experiences. they are generally thought to represent a discon-
Hence, associative visual agnosia refers to the nection type syndrome involving the temporal,
inability to identify or categorize a visually pre- occipital, and/or parietal regions of the left hemi-
sented stimulus despite adequate visual perception. sphere with some disruption of fiber pathways or
connections between the unimodal (visual) and
heteromodal cortices.
Current Knowledge

Individuals with this disorder should be able to Cross-References

match the visual stimulus to a sample and copy or
draw what is seen, thus distinguishing associative ▶ Alexia
from apperceptive visual agnosia. In the latter con- ▶ Apperceptive Visual Agnosia
dition, visual object recognition is also impaired, ▶ Color Agnosia
but primarily as a result of a disturbance of percep- ▶ Color Anomia
tion. In addition to having difficulty naming visu- ▶ Disconnection Syndrome
ally presented objects, a patient suffering from ▶ Heteromodal Cortex
associative visual agnosia would likely be unable ▶ Prosopagnosia
to describe their use or purpose, or indicate to ▶ Unimodal Cortex
which category of objects they may belong. How-
ever, in pure visual associative agnosia, identifica-
tion should be possible if the patient were allowed References and Readings
to hold the object(s) (tactile recognition).
An associative visual agnosia may differen- Bauer, R. M., & Demery, J. A. (2003). Agnosia. In
tially affect recognition of objects, words, colors, K. Heilman & E. Valenstein (Eds.), Clinical neuropsy-
chology (4th ed., pp. 236–295). New York: Oxford
or faces. In visual agnosia for words (also known University Press.
as pure alexia or pure word blindness), visual DeRenzi, E., & Spinnler, H. (1966). Visual recognition in
word recognition is impaired. But the individual patients with unilateral cerebral disease. Journal of
may be able to “read” if allowed to trace the letters Nervous and Mental Disease, 142, 513–525.
DeRenzi, E., Scotti, G., & Spinnler, H. (1969). Perceptual
with a finger, thus permitting tactile or kinesthetic and associative disorders of visual recognition. Rela-
recognition of individual letters. In associative tionship to the side of the cerebral lesion. Neurology,
color agnosia, the individual may be able to 19, 634–642.
376 Astasia-Abasia

Astasia-Abasia Astereognosis

Douglas I. Katz Melissa Amick

Department of Neurology, Boston University Department of Psychiatry and Human Behavior,
School of Medicine, Braintree, MA, USA Brown University, Providence, RI, USA

Synonyms Synonyms

Blocq’s disease Object agnosia; Tactile agnosia

Definition Short Description or Definition

An inability to stand and walk in a normal and Astereognosis is defined as the inability to iden-
coordinated manner. Astasia means inability to tify objects through touch without visual input.
maintain standing, and abasia refers to impaired
coordination of gait. The term is usually applied to
unusual, often bizarre patterns of gait and stance
that appear to have no neuropathophysiologic Categorization
basis. Conversion disorder is frequently the
underlying cause. Patients may sway in a stagger- Astereognosis has been subdivided into primary
ing, unstable manner, often catching themselves and secondary recognition deficits. Primary
before falling. This syndrome is also referred to as recognition deficits, also called morphognosia,
Blocq’s disease. reflect impairments in recognizing the physical
features of the object (e.g., weight or texture).
Secondary recognition deficits reflect a specific
impairment in object recognition with spared
Cross-References primary recognition (for review, see De Renzi
1982).
▶ Abasia
▶ Gait Disorders
▶ Psychogenic Disorder
Epidemiology

Astereognosis can be common after stroke with

References and Readings one report indicating that up to 90% of patients
demonstrate astereognosis (Connell et al. 2008).
Morris, J. G., Mark de Moore, G., & Herberstein,
Damage to the cortical regions important for hap-
M. (2006). Psychogenic gait: An example of deceptive
signaling. In C. R. Cloninger & M. Hallett (Eds.), tic input integration can cause astereognosis. This
Psychogenic movement disorders: Neurology and neu- disorder, therefore, is common and can occur in
ropsychiatry. Philadelphia: Lippincott Williams & the presence of many neurological disorders
Wilkins.
including brain (e.g., Knecht et al. 1996) or spinal
Okun, M. S., & Koehler, P. J. (2007). Paul Blocq and
(psychogenic) astasia abasia. Movement Disorders, cord tumors (Lesoin et al. 1986) and traumatic
22, 1373–1378. brain injury (Hom and Reitan 1982).
Astereognosis 377

Natural History, Prognostic Factors, and Battery (Reitan and Wolfson 1993) requires par-
Outcomes ticipants to manipulate a flat plastic shape with
one hand obscured from vision, while the other A
Connell et al. (2008) followed 58 stroke survivors hand points to the same shape mounted on a
over a period of 6 months (baseline, 2, 4, and board with three other potential distractors. In
6 months), and at each time period, participants the Benton Stereognosis Test (Benton 1969),
completed the Nottingham Sensory Assessment ten cards with fine-grain, sandpaper figures
(see below). Stereognosis significantly improved pasted on top are felt by the participant out of
during the observation period, with the greatest view. The participant has 30 s to explore the card
changes occurring within the first 4 months and 45 s to respond. Responses are made by
(baseline relative to 4-month performance). pointing to the corresponding line drawing
Regression analyses indicated that stroke severity mounted in full view of the respondent. The
and motor performance of the upper limb were Nottingham Sensory Assessment includes an
predictive of the presence of impaired stereo- assessment of astereognosis (Gaubert and
gnosis at the baseline assessment. Mockett 2000). In this task, the participant is
blindfolded and asked to name the object placed
in his/her hand. Presentation of the objects is
Neuropsychology and Psychology of time limited. Objects to be identified include
Astereognosis coins, comb, sponge, pencil, scissors, a cup,
and a glass. Responses are scored on a scale of
Astereognosis can occur after injury to either the 0–2 depending upon the quality of the verbal
left or right hemisphere. A specialized role for the response.
right hemisphere in stereognosis has been pro-
posed; however this finding has not been consis-
tently observed (for review, see Zaidel 1998 and Treatment
De Renzi 1982). Initially astereognosis was
thought to be due to damage to the primary Astereognosis has been observed to spontane-
somatosensory cortex; however, posterior parietal ously improve over time (Connell et al. 2008).
lesions have also been associated with this impair- One study has found that stereognosis improves
ment (Knecht et al. 1996). following systematic hand retraining in stroke
survivors who were at least 2 years post stroke.
Yekutiel and Guttman (1993) had 25 participants
Evaluation receive three 45-min hand-retraining sessions
weekly for a period of 6 weeks. The therapy was
Astereognosis is often examined with non- customized for each participant, but everyone
standardized methods. In the typical neurologi- received education to improve insight about their
cal examination, astereognosis is assessed by impairment, and exercises were intended to be
asking the patient to identify an object through appropriately challenging and designed to pro-
touch without visual input. Common objects mote self-efficacy, used vision and the less
used for identification can include coins, keys, affected hand to aid sensory function, and pro-
paper clips, or screws. For patients with vided frequent breaks and novel stimuli. Unlike
hemiparesis, the examiner may manipulate the the control group, the patient group showed a
patient’s hand to assist in object identification. statistically significant improvement on the
Standardized assessments of astereognosis do stereognosis assessment. These findings suggest
exist. The Tactile Form Recognition Test from that functional gains through therapy can occur in
the Halstead-Reitan Neuropsychological Test the years following stroke.
378 Astrocytoma

Cross-References
Astrocytoma
▶ Ahylognosia
▶ Amorphognosis Robert Rider1 and Carol L. Armstrong2
▶ Parietal Lobe 1
Department of Psychology, Drexel University,
▶ Somatosensory Cortex Philadelphia, PA, USA
▶ Stereognosis 2
Child and Adolescent Psychiatry and Behavioral
▶ Tactile Agnosia Sciences, The Children’s Hospital of
▶ Tactile Form Recognition Philadelphia, Philadelphia, PA, USA
▶ Tactual Performance Test

Definition
References and Readings
Astrocytomas are the most frequently diagnosed
Benton, A. L. (1969). Stereognosis test; Manual of instruc- tumors, are usually slow growing, and may
tions. Victoria: Neuropsychology Laboratory, Depart-
develop a cystic component. Arising in astrocytic
ment of Psychology, University of Victoria.
Connell, L. A., Lincoln, N. B., & Radford, K. A. (2008). cells anywhere throughout the central nervous
Somatosensory impairment after stroke: Frequency of system, they may occur in any age group but are
different deficits and their recovery. Clinical Rehabili- most frequently diagnosed in middle-aged males.
tation, 22, 758–767.
The highest incidence of brain stem astrocytomas
De Renzi, E. (1982). Disorders of space exploration and
cognition. New York: Wiley. is found in children. Grading systems focus on the
Gaubert, C. S., & Mockett, S. P. (2000). Inter-rater reliabil- degree of resemblance to normal astrocytes, with
ity of the Nottingham method of stereognosis assess- higher grades associated with more rapid growth
ment. Clinical Rehabilitation, 14(2), 153–159.
and greater likelihood of metastasis. Three com-
Hom, J., & Reitan, R. M. (1982). Effect of lateralized
cerebral damage upon contralateral and ipsilateral sen- mon types of astrocytomas are low-grade astrocy-
sorimotor performances. Journal of Clinical Neuropsy- tomas, which are often benign and tend to occur in
chology, 4(3), 249–268. the cerebellum (especially in children) but may
Knecht, S., Kunesch, E., & Schnitzler, A. (1996). Parallel
and serial processing of haptic information in man:
also occur in the cerebrum in adults; anaplastic
Effects of parietal lesions on sensorimotor hand func- astrocytomas, which are malignant; and glioblas-
tion. Neuropsychologia, 34, 669–687. toma multiforme, which are thought to arise from
Lesoin, F., Rousseaux, M., Martin, H. J., Petit, H., & astrocytomas and are the most malignant.
Jomin, M. J. (1986). Astereognosis and amyotrophy
The specific symptoms associated with astro-
of the hand with neurinoma of the second cervical
nerve root. Neurology, 233, 57–58. cytomas depend on the region of the CNS that is
Lincoln, N. B., Crow, J. L., Jackson, J. M., Waters, G. R., affected. A low-grade astrocytoma may remain
Adams, S. A., & Hodgson, P. (1991). The unreliability quiescent throughout the lifespan of the person,
of sensory assessment. Clinical Rehabilitation, 5,
especially when diagnosed at a young age, but the
273–282.
Reitan, R. M., & Wolfson, D. (1993). The Halstead- effects of surgery and radiation on the region of the
Reitan neuropsychological test battery: Theory and tumor may cause progressive injury; surgical
clinical interpretation. Tucson: Neuropsychology effects on brain and behavior tend to occur within
Press.
a year after surgery, but radiation effects may cause
Yekutiel, M., & Guttman, E. J. (1993). A controlled trial of
the retraining of the sensory function of the hand in progression of the deficits caused by the original
stroke patients. Journal of Neurology, Neurosurgery, tumor location for decades after. In cases of pro-
and Psychiatry, 56, 241–244. gressive cognitive injury in patients with high-
Zaidel, E. (1998). Stereognosis in the chronic split brain:
grade supratentorial astrocytomas, deterioration
Hemispheric differences, ipsilateral control and sen-
sory integration across the midline. Neuropsychologia, in information processing speed, attention, work-
36, 1033–1047. ing memory, long-term memory, and executive
Asymmetry 379

functioning has been reported. The extent of injury Definition

is in part dependent on the size of the tumor and
how much normal tissue it has invaded. In cases of Asymmetry is the discordance between the right A
cerebellar gliomas (astrocytomas and medullo- and left sides of the brain in respect to structure
blastomas), the location of the tumor in the cere- and/or function.
bellum again predicts the type of deficit, for
example, visuospatial memory and attention, anx-
iety with left cerebellar tumors, and verbal mem- Current Knowledge
ory and fluency in right cerebellar tumors.
Although not initially linked to brain asymmetry,
the first behavioral asymmetry that was likely
Cross-References
noted was the superiority of motor skills exhibited
by one hand, most commonly the right, over the
▶ Fibrillary Astrocytoma
other. The next real breakthrough with regard to
▶ Oligoastrocytoma
asymmetry is generally thought to have occurred
▶ Pilocytic Astrocytoma and Juvenile Pilocytic
in the nineteenth century with the discovery that
Astrocytoma
acquired language deficits (aphasia) were typi-
cally associated with lesions of the left hemi-
sphere. Since then, other asymmetries, both
References and Readings
functional and structural, have been identified
Bosma, I., Vos, M. J., Heimans, J. J., Taphoorn, J. B., with regard to the two cerebral hemispheres.
Aaronson, N. K., Postma, T. J., et al. (2007). The course
of neurocognitive functioning in high-grade glioma Structural Asymmetries
patients. Neuro-Oncology, 9(1), 53–62. Structural asymmetries of the brain were first
Iuvone, L., Peruzzi, L., Colosimo, C., Tamburrini, G.,
Caldarelli, M., DiRocco, C., et al. (2011). Pretreatment noted around the beginning of the twentieth cen-
neuropsychological deficits in children with brain tury, but it was not until the late 1960s that these
tumors. Neuro-Oncology, 13(5), 517–524. were first strongly correlated with functional dif-
Louis, D., Ohgaki, H., Cavenee, W., & Wiestler, O. (2007). ferences between the hemispheres. In a study of
WHO classification of tumours of the central nervous
system (4th ed.). Louis: World Health Organization. 100 postmortem brains, Geschwind and Levitsky
Moitra, E., & Armstrong, C. L. (2013). Neural substrates (1968) noticed that the planum temporale, located
for heightened anxiety in children with brain tumors. in the temporal operculum, was larger in 65% of
Developmental Neuropsychology, 38(5), 337–351. the brains studied as compared with only 11% in
which the right was larger. They concluded that
this difference was likely related to the left hemi-
sphere’s association with the production of lan-
Asymmetry guage in most individuals. Subsequent studies
have demonstrated that this asymmetry can be
Maryellen Romero shown to present even prior to birth, reinforcing
Department of Psychiatry and Behavioral the genetic predisposition to left-hemispheric
Sciences, Tulane University School of Medicine, dominance for language.
New Orleans, LA, USA Since the advent of more sophisticated imag-
ing techniques that allow for large-scale in vivo
studies of the brain, other structural differences
Synonyms have been documented. The inferior frontal gyrus
in the left hemisphere, corresponding to Broca’s
Hemispheric specialization area, has been shown to be more highly developed
380 Asymmetry

on the left side for most individuals. The gyri and point when speaking or writing. It appears to be
sulci associated with the motor strip (Brodmann’s important in appreciating verbal (as well as non-
area 4) are more prominent in the left hemisphere verbal) humor and in detecting meaning from the
of right-handers. Fairly consistent differences in differential inflections given to individual words
the lateral fissure have been found, with the pos- in speech.
terior ascending ramus of this sulcus making a In addition to words, numbers also have their
more abrupt upward turn in the right hemisphere own symbolic meaning. Hence, as might be
as compared with the left. This would suggest expected, the ability to use numbers is thought to
likely differences in the distribution of the supra- be a function normally carried out by the left
marginal and angular gyri in the inferior parietal hemisphere, the disturbance of which following
lobules of the two hemispheres. Even on a more a lesion to the left hemisphere may be defined as
microlevel, differences in the size and organiza- acalculia (dyscalculia). However, most complex
tion of individual cells or cell columns have been arithmetical operations also have a spatial compo-
identified in the two hemispheres. nent. For example, precise alignment of rows and
It is reasonable to speculate that some struc- columns of numbers is critical in mathematical
tural differences likely relate to functional differ- operations, whether completed mentally or on
ences between the two hemispheres, particularly paper. These spatial relations can be disturbed
behaviors such as language and handedness. following right-hemispheric lesions, resulting in
However, functional asymmetries have either what has been termed spatial dyscalculia.
been demonstrated or are suspected well beyond It is known that the hemisphere contralateral to
those which can currently be explained by struc- the hand being used to carry out some motor tasks
tural differences. The following represent a sam- is immediately responsible for the execution of
pling of some of the functional differences that these movements. However, the motor programs
have been observed. or engrams for overlearned motor skills are
believed to reside in the left hemisphere, certainly
Functional Asymmetries for the vast majority of right-handers, as well as
It has been well established that language expres- many left-handers. Thus, any lesion that either
sion and comprehension are normally mediated directly interferes with those engrams or the abil-
primarily, if not exclusively, by the left hemi- ity of that information to reach the premotor cor-
sphere, even among left-handers. However, the tex of either hemisphere can result in an impaired
right hemisphere has also been shown to play an performance, especially if the individual is asked
important role in communication. Verbal commu- to demonstrate the action in the absence of the
nication is not just about using words in sentences actual object. This latter condition is referred to as
or paragraphs; emotional tone or nuances of the an ideomotor apraxia.
speaker often convey important meaning. In some Perceptual abilities appear to be differentially
communications, such as those with a sarcastic distributed between the two hemispheres. It has
intent, the real message is carried by the tone already been noted that the left hemisphere is
rather than by the words, which, if interpreted normally the leading hemisphere in interpreting
literally, might actually convey a very different verbal (semantic) information, while the right
message. The ability to use as well as interpret appears to be better adapted to processing certain
these emotional components of speech, known as types of emotional cues. It seems that the right
prosody, is primarily mediated by the right hemi- hemisphere is also the more proficient in pro-
sphere; damage to this side of the brain may cessing many types of visual-spatial or visual-
produce various forms of aprosodia. With regard gestalt information. Thus, the right hemisphere
to using or interpreting the language of others, the has been found to be generally superior in carry-
right hemisphere is also believed to play an impor- ing out certain constructional tasks, making judg-
tant role in identifying the central theme or point ments regarding the orientation of lines in space,
of the discourse of others and being able to stay on in making discriminations regarding unfamiliar
Asymmetry 381

faces, and in recognizing familiar tunes or envi- with brain injury that individuals with right
ronmental sounds. On the other hand, the left hemisphere lesions often behave differently
hemisphere appears to be the leading hemisphere than those with left-sided lesions. While the lat- A
when it comes to perception of certain aspects of ter seem to remain emotionally attached, even if
one’s own body. Problems of right-left orientation that emotion is often one of anger, frustration, or
and difficulty recognizing individual fingers of sadness, right hemispherically damaged patients
one’s hands (finger agnosia) are typically associ- are more likely to be described as apathetic,
ated with lesions of the left inferior parietal lobule. indifferent, emotionally flat, both in terms of
Functional MRI studies have demonstrated con- their verbal and facial expressions and their inter-
sistent activation of right hemisphere structures personal relationships.
during tests of vigilance and directed attention.
However, divided attention tasks have been
shown to selectively activate left prefrontal cor- Cross-References
tex. PET imaging studies have demonstrated
increased blood flow in the right prefrontal and ▶ Anosognosia
superior parietal cortex during tasks requiring ▶ Directed Attention
sustained attention, regardless of the type of stim- ▶ Dominance (Cerebral)
ulus (verbal, visual, etc.) or where it is introduced ▶ Language
(left vs. right). ▶ Wada Test
Differences between the two hemispheres have
also been demonstrated in learning and memory
tasks and other cognitive domains. Of the two, the References and Readings
left hemisphere has been more strongly associated
with learning verbal information. While many Corballis, P. M. (2003). Visuospatial processing and the
studies have shown that the right hemisphere is right-hemisphere interpreter. Brain and Cognition, 53,
171–176.
perhaps better at learning certain “nonverbal” or Davidson, R. J. (1992). Emotion and affective style: Hemi-
“visual-spatial” type information, the findings are spheric substrates. Psychological Science, 3, 39–43.
generally less robust compared to the left hemi- Davidson, R. J., & Hugdahl, K. (Eds.). (1996). Brain
sphere and verbal memory. One frequent explana- asymmetry. Cambridge, MA: Bradford Books.
Gazzaniga, M. S. (2000). The new cognitive neurosciences.
tion for this is that when faced with any memory Boston: MIT Press.
task, humans have a natural tendency to try to Gazzaniga, M. S., Ivry, R. B., & Mangun, G. R. (2002).
verbally encode the stimulus, thus bringing the Cognitive neuroscience: The biology of the mind. New
left hemisphere into play. York: W. W. Norton & Company.
Geschwind, N., & Levitsky, W. (1968). Left-right asym-
It has also been suggested that the two hemi- metry in temporal speech region. Science, 161,
spheres play different roles in attention. The much 186–187.
more frequent association of disorders such as Good, C. D., Johnsrude, I., Ashburner, J., Henson, R. N.
unilateral neglect and anosognosia with right A., Friston, K. J., & Frackowiak, R. S. J. (2001).
Cerebral asymmetry and the effects of sex and handed-
hemispheric lesions has led to the hypothesis ness on brain structure: A voxel-based morphometric
that while, as might be expected, the left hemi- analysis of 465 normal adult human brains.
sphere attends to the right side of space (both NeuroImage, 14, 685–700.
personal and extrapersonal), the right hemisphere Kinsbourne, M. (Ed.). (1978). Asymmetrical function of
the brain. New York: Cambridge University Press.
focuses on both right and left space. Mendoza, J. E., & Foundas, A. L. (2008). Clinical neuro-
Finally, the association of the right hemi- anatomy: A neurobehavioral approach. New York:
sphere and emotional expression would appear Springer.
to go beyond the affective intonations of speech Ross, E. (2000). Affective prosody and the aprosodias. In
M. Mesulam (Ed.), Principles of behavioral and cog-
as described above. It is commonly observed, nitive neurology. New York: Oxford University Press.
both by health-care professionals as well as the Walsh, K. (1994). Neuropsychology: A clinical approach.
spouses and other family members of persons New York: Churchill Livingstone.
382 Ataxia

associated with seizures. The symptoms may

Ataxia respond to Coenzyme Q10 treatment. There are a
number of hereditary cerebellar ataxias. Most of
Anna DePold Hohler1 and the autosomal recessive and autosomal dominant
Marcus Ponce de Leon2 ataxias have no treatments. An exception is vitamin
1
Boston University Medical Center, Boston, E deficiency, which is an autosomal recessive dis-
MA, USA order. It is due to a mutation in the gene coding for
2
Madigan Army Medical Center, Tacoma, the alpha tocopherol transfer protein located on the
WA, USA long arm of chromosome 8. It is characterized by
childhood onset of ataxia, dysarthria, areflexia,
proprioceptive deficits, extensor plantar responses,
Synonyms and skeletal deformities.
The episodic ataxias, which are inherited in an
Clumsiness autosomal dominant fashion, may also have some
symptomatic treatment regimens. Episodic ataxia
type 1 is related to a chromosome 12 mutation in
Definition the potassium channel gene. Clinically, the disease
manifests with episodes of ataxia lasting seconds to
Ataxia describes a lack of coordination while minutes. Patients may also suffer from myokymia
performing voluntary movements. It is associated during and between attacks of ataxia. The ataxia
with damage to the cerebellum or its afferent or may be induced by startle or exercise. Episodic
efferent pathways. It may appear as clumsiness, ataxia type 2 is related to a defect located on chro-
inaccuracy, or instability. It may affect any part of mosome 19. It is due to a mutation in a voltage-
the body. When ataxia affects the arms and hands, dependent calcium channel. Clinically, patients pre-
it may cause tremor due to overcorrection of inac- sent with nystagmus. Attacks last minutes to hours
curate movements. It may produce dysmetria or an and may be induced by a change in posture.
inability to gauge distance correctly. It may cause Patients may also complain of vertigo. As the dis-
past-pointing when an attempted reach overshoots ease progresses, ataxia becomes permanent.
the target. It may also cause dysdiadochokinesia or
poor performance of regular, repeated movements.
Cerebellar injury may contribute to nystagmus, Epidemiology
hyper- and hypometric saccades, scanning speech,
titubation, and difficulties with gait and balance. Ataxia is a common sign associated with
inherited, acquired, toxic, and traumatic events.

Current Knowledge
Natural History
There are a number of different types of damage to
the cerebellum. These range from fixed damage The genetic syndromes that are associated with
(e.g., stroke, trauma, hypoxic injury) to chemical, ataxia tend to be progressive. Individuals with
metabolic, and degenerative. Cerebellar injury static insults such as strokes or trauma may show
related to vitamin deficiency (e.g., E, B12, and improvement in function over time.
thiamine) may be reversible and should be identi-
fied and treated. Metabolic diseases such as
Hartnup’s, Refsum’s, and the mitochondrial disor- Neuropsychology
ders are less treatable. A deficiency of Coenzyme
Q10 has been described in patients with cerebellar Cerebellar syndromes may be associated with
ataxia, usually with childhood onset and often cognitive slowing.
Atherosclerosis 383

Evaluation includes a detailed neurological calcium, and fibrin, a stringy material found nor-
examination, magnetic resonance imaging, and mally in the blood to help clot the blood. The
laboratory investigation for reversible or genetic plaque formation process stimulates the cells of A
causes. the artery wall to produce substances that then
Treatment depends on the underlying insult. accumulate in the vessel wall. Fat builds up within
these cells and around them, and they form con-
nective tissue and calcium. The artery wall
Cross-References thickens, the artery’s diameter is reduced, and
blood flow and oxygen delivery are decreased.
▶ Cerebellum Plaques can rupture or crack open, causing the
▶ Dysdiadochokinesia sudden formation of a blood clot (thrombosis).
Atherosclerosis can cause angina or myocardial
infarction if it blocks the blood flow in the coro-
References and Readings nary arteries that supply the heart muscle, stroke if
it blocks the carotid arteries that supply the brain,
Gilman, S. (2004). Clinical features and treatment of cere- kidney disease if it blocks the renal arteries or
bellar disorders. In R. L. Watts & W. C. Koller (Eds.), gangrene possibly leading to amputation if it
Movement disorders (2nd ed., pp. 723–736).
New York: McGraw-Hill.
blocks the peripheral arteries that supply the
limbs.
Atherosclerosis may be asymptomatic for
many years. Risk factors for this disease have
been well studied. It is thought that atherosclero-
Atherosclerosis sis is caused by a response to damage to the
endothelium from high cholesterol, high blood
Elliot J. Roth
pressure, and cigarette smoking. A person who
Department of Physical Medicine and
has all three of these risk factors is eight times
Rehabilitation, Northwestern University,
more likely to develop atherosclerosis than is a
Feinberg School of Medicine, Chicago, IL, USA
person who has none. Physical inactivity, diabe-
tes, and obesity are also risk factors for athero-
sclerosis. Heredity, advancing age, and racial
Synonyms
background are less-significant risk factors.
Treatment options include lifestyle changes,
Arteriosclerotic vascular disease or ASVD; Ath-
use of lipid-lowering and other drugs, angioplasty,
eromatous plaque; Hardening of the arteries
and various surgical procedures, depending on
the location of the plaque. Many lifestyle
changes that prevent disease progression also
Definition prevent the onset of the disease; these include a
low-fat, low-cholesterol diet, weight loss, exer-
Atherosclerosis is the progressive pathological cise, blood pressure control, diabetes manage-
process of buildup of plaque inside the blood ment, and smoking cessation.
vessels, resulting in blockage of blood flow
through the vessels.
Cross-References
Current Knowledge ▶ Angioplasty
▶ Anticoagulation
The plaque that causes atherosclerosis is com- ▶ Antiplatelet Therapy
prised of fatty substances, cholesterol, cells, ▶ Cerebrovascular Disease
384 Atkins v. Virginia

▶ Cholesterol Thus, Atkins was charged and convicted of

▶ Coronary Disease abduction, armed robbery, and capital murder.
▶ Ischemic Stroke This took place despite the results of an IQ test
▶ Myocardial Infarction completed by a clinical psychologist, in which
▶ Peripheral Vascular Disease Atkins’ score of 59 placed him in the mildly
▶ Stent mentally retarded range. Nonetheless, he was
▶ Thrombolysis sentenced to death.
▶ Thrombosis The Supreme Court of Virginia was in agree-
ment with the judgment of the trial court, and the
appeal was taken to the US Supreme Court. In
References and Readings July of 2002, the US Supreme Court reversed the
judgment of the trial court and the Supreme Court
Stary, H. C., Chandler, A. B., Dinsmore, R. E., Fuster, V., of Virginia and referred the case back to the sen-
Glagov, S., Insull, W., et al. (1995). A definition of
tencing court to render a sentence other than the
advanced types of atherosclerotic lesions and a histo-
logical classification of atherosclerosis: A report from death penalty. The US Supreme Court ruled that
the Committee on Vascular Lesions of the Council on the punishment was excessive and thus prohibited
Arteriosclerosis, American Heart Association. Circula- by the eighth Amendment as cruel and unusual if
tion, 92, 1355–1374.
it is not “graduated and proportioned to the
offense.” An excessive judgment is judged by
current societal standards. Thus, society’s stan-
dards of decency, albeit subject to change, must
Atkins v. Virginia prove that they are influenced by “objective fac-
tors to the maximum possible extent.” Further-
Robert L. Heilbronner
more, it was ruled that mental retardation does
Chicago Neuropsychology Group, Chicago, IL, not preclude a person’s capability to discriminate
USA right from wrong, though mental retardation
does lead to a diminished capacities to process
and comprehend information, reduces communi-
Synonyms cation abilities, and decreases one’s ability to
learn from mistakes and experiences, reason log-
Mental retardation defense ically, inhibit impulses, and understand the emo-
tions and behaviors of others. The US Supreme
Court concluded that mentally retarded individ-
Historical Background uals are not exempt from criminal sanctions,
though a decrease in personal culpability is
Daryl Atkins and William Jones abducted Eric warranted. Thus, due to the conclusions that the
Nesbitt from a convenience store, and after find- purposes of retribution and deterrence are not
ing only $60 in his wallet, Atkins and Jones used accomplished in the execution of mentally
Nesbitt’s vehicle to drive to an ATM and forced retarded individuals, coupled with the increased
him to withdraw $200. Thereafter, Atkins and risk that the death penalty will be imposed erro-
Jones drove Nesbitt to an isolated location neously, the US Supreme Court ruled that the
where he was shot eight times and subsequently eighth Amendment precludes execution of men-
died. Atkins and Jones were quickly tracked tally retarded persons.
down by police, and in custody, it was deter- Despite the court’s ruling, in July of 2005, a
mined that Jones’ story claiming that Atkins Virginia jury determined that Atkins was intelli-
pulled the trigger was more coherent than gent enough to be executed due to the fact that
Atkins’ story implicating Jones as the shooter. another IQ score had been recorded at above 70.
Atomoxetine 385

Moreover, the prosecution claimed that his poor

performance in school was related to use of alco- Atomoxetine
hol and drugs and that earlier assessments of his A
IQ were “tainted.” Thus, Atkins was set to be Efrain Antonio Gonzalez
executed on 2 December 2005. However, the College of Psychology, Nova Southeastern
decision was recently reversed again by the Vir- University, Fort Lauderdale, FL, USA
ginia Supreme Court, as a result of state proce- Utah State University, Logan, UT, USA
dural grounds.

Generic Name
Current Knowledge
Atomoxetine
Forensic psychological and neuropsychological
assessments of mentally retarded individuals
being considered for the death penalty are highly Brand Name
important. Specifically, the US Supreme Court
did not specify the degree of mental retardation Strattera
required to circumvent the death penalty and
instead left such determinations up to the discre-
tion of the states. It is important to note that Class
subaverage intelligence alone does not warrant
a label of mental retardation. Impairments in ADHD agents
adaptive functioning and evidence of mental
retardation prior to the age of 18 years are
needed for a diagnostic determination of mental Proposed Mechanism(s) of Action
retardation.
Inhibits the presynaptic reuptake of norepineph-
rine and theoretically increases dopamine in the
prefrontal cortex via the same mechanism.
Cross-References

▶ Intellectual Disability Indication

▶ Intelligence
Attention deficit/hyperactivity disorder.

References and Readings

Off-Label Use
Atkins v. Virginia, 153 L. Ed 2d 335 (2002).
Cunnningham, M. D., & Goldstein, A. M. (2003). Sen-
tencing determinations in death penalty cases. In Treatment-resistant depression and anxiety.
A. Goldstein (Ed.), Forensic psychology (vol 11).
Handbook of psychology. Hoboken: Wiley.
Denney, R. L. (2005). Criminal responsibility and other
criminal forensic issues. In G. Larrabee (Ed.), Forensic Side Effects
neuropsychology: A scientific approach. New York:
Oxford University Press. Serious
Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C.
Increased cardiac rate, potential hypertension,
(2007). Psychological evaluations for the courts:
A handbook for mental health professionals and law- orthostatic hypotension, rare liver damage, poten-
yers (3rd ed.). New York: Guilford Press. tial for induction of mania, and suicidal ideation.
386 Atrophy

Common
Sedation in children, decreased appetite, dry
mouth, constipation, nausea, vomiting, dysmen-
orrhea, erectile dysfunction, and impaired libido.

References and Readings

Physicians’ Desk Reference (71st ed.). (2017). Montvale:

Thomson PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The
prescriber’s guide (2nd ed.). New York: Cambridge
University Press.

Additional Information
Drug Interaction Effects: http://www.drugs.com/drug_
interactions.html.
Drug Molecule Images: http://www.worldofmolecules.
com/drugs/.
Free Drug Online and PDA Software: www.epocrates.
com.
Free Drug Online and PDA Software: www.medscape.
com. Atrophy, Fig. 1 Displays diffuse atrophy of the cerebral
Gene-Based Estimate of Drug interactions: http:// hemispheres. Note the shrunken gyri and prominent, wid-
mhc.daytondcs.com:8080/cgibin/ddiD4?ver=4&task= ened sulci (Photo courtesy of Steven S. Chin, M.D., Ph.D.,
getDrugList. University of Utah Health Sciences Center)
Pill Identification: http://www.drugs.com/pill_identifica
tion.html.
occur as a result of trauma or cerebrovascular
lesions, for example. Generalized atrophy may
occur with neurodegenerative conditions such as
Atrophy Alzheimer’s disease. With atrophy, there is also
corresponding loss of neural connections (synap-
JoAnn Tschanz1,2 and Stephanie Behrens1 ses). Visual features of atrophy include sulcal wid-
1
Department of Psychology, Utah State ening, shrunken gyri, and enlarged ventricles.
University, Logan, UT, USA Atrophy may be viewed on gross inspection of
2
Center for Epidemiologic Studies, Utah State the brain post-mortem or antemortem with struc-
University, Logan, UT, USA tural imaging techniques such as MRI or CT scan.
Figure 1 displays diffuse brain atrophy of the cere-
bral hemispheres viewed from the top.
Synonyms

Degenerative; Wasting References and Readings

Smits, L. L., Tijms, B. M., Benedictus, M. R., Koedam, E.

L. G. E., Koene, T., Reuling, I. E. W., Barkhof, F.,
Definition Scheltens, P., Pijnenburg, Y. A. L., Wattjes, M. P., &
van der Flier, W. M. (2014). Regional atrophy is asso-
Atrophy is a loss of cells of any tissue. In the brain, ciated with impairment in distinct cognitive domains in
Alzheimer’s disease. Alzheimer’s & Dementia, 10,
atrophy refers to a loss of neurons that may be ge- S299–S305.
neralized (e.g., diffuse atrophy) or focal, reflecting
circumscribed regional loss. Focal atrophy may
Attendant Care 387

an attendant, and financial issues including

Attendant Care paying a competitive wage to personal atten-
dants (Rodriguez-Banister 2006). Funding A
Amy J. Armstrong sources of attendant care may include private
Department of Rehabilitation Counseling, resources, such as health insurance, auto insur-
Virginia Commonwealth University, Richmond, ance, and worker’s compensation, or public
VA, USA resources such as Medicaid, Department of
Vocational Rehabilitation, Department of Vet-
erans Affairs, crime victims compensation,
Definition and/or other state-funded programs.
Federal legislation provides regulations that
Attendant care involves the provision of ser- are relevant to attendant care services. For
vices to assist individuals with mental and/or example, The Home and Community-Based
physical disabilities in the performance and/or Services, as mandated by 1915 (i) and 1915
conduct of activities of daily living in order to (c), provides for long-term community-based
maximize community inclusion and indepen- services and state-wide waivers under the Med-
dent living. The intent of attendant care is to icaid program, focused upon an individual’s
promote independence, participation, sustain- right to live an independent life, within a com-
ability, and quality of life of the individual munity of choice. Subpart K, Part 441 of the
while also preventing or reducing the impact of Community First Choice Option, CMS-2337
medical problems. Typically, the individual F implements Section 2401 of the Affordable
receiving attendant services is unable to perform Care Act. Subpart K provides for the develop-
such tasks independently or may perform them ment of state plans to provide home and com-
with great difficulty. Attendant services include munity attendant services and supports.
but are not limited to activities such as bathing, Developing familiarity with relevant legisla-
dressing, feeding, toileting, transferring, mobil- tion on the federal and state levels as well as
ity, cooking, cleaning, and laundering. Services the policies and procedures of specific funders
may also relate to sustaining health such as of attendant care is necessary for those provid-
dispensing medications. However medical ing professional and family-based supports for
services typically are not provided by personel eligible individuals.
care attendants.
Attendant care may be provided by a family
member such as a spouse, partner, sibling, or
parent or by a hired employee. Typically, atten- Cross-References
dant care is provided by persons who have been
trained to provide the service/s within the home ▶ Assisted Living
and/or community. The independent living
model of attendant care contends that individ-
uals with disabilities should be empowered, to References and Readings
the highest degree possible, to recruit, screen,
and hire, train, and terminate their respective Federal Register. Medicaid Program; Community First
personal attendants, thereby ensuring self- Choice Program, Subpart K. https://www.federalregister.
determination and choice. Additional consider- gov/articles/2012/05/07/2012-10294/medicaid-program-
community-first-choice-option#h-57
ations related to the provision of attendant care
Rodriguez-Banister, K. (2006). The personal care atten-
include where and how to locate and access dant guide: The art of finding, keeping, or being one.
quality service providers, adequate training of New York: Demos Medical Publishing.
388 Attention

some things in order to deal effectively with

Attention others.
While written over 100 years ago, this descrip-
Ronald A. Cohen tion very succinctly captures essential aspects of
Department of Clinical and Health Psychology, the phenomena of attention, and remains apropos
College of Public Health and Health Professions, even today. The understanding of cognitive,
University of Florida, Gainesville, FL, USA behavioral, and neuropsychological bases, influ-
Center for Cognitive Aging and Memory, ences, and effects of attention have dramatically
McKnight Brain Institute, University of Florida, evolved since the time of William James. Yet, the
Gainesville, FL, USA underlying subjective and behavioral experi-
ences characterized by James and the other psy-
chologists of his time remain largely consistent
Synonyms with current phenomenology of attention. Differ-
ent types of attention were described, such as
Concentration; Focus; Vigilance directed, divided, focused, sustained, selective,
and volitional attention, many of which continue
to be used to describe the varieties of attentional
Definition experience. The primary limitation of these early
efforts was the lack of experimentation that
Cognitive processes that enable the selection of, would have enabled operationalizing of these
focus on, and sustained processing of information. constructs and understanding of the processes
The object of attention can either be environmen- underlying them.
tal stimuli actively being processed by sensory Following the initial efforts of early psycholo-
systems, or associative information and response gists to study attention from perspectives of struc-
alternatives generated by ongoing cognitive turalism and functionalism, a rather long period
activity. ensued dominated by behaviorism during which
cognitive processes, like attention, were largely
viewed as outside of the realm of empirical psy-
Historical Background chological inquiry. Attention was considered to be
a construct that could be explained by more basic
Attention is subjectively self-evident to all people, behavioral principles, such as discrimination
and terms that referred to attention-type experi- learning, cue dominance, anticipation, and expec-
ences have been described by philosophers tation. Classical conditioning theory provided an
through the ages. The concept of attention is essential framework for behavioral analysis of
strongly linked in the philosophy to the nature of attention, as the orienting response to novel stim-
consciousness, self-awareness, and most theories uli, and its subsequent habituation, provided the
of the “mind.” Accordingly, attention has been the behavioral and neural building blocks for simple
subject of psychological inquiry from the begin- forms of attention, in the absence of long-term
ning of this scientific discipline. The writings of memory formation (i.e., conditioning). The con-
William James captured this fact, as evident from cepts of motivation and drive which played a
this well-known excerpt from his Principles of major role in neobehaviorism, also helped to
Psychology (1898). bridge attention theory and learning principles.
Everyone knows what attention is. It is the Information theory (Shannon and Weaver
taking possession by the mind, in clear and vivid 1949), which evolved out of technological
form, of one out of what seem several simulta- advances in radio communication and also radar
neously possible objects or trains of thought. detection during World War II, was a major impe-
Focalization, concentration, of consciousness tus for the subsequent re-emergence of cognitive
are of its essence. It implies withdrawal from science. In particular, the application of
Attention 389

information processing models and signal detec- that followed, a number of variations on this
tion methods to the study of communication led to model of attention were proposed by other inves-
a resurgence of research interest in attention. This tigators working in the newly emerging field of A
is not surprising considering the fact that signal cognitive psychology.
detection and selection, the basic elements of Most notably, Treisman proposed an attenua-
almost all theories of selective attention, are also tion theory of attention, which was similar to
central to information and communication theory. Broadbent’s model in which he postulated a single
This approach emphasized the probabilistic nature process that occurred early in the information
of information detection and selectivity, a concep- processing stream, soon after sensory registration
tual departure from earlier psychophysical (Treisman and Gelade 1980). According to atten-
methods used to study perception. The application uation theory, selective attention requires
of information processing approaches to the study distinguishing between messages on the basis of
of attention was a logical step, as one of the their physical characteristics, such as location,
primary problems for any communication or intensity, and pitch, as well as content. In this
information processing system is reducing the model of attention, stimuli naturally differ in
total amount of incoming signal to manageable their threshold for activating awareness of a stim-
levels to enable subsequent processing of this ulus, and the process of attention effectively
information. decreases (i.e., attenuates) the strength (e.g., loud-
Broadbent (1958) proposed the first formal ness) of irrelevant stimuli. This attenuation pro-
model of selective attention based on the informa- cess was considered to occur in conjunction with a
tion processing theory. He maintained that atten- feature integration process that enabled perceptual
tion occurs because there is an information experience. This line of research was noteworthy
“bottleneck” as the large quantity of environmen- for the use of dichotic listening paradigms in
tal information that is available during parallel which attention is divided between the two ears,
processing is subject to channel capacity limita- and information must be selected from one of the
tions later in the stream of processing due to serial two channels of input.
processing constraints. Broadbent posited that the The bottleneck models proposed by Broadbent
primary requirement for attention to occur was a and Treisman proposed that selection occurs at a
filtering process (as shown in Fig. 1) that occurred very early stage of processing soon after sensory
soon after sensory registration and served to sep- registration, thereby linking attention squarely
arate relevant from irrelevant signals in order to with sensory selection. Essentially, selective
enable meaningful information to be available for attention filters inhibits focus on information
subsequent serial processing through limited occurring in the unattended ear in dichotic listen-
capacity information channels. This model pre- ing experiments before semantic analysis and
sumed a somewhat passive system by which this other cognitive processes have time to occur.
filtering occurred, with selection driven by the Other investigators (e.g., Deutsch and Deutsch
salience of the stimuli themselves. However, the (1963) argued that attention is strongly influenced
nature of this filtering process was not fully by the response demands of a situation and that it
operationalized in this initial model. In the years likely occurred at a later stage of processing, and

Sensory
Messages Filter Detector To memory
store

Attended
message

Attention, Fig. 1 Model depicting filtering process as proposed by Broadbent (1958)

390 Attention

that in reality both ears analyze incoming infor- demonstrate the costs associated with these atten-
mation semantically, though response demands tion shifts. His research also made a distinction
creates a bias toward one ear over the other. This between two primary processes, selection and
led to heated debates in the 1960s and 1970s over focus, that were necessary to account attention’s
the location of the bottleneck. While considerable intensity and spatial distribution.
experimental evidence indicated that early sen- Shiffrin and Schneider (1979) conducted sem-
sory selection occurs prior to a point in time inal studies that distinguished automatic from
when semantic information has been processed, controlled attention. They varied the number of
there is also other paradigms that demonstrate that targets to be detected and the consistency of target
in most situations selection is greatly influenced location based on either fixed or variable memory
by semantics and the response requirements that demands. By creating greater variability in task
exist. characteristics, subjects could not rely on memory
Subsequent researchers took this a step further to facilitate performance, which slowed their
by demonstrating that capacity limitations con- response time. Under these conditions, automatic-
strain attention and the intensity of attentional ity was no longer feasible. Besides demonstrating
focus that is possible at any given point in time. the distinction between automatic and controlled
Kahenman’s (1983) capacity theory of attention attention, these findings also illustrated the rela-
proposed that people’s capacity for attentional tionship between attention and memory, and set
focus is not static, but instead varies as a function the stage for a long line of research examining
of factors such as the reward characteristics of the working memory in relationship to attention.
task, arousal level, and other biological determi-
nants. This theory of attention was extremely
important in that it brought to the forefront the Neuropsychological Models and
fact that attention should not be conceptualized in Frameworks
purely mechanical terms as was the case in early
attention models based solely on information pro- Over the past two decades, research efforts have
cessing theory. Rather attention needed to be been directed at organizing these varieties of
viewed in the context of the biological factors attention into coherent frameworks. Furthermore,
that drive it. This helped to catalyze an emphasis researchers have proposed neuropsychological
on the study of focused attention, a shift that models of attention that seek to characterize the
coincided with information coming from psycho- functional neuroanatomic systems involved in
physiological studies that showed linkages attention, the processes for which these systems
between arousal, activation, and effort in the con- are responsible, and also how these functional
trol of attention (Pribram and McGuinness 1979). brain areas interact. The models described below
A large body of cognitive studies of attention are not meant to be an exhaustive review of the
followed this pioneering work. Several of these literature in this regard, but rather highlights some
are particularly important in a historical context. of the key elements of current theoretical frame-
Posner (1979) made an important distinction works and the extent to which there is consistency
between overt and covert shifts of attention that across models.
occur in the context of visual selective attention. Alan Mirsky provided one of the first neuro-
Overt attention is characterized by the act of inten- psychological frameworks to account for what he
tionally directing attention (i.e., looking) toward a described as the “elements” of attention. This
stimulus, whereas covert attention occurs without framework proposed five elements of attention:
intention when focus is drawn to a particular stim- (1) selection, (2) focus, (3) execute, (4) switch,
ulus or location, typically as a result of cues or and (5) sustain. This theoretical framework was
other types of information of which the person derived from factor analyses of neuropsychologi-
may have little conscious awareness. Posner also cal test results obtained from a large sample from
refined the use of chronometric methods to his clinical practice.
Attention 391

Sustained
attention
A

Sensory Sensory selection- Attentional Response selection-

Response
input focusing capacity control

Energetic Structural
factors factors

Attention, Fig. 2 Simplified neuropsychological model of the components of attention

Cohen (1993) proposed a similar component particular tasks may require minimal demands
process framework of attention that hypothesized for sustained attention, but intense demands on
four primary components of attention (Fig. 2): capacity and focus. Validation efforts directed at
(1) sensory selective attention; (2) response inten- this framework have shown the principal factors
tion, selection, and control; (3) capacity-focus; to be highly reliable, internally consistent, and
and (4) sustained attention. A primary goal of valid with respect to their weighting relative to
Cohen’s model was to include components specific brain disorders and conditions. For exam-
reflecting similar levels of analysis. The compo- ple, patients with attention-deficit disorder have
nents of this framework were also derived from greatest impairment on tasks requiring sustained
factor analysis of clinical neuropsychological data attention, whereas patients with diminished speed
with efforts made to retain only the minimum of processing have greatest problems on tasks
number of factors necessary to account for maxi- requiring capacity and focus. It is noteworthy
mum variance in the data, with an effort to make that the analyses conducted by both Mirsky and
conservative interpretation of the component pro- Cohen yielded very similar factor structures and
cesses associated with each factor. Each compo- validity data, providing strong evidence that four
nent was hypothesized to be a function of other to five primary components processes exist that
more basic subcomponent processes. This model account for most varieties of attention. These
posits that these four components of attention are attentional component processes are described in
not completely orthogonal or functionally inde- greater detail below.
pendent, but instead rather share common compo-
nent subprocesses, processes depending on the Selective Attention
task at hand. A simplified version of the model is A fundamental aspect of all attentional processes
shown. is that it is selective. Attention enables the selec-
In everyday situations, attention depends on tive deployment of cognitive resources for the
the interaction of all four of these component processing of information from either the external
processes. However, for some tasks, the primary environment or internal cognitive processes or
demand may be for sustained attention or vigi- associative representations. Attention also
lance, whereas for another task it may be efficient requires a shift from less salient information. Pro-
use of available attention capacity and the inten- cesses that enable or facilitate the selection of
sity of focus. Similarly, some tasks that are salient information for further cognitive pro-
weighted more demand for sensory selective cessing are collectively referred to as selective
attention, while others place greater demand on attention (Treisman 1969; Triesman and Geffen
response intention and selection. In other words, 1967). Individuals are constantly flooded with an
while these four components need to be accounted infinite number of signals from both outside and
for in explaining attention across all situations, within. By reducing the amount of information
392 Attention

that will receive additional processing, attention making an actual motor response, leading to
constrains incoming information to the individ- response bias, that is, the probability of selecting
ual’s available capacity at a given point in time, specific responses.
thereby keeping the level of information to be The attentional processes involved in
processed at a manageable level. While selective response selection and control are related to a
attention is necessary and beneficial for cognitive broader class of cognitive processes, commonly
function, there are costs associated with selec- referred to as executive functions (Fuster 1989;
tively attending. By attending to a particular Luria 1966). Several processes associated with
stimulus, the likelihood of detecting other poten- response generation underlie executive control:
tially relevant stimuli or choosing an alternative intention, selection, initiation, inhibition, facili-
response strategy is reduced. Optimal selective tation, and switching. Not only do these pro-
attention depends on the system being flexible cesses account for the control of simple motor
and adaptive, with the capacity to select and responses, they also provide the foundation for
focus on certain stimuli, but then to shift to more complex cognitive processes, such as plan-
other stimuli or cognitive processing when task ning, problem solving, and decision making, as
conditions change. Selective attention thereby well as conceptual processes such as categoriza-
serves as a gating mechanism for the flow of tion, organization, and abstraction. Executive
information processing and the control of control is strongly dependent on the actions of
behavior. prefrontal-subcortical systems. Executive con-
trol is dependent on the ability of the system to
Response Selection and Control act with intention, to initiate responding, to
Attention has traditionally been viewed as a pro- inhibit responding based on new information,
cess closely related to perceptual processing. It and to efficiently shift from one response alter-
prepares the individual for sensory intake, percep- native to another in accordance with changing
tual analysis, and integration with other cognitive environmental demands.
processes. Yet, there are many situations in which
attention is not directed at incoming sensory infor- Focused Attention and Capacity Limitations
mation, but rather selection response alternatives, Attention is also characterized by having intensity
and the control of responding once a selection has and by the extent to which it is allocated in either a
been made. Even when a task primarily requires focal or diffuse manner. The intensity of atten-
selective attention, there are usually coexisting tional focus is a function of both situational and
response demands. While sensory selection may task demands and organismic factors, such as
be automatically elicited by the occurrence of motivation and drive. Focused attention is
salient external stimuli, more often than not the constrained by capacity limitations (Kahneman
act of attending is linked to a planned, goal- 1973) that limit the intensity of focus that is pos-
directed course of action. In this regard, attention sible on a moment-by-moment basis. Attentional
and responding are directed to obtain information capacity is influenced by both structural and ener-
that will optimize behavior. getic factors (Cohen 1993). Energetic capacity
The processes associated with response selec- limitations tend to be state dependent and reflect
tion and control range from simple behavioral the changing energetic conditions of the brain,
orienting, such as turning one’s head in response including motivation, and the incentives to attend
to a sound source to more complex cognitive that are present in the situation. Structural factors
processes involving intention, planning, and deci- tend to be more stable and dependent on each
sion making. Response selection and control form person’s intrinsic information processing capac-
the basis for what humans typically experience as ity. Factors that influence structural capacity
volitional action. Before responding, individuals include the processing speed capacity that is a
generate a large number of response alternatives. function of the integrity of neural transmission,
These response alternatives are evaluated prior to memory encoding, storage and retrieval
Attention 393

limitations, and temporal-spatial processing response intention, selection, and control are not
dynamics that vary across people. Given these very amenable to automatic attentional pro-
factors that limit attentional capacity, focused cessing, as behavioral responding typically A
attention varies relative to the cognitive demands requires complex motor sequencing with execu-
and type of information to be processed, and sit- tive control demands. However, the fact people
uational incentive. Focused attention can occur are able to perform certain tasks such as typing or
relative to either sensory selective attention, or playing a musical instrument with considerable
intention and response selection, and in fact automaticity illustrates that automaticity is attain-
often involves the coordination of sensory and able for well-learned motor programs.
response selection. Such coordination is quite
effortful (Pribram and McGuinness 1975). Sustained Attention
Arousal and activation vary as a function of the Attention varies as a function of the temporal
existing demands for focused attention, with dynamics of the task to be performed and the
greater activation occurring when there is more situation, and all humans experience some degree
utilization of available capacity because of the of performance variability, particularly when long
need to focus. periods of sustained performance are required.
Sustained attention refers to processes that enable
Automatic Versus Controlled Attention the maintenance of performance over time. Com-
An important distinction exists between automatic pared to other cognitive processes, such as lan-
and controlled attentional processing (Schneider guage and visual perception, attention is
and Shiffrin 1977; Hasher and Zacks 1979). Auto- inherently variable by necessity, as it must be
maticity occurs most commonly in the context of responsive to changing stimulus conditions, task
sensory selective attention, particularly for tasks demands, and motivational and energetic states.
requiring simple detection of a target from a set of Problems with sustained attention commonly
stimuli, and also on tests of attention span. With occur on tasks requiring attentional persistence
automaticity, there is usually relatively little for long durations when there are high levels of
demand placed on attentional capacity, and often demand for effortful processing. All people have
attention can occur without much awareness or limits in their capacity for sustained attention.
subjective effort (e.g., attending to other cars Sitting in a 1-h lecture is not a problem for most
while driving on an empty highway). Automatic- bright college students, but even the brightest
ity can be interfered with increase in size and students would encounter tremendous difficulties
complexity of the environment to be attended sustaining their focus for a lecture that lasted
to. Spatial selective attention is particularly well 12 consecutive hours.
suited for automatic attentional processing since Vigilance refers to sustained attention directed
visual information typically occurs in parallel toward specific targets, in which a state of readiness
with a vast array of information reaching the is required to detect and respond to stimuli occur-
brain almost instantaneously. Automaticity is ring at variable and often infrequent intervals
more difficult to achieve for tasks that require (e.g., Colquhoun and Baddeley 1967; Corcoran
sequential cognitive operations, though some et al. 1977). Detecting rare targets with lengthy
degree of automaticity may be attainable through intervals between responses can be difficult. This
practice. Controlled attention is typically required type of sustained attention is quite common in
for tasks in which there are working memory everyday life. For example, a watchman may
demands, or other requirement of other cognitive spend the entire night attending to the possibility
processes, such as memory encoding and of an intruder without this event ever occurring.
retrieval, rapid processing speed, or executive Attention to low-frequency events has different
control. The demand for focused intensity varies processing requirements than responding to
as a function of requirements for controlled atten- high-frequency events and, for many people, is
tion that exist for a particular task. Generally, more difficult. Vigilance and sustained attention
394 Attention

are under the influence of sustained motivational occurs when impaired attention is directly associ-
level, boredom, and fatigue, which are sensitive ated with a particular type of cognitive operation,
to the dynamics of temporal tasks. such as spatial processing. These impairments are
often associated with focal brain disturbances
affecting specific cortical or subcortical systems
Current Clinical and Experimental necessary for the cognitive operation. Nonspecific
Evidence disturbances of attention are much more common,
often occurring due to disorders that affect
Neuropsychological Studies arousal, motivation, or other factors that reduce
Twenty years ago the clinical and experimental attentional capacity, and as a result of more dif-
neuropsychological literature on impairments of fused nonlocalized brain disorders. Both types of
attention associated with neurological and psy- attentional disturbance provide insights into the
chiatric disorders affecting the brain was quite cognitive processes of attention and the brain
limited. Much of the neuropsychological focus mechanisms that underlie these processes.
on attention was on the assessment of attention Though localized lesions provide the best vehicle
span in the context of psychometric analysis of for analysis of the role of specific brain structures
performance on tests such as digit span. This in attentional control, nonspecific attentional
probably reflected the fact that adequate atten- impairments illustrate the influence of metabolic
tion was once viewed more as a necessary con- and neurotransmitter abnormalities on informa-
dition for other cognitive functions to occur tion processing rate, arousal, and other energetic
optimally, but not particularly important in its and structural factors that may affect attentional
own right in considerations of brain-behavior capacity and focus. Attentional capacity is a direct
relationships. This attitude has changed dramat- function of level of consciousness, making this an
ically, and attention is now widely regarded as a essential part of the clinical assessment of atten-
critical cognitive process that reflects not only tion. Levels of consciousness range from normal
the interface between both the external environ- states of alertness and awareness to coma.
ment and internal cognitive functions, but also A brief summary of the attentional distur-
moment-by-moment information processing. bances associated with several common neuro-
A literature review conducted about two decades logical and psychiatric conditions is provided
ago revealed less than 500 studies focused on the below. For more detailed consideration see
neuropsychology of attention. Recent literature Cohen (1993).
reviews suggest that this number is now over
40, 000. This increase in interest in attention Stroke and Neglect Syndrome
reflects the fact that: (1) attention disturbances Unilateral stroke affecting the nondominant cor-
are one of the most common by-products of tex often causes hemi-neglect syndrome, perhaps
brain, (2) attention is closely tied to the human the most well known and dramatic form of atten-
experiences of consciousness, awareness, and tion disturbance. The defining feature of neglect
cognitive control, (3) major advances have syndrome is the failure to attend to, respond to,
occurred in the methodology for studying and or be aware of stimuli on one side of space.
assessing attention, and (4) for a number of Many variants of neglect syndrome may be
reasons, there has been an increased societal observed clinically. Most patients with neglect
interest in attention disturbances, perhaps in exhibit impairments of sensory selective atten-
part because of the intense information pro- tion, although some may have primary problems
cessing demands and pace of life that people with hemi-spatial response selection and con-
now experience. trol. Experimental investigations have con-
Impairments of attention may be either specific firmed the role of attention in hemi-neglect
or nonspecific. Specific impairments occur when syndrome. Manipulation of attentional parame-
only aspect of attention is affected. Often this ters demonstrates that symptoms of hemi-
Attention 395

neglect change as attentional demands are MS and is associated not only with motor effort
modified (Kaplan et al. 1990). Regardless of but also with attending to and performing cogni-
which attentional process is most affected, all tive tasks. Patients with MS experience difficulty A
patients with neglect syndrome have a funda- maintaining consistent effort on tasks.
mental disorder involving the spatial distribu-
tion and allocation of attention. HIV
Similar to MS, HIV-infected patients who have
Alzheimer’s and Neurodegenerative Dementias not developed severe AIDS dementia typically
Attention disturbance is usually not described as a show primary impairments in the areas of psycho-
primary feature of Alzheimer’s disease (AD) and motor and information processing speed, focused
historically tended to be viewed as one cognitive and sustained attention, and executive function-
function that was largely spared. This conclusion ing. This reflects the fact that when not adequately
is misleading. While patients with early-stage AD treated, HIV tended to initially have greatest
typically do not show overt symptoms of severe effects on subcortical systems, including the
inattention, they frequently have marked diffi- basal ganglia.
culty with focused attention and executive con-
trol, particularly when tasks required controlled Closed Head Injury
attentional processing. This reflects a distinction The most common effects of closed head trauma
between performance on tests of simple and com- are diffuse axonal damage due to shearing forces
plex attention, as conclusions about spared atten- and frontal lobe disturbances. Consequently,
tion in AD have often been based on the attention and executive dysfunction are among
observation of preserved attention span on tests the most common associated cognitive problems.
such as digit span. Patients with early AD are Persistent distractibility, poor concentration, apa-
often usually alert, energetic, and able to maintain thy, and fatigability are prominent sequelae. Def-
their general focus on the assessment process. Yet, icits of arousal and poor performance on measures
most will have considerable difficulty on tasks of selective, focused, divided and sustained atten-
requiring focused and divided attention, suppres- tion, processing speed, and executive functioning
sion of interference (e.g., Stroop), information tend to occur, which may contribute to associated
processing speed and efficiency (e.g., Symbol learning and memory retrieval problems as well.
Coding), and working memory. As the disease
progresses, performance becomes impaired on Epilepsy
most tasks requiring effortful attentional pro- Transient changes in the level and quality of con-
cessing. Pervasive disturbance eventually sciousness, common in seizure disorder, typically
develops affecting all aspects of attention, includ- cause marked alterations in attention around the
ing self-awareness. time of the seizure. During the time between sei-
zures, patients with epilepsy may have greater
Multiple Sclerosis problems than healthy individuals on tests of
Multiple sclerosis (MS), one of the most com- focused and divided attention. These deficits
mon neurologic in young adults, often affects appear to be related in part to slowed speed of
learning, memory, and executive control. Given processing and its effects on attentional capacity.
the fact that the disease affects the myelin of the Pharmacological effects associated with anticon-
white matter, deficits in these areas are often vulsant therapy likely contribute in part to these
strongly associated with attentional impairments attentional effects.
and slowed inefficient information processing.
Attentional capacity is typically reduced with Metabolic Disturbances
performance decrements usually evident under Factors that affect the metabolic function often
conditions of increased informational load. cause delirium, or more subtle alterations in
Fatigue is the most common of all symptoms in attention and arousal. Accordingly, metabolic
396 Attention

disturbance is one of the most common reasons pathophysiology, particularly in light of the fact
for transient alterations in attention among peo- that ADD tends to occur along with other comor-
ple without other neurological or psychiatric ill- bid conditions.
ness. Metabolic disturbances that affect the brain
can be the result of a wide variety of factors, Primate Studies
including drug effects and systemic illnesses, Understanding of the neural substrates of atten-
such as liver and kidney disease, and diabetes. tion was greatly enhanced by the use of neuro-
physiological methods in primates. The value of
Psychiatric Disorders these studies is that they provided directed record-
Difficulties with focused and sustained attention ing of electrical activity from brain areas impli-
are extremely common among patients with psy- cated in attention both by past clinical studies of
chiatric disorders, including affective disorders patients with neurological disorders and also abla-
(major depression and bipolar disturbance) and tion studies involving laboratory animals. In the
schizophrenia. Severe anxiety states can also 1970s, Robert Wurtz, Michael Goldberg and their
interfere with attention. A strong relationship colleagues (Wurtz et al. 1982) began electrophys-
exists between expenditure of effort and perfor- iological studies from the brain of monkeys
mance on tests of attention and other demanding trained on specific attention paradigms. The earli-
cognitive functions for patients with major est of these studies showed that the superior
affective disorders. Impairments tend to be colliculus exhibits increased firing rates during
somewhat proportional to severity of depres- visual attention, providing the first direct evidence
sion, with performance improving when the of the involvement of a neural area in this process.
depression resolves. Diminished attentional Subsequently, a large number of studies were
capacity is particularly evident on tasks that conducted that showed the contribution of other
require psychomotor speed, attentional focus, brain regions, particularly in posterior visual areas
and effortful demands for mental control. to specific aspects of visual selective attention.
Abnormal attention is also a central feature of This work both confirmed the role of areas like
schizophrenia, as filtering of irrelevant stimuli the inferior parietal cortex that had been suspected
and thoughts has long been considered to be a of being involved in visual selective attention
major element of the disorder, which has been based on studies of hemi-neglect syndrome.
linked to the dopamine system. Schizophrenics Over time, there has been increasing emphasis
often encounter difficulties on tests of sensory on the role of frontal brain systems in relationship
selective attention because of their susceptibility to these posterior brain areas. There is now a large
to distraction. Slowed reaction time and pro- body of research on this topic, supporting to gen-
cessing speed also contribute to problems with eral conclusions about selective attention:
attentional capacity, and both focused and (1) Visual selective attention is controlled by mul-
sustained attention (Nuechterlein 1977). tiple interacting brain areas that comprise a func-
tional system. (2) Selective attention involves not
Attention-Deficit Disorder (ADD) only posterior visual brain areas, but also frontal-
A developmental disorder of attention, ADD is striatal systems that provide executive response
the most widely recognized of all attention distur- control. Active investigation continues using pri-
bance. Problems with sustained attention and dis- mate models with particular emphasis on source
tractibility are key features of the disorder, along analysis of how particular types of neurons are
with hyperactivity among a subset of children. tuned to optimize attention to particular types of
While there is general agreement regarding the signals. This research has been instrumental in
existence of ADD, there continues to be consid- characterizing the functional brain systems
erable debate about its manifestations and governing attention in humans.
Attention 397

Functional Neuroimaging other cognitive domains. Therefore, pure tests of

Attention was one of the first cognitive functions attention do not exist, and attention usually must
to be demonstrated through the use of functional be assessed within the context of performance on A
imaging methods, such as functional MRI and tasks that load on one or more these other
PET. The fact that attentional parameters can be domains. Attentional performance is often
easily manipulated in the context of the scanner assessed as derived measure obtained by com-
and that attention reflects the moment-by- paring performance across tasks that control for
moment information processing of the brain key attentional parameters (e.g., target-distractor
makes it very conducive to study through func- ratio). Absolute performance often provides less
tional brain imaging. These efforts have largely informative measures of performance inconsis-
confirmed the involvement of inferior parietal tencies in the assessment of attention. For exam-
and frontal brain systems in attention, with stud- ple, how performance varies as a function of
ies showing the relative contribution of specific time, spatial characteristics, or memory load pro-
areas in selective, focused, and sustained atten- vides more information about attentional
tion. This is a rapidly growing area of neuropsy- dynamics than simply considering total errors
chological inquiry. To date, results of functional on a visual detection task. Since attention is not
neuroimaging experiments have largely the by-product of a unitary process, or a single
supported evidence from earlier cognitive, neu- sensory modality, it cannot be adequately
ropsychological, psychophysiological, and pri- assessed on the basis of findings from one spe-
mate studies with respect to the neural substrates cific test. For example, conclusions based on
of attention. digit span performance are misguided. Atten-
tional assessment requires a multifactorial
approach. The specific attention measures used
Clinical Assessment Considerations in an evaluation depends on the overall level of
functioning of the particular patient. For patients
Although an essential cognitive process, with global cognitive dysfunction, it may be
attention is more difficult to directly observe or difficult to use certain tasks that require overly
measure than other cognitive functions like lan- complex responses. For patients with relatively
guage, visual perception, or memory. Attention high overall cognitive abilities, tasks should be
fluctuates in accordance with changes in task chosen that require multiple component pro-
demands and the processing capacity of the cesses. If the patient is able to perform well on
patient over time. Unlike other cognitive func- these tasks, then severe attention disturbance
tions, performance may be quite different across involving specific attentional component pro-
different points in time, and it is this variability cesses can be ruled out. The Stroop and Trail-
that in fact defines attention. Attention is often Making tests are examples of tasks that require
situation specific. This accounts for why some multiple attentional processes. If impairments
children with ADD perform well in a controlled are found on such tasks, then more extensive
laboratory setting, despite reports of gross prob- testing of specific component processes can be
lems with inattention in school or the home. conducted. When possible, efforts should be
Unlike most other cognitive processes, atten- made to use tasks that incorporate signal detec-
tion primarily serves a facilitative function. tion methods, even when not evaluating sensory
Attention enhances or inhibits perception, mem- selective attention per se. This methodology pro-
ory, motor output, and executive functions, vides the best means of accurately summarizing
including problem solving. Yet, attention is performance relative to all types of possible
always measured as a function of performance errors, and easily integrates with response time
on tasks that also loads on one or more of these measures.
398 Attention

Attentional Parameters that Should be Cross-References

Considered A thorough assessment of attention
should be based on analysis of data from a com- ▶ Attention Deficit Hyperactivity Disorder
prehensive battery of attentional tests that sample ▶ Automaticity
underlying component processes (Cohen 1993). ▶ Consciousness
Accordingly, tasks should be used that are differ- ▶ Directed Attention
entially sensitive to the following attentional ▶ Divided Attention
parameters: (1) spatial characteristics, (2) temporal ▶ Effort
dynamics, (3) memory demands, (4) processing ▶ Focused Attention
speed requirements, (5) perceptual complexity, ▶ Habituation
(6) demands for response sequencing and control, ▶ Hemi-attention Syndrome
(7) cognitive complexity of the task, (8) effort ▶ Intention Tremors
required to complete task, and (9) task salience, ▶ Orienting Response
relevance, and reward value. ▶ Selective Attention Models
While multifactor neuropsychological assess- ▶ Sustained Attention
ment provides the best means of evaluating atten-
tional impairments, a comprehensive attentional
evaluation may not be feasible in everyday clin- References and Readings
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Mesulam, M. A. (1981). A cortical network for directed ADD; ADHD; ADHD, combined; ADHD, pre-
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Schneider, W., & Shiffrin, R. M. (1977). Controlled and Categorization
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I. Detection, search, and attention. Psychological
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Shannon, C. E., & Weaver, W. (1949). The mathematical dominantly inattentive (ADHD-I), predominantly
theory of communication. Urbana: The University of hyperactive/impulsive (ADHD-H/I), and com-
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bined (ADHD-C). ADHD-C is the most prevalent
Treisman, A., & Gelade, G. (1980). A feature-integration
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Watson, R. T., Heilman, K. M., Cauthen, J. C., & King, observed in preschool and early elementary
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400 Attention Deficit Hyperactivity Disorder

children age (although feelings of restlessness attention deficit disorder with and without
may persist), but inattentive symptoms remain hyperactivity.
relatively constant. ADHD can exist without other psychiatric dis-
Children with ADHD-H/I and ADHD-C are at orders in 20–30% of ADHD cases (Barkley 2014)
higher risk for disruptive behavior. Youth with but is more often associated with comorbidity.
ADHD-I is at higher risk for learning disorders, Oppositional defiant disorder (45–65%) is the
anxiety, and possibly depression. While some most common psychiatric comorbidity in
argue that ADHD-I is a distinct disorder from ADHD. As many as half of these oppositional
ADHD-C and ADHD-H/I, others have not found children will progress to conduct disorder such
consistent differences between the subtypes on as lying, stealing, fighting, and otherwise violat-
neuropsychological or laboratory measures. ing the rights of others. Major depressive disorder
Though diagnosed as a categorical disorder, (20–30%) and anxiety disorders (20–30%) are
ADHD may actually represent an extreme end also relatively common comorbid conditions in
along a normal continuum for the traits of atten- pediatric ADHD.
tion, inhibition, and the regulation of motor Longitudinal research following children with
activity. ADHD into adulthood suggests that approxi-
mately two-thirds of children with ADHD con-
tinue to show impairing symptoms as they age
Epidemiology (Faraone et al. 2006). The fact that some children
do not continue to have an ADHD diagnosis may
The population prevalence of ADHD is estimated be due in part to the finding that ADHD symptoms
to be 5% of school-age children and 2–4% of decline as a function of age in typically develop-
adults (Polanczyk et al. 2007). ADHD is a world- ing populations. However, it may also simply
wide disorder found in most countries with rates reflect that DSM symptoms and symptom thresh-
similar to those found in North America. ADHD olds may be developmentally inappropriate and
is more prevalent in males in childhood yet this too restrictive, respectively, to be applied outside
sex discrepancy wanes in adulthood. Differences of childhood. For example, DSM-5 inattentive
across ethnic groups within the North America are symptoms are more common in adolescents than
sometimes found but seem to be more a function DSM-5 hyperactive/impulsive symptoms. While
of social class than ethnicity. ADHD is heritable; this may infer that inattention persists more than
parents and siblings of individuals with ADHD hyperactivity/impulsivity, it may also simply
have between and five- and tenfold increased risk reflect the developmental insensitivity of the
of developing ADHD. Environmental risk factors DSM-5 symptoms.
associated with ADHD include prenatal maternal Genetics also appear to be a large factor in
smoking or alcohol use, low birth weight, and those who continue to demonstrate clinically sig-
exposure to environmental toxins. nificant ADHD post-childhood versus those
whose symptoms are in remission. For example,
prevalence rates of ADHD among the relatives of
Natural History, Prognostic Factors, and children with persistent ADHD are significantly
Outcomes higher than rates in relatives of children with
remitted ADHD. In addition, a history of major
The syndrome of attention difficulties, impulsive depressive disorder in childhood is a predictor of
behavior, and overactivity has been known since the syndromic persistence of ADHD into adoles-
the late 1700s and certainly since the early 1900s. cence, as is having a below average IQ.
Numerous attempts have been made at definition By definition, individuals with ADHD need to
and nomenclature, including Strauss syndrome, be functionally impaired in two or more domains
minimal brain dysfunction or damage, hyperki- of major life activities. In children, academic,
netic child syndrome (or hyperkinesis), and social, and family functioning domains are the
Attention Deficit Hyperactivity Disorder 401

most frequently impaired (MTA Collaborative laboratory tasks that assess vigilance, motoric
Group 1999). Educational impairments including inhibition, organization, planning, complex prob-
academic underachievement and learning disabil- lem solving, and verbal learning and memory. A
ities are well documented in the pediatric ADHD Both children and adults with ADHD perform
literature. less well on tasks that require vigilance, or the
In adolescents and young adults, academic ability to sustain attention.
impairments continue to persist; young adults Response inhibition has been hypothesized to
with ADHD completed fewer years of education, play a central role in ADHD. Continuous perfor-
with nearly one-fourth failing to complete high mance test (CPT) commission errors are a com-
school (Kuriyan et al. 2013). Compared to chil- mon laboratory measure of this construct. Unlike
dren with ADHD who are followed into adult- attention deficits which seem to emerge more
hood, clinically diagnosed adults with ADHD reliably in rare target CPTs like the Gordon Diag-
appear to have higher intellectual levels and nostic System (Gordon 1983), response inhibition
have done better academically (Barkley 2014). deficits emerge more reliably in higher signal
In addition to educational impairments, impair- probabilities such as the Conners CPT-3rd edition
ments in domains such as occupational, dating/ (Conners 2014). Several studies have reported
marital relations, financial management, driving, that adults with ADHD make more errors of com-
child-rearing, managing a household, and mission on high signal CPTs relative to both clin-
maintaining health are also consistently reported ical and community control participants.
in adults with ADHD. For example, employer Executive functioning deficits are present in
ratings are lower for adults with ADHD, and both pediatric and adult ADHD. Thus, it is sur-
adults with ADHD have more part-time employ- prising that performance on one of the most well-
ment and change jobs more often (Barkley established tests of executive functioning, the
et al. 2007). Wisconsin Card Sorting Test (WCST; Heaton
There are some data to suggest that ADHD is et al. 1993), is not impaired in adults with
more functionally impairing than most other out- ADHD. Multiple studies have failed to report a
patient psychiatric disorders in these domains. significant difference between adults with ADHD
While the relationship between ADHD symptoms and community controls on WCST categories
and impairment in children with ADHD is modest completed and number of errors, both persevera-
(r = 0.3), these relationships may be more robust tive and non-perseverative (see Hervey et al. 2004
in adults (r = 0.7) (Barkley et al. 2007). for a meta-analysis).
Verbal fluency is impaired in adult ADHD. The
most widely used verbal fluency task in adult
Neuropsychology and Psychology ADHD populations has been the Controlled Oral
of ADHD Word Association Test (Benton et al. 1983). Mul-
tiple studies have reported significant differences
A meta-analysis suggested that children with between community controls and adults
ADHD have an IQ about nine points lower than with ADHD.
typically developing peers (Frazier et al. 2004). Given the importance of attention and working
Similar data have been reported in adults with memory to memory encoding and storage, it is not
ADHD. Lower performance on the Wechsler Pro- surprising that adults with ADHD have been dem-
cessing Speed and Working Memory indices may onstrated to have memory deficits. They also
account for a substantial portion of the IQ differ- appear to have more difficulty managing audi-
ences noted between children/adults with ADHD tory/verbal information relative to visual informa-
and community controls. tion. Although differences emerge between adults
Controlled processing deficits are commonly with ADHD and community controls on the
observed in both pediatric and adult ADHD. Chil- WAIS-IV Digit Span, the effect size of the differ-
dren and adults with ADHD perform less well on ences is much larger on the California Verbal
402 Attention Deficit Hyperactivity Disorder

Learning Test-2nd edition (Delis et al. 2000). For checklists on which normative data are available.
example, adults with ADHD perform less well on These include “broadband” questionnaires, such
overall rates of learning, recall, recognition, and as the Behavioral Assessment System for
semantic clustering. The weaker performance on Children-3rd edition (Reynolds and Kamphaus
the semantic clustering index may indicate failure 2015) or Child Behavior Checklist (Achenbach
to adopt a strategy. and Rescorla 2001) for screening the major
Finally, both children and adults with ADHD dimensions of childhood psychopathology (e.g.,
demonstrate reward dysregulation. Individuals anxiety, depression, attention, hyperactivity,
with ADHD have decision-making impairments aggression, etc.). “Narrowband” questionnaires
related to a preference for immediate rather than specifically evaluate the symptoms of ADHD as
delayed rewards that are thought to be indepen- set forth in DSM-5. Rating scales can reliably,
dent of the deficits in cognitive control. validly, and efficiently measure DSM-5-based
ADHD symptoms. Some examples of instruments
demonstrating appropriate psychometric proper-
Evaluation ties with a strong normative base include the
ADHD Rating Scale-5th edition (DuPaul et al.
The American Academy of Child and Adolescent 2016) and the Conners Rating Scales-3rd edition
Psychiatry (Pliszka 2007) has established guide- (Conners 2008).
lines for the assessment and treatment of ADHD. The diagnostic process for adults is very simi-
No neurological, genetic, neuropsychological, or lar to the process for children and adolescents.
behavioral tests have sufficient positive and neg- Structured diagnostic interviews such as the Diag-
ative predictive power to accurately classify nostic Interview for Adult ADHD-2nd edition
ADHD cases with sufficient success to recom- (DIVA-2; Kooij and Francken 2010) along with
mend them for clinical diagnosis. Clinical diag- ADHD rating scales such as the World Health
nosis is based largely on careful history taking, Organization Adult ADHD Self-Report Scale
use of structured interviews containing DSM-5 (ASRS; Kessler et al. 2005) for patients and col-
criteria for ADHD and related disorders, and the lateral reporters (e.g., spouse) are commonly
expert knowledge of the clinician in the differen- utilized.
tial diagnosis among other mental disorders. Par- A number of specific tests have been devised to
amount in the evaluative process for children and provide objective measures of a subject’s vigi-
adolescents is the time to listen to parental and lance and impulse control, such as the Gordon
patient concerns; probe for details concerning Diagnostic System, Conners Continuous Perfor-
nature, onset, and course; elaborate the specific mance Test, or the Test of Variables of Attention
impairments resulting from these concerns; and (Greenberg 2015), among others. Research sug-
place them in the larger framework of the clinical gests that these tests are not especially accurate at
taxonomy of mental disorders. The clinical inter- classifying individuals as having ADHD; while
view is then supplemented with the use of parent the presence of abnormal scores on such tests
and teacher behavior rating scales to assess indicates the presence of a disorder in as many
developmental deviance of symptoms, screening as 90% of individuals who perform poorly, such
of intelligence and academic achievement skills scores cannot indicate the specific disorder pre-
by standardized testing, brief observation of the sent (Barkley and Grodzinsky 1994). Moreover,
child during unstructured and structured activi- the ecological validity of these tests is low thus
ties, contact with school personnel concerning precluding the ability to predict from the test
classroom functioning, and compilation of prior scores how the individual will function in more
school and mental health records available on the natural settings, such as home, school, and work.
child. These tests are therefore not recommended for
Other sources of information essential for the routine diagnostic evaluations for individuals
diagnostic process are behavioral rating scales or with ADHD, although they may be used in clinics
Attention Deficit Hyperactivity Disorder 403

specializing in ADHD as part of research or drug Atomoxetine is a nonstimulant approved for

trials. More useful information is likely to be management of ADHD. Atomoxetine is an
obtained from the clinical interview and the rating exclusive noradrenergic reuptake inhibitor A
scales discussed above. and is a Schedule II controlled substance with
low potential for abuse, making it more conve-
nient than the stimulants for prescribing.
Treatment Clonidine and guanfacine are alpha2-noradren-
ergic agonists that are FDA approved for
Treatment for ADHD in children typically treating ADHD and are more effective for the
involves three components: parent and child management of hyperactive-impulsive ADHD
education and support, classroom accommoda- symptomatology.
tions, and medication. Substantial evidence In adults, stimulant medications are effective in
exists to show that training parents in child approximately 70% of individuals with ADHD
behavior management skills can be of signifi- (Spencer et al. 1996). Atomoxetine is FDA
cant benefit in the reduction of parent-child approved and prescribed most often for adults
conflict and improvement in child success with ADHD and comorbid depression or for
within the home (MTA Collaborative Group those with a comorbid substance use disorder.
1999). The school setting frequently requires Managing psychiatric comorbidity is a signifi-
adjustment to meet the special needs of the cant component of pediatric ADHD. The same
child with ADHD. School interventions often dictum appears central to managing ADHD in
include alterations to the curriculum and work- adults. While “uncomplicated” ADHD exists in
load to better mesh with the limited attention, about 25% of the adults with ADHD, most adults
persistence, and disorganization of the child with ADHD have significant psychiatric comor-
with ADHD, increases in sources of positive bidity that requires clinical attention and manage-
reinforcement for work productivity, occa- ment. One aspect in which the psychiatric
sional use of immediate and systematic nega- comorbidity is evident in treatment strategies is
tive consequences for disruptive or pharmacotherapy. Although the evidence for the
inappropriate behavior, and implementation of efficacy of polypharmacy is limited at this time,
a daily school behavior report card (the ratings multiple researchers have asserted that poly-
on which are linked to a home token economy). pharmacy may be more likely in adult ADHD
The mainstay of treatment for many children than pediatric ADHD.
with ADHD is medication, frequently Similar to pediatric ADHD, a psychosocial
psychostimulants. Three classes of medication treatment component is typically recommended
appear to be useful for management of ADHD, in adult ADHD. What constitutes the psycho-
these being psychostimulants (methylphenidate, social component, however, appears to be
amphetamines), noradrenergic reuptake inhibitors somewhat different in adult ADHD relative to
(atomoxetine), and antihypertensive medications pediatric ADHD. For example, neither cogni-
(clonidine, guanfacine). tive behavioral therapy (CBT) nor cognitive
Stimulant medications, especially extended therapy has much research support in pediatric
release formulations, are a frontline management ADHD. Nonetheless, there are some data to
strategy in pediatric ADHD; approximately 70% suggest that CBT may be more efficacious in
of children with ADHD will show an efficacious adolescents and adults with ADHD (Antshel
response to stimulant medications (Spencer et al. et al. 2014; Boyer et al. 2015; Safren et al.
1996). The side effects of stimulants are fairly 2010; Solanto et al. 2010). For example, in the
benign, short-lived, dose related, and often man- adult ADHD literature, there is some evidence
aged through dose or timing adjustments or by that CBT is efficacious for reducing functional
switching to a different delivery system or impairments in adults concurrently treated with
stimulant. stimulants.
404 Attention Deficit Hyperactivity Disorder

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(2000). California verbal learning test – second edi-
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Barkley, R. A. (2014). Attention deficit hyperactivity dis- Waschbusch, D. A., Gnagy, E. M., Sibley, M. H.,
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Barkley, R. A., & Grodzinsky, G. M. (1994). Are tests of tional outcomes of children diagnosed with ADHD.
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Attention Network Test (ANT) 405

analysis. American Journal of Psychiatry, 164, associated with superior parietal, right frontal, and
942–948. thalamic brain regions and the norepinephrine
Reynolds, C., & Kamphaus, R. (2015). Behavior assess-
ment system for children, third edition (BASC-3). San neurotransmitter system. A
Antonio: Pearson. The orienting system is responsible for
Safren, S. A., Sprich, S., Mimiaga, M. J., Surman, C., selecting and giving preference to specific sensory
Knouse, L., Groves, M., & Otto, M. W. (2010). Cog- information, often in terms of spatial location.
nitive behavioral therapy vs relaxation with educational
support for medication-treated adults with ADHD and Attentional orienting in space may be done
persistent symptoms: A randomized controlled trial. overtly by, for example, moving the head or
Journal of the American Medical Association, 304, covertly, that is, without moving the eyes or
875–880. head. For example, a football player might look
Solanto, M. V., Marks, D. J., Wasserstein, J., Mitchell, K.,
Abikoff, H., Alvir, J. M., & Kofman, M. D. (2010). down the field with his eyes while attending
Efficacy of meta-cognitive therapy for adult ADHD. covertly to the location and movements of other
American Journal of Psychiatry, 167, 958–968. players in his peripheral vision. Attended items
Spencer, T., Biederman, J., Wilens, T., Harding, M., are generally processed faster and more accurately
O’Donnell, D., & Griffin, S. (1996). Pharmacotherapy
of attention-deficit hyperactivity disorder across the life than nonattended items. Brain areas that have
cycle. Journal of the American Academy of Child and been linked to the orienting system include areas
Adolescent Psychiatry, 35, 409–432. of the parietal cortex and the frontal eye fields, and
Wilcutt, E. (2012). The prevalence of DSM-IV attention- the cholinergic neurotransmitter system appears
deficit/hyperactivity disorder: A meta-analytic review.
Neurotherapeutics, 9, 490–499. to play an important role.
The executive attention system is involved in
monitoring one’s performance in the context of
current task demands and providing control sig-
nals that help other systems adapt to changing
Attention Network Test (ANT) contexts and conflicting information. Executive
attention is especially important for detecting
Michael S. Worden and responding to situations in which there is
Department of Neuroscience, Brown University, stimulus-response conflict. Such conflict arises
Providence, RI, USA when two or more stimuli or two or more aspects
of the same stimulus are associated with different
behavioral responses. A common example is the
Attention is often subdivided by researchers into a Stroop task in which subjects are presented with
number of separate systems. Although there is printed words, and they must name the color of the
certainly some interaction between them, these ink in which the word is printed (e.g., red ink)
systems play different roles in terms of their effect when the word itself spells out a different color
on information processing and the control of (e.g., BLUE). Brain areas implicated in the exec-
behavior. Further, there is evidence that different utive attention system include frontal midline
attentional systems are associated with different, regions such as the anterior cingulate cortex and
largely nonoverlapping brain regions and rely to a the lateral prefrontal cortex. The neurotransmitter
large extent on different neurotransmitter systems. dopamine is important in the functioning of this
One such framework advanced by Michael Posner network.
and colleagues defines three separate attention The attention network task (ANT) was devel-
systems or networks: alerting, orienting, and oped by Jin Fan, Michael Posner, and colleagues
executive control. at the Sackler Institute for Developmental Psycho-
The alerting system is responsible for helping biology. Using subtractive methodology, the ANT
the organism reach and maintain an alert state. is designed to assess each of these three atten-
This state, which is separate from arousal, is char- tional networks using a single reaction-time para-
acterized by a readiness to perceive and process digm. The fundamental task of the participant is
incoming stimuli. The alerting system has been simple. On each trial, the participant looks at a
406 Attention Network Test (ANT)

small fixation cross in the center of a computer which the orienting system could take advan-
screen and a small arrow, called the target, is tage of the predictive cues to orient to a specific
briefly displayed either above or below the fixa- spatial location. In the case of the non-orienting
tion. The participant is required to respond by cues, the participant could not predict whether
pressing one of two buttons as quickly and accu- the target would appear above or below the
rately as possible indicating whether the arrow is fixation point and therefore could not improve
pointing to the left or right. On some presenta- performance by orienting to one or the other
tions, the target is preceded by a briefly presented spatial location. An efficiency score is derived
cue stimulus while on other trials it is presented for the executive attention system by comparing
with no advanced warning. These cues are either scores on trials with congruent flankers to trials
predictive or non-predictive. Orienting cues are with incongruent flankers. Subjects will tend
presented either above or below the central fixa- to be slower and less accurate for incongruent
tion and indicate the location at which the upcom- trials than for congruent trials, and the size of
ing arrow will be shown. Non-orienting cues are these differences indicates the extent to which
presented either at the center of the screen or else the individual is able to suppress conflicting
both above and below fixation simultaneously. response tendencies.
Both types of cues indicate that the target is A number of intriguing findings have come
about to appear but only orienting cues provide from studies that have utilized the ANT.
information regarding the location of the Supporting the notion that the three attention net-
impending target. Finally, in some cases, the tar- works assessed by the ANT constitute indepen-
get arrow is flanked on either side by other stimuli. dent systems, a large-scale study of over
These flanking stimuli may be arrows pointing in 200 individuals found that there was very little
the same direction as the target (called congruent correlation in efficiency scores among the three
trials) or they may be arrows pointing in the oppo- networks. In other words, the particular score of
site direction as the target (called incongruent an individual on any one of the three attention
trials). networks does not tend to predict the individual’s
The efficiency of the three attention networks scores on the other two networks. A high effi-
may be assessed independently for each partici- ciency score for the alerting network, for example,
pant by use of the subtractive method. Both reac- does not suggest what one’s scores are likely to be
tion time and accuracy may be examined. To for either the orienting or executive attention net-
assess the alerting network, scores from trials in works. Using electroencephalographic (EEG)
which no cue was presented are compared to recordings from the surface of the scalp, it was
scores from trials in which there was a cue pre- found that each of these three attention systems is
sented. The difference in mean reaction times associated with distinct patterns of neural oscilla-
between these two trial types constitutes an effi- tions. A number of variations on the original ANT
ciency score for the alerting network and is indic- have been developed to address specific questions
ative of the extent to which the alerting network and for the study of special populations. For
was able to use the information provided by the example, child-friendly versions of the ANT that
cue to improve behavioral performance. In a use cartoon pictures of fish instead of arrows have
similar manner, an efficiency score for the been used to study the development of attention
orienting network may be derived by sub- systems.
tracting mean scores from trials with orienting Attentional deficits are a hallmark of many
cues from the scores for trials with non- psychiatric and neurological disorders. The ANT
orienting cues. Both of these trial types include has been used to assess the relative impact of
a cue so there should be no difference in terms of many disorders on the different attention systems
a contribution from the alerting network. The and to help distinguish between or establish sub-
difference in scores measures the degree to types of particular disorders. Among others,
Attention Training 407

variations on the ANT have proven useful in the Current Knowledge

study of attention deficit hyperactivity disorder,
Alzheimer’s disease, autism, borderline personal- The aspects of attention that are trained vary A
ity disorder, traumatic brain injury, substance widely among interventions and frequently
abuse, and schizophrenia. depend upon a theoretical model of attention.
Attention models, regardless of their operational
framework, appear to include functions related to
References and Readings sustaining attention over time (vigilance), capac-
ity for information, shifting attention, speed of
Fan, J., McCandliss, B. D., Sommer, T., Raz, A., & Posner, processing, and screening out distractions. Some
M. I. (2002). Testing the efficiency and independence attention efficacy studies evaluate attention inter-
of attentional networks. Journal of Cognitive Neurosci-
ence, 14(3), 340–347.
ventions that focus on particular attention compo-
Fan, J., McCandliss, B. D., Fossella, J., Flombaum, J. I., & nents such as reaction time and sustained attention
Posner, M. I. (2005). The activation of attentional net- for visual information (e.g., Ponsford and Kinsella
works. NeuroImage, 26(2), 471–479. 1988). Other efficacy studies use attention train-
http://www.sacklerinstitute.org/users/jin.fan/
Posner, M. I., & Rothbart, M. K. (2007). Research on
ing programs that include hierarchical tasks to
attention networks as a model for the integration of address a continuum of attention components
psychological science. Annual Review of Psychology, from basic sustained attention to more complex
58, 1–23. mental control (e.g., Park et al. 1999; Sohlberg
et al. 2001).
Evidence supports the effectiveness of atten-
tion training beyond the effects of nonspecific
Attention Training cognitive stimulation for patients with traumatic
brain injury or stroke during the postacute phase
McKay Moore Sohlberg of recovery and rehabilitation (Butler et al.
Communication Disorders and Sciences, 2008; Cicerone et al. 2000), and preliminary
University of Oregon, Eugene, OR, USA evidence suggests attention training helps alle-
viate symptoms in psychiatric disorders such as
schizophrenia (e.g., Knowles et al. 2016).
Synonyms Recent studies have sought to investigate under-
lying changes in neural processes following
Attention process training; Direct attention train- attention training (e.g., Hopfinger 2017).
ing; Process training Evidence-based practice guidelines for attention
training were generated from examination of the
intervention research literature (Sohlberg et al.
Definition 2003). Analysis of nine Class I and Class II
studies suggested that certain aspects of atten-
Attention training is based on the premise that tion training are helpful in improving attention
attentional abilities can be improved by activat- performance in some adults with traumatic brain
ing particular aspects of attention through a injury. Treatment parameters found to influence
stimulus drill approach. The repeated stimula- positive outcomes included high frequency
tion of attentional systems via graded attention of attention training, combining attention
exercises is hypothesized to facilitate changes in training with metacognitive training (e.g., self-
attentional functioning. Most attention training monitoring and strategy training), and individu-
programs assume that aspects of cognition can alizing training to match the client's attention
be isolated and discretely targeted with training profile. The effects of attention training may be
exercises. relatively small or task-specific, and the research
408 Attentional Blink

encourages clinicians to actively facilitate and

monitor the impact of attention training on func- Attentional Blink
tional, everyday activities.
Eric S. Porges
Department of Clinical and Health Psychology,
Cross-References University of Florida, Gainesville, FL, USA
Center for Cognitive Aging and Memory,
▶ Attention McKnight Brain Institute, University of Florida,
▶ Neuropsychological Rehabilitation Gainesville, FL, USA
▶ Plasticity Department of Neurology, University of Florida,
▶ Process Training Gainesville, FL, USA

References and Readings Definition

Butler, R. W., Copeland, D. R., Fairclough, D. L., Mulhern, Attentional blink (AB) is a phenomenon primarily
R. K., Katz, E. R., Kazak, A. E., et al. (2008).
reported in the visual domain (Horváth and
A multicenter, randomized clinical trial of a cognitive
remediation program for childhood survivors of a pedi- Burgyán 2011), in which attention to a primary
atric malignancy. Journal of Consulting and Clinical target results in a reduced likelihood of identifying
Psychology, 76(3), 367–378. a secondary target presented a short duration after.
Cicerone, K. D., Dahlberg, C., Kamar, K., Langenbahn,
The effect is most pronounced in a 200–600 ms
D. M., Malec, J. F., Bergquist, T. F., et al. (2000).
Evidence-based cognitive rehabilitation: Recommen- window after the initial target is presented
dations for clinical practice. Archives of Physical Med- (Nieuwenstein et al. 2009). The classic paradigm
icine & Rehabilitation, 81, 316–321. involves the rapid serial visual presentation
Galbiati, S., Recla, M., & Pastore, V. (2009). Attention
remediation following traumatic brain injury in child-
(RSVP) of letters, with a primary target letter
hood and adolescence. Neuropsychology, 23(1), and secondary target letter embedded within the
40–49. RSVP. When the secondary target in the RSVP
Hopfinger, J. (2017). Introduction to special issue: appears during the AB window, the likelihood of
Attention and plasticity. Cognitive Neuroscience, 8,
successful identification is dramatically reduced.
69–71.
Knowles, M., Foden, P., El-Deredy, W., & Wells, If the secondary target is presented outside the
A. (2016). A systematic review of efficacy of the 200–600 ms window, a deficit in identification
attention training technique in clinical and non- does not occur. The initial reports of the AB
clinical samples. Journal of Clinical Psychology, 72,
reported that the effect depended on the inclusion
999–1025.
Park, N. W., & Ingles, J. L. (2001). Effectiveness of atten- of distractor letters in the RSVP (Raymond et al.
tion rehabilitation after acquired brain injury: A meta- 1992), though more recent reports have suggested
analysis. Neuropsychology, 15, 199–210. that this may not be the case (Visser 2007). Mech-
Park, N. W., Proulx, G., & Towers, W. M. (1999). Evalu-
anistically, the AB is thought to reflect a constraint
ation of the attention process training programme. Neu-
ropsychological Rehabilitation, 9, 135–154. in the ability of the nervous system to deploy
Sohlberg, M. M., McLaughlin, K. A., Pavese, A., selective attention (Dux and Marois 2009) and
Heidrich, A., & Posner, M. (2001). Evaluation of not to be constrained by sensory limitations.
attention process training and brain injury education
in persons with acquired brain injury. Journal of
Clinical and Experimental Neuropsychology, 22,
656–676. References and Readings
Sohlberg, M. M., Avery, J., Kennedy, M., Ylvisaker, M.,
Coelho, C., Turkstra, L., & Yorkston, K. (2003). Dux, P. E., & Marois, R. (2009). The attentional blink:
Practice guidelines for direct attention training. A review of data and theory. Attention, Perception &
Journal of Medical Speech Language Pathology, Psychophysics, 71(8), 1683–1700. https://doi.org/
11(3), 19–39. 10.3758/APP.71.8.1683.
Attentional Response Bias 409

Horváth, J., & Burgyán, A. (2011). Distraction and the affected by sensitivity of the perceptual system to
auditory attentional blink. Attention, Perception, & certain stimuli in the environment but also to an
Psychophysics, 73(3), 695–701. https://doi.org/
10.3758/s13414-010-0077-3. inclination to respond in one manner versus A
Nieuwenstein, M. R., Potter, M. C., & Theeuwes, J. (2009). another to these stimuli. Response bias is a pri-
Unmasking the attentional blink. Journal of Experi- mary element of signal detection theory, which
mental Psychology. Human Perception and Perfor- maintains that signal detection, and more broadly
mance, 35(1), 159–169. https://doi.org/10.1037/0096-
1523.35.1.159. the accuracy of attention to target stimuli, is not
Raymond, J. E., Shapiro, K. L., & Arnell, K. M. (1992). only a function of discriminability (d0 ) associated
Temporary suppression of visual processing in an with perceptual sensitivity but also the tendency
RSVP task: an attentional blink? Journal of Experimen- to either respond or not respond in the situation
tal Psychology. Human Perception and Performance,
18(3), 849–860. Retrieved from http://www.ncbi.nlm. (Beta). Response bias may be determined by
nih.gov/pubmed/1500880. various factors related to a given person’s behav-
Visser, T. A. W. (2007). Masking T1 difficulty: Processing ioral disposition, including their tendency to be
time and the attentional blink. Journal of Experimental accepting of errors of one type or another.
Psychology: Human Perception and Performance, 33(2),
285–297. https://doi.org/10.1037/0096-1523.33.2.285. A person who is inclined to never make an incor-
rect response will tend to miss targets while
attending, but will have few false-positive errors
of responding when a response was not called for.
Attentional Response Bias Conversely, a person with a response bias of never
missing a target will tend to miss fewer targets, but
Ronald A. Cohen will make many more false positive responses.
Department of Clinical and Health Psychology, While overall stimulus detection accuracy (d0 ) is
College of Public Health and Health Professions, largely a function of perceptual and attentional
University of Florida, Gainesville, FL, USA selection processes that occur quite early after
Center for Cognitive Aging and Memory, initial sensory registration, attentional response
McKnight Brain Institute, University of Florida, bias can be influenced by factors occurring at
Gainesville, FL, USA various stages of cognitive processing, including
the response demands inherent in the situation.
Response bias can be altered by changing physi-
Synonyms ological (e.g., wakefulness) and psychological-
emotional state, incentives, and a variety of other
Behavioral predisposition; Beta (b); Response factors. The fact that response bias plays an
tendency important role in signal detection and sensory
selection more broadly provides evidence for the
involvement of attentional processes in addition
Definition to sensory registration and perception. This is
reinforced by the fact that response biases play a
Attentional response bias refers to the tendency or major role when sustained attention and vigilance
increased likelihood of selecting one response are required over time, with this bias subject to
over others. change under conditions of fatigue. The concept
of response bias has its roots in statistical theory,
specifically the distinction between type I and II
Summary errors. When assessing attention in a clinical con-
text, it is essential that both discriminability and
The concept of response bias is essential when response bias be determined in order to fully assess
considering or assessing attention, as it accounts the performance characteristics. Tasks designed to
for the fact that attentional selection is not only assess sustained attention, such as continuous
410 Attorney

performance tests, usually provide measures of

response bias as a way of fully measuring and Attorney
characterizing error types associated with attention
disturbances. Brain disorders that impair frontal Moira C. Dux
lobe function often affect response bias with US Department of Veteran Affairs, Baltimore,
greater propensity to false-positive errors reflecting MD, USA
impulsivity. However, disturbances of intention
associated damage to the frontal cortex and other
brain regions can cause reductions in spontaneous
behavior and behavioral inertia, which would tend Definition
to increase the likelihood of missing targets during
attention tasks. This response tendency is also com- An attorney is defined as one who is legally
mon with psychiatric disorders, most notably appointed on another’s behalf. An attorney-at-
major depression. There has been a recent surge law is an individual who has achieved the nec-
in therapeutic approaches aimed at modifying essary educational requirements (J.D.) and is
attentional response bias. Malingering is often licensed to practice law by the highest court of
assessed by determining if there are extreme a state or some other forms of jurisdiction. In
response biases that fall outside the range of dis- civil cases (e.g., personal injury, medical mal-
turbances observed in patients with neurological or practice), there are plaintiff and defense attor-
psychiatric disorders. neys. The plaintiff attorney represents the
injured party (e.g., plaintiff) in an action
against the party they allege to be responsible
Cross-References for the damages; the defense attorney repre-
sents the defendant (e.g., insurance company,
▶ Attention hospital, and doctor). In criminal matters, there
▶ Continuous Performance Tests are prosecution and defense attorneys. The
▶ Malingering prosecuting attorney represents the party (e.g.,
▶ Signal Detection Theory federal, state, or local government) who has
accused and wants to convict the offender of
some type of criminal action (e.g., murder,
References and Readings assault). The defense attorney represents the
party (e.g., defendant) who has been accused
Cohen, R. A. (2014). Neuropsychology of attention of committing the crime.
(2nd ed.). New York: Plenum Publishing.
Green, D. M., & Swets, J. A. (1989). Signal detection theory
and psychophysics. Los Altos: Peninsula Publishing.
Heeren, A., De Raedt, R., & Koster, E. H. W. (2013). The
(neuro) cognitive mechanisms behind attention bias Cross-References
modification in anxiety: Proposals based on theoretical
accounts of attentional bias. Frontiers in Human Neu-
▶ Litigation
roscience. Lausanne. journal.frontiersin.org
Heilbronner, R. L., Sweet, J. J., & Morgan, J. E. (2009).
American Academy of Clinical Neuropsychology con-
sensus conference statement on the neuropsychological
assessment of effort, response bias, and malingering.
The clinical neuropsychologist. New York: Taylor and References and Readings
Francis.
Newman, D. P., O’Connell, R. G., & Bellgrove, M. A. Larrabee, G. (2005). Forensic neuropsychology:
(2013). Linking time-on-task, spatial bias and hemi- A scientific approach. New York: Oxford University
spheric activation asymmetry: A neural correlate of Press.
rightward attention drift. Neuropsychologia: Elsevier: Stern, B. H., & Brown, J. (2007). Litigating brain injuries.
Amsterdam. New York: Thomson Reuters.
Auditory Agnosia 411

Rorke, L. B., & Biegel, J. A. (2000). Atypical teratoid/

Atypical Teratoid/Rhabdoid rhabdoid tumour. In P. Kleihues & W. K. Cavenee
(Eds.), World health organization classification of
Tumor (AT/RT) tumours. Pathology & genetics. Tumours of the ner- A
vous system (pp. 145–148). Lyons: IARC Press.
Jennifer Tinker Rorke, L. B., Packer, R. J., & Biegel, J. A. (1996). Central
Department of Neurology, Thomas Jefferson nervous system atypical teratoid/rhabdoid tumors of
infancy and childhood: Definition of an entity. Journal
University, Philadelphia, PA, USA of Neurosurgery, 85, 56–65.
Torchia, J., et al. (2015). Molecular subgroups of atypical
teratoid rhabdoid tumours in children: An integrated
Definition genomic and clinicopathological analysis. Lancet
Oncology, 16(5), 569–582.

Atypical teratoid/rhabdoid tumor (AT/RT) is a rare,

highly malignant tumor of early childhood, most
commonly diagnosed in infants who are less than
3 years. First described by Rorke and colleagues in Auditory Agnosia
1987, the AT/RT received its designation because
of its complex histological components. Prognosis John E. Mendoza
is extremely poor with a median survival of 6–- Department of Psychiatry and Neuroscience,
11 months. Factors associated with improved prog- Tulane Medical School and SE Louisiana
nosis include supratentorial location, localized Veterans Healthcare System,
disease at the time of presentation, and complete New Orleans, LA, USA
resection (Torchia et al. 2015). Over half of AT/RTs
identified are located within the posterior fossa
(brainstem, cerebellum, and predominantly the Synonyms
cerebellopontine angle) (Rorke et al. 1996).
Roughly one-fourth are supratentorial and 8% Auditory-sound agnosia; Auditory-verbal agnosia;
may be multifocal. Clinical presentation varies Pure word deafness
largely by tumor location and size. Infants, in par-
ticular, may present with nonspecific symptoms,
including lethargy, vomiting, and failure to thrive. Definition
Older children (>3 years of age) may demonstrate
more specific problems, including head tilt, diplo- Rare condition in which sounds, although heard,
pia, cranial nerve palsy, headache, and hemiplegia are not properly interpreted and thus have little or
(Rorke and Biegel 2000). Often histologically con- no meaning for the patient.
fused with PNET/medulloblastoma.

Current Knowledge

Cross-References When present, auditory agnosia is usually pri-

marily limited to impaired recognition of either
▶ Medulloblastoma language sounds or nonlanguage (environmental)
▶ Primitive Neuroectodermal Tumor sounds. The former is known as auditory-verbal
agnosia or pure word deafness. No commonly
used term is applied to the latter. In either
References and Readings condition, appreciation of certain aspects of
musical sounds might also be compromised
Lefkowitz, I. B., Rorke, L. B., & Packer, R. J. (1987). (amusia). For this syndrome to be diagnosed,
Atypical teratoid tumor of infancy: Definition of an
entity. Annals of Neurology, 22, 56–65. other higher-order deficits that might more readily
412 Auditory Comprehension

explain the deficit (such as aphasic disorder) Cross-References

should be ruled out. In auditory-verbal agnosia,
there is impairment of one’s ability to process, ▶ Agnosia
interpret, or comprehend speech sounds or spoken ▶ Amusia
language. Patients may report that it is like hearing ▶ Disconnection Syndrome
someone speaking in a foreign language. Read-
ing, writing, and speaking are intact, although
speaking may be slightly problematic due to the References and Readings
distortions in auditory feedback heard as speech is
attempted. In auditory-verbal agnosia (pure word Bauer, R. M., & Demery, J. A. (2003). Agnosia. In K. Heilman
& E. Valenstein (Eds.), Clinical neuropsychology (4th
deafness), the ability to match nonspeech or
ed., pp. 236–295). New York: Oxford University Press.
“environmental” sounds (e.g., a barking dog, the Slevc, L., & Shell, A. (2015). Auditory agnosia. In
ringing of a bell, or a train whistle) to M. Aminoff, F. Boller, & D. Swaab (Eds.), Handbook
corresponding pictures may remain intact. Con- of clinical neurology (Vol. 129, pp. 573–587).
versely, one may have difficulties identifying or
matching nonspeech sounds, while retaining the
ability to process and interpret spoken language.
Some degree of impairment in one’s ability to rec- Auditory Comprehension
ognize musical sounds is commonly, but not invari-
ably, present in these disorders. Select patients may Kelly Knollman-Porter
have difficulty recognizing familiar tunes or melo- Department of Speech Pathology and Audiology,
dies, while retaining their ability to produce them Miami University, Oxford, OH, USA
spontaneously. Others may be impaired at matching
tones, rhythms, or timbre, for example, identifying
the sound of a particular musical instrument. Definition
Auditory agnosia is thought to result from
either (1) unilateral or bilateral lesions of the The ability to decode and understand spoken lan-
unimodal (secondary) auditory association cortex guage at the word (e.g., Stop!), sentence (e.g., Turn
in the middle portions of the superior temporal left at the next intersection), and discourse (e.g.,
gyrus and/or (2) a disconnection syndrome in- conversation) levels. Linguistic factors influencing
volving the primary auditory cortex (Heschl’s auditory comprehension can include a word’s fre-
gyrus) of one hemisphere and the subcortical quency of occurrence (e.g., cat vs. omnivore), se-
projections from the opposite hemisphere to the mantic or acoustic similarities to competing words
unimodal auditory association cortex on that same (e.g., car vs. bus), sentence length, and syntactic
side. Such lesions would allow elementary sounds complexity. Attention, auditory memory, and a lis-
to be heard (as one or both of Heschl’s gyri are tener’s ability to apply the spoken word to previous
intact), but would produce impaired higher-level experiences or knowledge base can influence effec-
processing due to damage or inaccessibility to tive and efficient auditory comprehension. Auditory
the unimodal cortex. With critically placed bi- comprehension can be impaired to varying degrees
lateral lesions of the superior temporal gyri, an following acquired neurogenic disorders such as
agnosia for all types of complex auditory input stroke, traumatic brain injury, and dementia.
may be present. Auditory-verbal agnosia is
more likely to result from left-sided lesions as
described above, while auditory agnosia for non- Cross-References
speech sounds is more likely to be associated with
right hemispheric lesions. Agnosia for musical ▶ Aphasia
sounds may also be differentially affected, but in ▶ Attention
an even less consistent manner. ▶ Language
Auditory Discrimination 413

References and Readings Lesions of Wernicke’s area (left hemisphere) are

associated with severe comprehension and other
Brookshire, R. H. (Ed.). (2007). Introduction to neurogenic language-related deficits, whereas comparable
communication disorders (7th ed.). St. Louis: Mosby. A
lesions in the right hemisphere may be associ-
Helm-Estabrooks, N., Albert, M. L., & Nicholas,
M. (Eds.). (2014). Manual of aphasia and aphasia ated with difficulty recognizing or interpreting
therapy (3rd ed.). Austin: Pro-Ed. nonlanguage sounds. Such lesions in the right
hemisphere might help account for the inability
of some patients to comprehend or interpret the
emotional tones or inflections in spoken lan-
Auditory Cortex guage, which may convey more meaning than
the actual words themselves (i.e., receptive
John E. Mendoza aprosodia).
Department of Psychiatry and Neuroscience,
Tulane Medical School and SE Louisiana
Veterans Healthcare System, New Orleans, LA,
USA Cross-References

▶ Aprosodia
Definition ▶ Auditory Agnosia
▶ Homotypic Cortex
That portion of the cerebral cortex devoted exclu- ▶ Idiotypic Cortex
sively to the processing of input from the medial
geniculate nuclei (auditory information).

Auditory Discrimination
Current Knowledge
Kelly Broxterman1, Beth Kuczynski2, Stephanie
Located in the superior portion of the temporal A. Kolakowsky-Hayner3 and Alyssa Beukema1
1
lobe of each hemisphere, the auditory cortex con- School Psychology, The Chicago School of
sists of both primary (idiotypic) and secondary Professional Psychology, Chicago, IL, USA
2
(unimodal homotypic) cortices. The former is Imaging of Dementia and Aging (IDeA)
located in the temporal operculum (Brodmann’s Laboratory, Department of Neurology and Center
area 41 and part of 42) and is referred to as for Neuroscience, University of California, Davis,
Heschl’s gyrus. The primary auditory cortex CA, USA
3
receives direct input from the medial geniculate Department of Rehabilitation Medicine, Icahn
nuclei of the thalamus, which it is thought to School of Medicine at Mount Sinai, New York,
process auditory input at a very basic level NY, USA
with little, if any, distinction between the right
and left hemispheres. The secondary auditory
cortex (primarily Brodmann’s area 22) sur- Synonyms
rounds the primary cortex and, for the most
part, is located in the lateral portion of the supe- Auditory processing
rior temporal gyrus. The posterior portion of this
secondary cortex in the left hemisphere consti-
tutes Wernicke’s area. These secondary cortices Definition
are thought to be responsible for the further
refinement of auditory input, organizing it into Auditory discrimination is part of phonology,
meaningful or potentially meaningful percepts. which is one of the five components of language.
414 Auditory Pathway

It is the ability to recognize differences in pho-

nemes (the smallest unit of sound in a language), Auditory Pathway
including the ability to identify words and
sounds that are similar and those that are differ- Woon N. Chow
ent. Auditory discrimination tests are performed Department of Pathology, Microbiology, and
to measure a person’s phonological awareness, Immunology, Vanderbilt University Medical
such as the ability to compare and contrast Center, Nashville, TN, USA
speech sounds, separate and blend phonemes,
identify phonemes within spoken words, and
combine phonemes into spoken words. Impaired Definition
auditory discrimination should be addressed
early in child development, as it is pertinent to The auditory neural pathway in the central nervous
learning. Auditory discrimination ability or pho- system transmits and processes sound signals from
nological awareness skills are correlated with the ear to the cortex. The configuration of the
reading performance. pathway is multisynaptic and bilaterally projecting.

Current Knowledge
Cross-References
From the Outer Ear to the Cochlear Nuclei
▶ Central Auditory Processing Disorder Sound is transmitted as longitudinal waves through
▶ Language the air, enters the outer ear, and vibrates the tym-
▶ Phonemic Awareness panic membrane. The three “tiny bones” of the
▶ Phonological Disorder middle ear, the ossicles (malleus, incus, and stapes),
▶ Phonology amplify and transmit these vibrations to the oval
window, producing waves in the scala vestibuli, a
fluid-filled compartment within the coil-shaped
cochlea of the inner ear. These fluid waves distort
References and Readings the stiff basilar membrane. Residing on this mem-
brane, hair cells within the organ of Corti transduce
Fromkin, V., & Rodman, R. (1974). An introduction the minute movements of the membrane into the
to language. New York: Holt, Rinehart and Winston.
graded release of glutamate onto the peripheral pro-
Gordon-Brannan, M. E., & Weiss, C. E. (2008). Clinical
management of articulatory and phonologic disor- cesses of bipolar afferent fibers, whose cell bodies
ders (3rd ed.). Philadelphia: Lippincott Williams & are located in the spiral ganglion. The central pro-
Wilkins. cesses exit the base of the cochlea, form the auditory
Moller, A. R. (2000). Hearing: Its physiology and patho-
physiology. San Diego: Academic Press.
trunk of the vestibulocochlear nerve (eighth cranial
Ouimet, T., & Balaban, E. (2009). Auditory stream biasing nerve, CN VIII), and project ipsilaterally to the
in children with reading impairments. Dyslexia, 16, ventral and dorsal cochlear nuclei in the brainstem.
45–65.
Sharma, M., Purdy, S. C., & Kelly, A. S. (2009). Comor-
From the Cochlear Nuclei to the Superior
bidity of auditory processing, lauguage, and reading
disorders. Journal of Speech Language and Hearing Olivary Nuclei
Research, 52, 706–722. Fibers from the dorsal cochlear nucleus decussate
Warren, R. M. (1999). Auditory perception: A new syn- to the contralateral inferior colliculus via the lateral
thesis (2nd ed.). New York: Cambridge University
lemniscus. Fibers from the ventral cochlear nuclei
Press.
Warren, R. M. (2008). Auditory perception: An analysis project ipsilaterally to the superior olivary nucleus
and synthesis (3rd ed.). New York: Cambridge Univer- and also decussate via the trapezoid body to the
sity Press. contralateral superior olivary nucleus. This circuit
Auditory Processing 415

provides temporal and intensity differences in the organization is preserved systematically all the
horizontal plane between right and left ear to aid in way up to the primary auditory cortex, where
sound source localization. Because of the bilateral higher-frequency sounds are mapped to a more A
nature of these afferent projections, central lesions medial location on the superior temporal gyrus,
rarely result in total unilateral hearing loss. whereas lower-frequency sounds are mapped to a
more anterolateral location.
From the Superior Olivary Nuclei to the Medial
Geniculate Nuclei
Afferent fibers from the superior olivary nuclei Cross-References
merge with other audition-associated ascending
fibers and project via the lateral lemniscus to the ▶ Auditory Cortex
inferior colliculus. The inferior colliculus receives ▶ Auditory System
bilateral inputs from almost all audition-related ▶ Cochlea
nuclei and acts as an almost obligatory relay in ▶ Cochlear Nuclei (Dorsal and Ventral)
the ascending auditory pathway. It is here that ▶ Heschl’s Gyrus
horizontally oriented and vertically oriented ▶ Inferior Colliculi
sound source localization data is fully and finally ▶ Internal Capsule
integrated. Ascending fibers from the inferior ▶ Lateral Lemniscus
colliculus project ipsilaterally to the last subcorti- ▶ Medial Geniculate Nuclei
cal relay station, the medial geniculate nucleus. ▶ Trapezoid Body
Located in the posteroinferior portion of the ▶ Vestibulocochlear Nerve
thalamus, the medial geniculate nucleus is a
relay between the inferior colliculus in the
brainstem and the auditory cortex. The medial
geniculate nucleus plays a role in directing and
maintaining attention. Auditory Processing

From the Medial Geniculate Nuclei to Scott L. Decker and Rachel M. Bridges
Heschl’s Gyri Department of Psychology, University of South
Outputs from the medial geniculate nucleus pro- Carolina, Columbia, SC, USA
ject via the internal capsule to the ipsilateral pri-
mary auditory cortex located in the posterior
portion of the superior temporal gyrus of Heschl. Definition
At the cortical level, detected sound is finally
perceived. Bilateral lesions of the auditory cortex Auditory processing is used to describe the manner
remove the conscious perception of sounds, but in which sound waves are transformed into neuro-
because of extensive subcortical processing, an logical impulses and subsequently decoded by the
individual may still react reflexively to a sound primary auditory cortex in the temporal lobe of the
without actually “hearing” it. brain. Simply put, object vibration causes surround-
ing molecules of air to condense and pull apart,
Tonotopic Mapping producing waves that travel away from the object.
One idea of note is tonotopy, which is the spatial Receptor cells within our ears will be stimulated if
arrangement of where particular frequencies of the vibration ranges between approximately 30 and
sound are relayed and processed within the audi- 20,000 times per second (Carlson 2007). These
tory system. In the cochlea, high-frequency waves will then be perceived as sound.
sounds are detected by hair cells at the base and There are three dimensions of sound: pitch,
low-frequency sounds at the apex. This tonotopic loudness, and timbre. The pitch of an auditory
416 Auditory Selective Attention Test

stimulus is determined by the frequency of repet- these studies, as well as much of the research that
itive (cyclic) vibrations per second (Hertz); a has followed, was to examine individual differ-
“high-pitch” sound has a high frequency of vibra- ences in selective attention as related to the oper-
tions per second, whereas a “low-pitch” sound has ator’s driving and flight operation performance
a low frequency of vibrations per second. The (Gopher and Kahneman 1971; Mihal and Barrett
loudness, or intensity, of a sound determines if it 1976). Selective auditory attention is often tested
is perceived as “loud” or “soft” – vigorous vibra- by a dichotic listening task such as the ASAT.
tions of an object produce more intense sound Dichotic listening tasks require the examinee to
waves, resulting in louder sounds. Finally, timbre focus in on relevant auditory information while
is the quality of sound, which further differenti- ignoring irrelevant auditory information that is
ates two sounds (e.g., voice vs. piano) when they being presented. The most updated version of
have identical pitch and loudness. the ASAT was compiled by Arthur and
Our ears are able to detect stimuli, determine the Doverspike in 1993.
spatial location of those stimuli (by differentiating The ASAT is administered through an audio
interaural time and interaural sound intensity; player where the examinee listens to the instruc-
Gazzaniga et al. 2014), and recognize the identity tions as well as the entire test through headphones.
of such stimuli. The examinee is instructed to repeat the message
they hear back to the examiner immediately after
each trial. A tone cue is presented at the beginning
References and Readings of each trial to identify whether the individual
should focus on the left or right ear input. A
Carlson, N. R. (2007). Physiology of behavior (8th ed.).
250 Hz cue indicates that the examinee should
Boston: Pearson.
Gazzaniga, M. S., Ivry, R. B., & Mangun, G. R. (2014). attend to the left ear sound, while a 2500 Hz cue
Cognitive neuroscience: The biology of the mind tone indicates that the participant should attend to
(4th ed.). New York: W.W. Norton & Company. the right ear sound. There is a practice portion to
the ASAT comprised of four messages. Overall, the
examinee hears 24 dichotic messages that consist
of various combinations of number and letter pairs.
Auditory Selective Once the cue is presented, 16 pairs (a single-digit
Attention Test number and a letter) are presented at the rate of two
per second. Auditory stimuli are presented on both
Elena Polejaeva1 and Adam J. Woods2,3,4 sides but not simultaneously. Thus, the examinee
1
Department of Clinical and Health Psychology, must attend to the input direction denoted by the
University of Florida, Gainesville, FL, USA cue prior to the trial while ignoring the stimuli
2
Department of Clinical and Health Psychology, presented from the other direction (left/right). The
College of Public Health and Health Professions, examinee is instructed to immediately repeat the
University of Florida, Gainesville, FL, USA numbers they heard aloud to the examiner at the
3
Center for Cognitive Aging and Memory, completion of each trial. The examinee has five
McKnight Brain Institute, University of Florida, seconds to do so before the next trial begins. The
Gainesville, FL, USA next portion of the ASAT presents another cue
4
Department of Neuroscience, University of followed by three pairs of numbers that the exam-
Florida, Gainesville, FL, USA inee must attend to. These pairs are preceded by an
additional pair of letters, two additional pairs, or no
pairs. Once again the examinee must repeat the
The Auditory Selective Attention Test (ASAT) numbers they heard at the end of each trial
was developed by Gopher and Kahneman in Israel (Doverspike et al. 1986).
and translated into English in 1976 by Mihal and Scores for the ASAT can be subdivided into a
Barrett. The primary focus of the ASAT within variety of categories: sum of correct items,
Auditory System 417

errors, directionality of cue performance accu- References

racy, and part one or two of the test. The error
scores are further subdivided into omission, Arthur, W. J., & Doverspike, D. (1992). Locus of control
and auditory selective attention as predictors of driving A
intrusion, and switching errors. An omission
accident involvement: A comparative longitudinal
error occurs when the examinee does not report investigation. Journal of Safety Research, 23, 73–80.
a number that was presented in the cue desig- Arthur, W. J., & Doverspike, D. (1993). ASAT: The Audi-
nated ear. An intrusion error indicates that the tory Selective Attention Test manual. Psychology
Department: Texas A&M University.
number reported was not part of the message or
Aviolio, B. J., Alexander, R. A., Barrett, G. V., & Sterns,
not reported in the correct sequence. Switching H. L. (1981). Designing a measure of visual selective
errors occur when the examinee omits the cue’s attention to assess individual differences in information
direction to switch attention from one ear to processing. Applied Psychological Measurement, 5,
29–41.
another (Doverspike et al. 1986).
Doverspike, D., Cellar, D., & Barrett, G. V. (1986). The
A reliability study of the ASAT was conducted auditory selective attention test: A review of field and
with a sample of 20 undergraduate students where laboratory studies. Educational and Psychological
the ASAT was administered at an initial time point Measurement, 46, 1095–1104.
Gopher, D., & Kahneman, D. (1971). Individual differ-
and then again two weeks later. The results were
ences in attention and the prediction of flight criteria.
r = 0.71 for total errors, r = 0.81 for omissions, Perceptual and Motor Skills, 33, 1335–1342.
and r = 0.39 for intrusions. However, a practice Kahneman, D., Ben-Ishai, R., & Lotan, M. (1973). Rela-
effect seemed to be present since performance tion of a test of attention to road accidents. Journal of
Applied Psychology, 58, 113–115.
increased from the initial test (Doverspike et al.
Mihal, W., & Barrett, G. V. (1976). Individual differences
1986). Studies that examined correlations in perceptual information processing and their –relation
between the various outcome scores for the to automobile accident involvement. Journal of
ASAT showed mixed results ranging from 0.2 to Applied Psychology, 61, 229–233.
Wahlberg, A. E. (2003). Some methodological deficiencies
0.8 (Avolio et al. 1981).
in studies of traffic accident predictors. Accident Anal-
As noted earlier, the ASAT was initially used as ysis and Prevention, 35, 473–486.
a predictive factor on how individuals performed
in flight school. Two of the ASAT scores were
significantly correlated with flight school perfor-
mance at r = 0.26 and r = 0.36 (Gopher and
Kahneman 1971). The ASAT has additionally Auditory System
been used to predict traffic accidents. A study of
bus drivers’ attention and driving accidents found Maryellen Romero
that ASAT scores significantly correlated with Department of Psychiatry and Behavioral
accidents at r = 0.29–0.37 (Kahneman et al. Sciences, Tulane University School of Medicine,
1973). Mihal and Barrett utilized the ASAT as a New Orleans, LA, USA
predictive factor for vehicle accidents and found a
moderate correlation (Mihal and Barrett 1976).
Another study supported these results via their Structure
own findings of poorer performance on the
ASAT as a predictor of vehicular accident The structure and function of the human auditory
involvement with r = 0.24, p < 0.01 and at system was first postulated by the physicist George
r = 0.20, p < 0.01 in cases where the accident Ohm more than 100 years ago. Dr. Ohm theorized
was that individual’s fault (Arthur and Doverspike that the auditory system’s main function was to
1992). A more extensive review and critique of translate complex sound material into highly spe-
studies examining predicting factors in traffic cialized vibratory signals that could then be pro-
accidents was conducted by Wahlberg and cessed in the brain and recoded as recognizable
includes a summary of studies utilizing the entities. At a very basic level, the auditory system
ASAT as a predictor variable (Wahlberg 2003). might be considered as being composed of three
418 Auditory System

primary structures and their interconnections. The the auditory system. What is important to note is
first of these is the ear, which itself is typically that while most fibers cross the midline, some
divided into three components. The outer or exter- remain ipsilateral, thus at a very early stage there
nal ear is that which is visible, the pinna and the is bilateral input from each ear. The trapezoid body
auditory meatus or ear canal which terminates at of the pons represents one such major crossing of
the tympanic membrane or ear drum. Next is the these auditory fibers (primarily those from the ven-
middle ear which primarily consists of a linked tral acoustic stria). Most of these second-order fibers
series of three small bones, the malleus, incus, synapse in the superior olivary nuclei, although
and stapes, which act together as a system of some proceed directly to the inferior colliculi. The
levers. The former is attached to the tympanic lateral lemniscus, again consisting of both crossed
membrane and the latter to the oval window of and uncrossed fibers, interconnects the superior
the inner ear. The middle ear is connected to the olivary nuclei with the inferior colliculi. From
oral cavity by the eustachian tube which allows for there, the brachium of the inferior colliculi carries
equalization of pressure on either side of the tym- auditory signals to the medial geniculates which, in
panic membrane. The semicircular canals, the ves- turn, project ipsilaterally to the primary auditory
tibule, and the cochlea comprise the inner ear. The cortices. It should be noted that, due to the arrange-
first two constitute the end organs for the vestibular ment of the auditory pathways, by the time these
system, whereas the cochlea and organ of Corti signals reach the cortex they are derived from both
contained within it represent the origin of the nerve ears, with approximately 60% coming from the
impulses that eventually are translated into sounds. contralateral ear and 40% from the ipsilateral one.
The second set of structures in the auditory
system is the brainstem nuclei associated with hear-
ing. The dorsal and ventral cochlear nuclei located Function
in the region of the pontine-medullary junction
represent the origin of the second-order auditory Joseph Fourier, a French mathematician, identi-
fibers. Next in line are the superior olivary nuclei, fied the physical and mathematical properties of
which lie in the pons and are the first nuclear group sound waves and described the transformation of
to receive auditory input from both ears. The next such stimuli into frequency, amplitude, and phase,
and final major nucleus concerned with hearing in which govern discrete elements of sound such as
the brain stem is the inferior colliculus, a paired loudness and pitch. In its raw, unprocessed state,
structure in the dorsal portion of the midbrain. sound exists in the form of vibration that results in
The brain itself might be considered the third alterations in the pressure of the air in the imme-
portion of the auditory system. The two most critical diate environment. These alterations in pressure
structures here are the medial geniculates of the take the form of waves that have a specific fre-
thalamus, and Heschl’s gyri (Brodmann’s area 41) quency or combination of frequencies as well as
which lie in the temporal operculum (within the intensity. The frequency of the sound wave, as
lateral fissure) of each hemisphere. It is this last measured by hertz (Hz) is the major determinant
structure, in conjunction with its adjacent secondary of the pitch of the resulting sound, experienced by
auditory cortices, which is responsible for processing the listener as high or low. The amplitude of the
the auditory input into meaningful information. wave, or its height, is the major determinant of the
Finally, there are the major pathways that inter- loudness of the resulting sound, measured in deci-
connect these various structures. The auditory bels (dB). The human ear is capable of capturing
portion of the vestibulo-cochlear nerve (CN sound over a considerable frequency range,
VIII) is the first-order neuronal pathway in the approximately 20–20,000 Hz.
auditory system. It has its origins in the organ of The transduction of sound waves into the per-
Corti and terminates in the dorsal and ventral ception of sound is complex. Vibrations entering
cochlear nuclei. The acoustic stria (dorsal, ventral, the external auditory meatus strike the tympanic
and intermediate) form the second-order neurons of membrane, causing it to vibrate. This vibration is
Auditory System 419

transferred directly to the ossicles; first the malleus, assessments of hearing loss are best left to audi-
which is attached to the tympanic membrane, ologists, a gross assessment of hearing acuity is
followed by the incus and then the stapes which important to better understand why a particular A
sets the oval window of the inner ear in motion. The patient may be having difficulty either on examina-
vibration is then picked up by the fluids (perilymph tion of mental status or coping at home or on the
and endolymph) of the cochlea, first setting the job. Given a hearing loss, neurologists will often try
perilymph of the scala vestibuli and then the endo- to differentiate its particular nature. Two types of
lymph of the organ of Corti and basilar membrane peripheral hearing loss (i.e., not due to a lesion of
upon which its rests, and finally the perilymph of the brain stem or above) are typically identified,
the scala tympani from where it is dissipated via the conductive and sensorineural. The former, which is
round window of the inner ear. In the course of this generally more amenable to treatment, is a result of
activity, the basilar membrane is differentially a problem with the external or middle ear, while the
affected depending on the frequency of the waves latter implies damage to the inner ear. These can
causing the hair cells along its length to be stimu- often be distinguished by a couple of procedures
lated, initiating patterns of nerve impulses that cor- using a tuning fork (preferably 512 Hz). In the first,
respond to the particular pitch. This very discrete the ability of the patient to hear the vibration is
information is picked up by the auditory nerve (CN tested by comparing air to bone conduction
VIII) in the form of bioelectrical nerve impulses, (Rinne test). Here the base of the vibrating tuning
which then are propagated through the various fork is applied to the mastoid process just behind
pathways described above until eventually reaching the ear. When the sound is said to have dissipated,
the cerebral cortex where they are eventually the ends of the fork are immediately moved near the
interpreted as speech or other sounds. auditory canal (air conduction). If the problem is in
the middle ear, the sound will not be heard. Con-
versely, if the sound is heard better via air than bone
Illness conduction, a sensorineural (inner ear) deficit is
suspected. It should be noted that for normals, air
Damage to any part of the auditory system, from conduction will be superior to bone conduction, but
cerumen (wax) in the auditory canal to bilateral one should be looking for relative differences in
cortical lesions (exceedingly rare) can result in acuity, not absolute auditory thresholds as the latter
hearing deficits. Because of the multiple crossings will likely lowered in the affected ear. A second
and ipsilateral connections within the system, procedure is to press the base of the tuning fork on
hearing loss which is confined to one ear normally the middle of the forehead. If there is a sensorineu-
implies damage no higher than the cochlear ral loss, the sound will be localized to the unaf-
nuclei. Pure word deafness (intact hearing with fected ear, while it will be localized (sound louder)
the inability to understand spoken language with- in the affected ear in a conductive hearing loss. This
out other major aphasic deficits) can result from a latter procedure is referred to as the Weber test.
relatively rare occurrence of damage to Heschl’s Another common problem associated with hear-
gyrus on the left and a dissociation of input to the ing is tinnitus, a buzzing, ringing, or other repetitive
secondary association areas from the non-domi- noxious sound in one or both ears. It can be rela-
nant hemisphere. Damage at intermediate levels tively brief or chronic. If the latter, it can be very
may result in poor localization of sounds. Aside disturbing to the patient. The causes can be multi-
from ponto-medullary strokes, unilateral (or bilat- ple, including certain drugs (e.g., aspirin), after
eral) hearing loss is most commonly the result of effects of exposure to loud noises, infections, or
damage to the middle or inner ear or the nerves occasionally may represent the initial symptoms of
that emanate from the latter. Any of many causes a more serious condition such as a brainstem tumor.
could be the problem, from prolonged exposure to Unfortunately, treatment options for this condition
loud noises, trauma, infections, medications, and, are quite limited. Having background noise, such as
of course, simply aging. While formal music, is often helpful.
420 Auditory Verbal Learning

Cross-References over short- or long-time intervals, and subsequent

access to the information either by free retrieval or
▶ Aphonia recognition. The nature of the test composition,
▶ Auditory Cortex the instructions to the individual, and the scoring
▶ Auditory Pathway dictate what conclusions are drawn from the spe-
▶ Cochlea cific task administered.
▶ Pure Word Deafness Auditory verbal learning tasks (AVLTs) are
▶ Tinnitus widely used in both clinical and research settings
▶ Weber Test and constitute a hallmark of memory assessment.
Different tests include the California Verbal
Learning Test-II (CVLT-II; Delis et al. 2000),
References and Readings Hopkins Verbal Learning Test-R (HVLT-R;
Brandt and Benedict 2001), World Health Orga-
Bradley, W. G., Daroff, R. B., Fenichel, G. M., & Jankovic, J. nization/UCLA Auditory Verbal Learning Test
(2004). Neurology in clinical practice: Principles of
(WHO/UCLA AVLT; Maj et al. 1993), Rey Audi-
diagnosis and management (4th ed.). Philadelphia:
Butterworth-Heinemann. tory Verbal Learning Test (RAVLT; Schmidt
Wilson-Pauwek, L., Akesson, E. J., Stewart, P. A., & 1996), Neuropsychological Assessment Battery
Spacey, S. D. (2002). Cranial nerves in health and (NAB; Stern and White 2003), list learning in
disease. Hamilton: B.C. Decker.
the Center to Establish Registry for Alzheimer’s
Disease (CERAD; Morris et al. 1989; Welsh et al.
1991), Repeatable Battery for the Assessment of
Neuropsychological Status (Randolph et al.
Auditory Verbal Learning 1998), and Wide Range Assessment of Memory
and Learning – Second Edition (WRAML-2;
Nancy S. Foldi1,2, Clara Vila-Castelar1, Emnet Sheslow and Adams 2003). Other commonly
Gammada1, Joan C. Borod3,4 and used list-learning tasks, e.g., the Alzheimer’s Dis-
Heidi A. Bender4 ease Assessment Scale – Cognition (ADAS-
1
Department of Psychology, Queens College and COG; Rosen et al. 1984) and the Free and Cued
The Graduate Center, The City University of Selective Reminder Task (FCSRT; Buschke et al.
New York, New York, NY, USA 2006; Grober et al. 1997), are not solely auditory,
2
Department of Medicine, Winthrop University as they include visual presentation of words or
Hospital, Stony Brook School of Medicine, pictures of items.
Mineola, NY, USA List-learning tasks can share many common
3
Department of Psychology, Queens College and features. To capture the characteristics of learning
The Graduate Center of the City University of and memory – and not just attentional skill – the
New York (CUNY), New York, NY, USA number of words included in the list should
4
Department of Neurology, Icahn School of exceed the typical working memory span (7  2
Medicine at Mount Sinai, New York, NY, USA items; Miller 1956). The learning phase is the
presentation of the list either once or across mul-
tiple trials. Following each trial, the examinee is
Description asked to recall as many items as possible. Once
the learning is complete, a short-time interval
An auditory verbal learning task typically requires elapses, usually including interference tasks
individuals to hear a list of items, learn those designed to prevent rehearsal of the list items.
items, and recall and/or recognize them at a later The examinee is then asked to recall items from
time. These tasks assess acquisition and retrieval the list, constituting a short-term recall. After
components of memory, including encoding, another longer distractor-filled interval, a second
learning characteristics, storage, consolidation recall is requested. These short- and long-term
Auditory Verbal Learning 421

retrieval assessments capture the examinee’s ability curve, indicating whether information learned on
to store, consolidate, and maintain information, as an earlier trial is consistently maintained and later
well as to retrieve it on command. Tests can also appended with new information. Learning char- A
include a multiple- or forced-choice task to facili- acteristics, such as serial position effects (i.e.,
tate access, capturing the items that were encoded recall from primacy and recency list positions),
but could not be accessed on free retrieval. provide insight into an individual’s learning. For
Despite these commonalities, instruments vary instance, the dual-storage model (Glanzer and
in content and administration. List construction on Cunitz 1966; Raaijmakers 1981) suggests that
some tests (e.g., CVLT-II, HVLT-R, WHO/CVLT items from primacy list positions are thought to
AVLT, and NAB) incorporates semantic catego- reflect long-term storage relying on successful
ries, whereas others do not (e.g., RAVLT, semantic encoding, whereas recent items remain
CERAD, RBANS, WRAML-2, and ADAS- in immediate working memory. The position of an
COG). Examinees are not initially informed of item in the list, known as a distinctiveness feature
semantic categories, in order to determine (Neath 1993), can also aid in later recall, the first
whether they can exploit categorical information or last items – which have only one adjacent
to their advantage and facilitate their ability to item – are learned and retained more easily. Sus-
organize, encode, or learn more items. To ensure ceptibility to proactive and/or retroactive interfer-
and document that any particular item is fully ence of the alternate list or shared semantic
encoded with semantic knowledge, the FCSRT, categories of target items can be analyzed. Long-
for example, adopts an alternate use of semantic term retention of verbal information can be parsed
organization by cueing examinees with the over- into storage and retrieval components via exami-
arching semantic category while the word is being nation of free recall versus recognition scores.
learned and by prompting the category immedi-
ately afterward. Another variation among tests is
the use of interference lists. For instance, after the Historical Background
initial learning phase of the target list in the CVLT-
II and NAB, an alternate list is administered, Word lists have been used to assess learning and
designed to share some but not all of the semantic memory for well over a century. Ebbinghaus
categories. This helps to address susceptibility to (1885) observed and described the serial position
proactive and retroactive interference and source phenomenon. Eduoard Claparède (Boake 2000)
learning. Other tests (e.g., HVLT-R) do not have assessed learning and memory in his work on
prescribed interference tasks, although other word child pedagogy in 1916 using a 15-item word
lists or naming tasks should be avoided. Delayed list, which was adapted by André Rey to develop
recall is commonly tested after a 20–30 min inter- the RAVLT in 1941. The RAVLT, first published
val. There are various methods to assess the in France, has been adapted since its development
knowledge of target list items. Examinees can and modified for use in multiple languages.
report items on free recall, identify target words A RAVLT manual (Schmidt 1996) was published
among a list of distracters (CVLT-II, HVLT-R, to provide standard instructions on administra-
NAB, RBANS, and WRAML-2), or identify tar- tion, scoring, and interpretation. The original
gets in forced- (CVLT-II) or multiple-choice CVLT (Delis et al. 1987) incorporated semantic
(FCSRT) recognition trials. While most tasks use categories, scorings of learning characteristics,
recognition after short- (NAB) or long-term the use of semantic strategy, and contrast mea-
(CVLT-II and HVLT-R) free recall, one test sures of learned and retrieved items. The CVLT-
(ADAS-COG) relies exclusively on the immediate II revision (Delis et al. 2000) adopted new norms.
recognition to assess learning. Lists have been developed to address the needs
AVLTs reveal significant information about of populations of different ages, cultures, and
learning and retrieval processes. The multiple diseases. The CVLT-Children’s Version (Delis
trial exposure generates an individual’s learning et al. 1994) is appropriate for children in the age
422 Auditory Verbal Learning

group of 5–16 years. The HVLT-R (Brandt and Reliability

Benedict 2001) contains six alternate forms Verbal learning tests are used to evaluate memory
designed for longitudinal, repeated testing and performance over time. Test-retest reliability
incorporates delayed recall and recognition trials. using the same version of the test has been eval-
Some AVLTs are targeted for certain populations uated for 1-month as well as 1-year intervals.
using age-appropriate words (e.g., CVLT-C). Many tests have adopted alternate or multiple
Shorter forms have also been adopted for more forms (e.g., CVLT-II or RBANS). Whereas alter-
impaired individuals (e.g., CVLT-II, Short Form; nate versions can reduce practice effects, there is
Delis et al. 2000). The WHO/UCLA AVLT was evidence that these effects are not completely
designed to better evaluate examinees worldwide eliminated (Houx et al. 2002) due to procedural
(Maj et al. 1993). In this instrument, the authors learning. Therefore, examiners must be very
were careful to select words that were familiar aware of practice effects. Even after 2 years, healthy
across multiple cultures. Similar to the CVLT-II, older adults showed practice effects on the CVLT-II
the words comprising the WHO/UCLA AVLT can (Blasi et al. 2009). For within-subject test-retest
be classified into universally familiar categories measures, reliable change indices (RCI; Iverson
(i.e., body parts, animals, tools, household 2001) have been applied to changes of AVLT scores
objects, and transportation vehicles). Of note, the in some populations, e.g., pre- and posttemporal
WHO/UCLA AVLT is a component of the Neu- lobe epilepsy surgery (Shah et al. 2015), progression
ropsychological Screening Battery for Hispanics in multiple sclerosis (Andersson-Roswall 2012),
(Ponton et al. 1996). A similar approach was and dementia (Gonçalves et al. 2015).
adopted when developing the International Shop-
ping List (Lim 2009), a list-learning task to assess Validity
individuals from diverse cultural and language Construct validity of AVLTs has also been exam-
groups (i.e., English, French, Malay, and ined. For example, a factor analysis in a sample of
Chinese-speaking cultures). children with traumatic brain injury using the
CVLT-C yielded four factors: attention span, learn-
ing efficiency, delayed recall, and inaccurate recall
Psychometric Data (Mottram and Donders 2005). Also, while AVLTs
are not interchangeable because administrations
Norms vary significantly, correlations among word lists
Normative data for different AVLTs span an age have been documented (e.g., RAVLT and CVLT-
range of 5–97 years. For example, the NAB has II, Crossen and Wiens 1994; HVLT-R and CVLT-II,
been normed on individuals up to 97 years of age; see Lacritz and Cullum 1998) demonstrating that
similarly, the WRAML-2 is used in children and these tests measure common constructs.
adults and has been normed for individuals
between 5 and 90 years of age. Standardization
samples include healthy adults of different lan- Clinical Uses
guage or culture groups, stratified by age, sex,
ethnicity, educational level, and/or geographic AVLTs are ubiquitous in assessments of memory-
region of a country (e.g., northeast of the United impaired populations. Amnesic disorders, degen-
States). Many tests (e.g., CVLT-II and CERAD) erative dementias (including Alzheimer’s,
have been normed for European, Asian, and Parkinson’s, and Huntington’s disease), mild
Southeast Asian groups. Direct translation of a cognitive impairment, temporal lobe epilepsy,
word list into other languages should be avoided, traumatic brain injury, depression, and focal
as words may have been selected to accommodate stroke are diseases that have not only benefitted
word frequency within a language or appropriate- from these tests but also have promoted refine-
ness within a culture. There are also norms for ments and further development to extend our
many neurological and psychiatric populations. knowledge of the neuropsychological and
Auditory Verbal Learning 423

neural underpinnings of memory function. memory as a prerequisite for the diagnosis of mild cog-
Such tests have been instrumental in assessing nitive impairment (MCI). Neuropsychology, 23,
189–200. https://doi.org/10.1037/a0014079.
change in memory over time, as well as being Boake, C. (2000). Edouard Claparède and the auditory A
very sensitive in discriminating between verbal learning test. Journal of Clinical and Experi-
healthy and memory-impaired groups. A vast mental Neuropsychology, 22, 286–292. PMID:
literature demonstrates the sensitivity of these 10779842.
Brandt, J., & Benedict, R. (2001). Hopkins verbal learning
tests to the detection of prodromal Alzheimer’s test-revised. Lutz: Psychological Assessment
disease. Resources.
These instruments evaluate both qualitative Bruno, D., Reiss, P. T., Petkova, E., Sidtis, J. J., & Pomara, N.
and quantitative, procedural aspects of verbal (2013). Decreased recall of primacy words predicts cog-
nitive decline. Archives of Clinical Neuropsychology,
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solidate, store, and retrieve information, thus Verghese, J., & Lipton, R. B. (2006). Retention weighted
revealing significant aspects of the learning and recall improves discrimination of Alzheimer’s disease.
Journal of the International Neuropsychological Soci-
retrieval processes. Learning characteristics, ety, 12, 436–440. PMID: 16903137.
particularly primary and recency serial position Crossen, J. R., & Wiens, A. N. (1994). Comparison of the
effects (Foldi et al. 2003), are highly informative auditory-verbal learning test (AVLT) and California
in differentiating clinical populations and pro- verbal learning test (CVLT) in a sample of normal
subjects. Journal of Clinical and Experimental Neuro-
vide insight about cognitive learning, as well as psychology, 16(2), 190–194. PMID: 8021306.
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Grober, E., Merling, A., Heimlich, T., & Lipton, R. B. Schmidt, M. (1996). Rey auditory verbal learning test:
(1997). Free and cued selective reminding and selective A handbook. Los Angeles: Western Psychological
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Young, R., et al. (1996). Normative data stratified by
age and education for the neuropsychological screening which an individual’s communication skills can
battery for hispanics (NeSBHIS): Initial report. Journal be maximized for functional and effective commu-
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Augmentative and Alternative Communication (AAC) 425

Historical Background Most recently, the emergence of affordable

mobile technologies and “apps” that can be con-
Prior to about 1970, AAC was not a widely figured to serve as an AAC device have increased A
accepted intervention technique and could the awareness and availability of technological
even be described as contraindicated in the pro- solutions to significant communication impair-
fessional literature. At that time, it was thought ment. Advances in access technologies such as
that the act of vocal production was a critical eyegaze and eye tracking and emerging work in
building block of human language develop- the area of brain–computer interface continue to
ment. As a result, interventionists believed that offer solutions to those whose communication
providing an alternative to speech production disability is accompanied by significant physical
would deter speech (and thus language) devel- disability.
opment because the child would choose to use
the “easier” alternative mechanism (Bates 1976;
Fourcin 1975). Rationale or Underlying Theory
In the late 1960s and in the 1970s, research
evidence indicated speech was actually a second- Today, the widespread acceptance of AAC is a
ary component to language function and that valid intervention option to develop viable means
robust receptive and expressive language could of effective communication for any individual
be developed without vocal production. In many with limited “natural” speech, as well as to
cases, the use of alternatives to speech production enhance comprehension for those who are not
was found to actually support (and in no way hearing impaired, but who have difficulty under-
deter) vocal production (Schlosser and Wendt standing spoken language. In 1992, the National
2008; Silverman 1980; Zangari et al. 1994). In Joint Committee for the Communication Needs of
1980, the American Speech-Language-Hearing Persons with Severe Disabilities issued a Com-
Association (ASHA) established an Ad Hoc Com- munication Bill of Rights that unequivocally
mittee on Communication Processes and Non- states, “All persons, regardless of the extent or
speaking Persons that developed a position severity of their disabilities, have a basic right to
statement outlining the concept of AAC as a set affect, through communication, the conditions of
of intervention techniques using a variety of sym- their own existence.” Revised in 2016, a set of 15
bol sets and communication interaction behaviors. specific rights are described in the Bill of Rights
This became the framework for the field of AAC including, “the right to have access to functioning
today. AAC (augmentative and alternative communica-
At about the same time, new computer tech- tion) and other AT (assistive technology) services
nologies were exploding onto the scene creating and devices at all times.”
previously unimaginable opportunities for AAC
device development. The Trace Research and
Development Center, part of the College of Goals and Objectives
Engineering at the University of Wisconsin-
Madison, was formed in 1971 to address the Most of the early history of AAC focused on indi-
communication needs of people with severe viduals with neuromotor impairments that limited
disabilities who were nonspeaking. The Center oral-motor skills such as cerebral palsy and
was an early leader and innovator in the aug- amyotrophic lateral sclerosis (ALS). However,
mentative communication field and pioneered with the passage of landmark legislation such as
development of electronic communication aids the Education of Handicapped Children’s Act (P.L.
in the 1970s and 1980s that became prototypes 94–142), Section 504 of the Rehabilitation Act,
for the speech generating devices (SGDs) of and later the Americans with Disabilities Act, indi-
today (Vanderheiden 1978; Vanderheiden and viduals with all types of disabilities have become
Grilley 1976). more integrated into education, employment,
426 Augmentative and Alternative Communication (AAC)

community living, and society in general. This communication opportunities and environments,
change created a widespread need for individuals and providing supports sufficient to ensure effec-
with all types of disabilities to have an effective, tive use of the system.
functional communication system. More complex Consideration for aided AAC intervention
and efficient AAC systems have been developed to begins with assessment by a qualified team of
meet this need with some specifically focused on individuals who are knowledgeable about the
individuals with neuropsychological disabilities individual and his other strengths and limitations
such as autism (Glennen and DeCoste 1997). especially in the areas of speech, language, and
While the core goal of AAC is to provide effective motor skills. One or more team members should
communication, related objectives can include be knowledgeable about the range of potential
decreasing problem behaviors and increasing suc- AAC alternatives available and those that are via-
cessful education (e.g., literacy), employment, and ble options to meet the individual’s communica-
community living outcomes. tion needs. Appropriate practice in assessment
includes conducting structured device trials with
various AAC devices in the environment(s) in
Treatment Participants which the individual will be using the technology
(e.g., home, school, community, etc.). This allows
Early in the history of AAC, two misconceptions for comparative analysis of different device fea-
thrived regarding candidacy for AAC – that a set tures and functions to determine which best
of prerequisite skills (usually cognitive and address the individual’s functional communica-
motor) was required before AAC could be con- tion needs, answer any clinical questions about
sidered and AAC should only be implemented the device-person “match” that remain after the
after all traditional forms of speech therapy had formal assessment, and establish user preferences,
failed. Both have been proven unsubstantiated as as appropriate.
many successful AAC users have severe motor The result of an AAC assessment is identifica-
and/or cognitive impairments, and research has tion of the system features appropriate for an
shown no justification for waiting to implement individual including specification of device input
AAC as it can support speech development features (selection techniques), language system,
(Shane and Bashir 1980). As a result, candidacy representational format (picture/symbol/orthogra-
for AAC is not limited by age, disability diagnosis phy), and output features. Once an appropriate
or prerequisite cognitive or motor skills. Individ- AAC system has been acquired, training and sup-
uals who can benefit from AAC may be of port for the user, their family, and others (e.g.,
all ages, including infants and toddlers with dis- teachers, therapists, etc.) must be implemented.
abilities and may have diagnoses including More complex AAC systems frequently require
apraxia, dysarthria, aphasia, autism, ALS, cere- customization as part of user support services.
bral palsy, multiple sclerosis, Parkinsons, intellec- Short- and long-term communication goals
tual disabilities, etc. should be developed using the AAC system and
therapy services implemented to support goal
achievement (Beukleman et al. 2007; Beukelman
Treatment Procedures and Mirenda 2013; www.aac-rerc.com).

The challenges for those providing intervention

are maintaining current knowledge of the vast Efficacy Information
array of available AAC device options, appropri-
ately matching the skill sets of individuals with Efficacy research on AAC ranges from observa-
disabilities to available AAC systems (hardware, tion of changes in functional communication
software/apps [language system]), securing skills to potential secondary improvements in aca-
funding to acquire the system, improving demic, social, behavioral, and other areas. For
Augmentative and Alternative Communication (AAC) 427

individuals with limited or no functional commu- Qualifications of Treatment Providers

nication, an AAC system that delivers basic com-
munication ability can be deemed effective by AAC intervention is typically provided by A
self-verification of communication occurring speech-language pathologists (SLPs) who are
(Fried-Oken and Bersani 2000). Beyond this licensed by states as health care providers, edu-
basic gauge of AAC efficacy, research has been cated at the graduate level in the study of human
done on a variety of specific outcomes such as communication, its development and its disor-
decreasing problem behaviors through the use of ders. Medicare requires an SLP who provides
AAC (Vaughn and Horner 1995), enhancing the AAC assessments or treatment to hold the Certif-
rate of AAC communication, (Venkatagiri 1993), icate of Clinical Competence (CCC) in speech-
and even nuances such as speech synthesizer language pathology from the American Speech-
intelligibility (Mirenda and Beukelman 1990) all Language-Hearing Association. In addition to
in an effort to support AAC efficacy. SLPs, some other types of professional providers
Seminal work on AAC efficacy done by Ralf may be members of the intervention team provid-
Schlosser (2003) addressed a wide range of ing AAC services, especially in the educational
AAC efficacy issues including the role of AAC environment, e.g., special educators, occupational
in facilitating or hindering natural speech devel- therapists, assistive technology practitioners, etc.
opment, literacy development in AAC users, and (ASHA 2004).
the effects of speech output (use of speech gen-
erating devices). In 2001, Medicare began cov-
erage of speech generating devices (SGDs)
based on acceptance of AAC efficacy research. Cross-References
Since then, a number of private insurance car-
riers have followed suit and now cover SGDs as ▶ Articulation
do most state Medicaid programs. In 2015, ▶ Articulation Disorders
Medicare affirmed that communication augmen- ▶ Assistive Technology
tation may include text, stating “We believe that ▶ Speech
a written message or phone message from an ▶ Speech Sound Disorder
individual lacking the ability to speak serves ▶ Speech/Communication Disabilities
the same purpose in communicating with indi- ▶ Speech-Language Pathology
viduals not in close proximity to the patient as ▶ Speech-Language Therapy
generation of speech does in communicating
with individuals who are in close proximity to
the patient.” References and Readings

AAC-RERC. (2011). Mobile devices and communication

Outcome Measurement apps: An RERC white paper. Downloaded from http://
aac-rerc.psu.edu/index.php/pages/show/id/46
American Speech-Language-Hearing Association. (2004).
Current technologies may include built in (or the Preferred practice patterns for the profession of
option to add-on) language activity monitoring speech-language pathology [Preferred Practice
systems that can provide ongoing data as to Patterns]. Available from www.asha.org/policy.
American Speech-Language-Hearing Association. Aug-
device usage and message construction as well
mentative and alternative communication decisions.
as quantitative data on selection rates. The most Downloaded 2. 23. 2018.
direct outcome measure for AAC intervention is Bates, E. (1976). Language and context: The acquisition of
demonstration of effective and efficient commu- pragmatics. New York: Academic.
Beukelman, D., & Mirenda, P. (2013). Augmentative &
nication, for a variety of communicative pur-
alternative communication: Supporting children&
poses and with a variety of communication adults with complex communication needs (4th ed.).
partners AAC. Baltimore: Paul H. Brookes Publishing Company.
428 Aura

Beukleman, D., Garrett, K., & Yorkston, K. (2007). Aug- Preliminary considerations. Journal of Speech and
mentative and alternative communication strategies for Hearing Disorders, 45, 408–414.
adults with acute or chronic medical conditions. Silverman, F. (1980). Communication for the speechless.
Baltimore: Paul H. Brookes Publishing Company. Englewood Cliffs: Prentice-Hall.
Brady, N. C., Bruce, S., Goldman, A., Erickson, K., Vanderheiden, G. C. (1978). Non-vocal communication
Mineo, B., Ogletree, B. T., Paul, D., Romski, M., resource book. Baltimore: University Park Press.
Sevcik, R., Siegel, E., Schoonover, J., Snell, M., Vanderheiden, G. C., & Grilley, K. (1976). Non-vocal
Sylvester, L., & Wilkinson, K. (2016). Communication communication techniques and aids for the severely
services and supports for individuals with severe dis- physically handicapped. Austin: Pro-Ed.
abilities: Guidance for assessment and intervention. Vaughn, B., & Horner, R. (1995). Effects of concrete
American Journal on Intellectual and Developmental versus verbal choice systems on problem behavior.
Disabilities, 121(2), 121–138. Augmentative and Alternative Communication,
Brumberg, J. S., Pitt, K. M., Mantie-Kozlowski, A., & 11, 89–92.
Burnison, J. D. (2018). Brain–computer interfaces for Venkatagiri, H. S. (1993). Efficiency of lexical prediction
augmentative and alternative communication: A tutorial. as a communication acceleration technique.
American Journal of Speech-Language Pathology, 27(1), Augmentative and Alternative Communication, 9,
1–12. https://doi.org/10.1044/2017_AJSLP-16-0244. 161–167.
Centers for Medicare and Medicaid Services. (2015). Zangari, C., Lloyd, L. L., & Vicker, B. (1994). Augmen-
National coverage determination of speech generating tative and alternative communication: A historic
devices. Available from https://www.cms.gov/medicare- perspective. Augmentative and Alternative
coverage-database/details/medicare-coverage-document- Communication, 10, 27–59.
details.aspx?MCDId=26&mcdtypename=National+
Benefit+Category+Analyses&MCDIndexType=3&bc=
AgAEAAAAAAAAAA%3d%3d&#final
Fourcin, A. J. (1975). Language development in the Aura
absence of expressive speech. In E. H. Lenneberg &
E. Lenneberg (Eds.), Foundations of language devel- Kenneth R. Perrine
opment (Vol. II). New York: Academic.
Fried-Oken, M., & Bersani, H. (2000). Speaking up and
Neurological Surgery, Weill Cornell Medicine,
spelling it out: Personal essays on augmentative and New York, NY, USA
alternative communication. Baltimore: Paul H.
Brookes Publishing Company.
Glennen, S. L., & DeCoste, D. C. (1997). Handbook of
augmentative and alternative communication. San
Definition
Diego: Singular Publishing Group.
Hill, K., Kovacs, T., & Shin, S. (2015). Critical issues using An aura is a paroxysmal episode that occurs
brain-computer interfaces for augmentative and alter- before several types of neurologic events. It is a
native communication. Archives of Physical Medicine
and Rehabilitation, 96(3), S8–S15.
type of warning heralding the onset of the ictal
Mirenda, P., & Beukelman, D. (1990). A comparison of event such as a migraine or an epileptic seizure.
intelligibility among the natural speech and seven Auras usually last longer in migraines (up to
speech synthesizers with listeners from three age minutes) than in seizures (typically several sec-
groups. Augmentative and Alternative Communication,
6, 61–68.
onds). Episodes longer in duration or more remote
National Joint Committee for the Communication Needs of from the ictus in both migraine and seizures are
Persons With Severe Disabilities. (1992). Guidelines called prodromes. In epilepsy, this simple partial
for meeting the communication needs of persons with seizure (focal seizure with retained awareness/
severe disabilities [Guidelines]. Available from www.
asha.org/policy or www.asha.org/njc.
responsiveness)1 can lead to a complex partial
Schlosser, R. W. (2003). The efficacy of augmentative and seizure (focal seizure with altered/dyscognitive
alternative communication: Toward evidence-based awareness/responsiveness), or a generalized
practice. San Diego: Academic. tonic-clonic seizure (bilateral convulsive seizure).
Schlosser, R. W., & Wendt, O. (2008). Effects of augmen-
tative and alternative communication intervention on
speech production in children with autism: A system-
1
atic review. American Journal of Speech-Language The International League Against Epilepsy suggested new
Pathology, 17, 212–230. terminology for seizure types (Berg et al. 2010). These new
Shane, H., & Bashir, A. S. (1980). Election criteria for the terms have not yet been fully adopted but are given in
adoption of an augmentative communication system: parentheses.
Autism Diagnostic Interview, Revised 429

In both disorders, auras can represent any disrup- epilepsy, auras are actually simple partial seizures
tion of networks limited to one hemisphere, the (focal partial seizures with retained awareness/
specific phenomena of which arise from the local- responsiveness) produced by epileptiform electri- A
ization of their onset in the brain. The term aura is cal discharges that affect just one brain region
attributed to the Roman physician Galen alone; they do not disrupt consciousness and can
(130–200AD) who reportedly overheard a boy be recalled by the patient after the ictus.
say just before a seizure that he felt a cool breeze,
“aura” in Latin (Haynes and Bennett 1992).
Cross-References

Current Knowledge ▶ Epilepsy

▶ Simple Partial Seizure
Auras can consist of disruptions or activations of
primary sensory modalities (touch, hearing, smell,
taste, vision), including paresthesias (somatosen- References and Readings
sory hallucinations that feel like tingling or “pins
and needles”) or numbness, unformed (noises, Berg, A. T., Berkovic, S. F., Brodie, M. J., Buchhalter, J.,
Cross, J. H., van Emde, B. W., Engel, J., French, J.,
distortions) or formed (voices, songs, commercial Glauser, T. A., Mathern, G. W., Moshe, S. L., Nordli,
jingles) auditory hallucinations or transient deaf- D., Plouin, P., & Scheffer, I. E. (2010). Revised termi-
ness, and olfactory or gustatory hallucinations nology and concepts for organization of seizures and
(usually noxious, such as burned rubber). Visual epilepsies: Report of the ILAE Commission on Classi-
fication and Terminology, 2005–2009. Epilepsia, 51
hallucinations are especially common in migraine (4), 676–685.
and can include loss of vision such as blind spots Haynes, S. D., & Bennett, T. L. (1992). Historical perspec-
or hemianopsia (loss of vision on one side), pos- tive and overview (p. 7). In T. L. Bennett (Ed.), The
itive phenomena such as “scintillating scotoma” Neuropsychology of Epilepsy. New York: Plenum
Press.
(flickering spots of light that may begin centrally www.epilepsyfoundation.org
and extend to arcs of flickering white or colored www.ilae.org
lights), or zigzag or other geometric lines or pat- Wyllie, E. (Ed.). (2015). Wyllie’s treatment of epilepsy:
terns. Formed visual hallucinations can occur Principles and practice (6th ed.). New York: Lippincott
Williams & Wilkins.
(especially in epilepsy), which are usually
described as animals or cartoon characters. Visual
distortions can also occur, such as macropsia/
micropsia (seeing objects larger/smaller) and tele-
scopia/micropsia (seeing objects farther away/ Autism Diagnostic Interview,
closer). In epilepsy, more complex somatosensory Revised
auras can occur, such as a rising epigastric sensa-
tion (feeling the stomach rising up to the mouth) So Hyun Kim1 and Catherine Lord2
1
or ineffable “feelings” that the patient cannot elu- Yale Child Study Center, Yale School of
cidate. Complex experiential psychic auras can Medicine, New Haven, CT, USA
2
also occur (especially in epilepsy), such as déjà Center for Autism and the Developing Brain,
vu, out-of-body experiences, depersonalization, New York-Presbyterian Hospital/Westchester
derealization, bizarre perceptual phenomena, etc. Division, White Plains, NY, USA
Psychological symptoms such as anxiety, panic,
and fear are also common. In migraines, auras are
thought to be caused by the vascular phenomena Synonyms
causing the headache. Of note, migraine auras can
occur without any subsequent headache. In ADI-R
430 Autism Diagnostic Interview, Revised

Description 1994), which was based on the original Autism

Diagnostic Interview (ADI; Le Couteur et al.
The current edition of the Autism Diagnostic 1989). The 1994 version was somewhat shorter
Interview-Revised (ADI-R; Rutter et al. 2003) is a than the original in order to make the interview
standardized, semistructured, and investigator- more appropriate for clinical, as well as research,
based interview for parents or caregivers of indi- usage. The diagnostic algorithm developed for the
viduals with autism. It provides a diagnostic algo- 1994 version remains unaltered (apart from minor
rithm for the ICD-10 definition of autism (World changes in age cutoff). However, a recent study
Health Organization [WHO] 1992) and DSM-IV has suggested that alternative algorithms devel-
(American Psychiatric Association [APA] 1993). oped based on machine learning techniques show
The interview is appropriate for the diagnostic slightly improved validity compared to the origi-
assessment of any person within the age range nal algorithms (Bone et al. 2016). In addition, new
extending from early childhood to adult life, pro- algorithms have been developed specifically for
vided that they have a nonverbal mental age above toddlers and preschoolers with ASD (Kim and
2 years. The ADI-R includes 93 items in three Lord 2012; Kim et al. 2013). The new algorithms
domains of functioning – language/communica- have shown improved sensitivity and specificity
tion, reciprocal social interactions, and restricted, compared to the original algorithms for these
repetitive, and stereotyped behaviors and interests, young children from 12 to 47 months of age.
as well as other aspects of behaviors. Up to 42 of
the interview items are systematically combined to
produce a formal, diagnostic algorithm for autism Psychometric Data
as specified by the authors, or a general diagnosis
of autism spectrum disorders (ASD) as used in Psychometric properties for the original ADI were
several collaborative studies (Risi et al. 2006). All provided for a carefully selected, blindly
items in the ADI-R are coded in terms of whether interviewed and coded, sample of 16 autistic and
the behavior is “currently” occurring, and whether 16 mentally handicapped children and adults cov-
it “ever” occurred, or occurred during a specifically ering a range of IQs and chronological ages. Inter-
defined period in preschool years. The diagnostic rater reliability was assessed for a sample of ten
algorithm is based on the “ever/most abnormal” children with autism and ten without, with multi-
codes in preschool years, but current scores can rater kappas ranging from 0.55 to 0.94 for each
be used to facilitate a clinical diagnosis. item and intraclass correlations above 0.94 for all
Most of the ADI-R pertains to behaviors that subdomain and domain scores. The majority of
are rare in individuals who do not have ASD individual items showed good discriminative
and/or who do not have profound intellectual dis- validity showing diagnostic differences across
abilities. Thus, numerical estimates of the typical autistic and mentally handicapped groups
scores of general population have not been (Le Courteur et al. 1989).
obtained. Researchers have used scores in the Psychometric properties for the current ADI-R
domains or overall as estimates of severity of were provided for a carefully selected, blindly
autistic symptoms. However, the validity of this interviewed and coded, sample of 25 autistic and
approach has not been directly tested. Scores have 25 mentally handicapped children ranged in chro-
been published for many research populations but nological age from 36 to 59 months, with mental
not yet systematically dimensionalized. ages ranging from 21 to 74 months. Inter-rater
reliability was assessed, with multirater kappas
ranging from 0.63 to 0.89 for each item and
Historical Background intraclass correlations above 0.92 for all sub-
domain and domain scores. Following the initial
The WPS Edition of the ADI-R (2003) is a mod- standardization study of the ADI-R, a further
ified version of the 1994 version (Lord et al. study was undertaken of a separate sample of
Autism Diagnostic Interview, Revised 431

53 children with autism and 41 nonautistic chil- Current Behavior Algorithms can be used to
dren with mental handicap or language impair- assess the participant’s current behavior. This can
ments (Lord et al. 1993). Inter-rater reliability be used in clinical settings to assess changes A
was as high as the initial study, with multirater brought about by intervention or changes
kappas ranging from 0.62 to 0.96 for individual reflecting increasing developmental maturity or
items. Test-retest reliability was very high, with changing life circumstances.
all coefficients being in the 0.93–0.97 range. The ADI-R should only be used by appropri-
Majority of individual items showed good dis- ately experienced clinicians. Interviewers must be
criminative validity showing diagnostic differ- familiar with the concepts of ASD and relevant
ences across autistic and mentally handicapped behaviors. Training workshops and videotapes are
groups (see Lord et al. 1994). The algorithm available to help clinicians understand the scoring
cutoffs were determined by identifying the and administration of the ADI-R.
point within each area that yielded the best com-
bination of sensitivity and specificity both
exceeding 0.90.
Cross-References

▶ Autism Diagnostic Observation Schedule

Clinical Uses ▶ Autistic Disorder
▶ Childhood Autism Rating Scales
The ADI-R offers a profile of a child in different
▶ Modified Checklist for Autism in Toddlers,
areas including language/communication, recip-
Revised, with Follow-Up (M-CHAT-R/F), also
rocal social interactions, and restricted, repetitive,
M-CHAT
and stereotyped behaviors and interests based on
the parents’ detailed descriptions of the history
and behaviors of the child. It can provide a com-
References and Readings
prehensive description of a child both currently
and in earlier ages but must be used in conjunction American Psychiatric Association. (1993). Options book
with observations and/or direct testing in making for DSM-IV. Washington, DC: Author.
a diagnosis of ASD. The ADI-R can provide a Bone, D., Biship, S., Black, M. P., Goodwin, M. S., Lord, C.,
& Narayanan, S. S. (2016). Use of machine learning to
useful structure to obtain history and understand a
improve autism screening and diagnostic instruments:
parent’s perspective on their children’s symptoms Effectiveness, efficacy, and multi-instrument fusion. Jour-
associated with ASD but requires approximately nal of Child Psychology and Psychiatry, 57(8), 927–937.
2 h to administer and substantial practice to do so DiLavore, P., Lord, C., & Rutter, M. (1995). The pre-
linguistic autism diagnostic observation schedule
reliably.
(PL-ADOS). Journal of Autism and Developmental
The Diagnostic Algorithms are sets of rules Disorders, 25, 355–379.
that allow classification of patterns of behavior Kim, S. H., & Lord, C. (2012). New autism diagnostic
according to whether or not they meet the current interview-revised algorithms for toddlers and young
preschoolers from 12 to 47 months of age. Journal of
DSM-IV or ICD-10 diagnostic criteria of autism
Autism and Developmental Disorders, 42(1), 82–93.
and nonautistic ASD. One caveat for clinical users Kim, S. H., Thurm, A., Shumway, S., & Lord, C. (2013).
is that they should be aware that diagnostic algo- Multisite study of new autism diagnostic interview-
rithm result and a true clinical diagnosis are not revised (ADI-R) algorithms for toddlers and young
preschoolers. Journal of Autism and Developmental
the same. Clinical diagnosis is based on multiple Disorders, 43(7), 1527–1538.
sources of information, including direct observa- Le Couteur, A., Rutter, M., Lord, C., Rios, P., Robertson,
tion. Thus, even though the ADI-R provides S., Holdgrafer, M., et al. (1989). Autism diagnostic
broader contexts including the information about interview: A semistructured interview for parents and
caregivers of autistic persons. Journal of Autism and
history or functioning of a child than observa-
Developmental Disorders, 19, 363–387.
tions, ADI-R alone cannot be used to make a Lord, C., Rutter, M., & Le Couteur, A. (1994). Autism
complete standard diagnosis. diagnostic interview-revised: A revised version of a
432 Autism Diagnostic Observation Schedule

diagnostic interview for caregivers of individuals with and social role-play. A variety of structured activ-
possible pervasive developmental disorders. Journal ities and materials, and less structured interac-
of Autism and Developmental Disorders, 24(5),
659–685. tions, provide standard contexts within the
Risi, S., Lord, C., Gotham, K., Corsello, C., Chrysler, C., ADOS in which the social, communicative, and
Szatmari, P., et al. (2006). Combining information from other behaviors relevant to the understanding of
multiple sources in the diagnosis of autism spectrum ASD are observed.
disorders. Journal of the American Academy of Child
and Adolescent Psychiatry, 45, 1094–1103. The previous version of the ADOS-Generic
Rutter, M., Le Couteur, A., & Lord, C. (2003). Autism consisted of four Modules (Module 1–4). The
diagnostic interview-revised. Los Angeles: Western newly revised ADOS-2 now includes five Modules
Psychological Services. (Toddler Module, Module 1–4; Lord et al. 2012).
World Health Organization. (1992). The ICD-IO classifi-
cation of mental and behavioral disorders: Clinical Each Module is appropriate for children and adults
descriptions and diagnostic guidelines. Geneva: at different developmental and language levels,
Author. ranging from no expressive or receptive use of
words, to fluent, complex language in an adult.
Only one Module, lasting about 30 min, is adminis-
tered to any individual at a given point of time. In the
Autism Diagnostic ADOS, the examiner uses the Module that best
Observation Schedule matches the expressive language skills of the
individual child or adult in order to make judg-
So Hyun Kim1 and Catherine Lord2 ments about social and communicative abilities as
1
Yale Child Study Center, Yale School of independent as possible from the effects of abso-
Medicine, New Haven, CT, USA lute level of language delay. Each Module has its
2
Center for Autism and the Developing Brain, own protocol, which contains a schedule of activ-
New York-Presbyterian Hospital/Westchester ities designed for use with children or adults at
Division, White Plains, NY, USA particular developmental and language levels.
Recently, the Toddler Module of the ADOS was
developed for use in children between 12 and
Synonyms 30 months of age in addition to the original four
Modules (Lord et al. 2012).
ADOS Module 1 is intended for children who do not
use spontaneous phrase speech consistently. It con-
sists of 10 activities with 29 accompanying ratings.
Description Module 2 is intended for children with some flex-
ible phrase speech who are not verbally fluent. It
The Autism Diagnostic Observation Schedule consists of 14 activities with 28 accompanying rat-
(ADOS; Lord et al. 2001) is a semistructured, ings. Module 3 provides 13 activities and 28 ratings.
standardized assessment of communication, It is intended for verbally fluent children for whom
social interaction, and play or imaginative use playing with toys is age-appropriate. The opera-
of materials for individuals who have been tional definition of verbal fluency is the spontane-
referred because of possible autism spectrum ous, flexible use of sentences with multiple clauses
disorders (ASD). As part of the schedule, that describe logical connections within a sentence.
planned social occasions, referred to as “presses” It requires the ability to talk about objects or events
(Lord et al. 1989), are created in which a range of not immediately present. Module 4 contains the
social initiations and responses is likely to socioemotional questions, along with interview
appear. In the same way, communication oppor- items about daily living and additional tasks. It is
tunities are designed to elicit a range of inter- intended for verbally fluent adults and for adoles-
changes. Play situations are included to allow cents who are not interested in playing with toys
observation of a range of imaginative activities such as action figures (usually over 12–16 years).
Autism Diagnostic Observation Schedule 433

This Module consists of 10–15 activities with developed phrase speech, they should be admin-
31 accompanying ratings. The difference between istered Module 2. Since differential diagnosis can
Modules 3 and 4 lies primarily in whether infor- be challenging especially in toddlers, the toddler A
mation about social communication is acquired Module algorithms generate range of concern
during play or through a conversational inter- (little-or-no concern; mild-to-moderate concern;
view. It is important to note that adolescents or moderate-to-severe concern) rather than strict
adults may feel uncomfortable when presented classifications.
with the toys for young children that are available Most of the ADOS pertains to behaviors that
in Modules 1 and 2; suggestions for modifying are rare in individuals who do not have ASD
the earlier Modules to be appropriate for older and/or who do not have profound intellectual dis-
children or adults who are less verbal are avail- abilities. Thus, numerical estimates of the typical
able from the authors. In addition to the four scores of general population have not been
Modules, the Toddler Module is intended for obtained. Both algorithm total and domain scores
children between 12 and 30 months of age who for Toddler Module, Module 1–3 have now been
should have a nonverbal age equivalent of at least calibrated for children with ASD to yield a stan-
12 months and be walking independently. It con- dard severity score based on a large sample (see
sists of 11 activities with 41 accompanying rat- below; Esler et al. 2015; Gotham et al. 2009; Hus
ings (Lord et al. 2012). et al. 2014).
The ADOS provides the diagnostic algorithms
that are sets of rules that allow classification of
autism or ASD. Separate diagnostic algorithms Historical Background
for each Module can be generated using subsets
of items in each Module. Items and the thresholds In its present form, the current WPS Edition of the
for the classification of autism and of ASD in the ADOS-2 (Lord et al. 2012) is a second edition of
algorithms differ for each Module. However, the the original ADOS, which was a combination of
general principles and procedures for computation two similar diagnostic instruments: the 1989 ver-
are the same across Modules and similar to the sion of the ADOS (Lord et al. 1989) and the Pre-
DSM-IV (American Psychiatric Association Linguistic ADOS (PL-ADOS; DiLavore et al.
1993) and ICD-10 (World Health Organization 1995). The ADOS was first introduced in the
1992). The algorithms for Module 1, 2, and 1980s as a method of standardizing direct obser-
3 were recently revised from the previous algo- vations of social behavior, communication, and
rithms (Gotham et al. 2007). Reflecting recent play in children suspected of having autism. It
research, the revised algorithms now consist of was intended to be administered to children
two new domains, Social Affect and Restricted, between the ages of 5 and 12, who had expressive
Repetitive Behaviors, combined to one score to language skills at least at the 3-year-old level. It
which thresholds are applied, resulting in gener- was proposed as a complementary instrument to
ally improved predictive validity compared to the the Autism Diagnostic Interview (ADI; Le
previous algorithms. The Module 1 consists of no Couteur et al. 1989), an investigator-based parent
words and some words algorithms by language or caregiver interview that yielded a description of
level. The Module 2 includes “Younger than 5” history, as well as current functioning, in areas of
and “Greater or Equal to 5” algorithms by chro- development related to autism. Because children
nological age. Module 3 includes a single algo- under age 5 constitute the bulk of referrals for a
rithm. All items appearing on the new algorithms first diagnosis of autism, there was a need to
contribute to a single score with two classification extend the age and verbal limits of the ADOS to
thresholds, one for autism and another for ASD. be appropriate for younger and nonverbal chil-
There are the Toddler Module algorithms for dren. The PL-ADOS was then created based on
children between 12 and 30 months, who do not the growing interest in using the instruments in
have phrase speech; once children have clinical settings, which addressed the concerns of
434 Autism Diagnostic Observation Schedule

parents and fit the abilities of children functioning in increased specificity and sensitivity proving
at infant and toddler levels. As a result, it included increased diagnostic validity compared to the pre-
more flexible, briefer activities and greater use of vious algorithms. Furthermore, even though the
play materials for nonverbal young children that inclusion of the RRB domain did not improve
served as a downward extension for the ADOS, predictive value of the ADOS in differentiating
rather than a replacement. The PL-ADOS was individuals with autism from those with pervasive
effective in discriminating 2–5-year-old-children developmental disorder – not otherwise specified
with autism from children with non-autism spec- (PDD-NOS; also referred as ASD), it aided in
trum developmental delays (DiLavore et al. distinguishing PDD-NOS from non-spectrum
1995). However, it tended to be underinclusive cases.
for children with autism who had some expressive
language. Thus, a tool was required to address
the needs of children who fell between the Psychometric Data
PL-ADOS and ADOS in language skills. Fur-
thermore, the ADOS consisted primarily of Psychometric properties for the original ADOS
activities intended for school-age children. Addi- were provided for a carefully selected, blindly
tional or alternative tasks were needed for ado- interviewed and coded, sample of 223 children
lescents and adults. The current edition of the and adults with autistic disorder (autism), pervasive
ADOS was designed in response to these factors. developmental disorder – not otherwise specified
The current ADOS differs from the preceding (PDD-NOS) or non-spectrum (NS) diagnoses.
instruments in a way that it is aimed at providing Inter-rater reliability was assessed, with mean
standard contexts for the observation of behavior multirater kappas of all items for each Module
for a broader developmental and age range of ranging from .65 to .78 and intraclass correlations
individuals suspected of having autism. Thus, above .82 for all subdomain and domain scores.
the current ADOS includes additional items Test-retest reliability varied by subdomain ranging
developed for verbally fluent, high-functioning from .59 to .82. In the original sample, the ADOS
adolescents and adults as well as younger and algorithms generally achieved 94% correct classifi-
nonverbal children. cation. The exceptions were the ASD versus non-
However, even though this updated version of spectrum (NS) Module 2 specificity of 87% and
the ADOS did indeed extend the usefulness of Module 3 sensitivity of 90%, and the PDD-NOS
the original ADOS below a language level of versus NS Module 2 specificity of 88% and sensi-
3 years, research has indicated that it remained tivity of 89% and Module 3 sensitivity of 80%
of limited value for children with nonverbal men- (Lord et al. 2001).
tal age below 16 months. Thus, a standardized Psychometric properties for the newly revised
diagnostic measure applicable for infant and algorithms were provided for a sample of 1,139
young toddlers was also needed for early identi- different participants. The revised algorithms
fication (Gotham et al. 2007). The recent devel- resulted in increased specificity in classifying
opment of the Toddler Module, now included in non-autism ASD in lower functioning
the ADOS-2, reflects this need for the measure to populations, evidenced by the 12–31% increase
be applicable to very young children from 12 to in specificity for children without any words
30 months. (depending on nonverbal mental age) and the
The original algorithms included two domains, modest gain in specificity for older children who
social interaction and communication. Recently, have not progressed beyond phrase speech. Dur-
Gotham et al. (2007) revised algorithms for Mod- ing Module 1, no words improved in each diag-
ule 1, 2, and 3, the existing social and communi- nostic comparison (e.g., from the sensitivity of
cation domains were merged, and the domain of 19–50% for children with nonverbal mental age
Restricted Repetitive Behaviors (RRB) was of 15); the specificity of both Module 2 groups
newly included. The revised algorithms resulted improved for non-autism ASD versus NS (e.g.,
Autism Diagnostic Observation Schedule 435

from 77% to 83% for children greater or equal to the room, which provides an opportunity to show
5). For autism versus non-spectrum and for ASD a parent, examples of behaviors that define ASD,
versus NS, the new and old algorithms performed and get information from a parent about the valid- A
approximately equally well in terms of sensitivity. ity of the child’s behaviors during the testing
For non-autism ASD versus non-spectrum, sensi- session. Because the ADOS consists of codings
tivity of the new algorithm was somewhat lower in made from a single observation, it does not
Module 1, no words (as was necessary to raise include information about history or functioning
specificity; e.g., 100% in old algorithm versus in other contexts. This means that the ADOS
97% in new algorithm for children under nonver- alone cannot be used to make a complete standard
bal mental age under 15), but it showed improve- diagnosis, but used in conjunction with other
ment from the old algorithm in the higher- testing.
functioning Module 1 (AUT versus NS; from Lord and her colleagues suggested several
88% to 97%) and Module 2 (ASD versus NS; strategies that clinicians or researchers may take
from 76% to 84%) cells. Inter-rater reliability on to measure how behaviors of an individual may
the ADOS was monitored through joint adminis- have changed over time by using the ADOS item
tration and scoring by two different examiners for and domain scores (Lord et al. 2000). If an indi-
at least 1 in 10 cases and, in some cases, through vidual has been administered the same Module
scoring of videotapes. Agreement remained at more than once, raw scores on individual items
greater than 85% (Gotham et al. 2007). and on algorithm domains can be compared. If an
Psychometric properties for the Toddler Mod- individual has changed Modules, raw scores on
ule were provided for a sample of 182 different items that remain constant across Modules (about
participants. The sensitivity of each algorithm two thirds of each contiguous Module) can be
ranged from 83% to 91% and specificity from compared, yet comparison of raw domain scores
86% to 94%. Inter-rater item and domain reliabil- is not meaningful. However, the ADOS cali-
ity was greater than .71, and inter-rater algorithm brated scores developed by Gotham et al.
reliability ranged from .60 to .90. Intraclass cor- (2009) can be used in this case to compare assess-
relations ranged from .74 to .99 for all algorithm ments across Modules and time. The calibrated
domains and total scores (Lord et al. 2012). scores have more uniform distributions across
age- and language-groups compared to raw
totals, which make it possible to compare chil-
Clinical Uses dren’s scores longitudinally across distinct algo-
rithms. Thus, calibrated scores can be useful in
Use of the ADOS is related to the examiner’s clinical settings to test treatment responsiveness
clinical skills and experience with the instrument. and other clinical outcomes in individuals with
Examiners need to be sufficiently familiar with the ASD. However, as calibrated scores may not be
ratings and the activities so that they can focus sensitive enough to capture the changes that
their attention on observation of the individual occur over the course of treatment, development
being assessed, rather than on administration of of a new measure adapted from the ADOS, which
tasks. The examiner should have sufficient prac- has been designed to capture treatment respon-
tice in observation of ASD symptoms and scoring siveness, brief observation of social communica-
of the ADOS items, as well as in administering the tion change (BOSCC), is currently underway.
activities. Examiners are encouraged to attend Besides the calibrated scores for the algorithm
workshops, use videotapes, or work with col- totals, domain calibrated scores separate for
leagues to obtain inter-rater reliability before social communication and restricted and repeti-
administering the ADOS for clinical or research tive behaviors have been also developed (Esler
purposes (Lord et al. 2001). Examiners should et al. 2015; Hus et al. 2014).
note that the Toddler Module and Module 1 are In addition, it was suggested that more
always administered with parents or caregivers in detailed coding of communication samples or
436 Autism Diagnostic Observation Schedule

particular behaviors (e.g., pragmatics, sentence References and Readings

structure, gestures) may also be carried out from
videotapes of the ADOS. Other observational American Psychiatric Association. (1993). Options book
coding schemes that address specific aspects of for DSM-IV. Washington, DC: Author.
behavior in more detail may also be applied DiLavore, P., Lord, C., & Rutter, M. (1995). Pre-linguistic
autism diagnostic observation schedule (PL-ADOS).
using the ADOS as a way of obtaining a discrete Journal of Austism and Developmental Disorders, 25,
sample of behavior in standard contexts. Often, 355–379.
clinicians carrying out diagnostic assessments Esler, A. N., Bal, V. H., Guthrie, W., Wetherby, A.,
may wish to make programming suggestions Weismer, S. E., & Lord, C. (2015). The autism diag-
nostic observation schedule, toddler module: Standard-
for parents/caregivers, therapists, or teachers. ized severity scores. Journal of Autism and
Many of the activities and codes of the earlier Developmental Disorders, 1–17.
Modules have fairly straightforward implica- Gotham, K., Risi, S., Pickles, A., & Lord, C. (2007). The
tions both for how to teach an individual child autism diagnostic observation schedule: Revised algo-
rithms for improved diagnostic validity. Journal of
and for the content of appropriate goals. For Autism and Developmental Disorders, 37, 613–627.
example, Module 1 provides opportunities for Gotham, K., Pickles, A., & Lord, C. (2009). Standardizing
children to make requests in a number of cir- ADOS scores for a measure of severity in autism spec-
cumstances, including requests for action (i.e., trum disorders. Journal of Autism and Developmental
Disorders, 39(5), 693–705.
the examiner to blow a balloon), requests for Hus, V., Gotham, K., & Lord, C. (2014). Standardizing
food, requests to continue a social game, and ADOS domain scores: Separating severity of social
requests for an object or activation of that object affect and restricted and repetitive behaviors. Journal
(i.e., operating a bubble gun). Noting how chil- of Autism and Developmental Disorders, 44(10),
2400–2412.
dren make requests and in what circumstances Le Couteur, A., Rutter, M., Lord, C., Rios, P., Robertson,
they are most easily able to communicate their S., Holdgrafer, M., et al. (1989). Autism diagnostic
interest or needs, allows the clinician to create interview: A semistructured interview for parents and
goals to teach new request behaviors and to help caregivers of autistic persons. Journal of Autism and
Developmental Disorders, 19, 363–387.
the children generalize existing behaviors across Lord, C., Rutter, M., Goode, S., & Heemsbergen, J. (1989).
contexts. Generating programming goals from Autism diagnostic observation schedule:
Modules 3 and 4 may be somewhat more com- A standardized observation of communicative and
plex, because fewer codes describe specific social behavior. Journal of Autism and Developmental
Disorders, 19(2), 185–212.
behaviors that may be usefully taught in a direct Lord, C., Rutter, M., & Le Couteur, A. L. (1994). Autism
fashion. Realizing the degree to which adults diagnostic interview-revised: A revised version of a
with autism have limited insight into the nature diagnostic interview for caregivers of individuals
of social relationships, or having the opportu- with possible pervasive developmental disorders.
Journal of Autism and Developmental Disorders,
nity to observe adolescents describing the emo- 24(5), 659–685.
tions of the main characters in a story, can be Lord, C., Risi, S., Lambrecht, L., Cook, E. H., Leventhal,
helpful in representing the strengths they may B. L., DiLavore, P., et al. (2000). The autism diagnostic
have and difficulties they experience in social observation schedule-generic: A standard measure of
social and communication deficits associated with the
interaction. spectrum of autism. Journal of Autism and Develop-
mental Disorders, 30(3), 205–223.
Lord, C., Rutter, M., DiLavore, P. C., & Risi, S. (2001).
Cross-References Autism diagnostic observation schedule. Los Angeles:
Western Psychological Services.
Lord, C., Rutter, M., DiLavore, P., Risi, S., Gotham, K., &
▶ Autism Diagnostic Interview, Revised Bishop, S. (2012). Autism diagnostic observation
▶ Autistic Disorder schedule–2nd edition (ADOS-2). Los Angeles: Western
▶ Childhood Autism Rating Scales Psychological Corporation.
World Health Organization. (1992). The ICD-IO classifi-
▶ Modified Checklist for Autism in Toddlers, cation of mental and behavioral disorders: Clinical
Revised, with Follow-Up (M-CHAT-R/F), also descriptions and diagnostic guidelines. Geneva:
M-CHAT World Health Organization.
Autistic Disorder 437

are no longer recognized but cases are

Autistic Disorder “grandfathered” in if they had a well-established
diagnosis, i.e., essentially retaining the DSM-IV A
Fred R. Volkmar system for cases with a diagnosis. The atypical/
Child Study Center, Child Psychiatry, Pediatrics subthreshold category is eliminated. A new cate-
and Psychology, Yale University School of gory, social communication disorder, is included
Medicine, New Haven, CT, USA but with limited empirical justification.

Synonyms Epidemiology

Autism spectrum disorder; Childhood autism; A number of epidemiological studies have been
Infantile autism; Kanner’s syndrome. undertaken around the world. Their interpretation
is complicated by methodological differences
including case finding and definitions used. The
Short Description/Definition earliest studies reported rates on the order of 1 in
2000 children, but more recent work suggests that
Autistic disorder is a neurodevelopmental condi- a figure of 1 in 800–1000 children is probably
tion characterized by marked problems in social more accurate; the broader PDD spectrum is
interaction, communication/play, and a set of much more ambiguously defined and probably
unusual behaviors related to difficulties in tolerat- affects as many as 1 in 150 children if not more
ing change in the environment. The condition is of (Presmannes et al. 2014). Much debate has cen-
early onset. In most cases, it appears to be con- tered on whether autism is increasing in fre-
genital, but perhaps in 20% of cases, a period of quency, but this issue remains unclear despite
normal development is observed. The condition better methods of case detection and greater pub-
almost always appears before 3 years of age – lic awareness.
usually before 2 years. Rates of autistic disorder are typically three to
four times higher in boys than in girls. The nature
of this gender difference remains unclear, but
Categorization speculation has centered on lower thresholds for
expression of the condition in boys. An early
Autism was first described by Leo Kanner in 1943 impression of increased rates in better educated
(Kanner 1943). Early controversy centered around families appears to have been due to referral bias
the idea that autism might be a form of schizophre- and has not been supported by later work.
nia, but several lines of evidence suggest this is not
the case. Changes in approaches to the definition of
autism have occurred over time. The American Natural History, Prognostic Factors, and
Psychiatric Association (DSM-IV-TR) (APA Outcomes
2000) and International (ICD-10) (World Health
Organization 1994) categorization systems define Issues of diagnosis can be complex in infants as not
autistic disorder in essentially the same way. The all required features may be exhibited until around
new DSM-5 (APA 2013) adopts a new approach age three (Lord and Venter 1992). After that time,
with a single disorder – autism spectrum disorder diagnostic agreement increases substantially. By
with several numeric modifiers, e.g., with Rett’s. school age, autistic children become more sociable
This approach has been controversial for several and may make significant academic gains although
reasons in that it results (somewhat paradoxically) behavioral difficulties are prominent. During ado-
in a more restricted diagnostic approach. Subtypes lescence, some children make substantial gains and
previously identified, such as Asperger’s disorder, others lose skills. There is increased risk for
438 Autistic Disorder

development of epilepsy throughout the develop- understanding and empathizing with others
mental period, with peak frequencies of new onset (Baron-Cohen 1989). This Theory of Mind
of epilepsy in early childhood and adolescence hypothesis has been very productive for research.
(Volkmar and Nelson 1990). It presumes that difficulties arise as a result of an
The first studies of long-term outcome in chil- inability to understanding feelings, intention, and
dren with autism were relatively pessimistic with social meaning. Weaknesses of this approach
only 2–3% of cases being able to achieve adult include the fact that more able individuals with
independence and self-sufficiency. Several factors autism can solve usual theory of mind type prob-
appear to significantly improve prognosis: cases lems; a second problem arises because many of
are now detected at early ages when intervention the first features of autism appear before usual
may be more effective (National Research theory of mind skills are established in typically
Council 2001), and in many countries, educa- developing infants. A relatively newer approach,
tional services are now mandated. It appears that Enactive Mind, has attempted a synthesis of
at least 20% or more of children with autism are insights from studies of social cognitive informa-
capable of self-sufficiency in adulthood with at tion processing in autism with normal develop-
least another 15–20% able to be largely indepen- mental perspectives (Klin et al. 2003) (Fig. 1).
dent (Howlin 2005). Major predictors of long- While Asperger’s disorder was removed from
term outcome include nonverbal cognitive ability DSM-5, it remains in ICD-10, and studies have
and the capacity to use language to communicate now shown differences between it and higher
by age five. Adaptive abilities (the ability to cope functioning autism, e.g., Chiang et al. (2014) in
with real-world situations) are also important par- a meta-analysis of IQ profiles.
ticularly as the person becomes older. A research focus on specific brain mechanisms
was suggested by high rates of epilepsy and various
neurological signs and symptoms (e.g., persistence
Neuropsychology and Psychology of of “primitive” reflexes, delayed development of
Autistic Disorder hand dominance, etc.). A range of abnormalities
have been found in postmortem studies. Lesion
The first attempts to develop psychological
models of autism centered around the notion
that experiential factors might be involved. As
evidence of brain involvement accumulated, the-
ories shifted to focus on neurocognitive and
brain-based mechanisms.
Several neurocognitive models/theories have
been proposed. One approach posits difficulties
in executive functioning skills; this model would
account for some of the problems with shifting set
and perseveration typical of individuals with
autism (Ozonoff et al. 2005). However, deficits
in these areas are not specific to autism and are not
strongly related to the extent of social vulnerabil-
ity. Another approach has focused on difficulties
in what is termed “central coherence” or the Autistic Disorder, Fig. 1 Visual focus of an autistic man
capacity to integrate information into coherent or and a normal comparison subject showing a film clip of a
meaningful wholes (Happe 2005). This model conversation. Typically developing person (top line) goes
back and forth between the eyes in viewing a social scene, a
centers on problems resulting from difficulties in
high functioning person with autism goes back and forth
selective attention and appreciation of social between the mouths of the speakers (Reprinted with per-
meaning. Another approach posits difficulties in mission from Klin et al. (2002))
Autistic Disorder 439

studies, e.g., of the amygdala or hippocampus, Treatment

have produced some behaviors in monkeys sim-
ilar to some of those seen in autism (Bachevalier Over the past decade a considerable body of work A
1996). Other studies have focused on abnormal- on intervention has become available. In its influ-
ities in the cerebellum and overall brain size, ential 2001 review, a panel from the US National
which appears to be increased in autism Research Council systematically evaluated ten
(Courchesne et al. 2004). treatment programs for younger children with
Other approaches have focused on specific autism. Although differing in some respects,
neuropsychological processes. For example, these programs shared many similarities including
Schultz and colleagues (Schultz et al. 2000) intensive individualized programs and structured
used fMRI techniques to demonstrate that more teaching. Many, although not all, of these pro-
cognitively able individuals with autism process grams make extensive use of applied behavior
faces differently than typical controls; essen- analytic principles to teach basic skills, which
tially they fail to activate the fusiform “face can then be expanded. Increasing social and com-
area.” This observation is of interest given a munication abilities are important goals. Psycho-
large body of experimental work on differences therapy is not a mainstay of treatment but is
in face processing in autism. Another work, e.g., sometimes used in older and more able individ-
using eye-tracking technology, has revealed uals, often problem-focused in nature.
marked differences in scanning of the environ- Drug treatments can be helpful relative to cer-
ment during social situations with more able tain symptoms (e.g., agitation, stereotyped man-
individuals with autism tending to focus on the nerisms) but do not address the core social deficit
lower half of the face or objects, thus losing a (Scahill and Martin 2005).
considerable amount of social-affective informa-
tion (Klin et al. 2002).
Beginning with the first twin studies of autism Cross-References
in the late 1970s, a considerable body of work
has strongly implicated genetic factors in the ▶ Applied Behavior Analysis
pathogenesis of autism. There are significantly ▶ Asperger’s Disorder
increased rates of autism in identical twins and a ▶ Behavior Modification
higher risk in siblings both of autism and a range ▶ Epilepsy
of other developmental problems. It appears that ▶ Executive Functioning
multiple genes are involved and several candi- ▶ Intellectual Disability
date genes are now being studied (Rutter 2005). ▶ Social (Pragmatic) Communication Disorder
▶ TEACCH

Evaluation
References and Readings
Evaluation of the child with autism typically
involves the efforts of members of several different American Psychiatric Association. (2000). Diagnostic and
disciplines – psychology, speech-language pathol- statistical manual (4th ed., Text Rev.). Washington,
ogy, medicine, occupational and physical therapy, DC: APA Press.
American Psychiatric Association. (2013). Diagnostic and
and special education. Goals for evaluation include
statistical manual (5th ed.). Washington, DC: APA
clarification of the diagnosis and establishment of Press.
patterns of strengths/weakness that have implica- Bachevalier, J. (1996). Brief report: Medial temporal lobe
tions for programming. Medical evaluations are and autism: A putative animal model in primates. Jour-
nal of Autism and Developmental Disorders, 26(2),
indicated to look for conditions like Fragile
217–220.
X syndrome and seizures sometimes associated Baron-Cohen, S. (1989). The theory of mind hypothesis of
with autism (Volkmar et al. 1999). autism: A reply to Boucher [comment]. The British
440 Autobiographical Memory

Journal of Disorders of Communication, 24(2), Schultz, R. T., Gauthier, I., Klin, A., Fulbright, R. K., Ander-
199–200. son, A. W., & Volkmar, F. (2000). Abnormal ventral
Chiang, H.-M., Tsai, L. Y., Cheung, Y. K., Brown, A., & temporal cortical activity during face discrimination
Li, H. (2014). A meta-analysis of differences in IQ among individuals with autism and Asperger syndrome.
profiles between individuals with Asperger’s disorder Archives of General Psychiatry, 57(4), 331–340.
and high-functioning autism. Journal of Autism and Smith, I. C., Reichow, B., & Volkmar, F. R. (2015). The
Developmental Disorders, 44(7), 1577–1596. effects of DSM-5 criteria on number of individuals diag-
Courchesne, E., Redcay, E., & Kennedy, D. P. (2004). The nosed with autism spectrum disorder: A systematic
autistic brain: Birth through adulthood. Current Opin- review. Journal of Autism and Developmental Disor-
ion in Neurology, 17(4), 489–496. ders, 45(8), 2541–2552.
Happe, F. (2005). The weak central coherence account of Volkmar, F. R., & Nelson, D. S. (1990). Seizure disorders
autism. In F. R. Volkmar, A. Klin, R. Paul, & D. J. Cohen in autism. Journal of the American Academy of Child
(Eds.), Handbook of autism and pervasive developmen- and Adolescent Psychiatry, 29(1), 127–129.
tal disorders (Vol. 1, pp. 640–649). Hoboken: Wiley. Volkmar, F., Cook, E., Jr., Pomeroy, J., Realmuto, G., &
Howlin, P. (2005). Outcomes in autism spectrum disorders. Tanguay, P. (1999). Summary of the practice parameters
In F. R. Volkmar, A. Klin, R. Paul, & D. J. Cohen for the assessment and treatment of children, adoles-
(Eds.), Handbook of autism and pervasive developmen- cents, and adults with autism and other pervasive devel-
tal disorders (Vol. 2, pp. 201–222). Hoboken: Wiley. opmental disorders. Journal of the American Academy
Kanner, L. (1943). Autistic disturbances of affective con- of Child and Adolescent Psychiatry, 38(12), 1611–1616.
tact. Nervous Child, 2, 217–250. World Health Organization. (1994). Diagnostic criteria for
Klin, A., Jones, W., Schultz, R., Volkmar, R., & Cohen, research. Geneva: World Health Organization.
D. (2002a). Visual fixation patterns during viewing of
naturalistic social situations as predictors of social com-
petence in individuals with autism. Archives of General
Psychiatry, 59(9), 809–816.
Klin, A., Jones, W., Schultz, R., Volkmar, F., & Cohen, Autobiographical Memory
D. (2002b). Defining and quantifying the social pheno-
type in autism. American Journal of Psychiatry, 159, Katherine Tyson
895–908.
Klin, A., Jones, W., Schultz, R., & Volkmar, F. (2003). The Department of Psychology, University of
enactive mind, or from actions to cognition: Lessons Connecticut, Storrs, CT, USA
from autism. Philosophical Transactions of the Royal
Society of London, Series B: Biological Sciences,
358(1430), 345–360.
Lord, C., & Venter, A. (1992). Outcome and follow-up Synonyms
studies of high-functioning autistic individuals. In
E. Schopler & G. B. Mesibov (Eds.), High-functioning Memory; Personal memory; Recollective memory
individuals with autism current issues in autism (Vol.
xviii, pp. 187–199, 316). New York: Plenum.
National Research Council. (2001). Educating young chil-
dren with autism. Washington, DC: National Academy Definition
Press.
Ozonoff, S., South, M., & Provencal, S. (2005). Executive Autobiographical memory (AM) is the memory
functions. In F. R. Volkmar, A. Klin, R. Paul, & D. J.
Cohen (Eds.), Handbook of autism and pervasive of events or information involving the self.
developmental disorders (3rd ed., pp. 606–627). Researchers generally conceptualize AM as epi-
New York: Wiley. sodic, as opposed to semantic. AMs are temporally
Presmanes Hill, A., Zuckerman, K., & Fombonne, defined (e.g., by the date of the remembered event)
E. (2014). Epidemiology of Autism Spectrum Disor-
ders. In F. R. Volkmar, R. Paul, S. J. Rogers, & K. A. and involve a sense of “recollection or reliving” of
Pelphrey (Eds.), Handbook of Autism and Pervasive the original event (Greenberg and Rubin 2003).
Developmental Disorders (p. 2). Hoboken: Wiley.
Rutter, M. (2005). Genetic influences and autism. In F. R.
Volkmar, A. Klin, R. Paul, & D. J. Cohen (Eds.),
Handbook of autism and pervasive developmental dis- Historical Background
orders (Vol. 1, pp. 425–452). Hoboken: Wiley.
Scahill, L., & Martin, A. (2005). Psychopharmacology. In Levin et al. (1982) are sometimes credited with
F. R. Volkmar, A. Klin, R. Paul, & D. J. Cohen (Eds.), originating the term AM. However, AM research
Handbook of autism and pervasive developmental dis-
orders (Vol. 2, pp. 1102–1122). Hoboken: Wiley. dates back to Francis Galton’s 1879 study of his
own recall of events in his personal past. Galton
Autobiographical Memory 441

sampled his own episodic memories by finding appears to emerge around three-and-a-half years
associations between words and events from his of age, as adults begin to share memories with
past and dating those events. In 1974, Crovitz their children. Some cultural differences have A
and Schiffman modified Galton’s technique to emerged in the nature of AM. Asian societies,
create what became a widely used method for for example, may report fewer AMs and have
studying AM (see Rubin 1999). Their revised fewer and later memories from earlier childhood
technique involved asking participants to think compared to Euro-Americans. Whereas collec-
of memories associated with words presented to tive identity may be the focus in these societies,
them. In 1983, Nigro and Neisser pioneered Americans tend to focus on creating a unique
studies examining the effect of point of view identity; AM is essential to this development of
on AM in their studies of field memories a self.
(viewed from the same viewpoint as originally In its role of aiding self-development, AM
experienced) and observer memories (viewed may also drive positive perceptions of self and
from an observer’s perspective). They found emotion regulation. Research by Wilson and
that older memories were more often viewed Ross (Bluck 2003) has shown that remembering
from the observer point of view than recent positive events often brings about a positive
memories (see Rubin 1999). Current research mood. Furthermore, the third person, observer’s
has spanned a variety of areas, including exam- perspective from which people often remember
ining AM’s functional mechanisms, studying negative life events gives them distance from
psychopathology’s potential effects on AM, those events, which may also promote well-
and investigating AM’s neuropsychological being. Sharing of AMs with others may aid emo-
underpinnings through imaging studies. tion regulation.
As a facilitator of social interaction AM helps
people to reflect on and share recollections of the
Current Knowledge past with one another. Fivush et al. (Bluck 2003)
have suggested that in mother-child relationships,
Phenomenology sharing of AMs may help children to learn how to
Much of the recent research on AM has concen- deal with and express emotions, particularly
trated on AM’s function. Pillemer (1992) posited negative ones.
that AM has three basic functions: self-related, In its directive function, AM guides current
communicative (social), and directive (planning behavior and functioning. Both everyday and
for present and future events) (Bluck 2003). In traumatic memories guide people’s present deci-
serving the self, AM helps people to develop a sions and actions.
sense of coherence and continuity in defining
who they are through memories. In its commu- Methods in AM Research
nicative role, AM provides the content of con- Several methods have been developed for study-
versations and facilitates building intimacy in ing AM. Given its complexity and the lack of
social relationships. Sharing of AMs can also consensus about how AM works, no single
inform and teach others about the sharer’s method has emerged as a gold standard; rather,
world. As a directive tool, AM can help people these methods are often used in combination.
solve problems as they examine lessons from Open-ended methods include the word-cue
past events and think about how future events method, similar to Galton’s original method. Par-
and behavior might turn out. ticipants are presented with cue words or other
As a cultural mechanism, in particular, AM stimuli and asked to think of memories. Typically,
helps not only to shape the individual self, but after the cued portion of such a study, the
also to provide the individual with a sense of researcher will ask the participants to date the
identity in relation to a wider community memories. This method has tended to provide
(Bluck 2003). In Euro-American societies, AM consistent results, lending support to expected
442 Autobiographical Memory

findings: childhood amnesia of early life memo- people without psychopathology (Dalgleish and
ries, retention of the memories of the most recent Brewin 2007).
two decades, and for people over age 40, an
increase in memories about adolescence and AM and Psychopathology
early adulthood (Wenzel and Rubin 2005). This In studying the relationship between psychopa-
cueing method is most commonly applied using thology and AM, researchers have found that
the autobiographical memory test, first described certain aspects of AM in clinical populations do
in 1986 by Williams and Broadbent (Wenzel and differ from those of healthy populations. Evidence
Rubin 2005). A second open-ended method suggests that AM in patients with suicidal idea-
involves simply asking a participant about his or tion, current or past depression, and trauma his-
her life. A more structured approach, the tory may be overgeneral compared to the specific
involuntary-memory-diary method, asks partici- memories that healthy individuals recall
pants to keep a diary record of involuntary AMs (Hermans et al. 2006). For example, a depressed
as they occur. patient might report a memory of going to lunch
Some other methods for delving into AM are with her mother on Tuesdays, as opposed to
more closed-ended. The autobiographical mem- remembering a specific one of those Tuesday
ory interview, developed by Kopelman, Wilson, lunches.
and Baddeley, was designed to be used with neu- Research also indicates that trauma and non-
ropsychological patients (Wenzel and Rubin trauma memories differ substantially in clinical
2005). The interview asks for specific kinds of but not in healthy populations (Dalgleish and
memories from specific time periods. The partic- Brewin 2007). While involuntary memory may
ipant is not provided a choice as to the types of be enhanced in some clinical populations, volun-
memories he or she will share. In the diary recall tary memory is often fragmented, incomplete, and
method, participants record events and subse- disorganized, particularly in people with a trauma
quently receive a memory test for these events. history. PET and fMRI studies have suggested that
Unlike the other methods, the diary recall method the retrieval of trauma memories in PTSD patients
can provide some measure of the accuracy of is characterized by increased activity of limbic
memories. A final method, the questionnaire and paralimbic areas, including the amygdala.
method, asks participants to report on a series of Additionally, researchers have found deactivation
properties of AMs; this method is often used in of the medial prefrontal areas and Broca’s area and
conjunction with other approaches. Recently, decreased hippocampal activity in PTSD patients
Sutin and Robins (2007) have developed the when they processed emotional, rather than neu-
memory experiences questionnaire, a measure tral material.
designed to assess a comprehensive range of In looking at depressed individuals, studies
dimensions of AM. have suggested that cues reflecting personal char-
In developing methods to study such a multi- acteristics are more likely to promote a shift to
faceted phenomenon as AM, researchers focus on processing of information within the long-term
several variables of interest. These variables view of the self, increasing the likelihood that
include whether the memory is general or specific, self-related semantic information will be provided
latency to retrieve a memory, number of omis- in response to cues on the autobiographical mem-
sions (i.e., when a person does not present a spe- ory test. In a different, but related line of research,
cific personal memory for certain stimuli euthymic individuals with a history of depression
presented), age of memories, and affective tone. and patients with a borderline personality disorder
Studies have shown that the last of these variables, retrieved less specific AMs in response to cue
affective tone, can potentially differentiate AMs words that matched highly endorsed attitudes or
of people with psychopathology from AMs of schema. This finding suggests that an impaired
retrieval of specific memories may be the result
Autobiographical Memory 443

of certain cues activating generic, higher-order and the frontal lobes have been implicated in
mental representations in people with both psy- case study research examining visual imagery’s
chopathology histories and present diagnoses role in AM. Auditory imagery may also be A
(Dalgleish and Brewin 2007; Hermans et al. involved in AM, but so far studies have not
2006). Generally dysfunctional attitudes, whether shown autobiographical amnesias to be related
in an individual exhibiting psychopathology or in specifically to damage of the auditory cortices.
a healthy individual, could play a part in an indi- As with visual imagery, further research may pro-
vidual’s inability to retrieve specific memories. vide more information on this aspect of AM.
In addition to its sensory dimensions, AM also
Neuropsychology seems to be closely related to language. However,
Although researchers have studied the neuropsy- with only one exception, semantic dementia, AM
chology of AM specifically, knowledge about the impairment does not seem to be related to
neuropsychology of memory in general is much language-related neuropsychological impair-
more substantial. By looking at the broad memory ments (Greenberg and Rubin 2003). In semantic
literature, researchers have been able to make dementia, patients display better recall for recent
some claims about the neuropsychology of AM memories than for older ones. A patient with
and to suggest areas for future study. semantic dementia experiences loss of AM, as
AM appears to be distributed throughout the well as a loss of the ability to maintain semantic
brain. Retrieval of personally experienced events memories in storage. While AM deficits have
has been linked to medial temporal lobe, visual been documented in both Alzheimer’s disease
cortex, posterior parietal midline, and prefrontal and frontotemporal dementia, the underlying cor-
cortex activity (Daselaar et al. 2008; Greenberg tical changes responsible for these deficits may be
and Rubin 2003). AM’s emotional and sensory disease specific (Irish et al. 2017).
components may involve still other brain areas.
Daselaar et al. (2008) have worked to map the
time course of AM, including emotional and Future Directions
reliving aspects of AM. Through functional mag-
netic resonance imaging (fMRI), Daselaar et al. Future research on AM should concentrate on
examined both initial accessing of memories and defining and specifying AM both behaviorally
subsequent elaboration of the memories. As a and through neuropsychological techniques,
person first began to recall a personal memory, including functional and structural imaging. Con-
hippocampal, retrosplenial, and medial and right tinuing to consider and revise a conceptual model
prefrontal cortex activation occurred (Daselaar of AM, such as Pillemer’s, is important to provid-
et al. 2008). As participants rated memories, ing researchers a better, more definite way to
brain areas associated with emotion and sensory conceptualize AM. Looking at AM cross-
function were activated, including the amygdala culturally may help to determine whether this
and hippocampus for initial emotion ratings, and type of memory plays distinct roles in different
visual cortex and ventromedial and inferior pre- cultures and societies. Individual differences in
frontal cortex for reliving ratings. This line of AM are also an important area for study, given
research underlines AM’s dynamic involvement researchers’ focus on AM as important to the
of multiple brain areas. formation of self. In research on psychopathology,
The visual, auditory, and olfactory systems all looking at schema activation and overgeneral
appear to be potential parts of the broad AM AMs may be important to understanding why
system. Research has demonstrated that visual clinical populations remember AMs differently
imagery is central to AM, especially when con- from nonclinical populations.
sidering long-term visual memories (Greenberg Taking a closer look at the neuropsychology of
and Rubin 2003). The medial-temporal lobes AM will be necessary as we find better ways to
444 Automated Neuropsychological Assessment Metrics

define AM behaviorally. Correlating behavioral

changes with the brain changes, we can see through Automated
imaging will be a significant area for future study Neuropsychological
so that we develop a clearer idea of what structures Assessment Metrics
make up the AM circuitry in the brain.
Summer Ibarra
Rehabilitation Hospital of Indiana, Indianapolis,
Cross-References IN, USA

▶ Declarative Memory
▶ Episodic Memory Synonyms
▶ False Memory
▶ Forgetting ANAM
▶ Memory Impairment
▶ Remote Memory
▶ Working Memory Definition

The Automated Neuropsychological Assessment

References and Readings Metrics (ANAM) is a computer-based battery of
tests designed to measure an individual’s
Bluck, S. (Ed.). (2003). Autobiographical memory:
neurocognitive skills including areas such as
Exploring its functions in everyday life. [Special
issue]. Memory, 11(2), 113–229. sustained attention, processing speed, working
Dalgleish, T., & Brewin, C. R. (Eds.). (2007). Autobio- memory, and visuospatial ability. The fourth
graphical memory and emotional disorder. [Special and current version, ANAM4, consists of 22 test
issue]. Memory, 15(3).
Daselaar, S. M., Rice, H. J., Greenberg, D. L., Cabeza, R.,
modules as well as forms for recording demo-
LaBar, K. S., & Rubin, D. C. (2008). The spatiotempo- graphic information (see Fig. 1; VistaLifeSciences
ral dynamics of autobiographical memory: Neural cor- 2015). The entire battery of tests can be adminis-
relates of recall, emotional intensity, and reliving. tered, or the administrator can elect to customize
Cerebral Cortex, 18, 217–229.
a subset of the ANAM tests in order to assess
Greenberg, D. L., & Rubin, D. C. (2003). The neuropsy-
chology of autobiographical memory. [Special issue]. more specific areas of functioning (Vincent et al.
Cortex, 39, 687–728. 2008). The ANAM General Neuropsychological
Hermans, D., Raes, F., Philippot, P., & Kremers, I. (Eds.). Screening Battery (ANAM-GNS), for example,
(2006). Autobiographical memory specificity and psy-
consists of a subset of tests from the ANAM
chopathology. New York: Psychology Press.
Irish, M., Landin-Romero, R., Mothakunnel, A., Ramanan, battery and is designed for general clinical assess-
S., Hsieh, S., Hodges, J., & Piquet, O. (2017). Evolu- ment of cognition (Woodhouse et al. 2013). Addi-
tion of autobiographical memory impairments in tional versions specific to particular disorders
Alzheimer’s disease and frontotemporal dementia-A
(ANAM-MS [multiple sclerosis] and ANAM-
longitudinal neuroimaging study. Neuropsychologia.
Levin, H. S., Benton, A. L., & Grossman, R. G. (1982). TBI-MIL [TBI in a military population]) have
Neurobehavioral consequences of closed head injury. also been developed (Settle et al. 2015; Vincent
New York: Oxford University Press. et al. 2012). The ANAM4 is available through
Rubin, D. C. (Ed.). (1999). Remembering our past: Studies
VistaLifeSciences (2015).
in autobiographical memory. New York: Cambridge
University Press. Administration time can range from a few
Sutin, A. R., & Robins, R. W. (2007). Phenomenology of minutes for a single subtest to 90+ minutes
autobiographical memories: The memory experiences for the entire battery (U.S. Army Medical
questionnaire. Memory, 15(4), 390–411.
Wenzel, A., & Rubin, D. C. (Eds.). (2005). Cognitive
Department 2009). In 95% of test takers in the
methods and their application to clinical research. US Department of Defense for cognitive mea-
Washington, DC: American Psychological Association. surement, typical administration time was
Automated Neuropsychological Assessment Metrics 445

Automated Neuropsychological Assessment Metrics, Fig. 1 Automated neuropsychological assessment metrics

20–25 min (VistaLifeSciences 2015). Scoring Current Knowledge

for the ANAM is computer generated. Scores
for ANAM subtests can be calculated in a vari- Various combinations of ANAM subtests have
ety of ways, including the percentage of correct been employed to investigate neurocognitive
responses (accuracy score), mean response time changes and impairment in medical and neuro-
for accurate responses (MS), and the ratio of logical conditions including acquired brain
accuracy and speed or number of correct injury, multiple sclerosis, Parkinson’s disease,
responses per minute (throughput score) systemic lupus erythematosus (Kane et al.
(Jones et al. 2008). An ANAM4 Performance 2007), migraine headache (Roebuck-Spencer
Report (APR), which provides full reports on et al. 2007), and Alzheimer’s dementia
current neurocognitive status as well as compar- (Levinson et al. 2005). Currently, in an effort to
isons to previous administrations for the same better identify the occurrence of traumatic brain
individual and comparisons to various refer- injury (TBI), the ANAM is also being used by
ence/normative groups, is also available the US military to establish a baseline of
(VistaLifeSciences 2015). neurocognitive functioning prior to deployment
for all service members (U.S. Army Medical
Department 2009).
Historical Background Data from over nine studies suggest that vary-
ing combinations of ANAM subtest batteries are
The ANAM was originally developed by the US sensitive and specific in detecting neurocognitive
Department of Defense as a means of monitoring change among individuals with neurological dis-
changes in human performance when encounter- orders (Kane et al. 2007). Common uses include
ing environmental challenges but has now screening and triage, monitoring of disease pro-
become a common assessment instrument for gression, and detection of treatment and medica-
use in several clinical populations (Kane et al. tion effects (Kane et al. 2007).
2007) and research applications (Vincent et al., Other uses of the ANAM include evaluation of
2008). The current ANAM is the result of 30+ cognitive functioning in determining fitness for
years of research and is directly linked to older duty, neurotoxicology, human factors engineer-
standardized test batteries, including the Unified ing, and various fields of medicine such as aero-
Tri-Service Cognitive Performance Assessment space, undersea, military operations, and sports
Battery (Reeves et al. 2007). (Reeves et al. 2007). The ANAM4-TBI,
446 Automated Neuropsychological Assessment Metrics

especially reaction time-based tests, has also been Battery, the Air Force Criterion Task Set, Navy
found to have some clinical utility in return to Performance Evaluation Tests for Environmental
duty decisions in the military following concus- Research) with research supporting their respec-
sion (Norris et al. 2013). tive sensitivity, reliability, and validity (Reeves
et al. 2007). As researchers have attempted to
Advantages gather psychometric data for the current ANAM,
The ANAM has been noted as an ideal instru- many have included only subsets of the subtests in
ment for assessing change in neurocognition their studies rather than the entire ANAM battery.
(Roebuck-Spencer et al. 2007). Through ran- For example, a large normative data set has been
domization of stimuli, practice effects are mini- established for the ANAM-TBI-MIL (Vincent
mized across numerous testing sessions et al. 2012).
(Roebuck-Spencer et al. 2007). Further, subtle Various combinations of ANAM subtests have
changes in response time can be more precisely been shown to be both sensitive and specific in
detected as compared to manual calculation of detecting cognitive changes in a number of neu-
response time (Roebuck-Spencer et al. 2007). rological conditions (Kane et al. 2007).
Other advantages include time efficiency and Through the process of multiple baseline
cost-effectiveness, both of which are helpful administrations, test-retest reliabilities across sev-
when attempting to triage large numbers of eral ANAM subtest throughput scores ranged
patients (Kane et al. 2007). from 0.50 to 0.91 with 9 of the 10 estimates
<0.77 (Short et al. manuscript in preparation).
Limitations Construct validity has been established between
Some researchers (e.g., Woodhouse et al. 2013) several of the commonly used ANAM subtests
have suggested that use of computerized assess- (e.g., Math, Running Memory, Code Substitution
ment measures such as the ANAM may not be Delayed Memory, and Logical Reasoning) and
appropriate for some people who exhibit clinical more traditional measure of neurocognitive
signs of a neurological disorder that may interfere function such as Trail Making Test A&B, Ani-
with their ability to complete the assessment in a mal Naming, Controlled Oral Word Association
standardized format (i.e., wide fluctuations in Test, and the Digits Backward and Digit Symbol
attention, disinhibition, disorganized thinking, subtests of the WAIS-III (Short et al. 2007).
language disturbances, etc.). Similarly, the ANAM-GNS has demonstrated a
strong relationship with the Repeatable Battery
Administration for the Assessment of Neuropsychological Sta-
Administration time can range from a few minutes tus (RBANS; Woodhouse et al. 2013). Further-
for a single subtest to 90+ minutes for the entire more, in a mixed clinical sample, the ANAM-
battery (U.S. Army Medical Department 2009). GNS correctly classified 87.9% of patients as
Scoring for the ANAM is computer generated. impaired or not, while sensitivity and specificity
Scores for ANAM subtests can be calculated in a was found to be 81% and 89.1%, respectively
variety of ways, including the percentage of cor- (Woodhouse et al. 2013).
rect responses (accuracy score), mean response
time for accurate responses (MS), and the ratio
of accuracy and speed or number of correct Future Directions
responses per minute (throughput score) (Jones
et al. 2008). The use of the ANAM in various fields of med-
icine and science continues to develop as
Psychometrics evidenced by recent studies attempting to vali-
The subtests of the ANAM were selected from date specified subsets of the ANAM battery.
previously established assessment instruments Examples include validation of the ANAM-
(e.g., Walter Reed Performance Assessment sports medicine battery (ASMB) designed for
Automated Neuropsychological Assessment Metrics (ANAM) 447

surveillance and management of sports-related (ANAM): Issues and challenges. Archives of Clinical
concussions (Cernich et al. 2007); use of ANAM Neuropsychology, 22, S79–S87. References – ANAM.
Settle, J. R., Robinson, S. A., Kane, R., Maloni, H. W., &
tests to assess the effects of extreme environ- Wallin, M. T. (2015). Remote cognitive assessments for A
mental stressors such as high altitude, toxins, patients with multiple sclerosis: A feasibility study.
and radiation exposure (Lowe et al. 2007); and Multiple Sclerosis Journal, 21, 1072–1079.
assessment of medication efficacy and potential Short, P., Cernich, A., Wilken, J. A., & Kane, R. L. (2007).
Initial construct validation of frequently employed
medication side effects, specifically for CNS- ANAM measures through structural equation model-
active drugs (Wilken et al. 2007). ing. Archives of Clinical Neuropsychology, 22S,
S63–S77.
Short, P., Ivins, B. J., & Kane, R. L. (n.d.). (manuscript in
preparation). Reliability characteristics of select Auto-
Cross-References mated Neuropsychological Assessment Metrics
(ANAM) measures.
▶ Cognitive Functioning U.S. Army Medical Department. (2009). Automated neuro-
▶ Concussion psychological assessment metrics (ANAM). www.medi
cine.army.mil/prr/anam.html. Retrieved 10 Mar 2009.
▶ Mild Traumatic Brain Injury Vincent, A. S., Bleiberg, J., Yan, S., Ivins, B., Reeves,
▶ Traumatic Brain Injury (TBI) D. L., Schwab, K., et al. (2008). Reference data
from the automated neuropsychological assessment
metrics for use in traumatic brain injury in an
active duty military sample. Military Medicine,
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Vincent, A. S., Roebuck-Spencer, T., Gilliland, K., & Schle-
Cernich, A., Reeves, D., Sun, W., & Bleiberg, J. (2007). gel, R. (2012). Automated neuropsychological assessment
Automated neuropsychological assessment metrics metrics (v4) traumatic brain injury battery: Military nor-
sports medicine battery. Archives of Clinical Neuropsy- mative data. Military Medicine, 177, 256–269.
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Jones, W. P., Loe, S. A., Krach, K., Rager, R. Y., & Jones, fesciences.com/anam-faq.html. Retrieved 3 Oct 2015.
H. M. (2008). Automated neuropsychological assess- Wilken, J. A., Sullivan, C. L., Lewandowski, A., & Kane,
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of cognitive ability: A concurrent validity study. The effect profiles and efficacy of medication. Archives of
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Wilken, J. (2007). Identifying and monitoring cognitive Roebuck-Spencer, T., Domboski-Davidson, K.,
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psychological assessment metrics (ANAM) tests. ANAM General Neuropsychological Screening battery
Archives of Clinical Neuropsychology, 22S, (ANAM GNS) for detecting neurocognitive impair-
S115–S126. ment in a mixed clinical sample. The Clinical Neuro-
Levinson, D., Reeves, D., Watson, J., & Harrison, psychologist, 27, 376–385.
M. (2005). Automated neuropsychological assessment
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Lowe, M., Harris, W., Kane, R. L., Banderet, L., Levinson, Automated
D., & Reeves, D. (2007). Neuropsychological assess- Neuropsychological
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Neuropsychology, 22S, S89–S99.
Norris, J. N., Carr, W., Herzig, T., Labrie, D. W., & Sams,
R. (2013). ANAM4 TBI reaction time-based tests have Tamara McKenzie-Hartman
prognostic utility for acute concussion. Military Medi- Defense and Veterans Brain Injury Center, James
cine, 178, 767–774. A. Haley, VA Hospital, Tampa, FL, USA
Reeves, D. L., Winter, K. P., Bleiberg, J., & Kane, R. L.
(2007). ANAM genogram: Historical perspectives,
description, and current endeavours. Archives of Clin-
ical Neuropsychology, 22S, S15–S37. Synonyms
Roebuck-Spencer, T., Sun, W., Cernich, A. N., Farmer, K.,
& Bleiberg, J. (2007). Assessing change with the auto-
mated neuropsychological assessment metrics ANAM4
448 Automated Neuropsychological Assessment Metrics (ANAM)

Description assessment of cognitive changes secondary to

injury, exposure, or environmental factors.
The Automated Neuropsychological Assessment The DoD currently uses the ANAM Version
Metrics (ANAM) is a computerized assessment of 4.0 (ANAM4), which is the traumatic brain injury
cognitive functioning originally developed by the military battery. The ANAM4 can be adminis-
Department of Defense (DoD). The ANAM was tered in approximately 15–20 min and contains a
initially developed in 1984 and has undergone specialized subset of tests and questionnaires from
multiple revisions. The original version contained the full ANAM library (see Table 1). The trau-
over 30 test modules and has four standardized matic brain injury (TBI) military battery collects
batteries for the assessment of astronauts in space demographic information and mood and sleep
(ANAUT), mild traumatic brain injuries (MILD), responses and tests cognitive domains including
moderate to severe traumatic brain injuries processing speed, working memory, visuospatial
(MODERATE), or neurologically normal individ- ability, and memory (Rice et al. 2011). Modules
uals (STANDARD) (Levinson and Reeves 1997). contain parameters that are modifiable (i.e., num-
The ANAM’s modules can be grouped into flex- ber and rate of stimuli, appearance of some stim-
ible or standardized fixed batteries for the uli, etc.), and ANAM software creates

Automated Neuropsychological Assessment Metrics (ANAM), Table 1 ANAM4 TBI battery test descriptions
Test (abbreviation) Description
Demographics/history module An array of information including name, age, gender, ethnicity, education, and
(SUB) relevant historical and medical information are collected here. See Fig. 1a
TBI questionnaire (TBQ) Questions to assess injury history and symptomatology
Sleepiness scale (SLP) The scale provides a state and/or trait evaluation of energy-fatigue level. See Fig. 1b
Mood scale II-revised (MOO) The scale assesses mood state or trait among seven categories including vigor (high
energy), happiness (positive disposition), depression (dysphoria), anger (negative
disposition), fatigue (low energy), anxiety (worry), and restlessness (motor
agitation). See Fig. 1c
Simple reaction time (SRT) The test serves as a measure of visuomotor reaction time. Simple reaction time is
assessed by presenting the examinee with a series of symbols and instructing him/
her to respond as quickly as possible once the target symbol appears. See Fig. 1d
Code substitution-learning Measures visual search, sustained attention, and working memory. The examinee is
(CDS) asked to compare a displayed symbol-digit pair against a symbol-digit key and
decide whether the stimulus in question represents a correct or incorrect match. See
Fig. 1e
Procedural reaction time (PRO) This test measures information processing speed, visuomotor speed, and attention.
The examinee is presented with a stimulus on the screen (either a 2, 3, 4, or a 5) and
asked to press the left mouse key for a “low” number (either 2 or 3) or the right
mouse key for a “high” number (either a 4 or 5). See Fig. 1f
Math processing (MTH) This task assesses basic computational skills, concentration, and working memory.
The examinee is asked to solve mathematical operations requiring an addition and
subtraction sequence in the form of “x þ y  z=”. The examinee must indicate if
the solution to the problem is greater than or less than five. See Fig. 1g
Matching to sample (M2S) The measure assesses spatial processing and visuospatial working memory. The
examinee is instructed to view a pattern that is produced in eight shaded blocks in a
4  4 grid and then compare two differing patterns presented side by side. The
examinee is asked to choose the pattern that matched the initial stimulus. See Fig. 1h
Code substitution- delayed The test measures delayed memory. The examinee is asked to compare a displayed
recognition (CDD) symbol-digit pair with previously learned symbol-digit pairs (the key). The
examinee indicates whether the symbol or the digit pair is a correct or incorrect
combination. See Fig. 1i.
Simple reaction time repeat The test is a repeat of the simple reaction test earlier in the battery and is used as
(SR2) another measure of visuomotor response speed
Automated Neuropsychological Assessment Metrics (ANAM) 449

Automated Neuropsychological Assessment Metrics (ANAM), Fig. 1 (continued)

“randomized stimuli across tests sessions, thereby computer keyboard and mouse are used for
producing multiple alternate forms” (Reeves et al. responding to the test. Administration procedures
2007). The ANAM4 manual also reports that the follow the general guidelines of the American
test is automated and largely self-administered, Psychological Association (APA) and encourage
requires minimally demanding motor responses a quiet, comfortable environment without
(mouse click), and has millisecond timing accu- distractions.
racy and large capacity data collection. ANAM software produces a report that
ANAM operates on a variety of platforms includes a comparison to an individual’s baseline
including desktop computers, laptops, wireless data (if available) or military normative scores.
networks, handheld devices, and the web. The The ANAM Access Database (AADB) automates
450 Automated Neuropsychological Assessment Metrics (ANAM)

Automated Neuropsychological Assessment Metrics (e) Code substitution-learning (CDS). (f) Procedural reac-
(ANAM), Fig. 1 ANAM4-TBI battery module visual tion time (PRO). (g) Math processing (MTH). (h)
descriptions. (a) Demographics module. (b) Sleepiness Matching to sample (M2S). (i) Code substitution-delayed
scale. (c) Mood scale. (d) Simple reaction time (SRT). recognition (CDD)

the import of raw and summary data and generates graphs for evaluating an individual’s serial
user interface screens that assist the examiner in ANAM performance.
viewing tables (including file and error log tables
for viewing questionable raw or summary data),
as well as subtest level data. Scores produced Historical Background
within the report include (1) mean response time
for all responses, (2) percent of correct responses, Development of the ANAM test battery began in
(3) mean response time for correct responses, (4) 1984 and was derived from computerized tests
standard deviation of the mean response time for developed by the joint military services. Prior to
all responses, (5) standard deviation of the mean its development, the DoD explored initiatives dat-
response time for correct responses, (6) median ing back to the 1970s to evaluate cognition to
response time for all responses, (7) median determine the impact of chemical warfare and
response time for correct responses, (8) the calcu- characterize war fighter capabilities (Reeves
lated number of correct responses per minute (also et al. 2007). The need for a neurocognitive assess-
referred to as “throughput,” which measures cog- ment tool (NCAT) was underscored in the 1990s
nitive efficiency), (9) response omissions, and with the return of service members with persistent
(10) premature responses (i.e., responses of less cognitive complaints following the Gulf War. In
than 130 ms). ANAM ClinicView is a software 1995, the Office of Military Assessment devel-
that can also be utilized in creating tables and oped the first iteration of the ANAM. A research
Automated Neuropsychological Assessment Metrics (ANAM) 451

emphasis on ANAM computerized assessment inconclusive evidence to support conducting rou-

following TBI beginning in 2001. tine pre-deployment baseline testing with the
Signed into public law on January 28, 2008, ANAM4, inconclusive evidence illustrating A
Section 1673 of the National Defense Authoriza- advantages of using the ANAM for the assess-
tion Act (NDAA HR 4986) instructed the secre- ment of mTBI versus a normative dataset, limita-
tary of defense to establish a protocol for tions of the ANAM4 dataset variables, and a lack
assessing and documenting pre-deployment cog- of data supporting the ANAM4’s utility in consis-
nitive functioning for service members deploying tently or significantly contributing to the long-
outside the USA to be later used as a reference term prognosis after a mTBI, were highlighted.
point following a TBI (DoD 2008). In accordance Two approaches have been used to evaluate the
with the statute, and in advance of evidence sensitivity of neurocognitive assessment tools to
supporting any single neurocognitive assessment assess mild TBI with inconclusive results. One
tool (NCAT), the ANAM was selected by a DoD approach includes comparing performance to
consensus panel as the interim measure to be population normative data, and the second
utilized pending further research. As it stands, includes intraindividual performance that com-
the ANAM must be administered within pares post-injury results to baseline performance.
12 months prior to deployment; however, it is not Arguments for both approaches have ensued
routinely administered upon return from deploy- (Hinton-Bayre 2015; Louey et al. 2014; Roe-
ment unless the service member endorses having a buck-Spencer et al. 2013; Broglio et al. 2007;
potentially concussive event on the Post-Deploy- Kelly et al. 2012; Iverson and Schatz 2015).
ment Health Reassessment (PDHRA). The ANAM Thus, the continued utility of pre-deployment
must be readministered prior to a subsequent baseline cognitive assessments remains uncertain.
deployment if it has been more than 12 months Furthermore, the ANAM4 dataset has been crit-
since the previously established baseline. icized for the limited stratification of test data. In
Currently, the DoD uses both the ANAM and 2008, a reference set of baseline tests with 107,000
the Immediate Post-Concussion Assessment and test scores were stratified by age and sex. Expan-
Cognitive Testing (ImPACT) tool to evaluate sion efforts that include additional factors such as
baseline and post-injury cognitive functioning. education, race, handedness, ethnicity, socioeco-
ImPACT is utilized specifically for service mem- nomic status, and rank with approximately 1.1 mil-
bers who are part of the US Military Special lion ANAM4 test scores are reportedly being
Operations units. Studies thus far have not planned (Defense Health Board 2016). Due to the
shown either tool to have a distinct advantage in limitations in stratifying the data, the ANAM4 has
assisting with the assessment or management of further been criticized for an inability to accurately
mild traumatic brain injury (mTBI) (Defense estimate baseline cognitive functioning for individ-
Health Board 2016). As of September 2015, the uals who score at either the high or low ends of the
DoD has reportedly collected over 1.8 million cognitive spectrum.
ANAM4 test results (2016). Published studies evaluating ANAM normative
data show strong age-related effects on reaction
time scores (i.e., slower processing/efficiency
Psychometric Data with increased age) (Vincent et al. 2012). The effect
of gender has been reported to be minimal on most
The ANAM4 is extensively used for the assess- subtests; however, some evidence supports faster
ment of mTBI within the DoD. Research has responding among males as compared to females
posited that many challenges remain in improving (Vincent et al. 2012). Some evidence also suggests
the test’s sensitivity and specificity (Coldren et al. that the effect of education is minimal when con-
2012; Cole et al. 2017; Kelly et al. 2012). In a trolling for age; however, higher education levels
report from the Defense Health Board (2016), a have been associated with better mathematical pro-
number of critical findings, including cessing (Roebuck-Spencer et al. 2008).
452 Automated Neuropsychological Assessment Metrics (ANAM)

Early research has highlighted the lack of data a recent study comparing four neurocognitive
supporting the ANAM’s reliability and sensitivity assessment tools did not support significant con-
in detecting individual impairment after a head vergent or discriminant validity between any of
injury. Test-retest reliability for the ANAM4 has the computerized measures and traditional neu-
been reported to range from 0.68 to 0.74 ropsychological tests (Cole et al. 2017). Overall,
depending on the timeframe between assessment the reliability and validity for the ANAM4 are
sessions (e.g., several months to 1 year), though a similar to other neurocognitive assessment tools
recent study reported the reliability across (Cole et al. 2013).
neurocognitive assessment tools to be “less than
suggested for clinical use” (Cole et al. 2013).
Other factors such as fatigue, pain, mood, effort, Clinical Uses
medication, and reported symptom severity have
also been fond to negatively impact the reliability The ANAM reportedly has a wide range of mili-
of ANAM4 test results (Bruce and Echemendia tary and clinical applications. The predominant
2009; Cooper et al. 2014; Ivins et al. 2009; Suhr use of the ANAM is within the military setting
and Gunstad 2005). Additionally, the current pol- to obtain pre-deployment baseline scores for com-
icy of administering the ANAM4 in a group set- parison in the event of subsequent injury during
ting is also believed to negatively impact baseline deployment. Baseline scores on the measure are
test scores (Moser et al. 2011). stored on a master database and are reported to be
Research suggests that the ANAM4 does suc- available with a quick turnaround time to any
cessfully identify cognitive deficits among clinician who needs them. Scores obtained in the-
concussed individuals, with specificity for indi- ater can be compared to an individual’s own base-
vidual subtests, as well as the combined battery, line data so that better treatment and return-to-
reported at greater than 0.80 (Register-Mihalik et duty (RTD) decisions can be made (DCoE 2011).
al. 2013). In contrast, sensitivity was found to be However, while having a cognitive baseline
low for both individual subtests and the test post-injury theoretically makes sense, evidence
battery as a whole (Broglio et al. 2007; Regis- demonstrating the advantage of this method for
ter-Mihalik et al. 2013). Register-Mahilik and evaluating mTBI has been reported to be inconsis-
colleagues (2013) found that while sensitivity tent (Defense Health Board 2015). Additionally,
increased by 50% when the individual’s symp- while the majority of ANAM tests administered
toms were taken into account, it was not signif- are for establishment of a baseline of cognitive
icant enough to warrant the utilization of the performance, recent findings suggest that baseline
ANAM4 as an independent measure of mTBI. evaluation are not assessed for the majority of the
Several research studies support the simple reac- population that has undergone testing post-injury.
tion time subtest as the most sensitive and effec- The primary explanation is that most injuries have
tive subtest within the ANAM, in differentiating occurred stateside (e.g., secondary to training acci-
concussed versus non-concussed service mem- dents) where baseline cognitive assessments are not
bers (Bryan and Hernandez 2012; Eckner et al. required (Helmick et al. 2015).
2014; Norris et al. 2013), particularly when Variation across military settings exists. The
administered within 72 h of injury (Coldren et US Naval Academy (USNA) also requires
al. 2012; Kelly et al. 2012). No studies to date that their midshipmen undergo baseline
assessing the usefulness of the ANAM4 in pre- cognitive testing with a slightly different version
dicting long-term prognosis have been published of the ANAM4 that utilizes additional subtests
(Defense Health Board 2016). assessing executive functioning, visuospatial
Some evidence supports construct validity processing, working memory, and effort (Defense
with traditional neuropsychological measures of Health Board 2016). When midshipmen experi-
information processing speed, attention, and ences a TBI, they are removed from normal activ-
working memory (Vincent et al. 2012). However, ity until complete resolution of their symptoms
Automated Neuropsychological Assessment Metrics (ANAM) 453

(as assessed by repeated ANAM4 assessments); References

if scores remain below their baseline, they are
then sent for additional testing, treatment, and Broglio, S. P., Macciocchi, S. N., & Ferrara, M. S. (2007). A
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document cognitive changes secondary to multi- metrics subtest scores relative to predeployment base-
ple sclerosis, Parkinson’s disease, Alzheimer’s line performance among service members evaluated for
traumatic brain injury in Iraq. The Journal of Head
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diagnostic or screening tool for concussion more than
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(Echemendia et al. 2013). ANAM can be admin- 179–183. Retrieved from http://militarymedicine.
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F. M., & Lewis, S. C. (2013). Test-retest reliability of
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decisions (DCoE 2011). Lewis, J. D., & Bowles, A. O. (2014). Factors
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OIF/OEF service members with postconcussive
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Defense Centers of Excellence (DCoE) for Psychological
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Recommendations_Post_Injury_NCAT_05-31-2011_
See Also f.pdf
Defense Health Board. (2016, February). Review of the
▶ Battlefield Assessment scientific evidence of using population normative
values for post-concussive computerized
▶ Defense and Veterans Brain Injury Center neurocognitive assessments. Retrieved from http://
▶ Military Acute Concussion Evaluation health.mil/Reference-Center/Reports/2016/02/10/Post-
▶ Pre-deployment Cognitive Testing Concussive-Computerized-Neurocognitive-Assessments
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Kelly, M. P., Coldren, R. L., Parish, R. V., Dretsch, M. N., individuals with mild head injury. Journal of the Inter-
& Russell, M. L. (2012). Assessment of acute concus- national Neuropsychological Society, 11(1), 23–29.
sion in the combat environment. Archives of Clinical https://doi.org/10.1017/S1355617705050010.
Neuropsychology, 27(4), 375–388. https://doi.org/ Vincent, A. S., Roebuck-Spencer, T., Gilliland, K., &
10.1093/arclin/acs036. Schlegel, R. (2012). Automated neuropsychological
Levinson, D. M., & Reeves, D. L. (1997). Monitoring assessment metrics (v4) traumatic brain injury
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Automaticity 455

Chapey, R. (Ed.). (2001). Language intervention strategies in

Automatic Language aphasia and related neurogenic communication disorders
(4th ed.). Philadelphia: Lippincott, Williams & Wilkins.
Davis, G. A. (2014). Aphasia and related cognitive- A
Roberta DePompei communicative disorders. Boston: Pearson.
School of Speech-Language, Pathology and Papathanasiou, I., Coppens, P., & Potagas, C. (2013).
Audiology, University of Akron, Akron, OH, Aphasia and related neurogenic communication disor-
ders. Burlington: Jones and Bartlett Learning.
USA

Synonyms
Automaticity
Nonpropositional language
Anna MacKay-Brandt
Nathan S. Kline Institute for Psychiatric Research,
Orangeburg, NY, USA
Definition
Taub Institute for Research on Alzheimer’s
Disease and the Aging Brain, Columbia
Automatic language is the use of nonpropositional
University, New York, NY, USA
language forms. Even if the patient is unable to
converse at all, he or she may produce automatic
responses. These responses may be (a) automatized
sequences, counting, reciting the alphabet, and
Definition
saying the days of the week; (b) memorized
sequences, prayers pledge of allegiance; (c) recur-
A mental operation that proceeds without volun-
rent social speech, “Have a nice day” and “How are
tary control and without requiring capacity or
you?”; and (d) emotional speech: cursing or a
processing resources.
typically stated sentence when emotionally upset.
It is important to note that these types of responses
are not clearly thought out and are not under the
cognitive control of the patient. These responses do
not represent propositional language skill and
Current Knowledge
should not be considered as a conscious attempt
to participate in conversational situations. Auto- Automatic processes are usually found in the context
of stimulus information that is well integrated into
matic language can be found in severe aphasias
and in many dementias. It may also occur in mental the individual’s memory through either a classical
health problems such as schizophrenia. conditioning, an overlearned behavior (e.g., reading),
or an evolutionarily adaptive response (e.g., orienting
response). The Stroop effect (Stroop 1935; MacLeod
1992) is a good example of the influence of automa-
Cross-References
ticity on behavior. Reading becomes automatic at a
▶ Stereotypy level of proficiency acquired by most school-aged
children, such that it is out of an individual’s control
not to read a presented word. This involuntary
References and Readings response is captured in the interference it produces
when one attempts to ignore a color word and instead
Alajouanine, T. (1956). Verbal realization in aphasia. name the color of the stimulus. Color naming is
Brain, 79, 1–28. slower when the color word and the color of the
Blanken, G., & Marini, V. (1997). Where do lexical speech stimulus are incongruent when compared to the
automatisms come from? Journal of Neurolinguistics,
stimulus which is neutral (a series of Xs or a noncolor
10(1), 19–31.
456 Automatism

word) or congruent (the color word is the same as the automatisms. Automatisms may occur during sei-
stimulus color). zures or as postictal phenomena. Speech automa-
tisms tend to lateralize to the left hemisphere, but
lateralization is not predictable for other automa-
Cross-References tisms (Rasonyi et al. 2006). Responsiveness is
usually lost when automatisms occur during sei-
▶ Controlled Attention zures. Rarely, patients may have preserved respon-
▶ Orienting Response siveness in the presence of seizure-induced
▶ Reading Fluency automatisms and only with seizures that arise
▶ Stroop Effect from right hemisphere foci (Ebner et al. 1995).
In addition to epileptic seizures, automatisms
may also be observed in other situations including
References and Readings intoxication, sleep walking, hypoglycemia, and
psychological disorders, such as dissociative
MacLeod, C. M. (1992). The Stroop task: The “gold stan- fugue states. Forensic assessments aimed at deter-
dard” of attentional measures. Journal of Experimental
Psychology: General, 121, 12–14. mining culpability often center around the differ-
Stroop, J. R. (1935). Studies of interference in serial verbal ential diagnosis of automatisms (Fenwick 1990).
reactions. Journal of Experimental Psychology, 18,
643–662.
Cross-References

▶ Complex Partial Seizure

Automatism

Douglas I. Katz References and Readings

Department of Neurology, Boston University
School of Medicine, Braintree, MA, USA Ebner, A., Dinner, D. S., Noachtar, S., & Luders, H.
(1995). Automatisms with preserved responsiveness:
A lateralizing sign in psychomotor seizures. Neurology,
45(1), 61–64.
Synonyms Fenwick, P. (1990). Automatism, medicine and the law. Psy-
chological Medicine. Monograph Supplement, 17, 1–27.
Automatic behavior Rasonyi, G., Fogarasi, A., Kelemen, A., Janszky, J., &
Halasz, P. (2006). Lateralizing value of postictal autom-
atisms in temporal lobe epilepsy. Epilepsy Research, 70
(2–3), 239–243.
Definition

This is a complex movement that occurs without

conscious awareness or purposeful intent. Autonomic Nervous System

Scott Vota
Current Knowledge Department of Neurology, Virginia
Commonwealth University, Richmond, VA, USA
Automatisms may occur in the setting of complex-
partial seizures. Typical simple movements include
lip smacking, chewing, or finger rubbing. More Synonyms
complex automatisms include walking, running,
undressing, and speaking. Emotional expressions, Internal regulation system; Involuntary nervous
such as laughing or crying, may also occur as system; Visceral nervous system
Autonomic Nervous System 457

Definition

The autonomic nervous system is a complex and Insular cortex

A
vital system that helps to maintain homeostasis
and adaptation throughout the human body. It is
composed of both central and peripheral compo- Paraventricular
nents that provide thermoregulation, arterial nucleus
blood pressure adaptation, as well as alterations
Central nucleus
in regional blood flow in response to metabolic of the amygdala
demands, micturition, gastrointestinal motility,
and sexual function. Lateral hypothalamic area

Current Knowledge Periaqueductal

gray matter

Central Component
The central components of the autonomic nervous
system are located within the cerebral cortex, thal-
Parabrachial
amus, hypothalamus, hippocampus, and cerebel- region
lum. These components are integrally connected
via a network of ascending and descending path-
ways (see Fig. 1). This provides a high level of
control over autonomic function. These intercon- Nucleus of the
nections ultimately descend to specific cells within tractus solitarius
the brainstem and spinal cord. The thoracolumbar
Nucleus ambiguus
outflow consists of fibers that arise in the
intermediolateral cell column of the thoracic and Ventrolateral
first two lumbar segments of the spinal cord. This is medulla
the origin of the sympathetic division of the auto-
nomic nervous system. The cranial outflow, arising Autonomic Nervous System, Fig. 1 Central compo-
from the cranial nerve nuclei III, VII, IX, and X, nents of the autonomic nervous system (Benarroch et al.
and the sacral outflow, arising from cell bodies in 1999)
the intermediate cell column of sacral segments
2 through 4, form the parasympathetic division of parasympathetic and sympathetic divisions
the autonomic nervous system. release acetylcholine, but the difference lies in
the postganglionic neurotransmitter release. The
Peripheral Component parasympathetic postganglionic fibers release
The peripheral part of the autonomic nervous norepinephrine and epinephrine and thus are
system is then composed of sympathetic and para- referred to as cholinergic. The sympathetic post-
sympathetic pathways. These pathways arise from ganglionic fibers release norepinephrine and epi-
two distinct anatomic portions of the brainstem nephrine and thus are classified as adrenergic. The
and spinal cord. The parasympathetic fibers arise terminals of sympathetic fibers on sweat glands,
from the craniosacral portion, and the sympathetic however, do not follow this pattern and are cho-
fibers arise from the thoracolumbar region. linergic (see Figs. 2 and 3).
Although anatomically separated, the two parts
are complementary in maintaining a balance in Parasympathetic Nervous System
the activities of many visceral structures and Parasympathetic outputs arise from the pregangli-
organs. The preganglionic neurons for both the onic neurons located in the nuclei of the brainstem
458 Autonomic Nervous System

Autonomic Nervous Ciliary ganglion

System, Fig. 2 Autonomic
nervous system. Ciliary muscle
Parasympathetic nervous Sphenopalatine CN III
system (Benarroch et al. ganglion
1999) Lacrimal gland
Submandibular CN VII
ganglion
Salivary glands

Parotid gland
CN IX
Otic ganglion
1
2
Larynx and trachea (CN X) 3
Lungs Vagus 4
Heart 5
6

Gastrointestinal tract 7

8
Abdominal organs
9
10
11
12
Large intestine 1
2
3

S2–4

Kidney
Bladder
Sex organs

and sacral spinal cord. Preganglionic parasympa- (producing lacrimation) and the cerebral and
thetic axons travel a long distance before eventually cranial blood vessels (eliciting vasodilatation).
reaching their target ganglia, which are typically Axons also travel to the submandibular gan-
close to or within the target end organ. glion, providing secretomotor and vasodilator
The cranial preganglionic parasympathetic inputs to the corresponding salivary glands.
nuclei (Edinger-Westphal nuclei) project The inferior salivatory nucleus sends axons via
through the oculomotor nerve. These pregangli- the glossopharyngeal nerve to ultimately syn-
onic axons synapse on neurons of the ciliary apse on the otic ganglion, stimulating parotid
ganglion. The neurons innervate the iris and gland secretion. Most preganglionic parasympa-
ciliary muscles, eliciting pupillary constriction thetic output from the brainstem is mediated by
and accommodation of the lens. The superior the vagus nerve, which receives input from the
salivatory nucleus located in the pons projects dorsal motor nucleus of the vagus and the lateral
via the facial nerve to the sphenopalatine gan- portion of the nucleus ambiguus. The vagus
glion. This innervates the lacrimal gland nerve innervates the heart, respiratory tract, and
Autonomic Nervous System 459

Autonomic Nervous
System, Fig. 3 Autonomic
nervous system.
Sympathetic nervous A
system (Benarroch et al.
1999) Ciliary muscle
Lacrimal gland
Salivary glands C1

Larynx and 1
T1
trachea 2
3
Lungs 4
5
Celiac
ganglion 6
Heart
7
Stomach 8
Small intestine 9
10
Adrenal medulla 11
12
1
Superior mesenteric 2
ganglion 3

Large intestine
L1
Kidney
Bladder
Inferior
Sex organs mesenteric
ganglion

the entire gastrointestinal tract with the excep- Sympathetic Nervous System
tion of the descending colon and rectum. The sympathetic preganglionic neurons are pri-
The sacral preganglionic output arises from marily located in the intermediolateral nucleus
neurons of the sacral preganglionic nucleus in the thoracic and upper lumbar regions of the
located in the lateral gray matter of the sacral spinal cord. The preganglionic sympathetic
spinal cord. These axons travel to the pelvic axons exit through the ventral roots and pass
splanchnic nerves, which join the inferior hypo- on to the corresponding spinal nerve to reach
gastric plexus to innervate the descending colon, the paravertebral sympathetic chain. The major-
bladder, and sexual organs. These outputs elicit ity of the presynaptic fibers branch and run ros-
contraction of the bladder detrusor muscle and trally or caudally along the sympathetic chain
circular smooth muscle of the rectum as well as and synapse on the paravertebral ganglia. The
regulating vasodilatation of the cavernous tissue remaining fibers pass through the paravertebral
of the penis required for erection. chain without synapsing. These form the
460 Autonomic Nervous System

splanchnic nerves which innervate prevertebral help develop a proper differential diagnosis and
ganglia. laboratory evaluation. The goals of the clinical
The paravertebral sympathetic ganglia are pri- evaluation are to identify the presence, location,
marily a relay station for preganglionic inputs. and time course of autonomic dysfunction. This
They innervate all tissues and organs except those will help to determine which part(s) of the auto-
in the abdomen, pelvis, and perineum. For exam- nomic nervous system may be involved: sympa-
ple, the superior cervical ganglion sends postgan- thetic noradrenergic, sympathetic cholinergic,
glionic axons to innervate the eye, facial sweat parasympathetic cholinergic, or adrenomedullary.
glands, salivary glands, and pineal, thyroid, and Specific questions should be asked to determine if
parathyroid glands. These outputs elicit pupil dila- the patient may have symptoms of orthostatic
tation, contraction of the Muller muscle of the hypotension, anhydrosis, weight change, consti-
eyelid, facial sweating, and vasoconstriction in pation, sexual dysfunction, sialorrhea, or urinary
facial and cerebral circulation. The stellate gan- retention. Questions related to aggravating and
glion, which receives preganglionic input from relieving factors need to be considered. Examples
the mid-thoracic segment, sends postganglionic include relationship to meals, environmental tem-
axons to innervate blood vessels and sweat glands perature, and diurnal variation. A complete listing
in the upper limbs and trunk. These outputs pro- of all prescribed medications as well as over-the-
duce either vasoconstriction or vasodilatation in the counter herbal and dietary supplements need to be
skin and muscle, sweating, or piloerection. Outputs reviewed.
from the stellate ganglion also elicit cardiac accel-
eration and bronchodilation. The lumbar para- Examination
vertebral ganglia subsequently innervate the An exam should start with a general overview of
blood vessels and sweat glands in the lower limb. the patient making note of facial expression, pos-
The prevertebral ganglia are located anterior ture, and height. Vital signs should be checked in
to the abdominal aorta. Preganglionic input from the supine, seated, and standing positions.
the lower thoracic segments is carried by the A thorough skin examination making note of
splanchnic nerves to the celiac and superior mes- acrocyanosis, pallor, mottling, diaphoresis, alope-
enteric ganglia and provides postganglionic cia, or erythema should be performed. An eye
fibers to the celiac plexus that innervates all exam can also be valuable. Attention should be
abdominal viscera, with the exception of the given to pupillary shape, size, and the response to
descending colon. These outputs produce vaso- light and accommodation.
constriction and inhibition of the gastrointestinal
tract motility. Preganglionic axons from the lum- Diagnostic Testing
bar spinal segments travel via the lumbar A workup to uncover an etiology for autonomic
splanchnic nerves to synapse in the inferior mes- dysfunction should begin with routine serologic
enteric ganglion. These axons innervate the testing. This includes serum electrolytes, glucose,
descending colon, rectum, bladder, and sexual hepatic function tests, protein electropheresis, and
organs eliciting vasoconstriction, smooth muscle a complete blood count. Further serologic testing
relaxation of the bladder and rectum, constriction may include cortisol levels, paraneoplastic auto-
of the internal sphincter of the bladder and rec- antibodies, and plasma catecholamines. An EKG
tum, and ejaculation. and echocardiogram should also be performed.
A variety of more specialized tests, both inva-
Diagnosing Autonomic Dysfunction sive and noninvasive, may also need to be consid-
ered. These include but are not limited to the
Medical History following: deep breathing and Valsalva ratio, iso-
As the autonomic nervous system innervates all metric handgrip and cold pressor tests, thermoreg-
organ systems, a detailed medical history and ulatory sweat and skin sympathetic tests,
physical examination is paramount. This will quantitative sudomotor axon reflex testing,
Autoreceptor 461

power spectral analysis of heart rate variability, tilt Ropper, A. H., & Brown, R. H. (2005). Adams and Victor’s
table testing, and neuroimaging such as PET principles of neurology (8th ed.). New York: McGraw-
Hill.
scanning. Rowland, L. P. (2005). Merritt’s neurology (11th ed.). Phil- A
adelphia: Lippincott Williams and Wilkins.
Treatment
Both nonpharmacologic and pharmacologic treat-
ments are available to treat patients with auto-
nomic dysfunction. For certain disorders, Autoreceptor
surgical intervention may be needed. The goal is
to ameliorate all symptoms while avoiding side Maya Balamane1, Beth Kuczynski2 and
effects. Stephanie A. Kolakowsky-Hayner3
1
Nonpharmacologic measurements start with Mount Sinai Brain Injury Research Center, San
patient education. Symptoms such as rising Francisco, CA, USA
2
slowly from a seated position or modifying Imaging of Dementia and Aging (IDeA)
sodium intake may be enough in some autonomic Laboratory, Department of Neurology and Center
disorders to provide patients with a symptom- for Neuroscience, University of California, Davis,
free life. CA, USA
3
Pharmacotherapy may include medications to Department of Rehabilitation Medicine, Icahn
increase central blood volume, such School of Medicine at Mount Sinai, New York,
fludrocortisones, vasopressin analogues, acetyl- NY, USA
cholinesterase inhibition, or caffeine.

Synonyms
Cross-References
Receptor
▶ Anticholinergic
▶ Arousal
▶ Cerebellum Definition
▶ Cholinergic System
▶ Hippocampus An autoreceptor is a receptor located on the neu-
▶ Hypothalamus ron (terminals, soma, and/or dendrites), and the
▶ Thalamus function is to bind a specific ligand (such as neu-
rotransmitters or hormones) released by that same
neuron. The autoreceptor is mainly used as a
References and Readings feedback mechanism to monitor neurotransmitter
synthesis and/or release. In most cases, a negative
Benarroch, E. E., Westmoreland, B. F., Daube, J. R., Rea- feedback happens, inhibiting the release of the
gan, T. J., & Sandok, B. A. (1999). Medical neurosci- neurotransmitter. Dopaminergic neurons can
ences: An approach to anatomy, pathology, and
have autoreceptors that regulate the release of
physiology by systems and levels (4th ed.). Philadel-
phia: Lippincott Williams and Wilkins. dopamine. Autoreceptor regulation is very effec-
Bradley, W. G., Daroff, R. B., Fenichel, G., & Jankovic, tive in modulating neurotransmission and is of
J. (2004). Neurology in clinical practice (4th ed.). Bos- interest for pharmacological intervention.
ton: Butterworth-Heinemann.
Gilman, S., Newman, S. W., Manter, J. T., & Gatz, A. J.
(2003). Manter and Gatz’s essentials of clinical neuro-
anatomy and neurophysiology (10th ed.). Philadelphia: Cross-References
F.A. Davis Company.
Netter, F. H. (1991). Nervous system, part 1: Anatomy and ▶ Hormones
physiology (Ciba collection of medical illustrations,
Vol. 1). Summit: Ciba-Geigy Corporation. ▶ Neurotransmitters
462 Autotopagnosia

References and Readings disorientation are frequently present at the same

time, particularly following lesions of the left
Carey, R., DePalma, G., Damianopoulos, E., Müller, C., & angular gyrus and may be a part of what has
Huston, J. (2004). The 5-HT1A receptor and behavioral
been defined as Gerstmann’s syndrome. The latter
stimulation in the rat: Effects of 8-OHDPAT on spon-
taneous and cocaine-induced behavior. Psychopharma- would also include deficits in writing (agraphia)
cology, 177(1/2), 46–54. https://doi.org/10.1007/ and arithmetical operations (acalculia).
s00213-004-1917-4.
Meltzer, H. (1980). Relevance of dopamine autoreceptors
for psychiatry: Preclinical and clinical studies. Schizo-
phrenia Bulletin, 6(3), 456–475. Cross-References
Schilcker, E., & Feuerstein, F. (2016). Human presynaptic
receptors. Pharmacology and Therapeutics. https://doi.
▶ Finger Agnosia
org/10.1016/j.pharmthera.2016.11.005. (in press).
▶ Gerstmann’s Syndrome
▶ Right Left Disorientation

Autotopagnosia
References and Readings
John E. Mendoza Benton, A. L., & Sivan, A. B. (1993). Disturbances of the
Department of Psychiatry and Neuroscience, body schema. In K. M. Heilman & E. Valenstein (Eds.),
Tulane Medical School and SE Louisiana Clinical neuropsychology (pp. 123–140). New York:
Veterans Healthcare System, New Orleans, LA, Oxford University Press.
Denberg, N. L., & Tranel, D. (2003). Acalculia and distur-
USA bances of the body schema. In K. M. Heilman &
E. Valenstein (Eds.), Clinical neuropsychology
(pp. 161–184). New York: Oxford University Press.
Definition

Disturbance of body schema involving the loss of

ability to localize, recognize, or identify the spe- Avoidant/Restrictive Food
cific parts of one’s body. Intake Disorder

Kristin M. Graham
Current Knowledge Department of Physical Medicine and
Rehabilitation, Virginia Commonwealth
While some reported cases exhibit impaired University, Richmond, VA, USA
knowledge of most body parts, autotopagnosia is
most frequently manifested as difficulty in identi-
fying or naming specific fingers (finger agnosia), Synonyms
especially the three middle fingers. The problem
extends to identifying comparable body parts on Feeding disorder of infancy or early childhood
the examiner or graphic representations of body
parts. The deficit usually involves both sides of
the body, thus distinguishing it from unilateral Definition
neglect. While not typically classified as such,
right-left disorientation likely reflects another Avoidant/restrictive food intake disorder
form or subtype of autotopagnosia. In this condi- (ARFID) is defined in the Diagnostic and Statis-
tion, patients are unable to reliably identify the tical Manual of Mental Disorders (5th ed.; DSM-
right and left sides of their bodies or those of 5; American Psychiatric Association 2013) as a
others. Both finger agnosia and right-left feeding and eating disorder characterized by
Avolition 463

avoidance or restriction of food intake. Symptoms Because ARFID is a new diagnostic condition,
often manifest as a lack of interest, sensory based effective treatment is still being researched. Treat-
avoidance (e.g., color, smell, texture), or concern ment typically involves both medical and psycho- A
of adverse consequences. Avoidance and/or logical interventions. Psychological interventions
restriction of food intake must also be accompa- are guided by treatment of similar eating disorders
nied by one or more key features, such as signif- such as anorexia nervosa.
icant weight loss or nutritional deficiency, to meet
diagnostic criteria.
See Also

Categorization ▶ Anorexia Nervosa

▶ Feeding and Eating Disorders
The disorder is classified with the feeding and
eating disorders in DSM-5. The disorder replaces
the DSM-IV diagnosis of feeding disorder of References and Readings
infancy or early childhood.
American Psychiatric Association. (2013). Diagnostic and
statistical manual of mental disorders (DSM-5 ®).
Washington, DC: American Psychiatric Association.
Current Knowledge Norris, M. L., & Katzman, D. K. (2015). Change is never
easy, but it is possible: Reflections on avoidant/restric-
Development and Course tive food intake disorder two years after its introduction
ARFID typically develops in infancy or early in the DSM-5. Journal of Adolescent Health, 57(1), 8–9.
Williams, K. E., Hendy, H. M., Field, D. G., Belousov, Y.,
childhood but may continue into adulthood. Riegel, K., & Harclerode, W. (2015). Implications of
The majority of individuals are female. In avoidant/restrictive food intake disorder (ARFID) on
infants and young children, associated features children with feeding problems. Children’s Health
may manifest as irritability, distress, or agitation Care, 44(4), 307–321.
during feeding, lack of engagement with care-
giver, or lack of communication of hunger.
Older children and adolescents may present
with generalized emotional difficulties and fail- Avolition
ure to proceed along the expected developmen-
tal trajectory (e.g., growth delay). The condition Irene Piryatinsky1 and Paul Malloy2
1
can cause failure to thrive and nutritional defi- Butler Hospital and Alpert Medical School of
ciencies. In severe cases, malnutrition can be Brown University, Providence, RI, USA
2
life-threatening and may require enteral feeding. Department of Psychiatry and Human Behavior,
Common comorbid conditions include anxiety Brown University, Providence, RI, USA
disorders, obsessive-compulsive disorder, atten-
tion-deficit/hyperactivity disorder, and autism
spectrum disorders. Synonyms

Assessment and Treatment Apathy

Clinical assessment involves physical examina-
tion, laboratory testing, and evaluation of dietary
intake to determine nutritional deficiency. Differ- Definition
ential diagnoses include other medical conditions,
reactive attachment disorder, autism spectrum dis- Avolition is a severe problem with initiation,
order, anxiety disorders, mood disorders, and volitional or willed action, and production of
other eating disorders such as anorexia nervosa. goal-directed behavior. It may reflect a general
464 Avolition

lack of motivation and drive. Avolition is com- Further Reading

monly seen as one of the negative symptoms in
patients with schizophrenia and is also common Foussias, G., & Remington, G. (2008). Negative symp-
toms in schizophrenia: Avolition and Occam’s
in frontal lobe disorders affecting medial frontal
Razor. Schizophrenia Bulletin Advance Access. 10.
systems. https://doi.org/10.1093/schbul/sbn094.
Liddle, P. F. (1994). Volition and schizophrenia. In A. S.
David & J. C. Cutting (Eds.), The neuropsychology of
See Also schizophrenia (pp. 39–48). Psychology Press.
Rummel, C., Kissling, W., & Leucht, S. (2005). Antide-
▶ Abulia pressants as add-on treatment to antipsychotics for peo-
ple with schizophrenia and pronounced negative
▶ Apathy symptoms: A systematic review of randomized trials.
▶ Cingulate gyrus Schizophrenia Research, 80, 85–97.
B

Babcock, Harriet (1807–1952) psychology to study the cognitive effects of

neurological disease. Her research methods
Anthony Y. Stringer were well characterized and repeatable, she
Department of Rehabilitation Medicine, Emory utilized standardized psychometric measures,
University, Atlanta, GA, USA and she incorporated normal control compari-
son groups in her research. Anticipating later
batteries of neuropsychological tests, Babcock
Major Appointments attempted to quantify deficits in discrete men-
tal abilities and used an “efficiency index” to
• Manhattan State Hospital, New York, summarize the overall functioning of her
1923–1925 patients.
• New York University, New York, 1931–1952 • Babcock based her efficiency index on the idea
that intellectual function varies over time.
More specifically, people may exhibit a higher
Major Honors and Awards
level of intellectual function while healthy and
in the prime of life, than they do after suffering
• Babcock was elected to the New York Acad-
neurological or psychiatric disorders. Babcock
emy of Science and was a Diplomate of the
believed that mental disorders do not affect
American Board of Examiners in Professional
tests of prior knowledge acquisition (e.g.,
Psychology.
vocabulary). She further identified a number
of tests that she thought were sensitive to men-
Landmark Clinical, Scientific, and tal disorders, including tests familiar to con-
Professional Contributions temporary neuropsychologists (e.g., reverse
digit span and various reasoning tasks).
• In the 1930s, Babcock began a longitudinal Babcock quantified mental efficiency by
study of syphilitic patients, a project that was contrasting performance on these two kinds
less notable for its outcomes (many of which of tests, a forerunner of the hold-don’t hold
were not subsequently replicated) than for its test comparison (▶ Hold-Don’t Hold Tests).
methodology. Classic neurological studies • Babcock’s contemporary influence is also evi-
from the time of Paul Broca and Karl Wernicke dent in her story memory format. In this for-
were centered around clinical case observation. mat, a story is initially presented and recall is
In a departure from this classic tradition, tested. The story is presented a second time
Babcock adopted the methods of scientific followed by 10 min of interpolated activity
# Springer International Publishing AG, part of Springer Nature 2018
J. S. Kreutzer et al. (eds.), Encyclopedia of Clinical Neuropsychology,
https://doi.org/10.1007/978-3-319-57111-9
466 Babinski Reflex

and a final recall test. This format has been

adopted in some contemporary memory bat- Babinski Reflex
teries and has the advantage of allowing
the neuropsychologist to test both immediate Edison Wong1 and Richard Kunz2
1
and delayed recall, as well as learning Center for Pain and Medical Rehabilitation,
with repetition. Although the original Fitchburg, MA, USA
2
Babcock Story is rarely used today, some Department of Physical Medicine and
current memory batteries incorporate its Rehabilitation, Virginia Commonwealth
format (▶ Wechsler Memory Scale All Ver- University, Richmond, VA, USA
sions). In this and other respects, Babcock’s
work continues to influence clinical and sci-
entific neuropsychology. Synonyms

Long tract sign; Plantar reflex; Upper motor neu-

Short Biography
ron sign
Little has been written concerning Babcock’s
personal life. She was born in 1877 in Westerly, Definition
Rhode Island. She began her career late in life,
earning her doctoral degree in her 50s. Prior to The Babinski reflex is a component of the neuro-
this, she lived a traditional life as a homemaker. logical exam, used to assess the adequacy of the
She initially gained experience working in psy- pyramidal tract (upper motor neuron). This reflex is
chiatric facilities, but after earning her doctorate, elicited by making contact along the lateral side of
she spent the balance of her career on the faculty the plantar foot with a blunt implement and not
at New York University. Despite her late begin- causing pain, discomfort, or injury to the skin; the
ning, Babcock’s work was an important forerun- implement is run from the heel along a curve to the
ner to the emergence of neuropsychology as a metatarsal pads. There are three responses possible:
scientific field. Babcock died on December 12,
1952. • Extensor (positive or pathological): hallux
(great toe) extension and the other toes abduct
(fanning)
Cross-References • Flexor (negative or normal): all toes flex and
the foot everts
▶ Hold-Don’t Hold Tests • Indifferent: no response
▶ Intelligence
▶ Intelligence Quotient Current Knowledge
▶ Wechsler Memory Scale All Versions
An extensor (positive) response signifies pathology
in the upper motor neuron pathways, either in the
References and Readings spinal cord and/or brain, such as in multiple sclero-
sis, stroke, traumatic brain injury, or spinal cord
Hartman, D. E. (1991). Reply to reitan: Unexamined injury. It may be the sole sign of upper motor neuron
premises and the evolution of clinical neuropsy-
chology. Archives of Clinical Neuropsychology, 6,
damage and is the most popular reflex for evaluation
147–165. of these pathways for the lower limbs. All infants
Stringer, A. Y., & Cooley, E. L. (2002). Neuropsychology: exhibit an extensor response from birth, which con-
A twentieth-century science. In A. Y. Stringer, E. L. verts to a flexor response during ages 12–18 months
Cooley, & A.-L. Christensen (Eds.), Pathways to prom-
inence in neuropsychology: Reflections of twentieth
as the nervous system matures given normal devel-
century pioneers (pp. 3–26). New York: Psychology opment; developmental delay may result in a persis-
Press. tent positive response. Indifferent responses may be
Bacterial Ventriculitis 467

found in normal individuals but may also indicate backward masking paradigm, a visual stimulus
the presence of a lower motor neuron or other (such as a letter) is rapidly presented and followed
peripheral nervous system injury that interferes by a mask that encompasses the area of the visual
with the expression of a normal flexor response. field where the initial stimuli was presented
(Breitmeyer and Ogmen 2000). The presentation B
of the initial stimulus, while rapid, is sufficiently
Cross-References
long enough for a non-backward masked presen-
tation to be perceptible. The mechanisms under-
▶ Developmental Delay
lying backward masking are an active area of
▶ Multiple Sclerosis
research; however, it is well established that cen-
▶ Spinal Cord Injury
tral and likely cortical mechanisms are involved,
▶ Stroke
given the time course of the effect as well as its
▶ Traumatic Brain Injury (TBI)
ability to be produced with dichoptic presentation
(stimulus and mask presented to separate eyes).
References and Readings
References and Readings
Babinski, J. (1896). Sur le reflexe cutane plantaire dans
certaines affections organiques du systeme nerveux
Breitmeyer, B. G., & Ogmen, H. (2000). Recent models
central. Comptes Rendus des Seances de la Societe de
and findings in visual backward masking: a compari-
Biologie et de Ses Filiales, 48, 207–208.
son, review, and update. Perception & Psychophysics,
Larner, A. J. (2016). A dictionary of neurological signs
62(8), 1572–1595. Retrieved from http://www.ncbi.
(4th ed.). Basel: Springer.
nlm.nih.gov/pubmed/11140180
Pearson, K., & Gordon, J. (2000). Spinal reflexes. In E. R.
Kandel, J. H. Schwartz, & T. M. Jessell (Eds.), Princi-
ples of neural science (4th ed., pp. 713–736).
New York: McGraw-Hill.
Bacterial Ventriculitis

Courtney Murphy
Backwards Masking Belmont Behavioral Hospital, Philadelphia,
PA, USA
Eric S. Porges
Department of Clinical and Health Psychology,
University of Florida, Gainesville, FL, USA Synonyms
Center for Cognitive Aging and Memory,
McKnight Brain Institute, University of Florida, Intraventricular infection; Intraventricular inflam-
Gainesville, FL, USA mation; Ventriculomeningitis
Department of Neurology, University of Florida,
Gainesville, FL, USA
Definition

Definition Bacterial ventriculitis refers to inflammation of

the cerebral ventricles, typically resulting from
Backward masking occurs when the perception of intraventricular infection or bacterial infection of
a stimulus is attenuated by the rapid presentation cerebral spinal fluid.
of a subsequent stimulus (the “mask”). Within the
domains of neuropsychology and psychology,
backward masking typically refers to visual phe- Current Knowledge
nomena. However, backward masking has been
explored in other sensory domains such as . . . Bacterial ventriculitis is a potential life-threatening
(may want to list other domains here). In a typical condition that can result from the rupture of a cerebral
468 Balance Disorders

abscess, an infection of an external ventriculostomy inner ear), and somatosensory (sensations from
catheter, an infection of cerebral spinal fluid, and the skin, muscles, tendons, and joints) – in addi-
other infectious CNS conditions. Bacterial infection tion to muscle strength. When these systems are
produces an immune response in the lining of the impaired, individuals may experience episodes of
ventricles, resulting in inflammation. spinning, light headedness, trouble focusing their
Presenting symptoms can be headaches, dizzi- eyes, and/or poor balance or falls.
ness, confusion, photophobia, and neck and upper
back pain and nausea and vomiting in children. In Categorization
infancy, it can cause unrecognized hydrocephalus.
Ventriculitis must be confirmed by examination of Balance may be affected by disturbances of
the cerebrospinal fluid. strength in the trunk or legs, sensation deficits,
or difficulties with coordination. Multiple sys-
tems may be affected. A detailed history and
Cross-References neurological examination may help detect the
affected area. Balance may be impaired after a
▶ Encephalitis (Viral) focal event such as a stroke or may develop
▶ Meningitis during the course of a neurodegenerative disease
such as Parkinson’s disease. Medications and
infections of the brain or inner ear may also
References and Readings contribute to balance difficulties.
Agrawal, A. M., Cincu, R., & Jake, R. (2008). Current
concepts and approach to ventriculitis. Infectious Dis-
eases in Clinical Practice, 16(2), 100–104. Epidemiology
Centers for Disease Control and Prevention (CDC). (2017).
CDC/NHSN surveillance definitions for specific types
Aging may also affect balance. Approximately
of infections. Retrieved from http://www.cdc.gov/nhsn/
PDFs/pscManual/17pscNosInfDef_current.pdf. 40% of people older than age 65 suffer falls each
Tabuchi, S., & Kadowaki, M. (2015). Neuroendoscopic year. Vertigo is the most common form of
surgery for ventriculitis and hydrocephalus after shunt dizziness.
infection and malfunction: Preliminary report of a new
strategy. Asian Journal Endoscopic Surgery, 8,
180–184. https://doi.org/10.1111/ases.12162.
Weerakkody, Y., & Gaillard, F. (n.d.). Ventriculitis. Natural History
Retrieved 9 Dec 2016, from https://radiopaedia.org/
articles/ventriculitis.
Balance disorders associated with neurodegener-
ative diseases tend to be progressive.

Balance Disorders
Neuropsychology and Psychology of
Anna DePold Hohler1 and Marcus Ponce de Leon2 Balance
1
Boston University Medical Center, Boston,
MA, USA Neurodegenerative disorders associated with bal-
2
Madigan Army Medical Center, Tacoma, ance that affect the cortex can also be associated
WA, USA with cognitive difficulties.

Definition Evaluation

Normal balance requires the integration of three The history and physical examination often
sensory systems: visual, vestibular (found in the lead to a diagnosis. At times, laboratory tests
Balint, R. (Rezso (Rudolf) Balint) (1874–1929) 469

and imaging are obtained for confirmation or Major Honors and Awards
to rule out harmful diagnoses. If a reversible
cause is found and treated, significant recov- • Balint’s work was honored by the later naming
ery may occur. However, if the balance prob- of his “triple-syndrome complex” as “Balint’s
lem is due to a permanent or progressive Syndrome” by Hecaen and Ajuriaguerra (1954). B
neurological deficit, the patient may need
training to manage their gait and balance
Landmark Clinical, Scientific, and
difficulties.
Professional Contributions

• Hungarian physician Rezso Balint’s first writ-

Treatment ings, published while he was still a medical
student, were case studies examining muscular
Physical therapy and vestibular rehabilitation atrophy in hemiplegia. He went on to study
may be useful in appropriate cases. They tabes dorsalis and the treatment of epilepsy.
may improve current functioning and In 1907, Dr. Balint recorded his observations
potentially decrease the potential for of a patient who suffered from a unique con-
progression of deficits and complications stellation of neurologic symptoms including
from falls. fixation of gaze, neglect of objects in his
periphery, and misreaching for target objects.
The patient was noted to first experience these
symptoms following damage to the posterior
Cross-References parietal lobes. This “triple-syndrome complex”
was later named “Balint’s Syndrome.”
▶ Ataxia
▶ Parkinson’s Disease
Short Biography

References and Readings Rezso Balint was born in 1874 to a German-Jewish

family in Budapest, Hungary. He attended the Uni-
Ackley, S., Newell Decker, T., & Limb, C. J. (2007). An versity of Budapest, where he received his degree in
essential guide to hearing and balance disorders. Psy- medicine in 1897. Balint was a student of Friedrich
chology Press. von Koranyi. He was employed as a Lecturer at the
University of Budapest in 1910 and was promoted
to Professor of Internal Medicine in 1917.
At the onset of World War I, Dr. Balint turned his
research focus from neurology to tuberculosis and
Balint, R. (Rezso (Rudolf) metabolism and the treatment of diabetes. He is
Balint) (1874–1929) most well known in his home country of Hungary
for the treatment of gastric ulcer with the use of
Alyssa Eidson alkali.
Emory University/Rehabilitation Medicine, Rezso Balint died of thyroid cancer in 1929 at
Atlanta, GA, USA the age of 56.

Major Appointments Cross-References

• University of Budapest, Budapest, Hungary, ▶ Neglect Syndrome

1910–1929 ▶ Optic Ataxia
470 Balint’s Syndrome

References and Readings Natural History, Prognostic Factors, and

Outcomes
Hecaen, H., & Ajuriaguerra, J. (1954). Balint Syndrome
(psychic paralysis of visual fixation) and its minor
The prognosis for patients with Balint’s syndrome
forms. Brain, 77, 373–400.
Husain, M., & Stein, J. (1988). Reszo Balint and his most varies depending on the etiology of the syndrome.
celebrated case. Archives of Neurology, 45, 89–93. Patients with posterior cortical atrophy usually
Rezso Balint (physician). From Wikipedia. http://en. experience a declining course, while some
wikipedia.org/wiki/rezs. Retrieved 7 Jan 2009.
patients with acute infarction may demonstrate
improved functioning with time.

Balint’s Syndrome Neuropsychology and Psychology of

Balint’s Syndrome
Uraina S. Clark
Department of Neurology, Icahn School of As noted above, individuals with Balint’s syn-
Medicine at Mount Sinai, New York, NY, USA drome display three classic symptoms, including
simultanagnosia, optic ataxia, and ocular motor
apraxia. Simultanagnosia is generally considered
Short Description or Definition to be a disruption in spatial attention, which is
associated with an inability to direct one’s atten-
Balint’s syndrome was first described by Rezső tion to more than one or a few objects at a time. It
Bálint in 1909. It consists of three visuospatial is not uncommon for patients with this syndrome
abnormalities: simultanagnosia, optic ataxia, to ignore or neglect all other objects once one
and ocular motor apraxia. The syndrome typi- object in the visual field has been fixated upon.
cally occurs in the absence of visual field defi- Although patients can perceive and name individ-
cits. Individuals with Balint’s syndrome ual objects regardless of the object’s location
experience significant perceptual limitations. within the visual field, they exhibit an inability
Patients with this syndrome cannot perceive to perceive and interpret the gestalt of the scene.
more than one object at a time. They experience The second symptom associated with Balint’s
great impairments in their ability to explore syndrome is optic ataxia, which is defined as a
visual space: they have difficulty navigating deficit in reaching under visual guidance despite
through their environment; they get lost easily; normal limb strength and position sense. As a
and they experience difficulty reaching for or result of this symptom, patients demonstrate an
grasping items in need. inability to manually respond to visual stimuli,
Balint’s syndrome is usually associated with and they often make location errors when pointing
large bilateral lesions in the dorsal occipitoparietal to or grasping for visual targets. Some of the
region and is consequently rare. The most com- impairments noted on tests of reaching abilities
mon causes of Balint’s syndrome include ische- include increased action latency, poor control of
mia (particularly watershed infarctions) and hand trajectory, increased variability at the end of
degenerative disorders (e.g., Alzheimer’s disease, the reach, tendency to reach to one side, and
posterior cortical atrophy). Balint’s syndrome can dissociations of distance and direction control.
also result from trauma, tumors, leukoencepha- The third symptom of Balint’s syndrome includes
lopathies, and prion disorders. In individuals ocular apraxia, which is manifested by an inability
with HIV/AIDS, Balint’s syndrome can develop to voluntarily shift gaze toward a new visual tar-
secondary to HIV encephalitis or progressive get. The ability to make a saccade on command is
multifocal leukoencephalopathy. Transient symp- significantly impaired and is next to impossible
toms of Balint’s syndrome have been reported in for patients with Balint’s syndrome, whereas the
association with migraine onset. ability to make reflexive saccades (e.g., those
Balint’s Syndrome 471

made to suddenly appearing visual objects or sud- the other. Patients with this syndrome are noted to
den noises) and random spontaneous saccades be clumsy when grasping for items, and they may
remains intact. often mislocate objects in space when reaching for
or pointing to items. In contrast, reaching to
somatosensory targets such as parts of the patient’s B
Evaluation own body (e.g., knee, shoulder) on command is
frequently intact; however, patients with significant
Before a diagnosis of Balint’s syndrome can be parietal spatial representation abnormalities may
made more general, cognitive dysfunction (e.g., indeed demonstrate impairments in both reaching
hemineglect, visual impairments) should be ruled for objects as well as reaching to somatosensory
out. It is important that the patient’s visual fields targets.
be assessed fully as some types of visual field In assessing for ocular motor apraxia, the
abnormalities (e.g., extensive peripheral scoto- patient’s ability to make saccadic eye movements
mata) can result in symptoms that are very similar to targets on command can be compared to
to Balint’s syndrome. his/her ability to make reflexive saccades to tar-
A typical method of assessing for gets that appear suddenly in their field of vision.
simultanagnosia includes asking the patient to The former can be tested by asking the patient to
examine and describe the events depicted in a saccade between the clinician’s left and right
complex visual image (e.g., the Cookie Theft Pic- index fingers, spaced far apart and held at various
ture from the Boston Diagnostic Aphasia Exami- locations across the patient’s visual field. The
nation). In such a task, it is helpful if key elements latter can be tested in response to a person pass-
of the image are presented in all four quadrants of ing by or to a loud unexpected noise occurring
the picture in order to assess visual attention more in the periphery.
fully across the quadrants. Individuals with
hemineglect may describe items on one side of
the picture only. Patients with Balint’s syndrome Treatment
often are able to identify discrete items in the
picture; however, they are frequently unable to Relatively little is known about treatment of
integrate the various elements of the picture into patients with Balint’s syndrome. Rehabilitation
a coherent story. Patients will also show impair- often utilizes a functional approach in which the
ments on visual search and counting tasks. Letter patient’s strengths are used to offset impairments.
identification and reading abilities should be There is some evidence to suggest that cognitive
assessed for functional purposes. and perceptual rehabilitation approaches using
In assessing for optic ataxia, one may place verbal cues and organizational search strategies
several items at different locations on a table and can improve visual function and reaching abilities
ask the patient to touch or grasp each of the items. It (see Perez et al. 1996). Case report studies, of
is important to assess whether the patient is able to which there are few, suggest that various rehabil-
grasp items within both hemifields with each hand itation strategies may be employed (see Rose
independently. Patients with unilateral lesions typ- et al. 2016; Zgaljardic et al. 2011), with minimal
ically demonstrate greater impairment when recovery of functional and physical abilities
reaching for items located in the hemispace that is reported.
contralateral to the lesion, using the contralateral
hand. Individuals with Balint’s syndrome, by con-
trast, are typically impaired at reaching for visual See Also
targets for all locations within the visual field;
however, it has been noted that some patients ▶ Neglect Syndrome
with Balint’s syndrome do demonstrate reaching ▶ Simultanagnosia
difficulties in which one arm is more affected than ▶ Visual Field Deficit
472 Barbiturates

Further Reading functions, particularly at higher doses (Feldman

et al. 1997).
Perez, F. M., Tunkel, R. S., Lachmann, E. A., & Nagler, W. The psychoactive effects of barbiturates
(1996). Balint’s syndrome arising from bilateral poste-
increase their risk for drug dependence and
rior cortical atrophy or infarction: Rehabilitation strate-
gies and their limitation. Disability and Rehabilitation, abuse. Symptoms of tolerance and withdrawal
18, 300–304. develop with chronic use. Reportedly, tolerance
Rose, A., Wilson, B. A., Manolov, R., & Florschutz, G. develops to the psychoactive effects of barbitu-
(2016). Seeing red: Relearning to read in a case
rates, but less to the respiratory depressant
of Balint’s syndrome. NeuroRehabilitation, 39,
111–117. effects, thereby increasing the risk of a toxic
Zgaljardic, D. J., Yancy, S., Levinson, J., Morales, G., & overdose (Feldman et al. 1997). Cross-tolerance
Masel, B. E. (2011). Balint’s syndrome and post-acute with other substances may also occur. For exam-
brain injury rehabilitation: A case report. Brain Injury,
ple, alcohol use may also increase tolerance to
25, 909–917.
barbiturates, further increasing the risk of a toxic
overdose.

Barbiturates Current Knowledge

JoAnn Tschanz The use of barbiturates has declined signifi-

Department of Psychology, Utah State University, cantly with the development of other anxiolytic
Logan, UT, USA and anticonvulsant medications. Benzodiaze-
Center for Epidemiologic Studies, Utah State pines, which are also anxiolytic compounds
University, Logan, UT, USA that interact with the GABAA receptor
(although a different site than barbiturates),
have a larger therapeutic window than barbitu-
Synonyms rates and have replaced their use as a safer
alternative for the treatment of anxiety. Some
Central nervous system depressants; Sedative- studies suggest a potential role for barbiturates
hypnotics in alcohol withdrawal. A recent review reported
potential benefit of barbiturates, most notably
for severe withdrawal and for treating seizures
Definition (Martin and Katz 2016).

Barbiturates belong to a class of medications

known as sedative-hypnotics. Initially they were
See Also
prescribed for their anxiolytic and relaxing prop-
erties. Later, they were also used as anticonvul-
▶ Benzodiazepines
sants, and shorter-acting forms were developed
for use as anesthetics in surgery (Feldman
et al. 1997).
References and Readings
Barbiturates affect a subtype of the receptors of
the neurotransmitter, gamma aminobutyric acid Feldman, R. S., Meyer, J. S., & Quenzer, L. F. (1997).
(GABA), one of the most common inhibitory Sedative-hypnotic and anxiolytic drugs. In Principles
neurotransmitter systems in the brain. Their of Neuropsychoparhmacology (pp. 673–729). Sunder-
behavioral effects include relaxation, drowsiness, land, MA: Sinauer Associates.
Martin, K., & Katz, A. (2016). The role of barbiturates for
and feelings of euphoria. However, their wide- alcohol withdrawal syndrome. Psychosomatics. Epub
spread effects also result in the depression of ahead of print. Mar 2. pii: S0033–3182(16)00041–4.
reflexes and cardiovascular and respiratory https://doi.org/10.1016/j.psym.2016.02.011.
Barona Index 473

future. The US Supreme Court ruled that psychi-

Barefoot v. Estelle (1983) atrists are no less reliable than laypersons and that
laypersons’ testimony of future dangerousness is
Robert L. Heilbronner indeed permissible. The Court upheld that the use
Chicago Neuropsychology Group, Chicago, of hypothetical questions to establish future dan- B
IL, USA gerousness is just because such testimony is
supported by the Federal Rules of Evidence
(FRE) that death penalty cases do not present
Synonyms special evidentiary problems. Furthermore, there
is evidence (e.g., Monahan 1992; Monohan and
Prediction of future dangerousness Steadman 1994; Mossman 1994) to suggest that
mental health professionals do indeed predict vio-
lence significantly better than chance when “rele-
Historical Background vant” factors are included in the determination.

Thomas A. Barefoot burned down a bar and shot

and killed a police officer who was investigating References and Readings
the arson. Barefoot was convicted by the jury of
capital murder of a police officer. During the death Denney, R. L. (2005). Criminal responsibility and other
criminal forensic issues. In G. Larrabee (Ed.), Forensic
penalty phase of the case, the state used psychiat-
neuropsychology: A scientific approach. New York:
ric testimony to demonstrate that Barefoot posed a Oxford University Press.
threat to society in the future. Specifically, the Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C.
state had Drs. John Holbrook and James Grigson (1997). Psychological evaluations for the courts:
A handbook for mental health professionals and law-
review a hypothetical fact situation based on evi-
yers. New York: Guilford.
dence from the case and asked each of the doctors Monahan, J. (1992). Mental disorder and violent behavior:
if the convicted individual would commit violent Perceptions and evidence. American Psychologist, 47,
acts in the future or would pose a threat to society. 511–521.
Monahan, J., & Steadman, H. J. (1994). Toward a rejuve-
Both doctors testified that the criminal would be a nation of risk assessment research. In J. Monahan &
continued threat to society. In fact, Dr. Grigson H. J. Steadman (Eds.), Violence and mental disorder:
concluded that there was a “one hundred percent Developments in risk assessment. Chicago: University
and absolute” probability that Barefoot would of Chicago Press.
Mossman, D. (1994). Assessing predictors of violence:
commit violent acts in the future and thus pose a
Being accurate about accuracy. Journal of Consulting
continued threat to society. The judge sentenced and Clinical Psychology, 62, 783–792.
Thomas A. Barefoot to death. Barefoot appealed
the decision and in the Court of Criminal Appeals
raised several concerns about the way his trial was
handled, most notably with respect to the proba- Barona Index
bility that he would commit future violent acts.
Barefoot argued that the psychiatrists testifying Glen E. Getz
against him had not even examined him and Department of Psychiatry, Allegheny General
were making determinations based on a hypothet- Hospital, Pittsburgh, PA, USA
ical fact-based situation. Moreover, Barefoot Neuropsychology Specialty Care, LLC,
called into question the ability of psychiatrists to Pittsburgh, PA, USA
predict future dangerousness. The Court of Crim-
inal Appeals rejected all of Barefoot’s arguments,
and the US Supreme Court rejected Barefoot’s Synonyms
suggestion that psychiatrists are not competent to
make determinations regarding dangerousness in Premorbid intelligence regression model
474 Barona Index

Definition from non-neurologically based patients utilizing

the WAIS-R. As demonstrated in Fig. 1, the predic-
Barona Index is a demographically based regres- tor variables incorporated into the model included
sion method to estimate premorbid intelligence in those originally utilized by Wilson et al. (1978) as
terms of index scores on the Wechsler Adult Intel- well as urban/rural residency, geographic location,
ligence Scale-Revised (WAIS-R). and handedness. Although these equations resulted
in less IQ variance and larger standard errors of
estimate, cross validation studies were successful.
Historical Background

Attempts have long been made to estimate pre- Current Knowledge

morbid intellectual functioning. A frequent
method in clinical practice is to estimate the Currently, premorbid estimation of IQ functioning
level of premorbid cognitive skill by subjectively includes the WAIS-IV (Wechsler 2008). Algo-
considering aspects of the individual’s history rithms derived from the WAIS-IV with demo-
such as education and occupation. Another com- graphic variables have been developed by the
mon approach to estimate premorbid IQ is to use Advanced Clinical Solutions (ACS; Pearson
tests of present ability, which are thought to be 2009). Holdnack et al. (2013) discuss the clinical
relatively resistant to change even during the utility of the Test of Premorbid Functioning
phases of a psychiatric disorder or those following (TOPF) to determine if the a patient’s current per-
a neurologically based disorder. A variant is the formance is expected or represents a decline from a
best performance method in which the highest previous estimated level of ability. The TOPF can
score obtained by an individual is assumed to be be used alone or in conjunction with demographic
the most likely premorbid level (▶ Best Perfor- characteristics to estimate premorbid level of func-
mance Method). Research has been inconsistent tioning. Research consistently suggests that TOPF
as to the effectiveness of this approach. In an estimates from the ACS are reasonably effective
attempt to reduce the error in estimating intelli- in estimating premorbid intelligence.
gence based on current functioning and eliminate
the subjectivity inherent in clinical judgment,
demographically based regression equations Future Directions
were created to statistically predict intelligence
test scores. A later method of combining demo- As we are on the brink of the release and utiliza-
graphic information and current performance on tion of the Wechsler Adult Intelligence Scale-V, it
IQ has also been found to be relatively effective. is quite likely that future regression models to
It is well established that demographic variables, estimate premorbid functioning as indexed by
such as education, social class and education, are scores on this test will be developed. It is neces-
correlated with measured IQ. Wilson et al. (1978) sary to continue to improve our methods of esti-
created a regression equation to predict WAIS IQ mating premorbid abilities. Future models will
from demographic variables. They used regression most likely consider other variables and/or
modeling with WAIS Full Scale IQ, Verbal IQ, and include more specific criteria for the existing
Performance IQ as criteria and age, education, sex, models. For example, the expansion of technol-
race, and occupation as predictors. With the devel- ogy along with fewer labor-based jobs and more
opment of the WAIS-Revised (WAIS-R), further technology-based jobs will very likely influence
models were needed to estimate premorbid intelli- the occupations used for the equation. Similarly,
gence. Barona et al. (1984) generated demographic as online education expands, an understanding of
equations for the estimation of premorbid WAIS-R the type of education rather than amount of edu-
IQ. Subsequently, research demonstrated successful cation may change the weighting of the model
discrimination of neurologically based patients algorithms. As age expectancy increases, the role
Barrow Neuropsychological Screen 475

WAIS-R VIQ = 54.23 + .49 (age) + 1.92 (sex) + 4.24 (race) + 5.25 (education) + 1.89
(occupation) + 1.24 (U-R residence.)
2
Standard Error of Estimate = 11.79; R = .38

WAIS-R PIQ = 61.58 + .31 (age) + 1.09 (sex) + 4.95 (race) + 3.75 (education) + 1.54
(occupation) + .82 (region) B
Standard Error of Estimate = 13.23; R2= .24

WAIS-R PIQ = 54.96 + .47 (age) + 1.76 (sex) + 4.71 (race) + 5.02 (education) + 1.89
(occupation) + .59 (region)
2
Standard Error of Estimate = 12.14; R = .36

Sex: Female = 1.Male = 2

Race: Black = 1, Other ethnicity = 2, White = 3
Education 0–7 years = 1,8 = 2,9–11 = 3, 12=4, 13–15 = 5, 16+ =6
Age: 16–17 years = 1,18–9 = 2, 20–24 = 3, 25–34 = 4, 35–44 = 5, 45–54 = 6,
55–64 = 7, 65–69 = 8, 70–74 = 9
Region: Southern = 1, North Central = 2, Western = 3, Northeastern = 4.
Residence: Rural = 1, Urban = 2
Occupation: Farm Laborers, Farm Foremen & Laborers (unskilled) = 1
Operatives, Service Workers, Farmers, & farm Managers (semiskilled) = 2
Not in Labor Force = 3
Craftsmen & Foremen (skilled workers) = 4
Managers, Officials, Proprietors, Clerical & Sales Workers = 5
Professional & Technical = 6

Barona Index, Fig. 1 Barona et al. (1984) regression formulas for pre-morbid IQ

of age on premorbid functioning will quite likely Schoenberg, M. R., Scott, J. G., Duff, K., & Adams, R. L.
become a more important variable as well. (2002). Estimation of WAIS-III intelligence from
combined performance and demographic variables:
Development of the OPIE-3. The Clinical Neuropsy-
chologist, 16, 426–438.
Cross-References Wilson, R. S., Rosenbuam, G., Broan, G., Rourke, D.,
Whitman, D., & Grisell, J. (1978). An index of pre-
morbid intelligence. Journal of Consulting and Clini-
▶ Best Performance Method cal Psychology, 46, 1554–1555.
▶ Intelligence
▶ Premorbid Estimate
▶ Premorbid Functioning
Barrow Neuropsychological
Screen
References and Readings
George P. Prigatano
Advanced Clinical Solutions for WAIS-IV and WMS-IV. Department of Clinical Neuropsychology, Barrow
(2009). Administration and scoring manual.
Barona, A., & Chastin, R. L. (1986). An improved estimate of
Neurological Institute, St. Joseph’s Hospital and
premorbid IQ for black and whites on the WAIS-R. Inter- Medical Center, Phoenix, AZ, USA
national Journal of Clinical Neuropsychology, 8,
169–173.
Barona, A., Reynolds, C. R., & Chastain, R. (1984).
A demographically based index of premorbid intelli-
Synonyms
gence for the WAIS-R. Journal of Consulting and
Clinical Psychology, 52, 885–887. BNIS
476 Barrow Neuropsychological Screen

Description performance on memory items plus the total score

on the BNIS successfully identified many normal
The Barrow Neurological Institute (BNI) Screen functioning individuals.
for Higher Cerebral Functions (BNIS) was devel- Two doctoral dissertations have documented the
oped to rapidly, but reliably and validly, assess reliability and validity of the BNIS. Wass (1997)
disturbances in higher integrative brain functions demonstrated that performance on the BNIS corre-
(Prigatano et al. 1995). In addition to sampling lated with independent and lengthier measures of
speech/language, orientation, attention/concentra- neuropsychological test performance. BNIS sub-
tion, visual spatial, and visual problem-solving, test scores were also positively correlated with the
and memory functions, it is unique as a neuropsy- Functional Independence Measure (FIM) and the
chological screening instrument insofar as it also adjunct of the Functional Assessment Measure
assesses affect expression and perception as well (FIM + FAM of the Uniform Data Set for Medical
as the person’s awareness of memory abilities. Rehabilitation). Nearly 50% of the psychosocial-
This provides for seven subtest scores and a pos- cognition score of the FIM-FAM was predicted by
sible total score of 50/50 points. The latter score the seven independent subtests of the BNIS.
can be converted to an age-adjusted T score. The Denvall et al. (2002) administered a Swedish
test has been translated into eight different lan- translation of the BNIS to 52 normal controls and
guages and typically takes between 10 and 15 to 36 patients with well-documented brain disorders
administer (Prigatano et al. 2013). (the majority being those with traumatic brain
injury and stroke). Swedish controls performed
almost identically to American controls on this
Historical Background test. Swedish brain dysfunctional patients
performed worst on the BNIS than Swedish con-
While several screening tests of higher cerebral or trols. Hofgren (2009) further studied the Swedish
integrative brain functions exist (see Lezak et al. version of the BNIS for her doctoral dissertation.
2004), they do not assess both cognitive and The first study (Hofgren et al. 2007b) utilized
affective functions. Various brain disorders affect 92 controls and 120 patients from a neuroreh-
both dimensions, but differentially. At the BNI, a abilitation clinic. Significant differences were
wide variety of brain dysfunctional patients are found between the control group and the patient
evaluated and treated. This led Prigatano and col- group. Sensitivity was 88% and specificity was
leagues to develop a screening test that assess, in 78%. In a second study (see Hofgren 2009), the
brief fashion, cognitive and affective functions BNIS was compared to the Mini-Mental State
that could be negatively influenced by various Examination as well as to the FIM. Concordance
brain disorders. In doing so, they attempted to between the BNIS total score and MMSE was good
provide the experienced clinician with both quan- (r = 0.744). Both measures discriminated ADL-
titative and qualitative information useful in dependent from nondependent patients. A third
patient evaluations, management, and research. study (Hofgren et al. 2007a) used the BNIS as a
predictor of return to work and level of activities of
daily living (ADL) in 58 stroke victims. At 1 year
Psychometric Data follow-up, the correlation of the BNIS total score
and the psychosocial-cognitive scale of the FIM
The initial standardization study (Prigatano et al. was r = 0.376 (p = 0.001). BNIS total score did not
1995) reported good test-retest reliability predict ability to return to work, but most of the
(r = 0.94) and good sensitivity for identifying patients studied did not return to work. In a fourth
brain dysfunctional patients (i.e., 92%). The spec- study, Hofgren et al. (2008) studied ADL, housing,
ificity of the instrument was modest (48%). Spec- and return to work 2 years after cardiac arrest in
ificity was increased if performance on memory 22 patients. The BNIS total score was higher in
tests was taken into account (83%). That is, good patients living in their home and who were able to
Barrow Neuropsychological Screen 477

return to work (mean total score was 43/50 points, Rosenstein et al. (1997) compared 41 patients with
range 41–47). In contrast, the mean BNIS total known cerebral dysfunction, with 22 psychiatric
score was notably lower in those living in their patients (some who were psychotic) and 22 medi-
own home but not able to return to work (mean cal inpatients. Psychiatric and medical patients
total score 37, range 35–42) and even lower for scored significantly higher on the BNIS total B
those living in sheltered accommodations (mean score compared to the brain dysfunctional patients.
Total score was 24, range of 19–32). Using the recommended cutoff score of 47/50
A study from the Netherlands further supported points, 40 of the 41 brain dysfunctional patients
the clinical utility and validity of the BNIS when were correctly classified (97.5%). The specificity
measuring outcome after stroke (Boosman et al. for medical controls was 68%. The specificity for
2013). The BNIS showed good internal consis- psychiatric patients was much lower (40.9%).
tency (alpha = 0.82) and no floor or ceiling effects These findings suggest that multiple factors can
in stroke patients described as having a good func- influence the patient’s BNIS total score, including
tional outcome using the Barthel Index. Selected the age, education, and psychiatric status of the
subtests correlated with more time-consuming and patient.
extensive tests of different cognitive domains. For In a French study, Prigatano et al. (2014a) dem-
example, the Boston Naming Test scores correlated onstrated that patients with mild cognitive impair-
0.538 (p = 0.000) with the speech/language subtest ment of the amnestic type (MCI) had poorer scores
scores of the BNIS. Likewise, the memory subtest on the BNI screen than age-matched patients who
scores correlated with the total scores obtained did not have MCI. MCI patients showed not only
from the Rey Auditory Verbal Learning Test disturbance in memory functioning but impaired
(r = 0.548). These findings replicated the earlier awareness and affect expression and perception.
observations of Wass (1997). The study demonstrated the potential importance
Recently, a normative study using the French of assessing both cognitive and affective functions
translation of the BNIS also reported findings very in cases of differential diagnosis.
similar to what was observed in the original Ameri- Also, recent case studies have suggested that
can standardization study (see Prigatano et al. 2013). performance on the BNIS may help identify patients
with anosognosia (e.g., Prigatano et al. 2014b).

Clinical Uses
References
Prigatano and Wong (1999) studied 95 heteroge-
neous brain dysfunctional patients treated on an Boosman, H., Visser-Meily, J. M. A., Post, M. W. M.,
Duits, A., & van Heugten, C. M. (2013). Validity of
inpatient neurorehabilitation unit who were clas-
the Barrow Neurological Institute (BNI) screen for
sified as having achieved their rehabilitation goals higher cerebral functions in stroke patients with good
or not. Patients who achieved their rehabilitation functional outcome. The Clinical Neuropsychologist,
goals had higher BNIS total scores at admission 27(4), 667–680.
Denvall, V., Elmstahl, S., & Prigatano, G. P. (2002). Rep-
compared to patients that did not achieve their
lication and construct validation of the BNI Screen for
rehabilitation goals. Impaired emotional function- higher cerebral function with the Swedish population.
ing was equally important as impaired cognitive Journal of Rehabilitative Medicine, 34, 153–157.
functioning when predicting goal attainment. Hofgren, C. (2009). Screening of cognitive functions:
Evaluation of methods and their applicability in neuro-
Interestingly, both groups were equally impaired logical rehabilitation (Doctoral Dissertation, University
in their awareness of the memory functioning on of Gothenburg, Gothenburg, Sweden).
admission. However, the group that eventually Hofgren, C., Bjorkdahl, A., Esbjornsson, E., & Stibrant-
achieved their goals showed improved awareness Sunnerhagen, K. (2007a). Recovery after stroke: Cogni-
tion, ADL function and return to work. Acta
after the rehabilitation experience.
Neurologica, 115, 73–80.
Studies have also documented the potential Hofgren, C., Esbjornsson, E., Aniansson, H., &
value of the BNIS in cases of differential diagnosis. Sunnerhagen, K. S. (2007b). Application and
478 Barthel Index

validation of the Barrow Neurological Institute Screen Description

for higher cerebral functions in a control population and
in patient groups commonly seen in neuroreh-
abilitation. Journal of Rehabilitative Medicine, 39, The Barthel Index (BI) measures ten functions that
547–553. are important for independent living – feeding, bath-
Hofgren, C., Lundgren-Nilsson, A., Esbjornsson, E., & ing, grooming, dressing, bowel and bladder conti-
Sunnerhagen, K. S. (2008). Two years after cardiac nence, toileting, transfers, mobility, and stair use.
arrest; cognitive status, ADL function and living situa-
tion. Brain Injury, 22(12), 972–978. Items are weighted and scored according to their
Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004). perceived importance. Higher scores indicate better
Neuropsychological assessment (4th ed.). New York: performance. In the most commonly used version,
Oxford University Press. the maximum score of 100 indicates full indepen-
Prigatano, G. P., & Wong, J. L. (1999). Cognitive and
affective improvement in brain dysfunctional patients dence. Several versions of the Barthel Index and their
who achieve inpatient rehabilitation goals. Archives of associated scoring methods exist. Shah et al. (1989)
Physical Medicine and Rehabilitation, 80, 77–84. expanded the scoring categories to improve the scale
Prigatano, G. P., Amin, K., & Rosenstein, L. D. (1995). discriminability. Others have simplified the scoring
Administration and scoring manual for the BNI Screen
for higher cerebral functions. Phoenix: Barrow Neuro- system, while incorporating additional categories, to
logical Institute. sum to a maximum of 20 points.
Prigatano, G. P., Tonini, A., Truelle, J. L., & Montreuil, M.
(2013). Performance of a French sample on the French
translation of the BNI Screen for higher cerebral func- Historical Background
tions. Brain Injury, 27(12), 1435–1440.
Prigatano, G. P., Montreuil, M., Chapple, K., Tonini, A.,
The BI evolved over a 10-year period from the mid-
Toron, J., Paquet, C., Dumurgier, J., Hugon, J., &
Truelle, J. L. (2014a). Screening for cognitive and 1950s until its publication in 1964. It was devel-
affective dysfunction in patients suspected of mild cog- oped to permit nursing staff to assess the ability of
nitive impairment. International Journal of Geriatric patients with neuro-muscular and musculoskeletal
Psychiatry, 29(9), 936–942.
disorders to care for themselves. It was one of the
Prigatano, G. P., Hendin, B. A., & Heiserman, J. E.
(2014b). Denial or unawareness of cognitive deficit first measures of activities of daily living (ADL) to
associated with multiple sclerosis? A case report. Jour- be developed. Since its initial publication, it has
nal of Clinical and Experimental Neuropsychology, been modified to both expand and restrict the item
36(4), 335–341.
scoring. The BI is widely used in rehabilitation
Rosenstein, L. D., Prigatano, G. P., & Nayak, M. (1997).
Differentiating patients with higher cerebral dysfunc- centers, despite subsequent investigations identify-
tion from patients with psychiatric or acute medical ing problems with the scaling and sum-scoring
illness with the BNI Screen for higher cerebral func- system. The BI remains popular as it includes the
tions. Neuropsychiatry, Neuropsychology, and Behav-
key physical and self-care items important for dis-
ioral Neurology, 10(2), 113–119.
Wass, P. J. (1997). An analysis of the construct-related and charge planning and is simple to use.
ecological validity of the Barrow Neurological Institute Following the appearance of the BI, many
Screen for higher cerebral functions (Doctoral Disser- other indices of function have been developed,
tation, University of Windsor, Windsor).
underlining the importance of this type of tool in
rehabilitation practice. The BI and the Functional
Independence Measure (FIM) are the two most
Barthel Index
widely used measures of ADL in stroke research.
The BI tends to be used more frequently in
Gavin Williams
Europe, while the FIM is more likely to be used
Epworth Rehabilitation Centre Epworth Hospital,
in North America.
Richmond Melbourne, VIC, Australia

Psychometric Data
Synonyms
The original version of the BI was developed
BI without the investigation of content validity for
Basal and Ceiling Rules 479

item inclusion or validity of the scoring system. Mahoney, F., & Barthel, D. (1965). Functional evaluation:
Many authors have questioned and subsequently The Barthel index. Maryland State Medical Journal,
14, 61–65.
suggested modifications to the scoring system. McDowell, I., & Newell, C. (1996). Measuring health - a
Most recently, de Morton et al. (2008) used guide to rating scales and questionnaires (2nd ed.
Rasch analysis to investigate the validity of item pp. 56–63). New York: Oxford University Press. B
score summation for the BI’s original and modi- Sangha, H., Lipson, D., Foley, N., Salter, K., Bhogal, S.,
Pohani, G., & Teasell, R. W. (2005). A comparison of the
fied versions. They found that score summation Barthel index and the functional independence measure
was not valid and although rescoring may as outcome measures in stroke rehabilitation: Patterns of
improve the validity of the data collected at dis- disability scale usage in clinical trials. International
charge, methods for rescoring outcome measures Journal of Rehabilitation Research, 28(2), 135–139.
Shah, S., Vanclay, F., & Cooper, B. (1989). Improving the
are not commonly used in rehabilitation. sensitivity of the Barthel index for stroke rehabilitation.
Many studies have found the BI to have Journal of Clinical Epidemiology, 42(8), 703–709.
high inter-rater and retest reliability. The low
number of scoring categories for some individ-
ual items means that the BI is less likely to be
as discriminative or responsive to change as Basal and Ceiling Rules
scales such as the Functional Independence
Measure (FIM), which has seven scoring cate- Matthew J. L. Page
gories for each item. Allegheny General Hospital, Pittsburgh, PA, USA
Despite problems with some psychometric Psychology, Allegheny Health Network,
properties of the BI, it has good clinical utility in Pittsburgh, PA, USA
that it requires little staff training, is quick and
easy to administer, and costs nothing.
Synonyms

Clinical Uses Entry and discontinue rules

The BI is widely used in inpatient rehabilitation

settings. It encompasses most of the important Definition
physical aspects of daily function but does not
directly address impairment to communication, A basal and ceiling rule refers to the entry point
cognition, or hearing and vision. The BI is simple and discontinue point of a psychometric test. The
and easy to use with well-defined categories; so purpose of basal and ceiling rules is to reduce the
minimal training or familiarization is required. number of items an examinee is required to
attempt, by eliminating items that are too easy
and too difficult. Doing so reduces administration
Cross-References time and burden on the examinee.
Although specific start and stop rules and
▶ Functional Independence Measure administration procedures vary across tests, basal
▶ Rivermead Mobility Index and ceiling rules are generally used for tests in
which the items are ordered from easiest to most
difficult. The most common basal procedure is to
References and Readings first start at an early, easier item based on the
examinee’s age. The examinee is then required to
de Morton, N., Keating, J., & Davidson, M. (2008). Rasch establish a basal by completing a predetermined
analysis of the Barthel index in the assessment of hos-
pitalized older patients after admission for an acute
number of consecutive items correctly (e.g., three
medical condition. Archives of Physical Medicine and correct items in a row). In general, items are
Rehabilitation, 89(4), 641–647. administered in reverse order, so that they are
480 Basal Forebrain

increasingly easier, until the basal is established. In low and revised upward in the standardization pro-
doing so, the examiner can refrain from adminis- cedure to ensure that a minimal number of exam-
tering easier items below the basal, assuming that inee raw scores (commonly 5%) change by moving
the examinee would be able to answer them cor- the start point forward. The ideal starting item has a
rectly. Once the basal has been established, items high pass rate in the normative sample, to minimize
are then administered in forward order, becoming the occurrence of reversal procedures. Discontinue
increasingly more difficult. The test continues in rules in the standardization procedure are also ini-
this fashion until a ceiling rule has been met. Ceil- tially conservative and then adjusted down to min-
ing rules typically require that an examinee answer imize changes in examinee raw and age-adjusted
a predetermined number of consecutive items standard scores. Additionally, discontinue rules are
incorrectly (e.g., three misses in a row). Some developed to maintain a high rank-order correlation
ceiling rules require a certain number of misses (e.g., 0.98) of total raw scores before and after the
out of a larger number of consecutive items (e.g., adjustment. This ensures that the standardization
four misses across five consecutive items). Once sample subjects maintain the same position in their
the ceiling rule has been met, the examiner rank order relative to others in their age group.
discontinues the test under the assumption that
the examinee would continue to answer the
remaining, more difficult items incorrectly. See Also
After administration is complete, some tests
follow a double basal rule. In this situation, the ▶ Ceiling Effect
examinee has established an initial basal (by com- ▶ Floor Effect
pleting a set number of consecutive items correctly) ▶ Item Difficulty
and then subsequently completed an additional ▶ Standard Scores
string of correct items to meet a second basal. ▶ Test Construction
Depending on the test, some procedures allow for ▶ Testing the Limits
the examiner to count all items below the second
basal as correct, even if the examinee actually
responded to some of them incorrectly. Because References and Readings
of the wide variability across administration pro-
tocols, it is vital for the examiner to be familiar with Wechsler, D. (2008). Wechsler adult intelligence scale
basal and ceiling rules prior to administration. (4th ed.). Bloominton: Pearson.
Wechsler, D. (2009). Wechsler memory scale (4th ed.).
Bloominton: Pearson.
Wechsler, D. (2014). Wechsler intelligence scale for chil-
Current Knowledge dren (5th ed.). Bloomington: Pearson.

Although many test companies do not publish

details regarding the development of their basal
and ceiling rules, the general goal of the rules is Basal Forebrain
to reduce the number of administered items while
minimizing the effects of these rules on raw and Randall E. Merchant
standard scores. The Wechsler tests (e.g., WAIS-IV, Department of Neurosurgery, Virginia
WMS-IV, WISC-V) describe one such develop- Commonwealth University, Richmond, VA, USA
ment procedure that may be commonly used
among other test publishers. For these tests,
national tryout data are used to determine the diffi- Definition
culty of all test items, to order them from easiest to
hardest based on how frequently they are answered The basal forebrain is a collection of nuclei and
correctly in the sample. Start points are then set tracts that lie near the bottom and front of the
Basal Ganglia 481

brain. It includes the nucleus basalis, diagonal Current Knowledge

band of Broca, and medial septal nuclei. This
area’s neurons are major producers of acetylcho- Role in behavior and cognition. Rosvold demon-
line which is then distributed throughout the brain strated a topographical coupling between the pre-
and most importantly to the cerebral cortex and frontal cortex and basal ganglia (Rosvold 1972; B
amygdala. The basal forebrain is most commonly Johnson et al. 1968; Middleton and Strick 2000;
damaged by an aneurysm of the anterior commu- Averbeck et al. 2014). Recent neuroimaging find-
nicating artery. When this occurs, there is a reduc- ings using functional magnetic resonance imaging
tion in the amount of acetylcholine in the brain, (Arsalidou et al. 2013) and diffusion tensor imag-
leading to impaired learning, amnesia, and con- ing tools (Kotz et al. 2013) confirmed such topo-
fabulation. A decrease in cholinergic output by graphical organization between the basal ganglia
neurons of the basal forebrain is also known to and the prefrontal cortex. Considering the major
occur in cases of Alzheimer’s disease and senile outflow of the basal ganglia to the thalamus
dementia. (Haber and Calzavara 2009), it is not surprising
that a substantial amount of research strongly
supports the role of the basal ganglia in higher-
order behavioral and cognitive tasks (Haber and
Cross-References
Knutson 2010). Much of this research relies on
striatal dopaminergic deficit and cortical lesion
▶ Anterior Communicating Artery
models in both human patients and animal
models.

Cortex
Basal Ganglia

Christina R. Marmarou1, Matthew R. Parry1 and

Ekaterina Dobryakova2 Putamen
1 Indirect
Neurosurgery, Virginia Commonwealth Thalamus
University, Richmond, VA, USA VL / VA / CM
2 Direct
Traumatic Brain Injury Research, Kessler
Foundation, West Orange, NJ, USA

Synonyms
Globus pallidus
Basal nuclei
Int Ext

Definition Subthalamic nucleus

The basal ganglia refer specifically to a group of

subcortical structures considered as extrapyrami- Dopaminergic, excitatory
dal motor components. These components Glutamatergic, excitatory
include caudate and putamen, substantia nigra, GABAergic, inhibitory
subthalamic nucleus, and globus pallidus (GP).
Basal Ganglia, Fig. 1 Basal ganglia circuitry. Diagram
Figure 1 depicts major circuitry within the basal illustrates only major direct and indirect circuits. Signifi-
ganglia. cant cortical input is active at every level (not shown)
482 Basal Ganglia

Studies in Parkinson’s disease (PD) patients ganglia (the putamen and GP) are involved in
uncover the importance of the basal ganglia in learning through feedback presented with a
attention – the behavior of target focusing in the delay between action and outcome (Dobryakova
presence of distractors (Brown et l. 1998). Levo- and Tricomi 2013). The basal ganglia are also
dopa therapy among PD patients improves motor involved in a number of other cognitive functions
behavior and attentional set-shifting; the absence including working memory (e.g., Baier et al.
of striatal dopamine has been shown to impair 2010), attentional systems (Sarter et al. 2006),
dual-task performance, self-monitoring (Brown and executive decision-making and control (Ino
and Marsden 1991; Brown et al. 1998; Taylor et al. 2010; Kim and Hikosaka 2013). While many
et al. 1986), and certain types of learning of the behaviors engaged in seem simple and are
(Shohamy 2011). For example, PD patients dem- taken for granted, these daily behaviors are really
onstrate significant impairment in Petrides’ self- patterns of highly organized behaviors with very
ordered pointing task (Petrides and Milner 1982; specific goals and purposes. As tasks are learned
West et al. 1998). and practiced, they become automated and require
The basal ganglia have been shown to regulate little to no conscious control. The basal ganglia
temporal coupling and ordering of both motor and play a critical role in the smooth and efficient
nonmotor sequences (Malapani et al. 1998; Kotz operation of such highly automated behaviors
et al. 2009). Interestingly, a role in auditory and as such are part of the complex “executive”
rhythm detection and generation has been system of the brain. Thus, the basal ganglia are
supported (Grahn and Brett 2007, 2008); this is critical in performing everyday practical tasks in
analogous to the well-established role of the basal an effortless and efficient manner (Koziol and
ganglia in motor timing and pattern generation, Budding 2009).
making the circuitry a “rhythm-pattern generator” Organization. The striatal complex is com-
both in executive (motor) and perceptual posed of the caudate nucleus and the putamen
(cognitive) realms. The implications of this and (Graybiel 2000). The caudate nucleus can be fur-
similar work for the perceptual and executive ther subdivided into the head, body, and tail that
aspects of language are well demonstrated (Kotz play separable roles in cognition (Seger 2008).
et al. 2009). For example, Smits-Bandstra et al. Embryologically the same, the caudate and puta-
have described the basal ganglia in the setting of men are separated by the internal capsule.
persons who stutter (Smits-Bandstra and De Nil Striosomes and matrix constitute a chemical and
2007). functional separation of the striatal complex:
The basal ganglia are involved in a number of striosomes are areas of low acetylcholinesterase
other higher-order cognitive functions. For and high neuropeptide content, whereas matrix
instance, problem-solving tasks that activate the regions are rich in acetylcholinesterase (Bernacer
prefrontal cortex also activate the basal ganglia. et al. 2007). This difference in acetylcholinester-
Recent research has shown that the basal ganglia ase content provides a convenient histochemical
are significantly involved in learning, including differentiation between neostriatal regions
motor skill learning, sequence learning, habit (DiFiglia et al. 1976).
learning, automaticity, and category learning Striatal function. The GABAergic cells of the
(Ashby et al. 2010; Seger 2008; Tricomi et al. striatum project to the internal segment of GP and
2009; Tricomi and Fiez 2008). Further, different substantia nigra (striosomes project mainly to pars
subregions of the basal ganglia have been shown compacta; matrix projects mainly to pars
to process learning stimuli under different time reticulata). These nuclei also receive substance-P
scales and fulfill different roles during learning. and enkephalinergic input from the striatum
For example, it has been shown that the anterior (Menguala et al. 1999). The striatum tonically
part of the basal ganglia (head of the caudate inhibits its pallidal and nigral targets.
nucleus) is involved in learning through immedi- The striatum itself receives inhibitory
ate feedback, while posterior regions of the basal GABAergic projections from substantia nigra
Basal Ganglia 483

pars reticulata (Boyes and Bolam 2007). Major capsule and laterally by the putamen (Haines
excitatory input is found in glutamatergic projec- 2004). Frequently, the term “lentiform nucleus”
tions from thalamus (centromedian and para- is used to refer to the GP and putamen together.
fascicular nuclei) and cortex (several motor Pallidal function. The internal segment toni-
areas), as well as dopaminergic input from sub- cally inhibits the ventroanterior and ventrolateral B
stantia nigra pars compacta (Kubota et al. 1987). nuclei of the thalamus. The external segment ton-
The latter dopaminergic input terminates in both ically inhibits the STN and provides transient
D1 and D2 dopamine receptor subtypes, an inhibition to the internal segment (DeLong and
important determinant in excitation or inhibition Wichmann 2007). It is convenient to consider the
of striatal neurons (Surmeier et al. 2007). GP as the “gateway” between the basal ganglia
The substantia nigra (SN) generally refers to and the thalamus. The thalamus, in turn, relays to
two nuclei, pars compacta and pars reticulata the motor areas of the cortex.
(SNpc, SNpr, respectively). The SN lies within The basal ganglia have been described in terms
the midbrain, caudal to the crus cerebri and rostral of functionally opposing direct and indirect path-
to the red nucleus (Haines 2002). The SNpc con- ways. Broadly, the direct pathway promotes
tains dopaminergic neurons, while the SNpr con- VA/VL thalamic relay to cortex, while the indirect
tains mostly GABAergic neurons. Intra-nigral pathway inhibits such traffic. The following
connections serve as modulatory loops: description of direct and indirect pathways is a
GABAergic input to SNpc decreases dopaminer- summary and integration of previous sources.
gic activity within the pars compacta; dopaminer- Direct pathway. The VA/VL thalamic complex
gic input to SNpr decreases GABAergic activity is under tonic inhibition from both GPi and SNpr;
(Boyes and Bolam 2007; DeLong and Wichmann transient inhibition of these nuclei is provided by
2007). the striatum. In this way, excitation of the striatum
Nigral function. The pars reticulata provides inhibits GPi output to the thalamus, and the net
tonic inhibition of the thalamus, while the major effect is disinhibition of the VA/VL thalamic com-
function of the pars compacta is dopaminergic plex. The activation of striatal GABAergic pro-
input to the striatum (Haines 2002). jections to SNpr and GPi has two sources: cortical
The subthalamic nucleus (STN) is inferior to glutamatergic stimulation and nigral dopaminer-
the thalamus and medial to the GP; a biconvex- gic stimulation acting upon D1 striatal receptors.
shaped structure, the STN is surrounded by dense In this way, the direct pathway is a case of tha-
bundles of myelinated fibers. The internal capsule lamic disinhibition by suppression of GPi activity.
separates the STN from the GP (Haines 2004). Indirect pathway. If the direct pathway is con-
Three major fiber tracts are associated with the sidered as a suppression of GPi activity leading to
STN: the subthalamic fasciculus (STF), the ansa disinhibition of the thalamus, the indirect pathway
lenticularis (AL), and the lenticular fasciculus is described as suppression of the GPe leading to
(LF). The STF connects the STN and GP, crossing disinhibition of STN. Tonic inhibition of STN
the internal capsule; the AL connects the GPi and comes from GPe (whereas tonic inhibition of thal-
the thalamus and differs from the STF in that it amus comes from GPi). The striatum serves to
does not directly cross the internal capsule. Lastly, transiently inhibit GPe (as well as inhibit GPi as
the LF crosses the internal capsule and ultimately previously described). The striatum contains both
joins the AL to form the thalamic fasciculus D1 and D2 dopamine receptors. While the direct
(or the H1 field of Forel). pathway uses D1 receptors, the D2 subtype is the
Subthalamic function. The STN is thought to main striatal receptor of the indirect pathway.
modulate the entire circuitry of the basal ganglia SNpc inhibits striatal output to GPe through
(Hamani et al. 2004). these D2 receptors.
The GP consists of two segments: internal In general terms, activity through the direct
(medial, GPi) and external (lateral, GPe). The pathway promotes thalamocortical activity by dis-
nucleus is bounded medially by the internal inhibition of the thalamus; the indirect pathway
484 Basal Ganglia

suppresses thalamocortical activity. This oppos- Corticostriatal: glutamatergic, from primary-,

ing circuitry is thought to modulate the net effect pre-, supplementary-, and cingulate-motor areas
of the basal ganglia on thalamic output. Nigrostriatal: dopaminergic from pars
compacta, fibers terminate on two separate dopa-
mine receptor types, also GABAergic from pars
Illness reticulata

Huntington disease, hyperkinetic, choreiform dis- Efferent

ease, autosomal dominant inheritance, and path- Striatopallidal: GABAergic and substance-P pro-
ological CAG trinucleotide repeats (Shao and jections to internal segment, GABAergic and
Diamond 2007). Mechanism of disease may enkephalin projections to external segment of
include enhanced corticostriate activity and globus pallidus
enhanced thalamic disinhibition (Centonze et al. Striatonigral: striosomal GABAergic projec-
2007). The Unified Huntington’s Disease Rating tions to pars compacta, matrix GABAergic and
Scale is widely accepted to represent an array of enkephalinergic projections to pars reticulata
disease signs and symptoms (Huntington Study
Group 1996). Dopamine and glutamate antago- Globus Pallidus: Internal, External Segments
nists as well as GABAergic therapy have been
described (Bonelli et al. 2004). Speech and gait Afferent
therapy are often employed. Depression is com- Striatopallidal (see above)
mon among Huntington’s disease patients, and Subthalamopallidal: glutamatergic mainly to
antidepressant treatment has been described internal segment
(Korenyi and Whittier 1967). Nigropallidal: dopaminergic to external
PD, late idiopathic onset, and early-onset segment
signs include resting tremor, oculomotor distur-
bance, and loss of postural reflexes, among other Efferent
dyskinesias. Pathology includes loss of nigral Pallidothalamic: GABAergic from internal seg-
dopaminergic neurons, although the cause is mul- ment mainly to ventral anterior nucleus of
tivariable (Nagatsu and Sawada 2007; Bergman thalamus
et al. 1998). Treatment can involve levodopa ther- Pallidonigral: GABAergic from external seg-
apy and decarboxylase antagonists, among a vari- ment to pars reticulata
ety of other pharmacological agents (Pahwa Pallidosubthalamic: GABAergic from external
2006). Surgical intervention is a relatively recent segment to subthalamic nucleus
development, often targeting STN and GPi (Kern
and Kumar 2007). Substantia Nigra: Pars Compacta, Pars
Other basal ganglia disorders: Wilson disease, Reticulata
Sydenham chorea, and ballismus.
Afferent
Striatonigral and pallidonigral (see above)
Summary of Major Components and Subthalamonigral: glutamatergic to pars
Circuitry (See Fig. 1) reticulata

Striatum: Caudate, Putamen Efferent

Nigrostriatal and nigropallidal (see above)
Afferent Nigrosubthalamic: dopaminergic from pars
Thalamostriatal: glutamatergic, mainly from cau- compacta to subthalamus
dal intralaminar nuclei (centromedian and para- Nigrothalamic: GABAergic to ventromedian
fascicular nuclei); glutamatergic and ventrolateral nuclei of thalamus
Basal Ganglia 485

Subthalamic Nucleus ▶ Rigidity

▶ Striatum
Afferent ▶ Substantia Nigra
Pallidosubthalamic and nigrosubthalamic (see ▶ Supplementary Motor Area (SMA)
above) ▶ Tardive Dyskinesia B
▶ Thalamus
Efferent ▶ Tremor
Subthalamopallidal and subthalamonigral (see
above)
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cortico- striato-thalamo-cortical dysfunction. Journal 1. A Teacher Rating Scale (TRS) and a Parent
of Fluency Disorders, 32(4), 251–278. Rating Scale (PRS) that gather multiple per-
Surmeier, D. J., Ding, J., Day, M., Wang, Z., & Shen, W.
(2007). D1 and D2 dopamine-receptor modulation spectives of observable behavior across set-
of striatal glutamatergic signaling in striatal medium tings and raters, using age-appropriate forms
spiny neurons. Trends in Neurosciences, 30(5), 2. A Self-Report of Personality (SRP) that a B
228–235. child, adolescent, or young adult can use to
Taylor, A., Saint-Cyr, J., & Lang, A. (1986). Frontal lobe
dysfunction in Parkinson’s disease: The cortical focus describe his or her behaviors, emotions, and
of neostriatal outflow. Brain, 109, 845–883. self-perceptions
Tricomi, E., & Fiez, J. a. (2008). Feedback signals in the 3. A Structured Developmental History (SDH)
caudate reflect goal achievement on a declarative mem- form that provides information about the
ory task. NeuroImage, 41(3), 1154–1167. https://doi.
org/10.1016/j.neuroimage.2008.02.066. course of development and family history that
Tricomi, E., Balleine, B. W., & O’Doherty, J. P. (2009). are important to make accurate diagnosis
A specific role for posterior dorsolateral striatum in 4. A Student Observation System (SOS) form
human habit learning. The European Journal of Neu- that can be used for recording and classifying
roscience, 29(11), 2225–2232. https://doi.org/10.1111/
j.1460-9568.2009.06796.x. directly observed classroom behavior, using a
West, R., Ergis, A., Winocur, G., & Saint-Cyr, J. (1998). smartphone, laptop computer, or paper form
The contribution of impaired working memory moni-
toring to performance of the self-ordered pointing task The BASC-3 is multidimensional in that it
in normal aging and Parkinson’s disease. Neuropsy-
chology, 12, 546–554. measures numerous aspects of behavior and per-
sonality, including positive (adaptive) as well as
negative (clinical) dimensions. Like its previous
editions (BASC-2, Reynolds and Kamphaus
BASC-3 2004; BASC, Reynolds and Kamphaus 1992),
the BASC-3 forms remain psychometrically
Robert A. Altmann1, Cecil R. Reynolds2, Randy strong instruments that are easy to complete and
W. Kamphaus3 and Kimberly J. Vannest4 relevant to both school-based and clinically based
1
A-PsychEd Publication Services, Minneapolis, settings. The norm samples are new and reflect the
MN, USA latest US Census estimates available at the time of
2
Texas A&M University, College Station, TX, the standardization project. In addition to new test
USA items, the BASC-3 TRS, PRS, and SRP now offer
3
College of Education, The University of Oregon, Clinical Indexes and new Executive Functioning
Eugene, OR, USA Indexes. The Clinical Indexes were developed
4
Department of Educational Psychology, Texas based on items that discriminated between clinical
A&M University, College Station, TX, USA and nonclinical samples and may be particularly
useful for helping to rule in or rule out certain
clinical diagnoses or educational classifications
Description and for assessing the amount of functional impair-
ment being experienced by the child or adoles-
The Behavior Assessment System for Children, cent. The Executive Functioning Indexes found
Third Edition (BASC-3; Reynolds and Kamphaus on the TRS and PRS provide insight into specific
2015) is a multimethod, multidimensional system executive functioning domains that are important
of related instruments that can be used to conduct when working with deficits such as attention def-
a comprehensive assessment of behavioral and icit hyperactivity disorder (ADHD), without the
emotional functioning of children, adolescents, need for additional rating scales. The Self-Report
and young adults aged 2–25 years. The BASC-3 of Personality Interview form, for ages 6–7, has
is a multimethod in that it has the following com- been redesigned. Rather than simply reading a
ponents, which may be used individually or in any series of items to the child, a total of 14 items
combination: are read to the child. Responses are obtained using
488 BASC-3

a semi-structured format that helps to elicit more hallmark of the BASC tools has been the compre-
natural responses by the child that can be used to hensiveness and breadth of behavioral and emo-
supplement findings from the BASC-3 TRS and tional problems covered. The number of problem
PRS and aid in treatment planning. The SDH form areas included on the BASC-3 tools is useful for
now offers an option for paired administration helping to rule in (and out) behavioral and emo-
with the PRS. When both are administered digi- tional functioning deficits that can look similar in
tally, additional items will be automatically nature, providing a distinct advantage over more
included during the SDH administration based narrowband classification instruments. The infor-
on PRS results, providing additional context that mation contained on the BASC-3 tools are
can be helpful for making accurate classification directly relevant to behavioral disorders found in
or diagnostic decisions. the Diagnostic and Statistical Manual of Mental
While paper administration and hand scoring Disorders, Fifth Edition (American Psychiatric
options are available for the TRS, PRS, SRP, SOS, Association 2013), as well as general categories
and SDH forms, the primary way to administer of problems addressed in legislation such as the
and score BASC-3 forms is digitally using the Q- Individuals with Disabilities Education Act (e.g.,
global web-based scoring and reporting platform. the diagnosis of severe emotional disturbance). In
Forms can be administered locally on a laptop or addition, the inclusion of adaptive behaviors on
web-enabled digital handheld device, or a web the BASC-3 TRS, PRS, and SRP forms provides
link can be emailed to a respondent to complete clinicians with information that can be used to
a form via a secured testing portal. Upon comple- help leverage a child’s or adolescent’s existing
tion, forms can be immediately scored, and strengths when developing individualized inter-
reports generated. Report options have been con- vention or treatment plans. Another key BASC-3
solidated from previous editions. The basic report feature is a grounded development approach that
offered is the Interpretive Summary Report, emphasizes a balance of both theory and statistics,
which provides extensive score profiles, along resulting in tools with strong psychometric prop-
with basic interpretive and clinical interpretive erties and clinical utility. Finally, the BASC-3
information, critical items, and item-by-scale list- tools promote ease of administration and scoring,
ings. The most comprehensive report offered is and the inclusion of scales that can help detect
the Interpretive Summary Report with Interven- threats to the validity and usefulness of obtained
tion Recommendations. This report provides responses makes the BASC-3 applicable to
intervention recommendations based on the numerous school, clinical, and forensic
obtained score profiles and is based on the applications.
BASC-3 Behavior Intervention Guide (Vannest
et al. 2015a; see below for more detailed
information). Historical Background
Like its previous editions, the BASC-3 remains
committed to a triangulated view of the child’s The original BASC (Reynolds and Kamphaus
behavioral and emotional functioning by examin- 1992) was published by American Guidance Ser-
ing behavior in multiple settings (at home and vice, following 7 years of development work. It
school) and evaluating the child’s emotions, per- was standardized for use with children and ado-
sonality, and self-perceptions. lescents ages 4–18 years and was rapidly adopted
as the most frequently administered behavior
scales in the schools in the United States. Spanish
Key Features of the BASC-3 versions were subsequently developed for inter-
national applications, as well as smaller research-
The BASC-3 has numerous features that make it only adaptations in several additional languages.
one of the most sophisticated and reliable systems The release of the second edition (BASC-2, Reyn-
of behavior assessment available today. A olds and Kamphaus 2004) continued to be well
BASC-3 489

received by users in both the United States and a reliable for application to diagnostic and treatment
number of other countries. Several other tools in issues. Additionally, the BASC-3 offers various
the BASC-2 family were released in subsequent types of validity checks to help the clinician detect
years, including the Parenting Relationship Ques- careless or untruthful responding, misunderstand-
tionnaire (PRQ, Kamphaus and Reynolds 2006), ing, or other threats to validity. The BASC-3 B
the Behavioral and Emotional Screening System Manual demonstrates validity evidence for the
(BESS; Kamphaus and Reynolds 2007), the proposed applications of the BASC-3 scales that
BASC-2 Intervention Guide (Vannest et al. is extensive and covers both theoretical and actu-
2008), and the BASC-2 Progress Monitor (Reyn- arial bases. Correlations with numerous other rat-
olds and Kamphaus 2010). These tools were con- ing scales and self-reports are given as well as
sistent with the Response to Intervention studies of a large number of clinical groups.
movement in the US educational system that
emphasized a screening, intervention, and moni-
toring approach to addressing a student’s func- BASC-3 Uses
tional deficits. The BASC-3 continues the
tradition of innovation with improvements to Clinical Diagnosis
existing instruments and the development of the The BASC-3 aids in the clinical diagnosis of
new components described below. disorders that are usually first apparent in child-
hood or adolescence. It assesses a variety of
symptoms that are noted in the DSM-5. Because
Psychometric Data the components of the BASC-3 can be used sep-
arately or in combination, the BASC-3 may be
The scales included on the TRS, PRS, and SRP easily used in residential settings, in clinics, or by
are designed to be highly interpretable and are private practitioners. The PRS and SDH can be
built around clearly specified constructs with completed by a parent while the child is being
matching item content, developed through a bal- evaluated by the practitioner, thus reducing the
ance of theory and empirical data. The ease of practitioner’s time in the data collection process.
scale interpretation is partly attributable to the The rating scales, the SRP, and the SOS can be
items which comprise them. The approach used repeated on a regular basis to monitor a child’s
to develop the original BASC items involved sur- progress and response to treatment. It is highly
veying teachers, parents, and students about desirable that diagnosis be linked clearly to inter-
behaviors that were the most difficult to manage vention. In this respect, treatment planning can
or behaviors that were the most disruptive; in also be facilitated by the BASC-3. Problem
addition, respondents were asked to provide behaviors can be delineated and targeted in a
examples of positive behaviors that were program leading to their reduction. A similar strat-
observed. This survey process was repeated dur- egy can be used with deficits in adaptive skills.
ing the BASC-3 standardization project, helping
to ensure that the items written during the devel- Educational Classification
opment of the original BASC remain relevant and Differential diagnosis is becoming an increasingly
that new behaviors deemed important were also important issue in school settings. This is partly
included on the BASC-3 edition. Factor-analytic because the complexity of many children’s prob-
evidence presented in the BASC-3 Manual pro- lems requires an array of interventions that must
vides support for the overall scale and composite be tailored to the individual child’s needs. Conse-
structure used for reporting results. quently, the BASC-3 is designed to be sensitive to
The BASC-3 scales and composites have high numerous presenting problems in the classroom,
internal consistency and test-retest reliability. including deficiencies in social skills, study skills,
Most alpha coefficients for the BASC-3 subscales or other adaptive skills. Academic difficulties
and composites exceed 0.80 and are sufficiently are frequently linked to behavior problems.
490 BASC-3

Syndromes such as ADHD and depression have which are considered by judges in determining
known academic consequences; learning disabil- admissibility of testimony based partially or wholly
ities and intellectual disability are often associated on test data. Also presented are additional crucial
with adjustment problems such as low self-con- data on the ability of the BASC-3 scale scores to
cept or anxiety. It is strongly suggested that every measure child and adolescent psychopathology
child experiencing academic difficulties receives and to discriminate among various diagnostic
a behavioral assessment. Additionally, research groups, capabilities that also are included in the
demonstrates that good behavioral assessment of consideration of admissible evidence. The BASC-
constructs such as attitude to school, attitude to 3 is well established in clinical environments such
teachers, study skills, attention problems, and as schools, child guidance centers, university
adaptability, in tandem with cognitive assessment, clinics, and private practice settings in the United
improves the prediction of both school perfor- States and abroad. The use of tests in a wide variety
mance and response to intervention. of settings is important in establishing credibility
and admissibility in various legal proceedings.
Program Evaluation When choosing instruments for forensic eval-
Repeated use of the BASC-3 TRS, PRS, SRP, and uations, it is also important for clinicians to eval-
SOS can aid in identifying a child’s progress in uate the instruments’ ability to detect
specific programs. Improvement in designated dissimulation (Reynolds and Kamphaus 2002).
areas of behavior and in affective states may be In court proceedings, individuals may have
noted, and the strengths and weaknesses of pro- much to gain by appearing to have more or
grams thus identified. The original BASC was fewer problems than what actually exist. Because
shown in a number of evaluation studies to be nearly any behavioral or emotional problem or
sensitive to the effects of various intervention pro- disorder can be minimized or exaggerated, objec-
grams for young children (including the evalua- tive methods are needed to determine whether
tion component of Head Start’s Project Mastery) dissimulation has occurred. The BASC-3 has
and adolescents (e.g., the evaluation by the Civil- scales designed and tested for the detection of
ian Health and Medical Program of the Uniformed dissimulation in responding by parents, teachers,
Services, or CHAMPUS, of the effectiveness of and children. In particular, the BASC-3 validity
residential treatment for adolescents). These and scales can identify exaggerated responding, min-
other applications of the BASC in program eval- imization of problem reporting, inconsistencies,
uation are reviewed in Reynolds and Kamphaus random answering patterns, and other response
(2002). methods that lead to inaccurate depictions of the
child’s or adolescent’s behavior.
Forensic Evaluation
The BASC-3 is appropriate for use in legal or
forensic settings. According to several US Additional BASC-3 Components
Supreme Court rulings of the 1990s, evidence of
the psychometric properties of tests used in a The BASC-3 includes a variety of other instru-
forensic setting is crucial for determining the ments that can be used to help identify and improve
admissibility of expert testimony based on test behavioral and emotional functioning. Each of
results. Reynolds and Kamphaus (2002) provide these instruments is described briefly below.
examples of uses of the original BASC in forensic
situations such as child custody evaluations, per- BASC-3 Behavioral and Emotional Screening
sonal injury litigation, and juvenile certification. System (BESS)
The BASC-3 Manual contains considerable The BASC-3 BESS (Kamphaus and Reynolds
information on the reliability of scale scores and 2015b) is designed to quickly and efficiently iden-
associated standard errors of measurement, on the tify risk for behavioral or emotional problems and
normative samples, and on validation studies, all of predict mental health and educational outcomes.
BASC-3 491

The BASC-3 BESS consists of two teacher forms BASC-3 Parenting Relationship Questionnaire
(ages 3–5 and ages 6–18), two parent forms (ages (PRQ)
3–5 and ages 6–18), and one self-report form The BASC-3 Parenting Relationship Question-
(ages 8–18). Each form of the BASC-3 BESS is naire (PRQ; Kamphaus and Reynolds 2015a) is
brief and requires no prior training and coaching designed to capture a parent’s perspective of the B
of the informant. parent-child relationship (or the perspective of a
Each BASC-3 BESS form provides a Behav- person serving a similar role). It assesses tradi-
ioral and Emotional Risk Index (BERI), which tional parent-child dimensions such as attachment
indicates the amount of risk a child or adolescent and involvement and also provides information on
has of having or developing a behavioral or emo- parenting style, parenting confidence, stress, and
tional problem. The teacher and parent forms offer satisfaction with the child’s school. The BASC-3
additional subindex scores, including an External- PRQ is used in clinical, pediatric, counseling,
izing Risk Index, Internalizing Risk Index, and school, and other settings where there is a need
Adaptive Skills Risk Index. In addition to the to understand the nature of the parent-child rela-
BERI, the self-report form also provides subindex tionship. It is particularly important when
scores for an Internalizing Risk Index, a Self- implementing home-based intervention strategies
Regulation Risk Index, and a Personal Adjust- and/or treatment monitoring. The BASC-3 PRQ
ment Risk Index. can be completed in approximately 15 minutes
Using the same item response formats as the and is available in English and Spanish. It should
BASC-3 TRS and PRS, each BASC-3 BESS form be administered to mothers and fathers (or care-
produces a single score indicating “normal risk” givers) of children ages 2–18 years. Administra-
(T = 20–60), “elevated risk” (61–70), or tion, scoring, and reporting are available on the Q-
“extremely elevated risk” (T = 71 or higher). global platform. The BASC-3 PRQ Manual pro-
Validity indexes are provided for each form, and vides information about the reliability and validity
Spanish adaptations and translations are available of evidence collected during the standardization
for parent and student forms. Administration, stage of development. Internal consistency reli-
scoring, and reporting (both individual- and ability coefficients for each scale were typically
group-level reports) are available on the Q-global in the mid-.80s or higher. A variety of correla-
testing platform. tional studies are also presented.
The BASC-3 BESS manual includes a detailed
discussion of development procedures and a sep- BASC-3 Flex Monitor
arate chapter devoted to validity and reliability The BASC-3 Flex Monitor (Reynolds and
evidence collected to date. All BERI reliability Kamphaus 2016) is used to monitor and track
coefficients exceed 0.90, and test-retest correla- the effect of behavioral interventions
tions are in the upper .80s or higher. A variety of implemented by a psychologist or other profes-
correlational studies are presented, including the sionals in a school or clinical environment. Avail-
BASC-3 TRS, PRS, and SRP, along with other able via Q-global, the BASC-3 Flex Monitor
behavioral/emotional functioning tests. The provides a bank of over 700 behaviorally or emo-
BASC-3 BESS manual also provides a detailed tionally based items that can be selected to create a
discussion of promising screening practices, customized monitoring form for teachers, parents,
including the use of multiple "gates" (i.e., assess- or students (via a self-report form) that enable
ment stages that range from broad-based screen- score comparisons to a nationally representative
ing on all students to more detailed assessment/ population sample. While creating forms, users
evaluation on students identified at previous can automatically calculate reliability estimates
gates). In addition, the Manual discusses linking that are based on a normative sample. In addition,
screening results with early intervention strategies the BASC-3 Flex Monitor offers a variety of stan-
aimed at preventing the onset of mental health dard forms that are available for immediate use,
disorders or unsuccessful educational outcomes. including inattention/hyperactivity, internalizing
492 BASC-3

problems, disruptive behaviors, developmental guide provides tier one and tier two intervention
social disorders, and school problems. Parent strategies in a classroom curriculum format, as
and self-report forms are available in both English well as additional strategies that are targeted for
and Spanish. Individual reports tracking progress small group settings. Teachers can follow the
on up to ten administrations of a form or aggre- lesson plans provided in the guide to teach
gated group-based reports can be easily generated schoolwide expectations using activities that are
on the Q-global platform. fast-paced and brief, lasting around 5 minutes
each. Additional instructional strategies for
classrooms and small groups are also available
BASC-3 Behavior Intervention Guide for the behavioral and emotional problems
included in the BASC-3 Behavior Intervention
The BASC-3 Behavior Intervention Guide Guide.
(Vannest et al. 2015a) provides evidence-based
intervention strategies for 11 common types of
emotional and behavioral problems: aggression, References and Readings
conduct problems, hyperactivity, attention prob-
lems, academic problems, anxiety, depression,
American Psychiatric Association. (2013). Diagnostic and
somatization, functional communication, adapt-
statistical manual of mental disorders (5th ed.). Wash-
ability, and social skills. These interventions rep- ington, DC: American Psychiatric Association.
resent a compendium of the most effective Kamphaus, R. W., & Reynolds, C. R. (2006). Parenting
strategies that have been published in empirically relationship questionnaire. Minneapolis: Pearson.
Kamphaus, R. W., & Reynolds, C. R. (2007). Behavioral
based research studies.
and emotional screening system. Minneapolis: Pearson.
In addition to providing background character- Kamphaus, R. W., & Reynolds, C. R. (2015a). BASC-3
istics and conditions of each behavioral or emo- parenting relationship questionnaire. Bloomington:
tional problem area, each chapter provides a NCS Pearson Inc.
Kamphaus, R. W., & Reynolds, C. R. (2015b). BASC-3
number of intervention strategies that are pre-
behavioral and emotional screening system. Bloom-
sented in a preparation, implementation, and eval- ington: NCS Pearson Inc.
uation format. The intervention steps that are Reynolds, C. R., & Kamphaus, R. W. (1992). Behavior
provided can be easily used by behavior experts assessment system for children. Bloomington: Pearson
Assessments.
(e.g., psychologists, counselors, behavioral spe-
Reynolds, C. R., & Kamphaus, R. W. (2002). The clini-
cialists) to promote more desirable behavior and cian’s guide to the behavior assessment system for
reduce problem behaviors. The BASC-3 Behavior children. New York: Guilford.
Intervention Guide also offers accompanying Reynolds, C. R., & Kamphaus, R. W. (2004). Behavior
assessment system for children (2nd ed.). Bloomington:
tools that are designed to promote intervention
Pearson Assessments.
fidelity and positive outcomes, including parent Reynolds, C. R., & Kamphaus, R. W. (2010). BASC–2
tip sheets that promote and provide structured progress monitor. Bloomington: NCS Pearson Inc.
involvement by parents or caregivers, supplemen- Reynolds, C. R., & Kamphaus, R. W. (2015). Behavior
assessment system for children (3rd ed.). Bloomington:
tal forms that accompany the intervention strate-
NCS Pearson, Inc. (BASC–3).
gies (e.g., daily log journals, activities, sample Reynolds, C. R., & Kamphaus, R. W. (2016). BASC–3 Flex
forms, etc.), and a fidelity documentation Monitor. Bloomington: NCS Pearson, Inc.
checklist. Vannest, K. J., Reynolds, C. R., & Kamphaus, R. W.
(2008). Behavior assessment system for children – sec-
For small group or classroom-based solutions,
ond edition (BASC-2) intervention guide for emotional
the BASC-3 Behavioral and Emotional Skill and behavioral problems. Bloomington: Pearson.
Building Guide (Vannest et al. 2015b) can be Vannest, K. J., Reynolds, C. R., & Kamphaus, R. W.
used in general or special education settings to (2015a). BASC-3 behavior intervention guide. Bloom-
ington: Pearson.
help promote positive behavioral and emotional
Vannest, K. J., Reynolds, C. R., & Kamphaus, R. W.
functioning. Based on the foundations established (2015b). BASC-3 behavioral and emotional skill build-
in the BASC-3 Behavior Intervention Guide, this ing guide. Bloomington: Pearson.
Basic Achievement Skills Inventory 493

Cross-References
Base Rate (Population)
▶ Sensitivity
Molly E. Zimmerman
Department of Psychology, Fordham University, B
Bronx, NY, USA References and Readings

Gouvier, W. D. (1999). Base rates and clinical decision

making in neuropsychology. In J. J. Sweet (Ed.),
Definition Forensic neuropsychology (pp. 27–38). New York:
Taylor & Francis.
The population prevalence of a variable of interest Lezak, M. D., Howieson, D. B., Bigler, E. D., & Tranel, D.
is known as the base rate. (2012). Neuropsychological assessment. Oxford:
Oxford University Press.
Podell, K., Defina, P. A., Barrett, P., McCullen, A., &
Goldberg, E. (2003). Assessment of neuropsychologi-
cal functioning. In I. B. Weiner, D. K. Freedheim, J. A.
Current Knowledge Schinka, & W. F. Velicer (Eds.), Handbook of psychol-
ogy (pp. 443–466). New York: Wiley.
Base rates can be calculated using the following
formula (Gouvier 1999):

Base rate Basic Achievement Skills

¼ #cases with condition of interest= Inventory
#cases in a population
Kelly Broxterman1, Doris S. Mok2 and Alyssa
In neuropsychological settings, base rates Beukema1
1
are often used to characterize diagnostic accu- School Psychology, The Chicago School of
racy and interpret the sensitivity and specificity Professional Psychology, Chicago, IL, USA
2
of a clinical assessment. The sensitivity of a Department of Psychology, Faculty of Social
test is the probability of correctly identifying Sciences and Humanities University of Macau,
an individual with impaired functioning as Taipa, Macau SAR, China
actually being impaired, while the specificity
of a test is the probability of correctly identi-
fying an individual with normal functioning as Synonyms
actually being normal (Lezak et al. 2012).
When the base rates of a condition are low, BASI
the sensitivity of a test may be misleading.
When the base rates of a condition are high,
the specificity of a test may be misleading Description
(Podell et al. 2003). The neuropsychologist
should consider base rates of a disorder when The Basic Achievement Skills Inventory (BASI)
selecting tests for use in a specific population. is a commercially published, norm-referenced
Knowledge of base rates may also indicate that achievement test that assesses math, reading, and
impairment cutoff scores should be adjusted to language skills for children and adults. It is
interpret diagnostic accuracy. Assessments of published by Pearson and was first made available
malingering or suboptimal effort should also in 2004. Information on the test is easily accessi-
be conducted with consideration of base rates ble through the publishers’ webpage (http://www.
for a particular condition of interest (Gouvier pearsonassessments.com/basi.aspx), which includes
1999). relevant excerpts from the manual, a flash
494 Basic Achievement Skills Inventory

demonstration, training modules, sample reports, scores of a census-matched national sample at

and others. the student’s grade level.
The adult summary report is a one-page report
Forms that summarizes an adult’s performance by skills
There are two forms: a comprehensive form and a composite, subtest, and learning objectives. It
survey form. The comprehensive form comprises includes percent correct, grade equivalent, and
six timed subtests: vocabulary, spelling, language classification by achievement area.
mechanics, reading comprehension, math compu-
tation, and math application. The subtests can be
administered independently to measure specific Historical Background
skills or in any combination. There are four
grade levels (I–IV), 3rd–4th grade, 5th–6th Achilles N. Bardos, PhD, is the author of the test
grade, 7th–8th, and 9th–12th. The survey form is (http://www.unco.edu/cebs/SchoolPsych/faculty/
a screening tool comprising two subtests: verbal BASI/index.html). The BASI was published in
skills and math skills. Verbal skills are assessed 2004. Content was based on curriculum standards
using vocabulary, language mechanics, and read- from The Model Curriculum and Assessment
ing comprehension questions, and math skills are Database (MCAD), a database used by educators
assessed using math computation and math appli- to align with district, state, and national curricu-
cation questions. Student progress can be assessed lum requirements and standards.
through Form A with Fall norms (August to
December) and Form B with Spring norms
(January to July). A growth scale value (GSV) is Psychometric Data
made available to measure the progress of
students. Standardization is reportedly based on stratified
random sampling to match closely with the US
Administration Census 2000. For the comprehensive form, a
The tests can be administered individually or in grade-appropriate sample was stratified according
groups, timed or untimed; the comprehensive to gender, race, parental education, and region.
form takes about 2 h, and the survey form takes Standardization of Form A was based on 2,439
about 50 min to complete. students tested during Fall 2002, and standardiza-
tion of Form B was based on 2,130 students tested
Scoring and Report in Spring 2003. The survey form included a
Scoring for the comprehensive form is available school-age standardization sample of 2,518 stu-
through Q-global web-based administration, dents (aged 8–18) tested in school settings and an
Q local software, or mail-in scoring. The student adult sample of 2,452 adults (aged 19–80)
summary report is a one-page report that summa- recruited in a variety of settings.
rizes the student’s performance by skills compos- Buros Institute test reviewers (Rhoades 2007;
ite, subtest, and learning objectives. The student Trevisan 2007) reported the test-retest stability,
summary report includes standard scores, percen- internal consistency, and alternate-forms reliabil-
tile scores, age equivalents, and grade equivalents ity to be fairly strong, with estimates ranging from
as well as a performance classification (low aver- 0.54 to 0.96 for individual subtest scores and
age, average to above average) by achievement 0.67–0.98 for composite scores. Test validity is
area. A parent’s report is included with each stu- established through the Iowa Tests of Basic Skills
dent report. The parent’s report graphs percentile (ITBS), the Iowa Tests of Education Development
scores and includes a space for written comments. (ITED), the Tests of Adult Basic Education
There is also an optional report available for level (TABE), the Wechsler Individual Achievement
4 of the BASI comprehensive version, titled the Test Second Edition (WIAT-II), and the Wood-
BASI college report. The college report shows cock Johnson Psychoeducational Battery III
how a student’s BASI scores compared to the (WJ-III).
Basilar Artery 495

Clinical Uses
Basilar Artery
The author proposes that the comprehensive form
provides a complete evaluation of academic skills Elliot J. Roth
to “(1) determine academic strengths and weak- Department of Physical Medicine and B
nesses; (2) screen for and assist in diagnosing Rehabilitation, Northwestern University,
learning disabilities in reading, writing and Feinberg School of Medicine, Chicago, IL, USA
math; (3) place for college students; (4) make
placement decisions for ESL, GED, and program
placement; (5) track academic progress, (6) effi- Definition
ciently complete triennial evaluations for students
with an IEPs or 504 plans; and (7) practice for or The basilar artery provides blood to the brain.
predict performance on high-stakes tests.” Spe- This artery and the two vertebral arteries comprise
cific applications in four settings are proposed in the vertebrobasilar system, which supplies blood
the BASI Flash demonstration (http://www. to the posterior part of circle of Willis and con-
pearsonassessments.com/basidemo/basi.swf): nects (“anastomoses”) with blood supplied to the
(1) K-12 school/educational setting, (2) correc- anterior part of the circle of Willis from the carotid
tions setting for intake and evaluation of offenders arteries. It arises from the confluence of the two
for placement in programs, (3) public safety for vertebral arteries, next to the lower brain stem,
employment screening, and (4) adult and child ascends parallel to the brain stem, and gives rise
clinical setting. In adult and child clinical settings, to the anterior inferior cerebellar artery, which
the BASI Comprehensive Form is recommended supplies part of the cerebellum, some smaller
to be used as a time- and cost-effective screening, branches that supply the brain stem, and the supe-
providing an overview of achievement or alterna- rior cerebellar artery. It finally divides into the two
tive for individually administered achievement posterior cerebral arteries (PCA). These supply
test when detailed information is not needed. the upper brain stem, the occipital lobe, and the
posterior portion of the temporal lobes.
Cross-References
Current Knowledge
▶ Academic Skills
The clinical manifestations of basilar artery occlu-
sion depend on the location of the occlusion, the
References and Readings
extent of thrombus, and the collateral flow. Nor-
Griffith, R. (2006). An examination of factors influencing mally, the blood flows in an anterograde fashion
differences in academic performance among active from the vertebral arteries to the basilar artery up
duty military students and naval reserve officer training to its terminal branches. This pattern of flow may
corps scholarship students in a university setting. Dis- vary. If the proximal segment of the basilar artery
sertation Abstracts International Section A 67, 2071.
Retrieved from PsycINFO database. is occluded and the occlusion resulted from a
Rhoades, E. K. (2007). Test review of the basic achieve- slowly progressive stenosis, collateralization
ment skills inventory. In K. F. Geisinger, R. A. Spies, occurs within the cerebellum into the circumfer-
J. F. Carlson, & B. S. Plake (Eds.), The seventeenth ential branches of the basilar artery. In addition,
mental measurements yearbook [Electronic Version].
Retrieved 17 Feb 2009 from the Buros Institute’s Test flow can be reversed from the PCAs into the distal
Reviews Online website: http://unl.edu/buros basilar artery. Thrombosis of the basilar artery
Trevisan, M. S. (2007). Test review of the basic achieve- causes various clinical syndromes that result
ment skills inventory. In K. F. Geisinger, R. A. Spies, from brainstem ischemia, including cranial nerve
J. F. Carlson, & B. S. Plake (Eds.), The seventeenth
mental measurements yearbook [Electronic Version]. dysfunction, difficulty in swallowing and breath-
Retrieved 17 Feb 2009 from the Buros Institute’s Test ing, and at its most severe, locked-in syndrome.
Reviews Online website: http://unl.edu/buros Basilar artery thrombosis is the most common
496 Battery Approach

cause of locked-in syndrome. Mortality rate of battery is very likely to depend on the assessment
basilar artery occlusion is 70%, but this can be setting, nature of the presenting problem and dif-
reduced substantially through the use of anti- ferential diagnosis, and the theoretical orientation
thrombotic agents. of the clinician.
One of the first battery approaches was what is
commonly referred to today as the “fixed battery.”
Cross-References In the fixed battery approach, test selection is
predetermined irrespective of the patient’s pre-
▶ Circle of Willis senting problem. A comprehensive battery of
▶ Posterior Cerebral Artery tests is administered to all patients in the same
▶ Vertebrobasilar System standardized manner. Collection of collateral
medical and social history is obtained following
administration and scoring of the neuropsycho-
logical data to avoid response bias on the part of
the test administrator. Examples of this psycho-
Battery Approach metrically oriented, data-driven approach include
the Luria-Nebraska Battery and the Halstead-
Molly E. Zimmerman Reitan Battery. An advantage of the fixed battery
Department of Psychology, Fordham University, approach is that it facilitates comparison of test
Bronx, NY, USA scores across patient groups and assessment set-
tings. Another advantage of the battery approach,
when using standardized tests, is that this
Definition approach facilitates the use of technicians in the
administration of the tests. This approach can also
A battery approach to neuropsychological assess- facilitate the development of data banks for
ment is the administration of multiple measures research purposes. A disadvantage, however, is
that cover a wide range of cognitive abilities to that it is often time-consuming, cost-prohibitive,
fully characterize an individual’s neuropsycho- and may produce excessive testing sessions that
logical strengths and weaknesses. are poorly tolerated by patients (Mitrushina
et al. 2005).
An alternative neuropsychological assess-
Current Knowledge ment method is the “flexible battery” approach.
In this hypothesis-driven approach, initial test
The battery approach is predicated on the exis- selection is guided by the patient referral ques-
tence of a variety of instruments that have been tion, presenting problem, and the clinical inter-
empirically developed to measure myriad aspects view. A modest range of measures that survey a
of neuropsychological function. Neuropsycholog- broad range of cognitive functions is specifically
ical batteries generally contain a measure of gen- chosen to probe and characterize the patient’s
eral intellectual functioning or premorbid presumed strengths and weaknesses. Following
functioning as well as assessments of basic neu- this initial assessment, which is sometimes
ropsychological functions that may include atten- referred to as a “core” or “screening” battery,
tion, executive function, language, memory, the clinician will then select additional tests
visuospatial perception and construction, and psy- based on the patient’s performance on the core
chomotor function. Performance on a test of gen- battery and reported cognitive concerns (Strauss
eral intellectual function serves as a context in et al. 2006). The flexible battery approach is
which performance across neuropsychological more focused on each individual patient’s pre-
domains can be considered. Selection of individ- senting problem and differential diagnosis than
ual tests that comprise a neuropsychological the fixed battery approach. As a result, the total
Battle’s Sign 497

assessment period is restricted and may be more References and Readings

cost-effective. However, inherent in the flexible
battery approach is the inconsistent administra- Lezak, M. D., Howieson, D. B., Bigler, E. D., & Tranel,
D. (2012). Neuropsychological assessment. Oxford:
tion of tests across patient groups. That is, not all
Oxford University Press.
of a neuropsychologist’s patients will receive the Mitrushina, M., Boone, K. B., Razani, J., & D’Elia, L. F. B
same tests, thereby limiting comparisons of find- (2005). Handbook of normative data for neuropsycho-
ings across patient groups or settings (Mitrushina logical assessment. Oxford: Oxford University Press.
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A
et al. 2005).
compendium of neuropsychological tests: Administration,
A variant of the flexible battery approach is the norms, and commentary. Oxford: Oxford University Press.
“process” approach, also known as the Boston Sweet, J. J., Meyer, D. G., Nelson, N. W., & Moberg, P. J.
process approach (Lezak et al. 2012). This method (2011). The TCN/AACN 2010 “salary survey”: Profes-
sional practices, beliefs, and incomes of U.-
entails emphasis on the more qualitative aspects
S. neuropsychologists. The Clinical Neuropsychologist,
of neuropsychological performance. When 25, 12–61.
completing a task, patients are closely observed
for strategy formation and execution. Atypical
performances will be further probed by the
clinician with direct questioning or modified Battle’s Sign
re-administration of the task to more fully
examine the nature of the behavioral dysfunc- Beth Rush
tion. This approach affords a more in-depth Psychiatry and Psychology, Mayo Clinic,
characterization of the patient’s neuropsycho- Jacksonville, FL, USA
logical abilities. However, it has been criti-
cized for its lack of normative data and
standards for the reliability and validity of its Synonyms
methods (Strauss et al. 2006).
Periauricular or mastoid ecchymosis

Future Directions Definition

Although all battery approaches to neuropsycho-
Named after English surgeon, Dr. William Henry
logical assessment have advantages and disadvan-
Battle, this is a clinical symptom suggestive of
tages, results from a survey from Sweet et al.
basilar skull/middle cranial fossa fracture. After
(2011) suggest that the flexible battery approach
blunt force head trauma, leaking of blood from the
is the method that is most preferred by clinicians.
blood vessels in the skull, typically the posterior
According to this report, the percentage of clini-
auricular artery, leads to a crescent-shaped bruise
cians who endorsed the flexible battery approach
wrapping behind the base of the earlobe and
increased from 54% in 1989 to 78% in 2010.
extending posteriorly toward the point of the
These data reflect the relative popularity of this
neck where the base of the skull meets the neck.
approach and suggest that it is likely to remain in
A patient with this symptom may present with
favor in the coming years.
acute bloody discharge of the ear and/or nose.
Battle’s sign may occur a few days following the
onset of the skull fracture.
Cross-References

▶ Boston Process Approach Cross-References

▶ Fixed Battery
▶ Flexible Battery ▶ Depressed Skull Fracture
498 Battlefield Assessment

References and Readings more than one blast event (the service member’s
commander shall direct a medical evaluation).
Victor, M., & Ropper, A. H. (2001). Principles Beginning with recognition, the policy outlines
of neurology (7th ed.pp. 925–953). New York:
additional steps including, refer, report, rest, and
McGraw-Hill.
return to duty.

Command Guidance

Battlefield Assessment Recognize

Military leadership is required to recognize all
Tamara McKenzie-Hartman personnel involved in any potentially concussive
Defense and Veterans Brain Injury Center, James event, including those without apparent injuries,
A. Haley, VA Hospital, Tampa, FL, USA as soon as safely possible using the IED/HEADS
checklist (Table 1).

Description Refer
Leaders refer any service member involved in a
Researchers report that “Due to enemy tactics and potentially concussive event to be evaluated by
the frequency of operational missions, many ser- a medic or health care provider and if applicable,
vice members are at risk of sustaining more than be re-evaluated and medically cleared before
one concussion during deployment” (Barth et al. returning to duty.
2010). It is further noted that as numerous service
members go on multiple deployments, the oppor- Report
tunity for injury is increased. According to the Military leaders are required to report all service
Defense and Veterans Brain Injury Center members involved in a potentially concussive
(DVBIC), 40% of all blast injuries in the Opera- event by completing the significant activities
tion Enduring Freedom/Operation Iraqi Freedom (SIGACT) report within 24 h of the injury.
(OEF/OIF) conflicts involve traumatic brain Depending on the command, reports may be
injury (TBI). Furthermore, many mild and mod- required using the Blast Exposure and Concus-
erate head injuries are reportedly overlooked due sion Incident Report (BECIR) module, located
to more imminent medical treatments focused on
polytrauma injuries including amputation and
burns (Martin et al. 2008).
Battlefield Assessment, Table 1: IED/HEADS
DoD instructional policy (DoDi 6490.11), enti- checklist
tled “Guidance for Management of Mild Trau-
Was the service member injured Yes/
matic Brain Injury/Concussion in the Deployed I-Injury during the event? no
Setting,” is intended to protect service members E- Are any of the “HEADS” Yes/
involved in potentially concussive events, direct evaluation symptoms present? no
leaders on mandated screening and reporting H-headaches and/or vomiting?
(yes/no)
requirements, guide medical evaluation and treat- E-ears ringing? (yes/no)
ments, and outline minimum mandatory rest A-amnesia, altered/loss of
periods. Specifically, the policy mandates that a consciousness? (yes/no)
service member be medically evaluated if exposed D-double vision and/or
dizziness? (yes/no)
to a potentially concussive event such as
S-something feels wrong or is not
(1) involvement in a vehicle blast, collision, or right? (yes/no)
rollover, (2) a direct blow to the head or witnessed D-distance/ Was the service member within Yes/
loss of consciousness, (3) presence within 50 m of proximity 50 m of the blast? Record no
a blast (inside or outside), and/or (4) exposure to distance from blast
Battlefield Assessment 499

within the Combined Information Data Network service member should receive seven additional
Exchange (CIDNE). days of rest after symptoms resolve. If three or
more concussions have been diagnosed within the
Medical Guidance previous 12 months, the service member is man-
Medical requirements include (1) utilization of the dated to receive a recurrent concussion evaluation B
Military Acute Concussion Evaluation (MACE) before returning to duty. Of note, commanders
for screening of a potentially concussive event, may determine that mission requirements super-
(2) documentation and appropriate International sede an individual’s welfare in certain circum-
Classification of Diseases (ICD) coding of the stances and can waive or postpone the
medical encounter within the electronic health mandatory rest period.
record, (3) and utilization of the “Concussion The recurrent concussion evaluation can be
Management in Deployed Settings” algorithm initiated at any time that it is clinically warranted
(DCoE 2011; Fig. 1). The algorithm outlines and should be used to inform treatment and return-
three levels of intervention: (1) Level I: Combat to-duty (RTD) decisions. Recurrent concussion
Medic/Corpsman Concussion Triage, (2) Level II: evaluations are to include (1) neurological exam-
Initial Management of Concussion in Deployed ination, including completion of the
Setting, and (3) Level III: Comprehensive Con- Neurobehavioral Symptom Inventory (NSI), a
cussion Evaluation. validated acute stress reaction assessment, and a
Medical personnel are instructed to use sec- vestibular assessment; (2) neuroimaging; (3) neu-
tion one of the MACE (Fig. 2), which is used to ropsychological assessment; (4) functional
assess the service member’s potential concus- assessment, including evaluation of cognitive,
sion/mild traumatic brain injury (mTBI). Ques- sensorimotor, and physical endurance; (5) and a
tions on the MACE guide the provider to obtain a duty status determination by a neurologist or other
description of the incident, as well as assess of qualified licensed independent practitioner trained
any alterations or losses of consciousness according to service policies in the care of mTBI/
(AOC/LOC), and/or post-traumatic amnesia concussion.
(PTA). Assessments are to be completed as Regarding neuropsychological assessment, the
close to the time of injury as feasible. The Clinical Recommendation (DCoE 2011) indicates
MACE is currently the primary instrument, that a neurocognitive assessment tool (NCAT)
used mostly by corpsmen/medics, to assess should be considered if symptoms persist. In
in-theater concussive events and determine the accordance with the National Defense Authoriza-
need for additional levels of care. tion Act (NDAA HR 4986), the DoD selected the
Automated Neuropsychological Assessment Met-
Rest rics (ANAM) as the NCAT to be utilized for pre-
Service members must receive a minimum of deployment baseline assessments and for post-
24 h of rest/downtime after a potentially concus- concussion testing in theater.
sive event. The 24-h clock starts at the time of the In theater, clinical guidelines indicate that the
event, not at the time of the evaluation. Recovery ANAM test battery be administered if symptoms
care is to include sleep and pain management. As of concussion are present 24-h post-injury. The
current research supports the return to first administration of the test should be within
neurocognitive baseline as soon as a few days 24–72 h from injury, and the test can be
post-injury, and many times without formal inter- readministered on a regular basis to assess for
vention (Mittenberg and Strauman 2000), the cognitive deficits and symptom resolution (Kelly
service member should remain in place for sev- et al. 2012). To this end, the service member’s
eral days to allow for this recovery (Barth post-injury test scores can be compared to his/her
et al. 2010). own baseline data, if possible, or to the norma-
If the service member has been diagnosed with tive database to determine recovery (DCoE
two concussions within the prior 12 months, the 2011).
500 Battlefield Assessment

Battlefield Assessment, Fig. 1 (continued)

Battlefield Assessment 501

Battlefield Assessment, Fig. 1 (continued)

502 Battlefield Assessment

Battlefield Assessment, Fig. 1 (continued)

Battlefield Assessment 503

Battlefield Assessment, Fig. 1 (continued)

504 Battlefield Assessment

Battlefield Assessment, Fig. 1 (continued)

Battlefield Assessment 505

Battlefield Assessment, Fig. 1 (continued)

506 Battlefield Assessment

Battlefield Assessment, Fig. 1 (continued)

Battlefield Assessment 507

Battlefield Assessment, Fig. 1 DVBIC concussion-management-algorithm pocket-cards version-4.2

508 Battlefield Assessment

Battlefield Assessment, Fig. 2 (continued)

Battlefield Assessment 509

Battlefield Assessment, Fig. 2 (continued)

510 Battlefield Assessment

Battlefield Assessment, Fig. 2 (continued)

Battlefield Assessment 511

Battlefield Assessment, Fig. 2 (continued)

512 Battlefield Assessment

Battlefield Assessment, Fig. 2 (continued)

Battlefield Assessment 513

Battlefield Assessment, Fig. 2 (continued)

514 Battlefield Assessment

Battlefield Assessment, Fig. 2 (continued)

Battlefield Assessment 515

Battlefield Assessment, Fig. 2 DVBIC military-acute-concussion-evaluation pocket-card

516 Battlefield Assessment

When the concussed service member is no consideration mission goals and iatrogenic effects
longer reporting symptoms, physical exertion of imposed rest:
testing is recommended. Exertional testing is Unit cohesion is an important component of mili-
typically conducted by having the service mem- tary life, lengthy separations can reduce expecta-
ber exert 65–85% of their target heart rate by tions of return to duty, and service members may
engaging in aerobic activities (i.e., treadmill become less likely to recover and return to full duty.
Keeping people out of action or evacuating them so
running, push-ups, or stationary biking), which they can recover must be balanced with the negative
is theorized to increase intracranial pressure and expectations about not returning to duty that may
activate dormant symptoms (Barth et al. 2010). arise when they are removed from their units. (Barth
Immediately after exertion (after approximately et al. 2010, pp. 135)
2 min), the medical provider assesses for the
presence of any symptoms (i.e., headache, diz- Historical Background
ziness, vision changes, vertigo, etc.). If symp-
toms are present, then continued rest and The assessment of mTBI can be challenging to
observation is recommended, while those who diagnose as symptoms can vary from person to
remain asymptomatic may be considered person and may not seem sufficiently “bad
for RTD. enough” for a service member or their command
Service members exhibiting symptoms of to discern that an injury has occurred. The Army
concussion for extended periods of time post- Research Laboratory’s report on the use of the
injury may require referral to a higher-level facil- ANAM for TBI assessment highlighted the
ity, where neuropsychological assessment in importance of assessment:
conjunction with a clinical examination and
input from various disciplines (e.g., physical Some service members who are determined to
and occupational therapies) is strongly encour- accomplish their mission and feel a strong desire
to remain in-country and support their unit, may
aged to determine return-to-duty (RTD) recom- mask their symptoms (e.g., cognitive deficiency,
mendations. After treatment in theater and/or via chronic daily headaches) by simply not seeking
combat support hospital, the wounded service care. The motivation not to leave one’s fellow ser-
member requiring greater intensity of care is vice members behind is strong, even when an indi-
vidual has been injured, and perhaps even more so
transported to Landstuhl Regional Medical Cen- when the injured service member is uncertain
ter (LRMC) in Germany, and then later to Walter whether their injury is real or an imagined set of
Reed National Military Medical Center symptoms related to stress. Undiagnosed mTBI can
(WRNMMC) in Washington, D.C. From there, endanger not only the individual, but also the entire
unit. A soldier’s cognitive as well as physical and
service members are assessed, treated, and emotional deficits may not be evident until a mis-
transferred to other military and Veterans take is made that could put both the service member
Administration (VA) facilities as needed and his or her team in jeopardy. (Rice et al. 2011,
(French et al. 2012). pp. 1)

Return to Duty In 2006, the Defense and Veterans Brain Injury

While recovering from TBI, service members Center and Brain Trauma Foundation in collabo-
should not return to duty or engage in other activ- ration with academic experts developed Guide-
ities that place them at risk for concussion (i.e., lines for the Field Management of Combat-
sports, combatives, etc.). Military leaders are Related Head Trauma. This guideline included
instructed to consult with medical personnel for the development of the Military Acute Concus-
RTD recommendations. sion Evaluation (MACE) tool (French et al. 2008)
While service members may need to be and a decision tree for determining additional
removed from combat to ensure safety of the evaluation and treatment.
individual as well as of others, Barth et al. In 2007, mandatory concussion screening
(2010) caution that clinicians must also take into protocols (i.e., MACE) were implemented
Battlefield Assessment 517

throughout the DoD. Consequently, this led to mild TBI and return-to-duty evaluations. In C. H.
abrupt increases in the reporting of TBI in the Kennedy & J. Moore (Eds.), Military neuropsychology
(pp. 127–174). New York: Springer.
deployed setting as well as across military instal- Bryan, C., & Hernandez, A. M. (2012). Magnitudes of
lations, both before and after deployment decline on automated neuropsychological assessment
(Helmick et al. 2015). Research has also consis- metrics subtest scores relative to predeployment base- B
tently shown the majority of TBI occurs in non- line performance among service members evaluated for
traumatic brain injury in Iraq. The Journal of Head
deployed settings secondary to military training Trauma Rehabilitation, 27(1), 45–54. https://doi.org/
accidents, auto accident (private and military 10.1097/HTR.0b013e318238f146.
vehicles), falls, sports, and recreational activities. Defense and Veterans Brain Injury Center. In DoD world-
However, many of those injuries diagnosed post- wide numbers for TBI. Retrieved from http://Dvbic.
Dcoe.Mil/Dod-Worldwide-Numbers-TBi
deployment have been found to be deployment- Defense and Veterans Brain Injury Center. (2012,
related events that were diagnosed weeks or November). Policy guidance for management of mild
months after return from deployment (Scholten traumatic brain injury/concussion in the deployed setting
et al. 2012). Prior to DoD instruction on concus- (line leader fact sheet). Retrieved from http://dvbic.Dcoe.
Mil/files/line-leader-fact-sheet-2012_V3_Final.Pdf
sion management in the deployed setting, the Defense Centers of Excellence (DCoE) for Psychological
identification of concussion was somewhat chal- Health and Traumatic Brain Injury. (2011, May). Indica-
lenging as the military culture traditionally dis- tions and conditions for in-theater post-injury
couraged admitting to being injured, so that the neurocognitive assessment tool (NCAT) testing (DCoE
clinical recommendation). Retrieved from http://dvbic.
service member could “get back to the fight.” Dcoe.Mil/files/resources/DCoE_clinical_Recommen
In 2010, the DoD responded to this trend by dations_post_injury_NCAT_05-31-2011_f.Pdf
implementing an incident-based system of Department of Defense. (2008). National defense authori-
reporting (DoDi 6490.11) in which command zation act for fiscal year 2008 (HR 4986, section 1673).
Retrieved from https://www.Congress.Gov/Bill/110th-
leaders were required to remove service members congress/house-bill/4986
from combat and report all service members who Department of Defense. (2012, September). DoD policy
had been exposed to a potentially concussive event guidance for management of mild traumatic brain
(DoD 2012). This policy, as described in the injury/concussion in the deployed setting (DoDi
6490.11). Retrieved from http://www.Dtic.Mil/whs/
description in the above section, has reportedly directives/corres/pdf/649011p.Pdf
increased awareness of mTBI and consequently Eckner, J. T., Kutcher, J. S., Broglio, S. P., & Richardson,
decreased the stigma, which will optimistically J. K. (2014). Effect of sport-related concussion on
mitigate any potential long-term effects of second- clinically measured simple reaction time. British Jour-
nal of Sports Medicine, 48(2), 112–118. https://doi.org/
ary to mTBI (Helmick et al. 2015). 10.1136/bjsports-2012-091579.
French, L., McCrea, M., & Baggett, M. (2008). The mili-
tary acute concussion evaluation (MACE). Journal of
Special Operations Medicine, 8(1), 68–77.
See Also French, L. M., Anderson-Barnes, V., Ryan, L. M.,
Zazeckis, T. M., & Harvey, S. (2012). Neuropsycho-
▶ Automated Neuropsychological Assessment logical practice in the military. In C. H. Kennedy &
E. A. Zillmer (Eds.), Military psychology: Clinical and
Metrics (ANAM) operational applications (2nd ed., pp. 185–210).
▶ Blast Effects New York: Guilford Press.
▶ Concussion Helmick, K. M., Spells, C. A., Malik, S. Z., Davies, C. A.,
▶ Defense and Veterans Brain Injury Center Marion, D. W., & Hinds, S. R. (2015). Traumatic brain
injury in the US military: Epidemiology and key clin-
▶ Mild Traumatic Brain Injury ical and research programs. Brain Imaging and
▶ Military Acute Concussion Evaluation Behavior, 9, 358–366. https://doi.org/10.1007/
s11682-015-9399-z.
Joint Mental Health Advisory Team 7 (J-MHAT 7). (2011).
Report of the advisory team on Operation Enduring
References and Readings Freedom 2010 Afghanistan. Retrieved from http://
armymedicine.Mil/documents/J_MHAT_7.pdf
Barth, J., Isler, W., Helmick, K., Wingler, I., & Jaffee, M. Kelly, M. P., Coldren, R. L., Parish, R. V., Dretsch, M. N.,
(2010). Acute battlefield assessment of concussion/ & Russell, M. L. (2012). Assessment of acute
518 Baxter v. Temple (2005)

concussion in the combat environment. Archives of injury or mental defect was Jenkins v. United
Clinical Neuropsychology, 27(4), 375–388. https:// States (1962). This was a criminal trial in which
doi.org/10.1093/arclin/acs036.
Martin, E. M., Lu, W. C., Helmick, K., French, L., & the jury was instructed to disregard the testimony
Warden, D. (2008). Traumatic brain injuries sustained of the psychologists on the grounds that they
in the Afghanistan and Iraq wars. American Journal of could not give a medical opinion as to mental
Nursing, 108(4), 40–47. https://doi.org/10.1097/01. disease or defect because they did not have med-
NAJ.0000315260.92070.3f.
Mittenberg, W., & Strauman, S. (2000). Diagnosis of mild ical training. The appellate court reversed the
head injury and the postconcussion syndrome. The decision holding that the expert did not need to be
Journal of Head Trauma Rehabilitation, 15(2), a medical practitioner. A later opinion, in United
783–791. Retrieved from http://journals.Lww.Com/ States v. Riggleman (1969) supported the position
headtraumarehab/abstract/2000/04000/Diagnosis_of_
mild_Head_injury_and_the.3.Aspx. that psychologists were not excluded from testify-
Norris, J. N., Carr, W., Herzig, T., Labrie, D. W., & Sams, ing about criminal sanity solely because they
R. (2013). ANAM4 TBI reaction time-based tests have lacked medical training. Simmons v. Mullins
prognostic utility for acute concussion. Military Medi- (1975) was an early appellate court decision that
cine, 178(7), 767–774. https://doi.org/10.7205/
MILMED-D-12-00493. essentially reversed a trial court opinion that neu-
Rice, V. J., Lindsay, G., Overby, C., Jeter, A., Alfred, P. E., ropsychologists were not competent to offer expert
Boykin, G. L., & Bateman. R. (2011, July). Automated testimony on brain malfunctions from motor vehi-
neuropsychological assessment metrics (ANAM) trau- cle accidents. The appellate court held that to
matic brain injury (TBI): Human factors assessment
(Army Research lab report ARL-TN-0440). Retrieved exclude such testimony on physical matters by
from http://www.Dtic.Mil/Cgi-bin/GetTRDoc?AD= psychologists would be to ignore present medical
ADA549141 and psychological practice. Most states allow neu-
Scholten, J. D., Sayer, N. A., Vanderploeg, R. D., ropsychological testimony about brain damage
Bidelspach, D. E., & Cifu, D. X. (2012). Analysis of
US veterans health administration comprehensive eval- (Richardson and Adams 1992) while there is a
uations for traumatic brain injury in operation enduring greater diversity of opinion as to testimony about
freedom and operation Iraqi freedom veterans. Brain causation.
Injury, 26(10), 1177–1184. https://doi.org/10.3109/
02699052.2012.661914.

Current Knowledge

In Baxter v. Temple (2005), defense filed a motion

Baxter v. Temple (2005) in limine to exclude the testimony of a neuropsy-
chologist in a case of lead exposure as insuffi-
Robert L. Heilbronner ciently unreliable because opinions were based
Chicago Neuropsychology Group, Chicago, on results from a flexible neuropsychological test
IL, USA battery. The defense argued successfully that
the neuropsychologist’s testimony should be
excluded because the Boston approach had not
Synonyms been subject to peer review and publication, has
no known or potential error rate, and is not gen-
Admissibility of psychological/neuropsychologi- erally accepted in the appropriate scientific litera-
cal evidence ture. In other words, Daubert factors were used by
the trial judge to exclude expert neuropsycholog-
ical evidence. Furthermore, the court made an
Historical Background important distinction between the roles of a clin-
ical provider and forensic examiner, emphasizing
One of the first decisions to address the admissi- that neuropsychologists in forensic practice must
bility of expert testimony by a psychologist or employ objective methods that allow them to be
neuropsychologist as to the existence of a brain unbiased truth seekers. The defendant motion in
Bayley Scales of Infant and Toddler Development 519

limine was granted. Some (Reed 1996) have

argued that Daubert challenges of idiosyncratic Bayley Scales of Infant and
(flexible) test combinations will eliminate the Toddler Development
use of flexible neuropsychological batteries in
forensic consulting. However, recent surveys of Glen P. Aylward B
neuropsychologists show that the majority of neu- SIU School of Medicine- Developmental-
ropsychologist practitioners use a carefully Behavioral Pediatrics, Springfield, IL, USA
constructed battery approach specifically tailored
to the patient/examinee’s specific issues. In 2008,
the New Hampshire Supreme Court reviewed the Synonyms
neuropsychological literature and practices of
neuropsychologists, considered relevant Daubert Bayley; BSID-III
standards and various amicus briefs, and con-
cluded that the exclusion of the neuropsycholog-
ical testimony in Baxter v. Temple (2005) was in Description
error.
The Bayley Scales of Infant and Toddler Devel-
opment-Third Edition (BSID-III; 2006) is consid-
ered to be the reference standard for
Cross-References
developmental assessment. It is an individually
administered test, applicable from 1 to 42 months
▶ Admissibility
of age. The primary purpose of the BSID-III is to
▶ Daubert v. Merrell Dow Pharmaceuticals (1993)
identify children with developmental delay and to
▶ Expert v. Treater Role
provide information for interventions.
▶ Federal Rules of Evidence
The BSID-III was normed on 1700 children
▶ Kumho Tire v. Carmichael
(divided into 17 age groups) and development is
assessed across five domains: Cognitive (91
items), Language (49 receptive and 48 expres-
References and Readings
sive), Motor (66 fine motor and 72 gross motor),
Chapple v. Ganger, 851 F. Suppl. 1481 (E. D. Wash, Social-Emotional, and Adaptive. Like its prede-
1994). cessors, the BSID-III is a modified power test.
Greiffenstein, M. F. (2009). Basics of forensic neuropsy- Assessment of the first three domains is accom-
chology. In J. Morgan & J. Ricker (Eds.), Textbook of plished by item administration, while the latter
clinical neuropsychology. New York: Taylor &
Francis. two are completed using caregiver response to a
Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychol- questionnaire. A Behavior Observation Inventory
ogy and the law: Principles of productive attorney- can be completed by both the examiner and the
neuropsychologists relations. In G. Larrabee (Ed.), caregiver and allows assessment of the child’s
Forensic neuropsychology: A scientific approach.
New York: Oxford University Press. behavior during testing and at home. The Lan-
Jenkins v. United States (1962). 307 F. 2d 637. guage scale includes Receptive Communication
Kaufmann, P. M. (2008). Admissibility of neuropsycho- and Expressive Communication subtests; the
logical evidence in criminal cases: Competency, insan- Motor scale includes a Fine Motor and a Gross
ity, culpability, and mitigation. In R. Denney &
J. Sullivan (Eds.), Clinical neuropsychology in the Motor subtest. The BSID-III Social-Emotional
criminal forensic setting. New York: Guilford Press. scale is an adaptation of the Greenspan Social-
Richardson, R. E. L., & Adams, R. L. (1992). Neuropsy- Emotional Growth Chart: A Screening Question-
chologists as expert witnesses: Issues of admissibility. naire for Infants and Young Children (Greenspan
The Clinical Neuropsychologist, 6, 295–308.
Simmons v. Mullins (Pa. Super Ct. 1975). 331 A2D 2004). The first eight items yield a Sensory Pro-
892, 897. cessing Score. The Adaptive Behavior scale is
United States v. Riggleman (4th Cir. 1969). 411 F.2d 1190. composed of items from the Parent/Primary
520 Bayley Scales of Infant and Toddler Development

Caregiver Form of the Adaptive Behavior Assess- child was not automatically given credit for pass-
ment System-Second Edition (Harrison and Oak- ing the lower item set. The BSID-II was also
land 2003). This scale measures areas such as criticized because it did not provide area scores
communication, community use, health and compatible with IDEA Part C requirements for
safety, leisure, self-care, self-direction, functional estimates of cognitive, motor, communication,
pre-academics, home living, social and motor, and social, and adaptive function.
yields a General Adaptive Composite (GAC).
Discrepancies between scaled scores can be
reviewed to determine whether the differences Psychometric Data
between subtests are statistically significant.
On the BSID-III, norm-referenced scaled scores
(M = 10, SD = 3), composite scores (M = 100,
Historical Background SD = 15), percentile ranks, and growth scores are
provided, in addition to confidence intervals for the
The original BSID (Bayley 1969) evolved from scales and developmental age equivalents. Com-
versions of developmental tests such as the Cali- posite scores range from 55 to 155, depending on
fornia Scales that were administered to infants the scale. Internal consistency of the subtests range
enrolled in the landmark National Collaborative from 0.86 to 0.93; the intercorrelation between
Perinatal Project. It was considered the reference Cognitive and Language composites is 0.52, for
standard for the assessment of infant develop- Cognitive and Motor composites, 0.50, and the
ment, administered to infants over the first intercorrelation between Language and Motor
2½ years. The BSID was theoretically eclectic composites is 0.49. Growth scores are provided
and borrowed from different research and test and are used to longitudinally plot the child’s
instruments. The test contained three components: growth over time for each subscale. This metric
the Mental Developmental Index (MDI), the Psy- is calculated based on the subtest total raw score
chomotor Developmental Index (PDI) (M = 100, and ranges from 200 to 800 (M = 500, SD = 100).
SD = 16) and the Infant Behavior Record, and Similar to the original BSID, there are basal rules
was applicable from 2 to 30 months. (passing the first three items at the appropriate age
The BSID subsequently was revised into start-point) and ceiling or discontinue rules (a
the BSID-II (Bayley 1993), this due in part to score of 0 for five consecutive items).
the upward drift of approximately 11 points on The correlation between the BSID-III Lan-
the MDI and 10 points on the PDI, reflecting the guage Composite and the previous BSID-II MDI
Flynn effect. Although the mean remained the is 0.71, the Motor Composite and the BSID-II
same (100), the SD was now 15. When compared PDI = 0.60, and the Cognitive Composite and
to the original BSID, the BSID-II MDI scores the BSID-II MDI = 0.60. However, in contrast
were 12 points lower and the PDI was10 points to the expected Flynn effect, the Bayley-III Men-
lower. The Behavior Rating Scale was developed tal and Motor composite scores, on average, are
to enable the assessment of state, reactions to the approximately seven points higher than the
environment, motivation, and interaction with corresponding BSID-II MDI and PDI. This phe-
people. The age range of the BSID-II was nomenon has also been reported with other devel-
expanded to span 1–42 months. The instrument opmental tests and has been termed the “reverse
contained 22 item sets and basal and ceiling rules Flynn effect.”
that differed from the original BSID. These rules The increase in scores may be due to inclusion
were controversial because if correction for pre- of infants at risk for developmental delay in the
maturity was used to determine the item set to standardization sample (10%). These “mixed
begin administration, or if an earlier item set was norms” inflate scores and decrease diagnostic
employed because of developmental problems, accuracy. In addition, there are concerns regarding
scores tended to be somewhat lower, because the a weak test floor. However, despite at-risk infants
Beck Anxiety Inventory 521

receiving “normal” scores, these still are below Greenspan, S. I. (2004). Greenspan social-emotional
comparison group scores, which typically are growth chart. A screening questionnaire for infants
and young children. San Antonio: Harcourt Assessment.
higher than the standardization mean (as seen in Harrison, P. L., & Oakland, T. (2003). Adaptive behavior
comparison of preterm infants and term controls). assessment system (2nd ed.). San Antonio: The Psy-
This conundrum becomes further complicated by chological Corporation. B
the possibility that the Bayley-II was too conser- Weiss, L. G., Oakland, T., & Aylward, G. P. (Eds.). (2010).
Bayley III: Clinical use and interpretation. Boston:
vative and underestimated development. Elsevier.

Clinical Uses
Beck Anxiety Inventory
Administration of the BSID-III yields quantitative
and qualitative data that provide insight into the Amy J. Starosta1 and Lisa A. Brenner2,3
child’s current levels of development. Repeated 1
Departments of Psychiatry and Physical
administration can document the effects of an Medicine and Rehabilitation, University of
intervention program. However, changes in test Colorado Denver, Aurora, CO, USA
content and alteration of scales in conjunction 2
Rocky Mountain Mental Illness Research
with the Flynn effect and the more recent increase Education and Clinical Center, Denver, CO, USA
in mean scores (in comparison to the previous 3
University of Colorado, Anschutz Medical
version) make longitudinal comparisons of scores Campus, Aurora, CO, USA
difficult in individual children or cohorts. There
also are concerns that the Bayley-III under-iden-
tifies children who could qualify for intervention Description
services. Extracting language items from the cog-
nitive scale also affects comparability with the The Beck Anxiety Inventory (BAI) (Beck et al.
MDI found in previous versions. Conversely, the 1988; Beck and Steer 1993) is a 21-item inventory
five domains now allow the BSID-III to be more which identifies anxiety symptoms and quantifies
compatible with early intervention requirements their intensity. Respondents are asked to rate how
(IDEA; PL 108–446, Part C). A criticism of the much they have been bothered by each item over
test is that it can take an exceptionally long time to the past week, including today, on a four-point
administer (e.g., >90 min at 13 months) and this is scale ranging from 0 (“not at all”) to 3 (“severely
problematic when testing infants and toddlers. – I could barely stand it”). Items are summed,
The BSID-III can be used in multidisciplinary resulting in a total score ranging from 0 to 63,
clinics, NICU follow-up programs, or as a fol- with higher scores representing greater levels of
low-up evaluation after a child has been identified anxiousness (Table 1).
by the use of a screening test. This assessment generally takes adults
5–10 min to complete. It can be self-report or
interviewer administered. Traditionally, this
References and Readings assessment is administered in a paper-and-pencil
or interview formats, but it is also increasingly
Aylward, G. P. (2013). Continuing issues with the Bayley-
III: Where to go from here. Journal of Developmental given via the computer.
and Behavioral Pediatrics, 9, 697–701.
Bayley, N. (1969). The Bayley scales of infant develop-
ment. San Antonio: The Psychological Corporation. Beck Anxiety Inventory, Table 1 Anxiety categoriza-
Bayley, N. (1993). The Bayley scales of infant development tion by score (Beck and Steer 1993)
(2nd ed.). San Antonio: The Psychological Corporation. Anxiety
Bayley, N. (2006). Bayley scales of infant and toddler level Minimal Mild Moderate Severe
development (3rd ed.). San Antonio: The Psychological
Corporation. BAI score 0–7 8–15 16–25 26–63
522 Beck Anxiety Inventory

Historical Background other types of psychopathology in both clinical

and nonclinical samples (Steer 2009). Discrimi-
The BAI was designed to assess anxiety symp- nant validity with depression symptoms is more
toms independent of depressive symptoms. variable based on populations, with lower dis-
Authors compiled a pool of 86 items from three criminant validity among older adults (Morin et
preexisting anxiety symptom checklists (the Anx- al. 1999; Wetherell and Gatz 2005) and non-
iety Checklist (Beck et al. 1985), the Physician’s clinical Spanish speakers (Magán et al. 2008).
Desk Reference Checklist (Beck 1978), and the Scores on the BAI are linearly related to depres-
Situational Anxiety Checklist (Beck 1982)). They sion scales; however, individual items from these
eliminated repetitive items, conducted successive assessments have a strong tendency to load onto
iterative principal factor analyses, and completed different factors (Beck et al. 1988).
a series of validity analyses to whittle the item list Among clinical populations, factor analytic
down to 21. This final 21-item BAI was found to studies generally support a two-factor structure,
have high internal consistency. It also demon- with one factor representing cognitive symptoms
strated both convergent validity with non-symp- of anxiety and the other representing somatic
tom constructs theoretically associated with symptoms (Wilson et al. 1999). Among non-
anxiety and discriminant validity with those clinical populations, the factor structure is more
constructs associated with depression among a varied, with evidence to support four (subjective,
psychiatric outpatient population. neurophysiological, autonomic, and panic
(Osman et al. 1993)), five (subjective fear, somatic
nervousness, neurophysiological, muscular/
Psychometric Data motoric, respiration (Borden et al. 1991)), and
six (somatic, fear, autonomic hyperactivity,
In the years since its original publication, the BAI panic, nervousness, and motor tension (Morin
has consistently shown good reliability in a vari- et al. 1999)) factor models. The broad categories
ety of both clinical and nonclinical populations. A of subjective and physiological symptoms still
meta-analysis by de Ayala et al. (2005) found the apply, but findings suggest that at nonclinical
average coefficient alpha to be 0.91. Test-retest levels of anxiety, respondents may experience
values showed significantly more heterogeneity, more nuanced physiological symptoms of anxi-
ranging from 0.35 to 0.83, with the greatest vari- ety. Given the lack of consensus in the literature
ability among nonpsychiatric noncollege regarding factor structure, the use of the total
populations. Given increasing use of computer- score remains the recommended approach for
based assessment administration, it is critical to measuring anxiety symptoms with this scale
consider the impact of the mode of administration (Steer 2009).
on the psychometrics of questionnaires. Prelimi-
nary studies evaluating effect of administration
mode found comparable internal consistencies Clinical Uses
but lower mean scores when the BAI was admin-
istered via the internet compared to paper-and- Overall, the BAI’s strongest qualities are its abil-
pencil versions (Carlbring et al. 2007). This sug- ity to assess panic symptomology and distinguish
gests that it may be necessary to use “internet between panic disorder and non-panic disorder
norms” when administering the BAI in a com- symptom profiles (Leyfer et al. 2006). It is sensi-
puter format. tive to changes in anxiety symptoms both in psy-
The BAI shows strong convergent validity chiatric (Brown et al. 1997) and medical
with anxiety symptom self-report instruments, populations (Lee et al. 2010). Because of its brev-
clinical ratings, and diaries. It has also shown ity and ease of administration, the BAI is com-
moderate discriminant validity with measures of monly used as an anxiety screening instrument.
Beck Anxiety Inventory 523

However, the BAI is not a diagnostic measure, Hewitt and Norton 1993; Osman et al. 1993;
and research suggests it has limited utility when Morin et al. 1999; Vázquez-Morejón et al.
used in isolation as a measure of anxiety (Manne 2014). This gender difference remains even after
et al. 2001; Hoyer et al. 2002). differential item analysis identified and removed
In addition to its use with general clinical potentially biased items (Magán et al. 2008). B
populations, the BAI has demonstrated utility in These findings are consistent with lifetime preva-
neuropsychological populations as well. The BAI lence data, which suggests that women have
has been used in clinical trials of psychotropic higher rates of anxiety (Kessler et al. 2005).
interventions for depression following traumatic While the BAI is one of the most widely used
brain injury (TBI) (Ashman et al. 2009) and as a tool for measuring anxiety symptomology, there
measure of anxiety following TBI (Zhou et al. is little research regarding its use in ethnic minor-
2013; Cantor et al. 2005). The BAI has been ity populations. An initial study examining the
used to assess anxiety among Veterans with a factor structure of the BAI for African Americans
history of TBI and was found to be associated (Chapman et al. 2009) found that the originally
with increased neuropsychiatric symptoms (King proposed two factor structure did not hold for an
et al. 2012). It has also been used to assess anxiety African American nonclinical sample. Rather,
poststroke (Baker-Collo 2007). they proposed an alternative two factor model
While the BAI has been used often with med- with more items loading onto the somatic factor.
ical and neuropsychiatric populations, research Examination of the psychometric properties of
suggests that there may be some overlap with the BAI in Latino populations (Contreras et al.
somatic symptoms, which would be potentially 2004) supported the original factor structure and
problematic in a medical setting. As the BAI was found that the BAI had strong internal reliability.
developed to assess anxiety independent of Of note, nonclinical Latino participants’ average
depression, it excludes many anxiety symptoms scores were within normal ranges but signifi-
which overlap with depression. It has been criti- cantly higher than Caucasian American
cized for placing too heavy emphasis on somatic populations.
symptoms of anxiety, which may be more charac- The BAI has been translated and validated in
teristic of panic as opposed to the overall construct several other languages, including Spanish
of anxiety. Of the 21 items, 14 assess somatic (Fernández and Navarro 2003), French (Freeston
symptoms, and patients with panic disorder have et al. 1994), Turkish (Ulusoy et al. 1998), Norwe-
been shown to score higher on the BAI (Leyfer et gian (Nordhagen 2001), and Icelandic
al. 2006). Because of its emphasis on somatic (Sæmundsson et al. 2015). While there are some
symptoms, the BAI has less utility in populations reported differences in factor structures, the over-
with greater medical illnesses (such as older adults all findings suggest comparable psychometric
Wetherell and Gatz 2005). These populations properties to the English version of the BAI. Find-
endorse more physical complaints, which results ings from studies examining the utility of the BAI
in inflated scores on the BAI. Providers should use in the international community have varied, with
caution when using the BAI as a broad anxiety some finding comparable normative values and
screening tool, particularly with populations with others showing significant variability between
increased medical complications. cultures (Pillay et al. 2001; Hoge et al. 2006).
The BAI has demonstrated some cross-cultural
utility, but it should continue to be used with
Diversity Considerations caution in diverse settings.

Internal reliability is comparable between the gen- See Also

ders; however, women consistently score higher
on the BAI than men (Beck and Steer 1993; ▶ Anxiety
524 Beck Anxiety Inventory

References Fernández, J. S., & Navarro, M. E. (2003). Propiedades

psicométricas de una versión española del Inventario de
Ashman, T. A., Cantor, J. B., Gordon, W. A., Spielman, Ansiedad de Beck (BAI) en estudiantes universitarios.
L., Flanagan, S., Ginsberg, A., Engmann, C., Egan, Ansiedad y Estrés, 9(1), 59–84.
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depression in persons with traumatic brain injury. psychométriques d’une traduction française.
Archives of Physical Medicine and Rehabilitation, L’Encéphale: Revue de psychiatrie clinique biologique
90(5), 733–740. et thérapeutique.
Barker-Collo, S. L. (2007). Depression and anxiety 3 Hewitt, P. L., & Norton, G. R. (1993). The Beck anxiety
months post stroke: Prevalence and correlates. Archives inventory: A psychometric analysis. Psychological
of Clinical Neuropsychology, 22(4), 519–531. Assessment, 5(4), 408.
Beck, A. T. (1978). PDR checklist. Philadelphia: Univer- Hoge, E. A., Tamrakar, S. M., Christian, K. M., Mahara,
sity of Pennsylvania, Center for Cognitive Therapy. N., Nepal, M. K., Pollack, M. H., & Simon, N. M.
Beck, A. T. (1982). Situational anxiety checklist (SAC). (2006). Cross-cultural differences in somatic presenta-
Philadelphia: University of Pennsylvania, Center for tion in patients with generalized anxiety disorder. The
Cognitive Therapy. Journal of Nervous and Mental Disease, 194(12),
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Beck, A. T., Steer, R. A., & Brown, G. (1985). Beck anxiety Margraf, J. (2002). Screening for anxiety in an epide-
checklist. Unpublished manuscript, University of miological sample: Predictive accuracy of question-
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Beck, A. T., Epstein, N., Brown, G., & Steer, R. A. (1988). Kessler, R. C., Berglund, P., Demler, O., Jin, R.,
An inventory for measuring clinical anxiety: Psycho- Merikangas, K. R., & Walters, E. E. (2005). Life-
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Psychology, 56(6), 893. DSM-IV disorders in the National Comorbidity Sur-
Borden, J. W., Peterson, D. R., & Jackson, E. A. (1991). vey Replication. Archives of General Psychiatry, 62
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Initial psychometric properties. Journal of Psychopa- King, P. R., Donnelly, K. T., Donnelly, J. P., Dunnam, M.,
thology and Behavioral Assessment, 13(4), 345–356. Warner, G., Kittleson, C. J., Bradshaw, C. B., Alt, M.,
Brown, G. K., Beck, A. T., Newman, C. F., Beck, J. S., & & Meier, S. T. (2012). Psychometric study of the
Tran, G. Q. (1997). A comparison of focused and neurobehavioral symptom inventory. Journal of Reha-
standard cognitive therapy for panic disorder. Journal bilitation Research and Development, 49(6), 879.
of Anxiety Disorders, 11(3), 329–345. Lee, Y. W., Park, E. J., Kwon, I. H., Kim, K. H., & Kim, K.
Cantor, J. B., Ashman, T. A., Schwartz, M. E., Gordon, W. A., J. (2010). Impact of psoriasis on quality of life: Rela-
Hibbard, M. R., Brown, M., Spielman, L., Charatz, H. J., tionship between clinical response to therapy and
& Cheng, Z. (2005). The role of self-discrepancy the- change in health-related quality of life. Annals of Der-
ory in understanding post-traumatic brain injury affec- matology, 22(4), 389–396.
tive disorders: A pilot study. The Journal of Head Leyfer, O. T., Ruberg, J. L., & Woodruff-Borden, J. (2006).
Trauma Rehabilitation, 20(6), 527–543. Examination of the utility of the Beck anxiety inventory
Carlbring, P., Brunt, S., Bohman, S., Austin, D., Richards, and its factors as a screener for anxiety disorders. Jour-
J., Öst, L. G., & Andersson, G. (2007). Internet vs. nal of Anxiety Disorders, 20(4), 444–458.
paper and pencil administration of questionnaires com- Magán, I., Sanz, J., & García-Vera, M. P. (2008).
monly used in panic/agoraphobia research. Computers Psychometric properties of a Spanish version of
in Human Behavior, 23(3), 1421–1434. the Beck Anxiety Inventory (BAI) in general pop-
Chapman, L. K., Williams, S. R., Mast, B. T., & Woodruff- ulation. The Spanish Journal of Psychology, 11(02),
Borden, J. (2009). A confirmatory factor analysis of the 626–640.
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pean American young adults. Journal of Anxiety Dis- Martini, R., Williams, S., Mee, L., Sexson, S., Lewis, J.,
orders, 23(3), 387–392. Vickberg, S. J., & Redd, W. H. (2001). Anxiety and
Contreras, S., Fernandez, S., Malcarne, V. L., Ingram, depression in mothers of children undergoing bone
R. E., & Vaccarino, V. R. (2004). Reliability and valid- marrow transplant: Symptom prevalence and use of
ity of the Beck depression and anxiety inventories in the Beck Depression and Beck anxiety inventories as
Caucasian Americans and Latinos. Hispanic Journal of screening instruments. Journal of Consulting and Clin-
Behavioral Sciences, 26(4), 446–462. ical Psychology, 69(6), 1037.
de Ayala, R. J., Vonderharr-Carlson, D. J., & Kim, D. Morin, C. M., Landreville, P., Colecchi, C., McDonald, K.,
(2005). Assessing the reliability of the Beck anxiety Stone, J., & Ling, W. (1999). The Beck anxiety inven-
inventory scores. Educational and Psychological Mea- tory: Psychometric properties with older adults. Jour-
surement, 65(5), 742–756. nal of Clinical Geropsychology, 5(1), 19–29.
Beck Depression Inventory 525

Nordhagen, T. (2001). Beck anxiety inventory: Translation Description

and validation of a Norwegian version (Master’s thesis,
The University of Bergen).
Osman, A., Barrios, F. X., Aukes, D., Osman, J. R., & The Beck Depression Inventory (BDI; Beck et al.
Markway, K. (1993). The Beck anxiety inventory: Psy- 1961) is one of the most widely used self-report
chometric properties in a community population. Jour- measures to assess depressive symptom severity B
nal of Psychopathology and Behavioral Assessment, 15 in adolescents and adults. It was amended in 1979
(4), 287–297.
Pillay, A. L., Edwards, S. D., Sargent, C., & Dhlomo, R. M. to allow for simpler administration and scoring
(2001). Anxiety among university students in South (BDI-IA; Beck et al. 1979). In 1996, a more
Africa. Psychological Reports, 88(3c), 1182–1186. substantial revision was made so it would corre-
Sæmundsson, B. R., Þórsdóttir, F., Kristjánsdóttir, H., spond to the Diagnostic and Statistical Manual of
Ólason, D. Þ., Smári, J., & Sigurðsson, J. F. (2015).
Psychometric properties of the Icelandic version of the Mental Disorders – Fourth Edition (DSM-IV;
Beck anxiety inventory in a clinical and a student American Psychiatric Association 1994) criteria
population. European Journal of Psychological for clinical depression (BDI-II; Beck et al. 1996b).
Assessment, 27, 133–141. The BDI-II is a self-report measure comprised
Steer, R. A. (2009). Amount of general factor saturation in
the Beck anxiety inventory responses of outpatients of 21 items reflecting specific cognitive, affective,
with anxiety disorders. Journal of Psychopathology and physical symptoms of depression. Scores
and Behavioral Assessment, 31(2), 112–118. range from 0 to 3, with higher numbers indicating
Ulusoy, M., Sahin, N. H., & Erkmen, H. (1998). Turkish greater symptom severity. If more than one state-
version of the Beck anxiety inventory: Psychometric
properties. Journal of Cognitive Psychotherapy, 12(2), ment from a given item is chosen by the patient,
163–172. the statement of greatest severity is scored. The
Vázquez Morejón, A. J., Vázquez-Morejón Jiménez, R., & maximum total score is 63.
Zanin, G. B. (2014). Beck anxiety inventory: Psycho- The BDI-II takes approximately 5–10 min to
metric characteristics in a sample from the clinical
Spanish population. The Spanish Journal of Psychol- complete and can be administered to individuals
ogy, 17, E76. 13–80 years old. It is typically self-administered,
Wetherell, J. L., & Gatz, M. (2005). The Beck anxiety although if clinically indicated, the examiner may
inventory in older adults with generalized anxiety dis- read the items to the individual.
order. Journal of Psychopathology and Behavioral
Assessment, 27(1), 17–24.
Wilson, K. A., De Beurs, E., Palmer, C., & Chambless, D.
(1999). Beck anxiety inventory. The use of psycholog- Historical Background
ical testing for treatment planning and outcomes
assessment, 2, 971–992.
Zhou, Y., Kierans, A., Kenul, D., Ge, Y., Rath, J., Reaume, The original BDI (Beck et al. 1961) was devel-
J., Grossman, R. I., & Lui, Y. W. (2013). Mild traumatic oped with the use of descriptors provided by cli-
brain injury: Longitudinal regional brain volume nicians and patients with depression. These
changes. Radiology, 267(3), 880–890. descriptors were then consolidated into 21 items.
Directions for the assessment instructed the indi-
vidual to choose the descriptor that best described
how they felt at the moment. Originally, it was a
Beck Depression Inventory measure administered by the examiner reading the
statements to the examinee. Revisions on the
Joyce Suh and Jennifer Linton Reesman BDI-IA (1979) turned it into a self-report, pen-
Kennedy Krieger Institute/Johns Hopkins cil-and-paper measure, and made the instrument
University School of Medicine, Baltimore, easier to understand, such as by removing double
MD, USA negatives. In total, 15 of the original 21 items were
modified. Additionally, directions were revised to
instruct the individual to choose the descriptor
Synonyms that best described how they have felt in the past
week, including the current day. A criticism of the
BDI; BDI-II BDI-IA, however, was that it only addressed six
526 Beck Depression Inventory

out of the nine DSM-III criteria for depression Depression (HRSD; Hamilton 1960), and Hamil-
(e.g., Moran and Lambert 1983). Also, inconsis- ton Rating Scale for Anxiety (HAM-A; Hamilton
tent with DSM-III criteria for clinical depression, 1959). The BDI-II was more positively correlated
the BDI-IA did not address symptoms such as with the HRSD (r = 0.71) than the HAM-A
agitation and feelings of worthlessness, and it (r = 0.47).
only addressed decreases (not increases) in appe- Factor validity of the BDI-II was also assessed
tite and sleep. by Beck and colleagues (1996b), who found a
Therefore, the measure was again revised. The two-factor solution using their outpatient stan-
BDI-II reworded select statements and introduced dardization sample. Dozois et al. (1998)
items to assess agitation, worthlessness, concen- suggested that, overall, “somatic-affective” and
tration difficulties, and loss of energy. It also “cognitive” are the two factors that tend to emerge
included questions to reflect increases in sleep in clinical samples, whereas “cognitive-affective”
and appetite. Furthermore, items assessing body and “somatic” are the two factors that tend to
image, work difficulty, weight loss, and somatic emerge in nonclinical samples.
preoccupations were removed, and the directions Overall, the BDI-II has demonstrated good
were modified so that the individual was internal consistency, test-retest reliability, conver-
instructed to choose the descriptor that best gent and discriminant validity, and factor validity.
described how they have felt in the past 2 weeks.
These changes improved correspondence to
DSM-III-R (1987) and-DSM-IV (1994) criteria Clinical Uses
for clinical depression.
The purpose of the BDI-II is to measure depres-
sion symptom severity. It can be used as part of a
Psychometric Data diagnostic battery or as a repeated measure to
track treatment efficacy. Additionally, clinicians
Standardization data for the BDI-II was obtained are advised to be aware that a score of “2” or “3”
from 500 psychiatric outpatients and 120 under- on item 2 (pessimism) or 9 (suicidal thoughts or
graduates. Internal consistency was high for each wishes) is associated with greater risk for suicide
sample (a = 0.92 and 0.93, respectively). This is (Beck et al. 1996b). Overall, the manual desig-
consistent with later independent study samples, nates the following total raw score classifications
which have found alphas ranging from 0.86 to for depression severity: 0–13 = minimal,
0.93 when assessing nonclinical populations, 14–19 = mild, 20–28 = moderate, and
including high school-aged students (ages 29 = severe. However, the instrument’s devel-
14–18 years; Osman et al. 2008), undergraduates opers suggest that different cutoff scores may be
(ages 17–39 years; Storch et al. 2004), and older required depending on the characteristics of the
adults (ages 59–90 years; Segal et al. 2008), as sample and the purpose for using the instrument
well as clinical samples, including adolescents (e.g., lower thresholds for greater sensitivity in
(ages 13–17 years; Osman et al. 2004) and adults identifying depression, greater thresholds for
(mean age = 37.6 years; Beck et al. 1996a). greater specificity, such as in research). Other
Test-retest reliability of the BDI-II was factors to consider when interpreting the BDI-II
assessed by Beck and colleagues (1996b), yield- include individual characteristics, such as ethnic
ing correlation coefficients of 0.92 in a sample of and cultural background, gender, age, and pres-
26 psychiatric outpatients, and 0.93 for their sam- ence of additional medical conditions.
ple of college students. Given the ethnic and cultural diversity of psy-
Convergent and discriminant validity of the chiatric and neurological patient populations,
BDI-II was demonstrated by Beck and colleagues there is a need for linguistically diverse and cul-
(1996b), who assessed 87 psychiatric outpatients turally sensitive psychiatric inventories. The BDI-
with the BDI-II, Hamilton Rating Scale for II has been translated into numerous languages
Beck Depression Inventory 527

including Arabic (e.g., Hamdi et al. 1988), Chi- more likely to score higher on sadness and self-
nese (e.g., Wu and Chang 2008), Dutch (e.g., criticalness, while men are more likely to endorse
Roelofs et al. 2013), Japanese (e.g., Kojima et al. past failure and loss of pleasure. However, studies
2002), Korean (e.g., Hong and Wong 2005), Por- with other populations have not found similar
tuguese (e.g., Gomes-Oliveira et al. 2012), Span- gender differences (e.g., chronic pain; Harris and B
ish (e.g., Gonzalez et al. 2015; Wiebe and Penley D’Eon 2008). Likewise, among US college stu-
2005), Turkish (e.g., Canel-Çınarbaş et al. 2011), dents, the BDI-II provided an assessment of the
and Xhosa (e.g., Edwards and Steele 2008). Some severity of depression symptoms that was equiv-
studies have suggested that BDI-II responding in alent across gender, race, and ethnicity (Whisman
different languages and cultures may have differ- et al. 2013). Consistent with this finding, in terms
ent psychometric properties. For example, studies of BDI-II reporting by patients of different ages,
have found that a three-factor model (instead of a studies have found it to also have strong psycho-
two-factor model) may emerge among some eth- metric support among geriatric patients (Segal
nic groups (e.g., Mexicans: Gonzalez et al. 2015) et al. 2008; Steer et al. 2000).
or more ethnically diverse groups (e.g., ethnically It is also important to consider the possible
diverse group of college students: Carmody 2005; differences in items endorsed among individuals
Whisman et al. 2013); other studies, however, with specific medical conditions. Physical
have confirmed the two-factor model (e.g., Chi- sequelae of certain conditions may mimic somatic
nese-heritage and European-heritage college stu- symptoms of depression, resulting in false classi-
dents in Canada: Dere et al. 2015; Japanese: fications of depressive symptomatology. Despite
Kojima et al. 2002). Nevertheless, overall, studies this possibility, overall, the BDI-II has been found
have shown that the psychometric properties of to be useful across medical populations, including
the BDI-II in other languages and cultures are individuals with chronic pain (Harris and D’Eon
often comparable to that of the English version. 2008), multiple sclerosis (Sacco et al. 2016), myo-
Clinicians utilizing a translated measure should be cardial infarction (Huffman et al. 2010), and trau-
aware of the different ways diverse groups may matic brain injury (Rowland et al. 2005). Some
describe and experience symptoms of depression. studies have suggested, however, that there may
For example, although Canel-Çınarbaş et al. be different optimal cutoff scores for different
(2011) found many of the psychometric properties populations (e.g., Huffman et al. (2010) found
of the Turkish version of the BDI-II to be compa- >=16 to be the optimal cutoff for patients with a
rable to its English counterpart, they noted that the history of myocardial infarction). Patterson et al.
Turkish word for depression connotes somatic (2011) found that, among patients with hepatitis
symptoms such as “bodily tightness”; consistent C, questions targeting cognitive and affective
with this, somatic symptoms were more likely be symptoms (rather than somatic symptoms) may
endorsed in this population. be a more valid measurement of depression.
Some studies have found gender differences in While the reading level requirement for the
reporting on the BDI-II. Beck and colleagues BDI-II is reported at a fifth to sixth grade level,
(1996b) found that, among their sample of 500 examination of the cognitive complexity of this
outpatients, there was a significant mean differ- measure may require more scrutiny with certain
ence among sexes, with women having higher clinical populations. The presence of multiple
overall scores than men (23.61 (SD = 12.31) for response options increases the complexity of this
females, 20.44 (SD = 13.28) for males). The same self-administered measure, which may impact its
pattern was found among their sample of 120 appropriateness for specific populations or settings
college students. Other studies have also found in which motivation to respond may be low, even
higher overall scores for women (e.g., Kojima et when the individual possesses the literacy skills
al. 2002; Roelofs et al. 2013). Additionally, necessary for response (Shumway et al. 2004).
Wagener et al. (2016) found that, in terms of The BDI-II was developed to correspond
specific symptom endorsements, women are with depressive disorder criteria set forth by the
528 Beck Depression Inventory

DSM-IV. The reliability and validity of the instru- inpatients with the Beck Depression Inventory for primary
ment have been established across several studies care. Behavior Research and Therapy, 35, 785–791.
Canel-Çınarbaş, D., Cui, Y., & Lauridsen, E. (2011).
including psychiatric and neurological patients as Cross-cultural validation of the Beck Depression
well as nonclinical community-dwelling individ- Inventory–II across U.S. and Turkish samples. Mea-
uals. This generally appears to extend to ethnic surement and Evaluation in Counseling and Develop-
and culturally diverse populations as well, ment, 44(2), 77–91.
Carmody, D. P. (2005). Psychometric characteristics of the
although research is ongoing. Of note, the BDI- Beck Depression Inventory-II with college students of
II is not intended to be used for the sole purpose of diverse ethnicity. International Journal of Psychiatry in
“specifying a clinical diagnosis,” but as an indi- Clinical Practice, 9(1), 22–28.
cator of the severity of depressive symptoms Dere, J., Watters, C. A., Yu, S. C., Bagby, R. M., Ryder, A.
G., & Harkness, K. L. (2015). Cross-cultural examina-
(Beck et al. 1996b). Therefore, it is important for tion of measurement invariance of the Beck Depression
clinicians to use clinical judgment, consider the Inventory–II. Psychological Assessment, 27(1), 68–81.
demographic characteristics and medical condi- Dozois, D. J. A., Dobson, K. S., & Ahnberg, J. L. (1998). A
tion of their patients, and consult current research psychometric evaluation of the Beck Depression
Inventory–II. Psychological Assessment, 10, 83–89.
when evaluating a patient for depression and Edwards, D. A., & Steele, G. I. (2008). Development and
interpreting BDI-II results. validation of the Xhosa translations of the Beck inven-
tories: 3. Concurrent and convergent validity. Journal
of Psychology in Africa, 18(2), 227–236.
Cross-References Gomes-Oliveira, M. H., Gorenstein, C., Neto, F. L.,
Andrade, L. H., & Wang, Y. P. (2012). Validation of
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▶ Center for Epidemiological Studies: Depression
sion Inventory-II in a community sample. Revista
▶ Geriatric Depression Scale Brasileira de Psiquiatria, 34(4), 389–394.
▶ Hamilton Depression Rating Scale González, D. A., Rodríguez, A. R., & Reyes-Lagunes, I.
▶ Self-Report Measures (2015). Adaptation of the BDI–II in Mexico. Salud
Mental, 38(4), 237–244.
▶ Zung Self-Rating Depression Scale
Hamdi, N., Abu-Hajlah, N., & Abu-Talib, S. (1988). The
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(2008). Psychometric properties of the Beck Depression designed to assess the integration of visual and
Inventory II (BDI-II) among community-dwelling older motor abilities. The current version includes two
adults. Behavior Modification, 32(1), 3–20. forms for the Beery VMI and two supplemental
Shumway, M., Sentell, T., Unick, G., & Bamberg, W. subsections, motor coordination and visual per-
(2004). Cognitive complexity of self-administered
depression measures. Journal of Affective Disorders, ception. The supplemental tests may be adminis-
83(2–3), 191–198. tered after results from the VMI test indicate the
Steer, R. A., Rissmiller, D. J., & Beck, A. T. (2000). Use of need for further assessment in order to separate an
Beck Depression Inventory-II with depressed geriatric individual’s pure motor and visual abilities. For
inpatients. Behaviour Research and Therapy, 38(3),
311–331. the VMI, examinees are administered either a
Storch, E. A., Roberti, J. W., & Roth, D. A. (2004). Factor 21-item short form or a 30-item long form; each
structure, concurrent validity, and internal consistency requires copying geometric forms that become
of the Beck Depression Inventory-Second Edition in a increasingly complex. The short form is designed
sample of college students. Depression and Anxiety, 19
(3), 187–189. for use with children aged 2–7 years, and the long
Wagener, A., Baeyens, C., & Blairy, S. (2016). Depressive form for individuals up to age 100. The long form
symptomatology and the influence of the behavioral takes approximately 10–15 min to administer, and
avoidance and activation: A gender-specific investiga- the short form takes approximately 10 min. The
tion. Journal of Affective Disorders, 193, 123–129.
Whisman, M. A., Judd, C. M., Whiteford, N. T., & test may also be administered to a group; however,
Gelhorn, H. L. (2013). Measurement invariance of the the authors recommend individual testing for
Beck Depression Inventory–Second Edition (BDI-II) children who have developmental delays or neu-
across gender, race, and ethnicity in college students. rological impairments. For children at or over the
Assessment, 20(4), 419–428.
Wiebe, J. S., & Penley, J. A. (2005). A psychometric compar- functional age of 5, administration begins with
ison of the Beck Depression Inventory-II in English and item 7. If the examinee is unable to complete
Spanish. Psychological Assessment, 17(4), 481–485. item 7 correctly, the manual provides instructions
Wu, P., & Chang, L. (2008). Psychometric properties of the for how to proceed. The examinees use a pen or
Chinese version of the Beck Depression Inventory-II
using the Rasch model. Measurement and Evaluation pencil to complete the geometric forms. One point
in Counseling and Development, 41(1), 13–31. is given for each correctly drawn figure, and
530 Beery Developmental Test of Visual-Motor Integration (VMI), Sixth Edition

testing is discontinued after three consecutive fail- Clinical Use

ures. A composite standard score is obtained.
The Beery VMI is a useful early screening tool
for psychologists, learning disability specialists,
Background school counselors, teachers, and other profes-
sionals to identify children with visual-motor
The first edition of the Beery VMI was published impairments. Test results assist in making appro-
in 1967 (Beery, Buktenica, and Beery). While priate referrals for services, or to test the effec-
other measures of visual-motor integration were tiveness of educational and other intervention
available at the time, none involved a sequence programs. Researchers use the test to examine
of increasingly complex geometric forms. deficits in visual-motor integration in specific
Although the Beery VMI is currently in its sixth neurodevelopmental disorders. In one study, the
edition, the test items found in the current edition Beery VMI was used to compare visual-motor
are almost identical to the original stimuli. The integration in children diagnosed with ADHD
1997 edition added the two supplemental forms and those with comorbid ADHD and reading
so that visual-motor integration could be com- disability, and/or oppositional defiant disorder
pared to pure visual or pure motor performance. (Kooistra et al. 2005). This study found increases
The sixth and most recent edition includes sug- in motor impairments among children with
gestions for teaching and improving visual- ADHD as a function of comorbid diagnoses,
motor integration. particularly reading disability. Another study
examined differences in VMI performance
between children with traumatic brain injury
Psychometric Data and ADHD in order to examine the instrument’s
validity, and found support for the use of the
The Beery VMI manual reports internal consis- VMI in children with both developmental and
tency reliabilities averaging 0.92 for visual- acquired brain dysfunction (Sutton et al. 2011).
motor integration, 0.91 for visual perception, The Beery VMI has also been used in research
and 0.90 for motor coordination. Analyses of studies of the neuropsychological outcomes for
convergent validity found the Beery VMI corre- children born preterm (Baron et al. 2009), and
lates 0.52 with the drawing subtest of the Wide individuals with Autism Spectrum Disorder
Range Assessment of Visual Motor Abilities (Green et al. 2015). Performance on the Beery
(WRAVMA) and 0.75 with the copying subtest VMI can inform diagnostic decisions across a
of the Developmental Test of Visual Perception wide spectrum of disorders.
(DTVP-2).
Normative data for the Beery VMI were
updated in the sixth edition (2010) with a sample
Cross-References
of 1,700 individuals with demographic charac-
teristics closely matching those from the 2010
▶ Rey Complex Figure Test
US Census. From ages 2–13, standard scores are
provided in 2-month intervals for the Beery
VMI, and in 3-month intervals for the two sup-
References and Further Readings
plemental tests. For ages 13–19, Beery VMI
norms are by year, and the supplemental tests Baron, I. S., Erickson, K., Ahronovich, M., Coulehan, K.,
are by 2-year periods. For adults, norms are by Baker, R., & Litman, F. (2009). Visuospatial and verbal
decade. Standard scores have a mean of 100 and fluency relative deficits in ‘complicated’ late-preterm
preschool children. Early Human Development, 85,
standard deviation of 15, and scores may be
751–754.
converted to other scales (e.g., scaled scores, Beery, K. E., Buktenica, N. A., & Beery, N. A. (2004). The
percentiles). Beery-Buktenica developmental test of visual-motor
Behavior Modification 531

integration: Administration, scoring, and teaching as a result of their TBI, the traditional behavior
manual (5th ed.). Minneapolis: NCS Pearson, Inc.. management approaches, which are based on learn-
Beery, K. E., Buktenica, N. A., & Beery, N. A. (2010). The
Beery-Buktenica developmental test of visual-motor ing theory principles, are modified. For example,
integration: Administration, scoring, and teaching behavior management approaches with TBI survi-
manual (6th ed.). Minneapolis: NCS Pearson, Inc.. vors may focus more on stimulus control (e.g., B
Green, R. R., Bigler, E. D., Froehlich, A., Prigge, M. B., controlling environmental (antecedent) cues) than
Travers, B. G., Cariello, A. N., & Lainhart, J. E. (2015).
Beery VMI performance in autism spectrum disorder. operant conditioning (e.g., recalling the contingency
Child Neuropsychology. https://doi.org/10.1080/ between behaviors and the resulting consequences).
09297049.2015.1056131.
Kooistra, L., Crawford, S., Dewey, D., Cantell, M., &
Kaplan, B. J. (2005). Motor correlates of ADHD contri-
bution of reading disability and oppositional defiant
disorder. Journal of Learning Disabilities, 38, 195–206. Cross-References
Sutton, G. P., Barchard, K. A., Bello, D. T., Thaler, N. S.,
Ringdahl, E., Mayfield, J., & Allen, D. N. (2011). ▶ Applied Behavior Analysis
Beery-Buktenica developmental test of visual-motor
integration performance in children with traumatic
▶ Behavior Modification
brain injury and attention-deficit/hyperactivity disor- ▶ Behavioral Therapy
der. Psychological Assessment, 23, 805.

References and Readings

Behavior Management Jacobs, H. E. (1993). Behavior analysis guidelines and

brain injury rehabilitation: People, principles and pro-
grams. Gaithersburg: Aspen.
Glenn S. Ashkanazi Karol, R. L. (2003). Neuropsychological intervention: The
Department of Clinical and Health Psychology, practical treatment of severe behavioural dyscontrol
Clinical and Health Psychology Clinic, College of after acquired brain injury. Boca Raton: CRC Press.
Novack, T., PhD. (n.d.). Management of behavioral prob-
Public Health and Health Professions, University
lems during acute rehabilitation of individuals with TBI.
of Florida, Gainesville, FL, USA Retrieved 30 Nov 2016, from http://www.brainline.org/
content/2008/07/management-behavioral-problems-dur
ing-acute-rehabilitation-individuals-tbi_pageall.html
Definition

Techniques used to control or modify an action or

performance of a subject. This is a less-intensive Behavior Modification
version of behavior modification in which the goal
is to develop, strengthen, maintain, decrease, or Chava Creque1 and Stephanie A. Kolakowsky-
eliminate behaviors in a planned or systematic Hayner2
1
way. Behavior management skills are particularly Department of Psychology and Neuroscience,
important to enhance the probability that individ- University of Colorado Boulder, Boulder,
uals, or groups, choose behaviors that are prosocial. CO, USA
2
Prosocial behaviors are typically seen as personally Department of Rehabilitation Medicine,
fulfilling, productive, and socially acceptable. The Icahn School of Medicine at Mount Sinai,
process typically includes identifying negative New York, NY, USA
behaviors, raising awareness about alternative
behaviors, and changing the environment by modi-
fying antecedents to behaviors or the consequences. Synonyms
Persons surviving a traumatic brain injury (TBI)
often have behavioral disturbances such as disinhi- Applied behavioral analysis; Behavior therapy;
bition and/or agitation. Due to learning impairments Cognitive-behavioral modification
532 Behavior Rating Inventory for Executive Function

Definition hepatitis C infection. American Journal of Health

Behavior, 29(6), 512–519.
Martin, G. L., & Pear,J.J. (2015). Behavior modification:
Behavior modification is the use of basic learning What it is and how to do it (10th ed.). New York, NY:
techniques, such as conditioning, biofeedback, Routledge Psychology Press.
assertiveness training, positive or negative rein- Ntinas, K. (2007). Behavior modification and the principle
forcement, hypnosis, or aversion therapy, to of normalization: Clash or synthesis? Behavioral Inter-
ventions, 22(2), 165–177.
change unwanted individual or group behavior
and improve daily functioning. These techniques
are typically based on functional assessment and
used to reinforce adaptive behaviors while
diminishing or extinguishing maladaptive behav- Behavior Rating Inventory for
iors. Behavioral modification techniques can be Executive Function
used to address learning issues as well as social,
emotional, behavioral, or psychiatric problems. Gerard A. Gioia1, Peter K. Isquith2 and
Seven characteristics of behavior modification, Robert M. Roth3
1
identified by Martin and Pear (2015), include: Children’s National Medical Center, Rockville,
MD, USA
2
• A strong emphasis on defining problems in Dartmouth Medical School, Lebanon, NH, USA
3
terms of measurable behavior Geisel School of Medicine at Dartmouth /
• Making environmental adjustments to improve DHMC, Lebanon, NH, USA
functioning
• Precise methods and rationales
• Dynamic real-life application of techniques Synonyms
• Techniques grounded in learning and behavior
theory BRIEF; BRIEF2; BRIEF-A; BRIEF-P; BRIEF-SR
• Scientific demonstration linking the imposed
technique with behavior change
• Strong emphasis on accountability Description

The Behavior Rating Inventory of Executive

Cross-References Function (BRIEF) family of measures are rating
scales designed to facilitate assessment of the
▶ Applied Behavior Analysis behavioral manifestations of executive dysfunc-
▶ Behavioral Assessment tion in everyday environments such as home,
▶ Behavior Management school, and work. First published in 2000 as par-
▶ Behavioral Therapy ent and teacher rating scales of executive function
in children and adolescents, the family of mea-
References and Readings sures has grown to include versions for assessing
preschool children, adolescents’ self-report, and
Crum, C. (2004). Using a cognitive-behavioral modifica- adults.
tion strategy to increase on-task behavior of a student The original BRIEF consists of two forms,
with a behavior disorder. Intervention in School and
a parent questionnaire and a teacher question-
Clinic, 39(5), 305.
Hicinbothem, J., Gonsalves, S., & Lester, D. (2006). Body naire, designed to assess executive function
modification and suicidal behavior. Death Studies, behaviors in children and adolescents aged
30(4), 351. 5–18 years in home and school environments.
Kazdi, A. E. (2012). Behavior modification in applied
It includes 86 items with 8 theoretically and
settings. Long Grove: Waveland Press.
Lindsey, N., Reif, J., Bachand, A., & Seys, S. (2005). empirically derived clinical scales measuring
Behavior modification following a diagnosis of Inhibit, Shift, Emotional Control, Initiate,
Behavior Rating Inventory for Executive Function 533

Working Memory, Plan/Organize, Monitor, and Organize. The clinical scales form three indexes,
Organization of Materials. The BRIEF also the Behavior Regulation Index (BRI), Emotion
includes two validity scales, Inconsistency Regulation Index (ERI), and Cognitive Regula-
and Negativity. The eight scales form two tion Index (CRI), and an overall summary score,
broader indexes based on the factor structure, the Global Executive Composite (GEC). B
Behavioral Regulation and Metacognition, as The BRIEF2 Self-Report also includes three
well as an overall score, the Global Executive validity scales – Infrequency, Inconsistency,
Composite (GEC). and Negativity.
In 2015, the first revision of the BRIEF, the An important enhancement in the BRIEF2 is
BRIEF2, was published, reducing the length of the inclusion of three 12-item screening forms
the measure by approximately one quarter while for parents, teachers, and adolescents. These
adding numerous enhancements. These were concise forms were created to meet the needs
informed by the hundreds of peer-reviewed of large-scale assessment in education, health,
papers that have employed the measure in a wide and research settings. Each correlates strongly
range of clinical and normative groups in multiple with the BRIEF2 Global Executive Composite
languages on six continents; tested the factor score (r > 90) and discriminates between typi-
structure; explored relationships with academic, cally developing children and those with exec-
behavioral, emotional, social, and adaptive func- utive function deficits with large effect sizes.
tioning; documented associations with biological Reliabilities are strong, there are multiple lines
factors including brain structure and function; and of evidence for validity, and the standardization
demonstrated sensitivity to change with recovery sample was large and stratified by gender, race/
or treatment. The BRIEF2 includes parallel Par- ethnicity, parent education, and geographic
ent and Teacher forms and incorporates the pre- region. Classification statistics including sensi-
viously separate adolescent self-report form. tivity/specificity and likelihood ratios are used
Parent and Teacher forms are composed of to identify children at risk for executive func-
63 items within 9 theoretically and empirically tion problems who should be more fully
derived clinical scales that are largely consistent assessed.
with those of the BRIEF, with the exception that The BRIEF-Preschool Version (BRIEF-P)
the Monitor scale was separated into Self- measures the behavioral manifestations of execu-
Monitor and Task Monitor scales. The BRIEF2 tive function in preschool-aged children, ages
includes three validity scales, Inconsistency, 2–5. It consists of a single form completed by
Negativity, and a new Infrequency scale. Finally, parents and/or teachers/caregivers to rate the
the nine scales form three broader indexes based child’s executive functions within the home and
on the factor structure, Behavior Regulation, preschool settings. The questionnaire consists of
Emotion Regulation, and Cognitive Regulation 63 items comprising 5 theoretically and empiri-
(similar to the metacognition index on the cally derived clinical scales measuring Inhibit,
BRIEF), as well as a Global Executive Compos- Shift, Emotional Control, Working Memory, and
ite score, or the GEC. Plan/Organize. These scales form three factor-
The BRIEF2 also includes a revised and derived indexes, Inhibitory Self-Control, Flexibil-
co-normed version of the BRIEF Adolescent ity, and Emergent Metacognition, and one com-
Self-Report. This is a 55-item Self-Report form posite score, the GEC. The BRIEF–P also
designed to complement the BRIEF2 Parent and includes two validity scale, Inconsistency and
Teacher forms. It is appropriate for older children Negativity.
and adolescents ages 11–18 years with a fifth- The BRIEF-A measures an adult’s executive
grade or higher reading ability. The items yield functions in his or her everyday home and work
information for seven clinical scales: Inhibit, environment. Two forms are available, a Self-
Self-Monitor, Shift, Emotional Control, Task Report and an Informant Report. The Self-Report
Completion, Working Memory, and Plan/ form is designed to be completed by adults
534 Behavior Rating Inventory for Executive Function

18–90 years of age, while the Informant Report everyday executive problem-solving in natural
form is administered to an adult who is familiar settings offer a complementary approach to clini-
with the rated individual’s everyday functioning. cal performance-based assessment.
The latter form can be used alone when the rated Executive function is generally viewed as a
individual is unable to complete the Self-Report broad umbrella term that encompasses a set of
form or has limited awareness of his or her own interrelated subdomains. Although authors vary
difficulties or with the Self-Report form to gain with respect to which cognitive and behavioral
multiple perspectives on the individual’s function- processes are viewed as part of the executive
ing. The BRIEF-A is composed of 75 items within function domain, they typically include initiation
9 clinical scales measuring: Inhibit, Self-Monitor, of goal-directed behavior, inhibition of competing
Shift, Emotional Control, Initiate, Working Mem- actions or stimuli, planning and selection of rele-
ory, Plan/Organize, Task-Monitor, and Organiza- vant task goals, organization of behavior to solve
tion of Materials. The clinical scales form novel and/or complex problems, flexible shifting
two broader factor-based indexes: Behavioral of behavior and problem-solving strategies when
Regulation (BRI) and Metacognition (MI), and necessary, monitoring and evaluation of problem-
these indexes form the overall summary solving behavior and task performance more gen-
score, the GEC. The BRIEF-A also includes erally, as well as monitoring the effects of one’s
three validity scales: Negativity, Inconsistency, own behavior on others. In support of these
and Infrequency. behaviors, working memory capacity plays a fun-
damental role in holding information actively
“online” in the service of problem-solving,
Historical Background including planning and organization. Importantly,
the executive functions are not exclusive to cog-
Executive functions have been historically evalu- nition; emotional control is also relevant to effec-
ated using laboratory-based performance tests. tive problem-solving activity and should be
While these types of measures offer the advan- considered in any definition. Historically, execu-
tages of control over extraneous variables and tive functions have been closely associated with
potential to fractionate and examine components the integrity of the frontal lobes of the brain. Much
of executive function separately such as planning of the evidence supporting a role for the frontal
versus working memory, they are limited in lobes in executive functions has come from stud-
ecological validity or ability to predict functioning ies of individuals with acquired focal damage to
in the everyday environment. Fundamentally, this region, as well as studies using advanced
executive functions are necessary for organization brain imaging techniques such as positron emis-
of goal-directed behavior in the everyday, “real- sion tomography (PET) and functional magnetic
world” environment. Thus, in addition to resonance imaging (fMRI). However, these same
assessing these functions with clinical perfor- studies have also clearly shown that executive
mance measures, it is important to also capture functions are not subserved by the frontal lobes
behavioral manifestations of executive function or alone, but rather by distributed neural circuitry
dysfunction. The BRIEF was developed to mea- that includes other cortical regions and subcortical
sure executive functions through the assessment structures as well as the cerebellum. Damage to
of an individuals’ behavior in their everyday envi- any given component of this circuitry may result
ronments. Given the challenges of executive func- in executive dysfunction.
tion assessment in the laboratory and inherent The BRIEF was originally developed begin-
limitations to applicability in the everyday envi- ning in 1994 following a commonly accepted
ronment and to treatment, attention has increas- developmental model of executive function
ingly turned to alternative methods of evaluation (Welsh and Pennington 1988; Holmes-Bernstein
that offer enhanced ecological validity. Assess- and Waber 1990). The impetus arose from the
ment methods that reliably tap the individual’s authors’ frequent observations in clinical practice
Behavior Rating Inventory for Executive Function 535

that parent and teacher reports of a child’s func- ratings (mean r = 0.39 for normative sample,
tioning in the everyday environment did not mean r = 0.56 for clinical sample).
always, or even often, fit with the same child’s Validity: Evidence of validity is demonstrated
test performance on putative executive function by several lines of evidence including high inter-
performance tests. The measure found acceptance rater agreement for item-scale assignments by B
initially within the field of pediatric neuropsychol- expert panel, factor analytic studies, and structural
ogy and was published first in 2000. Since then, equation modeling. Convergent and divergent
the several versions of the BRIEF have become validity evidence is demonstrated by convergence
widely used across the age spectrum and across with scales of inattention and impulsivity and
clinical, school, and research settings. Since pub- divergence of behavioral/emotional functioning
lication, a substantial body of literature has devel- from executive functioning using the ADHD-IV,
oped examining BRIEF profiles with a wide range BASC, CBCL, and CRS. Exploratory and confir-
of clinical groups (Roth et al. 2014; Strauss matory factor analysis of the BRIEF2 Parent,
et al. 2006). Teacher, and Self-Report forms yielded a consis-
tent three-factor solution (i.e., Behavior Regula-
tion, Emotion Regulation, Cognitive Regulation)
Psychometric Data for normative and clinical samples. Two of the
scales, Working Memory and Inhibit, are clini-
BRIEF2 (Ages 5–18 Years: Parent and Teacher cally useful in detecting and predicting the diag-
Forms) nosis of attention-deficit/hyperactivity disorder
Standardization: Normative data are based on (ADHD).
1,400 parents and 1,400 teachers from rural, sub-
urban, and urban areas. The samples were diverse BRIEF2 Self-Report (BRIEF2-SR)
to match proportions of race/ethnicity, parental Standardization: The BRIEF2-SR was standard-
education level, geographic region, and gender ized and validated for use with children and ado-
across all 50 states, based on the US population lescents aged 11–18 years. The normative sample
data from the Current Population Survey, March includes 803 participants using the same compre-
2013 by the US Census Bureau, 2012, hensive sampling as the Parent and Teacher forms
Washington, DC. Separate normative tables, matched to the US Census data. Clinical data are
including T scores, percentiles, and confidence based on 473 children and adolescents with a
intervals, are provided for four age groups for variety of developmental disorders or acquired
boys and girls separately, with norms for both neurological disorders (e.g., learning disabilities,
the Parent and Teacher forms. Clinical data are ADHD, TBI, Tourette’s syndrome, autism spec-
based on 2,892 parents and 1,889 teachers rating trum disorders, epilepsy, and brain tumor
children with developmental disorders or acquired disorders).
neurological disorders (e.g., learning disabilities, Reliability: The BRIEF2-SR scales demon-
ADHD, TBI, Tourette’s syndrome, mental retar- strate appropriate reliability. Internal consistency
dation, epilepsy, and language disorders). is high for the GEC (a = 0.97) and moderate to
Reliability: High internal consistency high for the clinical scales (a = 0.81–0.88). Tem-
(Cronbach’s alpha >0.90 for Parent and Teacher poral stability is strong (r = 0.85 for the GEC over
Index Scores). Test-retest reliability for compos- a period of 3.7 weeks), and there is strong inter-
ites was r = 0.82–0.89 for parent normative rat- rater agreement for the GEC with parent ratings
ings and r = 0.83–0.90 for teacher normative on the BRIEF (r = 0.71). Teacher ratings on the
ratings. Interobserver reliability reflected moder- BRIEF2-SR correlated moderately with adoles-
ate to high correlations for parent-parent ratings cent ratings on the BRIEF-SR (GEC r = 0.57).
(mean r = 0.77 for normative sample, 0.59 for Validity: Principal factor analysis of the
clinical sample), moderate correlations for parent- BRIEF2-SR yielded a three-factor solution (i.e.,
teacher (mean r = 0.30–0.50), teacher-teacher Behavior Regulation, Emotion Regulation,
536 Behavior Rating Inventory for Executive Function

Cognitive Regulation) for normative and clinical indexes in the parent and teacher normative groups,
samples. Correlational analyses with other self- respectively. The Working Memory and the Plan/
report behavior rating scales (i.e., Child Behavior Organize scales define the first component, the Shift
Checklist/Youth Self-Report [CBSL/YSR], and Emotional Control scales comprise the second
Behavior Assessment System for Children Self- component, and the Inhibit and Emotional Control
Report of Personality [BASC-SRP], Child Health scales define the third component.
Questionnaire [CHQ], Profile of Mood States-
Short Form [POMS-SF]) provide evidence of BRIEF-Adult (BRIEF-A: Self-Report and
convergent and divergent validity for the Informant Report)
BRIEF-SR. Examination of BRIEF2-SR profiles Standardization: The BRIEF-A was standardized
in a variety of clinical groups provides further and validated for use with men and women from
evidence of validity based on clinical utility. ages 18–90 years. The normative sample includes
BRIEF2-SR ratings for groups of adolescents 1,050 adult self-reports and 1,200 informant reports
with ADHD-I, ADHD-C, insulin-dependent dia- from a wide range of racial/ethnic backgrounds,
betes mellitus, autism spectrum disorders, and educational backgrounds, as well as geographic
anxiety and depressive disorders showed different regions that are matched to US Census data.
patterns of scale elevations for each group com- Reliability: The BRIEF-A has demonstrated
pared to matched control groups. Correlations multiple lines of evidence for reliability. Internal
between adolescent and parent ratings for consistency was moderate to high for the Self-
the clinical groups were low to moderate Report normative sample (a = 0.73–0.90 for clin-
(r = 0.25–0.35), suggesting agreement yet differ- ical scales; 0.93–0.96 for indexes and GEC) and
ent perspectives as well. high for the Informant Report normative sample
(a = 0.80–0.93 for clinical scales; 0.95–0.98 for
BRIEF-Preschool (BRIEF-P: Ages 2–5 Years, indexes and GEC). Using a mixed sample of
Parent and Caretaker Forms) clinical or healthy adults who were seen for clin-
Standardization: Normative data based on child ical evaluation or research study participation,
ratings from 460 parents and 302 teachers from internal consistency was high for the Self-Report
urban, suburban, and rural areas, reflecting form (a = 0.80–0.94 for clinical scales; 0.96–0.98
1999 US Census estimates for race/ethnicity, gen- for indexes and GEC) and the Informant Report
der, socioeconomic status, and age. Clinical sam- form (a = 0.85–0.95 for clinical scales; 0.96–0.98
ples included children in the following diagnostic/ for indexes and GEC). Test-retest correlations
clinical groups: ADHD, low birth weight/prema- over a 4-week period across the clinical scales
turity, language disorders, autism spectrum disor- ranged from r = 0.82–0.93 for the Self-Report
ders, and a mixed clinical group. form (n = 0.50) and from r = 0.91–0.94 for the
Reliability: High internal consistency Informant Report Form (n = 0.44). Correlations
(a = 0.80–0.95 for parent sample and between Self-Report ratings and Informant Report
a = 0.90–0.97 for teacher sample), test-retest ratings were moderate, ranging from
reliability (r = 0.78–0.90 for parents and r = 0.44–0.68 for the clinical scales and from
0.64–0.94 for teachers), and modest correlations 0.61–0.63 for the indexes and the GEC.
between parent and teacher ratings Validity: The BRIEF-A exhibits multiple lines
(r = 0.14–0.28). of validity evidence as an ecologically sensitive
Validity: Convergent and discriminant validity measure of executive functioning in individuals
evidence established with other measures of inatten- with a range of conditions across a wide age
tion, hyperactivity-impulsivity, depression, atypi- range. In terms of convergent validity evidence,
cality, anxiety, and somatic complaints (ADHD- the Self- and Informant Report Form of the
IV-P, CBCL/1½–5, BASC–PRS). Factor analytic BRIEF-A scales, indexes, and GEC demonstrated
studies provide support for a three-factor model of significant correlations in the expected direction
executive functioning embodied by the three with Self-Report and Informant Report on the
Behavior Rating Inventory for Executive Function 537

Frontal Systems Behavior Scale, Dysexecutive functioning in individuals with developmental

Questionnaire, and Cognitive Failures Question- disabilities, scholastic achievement and perfor-
naire. Validity has been further demonstrated via mance on high-stakes testing in children, as well
studies of clinical populations. Factor analysis of as college adjustment and academic procrastina-
Self-Report form data yielded a two-factor solu- tion in young adults. While there are modest cor- B
tion (i.e., Behavioral Regulation, Metacognition) relations between the BRIEF and performance
for normative and mixed clinical/healthy adult tests that tap aspects of executive functions, the
samples, accounting for 73% and 76% of the BRIEF shows significant associations with bio-
variance, respectively. Factor analysis of Infor- logical markers such as lead levels, structural and
mant Report form data also yielded a similar functional neuroimaging (e.g., frontal lobe vol-
two-factor solution for the normative and mixed ume, white matter integrity), and genetic markers
clinical/healthy adult samples, accounting for (e.g., polymorphisms of the monoamine oxidase
81% and 78% of the variance, respectively. A gene). Finally, certain BRIEF profiles of exec-
utive function in the everyday environment can
help predict diagnoses such as ADHD and autism
Clinical Uses spectrum disorder.
Data from the BRIEF can help the clinician
Given the central importance of the executive focus on potentially problematic areas requiring
functions to the direction and control of dynamic further assessment. The same data may inform
“real-world” behavior, the BRIEF family of decisions about targets for treatment and types of
instruments was designed for a broad range of interventions based on the potential for ameliorat-
individuals with developmental, neurological, ing real-world problems. An understanding of the
psychiatric, and medical conditions. Deficits in individual’s profile of executive function
various subdomains of the executive functions strengths and weaknesses can lead to targeted
are central characteristics of many developmental pharmacological, behavioral, cognitive, or other
and acquired neurological disorders across the life therapeutic interventions. Such strategies may be
span. Executive function deficits measured via the specifically targeted toward one area of executive
BRIEF have been demonstrated in a variety of functions, such as antecedent management for
populations such as ADHD, traumatic brain children with inhibitory control deficits, or may
injury, lesions of the frontal lobes, type 1 diabetes be more programmatic, such as the comprehen-
mellitus, autism spectrum disorders, learning dis- sive cognitive rehabilitation programs. For exam-
abilities, myelomeningocele and hydrocephalus, ple, an individual who is described as disinhibited
Tourette’s syndrome, phenylketonuria, bipolar in the everyday world might have treatments and
disorder, obstructive sleep apnea, 22q11 deletion supports targeted specifically toward boosting
syndrome, galactosemia, sickle cell disease, and inhibitory control or limiting opportunity for
prenatal alcohol exposure. The BRIEF-A has impulsive behavior. A child with difficulties
been examined in clinical populations such as shifting set might benefit from teaching and inter-
mild cognitive impairment, ADHD, epilepsy, vention strategies that incorporate use of routines
traumatic brain injury, schizophrenia, and cancer and schedules to reduce agitation and anxiety
survivors. when change is needed.
The measures also show promise for veridical- Finally, assessment of executive function with
ity, that is, predicting behavior in the natural envi- the BRIEF can inform clinical treatment design,
ronment. For example, correlational analyses monitoring, and outcome evaluation. Given the
suggest strong, logical relationships between the inherent difficulty in administering performance
Inhibit scale and aggression and the Working measures of executive function in a repeated fash-
Memory scale with attention problems. Correla- ion, behaviorally anchored measures may be
tions have also been reported between BRIEF and well suited to such within-subject methods. For
aspects of real-world functioning such as adaptive example, a patient concerned about attentional
538 Behavioral Assessment

difficulties might reveal problems with inhibi- Gioia, G. A., Kenworthy, L., & Isquith, P. K. (2010).
tory control and working memory on the Executive function in the real world: BRIEF lessons
from mark Ylvisaker. The Journal of Head Trauma
BRIEF. After appropriate interview and clinical Rehabilitation, 25(6), 433–439.
diagnosis, treatment methods might include Holmes-Bernstein, J., & Waber, D. (1990). Developmental
medication and cognitive behavior therapy. To neuropsychological assessment: A systemic approach.
evaluate effectiveness of treatment, the measure NeuroMethods, 17, 311–372.
Isquith, P. K., Crawford, J. S., Espy, K. A., & Gioia, G. A.
may be administered again after starting medica- (2005). Assessment of executive function in preschool
tion and again after a longer period to determine children. Mental Retardation and Developmental Dis-
whether the effects of treatment are maintained. ability Research Review, 11, 209–215.
Ratings can be provided by the individual them- Isquith, P. K., Roth, R. M., & Gioia, G. (2013). Contribu-
tion of rating scales to the assessment of executive
selves or an informant in their environment who functions. Applied Neuropsychology: Child, 2(2),
has the opportunity to regularly observe their 125–132.
behavior (e.g., parent, teacher, spouse). More Isquith, P. K., Roth, R. M., Kenworthy, L., & Gioia, G.
frequent monitoring might also be appropriate (2014). Contribution of rating scales to intervention for
executive dysfunction. Applied Neuropsychology:
in some cases, such as for individuals who sus- Child, 3(3), 197–204.
tain a mild TBI, where full neuropsychological Malloy, P., & Grace, J. (2005). A review of rating scales for
evaluation may not be feasible or appropriate at measuring behavior change due to frontal systems dam-
the time, but rapid, timely assessment of func- age. Cognitive and Behavioral Neurology, 18, 18–27.
Ransom, D. M., Burns, A., Youngstrom, E. A., Sady,
tioning is important for determining when the M. D., Vaughan, C. G., & Gioia, G. A. (2016). Apply-
individual may return to normal activities ing an evidence-based assessment model to identify
(Ransom et al. 2016). The BRIEF2 monitoring students at risk for perceived academic problems fol-
form may be especially useful for such situations lowing concussion. Journal of the International Neu-
ropsychological Society, 22(10), 1038–1049.
where frequent reassessment is needed in a time- Roth, R. M., Isquith, P. K., & Gioia, G. A. (2014). Assess-
and resource-sensitive manner. ment of executive functioning using the behavior rating
inventory of executive function (BRIEF). In
S. Goldstein & J. A. Naglieri (Eds.), Handbook of
executive functioning (2nd ed., pp. 301–331).
See Also New York: Springer.
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). Behav-
▶ Attention Deficit Hyperactivity Disorder ior rating inventory of executive function (BRIEF). In A
▶ Concussion compendium of neuropsychological tests, administra-
tion, norms, and commentary (3rd ed.,
▶ Executive Functioning pp. 1090–1099). Oxford: Oxford University Press.
▶ Traumatic Brain Injury (TBI)

Further Reading
Behavioral Assessment
Gioia, G. A., Isquith, P. K., & Guy, S. C. (2001). Assess-
ment of executive functions in children with neurologic
Dawn E. Bouman
impairment. In R. J. Simeonsson & S. Rosenthal (Eds.),
Psychological and developmental assessment: Chil- Neuropsychology and Medical Psychology,
dren with disabilities and chronic conditions. University of Cincinnati, Department of
New York: Guilford Press. Neurology and Rehabilitation Medicine,
Gioia, G. A., Isquith, P. K., Kenworthy, L., & Barton, R. M.
Cincinnati, OH, USA
(2002). Profiles of everyday executive function in
acquired and developmental disorders. Child Neuro-
psychology, 8, 121–137.
Gioia, G. A., Isquith, P. K., & Kenealy, L. (2008). Assess- Synonyms
ment of behavioral aspects of executive function. In
V. Anderson, R. Jacobs, & P. Anderson (Eds.), Execu-
tive functions and the frontal lobes: A life span Behavior/behavioral analysis; Behavior/behav-
approach. Sussex: Psychology Press. ioral observation
Behavioral Assessment of the Dysexecutive Syndrome 539

Definition
Behavioral Assessment of the
Behavioral assessment is a systematic Dysexecutive Syndrome
collection of data, obtained through direct
observation, often in natural settings, rather Shahal Rozenblatt B
than sole administration of standardized Advanced Psychological Assessment P. C.,
tests. Behavior assessment can be informal Smithtown, NY, USA
or formal and standardized. Based on learning
theory, behavioral assessment considers the
context of a person’s actions, including ante- Synonyms
cedents that precede and might trigger the
action, as well as consequences that follow BADS
the behavior which might reinforce the behav-
ior. Behavior assessment can be used to
describe a person’s functioning (i.e., arousal, Description
initiation, or agitation) and evaluate effective-
ness of therapy interventions or medications. The BADS (Wilson et al. 1996) is a test battery
In persons who have behavioral disorders due aimed at predicting everyday difficulties that arise
to neurological causes, behavior assessment is as a result of the Dysexecutive Syndrome (DES).
the first step for evaluating the situation so It consists of six subtests and a 20-item question-
that remediation recommendations can be naire that tap executive functioning in an ecolog-
made. Patients are often directly observed in ically valid way. The subtests are as follows: The
physical or occupational therapy sessions and Rule Shift Cards Test is a measure of cognitive
in the home or classroom. flexibility that consists of 21 spiral-bound cards
that are used to assess the individual’s ability to
respond correctly to a rule and to shift from one
rule to another. It is scored based on the time taken
Cross-References and number of errors made. In the first part, the
individual is asked to respond “Yes” to a red card
▶ Applied Behavior Analysis and “No” to a black card. This component estab-
▶ Behavior Management lishes a pattern of behavior that is geared to
▶ Behavior Modification increase the probability of perseverative errors in
▶ Behavior Rating Inventory for Executive the second part, when the rules are changed. In the
Function second part, the individual is asked to respond
▶ Behavioral Assessment of the Dysexecutive “Yes” if the card just turned over is the same
Syndrome color as a previously turned card and “No” if it
▶ Behavioral Therapy is different.
▶ Conners Comprehensive Behavior Rating The Action Program Test involves five steps
Scales™ that require simple skills that are typically part of
▶ Functional Assessment most people’s repertoires. It requires the individ-
▶ Functional Assessment Measure ual to determine what needs to be done prior to
concentrating on how that end is to be achieved.
The test consists of a rectangular stand with a thin
transparent tube with a removable lid and a cork
on the bottom, while at the other end there is a
References and Readings
beaker that is two-thirds full of water. An
Jacobs, H. E. (1993). Behavior analysis guidelines and L-shaped rod that is not long enough to reach the
brain injury rehabilitation. Gaithersburg: Aspen. cork is to the left of the stand. The individual is
540 Behavioral Assessment of the Dysexecutive Syndrome

asked to get the cork out of the tube using any of ranging from “Never” to “Very Often.” Two ver-
the objects around without lifting the stand, the, sions are available, one completed by the individ-
tube or the beaker and without touching the lid ual and the other by an informant.
with their fingers.
In the Key Search Test, the individual is pre-
sented with an A4-sized piece of paper with a Historical Background
100 mm square in the middle and a small black
dot 50 mm below it. The individual is told to The BADS is designed to evaluate the pattern of
pretend that the square is a field in which they deficits that are typically subsumed under the
lost their keys and are asked to draw a line, functions of the frontal lobes. Rylander (1939)
starting at the black dot, demonstrating how they enumerated the deficits as involving disturbances
would go about searching the field. The individual in attention, increased distractibility, impaired
is scored based on how efficient the search ability to learn new tasks, and deficits contending
process is. with complex information. Shallice (1982)
The Temporal Judgment Test comprises four described this pattern of deficits as comprising
questions concerning everyday events which impairment in attentional control, which he
range from requiring a few seconds to several termed the supervisory system. Baddeley (1986)
years. The individual is asked to make a sensible analogized the supervisory system to the central
guess as to how long an event will take (e.g., How executive component of working memory and
long do most dogs live?). suggested the term Dysexecutive Syndrome as a
In the Zoo Map Test, subjects are asked to way of characterizing patients with this pattern of
show how they would visit a series of designated impairment. Such patients are likely to present as
locations on a map of a zoo while following impulsive, distractible, and unable to use feed-
certain rules. In the high demand component, the back to modify their responses and behave inap-
individual will incur a high number of errors by propriately in social situations.
simply visiting the locations in the order given in The BADS was developed due to the fact that
the instructions. In the low demand component, patients with impaired executive functioning
the individual is simply required to follow the often performed adequately on tests such as the
instructions to produce an error-free performance. Wisconsin Card Sorting Test or the Stroop Test.
The goal of the test is to assess the individual’s These same individuals, however, exhibited obvi-
spontaneous planning abilities. ous impairment in their day-to-day functioning.
The Modified Six Elements Test requires the To this end, Shallice and Burgess (1991) devel-
completion of three tasks (i.e., dictation, arith- oped the Six Elements Test, which required the
metic, and picture naming), each of which is individual to carry out six tasks in a limited time
divided into parts A and B. The individual is frame without violating certain rules. It was tai-
required to attempt at least a part from each of lored to a difficulty level that was in line with the
the six subtests within a 10-minute period and is high level of functioning of Shallice and Burgess’
instructed not to do the two parts of the same task patients. Wilson et al. (1996) modified the Six
consecutively. The goal of this component is to Elements Test, simplifying it for more severely
determine the person’s ability to plan, organize, impaired and less intellectually able patients that
and monitor their behavior. are often seen by neuropsychologists. This
The Dysexecutive Questionnaire (DEQ) con- evolved into the BADS.
sists of 21 items that sample the range of problems
commonly associated with the Dysexecutive Syn-
drome. Four broad areas are sampled: emotional Psychometric Data
or personality changes, motivational changes,
behavioral changes, and cognitive changes. Multiple studies attest to the psychometric prop-
Items are scored on a 5-point (0–4) Likert scale, erties of the BADS. Wilson et al. (1996) found
Behavioral Assessment of the Dysexecutive Syndrome 541

that inter-rater reliability was high, ranging from most components of the measure, including task
0.88 to 1.00. Test-retest reliability was also exam- switching, time monitoring, and rule-shifting sub-
ined with subjects generally performing slightly tests. The highest level of discrimination between
higher after the second administration, but the controls and patients was found on the Modified
differences were not statistically significant. Cor- Six Elements, with a sensitivity index of 80% and B
relations between the first and second test admin- specificity index of 90%.
istrations were moderate, with the exception of the
Zoo Map Test, where virtually no correlation was
found. This was attributed to the presence of out- Clinical Uses
liers and small sample size (n = 25). The test-
retest reliability of the BADS was similar in pat- Wilson et al. (1996) developed the BADS to aid
tern to other tests of frontal lobe functioning those involved in the assessment of individuals
administered at the same time (e.g., Modified with brain injury to determine the extent of exec-
Card Sorting Test; Nelson 1976). utive dysfunction that is present and the likelihood
The validity of the BADS was assessed across that it will interfere with everyday life. It can also
varied populations. Bennett et al. (2005) investi- be used to determine the presence of executive
gated the sensitivity of the BADS to executive dysfunction in other patient groups, such as
dysfunction in a sample of 64 Australian patients schizophrenics and substance abusers. The
who were involved in motor vehicle or workplace BADS can be a useful part of the rehabilitation
accidents. All experienced loss of consciousness process as a tool that can pick up subtle difficulties
and varying degrees of post-traumatic amnesia with planning and organization, which are then
(PTA). Based on their findings, the authors con- amenable to intervention. For example, Baba et al.
cluded that scores derived from the BADS and (2010) found that the executive functioning of
other measures used in their study were only 20 Japanese adults with remitted major depressive
moderately useful in assessing executive dysfunc- disorder were more impaired on the Modified Six
tion. On the other hand, several studies have Elements subtest relative to 29 healthy compari-
found the BADS to discriminate between patients son subjects.
and controls. Krabbendam et al. (1999) were able
to discriminate between schizophrenic patients
and controls, while Katz et al. (2007) were able See Also
to discriminate between acute and chronic schizo-
phrenics, the latter evidencing greater executive ▶ Frontal Lobe
dysfunction. Verdejo-Garcia and Perez-Garcia
(2007) examined the usefulness of the BADS in
determining executive dysfunction in a Spanish Further Reading
sample of substance-dependent individuals (SDI).
They concluded that the BADS yielded greater Baba, K., Baba, H., Noguchi, I., Arai, R., Suzuki, T., &
Mimura, M. (2010). Executive dysfunction in remitted
effect sizes for differences between SDI and con-
late-life depression: Juntendo University mood disor-
trols than traditional measures of executive func- der projects (JUMP). The Journal of Neuropsychiatry
tion. SDI performance on the BADS was also and Clinical Neurosciences, 22, 70–74.
useful as a predictor of problems in daily activi- Baddeley, A. D. (1986). Working memory. Oxford:
Clarendon Press.
ties. Third, deficits in BADS scores persisted fol- Bennett, P. C., Ong, B., & Ponsford, J. (2005). Assessment
lowing protracted abstinence, even when other of executive dysfunction following traumatic brain
neuropsychological indices showed recovery. injury: Comparison of the BADS with other clinical
Canali et al. (2011) examined the reliability of neuropsychological measures. Journal of the Interna-
tional Neuropsychological Society, 11, 606–613.
the BADS in its ability to discriminate Brazilian
Canali, F., Brucki, S. M. D., Bertolucci, P. H. F., & Bueno,
older adults with and without mild Alzheimer’s O. F. A. (2011). Reliability study of the behavioral
disease. Intergroup differences were reported on assessment of the dysexecutive syndrome adapted for
542 Behavioral Inattention Test (BIT)

a Brazilian sample of older-adult controls and probable spatial neglect (Wilson et al. 1987b; Halligan
early Alzheimer’s disease patients. Revista Brasileira et al. 1991). Unilateral spatial neglect is com-
de Psiquiatria, 33, 338–346.
Katz, N., Tadmor, I., Felzen, B., & Hartman-Maeir, A. monly defined as an inability to respond to or
(2007). The behavioural assessment of the dysexecutive notice stimuli that is present on the side opposite
syndrome (BADS) in schizophrenia and its relation to of the brain lesion location. This spatial neglect is
functional outcomes. Neuropsychological Rehabilita- not attributed to motor or sensory deficits
tion, 17, 192–205.
Krabbendam, L., de Vugt, M. E., Derix, M. M. A., & Jolles, J. (Heilman et al. 1993). In an attempt to improve
(1999). The behavioural assessment of the dysexecutive ecological validity, the BIT incorporated nine
syndrome as a tool to assess executive functions in behavioral subtests in addition to six conventional
schizophrenia. The Clinical Neuropsychologist, 13, subtests. The behavioral subtests aim to assess
370–375.
Nelson, H. E. (1976). A modified card sorting test sensitive unilateral spatial neglect as well as an individual’s
to frontal lobe defects. Cortex, 12, 313–324. functioning on activities of daily living.
Rylander, G. (1939). Personality changes after operation The BIT takes approximately 40 min to com-
on the frontal lobes. Acta Psychiatrica Neurologica, plete and can be administered to individuals ages
(30).
Shallice, T. (1982). Specific impairments of planning. Phil- 19–83. The conventional subtests consist of line
osophical Transactions of the Royal Society of London. crossing, star cancellation, letter cancellation, line
Series B, Biological Sciences, 298, 199-209. bisection, figure/ shape copying, and representa-
Shallice, T., & Burgess, P. (1991). Deficits in strategy tion drawing. Line crossing and the cancellation
application following frontal lobe damage in man.
Brain, 114, 727–741. subtests require the examinee to cross out the
Verdejo-Garcia, A., & Perez-Garcia, M. (2007). Ecological target items, where the cancellation subtests add
assessment of executive functions in substance depen- a level of difficulty with the presence of various
dent individuals. Drug and Alcohol Dependence, 90, nontarget items. Line bisection requires the exam-
48–55.
Wilson, B. A., Alderman, N., Burgess, P. W., Emslie, H., & inee to estimate and mark the center of three
Evans, J. J. (1996). Behavioural assessment of the horizontal lines. In the figure copying portion of
dysexecutive syndrome. London: Harcourt Assessment. the subtest, the examinee is presented with a
drawing of a four-pointed star, a cube, and a
daisy in a vertical orientation where each of the
items are pointed out to the examinee prior to
Behavioral Inattention Test asking the examinee to draw the items. The
(BIT) shape copying portion of the same subtests con-
sists of the examinee drawing three geometric
Elena Polejaeva1 and Adam J. Woods2,3,4 shapes that are presented but not distinctly pointed
1
Department of Clinical and Health Psychology, out to the examinee. The representation drawing
University of Florida, Gainesville, FL, USA subtest requires the examinee to draw a clock face
2
Department of Clinical and Health Psychology, with numbers, a man or woman, and a butterfly.
College of Public Health and Health Professions, Both of the drawing subtests include images that
University of Florida, Gainesville, FL, USA tend to be bilaterally symmetric (Halligan et al.
3
Center for Cognitive Aging and Memory, 1991).
McKnight Brain Institute, University of Florida, The behavioral subtests of the BIT are com-
Gainesville, FL, USA prised of: menu reading, article reading, address/
4
Department of Neuroscience, University of sentence copying, telling/setting the time, tele-
Florida, Gainesville, FL, USA phone dialing, picture scanning, coin sorting,
card sorting, and map navigation. Menu reading
consists of a list of common food items presented
The Behavioral Inattention Test (BIT) was devel- in columns. The article reading subtest contains
oped in the United Kingdom in 1987 to assess three columns of text that are to be read by the
hemi-inattention and has predominantly been examinee. Address/Sentence copying asks the
used with stroke patients to assess unilateral examinee to copy four lines of an address and
Behavioral Inattention Test (BIT) 543

three lines of sentences. Telling/setting time rehabilitation, 0.385 (P = 0.004) for the conven-
requires the examinee to read the time on a digital tional BIT and 0.396 (P = 0.003) for the behav-
clock as well as analogue clock and to set time on ioral BIT subtests (Di Monaco et al. 2011). These
an analogue clock with moveable hands based on results indicate that the severity of unilateral spa-
the examiner’s verbal instructions. Telephone tial neglect should be accounted for when estimat- B
dialing utilizes a disconnected telephone and ing functional outcome poststroke and is
requires the examinee to dial three numbers pre- consistent with prior findings (Buxbaum et al.
sented in large print on separate cards. The picture 2004; Cherney et al. 2001). In general, studies
scanning subtest presents the examinee with three have found that unilateral spatial neglect contrib-
large color photographs of a plate of food, a bath- utes to worse functional outcomes and longer
room, and a hospital room. The examinee is asked rehabilitation durations (Gillen et al. 2005;
to look at each of the photos one at a time and to Franceschini et al. 2010). In fact, having unilateral
point as well as name the major items in each of spatial neglect was indicative of poorer functional
the photos. Coin sorting presents three rows of outcomes in 25 out of 26 studies examined and the
coins with six different denominations where the BIT has been shown to be the greatest predictor of
examinee is asked to identify and locate the coins function poststroke at 3, 6, and 12 months post-
as the examiner names various coins. The card injury (Jehkonen et al. 2006; Jehkonen et al.
sorting subtest involves the examiner pointing out 2000). To examine the ecological validity of the
each of the 16 cards to the examinee and then BIT, the behavioral subtests have been compared
asking the examinee to point to the card being to task performance as well as to Activities of
named by the examiner. Map navigation contains Daily Living (ADLs) checklist in patient samples.
a grid of different paths marked by a letter and as The results found that six out of the nine subtests
the examiner says letter pairs the examinee is correlated with task performance and ADLs.
asked to follow the path using their finger Additionally, seven out of the nine behavioral
(Halligan et al. 1991; Lezak et al. 2012). subtests were able to differentiate between indi-
The reliability of the BIT was initially based on viduals with and without spatial neglect
a small sample size but contained excellent test- (Hartman-Maeir and Katz 1995).
retest reliability with the behavioral subtest at Research studies often implement one or sev-
r = 0.97 and the conventional subtests at eral of the BIT subtests but this may not be an
r = 0.89. The conventional and behavioral sub- accurate way to distinguish unilateral neglect
tests are also highly correlated with each other at (Lopes et al. 2007). In cases where only one
r = 0.75. In terms of inter-rater reliability, the BIT subtest is administered, the sensitivity of the mea-
is also highly reliable with both the behavioral and sure may be lost. Lopes and colleagues found that
conventional subtests being r = 0.99 (Halligan all of the patients with hemi-neglect were properly
et al. 1991). Thus, the BIT has been a common identified using figure and shape copying as well
neuropsychological measure used to assess uni- as the representational drawing subtests. How-
lateral neglect postinjury and throughout recovery ever, this was not the case with other subtests of
(Azouvi 2016). Maximum total score for the con- the BIT when examined in a stand-alone manner.
ventional subtests is 146 with a clinical cutoff of Ultimately, the full BIT test administration is still
129. While the behavioral subtests total maximum recommended for greater sensitivity.
score is 81 with a clinical cutoff score of 67. When
an individual scores lower on either one of these
they are classified as having unilateral spatial References
neglect via BIT (Wilson et al. 1987a).
Using the BIT to predict functional outcomes, Azouvi, P. (2016). The ecological assessment of unilateral
neglect. Annals of Physical and Rehabilitation Medi-
one study found BIT scores to be significantly
cine. https://doi.org/10.1016/j.rehab.2015.12.005.
correlated with Functional Independence Measure Buxbaum, L. J., Ferraro, M. K., Veramonti, T., Farne, A.,
(FIM) scores at the time of discharge from Whyte, J., Ladavas, E., et al. (2004). Hemispatial
544 Behavioral Therapy

neglect: Subtypes, neuroanatomy, and disability. Neu-

rology, 62, 749–756. Behavioral Therapy
Cherney, L. R., Halper, A. S., Kwasnica, C. M., Harvey, R. L.,
& Zhang, M. (2001). Recovery of functional status
after right hemisphere stroke: Relationship with unilat- Glenn S. Ashkanazi
eral neglect. Archives of Physical Medicine and Reha- Department of Clinical and Health Psychology,
bilitation, 82, 322–328. Clinical and Health Psychology Clinic, College of
Di Monaco, M., Schintu, S., Dotta, M., Barba, S.,
Tappero, R., & Gindri, P. (2011). Severity of uni- Public Health and Health Professions, University
lateral spatial neglect is an independent predictor of of Florida, Gainesville, FL, USA
functional outcome after acute inpatient rehabilita-
tion in individuals with right hemispheric stroke.
Archives of Physical Medicine and Rehabilitation,
92, 1250–1255. Synonyms
Franceschini, M., La Porta, F., Agosti, M., &
Massucci, M. (2010). Is health-related-quality of Behavior management; Behavior modification
life of stroke patients influenced by neurological
impairments at one year after stroke? European
Journal of Physical and Rehabilitation Medicine,
46, 389–399. Definition
Gillen, R., Tennen, H., & McKee, T. (2005). Unilateral
spatial neglect: Relation to rehabilitation outcomes in Behavioral therapy is a type of psychotherapy
patients with right hemisphere stroke. Archives of Phys-
ical Medicine and Rehabilitation, 86, 763–767. that focuses on changing and gaining control over
Halligan, P. W., Cockburn, J., & Wilson, B. (1991). The unwanted behaviors based upon the principles of
behavioural assessment of visual neglect. Neuropsy- classical and operant conditioning. It is useful in
chological Rehabilitation, 1, 5–32. the treatment of depression, anxiety disorders, pho-
Hartman-Maeir, A., & Katz, N. (1995). Validity of the
behavioral inattention test (BIT): Relationships with bias, smoking cessation, weight loss, stuttering,
functional tasks. American Journal of Occupational enuresis, tics, and other medical conditions.
Therapy, 49, 507–516.
Heilman, K. M., Watson, R. T., & Walenstein, E. (1993).
Neglect and related disorders. In K. M. Heilman & E.
Valenstein (Eds.), Clinical neuropsychology (pp. Historical Background
279–336). New York: Oxford University Press.
Jehkonen, M., Ahonen, J. P., Dastidar, P., Koivisto, A. M., Attempts to help people solve behavioral prob-
Laippala, P., Vilkki, J., & Molnar, G. (2000). Visual lems through attempts that closely mirror today’s
neglect as a predictor of functional outcome one year
after stroke. Acta Neurologica Scandinavica, 101, “behavioral therapy” have a very long history. It is
195–201. based on the idea that all behaviors are learned and
Jehkonen, M., Laihosalo, M., & Kettunen, J. E. (2006). in the case of psychotherapy, these unhealthy
Impact of neglect on functional outcome after stroke: A behaviors can be changed.
review of methodological issues and recent research
findings. Restorative Neurology and Neuroscience, Nineteenth-century British penal colonies used
24, 209–215. “token economies” to reinforce inmates for obey-
Lezak, M. D., Howieson, D. B., Bigler, E. D., & Tranel, D. ing prison rules. The early Romans used “aversive
(2012). Neuropsychological assessment (5th ed.pp. conditioning” (e.g., placement of “putrid” spiders
428–439). New York: Oxford University Press.
Lopes, M. A., Ferreira, H. P., Carvalho, J. C., Cardoso, L., in the glasses of alcohol abusers) in order to
& Andre, C. (2007). Screening tests are not enough to decrease problem drinking. Seventeenth-century
detect hemineglect. Arquivos de Neuro-Psiquiatria, 65, French physicians were using “thought stopping”
1192–1195. to treat cases of obsessional thinking.
Wilson, B., Cockburn, J., & Halligan, P. W. (1987a).
Behavioural inattention test manual. Hants/Los Behavioral therapy’s philosophical roots are
Angeles: Thames Valley Test Company/Western Psy- from the school of behaviorism, which posits
chological Services. that psychological matters can be studied scientif-
Wilson, B., Cockburn, J., & Halligan, P. W. (1987b). ically by observing overt behaviors and without
Development of a behavioural test of visuospatial
neglect. Archives of Physical Medicine and Rehabilita- reference to internal mental states. Some of the
tion, 68, 98–102. early behavior therapists included Joseph Wolpe
Behavioral Therapy 545

(South Africa) and Hans Eysenck (United King- the rat is pressing the lever repeatedly to obtain the
dom). Perhaps the most well-known contributors food. Through “operant conditioning,” the rat’s
to the early development of behavioral therapy are behavior of pressing the lever is reinforced as the
Ivan Pavlov and B. F. Skinner. rat learns to pair the pressing of the lever with the
Ivan Pavlov (1849–1936) was a Russian phy- reward. B
sician and physiologist who published extensively In terms of behavioral therapy, human behav-
in the early part of the twentieth century on his ior can be affected by reinforcement in that
conditioned learning experiments, later to be desired behaviors can be rewarded (reinforced)
termed “classical conditioning.” In classical con- and thereby increase in frequency while undesired
ditioning, also called respondent conditioning, behaviors can be cut off from their reinforcement
Pavlov found that dogs would naturally salivate and extinguished. Skinner found that the fre-
(“unconditioned response”) when presented with quency and timing of the rewards given also
food (“unconditioned stimulus”). If he paired the affected how fast the new behaviors were acquired
presentation of the unconditioned stimulus with a and how hard it was to extinguish them. These
previously neutral stimulus, like a bell (“condi- became known as “schedules of reinforcement.”
tioned stimulus”), the previously neutral stimulus The work of Skinner also led to what is called
produced the same unconditioned response as the “shaping,” in which the desired behavior (e.g.,
unconditioned stimulus, even if the unconditioned training a chicken to peck a piano) could be grad-
stimulus was absent. The unconditioned response ually acquired by rewarding approximations to
thus became the “conditioned response” to the the behavior.
newly acquired conditioned stimulus. In other
words, Pavlov found that if he rang a bell before
feeding the dogs (who naturally salivated when Current Knowledge
the food was presented), eventually the bell ring-
ing alone would make the dogs salivate whether Behavioral therapy has been successfully used for
or not the food appeared. An important behavioral a variety of problem behaviors including, but not
therapy principle derived from this work is that if limited to, chronic pain, substance abuse, depres-
the conditioned stimulus (bell) is repeatedly pre- sion, phobias, autism, obesity, managing stress,
sented without the unconditioned stimulus (food), smoking cessation, anorexia, obsessive-
the conditioned response (salivation) decreases in compulsive disorder, and attention deficit/hyper-
intensity. This process is termed “extinction” and activity disorder. It has been extensively used in
can be found in human behavioral therapy in the patients with developmental disabilities, severely
treatment of phobias. For example, Wolpe treated disturbed psychotic patients, survivors of brain
phobic patients with a technique he named “sys- injury, and others where insight-oriented or cog-
tematic desensitization,” which involves gradu- nitive therapies may not be effective. There are a
ally exposing a patient to an anxiety-provoking myriad of methods involved including (but not
stimulus until the anxiety reaction is extinguished. limited to):
Burrhus Frederic (B. F.) Skinner (1904–1990)
expanded on the work of Pavlov with his concept • Self-monitoring
of “operant conditioning,” which postulates that • Systematic desensitization (SD)
behavior can be affected by rewards and punish- • Exposure and response prevention
ments. In a famous operant conditioning experi- • Contingency management
ment, a rat is in a box equipped with an automatic • Flooding
food dispenser. When the rat hears the dispenser • Modeling
releases food pellets, it moves to the food tray and • Applied behavior analysis
eats. Next, a lever is placed in the box that dis- • Operant conditioning
penses a few pellets of food when pressed. When • Respondent conditioning
the rat touches the lever, food is dispensed. Soon • Role-playing
546 Behavioral Therapy

Some of these techniques are used in everyday patients are taught relaxation skills to control
life. For example, parents and teachers place stars fear responses during exposure to the hierarchy.
on a refrigerator chart or bulletin board to reward Behavioral therapy treatment tends to be of
desirable behavior by children. Some techniques shorter duration than more traditional (e.g.,
involve accumulating points for performing a insight oriented) modes of psychotherapy (e.g.,
desired behavior, points that can later be psychodynamic). Initial sessions are dedicated to
exchanged for some desirable reinforcer. These the explanation of the basic tenets of behavioral
“token economies” are a variation of operant con- change (e.g., reinforcement, extinction, punish-
ditioning and are used in a variety of settings. In ment, etc.). Once established, a variety of tech-
addition, extinction of undesired behavior has niques may be utilized including:
penetrated the mainstream as seen by the use of
“time-out,” a technique involving the removal of a • Role-playing – therapist models desired behav-
child from reinforcement, seen by the child as iors or reactions.
somewhat aversive, or punishing, with the hope • Skills training – patient is taught new desired
of decreasing the unwanted behavior. behaviors to replace undesired ones for parent-
Behavioral therapy is based on the concepts ing, social situations, public speaking, etc.
that (1) targeted behaviors can be modified by a • Flooding – form of systematic desensitization
variety of behavioral techniques and (2) that the where the patient is exposed directly to the
newly acquired behaviors will be more adaptive feared stimulus to extinguish the fear response.
than the undesired ones. These techniques tend to • Modeling – patients learn responses simply by
be empirical (data-driven) and observable. They observing other individuals and repeating their
do not rely for their effectiveness on any mental behavior.
(cognitive) constructs like unconscious motiva- • Homework – patients are to try out new behav-
tions. They simply identify a behavior to change iors learned in therapy in real-life situations.
and change it rather than trying to understand why • Conditioning – application of reinforcement to
the individual was performing that behavior. An increase a desired behavior or the removal of
example of one of these techniques is the use of reinforcement to decrease an unwanted behav-
systematic desensitization. ior (e.g., token economies).
This technique is often used with people who • Relaxation training – used to help patients
have a specific phobia (e.g., fear of snakes, fear of relieve anxiety/tension, an important compo-
closed spaces, fear of heights, etc.). The phobic nent of systematic desensitization.
behavior can be defined as avoidance of, or escape
from, the phobic stimulus (e.g., escaping/running The use of behavioral therapy in the treatment
away from a spider or avoiding situations involv- of survivors of severe traumatic brain injury (TBI)
ing public speaking). By escaping from the phobic can be problematic. These problems can range
stimulus, patients can reduce their anxiety. The from aggression to agitation and from depression
behavior of escape/avoidance is reinforced since to nonadherence. Those who demonstrate severe
the reduction of the anxiety is reinforcing for the behavioral dyscontrol as a result of their TBI also
individual (negative reinforcement is a concept likely possess cognitive sequelae that hinder the
derived from operant conditioning). In SD, successful therapeutic use of these techniques.
patients are gradually exposed to the phobic stim- Persons with severe memory deficits may not be
uli, allowing them to acclimate themselves to it, able to recall the behavior they performed to earn
until they are able to tolerate it. Patients create a a reinforcer in a contingency management system.
hierarchy of fear steps that they must overcome to Memory problems may also interfere with a sur-
reach the last step, the phobic stimulus. These vivor’s ability to recall that a particular behavior
hierarchies can be imaginable pictures or actual led to a particular consequence. Without this abil-
exposure. Patients deal with each successive step ity to recall contingencies, survivors are likely to
until the hierarchy is completed. Typically, not be able to make different choices (i.e., make
Behaviorism 547

behavior changes) for which behavior they exhibit Cross-References

in given situations. Therefore, behavior manage-
ment strategies place special emphasis on control- ▶ Applied Behavior Analysis
ling environmental stimuli in order to reduce ▶ Behavioral Assessment
problem behaviors (e.g., disinhibition and agita- ▶ Behaviorism B
tion). One approach to examining these behaviors ▶ Cognitive Behavioral Therapy
sees behavioral dysfunction as more of a signal ▶ Homework
that a person is beyond their personal capacities to ▶ Psychotherapy
manage presenting challenges and thus requiring ▶ Relaxation Training
support that is contextually relevant. In this para- ▶ Social Skills Training
digm, “behavior” is seen as both a person’s com-
petencies and incompetencies in managing their
environment, personal functioning, emotional/ References and Readings
behavioral stability, and independence.
The goal of behavior therapy with moderate or Gelder, M. (1997). The future of behavior therapy. Journal
of Psychotherapy Practice, 6(4), 285–293.
mild TBI survivors is to provide the patient with a
Jacobs, H. (1993). Behavior analysis guidelines and brain
behavioral repertoire that they can use to solve injury rehabilitation: People, principles and programs.
daily life problems as a result of cognitive deficits Gaithersburg: Aspen Publishing Company.
(i.e., compensatory approaches). Critical behav- Jacobs, H. (2014). Perspectives on behavior and acquired
brain injury. NeuroRehabilitation, 34, 597–599.
ioral therapy techniques utilized include self-
Kazdin, A., & Hersen, M. (1980). The current status of
monitoring, scheduling of activities, role-playing, behavior therapy. Behavior Modification, 4(3), 283–302.
modeling, and contingency contracting. Masters, J., Burish, T., Holton, S., & Rimm, D. (1987).
Behavior therapy: Techniques and empirical findings.
San Diego: Harcourt Press Jovanovich.
Sobell, L., & Sobell, M. (2016). Individualized behavior ther-
Future Directions apy for alcoholics. Behavior Therapy, 47(6), 937–949.
Wilson, K. (1997). Science and treatment development:
Chronic diseases have replaced acute illness as the Lessons from the history of behavior therapy. Behavior
Therapy, 28, 547–558.
leading cause of premature death. These chronic
conditions often have unhealthy behaviors at their
root cause. Examples include cigarette smoking,
obesity, lack of exercise, poor nutritional habits,
Behaviorism
substance abuse, and medical noncompliance. For
this reason, behavioral therapy has demonstrated
Anthony Y. Stringer
great clinical value in the treatment and preven-
Department of Rehabilitation Medicine, Emory
tion of chronic health problems. An example of
University, Atlanta, GA, USA
behavioral therapy’s potential can be seen in the
work of Carl Simonton in the treatment of cancer
patients. His results confirm that patients who
Synonyms
have received behavioral treatment plus conven-
tional oncology treatment live twice as long as
Behavioral psychology; Cognitive behaviorism
patients who had received conventional cancer
treatment alone. Mark and Linda Sobell view
alcoholic drinking as a discriminated, operant Definition
response that can be treated through aversive con-
ditioning (electric shocks). Their research has Behaviorism is a psychological theory (and
important implications for future treatments branch of psychology), focusing on observable
since the experimental subjects functioned signif- behavior rather than mental phenomena, that
icantly better than controls post-intervention. attempts to explain behavior by learning
548 Bell Curve

principles such as classical and operant condition- Skinner, B. F. (1950). Are theories of learning necessary?
ing. In classical conditioning, an unconditioned Psychological Review, 57(4), 193–216.
Staddon, J. E. R. (2000). The new behaviorism: Mind, mech-
stimulus already eliciting a response is paired with anism, and society. Philadelphia: Psychology Press.
a neutral stimulus. With repeated pairing, the neu-
tral (conditioned) stimulus begins to elicit the
same response as the unconditioned stimulus.
Operant conditioning focuses on environmental
Bell Curve
consequences that increase (positive reinforce-
ment) or decrease (negative reinforcement) the fre-
Ericka L. Wodka
quency of behavior. Early behaviorists focused
Center for Autism and Related Disorders,
exclusively on observable behavior, while more
Kennedy Krieger Institute and The Johns Hopkins
recent cognitive behaviorists have applied learning
University School of Medicine, Baltimore,
principles to patterns of thought. As behaviorism
MD, USA
historically attempted to account for behavior
solely in terms of environmental factors, neuropsy-
chology has had limited impact on the develop-
Synonyms
ment of this approach to psychology. In contrast,
neuropsychologists have attempted to understand
Gaussian distribution; Normal curve; Normal
the neural mechanisms of learning, a notable exam-
distribution
ple being Donald Hebb’s seminal postulate that
concordant firing in synaptically coupled neurons
increases the strength of the connection between Definition
the two neurons. Despite behaviorism’s historical
avoidance of physiological explanations of behav- A normal distribution of observations/scores is
ior (Skinner 1950), those clinical neuropsycholo- shaped like a “bell,” with the majority of observa-
gists who include psychotherapy as part of their tions/scores occurring around the mean and
professional practice make use of classic and cog- increasingly fewer observations/scores occurring
nitive behavioral approaches in their work with farther (above/below) from the mean (68.26% of
brain injury survivors. observations/scores fall within one standard devi-
ation of the mean; 95.44% fall within two stan-
dard deviations of the mean). A normal
Cross-References distribution of observations is typical in large
samples acting additively and independently and
▶ Behavior Modification is assumed in parametric statistics (e.g., t-tests,
▶ Cognitive Behavioral Therapy ANOVA). Standardized scores derived from neu-
▶ Learning ropsychological measures are based upon
(assume) normal distribution of the standardiza-
tion sample. While this assumption provides a
References and Readings common metric that allows for direct comparison
of performance between different measures, it is
Beggs, J. M., Brown, T. Y., Byrne, J. H., Crow, T., LeDoux, important to note that score distributions for a
J. E., & LeBar, K. (1999). Learning and memory: Basic
number of neuropsychological tests are non-nor-
mechanisms. In M. J. Zigmond, F. E. Bloom, S. C.
Landis, J. L. Roberts, & L. R. Squire (Eds.), Funda- mal (e.g., Boston Naming Test, Wisconsin Card
mental neuroscience (pp. 1411–1454). San Diego: Sorting Test, Mini-Mental Status Exam, Test of
Academic. Memory Malingering). For this reason, selection
Mills, J. A. (1998). Control: A history of behavioural
of measures and interpretation of test findings
psychology. New York: New York University Press.
O’Donohue, W. T. (2001). The psychology of B.F. Skinner. must include consideration of score distributions
Thousand Oaks: Sage. (Strauss et al. 2006).
Bell’s Palsy 549

Cross-References to the anterior two thirds of the tongue and inner-

vates the stapedius muscle (a small muscle in the
▶ Base Rate (Population) middle ear, connecting the tympanic membrane to
▶ Cutoff Scores, Cutting Scores the stapes, that dampens excessive vibration in the
▶ Intelligence Quotient tympanic membrane due to loud noises). B
▶ Mental Age
▶ Percentiles Clinical Presentation
▶ Standard Scores The onset of paralysis may be preceded by pain
behind the ear for 1 or 2 days. The paralysis is
complete in 2 days in half the patients and by
References and Readings 5 days in almost all the patients. If the stapedius
muscle is involved, there may be sensitivity to
Lezak, M. D., Howieson, D. B., Bigler, E. D., & Tranel, D. noise. Taste is impaired in almost all patients.
(2012). Neuropsychological assessment (5th ed.). New
Clinically, the forehead is unfurrowed, the eye
York: Oxford University Press.
Sattler, J. M. (2001). Assessment of children: Cognitive cannot close fully, the lower eyelid droops, and
foundations (5th ed.). La Mesa: Jerome M. Sattler. tears may run down the cheek. Due to weakness of
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A the oral muscles, saliva may drip from the corner
compendium of neuropsychological tests: Administra-
of the mouth on the effected side.
tion, norms, and commentary (3rd ed., pp. 3–43). New
York: Oxford University Press. This is distinguished from a central facial palsy
(e.g., due to stroke), by forehead weakness and
weakness of eye closure. In a central facial weak-
ness, there is little or no forehead involvement. In
Bell’s Palsy the Bell’s palsy, the forehead is unfurrowed and
the eyebrow is lower than on the uninvolved side
Theslee Joy DePiero and cannot be voluntarily raised. In a central facial
Braintree Rehabilitation Hospital, Boston weakness, the eyelid closes fully, though closure
University School of Medicine, Boston, MA, USA may be weaker than on the uninvolved side. In
Bell’s palsy, eye closure is incomplete, and the
lower sclera and cornea may be reddened due to
Synonyms exposure to air without lubrication from tears.

Idiopathic facial paralysis Epidemiology

• Incidence: 23/100,000 annually.
• Cases in women and men are equal.
Definition • Season: no seasonal preference.
• Age: occurs equally in all age groups.
Bell’s palsy is the acute onset of paralysis of the
muscles innervated by the facial nerve, not due to Etiology
obvious causes such as trauma, stroke, or local The etiology of Bell’s palsy is thought to be viral.
infection. The genome of herpes simplex virus type 1 has
been identified in the fluid surrounding the facial
nerve in several cases, but there is no convincing
Current Knowledge evidence that this is the case in the majority of cases.
Lyme disease can also cause Bell’s palsy. In
Anatomy endemic areas, Lyme disease antibody tests
The facial nerve innervates the muscles that con- should be done.
trol the forehead and eyebrow, close the eyelids, Ramsay-Hunt syndrome refers to Bell’s palsy
and move the cheeks and lips. It also supplies taste caused by varicella zoster (the virus that causes
550 Bender Visual-Motor Gestalt Test II

chicken pox and shingles). The distinguishing Description

characteristic of Ramsay-Hunt is the presence of
vesicles (small fluid filled blisters) in the eternal The Bender-Gestalt test was first published in
auditory canal or on the eternal ear. 1938, as a brief measure of visual-motor func-
tioning. As with any measure, research identifies
Treatment various measurement, scoring, and standardiza-
Antiviral agents are not effective in idiopathic tion issues. Recent research culminated in the
cases. Steroids (prednisone is most common) revision of the test, the Bender-Gestalt, Second
decrease the probability of permanent paralysis or Edition (BG-II), which was revised by Branni-
aberrant reinnervation. Because of the paralysis of gan and Decker in 2003. The BG-II maintains
the muscles that close the eye, the cornea must be many historical properties that appealed to clini-
protected, especially at night. Artificial tears, liquid cians, while improving the psychometric ade-
or ointment, and taping the eye shut are common quacy of the test. The BG-II is divided into two
treatments. phases: copy and recall. The copy phase requires
Antiviral treatment is indicated in Ramsay- the duplication of 16 geometric images, shown
Hunt, as is antimicrobial treatment in Lyme- sequentially on separate 3  5 cards, onto a blank
positive patients. piece of paper with a No. 2 pencil. The recall
phase involves drawing these images from mem-
Prognosis ory on a new sheet of paper. Using the Global
Eighty percent recover within a few weeks to Scoring System, the drawing productions are
2 months. Recovery of some motor function in rated on a 5-point scale based on the similarity
the first week is a good prognostic sign. to the original image and yield percentile ranks,
scaled scores, T-scores, and confidence intervals.
Additionally, the BG-II also contains two sup-
Cross-References
plemental measures to screen for specific diffi-
culties and can be used to better understand low
▶ Lyme Disease
performance.
Like the original, the BG-II has high reliabil-
ity and validity and discriminates performance in
References and Readings
individuals with a variety of learning and psy-
Gilden, D. (2004). Clinical practice. Bell’s palsy. New chological problems. It is this latter finding – that
England Journal of Medicine, 351, 1323–1331. individuals from a wide variety of clinical con-
Hazin, R., Azizzadeh, B., & Bhatti, M. (2009). Medical ditions show poor performance on line copy
and surgical management of facial nerve palsy. Current tasks – that contributes to the test’s clinical util-
Opinion in Opthalmology, 20(6), 440–450.
ity. Unfortunately, theoretical explanations for
poor performance as well as explanations for
qualitative errors, such as figure rotations and
Bender Visual-Motor Gestalt perseverations, are still lacking. Although previ-
Test II ous research incorporated the use of psychody-
namic and personality paradigms, the most
Scott L. Decker and Rachel M. Bridges evidence-based supported inference of perfor-
Department of Psychology, University of South mance on the BG-II is as a measure of visual/
Carolina, Columbia, SC, USA perceptual-motor integration. Although many
subcomponents are required in performance
such as visual acuity and graphomotor skills,
Synonyms the integration of a visual percept with a motor
programming controlling seems to be the largest
Bender-Gestalt, Second Edition; BG-II source of variance on test performance (Decker
Benign Senescent Forgetfulness 551

et al. 2006). Additionally, research with the References and Readings

BG-II has shed insight on the development of
visual-motor abilities across the life-span(- Bender, L. (1938). A visual motor Gestalt test and its
clinical use. New York: American Orthopsychiatric
Decker 2008). Specifically, using this measure
Association.
it has been demonstrated that visual-motor inte- Decker, S. L. (2008). Measuring growth and decline in B
gration rapidly matures into adolescence, gradu- visual motor processes with the Bender-Gestalt, Sec-
ally declines through adulthood, and rapidly ond Edition. Journal of Psychoeducational Assess-
ment, 26, 3–15.
decreases in late adulthood.
Decker, S. L., Allen, R., & Choca, J. P. (2006). Construct
validity of the Bender-Gestalt II: Comparison with
Wechsler intelligence scale for children III. Perceptual
and Motor Skills, 102, 113–141.
Historical Background Koppitz, E. M. (1963). The Bender Gestalt test for young
children. New York: Grune and Stratton.
The Bender-Gestalt has historically been one of Lacks, P. (1999). Bender Gestalt screening for brain dys-
function (2nd ed.). New York: Wiley.
the most used measures in psychology. The Pascal, G. R., & Suttell, B. J. (1951). The Bender Gestalt
Bender-Gestalt originated from Lauretta test. New York: Grune & Stratton.
Bender’s research in perception and psychopa- Wertheimer, M. (1923). Studies in the theory of Gestalt
thology. She adapted designs used by psychology. Psychologische Forschung, 4, 301–350.
Wertheimer (1923) to be used as a measure of
development and psychopathology. Initially, per-
formance was qualitatively interpreted, but even-
Benign Senescent
tually the need for standardized scoring systems
Forgetfulness
emerged. Numerous scoring systems have been
developed, with the most notable being the Pas-
Richard F. Kaplan and Joshua Johnson
cal and Suttell (1951) method, the Koppitz
Department of Psychiatry (MC-2103), UConn
(1963) developmental scoring system, and
Health Center, Farmington, CT, USA
Lacks (1999) scoring system for screening for
brain dysfunction. The various scoring tech-
niques and the multifaceted use of the Bender-
Synonyms
Gestalt test, whether used as a “warm-up” prior
to more intellectually challenging tasks or to
Age-associated memory impairment (AAMI);
screen for brain injury, have contributed to the
Late-life forgetfulness
long-standing and sustained use of the measure.

Definition
Clinical Uses
The term “benign senescent forgetting” was
The Bender-Gestalt was initially utilized by coined by V.A. Kral (see Kral 1962) to describe
Lauretta Bender as a measure of perception and an age-related memory decline that is distinct
psychopathology. from memory impairment due to known neuro-
The BG-II is appropriate for use with chil- logical damage or disease.
dren as young as 4 years old to individuals over
the age of 85 years old and typically takes no
longer than 15 min to administer. It has been Current Knowledge
used extensively for educational, medical, and
other purposes, particularly in education as a Changes in cognitive functioning are prevalent in
determinant of fine motor or visual-spatial aging populations. It has become clear that there is
difficulties. most likely a continuum between normal and
552 Benton Visual Retention Test

abnormal mental function in those individuals Practice parameter: Early detection of dementia: Mild
who will ultimately develop dementia. Recent cognitive impairment (an evidence-based review)
report of the quality standards Subcommittee of the
studies focusing on the characterization of the American Academy of neurology. Neurology, 56,
earliest stages of cognitive impairment have 1133–1142.
identified an intermediate period between the Smith, G., & Rush, B. K. (2006). Normal aging and mild
cognitive changes of normal aging and dementia cognitive impairment. In D. K. Attix & K. A. Welch-
Bohmer (Eds.), Geriatric neuropsychology assessment
(see Petersen et al. 2001). This transitional zone and intervention (pp. 27–56). New York: Guilford.
has been described using a variety of terms,
including benign senescent forgetfulness (BSF),
age-associated memory impairment (AAMI),
age-associated cognitive decline (ACCD), cog-
nitive impairment-no dementia (CIND), and, Benton Visual Retention Test
most recently, mild cognitive impairment
(MCI). AAMI differs from BSF in that it includes Carlye B. G. Manna1, Carole M. Filangieri2,
specific memory test performance criteria of 1 SD Joan C. Borod3,4, Karin Alterescu1 and
below young-adult levels (see Larrabee and Crook H. Allison Bender4
1
1994). AACD expands the definition to decre- Department of Psychology, Queens College of
ments in performance in other cognitive domains. the City University of New York (CUNY),
MCI further refined the definition to include the Flushing, NY, USA
2
presence of memory complaints, normal activities Department of Behavioral Health, NYU
of daily living, normal global cognitive function- Winthrop Hospital, Mineola, NY, USA
3
ing, but abnormal memory performance compared Department of Psychology, Queens College and
to age- and education-matched controls (see Smith The Graduate Center of the City University of
and Rush 2006). The clinical concept of MCI is New York (CUNY), Flushing, NY, USA
4
important because it is a significant risk factor for Department of Neurology, Icahn School of
dementia. While conversion rates vary widely, Medicine at Mount Sinai, New York, NY, USA
most researchers estimate that individuals with
MCI develop dementia at a rate of 10–15% per
year, in contrast to the rate of 1–2% per year for Synonyms
age-matched controls.
Benton test; BVRT

Cross-References Description

▶ Age Decrements The Benton Visual Retention Test (BVRT) is a

▶ Mild Cognitive Impairment widely used test of visual memory, visual percep-
▶ Normal Aging tion, and/or visual construction. Now in its fifth
edition (Sivan 1992), the test consists of three
equivalent forms (Forms C, D, and E), each com-
References and Readings posed of ten items of visual stimuli. Most items
include three geometric forms presented along a
Kral, V. A. (1962). Senescent forgetfulness: Benign and
malignant. Journal of the Canadian Medical Associa-
horizontal plane, making the test particularly sen-
tion, 86, 257–260. sitive to visual neglect (Sivan 1992).
Larrabee, G. J., & Crook, T. H. (1994). Estimated preva- The following description of the BVRT
lence of age-associated memory impairment derived was adapted from Strauss et al. (2006). The
from standardized tests of memory function. Interna-
test includes four alternative methods of adminis-
tional Psychgeriatrics, 6, 95–104.
Petersen, R. C., Stevens, J. C., Ganguli, M., Tangalos, tration (A, B, C, and D) that assess different
E. G., Cummings, J. L., & DeKosky, S. T. (2001). aspects of functioning. The most common
Benton Visual Retention Test 553

administration (A) assesses immediate recall of a separate normative data. As an addition to the
visual display. After presenting a stimulus card for digit span test, the BVRT was intended to provide
10 s, the card is removed, and the examinee is a broader assessment of short-term memory, and
asked to draw the design from memory. Adminis- its format was selected for its resistance to emo-
tration B follows the same procedure as A, but tional influence, employment of different sensori- B
with a 5-s exposure interval. Administration motor components (graphomotor versus auditory-
C allows the examiner to dissociate memory func- vocal), and minimal examiner-subject interaction
tioning from perceptual and motor aspects of the (freedom from interpersonal demands). The initial
task by asking the examinee to reproduce the version included seven cards and two parallel
designs while each item is in plain view. There is forms. A 1955 revision increased the number of
no time limit, but individuals who work very designs and alternate forms and added norms for
slowly should be encouraged to increase their children aged 8–16. Later editions included a
speed. In Administration D, a 15-s interval is design copy administration and updated norms.
inserted between the 10-s encoding phase and The most recent revision was authored by Abigail
the figure reproduction, allowing the examiner to Benton Sivan (Sivan 1992) and is available from
assess short-term retention of visual information. its publisher, Pearson Assessments (http://
Scoring consists of both the number of correct pearsonassess.com).
designs and the number of six different types of
errors: omissions, distortions, perseverations,
rotations, misplacements, and size errors. Admin- Psychometric Data
istration time for each form is approximately
5 min. Several sets of norms are available and Information on reliability and validity may be
reflect different demographic characteristics, found in the manual. Test-retest reliability is
including age ranges and education levels 0.85. Alternate form reliability ranges from 0.79
(Mitrushina et al. 2005; Strauss et al. 2006). to 0.84. There is evidence that Form C is slightly
A multiple-choice recognition administration less difficult than Forms D and E under Adminis-
(Administration M, with alternate forms F and tration A. Correlations between immediate
G) is also sometimes used to assess visual mem- (Administration A) and delayed (Administration
ory without visuoconstructional or motor coordi- D) recall are positive and range from 0.40 to 0.83,
nation demands (Amieva et al. 2006). For depending on the combination of forms used.
Administration M, the examinee views a target Construct validity has been demonstrated through
stimulus for 10 s and, after it has been removed, moderate correlations (0.46–0.62) of the BVRT
is required to identify it from among four choices. with nonverbal subtests from the Wechsler Adult
Although not part of the English-language ver- Intelligence Scales.
sion, materials for this special administration are Child and adolescent normative data are
available in the German (Sivan and Spreen 1996) included for Administrations A and C. The nor-
and French (Benton 1965) editions. mative data for each method of administration are
based on different standardization samples, and
sample characteristics are provided for
Historical Background Administrations A, B, and C. (Normative data
for Administration D are not included in the man-
Dr. Arthur L. Benton developed the Visual Reten- ual.) The standardization sample for Administra-
tion Test as a brief measure of immediate nonver- tion A is based on a compilation of three separate
bal memory to supplement the popular auditory studies totaling over 1,300 participants, ranging in
digit span test in neuropsychological evaluations age from 8 to 69. (See manual for discussion of
(Benton 1945). It was first published in 1946. participant inclusion criteria for each of these
Memory-for-designs tasks had appeared earlier studies.) The standardization sample for Admin-
in the century as part of larger intelligence tests istration B is based on 103 medical inpatients and
but included only a few designs and did not have outpatients, aged 16–60 years, with no evidence
554 Benton Visual Retention Test

or history of brain disease. The standardization did not differ between the two administrations
samples for Administration C are 200 medical (Vakil et al. 1989).
patients with no history of brain disease for the Both copy and memory administrations are
adult norms and 236 children, aged 6–13 years, highly sensitive to early dementia and may also
enrolled in public schools in Iowa and Wisconsin help to identify individuals who are at risk for
for the child and adolescent norms. developing dementia in the future. In one such
study, participants with six or more errors on
Administration A were nearly twice as likely to
Clinical Uses develop Alzheimer’s disease 10–15 years later,
when compared to participants who had fewer
As it recruits a number of different cognitive errors (Kawas et al. 2003). The BVRT also aids in
functions, the BVRT is sensitive to many forms identifying children with a learning disability and
of brain damage and disease; however, its ability discriminating among types of learning disabilities,
to discriminate among diagnoses is low (for a with reading deficits associated with the lowest
review, see Mitrushina et al. 2005). An individ- levels of performance (Snow 1998). Poorer perfor-
ual’s global performance, quantified as either the mance on the BVRT in learning disabilities has
number correct score or error score, provides the been linked with deficits in the identification
best indicator of impairment. According to the of facial emotional expression (Dimitrovsky
manual, measures of specific error types, such as et al. 1998). Children with attention-deficit/
omissions, perseverations, and distortions, are not hyperactivity disorder receiving stimulant medica-
by themselves diagnostic but may raise hypothe- tion have also been shown to perform more poorly
ses for further testing. For example, a high number on the BVRT than healthy participants (Risser and
of perseverative errors suggests possible frontal Bowers 1993). Poorer performance is also evident
lobe damage, particularly if supported by other in a subset of patients with schizophrenia and may
test and behavioral data. Omission of peripheral result from abnormal patterns of visual scanning
figures may raise suspicion of brain damage and is and fixation related to deficient attention (Obayashi
most frequently associated with left hemispatial et al. 2003) or be related to poor executive func-
neglect as a result of damage to right parietal lobe tions (Egan et al. 2011). Another clinical applica-
regions. In contrast, global performance has not tion is the inclusion of the BVRT in a
been found to consistently distinguish between neuropsychological battery for the prediction of
patients with unilateral right and left brain dam- driving safety in patients with early dementia
age. Though the BVRT is sensitive to visuospatial (Dawson et al. 2009). The BVRT may also be
disturbance often observed in patients with right useful in detecting malingering, which has been
hemisphere damage, studies have shown that indi- characterized by a greater number of errors, partic-
viduals with unilateral left hemisphere damage ularly distortion errors, than seen in neuropsycho-
can exhibit similarly poor results on Administra- logically impaired patients (Suhr et al. 1997).
tion A (Vakil et al. 1989), as well as on copy and In evaluating results, it is important to consider
multiple-choice administrations (Arena and that the BVRT may also be sensitive to individual
Gainotti 1978). This indicates that memory for differences that do not reflect neuropathology.
the BVRT designs, many of which can be verbal- Stratified normative data confirm that age is neg-
ized, is mediated by both hemispheres. However, atively correlated and that baseline intellectual
the presence of a delay interval may differentially functioning is positively correlated with the
affect verbally and visually encoded material. Par- BVRT number correct score. The association
ticipants with right hemisphere damage achieved with baseline intellect is strongest in the lower
a lower total correct score on Administration than average IQ ranges. Education-stratified
D than Administration A, whereas individuals norms are also available and indicate a positive
with left hemisphere damage had the opposite relationship between years of education and the
pattern of performance, benefitting from the number correct score (Strauss et al. 2006).
delay. In contrast, scores from healthy participants Declines in executive function and attention
Benton Visual Retention Test 555

with normal aging have been associated with Dawson, J. D., Anderson, S. W., Uc, E. Y., Dastrup, E., &
lower BVRT scores and may be related to educa- Rizzo, M. (2009). Predictors of driving safety in early
Alzheimer disease. Neurology, 72, 521–527.
tional level or “cognitive reserve.” In a large Dimitrovsky, L., Spector, H., Levy-Shiff, R., & Vakil, E.
sample of healthy elderly adults, those with (1998). Interpretation of facial expressions of affect in
higher education performed better by using a children with learning disabilities with verbal or non- B
more exhaustive search strategy in the multiple verbal deficits. Journal of Learning Disabilities, 31,
286–292.
choice administration (Le Carret et al. 2003). The Egan, G. J., Hasenkamp, W., Wilcox, L., Green, A., Hsu, N.,
BVRT is used worldwide, and normative data Boshoven, W., Lewison, B., Keyes, M. D., & Duncan, E.
have been published from more than a dozen (2011). Declarative memory and WCST-64 perfor-
countries (Mitrushina et al. 2005). Most studies mance in subjects with schizophrenia and healthy con-
trols. Psychiatry Research, 188, 191–196.
have shown no gender differences. While rela- Kawas, C. H., Corrada, M. M., Brookmeyer, R.,
tively few in number, studies involving direct Morrison, A., Resnick, S. M., Zonderman, A. B., &
cross-cultural comparisons demonstrate gener- Arenberg, D. (2003). Visual memory predicts Alzhei-
ally good consistency; however, caution is mer’s disease more than a decade before diagnosis.
Neurology, 60, 1089–1093.
recommended when testing individuals with Le Carret, N., Rainville, C., Lechevailler, N., Lafont, S.,
very low levels of education (Mitrushina et al. Letenneur, L., & Fabrigoule, C. (2003). Influence of
2005). Results from a large Columbian sample of education on the Benton visual retention test perfor-
school-aged children did not differ from North mance as mediated by a strategic search component.
Brain and Cognition, 53, 408–411.
American norms (Rosselli et al. 2001), Mitrushina, M. N., Boone, K. B., Razani, J., & D’Elia, L. F.
suggesting that when educational quality is sim- (2005). Handbook of normative data for neuropsycho-
ilar, as is increasingly more common in devel- logical assessment (2nd ed.). New York: Oxford Uni-
oped countries, cross-cultural differences, if versity Press.
Obayashi, S., Matsushima, E., Ando, H., Ando, K., &
present, are relatively small. Kojima, T. (2003). Exploratory eye movements during
the Benton visual retention test: Characteristics of
visual behavior in schizophrenia. Psychiatry and Clin-
ical Neurosciences, 57, 409–415.
See Also Risser, M. G., & Bowers, T. G. (1993). Cognitive and
neuropsychological characteristics of attention deficit
▶ Short-Term Memory hyperactivity disorder children receiving stimulant med-
ications. Perceptual and Motor Skills, 77, 1023–1031.
▶ Visual-Motor Function Rosselli, M., Ardila, A., Bateman, J. R., & Guzman, M.
▶ Visuoperceptual (2001). Neuropsychological test scores, academic perfor-
▶ Wechsler Memory Scale All Versions mance, and developmental disorders in Spanish-speaking
children. Developmental Neuropsychology, 20, 355–373.
Sivan, A. B. (1992). Benton visual retention test (5th ed.).
San Antonio: Psychological Corporation.
Further Reading Sivan, A. B., & Spreen, O. (1996). Der Benton-Test
(7th ed.). Bern: Verlag Hans Huber.
Amieva, H., Gaestel, Y., & Dartigues, J. (2006). The Snow, J. H. (1998). Clinical use of the Benton visual retention
multiple-choice formats (forms F and G) of the Benton test for children and adolescents with learning disabilities.
visual retention test as a tool to detect age-related mem- Archives of Clinical Neuropsychology, 13, 629–636.
ory changes in population-based studies and clinical Strauss, E., Sherman, E. M. S., & Spreen, O. (2006).
settings. Nature Protocols, 1, 1936–1938. A compendium of neuropsychological tests: Adminis-
Arena, R., & Gainotti, G. (1978). Constructional apraxia tration, norms, and commentary (2nd ed.). New York:
and visuoperceptive disabilities in relation to laterality Oxford University Press.
of lesions. Cortex, 14, 463–473. Suhr, J., Tranel, D., Wefel, J., & Barrash, J. (1997). Mem-
Benton, A. L. (1945). A visual retention test for clinical ory performance after head injury: Contributions of
use. Archives of Neurology and Psychiatry, 54, malingering, litigation status, psychological factors,
212–216. and medication use. Journal of Clinical and Experi-
Benton, A. L. (1965). Manuel pour l’application du test de mental Neuropsychology, 19, 500–514.
rétention visuelle (1965). Paris: Les Editions du Centre Vakil, E., Blachstein, H., Sheleff, P., & Grossman,
de Psychologie Applique. S. (1989). BVRT-scoring system and time delay in the
Benton, A. L. (1974). Revised visual retention test: Clini- differentiation of lateralized hemispheric damage.
cal and experimental applications (4th ed.). New York: International Journal of Clinical Neuropsychology,
Psychological Corporation. 11, 125–128.
556 Benton, Arthur (1909–2006)

Major Appointments
Benton, Arthur (1909–2006)
• Dr. Benton volunteered for military service in
Steven W. Anderson the US Navy in 1941 and was commissioned as
University of Iowa Hospitals and Clinics, Iowa a lieutenant in the medical department. His
City, Iowa, USA active duty ended in 1945, but he continued to
serve in the US Navy Reserve for many years,
eventually retiring at the rank of captain. In
Landmark Clinical, Scientific, and 1946, he accepted a position in the Psychology
Professional Contributions Department at the University of Louisville. In
1948, he became a professor at the University of
• Arthur Benton was one of the pioneering Iowa, where he would remain for over 50 years.
figures in clinical neuropsychology. Begin- He initially was appointed Professor and Direc-
ning in the 1940s, he introduced and applied tor of Graduate Training in Clinical Psychology
novel and objective assessment techniques and then accepted a joint appointment in the
that provided a basis for fundamental brain- Departments of Psychology and Neurology in
behavior studies in aphasia, visuospatial 1958. He officially retired in 1978 but remained
abilities, hemispheric specialization, and active in research, teaching, and other profes-
other cognitive processes. Through the sional activities for another 20 years.
development of standardized tasks that
stressed specific abilities, together with the
collection of data from neurological patients Major Honors and Awards
and normal comparison subjects, he was
able to bring increased reliability and sensi- • President, American Orthopsychiatric Associ-
tivity to the mental status exam, helping to ation, 1965
establish neuropsychology as a valuable • President, International Neuropsychological
clinical entity. He developed a number of Society, 1970
neuropsychological tests that have been in • Secretary-General, Research Group on Apha-
wide use in clinical and research settings sia of the World Federation of Neurology,
worldwide for several decades, including the 1971–1978
Visual Retention Test, Judgment of Line Ori- • Distinguished Professional Contribution
entation, Three-Dimensional Block Construc- Award, American Psychological Association,
tion, and Facial Recognition. He advocated a 1978
flexible approach to clinical assessment, with • Outstanding Scientific Contribution Award,
the content and scope of testing determined by International Neuropsychological Society,
the referral question, context, and patient 1981
abilities. • Samuel Torrey Orton Award, Orton Dyslexia
Society, 1982
• Distinguished Service and Outstanding Contri-
Education and Training bution Award, American Board of Professional
Psychology, 1985
He received his B.A. and M.A. degrees from • Distinguished Clinical Neuropsychologist
Oberlin College and completed his Ph.D. at Award, National Academy of Neuropsychol-
Columbia University in 1935 under the mentor- ogy, 1989
ship of Carney Landis, followed by clinical train- • Gold Medal Award for Life Achievement in
ing at the Payne Whitney Psychiatric Clinic of the Application of Psychology, American Psy-
New York Hospital. chological Foundation, 1992 (Fig. 1)
Benton, Arthur (1909–2006) 557

the Division of Neurosurgery) and Dr. Maurice

Van Allen (Iowa City VA Hospital). From its
inception, his neuropsychology program was
dedicated to the tripartite goals of scientific
investigation, patient care, and student training, B
united by a focus on developing objective psy-
chological measures for the impairments
resulting from brain dysfunction. The beginnings
Benton, Arthur (1909–2006), Fig. 1 Benton, Arthur of the program were quite humble, with the orig-
(1909–2006) inal neuropsychology unit being housed in a
windowless 5  60 room shared with the Depart-
ment of Urology, which utilized it for “special
purposes.”
Biography The laboratory rapidly expanded, and with
access to the high volume of neurological
Arthur Benton was born in New York City on patients at the University Hospitals and other
October 16, 1909. Educated at Oberlin and nearby institutions, Benton and his students sys-
Columbia, he was a great historian who could tematically approached each of the primary
trace his academic lineage to the earliest psychol- domains of cognition, devising and validating
ogists. During his military assignment to the San tests of language, memory, attention, visual per-
Diego Naval Hospital prior to beginning his aca- ception, visuomotor abilities, auditory recogni-
demic career, he worked with neurologist Morris tion, tactile perception, body schema, and more.
Bender and examined servicemen with traumatic The enduring value of their empirical approach is
brain injury. This experience helped convince reflected in the fact that several of these tests
him of the value of standardized clinical tests remain in the batteries of most neuropsycholo-
and led to the development of the Benton Visual gists today.
Retention Test. Benton advocated a hypothesis-testing
During his first academic appointment at the approach to neuropsychological evaluation.
University of Louisville, Benton cowrote with According to this flexible approach, hypotheses
Spafford Ackerly the seminal paper on childhood- regarding the patient’s condition would arise from
onset damage to the prefrontal cortex. This detailed behavioral observations, the patient’s history, and
neuropsychological and neuroanatomical study of performances on an initial brief battery of tests.
a single patient dispelled the notion that early dam- These hypotheses would then be tested with sub-
age to the brain was always followed by good sequent targeted behavioral tests. “I think that we
recovery and presaged later work illuminating the should regard neuropsychological assessment in
prefrontal cortex as a critical region underlying the same way as we view the physical or neuro-
social and emotional behavior. logical examination, i.e., as a logical, sequential
In 1948, Benton began his long career at the decision-making process rather than as simply
University of Iowa when he took the position of the administration of a fixed battery of tests”
Professor and Director of Graduate Training in (Benton 1985). He was a strict empiricist and
Clinical Psychology. Two years later, A.L. Sahs, did not hesitate to challenge popular beliefs if
Chairman of the Department of Neurology at the his data indicated otherwise. Perhaps the best
University of Iowa Hospitals and Clinics, invited known was his characterization of the
him to set up a laboratory in the hospital for the Gerstmann syndrome as “. . . a fiction; it is sim-
purpose of studying behavioral impairments ply an artifact of defective and biased observa-
related to brain disease, a move strongly tions” (1961), based on his systematic
supported by Dr. Russell Meyers (Chairman of observation that the components of the
558 Benton, Arthur (1909–2006)

Gerstmann syndrome did not co-occur with one Department of Neurology remains a vital pro-
another anymore than with deficits not consid- gram for research, training, and patient care, in
ered part of the syndrome. the tradition established by Dr. Benton more
Benton was instrumental in bringing together than a half century ago.
the international neuropsychological community. Benton’s wife, Rita, was a professor of musi-
He used his knowledge of French, German, and cology at the University of Iowa, where she was
Italian to translate and bring to attention reports of the first head of the Music Library in 1957. Arthur
neurological syndromes that had been largely over- and Rita met in 1939 while they both were
looked because they were published in languages vacationing in Paris, and they married later that
other than English. He was a visiting scholar at the year. Upon Rita Benton’s death in 1980, the Music
University of Milan (1964); the Neurosurgical Library was named in her honor. They had three
Clinic, Hospital Sainte-Anne, Paris (1968); the children: Raymond, Abigail, and Daniel. Arthur
Hebrew University Medical School, Jerusalem Benton died in Glenview, Illinois, on December
(1969); the Free University of Amsterdam (1971); 27, 2006, from complications of emphysema, at
the University of Helsinki (1974); the Tokyo Met- the age of 97.
ropolitan Institute of Gerontology (1974); the Uni-
versity of Melbourne (1977); L’Ecole des Hautes
Etudes, Paris (1979); the University of Victoria, Cross-References
British Columbia (1980); the University of Minne-
sota Medical School (1980); and the University of ▶ American Board of Professional Psychology
Michigan (1986). (ABPP)
In the context of all of his professional accom- ▶ American Psychological Association (APA)
plishments, Dr. Benton’s dedication to education ▶ Aphasia
in neuropsychology was perhaps his greatest con- ▶ Benton Visual Retention Test
tribution. During neuropsychology’s formative ▶ Clinical Neuropsychology
years, he was instrumental in developing training ▶ Facial Recognition Test
standards for the field. At the first scientific ses- ▶ Flexible Battery
sion of the INS, held in Washington, D.C., in ▶ Frontal Lobe
1967, he moderated an afternoon symposium on ▶ Gerstmann’s Syndrome
the development of a comprehensive training pro- ▶ Hemispheric Specialization
gram in neuropsychology, and he remained active ▶ Hypothesis Testing Approach to Evaluation
in refining these standards over the years. At the ▶ Judgment of Line Orientation
University of Iowa, he supervised 46 doctoral dis- ▶ Mental Status Examination
sertations and 24 master’s theses, and he provided ▶ Multilingual Aphasia Examination
consultation to leading neuropsychology centers ▶ National Academy of Neuropsychology (NAN)
around the world. He was known for supervision ▶ Standardized Tests
characterized by frankly honest feedback, often
bruising to the student’s ego, but always accom-
panied by sage guidance for improving the References
situation.
Dr. Benton officially retired in 1978, at which Ackerly, S. S., & Benton, A. L. (1948). Report of a case of
time the Benton Laboratory of Neuropsychol- bilateral frontal lobe defect. In The frontal lobes; pro-
ceedings of the Association for Research in Nervous
ogy in the Department of Neurology was dedi-
and Mental Disease 1947, 27 (pp. 479–504). Balti-
cated. His retirement was incomplete, however, more: Williams and Wilkins.
as he continued to provide guidance for the Benton, A. L. (1945). A visual retention test for clinical
neuropsychologists at Iowa and elsewhere and use. Archives of Neurology and Psychiatry, 54,
212–216.
continued writing for more than another two
Benton, A. L. (1955). Right-left discrimination and finger-
decades. Today, the Benton Neuropsychology localization in defective children. Archives of Neurol-
Laboratory at the University of Iowa ogy and Psychiatry, 74, 383–389.
Ben-Yishay, Yehuda (1933–) 559

Benton, A. L. (1956). The concept of pseudo- • 1967–1974 Associate Professor of Clinical

feeblemindedness. Archives of Neurology and Psychi- Rehabilitation Medicine, New York University
atry, 75, 379–388.
Benton, A. L. (1960). Motivational influences on perfor- School of Medicine
mances in brain-damaged patients. American Journal • 1975–2011 Tenured Professor of Clinical
of Orthopsychiatry, 30, 313–321. Rehabilitation Medicine, New York University B
Benton, A. L. (1961). The fiction of the “Gerstmann syn- School of Medicine
drome”. Journal of Neurology, Neurosurgery, and Psy-
chiatry, 24, 176–181. • 1975–1976 Visiting Professor, Tel Aviv Uni-
Benton, A. L. (1962). Behavioral indices of brain injury in versity, Department of Psychology
school children. Child Development, 33, 199–208. • 1974–1976 Clinical Director of Israel Head
Benton, A. L. (1964a). Contributions to aphasia before Trauma Project, New York University Medi-
Broca. Cortex, 1, 314–327.
Benton, A. L. (1964b). Developmental aphasia and brain cal Center, Rusk Institute, and Israel Ministry
damage. Cortex, 1, 40–52. of Defense Joint Research Project, Afeka,
Benton, A. L. (1967). Problems of test construction in the Israel
field of aphasia. Cortex, 3, 32–58. • 1976–1983 Visiting Clinical Director,
Benton, A. L. (1969). Development of a multilingual apha-
sia battery: Progress and problems. Journal of Neuro- New York University Medical Center, Rusk
logical Sciences, 9, 39–48. Institute, and Israel Ministry of Defense Joint
Benton, A. L. (1977). Interactive effects of age and brain Research Project, Afeka, Israel
disease on reaction time. Archives of Neurology, 34, • 1995–1997 Clinical Director, Kurt Goldstein
369–370.
Benton, A. L. (1985). Some problems associated with Institute for Holistic Neuropsychological
neuropsychological assessment. Bulletin of Clinical Rehabilitation Steinach, Germany
Neurosciences, 50, 11–15. • 1996–2011 Assistant Chief of Behavioral Sci-
Benton, A. L., & Fogel, M. L. (1962). Three-dimensional ences, Rusk Institute of Rehabilitation
constructional praxis. Archives of Neurology, 7, 347–354.
Benton, A. L., & Howell, I. L. (1941). The use of psycho- • 1975–2011 Tenured Professor of Clinical
logical tests in the evaluation of intellectual function Rehabilitation Medicine, New York University
following head injury. Psychosomatic Medicine, 3, of School of Medicine
138–151.
Benton, A. L., & Van Allen, M. W. (1968). Impairment in
facial recognition in patients with unilateral cerebral
disease. Cortex, 4, 344–358. Major Honors and Awards
Benton, A. L., Hamsher, K. deS., Varney, N. R., & Spreen,
O. (1983). Contributions to neuropsychological assess- • 1976 Howard A. Rusk Award for Outstanding
ment. New York: Oxford University Press.
Levin, H. S., & Benton, A. L. (1975). Temporal orientation Accomplishments in Rehabilitation
in patients with brain disease. Applied Neurophysiol- • 1982 William F. Caveness Award for Distin-
ogy, 38, 56–60. guished Contributions in the field of Head
Injury, National Head Injury Foundation
• 1988 Thomas J. Dean Award of Excellence in
Head Injury Rehabilitation, Dallas, Rehabilita-
Ben-Yishay, Yehuda (1933–) tion Foundation
• 1991 Distinguished Career Achievement Award,
Amy Alderson1 and Christine Mullen2 American Board of Medical Psychotherapists
1
Department of Rehabilitation Medicine, Emory • 2006 Outstanding Lifetime Scientific Contri-
University, Atlanta, GA, USA butions to Rehabilitation Psychology. Ameri-
2
Emory Health Care, Atlanta, GA, USA can Psychological Association, Division 22

Major Appointments Landmark Clinical, Scientific, and

Professional Contributions
• 1964–1966 Assistant Professor of Clinical
Rehabilitation Medicine, New York University • Dr. Ben-Yishay is the father of holistic brain
School of Medicine injury rehabilitation. Initially developed in
560 Ben-Yishay, Yehuda (1933–)

Israel for war veterans with head injuries and abroad, and premiere rehabilitation institutes
later transitioned to the New York University around the world utilize his model of cogni-
School of Medicine at the Rusk Institute, tive rehabilitation as the foundation for their
Dr. Ben-Yishay’s treatment interventions with own brain injury programs. His teaching
individuals with brain injuries combined con- methods are studied by students and profes-
tributions from neuropsychology, behavioral sionals from all over the world, and he is
psychology, cognitive-behavioral psychother- internationally known as a clinician, teacher,
apy, special education, social psychology, and researcher, and expert in the field of holistic
psychodrama. He adapted these modalities to rehabilitation.
the needs and capabilities of his patients, sys-
tematically applying them in therapeutic com-
munity settings to reach maximal effectiveness.
Short Biography
Through his holistic approach to the treatment
of brain injury, a foundation for cognitive
and neuropsychological rehabilitation was
established.
• The holistic rehabilitation approach developed
by Dr. Ben-Yishay includes a number of com-
ponents in addition to traditional cognitive
retraining: development of a therapeutic milieu
or community, psychotherapy, regular involve-
ment of family and caregivers, psychoedu-
cation, and transitional work opportunities.
Within the therapeutic milieu or community,
persons with brain injury not only participate
in activities aimed at adaptation to and com-
pensation for their deficits but also meet regu-
larly with staff members to monitor their
progress. Interaction with other individuals
with brain injury is also an important part of
the therapeutic milieu. During individual and
group psychotherapy, persons with brain injury
address the many adjustment issues associated
with their deficits. In addition, the involvement
of family and caregivers in the rehabilitation
process not only provides additional support
for the person with a brain injury as they com-
plete therapies but also assists with the transi- Yehuda Bin-Yishay was born on February
tion back to the community by providing 11, 1933, in Cluj, Romania. He grew up in
realistic education and information regarding Israel and served in the Israeli army. In 1957,
the person’s progress and injury. Finally, tran- he received a B.A. degree in Sociology and
sitional work opportunities provide important Special Education from Hebrew University in
information regarding individuals’ abilities Jerusalem, Israel. Then, in 1958, he came to
outside of structured settings and help to pro- the United States on a scholarship from the
vide additional functional goals for rehabilita- New School University in New York City.
tion therapies. There, he studied under Kurt Goldstein. He
• Dr. Ben-Yishay’s work has been researched completed an internship in Clinical Psychology
and applied both within the United States and in 1960 at Trenton State Hospital in Trenton,
Ben-Yishay, Yehuda (1933–) 561

NJ. His master’s degree in Personality Psy- recognition for his work. He has received
chology was completed in 1961. numerous awards and honors, including the
After completing his master’s degree, 2006 Lifetime Scientific Contributions to Reha-
Dr. Ben-Yishay served as the psychologist bilitation Psychology Award from Division
for a research project in the Department of Reha- 22 of the American Psychological Association. B
bilitation at the Albert Einstein College of Med- In addition to his many international committee
icine in New York. The study tested the and consultant positions, Dr. Ben-Yishay has
effectiveness of a “therapeutic community” served on a number of important editorial
model of rehabilitation. boards, including Archives of Physical Medicine
Ben-Yishay obtained his Ph.D. from New York and Rehabilitation, Journal of Head Trauma
University, following the completion of studies Rehabilitation, Brain Injury, and Neuropsycho-
investigating the effects of normobaric oxygen logical Rehabilitation.
on stroke patients’ performances on neurologic, Of all of his achievements, Dr. Ben-Yishay
sensory-motor, and cognitive measures. In 1964, greatest satisfaction stems from the programs
Dr. Ben-Yishay joined the faculty at New York all over the world that subscribe to his philos-
University. While at New York University, ophy of brain injury rehabilitation and the
Dr. Ben-Yishay’s research over the next several many acknowledgments of his influence on
years focused on three key areas: (1) rehabilitation clinical practice (personal communication,
outcome prediction studies, (2) comparisons July 15, 2016).
between normal controls and brain-injured Dr. Ben-Yishay formally retired in 2009
individuals across a variety of measures, and and has since volunteered at the NYU Rusk
(3) development and efficacy studies of cognitive Rehabilitation Day Program. He continues to
rehabilitation modules. From 1974 to 1977, work on several publications, including work
Dr. Ben-Yishay conducted a pilot study in Israel identifying the major predictors of successful
to investigate the effects of holistic brain injury outcomes of intensive neuropsychological reha-
rehabilitation on Israeli war veterans. The results bilitation and patient acceptance of the limita-
of the study were impressive and were followed in tions imposed by brain injury. In regard to the
September of 1978 by a 5-year research grant on future of the field, Dr. Ben-Yishay believes the
brain injury rehabilitation at New York University “therapeutic community” portion of the holistic
(NYU) Rusk Rehabilitation Head Trauma approach merits a wider application in order to
Program. improve outcomes (personal communication,
Throughout his career, Dr. Ben-Yishay trained July 15, 2016).
numerous rehabilitation neuropsychologists, who
have gone on to institute his model of cognitive
rehabilitation. Individuals such as Anne-Lise Cross-References
Christensen, Ph.D., and George Prigatano, Ph.
D., have been greatly influenced by Ben-Yishay’s ▶ Christensen, Anne-Lise (1926– )
work and established programs built upon princi- ▶ Cognitive Rehabilitation
ples learned under his tutelage. Ben-Yishay ▶ Goldstein, Kurt (1878–1965)
maintains that the objective of all neuroreh-
abilitation interventions is to optimize the per-
son’s compensatory repertoire, including helping References and Readings
the individual in mastering and reliably applying
learned compensatory skills in his or her post- Ben-Yishay, Y. (1996). Reflections on the evolution of the
rehabilitation life. therapeutic milieu concept. Neuropsychological Reha-
bilitation, 6(4), 327–343.
Dr. Ben-Yishay’s work in the area of holistic Ben-Yishay, Y. (2000). Postacute neuropsychological
brain injury rehabilitation continues to the pre- rehabilitation: A holistic perspective. In
sent day, and he has earned worldwide A. Christensen & B. P. Uzzell (Eds.), International
562 Benzodiazepines

handbook of neuropsychological rehabilitation

(pp. 127–135). Dordrecht: Kluwer Academic/Plenum Benzodiazepines
Publishers.
Ben-Yishay, Y. (2008). Foreword. In F. Gracey and
T. Ownsworth (Eds). The self and identity in rehabili- JoAnn Tschanz
tation: A special issue of the journal Neuropsycholog- Department of Psychology, Utah State University,
ical Rehabilitation,18(5), 513–521. Logan, UT, USA
Ben-Yishay, Y., & Diller, L. (1993). Cognitive remediation
in traumatic brain injury: Update and issues. Archives Center for Epidemiologic Studies, Utah State
of Physical Medicine and Rehabilitation, 74(2), University, Logan, UT, USA
204–213.
Ben-Yishay, Y., & Diller, L. (2008). Kurt Goldstein’s holis-
tic ideas: An alternative, or complementary, approach
to the management of traumatically brain injured indi- Synonyms
viduals. US Neurology, 4(1), 79–80.
Ben-Yishay, Y., & Diller, L. (2016). Turning points: Anxiolytics; Sedative-hypnotics
Positive outcomes of insensitive psychotherapeutic
interventions in holistic neuropsychological rehabil-
itation settings. Youngsville: Lash and Associates
Publishing. Definition
Ben-Yishay, Y., & Gold, J. (1990). Therapeutic milieu
approach to neuropsychological rehabilitation. In Benzodiazepines belong to a class of medications
R. L. Wood (Ed.), Neurobehavioral sequelae of trau-
matic brain injury (pp. 194–215). London: Taylor and known as sedative-hypnotics. The benzodiaze-
Francis. pine molecule binds to the subtype A portion of
Ben-Yishay, Y., & Lakin, P. (1989). Structured group treat- the protein receptor of the primary inhibitory neu-
ment for brain-injury survivors. In D. Ellis & A. L. rotransmitter substance in the brain, gamma
Christensen (Eds.), Neuropsychological treatment
after brain injury (pp. 271–295). Boston: Kluwer aminobutyric acid (GABA). The simultaneous
Academic. binding of the endogenous neurotransmitter
Ben-Yishay, Y., Ben-Nachum, Z., Cohen, A., Gross, Y., GABA on the GABA-A postsynaptic receptor
Hoofien, D., Rattok, J., & Diller, L. (1978). Digest of a increases the frequency of the opening of the
two-year comprehensive clinical research program for
out-patient head injured Israeli veterans. NYU Rehabil- chloride channel, allowing greater amounts of
itation Monograph, 60, 1–61. this negatively charged anion, chloride, to rapidly
Ben-Yishay, Y., Rattok, J., Lakin, P., Piasetsky, E. B., Ross, enter the cell due to the concentration gradient.
B., Silver, S., . . . & Ezrachi, O. (1985). Neuropsy- The additional entry of chloride into the cyto-
chologic rehabilitation: Quest for a holistic approach.
Seminars in Neurology, 5(3), 252–259. plasm hyperpolarizes the cell, which reduces
Ben-Yishay, Y., Silver, S. M., Piasetsky, E., & Rattok, J. depolarization, or firing, of the cell. Hence, greater
(1987). Relationship between employability and voca- stimulation is required for cell firing. This is
tional outcome after intensive holistic cognitive reha- known as the GABA-benzodiazepine receptor
bilitation. The Journal of Head Trauma Rehabilitation,
2(1), 35–48. complex (Stahl 2004).
Ezrachi, O., Ben-Yishay, Y., Kay, T., Diller, L., & Rattok, J. Benzodiazepines have wide-ranging effects.
(1991). Predicting employment in traumatic brain Their popular use is reflected in their anxiolytic,
injury following neuropsychological rehabilitation. muscle relaxant, sedative, anesthetic, and anticon-
The Journal of Head Trauma Rehabilitation, 6(3),
71–84. vulsant properties. Due to their safety profile,
Prigatano, G. P., & Ben-Yishay, Y. (1999). Psychotherapy benzodiazepines became very popular in the
and psychotherapeutic interventions in brain injury 1970s, replacing older drugs such as barbiturates
rehabilitation. In M. Rosenthal, E. R. Griffith, and meprobamate for the treatment of anxiety
J. Korutzer, & B. Pentland (Eds.), Rehabilitation of
the adult and child with traumatic brain injury symptoms, insomnia and other sleep disorders
(3rd ed.). Philadelphia: F.A. Davis. (Iversen et al. 2009), and alcohol withdrawal syn-
Rattok, J., Ross, B., Ben-Yishay, Y., Ezrachi, O., Silver, S., drome (Ntais et al. 2005). However, negative
Lakin, P., & . . . Diller, L. (1992). Outcome of different effects of benzodiazepine use have also been
treatment mixes in a multidimensional neuropsycho-
logical rehabilitation program. Neuropsychology, 6(4), reported. Although these “side effects” vary
395–415. depending upon the original indication for
Berg Balance Scale 563

benzodiazepine use, some of the unwanted effects References

include drowsiness, decreased concentration,
memory impairment, psychomotor slowing Allain, H., Bentu’e-Ferrer, D., Polard, E., Akwa, Y., &
Patat, A. (2005). Postural instability and consequent
(Buffett-Jerrott and Stewart 2002), and postural
falls and hip fractures associated with use of hypnotics
instability (with increased risk of falls) among the in the elderly. A comparative review. Drugs in Aging, B
elderly (Allain et al. 2005). Chronic use also carries 22, 749–765.
the risk of substance dependence and abuse and Barker, M. J., Greenwood, K. M., Jackson, M., &
Crowe, S. F. (2004). Cognitive effects of long-
cognitive impairment with prolonged use at high
term benzodiazepine use. A meta-analysis. CNS
doses (Stewart 2005; Barker et al. 2004). For these Drugs, 18, 37–48.
and other reasons, medications in this class are now Bourin, M., & Lambert, O. (2002). Pharmacotherapy of
more commonly used on a short-term rather than a anxious disorders. Human Psychopharmacology: Clin-
ical and Experimental, 17, 383–400.
long-term basis (Iversen et al.).
Buffett-Jerrott, S. E., & Stewart, S. H. (2002). Cognitive
and sedative effects of benzodiazepine use. Current
Pharmaceutical Design, 8, 45–58.
Current Knowledge Gold, R., & Oreja-Guevara, C. (2013). Advances in the
management of multiple sclerosis spasticity: Multiple
sclerosis spasticity guidelines. Expert Review of
Current uses of benzodiazepines include the treat- Neurotherapeutics, 13(12 Suppl), 55–59.
ment of spasticity (Gold and Oreja-Guevara 2013) Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H.
and tremor (Meador et al. 2016) in patients with (2009). Antidepressants and anxiolytics. In Introduc-
tion to neuropsychopharmacology (pp. 306–335).
multiple sclerosis. As reported above, chronic use
New York: Oxford University Press.
of benzodiazepines has declined, particularly for the Meador, W., Salter, A. R., & Rinker, J. R., 2nd. (2016).
treatment of anxiety disorders and insomnia. Tricy- Symptomatic management of multiple sclerosis-
clic antidepressants (TCAs) and selective serotoner- associated tremor among participants in the
NARCOMS registry. International Journal of MS
gic agents are increasingly being prescribed over
Care, 18, 147–153.
benzodiazepines for the treatment of anxiety disor- Montplaisir, J., Hawa, R., Moller, H., Morin, C., Fortin, M.,
ders. For example, selective TCAs are reportedly as Matte, J., Reinish, L., & Shapiro, C. M. (2003).
effective as benzodiazepines in the treatment of Zopiclone and zaleplon vs benzodiazepines in the treat-
ment of insomnia: Canadian consensus statement.
generalized anxiety disorder, and certain selective
Human Psychopharmacology: Clinical and Experi-
serotonin reuptake inhibitors and TCAs are effec- mental, 18, 29–38.
tive in the treatment of panic and obsessive com- Ntais, C., Pakos, E., Kyzas, P., & Ioannidis, J. P. (2005).
pulsive disorder (Bourin and Lambert 2002). Benzodiazepines for alcohol withdrawal. Cochrane
Database of Systematic Reviews, 20, CD005063.
With respect to insomnia, benzodiazepines
Stahl, S. M. (2013). Anxiolytics and sedative hypnotics. In
were the treatment of choice over barbiturates. Essential psychopharmacology: Neuroscientific basis
However, negative effects such as the develop- and practical applications (pp. 297–333). New York:
ment of tolerance, residual daytime sleepiness, Cambridge University Press.
aggravation of respiratory conditions, and
reduced duration of slow-wave (restorative) and
REM sleep were also reported. Newer, non-
benzodiazepine hypnotic compounds such as Berg Balance Scale
zopiclone and zaleplon are also effective in treating
insomnia yet have fewer side effects than those of Kari Dunning
benzodiazepines (Montplaisir et al. 2003). Department of Rehabilitation Sciences,
University of Cincinnati, Cincinnati, OH, USA

See Also
Synonyms
▶ Anxiolytics
▶ Barbiturates 7-item BBS-3P; BBS
564 Berg Balance Scale

Description BBS scores are used when prescribing mobility

aids and treatment interventions, identifying safe
The Berg Balance Scale (BBS) is a 14-item per- and unsafe activities, and to measure treatment
formance observation measure that assesses bal- effect. When assessing the treatment effect for
ance on a scale from 0 to 4 for each item, yielding individual patients with stroke, a score change of
a total score range of 0–56, where higher scores 6 points has been shown to represent real change,
indicate better balance. The BBS tests both static beyond measurement error, with 90% confidence.
and dynamic balance with items meant to mimic For individuals with multiple sclerosis, the mini-
balance challenges encountered in daily life. mal clinically important difference has been deter-
mined to be 3 points.
Although originally designed to screen older
Historical Background adults for fall risk, the BBS has subsequently been
validated for persons with stroke, multiple sclero-
In 1989, Berg developed the BBS to fill the need sis, Parkinson’s disease, and chronic obstructive
for a quantitative balance assessment tool to pulmonary disease (COPD).
screen older adults for fall risk. The BBS has
subsequently become the best known clinical bal-
ance instrument. Shorter versions of the BBS,
Cross-References
such as the seven-item BBS-3P (which also has
a condensed rating scale), have also been devel-
▶ Balance Disorders
oped and validated.
▶ Multiple Sclerosis
▶ Parkinson’s Disease
▶ Sensitivity
Psychometric Data
▶ Specificity
▶ Stroke
The high reliability, validity, and sensitivity of the
BBS, including predictive validity for fall risk, are
well documented in the literature. Some authors
References and Readings
initially dichotomized the scale, using the thresh-
old value <45 points as an indication of fall risk. Alzayer, L., Beninato, M., & Portney, L. G. (2009). The
However, more rigorous study has determined accuracy of individual berg balance scale items com-
that a gradient of fall risk exists over the entire pared with the total berg score for classifying people
scale. A retrospective study of community-dwell- with chronic stroke according to fall history. Journal of
Neurologic Physical Therapy: JNPT, 33(3), 136–143.
ing persons with stroke demonstrated that chang- Berg, K., Wood-Dauphinee, S., Williams, J. I., & Gayton, D.
ing from 3 to 4 for the “standing on one leg” item (1989). Measuring balance in the elderly: Preliminary
had a sensitivity of 0.90 and a specificity of 0.50 development of an instrument. Physiotherapy Canada,
for predicting the history of multiple falls. 41, 304–311.
Berg, K., Wood-Dauphinee, S., & Williams, J. I. (1995).
The balance scale: Reliability assessment with elderly
residents and patients with an acute stroke. Scandina-
Clinical Uses vian Journal of Rehabilitation Medicine, 27(1), 27–36.
Blum, L., & Korner-Bitensky, N. (2008). Usefulness of the
berg balance scale in stroke rehabilitation: A systematic
The BBS is available online (Internet Stroke Cen- review. Physical Therapy, 88(5), 559–566.
ter 2007). Administration requires 10–20 min, a Chou, C. Y., Chien, C. W., Hsueh, I. P., Sheu, C. F., Wang,
chair, a step, a ruler, and a stopwatch. Balance C. H., & Hsieh, C. L. (2006). Developing a short form
ability is sometimes grossly categorized as good, of the berg balance scale for people with stroke. Phys-
ical Therapy, 86(2), 195–204.
fair, or poor for score ranges from 56 to 41, 40 to Gervasoni, E., Jonsdottir, J., Montesano, A., & Cattaneo, D.
21, and 20 to 0, respectively. As stated above, a (2016). Minimal clinically important difference of
gradient of fall risk exists over the entire scale. berg balance scale in people with multiple sclerosis.
Best Performance Method 565

Archives of Physical Medicine and Rehabilitation, the Best Performance Method. Using this method,
epub. data are collected from multiple sources, includ-
Internet Stroke Center. (2007). Berg balance scale. http://
www.strokecenter.org/Trials/scales/berg.html. Accessed ing, but not limited to, test scores, observations,
19 May 2010. interviews, reports from family, and historical
Jacome, C., Cruz, J., Olivera, A., & Marques, A. (2016). data. After the data are collected, the data source B
Validity, reliability, and ability to identify fall status of that yields the highest level of functioning is the
the berg balance scale, BESTest, Mini-BESTest, and
Brief-BESTest in patients with copd. Physical Therapy, set standard to which all other aspects of function-
96, 1807–1815. ing are compared. The Best Performance Method
Mao, H., Hsueh, I., Tang, P., Sheu, C., & Hsieh, C. (2002). assumes that one performance level exists for each
Analysis and comparison of the psychometric proper- person’s cognitive abilities. A notable discrep-
ties of three balance measures for stroke patients.
Stroke, 33(4), 1022–1027. ancy between a patient’s best and other perfor-
Muir, S. W., Berg, K., Chesworth, B., & Speechley, M. mances is indicative of neuropsychological
(2008). Use of the berg balance scale for predicting impairment. The Best Performance Method also
multiple falls in community-dwelling elderly people: assumes that performance should be consistent
A prospective study. Physical Therapy, 88(4),
449–459. across all areas of functioning. For example,
Stevenson, T. J. (2001). Detecting change in patients with very superior intellectual and other abilities
stroke using the berg balance scale. The Australian would be expected from a patient who has earned
Journal of Physiotherapy, 47, 29–38. a doctoral degree in engineering. The method has
Tyson, S. F., & Connell, L. A. (2009). How to measure
balance in clinical practice. A systematic review of the been criticized by some who believe that there is a
psychometrics and clinical utility of measures of bal- high likelihood of overestimating premorbid abil-
ance activity for neurological conditions. Clinical ity, and research does not support that perfor-
Rehabilitation, 23(9), 824–840. mance on cognitive testing is uniform across
different tests or cognitive domains. In fact,
abnormal performance on some proportion of
neuropsychological testing has proven to be psy-
Best Performance Method chometrically normal (Binder et al. 2009).

Glen E. Getz
Department of Psychiatry, Allegheny General
Cross-References
Hospital, Pittsburgh, PA, USA
Neuropsychology Specialty Care, LLC, ▶ Deficit Measurement
Pittsburgh, PA, USA
▶ Premorbid Estimate
▶ Premorbid Functioning
▶ Premorbid Intelligence
Synonyms

Cognitive potential References and Readings

Binder, L. M., Iverson, G. L., & Brooks, B. L. (2009). TO

Definition err is human: “Abnormal” neuropsychological scores
and variability are common in healthy adults. Archives
of Clinical Neuropsychology, 24, 31–46.
Neuropsychologists typically do not have an Lezak, M. D., Howieson, D. B., Bigler, E. D., & Tranel,
opportunity to evaluate patients before the D. (2012). The rationale of deficit measurement. In
onset of neurological illness or injury. Judgments Neuropsychological assessment (5th ed.). New York:
about impairment are often made by comparing Oxford University Press.
Mortensen, E. L., Gade, A., & Reinisch, J. M. (1991).
obtained test scores with estimates of premorbid “Best performance method” in clinical neuropsychol-
ability. There are several approaches to estimating ogy. Journal of Clinical and Experimental Neuropsy-
premorbid level of ability. One such approach is chology, 13, 361–371.
566 Beta-Interferons

Beta-Interferons Beyond a Reasonable Doubt

Kathleen L. Fuchs Robert L. Heilbronner

Department of Neurology, University of Virginia Chicago Neuropsychology Group, Chicago,
Health System, Charlottesville, VA, USA IL, USA

Synonyms Definition

Avonex ®; Betaseron ®; Rebif ® Beyond a reasonable doubt is the standard of

proof required in most criminal cases within an
adversarial system. Generally, the prosecution
Definition bears the burden of proof and is required to
prove their version of events to this standard.
Interferon b is a disease-modifying drug currently This means that the proposition being presented
indicated for treatment of relapsing forms of mul- by the prosecution must be proven to the extent
tiple sclerosis. Its mechanism of action is complex that there is no “reasonable doubt” in the mind of a
and is presumed to inhibit immune system T-cell reasonable person that the defendant is guilty.
activation and migration into the central nervous There can still be a doubt but only to the extent
system as well as modulate the action of some pro- that it would not affect a “reasonable person’s”
inflammatory proteins (cytokines). There are three belief regarding whether or not the defendant is
FDA approved beta interferons available in the guilty. The “shadow of a doubt” is sometimes
US - Avonex ® (INF-b1a), Betaseron ® (INF-b1b), used interchangeably with reasonable doubt, but
and Rebif ® (INF-b1a). These medications are this extends beyond the latter to the extent many
administered via injection, and each has been believe is an impossible standard. Reasonable
shown to reduce the frequency of MS relapses, doubt is therefore used. If doubt affects a “reason-
reduce MRI evidence of brain lesions, and possi- able person’s” belief that the defendant is guilty,
bly reduce disability progression. the jury is not satisfied beyond a “reasonable
doubt.” The precise meaning of words such as
“reasonable” and “doubt” is usually defined
Cross-References within jurisprudence of the applicable country.
The standard that must be met by the prosecu-
▶ Multiple Sclerosis tion’s evidence in a criminal prosecution is that no
other logical explanation can be derived from the
facts except that the defendant committed the
References and Readings crime, thereby overcoming the presumption that a
person is innocent until proven guilty. If the jurors
National Clinical Advisory Board of the National Multiple
Sclerosis Society. (2007). Disease management con-
or judge have no doubt as to the defendant’s guilt or
sensus statement. Retrieved 15 Feb 2010, from http:// if their only doubts are unreasonable doubts, then
www.nationalmssociety.org/download.aspx?id=8. the prosecutor has proven the defendant’s guilt
Noseworthy, J., Miller, D., & Compston, A. (2006). beyond a reasonable doubt, and the defendant
Disease-modifying treatments in multiple sclerosis.
In A. Compston, C. Confavreux, H. Lassman,
should be pronounced guilty. The term “reasonable
I. McDonald, D. Miller, J. Noseworthy, et al. (Eds.), doubt” connotes that evidence establishes a partic-
McAlpine’s multiple sclerosis (4th ed., pp. 729–802). ular point to a moral certainty and that it is beyond
Philadelphia: Elsevier. dispute that any reasonable alternative is possible.
Zhang, J., Hutton, G., & Zang, Y. (2002). A comparison of
the mechanisms of action of interferon beta and
It does not mean that no doubt exists as to the
glatiramer acetate in the treatment of multiple sclerosis. accused’s guilt, but only that no reasonable doubt
Clinical Therapeutics, 24, 1998–2021. is possible from the evidence presented.
Bias 567

Beyond a reasonable doubt is the highest stan- Definition

dard of proof that must be met in any trial. In civil
litigation, the standard of proof is either proof by Faust et al. (1991) and Wedding and Faust (1989)
a “preponderance of the evidence” or proof by explain chief forms of bias related to clinical
“clear and convincing evidence.” These are judgment and decision-making in neuropsychol- B
lower burdens of proof. A preponderance of the ogy. First, hindsight bias is the tendency to
evidence simply means that one side has more believe, after the outcome of an incident is deter-
evidence in its favor than the other, even by the mined, that the outcome could have been more
smallest degree. Clear and convincing proof is reliably predicted than is actually true. This form
evidence that establishes a high probability that of bias suggests that being aware of an event via a
the fact sought to be proven is true. The main client’s clinical history may lead the clinician to
reason that the high-proof standard of reasonable conclude that they can determine the outcome of
doubt is used in criminal trials is that such pro- the event and make diagnostic determinations.
ceedings can result in the deprivation of a defen- Confirmation bias refers to the tendency to seek
dant’s liberty or even in his or her death. These confirming evidence while failing to consider
outcomes are far more severe than in civil trials, disconfirming evidence when generating diagnos-
in which money damages are the common tic impressions. Thus, a clinician seeks to confirm
remedy. initial hypotheses while failing to gather informa-
tion related to alternative hypotheses. Moreover, it
has been demonstrated that clinicians tend to stop
Cross-References hypothesis evaluation once information in support
of an initial hypothesis has been gathered, thus
▶ Burden of Proof potentially terminating the evaluation prior to ade-
▶ Clear and Convincing Evidence quate consideration of competing hypotheses.
▶ Preponderance of the Evidence To combat against bias in neuropsychological
assessment and testimony, Wedding and Faust
(1989) and Sweet and Moulthrop (1999) provided
References and Readings a number of strategies for clinicians to consider
when testifying and preparing reports. First and
Denney, R. L. (2005). Criminal forensic neuropsychology foremost, they recommended that clinicians be
and assessment of competency. In G. Larrabee (Ed.), familiar with the scientific literature regarding
Forensic neuropsychology: A scientific approach. human judgment and decision-making. Moreover,
New York: Oxford University Press.
Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C.
they recommend that clinicians begin with con-
(2007). Psychological evaluations for the courts: sideration of the most valid information, generat-
A handbook for mental health professionals and law- ing alternative diagnostic hypotheses and then
yers (3rd ed.). New York: Guilford. gathering and considering evidence for each and
providing an outline of disconfirmatory informa-
tion. Thus, in the context of a neuropsychological
evaluation, it is recommended that clinicians gen-
Bias erate a list of test findings that support specific
hypotheses but also list data that disputes such
Robert L. Heilbronner hypotheses. Larrabee (2000) suggests a four-
Chicago Neuropsychology Group, Chicago, component consistency analysis for neuropsycho-
IL, USA logical decision-making, including asking the fol-
lowing four questions: (a) Are the data consistent
within and between neuropsychological domains?
Synonyms (b) Is the neuropsychological profile consistent
with the suspected etiologic condition? (c) Are
Partiality; Prejudice the neuropsychological data consistent with the
568 Bicycle Drawing Test

documented severity of injury? and (d) Are the freehand using a pencil. It can be a useful measure
neuropsychological data consistent with the sub- of visual-spatial and visual-motor impairments
ject’s behavioral presentation? Several pieces of and also has been used in the assessment of
data must be analyzed in order to address the hemi-neglect syndromes. Typically, the patient is
aforementioned questions: comprehensive inter- asked to draw a copy of a simple line drawn
view, meticulous record review, and comprehen- picture of a bicycle. Many clinicians first ask the
sive and redundant neuropsychological tests patient to draw a bicycle in freehand from their
within each domain (language, perception, senso- own memory, to assess their constructional ability
rimotor functioning, attention/information pro- in the absence of a model.
cessing, psychomotor speed, verbal and visual
learning and memory, intelligence, problem solv-
ing, motivation, and personality). History and Clinical Evidence

The bicycle drawing test is widely associated with

References and Readings Piaget’s (1955) investigations of cognitive devel-
opment, though similar tests seem to have been
Faust, D., Ziskin, J., & Hiers Jr., J. B. (1991). Brain employed earlier (Poppelreuter 1990; Veiders
damage claims: Coping with neuropsychological evi- 1934). Neuropsychological investigations of focal
dence. Marina del Rey: Law & Psychology Press. unilateral lesions (Hecaen and Assal 1970) have
Larrabee, G. J. (2000). Forensic neuropsychological
assessment. In R. D. Vanderploeg (Ed.), Clinicians demonstrated differences in performance between
guide to neuropsychological assessment (2nd ed., patients with left- and right-sided posterior brain
pp. 301–335). Mahwah: Lawrence Erlbaum. lesions. Such comparisons have also suggested
Sweet, J. J., & Moulthrop, M. A. (1999). Self-examination qualitative differences in the types of errors made
questions as a means of identifying bias in adversarial
assessments. Journal of Forensic Neuropsychology, 1, among patients with left- and right-sided lesions
73–88. (Angenent 1971). Such findings led to the inclu-
Van Gorp, W., & McMullen, W. (1997). Potential sources sion of this test as a measure of constructional
of bias in forensic neuropsychological evaluations. The ability. One study compared the bicycle drawing
Clinical Neuropsychologist, 11, 180–187.
Wedding, D., & Faust, D. (1989). Clinical judgment and test to the Bender-Gestalt test (Greenberg et al.
decision-making in neuropsychology. Archives of Clin- 1994) and found bicycle drawing to be more sen-
ical Neuropsychology, 4, 233–265. sitive to brain dysfunction in children with visual-
spatial problems than the Bender-Gestalt test. Inter-
estingly, improvements in bicycle drawing perfor-
mance have been described in studies of patients
Bicycle Drawing Test with Parkinson’s disease, multiple sclerosis, and
Tourette’s syndrome (Sandyk 1994, 1997a, b),
Ronald A. Cohen with reversal of spatial orientation in Parkinson’s
Department of Clinical and Health Psychology, patients when they received electromagnetic pulses
College of Public Health and Health Professions, to their brain (Sandyk 1998). The quality and com-
University of Florida, Gainesville, FL, USA plexity of the drawing produced by children and
Center for Cognitive Aging and Memory, adults has also been linked to their intellectual
McKnight Brain Institute, University of Florida, ability (Sharma 1972).
Gainesville, FL, USA

Current Clinical Use

Definition
Formal scoring systems exist for the bicycle draw-
As the name suggests, the bicycle drawing test ing test (Greenberg et al. 1994) providing a means
requires patients to draw a picture of a bicycle in for deriving quantitative results when using this
Bilingual Aphasia 569

test. Studies comparing the drawings of amateurs Poppelreuter, W. (1990). Disturbances of lower and higher
with artists have also shown that observational, visual capacities caused by occipital damage: With
special reference to the psychopathological, pedagog-
experimental, and neuropsychological methods ical, industrial, and social implications. Oxford:
for scoring drawings can provide systemic differ- Clarendon Press/Oxford University Press.
ences in cognitive skills among individuals (van Sandyk, R. (1994). Reversal of a visuoconstructional def- B
Sommers et al. 1995). Yet, most clinicians cur- icit in Parkinson’s disease by application of external
magnetic fields: A report of five cases. International
rently use the bicycle drawing test in conjunction Journal of Neuroscience, 75(3–4), 213–228.
with other constructional tests, including coping Sandyk, R. (1997a). Progressive cognitive improvement in
or freehand drawing tasks (e.g., cube, house), and multiple sclerosis from treatment with electromagnetic
examine results qualitatively for gross spatial dis- fields. International Journal of Neuroscience, 89(1–2),
39–51.
tortion or omissions. Other tests, such as copying Sandyk, R. (1997b). Reversal of a visuoconstructional
of the Rey complex figure, are now more widely disorder by weak electromagnetic fields in a child
used for visual-motor assessment. Yet, the bicycle with Tourette’s syndrome. International Journal of
drawing test is an easy-to-administer task that can Neuroscience, 90(3–4), 159–167.
Sandyk, R. (1998). Reversal of the bicycle drawing direc-
yield valuable information about the visual-spatial tion in Parkinson’s disease by AC pulsed electromag-
and constructional abilities of patients. It can also netic fields. International Journal of Neuroscience, 95
detect hemi-neglect syndrome, as some patients (3–4), 255–269.
may omit one side of the bicycle. It can yield Sharma, T. R. (1972). Measuring intelligence through
bicycle drawings. Indian Educational Review, 7(1),
information about additional information on intel- 1–30.
lectual development when used in the assessment van Sommers, P. (1995). Observational, experimental and
of children. Generally, it should not be used as a neuropsychological studies of drawing. In C. Lange-
stand-alone test but should rather be used in con- Küttner & G. V. Thomas (Eds.), Drawing and looking:
Theoretical approaches to pictorial representation in
junction with other tests of visual constructional children (pp. 44–61). Hertfordshire: Harvester
functioning. Wheatsheaf.
Veiders, E. (1934). Analyse der Fähigkeit zum räumlichen
Denken. Analysis of the ability for spatial thinking.
Psychotechnisches Zeitschrift, 9, 52–60.
Cross-References

▶ Bender Visual-Motor Gestalt Test II

▶ Block Design
▶ Clock Drawing Bilingual Aphasia
▶ Rey Complex Figure Test
Margarita Kaushanskaya1 and Henrike K.
Blumenfeld2
1
University of Wisconsin-Madison, Madison, WI,
References and Readings USA
2
School of Speech, Language and Hearing
Angenent, H. L. (1971). The development of thought
structure among normal and mentally retarded children.
Sciences, San Diego State University, San Diego,
Nederlands Tijdschrift voor de Psychologie en haar CA, USA
Grensgebieden, 26(4), 215–232.
Greenberg, G. D., Rodriguez, N. M., & Sesta, J. J. (1994).
Revised scoring, reliability, and validity investigations
of Piaget’s bicycle drawing test. Assessment, 1(1),
Definition
89–101.
Hecaen, H., & Assal, G. (1970). A comparison of construc- Bilingual aphasia is a term referring to aphasia in
tive deficits following right and left hemispheric an individual who is bilingual or multilingual. The
lesions. Neuropsychologia, 8(3), 289–303.
Piaget, J. (1955). Perceptual and cognitive (or operational)
degree and nature of impairment vary widely, and
structures in the development of the concept of space in depend on the interplay among a number of fac-
the child. Acta Psychologica, 11, 41–46. tors, including site and size of the lesion, the
570 Bilingual Aphasia

individual’s premorbid language learning and and experience interaction and interference
experience history, and proficiency and immer- between them. In addition, bilinguals frequently
sion in each language. Current evidence suggests switch and translate between languages.
that the same classification/diagnosis of aphasia There is still considerable debate regarding the
(e.g., fluent, nonfluent) tends to hold across both functional localization of language in bilinguals.
languages, with varying degrees of impairment The evidence to date indicates that the extent of
and recovery trajectories (Paradis 1998). In the overlap in representation of languages depends on
USA, 45,000 new cases of bilingual aphasia are the speaker’s language proficiency and the age at
expected each year (Paradis 2001). which the second language was acquired. Neuro-
imaging research suggests that different lan-
guages are most likely to share the same brain
Historical Background regions when the second language is acquired
earlier, with age of second-language acquisition
Knowledge of bilingual aphasia is primarily based treated as a continuous variable (Nichols and
on a history of case studies (for reviews, see Joanisse 2016) or as a categorical variable where
Ansaldo and Ghazi Saidi 2014; Lorenzen and a late age of acquisition is defined as 10 years or
Murray 2008; Pearce 2005), including older (e.g., Wartenburger et al. 2003). Bilinguals’
documented cases as early and varied as a patient languages also show more overlap when both are
who could read Latin but not German (Gesner highly proficient (e.g., Abutalebi and Green 2007;
1770); a patient in Southern France who, after Chee et al. 1999; Golestani et al. 2006; Klein et al.
brain damage, showed a selective deficit in French 1999; Perani et al. 2003). Even in languages that
but not Occitan (Lordat 1843); and a trilingual are structurally different from each other, at least
patient who recovered French and Spanish, but partially shared representations have been identi-
lost the ability to even understand Italian (Pitres fied (e.g., English/Chinese; English/ASL, Chee
1895). Based on early case studies, a number of et al. 1999; Emmorey et al. 2007).
predictions have been made about patterns of Additional brain areas have also been identi-
impairment and recovery in bilingual individuals fied during bilingual language processing,
with aphasia, including better recovery of the pointing to a complex neural network involved
mother tongue (Ribot’s Law 1882), the most in the cognitive control of bilinguals’ two lan-
familiar language (Pitres’ Rule 1895), the lan- guages (e.g., Green and Abutalebi 2013). For
guage dominant in the environment (Bychowsky example, bilinguals may engage the prefrontal
1919), and the language “closest to our heart” cortex to a larger extent when they process a less
(Minkowski 1927). proficient language than when they process a
more proficient language (e.g., Golestani et al.
2006; Indefrey 2006; Marian et al. 2007; Perani
Current Knowledge et al. 2003; Sakai et al. 2004). Increased activation
in dorsolateral prefrontal cortex, anterior cingu-
A systematic and theoretical understanding of late gyrus, and supramarginal gyrus has been
bilingual aphasia relies on an understanding of observed during language switching (Hernandez
the bilingual language system and its neural cor- et al. 2000; Price et al. 1999; Wang et al. 2007),
relates. While more similarities than differences while increased activation in anterior cingulate
have been observed with regard to linguistic pro- gyrus and basal ganglia has been noted during
cessing and neuroanatomical correlates of lan- translation (Price et al. 1999). Finally, bilinguals
guage for bilinguals and monolinguals, language show activation of the left caudate nucleus and
function of a bilingual speaker is not equivalent to anterior cingulate gyrus for naming tasks in a
that of a monolingual speaker. With two language bilingual context (Abutalebi et al. 2007). Alto-
systems instead of one, bilinguals have been gether, the neural network that supports language
shown to activate their two languages in parallel control in bilinguals likely includes anterior
Bilingual Aphasia 571

cingulate cortex, presupplementary motor area, languages). Pathological mixing, characterized

prefrontal and inferior frontal cortex, caudate by inadvertent and uncontrolled language
nucleus/putamen/thalamus, left inferior parietal switches, is typically associated with blended
lobule, and the cerebellum (Green and Abutalebi impairment. In contrast, pathological fixation is
2013). an inability to switch languages. Antagonistic B
Bilingual individuals with aphasia typically go recovery refers to a pattern where one language
through a variety of changes in their language recovers first and starts regressing when the other
abilities, where their languages are available to language starts to recover. Alternating antago-
different degrees during the acute phase of recov- nism refers to repetition of the antagonistic pat-
ery (up to 4 weeks postonset). During this phase, tern, with the two languages alternating in
availability of representations may vary because availability (cycles may range from hours to
of diaschisis. As impairment patterns stabilize months). Selective impairment refers to aphasia
during the postacute phase (up to 5 months post- in only one language, while the other language
onset), language impairment becomes more remains intact (relative to premorbid language
directly related to site of lesion and damage to proficiency). In addition, a variety of deficits
specific linguistic and cognitive representations. have been identified in bilingual aphasics’ ability
to translate from one of their languages to the
Clinical Variants and Recovery Patterns other. An inability to translate is reflected in bilin-
Bilingual individuals with aphasia show great guals’ inability to translate either forward (from
variability in impairment and recovery patterns. their native language to their second language) or
Paradis (2001), in a review of 132 cases of bilin- backward (from their second language to their
gual aphasia, found that 61% showed parallel native language). Paradoxical translation is an
recovery of their two languages, 18% showed ability to translate from one language to the
differential recovery of their two languages, 7% other, but not the other way around. Translation
showed blended recovery, and 5% showed selec- without comprehension is a preserved ability to
tive recovery (for similar distributions on a sample translate without an ability to comprehend the
of 20 Italian–Friulian patients, see Fabbro 2001). meaning of either translation. Finally, spontane-
Reports of atypical and pragmatically inappropri- ous translation is the involuntarily production of
ate language switching behaviors in bilingual translations that cannot be inhibited.
individuals with aphasia have also appeared The heterogeneity of the bilingual population
(Muñoz et al. 1999). makes it difficult to link language profiles and
Parallel impairment and recovery is the most lesion site/size with specific impairment and
prevalent pattern observed in bilingual aphasia recovery patterns in individuals with bilingual
(e.g., Paradis 2001), Parallel impairment refers aphasia. However, a number of linguistic factors
to aphasia of the same type and severity in both in impairment and recovery patterns have been
languages. The two languages are impaired and identified. Naming and translation of cognate
recover simultaneously (relative to premorbid lan- words (that share sound and meaning in the two
guage proficiency). Differential impairment refers languages, e.g., lamp-lámpara) is frequently less
to aphasia of the same type in both languages impaired in bilingual individuals with aphasia
(e.g., fluent vs. nonfluent) with crosslinguistic than naming and translation of noncognate
differences in severity levels. In contrast, differ- words (key – llave, Goral et al. 2006; Kohnert
ential aphasia refers to different aphasia symp- 2004; Roberts and Deslauriers 1999). However,
toms in each language. Differential recovery variability in such cognate effects has been dem-
refers to one language recovering better than the onstrated across individuals with aphasia, ranging
other (relative to premorbid levels). Blended from facilitation to interference effects (Hughes
impairment refers to the inappropriate combina- and Tainturier 2015). In general, aspects of bilin-
tion of two or more languages (e.g., the patient guals’ languages that are more shared are also
may lose the ability to discriminate between more resistant to impairment (e.g., Kiran and
572 Bilingual Aphasia

Tuctenhagen 2005). Linguistic features that differ There are currently no assessment measures for
between languages (e.g., different grammatical bilingual aphasia that meet all standards for mea-
systems) may result in differences in how symp- surement validity. The bilingual aphasia test
toms of aphasia are expressed even if the same (BAT, Paradis 1987) is the most comprehensive
underlying deficit exists. For example, a morpho- tool available, providing systematic ways to
logically rich language can theoretically undergo assess aphasia in more than 59 languages, includ-
greater morphological breakdown, and morpho- ing cross-linguistic interactions in an even larger
logical deficits may look more severe. Therefore, combination of language pairs. Tasks on the BAT
cross-linguistic differences in the symptoms and are equivalent in linguistic complexity across lan-
recovery patterns of bilingual aphasia frequently guages and cover assessment of multiple linguis-
occur at points where the two linguistic systems tic levels (phonological, lexical-semantic,
diverge. morphological, syntactic), linguistic skills
Another explanation for divergent recovery (comprehension, formulation, repetition, judg-
patterns in bilingual aphasia is the Cue Strength ment, lexical access), and linguistic units (words,
hypothesis (e.g., Wulfeck et al. 1991). According sentences, paragraphs). The BAT assumes that the
to this hypothesis, the linguistic importance of a test-taker has premorbid proficiency in each lan-
grammatical structure or the contribution it guage that is equivalent to at least 400 language-
makes to the linguistic message may account learning hours. The test is administered in each
for crosslinguistic differences in syntactic defi- language on different days. Where it is not feasi-
cits, with higher-ranked cues more likely to be ble to obtain all language versions of the BAT, its
preserved. For example, English-speaking indi- principles may be followed during assessment.
viduals with aphasia were found to be more sen- Additional tasks that may be useful in examin-
sitive to word-order errors during grammaticality ing bilingual individuals’ language impairments
judgments while Italian-speaking individuals include the type-token ratio in each language
with aphasia were more sensitive to morpholog- based on comparable language samples, number
ical errors. Similarly, differences in reading of verbs and grammatical clauses per utterance,
impairments have been found across languages semantic acceptability, confabulation, and total
with different orthographies. Readers are number of words or utterances within a set time
referred to reviews of bilingual aphasia by window (fluency measures). Preservation of links
Lorenzen and Murray (2008) and Ansaldo and between languages may be assessed by testing
Ghazi Saidi (2014). participants’ translation abilities from the native
language to the second language and vice versa.
Assessment As part of cognitive assessment, language
An important part of assessment in bilingual apha- switching behaviors may be examined. It may be
sia consists of establishing premorbid proficiency possible to distinguish pathological mixing
levels as accurately as possible and determining from nonpathological mixing, although such an
the nature and extent of impairment in each lan- analysis should be embedded within a careful
guage relative to these premorbid proficiency documentation of code-switching practices char-
levels. Self-reports, questionnaires about the his- acterizing the patient’s community.
tory of language use (e.g., code-switching), If, due to limitations in resources, assessment
reports from family members or friends, and writ- and treatment are done only in English, the clini-
ten or recorded samples of patients’ language cian may obtain information on the structure of
abilities are typically used to establish premorbid the clients’ other language in order to identify
proficiency levels. Once premorbid proficiency cross-linguistic influences in the clients’ English
levels have been established, it is important to output. This may allow the clinician to distinguish
assess both of the patients’ languages in order to low premorbid proficiency in English from a dis-
gauge their full linguistic capacity and impair- order. The dynamic assessment approach provides
ments across languages. an alternative method for examining deficits in
Bilingual Aphasia 573

situations of low premorbid language proficiency. are used in treatment (Kohnert 2004, but see
Dynamic assessment focuses on the ability to Kurland & Falcon for cognate interference during
learn new information, rather than the ability to treatment 2011), when semantic features are
retrieve known information. A clinician may treated (Edmonds and Kiran 2004, 2006; Knoph
explain a new grammatical rule and test the cli- et al. 2015), when general cognitive function is B
ent’s ability to generalize it. If the client general- treated (Kohnert 2004), and may be more likely
izes the rule easily, then weak linguistic when languages are structurally similar to each
performance is likely due to the influence of the other (e.g., Ansaldo and Ghazi Saidi 2014;
nontarget language or low proficiency in the target Knoph et al. 2015). However, generalization
language, rather than aphasia. from a stronger to a weaker language is less likely
and, in general, cross-linguistic generalization
Treatment does not always occur (e.g., Galvez and Hinckley
Assessment of both languages, together with the 2003). In contrast, within-language generalization
social communication needs of the client, will of treatment effects has been shown to be more
inform choice of therapy language and specific substantial in the more proficient language
therapy goals. A primary goal in the treatment of (Edmonds and Kiran 2006; Kurland and Falcon
bilingual individuals with aphasia is to maximally 2011), a result that must also be considered when
benefit both languages even if treatment occurs in selecting treatment languages. Although language
only one language. dominance patterns are frequently the same pre-
Treatment may be conducted to target both and postmorbidly, this is not always the case.
languages directly. During bilingual treatment, While much of the current treatment literature
language-switching may be encouraged as a com- suggests that premorbid proficiency levels influ-
pensatory strategy to allow the client to use his/her ence cross-linguistic generalization of treatment,
full linguistic capacity. Translation may be used in others have argued that generalization patterns
a similar manner to aid lexical access. For exam- may also be determined by postmorbid profi-
ple, switch-back through translation (SBT) treat- ciency levels (for a review, see Ansaldo and
ment (Ansaldo and Marcotte 2007) is a procedure Ghazi Saidi 2014).
where the client is cued to translate the word back
into the other language whenever an inadvertent
switch occurs. Future Directions
If resources are only available to treat in
English, the speech-language pathologist may In 2011, 21% of the population older than 5 years
work to identify outside resources in helping to of age (more than 60 million people) spoke a
rehabilitate the clients’ other languages. Such lin- language other than English at home, up from
guistic resources may include language-specific 18% in 2000, 14% in 1990, and 11% in 1980
community groups, or guidance of family mem- (Ryan 2013). As the bilingual population grows,
bers. Cross-linguistic generalization is most likely with special growth in older adults, the need for
to occur when shared representations are targeted accommodation of bilingual individuals with
for treatment, cross-linguistic associative links are aphasia will increase. Among Mexican Ameri-
used, or similar cognitive processes are a focus of cans, stroke incidence is slightly higher (1.63%)
intervention (e.g., reading in alphabetic lan- than in non-Latino white peers (1.36%), and tran-
guages). Current evidence suggests that treatment sient ischemic attacks are more frequent at youn-
in a patient’s weaker or equally dominant lan- ger ages (Lorenzen and Murray 2008). The US
guage may generalize to their other language, Department of Health and Human Services found
especially when treatment targets are similar that individuals of Latino origin were 33% less
across languages (e.g., Edmonds and Kiran likely to receive necessary health-care services,
2004). Generalization of treatment effects across compared to non-Latino white peers (Lorenzen
languages has been shown when cognate words and Murray 2008). With these changes in
574 Bilingual Aphasia

population dynamics, systematic evidence-based Cross-References

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approaches for bilingual aphasia has become ▶ Aphasia
increasingly necessary. ▶ Aphasia Tests
One avenue of research in bilingual aphasia ▶ Multilingual Aphasia Examination
that has been virtually unexplored is in the area ▶ Speech-Language Pathology
of cognitive control, and more broadly, in atten- ▶ Speech-Language Therapy
tion and executive function skills. There exists a
significant body of literature attempting to link
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ron, 37, 159–170.
Wulfeck, B., Bates, E., & Capasso, R. (1991). A cross-
linguistic study of grammaticality judgments in Broca’s The disorder is classified with the feeding and
aphasia. Brain and Language, 41, 311–336. eating disorders in DSM-5.
Zied, K. M., Phillipe, A., Karine, P., Valerie, H. T.,
Ghislaine, A., Arnaud, R., et al. (2004). Bilingualism
and adult differences in inhibitory mechanisms: Evi-
dence from a bilingual stroop task. Brain and Cogni- Current Knowledge
tion, 54, 254–256.
Zinn, S., Bosworth, H. B., Hoenig, H. M., & Swartwelder, Development and Course
H. S. (2007). Executive function deficits in acute
stroke. Archives of Physical Medicine and Rehabilita- The development of binge-eating disorder is com-
tion, 88, 173–180. mon in adolescents and young adults but can
Binocular Disparity 577

occur later in life. Individuals typically fall within Bulik, C., Brownley, K., & Shapiro, J. (2007). Diagnosis
a normal to obese weight range; however, binge- and management of binge eating disorder. World Psy-
chiatry, 6(3), 142–148.
eating disorder is distinct from obesity. The disor- Cossrow, N., Pawaskar, M., Witt, E. A., Ming, E. E.,
der is slightly more common in females (1.6%) Victor, T. W., Herman, B. K., ..., Erder, M. H. (2016).
than in males (0.8%; APA 2013). Binge-eating Estimating the prevalence of binge eating disorder in a B
disorder is persistent, but remission rates are community sample from the United States: Comparing
DSM-IV-TR and DSM-5 criteria. The Journal of Clin-
higher for than for anorexia nervosa or bulimia ical Psychiatry, 77(8), e968–e974.
nervosa. The condition is associated with social
maladjustment, poor quality of life, obesity, and
increased mortality. Mood disorders and anxiety
disorders commonly co-occur, as do substance
abuse disorders to a lesser extent. Binocular Disparity

Assessment and Treatment Sarah M. Szymkowicz1 and Adam J. Woods1,2,3

1
Diagnosis typically involves medical and psychi- Department of Clinical and Health Psychology,
atric evaluation. Individuals seeking treatment for College of Public Health and Health Professions,
binge-eating disorder are typically older than University of Florida, Gainesville, FL, USA
2
those seeking treatment for bulimia nervosa or Center for Cognitive Aging and Memory,
anorexia nervosa. Treatment typically involves McKnight Brain Institute, University of Florida,
pharmacotherapy and psychotherapy. Medica- Gainesville, FL, USA
3
tions with some empirical evidence include selec- Department of Neuroscience, University of
tive serotonin reuptake inhibitors, tricyclic Florida, Gainesville, FL, USA
antidepressants, anticonvulsants, and antiobesity
medications (Bulik et al. 2007). Empirically
supported psychotherapeutic interventions Human eyes are separated by about 50–75 mm
include cognitive-behavioral therapy and dialecti- between pupils (Dodgson 2004). Therefore, each
cal behavior therapy. eye views the world in a slightly different way.
The difference between these images is referred to
as binocular disparity and provides important
See Also information that is not available from either
image alone. The amount of disparity depends
▶ Anorexia Nervosa
on the difference in the distance of the two objects
▶ Bulimia Nervosa
and the distance of the fixation point. The greater
▶ Feeding and Eating Disorders
the disparity, or distance, between the two images,
the closer the object is to the fixation point. Bin-
ocular disparity is a necessary condition for stere-
References and Readings opsis, which is the sense of depth the brain
generates from information obtained by the left
American Psychiatric Association. (2013). Diagnostic and
statistical manual of mental disorders (DSM-5 ®). and right eye. This helps us to see the world in
Washington, DC: American Psychiatric Association. three dimensions, rather than two dimensions.
Berkman, N. D., Brownley, K. A., Peat, C. M., Lohr, K. N., The idea that binocular disparity contributes to
Cullen, K. E., Morgan, L. C., ..., Bulik, C. M. (2015).
Management and outcomes of binge-eating disorder.
depth perception was first described by Sir
Comparative Effectiveness Review No. 160. (Prepared Charles Wheatstone in the nineteenth century
by the RTI International-University of North Carolina after he invented the stereoscope, a device used
Evidenced-based Practice Center under Contract No. for observing pictures in three dimensions (Qian
290-2012-00008-I.) AHRQ Publication No. 15(16)-
EHC030-EF. Rockville, MD: Agency for Healthcare
1997). Since then, much research has focused on
Research and Quality; December 2015. www.effective- unraveling how the brain processes these dispar-
healthcare.ahrq.gov/reports/final.cfm. ities, particularly in animal models. A seminal
578 Binocular Disparity

study by Barlow et al. (1967) conducted in the be solely involved in relative disparity (Parker
cat’s primary visual cortex found that neurons are 2007), though a recent functional magnetic reso-
tuned, or excited, at different distances. A subse- nance imaging study showed that disparity pref-
quent study by Poggio and Fischer (1977) erences for depth perception were clustered in
described four types of depth cells in the striate dorsal visual areas, including V3A and V3B/KO
and prestriate cortex of the rhesus monkey: (1) (Goncalves et al. 2015).
“tuned excitatory neurons,” which respond to a
narrow range of depth around the fixation point,
(2) “tuned inhibitory neurons,” whose responses References
are suppressed by stimuli at or close to the fixation
point, (3) “near neurons,” which respond to stim- Barlow, H. B., Blakemore, C., & Pettigrew, J. D. (1967).
uli near the fixation point and suppress informa- The neural mechanism of binocular depth discrimina-
tion behind it, and (4) “far neurons,” which tion. The Journal of Physiology, 193(2), 327–342.
Dodgson, N. A. (2004). Variation and extrema of human
respond to information behind the fixation point interpupillary distance. In M. T. Bolas, A. J. Woods, J.
and suppress information near it. While Poggio O. Merritt, & S. A. Benton (Eds.), Proceedings of
and collaborators classified cells into these dis- SPIE: Stereoscopic displays and virtual reality systems
crete categories, additional research suggests XI (Vol. 5291, pp. 36–46). San Jose. https://doi.org/
10.1117/12.529999
there is a continuous distribution of these cells Goncalves, N. R., Ban, H., Sanchez-Panchuelo, R. M.,
(LeVay and Voigt 1988). Nevertheless, recordings Francis, S. T., Schluppeck, D., & Welchman, A. E.
indicate that disparity neurons are primarily (2015). 7 tesla FMRI reveals systematic functional
located in V2, V3/V3A, and MT/V5, with weak organization for binocular disparity in dorsal visual
cortex. The Journal of Neuroscience, 35(7),
clustering shown in V1 (Parker 2007). 3056–3072.
In humans, the architecture of disparity is less Janssen, P., Vogels, R., & Orban, G. A. (2000). Three-
understood. This is partially due to differences in dimensional shape coding in inferior temporal cortex.
neuronal firing for absolute versus relative dispar- Neuron, 27(2), 385–397.
Janssen, P., Vogels, R., Liu, Y., & Orban, G. A. (2001).
ities (Neri 2005). When looking at a pair of Macaque inferior temporal neurons are selective for
objects that are different distances apart, absolute three-dimensional boundaries and surfaces. The Jour-
disparity refers to the differences between the two nal of Neuroscience, 21(23), 9419–9429.
retinal images generated by the object alone with LeVay, S., & Voigt, T. (1988). Ocular dominance and
disparity coding in cat visual cortex. Visual Neurosci-
respect to the fixation point and relative disparity ence, 1(4), 395–414.
refers to the difference between the two absolute Neri, P. (2005). A stereoscopic look at visual cortex. Jour-
disparities (Neri 2005; Parker 2007). Humans are nal of Neurophysiology, 93(4), 1823–1826.
more sensitive to relative, compared to absolute, Parker, A. J. (2007). Binocular depth perception and the
cerebral cortex. Nature Reviews. Neuroscience, 8(5),
disparities (Westheimer 1979). Both the dorsal 379–391.
and ventral streams process binocular cues; how- Poggio, G. F., & Fischer, B. (1977). Binocular interaction
ever, each stream carries out different types of and depth sensitivity in striate and prestriate cortex of
processing. In animals, the dorsal stream is behaving rhesus monkey. Journal of Neurophysiology,
40(6), 1392–1405.
involved in processing relative disparity, particu- Qian, N. (1997). Binocular disparity and the perception of
larly as it relates to spatially extended surfaces depth. Neuron, 18(3), 359–368.
(Roy et al. 1992; Upadhyay et al. 2000). In con- Roy, J. P., Komatsu, H., & Wurtz, R. H. (1992). Disparity
trast, the ventral stream is also sensitive to relative sensitivity of neurons in monkey extrastriate area MST.
The Journal of Neuroscience, 12(7), 2478–2492.
disparity but appears to be selectivity involved in Uka, T., Tanabe, S., Watanabe, M., & Fujita, I. (2005).
the relative depth of objects and their three-dimen- Neural correlates of fine depth discrimination in mon-
sional configurations (Janssen et al. 2000, 2001; key inferior temporal cortex. The Journal of Neurosci-
Uka et al. 2005; Umeda et al. 2007). Neurons in ence, 25(46), 10796–10802.
Umeda, K., Tanabe, S., & Fujita, I. (2007). Representation
the dorsal and ventral streams do fire for both of stereoscopic depth based on relative disparity in
relative and absolute disparities, but, to date, no macaque area V4. Journal of Neurophysiology, 98(1),
single cortical region in humans has been found to 241–252.
Binswanger’s Disease 579

Upadhyay, U. D., Page, W. K., & Duffy, C. J. (2000). MST 2015). Although the precise cause of BD is
responses to pursuit across optic flow with motion unclear, it is frequently associated with diabetes,
parallax. Journal of Neurophysiology, 84(2), 818–826.
Westheimer, G. (1979). Cooperative neural processes cardiovascular disease, previous cerebrovascular
involved in stereoscopic acuity. Experimental Brain accident, malnutrition, and, most notably, hyper-
Research, 36(3), 585–597. tension. The age of onset for BD is typically B
between ages 60 and 79 years, with men and
women equally affected. Estimates about the inci-
dence of BD range from 3% to 12% (Babikian and
Binswanger’s Disease Ropper 1987).

Matthew Kraybill1 and Yana Suchy2

1
Neuropsychology, Cottage Rehabilitation Current Knowledge
Hospital, Santa Barbara, CA, USA
2
Department of Psychology, The University of Neuropathology
Utah, Salt Lake City, UT, USA Gross pathology of brain tissue affected by BD
is characterized by gyral atrophy and widening
of the sulci resulting from the loss of cerebral
Synonyms white matter. Lateral ventricles are also typically
enlarged. Lacunar infarctions can be found in
CADASIL; Multi-infarct dementia; Subcortical the white matter, pons, and basal ganglia as
leukoencephalopathy; Subcortical vascular well as occasionally in the cerebellum. Micro-
dementia scopic pathology of BD is marked by diffuse
and patchy white matter demyelination with
areas of reactive gliosis and decreased nerve
Definition fibers. The small arteries of the white matter
also show fibrous thickening, which is associ-
Binswanger’s disease (BD) is a type of subcortical ated with hypertension and cardiovascular dis-
vascular dementia caused by widespread, micro- ease. There is growing evidence that white
scopic damage to cerebral white matter. The dam- matter pathology in BD is related to endothelial
age is usually the result of atherosclerosis (i.e., dysfunction and neuroinflammation (Huisa and
narrowing of arterial blood vessels) that reduces Rosenberg 2014).
the supply of blood to subcortical areas of the
brain, causing tissue to die. The characteristic Clinical Symptoms
pattern of BD-damaged brain tissue can be seen BD typically has a slow, insidious onset that even-
using brain imaging techniques such as computed tually manifests in cognitive and motor dysfunc-
tomography (CT) or magnetic resonance imaging tions related to the disruption of subcortical neural
(MRI). CT imaging of BD often reveals symmet- circuits. Specifically, patients exhibit executive
ric, noncontrasting hypodensities also called dysfunction (e.g., impaired initiation, inhibition,
“leukoaraiosis,” and more sensitive MRI imaging monitoring of goal-directed behavior, and verbal
reveals diffuse white matter lesions and scattered fluency), psychomotor slowing, inattention, and
multiple lacunes (Akiguchi et al. 2014). short-term memory loss with poor retrieval but
There is some controversy in the literature intact recognition (Roman 2003). Other symp-
about whether BD constitutes a distinct clinical toms include changes in speech, an unsteady
entity or simply describes the result of different gait, postural instability, changes in personality
neuropathologies that affect subcortical white or mood (including apathy, irritability, and depres-
matter (Akiguchi et al. 2014; Caplan 1995; sion), as well as urinary incontinence (Babikian
Hachinski et al. 2006; Olsen and Clasen 1998; and Ropper 1987; Caplan 1995; Lezak et al. 2004;
Pantoni and Garcia 1995; Rosenberg et al. Roman 2003).
580 Biomechanics of Injury

Treatment Stroke-Canadian Stroke Network vascular cognitive

Treatment of BD is often targeted at specific impairment harmonization standards. Stroke, 37(9),
2220–2241.
symptoms. For example, medications such as Huisa, B. N., & Rosenberg, G. A. (2014). Binswanger’s
donepezil and memantine may be used to treat disease: Toward a diagnosis agreement and therapeutic
the cognitive symptoms associated with BD. Indi- approach. Expert Review of Neurotherapeutics, 14(10),
viduals with depression may be treated with anti- 1203–1213.
Lezak, M. D., Howieson, D. B., & Loring, D. (2004).
depressant medications (e.g., selective serotonin Neuropsychological assessment (4th ed.p. 1016). New
reuptake inhibitors (SSRIs) such as sertraline or York: Oxford University Press.
citalopram) and individuals with agitation or dis- Olsen, C. G., & Clasen, M. E. (1998). Senile dementia of
ruptive behavior can be treated with atypical anti- the Binswanger’s type. American Family Physician,
58(9), 2068–2074.
psychotic medications such as risperidone or Pantoni, L., & Garcia, J. H. (1995). The significance of
olanzapine (Sink et al. 2005). Antiplatelet therapy cerebral white matter abnormalities 100 years after
and statins have also been recommended for Binswanger’s report. A review. Stroke, 26(7),
stroke prevention in BD (Huisa and Rosenberg 1293–1301.
Roman, G. C. (2003). Neurological aspects of vascular
2014). Other treatment interventions are often dementia: Basic concepts, diagnosis, and management.
focused on reducing cardiovascular risk factors In P. A. Lichtenberg, D. L. Murman, & A. M. Mellow
by eating a healthy diet, exercising, and not (Eds.), Handbook of dementia – Psychological, neuro-
smoking or drinking too much alcohol. Control- logical, and psychiatric perspectives (pp. 149–171).
Hoboken: Wiley.
ling vascular risk factors can help improve cogni- Roman, G. C. (2005). Vascular dementia prevention: A risk
tion and may even help prevent the development factor analysis. Cerebrovascular Diseases, 20(Suppl.
of dementia (Roman 2005). 2), 91–100.
Rosenberg, G. A., Wallin, A., Wardlaw, J. M., Markus,
H. S., Montaner, J., Wolfson, L., Costantino, I.,
Prognosis Zlokovic, B. V., Joutel, A., Dichgans, M., Duering,
BD is a progressive disease and there is currently M., Schmidt, R., Korczyn, A. D., Grinberg, L. T.,
no cure. The course of BD can be variable and & Hachinski, V. (2015). Consensus statement for
deterioration can occur suddenly or gradually and diagnosis of subcortical small vessel disease. Jour-
nal of Cerebral Blood Flow and Metabolism, 36(1).
then progress in a stepwise manner (Santamaria 1–13.
Ortiz and Knight 1994). Santamaria Ortiz, J., & Knight, P. V. (1994). Review:
Binswanger’s disease, leukoaraiosis and dementia.
Age and Ageing, 23(1), 75–81.
Sink, K. M., Holden, K. F., & Yaffe, K. (2005). Pharma-
Cross-References cological treatment of neuropsychiatric symptoms of
dementia: A review of the evidence. JAMA, 293(5),
596–608.
▶ Leukoaraiosis

References and Readings Biomechanics of Injury

Akiguchi, I., Budka, H., Shirakashi, Y., Woehrer, A.,
Watanabe, T., Shiino, A., Yamamoto, Y., Kawamoto, Y., Beth Rush
Krampla, W., Jungwirth, S., & Fischer, P. (2014). MRI Psychiatry and Psychology, Mayo Clinic,
features of Binswanger’s disease predict prognosis and Jacksonville, FL, USA
associated pathology. Annals of Clinical and Transla-
tional Neurology, 1(10), 813–821.
Babikian, V., & Ropper, A. H. (1987). Binswanger’s dis-
ease: A review. Stroke, 18(1), 2–12. Definition
Caplan, L. R. (1995). Binswanger’s disease – Revisited.
Neurology, 45(4), 626–633.
An inclusive term to explore and describe the
Hachinski, V., Iadecola, C., Petersen, R. C., Breteler, M. M.,
Nyenhuis, D. L., Black, S. E., et al. (2006). mechanical and physical factors that result in trau-
National Institute of Neurological Disorders and matic brain injury.
Biopsy 581

Current Knowledge Cross-References

Biomechanical injuries typically occur without ▶ Acceleration Injury

the direct impact of an outside object on the ▶ Deceleration Injury
skull or brain, but rather in the context of ▶ Diffuse Axonal Injury B
acceleration-deceleration injuries or blast inju- ▶ Rotational Acceleration
ries. High-speed situations such as motor vehi- ▶ Traumatic Brain Injury (TBI)
cle accidents and sports provide mediums for
these inertia-based injuries. The structure of
the skull includes sinuses and bony protective References and Readings
regions. Underlying brain tissue is held in sus-
pension underneath the skull not only by the Bayly, P. V., Cohen, T. S., Leister, E. P., Ajo, D., Leuthardt,
E. C., & Genin, G. M. (2005). Acceleration-induced
meninges, but also by a cushion of cerebral
deformation of the human brain. Journal of
spinal fluid. Different inertial forces such as Neurotrauma, 22, 845–856.
linear acceleration, rotation of the head, or mas- Goriely, A., Geers, M. G., Holzapfel, G. A., Jayamohan, J.,
sive vibration or air pressure changes in the Jerusalem, A., Sivaloganathan, S., Squier, W., van
Dommelen, J. A., Waters, S., & Kuhl, E. (2015).
environment can result in a wide range of poten-
Mechanics of the brain: Perspectives, challenges,
tial damage to these underlying substances. and opportunities. Biomechanical Models of
These disruptions may include skull fracture, Mechanobiology, 14(5), 931–965.
linear acceleration injury, rotational injury, and Oeur, R. A., Karton, C., Post, A., Rousseau, P., Hoshizaki,
T. B., Marshall, S., Brien, S. E., Smith, A., Cusimano,
the effects of vibration of the skull and brain
M. D., & Gilchrist, M. D. (2015). A comparison of head
against one another. dynamic response and brain tissue stress and strain
Superficial or deep lesions may result in using accident reconstructions for concussion, concus-
parenchymal injury depending on the type of sion with persistent postconcussive symptoms, and
subdural hematoma. Journal of Neurosurgery, 123(2),
mechanical force that occurred at the time of
415–422.
head trauma. Linear acceleration injuries are Ommaya, A. K., Goldsmith, W., & Thibault, L. (2002).
most often associated with superficial brain inju- Biomechanics and neuropathology of adult and pediat-
ries such as cerebral contusions, while rotational ric head injury. British Journal of Neurosurgery, 16,
220–242.
injuries are most often associated with disrup-
tions to deep white matter tracts and projections,
and centrally located brain structures and neural
networks. Consequently, rotational injuries may
be more severe with regard to effects on cogni- Biopsy
tion, motor skills, and functional status. Concus-
sion with or without loss of consciousness is Bram Goldstein
also a consequence of biomechanical forces Department of Gynecologic Oncology, Hoag
and the subsequent effects on underlying brain Hospital Cancer Center, Newport Beach,
tissue. CA, USA
The biomechanics of injury differentially
affect initial and long-term recovery from
acquired brain injury. Understanding these differ- Definition
ent mechanical forces may help one to improve
understanding of injury severity. Increased under- A biopsy is a medical examination entailing
standing of the biomechanics underlying brain the removal of cellular tissue via a needle or
injury has led to the development of protective surgical resection. In particular, an incisional
headgear in high-speed or direct-impact sports or core biopsy involves a select sample of
such as biking, motor racing, football, and tissue, whereas an excisional biopsy necessi-
hockey. tates a larger specimen. The biopsy results are
582 Blast Effects

typically evaluated microscopically by a to brain injury and are classified as primary,

pathologist, who determines if a lesion’s secondary, tertiary, or quaternary (CDC 2016).
pathology is benign or malignant. Although Primary blast effects are unique to high-order
histological confirmation of tumor diagnosis explosives and may include injuries such as
can be achieved, a biopsy sampling error can concussion, eye rupture, or abdominal hemor-
result if the specific tissue section does not rhage (CDC 2016). Secondary and tertiary
contain the most representative cellular fea- effects may result from bomb fragments, flying
tures. When the biopsy is abnormal, the cell debris, or blast wind with any body part being
structure may be unusual and indicative of affected. Last, quaternary effects include explo-
malignancy. However, further pathological sion-related injuries, illness, or disease, such as
examination is often required to make a defin- burns, close or open brain injury, and breathing
itive diagnosis. problems due to toxic fumes, dust, or smoke
from a blast.

Cross-References
See Also
▶ Radiosurgery, Stereotactic Radiosurgery
▶ Blast Injury
▶ Mild Traumatic Brain Injury
References and Readings ▶ Severe Brain Injury
▶ Traumatic Brain Injury (TBI)
Yu, X., Liu, Z., Tian, Z., Li, S., Huang, H., Xiu, B.,
et al. (2006). Stereotactic biopsy for intracranial
space-occupying lesions: Clinical analysis of
550 cases. Stereotactic and Functional Neurosurgery,
References and Readings
75, 103–108.
Center for Disease Control Injury Prevention (2016).
Explosions and blast injuries: A primer for clinicians.
Retrieved from: https://www.cdc.gov/masstrauma/pre
paredness/primer.pdf
Blast Effects Lash, M. (2017). Understanding the effects of concussion,
blast, and brain injuries: A guide for families, veterans,
Kayla LaRosa and caregivers. Brainline Military. Retrieved from:
http://www.brainlinemilitary.org/content/2008/11/under
Educational and Psychological Studies/TBI standing-effects-concussion-blast-and-brain-injuries-gui
Model Systems, University of South Florida/J.A. de-families-veterans-and-caregi_pageall.html
Haley VA, Tampa, FL, USA

Synonyms Blast Injury

Blast injury Bradley J. Hufford

Neuropsychology, Rehabilitation Hospital of
Indiana, Indianapolis, IN, USA
Definition

Blast effects are injuries or symptoms resulting Synonyms

from a shock wave or blast caused by high-order
or low-order explosives such as dynamite, This term is highly associated (but technically not
bombs, or C-4 (CDC 2016). Effects resulting synonymous) with mild traumatic brain injury and
from blasts may vary from auditory problems post-concussive symptoms.
Blast Injury 583

Definition Current Knowledge

A trauma sustained as a result of exposure With improvements in medical care of trauma and
to an explosion or its effects. Technically, the development of more effective defensive
blast injury can affect any physical system/ equipment (i.e., body and vehicle armor), a B
function; its neurological effects are highlighted greater number of servicemen and women injured
here. in combat are surviving than ever before: The
mortality rate for wounded personnel has declined
from approximately 30% during the Second
Historical Background World War to approximately 10% during the
recent conflicts in Iraq and Afghanistan. As a
Blast injuries can occur in any setting, civilian result, a greater number of the wounded are sur-
or military. However, exposure to the effects viving with traumatic brain injury than in the
of explosive forces is much more associated past – from under 20% during the Vietnam con-
with military populations and has been since flict to perhaps near 50% in the recent conflicts.
the advent of modern warfare. Awareness of Overall, it has been estimated that up to 30% of all
the effect of blast injuries began to emerge in combat troops in Operations Iraqi Freedom and
earnest with the phenomenon of “shell shock” Enduring Freedom (OIF/OEF) may have incurred
during the First World War. That war exposed an acquired brain injury of some degree. The
a staggering number of soldiers to explosive majority of these combat-related brain injuries
injuries, far more than had previous conflicts. are sustained as a result of exposure to an
As a result, an ever-increasing number of mil- explosion.
itary personnel presented with vague but inca- Explosions may cause injury through four
pacitating complaints that prevented them from mechanisms:
returning to active (particularly front line)
duty. Initially, these symptoms were consid- 1. Primary Blast Injury
ered to be secondary to organic central ner- A primary injury is one sustained from expo-
vous system injury. Over time, however, others sure to the shock/pressure waves initiated by
favored a more psychological or even inten- the explosion. When explosive munitions are
tional (i.e., malingering) explanation, citing the detonated, a shock-wave approaching a speed
fact that many shell-shocked servicemen did of 8000 m/s is generated. The waves generated
not appear to have been as close to the explo- from a blast can cause life-threatening injuries
sion as would seem necessary to truly be neg- when they strike an individual directly or if
atively affected. The nature of the shell-shock they reflect off nearby surfaces and then come
symptoms was further obscured by the lack of into contact with the person. The force gener-
diagnostic methods, absence of a clear defini- ated is of such a magnitude that it often results
tion of the syndrome, and even political factors in an instant fatality or in trauma to multiple
(e.g., superiors being able to justify returning body systems. Body organs that are relatively
much-needed soldiers to frontline duty if their solid or fluid-filled tend to sustain a lesser
complaints reflected psychological or constitu- degree of injury than those that are gas-filled
tional weaknesses rather than neurological/ or have a gas-liquid interface, such as the tym-
organic injuries). This debate of “psychologi- panic membrane, lung, colon, etc. Although
cal versus neurological” causes has continued not fully understood, research suggests that
throughout subsequent wars and is a particular the explosion may injure the central nervous
focus of the recent conflicts in the Middle system directly, as in a concussion, but may
East, given the high incidence of explosives also indirectly affect the brain. The latter case
utilized by terrorists and non-Coalition may occur when peripheral somatic areas are
combatants. impacted by the blast, setting in motion events
584 Blast Injury

that ultimately impact the CNS, such as chem- the following symptoms: less than half an hour of
ical/metabolic cascades, physical sequelae loss of consciousness, less than 24 h of post-
(i.e., cerebral infarction caused by an air embo- traumatic amnesia, any retrograde or anterograde
lism), and/or kinetic events (e.g., transfer of amnesia, mental status changes immediately after
shock/pressure wave energy from the body, injury, and transient/permanent neurological
up the vasculature into brain tissue). It has impairments. The literature cautions that a mild
been postulated that the severity and number TBI from an explosion may not be equivalent to
of a person’s physical wounds from the pri- mild TBI from other etiologies (e.g., motor vehi-
mary blasts often overshadow symptoms of cle accidents, sports injuries), as the former may
traumatic brain injury, delaying diagnosis and affect the brain more diffusely and tend to involve
treatment for these injuries. trauma to other organ systems, thereby complicat-
2. Secondary Blast Injury ing the patient’s clinical presentation and recov-
Secondary injuries occur when shrapnel, ery. However, many studies have indicated that
debris, or other objects are caught up by the factors such as loss of consciousness, resultant
blast and propelled against/into an individual. symptom profiles, and recovery courses do not
Many of these injuries are therefore penetrat- appear to substantially differ between blast vic-
ing in nature. tims and those injured by other means, tentatively
3. Tertiary Blast Injury suggesting that knowledge gleaned from studying
This type of injury is sustained when the per- these other etiologies has at least some applicabil-
son is caught up and propelled by the blast ity to blast injury survivors.
wind that follows the initial shock wave and Cognitive (e.g., memory, attention), somatic
is thrown against an object, a structure, the (e.g., dizziness, headache, sleep initiation/main-
ground, other individuals, etc., often resulting tenance difficulties), and emotional (e.g., ner-
in blunt force wounds. vousness, irritability) symptoms are commonly
4. Quaternary Blast Injury seen initially after blast injuries. In civilian mTBI
Quaternary blast injuries arise from the after- samples, these symptoms usually resolve
effects of an explosion. Examples include quickly, with most individuals showing rapid
being exposed to radiation, fire, chemicals, recovery within the first week. However, over
dust, or toxic substances that were precipitated one-third may continue to experience significant
by the explosive event. post-concussion symptoms, and as many as 15%
may continue to experience persistent symptoms
Typically, an individual is exposed to more after 12 months (“Persistent Post-Concussion
than one mechanism, making the contributions Syndrome”). Unfortunately, these persistent
of one particular mechanism difficult to separate symptoms have not been consistently defined,
from others. and many point out that the constellation of
Approximately 60% of explosion-related inju- symptoms present are vague and lack specificity
ries in combat lead to an acquired brain injury. As needed to identify them as constituting a true
is the case with other etiologies, the majority of syndrome.
brain injuries resulting from explosions are clas- There is debate over whether the more chronic
sified as mild in nature. “Mild” traumatic brain symptom constellation after mild TBI reflects a
injury (mTBI) has not been consistently defined in true neurological condition; this has particular
the literature, which is a substantial limitation in relevance in blast injury, as the brief history of
making meaningful comparisons between studies. “shell shock” above illustrates. Those favoring a
Despite this, definitions such as that proposed by more neurological position cite animal models in
the American Congress of Rehabilitation Medi- which direct and indirect exposure to primary
cine (ACRM) are coming into wider acceptance blasts causes structural, chemical, and electro-
and have largely been adopted by the military. The physiological changes in the brain. Additionally,
ACRM definition of mTBI includes at least one of some studies using functional MRI and diffuse
Blast Injury 585

tensor imaging in humans have reported cerebral other symptoms (e.g., tinnitus) that place
alterations in some (albeit not all) persons who them at higher risk for having sustained a
have sustained blast injuries. Conversely, those TBI in a blast, to help ensure mTBIs are
weighing psychological factors more heavily in not underdiagnosed. The assessment process
terms of causation point to the mTBI literature that includes a thorough medical evaluation of the B
indicates non-neurological factors, such as pre- patient’s current condition and a comprehensive
morbid psychological coping resources and exter- interview that elicits historical information about
nal stressors, appear to influence the development past psychological treatment/coping, substance
of concussion symptoms in some individuals. The use, and combat exposure.
fact that mTBI symptoms overlap considerably Neuropsychological evaluation is recommended
with symptoms seen in disorders such as post- to occur as early as possible to help identify post-
traumatic stress disorder (PTSD) is particularly concussive symptoms and clarify the diagnostic
noteworthy, given the high incidence of PTSD in picture, enabling education and treatment efforts
military personnel who have experienced combat: to proceed more quickly. Whereas there are cog-
Gaylord et al. (2008) found that nearly 20% of nitive deficits commonly seen after most mTBIs
military persons who incurred blast and burn inju- (e.g., slowed attention and information processing
ries were appropriate for both mild brain injury speed, motor slowness, executive dysfunction,
and PTSD diagnoses. Hoge et al. (2008) reported and memory difficulties), the profile of cognitive
that approximately 15% of soldiers surveyed after weaknesses can be quite variable, necessitating a
being returned home might meet criteria for both broad-based neuropsychological assessment (i.e.,
mTBI and PTSD; these servicemen and women a sampling of all major cognitive domains). Addi-
were more likely to have been exposed to a blast tionally, as is the case in sports concussions, the
injury. In addition, their survey indicated that the symptom picture for many blast survivors may
presence of affective distress might be the major evolve relatively rapidly, arguing for use of tests
factor in maintaining chronic health difficulties, that have alternate forms (e.g., California Verbal
including mTBI symptomatology. A compromise Learning Test-2nd Edition, Hopkins Verbal
position of sorts posits mTBI symptoms are likely Learning Test-Revised). Tracking somatic symp-
neurological in origin but are subsequently toms (e.g., Neurobehavioral Symptom Inventory,
maintained by emotional/psychological factors Post-Concussion Scale-Revised) over time may
and that the presence of PTSD and similar affec- also have utility. Because of the high degree of
tive disturbances can complicate healing from and PTSD and other affective disorders, a thorough
coping with mTBI (and, concomitantly, mTBI psychological evaluation should always be
symptoms can exacerbate and prolong PTSD performed (including objective personality mea-
symptoms). The fact that PTSD symptoms can sures such as the MMPI-2 or PAI and instruments
arise long after the actual trauma indicates that such as the PTSD Checklist), and observation for
these emotional disturbances may influence a per- these symptoms should be an ongoing effort, not
son at virtually any point in his/her brain injury simply one restricted to an initial evaluation.
recovery. Given the high degree of lowered effort present
Treatment of blast injuries begins with a thor- in civilian mTBI cases, effort testing (e.g., Test of
ough diagnostic assessment. The armed services Memory Malingering) is often advocated, with
have made significant improvements in their the caveat that poor performance on an effort test
endeavors to standardize comprehensive screen- should not automatically be interpreted as an indi-
ing and interviewing methods to identify service cator of intentional feigning of symptoms, but as a
personnel who may have experienced an sign that further investigation is warranted as to
acquired brain injury, beginning on the battle- the cause of the lowered effort.
field and continuing throughout the military’s After a thorough diagnostic assessment has
medical system. Efforts have been made to been performed, treatments generally have
carefully screen every wounded individual for proceeded along the lines advocated for mild
586 Blast Injury

brain injuries attributed to non-blast causes. Spe- clearly needed. Within neuropsychology, devel-
cifically, reassurance and education regarding the opment of alternate forms for many tests is
nature and general recovery of cognitive and encouraged.
other symptoms after mTBI is delivered. Specific
treatments need to be tailored to the individual, in
recognition that not all mTBIs are expressed See Also
identically. For instance, in a cluster analysis
performed on 1341 servicemen who had ▶ Concussion
sustained an mTBI in combat over the previous ▶ Mild Traumatic Brain Injury
2 years, Bailie et al. (2016) found four different ▶ Post-concussive Syndrome
subtypes: good recovery (low overall cognitive ▶ Post-Traumatic Stress Disorder
and affective symptoms; 37.8% of the sample), ▶ Traumatic Brain Injury (TBI)
high PTSD but few cognitive symptoms
(21.9%), elevated cognitive but few affective
symptoms (21.5%), and mixed symptoms References and Readings
(18.6%). These results suggest an array of treat-
ment strategies that is necessary to effectively Bailie, J., Kennedy, J., French, L., Marshall, K., Pro-
khorenko, O., Asmussen, S., Reid, M., Qashu, F.,
address appropriate needs. Such treatment strat-
Brickell, T., & Lange, R. (2016). Profile analysis of
egies would include medication (e.g., analgesics the neurobehavioral and psychiatric symptoms follow-
for pain, soporific medication for insomnia, anti- ing combat-related mild traumatic brain injury: Identi-
depressants for affective symptoms), relaxation fication of subtypes. The Journal of Head Trauma
Rehabilitation, 31(1), 2–12.
strategies for anxiety symptoms, psychotherapy
Batten, S., Beal, S., Bleiberg, J., et al. (2009). Defense
for PTSD symptoms, and evidence-based cogni- centers of excellence for psychological health and trau-
tive rehabilitation. matic brain injury and defense and veterans brain
injury center consensus conference on cognitive reha-
bilitation for mild traumatic brain injury. Washington,
DC.
Future Directions Bogdanova, Y., & Verfaellie, M. (2012). Cognitive
sequelae of blast-induced traumatic brain injury:
The research literature in blast injury is still evolv- Recovery and rehabilitation. Neuropsychological
Review, 22, 4–20.
ing. The following is a partial list of necessary
Cernak, I., Wang, Z., Jiang, J., Bian, X., & Savic,
future research efforts: clarifying definitions of J. (2001). Ultrastructural and functional characteris-
mTBI and post-concussive symptom constella- tics of blast injury-induced neurotrauma. The Jour-
tions; separation of the effect of different blast nal of Trauma, Injury, Infection, and Critical Care,
50, 695–706.
mechanisms (e.g., primary, secondary) on the
Gaylord, K., Cooper, D., Mercade, J., Kennedy, J.,
brain; standardization of research methodology Yoder, L., & Holcomb, J. (2008). Incidence of post-
with respect to inducing blast injuries in animal traumatic stress disorder and mild traumatic brain
subjects; comparison of mTBI symptoms, course, injury in burned service members: Preliminary report.
The Journal of Trauma, Injury, Infection, and Critical
and recovery between blast injury survivors and
Care, 64, S200–S206.
those who have injuries from other sources; inves- Hoge, C., McGurk, D., Thomas, J., Cox, A., Engel,
tigation of the effect of multiple blast exposures; C., & Castro, C. (2008). Mild traumatic brain
and investigation of how PTSD/affective distress injury in U.S. soldiers returning from Iraq. The
New England Journal of Medicine, 358(5),
differs from and interacts with mTBI. Studies
453–463.
should take into account situational factors such Jackson, G., Hamilton, N., & Tupler, L. (2008). Detecting
as combat exposure, combat intensity, length and traumatic brain injury among veterans of operations
number of deployments, as well as potentially enduring and Iraqi Freedom. North Carolina Medical
Journal, 69(1), 43–47.
moderating variables on symptom expression
Jones, E., Fear, N., & Wessely, S. (2007). Shell shock and
and recovery (e.g., substance use, pain intensity, mild traumatic brain injury: A historical review. Amer-
sleep integrity). More prospective research is ican Journal of Psychiatry, 164, 1641–1645.
Blessed Dementia Scale 587

in habits section are scored on a 4-point scale (i.e.,

Blessed Dementia Scale 0–3), resulting in a stronger contribution to the
total score. Personality changes are scored 1 if
Avril J. Keller1, Elisabeth M. S. Sherman2 and present or 0 if absent (Blessed et al. 1968, 1988).
Esther Strauss3 A total cutoff score of 4 out of 28 is typically used B
1
Alberta Children’s Hospital, University of to differentiate patients with dementia versus
Calgary, Calgary, AB, Canada those without. Scores of 4–9 indicate mild impair-
2
Copeman Healthcare Centre, Calgary, AB, ment, whereas scores of 10 or higher suggest
Canada moderate to severe impairment (Eastwood et al.
3
Department of Psychology, University of 1983). Stern et al. (1987) have suggested 15 as the
Victoria, Victoria, BC, Canada threshold for moderate impairment.
The original DS also included a second
section comprised of a brief battery of simple
Synonyms cognitive tasks, called the information-memory-
concentration test (IMCT; Blessed et al. 1968,
Blessed dementia rating scale (BDRS); Blessed- 1988). Similar to other brief mental status
Roth DS; Dementia scale (DS); Modified Blessed instruments, the IMCT incorporates 12 items of
dementia scale (DS); Newcastle DS; Revised information/orientation, 11 items of long-term
dementia scale (RDS) memory, a brief test for the 5-min recall of a
person’s name and address, and 3 sequencing
tasks requiring concentration (Blessed et al.
Description 1968, 1988). This sub-component is typically no
longer included in the DS.
The Blessed dementia scale (DS) was developed
in 1968 by Blessed and colleagues in an attempt to
quantify the “degree of intellectual and personal- Historical Background
ity deterioration” (p. 799) in the elderly.
This rating scale consists of 22 items that The original dementia scale (DS) evaluated
reflect (1) changes in performance of everyday informant-reported changes in behavior and
activities (8 items; e.g., using money and finding daily functioning and also included cognitive
one’s way), (2) changes in habits including self- tasks given to the patient. It was developed by
care (3 items; i.e., eating, dressing and conti- Blessed, Tomlinson, and Roth in 1968 in an
nence), and (3) changes in personality, interests, attempt to compare the deterioration of intellect
and drives (11 items; e.g., evaluation of rigidity and personality with underlying brain neuropa-
and affect). A close friend or relative is asked to thology (Blessed et al. 1968, 1988). The revised
provide these behavior ratings of the examinee dementia scale (RDS) was introduced in 1988 and
over the past 6 months; when unavailable, medi- included only items reflecting informant-rated
cal records can be used. The DS is scored on a changes in everyday activities and habits (items
0–28-point scale, where higher numbers indicate a 1 through 11; Erkinjuntti et al. 1988). The sensi-
larger decrement in functional capacity. On every- tivity and specificity of the revised scale was
day activity items, a score of 1 is given for total higher than that of the original DS, possibly due
inability to perform a task; a score of 0.5 is given to lower dementia specificity of the excluded
for partial, variable, or intermittent inability to items (i.e., changes in personality, interests, and
perform an activity; and a score of 0 is given if drive; Lawson et al. 1977). However, the 4-week
the patient is able to perform the task. The changes test-retest reliability for the revised scale was
lower (r = 0.68) than the original (r = 0.79),
potentially due to the inclusion of fewer items
†
Esther Strauss: deceased. (Erkinjuntti et al. 1988).
588 Blessed Dementia Scale

Items from the DS have been included in the reported that disease progression can be moni-
standardized interview with relatives that is part tored using the DS; cognitive deficiencies affect-
of the Cambridge Mental Disorders of the ing instrumental activities of daily living (e.g.,
Elderly Examination (CAMDEX; Roth et al. handling money, remembering short lists) were
1986). Elements of this scale have also been evident early and worsened throughout the dis-
incorporated in the standardized battery of the ease course, whereas changes in basic self-care
Consortium to Establish a Registry for did not occur until 4–5 years into the illness
Alzheimer’s Disease (CERAD; Morris et al. (Stern et al. 1990).
1988). Additional analysis of the scale has indi- A cutoff of 1.5 on the RDS yields a sensitiv-
cated that the items can be subdivided into four ity of 93% and a specificity of 97% in discrim-
groups, each with its own score (cognitive, items inating between demented and non-demented
1–7, score range 0–7; personality change, items subjects, regardless of level of dementia
12–17, score range 0–6; apathy/withdrawal, (Erkinjuntti et al. 1988). The RDS is also highly
18, 20, and 21, score range 0–3; basic self-care, correlated with the Activities of Daily Living
9–11, score range 0–3), in order to aid in inter- Scale, the Instrumental Activities of Daily Liv-
pretation (Stern et al. 1990). ing Scale, and the Functional Activities Ques-
tionnaire (Juva et al. 1997).
The DS appears minimally affected by demo-
Psychometric Data graphic factors. Age correlates moderately with
DS scores (r = 0.31), but when degree of demen-
In community-dwelling individuals, test-retest tia is taken into account, age does not have a
reliability after 4 weeks was r = 0.79; the first significant effect (Erkinjuntti et al. 1988). Educa-
11 items show marginal reliability (r = 0.68; tion appears unrelated to DS scores (Erkinjuntti
Erkinjuntti et al. 1988). Cole (1990) found et al. 1988). African-American patients score
an interrater reliability of r = 0.59 when higher on the DS than white patients (Hargrove
comparing DS ratings by two independent et al. 1998). The DS has been translated
raters who each interviewed the caretakers of and validated in Chinese, Korean, and Czech
47 dementia patients. (Lam et al. 1997; Lee et al. 1999; Vajdickova
The initial study employing the DS showed et al. 1995).
that scores increased as the presence of senile
plaques increased (r = 0.77; Blessed et al.
1968). Also, the DS showed discriminative Clinical Uses
validity in identifying senile dementia patients
compared with depressed, paraphrenia, deliri- The DS offers a blend of items commonly found
ous, and physically ill patients (Blessed et al. on mental status exams, activities of daily living
1968). Others have also noted that the DS is scales, and instrumental activities of daily living
able to discriminate between dementia patients scales. It is quick and easy to administer and
and community residents (Erkinjuntti et al. 1988; additionally provides a quantification of the
Lam et al. 1997). When a cutoff of 4/28 was used, degree of dementia severity. As such, it is ideal
the DS was shown to have a sensitivity of 90% for use by general practitioners and specialized
and a specificity of 84% (Erkinjuntti et al. 1988). medical and mental healthcare professionals to
Moderate to high correlations have been reported gauge initial status, as well as to track disease
with other measures such as the CERAD total progression. The DS may also provide more use-
score (r = 0.40; Chandler et al. 2005), the Mini- ful information in a clinical setting than the
Mental State Exam (r = 0.80; Hendrie et al. MMSE and other cognitive assessment scales
1988), and the CAMDEX (r = 0.77; Hendrie (Mant et al. 1988) because it measures functional
et al. 1988). Additionally, Stern et al. (1987) aspects of dementia.
Blindsight 589

Cross-References Chinese version of the Blessed-Roth Dementia Scale.

International Psychogeriatrics, 9(1), 39–46.
Lawson, J. S., Rodenburg, M., & Dykes, J. A. (1977).
▶ Alzheimer’s Disease A dementia rating scale for use with psychogeriatric
▶ Bristol Activities of Daily Living Scale patients. Journal of Gerontology, 32, 153–159.
▶ Clinical Dementia Rating Lee, D. Y., Yoon, J. C., Lee, K. U., Jhoo, J. H., Kim, K. W., B
▶ Dementia Lee, J. H., et al. (1999). Reliability and validity of the
Korean version of Short Blessed Test (SBT-K) as a
▶ Dementia Rating Scale-2 dementia screening instrument. Journal of Korean
▶ Lawton-Brody Instrumental Activities of Daily Neuropsychiatric Association, 38, 1365–1375.
Living Scale Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004).
Neuropsychological assessment (4th ed.). New York:
Oxford University Press.
Mant, A., Eyland, E. A., Pond, D. C., Saunders, N. A., &
References and Readings Chancellor, A. H. B. (1988). Recognition of dementia
in general practice: Comparison of general practi-
Blessed, G., Tomlinson, B. E., & Roth, M. (1968). The asso- tioners’ opinion with assessments using the mini-
ciation between quantitative measures of dementia and of mental state examination and the Blessed Dementia
senile changes in the cerebral gray matter of elderly sub- Scale. Family Practice, 5(3), 184–188.
jects. British Journal of Psychiatry, 114(512), 797–811. Morris, J. C., Mohs, R. C., Rogers, H., Fillenbaum, G., &
Blessed, G., Tomlinson, B. E., & Roth, M. (1988). Blessed- Heyman, A. (1988). Consortium to establish a registry
Roth Dementia Scale (DS). Psychopharmacology for Alzheimer’s disease (CERAD) clinical and neuro-
Bulletin, 24(4), 705–708. psychological assessment of Alzheimer’s disease. Psy-
Chandler, M. J., Lacritz, L. H., Hynan, L. S., chopharmacology Bulletin, 24(4), 641–651.
Barnard, H. D., Allen, G., Deschner, M., et al. (2005). Roth, M., Tym, E., Mountjoy, C. Q., Huppert, F. A.,
A total score for the CERAD neuropsychological bat- Hendrie, H., Verma, S., et al. (1986). CAMDEX:
tery. Neurology, 65(1), 102–106. A standardized instrument for the diagnosis of mental
Cole, M. G. (1990). Interrater reliability of the Blessed disorders in the elderly with special reference to early
Dementia Scale. Canadian Journal of Psychiatry, detection of dementia. British Journal of Psychiatry,
35(4), 328–330. 149, 698–709.
Eastwood, M. R., Lautenschlaegar, E., & Corbin, S. Stern, Y., Mayeux, R., Sano, M., Hauser, W. A., &
(1983). A comparison of clinical methods for assessing Bush, T. (1987). Predictors of disease course in patients
dementia. Journal of the American Geriatrics Society, with probable Alzheimer’s disease. Neurology, 37(10),
31(6), 342–347. 1649–1653.
Erkinjuntti, T., Hokkanen, L., Sulkava, R., & Palos, J. Stern, Y., Hesdorffer, D., Sano, M., & Mayeux, R. (1990).
(1988). The Blessed Dementia Scale as a screening Measurement and prediction of functional capacity in
test for dementia. International Journal of Geriatric Alzheimer’s disease. Neurology, 40(1), 8–14.
Psychiatry, 3, 267–273. Vajdickova, K., Kolibas, E., Heretik, A., & Kosc, M.
Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975). (1995). Application of behavioural scale in the diagno-
Mini mental state: A practical method for grading the sis of dementia of advanced age. Ceska A Slovenska
cognitive state of patients for the clinician. Journal of Psychiatrie, 91(1), 7–14.
Psychiatric Research, 12(3), 189–198.
Hargrove, R., Stoeklin, M., Haan, M., & Reed, B. (1998).
Clinical aspects of Alzheimer’s disease in black and
white patients. Journal of the National Medical Asso-
ciation, 90, 78–84.
Hendrie, H. C., Hall, K. S., Brittain, H. M.,
Blindsight
Austrom, M. G., Farlow, M., Parker, J., et al. (1988).
The CAMDEX: A standardized instrument for the Sophie Lebrecht and Michael J. Tarr
diagnosis of mental disorder in the elderly: Visual Neuroscience Laboratory, Brown
A replication with a U.S. sample. Journal of the
University, Providence, RI, USA
American Geriatrics Society, 36(5), 402–408.
Juva, K., Maela, M., Erkinjuntti, T., Sulkava, R.,
Yukoski, R., Valvanne, J., et al. (1997). Functional
assessment scales in detecting dementia. Age and Short Description or Definition
Ageing, 26(5), 393–400.
Lam, L. C. W., Chiu, H. F. K., Li, S. W., Chan, W. F.,
Chan, C. K. Y., Wong, M., et al. (1997). Screening for Blindsight is a neuropsychological disorder that
dementia: A preliminary study on the validity of the results from damage to the primary visual cortex
590 Blindsight

(V1). Such localized cortical damage produces Neuropsychology and Psychology of. . .
localized visual impairment in the patient’s visual (Syndrome/Illness)
field contralateral to the site of the damage. Crit-
ically, despite the nominal loss of vision, patients The area of impaired vision in the visual field of a
with blindsight preserve the ability to detect and blindsight patient is referred to as a scotoma
discriminate visual stimuli presented in the – defined as an island of visual loss surrounded
impaired region of their visual field. Lawrence by an area of normal visual acuity (Fig. 1). It is
Weiskrantz’s (1986) observation of this ability to important to note that the visual impairment man-
“see” stimuli in a “blind” visual field led him to ifests in the region of the visual field contralateral
refer to this disorder as “blindsight.” to the hemisphere where the brain injury has
occurred. For example, damage to the left hemi-
sphere of V1 results in impairment to the right
Categorization visual field. Typically, because early visual brain
areas are retinotopically mapped, the extent of the
There are two types of blindsight, termed damage to the occipital lobe corresponds to the
Type I and Type II. Patients with Type extent of the impairment in the visual field. For
I blindsight report no conscious awareness of example, if an entire hemisphere’s occipital lobe
stimuli presented in the damaged region of is ablated, then the entire contralateral visual field
their visual field, yet preserve the ability to is damaged – such a condition is termed
detect stimuli presented there. Patients with hemianopia. Likewise, if a quarter of V1 is dam-
Type II blindsight report a faint conscious aged (i.e., one half of one hemisphere’s occipital
perception of stimuli in the damaged region lobe), a quarter of the contralateral visual field
of their visual field, yet preserve the ability is damaged – such a condition is termed
to detect stimuli with higher precision than quadranopia. Figure 2 illustrates the pattern of
their conscious perception.

Epidemiology

Blindsight results from brain damage to the primary

visual cortex (V1) located in the posterior region of
the occipital cortex, typically caused by a tumor, a
hemorrhage, or some sort of brain trauma.

Natural History, Prognostic Factors, and

Outcomes

The first cases of blindsight were observed in war

veterans with damage to their occipital lobe
(Pöppel et al. 1973). These veterans had no con-
scious perception of stimuli in the damaged por-
tion of their visual field yet were able to track a
moving light presented there. The most extensive
experimental work in this area was completed
with patient DB, who was diagnosed in the
1970s. DB’s case is extensively reviewed in the
seminal book on blindsight (Weiskrantz 1986). Blindsight, Fig. 1 The visual perception of a scotoma
Blindsight 591

Blindsight, Fig. 2 The

relationship between a
region of damage in the
visual cortex (V1) and the
corresponding impairment
in the visual field (Adapted Right optic tract
B
from Bear et al. 2006) Right LGN

Optic radiation
Scotoma

Area of damage

Primary visual cortex

visual impairment and the corresponding scotoma (LGN) directly to the extrastriate cortex. These
that arises when only a small region of the occip- pathways, unaffected by V1 damage, are potential
ital lobe is damaged. Although a patient with such mediators for the unconscious visual perception
a pattern of sparing and loss might experience observed in blindsight. The identification of this
blindsight in such a restricted scotoma, the most pathway has prompted a fascinating debate
interesting cases of blindsight have been where regarding the role of V1 in the neural representa-
patients have lost all conscious visual experience, tion of consciousness. Scientists have posited that
that is, there is injury covering early visual brain if there is perception, but not conscious percep-
areas across both hemispheres. tion, without V1, then V1 must play a critical role
Note that not all patients with scotomas expe- as a neural correlate of consciousness; this
rience blindsight. The functional definition is that remains an active area of research (for review
despite an absence of conscious perception, see Tong 2003).
patients with blindsight retain the ability to detect
and discriminate stimuli presented in their sco-
toma. For example, patients can localize moving Evaluation
and stationary stimuli using saccades or pointing.
They can also discriminate line orientations, Because blindsight patients experience no con-
detect motion, and recent evidence suggests scious awareness of stimuli presented in their
some patients can even differentiate between dif- scotoma, experimenters rely on a two-alternative
ferent wavelengths of color and form presented forced choice (2AFC) procedure to diagnose and
simultaneously in their scotoma (Trevethan et al. evaluate the symptoms of the disorder. The
2007). Primate studies support the claim that this 2AFC procedure, typically used to assess behav-
unconscious perception is not subserved by ioral performance in nonspeaking primates, pre-
islands of undamaged tissue. When the striate sents patients with a target stimulus, a probe
cortex of primates is cortically ablated, like stimulus (matched to target), and a distractor
humans, they have no conscious perception of stimulus (nonmatched to target); the target can
stimuli presented in their scotoma, but do retain be presented either prior to or simultaneously
unconscious perception. The strongest neural evi- with the paired probe and distractor. The patient
dence supporting the existence of blindsight must select either the probe or the distractor as
comes from the identification of subcortical con- matching the target. The patient is not allowed to
nections from the lateral geniculate nucleus respond, “I don’t know,” so in this way the task is
592 Blindsight

a forced-choice. In a variant of this procedure DB’s improvement in form perception is the

used to assess blindsight, experimenters present result of the large number of hours DB spent
an image both to the scotoma and the hemisphere completing experimental testing.
of normal visual acuity then ask subjects to One point to consider when diagnosing or
report whether the two stimuli are the same or treating patients with blindsight is that Type
different (Weiskrantz 1986). Given that chance I patients have no conscious access to the stimuli
performance in these procedures is 50%, it is presented in the scotoma. Consequently, experi-
interesting to note that patients estimate their menters should be cautious in asking for specific
success rate on these tasks to be roughly 50%, answers when running a 2AFC task in that this
but in reality their success rate is closer to 90%, task may be distressing to a patient who experi-
illustrating the disconnect between conscious ences no conscious visual perception. That is, they
and unconscious vision in blindsight. Similar may find such a task irrelevant to their personal
results have been observed using a somewhat experience.
different procedure designed to measure the
unconscious perception of visual motion in
blindsight patients: saccades tracking or pointing
in which a moving object is presented within the
Cross-References
visual field of the scotoma and the patient is
asked to track the object with their eyes or with ▶ Cortical Blindness
▶ Hemianopia
their finger.
▶ Scotoma
▶ Visual Field Deficit
Treatment

There is a period of spontaneous recovery for

References and Readings
neurovisual lesions, typically up to 3 months
Bear, M. A., Connors, B. W., & Paradiso, M. A. (2006).
post-lesion, but has been reported to extend to Neuroscience exploring the brain. Baltimore:
up to a year. Following this period, active dis- Lippincott Williams & Wilkins.
crimination of stimuli presented in the scotoma Dineen, J., & Keating, E. G. (1981). The primate visual
system after bilateral removal of striate cortex. Survival
seems to be the best strategy for improvement in
of complex pattern vision. Experimental Brain
humans (Sahraie et al. 2006) and nonhuman pri- Research. Experimentelle Hirnforschung. Expérimen-
mates (Dineen and Keating 1981). As such, tation Cérébrale, 41(3–4), 338–345.
blindsight patients that participate as experimen- Pöppel, E., Held, R., & Frost, D. (1973). Residual visual
function after brain wounds involving the central
tal subjects sometimes show large improvements
visual pathways in man. Letters to Nature, 243,
in their visual discrimination abilities. For exam- 295–296.
ple, patient DB, the first blindsight patient stud- Sahraie, A., Trevethan, C. T., MacLeod, M. J., Murray,
ied extensively (Weiskrantz 1986), was recently A. D., Olson, J. A., & Weiskrantz, L. (2006). Increased
sensitivity after repeated stimulation of residual spatial
retested, 30 years after his right striate cortex was
channels in blindsight. Proceedings of the National
surgically removed during the treatment of a Academy of Sciences of the United States of America,
nonmalignant venous tumor. Patient DB can 103(40), 14971–14976.
now discriminate complex circular forms pre- Tong, F. (2003). Primary visual cortex and visual aware-
ness. Nature Reviews Neuroscience, 4(3), 219–229.
sented in his scotoma, for example, he can Trevethan, C. T., Sahraie, A., & Weiskrantz, L. (2007). Can
discriminate a circle from an oval. Previously blindsight be superior to ‘sighted-sight’? Cognition,
the ability to distinguish form was accounted 103(3), 491–501.
for by DB’s ability to distinguish line orienta- Weiskrantz, L. (1986). Blindsight: A case study and its
implications. Net Library, USA: Oxford University
tions; however, this explanation cannot account
Press.
for now-present circular form discrimination Werner, J. S., & Chalupa, L. M. (2004). The visual neuro-
(Trevethan et al. 2007). One possibility is that sciences. Cambridge, MA: MIT Press.
Block Design 593

Historical Background
Block Design
Hutt (1925) notes that the first documented use
Brianne Magouirk Bettcher1,2, David J. Libon3, of block construction as a psychological test was
Edith Kaplan4, Rod Swenson5 and by Francis N. Maxfield, working at the Univer- B
Dana L. Penney6 sity of Pennsylvania Psychology Laboratory
1
Department of Neurosurgery and Neurology, and Clinic, who devised a “color cube” test to
University of Colorado School of Medicine, study “imageability in children.” The proce-
Denver, CO, USA dures devised by Maxfield were also used by
2
Rocky Mountain Alzheimer’s Disease Center, Clara Town (1921, cited in Hutt 1925). Both of
Aurora, CO, USA these researchers were interested in studying
3
Departments of Geriatrics, Gerontology, analytic problem-solving strategies in children.
and Psychology, Rowan University, However, it was Samuel Calmin Kohs
New Jersey Institute for Successful Aging, (1916–1960) who derived the block design
School of Osteopathic Medicine, Stratford, (BD) test that was ultimately adapted by David
NJ, USA Wechsler. It appears that Maxfield, Town, and
4
Department of Psychology, Suffolk University, Kohs used the same commercially available
Boston, MA, USA blocks, that is, all blocks were constructed with
5
Department of Psychiatry and Behavioral four colors – red, white, blue, and yellow. Kohs’
Science, University of North Dakota School of procedure differed from Maxfield and Town in
Medicine, Fargo, ND, USA that he asked children to use blocks to copy two-
6
Department of Neurology, The Lahey Clinic, dimensional designs printed on stimulus cards
Burlington, MA, USA rather than from models constructed by the
examiner using identical blocks, a method
adopted by Wechsler. Kohs (1920), 1923) spe-
Synonyms cifically used block construction as a means to
assess intelligence. Consistent with the pre-
Kohs blocks vailing views of the day, Kohs viewed intelli-
gence as a unitary or global construct. The Kohs
BD test consisted of a series of 17 designs
Description (culled from a corpus of 35 original designs).
Kohs (1920), 1923) clearly viewed his test as
The block design (BD) test is a subtest from the equal to the existing Binet scales in measuring
Wechsler corpus of intelligence tests that requires general intellectual ability. He also viewed the
the examinee to use three-dimensional blocks to “performance” (Kohs 1920) or nonverbal nature
construct a model from a two-dimensional stimu- of his test as a means to assess intelligence in
lus card. Blocks consist of sides that are all white, children where it was either not possible or
all red, or diagonally half red and white. Perfor- problematic to use language or language-related
mance is timed. Although bonus points are tests. As adopted by Wechsler later, Kohs
awarded for speed, the score is either all or none, awarded bonus points for speed. Interestingly,
that is, a score is awarded only if the model is a separate scoring system was also derived to
correctly produced within the prescribed time measure “moves” or “each separate and distinct
limit. change in the position of the block” (Kohs
1920). All these early researchers readily
acknowledged the multidimensional aspect
of their block construction procedures and
commented on the qualitative features of chil-
Edith Kaplan: deceased. dren’s block construction strategies.
594 Block Design

Psychometric Data the design reflecting an inattention of left hemi-

space suggestive right hemisphere dysfunction
Successful completion of the BD test requires a (Kaplan 1988, Figures 1–2). Very different
host of cognitive abilities (Kramer et al. 1991) errors occur with commissurotomized patients
including specific analytic and synthetic attempting BD using their left hand, that is,
problem-solving strategies (Schorr et al. 1982). when constructions are guided by the right hemi-
Analytic strategies refer to mental segmentation sphere with no input from the left hemisphere.
of the stimulus design into individual blocks. Now, the 2  2 or 3  3 grid matrix is rarely
After mentally dividing the blocks into segments, violated. However, blocks tend to be rotated so
blocks are subsequently arranged to match each that the internal details of individual blocks do not
unit. This strategy might capitalize on the presence match the model. Thus, Geschwind (1979) and
of perceptual edge cues and implicit grid informa- Kaplan (1988) show that regardless of which hand
tion when constructing the design (Kaplan 1988; is used, commissurotomized patients produce zero
Kaplan et al. 1991). Synthetic strategies emphasize point responses, but the underlying brain-behavior
the design as a whole and may not rely on segmen- relationships responsible for these response strate-
tation for test completion. Examinees who utilize gies are very different. Kaplan et al. (1981) noted
this strategy focus primarily on the gestalt or over- that similar behavior occurs in patients with focal
all form of the design. Specific BD test items tend right and left hemisphere lesions. Patients with
to “pull” for one strategy versus the other. How- right-sided lesions often break the 2  2 or 3 
ever, overreliance on either problem-solving 3 matrix inherent in the stimulus resulting in highly
approach will ultimately lower an examinee’s test distorted responses, blocks continue to collect on
score and could be highly suggestive of either focal the right side of hemi-space, and constructions are
or lateralized neurological insult. often initiated on the right side with patients work-
The BD test is often viewed as a measure of the ing from right to left. Patients with left-sided
so-called constructional apraxia (Kleist, 1923, lesions respect the inherent grid configuration of
cited in Benton and Tranel 1993) and has been the BD stimuli. These patients often make single-
naively associated with right parietal brain dam- block, rotational errors or misalign internal details
age (Kaplan 1988). Clear evidence of the multi- (Kaplan et al. 1991) with responses initiated on the
dimensional cognitive skills necessary for optimal left side of hemi-space.
performance on the BD test comes from two
sources: patients with cerebral disconnection
(Geschwind 1979; Kaplan 1988) and patients Clinical Uses
with focal brain lesions. For example, patients
who have undergone a commissurotomy Kaplan and colleagues (Kaplan 1988; Kaplan
(Geschwind 1979; Kaplan 1988) provided a et al. 1991) have suggested a number of additional
unique opportunity to study BD problem-solving testing and scoring procedures to extract detailed
strategies because these patients serve as their information from the BD test performance. These
own controls. Since these patients have under- are listed below and are part of the WAIS-R-NI
gone resection of the corpus callosum and the corpus (Kaplan et al. 1991).
anterior commissure, sensory information cannot
be transferred between the hemispheres. Illustra- 1. Providing Additional Blocks: Rather than
tions provided by Geschwind (1979) and Kaplan constraining the examinee’s performance by
(1988) show that when commissurotomized providing only four or nine blocks as pre-
patients use their right hand, that is, when BD scribed by the Wechsler test manual, Kaplan
constructions are guided by the left hemisphere et al. (1991) suggests presenting the patient
with no input from the right hemisphere, the inher- with nine blocks on all four-block test items
ent 2  2 or 3  3 matrix is violated, and there is a and 12 blocks on all nine-block test items.
tendency for blocks to pile up on the right side of Attempting to construct designs with too few
Block Design 595

or too many blocks conveys additional infor- 1. Orientation errors: Scored when a block(s) is
mation about possible spatial as well as exec- incorrectly oriented, that is, when the final
utive impairment. product or elements of the final product are
2. Flow Charting: Documenting the patient’s per- shifted or misoriented about 30 in relation to
formance with a flow chart is mandatory to the the model. Spatial, perceptual, or executive B
cogent analysis of BD test performance. Exam- problems might underlie this difficulty.
ples of the rich data which can be obtained with 2. Perseverations: Scored when incorrect block
a flow chart are illustrated by Kaplan et al. placements persist either within or between
(1991, Figure 6). As described above, focal successive BD trials. Gross perseverative
right-hemisphere lesioned patients tend to behavior is often seen in patients with frontal
break the 2  2 or 3  3 grid configuration of lobe or frontal systems lesions. Less severe
the stimulus matrix and often produce distorted perseverative behavior might occur in conjunc-
responses. Kaplan et al. (1991) provides exam- tion with rotational and broken configuration
ples of BD constructions produced by right- errors and may suggest dysexecutive behavior
anterior and right-posterior lesioned patients in associated with a specific brain region.
Figures 6c and 6d, respectively (see p. 90). The 3. Stimulus bound: Examples include instances
3  3 grid configuration is broken by both when the examinee is drawn to build their
patients. However, the construction of a patient construction either right next to or under the
with a right-posterior lesion is measurably stimulus booklet or even pile blocks on top of
more distorted than the construction produced the stimulus booklet. Less egregious but no
by a right-anterior lesioned patient suggesting less important stimulus-bound errors occur
greater perceptual-spatial impairment. Thus, as when patients are aware of but unable to self-
suggested many years ago by Kohs (1920, correct errors.
1923), an analysis of BD “moves” provides 4. Response latency: Patients with bradyphrenia
important information. may ultimately produce a correct construction
3. Errors Subtypes: The WAIS-R-NI (Kaplan and might be able to self-correct errors but may
et al. 1991) suggests a variety of error scores complete a correct design only after the time
that supplement the traditional total Wechsler limit as prescribed in the test manual has
scale score. The scoring techniques described passed. Such behavior might be associated
below are designed to supplement standard- with subcortical syndromes. However, slow
ized scoring procedures and help in identifying time to completion often occurs in patients
underlying brain pathology. with alcohol abuse, brain injury, multiple scle-
1. Rotational errors: Scored when a block’s rosis, or epilepsy.
surface coloring is incorrect. This type of 5. Start position: Using a flow chart,
internal detail error could be associated with documenting the start position of the first block
a left hemisphere lesion. also allows for examination of a “preferred” side
2. Broken configuration: Scored when the and can be indicative of lateralized brain dys-
2  2 or 3  3 grid matrix of the design is function (Akshoomoff-Haist et al. 1989).
violated. As noted above, such errors are
often seen in patients with right hemisphere
lesions. Block Design Use with Additional
Populations
While rotational and broken configuration
errors often occur in patients with circumscribed Healthy and Pathological Aging
stroke, patients with epilepsy (Zip-Williams et al. An observed pattern of developmental cognitive
2000) or brain injury (Wilde et al. 2000) change associated with age is the relative stability
lateralized to one side of the brain may also of verbal abilities coupled with a significant
make these errors. diminution in visuospatial and constructional
596 Block Design

abilities. Evidence suggests that the BD test dif- Benton, A., & Tranel, A. (1993). Visuoperceptual,
ferentiates between younger and older adults Visuospatial, and Visuoconstructional Disorders. In
K. M. Heilman & E. Valenstein (Eds.), Clinical
(Kaufman 1990; Troyer et al. 1994), but the spe- neuropsychology (3rd ed.). New York: Oxford Uni-
cific cognitive functions that underlie this behav- versity Press.
ior have been debated. Joy et al. (2001) provided a Caplan, B., & Caffery, D. (1992). Fractionating block
comprehensive evaluation of the reported age- design: Development of a test of visuospatial analysis.
Neuropsychology, 6, 385–394.
related decline in BD test performance and offered Geschwind, N. (1979). Specializations in the human brain.
normative data for the clinical interpretation of Scientific American, 241, 180–199.
BD in healthy older adults. In addition to standard Hutt, R. B. W. (1925). Standardization of a color cube test.
pass-fail scoring, these researchers also utilized The Psychological Clinic, 16, 77–97.
Joy, S., Fein, D., Kaplan, E., & Freedman, M. (2001).
proportional scoring methods as well as the sup- Quantifying qualitative features of block design perfor-
plemental measures detailed in the WAIS-R-NI. mance among healthy older adults. Archives of Clinical
Results confirmed a moderate negative correlation Neuropsychology, 16, 157–170.
between standard BD score and age (r = 0.455); Kaplan, E. (1988). A process approach to neuropsycholog-
ical assessment. In T. Boll & B. R. Bryant (Eds.),
however, the use of proportion scores, elimination Clinical neuropsychology and brain function:
of time constraints, and termination of time Research. Measurement, and practice: Master lectures.
bonuses significantly reduced the documented Washington, DC: The American Psychological
age differences. These authors interpreted this Association.
Kaplan, E., Palmer, E. P., Weinstein, C., & Baker,
finding as evidence for less severe age-related E. (1981). Block design: A brain-behavior based anal-
impairment in visuospatial and constructional ysis. Paper presented at the annual European meeting of
abilities in healthy older adults than traditional the International Neuropsychological Society, Bergen,
scoring techniques suggest. In general, it is impor- Norway.
Kaplan, E., Fein, D., Morris, R., & Delis, D. (1991). The
tant to carefully consider the role of psychomotor WAIS-R as a neuropsychological instrument. San
slowing and error types when administering the Antonio: The Psychological Corporation.
standard block design test to healthy older adults Kaufman, A. S. (1990). Assessing adolescent and adult
in order to avoid differently penalizing individuals intelligence. Boston: Allyn & Bacon.
Kohs, S. C. (1920). The block design tests. Journal of
based on age. Older adults diagnosed with a neu- Experimental Psychology, 3, 357–376.
rodegenerative disorder exhibit different patterns Kohs, S. C. (1923). Intelligence measurement. New York:
of errors depending upon their neuropsychologi- Macmillan.
cal profile and diagnosis. Stimulus-bound errors, Kramer, J. H., Kaplan, E., Blusewicz, M. J., &
Preston, K. A. (1991). Visual hierarchical analysis
broken configurations, and psychomotor slowing of block design configural errors. Journal of
are all more prevalent in individuals diagnosed Clinical and Experimental Neuropsychology, 13,
with a dementia relative healthy older adult 455–465.
controls. Lezak, M., Howison, D. B., & Loring, D. W. (2004).
Neuropsychological assessment (4th ed.). New York:
Oxford University Press.
Schorr, D., Bower, G. H., & Kiernan, R. (1982). Stimulus
Cross-References variables in the block design task. Journal of Consult-
ing and Clinical Psychology, 50, 479–487.
Troyer, A. K., Cullum, C. M., Smernoff, E. N., & Kozora,
▶ Constructional Apraxia E. (1994). Age effects on block design: Qualitative
performance features and extended-time effects. Neu-
ropsychology, 8, 95–99.
Wilde, M. C., Boake, C., & Sherer, M. (2000).
References and Readings Wechsler adult intelligence scale-revised block
design broker configuration errors in non-
Akshoomoff-Haist, N. A., Delis, D. C., & Kiefner, penetrating traumatic brain injury. Applied Neuro-
M. G. (1989). Block constructions of chronic alco- psychology, 7, 208–214.
holic and unilateral brain-damaged patients: A test Zip-Williams, E. M., Shear, P. K., Strongin, D., et al.
of the right hemisphere vulnerability hypothesis of (2000). Qualitative block design performance in epi-
alcoholism. Archives of Clinical Neuropsychology, lepsy patients. Archives of Clinical Neuropsychology,
4, 275–281. 15, 149–157.
Blood Flow Studies 597

function. The tendency to underestimate one’s

Blood Alcohol Level own blood alcohol level seems to pose an addi-
tional risk of impairment and injury risk. Addition-
Ross Zafonte1, Brad Kurowski2 and ally, speed of cognitive performance recovers as
Nathan D. Zasler3 alcohol is metabolized and BAL decrease; how- B
1
Department of Physical Medicine and ever, accuracy may continue to remain impaired.
Rehabilitation, Spaulding Rehabilitation
Hospital, Massachusetts General Hospital,
Brigham and Women’s Hospital, Harvard Cross-References
Medical School, Boston, MA, USA
2
Department of Physical Medicine and ▶ Coma
Rehabilitation, Spaulding Rehabilitation ▶ Executive Functioning
Hospital, Massachusetts General Hospital, ▶ Frontal Lobe
Brigham and Women’s Hospital, Harvard
Medical School, Cincinnati, OH, USA
3
Concussion Care Centre of Virginia, Ltd., References and Readings
Richmond, VA, USA
Domingues, S. C., Mendonca, J. B., Laranjeira, R., &
Nakamura-Palacios, E. M. (2009). Drinking and driv-
ing: A decrease in executive frontal functions in young
Synonyms drivers with high alcohol concentration. Alcohol,
43(8), 657–664.
Blood alcohol concentration; Blood alcohol content Harrison’s Online – Harrison’s principles of internal med-
icine (16th edn.). Chapter 372: Alcohol and alcoholism.
Laude, J. R., & Filmore, M. (2016). Drivers who self-
estimate lower blood alcohol concentrations are riskier
Definition drivers after drinking. Psychopharmacology (Berl),
233(8), 1387–1394. https://doi.org/10.1007/s00213-
016-4233-x.
Measure of alcohol in the blood.
Schweizer, T. A., & Vogel-Sprott, M. (2008). Alcohol-
impaired speed and accuracy of cognitive functions:
A review of acute tolerance and recover of
Current Knowledge cognitive performance. Experimental and Clinical
Psychopharmacology, 16(3), 340–350.

Blood alcohol level (BAL) is typically expressed

as milligrams or grams of ethanol per deciliter
(e.g., 100 mg/dL or 0.10 g/dL). A level of
20–30 mg/dL typically results from the ingestion Blood Flow Studies
of one to two drinks. One drink corresponds to
340 mL (12 oz.) of beer, 115 mL (4 oz) of wine, Cindy B. Ivanhoe1 and Ana Durand Sanchez2
1
and 43 mL (1.5 oz) of a shot. Blood alcohol levels Neurorehabilitation Specialists Baylor College
as low as 20–80 mg/dL can lead to decreased of Medicine, The Institute for Rehabilitation and
inhibitions and decreased cognitive and motor Research, Houston, TX, USA
2
performance, while levels of 300–400 mg/dL Physical Medicine and Rehabilitation, Baylor
can lead to coma or death. Blood alcohol levels College of Medicine, Houston, TX, USA
typically correlate inversely with cognitive and
motor performance (i.e., as blood alcohol levels
increase, cognitive and motor performance Synonyms
decrease). Specifically, increased blood alcohol
levels correlate with slower reaction time and Duplex/Doppler ultrasound (US); Vascular
inversely correlate with frontal executive ultrasound
598 Blood Flow Studies

Definition the flow of blood through vessels within solid

organs.
A blood flow study is a noninvasive imaging Transcranial Doppler (TCD) is used to mea-
technique which is used to measure blood flow sure blood flow through the brain’s blood vessels.
and pressure through arteries and veins, as well as It is becoming more widely used to evaluate for
chambers and valves of the heart. Doppler ultra- emboli, stenosis, vasospasm, and the risk of
sound (US) may be used to diagnose vascular stroke.
conditions such as cerebral vasospasm, cerebral Limitations to studies include obesity, cardiac
or limb thrombosis, vascular stenosis, valvular arrhythmias, heart disease, and smoking within an
heart disease, and peripheral vascular and aneu- hour of study. Studies are done in the inpatient and
rysmal disease. It may also be used to evaluate the outpatient settings monitoring.
condition of bypass grafts and blood flow to trans- Variations in blood flow can affect microvas-
planted organs. cular and macrovascular beds for a wide range of
clinical situations. There are new expanding tech-
niques to study blood flow but ultrasound remains
Current Knowledge the commonly used techniques in hospital an out-
patient clinical settings.
Blood flow studies are used most often to study
blood flow particularly in the legs, neck, and
brain. Blood flow studies such as Doppler US
See Also
uses a transducer that sends high-frequency
sound waves which bounce off of solid objects
▶ Cerebral Blood Flow
including red blood cells. The sound waves are
▶ Doppler Ultrasound
reflected back to the transducer. Moving objects,
▶ Regional Cerebral Blood Flow
such as the red blood cells, cause a change in pitch
▶ Transcranial Doppler
of the sound waves (also known as the “Doppler
effect”). These reflected waves are sent to and
processed by a computer which translates the
References and Readings
waves into pictures or graphs. The images are
representative of the flow of blood through the Blaivas, M. (2007). Ultrasound in the detection of venous
vessel. thromboembolism. Critical Care Medicine, 35(5),
There are different types of Doppler US studies S224–S234.
currently being utilized by physicians. Continu- Hamper, U. M., DeJong, M. R., & Scoutt, L. M.
(2007). Ultrasound evaluation of the lower extrem-
ous wave Doppler is typically used at the bedside ity veins. Radiologic Clinics of North America,
and only produces sound from the transducer 45(3), 525–547.
which the practitioner uses to listen for blockage Roberts, D. R., & Forfia, P. R. (2011). Diagnosis and
or stenosis of the vessel – usually a superficial assessment of pulmonary vasculature disease by dopp-
ler echocardiography. Pulmonary Circulation, 1(2),
one. Duplex Doppler produces both a picture of 160–181.
the blood vessel and a graph representing the Rubens, D. J., Bhatt, S., Nedelka, S., & Cullinan, J. (2006).
speed and direction of blood flow (hence the Doppler artifacts and pitfalls. Radiologic Clinics of
name “duplex”). Color Doppler uses a computer North America, 44(6), 805–835.
Webb, R. C., Ma, Y., Krishnan, L. Y., Yoon, S., et al.
to convert the Doppler sounds into colors and (2015). Epiderman devices for noninvasive, preise,
overlay those colors on an image of the blood and continuous mapping of macrovascular and
vessel. Power Doppler is more sensitive than microvascular blood flow. Science Advances, 1(9),
color Doppler in detecting blood flow. It combines 1–13.
Weber, T. M., Lockhart, M. E., & Robbin, M. L. (2007).
the results given by color Doppler with those of Upper extremity venous Doppler ultrasound. Radio-
duplex Doppler. It is commonly used to evaluate logic Clinics of North America, 45, 513–524.
Blood Oxygen Level Dependent (BOLD) 599

emission tomography (PET), in which radioactive

Blood Oxygen Level tracers are injected and their emitted radiation
Dependent (BOLD) detected. It was not until the discovery of BOLD
contrast in 1990 by Ogawa and colleagues at Bell
Alan Weintraub1 and John Whyte2 Laboratories that it was possible to measure neu- B
1
Craig Hospital, Rocky Mountain Regional Brain ron-mediated changes in blood flow without radi-
Injury System, Englewood, CO, USA ation exposure. While fMRI relies on an evolving
2
Moss Rehabilitation Research Institute, Albert understanding of both the physiologic and bio-
Einstein Healthcare Network, Elkins Park, physical origins of BOLD, this technique has
PA, USA become a powerful research modality in mapping
brain activation in animals and humans.

Synonyms
Current Knowledge
BOLD
Because of its dependence on the state of oxygen-
ation of the blood, the BOLD signal is several
Definition steps removed from the typical phenomenon of
interest: changes in neural activity. All measures
Blood–oxygen-level-dependent (BOLD) imaging of cerebral blood flow are indirect, in the sense
is a technique used to generate images in func- that they can be influenced by cardiovascular fac-
tional MRI (fMRI) studies. The goal of this tech- tors (e.g., changes in cardiac output, vascular
nique is to discern regional differences in cerebral resistance) as well as changes in metabolic
blood flow in an effort to delineate more specific demand by neuronal and glial tissue. BOLD tech-
regional activity. This version of magnetic reso- nique represents the relationship between oxygen
nance imaging depends on the different magnetic delivery and oxygen extraction, rather than oxy-
properties of oxygenated versus deoxygenated gen consumption itself – a more direct measure of
hemoglobin and thus, indirectly, on variations in tissue metabolic activity. The clinician and
local tissue perfusion. The utility of BOLD imag- research scientist should appreciate the delay of
ing for functional magnetic resonance imaging several seconds between the changes in neural
(fMRI) also depends on the physiological phenom- activity and changes in associated blood flow.
enon by which metabolically active cerebral tissue Thus, BOLD imaging technique requires mathe-
“demands” more perfusion than less-active tissue. matical modeling of the “hemodynamic response
Thus, populations of neurons that are particularly function” (the increase and subsequent return to
active during a cognitive or motor task actually baseline of flow associated with a neural event).
elicit a relative surplus of perfusion, which, in The derived BOLD signal should correlate to
turn, results in an increase in the ratio of oxygen- resting neuronal states or in response to specific
ated to deoxygenated hemoglobin, detectable as a behavioral and cognitive events that require neu-
change in the BOLD signal. ral processing. The hemodynamic response func-
tion can be modeled in a normative sense (i.e., the
shape of the blood flow response in a “typical”
Historical Background organism) or in the individual subject.
Although the BOLD signal is not a direct mea-
As early as 1890, Roy and Sherrington noted that sure of neuronal activity, its signal detected by
regional cerebral blood flow increased in areas of fMRI reflects changes in deoxyhemoglobin
neural activity. This increase in perfusion became derived from cerebral mediated changes in blood
detectable in vivo with the advent of positron oxygenation and blood flow. This phenomenon
600 Blood Oxygen Level Dependent (BOLD)

appears to be closely linked to neuronal activity, a across the two types of blocks, and a measure of
process referred to as neurovascular coupling. the difference between them is mapped onto each
Research exploring the neurovascular coupling voxel in the MR image, thus showing those areas
mechanisms and the BOLD signal are opportuni- of the brain that had the largest change in BOLD
ties to more completely understand the underlying signal between the two conditions. A contrasting
pathobiological mechanisms underlying brain rest block is typically used when one is interested
development, disease states, and aging. in the brain areas involved in all aspects of the
BOLD technique is also an important concept task, although this method has been criticized
in resting state fMRI studies. These concepts offer because there is no standardization of the subject’s
a broader understanding of human brain connec- mental activity during rest. Alternatively, if one is
tivity and especially how it is influenced by a interested in the brain areas involved with a spe-
variety of disease states and its inherent underly- cific task process, one might alternate the experi-
ing pathophysiologic mechanisms. In addition, mental task with a control task that shares most
BOLD imaging techniques and fMRI studies but not all of the features of the experimental task.
in human neuroscience most often make use of For example, if a research subject performs alter-
one of the two common experimental designs: nating blocks of finger tapping in response to a
blocked or event related (Fig. 1). In the blocked visual signal versus viewing the visual signal
design, the subject is asked to perform a particular without tapping, areas involved in the perception
cognitive or motor task in blocks that alternate of the visual signal will tend to be canceled out
with other blocks of a contrasting task or rest. across conditions whereas neural networks spe-
The BOLD signal is then statistically averaged cifically involved in the tapping response will be
highlighted. In this way, a wide range of cogni-
tive and motor tasks have been studied in normal
subjects as a way of localizing the neural net-
works involved in their performance and in
patient subjects, as a way of exploring how that
localization may have been altered by pathology
or recovery.
In event-related BOLD designs, experimental
trials of different types can be delivered in a
random sequence and averaged in a time-locked
fashion. The timing between trials is sometimes
“jittered” (i.e., randomly varied) so that even
though the hemodynamic responses from
individual trials overlap, their individual effects
can be separately modeled (deconvolved), by
incorporating the known temporal spacing
between them.
More recently, the BOLD signal has been used
to understand how activities in different parts of
the brain are interrelated. Modern neuroscience
posits the presence of distributed neural networks,
Blood Oxygen Level Dependent (BOLD), rather than focal regions, supporting specific cog-
Fig. 1 Blood–oxygen-level dependent. This axial slice nitive and motor processes. Since considerable
of the brain shows the areas of most significant BOLD distances may separate components of these neu-
activation across 18 control subjects, obtained while they
ral networks, it is of interest to understand how
attended to three randomly moving visual stimuli. Higher
visual areas in the occipital cortices (motion areas V5/MTþ) they communicate with each other in the perfor-
and superior colliculi show the greatest activation mance of specific cognitive activities. By
Blood-Brain Barrier 601

assessing how strongly changes in the BOLD Cross-References

signal in different regions are correlated over
time, one can derive a measure of “functional ▶ Functional Imaging
connectivity,” assessed either at rest or during ▶ Magnetic Resonance Imaging
the performance of specific tasks. Measures of B
functional connectivity do not specify the actual
anatomical connections between regions but References and Readings
merely demonstrate the degree to which their
activity levels are linked over time. Barkhof, F., Haller, S., & Rombouts, S. A. (2014). Resting-
state functional MR imaging: A new window to the
With any of these experimental designs, the
brain. Radiology, 272(1), 29–49.
BOLD signal must also be mapped to an anatom- Hillman, E. M. (2014). Coupling mechanism and signifi-
ical model of the brain. Modeling the signal sep- cance of the BOLD signal: A status report. Annual
arately in each voxel of the MRI image and then Review of Neuroscience, 37, 161–181.
Kida, I., & Hyder, F. (2006). Physiology of functional
contrasting the signal in each voxel between the
magnetic resonance imaging: Energetics and
experimental conditions of interest do this. This function. Methods in Molecular Medicine, 124,
may require additional manipulations, such as 175–195.
warping each subject’s image to a standard tem- Kim, S. G., & Ogawa, S. (2012). Biophysical and physio-
logical origins of blood oxygenation level-dependent
plate, “smoothing” the signal so that the activity in
fMRI signals. Journal of Cerebral Blood Flow and
collections of voxels rather than individual voxels Metabolism, 32(7), 188–1206.
is highlighted, and deriving statistical maps that Lee, M. H., Smyser, C. D., & Shimony, J. S. (2013).
code the reliability of the change of interest across Resting-state fMRI: A review of methods and clinical
applications. AJNR. American Journal of Neuroradiol-
brain regions and individual subjects. Several
ogy, 34(10), 1866–1872.
forms of computer software are available for pro- Mark, C. I., Mazerolle, E. L., & Chen, J. J. (2015). Meta-
cessing raw fMRI data into analyzable maps and bolic and vascular origins of the BOLD effect: Impli-
statistical results. cations for imaging pathology and resting-state brain
function. Journal of Magnetic Resonance Imaging, 42
(2), 231–246.
Veldsman, M., Cumming, T., & Brodtmann, A. (2015).
Conclusions Beyond BOLD: Optimizing functional imaging in
stroke populations. Human Brain Mapping, 36(4),
1620–1636.
Although BOLD and other fMRI techniques are
Yablonskiy, D. A., Sukstanskii, A. L., & He, X. (2013).
extremely powerful research tools, they incorpo- Blood oxygenation level-dependent (BOLD)-based
rate a large number of data transformations and techniques for the quantification of brain hemodynamic
assumptions between the raw signal acquisition and metabolic properties – Theoretical models and
experimental approaches. NMR in Biomedicine, 26(8),
and interpretations at the level of brain activity
963–986.
and behavior. A crucial perspective in interpreting
BOLD and fMRI results must comprehensively
consider BOLD’s vascular and metabolic under-
pinnings. This understanding is important to ana-
lyze under both resting conditions and in disease Blood-Brain Barrier
states. As noted above, conclusions reached by
these techniques can be undermined by alterations Nam Tran
in the coupling between neural activity and blood Neurosurgery, Virginia Commonwealth
flow, by failure to accurately understand the cog- University Medical Center, Richmond, VA, USA
nitive and motor processes required by the task
and by invalid application of the many analytical
and statistical methods that transform the mea- Synonyms
sured BOLD signal into statistical maps of brain
activity. Cerebral microvasculature
602 Body Dysmorphic Disorder

Definition tight junctions and increased electrical resis-

tance. Astrocytic membranes and supernatant
The blood-brain barrier (BBB) maintains brain from astrocytic cultures share similar inductive
homeostasis by regulating the movement of com- properties. The mechanisms of this induction
pounds across the endothelium of cerebral and the inductive factor(s) have yet to be fully
capillaries. elucidated.
In addition to its regulatory role, studies of
the BBB are beginning to emerge to demonstrate
Current Knowledge its function in establishing a unique brain
milieu. In vitro BBB models have shown
BBB serves to maintain brain homeostasis by decreased tissue plasminogen activator and
regulating the influx and efflux of compounds to then anticoagulant protein thrombomodulin
and from the brain. The presence of a barrier was expression and increased plasminogen activator
first documented by Paul Ehrlich in the late nine- inhibitor-1 expression by the brain endothelium
teenth century. However, it was not until the compared with the endothelium from the periph-
advent of the electron microscope that the makeup ery. These findings suggest a procoagulant envi-
of the BBB was begun to be understood. The brain ronment in the brain that may predispose the
microvascular endothelium comprises the BBB. brain to strokes.
In contrast to endothelium from other vascular
beds, the morphologic features unique to the
brain microvascular endothelium, such as tight
Cross-References
junctions, increased electrical resistance, and
lack of pinocytic vesicles, provide limited and
▶ Neuroglia
selective access to this highly specialized organ.
Only lipophilic molecules less than 600 Da can
passively diffuse through the BBB. This protects
the brain from toxins, microorganisms (i.e., bac-
teria), and peripheral neurotransmitters. This
Body Dysmorphic Disorder
selective barrier can potentially limit the entry of
large substances required for normal brain func-
Amma A. Agyemang
tion, including insulin, amino acids, and glucose.
Department of Physical Medicine and
In order to circumvent this problem, the BBB has
Rehabilitation, Virginia Commonwealth
developed highly specialized transport mecha-
University Medical Center, Richmond, VA, USA
nisms on both the luminal and abluminal mem-
brane surfaces, such as Na-K-Cl cotransporter,
g-glutamyl transpeptidase (GGTP), and the
Synonyms
GLUT-1 glucose transporter. The protective
BBB can be at a disadvantage in that it prevents
Dysmorphia
the entry of pharmacologic agents that are often
hydrophilic.
Also unique to the brain microvascular Definition
endothelium is their intimate association with
astrocytes, forming the glia limitans. Astro- Previously known a dysmorphia, body dysmor-
cytes are thought to participate in the induction phic disorder (BDD) is an obsessive-compulsive
and maintenance of the endothelial BBB phe- disorder (OCD)-related condition characterized
notype. In vitro studies have shown that astro- by a preoccupation with one or more perceived
cytes cocultured with endothelial cells can defects or flaws in one’s physical appearance that
induce BBB phenotypic features, including are not observable or appear slight to others. The
Body Dysmorphic Disorder 603

disorder is manifested through repetitive behav- greater psychiatric comorbidity, and poorer insight.
iors such as excessive grooming, skin picking, Associated/comorbid conditions include major
or mental acts such as comparing one’s appear- depressive disorder, social anxiety disorder, and
ance to others, in efforts to assuage appearance substance-related disorders.
concerns. Muscle dysmorphia is a subtype of B
BDD, in which there is a preoccupation with Assessment and Treatment
one’s body build being too small or insuffi- With regard to assessment, the primary rule out is
ciently muscular. eating disorders, however, BDD must also be
differentiated from other OCD-related disorders,
illness anxiety, depressive and anxiety disorders,
Categorization and psychotic disorders. It is recommended
that patients receiving mental health treatment
The disorder is classified with the obsessive- be screened for BDD, by asking whether indi-
compulsive and related disorders in the Diagnos- viduals are worried or unhappy with their
tic and Statistical Manual of Mental Disorders appearance and through use of standardized
(5th ed.; DSM-5; American Psychiatric measures such as the Yale-Brown Obsessive-
Association 2013). Compulsive Scale. Effective pharmacologic
interventions include serotonin reuptake inhib-
itors such as escitalopram and fluoxetine. Psy-
Current Knowledge chotherapeutic interventions include BDD-
specific cognitive-behavioral therapy (CBT).
Epidemiology There is emerging evidence for the utility of
National prevalence rates of BDD range internet-based CBT.
from 1.7% to 2.4%, with higher rates in outpa-
tient (1–8-6.7%) and inpatient (13.1–16%) clin-
ical samples, as well as in patients seeking
cosmetic surgery and dermatologic treatments See Also
(7.7–24.5%). Risk factors for BDD include
childhood neglect and abuse and a family history ▶ Obsessive-Compulsive and Related Disorders
of OCD. The mean age of onset is 16–17 years
and most individuals develop symptoms by age
18. Nevertheless, BDD does occur among the References and Readings
elderly as well, though much less is known
American Psychiatric Association. (2013). Diagnostic
about the nature of the disorder in this segment
and statistical manual of mental disorders
of the population. (DSM-5 ®). Washington, DC: American Psychiatric
Association.
Etiology and Clinical Issues Enander, J., Andersson, E., Mataix-Cols, D., Lichtenstein,
L., Alström, K., Andersson, G., ... & Rück, C. (2016).
The etiology of BDD is complex, encompassing
Therapist guided internet based cognitive behavioural
biological, psychological, and socioenvironmental therapy for body dysmorphic disorder: Single blind
factors. Biological factors that have been impli- randomised controlled trial. BMJ, 352, i241.
cated include hyperactivity in the left orbitofrontal Fang, A., Matheny, N. L., & Wilhelm, S. (2014). Body
dysmorphic disorder. Psychiatric Clinics of North
cortex and volume abnormalities in the America, 37(3), 287–300.
orbitofrontal cortex and anterior cingulate cortex. Harrison, A., de la Cruz, L. F., Enander, J., Radua, J., &
Additionally, maladaptive beliefs and cognitive Mataix-Cols, D. (2016). Cognitive-behavioral therapy
biases about physical appearance, reinforced for body dysmorphic disorder: A systematic review and
meta-analysis of randomized controlled trials. Clinical
through life experiences, likely play a role. Com-
Psychology Review, 48, 43–51.
pared to obsessive-compulsive disorder, BDD Phillips, K. A., & Hollander, E. (2008). Treating body
tends to be associated with higher suicidal ideation, dysmorphic disorder with medication: Evidence,
604 Body Schema

misconceptions, and a suggested approach. Body collective experiences with such discrete sensory
Image, 5(1), 13–27. input, it has been suggested that individuals even-
Phillips, K. A., Pinto, A., Menard, W., Eisen, J. L.,
Mancebo, M., & Rasmussen, S. A. (2007). Obsessive–- tually develop what might be considered a super-
compulsive disorder versus body dysmorphic disorder: ordinate sense of one’s own body, independent of
A comparison study of two possibly related disorders. its movement in space or time. This knowledge,
Depression and Anxiety, 24(6), 399–409. at least to some extent, transcends one’s own
Phillips, K. A., Keshaviah, A., Dougherty, D. D., Stout,
R. L., Menard, W., & Wilhelm, S. (2016). Pharmaco- body and allows insights into bodies in general.
therapy relapse prevention in body dysmorphic disor- Because awareness of body schema is such a
der: A double-blind, placebo-controlled trial. American fundamental operation of the central nervous sys-
Journal of Psychiatry, 173(9), 887–895. tem, it almost functions at a subliminal level. One
is normally only aware of its operation when it
becomes dysfunctional.
Disorders of body schema, known as
Body Schema asomatognosias, can take on various guises.
Although relatively rare, autotopagnosia repre-
John E. Mendoza sents what might be considered the quintessential
Department of Psychiatry and Neuroscience, body schema disturbance. This deficit involves
Tulane Medical School and SE Louisiana difficulties in identifying body parts and/or appre-
Veterans Healthcare System, New Orleans, ciating their relative relations to one another. Care
LA, USA should be taken to differentiate asomatognosia
from unilateral neglect or anomia. In the former,
the deficit is restricted to one side of the body; in
Synonyms the latter, difficulties with naming extend beyond
just parts of the body. More commonly, auto-
Somatognosis topagnosia is restricted to difficulty identifying
individual fingers, especially the middle three.
The deficit is usually bilateral and will frequently
Definition involve not only difficulties with regard to the
patient’s own fingers, but also those of the exam-
General term for the personal awareness of one’s iner or pictorial representations of a hand. Deficits
body, including the location and orientation of its are often found whether tested visually or tactu-
various parts and their relative motion in space ally and whether verbal or nonverbal (e.g.,
and time, as well as its functional integrity. matching to a model) responses are required. Uni-
laterally expressed deficits in finger recognition
using only tactile stimulation likely reflect a more
Current Knowledge basic somatosensory disturbance.
Right-left disorientation, the inability to reliably
Although usually taken for granted, to effectively distinguish the right from the left sides of one’s
carry out normal motor activities one needs to body in the absence of a more generalized aphasic
appreciate both the static and kinetic state of the disorder, is another commonly cited example of a
body as a whole as well as its individual parts. disturbance of body schema. As with finger agno-
This information is derived from a number of sia, difficulties extend beyond the patients them-
sensory feedback loops, including signals from selves to include problems with extrapersonal
receptors in the muscles, tendons, ligaments and right-left discriminations. Anosognosia and
the skin (proprioceptive, kinesthetic, and tactile anosodiaphoria (a milder form of anosognosia),
information), the inner ear or vestibular sense along with unilateral neglect or hemi-inattention
(orientation, direction, and speed of movement are sometimes viewed as specialized forms of a
of the head), and vision. Perhaps as a result of body schema disorder. One major difference is
Borderline Personality Disorder 605

that these latter syndromes are generally limited to

one side of the body, whereas autotopagnosia, the Borderline Personality
more restricted finger agnosia, and right-left disori- Disorder
entation affect both sides of the body. The one
notable exception to this rule is Anton’s syndrome, Cynthia Rolston B
a form of anosognosia in which the patient denies Department of PM&R, Virginia Commonwealth
blindness where both right and left visual fields University-Medical College of Virginia,
are involved. While there is some potential vari- Richmond, VA, USA
ability with regard to localizations of lesions,
asomatognosia, when bilaterally expressed, is
most commonly associated with lesions of the left Synonyms
parietal region, typically involving the inferior
parietal lobule. Unilateral neglect or hemi- Emotional intensity disorder
inattention syndromes may occur following ante-
rior or posterior lesions of either hemisphere,
although they are most common following right Definition
posterior lesions. Anton’s syndrome is typically
associated with bilateral lesions involving the pos- Borderline personality disorder (BPD) is charac-
terior cerebral arteries. terized in the Diagnostic and Statistical Manual of
Mental Disorders (DSM-5; American Psychiatric
Association 2013) by pervasive instability in rela-
Cross-References tionships, affect, and self-image, present in adult-
hood and across contexts. Criteria include frantic
▶ Allesthesia avoidance of real or imagined abandonment;
▶ Anosodiaphoria impulsivity; self-harm, including self-injury and
▶ Anosognosia suicidal behavior; marked emotional reactivity
▶ Autotopagnosia with intense, disproportionate anger; persistent
▶ Cortical Blindness feelings of emptiness; and transient paranoid ide-
▶ Finger Agnosia ation or dissociation.
▶ Hemiinattention
▶ Right Left Disorientation
Categorization

References and Readings BPD is classified with the cluster B personality

disorders in DSM-5.
Adair, J. C., Schwartz, R. L., & Barrett, A. (2003).
Anosognosia. In K. M. Heilman & E. Valenstein
(Eds.), Clinical neuropsychology (4th ed.,
pp. 185–214). New York: Oxford University Press.
Current Knowledge
Denburg, N. L., & Tranel, D. (2003). Acalculia and distur-
bances of body schema. In K. M. Heilman & Prevalence
E. Valenstein (Eds.), Clinical neuropsychology Rates of BPD are estimated at 1–5.9% in the
(4th ed., pp. 161–184). New York: Oxford University
Press.
community, with 75% female. Treatment set-
Goldenberg, G. (2003). Disorders of body perception and tings have higher rates: about 6% in primary
representation. In T. E. Feinberg & M. J. Farah (Eds.), care, 10% in outpatient mental health clinics,
Behavioral neurology and neuropsychology (2nd ed., and 20% in inpatient psychiatric programs.
pp. 285–294). New York: McGraw-Hill.
Prigatano, G. P., & Schacter, D. L. (Eds.). (1991). Aware-
Increased risk for BPD is found in first-degree
ness of deficit after brain injury: Clinical and theoret- relatives, Native Americans, and Blacks (Tomko
ical issues. New York: Oxford University Press. et al. 2014).
606 Borderline Personality Disorder

Diagnostic Considerations Problem-Solving (STEPPS) also frequently

Men with BPD may report greater symptom used. No treatment can boast a broad and sound
severity, separation anxiety, and body image con- evidence base, and replication studies are desper-
cerns in childhood and odd thinking in adoles- ately needed (Stoffers et al. 2012).
cence (Goodman et al. 2013; Busch et al. 2016). No medication is currently approved for BPD,
Impulsivity diminishes, but affective reactivity although common pharmacologic adjunctives
persists with aging (Arens et al. 2013). Symptoms may include mood stabilizers, antipsychotics,
vary across cultures, with self-harm/suicidality and antidepressants. When alcohol use disorder
more common in developed countries (Jani et al. co-occurs, anticonvulsants and second-generation
2016; Paris and Lis 2013). antipsychotics may be prescribed. Oxytocin
yields some promise, with some studies showing
Clinical Correlates reduced emotional reactivity, while others have
BPD has been proposed as a mood disorder, not- found increased interpersonal anxiety and
ing similar affective variability, impulsivity, and uncooperative behaviors (Amad et al. 2015).
related limbic dysregulation to bipolar disorder
(BD; Sjåstad et al. 2012; Perugi et al. 2013).
While comorbidity is high, both BD and BPD See Also
exist primarily without the other (Zimmerman
and Morgan 2013). Mood disorders, eating ▶ Personality Disorders
disorders, PTSD, ADHD, and other personality
diagnoses are frequent comorbid conditions. Pre-
mature death, suicide, and significant physical References and Readings
injuries are not uncommon.
Amad, A., Thomas, P., & Perez-Rodriguez, M. M. (2015).
Physiology and Neuropsychology Borderline personality disorder and oxytocin: Review
of clinical trials and future directions. Current Phar-
In BPD, the hippocampus, anterior cingulate cor-
maceutical Design, 21(23), 3311–3316. doi:CPD-
tex, dorsolateral prefrontal cortex, and amygdala EPUB-68145 [pii].
are implicated (Mak and Lam 2013; O’Neill and American Psychiatric Association. (2013). Diagnostic
Frodl 2012; Ruocco et al. 2016). Prefrontal gray and statistical manual of mental disorders (5th ed.).
Arlington: American Psychiatric Association
matter deficits may increase with age, while
Publishing.
parieto-occipital deficits may be more pronounced Arens, E. A., Stopsack, M., Spitzer, C., Appel, K.,
in younger individuals (Kimmel et al. 2016). This Dudeck, M., Volzke, H., ... Barnow, S. (2013). Borderline
population may also have atypical sensitivity to personality disorder in four different age groups:
A cross-sectional study of community residents in
stress hormones, dysregulation of the oxy-
Germany. Journal of Personality Disorders, 27(2),
tocinergic system, and atypical sleep patterns 196–207. 10.1521/pedi.2013.27.2.196
(Herpertz and Bertsch 2015; Winsper et al. 2016). Busch, A. J., Balsis, S., Morey, L. C., & Oltmanns, T. F.
Neurocognitive findings include increased selec- (2016). Gender differences in borderline personality
disorder features in an epidemiological sample of
tive attention to negative stimuli, difficulty with
adults age 55–64: Self versus informant report. Journal
dichotomous thinking, emotional processing, and of Personality Disorders, 30(3), 419–432. https://doi.
poor visuospatial working memory (Mak and Lam org/10.1521/pedi_2015_29_202.
2013; Winter et al. 2017; Thomsen et al. 2017). Goodman, M., Patel, U., Oakes, A., Matho, A., & Tri-
ebwasser, J. (2013). Developmental trajectories to
male borderline personality disorder. Journal of Per-
Treatment sonality Disorders, 27(6), 764–782. https://doi.org/
Dialectical behavior therapy (DBT) has been the 10.1521/pedi_2013_27_111.
most frequently studied model of psychotherapy, Herpertz, S. C., & Bertsch, K. (2015). A new perspective
on the pathophysiology of borderline personality dis-
with mentalization-based therapy (MBT),
order: A model of the role of oxytocin. The American
schema-focused therapy (SFT), and Systems Journal of Psychiatry, 172(9), 840–851. https://doi.org/
Training for Emotional Predictability and 10.1176/appi.ajp.2015.15020216.
Boston Diagnostic Aphasia Examination 607

Jani, S., Johnson, R. S., Banu, S., & Shah, A. (2016). Winsper, C., Tang, N. K., Marwaha, S., Lereya, S. T.,
Cross-cultural bias in the diagnosis of borderline per- Gibbs, M., Thompson, A., & Singh, S. P. (2016). The
sonality disorder. Bulletin of the Menninger Clinic, 80 sleep phenotype of borderline personality disorder: A
(2), 146–165. https://doi.org/10.1521/ systematic review and meta-analysis. Neuroscience
bumc.2016.80.2.146. and Biobehavioral Reviews, 73, 48–67.
Kimmel, C. L., Alhassoon, O. M., Wollman, S. C., Stern, Winter, D., Niedtfeld, I., Schmitt, R., Bohus, M., Schmahl, B
M. J., Perez-Figueroa, A., Hall, M. G., ... Radua, J. C., & Herpertz, S. C. (2017). Neural correlates of
(2016). Age-related parieto-occipital and other gray distraction in borderline personality disorder before
matter changes in borderline personality disorder: A and after dialectical behavior therapy. European
meta-analysis of cortical and subcortical structures. Archives of Psychiatry and Clinical Neuroscience,
Psychiatry Research, 251, 15–25. https://doi.org/ 267(1), 51–62. https://doi.org/10.1007/s00406-016-
10.1016/j.pscychresns.2016.04.005 0689-2.
Mak, A. D., & Lam, L. C. (2013). Neurocognitive profiles Zimmerman, M., & Morgan, T. A. (2013). The relationship
of people with borderline personality disorder. Current between borderline personality disorder and bipolar
Opinion in Psychiatry, 26(1), 90–96. https://doi.org/ disorder. Dialogues in Clinical Neuroscience, 15(2),
10.1097/YCO.0b013e32835b57a9. 155–169.
O’Neill, A., & Frodl, T. (2012). Brain structure and func-
tion in borderline personality disorder. Brain Structure
& Function, 217(4), 767–782. https://doi.org/10.1007/
s00429-012-0379-4.
Paris, J., & Lis, E. (2013). Can sociocultural and historical Boston Diagnostic Aphasia
mechanisms influence the development of borderline Examination
personality disorder?. Transcultural Psychiatry, 50(1),
140–151.
Perugi, G., Angst, J., Azorin, J. M., Bowden, C., Vieta, E., Nancy Helm-Estabrooks
Young, A. H., & BRIDGE Study Group. (2013). Is Department of Communication Disorders and
comorbid borderline personality disorder in patients Sciences, College of Health and Human Sciences,
with major depressive episode and bipolarity a develop-
Western Carolina University, Cullowhee, NC, USA
mental subtype? Findings from the international
BRIDGE study. Journal of Affective Disorders, 144
(1–2), 72–78. https://doi.org/10.1016/j.jad.2012.06.008.
Ruocco, A. C., Rodrigo, A. H., McMain, S. F., Page- Synonyms
Gould, E., Ayaz, H., & Links, P. S. (2016). Predicting
treatment outcomes from prefrontal cortex activation
for self-harming patients with borderline personality BDAE
disorder: A preliminary study. Frontiers in Human
Neuroscience, 10, 220. https://doi.org/10.3389/
fnhum.2016.00220.
Sjåstad, H. N., Grawe, R. W., & Egeland, J. (2012). Affec-
Description
tive disorders among patients with borderline person-
ality disorder. PloS One, 7(12), e50930. https://doi.org/ Boston Diagnostic Aphasia Examination (3rd ed.)
10.1371/journal.pone.0050930 [doi]. (BDAE-3) Authors: Harold Goodglass, Edith
Stoffers, J. M., Vollm, B. A., Rucker, G., Timmer, A.,
Kaplan, Barbara Barresi, 2001, Publisher: Pro-
Huband, N., & Lieb, K. (2012). Psychological thera-
pies for people with borderline personality disorder. Ed, 8700 Shoal Creek Blvd, Austin, TX
The Cochrane Database of Systematic Reviews, 8, 78757–6897, http://www.proedinc.com. The
CD005652. https://doi.org/10.1002/14651858. complete BDAE-3 test kit includes stimulus
CD005652.pub2.
cards, test booklets for Standard and Short
Thomsen, M. S., Ruocco, A. C., Uliaszek, A. A.,
Mathiesen, B. B., & Simonsen, E. (2017). Changes in forms, the 60-item Boston Naming Test with
neurocognitive functioning after 6 months of record booklets, a DVD, and a hardbound text
mentalization-based treatment for borderline personal- that contains the test manual.
ity disorder. Journal of Personality Disorders, 31(3),
The Boston Diagnostic Aphasia
306–324.
Tomko, R. L., Trull, T. J., Wood, P. K., & Sher, K. J. Examination-3 (BDAE-3; Goodglass et al.
(2014). Characteristics of borderline personality disor- 2001a) is a comprehensive, multiple subtests
der in a community sample: Comorbidity, treatment instrument for investigating a broad range of lan-
utilization, and general functioning. Journal of Person-
guage impairments that are common conse-
ality Disorders, 28(5), 734–750. https://doi.org/
10.1521/pedi_2012_26_093. quences of brain damage. It is designed as
608 Boston Diagnostic Aphasia Examination

a comprehensive measure of aphasia. The exam- was revised in 1983 and again in 2001. Changes
ination provides materials and procedures to eval- from the previous edition include the addition of
uate five language-related sections and an abbreviated and expanded testing formats,
additional section on praxis. The five language incorporation of the Boston Naming Test,
domains include conversational and expository addition of a Language Competence Index,
speech, auditory comprehension, oral expression, and clarification of scoring procedures and
reading, and writing. In addition to individual definitions. The revision also was designed to
subtest scores, the test yields three broader mea- integrate recent advances in neurolinguistics
sures: the Severity Rating Scale (a rating of research, including methods to assess narrative
the severity of observed language/speech and discourse complexity, category-specific
disturbance), the Rating Scale Profile of Speech dissociations in lexical production/comprehen-
Characteristics (a rating of observed speech char- sion, syntax comprehension, and analysis of
acteristics and of scores in two main language grapheme-phoneme conversion during reading.
domains), and the Language Competency Index The ultimate goal for the authors in developing
(a composite score of language performance on the test was clinical utility.
BDAE-3 subtests). The extended version The BDAE-3 consists of more than 50 subtests
includes a sixth section, “Praxis,” which exam- that can be administered in three different formats:
ines natural and conventional gestures, use of standard, short, and extended. The standard for-
pretend objects, and bucco-facial and respiratory mat most closely resembles earlier versions of the
movements. The test manual is part of the text by BDAE. The new short form of the test provides a
Goodglass et al. (2001b). It provides suggestions brief assessment. The extended version offers a
for administering, scoring, and interpreting per- comprehensive neurolinguistic profile that
formance on subtests, as well as directions for includes evaluation of spontaneous narrative, pro-
plotting and interpreting patient profiles. Percen- cessing of word categories, syntax comprehen-
tiles or standard scores can be derived for each sion, and reading/writing. The BDAE-3 allows
subtest. both a quantitative and a qualitative evaluation
of language. The examination is based on an
Administration assumption that the nature of the aphasic deficit
The 44-page test booklet provides instructions is determined by (1) organization of language in
for test administration. The short form and the brain, (2) the location of the lesion causing the
extended form items are specified in the test aphasia, and (3) interactions among parts of the
booklet and are also presented in different type- language system.
face; the short form items are presented in bold The BDAE has been adapted and translated
typeface, and the extended form items appear in for use in many languages including Spanish,
italics. The standard administration includes all French, German, Italian, Dutch, Greek, Hindi,
of the bold short form items in addition to regular Finnish, Mandarin Chinese, Japanese, and
typeface items. Portuguese.

Historical Background Psychometric Data

The BDAE is designed to meet three goals: to Norms

enable diagnosis of aphasia syndromes, to mea- Standardization of the BDAE-3 is based on a
sure the breadth and severity of aphasic distur- population of individuals with aphasia (IwA)
bance, and to provide a comprehensive who were referred concurrently by field exam-
assessment of language to guide therapy. Initially iners working in inpatient, outpatient, and private
published by Goodglass and Kaplan in 1972, it practice settings. Means and standard deviations
Boston Diagnostic Aphasia Examination 609

for the BDAE-3 subtests for IwA are provided in BDAE, Goodglass and Kaplan (1972) found a
the test manual. The number of IwA administered strong general language factor and factors cov-
the 50 subtests varies from a maximum of 85 to a ering spatial-quantitative-somatagnostic,
low of 31. Means are also provided for 15 non- articulation-grammatical fluency, auditory com-
clinical individuals who, on average, failed less prehension, and paraphasia domains. Goodglass B
than one item per subtest. Rosselli et al. (1990) and Kaplan (1983) described a second factor
and Pineda et al. (2000) provide norms for the analysis using a sample of 242 adults with apha-
Spanish version of the BDAE-2 (Goodglass and sia, concluding that auditory comprehension,
Kaplan 1986) that is based on 156 healthy indi- repetition-recitation, reading, and writing were
viduals living in Columbia, South America. factors of equal importance. Similar findings in
normal individuals were reported by Pineda et al.
Reliability (2000) for the BDAE-2 Spanish version.
Kuder-Richardson reliability coefficients for Correlations between earlier versions of the
subtests reflect variability, ranging between BDAE and other measures have been described.
<0.65 and <0.95 with about two-thirds of the For example, the BDAE oral apraxia task has
coefficients reported in the manual (Goodglass been correlated with other articulation tasks
et al. 2001a), ranging from 0.90 upwards. No (Sussman et al. 1986); correlations for the audi-
stability coefficients for test-retest are provided. tory comprehension measure on the BDAE and
The authors state that test-retest reliability is the Token Test and with respective measures of
difficult to attain with IwA. The current reliabil- the Porch Index of Communicative Ability
ity coefficients demonstrate very good internal (PICA) have been reported (Divenyl and
consistency in terms of what the items within the Robinson 1989). Brookshire and Nicholas
subtests are measuring (Goodglass et al. 2001b). (1984) found the BDAE auditory comprehension
For most subtests, correlations are very high subtest did not predict auditory paragraph
between the short and standard forms (>0.90; comprehension of independent standardized
Goodglass et al. 2001b). No reliability informa- material.
tion is provided in the BDAE-3 manual regarding Goodglass and Kaplan designed the BDAE to
the Severity Rating Scale, Language Compe- assess various components of language function
tency Index, praxis assessment, or Spatial- for the purpose of discriminating among different
Quantitative Battery. patterns of CNS lesions indicative of types of
aphasia. Studies to date have not determined deci-
Validity sion rules for the diagnosis of individual subtypes
A correlation matrix was obtained for all the of aphasia (Crary et al. 1992; Reinvang and
scores in the BDAE-3 battery, and the correlation Graves 1975).
coefficients 0.60 or greater are displayed in the Ecological validity of the BDAE for predicting
manual (Goodglass et al. 2001a), with severity progress with aphasia therapy has been described
partialled out, showing intercorrelations between by various authors (e.g., Davidoff and Katz 1985;
subtests for the standardization sample. Based on Marshall and Neuburger 1994).
these, “a number of sharply defined clusters” are
indicated by the authors (p. 16). Strauss et al.
(2006), however, pointed out that the lack of data Clinical Uses
on the entire correlational matrix makes it “difficult
to estimate convergent and discriminant validity The BDAE is derived from samples of 85 adult
within and across BDAE-3 clusters” (p. 896) individuals with stroke and 15 elderly nonclinical
especially given the fact that the more than volunteers. Therefore, it is most useful when
50 subtests were administered to just 31–85 sub- assessing adult populations with language impair-
jects. Based on data for earlier versions of the ments resulting from strokes, but it may be used
610 Boston Diagnostic Aphasia Examination

effectively with persons who have sustained trau- Davidoff, M., & Katz, R. (1985). Automated telephone
matic brain injury (e.g., Theodoros et al. 2008) therapy for improving comprehension in aphasic
adults. Cognitive Rehabilitation, 3, 26–28.
and forms of dementia (e.g., Tsantali et al. 2013). Divenyl, P. L., & Robinson, A. J. (1989). Nonlinguistic
The BDAE offers a comprehensive look at lan- auditory capabilities in aphasia. Brain and Language,
guage function from a neuropsychological per- 37, 290–326.
spective. Complete administration of this battery Goodglass, H., & Kaplan, E. (1972). Boston diagnostic
aphasia examination (BDAE). Philadelphia: Lea &
requires approximately 90 min. The short form Febiger.
requires approximately 40–60 min. The BDAE Goodglass, H., & Kaplan, E. (1983). The assessment of
is one of the most popular batteries for use by aphasia and related disorders (2nd ed.). Philadelphia:
speech-language pathologists for evaluation Lea & Febiger.
Goodglass, H., & Kaplan, E. (1986). La evaluacion de la
of aphasia and other neurologic language impair- afasia y transformos relacionados (2nd ed.). Madrid:
ments. In addition to its strength as a comprehen- Editorial Medica Panamericana.
sive assessment of language, the BDAE provides Goodglass, H., Kaplan, E., & Barresi, B. (2001a). Boston
useful instructions for observing and recording diagnostic aphasia examination (3rd ed.). Austin:
Pro-Ed.
specific types of error responses (e.g., paraphasia) Goodglass, H., Kaplan, E., & Barresi, B. (2001b). The
found in individuals with aphasia, reflecting what assessment of aphasia and related disorders (3rd ed.).
has been termed the “Boston school” approach to Austin: Pro-Ed.
aphasia classification. The detailed examination Helm-Estabrooks, N., Albert, M. L., & Nicholas,
M. (2014). Manual of aphasia and aphasia therapy
of conversational and expository speech is an (3rd ed.). Austin: Pro-ED.
important and unique aspect of the BDAE and is Marshall, R. C., & Neuburger, S. I. (1994). Verbal self-
well described in the manual (Goodglass et al. correction and improvement in treated aphasia clients.
2001b). Aphasiology, 8, 535–547.
Pineda, D. A., Rosselli, M., Ardila, A., Mejia, S. E.,
BDAE results can be used to guide aphasia Romero, M. G., & Perez, C. (2000). The Boston diag-
treatment programs (Helm-Estabrooks et al. nostic aphasia examination-Spanish version: The influ-
2014) and to measure the effects of treatment ence of demographic variables. Journal of the
(Robey 1998). International Neuropsychological Society, 6, 802–814.
Reinvang, I., & Graves, R. (1975). A basic aphasia exam-
ination: Description with discussion of first results.
Scandinavian Journal of Rehabilitation Medicine, 7,
129–135.
Cross-References Robey, R. R. (1998). A meta-analysis of clinical outcomes
in the treatment to aphasia. Journal of Speech, Lan-
▶ Anomic Aphasia guage, and Hearing Research, 41(1), 172–188.
Rosselli, M., Ardila, A., Florez, A., & Castro, C. (1990).
▶ Aphasia Normative data on the Boston diagnostic aphasia eval-
▶ Boston Naming Test uation in a Spanish speaking population. Journal of
▶ Broca’s Aphasia Clinical and Experimental Neuropsychology, 12,
▶ Conduction Aphasia 313–322.
Spreen, O., & Risser, A. H. (Eds.). (2003). Assessment of
▶ Praxis aphasia. New York: Oxford University Press.
▶ Wernicke’s Aphasia Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A
compendium of neuropsychological tests (3rd ed.).
New York: Oxford University Press.
Sussman, H., Marquardt, T., Hutchinson, J., &
References and Readings MacNeilage, P. (1986). Compensatoryarticulation in
Broca’s aphasia. Brain and Language, 27, 56–74.
Brookshire, R. H., & Nicholas, L. E. (1984). Comprehen- Theodoros, D., Hill, A., Russell, T., Ward, E., & Wootton,
sion of directly and indirectly stated main ideas and R. (2008). Assessing acquired language disorders in
details in discourse by brain-damaged and non-brain- adults via the internet. Telemedicine Journal and
damaged listeners. Brain and Language, 21, 21–36. E-Health, 14(6), 552–559.
Crary, M. A., Wertz, R. T., & Deal, J. L. (1992). Classifying Tsantali, E., Economidis, D., & Tsolaki, M. (2013). Could
aphasias: Cluster analysis of western aphasia battery language deficits really differentiate mild cognitive
and Boston diagnostic aphasia examination. impairment (MCI) from mild Alzheimer’s disease?
Aphasiology, 6, 29–36. Archives of Gerontology & Geriatrics, 57(3), 263–270.
Boston Naming Test 611

Administration
Boston Naming Test The Boston Naming Test assesses naming abili-
ties of children, adults with aphasia, and non-
Carole R. Roth1 and Nancy Helm-Estabrooks2 clinical adults. The drawings are shown to the
B
1
Otolaryngology Clinic, Speech Division, examinee one at a time, and the examinee is
Naval Medical Center, San Diego, asked to name each of them. Item familiarity
CA, USA decreases as the test progresses. Following pre-
2
Department of Communication Disorders and sentation of each picture stimulus, two types of
Sciences, College of Health and Human Sciences, cues may be presented when there is an error
Western Carolina University, Cullowhee, response: a “stimulus cue” (descriptive, e.g.,
NC, USA “used by a carpenter” for saw) and a “phonemic
cue” (the beginning sound of the target word, e.g.,
“s . . .” for saw) A stimulus cue is presented when
Synonyms the examinee clearly misperceives the picture
(e.g., “worm” for pretzel) or indicates a lack of
BNT recognition of the picture. A phonemic cue is
presented after each error response, including fol-
lowing a stimulus cue. The examinee is given up
Description to 20 s to respond following each stimulus pre-
sentation and after the cues. All responses are
Boston Naming Test (2nd (BNT-2) recorded as a “correct response” or as an error
Authors: Kaplan, Edith, Goodglass, Harold, with the actual error response written verbatim
Weintraub, Sandra for later coding by type. Types of cues (“stimulus
Second edition 2001 cue” or “phonemic cue”) presented are noted.
Publisher: Pro-Ed, 8700 Shoal Creek Blvd, Response latencies in seconds are also
Austin, TX 78757–6897 documented. The total correct score is the sum
http://www.proedinc.com of the accurate spontaneous responses given
Also available as part of the revised BDAE-3 within 20 s of picture presentation or following a
(Goodglass et al. 2001) from Pro-Ed. stimulus cue. Correct responses following a pho-
The Boston Naming Test (BNT) is a widely nemic cue are not included in the total correct
used tool for assessing confrontation naming score.
ability. The BNT consists of 60 black and
white line drawings of objects that are ordered
according to vocabulary word frequency from Historical Background
bed to abacus. The order of the pictured stimuli
takes into account the finding that individuals The test was originally published by Kaplan and
with dysnomia often have greater difficulties colleagues in 1978 as an experimental version
with the naming of low frequency objects. with 85 items. It was revised to a 60-item test in
Thus, instead of a simple category of anomia, 1983. The current version (BNT-2) retains the
naming difficulties may be rank ordered along a same 60 items and includes a short 15-item ver-
continuum.. This type of picture-naming vocab- sion as well as a multiple-choice version. Short
ulary test is useful in the evaluation of children forms of the BNT have been developed to reduce
with learning disabilities and adults with brain test time. These include Fastenau et al. (1998),
injury or dysfunction. When used in conjunction Graves et al. (2004), Lansing et al. (1999), Mack
with the Boston Diagnostic Aphasia Examina- et al. (1992), Saxton et al. (2000), Teng et al.
tion, inferences can be drawn regarding lan- (1989), and Williams et al. (1989). The 15-item
guage facility and possible localization of short-form 4 (Mack SF4) developed by Mack
cerebral damage. et al. (1992) was adopted by the authors of the
612 Boston Naming Test

BNT-2 and can be found at the beginning of the readministered between 9 and 24 months after
stimulus booklet and answer sheet. The Mack the baseline exam. During a 9–15-month retest
et al. 15- item version has been adopted by the period, a 4-point decline occurred. A 6-point
Consortium to Establish a Registry for decline occurred during a 16–24-month retest
Alzheimer’s Disease (CERAD). period. The participant’s age and family history
In a 2011 study, Hobson, et al. explored of dementia further characterized the cutoff values
whether the 15-item BNT/CERAD version and for reliable changes in BNT performance.
two 30-item (even and odd) versions could predict
scores earned on the 60-item version by partici- Validity
pants with and without AD. Estimated 60-item The BNT has been shown to correlate highly with
scores created from the shorter versions were other language-related measures, including the
then correlated with actual scores. The 60-item visual naming test of the Multilingual Aphasia
scores estimated from the 30-item versions had Examination (Axelrod et al. 1994; Schefft et al.
good predictive value for actual 60-item BNT 2003), as well as with measures of intelligence,
scores and the 15-item version less so. including the Verbal Comprehension Factor of the
The new BNT-2 also includes a multiple- WAIS-R and the Standard Raven Progressive
choice version that can be administered following Matrices in children aged 6–12 years (Storms
the standard presentation, specifically to further et al. 2004).
assess the examinee’s recognition of the lexicon Poor performance on the BNT has been
for items previously missed. The BNT-2 is avail- described in subjects with neurologic disease,
able separately and as part of the revised BDAE-3. including left-hemisphere and brainstem strokes,
The BNT has been adapted and translated for use anoxia, multiple sclerosis, Parkinson’s disease,
in at least a dozen languages including a 30-item Alzheimer’s disease, and closed head injuries.
adaptation for Spanish-speaking people in the
United States. Norms
The norms available in the test booklet are limited
to small groups of adults ranging in age between
Psychometric Data 18 and 79 (N = 178) and of children ranging in
age between 5.0 years and 12.5 years (N = 356).
Reliability, Validity, and Norms Information about geographical region, ethnicity,
or time reference for this normative data is not
Reliability provided.
Internal consistency for the 60-item form has been Data on BNT norms for children is limited. The
reported to range between 0.78 and 0.96. Reliabil- BNT record form presents norms for ages 5 years
ity coefficients have been lower for the abbrevi- and 0 months (5-0) through 12-5, based on small
ated versions; for example, the Mack SF4 version groups in successive 6-month age increments.
ranges between 0.49 and 0.84. Test-retest reliabil- The data were collected in 1987 and the normative
ity is high over short intervals. For longer time data are believed to be largely from Caucasian
intervals, such as 11–12 months, test-retest reli- boys and girls who were attending public and
ability was marginal to high; for example, in a private schools and living with middle-class fam-
healthy, elderly Caucasian adult population, test- ilies in suburban or urban areas of the northeastern
retest reliability ranged between 0.62 and 0.89 United States.
(Mitrushina and Satz 1995); and high retest reli- Martielli and Blackburn (2015) collected nor-
ability (0.92) in a normal or neurologically stable mative BNT-2 data for 100 male and 100 female
adult population (Dikmen et al. 1999). In 2012, adolescents aged 15–18 years. None of the
Sachs and colleagues published a BNT reliability 200 participants had neurologic, psychiatric, or
study of 844 cognitively unimpaired, Caucasian academic problems. No statistically significant
adults who were over age 55. The BNT was differences in BNT scores based on gender, age,
Boston Naming Test 613

or grade occurred. Martielli and Blackburn pro- individuals over 55 years (Steinberg et al.
vide normative means and standard deviations, 2005), and age- and education-adjusted norma-
collapsed across age and gender. tive data based on African Americans from the
Cross-sectional studies suggest that age Mayo Older African American Normative stud-
(Heaton et al. 2004; Ivnik et al. 1996; MacKay ies (MOAANS) project (Lucas et al. 2005; B
et al. 2005; Mitrushina et al. 2005) and verbal Strauss et al. 2006).
intelligence affect the BNT scores (Killgore and Pedraza and colleagues (2009) used item
Adams 1999; Steinberg et al. 2005; Tombaugh response theory (IRT) and methods to detect
and Hubley 1997). Gender has been reported to differential item functioning (DIF) of BNT
be unrelated to BNT performance (Henderson items with 336 Caucasian and 334 African
et al. 1998; Ivnik et al. 1996; Lucas et al. 2005; American participants. Twelve items were
Riva et al. 2000). Other studies suggest men shown to have DIF between the two groups.
outperform women in older samples, possibly Additional analyses showed that six of these
because of male-biased items (Randolph et al. items (dominoes, escalator, muzzle, latch, tripod,
1999). Reading vocabulary is strongly correlated and palette) represent the strongest evidence for
with BNT performance (Graves and Carswell race-/ethnicity-based DIF. This study demon-
2003; Senior et al. 2001). Geographic region and strates that psychometric and sociocultural fac-
ethnicity have been shown to affect performance tors can lead to BNT score discrepancies between
(Heaton et al. 2004; Lucas et al. 2005). Linguistic groups.
background also affects test scores according to Zec and colleagues (2007a) published the
Roberts et al. (2002). results of a BNT study conducted with 1111 “nor-
It can be found in the literature a number of mal elderly” adults aged 50–101 years and
normative reports for adult English speakers (see 61 younger adults aged 20–49 years. They found
pp. 905–907, Strauss et al. 2006). For example, both significantly lower scores and increasing
Heaton et al. (2004) reviewed studies over a variability among increasing age groups and
25-year period and presented age, gender, and with lower educational levels. In a subsequent
educational norms for two ethnicity groups: Cau- study (Zec et al. 2007b), BNT raw scores earned
casians and African Americans. Mitrushina et al. by 1,026 participants ranging in age from 50–95
(2005) compiled data from 14 studies, comprising were converted to scaled scores and percentiles.
a total of 1,684 educated participants with above- Zec and colleagues present these norms and
average intelligence who were administered the recommend them for use in assessing people
60-item version. Their data was presented in with suspected dementia.
5-year increments, ranging from ages
25–84 years. The data is considered to be similar
to those provided by Kaplan et al. (2001) and may Clinical Uses
overestimate expected performance for individ-
uals with lower educational and intellectual The BNT, a visual confrontation naming test, is
levels. Ivnik et al. (1996) provided age-corrected recommended as a supplement to the Boston
norms for 663 primarily Caucasian individuals Diagnostic Aphasia Examination. It can be used
older than 55 years of age, derived from the to assess naming abilities of children, individuals
Mayo Older Americans Normative Studies (the with aphasia a, and typical adults, although there
MOANS projects). Raw scores are converted to is limited and poorly described normative data
age-corrected scaled scores having a mean of ten and no test-retest reliability for children.
and a standard deviation (SD) of three (Strauss In their 2013 chapter on using a process
et al. 2006). Additional studies have expanded approach to aphasia, Helm-Estabrooks and Nich-
the utility of the MOANS project by providing olas describe the clinical and diagnostic utility of
age- and IQ-adjusted percentile equivalents response patterns to the BNT. Responses typical
of MOANS age-adjusted BNT scores, for of a person with Broca’s aphasia and a person with
614 Boston Naming Test

Wernicke’s aphasia are used to illustrate the clin- Henderson, L. W., Frank, E. W., Pigatt, T., Abramson,
ical value of looking beyond BNT scores to ana- R. K., & Houston, M. (1998). Race, gender and educa-
tional level effects on Boston Naming Test scores.
lyzing transcribed responses. Aphasiology, 12, 901–911.
Kaplan, E., Goodglass, H., & Weintrab, S. (1978, 1983).
The Boston naming test: Experimental edition (1978).
Boston: Kapan & Goodglass. (2nd ed.) Philadelphia:
Cross-References Lea & Febiger.
Kaplan, E., Goodglass, H., & Weintrab, S. (2001). The
Boston naming test (2nd ed.). Austin: Pro-Ed.
▶ Anomia Killgore, W. D. S., & Adams, R. L. (1999). Prediction of
▶ Boston Diagnostic Aphasia Examination Boston Naming Test performance form vocabulary
scores: Preliminary guidelines for interpretation. Per-
ceptual and Motor Skills, 89, 327–337.
Lansing, A. E., Ivnik, R. J., Cullum, C. M., & Randolph,
References and Readings C. (1999). An empirically derived short form of the
Boston Naming Test. Archives of Clinical Neuropsy-
Axelrod, B. N., Ricker, J. H., & Cherry, S. A. (1994). chology, 14, 481–487.
Concurrent validity of the MAE visual naming test. Lucas, J. A., Ivnik, R. J., Smith, G. E., Ferman, T. J., Willis,
Archives of Clinical Neuropsychology, 9, 317–321. F. B., Petersen, R. C., & Graff-Radford, N. R. (2005).
Dikmen, S. S., Heaton, R. K., Grant, I., & Temkin, N. R. Mayo’s older African Americans normative studies:
(1999). Test-retest reliability and practice effects of Norms for Boston Naming Test, controlled oral word
expanded Halstead-Reitan neuropsychological test bat- association, category fluency, animal naming, Token
tery. Journal of the International Neuropsychological test, WRAT-3 reading, trail making test, stroop test,
Society, 5, 346–356. and judgment of line orientation. The Clinical Neuro-
Fastenau, P. S., Denburg, N. L., & Mauer, B. A. (1998). psychologist, 19, 243–269.
Parallel short forms for the Boston Naming Test: Psy- Mack, W. J., Freed, D. M., Williams, B. W., & Henderson,
chometric properties and norms for older adults. Jour- V. W. (1992). Boston Naming Test: Shortened version
nal of Clinical and Experimental Neuropsychology, 20, for use in Alzheimer’s disease. Journal of Gerontology,
828–834. 47, 164–168.
Goodglass, H., Kaplan, E., & Barresi, B. (2001). Boston MacKay, A., Connor, L. T., & Henderson, V. W. (2005).
diagnostic aphasia examination (3rd ed.). Austin: Dementia does not explain correlation between age and
Pro-Ed. scores on Boston Naming Test. Archives of Clinical
Graves, R. E., Bezeau, S. C., Fogarty, J., & Blair, R. Neuropsychology, 20, 129–133.
(2004). Boston Naming Test Short Forms: A compari- Martielli, T. M., & Blackburn, L. B. (2015). When a funnel
son of previous forms with new item response theory becomes a martini glass: Adolescent performance on
based forms. Journal of Clinical and Experimental the Boston Naming Test. Child Neuropsychology:
Neuropsychology, 26, 891–902. A Journal on Normal and Abnormal Development in
Heaton, R. K., Miller, S. W., Taylor, M. J., & Grant, I. Childhood and Adolescence, 1–13.
(2004). Revised comprehensive norms for an expanded Mitrushina, M., & Satz, P. (1995). Repeated testing of
Halstead Reitan Battery: Demographically adjusted normal elderly with the Boston Naming Test. Aging
neuropsychological norms for African American and Clinical and Experimental Research, 7, 123–127.
Caucasian adults. Lutz: PAR. Mitrushina, M. M., Boone, K. B., Razani, J., & D’Elia,
Helm-Estabrooks, N., & Nicholas, M. (2013). The process L. F. (2005). Handbook of normative data for neuro-
approach to aphasia. In L. Ashendorf & D. J. Libon psychological assessment (2nd ed.). New York: Oxford
(Eds.), Neuropsychological assessment using the Bos- University Press.
ton process approach: A practitioner’s guide Morris, J. C., Mohs, R. C., Rogers, H., Fillenbaum, G., &
(pp. 170–199). New York: Oxford Press. Heyman, A. (1988). Consortium to establish a registry
Hobson, V. L., Hall, J. R., Harvey, M., Munro Cullum, C., for Alzheimer’s disease (CERAD) clinical and neuro-
Lacritz, L., Massman, P. J., Waring, S. C., & O’Bryant, psychological assessment of Alzheimer's disease. Psy-
S. E. (2011). An examination of the Boston Naming chopharmacology Bulletin, 24, 641–652.
Test: Calculation of “estimated” 60-item score from 30- Neils, J., Baris, J. M., Carter, C., Dell’aira, A. L., Nordloh,
and 15-item scores in a cognitively impaired popula- S. H., & Weiler, E. (1995). Effects of age, education, and
tion. International Journal of Geriatric Psychiatry, 26, living environment on Boston naming test performance.
351–335. Journal of Speech and Hearing Research, 38, 1143–1149.
Ivnik, R. J., Malec, J. F., Smith, G. E., Tangalos, E. G., & Nicholas, L. E., Brookshire, R. H., MacLennan, D. L.,
Peterson, R. C. (1996). Neuropsychological test norms Schumacher, J. G., & Porrazzo, S. A. (1988). The Bos-
above age 55: COWAT, BNT, MAE Token, WRAT-R ton naming test: Revised administration and scoring
Reading, AMNART, Stroop, TMT, and JLO. The Clin- procedures and normative information for non-brain-
ical Neuropsychologist, 10, 262–278. damaged adults. Clinical Aphasiology, 18, 103–115.
Boston Process Approach 615

Pedraza, O., Graff-Radford, N. R., Smith, G. E., Ivnik, Williams, B. W., Mack, W., & Henderson, V. W. (1989).
R. J., Willis, F. B., Petersen, R. C., & Lucas, J. A. Boston naming test in Alzheimer’s disease. Neuropsy-
(2009). Differential item functioning of the Boston chologia, 27, 1073–1079.
Naming Test in cognitively normal African American Zec, R. F., Burkett, N. R., Markwell, S. J., & Larsen, D. L.
and Caucasian older adults. Journal of the Interna- (2007a). A Cross-sectional study of the effects of age,
tional Neuropsychological Society, 15, 758–768. education, and gender on the Boston Naming Test. The B
Randolph, C., Lansing, A., Ivnick, R. J., Cullum, C. M., & Clinical Neuropsychologist, 21(4), 587–616.
Hermann, B. P. (1999). Determinants of confrontation Zec, R. F., Burkett, N. R., Markwell, S. J., & Larsen, D. L.
naming performance. Archives of Clinical (2007b). Normative data stratified for age, education,
Neuropsycology, 14, 489–496. and gender on the Boston Naming Test. The Clinical
Roberts, P. M., Garcia, L. J., Desrochers, A., & Hernandez, Neuropsychologist, 21(4), 617–637.
D. (2002). English performance of proficient bilingual
adults on the Boston Naming Test. Aphasiology, 16,
635–645.
Sachs, B. C., Lucas, J. A., Smith, G. E., Ivnik, R. J.,
Peterson, R. C., Graff-Radford, N. R., & Pedrazal, Boston Process Approach
O. (2012). Reliable change on the Boston Naming
Test. Journal of International Neuropsychological
Society, 18, 375–378.
Shahal Rozenblatt
Saxton, J., Ratcliff, G., Munro, C. A., Coffery, C. E., Becker, Advanced Psychological Assessment, P. C.,
J. E., Fried, L., & Kuller, L. (2000). Normative data on the Smithtown, NY, USA
Boston Naming Test and two equivalent 30-item short-
forms. The Clinical Neuropsychologist, 14, 526–534.
Schefft, B. K., Testa, S. M., Dualy, M. F., Privitera, M. D.,
& Yeh, H. S. (2003). Preoperative assessment of con- Synonyms
frontation naming ability and intrictal paraphasia pro-
duction in unilateral temporal lobe epilepsy. Epilepsy BPA
and Behavior, 4, 161–168.
Steinberg, B. A., Beiliauskas, L. A., Smith, G. E.,
Langellotti, C., & Ivnik, R. J. (2005). MAYO‘s older
Americans normative studies: Age- and IQ-adjusted Definition
norms for the Boston Naming Test, the MAE Token
test, and the judgment of line orientation test. The
Clinical Neuropsychologist, 19, 280–328.
Born out of the work of A. R. Luria (e.g., Higher
Storms, G., Saerens, J., & De Deyn, P. P. (2004). Norma- Cortical Function in Man, 1966), the Boston pro-
tive data for the Boston Naming Test in native Dutch- cess approach (BPA) to neuropsychological test-
speaking Belgian children and the relation with intelli- ing is a method of exploring the patient’s approach
gence. Brain and Language, 91, 274–281.
to a task and the process involved in attaining a
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A
compendium of neuropsychological tests: Administra- specific test score (Loring 1999). Its aim is to
tion, norms, and commentary (3rd ed.pp. 901–915). provide a more accurate characterization of neu-
New York: Oxford University Press. ropsychological function and dysfunction and the
Teng, E. L., Wimer, C., Roberts, E., Damasio, A. R., Eslinger,
nervous system components involved (Kaplan
P. J., Folstein, M. F., Tune, L. E., Whitehouse, P. J.,
Bardolph, E. L., Hui, H. C., & Henderson, V. W. (1989). 1988; Strauss et al. 2006).
Alzheimer’s dementia: Performance on parallel forms of
the dementia assessment battery. Journal of Clinical and
Experimental Neuropsychology, 11, 899–912.
Tombaugh, T. N., & Hubley, A. (1997). The 60-item Bos-
Current Knowledge
ton Naming Test: Norms for cognitively intact adults
aged 25 to 88 years. Journal of Clinical and Experi- According to Edith Kaplan (1988, 1990), the
mental Neuropsychology, 19, 922–932. “achievement”-oriented approach to assessment,
Van Gorp, W., Satz, P., Kiersch, M., & Henry, R. (1986).
where performance is based on the scores
Normative data on the Boston naming test for a group
of normal older adults. Journal of Clinical and Exper- obtained on a particular test, is flawed in that it
imental Neuropsychology, 8, 702–705. assumes that the scores obtained are reflective of
Welch, L. W., Doineau, D., Johnson, S., & King, D. (2002). an underlying unitary mechanism. As an example,
Educational and gender normative data for the Boston
two individuals could arrive at a similar score via
naming test in a group of older adults. Brain and
Language, 53(2), 260–266. distinctly different processes that are dependent
616 Brachytherapy

on distinctly different neural structures and/or also change how the patient approaches the test
pathways. The inherent loss of data that occurs when it is readministered.
by focusing on composite or total scores resulted
in the development of an approach that focused on
how a specific result was obtained. This led to the See Also
Boston process approach (BPA). In addition to
careful observation of the strategies used during ▶ Fixed Battery
the completion of a task, the BPA emphasizes the ▶ Flexible Battery
importance of demographic variables (e.g., age, ▶ Hypothesis Testing Approach to Evaluation
gender, socioeconomic status, education, and
occupational status), medical history, and mental
health history, as each of these variables can influ- Further Readings
ence a patient’s performance. According to
Delis, D. C., Kaplan, E., & Kramer, J. H. (2001). Delis-
Kaplan (1990), the BPA differs from the fixed Kaplan executive function system. San Antonio: The
and flexible battery approaches to testing in that Psychological Corporation.
the final score is deemphasized, that is, whether a Kaplan, E. (1988). A process approach to neuropsycholog-
response is right or wrong is less important than ical assessment. In T. Boll & B. K. Bryant (Eds.),
Clinical neuropsychology and brain function:
how it was attained. In addition, the test may be Research, measurement, and practice. Washington,
administered differently from the standardized DC: American Psychological Association.
approach, and additional measure may be intro- Kaplan, E. (1990). The process approach to neuropsycho-
duced in order to better understand the component logical assessment of psychiatric patients. Journal of
Neuropsychiatry, 2, 72–87.
processes that influence or are involved in a par- Korkman, M., Kirk, U., & Kemp, S. L. (2007). NEPSY
ticular task. Modified materials may also be used II. Administrative manual. San Antonio: Psychological
to gain a better understanding of the errors or Corporation.
unusual approaches that were noted on a task Loring, D. W. (1999). INS dictionary of neuropsychology.
New York: Oxford University Press.
(Milberg et al. 1986). Luria, A. R. (1966). Higher cortical function in man.
While right or wrong answers are deemphasized New York: Basic Books.
in the BPA, Kaplan (1990) felt that it was essential Milberg, W. P., Hebben, N., & Kaplan, E. (1986). The
for the qualitative observations to be quantifiable Boston process approach. In I. Grant & K. M. Adams
(Eds.), Neuropsychological assessment of neuropsychi-
and subjected to statistical analyses. This led to the atric disorders. New York: Oxford University Press.
development of a wide variety of measures includ- Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A
ing the NEPSY – Second Edition (Korkman et al. compendium of neuropsychological tests: Administra-
2007) and Delis-Kaplan Executive Function Sys- tion, norms, and commentary (3rd ed.). New York:
Oxford University Press.
tem (Delis et al. 2001). Each of these measures
provides a number of standard scores, enabling
comparisons with a normative sample. In addition,
they provide the clinician with a way of under-
standing the patient’s approach to the task, enabling Brachytherapy
complex processes to be broken down into simpler
components, so that the area(s) of weakness and Bram Goldstein
strength can be more readily identified. Department of Gynecologic Oncology, Hoag
Despite the growing popularity of the BPA, Hospital Cancer Center, Newport Beach,
there have been criticisms. As outlined by Strauss CA, USA
et al. (2006), criticisms of the approach include
insufficient norms, limited information about
reliability and validity, and problems with Synonyms
readministration due to nonstandard initial admin-
istration. This can result in practice effects but can Internal radiation therapy
Brain Abscesses 617

Definition seen in movements of small muscles when an

individual is asked to rapidly open and close a
Brachytherapy is a form of radiation therapy and hand, tap a finger, or move an arm back and forth
often indicated for the treatment of specific, recur- to grab an object. It can involve any limb in
rent brain tumors and head or neck cancers. The isolation, such as decreased arm swing during B
procedure involves the placement of radioactive gait evaluation or the entire body at once, evident
(e.g., iridium-192, palladium-103, or iodine-125) in the abnormal stillness of a patient with
seeds inside or adjacent to a targeted lesion. The Parkinson’s disease. It may fluctuate during the
primary advantage of brachytherapy is that the day depending on fatigue and medication levels in
treatment allows for a higher radioactive dose to the case of Parkinson’s disease.
be delivered to the tumor bed without damaging
the surrounding, healthy brain tissue (Sneed,
Prados, Phillips, Weaver, and Wara 1992). In par- Cross-References
ticular, high-dose rate brachytherapy utilizes cath-
eters to mitigate exposure and accelerate the ▶ Parkinson’s Disease
treatment time. Intracavitary brachytherapy is
another subtype that involves the use of a balloon
catheter which delivers localized radiation ther- References and Readings
apy to the affected area. Following the completion
of radiotherapy, the radiation source and balloon Fahn, S., & Jankovic, J. (Eds.). (2007). Parkinsonism:
catheter are then removed. Brachytherapy is a safe Clinical features and diagnosis. In Movement disorders
procedure, although reported side effects include (pp. 79–100). Philadelphia: Churchill Livingstone
Elsevier.
infection, seizures, and headaches.

References and Readings

Brain Abscesses
Sneed, P. K., Gutin, P. H., Prados, M. D., Phillips, T. L.,
Weaver, K. A., Wara, W. M., et al. (1992). Brachyther- Michael R. Villanueva and Susan K. Johnson
apy of brain tumors. Stereotactic and Functional Neu- Department of Psychology, University of North
rosurgery, 59, 157–165. Carolina at Charlotte, Charlotte, NC, USA

Definition
Bradykinesia
Brain abscesses are an intracranial mass of
1 2 immune cells, pus (i.e., collection of dead neutro-
Anna DePold Hohler and Marcus Ponce de Leon
1 phils), and other materials stemming from a bac-
Boston University Medical Center, Boston,
MA, USA terial or fungal infection.
2
Madigan Army Medical Center, Tacoma,
WA, USA
Current Knowledge

Definition Etiology
Brain abscesses may arise by direct infection of
Bradykinesia is a slowness of movement. It is organisms, local extension from adjacent focal
often seen in parkinsonian individuals and is a areas, or distribution by way of the bloodstream.
cardinal feature of Parkinson’s disease. It can be Moreover, they form as an inflammatory response
618 Brain Death

to bacteria or fungal infections within the brain. usually the treatment of choice. However, if the
This inflammatory response leads to a localization infection is determined to be of fungal origin, then
of infected brain cells, immune cells, and micro- antifungal medications may be prescribed. Sur-
organisms within an area of the brain (Kumaret al. gery is usually indicated if intracranial pressure
2014). This area becomes encapsulated by an continues to increase, medications fail to reduce
abscess wall, which is formed by adjacent cells the size of the abscesses, or the abscesses are at
to prevent further infection of neighboring struc- risk of rupture (www.nlm.nih.gov/medlineplus/
tures. This results in the formation of an encapsu- ency/article/000783.htm).
lated, purulent (pus-filled) mass within the brain.
While this inflammatory response can serve to
protect the brain from further injury, it can also Cross-References
have significant negative consequences. If the
abscess ruptures, it can lead to inflammation of ▶ Brain Swelling
the ventricles (i.e., fluid-filled cavities containing ▶ Cyst
cerebral spinal fluid) within the brain in addition ▶ Inflammation
to inflammation of the meninges (i.e., membranes
that surround the brain and spinal cord). If the
brain begins to swell, the mass may raise intracra- References and Readings
nial pressure and promote progressive herniation
within the brain, which can be fatal (Kumar Kumar, V., Abbas, A., & Fausto, N. (2014). Robbins and
et al. 2014). Cotran pathologic basis of disease (9th ed.). Philadel-
phia: W.B. Saunders Company.

Symptoms
Clinically, cerebral abscesses can be devastating
and often lead to an increase in intracranial pres-
sure and localized deficits (Kumar et al. 2014). Brain Death
Additionally, symptoms associated with brain
abscesses can develop slowly (i.e., within a Tiffany L. Powell
2-week period) or suddenly. A nonexhaustive list Department of Neurosurgery, Virginia
of symptoms may include the following: head- Commonwealth University, Richmond, VA, USA
aches, gait disturbances, disequilibrium, changes
in mental status, vomiting, and stiffness/aching of
the neck, shoulders, or back. Synonyms

Prognosis Death
If brain abscesses are left untreated, death is the
most likely outcome. On the other hand, treatment
can significantly reduce the mortality rate to about Definition
10%. Earlier treatment predicts a better outcome,
although long-term neurological deficits may per- Brain death is the irreversible loss of all brain
sist despite all intervention approaches (Kumar function. Including the lack of capacity for con-
et al. 2014 and http://www.nlm.nih.gov/ sciousness and respirations (Presidents Commis-
medlineplus/ency/article/000783.htm). sion for the Study of Ethical Problems in
Medicine 1981). Brain death is equivalent to tra-
Treatment ditional circulatory death, which is defined by
Brain abscesses are treated as medical emergen- cessation of tissue perfusion and the absence of
cies and may require hospitalization. If the infec- pulses. However, with brain death the heart will
tious agent is bacterial in nature, antibiotics are continue to beat and spinal cord reflexes may
Brain Death 619

persist for a short time (Canadian Neurocritical Brain Death, Table 1 Assessment of neurologic
Care Group 1999). devastation
Clinical or radiographic evidence of catastrophic and
irreversible brain injury
Exclusion of drug intoxication, sedatives, or paralytic
Current Knowledge
agents
B
Correction of severe electrolyte, acid-base, or endocrine
History of the Definition of Brain Death disturbances
In 1959, Mollaret and Goulon first introduced Core body temperature > 32  C
the term coma dépassé (beyond coma) to
describe irreversible brain damage (Mollaret
and Goulon 1959). The modern scientific con- Brain Death, Table 2 Clinical criteria for brain death
cept of brain death is largely based on this orig-
1. Coma, profound state of unconsciousness
inal description of 23 comatose patients who 2. Pupils fixed at midposition and dilated
exhibited loss of brainstem reflexes, respira- 3. Absence of papillary response to light
tions, and flat electroencephalograms (EEG). 4. Absence of pupil movement with head manipulation or
Several years later, the Harvard ad hoc commit- injection of cold water into the EAC (external auditory
tee formalized the definition of brain death using canal)
neurological criteria and published their land- 5. Absence of motor response
mark article in 1968. These publications helped 6. Absence of corneal and gag reflexes
to define current practice guidelines, now widely 7. Absence of coughing in response to tracheal suctioning
accepted by clinicians, involved in the diagnosis 8. Absence of respiratory drive at Paco2 60 mmHg or
20 mmHg above patients baselinea
of brain death. a
Paco2 is the partial pressure of arterial carbon dioxide
(Reprinted from Wijdicks (2001) with permission)
Criteria for the Diagnosis of Brain Death in
Adults
These often include cerebral angiography,
The determination of brain death is largely a clin-
transcranial doppler, electroencephalography
ical diagnosis. Any experienced physician should
(EEG), or nuclear imaging. These tests are not
be able to make the diagnosis; however, in some
required for the standard diagnosis of adult
states, a specialist in the field of neuroscience is
brain death.
required to make the assessment. Certain criteria
should be met before a diagnosis of brain death is
considered in order to determine the presence of
unequivocal neurologic devastation. These
References and Readings
include interpreting relevant imaging studies and
Ad Hoc Committee of the Harvard Medical School.
excluding the presence of conscious altering (1968). A definition of irreversible coma. Report of
drugs. (Table 1, Wijdicks 2000). the Ad Hoc Committee of the Harvard medical school
When the assessment for neurologic devasta- to examine the definition of brain death. Journal of the
American Medical Association, 205, 337–340.
tion is complete, a focused and methodical clinical
Canadian Neurocritical Care Group. (1999). Guidelines for
examination should follow with emphasis on the the diagnosis of death. Canadian Journal of Neurolog-
documentation of coma, absence of brainstem ical Sciences, 26, 64–66.
reflexes, and demonstration of apnea following Mollaret, P., & Goulon, M. (1959). Le coma dépassé.
Revue Neurologique, 101, 3–15.
maximal stimulation of respiratory centers President’s Commission for the Study of Ethical Problems
(Table 2). in Medicine. (1981). Guidelines for the determination
In some instances, the clinical determination of death. Journal of the American Medical Association,
of brain death is not possible because of a 246, 2184–2186.
Wijdicks, E. F. (2000). Brain death. Philadelphia:
patients’ extreme hemodynamic or respiratory
Lippincott Williams & Wilkins.
instability. In these cases, certain confirmatory Wijdicks, E. F. (2001). The diagnosis of brain death. New
testing can be completed to make the diagnosis. England Journal of Medicine, 344, 1215–1221.
620 Brain Injury Association of America

contributions was its success in securing congres-

Brain Injury Association of sional approval of the 1996 Traumatic Brain
America Injury Act (PL 104–166), later reauthorized as
Title XIII of the Children’s Health Act of 2000
Thomas R. Wodushek and Michael R. Greher (PL 106–310), the S. 793 TBI Act of 2008, and
School of Medicine, Department of Neurosurgery, most recently the TBI Reauthorization Act of
University of Colorado, Aurora, CO, USA 2014 (S. 2539). The original bill created the fed-
eral TBI program to address the struggles of many
persons with TBI in gaining access to appropriate
Synonyms community-based care. It is the only federal law
that addresses the millions of Americans who
BIAA suffer permanent disability as a result of traumatic
brain injury. The ability to achieve successive
appropriation bills has been due in part to the
Membership as of 2016 work of the BIAA and others to persuade approx-
imately 100 members of the congress to join the
The Brain Injury Association of America (BIAA) Congressional Brain Injury Task Force. The latest
consists of more than 27 divisions and state affil- version of the bill provided new emphasis on
iates across the USA, as well as hundreds of local brain injury management in children by tasking
chapters and support groups. A portion of the the CDC to study TBI care in children and identify
individuals involved at these various levels sub- potential opportunities for new research. The
scribe to the national mailing list which includes BIAA, in cooperation with the Mount Sinai
the names of approximately 25,000 individuals. Brain Injury Research Center, published a 2013
Approximately two-thirds of the list members position paper on this topic (Gordon et al. 2013).
are traumatic brain injury (TBI) survivors and In 1992, the BIAA was integral in shaping the
their family members, while the remaining repre- Defense and Veterans Head Injury Program, later
sents a wide variety of professional providers and renamed the Defense and Veterans Brain Injury
researchers (Ayotte, personal communication, Center (DVBIC). This organization’s mission is to
February, 2016). serve veterans and active-duty military TBI vic-
tims via clinical care, research initiatives, and
ongoing education of victims, families, providers,
Major Areas or Mission Statement and policy makers. The program has nearly tripled
in size from its 6 initial locations in 1992 to 16 that
“Our mission is to advance brain injury preven-
now offer specialized care; it acts as the opera-
tion, research, treatment and education and tional component of the Defense Centers of
to improve the quality of life for all individuals Excellence for Psychological Health and Trau-
impacted by brain injury. Through advocacy, matic Brain Injury.
we bring help, hope and healing to millions of
individuals living with brain injury, their families
In 1996, the BIAA founded the Academy of
and the professionals who serve them” (www. Certified Brain Injury Specialists (ACBIS) which
biausa.org). to date has certified over 6500 members. The
mission of ACBIS is to improve the care provided
to individuals with brain injury through enhanced
Landmark Contributions education and training of their health-care pro-
viders. Training is provided by volunteers and
The BIAA, formerly the National Head Injury based primarily upon The Essential Brain Injury
Foundation, was founded in 1980 by Marilyn Guide, which is now published in its fifth edition
and Marty Spivack and other family members of (Academy for the Certification of Brain Injury
brain injury survivors. Among BIAA’s landmark Specialists 2016). Certification is granted to
Brain Injury Association of America 621

those with appropriate work experience who have management for those suffering from moderate
successfully completed the training and written to severe TBI.
examination.
In 1999, the US Supreme Court decided the
case of L.C. & E.W. vs. Olmstead. The court held Major Activities B
that under Title II of the Americans with Disabil-
ities Act “states are required to place persons The BIAA has demonstrated a long-term commit-
with mental disabilities in community settings ment to shaping public policy and partnering with
rather than in institutions. . .” when appropriate. governmental agencies. It has repeatedly worked
The ruling tasked the states to plan reforms in to preserve and expand rehabilitation options for
treatment, transportation, housing, education, persons with brain injury, particularly Medicare
and social support, in order to integrate brain and Medicaid beneficiaries. It has worked to
injury survivors (among others) into the least secure federal funding for research and public
restrictive setting possible. To aid state agencies education on brain injury. The BIAA remains
working toward compliance, the BIAA partnered active in disability advocacy and has provided
with Independent Living Research Utilization to consultation and assistance in developing numer-
provide regional training workshops regarding ous legislative proposals that benefit those who
the content of the Olmstead decision. Although have sustained brain injury. Encouraging private/
the BIAA is no longer doing trainings specifi- public partnerships, particularly to facilitate clin-
cally for this purpose, their advocacy and legis- ical care for military service-related brain injury,
lative efforts continue to be driven toward has been a crucial area of intervention. Public
increasing access to medical care, including policy initiatives have also sought to address
rehabilitation, for all brain injury survivors. In trauma care, child abuse prevention, transportation
2006, these efforts included the publication Cog- safety, brain injury education, and respite care
nitive Rehabilitation: The Evidence, Funding, (Ayotte, personal communication, February, 2016).
and Case for Advocacy of Brain Injury (Katz The BIAA views brain injury prevention and
et al. 2006), which included ten recommenda- awareness as a primary component of its mission.
tions to increase access and delivery of cognitive The association has distributed information kits,
rehabilitation services across the nation. produced public service announcements, and pro-
In 2000, the BIAA in coordination with the vided access to subject matter experts for a number
Brain Trauma Foundation, the American Asso- of media outlets. In recent years it has focused on
ciation of Neurological Surgeons, and other Internet-friendly methods for disseminating infor-
professional contributors developed and mation and connecting survivors with educational
published Guidelines for the Management of materials and possible providers. The BIAA also
Severe Brain Injury (2000). The BIAA was publishes TBI Challenge!, a quarterly newsletter
also involved in authoring Management and with a distribution that includes 25,000 house-
Prognosis of Penetrating Brain Injury (Aarabi holds. It continues to host/cohost educational meet-
et al. 2001). These publications were created to ings and conferences and has added both live and
provide up-to-date, evidence-based guidelines recorded webinars to its array of education options.
and protocols to improve the outcome of TBI This webinar series, free to survivors, included
patients. The BIAA’s newest effort involves topics geared toward survivors and caregivers, as
partnering with the Icahn School of Medicine well as professional providers and researchers.
at Mount Sinai to provide recommendations for BIAA continues to maintain a comprehensive
post-acute TBI care; this will be the first guide- website and makes electronically available the
line focused upon treatment efforts after the National Directory of Brain Injury Rehabilitation
inpatient stage. These guidelines should be Services. On an annual basis, the BIAA responds to
published by 2017 and will address outpatient over 100,000 requests for assistance through either
rehabilitation efforts as well as chronic disease its national information call center or its website.
622 Brain Plasticity

See Also Current Knowledge

▶ Traumatic Brain Injury (TBI) Brain plasticity, or neuroplasticity, refers to the

brain’s ability to change in response to develop-
ment, to the environment (including learning),
References and Readings and in response to injury or aging. While it
was once conceptualized that once the brain
Aarabi, B., Alden, T. D., Chestnut, R. M., Downs J. H., ceases development, that it would then be resistant
Ecklund, J. M., Eisenberg, H. M., . . . Walters, B. C.
to change, or in effect be static. Research over
(2001). Management and prognosis of penetrating
brain injury – Guidelines. Journal of Trauma, Injury, the last several decades has demonstrated that
Infection and Critical Care, 51, S1–S86. the brain continues to be capable of change, or
Academy of certified brain injury specialists. (2016). The restructuring, throughout the life span. While
essential brain injury guide (5th ed.). McLean: Brain
much research with respect to brain plasti-
Injury Association of America.
Brain Injury Association of America. (2005). Academy of city focuses on outcomes following injury, brain
certified brain injury specialists (ACBIS). Retrieved plasticity also refers to developmental changes
from http://www.aacbis.net/index.html. that occur in the brain throughout the life span,
Brain Injury Association of America. (n.d.). Brain injury
including synaptic changes that occur in response
association USA home page. Retrieved from http://
www.biausa.org. to the acquisition of new learning and memories.
Brain Trauma Foundation, American Association of Neu- As such, plasticity is seen as an intrinsic property
rological Surgeons, Joint Section on Neurotrauma and of the central nervous system in that the brain
Critical Care. (2000). Guidelines for the management
is constantly restructuring and reorganizing in res-
of severe traumatic brain injury. Journal of
Neurotrauma, 17, 451–627. ponse to new learning. Specifically, studies of
Defense and Veterans Brain Injury Center. (n.d.). Defense learning new behaviors, such as learning Braille,
and veterans brain injury center: Home of defense and result in the rapid, but transient onset of cortical
veterans head injury program. Retrieved from http://
enlargement that gives way to a more stable but
www.dvbic.dcoe.mil.
Gordon, W. A., Oswald, J. M., Vaughn, S. L., Connors, S. H., less dramatic cortical enlargement associated with
& Brown, M. (2013). States of the states: Meeting the plasticity.
educational needs of children with traumatic brain Research has demonstrated that a variety of
injury. Retrieved from www.biausa.org/biaa-position-
factors affect plasticity of neural reorganization
papers.htm.
Katz, D. I., Ashley, M. J., O’Shanick, G. J., & Connors, S. H. and proliferation. One such environment includes
(2006). Cognitive rehabilitation: The evidence, funding, the richness of the environment in which an
and case for advocacy of brain injury. McLean: Brain organism is grown. Specifically, organisms that
Injury Association of America.
grow in a richly stimulating environment in
which a variety of experiences are encountered
have greater plasticity than individuals who are
Brain Plasticity reared in less-stimulating environments. Empiri-
cal experimentation in humans and animals alike
Jennifer Sue Kleiner have demonstrated that the dendrite length as
Department of Psychology, University of well as the density of synapses in organisms
Arkansas for Medical Sciences Blandford with enriched motor and sensory environ-
Physician Center, Little Rock, AR, USA ments surpass those raised in less-stimulating
environments. However, these differences appear
only to exist with early learning environments,
Definition as adolescents and adults show no such sen-
sitivity to environmental factors. Both gender
Plasticity refers to the brain’s ability to change its and hormone differences also appear to play a
structure in response to development, the environ- role in neural plasticity, with specific respect to
ment, or injury. cortical areas; for example, while males are more
Brain Plasticity 623

sensitive to experience related to the visual cortex, loss of a large area of the brain. The learning of
females are more sensitive to development in the alternative communication techniques, such as
hippocampal area. Braille, requires the adaptation of new behavior;
However, the concept of brain plasticity may research has demonstrated that individuals who
be best understood by examining the processes by have learned Braille have larger sensory maps B
which the brain changes in response to injury. related to the finger pad used in reading as com-
Responses to injury may result in the loss of a pared to the contralateral equivalent or as com-
previously held behavior, release of a previously pared to individuals who do not read Braille.
suppressed behavior, the assumption of a function Furthermore, not only do blind individuals dev-
by a neighboring neuronal network, or the dev- elop enlarged corresponding sensory maps, it has
elopment of new behaviors (which may be also been demonstrated that the occipital, or
adaptive or maladaptive). Physiologically, reorga- visual, cortex is subsequently recruited for tactile
nization can occur by changing the balance information processing, as well as auditory infor-
between excitatory and inhibitory synaptic and mation processing.
membrane responses as well as by strengthening The advancement of technology has furthered
or weakening synaptic connections. Brain plastic- our understanding of the existence of, and mech-
ity can also involve the growth of new dendrites anisms behind, neuroplasticity. The ability to
and axons to form new synaptic connections. specify and characterize brain function via visual-
Research suggests that the age of onset of the ization of glucose and oxygen metabolism has
injury is critical in the development of new con- allowed for exploration of mechanisms of plastic-
nections, as long connections are more difficult to ity. Processes of functional neuroimaging, in-
form in the mature brain, whereas the young brain cluding positron emission tomography as well as
may be more capable of forming long connections functional magnetic resonance imaging, allows
due to the existence of excess connectivity. for indirect visualization of synaptic activity;
Changes in connectivity can occur through the experimentation involving tasks being performed
strengthening or weakening of synaptic density while the brain is being imaged allows for exam-
or the rearrangement of synaptic connections. ination of synaptic changes. Magnetic resonance
While the concept of neuroplasticity does at spectroscopy is thought to be a promising
times result in recovery of adaptive behavioral technique that allows for analysis of the con-
changes, plasticity may also lead to unmasking nection between neurochemical changes and
of previous suppressed and maladaptive behav- behaviors. Electroencephalography and magneto-
iors as well as the development of dysfunctional encephalography allows to direct measurement of
behaviors. neuronal activity; however, it lacks structural
Brain plasticity may occur via multiple differ- specificity. Transcranial magnetic stimulation
ence mechanisms. Perhaps the most common, and also allows for direct analysis of neural activity
best understood, mechanism includes the expan- by temporarily suppressing brain regions, allo-
sion of a specified area of circuitry or the recruit- wing for direct assessment of brain-behavior
ment of either a local or distal area of circuitry. relationships in conjunction with functional neu-
Such reorganization of function is a common roimaging techniques.
post-injury response and occurs shortly following
the injury and continues to develop years follow-
ing the injury as the organism adapts. Remodeling References and Readings
or reorganization occurs both at the cortical and
subcortical level, and can occur both within and Galaburda, A., & Pascual-Leone, A. (2003). Mechanisms of
between functional modalities. For example, plasticity and behavior. In T. E. Feinberg & M. J. Farah
(Eds.), Behavioral neurology & neuropsychology
much literature exists examining the reorganiza-
(2nd ed., pp. 57–70). New York: McGraw-Hill.
tion of neuronal circuitry in response to blindness. Kolb, B. (1995). Brain plasticity and behavior. Mahwah:
Early onset blindness results in the functional Erlbaum.
624 Brain Reserve Capacity

Kolb, B., Gibb, R., & Robinson, T. E. (2003). Brain plas- brains were found to have a high degree of pathol-
ticity and behavior. Current Directions in Psychologi- ogy associated with Alzheimer’s disease did dem-
cal Science, 12(1), 1–5.
Kolb, B., & Whishaw, I. Q. (1998). Brain plasticity and onstrate minimal clinical symptoms associated
behavior. Annual Review of Psychiatry, 49, 43–64. with the disease. Interestingly, the results from
Nelson, C. A., & Luciana, M. (2001). Handbook of devel- this study suggested that the weight of the brains
opmental cognitive neuroscience. Boston: Massachu- in this subset of patients was higher. These patients
setts Institute of Technology.
were also found to have more neurons. It was
subsequently concluded that perhaps these
patients’ larger brains and their possession of
Brain Reserve Capacity more neurons were protective against dementia
symptoms. While subsequent studies have been
Glen E. Getz inconclusive, many studies have suggested that
Department of Psychiatry, Allegheny General head circumference, brain volume, intracranial vol-
Hospital, Pittsburgh, PA, USA ume, and genetic influences also play an important
role in brain reserve capacity (Stern et al. 2006).

Synonyms
Current Knowledge
Global reserve; Reserve
Research consistently demonstrates that the under-
lying neuropathology is not consistent with behav-
ioral disturbance caused by dementia. Brain reserve
Definition
capacity partially explains this phenomenon. Symp-
tomatic behaviors are less likely to be prevalent in
Brain reserve capacity is the brain’s resilience to
individuals with greater brain reserve capacity.
pathological damage or changes. The greater the
Research has consistently found that cognitive
brain reserve capacity, the less likely an individual
reserve capacity, that is, the lifestyle approaches
will demonstrate behavioral disturbance associ-
that encourage cognitive activity, plays an impor-
ated with a disease.
tant role in functional ability despite neuropatho-
logical changes. Brain reserve capacity, such as
increased amount of neurons and neuronal connec-
Historical Background
tions, is at least in part due to behaviors that encour-
age cognitive reserve capacity, such as education
Research has attempted to understand the role of
and occupation. It has also been argued that innate
various factors involved in cognitive decline. Fre-
intelligence of life experiences, including educa-
quent central nervous system disorders occur in
tional and professional achievements, may increase
the elderly, which increase the likelihood of cog-
cognitive reserve by helping a set of behavoiral
nitive decline. Age, in itself, is a factor known to
skills that allow people to manage their behaviors
alter cognitive functioning. Brain reserve capacity
better (Vasile 2013).The interplay among cognitive
is the brain’s ability to effectively manage the
activity, physical activity, diet, and brain reserve
increasing changes in normal aging and to cope
capacity is being carefully studied in an attempt to
with pathological damage.
understand the complex relationship.
Postmortem examination of elderly individuals
provides evidence that there is a discrepancy
between the clinical manifestation of Alzheimer’s Future Directions
disease and the neuropathology of the disorder
(Katzman et al. 1988). Specifically, this early Identifying factors that increase the likelihood of
study found that a subset of individuals whose brain reserve capacity has the possibility of being
Brain Swelling 625

an invaluable tool toward improving the quality of Current Knowledge

elderly people’s lives and potentially reducing the
risk of developing Alzheimer’s disease and other Brain swelling can elevate intracranial pressure
types of dementia. The National Institute of Aging immediately following brain injury and can con-
and other federally funded programs have tinue hours or days after the onset of brain injury. B
invested millions of dollars to better understand Once intracranial pressure is elevated, oxygen,
the factors in improving brain reserve capacity. glucose, and blood have difficulty reaching all
Studies will continue to better understand factors portions of the brain. Blood vessels are no longer
that increase brain cells, synaptic connections, efficient in carrying blood, oxygen, and nutrients
and other neurophysiological markers. The imple- throughout the brain. As a consequence, increased
mentation and advancement of technology will intracranial pressure complicates the degree of
assist in providing a clearer understanding of brain injury and also the brain’s natural response
these factors as well. to trauma.
Brain swelling can occur in 15–20% of
severe brain injuries. The exact mechanism
Cross-References that leads to brain swelling is poorly under-
stood, but once trauma is sustained, the brain
▶ Alzheimer’s Disease tissue swells to compress harder and harder
▶ Cognitive Reserve against the rigid skull. Brain swelling must be
managed emergently following brain injury
because patients experiencing brain swelling
References are at a higher risk of death. The brain may
swell to a point in which portions of the brain
Katzman, R., Terry, R., DeTeresa, R., Brown, T., Davies, P., herniate through openings in the skull. Brain
Fuld, P., et al. (1988). Clinical, pathological and
neurochemical changes in dementia: A subgroup
swelling may compress the brainstem, the area
with preserved mental status and numerous neo- of the brain that maintains consciousness, and
cortical plaques. Annals of Neurology, 23, critical life functions, such as cardiac function
138–144. and respiration. Mitochondrial function is
Stern, Y. (2006). In L. Bieliauskas (Ed.), Cognitive
now thought to be directly related to brain
reserve, theory and application. New York: Psychol-
ogy Press. edema. Acute management of brain swelling is
Vasile, C. (2013). Cognitive reserve and cortical plasticity. important at the gross and molecular level.
Procedia – Social and Behavioral Sciences, 78, Methods of managing brain swelling involve
601–604.
administering medications to constrict blood
vessels, drilling a burr hole or conducting
decompressive craniotomy to relieve pressure,
temporarily removing a portion of the skull in a
Brain Swelling decompressive craniectomy to relieve pressure
(and replacing the skull fragment once pressure
Beth Rush is normalized), placing an external drain to
Psychiatry and Psychology, Mayo Clinic, relieve pressure and excess fluid from the sur-
Jacksonville, FL, USA face of the brain, placing the patient on artifi-
cial respirator so that carbon dioxide does not
accumulate in the brain, inducing hypothermia,
Definition administering medications to reduce potential
oxidative stress, and using an electronic intra-
Expansion of the size of the brain that occurs cranial pressure monitor with a valve to adjust
following head trauma and brain injury. pressure over time.
626 Brain Training

Cross-References Cross-References

▶ Edema ▶ Cognitive Rehabilitation

▶ Intracranial Pressure

References and Readings

References and Readings
Simons, D. J., Boot, W. R., Charness, N., Gathercole, S.
Marmarou, A. (2007). A review of progress in understand- E., Chabris, C. F., Kambrick, D. Z., & Stine-Morrow,
ing the pathophysiology and treatment of brain edema. A. L. (2016). Do “brain-training” programs work?
Neurosurgery Focus, 22, E1. Psychological Science in the Public Interest, 17(3),
Vlodavsky, E., Palzur, E., Shehadeh, M., & Soustiel, 103–186.
J. F. (2015). Post-traumatic cytoxic edema is
directly related to mitochondrial function. Journal
of Cerebral Blood Flow and Metabolism, 37
(1):166–177.
Brain Tumor

Ethan Moitra1 and Daniel Smith2

1
Department of Psychiatry and Human Behavior,
Brain Training Brown University, Providence, RI, USA
2
Department of Psychology, Drexel University,
John DeLuca Philadelphia, PA, USA
Research Department, Kessler Foundation, West
Orange, NJ, USA
Definition

Synonyms An abnormal mass of tissue in which some cells

(glial or non-glial) grow and multiply uncontrol-
Brain games lably. A tumor can be benign or malignant. It is
associated with damage or mutation to the TP53
gene on human chromosome 17. P53 regulates
Brain training is a term used primarily by com- the cell cycle and functions in tumor suppression.
panies which market cognitive intervention A tumor can cause damage by increasing pres-
products or by the lay public, rather than clini- sure in the brain, by shifting the brain or pushing
cians or researchers. The term is somewhat of a against the skull, and by invading and damaging
misnomer as only a very small fraction of nerves and healthy brain tissue. Some tumors
published studies have assessed neural activity may be truly indolent in their growth, growing
directly. Companies use this term to refer to “. . . so slowly that they are present for an unknown
practicing core cognitive abilities with the goal length of time because symptoms are less gross
of improving performance on other cognitive and disruptive. Those that are actively growing
tasks, including those involved in everyday may be more likely to present with the following
activities. . .” (Simons et al. 2016, pp. 105). Sup- symptoms, depending on tumor locus: head-
port for the term and particularly its effectiveness aches; nausea or vomiting; seizures or convul-
is highly controversial, and scientific effective- sions; difficulty in thinking, speaking, or finding
ness should be differentiated from marketing words; personality changes; weakness or paraly-
and other claims. Care should be used in that sis in one part or one side of the body; loss of
the term brain training is not synonymous with balance; vision changes; confusion and disorien-
concepts like cognitive training or cognitive tation; and memory loss (Levin et al. 2001; Price
rehabilitation. et al. 2007).
Brainstem Auditory Evoked Responses 627

Cross-References Wave I: Cochlear nerve (CN VIII)

Wave II: Cochlear nucleus (CN VIII)
▶ Astrocytoma Wave III: Superior olivary complex
▶ Glioma Wave IV: Lateral lemniscus
▶ Neuroblastoma Wave V: Inferior colliculus B
▶ Neurocytoma
Waveform morphology and interwave differ-
ences are compared to healthy controls to estab-
References and Readings lish abnormality in function along the auditory
pathway. Unilateral delays suggest a lesion to
Levin, V. A., Leibel, S. A., & Gutin, P. H. (2001). Neo- cranial nerve VIII along its pathway or in the
plasms of the central nervous system. In V. T. DeVita,
brainstem. BAER may be abnormal in acoustic
S. Hellman, & S. A. Rosenberg (Eds.), Cancer: Prin-
ciples and practice of oncology (pp. 2100–2160). Phil- neuroma, demyelinating disease, migraine head-
adelphia: Lippincott, Williams, & Wilkins. aches, multiple sclerosis, brainstem tumor,
Price, T. R. P., Goetz, K. L., & Lovell, M. R. (2007). brainstem stroke, or brain injury of various etiol-
Neuropsychiatric aspects of brain tumors. In S. C.
ogies. Common uses of BAER include infant
Yudofsky & R. E. Hales (Eds.), The American Psychi-
atric Publishing textbook of neuropsychiatry and hearing screening, acoustic neuroma detection,
behavioral neurosciences (5th ed., pp. 735–764). multiple sclerosis diagnosis, and intraoperative
Washington, DC: American Psychiatric Association. monitoring during cerebellopontine angle tumor
resection. Magnetic resonance imaging (MRI)
may provide greater anatomic detail and would
Brainstem Auditory Evoked be preferable for detecting a small lesion. How-
Responses ever, BAER may be particularly useful in an indi-
vidual who cannot undergo MRI.
Flora M. Hammond and Sheryl Katta-Charles
Department of Physical Medicine and Current Knowledge
Rehabilitation, Indiana University School of
Medicine, Indianapolis, IN, USA BAER results are generally not affected by the
effect of anesthesia and medications or periph-
eral vestibular pathology. BAER is sometimes
Synonyms used for prognostic purposes after brain injury,
but its use is limited for this purpose. Complete
Auditory brainstem responses (ABR); Auditory absence of responses is considered an ominous
brainstem response audiometry; Auditory evoked sign (Lew et al. 2007), and abnormal BAER may
response (AER); BAER; Brainstem auditory evoked confirm suspicion of brainstem injury, while
potentials (BAEP); Brainstem response (BSR) normal BAER simply indicates preservation of
the auditory pathways through the brain. BAER
does not reveal information about damage that
Definition
may have occurred elsewhere in the brain, and
thus, normal BAER does not necessarily predict
Brainstem auditory evoked responses (BAER)
good outcome (Lew et al. 2007; Zafonte et al.
test the function of the auditory nerve and auditory
1996).
pathways of the brain by measuring the electro-
physiologic responses to repeated clicks pre-
sented to each ear. The response time of
electrical waves generated from different anatom- Cross-References
ical parts of the brain-ear system are plotted as
summarized below (Lew et al. 2007): ▶ Evoked Potentials
628 Brainstem Glioma

References and Readings

Huszar, L. (2006). Clinical utility of evoked potentials.

eMedicine. Retrieved 9 July 2007 from http://www.
emedicine.com/neuro/topic69.htm. Accessed 23 Mar 2017.
Lew, H. L., Lee, E. H., Pan, S. S. L., & Chiang, J. Y. P.
(2007). Electrophysiologic assessment techniques:
Evoked potentials and electroencephalography. In N.
D. Zasler, D. I. Katz, & R. D. Zafonte (Eds.), Brain
injury medicine (p. 158). New York: Demos.
Lew, H. L., Tanaka, C., Hirohata, E., & Goodrich, G. L.
(2016). Auditory, vestibular and visual impairments. In
D. X. Cifu (Ed.), Physical medicine and rehabilitation
(pp. 1137–1161). Philadelphia: Elsevier.
Luauté, J., Fischer, C., Adeleine, P., Morlet, D., Tell, L., &
Boisson, D. (2005). Late auditory and event-related
potentials can be useful to predict good functional
outcome after coma. Archives of Physical Medicine
and Rehabilitation, 86, 917–923.
Luaute, J., Maucort-Boulch, D., Tell, L., Quelard, F.,
Sarraf, T., Iwaz, J., Boisson, D., & Fischer, C. (2010). Brainstem Glioma, Fig. 1 (Picture credit: Michael Phil-
Long-term outcomes of chronic minimally conscious lips and Peter C. Fisher)
and vegetative states. Neurology, 75, 246–252.
Vernet, M., Bashir, S., Enam, S. F., Kumru, H., & Pascual- for survival, while tectal and cervicomedullary
Leone, A. (2012). Electrophysiologic techniques. In N. gliomas are associated with longer survival. Tec-
D. Zasler, D. I. Katz, & R. D. Zafonte (Eds.), Brain tal brainstem gliomas are often associated with
injury medicine (pp. 236–238). New York: Demos.
Zafonte, R. D., Hammond, F. M., & Peterson, J. (1996). hydrocephalus as a result of compression of the
Predicting outcome in the slow to respond traumati- fourth ventricle. Typical manifestations of
cally brain-injured patient: Acute and subacute param- cervicomedullary tumors include dysphagia,
eters. NeuroRehabilitation, 6, 19–32. unsteadiness, nasal speech, and sensory loss in
the face. Pontine brainstem gliomas are associated
with cranial nerve or long tract symptoms, includ-
ing problems with the control of facial muscles,
Brainstem Glioma
ocular movements, and swallowing. Diffuse
brainstem gliomas, once thought to be a single
Robert Rider
entity, are now thought to comprise a group of
Department of Psychology, Drexel University,
tumors with varying courses and outcomes.
Philadelphia, PA, USA
Brainstem gliomas can also occur in the
cervicomedullary junction, pons, midbrain, and
tectum; prognosis is worse and very grim for
Synonyms
diffuse brainstem gliomas. Diffuse brainstem gli-
omas do not typically enhance on MRI. They are
Midbrain glioma; Pontine glioma
not responsive to radiotherapy, and treatment is
usually limited to chemotherapy.
Definition
References and Readings
Brainstem gliomas are highly aggressive tumors
of the central nervous system occurring more fre- Albright, L., Pollack, I., Adelson, P., Humphreys, R.,
quently in children than in adults (Fig. 1). This George, T., Painter, M., et al. (2007). Principles and
type of tumors often originates from the left side practice of pediatric neurosurgery (2nd ed.).
New York: Thieme.
and typically involves one of three anatomical Donaldson, S., Laningham, F., & Fisher, P. (2006).
locations within the brainstem. Pontine brainstem Advances toward an understanding of brainstem glio-
gliomas are associated with the poorest prognosis mas. Journal of Clinical Oncology, 24(8), 1266–1272.
Brexipiprazole 629

blood pressure, and heart rate, a brainstem stroke

Brainstem Strokes has the potential to be fatal.
In its most severe form, an infarction of the
Elliot J. Roth ventral pons can interrupt the function of all motor
Department of Physical Medicine and pathways, causing locked-in syndrome, in which B
Rehabilitation, Northwestern University, the patient can receive and understand sensory
Feinberg School of Medicine, Chicago, IL, USA stimuli, but has no motor control, resulting
in complete total body paralysis and inability
to speak, while maintaining awareness and
Definition sensation.
MRI scanning usually facilitates the diagnosis
A stroke that is caused by ischemia or hemorrhage of brainstem stroke.
in the midbrain, pons, or medulla is called a
“brainstem stroke.” There are many brainstem
stroke clinical syndromes, the presentation of Cross-References
each depending on the specific location in the
brain stem that is involved. Most brainstem stroke ▶ Basilar Artery
syndromes result from ischemia due to partial ▶ Cerebrovascular Disease
blockage or complete occlusion of arteries in the ▶ Lacunar Infarction
vertebrobasilar system located at the posterior ▶ Locked-In Syndrome
region of the brain. ▶ Posterior Cerebral Artery
▶ Posterior Communicating Artery
▶ Pure Motor Stroke
Current Knowledge ▶ Thalamic Hemorrhage
▶ Vertebrobasilar System
Localization of the brainstem lesion can usually
be made by recognizing the specific pattern of
clinical deficits and understanding the anatomi- References and Readings
cal basis for these clinical manifestations. Many
of these strokes cause dysfunction of one or more Chua, K., & Kong, K. (1996). Functional outcome in brain
stem stroke patients after rehabilitation. Archives of
of the many cranial nerves that originate from the
Physical Medicine and Rehabilitation, 77, 194–197.
brain stem. The specific clinical dysfunction, Dauby, J.-D. (1996). The diving bell and the butterfly:
typically involving head and neck functions, A memoir of life in death. New York: Vintage.
localizes the tissue injury to the side that is ipsi- Nelles, G., et al. (1998). Recovery following lateral med-
ullary infarction. Neurology, 50, 1418–1422.
lateral to the clinical deficit. Some also involve
motor or sensory deficits of the body, which
localize the injury to the side that is contralateral
to the clinical deficit. When cerebellar signs such
as ataxia and discoordination are present in asso- Brexipiprazole
ciation with other brainstem findings, this local-
izes the lesion to the ipsilateral side, and usually Efrain Antonio Gonzalez
to the pons. When unilateral facial and contralat- College of Psychology, Nova Southeastern
eral body sensory deficits exist, this also local- University, Fort Lauderdale, FL, USA
izes the lesion to the brain stem. Other Utah State University, Logan, UT, USA
symptoms, such as vertigo, double vision, nau-
sea, and selected tremors, are also reflective of
dysfunction of certain specific brainstem struc- Generic Name
tures. Because the brain stem also contains
the life support centers that control respiration, Brexpiprazole
630 Brief Cognitive Rating Scale

Brand Name Additional Information

Rexulti CenterWatch: https://www.centerwatch.com/drug-
information/fda-approved-drugs/drug/100084/rexulti-
brexpiprazole.
Class http://www.drugs.com/drug_interactions.html.
Drug Molecule Images: http://www.worldofmolecules.
Atypical Neuroleptic, Serotonin-Dopamine Mod-
com/drugs/.
ulators (SDAM) Free Drug Online and PDA Software: www.epocrates.com.
Free Drug Online and PDA Software.
Gene-Based Estimate of Drug interactions: http://mhc.
daytondcs.com: 8080/cgi bin/ddiD4?ver=4&task=
Proposed Mechanism(s) of Action getDrugList.
Medscape Psychiatry.
The efficacy of brexpiprazole may be mediated Pill Identification.: http://www.drugs.com/pill_identifica
tion.html.
through a combination of partial agonist activity https://rexulti.com/us/mdd.
as serotonin 5-HT1A and dopamine D2 receptors,
and antagonist activity at serotonin 5-HT2A
receptors.
Brief Cognitive Rating Scale

Indication Megan Becker and Daniel N. Allen

Department of Psychology, University of Nevada,
Schizophrenia, adjunctive treatment of major Las Vegas, NV, USA
depressive disorder

Synonyms
Off Label Use
BCRS
No common offlabel use
Description

Side Effects The Brief Cognitive Rating Scale (BCRS;

Reisberg and Ferris 1988) is used to assess func-
Serious tional and cognitive abilities in both normal aging
Increased risk of death in elderly people with and progressive dementia. The BCRS is part of
dementia-related psychosis, CVA among elderly the Global Deterioration Scale Staging System
patients, hyperglycemia, low white blood cell (GDS; Reisberg et al. 1993) which is composed
count, orthostatic hypotension, seizures. of three separate rating scales that include the
GDS, the Functional Assessment Staging (FAST;
Common Reisberg 1988), and the BCRS. The BCRS is
Headache, weight gain, somnolence, dyspepsia, comprised of two parts and provides objective
constipation, fatigue, dizziness, anxiety, restless- ratings for a number of domains which include
ness, increased appetite. cognitive functions, functional abilities, mood,
and behavior. Part I includes ratings for concen-
tration, recent memory, remote memory, orienta-
References and Readings tion, and functioning and self-care, while Part II
allows for ratings of speech and language abilities,
Physicians’ desk reference (71st ed.) (2017). Montvale: motoric capacities, mood and behavior, praxis
Thomson PDR. ability, calculation ability, and feeding capacity.
Brief Psychiatric Rating Scale 631

Each of the domains is rated on a 1–7-point ▶ Alzheimer’s Disease

scale that ranges from normal (rating of 1) to ▶ Modified Mini-Mental State Examination
profound impairment (rating of 7). For each ▶ Multi-infarct Dementia
domain, a behavioral anchor is provided for each
point on the rating scale. The authors provided B
examples of questions that might be used to elicit References and Readings
information needed to complete the BCRS as well
as guidelines for scoring each domain. Ratings are Foster, J. R., Sclan, S., Welkowitz, J., Boksay, I., &
Seeland, I. (1988). Psychiatric assessment in medical
completed based on interviews with the patient
long-term care facilities: Reliability of commonly used
and an informant who is knowledgeable regarding rating scales. International Journal of Geriatric Psy-
the patient’s day-to-day activities and functioning. chiatry, 3, 229–233.
Interviews may be conducted in person or over the Ihl, R., Frölich, L., Dierks, T., Martin, E., & Maurer, K.
(1992). Differential validity of psychometric tests in
telephone. The BCRS has been translated into a
dementia of the Alzheimer type. Psychiatry Research,
number of languages including Chinese, French, 44, 93–106.
Polish, Spanish, and Swedish, among others. Reisberg, B. (1988). Functional assessment staging
(FAST). Psychopharmacology Bulletin, 24, 653–659.
Reisberg, B., & Ferris, S. H. (1988). Brief cognitive rating
Current Knowledge scale (BCRS). Psychopharmacology Bulletin, 24,
629–636.
Reisberg, B., Ferris, S. H., de Leon, M. J., & Crook, T.
From a psychometric standpoint, the BCRS has (1988). Global deterioration scale (GDS). Psychophar-
excellent interrater reliability when completed by macology Bulletin, 24, 661–663.
trained clinicians and high test-retest reliability Reisberg, B., Ferris, S. H., Steinberg, G., Shulman, E.,
(Foster et al. 1988; Reisberg et al. 1989). Validity de Leon, M. J., & Sinaiko, E. (1989). Longitudinal
study of dementia patients and aged controls.
studies indicate that the BCRS has strong correla- In M. P. Lawton & A. R. Herzog (Eds.), Special
tions with the GDS, the Mini-Mental State Exam- research methods for gerontology (pp. 195–231).
ination, some neuropsychological measures of Amityville: Baywood.
memory abilities, and measures of activities of Reisberg, B., Sclan, S. G., de Leon, M. J., Kluger, A.,
Torossian, C., Shulman, E., Steinberg, G., Monteiro, I.,
daily living and quality of life. Relationships have McRas, T., Mackell, J., & Ferris, S. H. (2007). The
also been demonstrated between BCRS scores and GDS staging system. In A. J. Rush (Ed.), Handbook
neuropathology measured using a variety of tech- of psychiatric measures (pp. 431–435). Washington,
niques (EEG, PET, SPECT, neurological examina- DC: American Psychiatric Publishers.
Tripathi, R. K., & Tiwari, S. C. (2013). Cognitive func-
tion). BCRS scores are sensitive to the progression tioning of community dwelling urban older adults with
of Alzheimer’s disease, with significant declines in reference to socio-demographic variables. Indian Jour-
scores as the disease progresses (Ihl et al. 1992). nal of Clinical Psychology, 40(2), 92–102.
The BCRS has been used with elderly persons in
India and compared to the Hindi Cognitive Screen-
ing Test (HCST) during its development, which
correlates with the BCRS total score (r = 0.87)
Brief Psychiatric Rating Scale
and composite axes (Tripathi and Tiwari 2013).
Thus, the BCRS is useful in both research and
Edward E. Hunter
clinical settings where it can provide valuable
Department of Psychiatry and Behavioral
information regarding progression of cognitive
Sciences, University of Kansas Medical Center,
decline, as well as the impact that such decline
Kansas City, KS, USA
has on behavior and function.

Cross-References Synonyms

▶ Alzheimer’s Dementia BPRS

632 Brief Psychiatric Rating Scale

Definition but is appropriate with other psychiatric conditions,

including bipolar disorder (Picardi et al. 2008) and
The Brief Psychiatric Rating Scale (BPRS) (Over- major depression (Zanello et al. 2013). It can also
all and Gorham 1962, 1988) consists of a series of be useful with persons having neurological condi-
18 items assessing the following psychiatric tions with psychotic or other psychiatric symptoms
symptoms: somatic concern, anxiety, emotional including Alzheimer’s disease, dementia with
withdrawal, conceptual disorganization, guilt Lewy bodies, Parkinson’s disease (Cummings
feelings, tension, mannerisms and posturing, et al. 2007; Devanand 1998; Tariot et al. 2004),
grandiosity, depressive mood, hostility, suspi- and traumatic brain injury (Diaz et al. 2012).
ciousness, hallucinatory behavior, motor retarda- Versions of the BPRS are widely available and
tion, uncooperativeness, unusual thought content, may be found online at http://uwaims.org/files/mea
blunted affect, excitement, and disorientation. sures/BPRS.pdf (18-item version) and http://www.
The instrument takes approximately 5–10 min to public-health.uiowa.edu/icmha/outreach/documents/
rate, following an interview with the patient. The BPRS_expanded.PDF (24-item expanded version).
clinician rates each item on a scale ranging from 1
(not present) to 7 (extremely severe). The inven-
tory is geared toward severe psychopathology. See Also

▶ Affective Disorder
Current Knowledge ▶ Alzheimer’s Disease
▶ Anxiety
The BPRS continues to be a very commonly used ▶ Clinical Interview
instrument. Between 2013 and 2015, there were ▶ Dementia with Lewy Bodies
well over 300 articles cited in MedLine which ▶ Parkinson’s Disease
employed the BPRS in clinical and experimental ▶ Psychosis
studies. Expanded versions of the BPRS have ▶ Psychotic Disorder
been developed. These include behavioral ▶ Structured Clinical Interview for DSM-IV
anchors and structured interview questions (SCID-I/SCID-II)
(Woemer et al. 1988). The BPRS has a well-
established history of acceptable psychometric
properties. For instance, using a behaviorally References and Readings
anchored 24-item version and no specific inter-
view format or rater training, Lachar et al. (2001) Cummings, K. R., Raman, R., & Thai, L. (2007).
Quetiapine for agitation or psychosis in patients with
obtained weighted kappa agreement between psy- dementia and parkinsonism. Neurology, 68,
chiatrists on the majority of items at above 0.75. 1356–1363.
Furthermore, scores on the BPRS are highly cor- Devanand, D. P. (1998). A randomized, placebo-controlled
related with those of other similar instrument con- dose-comparison of a trial of haloperidol for psychosis
and disruptive behaviours in Alzheimer’s disease.
structs although, as with all such clinician-rated
American Journal of Psychiatry, 155, 1512–1520.
scales, relationships with external criteria are Diaz, A. P., Schwarzbold, M. L., Thais, M. E., Hohl, A.,
modest (Mortimer 2007). Bertotti, M. M., Schmoeller, R., Nunes, J. C.,
In neuropsychological practice, the BPRS can Prediger, R., Linhares, M. N., Guarnieri, R., &
Walz, R. (2012). Psychiatric Disorders and Health-
enable the clinician to organize and quantify Related Quality of Life after Severe Traumatic Brain
observations of psychotic symptoms or other seri- Injury: A Prospective Study. Journal of Neurotrauma,
ously disordered behavior, both as part of an eval- 29(6):1029–1037
uation and in tracking to course of the clinical Dunayevich, E., Sethuraman, G., Enerson, M., Taylor, C. C.,
& Lin, D. (2006). Characteristics of two alternative
condition over time. It is most commonly used
schizophrenia remission definitions: Relationship to
with psychotic disorders such as schizophrenia clinical and quality of life outcomes. Schizophrenia
(e.g., Samara et al. 2015; Dunayevich et al. 2006), Bulletin, 86, 300–308.
Brief Symptom Inventory 633

Lachar, D., Bailley, S. E., Rhoades, H. M., Espandas, A., Checklist-90 (SCL-90; Derogatis et al. 1973)
Aponte, M., Cowan, K. A., Gummattira, P., Kopecky, C. that measures emotional-behavioral functioning
R., & Wassef, A. (2001). New subscales for an anchored
version of the Brief Psychiatric Rating Scale: Construc- in nine dimensions: somatization, obsessive-
tion, reliability and validity in acute psychiatric admis- compulsive, interpersonal sensitivity, depression,
sions. Psychological Assessment, 13, 384–395. anxiety, hostility, phobic anxiety, paranoid idea- B
Mortimer, A. M. (2007). Symptom rating scales and out- tion, and psychoticism. Four additional items not
come in schizophrenia. The British Journal of Psychi-
atry Supplement, 50, s7–14. specific to any one domain load on several differ-
Overall, J. E., & Gorham, D. R. (1962). The brief psychi- ent dimensions. In addition, three global indices –
atric rating scale. Psychological Reports, 10, 790–812. Global Severity Index (GSI), Positive Symptom
Overall, J. E., & Gorham, D. R. (1988). The Brief Psychi- Total (PST), and Positive Symptom Distress
atric Rating Scale (BPRS): Recent developments in
ascertainment and scaling. Psychopharmacology Bul- Index (PSDI) – provide more general assessment
letin, 24, 97–99. of psychological well-being. The BSI-18
Picardi, A., Battisti, F., de Girolamo, G., Morosini, P., (Derogatis 2000), an 18-item short form of the
Norcio, B., Bracco, R., & Biondi, M. (2008). Symptom BSI intended as a screen for psychiatric disorders
structure of acute mania: A factor study of the 24-item
Brief Psychiatric Rating Scale in a national sample of and psychological distress, consists of three
patients hospitalized for a manic episode. Journal of 6-item subscales: somatization, depression, and
Affective Disorders, 108, 183–189. anxiety. A GSI also can be calculated.
Samara, M. T., Leucht, C., Leeflang, M. M., et al. (2015). Not intended for use as diagnostic tools, both
Early improvement as a predictor of later response to
antipsychotics in schizophrenia: A diagnostic test instruments are designed to identify psychologi-
review. American Journal of Psychiatry, 172, 617–629. cal symptoms in medical populations, psychiatric
Tariot, P. N., Profenno, L. A., & Ismail, M. S. (2004). patients, and community non-patients, with sepa-
Journal of Clinical Psychiatry, 65(Suppl 11), 11–15. rate norms for males and females. Written at a
Woerner, M. G., Mannuzza, S., & Kane, J. M. (1988).
Anchoring the BPRS. Psychopharmacology Bulletin, sixth grade reading level and available in over
24, 112–117. 24 languages, these self-report measures can be
Zanello, A., Berthoud, L., Ventura, J., & Merlo, M. C. hand- or computer-administered to individuals
(2013). The Brief Psychiatric Rating Scale (version ages 13 and older (BSI) or 18 and older
4.0) factorial structure and its sensitivity in the treat-
ment of outpatients with unipolar depression. (BSI-18). Respondents rate the extent to which a
Pssychiatry Research, 15, 626–633. specific problem has distressed them in the past
7 days (although evaluations over other time inter-
vals may be specified), using a 5-point scale
(0 = not at all to 4 = extremely). Administration
Brief Symptom Inventory is straightforward, taking 4 (BSI-18) to 8–10 min
(BSI) to complete.
Joseph F. Rath and Lisa M. Fox Scores are determined by summing values for
NYU Langone Medical Center, Department of each symptom dimension and then dividing by
Psychology, Rusk Institute of Rehabilitation number of items endorsed in the respective dimen-
Medicine, New York, NY, USA sion. A GSI can be calculated for either measure by
adding the scores for all subscales, as well as the
additional items (in the BSI), and then dividing by
Synonyms number of responses. For the BSI only, the PST is
determined by counting the number of items
BSI; BSI-18 endorsed with a positive (nonzero) response, and
the PSDI is derived by dividing the sum of the item
values by the PST. Raw scores can be converted to
Description standardized T scores, generating a profile that
graphically illustrates a respondent’s current psy-
The BSI (Derogatis and Melisaratos 1983) is a chological symptom presentation. Interpretation of
shortened, 53-item version of the Symptom the BSI can be done at three levels: global scores,
634 Brief Symptom Inventory

primary symptom dimensions, and discrete symp- with spinal cord injury (Heinrich et al. 1994), Brit-
toms (Derogatis and Melisaratos 1983). Computer ish psychiatric outpatients (Ryan 2007) and
administration, scoring, and interpretation pro- community-dwelling adults (Francis et al. 1990),
grams are available for both instruments. Israeli adolescents (Canetti et al. 1994), and others
Advantages of the BSI and the BSI-18 are that (see Derogatis 1993). Internal consistency coeffi-
they can be completed quickly and used for cients are strong for both the BSI (0.71–0.83) and
repeated assessments. Also, both measures are BSI-18 (0.74–0.89). Test-retest reliability also is
reported to be sensitive to mild-to-severe psycho- good, ranging from 0.68–0.91 (BSI) to 0.68–0.84
logical distress, making them useful with many (BSI-18).
populations. Limitations include typical concerns BSI and BSI-18 manuals cite a variety of stud-
associated with self-report measures, such as pos- ies supporting validity in a range of settings and
sible patient response bias and over- or populations, including psychoneuroimmunology,
underreporting, as well as limited utility with psychopathology, pain assessment and manage-
some medical populations (e.g., neurologic), ment, HIV research, student mental health, and
given the paucity of acceptable norms and con- general clinical studies. For example, in symp-
cerns that certain items on the BSI may be closely tomatic adults, convergent validity between the
related to physical and cognitive symptoms BSI and the Minnesota Multiphasic Personality
(Slaughter et al. 1999). Inventory (MMPI) was shown to be 0.30–0.72
(Derogatis and Melisaratos 1983) for the Wiggins
content scales (i.e., 13 scales tapping content areas
Historical Background such as social maladjustment and authority con-
flict) and Tryon cluster scales (i.e., seven scales
In response to the need for briefer evaluation tools assessing conceptual clusters such as social intro-
relevant in a variety of assessment settings, version and bodily symptoms). Convergent valid-
including medical and industrial research studies, ity also has been demonstrated between the BSI
the BSI and BSI-18 were derived from the SCL- and several other scales in predicting affective
90, a 90-item checklist that includes the same nine status among chronic pain patients (Kremer et al.
symptom dimensions and three global indices as 1982). High correlations were also found between
the BSI. The SCL-90, itself, was developed in the SCL-90 and the BSI (0.92–0.96; Derogatis
1973 (Derogatis et al. 1973) and was derived 1993) and BSI-18 (0.91–0.96; Derogatis 2000).
from the Hopkins Symptom Checklist (Derogatis In terms of predictive validity, the BSI has been
et al. 1974). The BSI was published in 1983 shown to be a good predictor of psychopathology
(Derogatis and Melisaratos 1983), and the BSI- in several populations, including a community
18 followed in 2000 (Derogatis 2000). unipolar depression cohort (Amenson and
Lewinsohn 1981), drug-using adults (Buckner
and Mandell 1990), and the elderly (Hale et al.
Psychometric Data 1984). Screening studies completed with medical
cohorts (e.g., Kuhn et al. 1988) found the BSI to
The most recent BSI manual (Derogatis 1993) pro- be a strong and reliable predictor of psychological
vides normative data from four samples: (1) 1,002 distress, whereas the BSI-18 has been demon-
heterogeneous psychiatric outpatients, (2) 914 strated to predict levels of distress in cancer
adult non-patients, (3) 423 psychiatric inpatients, patients (e.g., Recklitis et al. 2006).
and (4) 2,408 adolescent non-patients. The BSI-18 Some concern has been raised about the factor
was normed on two samples: (1) 1,134 community structure and discriminant validity of the BSI and
adults and (2) 1,543 adult cancer patients. Addi- BSI-18. For example, Boulet and Boss (1991)
tional norms have been developed for such diverse found that BSI subscales correlated with non-
samples as older adults (Hale et al. 1984), college analogous scales on the MMPI, suggesting poor
students (Cochran and Hale 1985), individuals discriminant validity. In terms of factor structure,
Brief Symptom Inventory 635

moderate to high intercorrelations were found screening measure for the overall level of psycho-
among BSI subscales, with one factor explaining logical distress in both inpatients and outpatients
over 70% of the variance in a principal compo- with traumatic brain injury (TBI; Meachen et al.
nents analysis (Boulet and Boss 1991). Several 2008). The Federal Interagency TBI Outcomes
cross-cultural studies of the BSI-18 (e.g., Asner- Workgroup recommends the BSI-18 as a core B
Self et al. 2006) found only the GSI (versus the common data element for use in TBI research as
three subscales) to be a valid indicator of psycho- an indicator of psychological status and response
logical distress. These researchers suggested that to treatment (Hicks et al. 2013; Wilde et al. 2010).
the BSI and BSI-18 assess the degree, but not the However, the observation that most items in the
exact nature of psychopathology, and therefore BSI obsessive-compulsive scale are more reflec-
GSI scores should be considered the most useful tive of cognitive complaints (e.g., concentration
indicator of psychological distress derived from and memory problems) than classic obsessive-
the measures. compulsive disorder traits (Slaughter et al. 1999)
highlights an issue of particular concern to neuro-
psychologists. Given the overlap between many
Clinical Uses items and cognitive and physical symptoms, cli-
nicians are urged to interpret elevations cautiously
The BSI and BSI-18 are widely used measures and remain vigilant against misusing scale names
of psychological distress employed with a vari- for diagnostic purposes. It is crucial not to rely on
ety of populations including inpatient and out- psychiatric interpretations of elevated scales in
patient medical and psychiatric patients, neurological patients who have no history of emo-
individuals receiving treatment for substance tional difficulties; instead, BSI and BSI-18 item
abuse, and college students. Individuals who responses might best be examined individually
are of extremely low intelligence, delirious, and used to guide treatment.
and psychotic or have motivation to distort
their responses are not good candidates for either
measure. Given factor structure concerns noted
above (e.g., Boulet and Boss 1991), the instru- Cross-References
ments may be used most appropriately as screen-
ing tools to alert clinicians to elevated levels of ▶ Beck Anxiety Inventory
psychological distress, rather than as diagnostic ▶ Beck Depression Inventory
indicators. According to the BSI manual ▶ Brief Psychiatric Rating Scale
(Derogatis 1993), the measures are “most useful ▶ Center for Epidemiological Studies: Depression
in clinical and research settings where time is a ▶ Geriatric Depression Scale
major limiting variable.” ▶ Hamilton Depression Rating Scale
Both measures can be used as onetime assess- ▶ Millon Clinical Multiaxial Inventory
ments or administered repeatedly to evaluate ▶ Minnesota Multiphasic Personality Inventory
treatment efficacy or trends over time. Both are ▶ Personality Assessment Inventory
reported to have been used successfully in pri- ▶ Self-Report Measures
mary care settings to assess significant changes ▶ Symptom Checklist-90-Revised
in psychological distress and symptoms in ▶ Zung Self-Rating Depression Scale
patients with medical problems. The measures
can be used in nonclinical populations (e.g., to
assess caregiver distress) as well. References and Readings
Both the BSI and BSI-18 may be useful tools
Amenson, C. S., & Lewinsohn, P. M. (1981). An investi-
for inclusion in neuropsychological assessments, gation into the observed sex difference in prevalence of
given their brevity and utility for repeated admin- unipolar depression. Journal of Abnormal Psychology,
istrations. The BSI-18 was reported to be a valid 90, 1–13.
636 Brief Test of Attention

Asner-Self, K. K., Schreiber, J., & Marotta, S. A. (2006). injury. Archives of Physical Medicine and Rehabilita-
A cross-cultural analysis of the Brief Symptom tion, 89, 958–965.
Inventory-18. Cultural Diversity and Ethnic Minority Recklitis, C. J., Parsons, S. K., Shih, M., Mertens, A., &
Psychology, 12, 367–375. Robison, L. L. (2006). Factor structure of the Brief
Boulet, J., & Boss, M. W. (1991). Reliability and validity Symptom Inventory-18 in adult survivors of childhood
of the brief symptom inventory. Psychological Assess- cancer: Results from the childhood cancer survivor
ment, 3, 433–437. study. Psychological Assessment, 18, 22–32.
Buckner, C. J., & Mandell, W. (1990). Risk factors for Ryan, C. (2007). British outpatient norms for the Brief
depressive symptomatology in a drug-using popula- Symptom Inventory. Psychology and Psychotherapy:
tion. American Journal of Public Health, 80, 580–585. Theory, Research and Practice, 80, 183–191.
Canetti, L., Shalev, A. Y., & De-Nour, A. K. (1994). Israeli Slaughter, J., Johnstone, G., Petroski, G., & Flax, J. (1999).
adolescents’ norms of the Brief Symptom Inventory The usefulness of the Brief Symptom Inventory in the
(BSI). Israel Journal of Psychiatry and Related Sci- neuropsychological evaluation of traumatic brain
ences, 31, 13–18. injury. Brain Injury, 13, 125–130.
Cochran, C. D., & Hale, W. D. (1985). College student Wilde, E. A., Whiteneck, G. G., Bogner, J., Bushnik, T.,
norms on the Brief Symptom Inventory. Journal of Cifu, D. X., Dikmen, S., . . ., & von Steinbuechel,
Clinical Psychology, 41, 777–779. N. (2010). Recommendations for the use of common
Derogatis, L. R. (1993). Brief Symptom Inventory (BSI): outcome measures in traumatic brain injury research.
Administration, scoring, and procedures manual Archives of Physical Medicine and Rehabilitation, 91,
(3rd ed.). Minneapolis: National Computer Systems. 1650–1660.e1617.
Derogatis, L. R. (2000). Brief Symptom Inventory-18
(BSI-18): Administration, scoring, and procedures
manual. Minneapolis: National Computer Systems.
Derogatis, L. R., & Melisaratos, N. (1983). The Brief
Symptom Inventory: An introductory report. Psycho- Brief Test of Attention
logical Medicine, 13, 595–605.
Derogatis, L. R., Lipman, R. S., & Covi, L. (1973). SCL-90:
Molly E. McLaren1 and Adam J. Woods2,3,4
An outpatient psychiatric rating scale: Preliminary report. 1
Psychopharmacology Bulletin, 9, 13–28. Center for Cognitive Aging and Memory,
Derogatis, L. R., Lipman, R. S., Rickels, K., Uhlenhuth, Department of Clinical and Health Psychology,
E. H., & Covi, L. (1974). The Hopkins Symptom University of Florida, Gainesville, FL, USA
Checklist (HSCL): A self-report inventory. Behavioral 2
Department of Clinical and Health Psychology,
Science, 19, 1–15.
Francis, V. M., Rajan, P., & Turner, N. (1990). British College of Public Health and Health Professions,
community norms for the Brief Symptom Inventory. University of Florida, Gainesville, FL, USA
British Journal of Clinical Psychology, 29, 3
Center for Cognitive Aging and Memory,
115–116.
McKnight Brain Institute, University of Florida,
Hale, W. D., Cochran, C. D., & Hedgepath, B. E. (1984).
Norms for the elderly on the Brief Symptom Inventory. Gainesville, FL, USA
4
Journal of Clinical and Consulting Psychology, 52, Department of Neuroscience, University of
321–322. Florida, Gainesville, FL, USA
Heinrich, R. K., Tate, D. G., & Bucklew, S. P. (1994). Brief
Symptom Inventory norms for spinal cord injury. Reha-
bilitation Psychology, 39, 49–56.
Hicks, R., Giacino, J., Harrison-Felix, C., Manley, G., The Brief Test of Attention (BTA) is a test of
Valadka, A., & Wilde, E. A. (2013). Progress in devel- attention based on Cooley and Morris’s concep-
oping common data elements for traumatic brain injury
tualization of attentional processes (Cooley and
research: Version two–the end of the beginning. Jour-
nal of Neurotrauma, 30, 1852–1861. Morris 1990; Schretlen et al. 1996a). It was devel-
Kremer, E. F., Atkinson, J. H., & Ignelzi, R. J. (1982). Pain oped to be a pure measure auditory divided atten-
measurement: The affective dimensional measure of tion, and as such attempts to eliminate possible
the McGill pain questionnaire with a cancer pain pop-
confounds of other attentional tasks such as motor
ulation. Pain, 12, 153–163.
Kuhn, W. F., Bell, R. A., Seligson, D., Laufer, S. T., & and reasoning component (Schretlen et al. 1996a).
Lindner, J. E. (1988). The tip of the iceberg: Psychiatric It has also been suggested the BTA may be a
consultations on an orthopaedic service. International useful embedded measure of cognitive effort
Journal of Psychiatry in Medicine, 18, 375–382.
(Busse and Whiteside 2012). The BTA has been
Meachen, S. J., Hanks, R. A., Millis, S. R., & Rapport, L. J.
(2008). The reliability and validity of the Brief Symp- used to assess attention in a variety of populations
tom Inventory-18 in persons with traumatic brain including Parkinson’s disease, sleep apnea,
Brief Test of Attention 637

cancer, and traumatic brain injury (TBI; Aloia 1997; Strauss et al. 2006). Age is the largest
et al. 2003; Butler et al. 2008; Rao et al. 2010; demographic variable predicting performance on
Tröster et al. 1997; Wong 1999). Of note, the BTA the BTA, with older age associated with poorer
is not intended to measure normal attention but performance (Schretlen 1997; Schretlen et al.
instead to be a screening tool for attentional def- 1996a; Strauss et al. 2006). Other demographic B
icits (Schretlen 1997; Strauss et al. 2006). Addi- variables that may contribute to BTA performance
tionally, the BTA does not assess visual attention include ethnicity, education level, and gender
(Strauss et al. 2006). (Schretlen et al. 1996a; Schretlen 1997; Strauss
The BTA takes approximately 10 min to admin- et al. 2006). Demographic variables as a whole
ister and has two parts (Schretlen 1997; Strauss account for 17.5% of the variance in scores on the
et al. 2006). In both parts, individuals are asked to BTA, with age being the largest contributor to
listen to a voice on a recording read 10 lists of variance (Schretlen 1997).
letters and numbers. The length of each list ranges BTA has been shown to be sensitive to indi-
from 4 to 18 items. In the first part, individuals are viduals with mild head injury (Wong 1999). A
asked count how many numbers are read, ignoring report examining the validity of the BTA in
the letters in each list. In the second part, individ- Huntington’s disease patients found this group
uals count how many letters are read, ignoring the performed significantly worse than controls on
number for each list. The specific numbers and the BTA. In contrast, a small group on amnestic
letters do not need to be recalled, just the total patients were not found to perform differently
amount read per list. One point is given for each from controls on the BTA, suggesting intact mem-
correctly counted trial. Possible scores range from ory function may not be needed to successfully
0 to 20 points. Normative data is available for complete the BTA (Schretlen et al. 1996b).
individuals age 6–14 and 17–82 (Strauss et al. Overall, the BTA appears to be a valid and
2006). Recently, normative data of the BTA was relatively consistent measure of divided auditory
published for Spanish speaking adults in 11 Latin attention. More research examining validity and
America countries (Rivera et al. 2015). reliability in minority populations is needed, as is
The BTA has been shown to correlate most further evaluation of test-retest reliability in dif-
strongly with other known attentional test, and ferent populations.
specifically may be more related to more complex
attentional tasks (Trails B; digit backwards;
Schretlen et al. 1996a). Initial validity and reli- References
ability measures for the BTA indicate acceptable
internal consistency (coefficeint a = 0.82) in Aloia, M. S., Ilniczky, N., Di Dio, P., Perlis, M. L.,
Greenblatt, D. W., & Giles, D. E. (2003). Neuropsy-
adults (Schretlen et al. 1996a). When both clinical
chological changes and treatment compliance in older
and healthy populations were combined internal adults with sleep apnea. Journal of Psychosomatic
consistency was high (coefficient a = 0.91; Research, 54(1), 71–76. https://doi.org/10.1016/
Schretlen et al. 1996a). There have been variable S0022-3999(02)00548-2.
Busse, M., & Whiteside, D. (2012). Detecting suboptimal
results from examination of test-retest reliability
cognitive effort: Classification accuracy of the
for the BTA. In one study of adolescent girls Conner’s continuous performance test-II, brief test of
tested 3 months apart, test-retest reliability was attention, and trail making test. The Clinical Neuropsy-
low (r = 0.45), however it was suggested that chologist, 26(4), 675–687. https://doi.org/10.1080/
13854046.2012.679623.
limited range may have contributed to this finding Butler, R. W., Copeland, D. R., Fairclough, D. L., Mulhern,
(Schretlen 1997). In contrast, an examination of R. K., Katz, E. R., Kazak, A. E., Noll, R. B., Patel, S. K.,
older adults assessed at baseline and 9 months & Sahler, O. J. Z. (2008). A multicenter, randomized
reported adequate test-retest reliability (r = 0.70; clinical trial of a cognitive remediation program for
childhood survivors of a pediatric malignancy. Journal
Schretlen 1997). While practice affects appear to
of Consulting and Clinical Psychology, 76(3), 367.
be small or nonexistent, there have been concerns Cooley, E. L., & Morris, R. D. (1990). Attention in children:
regarding a ceiling effect in the test (Schretlen A neuropsychologically based model for assessment.
638 Bristol Activities of Daily Living Scale

Developmental Neuropsychology, 6(3), 239–274. Description

https://doi.org/10.1080/87565649009540465.
Rao, V., Bertrand, M., Rosenberg, P., Makley, M.,
Schretlen, D. J., Brandt, J., & Mielke, M. M. (2010). The Bristol ADL scale is an informant-rated mea-
Predictors of new-onset depression after mild traumatic sure that covers 20 ADLs, both basic and instru-
brain injury. The Journal of Neuropsychiatry and Clin- mental. Items are rated on a four-point scale (from
ical Neurosciences, 22(1), 100–104. https://doi.org/ totally dependent to totally independent, with an
10.1176/appi.neuropsych.22.1.100.
Rivera, D., Perrin, P. B., Aliaga, A., Garza, M. T., Saracho, additional “not applicable” option).
C. P., Rodriguez, W., Justo-Guillen, E., Aguayo, A.,
Schebela, S., Gulin, S., Weil, C., Longoni, M.,
Ocampo-Barba, N., Galarza-del-Angel, J., Rodriguez, D., Historical Background
Esencarro, L., Garcia-Egan, P., Martinez, C., &
Arango-Lasprilla, J. C. (2015). Brief test of attention:
Normative data for the Latin American Spanish speak- The BADLS was developed specifically for use in
ing adult population. Neuropsychological Rehabilita- people with dementia, as existing scales were felt
tion, 37, 663–676. to be insensitive to change in this group, having
Schretlen, D. (1997). Brief test of attention professional
manual. Odessa: Psychological Assessment Resources. been designed for healthy older adults or people
Schretlen, D., Bobholz, J. H., & Brandt, J. (1996a). Devel- with physical disabilities. Initially, 22 items were
opment and psychometric properties of the brief test of included based on the rationale that they appeared
attention. The Clinical Neuropsychologist, 10(1), in at least two existing ADL measures. Caregivers
80–89. https://doi.org/10.1080/13854049608406666.
Schretlen, D., Brandt, J., & Bobholz, J. H. (1996b). Vali- of people with dementia completed the question-
dation of the brief test of attention in patients with naire by mail, including feedback on the relevance
Huntington’s disease and amnesia. The Clinical Neu- and importance of the items and response options.
ropsychologist, 10(1), 90–95. https://doi.org/10.1080/ Some modifications were made to the scale, with
13854049608406667.
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A the next version incorporating different response
compendium of neuropsychological tests: Administra- options. Two items on which participants scored
tion, norms, and commentary. New York: Oxford Uni- at floor and ceiling respectively were removed,
versity Press. leading to the final 20-item version. Bucks and
Tröster, A. I., Fields, J., Wilkinson, S., Pahwa, R.,
Miyawaki, E., Lyons, K., & Koller, W. (1997). Unilat- Haworth (2002) stated that the measure is regularly
eral pallidal stimulation for Parkinson’s disease: used in 58% of memory clinics in the United King-
Neurobehavioral functioning before and 3 months after dom, but that a revision was needed in order to
electrode implantation. Neurology, 49(4), 1078–1083. increase sensitivity to mild cognitive impairment
Wong, T. M. (1999). Validity and sensitivity of the brief
test of attention with acute brain injury and mild head and to reflect changes in understanding of disability
injury patients. Archives of Clinical Neuropsychology, (particularly in light of the 2001 WHO framework)
14(8), 617–818. [Abstract]. since the scale was developed. Bucks and Haworth
(2002) also stated that studies evaluating a revised
BADLS are underway, but no papers reporting
these studies have been published to date
Bristol Activities of Daily (information correct as of 02.06.09).
Living Scale

Jessica Fish Psychometric Data

Medical Research Council Cognition and Brain
Sciences Unit, Cambridge, UK The 22-item preliminary version of the BADLS
had good test-retest reliability (r = 0.95, for kappa
scores; for individual items, see Bucks et al.
Synonyms 1996), and evidence of its validity was found
through correlations between the BADLS and
Bristol ADL scale (BADLS); Revised Bristol MMSE scores (r = 0.55) and between BADLS
activities of daily living scale (BADLS-R) and observed performance ratings (r = 65). The
Bristol Activities of Daily Living Scale 639

final 20-item version of the BADLS, completed dementias. Bucks and Haworth (2002) have
by 50 caregivers of people with dementia (mixed noted that completing the questionnaire may be
diagnoses), found estimates of reliability and in itself helpful for caregivers, as it can help them
validity consistent with the previous version, to understand the effects of dementia in real-life
with BADLS-MMSE scores correlating at 0.67. terms. B
Principal components analysis identified a four-
factor structure consisting of instrumental ADLs
(seven items explaining 40.3% of variance), self Cross-References
care (six items explaining 10.3% of variance),
orientation (five items explaining 7.5% of vari- ▶ Activities of Daily Living Questionnaire
ance), and mobility (two items explaining 7% of ▶ Alzheimer’s Disease Cooperative Study ADL
variance). Byrne et al. (2000) found that the Scale
BADLS was a good measure of change in ADL ▶ Disability Assessment for Dementia
proficiency over time in people with Alzheimer’s ▶ Lawton-Brody Instrumental Activities of Daily
disease (AD) receiving anticholinesterase inhibi- Living Scale
tors, as judged by its correlations with MMSE and
ADAS-Cog scores and sensitivity of 74% and
specificity of 65% in detecting improvement/sta- References and Readings
bility versus decline, in comparison with
clinician-rated judgments. AD2000 Collaborative Group. (2008). Aspirin in
A recent systematic review of 12 instrumental Alzheimer’s disease (AD2000): A randomised open-
label trial. Lancet Neurology, 7, 41–49.
ADL scales for persons with dementia (Sikkes et al.
Ballard, C., Lana, M. M., Theodoulou, M., Douglas, S.,
2009) concluded that the BADLS was of “moderate McShane, R., Jacoby, R., et al. (2008). A randomised,
quality,” the highest rating awarded in the review, blinded, placebo-controlled trial in dementia patients
which was given to only two measures, BADLS and continuing or stopping neuroleptics (the DART-AD
trial). PLoS Medicine, 5, 587–599.
the Disability Assessment for Dementia.
Bucks, R. S., & Haworth, J. (2002). Bristol activities of
daily living scale: A critical evaluation. Expert Reviews
in Neurotherapeutics, 2, 669–676.
Clinical Uses Bucks, R. S., Ashworth, D. L., Wilcock, G. K., & Sieg-
fried, K. (1996). Assessment of activities of daily liv-
ing: Development of the Bristol activities of daily
Wicklund et al. (2007) noted that the Bristol ADL living scale. Age and Ageing, 25, 113–120.
scale is heavily weighted toward basic ADLs Burns, A., Guthrie, E., Marino-Francis, F., Busby, C.,
rather than instrumental ADLs, so this should Morris, J., Russell, E., et al. (2005). Brief psychother-
apy in Alzheimer’s disease. British Journal of Psychi-
be borne in mind when considering using
atry, 187, 143–147.
it. Nonetheless, the BADLS has been used as a Byrne, L. M. T., Wilson, P. M. A., Bucks, R. S., Hughes,
primary or secondary outcome measure in a num- A. O., & Wilcock, G. K. (2000). The sensitivity to
ber of clinical trials, including those of pharma- change over time of the Bristol activities of daily living
scale in Alzheimer’s disease. International Journal of
ceutical and psychosocial interventions in people
Geriatric Psychiatry, 15, 656–661.
with dementia. Recent examples include open- Jones, R., Sheehan, B., Phillips, P., Juszczak, E., Adams, J.,
label and controlled trials on the safety of aspirin Baldwin, A., et al. (2009). DOMINO-AD protocol:
(AD2000 Collaborative Group 2008) and neuro- Donepezil and memantine in moderate to severe
Alzheimer’s disease – A multicentre RCT. Trials, 10, 57.
leptic treatments (Ballard et al. 2008) in people Sikkes, S. A. M., de Lange-de Klerk, E. S. M., Pijnenburg,
with AD, a comparison of cholinesterase inhibitor Y. A. L., Scheltens, P., & Uitdehaag, B. M. J. (2009).
and glutamate agonist treatment in moderate- A systematic review of instrumental activities of daily
severe AD (Jones et al. 2009), and RCTs of rem- living scales in dementia: Room for improvement.
Journal of Neurology Neurosurgery and Psychiatry,
iniscence therapy (Woods et al. 2009) and inter-
80, 7–12.
personal psychotherapy (Burns et al. 2005) for Wicklund, A. H., Johnson, N., Rademaker, A., Weitner,
people with Alzheimer’s disease and other B. B., & Weintraub, S. (2007). Profiles of decline in
640 Broca, Pierre Paul (1824–1880)

activities of daily living in non-Alzheimer’s dementia. Medicine in Paris. He lectured on topics in

Alzheimer’s Disease and Associated Disorders, 21, anatomy and surgery until a formal competi-
8–13.
Woods, R. T., Bruce, E., Edwards, R. T., Hounsome, B., tion for a professorship at the Faculty of Med-
Keady, J., Moniz-Cook, E. D., et al. (2009). Reminis- icine opened in 1853. That year, at the age of
cence groups for people with dementia and their family 29, Broca successfully competed to achieve the
carers: Pragmatic eight-centre randomised trial of joint distinction of Professor Agrégé and Chirurgien
reminiscence and maintenance versus usual treatment:
A protocol. Trials, 10, 64. du Bureau Central (also known as Chirurgien
des Hôpitaux or Surgeon of the Hospitals) at
the Faculty of Medicine. In 1867, he was
selected to chair the pathologie externe.
Broca received the distinction of a professor
Broca, Pierre Paul of clinical surgery in 1868. That same year, he
(1824–1880) was elected a member of the Académie de
Médicine and resigned his chair of the
Michael J. Larson pathologie externe in order to accept the chair
Brigham Young University, Provo, UT, USA of Clinical Surgery. He held this position until
his death. During his tenure as the chair of
Clinical Surgery, Broca worked in several Pari-
Name and Degrees sian hospitals, including the Hôpital
St. Antoine, the Pitié, the Hôtel des Cliniques,
Pierre Paul Broca received a bachelor’s degree of and the Hôpital Necker.
letters (a subject that includes history and litera-
ture) in 1840 from his hometown Sainte-Foy-la-
Major Honors and Awards
Grande College and subsequently received a
Bachelor of Science degree in mathematics. He
• Broca became widely recognized throughout
began his study of medicine in 1841 at the age of
France for his work. In 1865, he was elected
17 at the Faculty of Medicine at the University of
president of the Paris Société de Chirurgie. In
Paris. He completed his formal medical training
1868, he was appointed to the Académie de
there in 1848. Broca was studious and progressed
Médicine and named a member of the French
rapidly during his medical studies. He was named
Legion of Honor. He was elected to a perma-
externe of the Faculty of Medicine hospitals fol-
nent seat in the French Senate in 1880, just
lowing a competitive application in 1843, interne
before his death. Broca also received many
in 1844, and interne laureate, with a 1-year exten-
posthumous honors, including the eponymous
sion in 1847. He competed successfully to receive
naming of Broca’s area, Broca’s aphasia, and
the positions of Anatomy Assistant of the Faculty
the diagonal band of Broca.
of Medicine in 1846 and Prosector of Anatomy to
the Faculty in 1848. His mentors included such
renowned individuals as François Leuret at the Landmark Clinical, Scientific, and
Bicêtre, Philippe Ricord at the Hôpital du Midi, Professional Contributions
Langier at the Hôpital Beaujon, Pierre Nicolas
Gerdy at the Faculty of Medicine (Paris), and Early Career
Philippe-Frédéric Blandin at the Hôtel-Dieu. • Although Broca is best known for his work on
speech and the localization of brain functions,
he first established his reputation as a physician
Major Appointments and scientist using the microscope to study
diseases (Finger 2004). He described in detail
• Following the completion of his medical stud- the histology of articular cartilage (the type of
ies, Broca served as a lecturer at the Faculty of cartilage that covers the end of bones) and the
Broca, Pierre Paul (1824–1880) 641

histology of Rickets and demonstrated that willing to accept the idea that all parts of the
muscular dystrophy is primarily a disease of cerebral hemispheres function in the same way
the muscles. Broca was among the first to use a (Finger 2000).
microscope to show that cancer cells can pen- • On April 12, 1861, a Monsieur Leborgne was
etrate the venous and lymphatic systems as admitted to Broca’s surgical service at the B
they metastasize. In the early 1850s, he Bicêtre for cellulitis and gangrene of the right
performed the first experiment in Europe leg. Affected by epilepsy since childhood,
using hypnotism as surgical anesthesia. Leborgne developed considerable limitations
• Broca was a prolific writer. He wrote several in his ability to speak along with right
medical classics early in his career, including hemiparesis at age 30. He could comprehend
an extensive treatise on brain aneurysms, Des speech and communicate using pantomime,
aneurysms et de leur traitment, published in but his speech output was limited to the mono-
1856 and a memoir on cancer, Memoir sur syllabic phrase “tan,” which became his
l’anatomie pathologique du cancer, published nickname.
in 1850. • Leborgne died due to complications from the
cellulitis and gangrene on April 17, 1861.
Speech and Localization of Function Broca quickly completed an autopsy and pre-
• Broca’s most well-known observations were sented his preliminary findings at the meeting
made in 1861 and the several years that of the Société d’Anthropologie de Paris the
followed. During that time, there was consid- following day. He reported atrophy of both
erable fervor regarding the plausibility of hemispheres of Leborgne’s brain, with exten-
cortical localization of functions, as Franz sive softening of left-frontal areas originating
Joseph Gall’s early nineteenth-century phre- from the third left-frontal convolution. He fur-
nology had fallen out of favor. Gall, based on ther examined Leborgne’s brain specimen and
his observations of skull shape, placed the presented his in-depth findings at the Société in
ability to speak and recall words in the infe- August 1861. His presentation included a
rior aspect of the frontal lobes. Jean Baptiste description of Leborgne’s epilepsy and physi-
Bouillaud followed Gall’s localizationist cal difficulties, including right-sided paralysis
views and hypothesized that the anterior and loss of speech, along with a description of
lobes of the brain contained a center for the growth of a lesion from the third left-frontal
speech production. Bouillaud even offered a convolution to other areas of the brain. Over
prize to the first individual who reported a time, the area of the third left-frontal convolu-
case with loss of speech without lesion to the tion became known as “Broca’s area” as a
frontal lobes. result of this case.
• In February 1861 at a meeting of the Société • Later in 1861, Broca’s surgical service was
d’Anthropologie de Paris, a heated debate referred a Monsieur Lelong who had fractured
ensued when Pierre Gratiolet, another well- his left femur after a fall. Lelong was an
respected scientist of the time, proposed total 84-year-old man who had been admitted to
brain volume as a meaningful correlate of intel- the Bicêtre 8 years previously for “senility.”
ligence and indicated that the functions of all In the spring of 1860, Lelong had suddenly
parts of the brain were essentially identical. collapsed and fallen unconscious. Upon recov-
These views were vehemently opposed by ery, he was able to produce only four French
Bouillaud and his student and son-in-law words: “oui,” “non,” “toujours,” and “trios,”
Simon Alexandre Ernest Aubertin. Broca was though his pantomimes were nearly always
present during these debates as the secretary of correct (Lee 1981). Lelong lived for only
the Société d’Anthropologie. As he considered 12 days after he was referred to Broca’s ser-
the views presented, Broca eventually sided vice. Following Lelong’s death, Broca
with Bouillaud and Aubertin and became less performed an autopsy and found lesions in
642 Broca, Pierre Paul (1824–1880)

the second and third frontal convolutions. Pre- and lapsed into a coma. Broca suspected an
senting the findings from the case of Lelong to abscess in the area of the third frontal convolu-
the Société d’Anthropologie de Paris in tion and performed a craniotomy at this approx-
November 1861, Broca indicated that the find- imate location based on his hypothesis. He
ings confirmed those from his study of successfully drained the abscess, but the patient
Leborgne and hypothesized Lelong’s left- slipped back into coma after approximately
frontal lesion was due to an old hemorrhage 11 h and died. Autopsy revealed a left-sided,
that had occurred at the time Lelong lost his predominantly frontal, meningoencephalitis
speech in 1860 (Lee 1981). (Jay 2002). This surgery based on Broca’s find-
• Broca called the inability to produce language ings regarding the localization of speech func-
in the context of intact comprehension, as seen tions is likely the first practical application of
in the cases of Leborgne and Lelong, the theory of cortical localization (Finger 2004;
“aphémie” (Armand Trousseau subsequently Stone 1991).
renamed such disturbances “aphasia” in
1864). Broca published several additional
cases of aphémie with lesions to the left hemi- Anthropology
sphere. For example, in 1863, he published a
series of eight cases showing primarily left- From approximately 1866 until his death, Broca
frontal lesions with language production defi- focused the majority of his efforts on the advance-
cits. In an 1865 manuscript, Broca firmly ment of anthropology. Indeed, due to his interest
asserted that the left hemisphere is the domi- in anthropology and the remains of early humans,
nant seat for language production. he did not write any papers at all on speech and the
• Broca’s declaration that the left hemisphere is brain after 1877 (Finger 2000). Broca’s initial
predominantly responsible for language is interest in anthropology was piqued after serving
among the clearest and most dramatic exam- on a commission examining excavations in the
ples of localization of neural functions. Broca cemetery of the Celestins in 1847. The discovery
continues to receive the primary credit for of Neanderthal Man in 1856, the publishing of
reporting on the localization of language func- Charles Darwin’s controversial ideas in On the
tions, although there were others who may Origin of Species in 1859, and the subsequent
have preceded him. In 1836, Marc Dax pre- controversy on the origins of man furthered
sented a work indicating that disturbances in Broca’s desire to study anthropology.
language production were due to lesions of the Much of Broca’s anthropological research
left hemisphere. Dax’s work remained largely focused on the comparative study of skulls and
unknown until his son Gustave Dax presented the cranium circumference across ethnic groups.
and published his deceased father’s work in the He devised various instruments, standardized
years after 1863 (see Buckingham 2006 and techniques, and methods to examine the structure
Finger 2000). and topography of the brain based on measure-
ments from prehistoric craniums. He invented at
Surgery least 27 instruments to determine the relation
Broca focused heavily on the relation between between the brain and skull, including a goniom-
the skull and the brain. In June 1871, he treated eter (instrument to measure angles), craniograph
a 38-year-old laborer who was kicked in the (instrument used to depict the outline of the skull),
left-frontal region of the skull by a horse. and several stereographic instruments (Cowie
There was no fracture; nevertheless, the patient 2000).
showed difficulties with speech production after In 1869, Broca published the first descrip-
approximately 1 month. He eventually lost his tion of the Gibraltar skull. Discovered in 1848,
full ability to express himself through speech the Gibraltar skull was among the earliest
Broca, Pierre Paul (1824–1880) 643

skeletal remains identified as belonging to the Broca showed considerable interest in the sci-
early species of Homo sapiens neanderthlensis. entific societies that prevailed in Paris both during
Broca was also fascinated with the topic of his study of medicine and throughout his career.
neolithic trephination, the process, whereby a He joined the Société Anatomique (Anatomical
hole is scraped or drilled into the skull. His Society) in 1847 and the Société de Chirurgie B
interest in trephination began in 1867 after he (Surgical Society) in 1849. He also founded sev-
examined an Incan skull with cross-hatched eral societies, schools, and laboratories. In 1848,
cuts. He hypothesized that the operations were he established a society of free-thinking individ-
performed to treat “internal maladies” in chil- uals, many of whom were sympathetic to Charles
dren (Finger 2004) and was among the first to Darwin’s controversial theories. He started the
speculate that trephination was a therapeutic anthropology laboratory at the École des Hautes
practice that was survived postoperatively Études in Paris in 1858, the Société
based on the signs of inflammation at the d’Anthropologie de Paris, the first-known anthro-
wound margins (Cowie 2000). pological Société in the world, in 1859, the Revue
Broca was very active in the study of anthro- d’Anthropologie in 1872, and the École
pology during the final years of his life. Indeed, he d’Anthropologie in Paris in 1876. Broca held
was known to spend many hours per day in the leadership positions in many of these societies,
École d’Anthropologie he founded. During the including secretary of the Société Anatomique,
last two decades of his life, Broca published over general secretary of the Société d’Anthropologie
240 papers and monographs on anthropological de Paris, president of the Société de Chirurgie, and
topics (Schiller 1992), including a five-volume director of the École d’Anthropologie.
work entitled, Mémoires d’Anthropologie, Broca married Lugol Augustine, the daughter
published in 1871. of Dr. Jean Guillaume Auguste Lugol, who prop-
agated the use of iodine in the treatment of dis-
ease, on July 6, 1857. The couple had three
Short Biography children, one daughter and two sons. Just as
Broca followed in his father’s footsteps by becom-
Pierre Paul Broca was born on June 28, 1824, in ing a physician, his two sons succeeded him as
Sainte-Foy-la-Grande, a small town near Bor- well-respected medical scientists.
deaux, France. He was raised under the Calvinist Pierre Paul Broca died on July 9, 1880, in Paris
Protestant tradition. His maternal grandfather, in at the age of 56. Autopsy showed that all organs
addition to serving as mayor of Bordeaux during were apparently sound, although some have spec-
the French revolution, was a pastor. His mother, ulated his cause of death to be heart disease
Annette Thomas, was the sister of a Protestant (Finger 2000, 2004). Following his autopsy one
minister. His father, Jean Pierre (known as Benja- of his students remarked, “We shall probably not
min) Broca, was a physician who served for sev- be far from the truth in attributing the catastrophe
eral years as a surgeon in the French Army and to cerebral exhaustion, arising from too protracted
was present at the Battle of Waterloo (Finger a course of severe intellectual exertion” (Memoir
2000). of Paul Broca 1881). He was buried at the Mont-
Following his undergraduate education, Broca parnasse Cemetery in Paris. In his life, Broca
sought to study engineering at the École Poly- published over 500 books and articles. His influ-
technique in Paris (Schiller 1992). The death of ence on ideas regarding cortical localization,
his only sibling, a sister named Léontine, in 1840, speech, and anthropology endures today. Indeed,
along with pressure from his parents to remain many scientists would agree that the foundations
closer to home and follow his father’s career of modern neuropsychology and cognitive neuro-
path, led to his decision to change his course of science were laid by Pierre Paul Broca (Dronkers
study to medicine in 1841. et al. 2007).
644 Broca’s Aphasia

Cross-References Hothersall, D. (2004). History of psychology (4th ed.).

New York City: McGraw-Hill.
Jay, V. (2002). Pierre Paul Broca. Archives of Pathology
▶ Aphasia and Laboratory Medicine, 126, 250–251.
▶ Broca’s Aphasia Lee, D. A. (1981). Paul Broca and the history of aphasia:
▶ Localization Roland P. Mackay award essay, 1980. Neurology, 31,
▶ Speech 600–602.
Memoir of Paul Broca. (1881). The Journal of the Anthro-
▶ Tan pological Institute of Great Britain and Ireland, 10,
▶ Wernicke’s Aphasia 242–261.
Schiller, F. (1983). Paul Broca and the history of aphasia.
Neurology, 33, 667.
Schiller, F. (1992). Paul Broca: Founder of French anthro-
pology, explorer of the brain. New York: Oxford Uni-
References and Readings versity Press.
Schreider, E. (1966). Brain weight correlations calculated
Broca, P. P. (1850). Memoire sur l’anatomie pathologique from original results of Paul Broca. American Journal
du cancer. Bulletin de la Societe Anatomique de Paris, of Physical Anthropology, 25, 153–158.
25, 45. Stone, J. L. (1991). Paul Broca and the first craniotomy
Broca, P. P. (1856). Traite des anevrismes et leur based on cerebral localization. Journal of Neurosur-
traitement. Paris: Labe & Asselin. gery, 75, 154–159.
Broca, P. P. (1861a). Sur le principe es localisations
cerebrales. Bulletin de la Societe d’Anthropologie, 2,
190–204.
Broca, P. P. (1861b). Nouvelle observation d’aphemie pro-
duite par une lesion de la moitie posterieure de
deuxieme et troisieme circonvolution frontales
Broca’s Aphasia
gauches. Bulletin de la Societe Anatomique, 36,
398–407. Lyn S. Turkstra
Broca, P. P. (1863). Localisations des fonctions cerebrales. School of Rehabilitation Science, McMaster
Siege de la faculte du language articule. Bulletin de la
University, Hamilton, ON, Canada
Societe d’Anthropologie, 4, 200–208.
Buckingham, H. W. (2006). The Marc Dax
(1770–1837)/Paul Broca (1824–1880) controversy
over priority in science: Left hemisphere specificity Synonyms
for seat of articulate language and for lesions that
cause aphemia. Clinical Linguistics & Phonetics,
20, 613–619. Anterior aphasia; Expressive aphasia; Motor
Clower, W. T., & Finger, S. (2001). Discovering trepana- aphasia
tion: The contributions of Paul Broca. Neurosurgery,
49, 1417–1425.
Cowie, S. E. (2000). A place in history: Paul Broca and
cerebral localization. Journal of Investigative Surgery,
Short Description or Definition
13, 297–298.
Dronkers, N. F., Plaisant, O., Iba-Zizen, M. T., & It is a type of aphasia that is characterized by
Cabanis, E. A. (2007). Paul Broca’s historic cases: speech that is effortful, sparse, and halting, and
High resolution MR imaging of the brains of Leborgne
impaired repetition, with relatively intact lan-
and Lelong. Brain, 130, 1432–1441.
Finger, S. (1994). Origins of neuroscience. New York City: guage comprehension. The spoken output of indi-
Oxford University Press. viduals with Broca’s aphasia often is described as
Finger, S. (2000). Minds behind the brain. New York City: telegraphic, as it contains primarily content words
Oxford University Press.
and lacks functors, bound morphemes, and other
Finger, S. (2004). Paul Broca (1824–1880). Journal of
Neurology, 251, 769–770. grammatical elements. Paraphasic errors are also
Greenblatt, S. H. (1970). Hughlings Jackson's first encoun- present. Reading and writing performance gener-
ter with the work of Paul Broca: The physiological and ally mirrors that of auditory comprehension and
philosophical background. Bulletin of the History of
Medicine, 44, 555–570.
oral expression. Some individuals with Broca’s
Grodzinsky, Y., & Amunts, K. (2006). Broca’s region. aphasia have agrammatism, a lack of grammatical
New York City: Oxford University Press. structure in their extemporaneous or repeated
Broca’s Aphasia 645

output that is often associated with impaired com- from slow lexical activation) (Patil et al. 2016).
prehension of grammatical structures. Personality For the treatment implications of this debate, see
and intelligence are typically intact, and, in gen- discussion in Basso and Marangolo (2000).
eral, nonlinguistic cognitive functions are rela- Depression is a common psychological conse-
tively preserved, but this is difficult to test the quence of aphasia and is significantly more com- B
given role of language in cognitive functions. mon after anterior left-hemisphere lesions
(including those associated with nonfluent apha-
sia) than lesions in other areas (Carson et al.
Categorization 2000). The most commonly used tools for evalu-
ation of depression rely heavily on language pro-
Broca’s aphasia is a type of aphasia that is char- cesses and thus have limited utility for individuals
acterized by speech that is effortful, sparse, and with aphasia (Turner-Stokes and Hassan 2002).
halting, with impaired repetition and relatively Scales designed to limit verbal demands, such as
intact language comprehension. the Cornell Depression Scale (Alexopoulos et al.
1988), have been used in studies of aphasia but
have not been validated for this population
Natural History, Prognostic Factors, and (Townend et al. 2007). A systematic review of
Outcomes measures of depression in aphasia (Townend
et al. 2007) indicated that adaptation of existing
The prognosis for recovery of functional com- scales and use of other informants were common
munication in individuals with Broca’s aphasia approaches to the diagnosis of depression in indi-
depends on the underlying cause of the aphasia viduals with aphasia and recommended collabo-
as well as factors such as the size of the lesion ration between mental health and language
and the patient’s age, premorbid language skills, experts in the diagnostic process.
and comorbid health conditions. Individuals who
initially present with Broca’s aphasia often
evolve to a clinical profile of anomic aphasia, Evaluation
with relatively good auditory and reading com-
prehension, and deficits primarily in word- Aphasia is typically evaluated using a combina-
finding and the comprehension and production tion of standardized language tests and careful
of complex syntax. observation of extemporaneous communication.
Assessment of cognitive functions such as atten-
tion, memory, and executive functions is chal-
Neuropsychology and Psychology of lenging in this group, given both the verbal
Broca’s Aphasia demands inherent in the structure of most neuro-
psychological tests and the complex interplay of
Broca’s aphasia has been traditionally associated language and other cognitive functions. Cognitive
with lesions to Brodmann’s areas 44 and 45 in the tests considered to have relatively low language
frontal lobe of the dominant (typically left) hemi- demands (e.g., the Cognitive Linguistic Quick
sphere. Autopsy data and neuroimaging studies, Test, Helm-Estabrooks 2001; or Raven’s Standard
however, have shown both the absence of Broca’s Progressive Matrices, Raven 1938, included in the
aphasia in individuals with lesions in this region Western Aphasia Battery) are sometimes used to
and also the reverse (Yang et al. 2008). The debate test cognitive abilities other than language, with
about localization of Broca’s aphasia is part of a the caveat that language impairments are likely to
larger theoretical discussion of the modularity of influence performance on these tests as well
language and other cognitive functions, in which (Beeson et al. 1993).
localizationist views are contrasted with pro- The specific tests and measures used depend on
cessing accounts (e.g., that Broca’s aphasia results the goals of the assessment (e.g., diagnosis
646 Broca’s Aphasia

vs. prediction of functional performance Alexopoulos, G. S., Abrams, R. C., Young, R. C., &
vs. treatment planning), the time postonset (e.g., Shamoian, C. A. (1988). Cornell scale for depression
in dementia. Biological Psychiatry, 23(3), 271–284.
comprehensive test batteries are not appropriate in Basso, A., & Marangolo, P. (2000). Cognitive neuropsy-
the context of acute stroke), and the patient’s chological rehabilitation: The emperor’s new clothes?
clinical presentation. As lesions typically associ- Special issue: Cognitive neuropsychology and lan-
ated with Broca’s aphasia affect motor structures guage rehabilitation. Neuropsychological Rehabilita-
tion, 10(3), 219–229.
in the frontal lobe, many patients with Broca’s Beeson, P. B., Bayles, K. A., Rubens, A. B., & Kaszniak,
aphasia also have apraxia of speech and hemiple- A. W. (1993). Memory impairment and executive con-
gia or hemiparesis, which poses a particular chal- trol in individuals with stroke-induced Aphasia. Brain
lenge in assessment of language and other and Language, 45, 253–275.
Carson, A. J., MacHale, S., Allen, K., Lawrie, S. M.,
cognitive functions. Dennis, M., House, A., et al. (2000). Depression after
stroke and lesion location: A systematic review. Lancet,
356(9224), 122–126.
Treatment Cherney, L. R., Patterson, J. P., Raymer, A., Frymark, T., &
Schooling, T. (2008). Evidence-based systematic
review: Effects of intensity of treatment and
There is a wide variety of validated treatment tech- constraint-induced language therapy for individuals
niques for nonfluent aphasia, particularly for with stroke-induced Aphasia. Journal of Speech, Lan-
Broca’s aphasia. These range from traditional guage, and Hearing Research, 51(5), 1282–1299.
Goodglass, H. (1993). Understanding aphasia. San Diego:
stimulation-type therapies, which have been the Academic.
staple of aphasia therapy since the Second World Helm-Estabrooks, N. (2001). Cognitive linguistic quick
War, to current treatments such as conversational test (1st ed.). San Antonio: Psychological Corporation.
script training (Manheim et al. 2009), constraint- Kagan, A., Black, S., Duchan, J., Mackie, N., & Square, P.
(2001). Training volunteers as conversation partners
induced aphasia therapy (Cherney et al. 2008), using “supported conversation for adults with Aphasia”
training of communication partners (Kagan et al. (SCA): A controlled trial. Journal of Speech, Lan-
2001), and direct training of underlying grammati- guage, and Hearing Research, 44, 624–638.
cal structures (Thompson and Shapiro 2005). Most Manheim, L. M., Halper, A. S., & Cherney, L. (2009).
Patient-reported changes in communication after
of the treatment literature has focused on individ- computer-based script training for aphasia. Archives of
uals with vascular disorders, primarily stroke. For Physical Medicine and Rehabilitation, 90(4), 623–627.
these patients, speech-language therapy interven- Patil, U., Hanne, S., Burchert, F., De Bleser, R., &
tions have been found to be effective in improving Vasishth, S. (2016). A computational evaluation of
sentence processing deficits in aphasia. Cognitive Sci-
both impairments and functional communication ence, 40(1), 5–50.
ability even several years after the stroke. Raven, J. C. (1938). Progressive matrices: A perceptual
test of intelligence. London: H.K. Lewis.
Thompson, C. K., & Shapiro, L. P. (2005). Treating
agrammatic aphasia within a linguistic framework:
Cross-References Treatment of underlying forms. Aphasiology, 19
(10/11), 1021–1036.
▶ Aphasia Townend, E., Brady, M., & McLaughlan, K. (2007).
A systematic evaluation of the adaptation of depression
▶ Nonfluent Aphasia diagnostic methods for stroke survivors who have
▶ Paraphasia aphasia. Stroke, 38(11), 3076–3083.
▶ Speech-Language Therapy Turner-Stokes, L., & Hassan, N. (2002). Depression after
stroke: A review of the evidence base to inform the
development of an integrated care pathway. Part 1:
Diagnosis, frequency and impact. Clinical Rehabilita-
References and Readings tion, 16(3), 231–247.
Yang, Z. H., Zhao, X. Q., Wang, C. X., Chen, H. Y., &
Academic of Neurologic Coaammunication Disorders and Zhang, Y. M. (2008). Neuroanatomic correlation of the
Sciences. Evidence-based practice guidelines post-stroke aphasias studied with imaging. Neurologi-
(association). www.ancds.org. Retrieved 1 Oct 2008. cal Research, 30(4), 356–360.
Bromocriptine 647

Cross-References
Brodmann’s Areas of the
Cortex ▶ Auditory Cortex
▶ Cerebral Cortex
Kimberle M. Jacobs ▶ Neocortex B
Department of Anatomy and Neurobiology, ▶ Somatosensory Cortex
Virginia Commonwealth University, Richmond, ▶ Visual Cortex
VA, USA

References and Readings

Definition
Brodmann, K. (2005). Brodmann’s: Localisation in the
cerebral cortex (trans: Carey L. J.). Berlin:
Brodmann’s areas of the cortex refer to 52 regions
Springer.
of the cerebral cortex that were identified in 1909 Falk, D., & Gibson, K. R. (Eds.). (2008). Evolutionary
by German Neurologist, Korbinian Brodmann, anatomy of the primate cerebral cortex. Cambridge:
based on cytoarchitectonic (cell size, spacing or Cambridge University Press.
packing density, and lamination) differences.
Brodmann’s areas are typically shown on a map
of the brain surface, but each region is continued
through the depth of cerebral cortex. These Bromocriptine
regions were originally identified based on Nissl-
stained sections of human brain; however, David J. Libon
Brodmann believed that they applied to all Departments of Geriatrics, Gerontology, and
mammals. Psychology, Rowan University, New Jersey
Institute for Successful Aging, School of
Osteopathic Medicine, Stratford, NJ, USA
Current Knowledge
Definition
In some cases, the boundary identified by
Brodmann is also a functional boundary. For
Bromocriptine is one of the groups of medicines
instance, primary visual cortex is contained in
classified as ergot alkaloids. Bromocriptine acts to
Brodmann’s area 17. Brodmann’s area 18 is con-
block the release of prolactin which is produced
sidered to be higher-order visual cortex. Somato-
by the pituitary gland. Bromocriptine is used to
sensory functions are associated with Brodmann’s
treat a variety of medical conditions including
areas 3, 1, and 2, with part of area 3 being recog-
problems with menstruation, infertility,
nized as primary somatosensory cortex.
Parkinson’s disease, neuroleptic malignant syn-
Brodmann’s areas 41 and 42 are associated with
drome, and pituitary adenomas. When used in
audition (hearing). Primary motor cortex (the out-
conjunction with diet, bromocriptine can also be
put for motor commands) is associated with
used to treat type 2 diabetes.
Brodmann’s area 4, while premotor cortex
(where the decision to move likely arises) is
found in Brodmann’s area 6.
A different interpretation of cytoarchi- References and Readings
techtonic regions (107 areas) was published
Ropper, A. H., & Samuels, M. A. (2009). Adams and victor
by Constantin von Economo and Georg principles of neurology (9th ed.). New York: McGraw
N. Koskinas in 1925. Hill.
648 Brown-Séquard Syndrome

commissure and then ascend contralaterally as

Brown-Séquard Syndrome the ventral and lateral spinothalamic tracts
(anterolateral system).
John E. Mendoza Thus, a lesion that transects one-half of the
Department of Psychiatry and Neuroscience, spinal cord will cause motor symptoms on the
Tulane Medical School and SE Louisiana same side of the body as a result of severing
Veterans Healthcare System, New Orleans, the lateral corticospinal tract on that side. This
LA, USA will result in residual upper motor neuron type
deficits below the level of the lesion (e.g.,
spastic paralysis, hyperreflexia, clonus, loss of
Synonyms superficial reflexes, and a positive Babinski).
As the lesion also affects the ventral horns,
Hemisection of spinal cord lower motor neuron signs (flaccid paralysis,
severe atrophy, hyporeflexia, and fascicula-
tions) are potentially discernable at the level
Definition of the lesion. Because the posterior columns
are affected, the individual will also demon-
Brown-Séquard syndrome is a neurological strate a loss of proprioception, fine tactual
condition in which, as a result of a lesion discrimination, and vibratory sense below the
affecting one half of the spinal cord, there is level of the lesion on that same side. Finally,
paralysis and loss of proprioception, vibration, as a result of a disruption of the ascending
and fine tactile discrimination on one side of spinothalamic tracts, there will be a loss of
the body and loss of pain and temperature on pain and temperature. However, because these
the other. latter tracts represent sensory information that
has crossed over from the opposite side of the
cord, the loss of pain and temperature will be
Current Knowledge contralateral to the lesion (and one of the sides
opposite to the motor and posterior column
To fully appreciate this syndrome, it is helpful to symptoms). Because the fibers carrying signals
understand some basic anatomy of the spinal cord. for pain and temperature ascend and descend a
Recall that the lateral corticospinal tract, which couple of spinal segments before decussating,
carries voluntary motor impulses originating in the level of loss of pain and temperature will
the cortex, descends in the lateral portion of the be slightly below that of proprioception and
cord after having crossed the midline (decussated) stereognosis.
in the medulla. On the sensory side, fibers that A Brown-Séquard syndrome usually results
mediate position sense (proprioception), fine tac- from a penetrating injury as might be found in a
tual discrimination (stereognosis), and vibration knife or bullet wound. Because such wounds lack
enter the cord through the dorsal nerve roots and, anatomical precision, exactly one half of the cord
without synapsing, travel up the same side of the is rarely severed, but the term is applied if the
cord from which they enter (via the posterior clinical picture generally matches that which was
columns or lemniscal system) until they synapse described above.
in the medulla. By contrast, those dorsal root
(sensory) fibers that carry information regarding
pain and temperature synapse in the dorsal horn of Cross-References
the cord on the same side in which they entered.
From there, their second-order neurons cross the ▶ Anterolateral System
midline of the cord in the ventral while ▶ Posterior Columns
Brunel Balance Assessment 649

Reliability: Test-retest reliability was assessed

Brunel Balance Assessment using observations on consecutive days, while
inter-rater reliability was assessed using two
Tamara Bushnik independent raters. There was 100% agreement for
Inter-Hospital Research and Knowledge both forms of reliability (Tyson and DeSouza 2004). B
Translation, Rusk Rehabilitation, New York, Validity: Criterion validity was assessed by
NY, USA comparison with the sitting section of the Motor
Assessment Scale (sitting balance), the Berg Bal-
ance Test (standing balance), and the Rivermead
Synonyms Mobility Index (stepping balance/functional
mobility). The correlation coefficients were 0.83
BBA (Motor Assessment Scale), 0.97 (Berg Balance
Test), and 0.95 (Rivermead Mobility Index).
Predictive validity was assessed by comparing
Definition BBA scores during in-hospital admission within
2–4 weeks after stroke to scores on the Barthel
The Brunel Balance Assessment (BBA) clinical Index and Rivermead Mobility Index at 3 months
assessment tool is designed as an outcome poststroke in 102 individuals (Tyson et al. 2007).
measure to assess balance before and after Individuals who had limited sitting balance during
stroke physiotherapy interventions. It consists of hospitalization showed little recovery of func-
12 items that progress from easy to difficult in a tional mobility independence. Individuals who
hierarchical manner to form an ordinal scale. The were able to walk (with or without assistive equip-
easiest item is “static sitting balance with upper ment) during hospitalization were mostly inde-
limb support”; a mid-range item is “dynamic stand- pendent at 3 months poststroke in transfers,
ing balance”; the hardest item is “advanced change walking, and stairs. For those individuals with
of the base of support.” Each item is assessed by limited standing balance during hospitalization,
evaluating performance on a specific task with task- the majority regained the ability to walk, conduct
specific criteria for succeeding; for example, transfers, and navigate stairs, although more of
dynamic standing balance is assessed by evaluating these individuals required assistance.
the distance that the individual can reach beyond Minimal Clinically Important Difference
arm’s length. Success at this task is set at a mini- (MCID): Due to the hierarchical nature of the
mum reach of 7 cm. Each item is scored using scale, the MCID is considered to be a change of
a pass/fail criteria based upon task-specific one level.
performance or time standards. The BBA items
are arranged into three subscales which can be
used individually: sitting, standing, and stepping Cross-References
balance.
▶ Barthel Index
▶ Berg Balance Scale
Current Knowledge ▶ Motor Assessment Scale
▶ Rivermead Mobility Index
Homogeneity of the scale: All items have item-
total correlations of more than 0.20. Cronbach’s
alpha, a measure of internal consistency, was References and Readings
0.93 (Tyson and DeSouza 2004). Therefore, the
Tyson, S. F., & Connell, L. A. (2009). How to measure
scale was deemed homogeneous and internally balance in clinical practice. A systematic review of
consistent. the psychometrics and clinical utility of measures of
650 Bulimia Nervosa

balance activity for neurological conditions. Clinical Current Knowledge

Rehabilitation, 23, 824–840.
Tyson, S. F., & DeSouza, L. H. (2004). Development of the
Brunel Balance Assessment: A new measure of balance Development and Course
disability post stroke. Clinical Rehabilitation, 18, The development of bulimia nervosa is com-
801–810. mon during adolescence and young adulthood
Tyson, S. F., Hanley, M., Chillala, J., Selley, A. B., & and is often associated with stressful life events
Tallis, R. C. (2007). The relationship between balance,
disability, and recovery after stroke: Predictive validity or the occurrence of binge eating behavior dur-
of the Brunel Balance Assessment. Neurorehabilitation ing or following a period of dieting. The disor-
and Neural Repair, 21, 341–346. der is 10 times more common in females than
males, with a prevalence of approximately
1–3% (APA 2013). Risk of suicidal ideation
or behaviors is greater in individuals with this
Bulimia Nervosa disorder.

Kristin M. Graham Associated Features and Current Research

Department of Physical Medicine and Individuals with bulimia nervosa are typically
Rehabilitation, Virginia Commonwealth within the normal weight to overweight range
University, Richmond, VA, USA (body mass index 18.5 and <30). The disorder
can produce a number of medical problems,
including amenorrhea, electrolyte imbalance,
Synonyms and gastrointestinal dysfunction, and there is a
significant risk of mortality. A wide range of func-
Bulimia tional limitations, such as social disturbances, are
associated with bulimia nervosa. Additionally, stud-
Definition ies have identified neuropsychological impairments
in the areas of attention and executive functioning
Bulimia nervosa is defined in the Diagnostic and that are associated with bulimia nervosa (Lauer
Statistical Manual of Mental Disorders (5th ed.; 2002). Common comorbid conditions include
DSM-5; American Psychiatric Association 2013) mood disorders, anxiety disorders, substance
as a feeding and eating disorder characterized by abuse, and personality disorders (most commonly
episodes of binge eating that occur during a dis- borderline personality disorder).
crete period of time and are accompanied by a
sense of lack of control. Behaviors to expel Assessment and Treatment
food eaten (e.g., self-induced vomiting, laxatives) Diagnosis typically involves psychiatric assess-
and/or restrictive caloric intake behaviors typi- ment, physical examination, and laboratory test-
cally follow binge eating episodes. Additionally, ing for associated medical conditions. Course of
individuals engage in inappropriate behaviors to treatment is also impacted by the information
prevent weight gain, and self-evaluation is dispro- gathered in the diagnostic phase, as well as factors
portionately influenced by body shape and such as interpersonal history and functioning,
weight. Individuals typically experience fear of medical and psychiatric comorbidity, and previ-
gaining weight and a desire to lose weight, as is ous treatment attempts. Treatment often combines
common in anorexia nervosa. pharmacological (e.g., antidepressants) and psy-
chological interventions. Cognitive behavioral
therapy has emerged as the superior treatment
Categorization approach (McGilley and Pryor 1998). Differential
diagnoses include anorexia nervosa, binge eating
The disorder is classified with the Feeding and disorder, major depression, and borderline per-
Eating Disorders in DSM-5. sonality disorder.
Bupropion 651

See Also Class

▶ Anorexia Nervosa Antidepressants, smoking cessation aids, and

▶ Binge-Eating Disorder dopamine reuptake inhibitors
▶ Body Dysmorphic Disorder B
▶ Feeding and Eating Disorders
▶ Rumination Disorder Proposed Mechanism(s) of Action

Increases norepinephrine/noradrenaline and

References and Readings dopamine, blocks norepinephrine reuptake
pump, may increase dopamine neurotransmission
American Psychiatric Association. (2013). Diagnostic and in the frontal cortex, and blocks dopamine
statistical manual of mental disorders (DSM-5 ®).
reuptake pump.
Washington, DC: American Psychiatric Association.
Jenkins, P. E., Luck, A., Cardy, J., & Staniford, J. (2016).
How useful is the DSM-5 severity indicator in bulimia
nervosa? A clinical study including a measure of Indication
impairment. Psychiatry Research, 246, 366–369.
Lauer, C. J. (2002). Neuropsychological findings in eating
disorders. In Biological psychiatry (pp. 1167–1172). Major depressive disorder, seasonal affective dis-
New York: Wiley. order, and smoking cessation.
McGilley, B. M., & Pryor, T. L. (1998). Assessment and
treatment of bulimia nervosa. American Family Physi-
cian, 57(11), 2743–2750.
Wonderlich, S. A., Peterson, C. B., Crosby, R. D., Smith, T. Off-Label Use
L., Klein, M. H., Mitchell, J. E., & Crow, S. J. (2014).
A randomized controlled comparison of integrative
cognitive-affective therapy (ICAT) and enhanced cog- Bipolar disorder, ADHD, and neuropathic pain.
nitive-behavioral therapy (CBT-E) for bulimia nervosa.
Psychological Medicine, 44(03), 543–553.
Side Effects

Serious
Bupropion Seizures, hypomania, induction of mania, and
activation of suicidal ideation (controversial).
Cristy Akins1 and Efrain Antonio Gonzalez2,3
1
Mercy Family Center, Metarie, LA, USA
2
College of Psychology, Nova Southeastern
University, Fort Lauderdale, FL, USA Common
3
Utah State University, Logan, UT, USA
Dry mouth, constipation, nausea, weight loss,
insomnia, dizziness, headache, agitation, tremor,
Generic Name abdominal pain, tinnitus, tremor, palpitation,
anorexia, urinary frequency, and sweating.
Bupropion, Bupropion hydrobromide

References and Readings

Brand Name
Physicians’ Desk Reference (71st ed.). (2017). Montvale:
Thomson PDR.
Wellbutrin, Wellbutrin SR, Wellbutrin XL,
Stahl, S. M. (2007). Essential psychopharmacology: The
Zyban, Aplenzin, Buproban, Budeprion SR, and prescriber’s guide (2nd ed.). New York: Cambridge
Forfivo XL University Press.
652 Burden of Proof

Additional Information appellate courts when reviewing trial court

Centerwatch: https://www.centerwatch.com/drug- records. Under the current Mental Penal Code
information/fda-approved-drugs/drug/986/aplenzin-
standard for insanity, “The defendant has the bur-
bupropion-hydrobromide.
Drug Interaction Effects: http://www.drugs.com/drug_ den of providing the defense of insanity by clear
interactions.html. and convincing evidence.”
Drug Molecule Images: http://www.worldofmolecules.
com/drugs/.
Free Drug Online and PDA Software: www.epocrates.com.
Free Drug Online and PDA Software: www.medscape.com. Cross-References
Gene-Based Estimate of Drug interactions: http://
mhc.daytondcs.com:8080/cgibin/ddiD4?ver=4&task= ▶ Beyond a Reasonable Doubt
getDrugList.
▶ Clear and Convincing Evidence
Pill Identification: http://www.drugs.com/pill_identifica
tion.html. ▶ Preponderance of the Evidence

References and Readings

Burden of Proof Denney, R. L. (2005). Criminal forensic neuropsychology
and assessment of competency. In G. Larrabee (Ed.),
Moira C. Dux Forensic neuropsychology: A scientific approach.
New York: Oxford University Press.
US Department of Veteran Affairs, Baltimore,
Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin, C.
MD, USA (2007). Psychological evaluations for the courts:
A handbook for mental health professionals and law-
yers (3rd ed.). New York: Guilford Press.
Synonyms

Standards of proof
Buspirone

Efrain Antonio Gonzalez

Definition
College of Psychology, Nova Southeastern
University, Fort Lauderdale, FL, USA
This refers to the duty to provide evidence for
Utah State University, Logan, UT, USA
allegations raised in the context of legal action.
The standard of proof is the degree of proof
needed in a legal action to persuade the court
Generic Name
(e.g., judge or jury) that a given allegation is
indeed founded or true. There are three main
Buspirone
types of standards of proof: beyond a reasonable
doubt, clear and convincing evidence, and a pre-
ponderance of the evidence. Artificial percentages
have been associated with each of these standards Brand Name
of proof with beyond reasonable doubt coinciding
with 90–95% certainty, clear and convincing evi- BuSpar, Buspirex, Bustab, and Linbuspirone
dence of 75%, and a preponderance of the evi-
dence associated with just over 50%. Each of
these standards is used during different inquiries Class
in criminal procedure (e.g., insanity defense, com-
petency to stand trial, and competency to be exe- Antianxiety agents, anxiolytics, and
cuted), and there are other standards used by nonbenzodiazepines
Butters, Nelson (1937–1995) 653

Proposed Mechanism(s) of Action

Butters, Nelson (1937–1995)
Serotonin 1A partial agonist, thus diminishing the
overall serotonergic activity at those receptor Meryl A. Butters and James T. Becker
sites. Department of Psychiatry, University of B
Pittsburgh School of Medicine, WPIC, Pittsburgh,
PA, USA
Indication

Anxiety disorders.
Major Appointments

• NIMH Postdoctoral Research Fellow at the

Neuropsychology Section of NIMH, Bethesda,
Off-Label Use MD (1964–1966)
• Instructor, College of General Studies, George
Mixed anxiety and depression, treatment-resistant Washington University (1965–1966)
depression, and smoking cessation. • Assistant Professor, Ohio State University
(1966–1967)
• Lecturer in Psychology, Antioch College
Side Effects (1966–1967)
• Lecturer in Psychology, Wellesley College
Serious (1967–1968)
Very rare cardiac symptoms. • Lecturer in Psychology, University of Massa-
chusetts (Boston) (1967–1983)
• Research Career Scientist, Boston Veterans
Common
Administration Medical Center (1967–1983)
Dizziness, sedation, nervousness, and nausea.
• Professor of Neurology (Neuropsychology),
Boston University School of Medicine
(1967–1983)
References and Readings • Senior Lecturer, Northeastern University, Uni-
versity College (1967–1983)
Physicians’ Desk Reference (71st ed.). (2017). Montvale: • Affiliate Professor of Psychology, Clark Uni-
Thomson PDR. versity (1973–1983)
Stahl, S. M. (2007). Essential psychopharmacology: The
prescriber’s guide (2nd ed.). New York: Cambridge • Chief, Psychology Service, San Diego Depart-
University Press. ment of Veteran Affairs Medical Center
(1983–1995)
• Professor of Psychiatry, University of California
Additional Information
School of Medicine (San Diego) (1983–1995)
Drug Interaction Effects: http://www.drugs.com/drug_
interactions.html.
Drug Molecule Images: http://www.worldofmolecules.
com/drugs/. Major Honors and Awards
Free Drug Online and PDA Software: www.epocrates.
com.
Free Drug Online and PDA Software: www.medscape. • Phi Beta Kappa, Summa Cum Laude, A.B..
com. with Honors
Gene-Based Estimate of Drug interactions: http:// • NIH Predoctoral Research Fellowship
mhc.daytondcs.com:8080/cgibin/ddiD4?ver=4&task=
(1961–1964)
getDrugList.
Pill Identification: http://www.drugs.com/pill_identifica • NIMH Postdoctoral Research Fellowship
tion.html. (1964–1966)
654 Butters, Nelson (1937–1995)

• Member of the Collegium of the Distinguished practicing clinicians. He was especially proud
Alumni of the College of Liberal Arts of Bos- of this “cross-professional” appeal.
ton University (elected 1974) • Butters’ earliest work was conducted in pri-
• Fellow, American Association for the mates. Two tests in particular could reveal
Advancement of Science memory loss in monkeys – the delayed
• American Psychological Association (Fellow response (DR) and delayed alternation
Divisions 3, 6, 40; President of Division (DA) tasks. For both DR and DA, the animals
40 1982–1983; Representative to APA Council had to hold information in memory for a short
1990–1992) time before making a response to obtain a
• International Neuropsychological Society reward. Lesions in the prefrontal cortex, in
(Secretary-Treasurer 1974–1977; Board of particular along the sulcus principalis, severely
Governors 1978–1981; Treasurer 1980–1983; disrupted the monkeys’ ability to either per-
President, 1984–1985) form or learn the tasks. In 1969, Butters, in
• National Academy of Neuropsychology collaboration with Deepak Pandya, demon-
(Fellow; President 1992–1993) strated that the middle third of the sulcus
• American Psychological Society (Fellow, principalis was the critical region associated
1988) with impairments of DR and DA. In 1971,
• American Board of Clinical Neuropsychology they described functional differentiation along
(Founding Fellow, Vice-President 1991–1993) the axis of the sulcus principalis; the middle
• Distinguished Clinical Neuropsychologist third differed from the anterior and posterior
Award from the National Academy of Neuro- portions with regard to their efferent
psychology (1991) (outgoing) projections of the prefrontal cortex.
• Meritorious Service Award from the Depart- In 1972, with their student Gary Van Hoesen,
ment of Veteran Affairs (1993) they reported on the afferent (incoming) pro-
• Distinguished Service Award from the Ameri- jections to the entorhinal cortex around the
can Board of Professional Psychology (1993) hippocampus – another brain region critical
for memory functions.
• At the same time, Butters was working closely
Landmark Clinical, Scientific, and with Donald Stein and Jeffrey Rosen on
Professional Contributions recovery of function following frontal lobe
lesions in nonhuman primates. They showed
• Nelson Butters authored or coauthored over that if one removed sections of the frontal
200 peer-reviewed scientific articles, 60 invited lobes in monkeys in serial fashion, that is,
monographs and book chapters, and reams over a series of operations, the resulting def-
of abstracts. He coedited or coauthored six icit was less than that exhibited by monkeys
books and delivered a multitude of invited who experienced the same lesion, in one step.
lectures and presentations. Butters expended They concluded that these results demon-
much professional energy demonstrating the strated at least partial recovery of function.
existence of distinct dissociations among This finding in adult monkeys was important
cognitive functions, especially memory, within because, at the time, it was believed that if a
and between patients with various forms of brain lesion occurred after 12 months of age
cerebral dysfunction. He was unusually suc- (in the monkey), recovery was not possible.
cessful (perhaps uniquely so) at integrating Patricia Goldman was showing that infant
neuroanatomy and cognitive theory with macaques with brain lesions could fully
applied neuropsychology. As a result, one of recover some functions, but not others – the
the most distinguishing features of his career data from the Rosen, Stein, and Butters series
was that his work was very highly regarded by shed light on the question of whether, and by
cognitive and clinical researchers as well as how much, older animals (and by extension,
Butters, Nelson (1937–1995) 655

humans) could recover function after a brain psychologists were debating the relative merits
lesion. of serial versus parallel processing in normal
• One of his earliest human studies (published human memory. Butters’ work with Laird
with Melvin Barton in 1970) on the role of Cermak on patients with amnesic disorders
the frontal and parietal lobes in concrete oper- was among the first to examine this and other B
ations shaped much of Butters’ philosophy of central topics of cognitive psychological
neuropsychology and laid the groundwork research. The Butters and Cermak collabora-
for his career examining the brain structures tion was particularly fruitful because it directly
that mediate abnormal cognition. They took influenced the development of models of nor-
concepts and methods that were popular in mal human memory – particularly the notion
human cognition at that time and used them that memory is neither a serial nor parallel
to examine the role of various brain structures process but rather that the type or intensity of
in these cognitive processes. For example, the processing was what was critical (i.e.,
humans with damage to the parietal lobes “levels of processing” argument espoused by
have difficulty reversing – or changing – their Fergus Craik).
behavior. That is, once taught a rule, they have • While in Boston, Butters and his colleagues
difficulty deviating from that rule. What was made great strides in elucidating the neuropsy-
unclear at the time was whether this deficit was chological effects of alcoholism. The papers
a fundamental deficit in reversal or a conse- that emanated from studies of chronic, non-
quence of a deficit in retention – the ability to amnestic alcoholics (in collaboration with
remember the old rule or learn the new one. Christopher Ryan, James Becker, Kathleen
The results of these experiments not only Montgomery, and Barbara Jones) had a lasting
informed investigators on the nature of the influence on the way that the neuropsychology
behavioral and cognitive changes that follow of alcoholism was viewed and studied. Butters’
focal brain damage but lent insight into the work also focused on the amnesic syndrome
cognitive processes themselves. associated with chronic, severe alcoholism.
• Butters made exemplary use of what Hans- With Laird Cermak, his systematic series of
Lukas Teuber referred to as the “natural frac- studies focused on the role of interference and
ture lines of behavior.” That is, when a patient encoding in the short-term memory defects of
suffers a brain injury, behavior and cognition patients with alcoholic Korsakoff’s syndrome.
fail neither completely nor in a random man- It is noteworthy that Butters developed per-
ner. Rather, the breakdown occurs at points sonal relationships with many of these patients,
where different cognitive processes intersect. venturing out to their homes (sometimes state
By comparing and contrasting the nature and hospitals or nursing homes) and repeatedly
extent of changes in cognition across patients reevaluating them for different projects. This
with different forms of brain damage, we work was important not only because of what it
advance our understanding of the neuroana- revealed about both normal and pathological
tomical basis of the cognitive process in ques- memory but also because it clearly demon-
tion, the organization of the process itself, and strated that a long-term consequence of alco-
how these affect the individual patient. This holism can be an amnestic disorder (a matter
concept became a theme – sometimes explicit that was hotly debated at the time). Perhaps the
and sometimes implicit – that was woven into most enduring legacy of Butters and Cermak’s
the fabric of Butters’ research career. work from this period was the 1980 publication
• An early series of studies in the 1970s with Ina of Alcoholic Korsakoff’s Syndrome: An Infor-
Samuels exemplified this approach. Together mation Processing Approach to Amnesia. The
they systematically examined visual and audi- title was not an accident – they wanted to
tory short-term memory in individuals with a emphasize the role of neuropsychology in ana-
variety of lesions. In the early 1970s, cognitive lyzing information processing and how this
656 Butters, Nelson (1937–1995)

research informed our models of normal mem- he relished the opportunity to develop a clini-
ory and memory systems. The publication of cal service with neuropsychologists who
this text marked the beginning of the modern conducted research as well as provided clinical
era of “cognitive neuroscience.” care. In addition to developing a first-rate psy-
• Another trend in Butters’ research during the chology service, Butters maintained his pro-
middle to late 1970s was prompted by his lific research publication rate. Soon after
desire to better understand retrograde amnesia, arriving in San Diego, UCSD was designated
which had not yet been studied in any system- an Alzheimer’s Disease Research Center,
atic way, due, in part, to the lack of suitable test which provided Butters with the opportunity
instruments. He collaborated with Marilyn to expand his research on memory. His studies
Albert, who took on the task of developing now included Alzheimer’s disease, which he
the Boston Retrograde Amnesia Battery, considered the prototypical “cortical” demen-
which became the first carefully validated and tia. In San Diego his work with David Salmon,
well-normed retrograde memory battery William Heindel, William Beatty, Munro
applicable to individuals of various ages. This Cullum, Eric Granholm, Alexander Troster,
productive collaboration, which later included Agnes Chan, Andreas Monsch, and a host of
Jason Brandt and Donald Stuss, firmly other students and colleagues focused on three
established that the retrograde memory impair- main areas, yielding a significant scientific
ment exhibited by Korsakoff’s patients had a contribution in each.
clear temporal gradient, suggesting that the • Butters’ work with David Salmon and their
neural substrates of memory change with the colleagues demonstrated that the memory dis-
passage of time. That is, over time, episodic orders of cortical and subcortical dementias
memories mediated by the hippocampal cir- are dissociable, with Alzheimer’s disease
cuitry are actively recalled, thereby losing characterized by poor consolidation and rapid
their spatial and temporal markers, becoming forgetting due to limbic damage and
part of semantic memory, stored elsewhere Huntington’s disease by poor retrieval associ-
(likely the temporal-parietal association ated with fronto-striatal dysfunction. Butters’
cortices). work with trainee Mark Bondi and others in
• During his last years in Boston, Butters his research group was among the first to show
devoted considerable time to studying the that the neuropsychological characteristics of
cognitive effects of Huntington’s disease very early Alzheimer’s disease differed from
(HD), demonstrating a functional dissociation the benign cognitive changes of normal aging
between the locus of the lesions in HD (the and could therefore be used for the early and
basal ganglia) and those found in Korsakoff’s even preclinical detection of the disease, pre-
syndrome (the limbic system). This research saging similar findings in HD. Finally,
predated the identification of the HD gene researchers were beginning to investigate the
and development of a test to determine whether phenomenon of implicit memory, and Butters’
the offspring of HD patients were destined to work with William Heindel, David Salmon,
develop the disease. As part of the “Center Jane Paulsen, and others showed that various
Without Walls,” Butters worked with people forms of implicit memory could be dissociated
“at risk” for HD (i.e., who had a parent with in Alzheimer’s disease, Huntington’s disease,
the disease) to determine whether measures of and Parkinson’s disease. These studies were
cognition administered earlier in life could the first to dissociate priming and procedural
predict those who would ultimately develop learning in the brain, showing that procedural
the disease. learning deficits were associated with basal
• In 1983 Butters accepted an offer to join ganglia dysfunction while priming deficits
the Department of Psychiatry at the University were linked with neocortical damage that
of California-San Diego (UCSD), where occurs in Alzheimer’s disease. Any one of
Butters, Nelson (1937–1995) 657

these contributions would have been impres- • Butters was blunt, brash, and famously irrev-
sive; together they represent a truly remarkable erent. While his lifestyle was decidedly main-
accomplishment. stream, he reveled in characterizing himself
• In 1986 the American Psychological Associa- as something of a rebel. He was unendingly
tion (APA) acquired the journal Neuropsychol- curious about those who walked to the beat of B
ogy, and Butters was appointed editor. APA a different drummer. His personal role models
tradition allows new editors to choose the included Marlon Brando, Lenny Bruce, and
colors of the journal’s binding – and Butters Woody Allen. He had a keen sense for and
chose a white background with (Boston) Celtic appreciation of the absurd and ironic and
green for the text (he was a lifelong fan of his found humor in the darker side of life, though
hometown basketball team). Butters’ goal he never took himself too seriously. On more
for the journal was that it should become one than one occasion, he was heard saying:
of the journals of record for basic, applied, and “If I hadn’t become a neuropsychologist,
clinical research in neuropsychology. This will I would’ve been a comedian.” At every APA
be another of his lasting legacies. and INS meeting social hour, Butters could be
• Most important to Butters were his students – found, beer in hand, listening to and recounting
his academic children (and in some cases hilarious stories about friends, colleagues, and
grandchildren) were almost as important to family. Most of the time, he played a leading
him as his biological children, Meryl, Paul, role in these comedic tales. In sum, Butters’
and Lisa. His attraction was international rare combination of intellectual creativity,
(e.g., John Hodges, Narinder Kapur, Matti drive, irreverence, and appreciation of satire
Laine), and his mentees continue to lead the allowed him to make his mark both in the
field (e.g., Kathie Welsh-Bohmer, Terry field of neuropsychology and in the hearts of
Jernigan). his contemporaries.
• A narrative of Butters’ contributions to neu-
ropsychology would be woefully incomplete
without a personal description. He possessed Short Biography
tremendous internal drive and held both his
students and colleagues to the high standards Nelson Butters was born on May 7, 1937, in
he applied to himself. Every Butters’ student Boston, MA. He initially attended public school
carries distinct memories of the red ink and in Brookline, MA, and then Worcester Academy,
blunt reviews accompanying their manuscript a private boarding school, graduating first in his
drafts. His academic rigor notwithstanding, class. He was an accomplished athlete and
Butters was universally known as an scholar. A concussion sustained playing football
involved, supportive mentor and colleague. left him with lifelong anosmia, an irony not lost on
His role extended to that of job broker, and him when he later published articles on the impor-
he devoted an inordinate amount of time and tance of assessing olfaction in brain-damaged
energy to assisting and advising a vast array patients. In addition to his obvious academic
of students and colleagues about both profes- talent, he took great pride in his carefully crafted
sional and personal matters. He was image as a motor scooter-riding “bad boy,” emu-
described as being biologically incapable of lating James Dean and Marlon Brando. Later
tolerating an unhappy “student” (a term that in life, he took great pleasure in recounting tales
he applied quite broadly); he had to help of his friendship with his classmate, the late social
make things right (even if the student did and political activist Abbie Hoffman. Butters par-
not immediately appreciate his wisdom). In ticularly enjoyed retelling stories of “drag racing”
his later years, he took tremendous pleasure against Hoffman from Worcester to Boston, MA,
in referring to himself as the “Godfather of and attending wild parties at Hoffman’s home.
Neuropsychology.” Somehow surviving high school, he went on to
658 Butters, Nelson (1937–1995)

attend the University of Chicago and Boston caught the attention of Harold Goodglass and
University. Norman Geschwind of the Boston Veterans
Butters was at first unsure of his professional Administration Hospital and Department of
goals. His parents had pushed for him to become Neurology of the Boston University School of
a physician or lawyer, but neither profession held Medicine. Moreover, Butters and Goodglass had
much appeal. Public speaking came rather easily become acquainted during the former’s years at
to him, and he was excited by the idea of being Clark. The personal relationship, combined with
a positive influence in the lives of college stu- Butters’ cutting-edge animal work, led to an invi-
dents. Therefore, during the second or third year tation from Geschwind and Goodglass to join
of college, he decided to become a psychology their burgeoning Aphasia Research Center.
teacher. Butters eagerly accepted the opportunity to join
Butters entered the doctoral program in psy- this exciting group and to return home to Boston.
chology at Clark University in the fall of 1960. While he initially studied nonhuman primates,
At the time Clark had one of the leading psychol- he took the opportunity to learn about human
ogy programs in the world. He was awarded a neuropsychology from the early pioneers, many
Woodrow Wilson Fellowship for his first year of of whom resided in Boston. In addition to
graduate school because of his commitment to Geschwind and Goodglass, he reveled in learning
college teaching. During his second or third year from and exchanging ideas with the likes of
in graduate school, he ran across a research article Edith Kaplan, Marlene Oscar Berman, Howard
by Mortimer Mishkin and H. Enger Rosvold Gardner, Edgar Zurif, and many others. The
about delayed alternation, reversal learning, and unparalleled atmosphere at the Boston VA Hospi-
the frontal lobes in monkeys. Butters became fas- tal led to Butters’ first studies in human neuropsy-
cinated with the concept that one could examine chology. During 1967–1970 he conducted both
the neurological structures that underlie cognitive animal and human research, and after 1970 his
and psychological processes. At the time he was work focused exclusively on human cognition.
particularly interested in what went on in the brain In 1983 Butters moved to San Diego, CA, to
and what brain structures played a part in the join the Department of Psychiatry at UCSD,
development of concrete or formal operations where he continued to flourish. Continuing his
in the thinking processes of children. research program, Butters also built a psychology
At the end of his third year of graduate school, service with a particular emphasis on training.
Butters wrote to Hal Rosvold, a researcher at He surrounded himself with superb colleagues
the National Institutes of Health (NIH), asking including, among others, Robert Heaton and
whether he would consider taking him as a post- Dean Delis.
doctoral fellow. A visit to Rosvold’s lab led to a In early 1993 Butters developed oral motor
postdoctoral fellowship with Rosvold and Mis- weakness, and by March 1993 it was clear that
hkin from 1964 to 1966. His work at the NIH he had amyotrophic lateral sclerosis. He was
focused on the roles of the septal nuclei, basal 55 years old and at the height of his career.
forebrain, and caudate nucleus in reversal learning He handled his nearly 3-year battle with ALS in
and delayed alternation performance. Butters was typical Butters fashion, continuing to work and
fulfilling his plan to spend “a couple of years” socialize until the week before his death. He took
studying physiological psychology and perhaps the opportunity to tell his students, colleagues,
do “a few studies” on the neurological bases and family how grateful he was to have had
of cognition before resuming the path toward his them in his life. When he lost the ability to
teaching career. speak, he used adaptive computer equipment to
Butters resumed his teaching path in 1966 by communicate. The week before he died, he was
taking teaching positions at Wright State Univer- still telling off-color and self-deprecating jokes by
sity and Antioch College in Ohio. However, the laboriously typing with his big toe, irreverent and
“few studies” he had conducted while at NIH irrepressible until the end.
Butters, Nelson (1937–1995) 659

Cross-References prominence: Reflections of 20th century neuropsychol-

ogists. New York: Psychology Press.
Butters, N., & Cermak, L. S. (1974). The role of cognitive
▶ Alzheimer’s Disease factors in the memory disorders of alcoholic patients
▶ Amnesia with the Korsakoff syndrome. Annals of the New York
▶ Amnestic Disorder Academy of Sciences, 233, 61–75. PMID: 4523804. B
▶ Amnestic Syndromes Butters, N., & Pandya, D. (1969). Retention of delayed-
alternation: Effect of selective lesions of sulcus
▶ Anterograde Amnesia principalis. Science, 165(3899), 1271–1273. PMID:
▶ Dementia 4979528.
▶ Episodic Memory Butters, N., & Rosvold, H. E. (1968). Effect of caudate and
▶ Goodglass, Harold (1920–2002) septal nuclei lesions on resistance to extinction
and delayed-alternation. Journal of Comparative and
▶ Implicit Memory Physiological Psychology, 65(3), 397–403. PMID:
▶ Kaplan, Edith (1924–2009) 4970002.
▶ Korsakoff’s Syndrome Butters, N., Lewis, R., Cermak, L. S., & Goodglass,
▶ Mammillary Bodies H. (1973). Material-specific memory deficits in alco-
holic Korsakoff patients. Neuropsychologia, 11(3),
▶ Medial Temporal Lobe 291–299. PMID: 4792180.
▶ Memory Butters, N., Tarlow, S., Cermak, L. S., & Sax, D. (1976).
▶ Memory Impairment A comparison of the information processing deficits of
▶ Mishkin, Mortimer (1926–) patients with Huntington’s chorea and Korsakoff’s syn-
drome. Cortex, 12(2), 134–144. PMID: 133786.
▶ Parkinson’s Dementia Butters, N., Wolfe, J., Martone, M., Granholm, E., &
▶ Parkinson’s Disease Cermak, L. S. (1985). Memory disorders associated
▶ Procedural Memory with Huntington’s disease: Verbal recall, verbal recog-
▶ Retrograde Amnesia nition and procedural memory. Neuropsychologia,
23(6), 729–743. PMID: 2934642.
▶ Semantic Memory Butters, N., Granholm, E., Salmon, D. P., Grant, I., &
▶ Subcortical Dementia Wolfe, J. (1987). Episodic and semantic memory:
▶ Temporal Lobe A comparison of amnesic and demented patients. Jour-
▶ Thalamus nal of Clinical and Experimental Neuropsychology,
9(5), 479–497. PMID: 2959682.
Butters, M., Becker, J. T., & Brandt, J. (1996). A legend in his
own time: tribute to Nelson Butters, in Nelson Butters
remembered. APA Division 40 Newsletter, 14(3), 2, 7–8.
References and Readings Cermak, L. S. (Ed.). (1994). Neuropsychological explora-
tions of memory and cognition: Essays in honor of
Albert, M. S., Butters, N., & Brandt, J. (1981). Patterns Nelson Butters. New York: Plenum.
of remote memory in amnesic and demented patients. Chan, A. S., Butters, N., Paulsen, J. S., Salmon, D. P.,
Archives of Neurology, 38(8), 495–500. PMID: Swenson, M. R., & Maloney, L. T. (1993). An assess-
6454407. ment of the semantic network in patients with
Brandt, J., Butters, N., Ryan, C., & Bayog, R. (1983). Cog- Alzheimer’s disease. Journal of Cognitive Neurosci-
nitive loss and recovery in long-term alcohol abusers. ence, 5(2), 254–261. https://doi.org/10.1162/
Archives of General Psychiatry, 40(4), 435–442. jocn.1993.5.2.254. PMID: 23972157.
Butters, N. (1966). The effect of LSD-25 on spatial and Granholm, E., & Butters, N. (1988). Associative encoding
stimulus perseverative tendencies in rats. Psychophar- and retrieval in Alzheimer’s and Huntington’s disease.
macologia, 8(6), 454–460. Brain and Cognition, 7(3), 335–347. PMID: 2969744.
Butters, N. (1984). The clinical aspects of memory disor- Heindel, W. C., Salmon, D. P., Shults, C. W., Walicke,
ders: Contributions from experimental studies of amne- P. A., & Butters, N. (1989). Neuropsychological
sia and dementia. Journal of Clinical Neuropsychology, evidence for multiple implicit memory systems:
6(1), 17–36. PMID: 6230375. A comparison of Alzheimer’s, Huntington’s, and
Butters, N. (1992). Memory remembered: 1970–1991. Parkinson’s disease patients. The Journal of Neurosci-
Archives of Clinical Neuropsychology, 7(4), 285–295. ence, 9(2), 582–587. PMID: 2521896.
PMID:14591284. Hodges, J. R., Salmon, D. P., & Butters, N. (1990). Differ-
Butters, N. (1996). Memoirs, in Nelson Butters remem- ential impairment of semantic and episodic memory in
bered. APA Division 40 Newsletter, 14(3), 1, 3–7. Alzheimer’s and Huntington’s diseases: A controlled
Butters, M. A., & Butters, N. M. (2002). Nelson prospective study. Journal of Neurology, Neurosur-
M. Butters: One step ahead. In A. Y. Stringer, E. L. gery, and Psychiatry, 53(12), 1089–1095. PMID:
Cooley, & A. L. Christensen (Eds.), Pathways to 2149861.
660 Butters, Nelson (1937–1995)

Jernigan, T., & Butters, N. (1989). Neuropsychological and Shimamura, A. P., Salmon, D. P., Squire, L. R., & Butters, N.
neuroradiological distinctions between Alzheimer’s (1987). Memory dysfunction and word priming in
and diseases. Neuropsychology, 3, 283–290. dementia and amnesia. Behavioral Neuroscience,
Moss, M. B., Albert, M. S., Butters, N., & Payne, M. 101(3), 347–351. PMID: 2955793.
(1986). Differential patterns of memory loss among Tröster, A. I., Butters, N., Salmon, D. P., Cullum, C. M.,
patients with Alzheimer’s disease, Huntington’s dis- Jacobs, D., Brandt, J., & White, R. F. (1993). The
ease, and alcoholic Korsakoff’s syndrome. Archives of diagnostic utility of savings scores: Differentiating
Neurology, 43(3), 239–246. PMID: 2936323. Alzheimer’s and Huntington’s diseases with the logical
Rosen, J., Stein, D., & Butters, N. (1971). Recovery of memory and visual reproduction tests. Journal of
function after serial ablation of prefrontal cortex in the Clinical and Experimental Neuropsychology, 15(5),
rhesus monkey. Science, 173(3994), 353–356. PMID: 773–788. PMID: 8276935.
4997798.
C

CADASIL variability among patients, the initial clinical man-

ifestation often begins with migraines with aura
Angela Eastvold1 and Yana Suchy2 and slowly progresses to transient ischemic attacks
1
Department of Neurology, The University of (TIA) and recurrent strokes. The migraine attacks
Utah, Salt Lake City, UT, USA are often reported to be particularly long lasting or
2
Department of Psychology, The University of severe and may even include symptoms of hemi-
Utah, Salt Lake City, UT, USA plegia. The strokes are typically lacunar, occurring
in subcortical white matter or basal ganglia and, in
some cases, in the brain stem and spinal cord.
Synonyms Recurrent subcortical infarcts lead to cognitive
decline, pseudobulbar palsy, motor impairment,
Agnogenic medial arteriopathy; Chronic familial psychiatric symptoms (most commonly depres-
vascular encephalopathy; Familial Binswanger’s sion), and ultimately total motor impairment and
disease; Familial disorder with subcortical ische- subcortical vascular dementia. Cognitive decline is
mic strokes, dementia, and leukoencephalopathy; most prominently seen as executive dysfunction,
Hereditary multi-infarct dementia slowed processing speed, and reduced attentional
abilities. As the disease progresses, memory and
other areas of cognitive functioning begin to
Short Description or Definition decline. The total amount of white matter involve-
ment associated with the lacunar lesions and the
Cerebral autosomal dominant arteriopathy with degree of atrophy predict severity of cognitive and
subcortical infarcts and leukoencephalopathy motor impairment.
(CADASIL) is a rare (prevalence 4.6 per 100,000) Cause: CADASIL is caused by mutations or
autosomal dominant, adult-onset inherited cerebral deletions in the Notch3 gene on chromosome
vascular disease, characterized by migraines, recur- 19, which plays an important role in cell differen-
rent transient ischemic attacks, and strokes leading tiation during development. There is a consider-
to cognitive decline and dementia. able range in the types of deletions or mutations,
with as many as 21 different types identified.
While the pathogenetic mechanism has yet to
Current Knowledge be determined, the resulting pathophysiology
includes thickening of arterial walls, accumula-
Clinical manifestation: The typical age of onset is tion of granular osmiophilic material (GOM) in
30–50 years of age. Although there is considerable arterial walls (this distinguishes it from arterial
# Springer International Publishing AG, part of Springer Nature 2018
J. S. Kreutzer et al. (eds.), Encyclopedia of Clinical Neuropsychology,
https://doi.org/10.1007/978-3-319-57111-9
662 CAGE Questionnaire

hypertension), gradual destruction of vascular

smooth muscle cells leading to fibrosis, progres- CAGE Questionnaire
sive thickening of arterial walls, and narrowing of
the lumen of cerebral arteries. This eventually Myron Goldberg
causes thrombosis, reduced blood flow, destruc- Department of Rehabilitation Medicine,
tion of small- and medium-sized arteries, and University of Washington Medical Center,
consequently focal infarcts. MRI typically reveals Seattle, WA, USA
characteristic periventricular or white matter
hyperintensities, as well as infarcts in the basal
ganglia and brain stem. The cerebral cortex Definition
remains relatively intact.
Diagnosis: Identification of a Notch3 mutation The CAGE is one of a number of brief screening
provides the most certain diagnosis, in addition to instruments designed to help in the detection of
the presence of GOM in arterial walls, which can alcohol misuse. The instrument’s name is an acro-
be detected with a skin biopsy. Positive MRI nym for questions about: Cutting down on drinking;
findings are often detected in even asymptomatic Annoyance at other’s concern about drinking; feel-
individuals. History of particularly severe ing Guilty about drinking; and using alcohol as an
migraines may be the earliest indication. Eye-opener in the morning. The CAGE can be
Treatment and prognosis: Currently, there is no rapidly administered in an interview format or writ-
cure or disease-modifying therapy for CADASIL, ten format and consists of the following four items:
and only symptom management and supportive (1) “Have you ever felt that you should cut down on
care are available for affected individuals. Death your drinking?”; (2) “Have people annoyed you by
typically occurs 10–20 years after the onset of criticizing your drinking?”; (3) “Have you ever felt
symptoms. Angiography and anticoagulants bad or guilty about your drinking?”; and (4) “Have
should be avoided as they may provoke cerebro- you ever had a drink first thing in the morning to
vascular accidents. steady your nerves or to get rid of a hangover
(eye-opener)?” Individual item responses are scored
in a binary fashion (“0” = “no” and “1” = “yes”).
Cross-References The total score can range from 0 to 4. A score of 2 or
greater is typically considered a positive finding,
▶ Binswanger’s Disease that is, an indication of alcohol misuse.
▶ Lacunar Infarction
▶ Small Vessel Ischemic Disease
Historical Background

References and Readings The CAGE was developed by Ewing and Rouse
(1968) for detection of “alcoholism” and was first
Kalaria, R. N., Viitanen, M., Kalimo, H., Dichgans, M., introduced as a formal screening instrument
& Tabira, T. (2004). The pathogenesis of CADASIL: 2 years later (Ewing and Rouse 1970). Final
An update. Journal of Neurological Sciences, 226, item selection for the CAGE was based on exam-
35–39.
ination of 130 randomly selected, general hospital
Kalimo, H., Ruchoux, M. M., Viitanen, M., & Kalaria,
R. N. (2002). CADASIL: A common form of heredi- patients; items selected were those that resulted in
tary arteriopathy causing brain infarcts and dementia. a “minimal” set of items that “usefully divided”
Brain Pathology, 12(3), 371–384. responders into two groups: patients with “alco-
Moreno, F. C., Raxvi, S. S., Davidson, R., & Muir, K. W.
(2014). Changing clinical patterns and increasing prev-
holism” (confirmed by physician impressions and
alence in CADASIL. Acta Neurologica Scandinavica, chart study) and patients without indication of
130(3), 197–203. “alcoholism” (Ewing 1984).
CAGE Questionnaire 663

Over the years, several modifications to the different cutoff scores. The authors concluded
original instrument have been recommended, that the CAGE has “adequate validity” in screen-
including placing a time-frame reference on the ing medical and surgical inpatients, psychiatric
four questions (e.g., in the last year) as well as inpatients, and ambulatory medical patients for
adding questions regarding frequency of use, tol- alcohol misuse and that use of a cutoff score of
erance, and perceived history of drinking prob-
2 affords the best combination of sensitivity,
lems (Bradley et al. 2001; National Institute on specificity, and positive predictive value. At the C
Alcohol Abuse and Alcoholism 1995; McQuade same time, they cautioned that the CAGE has not
et al. 2000). performed well with Caucasian women, prenatal
women, and college students.
Fiellin et al. (2000) also provide a noteworthy
Psychometric Data review of validity studies, concluding that in pri-
mary care settings, the CAGE questionnaire was
Test-retest reliability of the CAGE over a 7-day more effective in identifying patients with alcohol
period was 0.80 in a psychiatric sample and 0.95 abuse or dependency than in detecting patients
in a nonclinical sample (Teitelbaum and Carey with at risk, hazardous, or harmful drinking. In
2000); mean CAGE score changes for each another systematic review of the literature, Berks
group across this same time period were nonsig- and McCormick (2008) reached similar conclu-
nificant. Convergent validity has been reasonably sions regarding the utility of the CAGE in elderly
good, though somewhat variable, with reported primary care populations – i.e., the CAGE is bet-
correlations ranging from 0.48 to 0.70 with other ter in detecting alcohol abuse or dependency
alcohol-screening instruments (see Dhalla and rather than hazardous drinking.
Kopec 2007 for review).
A number of studies have examined the valid-
ity of CAGE in detecting alcohol misuse. Clinical Uses
Aertgeerts et al. (2004) performed a meta-analysis
of ten studies of the utility of the CAGE in The CAGE has enjoyed wide popularity in pri-
detecting alcohol abuse or alcohol dependency mary care settings as an alcohol-screening instru-
in general clinical populations using criteria ment for a number of reasons, as it is brief, easy to
from the Diagnostic and Statistical Manual for administer, and can be incorporated into more
Mental Disorders (DSM-III-R’, APA 1987). extensive interviews or questionnaires (Bradley
With a cutoff score at
2, pooled sensitivities et al. 2001). It has been utilized in a large-scale
across studies were 0.87 in hospital inpatients, prospective study of older persons (Health and
0.71 in primary care patients, and 0.60 in ambu- Retirement Study, 1996–2010) to document alco-
latory medical patients; specificities were 0.77, hol use and its association with outcomes such as
0.91, and 0.92, and positive predictive validities cognitive impairment (Kuzma et al. 2014). It has
were 0.57, 0.74, and 0.82, respectively. Aertgeerts also been incorporated in research with individ-
et al. (2004) concluded that the CAGE is only of uals having neurological conditions (e.g., multiple
“limited value” as a screening instrument using a sclerosis) to document the relationship between
cutoff score of
2 and recommended that addi- alcohol abuse/dependence and emotional distress
tional information about alcohol use patterns be (McKay et al. 2015). However, support for its
obtained from any patient who gives one positive validity across different populations has been
answer on the instrument. mixed. It appears to perform best when used to
Dhalla and Kopec (2007) provided a more screen for alcohol abuse or dependence in clinical
recent review of the CAGE validity literature, populations and less well in detecting current
considering, in part, the sensitivity, specificity, hazardous drinking. Caution should be used espe-
and positive predictive value associated with cially when interpreting results for nonclinical
664 Calcarine Cortex

respondents (i.e., general population) as well as Ewing, J. A. (1984). Detecting alcoholism: The CAGE
for women and college students, as the CAGE questionnaire. Journal of the American Medical
Association, 252, 1905–1907.
has been noted to underperform in these Ewing, J. A., & Rouse, B. A. (1970). Identifying the hidden
populations. In addition, as several authors have alcoholic. Presented at the 29th international
recommended, a positive finding on the CAGE, congress on alcohol and drug dependence, Sydney,
regardless of cutoff score level (i.e.,
1 or 2), 3 Feb 1970.
Fiellin, D., Carrington, R., & O’Conner, P. (2000).
should be followed up by further examination of Screening for alcohol problems in primary care:
alcohol consumption patterns, using established A systematic review. Archives of Internal Medicine,
standard criteria. 160, 1977–1989.
Kuźma, E., Llewellyn, D. J., Langa, K. M., Wallace, R. B.,
& Lang, I. A. (2014). History of alcohol use disorders
and risk of severe cognitive impairment: A 19-year
Cross-References prospective cohort study. The American Journal of
Geriatric Psychiatry, 22(10), 1047–1054.
▶ Alcohol Abuse McKay, K. A., Tremlett, H., Fisk, J. D., Patten, S. B.,
▶ Alcohol Dependence Fiest, K., Berrigan, L., & Marrie, R. A. (2015). Adverse
health behaviours are associated with depression and
▶ Alcoholic Brain Syndrome anxiety in multiple sclerosis: A prospective multisite
▶ Alcoholism study. Multiple Sclerosis Journal. https://doi.org/
▶ Blood Alcohol Level 10.1177/1352458515599073.
▶ Fetal Alcohol Spectrum Disorder National Institute on Alcohol Abuse and Alcoholism
(1995). The physician’s guide to helping patients with
▶ Korsakoff’s Syndrome alcohol problems (NIH publication 95–3769).
▶ Michigan Alcoholism Screen Test Bethesda: U.S. Department of Health and Human Ser-
▶ Substance Abuse vices, Public Health Service, National Institutes of
▶ Substance Use Disorders Health.
Pokorny, A., Miller, B., & Kaplan, H. (1972). The brief
▶ Wernicke-Korsakoff Syndrome MAST: A shortened version of the Michigan Alcohol-
ism Screening Test. American Journal of Psychiatry,
129, 342.
References and Readings Saunders, J. B., Aasland, O. G., Babor, T. F., De La
Fuente, J. R., & Grant, M. (1993). Development of
the alcohol use disorders identification test (AUDIT):
Aertgeerts, B., Buntinx, F., & Kester, A. (2004). The
WHO collaborative project on early detection of per-
value of the CAGE in screening for alcohol abuse and
sons with harmful alcohol consumption-II. Addiction,
alcohol dependence in general clinical populations:
88, 791–804.
A diagnostic meta-analysis. Journal of Clinical
Teitelbaum, L., & Carey, K. (2000). Temporal stability of
Epidemiology, 57, 30–39.
alcohol screening measures in a psychiatric setting.
American Psychiatric Association. (1987). Diagnostic and
Psychology of Addictive Behaviors, 14, 401–404.
statistical manual of mental disorders (3rd rev. ed.).
Washington, DC: American Psychiatric Press.
Berks, J., & McCormick, R. (2008). Screening for
alcohol misuse in elderly primary care patients:
A systematic review. International Psychogeriatrics,
20, 1090–1103.
Calcarine Cortex
Bradley, K., Kiviahan, D., Bush, K., McDonell, M., &
Fihn, S. (2001). Variations on the CAGE alcohol Mary-Ellen Meadows
screening questionnaire: Strengths and limitations in Division of Cognitive and Behavioral Neurology,
VA general medical patients. Alcoholism: Clinical
and Experimental Research, 25, 1472–1478.
Brigham and Women’s Hospital, Boston, MA,
Cherpitel, C. J. (2000). A brief screening instrument for USA
problem drinking in the emergency room: The RAPS4.
Journal of Studies on Alcoholism, 61, 447–449.
Dhalla, S., & Kopec, J. (2007). The CAGE
questionnaire of alcohol misuse: A review of reliability
Synonyms
and validity studies. Clinical & Investigative Medicine,
30, 33–41. Primary visual cortex; Striate cortex
Calcarine Cortex 665

Structure instance, area V2 is important for organizing this

visual information to discrete perceptions and
This is the term for the primary visual cortex, V1, combines both the physical and any illusory com-
or Brodmann’s area 17. The area encompasses ponents. Information is further streamed via trans-
the medial surface and a small lateral surface of mission to the dorsal (where) and the ventral
the occipital lobe and is within the calcarine (what) streams to the parieto-occipital association
sulcus. It is located at the most posterior portion cortex and occipitotemporal association cortices, C
of the cerebral hemisphere. The optic radiations respectively.
terminate in layer IV of the calcarine cortex.
Layer IV is rather thick and is subdivided into
sublaminae. The calcarine cortex is also some- Illness
times referred to as the striate cortex because of a
strip of myelin (stria of Gennari) that can be Our visual system has evolved such that damage
visualized. The area is organized in a retinotopic to one eye does not result in blindness in one
fashion; that is, there is point-to-point represen- visual field. The calcarine cortex is perfused by
tation from the retina to the cortex. For instance, the calcarine artery, which is a limb of the poste-
fibers in the right half of each retina (which rior cerebral artery. Damage to either the right or
perceives information in the left visual field) left calcarine cortex can result via a stroke or by
project to the right calcarine cortex, and fibers other head injury [i.e., projectile (bullet)]. Dam-
in the left half of each retina (perceives informa- age to the cortex results in a contralateral field cut,
tion in the right visual field) project to the left a hemianopia. Macular sparing usually occurs
calcarine cortex. Connections from the macula of because of collateral blood supply from branches
the retina are rich to the striate cortex, in that of the middle cerebral artery. Isolated lesions of
approximately 2% of the total visual field encom- the primary visual cortex result in discrete blind
passes 55–60% of the total area of the calcarine spots (scotomas) in the corresponding area of the
cortex. The peripheral visual field is represented visual field.
in the more anterior regions of the striate cortex.

Cross-References
Function
▶ Calcarine Fissure
From a functional perspective, the calcarine cor- ▶ Occipital Lobe
tex is important in determining orientation, spatial ▶ Scotoma
frequencies, and color properties of the visual ▶ Unimodal Cortex
stimulus. Vision is a complex process that requires ▶ Visual Cortex
parallel processing of neural networks, and the
initial input to the calcarine cortex is integral to
further processing. The context of a particular References and Readings
visual stimulus is also important to eventual per-
ception of that stimulus, and the responses can be Horton, J. C., & Hoyt, W. F. (1991). The representation of
the visual field in human striate cortex. A revision of the
facilitated or inhibited. When there is little con-
classic Holmes map. Archives of Ophthalmology, 109,
trast of the stimulus within the surrounding 816–824.
environment, a reduction of response occurs. Netter, F. (1991). The CIBA collection of medical illustra-
However, when there is high contrast, an enhance- tions: Volume I – nervous system, part I: Anatomy and
physiology. West Caldwell: CIBA-Geigy.
ment of responses occurs. The information from Prasad, S., & Rizzo, J. F. (2015). Anatomy & physiology of
primary visual cortex is projected to other areas in the human visual system. Boston: Modern Neurology,
the occipital lobe for further visual analysis. For LLC.
666 Calcarine Fissure

gyrus) will produce upper field deficits. Lesions

Calcarine Fissure destroying tissue along both the upper and lower
banks may result in a contralateral homonymous
John E. Mendoza hemianopia.
Department of Psychiatry and Neuroscience,
Tulane Medical School and SE Louisiana
Veterans Healthcare System, New Orleans, LA, Cross-References
USA
▶ Cuneus
▶ Lingual Gyrus
Synonyms ▶ Visual System

Calcarine sulcus

Definition California Computerized

Assessment Package
The calcarine fissure is a deep sulcus located on
the medial surface of the occipital lobe (see Eric N. Miller
Fig. 1). The superior (cuneus) and inferior Palm Springs, CA, USA
(lingual gyrus) banks of this sulcus represent the
primary cortical projection area for vision. Visual
information that is first received in the upper por- Synonyms
tions of the retina is represented along the upper
banks of the fissure (cuneus), while that derived CalCAP
from the lower retina projects to its lower bank.
Thus, lesions confined to the upper bank (cuneus)
will result in contralateral inferior visual field Description
defects, while damage to the lower bank (lingual
The California Computerized Assessment Pack-
age (CalCAP; 1999) presents a series of brief
reaction time tasks designed to assess speeded
information processing and psychomotor func-
tioning. The standard CalCAP consists of four
Simple and six Go-No Go reaction time subtests
that require 20–25 min to complete. The individ-
ual reaction time measures were designed to
assess a number of cognitive domains, including
speed of processing (reaction time), lexical dis-
crimination (real word vs. nonsense word), rapid
visual scanning, form discrimination and
matching, working memory (1-back and 2-back
tasks), and sustained and divided attention. Each
task includes a practice session that must be com-
pleted with 100% accuracy to proceed to the main
Calcarine Fissure, Fig. 1 Mid-sagittal view of the brain
(MRI) showing calcarine fissure separating the cuneus and 2-min procedure, a method that ensures that sub-
the lingual gyrus of the occipital lobe jects understand the task instructions and that
California Computerized Assessment Package 667

minimizes practice effects in longitudinal study shown that the tasks correlate only modestly
designs. Subjects are asked to focus on a display (0.2–0.4) with traditional neuropsychological
field and respond only to specific types of visual measures (Miller et al. 1991). Factor analyses
stimuli. For example, in the form discrimination using the CalCAP and other neuropsychological
task, they are asked to press a key only when two test batteries show that the reaction time indices
out of three non-nameable figures are identical. form two primary factors best characterized as
The core measures of reaction time, hits and simple reaction time and decision speed. These C
false-positives, and signal detection parameters factors are distinct from traditional neuropsycho-
allow investigators to measure accuracy and gen- logical measures, and most researchers and cli-
eral speed of processing, as well as relative differ- nicians now use the CalCAP and other reaction
ences among conceptually distinct decision tasks. time measures primarily as indices of these types
Four iterations of a Simple reaction time routine at of speeded information processing and attention.
various points in the test allow direct measurement The abbreviated version of the CalCAP specifi-
of the subject’s ability to maintain focus throughout cally excludes measures designed to look at
the 20-min testing procedure. The computer scores visuoperceptual and language skills and focuses
each task using age- and education-specific norms primarily on these core indices of reaction time,
derived from 641 men ranging from 21 to 58 years working memory, and attention.
of age, with a mean education of 16 years. Final
scores are available immediately in tabular and
graphical formats. Additional norms have been Psychometric Data
derived for elementary school children (third,
fifth, and sixth grades), women, and older individ- All the subtests in the CalCAP have high internal
uals. The CalCAP also includes a four subtest consistency reliability (0.77–0.96). Six-month
language-independent abbreviated battery test-retest reliability for the Go-No Go paradigms
weighted toward measures of speeded processing is comparable with levels seen for conventional
and working memory. These test batteries are well neuropsychological procedures (0.43–0.68), but
suited for collecting reliable information on psy- there is less evidence of the practice effects com-
chomotor functioning in a brief period of time and monly seen with psychomotor measures. The
can be used effectively for assessing changes over reduced practice effects may be due to the require-
time. Stimulus materials are available in English, ment that all subjects complete practice trials with
Spanish, French, Norwegian, Danish, and Flemish. 100% accuracy before proceeding to the actual
test. Unlike the Go-No Go paradigms, the simple
reaction time measures have relatively low test-
Historical Background retest reliability (0.20–0.29), suggesting that the
psychomotor skills measured by the simple reac-
The CalCAP was originally developed by tion time tasks vary considerably depending on
Dr. Eric Miller in the late 1980s as an automated state variables such as mood, attention, fatigue,
substitute for traditional neuropsychological and time of day (Miller 2008).
testing. The Standard battery, developed in con- CalCAP reaction time correlates most highly
sultation with Dr. Paul Satz and Dr. Ola Selnes, with age, and, to a lesser extent, with years of
was designed to measure aspects of language education. Two studies of gender effects on
and visuoperceptual skills, working memory, CalCAP reaction time have shown no differences
speeded information processing, attention, learn- between men and women on any of the CalCAP
ing and memory, visual scanning, and reaction indices (Berg 1994). The psychometric properties
time. While the reaction time tasks that comprise of the CalCAP are unstable for third graders but
the Standard CalCAP battery do assess many of essentially the same as found in adults by the fifth
these areas of cognitive functioning, studies have grade (Budzinski 1994).
668 California Computerized Assessment Package

Clinical Uses References and Readings

The CalCAP has been widely used in cross- Berg, D. (1994). Adults’ reaction time as affected by age
and education level. B.A. Honours Thesis supervised
sectional and longitudinal studies of HIV/AIDS
by Dr. Frank Spellacy, University of Victoria.
(Miller et al. 1991; Gonzalez et al. 2003), drug Budzinski, L. M. (1994). An exploration of simple and
abuse (Chang et al. 2002; Volkow et al. 2001), choice reaction times in children. B.A. Honours Thesis
depression (Stordal et al. 2004), epilepsy supervised by Dr. Frank Spellacy, Victoria, B.C., Uni-
versity of Victoria.
(Hessen et al. 2008), traumatic brain injury
Chang, L., Ernst, T., Speck, O., Petal, H., DeSilva, M.,
(Waterloo et al. 1997), and hyperbaric oxygen Leonido-Yee, M., et al. (2002). Perfusion MRI and
treatments (Hjalmarsen et al. 1999; Van Hoof computerized cognitive tests abnormalities in abstinent
et al. 2002). It is particularly sensitive to the methamphetamine users. Psychiatry Research, 114,
65–79.
psychomotor changes seen in these disorders
Gonzalez, R., Heaton, R. K., Moore, D. J., Letendre, S.,
and, unlike most psychomotor tasks, has minimal Ellis, R. J., Wolfson, T., et al. (2003). HIV
practice effects, making it particularly appropriate Neurobehavioral Research Center Group. Computer-
for research paradigms such as clinical trials and ized reaction time battery versus a traditional neuropsy-
chological battery: Detecting HIV-related impairments.
epidemiologic studies that require repeated
Journal of International Neuropsychological Society,
testing. 9, 64–71.
The cognitive functions assessed by the CalCAP Hessen, E., Lossius, M. I., Reinvang, I., & Gjerstad, L.
program are best described as timed psychomotor (2008). Improvement in speeded cognitive processing
after anti-epileptic drug withdrawal – a controlled study
skills requiring focused or sustained attention.
in mono-therapy patients. Progress in Neurother-
Impaired reaction time across multiple measures is apeutics and Neuropsychopharmacology, 3, 199–209.
usually indicative of generalized motor slowing or Hjalmarsen, A., Waterloo, K., Dahl, A., Jorde, R., &
slowed information processing. Impaired reaction Viitanen, M. (1999). Effect of long-term oxygen ther-
apy on cognitive and neurological dysfunction in
time on specific measures, particularly when
chronic obstructive pulmonary disease. European Neu-
coupled with scores outside of normal bounds on rology, 42, 27–35.
true-positive responding, is suggestive of a more Miller, E. N. (1999). CalCAP California computerized
specific functional deficit, such as language skills assessment package manual (2nd ed.). Los Angeles:
Norland Software.
(lexical discrimination task), visuoperceptual defi-
Miller, E. N. (2008). CalCAP California computerized
cits (form discrimination), or working memory assessment package. Retrieved 16 Oct 2008 from
(1-back and 2-back tasks). http://www.calcaprt.com
The standard CalCAP program classifies sub- Miller, E. N., Satz, P., & Visscher, B. (1991). Computerized
and conventional neuropsychological assessment of
jects as “outliers” if they perform two standard
HIV-1 infected homosexual men. Neurology, 41,
deviations or lower on two or more of the tasks. 1608–1616.
Using these criteria, approximately 10% of sub- Stordal, K. I., Lundervold, A. J., Egeland, J., Mykletun, A.,
jects are classified as outliers. This base rate of Asbjornsen, A., Landro, N. I., et al. (2004). Impairment
across executive functions in recurrent major depres-
10% includes individuals with premorbid condi-
sion. Nordic Journal of Psychiatry, 58, 41–47.
tions such as prior head injury, learning disability, Van Hoof, E., Coomans, D., De Becker, O., De Meirleir,
preexisting neurologic conditions, as well as indi- K., & Cluydts, R. (2002). Hyperbaric oxygen therapy
viduals who are simply on the low end of normal for chronic systemic infections in chronic fatigue
syndrome. International Journal of Psychophysiology,
functioning.
45, 82–83.
Volkow, N. D., Chang, L., Wang, G. J., Fowler, J. S.,
Leonido-Yee, M., Francesci, D., et al. (2001). Associ-
Cross-References ation of dopamine transporter reduction with psycho-
motor impairment in methamphetamine abusers.
▶ Continuous Performance Tests American Journal of Psychiatry, 158, 377–382.
Waterloo, K., Ingebrigtsen, T., & Romner, B. (1997). Neu-
▶ Executive Functioning
ropsychological function in patients with increased
▶ Information Processing Speed serum levels of protein S-100 after minor head injury.
▶ Visual-Motor Function Acta Neurochirurgica, 139, 26–32.
California Verbal Learning Test – Children’s Version 669

three semantic categories (i.e., fruits, furniture,

California Verbal Learning and desert). The Tuesday trial is followed by
Test – Children’s Version short-delay free- and cued-recall trials of the first
(Monday) list. For cued-recall trials, the examinee
Eric M. Fine1 and Dean C. Delis2 is asked to recall words from the three semantic
1
Department of Neurology, University of categories contained in List A. A 20 min delay
California, San Francisco, CA, USA occurs next, during which nonverbal measures C
2
School of Medicine, University of California- should be administered. After the delay interval,
San Diego, La Jolla, CA, USA long-delay free-recall, long-delay cued-recall, and
yes/no recognition memory trials of the Monday
list (List A) are administered.
Synonyms With these procedures, the CVLT-C evaluates
not only the level of a child’s memory perfor-
CVLT-C mance, but also the learning strategies used and
types of errors made (Delis et al. 1994). Numer-
ous learning and memory variables are quanti-
Description fied on the CVLT-C, including level of total
recall and recognition on all trials, type of learn-
Overview of Test Procedures ing strategy employed (e.g., semantic clustering
The California Verbal Learning Test – Children’s and serial clustering), serial position effects,
Version (CVLT-C) is a relatively brief, individ- degree of vulnerability to proactive and retroac-
ually administered measure designed to assess tive interference, retention of information
the strategies and processes involved in learning over short and longer delays, enhancement
and remembering verbal materials (Delis et al. of recall performance by category cuing and
1994). Like the adult versions of this measure recognition testing, perseveration and intrusion
(CVLT; Delis et al. 1987; CVLT-II; Delis et al. errors in recall, and false-positive errors in
2000; “▶ California Verbal Learning Test recognition memory (Table 1 for CVLT-C vari-
(California Verbal Learning Test-II),” the able definitions).
CVLT-C adopts a process-oriented approach for
parsing a variety of learning and memory com- Standardization Sample
ponents, which facilitates the identification of The CVLT-C was normed on a sample of 920 chil-
distinct memory profiles associated with clinical dren from 12 age groups ranging from 5 through
disorders. 16 years of age. The sample was stratified based
The CVLT-C uses words presented as part of on data from the 1988 US Census (for additional
two shopping lists (i.e., a “Monday list” and a information regarding the sample characteristics,
“Tuesday list”) and measures both recall and rec- see the test manual; Delis et al. 1994). In addition,
ognition of the words over a number of trials. The normative data for 4-year-olds was provided by a
use of a “shopping-list” format makes the proce- study by (Goodman et al. 1999).
dure more relevant for a child and provides infor-
mation regarding how the child approaches an Score Conversions and Contrast Scores
everyday memory task. Specifically, in the first Raw scores for the various CVLT-C indices are
five trials, the child is asked to recall words from converted into an age-based T or z scores (see test
the Monday list (List A), which consists of manual for description of procedures used to
15 words, with five words from each of three derive these standardized scores; Delis et al.
semantic categories (i.e., fruits, clothing, and 1994). Although the test manual includes tables
toys). An interference Tuesday list (List B) of for converting the numerous raw scores to stan-
15 words is then presented on one trial. Words dardized scores, these scores are computed auto-
from the Tuesday list are divided equally across matically using the CVLT-C computer scoring
670 California Verbal Learning Test – Children’s Version

California Verbal Learning Test – Children’s Version, Table 1 CVLT-C variable definitions
Variable
List A total Total number of words recalled across the five learning trials
List A1 Number of words recalled from the first trial
List A5 Number of words recalled from the fifth trial
List B Number of words recalled from the interference list (List B)
List A short-delay free recall Number of words recalled from List A immediately after the presentation of the
interference list (List B)
List A short-delay cued recall Number of words recalled from List A with semantic cueing
List A long-delay free recall Number of words recalled from List A after a 20 min delay
List A long-delay cued recall Number of words recalled from List A with semantic cueing after a 20 min delay
Semantic clustering Number of consecutively recalled words from the same semantic category (i.e.,
consecutive words from the same semantic category), which reflects the extent to
which the subject has actively imposed a semantic organization on the list of words
Serial clustering Number of consecutively recalled words in the same order as they were presented
(i.e., a serial cluster)
Primacy % Percentage of words correctly recalled from the beginning of List A (first four words)
Middle % Percentage of words correctly recalled from the middle of List A (middle seven
words)
Recency % Percentage of words correctly recalled from the end of List A (last four words)
Learning slope Average number of new words acquired across the five List A immediate-recall trials
(e.g., a score of 1 means that the examinee learned approximately one new word per
trial)
Consistency % Percentage of target words recalled once on each of the four learning trials that were
also recalled on the very next trial; reflects ability to maintain a consistent learning
strategy
Perseverations Total number of target words repeated within a trial (called “repetitions” on the
CVLT-II; Delis et al. 2000)
Free-recall intrusions Total number of extra-list intrusions on all the free-recall trials
Cued intrusions Total number of extra-list intrusions on all the cued-recall trials
Total intrusions Total number of extra-list intrusions made on free- and cued-recall trials
Recognition hits Total number of target words correctly identified on recognition testing as belonging
to List A (yes/no format)
Recognition discriminability Accuracy of distinguishing target from distracter words on recognition testing;
calculated using signal detection methods
False positives Total number of distractor words incorrectly identified as belonging to List A during
recognition testing
Response bias Tendency to favor “yes” or “no” responses on recognition testing (positive scores
reflect a “yes” bias)

software. The standard score for List A trials 1–5 processes. For example, comparing List
total is presented in a T-score metric, with a mean B (Tuesday list) recall with List A (Monday list)
of 50 and a standard deviation of 10. The Trial 1 recall provides a measure of a child’s
remaining standardized scores are presented in a susceptibility to proactive interference. As
z-score metric, with a mean of 0 and a standard another example, contrasting List A long-delay
deviation of 1. free recall with List A short-delay free recall can
Examination of contrast scores (i.e., z-score be used to identify rapid forgetting across
differences between two variables) allows for the delays (Delis et al. 1994, 2000; Donders and
assessment of particular learning and memory Minnema 2004).
California Verbal Learning Test – Children’s Version 671

Historical Background five words for 8-year-olds, by six words for

12-year-olds, and by nine words for 16-year-
In the past, the clinical neuropsychological assess- olds. The average improvement on List B, the
ment of memory relied on tests designed primarily short-delay, and long-delay trials ranged from
to assess the presence or absence of memory dys- one to two words across all the groups.
function per se. This goal was accomplished by Evidence supporting the validity of CVLT-C
scoring memory tests only in terms of the level of comes from factor analyses of the original C
correct recall or recognition. However, over the standardization sample and studies of CVLT-C
past 25 years or so, numerous studies from cogni- performance in various neurological and
tive neuropsychology have documented qualita- neurodevelopmental populations. As described in
tively distinct patterns of memory dysfunction the test manual, exploratory principal components
associated with various neurological and psychi- analysis of the primary CVLT-C performance indi-
atric populations. These findings emphasize the ces produced a six-factor solution that closely
multicomponential nature of learning and mem- paralleled the adult version (CVLT; Delis et al.
ory, and, as such, the importance of developing 1987). In addition, Donders (1999) employed con-
clinical memory tests that allow for the evaluation firmatory factor analysis to reanalyze the CVLT-C
of both qualitative and quantitative features of standardization sample and found a five-factor
memory performance. Informed by principles of solution that included attention span (List A,
learning/memory from cognitive science and cog- Trial 1; List B; middle region recall), learning
nitive neuroscience, and modeled in part after the efficiency (List A, Trial 5; semantic clustering;
“▶ Rey Auditory Verbal Learning Test, Rey recall consistency), free delayed recall (ahort-
AVLT” (Rey AVLT; Rey 1964), the CVLT-C, delay free recall, long-delay free recall), cued-
like its adult counterpart (“▶ California Verbal delay recall (short-delay cued recall, long-delay
Learning Test (California Verbal Learning Test- cued recall), and inaccurate recall (total intrusions,
II)”), was developed to facilitate the quantification recognition false positives).
of multiple learning and memory parameters
(Delis et al. 1987, 1988, 1994, 2000).
Clinical Uses

Psychometric Data The CVLT-C was designed to assess subtle to

severe verbal learning and memory deficits in
Reliability and Validity child clinical populations. The extant literature
The reliability of the CVLT-C was assessed using indicates that the CVLT-C has utility for charac-
measures of internal consistency and test-retest terizing the learning and memory deficits associ-
reliability (Delis et al. 1994). The internal consis- ated with a wide-range of clinical disorders
tency coefficient for the five trials of the Monday (for review, see Strauss et al. 2006). In addition,
list ranged from 0.84 to 0.91 (with a mean of 0.88) CVLT-C performance has been shown to be
and the across-semantic-category consistency predictive of long-term educational outcomes in
coefficient ranged from 0.64 to 0.80 (with a children who have suffered a traumatic brain
mean of 0.72). Test-retest stability (median retest injury (Miller and Donders 2003).
interval of 28 days) ranged from 0.90 to 0.17, with Because the reliability characteristics of the
higher test-retest correlations typically occurring primary CVLT-C performance indices (e.g., the
for measures of overall level of performance (e.g., total words recalled during the learning trials)
total words recalled during the five learning trials are stronger than for the “process” or strategy-
and long-delay free recall). Practice effects were use variables (e.g., semantic clustering), it has
fairly large for certain conditions. For example, been recommended that clinicians place greater
trials 1–5 total recall improved by an average of emphasis on the main performance variables and
672 California Verbal Learning Test (California Verbal Learning Test-II)

interpret process-variables cautiously (Strauss et al.

2006). In order to evaluate learning and memory California Verbal Learning
in other formats (e.g., story memory) or modali- Test (California Verbal
ties (visual), the CVLT-C can be complemented Learning Test-II)
with measures from other standardized children’s
memory assessment batteries (e.g., Children’s Angela Yi
Memory Scale and Wide Range Assessment of Department of Rehab Medicine, Mount Sinai
Memory-Second Edition). School of Medicine, New York, NY, USA

Cross-References Synonyms

▶ California Verbal Learning Test (California CVLT-II

Verbal Learning Test-II)
▶ Children’s Memory Scale
▶ Rey Auditory Verbal Learning Test, Rey AVLT Description

The California Verbal Learning Test-II (CVLT-

References and Readings II) (Delis et al. 2000) is a widely used verbal
learning and memory test. The current version
Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. requires recalling and recognition of two lists of
(1987). The California verbal learning test – Adult
version. San Antonio: The Psychological Corporation.
words over immediate and delayed trials. List
Delis, D. C., Freeland, J., Kramer, J. H., & Kaplan, A includes 16 words administered over five tri-
E. (1988). Integrating clinical assessment with cogni- als. List B (interference), which is also 16 words,
tive neuroscience: Construct validation of the Califor-
nia verbal learning test. Journal of Consulting and Editorial Addendum: The text below pertains primarily to
Clinical Psychology, 53(1), 123–130. the CVLT-II (2000). While this edition of the Encyclopedia
Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. was in preparation, the CVLT-3 was published. The new
(1994). The California verbal learning test-Children’s version has two parallel forms of 16 items each and a
version. San Antonio: The Psychological Corporation. 9-item brief form. The former follow the same format and
Delis, D. C., Kramer, J., Kaplan, E., & Ober, B. A. (2000). employ the same content as the CVLT-II described below,
California verbal learning test – Second edition. San while the latter consists of 4 learning trials followed by a
Antonio: The Psychological Corporation. short-delay free recall trial (NB: there is no short-delay
Donders, J. (1999). Structural equation analysis of the cued recall) and long-delay recall without and with
California verbal learning test – Children’s version in categorical cueing. The test can also be administered in
the standardization sample. Developmental Neuropsy- digital format. This version was normed on 700 individuals
chology, 15, 395–406. aged 16–90 years. The Manual states that the test was
Donders, J., & Minnema, M. (2004). Performance discrep- updated in several ways including development of
ancies on the California verbal learning test – Chil- additional intrusion and yes/no recognition memory
dren’s version (CVLT-C) in children with traumatic measures, use of scaled score metric to permit comparison
brain injury. Journal of the International Neuropsycho- with performance on other tests that employ scaled scores,
logical Society, 10, 482–488. addition of index scores in standard score format. The
Goodman, A. M., Delis, D. C., & Mattson, S. N. (1999). Manual characterizes alternate form reliability as “robust”
Normative data for 4-year-old children on the Califor- and similar to figures obtained with the earlier version of
nia verbal learning test – Children’s version. The Clin- the test. There is discussion concerning the matter of
ical Neuropsychologist, 13(3), 274–282. demographic adjustments and the use of the CVLT-3 as a
Miller, L. J., & Donders, J. (2003). Prediction of educa- measure of “performance validity.” Chapter 6 of the
tional outcome after pediatric traumatic brain injury. Manual offers a detailed review of studies from 1999 to
Rehabilitation Psychology, 48, 237–241. 2017 that used a version of the CVLT to study patterns of
Rey, A. (1964). L’;examen clinique en psychologie. Paris: performance in a wide variety of clinical groups. As would
Presses Universitaires de France. be expected, the bibliography is quite extensive. At this
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). A time, the test is too new for additional studies beyond that
compendium of neuropsychological tests (3rd ed.). of the standardization sample to have appeared in the peer-
New York: Oxford University Press. reviewed literature.
California Verbal Learning Test (California Verbal Learning Test-II) 673

is administered once after List A. Short-delay principles from cognitive science to measure mul-
free recall and cued recall are administered tiple aspects of learning and memory. This test
after List B. A 20-min delay follows the short- provided a measurement of not only what an
delay recalls, an interval filled by nonverbal test- individual remembers, but how they remember
ing. Long-delay free recall, long-delay cued i.e., memory strategy) and what errors are made.
recall, and yes/no-recognition trials of List This refuted previous beliefs that memory dys-
A items follow the 20-min delay. A revision of function was limited to recall and recognition. C
the CVLT-II is the addition of a forced choice Elwood (1995) provided a review of the first
recognition after a 10-min delay following the several years' worth of findings using the original
yes/no trial. CVLT.
Another modification of the CVLT-II is the
inclusion of a short form (nine words) and an
alternate form. The short form was created for Psychometric Data
the purpose of screening or for patients who may
have more severe brain damage and may feel CVLT-II: Split-half reliability coefficients based
overwhelmed by the long form. This short form on splitting immediate-recall trials ranged from
takes 15 min to administer and also has a 15-min 0.89 to 0.94. Coefficient alphas based on word
delay. The alternate form has been statistically category scores across immediate-recall trials
equated with the standard form. ranged from 0.71 to 0.82. The split-half reliability
The CVLT-II was normed on a national stan- based on the number of times each word was
dardization sample of 1087 individuals aged correctly recalled across immediate-recall trials
16–89, which was demographically matched to ranged from 0.68 to 0.79. The CVLT-II is corre-
the US population. The test takes approximately lated with the Wechsler Abbreviated Scale of
30 min to administer. The test is administered in Intelligence (WASI).
paper and pencil format, with the examiner record- CVLT-C: The internal consistency reliability
ing the examinee’s responses. The responses are across five trials ranged from 0.84 to 0.91. Reli-
scored using the Comprehensive Scoring System, ability coefficients for across-semantic category
which computes raw scores and standardized consistency ranged from 0.64 to 0.80.
scores for over 50 learning and memory variables. Test-retest reliability of the standard and alter-
The raw scores can be scored manually, although nate forms indicated smaller practice effects
there are limits to how much information can be (Cohen’s d range = 0.01–0.18) on the primary
derived. indices compared to those who received the stan-
The CVLT-children’s (CVLT-C) (Delis et al. dard form on two occasions (Cohen’s d range
1993) version can be administered to children 0.27–0.61) (Woods et al. 2006).
aged 5–16 and can assist professionals in diag- Norms controlled for demographic variables
nosing memory impairment secondary to learning are also available from 906 subjects (Norman
disabilities, attention-deficit disorder, mental et al. 2010).
retardation, and other neurological disorders and
psychiatric problems. The administration is simi-
lar to the format of the CVLT-II, although forced Clinical Uses
choice recognition is not included.
The CVLT-II manual states that the test measures
“multiple aspects of how verbal memory occurs
Historical Background or fails to occur, therefore providing a compre-
hensive assessment of each patient’s profile of
The first edition of the CVLT was originally verbal learning and memory strengths and weak-
published in 1987 by Delis et al. (1987). They nesses.” The manual reports a review of the
created one of the first tests to incorporate literature of clinical populations from 1987 to
674 Cambridge Neuropsychological Testing Automated Battery

1999, summarizing the key findings of

CVLT performance across various clinical Cambridge
populations, which include anterior temporal Neuropsychological Testing
lobectomy, Korsakoff’s syndrome, Alzheimer’s Automated Battery
disease, Huntington’s disease, Parkinson’s dis-
ease, head injury, schizophrenia, depression and Mark A. Sandberg
other affective disorders, chronic alcohol and Neuropsychology, Northport VA Medical Center,
drug abuse, posttraumatic stress disorder, sys- Smithtown, NY, USA
temic medical disease (HIV, chronic fatigue
syndrome, Lyme disease, eosinophilia myalgia
syndrome, cardiac transplant candidates), insuf- Synonyms
ficient effort, and predictor for everyday
functioning. CANTAB

Description
Cross-References
The Cambridge Neuropsychological Testing
▶ Children’s Memory Scale
Automated Battery (CANTAB) is a neuropsy-
▶ Hopkins Verbal Learning Test
chological measure developed at the University
▶ Rey Auditory Verbal Learning Test, Rey AVLT
of Cambridge and currently marketed by Cam-
▶ Rivermead Behavioral Memory Test
bridge Cognition Limited (CCL). The CANTAB
▶ Selective Reminding Test
is a theoretically derived instrument, predomi-
▶ Wechsler Memory Scale All Versions
nantly measuring nonlanguage functions includ-
ing memory, executive function, attention,
decision-making, and social cognition. The
References and Readings current versions are validated for use online and
by the use of tablet technology. A tablet-based
Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. memory screening device labeled CANTAB
(1987). The California verbal learning test: Research
Mobile was recently awarded FDA clearance
edition, adult version. San Antonio: The Psychological
Corporation. to be marketed as a medical devise in USA.
Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, CANTAB tests are described as having sufficient
B. A. (1993). The California verbal learning test sensitivity to discern changes in cognitive func-
for children. San Antonio: The Psychological
tioning brought about by CNS disorders and
Corporation.
Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, medications. The publisher regards performance
B. A. (2000). The California verbal learning test – on CANTAB tests to be independent of language
second edition. San Antonio: The Psychological and culture.
Corporation.
Elwood, R. W. (1995). The California verbal learning test:
Psychometric characteristics and clinical application.
Neuropsychology Review, 5(3), 173–201.
Norman, M., Evans, J., Miller, W., & Heaton, R. (2010). Historical Background
Demographically corrected norms for the California
verbal learning test. Journal of Clinical and Experi-
mental Neuropsychology, 22, 80–94. Originally created in the late 1980s to diagnose
Woods, S., Delis, D., Scott, J., Kramer, J., & Holdnack, dementia in elderly individuals (Fray et al.
J. (2006). The California verbal learning test-second 1996), the CANTAB is used, and has been stud-
edition: Test-retest reliability, practice effects, and
ied, across age groups and with patients pre-
reliable change indices for the standard and
alternate forms. Archives of Clinical Neuropsychology, senting with both psychiatric and neurological
21, 413–420. conditions.
Cambridge Neuropsychological Testing Automated Battery 675

Current Knowledge CANTAB complete portfolio of measures

includes 24 tests grouped into specific cognitive
The CANTAB offers assessment products dimensions measuring memory, executive func-
designed for use in healthcare encounters and tion, attention, decision-making, and social cog-
research. CANTAB Mobile is a touchscreen device nition. A separate functional category labeled
which combines an assessment of episodic mem- “induction” is comprised of two short tests
ory and mood with the added evaluation of ADL whose purpose is to familiarize examinees with C
independence. It is used for the identification of the general idea of responding by touching the
mild cognitive impairment and is suitable for per- screen. Induction measures are also used to iden-
sons aged 50–90. CANTAB Insight is described as tify those examinees who cannot reliably partici-
a Class II medical device and normed for person pate in the examination due to sensorimotor or
18 and older. It is designed to “measure an individ- comprehension issues. Details of each subtest
ual’s cognitive health.” CANTAB also offers a are described in Table 1. The CANTAB offers
cloud-based research assessment product labeled flexibility by encouraging users to select subtests
Connect Research, which incorporates up to to address specific clinical questions or research
13 tests to assess cognition in research applications. applications. All subtest stimuli are delivered

Cambridge Neuropsychological Testing Automated Battery, Table 1 CANTAB tests

CANTAB test Functional category Cognitive function measured
Motor screening Induction Sensory motor function and
comprehension
Big little circle Induction Sensory motor function and
comprehension
Delayed matching to sample Visual memory Attention/short term visual memory
Paired associates learning Visual memory Visual episodic memory
Pattern recognition memory Visual memory Visual recognition memory
Spatial recognition memory Visual memory Visual spatial memory
Attention switching task Executive function Alternating attention
Intra-extra dimensional shift Executive function Set shifting
One touch stocking of Cambridge Executive function Planning
Spatial span Executive function Visuospatial working memory
Spatial working memory Executive function Working memory and strategy
One touch stockings Executive function Planning
Reaction time Attention Motor and mental response speed
Match to sample visual search Attention Speed/accuracy trade-off
Choice reaction time Attention General alertness and motor speed
Simple reaction time Attention General alertness and motor speed
Rapid visual information Attention Sustained attention
processing
Grading naming test Semantic/verbal memory Naming
Verbal recognition memory Semantic/verbal memory Verbal memory and new learning
Cambridge gambling task Decision-making and response Decision-making and risk-taking
control
Information sampling task Decision-making and response Impulsivity and decision-making
control
Stop signal task Decision-making and response Response inhibition
control
Affective go no go Social cognition Information processing biases
Emotional recognition Social cognition Identify emotions in facial expressions
676 Cancellation Tests

nonverbally, although adequate receptive lan- Future Directions

guage functions are necessary to understand task
demands. Pharmaceutical companies have been using
Research supporting the use of the CANTAB CANTAB internationally in multisite clinical tri-
in the evaluation of brain-behavior relations is als for more than 20 years.
reasonably extensive, with a bibliography of
peer-reviewed articles searchable by disorder or
intervention, and is available for review on the References and Readings
company’s website www.cantab.com. Studies
are available supporting the validity and Elliott, R., McKenna, P. J., Robbins, T. W., &
Sahakian, B. J. (1995). Neuropsychological evidence
utility of the CANTAB in measuring the impact
for frontostriatal dysfunction in schizophrenia.
of pharmacotherapy on neuropsychological Psychological Medicine, 25, 619–630.
performance and in the assessment of attention Luciana, M. (2003). Practitioner review: Computerized
deficit hyperactivity disorder, affective disor- assessment of neuropsychological function in children:
Clinical and research applications of the Cambridge
ders, schizophrenia, senile dementia of the
Neuropsychological Testing Automated Battery
Alzheimer’s type, Parkinson’s disease, among (CANTAB). Journal of Child Psychology and
other diagnostic groups. Research is available Psychiatry, 44(5), 649–663.
showing the usefulness of CANTAB with both Luciana, M., & Nelson, C. A. (2002). Assessment of neu-
ropsychological function through use of the Cambridge
child and adult populations. Normative data is
Neuropsychological Testing Automated Battery: Per-
not currently available for CANTAB Connect formance in 4- to 12-year-old children. Developmental
Research. Neuropsychology, 22(3), 595–624.
Reliability studies have been completed inter- Prouteau, A., Verdoux, H., Briand, C., Lesage, A.,
Lalonde, P., Nicole, L., Reinharz, D., &
nally by Cambridge Cognition which described
Stip, E. (2004). The crucial role of sustained attention
test-retest reliability coefficients ranging from in community functioning in outpatients with schizo-
0.4–0.87. Those findings are consistent with sta- phrenia. Psychiatry Research, 129, 171–177.
bility coefficients reported by Lowe and Rabbitt Sweeney, J. A., Kmiec, J. A., & Kupfer, D. J. (2000).
Neuropsychologic impairments in bipolar and unipolar
(1998). Luciana (2003) reported consistency coef-
mood disorders on the CANTAB neurocognitive bat-
ficients ranging from 0.73 for a measure of reac- tery. Biological Psychiatry, 48, 674–685.
tion time latency to 0.95 for performance on the
self-ordered search task.
Limitations of CANTAB include its exclusion
of language based measures, thus leaving the
examiner to supplement the battery with addi- Cancellation Tests
tional tests to assess relevant brain-behavior
issues (e.g., verbal fluency). The absence of per- Richard F. Kaplan
formance validity measurement is also a limita- Department of Psychiatry (MC-2103), UConn
tion. CANTAB’s cost will make it prohibitive for Health Center, Farmington, CT, USA
most private practitioners and organizations.
CANTAB cognitive tests are automated
using voice-over directions available in multiple
Synonyms
languages. The Research Suite software is
designed to work with Windows 7, 8, and
Vigilance tests
10 touchscreen devices. A 9.700 iPad Pro is
recommended for use with CANTAB Insight.
Testing can occur away from a research study
site through a recently released web-based Description
method of assessment which uses a desktop com-
puter or laptop. A cloud-hosted infrastructure is Cancellation tests are designed to measure
used to maintain data. sustained and selective attention.
Capacity 677

Historical Background References and Readings

Numerous variations of cancellation tests have Kaplan, R. F., Verfaellie, M., Meadows, M. E., Caplan,
L. R., Pessin, M. S., & DeWitt, L. D. (1991). Changing
been developed to assess sustained, selective
attentional demands in left hemispatial neglect.
attention and spatial inattention following hemi- Archives of Neurology, 48, 1263–1266.
spheric lesions. The patient is typically required to Mitrushina, M., Boone, K. B., Razani, J., & D’Elia, L. F.
scan through an array of stimuli and find (cancel) (2005). Handbook of normative data for neuropsycho- C
logical assessment (2nd ed., pp. 160–170). New York:
specific target stimuli (e.g., bells).
Oxford.
Weintraub, S. (2000). Neuropsychological assessment of
mental state. In M. Mesulam (Ed.), Principles of behav-
Psychometric Data ioral neurology (2nd ed., pp. 121–173). New York:
Oxford.
There is relatively little normative data for cancel-
lation tests, and most comparative studies show
that normal individuals make few, if any, errors Capacity
(Weintraub 2000). Standardized versions of can-
cellation tests, such as the Ruff 2 & 7, show good Robert L. Heilbronner
test-retest reliability. In addition, on the Ruff 2 & Chicago Neuropsychology Group, Chicago, IL,
7, younger adults performed better than older USA
adults, and performances improved with higher
levels of education. There were no gender effects
(Mitrushina et al. 2005). Synonyms

Competency
Clinical Uses

Cancellation tests have been shown to be sensitive

in detecting deficits in attention related to right
Definition
hemisphere lesions, traumatic brain injuries, schizo-
In the most basic sense, capacity refers to the ability
phrenia, and AIDS-related cognitive impairment.
to make decision(s) with regard to oneself. Specif-
Cancellation tests are particularly useful in
ically, this refers to one’s ability to understand and
assessing visuospatial neglect. Unlike normal indi-
appreciate the consequences of one’s actions. Legal
viduals who begin searching for target stimuli on
capacity remains in effect until death, unless a court
the left side of the page and systematically move
rules that one is “incapacitated.” If a person is ruled
rightward, neglect patients begin on the right using a
by a court of law to be legally incapacitated, this
disorganized search pattern omitting many targets
can remove all or part of a person’s right to make
on the left side of the page (Weintraub 2000). By
decisions. Specifically, one can be deemed incapa-
decreasing the attentional demands of a letter can-
ble of managing financial affairs but ruled capable
cellation test by reducing the number of nontarget
of making medical decisions, for example. If a
stimuli, right-hemisphere-damaged patients showed
person is ruled to lack full legal capacity, then
decreased left-sided neglect, suggesting that the
they are prohibited from entering into a contract,
neglect syndrome is the result of an attentional
giving a power of attorney, creating a will, or
bias (Kaplan et al. 1991).
consenting to medical treatment. A ruling of legal
incapacity typically results in the appointment of a
Cross-References guardian or conservator to make decisions for the
person. There are several types of capacity that are
▶ Attention relevant to forensic neuropsychology including
▶ Neglect Syndrome capacity to consent to treatment, to manage finan-
▶ Vigilance cial affairs, and others.
678 Capacity Limitations

Cross-References communication theorists in engineering.

Broadbent used the communication system as a
▶ Testamentary Capacity metaphor for relationships within the human
brain. Each brain system (i.e., sensory, memory,
response generation) was conceptualized in
References and Readings terms of a communication system, with an infor-
mation source, transmission channel(s), and a
Marson, D. C., & Hebert, K. (2005). Assessing civil com- receiver. The channel by which a message is
petencies in older adults with dementia: Consent capac-
transmitted has a capacity, which limits the
ity, financial capacity, and testamentary capacity. In
G. Larrabee (Ed.), Forensic neuropsychology: rate by which information can be transmitted.
A scientific approach. New York: Oxford University A property of communication systems is that
Press. the transmission of information within a system
Marson, D. C., Sawrie, S., Snyder, S., McInturff, B.,
can never exceed the capacity of the channel
Stalvery, T., Boothe, A., et al. (2000). Assessing finan-
cial capacity in patients with Alzheimer’s disease: divided by the information source output. This
A conceptual model and prototype instrument. theoretical conceptualization sets the stage for
Archives of Neurology, 57, 877–884. future research, describing the limits in sensory
Willis, S. (1996). Everyday cognitive competence in
and cognitive systems and mechanisms to deal
elderly persons: Conceptual issues and empirical find-
ings. The Gerontologist, 36, 595–601. with the processing of information in these
systems.

Current Knowledge
Capacity Limitations
In response to the observation that one is not
Anna MacKay-Brandt able to attend to all stimuli in the environment at
Nathan S. Kline Institute for Psychiatric Research, the same time, hypotheses have developed to
Orangeburg, NY, USA explain the limitations on the capacity for cog-
Taub Institute for Research on Alzheimer’s nitive processing, particularly in the areas of
Disease and the Aging Brain, Columbia attention and memory (Broadbent 1971; Miller
University, New York, NY, USA 1956; Shiffrin and Schnieder 1977; Kahneman
1973). Cohen (1993) organized attentional
capacity in terms of structural and energetic
limitations. Structural capacity limitations can
Definition be thought of in terms of optimal processing
characteristic of the system such as channel
The constraints on processing of internal and
capacity, working-memory capacity, processing
external stimuli that are dependent upon the struc-
speed, and temporal-spatial characteristics of
ture of, and the processes related to, the cognitive
the system. These structural elements are
system.
influenced by variables such as performance
required on more than one task (e.g., dual
task): task complexity, memory demand, high
Historical Background or low rate of target event occurrence, and task
duration. Energetic capacity limitations are con-
Fundamental research in attention emerged in the sidered to be natural or imposed variations
1950s with information processing theories. within an individual that includes arousal, moti-
D.E. Broadbent published an influential book in vation, and generated effort. A clear indicator of
1958, Perception and Communication, which was the influence of energetic factors on perfor-
in turn influenced by the contemporary work of mance is performance variability over time.
Capgras Syndrome 679

Researchers of cognition have used the debate References and Readings

over whether particular processes are limited or
unlimited in capacity as a fruitful ground for Broadbent, D. E. (1958). Perception and communication.
London: Pergamon.
study. For example, theories of serial and parallel
Broadbent, D. E. (1971). Decision and stress. London:
processing have emerged in both the attention and Academic.
memory literature in support and rejection of Cohen, R. (1993). The neuropsychology of attention. New
capacity-limited processes. Although not strictly York: Plenum. C
Duncan, J., & Humphreys, G. W. (1989). Visual search and
coupled, serial processing is often considered in
stimulus similarity. Psychological Review, 96,
the context of limited capacity, whereas parallel 433–458.
processing is thought to be unlimited in capacity. Jacoby, L. L. (1991). A process dissociation framework:
This coupling bears out in visual search studies Separating automatic from intentional uses of memory.
Journal of Memory and Language, 30, 513–541.
that have found preattentive processes that are
Kahneman, D. (1973). Attention and effort. Englewood
thought to be parallel and unlimited in capacity, Cliffs: Prentice-Hall.
versus focal attentive processes that are serial and Lovden, M., Backman, L., Lindenberger, U., Schaefer, S.,
limited in capacity (Duncan and Humphreys & Schmiedek, F. (2010). A theoretical framework for
the study of adult cognitive plasticity. Psychological
1989; Treisman and Gelade 1980; Wolfe 1994).
Bulletin, 136(4), 659–676.
Similarly, in memory research, Jacoby (1991) dis- Miller, G. A. (1956). The magical number seven, plus or
tinguished automatic from controlled processing, minus two: Some limits on our capacity for processing
with similar parallel and unlimited capacity information. Psychological Review, 63, 81–97.
Shiffrin, R. M., & Schnieder, W. (1977). Controlled and
(automatic) versus serial and limited capacity
automatic human information processing: 2. Perceptual
(controlled) distinctions. learning, automatic attending and a general theory.
Psychological Review, 84, 127–190.
Treisman, A., & Gelade, G. (1980). A feature integration
theory of attention. Cognitive Psychology, 12, 97–136.
Future Directions Wolfe, J. M. (1994). Guided search 2.0: A revised model of
visual search. Psychonomic Bulletin & Review, 1,
A relatively recent emphasis has been placed on 202–238.
the interaction of neural and cognitive limitations
with factors such as arousal, motivation, and
effort.
Further, a framework for understanding cogni- Capgras Syndrome
tive plasticity proposes changes in capacity that
arise from supply-demand mismatches in the cog- Paul Malloy
nitive/brain system in relation to environmental Department of Psychiatry and Human Behavior,
demands that occur over prolonged periods of Brown University, Providence, RI, USA
time and thus bring about plastic (structural)
changes (Lovden et al. 2010).
Synonyms

Cross-References Reduplication delusion; Reduplicative paramnesia

▶ Attention
▶ Behavior Rating Inventory for Executive Short Description or Definition
Function
▶ Parallel Processing Delusions are defined as false beliefs based on
▶ Plasticity incorrect inference about external reality and
▶ Serial/Sequential Processing firmly sustained in spite of the opinions of others
▶ Short-Term Memory or contrary evidence (American Psychiatric
▶ Working Memory Association 1987).
680 Capgras Syndrome

Capgras syndrome (Capgras and Reboul- often admit to puzzlement or bemusement regarding
Lachaux 1923) is a type of reduplication delusion aspects of the delusion. Rather than escalate their
involving the belief that persons well-known to the defenses by becoming hostile, they are more likely
patient, such as family members, have identical to confabulate an explanation. For example, a
doubles or are imposters. The double or imposter patient with a delusion of duplication (Malloy
is sometimes perceived as differing slightly in 1991) was asked how she could have two sets of
some physical characteristic from the “genuine” children with identical names. She appeared
person, but the patient may have difficulty verbal- momentarily puzzled and then stated, “My husband
izing the precise nature of this “difference.” was in the Navy, and we moved around a lot; it was
hard to keep that straight.”

Categorization
Epidemiology
Several variations of Capgras syndrome have
been identified. Doppelganger or subjective dou- Dohn and Crews (1986) observed that Capgras
ble is the belief that the patient himself/herself has syndrome was frequently overlooked in psychiat-
a double or impersonator (Christodoulou 1978). ric patients and found that the delusion actually
Fregoli syndrome is the belief that a person is had a 15% incidence in their sample of adult
capable of taking on the appearance of others inpatients previously diagnosed as having schizo-
while retaining his/her own psychological identity phrenia. Several researchers have found that about
(Courbon and Fail 1927). Intermetamorphosis is 25% of Alzheimer patients display delusions
the belief that people are changing in both phys- involving misidentification of people (e.g.,
ical and psychological identity to become another Mendez et al. 1992). Large-scale epidemiological
person (Courbon and Tusques 1932). studies are lacking to date.
Capgras syndrome must be distinguished from
purely perceptual or hallucinatory disturbances
and from generalized disturbance of cognition. Natural History, Prognostic Factors, and
That is, in order to be properly and convincingly Outcomes
diagnosed as a delusion, the disturbance must
involve a mistaken belief (not merely a mis- About 58% of Capgras patients who receive ade-
perception) and must be persistent (not a transitory quate neurodiagnostic workups are found to dis-
effect of confusion). For example, in autoscopy, play primary psychiatric disorder, uncomplicated
the patient experiences a second self, as in the by demonstrable neurologic disease (Dohn and
subjective double variant of Capgras. However, Crews 1986). Although psychological factors can
the phenomena differ in that the double is actually be important in the production of delusions, a crit-
seen in autoscopy, rather than believed to be active ical review of the literature by Malloy and Rich-
elsewhere, as in subjective doubles. The pro- ardson (1994) demonstrated that delusions can also
sopagnosic person may fail to recognize his wife, result from identifiable neurologic disease, from
whereas the Capgras patient will insist that the generalized disturbances to focal lesions.
present person is an imposter and that the “real” They found that Capgras and its variants
wife is somewhere else. Patients in confusional have been reported in association with a variety
states or dementia may express strange beliefs, but of systemic diseases and diffuse neurologic disor-
the beliefs typically change from hour to hour and ders. Systemic etiologies have included metabolic
do not persist once the confusion resolves. Thus disturbances such as myxedema, pseudo-
this problem should not be termed delusional. hypoparathyroidism, anemia, hepatic dysfunction,
Patients with Capgras syndrome are usually and B12 deficiency; intoxication and reactions to
described as forthcoming and cooperative. Although drugs including cocaine, chloroquine, disulfiram,
they insist that their delusional beliefs are true, they digoxin, and lithium; cerebral infections such as
Capgras Syndrome 681

encephalitis and AIDS; subarachnoid hemorrhage; delusion clearly related to a specific neurologic
migraine; post-ECT confusion; minor head structural lesion, involving the right hemisphere
trauma; and degenerative dementia. with predominantly frontal and temporal lobe
In terms of focal lesions such as tumors and damage. They noted the importance of frontal
stroke, that review demonstrated that the right damage in Capgras, both in terms of the inability
hemisphere or bilateral lesions were invariably to resolve conflicts and confabulation of a second
found on neuroimaging, with no exclusively left persona. C
hemisphere lesions. EEG and neurologic exam
findings also implicated right hemisphere pathol-
ogy. In terms of specific localization, 72% of cases Evaluation
with CT or MRI scans had right frontal, temporal,
or frontotemporal involvement. Neuropsycholog- Careful clinical interview with both patient and
ical testing documented spatial, executive, and family members will help to elicit evidence of
nonverbal memory problems, consistent with the Capgras delusions. In the course of family dis-
right frontotemporal localization on neuroimag- putes and initial evaluations, patients may learn
ing studies. to minimize or deny their delusions. Demented
patients may forget instances of misidentification.
Hence, family informants may be extremely help-
Neuropsychology and Psychology of ful. The literature is replete with case reports
Capgras Syndrome positing a psychodynamic explanation for
Capgras, but with no workup to rule out neuro-
Capgras and its variants represent either logic etiology. Since Capgras is commonly asso-
underidentification or overidentification of the ciated with neurologic illness, full workup
object of the delusion (Vie 1930). Thus, in Capgras including neuroimaging and neuropsychological
syndrome, the patient mistakenly perceives the testing is essential. Neuropsychological testing
person as unfamiliar due to underidentification. In often reveals deficits in frontal/executive and
Fregoli syndrome, on the other hand, the patient visuospatial functions (Malloy and Richardson
misperceives diverse persons as the same person 1994). Facial recognition and memory should be
due to overidentification. tested to rule out alternative explanations for the
Feinberg and Shapiro (1989) emphasized the patient’s problems, such as prosopagnosia.
importance of the right temporal lobe in produc-
ing misidentification delusions. They reviewed
the evidence from stimulation and seizure studies Treatment
indicating that the right temporal lobe plays an
important role in producing the experience of In degenerative dementia, duplication delusions
familiarity. Cutting (1991) has put forth a similar are usually transitory phenomena, occurring in the
argument regarding the role of the right hemi- early-to-middle stages and disappearing when
sphere in identification. cognitive deficits become severe. In other etiolo-
Crucial factors in the persistence of delusions gies such as cerebrovascular disease, they often
may be the length of time the perceptual distor- occur acutely and persist for many months or
tion continues and the ability of the patient to years. Prognosis appears to vary with the type of
correct the misperception on the basis of new delusion and the underlying etiology.
information. Frontal lesions may impact on the Many underlying systemic causes (e.g., infec-
latter self-corrective function, making it impos- tions, toxic reactions, metabolic disturbances) of
sible to resolve conflicting information, resulting duplication delusions are readily treated, resulting
in unconcern and confabulation when the con- in elimination of the delusion. For example, San-
flicts are confronted (Joseph 1986). Alexander tiago et al. (1987) reported resolution of Capgras
et al. (1979) were the first to report a Capgras following treatment of underlying thyroid disease.
682 Carbamazepine

Spontaneous resolution of Capgras delusions has Foerstl, H. (1990). Capgras’ delusion: An example
also been reported (Ruff and Volpe 1981). of coalescent psychodynamic and organic factors.
Comprehensive Psychiatry, 31, 447–449.
On the other hand, Joseph (1987) described a Joseph, R. (1986). Confabulation and delusional denial:
patient whose chronic psychosis and intermittent Frontal lobe and lateralized influences. Journal of Clin-
psychotic misidentification of the Capgras and ical Psychology, 42, 507–520.
intermetamorphosis types were refractory to neu- Joseph, A. B. (1987). Delusional misidentification of the
Capgras and intermetamorphosis types responding to
roleptic treatment. Upon administration of a trial clorazepate. A case report. Acta Psychiatrica
of clorazepate, complete remission of psychotic Scandinavica, 75, 330–332.
symptoms was achieved for the first time in Malloy, P. (1991). Differential diagnosis of primary
19 years, but these recurred when the patient and secondary Capgras delusions. Neuropsychiatry,
Neuropsychology, and Behavioral Neurology, 4,
discontinued her clorazepate. 90–108.
The effectiveness of psychological interven- Malloy, P. F. & Richardson, E. D. (1994). The frontal
tions may vary with the type of delusion and the lobes and content-specific delusions. Journal of
degree to which neurologic factors are involved. Neuropsychiatry and Clinical Neuroscience, 6,
455–466.
Unfortunately, there has been no systematic treat- Mendez, M. F., Martin, R. J., Smyth, K. A., & Whitehouse,
ment follow-up research, and data are limited to P. J. (1992). Disturbances of person identification in
uncontrolled case studies. Alzheimer’s disease. A retrospective study. The Jour-
nal of Nervous and Mental Disease, 180, 94–96.
Ruff, R. L., & Volpe, B. T. (1981). Environmental redupli-
cation associated with right frontal and parietal lobe
Cross-References injury. Journal of Neurology, Neurosurgery, and Psy-
chiatry, 44, 382–386.
Santiago, J. M., Stoker, D. L., Beigel, A., Yost, D., & Spen-
▶ Reduplicative Paramnesia cer, P. (1987). Capgras’ syndrome in a myxedema patient.
Hospital & Community Psychiatry, 38, 199–201.
Vie, J. (1930). Un trouble de l’identification des personnes:
L’illusion des sosies. Annales Médico-Psychologiques,
References and Readings 88, 214–237.

Alexander, M., Stuss, D. T., & Benson, D. F. (1979).

Capgras syndrome: A reduplicative phenomenon. Neu-
rology, 29, 334–339.
American Psychiatric Association. (1987). Diagnostic and
statistical manual of mental disorders-third edition-
revised(DSM-III-R). Washington, DC: American Psy- Carbamazepine
chiatric Press.
Capgras, J., & Reboul-Lachaux, J. (1923). L’illusion des Efrain Antonio Gonzalez
“sosies” dans un delire systematise. Bulletin de Societe
College of Psychology, Nova Southeastern
Clinical Medicine Mentale, 11, 6–16.
Christodoulou, G. N. (1978). Syndrome of subjective dou- University, Fort Lauderdale, FL, USA
bles. The American Journal of Psychiatry, 135, 249–251. Utah State University, Logan, UT, USA
Courbon, P., & Fail, G. (1927). Syndrome “d’illusion de
Fregoli” et schizophrenie. Bulletin de Societe Clinical
Medicine Mentale, 88, 214–237.
Courbon, P., & Tusques, J. (1932). L’illusion de Generic Name
intermetamorphose et de charme. Annales Médico-
Psychologiques, 90, 401–406. Carbamazepine
Cutting, J. (1991). Delusional misidentification and the role
of the right hemisphere in the appreciation of identity. The
British Journal of Psychiatry, 159(Suppl. 14), 70–75.
Dohn, H. H., & Crews, E. L. (1986). Capgras syndrome: Brand Name
A literature review and case series. The Hillside Jour-
nal of Clinical Psychiatry, 8, 56–74.
Tegretol, Carbatrol, Equetro, Epitol, Tegretol XR,
Feinberg, T. E., & Shapiro, R. M. (1989). Misidentification-
reduplication and the right hemisphere. Neuropsychiatry, Carbamazepine Chewtabs, Carbamazepine CR,
Neuropsychology, and Behavioral Neurology, 2, 39–48. Teril, and Carnexiv
Carbon Monoxide Poisoning 683

Class Additional Information

Drug Interaction Effects. http://www.drugs.com/drug_
interactions.html.
Anticonvulsants, antimanic agents, and bipolar
Drug Molecule Images. http://www.worldofmolecules.
disorder agents com/drugs/.
Free Drug Online and PDA Software. www.epocrates.com.
Free Drug Online and PDA Software. www.medscape.com.
Proposed Mechanism(s) of Action Gene-Based Estimate of Drug interactions. http:// C
mhc.daytondcs.com:8080/cgibin/ddiD4?ver=4&task=
getDrugList.
Carbamazepine is a use-dependent blocker of Pill Identification. http://www.drugs.com/pill_identifica
voltage-sensitive sodium channels; it interacts tion.html.
with the open channel conformation of voltage-
sensitive sodium channels; it interacts at alpha
pore-forming subunit of voltage-sensitive sodium Carbon Monoxide Poisoning
channels, and it inhibits release of glutamate.
George C. Wagner
Department of Psychology, Rutgers University,
Indication
New Brunswick, NJ, USA
Complex partial seizures, generalized tonic-clonic
seizures, mixed seizure patterns, bipolar mania,
Synonyms
restless legs syndrome, postherpetic neuralgia,
trigeminal neuralgia pain, and intravenous carba-
Carboxyhemoglobinemia
mazepine (Orphan).

Description
Off-Label Use
Carbon monoxide (CO) is a colorless, odorless
Glossopharyngeal neuralgia, psychosis, schizo-
gas generated during the combustions of carbon-
phrenia, and personality disorders.
containing fuels. When inhaled into the lungs, it
readily competes with oxygen for binding sites on
Side Effects hemoglobin. The affinity for carbon monoxide
binding to hemoglobin is more than 200-fold
Serious greater than that for oxygen. Thus, at atmospheric
Aplastic anemia, agranulocytosis, Stevens-Johnson concentrations as low as 0.1%, carbon monoxide
syndrome, cardiac problems, induction of psycho- will achieve a 50% saturation of the hemoglobin,
sis or mania, and increased frequency of seizures. resulting in carboxyhemoglobinemia and a signif-
icant reduction in the blood oxygen levels.
Common Acute carbon monoxide poisoning as, for
Sedation, dizziness, confusion, headache, nausea, example, following exposure to automobile
and vomiting. exhaust (which generates about 5–7% carbon
monoxide) will rapidly saturate the hemoglobin
and cause death within minutes with virtually no
References and Readings prior symptoms.

Physicians’ Desk Reference (71st ed.). (2017). Montvale:

Thomson PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The
Categorization
prescriber’s guide (2nd ed.). New York: Cambridge
University Press. Poison; neurotoxin
684 Carbon Monoxide Poisoning

Epidemiology Neuropsychology of Carbon Monoxide

Syndrome
Exposure to low concentrations of carbon mon-
oxide consequent to the operation of faulty fur- The Carbon Monoxide Neuropsychological
naces or gas-powered engines is the leading cause Screening Battery (CONSB) has been developed
of accidental poisoning in the United States. to screen for cognitive impairment following
Exposure to high concentrations of carbon mon- acute carbon monoxide poisoning (Messier and
oxide is the most common form of intentional Myers 1991). The CONSB battery begins with an
poisoning in the United States. Exposure to car- assessment of general orientation of the patient,
bon monoxide is the most common form of poi- and this is followed by the Digit Span, Trail Mak-
soning worldwide. With increased awareness of ing, Digit Symbol, Aphasia Screening, and Block
its potential dangers, the majority of these expo- Design tests. Use of this battery in an emergency
sures can be prevented. room setting allows for the early detection of
cerebral impairment in the exposed individuals.

Natural History, Prognostic Factors, and Evaluation

Outcomes
The long-term consequences of acute carbon
Compared to normal oxyhemoglobin (i.e., when monoxide poisoning may, in part, be consequent
oxygen binds to hemoglobin), carboxyhemoglobin to damage to the blood-brain barrier during the
is bright red; thus, an early sign of carbon monox- period of hypoxic coma. Following apparent
ide poisoning is a cherry-red skin color. recovery from the acute exposure, a delayed tox-
Acute exposure to lower concentrations of icity with abrupt onset may appear with symptoms
carbon monoxide will result in a slowly develop- of confusion together with motoric symptoms
ing hypoxia that triggers peripheral vasodilation. resembling Parkinson’s disease (incoordination,
Paradoxically, when there is a slow increase in muscular weakness, and muscular rigidity).
carboxyhemoglobin saturation, compensatory These neurological signs reflect extensive damage
changes in respiratory rate may lag. Thus, the to the basal ganglia and white matter of the brain
symptoms of dizziness, weakness, headache, and with a demyelination that spares the neuronal
nausea will precede fainting. Once unconscious, axons. Neuroimaging scans will most likely
increased respiration and tachycardia will be appear normal 24 h after exposure; lesions may
followed by convulsions, and coma and death begin to appear 2 weeks later. Functional changes
will ensue as the carboxyhemoglobin climbs and associated with these later-appearing lesions are
remains above 50% saturation. variable, but attempts have been made to relate
Chronic exposure to low concentrations of these to the severity of the initial exposure. Acute
carbon monoxide can occur in heavy smokers exposure resulting in carboxyhemoglobin satura-
as well as in individuals whose occupations tion of 25% or more will result in later-onset
involve protracted exposure to exhaust fumes. cognitive impairments in as many as 50% of the
The binding of carbon monoxide to hemoglobin patients. The cognitive deficits include agnosia,
is fully dissociable though these individuals aphasia, and apraxia as well as impaired memory,
may manifest carboxyhemoglobin saturation at impaired executive function, and a general
10%, which is 20-fold higher than normal. decrease in intellect. In addition, visuomotor per-
Symptoms associated with chronic exposure formance deteriorates. Finally, late-appearing
include headache, fatigue, nausea, difficulty changes in affect are frequently reported as are
concentrating, and impaired memory (Kao and obsessive-compulsive tendencies and anxiety
Nanagas 2005). (Hopkins and Woon 2006).
Cariprazine 685

Treatment Brand Name

Vraylar
Effective treatment entails removal from the
source of the carbon monoxide and providing Class
oxygen; when breathing air, the half-life of Antipsychotics, second generation; bipolar agents
carboxyhemoglobin is about 5 h, and this time
can be reduced to 1.5 h with oxygen supplemen- C
tation. Indeed, supplementation with oxygen Proposed Mechanism(s) of Action
immediately after exposure remains as the most
effective strategy for reducing the severity of the The efficacy of cariprazine could be mediated
later-appearing neural and functional conse- through a combination of partial agonist activity
quences following carbon monoxide poisoning at central dopamine D2 and serotonin 5-HT1A
(Prockop and Chichkova 2007). receptors and antagonistic activity at serotonin
5-HT2A receptors.

See Also
Indication
▶ Neurotoxins
For the treatment of schizophrenia and for the
acute treatment of manic or mixed episodes asso-
References and Readings ciated with bipolar I disorder.

Hopkins, R. O., & Woon, F. L. M. (2006). Neuroimaging,

cognitive and neurobehavioral outcomes following car- Off-Label Use
bon monoxide poisoning. Behavioral and Cognitive
Neuroscience Reviews, 5(3), 141–155.
Kao, L. W., & Nanagas, K. A. (2005). Carbon monoxide No common off-label use
poisoning. Medical Clinics of North America, 89,
1161–1194.
Messier, L. D., & Myers, R. A. M. (1991).
Side Effects
A neuropsychological screening battery for emergency
assessment of carbon-monoxide-poisoned patients.
Journal of Clinical Psychology, 47(5), 675–684. Serious
Prockop, L. D., & Chichkova, R. I. (2007). Carbon mon- Increased risk of death in elderly people with
oxide intoxication: An updated review. Journal of the
dementia-related psychosis, extrapyramidal
Neurological Sciences, 262, 122–130.
symptoms, Parkinsonism, akathisia.

Common
Cariprazine Headache, insomnia, nausea, constipation,
somnolence.
Efrain Antonio Gonzalez
College of Psychology, Nova Southeastern
University, Fort Lauderdale, FL, USA References and Readings
Utah State University, Logan, UT, USA
Physicians’ desk reference (71st ed.) (2017). Montvale:
Thomson PDR.

Generic Name Additional Information

CenterWatch. https://www.centerwatch.com/drug-informa
Cariprazine tion/fda-approved-drugs/drug/100094/vraylar-cariprazine
686 Carotid Angiography

Drug Molecule Images. http://www.worldofmolecules. dissections and pseudoaneurysms which may be

com/drugs/ associated with classic signs of pain, bruits, and/or
Free Drug Online and PDA Software. www.epocrates.com
Free Drug Online and PDA Software. www.medscapep cranial nerve palsies. Carotid angiography is also
sychiatry.com useful for imaging of carotid-cavernous fistulas
Gene-Based Estimate of Drug interactions. http://mhc. which if not found early can cause blindness and
daytondcs.com:8080/cgibin/ddiD4?ver=4&task=get may present with an ocular bruit, scleral injection,
DrugList
http://www.drugs.com/drug_interactions.html and ocular proptosis.
http://www.vraylar.com/
Pill Identification. http://www.drugs.com/pill_identifica
tion.html
Current Knowledge

Can be part of the evaluation process of patients

with cerebrovascular disease or traumatic vascu-
lar insult.
Carotid Angiography
Cross-References
Nathan D. Zasler1 and Paul E. Kaplan2
1
Concussion Care Centre of Virginia, Ltd., ▶ Angioma, Cavernous Angioma
Richmond, VA, USA ▶ Glioma
2
Capitol Clinical Neuroscience, Folsom, CA, ▶ Hemangioma
USA ▶ Hemiplegia

Synonyms References and Readings

Angio http://www.radiologyinfo.org/en/info.cfm?pg=angiocerebral.
Accessed 10 Apr 2016.
Ahn, S. O., Prince, E. A., & Dubel, G. J. (2013). Basic
neuroangiography: Review of technique and perioper-
Definition ative patient care. Seminars in Interventional Radiol-
ogy, 30(3), 225–233.
Kaufmann, T. J., & Kallmes, D. F. (2008). Diagnostic
Angiography is the evaluation of the blood ves-
cerebral angiography: Archaic and complication-
sels of the central nervous system and associated prone or here to stay for another 80 years? AJR. Amer-
cervicocerebral vasculature via radiographic ican Journal of Roentgenology, 190(6), 1435–1437.
imaging of intravascular contrast media injected
prior to the imaging procedure. Femoral or axil-
lary nonselective approaches can be used to cath-
eterize the aortic arch or selective means
employed to catheterize the carotid artery. Digital Carotid Endarterectomy
subtraction, computed tomography
(CT) scanning, and MRI techniques can be Alan Weintraub1 and Anuj Sharma2
1
applied as adjutant imaging techniques once con- Craig Hospital, Rocky Mountain Regional Brain
trast is injected. Obstructions, stenosis, aneu- Injury System, Englewood, CO, USA
2
rysms, and A-V malformations can be identified Virginia Commonwealth University School of
through this technique. Finer and more selective Medicine, Richmond, VA, USA
views are accomplished by using microcatheters.
Some of the disease entities studied include ische-
mic cerebrovascular disease, aneurysms, vascular Synonyms
malformations, neoplasms, and brain injuries.
Angiography is the test of choice for arterial CEA
Carotid Endarterectomy 687

Definition speech, or loss of vision in one eye described as

a shade coming down over one eye (amaurosis
Carotid Endarterectomy (CEA) is an elective sur- fugax), last for a few minutes to hours and resolve
gical procedure that removes plaque from the completely in 24 h. Patients with a history of
lumen of the carotid artery. After anesthesia, the stroke or TIA are at increased risk of a subsequent
surgeon clamps the carotid artery proximal and stroke and should be further evaluated with imag-
distal to the stenosis temporarily. The surgeon ing studies. According to the North American C
may place a shunt proximal to the clamp to reroute Symptomatic Carotid Endarterectomy Trial
blood to the brain. Next, an incision is made over (NASCET), patients with symptomatic carotid
the area of blockage. The plaque is scraped out artery stenosis of greater than 70% have a 26%
and separated from the inner lining of the artery. risk of recurrent stroke over 2 years.
After it is removed, the artery is sutured together, The diagnosis of a TIA is made by carotid
the clamps are removed, and any bleeding is duplex ultrasound. This type of imaging bounces
stopped. Finally, the skin incision is closed. high-frequency sound waves off blood vessels
and the blood within the lumen to determine
blood flow and any abnormalities within the ves-
Current Knowledge sels themselves. Other modalities useful in the
diagnosis of a TIA include computed tomography
The arch of the aorta gives off three branches: the angiography (CTA), magnetic resonance angiog-
innominate, the left common carotid, and the left raphy (MRA), and angiography. In each of these,
subclavian. The innominate artery, also known as a contrast dye, or gadolidium in the case of MRA,
the brachiocephalic artery, gives rise to the right is injected into the arteries. This helps identify any
subclavian artery and the right common carotid areas of poor blood flow and determine the degree
artery. The common carotid arteries bilaterally of stenosis.
split into internal and external carotid arteries. If there is greater than 70% blockage of the
The right and left internal carotid arteries, along carotid artery, a CEA is recommended if the patient
with the vertebral arteries, branches of the subcla- is symptomatic with a history of TIA or non-
vian artery, are the major blood vessels supplying disabling stroke, or even if the patient is
the brain. asymptomatic. However, a CEA should not be
As plaque builds in the carotid artery, athero- performed during a stroke or TIA or if the patient
sclerosis, or hardening of arteries, develops. experiences a stroke that leaves him severely
Carotid stenosis, or narrowing of the carotid disabled. If there is less than a 70% blockage
artery, may also develop and is most common at and the patient is asymptomatic, a CEA is not
the origin of the internal carotid artery or less recommended. In this case, the patient should be
commonly at the distal common carotid artery. If treated medically with a baby aspirin daily. In addi-
the stenosis is severe, it may result in decreased tion, other risk factors that may cause further dam-
perfusion of brain tissue and consequently ische- age to the vessels, such as smoking, diabetes,
mia. Another mechanism by which ischemia can hypertension, and hypercholesterolemia, should
develop is by the development of a thrombus over be treated medically. A CEA is only recommended
the plaque. When this occurs, an embolus may for 50–69% stenosis if the patient has had recurrent
break off and may result in the occlusion of a TIAs unresponsive to medical management.
vessel distally. For patients that are high risk for the CEA, other
A stroke may develop if the brain is deprived of surgical interventions, such as angioplasty and
its blood supply, resulting in a sudden loss of stenting, can be considered. During this procedure,
neurologic function. However, transient ischemic a catheter is inserted through the groin and is guided
attacks (TIA) may be the diagnosis if symptoms, until it reached the site of stenosis. After the loca-
such as loss of sensory or motor function in the tion of the catheter is confirmed, a balloon inflates
extremities, inability to comprehend or initiate and attaches a metal-mesh stent into the artery. The
688 Carrie Kennedy

balloon is then deflated and the catheter is gently Major Appointments (Institution,
removed. However, long-term studies have not Location, Dates)
proven this method to be superior to a CEA.
• Director, Deployment Health Clinical Center,
Defense Centers of Excellence for Psycholog-
Cross-References ical Health and Traumatic Brain Injury, Silver
Spring, MD (October 2016–present)
▶ Ischemia • Head, Mental Health Department, Naval
▶ Magnetic Resonance Angiography Branch Health Clinic, Bahrain (2015–2016)
▶ Stroke • Group Psychologist, Marine Corps Embassy
Security Group (2011–2015)
• Aerospace Neuropsychologist, Assistant
References and Readings Director of Clinical Services, Naval Aerospace
Medical Institute (2006–2011)
Chaturvedi, S., Bruno, A., Feasby, T., Holloway, R., • Head, Substance Abuse Rehabilitation Depart-
Benavente, O., Cohen, S. N., et al. (2005). Carotid
endarterectomy – an evidence-based review: Report
ment, United States Naval Hospital, Okinawa,
of the Therapeutics and Technology Assessment Sub- Japan (2002–2004)
committee of the American Academy of Neurology. • Division Officer/Psychologist, Mental Health
Neurology, 65, 794–801. Department, United States Naval Hospital,
Roffi, M., & Lüscher, T. F. (2008). Management of carotid
Okinawa Japan (2001–2002)
artery stenosis. Herz, 33, 490–497.
Rothwell, P. M., Eliasziw, M., Gutnikov, S. A., Fox, A. J., • Postdoctoral Supervision, Behavioral
Taylor, D. W., Mayberg, M. R., et al. (2003). Analysis Healthcare and Infectious Disease Special
of pooled data from the randomised controlled trials Immunology Clinic, National Naval Medical
ofendarterectomy for symptomatic carotid stenosis.
Center (2000–2001)
Lancet, 361, 107–116.
• Case Manager/Program Consultant, Chesa-
peake Head Injury Center (1991–1999)

Carrie Kennedy
Major Honors and Awards
Leah Drasher-Phillips
Center of Innovation on Disability and • Sigma Xi First Dean of the College of Arts and
Rehabilitation Research, James A. Haley Sciences Research Award (1997)
Veterans’ Hospital, Tampa, FL, USA • Sigma Xi Departmental Research Award
(1997)
• Pennsylvania Psychological Association Grad-
Name and Degrees uate Student Research Award (1997)
• National Academy of Neuropsychology Grad-
Carrie Hill Kennedy, PhD, received a Bachelor in uate Student Research Award (1997)
Science (B.S.) degree in Psychology (1991) from • Philadelphia Neuropsychology Society Grad-
York College, York, Pennsylvania. She received a uate Student Research Award (1998)
Master’s in Arts (M.A.) degree in Psychology • Navy and Marine Corps Achievement Medal
(1993) from Washington College, Chestertown, (2003)
Maryland. She received a Master’s in Education • Medical Service Corps Officer of the Year,
(M.Ed.) degree in Guidance and Counseling Okinawa, Japan (2003)
(1995) from the University of Maryland Eastern • Navy and Marine Corps Commendation Medal
Shore, Princess Anne, Maryland. She was awarded (May 2004, September 2009, December 2010,
a PhD in Clinical Psychology from Drexel Univer- September 2016)
sity, Philadelphia, Pennsylvania (2000). • Defense Meritorious Service Medal (2007)
Carrie Kennedy 689

• Navy Junior Clinical Psychologist of the Year Afghanistan. Stationed in the British combat hos-
(2007) pital on Camp Bastian, she and her technician
• American Psychological Association Division were responsible for the blast concussion evalua-
19, Charles S. Gersoni Award (2012) tion of every service member who had been in or
• Navy Senior Clinical Psychologist of the Year near a blast. 2010 was a particularly kinetic time
(2012) in the combat zone, and she saw approximately
• Meritorious Service Medal (2015) 400 US service members acutely for evaluation C
during her 7-month deployment. She also trav-
elled through the combat zone providing training
Landmark Clinical, Scientific, and in acute concussion assessment to Navy corpsmen
Professional Contributions and trained both the leaders and medical person-
nel of arriving Marine units in various aspects of
Captain Kennedy has been a staunch advocate of concussion (i.e., policy, assessment, and what
neuropsychology in the military. She served as happens to service members following evacuation
the Navy’s neuropsychology subspecialty leader from the point of injury).
from 2006 to 2015. During that time, she tripled Following her return from deployment, she
the number of active duty neuropsychologists in was again tapped by BUMED to train corpsmen
the Navy, facilitated the offering of at least one deploying to the combat zone on use of the Mili-
new neuropsychology fellowship annually for tary Acute Concussion Evaluation, and she has
Navy psychologists, ensured coded billets for consulted a subject matter expert on the Navy’s
neuropsychologists, and established a permanent concussion policies since that time. She continues
designation for a winged neuropsychologist for to advocate for the field of neuropsychology in her
the billet at the Naval Aerospace Medical Insti- current position as Director, DoD Deployment
tute. In this billet, Navy neuropsychologists are Health Clinical Center.
now provided the 6-month aeromedical officer In addition to her military accomplishments,
training in aerospace psychology. This training she considers one of her greatest achievements
involves survival training, aviation-related to be her Master’s Thesis, in which she created
academics, flight training, and training in aero- and validated an assessment of capacity to consent
space medical, physiological, and psychological to sexual activity, a thesis spurred by very real
topics. practical problems at the TBI rehabilitation center
Throughout her naval career, and particularly where she worked while going to graduate school.
when the number of blast concussed service She designed the Sexual Consent and Education
members began increasing due to the war, she Assessment (SCEA), which was used in a case of
provided training in neuropsychological topics a man accused of sexually abusing a severely
throughout the Navy and Marine Corps. In 2008 cognitively and physically disabled woman and
she was tapped by the Navy’s Bureau of Medicine impregnating her. Thus, the case hinged on
and Surgery (BUMED) to provide training to both whether or not she could consent, and the findings
garrison and deploying providers in such topics as of the SCEA were that she could not. On appeal,
acute concussion assessment, physiology of based on a challenge of the instrument’s validity,
traumatic brain injury (TBI), combat stress, and and specifically on 27 May 2014, the SCEA met
use of the Automated Neuropsychological the Daubert standard as set out by the Court of
Assessment Metric (ANAM). Appeals of the State of Oregon in the case of State
Her previous employment at a community- of Oregon vs. George Woody Reed, [State v.
based TBI rehabilitation center, her graduate Brown, 297 Or 404, 687 P2d 751 (1984), and
training in neuropsychology, and the focus of State v. O’Key, 321 Or 285, 899 P2d 663
UVA’s neuropsychology fellowship on sport’s (1995), for the admission of scientific evidence
concussions provided the trifecta of professional under OEC 702 and OEC 401] and the individ-
preparation for neuropsychological services in ual’s sentence was upheld.
690 Carrie Kennedy

Short Biography See Also

Navy Captain (Dr.) Carrie Kennedy is the director ▶ Automated Neuropsychological Assessment
of the Deployment Health Clinical Center Metrics
(DHCC), one of three centers of the Defense ▶ Battlefield Assessment
Centers of Excellence for Psychological Health ▶ Department of Defense (DoD)
and Traumatic Brain Injury (DCoE). ▶ Military Acute Concussion Evaluation
Kennedy was commissioned as a lieutenant in ▶ Military Neuropsychology
the fourth year of her PhD program in clinical ▶ Traumatic Brain Injury (TBI)
psychology at Drexel University. She completed
her internship at Naval Medical Center Ports-
mouth, Virginia, in 2000 and transferred to References and Readings
National Naval Medical Center where she
worked in the HIV clinic for 8 months. Opera- Peer-Reviewed Papers
tional requirements prompted her early transfer Campbell, J. S., Moore, J. L., Poythress, N. G., & Kennedy,
to United States Naval Hospital, Okinawa, in C. H. (2009). Personality traits in clinically referred
aviators: Two clusters related to occupational suitabil-
2001, where she served as department head of ity. Aviation, Space and Environmental Medicine, 12,
the Substance Abuse Rehabilitation Program 1049–1054.
until 2004. Hill, S. K., Ryan, L. M., Kennedy, C. H., & Malamut, B. L.
Following her tour in Okinawa, she was (2003). The relationship between measures of declara-
tive memory and the test of memory malingering in
selected for Duty Under Instruction (DUINS) patients with and without temporal lobe dysfunction.
and completed postdoctoral fellowship training Journal of Forensic Neuropsychology, 3, 1–18.
in neuropsychology at the University of Virginia Johnson, W. B., & Kennedy, C. H. (2010). Preparing
School of Medicine in 2006. She was then psychologists for high-risk jobs: Key ethical consider-
ations for military clinical supervisors. Professional
assigned to Naval Aerospace Medical Institute Psychology: Research and Practice, 41, 298–304.
(NAMI), Pensacola, Florida, where she com- Kennedy, C. H. (1999). Assessing competency to consent
pleted aeromedical officer training, was winged to sexual activity in the cognitively impaired popula-
as aerospace experimental psychologist #133, and tion. Journal of Forensic Neuropsychology, 1, 17–33.
Kennedy, C. H. (2001a). Test review: d2 test of attention.
served as aerospace neuropsychologist until 2011. Applied Neuropsychology, 8, 256–259.
While stationed at NAMI, she was deployed Kennedy, C. H. (2001b). Test review: Tower of London –
twice, first to Guantanamo Bay, Cuba, in 2006 as Drexel University. Journal of Forensic Neuropsychol-
chief of behavioral health services and then to ogy, 2, 90–98.
Kennedy, C. H. (2003). Legal and psychological implica-
Afghanistan with 1st Medical Battalion in 2010, tions in the assessment of sexual consent in the cogni-
where she was assigned to the Role III hospital on tively impaired population. Assessment, 10, 352–358.
Camp Bastian and evaluated individuals with Kennedy, C. H. (2006, September 20). Understanding Our
blast concussions in the emergency department. Nation’s Greatest Resource: Military Personnel.
(Review of the 4-volume set of books Military Life:
Next, she served as group psychologist of the The Psychology of Serving in Peace and Combat).
Marine Corps Embassy Security Group, Quantico, PsycCRITIQUES-Contemporary Psychology: APA
Virginia, and before coming to DHCC, she served Review of Books, 51 (No. 38), Article 1. Retrieved
as mental health department head at Naval Branch September 20, 2006, from the PsycCRITIQUES
database.
Health Clinic, Bahrain. Kennedy, C. H. (2007a, September 26). An Overview of
Kennedy’s personal awards include the Mental Health Diagnoses for First Responders.
Defense Meritorious Service Medal, Meritorious (Review of the book First Responder’s Guide to Abnor-
Service Medal, Navy Commendation Medal (four mal Psychology: Applications for Police, Firefighters
and Rescue Personnel). PsycCRITIQUES-Contempo-
awards), and the Navy Achievement Medal. She rary Psychology: APA Review of Books, 52 (No. 39),
is board certified in clinical psychology and police Article 8. Retrieved September 26, 2007, from the
and public safety psychology. PsycCRITIQUES database.
Case Management 691

Kennedy, C. H. (2007b, August 29). The Definitive Hand- Tsao, J. W., Perry, B. N., Kennedy, C. H., & Beresford, R.
book for the Cognitive Behavioral Treatment of PTSD. (2014). Predicting prolonged recovery after concus-
(Review of the book Cognitive-Behavioral Therapy for sion. Neurology, 83, 2196–2197.
PTSD: A Case Formulation Approach).
PsycCRITIQUES-Contemporary Psychology: APA
Books
Review of Books, 52 (No. 35), Article 14. Retrieved
Kennedy, C. H., & Kay, G. (2013). Aeromedical psychol-
August 30, 2007, from the PsycCRITIQUES database.
ogy. England: Ashgate.
Kennedy, C. H. (2007c, May 23). Components of Adult
ADHD Assessment and Treatment. (Review of the
Kennedy, C. H., & Kay, G. G. (2016). Aeromedical psy- C
chology (Chinese translation). Beijing: Military Medi-
book Understanding and treating adults with Attention
cal Science Press.
Deficit Hyperactivity Disorder). PsycCRITIQUES-
Kennedy, C. H., & Moore, J. L. (2010). Military neuropsy-
Contemporary Psychology: APA Review of Books, 52
chology. New York: Springer.
(No. 21), Article 13. Retrieved May 23, 2007, from the
Kennedy, C. H., & Williams, T. J. (2011). Ethical practice
PsycCRITIQUES database.
in operational psychology: Military and National Intel-
Kennedy, C. H. (2008, July 30). A succinct desk reference
ligence Applications. Washington, DC: American Psy-
for pathological gambling. (review of the book problem
chological Association.
and pathological gambling). PsycCRITIQUES-Con-
Kennedy, C. H., & Zillmer, E. A. (2001). Study guide for
temporary Psychology: APA Review of Books, 53
Zillmer and Spiers principles of neuropsychology. Bel-
(no. 31), article 7. Retrieved July 30, 2008 from the
mont: Wadsworth.
PsycCRITIQUES database.
Kennedy, C. H., & Zillmer, E. A. (2006). Military psychol-
Kennedy, C. H. (2009, February 18). The Psychology of
ogy: Clinical and operational applications. New York:
September 11, 2001. (Review of the book Therapy
Guilford Publishing.
after Terror). PsycCRITIQUES-Contemporary Psy-
Kennedy, C. H., & Zillmer, E. A. (2007). Military psychol-
chology: APA Review of Books, 54 (No. 7), Article 5.
ogy: Clinical and operational applications (Chinese
Retrieved March 7, 2009 from the PsycCRITIQUES
translation). Beijing: East China Normal University
database.
Press.
Kennedy, C. H. (2016). The future is here. (Review of the
Kennedy, C. H., & Zillmer, E. A. (2009). Military psychol-
book Humans in Space: The Psychological Hurdles).
ogy: Clinical and operational applications (Portu-
PsycCRITIQUES-Contemporary Psychology: APA
guese translation). Rio de Janeiro: Biblioteca do
Review of Books, 61 (No. 9). Retrieved June 2, 2016
Exercito.
from the PsycCRITIQUES database.
Kennedy, C. H., & Zillmer, E. A. (2012). Military psychol-
Kennedy, C. H., & Johnson, W. B. (2009). Mixed agency
ogy: Clinical and operational applications (2nd ed.).
in military psychology: Applying the American Psy-
New York: Guilford Publishing.
chological Association’s ethics code. Psychological
Kennedy, C. H., & Zillmer, E. A. (2016). Military psychol-
Services, 6, 22–31.
ogy: Clinical and operational applications (2nd ed.,
Kennedy, C. H., & Moore, B. A. (2008). Evolution of
Korean translation). Seoul: Hakjisa Publisher.
clinical military psychology ethics. Military Psychol-
Moore, B. A., & Kennedy, C. H. (2011). Wheels down:
ogy, 20, 1–6.
Adjusting to life after deployment. Washington, DC:
Kennedy, C. H., & Niederbuhl, J. (2001). Establishing
American Psychological Association.
criteria for sexual consent capacity in the mentally
retarded population. American Journal on Mental
Retardation, 106, 503–510.
Kennedy, C. H., Cook, J. H., Poole, D. R., Brunson, C. L.,
& Jones, D. E. (2005). Review of an overseas military
gambling treatment program. Military Medicine, 170,
Case Management
683–687.
Kennedy, C. H., Jones, D. E., & Arita, A. A. (2007). Brian T. McMahon
Multicultural experiences of U.S. military psycholo- Department of Rehabilitation Counseling,
gists: Current trends and training target areas. Psycho-
Virginia Commonwealth University, Richmond,
logical Services, 4, 158–167.
Kennedy, C. H., Malone, R. C., & Franks, M. J. (2009). VA, USA
Provision of mental health services at the detention
hospital in Guantanamo Bay. Psychological Services,
6, 1–10.
Case managers are professionally trained
Kennedy, C. H., Evans, J. P., Lynch-Chee, S., Moore, J. L.,
Barth, J., & Stuessi, K. (2012). Return to combat duty healthcare providers who work with individuals
following concussive blast injury. Archives of Clinical with neurological impairments and many other
Neuropsychology, 27, 817–827. stakeholders to help them understand fully:
692 Catastrophic Reaction

• The nature and scope of the impairment • Rehabilitation concepts and strategies
• The composition of the interdisciplinary team • Ethical, legal, and practice standards
• Their particular role and value on the interdis-
ciplinary team There are now over 60,000 CCMs in the USA,
• The issues and barriers to restoring function and case management continues to grow and
• The solutions to removing or mitigating these evolve in response to changing healthcare circum-
issues and barriers stances. Without question, the mission of case
managers is highly consistent with the spirit and
Above all, the case manager is frequently the intent of the Affordable Healthcare Act due to its
main architect of the rehabilitation plan as well as inherent emphases on cost containment and qual-
the coordinator of all of the services and service ity. The Commission on Case Management Certi-
providers required by the plan. As such, the case fication makes available an abundance of accurate
manager is a true manager and is trained in man- and helpful information about the ongoing profes-
agement theory including how to plan, organize, sionalization of the case management profession
direct, and control. In executing these manage- at www.ccmcertification.org.
ment functions, the case manager is “not” manag-
ing the person or the impairment but rather is
working in partnership with the individual
with the impairment to manage the entire rehabil- Catastrophic Reaction
itation process, from outreach and evaluation
through the myriad of restorative therapies to the Dawn E. Bouman
point of maximum functioning in the community Neuropsychology and Medical Psychology,
in terms of family life and/or employment. University of Cincinnati, Department of
Typically, a case manager has been trained Neurology and Rehabilitation Medicine,
in the “first profession” and is licensed or Cincinnati, OH, USA
certified in a relevant healthcare specialization.
Most professional case managers rise through
the ranks from nursing, rehabilitation counseling, Synonyms
social work, or an allied health specialization. But
to become a certified case manager, one must pass Catastrophic condition
an examination in case management principles
and practices and also accumulate several months
or years of supervised case management experi- Definition
ence. The certified case manager (CCM) does not
ever abandon the first profession which provides This term coined by Goldstein (1948) describes
the ethical and regulatory basis of their practice, acute distress, agitation, and disorganized behav-
and as such the CCM is considered an “overlay” ior occurring when overwhelmed by a situation
credential which adds value and case management with which the person cannot cope, typically fol-
expertise to one’s repertoire. lowing brain injury or other neurological impair-
In 2014, the Commission on Case Manage- ment. Rapid and extreme anxiety, depression, and
ment Certification published a revised list of key frustration can result when a person becomes
knowledge and practice domains for the CCM. overstimulated or overwhelmed with a task that
The new list includes: has become too difficult or is perceived as being
too difficult. Typically, persons experiencing
• Care delivery and reimbursement methods catastrophic reactions are not fully aware of their
• Psychosocial concepts and support systems increasing lability and cannot respond to logic and
• Evaluation and measurement of quality and reason, but they benefit from decreased demands
outcomes and calm reassurance. Catastrophic reactions were
Catatonic Behavior 693

initially thought to be associated only with domi- Short Description

nant hemisphere damage and accompanying lan-
guage impairment, but they can follow any Catatonic behavior is characterized by marked
neurological problem that interferes with adaptive disturbances in psychomotor movements that
coping and executive functioning. occur within the context of a psychiatric or med-
ical condition. According to the Diagnostic and
Statistical Manual of Mental Disorders-Fifth C
Edition (DSM-5), catatonic features are identified,
Cross-References
and the catatonic specifier or residual category is
appropriate, when there are at least three of the
▶ Agitation
following:
▶ De-Escalation
▶ Executive Functioning
• Stupor (no psychomotor activity, not relating
▶ Frustration Tolerance
to environment)
• Catalepsy (passive induction of a posture held
against gravity)
References and Readings
• Waxy flexibility (resistance to positioning by
Callahan, C. D. (2009). The assessment and rehabilitation examiner)
of executive function disorders. In B. Johnstone & • Mutism (no, or very little, verbal response)
H. H. Stonnington (Eds.), Rehabilitation of neuropsy- • Negativism (opposition or no response to
chological disorders (2nd ed., pp. 75–106). Philadel- instructions or external stimuli)
phia: Psychology Press.
Goldstein, K. (1948). Language and language distur- • Posturing (spontaneous and active mainte-
bances: Aphasic symptom complexes and their signifi- nance of a posture against gravity)
cance for medicine and theory of language. New York: • Mannerism (peculiar, circumstantial caricature
Grune and Stratton. of normal actions)
Holland, D., & Larimore, C. (2009). The assessment and
rehabilitation of language disorders. In B. Johnstone & • Stereotypy (repetitive, abnormally frequent,
H. H. Stonnington (Eds.), Rehabilitation of neuropsy- non-goal-directed movements)
chological disorders (2nd ed., pp. 137–166). Philadel- • Agitation, not influenced by external stimuli
phia: Psychology Press. • Grimacing
Lezak, M. D., Howieson, D. B., Bigler, E.D., & Tranel
D. (2012). Neuropsychological assessment (5th ed., • Echolalia (repetition of a word or phrase just
p. 66). New York: Oxford University Press. spoken by another)
• Echopraxia (repetitive imitation of movements
of others)

Catatonic Behavior Categorization

Farzin Irani1 and Solomon Kalkstein2 The DSM-5 does not treat catatonia as an inde-
1
Psychology Department, West Chester pendent category but recognizes, under the same
University of Pennsylvania, West Chester, PA, code (293.89) and using the uniform criteria
USA above, several conditions where catatonic features
2
Psychiatry, University of Pennsylvania, may be observed:
Philadelphia, PA, USA
1. Catatonia associated with another mental dis-
order (catatonia specifier)
Synonyms (a) This specifier may be used when catatonia
occurs during the course of a psychotic,
Catatonia mood, or other mental disorder.
694 Catatonic Behavior

2. Catatonic disorder due to another medical are used and catatonia rating scales are applied,
condition this range narrows from 7% to 15% (Fink and
(a) When there is evidence from the history, Taylor 2006). While rarer, reports of catatonia
physical examination, or laboratory find- among children and adolescents have been
ings that the catatonia is attributable to documented, particularly amongst autism spec-
another medical condition, this specifier trum, pervasive developmental disorders, and
may be used. children with co-occurring medical conditions
3. Unspecified Catatonia (Consoli et al. 2012; Wing and Shah 2006;
(a) This residual category is used to docu- Weder et al. 2008).
ment the presence of catatonia when the
nature of the underlying mental disorder
or medical condition is unclear or when Natural History, Prognostic Factors, and
full criteria for catatonia are not met but Outcomes
distress or functional impairment are
evident. Catatonia was first formally described in the late
nineteenth century by the German physician,
Diagnostically, since catatonic behavior has Dr. Karl Ludwig Kahlbaum, as a disorder char-
numerous disease causes (Gelenberg 1976), care acterized by mood symptoms, stupor, confusion,
must be taken to distinguish the above-listed con- and eventually, dementia. Additionally, he
ditions from other syndromes which may present noted unusual motor symptoms and carefully
with similar features. Specifically, DSM-5 notes documented the character and course of the ill-
that a separate diagnosis is not given if the cata- ness. Subsequently, Kraepelin classified patients
tonia occurs exclusively during the course of a who exhibited symptoms of catatonia within
delirium. Additionally, catatonia-like symptoms his dementia praecox disorder, and Bleuler,
may occur in the context of one of the adopting this formulation, interpreted catatonic
medication-induced movement disorders, such symptoms as features of his newly named
as neuroleptic-induced parkinsonism or neurolep- “schizophrenia.” This model of catatonia as a
tic malignant syndrome, or as a feature of akinetic subtype within schizophrenia persisted through
parkinsonism, malignant hyperthermia, locked-in early and recent versions of the DSM. Only with
syndrome, stiff-person syndrome, or elective mut- the publication of DSM-IV was consideration
ism (Taylor and Fink 2003). given to catatonia occurring within the context
of other psychiatric and medical conditions. This
was due to important articles published in the
Epidemiology 1970s, which established co-occurrence of cata-
tonia and mood disorders (Abrams and Taylor
Catatonia is currently rare in North America and 1976) and emphasized the association between
Europe; however, reports of its prevalence vary catatonia and neurological or general medical
widely among studies. Bleuler’s initial estimates conditions (Gelenberg 1976). In an effort to
of catatonic symptomatology among schizophre- improve simplicity and clinical utility, DSM-5
nia patients were significantly higher than those further expanded the psychotic and mood
reported today. Numerous surveys of catatonia conditions under which catatonia can be used as
among psychiatric patients using duration a specifier and adopted a single set of criteria to
criteria of several hours to more than 24 h have be used across the diagnostic manual (Tandon
yielded prevalence rates ranging from 7.6% to et al. 2013). Along with the addition of a
38% (Taylor and Fink 2003). When including residual category, these changes in the direction
studies in which systematic rules of examination of establishing catatonia as an independent
Catatonic Behavior 695

syndrome, rather than a subtype of schizophre- Evaluation

nia, addressed a longstanding controversy about
the evolving conceptualization and classification Although DSM-5 requires 3 of 12 symptoms of
of catatonia (Fink 2013). catatonic behavior listed previously in order to
Numerous etiological mechanisms and risk establish presence of catatonia, definitions of cata-
factors for catatonia have been discussed includ- tonia, as well as its basic signs and symptoms, have
ing a history of perinatal infections, epilepsy, long been the subject of debate (Caroff and Ungvari C
medication effects, and frontal or basal ganglia 2007). Several rating scales have been developed to
diseases (Weder et al. 2008; Dhossche et al. assess for the presence of catatonia; however, the
2010). Additionally, various aspects of comorbid number of signs and symptoms that are included
psychiatric conditions including age of onset and range from 10 to 40 across these instruments
severity of symptoms are considered risk factors (Taylor and Fink 2003). Several reviews have listed
and contribute to prognosis. Although highly var- the most commonly listed signs and symptoms of
iable, overall prognosis appears to be relatively the syndrome as mutism, posturing, negativism,
better for recurrent catatonia and mood disorders staring, rigidity, echophenomena, stereotypes,
with catatonia as compared to catatonic schizo- grimacing, and perseveration (Weder et al. 2008).
phrenia. While acute treatment prognosis may be In terms of the number of symptoms required to
excellent, long-term prognosis depends on the justify a diagnosis, minimum thresholds vary
underlying condition that elicited catatonia among scales. While some scales resemble the
(Taylor and Fink 2003). DSM-5 in requiring the presence of 2 or 3 symp-
toms out of a list of 11 or 12 (Lohr and Wisniewski
1987; Rosebush et al. 1990), other instruments
Neuropsychology and Psychology of assign greater weight to certain cardinal symptoms
Catatonic Behavior over other secondary symptoms (Bush et al. 1996).
Other scales group symptoms by category (i.e.,
Although the pathophysiology of catatonia motor, affective, and behavioral) and require a
remains poorly understood, both the GABA and symptom from each category in order to establish
dopaminergic neurotransmitter systems have been a diagnosis (Northoff et al. 1999). Most authors
implicated in psychopharmacological studies accept a range from several to 24 h duration of
(Dhossche et al. 2010). Neuroimaging studies symptoms as being necessary to definitively estab-
have not been conclusive and have revealed var- lish the presence of catatonia (Weder et al. 2008).
ious cortical and subcortical brain regions to be Attempts have been made to identify individual
associated with catatonia, which may explain clusters within catatonia based on discrete
observed clinical differences in symptom presen- symptom-groups and duration of illness (acute/
tation (Weder et al. 2008). Neuropsychological chronic); however, further research in this area is
evaluation of psychiatric inpatients with catatonia necessary before the existence of subtypes can be
compared to psychiatric controls revealed rela- established (Weder et al. 2008).
tively poorer performance on measures of work-
ing memory and visual-spatial abilities related to
right parietal functioning. Additionally, signifi- Treatment
cant differences between catatonic patients and
healthy controls were observed on attentional Treatment for catatonic symptoms differs
and executive tests associated with frontal func- depending on the underlying cause. Catatonia is
tioning. These results suggest attentional-motor currently viewed by most clinicians from a predom-
and frontoparietal dysfunction in catatonia inantly biological framework (Penland et al. 2006).
(Northoff et al. 1999). Generally, benzodiazepines such as lorazepam are
696 Catatonic Behavior

considered to be the first treatment of choice. If Caroff, S. N., & Ungvari, G. S. (2007). Expanding
patients fail their initial trial, the use of bilateral horizons in catatonia research. Psychiatric Annals,
37(1), 7–9.
electroconvulsive therapy is usually considered. Consoli, A., Raffin, M., Laurent, C., Bodeau, N., Campion,
Although these are the best-studied treatments, the D., Amoura, Z., Sedel, F., An-Gourfinkel, I., Bonnot,
efficacy of other approaches such as transcranial O., & Cohen, D. (2012). Medical and developmental
magnetic stimulation continues to be explored. Cat- risk factors of catatonia in children and adolescents:
A prospective case-control study. Schizophrenia
atonic schizophrenia has been treated by a variety Research, 137(1–3), 151–158.
of pharmacotherapeutic and psychotherapeutic Dhossche, D. M., Stoppelbein, L., & Rout, U. K. (2010).
methods. Hospitalization may be necessary to pro- Etiopathogenesis of catatonia. The Journal of ECT, 26,
tect the patient’s safety and supportive psychother- 253–258.
Fink, M. (2013). Rediscovering catatonia: The biography of
apy, and family education may help patients and a treatable syndrome. Acta Psychiatrica Scandanavica,
their families adjust to problems created by catato- 127(Suppl 441), 1–47.
nia. Other supportive services as sheltered work- Fink, M., & Taylor, M. A. (2003). Catatonia: A clinician’s
shops and special education may also be helpful. guide to diagnosis and treatment. Cambridge: Cam-
bridge University Press.
When catatonic symptoms are due to a mood dis- Fink, M., & Taylor, M. A. (2006). Catatonia: Subtype or
order, episodes may be treated with mood stabi- syndrome in DSM? American Journal of Psychiatry,
lizers or antidepressant medications, or with 163, 1875–1876.
psychotherapy. Catatonic symptoms caused by a Francis, A., Fink, M., Appiani, F., Bertelsen, A., Bolwig,
T. G., Bräunig, P., . . ., & Wachtel, L. (2010). Catatonia
medical disorder require correct diagnosis of the in diagnostic and statistical manual of mental disorders,
underlying medical condition, followed by appro- fifth edition. Journal of ECT, 26(4), 246–247.
priate treatment. For example, levodopa and aman- Gelenberg, A. J. (1976). The catatonic syndrome. Lancet,
tadine (Symmetrel) have shown some effectiveness 1(7973), 1339–1341.
Lohr, J., & Wisniewski, A. A. (1987). Catatonia. In
in reducing catatonia due to postencephalitic J. Lohr & A. A. Wisniewski (Eds.), Movement
Parkinson’s disease. Hospitalization and careful disorders: A neuropsychiatric approach. New York:
supervision of persons with catatonia may be nec- Guilford Press.
essary to ensure that they do not harm themselves Northoff, G., Nagel, D., Danos, P., Leschinger, A., Lerche,
J., & Bogerts, B. (1999). Impairment in visual-spatial
or others and to prevent malnutrition, exhaustion, function in catatonia: A neuropsychological investiga-
or fever. tion. Schizophrenia Research, 37, 133–147.
Penland, H. R., Weder, N., & Tampi, R. R. (2006).
The catatonic dilemma expanded. Annals of General
Cross-References Psychiatry, 5(14), 1–9.
Rosebush, P. I., Hildebrand, A. M., Furlong, B. G., &
Mazurek, M. F. (1990). Catatonic syndrome in a
▶ Delusion general psychiatric inpatient population: Frequency,
▶ Mood Disorder clinical presentation, and response to lorazepam. Jour-
▶ Schizophrenia nal of Clinical Psychiatry, 51, 357–362.
Tandon, R., Heckers, S., Bustillo, J., Barch, D. M., Gaebel,
W., Gur, R. E., Malaspina, D., Owen, M. J., Schultz, S.,
Tsuang, M., van Os, J., & Carpenter, W. (2013). Cata-
References and Readings tonia in DSM-5. Schizophrenia Research, 150(1),
26–30.
Abrams, R., & Taylor, M. A. (1976). Catatonia: Taylor, M. A., & Fink, M. (2003). Catatonia in psychiatric
A prospective clinical study. Archives of General Psy- classification: A home of its own. American Journal of
chiatry, 33(5), 579–581. Psychiatry, 160, 1233–1241.
American Psychiatric Association. (2013). Diagnostic and Weder, N. D., Muralee, S., Penland, H., & Tampi, R. R.
statistical manual of mental disorders (5th ed.). (2008). Catatonia: A review. Annals of Clinical Psychi-
Washington, DC: American Psychiatric Association. atry, 20(2), 97–107.
Bush, G., Fink, M., Petrides, G., Dowling, F., & Francis, Wing, L., & Shah, A. (2006). A systematic examination of
A. (1996). Catatonia. I. Rating scale and standardized catatonia-like clinical pictures in autism spectrum dis-
examination. Acta Psychiatrica Scandanavica, 93, orders. International Review of Neurobiology, 72,
129–136. 21–39.
Catecholamines 697

production, and circulation of catecholamines in

Catecholamines the central nervous system, and/or lesions of nuclei
affecting the sympathetic nervous system in the
Marla Sanzone1 and Efrain Antonio Gonzalez2,3 brainstem.
1
Independent Practice, Loyola College of Catecholamines affect metabolic rate, tempera-
Maryland, Annapolis, MD, USA ture regulation, smooth muscle functions, and car-
2
College of Psychology, Nova Southeastern diovascular and nervous systems. Epinephrine and C
University, Fort Lauderdale, FL, USA norepinephrine autonomically prepare the body for
3
Utah State University, Logan, UT, USA crisis such as cold, fatigue, danger, and shock.
Dopamine is produced as an intermediate process
in the synthesis of epinephrine and is critical to the
Synonyms regulation of many neurological processes, includ-
ing smooth fine and gross motor movements,
Adrenergic agonists; Direct- and indirect-acting energy regulation, motivation, executive function-
adrenergic receptor agonists; Dopamine agonists; ing, and formal thought regulation. Sympathomi-
Dopaminergic agonists; Sympathomimetic metic drugs used to treat conditions associated
amines/drugs/agents/compounds with these biological functions mimic the actions
of epinephrine, norepinephrine, or dopamine
(Sympathomimetic drug 2008; Venes et al. 2001).
Definition Such drugs include those used to treat a variety of
abnormalities associated with central and sympa-
Catecholamines are a class of biologically active thetic nervous system processes (e.g., blood pres-
water-soluble hormones comprising catechol and sure, cardiac anomalies, premature labor, glaucoma,
amine compounds. They are derivatives of the bronchitis, asthma, emphysema, blood glucose
amino acid tyrosine. Tyrosine is converted from metabolism, movement disturbances, and psycho-
phenylalanine as a function of the hydroxylation sis). In addition, numerous disorders involve cate-
by the enzyme phenylalanine hydroxylase and cholamine disturbances of congenital, genetic, or
can also be directly ingested from dietary proteins familial origin such as dopamine-b-hydroxylase
(Catecholamines 2002, 2008, 2009a, b). deficiency, paraganglioma syndrome, and tetra-
Catecholamines are sympathomimetic amines, a hydrobiopterin deficiency, but also those with
group of compounds including dopamine, epineph- unknown precipitating mechanisms, including
rine, and norepinephrine whose molecular structure chemodectina, neuroblastoma, and pheochromocy-
is similar to that of a larger class of neurotransmit- toma (Catecholamines 2002).
ters, the monoamines. The specific molecular struc-
ture of catecholamines is a benzene ring with two
hydroxyl groups, an intermediate ethylamine to the Catecholamine-Related Conditions
side and an amine terminal group. The chromaffin
cells in the adrenal medulla and sympathetic ner- Benign familial tremor/essential tremor is an
vous system postganglionic fibers are the primary inherited autosomal dominant condition sugges-
site of catecholamine production (Hoffman 2004). tive of excessive systemic adrenergic activity. It is
During times of physiological and/or psycholog- the most common involuntary movement disorder
ical stress, neurons in the central and peripheral and tends to develop during middle adulthood.
sympathetic nervous systems secrete catechol- Anxiety can precipitate and exacerbate the ampli-
amines via hypothalamic and adrenomedullary tude of the tremor. It is generally treated with beta-
activation. Catecholamine toxicity, also referred blockers such low doses of propranolol and with
to as catecholamine dump or storm, can occur lesser efficacy with atenolol and anxiolytics such
from trauma, causing overstimulation, excessive as alprazolam (Kaufman 2007).
698 Catecholamines

Chemodectoma (nonchromaffin para- inhibit one or more of the actions of these recep-
ganglioma) is a benign chemoreceptor system tors. Some agents have stimulating and blocking
tumor. The most common types are glomus actions on different receptors simultaneously.
jugulare tumor and carotid body tumor. Receptor selectivity addresses strength of affinity
Dopamine-b-hydroxylase deficiency is a severe toward a particular receptor rather than absolute
orthostatic hypotension of a congenital nature specific selectivity of one receptor only.
caused by the inability to generate the enzyme, Direct-acting dopamine agonists are used to
dopamine-b-hydroxylase. treat hypertensive crisis and parkinsonian signs
Familial paraganglioma syndrome is a genetic and symptoms.
slow-growing chromosomal (11q23) benign Indirect-acting, norepinephrine transporter
tumor primarily of the head and neck. These antagonists such as ephedra, cocaine, and
unusual conditions are inherited from the father. amphetamines. They block and reverse the activ-
Disfiguring facial swelling, hearing loss, tinnitus, ity of the norepinephrine transporter proteins.
pain, persistent cough, or other head/neck anom- These proteins functionally terminate the effects
alies as a function of cranial nerve damage from of norepinephrine and to a lesser degree, dopa-
the tumor. mine, by removing these neurotransmitters from
Neuroblastoma produces catecholamines and, the synapse and repackaging them in their vesicles
following brain tumors, is the second most com- for later use (Katzung 2004).
mon solid tumor in childhood. Testing for the Indirectly inhibiting epinephrine and norepi-
catecholamine metabolites, vanillylmandelic acid nephrine metabolism such as COMT inhibitors
and homovanillic acid, is identified in the urine. (e.g., entacapone and tolcapone) and MAOIs
Pheochromocytoma is a benign tumor that such as Parnate and Nardil (Aminoff 2004) that
secretes norepinephrine and epinephrine. It origi- raise the level of all the catecholamines in the
nates in sympathetic paraganglia or adrenal medulla. blood. Monoamine oxidase (MAO) is the enzyme
Tetrahydrobiopterin deficiency is a genetic con- primarily responsible for metabolism of epineph-
dition that results in the inability to manufacture rine and norepinephrine. If the enzyme is
the enzymes required to synthesize catechol- inhibited, it prevents the removal of epinephrine
amines. This leads to a deficiency of the neuro- and norepinephrine from the system which
transmitters, norepinephrine, epinephrine, and induces sympathomimetic effects. Similarly,
dopamine (Catecholamines 2002; Myers 2006). with COMT inhibitors, the enzyme catechol-
O-methyl transferase (COMT) is an intracellular
enzyme in the postsynaptic neuron that degrades
Mechanisms of Action epinephrine and norepinephrine. This enzyme
effectively deactivates them by inducing
The adrenergic or sympathomimetic drugs act at S-adenosyl methionine (SAM) to add a methyl
sympathetic postganglionic terminal by activating group to the catecholamines. The COMT inhibi-
the catecholaminergic hormones, epinephrine tors prevent this deactivation by blocking the
(adrenaline), norepinephrine (noradrenaline), breakdown/reuptake process and enabling the
and/or dopamine in various ways. Some com- utility of the catecholamines (Catechol-O-methyl
pounds have cross-reactivity such that they act transferase 2009).
on catecholamines by more than one mechanism Stimulating production and release of cate-
of action (Sympathomimetic drug 2008). cholamines as do MAOIs and amphetamines.
Directly activating adrenergic postsynaptic These agents are known to increase cardiac output
receptors (direct-acting adrenergic agonists) and blood pressure as a function of constricting
include a-adrenergic agonists and b-adrenergic peripheral blood vessels which increases the force
agonists. There are five types: a1, a2, b1, b2, and and rate of cardiac muscle contractions. They can
b3. Adrenergic agonists stimulate one or more of also lead to elevations in blood lipid levels due to
these receptor types. Adrenergic antagonists fat catabolism and blood glucose levels due to
Catecholamines 699

Catecholamines, Table 1 Sympathomimetic action and function

Primary
neurotransmitter
actions Mechanism of action Examples of compounds Clinical uses
Alpha (a)- Direct-acting alpha- Alpha (a1, a2)-adrenergic Used to treat glaucoma by
adrenergic agonists adrenergic agonists – agonists decreasing the production of
promote vasoconstriction, aqueous fluid; as
mydriasis, body tissue vasopressors, nasal C
building, inhibition of decongestants and to dilate
endogenous testosterone the pupil for eye exams
release
a1-Agonists a1-Agonists – stimulate Oxymetazoline, Used to treat anemias caused
phospholipase C activity phenylephrine by deficient production of red
blood cells, aplastic anemia,
hypotension, shock,
paroxysmal supraventricular
tachycardia
a2-Agonists a2-Agonists – inhibit Clonidine – (a2- and a2-Agonists reduce
adenylyl cyclase activity imidazoline-I1 agonist) sympathetic nervous system
Guanfacine – (affinity for activation. They are used to
preference for a2a treat opiate and alcohol
adrenoceptor) withdrawal symptoms, as
Methyldopa is antihypertensives,
approximately 50% gestational hypertension, to
absorbed from the gut, decrease peripheral
metabolized in the intestines resistance and as sedatives.
and liver and alpha- More recently they are being
methylnorepinephrine, its used to treat neuropathic
metabolite, stimulates pain, sleep hyperhidrosis,
central a2- receptors and off-label, to counter the
side effects of stimulant
medications
Mixed a, b1, and b2- Undetermined or mixed Epinephrine, amidephrine, Mixed alpha- and beta-
Agonists alpha-, beta- stimulation ergotamine, norepinephrine, agonists such as epinephrine
synephrine are used to treat anaphylaxis,
acute asthmatic reactions,
cardiac arrest, open-angle
glaucoma and nasal
congestion. It stimulates
alpha, beta1, and beta2
adrenergic receptors,
increasing cardiac output,
dilating bronchials, skeletal
muscle vasculature, and
pupils dilation due to
constriction of dilatory
muscles
b-Antagonists Direct-acting beta-adrenergic Cardiac stimulants Beta-blockers are used to
(beta-blockers) – agonists – stimulate adenylyl treat heart block, ventricular
block the action of cyclase activity and open tachycardia, cardiac arrest,
epinephrine and calcium channels asthma, chronic bronchitis,
norepinephrine emphysema, hypovolemic
and septic shock, low cardiac
output or hypoperfusion,
congestive heart failure
b1-Agonists Direct-acting b1-adrenergic Albuterol, dobutamine Asthma, chronic obstructive
agonists pulmonary disease (COPD),
sinus congestion
(continued)
700 Catecholamines

Catecholamines, Table 1 (continued)

Primary
neurotransmitter
actions Mechanism of action Examples of compounds Clinical uses
b2-Agonists Direct-acting b2-adrenergic Metaproterenol, formoterol, A moderately selective b2-
agonists – stimulate salmeterol, terbutaline agonist. It acts on smooth
postsynaptic b2 receptors of muscle in the lungs, uterus,
the intracellular enzyme, and skeletal muscle
adenylyl cyclase. Closes vasculature. Used to treat
calcium channels, relaxing asthma, COPD, premature
smooth muscle labor
The enzyme intracellular
adenyl cyclase catalyzes the
conversion of ATP to cAMP.
Elevated cAMP levels are
associated with bronchial
smooth muscle relaxation
and regulation of mast cells
activation
Mixed Isoproterenol (b1- and b2- Cardiogenic shock,
b-antagonists agonist) bradyarrhythmias, heart
block, cardiac arrest,
bronchospasm associated
with anesthesia, asthma,
chronic bronchitis,
emphysema, hypovolemic
and septicemic shock
COMT inhibitors Indirectly inhibiting Entacapone, tolcapone Adjunctive Parkinson’s
epinephrine and treatment
norepinephrine metabolism
Dopamine agonists Stimulate production and Bromocriptine, Hypertensive crisis through
release at D1 receptors apomorphine, fenoldopam vasodilation in coronary,
renal, mesenteric and
peripheral arteries
Pramipexole – (pre- and Pramipexole used to treat
postsynaptic D2 and 3 idiopathic parkinsonism
receptor agonism) signs. It stimulates caudate
neurons by D3 agonism
Prolongs dopaminergic Levodopa (I-Dopa) Parkinsonism – Levodopa’s
activity when combined with efficacy is as a prodrug. It is a
COMT inhibitors and dopa precursor of catecholamines
decarboxylase inhibitors
(e.g., benserazide or
carbidopa)
Dopamine reuptake Increase norepinephrine Cocaine, methylphenidate Cocaine used recreationally
inhibitors (DRIs) release at central amphetamines and highly subject to abuse.
noradrenergic neurons. Ophthalmically used as local
Release of dopamine at anesthetic
mesolimic areas in high Amphetamines and
doses methylphenidate are used
primarily to treat ADHD,
narcolepsy, occasionally in
geriatric depression, post-
stroke and cancer to increase
alertness and counteract
chemotherapy lethargy. All
DRIs and stimulant-acting
(continued)
Catecholamines 701

Catecholamines, Table 1 (continued)

Primary
neurotransmitter
actions Mechanism of action Examples of compounds Clinical uses
drugs elevate mood, increase
focusing ability and physical
energy in most, increase
respiration and heart rate,
C
blood pressure and decrease
appetite. They can cause
euphoria, rebound
depression and anxiety
particularly if overused or
used inappropriately to treat
depressive disorders
Dopamine Blockade of dopamine (more Antipsychotic agents Schizophrenia, bipolar I,
antagonists D2 than D1 receptor affinity) mania
Moderate a adrenergic and
histaminic antagonism
Monoamine oxidase Stimulate production and Phenelzine (Nardil) Treatment resistant
inhibitors (MAOIs) release of catecholamines in depression, atypical
CNS depression, panic disorder
Chronic use downregulates Tranylcypromine (Parnate)
a2 or b adrenergic and
serotonin receptors
Norepinephrine Prevent reuptake of Most non-SSRI Atypical depression,
reuptake inhibitors norepinephrine at antidepressants: Tricyclic dysthymia, anxiety, ADD,
postsynaptic receptors antidepressants (TCAs – post-traumatic stress disorder
mixed catecholamine
stimulation and inhibition)
atomoxetine (Strattera) –
serotonin and
norepinephrine reuptake
inhibition duloxetine
(Cymbalta) venlafaxine
(Effexor) – selective
norepinephrine reuptake
inhibition
Norepinephrine- Increase availability of Bupropion, pyrovalerone, ADHD, depression, chronic
dopamine reuptake monoamines, dopamine and mazindol (also classified as a fatigue, obesity
inhibitor norepinephrine, due to TCA), phenethylamines
inhibiting reuptake, causing a
stimulating effect
Norepinephrine Stimulate production and Mirtazapine (classified as a Depression, mixed anxiety-
releasers release of catecholamines tetracyclic and a depression with sleep
noradrenergic specific disruption
serotonergic
antidepressant – NaSSA
Mianserin is a tetracyclic
antidepressant
(continued)
702 Catecholamines

Catecholamines, Table 1 (continued)

Primary
neurotransmitter
actions Mechanism of action Examples of compounds Clinical uses
Stimulants Stimulate direct production Amphetamine salts, ADD/ADHD – increases
and release of methylphenidate, alertness, concentration,
catecholamines, particularly dexamphetamine, focus, attention, executive
norepinephrine and dextroamphetamine, functions, endurance
dopamine from storage phentermine mentally and physically.
vesicles Diminishes verbal and
physical impulsivity
Narcolepsy – to help
maintain alertness
Major depressive disorder –
occasionally used to augment
antidepressant treatment
Weight management –
phentermine is used to
suppress appetite
Also increase norepinephrine Schedule IV controlled
and dopamine levels via substances in the USA
reuptake inhibition and
binding to the MAO protein
transporter
Stimulate production and Modafinil, adrafinil Narcolepsy – to maintain
release of catecholamines alertness, and counteract
abnormal states that diminish
alertness
Night shift work – to
counteract fatigue
Over-the-counter Synthetic- and plant-based Ephedrine, To suppress appetite,
stimulants herbal preparations with pseudoephedrine, MDMA, increase alertness, enhance
significant abuse potential cocaine, ephedra, ma huang, athletic performance
thought to stimulate release guarana Cocaine, a tropane
of catecholamines derivative, is made from
South American coca bush
leaves. It is occasionally used
legally as an ophthalmic local
anesthetic, but no longer
prescribed for its stimulant
properties
Aminoff (2004), Hoffman (2004), Kaufman (2007), Katzung (2004), Psychoactive drug (2009), Stimulant (2009),
Sympathomimetic drug (2008), Williams and Turner (2008).

glycogenolysis of skeletal and hepatic muscle reactivity. The production of all the catechol-
(Sympathomimetic drug 2008). As discussed amines, dopamine, epinephrine, and norepineph-
above, monoamine oxidase (MAO) is the enzyme rine is stimulated and the reuptake, particularly of
primarily responsible for degrading catechol- norepinephrine, is inhibited.
amines. It has a half-life of several minutes.
MAOIs and psychoactive stimulants bind to the
enzyme, inhibiting the breakdown of the catechol- Specific Compounds and Properties
amines, and largely for this reason, the effects of
amphetamines last longer than those of cocaine or All sympathomimetic amines can be conceptual-
crack. Amphetamines are among the adrenergic ized to be part of a broad group of stimulant drugs
agents with dual mechanisms of action or cross- due to their sympathetic nervous system and/or
Category Test 703

central nervous system-activating properties. Sympathomimetic drug. (2008). Wikipedia. Retrieved

However, due to multiple mechanisms of action, January 13, 2009, from http://en.wikipedia.org/wiki/
Sympathomimetic
sympathomimetics are classified accordingly and Venes, D., Thomas, C., Egan, E., & Houska, A. (2001).
as a function of their use in the treatment of Catecholamine (definition). In D. Venes et al. (Eds.),
specific conditions (Table 1). Taber’s medical dictionary (19th ed., p. 357). Philadel-
phia: FA Davis Company.
Williams, F. M., & Turner, T. J. (2008). Adrenergic phar-
macology: Biochemistry & physiology of adrenergic
C
function. In D. E. Golan, A. H. Tashjian, E. J. Arm-
Cross-References strong, & A. W. Armstrong (Eds.), Principles of phar-
macology: The pathophysiologic basis of drug therapy
▶ Dopamine (pp. 129–139). Philadelphia: Lippincott Williams &
▶ Epinephrine Wilkins.
▶ Monoamine Oxidase
▶ Norepinephrine

Category Test
References and Readings

Aminoff, M. J. (2004). Pharmacologic management of Nick A. DeFilippis

parkinsonism & other movement disorders. In Georgia School of Professional Psychology,
B. Katzung (Ed.), Basic and clinical pharmacology Atlanta Psychological Associates, Atlanta, GA,
(9th ed., pp. 447–461). New York: Lange Medical USA
Books/McGraw-Hill.
Catecholamines. (2002). MedicineNet. Retrieved January
15, 2009, from http://www.medterms.com
Catecholamines. (2008). Wikipedia. Retrieved January Synonyms
13, 2009, from http://en.wikipedia.org/wiki/
Catecholamines
Catecholamines. (2009a). The free dictionary by Farlex. BCT; CT; HCT
Retrieved January 13, 2009, from http://medical-
dictionary.thefreedictionary.com/Catecholamines
Catecholamines. (2009b). Merriam-Webster online dictio- Description
nary. Retrieved January 13, 2009, from http://www.
merriam-webster.com/dictionary/catecholamines
The category test (CT) was first published by Ward
Catechol-O-methyl transferase. (2009). Wikipedia.
Retrieved January 15, 2009, from http://www. Halstead (Halstead and Settlage 1943). Over the
answers.com/topic/catechol-o-methyl-transferase years, there have been several versions of the test,
Hoffman, B. B. (2004). Adrenoceptor-activating & other all retaining the essential format of the original and
sympathomimetic drugs. In B. Katzung (Ed.), Basic
the goal of measuring concept formation ability. All
and clinical pharmacology (9th ed., pp. 122–141).
New York: Lange Medical Books/McGraw-Hill. versions involve the presentation of visual images
Katzung, B. G. (2004). Introduction to autonomic pharma- of different shapes to the examinee. The examinee
cology. In B. Katzung (Ed.), Basic and clinical phar- is to determine which underlying concept is pre-
macology (9th ed., pp. 75–93). New York: Lange
sented by the image and choose a number from 1 to
Medical Books/McGraw-Hill.
Kaufman, D. M. (2007). Clinical neurology for psychia- 4 to identify the concept. For example, the exam-
trists (6th ed.., pp. 97, 190, 193, 430–431). Philadel- inee may choose the number corresponding to the
phia: Saunders Elsevier. number of items in the image, the proportion of the
Myers, T. (2006). Catecholamine (definition). In T. Myers
image that is drawn continuously, etc. The exam-
(Ed.), Mosby’s dictionary of medicine, nursing &
health professions (7th ed., p. 323). Missouri: Mosby inee is given feedback after each choice to indicate
Elsevier. if he or she was correct in their decision. By a
Psychoactive drug. (2009). Wikipedia. Retrieved January process of utilizing this feedback to monitor per-
16, 2009, from http://en.wikipedia.org/wiki/Psychoac
formance, the examinee then learns the concepts.
tive_drug
Stimulant. (2009). Wikipedia. Retrieved January 15, 2009, The number of errors is used to determine the
from http://en.wikipedia.org/wiki/Stimulant overall performance.
704 Category Test

The original version of the test was adminis- measured abstraction and the process of developing
tered by way of a drum with images on it and a sets or frames of reference on which to base
slit for examinees to view them. Feedback was approaches to new and unfamiliar stimuli.
given with a bell (correct) or buzzer (incorrect). Although Halstead found his test to discriminate
Sometime during the 1940s or 1950s (the exact frontal lobe-damaged patients from others, this
date being unclear), the test was reduced from its finding was never validated by other researchers.
original 360 items and 9 subtests to 208 items Various researchers have, however, identified the
and 7 subtests. The final subtest asks the exam- CT as one of the most sensitive measures of brain
inee to recall previously presented concepts in injury in the Halstead Reitan Battery (Choca et al.
order to respond correctly, constituting a mem- 1993). Santos et al. (2016) did find unique ERP
ory component to the test. More recent versions correlates to correct responses on the CT in nor-
have included a projection of images using mals, suggesting frontal lobe involvement. How-
slides, a card format, a self-administered version, ever, this research would need to be replicated and
a booklet version, and various computer ver- expanded to link CT performance to the frontal
sions. The various versions are available from lobes.
different publishers: slide projector version The existence of various versions of the CT has
(Reitan Labs), booklet version (Psychological raised the issue of comparability of these newer
Assessment Resources), and computer versions forms with the original CT. To date, there has
(Psychological Assessment Resources, The Neu- been no research indicating effects of CT test appa-
ropsychology Center, and Mental Health Sys- ratus on the performance of examinees. Numerous
tems). Feedback has varied by version and studies demonstrated comparable results, regard-
includes the original bell or buzzer, computer less of the test format. Kupke (1983) pointed out
approximations of the bell or buzzer, or examiner that the modification of a test apparatus in a purely
feedback of “correct” and “incorrect.” Test cognitive task, such as that presented by the CT,
administration time is 30–45 min. should have little effect on performance. However,
A French edition of the test was published by this analysis would only pertain to versions that
ECPA in 2002 (DeFilippis and McCampbell), and retain the original test stimuli and administration
there were significant differences found in an instructions. A self-administered version of the test
analysis of the two sets of norms (DeFilippis and that drastically changed instructions and allowed
Reece 2015). Other sets of norms from Portu- the examinee to view earlier responses does not
guese and Hispanic populations also identified meet this requirement. Also, various short forms of
significant normative differences, even though the CT have not been studied sufficiently to deter-
the test is nonverbal (Mungia and DeFilippis mine their comparability to the original length test.
2013; Costa et al. 2014). Clearly, the use of the A number of investigators have attempted to
test in different countries will require obtaining determine if the CT can generate more scores than
new norm sets. Currently, the test remains one of just the number of errors. Factor analytic studies
the most commonly used measures of executive have indicated that there may be different abilities
function (LaDuke et al. 2016). tapped by the test, prompting research into the
possibility of developing scores for different abil-
ities. Scales for spatial positional reasoning, pro-
Historical Background portional reasoning, perseveration, loss of set, and
memory have all been proposed, along with a
Halstead (1940) reported the preliminary findings measure of effort. Recent research has found con-
of studies dating back to the 1920s using concept current validity for a number of these measures,
formation tests in which brain-damaged partici- and efforts to standardize them for clinical use
pants grouped objects into categories. It was clear continue (Minassian et al. 2003).
from subjective analyses that brain damage affected Researchers at NIH validated the ability of
this ability. Halstead hypothesized that his test a number of new scales that measure perseveration,
Category Test 705

categorization, and other variables in discriminat- functioning.” This concept can be loosely
ing head injured from normal populations defined as the ability to utilize feedback to orga-
(McNally et al. 2015). Research at NYU is devel- nize and plan one’s approach to deal with a novel
oping norms for the new scales in order to have problem-solving task. Taking this definition, the
them be of clinical utility. CT seems to qualify as a measure of this ability.
In fact, clinicians who use the test typically
include it in their battery of tests as an executive C
Psychometric Data functioning measure. This approach is supported
by the test format and some research but should
Demonstrated test-retest validity of the CT ranges not involve reliance on the CT as the sole mea-
from 0.60 in normal populations to 0.96 for brain- sure of executive functioning. As previously
damaged participants. A problem in identifying discussed, the test does not identify only frontal
retest stability for the CT has to do with the sub- lobe dysfunction but is sensitive to any type of
stantial learning aspect of the test. Although there brain injury.
has been no adequate analysis of expected gain on Unfortunately, the only validated and normed
re-administration of the test, reliability data suggest score for the CT is the total error score. The
an improvement of about 15 points for normal original cutoff of 50 errors should not be used
individuals and 25 points for brain-damaged indi- without also looking at age- and education-
viduals, with a retest interval of 2–3 months. Inter- adjusted scores. The sex of the examinee does
nal consistency, perhaps a better marker of not appear to have a significant effect on test
reliability for this test, has been shown to be very performance, and although norms are frequently
high at 0.97, as is split half reliability at 0.98. broken down by sex, this demographic variable
Numerous studies have demonstrated the CT’s can largely be ignored. The clinician can view CT
ability to discriminate brain-damaged from nor- performance as indicative of the overall cortical
mal examinees, with analyses indicating statisti- integrity of his or her patient. There is also some
cally significant discrimination at the 0.05–0.001 evidence that the test assesses fluidity of thinking
levels. However, utilizing only the suggested cut- and may be related to rehabilitation outcome.
off score of 50 errors to separate groups has Ongoing research will hopefully provide the
resulted in a false-positive rate of as high as clinician more information concerning his or her
18%. The need to correct for age and education patient’s abilities related to perseveration, atten-
has been firmly established, as these variables tion, and possibly other aspects of their perfor-
account for a significant variance of CT error mance on the CT.
scores. Including these corrections significantly
reduces classification errors (Heaton et al. 1991).
The original intent of Halstead to utilize the CT
Cross-References
as a measure of frontal lobe functioning has not
been validated by researchers. Also, the CT has
▶ Figural Fluency Test
been found to be relatively ineffective in
▶ Tower of London
lateralizing damage to the brain. The test, as is
▶ Trail Making Test
the case with many neuropsychological instru-
▶ Wisconsin Card Sorting Test
ments, is significantly impacted by severe psychi-
atric disturbance and inadequate effort.

References and Readings

Clinical Uses
Choca, J. P., Laastch, L., Wetzel, L., & Agresti, A. (1993).
The Halstead category test: A fifty year perspective.
The CT is generally grouped in most textbooks in Paper presented at the Annual Meeting of the American
the field with other measures of “executive Psychological Association, Toronto.
706 Caudal

Costa, J., Santos, I., Silva, C., & DeFilippis, N. (2014).

Portuguese norms of the Halstead category test: Caudal
Preliminary data. Presented at the 2014 National
Academy of Neuropsychology Conference, Puerto
Rico. John Bigbee
DeFilippis, N. A., & McCampbell, E. (2002). Booklet Anatomy and Neurobiology, Virginia
category test. Paris: ECPA. French version of test Commonwealth University, Richmond, VA, USA
with new norms and scales.
DeFilippis, N., & Reece, T. (2015). A statistical
comparison of French vs US norms for the Booklet
category test. Presented at the National Academy of Synonyms
Neuropsychology Annual Convention, Austin, Nov
2015
Halstead, W. C. (1940). Preliminary analysis of Posterior
grouping behavior in patients with cerebral injury
by the method of equivalent and non-equivalent
stimuli. American Journal of Psychiatry, 96, Definition
1263–1294.
Halstead, W. C., & Settlage, P. H. (1943). Grouping behav- Anatomical term indicating direction. With refer-
ior of normal persons and of persons with lesions of the
ence to quadrupeds, caudal indicates direction
brain. Archives of Neurology and Psychiatry, 49,
489–503. toward the tail and is used synonymously with
Heaton, R. K., Grant, I., & Matthews, C. G. (1991). Com- posterior. The opposite direction is rostral, indicat-
prehensive norms for an expanded Halstead-Reitan ing direction toward the head and is used synony-
battery: Demographic corrections, research findings,
mously with anterior. In human anatomy, caudal is
and clinical applications. Odessa: Psychological
Assessment Resources. only commonly used in reference to the embryo
LaDuke, C., Barr, W., Brodale, D., & Robin, L 2016. and the brain and cranium. Due to the tilting of the
Common test utilization in forensic neuropsychological central nervous system, for reference to the brain,
assessment: A survey of National Academy of Neuro-
caudal, or alternatively posterior, indicates direc-
psychology (NAN) and International Neuropsycholog-
ical Society (INS) members. Presented at the 2016 tion toward the back of the head. In contrast, ros-
National Academy of Neuropsychology Annual Meet- tral, or anterior, indicates direction toward the face.
ing, Seattle.
Kupke, T. (1983). Effects of subject sex, examiner sex, and
test apparatus on Halstead category and tactual perfor-
mance tests. Journal of Consulting and Clinical Psy- See Also
chology, 51, 624–626.
McNally, S., Dsurney, J., McGovern, J., DeFilippis, N., & ▶ Rostral
Chan, L. (2015). Concurrent validity of new
subscale scores for the Booklet category test Assess-
ment, 1–9. https://doi.org/10.1177/073191115588783.
Minassian, A., Perry, W., Carlson, M., Pelham, M., &
DeFilippis, N. (2003). The category test perseveration, Caudate Nucleus
loss of set, and memory scales: Three new scales and
their relationship to executive functioning measures.
Assessment, 10, 213–221. Seema Shroff
Mungia, M., & DeFilippis, N. (2013). The effects of Department of Anatomy and Neurobiology,
demographics on a Spanish version of the Booklet Virginia Commonwealth University, Richmond,
category test. Presented at the 2013 Meeting of the
VA, USA
American Psychological Association. Honolulu,
Hawaii.
Santos, I. M., Teixeira, A. R., Tomé, A. M., Pereira, A. T.,
Rodrigues, P., Vagos, P., Costa, J., Carrito, M. L., Definition
Oliveira, B., DeFilippis, N. A., & Silva, C. F. (2016).
ERP correlates of error processing during perfor-
mance on the Halstead category test. International The caudate nucleus is an arcuate mass deep into
Journal of Psychophysiology, 106, 97–105. the cortical hemispheres forming a part of the
Caudate Nucleus 707

basal ganglia. Apart from being involved in the execution project to the caudate and putamen.
smooth orchestration of motor actions, it has been Striatal neurons relay to the globus pallidus that
recently implicated in other functions like learn- sends information to the thalamus (VA/VL),
ing, memory, emotion, and language. which in turn feeds back to cortical motor areas
forming the “direct pathway” that increases motor
activity. An indirect pathway, involving the sub-
Nomenclature thalamic nucleus, decreases motor activity. The C
activity of these pathways is further modulated
Striatum/neostriatum = Caudate nucleus (nucleus by dopamine from the nigrostriatal tract and
caudatus) + putamen ACh from the interneurons.
Corpus striatum (dorsal division) = Caudate
nucleus + putamen + globus pallidus Physiology and Pathophysiology
The caudate nucleus is mainly involved in motor
planning and execution of smooth movement.
Current Knowledge
Degeneration of the caudate is associated with
dyskinesias and involuntary movements. Caudate
Anatomy
pathology manifests in choreiform movements
The caudate nucleus has a globular head, tapering
(brisk, jerky, and purposeless), as seen in
body, and down curving tail. The head lies in the
Sydenham’s chorea (minute caudate hemorrhages
floor and lateral wall of the anterior horn of the
and capillary emboli post-streptococcal infection
lateral ventricle, whereas the body runs in the floor.
in children) or Huntington’s disease (an adult-
Medially, the caudate nucleus abuts the thalamus;
onset degenerative hereditary disorder). Athetosis
in the floor of the ventricle, this junction forms a
(slow, sinuous, and aimless movements involving
groove known as the sulcus terminalis that lodges
distal musculature) is also seen in striatal pathol-
the stria terminalis of the choroids plexus. The
ogy. Loss of nigrostriatal input in Parkinson’s
corpus callosum runs above the head and body.
disease leads to akinesia and rigidity characteristic
The caudate nucleus is separated from the lentiform
of the disease.
nucleus by the anterior limb of the internal capsule.
Recently, the caudate nucleus has been impli-
cated in functions other than motor planning.
Histology Using functional imaging, Crinion et al. (2006)
The caudate nucleus and putamen show similar have shown activation of the caudate nucleus dur-
histology. Small and large neurons (in a 20:1 ing language processing in bilingual persons. Ini-
ratio) with spherical or ovoid dendritic fields tial degeneration in the caudate is thought to be
populate the neostriatum making connections responsible for the dysphoria in early Huntington’s
within the nucleus or with the globus pallidus. disease (Paradiso et al. 2008). The caudate nucleus
Most small neurons contain GABA and either has also been theorized to envision positive emo-
enkephalin or substance P. Enkephalinergic neu- tional events in the near future (D’Argembeau et al.
rons express D2 dopamine receptors, whereas 2007) and provide complimentary information of
those with substance P have D1 receptors. the outcomes of actions (Lau and Glimcher 2007).
Large neurons with spiny dendrites contain ace-
tylcholine esterase (AChE) and choline
acetyltransferase (CAT).
Cross-References
Circuitry
Corticostriate, thalamostriate, and nigrostriate ▶ Globus Pallidus
fibers form the major input to the striatum. ▶ Putamen
Cortical areas involved in motor planning and ▶ Thalamus
708 Ceiling Effect

References and Readings compared with others in the standardization sam-

ple because the maximum level of performance
Crinion, J., Turner, R., Grogan, A., Hanakawa, T., within the sample cannot be assessed.
Noppeney, U., Devlin, J. T., et al. (2006). Language
For example, on a list-learning memory test
control in the bilingual brain. Science, 312(5779),
1537–1540. that contains only four words, the majority of
D’Argembeau, A., Xue, G., Lu, Z.L., Van der Linden, M., & examinees will most likely recall most or all of
Bechara, A. (2007). Neuroimage [Epub ahead of print]. the words. Four “bits” of information (in this case,
Gray’s Anatomy (1995). (38th ed.). Pearson Professional
words in a list) place very little demand on the
Limited.
Lau, B., & Glimcher, B. W. (2007). Action and outcome average person’s memory ability. To say that any
encoding in the primate caudate nucleus. Journal of particular examinee who learns all four words is
Neuroscience, 27(52), 14502–14514. demonstrating intact memory abilities may under-
Murray, B., & John, K. (1983). The human nervous
estimate that examinee’s actual memory span.
system – An anatomical viewpoint (4th ed.). Philadel-
phia: Harper and Row, Publishers, Inc.. Adding at least five more words would allow for
Paradiso, S., Turner, B. M., Paulsen, J. S., Jorge, R., Ponto, an investigation of that individual’s upper limit of
L. L., & Robinson, R. G. (2008). Neural bases of learning or memory capacity.
dysphoria in early Huntington’s disease. Psychiatry
Research, 162(1), 73–87.

Cross-References

▶ Floor Effect
Ceiling Effect ▶ Testing the Limits

Sandra Banks
Department of Psychiatry, Allegheny General
Hospital, Pittsburgh, PA, USA
Center for Epidemiological
Studies: Depression
Synonyms
Lisa A. Brenner and Molly Penzenik
Ceiling level Rocky Mountain Mental Illness Research
Education and Clinical Center, Denver, CO, USA
University of Colorado, Anschutz Medical
Definition Campus, Aurora, CO, USA

A ceiling effect is observed when an examinee

obtains very high or maximum scores on a partic- Synonyms
ular test. This may lead to an underestimation of
the examinee’s true ability level because the test CES-D
does not allow for higher levels of performance to
be assessed.
Description

Current Knowledge The Center for Epidemiological Studies-

Depression Scale (CES-D; Radloff 1977) is a
A ceiling effect in a large number of participants 20-item self-report measure that assesses the
in a normative sample may prevent the examiner’s presence and severity of depressive symptoms
ability to gauge a particular individual’s personal over the previous week. The CES-D has been
ceiling, or highest level of performance, when used with adults and adolescents. Individuals
Center for Epidemiological Studies: Depression 709

completing the scale rate each item on a four- Psychometric Data

point Likert scale ranging from 0 (rarely or none
of the time) to 3 (most or all of the time). Four Psychometric properties of the CES-D were ini-
items require reverse scoring. Administration tially established with members of the general
time is approximately 5 min. Responses are population (household interview survey) and
summed to obtain a total score of 0–60, with those receiving services in a psychiatric setting
higher scores indicating a greater frequency (Radloff 1977). Validity (content, construct, and C
of symptoms. Scores of 16 or higher were criterion) was confirmed via item choice and
suggested to identify subjects with depressive patterns of correlations with clinical ratings and
illness (Radloff 1977). Work by Pandya et al. alternate self-report measures. CES-D scores
(2005) supports the use of this cut-off in those differentiated between psychiatric inpatients and
with multiple sclerosis (MS). Earlier work by members of the general population (Radloff
Zich et al. (1990) suggests that alternate cut-off 1977): 70% of the patients versus 21% of the
scores may be more appropriate with medical general population scored above 16. Internal con-
populations. sistency, based on coefficient alpha and Spear-
man-Brown split-halves method, is generally
high – approximately 0.85 in the general popula-
Historical Background tion and approximately 0.90 in the patient sample.
Consistent with the expectation that shorter test-
In 1971, the National Institute of Mental Health retest intervals would produce higher correlations,
(NIMH) began the development of the CES-D to test-retest reliabilities ranged from 0.32
measure depressive symptoms in epidemiological (12 months) to 0.67 (4 weeks). Follow-up studies
research (Brantley et al. 2000). Selection of orig- appear to support Radloff’s (1977) original reli-
inal components of depressive symptomatology ability and validity statistics (Brantley et al. 2000).
(e.g., depressed mood, worthlessness) was based A four factor structure (depressed affect, positive
on factor analytic studies and clinical literature affect, somatic and retarded activity, and interper-
(Radloff 1977); specific items were chosen from sonal) was initially reported (Radloff 1977) and
established measures. Following minor revisions, has been supported by subsequent confirmatory
items were added to the NIMH structured inter- analyses. However, findings suggest that among
view and used in a large-scale study (Brantley minority populations, alternate models may pro-
et al. 2000). vide a better fit (Brantley et al. 2000).
Follow-up studies support use of the CES-D
with diverse populations, including those with
neurological compromise. Recent efforts have Clinical Uses
also focused on creating shorter versions of this
measure (e.g., Iowa, Boston) to facilitate use and The CES-D is a widely accepted measure of
decrease participant burden. Kohout et al. (1993) depressive symptoms that has been used with a
found that when assessing older adults (65 range of populations, including those with a his-
and older), shorter versions adequately evaluated tory of neuropsychological impairments second-
the same symptom dimensions as the original ary to disease (e.g., MS), acquired insult (e.g.,
measure. Findings from Carpenter et al. (1998), stroke), or injury (e.g., traumatic brain injury,
who pooled data from 832 women (six popula- TBI). The CES-D has been relied on to document
tion), support use of the Iowa form over the the incidence and severity of depression in indi-
Boston. In a recent study, a computerized adap- viduals with MS, including those who received
tive methodology was successfully applied to the disease-modifying treatments (Patten et al. 2003;
CES-D; the computerized version also showed Chwastiak et al. 2002), and to assess for potential
the potential for greater clinical efficiency (Smits adverse psychiatric side effects of interferon treat-
et al. 2011). ment (Patten and Metz 2001). It has also been
710 Center for Epidemiological Studies: Depression

used to explore the relationship between depres- epidemiological studies depression scale (CES-D). In
sion and cognitive complaints in individuals with M. E. Maruish (Ed.), Handbook of psychological
assessment in primary care settings (pp. 391–422).
MS (Maor et al. 2001) and study whether depres- Mahwah: Lawrence Erlbaum Associates, Inc..
sion may be a risk factor for increased mortality Bush, B. A., Novack, T. A., Schneider, J. J., & Madan, A.
after stroke (Gump et al. 2005). (2004). Depression following traumatic brain injury:
Confirmatory factor analysis supports the use The validity of the CES-D as a brief screening device.
Journal of Clinical Psychology in Medical Settings, 11,
of this measure for those with mild to moderate 195–201.
TBI (McCauley et al. 2006); acceptable reliability Carpenter, J. S., Andrykowski, M. A., Wilson, J., Hall, L.
of the CES-D with individuals with TBI has also A., Rayens, M. K., Sachs, B., et al. (1998). Psychomet-
been documented (Bush et al. 2004). Moreover, rics for two short forms of the center for epidemiologic
studies-depression scale. Issues in Mental Health Nurs-
Bay et al. (2007) argue that the CES-D’s psycho- ing, 19, 481–494.
metric properties and ease of use render it an Chwastiak, L., Ehde, D. M., Gibbons, L. E., Sullivan, M.,
appropriate measure for depression screening in Bowen, J. D., & Kraft, G. H. (2002). Depressive
persons with TBI. The CES-D has also been used symptoms and severity of illness in multiple
sclerosis: Epidemiologic study of a large community
in longitudinal research on the incidence of sample. The American Journal of Psychiatry, 159(11),
depression following TBI (Dikmen et al. 2004) 1862–1868.
and in studies of depression in caregivers of indi- Dikmen, S. S., Bombardier, C. H., Machamer, J. E., Fann,
viduals with TBI (Rivera et al. 2007). J. R., & Temkin, N. R. (2004). Natural history of
depression in traumatic brain injury. Archives of Phys-
Of note, although findings from the CES-D ical Medicine and Rehabilitation, 85(9), 1457–1464.
may be useful in identifying certain symptoms of Gump, B. B., Matthews, K. A., Eberly, L. E., Chang, Y. F.,
depression, the measure only addresses mood & MRFIT Research Group. (2005). Depressive symp-
during the week prior to administration and, toms and mortality in men: Results from the multiple
risk factor intervention trial. Stroke, 36(1), 98–102.
therefore, does not permit the clinician to assign Kohout, F. J., Berkman, L. F., Evans, D. A., & Cornoni-
a formal diagnosis of a mood disorder. As such, Huntley, J. (1993). Two shorter forms of the CES-D
in a clinical setting, it may be best used in con- depression symptoms index. Journal of Aging and
junction with additional findings (e.g., structured Health, 5, 179–193.
Maor, Y., Olmer, L., & Mozes, B. (2001). The
clinical interview, additional measures) to diag- relation between objective and subjective impairment
nose depressive disorders and assess treatment in cognitive function among multiple sclerosis
needs. patients – The role of depression. Multiple Sclerosis,
7(2), 131–135.
McCauley, S. R., Pedroza, C., Brown, S. A., Boake, C.,
Cross-References Levin, H. S., Goodman, H. S., et al. (2006).
Confirmatory factor structure of the center for epide-
miologic studies-depression scale (CES-D) in mild-to-
▶ Beck Depression Inventory moderate traumatic brain injury. Brain Injury, 20,
▶ Geriatric Depression Scale 519–527.
▶ Hamilton Depression Rating Scale Pandya, R., Metz, L., & Patten, S. B. (2005). Predictive
value of the CES-D in detecting depression among
▶ Structured Clinical Interview for DSM-IV
candidates for disease-modifying multiple sclerosis
(SCID-I/SCID-II) treatment. Psychosomatics, 46, 131–134.
▶ Zung Self-Rating Depression Scale Patten, S. B., & Metz, L. M. (2001). Interferon beta-1 a and
depression in relapsing-remitting multiple sclerosis: An
analysis of depression data from the PRISMS clinical
trial. Multiple Sclerosis, 7(4), 243–248.
References and Readings Patten, S. B., Fridhandler, S., Beck, C. A., & Metz, L. M.
(2003). Depressive symptoms in a treated multiple
Bay, E., Hagerty, B. M., & Williams, R. A. (2007). Depres- sclerosis cohort. Multiple Sclerosis, 9, 616–620.
sive symptomatology after mild-to-moderate traumatic Radloff, L. S. (1977). The CES-D scale: A self-report
brain injury: A comparison of three measures. Archives depression scale for research in the general population.
of Psychiatric Nursing, 21(1), 2–11. Applied Psychological Measurement, 1, 385–401.
Brantley, P. J., Mehan, J., & Thomas, J. L. (2000). The beck Rivera, P., Elliott, T. R., Berry, J. W., Grant, J. S., &
depression inventory (BDI) and the center for Oswald, K. (2007). Predictors of caregiver depression
Center for Outcome Measurement in Brain Injury (COMBI) 711

among community-residing families living with Center for Outcome Measurement in Brain Injury
traumatic brain injury. NeuroRehabilitation, 22(1), (COMBI), Table 1 COMBI-featured scales/measures
3–8.
Advocacy activity scale (AAS)
Smits, N., Cuijpers, P., & van Straten, A. (2011). Applying
computerized adaptive testing to the CES-D scale: A Agitated behavior scale (ABS)
simulation study. Psychiatry Research, 188(1), Apathy Evaluation Scale (AES)
147–155. Awareness Questionnaire (AQ)
Zich, J. M., Attkisson, C. C., & Greenfield, T. K. (1990).
Screening for depression in primary care clinics: The
Cognitive Log (Cog-Log) C
Coma/Near-Coma Scale (CNC)
CES-D and the BDI. International Journal of Psychia-
try in Medicine, 20, 259–277. Coma Recovery Scale-Revised (CRS-R)
Confusion Assessment Protocol (CAP)
Community Balance and Mobility Scale (CB&M)
Community Integration Questionnaire (CIQ)
Craig Handicap Assessment and Reporting Technique
Center for Outcome (CHART)
Measurement in Brain Injury Craig Handicap Assessment and Reporting Technique
Short Form (CHART SF)
(COMBI)
Craig Hospital Inventory of Environmental Factors
(CHIEF)
Jerry Wright Disability Rating Scale (DRS)
Rehabilitation Research Center, Santa Clara (Studying) Employment Variables after TBI
Valley Medical Center, San Jose, CA, USA Family Needs Questionnaire (FNQ)
Functional Assessment Measure (FAM)
Functional Independence Measure (FIM)(TM)
Membership Glasgow Outcome Scale (GOS)
Extended Glasgow Outcome Scale (GOS-E)
The Center for Outcome Measurement in Brain High-Level Mobility Assessment Tool (HiMAT)
Injury (COMBI) is a collaborative project of Independent Living Scales (ILS)
16 brain injury facilities or centers, most of them Level of Cognitive Functioning Scale (LCFS)
Traumatic Brain Injury Model Systems (funded Mayo-Portland Adaptability Inventory (MPAI)
by the National Institute on Disability and Reha- Mississippi Aphasia Screening Test (MAST)
bilitation Research). The product is an informa- Moss Attention Rating Scale (MARS)
Neurobehavioral Functioning Inventory (NFI)
tional web site that is oriented primarily toward
Orientation Log (O-Log)
clinicians and researchers but is also freely avail-
Overt Behavior Scale (OBS)
able to the general public.
Patient Competency Rating Scale (PCRS)
Participation Assessment with Recombined Tools-
Objective (PART-O)
Major Areas Participation Objective, Participation Subjective
Perceived Control Scale for Brain Injury (PCS-BI)
The COMBI is an online resource for those Satisfaction With Life Scale (SWLS)
needing detailed information and support in (Problematic) Substance Use Identified in the TBI Model
regard to outcome measures for persons with Systems National Dataset
brain injury. The measures included in the Service Obstacle Scale (SOS)
COMBI are commonly used in the field of brain Supervision Rating Scale (SRS)
injury rehabilitation and assessment. The COMBI
is a collaborative project of 16 brain injury facil- information on validity and reliability, a reference
ities or centers, with each center contributing list of published studies, and testing materials.
information on one or more measures. For most A Frequently Asked Question (FAQ) section is
supported measures, there are syllabus and train- also included, compiled from past training infor-
ing information, rating forms, background mation and submitted questions. The COMBI was
712 Centers for Medicare and Medicaid Service

designed to provide accessible and consistent

information regarding brain injury outcome mea- Centers for Medicare and
sures to clinicians and researchers. Medicaid Service

Robert G. Frank
Landmark Contributions University of New Mexico, Albuquerque, NM,
USA
The COMBI is coordinated by Santa Clara
Valley Medical Center and is supported by
funds from the National Institute on Disability Membership
and Rehabilitation Research (NIDRR). It has
been a collaborative project of the NIDRR- The Centers for Medicare and Medicaid (CMS)
funded Traumatic Brain Injury Model Systems served 125 million Americans enrolled in Medi-
since 1998. care, Medicaid, and the Children’s Health Insur-
ance Program (CHIP) in FY 2017.

Major Activities Major Areas

Currently, the COMBI has 37 featured scales. CMS is part of the Department of Health and
Table 1 shows the COMBI-featured scales as of Human Services. The primary offices are not
this writing. The COMBI web site also conducts located in Washington D.C. but in Baltimore.
testing and certification for the Disability Rating With a budget of approximately $681.6 billion,
Scale (DRS). The COMBI web site (www.tbims. serving almost 125 million beneficiaries, CMS
org/combi) receives over 1200 visitors per day, has a dominant role in American health care.
with well over one million visits in total. The top position in CMS, the Administrator, is
nominated by the President of the USA but must
be confirmed by the Senate. Most administrators
Cross-References have come to CMS from academia or have been
industry lobbyists. The position of Administrator
▶ Agitated Behavior Scale is complex and demanding. Nancy-Ann DePearle,
▶ Coma Recovery Scale who served as Administrator at the end of the
▶ Coma/Near Coma Scale Clinton administration, during one of the few
▶ National Institute on Disability Independent periods in which federal spending for CMS
Living and Rehabilitation Research (NIDILRR) declined, noted that the Administrator has
▶ Neurobehavioral Functioning Inventory “. . .many bosses, including 535 members of Con-
▶ Orientation Log gress, the White House, the Inspector General, the
▶ Rancho Los Amigos Scale US Government Accountability Office (GAO)”
▶ Traumatic Brain Injury (TBI) (Health Affairs: W-5-337).
▶ Traumatic Brain Injury Model System The Department of Health and Human Ser-
vices, through CMS, issues regulations and policy
clarifications guiding the provision of services for
References and Readings Medicare beneficiaries. All psychologists who
provide health-care services to Medicare recipi-
http://www.tbims.org/combi ents, particularly neuropsychologists, interact
Wright, J. M., Bushnik, T., & O’Hare, P. (2000). The center
with CMS. Each psychologist who provides ser-
for outcome measurement in brain injury (COMBI): An
internet resource you should know about. Journal of vices to Medicare beneficiaries must obtain
Head Trauma Rehabilitation, 15(8), 734–738. National Provider Identification (NPI) from
Centers for Medicare and Medicaid Service 713

CMS. Medicare fiscal intermediaries oversee pay- Medicare and Medicaid were administered sep-
ment for Medicare services including the elec- arately during the Johnson and Nixon administra-
tronic fund transfer. Each state has a fiscal tions. Joseph Califano, Secretary of Health
intermediary overseeing Medicare Part A (inpa- Education and Welfare (HEW) under Jimmy Car-
tient services) and Part B (professional services). ter, believed that ineffective oversight of health
CMS regulations now guide the care of all Medi- programs permitted spiraling health costs and
care beneficiaries. In addition, the size and impact health-care spending inflation (Derzon 2005). C
of Medicare have made the agency a predictor of Califano knew the separate administration of Medi-
many coverage choices by private insurers. When care and Medicaid reflected the political compro-
CMS issues proposed rules in the Federal Regis- mises needed to create coverage for the elderly and
ter (the federal government’s daily journal), all the poor through linking coverage for the elderly to
providers have the opportunity to comment. welfare. The split administration of Medicare and
Final rules that guide reimbursement by CMS’s Medicaid, however, made the two mammoth pro-
fiscal intermediaries are then issued. grams less manageable. Califano moved quickly, in
secret and combined Medicare and Medicaid,
forming the Health Care Financing Administration
Landmark Contributions (HCFA). HCFA provided oversight to the Medi-
care program (health insurance for people aged 65
In July 1965, at the home of President Harry and over, younger people receiving social security
Truman, President Lyndon B. Johnson signed disability benefits, and persons with end-stage kid-
the Social Security Act of 1965. Titles XVIII ney disease) as well as the Medicaid program (pro-
and XIX of the Act fostered a new view of health viding medical assistance from state and federal
care in the USA, responding to more than 20 years governments for eligible low-income persons).
of legislative initiatives aimed at creating an insur- Although the federal government regulates Medic-
ance program to cover hospitalization, health ser- aid, state governments actually operate the pro-
vices, and skilled nursing care for the elderly as gram. HCFA also provided federal oversight for
well as coverage for low-income children. When quality control initiatives.
implemented in 1966, Medicare (created by Title Between 1989 and 2000, the number of Medi-
XVIII) provided coverage for more than 19 mil- care claims rose from 70% to more than 800
lion elderly Americans. Medicaid (created in Title million claims. Despite this staggering volume,
XIX) covered almost 15 million people and was Medicare’s administrative costs were only 2%.
administered by the Social Rehabilitation Admin- HCFA was viewed as having a bias toward pro-
istration, an agency managing poverty and wel- viders. In 2001, the Bush administration, believ-
fare programs. ing that HCFA was perceived as bureaucratic,
The inclusion of Medicare and Medicaid within unresponsive, and biased toward physicians and
the Social Security Act reflected political compro- hospitals, sought a new image for the agency. In
mises needed for the passage of both programs. an effort to improve the agency’s image, the Bush
Wage and price controls imposed during World administration changed the name to the Centers
War II prompted many employers to offer health- for Medicare and Medicaid – CMS (Scully 2005),
care coverage. This “de facto” wage increase deter- heralding an effort to streamline the many admin-
mined that health insurance became a common istrative processes overseen by CMS. Despite the
employer benefit, but one that excluded the elderly new name, CMS continued the responsibilities of
and unemployed. By 1960, the inadequacy of HCFA: Medicare, end-stage renal disease, quality,
health services for older Americans had become a and coordination of Medicaid with the states. In
political issue. In order to secure enough votes to January 2011, CMS became responsible for the
pass Medicare, President Johnson created the con- implementation of the Affordable Care Act pro-
cept of the “medically indigent” thereby linking visions that provided coverage for previously
welfare to health care for the elderly. uninsured Americans with preexisting conditions,
714 Centigray

reimbursement of employers for employers to the differential recovery rates for normal and neo-
help pay part of the cost of for early retirees, plastic tissue, thereby permitting repopulation of
their spouses and dependents. In 2014, CMS normal cells and inducing radiosensitivity via
worked with states to create health insurance mar- increased oxygen to the remaining tumor cells.
kets and operate through Health Insurance Mar- Fractionated dose radiotherapy enhances the treat-
ketplaces to provide health coverage. More ment efficacy by targeting the cancer cells while
recently, CMS began the Merit-based Incentive mitigating the damage to healthy tissue. This is
Payment System (MIPS) in Medicare to reward determined using a therapeutic ratio, which com-
providers for high quality efficient care. pares the damage to both cancerous and healthy
cells (Potters et al. 2005). Moreover, the biological
effects on the relevant tissue vary according to the
References and Readings radiation type and intensity.

DePearle, N. A. (2005). What does it take to run Medicare

and Medicaid? Health Affairs, Published on-line July
26, 2005, W-5-337–338.
References and Readings
Derzon, R. A. (2005). The Genesis of HCFA. Health
Affairs, Published on-line July 26, 2005,W5–326. Potters, L., Timmerman, R., & Larson, D. (2005). Stereo-
Scully, T. A. (2005). Policy high points: Medicare and tactic body radiation therapy. Journal of the American
Medicaid in the New Millennium. Health Affairs, College of Radiology, 2, 676–680.
Published on-line July 26, 2005, W5–339.

Central Auditory Processing

Centigray Disorder

Bram Goldstein Judith A. Shechter1, Bruce Caplan2 and

Department of Gynecologic Oncology, Hoag Sarah J. Leinen3
1
Hospital Cancer Center, Newport Beach, CA, Wynnewood, PA, USA
2
USA Independent Practice, Wynnewood, PA, USA
3
Institute for Graduate Clinical Psychology,
Widener University, Chester, PA, USA
Synonyms

cGY Synonyms

Auditory perceptual disorder (APD); Auditory

Definition processing disorder (APD); CAPD; Sensory
integration-C/APD (SI-C/APD)
Centigray (cGY) is the preferred measurement of
absorbed radiation and is equivalent to one-
hundredth (102) of a gray, or 1 rad. The gray Short Description or Definition
measures the deposited energy of radiation. The
daily dose of radiation is also referred to as a Central Auditory Processing Disorder (CAPD) is
fraction, since each dose is a percentage of the not a neuropsychological diagnosis. Indeed, its
cumulative prescribed dose. The dose is given in very existence is controversial, and among those
sublethal fractions, which protract the dose to facil- who grant its reality, there is no consensus about
itate the occurrence of repair kinetics. Hence, radi- its components. The term refers to an amalgam of
ation oncologists use fractions to take advantage of symptoms diagnosed primarily by audiologists
Central Auditory Processing Disorder 715

and/or speech and language specialists previously Categorization

using the ICD-9 audiology code 388.4 (Abnormal
Auditory Processes). It is included in ICD-10 as Neither CAPD nor sensory-integration (SI) disor-
code 93.25 with the following definition: “A der is listed in the DSM-IV, DSM-IV-TR, or
disorder characterized by impairment of the audi- DSM-V manuals which provide diagnostic codes
tory processing, resulting in deficiencies in the for psychologists, psychiatrists, and speech and
recognition and interpretation of sounds by the language specialists. When these specialists assess C
brain. Causes include brain maturation delays language-based problems, they tend to assign ICD
and brain traumas or tumors.” However, the dif- diagnostic codes associated with specific language
ferent training and expertise among members of a disorders (e.g., ICD-10 F80.2, Receptive Language
multidisciplinary treatment team may produce Disorder).
differences in diagnosis (McNamaraa et al. 2008; While the diagnosis of CAPD has been debated
Richard 2012). Some other representative posi- for almost 80 years, controversy about its legiti-
tions follow in this and the next section. macy remains (Carneol 2008; see American Acad-
The American Speech-Language Hearing As- emy of Audiology (2010, p. 5) for a statement of the
sociation (ASHA 2005) defined CAPD as dif- position that CAPD “has been definitively
ficulties in the perceptual processing of auditory established as a ‘true’ clinical disorder.”). In part,
information in the central nervous system (CNS). this stems from its extensive comorbidity with a
In this view, the condition presents in the form of variety of impairments in attention/concentration,
poor performance in one or more of the following language, memory, IQ, academic achievement, and
abilities or skills: sound localization and laterali- other behavioral/emotional disorders (American
zation, auditory discrimination, auditory pattern Academy of Audiology 2010). The AAA document
recognition, temporal aspects of audition (in- lists more than one dozen behavioral manifestations
cluding temporal integration, temporal discri- of CAPD including poor listening skills, difficulty
mination/gap detection, temporal ordering, and filtering linguistic information from background
temporal masking), auditory performance in com- noise, problems with sound localization, impaired
peting acoustic signals (including dichotic listen- ability to detect subtle prosodic changes that signal
ing), and auditory performance with degraded humor and sarcasm, difficulty hearing on the phone,
acoustic signals. A Task Force appointed by the problems following rapid speech, problems follow-
American Academy of Audiology (2010) noted ing oral instructions, poor auditory discrimination
the several etiologies of CAPD (e.g., degen- skills, and distractibility/inattentiveness. Children
erative disease, toxic exposure, developmental diagnosed with CAPD often need additional time
disorders), but also acknowledged that many indi- to complete tasks (Bloom and Hynd 2008).
viduals who present with CAPD symptoms have No compelling research reliably provides spe-
no identifiable structural brain impairment. cific neurobiological bases for CAPD as opposed
Largely incorporating the ASHA definition, to findings that link specific brain regions with
Belis and Belis (2015) describe CAPD as “. . .a certain language-based learning disabilities and
neurobiologic deficit in the central auditory ner- Attention Deficit Hyperactivity Disorder (Bloom
vous system (CANS) that affects those mecha- and Hynd 2008). Together, these factors have
nisms that underlie fundamental auditory called into question the validity of CAPD as a
perception (p. 537).” Stefanatos and DeMarco distinct diagnosis. That is, despite persistent pro-
(2012) consider CAPD to be “. . .a collection fessional disagreement about the validity of the
of conditions in which the ability to detect diagnosis and over one million citations on Goo-
sounds, localize their sources, or determine their gle, CAPD remains a collection of loosely defined
identity and meaningfulness is impaired due to information-processing difficulties (Kamhi et al.
a functional compromise of the central audi- 2016). Even the National Coalition of Auditory
tory nervous system by disease, damage, or Processing Disorders (NCAPD) acknowledges:
maldevelopment (p. 441).” “There is no clear agreed-to definition of Auditory
716 Central Auditory Processing Disorder

Processing Disorder” (NCAPD website, retrieved Some researchers have proposed CAPD sub-
April 5, 2018). Nonetheless, they state (contra; groups such as Auditory Decoding Deficit
Bloom and Hynd 2008) that auditory processing (primary left auditory cortex dysfunction), Pro-
disorder “. . .is a neurological defect that affects sodic Deficit (nonprimary right auditory cortex
how the brain processes spoken language.” It and associated areas dysfunction), and Integration
should be noted that the behaviors the NCAPD Deficit (corpus callosum dysfunction) (Bellis
lists as characteristic of CAPD are nonspecific; 2003; Bellis and Ferre 1999; Katz 1992). These
virtually all are characteristic of other impair- subtypes may help clinicians design intervention
ments such as ADD with or without hyperactivity strategies specific to an individual’s presenting
or forms of dyslexia. problems. However, these models are theoretical
DeBonis (2015) reviewed the relevant literature in nature and not universally agreed upon (ASHA
and concluded that assessment of CAPD “. . . is 2005; Jutras et al. 2007).
highly influenced by nonauditory factors including
memory, attention, and language functions”
(p. 124). His ultimate conclusion was that “routine Epidemiology
use of CAPD test protocols cannot be supported.”
Banai and Yifat (2010) stated unequivocally: Given the elasticity of the diagnosis, it is not
“There is currently little data to support diagnosing surprising that no truly authoritative population
APD as a “stand alone” disorder. (p.2),” a position or prevalence studies of CAPD are available
endorsed by Kamhi (2011) and associates Kamhi (Castragiovanni 2008; Stach et al. 1990), and
et al. (2016). However, Dawes and Bishop (2009), those that do exist contain strikingly disparate
after a review of relevant literature, while asserting estimates, in part as a function of age. Chermak
that CAPD “is not a coherent category,” argued that and Musiek (1997) estimated a prevalence rate of
the construct should not be discarded, and clini- 2–3% in children, with the disorder occurring
cians should “. . . develop improved methods for twice as frequently in males than females. Coo-
assessment and diagnosis (p. 440),” although they per and Gates (1991) estimate that the prevalence
did not propose concrete steps to be taken toward in older adults is 10–20%, while Stach et al.
those ends. reported an increasing prevalence of the related
Another aspect of the controversy surrounding construct of “central presbycusis” among adults
CAPD involves debate over whether it is modality- aged 50 (17% incidence) to 80+ years (95%
specific. The ASHA working group concluded: incidence).
“. . .definition of CAPD that specifies complete
modality-specificity as a diagnostic criterion is neu-
rophysiologically untenable (ASHA 2005, p. 3).” Natural History, Prognostic Factors, and
It is important to understand the complicated Outcomes
neurophysiological components of hearing to
understand the etiological basis of CAPD. That The etiology of CAPD is unknown. CAPD may
is, one must know how sound travels from the present as a developmental or acquired disorder.
outer ear through the middle and inner ear struc- The maturation of the central auditory pathway
tures through the eighth auditory nerve to may be delayed (Bamiou et al. 2001). Prenatal or
Heschl’s gyrus in the left temporal lobe of the perinatal factors (e.g., hyperbilirubinemia, anoxia
brain. At that point, the brain begins to recognize or hypoxia, ototoxic drugs, Rh incompatibility,
nerve impulses as sound and then initiates prematurity/low birth weight, birth complications,
interpretation of these impulses as either maternal diabetes, or infections), ear infections,
speech or nonverbal auditory stimuli. These heavy metal exposure, cerebrovascular disorders,
stimuli are then analyzed bilaterally by auditory epilepsy, Lyme disease, and traumatic brain injury
stimulus networks distributed within the brain may be risk factors for the constellation of symp-
(Carneol 2008). toms that characterize the CAPD diagnosis
Central Auditory Processing Disorder 717

(Bamiou et al. 2001; Musiek and Chermak 2009; associated with a variety of functional deficits in
Riccio and Hynd 1996; Chermak et al. 2017). speech and language. Differential diagnosis
It is not clear if problems in auditory processing between CAPD and language disorders can be
resolve with age, if children are able to compensate quite challenging due to shared symptomatology.
for auditory processing deficits, and what factors For example, a core deficit in phonological pro-
may contribute to outcome trajectories (e.g., cessing underlies dyslexia. Similarly, children
comorbid ADHD, LD; Bloom and Hynd 2008). with CAPD may have difficulty discriminating C
Interventions offered when CAPD has been and manipulating the phonetic aspects of auditory
diagnosed may include encouraging the develop- input. It has been suggested that auditory pro-
ment of compensatory abilities, modifying the cessing problems in developmental dyslexia are
environment in which the child is being taught, specific to the encoding of speech, whereas CAPD
and direct remediation of the auditory deficit. is characterized by a general dysfunction
However, it must be acknowledged that there is encoding all auditory stimuli.
a paucity of rigorously controlled research Academic difficulties are often characteristic
supporting these interventions (Choudhury and of children who carry a CAPD diagnosis (ASHA
Chavira 2017; Fey et al. 2001). 2005). They may have a difficult time encoding/
learning spoken information or information pre-
sented with background noise. They are more
Neuropsychology and Psychology likely to have behavioral, emotional, and social
of CAPD difficulties secondary to poor communication
skills (ASHA 2005). The preceding, combined
The very considerable overlap of CAPD symp- with associated learning difficulties, can compro-
toms with other developmental disorders such as mise self-esteem and contribute to emotional
ADHD continues to fuel debate among psychol- withdrawal, somatization, conduct disorders, de-
ogists, neuropsychologists, audiologists, and pression, anxiety, and interpersonal problems
speech-language pathologists over the existence (Riccio et al. 2005).
of this diagnosis. While a definition of CAPD as a
unimodal disorder is a useful tool in the concep-
tualization of the symptoms associated with it, the Evaluation
notion of CAPD as separate and distinct from
language-based LD and ADHD has not been well- Since CAPD is generally considered to be an
documented in the literature (Chermak et al. 2017). auditory deficit, an audiologist is the profes-
Failures in functions such as attention, cognition, sional who has historically been regarded as
working memory, and efficiency of neural pro- best-qualified to diagnose CAPD (ASHA 2005).
cessing can individually or in combination Although psychologists and speech-language
account for an inability to translate spoken lan- pathologists (SLPs) may screen for auditory pro-
guage accurately (DeBonis 2015). cessing difficulties, speech-language and psycho-
In a sample of 30 9–13-year-olds, approxi- logical measures should not be used to diagnose
mately 50% of children diagnosed with CAPD CAPD (ASHA 2005). Shinn (2012) stated that
also met diagnostic criteria for ADHD (Riccio only children with “normal cognitive abilities”
et al. 1994). Based on ratings from audiologists (including receptive and expressive language
and pediatricians, Chermak et al. (2009) identified skills) should be tested for CAPD. Screening
exclusive behavior sets characterizing CAPD and processes involve systematically observing listen-
ADHD. CAPD was not characterized by hyperac- ing behavior and assessing performance on tests
tivity and difficulties with impulse control. of auditory function (ASHA 2005). Multidis-
Some individuals with CAPD may have diffi- ciplinary assessment including other profes-
culties with speech and language. Varying combi- sionals such as psychologists and SLPs should
nations of auditory processing deficits may be be conducted to help delineate cognitive
718 Central Auditory Processing Disorder

communication and language-related factors environmental modifications (e.g., preferential

associated with CAPD, determine the functional seating, use of a stereo system in the class-
impact of CAPD, and guide treatment (ASHA room, use of area rugs), assistive technology
2005). Nonetheless, ASHA has stated: “There is alternatives, and specific educational program-
currently no reference standard for diagnosing ming (Shinn 2012). These would be written in
CAPD,” citing their own 2005 document as well the form of an Individual Education Program
as that of the AAA (2010) and the work of (Individuals with Disabilities Education Improve-
Vermiglio (2016). ment Act of 2004, 20 U.S.C. 1400; Public Law
The audiologist’s central auditory diagnostic 108–446) that would provide such accommoda-
test battery, which aims to examine the integrity tions under the category of Other Health Impaired.
of the central and peripheral auditory nervous The American Academy of Audiology Clini-
systems (ASHA 2005), may include auditory dis- cal Practice Guideline encourages an individual-
crimination tests, auditory temporal proces- ized approach initiated as soon as CAPD has been
sing and patterning tests, dichotic speech tests, detected. Interested readers are referred to p. 25 of
monaural low-redundancy speech tests, binaural their Guideline for discussion of the use of “audi-
interaction tests, electroacoustic measures, and tory training” in cases of CAPD.
electrophysiologic measures (ASHA 2005).
Auditory processing tests include elements of at-
tention and memory, but also appear to assess Cross-References
processes not tapped by measures of these con-
structs (Riccio et al. 2005). Shinn (2012) argued ▶ American Speech-Language-Hearing Associa-
that evaluations should be individualized based on tion (ASHA)
the particular patient’s behavioral manifestations ▶ Americans with Disabilities Act of 1990
of CAPD. A diagnosis of CAPD typically requires ▶ Auditory System
performance two standard deviations below the ▶ Cognitive-Communication Disorder
mean on two or more auditory processing tests ▶ D-amphetamine
(Shinn 2012). The audiologist must also consider ▶ Dyslexia
the confounding effects of fatigue, poor attention, ▶ Executive Functioning
memory, and motivation on test performance. ▶ Learning Disability
There may also be a role for behavioral and ▶ Section 504 of the Rehabilitation Act of 1973
electrophysiologic measures (McNamara and ▶ Stimulants
Hurley 2017).

References and Readings

Treatment
American Speech-Language-Hearing Association. (2005).
Collaboration among educators, school psycholo- (Central) auditory processing disorders [Technical
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Auditory processing disorders. In J. H. Stone &
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Encyclopedia of human behavior (2nd ed., weaknesses of previous short-term memory

pp. 441–453). New York: Academic Press. (STM) models, including the failure to address
Vermiglio, A. (2016). On diagnostic accuracy in audiol-
ogy: Central site of lesion and central auditory pro- nonverbal processing. Baddeley’s model, which
cessing disorder studies. Journal of the American has undergone changes throughout the years, is a
Academy of Audiology, 27, 1–16. theoretical concept and was not originally devel-
oped to directly correspond with specific neuro-
anatomical regions, though research that attempts
to do so has been completed. The original theory
Central Executive proposed the existence of three components
(Fig. 1). Baddeley envisioned this system as
Nicole C. R. McLaughlin consisting of a central executive, which is a lim-
Butler Hospital Alpert Medical School of Brown ited capacity subsection that controls certain sub-
University, Providence, RI, USA systems. The central executive controls “slave”
systems, which are mainly used for the temporary
storage of information. Information that is not
Definition needed right now, but will soon be needed, can
be stored within these “slave” systems to free up
Working memory (WM) has been defined as the the central executive for other tasks. One of the
“blackboard of the mind” and the “mental slave systems is the articulatory or phonological
sketchpad” (Baddeley 1986). It enables the online loop, which is a verbal store. Subvocalization of
holding and mental manipulation of information. verbal material creates a record in a phonological
Human beings use WM processes all the time. For buffer. The central executive then reads the pho-
example, WM is used to perform rapid mathemat- nological buffer, and the cycle begins again. For
ical functions in our heads and to understand the most of this cycle, the central executive is not
inherent meaning in speech and writing. WM is needed. Another slave system is the visuospatial
also important for reasoning and problem solving sketchpad, which is used to rehearse visual or
(Baddeley 1999). Psychologists have posited sev- spatial materials. Manipulation of information
eral types of memory in the intact human mind. within either the phonological loop or visuospatial
Although philosophers have long been theorizing sketchpad does not affect information being
about distinctions within memory, there has retained in the other system; they have been
been experimental evidence supporting the divi- shown to be distinct systems in regard to interfer-
sions of memory for only the past 30–40 years ence effects (Brooks 1968). Another component,
(Baddeley 1999). the episodic buffer (described in detail below),
was added in 2000 to address some of the per-
ceived weaknesses of the earlier model. The cur-
Historical Background rent multicomponent model describes “fluid”
capabilities (such as temporary storage) and
Baddeley and Hitch (1974) developed a theory of “crystallized” abilities that are involved in long-
a WM system that has become the dominant the- term knowledge (Fig. 2).
ory in cognitive psychology for the organization Phonological Loop. The phonological loop is
of WM (Fig. 1). Baddeley’s model addressed most similar to the earlier concept of STM

Visuospatial Central executive Phonological

sketchpad loop

Central Executive, Fig. 1 Initial three-component model of working memory (WM) (Baddeley and Hitch 1974)
Central Executive 721

Central Executive,
Fig. 2 Multicomponent Central executive
model of working memory
(WM) (Baddeley 2000)

Phonological Loop Episodic buffer Visuospatial sketchpad

C

Visual Episodic Language

semantic long-term memory

(Baddeley 1992) and is the most studied compo- by being required to state an irrelevant word (such
nent within this theory. There are two components as the. . .the. . .the), performance declines. There
within the phonological loop: a phonological store also appears to be a word-length effect such that
and an articulatory rehearsal system. The phono- longer words are more difficult to remember,
logical store can temporarily hold acoustic mate- potentially because participants are subvocalizing
rial for 1–2 s and is involved in speech perception. words, and thus, there is more time for informa-
The articulatory rehearsal system can maintain tion to deteriorate (Baddeley 2000).
material by subvocal repetition and can take visu- People frequently use the phonological store in
ally presented material and register this material everyday life, subvocalizing when counting and
by subvocalization. There are several pieces of when reading. Adult fluent readers use this com-
evidence that have supported the presence of the ponent less than poor readers, or individuals learn-
phonological loop. The simplest piece of evidence ing to read, but show difficulties picking up errors
is that it appears clear that our verbal store holds in written text when their subvocalization capa-
only a limited amount of information. The phono- bilities are disrupted (Baddeley 1999). The pho-
logical similarity effect indicates that sequences of nological store may also be important for new
items with similar phonological sounds are more language acquisition as well as native language
difficult to remember than those with disparate acquisition (Baddeley 1999); some researchers
sounds (e.g., “mad can cap man” is more difficult have indicated that the phonological loop’s pri-
than “pen day cow bar rig”) (Baddeley 1966b). In mary purpose is for language acquisition
addition, it demonstrates the tendency for partici- (Baddeley et al. 1998).
pant errors to be phonologically similar to the A deficit in phonological STM appears to stem
correct item (i.e., F for S and B for G). Similarity from a defective phonological store. Articulatory
of meaning does not seem to be important for the rehearsal appears to be defective in aphasic
phonological store (Baddeley 1966b), whereas patients with dyspraxia, as they are unable to
long-term storage is affected by similarity of carry out the speech motor codes needed for artic-
meaning, but not sound (Baddeley 1966a). The ulation (Waters et al. 1992). Dysarthric patients do
irrelevant speech effect shows that exposure to not appear to have a deficit in articulatory
irrelevant speech either at the same time or rehearsal, likely because their deficits are periph-
directly after stimuli material can disrupt immedi- eral, not central (Baddeley and Wilson 1985).
ate recall of the stimulus; meaningless noise Neuroanatomically, based upon lesion studies,
does not disrupt stimuli material. This effect is the inferior parietal cortex appears to be related
the same for phonologically similar or dissimilar to the temporary phonological store, whereas the
items (Salame and Baddeley 1987). Preventing articulatory rehearsal system uses brain areas nec-
rehearsal (articulatory suppression) further essary for speech production, such as Broca’s area
decreases performance (Baddeley 1999); when and/or the supplementary motor area (Muller and
participants are prevented from rehearsing items Knight 2006).
722 Central Executive

Visuospatial Sketchpad. Similar to the function Baddeley has compared the central executive
of the phonological loop for verbal material, the to Norman and Shallice’s ideas of the supervisory
visuospatial sketchpad allows for the maintenance attentional system (SAS; Shallice 1982), which is
of temporary representations of visuospatial infor- used in planning, decision-making, novel situa-
mation. The visuospatial sketchpad is involved in tions, and difficult situations. Contention sched-
such tasks as visual imagery and mental rotation. uling (CS) is a process that chooses one response
Evidence for this system comes from the finding and inhibits another, in a “crude and fast” way. CS
that visuospatial immediate memory can be modulates the selection of an action schema when
disrupted by visual tracking, but not by verbal it is routine, or unconscious, selecting the schema
coding (Baddeley 1999). There seems to be sepa- with the “strongest triggers.” The SAS is a higher-
rate subsystems involved in the maintenance of level system that is “slow and flexible.” It is uti-
visual information (shape, color) and spatial infor- lized when a selection is more complex and
mation, independent of the central executive adjusts the activation level of the action schemas.
(Klauer & Zhao 2004). In addition, there also Therefore, the SAS can actually “override” the CS
appears to be a dissociation of this system into when the CS fails or no known schema exists
two components, a passive store that maintains (Shallice 1982).
information and a more active device that manip- Additional attentional processes that have been
ulates it (Bruyer and Scailquin 1998). ascribed to the central executive include focusing,
The visuospatial sketchpad appears to be prin- dividing, and switching attention, as well as serv-
cipally represented within the right hemisphere ing as the interface between the subsystems
(Baddeley 2000). Within this component, as described above and long-term memory
noted above, past research has indicated that (Baddeley 2001). With regard to focusing atten-
there is a neuroanatomical differentiation between tion, participants in a chess game were impaired
object and spatial information. Using evidence by interference from a random digit generation
from the parietal and temporal visual streams, it task; this was thought to place a heavy load on
is likely that the parietal lobe (dorsal stream) pro- the central executive (Robbins et al. 1996). With
cesses spatial information (i.e., where – the rela- regard to dividing attention, participants with
tion of objects across coordinates), while the Alzheimer’s disease who have long-term memory
temporal lobe (ventral stream) processes non- and attentional deficits are impaired on dual-task
spatial (i.e., what – as in a visual image or object paradigms, yet are able to do the same tasks indi-
information); this subdivision also possibly vidually (MacPherson et al. 2007). There is a
extends into dorsal and ventral regions of the question as to whether switching is primarily an
prefrontal cortex, and these regions are most rel- executive process, though there also appears to be
evant for short-term or working memory pro- a strong relationship between the phonological
cesses (Goldman-Rakic and Leung 2002). loop and switching.
Central Executive. The central executive has Research has indicated that the prefrontal cor-
been described as a “homunculus” or “little man” tex, especially the dorsolateral prefrontal region,
who makes decisions as to how the slave systems is critical for executive functioning (Collette et al.
should be used. It is a limited capacity attentional 1999; D’Esposito et al. 1995; Owen et al. 1996;
system that is in charge of the phonological loop Salmon et al. 1996). However, more recent studies
and visuospatial sketchpad (Baddeley 1999). have indicated that, although the PFC appears
Although the central executive may be consid- essential for executive functioning, other brain
ered the most important component of this regions may also be important for these functions
model, given the apparent complexity of this (Baddeley and Wilson 1988; Baker et al. 1996;
system, it is difficult to investigate. Baddeley Berman et al. 1995; Nagahama et al. 1996).
(1986) coined the term dysexecutive syndrome Episodic Buffer. As mentioned above, the epi-
(DES) to describe dysfunctions of the central sodic buffer was developed in response to a need
executive. for a component to relate between working and
Central Executive 723

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Baddeley, A. D., & Hitch, G. (1974). Working memory. In
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724 Central Venous Thrombosis

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Robbins, T. W., Anderson, E. J., Barker, D. R., Bradley, stroke such as weakness of the face and limbs
A. C., Fearnyhough, C., Henson, R., et al. (1996). on one side of the body. Diagnosis is usually
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Cerebellar Hemorrhage 725

If raised intracranial pressure results from the posteriorly, that controls balance, coordination,
thrombosis, then surgical placement of a ventricu- and related functions.
loperitoneal shunt is considered. Survival rate
exceeds 90%, full recovery occurs in 88% of the
survivors, and recurrence rate is about 2%.
Current Knowledge
C
It is estimated that 10% of all intracerebral hem-
Cross-References
orrhages, or about 1–2% of all strokes, are cere-
bellar hemorrhages. It can be caused by high
▶ Anticoagulation
blood pressure, heavy alcohol consumption,
▶ Antiplatelet Therapy
cocaine use, anticoagulant use, clotting disor-
▶ Cerebrovascular Disease
ders, cerebral vascular abnormalities such as
▶ Heparin
arteriovenous malformations and aneurysms,
▶ Ischemic Stroke
and cerebral amyloid angiopathy. Approxi-
▶ Thrombolysis
mately, two-thirds are thought to result from
▶ Thrombosis
hypertension. Symptoms of the hemorrhage
▶ Venous Thrombosis
include headaches, especially at the posterior
▶ Warfarin (Coumadin)
and inferior area of the skull, nausea and emesis,
stiff neck, dizziness and vertigo, blurred or
double vision, balance and coordination deficits,
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Ferro, J. M., Canhão, P., Bousser, M. G., Stam, J., & onset of symptoms is generally abrupt and
Barinagarrementeria, F. (2005). Cerebral vein and dramatic. This is a medical emergency, requiring
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Cerebellar Hemorrhage
Cross-References
Elliot J. Roth
Department of Physical Medicine and ▶ Hemorrhagic Stroke
Rehabilitation, Northwestern University, ▶ Intracerebral Hemorrhage
Feinberg School of Medicine, Chicago, IL, USA ▶ Intracranial Hemorrhage

Synonyms
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726 Cerebellar Mutism

Pathophysiology
Cerebellar Mutism Information obtained from single photon emis-
sion computerized tomography (SPECT) studies
Jacqueline L. Cunningham have supported the theory that cerebellar mutism
Department of Psychology, Children’s Hospital results from the effects of decreased cerebral
of Philadelphia, Philadelphia, and cerebellar blood flow upon cell functioning
PA, USA in particular brain pathways. These cause disrup-
tion in the cerebellar modulation of neural
circuits that link prefrontal, posterior parietal,
Definition superior temporal, and limbic cortices with the
cerebellum.
A transient speech disorder typically associated
with resection of cerebellar tumors as an operative Treatment
complication, particularly resection of medullo- The treatment of cerebellar mutism resides in
blastomas involving the cerebellar vermis or speech-language therapy, with early goals of
brainstem, and was reported to be 24%. It is asso- therapy including the teaching of nonverbal
ciated with the integrity of the dentate-thalamo- communication as a compensatory strategy as
cortical tracts, especially the tract that originates well as the direct strengthening of oral-motor
in the right cerebellar hemisphere. Cerebellar functioning through the systematic practicing of
mutism can also result from stroke in the cerebro- tongue and lip movements. Moreover, since cer-
vascular distribution, affecting the cerebellar ebellar mutism occurs within a context of broad
peduncles and brainstem. Cerebellar mutism cognitive and affective change, a comprehensive
forms part of a syndrome of deficits, known as assessment of speech and language skills is
the posterior fossa syndrome (PFS). important to identify and treat language deficits
more broadly. Problems in higher-level
cognitive-linguistic functioning can include dif-
Current Knowledge ficulty in areas like planning and initiating com-
munication, verbal fluency, abstract reasoning,
Symptoms and working memory.
As part of PFS, cerebellar mutism is associated
with decreased or absent speech, irritability, hypo-
tonia, ataxia, and the inability to coordinate vol- Cross-References
untary movements, including the volitional motor
aspects of speech. Mutism occurs within the first ▶ Brain Tumor
week of surgery (or cerebrovascular event) and its ▶ Cerebellum
duration may be a matter of days or weeks. It is ▶ Cognitive Affective Syndrome
expected to resolve within 4 months. However, ▶ Medulloblastoma
even with the return of functional speech, the ▶ Posterior Fossa
quality of vocalizations may lack normalcy in ▶ Posterior Fossa Syndrome
being hypernasal, monotone, high pitched,
slowed, and/or sparse. A small study but carefully
case-matched study of neurocognitive outcomes References and Readings
of children with posterior fossa embryonal tumors
who did or did not manifest cerebellar mutism Ersahin, Y., Mutluer, S., et al. (1996). Cerebellar mutism:
syndrome reported lower performances in the Report of seven cases and review of the literature.
Neurosurgery, 38, 60–66.
mutism group in processing speed, attention,
Ferrante, L., Mastronardi, L., et al. (1990). Mutism after
working memory, executive processes, cognitive posterior fossa surgery in children. Journal of Neuro-
efficiency, and academic achievement. surgery, 72, 959–963.
Cerebellum 727

Keating, R. F., Goodrich, J. T., & Packer, R. J. (2001). To thalamus and red nucleus
Tumors of the pediatric central nervous system.
Corticopontine
New York: Thieme. fibers Superior cerebellar
Palmer, S. L., Hassall, T., Evankovich, K., Mabbott, D. J.,
peduncle
Bonner, M., Deluca, C., Cohn, R., Fisher, M. J., Morris,
Cerebellum
E. B., Broniscer, A., & Gajjar, A. (2010). Neuro-
Oncology, 12(12), 1311–1317.
Pons
Pitsika, M., & Tsitouraas, V. (2013). Cerebellar mutism:
A review. Journal of Neurosurgery: Pediatrics, 12(6),
To vestib. C
nuclei
604–614. Pontine
Dentate
Schmahmann, J. D., & Caplan, D. (2006). Cognition, emo- mossy fibers Interposed
tion and the cerebellum. Brain, 129, 290–292. Fastigial
Schweizer, T. A., Levine, B., Rewilak, D., et al. (2008). Middle
Rehabilitation of executive functioning after focal dam- cerebellar
age to the cerebellum. Neurorehabilitation and Neural peduncle
Repair, 22, 72–77.
Inferior cerebellar
Yildiz, O., Kabatas, S., Yilmaz, C., Altinors, N., & peducncle
Agaoglu, B. (2010). Cerebellar mutism syndrome and
Climbing fibers Proprioceptive
its relation to cerebellar cognitive and affective func- from inferior olive information from
tion: Review of the literature. Annals of Indian Acad- spinocerebellar tract
emy of Neurology, 13(1), 23–27. (mossy fibers)

Cerebellum, Fig. 1 Cerebellum

Cerebellum
small lobules: lingula, folium, central lobule, tuber,
Islam Zaydan culmen, pyramid, declive, uvulae, and tonsils.
Neurology, Virginia Commonwealth University,
Richmond, VA, USA Cerebellar Peduncles
The cerebellar peduncles are bundles of nerve
fibers, connecting the cerebellum with the brain
Definition stem. There are three bundles: inferior, middle,
and superior cerebellar peduncles.
The cerebellum, one of the three major portions of The inferior cerebellar peduncle (ICP) con-
the brain, is involved with the coordination of tains the dorsal spinocerebellar tract (DSCT),
voluntary movements as well as the control of cuneocerebellar tract (CCT), olivocerebellar
equilibrium (Fig. 1). tract (OCT), and vestibulocerebellar tract
(VCT). DSCT fibers arise from cells in the ipsi-
lateral Clarke’s column in the spinal cord
Current Knowledge (C8-L3). CCT fibers arise from the ipsilateral
accessory cuneate nucleus. The largest compo-
Embryology nent of the OCT fibers arises from the contralat-
The cerebellum originates from the metenencephalic eral inferior olive. VCT fibers arise from cells in
division of the rhombencephalon, sharing the same both the vestibular ganglion and the vestibular
embryologic origin with the pons. nuclei, and pass in the inferior cerebellar pedun-
cle to reach the cerebellum.
Anatomy The middle cerebellar peduncle (MCP) con-
The cerebellum consists of three main lobes: ante- tains the pontocerebellar tract (PCT). These
rior (paleocerebellum or spinocerebellum), poste- fibers arise from the contralateral pontine gray
rior (neocerebellum or cerebrocerebellum), and matter.
flocculonodular (archicerebellum or vestibulo- The superior cerebellar peduncle (SCP) is
cerebellum). These lobes are further divided to ten the primary efferent peduncle of the cerebellum.
728 Cerebellum

It contains fibers that arise from several deep lateral nucleus, dentate, receives its input from
cerebellar nuclei. These fibers pass ipsilaterally the OCT and PCT and carries planning informa-
and then cross at the level of the inferior colliculus tion from the posterior parietal area. The
to form the decussation of the SCP. From the SCP, interpositus nucleus (globose and emboliform)
these fibers will then continue rostrally to termi- receives its Purkinje cell input from the OCT
nate in the red nucleus and the motor nuclei of the and PCT fibers carrying information from pri-
ventral anterior (VA) and ventral lateral mary motor cortex (area 4), DSCT, and CCT.
(VL) thalamus. Medially located fastigial nucleus receives
input from the DSCT and CCT. Vestibular nuclei
receive proprioceptive input from the spinal cord
Histology and medullary olive.

Cortex Fibers
The cerebellar cortex consists of three layers from Climbing fibers go to all parts of the cerebellum.
outermost to innermost: molecular, Purkinje They are not restricted to a particular zone.
(pyriform), and granular layers. The molecular A climbing fiber sends a collateral synapse to
layer consists mainly of neuropil and is the site the deep cerebellar nuclei, which is excitatory.
of synapses. The majority of cells in this layer are The climbing fiber then “climbs up,” synapsing
stellate and basket cells in addition to a few neu- on the dendrites of the Purkinje cell. Each
rons. Purkinje cell layer consists of a single layer Purkinje cell receives input from only one
of large (25 micrometer) pear-shaped neurons. It climbing fiber axon, but each climbing fiber
is considered the largest cells in the nervous sys- axon can split to innervate several Purkinje
tem. The granular layer is dense with 3-7 million cells. The climbing fiber-Purkinje cell synapses
neurons per cubic mm, consisting of small cells are excitatory. The OCT terminates directly on
with a granular cytoplasm. Beneath the cortex lies Purkinje cells, by-passes granule cells, and
white matter that forms the core of the foliae. causes complex spikes in Purkinje cells.
Mossy fibers are the axons of DSCT, CCT,
Cells vestibulocerebellar (VCT) and PCT carrying input
The cerebellum is formed of several complex to the cerebellar cortex. They terminate and excite
cells. Stellate cells project local inhibitory output granule cells. Each mossy fiber branches profusely
(taurine). Basket cells also project local inhibitory in the white matter. Each Purkinje cell receives
output (GABA). They feed forward inhibition on input from approximately >20,000 mossy fibers
Purkinje cells. Purkinje cells are stimulatory, and only one climbing fiber.
transmitting impulses from the cerebellar cortex Parallel fibers are the long axons of granule
via efferent pathways. They project inhibitory out cells that pass dorsally through the granule and
(GABA). Granule cells have axons that run paral- Purkinje cell layers to reach the molecular layer of
lel to the longitudinal axis of the lobes. Granule the cerebellar cortex, where they bifurcate and run
cell excite by way of glutamate. Granule cells are parallel to the long axis of the folium. Parallel
only excitatory in the cerebellar cortex, terminat- fibers excite a row of Purkinje cells and in addition
ing on Golgi, basket, and Purkinje cells. Golgi to a few basket cells that in turn will inhibit distant
cells are intermediary cells located in the granular Purkinje cells outside the field of excitation.
layer. They receive stimulatory input (GABA) The aminergic fibers originate in the
from the granular layer to inhibit granule cells. Raphe nuclei and possess serotonergic input, mod-
ulating the granule and molecular layers. This cat-
Nuclei egory of fibers also includes those originating from
Purkinje cells can transmit inhibitory signals to the locus ceruleus possessing noradrenergic input
the deep nuclei of the cerebellum. The most and terminating in all three cortical layers.
Cerebral Amyloid Angiopathy 729

Function Cross-References
The cerebellum receives input from all areas of
the central and peripheral nervous systems. Con- ▶ Ataxia
tinuous flow of information from the spinal cen- ▶ Dysdiadochokinesia
ters and cortical areas are integrated in the ▶ Glutamate
cerebellar cortex. The cerebellar output then ▶ Nystagmus
guides the precision of different cerebral func- ▶ Proprioception C
tions namely equilibrium, planned voluntary
movements, and muscle tone. The cerebellar
modulation of motor control is executed through References and Readings
its inhibitory output to the motor cortex and the
descending motor tracts. Guided by visual, pro- Albus, J. S. (1971). A theory of cerebellar function. Math-
ematical Biosciences, 10, 25–61.
prioceptive, and vestibular spinal input, the cer-
Miller, N., & Newman, N. (2005). Walsh and Hoyt’s clin-
ebellum compares the intended force needed to ical neuro-ophthalmology (6th ed.). Philadelphia:
execute a planned voluntary movement with the Lippincott Williams and Wilkins.
appropriate muscle power needed to execute Ramnani, N. (2006). The primate cortico-cerebellar system:
Anatomy and function. Nature Reviews Neuroscience, 7,
it. It then modulates the tone of the agonist and
511–522.
antagonist muscles through inhibitory input to Ropper, A., & Brown, R. (2005). Adams and Victor’s prin-
the motor cortex, the pyramidal and extrapyra- ciples of neurology (11th ed.). New York: McGraw-Hill.
midal tracts, aiming at the execution in a precise Strick, P. L., Dum, R. P., & Fiez, J. A. (2009). Cerebellum
and nonmotor function. Annual Review of Neurosci-
manner. While this voluntary movement is exe-
ence, 32, 413–434.
cuted, maintenance of equilibrium regardless of
movement or body position is achieved through
the cerebellar output to the antigravity muscles
and the vestibular centers. Eye movements are Cerebral Amyloid Angiopathy
also maintained during body movement via
extensive connections with the occulomotor Elliot J. Roth
nuclei in the brain stem. More recent data has Department of Physical Medicine and
shown that the cerebellum is involved in cogni- Rehabilitation, Northwestern University,
tive, behavioral, and emotional processing, Feinberg School of Medicine, Chicago, IL, USA
including executive control, attention, working
memory, learning, language, pain, and emotion
(Strick et al. 2009). Synonyms

Lesions CAA
Damage to the cerebellar center or to either its
inflow or outflow tracts leads to loss of cerebellar
fine tuning modulation on different cerebral Definition
functions. Vestibulocerebellar lesions can
result in disequilibrium, nystagmus, abnormal Cerebral amyloid angiopathy is a syndrome char-
gait, and recurrent falls. Truncal ataxia and acterized by recurrent spontaneous lobar cerebral
scanning speech are seen with spinocerebellar hemorrhages of various sizes and in various
lesions. Patients with corticocerebellar lesions locations. Each hemorrhage may be asymptomatic
can display signs of dysmetria, asynergia or may cause all of the symptoms of lobar
(decomposition of the voluntary movement), hemorrhages resulting from increased intracranial
hypotonia, dysdiadochokinesia, and intention pressure, including severe headache, seizure,
tremors. stiff neck, and vomiting, altered consciousness,
730 Cerebral Angiitis

paralysis or weakness and sensory loss, and cog-

nitive and language dysfunction, often leading to Cerebral Angiitis
dementia after multiple episodes.
Elliot J. Roth
Department of Physical Medicine and
Current Knowledge Rehabilitation, Northwestern University,
Feinberg School of Medicine, Chicago, IL, USA
The pathological process that causes this disease
is the deposition of a protein, beta-amyloid, in the
walls of the medium-sized arteries of the brain. Synonyms
Interestingly, this protein is identical to the one
found in high quantities in the brains of patients Cerebral vasculitis
with Alzheimer’s disease.
The incidence of cerebral amyloid angiopathy
is difficult to estimate but is known to increase with Definition
advancing age. It is thought to account for 15% of
all intracerebral hemorrhages in patients over Cerebral angiitis or cerebral vasculitis is a rela-
60 years and up to one-half of lobar intracerebral tively rare disease, characterized by inflamma-
hemorrhages in patients older than 70, totaling tion of the blood vessels inside and leading to
about 20 per 100,000 per year in that group. Diag- the brain. It may be caused either by a primary
nosis is usually made based on the clinical presen- disease of the blood vessel walls producing
tation and imaging of recurrent spontaneous lobar inflammation or as a secondary phenomenon
hemorrhages, with no other predisposing prob- resulting from a systemic inflammatory disease
lems, usually associated with progressive decline such as systemic lupus erythematosus or certain
in function and most often associated with demen- infections.
tia. The recurrences can occur simultaneously,
clustered in time, or separated by years. The defin-
itive diagnosis, based on pathological findings, is Current Knowledge
most typically made postmortem. Treatment is
similar to that for intracerebral hemorrhage stroke Angiitis that is confined to the brain is relatively
usually consisting of acute medical management, uncommon, and is called primary angiitis of the
symptom relief, and rehabilitation. central nervous system (PACNS), isolated CNS
vasculitis, primary CNS vasculitis, or granuloma-
tous angiitis of the nervous system. It usually affects
See Also
small- and medium-sized cerebral blood vessels,
▶ Hemorrhagic Stroke but does not involve blood vessels outside of the
CNS. Headache and encephalopathy are the most
▶ Lobar Hemorrhage
frequent symptoms. Stroke occurs in about 20% of
patients. Blood tests reflecting inflammation are
usually normal, but magnetic resonance imaging
References
of the brain is abnormal in more than 90% of
Charidimou, A., Gang, Q., & Werring, D. J. (2012). Sporadic patients. However, the pattern of abnormal findings
cerebral amyloid angiopathy revisited: Recent insights is not specific. Cerebrospinal fluid analysis usually
into pathophysiology and clinical spectrum. Journal of reveals elevations in total protein level or white
Neurology, Neurosurgery, and Psychiatry, 83, 124.
Viswanathan, A., & Greenberg, S. M. (2011). Cerebral
blood cell count. Angiography has a low sensitivity
amyloid angiopathy in the elderly. Annals of Neurology, and low specificity. Treatment usually includes
70, 871. cyclophosphamide and prednisone.
Cerebral Cortex 731

Cross-References blood flow is highly regulated, through “auto-

regulation,” in order to meet the metabolic
▶ Lupus Cerebritis demands of the functioning brain. If it is too
▶ Moyamoya Disease high, it can cause elevated intracranial pressure,
▶ Vasculitis which will compress and damage brain tissue. If it
▶ Vasospasm is too low, it will fail to meet the demands of the
brain, resulting in cerebral ischemia if blood flow C
is less than 20 ml per 100 g of brain tissue per
References and Readings minute and in cerebral infarction if blood flow is
less than 10 ml per 100 g of brain tissue per
Birnbaum, J., & Hellmann, D. B. (2009). Primary angiitis minute. Cerebral blood flow is affected by blood
of the central nervous system. Archives of Neurology,
viscosity, blood vessel size, intracranial pressure
66, 704–709.
Calabrese, L. H., Duna, G. F., & Lie, J. T. (1997). Vasculitis level, and systemic blood pressure.
in the central nervous system. Arthritis & Rheumatism,
40, 1189–1201.
Younger, D. S. (2004). Vasculitis of the nervous system.
Current Opinion in Neurology, 17, 317–336.
Cross-References

▶ Atherosclerosis
▶ Diffusion-Weighted Imaging
▶ Ischemic Penumbra
Cerebral Blood Flow ▶ Ischemic Stroke
▶ Perfusion-Weighted Imaging
Elliot J. Roth ▶ Transcranial Doppler Ultrasonography
Department of Physical Medicine and ▶ Vasospasm
Rehabilitation, Northwestern University,
Feinberg School of Medicine, Chicago, IL, USA
References and Readings

Synonyms Aaslid, R., Lindegaard, K. F., Sorteberg, W., & Nornes,

H. (1989). Cerebral autoregulation dynamics in
humans. Stroke, 20, 45–52.
Cerebral autoregulation; Cerebral perfusion Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2000).
pressure Principles of neural science (4th ed.p. 1305).
New York: McGraw-Hill.

Definition

Cerebral blood flow is the amount of blood that Cerebral Cortex

goes through the arterial tree in the brain in a given
amount of time. Kimberle M. Jacobs
Department of Anatomy and Neurobiology,
Virginia Commonwealth University, Richmond,
Current Knowledge VA, USA

In adults, cerebral blood flow is typically 750 ml

per minute, or about 50 ml per 100 g of brain Synonyms
tissue per minute. This amount is equivalent to
about 15% of the total cardiac output. Cerebral Cerebrum surface; Cortex
732 Cerebral Cortex

Definition The cerebral cortex can also be divided on the

basis of phylogeny into archicortex, paleocortex,
The cerebral cortex is a structure lying on the and neocortex (oldest to newest). Archicortex
outer surface of the vertebrate cerebrum that is consists of the hippocampus, which is associated
responsible for consciousness and higher brain with the acquisition of memories. Paleocortex is
functions. primarily associated with the function of olfac-
tion. Only mammals have neocortex. In humans,
the majority of the cerebral cortex is made up of
Historical Background neocortex. In addition, as a percentage of total
brain tissue, humans have more neocortex than
The cerebral cortex is a structure lying on the outer other species (see for example, human relative to
surface of the vertebrate cerebrum that is responsi- rat, Swanson 1995). This is unique to the neocor-
ble for consciousness and higher brain functions, tex, since evolution has not increased the size of
including sensory perception, voluntary move- other brain structures, such as the cerebellum
ment, language, reasoning, memory, and planning. (Clark et al. 2001). This increase in proportion is
Cerebral comes from the Latin word cerebrum, due to increased surface area, and not to a change
meaning brain. Cortex comes from the Latin word in the thickness of the cortex, which is from 1 to
for bark, which is typically an outer layer or cover- 3 mm thick in all species.
ing. In large mammals, this structure is folded Cortex is made up of gray matter, where cell
forming ridges known as gyri and grooves known bodies predominate, and white matter that con-
as sulci. Gyri and sulci normally form in the same sists primarily of myelinated axons. All cortex is
relative locations from one individual to another. laminated, but the gray matter of neocortex has six
This folding increases the cortical surface area layers (Fig. 1), while that of the older archi-and
while allowing for constraints on skull circumfer- paleocortices has three layers. Cortical layers are
ence. Abnormal folding of the cortex is associated differentiated based on their cellular components.
with neurological deficits. Absent or reduced fold- The basic components and lamination of cortex
ing in humans is known as lissencephaly (smooth are consistent across phylogeny. Within neocor-
brain) and is associated with mental retardation and tex, the layers are given names that represent the
epilepsy (Leventer et al. 2000). The abnormality of predominant neuronal cell type. The outermost
small regions of increased folding is known as layer (identified by Roman numeral I), contains
polymicrogyria (many small ridges), and can also mainly dendrites and axons and is called the
be associated with developmental delay and epi- molecular layer. Layer II is called the external
lepsy (Piao et al. 2005). granule layer and consists of small, spherical
cells. Layer III primarily contains small to
medium pyramidal neurons and is called the
Current Knowledge external pyramidal layer. Layer IV contains
spiny stellate neurons and is called the internal
Structurally, the cerebral cortex can be divided granule cell layer. Layer V contains large pyrami-
into four lobes named after the overlying cranial dal neurons and is called the internal pyramidal
bones: frontal, parietal, temporal, and occipital. layer. Layer VI has a variety of morphological cell
Prominent sulci define the borders of these types and is therefore called the polymorphic cell
lobes. Primary functions of the lobes can be layer. These layers have differential functions that
ascribed as follows: occipital: vision; parietal: are consistent across different neocortical areas
sense of touch (somatosensation) and body posi- (Fig. 2). Layer I is a modulatory region and
tion; frontal: planning of action and control of receives input from higher order cortical regions.
movement; and temporal: hearing, visual identifi- Layers II and III perform intracortical processing,
cation, and memory. These lobes are present in receiving input from the deeper layer IV, as well as
each of the two hemispheres (left and right). from adjacent layers II and III and from the
Cerebral Cortex 733

II

Callosal C
III

IV

Callosal
V

Cerebral Cortex, Fig. 1 Cortical Lamination. Cresyl

Violet stained coronal section from rat, showing neocortex
above hippocampus (archicortex). Neocortical layers are VI
indicated by Roman numerals. Layer V is commonly
divided into subparts with layer Va containing callosal
Modulatory
projection neurons, and Vb containing the largest pyrami- Specific Nonspecific
DA
dal neurons that project to spinal cord and other subcortical To Thalamic Thalamic
NE
locations. Within this section of neocortex, slight differ- Spinal Cord Afferents Afferents
5-HT
ences in cytoarchitectonics can be seen between the ACh Superior Colliculus
somatosensory cortex (Brodmann’s area 3) to the right
and motor cortex (Brodmann’s area 4) to the left. Most Cerebral Cortex, Fig. 2 Diagram of typical excitatory
obvious is the lack of a clear layer IV within motor cortex. neuronal cell types and connections of neocortex. Layer I,
WM neocortical white matter; s.o. stratum oriens; the modulatory cell layer, contains the tufts of deeper lying
s.p. stratum pyramidale; s.r. stratum radiatum, all of the pyramidal neurons, nonspecific thalamic afferents, and
CA1 region of the hippocampus input from brainstem modulatory transmitter systems.
Layer II contains primarily small granule cells. Layer III
has small pyramidal neurons that perform intracortical
homologous cortical region in the opposite hemi- processing, sending their axons horizontally within layer
sphere. Layer IV is the major input layer and III. Layer IV contains spiny stellate neurons that send their
output to layer III. Specific thalamic afferents make excit-
receives specific thalamocortical afferents in sen-
atory synapses within layer IV on the spiny stellate cells as
sory areas of cortex. Layer V is the major cortical well as on the apical dendrites of deeper lying pyramidal
output, for instance sending the result of motor neurons. These specific thalamic afferents have a smaller
cortical processing to the motor neurons of the projection to layer VI, near the border with layer V. Layer
V is the major output layer for the cortex, and contains
spinal cord. Layer VI provides a return feedback
medium and large pyramidal neurons. Layer VI contains
to the thalamus. neurons with a variety of shapes. Note that inhibitory cells
Different functional regions of cortex are con- that make up 20% of the neurons in the neocortex are not
sidered to have primary, secondary, and associa- shown here. Modulatory: Modulatory neurotransmitters;
DA: Dopamine; NE: Norepinephrine; 5-HT: Serotonin;
tion components. In sensory cortex, the primary
and ACh: Acetylcholine
cortical area is the region that first receives infor-
mation about that sense from the periphery
(traveling by way of the thalamus). The secondary processing from the primary cortical area. Asso-
cortical area is considered “higher order” because ciation cortex receives input from several different
the input it receives is the result of cortical cortical regions
734 Cerebral Edema

The general function of the layers is ▶ Neocortex

maintained across cortical regions; however, ▶ Prefrontal Cortex
there are slight changes in cell size and packing ▶ Primary Cortex
density (cytoarchitecture) from one cortical area ▶ Secondary Cortex
to another. These cytoarchitectonic differences ▶ Somatosensory Cortex
were used by Korbinian Brodmann in 1909 to ▶ Striate Cortex
draw boundaries presumed to identify function- ▶ Tertiary Cortex
ally different cortical areas. ▶ Unimodal Cortex
Perpendicular to the plane of the cortical ▶ Visual Cortex
layers are functional modules called cortical col-
umns. The idea that a column of cortex repre-
sents a fundamental processing unit was brought References and Readings
to light by Vernon Mountcastle of Johns Hopkins
University (Mountcastle 1957). Within a col- Clark, D. A., Mitra, P. P., & Wang, S. S. (2001). Scalable
architecture in mammalian brains. Nature, 411,
umn, neurons tend to have similar response prop-
189–193.
erties. For instance, within somatosensory Jones, E. G., & Peters, A. (Eds.). (1990a). Cerebral cortex:
cortex, the neurons within a column have similar volume 8A: Comparative structure and evolution of the
receptive fields (area of the receptive surface that cerebral cortex, part I. New York: Springer.
Jones, E. G., & Peters, A. (Eds.). (1990b). Cerebral cortex:
causes the neuron to fire action potentials). Neu-
volume 8B: Comparative structure and evolution of the
rons of different columns have nonoverlapping cerebral cortex, part II. New York: Springer.
receptive fields. The result of evolution then has Leventer, R. J., Mills, P. L., & Dobyns, W. B.
been to add cortical columns or additional pro- (2000). X-linked malformations of cortical develop-
ment. American Journal of Medical Genetics, 97,
cessing units.
213–220.
Head trauma, stroke, and tumor may all result Mountcastle, V. B. (1957). Modality and topographic prop-
in lesions of the cerebral cortex. The function lost erties of single neurons in cat’s somatic sensory cortex.
will be dependent on the location of the lesion. For Journal of Neurophysiology, 20, 408–434.
Piao, X., Chang, B. S., Bodell, A., Woods, K., Benzeev, B.,
example, lesion of Brodmann’s area 17 will result
Topcu, M., et al. (2005). Genotype-phenotype analysis
in loss of vision, while lesion of Brodmann’s area of human frontoparietal polymicrogyria syndromes.
3 will result in some loss of somatosensation Annals of Neurology, 58(5), 680–687.
including touch and pain discrimination. Damage Rasmussen, W., & Penfield, T. (1957). The cerebral cortex
of man: A clinical study of localization of function.
to Brodmann’s area 4 will result in loss of motor
New York: Macmillan Company.
function. Lesions of the frontal cortex can cause Swanson, L. W. (1995). Mapping the human brain: Past,
severe personality changes. Memory loss is typi- present, and future. Trends in Neurosciences, 418,
cally associated with cortical lesions. The inabil- 471–474.
ity to speak occurs after destruction of Broca’s
area in the ventral portion of the frontal lobe,
typically in the left hemisphere (Brodmann’s
areas 44 and 45). Incoherent speech or “word
salad” results from the destruction of Wernicke’s Cerebral Edema
area in the upper portion of the temporal lobe (part
of Brodmann’s area 22). Gary Tye1 and John Brown2
1
Neurosurgery, Virginia Commonwealth
University, Richmond, VA, USA
2
Cross-References Medical College of Georgia, Augusta, GA, USA

▶ Auditory Cortex
▶ Brodmann’s Areas of the Cortex Synonyms
▶ Heteromodal Cortex
▶ Homotypic Cortex Cytotoxic edema; Vasogenic edema
Cerebral Embolism 735

Definition originates and stops in an artery that leads to or

rests within the brain. The result is occlusion of the
Cerebral edema is an increase in the water content vessel and obstruction of the flow of oxygen and
of the brain that leads to brain swelling. It may be blood to the brain tissue supplied by that artery.
divided into two broad categories: vasogenic and
cytotoxic.
Vasogenic edema involves a disruption in the Current Knowledge C
blood-brain barrier with leakage of fluid from the
intravascular space. Cerebral embolisms cause about 15–20% of all
In cytotoxic edema, the blood-brain barrier is strokes and about one-quarter of all ischemic
intact, and there is an increase in the intracellular strokes. It occurs most frequently in patients
fluid compartment. who have known heart disease, including atrial
fibrillation and other arrhythmias, valve disease,
“mural thrombus” (a blood clot sitting in the left
Cross-References ventricle of the heart), or other conditions. It
causes symptoms similar to those of thrombotic
▶ Cerebral Perfusion Pressure strokes, but the presentations of embolic strokes
▶ Intracranial Pressure tend to be more abrupt and dramatic. These can
include sudden onset of hemiplegia, sensory loss,
facial weakness, cognitive deficits, or speech dis-
References and Readings turbance. Seizures or headaches are relatively
common in embolic strokes, and both of these
Beaumont, A., Marmarou, A., & Ward, J. D. (2001). Intra-
cranial hypertension mechanisms and management. In symptoms are relatively rare in ischemic strokes.
D. G. McClone (Ed.), Pediatric neurosurgery In addition, there may be multiple diffuse simul-
(pp. 619–633). Philadelphia: W. B. Saunders. taneous neurological findings, which may result
Greenberg, M. S. (1997). Handbook of neurosurgery. from multiple simultaneous emboli, known as
Lakeland: Greenberg Graphics.
Rosenblum, W. I. (2007). Cytotoxic edema: Monitoring its “showers of emboli.” Usually, management
magnitude and contribution to brain swelling. Journal requires addressing the cardiac condition and pre-
of Neuropathology and Experimental Neurology, venting subsequent emboli by using anticoagu-
66(9), 771–778. lants, in addition to the treatment of the cerebral
infarction and its neurological consequences.

Cerebral Embolism

Elliot J. Roth Cross-References

Department of Physical Medicine and
Rehabilitation, Northwestern University, ▶ Anticoagulation
Feinberg School of Medicine, Chicago, IL, USA ▶ Echocardiogram
▶ Infarction
▶ Ischemic Stroke
Synonyms ▶ Myocardial Infarction
▶ Thrombosis
Embolic stroke ▶ Warfarin (Coumadin)

Definition References and Readings

DiTullio, M. R., & Homma, S. (2002). Mechanisms of

A cerebral embolism is a blood clot (thrombus) that cardioembolic stroke. Current Cardiology Reports, 4,
starts from the heart or blood vessel where the clot 141–148.
736 Cerebral Palsy

Fuster, V., Rydén, L. E., Cannom, D. S., Crijns, H. J., change in function, and provide prognostic infor-
Curtis, A. B., & Ellenbogen, K. A. (2006). mation (Rosenbaum et al. 2007). Historically,
ACC/AHA/ESC 2006 guidelines for the management
of patients with atrial fibrillation: A report of the Amer- classification has focused on two features: (a)
ican College of Cardiology/American Heart Associa- tone and (b) body part involvement (Menkes and
tion Task Force on Practice Guidelines and the Sarnat 2000). See Table 1 for a summary. Spastic
European Society of Cardiology Committee for Prac- forms of CP are more common, with spastic diple-
tice Guidelines (Writing Committee to Revise the 2001
guidelines for the management of patients with atrial gia being the most common (Menkes and Sarnat
fibrillation): Developed in collaboration with the 2000). However, there is disagreement regarding
European Heart Rhythm Association and the Heart classification schemes, largely due to poor reli-
Rhythm Society. Circulation, 114, e257–e354. ability (Accardo and Hoon 2008). Recent
Hart, R. G., Pearce, L. A., & Aguilar, M. I. (2007). Meta-
analysis: Antithrombotic therapy to prevent stroke in attempts to improve classification schemes
patients who have nonvalvular atrial fibrillation. Annals include: (a) development of standardized exami-
of Internal Medicine, 146, 857–867. nation procedures and diagnostic algorithms and
(b) use of the Gross Motor Functional Classifica-
tion System (GMFCS), which focuses on func-
tional mobility (Rosenbaum et al. 2007).
Cerebral Palsy

Kathleen K. M. Deidrick Epidemiology

Neuro- and Behavioral Psychology, St. Luke’s
Children’s Hospital, Boise, ID, USA Prevalence rates vary from 1.3 to 3/1000 and are
stable across country of origin (Clark and Hankins
2003). Preterm birth raises the risk of CP. For
Synonyms example, Ancel et al. (2006) report diagnosis of
cerebral palsy among 20% of children born at or
Static encephalopathy before 27 weeks of gestation versus diagnosis of

Cerebral Palsy, Table 1 Traditional categorization of

Short Description or Definition cerebral palsy
Type Description
As defined by the International Workshop on the
Spastic cerebral Increased muscle tone with
Definition and Classification of Cerebral Palsy, palsy movement
Cerebral Palsy (CP) is: “a group of permanent Spasticity of upper and lower
disorders of the development of movement and Spastic quadriplegia limbs
posture, causing activity limitation, that are attrib- Spastic diplegia Greater involvement of the legs
uted to non-progressive disturbances that than the arms
occurred in the developing fetal or infant brain. Greater involvement of one side
Spastic hemiparesis of the body (more often the
The motor disorders of cerebral palsy are often
right); greater impairment of the
accompanied by disturbances of sensation, per- arm than the leg
ception, cognition, communication, and behavior, Extraparamidal Involuntary and abnormal
by epilepsy, and by secondary musculoskeletal cerebral palsy muscle movements: Dystonia
problems” (Rosenbaum et al. 2007). (fluctuating tone and abnormal
body postures) and/or athetoid
movements (writhing
movements in the extremities)
Categorization Hypotonic cerebral Persistent, low muscle tone
palsy
Classification schemes are critical to providers Mixed and atypical Mixture of spasticity and
cerebral palsy extrapyramidal symptoms
attempting to describe the disorder, measure
Cerebral Palsy 737

5–6% of children born between 28 and 31 weeks. Cerebral Palsy, Table 2 Symptoms associated with CP
Reviewers note that overall rates of CP are Domain Symptoms
climbing, while rates of CP among full-term infants Secondary muscular Delayed development of
have remained stable (1.1/1000). This suggests that and orthopedic adaptive motor skills
increases are largely due to greater survival of pre- symptoms Gait abnormalities
Oral-motor difficulties and
term infants (Mukherjee and Gaebler-Spira 2007). problems with speaking and
drooling C
Contracture (shortening of the
Natural History, Prognostic Factors, muscle)
Bone deformities (e.g., hip
Outcomes subluxation/dislocation)
Scoliosis
Etiology varies by birth status (preterm or full- Osteoporosis
term) and type of CP (Menkes and Sarnat 2000). Reduced limb growth
For preterm infants, the most common causes of Neurologic symptoms Seizure disorder
Sensory Visual problems
CP are intraventricular hemorrhage and/or peri-
Homonymous hemianopia
ventricular leukomalacia. Risk factors for CP in (in spastic hemiplegia)
full-term infants include prenatal infections, Strabismus
anoxic or ischemic injuries, genetic syndromes, Nystagmus
Visual sequela related to
brain malformations, or stroke. Atypical CP with
prematurity
athetoid movements is typically caused by basal Tactile/perceptual deficits
ganglia damage secondary to hyperbilirubinemia Stereognosis
(Mukherjee and Gaebler-Spira 2007). A variety of Poor two-point
discrimination (in spastic
symptoms are associated with CP, which vary by
hemiplegia)
severity and type of CP (Menkes and Sarnat 2000; Neglect of affected side of
Mukherjee and Gaebler-Spira 2007). See Table 2 the body (in spastic hemiplegia)
for a summary. Hearing loss
Feeding/ Dysphagia and aspiration
gastrointestinal Malnutrition requiring
gastrostomy
Neuropsychology and Psychology of Gastroesophageal reflux
Cerebral Palsy Constipation
Incontinence or difficulty
voiding
As many as 30–50% of children with CP may
Dental Malocclusion
have a diagnosis of intellectual disability, with Poor tooth enamel
increased risk for children with quadriplegia, Pain and fatigue Pain associated with primary (e.
more severe motor deficits, full-term birth, and/ g., spasticity and contractures)
or a coexisting seizure disorder (Menkes and and secondary (e.g.,
Sarnat 2000; Mukherjee and Gaebler-Spira, constipation) disease processes
Pain related to medical
2007; Warschausky and Kaufman 2010). Esti- procedures/therapies
mates of cognitive functioning can be difficult Fatigue secondary to poor
to obtain, as speech, vision, and motor deficits can mobility
limit participation in traditional tests (Yin Foo et al.
2013). Efforts are ongoing to develop cognitive
tests that limit demands for speeded motor and/or and language, short-term and working memory,
verbal response (Kaufman et al. 2014; Warschausky slowed processing speed, and executive function-
et al. 2012). ing (e.g., focused and sustained attention, inhibi-
Regardless, difficulties with visual-perceptual tion, effective strategies for learning, cognitive
processing (particularly for children with a flexibility) are described in the literature (Deidrick
history of PVL), visual-motor integration, speech and Harlan Drewel 2012; Ego et al. 2015;
738 Cerebral Palsy

Warschausky et al. 2013). Problems with learning tests of intelligence that minimize requirements
and academic achievement in this population, for motor output; see Yin Foo et al. 2013 for
including difficulties in math (e.g., numeracy, guidance). In children with marked communica-
math fact fluency, computation) and reading, tion deficits, parents and educators may be inter-
may be linked to core cognitive deficits that are ested in possible methods for alternative
similar to those found in children without CP who communication (e.g., picture exchange systems,
have learning disorders. complex computerized devices), a question which
Emotionally and behaviorally, a subset of can be addressed through a multidisciplinary eval-
parents endorse clinically significant internaliz- uation including a psychologist, speech-language
ing (poor emotional regulation, dependence, pathologist, and occupational therapist (Berninger
anxiety) and externalizing (behavior and activ- 2004). For children who are less impaired, evalu-
ity level) concerns for children with CP ations should include a broad overview of neuro-
(Deidrick and Harlan Drewel 2012). Factors psychological functions with attention to
associated with higher rates of emotional and executive functioning, visual-perceptual pro-
behavioral difficulties in this population include cessing, and academics. Assessments should
co-occurring epilepsy, intellectual disability, include formal or informal evaluation of pain,
high levels of pain, and family factors. Studies fatigue, quality of life, and psychological and
of emotional adjustment suggest concerns about behavioral functioning.
self-concept in areas directly impacted by the
physical disability (e.g., attractiveness, social
interaction, athletics, academics) (Deidrick and Treatment
Harlan Drewel 2012). Adolescent girls may be at
particularly increased risk for low self-concept Multidisciplinary treatment is considered the
(Shields et al. 2006). Studies of Quality of Life standard of care for children with CP (Braddom
(QOL) suggest lower QOL for children with CP, 2007). Children are involved in medical and
particularly in areas associated with CP and its therapeutic treatments designed to decrease spas-
sequela (e.g., academics, social interaction) and ticity and increase function (e.g., Botox injec-
most notably for children with quadriplegia/more tions, baclofen pump, surgical interventions,
severe CP (Livingston et al. 2007). Transition to splinting and casting, physical and occupational
adulthood is understudied, but issues regarding therapies, speech-language therapy, early inter-
reduced involvement in age-appropriate social vention services). Information regarding the effi-
activities and roles, employment, and leisure activ- cacy of these interventions is emerging and very
ities are of concern (Liptak 2008; Rutkowski and limited (Tupper 2007). For example, recent
Riehle 2009). reviews indicate emerging evidence that intra-
thecal baclofen may reduce spasticity, improve
motor movement, and make young people feel
Evaluation more comfortable and caretaking easier (Hasnat
and Rice 2015).
Given the broad variability in etiology and the Interventions developed from a rehabilitation
sparse knowledge base regarding neuropsycho- psychology perspective are integral to the treat-
logical functioning in CP, evaluations should be ment plan, including behaviorally based treat-
tailored to the child and situation. Prior to the ments to increase function and assessment and
evaluation, medical evaluations clarifying the intervention of pain and fatigue. Rehabilitative
child’s vision and hearing will be critical. Assess- therapies focusing on upper limb function, such
ment measures should be chosen carefully to as constraint-induced movement therapy (CIMT)
avoid underestimates of function due to motor or and bimanual training, are promising approaches
verbal output problems (e.g., use of nonverbal that attempt to promote increased use of the
Cerebral Palsy 739

impacted limb (Sakzewski et al. 2014), though Berrin, S. J., Malcarne, V. L., Varni, J. W., Burwinkle, T.
questions about treatment modality, intensity, M., Sherman, S. A., Artavia, K., & Chambers, H. G.
(2007). Pain, fatigue, and school functioning in chil-
and the mechanisms responsible for improvement dren with cerebral palsy: A path-analyticmodel. Jour-
remain under investigation (Reid et al. 2015). nal of Pediatric Psychology, 32(3), 330–337. https://
Also promising are behavioral treatments that doi.org/10.1093/jpepsy/jsl017.
address problems with drooling (Van der Burg et Braddom, R. L. (Ed.). (2007). Physical medicine & reha-
al. 2007). Pain can be life-limiting and may be
bilitation (3rd ed.). Philadelphia: Elsevier.
Clark, S. L., & Hankins, G. D. V. (2003). Temporal
C
underrecognized due to communication deficits and demographic trends in cerebral palsy – Fact
and atypical pain responses in children with CP and fiction. American Journal of Obstetrics & Gyne-
(Houlihan et al. 2004). Measures for the evalua- cology, 188(3), 628–633. https://doi.org/10.1067/
mob.2003.204.
tion of pain adapted for children with wide range Deidrick, K. M., & Harlan Drewel, E. (2012).
of motor and communication skills may help the Children with chronic health conditions. In P. Kennedy
team to adequately evaluate and treat pain (Ed.), The Oxford handbook of rehabilitation psychol-
(Kingsnorth et al. 2015). Fatigue due to increased ogy (pp. 171–188). New York: Oxford University
Press.
energy expenditure during daily tasks can also Ego, A., Lidzba, K., Brovedani, P., Belmonti, V., Sibylle,
impact function and should be addressed (Berrin G-M., Boudia, B.,   , & Cans, C. (2015). Visual-per-
et al. 2007). ceptual impairment in children with cerebral palsy: A
systematic review. Developmental Medicine and Child
Neurology, 57(Suppl 2), 46–51. https://doi.org/10.111/
dmcn.12687.
See Also Hasnat, M. J., & Rice, J. E. (2015). Intrathecal baclofen
for treating spasticity in children with Cerebral
Palsy. The Cochrane Database of Systematic
▶ Assistive Technology Reviews, 11, 1–47. https://doi.org/10.1002/14651858.
▶ Augmentative and Alternative Communication CD004552.pub2.
(AAC) Houlihan, C. M., O’Donnell, M., Conaway, M., & Steven-
son, R. D. (2004). Bodily pain and health-related qual-
▶ Constraint Induced Therapy
ity of life in children with cerebral palsy.
▶ Encephalopathy Developmental Medicine & Child Neurology, 46(5),
▶ Hemiparesis 305–310. https://doi.org/10.1111/j.1469-8749.2004.
▶ Hemiplegia tb00490.x.
Kaufman, J. N., Donders, J., & Warschausky, S. (2014). A
▶ Interdisciplinary Team Rehabilitation
comparison of visual inspection time measures in chil-
▶ Periventricular Leukomalacia dren with cerebral palsy. Rehabilitation Psychology, 54
▶ Prematurity and Low Birth Weight (2), 147–154. https://doi.org/10.1037/a0036019.
Kingsnorth, S., Orava, T., Provvidenza, C., Adler, E., Ami,
N., Greseley-Jones, T.,   , & Fehlings, D. (2015).
Chronic pain assessment tools for cerebral palsy: A
Further Reading systematic review. Pediatrics, 135, e947–e960.
https://doi.org/10.1542/peds.2015-0273.
Accardo, P. J., & Hoon, A. H., Jr. (2008). The challenge of Liptak, G. S. (2008). Health and well being of
cerebral palsy classification: The ELGAN study. Jour- adults with cerebral palsy. Current Opinion in
nal of Pediatrics, 153, 451–452. Neurology, 21, 136–142. https://doi.org/10.1097/
Ancel, P.-Y., Livinec, F., Larroque, B., Marret, S., Arnaud, WCO.0b013e3282f6a499.
C., Pierrat,   , & Kaminski, M. (2006). Cerebral palsy Livingston, M. H., Rosenbaum, P. L., Russell, D. J., &
among very preterm children in relation to gestational Palisano, R. J. (2007). Quality of life among adoles-
age and neonatal ultrasound abnormalities: The cents with cerebral palsy: What does the literature tell
EPIPAGE cohort study. Pediatrics, 117, 828–835. us? Developmental Medicine & Child Neurology,
https://doi.org/10.1542/peds.2005-0091. 49(3), 225–231. https://doi.org/10.1111/j.1469-
Berninger, V. A. (2004). Understanding the “Graphia” in 8749.2007.00225.x.
developmental dysgraphia. In D. Dewey & D. E. Tup- Menkes, J. H., & Sarnat, H. B. (2000). Perinatal asphyxia
per (Eds.), Developmental motor disorders: A neuro- and trauma. In J. H. Menkes & H. B. Sarnat (Eds.),
psychological perspective (pp. 328–350). New York: Child neurology (6th ed., pp. 401–466). Philadelphia:
Guilford Press. Lippincott Williams & Wilkins.
740 Cerebral Perfusion Pressure

Mukherjee, S., & Gaebler-Spira, D. J. (2007). Cerebral

palsy. In R. L. Braddom (Ed.), Physical medicine & Cerebral Perfusion Pressure
rehabilitation (3rd ed., pp. 1243–1267). Philadelphia:
Elsevier.
Reid, L. B., Rose, S. E., & Boyd, R. N. (2015). Rehabili- Gary Tye1 and John Brown2
1
tation and neuroplasticity in children with unilateral Neurosurgery, Virginia Commonwealth
cerebral palsy. Nature Reviews Neurology, 11, University, Richmond, VA, USA
390–400. https://doi.org/10.1038/nrneurol.2015.97. 2
Rosenbaum, P., Paneth, N., Leviton, A., Goldstein, M., & Medical College of Georgia, Augusta, GA, USA
Bax, M. (2007). A report: The definition and classifica-
tion of cerebral palsy April 2006. Developmental Med-
icine & Child Neurology – Supplementum, 109, 8–14. Definition
https://doi.org/10.1111/j.1469-8749.2007.tb12610.x.
Rutkowski, S., & Riehle, E. (2009). Access to employment
and economic independence in cerebral palsy. Cerebral perfusion pressure (CPP) is the net pres-
Physical Medicine and Rehabilitation Clinics of sure of flow of the blood to the brain, which is the
North America, 20, 535–547. https://doi.org/10.1016/ difference between the mean arterial pressure
j.pmr.2009.06.003.
Sakzewski, L., Ziviani, J., & Boyd, R. N. (2014). Efficacy (MAP) and the intracranial pressure (ICP).
of upper limb therapies for unilateral cerebral palsy: A
meta-analysis. Pediatrics, 133, e175–e204. https://doi.
org/10.1542/peds.2013-0675. Cross-References
Shields, N., Murdoch, A., Loy, Y., Dodd, K. J., & Taylor,
N. F. (2006). A systematic review of the self-concept of
children with cerebral palsy compared with children ▶ Cerebral Blood Flow
without disability. Developmental Medicine & Child ▶ Intracranial Pressure
Neurology, 48, 151–157. https://doi.org/10.1017/
S0012162206000326.
Tupper, D. E. (2007). Management of children with disor-
ders of motor control. In S. J. Hunter & J. Donders References and Readings
(Eds.), Pediatric neuropsychological intervention: A
critical review of science and practice. Cambridge: Diringer, M. N., & Axelrod, Y. (2007). Hemodynamic
Cambridge University Press. manipulation in the neuro-intensive care unit: Cerebral
Van der Burg, J. J. W., Didden, R., Jongerius, P. H., & perfusion pressure therapy in head injury and hemody-
Rotteveel, J. J. (2007). Behavioral treatment of namic augmentation for cerebral vasospasm. Current
drooling: A methodological critique of the literature Opinion in Critical Care, 13(2), 156–162.
with clinical guidelines and suggestions for future Wright, W. L. (2007). Multimodal monitoring in the ICU:
research. Behavior Modification, 31, 573–594. https:// When could it be useful? Journal of the Neurological
doi.org/10.1177/0145445506298723. Sciences, 261(1–2), 10–15.
Warschausky, S., & Kaufman, J. (2010). Neurodeve-
lopmental conditions in children. In R. G. Frank, M.
Rosenthal, & B. Caplan (Eds.), Handbook of rehabili-
tation psychology (2nd ed., pp. 329–335). Washington,
DC: American Psychological Association. Cerebrovascular Disease
Warschausky, S., Kaufman, J. N., & Felix, L. (2013).
Cerebral palsy. In I. S. Baron & C. Rey-Casserly Elliot J. Roth
(Eds.), Pediatric neuropsychology medical advances
and lifespan outcomes (pp. 80–98). New York: Oxford Department of Physical Medicine and
University Press. Rehabilitation, Northwestern University,
Warschausky, S., Van Tubbergen, M., Asbell, S., Kaufman, Feinberg School of Medicine, Chicago, IL, USA
J., Ayyangar, R., & Donders, J. (2012). Modified test
administration using assistive technology: Preliminary
psychometric findings. Assessment, 19, 472–479.
https://doi.org/10.1177/1073191111402458. Definition
Yin Foo, R., Guppy, M., & Johnston, L. M. (2013). Intel-
ligence assessments for children with Cerebral Palsy: Cerebrovascular disease refers to the group of
A systematic review. Developmental Medicine &
Child Neurology, 55, 911–918. https://doi.org/ conditions characterized by disease of the blood
10.1111/dmcn.12157. vessels that supply blood to the brain. It can occur
Chandler Exterminators v. Morris (1992) 741

in the blood vessels that lead to the brain or in the ▶ Subarachnoid Hemorrhage
blood vessels inside the brain. While it usually ▶ Thrombosis
presents with symptoms of a stroke (the group of ▶ Transcranial Doppler Ultrasonography
clinical manifestations of cerebrovascular dis- ▶ Vascular Dementia
ease), it can be asymptomatic, in which case it is ▶ Vascular Malformations
usually detected either by physical examination or ▶ Vasculitis
selected imaging techniques. C
The term “cerebrovascular accident” (or CVA)
is incorrect and should be avoided, as there is References and Readings
nothing accidental about a stroke. The term “cere-
brovascular disease” is a more general term than is Wolf, P. A., & Grotta, J. C. (2000). Cerebrovascular dis-
ease. Circulation, 102, IV-75.
“stroke,” because “cerebrovascular disease”
includes asymptomatic or subclinical disease, in
addition to the clinically manifest strokes.
Most cerebrovascular disease is obstructive in
Chandler Exterminators
nature, caused by atherosclerotic plaques that line
v. Morris (1992)
the blood vessel walls and block the blood flow. If
the blockage is only partial, and is not severe
Robert L. Heilbronner
enough to impair brain function, then the disease
Chicago Neuropsychology Group, Chicago, IL,
remains asymptomatic. However, if the obstruc-
USA
tion is severe enough to reduce blood supply to the
extent that brain injury occurs, then symptoms
suggesting a stroke ensue. If these symptoms are
Definition
temporary and completely reversed, the phenom-
enon is known as a “transient ischemic attack.” If
The testimony of neuropsychologists is commonly
the brain injury is irreversible, this causes a com-
challenged by defense attorneys in cases relating to
pleted “stroke,” which is defined as the neurolog-
inferences of subtle brain changes associated with
ical manifestations of disease of blood vessels of
neurotoxic brain injury. In the case of Schudel
the brain. Other forms of cerebrovascular disease
v. General Electric (1995), plaintiffs accepted neu-
also can occur. Inflammation of blood vessel walls
ropsychological evidence for brain damage caused
(“vasculitis”), bleeding into the cerebral vessel
by organic solvents and polychlorinated biphenyls
walls (“dissection”), and hemorrhage, or extrava-
(PCBs). However, the federal appeals court from
sation of blood outside of the vessels themselves
the Ninth Circuit ruled that neuropsychological
and into the brain tissue, also can cause brain
testimony is limited only to damages and cannot
damage. These can give rise to strokes.
determine physical causation. The court opined that
determination of causation is relegated to medical
Cross-References doctors (MDs) or left to the discretion of the jury to
make connections between neurocognitive deficits
▶ Atherosclerosis presented and exposure to toxins. In the case of
▶ Cerebral Angiitis Chandler Exterminators v. Morris (1992), the
▶ Cerebral Embolism Georgia Supreme Court ruled in favor of the trial
▶ Dissection court’s decision to prohibit neuropsychological tes-
▶ Hemorrhagic Stroke timony that proposed a link between neurotoxicants
▶ Infarction and impaired neuropsychological test scores. In
▶ Intracerebral Hemorrhage response to this case, Georgia legislature wrote a
▶ Ischemic Stroke new law permitting neuropsychologists to provide
▶ Stroke testimony related to causation of brain injuries in
742 Chapple v. Ganger

Georgia. Challenges to specific neuropsychological flexible battery approach; thus, contradicting

tests and test batteries occur with some degree of Reed’s assertions implying that most neuropsy-
frequency, and they should be taken seriously by all chologists would not be suited for involvement in
parties involved, especially neuropsychologists. forensic work. In support of his conclusion, Reed
These types of challenges question the scientific referenced the case of Chapple v. Ganger (1998), a
basis of one or more of the expert’s methods, mea- brain injury claim. Review of the judge’s written
sures, or conclusions. Challenges to specific decision in Chapple v. Ganger outlined that all
methods are brought under Frye v. United States neuropsychological testimony (even partial HRB
(1923) and Daubert v. Merrell Dow (1993) rulings. protocols from two other neuropsychologists) was
admitted into evidence and the fact that the judge
had placed more emphasis on testimony from a
Cross-References fixed battery advocate was completely unrelated
to the determination of the test battery. Indeed,
▶ Daubert v. Merrell Dow Pharmaceuticals (1993) there was no Daubert challenge to a flexible test
battery approach. In this particular case, only the
testimony of a vocational specialist who conducted
References and Readings no testing and provided no evidence in the form of
a peer-reviewed study to support his claims was
Chandler Exterminators Inc. v. Morris, 200 Ga. subject to a Daubert hearing from the defense.
App. 816 (1992).
Schudel v. General Electric, 120 F. 3d 991 (1995).

References and Readings

Chapple v. Ganger Chapple v. Ganger, 851 F. Supp. 1481, E.D. of Washington

(1994).
Daubert v. Merrell Dow Pharmaceuticals,
Robert L. Heilbronner 509 U.S. 579 (1993).
Chicago Neuropsychology Group, Chicago, IL, General Electric Co. v. Joiner, 522 U.S. 136 (1997).
USA Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychol-
ogy and the law: Principles of productive attorney-
neuropsychologists relations. In G. Larrabee (Ed.),
Forensic neuropsychology: A scientific approach.
Historical Background New York: Oxford University Press.
Kumho Tire Co. v. Carmichael, 526 U.S. 137 (1999).
Reed, J. E. (1996). Fixed versus flexible neuropsycholog-
In the case of Daubert v. Merrell Dow (1993), it
ical test batteries under the Daubert standard for
was ruled that for scientific testimony to be admis- the admissibility of scientific evidence. Behavioral
sible, it has to be (a) scientifically valid and Sciences and the Law, 14, 315–322.
(b) relevant to the case at hand. The court provided
a list of guidelines intended to aid in the determi-
nation of scientific validity (e.g., peer reviewed,
falsifiability, acceptable error rate, etc.). The Charles Bonnet Syndrome
Daubert ruling along with subsequent related rul-
ings (e.g., General Electric v. Joiner 1997; Kumho Melissa Buttaro
Tire v. Carmichael 1999) generated significant Department of Psychiatry, The Miriam Hospital,
debate among psychologists and neuropsycholo- Providence, RI, USA
gists and many other disciplines. Specifically,
Reed (1996) viewed the Daubert ruling to necessi-
tate the utilization of commercially available fixed Synonyms
batteries only, such as the Halstead-Reitan Battery.
However, most neuropsychologists employ a Bonnet syndrome
Charles Bonnet Syndrome 743

Short Description or Definition Charles Bonnet Syndrome, Table 1 Types of

Hallucinations
Charles Bonnet syndrome (CBS) is a condition in Hallucination category Description
which visually impaired individuals experience Tessellopsia Regular, overlapping
complex visual hallucinations. It is characterized patterns
by the following features (Eperjesi and Akbarali Hyperchromatopsia Hyperintense, vivid,
2004):
brilliant colors
C
Prosopometamorphopsia Facial distortions
Dendropsia Branching forms
1. The presence of well-formed, complex, repet- Perseveration True percept that persists
itive, or persistent visual hallucinations after the individual looks
2. Full or partial retention of insight into the away
unreal nature of the hallucinations Illusory visual spread Spread of a non-
hallucinated pattern
3. The absence of hallucinations in other sensory
Polyopia Multiple copies of a percept
modalities (e.g., auditory, olfactory)
Micropsia/macropsia Miniaturized/“larger than
4. The absence of delusions life” images

Categorization related macular degeneration, glaucoma, and

cataracts (Rovner 2006). It has also been
The images associated with CBS are often rich in argued that past prevalence estimates of CBS
detail, and their clarity frequently contrasts sharply were spuriously low due to a general lack of
with sufferers’ blurred perception of real objects awareness of the syndrome in the medical
(Menon et al. 2003). They are sometimes referred community, as well as patients’ reluctance to
to as “pseudohallucinations” to indicate that the disclose their hallucinatory symptoms for fear
person experiencing them is aware that the images of being labeled psychotic or demented
are not real. Hallucinations may vary greatly in (Plummer et al. 2007). One estimate suggests
terms of color, clarity, movement, and bizarreness that the frequency of CBS in patients with
(Plummer et al. 2007). Nevertheless, common visual impairment ranges from 0.4% to 34%
themes and figures have been described, including (Lapid et al. 2013).
humans and animals, extended landscapes, and 2. Age of onset: CBS may occur at any age, but it
ornate structures (Plummer et al. 2007). Ffytche is more common in the elderly. Average age of
and Howard (1999) classified their patients’ hallu- onset tends to be in the seventies and eighties
cinations into eight categories (Table 1). (Plummer et al. 2007). The increased preva-
While the clinical validity of this classification lence of CBS in older adults is likely related to
system has not yet been established, it does share the greater incidence of sudden visual loss
some similarities with known functional and ana- and/or isolation in this age group (Menon
tomical networks within the visual association et al. 2003).
cortex (Plummer et al. 2007).

Natural History, Prognostic Factors, and

Epidemiology Outcomes

1. Prevalence: Once considered rare, CBS is Historical background: Charles Bonnet syndrome
becoming increasingly more common is named after the eminent Swiss philosopher and
(Rovner 2006). The larger number of reported naturalist who first described this phenomenon in
CBS cases may be related to the growing pop- 1760 (Hedges 2007). In a book entitled Essai
ulation of older adults and the more common Analytique sur les Facultes de L’Ame [Analytical
occurrence of visual disorders such as age- Essays Concerning the Faculties of the Mind],
744 Charles Bonnet Syndrome

Charles Bonnet described how his cognitively It has been argued that CBS is more commonly
intact, 89-year-old grandfather with failing eye- associated with higher degrees of visual impair-
sight began to experience well-formed visual hal- ment and with bilateral as opposed to unilateral
lucinations, which he was aware were not actually ocular pathology (Menon et al. 2003). It has also
physically present. Interestingly, Charles Bonnet been suggested that it is not the specific lesion site
began to have similar experiences later in his own or the severity of impairment, but rather the rate of
life. At the age of 22, he began to experience development of the visual impairment that best
severe eye pain and progressively worsening predicts CBS (Plummer et al. 2007). That is, hal-
loss of vision that made it difficult for him to use lucinations may be more common in the context
a microscope, and he ultimately turned to more of sudden or unexpected decrease in visual func-
abstract philosophical pursuits and theoretical tion (Menon et al. 2003).
questions in biology. In his retirement, he experi- Outcomes: The course of CBS can be
enced formed visual hallucinations associated unpredictable. While the onset is generally sud-
with many of the common attributes of the syn- den, it may also be gradual (Menon et al. 2003).
drome that shares his name, including blindness, Hallucinations can last from seconds to hours, or
intact cognition, and occurrence in quiet and even days. Clustering of episodes across days or
reflective settings. Another native of Geneva, weeks is not unusual. Three patterns of the syn-
George de Morsier, proposed in 1967 that visual drome have been described (Menon et al. 2003).
hallucinations in older men without mental defi- The episodic pattern, characterized by hallucina-
ciency be designated the syndrome of Charles tions that happen over a period of days to months
Bonnet. and then permanently cease, is reportedly the
Current thinking/prognostic factors: The ques- least common. In the periodic pattern, phases of
tion of whether visual impairment is necessary for hallucinatory activity alternate with phases of
the development of CBS has been the matter of remission. The continuous pattern, as its name
debate. Some argue that CBS is almost invariably suggests, is characterized by unremitting hallu-
associated with impaired vision, and it may occur cinations (i.e., no hallucination-free intervals)
whenever sensory input to the brain is decreased (Menon et al. 2003). Overall, the duration of
sufficiently to allow release phenomena. Other CBS can extend from days to years, and sponta-
researchers report that visual dysfunction, though neous recurrence after a symptom-free interval is
common, is not mandatory for diagnosis, and note possible. Interestingly, some sufferers have
that CBS has been found in individuals with intact reported permanent remissions of CBS in con-
vision (Terao and Collinson 2000) (Tables 2 and 3). junction with ongoing visual decline (Plummer
et al. 2007). Lapid et al. (2013) found that 26% of
patients with CBS ultimately developed some
Charles Bonnet Syndrome, Table 2 Factors favoring
the recurrence of hallucinations form of dementia, most commonly Lewy body
dementia.
Dimly lit conditions
States of drowsiness
Physical and social isolation
Neuropsychology and Psychology of
Charles Bonnet Syndrome
Charles Bonnet Syndrome, Table 3 Factors that may
help relieve hallucinations
The exact pathophysiology of CBS is unclear.
Rapid blinking Although Charles Bonnet suggested that the pri-
Sustained eye closure
mary pathology was restricted to the eye, subse-
Diversionary activities
quent research has suggested that complex
Limiting exposure to dim lighting
hallucinations can occur in the context of visual
Walking away
impairment secondary to pathology anywhere
Looking at or approaching images
along the central visual pathway, from the orbit
Charles Bonnet Syndrome 745

to the occipital cortex (Menon et al. 2003). Treatment

A leading hypothesis is that complex visual hal-
lucinations result from deafferentation of the Treatment for CBS may not always be necessary,
visual association cortex following lesions since visual hallucinations often resolve sponta-
among the central visual pathway. Age-related neously, either in response to improvement or
macular degeneration is a commonly cited cause further deterioration of visual function (Menon
of CBS, but other ocular pathologies include glau- et al. 2003). In addition, many patients are not C
coma, central retinal artery occlusion, and optic distressed by their hallucinations and may even
neuritis (Plummer et al. 2007). Extraocular and enjoy them. However, if hallucinations are fre-
central visual axis pathologies associated with quent or distressing, the following treatment
CBS include lesions of the pituitary and optic options are available:
chiasm, meningioma, and occipital stroke.
1. Optimizing visual acuity: Patients should ini-
tially be referred to a low-vision specialist, who
Evaluation may be able to reduce or alleviate hallucinations
by optimizing visual function (e.g., via prescrip-
The evaluation of CBS should begin with a clin- tion eyeglasses or visual aids). If appropriate,
ical interview, which should be approached care- the patient might be considered for surgery (e.g.,
fully in light of sufferers’ frequent reluctance to cataract surgery or neurosurgical procedures).
disclose hallucinatory experiences. The clinician Several reports indicate that improvement of
should assess the nature of the hallucinations, the visual function, either spontaneously or by
modalities in which they occur, the presence of intervention, can effectively decrease or even
delusions, and the patient’s insight. It is important eliminate hallucinations (Menon et al. 2003).
to note that insight into the illusory nature of the 2. Supportive treatment: A key component in the
hallucinations may not occur immediately; in fact, management of CBS is supportive. Patients
there may be a period of initial deception, espe- may derive comfort from sympathetic explana-
cially if the perceived images are not uncommon tions that their hallucinations are not uncom-
and fit realistically into the patient’s surroundings mon, are not necessarily a marker of
(Menon et al. 2003). Referrals to an ophthalmol- psychiatric disease, and may represent a
ogist, low-vision specialist, and neuropsychiatrist release phenomenon in the context of visual
may be helpful. impairment. Using the analogy of “phantom
A key issue for clinical neuropsychologists is visions,” similar to a phantom limb syndrome,
the differential diagnosis of CBS from other may be helpful (Rovner 2006).
causes of visual hallucinations. Conditions 3. Psychotherapeutic strategies: Psychothera-
belonging in the differential include migraine, peutic techniques used for phantom limb
occipital seizures, peduncular hallucinosis pain, including distraction, hypnosis, relaxa-
(usually from rostral brainstem infarct), drug- tion training, and cognitive restructuring, can
induced states, psychiatric disease, delirium, and help reduce the unpleasant effects of intrusive
dementia. In particular, CBS may occur in the and upsetting visual hallucinations (Menon
early stages of dementia with Lewy bodies et al. 2003). Support or psychoeducational
(DLB), and as cognitive function declines, insight groups are useful settings in which sufferers
about the unreal nature of the hallucinations van- can meet, obtain reassurance, and be given
ishes (Terao and Collinson 2000). Some have advice about specific techniques for reducing
suggested the term Charles Bonnet syndrome hallucinations (Eperjesi and Akbarali 2004).
plus or CBS plus to describe visual hallucinations 4. Behavioral/environmental modifications:
that occur in the presence of a neuropsychiatric Approaches such as rapid eye blinking,
disorder (Eperjesi and Akbarali 2004; Menon sustained eye closure, minimizing fatigue and
et al. 2003). stress, and engaging in distracting activities
746 CHART Short Form

(e.g., listening to the radio and attending to Hedges, T. R. (2007). Charles Bonnet, his life, and his
household chores) may help reduce hallucina- syndrome. Survey of Ophthalmology, 52(1), 111–114.
Lapid, M. I., Burton, M. C., Chang, M. T., Rummans,
tions. Limiting exposure to dim lighting (e.g., T. A., Cha, S. S., Leavitt, J. A., & Boeve, B. F.
by increasing lighting in the home in the eve- (2013). Clinical phenomenology and mortality in
ning) and taking steps to reduce glare may also Charles Bonnet syndrome. Journal of Geriatric Psy-
be helpful. Looking directly at the images, chiatry and Neurology, 26(1), 3–9.
Menon, G. J., Rahman, I., Menon, S. J., & Dutton, G. N.
attempting to approach them, and conversing (2003). Complex visual hallucinations in the visually
with them have also been reported to stop impaired: The Charles Bonnet Syndrome. Survey of
hallucinations (Menon et al. 2003). Since sol- Ophthalmology, 48(1), 58–72.
itude and loneliness, particularly during the Plummer, C., Kleinitz, A., Vroomen, P., & Watts,
R. (2007). Of Roman chariots and goats in overcoats:
evening hours, tend to heighten hallucinations, The syndrome of Charles Bonnet. Journal of Clinical
strengthening social networks and increasing Neuroscience, 14(8), 709–714.
the amount of time spent interacting with Rovner, B. W. (2006). The Charles Bonnet syndrome:
others may be useful (Plummer et al. 2007). A review of recent research. Current Opinion in Oph-
thalmology, 17(3), 275–277.
5. Pharmacological interventions: Referral to a Terao, T., & Collinson, S. (2000). Charles Bonnet syn-
specialist for pharmacological therapy may be drome and dementia. Lancet, 355(9221), 2168.
helpful. Atypical antipsychotics, anticonvul-
sants, selective serotonin reuptake inhibitors
(SSRIs), and serotonin and norepinephrine reup-
take inhibitors (SNRIs) have been used to treat
CBS with variable benefits (Lapid et al. 2013). CHART Short Form
6. Follow-up: Since some cases of CBS do go on
to develop dementia, it is recommended that Angela M. Philippus and Gale G. Whiteneck
clinicians follow patients with complex visual Craig Hospital, Englewood, CO, USA
hallucinations carefully over time (Menon
et al. 2003). Though most patients experience
no practical problems associated with CBS, Synonyms
continuous visual hallucinations can interfere
with navigation and driving, and patients’ abil- CHART-SF; Craig Handicap Assessment and
ity to perform daily activities safely should be Reporting Technique (CHART) Short Form
monitored over time (Menon et al. 2003).

Definition
Cross-References
The Craig Handicap Assessment and Reporting
▶ Dementia with Lewy Bodies Technique Short Form (CHART-SF) is a 19-item
▶ Macropsia measure of handicap or level of societal participa-
▶ Micropsia tion. Released in 1998, the CHART-SF is the short
▶ Visual Hallucinations version of the 32-item CHART instrument
designed to provide a simple, objective measure
of the degree to which impairments and disabil-
References and Readings ities result in handicaps (societal participation
limitations) for adolescents and adults (15 years
Eperjesi, F., & Akbarali, N. (2004). Rehabilitation in Charles and older) in the years after initial rehabilitation.
Bonnet syndrome: A review of treatment options. Clin- Like its precursor, the CHART-SF includes
ical and Experimental Optometry, 87(3), 149–152.
Ffytche, D. H., & Howard, R. J. (1999). The perceptual
sixsubscales (physical independence, cognitive
consequences of visual loss: ‘Positive’ pathologies of independence, mobility, occupation, social inte-
vision. Brain, 122(Pt 7), 1247–1260. gration, and economic independence), which
Charter School 747

closely reflect the disablement model developed variance except economic self-sufficiency, which
by the World Health Organization, published in using the main variables could only explain 45%.
1980 and revised in 2001. Each subscale contains
from 2 to 5 questions, which together quantify the
extent to which individuals fulfill various social Cross-References
roles. CHART-SF focuses on objective, observ-
able criteria that are easily quantifiable and ▶ Craig Handicap Assessment and Reporting C
unlikely to be open to subjective interpretation. Technique
Each of the domains or subscales of the instru-
ment has a maximum score of 100 points, which is
considered the level of performance typical of the References and Readings
average nondisabled person. High subscale scores
Whiteneck, G., Brooks, C.A., Charlifue, S., Gerhart, K.A.,
indicate less handicap or higher social and com-
Mellick, D., Overholser, D., et al. (1998). Guide for use
munity participation. of the CHART: Craig handicap assessment and
Although originally developed for use with reporting technique. https://craighospital.org/pro
persons with spinal cord injury, the CHART and grams/research/research-instruments. 20 April 2017.
the CHART-SF have proven to be appropriate
measures of societal participation that can be
used with individuals having a range of physical
or cognitive impairments. The CHART-SF was Charter School
designed to be administered by interview, either
in person or by telephone, and takes approxi- Gail Malvestuto1 and Rik Carl D’Amato2
1
mately 5–7 minutes to administer. There is no School of Psychology, The Chicago School of
set time period for administering the CHART- Professional Psychology, Chicago, IL, USA
2
SF; however, it is recommended that multiple School Psychology, Clinical Neuropsychology,
measurements be taken over the course of a Clinical Psychology, The Chicago School of
person’s lifetime to assess the changes with Professional Psychology, Chicago, IL, USA
adaptation to the disability and to gain insight
into changes in participation, which may occur
over time. A charter school is a public school developed with
The 19-item CHART-SF with subscales a specialized mission in mind (U.S. Department of
closely approximating the subscale scores for the Education 2017). Examples of such missions may
CHART long form is recommended for those include a focus on math and science, arts, and/or
populations for whom time is at a minimum. college preparation. The unique mission of the
school and the population the school draws from
make it different than any other district school.
Current Knowledge However, the uniqueness of the school’s charter is
both its strength and weakness. Charter schools
In an effort to reduce the number of items in the are publicly funded and governed by a specific
original CHART, a short form was developed. group or organization under a legislative contract
A multidimensional analysis was performed which (U.S. Department of Education 2016). This
showed that fewer variables were needed to obtain allows charter schools to be exempt from follow-
CHART scores. Regression analyses were ing traditional public school regulations. For
performed on each subscale with the dependent example, certain types of children may not be
measure being the scale score and the variables served in these schools. Charters typically last
contributing to the subscale acting as the predictor three to five years and must be renewed. Charter
variables. All CHART subscale scores could be schools are funded by transferring funds from
reduced by fewer questions to reach 90% explained current school district budgets to them.
748 Chelation

References Categorization

U.S. Department of Education. (2016). National Center for While chelation therapy has been used for
Education Statistics. The condition of education 2016
treating lead poisoning and vascular occlusive
(NCES 2016–144), Charter school enrollment.
Retrieved from: https://nces.ed.gov/fastfacts/display. disease, oral chelation therapy with the
asp?id=30 a-ketohydroxypyridine chelator 1,2-dimethyl-3-
U.S. Department of Education. (2017). Charter schools. hydroxypyrid-4-one (L1, INN/BAN: deferiprone)
Retrieved from: https://www2.ed.gov/parents/schools/
has also been used in iron- and aluminum-
choice/definitions.html#cs
overloaded patients. A number of iron (III) chela-
tors have also shown antimalarial activity in vitro
with the proposed mechanism of activity involv-
ing the withholding of iron from metabolic path-
Chelation ways of the intra-erythrocytic parasite and the
formation of toxic complexes with iron (Mabeza
Bruce J. Diamond, Emily Desbiens and et al. 1999).
Rebecca Pavlick
Department of Psychology, William Paterson
University, Wayne, NJ, USA History

Chelation therapy began in the early 1950s and

Synonyms was primarily used to treat metal poisoning of the
blood. However, CAIM practitioners have used it
Chelation; Chelation therapy; EDTA therapy to reverse the arteriosclerotic disease process
(e.g., peripheral arterial occlusive disease
(PAOD) (Ernst et al. 2001). The use of novel and
Short Description or Definition unconventional treatments for ASD is common,
with up to 74% of children using these treatments
Chelation therapy has applications in allopathic (Rossignol 2009). It is within this context that
medicine, and the technique has also been chelation therapy has been explored as a treatment
embraced by practitioners of complementary, for ASD.
alternative, and integrative medicine (CAIM).
While CAIM practitioners have used this tech-
nique to treat cardiovascular disease, allopathic Evaluation
practitioners consider chelation therapy to be
highly effective and is the treatment of choice in Studies examining the efficacy of chelation ther-
treating heavy metal poisoning (Ernst et al. 2001) apy have shown mixed results. In one authorita-
although more recent work suggests that chelation tive systematic review, it was stated that
plus antioxidant supplementation to be more proponents of chelation therapy adhere to patho-
effective than monotherapeutic interventions physiological models of arteriosclerosis, which
(Flora et al. 2008). Recent clinical applications are inconsistent with contemporary knowledge
have included autism spectrum disorder (ASD) and practice (Ernst et al. 2001). In a systematic
(James et al. 2015; Rossignol 2009), although review of chelation therapy in the treatment of
more extensive research is needed. Some research malaria, it was concluded that when used via
also suggests that iron chelation therapy with oral administration, its efficacy and low cost
desferrioxamine may have application in the treat- make it more accessible than desferrioxamine for
ment of malaria (Mabeza et al. 1999). the majority of patients needing iron chelation
Chelation 749

(Mabeza et al. 1999). With respect to ASD, no six cases of reversible agranulocytosis, 0–30%
clinical trial evidence using randomized, placebo- incidence of transient musculoskeletal and joint
controlled (RPC) trials has been found suggesting pains, 0–6% of gastric intolerance, and 0–2% zinc
that pharmaceutical chelation is an effective inter- deficiency.
vention for ASD (James et al. 2015). Where evi- The use of chelation therapy in ASD is based
dence has been presented, it was based on non- on the idea that the severity of ASD symptoms is
RPC or case series trials and is thus less definitive positively correlated with the level of circulating C
(Rossignol 2009). or stored toxic metals and that chelation
therapy could help remove these heavy metals.
However, it was concluded that evidence
Treatment and Mechanisms supporting a causal link between heavy metals
and autism should be established, in addition to
Typically, chelation therapy is administered in methods that ensure participant safety are needed
multiple sessions with each treatment lasting for before further trials are conducted (James
over an hour. The putative mechanism underly- et al. 2015).
ing chelation therapy is the binding of ions in the
blood by EDTA. The therapy is generally con-
sidered effective in treating heavy metal poison- See Also
ing. In CAIM applications, it has been used as an
alternative to bypass surgery, based on the idea ▶ Lead Exposure
that chelation therapy removes harmful plaque
buildup in the arteries (unblocking arterioscle-
rotic arteries) and helps prevents strokes. The Further Reading
mechanism is believed to involve the extraction
of calcium out of arteriosclerotic plaques via the Ernst, E., Pittler, M. H., Stevinson, C., White, A., &
chelating mechanism. However, EDTA treat- Eisenberg, D. (Eds.). (2001). The desktop guide to
ment may be associated with life-threatening complementary and alternative medicine: An evidence
based approach. Amsterdam: Elsevier Health
adverse effects, such as hypocalcemia and severe Sciences.
kidney damage, in addition to prolonged bleed- Flora, S. J. S., Mittal, M., & Mehta, A. (2008). Heavy metal
ing and respiratory distress. In reviewing ran- induced oxidative stress & its possible reversal by
domized, placebo-controlled (RPC), double- chelation therapy. Indian Journal of Medical Research,
128(4), 501–523.
blind trials, it was concluded that chelation ther- James, S., Stevenson, S. W., Silove, N., & Williams,
apy for PAOD is not superior to placebo, that it is K. (2015). Chelation for autism spectrum disorder
associated with considerable risks and costs, and (ASD). Cochrane Database Syst Reviews, 5,
that it should now be considered obsolete (Ernst CD010766.
Kontoghiorghes, G. J. (1995). New concepts of iron
et al. 2001). and aluminum chelation therapy with oral L1
However, it should also be noted that using oral (deferiprone) and other chelators: A review. Analyst,
chelation therapy, in doses ranging from 55 to 120, 845–851.
100 mg kg1 of L1 (a-ketohydroxypyridine che- Mabeza, G. F., Loyevsky, M., Gordeuk, V. R., & Weiss,
G. (1999). Iron chelation therapy for malaria: A review.
lator 1,2-dimethyl-3-hydroxypyrid-4-one (L1, Pharmacology & Therapeutics, 81, 53–75.
INN/BAN: deferiprone)), a majority of iron- Rossignol, D. A. (2009). Novel and emerging treatments
loaded patients showed urinary iron excretion for autism spectrum disorders: A systematic review.
levels greater than those accumulating from trans- Annals of Clinical Psychiatry., 21(4), 213–236.
Seely, D. M., Wu, P., & Mills, E. J. (2005). EDTA
fusions (15–35 mg day1) and also reductions in chelation therapy for cardiovascular disease:
serum ferritin and liver iron to near normal levels A systematic review. BMC Cardiovascular Disorders,
(Kontoghiorghes 1995). Toxic side effects include 5, 32–38.
750 Chemo Brain

face (Ahles et al. 2012). Current research is unit-

Chemo Brain ing neuropsychological tests with radiological
brain imaging and molecular analysis to aid the
Samantha Knight1, Daniel Smith2,3 and development of treatment strategies to reduce
Carol L. Armstrong4 the long-term effect on survivors’ quality of life
1
Medicine, Royal College of Surgeons in Ireland, (Hede 2008).
Dublin, Ireland
2
Department of Psychology, Drexel University,
Philadelphia, PA, USA Proposed Mechanisms
3
Winship Cancer Institute, Emory University,
Atlanta, GA, USA Specific etiologies of PCCI remain poorly defined
4
Child and Adolescent Psychiatry and Behavioral as so many confounding factors are present in the
Sciences, The Children’s Hospital of multifaceted nature of cancer treatment protocols
Philadelphia, Philadelphia, PA, USA (Taillibert and Voillery 2007). Despite this, two
major theories have proven popular among
researchers: direct effect of chemotherapy on the
Synonyms patient’s brain and the effect chemotherapy has on
the hormones so vital in proper nervous system
“chemobrain”; “chemo fog”; Post-chemotherapy functioning (Matsuda et al. 2005). Other theories
cognitive impairment include chemotherapy-induced anemia, vascular
injury, inflammation, autoimmune response,
and the presence of epsilon 4 variation of
Definition and Overview apolipoprotein E gene (Hede 2008; Nelson
et al. 2007; Scherling and Smith 2013). Important
“Chemo brain” is the widely used lay term for confounding factors researchers must take into
post-chemotherapy cognitive impairment (PCCI). account when investigating PCCI include emo-
It is experienced by approximately 20–30% of tional states and glucocorticoids, paraneoplastic
cancer survivors treated with chemotherapy syndromes, menopause/premature ovarian failure,
(Ganz et al. 2013; McDougall et al. 2014). This and comorbidities (Scherling and Smith 2013).
phenomenon first came to light in breast cancer
survivors who reported cognitive deficits in mem-
ory, attention, and verbal fluency after their treat- Current Research
ments (Tannock et al. 2004). A review by Ahles
et al. (2012) found that 17–75% of women expe- Diverse theories have been proposed for the long-
rienced deficits in attention, concentration, work- term PCCI of patients. Studies utilizing radiolog-
ing memory, and executive function 6 months to ical imaging have significantly expanded the cur-
20 years after chemotherapy and that a significant rent knowledge of PCCI. A study done by
proportion of patients have cognitive impairment Silverman and colleagues used positron emission
prior to any treatment. Cognitive complaints have tomography to compare the metabolic activity of
corresponded with depression, but not with objec- long-term breast cancer survivors, both those who
tive neurological deficits (Peralta 2013). PCCI is were and were not treated with chemotherapy, to
most widely reported in cancers treated aggres- healthy control subjects (Hede 2008; Silverman
sively with chemotherapy: colorectal, prostate, et al. 2007). The researchers were blinded to the
breast, ovarian, and other reproductive cancers medical history of the patient and administered a
(Matsuda et al. 2005; McDougall et al. 2014). visual delayed recall memory test [Rey Osterrieth
With the growing number of long-term survivors Complex Figure Delayed Recall (ROCF)] while
of cancer, it is advantageous to better understand observing the metabolic activity (Silverman et al.
the potential cognitive deficits these patients may 2007). This breakthrough study demonstrated
Chemo Brain 751

lower metabolic activity in post-chemotherapy these cognitive deficits can be debilitating in

survivors and lower ROCF scores but signifi- many facets of patients’ lives from academic or
cantly increased activity during recall in inferior workplace performance to inter-personal relation-
and superior frontal gyri and contralateral poste- ships (Nelson et al. 2007; Scherling and Smith
rior cerebellum, and untreated patients had greater 2013). There is currently no treatment protocol
activation in the dominant parietal cortex and for PCCI, however many hypothesized treatments
contralateral primary visual cortex (The authors have been proposed. These include antioxidants, C
suggested that the increased frontal activation cognitive behavioral therapy, erythropoietin, and
during the ROCF task may represent a compensa- stimulant drugs such as methylphenidate; it is
tory response to lower resting metabolism important to note however that these remain the-
(Silverman et al. 2007). Similar results have oretical options all of which address the underly-
been shown in various functional magnetic reso- ing proposed mechanisms of inflammation,
nance imaging studies (Askren et al. 2014; emotional stress, chemotherapy-induced anemia,
Inagaki et al. 2007; Pomykala et al. 2013). and reduced metabolic activity, respectively
Another major area of research focuses on the (Kohli et al. 2007; Nelson et al. 2007). A recent
reactive oxygen species used to induce oxidative study aimed at testing the stimulant treatment
stress in malignant cells, which are produced by option on breast cancer survivors using modafinil,
56 of the 132 chemotherapy agents currently widely used for treatment of narcolepsy, found
used (Aluise et al. 2010; Joshi et al. 2007; statistically significant improvement in cognitive
Myers et al. 2008). Neural progenitor cells scores (Kohli et al. 2007). Estrogen hormone
which give rise to the neurons and glia of the replacement has shown to aid reversal of PCCI
brain have been shown to be particularly suscepti- symptoms in breast cancer survivors; however by
ble to the cytotoxic effects of chemotherapy agents doing so, there is increased risk for endothelial
(Dietrich et al. 2006). Specifically, 5-fluorouracil carcinoma as well as estrogen-responsive
has been shown to significantly reduce the viability breast carcinoma (Matsuda et al. 2005). Other
of these cells as opposed to malignant cells which researchers insist that cognitive rehabilitation is
at the same dose experience no change in viability the treatment method of choice as well as devel-
(Dietrich et al. 2006; Han et al. 2008). The hippo- oping coping strategies to improve working mem-
campus has received dedicated research on neuro- ory (Ferguson et al. 2007; Hede 2008). Continued
toxic effects of chemotherapy due to its vital research is required to determine definitive causes
function in memory formation (Seigers et al. of PCCI, which will allow further insight into
2008). The new neurons in the hippocampus are treatment developments. Although frustrating,
created through neurogenesis requiring a brain- overall prognosis of PCCI is good with the major-
derived neurotrophic factor (BDNF) to properly ity of symptoms disappearing after an average
form. Two commonly utilized chemotherapy of 4 years; in some cases, however, deficits
agents interfere with this process; 5-fluorouracil have been subjectively reported a decade post-
has been shown in animal models to significantly chemotherapy when aging processes are also
reduce levels of BDNF, and methotrexate causes progressing (Matsuda et al. 2005; Silverman
dose-dependent long-term damage on hippocam- et al. 2007; Ahles et al. 2012).
pal cell proliferation (Mustafa et al. 2008; Seigers
et al. 2008).
References

Symptoms, Management, and Prognosis Ahles, T. A., Root, J. C., & Ryan, E. L. (2012). Cancer- and
cancer treatment-associated cognitive change: An
update on the state of the science. Journal of Clinical
PCCI is widely reported to affect visual and
Oncology: Official Journal of the American Society of
semantic memory, attention span, and motor coor- Clinical Oncology, 30(30), 3675–3686. https://doi.org/
dination (Nelson et al. 2007). Understandably 10.1200/JCO.2012.43.0116.
752 Chemo Brain

Aluise, C. D., Sultana, R., Tangpong, J., Vore, M., St Clair, impairment after adjuvant chemotherapy in breast can-
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Chemotherapy 753

and -thalidomide. The specific manner in which

Chemotherapy chemotherapy achieves the intended effect is con-
tingent upon the particular drug(s) employed.
Bram Goldstein However, cytotoxicity usually occurs when the
Department of Gynecologic Oncology, Hoag cell attempts to divide and before the repair occurs
Hospital Cancer Center, Newport Beach, CA, (Chabner and Longo 2004). The probability of the
USA intended effect on the targeted molecules reflects C
the appropriate concentration of drugs, amount or
dose, and timing of drug administration. Drug
Synonyms absorption, distribution, and penetration are also
significant factors inherent in the efficacy of che-
Systemic therapy motherapy. The precise drug dosage can be com-
plicated because if the amount is too low, it may
be ineffective against the tumor. Conversely, if the
Definition dosage is too high, patients may suffer from
excessive toxicity. Since chemotherapy damages
Chemotherapy is a systemic treatment for cancer, healthy cells during the therapeutic process, the
comprising cytotoxic agents that target cancer treatment is associated with several harmful side
cells. Normally, cells develop and die in an effects, such as myelosuppression. For example,
orderly and determined fashion. However, when bone marrow, which produces white blood cells,
cancer manifests itself, the cells intractably divide red blood cells, and blood platelets, can be dam-
and proliferate. Chemotherapy drugs target these aged during chemotherapy treatment. In particu-
cancer cells by destroying them before they con- lar, white blood cells and platelets frequently drop
tinually multiply and divide. In particular, chemo- transiently after chemotherapy, so that patients are
therapy interferes with or impairs the targeted at increased risk for infection and bleeding during
molecules (e.g., DNA, proteins) during desig- and post chemotherapy. Many chemotherapy
nated cellular stages, such as synthesis or mitosis. patients also suffer from nausea and vomiting
The majority of chemotherapy drugs damage or because the drugs irritate the stomach lining and
interfere with the replication of DNA and/or bowel. Certain chemotherapy drugs also cause
RNA, and are used to treat several malignancies, alopecia, or hair loss. This condition results from
particularly brain tumors, lymphomas, and leuke- the chemotherapy agent adversely affecting the
mias. Some of the chemotherapies include growth of hair cells, causing them to become
alkylating agents (such as cisplatin, carboplatin, brittle and eventually break. Several chemother-
cyclophosphamide, and temozolomide) to treat apies also result in anorexia, severe loss of appe-
brain tumors, lymphomas, and leukemias; tite, and significant weight loss. Fatigue, diarrhea,
nitrosoureas (e.g., carmustine and lomustine) are and constipation are also very common side
indicated for the treatment of brain tumors and effects from cancer and chemotherapy. Addition-
lymphomas; antimetabolites (such as methotrex- ally, specific chemotherapy agents can cause sto-
ate) to treat leukemias; anthracycline and related matitis, a condition that results in sores
drugs (e.g., doxorubicin), which have toxic manifesting inside the mouth or throat. Chemo-
effects on the heart; topoisomerase inhibitors therapy is most often given intravenously,
(such as topotecan, irinotecan, and etoposide); whereby a thin needle is inserted into a patient’s
mitotic inhibitors (e.g., vinblastine and vincris- vein on the hand or lower arm. Intravenous che-
tine), which can cause peripheral nerve damage; motherapy can also be delivered through cathe-
and corticosteroid hormones, which can be used ters, ports, and pumps. The treatment is frequently
to kill or slow the growth of cancer cells. There are given in cycles (i.e., specified treatment periods)
other chemotherapies that are excluded from these that reflect alternating rest periods. This is neces-
categories, namely, L-asparaginase, -hydroxyurea, sary because patients require substantial relief to
754 Chemotherapy

permit the body to recuperate, build healthy new malignancies, particularly brain tumors,
cells, and restore strength. Treatment regimens lymphomas, and leukemias. Some of the chemo-
may be given daily, weekly, or monthly and therapies include alkylating agents (such as
are based upon a drug’s efficacy or toxicity. cisplatin, carboplatin, cyclophosphamide, and
Chemotherapy is usually administered before temozolomide) to treat brain tumors, lymphomas,
(neoadjuvant) surgery or post (adjuvant) surgery. and leukemias; nitrosoureas (e.g., carmustine and
Neoadjuvant chemotherapy is intended to lomustine) to treat brain tumors and lymphomas;
decrease the primary tumor’s size. This poten- antimetabolites to treat leukemias (such as
tially mitigates the harmful effects of surgery or methotrexate); anthracycline and related drugs
radiotherapy and enhances the efficacy of (e.g., doxorubicin), which have toxic effects on
chemotherapy. the heart; topoisomerase inhibitors (such as
Adjuvant chemotherapy may also reduce the topotecan, irinotecan, and etoposide); mitotic
probability of tumor resistance to drug therapy in inhibitors (e.g., vinblastine and vincristine),
the event of disease recurrence (Chabner and which can cause peripheral nerve damage; and
Longo 2004). Furthermore, adjuvant chemother- corticosteroid hormones, which can be used to
apy is effective at destroying residual cancer cells kill or slow the growth of cancer cells. There are
that have spread to distal parts of the body (i.e., other chemotherapies that are excluded from these
metastasis), particularly because rapidly prolifer- categories, such as L-asparaginase, -hydroxyurea,
ating lesions are very amenable to treatment. Pal- and -thalidomide. The specific manner in which
liative chemotherapy is indicated when the chemotherapy achieves the intended effect is con-
curative potential is very low and the primary tingent upon the particular drug(s) employed.
goals are to decrease the patient’s tumor burden However, cytotoxicity usually occurs when the
and prolong life expectancy. cell attempts to divide and before repair occurs
(Chabner and Longo 2004).
The probability of the intended effect on the
Current Knowledge targeted molecules reflects the appropriate con-
centration of drugs, amount or dose, and timing
Recent neuropsychological research has indi- of drug administration. Drug absorption, distribu-
cated that chemotherapy can also adversely tion, and penetration are also significant factors
impact cognitive functioning, both short-term inherent in the efficacy of chemotherapy.
and delayed. In particular, neuropsychological The precise drug dosage can be complicated
research studies have provided evidence because if the amount is too low, it may be inef-
discussing the impact of chemotherapy on atten- fective against the tumor. Conversely, if the dos-
tion, memory, and concentration (Armstrong age is too high, patients may suffer from excessive
et al. 2004). Consequently, many of these toxicity.
chemotherapy-induced cognitive impairments Since chemotherapy damages healthy cells
can significantly impair patients’ daily activities, during the therapeutic process, the treatment is
such as working, being involved in a committed associated with several harmful side effects, such
relationship, and attending to personal responsi- as myelosuppression. For example, bone marrow,
bilities. Research has suggested that many of which produces white blood cells, red blood cells,
these impairments are temporary but some may and blood platelets, can be damaged during che-
be more long-term or even permanent. The motherapy treatment. In particular, white blood
cognitive effects are not uniform, and the sever- cells and platelets frequently drop transiently
ity appears to reflect a higher concentration after chemotherapy, so that patients are at
and/or larger dose of chemotherapy. increased risk for infection and bleeding during
Most of the different types of chemotherapy and after chemotherapy.
drugs damage or interfere with the replication of Many chemotherapy patients also suffer from
DNA and/or RNA, and are used to treat several nausea and vomiting because the drugs irritate the
Chief Sensory Nucleus of V 755

stomach lining and bowel. Certain chemotherapy References and Readings

drugs also cause alopecia or hair loss. This condi-
tion results from the chemotherapy agent Armstrong, C. L., Gyato, K., Awadalla, A. W., Lustig, R.,
& Tochner, Z. A. (2004). A critical review of the
adversely affecting the growth of hair cells, caus-
clinical effects of therapeutic irradiation damage to
ing them to become brittle and eventually break. the brain: The roots of controversy. Neuropsychology
Several chemotherapies also result in anorexia, Review, 14, 65–86.
severe loss of appetite, and significant weight Chabner, B. A., & Longo, D. L. (2004). Cancer chemo- C
therapy and biotherapy: Principles and practice.
loss. Fatigue, diarrhea, and constipation are also
Hagerstown: Lippincott, Williams & Wilkins.
very common side effects from cancer and che-
motherapy. Additionally, specific chemotherapy
agents can cause stomatitis, a condition that
results in sores manifesting inside the mouth or
throat. Chief Sensory Nucleus of V
Chemotherapy is most often given intrave-
nously, involving a thin needle, which is inserted John E. Mendoza
into a patient’s vein on the hand or lower arm. Department of Psychiatry and Neuroscience,
Intravenous chemotherapy can also be delivered Tulane Medical School and SE Louisiana
through catheters, ports, and pumps. The treat- Veterans Healthcare System, New Orleans, LA,
ment is frequently given in cycles that reflect USA
specified treatment periods which are alternated
with rest periods. This is necessary because
patients require substantial relief to permit the Synonyms
body to recuperate, build healthy new cells, and
restore strength. Principal sensory nucleus of the trigeminal nerve;
Treatment regimens may be given daily, Principal sensory nucleus of V
weekly, or monthly and are based upon a drug’s
efficacy or toxicity. Chemotherapy is usually
administered before (neoadjuvant) surgery or Definition
post (adjuvant) surgery. Neoadjuvant chemother-
apy is intended to decrease the primary tumor’s Nucleus responsible for proprioceptive feedback
size. This potentially mitigates the harmful effects from the muscles of facial expression, stereo-
of surgery or radiotherapy and enhances the effi- gnosis or fine tactual discrimination, and vibratory
cacy of chemotherapy. sensations from the face. Located in the dorsolat-
Adjuvant chemotherapy is employed when eral pons just medial to the middle cerebellar
there is scant evidence of residual disease, but peduncle and inferior to the superior cerebellar
there is an increased risk of cancer recurrence. peduncle, it is the functional equivalent of the
Adjuvant chemotherapy may also reduce the nuclei cuneatus and gracilis in the medulla,
probability of tumor resistance to drug therapy in which mediate similar input from the trunk and
the event of disease recurrence (Chabner and extremities. It gives rise to trigeminothalamic
Longo 2004). Furthermore, adjuvant chemother- fibers, which terminate in the ventral posterior
apy is effective at destroying residual cancer cells medial nucleus of the thalamus.
that have spread to distal parts of the body (i.e.,
metastasis), particularly since rapidly proliferat-
ing lesions are very amenable to treatment. Palli- Current Knowledge
ative chemotherapy is indicated when the curative
potential is very low and the primary goals are to Because of its size and density, it is rare for
decrease the patient’s tumor burden and prolong brainstem lesions to be isolated to a single nucleus
life expectancy. or pathway. Theoretically, lesions which involve
756 Childhood Autism Rating Scales

this nucleus might most readily be distinguished (Standard Version) and the CARS2-HF (High
on a routine neurological exam by changes Functioning). The content of the CARS2-ST
(asymmetries) in two-point discrimination on the remains unchanged from that of the original
ipsilateral face. In practice, however, such lesions CARS, published in 1988, and continues to be
are likely to involve other brainstem nuclei and used with children aged 6 and older. The CARS2-
pathways, including the adjacent motor nucleus HF was developed as an alternative measure to
of V, spinal trigeminal tract and/or nucleus, spinal differentiate higher-functioning and verbally fluent
thalamic tracts, lateral portions of the medial lem- (estimated overall IQ scores
80) individuals with
niscus, and middle cerebellar peduncles resulting autism spectrum disorders from comorbid con-
in ipsilateral muscle weakness of the jaw muscles, cerns (Schopler et al. 2010). The CARS2 measures
ipsilateral changes in pain and temperature in the 15 core deficit behaviors associated with autism
face and diminished or abolished corneal reflex, spectrum disorders including social-emotional
contralateral loss of pain and temperature in the understanding, expression and regulation of emo-
extremities, diminished or loss of proprioception, tion, relationship to people, imitation, body use,
stereognosis, and vibration in the contralateral object use, adaptation to change, visual response,
extremities (leg > arm), and ipsilateral cerebellar listening response, sensory use (taste, touch,
signs. smell), fear and anxiety, verbal communication,
nonverbal communication, activity level, consis-
tency of intellectual response, and clinical impres-
References and Readings sions. CARS2 scales quantify the peculiarity,
frequency, and severity of behaviors with each
Gilman, S., & Newman, S. W. (2003). Manter and Gatz’s category being rated on a 7-point scale from 1
essentials of clinical neuroanatomy and neurophysiol-
(within normal limits) to 4 (severely abnormal) in
ogy. Philadelphia: F.A. Davis.
Wilson-Pauwek, L., Akesson, E. J., Stewart, P. A., & 0.5 increments. Ratings on the CARS2-ST and
Spacey, S. D. (2002). Cranial nerves in health and CARS2-HF yield a total score ranging from 15 to
disease. Hamilton: B.C. Decker. 60, with scores of 15–29.5 and 15–27.5 reflective
of minimal-to-no symptoms, 30–36.5 and 28–33.5
reflective of mild-to-moderate symptoms, and
37–60 and 34–60 reflective of severe symptoms
Childhood Autism Rating of autism spectrum disorder, respectively. As the
Scales CARS2 is recommended to be used in conjunction
with developmental history and medical symp-
John Parkhurst1 and Jacqueline M. Kawa2 toms, a 36-item structured Questionnaire for Par-
1
Psychiatry and Behavioral Medicine, Children’s ents and Caregivers (CARS2-QPC) is available to
Hospital of Wisconsin Medical College of support data collection.
Wisconsin, Milwaukee, WI, USA
2
Psychiatry and Behavioral Medicine, Children’s
Hospital of Wisconsin, Milwaukee, WI, USA Historical Background

The first edition of the CARS was published in

Description 1988 after approximately 15 years of use as a
research instrument, initially referred to as the child-
The Childhood Autism Rating Scale, Second Edi- hood psychosis rating scale (Schopler et al. 1980).
tion (CARS2) is 15-item observation-based rating The CARS was used to evaluate children
system designed to assist in diagnostic assessment referred to a statewide program for children and
and intervention for autism spectrum disorders adolescents with autism and communication
(Schopler et al. 2010). Two observational rating delays through the University of North Carolina
forms are available including the CARS2-ST at Chapel Hill program Division TEACCH.
Childhood Autism Rating Scales 757

The measure has historically been intended for 80, with 19 individuals achieving standard scores
use by trained mental health and educational pro- between 80 and 85. A meta-analysis of research
fessionals (e.g., physician, psychologist, school using the CARS between 1980 and 2012 indi-
psychologist, special educator, speech patholo- cated good inter-rater reliability (0.79) and inter-
gist, etc.) along with parent or caregiver interview, nal consistency (0.89) (Breidbord and Croudace
behavioral observation, and case history review 2013). The CARS2 manual describes a high
(Schopler et al. 2010). degree of internal consistency (Cronbach C
The CARS2 was developed to increase the alpha = 0.93) for the CARS2-ST. Corrected
utility of the measure when evaluating and dif- item total reliability values for the 15 categories
ferentiating individuals with behavioral markers ranged from 0.43 to 0.81. Inter-rater reliability
of autism spectrum disorders, Asperger’s disor- was not completed with the CARS2-ST verifica-
der, or pervasive developmental disorder-not tion sample; however, previously reported inter-
otherwise specified (Schopler et al. 2010). The rater reliability on the original data suggested
CARS2-HF was built upon the 15-category total correlation of 0.84. Mayes et al. (2014)
structure of the CARS while taking into account addressed the utility of the CARS2-ST measure
some of the more subtle behaviors exhibited given diagnostic changes to the DSM-5 (APA
by someone with near-average to average intel- 2013) and found 84% diagnostic agreement
ligence. Notably, the CARS2-HF uses a lower between the CARS2-ST and the DSM-5 in a
clinical cutoff score compared to the CARS2-ST. sample of individuals between the ages of 1 and
18. Additional work has shown adequate
diagnostic sensitivity (0.84) of the CARS2-ST
Psychometric Data using DSM-5 criteria for autism spectrum disor-
der (Dawkins et al. 2016). Park and Kim (2016)
The CARS was originally developed from a sam- expressed that while the CARS was developed
ple of 1,606 children, 72% of whom were male. prior to the introduction of the DSM-5, psycho-
Approximately 62% of the sample identified metric properties, and factor structure support,
their ethnic background as White, 28% as the CARS2-ST continued relevance for
Black, and 3% as other races. One thousand assessment.
nine-hundred ninety-nine individuals were col-
lected from clinical and nonclinical settings to CARS2-HF
evaluate both the CARS2-ST and CARS2-HF. The CARS2-HF development sample included
Since the original CARS and CARS2-ST 994 individuals with a variety of clinical diagno-
are identical, historical CARS data continues to ses including high-functioning autism (n = 248),
be relevant in the examination of CARS-ST Asperger’s disorder (n = 231), pervasive devel-
psychometric properties (Moulton et al. 2016; opment disorder-not otherwise specified (n = 95),
Schopler et al. 2010). ADHD (n = 179), learning disorders (n = 111),
and other internalizing and externalizing clinical
CARS2-ST disorders (n = 69). A small group of general
The reported CARS2-ST verification sample education and special education classroom stu-
included 1,034 children with a diagnosis of dents without autism were also included
autism spectrum disorder ranging in age from 2 (n = 61). Two thirds of the sample were male
to 36 (78% male, 22% female). Ethnic back- (78%) and between the ages of 6 and 57. Ethnic
grounds of the sample were reported as White backgrounds of the sample were reported as
(60%), Black/African-American (16%), His- White (73%), Black/African-American (14%),
panic/Latino (13%), Asian/Pacific Islander Hispanic/Latino (6%), Pacific Islander (3%),
(7%), and others (4%). Full-scale cognitive mea- Native American (1%), and others (3%). The
sure estimates suggested that 81% of the sample CARS2 manual describes a high degree of inter-
achieved cognitive ability standard scores below nal consistency for the CARS2-HF scale
758 Children’s Category Test

(Cronbach alpha = 0.96). Corrected item total and Developmental Disorders, 46, 3361–3368. https://
reliability values between the 15 categories doi.org/10.1007/s10803-016-2860-z.
Mayes, S. D., Calhoun, S. L., Murray, M. J., Pearl, A.,
ranged from 0.53 to 0.88. Inter-rater reliability Black, A., & Tierney, C. D. (2014). Research and
was examined for ratings made by several sets of autism spectrum disorders final DSM-5 under – Iden-
two independent, trained examiners across 239 tifies mild autism spectrum disorder: Agreement
participants. High inter-rater reliability was between the DSM-5, CARS, CASD, and clinical
diagnoses. Research in Autism Spectrum Disorders, 8,
found with total correlation of 0.95 (category 68–73.
range 0.53–0.93). The CARS2-HF development Moulton, E., Bradbury, K., Barton, M., & Fein, D. (2016).
sample identified effective overall discrimination Factor analysis of the childhood autism rating scale in a
between individuals with and without autism sample of two year olds with an autism spectrum dis-
order. Journal of Autism and Developmental Disorders,
spectrum disorders. Dawkins et al. (2016) identi- 1–14.
fied high sensitivity (100) and specificity (0.83 Park, E. Y., & Kim, J. (2016). Factor structure of the
and 0.71) using DSM-IV-TR and DSM-5 criteria, childhood autism rating scale as per DSM-5. Pediatrics
respectively. Other gold standard assessments of International, 58, 139–145.
Schopler, E., Reichler, R. J., DeVellis, R. F., & Daly, K.
autism spectrum disorders including the ADOS (1980). Toward objective classification of childhood
correlated well with the CARS2-HF (0.77), dem- autism: Childhood autism rating scale (CARS). Jour-
onstrating reasonably strong relationships nal of Autism and Developmental Disorders, 10,
between the two clinical rating systems. 91–103.
Schopler, E., Van Bourgondien, M., Wellman, G., & Love,
S. (2010). Childhood autism rating scale-second edi-
tion (CARS2): Manual. Los Angeles: Western Psycho-
logical Services.
Clinical Uses of Psychometric Stability

The CARS2 is one of the most widely researched

assessment tools for autism spectrum disorders.
It is appropriate for use in conjunction with diag-
Children’s Category Test
nostic interviews, caregiver reports, and other
social-emotional, behavioral, and cognitive mea-
Vanessa L. Ramos Scarborough1 and Keith Owen
sures for the identification of individuals with
Yeates2
autism spectrum disorders (Dawkins et al. 1
Department of Neuropsychology, Kennedy
2016). Although the definition of autism has
Krieger Institute, Baltimore, MD, USA
evolved over the last 70 years, the CARS2 rating 2
Department of Psychology, University of
scales continue to assess the features of autism
Calgary, Calgary, AB, Canada
that have remained stable over time (Schopler
et al. 2010).
Synonyms

References and Readings CCT

American Psychiatric Association. (2013). Diagnostic and

statistical manual of mental disorders: DSM-5 (5th ed.). Description
Washington, DC: American Psychiatric Association.
Breidbord, J., & Croudace, T. J. (2013). Reliability
generalization for childhood autism rating scale. Jour- The Children’s Category Test (CCT) is an abbre-
nal of Autism and Developmental Disorders, 43, viated version of the original Halstead Category
2855–2865. Test (HCT; Reitan and Wolfson 1992). The CCT
Dawkins, T., Meyer, A., & Van Bourgondien, M. (2016).
The relationship between the childhood autism rating
is an individually administered instrument
scale: Second edition and clinical diagnosis utilizing designed to measure nonverbal learning and
the DSM-IV-TR and the DSM-V. Journal of Autism memory, concept formation, and problem-solving
Children’s Category Test 759

abilities. The CCT consists of two levels. Level other measures of achievement or cognitive ability,
1 is given to children aged 5–8 and consists of five such as the WISC-R and CVLT-C.
subtests and 80 items. Level 2 is given to children
aged 9–16 and consists of six subtests and
83 items. The child’s task is to identify the single Clinical Uses
conceptual rule underlying the items in each sub-
test. The last subtest on both levels requires the The CCT is a widely used test of the ability to solve C
child to remember and reapply the conceptual problems by developing and modifying strategies
rules from previous subtests. of responding to various visual designs and pat-
The CCT was normed on a stratified represen- terns (Nesbit-Greene and Donders 2002). The CCT
tative sample of 920 children in 12 age groups does not require demonstration of acquired skills,
ranging from 5 years to 16 years, 11 months. ability, or knowledge, and eliminates potential
Administration requires approximately confounding variables because it can be used with
15–20 min. The raw score is the total number of children with motor deficits or speech/language
errors (CCT Total), which is converted into an difficulties (Boll 1993). The CCT can provide
age-normed T-score (M = 50, SD = 10). The insights regarding a child’s cognitive abilities and
CCT is easy to administer and score. learning strategies in terms of difficulties in mem-
ory or shifting between conceptual ideas (MacNeil
Horton 1996). However, a poor score on the CCT
Historical Background does not necessarily indicate a neurologically
based disorder; rather it indicates a disruption in
The CCT was developed in an effort to provide an mental processing (Boll 1993).
efficient and well-normed children’s version of the Studies of the CCT’s sensitivity to brain dys-
HCT, which is well documented to be sensitive to function indicate that the measure is not consis-
cerebral impairment (Reitan and Wolfson 1992), tently sensitive to structural brain damage or
and the previous children’s versions of the Cate- neurodevelopment disorders in children (Bello
gory Test (Reitan and Wolfson 1993). Concerns et al. 2008; Donders 1996). Results from studies
about lengthy administration times and expensive, examining the sensitivity of the CCT to various
bulky equipment led to the development of various forms of brain dysfunction suggest that the CCT
short forms of these tests (e.g., Short Category Test assesses multiple dimensions of problem solv-
Booklet Format), with the most comprehensive of ing, rather than a general construct of abstraction
these efforts resulting in the CCT (Boll 1993). The (Nesbit-Greene and Donders 2002), which has
CCT and California Verbal Learning Test-Chil- led some to caution against relying on the total
dren’s Version (CVLT-C) were standardized and error score as the sole index of brain dysfunction
normed on the same population. (Allen et al. 2006; Bello et al. 2008). The use of
the CCT with brain-injured children may be ham-
pered by the fact that the overall T-score is based
Psychometric Data on six different subtests that differ in their sensi-
tivity to the severity of the injury (Nesbit-Greene
Median internal consistency reliability for the CCT and Donders 2002). Another problem with using
Total score is 0.88 for Level 1 and 0.86 for Level 2, the CCT with brain-injured children is that it is
with average standard errors of measurement of untimed and children are provided with correc-
3.46 and 3.74, respectively (Boll 1993). The sepa- tive feedback throughout the test administration,
rate age-level values and averaged coefficients and these features may compensate for any def-
indicate that the CCT possesses a high degree of icits in processing speed or executive function
internal consistency across ages. The manual that the child may be experiencing (Donders and
reports a variety of studies demonstrating that the Nesbit-Greene 2004). Overall, studies investi-
CCT consistently and significantly correlates with gating the use of the CCT with brain-injured
760 Children’s Memory Scale

children suggest that caution is needed in

interpreting the results, and that it should be Children’s Memory Scale
supplemented with psychometric data from addi-
tional neuropsychological tests (Donders and Morris J. Cohen
Nesbit-Greene 2004; Moore et al. 2004). Neurology, Pediatrics and Psychiatry, Pediatric
Neuropsychology, Medical College of Georgia
and BT-2601 Children’s Medical Center,
Augusta, GA, USA
Cross-References

▶ Concept Learning
Synonyms
▶ Delis-Kaplan Executive Functioning System
▶ Halstead-Reitan Neuropsychological Test
CMS
Battery
▶ Memory Impairment
▶ Nonverbal Learning Disabilities
Description
▶ Problem Solving
The Children’s Memory Scale (CMS), published
in 1997, provides a comprehensive assessment of
References and Readings learning and memory in children and adolescents
of ages 5 through 16 years. The CMS is individ-
Allen, D. N., Knatz, D. T., & Mayfield, J. (2006). Validity
of the children’s category test-level 1 in a clinical sam-
ually administered and designed to be used as part
ple of heterogeneous forms of brain dysfunction. of a standard psychological or neuropsychologi-
Archives of Clinical Neuropsychology, 21, 711–720. cal evaluation. It assesses declarative learning and
Bello, D. T., Allen, D. A., & Mayfield, J. (2008). Sensitiv- memory functions across three domains: auditory/
ity of the children’s category test level 2 to brain dys-
verbal, visual/nonverbal, and attention/concentra-
function. Archives of Clinical Neuropsychology, 23,
329–339. tion (working memory). Each domain contains
Boll, T. (1993). Children’s category test. San Antonio: two core subtests and one supplemental subtest.
Psychological Corporation. The subtests comprising the attention/concentra-
Donders, J. (1996). Validity of short forms of the interme-
tion domain provide measures of attention and
diate Halstead category test in children with traumatic
brain injury. Archives of Clinical Neuropsychology, 11, working memory. Each subtest in the auditory/
131–137. verbal and visual/nonverbal domains provide
Donders, J., & Nesbit-Greene, K. (2004). Predictors of measures of both immediate and delayed
neuropsychological test performance after pediatric
(30 min) recall. Each auditory/verbal subtest also
traumatic brain injury. Assessment, 11(4), 275–284.
MacNeil Horton, A. (1996). Book and test reviews. provides a measure of recognition recall.
Archives of Clinical Neuropsychology, 11, 171–173. After administration of the core subtests
Moore, B. A., Donders, J., & Thompson, E. H. (2004). (Table 1), the examiner can derive eight index
Validity of the children’s category test-level 1 after
scores: attention/concentration, verbal immediate,
pediatric traumatic brain injury. Archives of Clinical
Neuropsychology, 19, 1–9. verbal delayed, delayed recognition, visual imme-
Nesbit-Greene, K., & Donders, J. (2002). Latent structure diate, visual delayed, learning, and general mem-
of the children’s category test after pediatric traumatic ory (Fig. 1). The Learning Index is derived using
head injury. Journal of Clinical and Experimental Neu-
ropsychology, 24(2), 194–199.
subtest scores from the auditory/verbal (word
Reitan, R. M., & Wolfson, D. (1992). Neuropsychological pairs) and the visual/nonverbal (dot locations)
evaluation of older children. South Tucson: Neuropsy- domains. The General Memory Index is a mea-
chology Press. sure of global memory functioning and is gener-
Reitan, R. M., & Wolfson, D. (1993). The Halstead-Reitan
ated using both the immediate and delayed
neuropsychological test battery: Theory and clinical
interpretation (2nd ed.). South Tucson: Neuropsychol- memory indexes from the Auditory/Verbal and
ogy Press. Visual/Nonverbal domains.
Children’s Memory Scale 761

Children’s Memory Scale, Table 1 Description of CMS core index and subtest components
Core index Core subtest Subtest description
Verbal memory indexes Stories Two stories (age-dependent 5–8-, 9–12-, and 13–16-year olds) are read.
(immediate, delayed, and Immediately after presentation of each story, the child is asked to repeat as
recognition) much of the story as can be remembered. In the delayed portion, the child
retells the stories and then answers questions about the stories (recognition
recall)
Word pairs A list of 10 or 14 (age-dependent 5–8-year olds; 9–16-year olds) related
C
and unrelated word pairs are read; thereafter the stem is read and the child
recalls the associate. Three learning trials are administered followed by a
free recall. In the delayed portion, the child is asked to recall the word pairs
spontaneously followed by a recognition section
Visual/nonverbal memory Dot The child is shown an array of dots (blue) located within a rectangle in a
indexes (immediate and locations stimulus book. This page is removed and the client is asked to replicate the
delayed) spatial location of the dots by placing chips on a 3  4 or 4  4 rectangular
grid (depending on age, 6 dots for 5–8-year olds; 8 for dots 9–16-year
olds). Three learning trials are administered followed by presentation of a
distractor array (red dots) after which an immediate recall trial is presented.
In the delayed portion, the child is asked to reproduce the original blue dot
array
Faces The child is presented with a series of 12 (5–8-year olds) or 16 (9–16-year
olds) pictured human faces one at a time. In the immediate and delayed
recall sections, the child is asked to identify the stimulus faces from a
different set of foils (36 or 48 colored photos)
Attention/concentration Numbers A digit span forwards and backwards task (similar to the WISC-III subtest)
index Sequences The client is asked to mentally sequence or manipulate information as
quickly as possible. The 12 items include such tasks as reciting numbers,
days of the week and months in forward and reverse order, and counting by
2 s, 4 s, and 6 s. Scoring is based upon accuracy and speed

The immediate portion of the core battery takes psychological evaluation of children with neuro-
approximately 30–40 min to administer, with an logical and neurodevelopmental disorders
additional 10–20 min required for administration of included tests of intelligence, achievement, and
the delayed recognition sections. Two record forms behavior/emotional functioning with little if any
are provided for students of 5–8 and 9–16 years. attention paid to the child’s ability to learn and
Scoring tables in the manual or computer software remember new information. This was the case
allow for conversion of raw scores to scaled scores despite the fact that most referrals were in some
(mean = 10; SD = 3) at the individual subtest level way related to the student’s inability to learn and
and standard scores (mean = 100; SD = 15) at the remember school-related content. As a result, the
index level. Table 1 provides a brief description of CMS was developed with five goals in mind:
the core subtests.
1. The development of an instrument that was
consistent with current theoretical models of
Historical Background learning and memory.
2. The development of an instrument that was
Development of the CMS began in 1985 to pro- sensitive to developmental changes over time.
vide clinicians with a comprehensive, well- 3. To evaluate the relationship between memory
standardized, individually administered instru- and intelligence and provide the clinician
ment that would assess the important processes with a mechanism to meaningfully evaluate
involved in learning and memory within the discrepancies between IQ and learning/mem-
pediatric population. Prior to this, traditional ory performance.
762 Children’s Memory Scale

Children’s Memory Domain Subtests Indexes

Scale, Fig. 1 Structure of
Stories* Verbal
the children’s memory scale
Word pairs* Immediate
Word lists**
Auditory/verbal

Stories 2* Verbal
Word pairs 2* Delayed
Word lists 2**

Delayed
Recognition

Learning

Dot locations* Visual

Faces* Immediate
Family pictures**
Visual/nonverbal

Dot locations 2* Visual

Faces 2* Delayed
Family pictures 2**

Numbers* Attention/
Attention/concentration Sequences* Concentration
Picture locations**
Note: *Core subtest; **Supplemental subtest

4. The inclusion of a diversified selection of clin- Psychometric Data

ically and educationally relevant tasks that
would allow clinicians to identify and charac- The CMS was standardized on a representative
terize learning and memory disorders in chil- US sample of 1000 children. The sample was
dren and help them to design remedial and stratified according to age (10 age groups ranging
compensatory programs based upon the child’s in age from 5 to 16 years, 100 per age group), sex
performance. (equal number of males and females in each age
5. The development of an instrument that could be group), race/ethnicity (White, African American,
successfully administered within a standardized Hispanic, and other), geographic region
testing situation and also be child friendly. (northeast, north central, south, west), and parent
education level (five categories ranging from
As such, the CMS focused upon the assess- <8th grade to university degree). Further, the
ment of declarative memory with no attempt CMS is the only memory assessment instrument
made to formally evaluate procedural memory, to provide a linking sample co-normed with an
which involves skill learning and classical condi- individually administered intelligence scale
tioning. Further, the CMS was unable to provide (WISC-III and WPPSI-R). This sample was com-
measures of long-term memory beyond 30 min prised of 300 children (ages 5–16; 50% male 50%
due to the time restriction of a traditional assess- female) and provided the examiner with an empir-
ment and the logistical problems inherent in the ically grounded basis for predicting the level of
reevaluation of the standardization sample over a memory performance from IQ and determining
longer time interval. when a child’s memory performance deviated
Children’s Memory Scale 763

significantly from IQ expectancy. With the release Clinical Uses

of the WISC-IV in 2004, a smaller correlation
study was conducted involving 126 children of As previously stated, the CMS was designed to be
ages 6–16 years (Drozdick et al. 2005). The used as part of a standard psychological or neuro-
authors provide tables which allow for ability- psychological evaluation in order to provide a com-
memory discrepancy analysis using the predicted prehensive assessment of learning and memory in
actual or simple difference methods and base children and adolescents of ages 5–16 years. The C
rates. clinical sensitivity and usefulness of the CMS was
The CMS manual provides both split-half and demonstrated by the inclusion of case studies and
test-retest reliability coefficients for the index clinical validity studies in the test manual. These
scores and subtests. For the indexes, average included individual studies comparing the perfor-
split-half reliability estimates ranged from 0.76 mance of children with temporal lobe epilepsy,
to 0.91. Average split-half reliability estimates traumatic brain injury, brain tumors, learning dis-
for the subtests ranged from 0.71 to 0.91. Test- abilities, ADHD, and specific language impairment
retest reliability (mean retest interval 59.6 days) to that of normal controls. Additional studies have
was assessed across three age bands using a sam- been published examining learning and memory
ple of 125 students. Reliability estimates ranged performance in children with dyslexia and/or
from 0.29 to 0.89 for the indexes. Due to the ADHD (Kibby and Cohen 2008) and specific lan-
nature of memory assessment and psychometric guage impairment (Riccio et al. 2007a). The rela-
considerations (restriction of range), decision con- tionship between continuous performance testing
sistency test-retest coefficients were also calcu- and performance on the CMS has been investigated
lated. These ranged from 0.61 to 0.93 for the in a clinic sample (Riccio et al. 2007b). Studies have
indexes and from 0.71 to 0.93 for the core sub- also been reported on learning and memory perfor-
tests. Results indicated a general practice effect of mance of children with complex partial epilepsy of
up to one standard deviation, similar to what was temporal origin, using an experimental version of
obtained on the WISC-III. Inter-rater reliability the CMS (Cohen 1992; Cohen et al. 1990).
was also assessed on subtests requiring subjective
scoring (e.g., stories) and was found to be high.
With respect to validity, the results of confir-
Cross-References
matory factor analysis yielded a three-factor solu-
tion consisting of auditory/verbal memory, visual/
▶ Memory
nonverbal memory, and attention/concentration.
▶ Wechsler Memory Scale All Versions
The manual also provides concurrent validity
▶ Wide Range Assessment of Memory and
studies with different measures of intelligence
Learning
and achievement, which consistently show a mod-
erate positive correlation. The CMS correlations
with measures of executive functioning and lan-
References and Readings
guage were low to moderate. Finally, with respect
to other measures of memory, moderate to high Cohen, M. J. (1992). Auditory/verbal and visual/spatial
correlation were obtained across the indexes of memory in children with complex partial epilepsy of
the CMS and Wechsler Memory Scale-III, and temporal lobe origin. Brain and Cognition,
20, 315–326.
low to moderate correlations were obtained across
Cohen, M. J. (1997). Children’s memory scale. Adminis-
the indexes of the CMS and the Wide Range tration manual. San Antonio: The Psychological
Assessment of Learning and Memory. More Corporation.
recently, performance on both the CMS and Cohen, M. J., Holmes, G. L., Campbell, R., Smith, J. R., &
Flanigan, H. F. (1990). Memory performance following
WRAML-2 was reported as low to moderate in
unilateral electrical stimulation of the hippocampus in a
the latter test’s Examiner’s Manual (Sheslow and child with right temporal lobe epilepsy. Journal of
Adams 2003). Epilepsy, 3, 115–122.
764 Chi-square

Drozdick, L. W., Holdnack, J., Rolfus, E., & frequency and dividing by the expected fre-
Weiss, L. (2005). Technical report #5 WISC-IV and chil- quency, and then summing each result.
dren’s memory scale. San Antonio: Harcourt Assessment.
Kibby, M. Y., & Cohen, M. J. (2008). Memory functioning
in children with reading disorders and/or attention-
deficit/hyperactivity disorder: A clinical investigation Current Knowledge
of their working memory and long-term memory func-
tioning. Child Neuropsychology, 14, 525–546. An underlying assumption of the chi-square test is
Riccio, C. A., Cash, D. L., & Cohen, M. J. (2007a).
that the observations in the sample are indepen-
Learning and memory performance of children with
specific language impairment (SLI). Applied dent of each other. Additionally, the chi-square
Neuropsychology, 14, 255–261. test requires that the sample is sufficiently large.
Riccio, C. A., Garland, B. H., & Cohen, M. J. (2007b). Although various rules of thumb are available to
Relations between the test of variables of attention
determine an adequate sample size, a common
(TOVA) and the children’s memory scale (CMS).
Journal of Attention Disorders, 11, 167–171. guideline is to have expected frequencies of at
Sheslow, D., & Adams, W. (2003). Wide range assessment least five in at least 80% of cells, with no expected
of memory and learning – 2. Administration manual. frequencies less than one.
Wilmington: Jastak Associates.

See Also

▶ Contingency Table
Chi-square ▶ Correlation Coefficients
▶ Nonparametric Statistics
Matthew J. L. Page ▶ Statistical Significance
Allegheny General Hospital, Pittsburgh, PA, USA
Psychology, Allegheny Health Network,
Pittsburgh, PA, USA Further Readings

Campbell, I. (2007). Chi-squared and Fisher-Irwin tests of

Definition two-by-two tables with small sample recommenda-
tions. Statistics in Medicine, 26, 3661–3675.
Cochran, W. G. (1952). The w2 test of goodness of fit.
The chi-square (w2) test is a nonparametric statis- Annals of Mathematical Statistics, 25, 315–345.
tical method primarily used to evaluate frequency McHugh, M. L. (2013). The chi-square test of indepen-
data for categorical variables, by examining the dence. Biochemical Medicine, 23, 143–149.
differences between observed and expected fre-
quencies for each category. A one-way chi-square
test is used to determine whether differences in
frequencies across levels of a nominal variable are Chlordiazepoxide
due to chance (the null hypothesis) or represent a
true difference (the alternative hypothesis). The John C. Courtney1 and Efrain Antonio Gonzalez2,3
1
chi-square is calculated by dividing the squared Socorro Mental Health, Presbyterian Medical
difference between the observed and expected Services, Socorro, NM, USA
2
frequency by the expected frequency in each College of Psychology, Nova Southeastern
category and summing the results University, Fort Lauderdale, FL, USA
(w = S((O  E) /E)). When two variables are
2 2 3
Utah State University, Logan, UT, USA
involved, a contingency table is constructed,
depicting the observed frequency and the
expected frequency in each cell. The chi-square Generic Name
is calculated again by, within each cell, squaring
the difference between the observed and expected Chlordiazepoxide
Chlorpromazine 765

Brand Name
Librium and Librax Chlorpromazine
Class John C. Courtney1 and Cristy Akins2
Antianxiety agents, anxiolytics, and 1
Socorro Mental Health, Presbyterian Medical
benzodiazepines Services, Socorro, NM, USA
2
Mercy Family Center, Metarie, LA, USA C
Proposed Mechanism(s) of Action
Generic Name
Chlordiazepoxide binds to the GABA-A ligand-
gated chloride channel complex and, thereby, Chlorpromazine
enhances the inhibitory effects of GABA.
Brand Name
Thorazine
Indication
Class
Anxiety disorders, symptoms of anxiety, preoper- Conventional antipsychotic
ative apprehension and anxiety, and withdrawal
from acute alcoholism
Proposed Mechanism(s) of Action
Side Effects Blocks dopamine 2 receptors, dopamine D2, his-
tamine H1, and cholinergic M1 blockade in the
Serious vomiting center (area postrema)
Respiratory depression, kidney dysfunction, and
liver disorders (rare)
Indication
Common
Sedation, dizziness, depression, forgetfulness, Schizophrenia, nausea, vomiting, restlessness
confusion, and hyperexcitability before surgery, manic episodes of bipolar disorder,
and tetanus
References and Readings

Physicians’ desk reference (71st ed.). (2017). Montvale: Off-Label Use

Thomson PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The
Bipolar disorder
prescriber’s guide (2nd ed.). New York: Cambridge
University Press.

Additional Information Side Effects

Drug Interaction Effects. http://www.drugs.com/drug_
interactions.html Serious
Drug Molecule Images. http://www.worldofmolecules.
Neuroleptic malignant syndrome, jaundice,
com/drugs/
Free Drug Online and PDA Software. www.epocrates.com agranulocytosis, and seizures
Free Drug Online and PDA Software. www.medscape.com
Gene-Based Estimate of Drug interactions. http://mhc. Common
daytondcs.com:8080/cgi bin/ddiD4?ver=4&task=
Neuroleptic-induced deficit syndrome, akathisia,
getDrugList
Pill Identification. http://www.drugs.com/pill_identifica extrapyramidal symptoms, priapism, and
tion.html amenorrhea
766 Cholesterol

References and Readings lipoprotein molecules. Low-density lipoprotein

(LDL) is the major carrier of cholesterol. In the
Physicians’ desk reference (62nd ed.). (2007). Montvale: presence of high circulating concentrations, LDL-
Thomson PDR.
cholesterol gradually builds up in and on the walls
Stahl, S. M. (2007). Essential psychopharmacology: The
prescriber’s guide (2nd ed.). New York: Cambridge of the coronary, cerebrovascular, or peripheral
University Press. arteries. Together with coagulation factors and
platelets, cholesterol deposits on the vessel walls
Additional Information can form thick hard “plaques” which, over time,
Drug Interaction Effects. http://www.drugs.com/drug_ can occlude the blood vessels in a process called
interactions.html
“atherosclerosis.” Therefore, a high level of LDL-
Drug Molecule Images. http://www.worldofmolecules.
com/drugs/ cholesterol (usually greater than 160 mg/dL) indi-
Free Drug Online and PDA Software. www.epocrates.com cates an increased risk of heart disease and, to a
Gene-Based Estimate of Drug interactions. http://mhc. lesser extent, stroke. For this reason, LDL-
daytondcs.com:8080/cgi bin/ddiD4?ver=4&task=
cholesterol is often called “bad cholesterol.”
getDrugList
Pill Identification. http://www.drugs.com/pill_identifica About one-third of the circulating cholesterol is
tion.html transported by high-density lipoprotein (HDL),
which more commonly carries the cholesterol
away from the arteries, and toward the liver
where it is metabolized and eliminated. It has
Cholesterol been suggested that HDL removes excess choles-
terol from plaques, and consequently, HDL-
Elliot J. Roth cholesterol is known as “good cholesterol”
Department of Physical Medicine and because a high HDL-cholesterol level seems to
Rehabilitation, Northwestern University, protect against coronary heart disease. Typically,
Feinberg School of Medicine, Chicago, IL, USA the liver meets all of the body’s requirements for
cholesterol by manufacturing it, which means that
dietary cholesterol is not needed for nutritional
Synonyms purposes. In foods, saturated fatty acids, and to a
lesser extent, trans fats, are the main sources of
Fats; Lipids elevated blood cholesterol levels. Measures to
reduce elevated cholesterol levels include reduc-
tions in dietary cholesterol intake, cholesterol-
Definition lowering medications, increases in physical activ-
ity levels (which increase HDL-cholesterol), and
Cholesterol is a naturally occurring lipid found in cessation of smoking.
the bloodstream and in cells throughout the body.
It is an important component of cell membranes
and some hormones. However, hypercholester- Cross-References
olemia, or high blood concentrations of choles-
terol, is a major risk factor for heart disease and ▶ Atherosclerosis
stroke. ▶ Cerebrovascular Disease
▶ Coronary Disease
▶ Ischemic Stroke
Current Knowledge ▶ Myocardial Infarction
▶ Peripheral Vascular Disease
Cholesterol does not typically exist on its own in ▶ Stent
the blood; it is transported to and from cells by ▶ Thrombosis
Cholinergic System 767

References and Readings metabolic reactions and an acceptor and donor of

acetyl groups. These molecules are catalyzed by
Fletcher, B., Berra, K., Ades, P., Braun, L. T., Burke, L. E., choline acetyltransferase, an enzyme found only
Durstine, J. L., et al. (2002). Managing abnormal blood
in acetylcholinergic cells, in order to produce
lipids: A collaborative approach. Circulation, 112,
3184–3209. acetylcholine.
National Cholesterol Education Program Expert Panel on In the metabolism of acetylcholine, acetylcho-
Detection, Evaluation, and Treatment of High Blood linesterase degrades the molecule to produce cho- C
Cholesterol in Adults (Adult Treatment Panel III).
line and acetic acid. The choline molecules
(2002). Third report of the National Cholesterol Edu-
cation Program (NCEP) expert panel on detection, generated through this reaction are transported,
evaluation, and treatment of high blood cholesterol in via a high-affinity choline uptake protein, back
adults (adult treatment panel III). Circulation, 106, to the nerve terminal. They are then used to syn-
3143–3421.
thesize new acetylcholine molecules.

Cholinergic Receptor Types and Subtypes

Nicotinic: The nicotinic acetylcholine receptor
Cholinergic System type forms ligand-gated ion channels in the mem-
branes of neurons receptive to acetylcholine. As
Colleen E. Jackson an ionotropic receptor, the nicotinic receptor is
VA Boston Healthcare System, Boston, MA, USA directly linked to an ion channel. When acetyl-
choline binds to the nicotinic receptor, it generates
the opening of the ion pore, causing a rapid influx
Synonyms of cations. There are four nicotinic receptor sub-
types (N1, N2, N3, and N4), as well as a, b, d, and
Acetylcholinergic system g subunits for each subtype.
Muscarinic: The muscarinic acetylcholine recep-
tor type forms G protein-coupled channels in the
Definition membranes of neurons receptive to acetylcholine.
When acetylcholine binds to one of these meta-
The cholinergic system is composed of organized botropic channels, it generates a cascade of infor-
nerve cells that use the neurotransmitter acetyl- mation transduction within the cell via intracellular
choline in the transduction of action potentials. proteins. There are five muscarinic receptor sub-
These nerve cells are activated by or contain and types (M1, M2, M3, M4, and M5). All five receptor
release acetylcholine during the propagation of a subtypes are present in the central nervous system;
nerve impulse. The cholinergic system has been however, M1, M2, and M4 are more predominant.
associated with a number of cognitive functions,
including memory, selective attention, and emo- Cholinergic Projections
tional processing. The cholinergic system is formed by a broadly
projecting circuitry, as well as local circuitry.
Long-projection cholinergic neurons originating
Current Knowledge in the nuclei of the basal forebrain project widely
throughout the brain. For example, the nucleus
Acetylcholine Synthesis and Metabolism basalis of Meynert and the diagonal band of
The synthesis of acetylcholine, the neurotransmit- Broca, both structures within the basal forebrain,
ter used by nerve cells in the cholinergic system, transmit acetylcholine to the cerebral cortex. In
requires choline, a natural amine found in the lipid addition, cholinergic projections exist between
bilayer of the cell membrane, and acetyl coen- the septal nucleus and the hippocampus. Local
zyme A (acetyl-CoA), a thioester used in cholinergic circuitry within the striatum has
768 Cholinergic System

important interactions with nigrostriatal dopa- receptors in the central nervous system. Nicotinic
mine neurons and striatal GABAergic neurons acetylcholine antagonists acting on cells in the
involved in extrapyramidal movement. central nervous system are rarely used in clinical
practice.
Cognitive Role of the Cholinergic System Pilocarpine is an example of a muscarinic ace-
The cholinergic system has been implicated in a tylcholine agonist that acts on the parasympa-
number of cognitive abilities, including attention, thetic nervous system. While pilocarpine is not
memory, and emotional processing. Both human used clinically to treat central nervous system
and animal studies indicate that cholinergic input disorders, it has a range of side effects, including
originating in the basal forebrain mediates sustained excessive sweating and salivation, which are
attentional performance (see Sarter et al. 2001 for related to its action on muscarinic receptors in
review). Acetylcholine neuron activation has also the parasympathetic nervous system. Muscarinic
been associated with response to novel stimuli, acetylcholine antagonists, such as scopolamine
although there is evidence that this response varies and atropine, block muscarinic receptors. Their
based on brain region (Rangel-Gomez and Meeter anticholinergic effects on the parasympathetic
2016). In addition, the cholinergic system also acts nervous system result in side effects such as dry
as a modulator of level of processing (e.g., primitive mouth, constipation, and tachycardia.
responses such as reflexes vs. limbic system Acetylcholinesterase inhibitors, such as tacrine
responses vs. evaluative and discriminative execu- and donepezil, block the breakdown of acetylcho-
tive functioning processes). Broadly, activation of line in the synaptic cleft. The result is sustained
the cholinergic system supports attentional pro- levels of acetylcholine in the synapse that are
cessing of threat-related stimuli (Berntston et al. capable of transmitting chemical information to
1998), while specific projections to the medial pre- other cells. Acetylcholinesterase inhibitors are
frontal cortex influence anxious responses to con- commonly used in the treatment of Alzheimer’s
textual stimuli (Hart et al. 1999). By influencing disease, as well as Lewy body dementia.
arousal and attention, acetylcholine also impacts Presently, there is a developing focus on the
working memory and the attentional processes cholinergic system in the treatment of schizophrenia
required for error detection (see Sarter et al. 2006 (see Gibbons and Dean 2016 for review). For exam-
for review). Emotional processing is also intricately ple, xanomeline, an M1/M4 muscarinic acetylcho-
related to the cholinergic system; cholinergic inputs line agonist that was initially assessed as a possible
to the frontoparietal cortex may influence how treatment for Alzheimer’s disease, has shown
attention is directed toward emotional information efficacy in treating psychotic symptoms (Bodick
(Bentley et al. 2003). As would be expected from a et al. 1997). In addition, N-desmethylclozapine
system influencing such a variety of cognitive func- (norclozapine, NDMC), a metabolite of the antipsy-
tions, decreased cholinergic tone, associated with chotic clozapine, is a partial M1 agonist. This agent
Alzheimer’s disease, results in impaired cognitive is currently being assessed as a treatment for schizo-
performance broadly extending to memory, atten- phrenia (Lameh et al. 2007).
tion, and executive functioning (Terry and
Buccafusco 2003).
Future Directions
Pharmacological Agents Acting on the
Cholinergic System Future research focused on the interaction between
Pharmacological agents impact the cholinergic the cholinergic system and other neurotransmitters
system in a number of different ways. At the (e.g., norepinephrine, dopamine, and serotonin) and
receptor level, nicotinic acetylcholine agonists neuromodulators (e.g., substance P) will be impor-
stimulate cholinergic activity largely in peripheral tant in understanding the complexities that exist
acetylcholine neurons. However, nicotine, a nico- within the brain and body regarding the commu-
tinic acetylcholine agonist, acts at nicotinic nication of chemical signals. Further development
Cholinesterase Inhibitors 769

of biomarkers (e.g., behavioral, electrophysiolog- Sarter, M., Gehring, W. J., & Kozak, R. (2006). More
ical, and neuroimaging) associated with choliner- attention must be paid: The neurobiology of attentional
effort. Brain Research Reviews, 51, 145–160.
gic decline will allow for improved identification Terry, A., & Buccafusco, J. (2003). The cholinergic
of disorders associated with the cholinergic sys- hypothesis of age and Alzheimer’s disease-related cog-
tem. A continued focus on the role of the cholin- nitive deficits: Recent challenges and their implications
ergic system in Alzheimer’s disease, as well as the for novel drug development. Journal of Pharmacology
development of pharmaceutical interventions
and Experimental Therapeutics, 306, 821–827.
C
targeting the cholinergic system in the treatment
of this disease (e.g., alpha-7 subunit nicotinic ago-
nists), remains critical, particularly with its con-
tinued rise in the elderly population. Finally, Cholinesterase Inhibitors
research on the role of the cholinergic system in
a number of psychological disorders, including Stephanie Behrens1 and JoAnn Tschanz1,2
1
stress, affective and panic disorders, and schizo- Department of Psychology, Utah State
phrenia, will continue to highlight the broad impli- University, Logan, UT, USA
2
cations on mental health that this system has. Center for Epidemiologic Studies, Utah State
University, Logan, UT, USA

Cross-References Synonyms
▶ Alzheimer’s Disease
Acetylcholinesterase inhibitors; AchEIs; CHEIs;
▶ Cholinesterase Inhibitors
ChEIs
▶ Memory
▶ Memory Impairment
▶ Mild Cognitive Impairment
Definition

A class of medications that targets the cholinergic

References and Readings neurotransmitter system and is used in the treat-
ment of Alzheimer’s disease and other dementias.
Bentley, P., Vuilleumier, P., Thiel, C., Driver, J., & Dolan,
R. (2003). Cholinergic enhancement modulates neural The treatment is based on the observation of a
correlates of selective attention and emotional pro- cholinergic deficiency in the condition. Cholines-
cessing. Neuroimage, 20, 58–70. terase inhibitors (CHEI) block the activity of ace-
Bodick, N. C., Offen, W. W., Levey, A. I., Cutler, N. R.,
Gauthier, S. G., Satlin, A., et al. (1997). Effects of
tylcholinesterase, the primary enzyme that breaks
xanomeline, a selective muscarinic receptor agonist, down acetylcholine, allowing the neurotransmit-
on cognitive function and behavioral symptoms in ter substance to remain in the synaptic cleft longer
Alzheimer disease. Archives of Neurology, 54, in order to stimulate postsynaptic receptors. The
465–473.
oldest CHEI, Tacrine (Cognex), is infrequently
Gibbons, A., & Dean, B. (2016). The cholinergic system:
An emerging drug target for schizophrenia. Current prescribed due to its unsafe side effects. Other
Pharmaceutical Design, 22, 2124–2133. CHEIs include Donepezil (Aricept), Rivastigmine
Lameh, J., Burstein, E. S., Taylor, E., Weiner, D. M., (Exelon), and Galantamine (Razadyne). The
Vanover, K. E., & Bonhaus, D. W. (2007). Pharmacol-
ogy of N-desmethylclozapine. Pharmacology & Ther-
newest addition to the CHEI class is a combina-
apeutics, 115, 223–231. tion treatment, Namzaric, consisting of donepezil
Rangel-Gomez, M., & Meeter, M. (2016). Neurotransmit- and memantine, the latter being an N-methyl-D-
ters and novelty: A systematic review. Journal of Psy- aspartate-receptor antagonist. CHEIs are modestly
chopharmacology, 30, 3–12.
Sarter, M., Givens, B., & Bruno, J. P. (2001). The cognitive
effective in short-term (6–12 months) improve-
neuroscience of sustained attention: Where top-down ment of cognitive processes (attention, concentra-
meets bottom-up. Brain Research Reviews, 35, 146–160. tion, memory), functional abilities (activities of
770 Chorea

daily living), and possibly, neuropsychiatric appear to flow from one muscle to the next. They
symptoms. To date, research has shown these may appear as dance-like movements of the limbs,
drugs do not show efficacy in treating mild cog- trunk, or head. Typical movements include facial
nitive impairment (MCI). The drugs do not pre- grimacing, shoulder adduction, and finger exten-
vent the further degeneration of cholinergic sion and contractions. They can be associated
neurons or stop the progression of Alzheimer’s with snakelike writhing movements of the hands
disease. or feet known as athetosis.

Current Knowledge
See Also
Chorea is a feature of Huntington’s disease and
▶ Alzheimer’s Dementia
may be present with rheumatic fever. It can be
seen as a side effect of the medication levodopa or
the dopamine agonists and may result from meta-
References and Readings
bolic disorders, endocrine disorders, and vascular
Orgogozo, J.-M. (2003). Treatment of Alzheimer’s disease incidents.
with cholinesterase inhibitors. An update on currently
used drugs. In K. Iqbal & B. Winblad (Eds.),
Alzheimer’s disease and related disorders: Research Cross-References
advances (pp. 663–675). Bucharest: Ana Asian Intl.
Acad. of Aging.
Rountree, S. D., Atri, A., Lopez, O. L., & Doody, R. S. ▶ Huntington’s Disease
(2013). Effectiveness of antidementia drugs in delaying
Alzheimer’s disease progression. Alzheimer’s &
Dementia, 9, 338–345.
Small, G., & Bullock, R. (2011). Defining optimal treat- References and Readings
ment with cholinesterase inhibitors in Alzheimer’s dis-
ease. Alxheimer’s & Dementia, 7, 177–184. Marshall, F. J. (2004). Clinical features and treatment of
Huntington’s disease. In R. L. Watts & W. C. Koller
(Eds.), Movement disorders (2nd ed., pp. 589–603).
New York: McGraw-Hill.
Chorea

Anna DePold Hohler1 and Marcus Ponce de

Leon2 Christensen, Anne-Lise
1
Boston University Medical Center, Boston, MA, (1926– )
USA
2
Madigan Army Medical Center, Tacoma, Anthony Y. Stringer1 and Christine Ghilain2
1
WA, USA Department of Rehabilitation Medicine, Emory
University, Atlanta, GA, USA
2
Department of Neuropsychology, Children’s
Synonyms Healthcare of Atlanta, Atlanta, Georgia, USA

Dance-like
Landmark Clinical, Scientific, and
Professional Contributions
Definition
• In 1966, Anne-Lise Christensen reviewed
Chorea is characterized by brief, irregular muscle a newly published English translation of
contractions that are not repetitive or rhythmic but Aleksandr Luria’s (1966) Higher Cortical
Christensen, Anne-Lise (1926– ) 771

Functions in Man and instantly realized its Education and Training

value in the clinical bedside examination of
cognitive function in neurological patients. • 1954–1955 – Visiting research fellow at Rad-
Luria provided a comprehensive theory of cliffe University
brain organization, from which cognitive • 1956 – Master of Arts in Psychology, Univer-
tasks could be developed to measure various sity of Copenhagen, Denmark
cortical functions. However, Luria’s scholarly • 1957 – Doctor of Philosophy, University of C
presentation required some adaptation before it Copenhagen, Denmark
could be practically applied by clinicians.
Guided by her experience working with neuro- Christensen began attending the University of
surgeon Richard Malmros, Christensen began Copenhagen in 1945, shortly after the liberation
to translate Luria’s methods into her native of Denmark from the Nazi occupation. She writes
Danish as well as adapt them for use in the about the “overwhelming experience of freedom
clinic. Responding to Luria’s invitation, and peace . . . [when] the borders were opened,
Christensen visited him in Moscow and pre- and we were full of hope and expectations for the
sented her Danish translation. Luria labeled it a future” (Christensen 2002, p. 119). Courses in
“vulgarization” of his method, but added he philosophy progressed to courses in Experimental
had always wanted someone to do this. He and Gestalt Psychology, and she credits the initial
encouraged Christensen to do an English trans- piquing of her interests in neuropsychology to
lation. Five years later, Christensen presented Professor Franz From at the University of Copen-
the first English draft to Luria on her second hagen. Focusing on the phenomenology of human
visit to Moscow. Luria made edits and pro- behavior, From described the need to interpret the
vided a paper for Christensen to translate and intentions of others, to best understand human
include in the final draft. Christensen published behavior and interactions, which aligned with
Luria’s Neuropsychological Investigation her prior studies of Danish philosopher Soren
(LNI) in 1975, including a textbook, manual, Kierkegaard. Her studies were interrupted for 6
and stimulus cards. years by marriage and motherhood, but she
• The LNI introduced a qualitative approach to returned to the university in 1952, dividing her
neuropsychological examination, which time between literature and psychology.
contrasted with the predominant quantitative Christensen was accepted at Radcliffe University
batteries used in the USA. The LNI is one of in 1954, where she was exposed to the work of
the few theory-based assessment approaches Talcott Parsons, Gordon Allport, Gardner
in neuropsychology and has been lauded for Lindzey, and George Mandler. She cites, Jerome
its flexible administration, brevity, and quali- S. Bruner, however, as her greatest influence. In
tative focus (Kolb and Wishaw 1990). It has his work, Christensen was exposed to “New Look
also been criticized for its lack of norms Psychology” which took the methods of the psy-
and insensitivity to mild impairment (Lezak chophysics laboratory and applied them to every-
1983). Though Christensen declined to col- day perceptual experience.
laborate, Charles Golden and colleagues Christensen returned to Denmark in 1955 and
(Golden et al. 1979) in the USA attempted to completed her doctoral studies at the University of
standardize the administration of the LNI and Copenhagen in 1957. Bruner continued to influ-
establish a normative base for interpretation. ence Christensen’s career for more than a decade
This unfortunately violated the original qual- later when he insisted she introduce herself to
itative focus of the LNI and generated consid- Luria at a 1969 conference in London. Impressed
erable controversy and criticism. Nonetheless, with her attempts at using his method in Denmark,
Christensen’s original qualitatively oriented Luria invited Christensen to visit him in Moscow,
LNI continues to be used in Europe, and but a sudden heart attack prevented his participa-
somewhat less frequently in the USA. tion in the conference. Nonetheless, an official
772 Christensen, Anne-Lise (1926– )

invitation arrived in Denmark from the Russian at the University of Aarhus together beginning in
Ministry of Health, and Christensen made her visit 1959, and Niels became the Chair of the Philoso-
to the Bourdenko Neurosurgical University Insti- phy Department just one year before Anne-Lise
tute to work with Luria in September 1970 became the Chair of Clinical Psychology. Over
(Christensen 2002). This began the collaboration the course of her career, Christensen has had many
between the two, which resulted in the introduc- distinguished collaborators, colleagues, and men-
tion of the LNI to the West. tors. Besides Bruner and Luria, she cites the noted
neuropsychologists Elkhonon Goldberg (whom
she met in Moscow while training with Luria),
Major Appointments Edith Kaplan, and Muriel Lezak, and neuroscien-
tists Donald Stein and Stanley Finger
• University Psychiatric Hospital, Copenhagen (Christensen 2002). Her collaborations have
1957–1959 always been international in scope, stretching
• University Hospital of Aarhus (Psychiatry and across Europe and the Americas. Her collabora-
Neurosurgery Departments), Jutland, Den- tion with her husband Niels came to a sad ending
mark, 1959–1968 with his suicide in 1980 after battling bipolar
• University Hospital of Aarhus (Head of Clini- disorder. Yet, even after retiring, her international
cal Psychological Department), Jutland, Den- collaborations continued, with Christensen serv-
mark, 1969–1981 ing on the Board of Consultants for the SARAH
• University of Copenhagen (Research Neuro- Network Hospitals in Brazil, a complex of facili-
psychologist), Denmark, 1981–1985 ties, she believes bridge “the chasm between
• Center for Neuropsychological Rehabilitation humanistic and empirical scientific approaches”
(CRBI; Founder and Director), University of to rehabilitation (Christensen 2002, p. 134).
Copenhagen, Denmark, 1985–1998
• University of Copenhagen (Professor of Neu-
ropsychological Rehabilitation), Denmark,
Cross-References
1985–1998
▶ Kaplan, Edith (1924–2009)
Major Honors and Awards ▶ Lezak, Muriel
▶ Luria Nebraska Neuropsychological Battery
• 1987 – Lady of the Dannebrog Order ▶ Luria, Alexander Romanovich (1902–1977)
(bestowed by the Queen of Denmark) ▶ Qualitative Neuropsychological Assessment
• 1994 – Philosophia Doctor Honoris Causa,
University of Lund, Sweden
• 2012 – Lifetime Achievement Award (pre- References and Readings
sented by the International Brain Injury Asso-
ciation, Edinburg, Scotland) Christensen, A.-L. (1975). Luria’s neuropsychological
investigation. Manual and test materials. New York:
Spectrum Publications.
Short Biography Christensen, A.-L. (2002). Lifelines. In A. Y. Stringer, E. L.
Cooley, & A.-L. Christensen (Eds.), Pathways to prom-
inence in neuropsychology: Reflections of twentieth-
A deep and lasting penchant for collaboration is century pioneers (pp. 119–137). New York: Psychol-
evident both in Anne-Lise Christensen’s personal ogy Press.
and professional lives. At 19, she married Niels Golden, C. J., Purisch, A. D., & Hammeke, T. A. (1979).
The Luria-Nebraska neuropsychological battery. Lin-
Egmont Christensen, a former classmate. Their coln: University of Nebraska Press.
careers progressed in tandem. While Anne-Lise IBIA. (2012). Honors Anne-Lise Christensen with 2012
was at Radcliffe, Niels was at Harvard. They were Lifetime Achievement Award. 11 Dec 2012. Retrieved
Chronic Effects of Neurotrauma Consortium 773

November 11, 2016, from http://www.internationalbrain.

org/articles/ibia-honors-annelise-christensen-with-2012- Chronic Effects of
lifetime-achievement-award/
Kolb, B., & Wishaw, I. Q. (1990). Fundamentals of human Neurotrauma Consortium
neuropsychology (3rd ed.). New York: Freeman.
Lezak, M. (1983). Neuropsychological assessment (2nd Kevin Sickinger
ed.). New York: Oxford University Press. Chronic Effects of Neurotrauma Consortium
Luria, A. R. (1966). High cortical functions in man (2nd
ed.). New York: Basic Books. (CENC), Virginia Commonwealth University, C
Richmond, VA, USA

Membership
Chromosome
The Chronic Effects of Neurotrauma Consortium
Martin Hahn1 and Rohan Palmer2 (CENC) is a coordinated, multicenter research
1
Department of Biology, William Paterson collaboration linking basic, translational, and clin-
University, Wayne, NJ, USA ical neuroscience researchers from the Veterans
2
Institute for Behavioral Genetics, University of Health Administration (VHA), military, the pri-
Colorado at Boulder, Boulder, CO, USA vate sector, and academia. The Consortium aims
to effectively address the knowledge gaps in diag-
nosis and therapy for mild traumatic brain injury
Definition (mTBI) and its long-term effects. Unique features
of the Consortium include (1) its centralized orga-
Chromosomes are threadlike structures made of nization, with a coordinating center located at
proteins and nucleic acids. They are found in the Virginia Commonwealth University, directed by
nucleus of eukaryotic cells and carry genetic senior academic TBI leaders of the Department of
information along their length in the form of Veterans Affairs (VA) and Department of Defense
genes. In the early 1900s, Walter Sutton and (DoD); (2) nationwide linkages between eight
Theodor Boveri argued that the understanding of major VA TBI/Polytrauma Centers, multiple
chromosomes was consistent with Mendelian DoD Centers, and over two dozen academic and
genetics, and the result of their thinking is called private research centers; (3) extensive, long-term
the chromosome theory of heredity. A part of that track record of collaborative TBI research; (4)
theory is that Mendelian genes have specific loca- access to large military/VA-relevant research sub-
tions (or loci) on chromosomes - a topic under ject populations; and (5) ten innovative and
heavy research since that time. intersecting research projects that are designed to
Chromosomes differ in overall length and the advance knowledge of traumatic brain injury in
length of their parts, and they have distinctive the near term and lay the groundwork for subse-
banding patterns that allow them to be recognized. quent investigation.
Humans have 23 pairs or 46 chromosomes. Of
those 23 pairs, one pair is called the sex chromo-
somes, and the remaining 22 pairs are called Major Areas or Mission Statement
autosomes.
The mission of the CENC is to fill gaps in knowl-
edge about the basic science of mTBI (also termed
Cross-References concussion or mild TBI), determine its effects on
late-life outcomes and neurodegeneration, iden-
▶ Deoxyribonucleic Acid (DNA) tify service members most susceptible to these
▶ Gene effects, and identify the most effective treatment
774 Chronic Effects of Neurotrauma Consortium

strategies. This project is explicitly designed to retrospective cohort study integrating

understand the linkages between mTBI, chronic existing federal healthcare databases to
effects, and neurodegeneration to enhance current study the chronic effects of mTBI on neuro-
and future care, guide the development of novel degenerative disease and other comorbidities
interventions, prevent or mitigate cognitive and and the methods to treat and rehabilitate
behavioral decline, and contribute to long-term adverse effects of mTBI in veterans over time.
planning for service members and veterans. 3. The Tau Modifications Study (CENC0005C)
The chronic effects from mTBI, whether single is a basic science project to identify the key
or repeated, on chronic disabling symptoms, on molecular events in the processing of tau after
recovery from combat and trauma-related TBI in rodents and humans, with the goal of
comorbidities, and on long-term brain function developing novel biomarker tools to assess
in veterans and service members are not known. tau dysregulation after TBI.
The goals of CENC are to definitively identify and 4. The Otolith Dysfunction and Postural Stabil-
characterize the anatomic, molecular, and physio- ity Study (CENC0008P) is a prospective
logical mechanisms of chronic brain injury and case-controlled study to determine the effect
potential neurodegeneration. of inner ear (vestibular) dysfunction on bal-
The specific research studies have been ance, gait, and quality of life in veterans. This
designed to directly address Consortium objec- study is located at the Mountain Home Vet-
tives, to build on and leverage existing TBI eran’s Affairs Medical Center in Johnson
research activities, to provide meaningful answers City, TN.
to the current questions facing individuals and 5. The Novel White Matter Imaging to Improve
organizations affected by neurotrauma, and to Diagnosis of Mild TBI Study (CENC0020P)
identify and lead a way ahead. is an observational cohort study assessing the
Current approved and active studies include diagnostic utility of multicomponent-driven
the following: equilibrium single pulse observation of T1
and T2 (mcDESPOT) on brain volume after
1. The Observational Study on Late Neurologic mTBI in veterans with a history of mTBI,
Effects of OEF/OIF/OND Combat posttraumatic stress, or both. This study is
(CENC0001C) is a large 1100-participant located at the VA San Diego Healthcare
observational cohort study with the objective System.
of identifying and assessing the long-term 6. The ADAPT/EVOLVE Study (CENC0025P)
effects of mild TBI in a population of veterans is a follow-up to an existing prospective
and service members with a history of case-controlled study of advanced MR imag-
deployment and combat exposure in recent ing and clinical outcome measures 3–5 years
conflicts such as Operation Enduring after concussive traumatic brain injury
Freedom or Operation Iraqi Freedom. Data (TBI) in US military personnel injured
collected include a variety of clinical mea- during deployment. This study is located
sures, cognitive and neurological functioning at the University of Washington in Seattle,
assessments, patient-reported outcomes, and WA.
biological measures including biospecimen 7. The Structural and Functional Neurobiology
and MRI analysis. This study is taking place of Veterans Exposed to Primary Blast Forces
at seven Veteran’s Affairs Medical Centers Study (CENC0034P) is an observational
located in Richmond, Tampa, Houston, San cohort study designed to investigate the
Antonio, Portland, Minneapolis, and Boston microstructural nature and functional effect
as well as one DoD site located at Fort of diffuse heterogeneous white matter abnor-
Belvoir, VA. malities following mTBI in veterans of recent
2. The Epidemiology of mTBI and Neurosen- conflicts, using advanced multimodal neuro-
sory Outcomes Study (CENC0004C) is a imaging, structured interview, and cognitive
Chronic Effects of Neurotrauma Consortium 775

testing and questionnaires. This study is the overall function of all components of the
located at the WG Hefner VA Medical Center CENC and is the primary point of contact to
in Salisbury, NC. the sponsors. The primary goal of the VCU
8. The DTI Phantom Study (CENC0039P) is an Coordinating Center is to insure completion
observational study to cross-validate the of all activities, sponsor required reporting,
many different scanners across the VA hospi- and compliance for the CENC.
tal system to provide the same imaging infor- 2. Neuroimaging Core: The Neuroimaging Core C
mation in suspected cases of TBI. is located at the Baylor College of Medicine
9. The Clinical and Neuroimaging Correlates of (BCM) and the Michael E. DeBakey VA Med-
Neurodegeneration in Military mTBI Study ical Center in Houston, Texas. It is led by Drs.
(CENC0049P) is an observational cohort Elisabeth Wilde and Harvey Levin, but utilizes a
study designed to test potential markers of group of sub-cores for data analysis, including
mTBI and assess self-report measures by re- some forms of volumetric and FLAIR analysis
assessing an existing cohort of veterans and by Drs. Erin Bigler and Mr. Tracy Abildskov
service members by collecting data through (Brigham Young University), diffusion analysis
clinical interviews, self-reporting measures, by Dr. David Tate (University of Missouri, St.
neuroimaging, and blood-based protein Louis), additional diffusion and volumetric
expression. This study is located at the Min- analysis by Drs. James Stone and Nick Tustison
neapolis VA Healthcare System and the Uni- (University of Virginia), and functional connec-
versity of Minnesota. tivity analysis by Dr. Mary Newsome (Baylor
10. The Visual Sensory Impairments and Pro- College of Medicine and MEDVAMC). The
gression Following Mild Traumatic Brain Core includes experts from a wide spectrum of
Injury Study (CENC0056P) is an observa- neuroimaging to include neuroradiology, neuro-
tional cohort study to identify the spectrum psychology, magnetic resonance imaging
of visual sensory disturbances after mTBI (MRI) physics, information technology (IT)
using a new imaging technology and further and computer programming, and statistics. The
to identify potential therapeutic modalities Core has facilitated sequence development and
including focal transcranial magnetic stimu- pulse programming, training, and supervision of
lation, visual behavioral tasks that may technologists and support personnel and quality
strengthen synaptic connections, chemical assurance (QA) in overall support of CENC
neuromodulation, and peripheral and central studies.
nerve stimulation. This study is 3. Neuropathology Core: The Neuropathology
headquartered out of the Iowa City VA Core is co-located at the Uniformed Services
Healthcare System with study sites also University of the Health Sciences (USUHS)
located in Minneapolis and Palo Alto. led by Drs. Dan Perl and Kimbra Kenney and
the VA Boston Biorepository Brain Bank led
There are five research cores in support of these by Dr. Ann McKee. This Core manages the
studies: collection of brain specimens from participants
using an existing national network of donors
1. VCU Coordinating Center: The Coordinating and neuropathologists. The Core also catalogs
Center at VCU serves both to implement a and stores these tissues for use by qualified
specific program of research designed to pro- investigators from within or outside the
vide clinically relevant answers and interven- CENC. The Core administers requests for use
tions for current service members and veterans of these tissues according to sample sharing
and provides leadership in developing innova- policies of the Consortium and tracks the
tive research proposals and programs to define results of these collaborative studies.
the long-term solutions to the chronic effects of 4. Biorepository Core: The Biorepository Core is
TBI. The Coordinating Center at VCU insures located at the Uniformed Services University
776 Chronic Effects of Neurotrauma Consortium

of the Health Sciences (USUHS) led by Drs. Edition highlighting eleven CENC-related articles
Brian Cox and Kimbra Kenney. The and a preface by Consortium Director David X.
Biorepository Core manages the storage and Cifu, M.D.
processing of blood and saliva samples col- CENC actively participates in national and
lected through all CENC protocols. Blood international neuropsychological specialty initia-
samples consist of plasma, serum, and cells, tives revolving around the science and research of
which will be processed to extract DNA and mild traumatic brain injury.
other biomarkers. These biological fluids
will be catalogued, tracked, and stored at
80  C in a dedicated biorepository facility Major Activities
maintained by Center for Neuroscience and
Regenerative Medicine (CNRM) at USUHS. CENC holds an annual conference during which
The Core will administer requests for use of the entire Consortium assembles to share in a
these biological samples from investigators public forum of what has been accomplished in
inside or outside the CENC, according to the the past year and to discuss relevant topics likely
data and sample sharing policies of the to be encountered in the future.
Consortium. CENC leaders and selected principal investi-
5. Biostatistics [B], Data Management [DM], gators present current study status and Consor-
and Study Management [SM] Core: The tium updates on a quarterly basis to the
Biostatistics, Data Management, and Study Government Steering Committee (GSC). The
Management Core (BDMSM) is operated by GSC is a DoD/VA-appointed and DoD/VA-
RTI International and led by Dr. Rick Williams. chaired steering committee that provides over-
The Biostatistics Core provides analytic exper- sight to the CENC. The GSC is co-chaired by
tise and statistical programming support for DoD and VA representatives and comprises gov-
CENC-supported studies. This support includes ernment representatives as well as non-DoD and
study design and protocol development, ongo- VA subject matter experts. The GSC is the overall
ing study monitoring, data analysis, reporting, main governing and management body and the
harmonization with the Federal Interagency committee through which the DoD and VA inter-
Traumatic Brain Injury Research (FITBIR) act and collaborate with the CENC.
informatics system, and manuscript develop- CENC conducts a biannual Consumer Advi-
ment of basic science, preclinical, translational, sory Board (CAB). The mission of the CAB is to
and observational studies as well as randomized advise and make nonbinding recommendations to
clinical trials. It also securely maintains all the leaders of CENC. The members of the board
CENC-collected data, oversees the clinical mon- are selected due to their awareness of mTBI and to
itoring of research sites, and interacts with the provide valuable input in the planning and con-
clinical research coordinators from the study duct of the studies.
sites to expedite and guide clinical protocols
through regulatory approval processes and coor-
dinates patient accrual and study activities across
sites. References and Readings

Akin, F., et al. (2016). Vestibular, balance, microvascular,

and white matter neuroimaging characteristics of blast
Landmark Contributions injuries: Four case reports. CENC Special Issue of Brain
Injury, 30, 1501–1514.
Brain Injury, the peer-reviewed, official Cifu, D. X., Diaz-Arrastia, R., Williams, R. L., Carne, W.,
West, S. L., McDougal, M., & Dixon, K. (2015). The
research journal of the International Brain Injury VA/DoD chronic effects of neurotrauma consortium: An
Association (IBIA), published a CENC Special overview at year 1. Federal Practitioner, 32(8), 70–74.
Chronic Fatigue Syndrome 777

Davenport, N. D., Lamberty, G. J., Nelson, N. W., Lim, K.

O., Armstrong, M. T., & Sponheim, S. R. (2016). PTSD Chronic Fatigue Syndrome
confounds detection of compromised cerebral white
matter integrity in military veterans reporting a history
of mild traumatic brain injury. CENC Special Issue Gudrun Lange
of Brain Injury, 30, 1491–1500. Pain and Fatigue Study Center, New York,
https://cenc.rti.org/ NY, USA
Jurick, S. M., Bangen, K. J., Evangelista, N. D.,
Sanderson-Cimino, M., Delano-Wood, L., & Jak, A. Mount Sinai Beth Israel Medical Center, C
J. (2016). Advanced neuroimaging to quantify myelin New York, NY, USA
in vivo – application to mild TBI. CENC Special issue
of Brain Injury, 30, 1452–1457.
Lynch, C. E., Crynen, G., Ferguson, S., Mouzon, B., Paris,
D., Ojo, J., Leary, P., Crawford, F., & Bachmeier, C. Synonyms
(2016). Chronic cerebrovascular abnormalities in a
mouse model of repetitive mild traumatic brain injury. Chronic fatigue immune deficiency syndrome
CENC Special Issue of Brain Injury, 30, 1414–1427. (CFIDS); Medically unexplained symptoms
Pugh, M. J., Finley, E. P., Wang, C. P., Copeland, L. A.,
Jaramillo, C. A., Swan, A. A., Elnitsky, C. A., Leykum, (MUS); Myalgic Encephomyelitis (ME); Post-
L. K., Mortensen, E. M., Eapen, B. A., Noel, P. H., infectious fatigue syndrome (PFIS); Myalgic
Pugh, J. A., & the TRACC Research Team. (2016). A Encephomyelitis/Chronic Fatigue Syndrome
retrospective cohort study of comorbidity trajectories (ME/CFS); Systemic Exertion Intolerance Dis-
associated with traumatic brain injury in veterans of the
Iraq and Afghanistan wars. CENC Special Issue ease (SEID). Nomenclature used by patients or
of Brain Injury, 30, 1481–1490. healthcare providers is generally based on their
Stone, J. R., Wilde, E. A., Taylor, B. A., Tate, D. F., Levin, etiologic perspective.
H., Bigler, E. D., Scheibel, R. S., Newsome, M. R.,
Mayer, A. R., Abildskov, T., Black, G. M., Lennon, M.
J., York, G. E., Agarwal, R., DeVillasante, J., Ritter, J.
L., Walker, P. B., Ahlers, S. T., & Tustison, N. J. (2016). Short Description or Definition
Supervised learning technique for the automated iden-
tification of white matter hyperintensities in traumatic
brain injury. CENC Special Issue of Brain Injury, 30, Chronic fatigue syndrome is a complex illness
1458–1468. defined by unexplained disabling fatigue and a
Tzekov, R., Pifer, J., Myers, A., Mouzon, B., & Crawford, combination of nonspecific accompanying
F. (2016). Inflammatory changes in optic nerve after
symptoms that can have sudden or gradual
close-head repeated traumatic brain injury. CENC Spe-
cial Issue of Brain Injury, 30, 1428–1435. onset. The diagnosis of the condition was ini-
Uchendu, U. S., Omalu, B. I., Cifu, D. X., & Egede, L. E. tially defined by the Centers for Disease Control
(2016). Repeated concussions: time to spur action (CDC) study group (Holmes et al. 1988); they
among vulnerable veterans. American Journal of Pub-
named the condition chronic fatigue syndrome
lic Health, 106(8), 1366–1368.
Walker, W. C., Carne, W., Franke, L. M., Nolen, T., (CFS). In subsequent years, case definitions for
Dikmen, S. D., Cifu, D. X., Wilson, K., Belanger, H., CFS were created in Australia, Great Britain
Williams, R., & the CENC Observational Study Group. (Sharpe et al. 1991; Wessely 1995), and Canada
(2016). The Chronic effects of neurotrauma consortium
(Carruthers et al. 2003), and a pediatric case
(CENC) observational study: Description of study and
characteristics of early participants. CENC Special definition for ME/CFS was published in 2006
Issue of Brain Injury, 30, 1469–1480. (Jason et al. 2006). Currently, the most common
Wilde, E. A., Bigler, E. D., Huff, T., Wang, H., Black, G. case definition used in the United States for the
M., Christensen, Z., Goodrich-Hunsaker, N., Petrie, J.,
clinical diagnosis of CFS is a version of the
CENC Neuroimaging Core Investigators including,
Abildskov, T., Taylor, B. A., Stone, J. R., Tustison, N. original 1988 CDC case definition revised in
J., Newsome, M. R., Levin, H. S., Chu, Z. D., York, G. 1994 by an International CFS Study Group
E., & Tate, D. F. (2016). Quantitative structural neuro- (Fukuda et al. 1994) as described below:.
imaging of mild traumatic brain injury in the chronic
The diagnosis of CFS cannot be made if the
effects of neurotrauma consortium (CENC): Compari-
son of volumetric data within and across scanners. following are present and could account for the
CENC Special Issue of Brain Injury, 30, 1442–1451. presence of persistent fatigue:
778 Chronic Fatigue Syndrome

1. Permanent medical exclusions include organ accompanying redness or swelling, headaches

failure, chronic infections, rheumatic and of a new type, unrefreshing sleep, post-exer-
chronic inflammatory diseases, major neuro- tional malaise lasting more than 24 h.
logic diseases requiring systemic treatment,
major endocrine diseases, and primary sleep These symptoms are nonspecific and variable in
disorders; both nature and severity over time. They were
2. Temporary medical exclusions include treat- selected on the basis of consensus clinical opinion
able conditions that require evaluation over and were not identified empirically.
time to determine the extent to which they Most recently, the Institute of Medicine (IOM)
contribute to the fatiguing illness such as con- was tasked to re-evaluate research available
ditions discovered at onset or initial evaluation addressing ME/CFS. In their publication:
(e.g., effects of medications, sleep deprivation, “Beyond Myalgic Encephalomyelitis/Chronic
untreated hypothyroidism, untreated or unsta- Fatigue Syndrome: Redefining an Illness”
ble diabetes mellitus, active infection), condi- (2015), the IOM proposes a revised set of diag-
tions that resolve (e.g., pregnancy), cardiac nostic criteria and a new name for the illness.
conditions, and morbid obesity specified as Taken from the IOM report, “the proposed
BMI >45; Diagnostic Criteria for ME/CFS Diagnosis requires
3. Permanent psychiatric exclusions include life- that the patient have the following three symptoms:
time diagnoses of bipolar affective disorders,
schizophrenia of any subtype, delusional dis- 1. A substantial reduction or impairment in the
orders of any subtype, dementias of any sub- ability to engage in preillness levels of occupa-
type, organic brain disorders, and alcohol or tional, educational, social, or personal activities,
substance abuse within 2 years before onset of that persists for more than 6 months and is
the fatiguing illness, any past or current diag- accompanied by fatigue, which is often pro-
nosis of major depressive disorder with psy- found, is of new or definite onset (not lifelong),
chotic or melancholic features, anorexia is not the result of ongoing excessive exertion,
nervosa, or bulimia. and is not substantially alleviated by rest,
2. Post-exertional malaise,
If none of the exclusions apply, using the 1994 3. Unrefreshing sleep At least one of the two
case definition, CFS is diagnosed based on the following manifestations is also required:
following criteria:
1. Cognitive impairment or 2. Orthostatic
1. Fatigue is of new or definite onset, not due to intolerance Frequency and severity of symptoms
exertion, not relieved by rest, and must result in should be assessed.
substantial reductions in previous levels of The diagnosis of ME/CFS should be
educational, occupational, social, or personal questioned if patients do not have these symptoms
activities, at least half of the time with moderate, substantial,
2. Fatigue is of at least 6 months duration, and or severe intensity”. (IOM 2015).
3. Concurrent with at least four of the following The committee also felt that the current name
eight symptoms that could not have predated the of the illness ME/CFS does not capture a “central
onset of fatigue: impairment in short-term mem- characteristic of the disease: the fact that exertion
ory or concentration severe enough to result in of any sort – physical, cognitive, or emotional –
substantial reductions in previous levels of can adversely affect patients in many organ sys-
educational, occupational, social, or personal tems and in many aspects of their lives.” Thus,
activities, painful lymph nodes in front or back they proposed that the name “systemic exertion
of the neck or under the arms, sore throat, mus- intolerance disease, or SEID” be used for the
cle pain, pain in more than one joint without illness.
Chronic Fatigue Syndrome 779

Categorization dysfunction or abnormalities within the central

nervous system (CNS). Abnormalities identified
Only a small percentage of patients complaining of in individuals with CFS include hypothalamic-
fatigue will be categorized as having CFS. Most pituitary-adrenal axis dysfunction, cortisol
patients either have prolonged fatigue, defined as dysregulation, small white matter lesions in the
self-reported, persistent fatigue of 1 month or lon- frontal regions of the brain, and orthostatic and
ger, or chronic fatigue defined as self-reported per- cognitive dysfunction. Most abnormalities are C
sistent or relapsing fatigue of six or more found in CFS patients who do not suffer from
consecutive months (Fukuda et al. 1994). Other comorbid psychiatric disorder, most commonly
conditions of unexplained etiology with similar depression. Treatments, especially cognitive
symptom profiles are often comorbid with CFS behavioral and graded exercise treatments,
and can include fibromyalgia syndrome (FMS), enhance the prognosis for improvement. If
temporomandibular syndrome (TMS), irritable untreated, complete recovery from CFS is rare.
bowel syndrome (IBS), multiple chemical sensitiv-
ity (MCS), gulf war syndrome (GWS), major
depressive disorder (MDD), and anxiety disorders. Neuropsychology and Psychology of
Chronic Fatigue Syndrome

Epidemiology CFS patients typically complain of difficulties

with concentration, memory, and thinking, yet
In the United States, CFS occurs in up to about neuropsychological testing does not generally
0.5% of the general population. It is most com- confirm the reported cognitive dysfunction
monly found in middle-aged women and is most (Cockshell and Mathias 2014). Available data
common in Latinos, followed by African Ameri- suggest that the main cognitive deficit in individ-
cans, and Whites. The illness affects women (pre- uals with CFS is slowed information processing,
dominantly between the ages of 40 and 59) more which can affect memory as well as executive
often than men (Reyes et al. 2003). In general, the function. Depression is a very common comorbid
expression of the syndrome is not gender-specific condition (Tiersky et al. 1997; IOM Report 2015).
(Buchwald et al. 1994). Chronic fatigue syndrome Neuroimaging data increasingly provide evidence
can also occur in children and adolescents. While for decreased cerebral blood flow and functional
gender distribution is similar to that of adults, activation of brain areas suggesting increased cog-
prevalence rates are significantly lower. nitive effort (Lange et al. 1998, 2005; Cook et al.
2007).

Natural History, Prognostic Factors, and

Outcomes Evaluation

Disorders with similar symptom profiles have A neuropsychological testing battery for individ-
been described for at least two centuries and uals with CFS should include measures of overall
have been known under a variety of names includ- current and premorbid cognitive function (i.e.,
ing neurasthenia, Akureyri disease, Epstein-Barr Test of Premorbid Function, Wechsler Adult Intel-
syndrome, and chronic mononucleosis. Although ligence Scale IV), simple and complex attention,
many hypotheses exist about the causes for CFS, as well as information processing and working
the etiology of the condition is still unclear. Some memory (i.e., Continuous Performance Test, Gor-
believe that CFS is a latent form of depression and don Diagnostic System, Trails, Paced Auditory
anxiety disorder, while others view the syndrome Serial Addition Test), executive function (i.e.,
as a sleep disorder, attribute it to endocrine subtests of Delis-Kaplan Executive Function
780 Chronic Fatigue Syndrome

System including verbal fluency, towers test; Wis- CFS-defining symptoms reflect pain (headaches
consin Card Sort Test), memory (i.e., Wechsler of a new type, pattern, or severity, muscle pain,
Memory Scale IV, California Verbal Learning and multi-joint pain without swelling or redness,
Test II, Rey Osterrieth Complex Figure Test), sore throat, tender cervical/axillary lymph
language function (i.e., Boston Naming Test), nodes). In many cases, pain may be the primary
visual-perceptual function (i.e., Judgment of determinant of disability for some individuals
Line Orientation, Hooper), and motor function with CFS. The McGill Pain Questionnaire
(i.e., grip strength, finger tapping, pegboard). It (MPQ) is a well-validated questionnaire that
is also recommended to test the level of motiva- can be used to further characterize pain or follow
tion and effort expanded during neuropsycholog- the course of pain in CFS (Melzack 1975). The
ical testing (Validity Indicator Profile) as well as MPQ includes four components: (1) a human
emotional functioning (Beck Depression Scale II, figure drawing on which patients are asked to
State Trait Anxiety Inventory, MINI International mark the location of their pain; (2) a series of
Neuropsychiatric Interview 6.0) to improve inter- adjectives divided into groups from which
pretability of test results. patients identify their experience by circling
When an individual is diagnosed with CFS, it word descriptors; (3) questions about prior pain
may be desirable to evaluate the intensity and experience, pain location, and information on the
severity of symptoms associated with CFS use of pain medication; and (4) a present pain
using self-report questionnaires (IOM report intensity index.
2015). To assess fatigue intensity, several mea-
sures have been used including the Chalder
Fatigue Scale and the Krupp Fatigue Scale; Treatment
both have acceptable psychometric properties.
The Chalder Fatigue Scale is a 14-item instru- Effective treatment needs to be tailored to each
ment with a four-choice format and separates individual diagnosed with CFS and often consists
mental and physical fatigue (Chalder et al. of a combination of behavioral, pharmacological,
1993). The Krupp Fatigue Severity Scale and physical interventions. Behavior modification
includes nine items rated on seven-point scales or cognitive restructuring are two cognitive
and is sensitive to different aspects and grada- behavioral therapy (CBT) approaches used to
tions of fatigue severity. Most items in the Krupp treat CFS. Using this modality, reductions in the
scale are related to behavioral consequences of effect of fatigue on functional ability and quality
fatigue (Krupp et al. 1989). The Checklist Indi- of life have been shown in CFS (Kroenke et al.
vidual Strength (CIS) is a 20-item inventory with 2000). Medication management of fatigue is in its
four subscales commonly used to measure infancy; presently, there is no FDA-approved drug
fatigue severity, concentration, reduced motiva- for fatigue. Over the counter medications offer a
tion, and physical activity. The CIS focuses on first-line of therapeutic possibilities. Stronger
fatigue over the preceding 2 weeks (Vercoulen et medications, including stimulants and antidepres-
al. 1994). Another commonly used instrument to sants, require a physician’s prescription. In gen-
measure fatigue severity is the Multidimensional eral, medications used to treat depression, anxiety,
Fatigue Inventory, also a 20-item questionnaire and pain are very often used for the pharmacologic
providing scores for severity of general treatment of CFS. It is important to recognize that
fatigue, physical fatigue, mental fatigue, as fatigue is not solely due to disease processes but
well as reduced motivation and activity (Smets can occur as an indirect consequence of decreased
et al. 1995). physical activity and conditioning. Graded aero-
Another symptom that might warrant addi- bic exercise training is a safe and effective treat-
tional investigation is pain. Five of the eight ment for CFS and has been shown to improve
Chronic Fatigue Syndrome 781

quality of life. The primary goal of exercise is to Holmes, G. P., Kaplan, J. E., Gantz, N. M., Komaroff, A.
avoid the spiral of deconditioning that is common L., Schonberger, L. B., Straus, S. E., et al. (1988).
Chronic fatigue syndrome: A working case definition.
in most fatiguing diseases. Annals of Internal Medicine, 108, 387–389.
IOM Report. (2015). Review of the evidence on major ME/
CFS symptoms and manifestations. In Beyond myalgic
encephalomyelitis/chronic fatigue syndrome:
Cross-References Redefining an illness. Washington, DC: National Acad-
C
emy Press.
Jason, L. A., Bell, D. S., Rowe, M. D., van Hoof, E. L. S. J.
▶ Epstein-Barr Virus
K., Lapp, C., et al. (2006). A pediatric case definition
▶ Gulf War Syndrome for myalgic encephalomyelitis and chronic fatigue syn-
▶ Neurasthenia drome. Journal of Chronic Fatigue Syndrome, 13,
▶ Unexplained Illness 1–44.
Kroenke, K., Taylor-Vaisey, A., Dietrich, A. J., & Oxman,
T. E. (2000). Interventions to improve provider diag-
nosis and treatment of mental disorders in primary care.
References and Readings A critical review of the literature. Psychosomatics, 41,
39–52.
Buchwald, D., Pearlman, T., Kith, P., & Schmaling, K. Krupp, L. B., LaRocca, N. G., Muir-Nash, J., & Steinberg,
(1994). Gender differences in patients with chronic A. D. (1989). The fatigue severity scale. Application to
fatigue syndrome. Journal of General International patients with multiple sclerosis and systemic lupus
Medicine, 9, 397–401. erythematosus. Archives of Neurology, 46, 1121–1123.
Carruthers, B. M., Jain, A. K., De Meirleir, K. L., Peterson, Lange, G., Wang, S., Deluca, J., & Natelson, B. H. (1998).
D. L., Klimas, N. G., Lerner, A. M., et al. (2003). Neuroimaging in chronic fatigue syndrome. American
Myalgic encephalomyelitis/chronic fatigue syndrome: Journal of Medicine, 105, 50S–53S.
Clinical working case definition, Diagnostic and treat- Lange, G., Steffener, J., Cook, D. B., Bly, B. M.,
ment protocols. Journal of Chronic Fatigue Syndrome, Christodoulou, C., Liu, W. C., et al. (2005). Objective
11, 7–115. evidence of cognitive complaints in chronic fatigue
Chalder, T., Berelowitz, G., Pawlikowska, T., Watts, L., syndrome: A BOLD fMRI study of verbal working
Wessely, S., Wright, D., et al. (1993). Development of a memory. NeuroImage, 26, 513–524.
fatigue scale. Journal of Psychosomatic Research, 37, Melzack, R. (1975). The McGill pain questionnaire: Major
147–153. properties and scoring methods. Pain, 1, 277–299.
Cockshell, S. J., & Mathias, J. L. (2012). Test effort in Reyes, M., Nisenbaum, R., Hoaglin, D. C., Unger, E. R.,
persons with chronic fatigue syndrome when assessed Emmons, C., Randall, B., et al. (2003). Prevalence and
using the validity indicator profile. Journal of Clinical incidence of chronic fatigue syndrome in Wichita, Kan-
and Experimental Neuropsychology, 34, 679–687. sas. Archives of Internal Medicine, 163, 1530–1536.
Cockshell, S. J., & Mathias, J. L. (2013). Cognitive deficits Sharpe, M. C., Archard, L. C., Banatvala, J. E.,
in chronic fatigue syndrome and their relationship to Borysiewicz, L. K., Clare, A. W., David, A., et al.
psychological status, symptomatology, and everyday (1991). A report – chronic fatigue syndrome: Guide-
functioning. Neuropsychology, 27, 230–242. lines for research. Journal of the Royal Society of
Cockshell, S. J., & Mathias, J. L. (2014). Cognitive func- Medicine, 84, 118–121.
tioning in people with chronic fatigue syndrome: A Smets, E. M., Garssen, B., Bonke, B., & De Haes, J. C.
comparison between subjective and objective mea- (1995). The Multidimensional Fatigue Inventory (MFI)
sures. Neuropsychology, 28(3), 394–405. psychometric qualities of an instrument to assess
Cook, D. B., O’Connor, P. J., Lange, G., & Steffener, J. fatigue. Journal of Psychosomatic Research, 39,
(2007). Functional neuroimaging correlates of mental 315–325.
fatigue induced by cognition among chronic fatigue Tiersky, L. A., Johnson, S. K., Lange, G., Natelson, B. H.,
syndrome patients and controls. NeuroImage, 36, & DeLuca, J. (1997). Neuropsychology of chronic
108–122. fatigue syndrome: A critical review. Journal of Clinical
DeLuca, J. (2008). Fatigue as a window to the brain. and Experimental Neuropsychology, 19, 560–586.
London: MIT Press. Vercoulen, J. H., Swanink, C. M., Fennis, J. F., Galama, J.
Fukuda, K., Straus, S. E., Hickie, I., Sharpe, M. C., Dobbins, M., Van der Meer, J. W., & Bleijenberg, G. (1994).
J. G., & Komaroff, A. (1994). The chronic fatigue syn- Dimensional assessment of chronic fatigue syndrome.
drome: A comprehensive approach to its definition and Journal of Psychosomatic Research, 38, 383–392.
study. International Chronic Fatigue Syndrome Study Wessely, S. (1995). The epidemiology of chronic fatigue
Group. Annals of Internal Medicine, 121, 953–959. syndrome. Epidemiological Review, 17, 139–151.
782 Chronic Obstructive Pulmonary Disease

volume in 1 s/forced vital capacity (FEV1/FVC

Chronic Obstructive ratio)) is required for clinical diagnosis of COPD.
Pulmonary Disease Classification of the severity of airflow limitation
in COPD ranges from GOLD 1/mild to GOLD
Elizabeth Kozora1 and Karin F. Hoth2 4/very severe. The current GOLD report defines
1
Department of Medicine, National Jewish grade of COPD (A, B, C, or D) based on a com-
Medical and Research Center, National Jewish bined COPD assessment including spirometric
Health, Denver, CO, USA classification, symptoms, breathlessness, and
2
Department of Medicine, University of Iowa, risk of exacerbations. Pathological changes in
Iowa City, IA, USA COPD are driven by a chronic inflammatory
response and include parenchymal tissue destruc-
tion (resulting in emphysema), changes to small
Synonyms airways, and alterations in the pulmonary vascu-
lature. Assessment of comorbidities is recognized
Chronic bronchitis; COPD; Emphysema as an important aspect of COPD management.
Common comorbidities include cardiovascular
disease, osteoporosis, anxiety and depression,
Short Description or Definition lung cancer, infections, metabolic syndrome and
diabetes, bronchiectasis, and impaired cognitive
The Global Initiative for Chronic Obstructive function. The January 2015 GOLD report noted
Lung Disease (GOLD) statement regarding the explicitly that impaired cognitive function is a
diagnosis, management, and prevention of feature of COPD and that the presence of COPD
COPD (GOLD 2015) defines COPD as a disease increases the risk of developing mild cognitive
that is “characterized by persistent airflow limi- impairment (GOLD 2015; Dodd et al. 2010;
tation that is usually progressive and associated Singh et al. 2014).
with an enhanced chronic inflammatory response
in the airways and the lung to noxious particles or
gases.” The definition includes the fact that exac- Epidemiology
erbations and comorbidities contribute to the
overall severity of disease in individual patients. COPD is the third leading cause of death in United
The GOLD initiative was organized by the States. Worldwide mortality from COPD is pre-
World Health Organization (WHO) and the US dicted to increase owing to the increased tobacco
National Heart Lung and Blood Institute consumption in third world countries, and COPD
(NHLBI) with the first GOLD report published mortality among women is increasing faster than
in 2001. The most recent GOLD report and mortality among men (Anthonisen and Manfred
additional information about definitions, diagno- 2004). The third National Health and Nutrition
sis, treatment, and research can be found at www. Examination Survey, conducted between 1988
goldcopd.com. and 1994, demonstrated that between 5% and
8% of the US population had COPD as defined
by physiological parameters (NHANES III). The
Categorization worldwide prevalence of COPD in 1990 was esti-
mated by the WHO/World Global Burden of Dis-
COPD has traditionally been defined by severity ease Study to be 9.34 per 1,000 in men and 7.33
of airflow limitation. Indeed, spirometry to obtain per 1,000 in women. In the United States, COPD
measures of airflow limitation (i.e., forced expira- death rates are low among people under the age of
tory volume in 1 s (FEV1) and forced expiratory 45 but increase with age.
Chronic Obstructive Pulmonary Disease 783

Natural History, Prognostic Factors, evidence that cognitive impairment has an inde-
Outcomes pendent impact on patients’ daily functioning,
medical regimen adherence, and quality of life,
COPD results from a gene-environment interac- although results have been mixed (McSweeny
tion. Only a subset of smokers ultimately develops and Labuhn 1996).
COPD depending in part upon their environmental Psychological changes and emotional distress
exposure, genetic predisposition, and how long have also been noted in COPD patients. To date, C
they live. Cigarette smoke is the most common depression and anxiety are the most commonly
and well-studied external risk factor, followed by observed psychological problems in COPD
pipe and cigar smoke, occupational dusts and (Hynninen et al. 2005) with estimates of the prev-
chemicals, history of severe childhood respiratory alence of depression ranging from approximately
infections, HIV infection, outdoor pollution, and 25–50%. Some of the discrepancies in prevalence
IV drug use. Host-related factors include airways estimates across studies may be related to differ-
hyperresponsiveness, genetic factors, severe hered- ences in the method used to assess depression. In
itary alpha1-antitrypsin deficiency, low birth addition to emotional distress, multiple studies
weight, and maternal cigarette smoking during have demonstrated poor quality of life in patients
gestation (Anthonisen and Manfred 2004). with COPD, which has been associated with
restrictions in daily activity, increased disease
severity, and impaired health status (Hopkins
Neuropsychology and Psychology and Bigler 2001; McSweeny and Labuhn 1996).
of COPD

Empirical studies have documented neuropsycho- Evaluation

logical (i.e., cognitive) deficits in patients with
chronic airway obstruction and COPD. Two of Neuropsychological evaluation for cognitive prob-
the largest studies conducted in the 1980s were lems associated with COPD typically involves
the Nocturnal Oxygen Therapy Trial (NOTT) and measurement of attention, learning and memory,
the Intermittent Positive Pressure Breathing Trial reasoning and executive functioning skills,
(Prigatano and Levin 1988). The pattern and extent visuomotor speed, and visuoperceptual function.
of cognitive dysfunction reported in COPD vary Psychological evaluation typically involves mea-
across patients and appear to be associated with sures of depression, anxiety, and health-related
disease severity. In COPD patients with moderate quality of life.
to severe hypoxemia, deficits have been identified
in simple motor movement and overall strength,
perceptual-motor integration, abstract reasoning, Treatment
attention to auditory stimuli, learning and memory,
and language skills. In patients with mild hypox- There is research to suggest that a variety of ther-
emia, impairments in higher cerebral functioning apeutic approaches utilized in COPD patients
include abstract reasoning, auditory and visual (including oxygen therapy, comprehensive rehabil-
attention, verbal and nonverbal learning and recall, itation programs, and surgical techniques) improve
and reasoning and motor skills (Kozora et al. 2008; psychological and cognitive functioning. Long-
Kozora and Hoth 2013). In a large review of COPD term (greater than 6 months) use of oxygen therapy
studies with and without hypoxemia, the correla- improves cognitive performance in COPD, proba-
tions between cognitive functions and degree of bly due to direct effects of improved oxygen deliv-
hypoxemia were less impressive and thought to ery to the central nervous system (Prigatano and
be inconsistent (Dodd 2010). There is some Levin 1988). Early studies reported improvement
784 Chronic Obstructive Pulmonary Disease

in visual memory, verbal memory, and motor speed and psychological status following comprehensive
among the COPD subjects following 6 months of rehabilitation with an exercise component. Many
continuous oxygen therapy. Large multisite studies studies have also reported increased quality of life
have also demonstrated benefits of oxygen for cog- following comprehensive rehabilitation (Make
nitive function in COPD. For example, in the Noc- 2004).
turnal Oxygen Therapy Trial, COPD patients Finally, studies have suggested some improve-
receiving continuous oxygen therapy for 12 months ment in cognition for moderate to severe COPD
experienced greater improvements in cognitive patients following lung volume reduction surgery
performance than did patients receiving only noc- (LVRS). In an ancillary study of the National
turnal oxygen therapy. Emphysema Treatment Trial (NETT), Kozora
There is also evidence suggesting that compre- and colleagues (Kozora et al. 2008) examined
hensive multidisciplinary rehabilitation programs neuropsychological and psychological function-
can improve cognitive functioning and psycho- ing of patients receiving LVRS when compared
logical status in emphysema patients. Compre- to patients receiving only medical therapy (MT).
hensive rehabilitation programs for treatment of The LVRS group showed significant improve-
COPD are well established and typically include ment compared to the MT group at 6 months on
assessment, education, instruction on respiration, a measure of psychomotor speed, delayed recall
psychosocial support, and exercise training with for verbal information, trends toward improved
the goal of restoring patients to the highest level of sequential thinking, and psychomotor speed and
independent function (Make 2004). As noted in a naming to confrontation. LVRS patients also
review article (Kozora et al. 2008), Emery and experienced significant reduction in depression
colleagues first reported in 1991 improved com- at 6 months, as reflected in total Beck Depression
plex attention in COPD patients following a Inventory score. There was no direct evidence that
30-day exercise rehabilitation program that improved cognition in LVRS was related to
included instructional/educational components, improved physical capacity (workload and 6 min
psychosocial counseling, and stress reduction. In walk) or pulmonary function. At 6 months we did
a subsequent study published in 1998, they report that the LVRS group had more improve-
reported improvement in verbal fluency and ment in cognitive function; however, over a
reduction in symptoms of anxiety and depression 3-year period, we did not find differences between
in a group participating in exercise, stress reduc- the two groups on a visuomotor sequencing task
tion, and education programs when compared to a (Kozora et al. 2010). Taken together, treatment
control group participating in stress reduction and studies provide some modest evidence for cogni-
education treatment only. This finding highlighted tive improvement, although currently the litera-
the utility of the exercise component toward ture does not enable firm conclusions on which to
improved cognitive and psychological functions. base treatment decisions.
In 2002, Kozora and colleagues also reported
improvement in visual attention and semantic flu-
ency, among COPD patients following a 3-week
Cross-References
comprehensive rehabilitation program when com-
pared to untreated COPD and healthy control sub-
▶ Anoxia
jects similar in age, education, and gender. This
program included exercise, educational, instruc-
tional, and psychosocial components. In addition
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Medical neuropsychology (2nd ed., pp. 247–266). The cingulate gyrus, first named by Burdach in
New York: Kluwer/Plenum.
Hynninen, K. M., Breitve, M. H., Wiborg, A. B., Pallesen,
1822, was combined with the anterior olfactory
S., & Nordhus, I. H. (2005). Psychological characteris- region and hippocampus by Broca to form the ring
tics of patients with chronic obstructive pulmonary of olfactory processing he termed the grand lobe
disease: A review. Journal of Psychosomatic Research, limbique. Anatomic studies revealed extensive
59(6), 429–443.
Kozora, E., & Hoth, K. F. (2013). Evaluating cognition in
connections between the anterior thalamus,
patients with chronic obstructive pulmonary disease. In known to be associated with the hippocampus
L. D. Ravdi & H. L. Katzen (Eds.), Handbook on the and hypothalamus, and the cingulate. In 1937,
neuropsychology of aging and dementia (pp. 455–466). Papez combined these anatomic results with the
New York: Springer.
Kozora, E., Emery, C., Kaplan, R. M., Wamboldt, F. S.,
clinical reports of emotional disturbances follow-
Zhang, L., & Make, B. J. (2008). Cognitive and psy- ing lesions to the cingulate and other limbic struc-
chological issues in emphysema. Proceedings of the tures to propose a mechanism of emotion based on
ATS, 5(4), 556–560. a limbic circuit. For Papez, the integration of
Kozora, E., Emery, C. F., Zhang, L., & Make, B. (2010).
Improved neurobehavioral functioning in emphysema
internal feelings and emotional responsiveness
patients following medical therapy. Journal of Cardio- with the functions of the lateral cerebral cortex
pulmonary Rehabilitiation, 34, 291–302. occurred in the cingulate. The limbic circuit of
Make, B. (2004). Pulmonary rehabilitation. In J. D. Crapo, Papez however did not find anatomical evidence
J. Glassroth, J. B. Karlinsky, & T. E. King (Eds.), Baum’s
textbook of pulmonary diseases (7th ed., pp. 289–307).
to support the closing connection of the cingulate
Philadelphia: Lippincott Williams and Wilkins. to the hippocampus until 1975, when Shipley and
McSweeny, A. J., & Labuhn, K. T. (1996). The relationship Sørensen documented that the presubiculum,
of neuropsychological functioning to health-related which receives a dense cingulate outflow, projects
quality of life in systemic medical disease: The exam-
ple of chronic obstructive pulmonary disease. In
heavily to layer III of the entorhinal cortex – the
I. Grant & K. M. Adams (Eds.), Neuropsychological origin of the perforant pathway into hippocampal
assessment of neuropsychiatric disorders pyramidal cells.
(pp. 577–602). New York: Oxford University Press. Understanding the function of the cingulate in
Prigatano, G. P., & Levin, D. C. (1988). Pulmonary system.
In R. E. Tarter, D. H. Van Theiel, & K. L. Edwards (Eds.),
the integration of internal feelings and emotional
Medical neuropsychology (pp. 11–26). New York: responsiveness with movement and thought
Plenum. begins with an appreciation of its cytoarch-
Singh, B., Mielke, M. M., Parsaik, A. K., Cha, R. H., itecture. Brodmann’s original cytoarchitectonic
Roberts, R. O., Scanlon, P. D., et al. (2014).
A prospective study of chronic obstructive pulmonary
separation of anterior and posterior cingulate
disease and the risk for mild cognitive impairment. cortex into areas 24 and 23 based upon the pres-
JAMA Neurology, 71(5), 581–588. ence of agranular cortex in area 24 contrasted
786 Cingulate Gyrus

with the granular cortex of area 23 has been Appreciating that the major reciprocal connec-
refined by more accurate studies of the progres- tions between the orbitofrontal trends are with
sive cytoarchitectonic elaboration in the ventral the anterior cingulate, while the hippocampal
to dorsal direction. Two main centers of iso- trends are with the posterior cingulate, will assist
cortical development can be traced phylogeneti- the understanding of cingulate function.
cally and through cytoarchitectonic progression. Three anterior effector regions and a posterior
These two developmental trends, termed para- processing region also emerge through a review of
limbic belts, are transitional cortical zones from the efferent and afferent connections of the cingu-
less-differentiated allocortex to more-differenti- late. The three anterior regions include a visceral
ated isocortex with two functional centers: the effector region inferior to the genu of the corpus
more rostral olfactory piriform paleocortex callosum encompassing area 25, the anterior sub-
unites the orbitofrontal, insular, and callosal portions of 24a-b, and 32; a cognitive effec-
temporopolar regions, while the more caudal tor region, which includes most of the supra-
archicortex of the hippocampus provides the callosal area 24, and areas 24a0 -b0 and 320 ; and a
nidus for developmental spread through para- skeletomotor effector region within the depths of the
hippocampal and entorhinal regions into the pos- cingulate sulcus that includes areas 24c0 /23c on the
terior cingulate. Both paralimbic belts reflect a ventral bank, with 24c0 g and 6c on the dorsal bank.
different emphasis within the cingulate (Fig. 1). These three cingulate effector regions integrate
The orbitofrontal-centered belt processes the ascending input concerning the internal milieu of
internal affective state of the organism. The the organism with visceral motor systems, cogni-
more recent hippocampal-centered belt is the tive-attentional networks, and skeletomotor centers
externally directed evaluative arm of the limbic to produce the affective motivation necessary for
system. the organism’s engagement in the environment. The
Both work in concert, enabling the selection of posterior sensory processing region (areas 23a-b
environmental stimuli based on the internal rele- and 29/30) assists in the memory and processing
vance those stimuli have for the organism. of environmental stimuli targeted as relevant to the
Although both areas 24 and 32 are part of the organism based on their motivational valence. The
hippocampal belt, the more rostral connections following sections will explore the connections of
of area 24 contrast with the more caudal sensory these four cingulate regions (Figs. 2 and 3) and their
connections of area 23, distinguishing the anterior function as observed from electrical stimulation,
executive from the posterior evaluative cingulate. imaging, and clinical data.

Cingulate Gyrus,
Fig. 1 The orbitofrontal
(red) and hippocampal
(blue) paralimbic trends
Cingulate Gyrus 787

Cingulate Gyrus,
Fig. 2 Cytoarchitectonic
divisions of the cingulate
and adjacent areas

Cingulate Gyrus,
Fig. 3 The four functional
divisions of the cingulate.
The visceral effector region
1, the cognitive effector
region 2, the skeletomotor
effector region 3, and the
posterior cingulate 4

Function from their amygdalar connections that convey

the visceral state of the organism to paralimbic
Visceral effector region. Major reciprocal connec- areas. The orbitofrontal cortex mediates empathic,
tions with the visceral effector region are with the civil, and socially appropriate behavior. Rostral
basal and accessory basal amygdala, medial auditory association cortex in the superior tempo-
orbitofrontal cortex areas 11, 12, and 13, anterior ral area also provides auditory information to the
superior temporal pole area 38, and the anterior visceral effector region. No visual information has
ventral claustrum. Major nonreciprocal projec- direct access to the subcallosal area.
tions from the visceral effector region target the The dorsolateral prefrontal lobe, functioning as
parasympathetic nucleus of the solitary tract, the an “executive processor,” provides nonreciprocal
sympathetic thoracic intermediolateral column, input from areas 9 and 46 to the subcallosal ante-
the dorsal motor nucleus of the vagus, and the rior cingulate region. Executive functions permit
nucleus accumbens/olfactory tubercle of the ven- an organized behavioral response to solve a com-
tral striatum. plex problem. This includes the activation of
Brain areas that have reciprocal connections remote memories, self-direction, and indepen-
with the visceral effector region, except the claus- dence from environmental contingencies, shifting
trum that supplies auditory input, also influence and maintaining behavioral sets appropriately,
visceral function when stimulated. This results generating motor programs, and using verbal
788 Cingulate Gyrus

skills to guide behavior. Dorsolateral prefrontal areas 8, 9, 10, and 46 devoted to executive func-
efferents into the subcallosal cingulate provide tion. The amygdala provides internal affective
feedback inhibition on the basic drives of hunger, input to the supracallosal anterior cingulate. The
aggression, and reproductive urges. Table 1 for a distribution of amygdala efferents delineates the
summary of these anatomic connections. dorsal boundary of the cingulate as a functional
Subcallosal cingulate processing modulates system. Auditory input arises from the anterior
visceral output from brain-stem sympathetic and medial claustrum as well as a minor link with the
parasympathetic centers. Access to the basal auditory association area of the superior temporal
ganglia, via the ventral striatum, allows pro- gyrus. The rostral insula and anterior para-
cessing of the internal milieu of the organism to hippocampal areas provide additional reciprocal
influence the skeletal motor system as well. This connections with the cognitive effector region not
visceral motor network encompasses the bulk of associated with the subcallosal region. Rostral
the orbitofrontal-centered paralimbic belt dedi- insular cortex is a transitional paralimbic region
cated to assessing the emotional valence of that integrates visceral alimentary input with
objects based upon internal motivating drives. olfactory and gustatory afferents. Connections
Patients with lesions in this area are often with the anterior parahippocampal areas 35 and
disinhibited with irritability, lability, tactlessness, 36 allow the supracallosal cingulate to influence
and fatuous euphoria. Patients act upon visceral multimodal sensory afferents entering the
drives without regard to social decorum. hippocampus.
Cognitive effector region. Major reciprocal Major nonreciprocal projections of the supra-
connections with the cognitive effector region callosal anterior cingulate include the auditory
are with the basal amygdala, prefrontal areas 8, association cortex of anterior superior temporal
9, 10, and 46, caudal orbitofrontal area 12, inferior area 22, allowing the cognitive effector region to
temporal pole area 38, rostral insula, anterior para- influence language and the access of semantic
hippocampal areas 35 and 36, and the anterior stores. The posterior parietal area 7a and the
medial claustrum. Areas reciprocally connected dorsomedial head of the caudate are also targets.
to the cognitive effector region share a general Parietal area 7a is the sensory component in the
similarity with the subcallosal anterior region extrapersonal attentional network linked with the
underscoring their common membership in the dorsolateral prefrontal “executive system.” The
orbitofrontal paralimbic belt. The cognitive effec- head of the caudate is also a target of this execu-
tor region is more developed in its cytoarch- tive prefrontal cortex. Cingulate input to the cau-
itecture, than the subcallosal cingulate, and thus date assists in the initiation of vocalization
has stronger connections with more phylogeneti- behavior as well as executive function. Emotional
cally recent neocortex of dorsolateral prefrontal vocalizations occurring during stimulation in
monkeys requires intact cingulate efferents to the
Cingulate Gyrus, Table 1 Major reciprocal connections periaqueductal gray that produce similar behav-
and nonreciprocal targets for the visceral effector region of iors when stimulated. The most caudal amygdalar
the cingulate cortex projections to 24c, extending into anterior 24c0 ,
Reciprocal connections innervate a face representation region that may
Basal and accessory basal amygdala have direct connections with the facial nucleus
Medial orbitofrontal areas 11, 12, and 13 in the pons. Efferents to the dorsomedial pons
Superior temporal pole area 38 provide cingulate influence on the reticular acti-
Anterior ventral claustrum vating system and its control over arousal. Table 2
Nonreciprocal targets for a summary of these anatomic connections.
Parasympathetic nucleus of solitary tract Skeletomotor effector region. Major reciprocal
Sympathetic intermediolateral column connections with the skeletomotor effector region
Dorsal motor nucleus of the vagus are with the primary and supplementary/premotor
Nucleus accumbens and olfactory tubercle
motor cortex areas 4 and 6, prefrontal areas 8, 9,
Cingulate Gyrus 789

Cingulate Gyrus, Table 2 Major reciprocal connections Cingulate Gyrus, Table 3 Major reciprocal connections
and nonreciprocal targets for the cognitive effector region and nonreciprocal targets for the skeletomotor effector
of the cingulate cortex region of the cingulate cortex
Reciprocal connections Reciprocal connections
Basal amygdale Primary motor area 4
Prefrontal areas 8, 9, 10, and 46 Supplementary motor area 6
Caudal orbitofrontal cortex area 12 Prefrontal areas 8, 9, and 46 C
Inferior temporal pole area 38 Parietal areas 1, 2, 3a, 5, and 7b
Rostral insula Caudal insula
Anterior parahippocampal areas 35 and 36 Nonreciprocal targets
Anterior medial claustrum Lateral putamen
Nonreciprocal targets Spinal cord
Anterior superior temporal area 22 Red nucleus
Parietal area 7a Ventrolateral pontine gray matter
Dorsomedial head and body of caudate
Periaqueductal gray
Dorsomedial pontine gray matter neurons are found in the cingulate than are found
in the supplementary motor cortex, and the cingu-
late has about 40% of the amount found in pri-
and 46, parietal areas 1, 2, 3a, 5, and 7b, and mary motor cortex. Table 3 for a summary of these
caudal insula. Major nonreciprocal projections anatomic connections.
from the skeletomotor area target the lateral puta- Sensory processing region. Major reciprocal
men, spinal cord, ventromedial parvocellular divi- connections with the sensory processing region
sion of the red nucleus, and the ventrolateral are with caudal parietal area 7a, frontal eye fields
pontine gray matter. area 8, posterior perirhinal area 35, presubiculum,
Primary motor cortex has very limited input. posterior parahippocampal area 36, prefrontal
The medial supplementary, lateral premotor, and area 46, and the ventral caudal claustrum. Major
cingulate skeletal motor regions are the only fore- nonreciprocal projections from the sensory pro-
brain inputs to the primary motor cortex. The cessing region target the dorsal caudate, posterior
skeletomotor region in the banks of the cingulate superior temporal gyrus area 22, and orbitofrontal
sulcus conveys limbic influence to the medial area 11. These regions are shown in Table 4.
supplementary, lateral premotor, and primary The posterior granular sensory cortices are dis-
motor cortex. Frontal eye fields in area 8 also tinguished from the anterior agranular executive
share reciprocal connections with the skeletal cortices. The posterior cingulate, with its promi-
motor effector region. Areas 9 and 46 of the dor- nent granular layer IV, is dedicated to visuospatial
solateral prefrontal cortex contribute executive and memory processing. Major reciprocal con-
input to the limbic motor system. Thus, executive nections are with the dorsal visual system of the
and limbic systems gain access to primary motor inferior parietal lobe dedicated to spatial pro-
area 4 indirectly. The cingulate skeletal motor cessing and with the frontal eye fields in area 8.
region receives the greatest outflow from execu- Reciprocal connections with lateral prefrontal
tive prefrontal cortex than all other motor cortices area 46 allow an interaction between executive
underscoring its influence over goal-directed and sensory/mnemonic processing, which may
behavior. Sensory-motor parietal areas 1, 2, 3a, mediate perceptual working memory tasks. Pos-
and 5 also have reciprocal connections with the terior parahippocampal and perirhinal areas 36
skeletal motor center within the banks of the cin- and 35, as well as the presubiculum, are recipro-
gulate sulcus. The rostral parietal area 7b has a cally connected to the sensory processing region
strong relationship with the premotor cortex, of the posterior cingulate. These connections
while the granular cortex of the caudal insula is a modulate the multimodal efferents entering the
somatosensory limbic region. More corticospinal entorhinal layer III cells that form the perforant
790 Cingulate Gyrus

Cingulate Gyrus, Table 4 Major reciprocal connections stimulation of primary motor cortex, which can-
and nonreciprocal targets for the sensory processing region not be controlled, respiratory arrest from cingulate
of the cingulate cortex
stimulation can be overcome volitionally
Reciprocal connections (Penfield and Jasper 1954). Automatic behaviors
Caudal parietal area 7 noted include unilateral and bilateral movements
Frontal eye fields area 8
and repetitive “tic-like” movements of the hands,
Prefrontal area 46
lips, or tongue. These movements can also be
Posterior parahippocampal areas 35 and 36
consciously suppressed; implicating the cingulate
Presubiculum
as an “unconscious” effector supports its role in
Ventral caudal claustrum
Nonreciprocal targets
the pathophysiology of obsessive-compulsive dis-
Dorsal caudate order (behaviors that respond well to
Posterior superior temporal area 22 cingulotomy). Fear, pleasure, agitation, euphoria,
Orbitofrontal area 11 and a sense of well being – affective phenomena
also common after limbic stimulation – have been
reported (Meyer et al. 1973). Involuntary vocali-
pathway into the hippocampus. Feedback from zations and speech arrests are less common in
these areas to the cingulate provides highly pro- humans than in animals with stimulation of areas
cessed sensory information, and the ventral visual 32, 24, and the rostral part of 25 (Vogt and Barbas
system involved in feature analysis can influence 1988).
the posterior cingulate through these connections. Functional activation of the cingulate. In func-
Although in cats dorsal caudal claustrum is related tional activation studies, the cognitive effector
to visual processing, while the ventral caudal claus- region of the anterior cingulate is activated when
trum receives auditory input, it is possible that in sustained attention to novel tasks is required.
primates visual information may reach the posterior Tasks spanning motor, language, memory, and
cingulate via the ventral caudal claustrum. visuospatial paradigms all produce supracallosal
The nonreciprocal targets of the posterior sen- anterior cingulate activation. When memory
sory processing region include the dorsal caudate encoding is combined with a motor task demand-
which also receives input from area 7a of the ing sustained divided attention (Fletcher et al.
caudal inferior parietal lobe. This shared connec- 1995), only the anterior cingulate is activated
tion between the dorsal head of the caudate and the due to the sustained vigilance demanded by divid-
dorsal visual system of area 7a supports the role of ing effort between the two tasks. When motivation
the posterior cingulate in visual attention. Output to master a task is no longer required, and accurate
to posterior superior temporal area 22 will influ- performance of a task becomes routine, the ante-
ence auditory association cortex. Limited effer- rior cingulate returns to a baseline activity level
ents to the rostral portion of area 11 provide the (Raichle et al. 1994). The acquisition of novel
only overlap with the orbitofrontal-centered belt. cognitive strategies requires the “dynamic vigi-
Electrical stimulation of the cingulate. Electri- lance” of the supracallosal cingulate, but with
cal stimulation studies of the cingulate in humans practice the motivation required to entrain new
and animals are difficult to interpret because dif- cognitive networks to a novel task is no longer
fering techniques have been used in these investi- necessary. A distinction between motivation and
gations. With varying intensity, time course, and attention is important. A task is still attended to
location of stimulation, it is not surprising that a and completed correctly after the motivating influ-
spectrum of results is noted. Despite technical ence of the supracallosal cingulate has initiated
variations, stimulation of the anterior cingulate the acquisition of an efficient cognitive routine.
in humans regularly produces visceral motor Through the activation of the anterior supra-
and affective changes, speech alterations, and callosal cingulate limbic motivation directs the
automatic motor behaviors (Meyer et al. 1973). selection of the best cognitive strategy among
In contrast to inhibitory responses elicited by the many competing contingencies. Thus, activation
Cingulate Gyrus 791

studies using varied tasks consistently activate the frontal pole as well. Consciousness may be
cognitive effector region in normals motivated to altered, and automatisms can be voluntarily
succeed in whatever task is given them. The con- inhibited or integrated with ongoing movements
tribution to an extrapersonal attentional network – (Geier et al. 1977).
involving direct links between the anterior cingu- An 11-year-old girl who initially had atonic
late, dorsolateral executive frontal area, and the seizures at age 30 months was reported to develop
inferior parietal lobule – provided by the cognitive complex partial seizures with blinking, lip smack- C
effector region is the motivation to engage in a ing, automatisms, and humming (Levin and
cognitive challenge. Duchowny 1991). An obsessive-compulsive dis-
Functional imaging has also confirmed the role order developed over a 5-year period, and by age
of the skeletomotor effector region in the prepa- 8, she became preoccupied with Satan and her
ration of motor output and motor learning. When a personal hygiene. Seizure focus, recorded from
motor task is only imagined, the cingulate cortex depth electrodes, was in the right anterior cingu-
inferior and anterior to the supplementary motor late. The patient’s behavioral abnormalities
area (dorsal bank of the cingulate sulcus) shows responded well to a 4-cm ablation of the right
significant activation. During the acquisition of anterior cingulate.
procedural learning in a rotary pursuit task, the Another case of a right anterior cingulate focus
cingulate skeletomotor region is also activated with accompanying behavioral abnormalities has
(Grafton et al. 1994). been described (Devinsky et al. 1995). One year
after mild head trauma, a 42-year-old male devel-
oped, over a 15-year period, sociopathic behavior
Illness and complex partial seizures unresponsive to
medical treatment. Seizures were usually noctur-
Structural and functional abnormalities. Seizures nal and frequent (10–20 per night), with stereo-
originating in the anterior cingulate can alter vis- typic motor output: facial contortions, tongue
ceral activity, produce involuntary skeletomotor thrusting, a strangulated yell, flexion of the neck
output, result in disturbed attention, and cause and trunk, bilateral extremity extension, and
interictal behavior abnormalities. The severity thrashing with preserved consciousness. Occa-
and specific abnormality will depend upon the sionally, generalization to tonic-clonic seizures
location of the seizure focus and ensuing damage developed with loss of consciousness.
that affects interictal brain function. A diverse Irritability, disinhibition, and sexual deviancy
assortment of atonic, absence, speech arrest, auto- were behavioral complications in a police officer
nomic, and complex partial seizures with second- who was dismissed from the force because of
ary generalization have been described. brutality and the use of confiscated drugs. Sur-
Inaccessibility of the medial hemisphere to sur- face and sphenoidal electroencephalogram
face electrode recording is the greatest obstacle to showed rhythmic bifrontal theta. Magnetic reso-
the elucidation of cingulate seizures. nance imaging (MRI) and [18F]-fluorodeox-
In a study involving 36 cases (Mazars 1970), yglucose positron emission tomography (FDG-
depth electrodes revealed near-instantaneous PET) were essentially normal, but depth elec-
bilateral spread to the frontal poles when the trodes revealed a right cingulate focus which
focus was in the anterior cingulate; posterior foci spreads to the ipsilateral orbitofrontal area and
spread to the contralateral cingulate within sec- contralateral anterior cingulate in 300 ms. Resec-
onds, followed by involvement of the convexities tion of the right cingulate and anterior corpus
with generalized tonic-clonic seizures. Emotional callosum relieved 90% of the spells with only
stress often precipitated the seizures. Psychoses brief axial flexion being the residual seizures.
and episodic rage were common interictal behav- The behavioral abnormalities were reported to
ioral abnormalities that responded to the removal improve with the patient, married and employed
of the anterior cingulate and occasionally the as a fast-food restaurant manager.
792 Cingulate Gyrus

Both stimulation and seizure activity can demonstrate profound indifference, docility, and
discharge the functional centers of the cingulate the loss of motivation to engage in a task. They
to produce a visceral effect, a cognitive or behav- can be led by the examiner to engage in a task but
ioral change, and a speech or motor output. will fail to self-generate sustained directed atten-
Appreciating the functional centers within the tion. They lack cognitive motivation.
cingulate assists the interpretation of the signs The role of the anterior cingulate as a cognitive
and symptoms exhibited when it discharges. The effector is appreciated within the realm of lan-
interictal behavioral abnormalities of anterior guage. Language, a cognitive function, is distin-
cingulate epilepsy reflect the dysfunction of lim- guished from the motor function of speech.
bic networks which, if affecting infracallosal and Transcortical motor aphasia (TCMA) is the usual
orbitofrontal cortex, will result in visceral motor result of left anterior medial or anterior dorsolat-
disturbances and disinhibition with socially eral prefrontal lesions. The classic syndrome of
inappropriate behavior. Obsessive-compulsive TCMA is initial mutism that resolves in days to
features may occur with dysfunction of the cog- weeks, yielding a syndrome featuring delayed
nitive component of the supracallosal cingulate. initiation of brief utterances without impaired
This abnormal “dynamic vigilance” exerted by articulation, excellent repetition, inappropriate
the cognitive effector region in obsessive-com- word selection, agrammatism, and poor compre-
pulsive disorders can occur from a well- hension of complex syntax. Activation of dorso-
circumscribed seizure focus in this region lateral prefrontal cortices enabling language and
(Levin and Duchowny 1991) and is relieved by speech arises from two sources: the anterior cin-
surgical ablation of this region or its outflow gulate and the supplementary motor area (with the
(Tow and Whitty 1953). cingulate skeletomotor effector region). When the
Focal lesions and syndromes. Well- executive prefrontal cortex (areas 9, 10, and 46) is
circumscribed lesions in humans are rarely con- disrupted, cognitive language deficits are promi-
fined to one region of the cingulate. With an nent (TCMA, type I); when motor neurons in area
anterior lesion, the cognitive, skeletomotor, and 4, devoted to the speech apparatus, are discon-
visceral effector regions are often affected. Bilat- nected from their activation, speech hesitancy
eral lesions result in an akinetic mute state and impoverished output ensues (TCMA, type
(Akinetic Mutism). Patients are profoundly apa- II). These two functional realms are separable
thetic. Rarely moving, and incontinent, they eat and can be disconnected anywhere along two
and drink only when fed, and if speech occurs it is pathways. Direct damage to the supplementary
limited to monosyllabic responses to questioning. motor area or its efferent pathway to the motor
Patients appear awake with eyes tracking objects. cortex traveling in the anterior superior para-
Displaying no emotions, even when in pain, ventricular white matter will produce TCMA
patients show complete indifference to their cir- type II. Direct damage to the anterior cingulate,
cumstance. Transient akinetic mutism with simi- its outflow to areas 9, 10, and 46, or to the caudate
lar features occurs with unilateral lesions. The – via the subcallosal fasciculus, just inferior to the
akinetic mute state can also result from bilateral frontal horn of the lateral ventricle – will disrupt
paramedian diencephalic and midbrain lesions, frontal-subcortical circuits involved in motivation
possibly affecting the ascending reticular core. and executive cognitive functions. The initial
Failure of response inhibition on go-no-go tests muteness has been described by a patient after
is the major neuropsychological deficit in the recovering from an anterior cingulate/supplemen-
patient with an anterior medial frontal damage. tary motor infarction as a loss of the “will” to reply
The loss of spontaneous motor activity results to her examiners, because she had “nothing to
when the lesion involves the supplementary say,” her “mind was empty,” and “nothing
motor area and the skeletomotor effector region. mattered” (Akinetic Mutism).
When these two motor regions are spared, motor The cingulum bundle has also been the site of
activity will be normal but the patient will surgical lesions (cingulumotomy, or cingulotomy
Cingulate Gyrus 793

when cingulate cortex is also removed) to treat The analysis of rare circumscribed lesion in
psychiatric and pain disorders. The cingulum con- humans cannot determine if the posterior cingu-
tains the efferents and afferents of the cingulate to late cortex, rather than the cingulum or neighbor-
the hippocampus, basal forebrain, amygdala, and ing members of Papez’s circuit, result in amnesia
all cortical areas, as well as fibers of passage when lesioned due to the location of fiber path-
between hippocampus and prefrontal cortex, and ways to the hippocampus that are buried in the
from the median raphé to the dorsal hippocampus. posterior cingulate. Excitotoxic lesions in ani- C
Surgical ablation of the anterior portion (sparing mals that destroy neurons but spare fibers of
fibers relevant to memory function) is most suc- passage can clarify this issue. Based upon poste-
cessful when treating aggression, extreme anxiety, rior cingulate cortical lesions, using the selective
obsessive-compulsive behaviors, and severe pain. cytotoxin quisqualic acid (Sutherland and
Psychotic symptoms show only a temporary Hoesing 1993), results in animal studies reveal
response. The three anterior cingulate regions, that area 29 neurons are necessary for the acqui-
by virtue of the distinct functional systems they sition and retention of spatial and nonspatial
access, are the conduits through which limbic memory. Furthermore, the posterior cingulate
motivation can activate feeling, thought, and acts in concert with the anterior thalamus and
movement. the hippocampus during encoding and may also
Lesions of the posterior cingulate disrupt mem- be important in the storage of long-term
ory function in animals and humans. The closing information.
link in the circuit of Papez, from the anterior Synthesizing cytoarchitectonic refinements,
thalamic efferents traveling through the posterior nonhuman primate tracer studies, clinical-behav-
cingulum to areas 32 and 29/30, is the cingulate ioral correlation data, and functional neuroimag-
projection sent to the presubiculum. Anterior ing results have been refined but have not
cingulotomy will not disrupt this memory circuit significantly added to the basic description of
but rarely pathologic lesions will extend into, and cingulate function offered by Papez.
beyond, the posterior cingulate. If the lesion “It is thus evident that the afferent pathways
extends inferior to the splenium of the corpus from the receptor organs split at the thalamic
callosum, it may also disrupt the fornix, thus level into three routes, each conducting a
disconnecting the efferents from the hippocampus stream of impulses of special importance. One
to the diencephalon. If the lesion extends posteri- route conducts impulses through the dorsal
orly, it may damage the supracommissural portion thalamus and the internal capsule to the corpus
of the hippocampus – the gyrus fasciolaris and the striatum. This route represents “the stream of
fasciola cinerea. A large left-sided lesion that movement.” The second conducts impulses
extended beyond the posterior cingulate into the from the thalamus through the internal capsule
fornix and supracommissural hippocampus after to the lateral cerebral cortex. This route repre-
the surgical repair of an arteriovenous malforma- sents “the stream of thought.” The third con-
tion resulted in a persistent amnesia (Cramon and ducts a set of concomitant impulses through the
Schuri 1992). Disruption of septo-hippocampal ventral thalamus to the hypothalamus and by
pathways in the cingulum and fornix were thought way of the mamillary body and the anterior
by the authors to play a significant role in the thalamic nuclei to the gyrus cinguli, in the
patient’s clinical deficit, but other important com- medial wall of the cerebral hemisphere.
ponents of Papez’s circuit had clearly been dam- This route represents “the stream of feeling.”
aged. A rare lesion restricted to the left posterior In this way, the sensory excitations which reach
cingulate, the cingulum, and the splenium of the lateral cortex through the internal capsule
the corpus callosum (but possibly sparing the receive their emotional coloring from the
fornix) resulted in a severe amnesia after the repair concurrent processes of hypothalamic origin
of an arteriovenous malformation (Valenstein which irradiate them from the gyrus cinguli
et al. 1987). (Papez 1937)”.
794 Cingulum

References and Readings

Cingulum
Devinsky, O., Morrell, M. J., & Vogt, B. A. (1995). Con-
tributions of anterior cingulate cortex to behavior.
Irene Piryatinsky
Brain, 118, 279–306.
Fletcher, P. C., Firth, C. D., Grasby, P. M., Shallice, T., Butler Hospital and Alpert Medical School of
Frackowiak, R. S. J., & Dolan, R. J. (1995). Brain Brown University, Providence, RI, USA
systems for encoding and retrieval of auditory-verbal
memory. An in vivo study in humans. Brain, 118,
401–416.
Geier, S., Bancaud, J., Talairach, J., Bonis, A., Szikla, G., Definition
& Enjelvin, M. (1977). The seizures of frontal lobe
epilepsy. A study of clinical manifestations. Neurology, The cingulum is a collection of white matter fibers
27, 951–958.
projecting from the cingulate gyrus to the entorhi-
Grafton, S. T., Woods, R. P., & Tyszka, M. (1994). Func-
tional imaging of procedural motor learning: Relating nal cortex in the brain, allowing for communica-
cerebral blood flow with individual subject perfor- tion between components of the limbic system.
mance. Human Brain Mapping, 1, 221–234. The cingulum connects the medial temporal lobe
Levin, B., & Duchowny, M. (1991). Childhood obsessive-
with the posterior cingulate gyrus. Diffusion ten-
compulsive disorder and cingulate epilepsy. Biological
Psychiatry, 30, 1049–1055. sor imaging studies have reported cingulum bun-
Mazars, G. (1970). Criteria for identifying cingulate epi- dle disruption in mild cognitive impairment and
lepsies. Epilepsia, 11, 41–47. Alzheimer’s disease. In addition, some research
Meyer, G., McElhaney, M., Martin, W., & McGraw, C. P.
indicates that in Alzheimer’s disease, the posterior
(1973). Stereotactic cingulotomy with results of acute
stimulation and serial psychological testing. In L. V. cingulate cortex hypofunction is due to the indi-
Laitinen & K. E. Livingston (Eds.), Surgical rect effect of the degeneration of cingulum fibers
approaches in psychiatry (pp. 39–58). Baltimore: Uni- secondary to medial temporal lobe atrophy. Dam-
versity Park Press.
age to the cingulum has also been found to be
Papez, J. W. (1937). A proposed mechanism of emotion.
Archives of Neurology and Psychiatry, 38, 725–733. associated with cognitive impairment in other dis-
Penfield, W., & Jasper, H. (1954). Epilepsy and the func- eases of the brain such as multiple sclerosis.
tional anatomy of the human brain. Boston: Little
Brown.
Raichle, M. E., Fiez, J. A., Videen, T. O., MacLeod, A.-M.
Cross-References
K., Pardo, J. V., Fox, P. T., et al. (1994). Practice-related
changes in human brain functional anatomy during
nonmotor learning. Cerebral Cortex, 4, 8–26. ▶ Cingulate Gyrus
Sutherland, R. J., & Hoesing, J. M. (1993). Posterior cin-
gulate cortex and spatial memory; a microlimnology
analysis. In B. A. Vogt & M. Gabriel (Eds.), Neurobi-
ology of cingulate cortex and limbic thalamus: A com- References and Readings
prehensive handbook (pp. 461–477). Boston:
Birkhäuser. Catani, M., Howard, R. J., Pajevic, S., & Jones, D. K.
Tow, P. M., & Whitty, C. W. M. (1953). Personality (2002). Virtual in vivo interactive dissection of white
changes after operations of the cingulate gyrus in matter fasciculi in the human brain. NeuroImage, 17(1),
man. Journal of Neurology Neurosurgery & Psychia- 77–94.
try, 16, 186–193. Fellgiebel, A., Müller, M. J., Wille, P., Dellani, P. R.,
Valenstein, E., Bowers, D., Verfaellie, M., Heilman, K. M., Scheurich, A., Schmidt, L. G., et al. (2005). Color-
Day, A., & Watson, R. T. (1987). Retrosplenial amne- coded diffusion-tensor-imaging of posterior cingulate
sia. Brain, 110, 1631–1646. fiber tracts in mild cognitive impairment. Neurobiology
Vogt, B. A., & Barbas, H. (1988). Structure and connec- of Aging, 26(8), 1193–1198.
tions of the cingulate vocalization region in the rhesus Firbank, M. J., Blamire, A. M., Krishnan, M. S.,
monkey. In J. D. Newman (Ed.), The physiological Teodorczuk, A., English, P., Gholkar, A., et al.
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New York: Plenum Press. white matter disruption in dementia with Lewy bodies
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pocampal pathways and their relevance to human mem- Rose, S. E., McMahon, K. L., Janke, A. L., O’Dowd, B., de
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Circadian Rhythms 795

Diffusion indices on magnetic resonance imaging and with the 24-h circadian rhythms figuring promi-
neuropsychological performance in amnestic mild cog- nently in the literature. These rhythms impact
nitive impairment. Journal of Neurology, Neurosurgery
& Psychiatry, 77(10), 1122–2112. daily life (e.g., work, school, medical–psy-
Syc, S. B., Harrison, D. H., Saidha, S., Seigo, M., chological status) and are of relatively brief dura-
Calabresi, P. A., & Daniel, S. R. (2013). Quantitative tion, so they are amenable to study (Clark 2005).
MRI demonstrates abnormality of the fornix and cin- There is also a developmental progression in how
gulum in multiple sclerosis. Multiple Sclerosis Interna-
tional. https://doi.org/10.1155/2013/838719. Published rhythmicity is expressed from birth to old age C
online 16 Feb 2013. (Weinert 2010), and there are a number of biolog-
Wakana, S., Jiang, H., Nagae-Poetscher, L. M., van Zijl, ical rhythms that are characterized by different
P. C. M., & Mori, S. (2004). Fiber tract-based atlas of time periods (see Table 1).
human white matter anatomy. Radiology, 23(1), 77–87.
Zhang, Y., Schuff, N., Jahng, G. H., Bayne, W., Mori, S.,
Schad, L., et al. (2007). Diffusion tensor imaging of
cingulum fibers in mild cognitive impairment and Mechanisms
Alzheimer disease. Neurology, 68(1), 13–19.
Circadian rhythms are modulated by both inter-
nal clocks (e.g., pacemakers) and external trig-
gers that can entrain biorhythms, acting as
Circadian Rhythms zeitgebers (e.g., changes in illumination). The
superchiasmic nucleus (SCN) of the hypothala-
Bruce J. Diamond and Walter Barr mus has been identified as the principal biologi-
Department of Psychology, William Paterson cal clock (Chan et al. 2012; Carlson 1999) based
University, Wayne, NJ, USA on lesion studies and day–night changes in activ-
ity levels. The mechanisms mediating communi-
cation and synchronization between neurons
Synonyms appear to be chemical in nature. Both the SCN
and the pineal gland exert an influence on sea-
Biological cycles; Biorhythms; Circadian clock sonal rhythms with SCN-induced melatonin
secretion involved in synchronizing circadian
rhythms (Chan et al. 2012). Developmental fac-
Short Description or Definition tors may also mediate variations in circadian
rhythms. For example, the aging process is
One of the pervasive characteristics of living often accompanied by changes in circadian
organisms are rhythmic biological and behavioral rhythms that may affect the sleep patterns of
changes, which are expressed at varying levels of older adults placing them at a higher risk for
organization ranging from the cellular to highly sleep disturbance (Lee-Chiong 2005).
complex multicellular systems. These rhythms
are generally referred to as circadian rhythms,
and they organize a variety of behaviors, includ-
ing sleep, which is, for example, characterized Circadian Rhythms, Table 1 Circadian Rhythms: Time
Period and Function
by a 90-min rapid eye movement (REM)
cycle and the wakefulness–sleep cycle, which is Biological
rhythms Time period Activity
organized around an approximate 24-h cycle
Infradian Period of less Eating behaviors
(Carlson 1999). than 24 h
Circadian Period of about Sleep–wake
Categorization 24 h
The core body temperature rhythm and the Ultradian Period of about Human female
sleep–wake cycle are among the most extensively 28 days menstrual cycle
studied of the human biorhythms (Weinert 2010) Circannual Yearly Migratory birds
796 Circadian Rhythms

History and Impact Treatment

Endogenous biological clocks were demonstrated While the circadian clock of healthy humans is
over 300 years ago (Kolb and Wishaw 2009), and entrained to a period of about 24 h, the precise
entrainment was identified as the most important timing varies on an intra- and interindividual
property for determining the phase relationship of basis. Treatment interventions should be respon-
a circadian clock (Johnson et al. 2004). Circadian sive to this variability. Thus, seasonal affective
rhythms may confer an adaptive value on an disorder has been treated using phototherapy,
organism since the organism can anticipate envi- which involves the use of light boxes, whereby a
ronmental changes (Golombek and Rosenstien patient is exposed to light each winter morning or
2010), and physiological functions synchronized evening, and the circadian rhythm becomes
with the time of day are associated with enhanced entrained in ways that induce circadian phase
efficiency (Quigg 2006). Disruption in circadian shifts (Kolb and Wishaw 2009).
rhythms can adversely impact individuals Individuals who make substantial changes to
involved in shift and night work, who suffer jet their sleep–wake cycles during night work or after
lag or whose schedules are temporally irregular. transmeridian travel can be helped using a chro-
The impact is more serious when task demands nobiological treatment. That is, treatment
involve vigilance and reaction time (Costa 1999) involves exposure to appropriate circadian syn-
which are more vulnerable to fatigue effects. chronizers and with therapy based on phase
Attentional regulation over both incoming infor- response curves for light and melatonin
mation and outgoing responses may also be vul- (Waterhouse and DeCoursey 2004). By making
nerable to time of day effects. Disturbances in accommodations in the timing of work-related
sleep–wake cycles and biological rhythms have activities (Hasher et al. 2005), performance effi-
also been associated with affective disorders ciency can be improved and fatigue decreased,
including depression, as well as being implicated thus enhancing health and safety (Costa 1999).
as risk factors for cancer (e.g., breast and prostate Other possible treatments for circadian disruption
cancer) (LeGates et al. 2014; Sigurdardottir currently being investigated are the use of antide-
et al. 2012). pressants, cognitive behavioral therapy (CBT),
antipsychotics, and hypnotic drugs (Wilson et al.
2010). Also, in treating patients with bipolar dis-
order, psychosocial therapies should identify
Evaluation areas of vulnerability including unhealthy circa-
dian rhythms (Newman 2006).
Younger and older adults exhibit large differ-
ences in circadian cycles. Clinicians should
assess the quantitative and qualitative nature of References and Readings
cognitive decline in the elderly with attention to
circadian influences (with the elderly tending to Carlson, N. R. (1999). Foundations of physiological psy-
be morning oriented) (Hasher et al. 2005). In chology (4th ed.). Boston: Allyn & Bacon.
Chan, M.-C., Spieth, P. M., Quinn, K., Parotto, M., Zhang,
evaluating clients for possible disruptions in cir-
H., & Slutsky, A. S. (2012). Circadian rhythms: From
cadian rhythms, clinicians would be well advised basic mechanisms to the intensive care unit. Critical
to determine if clients engage in shift work, have Care Medicine, 40(1), 246–253. https://doi.org/
experienced jet lag or changes in schedule, or 10.1097/CCM.0b013e31822f0abe.
Clark, A. V. (Ed.). (2005). Causes, role and influence of
exhibit fatigue, sleep disorders, excessive daytime
mood states. Hauppauge: Nova Biomedical Books.
drowsiness, or decrements in job-related perfor- Costa, G. (1999). Fatigue and biological rhythms. In D. J.
mance (Costa 1999). Garland, J. A. Wise, & D. V. Hopkin (Eds.), Handbook
Circle of Willis 797

of aviation human factors (pp. 235–255). Mahwah:

Lawrence Erlbaum. Circle of Willis
Golombek, D. A., & Rosenstein, R. E. (2010). Physiology
of circadian entrainment. Physiological Reviews, 90(3),
1063–1102. Elliot J. Roth
Hasher, L., Goldstein, D., & May, C. P. (2005). It’s about Department of Physical Medicine and
time: Circadian rhythms, memory, and aging. In Rehabilitation, Northwestern University,
C. Izawa & N. Ohta (Eds.), Human learning and mem-
ory: Advances in theory and application: The 4th Feinberg School of Medicine, Chicago, IL, USA C
Tsukuba international conference on memory
(pp. 199–217). Mahwah: Lawrence Erlbaum.
Huang, W., Ramsey, K. M., Marcheva, B., & Definition
Bass, J. (2011). Circadian rhythms, sleep, and
metabolism. The Journal of Clinical Investigation,
121(6), 2133. The circle of Willis is the anatomical name given
Johnson, C.H. (2004). Precise circadian clocks in prokary- to the formation of arteries at the base of the brain
otic cyanobacteria. Curr Issues Mol Biol 6, 103–110. that contribute the overwhelming majority of
Kolb, B., & Whishaw, I. (2009). An introduction to brain
and behavior (3rd ed.). New York: Worth Publishers. blood supply to the brain.
Lee-Chiong, T. L. (2005). Sleep: A comprehensive hand-
book. Hoboken: Wiley.
LeGates, T. A., Fernandez, D. C., & Hattar, S. (2014). Current Knowledge
Light as a central modulator of circadian rhythms,
sleep and affect. Nature Reviews Neuroscience, 15(7),
443–454. The circle of Willis is formed by the connections
Newman, C. F. (2006). Bipolar disorder. In F. Andrasik between the predominantly horizontal branches
(Ed.), Comprehensive handbook of personality and that derive from the middle cerebral arteries
psychopathology, Adult psychopathology (Vol. 2,
pp. 244–261). Hoboken: Wiley. anteriorly and from the basilar artery posteriorly.
Quigg, M. (2006). Circadian rhythms: Problems with the The right and left middle cerebral arteries each
body clock. In N. F. Watson & B. V. Vaughn (Eds.), give off an anterior cerebral artery (forming the
Clinicians guide to sleep disorders (pp. 277–304). Phil- anterolateral borders of the circle of Willis),
adelphia: Taylor & Francis.
Sigurdardottir, L. G., Valdimarsdottir, U. A., Fall, K., Rider, which goes forward to supply blood to the fron-
J. R., Lockley, S. W., Schernhammer, E. S., & Mucci, tal lobe. These anterior cerebral arteries are
L. A. (2012). Circadian disruption, sleep loss and pros- connected to each other by the anterior commu-
tate cancer risk: A systematic review of epidemiological nicating artery, which forms the front of the
studies. Cancer Epidemiology, Biomarkers & Preven-
tion : A Publication of the American Association for circle. Posteriorly, the basilar artery bifurcates
Cancer Research, Cosponsored by the American Society into the right and left posterior cerebral arteries,
of Preventive Oncology, 21(7), 1002–1011. https://doi. which supply the occipital and posterior tempo-
org/10.1158/1055-9965.EPI-12-0116. ral lobes and the cerebellum, forming the poste-
Waterhouse, J. M., & DeCoursey, P. J. (2004). Human
circadian organization. In J. C. Dunlap, J. J. Loros, & rior border of the circle. Each posterior cerebral
P. J. DeCoursey (Eds.), Chronobiology: Biological artery is connected to the middle cerebral artery
timekeeping (pp. 291–323). Sunderland: Sinauer. on its corresponding side by a posterior commu-
Weinert, D. (2010). Circadian temperature variation and nicating artery, forming the posterolateral bor-
ageing. Ageing Research Reviews, 9(1), 51–60.
Wilson, S. J., Nutt, D., Alford, C., Argyropoulos, S., ders of the circle. There are several clinical
Baldwin, D., Bateson, D., Britton, T., Crowe, C., implications of the circle pattern of these arter-
Dijk, D., Espie, C., Gringras, P., Hajak, G., Idzikowski, ies. Perhaps most importantly, because of the
C., Krystal, A., Nash, J., Selsick, H., Sharpley, A., & interconnectedness of the arteries that result
Wade, A. (2010). British Association for Psychophar-
macology consensus statement on evidence-based from this circle format, if one of the main arteries
treatment of insomnia, parasomnias and circadian is occluded, the distal smaller arteries that it
rhythm disorders. Journal of Psychopharmacology, supplies can potentially receive blood from
24(11), 1577–1601. ISSN 0269-8811. the other arteries that make up the circle, a
798 Circles of Support

phenomenon known as collateral circulation. (Falvey et al. 1994). It is one of many tools
This helps to prevent cerebral ischemia and addressing life planning from a functional or stra-
stroke. The circle of Willis also is a common tegic assessment approach known as person-
site for cerebral aneurysms, with the greatest centered planning. Person-centered planning
numbers involving the anterior communicating replaces more traditional assessment approaches
artery, posterior communicating arteries, and associated with the medical model of services.
middle cerebral arteries. Circles of support originated in Canada and have
experienced widespread use in North America.
Circles view people as individuals and assist
them to attain self-determination focusing upon
Cross-References
empowerment and not dependence of the individ-
ual (O’Brien and Lyle O’Brien 1998). It is capac-
▶ Anterior Cerebral Artery
ity oriented and identifies strengths, preferences,
▶ Anterior Communicating Artery
likes, and dislikes of the individual. The circle will
▶ Basilar Artery
also identify support needs in order to achieve a
▶ Internal Carotid Artery
particular goal.
▶ Middle Cerebral Artery
The focus person leads the process and decides
▶ Posterior Cerebral Artery
who will participate in the circle and the direction
▶ Posterior Communicating Artery
which the planning will take. Typically, a facilita-
▶ Vertebrobasilar System
tor is selected from within the circle to help ener-
gize the group. The first circle is the circle of
intimacy and includes the people most intimate
in the focus person’s life. The second circle, the
circle of friendship, includes good friends and
Circles of Support close relatives. The third circle, the circle of par-
ticipation, includes the people and organizations
Amy J. Armstrong the focus person is involved with. The fourth
Department of Rehabilitation Counseling, circle is the circle of exchange and includes
Virginia Commonwealth University, Richmond, those that are paid to be in the focus person’s life
VA, USA (Falvey et al. 1994). Members are not paid to be
involved in a circle of support but are involved in
the focus person's life in some capacity. Members
Synonyms use their skills, knowledge, and networks to help
the focus person accomplish goals. The circle
Circle of friends develops and monitors the plan, making sure that
it is current with the wishes of the focus person.
Circle of supports is an ongoing process that uses
Definition a specific protocol, yet it is dynamic and organic
to respond to the changing needs and interests of
Researchers have long indicated the importance the individual.
of social relationships and supports to the well-
being and inclusion of human beings (Rath and
Harter 2011). A circle of support is a group of
people that forms a community around a specific Cross-References
individual (focus person) with significant disabil-
ities to assist him or her to achieve personal goals ▶ Medical Model
Circumlocution 799

References and Readings References and Readings

Falvey, M. A., Forest, M., Pearpoint, J., & Rosenberg, R. Victor, M., & Ropper, A. H. (2001). Adams and victor’s
(1994). All my life’s a circle. Using the tools: Circles, principals of neurology (7th ed.). New York: McGraw-
MAP’s and PATH. Toronto: Inclusion Press. Hill.
O’Brien, J., & Lyle O’Brien, C. (Eds.). (1998). A little book
about person centered planning. Toronto: Inclusion Press.
O’Brien, C. L., & O’Brien, J. (2000). The origins of person- C
centered planning: A community of practice perspective.
Retrieved from http://thechp.syr.edu/PCP_History.pdf
Rath, T., & Harter, J. (2011). Wellbeing: The five essential Circumlocution
elements. New York: Gallup Press.
Sarah S. Christman Buckingham and Kayle E.
Sneed
Department of Communication Sciences and
Circumduction Disorders, The University of Oklahoma Health
Sciences Center, Oklahoma City, OK, USA
Theslee Joy DePiero
Braintree Rehabilitation Hospital, Boston
University School of Medicine, Boston, MA, USA Synonyms

Periphrasis; Pleonasm; Prolix

Synonyms

Spastic gait Definition

Circumlocution is the use of more words than

Definition necessary to express what could be said precisely
and directly. Frequently present during word-
Circumduction describes the movement of the leg finding difficulties, circumlocutions typically
of a person with hemiplegia, hemiparesis or para- involve production of functional or attributive
plegia, and paraparesis. Lesions of the pyramidal descriptions in place of content words that cannot
tract cause more weakness in the flexors of the leg be immediately accessed (Benson and Ardila
than the extensors (hip and knee flexors and ankle 1996). Examples include saying, “the thing that
dorsiflexors). Because of this weakness, the foot you use to tell time” instead of “clock” or saying
cannot be raised from the floor, and the leg cannot “the thing that is red, white, and blue” instead of
be advanced in a straight line forward, as it would “American flag.”
do normally. The leg moves away from the trunk, Circumlocution is found in neurotypical indi-
then it is advanced toward it during walking, in a viduals who occasionally have a word on the “tip
circular pattern. The medial side of the shoe scrapes of the tongue,” that is, when the semantics of a
the floor, causing excessive wear in that area. needed word can be accessed but not the phono-
logical form. It is also frequently present, how-
ever, as a symptom of anomia in individuals with
Cross-References fluent aphasias and cognitive-communication
disorders (Davis 2013). In these circumstances,
▶ Hemiparesis circumlocution can be viewed as both a symp-
▶ Hemiplegia tom and a compensatory strategy to circumvent a
▶ Pyramidal System failure of phonological access (Raymer 2015).
800 Circumstantiality

In bilingual speakers who experience unwanted

language switching, it can also serve to Citalopram
facilitate interlanguage access via the common
conceptual store to which related words in dif- John C. Courtney1 and Efrain Antonio Gonzalez2,3
1
ferent languages are linked (Kohnert and Socorro Mental Health, Presbyterian Medical
Peterson 2012). Services, Socorro, NM, USA
2
College of Psychology, Nova Southeastern
University, Fort Lauderdale, FL, USA
3
Utah State University, Logan, UT, USA
Further Reading

Benson, D. F., & Ardila, A. (1996). Aphasia: A clinical

perspective. New York: Oxford University Press. Generic Name
Davis, G. A. (2013). Aphasia and related cognitive-
communication disorders. New York: Pearson. Citalopram
Kohnert, K., & Peterson, M. (2012). Generalization in
bilingual aphasia treatment. In M. R. Gitterman,
M. Goral, & L. K. Obler (Eds.), Aspects of Brand Name
multilingual aphasia (pp. 89–105). Bristol: Multilin- Celexa
gual Matters.
Raymer, A. M. (2015). Clinical diagnosis and treatment of
Class
naming disorders. In A. E. Hillis (Ed.), The handbook
of adult language disorders (2nd ed., pp. 161–183). Antidepressants and selective serotonin reuptake
New York: Psychology Press. inhibitors

Proposed Mechanism(s) of Action

Circumstantiality Citalopram blocks the presynaptic serotonin reup-

take pump and desensitizes serotonin receptors,
Robert G. Frank theoretically increasing serotonin neurotransmis-
University of New Mexico, Albuquerque, NM, sion. Citalopram is also a mild antihistamine.
USA
Indication
Definition
Depression
Circumstantiality is circuitous thinking and
speech that digresses from the essential point.
Off-Label Use
It differs from tangentiality in which the individ-
ual ultimately fails to address the main idea.
Premenstrual dysphoric disorder, obsessive com-
In circumstantiality, the main point is never lost
pulsive disorder, panic disorder, generalized anx-
but may be “clouded” and its appearance
iety disorder, posttraumatic stress disorder, social
delayed by excess and repeated material. Cir-
anxiety disorder, alcoholism, binge eating disor-
cumstantial thinking is a characteristic of thought
der, and hot flashes
disorders.

Side Effects
Cross-References
Serious
▶ Tangentiality Seizures, mania, and suicidal ideation (all rare)
Classical Test Theory 801

Common organizations. Civil litigation primarily aims to

Sexual dysfunction, gastrointestinal upset, insom- correct an injustice, uphold an agreement, or settle
nia, sedation, tremor, headache, dizziness, sweat- a dispute. If compensation is awarded to the victim,
ing, bruising and very rare bleeding, rare then the person/organization responsible for the
hyponatremia, and a potential for SIADH (syn- injustice is responsible for covering the compensa-
drome of inappropriate antidiuretic hormone tion. In civil litigation, the burden of proof is usu-
secretion) ally placed on the plaintiff, though exceptions do C
exist. Punishment related to civil litigation is typi-
cally limited to reimbursement for losses incurred
References and Readings by the plaintiff as a result of actions/inactions com-
mitted by the defendant. Incarceration is not a
Physicians’ desk reference (71st ed.). (2017). Montvale: punishment rendered via civil litigation. Civil liti-
Thomson PDR.
gation and criminal litigation are not mutually
Stahl, S. M. (2007). Essential psychopharmacology: The
prescriber’s guide (2nd ed.). New York: Cambridge exclusive entities. For example, an individual
University Press. involved in a criminal case may seek compensation
in civil court. For neuropsychologists, civil litiga-
Additional Information tion typically involves determination of causation,
Drug Interaction Effects. http://www.drugs.com/drug_ damages, and disability in disputes in which neu-
interactions.html
ropsychological functioning is of relevance (e.g.,
Drug Molecule Images. http://www.worldofmolecules.
com/drugs/ personal injury, medical malpractice).
Free Drug Online and PDA Software. www.epocrates.com
Free Drug Online and PDA Software. www.medscape.com
Gene-Based Estimate of Drug interactions. http://
mhc.daytondcs.com:8080/cgibin/ddiD4?ver=4&task=
References and Readings
getDrugList
Pill Identification. http://www.drugs.com/pill_identifica Greiffenstein, M. F. (2009). Basics of forensic neuropsy-
tion.html chology. In J. Morgan & J. Ricker (Eds.), Textbook of
clinical neuropsychology. New York: Psychology
Press.
Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychol-
ogy and the law: Principles of productive attorney-
neuropsychologists relations. In G. Larrabee (Ed.),
Civil Litigation Forensic neuropsychology: A scientific approach.
New York: Oxford University Press.
Moira C. Dux Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin,
US Department of Veteran Affairs, Baltimore, C. (2007). Psychological evaluations for the courts
(3rd ed.). New York: Guilford Press.
MD, USA

Definition
Classical Test Theory
Civil law is a division of the law that deals primar-
ily with disputes between individuals and/or orga- Michael Franzen
nizations, in which some form of compensation Allegheny General Hospital, Pittsburgh, PA, USA
may be awarded to the victim. Typically, civil law
involves filing of a lawsuit by a private party, called
“the plaintiff.” Civil litigation commonly involves Definition
hearing related to disputes regarding torts, con-
tracts, probate of wills, trusts, property, administra- Classical test theory is the body of concepts and
tive law, commercial law, as well as a plethora of methods that have formed the basis for psycholog-
other matters related to private parties and ical assessment. Classical test theory posits that
802 Clear and Convincing Evidence

observed scores are the additive function of true opinion to one’s own position: it may only be
scores and error terms. True scores are the ideal or fulfilled by evidence. Under the Latin maxim,
“true” value of a construct in a particular person or necessitas probandi incumbit ei qui agit, the gen-
situation. The error term is the effect of factors eral rule is that “the necessity of proof lies with
extraneous to the construct of interest but which he who complains.” The burden of proof, there-
are elicited by the measurement process. Error fore, usually lies with the party making the claim.
terms are assumed to be independent of (or The exception to this rule is when a prima facie
uncorrelated with) the true scores. Analysis of the case has been made. He who does not carry the
reliability of a score can be accomplished by manip- burden of proof carries the benefit of assumption,
ulating factors thought to be influencing the error meaning he needs no evidence to support his
term. For example, in order to examine the effect of claim. Fulfilling the burden of proof effectively
factors related to time or instance of measurement, a captures the benefit of assumption, passing the
test might be administered to the same individuals burden of proof off to another party. Clear and
on two different occasions. The relation between the convincing evidence is a burden of proof
two observed scores, determined by calculating a required of a plaintiff for him to win the lawsuit.
correlation coefficient or by performing an analysis This standard is higher than mere preponderance
of variance, helps to estimate the magnitude of the of the evidence. Proof of fraud, for example,
error term and the proportion of the observed score usually requires clear and convincing evidence.
that is likely to be true score. Clear and convincing evidence is the higher level
of burden of persuasion and is most often
employed in civil litigation. To prove something
Cross-References
by “clear and convincing evidence,” the party
with the burden of proof must convince the trier
▶ Error, Sources of
of fact that it is substantially more likely than not
▶ Item Response Theory
that the thing is in fact true. This is a lesser
requirement than “proof beyond a reasonable
doubt,” which requires that the trier of fact be
References and Readings
close to certain of the truth of the matter asserted,
Embretson, S. E. (Ed.). (2010). Measuring psychological but a stricter requirement than proof by “prepon-
constructs: Advances in model-based approaches. derance of the evidence,” which merely requires
Washington, DC: American Psychological Association. that the matter asserted seems more likely true
Lord, F. M., & Novick, M. R. (2008). Statistical theories of than not.
mental test scores. New York: Information Age
Publishing.

Cross-References
Clear and Convincing
Evidence ▶ Beyond a Reasonable Doubt
▶ Burden of Proof
Robert L. Heilbronner ▶ Preponderance of the Evidence
Chicago Neuropsychology Group, Chicago, IL,
USA

References and Readings

Definition
Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin,
C. (2007). Psychological evaluations for the courts:
The burden of proof is the obligation to shift the A handbook for mental health professionals and law-
assumed conclusion away from an oppositional yers (3rd ed.). New York: Guilford Press.
Clinical Dementia Rating 803

MCI); CDR = 1 (mild dementia); CDR = 2

Clinical Dementia Rating (moderate dementia); and CDR = 3 (severe
dementia). CDR = 4 (profound) and CDR = 5
Jing Ee Tan1,2,3, Esther Strauss3 and (terminal) may be used to classify the later stages
Elisabeth M. S. Sherman4 of dementia. An alternative method that gener-
1
Division of Neurology, University of British ates a total score (range 0–18) from the sum of
Columbia, Vancouver, BC, Canada boxes (CDR-SB) is commonly used for quantifi- C
2
Vancouver General Hospital, Vancouver, BC, cation purposes in longitudinal studies (e.g.,
Canada Cortes et al. 2008). A scoring method based on
3
Department of Psychology, University of item response theory (IRT) is available if precise
Victoria, Victoria, BC, Canada measurement of dementia severity is needed
4
Copeman Healthcare Centre, Calgary, AB, Canada (Lowe et al. 2012). The CDR takes about
90 min to administer.
The CDR has been used in clinical practice and
Synonyms multicenter clinical trials, as well as in cross-cul-
tural dementia studies around the world. The CDR
CDR protocol is available in over 60 languages and
dialects. These translations can be downloaded
free of cost for clinical and research use from the
Description CDR Web site (http://alzheimer.wustl.edu/cdr/
CDR.htm).
The Clinical Dementia Rating (CDR; Hughes The authors recommend live, in-person train-
et al. 1982) is a semi-structured, clinician-rated ing in order to use the CDR. An online training
interview widely used to stage the progression of video on the use of the CDR is available free for
dementia using information provided by the registered individual users. Detailed scoring
patient and an informant. A global CDR score algorithms, including “tiebreak” rules, and an
is generated to stage the severity of dementia. It online scoring worksheet are available on the
is based on ratings of the patient’s functioning in CDR Web site.
six domains commonly affected in Alzheimer’s
disease (AD): memory, orientation, judgment
and problem solving, community affairs, home Historical Background
and hobbies, and personal care. The CDR rates
only impairments due to cognitive deficits rather The CDR was originally developed at the Wash-
than to physical disability. A number of scoring ington University School of Medicine in 1979 to
methods have been developed over the years. In evaluate the progression of AD (Hughes et al.
the original protocol, a box score describing the 1982). The original protocol has evolved some-
level of impairment is generated for each domain what over the years, with box descriptors
using clinical information based solely from the updated to sharpen the distinction between sever-
patient and informant and without reference to ity levels within each domain and new scoring
psychometric performance. The box score ranges rules added to resolve scoring ambiguity (Morris
from 0 to 3, representing “none” to “severe” 1993). Alternative scoring methods have also
impairment. Using a scoring algorithm, one of been suggested to improve scoring accuracy
five possible stages is then derived from the (Gelb and St. Laurent 1993). A total score gen-
individual box scores as follows: CDR = 0 (no erated from the sum of boxes (CDR-SB) has
dementia); CDR = 0.5 (questionable dementia or showed promise as a single primary outcome
measure in clinical trials in predementia as well
as very mild to moderate AD (Cedarbaum et al.
Esther Strauss: deceased. 2013; Coley et al. 2011).
804 Clinical Dementia Rating

Psychometric Data et al. 2010). Adding Language as well as Behavior

domains to the CDR-SB improves the classifica-
Interrater Reliability tion accuracy of AD and frontotemporal dementia
Experience using the CDR increases reliability from 65% to 94% compared to Memory domain
estimates, although adequately trained inexperi- alone (Russo et al. 2014). Those who are
enced raters may also demonstrate a high level of CDR = 0.5 with impaired CDR IADL items are
agreement (kappa = 0.83 or higher; Schafer et al. more likely to progress to AD over 2 years than
2004). The CDR also shows good reliability those with intact IADL (Chang et al. 2011). Sur-
among raters of various qualifications. In one vival in individuals with suspected dementia may
study, there were no major differences in reliabil- be predicted by CDR: the median survival is
ity among physicians, nurses, PhDs, social 1 year for CDR = 5, 2 years for CDR = 4,
workers, psychometrists, or research assistant 2.5 years for CDR = 3, 3 years for CDR = 2,
raters, with kappas ranging from 0.66 to 0.94 and 3.5 years for CDR = 1 (Dooneief et al. 1996).
(Oremus et al. 2000).

Construct Validity Clinical Uses

Evidence for construct validity of the CDR
appears solid. In the original study, the CDR The original focus of the CDR was to assess
had strong correlations with the Blessed Demen- community-dwelling older adults, since its anchor
tia Scale (BDS; r = 0.74) and the Pfeiffer Short points probe for examples of one’s engagement
Portable Mental Status Questionnaire (SPMSQ; with the home and community. It has been
r = 0.84) among individuals with CDR ratings adapted for use in chronic long-term care facilities
between no dementia and very mild dementia (Marin et al. 2001). In addition to AD, the CDR
(Hughes et al. 1982). Correlations with various has also been used to stage Parkinson’s disease
cognitive measures ranged from small to large in and frontotemporal dementia (Knopman et al.
community-dwelling samples (MMSE = 0.33; 2011). In terms of longitudinal studies of AD
BDS = 0.74; SPMSQ = 0.84). Similar correla- progression, both the global CDR and the CDR-
tions were found with neuropsychological SB appear to be useful for tracking cognitive
measures such as the CERAD (Oremus et al. changes over a 2–3-year period (e.g., Cortes
2000). There is also evidence that the CDR et al. 2008). Annual rate of change in CDR-SB
remains stable over a 30-year period (Williams among symptomatic AD (global CDR = 0.5
et al. 2009). at baseline) has been reported to be 1.43 points.
In terms of neuropathology, CDR = 0.5 has Those who were CDR = 0.5 at baseline
been associated with multiple pathological signs (3.75 years) progressed to a higher global CDR
including those related to AD, Lewy body demen- more slowly than CDR = 1.0 (2.98 years) (Wil-
tia, and vascular dementia, as well as nonspecific liams et al. 2013).
pathology (Saito and Murayama 2007). CDR Of the two scoring methods, the CDR-SB is
IADL items are associated with widespread gray more commonly used in clinical drug trials
matter loss in the frontal and parietal regions because it was found to be sensitive to changes
among those who are CDR = 0.5 (Chang et al. within 12 months following baseline measure-
2011). A negative association is also found ment in donepezil drug trials, whereas the global
between the CDR-SB score and glucose metabo- CDR was not (e.g., Petersen et al. 2005). CDR-SB
lism in the right posterior cingulate gyrus appears more useful than the global CDR in
(Perneczky et al. 2007). distinguishing mild cognitive deficits from
dementia (Lynch et al. 2006).
Predictive Validity In addition to Western populations, the CDR
CDR-SB yields an overall 94% classification rate has also been accepted as an appropriate compre-
for heterogeneous dementia samples (O’Bryant hensive measure for studies of dementia patients
Clinical Dementia Rating 805

in Asian populations (Senanarong et al. 2006), Gelb, D. J., & St. Laurent, R. T. (1993). Alternative calcu-
although empirical validation of various transla- lation of the Global Clinical Dementia Rating. Alzheimer
Disease and Associated Disorders, 7(4), 202–211.
tions is needed. Hughes, C. P., Berg, L., Danziger, W. L., Coben, L. A., &
The CDR presents several advantages over Martin, R. L. (1982). A new clinical scale for the
psychometric tests. First, it is an assessment staging of dementia. British Journal of Psychiatry,
option for patients who are illiterate and/or have 140, 566–572.
limited English language proficiency. Moreover,
Knopman, D. S., Weintraub, S., & Pankratz, V. S. (2011).
Language and behavior domains enhance the value of
C
it can also be used in the presence of aphasia, a the Clinical Dementia Rating scale. Alzheimer’s &
condition common among patients with Dementia, 7(3), 293–299.
dementing disorders. Lastly, the administration Lowe, D. A., Balsis, S., Miller, T. M., Benge, J. F., &
Doody, R. S. (2012). Greater precision when measuring
of the CDR does not require a standardized set dementia severity: Establishing item parameters for the
of instructions, but is dependent upon a set of Clinical Dementia Rating scale. Dementia and Geriat-
guidelines. As such, the CDR is easily adapted ric Cognitive Disorders, 34(2), 128–134.
for cross-cultural use. Given these advantages, the Lynch, C., Walsh, C., Blanco, A., Moran, M., Coen, R.,
Walsh, J., et al. (2006). The Clinical Dementia Rating
CDR is considered one of the best scales for sum of box score in mild dementia. Dementia and
staging Alzheimer’s dementia (Rikkert et al. Geriatric Cognitive Disorders, 21(1), 40–43.
2011). A disadvantage of the CDR is that it is Marin, D., Flynn, S., Mare, M., Lantz, M., Hsu, M.,
somewhat lengthy to administer. Laurans, M., et al. (2001). Reliability and validity of a
chronic care facility adaptation of the Clinical Demen-
tia Rating scale. International Journal of Geriatric
Cross-References Psychiatry, 16(8), 745–750.
Morris, J. C. (1993). The Clinical Dementia Rating (CDR):
Current version and scoring rules. Neurology, 43(11),
▶ Alzheimer’s Disease 2412–2414.
▶ Dementia O’Bryant, S. E., Lacritz, L. H., Hall, J., Waring, S. C.,
Chan, W., Khodr, Z. G., et al. (2010). Validation of
the new interpretive guidelines for the Clinical Demen-
tia Rating scale sum of boxes score in the national
References and Readings Alzheimer’s coordinating center database. Archives of
Neurology, 67(6), 746–749.
Cedarbaum, J. M., Jaros, M., Hernandez, C., Coley, N., Oremus, M., Perrault, A., Demers, L., & Wolfson, C.
Andrieu, S., Grundman, M., & Vellas, B. (2013). Ratio- (2000). A review of outcome measurement instruments
nale for use of the Clinical Dementia Rating sum of in Alzheimer’s disease drug trials: Psychometric prop-
boxes as a primary outcome measure for Alzheimer’s erties of global scales. Journal of Geriatric Psychiatry
disease clinical trials. Alzheimer’s & Dementia, 9(1), and Neurology, 13(4), 197–205.
S45–S55. Perneczky, R., Hartmann, J., Grimmer, T., Drzezga, A., &
Chang, Y., Bondi, M. W., McEvoy, L. K., Fennema- Kurz, A. (2007). Cerebral metabolic correlates of the
Notestine, C., Salmon, D. P., Galasko, D., et al. Clinical Dementia Rating scale in mild cognitive
(2011). Global Clinical Dementia Rating of 0.5 in impairment. Journal of Geriatric Psychiatry and Neu-
MCI masks variability related to level of function. rology, 20(2), 84–88.
Neurology, 76(7), 652–659. Petersen, R. C., Thomas, R. G., Grundman, M., Bennett,
Coley, N., Andrieu, S., Jaros, M., Weiner, M., Cedarbaum, D., Doody, R., Ferris, S., et al. (2005). Vitamin E and
J., & Vellas, B. (2011). Suitability of the Clinical donepezil for the treatment of mild cognitive impair-
Dementia Rating-sum of boxes as a single primary ment. New England Journal of Medicine, 352(23),
endpoint for Alzheimer’s disease trials. Alzheimer’s & 2379–2388.
Dementia, 7(6), 602–610. Rikkert, M. G. M. O., Tona, K. D., Janssen, L., Burns, A.,
Cortes, F., Nourhashémi, F., Guérin, O., Cantet, C., Gil- Lobo, A., Robert, P., et al. (2011). Validity, reliability,
lette-Guyonnet, S., Andrieu, S., et al. (2008). Prognosis and feasibility of clinical staging scales in dementia: A
of Alzheimer’s disease today: A two-year prospective systematic review. American Journal of Alzheimer’s
study in 686 patients from the REAL-FR study. Disease and Other Dementias, 26(5), 357–365.
Alzheimer’s & Dementia, 4(1), 22–29. Russo, G., Russo, M. J., Buyatti, D., Chrem, P., Bagnati, P.,
Dooneief, G., Marder, K., Tang, M. X., & Stern, Y. (1996). Suarez, M. F., et al. (2014). Utility of the Spanish
The Clinical Dementia Rating scale: Community-based version of the FTLD-modified CDR in the diagnosis
validation of ‘profound’ and ‘terminal’ stages. Neurol- and staging in frontotemporal lobar degeneration. Jour-
ogy, 46, 1746–1749. nal of the Neurological Sciences, 344(1–2), 63–68.
806 Clinical Interview

Saito, Y., & Murayama, S. (2007). Neuropathology of mild current life circumstances, including the reason
cognitive impairment. Neuropathology, 27(6), 578–584. for referral and history of the presenting problem,
Schafer, K., Tractenberg, R., Sano, M., Mackell, J.,
Thomas, R., Gamst, A., et al. (2004). Reliability of as well as an account of developmental/medical/
monitoring the Clinical Dementia Rating in multicenter family history, educational and occupational
clinical trials. Alzheimer Disease and Associated Dis- achievement, legal problems, sociocultural/reli-
orders, 18(4), 219–222. gious considerations, substance abuse, and other
Senanarong, V., Chen, C., & Orgogozo, J. (2006). Third
Asia-Pacific regional meeting of the International relevant psychiatric issues. Together with test data
Working Group on Harmonization of Dementia Drug and collateral information, interview material is an
Guidelines: Meeting report summary. Alzheimer Dis- invaluable tool for clinical hypothesis formulation
ease and Associated Disorders, 20(4), 311–312. and testing, as well as treatment planning.
Williams, M. M., Roe, C. M., & Morris, J. C. (2009).
Stability of the Clinical Dementia Rating, 1979–2007.
Archives of Neurology, 66(6), 773–777.
Williams, M. M., Storandt, M., Roe, C. M., & Morris, J. C. Current Knowledge
(2013). Progression of Alzheimer’s disease as mea-
sured by Clinical Dementia Rating sum of boxes
scores. Alzheimer’s & Dementia, 9(1), S39–S44. There are three types of clinical interview,
reflecting the degree to which the content and
questions are scripted: structured, semi-struc-
tured, and unstructured. A structured interview
Clinical Interview (e.g., the Structured Clinical Interview for DSM-
5 [SCID-5-CV]; First et al. 2015), like any stan-
Kimberly A. Gorgens dardized assessment tool, gathers specific data
Graduate School of Professional Psychology, that allows clinicians to make comparisons
University of Denver, Denver, CO, USA between client and normative group function.
Criticisms of structured clinical interviews
include a frustration with lengthy questionnaires
Synonyms and the missed opportunity for meaningful dia-
logue (Maruish 2008). An unstructured clinical
Diagnostic interview; Intake; Intake interview; interview, on the other hand, is principally reliant
Unstructured clinical interview on clinical skill for direction. An optimal unstruc-
tured clinical interview involves moving from
broad content areas to more specific ones, from
Definition open-ended to more directive questions seeking
yes/no responses. While the goals of clinical
A skillfully conducted clinical interview is the interviewing remain much the same regardless of
cornerstone of psychological assessment. This format, critics have argued that bias is more easily
interaction, typically a face-to-face meeting that introduced into unstructured clinical interviews
lasts between 30 minutes and 2 hours, generates a than standardized approaches. A hybrid approach,
tremendous amount of data for the clinician via the semi-structured clinical interview, offers many
both observation and direct questioning. Informa- of the benefits of its structured and unstructured
tion obtained through observation during the counterparts, with breadth and depth chief among
clinical interview is considered qualitative or them. The semi-structured format ensures that all
descriptive and can include impressions about cog- areas of potential clinical concern are assessed
nition, attention, orientation, language, sensorimo- while affording the clinician the flexibility to dic-
tor functioning, affect, insight, attitude toward tate the degree of attention each content area
assessment, acculturation, hygiene, interpersonal receives. In addition, the semi-structured clinical
relations, and coping mechanisms, among other interview can be altered to accommodate disabil-
variables. In addition, the verbal exchange between ities, it can be abbreviated to meet the needs of the
patient and clinician yields information about client (e.g., fatigue) or the setting (e.g., bedside
Clinical Neuropsychology 807

assessment), and it can be amended to include interview for DSM-5 disorders – Clinician version
additional lines of inquiry. (SCID-5-CV). Arlington: American Psychiatric
Association.
As well as yielding information regarding Lezak, M. D., Howieson, D. B., Bigler, E. D., & Tranel, D.
patient history and current functioning, a clinical (2012). Neuropsychological assessment (5th ed.). New
interview offers opportunities to build rapport and York: Oxford University Press.
foster a working alliance. In addition to promoting Maruish, M. M. (2008). The clinical interview. In R. P.
satisfaction with the assessment process, the
Archer & S. R. Smith (Eds.), Personality assessment.
New York: Routledge.
C
development of rapport may promote compliance Rogers, R. (2001). Diagnostic and structured interviewing.
from a reluctant patient and provide a foundation A handbook for psychologists. New York: Guilford
for follow-up discussions and interventions that Press.
Sbordone, R. J. (2000). The assessment interview in clin-
may be indicated. Also, the dialogue during a ical neuropsychology. In G. Groth-Marnat (Ed.), Neu-
clinical interview allows a clinician to provide ropsychological assessment in clinical practice (pp.
important patient education. The initial conversa- 94–126). New York: Wiley.
tion may explicitly address confidentiality, insur- Shedler, J. (2002). A new language for psychoanalytic
diagnosis. Journal of the American Psychoanalytic
ance/fee setting, the nature and purpose of the Association, 50, 429–456.
examination, the intended use of assessment Zimmerman, M. (1994). Interview guide for evaluating
data, and a summary of follow-up plans including DSM-IV psychiatric disorders and the mental status
feedback sessions (Lezak et al. 2012). examination. East Greenwich: Psych Products Press.
Zimmerman, M., & Mattia, J. I. (1999). Psychiatric diag-
Despite routine use in clinical practice, there is nosis in clinical practice: Is comorbidity being missed?
considerable debate about the reliability of clinical Comprehensive Psychiatry, 40(3), 182–191.
interviews. Many believe the variability in
questioning undermines the utility of the tool itself.
Some research has suggested that unstructured
clinical interviews often fail to detect psychiatric Clinical Neuropsychology
and comorbid conditions (Zimmerman and Mattia
1999). Other researchers find “empirical rigor” in Anthony Y. Stringer
skillful clinical interviewing (Shedler 2002; p. Department of Rehabilitation Medicine, Emory
429). This argument notwithstanding, the clinical University, Atlanta, GA, USA
interview remains a staple assessment tool, as fal-
lible or effectual as the clinician.
Definition

Clinical neuropsychology is a specialty within

Cross-References
psychology that applies the science of brain-
behavior relations to the assessment, diagnosis,
▶ Behavioral Assessment
treatment, and rehabilitation of patients across
▶ Mental Status Examination
the life span with neurological, medical,
▶ Referral Question
neurodevelopmental, psychiatric, or other cogni-
▶ Self-Report Measures
tive and learning disorders (Barth et al. 2003). The
▶ Structured Clinical Interview for DSM-IV
American Psychological Association (APA)
(SCID-I/SCID-II)
defines a clinical neuropsychologist as “a profes-
▶ Structured Interview of Reported Symptoms
sional psychologist who applies principles of
(SIRS)
assessment and intervention based upon the sci-
entific study of human behavior as it relates to
normal and abnormal functioning of the nervous
References and Readings
system” (APA 1989, p. 22).
First, M., Williams, J. B. W., Karg, R. S., & Spitzer, R. L. Clinical neuropsychology is recognized as a
(2015). User’s guide for the structured clinical specialty by APA, the American Board of
808 Clinical Neuropsychology

Professional Psychology, and the Canadian Psy- instrumental in establishing a psychological labo-
chological Association. Though there is no agreed ratory at Mclean Hospital in Boston. This was the
upon date for the emergence of the field, clinical first such laboratory in a hospital setting in
neuropsychology began to be recognized as a the USA.
distinct professional discipline following a 1948 In 1935, the experimental psychologist Ward
symposium at the APA annual meeting appropri- Halstead opened a laboratory at the University of
ately entitled “Neuropsychology.” In this sympo- Chicago for the psychological study of neurology
sium, Hans-Lukas Teuber described procedures and neurosurgery patients. Adopting techniques
he and Morris Bender developed to study the used to test animals in ablation studies, Halstead
behavioral effects of penetrating missile wounds designed a series of tests intended to measure what
to the brain (Benton 1987). he termed “biological intelligence.” The influence
Clinical neuropsychology had many forerun- of Galton’s statistical methods is seen in Halstead’s
ners. In the 1880s, Sir Francis Galton opened a factor analysis of his test battery. Halstead pro-
laboratory in London where for a few pennies, posed a four-factor theory of biological intelligence
people could take tests of visual acuity, reaction in his 1947 book Brain and Intelligence. Halstead’s
time, and various psychophysical abilities. book was severely criticized by contemporary
A cousin of Charles Darwin, Galton’s ideas scholars and ultimately had little influence on the-
about eugenics have made him a historically con- ories of intelligence (Hartman 1991). Halstead’s
troversial figure. Nonetheless, factor analytic sta- test battery, however, did prove highly influential.
tistical methods grew out of his work and became Ralph Reitan, a student of Halstead, established a
critical for the development and validation of laboratory at the University of Indiana Medical
mental ability tests. His work was put to practical Center in 1950. Over the course of several decades,
use in early twentieth-century France when psy- Reitan expanded upon Halstead’s initial battery,
chologists Alfred Binet and Théodore Simon adding procedures for detecting aphasia and sen-
developed intellectual tests to identify and place sory perceptual impairments and for comparing
children in need of special education. World War performances of the two sides of the body. Reitan
I also stimulated interest in his work in the USA, developed adaptations of the original adult battery
as the military sought tests that could efficiently for children and adolescents, collected normative
identify the strengths and weaknesses of large data, and used discriminant function analysis to
numbers of military recruits. As many as one validate the ability of the various batteries to dis-
million soldiers underwent mental ability testing criminate brain damaged from neurologically
during World War I (Hartman 1991). healthy individuals. The Halstead-Reitan Neuro-
Just after World War I, the German American psychological Test Battery set a standard of excel-
psychologist Shepherd Ivory Franz lence for test development in neuropsychology and
(1919) published detailed descriptions of tests of for a time was the most widely used approach in
tactile sensation, motor coordination, praxis, lan- clinical neuropsychological assessment.
guage, attention, memory, visuospatial percep- Reitan’s students were also prolific (Reed
tion, reasoning, and intelligence. By 1924, hand 1985). They include Hallgrim Kløve who studied
dynamometers, finger tapping keys, motor steadi- with Reitan in the 1950s and then established a
ness tests, form perception boards, and tests of laboratory at the University of Wisconsin.
color vision, vibration sense, attention, and mem- Another student, Homer Reed, directed the Neu-
ory were available (Hartman 1991). Though these ropsychology Laboratory at the New England
tests were quickly adopted by researchers (see Medical Center in Boston where he concentrated
Neuropsychology, Science of), clinical application on use of the battery with pediatric patients.
came a few decades later. Franz advocated for Phillip Rennick, who did fellowship training
their clinical use in a series of lectures to the with Reitan, went on to establish a laboratory
Government Hospital for the Insane, starting in at the former (now defunct) Lafayette Clinic
1910 (Hartman 1991) and in 1904 was in Detroit, and developed a repeatable
Clinical Neuropsychology 809

neuropsychological battery for situations in which In 1948, the year of Teuber’s seminal APA
serial testing is needed. presentation, Arthur Benton accepted an
Just as World War I provided an impetus for the appointment as Professor of Psychology at the
development of psychological ability tests, World University of Iowa, and by 1950 established a
War II stimulated the development of neuropsy- neuropsychological testing unit at the University
chological assessment and treatment methods of Iowa Hospitals (Hamsher 1985). There, Ben-
because of the large number of veterans who ton and his students and colleagues conducted C
returned having survived penetrating missile normative studies, examining the effects of age,
wounds to the brain. Reitan’s early work involved gender, and education. They also developed a
the examination of brain-injured World War II variety of tests for use in studying what had
veterans. This population also provided the impe- previously been vaguely defined clinical disor-
tus for Hans-Lukas Teuber’s work in the USA and ders such as the Gerstmann syndrome (See
Aleksandr Romanovich Luria’s work in Russia. Gerstmann Syndrome). Over the next two
Teuber immigrated from Germany and served decades, Benton’s laboratory was home to
as a noncommissioned naval officer before numerous neuropsychology pioneers including
establishing the Psychophysiological Laboratory Max Fogel, Donald Shankweiler, Kerry deS.
with the neurologist Morris Bender at New York Hamsher, Nils Varney, Scott Lindgren, Otfried
University (Weinstein 1985). Besides being the Spreen, and Harvey Levin (Hamsher 1985).
focal point for numerous seminal studies, Benton’s laboratory conducted important studies
Teuber’s laboratory was the incubator for many of aphasia using control group designs, psycho-
neuropsychologists who went on to make impor- logical test construction methods, statistical
tant contributions including Joseph Altman, Lila analysis, and psycholinguistic theory.
Ghent, Rita Rudel, Josephine Semmes, and Sid- The behavioral neurologist Norman
ney Weinstein. Meanwhile, working with Russian Geschwind, along with his colleagues Davis
World War II veterans at the Burdenko Neurosur- Howes and Harold Goodglass, established an
gical Institute in Moscow, Luria developed a aphasiology center at the Boston Veterans Admin-
richly qualitative approach to neuropsychological istration Hospital, continuing the more rigorous
assessment that was in stark contrast to the quan- neuropsychological approach to language disor-
titative and normatively based test batteries that ders. The Boston VA became a major center for
were in use in the USA. Luria also was an expo- neuropsychological training and research with
nent of neuropsychological approaches to rehabil- Dr. Edith Kaplan famously serving there as
itation and to use of pharmacologic agents to “mother” to a generation of neuropsychology
enhance recovery of function (Gualtieri 1988). practitioners and researchers. Dr. Kaplan and her
Besides having cognitive disorders, many associates in Boston developed the process-
injured World War II veterans were aphasic, approach to neuropsychological assessment, rec-
sparking neuropsychological interest in language ognizing that tests are complex and multifactorial
and the brain. Kurt Goldstein’s (See Goldstein, and that patients can take different paths to the
Kurt) book Language and Language Disorders, same test score. According to this approach, only
published in 1948, combined his theories about by systematically analyzing the process(es) by
abstracting ability with neurology’s classic which patients arrive at their responses, often by
anatomico-clinical syndrome approach to apha- parsing a test into fine-grained components, can a
sia. The numbers of aphasic veterans available neuropsychologist truly understand what aspect
for study along with Goldstein’s influential book of brain functioning is compromised.
attracted experimental neuropsychologists and Activity was not confined to North America.
psycholinguists to the study of language disorders Clinical neuropsychology got its South American
(Goodglass 1985). Aphasia research centers start when C. Mendilaharsu and S. Acevedo de
began to appear in the USA, among them being Mendilaharsu established the first South Ameri-
a laboratory established by Arthur Benton. can neuropsychological laboratory in 1958 at the
810 Clinical Neuropsychology

Neurological Institute in Montevideo, Uruguay and practice of clinical psychologists seeking sub-
(Ardila 1990). Despite sometimes challenging specialty certification in the USA.
economic conditions, South American neuropsy- In 1987, APA Division 40 published guide-
chologists conducted investigations of construc- lines for doctoral, internship, and postdoctoral
tional ability, dementia, and language. The field training in neuropsychology and a year later
spread to Mexico, Peru, Columbia, Chile, Argen- formally adopted the definition of a clinical neu-
tina, Brazil, Honduras, Nicaragua, and elsewhere. ropsychologist quoted above. Included in this
Clinical neuropsychology as a profession has definition (but not quoted) were explicit training,
become increasingly organized since its inception. supervision, licensing, and peer review require-
The International Neuropsychological Society ments that must be met by neuropsychologists.
(INS), the National Academy of Neuropsychology APA also recognized attainment of the ABCN/
(NAN), and the APA Division of Clinical Neuro- ABPP diploma as “the clearest evidence of com-
psychology (Division 40) are the most well-known petence as a Clinical Neuropsychologist” (APA
professional neuropsychological organizations Division 40 1989). As of 2017, over 1500 prac-
within the USA. Founded in 1967, INS has a ticing clinicians have attained ABPP/ABCN
membership that exceeds 3500. NAN, formed in diplomate status. Though ABCN and ABN ini-
1974, includes more than 3000 members. Division tially differed in their examination procedures,
40 of the American Psychological Association, currently both boards now require a peer review
incorporated in 1980, is the most recent of these of credentials, a multiple-choice written exam, a
professional organizations, with a membership of review of submitted work samples, and an oral
over 4000 neuropsychologists. Although smaller in examination. Nonetheless, the two boards have
membership, neuropsychologists have formed sim- not shown comparable growth. As of 2017, over
ilar professional organizations throughout Europe, 1500 practicing clinicians have attained ABPP/
Asia, South America, Australia, and Africa (see, ABCN diplomate status, while ABN diplomates
for example, Jodzio 1998; Nihashi 1998; number in the lower hundreds. While a merger of
Preilowski 1997). the two boards has been discussed, no active
Formal courses and organized programs of efforts in this direction are underway. ABCN
instruction in clinical neuropsychology began to continues to grow at a rapid pace, making neu-
appear in the 1960s, with one of the first offered ropsychology the fastest growing ABPP spe-
in the Biological Psychology Doctoral Program at cialty. One milestone likely to occur in the
the University of Oklahoma Health Sciences Center USA in the twenty-first century is the achieve-
(Parsons 1991). Quality and content of instruction ment of widespread ABPP/ABCN diplomacy
varied from program to program as they multiplied among those identifying neuropsychology as
in the 1970s. In 1979, Dr. Manfred Meier initiated their primary area of specialization. This mile-
an effort to establish standards of training and com- stone would signal the professional and organi-
petence for neuropsychologists in the USA. This zational maturity of clinical neuropsychology.
effort culminated first in the establishment of the Neuropsychology in the twenty-first century is
American Board of Clinical Neuropsychology responding to changes in population demo-
(ABCN) in 1981. A year later, the American graphics. In the USA, the growing Hispanic/
Board of Professional Neuropsychology (ABN) Latino population has brought recognition of the
was established with a similar goal of establishing limited assessment tools available for Spanish-
standards of professional expertise in neuropsy- speaking populations. The American Academy
chology. These two certification bodies continue of Clinical Neuropsychology (AACN) estimates
to function autonomously, though ABCN affiliated that if appropriate assessment tools are not devel-
with the American Board of Professional Psychol- oped, by the year 2050, 60% of the American
ogy (ABPP) in 1984, joining other boards that population will not be able to undergo neuropsy-
conduct peer review of the credentials, knowledge, chological testing. The AACN Relevance 2050
Clinical Neuropsychology 811

Initiative, launched in 2016, attempts to address eloquent cortex. As has happened with many
this shift by supporting among other things the other fields, clinical neuropsychology is likely to
development of new assessment methods, training be significant transformed in coming years by
models, and clinical strategies to maintain the technological innovation.
field’s vital role in US healthcare. As neuropsy- A final emerging trend that deserves highlight-
chology spreads worldwide, the need for language ing is clinical neuropsychology’s transition from a
and culture appropriate test batteries grows. Sim- predominantly diagnostic field to one that is at the C
ilar initiatives are needed now in developing forefront of intervention. Cognitive rehabilitation,
countries with large neurological populations in the application of remedial exercises and compen-
need of neuropsychological services. satory strategies to address cognitive impairment,
The expansion in information technology is has become an integral part of neuropsychology.
also challenging neuropsychology. Increasingly Clinical neuropsychologists work in rehabilitation
neuropsychology test publishers are introducing and outpatient clinic settings developing and
tests that are administered or scored by computer, guiding the rehabilitation of patients with cogni-
while standard paper-and-pencil versions of tests tive impairment due to stroke, brain injury, and
are slowly phased out. Computer administration numerous other neurological conditions. Technol-
brings many challenges, but also opportunities. ogy plays a large role here as well, as increasingly
“Big Data” analysis is having a huge impact on neuropsychologists make use of smartphones and
economics, public health, and marketing fields, a host of other adaptive aids to foster patient
and could impact neuropsychology in as yet independence. The aging of the US population
unforeseen ways as test data is captured for future will likely bring more opportunities for expansion
analysis by test developers. This also poses sig- of an interventional and technologically oriented
nificant privacy and ethical challenges for a field clinical neuropsychology.
that maintains strict standards with regards to
patient confidentiality.
Information technology also makes possible Cross-References
entirely new methods of test administration.
Rather than every patient getting the same ▶ American Academy of Clinical Neuropsychol-
sequence of test items, technology makes it pos- ogy (AACN)
sible to adjust item difficulty in response to a ▶ American Board of Clinical Neuropsychology
predetermined criterion of success or failure. (ABCN)
A patient’s response ceiling can be determined ▶ American Board of Professional Neuropsy-
much more rapidly, allowing testing to be chology (ABN)
discontinued or shifted to another cognitive ▶ American Psychological Association (APA),
domain before the assessment becomes overly Division 40
frustrating. Such a strategy could greatly reduce ▶ Benton, Arthur (1909–2006)
the length of test batteries without necessarily ▶ Forensic Neuropsychologist
sacrificing accuracy or comprehensiveness. Neu- ▶ Forensic Neuropsychology
ropsychology also increasingly utilizes functional ▶ Geschwind, Norman (1926–1984)
magnetic resonance imaging (fMRI) and other ▶ Halstead, Ward (1908–1968)
technologies to elucidate brain-behavior relation- ▶ International Neuropsychological Society
ships in the research lab. This use is only begin- ▶ Luria, Alexander Romanovich (1902–1977)
ning to extend to the clinical setting where ▶ National Academy of Neuropsychology (NAN)
neuropsychologists may be actively involved in ▶ Neuropsychiatry
fMRI language mapping as part of the evaluation ▶ Neuropsychology
of patients who are candidates for tumor resec- ▶ Reitan, Ralph (1922–)
tions or palliative seizure surgeries that involve ▶ Teuber, Hans-Lukas (1916–1977)
812 Clinical Practice Guidelines

References and Readings

Clinical Practice Guidelines
American Psychological Association Division 40. (1989).
Definition of a clinical neuropsychologist. The Clinical
Orlando Sánchez1 and Martha Brownlee-Duffeck2
Neuropsychologist, 3, 22. 1
Ardila, A. (1990). Neuropsychology in Latin America. The Minneapolis VA Health Care System,
Clinical Neuropsychologist, 4, 121–132. Minneapolis, MN, USA
Barth, J. T., Pliskin, N., Axelrod, B., Faust, D., Fisher, J., 2
Harry S. Truman Memorial, Columbia, MO,
Harley, J. P., et al. (2003). Introduction to the NAN
USA
2001 definition of a clinical neuropsychologist.
Archives of Clinical Neuropsychology, 18, 551–555.
Benton, A. (1987). Evolution of a clinical specialty. In
K. M. Adams & B. P. Rourke (Eds.), The TCN guide Synonyms
to professional practice in clinical neuropsychology
(pp. 1–4). Amsterdam: Swets & Zeitlinger. Clinical guideline; Evidence-based guidelines;
Goldstein, K. (1948). Language and language disorders. Individualized guidelines; Medical guideline;
Orlando: Grune & Stratton.
Goodglass, H. (1985). Aphasiology in the United States. Practice guidelines; Practice parameters
International Journal of Neuroscience, 25, 307–311.
Groth-Marnat, G. (2000). Introduction to neuropsychological
assessment. In G. Groth-Marnat (Ed.), Neuropsycholog- Definition
ical assessment in clinical practice: A guide to test inter-
pretation and integration (pp. 3–25). New York: Wiley. The Institute of Medicine (IOM) revised its original
Gualtieri, C. T. (1988). Pharmacotherapy and the definition of clinical practice guidelines (CPGs) in
neurobehavioural sequelae of traumatic brain injury.
Brain Injury, 2, 101–129. 2011. According to this new definition, CPGs are
Hamsher, K. D. (1985). The Iowa Group. International “statements that include recommendations
Journal of Neuroscience, 25, 295–305. intended to optimize patient care that are informed
Hartman, D. E. (1991). Reply to Reitan: Unexamined pre- by a systematic review of evidence and an assess-
mises and the evolution of clinical neuropsychology.
Archives of Clinical Neuropsychology, 6, 147–165. ment of the benefits and harms of alternative care
Jodzio, K. (1998). Neuropsychology in Poland: Past and options.” Systematic review of evidence was
present. International Neuropsychological Society defined as “a scientific investigation that focuses
Liaison Committee Newsletter, 5, 1–3. on a specific question and uses explicit, pre-
Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004).
The practice of neuropsychological assessment. In specified scientific methods to identify, select,
Neuropsychological assessment (4th ed., pp. 3–14). assess, and summarize the findings of similar but
New York: Oxford University Press. separate studies.” This two-part definition empha-
Nihashi, N. (1998). Neuropsychology in Japan. Interna- sizes the importance of (1) a thorough systemic
tional Neuropsychological Society Liaison Committee
Newsletter, 5, 1–3. research review carefully scrutinizing the strength
Parsons, O. A. (1991). Clinical neuropsychology of the evidence to then (2) us this evidence to device
1970–1990: A personal view. Archives of Clinical Neu- highly specific recommendations that, among other
ropsychology, 6, 105–111. things, considers the benefits and harms of
Preilowski, B. (1997). Establishing clinical neuropsychol-
ogy in Germany: Scientific, professional, and legal healthcare options. Thus, in practical terms, clinical
issues. Neuropsychology Review, 7, 187–199. practice guidelines are subject specific (e.g., diabe-
Reed, J. (1985). The contributions of Ward Halstead, Ralph tes mellitus care plan, treatment and management
Reitan and their associates. International Journal of of adult allergic rhinitis, etc.), research-based rec-
Neuroscience, 25, 289–291.
Stringer, A. Y., & Cooley, E. L. (2002). Neuropsychology: ommendations intended to assist healthcare pro-
A twentieth-century science. In A. Y. Stringer, E. L. viders in the delivery of optimal patient care.
Cooley, & A.-L. Christensen (Eds.), Pathways to prom-
inence in neuropsychology: Reflections of twentieth cen-
tury pioneers (pp. 3–26). New York: Psychology Press. Historical Background
Weinstein, S. (1985). The influence of Hans-Lukas Teuber
and the psychophysiological laboratory on the estab-
lishment and development of neuropsychology. Inter- Recommendations for appropriate care have been
national Journal of Neuroscience, 25, 277–288. found in ancient writings (IOM 1992). Modern
Clinical Practice Guidelines 813

guidelines have been developed by professional development. The last update on clinical practice
organizations for over 50 years. It was only in the guidelines from the IOM took place in 2011 with a
1990s, however, that the systematic, evidence- report called Clinical Practice Guidelines We Can
based guidelines began to appear with any regu- Trust. This report offered a revised definition of
larity. In November 1989, the Agency for Health CPGs and addressed several factors including the
Care Policy and Research (AHCPR), currently lack of multidisciplinary representation in guide-
known as Agency for Healthcare Research and line development, failure to include a comprehen- C
Quality (AHRQ), was created with, among other sive external review process, and lack of
responsibilities, a mandate to develop, dissemi- transparency concerning recommendations and
nate, and evaluate clinical practice guidelines. how these are derived and rated.
The AHCPR then enlisted the IOM for advice. While CPGs were initially intended to assist
The result was the 1990 report generated by the clinicians in the delivery of quality care, insurance
IOM called Clinical Practice Guidelines: Direc- companies, healthcare administrators, and attor-
tions for a New Program that aimed to encourage neys also routinely use them. Insurances and
standardization and consistency in the develop- healthcare administrators have begun to rely on
ment of guidelines. From inception, the five major well-established CPGs to implement Pay for Per-
purposes of clinical practice guidelines has been formance programs (Rosenthal et al. 2005). The
to (1) aid in clinical decision-making by patients goal of these programs is to reduce costs while
and healthcare providers, (2) educate individuals improving care by linking the clinician’s payment
or groups, (3) assess and ensure quality of care, (4) to care quality via performance measures derived
guide the allocation of healthcare resources, and from CPG recommendations. Currently, research
(5) reduce the risk of liability for negligent care is insufficient to validate the utility of Pay for
(IOM 1992). Performance programs and/or whether they actu-
In 1992, the IOM published a second report ally accomplish their goal of reducing costs and
that expanded on their 1990 report by emphasiz- improving care. While attorneys have attempted
ing the importance of credibility and utility with to use CPGs in malpractice litigations, due to a
respect to the guideline development process. plethora of CPGs on similar topics with little if
Over the next few years, guideline efforts were any consensus in their recommendations, their use
thwarted primarily by concerns associated with for this purpose has not been successful.
inadequacies in the selection of guideline topics.
Consequently, in 1995, the IOM released a third
report recommending set principles and methods Current Knowledge
for prioritizing topics. Though many of the 1995
recommendations were largely debated and Since the first IOM report in 1990, practice guide-
ignored, one conclusion was highly influential – lines have rapidly proliferated nationally and
agencies act as clearinghouses and disseminate across international boundaries with approxi-
guidelines. Clinical practice guidelines were mately 2,700 national guidelines and 3,700 inter-
again reviewed by the IOM in 2008 and con- national guidelines covering a wide range of
cluded that many problems identified by earlier specialties (IOM 2011). As national and interna-
reports persisted. As a result, the IOM tional CPG organizations became well
recommended a public-private program to (a) cre- established, they began to promote CPG develop-
ate a set of standards to aid the process of devel- ment via a highly intensive and systematized
oping guidelines and (b) develop a method for review of current research and knowledge. Con-
documenting adherence to these standards. In sequently, CPGs gained both momentum and
addition, the 2008 IOM report, in conjunction influence. However, though CPGs have abun-
with a subsequent IOM report published in dantly flourished, to this day, they vary greatly in
2009, sought to address issues associated with quality and objectiveness. To confront this issue,
conflict of interests pertaining to guideline the following eight standards were proposed to
814 Clinical Practice Guidelines

ensure high quality, trustworthy clinical practice expressed particular concern in their ability to
guidelines that could increase quality of care: meet such standards given the complex develop-
ment process.
1. Transparency – how CPGs are developed and The Agency for Healthcare Research and
who funds them should be explicitly outlined Quality (AHRQ), formerly the AHCPR, in part-
and made public. nership with the American Medical Association
2. Conflict of Interest – managing conflict of and America’s Health Insurance Plans (formerly
interest can range from simple disclosure to the American Association of Health Plans) cre-
exclusion of CPG panel participation. ated a central public resource for evidenced-based
3. Guideline Development and Group Composi- clinical practice guidelines called the National
tion – panels should be multidisciplinary Guideline Clearinghouse (NGC) that can be
reflecting three to five disciplines and should accessed at http://www.guideline.gov/.
include the input of patients and public/con- The purpose of the NGC is to (a) offer acces-
sumer representatives. sible means of obtaining detailed objective infor-
4. Systematic Review of Evidence – CPGs mation concerning CPGs and (b) promote the
should be based on quality research that ongoing dissemination of CPGs, their implemen-
meets the IOM Committee on Standards for tation, and routine use. For a clinical practice
Systematic Reviews of Comparative Effective- guideline to be included on the NGC, the follow-
ness Research. ing 2013 revised criteria must be met:
5. How Recommendations are Made and Rated
– the evidence for each recommendation must 1. The guideline must contain systematically
be clearly articulated in addition to a clear developed recommendations aimed at optimiz-
outline of how a score, grade, or rating was ing patient care and assist in the decision-mak-
assigned. ing of appropriate healthcare in specific
6. Articulating Recommendations – all recom- clinical situations by healthcare providers and
mendations deriving from CPGs should be patients.
articulated in a clear and precise manner. 2. The guideline must be produced by a medical
7. External Review – CPGs should undergo an specialty association, professional societies,
external review by a diverse panel of stake- public or private organizations, government
holders including patients, public representa- agencies, or healthcare organizations or plans.
tives, agencies/organizations, and scientific 3. Guidelines are based on a systemic review of
and clinical experts. available evidence with specific documenta-
8. Updating – CPGs should be routinely updated tion provided verifying that such review was
to reflect the most current body of scientific performed during the guideline development.
knowledge available (IOM 2011). 4. Guidelines or supporting documentation
includes an assessment of the potential risks
In addition, at an international level, standards and benefits of recommended care and alterna-
for achieving high-quality CPGs have been set tive options.
forth by the Guidelines International Network 5. Upon request, the guideline (full text) should
(G-I-N), which is a network composed of 104 be available in English to the public.
organizations from 51 countries (G-I-N, 2015). 6. The guidelines should be up to date – pro-
At present, while the vision and aspiration to duced, reviewed, or revised within 5 years
achieve trustworthy, quality national and interna- (National Guideline Clearinghouse 2013).
tional CPGs has been received favorably, the main
criticism is in the practical implementation of such These criteria ensure minimum quality of
standards. Settings with limited resources have guidelines submitted to the NGC.
Clinical Significance 815

Future Directions Cross-References

An ongoing challenge is the implementation of clin- ▶ AACN Practice Guidelines

ical practice guidelines and ensuring their applica-
tion by healthcare providers. Factors such as
information overload, habitual practice patterns, References and Readings
fears of malpractice, and a lack of economic incen- C
tives create barriers to guideline application, and Eddy, D., Adler, J., Patterson, B., Lucas, D., Smith, K., &
Morris, M. (2011). Individualized guidelines: The
each must be addressed on an individual and sys-
potential for increasing quality and reducing costs.
temic level. With the birth of information technology Annals of Internal Medicine, 154, 627–634.
giving rise to electronic health records, CPGs must IOM. (1992). In M. J. Field & K. N. Lohr (Eds.), Guide-
become electronically compatible to ensure they do lines for clinical practice: From development to use.
Washington, DC: National Academy Press.
not become obsolete. The interface between CPGs
IOM (Institute of Medicine). (2011). Clinical practice
and clinical decision support (CDS), considered a guidelines we can trust. Washington, DC: The National
key factor in information technology as it pertains to Academies Press.
healthcare, will be significantly important. National Guideline Clearinghouse. (2013). Inclusion
criteria. Retrieved 17 Nov 2015, from the National
The concept of individualized guidelines has
Guideline Clearinghouse Web site: http://www.guide
also recently emerged as an area for future develop- line.gov/about/inclusion-criteria.aspx
ment (Eddy et al. 2011). The focus of individualized Rosenthal, M. B., Frank, R. G., Li, Z., & Epstein, A. M.
guidelines, as the name suggests, is on specific risk (2005). Early experience with pay-for-performance: From
concept to practice. JAMA: Journal of the American
factors for a particular individual as opposed to
Medical Association, 294(14), 1788–1793. https://doi.
general risk factors concerning the larger popula- org/10.1001/jama.294.14.1788.
tion. These person-specific risk factors are then Welcome to G-I-N – Guidelines International Network.
incorporated into mechanisms set to evaluate the (n.d.). Retrieved 24 Nov 2015, from http://www.g-i-n.net/
benefits and risks of medical decisions to subse-
quently guide clinicians in their treatment approach.
Individualized guidelines and their potential to
reduce costs and improve care will be greatly Clinical Significance
enhanced by further research in the following areas:
Monica Kurylo1 and Kimberly Fleming2
1
1. Risk calculators – devising adequate calcula- Departments of Psychiatry and Rehabilitation
tors to assist clinicians in their decision-mak- Medicine, University of Kansas Medical Center,
ing process will greatly advance the utility and Kansas City, KS, USA
2
quality of CPGs. Department of Psychiatry and Behavioral
2. Disease models – if useful CPGs are to be Sciences, The University of Kansas KU Medical
developed for specific conditions, ongoing Center, Kansas City, KS, USA
research concerning validated disease models
is needed (without adequate research to help us
understand how a particular disease works, Clinical significance is a perceived, valued, and
treatment advances cannot be made, and, as a functionally relevant discrepancy in symptoms/
result, an adequate CPG targeting that disease abilities that reflects an important change in func-
cannot be developed). tioning. This can involve either an improvement
3. Practical applications – more research is (usually as a result of treatment or intervention) or
needed to make the leap from theory to practice a decline (typically due progression of illness or
concerning the practical application of trust- disorder) as measured by symptoms or impair-
worthy, high quality CPGs. ment level.
816 Clock Drawing

Clinical significance also refers to a static con-

dition of import – for example, a functionally Clock Drawing
relevant discrepancy between cognitive abilities
in different domains (e.g., language vs. visual- David J. Libon1, Edith Kaplan2, Rod Swenson3
perceptual abilities). and Dana L. Penney4
1
While clinical significance may be supported Departments of Geriatrics, Gerontology, and
by statistically significant differences on quantita- Psychology, Rowan University, New Jersey
tive measures of functioning, statistical signifi- Institute for Successful Aging, School of
cance cannot be equated with clinical Osteopathic Medicine, Stratford, NJ, USA
2
significance. Department of Psychology, Suffolk University,
Boston, MA, USA
3
Department of Psychiatry and Behavioral
Cross-References Science, University of North Dakota School of
Medicine, Fargo, ND, USA
▶ Functional Assessment 4
Department of Neurology, The Lahey Clinic,
▶ Premorbid Functioning Burlington, MA, USA
▶ Quality of Life
▶ Reliable Change Index
▶ Response to Intervention Description
▶ Statistical Significance
Clock drawing test (CDT) is a widely used and
popular neuropsychological test. Rubin et al.
References and Readings (2005) reported that the CDT appears in the top
40 tests most commonly used by neuropsycholo-
American Psychiatric Association. (2013). Diagnostic and gists. The CDT is often considered to be a
statistical manual of mental disorders (5th ed.). Arling-
visuoconstructional test. Modern versions of the
ton: American Psychiatric Association.
Bowden, S. C., Harrison, E. J., & Loring, D. W. (2014). CDT usually contain at least two parts – clock
Evaluating research for clinical significance: Using drawing to command and clock drawing to copy.
critically appraised topics to enhance evidence-based In the command condition, patients are presented
neuropsychology. The Clinical Neuropsychologist, 28,
with a blank sheet of paper and are asked to “draw
653–668.
Jacobson, N. S., & Truax, P. (1991). Clinical significance: the face of a clock showing the numbers and the
A statistical approach to defining meaningful change in two hands set for ten after eleven”. In the copy
psychotherapy research. Journal of Consulting and condition, a pre-drawn model of a clock with num-
Clinical Psychology, 59, 12–19.
bers and hands set for 10 after 11 is presented, and
Jacobson, N. S., Roberts, L. J., Berns, S. B., &
McGlinchey, J. B. (1999). Methods for defining and the patient is asked to copy the model. Clock draw-
determining the clinical significance of treatment ing with hands set for 10 after 11 is an innovation
effects: Description, application, and alternatives. Jour- introduced by Edith Kaplan (1988, 1990). As
nal of Consulting and Clinical Psychology, 67,
described below, other versions of the CDT ask
300–307.
Kazdin, A. E. (1999). The meanings and measurement of the patient to set the hands for other times. Also,
clinical significance. Journal of Consulting and Clini- some versions of the CDT include a clock subtest in
cal Psychology, 67, 332–339. which patients are presented with pre-drawn clock
Kazdin, A. E. (2003). Clinical significance: Measuring
whether interventions make a difference. In A. E.
faces with and without numbers and/or hands and
Kazdin (Ed.), Methodological issues and strategies in are asked to either draw clock hands to designate
clinical research (3rd ed., pp. 691–710). Washington, specific times or read the specified time (Borod
DC: American Psychological Association. et al. 1980; Leach et al. 2000; Tuokko et al. 1992).
Spitzer, R. L., & Wakefield, J. C. (1999). DSM-IV diag-
nostic criterion for clinical significance: Does it help
solve the false positives problem? American Journal of
Psychiatry, 156, 1856–1864. Edith Kaplan: deceased.
Clock Drawing 817

Historical Background cortex. This is in stark contrast to the anecdotal

point of view that tends to automatically associate
Since the late 1980s, a profusion of research using defective clock drawing (or any other impaired
the CDT as an assessment tool for dementia has figure copying test for that matter) with a right
emerged. However, some of the more interesting parietal lesion. While it is certainly true that
historical roots of the CDT came from research patients with right parietal lesions often produce
with aphasic patients. Henry Head, in his magnum very spatially impaired clock drawings, it is naive C
opus Aphasia and Kindred Disorders of Speech to automatically associate impaired clock drawing
(1926), assessed aphasic patients using a wide with either a lesion in any single brain region, or
number of drawing tests including “the clock as a measure of any single cognitive operation. As
test” (p. 214) to assess deficits in understanding described below, defective clock drawings to
and executing complex propositional speech and command and copy can be associated with a
deficits associated with symbol formation. wide array of neurologic lesions and underlying
In describing propositional speech and symbolic cognitive disorders.
formation deficits associated with aphasia, Head Many time settings have been used in the CDT.
(1926) wrote “any act of mental expression, Kaplan (1988, 1990) recommends using “ten after
which demands symbolic formulation, tends to eleven.” First, clock setting for 10 after 11 requires
be defective and the higher its propositional the patient to disambiguate a complex proposi-
value the greater the difficulty it will present” tional command. Second, since the numbers
(p. 212). Head (1926) provided many examples “10” and “11” are on the clock, patients need to
of aphasic patients who demonstrated striking resist the temptation to be pulled to the numbers
impairment in executing the propositional “10” and “11.” Thus, clock setting to 10 after
command to set the clock hands for a specified 11 tends to elicit a variety of stimulus-bound
time. For example, Head described an aphasic errors. In a survey of neuropsychologists and neu-
patient who was able to set clock hands “correctly rologists described by Freedman et al. (1994),
at 3:40,” but not when he was told to place other commonly used clock settings include “20
the hands at “20 minutes to 4.” For this latter after 8” and “3 o’clock.”
test condition (“20 minutes to 4”), Head
commented that his patient appeared “doubtful
of the meaning of the words 20 minutes to.” Psychometric Data
Other researchers have used the CDT to assess
deficits in symbolic formation in neurologic Some scoring guidelines for the CDT can be
patients (Mayer-Gross 1935; McFie and Zangwill found as part of the Boston Diagnostic Aphasia
1960; Van Horst 1934). Examination supplementary language tests
Classically trained neurologists often associate (BDAE; Goodglass and Kaplan 1972, 1983;
the CDT as a means to assess constructional Goodglass et al. 2001). In the original BDAE
apraxia. Kleist (1912, cited in Benton and Tranel (with the rakishly purple cover [see Holland’s
1993) described constructional apraxia as deficits forward to the third edition of the BDAE,
in formative activities necessary to assemble parts 2001]), the CDT test was one of several tests
into a meaningful whole. For Kleist, the essential believed to be sensitive to parietal lobe injury.
defect in constructional apraxia was the ineffec- As described in the BDAE corpus, clock drawing
tive translation of visuoperceptual information is one of six figures where patients are asked to
into an effective motor act. In this sense, the draw to command and copy (i.e., a clock with
concepts of Kleist are consistent with the con- hands set for 10 after 11, a daisy, an elephant, a
structs Head (1926) used to understand impaired red cross, a three-dimensional cube, and a
clock drawings produced by aphasic patients. house). For the clock drawing portion of the
Interestingly, Kleist tended to associate construc- test, a three-point scoring system was described
tional apraxia with lesions in the left posterior awarding a point for an approximately circular
818 Clock Drawing

clock face, symmetry of number placement, and system. The pre-drawn clock face condition is
correctness of numbers. No scoring for the rep- scored using an 11-point scoring system. Thus,
resentation of the clock hands was suggested. for this portion of the test, scores have a 0–37
Normative data for the entire figure drawing point range. Each clock reading subtest contains
test (range 0–13 for the separate command and six test stimuli. Performance on the three clock
copy test conditions) is provided. Separate nor- drawing test conditions are combined with a score
mative data for the CDT is not included. Addi- measuring the copy of a complex figure for a
tional normative information is provided by combined age-corrected scale score. The two
Borod et al. (1980). In this report, norms are clock reading subtests are scored separately
also provided for two additional clock assess- (range 0–6). For these two tests, age-related per-
ment procedures – clock setting with numbers centile cut scores are provided.
and clock setting without numbers. In both tests, Freedman et al. (1994) described a very com-
the patient is presented with pre-drawn clock prehensive clock scoring system using a variety of
faces with and without numbers and are asked clock drawing conditions and clock settings. Nor-
to draw the hands to read 1:00, 3:00, 9:15, and mative data was collected and grouped by decade
7:30. Performance is assessed using a 12-point from age 20 to 80+. Separate scales were devel-
scoring system. Borod et al. (1980) described oped to assess the drawing of the clock face, the
both age and educational effects for this clock drawing of the numbers, the presence and drawing
assessment procedure. Other researchers have of the clock hands, and the degree to which the
commented on the effects of education on clock clock hands emanated from the center of the clock
drawing test performance (Marcopulos face. Base rates for a wide range of clock drawing
et al. 1997). behavior are provided. These data show that cer-
The Kaplan-Baycrest Neuropsychological tain errors occur more frequently with age. For
Survey (KBNS; Leach et al. 2000) contains a example, for clock setting using “ten after
comprehensive clock test consisting of five parts: eleven,” the representation of the clock hands
tends to be differentially affected by age.
1. Clock drawing to command where patients are As noted above, a wide number of clock draw-
asked to draw the face of clock put in all the ing procedures have been reported (Lezak et al.
numbers and set the hands for 10 after 11 2004); however, most researchers follow Kaplan’s
2. A clock drawing to copy condition where (1988, 1990) suggestion and ask patients to set the
patients are presented with a blank page and hands for “ten after eleven” (Freedman et al.
asked to draw a clock with numbers and set the 1994). It is important to understand that many
hands for 10 after 11 CDT scoring procedures are essentially atheoreti-
3. A pre-drawn clock face where patients are cal, that is, the administration and scoring pro-
asked to put in all the numbers and set the cedures were devised with an eye toward
hands for 20 after 8 sensitivity to brain damage or neurological insult
4. A clock reading test with hands, but without rather than to assess for deficits involving specific
numbers where patients are asked to identify a cognitive constructs. Recent research, particularly
specified time in using the CDT as part of a dementia evaluation,
5. A clock reading test with numbers and hands suggests that the command and copy conditions
where patients are, again, asked for the speci- are related to different underlying cognitive mech-
fied time anisms (Cosentino et al. 2004; Libon et al. 1993,
1996; Rouleau et al. 1992). Equally important,
For clock drawing to command and copy, different results are obtained depending on test
behavior related to the drawing of the clock face, instruction (see Cosentino et al. 2004 for a
the numbers, and hands and the representation of review). These considerations are critically
the clock hands originating from the center of the important when the task at hand is to differentiate
clock are each scored using a 13-point scoring between say, dementia subtypes.
Clock Drawing 819

Clinical Uses visuospatial impairment seen in the command

condition may be due to a deficit in visuospatial
Focal lesions – Clock drawing has not been exten- memory. Tranel et al. (2008) administered the
sively studied in non-dementia, focal-lesioned CDT to a large group of focal-lesioned patients.
patients. Nonetheless, specific patterns of deficits Imaging studies found errors on the CDT were
can be associated with specific neurologic lesions. associated with right parietal (supramarginal
Freedman et al. (1994) and Kaplan (1988, 1990) gyrus) and left inferior frontal-parietal opercular C
provide some instructive exemplars. For example, brain damage. These researchers also noted that
patients with left posterior brain lesion resulting in visuospatial errors were predominant in patients
a Wernicke’s aphasia often present with language with right hemisphere damage, whereas time-
comprehension deficits. While these patients may setting errors were predominant in patients with
demonstrate general understanding of the clock left hemisphere lesions.
drawing instructions, numbers may be omitted Dementia – As noted above, since the late
entirely with hatch marks used as substitutes 1980s, there has been a plethora of research dem-
(Freedman et al. 1994). Patients with a left ante- onstrating the value of the clock drawing test as
rior lesion presenting with a Broca’s aphasia often both a screening test for dementia as well as a
have difficulty in understanding functor words means of investigating cognitive constructs that
such as “to” and “after.” These patients, therefore, may differentiate between dementia subtypes (see
may be apt to draw the clock hands pointing to the Cosentino et al. 2004 for a review). Rouleau et al.
numbers “10” and “11.” Further assessment is (1992, 1996) examined patients with Alzheimer’s
required to see if this kind of error is caused by a disease (AD) and Huntington’s disease
language-related deficit or represents an executive (HD) administering a clock drawing test to com-
deficit. Patients with left hemisphere lesions mand and copy with hands set for 10 after 11. An
might initiate their drawing on the left side of the analysis of errors proved effective in differentiat-
clock, that is, on the side contralateral to their ing between dementia subtypes. AD patients
intact right hemisphere. Thus, numbers may be made more conceptual errors, while HD patients
written correctly but in a counterclockwise direc- produced more graphomotor errors. These authors
tion (Freedman et al. 1994). speculated that semantic knowledge deficits
Interesting dissociations can be found in clock might underlie the deficits produced on the CDT
drawings to command versus copy in focal lesion by AD patients whereas executive dysfunction
patients. Kaplan (1990) provides several instruc- might underlie the errors produced by HD
tive examples. An analysis of clock drawings patients. When the command and copy conditions
produced by a patient with a right parietal lesion were compared, AD, but not HD patients
demonstrates differential impairment in the copy improved from the command to copy test
versus the command test conditions. In the copy conditions.
test condition, many numbers were omitted on the Rouleau’s research was the impetus for a series
left side of the drawing. The clock drawing to of studies conducted by Libon and colleagues
command did not demonstrate this behavior and (Cosentino et al. 2004; Libon et al. 1993, 1996)
was generally intact compared to the copy test that examined differences on the CDT between
condition. Kaplan (1988) demonstrated the oppo- patients with AD and vascular dementia (VaD). In
site profile in a patient with a right temporal their original study, Libon et al. (1993) found no
lesion. Here, there was differential impairment in difference in errors between AD and VaD patients
the command condition. For this patient, the clock in the command condition. However, similar to
drawing to copy was generally intact. For the right Rouleau, AD patients improved, that is, made
parietal-lesioned patient, the differential impair- fewer errors than VaD patients in the copy condi-
ment in the copy condition likely reflected a deficit tion. These findings were replicated in a second
involving visually mediated neglect of left hemi- study (Libon et al. 1996), that is, AD patients
space. For the left temporal lobe patient, the generally improved from the command to copy
820 Clock Drawing

test conditions compared to VaD patients. interest included a variety of decision-making or

Cosentino et al. (2004) grouped dementia patients intra-component latencies that measure the time
diagnosed clinically with either AD or VaD on the elapsed between clock drawing components (i.e.,
basis of MRI white matter alterations time between last element drawn followed by the
(MRI-WMA). These groups were compared to first clock hand), inter-digit latency (i.e., average
dementia patients with Parkinson’s disease (PD). time between drawing numbers, and quartile
Patients presenting with minimal to mild MRI- drawing time (i.e., total drawing time divided
WMA continued to improve from the command into four equal segments. In the command condi-
to copy test conditions, that is, produce fewer tion impaired MS patients produced slower
errors in the copy versus the condition test condi- selected intra-component latencies and slower
tions, compared to patients with moderate to third and fourth quartile latencies. In the copy
severe MRI-WMA and PD patients. Errors pro- condition, impaired MS patients also displayed
duced the copy condition were correlated with slower selected intra-component latencies and
poor performance on executive tests. Errors pro- slower latencies in all four quartiles compared to
duced in the command condition were correlated NCs, but slower latencies only for the third and
with overall dementia severity and tests related to fourth quartiles compared to non-impaired
semantic knowledge. Cahn-Weiner (2003) corre- MS. These data underscore the notion that prob-
lated CDT performance with MRI measures of lems associated with processing speed underlie
atrophy and found that impaired CDT perfor- much of the neurocognitive impairment associ-
mance was attributable to impairment in multiple ated with MS. However, the data described
cognitive domains but was primarily related to above suggests that processing speed deficits in
volume loss involving the right temporal cortex. MS may be somewhat nuanced and can be shown
Taken as a whole, this research suggests that dif- to fluctuate as patients attempt to bring tests to
ferent cognitive constructs underlie impaired fruition.
clock drawing in patient with cortical versus sub- Cohen et al. (2014) looked at dCDT behavior
cortical dementia. in large group of patients with depression. Despite
equivalent total time to completion there was a
The Digital Clock Drawing System significant interaction such that younger
The traditional clock drawing test has recently depressed patients spent a smaller proportion of
been combined with digital assessment technol- time actually drawing, relative to non-drawing
ogy that uses new, innovative software. This soft- time, compared to the older depressed group.
ware now permits a more sophisticated analysis of Also, in the command and copy test conditions
clock drawing behavior and the neurocognitive percent time spent not drawing was negatively
constructs that underlie problems that emerged correlated with neuropsychological tests that
on the clock drawing test. Using machine learning assess attention/information processing speed.
algorithms Davis et al. (2014) demonstrated that These data are able to differentiated aspects of
the digit clock drawing test (dCDT) was able to psychomotor slowing in depressed patients.
differentiate between patients with Alzheimer’s A behavior often seen in clock drawing is the
disease or other dementia syndromes from normal tendency for patients to initiate their drawings
controls. using anchor digits (i.e., the numbers 12, 6, 3, 9).
Libon et al. (2014) used the digital clock draw- Lamar et al. (2016) studied a group of non-
ing test (dCDT) to examine clock drawing behav- demented/non-depressed adults who were
ior produced by patients with multiple sclerosis grouped on the basis of whether anchor digits
(MS). Clock drawings produced by MS patients were initially drawn before other digits. Partici-
was initially scored using a 10-point scale and pants who anchored had higher local efficiency
classified into impaired versus non-impaired MS involving the left medial orbitofrontal and trans-
clock drawing groups. Both MS groups were verse temporal cortical, right rostral anterior cin-
compared to a NC group. dCDT variables of gulate, and superior frontal gyrus versus
Clock Drawing 821

participants who did not anchor. These data sug- Goodglass, H., Kaplan, E., & Baresi, B. (2001). Assess-
gest a higher degree of modular integration among ment of aphasia and related disorders (3rd ed.). Phila-
delphia: Lippincott, Williams.
heteromodal regions of the ventral visual pro- Head, H. (1926). Aphasia and kindred disorders of speech.
cessing stream versus non-anchorers. In sum, New York: Macmillan.
combining clock drawing with new assessment Kaplan, E. (1988). A process approach to neuropsycholog-
technology has uncovered behavior previously ical assessment. In T. Boll & B. K. Bryant (Eds.),
unknown and suggests exciting avenues of
Clinical neuropsychology and brain function:
Research, measurement, and practice. Washington,
C
research to explore brain behavior relations. DC: American Psychological Association.
Kaplan, E. (1990). The process approach to neuropsycho-
logical assessment of psychiatric patients. Journal
of Neuropsychiatry and Clinical Neurosciences, 2,
Cross-References 72–87.
Lamar, M., Olusola, A., Cohen, J., Charlton, R.,
▶ Constructional Apraxia GadElkarim, J., Leow, A., Libon, D., & Kumar,
A. (2016). Merging digital technology, neuropsycho-
logical assessment and the human connectome to detect
preclinical markers of neurodegeneration. Neuropsy-
References and Readings chologia, 85, 301–309.
Leach, L., Kaplan, E., Rewilak, D., Richards, B., & Proulx,
Benton, A., & Tranel, D. (1993). Visuoperceptual, visuo- G.-B. (2000). The kaplan baycrest neurocognitive
spatial, and visuoconstructional disorders. In K. M. assessment. San Antonio: The Psychological Corp.
Heilman & E. Valenstien (Eds.), Clinical neuropsy- Lezak, M., Howison, D. B., & Loring, D. W. (2004).
chology (3rd ed.). New York: Oxford University Neuropsychological assessment (4th ed.). New York:
Press. Oxford University Press.
Borod, J. C., Goodglass, H., & Kaplan, E. (1980). Norma- Libon, D. J., Swenson, R., Barnoski, E., & Sands, L. P.
tive data on the Boston diagnostic aphasia examination, (1993). Clock drawing as an assessment tool for
parietal lobe battery, and the Boston naming test. Jour- dementia. Archives of Clinical Neuropsychology, 8,
nal of Clinical Neuropsychology, 2, 209–216. 405–416.
Cahn-Weiner, D. A., Williams, K., Grace, J., Tremont, G., Libon, D. J., Malamut, B. L., Swenson, R., & Cloud, B. S.
Westervelt, H., & Stern, R. A. (2003). Discrimination (1996). Further analyses of clock drawings among
of dementia with lewy bodies from Alzheimer disease demented and non-demented subjects. Archives of
and Parkinson disease using the clock drawing test. Clinical Neuropsychology, 11, 193–211.
Cognitive and Behavioral Neurology, 16, 85–92. Libon, D.J., Penney, D.L., Davis, R., Tabby, D.S., Eppig,
Cohen, J., Penney, D. L., Davis, R., Libon, D. J., Ajilore, J., Nieves, C., Wicas, G., Lamar, M., Price, C.C., Au,
O., Kumar, A., & Lamar, M. (2014). Differentiating R., Swenson, R., and Garrett, K.D. (2014). On behalf of
‘thinking’ versus ‘drawing’ in depression across the the Clock Sketch Consortium. Deficits in processing
lifespan. Journal of the International Neuropsycholog- speed and decision making in relapsing-remitting mul-
ical Society, 20, 1–9. tiple Sclerosis: The digit clock drawing test (dCDT).
Cosentino, S., Jefferson, A. J., Chute, D. L., Kaplan, E., & Journal of Multiple Sclerosis, 1, 113. https://doi.org/
Libon, D. L. (2004). Clock drawing errors in dementia: 10.4172/jmso.1000113.
Neuropsychological and neuroanatomic consider- Marcopulos, B. A., McLean, A., & Giuliano, A. J. (1997).
ations. Cognitive and Behavioral Neurology, 17, Cognitive impairment or inadequate norms: A study of
74–83. healthy, rural, older adults with limited education. The
Davis, R., Libon, D. J., Au, R., Pitman, D., & Penney, D. L. Clinical Neuropsychologist, 11, 111–131.
(2014). THink: Inferring cognitive status from subtle Mayer-Gross, W. (1935). Some observations on apraxia.
behaviors. Proceedings of the Conference of Artificial Proceeding of the Royal Society of Medicine, 28,
Intelligence, July, 2898–2905. 1203–1212.
Freedman, M., Leach, L., Kaplan, E., Shulman, K. I., & McFie, J., & Zangwill, O. L. (1960). Visuo-constructive
Delis, D. C. (1994). Clock drawing: disabilities associated with lesions of the left cerebral
A neuropsychological analysis. New York: Oxford hemisphere. Brain, 83, 243–260.
University Press. Rouleau, I., Salmon, D. P., Butters, N., Kennedy, C., &
Goodglass, H., & Kaplan, E. (1972). Assessment of apha- McGuire, K. (1992). Quantitative and qualitative ana-
sia and related disorders (1st ed.). Philadelphia: Lea lyses of clock drawings in Alzheimer’s and
and Febiger. Huntington’s disease. Brain and Cognition, 18, 70–87.
Goodglass, H., & Kaplan, E. (1983). Assessment of apha- Rouleau, I., Salmon, D. P., & Butters, N. (1996). Longitu-
sia and related disorders (2nd ed.). Philadelphia: Lea dinal analysis of clock drawing in Alzheimer’s disease
and Febiger. patients. Brain and Cognition, 31, 17–34.
822 Clomipramine

Rubin, L. A., Barr, W. B., & Burton, L. A. (2005). Assess- Indication

ment practices of clinical neuropsychologists in the
United States and Canada: A survey of INS, NAN,
and APA division 40 members. Archives of Clinical Obsessive-compulsive disorder, depression, cata-
Neuropsychology, 20, 33–65. plexy syndrome, premature ejaculation.
Tranel, D., Rudrauf, D., Vianna, E. P. M., & Damasio,
H. (2008). Does the clock drawing test have focal
neuroanatomical correlates? Neuropsychology, 22,
553–562. Off-Label Use
Tuokko, H., Hadjustavropoulos, T., Miller, J. A., & Beat-
tie, B. L. (1992). The clock test: A sensitive measure to Anxiety, insomnia, chronic pain.
differentiate normal elderly from those with Alzheimer
disease. Journal of the American Geriatrics Society, 40,
579–584.
Van der Horst, L. (1934). Constructional apraxia: Psycho- Side Effects
logical views on the conception of space. Journal of
Nervous and Mental Disease, 80, 645–650. Serious
Paralytic ileus, hyperthermia, lowered seizure
threshold and rare seizures, orthostatic hypo-
tension, sudden death, arrhythmias, tachycardia,
Clomipramine QTc prolongation, increased intraocular pressure,
hepatic failure, extrapyramidal symptoms, mania,
John C. Courtney1 and Efrain Antonio Gonzalez2,3 and suicidal ideation.
1
Socorro Mental Health, Presbyterian Medical
Services, Socorro, NM, USA Common
2
College of Psychology, Nova Southeastern Blurred vision, constipation, increased appetite,
University, Fort Lauderdale, FL, USA urinary retention, dry mouth, nausea, diarrhea,
3
Utah State University, Logan, UT, USA heartburn, strange taste in mouth, weight gain,
fatigue, weakness, dizziness, headache, anxiety,
nervousness, restlessness, sedation, sexual dys-
Generic Name function, sweating.

Clomipramine
References and Readings

Brand Name Physicians’ desk reference (71st ed.) (2017). Montvale:

Thomson PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The
Anafranil prescriber’s guide (2nd ed.). New York: Cambridge
University Press.

Class Additional Information

Drug Interaction Effects. http://www.drugs.com/drug_
Tricyclic antidepressant interactions.html.
Drug Molecule Images. http://www.worldofmolecules.
com/drugs/.
Free Drug Online and PDA Software. www.epocrates.com.
Proposed Mechanism(s) of Action Free Drug Online and PDA Software. www.medscape.
com.
Boosts neurotransmitters serotonin and norepi- Gene-Based Estimate of Drug interactions. http://mhc.
daytondcs.com:8080/cgi bin/ddiD4?ver=4&task=
nephrine/noradrelaline; blocks serotonin trans-
getDrugList.
porter; apparently desensitizes both serotonin 1A Pill Identification. http://www.drugs.com/pill_identifica
receptors and beta adrenergic receptors. tion.html.
Clonidine 823

sudden death, arrhythmias, tachycardia, QTc pro-

Clonazepam longation, increased intraocular pressure, hepatic
failure, extrapyramidal symptoms, mania, and sui-
Efrain Antonio Gonzalez cidal ideation.
College of Psychology, Nova Southeastern
University, Fort Lauderdale, FL, USA Common
Utah State University, Logan, UT, USA Blurred vision, constipation, increased appetite, C
urinary retention, dry mouth, nausea, diarrhea,
heartburn, strange taste in mouth, weight gain,
Generic Name fatigue, weakness, dizziness, headache, anxiety,
nervousness, restlessness, sedation, sexual dys-
Clomipramine function, and sweating.

Brand Name References and Readings

Anafranil Physicians’ Desk Reference (71st ed.). (2017). Montvale:

Thomson PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The
prescriber’s guide (2nd ed.). New York: Cambridge
Class University Press.

Antidepressants and tricyclic antidepressants Additional Information

Drug Interaction Effects. http://www.drugs.com/drug_
interactions.html.
Drug Molecule Images. http://www.worldofmolecules.
Proposed Mechanism(s) of Action com/drugs/.
Free Drug Online and PDA Software. www.epocrates.com.
Boosts neurotransmitters serotonin and norepi- Free Drug Online and PDA Software. www.medscape.
com.
nephrine/noradrenaline; blocks serotonin trans- Gene-Based Estimate of Drug interactions. http://mhc.
porter; apparently desensitizes both serotonin 1A daytondcs.com:8080/cgi bin/ddiD4?ver=4&task=
receptors and beta-adrenergic receptors. getDrugList.
Pill Identification. http://www.drugs.com/pill_identifica
tion.html.

Indication

Obsessive-compulsive disorder, depression, cata-

plexy syndrome, and premature ejaculation. Clonidine

John C. Courtney1 and Efrain Antonio Gonzalez2,3

1
Off-Label Use Socorro Mental Health, Presbyterian Medical
Services, Socorro, NM, USA
2
Anxiety, insomnia, and chronic pain. College of Psychology, Nova Southeastern
University, Fort Lauderdale, FL, USA
3
Utah State University, Logan, UT, USA
Side Effects

Serious Generic Name

Paralytic ileus, hyperthermia, lowered seizure
threshold and rare seizures, orthostatic hypotension, Clonidine
824 Clorazepate

Brand Name References and Readings

Duraclon, Catapres, Catapres-TTS,
Clorpres, Jenloga, Kapvay, Nexiclon Physicians’ desk reference (71st ed.) (2017). Montvale:
XRClass Thomson PDR.
Stahl, S. M. (2007). Essential psychopharmacology: The
Antihypertensive; alpha 2 agonists, central-act- prescriber’s guide (2nd ed.). New York: Cambridge
ing; ADHD agents University Press.

Additional Information
Drug Inter action Effects. http://www.drugs.com/drug_
Proposed Mechanism(s) of Action interactions.html
Drug Molecule Images. http://www.worldofmolecules.
Centrally acting alpha 2 agonist com/drugs/
Free Drug Online and PDA Software. www.epocrates.com
Free Drug Online and PDA Software. www.medscape.com
Gene-Based Estimate of Drug interactions. http://mhc.
daytondcs.com:8080/cgi bin/ddiD4?ver=4&task=
Indication getDrugList
Pill Identification. http://www.drugs.com/pill_identifica
Hypertension tion.html

Off-Label Use

Attention deficit hyperactivity disorder, Tourette’s Clorazepate

syndrome, anxiety disorders including PTSD and
social anxiety disorder, substance withdrawal John C. Courtney1 and Efrain Antonio Gonzalez2,3
including opiates and alcohol, smoking cessation, 1
Socorro Mental Health, Presbyterian Medical
restless legs syndrome, Tourette’s syndrome, dys- Services, Socorro, NM, USA
menorrhea, postherpetic neuralgia, psychosis, 2
College of Psychology, Nova Southeastern
pheochromocytoma, menopausal flushing, cloni- University, Fort Lauderdale, FL, USA
dine-induced hypersalivation, severe pain in can- 3
Utah State University, Logan, UT, USA
cer patients

Generic Name
Side Effects
Clorazepate
Serious
Brand Name
Sinus bradycardia, atrioventricular block during
withdrawal, hypertensive, encephalopathy, cere- Azene, Tranxene, Tranxene SD, and Tranxene T-
Tab
brovascular accidents, and death

Common Class
Anxiolytics, anticonvulsants, and
Dry mouth, dizziness, constipation, sedation,
benzodiazepines
major depression, weakness, fatigue, impotence,
loss of libido, insomnia, headache, dermatologic
reactions, hypotension, occasional syncope, ner-
vousness, agitation, tachycardia, nausea, and
Proposed Mechanism(s) of Action
vomiting
Binds to benzodiazepine receptors at the GABA-A
ligand-gated channel, thus allowing for neuronal
Closure 825

hyperpolarization. Benzodiazepines enhance the

inhibitory action of GABA via boosted chloride Closure
conductance. Clorazepate is also hypothesized to
inhibit neuronal activity in amygdala-centered fear Ronald A. Cohen
circuits. Department of Clinical and Health Psychology,
College of Public Health and Health Professions,
University of Florida, Gainesville, FL, USA C
Indication Center for Cognitive Aging and Memory,
McKnight Brain Institute, University of Florida,
Anxiety disorder, symptoms of anxiety, seizures, Gainesville, FL, USA
and acute alcohol withdrawal

Synonyms
Off-Label Use
Visual integration; Visual synthesis
Partial seizures (as an adjunct)

Definition
Side Effects
Visual closure refers to the ability to perceive and
Serious
recognize objects, shapers, features, or symbols
Respiratory depression, hepatic dysfunction
from incomplete or degraded visual stimuli. It
(rare), renal dysfunction and blood dyscrasias,
reflects the capacity of humans to fill in missing
and grand mal seizures
information from incomplete sensory input to
achieve a meaningful percept.
Common
Sedation, fatigue, depression, dizziness, memory
problems, dysinhibition, confusion, ataxia, and
slurred speech Historical Perspective

The principle of visual closure had its roots in

References and Readings Gestalt psychology (Ellis 1938; Harlow 1938;
Köhler 1929). Gestalt psychology theorized that
Physicians’ desk reference (71st ed.) (2017). Montvale: operationally brain functions (i.e., perception
Thomson PDR. and cognition) are holistic consisting of analog
Stahl, S. M. (2007). Essential psychopharmacology: The
processes that occur in a parallel manner and are
prescriber’s guide (2nd ed.). New York: Cambridge
University Press. self-organizing. This led to the well-known con-
clusion regarding perception, and cognition
Additional Information more generally, that “the whole is greater than
Drug Interaction Effects. http://www.drugs.com/drug_ the sum of its parts.” Based on this framework,
interactions.html all perceptual processes act to achieve optimal
Drug Molecule Images. http://www.worldofmolecules.
organization and reconciliation with the objects
com/drugs/
Free Drug Online and PDA Software. www.epocrates.com that are being perceived. A critical principle
Free Drug Online and PDA Software. www.medscape.com driving Gestalt perception is prägnanz (law of
Gene-Based Estimate of Drug interactions. http:// conciseness), which maintains that people orga-
mhc.daytondcs.com:8080/cgibin/ddiD4?ver=4&task=
nize their experience in an orderly, symmetric,
getDrugList
Pill Identification. http://www.drugs.com/pill_identifica and simple manner when possible. Visual clo-
tion.html sure was one of the five laws of prägnanz, with
826 Closure

others including the laws of similarity, proxim- demonstrating consistent impairments on tests
ity, symmetry continuity, and common fate. such as the Gollin Figures and Mooney Closure
While each of these laws has potential value tests. This may reflect the fact that impairments
in accounting for elements of visual integra- on this type of task tend to be embedded in
tion, the law of visual closure seems to have other visual perception deficits that are more
had the most direct impact, particularly with striking. However, it is also clear that closure
respect to clinical neuropsychology. Early paradigms have not been systematically
clinical studies of the effects of posterior corti- implemented into standard neuropsychological
cal lesions on visual perception indicated that batteries using modern computerized methods,
certain patients had difficulty in simultaneously so that definitive conclusions regarding impair-
processing all the elements of their visual ments of closure secondary to localized and
sensorium to achieve a unified percept, a global brain disorders cannot be reached at
syndrome that was labeled simultagnosia this point.
(Poppelreuter 1990).

Cross-References
Current Knowledge
▶ Gollin Figures
The idea that visual perception occurs as a ▶ Hooper Visual Organization Test
function by-product of active self-organizing ▶ Simultanagnosia
processes is now widely accepted by most
visual scientists, though many would reject a
pure holistic view. Instead, visual perception
and higher-order visual processes tend to be References and Readings
conceptualized as the by-product of computa-
tional processes carried out by modular neural Ellis, W. D. (1938). A source book of Gestalt psychology.
New York: Harcourt, Brace & World.
networks responsible for specific operations.
Foreman, N. (1991). Correlates of performance on the
Visual closure is thought to result from such Gollin and Mooney tests of visual closure. Journal of
processes occurring in extra-striatal systems General Psychology, 118(1), 13–20.
found primarily in the parietal cortex. Psycho- Harlow, R. F. (1938). Philosophy’s contribution to Gestalt
psychology. Journal of Psychology: Interdisciplinary
metric studies of closure have tended to employ
and Applied, 5, 185–200.
tests such as the Gollin Figures and Mooney test Holmes, D. S. (1968). Search for “closure” in a visually
(Foreman 1991; Holmes 1968; Jones and perceived pattern. Psychological Bulletin, 70(5),
Dennis 1972; Mooney and Ferguson 1951). 296–312.
Jones, E. C., & Dennis, M. E. (1972). Perceptual closure as
In healthy adults, the ability to recognize line
a function of gap size. Perceptual and Motor Skills,
drawings that have been degraded has 35(1), 126.
been shown to be a function of the size of Köhler, W. (1929). Gestalt psychology. New York:
gaps in the drawing (Jones and Dennis 1972), H. Liveright.
Mooney, C. M., & Ferguson, G. A. (1951). A new closure
which in turn reflects the amount of missing
test. Canadian Journal of Psychology/Revue
information. Performance on closure tests has Canadienne de Psychologie, 5(3), 129–133.
been shown to not be strongly associated with Poppelreuter, W. (1990). Disturbances of lower and
visual search performance, suggesting that higher visual capacities caused by occipital damage:
With special reference to the psychopathological,
these are distinct visual processes (Foreman
pedagogical, industrial, and social implications.
1991). While tests of closure have existed for Oxford/New York: Clarendon Press/Oxford Univer-
over 40 years, there are relatively few studies sity Press.
Clustering 827

Serious
Clozapine Agranulocytosis, neuroleptic malignant syn-
drome, seizures, pulmonary embolism, myocardi-
John C. Courtney1, Cristy Akins2 and tis, and hyperglycemia.
Efrain Antonio Gonzalez3,4
1
Socorro Mental Health, Presbyterian Medical Common
Services, Socorro, NM, USA Increased risk for diabetes, sweating, and increased C
2 salivation.
Mercy Family Center, Metarie, LA, USA
3
College of Psychology, Nova Southeastern
University, Fort Lauderdale, FL, USA References and Readings
4
Utah State University, Logan, UT, USA
Physicians’ Desk Reference. (2017). (71st ed.). Montvale:
Thomson PDR.
Generic Name Stahl, S. M. (2007). Essential psychopharmacology: The
prescriber’s guide (2nd ed.). New York: Cambridge
University Press.
Clozapine

Brand Name Additional Information

Drug interaction effects. (n.d.). http://www.drugs.com/
Clozaril, Leponex, FazaClo ODT, and Versacloz drug_interactions.html.
Drug molecule images. (n.d.). http://www.worldofmolecules.
Class com/drugs/.
Antipsychotics, second generation Free drug online and PDA software. (n.d.-a). www.
epocrates.com.
Free Drug Online and PDA software. (n.d.-b). www.
Proposed Mechanism(s) of Action medscape.com.
Gene-based estimate of drug interactions. (n.d.). http://
mhc.daytondcs.com:8080/cgibin/ddiD4?ver=4&task=
Blocks dopamine 2 receptors and inhibits seroto- getDrugList.
nin 2A receptors, thus increasing presynaptic Pill identification. (n.d.). http://www.drugs.com/pill_identi
release of related catecholamines. fication.html.

Indication
Clustering
Schizophrenia (treatment resistant) and reduction
Michael Franzen
of suicidal behavior.
Allegheny General Hospital, Pittsburgh, PA, USA

Off-Label Use
Synonyms
Bipolar disorder (treatment resistant), violence,
and aggression associated with psychosis or Cluster analysis
brain dysfunction.
Definition
Side Effects
Clustering can be thought of as the obverse of
Hypotension, tachycardia, constipation, nausea, factoring. In factor analysis, observations are cor-
sedation, appetite increase, heartburn, vomiting, related with each other, and the correlation matrix
and weight gain. is examined to see which items covary among
828 Cmax

themselves and which therefore can be combined Definition

into a simpler structure of factors composed of
items. In cluster analysis, the correlation matrix Plasma concentrations reflect a time curve from
is examined to see which individuals or observa- the administration of a drug through its peak effect
tions covary among themselves and can be and eventual elimination. The maximum concen-
represented by clusters composed of different tration of a drug in blood plasma represents drug’s
observations. Once the groups of individuals are peak effect. Cmax is one of the primary pharma-
composed, they are compared to each other in cokinetic measures for evaluating how the body
order to see if some external correlate exists. acts upon a drug.
For example, a large group of patients might be The same dose of a drug may result on different
administered a series of cognitive measures. The plasma levels because the body is not a passive
scores on those measures are examined to see recipient. Plasma levels of a drug can be altered by
which individuals seem to be most similar to the route of administration, the ease of absorption,
each other and can be clustered. Once the groups the distribution of the drug with the body, the
are empirically formed, their characteristics are bioavailability or accessible concentration of the
examined to see if age or diagnosis or injury drug, and the efficiency with which a drug is
severity discriminates among the groups. metabolized or eliminated.
Common factors that affect plasma levels of a
drug could include the size of the molecule and its
Cross-References
fat solubility; the patient’s gastric pH, physical
health, or age; and the presence of other medica-
▶ Correlation Coefficients
tions or foods that may expedite or slow absorp-
▶ Factor Analysis
tion from the gastrointestinal tract into general
circulation or alter the drug’s metabolism and
excretion. These factors may require changes in
References and Readings
dosing in order to achieve therapeutic levels of a
Corter, J. (1996). Tree models of similarity and association. drug or alterations in diet, such as to take a drug
Thousand Oaks: SAGE. with or without food. It may also include recom-
Kaufman, L., & Rousseeuw, P. (2005). Finding groups in mendations to avoid particular foods that are
data: An introduction to cluster analysis. Hoboken: Wiley.
known to induce or inhibit the specific enzyme
McIntyre, R. M., & Blashfield, R. K. (1980). A nearest-
centroid technique for evaluating the minimum-vari- pathways that metabolize the drug (e.g., grapefruit
ance clustering procedure. Multivariate Behavioral juice). Drug-drug interactions can alter the plasma
Research, 15, 2225–2238. levels of a drug, including its peak effect.
There are also mediations that inhibit metabo-
lism within a particular liver-mediated enzyme
Cmax system, thus altering the availability of other
agents of that drug itself. This can alter the avail-
Nadia Webb1 and Efrain Antonio Gonzalez2,3 ability of a drug, including its Cmax. Fluoxetine’s
1
Children’s Hospital of New Orleans, New impact on codeine is a good example. Codeine is
Orleans, LA, USA ultimately synthesized into morphine and via a
2
College of Psychology, Nova Southeastern transformation that requires an enzyme that
University, Fort Lauderdale, FL, USA makes this change possible. Fluoxetine appears
3
Utah State University, Logan, UT, USA to inhibit this process, thus dramatically reducing
the pain control intended via the administration of
codeine.
Synonyms For some drugs, there is no clear relationship
between the concentration of a drug in blood
Maximum concentration; Peak concentration plasma and its pharmacological effect. For other
Cochlear Nuclei (Dorsal and Ventral) 829

drugs, the concentration must be tightly moni- The acoustic division of the eighth cranial nerve
tored, typically through regular plasma assess- has its cell bodies in the spiral ganglion of the
ments of drug levels (assays). As a rule of cochlea.
thumb, adverse drug reactions and side effects
become more likely as the dose of a drug
increases. Consequently, adverse drug effects are Cross-References
more likely at the time of Cmax. C
▶ Auditory System

Cross-References
References and Readings
▶ Cytochrome P450
▶ Pharmacokinetics Ropper, A. H., & Brown, R. J. (2005). Deafness, dizziness,
and disorders of equilibrium. In Adams and Victor’s
principles of neurology. New York: McGraw-Hill.

References and Readings

Brunton, L. B., Lazo, J. S., & Parker, K. L. (Eds.). (2005). Cochlear Nuclei (Dorsal and
Goodman & Gilman’s the pharmacological basis of
therapeutics (11th ed.). New York: McGraw Hill.
Ventral)
Stahl, S. M. (2008). Stahl’s essential psychopharmacol-
ogy: Neuroscientific basis and practical applications. John E. Mendoza
New York: Cambridge University Press. Department of Psychiatry and Neuroscience,
Tulane Medical School and SE Louisiana
Veterans Healthcare System, New Orleans, LA,
USA

Cochlea
Definition
Kerry Donnelly
VA WNY Healthcare System, University of Cochlear nuclei is the nuclei that receive first-
Buffalo (SUNY) Behavioral Health Careline order auditory input from the organ of Corti in
(116B), Buffalo, NY, USA the cochlea of the inner ear.

Definition Current Knowledge

The cochlea, a small conical structure, is the part The cochlear nuclei are divided into a dorsal and a
of the inner ear that converts mechanical energy ventral group. The dorsal cochlear nuclei give rise
(vibrations) into nerve impulses sent to the brain. to the dorsal acoustic stria, which immediately
It is also known as the organ of hearing. The word cross the midline and contribute fibers that ascend
cochlea is a Latin word derived from the Greek contralaterally in the lateral lemniscus. The ven-
kokhlos, which refers to the land snail. A coiled tral cochlear nuclei are the source of two other
tube, the cochlea winds around a central axis, auditory pathways, the intermediate and the ven-
forming the anterior part of the labyrinth. It con- tral acoustic stria. The former also crosses the
tains the organ of Corti, which includes the midline and, like the dorsal acoustic stria, ascends
hair cells that constitute the primary mechanisms in the contralateral lateral lemniscus. Fibers mak-
by which pressure waves in the cochlea are ing up the ventral acoustic stria, the largest of
transduced into bioelectrical nerve impulses. these three pathways, take three different paths
830 Cogniform Disorder

after leaving the nucleus. They (1) synapse in both Definition

the ipsilateral or contralateral superior olivary
nuclei, which in turn send tertiary fibers to the In neuropsychology, the assessment of test-
inferior colliculi via the ipsilateral and contralat- taking effort has captured the focus of consider-
eral lateral lemniscus, and (2) send fibers directly able research and debate. In the past 20 years,
to the contralateral inferior colliculi, bypassing the over 500 studies have been published in peer-
superior olivary nuclei. reviewed neuropsychological journals that
The crossing fibers of the ventral acoustic stria address the breadth and scope of this problem
make up what is known as the trapezoid body of (see reviews by Hom and Denney 2002; Iverson
the pontine tegmentum. The dorsal and ventral and Binder 2000; Larrabee 2005; Sweet 1999).
cochlear nuclei themselves are located laterally Considerable advances have been made in the
in the rostral medulla at the pontine-medullary development of empirically based methods for
junction near the vestibulocochlear nerve. identifying individuals who are simulating cog-
Since the first-order neurons from the auditory nitive problems, including the use of instruments
nerve terminate in the cochlear nuclei and the designed specifically to assess cognitive validity
decussations within the auditory system only (Binder 1993; Frederick 1997; Green et al. 2001;
begin with the second-order neurons originating Tombaugh 1996), analysis of atypical perfor-
in the cochlear nuclei, these nuclei receive input mances on standard ability tests (Larrabee
only from one ear. Hence, unilateral pontine 2003; Millis et al. 1995), and analysis of test-
lesions affecting the dorsal and ventral cochlear retest profile inconsistencies (Hom and Denney
nuclei would be expected to result in ipsilateral 2002; Iverson and Binder 2000). In addition,
hearing deficits (loss). specific guidelines and criteria have been devel-
oped for diagnosing suboptimal effort and malin-
gering on neuropsychological tests (e.g., Slick
Cross-References et al. 1999). Using these methods and guidelines,
neuropsychologists have found that the fre-
▶ Auditory System quency of individuals exhibiting excessive or
exaggerated cognitive symptoms in medicolegal
evaluations often ranges from 20% to 40%
References and Readings (Miller 2001; Millis et al. 1995; Mittenberg
et al. 2002). In light of the pervasiveness of this
Wilson-Pauwek, L., Akesson, E. J., Stewart, P. A., & problem, it is now generally accepted that cogni-
Spacey, S. D. (2002). Cranial nerves in health and
tive validity testing is an important part of the
disease. Hamilton: B.C. Decker.
neuropsychological assessment process, particu-
larly for evaluations that occur in the context of
medicolegal or disability-application settings
(Bush et al. 2005).
Cogniform Disorder While considerable advances have been made
in the methods used to detect individuals who are
Dean C. Delis exhibiting inadequate effort and symptom exag-
School of Medicine, University of California-San geration on cognitive testing, neuropsychologists
Diego, La Jolla, CA, USA often find themselves in a quandary in terms of the
diagnostic labels to ascribe to these individuals
once they have been identified. The DSM-IV
Synonyms offers several possible categories for diagnosing
individuals with excessive cognitive symptoms
Conversion disorder; Malingering; Somatoform (e.g., Malingering and Conversion Disorder);
disorders however, shortcomings of these conditions have
Cogniform Disorder 831

been noted in the literature. In particular, Malin- 1. Somatization Disorder requires at least four
gering has been the subject of considerable debate pain symptoms, two gastrointestinal symp-
and criticism, especially with regards to the objec- toms, one sexual symptom, and one pseudo-
tivity with which clinicians can assess if feigned neurological symptom. However, many
symptoms were intentionally or unintentionally individuals who present with primarily exces-
produced. Improvements have been made in sive cognitive symptoms have few if any phys-
establishing criteria for this condition (e.g., Slick ical complaints (Larrabee 2005). C
et al. 1999), but clinicians nevertheless often 2. Undifferentiated Somatoform Disorder
remain reluctant to use any diagnosis that requires requires “one or more physical complaints,”
them to make judgments about intentionality of with no reference made to cognitive
symptom exaggeration. difficulties.
Clinicians often face three general problems in 3. Conversion Disorder requires “one or more
trying to use existing DSM-IV categories to clas- symptoms or deficits affecting voluntary motor
sify individuals with excessive cognitive symp- or sensory function” [emphasis added], with-
toms. These problems include (a) lack of a out mention of cognitive or memory difficul-
diagnostic category that adequately targets the ties among the specific criteria.
specific features of this relatively common condi- 4. Pain Disorder requires only excessive pain
tion, (b) the use of criteria that require the clini- symptoms.
cian to make judgments about internal states that 5. Somatoform Disorder NOS could conceiv-
are exceedingly difficult to evaluate in an objec- ably include individuals with predominantly
tive manner (e.g., intentional versus unintentional excessive cognitive symptoms; however,
production of excessive symptoms), and “soma” denotes physical rather than cognitive
(c) difficulties in determining the relative role problems, and the list of example cases pro-
that external incentive and sick-role factors may vided in the DSM-IV for this catchall category
play in the symptom production. makes no reference to excessive cognitive
Symptom Specificity. The existing DSM-IV symptoms.
categories addressing excessive symptomatology 6. Dissociative Amnesia requires one specific
can be divided into two general types: symptom- type of cognitive problem, namely, “an inabil-
specific versus symptom-nonspecific conditions. ity to recall important personal information,
Symptom-specific conditions are those that usually of a traumatic or stressful nature”
require amplification of only certain types of [emphasis added]. However, individuals pre-
symptoms. The DSM-IV offers a relatively small senting with excessive cognitive symptoms do
number of symptom-specific categories, which fall so in a myriad of ways (Bush et al. 2005; Delis
only among the somatoform disorders (e.g., and Jacobson 2000; Larrabee 2003). Some
Somatization Disorder and Conversion Disorder) people endorse problems in all cognitive
and dissociative disorders (e.g., Dissociative domains queried, including attention, lan-
Amnesia and Dissociative Fugue). In addition, guage, math, visual-spatial functions, higher-
the DSM-IV offers two symptom-nonspecific con- level executive functions, new learning and
ditions, Malingering and Factitious Disorder, memory, and remote recall of important per-
which are discussed in the next section. sonal information. In contrast, other individ-
A major problem in trying to subsume individ- uals endorse difficulties in only one or a few
uals with excessive cognitive complaints or inva- specific cognitive skills (e.g., short-term mem-
lid test performances into one of the symptom- ory and concentration), while denying prob-
specific diagnoses is that the cognitive symptoms lems in other cognitive domains, including
of many of these cases simply fail to fit adequately recall of important personal information. In
in these categories. Following are explanations of fact, cases of isolated difficulty in remember-
this problem for each of the symptom-specific ing important autobiographical information are
categories provided in the DSM-IV: relatively rare, illustrating the limited utility of
832 Cogniform Disorder

this diagnostic category for the vast majority of or symptoms. For example, a key required crite-
cases with excessive cognitive symptoms. rion for the two symptom-nonspecific categories –
7. Dissociative Fugue not only requires one spe- Malingering and Factitious Disorder – is that the
cific cognitive difficulty (“inability to recall clinician must determine if the excessive symp-
some or all of one’s past”) but carries the toms were generated in an intentional or volitional
added stipulation that this difficulty must sur- manner. The problem here is that this criterion
face in the context of a “sudden, unexpected, reflects a causative internal state that, for the
travel away from home or one’s customary majority of cases, is difficult if not impossible to
place of daily activities” [emphasis added]. assess in an objective manner. That is, the degree
These cases are extremely rare among individ- to which a person may be exhibiting excessive
uals presenting with excessive cognitive symp- symptoms or behaviors in an intentional, volun-
toms, thereby precluding the use of this tary, or conscious manner versus an unintentional,
category for almost all cases. involuntary, or unconscious manner represents an
8. Dissociative Identity Disorder is thought to untestable diagnostic hypothesis for many cases
occur in individuals with multiple personalities (see also Slick et al. 1999). A clinician may have a
in which they exhibit an inability to recall “hunch” about whether an individual’s excessive
important information about one or more per- complaints or symptoms were under the voluntary
sonality states when they are in a different or involuntary control of the person, but usually
personality state. However, cases of multiple these impressions are not substantiated by objec-
personalities are relatively rare, particularly in tive data, such as a disclosure or confession
clinical-neuropsychological practice, and thus made by the individual to a clinician or other
this diagnosis is seldom applicable to individ- uninvolved, reliable third party.
uals with excessive cognitive symptoms. Another difficulty in this area of diagnosis is
9. Dissociative Disorder NOS is another catchall that intentionality is likely multifactorial in nature.
category that, conceivably, could encompass For example, there may be at least two key com-
individuals with excessive cognitive com- ponents of intentionality that can be dissociated:
plaints. However, the tenor of this category is conscious awareness and goal-directed motiva-
for individuals who exhibit an inability to tion. An individual may be both conscious of
recall personal information that was of a trau- producing feigned behavior (e.g., is capable of
matic or stressful nature, thereby greatly limit- admitting to self and others that he or she is
ing the utility of this category for most cases of simulating symptoms) and motivated to do so for
excessive cognitive symptoms. some type of personal gain; these features would
meet criteria for a DSM-IV diagnosis of Malin-
Taken together, the aforementioned nine gering. However, someone may be largely uncon-
symptom-specific categories either fail to include scious of the feigned behavior (e.g., has
cognitive complaints, target only highly specific, convinced himself or herself that the excessive
relatively rare types of cognitive problems, or symptoms are real), yet the feigned behavior
require that other, qualitatively different symp- may still arise due to a specific, goal-directed
toms or conditions also be present (e.g., extensive purpose. For example, it was noted during World
physical symptoms for Somatization Disorder). War II that some soldiers, when faced with the
For these reasons, these diagnoses generally fail prospect of entering the frontlines of battle, would
to capture the vast majority of individuals pre- develop psychogenic paralysis (what would now
senting with excessive cognitive symptoms. be diagnosed as Conversion Disorder given that
Intentionality. Another difficulty in using the symptom amplification occurred primarily in
existing DSM-IV categories has to do with the motor domain). These individuals often
required criteria related to intentional/ appeared to truly believe they were paralyzed,
unintentional or voluntary/involuntary control thereby suggesting an unconscious (conversion)
over the production of the excessive complaints process. However, their exaggerated behavior
Cogniform Disorder 833

(paralysis) was clearly goal-directed, because it inclusionary criterion for Malingering and required
was manifested in the context of an external exclusionary criterion for Factitious Disorder.
incentive (avoidance of danger). In these cases, (If there is an absence of external incentive, then
the conscious component of intentionality may the clinician must make a further determination of
have been absent, but the goal-directed motiva- whether or not an individual has adopted the sick
tional component for producing the symptom was role in order to diagnose Factitious Disorders.)
likely present. However, the criterion of external incentive carries C
In neuropsychological practice, the same type its own inherent difficulties for clinicians to iden-
of dissociation may occur in which individuals tify when considering these diagnoses. First, for
may produce excessive cognitive symptoms in many cases, practitioners may not have access to
reaction to an external incentive (e.g., litigation), sufficient background information about a person’s
thereby suggesting goal-directed motivation for the life to be able to assess if external incentives are
symptom production. However, these individuals operative in the case. That is, a practitioner may be
may have nevertheless convinced themselves that unaware that a patient has or is planning to apply
their symptoms are real, thereby suggesting a lack for disability or to initiate a civil lawsuit in the
of a conscious component to the symptom produc- future, or has committed a crime and fears that he
tion. Thus, for these individuals, only certain com- or she may soon be apprehended. This lack of
ponents of intentionality may be present, with the knowledge about possible covert sources of exter-
lack of conscious awareness calling into question nal incentives makes it difficult to utilize the diag-
whether they would adequately meet the required noses of Malingering or Factitious Disorder for a
criteria for a diagnosis of Malingering. Another number of cases, especially given that such infor-
complicating factor in the assessment of intention- mation is a required criterion rather than an
ality is that conscious awareness likely exists on a optional one for these categories.
continuum, with individuals varying from being Second, as currently written, the DSM-IV
fully conscious, to semiconscious, to largely criteria do not allow for the possibility that a
unconscious of the production of the feigned comorbidity may occur between the adoption of
behavior. Although an operational definition of the sick role and the presence of external incen-
intentionality is beyond the scope of this entry, tives (see also Slick et al. 1999). For example,
the important point here is that intentionality of some individuals may gradually develop into a
symptom production not only refers to an elusive progressively worsening sick role without the
internal state but it likely has component features presence of external incentives. However, after a
that exist on a continuum (e.g., levels of conscious period of time, these individuals may present as so
awareness), thereby making this construct exceed- “disabled” that they begin to receive disability
ingly difficult for clinicians to assess in an objective payments, without necessarily having actively
manner. Consequently, many clinicians are reluc- sought out such compensation. The financial
tant to use diagnoses such as Malingering, Facti- gain, however, likely buttresses and propagates
tious Disorder, and Conversion Disorder at least in the continuation of the sick role. According to
part because of difficulty in objectively assessing the DSM-IV, these individuals would have started
the presence or absence of intentionality in the out as having Factitious Disorder, but as soon as
generation of the excessive symptom. the external incentive was initiated and became a
External Incentive. A third difficulty in using reinforcing factor, the diagnosis of Factitious Dis-
existing DSM-IV categories to diagnose individ- order would be called into question (again,
uals with excessive cognitive symptoms is related because external incentive is a required exclusion-
to another required criterion for the two symptom- ary criterion for this condition). However, for
nonspecific categories – Malingering and Facti- these cases, the predominant causative factor for
tious Disorder – regarding the presence or absence the excessive symptomatology may still be the
of external incentive in the production of the symp- adoption of the sick role, with the external incen-
toms. Specifically, external incentive is a required tive playing a secondary or supportive role in the
834 Cogniform Disorder

continuation of the symptoms. As another exam- test performances occur in the presence of a
ple, some individuals may begin to feign symp- known neurological or mental disorder or any
toms intentionally and consciously in reaction to other factor known to affect CNS function (e.g.,
an external incentive (e.g., a lawsuit). However, medication), the cognitive symptoms are in excess
these individuals may gradually, and perhaps of what would be expected from the history, phys-
unconsciously, assume a progressively worsening ical examination, laboratory tests, or psychomet-
sick role due to (a) a prolongation in obtaining the ric validity testing. Findings from the clinical
external incentive (e.g., caused by delays in the interview or psychometric testing of cognitive
lawsuit) and (b) increased skepticism and functions do not substantiate the degree of cogni-
questioning on the part of family members, tive complaints or symptoms because of the pres-
coworkers, or health providers about the authen- ence of at least two of the following features:
ticity of the individual’s complaints. This pro-
longed scrutiny may be overwhelming to these 1. Cognitive complaints or poor test perfor-
individuals, compelling them to adopt the sick mances that are rare for patients with
role and exhibit illness behavior in widespread documented mild to moderate generalized
areas of their lives, to the point where they may brain damage (e.g., loss of remote autobio-
even convince themselves of the authenticity of graphical memories and inability to perform
their symptoms. In other words, while the DSM- overlearned verbal skills like reading, spelling,
IV treats external incentive and sick role as mutu- or simple math).
ally exclusive diagnostic criteria for differentiat- 2. Inconsistencies between the individual’s
ing Malingering and Factitious Disorder, in excessive cognitive complaints or poor test
reality, as is the case for most psychiatric condi- performances and the relatively mild nature
tions, they may co-occur in varying degrees (Slick of the injury or illness as documented in the
et al. 1999). medical records.
Given these limitations in the DSM-IV, the 3. Inconsistencies between the individual’s
following two diagnostic categories were pro- excessive cognitive complaints or poor test
posed by Delis and Wetter (2007) to encompass performances and observed behavior.
cases of excessive cognitive complaints or poor 4. Delayed onset of excessive cognitive com-
(invalid) test performances in the absence of suf- plaints or symptoms after an injury and/or sig-
ficient evidence of intentionality of symptom pro- nificant worsening of symptoms over time
duction to warrant a diagnosis of Malingering. without an adequate explanation for the
decline in functioning (e.g., subsequent neuro-
logical complications).
Neuropsychology of Cogniform Disorder 5. Significant inconsistencies in cognitive test
scores or profiles across repeat evaluations.
The essential feature of Cogniform Disorder is a 6. Patterns of cognitive test scores within an
pattern of cognitive complaints or low scores on examination that are rare for brain-damaged
psychometric cognitive tests that are considered to patients.
be excessive because they cannot be fully 7. Significant inconsistencies in cognitive com-
explained by a neurological disorder, by another plaints or symptoms over time.
mental disorder that is associated with CNS dys- 8. Evidence of insufficient test-taking effort or
function (e.g., schizophrenia), by a general medi- exaggeration on tests designed specifically to
cal condition known to affect CNS function (e.g., assess validity of cognitive performance.
renal disease), by the direct effects of a substance 9. Evidence of insufficient test-taking effort or
(e.g., opioid medications), or by other factors exaggeration on specific measures obtained
known to affect cognitive functioning (e.g., devel- from standard ability tests that have been
opmental learning disorder, insomnia, and normal empirically found to assess validity of cogni-
aging process). If the cognitive complaints or poor tive performance.
Cogniform Disorder 835

Considerable individual differences are found Disorder but with the excessive symptoms
in the performances of people with this condition manifested primarily in terms of cognitive dys-
on psychometric tests of cognitive skills (Larrabee function rather than deficits affecting primarily
2003; Slick et al. 1999). Some individuals obtain motor or sensory functions (e.g., nonepileptic sei-
markedly low scores on most cognitive tests zures). For this reason, Cogniform Disorder
administered; these individuals are often less should be considered as a new subtype of the
sophisticated about medical and psychological somatoform disorders. C
conditions and more blatant in their symptom
amplification. Other people may obtain low and
invalid scores on only a few tests administered Neuropsychology of Cogniform
(e.g., memory tasks); these individuals may be Condition
more subtle in their symptom exaggeration and,
as a result, more difficult to identify. Occasionally, The essential features of Cogniform Condition are
an individual may perform within expected ranges the same as those of Cogniform Disorder in every
on most cognitive tests administered, including respect, with the exception of the degree to which
cognitive validity tests, and yet continue to com- the individual exhibits cognitive dysfunction in
plain of extensive cognitive problems and dys- widespread areas of his or her everyday life.
function in their daily lives. These individuals That is, in Cogniform Condition, there is (a) a
may have learned from other sources (e.g., Inter- lack of reasonable evidence that the individual
net; attorney coaching) that neuropsychological presents as cognitively dysfunctional in many
tests are capable of detecting poor test-taking areas of his or her life and (b) evidence of signif-
effort and consequently exert adequate effort on icant inconsistencies between the individual’s
psychometric tests despite reporting significant excessive cognitive complaints or poor test per-
cognitive complaints and dysfunction in their formances in an evaluation and his or her higher
daily lives. level of everyday functioning. For example, an
The primary distinguishing feature between individual may obtain severely deficient (and
Cogniform Disorder and Cogniform Condition likely invalid) scores on tests of visual-motor
(see below) concerns the degree to which the and visual-spatial functioning and yet continues
individual presents as cognitively impaired in to drive a vehicle without apparent difficulty. In
widespread areas of his or her life. Specifically, a other words, in Cogniform Condition, the individ-
diagnosis of Cogniform Disorder should be made ual is not given a diagnosis of “disorder,” because
if there is reasonable evidence that the individual there is a lack of reasonable evidence that the
exhibits excessive cognitive symptoms in most if individual is acting out the “sick role” of being
not all areas of his or her life and seemingly at all cognitively dysfunctional in widespread areas of
times, thereby suggesting a conversion-like adop- his or her life despite presenting to the clinician in
tion of the sick role manifested primarily as cog- a manner that suggests that he or she should be
nitive dysfunction. In addition, in Cogniform markedly impaired in everyday functioning.
Disorder, the degree of claimed disability in
performing activities of daily living will often Cogniform Disorder and Condition Versus
parallel the individual’s complaints of cognitive Malingering: Similarities and Differences
dysfunction and poor (invalid) cognitive test per- Cogniform Disorder, Cogniform Condition, and
formance. For example, the individual not only Malingering (when manifested in the form of cog-
obtains severely deficient (and likely invalid) nitive dysfunction) are similar in that the individ-
scores on tests of visual-motor and visual-spatial ual may present with excessive cognitive
functioning, but he or she also ceases to drive a complaints or exhibit evidence of inadequate
vehicle because of the perceived cognitive prob- effort and exaggeration on formal neuropsycho-
lems. In many ways, Cogniform Disorder is anal- logical testing. However, a diagnosis of
ogous to the somatoform condition of Conversion Cogniform Disorder or Cogniform Condition
836 Cogniform Disorder

should not be made if there is reasonable evidence imply only that there is insufficient evidence at the
that the excessive cognitive symptoms are pro- time of the assessment to formulate a diagnosis of
duced in an intentional or volitional manner, in intentionality and therefore Malingering. Indeed,
which case a diagnosis of Malingering may be an advantage of having diagnostic categories such
warranted. As noted above, however, this deter- as Cogniform Disorder and Cogniform Condition
mination can be difficult to make for many cases is that they allow the clinician to label the cognitive
due to inherent problems in objectively assessing symptoms as excessive using more neutral terms
the internal state of the intentionality of simulated that avoid the accusatory implications of Malinger-
behavior. For this reason, it is likely that many ing when there is a lack of clear evidence to make
cases of excessive cognitive symptoms would that diagnosis. In addition, as discussed above,
receive the more neutral diagnosis of Cogniform intentionality is likely multifactorial in nature and
Condition, and possibly a diagnosis of Cogniform is comprised of at least two key components: con-
Disorder if the individual exhibits cognitively scious awareness and goal-directed motivation.
dysfunctional behavior in widespread areas of The individual who has convinced himself or her-
his or her life. However, when evidence emerges self that the feigned behavior is real may not be
that implicates at least a conscious component fully or even partially conscious of his or her symp-
in the production of the excessive cognitive tom amplification, but this person may nevertheless
symptoms, then a diagnosis of Malingering have developed the symptoms in reaction to the
(or Malingered Neuropsychological Dysfunction; presence of external or interpersonal incentives
Slick et al. 1999) may be warranted. Following are for personal gain. The categories Cogniform Dis-
different examples of evidence that can be sup- order and Cogniform Condition allow the clinician
portive of a diagnosis of Malingering: to acknowledge the presence of incentives that may
have played a significant role in the goal-directed
1. On psychometric testing, an individual obtains motivation for the excessive symptomatology
an accuracy score on a forced-choice recogni- without having to make the difficult determination
tion memory test that falls significantly of whether the individual is conscious or uncon-
below a chance level. Such a score provides scious of these dynamics.
empirical evidence that the individual correctly It should be noted that this entry first appeared
remembered the right answers above a prior to the availability of DSM-5. However,
chance level and used this knowledge to fre- many of the lacunae discussed above pertaining
quently select the wrong answer (Larrabee to DSM-IV apply to its successor as well.
2003; Millis 1992). Despite some qualified enthusiasm for these
2. A person who is involved in two separate proposed categories expressed in commentaries
personal-injury lawsuits for different accidents by three experienced forensic neuropsychologists
complains of one set of symptoms and injuries (Boone 2007: Binder 2007: Larrabee 2007), it has
to doctors associated with one lawsuit and dif- not been widely adopted. While applauding Delis
ferent symptoms and injuries to other doctors and Wetter’s emphasis on the possible psychiatric
associated with the second lawsuit. Such selec- underpinnings of excessive symptom reporting,
tive reporting of symptoms that correspond to Boone (2007) expressed concern that distinct sub-
the different lawsuits suggests a conscious com- groups fit the Cogniform Disorder diagnosis,
ponent to the symptom amplification. potentially leading to a loss of distinction between
3. An individual “confesses” to intentionally factitious disorders and both conversion disorder
performing poorly when taking cognitive tests. and malingering. She also cites the absence of
recommendations concerning the number of fail-
As proposed here, a diagnosis of Cogniform ures on measures of effort required to apply the
Disorder or Cogniform Condition does not exclude proposed diagnosis. Boone raised the possibility
the possibility of intentional production of the that advances in methods of determining “non-
excessive symptoms; rather, these categories credible cognitive presentations” (including the
Cogniform Disorder 837

important distinction between self- and other- Delis, D. C., & Wetter, S. R. (2007). Cogniform disorder
deception) might lend a firmer basis for the pro- and cogniform condition: Proposed diagnoses for
excessive cognitive symptoms. Archives of Clinical
posed diagnosis of Cogniform Disorder. Neuropsychology, 22, 589–604.
Binder (2007) began by noting Delis and Wet- Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A.
ter’s acknowledgment that their recommendations (2000). The California verbal learning test (2nd ed.).
constituted “proposed diagnoses,” and he called San Antonio: The Psychological Corporation.
for refinement of the diagnostic criteria. He
Frederick, R. I. (1997). Validity indicator profile.
Minnetonka: NCS Assessments.
C
observed that inconsistent patterns of test results – Gervais, R. O., Russell, A. S., Green, P., Allen, L. M.,
i.e., discrepant performances on tests that purport Ferrari, R., & Pieschl, S. D. (2001). Effort testing in
to assess similar constructs – do not necessarily patients with fibromyalgia and disability incentives.
Journal of Rheumatology, 28, 1892–1899.
reflect incomplete effort but rather may result Green, P., Rohling, M. L., Lees-Haley, P. R., &
simply from the imperfect correlations between Allen, L. M. (2001). Effort has a greater effect on test
pairs of tests (citing the correlation of 0.36 scores than severe brain injury in compensation claim-
between the WMS-III Visual Memory Index and ants. Brain Injury, 15, 1045–1060.
Hom, J., & Denney, R. L. (2002). Detection of response
WMS-III Visual Immediate Index). Larrabee bias in forensic neuropsychology. Journal of Forensic
(2007) discussed similarities and divergences Neuropsychology, 2, 1–166.
between the criteria proposed by Slick et al. Iverson, G. L., & Binder, L. M. (2000). Detecting exagger-
(1999) for malingered neurocognitive dysfunction ation and malingering in neuropsychological assess-
ment. The Journal of Head Trauma Rehabilitation,
and Delis and Wetter’s proposed diagnoses, 15, 829–858.
Larrabee noted that the latter “. . . apply to those Iverson, G. L., & Franzen, M. D. (1996). Using multiple
cases of non-malingering persons manifesting objective memory procedures to detect stimulated
atypical or exaggerated cognitive symptoms who malingering. Journal of Clinical and Experimental
Neuropsychology, 18, 38–51.
heretofore did not fit in any meaningful diagnostic Larrabee, G. J. (2003). Detection of malingering using
category” (p. 686). atypical performance patterns on standard neuropsy-
chological tests. The Clinical Neuropsychologist,
17, 410–425.
References and Readings Larrabee, G. J. (2005). Assessment of malingering. In G. L.
Larrabee (Ed.), Forensic neuropsychology. New York:
Binder, L. M. (1993). Assessment of malingering after Oxford University Press.
mild head trauma with the Portland Digit Recognition Larrabee, G. (2007). Cogniform disorder and cogniform
Test. Journal of Clinical and Experimental condition: Proposed diagnoses for excessive cognitive
Neuropsychology, 15, 170–182. symptoms by Delis and Wetter. Archives of Clinical
Binder, L. (2007). Commentary on “Cogniform disorder Neuropsychology, 22(6), 683–687.
and cogniform condition: Proposed diagnoses for Millis, S. R. (1992). The recognition memory test in the
excessive cognitive symptoms” by Delis and Wetter. detection of malingered and exaggerated memory def-
Archives of Clinical Neuropsychology, 22(6), 681–682. icits. The Clinical Neuropsychologist, 6, 406–414.
Binder, L. M., Storzbach, D., Anger, W. K., Campbell, Millis, S. R., Putnam, S. H., Adams, K. M., & Ricker, J. H.
K. A., & Rohlman, D. S. (1999). Subjective cognitive (1995). The California verbal learning test in the detec-
complaints, affective distress, and objective cognitive tion of incomplete effort. Psychological Assessment,
performance in Persian Gulf War Veterans. Archives of 7, 463–471.
Clinical Neuropsychology, 14, 531–536. Mittenberg, W., Patton, C., Canyock, E. M., &
Boone, K. (2007). Commentary on “Cogniform disorder Condit, D. C. (2002). Base rates of malingering and
and cogniform condition: Proposed diagnoses for symptom exaggeration. Journal of Clinical and
excessive cognitive symptoms” by Delis and Wetter. Experimental Neuropsychology, 24, 1094–1102.
Archives of Clinical Neuropsychology, 22(6), 675–679. Slick, D. J., Sherman, E. M. S., & Iverson, G. L. (1999).
Bush, S. S., Ruff, R. M., Troster, A. I., Barth, J. T., Koffler, Diagnostic criteria for malingered neurocognitive
S. P., & Pliskin, N. H. (2005). Symptom validity assess- dysfunction: Proposed standards for clinical practice and
ment: Practice issues and medical necessity. Archives of research. The Clinical Neuropsychologist, 13, 545–561.
Clinical Neuropsychology, 20, 419–426. Sweet, J. J. (1999). Malingering: Differential diagnosis. In
Delis, D. C., & Jacobson, M. (2000). Neuropsychological J. J. Sweet (Ed.), Forensic neuropsychology. Lisse:
testing. Encyclopedia of psychology. New York: Swets and Zeitlinger.
American Psychological Association/Oxford Univer- Tombaugh, T. N. (1996). Test of memory malingering.
sity Press. New York: Multi Health Systems.
838 Cognistat

originally published, a number of studies have

Cognistat subsequently examined its sensitivity to brain dam-
age and the influence of demographic variables on
Megan Becker and Daniel N. Allen test performance. The Cognistat may be more sen-
Department of Psychology, University of Nevada, sitive to brain damage than the Mini-Mental State
Las Vegas, NV, USA Exam, Cognitive Capacity Screening Examina-
tion, and Mattis Dementia Rating Scale (e.g.,
Drane et al. 2003). The Cognistat has sensitivity
Synonyms for various neurological and psychiatric disorders
and age-related changes in cognitive abilities (for
Neurobehavioral cognitive status examination brief review see Doninger et al. 2006). Correlations
(NCSE) between the Cognistat’s subtests and neuropsycho-
logical measures of similar abilities provide evi-
dence for its construct validity (Nabors et al. 1997).
Description The Cognistat battery also has limitations. For
example, performance is influenced by demo-
The Cognistat test battery (Kiernan et al. 1995), graphic variables, including age and education.
formerly called the neurobehavioral cognitive sta- Although the original validation study of the
tus examination, is a screening tool designed to Cognistat demonstrated no differences in perfor-
assess a number of different cognitive domains mance between age groups (Kiernan et al. 1987),
including orientation, attention, language abilities further investigations found that older age is asso-
(comprehension, repetition, naming), construction, ciated with poorer performance on the construc-
memory, calculations, and reasoning (similarities, tion, memory, similarities, attention, and
judgment). A rating for level of consciousness is calculation domains, with construction and mem-
also provided. The various subscales are abbrevi- ory consistently impacted by age (Drane and
ated from well-validated neuropsychological tests. Osato 1997). Additionally, low levels of educa-
For example, attention is assessed using digit rep- tional attainment are associated with diminished
etition similar to that used on the Wechsler scales. performance (Macaulay et al. 2003; Ruchinskas
Unlike other screening procedures that yield a sin- et al. 2001). With limited normative data available
gle summary score, the Cognistat is designed to to correct for these influences (Drane et al. 2003),
yield a score for each domain and thus produces a interpretation of performance in the elderly and
differentiated profile of cognitive abilities. The those with limited education must be tentative.
Cognistat also employs an adaptive testing Finally, a recent study of community dwelling
approach (referred to as a screen and metric and hospitalized individuals with traumatic brain
approach) to decrease time spent in administration. injury suggests that the Cognistat should not rep-
In this approach, an item of average difficulty is resent a profile neurocognitive strengths and
first administered for each subtest. If that item is weaknesses because measurement error
passed, no other items are administered from that accounted for the majority of variance in subtest
subtest, but if it is failed, additional easier items are scores (Doninger et al. 2006).
administered. The raw scores for each subscale are The Cognistat’s clinical utility has extended
then plotted on a standard profile form, and perfor- cross-culturally. Scores on the Cognistat accurately
mance is classified in the average range or as indic- predicted secondary care referral for dementia
ative of mild, moderate, or severe impairment. patients in Swedish primary care settings
(Johansson et al. 2014). In Norway, the Cognistat
also predicted shifts from mild cognitive impair-
Current Knowledge ment to dementia (Nesset et al. 2014). The
Cognistat may also aid in differentiating late-life
Because extensive validity and normative informa- depression from late-onset Alzheimer’s disease, as
tion were not available when the Cognistat was demonstrated in Japan (Tsuruoka et al. 2016).
Cognitive Affective Syndrome 839

Additionally, characteristics of mild Parkinsonian Japanese patients with Parkinson’s disease. Neurology
cognitive impairments were detected using the and Clinical Neuroscience, 1, 103–108.
Nabors, N. A., Millis, S. R., & Rosenthal, M. (1997). Use
Cognistat-J, the Japanese translated version of the of the neurobehavioral cognitive status examination
Cognistat (Murakami et al. 2013). Thus, the (Cognistat) in traumatic brain injury. The Journal of
Cognistat provides a useful screening method for Head Trauma Rehabilitation, 12(3), 79–84.
a variety of neurological and psychiatric disorders Nesset, M., Kersten, H., & Ulstein, I. D. (2014). Brief test
and neurocognitive impairment. However, more
such as the clock drawing test or Cognistat can be
useful predictors of conversion from MCI to dementia
C
extensive normative data for the Cognistat is in the clinical assessment of outpatients. Dementia and
needed in addition to research regarding the eval- Geriatric Cognitive Disorders Extra, 4, 263–270.
uation of impaired discrete cognitive abilities. Schrimsher, G. W., Parker, J. D., & Burke, R. S. (2007).
Relation between cognitive testing performance and
pattern of substance use in males at treatment entry.
The Clinical Neuropsychologist, 21(3), 498–510.
Cross-References Tsuruoka, Y., Takahashi, M., Suzuki, M., Sato, K., &
Shirayama, Y. (2016). Utility of the neurobehavioral cog-
nitive status examination (COGNISTAT) in differentiat-
▶ Dementia Rating Scale-2 ing between depressive states in late-life depression and
▶ Mini-Mental State Exam late-onset Alzheimer’s disease: A preliminary study.
Annals of General Psychiatry, 15(3), 1–8.

References and Readings

Doninger, N. A., Ehde, D. M., Bode, R. K., Knight, K., Cognitive Affective Syndrome
Bombardier, C. H., & Heinemann, A. W. (2006). Mea-
surement properties of the neurobehavioral cognitive sta-
tus examination (Cognistat) in traumatic brain injury Robert Rider
rehabilitation. Rehabilitation Psychology, 51(4), 281–288. Department of Psychology, Drexel University,
Drane, D. L., & Osato, S. S. (1997). Using the Philadelphia, PA, USA
neurobehavioral cognitive status examination as a
screening measure for older adults. Archives of Clinical
Neuropsychology, 12(2), 139–143.
Drane, D. L., Yuspeh, R. L., Huthwaite, J. S., Klingler, Synonyms
L. K., Foster, L. M., Mrazik, M., & Axelrod, B. N.
(2003). Healthy older adult performance on modified Cerebellar cognitive affective syndrome
version of the Cognistat (NCSE): Demographic issues
and preliminary normative data. Journal of Clinical
and Experimental Neuropsychology, 25(1), 133–144.
Johansson, M. M., Kvitting, A. S., Wressle, E., & Definition
Marcusson, J. (2014). Clinical utility of Cognistat in
multiprofessional team evaluations of patients with
cognitive impairment in Swedish primary care. Inter- First described by Schmahmann and Sherman
national Journal of Family Medicine, 2014, 1–10. (1998), cerebellar cognitive affective syndrome
Kiernan, R. J., Mueller, J., Langston, J. W., & Van Dyke, (CAS) refers to a cluster of impairments involving
C. (1987). The neurobehavioral cognitive status examina- higher-order cognitive processes and affective
tion: A brief but quantitative approach to cognitive assess-
ment. Annals of Internal Medicine, 107(4), 481–485. functioning. Symptoms tend to cluster in executive
Kiernan, R. J., Mueller, J., & Langston, J. W. (1995). dysfunction, including problems with planning, set
Cognistat (neurobehavioral cognitive status examina- shifting, verbal fluency, abstract reasoning, persev-
tion). Lutz: Psychological Assessment Resources. eration, attentional dysregulation, hyperactivity,
Macaulay, C., Battista, M., Lebby, P. C., & Mueller, J. (2003).
Geriatric performance on the neurobehavioral cognitive impulsivity and disinhibition, and deficits in work-
status examination (Cognistat) what is normal? Archives ing memory. However, symptoms may also include
of Clinical Neuropsychology, 18, 463–471. visuospatial disorders, expressive language disor-
Murakami, H., Fujita, K., Futamura, A., Sugimoto, A., ders, affective abnormalities, difficulties with
Kobayakawa, M., Kezuka, M., Midorikawa, A., &
Kawamura, M. (2013). The Montreal cognitive assess- visuospatial organization, visual memory, logical
ment and neurobehavioral cognitive status examination sequencing, and blunted or inappropriate affect
are useful for screening mild cognitive impairment in (Schmahmann and Sherman 1998).
840 Cognitive Assessment System

Current Knowledge neurocognitive instrument designed to assess chil-

dren aged 5 years, 0 months to 18 years, and
Causes and Correlates of CAS 11 months. The theoretical basis of the CAS2 is
The co-occurrence of these cognitive and affective an extension of Alexander S. Luria’s work relating
symptoms arises from the disruption of neuroana- to the brain’s three functional units (Naglieri and
tomical circuits connecting the cerebellum with Otero 2012). It was modified and refined by Das,
frontal, parietal, temporal, and limbic cortices. Naglieri, and Kirby into four processing compo-
Damage to these connections can occur in associa- nents: Planning, Attention, Simultaneous, and Suc-
tion with cerebellar infarct (Schmahmann and cessive Processing, otherwise known as PASS, to
Sherman 1998), cerebellar atrophy associated explain differences in cognitive processing of chil-
with severe alcoholism (Fitzpatrick et al. 2008), dren (Naglieri 1999; Naglieri and Otero 2011).
cerebellar tumor or tumor resection (Levihson Each of the four PASS Composite Indexes is com-
et al. 2000; Konczak 2005), trauma, neurodegener- prised of two core subtests and one supplementary
ative disorders, or cerebellitis. Affective symptoms subtest for the Extended Battery. Thus, the Core
have been associated with damage to the cerebellar Battery utilizes 8 subtests, while the Extended Bat-
vermis (Levihson et al. 1997). Lesions of the ante- tery includes 12 subtests. Individual administration
rior lobe of the cerebellum tend to produce only time is approximately 40 or 60 min, respectively.
minor changes in executive and visual-spatial func- The Planning subtests require individuals to
tions. Children with a cognitive affective syndrome engage in a problem-solving sequence to com-
can also have autistic characteristics, and diagnosis plete novel tasks (Naglieri 1999). The selection
of autism can be confounded by cerebellar lesions. and/or application of strategies are reported by the
child for the clinician to evaluate strategies crucial
to the success or failure of performance (McGill
References and Readings 2015; Naglieri et al. 2014). The Planning Com-
posite Index consists of:
Schmahmann, J., & Sherman, J. (1998). The cerebellar
cognitive affective syndrome. Brain, 121, 561–579.
1. Planned Codes – The child is requested to com-
Schmahmann, J., Weilburg, J. D., Sherman, J. B., & Janet,
C. (2007). The neuropsychiatry of the cerebellum – plete a series of boxes according to a code
Insights from the clinic. Cerebellum, 6(3), 254–267. system provided at the beginning of each item.
2. Planned Connections – This subtest is similar
to the original trail making task.
a. Children aged 5–7 complete number
Cognitive Assessment System sequences only.
b. For children 8–18, both numerical and
Leesa V. Huang alphabetical sequences are utilized.
Department of Psychology, California State 3. Planned Number Matching – The child is
University, Chico, CA, USA asked to locate and underline a pair of
matching numbers. This subtest included in
the Extended CAS2 Battery only.
Synonyms
Simultaneous Processing subtests require the
CAS2 ability of an individual to incorporate and compre-
hend unconnected entities and its relation/position
to a collective whole (Naglieri 2005). The Simul-
Description taneous Processing Composite Index includes:

The Cognitive Assessment System – Second Edi- 1. Matrices – A variety of pictures with geometri-
tion (CAS2; Naglieri et al. 2014) is a cal shapes or patterns are shown to the child. The
Cognitive Assessment System 841

child needs to select one option that is consistent stimuli (Naglieri and Das 2005). The Successive
with the presented relationship or pattern. Processing Composite Index consists of:
2. Verbal-Spatial Relations – The individual
receives auditory information and determines 1. Word Series – Children are instructed to repeat
which picture best represents the verbal a series of commonly used words in the same
description given. Presented in a multiple- consecutive order given.
choice format, the series of pictures allows 2. Sentence Repetition – Administered to chil- C
the student to demonstrate understanding of dren aged 5–7 only. This subtest demands
logical, grammatical, and spatial information. that a child repeat sentences that gradually
3. Figure Memory – A child is required to trace become longer. The sentences in this subtest
geometric design previously observed, which utilized color words to reduce the contextual
is embedded within a larger and more intricate meaning and possible interference with simul-
geometrical design. This subtest included in taneous processing.
the Extended CAS2 Battery only. 3. Sentence Questions – Administered to children
aged 8–17 only. In a variation of the sentence
Subtests in the Attention scale require a com- repetition task, this subtest requires that chil-
bination of three components: focused, selective, dren respond to a question about a nonsensical
and sustained attention (Naglieri 2005). Focused sentence.
attention involves the act of attending to presented 4. Visual Digit Span – A child is asked to verbally
stimuli in the environment. Selective attention is repeat a series of numbers presented visually.
the concentration of attention to chosen stimuli This subtest included in the Extended CAS2
while disregarding nonessential or competing Battery only.
stimuli. Sustained attention is the differential
effort (over time, especially) an individual applies The CAS2 is arranged in three separate, yet
toward task completion. The Attention Composite interrelated levels of scores: individual subtest
Index encompasses: scaled scores, composite scores, and a full-scale
quotient. Thirteen subtests comprise the CAS2,
1. Expressive Attention and each subtest generates a scaled score (M = 10;
a. Children aged 5–7 are to identify the size of SD = 3). Each of the four PASS composite scores
an assortment of animals, in spite of the size (M = 100; SD = 5) is a combination of the subtests
depicted on the page. included in each respective process. Additionally,
b. For children aged 8–17, this subtest is similar the CAS2 includes five new supplemental compos-
to the Stroop Test. Color words are presented ite scores: Executive Functioning Without Working
in a different colors of ink (e.g., the word Memory, Executive Functioning With Working
“red” might be in blue ink) and children are Memory, Working Memory, Verbal Content, and
requested to name the color of the ink. Nonverbal Content with a mean standard score of
2. Number Detection – This subtest consists of 100 and a standard deviation of 15. The Full Scale
rows of numbers with both target and distracter Score (M = 100; SD = 15) is the aggregate total of
stimuli. At the top of each item page, a key is the four PASS cognitive processes scales, which are
printed with the target numbers. Children are equally weighed. The CAS2 also includes a com-
instructed to underline only the target specified. parison of differences between subtests relying on
3. Receptive Attention – Children must identify visual vs. auditory stimuli.
and underline identical stimuli (i.e., pictures or
letters). This subtest is included in the
Extended CAS2 Battery only. Historical Background

Successive Processing is described as the This is first revision of the Cognitive Assessment
unidirectional, consecutive organization of System (CAS; Naglieri and Das 1997). The
842 Cognitive Assessment System

rationale for the revision was to create a compre- of the PASS processes for two main purposes:
hensive set of tools based on the neuropsycholog- eligibility determination and academic interven-
ical foundation of the PASS theory to evaluate the tion (Naglieri et al. 2014; Power and D’Amato in
learning strengths and weaknesses in children and press). The scores obtained on the subtests and
adolescents. The CAS2 now incorporates a three- composites allow clinicians to determine pat-
part assessment system (CAS2, CAS2 Brief, and terns of intraindividual and normative strengths
CAS2 Rating Scale) for use across multiple settings and weaknesses. Additionally, the PASS scores
and tiers. Additionally, the CAS2 can be utilized in are sensitive to disorders in the basic psycholog-
conjunction with the intervention handbook ical processes related to academic success and
(Naglieri and Pickering 2010) to select empirically failure as defined by IDEIA (Naglieri and Otero
based cognitive strategies and interventions to 2012). The authors suggested that the CAS2 is a
improve academic performance and functioning. valuable alternative tool to the traditional
This current version offers updated norms, slight Wechsler or Stanford-Binet scales, when
changes of subtest formats, addition/deletion of assessing and determining whether individuals
items, inclusion of a new visual Successive subtest, may have specific learning disabilities, attention
and addition of the Supplementary Scales. deficit/hyperactivity disorders (ADHD; Gold-
stein and Naglieri 2015), intellectual disabilities,
serious emotional disturbance, giftedness, and
Psychometric Data traumatic brain injury (Naglieri et al. 2014). Fur-
thermore, possessing an understanding of an
The standardization sample of 1,342 children is individual’s PASS profile will provide relevant
representative of the US population from 2011 information for the selection and evaluation of
and is stratified according to age, gender, region, instructional recommendations (Naglieri 1999;
ethnicity, exceptionality status, and parent educa- Naglieri and Pickering 2010). Because the con-
tion level (McGill 2015; Naglieri et al. 2014). structs are based in neurocognitive theory that
Reliability coefficients for subtests ranged from underlies general human learning and function-
moderate to strong (0.80–0.91). The internal con- ing, the CAS2 may also be helpful when evalu-
sistency of the CAS2 subtests range from 0.80 to ating individuals from diverse backgrounds.
0.91, with a median reliability of 0.84. Average
coefficient values for the core and extended bat-
tery are strong and range from 0.86–0.95 and
See Also
0.90–0.97, respectively.
The theoretical premise of the CAS2 was ▶ Attention
constructed on a four-factor model, and confirma-
▶ Sequential Processing
tory factor analyses (CFA) generated empirical sup-
port for the four-factor models across all age
categories. Moderate to strong correlations were
References and Readings
found (0.65–0.88) between the CAS2 and the
CAS. Predictive validity was moderately established Goldstein, S., & Naglieri, J. A. (2015). Using the CAS2 in
with similar neurocognitive assessment instruments. the comprehensive assessment of ADHD. The ADHD
Obtained score differences across gender, race, and Report, 23(7), 8–10. 14.
McGill, R. J. (2015). Test review: Naglieri, J. A., Das, J. P.,
ethnicity were found to be insignificant. & Goldstein, S. (2014). Cognitive assessment system-
second edition (2nd ed.) Journal of Psychoeducational
Assessment, 33(4), 375–380.
Clinical Uses Naglieri, J. A. (1999). Essentials of CAS assessment. New
York, NY: Wiley.
Naglieri, J. A., & Das, J. P. (1997). Cognitive assessment
The CAS2 provides an analysis of an individ- system: Administration and scoring manual. Itasca,
ual’s cognitive abilities through the measurement NY: Riverside Publishing.
Cognitive Behavioral Couples Therapy 843

Naglieri, J. A. (2005). The cognitive assessment system. approaches for the treatment of marital and cou-
In D. P. Flanagan & P. L. Harrison (Eds.), Contempo- ple distress, with growing empirical support for
rary intellectual assessment: Theories, tests, and
issues (2nd ed., pp. 441–460). New York, NY: The its effectiveness. Theoretically grounded in both
Guilford Press. social learning and social exchange theories, the
Naglieri, J. A., & Das, J. P. (2005). Planning, attention, premise of CBCT is that an individual’s behav-
simultaneous, and successive (PASS) theory: A revi- ior both influences and is influenced by his/her
sion of the concept of intelligence. In D. P. Flanagan &
P. L. Harrison (Eds.), Contemporary intellectual environment. When applied to a marriage or C
assessment: Theories, tests, and issues (2nd ed., pp. other long-term relationship, this premise
120–135). New York, NY: The Guilford Press. suggests that one partner’s behavior influences
Naglieri, J. A., & Otero, T. (2011). Cognitive assessment and is influenced by the actions of the other.
system: Redefining intelligence from a neuropsycho-
logical perspective. In A. Davis (Ed.), Handbook of CBCT typically focuses on two aspects of
pediatric neuropsychology (pp. 320–333). New York, this process: (a) exchanges of positive and neg-
NY: Springer. ative behaviors and (b) communication skills
Naglieri, J. A., & Otero, T. M. (2012). The cognitive that influence the interaction process (Epstein
assessment system: From theory to practice. In D. P.
Flanagan & P. L. Harrison (Eds.), Contemporary intel- et al. 1997).
lectual assessment: Theories, tests, and issues (3rd ed.,
pp. 376–399). New York, NY: Guilford Press.
Naglieri, J. A., & Pickering, E. (2010). Helping children Current Knowledge
learn: Intervention handouts for use in school and at
home (2nd ed.). Baltimore, MD: Brooks.
Naglieri, J. A., Das, J. P., & Goldstein, S. (2014). Cognitive Couples and Health
assessment system–Second edition (2nd ed.). Austin, A patient’s ongoing, long-term relationship can
TX: Pro-Ed. influence a range of psychosocial variables related
Power, E. M., & D’Amato, R. C. (in press). Review of the
cognitive assessment system: Brief. In J. Impara & to health behaviors. The health-enhancing prop-
B. Plake (Eds.), Buros 20th measurements yearbook erties of intimate and long-term relationships have
(2nd ed.). Lincoln, NE: Buros Institute of Mental been repeatedly documented (Kiecolt-Glaser and
Measurements. Newton 2001; Wilson 2001). Various mecha-
nisms of action for this relationship have been
proposed, including selection and protection
(Kiecolt-Glaser and Newton 2001). That is,
Cognitive Behavioral Couples healthier people are more likely to be in and stay
Therapy in intimate relationships, and they tend to have
more resources and take care of themselves better
Tamara Goldman Sher than their counterparts without such relationships.
Institute of Psychology, Illinois Institute of Additional research has investigated other mech-
Technology, Chicago, IL, USA anisms for the protective benefits of long-term
relationships, including partner attitudes or
behaviors, and caretaking (Keefe et al. 1996;
Synonyms Wilson 2001).

Behavioral marital therapy; CBCT; Cognitive

behavioral marital therapy; Couples therapy; Treatment Procedures
Marital therapy
A CBCT approach to treatment with both relation-
ship distressed and health impaired couples focuses
Definition on three factors: behavioral factors, affective/emo-
tional factors, and cognitive factors. The behavioral
Cognitive Behavioral Couples Therapy (CBCT) component includes increasing positive behaviors
has become one of the most well-researched such as spending more time together and
844 Cognitive Behavioral Couples Therapy

decreasing negative behaviors such as criticizing or various populations. This includes neuropsy-
nagging. In addition, because communication chologists, clinical psychologists, marriage and
problems are the most commonly reported pre- family therapists, counselors, social workers,
senting complaint of distressed couples, the behav- and clergy.
ioral aspects of the treatment also typically involve
a skills-oriented approach to communication
change where the value and skills of working
together to solve a problem are the foci. Cross-References
Affect is a focus of therapy insomuch as it is an
indicator of significant relationship distress and ▶ Behaviorism
for its ability to direct the therapist in exploring ▶ Cognitive Behavioral Therapy
links between the emotions of the partners and
their behaviors. Affect can be approached with a
skills approach in helping partners learn to
express their own and listen to the other person’s References and Readings
emotions and by linking specific emotions to spe-
cific relationship issues. Baucom, D. H., Shoham, V., Mueser, K. T., Daiuto, A. D.,
& Stickle, T. (1998). Empirically supported couple and
The third factor in CBCT is cognition. As
family interventions for marital distress and adult men-
Epstein et al. (1997) note, “the importance of cog- tal health problems. Journal of Consulting and Clinical
nitive factors in relationship functioning lies in the Psychology, 66, 53–88.
fact that objectively observable behavioral events Epstein, N. B., & Baucom, D. H. (2002). Enhanced
cognitive-behavioral therapy for couples.
are often subjectively experienced quite differently
Washington, DC: American Psychological
by the partners.” The therapist works to uncover Association.
underling cognitive factors shaping the behavior Epstein, N. H., Baucom, D. H., & Daiuto, A. (1997).
and affect of the partners in order to increase under- Cognitive-behavioral couples therapy. In W. K. Halford
& H. J. Markman (Eds.), Clinical handbook of mar-
standing and promote behavioral change.
riage and couples intervention (pp. 415–449). West
Sussex: Wiley.
Efficacy Information Halford, W. K., & Markman, H. J. (Eds.). (1997). Clinical
CBCT and its predecessor, Behavioral Marital handbook of marriage and couples intervention.
New York: Wiley.
Therapy (BMT), have been one of the most
Keefe, F. J., Caldwell, D. S., Baucom, D. H., Salley, A.,
researched forms of couples therapy (Shadish Robinson, E., Timmons, K., et al. (1996). Spouse-
and Baldwin 2003, 2005). Results of efficacy tri- assisted coping skills training in the management of
als repeatedly demonstrate that those who receive osteoarthritic knee pain. Arthritis Care and Research,
9(4), 279–291.
either CBCT or BMT report less distress than
Kiecolt-Glaser, J. K., & Newton, T. L. (2001). Marriage
those who receive no treatment and that this find- and health: His and hers. Psychological Bulletin,
ing remains not only for couples presenting with 127(4), 472–503.
general marital distress but also for depression, Schmaling, K., & Sher, T. G. (2000). The psychology of
couples and illness: Theory, research, and practice.
agoraphobia, and alcohol abuse (Baucom et al.
Washington, DC: American Psychological
1998). Based upon recent meta-analyses of stud- Association.
ies using CBCT, Shadish and Baldwin (2003, Shadish, W. R., & Baldwin, S. A. (2003). Meta-analysis of
2005) reported an overall mean effect size ranging MFT interventions. Journal of Marital and Family
Therapy, 29, 547–570.
from 0.59 to 0.84 for couples therapy generally,
Shadish, W. R., & Baldwin, S. A. (2005). Effects of behav-
with no differential effectiveness across theoreti- ioral marital therapy: A meta-analysis of randomized
cal orientation found. controlled trials. Journal of Consulting and Clinical
Psychology, 73(1), 6–14.
Wilson, S. E. (2001). Socioeconomic status and the prev-
Qualifications of Providers
alence of health problems among married couples in
CBCT can be conducted by a variety of treatment later midlife. American Journal of Public Health,
providers, specifically trained in its use with 91(1), 131–135.
Cognitive Behavioral Therapy 845

(i.e., factors within the person such as a person’s

Cognitive Behavioral Therapy own intelligence and behavior) or external fac-
tors (i.e., factors external to the person such as
Taryn M. Stejskal the weather or luck). When internal attributions
Department of Physical Medicine and are made, people are said to have an internal
Rehabilitation, Virginia Commonwealth locus of control or hold cognitions that support
University Medical Center, Virginia, VA, USA their sense of efficacy in affecting what happens C
to them. When external attributions are para-
mount, people are said to have an external locus
Definition of control, that is, they believe that they exert less
control over their environment.
Cognitive behavioral therapy (CBT) is a theoretical
framework based on the premise that a person’s
cognitions influence their emotions and behavior.
Goals and Objectives
CBT provides considerable utility in addressing a
variety of common emotional consequences of
Neuropsychologists using CBT as a conceptual
neurological disorders including anxiety and
framework work toward modifying maladaptive
depression, as well as behavior modification for
cognitions such as negative attributions,
brain injury survivors.
unattainable expectations and standards, and
faulty belief systems. Through the modification
of these problematic (i.e., schemas), CBT seeks to
Historical Background
alter people’s emotional and behavioral responses
in service of symptom management, reduction,
CBT grew out of Albert Ellis’s (1975) work on
and alleviation. To reduce the emotional experi-
Rational Emotive Behavioral Therapy (REBT)
ence of frustration, a neuropsychologist working
and examination of irrational beliefs in the
with a brain-injured patient would encourage the
1950s. Ellis concluded that irrational beliefs
patient to appreciate the gains made since the
(e.g., I am powerless to solve my problems; I am
injury. In order to avoid unrealistic expectations
unlovable) were associated with the development
for post-injury functioning that could create
of mood disorders. Beck et al. (1979) developed
frustration; the patient would be cautioned against
Cognitive Therapy on the premise that cognitive
comparing present capabilities to preinjury
errors (e.g., over-generalizing, magnification,
functioning.
personalization) were associated with the devel-
opment of depression and anxiety. Further, they
viewed depression as accompanied by of a triad of
negative cognitions consisting of a negative view Treatment Participants
of self, the world, and the future.
Arnold Lazarus (1971) was the first to intro- CBT is broadly applicable to a variety of clinical
duce the term “behavior therapy” into the profes- neurological diagnoses including anxiety, depres-
sional literature. Further expanding the lens of sion, obsessive compulsive disorder (OCD), and
CBT, Lazarus and Folkman (1984) developed posttraumatic stress disorder (PTSD). CBT can be
the stress, appraisal, and coping model (1984) used with individuals, couples, and families. Fur-
that acknowledges the importance of how an ther, CBT can be used with patients at develop-
individual views the environment (primary mental levels from young children to older adults.
appraisal) and their available coping resources CBT therapists act more as coaches collaborating
(secondary appraisal). Finally, attribution theory, with patients alter processes of thinking, feeling,
proposed by Fritz Heider (1958), posits that peo- and action as opposed to an analyst making expert
ple can interpret events as caused by internal interpretations.
846 Cognitive Behavioral Therapy

Treatment Procedures surrounding the diagnosis. Communication skills

training teaches families how to communicate
CBT encompasses a variety of clinical interven- more productively with one another about com-
tions for individuals with a neurological disorder plex issues and reduce detrimental patterns of
as well as couples and families in which a member interaction such as EE.
has a neurological diagnosis or injury. Within all
CBT interventions, behaviors, cognitions, and Cognition-Focused Interventions
emotions are integrally related; though interven- The manner in which a person cognitively ascribes
tions may focus on behavior or cognition, these meaning to behavior is an important factor in CBT.
distinctions are often made for heuristic purposes Therapy often focuses on reassessing and
(Epstein and Baucom 2002). Further, CBT posits amending these cognitions. Areas of inquiry often
that change in one domain will produce changes in include attributions, expectancies, assumptions,
others domains. In the past, behavior-oriented ther- standards, and beliefs. In order to evaluate and
apies have been ripe with skills training in areas modify existing cognitions, clinicians intervene
such as problem-solving, communication, and using guided discovery during which clients are
relaxation with the idea being that maladaptive asked to identify and evaluate their cognitions
patterns arise around areas of skill deficits. Though (Epstein and Baucom 2002). When a patient is
CBT therapists also deliver a judicious amount of depressed about a neurological diagnosis or injury,
skills-based training, therapy moves beyond behav- clinicians may intervene at the cognitive level chal-
ior modification to the meaning and interpretations lenging catastrophic thinking (e.g., I will never get
made as a result of interactions and experience. better). A therapist may focus decreasing negative
self-talk (e.g., I am worthless the way I am now) by
Behavior-Focused Interventions encouraging the patient to keep a journal of
Patients with neurological diagnoses have a host thoughts occurred and the impact of the thoughts
of behavior patterns amenable to CBT interven- on the patient’s mood (Epstein and Baucom 2002).
tion. One such pattern, negative reciprocity, is the
idea that negative behavior increases the propen- Emotion-Focused Interventions
sity that a person will respond to expressed nega- Interventions within the realm of emotions may
tive behavior with more negative behavior range from expanding minimized emotional expe-
(Epstein and Baucom 2002). For example, family rience to containing heightened emotional experi-
members may respond angrily toward a patient ence. Clinicians may draw on a variety of
who acts aggressively after a brain injury. Over strategies to access, heighten, or limit emotional
time, negative reciprocity pervades relationships, experience including normalizing emotional
invading cognitions and emotions such that fam- responses, metaphor, acceptance of emotional
ily members make global negative attributions expression, enhancing tolerance for distressing
about another person’s intentions and behavior emotions, and encouraging healthy compartmen-
(Epstein and Baucom 2002). talization of emotion (Epstein and Baucom 2002).
An important aspect of CBT is skills-based In cases of neurological diagnosis or injury, emo-
training, meant to enhance positive behavior and tions may either be exacerbated or minimized. To
decrease negative behavior. In an instance where a enhance the expression of emotions, therapists
person receives a diagnosis of schizophrenia, a may ask probing questions to bring awareness to
CBT clinician may intervene with a family to emotional experience such as: What happens to
teach communication skills. Empirical literature you when. . .What is it like for you when. . .How
has discussed the detrimental impact of expressed do you feel as you listen to your son expressing
emotion (EE) in families with a schizophrenic his experience. . . (Epstein and Baucom 2002). In
family member. Further, the family members this way, individuals and family members can be
may be overwhelmed and have many questions, encouraged to share their emotional experience in
concerns, and emotions they need to express the context of a safer therapeutic environment.
Cognitive Behavioral Therapy 847

Efficacy Information (MFTs), counselors, and social workers. Treat-

CBT has been empirically validated for the treat- ment providers using CBT should have appropri-
ment of many disorders including anxiety (Barlow ate clinical training in the model. Further, clinical
et al. 1984), sexual dysfunction (Baucom et al. providers learning to use CBT as a conceptual
1998), depression (Beach et al. 1990), bipolar dis- framework to guide therapy should seek supervi-
order, schizophrenia, and bulimia nervosa (Baucom sion from an experienced individual trained in the
et al. 1998). CBT is often used in conjunction with model of CBT. C
medication for a variety of mental health concerns.
In addition, CBT effectively enhances coping
skills for adults with chronic illness (Rybarczyk Cross-References
et al. 2001) and caregivers (Gallagher-Thompson
et al. 2000).
▶ Behavior Modification
Recently, advances in computer software have ▶ Behaviorism
given rise to computerized versions of CBT.
▶ Psychotherapy
Though computerized cognitive behavioral ther-
apy (CCBT) is not meant to replace face-to-face
therapy, it does provide an additional treatment
References and Readings
option. CCBT allows clients to participate in ther-
apy when there is a paucity of available therapists, Barlow, D. H., O’Brien, G. T., & Last, C. G. (1984).
the associated costs are prohibitive, or the pros- Couples treatment of agoraphobia. Behavior Therapy,
pect of speaking to someone face-to-face seems 15, 41–58.
Baucom, D. H., Shoham, V., Mueser, K. T., Daiuto, A. D.,
off-putting. In 2006, the United Kingdom’s & Stickle, T. R. (1998). Empirically supported couples
National Institute of Health and Clinical Excel- and family therapies for adult problems. Journal of
lence (NICE) provided guidelines recommending Consulting and Clinical Psychology, 66, 53–88.
CCBT as a result of randomized controlled trials Beach, S. R. H., Sadeen, E. E., & O’Leary, K. D. (1990).
Depression in marriage: A model for etiology and
for mild to moderate depression and anxiety
treatment. New York: Guilford Press.
(NICE 2006). Beck, J. S. (1995). Cognitive therapy: Basics and beyond.
New York: Guilford.
Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979).
Cognitive therapy of depression. New York: Guilford.
Outcome Measurement Beck, A. T., Steer, R. A., & Brown, G. K. (1996). Manual
for the Beck depression inventory-II. San Antonio:
Many clinicians used standardized instruments to Psychological Corporation.
assess the presence and severity of a variety of Dattilio, F. M., & Freeman, A. (Eds.). (2003). Cognitive-
behavioral strategies in crisis intervention (3rd ed.).
neuropsychological diagnoses. With regard to
New York: Guilford.
depression, clinicians may use self-report inven- Ellis, A. (1975). A new guide to rational living. Englewood
tories such as the Beck Depression Inventory Cliffs: Prentice Hall.
(BDI II; Beck et al. 1996). Finally, the Beck Epstein, N. B., & Baucom, D. H. (2002). Enhanced
cognitive-behavioral therapy for couples. Washington,
Anxiety Inventory (BAI: Kabacoff et al. 1997)
DC: American Psychological Association.
has shown considerable utility in diagnosing anx- Gallagher-Thompson, D., Lovett, S., Rose, J., McKibbin,
iety and identifying the severity of the anxiety C., Coon, D., Futterman, A., & Thompson, L. W.
symptoms. (2000). Impact of psychoeducational interventions on
distressed family caregivers. Journal of Clinical
Geropsychology, 6, 91–110.
Heider, F. (1958). The psychology of interpersonal rela-
Qualifications of Treatment Providers tions. New York: Wiley.
Kabacoff, R. I., Segal, D. L., Hersen, M., & Van Hasselt,
V. B. (1997). Psychometric properties and diagnostic
CBT can be used by a variety of treatment pro-
utility of the Beck anxiety inventory and the state-trait
viders such as neuropsychologists, clinical psy- anxiety inventory with older adult psychiatric outpa-
chologists, marriage and family therapists tients. Journal of Anxiety Disorders, 11(1), 33–47.
848 Cognitive Behavioral Therapy for Insomnia

Lazarus, A. A. (1971). Behavior therapy and beyond. mental health condition. However, the majority of
New York: McGraw-Hill. insomnia cases co-occur with other mental or
Lazarus, R. S., & Folkman, S. (1984). Stress, appraisal
and coping. New York: Springer. physical health conditions. In the past, this form
Leahy, R. L. (Ed.). (1997). Practicing cognitive therapy: of insomnia was termed secondary insomnia, as it
A guide to interventions. Northvale: Jason Aronson. was perceived as a consequence of the other dis-
National Institute of Health and Clinical Intervention order. However, the National Institutes of Health
(NICE). (2006). Depression and anxiety computerized
cognitive behavioral therapy (CCBT). Retrieved on recommended that the term be changed to comor-
July 17, 2007 at http://guidance.nice.org.uk/TA97 bid insomnia in 2005 because of the absence of
O’Farrell, T. J., Choquette, K. A., Cutter, H. S. G., Brown, empirical evidence supporting a unidirectional
E. D., & McCourt, W. F. (1993). Behavioral marital relationship between insomnia and other health
therapy with and without additional couples relapse
prevention sessions for alcoholics and their wives. conditions. Insomnia has well-documented
Journal of Studies on Alcohol, 54, 652–666. adverse effects on physical health (e.g., metabolic
Rybarczyk, B., DeMarco, G., DeLaCruz, M., Lapidos, S., dysfunction) and mental health (e.g., increased
& Fortner, B. (2001). A classroom mind-body wellness depression symptoms), and other daytime symp-
intervention for older adults with chronic illness: Com-
paring immediate and one year benefits. Behavioral toms including fatigue, impaired attention, and
Medicine, 27, 15–27. memory deficits, as well as increased medical
visits and work absenteeism. Cognitive behav-
ioral therapy for insomnia (CBT-I) is the most
effective nonpharmacological treatment for both
Cognitive Behavioral Therapy primary and secondary insomnia and the
for Insomnia recommended first line of treatment.
Cognitive behavioral therapy-insomnia (CBT-I)
Allison Baylor1, Sarah Griffin1 and is a collection of interventions that address the
Bruce Rybarczyk2 cognitive, physiological, and behavioral factors
1
Virginia Commonwealth University, Richmond, that perpetuate insomnia. The core components of
VA, USA CBT-I are psychoeducation, sleep restriction, stim-
2
Department of Psychology, Virginia ulus control, sleep hygiene, and cognitive
Commonwealth University, Richmond, VA, USA restructuring. Treatment typically consists of
between four to eight 50-min sessions, following
a goal-oriented, collaborative format. CBT-I is flex-
Summary ible and can be tailored to fit a variety of treatment
settings, from standard therapy in traditional men-
Cognitive behavioral therapy for insomnia tal health practices to primary care settings.
(CBT-I) is a brief, evidence-based behavioral CBT-I generally follows a format of an intro-
treatment for insomnia. CBT-I includes ductory psychoeducational session, followed by
psychoeducation, healthy sleep habits, sleep sessions focused on behavioral targets combined
restriction, and cognitive restructuring. with cognitive targets (the emphasis of which
depends on the number of cognitive errors asso-
ciated with sleep). For the first session, the patient
Overview brings a sleep log that includes estimated times
when the person went to bed/got out of bed, when
Insomnia is a prevalent sleep disorder, with a they fell asleep, and daytime naps over the pre-
negative impact on physical and mental health. ceding 2 weeks. During the first session, the cli-
Insomnia is defined as dissatisfaction with either nician devotes substantial time to reviewing this
sleep quantity or quality, coupled with difficulties log and understanding the patient’s current sleep
with sleep onset or maintenance. For adults with habits and goals, which informs case conceptual-
primary insomnia, these sleep difficulties are not ization and the treatment plan. Psychoeducation is
likely caused by another independent physical or another core tenant of the first session of CBT-I
Cognitive Behavioral Therapy for Insomnia 849

and remains foundational to all of the subsequent Evidence for CBT-I

CBT-I sessions. The clinician outlines good sleep
hygiene tips and reviews the basic physiology of Cognitive behavioral therapy for insomnia is an
sleep, which is regulated by the homeostatic drive empirically supported treatment for primary and
(i.e., sleep pressure) and the circadian drives (i.e., comorbid insomnia and the recommended first
the wake drive). It is important for patients to have line of treatment for primary insomnia. When com-
a basic understanding of these drives, especially, pared to pharmacotherapy, CBT-I is equally effec- C
that the sleep pressure must build (which consti- tive in the short term and more effective in the long
tutes the rationale for sleep restriction) properly in term for primary insomnia. Further, as a purely
order for them to accept treatment rationale and to behavioral treatment, CBT-I is not subject to the
increase their compliance (Harvey 2013). side effects inherent to pharmacological treatments.
After the psychoeducational and basic premise Additionally, meta-analyses indicate that insomnia
of the treatment is conveyed, the focus begins which is comorbid with other medical or psychiat-
with the cornerstone of the therapy – sleep restric- ric conditions reaps similar benefits from CBT-I as
tion. In this approach, the patient curtails their compared to individuals who only have insomnia.
sleep duration (by pushing their bedtime later yet CBT-I has also been demonstrated to be efficacious
keeping wake time constant) to build sleep pres- across age groups, according to recent meta-
sure. This is the most difficult aspect of the treat- analyses showing older adults are equally likely to
ment, and Rybarczyk and colleagues have dubbed benefit. Finally, CBT-I remains effective when
this initial stage of treatment as the “bootcamp” administered by a variety of health professionals,
phase – which allows the sleep system to be including psychologists, nurses, physicians, and
“re-booted.” The idea is to drive sleep pressure social workers. Furthermore, CBT-I has yielded
at the earliest phase to consistently high enough positive treatment outcomes across settings that
level to allow for a retraining of the rapid falling include specialty clinics, veteran’s administrations,
asleep and staying asleep processes. The second primary care clinics, and traditional mental health
key aspect of treatment is stimulus control. centers. In summary, cognitive behavioral therapy
According to the neurocognitive model of insom- for insomnia is an effective treatment, delivered
nia, insomnia occurs because the bed/bedroom in-person or in group formats, for primary or
and sensory cues (darkness, pillow, laying comorbid insomnia, for diverse patient populations,
prone) cease be being “paired” exclusively with and across a wide range of treatment settings.
sleep and is instead paired with wake behaviors
(e.g., lying in bed worrying about falling asleep),
which in turn leads to conditioned cortical arousal
References
in the sleep environment. In CBT-I, the client
retrains their brain to associate the bed and those Bastien, C. H. (2011). Insomnia: Neurophysiological and
accompanying sensory cues with sleep by only neuropsychological approaches. Neuropsychology
sleeping in bed (no other activities including TV Review, 21(1), 22–40.
Kaplan, K. A., & Harvey, A. G. (2014). Treatment of sleep
watching) and by minimizing nonsleeping time in
disturbance. In D. H. Barlow (Ed.), Clinical handbook of
bed (e.g., if the patient cannot fall asleep within psychological disorders: A step-by-step treatment man-
15–20 min, he or she is instructed to get up and ual (pp. 640–669). New York: Guilford Publications.
read in another room until more drowsy). Finally, Rybarczyk, B., Lund, H. G., Garroway, A. M., & Mack,
L. (2013). Cognitive behavioral therapy for insomnia in
cognitive components that contribute to insomnia
older adults: Background, evidence, and overview of
are challenged and reframed, including: catastro- treatment protocol. Clinical Gerontologist, 36(1),
phization of daytime consequences of insufficient 70–93.
sleep, worry/rumination about sleep, dysfunc- Wu, J. Q., Appleman, E. R., Salazar, R. D., & Ong, J. C.
(2015). Cognitive behavioral therapy for insomnia
tional beliefs about sleep, safety behaviors,
comorbid with psychiatric and medical conditions:
and overestimating nocturnal wakefulness while A meta-analysis. JAMA Internal Medicine, 175(9),
underestimating sleep. 1461–1472.
850 Cognitive Correctors

Cognitive Correctors, Table 1 Kinds of cognitive

Cognitive Correctors correctors
Behavioral prosthetics – behaviors that remind a person
Rick Parente, Maria St. Pierre and to do something
Grace-Anna Chaney Cognitive robot – carries out the same task consistently
and correctly
Department of Psychology, Towson University,
Cognitive orthotic – performs a thinking task
Towson, MD, USA Cognitive trainers – teaches new skills and provides
practice
Cognitive archives – maintain knowledge and records of
Synonyms past experience

Behavioral memory aids; Behavioral prosthetics;

Cognitive archives; Cognitive assessors; Cognitive Cognitive robots carry out a repetitive task for an
monitors; Cognitive orthotics; Cognitive robots;
individual. Examples of cognitive robots: Calcula-
Cognitive trainers; External aids; Prosthetic devices
tors perform the same mathematical operations.
Cycling timers turn appliances on and off at
preset times. Telememo wrist watches remind a
Definition person of appointments at the same time every
day, week, month, or year. Motion-sensitive detec-
A device, external to the mind that enhances or
tors automatically turn lights on and off when
replaces a memory or cognitive function.
motion or the lack thereof is sensed. Smart irons
turn themselves off after a short period of disuse.
Cognitive orthotic devices replace some cog-
Current Knowledge nitive function. For example: Spell checkers find
the correct spelling by keying in a close match.
According to Kim et al. (2015), there are two Grammar checkers find flawed sentence struc-
types of cognitive interventions: single domain tures. Internet search engines scour the internet
and multi-domain. Single-domain cognitive cor- using key words and Boolean logic.
rectors solve a specific problem. For example, a Cognitive trainers and archives teach a skill
brain injury survivor may carry a sticky notepad to and/or stores large searchable databases. For
write down important information. Multi-domain example: Academic remediation software teaches
cognitive correctors provide a wider variety of basic academic skills. Cognitive remediation soft-
functions. For example, the same survivor may ware provides drill and practice exercises that
use a “smartphone” with a variety of features that improves cognitive skills. Skills training software
support a large number of cognitive functions. teaches skills like typing or use of specific soft-
Parente and Herrmann (2010) have summarized ware packages, e.g., Microsoft Office. Cognitive
the variety of cognitive correctors in Table 1. archives, e.g., electronic encyclopedias, store
Cognitive prosthetics are devices that take over large amounts of information and provide a search
some memory process. For example: Color coding engine for finding specific topics.
creates a simplistic visual organization. Checklists
improve consistency and sequential ordering. Med-
ication organizers organize medications and remind
a person which ones to take on each day. Notepads See Also
and post-it notes are useful for quickly writing down
a message or for placing a written message some- ▶ Assistive Technology
where where it will be seen later. Appointment cal- ▶ Learning
endars and diaries remind the person of important ▶ Prosthetic Memory Aids
appointments and provide a record of daily activity. ▶ Retrieval Techniques
Cognitive Functioning 851

Further Readings brain regulate distinct aspects of thought, person-

ality, and behavior. Later on in the 1800s and
Kim, G. H., Jeon, S., Im, K., Kwon, H., Lee, B. H., Kim, 1900s, scientists including Wilder Penfield,
G. Y., ... Na, D. L. (2015). Structural brain changes after
Hughlings Jackson, Paul Broca, and Carl
traditional and robot-assisted multi-domain cognitive
training in community-dwelling healthy elderly. PLoS Wernicke used epilepsy and lesion models to
One, 10(4), e0123251. delineate distinct neuroanatomical correlates of
Parente, R., & Herrmann, D. (2010). Retraining cognition: cognitive and motor functions. More recently, C
Techniques and applications (pp. 283–303, Chap. 24).
functional (e.g., fMRI, PET) and structural
Austin: ProEd Publishers.
(e.g., MRI, CT) neuroimaging techniques have
provided an even more well-defined understand-
ing of brain-behavior relationships.

Cognitive Functioning
Current Knowledge
Christina A. Palmese
Department of Neurology, Mount Sinai Beth Attention
Israel, New York, NY, USA Attention refers to the ability to concentrate on
information present in the world around us. It
allows us to concentrate on two things at once,
such as balancing a checkbook while talking on
Synonyms the phone. It is regulated by the frontal lobes,
although pathways involving the pons, parietal
Cognition; Mentation; Thinking lobe, and thalamus are involved in the mediation
of attention, as well. Dysfunction along any of
these pathways can contribute to various types of
Definition attention problems.
Attention is hierarchically organized. The abil-
Cognitive functioning is a general term used to ity to focus is the most rudimentary level of atten-
describe the different ways that people think. It tion that permits us to concentrate or be vigilant to
refers to faculties such as attention, mental pro- something in the environment for a very brief time
cessing speed, executive functions, language, period. Sustained attention refers to maintenance
visual-spatial skills, memory, and fine motor dex- of concentration for minutes or hours. Selective
terity. Different cognitive functions are supported attention requires even greater attention capacity
by distinct cortical and subcortical brain regions. that allows us to attend to a particular task while
Disruption of neural processes in these brain filtering out irrelevant, background information.
regions can result in a range of cognitive deficits For example, this form of attention is used when
and syndromes. we read the newspaper and are not distracted by
noises such as the radio or television nearby.
Divided attention allows us to pay attention to
two or more tasks simultaneously, otherwise
Historical Background known as multitasking. At the top of the hierarchy
is alternating attention, which is the most complex
In the 1600s, Descartes, a philosopher, was one form of attention that involves shifting of atten-
of the first scholars to establish the idea that the tion from one task to another.
brain controls behavior. In the late 1700s, Franz There exist many neuropsychological measures
Gall, a forefather of phrenology (the study of that measure attention. One such measure is the
behavior based on the size and shape of the digit span test. This task assesses basic attention
skull), helped identify that different parts of the capacity through repetition of series of numbers of
852 Cognitive Functioning

increasing length (e.g., 1-2-3-etc.). Continuous per- largely by the frontal lobes. They include skills
formance tests are computerized tools that evaluate such as problem-solving efficiency, impulse con-
attention capacity over an extended time period of trol, organization, mental flexibility, planning, and
10–15 min. Higher level attention skills can be conceptualization. Deficits in executive function-
examined using tests measures of mental arithmetic, ing can occur secondary to a neurodevelopmental
connecting of numbers and letters in alternating delay, such as seen in attention deficit disorder.
sequence (e.g., 1-A-2-B-3-etc.), and resequencing For the most part, however, executive dysfunction
of numbers and letters in numeric and alphabetic is acquired through acute brain injury (e.g., stroke)
order (e.g., transform “8-K-2” to 2-8-K). or associated with neurodegenerative syndromes,
Attention problems can be observed across the such as Alzheimer’s disease, multiple sclerosis,
lifespan. In children, poor concentration, distract- and Huntington’s disease.
ibility, and trouble regulating behavior can be
related to an attention deficit disorder, a diagnosis
that is made when pervasive attention difficulties Language
are idiopathic, demonstrated at a young age, and
observable in at least two different environments. At the most fundamental level, language can be
Attention difficulties in children also can develop broken down into two categories: receptive and
secondary to other medical or psychiatric disor- expressive language. Receptive language is the
ders such as anxiety, language disorders, or epi- ability to understand language. It is mediated by
lepsy. In adults, attention deficits may manifest the left posterior temporal lobe, which also is
secondary to a variety of neurological and medical referred to as Wernicke’s area. Expressive lan-
conditions, including subarachnoid hemorrhage, guage, on the other hand, pertains to oral and
epilepsy, dementia, head injury, diabetes, and written expression, and it is regulated by the pos-
hypothyroidism. Stress, depression, and medica- terior frontal/anterior temporal lobe. This region
tion side effects often contribute to attention prob- commonly is referred to as Broca’s area.
lems in adults, as well. Deficits in receptive and expressive language
can be idiopathic (i.e., of unknown origin) or
Mental Processing Speed acquired. If language problems are idiopathic,
Mental processing speed is a term used synony- they typically are identified during a child’s devel-
mously with reaction time, and it refers to the opment and are referred to as a developmental
speed at which individuals think and complete language delay. As some children mature, their
activities. It also often is referred to as language difficulties might resolve; however,
bradyphrenia (brady means “slow”; phrenia other children experience residual language defi-
means “mind”). It is largely regulated by the fron- cits throughout adulthood. On the other hand,
tal lobes and subcortical regions, and it has global acquired language deficits such as those resultant
effects on cognition. Reaction time can be evalu- from stroke, head injury, and tumor are character-
ated in several ways, with common measures ized as aphasia. Depending on the location of
including those of timed digit symbol transcrip- brain injury, different aphasia syndromes can be
tion, timed reading of color names and naming of observed.
colors, and timed symbol search. Bradyphrenia Traditionally, language skills in adults are
commonly is seen in various medical and neuro- assessed with an aphasia battery (e.g., Boston
logical conditions across the lifespan, including, Diagnostic Aphasia Examination (BDAE)), letter
yet not limited to, dementia, brain injury, and category fluency measures, and picture-
Parkinson’s disease, and epilepsy. naming tasks. Similar measures are used during
evaluation of pediatric populations, although
Executive Functions there often is added emphasis on assessment of
Executive functions are some of the most highly phonics, reading, grammar, syntax, language for-
complex aspects of thinking that are mediated mulation, and language organization skills.
Cognitive Functioning 853

Visual-Spatial Processing common dementia that is associated with a learn-

Visual-spatial skills include a range of abilities ing deficit. Retrieval deficits typically are seen in
such basic spatial perception, left-right orientation, people with a history of Parkinson’s disease and
visual construction, and nonverbal problem- Huntington’s disease, and they also commonly
solving ability. They involve an appreciation for occur in people who have major depression.
“what” and “where” items that are in space. Memory deficits secondary to the latter may be
The “what,” or ventral, pathway is mediated by reversible upon resolution of mood symptoms. C
the right (nondominant) temporal lobe. Disruption
of this pathway by acquired brain injury can result in Motor
agnosia, which is a loss of awareness and inability to Motor skills refer to hand-eye coordination, man-
recognize what things are. Agnosias can be domain ual dexterity, and visual-motor integration. These
specific, affecting auditory, visual, or somatosen- skills all have contralateral representation within
sory functioning. Prosopagnosia is a unique agnosia the parietal lobes. That is, right-sided motor func-
in which there is an inability to recognize faces. tions are regulated by left parietal lobe regions,
The “where” or dorsal pathway is regulated by and vice versa. Motor dysfunction can be observed
the parietal lobe. Dysfunction in the parietal lobe in children with developmental delay, as well as in
can contribute to spatial neglect in which a portion adults and children with medical conditions
of space is neglected or ignored. Neglect can be including cerebral palsy, spasticity, and dementia.
detected during visual field screening and on line It often manifests as clumsiness, poor handwriting,
bisection and drawing tasks. An individual with or trouble tying shoe laces and buttoning shirts.
spatial neglect will not respond to information Motor abilities can be evaluated using tasks requir-
presented in part or all of the visual field. Left ing rapid placement of pegs into a pegboard, draw-
hemispatial neglect, in which the entire left side of ing, finger tapping, and grip strength.
space is ignored, is the most commonly observed
form of neglect that results from damage to the
right parietal lobe.
Cross-References
Memory
Memory is a term used to described learning, ▶ Agnosia
retrieval, and retention of information. Verbal ▶ Agraphia
memory is regulated by left (dominant) temporal ▶ Alexia
regions and visual-spatial memory regulated by ▶ Amnesia
the right temporal lobe. Consolidation of new ▶ Anomia
information into long-term memory stores ▶ Aphasia
occurs within the CA1–CA3 regions of the hip- ▶ Apraxia
pocampus, a brain region rich in acetylcholine. ▶ Attention
Once consolidated, information then is stored in ▶ Dementia
various neural networks throughout the brain. ▶ Learning
Learning deficits occur when there is deple- ▶ Memory
tion of acetylcholine or a loss of brain cells in ▶ Processing Speed Index
the hippocampus. Retrieval deficits, on the ▶ Verbal Fluency
other hand, are associated with cell loss and ▶ Visuoperceptual
neurochemical depletion of dopamine and gluta-
mate in the basal ganglia and other subcortical
regions. References and Readings
When memory loss is severe enough to affect a
Heilman, K. M., & Valenstein, E. (2011). Clinical neuro-
person’s daily independence, it is referred to as psychology (5th ed.). New York: Oxford University
dementia. Alzheimer’s disease is the most Press.
854 Cognitive Linguistic Quick Test

Kolb, B., & Wishaw, I. (2015). Fundamentals of human Administration

neuropsychology (7th ed.). New York: Worth Pub- The CLQT can be administered while seated at a
lishers, Inc.
Lezak, M., Howieson, D. B., Bigler, E. D., & Tranel, table or at bedside in 15–30 min by experienced
D. (2012). Neuropsychological assessment (5th ed.). clinicians. The CLQT Examiner’s Manual pro-
New York: Oxford University Press. vides explicit directions for administering, scor-
Ravdin, L., & Katzen, H. L. (Eds.). (2013). Handbook on ing, and interpreting test results. It also provides
the neuropsychology of aging and dementia.
New York: Springer Publishers. scored samples of performance on each task from
Squire, L. R., & Schacter, D. L. (2003). Neuropsychology the five clinical groups tested.
of memory (3rd ed.). New York: The Guilford Press. The CLQT English and Spanish record forms
also provide precise instructions for administer-
ing, recording, and scoring each of the 10 task.
Cognitive Linguistic Instructions to be given to examinees are expli-
Quick Test cated stated. The Banners at the top of each task
summarize the use of the stimulus manual,
Nancy Helm-Estabrooks response booklet, additional materials, prompts,
Department of Communication Disorders and repetitions, and item limits for that task.
Sciences, College of Health and Human Sciences,
Western Carolina University, Cullowhee, NC, USA
Historical Background

Synonyms Field testing for the Cognitive Linguistic Quick

Test (CLQT) began in 1998 and consisted of one
CLQT pilot study and three research studies. The pur-
pose of the pilot study was to see whether
13 examinees with no known neurological dys-
Description function were able to respond correctly to the
original test items. Result of that study led to
Cognitive Linguistic Quick Test (CLQT). Author: revisions of test items, test format, and adminis-
Nancy Helm-Estabrooks 2001. Publisher: tration directions.
Pearson. P.O. Box 599700, San Antonio, TX CLQT Study 1 was conducted in 18 US states
78259. Pearsonclinical.com/language/. . ./cognitive- by 30 certified speech and language pathologists
linguistic-quick-test-clqt.html. The complete kit and psychologists. Of the 92 examinees tested,
consists of Examiner’s Manual, Stimulus Manual, 28 were diagnosed according to clinical evidence
15 English Record Forms or 15 Spanish Record of neurologic dysfunction (clinical) and 64 exam-
Forms, and 15 Response Forms. inees had no known clinical dysfunction
The Cognitive Linguistic Quick Test (CLQT) (nonclinical). The clinical group consisted of indi-
measures the status of cognitive-linguistic function- viduals diagnosed with left CVA, right CVA,
ing in five cognitive domains (Attention, Memory, bilateral CVA, closed head injury, or Alzheimer’s
Executive Functions, Language, and Visuospatial disease. With one exception, at least two non-
Skills) in English and Spanish-speaking adults ages clinical examinees were matched by age, race/
18–89 with known or suspected neurological dys- ethnicity, and education level to each clinical par-
function. CLQT’s ten tasks, five of which have ticipant. The age range for the two groups was
minimal language demands, tap specific cognitive 18–89 years. The resulting data were analyzed
skills within a short time period and with relatively according to five age groups for both clinical and
simple administration and scoring procedures. nonclinical participants leading to different cut
CLQT criterion cut scores (Within Normal Limits, scores for ages 18–69 and 70–89. Analysis of
Mild, Moderate, and Severe) are provided for each overall data showed clinical vs nonclinical differ-
cognitive domain. ences in mean performance of at least 1 standard
Cognitive Linguistic Quick Test 855

deviation on all tasks. Changes in the test material aphasia (PWA) along with the original testing and
for Study 2 were made on the basis of Study 1 data scoring procedures for other population with
and examiners’ feedback. known or suspected neurological impairments.
Study 2 was conducted by 61 clinicians in For this new study, 76 participants with aphasia
21 states who received training in CLQT admin- were tested at 1 month to 18 years following left
istration. The sample of 154 nonclinical exam- hemisphere (only) strokes by 12 CLQT trained
inees included African American, Hispanic, and examiners. Participants were distributed across C
White participants aged 18–89 years. Data analy- 15 US states and ranged from 36 to 88 years.
sis and examiner feedback resulted in changed to
the Generative naming task.
Study 3 was conducted between March and Psychometric Data
November 2000 with 30 trained examiners from
health-related professions administering the final Reliability
version of the CLQT to 119 participants (81 non- The stability of the CLQT test was measured with
clinical and 38 clinical examinees in 16 states. The a sample of 46 nonclinical examinees between the
clinical group consisted of individuals with one of ages of 19 and 89 (mean age = 50.13,
the following diagnosis: left CVA, right CVA, SD = 20.91). The test-retest interval was between
bilateral CVA, closed head injury, or Alzheimer’s 80 days and 140 days (mean interval was
disease. 100.43 days, SD = 11.92). This length of time
was chosen to minimize practice effects but to
Spanish Version keep the constructs stable for the individual.
From the earliest developmental stages of the Given the nonclinical sample, there was little dif-
CLQT, the appropriateness of each test task and ference, if any, in performance between test and
item was considered for both the English- retest. In addition, with the brevity of some of the
speaking and Spanish-speaking populations. The tasks, the correlation coefficients were affected.
instructions as well as the stimulus vocabulary for The test-retest stability coefficients ranged
the confrontation naming and story retelling tasks between 0.61 and 0.90 for the cognitive domains,
were designed to minimize socioeconomic and and between 0.03 and 0.81 for the tasks
cultural bias. Pilot testing resulted in minor item themselves.
changes to the final version that is based on results A better picture of stability can be obtained by
of 100 Spanish-speaking individuals from four calculating the absolute score difference. Results
regions of the United States. The Study 2 eight were generally small, with less than 1 point dif-
bilingual examiners were familiar with Spanish as ference for all tasks, indicating high consistency
it is spoken in Cuba, Mexico, Peru, Puerto Rico, of scores across administrations.
Venezuela, and the US southwest. Data from All CLQT test protocols were scored by two
CLQT Spanish Version Study 2 and the final trained scorers under the supervision of the test
version is presented in the CLQT Examiner’s developers. Eight of 10 tasks on the CLQT are
Manual. objectively scored. For the other two tasks, the
In addition to the Spanish version, two research overall correlation between scorers for the Clock
adaptations have been made: one in French- Drawing task was 0.86. The correlation coeffi-
Canadian and the other in Kannada. For more cient between the two scorers for Generative
information, contact the publisher. Naming was 0.99.

Revised CLQT Validity

As of the submission date to this encyclopedia, data CLQT tasks were designed to tap specific cogni-
analyses are underway on a revised version of the tive and language skills known to show utility in
CLQT. This version will yield nonlinguistic cogni- clinical practice, as evidenced by the research
tive ratings and language ratings for people with literature. The test manual documents the relevant
856 Cognitive Linguistic Quick Test

literature base for each task in the CLQT. At the socioeconomic, cultural, and educational back-
conclusion of the pilot study as well as after Study grounds. The score for each task, except Clock
1 and 2, the test was checked for evidence of Drawing, contributes to the severity rating for one
construct-irrelevant components and construct or more of the five cognitive domains. A Total
underrepresentation by various experts, including Composite Severity Rating for each age group
the author. Test modifications were made based on (18–69, 70–89) is derived from the severity rat-
these reviews. ings for each of the five cognitive domains.
A correlation analysis was performed to deter- A separate severity rating is obtained for the
mine the relationship between the Clock Drawing Clock Drawing task for each age group. The
Severity Rating and the Composite Severity Rat- Clock Drawing rating can serve as a quick mon-
ing. The Clock Drawing task is considered to be itor of progress or decline.
useful as a mini-screen of cognition. A Pearson
correlation coefficient of 0.74 was found between
the Clock Drawing Severity Rating and the Com- Clinical Uses
posite Severity Rating.
Confirmatory factor analysis was compiled and The Cognitive Linguistic Quick Test (CLQT) is a
a performance comparison between clinical and commonly used clinical assessment tool that pro-
nonclinical examinees was conducted. Structural vides a “snapshot” of the individual’s relative
equation modeling was used on each of the five strengths and weaknesses within five domains of
cognitive domain subscales. One-factor measure- cognition. Based on CLQT performance, deci-
ment models were constructed for each subscale sions can be made regarding further assessment
and fit to the standardization data. Fit indices for and recommendations for remediation and
several measurement models (chi-square/df counseling.
(Wheaton 1977), Non-Normed Fit Index (NNFI; Published studies of the clinical use of the
Bentler and Bonnet 1980), Root Mean Square CLQT include that of Parashos et al. (2009) who
Error of Approximation (RMSEA; Steiger administered the CLQT and the Mini-Mental State
1990), and Expected Cross-Validation Index Examination (MMSE) to 93 individuals with
(ECVI)) are reported in the CLQT manual and Parkinson’s disease (PD). The two measures cor-
provide strong support for the unidimensionality related well and their diagnostic value for demen-
of each subscale, each of which represents a dif- tia was similar. The CLQT, however, was superior
ferent cognitive domain. to the MMSE in that it provided cognitive-domain
A clinical study was completed to determine performance ratings. The authors concluded that
the degree to which the CLQT can differentiate the CLQT was a valuable tool for identifying
between clinical and nonclinical groups. dementia in people with PD.
A matched sample (n = 76) was created using Mupawose and Broom (2010) used the CLQT
each examinee from the CLQT Clinical Research to assess cognition in 16 individuals with HIV or
Sample paired with a nonclinical examinee. The AIDS in South Africa. They found that 87.5% of
results of the t-test procedure demonstrated a sig- the study participants were diagnosed with some
nificant difference between matched clinical and form of cognitive deficit according to CLQT
nonclinical examinees for all 10 CLQT tasks as scores. The authors concluded that this tool can
well as all five cognitive domains. be used with this population as a substitute for
more expensive and time-consuming neuropsy-
Norms chological assessment protocols.
CLQT criterion cut scores (Within Normal Limits, In a 2012 Australian study, Blyth et al. com-
Mild, Moderate, and Severe) were established for pared the clinical utility of the Cognistat (Kiernan
each cognitive domain based on the author’s et al. 1987) versus the CLQT is assessing
expertise informed by nonclinical and clinical cognitive-communicative disorders in 83 individ-
subjects representative of different ages, uals with posttraumatic brain injury. The CLQT
Cognitive Log 857

was superior to the Cognistat in identifying high- praxis. All responses are scored according to the
level cognitive-communicative deficits in the TBI following criteria: 3 points = spontaneously cor-
study population recruited from an acute trauma rect response, no errors; 2 points = correct on
center. logical cueing (e.g., “That was yesterday, so
today is?”) or in the presence of 1 error; 1
point = correct on multiple-choice cueing or in
References the presence of 2 errors; and 0 points = incorrect C
despite cueing, more than 2 errors, unable to com-
Blyth, T., Scott, A., Bond, A., & Paul, E. (2012). plete. Points for time estimation are calculated as
A comparison of two assessments of high level cogni-
follows: 3 points = correct within 5 s; 2
tive communication disorders in mild traumatic brain
injury. Brain Injury, 26(3), 234–240. points = correct within 10 s; and 1 point = cor-
Helm-Estabrooks, N. (2001). Cognitive linguistic quick rect within 15 s. Incorrect/absent responses are
test. San Antonio: Pearson Publishing. followed by cueing at the next level for the orien-
Kiernan, R. J., Mueller, J., Langston, J. W., & Van Dyke,
tation and delayed memory items. Multiple-
C. (1987). The neurobehavioral cognitive status exam-
ination, a brief but differentiated approach to cognitive choice cueing, used only with the orientation
assessment. Annals of Internal Medicine, 107, items, involves provision of three choices, vary-
481–485. ing the location of the correct response. Item
Mupawose, A., & Broom, Y. (2010). Assessing cognitive-
scores are summed to provide a total score ranging
linguistic abilities in South African adults living with
HIV: The cognitive linguistic quick test. African Jour- from 0 to 30. Daily scores can be plotted to permit
nal of AIDS Research, 9(2), 147–152. quick visual analysis of recovery trends.
Parashos, S. A., Johnson, M. L., Erickson-Davis, C., & The following specific items are included in
Wielinski, C. L. (2009). Assessing cognition in
the Cog-Log: three items assessing the orientation
Parkinson disease: Use of the cognitive linguistic
quick test. Journal of Geriatric Psychiatry and Neurol- to the date, time, and hospital name; two items
ogy, 22(4), 228–234. assessing immediate and delayed recall for a short
address; counting backward from 20; reciting the
months in reverse order; and estimating when 30 s
has passed. Two motor tasks involving hand ges-
Cognitive Log tures – a movement sequence (fist-edge-palm) and
a response inhibition task (go/no-go) – are also
Thomas A. Novack included.
Department of Physical Medicine and
Rehabilitation, University of Alabama at
Birmingham, Birmingham, AL, USA Historical Background

Measurement of orientation and higher

Synonyms neurocognitive processes are important aspects
of early neurorehabilitation. Reliable serial
C-Log; Cog-Log assessment is crucial to document the rapid
changes in behavior and cognition during recov-
ery from acquired brain disorders. Therefore,
Description there is a need for a brief, bedside evaluation
instrument to assess other areas of cognition that
The Cog-Log is a ten-item scale designed for are frequently affected by acquired brain injuries.
serial bedside measurement of cognitive functions Existing scales are typically too lengthy or
in individuals completing inpatient rehabilitation. involved to present as part of morning rounds.
The scale includes items assessing orientation, Other scales fail to adequately capture the primary
immediate and delayed verbal recall, concentra- limitations resulting from acquired brain injury.
tion, executive function, response inhibition, and The brief scales that have been created for serial
858 Cognitive Log

administration in an inpatient setting have been controlling for demographics and injury severity.
presented without adequate psychometric proper- The Cog-Log was also significantly correlated
ties or scaling. The Cog-Log was created to serve with the results of the Mini-Mental State Exami-
as a brief bedside measure to chart neurocognitive nation, a well-known cognitive screening test
recovery and assist in planning rehabilitation (r = 0.75, P < 0.001).
interventions with a wide variety of patients.

Clinical Uses
Psychometric Data
Individuals without known neurological insult
The reliability and validity of the Cog-Log have received average total Cog-Log scores of 28 ( 2),
been assessed in several ways. A sample of 150 and mean individual item scores were greater
individuals with acquired brain injury was exam- than or equal to 2.4. Age, education, and gender
ined with the Cog-Log. Most of the sample (80%) did not predict total or individual item scores
had sustained moderate to severe TBI, with the (p > 0.05). Stepwise discriminant analyses on a
remainder including patients with CVA and sample of 82 persons with brain injury and 82
anoxia. Internal consistency analysis (Cronbach’s normal controls matched for age, education, and
alpha) was conducted for the total Cog-Log score. gender revealed that a cut-off score of 25 correctly
Inter-rater reliability estimates (Spearman’s rho) classified 88.4% of individuals in their respective
were calculated using a subset of 19 patients (75 groups.
total observations). High internal consistency The Cog-Log is a companion instrument to the
(Cronbach’s alpha = 0.778) was demonstrated Orientation Log (O-Log). Generally, the Cog-Log
with a standard error of measurement of 0.53. is not administered until a score of at least 15 is
Inter-rater reliability coefficients for each of the achieved on the O-Log, indicating that the person
ten Cog-Log items ranged from 0.749 (go/no-go is responding and able to respond correctly to
task) to 1.0 (time estimation). Standard errors of some orientation questions. Administering the
measurement were no more than 0.10 for single Cog-Log prior to this point has not proven fruitful.
item scores, which range from 0 to 3. The Cog-Log can be administered every day, but
Factor analysis of the Cog-Log using principal typically three times a week is sufficient to mon-
components extraction (N = 150) revealed a uni- itor progress or detect deterioration.
tary factor (eigenvalue = 3.48), with all items Efficiency and ease of assessment were con-
loading on that factor. The highest loadings were sidered when choosing items; tasks requiring
for delayed recall of verbal information and reci- additional stimuli (e.g., block construction) or
tation of months backward, suggesting a stronger extended administration times were not included.
contribution of complex working memory and The Cog-Log was designed for flexible adminis-
verbal recall to this unitary factor. tration to patients with severe cognitive and
The Cog-Log exhibited a significant correla- behavioral disturbances. Administration time
tion with neuropsychological assessment com- ranges from 7 to 10 min for confused patients,
pleted on the same day, including tests such as but can be as short as 5 min for those who perform
immediate and delayed recall of the Wechsler well.
Memory Scale-III Logical Memory subtest, Rey
Auditory Verbal Learning Test, Digit Span subtest
of the Wechsler Adult Intelligence Test-III, and Cross-References
the Trail Making Test. The lowest Cog-Log score
obtained during acute rehabilitation also signifi- ▶ Cognitive Functioning
cantly predicted 1-year outcome in three of six ▶ Galveston Orientation and Amnesia Test
neuropsychological domains (attention, executive ▶ Modified Mini-Mental State Examination
functioning, and visuospatial abilities) after ▶ Traumatic Brain Injury (TBI)
Cognitive Processing 859

References and Readings complex flow of dynamics, including bottom-up

(sensory-driven) and top-down (concept-driven)
Alderson, A. L., & Novack, T. A. (2003). Reliable serial processes. One cognitive psychology approach
measurement of cognitive processes in rehabilitation:
to better understanding cognitive processing has
The cognitive-log. Archives of Physical Medicine and
Rehabilitation, 84, 668–672. been through the development of computational
Center on Outcome Measurement in Brain Injury models, such as artificial intelligence.
(COMBI). www.tbims.org/combi. Accessed 26 May In cognitive neuroscience research, cognitive C
2009.
processing concepts are used to explore the rela-
Lee, D., LoGalbo, A. P., Baños, J. H., & Novack, T. A.
(2004). Prediction of cognitive abilities one year tion between brain and behavior, as exemplified
following TBI based on cognitive screening by George Miller’s research (1956) on the capac-
during rehabilitation. Rehabilitation Psychology, 49, ity of short-term memory to hold seven plus or
167–171.
minus two items and Baddeley’s theory (1974) of
Penna, S., & Novack, T. (2007). Further validation of the
orientation and cognitive log relative to the mini mental a central executive, phonological loop, and visuo-
status exam. Archives of Physical Medicine and Reha- spatial sketchpad.
bilitation, 88, 1360–1361.

Current Knowledge

The cognitive processing model is currently used

Cognitive Processing in the assessment and treatment of learning
disabilities, alcohol and drug addictions, and
Denise Krch trauma and abuse. This model emphasizes how
Kessler Foundation, East Hanover, NJ, USA new information is processed, internalized, and
retrieved in the context of a person’s existing
mental representations of information and of
Definition his/her beliefs, desires, knowledge, preferences,
and intentions.
Cognitive processing is a general term to
describe a series of cognitive operations carried
out in the creation and manipulation of mental Cross-References
representations of information. Cognitive
processes may include attention, perception, ▶ Attention
reasoning, emoting, learning, synthesizing, ▶ Cognitive Functioning
rearrangement and manipulation of stored infor- ▶ Learning
mation, memory storage, retrieval, and metacog- ▶ Memory
nition. These functions can be conscious ▶ Metacognition
(e.g., learning a concept) or unconscious (e.g., ▶ Perception
learning a skill) and can be internally generated ▶ Reasoning
(e.g., recalling a memory) or initiated by a ▶ Retrieval Techniques
novel sensory input from the environment ▶ Short-Term Memory
(e.g., solving a problem).
From a cognitive psychology perspective, cog- References and Readings
nitive processing is approached as a sequence of
ordered stages wherein sensory input is trans- Coren, S., Ward, L., & Enns, J. (2004). Sensation and
formed, reduced, elaborated, stored, recovered, perception. New York: Harcourt Brace.
Groome, D., Brace, N., Edgar, H., Esgate, A., Pike, G.,
and utilized. Early views of cognitive processing Stafford, T., et al. (2006). An introduction to cognitive
emphasized linear temporal processing, whereas psychology: Processes and disorders (2nd ed.).
contemporary models assume a less linear, more London: Routledge.
860 Cognitive Rehabilitation

Sohlberg and Mateer 2001). However, current

Cognitive Rehabilitation trends in service delivery have resulted in an
“era of consolidation,” a term describing the sig-
Melanie M. Cochrane1, Marianne Hrabok2 and nificant downsizing of CR programs. It has been
Kimberly A. Kerns1 suggested that the reduced length of inpatient
1
Department of Psychology, University of stays, outpatient health coverage, and more lim-
Victoria, Victoria, BC, Canada ited support for CR programs have made evidence
2
Department of Psychology, Addiction and and theory-based CR practices increasingly rele-
Mental Health, Alberta Health Services, vant to contemporary practice (Cicerone et al.
Edmonton, AB, Canada 2005; Levine and Downey-Lamb 2002; Sohlberg
and Mateer 2001).

Synonyms
Rationale or Underlying Theory
Cognitive remediation
CR is multidisciplinary and draws from a range of
fields, including neuropsychology, learning theory,
Definition cognitive behavioral therapy and psychotherapy,
among many others. One main category of theories
Cognitive rehabilitation (CR) can be defined as underlying CR is those specific to the cognitive or
efforts to promote maximal adaptive cognitive func- behavioral domain of CR focus. For example,
tioning in people with neurologically induced cog- attention rehabilitation programs are based on the-
nitive deficits (Barrett and Gonzalez-Rothi 2002). oretical models of attention, memory rehabilitation
programs on theoretical models of memory, and so
on. A theory-driven approach provides a rational
Historical Background and empirical basis for intervention and guidance
on the structure and delivery of CR (Hart et al.
The field of CR has grown rapidly over the last 2014; Sohlberg and Mateer 2001).
few decades, but historically can be traced to the Another major theory underlying many forms
1800s (Ponsford 2004; Sohlberg and Mateer of CR is neuroplasticity (Kolb and Cioe 2004), the
2001). For example, Broca administered language concept that the brain is amenable to change in
rehabilitation in the 1800s, and until the 1980s structure and function. Neuroplasticity has many
most rehabilitation programs focused on remedi- implications for CR (see Kleim and Jones 2008
ation of language deficits (as reviewed by for discussion), including the type and timing of
Ponsford 2004). Many further developments in CR and the effect of environmental factors on
CR were a result of the confluence of societal recovery of cognitive function following brain
influences and scientific and technological injury (Barrett and Gonzalez-Rothi 2002).
advances. During WWI, Goldstein established
CR programs for brain-injured soldiers. During
WWII, Luria advanced the field of CR through Goals and Objectives
his theoretical model of brain functioning, recov-
ery, and rehabilitation (Ponsford 2004). CR aims to foster natural recovery, decrease the
Advances in medical practice and an increase development of maladaptive patterns, and
in the number of survivors of traumatic brain increase functional recovery (Sohlberg and
injury (TBI) led to a greater awareness of the Mateer 2001). The primary goal of CR is to help
needs of people who sustained TBI and an expan- people achieve an optimal level of functioning in
sion of the number and focus of CR programs (the the context of impairments, including fostering
“era of proliferation”; Coelho, 1997, as cited by change in specific neuropsychological deficits
Cognitive Rehabilitation 861

and improvement in day-to-day function. CR recovery and adjustment (Anson and Ponsford
emphasizes improving function in everyday con- 2006; Green et al. 2008; Rassovsky et al. 2015).
texts rather than on specific cognitive tasks per se. Gender: Some research suggests that women
have better recovery following left hemisphere
lesions than men (Kimura 1983). Circulating sex
Treatment Participants hormones have also been shown to have
neuroprotective effects; however, future research C
CR has been used with a variety of populations, is needed to better understand these processes
including but not limited to TBI, stroke, develop- (e.g., see Engler-Chiurazzi et al. 2016 for
mental disorders, Alzheimer’s dementia, and discussion).
schizophrenia. CR has been most commonly Culture: Culture influences beliefs regarding
used and found effective among people who the nature and cause of loss, service utilization,
have sustained TBI and stroke (Cicerone et al. degree of personal responsibility for health, role
2011). Recently, there has been significant growth of family, and many other facets of psychological
in treatment research aimed at rehabilitation of and behavioral functioning relevant to recovery
neurocognitive deficits in schizophrenia (e.g., and participation in CR (Sohlberg and Mateer
CR focused on executive functioning deficits; 2001).
Kluwe-Schiavon et al. 2013).
Variables contributing to the pattern and degree Injury-Related Variables
of recovery include demographic (e.g., age, edu- Time Since Injury: Time since injury has been
cation, gender, culture), injury-related (e.g., time found to be an important predictor of cognitive
since injury, extent, and severity of injury), and sequelae following mild TBI, with litigation iden-
psychological characteristics (e.g., therapeutic tified as a factor that may be associated with an
alliance, comorbid psychological disorders, atypical trajectory of recovery (see Belanger et al.
awareness). 2005). Spontaneous recovery typically occurs at a
faster rate immediately following brain injury,
Demographic Variables particularly within the first 6 months, with signif-
Age: Younger adults show better levels of recovery icant recovery also occurring up to 2 years follow-
than older adults (de la Plata et al. 2008; Green ing injury (Sohlberg and Mateer 2001). However,
et al. 2008; Teuber, 1975 as cited by Sohlberg and it is important to note that compensatory tech-
Mateer 2001). Acquired brain injury (ABI) in older niques can be implemented and underlying
adults may be complicated by a number of factors, motor and cognitive skills improved years after
including the superimposition of effects of ABI on injury (e.g., Shaw et al. 2005).
declining cognitive abilities (Richards, 2000 as Extent and Severity of Injury: In general, rela-
cited by Sohlberg and Mateer 2001), and psycho- tively mild injuries are associated with faster
social difficulties more prevalent in the population, recovery rate and better outcomes. Focal injuries
including reduced levels of social support and are often associated with more rapid recovery than
financial resources (Goleburn and Golden 2001). diffuse injury (Sohlberg and Mateer 2001). TBI
However, it has also been suggested that older severity is related to greater impairment in subse-
adults often have a greater degree of stability, cop- quent functional outcome (Husson et al. 2010;
ing skills, fewer life demands, and effective com- Rassovsky et al. 2015).
pensatory techniques, which may be helpful in
promoting recovery (Sohlberg and Mateer 2001). Psychological Factors
Older age has been found to be predictive of poorer Therapeutic Alliance: CR should be an interactive
functional ability (Meyer et al. 2015) and rehabil- partnership between the client, therapist, and sig-
itation outcome (Koh et al. 2013). nificant others (if indicated). Cultivating a rela-
Education and Intelligence: Premorbid intelli- tionship characterized by attentiveness, respect,
gence and education are significantly related to trust, commitment, and rapport is a critical
862 Cognitive Rehabilitation

component of CR. Open communication and The second category of CR interventions is

involvement of the client and family in goal set- compensatory techniques, which aim to compen-
ting can also enhance engagement in rehabilita- sate for or bypass deficits (Sohlberg and Mateer
tion (Sohlberg and Mateer 2001). 2001; Wilson and Zangwill 2003). These include
Comorbid Psychological Disorders: Depres- environmental supports (e.g., organization of
sion and anxiety are frequently associated with physical space, manipulation of physiological fac-
brain injury (e.g., Anson and Ponsford 2006). tors such as sleep, nutrition, etc.) and external aids
These can impede CR and adjustment following (e.g., calendars, checklists, etc.; Manly et al. 2002;
injury due to their propensity to decrease motiva- Wilson and Zangwill 2003). Compensatory tech-
tion and contribute to a feeling of hopelessness niques can be helpful in managing diverse types
(Sohlberg and Mateer 2001). of cognitive difficulties, including memory defi-
Awareness: Greater awareness of deficits fol- cits (McDonald et al. 2011; Sohlberg and Mateer
lowing TBI may be associated with better treat- 2001).
ment outcomes (see Ownsworth and Clare 2006 Another method is the use of specialized
for discussion). Methodological limitations have approaches to teaching and stabilizing new
been noted in the awareness literature, and further behaviors and knowledge in people with memory
research is required. difficulties. These include instructional tech-
niques such as errorless learning, in which mis-
takes are minimized (Wilson et al. 1994), the
Treatment Procedures method of vanishing cues (e.g., Kessels and
Haan 2003), and traditional behavioral shaping
Examples of domains that have been a focus of and training techniques.
CR include attention, memory, language, Psychosocial support or psychotherapy (e.g.,
visuoperceptual difficulties, executive functions, supported listening, brain injury education, relax-
and socioemotional and behavioral disturbances. ation training) can also be an integral part of a
CR encompasses a range of interventions. These rehabilitation program, depending on the needs of
can be broadly divided into two types of the client (Sohlberg and Mateer 2001). For
techniques. instance, a range of psychological interventions
The first are those that aim to restore or have been shown to be effective in addressing
enhance function, by targeting the underlying depressive symptoms in long-term rehabilitation
impairment (Glisky and Glisky 2002; Sohlberg after ABI (Stalder-Lüthy et al. 2013).
and Mateer 2001). For example, Attention Pro- Comprehensive-holistic rehabilitation programs
cess Training (APT) is a theoretically driven pro- have been found to be efficacious for addressing
gram that contends that attention can be improved behavioral and psychosocial disorders following
through repeated activation of attentional systems ABI (Cattelani et al. 2010).
(Sohlberg and Mateer 1987, 2001). APT consists Computer programs can be used as an adjunct
of a group of hierarchically organized tasks that to CR but should not be the sole form of CR
exercise different components of attention (e.g., (Cicerone et al. 2005). A recent systematic review
sustained, selective, alternating, divided atten- highlighted the insufficient evidence of computer-
tion). In CR of memory deficits, restorative/gen- based CR and the critical need for future research
eralized memory approaches aim to improve in this area (Politis and Norman 2016).
specific memory systems (e.g., Raskin & A successful rehabilitation program typically
Sohlberg, 1996, as cited by Sohlberg and Mateer involves a combination of interventions, specifi-
2001; Spreij et al. 2014). Various approaches to cally tailored to the individual’s level of disability
executive function rehabilitation focus on training and personal goals (Manly et al. 2002; Sohlberg
in formal problem-solving strategies as well as and Mateer 2001).
how these strategies can be applied to activities The duration and frequency of CR varies
of daily living (Cicerone et al. 2011). widely (e.g., Geusgens et al. 2007; Kurtz and
Cognitive Rehabilitation 863

Nichols 2007). CR has been delivered both on an specific language impairments (e.g., reading
individual and on a group basis. Significant others comprehension).
(e.g., family) are viewed as an integral part of Memory strategy training, such as internalized
treatment (Sohlberg and Mateer 2001). Family strategies (e.g., visual imagery) and external
and caregiver characteristics (e.g., family func- memory compensations (e.g., notebooks), had
tioning, caregiver distress, social support) are strong empirical support for mild memory impair-
associated with better community integration fol- ments from TBI. Metacognitive strategy training C
lowing mild/moderate TBI (Sady et al. 2010). (e.g., self-monitoring and self-regulation) for def-
icits in executive functioning after TBI was
supported, as was comprehensive-holistic CR
Efficacy Information programs (which address multiple aspects of
impairment).
Evidence-based standards of CR are frequently Although CR has found to be efficacious, there
identified as important in advancing the field of are still limitations. Further guidelines and stan-
CR, both in terms of quality of treatment and for dards are required to evaluate the quality of
fiscal support at an organizational level (e.g., methods used in cognitive rehabilitation research
Sohlberg and Mateer 2001). Cicerone et al. in order to inform best practices (e.g., see
(2000, 2005, 2011) conducted reviews on out- Cicerone et al. 2009).
comes of CR for people with TBI or stroke. There is less empirical study of CR with
Across studies, a total of 370 interventions populations beside TBI and stroke. A Cochrane
(65 Class I or Ia, 54 Class II, and 251 Class III review reported cognitive training was of limited
studies) were reviewed. Interventions were clas- benefit for dementia, but quality of studies was
sified as practice standards, practice guidelines, or low to moderate (Bahar-Fuchs et al. 2013). Cog-
practice options, based on quality of evidence (see nitive remediation in early schizophrenia may
Cicerone et al. 2011 for details). improve verbal memory and social cognition
Although implementation of CR programs fre- (Revell et al. 2015). A review of CR for people
quently results in positive change, a number of with multiple sclerosis suggested some promise
methodological problems have been identified in for CR, but methodological weaknesses limited
the CR literature, including sample characteristics conclusions (Mitolo et al. 2015).
(e.g., client variability, insufficient information
provided, small sample sizes) and treatment char-
acteristics (e.g., variability of settings, insufficient Outcome Measurement
description of interventions, lack of standardized
treatment protocols, absence of control Hart and Ehde (2015) recommend that rehabilita-
conditions). tion programs should explicitly include targets of
The results of Cicerone and colleagues’ the intervention (i.e., the desired outcome), active
reviews provide insight into the research support ingredients of the CR program (i.e., specific
for various CR methods. Specifically, remediation aspects of the program that exert the greatest
of attention focused on direct attention training impact on the desired outcome), and finally, the
and metacognitive training was supported. Strong mechanisms by which the outcomes are achieved.
empirical support was found for visuospatial reha- Measures should include specific outcome mea-
bilitation after right hemisphere stroke (e.g., sures related to the construct addressed by the
visual scanning) and interventions for apraxia intervention and general measures of functional
after left hemisphere stroke (e.g., specific gestural outcome (i.e., work/school return, interpersonal
or strategy training). A number of language inter- relationships; Levine and Downey-Lamb 2002).
ventions were shown to have empirical support, When possible, measures should have established
including cognitive linguistic therapies, pragmatic psychometric properties and be completed by
conversational skills, and interventions for both the client and significant others.
864 Cognitive Rehabilitation

Neuropsychological assessment can be a valu- ▶ Prosthetic Memory Aids

able tool at various points to predict outcome, ▶ Rehabilitation Psychology
guide appropriate rehabilitation strategies, guide ▶ Traumatic Brain Injury (TBI)
vocational and educational planning, interpret
behavior, and help evaluate the extent of injury
in conjunction with other information (Bergquist References and Readings
and Malec 2002).
Measurement of transfer of training to every- Anson, K., & Ponsford, J. (2006). Coping and emotional
adjustment following traumatic brain injury. The Jour-
day life has been measured through assessment of
nal of Head Trauma Rehabilitation, 21, 248–259.
performance on tasks similar to tasks used during Bahar-Fuchs, A., Clare, L., & Woods, B. (2013). Cognitive
training, standardized observations of simulated training and cognitive rehabilitation for mild to moder-
performance of daily tasks in a laboratory envi- ate Alzheimer’s disease and vascular dementia.
Cochrane Database Systemic Review, (6).
ronment, and standardized and non-standardized
Barrett, A. M., & Gonzalez-Rothi, L. J. (2002). Theoretical
reports of transfer to daily functioning (Geusgens bases for neuropsychological interventions. In P. J.
et al. 2007). There is a need for further develop- Eslinger (Ed.), Neuropsychological interventions:
ment of standardized measures of transfer with Clinical research and practice (pp. 16–37). London:
The Guilford Press.
good psychometric properties (Geusgens et al.
Belanger, H. G., Curtiss, G., Demery, J. A., Lebowitz,
2007). It has been recommended that generaliza- B. K., & Vanderploeg, R. D. (2005). Factors moderat-
tion should not be “expected” but should be “pro- ing neuropsychological outcomes following mild trau-
grammed” throughout the CR program (Sohlberg matic brain injury: A meta-analysis. Journal of the
International Neuropsychological Society: JINS,
and Mateer 2001).
11(3), 215.
Bergquist, T. F., & Malec, J. F. (2002). Neuropsychological
assessment for treatment planning and research. In P. J.
Qualifications of Treatment Providers Eslinger (Ed.), Neuropsychological interventions:
Clinical research and practice (pp. 38–58). London:
The Guilford Press.
CR is typically provided by registered psycholo- Cattelani, R., Zettin, M., & Zoccolotti, P. (2010). Rehabil-
gists and occupational therapists. Speech and lan- itation treatments for adults with behavioral and psy-
guage therapists typically provide rehabilitation for chosocial disorders following acquired brain injury:
language and communication deficits. Neuropsy- A systematic review. Neuropsychology Review, 20(1),
52–85.
chologists have a key role in CR, in terms of pro- Cicerone, K. D., Dahlberg, C., Kalmar, K., Langenbahn,
viding neuropsychological assessment (see above), D. M., Malec, J. F., Bergquist, T. F., . . . Herzog,
matching theoretical foundations with practice, and J. (2000). Evidence-based cognitive rehabilitation:
guiding empirically informed practice. Recommendations for clinical practice. Archives of
Physical Medicine and Rehabilitation, 81(12),
1596–1615.
Cicerone, K. D., Dahlberg, C., Malec, J. F., Langenbahn,
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866 Cognitive Reserve

injury. Archives of Physical Medicine and Rehabilita- Historical Background

tion, 91(10), 1542–1550.
Shaw, S. E., Morris, D. M., Uswatte, G., McKay, S.,
Meythaler, J. M., & Taub, E. (2005). Constraint-induced Historically, one of the earliest observations of
movement therapy for recovery of upper-limb function cognitive reserve was described in a study that
following traumatic brain injury. Journal of Rehabilita- found characteristic senile plaques and neurofi-
tion Research and Development, 42, 769–778. brillary tangles commonly associated with
Sohlberg, M. M., & Mateer, C. A. (1987). Effectiveness of
an attention training program. Journal of Clinical and Alzheimer’s pathology present in healthy, cogni-
Experimental Neuropsychology, 19, 117–130. tively unimpaired elderly (Blessed et al. 1968).
Sohlberg, M. M., & Mateer, C. A. (2001). Cognitive reha- Similar observations between brain pathology and
bilitation: An integrated neuropsychological performance variability frequently have been
approach. New York: Guilford Press.
Spreij, L. A., Visser-Meily, J., van Heugten, C. M., & described in the extant literature.
Nijboer, T. C. (2014). Novel insights into the rehabilita-
tion of memory post acquired brain injury: A systematic
review. Frontiers in Human Neuroscience, 8, 993. Current Knowledge
Stalder-Lüthy, F., Messerli-Bürgy, N., Hofer, H.,
Frischknecht, E., Znoj, H., & Barth, J. (2013). Effect of
psychological interventions on depressive symptoms in While the underlying mechanisms that support
long-term rehabilitation after an acquired brain injury: cognitive reserve remain unclear, current theories
A systematic review and meta-analysis. Archives of Phys- focus on how the brain may develop alternative or
ical Medicine and Rehabilitation, 94(7), 1386–1397.
Wilson, B. A., & Zangwill, O. (Eds.). (2003). Neuropsy- more efficient networks to compensate for pathol-
chological rehabilitation: Theory and practice. Exton: ogy. One theory proposed by Satz (1993) holds
Psychology Press. that brain mass and neuronal count – or brain
Wilson, B. A., Baddeley, A., Evans, J., & Shiel, A. (1994). reserve capacity (BRC) – may raise or lower the
Errorless learning in the rehabilitation of memory
impaired people. Neuropsychological Rehabilitation, brain’s threshold to withstand a lesion or degen-
4(3), 307–326. erative process. In this model, lower BRC would
make an individual more vulnerable to neurolog-
ical insult and increase test sensitivity in detecting
impairment. Similarly, greater BRC would pro-
Cognitive Reserve vide a higher threshold before the effects of neu-
ropathology are observed. For instance, one study
Jesse Chasman (Katzman et al. 1988) compared a high-
Department of Psychology, University of functioning group of nursing home residents
Connecticut, Storrs, CT, USA with Alzheimer’s pathology with a group of
healthy nursing home controls. When compared
across several cognitive domains, the Alzheimer’s
Synonyms group performed at or above the levels of healthy
controls. In this study, the observed cognitive
Brain reserve; Neural compensation; Neural deficits were much lower than predicted, given
reserve the level of brain pathology in these individuals.
This was explained, in part, by the finding that
those in Alzheimer’s group had larger brains with
Definition more neurons than the control group, which may
have helped those individuals compensate for
Cognitive reserve is a concept often used to their neuropathology. Genetics may play a pri-
describe how individual differences mediate the mary role in building greater BRC by increasing
clinical expression of brain damage. In this context, overall brain mass, synaptic density, or
some individuals may cope better than others and neurogenesis, all of which could provide greater
function within relatively normal limits, despite the resiliency against lesions or a degenerative
presence of neuropathology. process.
Cognitive Resilience 867

By contrast, the concept of cognitive reserve Cross-References

suggests that individual differences in genetics or
life experiences provide a buffer to the effects of ▶ Brain Plasticity
brain disease, including dementia. Neural reserve ▶ Brain Reserve Capacity
or neural compensation models (Stern 2003) are
proposed as potentially active processes that facil-
itate the brain’s attempts to adapt to disease pathol- References and Readings C
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this model noting the benefits of enriched environ- Blessed, G., Tomlinson, B. E., & Roth, M. (1968). The
association between quantitative measures of dementia
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and of senile change in the cerebral grey matter of
In humans, years of education and occupational elderly subjects. The British Journal of Psychiatry,
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compared to those with higher education (Stern Aging Neuroscience, 2, 145.
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P., Fuld, P., et al. (1988). Clinical, pathological, and
uals with dementia; however, it has also been dem-
neurochemical changes in dementia: A subgroup with
onstrated in people with vascular injury, preserved mental status and numerous neocortical
Parkinson’s disease, traumatic brain injury, HIV, plaques. Annals of Neurology, 23(2), 138–144.
and multiple sclerosis (Stern 2012). Satz, P. (1993). Brain reserve capacity on symptom onset
after brain injury: A formulation and review of evidence
One of the important implications of the cog-
for threshold theory. Neuropsychology, 7(3), 273–295.
nitive reserve construct is that lifetime experiences Stern, Y. (2003). The concept of cognitive reserve:
can influence individuals’ level of functioning. It A catalyst for research. Journal of Clinical and Exper-
is important to highlight that current research does imental Neuropsychology, 25(5), 589–593.
Stern, Y. (2006). Cognitive reserve: Theory and applica-
not suggest that cognitive reserve prevents neuro-
tion (studies on neuropsychology, neurology, and cog-
pathology from developing. Rather, it is believed nition). New York: Psychology Press.
that a lifetime spent engaging in stimulating activ- Stern, Y. (2012). Cognitive reserve in ageing and
ities, such as education, occupation, exercise, or Alzheimer’s disease. Lancet Neurology, 11, 1006–1012.
social involvement, may provide buffers within
neural networks to help delay the behavioral
symptoms associated with brain pathology. In Cognitive Resilience
contrast to brain reserve, cognitive reserve is an
active process in which preexisting cognitive pro- Kayla LaRosa
cessing approaches or compensatory approaches Educational and Psychological Studies/TBI
are enlisted (Stern 2012). Model Systems, University of South Florida/J.A.
Haley VA, Tampa, FL, USA

Future Directions
Synonyms
An important implication of this concept may be
the development of interventions that aim to Cognitive flexibility; Psychological resilience
enhances cognitive reserve. In aging research,
for instance, growing interest has revolved around
the effectiveness of brain “training” games, exer- Definition
cise, or lifestyle modifications that may strengthen
and/or expand neural networks, and improve cog- Cognitive resilience is the ability to overcome
nitive functioning (Blumen et al. 2010). negative effects or stress on cognitive functioning
868 Cognitive-Communication Disorder

(Staal et al. 2008). Associated factors include Short Description or Definition

a general positive cognitive appraisal of the
environment, the cognitive capacity to effectively The American Speech-Language-Hearing Associ-
deal with stress, as well as the ability and ation (ASHA) has defined cognitive-
self-efficacy to utilize coping strategies (Staal communication disorders (CCDs) as those that,
et al. 2008). Typically as levels of stress “. . .encompass difficulty with any aspect of com-
increase, cognitive performance decreases (Staal munication that is affected by disruption of cogni-
et al. 2008). However, prior experience and tion. Communication may be verbal or nonverbal
training to deal with high levels of stress and and includes listening, speaking, gesturing, read-
uncertainty may improve cognitive resilience ing, and writing in all domains of language
(Staal et al. 2008). (phonologic, morphologic, syntactic, semantic,
and pragmatic). Cognition includes cognitive pro-
cesses and systems (e.g., attention, perception,
See Also memory, organization, executive function). Areas
of function affected by cognitive impairments
▶ Blast Injury include behavioral self-regulation, social interac-
▶ Mild Traumatic Brain Injury tion, activities of daily living, learning and aca-
▶ Severe Brain Injury demic performance, and vocational performance.
▶ Traumatic Brain Injury (TBI) Cognitive-communication disorders may be con-
genital or acquired. Congenital etiologies include
but are not limited to genetic disorders and pre-,
peri-, and postnatal neurologic injuries and dis-
References and Readings
eases. Acquired etiologies include but are not lim-
Staal, M. A., Bolton, A. E., Yaroush, R. A., & Bourne, L. E. ited to stroke, brain tumor, traumatic brain injury,
(2008). Cognitive performance and resilience to stress. anoxic or toxic encephalopathy, and non-
In B. J. Lukey & V. Tepe (Eds.), Biobehavioral resil- degenerative and degenerative neurologic diseases
ience to stress (pp. 259–348). Boca Raton, FL: Taylor (including the dementias).” (ASHA 2005, p. 1).
& Francis Group, LLC.
CCDs were recognized in the early 1980s as
research mounted illustrating the interdependency
of cognition and language, particularly with
regard to the roles of attention and memory in
Cognitive-Communication language processing and with regard to the perva-
Disorder sive impact that cognitive impairments have on
functional communication abilities (Bayles and
Sarah S. Christman Buckingham and Tomoeda 2007; Myers and Blake 2008; Ylvisaker
Kayle E. Sneed et al. 2008). Speech-language pathologists (SLPs)
Department of Communication Sciences and now routinely assess and treat those aspects of
Disorders, The University of Oklahoma Health cognition that either support or are influenced
Sciences Center, Oklahoma City, OK, USA by, speech, language, and communication; other
clinicians such as neuropsychologists, rehabilita-
tion psychologists, and cognitive remediation spe-
cialists may do so as well.
Synonyms

Cognitive-communication impairment; Language Categorization

of confusion; Language of generalized intellectual
impairment; Right hemisphere impairment/ CCDs are differentiated from linguistic impair-
disorder ments (aphasias) and from motor speech disorders
Cognitive-Communication Disorder 869

(dysarthrias, apraxia of speech) by the use of greater initial severity have a poorer prognosis
overly concrete, poorly organized, and socially than CCD of mild or moderate initial severity,
insensitive communication despite preserved although in the case of recovery from TBI, degree
speech and language skills. CCDs may be caused of functionality at hospital discharge may be more
and/or complicated by impairments of attention, predictive than initial severity of injury (Testa
memory, executive functions, and pragmatics. et al. 2005). The presence of co-occurring ill-
Symptoms will vary by etiology, patterns of nesses may compromise the speed and extent of C
brain damage, and individual differences in the recovery from CCD at any severity level; CCDs
neural organization of cognitive functions. arising from traumatic injuries causing diffuse
brain damage, for example, are likely to be
accompanied by paralysis, motor speech disor-
Epidemiology ders, and injuries to vital organs.
Recovery from CCD differs by etiology.
It is estimated that, of the 795,500 individuals in Recovery after stroke is usually most rapid in the
the USA who will suffer stroke annually first 3 months post-onset. Recovery from throm-
(Mozaffarian et al. 2015), approximately 50% boembolic stroke may continue after 6 months
will experience a cognitive-communication disor- post-onset, whereas recovery from hemorrhagic
der (Hinckley 2014). CCD will also be evident in stroke may plateau at the 6 month point. Func-
two-thirds of the 1.7 million people who sustain tional improvement in cognitive-communication
traumatic brain injuries each year (O’Dell 2013; abilities after severe traumatic brain injury is gen-
Roozenbeek et al. 2013). Among children aged erally slower at the outset when compared with
0–14 years, nearly half a million will visit emer- stroke and typically proceeds in a stairstep fashion
gency rooms with traumatic brain injuries annu- over months or years. Recovery from mild stroke
ally (Faul et al. 2010), although this estimate is or brain injury often seems rapid in comparison.
probably low (Turkstra et al. 2015). The number Many individuals with mild brain injuries appear
of individuals expected to be living with dementia to recover quickly (Ylvisaker et al. 2008) but as
of the Alzheimer’s type (DAT), and thus living many as 15–20% suffer from persistent fatigue
with CCDs, is expected to increase from 4 million and reduced information processing speed for
(in the year 2000) to 31.2 million people by the years after injury. Frequently unrecognized and
year 2050. untreated, these deficits cause lifelong cognitive
challenges that threaten social adjustment and
successful community reentry.
Natural History, Prognostic Factors, In contrast to stroke and TBI, recovery from
Outcomes dementing illness is not expected. Evidence sug-
gests, however, that higher levels of education,
The natural history and prognosis for improve- environmental stimulation, intelligence, and liter-
ment of cognitive-communication dysfunction acy may afford a neuroprotective “cognitive
are tied to many factors, including etiology, initial reserve” (Stern 2002) that helps to reduce the
severity of disorder, the presence or absence of incidence of dementia and/or slow its onset in
comorbid illnesses, and the nature of specific indi- older individuals (Valenzuela and Sachdev
vidual variables such as age, gender, and psycho- 2006). Studies by Bialystok et al. (2007) and
logical state. In the absence of confounding (2010), for example, have shown that the onset
circumstances, improvement of CCD is antici- of DAT may be delayed by as many as 4 years on
pated when caused by stroke, excisable tumor, average in bilingual speakers.
remitting disease, or traumatic brain injury. Early stages of cognitive decline in DAT are
When caused by progressive debilitating condi- accompanied by forgetfulness, word-finding dif-
tions such as non-excisable tumors or dementing ficulties, and changes in social pragmatics in most
diseases, CCD will worsen over time. CCD of individuals. In bilingual speakers, early signs may
870 Cognitive-Communication Disorder

also include regression to the sole use of a first- may reduce the efficiency of auditory language
learned language (McMurtray et al. 2009) and processing if stimuli are complex or if they must
difficulty with appropriate code switching be processed quickly. Damage may also impair
(Kempler and Goral 2008). Mid-stages of cogni- the interpretation of affective prosody when pro-
tive decline are characterized by increased mem- duced by others. Lesions to prefrontal, parietal,
ory loss, anomia, and social withdrawal, whereas and temporal cortex have been associated with
late stages are associated with loss of most useable anosognosia, the failure to recognize the existence
cognitive and physical functions (Bayles and or presence of illness, and a problem that can
Tomoeda 2007). reduce compliance with treatment activities
(Myers 2001; Myers and Blake,2008; Tomkins
1995).
Neuropsychology and Psychology of When damage to the cerebral cortex is bilat-
Cognitive-Communication Disorder eral, deficits across multiple systems may interact
to impair communication to different degrees.
Damage to the prefrontal and frontal association Bilateral cortical damage can cause impairments
regions of the right (or non-language-dominant) in the self-regulation of communicative behaviors
hemisphere of the cerebrum may cause difficulty that range from failure to organize discourse effi-
with pragmatics, context-sensitive semantics, and ciently to failure to inhibit inappropriate utter-
expressive affective prosody, obscuring indica- ances and actions. Executive dysfunction in
tions of mood and compromising the ability to bilingual speakers, for example, may cause differ-
communicate successfully in social situations. ential impairments in language use and/or diffi-
Egocentrism may impair recognition of these culty with appropriate language switching
problems and reduce insight into the communica- (Kempler and Goral 2008). It can also diminish
tion needs of others. Deficits in vigilance, the ability to focus attention and memory so as to
sustained and selective attention, and/or in atten- make them useful during conversational
tion switching can cause salient information to be exchanges (Ylvisaker et al. 2008). If bilateral
missed and reduce the sequential or simultaneous damage involves subcortical hippocampal struc-
processing of information from multiple sources. tures, however, then fundamental disruptions of
Difficulties drawing inferences, extracting themes declarative (semantic, episodic, and lexical) and
and topics in discourse, interpreting nonliteral explicit memory may occur. Hippocampal dam-
language, and/or reading affective and prosodic age/deterioration is common with brain injury/
cues for meaning during conversational exchanges dementing disease, and it can lead to a host of
may be present (Ylvisaker et al. 2008). A tangen- impairments ranging from difficulty learning new
tial communication style often emerges, where information to the presence of a severe, unremit-
excessive, vaguely relevant details are inserted ting amnesia.
inappropriately into narratives and discourse Bilateral damage to lower brain stem reticular
(Myers and Blake 2008). activating circuits can severely compromise
Damage to the right parietal association cortex arousal, alertness, and awareness. This can lead
and to right parietal-temporal-occipital (PTO) cor- to brief losses of consciousness or to intractable
tex can lead to contralateral inattention, impeding coma. When caused by dementing disease, coma
reading, writing, and listening for stimuli in the is most likely followed by death. However, recov-
left hemispace. Lesions in PTO cortex can also ery from traumatic coma frequently leads to return
cause visual-spatial perception and recognition of function through increasing levels of
deficits (including topographical and geographi- responsivity, communication, orientation, self-
cal agnosias) which can impair navigation in regulation, and cognitive integration. A common
familiar environments if verbal mediation strate- sequela of traumatic brain injury is a period of
gies are not used to compensate. Damage to sec- post-traumatic amnesia (PTA) – i.e., inability to
ondary (superior temporal) association cortex form new memories of events happening after
Cognitive-Communication Disorder 871

brain injury with disorientation to time, place, or 2. Inferencing abilities are tested by asking
person. In individuals who are verbal, confabula- patients to interpret humor, to recognize indi-
tion may be present until disorientation and con- rect requests for actions, and to follow the
fusion diminish. As cognitive functioning themes of conversations.
improves, individuals with brain injuries will ben- 3. Orientation is assessed by asking patients to
efit from environmental structure and external respond to questions about time, place, and
direction to support increasingly purposive, flex- person. C
ible, and goal-oriented behavior. 4. Memory for facts, events, and procedures is
evaluated with yes/no questions, narratives,
and performance of familiar routines.
Evaluation 5. The ability to discriminate relevant from irrel-
evant detail and integrate disparate parts into a
Evaluation of a suspected CCD requires examina- coherent whole can be evaluated with scene
tion of cognition as it affects and interacts with description tasks.
skills of speech planning and execution, language 6. Cognitive flexibility and functional problem-
comprehension and production, and pragmatic/ solving abilities can be assessed with tasks that
discourse aspects of communication in everyday require the generation of multiple strategies for
social contexts (Turkstra et al. 2005). Tests of achieving a goal and that require repairs of
cognitive-communication skills are used to eval- failed communicative interchanges with others
uate the effects that deficits in attention, orienta- (Myers 1999).
tion, perception, memory, organization, and
executive functions can have on communication. Standardized tests used to assess cognitive-
It is important that any assessment be culturally communication functions subsequent to right
and linguistically appropriate if results are to be hemisphere impairment include the Mini-Inventory
valid (Goldstein 2000). In bilingual speakers, for of Right Brain Injury, Second Edition (Pimental
example, examinations should ideally be admin- and Kingsbury 2000), the RIC Evaluation of
istered in each language so that results can be Communication Problems in Right Hemisphere
compared (ASHA 2015). It is best to use assess- Dysfunction-Third Edition (Halper et al. 2010),
ment tools developed for each language – or else and The Burns Brief Inventory of Communication
adapt a single tool carefully for non-standardized and Cognition (Burns 1997). While these instru-
use – since many aspects of orientation (such as ments will elicit symptoms of CCD associated with
seasons), humor, and abstract language (especially right hemisphere damage, findings must be
idioms) may not be translate meaningfully across interpreted with a view toward evaluating impair-
cultures; furthermore, some types of memories ments of underlying neuropsychological processes
may be more easily assessed in one language but for it is here that treatment will be most profitably
not another (see Ardila et al. 2013; 1994 for neu- directed (Myers 1999).
ropsychological assessments in Spanish). Standardized tests used to assess CCD after TBI
Examples of tasks frequently included in for- include the American Speech-Language-Hearing
mal and informal assessments are provided for Association Functional Assessment of Communi-
illustration: cation Skills in Adults (Frattali et al. 1995), the
Behavioral Rating Inventory of Executive Function
1. Attention to the left hemispace is frequently (Roth et al. 2005) and its variations, the Brief Test
tested with line bisection, cancellation, and of Head Injury (Helm-Estabrooks and Hotz 1991),
drawing tasks as well as with more complex the Ross Information Processing Assessment-2
reading, writing, and listening tasks that (Ross-Swain 1996) and its variations, and the
require individuals to process communication Scales of Cognitive Ability for Traumatic Brain
stimuli from both right and left sides of body Injury (Adamonovich and Henderson 1992). The
midline. Glasgow Coma Scale (Jennett and Teasdale 1981)
872 Cognitive-Communication Disorder

and the Rancho Los Amigos Levels of Cognitive include the Mini-Mental State Examination
Function Scale (Hagen et al. 1979) or its revisions, (Folstein et al. 1975) and the Global Deteriora-
including a version adapted for children under tion Scale (Reisberg et al. 1982). Comprehensive
14 years of age (Blosser and DePompei 2003), assessment batteries include the Arizona Battery
are frequently used to assess consciousness and for Communication Disorders of Dementia
track recovery of cognitive functions after coma. (Bayles and Tomoeda 1993) and The Functional
The Pediatric Test of Brain Injury (Hotz et al. Linguistic Communication Inventory (Bayles and
2010) is a criterion-referenced, standardized tool Tomoeda 1994), the latter most useful for individ-
for assessment of the cognitive-linguistic skills that uals with severe dementia (Hopper and Bayles
children (ages 6–16) need for successful function 2008). Assessment findings can help families
in school. work with SLPs to understand and compensate
Informal, situational assessments of cognition for the symptoms of cognitive decline.
and communication may yield valuable informa-
tion that cannot be obtained from formal standard-
ized tests (Blosser and DePompei 2003; Turkstra Treatment
et al. 2005). This naturalistic approach to assess-
ment has been termed a “functional, collaborative, Treatment for CCD has traditionally been
context-sensitive, hypothesis-testing assess- decontextualized (implemented in rehabilitation
ment,” and it should be conducted with the pur- settings or at bedside) and deficit-oriented
pose of identifying situational variables that can (designed to improve/support impaired cognitive-
be manipulated to improve the successful partici- communication processes). Conventional pencil/
pation of injured individuals as they operate paper or computer tasks are used to stimulate
within their everyday environments (Ylvisaker underlying cognitive processes (e.g., attention,
et al. 2008). Best-practice assessment procedures memory) with the expectation that as they
for individuals who have suffered brain injuries improve, so will related functional skills (e.g.,
should, therefore, include (1) completion of for- readiness to listen to speakers taking turns,
mal testing in specific skill domains and (2) com- remembering a set of instructions given by one’s
pletion of observational checklists (or quality of boss). Myers (1999) advocates the use of
life inventories) where children (or adults) may be decontextualized treatments to facilitate cogni-
evaluated in natural environments (Blosser and tive-communication skills in individuals who
DePompei 2003; Turkstra et al. 2005). This type have acquired CCD from right hemisphere stroke.
of assessment might include administration of the She argues that although that the value of any
Functional Assessment of Verbal Reasoning and treatment approach “rests on its functional merits”
Executive Strategies test (MacDonald 2005), a (p. 209), improving fundamental cognitive pro-
tool that was developed for evaluation of cesses will have the greatest automatic generali-
cognitive-communication skills specifically zation to the many untrained tasks where those
related to reading, writing, and reasoning processes are needed. This is particularly true for
(Turkstra et al. 2005), and the Quality of Commu- bilingual speakers who may benefit from inter-
nication Life Scale (Paul et al. 2005). ventions that are focused in different languages
Assessment of CCD in dementia employs stan- for improvement on performance of different
dardized screening tests, severity staging instru- functional tasks (Bialystok and Barac 2013).
ments, and comprehensive assessment batteries Generalization may be more difficult to achieve
(Hopper and Bayles 2008). Screening tests when CCD is associated with diffuse brain injury
include the Story Retelling Subtest of the Arizona vs. focal stroke. Rehabilitation approaches that are
Battery for Communication Disorders of Demen- more contextualized (implemented in natural set-
tia (Bayles and Tomoeda 1993) and the FAS Ver- tings) and more function-oriented (designed to sup-
bal Fluency Test (Borkowski et al. 1967). Tests for port activities of daily living) than traditional
estimating the severity of cognitive decline methods are ideal for promoting rapid skill mastery
Cognitive-Communication Disorder 873

and transfer. Ylvisaker et al. (2008) suggest that Further Reading

treatment strategies designed to compensate for
impaired executive functions and self-regulation Adamonovich, B., & Henderson, J. (1992). Scales of cog-
nitive ability for traumatic brain injury. Chicago:
abilities will most often lead to successful rehabil-
Riverside.
itation after brain injury. They advocate practicing American Speech-Language-Hearing Association. (2005).
essential cognitive-communication tasks (such as Roles of speech-language pathologists in the identifi-
conversing with family members or taking notes cation, diagnosis, and treatment of individuals with C
cognitive-communication disorders: Position state-
during lectures) within supportive real-world envi-
ment [Position Statement]. www.asha.org/policy
ronments where stimuli likely to trigger errors have American Speech-Language-Hearing Association. (2015).
been removed and where the use of external aids is Bilingual service delivery: Key issues. Retrieved from
encouraged. http://www.asha.org/PRPSpecificTopic.aspx?folderid=
8589935225&section=Key_Issues
Intervention for CCD in DAT emphasizes man-
Ardila, A., Rosselli, M., & Puente, A. E. (2013). Neuro-
agement rather than rehabilitation. Goals are psychological evaluation of the Spanish speaker.
designed to help individuals maintain functional New York: Springer. (Reprint of the Plenum Press
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Bayles, K. A., & Tomoeda, C. (1993). The Arizona Battery
lized errorless learning activities that drill attention
for communication disorders of dementia. Austin:
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Intervention tasks that employ external memory linguistic communication Inventory. Austin: Pro-Ed.
Bayles, K. A., & Tomoeda, C. (2007). Cognitive-
aids, which recruit long-term (remote) memory
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on procedural memory for familiar routines (such Bialystok, E., & Barac, R. (2013). Cognitive effects. In
as describing how to get home), can help promote F. Grosjean & P. Li (Eds.), The psycholinguistics of
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Bialystok, E., Craik, F. I. M., & Freedman, M. (2007).
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▶ Attention Bourgeois, M. S. (1991). Communication treatment for
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▶ Mild Traumatic Brain Injury Delaying the onset of Alzheimer’s disease: Bilingual-
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Faul, M., Xu, L., Wald, M. M., & Coronado, V. G. (2010).
▶ Pragmatic Communication Traumatic brain injury in the United States: Emergency
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Color Agnosia 875

injury. In R. Chapey (Ed.), Language intervention The cause of most of these diseases is
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Lippincott Williams & Wilkins. autoimmunity, environmental antigens, infec-
tions, allergies, and antigen-antibody complexes
in various combinations are probably involved.

C
Collagen Vascular Disease
Cross-References
Elliot J. Roth
▶ Cerebral Angiitis
Department of Physical Medicine and
▶ Lupus Cerebritis
Rehabilitation, Northwestern University,
▶ Vasculitis
Feinberg School of Medicine, Chicago, IL, USA

References and Readings

Synonyms
Klippel, J. H., Stone, J. H., Crofford, L. J., & White, P. H.
Connective tissue disease (Eds.). (2008). Primer on the rheumatic diseases
(13th ed.). New York: Springer.

Definition

Collagen vascular diseases are a group of condi-

tions that are characterized by malfunction of the Color Agnosia
tendons, bones, and connective tissue, that are
supported by collagen. Their pathogenesis is auto- John E. Mendoza
immune in nature. Department of Psychiatry and Neuroscience,
Tulane Medical School and SE Louisiana
Veterans Healthcare System, New Orleans, LA,
Current Knowledge USA

The most common collagen vascular disorders

include rheumatoid arthritis, systemic lupus Definition
erythematosus, scleroderma, and dermatomyosi-
tis. Others include polymyositis, polyarteritis Literally, a loss of previous color knowledge.
nodosa, ankylosing spondylitis, and a number of
vasculopathies. These diseases are frequently
associated with diffuse inflammatory changes, Current Knowledge
abnormal immunity. Vascular abnormalities that
result from these conditions serve as frequent In pure color agnosia, patients have difficulty
causes of various types of vasculitis. Common naming or pointing to named colors, despite rela-
features include arthritis, skin changes, eye tively preserved color perception (i.e., retaining
changes, pericarditis, pleuritis, myocarditis, the ability to match colors or to identify the num-
nephritis, and vasculitis of the brain, peripheral bers on the Ishihara plates). They also have diffi-
nerves, or extremities. They also may have a vari- culty matching colors, either verbally or visually,
ety of hematological changes causing clotting or to familiar colored objects (e.g., identifying the
bleeding and a number of abnormal circulating color normally associated with cherries, lettuce, or
blood proteins. bananas).
876 Color Anomia

Relatively rare, pure color agnosia must be

distinguished from other disturbances of color Color Anomia
perception and color naming (color anomia). In
color blindness, the individual is unable to per- John E. Mendoza
ceive or distinguish either certain colors or pos- Department of Psychiatry and Neuroscience,
sibly all color. In the latter case, the world is seen Tulane Medical School and SE Louisiana
in shades of black and white. While color blind- Veterans Healthcare System, New Orleans, LA,
ness is usually congenital, it can also be acquired, USA
a condition known as central achromatopsia.
The latter is a perceptual deficit thought to result
from lesions in the visual cortices (e.g., lingual Definition
gyrus and the occipitotemporal (fusiform)
gyrus). In this disorder, the patient may have Anomia is the inability to name colors in the
difficulty verbally naming a visually presented absence of a more global anomia associated with
color, pointing to a color named by the examiner, an aphasic disorder.
or simply matching or sorting colored objects to
others of a similar hue, yet still be able to indicate
(name) the colors normally associated with com- Current Knowledge
mon objects (e.g., the colors of the outside,
inside, and seeds of a watermelon). In a milder To be classified as a color anomia, the disorder
form of this condition (dyschromatopsia), should occur in the absence of problems with
colors are described as “dull,” “washed out,” or color perception or recognition (i.e., the patient
“faded.” In color anomia, the problem is not one should be able to match or sort colors). Two sub-
of perceptions, but of language. The patient can types of the disorder have been identified. In one,
perceive and match colors, but has difficulty the problem is limited to an inability to name
naming specific colors or pointing to colors colors that are visually presented or to point to
named by the examiner. colors named by the examiner. This type of color
In the few published cases, lesions associated anomia is usually associated with the syndrome of
with color agnosia tend to occur in the left or alexia without agraphia and results from lesions
bilateral occipitotemporal area. involving the primary visual cortex of the domi-
nant hemisphere (resulting in a right homony-
mous hemianopsia) and the splenium of the
corpus callosum. Visual information is thus
Cross-References restricted to the left visual field (right hemisphere)
and the color information cannot cross the
▶ Achromatopsia
involved splenium of the corpus callosum to
▶ Color Anomia
reach the left (verbal) hemisphere. In the second
subtype, specific color anomia, the patient has
difficulty with purely verbal color naming tasks,
References and Readings in addition to difficulty in naming visually pre-
Bauer, R. M., & Demery, J. A. (2003). Agnosia. In
sented colors. Thus, there would be a naming
K. Heilman & E. Valenstein (Eds.), Clinical neuropsy- deficiency if the patient were asked to name the
chology (4th ed., pp. 236–295). New York: Oxford colors associated with the inside and outside of a
University Press. watermelon. As in the first case, color matching or
Tranel, D. (2003). Disorders of color processing. In T. E.
Feinberg & M. J. Farah (Eds.), Behavioral neurology
sorting should be intact. In specific color anomia,
and neuropsychology (pp. 243–256). New York: other aphasic (naming) deficits may be present,
McGraw-Hill. but color names are most affected.
Colored Progressive Matrices 877

Cross-References although the latter may be identified by its shape.

While the exact anatomical site responsible for
▶ Color Agnosia disturbances of color imagery has not been firmly
established, the left temporal-occipital cortex is
believed to be involved in most cases.
References and Readings
C
Bauer, R. M., & Demery, J. A. (2003). Agnosia. In Cross-References
K. Heilman & E. Valenstein (Eds.), Clinical neuropsy-
chology (4th ed., pp. 236–295). New York: Oxford
University Press. ▶ Apperceptive Visual Agnosia
Tranel, D. (2003). Disorders of color processing. In T. E. ▶ Associative Visual Agnosia
Feinberg & M. J. Farah (Eds.), Behavioral neurology & ▶ Color Agnosia
neuropsychology (pp. 243–256). New York: McGraw-
▶ Color Anomia
Hill.

References and Readings

Color Imagery
Farah, M. J. (2003). Disorders of visual-spatial perception
and cognition. In K. M. Heilman & E. Valenstein
John E. Mendoza (Eds.), Clinical neuropsychology (4th ed.,
Department of Psychiatry and Neuroscience, pp. 146–160). New York: Oxford University Press.
Tulane Medical School and SE Louisiana Tranel, D. (2003). Disorders of color processing. In T. E.
Veterans Healthcare System, New Orleans, LA, Feinberg & M. J. Farah (Eds.), Behavioral neurology
and neuropsychology (2nd ed., pp. 243–256).
USA
New York: McGraw-Hill.

Definition
Colored Progressive Matrices
The ability to visualize a color in its absence.
When asked, most individuals would be able to Victoria M. Leavitt1 and Erica Weber2
1
identify the outer color of a watermelon as well as Cognitive Neuroscience Division, Columbia
that of the inside of the rind, the fleshy part of the University Medical School, New York, NY, USA
2
melon, and its seeds. Color imagery is more than Department of Physical Medicine and
an ability to simply recall a particular visual Rehabilitation, Kessler Foundation, East
image; it also involves the capacity to mentally Hanover, NJ, USA
conjure up and manipulate colors at will. For
example, one may imagine a blue horse or a
person wearing an article of clothing of a specific Description
color, never having seen either before. While dis-
turbances of color perception and color imagery • The colored progressive matrices (CPM) are an
are frequently linked, in some cases the two can be alternate form of the Raven’s progressive
distinguished clinically. Thus, while a given matrices (RPM) that was published in the
patient may be able to name or match colors 1940s. Shorter and simpler than the original,
presented visually, that same patient may not be this version was designed for younger children
able to name the color of an apple in its absence. (ages 5–11 years), the elderly (over 65 years),
Similarly, while accurately identifying the color and people with moderate or severe learning
red from an array, the patient may not be able to difficulties. As such, it also tends to be used
match it to a black-and-white picture of the fruit, more frequently in research protocols,
878 Colored Progressive Matrices

although it is important to note that the CPM individuals who cannot understand English; peo-
and the RPM are not interchangeable nor may ple with physical disabilities, aphasias, cerebral
derived scores from the two tests be interpreted palsy, or deafness; and people with below normal
the same. CPM contains 36 items, grouped into intelligence. The colored backgrounds were
three sets (A, Ab, B) of 12 items each: A and introduced to attract the patient’s attention; the
B from the original version, with the addition test can be administered in the form of illustra-
of set Ab. Most items are presented on a col- tions in a booklet or as boards with moveable
ored background to make the test visually stim- pieces. Patients with left hemisphere damage
ulating for participants; the bright background perform better on the colored matrices than on
does not seem to detract from the clarity of the the standard form (as described in Lezak et al.
stimuli. As the last few items in set B are 2004). This is likely attributable to the fact that
exactly the same as they appear in the standard while only one-fifth of RPM items test visuospa-
version, an examinee who succeeds on these tial skills almost exclusively, fully one-third of
may go on to sets C, D, and E of the standard items on the CPM are predominantly visuospa-
progressive matrices (SPM) so that intellectual tial, with other items involving more problem-
capacity can be more accurately assessed (the solving. Also likely due to the visuospatial task
score for set Ab would be omitted to determine demands, individuals with Lewy body dementia
a percentile based on SPM scoring). tend to have more difficulty on the CPM than
Alzheimer’s patients with similar levels of
dementia. In Alzheimer’s disease, recent imag-
Historical Background
ing evidence has attributed CPM task impair-
ment to poor resting cerebral blood flow in
For information about the historical background
regions responsible for both visual perception
of the original test, please refer to “▶ Raven’s
and reasoning ability (i.e., bilateral inferior pari-
Progressive Matrices.”
etal lobes, right inferior temporal gyrus, and right
middle frontal gyrus; Yoshida et al. 2017).

Psychometric Data

Norms for ages 5.5–11.5 for North America are Cross-References

presented by Raven et al. (1998, 2000). By age
9 years, a nearly perfect score is obtained (35/36) ▶ Advanced Progressive Matrices
by the upper 5% of the sample. Education ▶ Raven’s Progressive Matrices
corrected norms are available for an abbreviated ▶ Standard Progressive Matrices
version (sets A and B, excluding Ab which is
correlated >0.90 with the sum of A and B) for
ages 55–85. In children, split-half reliability has References and Readings
been shown to be high (>0.80) (Raven et al.
Lezak, M. D., Howieson, D. B., & Loring, D. W. (2004).
1998), as is test-retest reliability following days
Neuropsychological assessment (4th ed.). New York:
or weeks (>0.80). Over longer intervals (6 months Oxford University Press.
to 1 year) these values decline (0.59–0.79). Raven, J. C. (1938, 1996). Progressive matrices:
A perceptual test of intelligence. Oxford: Oxford Psy-
chologists Press.
Raven, J., Raven, J. C., & Court, J. H. (1998). Raven
Clinical Uses manual: Section 2. Colored progressive matrices.
Oxford: Oxford Psychologists Press.
Raven, J., Raven, J. C., & Court, J. H. (2000). Raven
The CPM was designed for use with children,
manual research supplement 3: American norms, neu-
older people, for anthropological studies, and for ropsychological applications. Oxford: Oxford Psy-
clinical work. Its format makes it valuable for chologists Press.
Coma 879

Raven, J., Raven, J. C., & Court, J. H. (2003). Manual for absence of sleep-wake cycles on EEG (Giacino
Raven’s progressive matrices and vocabulary scales. et al. 2014). Several diagnostic scales are avail-
Section 1: General overview. San Antonio: Harcourt
Assessment. able for severity rating and include the Glasgow
Strauss, E., Sherman, E. M. S., & Spreen, O. (Eds.). (2006). Coma Scale (Teasdale and Jennett 1976) and the
A compendium of neuropsychological tests (3rd ed.). FOUR Score (Wijdicks et al. 2005).
New York: Oxford University Press.
Yoshida, T., Mori, T., Shimzu, H., Yoshino, Y., Sonobe, N.,
Matsumoto, T., et al. (2017). Neural basis of visual Prognosis
C
perception and reasoning ability in Alzheimer’s dis- Mortality rates for patients in coma vary with eti-
ease: Correlation between Raven’s colored progressive
ology, but commonly reach or exceed 50%. Early
matrices test and 123 I-IMP SPECT imaging results.
International Journal of Geriatric Psychiatry, 32, prognostic variables of poorer outcome include
407–413. coma duration, lower Glasgow Coma Scale scores
(Teasdale and Jennett 1976), increased age, absent
pupillary responses, systolic blood pressure
<90 mmHg, and computed tomography abnormal-
ities, including compression, effacement, or blood
Coma within the basal cisterns, or extensive traumatic
subarachnoid hemorrhage (Posner et al. 2007).
Travis Williams1 and Jacob Kean2 The comatose patients who survive typically
1
Department of Physical Medicine and transition to vegetative state or minimally con-
Rehabilitation, Indiana University, Indianapolis, scious state within 2–4 weeks (Giacino et al. 2014).
IN, USA
2
Department of Physical Medicine and
Rehabilitation, Indiana University School of
Medicine, Indianapolis, IN, USA Cross-References

▶ Decerebrate Posturing
Definition ▶ Decorticate Posturing
▶ Glasgow Coma Scale
Coma is a state of unconsciousness in which the ▶ Loss of Consciousness
patient is incapable of being awake, and is ▶ Minimally Conscious State
unarousable, even with vigorous stimulation. ▶ Stupor
Coma is a self-limiting state which is usually the ▶ Vegetative State (Persistent)
result of disease or injury and rarely lasts for more
than 4 weeks. While comatose, a patient may be
reflexive to painful stimuli but lack the ability to
demonstrate localized response or defensive References and Readings
movements (Posner et al. 2007).
Giacino, J. T., Fins, J. J., Laureys, S., & Schiff, N. D.
(2014). Disorders of consciousness after acquired
brain injury: The state of the science. Nature Reviews
Current Knowledge Neurology, 10(2), 99–114.
Posner, J. B., Saper, C. B., Schiff, N. D., & Plum, F. (2007).
Plum and Posner’s diagnosis of stupor and coma.
Diagnosis New York: Oxford University Press.
The diagnosis of patients in coma is clinical and Teasdale, G., & Jennett, B. (1976). Assessment and prog-
involves examination of physiological functions, nosis of coma after head injury. Acta Neurochirurgica,
including arousal, pupillary responses, respira- 34, 45–55.
Wijdicks, E. F. M., Bamlet, W. R., Maramattom, B. V.,
tion, motor function, and reflexes. Several clinical Manno, E. M., & McClelland, R. L. (2005). Validation
features of coma include the loss of spontaneous of a new coma scale: The FOUR score. Annals of
or induced arousal, no eye opening, and the Neurology, 58, 585–593.
880 Coma Recovery Scale

described as high for CRS-R total scores, although

Coma Recovery Scale some systematic scoring differences between raters
were found on the visual and oromotor/verbal sub-
Mark A. Sandberg scales. The CRS-R has been translated into Spanish,
Neuropsychology, Northport VA Medical Center, Italian, German, French, Dutch, and Norwegian.
Smithtown, NY, USA The CRS-R offers a reliable method for measuring
the trajectory of consciousness following severe
brain injury and in assisting in the differential diag-
Synonyms nosis of patients in a minimally conscious state from
those in a vegetative state. The CRS-R is regularly
CRS; CRS-R; JFK coma recovery scale used in clinical and research applications to mea-
sure changes in patient awareness over time (e.g.,
Estraneo et al. 2015).
Definition

The Coma Recovery Scale (CRS-R) is a 23-item Cross-References

instrument used to assist with differential diagno-
sis, prognostic assessment, and treatment planning ▶ Coma/Near Coma Scale
with patients having disorders of consciousness.

References and Readings

Current Knowledge
Estraneo, A., Moretta, P., Cardinale, V., DeTanti, A., Gatta,
G., Giacino, J. T., & Trojano, L. (2015). A multicentre
The Coma Recovery Scale was initially developed
study of intentional behavioural responses measured
by Giacino and colleagues in 1991 and then revised using the coma recovery scale-revised in patients with
in 2004 and re-named the JFK Coma Recovery minimally conscious state. Clinical Rehabilitation,
Scale-Revised (Giacino et al. 2004). The scale 29(8), 803–808.
Giacino, J. T., Kalmar, K., & Whyte, J. (2004). The JFK
was developed with the goal of helping to identify coma recovery scale-revised: Measurement character-
neurobehavioral characteristics of persons diag- istics and diagnostic utility. Archives of Physical Med-
nosed with disorders of consciousness, allowing icine and Rehabilitation, 85(12), 2020–2029.
for refined decision-making concerning treatment Kalmar, K., & Giacino, J. (2005). The JFK coma recovery
scale-revised. Neuropsychological Rehabilitation, 15
and prognosis. In its revised form, the CRS-R is
(3–4), 454–460.
composed of 23 items, which are assigned into six The CRS-R, including administration and scoring informa-
subscales addressing auditory, visual, motor, tion and rating forms, is available as a PDF file at www.
oromotor, communication, and arousal functions. tbims.org/combi/crs/index.html
Each subscale is composed of hierarchically
arranged items associated with the brain stem, sub-
cortical, and cortical processes. Items receiving
higher scores are more likely to reflect cognitively Coma/Near Coma Scale
mediated activity. The test syllabus offers behav-
ioral criteria, which provide the user with Mark A. Sandberg
operationalized characteristics used to determine Neuropsychology, Northport VA Medical Center,
whether a specific response to sensory stimuli has Smithtown, NY, USA
been demonstrated by the patient. A rating form is
included as part of the syllabus, which allows the
trained user to perform serial assessments. Synonyms
Based on the 2004 study by Giacino, Kalmar,
and Whyte, interrater and test-retest reliability were C/NC; CNC
Coma/Near Coma Scale 881

Definition Current Knowledge

The Coma/Near Coma (CNC) Scale was designed As described by Rappaport et al. (1992), interrater
to measure changes in neurobehavioral status reliability calculated at three time periods was
among patients who have sustained severe brain 0.97. The lowest interrater intercorrelation of
injuries and whose clinical functioning is consis- 0.86 was found to exist on item 8 (nasal swab).
tent with vegetative or near-vegetative states. The The internal consistency as determined using C
CNC Scale is useful when reliable, valid, and alpha coefficients was 0.43, 0.65, and 0.65 for
efficient assessment of patient’s functioning is CNC scores taken at 1-, 8-, and 16-week post-
required to substantiate clinical change or lack injury (Rappaport et al. 1992).
thereof in patients whose functioning is at mark- Although a rank order correlation between
edly low levels. The CNC Scale expands the CNC and DRS scores was found to be 0.69 in
levels of the Disability Rating Scale (DRS). It older research (p < 0.02) (Rappaport et al. 1992),
has five levels and is comprised of 11 items that a more recent study found lower correlations
assess dysfunction in the sensory and perceptual (Balconi and Arangio 2015). The correlation
dimensions and describes presence of primitive between CNC ratings and the prominence of sen-
reflexes. sory (auditory, visual, and somatosensory) abnor-
mality as determined through evoked potential
studies was 0.52 (p < 0.05) (Rappaport et al.
Historical Background 1992), and between CNC and N400 peak latency
during presentation of incongruous semantic
Recognizing a need for rehabilitation profes- associations was 0.40 (p < 0.01) (Balconi and
sionals to systematically identify and chart Arangio 2015).
changes in functioning in patients whose clinical It is recommended that proper use of the instru-
status is best characterized as approximately “veg- ment follow a period where testing is performed
etative,” the CNC was developed as a supplement simultaneously with several raters independently
to the Dementia Rating Scale (DRS). The use of offering judgments for each item. Interrater com-
the CNC Scale is recommended whenever the parisons and discussion concerning the reasons
DRS score is greater than 21 (Extremely Severe for making specific judgments is encouraged to
Disability). The scoring form also notes that in refine observational accuracy. Following this
cases where DRS scores are <21, CRC Scale training, it is noted that while single ratings can
ratings should be conducted monthly together be used, “a minimum of two independent ratings
with DRS scores. per patient is encouraged” for purposes of

Coma/Near Coma Scale, Table 1 CNS Scale Parameters

Item # Dimension assessed Stimulus used Response elicited
1 Auditory Ringing bell Eye opening/orientation
2 Command Verbal request Response to command
Responsivity
3 Visual Flashing light Fixation or avoidance
4 Visual Say “look at me” Fixation and tracking
5 Threat Quick movement of hand to eyes Eye blinking
6 Olfactory Ammonia capsule Withdrawal or grimacing
7 Tactile Shoulder tap Head/eye orientation or shoulder movement
8 Tactile Swab to each nostril Withdrawal/eye blink or mouth twitch
9 Pain Firm pinch to finger tip Withdrawal or agitation
10 Pain Firm ear pinch Withdrawal or agitation
11 Vocalization None; listen for any verbalization Words or sounds
882 Commission on Accreditation of Rehabilitation Facilities (CARF)

promoting reliability (Rappaport 2000). It is also

recommended that ratings be taken at approxi- Commission on Accreditation
mately the same time each day whenever possible. of Rehabilitation Facilities
CNC Scale includes 11 items representing eight (CARF)
response dimensions (see Table 1). Each item
includes three score options (0, 2, 4), 4 referring Sarah K. Lageman
to “no responsivity to sensory stimulation.” CNC Parkinson’s and Movement Disorders Center,
total score is computed by adding the ratings (0, 2, Department of Neurology, School Of Medicine,
4) from each of the 11 items and dividing that score Virginia Commonwealth University, Richmond,
by the number of items rated. Categorical descrip- VA, USA
tions are offered to coincide with the total score
attained (i.e., No Coma through Extreme Coma).
Membership

Future Directions Commission on Accreditation of Rehabilitation

Facilities (CARF) is an independent, nonprofit
Measuring level of awareness in an unconscious organization that is an accreditor of health and
person will continue to be a challenge, necessit- human services. It was formed in 1966 when the
ating technologically novel and sophisticated Association of Rehabilitation Centers (ARC) and
methods to be employed as well as behavioral the National Association of Sheltered Workshops
markers such as those gathered by the CNS and Homebound Programs (NASWHP) joined
scale. Studies that examine simultaneous use of forces to further develop their interests in setting
both methods may be particularly helpful in standards. Since its inception, CARF has grown
understanding the prognostic meaning of CNS significantly in size and informally adopted CARF
scale findings. International as its registered name after accrediting
programs in Canada, Europe, and South America.
CARF International currently provides accred-
See Also itation services in the following areas: aging ser-
vices; behavioral health; business and services
▶ Coma Recovery Scale management networks; child and youth services;
▶ Dementia Rating Scale-2 employment and community services; and medi-
cal rehabilitation. The CARF International group
of companies currently accredits more than
Further Readings 50,000 programs and services at 23,000 locations.
More than 8 million persons of all ages are served
Balconi, M., & Arangio, R. (2015). The relationship annually by 6800 CARF-accredited service pro-
between coma near coma, disability ratinghs, and viders. CARF accreditation now extends to coun-
event-related potentials in patients with disorders of
tries in North and South America, Europe, Asia,
consciousness: A semantic association task. Applied
Psychophysiology and Biofeedback, 40, 327–337. and Africa. Financial support for CARF includes
Rappaport, M. (2000). The coma/near coma scale. fees from applicant service providers, registration
The center for outcome measurement in brain fees from seminars and conferences, sales of pub-
injury. http://www.tbims.org/combi/cnc. Accessed
6 Jan 2008.
lications, contributions from International Advi-
Rappaport, M. (2005). The disability rating scale and sory Council (IAC) members, and grants from
coma/near coma scales in evaluating severe head public and private agencies.
injury. Neuropsychological Rehabilitation, 15(3/4), CARF is governed by its President/CEO and
442–453.
an 11-member Board of Directors. The Board of
Rappaport, M., Dougherty, A., & Kelting, D. L. (1992).
Evaluation of coma and vegetative states. Archives of Directors consists of individuals with expertise,
Physical Medicine and Rehabilitation, 73, 628–634. experience, and perspective on CARF-related
Commission on Accreditation of Rehabilitation Facilities (CARF) 883

issues. CARF leadership typically includes indi- • To develop and maintain current, field-driven
viduals with a diverse range of expertise, includ- standards that improve the value and respon-
ing individuals with psychology, physical therapy, siveness of the programs and services delivered
speech-language pathology, nursing, and social to people in need of life enhancement services.
work backgrounds, as well as past surveyors and • To recognize organizations that achieve
individuals with business and legal training. Other accreditation through a consultative peer-
perspectives on issues related to CARF-accredita- review process and demonstrate their commit- C
tion and other matters are gained through individ- ment to the continuous improvement of their
uals and organizations that are members of programs and services with a focus on the
CARF’s IAC. The IAC creates a partnership for needs and outcomes of the persons served.
CARF and IAC members to promote quality in • To conduct accreditation research emphasizing
human services and enhance the lives of persons outcomes measurement and management, and
served. It also provides a forum for guidance and to provide information on common program
input into standards development and the accred- strengths as well as areas needing improvement.
itation process and insight on issues affecting the • To provide consultation, education, training,
fields in which CARF provides accreditation ser- and publications that support organizations in
vices. IAC members support CARF’s mission, achieving and maintaining accreditation of
purposes, values, and vision. The IAC is com- their programs and services.
posed of organizational and individual members • To provide information and education to per-
who represent a broad spectrum of stakeholders, sons served and other stakeholders on the value
including persons served, providers, and profes- of accreditation.
sionals, in the health and human services field. • To seek input and to be responsive to persons
Current members of the IAC are detailed on the served and other stakeholders.
CARF website, http://www.carf.org/About/IAC/. • To provide continuous improvement services
to improve the outcomes for organizations and
the persons served and their community of
Major Areas or Mission Statement influence.

The mission of CARF is “to promote the quality, CARF also collaborates with partners who share
value, and optimal outcomes of services through a CARF vision and goals, while remaining politically
consultative accreditation process and continuous neutral. CARF partners include professional asso-
improvement services that center on enhancing ciations, advocacy groups, governmental agencies,
the lives of persons served” (retrieved October and individuals who are committed to enhancing
12, 2015, from http://www.carf.org/About/Mis the lives of persons who receive services.
sion/). CARF has identified three core values as
central to its mission, and these values are priori-
tized in all CARF accreditation, research, contin- Landmark Contributions
uous improvement services, and educational
activities. The following are the three CARF One of the key developments in the history of
core values: (1) all people have the right to be CARF was the passing of a resolution by the
treated with dignity and respect, (2) all people Council of State Administrators of Vocational
should have access to needed services that achieve Rehabilitation in April 1970, which urged state
optimum outcomes, and (3) all people should be agencies to support a CARF accreditation require-
empowered to exercise informed choice. ment for all organizations providing rehabilitation
In support of its mission, CARF has identified services. As CARF’s services became increas-
numerous purposes that are the focus of the agency, ingly recognized by organizations and agencies,
including the following (retrieved October 12, additional support of CARF accreditation services
2015, from http://www.carf.org/About/Mission/). has occurred. In November 1974, Goodwill
884 Commission on Accreditation of Rehabilitation Facilities (CARF)

Industries of America recognized CARF as the visibility, accountability, peer network, in addi-
accrediting organization for all Goodwill organi- tion to other benefits detailed on the CARF
zations. Another resolution, adopted in November website.
1980 by the Association of Trial Lawyers of
America, urged state workers’ compensation
agencies to require CARF accreditation for reha- Major Activities
bilitation organizations providing services to
workers with occupational disabilities. CARF accreditation outcomes for CARF, CARF
CARF has also expanded the types of services Canada, and CARF Europe consist of a 3-year
for which it provides accreditation. In September accreditation, a 1-year accreditation, provisional
1997, CARF was awarded a contract by the accreditation, nonaccreditation, and preliminary
Department of Health and Human Services, Sub- accreditation. CARF-CCAC accreditation out-
stance Abuse and Mental Health Services Admin- comes include a 5-year accreditation and non-
istration (SAMHSA) for the development and accreditation. CARF currently has close to 1400
implementation of Opioid Treatment Program surveyors throughout the North and South Amer-
accreditation. After successful development of ica, Europe, and Asia.
the program accreditation, CARF was recognized The steps to accreditation may involve a year or
in November 2001 by the SAMHSA/Center for more of preparation prior to the site survey and
Substance Abuse Treatment (CSAT) as an ongoing quality improvement following the sur-
approved accrediting organization for Opioid vey. CARF designates a CARF Resource Specialist
Treatment Programs. In 2003, CARF acquired to organizations seeking accreditation to provide
the Continuing Care Accreditation Commission guidance and technical assistance regarding the
(CCAC), which accredits continuing care retire- accreditation process. Other resources are also
ment communities and aging service networks. available to facilitate the preparation process,
Acquisition of the CCAC promoted CARF’s including standards manuals for the various pro-
vision of being an independent resource that iden- grams and services an organization can seek
tifies high-quality care providers for individuals of accreditation for, the CARF Accreditation Source-
all ages, including children and older adults. In book, which explains the accreditation process, and
February 2007, CARF began accrediting sup- the Survey Preparation Workbook, which helps
pliers of certain Durable Medical Equipment, organizations identify what practices must be in
Prosthetics, Orthotics, and Supplies (DMEPOS) place to demonstrate conformance to each stan-
after the Centers for Medicare & Medicaid Ser- dard. CARF accreditation requires that each pro-
vices (CMS) approved CARF as a national gram or service must implement and operate in
authority for DMEPOS suppliers. conformance to the standards and direct services
Over the decades, CARF has steadily grown toward the persons served for at least 6 months
and expanded its accreditation services to serve prior to the survey. During this time, the service
individuals in other countries. In 1969, CARF provider conducts a self-study and evaluation of its
accredited its first program in Canada and the conformance to the standards using the standards
first program in Europe was accredited in August manual in conjunction with the survey preparation
1996. CARF Canada and CARF Europe were questions. Then the organization submits the Sur-
incorporated in 2002 and 2008, respectively. Fur- vey Application, which includes detailed informa-
ther expansion of services included accreditation tion about leadership, programs and services that
of first programs in South America in 2005, Oce- the service provider is seeking to accredit, and
ania and the Middle East in 2008, the Asian con- service delivery location(s). CARF selects a survey
tinent in 2009, and the African continent in 2010. team by matching program or administrative exper-
The value of CARF accreditation is extensive and tise and relevant field experience with the service
includes benefits such as business improvement, provider’s unique requirements. During the survey,
risk management, funding access, positive the survey team determines the service provider’s
Commission on Accreditation of Rehabilitation Facilities (CARF) 885

conformance to all applicable standards on site Manual to also include the Behavioral Health Stan-
through the observation of services, interviews dards Manual and the Adult Day Services Stan-
with persons served and other stakeholders, and dards Manual. CARF’s public information policy
review of documentation. CARF then renders the was extended to include all areas later in 2003.
accreditation decision and a written survey report Since 2000, CARF has published new standards
approximately 6–8 weeks after the survey. Service manuals in many of its areas of accreditation, which
providers have 90 days after notification of an are detailed on the CARF website (http://www.carf. C
accreditation award to fulfill an accreditation con- org/About/History/).
dition by submitting to CARF a Quality Improve- CARF has implemented new electronic pro-
ment Plan (QIP) outlining actions that have been or grams designed to support and further develop its
®
will be implemented in response to the areas for mission. In 2007, CARF released the uSPEQ
improvement identified in the report. Service pro- (pronounced you speak; http://www.uspeq.org/)
viders accredited by CARF submit to CARF a Consumer Experience Survey, followed by the
signed Annual Conformance to Quality Report uSPEQ Employee Climate Survey. Both survey
(ACQR) on the accreditation anniversary date in tools are designed to assist organizations with per-
each of the years following the award. CARF formance improvement. CARF launched its extra-
maintains communication with service providers net Customer Connect (http://customerconnect.
throughout the tenure of accreditation. carf.org) for accredited organizations and those
CARF has published numerous standard man- seeking accreditation to manage their individual
uals that have identified program evaluation stan- contact information, view up-to-date information
dards, resulting in improved services and programs about their organization’s surveys, and access infor-
provided to clients receiving rehabilitation services. mation about the accreditation process. In 2008,
The first publication of a new section of standards CARF’s ASPIRE to Excellence™ quality frame-
manuals for Rehabilitation Facilities in November work was implemented in all standards manuals.
1973 became a springboard for future CARF con- This framework provides a logical, action-oriented
tributions to program evaluation. In January 1986, approach to ensure that organizational purpose,
standards for two new program areas (Respite Pro- planning, and activity result in desired outcomes.
grams and Alcoholism and Drug Abuse Treatment Each year, CARF sponsors numerous in-per-
Programs) were published in the 1986 Standards son and web-based seminars to help providers
Manual for Organizations Serving People with maintain conformance to the CARF standards.
Disabilities. The 1988 Standards Manual for Orga- The in-person seminars are held in cities across
nizations Serving People with Disabilities included the United States, Canada, and Europe.
new standards in areas of Post-Acute Brain Injury
Programs and Community Mental Health Pro-
grams. CARF published a separate volume of its Cross-References
1995 Standards Manual and Interpretive Guide-
lines for each of its accreditation areas (Behavioral ▶ Americans with Disabilities Act of 1990
Health, Employment and Community Support, and ▶ Individuals with Disabilities Education Act
Medical Rehabilitation). Then in 1996, CARF ▶ National Center for the Dissemination of Dis-
published the first edition of the Accreditation ability Research (NCDDR)
Sourcebook. A significant contribution to accredi- ▶ National Dissemination Center for Children
tation services occurred in 1998, when CARF with Disabilities
rewrote its standards to be unidimensional as part ▶ National Institute of Neurological Disorders
of its commitment to implementing the Standards and Stroke
Conformance Rating System. Then in 1999, CARF ▶ National Institute on Disability Independent Liv-
extended its practice of disclosing information to ing and Rehabilitation Research (NIDILRR)
the public regarding an organization’s survey report ▶ National Rehabilitation Information Center
from just the Medical Rehabilitation Standards (NARIC)
886 Commissures, Cerebral

▶ No Child Left Behind Act of 2001 commissure is a smaller bundle of nerve fibers that
▶ Rehabilitation Counseling interconnect parts of the temporal lobes. The pos-
▶ Rehabilitation Psychology terior commissure is another fiber bundle that
▶ Section 504 of the Rehabilitation Act of 1973 crosses beneath the pineal gland to connect the
midbrain regions of the cerebral hemispheres.

References and Readings

Cross-References
CARF accreditation. http://www.carf.org/Accreditation/
AccreditationProcess/StepstoAccreditation/
▶ Commissurotomy
CARF IAC. http://www.carf.org/About/IAC/
CARF mission. http://www.carf.org/About/Mission/ ▶ Corpus Callosum
CARF overview. http://www.carf.org/About/
CARF partners. http://www.carf.org/Resources/
IACResources/
CARF structure. http://www.carf.org/About/WhoWeAre/
Value of CARF accreditation. http://www.carf.org/Accred Commissurotomy
itation/ValueofAccreditation/
Christina Kwasnica
Barrow Neurological Institute, Phoenix, AZ, USA

Commissures, Cerebral
Synonyms
Martin R. Graf
Department of Neurosurgery, Virginia Split brain
Commonwealth University Medical Center,
Richmond, VA, USA
Definition

The term referring to the medical procedure in

Synonyms which interconnecting fibers between the cerebral
hemispheres are lesioned. The anatomic location
Brain commissures; Commissural fibers
includes either or both anterior and posterior
fibers. When posterior fibers are resected, connec-
tions to the hippocampus may also be affected.
Definition

The right and left cerebral hemispheres are Current Knowledge

connected by three tracts of nerve fibers or axons,
which are collectively referred to as commissures, The neurosurgical technique is based on the pre-
cerebral. These transverse, nerve fiber bundles con- mise that when stimuli enters the brain it is rapidly
nect to the homologous regions of each hemisphere communicated via the corpus callosum to the
and are known as the corpus callosum, the anterior other hemisphere. In refractory epilepsy, severing
commissure and the posterior commissure. The the corpus callosum may prevent the spread of
corpus callosum, also referred to as the great cere- electrical activity between hemispheres and gen-
bral commissure, is the largest, and it interconnects eralization of the seizure activity. This procedure
the greatest portion of the cerebral hemispheres, prevents the communication of the two hemi-
permitting the cerebral cortex to operate as a spheres thus resulting in a clinical scenario of a
whole. The corpus callosum is often the site for “split brain.” Clinical disconnection syndromes in
commissurotomy, surgical bisection, to treat cer- these patients have been studied across a large
tain psychiatric disorders and epilepsy. The anterior number of neurocognitive tasks. These surgical
Community Integration Questionnaire 887

lesions have allowed for the study of sensory between parties regardless of form, that is, commu-
perceptual processes and lateralization. Deficits nication may occur in the following forms: speak-
have been seen in the area of perception, attention, ing; writing; listening; gesturing; seeing; drawing,
memory, language, and reasoning. In studies of pointing to pictures, letters, and words;, or
these patients, it has become clear that the left selecting messages on computerized augmentative
hemisphere has limitations in perceptual functions and assistive communication devices. Human
while the right hemisphere has more striking lim- communication relies primarily on the preservation C
itations in cognitive functions. The split brain and maintenance of key social and interpersonal
studies have also led to theories of consciousness bonds (i.e., staying close and connected with indi-
and a neurocognitive framework for the human viduals who matter most in daily life). Thus, effec-
experience. Recent literature has sought to differ- tive communication depends as much on nonverbal
entiate between the surgical technique of severing behaviors such as facial expression, touch, and
only in corpus callosum, or a callostomy, versus vocal intonation as on the exchange of words.
procedures which disconnect the anterior or pos- Acquired communication deficits can occur in the
terior commisures, otherwise known as a true absence of a notable loss in intelligence or non-
commisurotomy, thus helping us better under- linguistic cognitive functions due to a loss of lan-
stand cognitive processing. guage ability, impaired motor speech skills, or
voice disorders (e.g., aphasia, dysarthria, dyspho-
nia/aphonia, and apraxia of speech).
Further Readings

Agrawal, D., Mohanty, B. B., Kumar, S., & Chinara, P. K. Cross-References

(2014). Split brain syndrome: One brain but two con-
scious minds? Journal of Health Research and
Reviews, 1, 27–33. ▶ Language
Gazzaniga, M. S. (2000). Cerebral specialization and ▶ Speech
interhemispheric communication: Does the corpus
callosum enable the human condition? Brain, 123,
1293–1213.
van der Knaap, L. J., & van der Ham, I. J. (2011). How does References and Readings
the corpus callosum mediate interhemispheric transfer?
A review. Behavioural Brain Research, 223, 211–221. Beukelman, D., & Mirenda, P. (2013). Augmentative and
Winter, T. J., & Franz, E. A. (2014). Implication of the alternative communication: Supporting children and
anterior commissure in the allocation of attention to adults with complex communication needs (4th ed.).
action. Frontiers in Psychology, 5, 432–435. Baltimore: Paul H. Brookes.

Community Integration
Communication Ability Questionnaire
Jon G. Lyon1 and Sarah E. Wallace2 Marcel P. J. M. Dijkers
1
Mazomanie, WI, USA American Congress of Rehabilitation Medicine,
2
John G. Rangos Sr. School of Health Sciences, Reston, VA, USA
Department of Speech-Language Pathology, Department of Rehabilitation Medicine, Icahn
Duquesne University, Pittsburgh, PA, USA School of Medicine at Mount Sinai, New York,
NY, USA

Definition
Synonyms
Commonly refers to the ease, efficiency, and accu-
racy of the exchange of information or content CIQ
888 Community Integration Questionnaire

Description (including stroke and brain tumors), spinal cord

injury, multiple sclerosis, Parkinson’s, burns,
The Community Integration Questionnaire (CIQ) trauma in general, and post-polio syndrome. The
measures what the International Classification of most common applications are in program evalu-
Disability, Functioning and Health (ICF) cur- ation and the study of the natural history of TBI
rently designates as participation. The CIQ con- and other impairments, but the CIQ has also been
sists of 15 items relevant to home integration used in clinical trials of interventions to improve
(H) (living), social integration (S) (loving), and post-injury functioning and in construct valida-
productive activities (P) (working). It is scored to tion studies of newly proposed participation
provide subtotals for each of these domains, as measures.
well as a total community integration score. The Because the assignment of items to subscales
basis for scoring is primarily frequency of by Willer et al. was based on a correlation matrix
performing activities or roles, with secondary calculated for a small sample, Sander et al.
weight given to whether or not activities are performed a factor analysis involving all CIQ
done jointly with others and the nature of these items for a much larger sample. The resulting
other persons (e.g., with/without disability). The instrument, sometimes designated the CIQ-R,
CIQ can be completed by either the index person dropped one item and reassigned two to different
or a proxy in 10–15 min. The optimal method of subscales (Sander et al. 1999). The CIQ-R has
data collection is an in-person interview, but tele- been used infrequently. A different CIQ-R incor-
phone interviewing is quite common, and the porated three new questions on “Electronic Social
Traumatic Brain Injury Model Systems have also Networking,” bringing the measure up to date for
utilized self-administered CIQs. No formal train- the twenty-first century (Callaway et al. 2014).
ing and credentialing process for the administra-
tion of the CIQ exist.
Psychometric Data

Historical Background Psychometric information for the CIQ is spread

out over a number of sources. In addition to the
The CIQ was developed in the early 1990s by three papers by Willer et al. (Willer et al. 1993,
Barry Willer, Ph.D., and a group of professionals 1994a, b), key texts are those by Corrigan and
and consumers to provide a measure of commu- Deming (1995), Sander et al. (1999), Sander
nity integration after traumatic brain injury (TBI) et al. (1997), and Tepper et al. (1996). Dijkers
that could be used in the TBIMS research program critically summarized psychometric information
(Willer et al. 1993, 1994a, b). They used the available through 1997 (Dijkers 1997), and some
following design criteria: brevity; suitable for later sources are given by Reistetter and
use in in-person or telephone interviews with the Abreu (2005).
person with TBI or a proxy; focus on behaviors
rather than feeling states; no biases resulting from Reliability Results of reliability studies have been
age, gender, or socioeconomic status; sensitive to mixed. Based on the (Pearson) correlations
a wide variety of living situations; and value neu- reported in the earliest study, the interrater reliabil-
tral. The instrument has been translated (not ity of the CIQ appears to be in the “acceptable”
always using formal backtranslation methods) range. However, the intraclass correlation coeffi-
into French, Arabic, Portuguese, Spanish, Japa- cient (ICC), a more appropriate measure, resulted
nese, Korean, Dutch, Swedish, and Norwegian, in much lower numbers, according to a later inves-
among others. It is the most extensively used tigation, especially for the Home (H) dimension.
measure of community integration/participation More recent research also suggests that in home
in research on TBI but has also been applied in integration, there is the greatest discrepancy
investigations of other types of brain injury between reports by subjects with TBI and those
Community Integration Questionnaire 889

by their proxies. In the latter study, the person with between CIQ and subjective quality of life. Most
TBI tended to report higher values than the proxy researchers find negative correlations between CIQ
for all three components. Subscale ICCs ranged and its subtotals (except sometimes H) and age.
from 0.43 (H) to 0.81 (P) – fairly low values. Females tend to have higher CIQ scores for total,
H and S than males, but lower P scores.
For the CIQ total score, a number of studies
have reported internal consistency levels that Sensitivity The available research shows that the C
exceed the criterion of a coefficient alpha above CIQ can validly distinguish between persons with
0.80. However, the corresponding values for the TBI and nondisabled people. Persons with TBI
S and P dimensions are much lower, especially for are less integrated along all dimensions than non-
the latter – quite likely due to the fact that alpha is disabled comparison groups in most research. In
based on only two variables – which are very one study, CIQ scores distinguished between
dissimilar from one another: work/study/ three groups of persons with TBI living in settings
volunteering and travel. differentiated by supervision/support level: inde-
pendent in the community, in the community with
Distribution Issues Corrigan and Deming noted some (natural) support, and in an institution such
negatively skewed distributions for the premorbid as a nursing home, rehabilitation facility, etc.
data for CIQ total, positive skews for H for all four
samples, negative skews for all samples for the Responsiveness Willer et al. reported gain in CIQ
S dimension, and negative skew for P for the TBI- (sub)scores for people with TBI receiving residen-
premorbid sample, but positive skew for the three tial rehabilitation services. Responsiveness also
others. Various kurtosis problems were also noted. has been shown in CIQ changes as a consequence
They recommended that the P subscale not be used of physical therapy in a multiple sclerosis sample,
independently from its contribution to the CIQ total treatment of mental health issues in a burn sample,
score. Distribution problems were also noted by peer support for patients with stroke, and
Willer et al. and Sander et al., among others. Unless cognitive-behavioral therapy for distress in a sam-
these can be resolved through transformations, non- ple with acquired brain injury.
parametric statistics need to be used in order to deal
with the nonnormal distributions. Norms For years, a self-selected small “normal
control” sample provided the only reference point
Validity No formal content or face validity stud- for judging “adequacy” of community integration,
ies of the CIQ have been done, but it was devel- even if only a mean score, SD, and Q1, Q2, and
oped utilizing a panel consisting of both Q3 were reported (Willer et al. 1994). A recent
consumers and professionals with expertise in quota sample (2,000 subjects) study of the
TBI outcome studies. An exercise in mapping Australian working-age population (Callaway
CIQ items to the ICF showed that the CIQ tapped et al. 2014) allows development of norms for
the content of household, family, and community age and gender subgroups, but they have not yet
integration. CIQ subscales and total score have been published.
been found to correlate with subscales and total
score on CHART (another measure of community
integration), impairment and disability, time since Clinical Uses
injury, CIM (a measure of subjective community
integration), Participation Assessment with In several TBI community integration programs,
Recombined Tools-Objective (PART-O), and simi- the CIQ is used to monitor patients’ progress.
lar integration measures. Similarly, expected corre- However, due to the lack of norms and the depen-
lations have been found between CIQ and measures dence of community functioning on the environ-
of, e.g., cognitive impairment, pain, balance, and ment, the clinical applicability of the CIQ is very
gait. Also found repeatedly were associations much limited.
890 Community Re-entry

Cross-References Sander, A. M., Fuchs, K. L., High Jr., W. M., Hall, K. M.,
Kreutzer, J. S., & Rosenthal, M. (1999). The
community integration questionnaire revisited: An
▶ Assessment of Life Habits (LIFE-H) assessment of factor structure and validity. American
▶ CHART Short Form Journal of Physical Medicine and Rehabilitation, 80,
▶ Community Re-entry 1303–1308.
▶ Craig Handicap Assessment and Reporting Tepper, S., Beatty, P., & DeJong, G. (1996). Outcomes in
traumatic brain injury: Self-report versus report of sig-
Technique nificant others. Brain Injury, 10, 575–581.
▶ Disability Rating Scale Willer, B., Rosenthal, M., Kreutzer, J. S., Gordon, W. A., &
▶ Frenchay Activity Index Rempel, R. (1993). Assessment of community
▶ Glasgow Outcome Scale integration following rehabilitation for traumatic
brain injury. Journal of Head Trauma Rehabilitation,
▶ Glasgow Outcome Scale: Extended 8, 75–87.
▶ Impact on Participation and Autonomy Willer, B., Linn, R., & Allen, K. (1994a).
Questionnaire Community integration and barriers to integration for
▶ Instrumental Activities of Daily Living individuals with brain injury. In M. A. J. Finlayson &
S. H. Garner (Eds.), Brain injury rehabilitation:
▶ Lawton-Brody Instrumental Activities of Daily Clinical considerations. Baltimore: Williams and
Living Scale Wilkins.
▶ Outcome, Outcome Measurement Willer, B., Ottenbacher, K. J., & Coad, M. L. (1994b). The
▶ Participation Measure for Post-acute Care community integration questionnaire. A comparative
examination. American Journal of Physical Medicine
▶ Participation Objective, Participation Subjective and Rehabilitation, 73, 103–111.
▶ Reintegration to Normal Living Index
▶ Social and Occupational Functioning Assess-
ment Scale (SOFAS)
▶ Traumatic Brain Injury Model System
Community Re-entry
References and Readings Allen N. Lewis Jr.1 and Pamela H. Lewis2
1
School of Health and Rehabilitation Science,
Callaway, L., Winkler, D., Tippett, A., Migliorini, C., University of Pittsburgh, Pittsburgh, PA, USA
Herd, N., & Willer, B. (2014). The community reinte- 2
gration questionnaire-revised: Australian normative Department of Rehabilitation Counseling,
data and measuring electronic social networking. School of Allied Health Professions, Virginia
Monash University/Institute for Safety, Compensation Commonwealth University, Richmond, VA, USA
and Recovery Research, report 074-0814-R01,
Melbourne.
Corrigan, J. D., & Deming, R. (1995). Psychometric char-
acteristics of the community integration questionnaire:
Replication and extension. Journal of Head Trauma
Synonyms
Rehabilitation, 10, 41–53.
Dijkers, M. (1997). Measuring the long-term outcomes of Community adjustment; Community integration
traumatic brain injury: A review of the community
integration questionnaire. Journal of Head Trauma
Rehabilitation, 12, 74–91.
Reistetter, T. A., & Abreu, B. C. (2005). Appraising evi-
dence on community integration following brain Definition
injury: A systematic review. Occupational Therapy
International, 12, 196–217.
Community reentry is the extent that an individ-
Sander, A. M., Seel, R. T., Kreutzer, J. S., Hall, K. M., High
Jr., W. M., & Rosenthal, M. (1997). Agreement ual who is initially unable to fully function in the
between persons with traumatic brain injury and their community due to disability is eventually
relatives regarding psychosocial outcome using the
community integration questionnaire. American Jour-
nal of Physical Medicine and Rehabilitation, 78,
353–357. The authors are not related by blood or marriage.
Community-Based Rehabilitation 891

returned to the community to work and live inde- President’s New Freedom Commission Report on Mental
pendently, using natural supports and exercising Health (2003). Achieving the promise: Transforming
mental health care in America. Substance abuse and
full access, choice, autonomy, and striving for mental health services administration of the U.S.
actualization. Actualization is the degree to Department of Health and Human Services.
which there is the achievement of a respectable
quality of life.
The Americans with Disabilities Act (ADA) C
of 1990 attempted to legislate community inte- Community-Based
gration by removing physical barriers related to Rehabilitation
access and making it illegal to discriminate on
the basis of disability. However, 30 years since Allen N. Lewis Jr.1 and Pamela H. Lewis2
1
the ADA’s passage and after the recent passage of School of Health and Rehabilitation Science,
the ADA Restoration Act in late 2008, there is University of Pittsburgh, Pittsburgh, PA, USA
2
still significant concern that US society does not Department of Rehabilitation Counseling,
fully possess nor embrace the attitudes and School of Allied Health Professions, Virginia
values commensurate with full inclusion and Commonwealth University, Richmond, VA, USA
community integration for individuals with
disabilities.
Community reentry programs teach skills nec- Synonyms
essary along a continuum of services that afford
persons the opportunity to learn behaviors needed In vivo services; Milieu-based services; Outpa-
to live full lives with a disability. Such programs tient rehabilitation
provide services and support to enable the suc-
cessful transition of an individual with a disability
from facility-based services to a viable commu- Definition
nity placement.
The provision of restorative or rehabilitative ser-
vices targeted toward the amelioration of a dis-
ability (disability: any illness, condition, or
Cross-References impairment [congenital or acquired] that inter-
feres with functioning in a major life domain)
▶ Quality of Life and/or the mitigation of functional limitation
resultant from a disability to the maximum extent
possible in a nonacute care, nonfacility-based
References and Readings service setting. Community-based rehabilitation
services attempt to maximize the individual’s
Americans with Disabilities Amendments Act of 2008. ability to function “in vivo” within major life
(2008). Pub. L. No. 110–325, 122 Stat. 3553.
pursuits such as independent daily living
Huey, K. (1980). Patient re-entry into the
community. Hospital and Community Psychiatry, 31, and work.
51–56. Community-based rehabilitation attempts to
Liberman, R. P., & Silbert, K. (2005). Community re-entry: enhance the quality of life for individuals with
Development of life skills. Psychiatry: Interpersonal
and Biological Processes, 68(3), 220–229.
disabilities and their families. This includes meet-
McColl, M. A., Carlson, P., Johnston, J., Minnes, P., Shue, ing basic needs but also going beyond to promote
K., Davies, D., et al. (1998). The definition of commu- inclusion and participation. Community-based
nity integration: Perspectives of people with brain inju- rehabilitation typically involves several domains
ries. Brain Injury, 12(1), 15–30.
National Institute on Disability and Rehabilitation
of functioning such as health, education, work,
Research. (2006). Long-range plan for fiscal years socialization, and one’s sense of empowerment.
2005 through 2009. Reaching a point of social acceptance in the 1970s
892 Compartmentalization

and 1980s, the original mission of community- compartment model, drugs are theoretically pre-
based rehabilitation was to offer individuals sumed to diffuse through tissues and the
with disabilities access to programming and sup- differences in absorption and retention of a
ports in their own home communities using drug are not treated as significant. This single-
local resources. Further, community-based reha- compartment model is sufficient in many situations
bilitation ostensibly attempts to optimize the but is less useful when drugs may be preferentially
provision of rehabilitative services, equalize retained in one type of tissue. Dosage predictions
opportunity, reduce poverty, and promote full fail if they do not account for the gradual ambient
social inclusion. leaching of the drug from fat or bone into general
circulation.
The instances in which a multicompartment
References and Readings model is most relevant are for individuals who
are medically ill, have unusually high or low
Church, J., Saunders, D., Wanke, M., & Pong, R. (1995). body fat, are pregnant, have an abnormality in
Organizational models in community based health
pH or illnesses which impact the liver or kidneys
care: A review of the literature. Health Promotion and
Programs Branch. Ottawa: Health Canada. (and thus profoundly alter the pharmacokinetics
World Health Organization, (2004). CBR: A strategy for of drug metabolism). Differences in the propor-
rehabilitation, equalization of opportunities, poverty tion of fatty tissue can influence dosing decisions
reduction and social inclusion of people with disabil-
since mg/kg may be less appropriate for drugs that
ities: Joint position paper/International Labour Organi-
zation, United Nations Educational, Scientific and are less fat-soluble. One common example of this
Cultural Organization and the World Health reduced alcohol tolerance in women since fatty
Organization. tissues do not readily absorb alcohol.
Another form of compartmentalization is ion
trapping, in which the pH alters the ease with
which a drug is transferred into or out of a partic-
Compartmentalization ular tissue. For example, neonatal blood is typi-
cally more acidic than adult blood, making it more
Nadia Webb1 and Efrain Antonio Gonzalez2,3 difficult for slightly alkaline drugs to diffuse back
1
Children’s Hospital of New Orleans, New into maternal circulation. Similarly, the GI tract is
Orleans, LA, USA more acidic than blood plasma. Weakly acidic
2
College of Psychology, Nova Southeastern drugs diffuse more readily to blood than weakly
University, Fort Lauderdale, FL, USA alkaline drugs.
3
Utah State University, Logan, UT, USA

Cross-References
Definition
▶ pH
Drugs do not saturate tissues within the body at ▶ Pharmacokinetics
the same rate. They are quickly absorbed into
blood plasma and into well-perfused organs. Mus-
cle, fat, and bone are saturated last. These tissues References and Readings
can serve as storage depots for substances, con-
tributing to the half-life of a drug and potentially Brunton, L. B., Lazo, J. S., & Parker, K. L. (Eds.). (2005).
to interaction effects days or weeks after a drug Goodman & Gilman’s the pharmacological basis of
therapeutics (11th ed.). New York: McGraw Hill.
has been discontinued.
Stahl, S. M. (2008). Stahl’s essential psychopharmacol-
The body may be inappropriately treated as ogy: Neuroscientific basis and practical applications.
a single entity or compartment. In a single- New York: Cambridge University Press.
Compensatory Education Approach 893

References and Readings

Compensation Neurosis
Brown, J. T. (1996). Compensation neurosis rides again:
1 2 A practitioner’s guide to defending PTSD claims (post
Chava Creque , Beth Kuczynski and
traumatic stress disorder). Defense Counsel Journal,
Stephanie A. Kolakowsky-Hayner3 63(4), 467–482.
1
Department of Psychology and Neuroscience, Hall, R. C., & Hall, R. C. (2012). Compensation neurosis:
University of Colorado Boulder, Boulder, CO, A too quickly forgotten concept? Journal of the Amer- C
ican Academy of Pyschiatry and the Law Online, 40(3),
USA
2 390–398.
Imaging of Dementia and Aging (IDeA) Hickling, E. J., Blanchard, E. B., & Hickling, M. T. (2006).
Laboratory, Department of Neurology and Center The psychological impact of litigation: Compensation
for Neuroscience, University of California, Davis, neurosis, malingering, PTSD, secondary traumatiza-
tion, and other lessons from MVAs. DePaul Law
CA, USA
3 Review, 55(2), 617–633.
Department of Rehabilitation Medicine, Icahn Rogers, R. (2008). Clinical assessment of malingering and
School of Medicine at Mount Sinai, New York, deception (3rd ed.). New York: Guilford Press.
NY, USA

Synonyms Compensatory Education

Approach
Accident neurosis; Litigation neurosis
Jill Snyder
Behavioral Health Services, Boston Public
Definition Schools, Roxbury, MA, USA

Compensation neurosis is a condition in which

symptoms are associated with a real or presumed Definition
disability (possibly exaggerated) that may bring
legally awarded financial compensation. This type Compensatory educational approaches include
of neurosis is believed to be motivated in part by the presentation of material in an alternative for-
the desire for, and hope of, monetary or interper- mat, providing students an alternative way to
sonal gain. However, many factors are involved in master a particular concept and demonstrate
compensation neurosis, such as the psychological knowledge.
factors before and after the presumed injury, the
additional effects on the quality of life, the possi-
ble influences of legal or insurance processes, Current Knowledge
secondary gains of victimhood, and a feeling of
being entitled to compensation. The condition The goal of education is to help students acquire
may or may not resolve after financial settlement skills and master concepts that will be useful in
occurs. The term is often used in litigation and daily living. Generally, two approaches are used
seems to be quite controversial in psychiatry, with when instruction fails to help students learn.
some researchers disputing its existence. These include compensatory education
approaches and/or remedial education approaches
(▶ Remedial Education Approach). Compensa-
Cross-References tory educational approaches require teachers to
present material in a different format, providing
▶ Fake Bad Scale students an alternative way to master a particular
▶ Malingering concept and demonstrate knowledge. They are
894 Compensatory Strategies

used when students lack the ability to acquire a

certain skill or concept. For example, a deaf stu- Compensatory Strategies
dent who is unable to speak may be taught sign
language as an alternate form of communication, Matthew M. Kurtz
or a student with a math calculation disability may Department of Psychology, Wesleyan University,
be taught to use a calculator. When students fail to Middletown, CT, USA
make progress in a certain skill area, evidence-
based strategies and methods must be employed to
help the student attain expected learning out- Definition
comes. In these cases, education must be adjusted
by offering different activities that facilitate the Compensatory strategies are environmental mod-
same results. This approach in isolation does not ifications or behavioral strategies designed to
represent best practice, and in keeping with the bypass persistent impairment in attention, mem-
educational and neurodevelopmental literature, ory, executive function, and/or other cognitive
practitioners should offer both remedial and com- skills as a means to achieve desired rehabilitation
pensatory approaches, depending on students’ goals. Environmental modifications could include
specific academic needs. Educators must be care- the use of external aids or modifying the setting in
ful to distinguish between the educational content which activities take place. The use of an alpha-
in which a student struggles (e.g., reading or numeric pager and a checklist for a person with
math) and the method in which a particular con- memory and executive-function deficits to ensure
cept may be successfully integrated. Offering a completion of daily tasks at specific times would
compensatory approach should be a last resort be an example of external aids. Working in a
on the educational continuum and should be distraction-free room to enhance concentration
supported by a comprehensive neuropsych- skills in a person with symptoms of disinhibition
ological evaluation. would be an example of modifying an environ-
ment. Examples of behavioral strategies would
include repeating phrases during social interac-
Cross-References tions to ensure accurate processing of conversa-
tion or associating words with images to enhance
recall.
▶ Academic Competency
▶ Academic Skills
▶ Compensatory Education Approach
▶ Remedial Education Approach Current Knowledge
▶ Strength-Based Education
Compensatory strategies have shown efficacy in
randomized, controlled studies for improving the
ability to remember to complete activities in the
References and Readings
future (prospective memory) in neurologically
D’Amato, R. C., & Rothlisberg, B. A. (1996). How edu- impaired people with cognitive difficulties. For
cation should respond to students with traumatic brain example, Wilson et al. (2001) used an external
injury. Journal of Learning Disabilities, 29(6), pager in 143 people between 8 and 83 with a
670–683.
D’Amato, R. C., Rothlisberg, B. A., & Work,
range of neurological illnesses or trauma. Results
P. L. H. (1999). Neuropsychological assessment for revealed that more than 80% of clients improved
intervention. In C. R. Reynolds & T. B. Gutkin (Eds.), in carrying out self-care activities and meeting
The handbook of school psychology (pp. 452–475). appointments, as well as other life skills, relative
New York: Wiley.
to the baseline period, and effects were maintained
Gaddes, W. H., & Edgell, D. (1994). Learning disabilities
and brain function: A neuropsychological approach 7 weeks after return of the pager. Environmental
(3rd ed.). New York: Springer. modifications, including use of signs, removal of
Competency 895

distracting environmental stimuli, and checklists, health-care professional) to make determinations/

have been used effectively in randomized, con- decisions or to perform certain functions. In a
trolled trials to enhance adaptive functioning and legal context, competency typically relates to
quality of life in people with severe psychiatric one’s understanding of issues related to involve-
illnesses as well (Velligan et al. 2002). ment in a legal proceeding (Reisner and Slobogin
1990). Such an understanding necessitates some
degree of acknowledgment regarding the nature C
Cross-References of the procedure, the risks involved, success esti-
mates, possible alternative options/approaches,
▶ Cognitive Rehabilitation and the pros and cons of specific courses of action.
▶ Environmental Modifications Issues related to competency can be raised at any
▶ Mnemonic Techniques time during the criminal judicial process. Specific
▶ Neuropsychological Rehabilitation competencies in the criminal realm include com-
▶ Prosthetic Memory Aids petence to confess (or waive rights at pretrial
investigations), competency to plead guilty, com-
petency to waive right to counsel, competency to
References and Readings stand trial, competency to be sentenced, compe-
tency to waive further appeal (when facing capital
Velligan, D. I., Prihoda, T. J., Ritch, J. L., Maples, N., Bow- punishment), and competency to be executed.
Thomas, C., & Dassori, A. (2002). A randomized,
Competency evaluations are the most common
single-blind pilot study of compensatory strategies in
schizophrenia outpatients. Schizophrenia Bulletin, 28, referral of mental health professional in criminal
283–292. forensics. A defendant’s competency can be
Wilson, B. A. (2008). Neuropsychological rehabilitation. questioned by attorneys and judges. In the civil
Annual Review of Clinical Psychology, 4, 141–162.
realm, impairment of competency, or decision-
Wilson, B. A., Emslie, H. C., Quirk, K., & Evans, J. J.
(2001). Reducing everyday memory and planning making capacity, is often a consequence of vari-
problems by means of a paging system: A randomised ous types of dementias and other organic brain
control crossover study. Journal of Neurology, Neuro- syndromes. Impairments in memory, judgment,
surgery and Psychiatry, 70, 477–482.
reasoning, and planning can affect a person’s
capacity to make medical decisions, consent to
research, manage financial affairs, execute a will,
drive, manage medications, live independently,
Competency and handle even the most basic activities of daily
life (ADLs).
Moira C. Dux In the criminal realm, competency relates to a
US Department of Veteran Affairs, Baltimore, defendant’s current ability to understand and par-
MD, USA take in legal proceedings. The Dusky standard
states that: “The test must be whether he (the
defendant) has sufficient present ability to consult
Synonyms with his lawyer with a reasonable degree of ratio-
nal understanding – and whether he has a rational
Capacity as well as factual understanding of the proceed-
ings against him.” (p. 402). The Dusky standard
outlines the minimal level of competency neces-
Definition sary in accordance with the US Constitution for all
criminal jurisdictions. Grisso (1988) outlined five
Competency is a legal determination to be made areas of analysis suggested for psychologists/neu-
by a legal professional (i.e., judge). It relates to a ropsychologists conducting competency evalua-
person’s capacity (a clinical status as judged by a tions: (1) functional description of specific
896 Complex Partial Seizure

abilities, (2) causal explanations for deficits in References and Readings

competency abilities, (3) interactive significance
of deficits in competency ability, (4) conclusory Denney, R. L. (2005). Criminal forensic neuropsychology
and assessment of competency. In G. Larrabee (Ed.),
opinions about legal competency and incompe-
Forensic neuropsychology: A scientific approach.
tency, and (5) prescriptive remediation for deficits New York: Oxford University Press.
in competency abilities. In an attempt to Dusky v. United States, 362 U.S. 402 (1960).
operationalize the Dusky ruling, the Group for Grisso, T. (1988). Competency to stand trial evaluations:
A manual for practice. Sarasota: Professional Resource
the Advancement of Psychiatry (1974) developed
Exchange.
a 21-point list of abilities derived from compe- Group for the Advancement of Psychiatry. (1974). Misuse
tency assessment instruments available at the time of psychiatry in the criminal courts: Competency to
and included items such as understand current stand trial. New York: Committee on Psychiatry and
Law.
legal situation, understand legal defenses avail-
Marson, D. C., & Hebert, K. (2005). Assessing civil
able in the defendant’s behalf, tolerate stress at competencies in older adults with dementia: Consent
the trial and while awaiting trial, and protect self capacity, financial capacity, and testamentary
by using available legal safeguards. As a result of capacity. In G. Larrabee (Ed.), Forensic neuropsychol-
ogy: A scientific approach. New York: Oxford Univer-
Wieter v. Settle (1961), the US District Court
sity Press.
outlined several minimal ability requirements for Reisner, R., & Slobogin, B. (1990). Law and the mental
criminal competency including (but not limited health system (2nd ed.). St. Paul: West.
to) mental capacity to appreciate his or her pres- Wieter v. Settle (1961). 193 F. Supp. 318 (W.D. Mo., 1961).
ence in relation to time, place, and thing; he or she
apprehends that there is a judge on the bench; he
or she apprehends that there is, or will be, a jury
present to pass on evidence adduced as to his or Complex Partial Seizure
her guilt or innocence of such charge; and he or
she has memory sufficient to relate those things in William B. Barr1, H. Allison Bender2 and
his or her own personal manner. Rebecca Bind3
1
Currently, there are a number of instruments NYU Langone Medical Center, Comprehensive
designed to assess competency (primarily in the Epilepsy Center, New York, NY, USA
2
criminal realm), which are referred to as compe- Department of Neurology, Icahn School of
tency assessment tools (CATs). Examples include Medicine at Mount Sinai, New York, NY, USA
3
the Competency Assessment Inventory-Revised, Department of Neurology, Mount Sinai Medical
the Fitness Interview Test-Revised, the Georgia Center, New York, NY, USA
Court Competency Test, the Competency Assess-
ment for Standing Trial for Defendants With Men-
tal Retardation, and the MacArthur Competency Definition
Assessment Tool-Criminal Adjudication. It is
important to note that none of the aforementioned Formerly known as “complex partial seizures,”
CATs have been validated with brain-injured or focal seizures with impaired consciousness or
neurological populations. Marson and colleagues awareness or responsiveness are defined by the
(cf. Marson and Hebert 2005) have developed International League Against Epilepsy as focal
instruments to assess consent capacity in older seizures with “dyscognitive” symptoms as their
adults. primary feature, i.e. an altered state of awareness,
consciousness, and/or responsiveness. This sei-
zure type is now commonly referred to as Focal
Cross-References dyscognitive seizures (FCS).
FDS originate in a single hemisphere of the
▶ Financial Capacity brain and may begin with a focal seizure with
Complex Partial Seizure 897

retained consciousness or awareness (formerly the brain. Vagus nerve stimulation is yet another
known as a simple partial seizure), also referred possible avenue for intervention. Surgical resec-
to as an aura. This commonly consists of feelings tion for patients with intractable focal seizures in
of emotional, ideational, or sensory changes. the temporal lobes may be an option if the origin
Once consciousness, awareness, or responsive- of seizure activity has been identified. This can
ness become impaired, individuals with FDS prove difficult and traditional methods are not
may experience automatisms, which are often always successful. Stereoelectroencephalography C
characterized as repetitive, semi-purposeful invol- (SEEG) is a recently developed surgical method
untary movements. The specific paroxysmal in which electrodes are inserted into 15–20 loci in
behavior changes correspond to the seizure focus the brain to determine the location of seizure
and the progression represents the spread of epi- activity. Though invasive, it can successfully
leptiform activity. These may be oropharyngeal map seizure activity and allow a patient to subse-
(e.g., lip smacking), emotional (e.g., fear), ges- quently undergo surgery. A more recent treatment
tural, ambulatory, or verbal. Additionally, auto- option for intractable seizures uses laser ablation
nomic symptoms may occur, including: pallor, technology (e.g., Visualase) to thermally destroy
flushing, and sweating. FDS can subsequently the epileptogenic foci.
spread throughout the brain and progress into a
generalized event (i.e., bilateral convulsive
seizure).
References and Readings

Berg, A., Berkovic, S., Brodie, M., Buchhalter, J., Cross,

Current Knowledge H., Boas, W., Engel, J., French, J., Glauser, T.,
Mathern, G., Moshe, S., Nordli, D., Plouin, P., &
Epidemiologically, FDS comprise ~50% of all Scheffer, E. (2010). Revised terminology and concepts
for organization of seizures and epilepsies: Report of
focal seizures and 33% of all epilepsies. Approx-
the ILAE commission on classification and terminol-
imately 80% of FDS arise from the temporal lobe, ogy, 2005–2009. Epilepsia, 51(4), 676–685.
particularly the neocortex and inferomedial Gonzalez-Martin, J., Vadera, S., Mullin, J., Enatsu, R.,
(limbic) structures. Focal seizures can originate Alexopoulos, A. V., Patwardhan, R., Bingaman, W.,
& Najm, I. (2014). Robot-assisted stereotactic laser
from other brain regions, most notably the frontal
ablation in medically intractable epilepsy: Operative
lobes; events can also begin in the parietal and technique. Neurosurgery, 10(2), 167–172.
occipital lobes, though it is quite rare. A diagnosis Morrell, M. J., & Halpern, C. (2016). Responsive direct
of FDS can be identified through a neurological brain stimulation for epilepsy. Neurosurgery Clinics of
North America, 21(1), 111–121.
history and description of the events as well as
Scheffer, I., Berkovic, S. F., Capovilla, G., Connolly, M. B.,
extensive workups, including neuroimaging. Guilhoto, L., Hirsch, E., Moshe, S. L., Nordli, D., Zhang,
However, the electroencephalogram (EEG) Y., Zuberi, S. M. The organization of the epilepsies:
remains the “gold standard” for diagnosis. Report of the ILAE Commission on Classification and
Terminology. http://www.ilae.org/visitors/centre/Docu
Patients with FDS often exhibit abnormal dis-
ments/OrganizationEpilepsy.pdf. Accessed 31 Mar 2017.
charges on interictal recordings and a characteris- Serletis, D., Bulacio, J., Bingaman, W., Najm, I., &
tic pattern of onset and spread of activity when Gonzalez-Martinez, J. (2014). The stereotactic
seizures are recorded. approach for mapping epileptic networks:
A prospective study of 200 patients. Journal of Neuro-
FDS are most commonly treated with one or
surgery, 121(5), 1239–1246.
more antiepileptic drugs (AEDs) and about half of The Epilepsy Foundation. New terms for seizure classifica-
patients are able to achieve a seizure-free state. tion. http://www.epilepsy.com/learn/types-seizures/new-
When seizures cannot be well controlled by AEDs terms-and-concepts-seizures-and-epilepsy. Accessed 31
Mar 2017.
alone, one treatment option is NeuroPace, a
Treiman, D. (2010). Treatment of refractory complex par-
neurostimulator implanted into the skull that mon- tial seizures: Current state of the art. Journal of Neuro-
itors and attempts to regulate electrical activity of psychiatric Disease and Treatment, 6, 297–308.
898 Computed Tomography

Cross-References
Computed Tomography
▶ PET
Nathan D. Zasler1 and Robin Sekerak2
1
Concussion Care Centre of Virginia, Ltd.,
Richmond, VA, USA References and Readings
2
Waikato District Health Board, Hamilton,
New Zealand American Academy of Neurology. (1991). SPECT and
neurosonology qualifications approved. Neurology,
41, 13A.
Kaufmann, H., & Schatz, I. J. (2004). Pure autonomic
failure.In D. Roberston (Ed.), Primer on the autonomic
Definition nervous system, (2nd ed., pp. 309–311). Amsterdam:
Elsevier. https://www.britannica.com/topic/tomography.
Tomography refers to sectional imaging through Accessed 10 Aug 2016.
the use of any type of waves with penetrative
properties. Tomography is used in radiology, biol-
ogy, and many other areas of science. The tech-
nique relies on production of images based on the
mathematical procedure of tomographic recon-
Computerized Assessment of
struction. In conventional radiology, X-ray
Response Bias
tomography is accomplished by making sectional
David R. Cox
images through of body parts by moving the
Neuropsychology and Rehabilitation Consultants,
X-ray source in the film in opposite directions
P.C., Chapel Hill, NC, USA
during the period of radiation exposure. As a
result, structures in the focal plane appear sharper,
while structures another planes appear blurred.
Synonyms
Current tomographic techniques typically rely on
gathering projection data from multiple directions
CARB
and feeding the data into a tomographic recon-
struction software algorithms which is processed
by computer that both requires the data and then
Description
generates a tomographic image. There are multi-
ple different technologies that integrate tomogra-
The Computerized Assessment of Response Bias
phy with some of the more common ones used in
(CARB) is a computer-based assessment tool for
the neurosciences being single photon emission
evaluating effort. The test is one of many tests
computerized tomography, computed tomogra-
characterized as symptom validity tests (SVT),
phy, ultrasonic tomography, and positron emis-
measures of response bias, tests used to assess
sion tomography.
possible malingering or poor effort, and tests of
exaggeration of deficit. The test is a computerized
version of the digit recognition paradigm using a
Current Knowledge forced choice format, akin to the procedure
described by Hiscock and Hiscock (1989) and
An imaging technique that produces views Binder (1990). Frequently, statistical determina-
through the internal aspects of solid objects tion of below chance performance (based on the
including the human body through application binomial theorem) has been used with tests such
and recording of energy waves of various sorts as these. However, CARB has been described as
through those structures. Images can be dimen- an easy test to perform, resulting in the ability to
sional or multidimensional. detect inadequate effort using above chance
Computerized Assessment of Response Bias 899

cut-off scores (Millis 2008, p. 896). The test has below the sample of individuals with documented
been studied with a wide variety of populations, brain injury that had been tested (Conder et al.
including head injury, chronic fatigue syndrome, 1992); performance below 90% was deemed to be
musculoskeletal injuries, pain disorders, and psy- biased.
chiatric or emotional disturbances such as depres- Subsequent versions of CARB include CARB-
sion. Published studies have included adults and 97 (Allen et al. 1997) and another revision
children. The test administration time of CARB referenced in Green and Iverson (2001). CARB- C
can vary depending on the protocol used; how- 97 added auditory feedback to the original version
ever, it typically can be completed in no more than such that correct responses are followed by a
10–15 min. CARB performance results reported pleasant tone and incorrect responses are followed
include percent correct for each group of trials as by an unpleasant tone. The third revision short-
well as the overall percentage correct. Also ened the delays between stimulus presentation
reported are the response latency time for each and forced choice presentation to 1.5, 2.5 and
item, average latency per group of trials and over- 3.5 s. Each of the CARB versions has been uti-
all, as well as other information. An interpretive lized in published studies, although the original
summary can also be optionally provided. version may continue to be the most widely used
(Larrabee 2007, p. 61).
The publisher of CARB (CogniSyst) has not
Historical Background further updated the test and no longer maintains a
web presence.
CARB was designed and published by Conder
et al. (1992) in an effort to provide a computerized
tool for administration of the forced-choice, digit Psychometric Data
recognition tasks that were gaining popularity in
assessment of effort among individuals undergo- As with many, if not most, symptom validity tests
ing neuropsychological testing. Hiscock and the nature of CARB – presentation of a relatively
Hiscock (1989) had reported on use of forced- easy task that may be perceived to be much more
choice methods in detecting malingering; Binder difficult than it actually is – leads to a distribution
(1990) had also been working on this method of of scores that is highly skewed toward the upper
assessing effort. The authors of CARB elected to end. Individuals who put forth effort on the test
name the test with the phrase “response bias” as get all, or nearly all, of the items correct. This
opposed to malingering or something else, to clar- appears to be true regardless of the presence or
ify that the test was not “diagnosing” malingering, absence of brain injury or other cognitive deficit.
but measuring a bias in responding. CARB was originally validated on a small sample
Several versions of CARB have been (8) of individuals who had documented severe
published and studied. The original version brain injury. That group performed at 98.6%
(Conder et al. 1992) utilized three distinct trials (SD = 3.6) correct (Conder et al. 1992). Internal
of 37 items each. Each item includes presentation consistency across items is therefore also quite
of a five digit number that is to be remembered high among individuals putting forth adequate
and, after a short delay during which the examinee effort; biased responding with suboptimal effort
is to count silently backward from 20, selected is presumed, by the nature of the construct, to be
from two choices – the target number and a foil. more variable. Individuals who perform at a
The groups of trails differ from one another in that “passing” level on CARB yielded 96.6–97.6%
the delay between stimulus presentation and accuracy across the blocks of trails in CARB,
forced-choice presentation increases from 3 to 6 whereas those who performed at a nonpassing
and 9 s, respectively. Initial studies of this version level yielded accuracy scores ranging from
of CARB reported that performance at or below 62.4% to 74.6% (Allen et al. 1997; Allen et al.
89% correct is more than two standard deviations 1998). An accuracy difference of 10% or more
900 Computerized Assessment of Response Bias

between any two blocks of the test was deter- studies in a given group exist or not. Clearly,
mined to correlate highly with poor (nonpassing) however, there is support for the use of CARB
scores on CARB (Allen et al. 1997). Test-retest with cut-off scores at above-chance levels in
reliability (1-week interval) is reported to be quite assessment of those groups of whom scientific
high (r = 0.97) (de Armas 1996). studies have been published. A valuable area of
Many additional studies have also been assessment using CARB includes those cases in
performed using samples of persons with brain which secondary gain such as litigation or disabil-
injury, alleging brain injury, or with or alleging ity benefits are at issue. Additional clinical appli-
other disorders that may impact cognition. The cation may be found in the review by Allen et al.
variable of seeking, or not seeking, compensation (2003). Several studies underscore the now
as a result of an injury or condition is a significant widely accepted practice of the use of multiple
one in the realm of assessing effort. Lending sup- symptom validity measures in clinical and/or
port to the notion that secondary gain can be a forensic assessment due to variation across mea-
major factor in these cases, Gervais et al. (2001) sures (Mossman et al. 2012; Harrison et al. 2015).
reported that 100% of the individuals with fibro-
myalgia and rheumatoid arthritis who were not
seeking compensation performed in a fashion
that indicated adequate effort. Age does not See Also
appear to be a significant factor influencing per-
formance on CARB. Flaro et al. (2000) reported ▶ Dissimulation
on children performing at or above normal adult ▶ Effort
performance levels on CARB. Allen et al. (2003) ▶ Forensic Neuropsychologist
reported on a number of studies providing valida- ▶ Forensic Neuropsychology
tion for the utility of CARB with a variety of ▶ Forensic Psychology
diagnostic groupings, and the reader is encour- ▶ Hiscock Forced-Choice Test
aged to read that review. ▶ Malingering
▶ Portland Digit Recognition Test
▶ Response Bias
Clinical Uses ▶ Rey 15 Item Test
▶ Symptom Validity Assessment
Clinically, CARB is used to assess response bias, ▶ Word Memory Test
level of effort and to assist in the detection of
symptom exaggeration and/or malingering. It has References and Readings
primarily been used (at least in published studies)
in populations of individuals alleging brain injury Allen, L. M., Conder, R. L., Green, P., & Cox, D. R.
via closed head trauma, although other diagnostic (1997). CARB' 97 manual for the Computerized Assess-
groupings have also been studied and published. ment of Response Bias. Durham: CogniSyst, Inc.
Allen, L. M., Richards, P. M., Green, W. P., Iverson, G. L.,
These include chronic fatigue syndrome, fibromy- & Conder, R. L. (1998). Performance patterns on the
algia, stroke, chronic pain, multiple sclerosis, Computerized Assessment of Response Bias in 1752
brain aneurysm, and brain tumor (Allen et al. compensation cases (Abstract). Archives of Clinical
2003). CARB appears to be an appropriate mea- Neuropsychology, 13, 15–16.
Allen, L. M., Iverson, G. L., & Green, P. (2003). Comput-
sure to use for assessing effort with adults or erized Assessment of Response Bias in forensic neuro-
children, and would in theory be appropriate in psychology. Journal of Forensic Neuropsychology, 3
any clinical population in which assessment of (2), 205–225.
effort might be of value. The concept of the bino- de Armas, A. (1996, July–August). Detection of malinger-
ing in forensic psychological evaluations. The Forensic
mial theorem and evaluation of performance Examiner, 5, 26–28.
against chance levels is a useful and reasonably Binder, L. M. (1990). Malingering following minor head
valid measure regardless of whether published trauma. The Clinical Neuropsychologist, 4, 25–36.
Computerized Treatment 901

Conder, R., Allen, L., & Cox, D. (1992). Manual for the electronic medium to either (1) directly improve a
Computerized Assessment of Response Bias. Durham: specific cognitive ability (restitution) or (2) serve as
CogniSyst, Inc.
Flaro, L., Green, P., & Allen, L. M., III. (2000). Symptom an external aid that reduces the impact of cognitive
validity test results with children: CARB and WMT. dysfunction on daily life (compensation). Today’s
Archives of Clinical Neuropsychology, 15(8), 840. computerized interventions, which include com-
Gervais, R., Green, P., Allen, L., & Iverson, G. (2001). puter software, smartphone, and tablet applications
Effects of coaching on symptom validity testing in
chronic pain patients presenting for disability assess- and video games, have been praised as a cost- C
ments. Journal of Forensic Neuropsychology, 2(2), 1–19. effective and easily accessible alternative to tradi-
Green, P., & Iverson, G. L. (2001). Validation of the Com- tional in-person treatments (Kueider et al. 2012).
puterized Assessment of Response Bias in litigating
patients with head injuries. The Clinical Neuropsychol-
ogist, 15, 492–497.
Harrison, A. G., Flaro, L., & Armstrong, I. (2015). Rates Historical Background
of effort test failure in children with ADHD: An
exploratory study. Applied Neuropsychology, 4, Lynch (2002) presents a detailed historical time-
197–210.
Hiscock, M., & Hiscock, C. K. (1989). Refining the forced- line of the development and evolution of CIs.
choice method for the detection of malingering. Jour- According to his comprehensive review, CI
nal of Clinical and Experimental Neuropsychology, 11, began with the popularization of video games
967–974. and personal computers in the late 1970s. Soon
Larrabee, G. J. (2007). Assessment of malingered
neuropsychological deficits. New York: Oxford Univer- after, brain injury programs that had traditionally
sity Press. relied on puzzles, word games, and board games
Millis, S. R. (2008). Assessment of incomplete effort and began incorporating computer software in tradi-
malingering in the neuropsychological examination. In tional cognitive rehabilitation. Historically, CI
J. E. Morgan & J. H. Ricker (Eds.), Textbook of clinical
neuropsychology. New York: Taylor & Francis. development can be categorized into two main
Mossman, D., Wygant, D. B., & Gervais, R. O. (2012). trends: (1) development of software content and
Estimating the accuracy of neurocognitive measures in adaptation of popular video games to remediate
the absence of a “gold standard”. Psychological Assess- specific cognitive deficits (Glisky et al. 1985;
ment, 24, 815–822.
Chute et al. 1988; Lynch 1986) and (2) utilization
of computers as “cognitive prosthetics” (Lynch
1990) to directly replace lost skills. Examples of
this latter trend have included computer-generated
Computerized Treatment speech for patients with expressive aphasia, or
external organization systems such as PEAT
Erica Kaplan1 and Melissa Shuman-Paretsky2 (planning and execution assistant and trainer;
1
Rehabilitation Medicine, Brain Injury Research Levinson 1997) to aid patients with executive
Center, Icahn School of Medicine at Mount Sinai, dysfunction. While CIs were historically used to
New York, NY, USA supplement in-person cognitive rehabilitation,
2
Department of Rehabilitation Medicine, Mount modern efforts on CIs have been advertised as
Sinai School of Medicine, New York, NY, USA free-standing interventions with generalizable
benefits that transcend geographic or economic
barriers (Hardy et al. 2015).
Definition

Harley and colleagues (1992) defined cognitive Rationale or Underlying Theory

rehabilitation as “systematic, functionally-oriented
service of therapeutic cognitive activities, based on Most CIs are based on the concept of
assessment and understanding of the person’s neuroplasticity – the idea that neural structures
brain-behavior deficits.” Computerized interven- and networks can be modified by repeated prac-
tions (CIs) for cognitive rehabilitation employ an tice of an increasingly difficult task over an
902 Computerized Treatment

extended period of time (Rabipour and Raz 2012). neurological and psychiatric conditions including
Generalization is also integral; CIs attempt to stroke (Yoo et al. 2015), dementia (Mahendra
transfer the effects from task- and domain-specific et al. 2005), traumatic brain injury (Bogdanova
computerized exercises to other cognitive et al. 2015), schizophrenia (Gomar et al. 2015),
domains and daily life skills (Roche and Johnson and major depressive disorder (Motter
2014; Lebowitz et al. 2012). More generally, CI et al. 2016).
theorists argue that increases in motivation and
self-efficacy gleaned from accessible and user-
friendly CIs will also help to facilitate this gener- Treatment Procedures
alization process (Rabipour and Raz 2012).
The frequency and duration of CIs is highly var-
iable. A recent review of computerized cognitive
Goals and Objectives programs for older adults indicated that optimal
benefit is achieved by 30–60 min CI sessions
In clinical populations, CIs are implemented with approximately three times per week (Lampit
the goal of either restoring lost functions or com- et al. 2014). CI programs are usually adaptive,
pensating for cognitive deficits in order to matching difficulty level to performance and
improve daily functional ability (Dams- consisting of tasks that increase in speed and/or
O’Connor and Gordon 2010). CIs have targeted complexity on a trial-by-trial basis (Roberts et al.
problems across cognitive domains including 2016; Roche and Johnson 2014; Lebowitz et al.
attention and working memory, memory, execu- 2012; Smith et al. 2009). Some programs focus on
tive functioning, language, and visuospatial abil- a specific domain of cognitive training, such as
ity. In healthy populations, CIs are implemented attention (Roberts et al. 2016; Roche and Johnson
with the goal of enhancing cognitive ability or 2014), while others include tasks that represent
preventing age-related cognitive decline (Kueider more generalized experiences that occur in the
et al. 2012). environment, such as rapid speech for auditory
processing (Smith et al. 2009; Merzenich et al.
2014). While CIs are often administered in isola-
Treatment Participants tion, recent reviews have recommended combin-
ing these programs with other effective
CIs have been implemented across a range of interventions, such as physical exercises for exec-
populations varying in age, diagnosis, and cogni- utive functioning, memory strategy training for
tive ability. In pediatric populations, computer- verbal memory, and lifestyle changes (Lampit
ized interventions have been implemented to et al. 2014).
enhance functioning in healthy children as well Many CIs are available without supervision by
as to restore specific abilities in those diagnosed a trained professional, including but not limited to
with ADHD, learning disabilities, cerebral palsy, Posit Science Brain Fitness, Lumosity, and
developmental coordination disorder, and HAPPYneuron. Other CIs are designed for use in
acquired brain injury (Rabipour and Raz 2012). conjunction with in-person treatment, including
CIs have also been applied to academic settings as attention process training (Sohlberg and Mateer
adjunct tools for improving reading and math 1987) and CogSMART (Twamley 2016). Recom-
functioning. In adult populations, CIs have been mendations for clinicians Given the increasing
implemented in nonclinical settings to improve popularity and variety of currently available
brain health in normal aging (Kueider et al. computerized cognitive interventions, there is a
2012; Lampit et al. 2014; Smith et al. 2009) and significant need for manualized treatment pro-
for older adults at risk for cognitive decline (Coyle gram and guidelines to increase the consistency
et al. 2015). Clinically, CIs have been integrated and accessibility of treatment (Bogdanova
into cognitive rehabilitation for individuals with et al. 2015).
Computerized Treatment 903

Efficacy Information Outcome Measurement

It is difficult to formulate conclusions about the Common outcome measures for CIs have included
efficacy of CIs; outcomes are often contingent on standardized neuropsychological tests across cog-
experimental design and vary according to the nitive domains (with an emphasis on attention and
cognitive domain being targeted. Many efficacy executive functioning), behavioral questionnaires,
studies also suffer from methodological limita- and changes in performance on typical tasks or C
tions including small sample and effect sizes and activities of daily living (Bogdanova et al. 2015;
the absence of random assignment, control Roberts et al. 2016; Roche and Johnson 2014;
groups, and controls for stimulants and other med- Zelinski et al. 2011). While some studies have
ications (Melby-Lervag and Hulme 2013; Roche also used more generalizable measures, such as
and Johnson 2014; Lampit et al. 2014). academic measures for school-aged children, and
The available literature provides adequate neuropsychological measures that are not directly
support for short-term, specific improvements related to training (Smith et al. 2009), these mea-
and limited support for long-term benefits that sures have yielded less promising results (Roberts
generalize beyond the targeted domain. CIs are et al. 2016).
frequently associated with short-term improve- Outcome measures that can demonstrate the
ments in attention, memory, working memory, generalizability of computerized cognitive train-
and executive functioning on measures that ing through clinically meaningful functional end-
directly relate to those domains (Bogdanova points are needed. Matched, active control groups
et al. 2015; Coyle et al. 2015; Melby-Lervag and are necessary in order to demonstrate that
Hulme 2013; Roche and Johnson 2014; Smith improvements are due to the actual computerized
et al. 2009; Bennett et al. 2013). However, evi- cognitive program and not due to the placebo
dence for generalizable benefit that continues effect of knowledge of participation in a program.
beyond 12 months is limited (Roberts et al. Outcomes targeting functional brain changes are
2016). Similarly, generalized improvements also recommended to evaluate neuroplastic pro-
from targeted CIs (Rabipour and Raz 2012) cesses (Rabipour and Raz 2012). Generally,
often do not extend beyond the short-term reviews of computerized interventions suggest
(Zelinski et al. 2011), with the majority of findings that further research is needed to define, standard-
opposing long-term benefit that generalizes ize, and assess outcome measures and to establish
beyond specific task performance (Owen et al. outcome measures related to functional and last-
2010; Zickefoose et al. 2013). ing long-term outcomes (Bogdanova et al. 2015).
One consistent exception to the poor general-
izability and stability of CI benefits are those
interventions that employ a contextualized and Qualifications of Treatment Providers
metacognitive (awareness of one’s cognitive pro-
cess) approach. According to the INCOG Most studies of CIs do not mandate the presence of a
(international cognitive) group, CIs that consist treatment provider, and those that do include treat-
of repeated practice of decontextualized tasks do ment providers do not have detailed information on
not produce sustainable or generalizable benefit. provider qualifications or interactions between the
However, CIs that include clinician emphasis on treating provider and participants (Bogdanova et al.
compensatory and metacognitive strategies have 2015). Most studies including treatment providers
been shown to produce significant benefit that were based on one treatment, Cogmed, which uses
generalizes to daily functional ability (Ponsford “coaches” to monitor client’s performance and pro-
et al. 2014; Zelinski et al. 2011). Thus, it is possi- gress, ensure that the environment is conducive to
ble that CI efficacy is more contingent on strate- training and that the program is working appropri-
gies gleaned from practice rather than specific ately, encourage feedback, and facilitate generaliza-
intervention content or type of CI. tion of learning (Roche and Johnson 2014).
904 Computerized Treatment

According to the INCOG (International Cog- Gomar, J. J., Valls, E., Radua, J., Mareca, C., Tristany, J.,
nitive) guidelines, while computerized interven- del Olmo, F., et al. (2015). A multisite, randomized
controlled clinical trial of computerized cognitive
tions may be utilized as supplement to cognitive remediation therapy for schizophrenia. Schizophrenia
rehabilitation, those interventions performed not Bulletin, 41(6), 1387–1396. https://doi.org/10.1093/
in the presence of a treating therapist will not lead schbul/sbv059.
to improvement in daily functioning (Ponsford Gross, A. L., Parisi, J. M., Spira, A. P., Kueider, A. M., Ko,
J. Y., Saczynski, J. S., et al. (2012). Memory training
et al. 2014). These guidelines advocate the pres- interventions for older adults: A meta-analysis. Aging
ence of a trained rehabilitation clinician who is & Mental Health, 16(6), 722–734. https://doi.org/
able to identify relevant compensatory and meta- 10.1080/13607863.2012.667783.
cognitive strategies. Hardy, J. L., Nelson, R. A., Thomason, M. E., Sternberg,
D. A., Katovich, K., Farzin, F., & Scanlon, M. (2015).
Enhancing cognitive abilities with comprehensive
training: A large, online, randomized, active-controlled
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10.1097/HTR.0000000000000072. Grace-Anna Chaney
Rabipour, S., & Raz, A. (2012). Training the brain: Fact Department of Psychology, Towson University,
and fad in cognitive and behavioral remediation. Brain Towson, MD, USA
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10.1016/j.bandc.2012.02.006.
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trial. JAMA Pediatrics, https://doi.org/10.1001/ Abstraction; Conceptualization; Ideas; Notion;
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R. F., Mahncke, H. W., & Zelinski, E. M. (2009). A concept is a special combination of ideas that
A cognitive training program based on principles of has a particular meaning (Hampton 1981, 1995;
brain plasticity: Results from the improvement in mem-
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an attention-training program. Journal of Clinical
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https://doi.org/10.1080/01688638708405352. ence and reasoning (Li et al. 2015). Concepts derive
Twamley, E. (2016). Cogsmart. Retrieved from from the integration of real-world entities with their
www.cogsmart.com.
Vermeij, A., Kessels, R. P., Heskamp, L., Simons, E. M., purpose and everyday uses (Li et al. 2015). Chil-
Dautzenberg, P. L., & Claassen, J. A. (2016). Prefrontal dren acquire their first concepts during the discov-
activation may predict working-memory training gain in ery language process that occurs between birth and
normal aging and mild cognitive impairment. Brain age of 3. During that period of development, chil-
Imaging and Behavior. https://doi.org/10.1007/s11682-
016-9508-7. dren start to recognize regularities in their world
Yoo, C., Yong, M. H., Chung, J., & Yang, Y. (2015). Effect and begin to identify labels or symbols to represent
of computerized cognitive rehabilitation program on them (Macnamara 1982). Thereafter, concept
906 Concept Learning

learning is governed by receptive language learn- forming global concept and then modifying them
ing whereby new concepts are created by asking in accordance with rewards and punishments. For
questions and expanding on acquired meanings example, a person may realize that speeding is
(Novak and Canas 2010). Rules are concepts that dangerous but will continue to do so until he or
direct behavior because there are consequences she gets a ticket. Trial and error is the tendency to
attached to them. A hypothesis relates two or “just keep trying until something works.” For
more concepts with a prediction. Hypothesis test- example, when our computer stops working unex-
ing, rule learning, concept learning, and problem- pectedly, we often press any and all of the various
solving are all interrelated skills (Bourne 1963; keys until it responds. Aspects of the task that
Bruner et al. 1956). Concept learning is how we improve concept acquisition include an orderly
as humans learn to divide our environment into arrangement of the items the person must use to
examples and non-examples of things we under- form the concept. A compact display in which all
stand (Smith 1990; Smith and Medin 1981). Rule the aspects of the concept are present also
learning is the process of associating concepts with improves acquisition. Sequential problems must
consequences. Hypothesis testing is a person’s abil- present a consistent concept. The saliency, nov-
ity to try out several possible concepts, solutions, or elty, and complexity of the concept and whether
rules in a systematic way to determine which is the feedback is provided also affect how quickly a
most useful. person learns it. Concept maps were created as
Cognitive psychologists describe concepts in graphic tools to organize and represent knowl-
terms of prototypes, schemas, attributions, or edge, as well as the relationship between concepts
exemplars. Prototypes are learned typical repre- (Novak and Canas 2010). Organized in a hierar-
sentations of a concept. For example, a compact chical fashion, the concepts at the top of the map
car is small, gets good gas mileage, and is a are more specific and the less general concepts are
Toyota or Mini Cooper. Schemas are scripts that arranged at the bottom. According to Novak and
we learn for behaving or for evaluating behavior. Canas (2010), the most powerful use of concept
For example, an introduction usually involves a maps is that they present a conceptually clear
greeting, a smile, and a handshake. Attributions visual or diagrammatic picture of the concept
are collections of behavioral adjectives and and how it relates to other concepts through the
adverbs that define our notion of a person, place, use of prior knowledge.
or behavior, (Medin 1989), For example, demo-
crats are liberals who promote social programs,
whereas republicans are conservatives, who sup- See Also
port the military. Exemplars are collections of
examples of concepts that are stored in memory. ▶ Learning
For example, observing people in public places ▶ Reasoning
defines our concept of “everyday people.” There ▶ Retrieval Techniques
are several strategies people use to form concepts.
Conservative focus involves gradual manipula-
tion of one aspect of a complex concept at a time Further Readings
until the concept clarifies. For example, when a
flashlight will not start then our first response may Bourne, L. E. (1963). Some factors affecting strategies
used in problems of concept formation. American Jour-
be to replace the batteries. If that does not solve nal of psychology, 75, 229–238.
the problem then we may replace the bulb. Focus Bruner, J. S., Goodnow, J., & Austin, G. A. (1956). A study
gambling tests several possible hypotheses at the of thinking. New York: Wiley.
same time instead of one at a time (Bruner et al. Hampton, J. A. (1981). An investigation of the nature of
abstract concepts. Memory and Cognition, 9, 149–156.
1956). For example, the same person may replace
Hampton, J. A. (1995). Psychological representation of
the batteries and bulb at the same time in their concepts. In M. A. Comway (Ed.), Cognitive models
effort to fix the flashlight. Scanning involves of memory. Cambridge, MA: MIT Press.
Concussion 907

Hunt, R. R., & Ellis, H. C. (2003). Fundamentals of cog- Giza and Hovda (2014) and Hovda et al. (1999)
nitive psychology. Madison: Brown & Benchmark. expertly describe the abnormal neurometabolic
Lamberts, K., & Shanks, D. (Eds.). (1997). Knowledge,
concepts, and categories. Cambridge, MA: MIT Press. processes associated with concussion. Early clin-
Li, J., Mei, C., Xu, W., & Qian, Y. (2015). Concept learning ical signs of concussion include alteration of men-
via granular computing: A cognitive viewpoint. Infor- tal status or behavior and can be accompanied by
mation Sciences, 298447–298467. https://doi.org/ other symptoms outlined below (see mild trau-
10.1016/j.ins.2014.12.010.
Macnamara, J. (1982). Names for things: A study of human matic brain injury). C
learning. Cambridge, MA: MIT Press.
Medin, D. L. (1989). Concepts and conceptual structure. Diagnosis
American Psychologist, 44, 1469–1481. Diagnosis of concussion is made based on identify-
Mervis, C. B., & Rosch, E. (1981). Categorization of natural
objects. Annual Review of Psychology, 32, 89–115. ing an event with adequate biomechanical force to
Nisbett, R. E. (Ed.). (1993). Rules for reasoning. Hillsdale: cause a concussive injury and by examining acute
Erlbaum. injury severity indicators. Common mechanisms
Novak, J. D., & Cañas, A. J. (2010). A teoria subjacente associated with concussion include a motor vehicle
aos mapas conceituais e como elabora-los e USA- los.
Revista Práxis Educativa, 5(1), 9–29. Website for the accident, fall, assault, or contact sports. In addition
reference above (in English) http://cmap.ihmc.us/Publi to a direct blow to the head, a concussion can result
cations/researchPapers/theorycmaps/Theoryunderlying from rapid acceleration, deceleration, rotational or
ConceptMaps.bck-11-01-06.htm. percussive forces that affect brain tissue. Injury
Smith, E. E. (1990). Categorization. In D. N. Osherson & E.
E. Smith (Eds.), Thinking: An invitation to cognitive severity indicators frequently used to diagnose con-
science (Vol. 3, pp 33–53). Cambridge, MA: MIT Press. cussion include alteration of consciousness (confu-
Smith, E. E., & Medin, D. L. (1981). Categories and sion), loss of consciousness (LOC), post-traumatic
concepts. Cambridge, MA: Harvard University Press. anterograde amnesia (PTA), retrograde amnesia,
Wason, P. C. (1960). On the failure to eliminate hypotheses
in a conceptual task. Quarterly Journal of Experimen- and Glasgow Coma Scale (GCS; Teasdale and
tal Psychology, 12, 129–140. Jennett 1974). Standard neurological examination
and neuroimaging studies are frequently normal
following concussion (i.e., have limited sensitivity)
so should not be relied on to diagnose concussion.
Concussion

Matthew R. Powell1 and Michael McCrea2 Current Knowledge

1
Division of Neurocognitive Disorders,
Department of Psychiatry and Psychology, Mayo Epidemiology
Clinic, Rochester, MN, USA Current epidemiology statistics likely grossly
2
Department of Neurosurgery and Neurology, underestimate the true incidence of concussion
Medical College of Wisconsin, Milwaukee, WI, because of imprecise surveillance systems (e.g.,
USA many individuals with concussive injury never
seek medical care and those who do seek care are
frequently not hospitalized), and because current
Synonyms estimates are clouded by variable research method-
ologies and inconsistent definitions of concussion
Mild traumatic brain injury; Sport-related (McCrea 2008; National Center for Injury Preven-
concussion tion and Control 2003). Epidemiology is discussed
further in the mild brain traumatic brain injury and
sport-related concussion entries.
Definition
Recovery and Outcome Post Concussion
A concussion is a trauma-induced alteration in Concussions fall under the general rubric of
neurological function (Giza and Hovda 2014). MTBI and are sometimes graded by severity
908 Concussion

(e.g., grade 1–3 concussion). More significant con- crucial for tracking recovery following injury.
cussive injury is thought to be associated with This will help providers determine when it is
greater length of altered consciousness, LOC, or appropriate for patients to resume prior activities,
amnesia, although concussive injury often occurs such as contact sports, academics, or work. Indi-
without observed LOC or measurable amnesia. viduals recovering from concussion appear to be
Generally speaking, acute neurologic, behavioral, more vulnerable for re-injury or catastrophic injury.
or cognitive symptoms begin acutely and resolve Neurocognitive testing can objectively track cog-
within 7–10 days, with a small percentage of nitive recovery over time and can contribute valu-
individuals exhibiting clinical symptoms beyond able information to the return to play decision-
3 months (Belanger and Vanderploeg 2005; making process. See McCrory et al. (2013) for an
Iverson 2005; McCrea 2008). Providers should excellent discussion of issues involved in manage-
expect a relatively rapid and full recovery for ment of sports-related concussion, principles of
patients following a concussion, but there is evi- which can be applied to management of concus-
dence of longer recovery periods for post- sions resulting from any mechanism.
concussive symptoms (Dikmen et al. 2016;
Williams et al. 1990). Although animal models
and functional imaging studies demonstrate a neu-
References and Readings
rophysiologic recovery curve that follows a very
similar timeframe as recovery of clinical symp- Belanger, H. G., & Vanderploeg, R. D. (2005). The neuro-
toms post-injury, the full timeframe for “brain psychological impact of sports-related concussion: A
recovery” remains a focus of ongoing study meta-analysis. Journal of the International Neuropsy-
chological Society, 11, 345–357.
(Giza and Hovda 2014).
Dikmen, S., Machamer, J., & Temkin, N. (2016). Mild
traumatic brain injury: Longitudinal study of cognition,
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Early evaluation of symptoms and neurological nal of Neurotrauma, 33, 1–7.
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status is essential following concussion to diag-
neurometabolic cascade of concussion. Neurosurgery,
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Bergsneider, M., & Martin, N. A. (1999). Neurobiol-
imaging of the brain is frequently ordered by
ogy of concussion. In J. E. Bailes, M. R. Lovell, & J. C.
medical specialists because it continues to be the Maroon (Eds.), Sports-related concussion (pp. 12–51).
most sensitive procedure for detecting acute intra- St. Louis: Quality Medical.
cranial abnormalities post injury. Iverson, G. L. (2005). Outcome from mild traumatic brain
injury. Current Opinion in Psychiatry, 18, 301–317.
While spontaneous improvement over days to
Kelly, J. P., & Rosenberg, J. H. (1997). Diagnosis and
weeks is expected for most patients, behavioral management of concussion in sports. Neurology, 48
management (e.g., education, cognitive-behavioral (3), 575–580.
therapy, or active rehabilitation approaches) may McCrea, M. (2008). Mild traumatic brain injury and post-
concussion syndrome: The new evidence base for diag-
minimize the likelihood of a suboptimal outcome
nosis and treatment. New York: Oxford University Press.
or increase quality of life for patients at risk for McCrea, M., & Powell, M. R. (2012). The concussion
postconcussive syndrome (Mittenberg et al. 2001, clinic: A practical, evidence based model for assess-
1996; McCrea and Powell 2012). Behavioral inter- ment and management of sport related concussion.
Journal of Clinical Sport Psychology, 6, 275–292.
ventions help patients develop accurate self- McCrory, P., Meeuwisse, W., Aubry, M., Cantu, B., Dvorak,
appraisals, hopefully early in the course of recov- J., Echemendia, R. J., et al. (2013). Consensus statement
ery, and promote gradual resumption of activities, on concussion in sport – the 4th international conference
which minimizes deconditioning. Pharmacologic on concussion in sport held in Zurich, November 2012.
Clinical Journal of Sport Medicine, 23(2), 89–117.
intervention for certain symptoms, such as pain,
https://doi.org/10.1097/JSM.0b013e31828b67cf.
insomnia, or mood disturbance, may also be indi- Mittenberg, W., Tremont, G., Zielinski, R. E., Fichera, S.,
cated. Post-acute evaluation and monitoring is & Rayls, K. (1996). Cognitive-behavioral prevention
Conduct Disorder 909

of postconcussion syndrome. Archives of Clinical Neu- Categorization

ropsychology, 11(2), 139–145.
Mittenberg, W., Canyock, E. M., Condit, D., & Patton, C.
(2001). Treatment of post-concussion syndrome fol- The disorder is classified with the disruptive,
lowing mild head injury. Journal of Clinical and Exper- impulse-control, and conduct disorders in DSM-5.
imental Neuropsychology, 23(6), 829–836.
National Center for Injury Prevention and Control. (2003).
Report to congress on mild traumatic brain injury in
the United States: Steps to prevent a serious public Current Knowledge C
health problem. Atlanta: Centers for Disease Control
and Prevention. Development and Course
Teasdale, G., & Jennett, B. (1974). Assessment of coma The prevalence rate of CD is estimated to be
and impaired consciousness: A practical scale. The
Lancet, 2(7872), 81–84. between 2% and 10% (American Psychiatric Asso-
Williams, D. H., Levin, H. S., & Eisenberg, H. M. (1990). ciation 2013). Symptoms of CD may begin in child-
Mild head injury classification. Neurosurgery, 27(3), hood or adolescence, with earlier onset being
422–428. predictive of a worse prognosis. Onset during child-
hood is more common among males and is associ-
ated with aggression, poorer relationships with
peers, and a higher risk for development of criminal
Conduct Disorder or antisocial behavior. There is less of a gender
discrepancy among individuals with onset during
Daniel W. Klyce adolescence. Onset during adolescence is also asso-
Virginia Commonwealth University – School of ciated with better peer relationships (though often
Medicine, Richmond, VA, USA with delinquent peers), more problems with author-
ity, and a lower likelihood of symptoms that persist
into adulthood. Symptoms of CD are associated
Synonyms with negative outcomes such as disruption in work
or school, negative health consequences (i.e., inju-
Delinquent or antisocial behavior; Externalizing ries, acquired disease), and legal consequences.
behavior Individuals with a diagnosis of CD tend to interpret
ambiguity in social situations as more threatening,
often contributing to a response they feel to be
Short Description or Definition justified though disproportionate to the situation.

Conduct disorder (CD) is defined in the Diagnostic Associated Disorders and Current Research
and Statistical Manual of Mental Disorders (5th The onset of CD is commonly preceded by symp-
ed.; DSM-5; American Psychiatric Association toms of oppositional defiant disorder; as such,
2013) by a pattern of behavior that violates the these two disorders are often studied together.
rights of others or societal norms. Symptoms of Childhood onset of CD is also associated with
CD involve aggression toward people or animals, attention deficit/hyperactivity disorder and other
destruction of property, deceitfulness or theft, and neurodevelopmental disorders. Individuals with
serious violations of rules. At least three symptoms CD are at higher risk for later development of
must have been present in the last 12 months. The multiple mental health disorders, including
pattern of behavior represents a significant disrup- mood, anxiety, somatic, substance use, psychotic,
tion in social function. The diagnosis may be spec- and trauma/stressor-related disorders.
ified “with limited prosocial emotions” if at least Several familial and community risk factors
two of the following characteristics are noted: (1) are associated with CD. Familial risk factors
lack of remorse or guilt, (2) callousness – lack of include a history of abuse or neglect, inconsistent
empathy, (3) unconcern about performance, or (4) parenting, and unstable living situations. Commu-
shallow or deficient affect. nity risk factors include exposure to violence,
910 Conduction Aphasia

poor peer influences, and peer rejection. Causal Nigg, J. T., & Huang-Pollock, C. L. (2003). An early-onset
factors are more likely to be interrelated than model of the role of executive functions and intelli-
gence in conduct disorder/delinquency. In B. B.
distinct and likely involve an interplay of biolog- Lahey, T. E. Moffitt, & A. Caspi (Eds.), Causes of
ical, emotional, familiar, peer, and community conduct disorder and juvenile delinquency (pp.
variables. Recent research on CD has focused on 227–253). New York: The Guilford Press.
callous-unemotional traits among individuals
with this diagnosis, as well as possible subtypes
of the childhood-onset type. Neuroimaging stud-
ies involving children with CD have implicated
Conduction Aphasia
dysfunction in frontal and temporal structures
Lyn S. Turkstra
(Moffitt et al. 2008), which is generally consistent
School of Rehabilitation Science, McMaster
with research associating deficits in executive
University, Hamilton, ON, Canada
function and emotional processing with a diagno-
sis of CD (Nigg and Huang-Pollock 2003).
Synonyms
Assessment and Treatment
Diagnosing CD should involve multiple informants
Associative aphasia
and assessment modalities. Such a method is par-
ticularly important to identify individuals who may
be specified to have “limited prosocial emotions,”
Short Description
as these individuals would be unlikely to endorse
this pattern of function through self-report. Treat-
Conduction aphasia is a subtype of fluent aphasia
ment for CD tends to focus on preventive interven-
that is characterized by fluent speech and relatively
tions for children who are at risk, implementation of
intact language comprehension, but significantly
contingency management programs, and parent
impaired repetition. Utterance length is normal or
training interventions with emphasis on behavior
increased, and speech has normal prosody and
management strategies (Frick and Dickens 2006).
grammar and is produced with normal effort.
There is a reduction in content words, paraphasic
errors are common, and oral reading is impaired.
See Also

▶ Antisocial Personality Disorder Categorization

▶ Disruptive, Impulse-Control, and Conduct
Disorders Conduction aphasia is differentiated from other
▶ Oppositional Defiant Disorder types of fluent aphasia (Wernicke’s aphasia, trans-
cortical sensory aphasia, and anomic aphasia) by
the disproportionate impairment in repetition rel-
References ative to comprehension and spontaneous produc-
tion. It is differentiated from Wernicke’s aphasia
American Psychiatric Association. (2013). Diagnostic and in particular by the patient’s awareness of his or
statistical manual of mental disorders (5th ed.). Arling- her paraphasic errors.
ton: American Psychiatric Association Publishing.
Frick, P. J., & Dickens, C. (2006). Current perspectives on
conduct disorder. Current Psychiatry Reports, 8,
59–72. Natural History, Prognostic Factors, and
Moffitt, T. E., Arseneault, L., Jaffee, S. R., Kim-Cohen, J., Outcomes
Koenen, K. C., Odgers, C. L., Slutske, W. S., & Viding,
E. (2008). Research review: DSM-V conduct disorder:
research needs for an evidence base. Journal of Child The prognosis for recovery of functional commu-
Psychology and Psychiatry, 49(1), 3–33. nication in individual with conduction aphasia
Confabulation 911

depends on the underlying cause of the aphasia as picture), and repetition, so that the relative perfor-
well as factors such as the size of lesion and the mance in these modalities can be compared.
patient’s age, premorbid language skills, and
comorbid health conditions. Individuals who ini-
tially present with conduction aphasia often evolve Treatment
to a clinical profile of anomic aphasia, with rela-
tively good auditory and reading comprehension, There is no specific treatment for conduction C
and deficits primarily in word-finding and the com- aphasia, beyond therapies that are appropriate
prehension and production of complex syntax. for aphasia in general (see “▶ Aphasia”).

Neuropsychology and Psychology of Cross-References

Conduction Aphasia
▶ Aphasia
Conduction aphasia historically has been attributed ▶ Nonfluent Aphasia
to the interruption of white matter pathways, nota-
bly the arcuate fasciculus (part of the superior
longitudinal fasciculus), which connects posterior References and Readings
and anterior cortical structures involved in lan-
guage comprehension and production. Thus, con- Catani, M., & Ffytche, D. H. (2005). The rises and falls of
disconnection syndromes. Brain, 128(Pt 10),
duction aphasia historically was referred to as a
2224–2239.
“disconnection syndrome” (Geschwind 1965). Geschwind, N. (1965). Disconnexion syndromes in ani-
Lesion and imaging studies have revealed, how- mals and man. II. Brain, 88, 585–644.
ever, that conduction aphasia may result from Goodglass, H. (1993). Understanding Aphasia. San Diego:
Academic.
lesions in a variety of locations and that arcuate
Quigg, M., Geldmacher, D. S., & Elias, W. J. (2006).
fasciculus lesions are instead implicated in the pro- Conduction aphasia as a function of the dominant pos-
duction of repetitive, stereotypic utterances (stereo- terior perisylvian cortex: Report of two cases. Journal
typies). This is consistent with the finding that the of Neurosurgery, 104, 845–848.
arcuate fasciculus is spared in many patients with
conduction aphasia (Quigg et al. 2006). By contrast
to the localization or modular view of Geschwind
and others, researchers in connectionist theory Confabulation
have conceptualized language as the product of a
distributed cortical network that can be disrupted in Farzin Irani1 and David J. Libon2
1
various ways to produce similar phenotypes. The Psychology Department, West Chester
advent of functional imaging resurrected the notion University of Pennsylvania, West Chester, PA,
of disconnection syndromes and more modular USA
2
notions of language (Catani and Ffytche 2005), Departments of Geriatrics, Gerontology, and
and the current view is somewhere in between a Psychology, Rowan University, New Jersey
modular and connectionist perspective. Institute for Successful Aging, School of
Osteopathic Medicine, Stratford, NJ, USA

Evaluation
Description
The signs and symptoms of conduction aphasia
will be revealed only with testing of auditory and Korsakoff initially described “pseudoreminiscences”
reading comprehension, connected language pro- in alcoholic patients with amnesia who made up
duction (e.g., asking the patient to describe a fictitious stories about events that did not occur. In
912 Confabulation

their translation of Kosakoff’s original work, Vic- often in the context of memory testing, or sponta-
tor and Yakovlev note that Korsakoff first identi- neous confabulations occurring without any exter-
fied patients with a “psychic disorder in nal trigger (Kopelman 1987). The boundaries
conjunction with multiple neuritis” who presented between provoked/spontaneous and momentary/
with “a derangement of memory and of the asso- fantastic confabulations are often blurred, with
ciation of ideas” along with other symptoms of the many authors mixing these characteristics when
now well-known Korsakoff syndrome (Korsakoff describing the symptoms. Some have argued
1955). Later, the term confabulation was intro- against such categorizations and instead suggested
duced and defined as the “falsification of memory that confabulation should be regarded as a contin-
occurring in clear consciousness in association uous variable, ranging from minor distortions to
with an organically derived amnesia” (Berlyne more dramatic fantasies (Metcalf et al. 2007).
1972). It has also been referred to as “true memo-
ries that have been misplaced in both time and
place” (Kopelman 1987) as well as the “spontane- Neuropsychology of Confabulation
ous narrative reports of events that never hap-
pened.” More recently, confabulation has been Studies using neuropsychological test performance
defined as “statements or actions that involve dis- to examine mechanisms of confabulation have not
tortions of memories” (Metcalf et al. 2007). yielded consistent results. Observations of persev-
Confabulation, as a symptom, has been erative responses in individuals who confabulate
described in a number of disorders including strokes have implicated frontal executive dysfunction (e.g.,
(particularly anterior communicating artery), trau- Kopelman et al. 1997). Others have argued for
matic brain injuries, dementia, metabolic disorders, more prominence of memory impairments rather
and psychiatric disorders. Confabulations are men- than executive dysfunction (e.g., Dalla Barba
tioned as a probable symptom in most of the 1993). A combination of executive and memory
descriptions of Korsakoff’s syndrome, despite deficits may be involved. Memory impairment may
ambiguous clinical diagnostic guidelines explain the presence or absence of confabulation,
(Borsutzky et al. 2008). For instance, the ICD-10 but the severity of confabulation may be influenced
mentions confabulations as a probable but not by the extent of executive dysfunction (Fischer
obligatory symptom for diagnosing an “alcohol- et al. 1995). Clinical lesion studies have implicated
induced amnesic syndrome,” while the Diagnostic the medial prefrontal cortex in spontaneous con-
and Statistical Manual of Mental Disorders- fabulations, particularly the orbitofrontal region
Fifth Edition (DSM-5) indicates diagnoses of (Schnider 2003). Damage to limbic structures
alcohol-induced major neurocognitive disorder, involved in memory is also likely to be required
nonamnestic-confabulatory type (F10.27, F10.97), for confabulations to occur (Fischer et al. 1995).
or amnestic-confabulatory type (F10.26, F10.96). The literature on anterior communicating artery
aneurysms (ACoA) has implicated frontal struc-
tures as a necessary site of neuropathology in con-
Categorization fabulation, although cases of nonamnestic ACoA
patients with frontal lesions who do not confabu-
There are different descriptions of confabulation late have suggested that both frontal lobe and basal
used by several authors. Momentary confabula- forebrain structures may be needed for spontaneous
tions have been described as brief, partially accu- confabulations (DeLuca and Diamond 1995).
rate responses often inaccurately localized in time Four types of cognitive models have been pro-
(Victor and Ropper 2001). Fantastic or productive posed to account for confabulations:
confabulations have been described as
more elaborate fictitious stories (Berlyne 1972). 1. Source monitoring theory. This view was ini-
Further distinctions have been made between con- tially promoted by Johnson et al. (1993) who
fabulations that are provoked by direct questions, argued that individuals who confabulate are
Confabulation 913

unable to accurately monitor the source of their confabulation. Specifically, confabulation is

memories which results in errors and confu- thought to be the result of a faulty “strategic
sion. According to this view, patients who con- retrieval” search and inaccurate ordering and
fabulate cannot accurately identify where or placement of memories in context. According
when events occur. They may also be unable to this view, strategic retrieval is dependent
to differentiate between whether a representa- upon executive processes and is self-initiated
tion is “real” or not due to impairments in being and goal directed, while associative retrieval is C
able to access qualitative characteristics of the automatic and independent of executive
representation such as details about perceptual, processes. Confabulators are thought to show
contextual, affective, and semantic informa- deficiencies in strategic retrieval, influenced
tion. Furthermore, secondary evaluation defi- by deficiencies in the neocortical/prefrontal/
cits may also lead to the over-inclusive hippocampal network hypothesized to be
acceptance of memories. Damage to frontal involved in strategic retrieval.
areas, especially ventromedial prefrontal cor- 4. Three-factor cognitive neuropsychological
tex, can result in profound source misattribu- theory. Metcalf et al. (2007) propose a three-
tions that are clinically classified as factor combined model that hypothesizes inter-
confabulations (Johnson et al. 2011). play between an executive control retrieval
2. Temporal context theory. Dalla Barba et al. deficit, an evaluation deficit, and a person’s
(1998) have suggested that the primary impair- individual emotional/motivational biases. Spe-
ment in confabulation is a difficulty with “tem- cifically, according to this view, confabulatory
poral consciousness.” According to this view, symptoms and content are the result of a failure
patients who confabulate are confused about of executive control that causes an impaired
the temporal order of information retrieved search and selection of appropriate memories
from memory. While knowledge of time is from the autobiographical episodic memory
preserved and patients are aware of a past, store. Confabulators are purportedly unable to
present, and future, they are unable to make critically evaluate material from their autobio-
correct temporal judgments about their memo- graphical or general semantic store and accept
ries, resulting in sequencing errors. Schnider confabulations as real memories. Further, per-
(2003) has also argued that there is confusion sonal biases may be involved in the preferen-
between presently relevant and irrelevant tial selection of memories that are emotionally
memories, resulting in a failure to suppress biased.
activated but presently irrelevant memory
traces. Neuroanatomically, Schnider et al.
have linked confabulation with the posterior Evaluation
orbitofrontal cortex and the anterior limbic
structures directly connected with it. Schnider Since Korsakoff’s initial description in 1955 of
argues that the adaptation of thought and “pseudoreminiscences” in alcoholic patients with
behavior to ongoing reality is mediated by the amnesia who made up fictitious stories about
anterior limbic system which acts by events that did not occur, there has been consid-
suppressing activated memory traces that do erable variability in how confabulation is defined,
not pertain to ongoing reality. In patients who identified, assessed, and understood. For instance,
confabulate, this monitoring of ongoing reality it remains debated whether confabulations are
in thought goes awry and appears to be related readily differentiated from delusions. Some have
to the brain’s reward system. argued that confabulations are not different from
3. Retrieval theory. This view has been primarily delusions since both are held firmly over time.
promoted by Moscovitch and Melo (1997) Others have viewed confabulations, delusions,
who argue that deficient strategic retrieval pro- hallucinations, and insight as part of a continuum.
cesses and monitoring deficits influence Still others have argued that delusions and
914 Confabulation

confabulations differ since confabulations tend to mild to moderate Alzheimer’s disease (El Haj and
be associated with partially valid memories that Laroi 2017). Overall, the concept of confabulation
can be traced to real events. Recent work has remains elusive, and its underlying mechanisms
indicated that confabulation associated with psy- remain an area requiring further understanding.
chiatric disorders (e.g., schizophrenia) differs
from that in other neuropsychiatric conditions
since schizophrenia patients tend to (1) restruc- Treatment
ture/reorganize the original information and are
constrained by the context of the original infor- Treatment is determined in part by etiology. Some
mation; (2) do not show a strong association with have proposed that rehabilitation efforts should
executive function deficit, but instead show avoid memory training and repeated questions
semantic memory and verbal comprehension def- about orientation. For instance, according to
icits associated with their confabulations; and Schnider (2003), it may be easier for a confabu-
(3) associate their confabulations with positive lating patient to “accept that her baby has already
symptoms like formal thought disorder and delu- received food than to convince her that her baby is
sions (Shakeel and Docherty 2015). over 30 years old.” Instead, it may be more ben-
Further debate ensues about whether confabu- eficial to promote the engagement of patients in
lations are deliberate attempts to compensate for common everyday activities and accept their false
“memory gaps” due to embarrassment or whether interpretation of reality until spontaneous confab-
they involve source monitoring, temporal context, ulations resolve (Schnider). Many spontaneous
or retrieval difficulties that result in an implausible confabulations eventually resolve. In a study of
or fictional output. Confabulation, particularly fol- eight spontaneous confabulators, almost all
lowing ACoA aneurysms, has also been viewed as stopped confabulating 18 months later and
representing differences in degree and not kind. regained correct orientation in time and place, as
Other important variables identified in the under- well as the ability to refer thinking and acting to
standing of confabulation have included making ongoing reality (Schnider et al. 2000). Specifi-
the distinction between an “unaware” or “aware” cally, “temporal context confusion” based on an
process, premorbid personality factors, the need for inability to suppress intrusions of currently irrele-
coexistence of amnesia, differentiation from an vant memory traces into ongoing thinking para-
acute confusional state, disconnection syndrome, lleled the course of spontaneous confabulations in
and whether indifference/apathy or deceit/lying is this study. Patients with isolated, less extensive,
involved (DeLuca 2000). There has been further orbitofrontal lesions stopped confabulating within
variability in decisions on how to label an individ- a few weeks and had the best neuropsychological
ual as a “confabulator.” Some have used the term outcomes. Patients with additional basal forebrain
based on clinical observations of spontaneous or lesions continued to confabulate for several
provoked production of fabricated stories follow- months and remained amnestic. One patient with
ing brain injury. Other researchers have labeled extensive orbitofrontal damage and perirhinal cor-
individuals as confabulators based on the number tex damage continued to confabulate after more
or quality of intrusions/confabulations produced than 3 years. Interdisciplinary approaches for the
during standardized neuropsychological tests or rehabilitation of confabulation in the treatment of
experimental tasks. Evaluation of confabulations patients with ACoA aneurysms have also been
in Alzheimer’s disease has also been conducted suggested, including a three-tiered approach
using the confabulatory interview which consists focused on improving (1) intellectual awareness,
of questions tapping general personal knowledge, the ability to understand that one has an impair-
specific personal memories, knowledge of famous ment; (2) emergent awareness, the ability to rec-
facts and famous people, and personal future plans ognize a problem when it is occurring; and (3) the
(Dalla Barba 1993). Provoked confabulations are ability to anticipate that a problem (confabulation)
more common than spontaneous confabulations in is going to occur (DeLuca 1992). In one case,
Confidentiality 915

improvements in executive functioning using this of their prevalence and relation with general cognitive
rehabilitation approach removed obstacles to and executive functioning. Psychiatry and Clinical
Neurosciences, 71, 61–69.
vocational activity and social functioning by Fischer, R. S., Alexander, M. P., D’Esposito, M., & Otto,
improving the patient’s awareness of his difficul- R. (1995). Neuropsychological and neuroanatomical
ties and enabling utilization of compensatory correlates of confabulation. Journal of Clinical and
strategies (DeLuca and Locker 1996). Recent Experimental Neuropsychology, 17(1), 20–28.
experimental work with children has indicated
Johnson, M. K., Hashtroudi, S., & Lindsay, D. S. (1993).
Source monitoring. Psychological Bulletin, 114(1), 3–28.
C
some benefits of metacognitive training to Johnson, M. K., Raye, C. L., Mitchell, K. J., &
resisting confabulation and promoting false- Ankudowich, E. (2011). The cognitive neuroscience
memory editing (Castelli and Ghetti 2014). of true and false memories. In R. F. Belli (Ed.), True
and false recovered memories: Toward a reconciliation
of the debate. Vol. 58: Nebraska symposium on moti-
vation (pp. 15–52). New York: Springer.
Cross-References Kopelman, M. D. (1987). Two types of confabulation.
Journal of Neurology, Neurosurgery, and Psychiatry,
50(11), 1482–1487.
▶ Capgras Syndrome Kopelman, M. D., Stanhope, N., & Kingsley, D. (1997).
▶ Delusion Temporal and spatial context memory in patients with
▶ Intrusion Errors focal frontal, temporal lobe, and diencephalic lesions.
Neuropsychologia, 35(12), 1533–1545.
▶ Reduplicative Paramnesia Korsakoff, S. S. (1955). Psychic disorder in conjunction
▶ Wernicke-Korsakoff Syndrome with peripheral neuritis. Neurology, 5, 394–406.
Metcalf, K., Langdon, R., & Coltheart, M. (2007). Models
of confabulation: A critical review and a new frame-
work. Cognitive Neuropsychology, 24(1), 23–47.
References and Readings Moscovitch, M., & Melo, B. (1997). Strategic retrieval and
the frontal lobes: Evidence from confabulation and
American Psychiatric Association. (2013). Diagnostic and amnesia. Neuropsychologia, 35(7), 1017–1034.
statistical manual of mental disorders (5th ed.). Schnider, A. (2003). Spontaneous confabulation and the
Washington, DC: American Psychiatric Association. adaptation of thought to ongoing reality. Nature
Berlyne, N. (1972). Confabulation. The British Journal of Reviews Neuroscience, 4(8), 662–671.
Psychiatry, 120(554), 31–39. Schnider, A., Ptak, R., von Daniken, C., & Remonda,
Borsutzky, S., Fujiwara, E., Brand, M., & Markowitsch, L. (2000). Recovery from spontaneous confabulations
H. J. (2008). Confabulations in alcoholic Korsakoff parallels recovery of temporal confusion in memory.
patients. Neuropsychologia, 46(13), 3133–3143. Neurology, 55(1), 74–83.
Castelli, P., & Ghetti, S. (2014). Resisting imagination and Shakeel, M., & Docherty, N. M. (2015). Confabulations in
confabulation: effects of metacognitive training. Journal schizophrenia. Cognitive Neuropsychiatry, 20(1), 1–13.
of Experimental and Child Psychology, 126, 339–356. Victor, M., & Ropper, A. H. (Eds.). (2001). Principles of
Dalla Barba, G. (1993). Different patterns of confabula- neurology (7th ed.). New York: The McGraw-Hill
tion. Cortex, 29(4), 567–581. Companies, Inc.
Dalla Barba, G., Mantovan, M. C., Cappelletti, J. Y., &
Denes, G. (1998). Temporal gradient in confabulation.
Cortex, 34(3), 417–426.
DeLuca, J. (1992). Rehabilitation of confabulation: The
issue of unawareness of deficit. NeuroRehabilitation,
2(3), 23–30.
Confidentiality
DeLuca, J. (2000). A cognitive neuroscience perspective on
confabulation. Neuro-psychoanalysis, 2(2), 119–132. Robert L. Heilbronner
DeLuca, J., & Diamond, B. J. (1995). Aneurysm of the Chicago Neuropsychology Group, Chicago, IL,
anterior communicating artery: A review of neuroanatom-
USA
ical and neuropsychological sequelae. Journal of Clinical
and Experimental Neuropsychology, 17(1), 100–121.
DeLuca, J., & Locker, R. (1996). Cognitive rehabilitation
following anterior communicating artery aneurysm Definition
bleeding: A case report. Disability and Rehabilitation,
18(5), 265–272.
El Haj, M., & Laroi, F. (2017). Provoked and spontaneous Confidentiality has been defined as “containing
confabulations in Alzheimer’s disease: An examination information whose unauthorized disclosure could
916 Confirmatory Bias

be prejudicial to the national interest.” In psychol- Melton, G. B., Petrila, J., Poythress, N. G., & Slobogin,
ogy, it is one of the most important components of C. (2007). Psychological evaluations for the courts
(3rd ed.). New York: Guilford.
the Ethical Principles of Psychologists and Code of
Conduct (2002) and the Specialty Guidelines for
Forensic Psychologists (1991). The boundaries of
confidentiality vary based on the setting, that is, Confirmatory Bias
whether it is in the clinical versus forensic realm or
whether it is in the civil versus criminal realm. In Molly E. Zimmerman
treatment settings, clinicians consider confidential- Department of Psychology, Fordham University,
ity of paramount importance, and they are reluctant Bronx, NY, USA
to disclose information obtained from a client even
when there are explicit legal or countervailing eth-
ical mandates to do so (such as when a patient may Definition
harm another). Such a position is unrealistic in the
forensic context because the results of forensic Confirmatory bias occurs when a clinician prefer-
evaluations (be it civil or criminal) are routinely entially accepts or seeks evidence that confirms an
disclosed to third parties. In both clinical and foren- initial hypothesis at the expense of thorough con-
sic contexts, psychologists provide examinees with sideration of emerging contradictory evidence
adequate “informed consent” prior to engaging in (Garb 2003). For example, a clinician may formu-
the examination. In the forensic context, it is the late an initial impression that a client has dementia
duty of forensic psychologists to inform clients of based on a referral question. During the clinical
their legal rights regarding the purpose of an eval- interview, the clinician may focus on questions
uation, the anticipated forensic service, the nature relating to memory and change in activities of
of procedures to be utilized, the limits of confiden- daily living while failing to ask questions that
tiality, who has retained the examiner for the eval- specifically pertain to differential diagnoses, such
uation, who the report may be directed to, and that as major depressive disorder. In neuropsychologi-
anything which is said during the examination cal settings, this generally unintentional bias may
could be included in a report or come up during impair judgment, hamper decision-making, pro-
deposition or trial testimony. Some jurisdictions do duce false reports, and negatively impact the
not provide for confidentiality of mental health assessment approach and interpretation of findings.
evaluations. For example, when an evaluation is To address this bias, the clinician should systemat-
conducted as a result of direct court order, confi- ically review all available data within a hypothesis-
dentiality is not provided. testing framework in an effort to remain as impar-
tial as possible (Weiner and Greene 2007).

Cross-References
Cross-References
▶ Privilege
▶ Hypothesis Testing Approach to Evaluation

References and Readings

References and Readings
American Psychological Association. (2002). Ethical prin-
ciples of psychologists and code of conduct. American Garb, H. N. (2003). Clinical judgment and mechanical pre-
Psychologist, 57, 1060–1073. diction. In I. B. Weiner, D. K. Freedheim, M. Gallagher,
Committee on Ethical Guidelines for Forensic J. A. Schinka, & R. J. Nelson (Eds.), Handbook of
Psychologists. (1991). Specialty guidelines for psychology (pp. 27–42). New York: Wiley.
forensic psychologists. Law and Human Behavior, 15, Weiner, I. B., & Greene, R. L. (2007). Handbook of per-
655–665. sonality assessment. New York: Wiley.
Confrontation Naming 917

Confounding Variables Confrontation Naming

James H. Baños Anastasia Raymer

Department of Medical Education, University of Communication Disorders and Special Education,
Alabama School of Medicine, Birmingham, AL, Old Dominion University, Norfolk, VA, USA
USA C

Synonyms
Synonyms
Word finding
Confound; Extraneous variable; Lurking variable

Definition
Definition
Confrontation naming refers to a type of task used
A confounding variable is an extraneous variable in assessment when problems with anomia or
that obscures the true relation between two other word retrieval are of concern. Confrontation nam-
variables or groups of interest. In experimental ing involves the selection of a specific label
research designs, a confounding variable often corresponding to a viewed picture of an object or
presents as an unintended or undesirable system- action.
atic difference between groups (the independent
variable) that is also systematically related to the
outcome of interest (dependent variable). It hin- Current Knowledge
ders the ability to infer a causal relation between
the variables and can lead to misattributing a Confrontation naming tasks often are incorporated
causal effect to the independent variable (a threat as part of clinical language testing for aphasia to
to internal validity). Potential confounding vari- detect impairments of word-finding abilities, or
ables are most effectively addressed during study anomia, in individuals with neurologic conditions
design (e.g., via random assignment, case control typically affecting the left hemisphere of the brain
matching), but may be addressed to some extent (Race and Hillis 2015). Although word finding
during statistical analysis (e.g., handled as a takes place during the course of sentence genera-
covariate). tion in conversational speech, it is most often tested
clinically in picture confrontation naming tasks
where the vocabulary tested is constrained to
Cross-References known, identified target words. Therefore, word-
finding functions are at times referred to as naming
▶ Analysis of Variance abilities (e.g., Raymer 2015).
▶ Error, Sources of The most common published test of confron-
tation naming is the Boston Naming Test (Kaplan
et al. 2001); other published confrontation nam-
References and Readings ing tests also exist for use in children and adults
with word-finding difficulties (Brownell 2010;
Kazdin, A. E. (Ed.). (2016). Methodological issues & German 2015). Confrontation naming tests
strategies in clinical research (4th ed.). Washington, assess the ability to retrieve different classes of
DC: American Psychological Association.
words, such as pictures of objects to test noun
Pearl, J. (2009). Causality: Models, reasoning, and infer-
ence (2nd ed.). Cambridge: Cambridge University retrieval, or pictures of actions to test verb
Press. retrieval. Although most tests of confrontation
918 Congestive Heart Failure

naming test stimuli from a variety of semantic Definition

categories, some tests can differentiate pictures
according to the semantic category to which they Congestive heart failure (CHF) or heart failure is a
belong, including pictures from a variety of nat- condition in which the heart muscle is unable to
ural categories such as animals, fruits, and vege- pump sufficient blood to adequately supply the
tables and man-made categories such as body’s organs.
furniture, clothing, tools, and transportation (e.
g., Goodglass et al. 2001).
Current Knowledge

Cross-References Common causes of CHF include coronary artery

disease, myocardial infarction, hypertension, car-
▶ Anomia diac valve disease, cardiomyopathy (heart muscle
▶ Anomic Aphasia disease), congenital heart disease, and endocardi-
tis (heart infection). In CHF, the heart continues to
pump, but exercise and activity cause shortness of
References and Readings breath (“dyspnea on exertion” or DOE), fatigue,
weakness, light-headedness, or syncope. Because
Brownell, R. (2010). Receptive and expressive one-word the heart is not pumping the blood completely and
picture vocabulary test (4th ed.). San Antonio: Pearson
effectively, the blood “backs up” into the heart
Publishing.
German, D. J. (2015). Test of word finding (3rd ed.). Aus- chambers and ultimately into the venous system.
tin: Pro-Ed. This causes congestion of the tissues and edema in
Goodglass, H., Kaplan, E., & Barresi, B. (2001). The the legs and internal organs, including the lungs
assessment of aphasia and related disorders (3rd ed.).
(“pulmonary edema”), often resulting in shortness
Philadelphia: Lippincott, Williams & Wilkins.
Kaplan, E., Goodglass, H., & Weintraub, S. (2001). The of breath, especially when lying supine (“ortho-
Boston naming test. Philadelphia: Lippincott, Williams pnea”). Electrocardiogram and certain blood tests
& Wilkins. are usually abnormal, and chest x-ray shows con-
Race, D. C., & Hillis, A. E. (2015). The neural mechanisms
underlying naming. In A. E. Hillis (Ed.), The handbook
gestion of the lungs. Echocardiography is nonin-
of adult language disorders (pp. 151–160). New York: vasive and highly revealing and has the potential
Psychology Press. to provide a quantitative measure of severity of
Raymer, A. M. (2015). Clinical diagnosis and treatment of heart failure as indicated by the proportion of
naming disorders. In A. E. Hillis (Ed.), The handbook
blood in the left ventricle that can be pumped
of adult language disorders (pp. 161–183). New York:
Psychology Press. out by the muscle (“ejection fraction”).
CHF is a chronic condition with acute exacer-
bations during which patients may experience
moderate or significant distress. Chronic conges-
tive heart failure can be managed using a combi-
Congestive Heart Failure nation of interventions that help the patient to
“compensate” for the problems caused by CHF.
Elliot J. Roth Acute pulmonary edema is a medical emergency.
Department of Physical Medicine and Treatment of acute CHF episodes usually consists
Rehabilitation, Northwestern University, of rest, salt reduction, identification, and removal
Feinberg School of Medicine, Chicago, IL, USA of the precipitating factor (such as infection, car-
diac arrhythmia, or other cause), and the use of
select medications that help to improve the
Synonyms pumping ability (“contractility”) of the heart mus-
cle and the capacity of the blood vessels to
Heart failure provide blood supply to other organs. These
Conjugate Gaze 919

medications include angiotensin-converting downward. Disorders in conjugate gaze refer to

enzyme inhibitors, beta-blockers, digoxin, the inability to look in a certain direction with
diuretics (water pills), and vasodilators. At times, both eyes.
valve disease warrants valve replacement surgery,
and extremely severe heart damage may require
cardiac transplantation to prevent death. Usually, Current Knowledge
mild to moderate congestive heart failure can be C
treated with medications, adjustments of exercise Conjugate gaze is mediated in the brain stem by
and activity levels, and medical supervision. the medial longitudinal fasciculus, which is a
nerve tract that connects the abducens, trochlear,
and oculomotor nuclei. These nuclei, in turn, are
Cross-References responsible for the muscles that control eye move-
ments. The left pontine center connects with the
▶ Coronary Disease right frontal center for conjugate gaze to the left,
▶ Echocardiogram and the right pontine center connects with the left
frontal center for conjugate gaze to the right. If
extraocular muscles are not working properly,
References and Readings dysconjugate gaze can result, which can then
cause diplopia. The mechanisms for horizontal
Jessup, M., Abraham, W. T., Casey, D. E., Feldman, A. M., eye movements are better understood than vertical
Francis, G. S., Ganiats, T. G., et al. (2009). Focused
eye movements. As individuals age, the ability to
update: ACCF/AHA guidelines for the diagnosis and
management of heart failure in adults: A report of the look upward tends to decline. Cerebral structures
American College of Cardiology Foundation/Ameri- control when and where the eyes move, and the
can Heart Association task force on practice guidelines, brain stem structures control how they move.
developed in collaboration with the International Soci-
The centers for lateral conjugate gaze are in the
ety for Heart and Lung Transplantation. Circulation,
119, 1977–2016. frontal and occipital cortices. In the frontal lobe,
this area is in the posterior aspect of the frontal
lobes, referred to as the frontal eye fields. This
area is close to the motor strip. The function of the
Conjugate Gaze frontal centers is to control voluntary conjugate eye
movements to the opposite side. The frontal eye
Mary-Ellen Meadows fields (FEF) receive inputs from peristriate, parietal
Division of Cognitive and Behavioral Neurology, and superior temporal cortex, medial pulvinar, and
Brigham and Women’s Hospital, Boston, MA, the dorsomedial nucleus of the thalamus. Stimula-
USA tion of FEF results in contralateral saccades. In
strokes that affect this area, one may see an eye
deviation toward the side of the lesion and away
Synonyms from the paralyzed limb. This usually occurs only
in the acute phase of an infarct. At some point, the
Eye movements; Versional movements patient may be unable to move the eyes away from
the lesion on command. However, they may be able
to follow an object to the opposite side if the occip-
Definition ital lobe center is not damaged. The occipital lobe
centers for lateral conjugate gaze control eye move-
Conjugate gaze is the ability of the eyes to work ment when an individual is following an object to
together or in unison. It refers to the motion of the opposite side. Lesions of the occipital lobe that
both eyes in the same direction at the same time. control lateral conjugate gaze are less common than
The eyes can look laterally (left/right), upward, or lesions of the frontal centers.
920 Conjugate Gaze

Conjugate gaze can be disrupted by stroke or Caloric test – This test can be done in the
trauma, depending on the location of the damage. comatose patient. The patient’s ear canal is irri-
For instance, an intracerebral hemorrhage in the gated with 20 ml of ice-cold water. The eyes
caudate nucleus or putamen will cause conjugate should move toward the ear that is irrigated. If
deviation of eye movements to the side of the the patient’s eyes do not move, the lesion is in the
lesion. Pineal tumors, which can press upon the brain stem. This test should not be used in a
midbrain, can cause paralysis of upward gaze. patient who has possible cervical injuries or who
Deeper damage can affect downward saccades. has blood in the ear canal or a perforated eardrum.
Given the extensive anatomy of control of the Conjugate eye movements allow the eyes to
visual system, damage or dysfunction along any get an image onto the fovea and keep it there. Fast
of the nuclei or tracts integral to eye movements movements or saccades allow images onto the
can result in abnormalities. Eye movements utilize fovea, and slower movements keep them there.
the basal ganglia and cerebellum in their planning Smooth pursuit movements compensate for target
and coordination. Patients with basal ganglia disor- movement. There are several ocular motor
ders may have involuntary, small, or slow eye systems:
movements. Patients with parkinsonian symptoms Saccadic system moves the eyes rapidly (up to
may have a restriction of upgaze. In patients with 800 /s) in order to fixate on new targets in the
progressive supranuclear palsy, a cardinal feature is visual fields. These can be voluntary or a response
the restriction of upgaze, and these patients initially to a verbal command. Reflex saccades can also
complain of difficulties with reading. The flocculus occur to stimuli that are threatening or to a sound
of the cerebellum is important for suppression of in the periphery.
vestibular reflex and for smooth pursuit move- Pursuit system enables the eyes to track slowly
ments. Parts of the vermis help to coordinate sac- moving targets (approximately 70 /s) so the
cades, and damage can result in dysmetric image is stable on the fovea.
saccades. Patients with long-standing frontal lobe Vestibular eye movement subsystem maintains
lesions cannot inhibit inappropriate saccades from a a stable image on the retina during head move-
fixation to a peripheral, visually attractive stimulus ments. The vestibulo-ocular reflex maintains the
that appears suddenly. Frontal seizures with a focus eyes in the same direction in space during head
in or near one eye field may manifest by turning of movements. This is controlled by the semicircular
the eye and head away from the side of the lesion. canals, which respond to rotational acceleration of
Evoked eye movements (doll’s eye test or the head.
oculocephalic reflex) and the caloric response can Optokinetic system complements the vestibular
be used in the examination of an unresponsive eye movement system. It uses reference points in
patient. However, if a patient is in a comatose state the environment to maintain orientation. This sys-
due to drug intoxication or hypothermia, these tests tem uses fixation and pursuit in humans.
may show no response. The assessment is as Vergence system enables the eyes to move
follows: dysconjugately (converge and diverge) in the hor-
Doll’s eye test – This test can be used in either izontal axis to maintain fixation on a moving
the comatose or conscious patient. Hold the target toward or away from the individual. These
patient’s eyes open and rapidly move/rotate the are critical for binocular single vision and depth
head to one side, and hold it there. If the brain perception.
stem reflexes are intact, the eyes will move con-
jugately in the direction opposite to the head rota-
tion. If the injury is in the brain stem, the eyes do Cross-References
not move. If a patient is conscious and can follow
commands, have them fixate on an object. This ▶ Dysconjugate Gaze
test should not be used in a patient who has ▶ Lateral Gaze Palsy
possible cervical injuries. ▶ Saccadic Eye Movements
Conners 3rd Edition (Conners 3; Conners 2008) 921

References and Readings defiance/aggression, and peer/family relations.

Symptoms of distinct diagnoses can be assessed
Lavin, P. J. M., & Weissman, B. (2000). Neuro- with scales that link directly to the Diagnostic and
opthalmology. In W. G. Bradley, R. B. Daroff, G. M.
Statistical Manual of Mental Disorders (DSM-5;
Fenichel, & C. D. Marsden (Eds.), Neurology in clini-
cal practice: Principles of diagnosis and management. American Psychiatric Association 2013) symp-
Boston: Butterworth-Heinemann. tomatic criteria for ADHD, conduct disorder
Marshall, K. G. (2006). Cranial nerve III, IV and VI: (CD), and oppositional defiant disorder (ODD)1. C
Disorders of conjugate gaze. Patient Care Canada,
Anxiety and depression screener items are also
17, 51–57.
Ross, R. T. (1999). How to examine the nervous system included in order to provide coverage of two
(3rd ed.). Stamford: Appleton and Lange. internalizing problems frequently associated
with ADHD. The Conners 3 also provides two
index scores: the Conners 3 ADHD Index and the
Conners 3 Global Index. The assessment also
Conners 3rd Edition (Conners includes validity scales (positive impression, neg-
3; Conners 2008) ative impression, and inconsistency index), severe
conduct critical items, impairment items (home,
C. Keith Conners1, Sara R. Rzepa2, Jenni school, and social settings), and open-ended addi-
Pitkanen3 and Stephanie Mears4 tional questions (additional concerns, strengths).
1
Duke University Medical School, Durham, NC, The Conners 3 offers full-length, short, and
USA index form options. The full-length forms convey
2
Clinical, Education, and Public Safety at MHS the most detailed information of all the forms. The
Inc, Toronto, ON, Canada short forms are useful when the administration of
3
Product Development at MHS Inc., Toronto, ON, the full-length version is not possible or practical
Canada (e.g., when multiple administrations over time are
4
MHS Inc, Toronto, ON, Canada required). The index forms are useful in screening
and treatment monitoring situations. Administra-
tion requires approximately 20 min for the full-
Description length forms, 10 min for the short forms, and
approximately 5 min for the index forms. Raw
The Conners 3rd Edition (Conners 3; Conners, scores are converted to age- and gender-based
2008, 2009), with the Conners 3rd Edition DSM- standard scores (including T-scores and percen-
5 Update (Conners 3 DSM-5 Update; Conners tiles). Results from the DSM-5 symptom scales
2014), the latest version of the Conners Rating are also reported in terms of symptom counts, that
Scales, is a thorough assessment of attention defi- is, whether or not the minimum symptom require-
cit/hyperactivity disorder (ADHD) and its most ments set by the DSM-5 have been met. The
commonly associated problems and disorders in Conners 3 ADHD Index produces a probability
school-aged youth. The Conners 3 is a multi-infor- score, which indicates whether the youth’s scores
mant assessment with forms for parents, teachers, are more like youth with ADHD or with those
and youth. Parent and teacher ratings can be from the general population.
obtained about youth aged 6–18 years, and youth The Conners 3 normative sample consists of
aged 8–18 years can complete the self-report. 3400 assessments (1200 parent, 1200 teacher, and
The assessment features multiple content 1000 self-report assessments) including 50 boys
scales that assess ADHD-related concerns such and 50 girls from each age (6–18 years for the
as inattention and hyperactivity as well as related
problems in executive functioning, learning, 1
An online scoring option remains available to obtain
symptom counts corresponding to the Diagnostic and Sta-
tistical Manual of Mental Disorders (DSM-IV-TR; Amer-
C. Keith Conners: deceased. ican Psychiatric Association 2000).
922 Conners 3rd Edition (Conners 3; Conners 2008)

parent and teacher report, 8–18 years for the self- revision of the Conners Rating Scales, incorpo-
report). The racial/ethnic distribution of this sam- rates the key features of its predecessors with
ple closely matches the US population. Approxi- updated normative data and psychometric proper-
mately 2100 clinical cases were also collected ties, an age range specific to the assessment of
from youth with the following diagnoses: school-aged children, and an increased focus on
ADHD (including all three ADHD subtypes: the assessment of ADHD, associated features, and
ADHD predominantly inattentive type, ADHD the disorders most commonly comorbid with
predominantly hyperactive-impulsive type, and ADHD. The Conners 3 DSM-5 Update outlines
ADHD combined type), disruptive behavior dis- scoring and reporting adjustments and interpreta-
orders, learning disorders, anxiety disorders, tive considerations corresponding to diagnostic
major depressive disorder, bipolar disorder, and criteria amendments published in the Diagnostic
pervasive developmental disorders. and Statistical Manual of Mental Disorders – 5th
Edition (American Psychiatric Association 2013).

Historical Background
Psychometric Data
The first versions of the Conners Parent and
Teacher Rating Scales were developed at the Results of reliability analyses revealed that the
Harriet Lane Clinic of the John Hopkins Hospital Conners 3 forms have high levels of internal con-
in the 1960s during Dr. Leon Eisenberg’s con- sistency, with Cronbach’s alpha ranging from 0.77
trolled studies of psychotherapy and medications. to 0.97 (mean Cronbach’s alpha = 0.90), and
The purpose of the original scales was to serve as excellent temporal stability, with test-retest corre-
the basis for a detailed interview about a child’s lations ranging from 0.71 to 0.98 (mean r = 0.83,
problems. The first version of the parent scale all correlations, p < 0.001). There is also a great
contained items grouped in terms of problems deal of consistency between multiple parent and
(e.g., sleep, eating, temper, friendships, school). teacher ratings of the same youth, with inter-rater
The teacher scale included items related to func- reliability coefficients ranging from 0.52 to 0.94
tioning within the classroom setting (e.g., group (mean r = 0.77, all correlations, p < 0.001).
participation, attitude toward authority). The ear- The Conners 3 Manual reports a variety of stud-
liest research studies on the scales supported the ies demonstrating convergent/divergent validity
research properties of the scales. For example, the through correlations of Conners 3 scales scores
very first study on the teacher scales (Conners with other related measures of childhood psycho-
1969) demonstrated adequate test-retest reliabil- pathology. Overall, scales that assess similar con-
ity. In addition, good sensitivity to drug treatment structs tended to be moderately to strongly
and nondrug therapy effects were established. intercorrelated, while scales that did not assess sim-
The scales were first formally published in ilar constructs tended to have smaller correlations.
1989 as the Conners Rating Scales (CRS™, Table 1 provides highlights from these analyses.
Conners 1989, 1990) and offered a standard for- Results from discriminative validity analyses
mat with normative data, detailed information indicated that the Conners 3 scores accurately
about the psychometric properties and the proper discriminate between relevant groups. Results
use of the scales, and the hand-scorable from a series of multivariate analysis of covari-
“QuikScore™” form allowing for easy adminis- ance revealed that, for all scales, the means for the
tration and scoring. The CRS was later revised target clinical groups were significantly higher
(CRS-R; Conners 1997) to offer a self-report com- than the means for the general population and
ponent and scales linked to the Diagnostic and other clinical groups (e.g., youth diagnosed with
Statistical Manual of Mental Disorders – Fourth ADHD, predominantly hyperactive-impulsive
Edition (American Psychiatric Association 1994) type scored significantly higher on the hyperac-
criteria for ADHD. The Conners 3, the latest tivity/impulsivity and ADHD hyperactive-
Conners 3rd Edition (Conners 3; Conners 2008) 923

Conners 3rd Edition (Conners 3; Conners 2008), The Conners 3 offers a scoring feature, which links
Table 1 Overview of correlations between the Conners the assessment results to areas of eligibility under
3 and other measures
the Individuals with Disabilities Education
Conners 3 scales Other measures r (range) Improvement Act of 2004 (IDEA 2004) making
Inattention, ADHD BASC-2: Attention 0.52–0.89 the assessment useful for identification of appro-
inattentive problems
priate educational classification and/or services for
ASEBA: Attention
problems
0.72–0.96
students in the public school system. The Conners C
Hyperactivity/ BASC-2: 0.41–0.91 3 can also be used as an assessment tool in screen-
impulsivity, ADHD Hyperactivity ing and research contexts.
hyperactive- BRIEF: Inhibit 0.76–0.92 In addition to being an assessment tool, the
impulsive
Conners 3 forms can be employed as a tool for
Executive BASC-2: Executive 0.43–0.68
functioning functioning
planning, monitoring, and evaluating treatment
BRIEF: Plan/ 0.70–0.87 plans. Elevated scores from the Conners 3 suggest
organize areas to target in treatment, with individual item
Aggression, conduct BASC-2:Aggression 0.59–0.95 responses that can be used to guide decisions
disorder, ASEBA: Aggressive 0.58–0.93 about specific behaviors requiring intervention.
oppositional defiant behavior The assessment can also be used in treatment
disorder
monitoring situations, for example, to monitor
Peer relations ASEBA: Social 0.72–0.84
problems the effectiveness of an individual’s response to
Note. All rs significant, p < 0.05 treatment or to evaluate an intervention program.
BASC-2 Behavior Assessment System for Children, Sec- Earlier versions of the Conners 3 forms have
ond Edition, ASEBA Achenbach System of Empirically demonstrated the utility of the assessment in treat-
Based Assessment, BRIEF Behavior Rating Inventory of ment outcome studies, epidemiological and etio-
Executive Function
logical studies of ADHD and other behavior
problems, construct and discriminative validity
impulsive scales than did youth without a clinical studies, correlational studies, and cross-cultural
diagnoses, as well as youth diagnosed with other studies. Since their publication, the Conners 3
disorders). The sizes of the group membership forms have generated research literature in simi-
effects (as determined with partial Z2) were mod- larly diverse areas including treatment outcome
erate to large, on average, accounting for 19.1% of studies (Christiansen et al. 2014; Nikles et al.
the variance in scores. In terms of the classifica- 2017; Steiner et al. 2014a, 2014b), community-
tion accuracy of the scores (as determined by a based studies of children with ADHD and other
series of discriminant function analyses), the disorders or impairments (Efron et al. 2014; Green
mean overall correct classification rate was et al. 2015; Sciberras et al. 2013, 2014, 2016), and
75.6% across all forms. validation studies (Christiansen et al. 2016; Mar-
tinez et al. 2013). There are correlational research
studies that include the Conners 3 forms (Bhide
Clinical Uses et al. 2017; Breau et al. 2015; Borsting et al. 2016;
Mulraney et al. 2016; Reinblatt et al. 2015), as
The Conners 3 can be used as an assessment tool as well as cross-cultural studies (Efron et al. 2016;
well as in planning and monitoring treatment plans. Schmidt et al. 2017). Research incorporating the
Standardized scores allow for the objective com- Conners 3 forms has also been done in the areas of
parison of an individual with age- and gender- parental perception (Wood 2012) and deception
based expectations. Correspondence of items with (Norfolk and Floyd 2016); concordance of parent-,
DSM-5 symptomatic criteria for ADHD, CD, and teacher-, and self-report ratings (Willard et al.
ODD in combination with information about asso- 2016); and exploring instruments for evaluating
ciated features and level of impairment facilitates pharmacotherapy intervention efficacy (Hambly
differential diagnosis decisions in clinical practice. et al. 2017).
924 Conners 3rd Edition (Conners 3; Conners 2008)

Cross-References Efron, D., Sciberras, E., Anderson, V., Hazell, P.,

Ukoumunne, O. C., et al. (2014). Functional status in
children with ADHD at age 6–8: A controlled commu-
▶ Attention Deficit Hyperactivity Disorder nity study. Pediatrics, 134, e992–e1000.
▶ Conners Comprehensive Behavior Rating Efron, D., Sciberras, E., Hiscock, H., Jongeling, B., Lycett,
Scales™ K., et al. (2016). The diagnosis of attention-deficit/
▶ Conners’ Continuous Performance Test Third hyperactivity disorder in Australian children: Current
paediatric practice and parent perspective. Journal of
Edition Paediatrics and Child Health, 52, 410–416.
▶ Individuals with Disabilities Education Act Green, J. L., Rinehart, N., Anderson, V., Nicholson, J. M.,
Jongeling, B., et al. (2015). Autism spectrum disorder
symptoms in children with ADHD: A community-
based study. Research in Developmental Disabilities,
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Hambly, J. L., Khan, S., McDermott, B., Bor, W., &
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American Psychiatric Association. (2013). Diagnostic and (2004). [Amending 20 U.S.C. 1400 et seq.].
statistical manual of mental disorders (5th ed.). Arling- Martinez, B. A., Gonzalez, V. B. A., & Sánchez, L. E. G.
ton: American Psychiatric Publishing. (2013). Calibración del Índice de Hiperactividad de
Bhide, S., Sciberras, E., Anderson, V., Hazell, P., & Nich- Conners mediate el modelo de Rasch. Universitas
olson, J. M. (2017). Association between parenting Psychologica, 12, 957–970.
style and social outcomes in children with and without Mulraney, M., Schilpzand, E. J., Hazell, P., Nicholson, J.
attention-deficit/hyperactivity disorder: An 18-month M., Anderson, V., et al. (2016). Comorbidity and cor-
longitudinal study. Journal of Developmental and relates of disruptive mood dysregulation disorder in
Behavioral Pediatrics, 38, 369–377. 6–8-year-old children with ADHD. European Child &
Borsting, E., Mitchell, G. L., Arnold, L. E., Scheiman, M., Adolescent Psychiatry, 25, 321–330.
Chase, C., et al. (2016). Behavioral and emotional Nikles, J., Mitchell, G., McKinlay, L., Waugh, M.-C., Epps,
problems associated with convergence insufficiency A., et al. (2017). A series of n-of-1 trials of stimulants in
in children: An open trial. Journal of Attention Disor- brain injured children. NeuroRehabilitation, 40, 11–21.
ders, 20, 836–844. Norfolk, P. A., & Floyd, R. G. (2016). Detecting parental
Breau, L. M., Clark, B., Scott, O., Wilkes, C., Reynolds, S., deception using a behavior rating scale during assessment
et al. (2015). Social communication features in children of attention-deficit/hyperactivity disorder: An experimen-
following moderate to severe acquired brain injury: A tal study. Psychology in the Schools, 53, 158–172.
cross-sectional pilot study. Journal of Child Neurology, Reinblatt, S. P., Mahone, E. M., Tanofsky-Kraff, M., Lee-
30, 588–594. Winn, A. E., Yenokyan, G., et al. (2015). Pediatric loss
Christiansen, H., Reh, V., Schmidt, M. H., & Rief, W. of control eating syndrome: Association with attention-
(2014). Slow cortical potential neurofeedback and deficit/hyperactivity disorder and impulsivity. Interna-
self-management training in outpatient care for chil- tional Journal of Eating Disorders, 48, 580–588.
dren with ADHD: Study protocol and first preliminary Schmidt, M., Reh, V., Hirsch, O., Rief, W., & Christiansen, H.
results of a randomized controlled trial. Frontiers in (2017). Assessment of ADHD symptoms and the issue of
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Christiansen, H., Hirsch, O., Drechsler, R., Wanderer, S., to children and parents with migration background? Jour-
Knospe, E.-L., et al. (2016). German validation of the nal of Attention Disorders, 21, 587–599.
Conners 3 Rating Scales for parents, teachers, and Sciberras, E., Efron, D., Schilpzand, E. J., Anderson, V.,
children. Zeitschrift für Kinder- und Jugendpsychiatrie Jongeling, B., et al. (2013). The Children’s attention
und Psychotherapie, 44, 139–147. project: A community-based longitudinal study of chil-
Conners, C. K. (1969). A teacher rating scale for use in dren with ADHD and non-ADHD controls. BMC Psy-
drug studies with children. American Journal of Psy- chiatry, 13, 18.
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Conners, C. K. (1989, 1990). Conners rating scales tech- son, V., et al. (2014). Language problems in children
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Conners, C. K. (2008, 2009). Conners 3rd edition manual. son, V., et al. (2016). Health-related impairments in
Toronto: Multi-Health Systems.
Conners Comprehensive Behavior Rating Scales™ 925

young children with ADHD: A community-based study. and youth aged 8–18 years can complete the
Child: Care, Health and Development, 42, 709–717. self-report. The assessment features multiple Con-
Steiner, N. J., Frenette, E. C., Rene, K. M., Brennan, R. T.,
& Perrin, E. C. (2014a). Neurofeedback and cognitive tent scales that assess emotional distress, defiant/
attention training for children with attention-deficit aggressive behaviors, academic difficulties,
hyperactivity disorder in schools. Journal of Develop- hyperactivity/impulsivity, social problems, sepa-
mental and Behavioral Pediatrics, 35, 18–27. ration fears, perfectionistic and compulsive
Steiner, N. J., Frenette, E. C., Rene, K. M., Brennan, R. T.,
& Perrin, E. C. (2014b). In-school neurofeedback train- behaviors, violence potential, and physical symp- C
ing for ADHD: Sustained improvements from a ran- toms. Scales are also included to assess the Diag-
domized control trial. Pediatrics, 133, 483–492. nostic and Statistical Manual of Mental Disorders
Willard, V. W., Conklin, H. M., Huang, L., Zhang, H., & (DSM-5; American Psychiatric Association; APA
Kahalley, L. S. (2016). Concordance of parent-,
teacher-, and self-report ratings on the Conners 3 in 2013)1 diagnostic criteria for symptoms of gener-
adolescent survivors of cancer. Psychological Assess- alized anxiety disorder, separation anxiety disor-
ment, 28, 1110–1118. der, social anxiety disorder (social phobia),
Wood, S. C. (2012). Examining parent and teacher percep- obsessive-compulsive disorder, major depressive
tions of behaviors exhibited by gifted students referred
for ADHD diagnosis using the Conners 3 (an explor- episode, depressive episode, with mixed features,
atory study). Roeper Review: A Journal on Gifted Edu- manic episode, manic episode, with mixed fea-
cation, 34, 194–204. tures, autism spectrum disorder, attention deficit/
hyperactivity disorder (ADHD), conduct disorder,
and oppositional defiant disorder. Other clinical
indicators are also included for other potential
Conners Comprehensive problem areas, including bullying, enuresis/
Behavior Rating Scales™ encopresis, panic attack, autism spectrum disorder
(Self-report), pica, post-traumatic stress disorder,
Sara R. Rzepa1, C. Keith Conners2, J. Pitkanen3 specific phobia, substance use, tics, and trichotil-
and Stephanie Mears4 lomania. The assessment also includes the
1
Clinical, Education, and Public Safety at MHS Conners Clinical Index (Conners CI), Severe
Inc, Toronto, ON, Canada Conduct and Self-Harm Critical items, Validity
2
Duke University Medical School, Durham, NC, scales (Positive Impression, Negative Impression,
USA and Inconsistency Index), Impairment items
3
Product Development at MHS Inc., Toronto, ON, (home, school, and social settings), and open-
Canada ended Additional Questions (additional concerns,
4
MHS Inc, Toronto, ON, Canada strengths, and skills).
In addition to the Conners CBRS form, the
assessment also offers the Conners CI as a
Description standalone form. The Conners CBRS forms pro-
vide a comprehensive view of a youth’s behav-
The Conners Comprehensive Behavior Rating ioral, social, emotional, and academic
Scales™ (Conners CBRS ®; Conners 2008, functioning. The Conners CI is a brief 24-item
2010) is a comprehensive assessment tool, which index with items from the Conners CBRS form
can be used to assess a wide range of behavioral, that best differentiate youth with a clinical diag-
emotional, social, and academic issues in school- nosis from youth in the general population.
aged youth. The Conners CBRS is a multi- Administration requires approximately 25 min
informant assessment with forms for parents, for the Conners CBRS forms and 10 min for the
teachers, and youth. Parent and teacher ratings
can be obtained about youth aged 6–18 years, 1
An online scoring option remains available to obtain
symptom counts corresponding to the Diagnostic and Sta-
tistical Manual of Mental Disorders (DSM-IV-TR; Amer-
C. Keith Conners: deceased. ican Psychiatric Association 2000).
926 Conners Comprehensive Behavior Rating Scales™

Conners Clinical Index form. Raw scores are Psychometric Data

converted to age- and gender-based standard
scores (including T-scores and percentiles). Results of reliability analyses revealed that the
Results from the DSM-5 symptom scales are Conners CBRS assessments have high levels of
also reported in terms of symptom counts, that internal consistency, with Cronbach’s alpha ranging
is, whether or not the minimum symptom require- from 0.69 to 0.97 (mean Cronbach’s alpha = 0.86),
ments set by the DSM-5 have been met. The and excellent temporal stability, with test-retest cor-
Conners CI produces a probability score, which relations ranging from 0.56 to 0.96 (mean r = 0.81,
indicates whether the youth’s scores are more like all correlations, p < 0.001). There is also a great
youth with a clinical diagnosis (disruptive behav- deal of consistency between multiple parent and/or
ior disorder, learning/language disorder, mood teacher ratings of the same youth, with inter-rater
disorder, anxiety disorder, or ADHD) or with reliability coefficients ranging from 0.53 to 0.89
those from the general population. (mean r = 0.74, all correlations, p < 0.001).
The Conners CBRS normative sample consists The Conners CBRS Manual reports a variety of
of 3400 assessments (1200 parent, 1200 teacher, studies demonstrating convergent/divergent valid-
and 1000 self-report assessments) including ity through correlations of Conners CBRS scale
50 boys and 50 girls from each age (6–18 years scores with other related measures of childhood
for the parent and teacher report, 8–18 years for psychopathology. Overall, scales that assess similar
the self-report). The racial/ethnic distribution of constructs tended to be moderately to strongly
this sample closely matches the US population. intercorrelated, while scales that did not assess sim-
Approximately, 2000 clinical cases were also col- ilar constructs tended to have smaller correlations.
lected from youth with the following DSM-IV-TR Table 1 provides highlights from these analyses.
diagnoses: ADHD, disruptive behavior disorders, Results from discriminative validity analyses
learning disorders, anxiety disorders, major indicated that the Conners CBRS scores accu-
depressive disorder, bipolar disorder, and perva- rately discriminate between relevant groups.
sive developmental disorders. Results from a series of multivariate analyses of
covariance revealed that, for all scales, the means
for the target clinical groups were significantly
Historical Background higher than the means for the general population
and other clinical groups (e.g., youth diagnosed
The Conners CBRS is a new assessment tool, with a disruptive behavior disorder scored signif-
which is built on the foundation of the Conners icantly higher on the defiant/aggressive behavior
Rating Scales. The Conners Rating Scales is a and Violence Potential scales than did youth with-
widely used and well-validated assessment of out a clinical diagnoses, as well as youth diag-
ADHD and related issues. When updating and nosed with other disorders). The sizes of the group
revising the latest version of the scales (Conners membership effects (as determined with partial
3rd Edition; Conners 2008, 2009), the need for a Z2) were moderate to large, on average, account-
comprehensive assessment of behavioral, social, ing for 14.5% of the variance in scores. In terms of
emotional, and academic concerns became evi- the classification accuracy of the scores
dent. The Conners CBRS was therefore devel- (as determined by a series of discriminant function
oped to provide clinicians with an assessment analyses), the mean overall correct classification
and treatment planning/monitoring tool, which rate was 78% across all forms.
would address a broad range of clinical issues in
school-aged youth and which could be linked to
diagnostic and intervention systems such as the Clinical Uses
DSM (APA 2000, 2013) and Individuals with
Disabilities Education Improvement Act of 2004 The Conners CBRS can be used as an assessment
(IDEA 2004). tool as well as in planning and monitoring
Conners Comprehensive Behavior Rating Scales™ 927

Conners Comprehensive Behavior Rating Scales™, Table 1 Overview of correlations between the Conners CBRS
and other measures
Conners CBRS Scale Other measures r
Conners CBRS content Emotional distress BASC-2: Anxiety 0.47–0.87
scales ASEBA: Anxious/depressed 0.53–0.85
Academic difficulties BASC-2: Learning problems 0.78–0.93
Defiant/aggressive behaviors, violence ASEBA: Aggressive behavior 0.60–0.96 C
potential
Physical symptoms BASC-2 somatization 0.59–0.78
DSMa symptom scales ADHD inattentive ASEBA: Attention problems 0.72–0.91
ADHD hyperactive-impulsive BRIEF: Inhibit 0.74–0.89
Major depressive episode BASC-2: Depression 0.38–0.71
ASEBA: Anxious/depressed 0.43–0.83
Generalized anxiety disorder BASC-2: Anxiety 0.46–0.67
ASEBA: Anxious/depressed 0.51–0.83
Social phobia MASC: Social anxiety 0.62–0.68
Separation anxiety disorder MASC: Separation/panic scale 0.42–0.53
Autistic disorder, Asperger’s disorder BASC-2: Developmental social 0.43–0.69
disorders
ASEBA: Social problems 0.64–0.80
Note. All rs significant, p < 0.05. BASC-2 = Behavior Assessment System for Children, Second Edition;
ASEBA = Achenbach System of Empirically Based Assessment; BRIEF = Behavior Rating Inventory of Executive
Function; MASC = Multidimensional Anxiety Scale for Children.
a
Data for the Conners CBRS were collected prior to the publication of the DSM-5; clinical sample diagnoses were based
on diagnostic criteria outlined in the DSM-IV-TR. Psychometric data for the DSM scales that required DSM-5 updates are
presented in the Conners Comprehensive Behavior Rating Scales DSM-5 Update (2014). Pearson product-moment
correlation coefficients between the DSM-5 and DSM-IV-TR Symptom Scales of the Conners CBRS ranged from
0.909 to 0.998 across norm groups and rater versions. These results suggest that analyses conducted on the DSM-IV-
TR Symptom Scales during the standardization and psychometric evaluation of the Conners CBRS would produce highly
similar results for the DSM-5 Symptom Scales.

treatment plans. Standardized scores allow for plans. Elevated scores from the Conners CBRS
the objective comparison of an individual with suggest areas to target in treatment, and individ-
age- and gender-based expectations. Correspon- ual item responses can be used to guide deci-
dence of items with DSM-5, symptomatic sions about specific behaviors requiring
criteria for a number of disorders in combination intervention. The assessment can also be used
with information about the youth’s level of in treatment monitoring situations, for example
impairment, facilitates differential diagnosis to monitor the effectiveness of an individual’s
decisions in clinical practice. The Conners response to treatment or to evaluate an interven-
CBRS offers a scoring feature, which links the tion program.
assessment results to areas of eligibility under the
IDEA 2004, making the assessment useful for
identification of appropriate educational classifi-
cation and/or services for students in the public Cross-References
school system. The Conners CBRS forms can
also be used as an assessment tool in screening ▶ Conners 3rd Edition (Conners 3; Conners 2008)
and research contexts. ▶ Conners’ Continuous Performance Test Third
In addition to being an assessment tool, the Edition
Conners CBRS can be employed as a tool for ▶ Differential Diagnosis
planning, monitoring, and evaluating treatment ▶ Individuals with Disabilities Education Act
928 Conners Rating Scales

References and Readings children. The Conners rating scales were initially
developed as comprehensive checklists of basic
American Psychiatric Association. (2000). Diagnostic and presenting problems of children. Several
statistical manual of mental disorders (text rev. 4 ed.).
re-standardizations have taken place over the
Washington, DC: American Psychiatric Publishing.
American Psychiatric Association. (2013). Diagnostic and years to provide a stronger empirical base and a
statistical manual of mental disorders (5th ed.). Arling- more narrowed focus of common behavioral prob-
ton: American Psychiatric Publishing. lems in childhood as well as specific challenges
Conners, C. K. (2008). Conners comprehensive behavior
associated with ADHD in childhood and adult-
rating scales manual. Toronto: Multi-Health Systems.
Conners, C. K. (2008, 2009). Conners 3rd edition manual. hood. The revised scales were developed with
Toronto: Multi-Health Systems. norms derived from a large representative norma-
Conners, C. K. (2010). Conners comprehensive behavior tive sample. The item content was updated to
rating scales manual. Toronto: Multi-Health Systems.
reflect the recent knowledge and developments
Conners, C. K. (2014). Conners comprehensive behavior
rating scales DSM-5 update. Toronto: Multi-Health concerning ADHD. The Conners is designed to
Systems. offer a thorough assessment of ADHD and related
Individuals with Disabilities Education Improvement Act challenges. It also has clinical application as it
of 2004 (IDEA), Pub. L. No. 108–446, 118 Stat. 2647
identifies children with not only ADHD but also
(2004). [Amending 20 U.S.C. 1400 et seq.].
behavioral challenges. The Conners 3 is the most
recent version of the child measure. There are
parent, teacher, and self-report forms, and all are
available in full-length and short version. The
Conners Rating Scales Conners Adult ADHD Rating Scale (CAARS) is
the adult version of this form. There is a self-report
Allison S. Evans1 and Andrew Preston2 version and an observer version. There are long,
1
Concord Comprehensive Neuropsychological short, and screening versions available for each.
Services, Concord, MA, USA
2
Department of Pediatrics, Chapel Hill Pediatric
Psychology, Chapel Hill, NC, USA Psychometric Data

The authors report that the psychometric properties

Synonyms of the Conners 3 and the CAARS are adequate as
demonstrated by good internal reliability coeffi-
CPRS; CRS cients, high test-retest reliability, effective discrimi-
natory power, and predictive and structural validity.
Various researchers have suggested three main areas
Description for the application of Conners scales: as a general
screening tool for the detection of problematic
The Conners Rating Scales are used as a multi- behaviors in children, as a complimentary tool for
informant (parent, teacher, self) screening tool for clarifying a specific diagnosis, and as a measure-
the detection of problematic behaviors and atten- ment tool for the assessment of treatment results.
tion deficit hyperactivity disorder (ADHD) symp-
toms in particular in children and adults.
Clinical Uses

Historical Background The Conners scales are designed to assess symp-

toms associated with ADHD as well as symptoms
Rating scales and symptom checklists provide an and other problems that are often comorbid with
effective, quick, and standard approach to the mea- ADHD. The Conners 3 provides a refined focus
surement of problematic behaviors observed in on ADHD in school-age children with a new age
Conners’ Continuous Performance Test Third Edition 929

range (6–18 for parent and teacher forms and 8–18 Cross-References
for self-report forms). There are short and long
forms. Forms are available in paper-and-pencil or ▶ Conners 3rd Edition (Conners 3; Conners
computerized format. There are two auxiliary 2008)
scales available for the long forms: the Conners ▶ Conners Comprehensive Behavior Rating
3 ADHD Index (ten-item ADHD Index) and the Scales™
Conners 3 Global Index (general psychopathol- C
ogy) in addition to a range of other scales, includ-
ing General Psychopathology, Inattention, References and Readings
Hyperactivity/Impulsivity, Learning Problems,
Executive Functioning, Defiance/Aggression, Conners, C. K. (1989). Conners’ rating scale manual.
New York: Multi-Health Systems.
Peer Relations, Family Relations, ADHD Inatten-
Conners, C. K. (2010). Test review. Journal of Psychoedu-
tive, ADHD Hyperactive-Impulsive, ADHD cational Assessment, 28(6), 598–602.
Combined, Oppositional Defiant Disorder, and Conners, C. K., Erhardt, D., & Sparrows, E. (1999).
Conduct Disorder. The short forms do not include Conners’ adult ADHD rating scales (CAARS). North
Tonawanda: Multi-Health Systems.
all of these indices, but they do provide evaluation
Conners, C., Sitarenois, G., Parker, J. D., & Epstein, J. N.
of the key areas of inattention, hyperactivity/ (1998a). The revised Conners’ Parent Rating Scale
impulsivity, learning problems/executive func- (CPRS-R): Factor structure, reliability, and criterion
tioning, aggression, and peer relations in parent validity. Journal of Abnormal Child Psychology, 26,
257–268.
and teacher versions but family relations in the
Conners, C., Sitarenois, G., Parker, J. D., & Epstein, J. N.
self-report version. Assessment reports, progress (1998b). Revision and restandardization of the
reports, and comparative reports are available for Conners’ Teacher Rating Scale (CTRS-R): Factor
purposes of assessing symptoms and monitoring structure, reliability, and criterion validity. Journal of
Abnormal Child Psychology, 26, 279–291.
symptom presentation over time.
The Conners Adult ADHD Rating Scale
(CAARS) was developed to measure the presence
and severity of ADHD symptoms in adults so that
one can determine whether the ADHD symptoms Conners’ Continuous
contribute to more generalized challenges. The Performance Test Third
CAARS scales quantitatively measure ADHD Edition
symptoms across clinically significant domains,
while examining the manifestation of those symp- C. Keith Conners1, Gill Sitarenios2 and
toms. There are self and observer rating scales as Lindsay E. Ayearst2
1
well as short and long versions of this form. The Duke University Medical School, Durham,
factor-derived subscales include Inattention/Mem- NC, USA
2
ory Problems, Hyperactivity/Restlessness, Impul- Multi-Health Systems Inc., Toronto, ON, Canada
sivity/Emotional Lability, and Problems with Self-
Concept. There are also DSM-IV ADHD Scales
that include DSM-IV Inattentive Symptoms, Description
DSM-IV Hyperactive-Impulsive Symptoms, and
DSM-IV Total ADHD Symptoms. There is an The Conners Continuous Performance Test – 3rd
ADHD Index and an Inconsistency Index. Edition ™ (Conners CPT 3; Conners 2014) is a
The Conners ratings have also been compared revision of its predecessor, the Conners Continu-
across cultures, including Italian, British, Chinese, ous Performance Test II (Conners CPT II;
Brazilian, and New Zealand cultures and, conse- Conners 2000) and was designed to assess
quently, translated into a number of different lan-
guages, including Sudanese Arabic, Turkish, and
Hindi. C. Keith Conners: deceased
930 Conners’ Continuous Performance Test Third Edition

attention-related problems in four domains of to respond to a target letter), commission errors

attention. The revision is similar to that of the (i.e., responding to a nontarget), perseverations
previous versions: individuals are seated in front (reaction times less than 100 ms), hit reaction
of a computer and required to respond (by press- time (the average speed of correct presses to target
ing the spacebar or the appropriate key on the letters), hit reaction time standard deviation
mouse) when any letter other than the letter “X” (which assesses the consistency of responses to
appears on the monitor (this is known as the non- targets), variability (change in response consis-
X paradigm). The Conners CPT 3 presents 360 tency as the test progresses), detectability (the
scored stimuli trials (i.e., individual letters) on the ability to discriminate between targets and non-
screen, with 1, 2, or 4 s between the presentation targets), hit reaction time block change (change in
of letters (i.e., the interstimulus interval; ISI). The reaction time as the test progresses), hit reaction
360 trials are divided into 6 blocks, with 3 sub- time by ISI (change in mean reaction time across
blocks each consisting of 20 trials. The ISIs are ISI), omissions and commission by block (rate of
counterbalanced across these blocks. The Conners missed targets and incorrect responses to nontar-
CPT 3 takes 14 min to administer excluding the gets, respectively, across blocks), and omissions
recommended practice test. The revision includes and commissions by ISI (rate of missed targets or
a modification to the paradigm, new age range, incorrect responses to nontargets, respectively, in
new normative data, scoring changes, a each of the three ISI trial types). These statistics,
reconceptualization of the assessed dimensions with the exception of omissions and commissions
of attention, and some improvements to the by block and ISI are converted to T-scores and can
usability of the program (see Table 1). be interpreted in terms of various aspects of atten-
Many statistics are computed including tion including inattention, impulsivity, vigilance,
response style (assesses speed vs. accuracy and new to the Conners CPT 3, sustained atten-
response tendencies), omission errors (i.e., failing tion. The Conners CPT 3 also provides a Clinical

Conners’ Continuous Performance Test Third Edition, Table 1 Main differences between the Conners CPT II and
the Conners CPT 3
Type of change Conners CPT II Conners CPT 3 Reason for change
Age range 6+ 8+ For 6- and 7-year-olds, the Conners K–CPT 2 was
found to be the more efficient assessment
Changes to White letter Black letter stimuli To reduce glare and to increase the visibility of the
the paradigm stimuli and and white background stimuli
black background
360 trials 361 trials presented An additional, unscored trial is presented at the
presented start of the test to prepare the respondent for
subsequent trials
90% targets/10% 80% targets/20% To improve the psychometric properties of the
nontargets nontargets commissions variable
Scoring Β C To improve the psychometric properties of the
changes HRT se HRT SD individual scores and interpretation of results
HRT SE Deleted overall
block change
HRT SE ISI Deleted
change
Confidence index Clinical likelihood
(CI) statement
Dimensions of Inattentiveness Inattentiveness The difference between vigilance and sustained
attention Impulsivity Impulsivity attention has been clarified and is distinctly
Vigilance Sustained attention assessed
Vigilance
Conners’ Continuous Performance Test Third Edition 931

Likelihood statement (replacing the Confidence Psychometric Data

Index provided by the Conners CPT II), which is
based on the number of atypical or very atypical Reliability. Split-half reliability results were com-
scores in a respondent’s overall profile. puted for the normative and clinical samples.
T-scores are computed using General Popula- Results were very strong across all scores (median
tion (not preidentified with a clinical condition) split-half estimate was 0.92 for the norm samples
norms (Conners 2014) obtained for children and and 0.94 for the clinical samples). Test-retest reli- C
adults aged 8 years and above. For children aged ability is reported based on a sample of 120
4–7 years, the Conners Kiddie Continuous Perfor- respondents from the general population sample
mance Test 2nd Edition™ (Conners K–CPT 2™; who completed the Conners CPT 3 twice with a 1-
Conners 2015) is the more efficient and to 5-week interval between administrations. The
recommended assessment. The scores are based median test-retest correlation was 0.67.
on a total of 1400 normative cases (including 800 Validity. Validation of the Conners CPT 3
youth ages 8–17 years, and 600 adults ages 18+ focused on its two primary clinical uses: to distin-
years), evenly proportioned between males and guish between clinical and nonclinical groups
females, and stratified based on the 2010 US Cen- (discriminative validity) and to assess how it
sus for region, race/ethnicity, and either parental works together with other measures of similar
education level (for youth) or education level (for constructs in the assessment of attention problems
adults). T-scores are computed based on the age (incremental validity).
and gender of the respondent. Youth and adult In order to determine the discriminative valid-
clinical samples were also collected. The youth ity of the Conners CPT 3, a sample of 346 children
clinical sample included 253 individuals diag- and adults with ADHD was collected and scores
nosed with ADHD and 96 with other clinical from this ADHD sample were compared to a
diagnoses. The adult sample included 93 adults matched sample from the general population sam-
diagnosed with ADHD and 52 with other clinical ple. Results indicated that significant differences
diagnoses. were found between the ADHD sample and the
normative matched sample on most measures with
small to moderate effect sizes (d = 0.10–0.49) with
Historical Background the ADHD sample performing more poorly (hav-
ing higher scores). In particular, the ADHD sample
The acronym “CPT” was first introduced by had more difficulty in distinguishing between tar-
(Rosvold et al. 1956) who used a particular ver- gets and nontargets, made a greater number of
sion to detect attention lapses in subjects with omission and commission errors, and showed
petit mal epilepsy. In early CPTs such as the one more viability in their responses overall and across
they used, subjects were required to press a key sub-blocks compared to the matched sample from
when a target letter (e.g., “X”) appeared or when the general population. The responses of the
the target letter appeared preceded by another ADHD sample were also more affected by changes
letter (e.g., “AX”). While the CPT was being in block and ISI.
explored in clinical settings, Mackworth (1957) To assess incremental validity, parent reports
initiated basic vigilance studies. By changing on the Conners 3rd Edition (Conners 3–P;
basic test parameters, different CPT paradigms Conners 2008) were collected for 112 general
could be constructed. The CPT literature refers to population and ADHD youth who also completed
the Conners’ CPT as a non-X paradigm (e.g., the Conners CPT 3. Self-reports for the Conners
Epstein et al. 2003). Compared to the X para- Adult ADHD Rating Scales (CAARS; Conners et
digm, the non-X paradigm has a higher propor- al. 1999) were also collected for a sample of 137
tion of targets to nontargets making it more nonclinical and ADHD adults who also completed
sensitive to impulsivity and problems with the Conners CPT 3. Logistic regressions were
response inhibition. conducted in order to determine how well scores
932 Conners’ Continuous Performance Test Third Edition

Conners’ Continuous Performance Test Third Edition, Table 2 Incremental validity of the Conners CPT 3
Conners 3- Conners 3-P and Conners CAARS and Conners
Classification statistic P CPT 3 CAARS CPT 3
Overall correct classification 83.9 88.4 89.1 92.7
(%)
Sensitivity (%) 86.0 89.5 65.4 73.1
Specificity (%) 81.8 87.3 94.6 97.3

from the Conners CPT 3 improve the diagnostic References and Readings
efficacy of the rating scales in predicting group
membership into ADHD or general population Balint, S., Czobor, P., Komlosi, S., Meszaros, A., et al.
(2009). Attention-deficit/hyperactivity disorder
groups. Table 2 shows that adding the Conners
(ADHD): Gender- and age- related differences in
CPT 3 to scores from the ratings scales increases neurocognition. Psychological Medicine, 39,
the ability to predict group membership. 1337–1345.
Bauermeister, J. J., Matos, M., Reina, G., Salas, C. C., et al.
(2005). Comparison of the DSM-IV combined and
inattentive types of ADHD in a school-based sample
Clinical Uses of Latin/Hispanic children. Journal of Child Psychol-
ogy and Psychiatry, 46, 166–179.
Although the Conners CPT 3 cannot be used alone Conners, C. K. (2000). Conners’ continuous performance
test II: Computer program for windows technical guide
to make a diagnosis, it provides performance
and software manual. Toronto: Multi-Health Systems.
based information that aids in the diagnostic pro- Conners, C. K. (2008). Conners 3rd edition manual.
cess. The performance based information from the Toronto: Multi-Health Systems.
Conners CPT 3 complements informant reports Conners, C. K. (2014). Conners continuous performance
test 3rd edition manual. Toronto: Multi-Health Systems.
commonly obtained from parents, teachers, or by
Conners, C. K. (2015). Conners kiddie continuous perfor-
self-report. Response patterns on the Conners CPT mance test 2nd edition manual. Toronto: Multi-Health
3 enable practitioners to better understand the man- Systems.
ifestation and presentation of attention deficits (e. Conners, C. K., Erhardt, D., & Sparrow, E. (1999).
Conners’ adult ADHD rating scales technical manual.
g., Hervey et al. 2006), developmental trajectories
Toronto: Multi-Health Systems.
of attention problems (e.g., Miller and Hinshaw Egeland, J., Johansen, S. N., & Ueland, T. (2009). Differ-
2010; Miller et al. 2012), differences between gen- entiating between ADHD sub-types on CPT measures
ders with respect to attention-related problems (e. of sustained attention and vigilance. Scandinavian
Journal of Psychology, 50, 347–354.
g., Balint et al. 2009), and across the different sub-
Epstein, J. N., Erkanli, A., Conners, C. K., Klaric, J.,
types of ADHD (Bauermeister et al. 2005; Egeland Costello, J. E., & Angold, A. (2003). Relations between
et al. 2009). The Conners CPT 3 has also com- continuous performance test performance measures
monly been used as a way of assessing treatment and ADHD behaviors. Journal of Abnormal Child Psy-
chology, 31, 543–554.
effectiveness. Careful charting of CPT scores while
Hervey, A. S., Epstein, J. N., Curry, J. F., Tonev, S., Arnold,
testing different drug dosages can often be helpful L. E., Conners, C. K., et al. (2006). Reaction time
in determining optimal dosage levels. distribution analysis of neuropsychological perfor-
mance in an ADHD sample. Child Neuropsychology,
12, 125–140.
Mackworth, N. H. (1957). Some factors affecting vigi-
Cross-References lance. Advancements in Science, 53, 389–393.
Miller, M., & Hinshaw, S. P. (2010). Does childhood
▶ Attention Deficit Hyperactivity Disorder executive function predict adolescent functional out-
comes in girls with ADHD? Journal of Abnormal
▶ Conners 3rd Edition (Conners 3; Conners
Child Psychology, 38, 315–326.
2008) Miller, M., Ho, J., & Hinshaw, S. P. (2012). Executive
▶ Conners Comprehensive Behavior Rating functions in girls with ADHD followed by prospec-
Scales™ tively into young adulthood. Neuropsychology, 26,
278–287.
▶ Continuous Auditory Test of Attention (CATA)
Consciousness 933

Rosvold, H. E., Mirsky, A. F., Sarason, I., Bransome, E. D., the ages. The ancient Greek philosophers contem-
Jr., & Beck, L. H. (1956). A continuous performance test plated questions regarding the relationship
of brain damage. Journal of Consulting Psychology, 20,
343–350. between external and objective reality. For exam-
ple, Plato recognized that humans can think and
speak and yet not be fully aware of their larger
realm and whether their observations were valid
Consciousness with respect to external reality. His cave allegory C
was an effort to describe this problem. For medi-
Ronald A. Cohen eval religious philosophers (e.g., Aquinas), it
Department of Clinical and Health Psychology, referred to the act of applying moral knowledge
College of Public Health and Health Professions, to one’s actions. Descartes extended the concept
University of Florida, Gainesville, FL, USA of “conscientia” to include the idea that it involves
Center for Cognitive Aging and Memory, a psychological state of mind and used separate
McKnight Brain Institute, University of Florida, terms to explain this level of experience from
Gainesville, FL, USA moral knowledge, though he did not formally
employ the modern concept of consciousness in
his dualism of mind-body interaction. John Locke
Synonyms later wrote “I may be held morally responsible for
the act of which I am conscious of having
Alertness; Awareness; Mindfulness; Self- achieved; and my personal identity; my-self goes
awareness; Wakefulness as far as my consciousness extends itself,” its first
modern usage associated with the idea of “self”
and personal identity. Interestingly, Locke still
Definition linked consciousness to the ideas of morality and
responsibility. The nature of consciousness was a
Consciousness comes from the Latin word recurrent theme of renaissance philosophers.
“conscientia” which means “knowledge-within” The quest to better understand the nature of
or knowledge that is shared. Today the term is consciousness dominated the new science of psy-
used to describe the experience of “self” as distinct chology as it evolved in the late nineteenth cen-
from the external environment. It is characterized tury. Wilhelm Wundt believed that identifying the
by experiences of alertness, self-awareness, and constituents of human consciousness was a pri-
attention of oneself relative to the environment mary task for psychology. He postulated that
relative to the self, i.e., identify, which in turn “apperception” represented the core activity of
involves awareness of one’s own perceptions, asso- the mind and was the interface between internal
ciations, emotional experience, and the cognitive and external experience. Notably, Wundt’s pri-
interpretation of these experiences. More narrowly, mary method for exploring these processes was
consciousness is often defined as level of arousal, introspection, which essentially is the process of
wakefulness, alertness, responsiveness, and adapt- looking inward or self-reflection. These ideas
ability in contrast to states of coma or sleep. evolved into structuralism, the first dominant the-
However, consciousness has defied unitary oretical school of psychology.
definition, perhaps because it is intrinsically A dramatic shift away from consideration of
bound to subjective experience. consciousness occurred during much of the twen-
tieth century as behaviorism became the dominant
perspective, as consciousness was viewed as
Historical Background metaphysical and beyond empirical observation.
Even cognitive scientists tended to steer away
The nature of human consciousness has been a from tackling this construct, probably because of
primary topic of philosophical inquiry throughout the difficulties associated with experimentally
934 Consciousness

studying it. Yet, for clinicians working with the subjective cognitive states, providing evidence
subjective experiences of their neurological and that these states have valid neurobiological under-
psychiatric patients, consciousness was difficult pinnings. Furthermore, growing recognition of
to avoid. When the neurologist Babinski the brain’s complexity has played an important
(1914) first described patients who were unaware role. There is now general consensus that cogni-
of their own deficits (i.e., anosognosia), he was tion involves interactions among large networks
essentially addressing the issue of consciousness of cortical neurons, which communicate across
and self-awareness. Initially, the problem of con- larger functional systems in an integrated manner.
sciousness was handled by narrowing the mean- This perspective enabled cognitive neuroscien-
ing of the term to refer to the state of being awake, tists to shift away from having to view conscious-
alert, and aware, in contrast to coma, stupor, or ness as a unitary process sitting on top of the
sleep, which in turn led to the idea of level of pyramid of cognitive functions.
consciousness, which remains a standard part of Several lines of research and clinical evidence
mental status examinations. have had particular bearing on current knowledge
regarding the neuropsychology of consciousness.
The effect of various types of drugs, most notably
Current Neuropsychological Knowledge hallucinogens, opiates, and alcohol on conscious
experience, provides one of the most clear -cut
Over the past two decades, there has been a major illustrations of the fact that even among healthy
resurgence of interest and research effort directed people consciousness is not a static phenomenon.
at the nature of consciousness, along with grow- One’s sense of reality, identity, and self-awareness
ing recognition that the construct is a necessary can be dramatically altered by drugs such as LSD,
one, as consciousness describes an important ele- presumably by altering the flow of information
ment of human experience, the sense of self. processing. Case studies have consistently
A number of scientific developments set the shown that disruption of self-awareness as a func-
stage for this shift in zeitgeist. The evolution of tion of damage to specific brain regions. Further-
the field of cognitive science provided empirical more, clinicians working with patients
methods for studying covert “mental” processes. experiencing neurodegenerative dementias have
Also as cognitive processes such as attention and long been aware of dramatic impoverishment in
memory were better understood, foundations the quality of conscious experience as the disease
were established for studying phenomena like progresses, corresponding with the extent of cor-
intention and self-awareness. Computational neu- tical atrophy. Among patients with Alzheimer’s
roscience was also influential in this regard. It is disease (AD) and other neuronal dementias, a loss
quite difficult to operationalize or conceptualize of “self” is one of the hallmark features of the end-
consciousness as a single node in a top-down stage condition. In fact, it is when AD patients
modular cognitive framework. This is less of a lose their ability to respond to people who are
problem for computational theories that take a familiar and meaningful to them and when they
bottom-up approach, such as the parallel distrib- lose awareness of their own identity, their per-
uted processing (PDP) models proposed by sonal memories, and the nature of their cognitive
Rummelhart and McClelland (1986), as con- problems that families typically experience
sciousness can be conceptualized as an emergent greatest despair. In fact, it is often this change,
by-product of associative networks acting along with an inability for self-care that leads to
together with feedback or feed-forward organiza- nursing home placement rather than the amnestic
tion. Another major impetus for consciousness disturbance per se. The loss of identity in AD
becoming an acceptable topic for scientific patients usually corresponds with personality
inquiry was advances in the field of neuroscience changes and profound impoverishment in abstrac-
itself. Functional imaging methods have made it tion and associative ability. While other cognitive
easier to measure brain responses associated with functions like language are often also severely
Consciousness 935

impaired at this point, it may be difficult to fully Compared to healthy people who are awake,
appreciate these changes, though the quality of patients with this syndrome have impaired con-
emptiness and loss of self may ultimately be the nectivity between the brain stem and thalamic
characteristic that best defines severe dementia areas and the cortex. This results in a reduced
rather than impairment in a particular cognitive cortical activation, with generalized slowing con-
domain. sistent with coma. These subcortical areas are
In contrast to AD, patients with certain other clearly essential for maintaining normal con- C
degenerative conditions often show general pres- sciousness, since disconnecting them from corti-
ervation of consciousness despite having marked cal areas impairs alertness, attention, and other
impairments of other functions. For example, cognitive functions linked to consciousness. The
patients with severe Parkinson’s disease typically activation and arousal associated with this func-
have major motor symptoms and cognitive con- tional anatomic system makes an essential contri-
trol problems, including executive and attention bution to is a necessary part of the maintaining
dysfunction. They may also show blunting of consciousness, though this activation is not suffi-
emotional response and altered emotional func- cient to account for the full dynamic of conscious-
tioning. Yet, they are often painfully aware of their ness (i.e., self-awareness and sense of identity).
deficits and have greater preservation of sense of The thalamus appears to play an important role
self than the AD patient. Similarly, patients with in consciousness but as a convergence site of
multiple sclerosis (MS) sometimes exhibit reticular activation from lower brain systems and
pseudobulbar affect. They are affectively labile because of its role in integrating this activation
with dramatic shift in the outward expression of with cortical input. Bilateral ablation of the central
emotion, but yet they report not feeling the emo- medial zone of the intralaminar nucleus of the
tion that corresponds to this expression. Despite thalamus produces coma and persistent vegetative
these problems with affective and behavioral con- states. This thalamic area is affected by general
trol, patients with MS typically are very aware of anaesthetics and drugs that cause sedation,
their deficits and may feel locked in because of suggesting that it is necessary for antipsychotic
their symptoms. drugs. This evidence suggests that a functioning
Alterations in self-awareness and conscious- thalamus is necessary, but not sufficient, for
ness also occur as a result of damage to specific human consciousness, though again this area
brain regions. This fact is significant since it sug- alone is not sufficient to account for all aspects
gests that certain functional anatomic systems of consciousness. Cortical and limbic functions
play an important role in the experience of con- are necessary elements of normal consciousness.
sciousness, though probably not as a function of Patients with bilateral occipital damage who
any one of these systems alone. Subcortical exhibit blind sight are clearly experiencing some
lesions affecting the midbrain, brain stem, and alteration in consciousness and self-awareness.
thalamus often cause dramatic alterations in Yet, this disturbance may be relative focal and
level of consciousness. The reticular system limited to vision. For these individuals, altered
which generates ascending activation to cortical consciousness has not affected all aspects of self-
areas plays a well-established role in this phenom- awareness and identity. Damage to other cortical
enon, with damage to this system contributing to areas may also produce specific impairments of
problems with arousal and alertness. Damage to awareness and self-consciousness. For example,
these areas frequently underlies coma, and the the neglect syndrome commonly associated with
electrical activity measured by EEG is amplified right inferior parietal damage often results in
by generators in these systems. Persistent vegeta- anosognosia and impaired awareness of what is
tive state is a clinical illustration of this, as these being neglected. For some of these patients, the
unfortunate patients exhibit impaired higher cor- alteration in awareness and consciousness extends
tical functions and have persevered circadian beyond the limits of the spatial disturbance that is
sleep-wake cycles and autonomic function. observed. Yet, typically patients with these lesions
936 Consciousness

do not lose their sense of self completely. They reduplicative paramnesia, patients may feel with
may show diminished ability for self-reflect but certainty that while the house in which they are
usually show abilities in this regard as long as not living looks identical to their real home, it is in
tied to the types of spatial processing that is fact a replica of their home. When queried these
affected. patients usually acknowledge the logical implau-
The frontal cortex seems to have the cortical sibility of their belief but state that they are certain
area with greatest influence on consciousness, because of some feeling they have, suggesting a
self-regulation, and self-referential processes. relationship between emotional response and the
The famous case of Phineus Gage, the railroad processing of these frontal systems. Primate stud-
worker who suffered severe frontal damage when ies support the role of the frontal cortex in this
a spike penetrated his brain, provided historical regard and led Crick and Koch (1995) to propose
illustration of this. Following his injury Gage that consciousness is largely dependent on the
became indifferent to social consequences and resonance of thalamocortical systems acting in a
showed little self-regard for his own behavior recursive manner.
(Harlow 1848). While it is impossible to accu- The role of memory and its underlying func-
rately evaluate the nature of change in his subjec- tional neuroanatomic systems raises a number of
tive sense of consciousness and self-awareness interesting issues for consciousness. Patients like
based on the historical record, it seems clear HM, who have suffered bilateral damage to hip-
from clinical descriptions that his self-awareness pocampal or paralimbic areas, lose their ability to
was dramatically altered. In modern case study, form new episodic memories. Yet, they typically
Eslinger and his colleagues (1986) have demon- retain retrograde memory for events that hap-
strated impaired empathy associated with frontal pened earlier in their life, which enables them to
lobe disturbance, which affects social reasoning, retain some sense of personal identity based on
judgment, and perspective taking. Interestingly, these recollections. Yet, they have lost the ability
this disorder of empathy also involves problems to update these memories or to adapt these mem-
with moral reasoning, a notion consistent with ories to new circumstances. Clearly this results in
early philosophical ideas regarding conscious- an alteration of consciousness, though they may
ness, which as discussed earlier conceptualized still report knowing who they are or what they
consciousness as tied to man’s capacity for think about certain topics.
moral knowledge. In addition to the contribution of specific cor-
There is strong evidence from studies of tical and subcortical areas to the experience of
neglect syndrome that medial frontal and anterior consciousness, there is a rich history of research
cingulate cortical areas play a major role in “inten- on brain laterality, specifically the effects of dis-
tion” (Cohen 1993). The intent and plan for action connection between the left and right hemisphere
seems to be an important element of conscious- of the brain. The corpus callosum provides the
ness, as this capacity is linked to the experience of white matter linkage between the hemispheres.
drive and spontaneity. An illustration of this is Roger Sperry observed remarkable alterations in
seen in patients who undergo cingulotomy, as consciousness and awareness among patients who
their primary long-term neurocognitive deficit underwent surgical severing of the corpus
involves diminished performance on tests requir- callosum (split brain) for treatment of intractable
ing intention and also reduced spontaneity, initia- seizures. When the two hemispheres are no longer
tive, and creative impulse. It is also noteworthy able to communicate, each processes and inter-
that syndromes that result in alterations of con- prets information presented to it in different ways.
sciousness that involve delusions and a fractured For example, the left hemisphere is typically more
sense of reality, such as reduplicative paramnesia involved in language processing and therefore
and Capgras syndrome, tend to occur among tended to be aware of verbal elements of informa-
patients with frontal lobe damage, often involving tion during tasks compared to the right hemi-
the non-dominant hemisphere. In cases of sphere. Because of a lack of integration between
Consciousness 937

the cortical hemispheres, it is possible to dissoci- control for gating of this information as it flows
ate elements of consciousness tied to each side of from posterior cortical systems. (4) Limbic areas,
the brain. Yet, following this procedure, it was such as the amygdala, likely play a significant role,
only under experimentally controlled conditions by linking emotional valence to particular associa-
that major dissociations occurred. Postsurgically, tive information. In interaction with cortical areas,
people still experience a single identity in every- these limbic areas enable amplification of affective
day experience, suggesting that splitting the two signals, and also their regulation, providing for the C
hemispheres does not completely disrupt the intensity and richness of emotional affective expe-
sense of a unified consciousness. rience. (5) Some type of mechanism that enables
temporal binding of associative experiences in an
integrated way likely occurs that creates the feeling
Neuropsychological Models of of a unified conscious experience and sense of
Consciousness single identity, “I.”
Some of the distinctions that exist between
Consideration of the neuropsychological literature theories of consciousness relate to the emphasis
to date has established the foundations for the that is placed on particular cognitive functions.
cognitive neuroscience of consciousness. Over Some recent investigators have emphasized the
the past 15 years, theoretical models have been role of posterior brain systems involved in visual
developed to explain how the brain creates processing to a greater extent. A number of theo-
“mind” and “consciousness.” These models ries emphasize the role of frontal brain systems.
include contributions from philosophers (Dennett For example, one of the first neuroscientific
1991; Churchland 2005), neuropsychologists/ models of consciousness proposed by Shalice
behavioral neurologists (Cohen 1993; Damasio (1978) viewed consciousness as a by-product of
1995, 2000), and cognitive neuroscientists dominant action systems that govern the stream of
(Shallice 1978; Eccles 1994; Crick and Koch thought processes. As discussed previously, many
1995; McClelland et al. 1997; Grossberg 1999). It models have focused on frontal systems with
is beyond the current scope to review each of their varying degrees of emphasis on particular pro-
models. However, there are several features com- cesses. Damasio’s model of consciousness
mon to each, as well as a few fundamental distinc- emphasizes the critical role of emotional pro-
tions between these models, as summarized below. cessing systems, as well as the somatic or visceral
Most current models of consciousness take the activity of the body as a whole.
perspective that consciousness is not localized to a Perhaps the greatest distinction between theo-
single brain region but rather is an emergent func- ries of consciousness stems from the extent to
tion of multiple systems acting in an integrated which it is viewed as distinct from the physical
fashion. (1) Almost all researchers and theorists processes that comprise, or essentially indistin-
agree that lower brain areas (e.g., reticular system) guishable from these physical processes, as
that energize the brain and lead to altering levels of Dennett argues. Furthermore, some of these
activation are a necessary requirement for con- models take more of a top-down approach, whereas
sciousness, but not sufficient to explain the phe- others view consciousness from a bottom-up per-
nomenon. (2) The thalamus seems to play and spective, as an emergent by-product of all of the
essential role, particularly as a nexus for this acti- more basic associative processes that underlie cog-
vation and for integration and gating of cortical nition. The PDP approach of McClelland and
information. (3) Frontal regions appear to play Rummelhart (1986, 1997) and other neurocompu-
several important roles, including the generation tational theories (e.g., Grossberg 1999) take a more
and sustaining of intention, switching and gating bottom-up approach and tend to view conscious-
of information, and the enabling of feedback and ness as the sum total of these distributed processes.
feed-forward mechanisms that enable reprocessing Despite these differences, there seems to be little
of certain associative information and feedback disagreement that consciousness is a complex
938 Consciousness

cognitive phenomenon that results from the inter- Cross-References

action of multiple brain systems and processes,
which in an integrated coherent manner provides ▶ Anosognosia
for the sense of self, universally experienced by ▶ Attention
healthy humans. ▶ Capgras Syndrome
▶ Minimally Conscious State
▶ Parallel Processing
Future Directions ▶ Reduplicative Paramnesia
▶ Reticular Activating System
The cognitive and neurobiological bases of con- ▶ Split-Brain
sciousness remain major frontiers in neuropsy-
chology. Clinicians evaluating patients following
acute brain injury routinely assess level of References and Readings
impaired consciousness (i.e., the degree of coma,
stupor or lethargy), though this level of analysis Churchland, P. S. (2002). Self-representation in nervous
does not fully capture the richness of normal con- systems. Science, 296, 308–310.
scious experience. Nonetheless, clinical research Churchland, P. S. (2005). A neurophilosophical slant on
consciousness research. Progress in Brain Research,
is likely to yield greater precision in the assess- 149, 285–293.
ment of “levels” of consciousness. Cohen, R. A. (1993). Neuropsychology of attention.
Some progress has been made in understanding New York: Plenum.
how consciousness arises as a by-product of other Crick, F., & Koch, C. (1990). A framework for conscious-
ness. Nature Neuroscience, 6(2), 119–126.
cognitive functions, most notably emotional expe- Damasio, A. R. (1995). Consciousness. Knowing how,
rience, attention, and executive functioning. Com- knowing where. Nature, 375, 106–107.
putation neuroscience has offered a perspective Damasio, A. R. (2000). The feeling of what happens: Body
for explaining consciousness as an emergent prop- and emotion in the making of consciousness.
New York: Vintage.
erty of complex neural systems. Yet, the measure- Damasio, H., Grabowski, T., Frank, R., et al. (1994). The
ment of the qualitative experience that comprises return of Phineas Gage: Clues about the brain from the
consciousness is still far from becoming part of skull of a famous patient. Science, 264, 1102–1105.
mainstream neuropsychological assessment or Dennett, D. (1991). Consciousness explained. Boston: Lit-
tle & Company.
from being fully operationalized as a cognitive Eccles, J. C. (1994). How the self controls its brain. Berlin:
construct or neuropsychological domain. Greatest Springer.
progress has been made with respect to the study Eslinger, P. J. (1998). Neurological and neuropsychologi-
of anosognosia and recent efforts to better under- cal bases of empathy. European Neurology, 39,
193–199.
stand the relationship between subjective experi- Grossberg, S. (1999). The link between brain learning,
ence of cognitive impairments and also cognitive attention, and consciousness. Consciousness and Cog-
and emotional experience and neuropsychological nition, 8, 1–44.
performance. This seems to be a fertile area of Harlow, J. M. (1848). Passage of an iron rod through the
head. Boston Medical and Surgical Journal, 39,
continued investigation. Functional imaging 389–393.
approaches have provided considerable insight Harlow, J. M. (1868). Recovery from the passage of an iron
into the neural bases of consciousness and likely bar through the head. Publications of the Massachu-
will continue to be on the cutting edge of these setts Medical Society, 2, 327–347.
McClelland, J. L., Cohen, J. D., & Schooler, J. W. (1997).
efforts, since they provide a means for observing The neural basis of consciousness and explicit memory:
brain response associated with subjective experi- Reflections on Kihlstrom, Mandler and Rumelhart. In
ence. Evidence of the attentional default network Scientific approaches to consciousness (pp. 499–509).
that emerged from functional imaging research Lawrence Erlbaum Associates.
Rumelhart, D. E., McClelland, J. E., & the PDP Research
illustrates the type of insight about the neural Group. (1986). Parallel distributed processing: Explo-
bases of consciousness that can be achieved from rations in the miccrostructure of cognition, vol. 1:
these approaches. Foundations. Cambridge, MA: Bradford/MIT Press.
Consolidation 939

Shallice, T. (1978). The dominant action system: An infor- that it takes time to form memories, but for
mation processing approach to consciousness. In K. S. some time after their formation, these new mem-
Pope & J. L. Singer (Eds.), The stream of conscious-
ness: Scientific investigations into the flow of experi- ories are susceptible to being disrupted (Lechner
ence. New York: Plenum. et al. 1999).
Wundt, W. (1902). Outlines of psychology (Trans.,
2nd ed.). Engelmann: Oxford.
Process of Consolidation
Two specific processes are involved in consolida-
C
tion, which differ by the amount of time needed to
create long-term memories from the short-term
memories (Dudai 2004). Synaptic consolidation
Consolidation is the quickest, consolidating memories within the
first few minutes to hours of learning. System
Elizabeth S. Gromisch consolidation, on the other hand, takes between
Psychology Service, VA Connecticut, West weeks to years for memories to become indepen-
Haven, CT, USA dent of the hippocampus. Consolidation can occur
more rapidly if new information is incorporated
with an already existent schema. There has been
Synonyms strong evidence with forms of procedural memory
and modest evidence with forms of declarative
Memory consolidation memory that consolidation occurs during sleep
(Stickgold 2005).

Definition Long-Term Memory

Studies in anterograde amnesia, such as with
Consolidation is the process of converting a short- patient H.M., have shown that lesions on the
term memory to a permanent long-term memory medial temporal lobe prevent long-term memory
through the formation of new synapses. formation (Corkin 2002). While consolidation is
initiated in the limbic system, specifically in the
hippocampus, long-term memories are stored
Current Knowledge throughout the cortex (Frankland and Bontempi
2005). When the memory is retrieved, it can be
History modified with recently acquired memories, thus
The first written evidence of consolidation strengthening the original memory (Tronson and
was by Marcus Fabius Quintilian, who stated Taylor 2007).
“curious fact, of which the reason is not obvious,
that the interval of a single night will greatly Assessment and Measurement
increase the strength of the memory” and “the Consolidation is assessed in a neuropsychological
power of recollection, which is the most impor- evaluation by measuring the immediate recall of
tant element of memory, undergoes a process recently presented information and then measur-
of ripening and maturing during the time ing recall after a delay and/or distraction. The
which intervenes” (Quintilian 1922). The term participant is given a list of words, for example,
“consolidation” was coined by Georg Elias and asked to repeat them back to the examiner.
Müller and Alfons Pilzecker, whose research After a period of time has passed, the participant
between 1892 and 1900 found that memory will be prompted to repeat the words again.
takes time to “consolidirung.” Published in A distraction (i.e., a second word list) may be
their article “Experimentelle Beiträge zur Lehre used to prevent the participant from rehearsing
vom Gedächtnis,” Müller and Pilzecker found the information.
940 Consortium to Establish a Registry on Alzheimer’s Disease

Neuroimaging
Takashima et al. (2005) found on functional mag- Consortium to Establish a
netic resonance imaging (fMRI) that as the brain Registry on Alzheimer’s
consolidates short-term memories into long-term Disease
memories, there is an increase in activity in the
hippocampus. Once the brain switches from con- Susan Vandermorris1, Esther Strauss2 and
solidation to memory retrieval, the hippocampal Elisabeth M. S. Sherman3
1
activity decreases, and the ventral medial prefron- Neuropsychology and Cognitive Health
tal region activity increases. By using fMRI to Program, Baycrest, Toronto, ON, USA
2
examine consolidation during sleep, Sterpenich Department of Psychology, University of
et al. (2009) showed that activation in the hippo- Victoria, Victoria, BC, Canada
3
campus decreased over time (three days compared Copeman Healthcare Centre, Calgary, AB,
to six months), indicating that the memories were Canada
being stored in the neocortex and were not hippo-
campus dependent. After six months, activity
increased in the ventral medial prefrontal region. Synonyms

CERAD
Cross-References
Description
▶ Memory
▶ Short-Term Memory
The Consortium to Establish a Registry for
Alzheimer’s Disease (CERAD) neuropsychologi-
cal battery was designed to provide an efficient,
References and Readings standardized method to evaluate cognitive func-
Corkin, S. (2002). What’s new with amnestic patient H.M.?
tioning in individuals with Alzheimer’s disease
Nature Reviews Neuroscience, 3, 153–160. (AD). Originally employed in a large-scale longi-
Dudai, Y. (2004). The neurobiology of consolidations, or, tudinal research program, tests were selected to
how stable is the engram? Annual Review of Psychol- provide coverage of the primary cognitive deficits
ogy, 55, 51–86.
Frankland, P. W., & Bontempi, B. (2005). The organization
associated with AD (e.g., memory, language,
of remote and recent memories. Nature Reviews Neu- praxis, and intellectual status) and to have a
roscience, 6, 119–130. range of difficulty appropriate for use through
Lechner, H. A., Squire, L. R., & Byrne, J. H. (1999). much of the course of the disease (Morris et al.
100 years of consolidation-remembering Müller and
Pilzecker. Learning and Memory, 6, 77–87.
1989). Individual tests within the battery include
Quintilian, M.F. (1922). The institution oratoria of Quin- well-known, commonly used measures such as the
tilian: Volume IV. (H.E. Butler, Trans). London: Wil- Mini-Mental State Exam (MMSE; Folstein et al.
liam Heinemann (Original work published in the 1st 1975), a 15-item modified Boston Naming Test
Center CE).
Sterpenich, V., et al. (2009). Sleep promotes the neural
(Kaplan et al. 1978), and an Animal Naming ver-
reorganization of remote emotional memory. The Jour- bal fluency test (Isaacs and Kennie 1973). Also
nal of Neuroscience, 29(16), 5143–5152. included are a ten-item word list memory test, with
Stickgold, R. (2005). Sleep-dependent memory consolida- free recall (immediate and delayed) and recogni-
tion. Nature, 437, 1272–1278.
Takashima, A., et al. (2005). Declarative memory consol-
tion (delayed) conditions, and a constructional
idation in humans: A prospective functional magnetic praxis test that requires examinees to copy four
resonance imaging study. Proceedings of the National line drawings of increasing complexity (Rosen
Academy of Sciences of the United States of America, et al. 1984). Administration time for the battery is
103(3), 756–761.
Tronson, N. C., & Taylor, J. R. (2007). Molecular mecha-
nisms of memory reconsolidation. Nature Reviews
Neuroscience, 8, 262–275. Esther Strauss: deceased.
Consortium to Establish a Registry on Alzheimer’s Disease 941

20–30 min for persons with AD; persons without intraclass correlation coefficients ranging from
AD may complete the battery in less time (Morris 0.92 to 1.0 (Morris et al. 1989). One month test-
et al. 1989). As may be expected given the retest data showed variable reliability (r’s from
brevity of the battery and the range of cognitive 0.36 to 0.90), with lower correlation coefficients
ability of the target populations, floor and ceiling for measures whose variance may have been
effects have been noted for individuals with later- constrained by ceiling effects (Morris et al.
stage AD and for individuals without AD, respec- 1989). The efficacy of CERAD battery measures C
tively (Morris et al. 1989). Normative data are (individually and in combination) for detecting
available based on the CERAD program control AD and for staging dementia severity has been
sample (Welsh et al. 1994), as well as from studies evaluated using discriminant function models
of specific demographic groups (see section (Welsh et al. 1991, 1992). The word list delayed
“Clinical Uses”). recall measure was shown to most effectively
differentiate those with AD from controls
(correctly identifying 94% of controls and 86%
of mild AD patients), although the ability of this
Historical Background
measure to distinguish dementia severity groups
was limited due to floor effects. For those with
The Consortium to Establish a Registry for
impaired scores on delayed recall, performance on
Alzheimer’s Disease (CERAD) was first funded
the naming measure was shown to modestly
by the National Institute on Aging in 1986 in
increase the discrimination of those with mild
response to a US Congressional mandate to col-
from moderate AD (improvement in overall accu-
lect epidemiological data concerning the inci-
racy from 65% to 71%). Verbal Fluency and Con-
dence of AD. A nationwide consortium of
structional Praxis performances were shown to
24 university medical centers (the CERAD pro-
increase discrimination of those with moderate
gram) developed, standardized, and evaluated
from severe AD (improvement in overall accuracy
methods for clinical, neuropsychological, neuro-
from 66% to 81%). Clinical-pathological correla-
pathologic, and neuroimaging assessments of
tions have shown association between CERAD
AD. Data from the study population, including
neuropsychological performance and AD pathol-
1094 patients with AD and 463 controls evaluated
ogy on autopsy (Hulette et al. 1998). The CERAD
annually between 1987 and 1996, are available for
battery has been extensively translated. Norma-
research purposes (for further information, see
tive and psychometric data for the CERAD are
http://cerad.mc.duke.edu). As the bulk of the
available for a wide range of racial/cultural/demo-
CERAD data collection took place before the
graphic groups (for review, see Fillenbaum et al.
widespread use of cholinesterase inhibitor treat-
2008; Liu et al. 2011).
ment for AD, these data provide a rich source of
information as to the natural history of AD. A
special issue of Neurology (49, suppl. 3)
Clinical Uses
published in 1997 commemorated the tenth anni-
versary of the CERAD program and reviewed
The chief objective of the CERAD neuropsychol-
study design, implementation, and key findings
ogy task force was “to develop a brief, reliable
from wide-ranging investigations of AD.
battery of neuropsychological tests that would be
widely used by researchers and clinicians to
assess the cognitive status of patients with AD at
Psychometric Data entry and during long-term annual follow-up”
(Welsh-Bohmer and Mohs 1997). The CERAD
Psychometric data for the CERAD neuropsycho- neuropsychological battery has been widely used
logical battery reported for participants enrolled in research studies, including those completed at
over the first 19 months of the study indicated many of the NIH-sponsored Alzheimer’s disease
good interrater reliability across all tests, with centers. Normative data based on 413 CERAD
942 Consortium to Establish a Registry on Alzheimer’s Disease

control subjects aged 50–89 have been published neuroimaging markers of pathology including
to facilitate clinical application (Welsh et al. white matter lesion load, gray matter atrophy,
1994). These data are stratified by age, education, and cortical thinning (Bilello et al. 2015; Paajanen
and gender, as these factors were shown to differ- et al. 2013). Normative data (Han et al. 2014) and
entially impact test performance. A constructional reliable change data for individuals with and with-
praxis recall measure was later added to address out AD (Rossetti et al. 2010; Stein et al. 2012) are
concerns regarding an overreliance of verbal abil- available.
ities in the assessment of memory, and normative In sum, the brevity of the CERAD neuropsycho-
data are available for this (Fillenbaum et al. 2011). logical battery, combined with the vast associated
Base rates of low performance in healthy older research base, makes the CERAD a useful tool for
adults are available (Mistridis et al. 2015). Nor- assessment of cognitive function in large-scale pop-
mative data for patients with AD have also been ulation studies and in individual cases of suspected
reported, in addition to annual rates of change on dementia where “factors such as fatigue, motivation,
CERAD test scores over a 4-year period (Morris or incapacity prevent a more extensive neuropsy-
et al. 1993). The CERAD has also shown to have chological examination of cognitive capacities”
some utility for evaluating cognitive impairment (Welsh et al. 1994). Assessment in specialized mem-
in schizophrenia (Davidson et al. 1996), ory clinics, however, would typically employ a
frontotemporal lobar degeneration (Haanpaa more extensive neuropsychological battery.
et al. 2015), Parkinson’s disease (Karrasch et al.
2013), Lewy body disease (Hellwig et al. 2013),
and late-onset depression (Kunig et al. 2006). Cross-References
Methods for deriving a single summary score for
the CERAD battery (excluding the MMSE) and ▶ Alzheimer’s Disease
normative data for this summary score for ▶ Blessed Dementia Scale
unimpaired, mild cognitive impairment (MCI) ▶ Clinical Dementia Rating
and AD groups have been published (Chandler ▶ Dementia Rating Scale-2
et al. 2005; a later version by Seo et al. 2010 ▶ Mini-Mental State Exam
includes the praxis recall measure). This total
score was reportedly more consistent at differenti-
ating these three groups from one another com- References and Readings
pared to the MMSE total score, which showed
limited ability to distinguish patients with MCI Aguirre-Acevedo, D. C., Jaimes-Barragan, F., Henao, E.,
from unimpaired individuals, and the word list Tirado, V., Munoz, C., & Reiman, E. M., et al. (2015).
Diagnostic accuracy of CERAD total score in a Colom-
delayed recall score, which showed limited ability
bian cohort with mild cognitive impairment and
to distinguish MCI from AD. Similar findings Alzheimer's disease affected by E280A mutation on
were seen in American (Roalf et al. 2013), Colum- presenilin-1 gene. International Psychogeriatrics,
bian (Aguirre-Acevedo et al. 2015), German 1–8. https://doi.org/10.1017/s1041610215001660.
Bilello, M., Doshi, J., Nabavizadeh, S. A., Toledo, J. B.,
(Ehrensperger et al. 2010; Wolfsgruber et al.
Erus, G., Xie, S. X., et al. (2015). Correlating
2014), South Korean (Seo et al. 2010), and multi- cognitive decline with white matter lesion and
national European (Paajanen et al. 2010) samples. brain atrophy magnetic resonance imaging measure-
The total score has been shown to be sensitive ments in Alzheimer’s disease. Journal of Alzheimer's
Disease, 48(4), 987–994. https://doi.org/10.3233/jad-
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moderate practice effects in healthy older adults, score for the CERAD neuropsychological battery. Neu-
rology, 65(1), 102–106.
improving over at least 4 years (Mathews et al.
Davidson, M., Harvey, P., Welsh, K. A., Powchik, P.,
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also been shown to correlate with various functioning in late-life schizophrenia: A comparison
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(1998). Neuropathological and neuropsychological psychological battery total score in multinational mild
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944 Constraint Induced Therapy

Geriatric Cognnitive Disorders, 3(1), 446–458. https://

doi.org/10.1159/000356725 Constraint Induced Therapy
Roalf, D. R., Moberg, P. J., Xie, S. X., Wolk, D. A., Moelter,
S. T., & Arnold, S. E. (2013). Comparative accuracies of
two common screening instruments for classification of Carley Borza1, Martin Mrazik2 and Marianne
Alzheimer’s disease, mild cognitive impairment, and Hrabok3
healthy aging. Alzheimer's & Dementia, 9(5), 529–537. 1
University of Alberta, Edmonton, AB, Canada
https://doi.org/10.1016/j.jalz.2012.10.001 2
Rosen, W. G., Mohs, R. C., & Davis, K. L. (1984). A new Department of Educational Psychology,
rating scale for Alzheimer’s disease. The American University of Alberta, Edmonton, AB, Canada
3
Journal of Psychiatry, 141(11), 1356–1364. Department of Psychology, Addiction and
Rossetti, H. C., Munro Cullum, C., Hynan, L. S., & Lacritz, Mental Health, Alberta Health Services,
L. H. (2010). The CERAD neuropsychologic
battery total score and the progression of Edmonton, AB, Canada
Alzheimer disease. Alzheimer Disease and Associated
Disorders, 24(2), 138–142. https://doi.org/10.1097/
WAD.0b013e3181b76415 Definition
Seo, E. H., Lee, D. Y., Lee, J. H., Choo, I. H., Kim, J. W.,
Kim, S. G., et al. (2010). Total scores of the CERAD
neuropsychological assessment battery: Validation for Constraint induced therapy (CIT), or more com-
mild cognitive impairment and dementia patients with monly termed constraint induced movement ther-
diverse etiologies. The American Journal of Geriatric apy (CIMT), is a neurorehabilitation technique
Psychiatry, 18(9), 801–809. https://doi.org/10.1097/
JGP.0b013e3181cab764. used primarily following stroke, in order to
Stein, J., Luppa, M., Luck, T., Maier, W., Wagner, M., improve functional use of the neurologically
Daerr, M., et al. (2012). The assessment of changes in weaker upper extremity (Etoom et al. 2016; Fritz
cognitive functioning: Age-, education-, and gender- et al. 2012; Taub and Uswatte 2006). CIMT typ-
specific reliable change indices for older adults tested
on the CERAD-NP battery: Results of the German ically involves the restraint of an unaffected upper
Study on Ageing, Cognition, and Dementia in Primary extremity combined with intensive practice with
Care Patients (AgeCoDe). American Journal of Geri- the affected extremity (Kwakkel et al. 2015; Taub
atric Psychiatry, 20(1), 84–97. https://doi.org/10.1097/ and Uswatte 2006). There are a number of excel-
JGP.0b013e318209dd08.
Welsh, K. A., Butters, N., Hughes, J., Mohs, R., & lent reviews and meta-analyses that have recently
Heyman, A. (1991). Detection of abnormal memory been published (see “References”).
decline in mild cases of Alzheimer’s disease using
CERAD neuropsychological measures. Archives of
Neurology, 48(3), 278–281.
Welsh, K. A., Butters, N., Hughes, J. P., Mohs, R. C., & Historical Background
Heyman, A. (1992). Detection and staging of dementia
in Alzheimer’s disease. Use of the neuropsychological
measures developed for the Consortium to Establish a CIMT was first documented in 1909 by Munk in
Registry for Alzheimer’s Disease. Archives of Neurol- nonhuman primates (Munk 1909, as cited in
ogy, 49(5), 448–452. Kwakkel et al. 2015). It was observed that animals
Welsh, K. A., Butters, N., Mohs, R. C., Beekly, D., Edland, avoided use of their affected limb unless the unaf-
S., Fillenbaum, G., et al. (1994). The Consortium to
Establish a Registry for Alzheimer’s Disease fected limb was restrained (Fritz et al. 2012; Taub
(CERAD). Part V. A normative study of the neuropsy- and Uswatte 2006). This idea was then applied to
chological battery. Neurology, 44(4), 609–614. patients with hemiplegia following stroke (Taub
Welsh-Bohmer, K. A., & Mohs, R. C. (1997). Neuropsy- and Uswatte 2006). Original CIMT consisted of
chological assessment of Alzheimer’s disease. Neurol-
ogy, 49(Suppl 3), S11–S13. three intensive components: immobilization of the
Wolfsgruber, S., Jessen, F., Wiese, B., Stein, J., Bickel, H., non-paretic arm, task-oriented training, and
Mosch, E., et al. (2014). The CERAD neuropsycholog- behavioral strategies to improve transfer of
ical assessment battery total score detects and skills from clinical to real world settings
predicts Alzheimer disease dementia with high diag-
nostic accuracy. American Journal of Geriatric Psychi- (see Etoom et al. 2016; Morris et al. 2006; Taub
atry, 22(10), 1017–1028. https://doi.org/10.1016/j. et al. 2013 for discussion). Given the intensity of
jagp.2012.08.021. conventional CIMT and practical barriers to
Constraint Induced Therapy 945

implementation, a modified constraint-induced Goals and Objectives

movement therapy (mCIMT) protocol has been
used, which uses component parts of conventional Research suggests upper extremity hemiparesis of
CIMT, such as repetitive task-specific training of the contralateral limb is the most common impair-
the affected upper extremity (Kwakkel et al. 2015; ment following stroke (see Hatem et al. 2016 for
Park et al. 2015). discussion). Therefore, CIMT’s major goal is to
restore independence to stroke survivors by C
increasing the use of the affected limb in real
Rational or Underlying Theory world environments. In contrast to rehabilitation
strategies that focus on developing compensatory
CIMT reflects the integration of a wide variety of techniques, CIMT aims to optimize and develop
research fields, including neuroplasticity, motor residual functions.
learning, and behavioral therapy (Sterr et al.
2006). Outcomes of CIMT are believed to be the
result of two separate mechanisms: overcoming Treatment Participants
learned nonuse and use-dependent cortical reor-
ganization (see discussion in Arya et al. 2011; Research has suggested CIMT may be indicated
Corbetta et al. 2015; Fritz et al. 2012; Kwakkel for individuals presenting with mild to moderate
et al. 2015). paresis of an upper limb who show some exten-
The theory of learned nonuse emerged from sion of wrist and fingers (Corbetta et al. 2015;
experiments with nonhuman primates. Learned Nijland et al. 2010). Extension in the wrist and
nonuse is said to occur post brain injury due to fingers is indicative of integrity of the
unsuccessful motor attempts with the affected corticospinal tract system, which is suggested to
extremity, which leads to punishment (e.g., pain, be associated with posttreatment improvement
incoordination, and failure to meet the goal of the (Kwakkel et al. 2015; Nijland et al. 2010).
movement). CIMT aims to counter learned nonuse Although this therapy was developed for indi-
by restraining the unaffected arm so the individual viduals post-stroke, CIMT has been modified and
uses the affected arm. Reinforcement contingen- extended to a number of clinical populations,
cies are thereby altered via CIMT training, and use including cerebral palsy (Case-Smith et al. 2012;
of affected limb is reinforced in the course of Taub et al. 2011; Uswatte and Taub 2013), TBI
treatment. (Cimolin et al. 2012; Shaw et al. 2005), multiple
Use-dependent cortical reorganization is the sclerosis (Mark et al. 2008, 2013; Uswatte and
second primary mechanism thought to underlie Taub 2013), aphasia (Uswatte and Taub 2013;
CIMT (Arya et al. 2011; Uswatte and Taub Woldag et al. 2017), and focal hand dystonia in
2013). Both animal studies and neuroimaging musicians (Berque et al. 2013). A form of CIMT
techniques have been used to study neural reorga- was developed for lower extremities and has
nization associated with CIMT. The relationship shown to be efficacious in a variety of populations
between neuroplasticity and the return of motor (Mark et al. 2013; Uswatte and Taub 2013; Zhu
function is not yet well understood; however, et al. 2016).
some researchers hypothesize that lesion site,
corticospinal tract involvement or alterations in
brain architecture may be associated factors Treatment Procedures
(Fritz et al. 2012). The precise underlying mech-
anism for motor improvement continues to be an CIMT is generally administered as a package
active area of investigation (see Buma et al. 2013; treatment, incorporating restraint of the unaf-
Laible et al. 2012; van Kordelaar et al. 2013; fected limb, structured practice (e.g., shaping
Uswatte and Taub 2013). and repetitive practice) with the affected limb,
946 Constraint Induced Therapy

and behavioral transfer strategies (see Morris et al. daily activities; Corbetta et al. 2015). Data on
2006; Uswatte and Taub 2013 for discussion). long-term effects of CIMT is limited. Taken
Specifically, structured practice involves every- together, it appears results for the efficacy of
day functional tasks, such as eating lunch and CIMT are mixed and further randomized control
throwing a ball. A “transfer package” refers to trials with larger sample sizes and methodological
the use of behavioral techniques (e.g., behavior rigor are needed to better understand this therapy.
contracts, diary logs) to promote the transfer of
motor improvements in a controlled laboratory
setting to daily life, in order to encourage treat- Outcome Measurement
ment adherence.
Conventional CIMT treatment aims for Overall, in the CIMT literature there are signifi-
restraint of the unaffected limb for 90% of waking cant discrepancies between improvement in dis-
hours and structured practice up to 6 h per day for ability (i.e., real world functioning) and motor
approximately 2 weeks (Kwakkel et al. 2015), functioning, measured in a laboratory setting. In
with variances noted (Corbetta et al. 2015). How- their review of RCTs and quasi-RCTs, Corbetta
ever, due to conventional CIMT’s intense proce- et al. (2015) reported the most commonly used
dures mCIMT has been developed to decrease measures of disability are the Functional Indepen-
cost, time, and patient burden. Modifications dence Measure (FIM), followed by the Barthel
have included group delivery (Henderson and Index (BI). The most common measures of arm
Manns 2012) and home-based protocols (Barzel motor function are the Action Research Arm Test
et al. 2015). Additional research suggests that (ARAT) and the Wolf Motor Function Test
CIMT paired with neurostimulation may be a (WFT). Arm motor impairment is most often
safe and efficacious motor rehabilitation treatment assessed by the Fugl-Meyer Assessment (FMA),
for children and adults post stroke (Gillick et al. and QOL via the Stroke Impact Scale (SIS).
2015; Rocha et al. 2016).
Research suggests that the dose of CIMT
varies from between 30 min and 6 h per day, 2–7 Qualifications of Treatment Providers
sessions per week for between 2 and 12 weeks
(Kwakkel et al. 2015). CIMT is most frequently facilitated by physio-
Improvements in existing motor abilities are therapists and occupational therapists (see
possible with both immediate and delayed CIMT Corbetta et al. 2015). In light of expertise in
(see Corbetta et al. 2015; Lang et al. 2013; Wolf behavioral theory and techniques, psychologists
et al. 2010 for discussion). However, CIMT early can have an important role in consultation and
in the post-stroke period may confer an advantage facilitation of behavioral techniques. In light of
(e.g., Lang et al. 2013). the intensive nature of CIMT, psychologists may
have an important role in supportive intervention
with patients undergoing CIMT.
Efficacy Information

Methodological limitations in CIMT literature

include sample size, inadequate statistical power,
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of reporting (see Corbetta et al. 2015; Etoom et al. Movement therapy induced neural reorganization and
2016). Despite these limitations, a Cochrane motor recovery in stroke: A review. Journal of Body-
review reported CIMT demonstrates superiority work and Movement Therapies, 15(4), 528–537.
https://doi.org/10.1016/j.jbmt.2011.01.023.
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Barzel, A., Ketels, G., Stark, A., Tetzlaff, B., Daubmann,
in terms of motor impairment and dexterity, but A., Wegscheider, K., . . ., & Scherer, M. (2015). Home-
not in overall disability (the ability to function in based constraint-induced movement therapy for
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tion intervention for upper extremity in stroke patients: G. R., Bryson, C. C., . . ., & Bowman, M. H. (2013).
Systematic review and meta-analysis. International Constraint-induced movement therapy for the lower
Journal of Rehabilitation Research. Internationale extremities in multiple sclerosis: Case series with
Zeitschrift Fur Rehabilitationsforschung.Revue 4-year follow-up. Archives of Physical Medicine and
Internationale De Recherches De Readaptation, Rehabilitation, 94(4), 753–760. https://doi.org/
39(3), 197–210. https://doi.org/10.1097/ 10.1016/j.apmr.2012.09.032.
MRR.0000000000000169. Morris, D. M., Taub, E., & Mark, V. W. (2006). Constraint-
Fritz, S. L., Butts, R. J., & Wolf, S. L. (2012). Constraint- induced movement therapy: Characterizing the inter-
induced movement therapy: From history to plasticity. vention protocol. Europa Medicophysica, 42(3),
Expert Review of Neurotherapeutics, 12(2), 191–198. 257–268.
https://doi.org/10.1586/ern.11.201. Nijland, R. H., van Wegen, E. E., Harmeling-van der Wel,
Gillick, B., Menk, J., Mueller, B., Meekins, G., Krach, L. B. C., Kwakkel, G., & EPOS Investigators. (2010).
E., Feyma, T., & Rudser, K. (2015). Synergistic effect Presence of finger extension and shoulder abduction
of combined transcranial direct current stimulation/ within 72 hours after stroke predicts functional recov-
constraint-induced movement therapy in children and ery: Early prediction of functional outcome after stroke:
young adults with hemiparesis: study protocol. Bio The EPOS cohort study. Stroke, 41(4), 745–750.
Med Central Pediatrics, 15(1), 178. https://doi.org/ https://doi.org/10.1161/STROKEAHA.109.572065.
0.1186/s12887-015-0498-1. Park, J., Lee, N., Cho, Y., & Yang, Y. (2015). Modified
Hatem, S. M., Saussez, G., Della Faille, M., Prist, V., constraint-induced movement therapy for clients with
Zhang, X., Dispa, D., & Bleyenheuft, Y. (2016). Reha- chronic stroke: Interrupted time series (ITS) design.
bilitation of motor function after stroke: A multiple Journal of Physical Therapy Science, 27(3), 963–966.
systematic review focused on techniques to stimulate https://doi.org/10.1589/jpts.27.963.
upper extremity recovery. Frontiers in Human Neuro- Rocha, S., Silva, E., Foerster, A., Wiesiolek, C., Chagas,
science. https://doi.org/10.3389/fnhum.2016.00442. A. P., Machado, G., . . ., & Monte-Silva, K. (2016). The
948 Constructional Apraxia

impact of transcranial direct current stimulation (tDCS)

combined with modified constraint-induced movement Constructional Apraxia
therapy (mCIMT) on upper limb function in chronic
stroke: A double-blind randomized controlled trial.
Disability and Rehabilitation, 38(7), 653–660. https:// Brittney Moore and Andrew S. Davis
doi.org/10.3109/09638288.2015.1055382. Department of Educational Psychology, Ball State
Shaw, S. E., Morris, D. M., Uswatte, G., McKay, S., University, Muncie, IN, USA
Meythaler, J. M., & Taub, E. (2005). Constraint-
induced movement therapy for recovery of upper-limb
function following traumatic brain injury. Journal of
Rehabilitation Research and Development, 42(6), Synonyms
769–778.
Sterr, A., Szameitat, A., Shen, S., & Freivogel, S. (2006).
Application of the CIT concept in the clinical environ- Constructional dyspraxia
ment: Hurdles, practicalities, and clinical benefits. Cog-
nitive and Behavioral Neurology: Official Journal of
the Society for Behavioral and Cognitive Neurology, Definition
19(1), 48–54. https://doi.org/00146965-200603000-
00006.
Taub, E., & Uswatte, G. (2006). Constraint-induced move- Constructional (or construction) apraxia results in
ment therapy: Answers and questions after two decades an inability to manipulate physical stimuli to con-
of research. NeuroRehabilitation, 21(2), 93–95. struct or build a design. Some patients with con-
Taub, E., Griffin, A., Uswatte, G., Gammons, K., Nick, J.,
& Law, C. R. (2011). Treatment of congenital struction apraxia may have isolated difficulties
hemiparesis with pediatric constraint-induced move- with construction depending on the task, while
ment therapy. Journal of Child Neurology, 26(9), others may be unsuccessful in all construction
1163–1173. https://doi.org/10.1177/ tasks (Lezak et al. 2012). Construction apraxia is
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Taub, E., Uswatte, G., Mark, V. W., Morris, D. M., Bar- one of the most common conditions resulting
man, J., Bowman, M. H., . . ., & Bishop-McKay, from a lesion to the parieto-temporo-occipital
S. (2013). Method for enhancing real-world use of a association cortex in either hemisphere (Benton
more affected arm in chronic stroke: Transfer package and Tranel 1993). Indeed, the most common def-
of constraint-induced movement therapy. Stroke, 44(5),
1383–1388. https://doi.org/10.1161/ icits seen in patients with lesions in the non-
STROKEAHA.111.000559. dominant hemisphere (usually the right) are
Uswatte, G., & Taub, E. (2013). Constraint-induced move- those involving construction abilities and visual-
ment therapy: A method for harnessing neuroplasticity spatial analysis (Blumenfeld 2002).
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63327-9.00015-1.
Woldag, H., Voigt, N., Bley, M., & Hummelsheim, See Also
H. (2017). Constraint-induced aphasia therapy in the
acute stage: What is the key factor for efficacy?
A randomized controlled study. Neurorehabilitation ▶ Apraxia
and Neural Repair, 31(1), 72–80. https://doi.org/ ▶ Visual-Motor Function
10.1177/1545968316662707. [pii]. ▶ Visual-Spatial Ability
Wolf, S. L., Thompson, P. A., Winstein, C. J., Miller, J. P.,
Blanton, S. R., Nichols-Larsen, D. S., . . ., & Taub,
E. (2010). The EXCITE stroke trial: Comparing early
and delayed constraint-induced movement therapy. References and Readings
Stroke (00392499), 41(10), 2309–2315. https://doi.
org/10.1161/STROKEAHA.110.588723. Benton, A. L., & Tranel, D. (1993). Visuoperceptual,
Zhu, Y., Zhou, C., Liu, Y., Liu, J., Jin, J., Zhang, S., . . ., & visuospatial, and visuoconstructive disorders. In
Wu, Y. (2016). Effects of modified constraint-induced K. M. Heilman & E. Valenstein (Eds.), Clinical neuro-
movement therapy on the lower extremities in patients psychology (3rd ed.). New York: Oxford University
with stroke: A pilot study. Disability and Rehabilita- Press.
tion, 38(19), 1893–1899. https://doi.org/10.3109/ Blumenfeld, H. (2002). Neuroanatomy through clinical
09638288.2015.1107775. cases. Sunderland: Sinauer Associates.
Contingency Table 949

Lezak, M. D., Howieson, D. B., Bigler, E. D., & Tranel, negatives and then dividing them by the
D. (2012). Neuropsychological assessment (5th ed.). number of total decisions ((TP + FN)/total
New York: Oxford University Press.
decisions). This allows for a relatively simple
way to assess the relationships between categor-
ical variables.
Contingency Table A concrete example would be a group of
100 patients, 40 of whom have a true diagnosis C
1,2 2
Christian Schutte and Bradley N. Axelrod of mild cognitive disorder. You give them a brief
1
Henry Ford Allegiance, Jackson, MI, USA test to diagnose the presence of the disorder.
2
John D. Dingell VA Medical Center, Psychology Using a cut you determined 55 patients are tagged
Section (11MHPS), Detroit, MI, USA as having the disorder and 45 as not having the
disorder. Using this information we can quickly
define a contingency table to find hit rate, sensi-
Synonyms tivity, and specificity, as well as positive and neg-
ative predictive power.
2  2 table
TBI No TBI
Test + 35 15 50
Definition Test  5 45 50
40 60 100
A contingency table generally is a representation Cond. Condition
of categorical data in a tabular format, such as a
2  2 table, though the table can have three or
One can then calculate hit rate (TP + FN)/total
more variables. There are row variables on the
decisions) or (35 + 5)/100 = 0.4, sensitivity
horizontal axis and column variables on the verti-
(TP/(TP + FN)) or 35/(35 + 5) = 0.875, specific-
cal axis. It represents mutually exclusive vari-
ity (TN/(TN + FP) or 45/(45 = 15) = 0.75,
ables. Good examples of contingency tables are
positive predictive power (TP/(TP + FP) or
hit rate, sensitivity, and specificity, as well as
35/(35 + 15) = 0.70 and negative predictive
positive and negative predictive power. In the
power (TN/(TN + FN) or 45/(45 + 5) = 0.90.
case of hit rates to assess the number of correct
More complex contingency tables can be used,
classification decisions that result from the use of
such as 3  3 or more, though relationships
a particular test or measure, one would enter the
between variables are less clear due to difficulties
number of true positives, true negatives, false
with interaction effects. More complex contin-
positives, and true negatives into a contingency
gency tables are often analyzed with more com-
table like the one below.
plex statistical procedures, such as log-linear
Cond. + Cond.  analysis.
Test True + False + Total + decisions
+ (TP) (FP)
Test False  True  Total  decisions
 (FN) (TN) See Also
Base rate Cond. Total of all
Absent decisions ▶ Multivariate Analysis of Variance
Cond. Condition ▶ Negative Predictive Power
▶ Positive Predictive Power
In this example hit rate would be calculated by ▶ Sensitivity
adding the number of true negatives and false ▶ Specificity
950 Continuous Auditory Test of Attention (CATA)

(the target). The remaining 20% (i.e., ten) are

Continuous Auditory Test of unwarned trials, in which the target high tone is
Attention (CATA) not preceded by the low tone warning. Respon-
dents are required to respond to high tones on
Lindsay E. Ayearst warned trials and ignore high tones (inhibit their
Multi-Health Systems Inc., Toronto, ON, Canada response) on unwarned trials. They are also asked
to listen for the target sound in the same ear in
which they heard the warning sound. The majority
Synonyms of warned trials (i.e., 75% or 30/40 warned trials
within each block) have the warning and target
Conners CATA sounds played sequentially in the same ear. These
are called nonswitch trials. In the remaining trails
(i.e., 25% or 10/40 warned trials within each
Description block), the warning and target sounds are played
in opposite ears. These are referred to as switch
The Conners Continuous Auditory Test of Atten- trials. On the switch trials, the warning sound is an
tion (Conners CATATM) assesses auditory pro- invalid cue to the location of the target sound,
cessing and attention-related problems in requiring the respondent to switch attention from
individuals 8 years of age and older. The one ear to the other.
14-min test consists of 200 trials divided into The Conners CATA was normed on a large,
four blocks of 50 trials each. The test provides demographically representative sample, including
specific information about the type of auditory 1,080 individuals from the general population as
attention deficits (e.g., inattentiveness, impulsiv- well as 193 individuals with clinical diagnoses.
ity, and sustained attention) and information Computer-generated reports describe the respon-
about auditory processing, including laterality dent’s performance in detail using Confidence
(i.e., relative effectiveness/efficiency in pro- Intervals, to provide information about the range
cessing left- or right-ear targets) and mobility of scores in which the respondent’s true score is
(i.e., the ability to shift attention from one ear to expected to fall, as well as empirical percentiles,
another) (see Table 1 below). to provide information about where the respon-
The Conners CATA paradigm includes 80% dent ranks among his or her peers in the normative
(i.e., 40) warned trails in each block, in which a group for a given variable. Two types of reports
low tone (the warning) is followed by a high tone (e.g., an Assessment Report and Progress Report)
can be generated based on the type of interpreta-
tion required. The Assessment Report provides
Continuous Auditory Test of Attention (CATA),
Table 1 A summary of the Conners Continuous Auditory
information about a single administration,
Test of Attention whereas the Progress Report combines results of
Administration 14 min
up to four Conners CATA administrations
time conducted on the same respondent and indicates
Paradigm Respond to warned high tone, whether the respondent’s scores have increased or
ignore unwarned high tone decreased significantly over time. For assessors
Areas of Inattention interested in the respondent’s raw score for each
attention Impulsivity variable, raw scores are available as an option
measured Sustained attention in both reports. Generally speaking, higher
Auditory laterality raw score values indicate worse performance. To
Auditory mobility facilitate interpretation of the results, raw scores
Normative N = 1,080
are converted to standardized scores in most
sample
instances.
Continuous Auditory Test of Attention (CATA) 951

Historical Background sample was equal to 0.98 for female adults and
0.97 for all other groups. For the clinical sample,
There are two modalities, visual and auditory, the median split-half reliability estimates ranged
that are used for information processing in daily from 0.95 to 0.97 across all groups.
life. For example, students attending a class need Respondents scores on the Conners CATA tend
to direct their eyes to the front of the classroom to remain similar across repeated assessments
and listen to the words spoken by the instructor. (i.e., median corrected test–retest r = 0.64) and C
This commonplace scenario illustrates the differ very little from Time 1 to Time 2 (i.e., mean
importance of both visual and auditory attention. differences in scores between Time 1 and Time
Breakdown in either of these modalities can lead 2 were small, ranging from 2.1 to 2.4 T-score
to difficulties in information processing. Individ- points, and median absolute values for Cohen’s
uals with attention deficits may exhibit problems d was 0.05 indicating little change across scores
across modalities because there are common ele- from Time 1 to time 2). Laterality and mobility
ments of attention that extend across both the classifications have also been found to be stable
visual and auditory domains (Aylward et al. across administrations. Thus, assessors can feel
2002). However, there are also aspects of atten- confident that the Conners CATA yields scores
tion that are modality specific (Bedi et al. 1994; that, in the absence of an intervention, will remain
Cooley and Morris 1990), and some individuals consistent over time.
may exhibit attention deficits in one modality but
not the other. A comprehensive assessment bat- Validity
tery intended to evaluate attention deficits should The manual reports results from a variety of stud-
ideally consist of objective performance tests in ies exploring the validity of the Conners CATA
both visual and auditory modalities (Doyle demonstrating that:
et al. 2000).
The Conners CATA (2014) was developed to 1. Scores relate in a meaningful manner with an
provide unique information to visually based con- assessment of visual attention, the Conners
tinuous performance tests, such as the Conners CPT 3 (convergent validity)
Continuous Performance Test 3rd Edition 2. Scores discriminate between clinical (youths
(Conners CPT 3TM; Conners 2014). and adults with an ADHD diagnosis) and non-
clinical groups (discriminative validity)
3. Scores contribute to the predictive ability of the
Psychometric Data scores from the Conners CPT 3 and Conners
3rd EditionTM – Parent Form (Conners 3-P;
Reliability Conners 2008) (incremental validity; see
The Conners CATA scores demonstrated strong Table 2 below)
internal consistency in both the normative and 4. Scores have a high generalizability across dif-
clinical samples for youth aged 8–17 years and ferent administration methods (i.e., input
adults aged 18+ years. The median split-half reli- device and computer type) and race/ethnic
ability estimate across all scores in the normative groups

Continuous Auditory Test of Attention (CATA), Table 2 Incremental validity

Classification Conners Conners 3-P and Conners 3-P and Conners 3-P, Conners CPT 3,
statistic 3-P Conners CATA Conners CPT 3 and Conners CATA
Overall correct 83.9 88.4 88.4 93.8
classification (%)
Sensitivity (%) 86.0 91.2 89.5 94.7
Specificity (%) 81.8 85.5 87.3 92.7
952 Continuous Performance Tests

5. Scores have negligible or small relationships Cross-References

with levels of intelligence as measured by the
Wechsler Intelligence scale for Children – ▶ Conners 3rd Edition (Conners 3; Conners
Fourth Edition (WISC-IVTM, Wechsler 2003) 2008)
6. Scores in the normative sample are not affected
by presentation of auditory stimuli in the left or
right ear, or by switching attention from one References and Readings
ear to the other
Aylward, G. P., Brager, P., & Harper, D. C. (2002).
Relations between visual and auditory continuous
performance tests in a clinical population: A
descriptive study. Developmental Neuropsychology,
21, 285–303.
Clinical Uses Bedi, G., Halperin, J. M., & Sharma, V. (1994). Investiga-
tion of modality specific distractibility in children.
International Journal of Neuroscience, 74, 79–85.
As noted in the manual, “The Conners CATA can Conners, C. K. (2008). Conners 3rd edition manual.
be a useful adjunct to the process of diagnosing Toronto: Multi-Health Systems Inc..
Attention-Deficit/Hyperactivity Disorder Conners, C. K. (2014). Conners continuous performance
test – Third edition manual. Toronto: Multi-Health
(ADHD) and other neurological conditions
Systems Inc..
related to auditory attention” (p. 1). The Conners Cooley, E. L., & Morris, R. D. (1990). Attention in
CATA is unique in that it offers information about children: A neuropsychologically based model for
how a respondent initiates, sustains, and inhibits assessment. Developmental Neuropsychology, 6,
239–274.
attention, as well as the respondent’s ability to
Doyle, A. E., Biederman, J., Seidman, L. J., Weber, W., &
shift attention from one ear to the other (i.e., Faraone, S. V. (2000). Diagnostic efficiency of
auditory mobility). From a clinical perspective, neuropsycho-logical test scores for discriminating
the Conners CATA has much to offer, including boys with and without attention deficit–hyperactivity
disorder. Journal of Consulting and Clinical Psychol-
not only important information about possible
ogy, 68, 477–488.
attentional deficits in the auditory modality of Wechsler, D. (2003). Wechsler intelligence scale for
single individual when used as part of a broader children – Fourth edition. San Antonio: Pearson.
assessment for educational, functional, mental
health, or other related reasons, but it can also be
used to screen individuals/groups, to monitor
change over time through multiple administra- Continuous Performance
tions, and to evaluate the effectiveness of an inter- Tests
vention or treatment.
It is important to recognize that poor perfor- Ronald A. Cohen
mance on the Conners CATA is not necessarily Department of Clinical and Health Psychology,
indicative of an ADHD diagnosis. A number of College of Public Health and Health Professions,
different disorders are characterized by deficits in University of Florida, Gainesville, FL, USA
attention that could lead to poor performance on Center for Cognitive Aging and Memory,
the Conners CATA. For example, a diagnosis of McKnight Brain Institute, University of Florida,
Schizophrenia or presence of an auditory pro- Gainesville, FL, USA
cessing disorder can negatively affect perfor-
mance on the Conners CATA. Poor performance
on the Conners CATA is an indication of an atten- Synonyms
tion problem, but not an indication of any partic-
ular disorder. CPT
Continuous Performance Tests 953

Description evaluations. In fact, the CPT was one of the first

neuropsychological paradigms widely adapted for
An attention paradigm that has evolved into a computerized assessment. Subsequently, impair-
class of neuropsychological tests used to assess ments on this paradigm were demonstrated across
sustained attention. There is not a single continu- various disorders, most notably schizophrenia
ous performance test (CPT), as a number of com- (Nuechterlein 1983) and attention deficit disorder
mercially available and research CPT tasks exist (Epstein et al. 2003). C
and have been published in the neuropsychologi-
cal literature. The common characteristic of all
CPT tests is that they involve sequential presen- Psychometric Data
tation of stimuli, usually letters or numbers, over
an extended period of time. The task demand is to In its original form, the CPT provided measures of
attend and respond to particular target stimuli, accuracy and response bias over the course of a
while ignoring other stimuli that serve as nontar- fixed time period using signal detection method-
get distractors. ology. Although the tests may vary in terms of
length and type of stimulus used, the underlying
paradigm is the same across versions of the test.
Historical Background Patients are presented with series of letters
(typically) or other stimuli on a screen and are
Early efforts by psychologists to assess attention told to push a response key only when they see
in the context of intellectual or other cognitive the “target” stimulus. They are instructed not to
testing typically relied on tests such as digit respond when they see any other stimuli. The
span, which provided a useful measure of atten- letter “x” has often been used as the target in
tional focus and span, but did not address other CPT paradigms, with the task to respond to this
important elements of attention, such as the letter while ignoring other letters that flash before
patients’ ability to selectively attend to informa- them. Several common variations of the standard
tion or to sustain attention (Cohen 2014). CPT paradigm exist, in particular, a conditional
Sustained attention was particularly difficult to task, in which the patient must only respond to the
assess using traditional paper-and-pencil tests, as target letter when another stimulus occurs imme-
it required the measurement of signal detection diately before it (e.g., A–X), which increases the
performance over extended periods of time. Psy- difficulty of the task.
chologists typically relied on behavioral observa- In recent years, a variety of tests based on
tion or analysis of patterns of inconsistency in test computerized CPT paradigms have been devel-
performance over time to derive evidence of oped, with varying degree of sensitivity and spec-
sustained attention problems. The development ificity to clinical disorders of attention. At the
of the tachistoscope for rapid presentation of present time, the most widely used commercially
visual stimuli with controlled timing provided a available CPT tests are versions by Conners et al.
means of circumventing this problem. Mirsky and (2003) and the test of variables of attention
his colleagues (1956) described the continuous (TOVA), though a variety of others exist, such as
performance paradigm and provided research VIGIL (1990) and the d2 test of attention
data supporting its sensitivity in detecting brain (Brickenkamp 1992). Typically, a CPT is included
damage. The advent and widespread availability as part of a more comprehensive battery of tests of
of computer technology in the decades that attention and executive functioning.
followed led to more widespread experimentation Given that the CPT paradigm is based on
with this paradigm and it eventually being more signal detection theory and method, there are
commonly used in standard neuropsychological certain indices common to all versions of the
954 Continuous Performance Tests

test: correct responses, errors of omission attention. While d0 and b provide excellent mea-
(misses), errors of commission (false positives), sures of detection accuracy, response deposition,
and response time (RT). Correct responses are and overall attention performance, they do not
based on the sum of the number of times the directly provide measures of performance over
patient correctly responds to the target and cor- time. Recent versions of the Conner and other
rectly avoids responding to distractors. Omission CPT tests tend to now include a measure of tem-
errors (misses) are errors involving a failure to poral variability in performance. While there are a
respond to the target, while commission errors variety of ways that the temporal nature of perfor-
(false positives) are errors involving a response mance can be determined, two general types of
to nontargets. Errors of commission reflect a measures exist: (1) performance decrement and
failure to inhibit responding. High omission (2) performance inconsistency. Performance dec-
rates indicate that either the patient is not focus- rement provides a measure of the change in per-
ing adequately on the stimuli or that their pro- formance between the beginning and end of the
cessing speed is slow and they are unable to test. In theory, if a person is failing to sustain
respond rapidly enough. CPT tests usually also attention, their performance should worsen the
provide a measure of mean response time (RT), longer they stay on the task. However, often this
which reflects the processing speed of the patient measure is not impaired except when there is a
during the task. Higher rates of correct detections severe problem with sustained attention and
indicate better attention performance. fatigue after several minutes of effort. Perfor-
From these primary measures, signal detection mance inconsistency indices provide an alterna-
indices are usually derived based on a comparison tive temporal measure based on variance across
of error types. Based on the total number of errors time, as opposed to linear decrement.
of commission and omission on the CPT, a dis- A primary problem in interpreting the meaning
crimination index (d0 ) is calculated which pro- and clinical significance of CPT findings stems
vides a measure of accuracy based on from the lack of consistency across versions of the
standardized scores (z-scores) from normative tests, particularly with respect to basic parameters
samples. A measure of response bias (b) is also such as the duration of the interstimulus interval
usually derived based on the difference in stan- (ISI), the total duration of the task, and the task
dard scores for each type of error. Response bias demand. For example, a task requiring detection
indices provide a better way of interpreting ten- of a single letter is much easier than a conditional
dencies to make one type of error or the other paradigm requiring detection of a letter sequence
because they account for the total number of (A–X). Furthermore, the duration of a typical CPT
errors of each type. Receiver operator character- test can range from several minutes to over
istic (ROC) metrics can also be derived, which 20 min. Versions with a long ISI tend to be rela-
provide a way of interpreting the tendency to tively easy to perform, but are tedious, with
make errors of each type as a function of the signal behavioral challenge arising from the monotony
detection parameters of the task, such as percent- of the task, which over a long test period is really a
age of targets to nontargets. General equations for test of vigilance. In contrast, versions that have a
d0 and b are shown below. short ISI with conditional task demands or other
characteristics that increase difficulty tend to be
d0 ¼ zðmissesÞ þ zðfalse positivesÞ more sensitive to sustained attention in the context
of greater information processing demand and
beta ¼ zðmissesÞ requirement for focused attention. Adaptive-rate
 zðfalse positivesÞ=zðtotal errorsÞ continuous performance methods provide a
means of circumventing this issue. For example,
In the past, many versions of the CPT provided the adaptive-rate continuous performance test
only these basic indices, which limited their use- (ARCPT; Cohen 1993) adjusts its ISI over the
fulness in characterizing problems with sustained course of the test based on the accuracy of
Continuous Performance Tests 955

response to compensate for the slow speed of consistency of stimulus presentation makes it a
processing. The final ISI that is maintained by valuable addition to standard paper-and-pencil
the end of the test provides a strong measure of tests of cognitive function.
capacity limitations related to processing speed Performance deficits on the CPT are evident in
deficits. Also the ARCPT provides separate vigi- patients with various forms of brain dysfunction
lance decrement and inconsistency indices to (Rosvold et al. 1956). The most obvious use for
enable assessment of the temporal dynamics of the CPT is in the assessment of attention deficit C
performance over ten blocks of time over the disorder (ADD), for which the objective assess-
duration of the test. The ARCPT measures atten- ment of sustained attention is central to the diag-
tional performance on a rapid and challenging nosis. However, there is now an extensive
task which is less subject to boredom. Therefore, research literature demonstrating deficits or out-
the ARCPT provides and enables the assessment right impairments of CPT performance among
of sustained attention during a cognitively patients with a wide range of neurological and
demanding task compared to standard CPT para- psychiatric conditions. For this reason, impaired
digms. Also, because the ISI adjusts to shorter CPT performance should be considered a highly
durations when a patient is performing well, the sensitive measure of functional attention impair-
test can typically be completed in about 10 min. ment and brain dysfunction, though not necessar-
The ARCPT also provides several metrics that ily specific to one type of neurological or
enable assessment of temporal inconsistencies in psychiatric condition.
performance. Impairments of CPT are evident in patients
Despite the fact that CPT tests vary in a variety with neurodegenerative disorders like
of ways, many of the commonly used measures Alzheimer’s disease, as well as disorders affecting
(e.g., Conner’s CPT) report good test-retest reli- subcortical and white matter brain systems, such
ability in healthy adults. CPT performance tends as multiple sclerosis, HIV, and cerebrovascular
to correlate well with performance on other infor- disease. In fact, patients with cardiovascular dis-
mation processing-based measures and perfor- ease show a relationship between cardiac output
mance on speeded tests of attention and and CPT performance (Jerskey et al. 2009).
executive function, such as the Stroop and trail- Among patients with severe affective disorders,
making test. Validation studies conducted with the CPT performance is often impaired and associated
ARCPT indicate strong reliability (r = 0.95) for with problems with effort (Cohen et al. 2001).
accuracy of performance (d0 ) across samples and CPT has been shown to be sensitive to sustained
strong validity as indicated by the sensitivity of attention and information processing deficits asso-
CPT indices to measures of structural and func- ciated with neurotoxic exposure to lead, solvents,
tional brain and systemic physiological distur- drugs, or other substances. An important clinical
bances as discussed in greater detail below. determination that needs to be made when exam-
ining performance on the CPT is whether there is
evidence of an actual problem with sustained per-
Clinical Uses formance or whether a broader problem with
focused and selective attention exists that occurs
CPT tests should be included in all comprehensive regardless of the time spend on task.
neuropsychological batteries designed to provide
a thorough assessment attention, executive func-
tioning, and processing speed. There is a well- Cross-References
established research and clinical literature demon-
strating that this paradigm is highly sensitive to ▶ Attention Deficit Hyperactivity Disorder
brain dysfunction. The fact that the CPT yields ▶ Signal Detection Theory
measures of information processing characteris- ▶ Sustained Attention
tics based on a task with controlled timing and ▶ Vigilance
956 Contraindication

References and Readings Definition

Brickenkamp, R. Z. E. (1992). The d2 test of attention. A contraindication is a circumstance, condition,

Seattle: Hogrefe & Huber.
symptom, or factor that increases the risk associ-
Cohen, R. A. (2014). Neuropsychology of attention (2nd
ed). New York: Springer. ated with a medical procedure, drug, or treatment.
Cohen, R., Lohr, I., Paul, R., & Boland, R. (2001). Impair- A contraindication refers to any intervention con-
ments of attention and effort among patients with major sidered inappropriate or inadvisable based upon
affective disorders. Journal of Neuropsychiatry and
unique factors of the situation such as potential
Clinical Neurosciences, 13(3), 385–395.
Conners, C. K., Epstein, J. N., Angold, A., & Klaric, harmful interactions between drugs or medical
J. (2003). Continuous performance test performance conditions that renders an individual vulnerable
in a normative epidemiological sample. Journal of if implemented.
Abnormal Child Psychology, 31(5), 555–562.
A contraindication may be absolute or relative.
Epstein, J. N., Erkanli, A., Conners, C. K., Klaric, J.,
Costello, J. E., & Angold, A. (2003). Relations between Absolute contraindications are those which are
continuous performance test performance measures inadvisable without exception or qualification.
and ADHD behaviors. Journal of Abnormal Child Psy- They are either permanently recommended
chology, 31(5), 543–554.
against, or temporarily until the disqualifying con-
Gunstad, J., Cohen, R. A., Paul, R. H., & Gordon,
E. (2006). Dissociation of the component processes of dition is remediated. The use of the atypical anti-
attention in healthy adults. Archives of Clinical Neuro- psychotic medication, clozapine carries a risk of
psychology, 21(7), 645–650. agranulocytosis, a severe low white blood cell
Jerskey, B., Cohen, R. A., Jefferson, A. L., Hoth, K. F.,
disorder condition. Clozopine would be an abso-
Haley, A. P., Gunstad, J. J., et al. (2009). Sustained
attention is associated with left ventricular ejection lute contraindication in an individual with a his-
fraction in older adults with heart disease. Journal of tory of bone marrow suppression.
the International Neuropsychological Society, 15(1), Relative contraindications refer to circum-
137–141.
stances in which procedures or treatments are
Leark, R. A., Greenberg, L. K., Kindschi, C. L., Dupuy,
T. R., & Hughes, S. J. (2007). Test of variables of considered in comparative terms. They are con-
attention: Clinical manual. Los Alamitos: The TOVA tingent upon a risk/benefit analysis of the relevant
Company. factors. The proportionate value of an intervention
Nuechterlein, K. H. (1983). Signal detection in vigilance
is compared with its potential for negative conse-
tasks and behavioral attributes among offspring of
schizophrenic mothers and among hyperactive chil- quences. An example of a relative contraindica-
dren. Journal of Abnormal Psychology, 92(1), 4–28. tion would be the use of an anti-convulsant/mood
Rosvold, H. E., Mirsky, A. F., Sarason, I., Bransome Jr., stabilizing medication in the ongoing treatment of
E. D., & Beck, L. H. (1956). A continuous performance
a pregnant woman with severe bipolar mania and
test of brain damage. Journal of Consulting Psychiatry,
20, 343–350. suicidality, but whose has been asymptomatic
VIGIL. (1990). A continuous performance test. New only while on lithium.
Hampshire: Forethought.

Cross-References
Contraindication
▶ Extrapyramidal Symptoms
Marla Sanzone ▶ Iatrogenic
Independent Practice, Loyola College of ▶ Signs
Maryland, Annapolis, MD, USA

References and Readings

Synonyms Mosby. (2006). Contra- (definition). In T. Myers (Ed.),
Mosby’s dictionary of medicine, nursing & health pro-
Conflict; Counterindicant fessions (7th ed., p. 453). St. Louis: Mosby Elsevier.
Controlled Attention 957

Venes, D., Thomas, C., Egan, E., & Houska, A. (2001).

Contraindication (definition). In D. Venes et al. (Eds.), Controlled Attention
Taber’s medical dictionary (19th ed., p. 479). Philadel-
phia: FA Davis Company.
Anna MacKay-Brandt1,2 and Tina Trudel3
1
Nathan S. Kline Institute for Psychiatric
Research, Orangeburg, NY, USA
2
Taub Institute for Research on Alzheimer’s C
Contrecoup Injury Disease and the Aging Brain, Columbia
University, New York, NY, USA
3
Beth Rush Northeast Evaluation Specialists, PLLC, Dover,
Psychiatry and Psychology, Mayo Clinic, DE, USA
Jacksonville, FL, USA

Definition Synonyms

Contrecoup injury is an injury to the brain tissue Central executive; Cognitive control; Supervisory
directly beneath the skull, opposite to the point of attentional system
impact. It results from acceleration-deceleration
events during which the force impacting the
head causes the brain to slam into the skull on Definition
the opposite side of the blow. Motor vehicle acci-
dents, falls, sports injuries, and physical assaults Higher-order cognitive processes that influence
with blunt objects frequently result in contrecoup the regulation of behavioral responses and the
injuries. Skull characteristics make the most prob- selection of information to be attended to are
able sites of injury in the frontal and temporal based on task-related goals.
lobes, as tips of the skull can more easily be forced
into the underlying brain tissue in the frontal and
temporal lobes. Neuropsychological evaluation
can help to identify cognitive impairments arising Current Knowledge
from both the primary and secondary sites of
injury. Neuroanatomical
From a neuroanatomical perspective, brain net-
works other than those related to frontal lobe func-
Cross-References tions can be involved in controlled aspects of
attention. For example, parietal lobe structures
▶ Acceleration Injury appear to be important for response intention and
▶ Biomechanics of Injury sensory selective attention. However, control
▶ Cortical Contusion behaviors such as response planning, selection,
▶ Traumatic Brain Injury (TBI) and execution are associated with networks of cor-
tical and subcortical regions linked to the frontal
lobes. It is these functions that are most commonly
References and Readings referred to when discussing control functions of the
brain. Although there is not a clear anatomical
Graham, D. I., Saatman, K. E., Marklund, N., Copnte, V., mapping, studies suggest that different regions of
Morales, D., Royo, N., & McIntosh, T. K. (2006). The the frontal lobe (and associated networks) relate to
neuropathology of trauma. In R. W. Evans (Ed.), Neu-
rology and trauma (2nd ed., pp. 45–94). New York: different aspects of control, such that there is a
Oxford University Press. heterogeneity of functioning that would argue
958 Controlled Oral Word Association Test

against any unitary conceptualization of attentional Miyake, A., Friedman, N. P., Emerson, M. J., Witzki,
control (Cohen 1993). A. H., Howerton, A., & Wager, T. D. (2000). The
unity and diversity of executive functions and their
contributions to complex “frontal lobe” tasks: A latent
Cognitive variable analysis. Cognitive Psychology, 41, 49–100.
Similarly, cognitive researchers have made an Monsell, S. (2015). Task-set control and task switching. In
effort to move away from a homunculus view of J. Fawcett, E. F. Risko, & A. Kingstone (Eds.), The
handbook of attention. Cambridge, MA: The MIT
control functions, pointing out that terms such as Press.
central executive (Baddeley and Hitch 1974), Monsell, S., & Driver, J. (2000). Attention and perfor-
supervisory attentional system (Shallice 1988), mance XVIII: Control of cognitive processes. Cam-
and executive control (e.g., Anderson and Green bridge, MA: MIT Press.
O’Reilly, R. C., Braver, T. S., & Cohen, J. D. (1999).
2001) all take on the role of a poorly defined A biologically-based neural network model of working
black box and give the impression of a unitary memory. In P. Shah & A. Miyake (Eds.), Models of
concept. These terms continue to be useful working memory. New York: Cambridge University
placeholders while cognitive researchers work Press.
Repovs, G., & Baddeley, A. (2006). The multi-component
out the details of related systems, such as the model of working memory: Explorations in experimen-
subcomponent or “slave systems” of Baddeley tal cognitive psychology. Neuroscience, 139(1), 5–21.
and Hitch’s (1974) model of working memory Shallice, T. (1988). Form neuropsychology to mental
or as the black box framework is incrementally structure. Cambridge: Cambridge University Press.
Shallice, T., Stuss, D. T., Picton, T. W., Alexander, M. P., &
replaced with new insights into specific control Gillingham, S. (2008). Mapping task switching in fron-
functions (Repovs and Baddeley 2006). New tal cortex through neuropsychological group studies.
tools for the direct study of phenomena such as Frontiers in Neuroscience, 2(1), 79–85.
task switching, response inhibition, goal forma-
tion, and planning in the form of functional
neuroimaging (e.g., Shallice et al. 2008), com-
putational modeling (O’Reilly et al. 1999), and Controlled Oral Word
statistical modeling techniques (Miyake et al. Association Test
2000) continue to clarify the processes involved
in these selection functions (Monsell and Driver Janet Patterson
2000; Monsell 2015). Audiology and Speech-Language Pathology
Service, VA Northern California Health Care
System, Martinez, CA, USA
Cross-References

▶ Divided Attention Synonyms

▶ Focused Attention
▶ Frontal Lobe Category fluency; CFL test; COWA; COWAT;
▶ Vigilance F-A-S test; Letter fluency; Phonemic fluency;
Verbal fluency

References and Readings

Description
Anderson, M. C., & Green, C. (2001). Suppressing
unwanted memories by executive control. Nature,
410, 366–369. The Controlled Oral Word Association Test
Baddeley, A. D., & Hitch, G. (1974). Working memory. In (COWAT) is a measure of verbal fluency and is a
G. H. Bower (Ed.), The psychology of learning and subtest of the Multilingual Aphasia Examination
motivation: Advances in research and theory (Vol. 8,
(MAE; Benton et al. 1994). The COWAT uses two
pp. 47–89). New York: Academic Press.
Cohen, R. (1993). The neuropsychology of attention. three letter sets – C, F, and L; and P, R, and W
New York: Plenum. (Ross et al. 2006) – to assess phonemic fluency.
Controlled Oral Word Association Test 959

Individuals are given 1 min to name as many Psychometric Data

words as possible beginning with one of the let-
ters. The procedure is then repeated for the Psychometric data for the COWAT and other pho-
remaining two letters (see Strauss et al. 2006; nemic fluency tests, as well as other verbal fluency
Benton et al. 1994 for specific administration tasks (e.g., semantic fluency), are readily available.
instructions). Several tests of phonemic fluency Norms have been published for children and adults
exist, some of which are part of larger test batte- of varying ages, levels of education, ethnic diver- C
ries (e.g., the MAE or the Neurosensory Center sity, and geographical diversity (Bolla et al. 1998;
Comprehensive Examination for Aphasia; Spreen Loonstra et al. 2001; Rodriguez-Aranda and
and Benton 1977) and others that can be admin- Martinussen 2006; Strauss et al. 2006). Some dif-
istered independently (e.g., the F-A-S Test). ferences have been noted between test forms, most
Verbal fluency is a cognitive function that facil- notably, between the COWAT and F-A-S Test
itates information retrieval from memory. Suc- (Barry et al. 2008); the CFL form appeared more
cessful retrieval requires executive control over difficult, while results for the F-A-S form appeared
cognitive process such as selective attention, men- more variable. In addition, COWAT scores have
tal set shifting, internal response generation, and been correlated with neuropsychological measures
self-monitoring. Tests of verbal fluency evaluate such as reading tests and IQ tests.
an individual’s ability to retrieve specific informa-
tion within restricted search parameters (Lezak
et al. 2004). The two most common parameters Clinical Uses
are semantic fluency and phonemic fluency.
Scoring for the COWAT and other verbal fluency
tests is straightforward. The examiner writes each
Historical Background word as it is produced by the individual. Many
examiners mark responses in 1500 intervals as a
Borkowski et al. (1967) were early proponents of way of evaluating sustained effort. The transcript
systematically examining word fluency in persons is reviewed and inadmissible words (i.e., repeti-
with brain damage. They recognized that so- tions, proper names, or slang) are eliminated. The
called word fluency tasks had been used in neu- test score is the total number of different words
ropsychological investigation of patients with produced for all three letters (see Strauss et al.
brain damage and undertook two studies of the 2006; Benton et al. 1994 for specific administra-
task. The first established the relations between tion instructions).
word fluency and various English letters; the sec- Supplementary scoring measures for the
ond examined word fluency data for persons with COWAT and other phonemic fluency tests provide
brain damage and control patients. They presented additional information in clinical diagnosis and
normative data for the first study and comparative treatment. Supplementary scorning measures are
data for the second, clearly supporting their error analysis, and cluster and switching analysis
hypotheses of the utility of word fluency (see Table 1). In error analysis, the examiner notes
assessment. any observable pattern of production of errors that
Since publication of these data, word fluency suggests a loosening of executive control over
tasks, and the COWAT in particular, have been cognitive processes that would result in errors.
investigated in detail. Spreen and Risser (2003) For example, a pattern of multiple repetitions of
suggest that this assessment tool in its various previous responses suggests perseveration and
forms has been one of the most frequently and inefficient self-monitoring. Error patterns provide
thoroughly investigated neuropsychological qualitative performance data and may appear as
assessment measures for unimpaired and neuro- common patterns such as repetition of a word or
logically impaired persons. A search of electronic idiosyncratic patterns. Clustering and switching
databases confirms this suggestion. analyses evaluate the depth of the searchable
960 Controlled Oral Word Association Test

Controlled Oral Word Association Test, Table 1 An Scores from the COWAT are useful in evalu-
example of F-A-S test results and cluster and switch scor- ating verbal fluency and persons with neurogenic
ing for a person with aphasia
communication disorders, such as aphasia fol-
Clusters and lowing stroke, traumatic brain injury, and
Responses switches
dementia. Studies have included COWAT in the
FAS-Test: “F” fast, fun, fickle, Clusters = 8 (mean
fuschsia, finger size = 1.1) diagnostic batteries given to several patient
of fate, fast populations and also in treatment studies as mea-
four, fifty-four, fun sures of behavioral change. The utility of the
forty, fornicate fickle COWAT in identifying the nature and severity
Words = 9 fuchsia
finger of fate of performance deficits in clinical populations
four has been supported; however, conflicting find-
fifty-four ings have been reported. Typically, the total
forty, fornicate number of acceptable responses is the reported
Switches = 7
test result; however, increasingly cluster and
FAS-Test: “A” apple, aardvark, Clusters = 5 (mean
alpaca, size = 1) switching scores are reported as well (Ross
ammonia, arsenic apple et al. 2007). The COWAT is valuable in detecting
Words = 5 aardvark cognitive dysfunction, but it requires further
alpaca study before definitive conclusions are possible
ammonia
arsenic with regard to performance patterns that can
Switches = 4 be linked with specific neurogenic behavioral
FAS-Test: “S” substantial, sum, Clusters = 5 (mean deficits.
subtraction, size = 1.8)
stuck, structure, substantial, sum,
symbol, subtraction
sympathy, stroke, stuck, structure
sixty symbol, sympathy Cross-References
Words = 9 stroke
sixty
▶ Aphasia
Switches = 4
Total Words = 23 Clusters = 18
▶ Aphasia Tests
Mean size = 1.27 ▶ Benton, Arthur (1909–2006)
Switches = 15 ▶ Boston Diagnostic Aphasia Examination
▶ Circumlocution
▶ Clustering
knowledge base (clusters) and the cognitive flexi- ▶ Cognitive Functioning
bility within and across categories (switching) ▶ Cognitive Processing
(Troyer, Moscovitcvh, & Winocur 1997). An exam- ▶ Cognitive-Communication Disorder
ple of an efficient search strategy would be identi- ▶ Cue
fying a cluster or subcategory within the category ▶ Cued Recall
(e.g., words that begin with “cr” in the COWAT task ▶ Error Recognition and Correction
of naming words that begin with C) and producing ▶ Free Recall
as many items in that category as possible and then ▶ Mayo’s Older Americans Normative Studies
switching clusters (e.g., to words beginning with (MOANS)
“cl”). Clusters are scored by counting the number of ▶ National Adult Reading Test and Orientation
clusters and calculating the mean cluster size; (Left–Right)
switches are scored by counting the number of ▶ Phonemic Cue
transitions between clusters. Rules for scoring clus- ▶ Semantic Cue
ter size and number of switches appear in Troyer et ▶ Semantics
al. (1997) and normative data for healthy adults ▶ Verbal Mediation
appear in Troyer (2000). ▶ Western Aphasia Battery
Conversational Treatments 961

References and Readings

Conversational Treatments
Barry, D., Bates, M. E., & Labouvie, E. (2008). FAS and
CFL forms of verbal fluency differ in difficulty: A
Julie Griffith
meta-analytic study. Applied Neuropsychology, 15,
161–166. Department of Speech Pathology and Audiology,
Benton, A. L., Hamsher, K., Rey, G. L., & Sivan, A. B. Ball State University, Muncie, IN, USA
(1994). Multilingual aphasia examination (3rd ed.). C
Iowa City: AJA Associates.
Bolla, K. I., Gray, S., Resnick, S. M., Galante, R., &
Kawas, C. (1998). Category and letter fluency in highly Synonyms
educated older adults. The Clinical Neuropsychologist,
12(3), 330–338. Conversation therapy
Borkowski, J. G., Benton, A. L., & Spreen, O. (1967).
Word fluency and brain damage. Neuropsychologia,
5, 135–140.
Goodglass, H., Kaplan, E., & Baressi, B. (2001). Boston Definition
diagnostic aphasia examination (3rd ed.). San
Antonio: Psychological Corporation.
(a) Conversational treatments for people with
Kertesz, A. (2006). Western aphasia battery. New York:
Grune & Stratton. aphasia strive to enhance the exchange of
Lezak, M. D., Howieson, D. B., Loring, D. W., Hannay, H. information between communication partners
J., & Fischer, J. S. (2004). Neuropsychological and create successful and fulfilling interac-
assessment (4th ed.). New York: Oxford University
tions by specifically practicing the necessary
Press.
Loonstra, A. S., Tarlow, A. R., & Sellers, A. H. (2001). elements of dialogue (e.g., conveying a mes-
COWAT metanorms across age, education and gender. sage, expanding upon an established topic)
Applied Neuropsychology, 8, 161–166. within conversation.
Rodriguez-Aranda, C., & Martinussen, M. (2006). Age-
(b) Conversation therapy is “‘direct’, planned
related differences in performance of phonemic verbal
fluency measured by Controlled Oral Word Association therapy that is designed to enhance conversa-
Task (COWAT): A meta-analytic study. Developmental tional skill and confidence” using activities
Neuropsychology, 30(2), 697–717. that directly address conversation and focus
Ross, T. P., Furr, A. E., Carter, S. E., & Weinberg, M.
on changing behaviors within the context of
(2006). The psychometric equivalence of two alternate
forms of the Controlled Oral Word Association Test. genuine conversation (Simmons-Mackie et al.
The Clinical Neuropsychlogist, 20, 414–431. 2014, p. 512)”.
Ross, T. P., Calhounn, E., Cox, T., Wenner, C., Kono, W.,
& Pleasant, M. (2007). The reliability and validity of
qualitative scores for the Controlled Oral Word Asso- Historical Background
ciation Test. Archives of Clinical Neuropsychology, 22,
475–488.
Spreen, O., & Benton, A. L. (1977). Neurosensory center There are distinct periods in the history of the
comprehensive examination for aphasia. Victoria: Uni- diagnosis and treatment of aphasia. Each time
versity of Victoria Neuropsychology Laboratory. period is marked by a movement that has laid
Spreen, O., & Risser, A. H. (2003). Assessment of aphasia.
the foundation for contemporary conversational
Oxford: Oxford University Press.
Strauss, E., Sherman, E. M. S., & Spreen, O. (2006). treatments. In the late nineteenth and early twen-
Compendium of neuropsychological tests: Administra- tieth centuries, physicians and scholars (e.g.,
tion, norms, and commentary (3rd ed.p. 502). Oxford: Paul Broca, Carl Wernicke) focused on the ana-
Oxford University Press.
tomical and physiologic nature of aphasia. Early
Troyer, A. K. (2000). Normative data for clustering
and switching on verbal fluency tasks. Journal of work in aphasiology aimed to explain language
Clinical and Experimental Neuropsychology, 22, deficits by exploring and dissecting lesioned
370–378. brains. Brain lesions were then mapped to create
Troyer, A. K., Moscovitch, M., & Winocur, G. (1997).
connectionist diagrams. These diagrams depict
Clustering and switching as two components of verbal
fluency: Evidence from younger and healthy adults. how brain centers may work together for speech
Neuropsychology, 11, 138–146. comprehension and production. Around the time
962 Conversational Treatments

Conversational Treatments, Table 1 Evidence-based conversational treatments for people with aphasia
Intervention name Intervention focus Brief description References
Promoting Person with The clinician and person with aphasia participate Davis (2005); Davis and
Aphasics’ Aphasia equally as senders and receivers of new Wilcox (1985)
Communicative information. Both may choose any
Effectiveness communication modality to convey a message
(PACE)
Response Person with People with aphasia are coached by clinicians to Kearns (1985);
Elaboration Aphasia expand the content of their conversations by Wambaugh and
Training (RET) increasing word retrieval, content words and Martinez (2000);
elaborating on ideas Wambaugh et al. (2001)
Script Training Person with A person with aphasia and clinician co-construct Cherney et al. (2008);
Aphasia a monologue or dialog that is rehearsed Lee et al. (2009);
repetitively using techniques such as phrase Youmans et al. (2005)
repetition and choral reading to improve fluency
Supported Communication Trains communication partners and people with Kagan (1998); Kagan
Conversation for Partners/ Dyad aphasia to get and give accurate information et al. (2001)
Adults with through various supportive techniques such as
AphasiaTM (SCA asking yes/no questions, giving extra time, and
using multiple modalities of communication
Group conversation People with Group therapy brings people with aphasia,
therapy aphasia and caregivers, friends, and clinicians together to
multiple have authentic communicative and social
communication interactions
partners
Facilitating People with People with aphasia, clinicians, and loved ones Damico et al. (2015)
Authentic aphasia and improve conversation skills by identifying
Conversation multiple strategies that enhance conversation. The
(FAC) communication treatment occurs between people with aphasia
partners and clinicians first and then is generalized to
other communication contexts such as
communicating with spouses and peer groups

of the Second World War, aphasiologists began disorders. The twentieth century ended with a
to make a distinction between speech and lan- pragmatic revolution in which the communica-
guage. Treatment during this period took on a tion deficits associated with aphasia are consid-
peripheralist notion in which specific speech ered in view of an individual’s culture and
sounds were trained through auditory stimula- participation in daily living (Duchan 2011). Cur-
tion and motor placement training. Peripheralist rently, aphasiology is thriving in the pragmatic
treatment was largely based on shaping commu- revolution period as the Life Participation
nicative behavior by creating specific stimulus- Approach to Aphasia (LPAA Project Group
response associations. During the mid-twentieth et al. 2000) is gaining momentum. Therefore,
century, aphasia treatment moved beyond train- presently aphasia treatment is becoming highly
ing specific stimuli to develop therapy focused on enhancing quality of life by achieving
approaches that aimed to improve the underlying meaningful goals that improve the discourse and
psychological processes required for communi- conversational abilities of people with aphasia.
cation (e.g., Hildred Schuell’s Stimulation
Approach) and is known as the procession
period. A linguistic era occurred in the mid- Current Knowledge
1960s and 1970s during which aphasia was
viewed and treated as a deficit in linguistic The overall goals of conversation treatments and
knowledge and separate from motor speech therapy are to improve communication skills,
Conversational Treatments 963

confidence, and life participation for people with See Also

aphasia. The aims of conversational treatments
are personalized and co-constructed by people ▶ Pragmatic Communication
with aphasia and clinicians to convey messages ▶ Social Communication
in efficient and socially acceptable manners ▶ Speech-Language Therapy
(Hinckley 2009; Simmons-Mackie et al. 2014).
Thus, the success of conversational therapy may C
be measured in a variety of ways, from increas- References and Readings
ing and improving syntax and turn-taking to
joke-telling and gossiping (Simmons-Mackie American Speech-Language Hearing Association. (2016).
Practice portal. Retrieved from http://www.asha.org/
2008). Some people with aphasia may choose
practice-portal/
to increase their conversational skills by improv- Cherney, L. R., Halper, A. S., Holland, A. L., &
ing the fluency of their verbal productions as well Cole, R. (2008). Computerized script training for
as the content and variety of their utterances aphasia: Preliminary results. American Journal of
Speech-Language Pathology, 17, 19–34.
(Hinckley 2009). Others may utilize conversa-
Damico, J., Tetnowski, J., Lynch, K., Hartwell, J.,
tional therapy to enhance communication by Weill, C., Heels, J., & Simmons-Mackie, N. (2015).
focusing on initiating, responding to, and con- Facilitating authentic conversation: An intervention
tinuing responses. People with aphasia may also employing principles of constructivism and conversa-
tion analysis. Aphasiology, 29, 400–421.
wish to use the context of conversational treat-
Davis, A. G. (2005). PACE revisited. Aphasiology, 19,
ments to practice and promote the use of multiple 21–38.
communication modalities (e.g., gesturing, Davis, A. G., & Wilcox, J. (1985). Adult aphasia rehabilita-
drawing or referring to an augmentative and tion: Applied pragmatics. San Diego: College Hill Press.
Duchan, J. (2011). A history of speech-language pathol-
alternative communication device) during com-
ogy. Retrieved from http://www.acsu.buffalo.edu/
municative exchanges to enhance information ~duchan/new_history/overview.html
transfer. Hinckley, J. J. (2009). Conversational treatments: Aphasia.
Many treatments have been developed that Seminar presented at the 2009 American Speech-Lan-
guage Hearing Association Convention, New Orleans.
target conversational abilities specifically for peo-
Kagan, A. (1998). Supported conversation for adults with
ple with aphasia and communication partners or aphasia: Methods and resources for training conversa-
dyads that can be generalized to group interven- tional partners. Aphasiology, 12, 816–830.
tions. Table 1 presents a few of the existing con- Kagan, A., Black, S., Duchan, J., Simmons-Mackie, N., &
Square, P. (2001). Training volunteers as conversation
versational treatments with evidence for efficacy
partners using ‘Supported Conversation for Adults with
obtained from well-conducted clinical studies and Aphasia’ (SCA): A controlled trial. Journal of Speech,
expert opinion (American Speech-Language Language, and Hearing Research, 44, 624–638.
Hearing Association 2016). Kearns, K. P. (1985). Response elaboration training for
patient initiated Utterances. In Clinical aphasiology
conference: Clinical aphasiology conference
Future Directions (1985:15th: Ashland: June 2–6, 1985).
Lee, J. B., Kaye, R. C., & Cherney, L. R. (2009). Conver-
sational script performance in adults with non-fluent
Conversation is dynamic and collaborative in aphasia: Treatment intensity and aphasia severity.
nature; therefore, creating outcome measures that Aphasiology, 23, 885–897.
truly reflect conversational skills, communicative LPAA Project Group, Chapey, R., Duchan, J. F.,
Elman, R. J., Garcia, L. J., Kagan, A., Lyon, J., &
success, and social acceptance are needed. Ideally, Simmons-Mackie, N. (2000). Life participation
future research will hone in on distinct conversa- approach to aphasia: A statement of values for the
tional behaviors such as turn-taking and repairs of future. The ASHA Leader, 5(3), 4–6.
communication breakdowns that generalize to Simmons-Mackie, N. (2008). Social approaches to aphasia
intervention. In R. Chapey (Ed.), Language interven-
increase confidence and participation in conversa- tion strategies in aphasia and related neurogenic com-
tions for people with aphasia with diverse com- munication disorders (4th ed., pp. 290–319).
munication partners and settings. Baltimore: Lippincott Williams & Wilkins.
964 Coping

Simmons-Mackie, N., Savage, M. C., & Cross-References

Worrall, L. (2014). Conversation therapy for aphasia:
A qualitative review of the literature. International
Journal of Language & Communication Disorders, ▶ Self-Regulation
49(5), 511–526. ▶ Stages of Adjustment
Wambaugh, J. L., & Martinez, A. L. (2000). Effects of ▶ Stress
modified response elaboration training with apraxic ▶ Stress Management
and aphasic speakers. Aphasiology, 14, 603–617.
Wambaugh, J. L., Martinez, A. L., & Alegre, M. N. (2001).
Qualitative changes following application of modified
response elaboration traing with apraxic-aphasic References and Readings
speakers. Aphasiology, 15, 965–976.
Youmans, G., Holland, A., Munoz, M., & Carver, C. S., Scheier, M. F., & Weintraub, J. K. (1989).
Bourgeois, M. (2005). Script training and automaticity Assessing coping strategies: A theoretically based
in two individuals with aphasia. Aphasiology, 19, approach. Journal of Personality and Social Psychol-
435–450. ogy, 56, 267–283.
Lazarus, R. S., & Folkman, S. (1984). Stress, appraisal
and coping. New York: Springer.

Coping

Joel W. Hughes Coronary Artery Bypass Graft

Department of Psychology, Kent State University,
Kent, OH, USA Richard Kunz
Department of Physical Medicine and
Rehabilitation, Virginia Commonwealth
Synonyms University, Richmond, VA, USA

Stress management
Synonyms

Definition CABG

Coping is responding to environmental stimuli,

events, and circumstances for the purpose of min- Definition
imizing or managing stress, solving problems, and
modulating physiological and emotional Coronary artery bypass graft (CABG) is a surgical
responses. Coping is often paired with stress procedure for coronary artery disease in which
(as the latter elicits the former) in what has arteries or veins from other parts of the body are
become the stress and coping literature associated grafted from the aorta to the coronary arteries in
with Richard Lazarus and Susan Folkman. Stress order to bypass the blocked portions. Indications
responses typically involve appraising the stimu- for surgery include disease of the left main coro-
lus or event, which begins the process of assigning nary artery and/or disease of all three coronary
value (e.g., distressing) and determining arteries and abnormal ventricular function. It
responses (e.g., fight, flight, freeze). Coping is a may be performed in patients with severe angina
process that follows stress appraisals, and coping which is unresponsive to medical management.
responses seek to manage stress with cognitive, Patients undergo general anesthesia, and a
physiological, and behavioral responses. Various midline incision (median sternotomy) allows the
coping strategies have been categorized, such as surgeon to visualize the heart and vessels. The
appraisal-focused, problem-focused, or emotion- artery or vein grafts are then harvested. Frequently
focused coping. used vessels include the internal thoracic arteries,
Coronary Disease 965

radial arteries, and saphenous veins. The heart is Tarter, R. E., Butters, M., & Beers, S. R. (2001). Medical
then stopped using a special mixture of chemicals, neuropsychology (2nd ed.pp. 69–71). New York:
Kluwer Academic.
and the patient is placed on cardiopulmonary http://www.nlm.nih.gov/medlineplus/ency/article/002946.
bypass where the blood flow returning to the htm. Accessed 11 Oct 2016.
heart is diverted through a heart–lung machine
that provides extracorporeal circulation and oxy-
genation. The graft is then sewn into place and the C
heart is restarted. The sternum is then closed with Coronary Disease
wires, and the incision is sutured.
Elliot J. Roth
Department of Physical Medicine and
Rehabilitation, Northwestern University,
Current Knowledge
Feinberg School of Medicine, Chicago, IL, USA
In the early years of cardiac surgery, several inves-
tigators noted transitive postoperative delirium,
Synonyms
whereas others reported immediate postoperative
neurological abnormalities; however, no well-
Atherosclerotic heart disease; Coronary artery
conducted or controlled studies were available.
disease; Coronary heart disease; Ischemic heart
More recent studies have shown a short-term neu-
disease
ropsychological decline 7–14 days after CABG,
including deficits in psychomotor speed, atten-
tion, verbal learning, and memory. Studies have
Definition
reported an 11–75% incidence of postoperative
cognitive decline (POCD) after cardiac surgery.
Coronary disease, or coronary artery disease
Age is considered to be the strongest predictive
(CAD), results from atherosclerosis, or narrowing
factor of postoperative cognitive dysfunction. It is
of the arteries that provide blood supply to the
hypothesized that “off-pump” surgery causes less
heart muscle (“myocardium”).
cognitive decline as it avoids extracorporeal cir-
culation, but studies have not shown this to be
true. Other potential causes of neurocognitive
Current Knowledge
decline include intraoperative cerebral oxygen
desaturation or microemboli.
Atherosclerosis, which is the process by which
cholesterol and fat deposits adhere to the inside
walls of blood vessels, creates “plaques” that
References and Readings block the blood supply through blood vessels.
When this narrowing or occlusive process blocks
Ellis, L., Murphy, G. J., Culliford, L., Dreyer, L., Clayton,
the coronary artery, the accompanying obstruction
G., Downes, R., Nicholson, E., Stoica, S., Reeves,
B. C., & Rogers, C. A. (2015). The effect of patient- to blood flow reduces the supply of oxygen and
specific cerebral oxygenation monitoring on postoper- nutrients to the heart muscle, creating ischemia
ative cognitive function: A multicenter randomized that causes chest pain (“angina pectoris”), or death
controlled trial. JMIR Research Protocols, 4(4), e137.
Hillis, L. D., Smith, P. K., Anderson, J. L., Bittl, J. A.,
of the cells of the heart (“myocardial infarction”).
Bridges, C. R., et al. (2011). http://circ.ahajournals.org/ At times, it can cause other problems such as
content/124/23/e652.full. Accessed 29 June 2016. arrhythmias (abnormal heart rhythm) or conges-
Slater, J. P., Guarino, T., Stack, J., Vinod, K., Bustami, tive heart failure, in which the heart is unable to
R. T., Brown III, J. M., et al. (2009). Cerebral oxygen
desaturation predicts cognitive decline and longer hos-
pump sufficient blood to the remainder of the
pital stay after cardiac surgery. Annals of Thoracic body. CAD is the most common type of heart
Surgery, 87(1), 36–44. discussion 44–45. disease and the leading cause of death in USA.
966 Corpus Callosum

Risk factors for CAD have been well studied;

these include smoking, diabetes, hypertension, Corpus Callosum
hyperlipidemia, obesity, sedentary lifestyle,
excessive alcohol intake, and family history. Jeff Dupree
Although chest pain is the most common symp- Anatomy and Neurobiology, Virginia
tom, dyspnea, palpitations, diaphoresis, nausea, Commonwealth University, Richmond, VA, USA
radiation of the pain to the neck and left arm,
and no symptoms at all, also are possible. The
diagnosis relies on electrocardiogram, blood Synonyms
levels of cardiac enzymes, echocardiography,
select cardiac stress tests, and direct visualization Commissural magna; Corporis callosi;
on coronary angiography or other imaging stud- Interhemispheric commissure
ies. The treatment includes the use of beta-
blockers, calcium channel blockers, angiotensin
converting enzyme inhibitors, nitroglycerine, Definition
aspirin, or other medications; antihypertensive
and lipid-lowering agents; diet, exercise, and life- Corpus callosum is the largest axonal tract of the
style changes; thrombolysis; angioplasty with cor- adult brain that provides symmetrical connections
onary stent placement; and coronary bypass graft between the two hemispheres.
surgery.

Current Knowledge
Cross-References The corpus callosum is the largest commissure of
the adult brain that provides a bridge for the passing
▶ Angioplasty
of information from one cerebral hemisphere to the
▶ Anticoagulation
other by 200–300 million myelinated and unmy-
▶ Antiplatelet Therapy
elinated axons. The size of the corpus callosum
▶ Atherosclerosis
varies greatly but is generally larger in females
▶ Cholesterol
than in males. In the human, the corpus callosum
▶ Congestive Heart Failure
begins development around the 11th week of ges-
▶ Infarction
tation and continues through adolescence. Initially,
▶ Ischemia
the corpus callosum is composed of astrocytic pro-
▶ Myocardial Infarction
cesses, which serve as conduits for growing axons
▶ Recombinant Tissue Plasminogen Activator
extending to the contralateral hemisphere. This
▶ Stent
interhemispheric commissure lies beneath the cor-
▶ Thrombosis
tex at the bottom of the cerebral longitudinal fis-
▶ Vasospasm
sure. It forms much of the roof of the lateral
ventricles and is composed of four parts: the ros-
trum, the genu, the body (also known as the trunk),
References and Readings and the splenium. Each portion of the corpus
Hansson, G. K. (2005). Inflammation, atherosclerosis, and
callosum is responsible for connecting symmetrical
coronary artery disease. New England Journal of regions of the two hemispheres with the rostrum
Medicine, 352, 1685–1695. and genu connecting portions of the prefrontal and
Virmani, R., Kolodgie, F. D., Burke, A. P., Farb, A., & premotor cotices, the body interconnecting the pre-
Schwartz, S. T. (2000). Lessons from sudden coronary
motor, motor, supplementary motor, and the poste-
death: A comprehensive morphological classification
scheme for atherosclerotic lesions. Arteriosclerosis, rior parietal cortices, while the splenium connects
Thrombosis, and Vascular Biology, 20, 1262–1275. portions of the temporal, occipital, and parietal
Correlation Coefficients 967

lobes. Although being the largest white matter tract

of the brain, the corpus callosum is not essential for Correlation Coefficients
life. The complete or partial absence of the corpus
callosum is known as agenesis of the corpus Christian Schutte1,2 and Bradley N. Axelrod2
1
callosum. This condition is rare, and estimates of Henry Ford Allegiance, Jackson, MI, USA
2
incidence vary widely but are generally reported to John D. Dingell VA Medical Center, Psychology
range between 0.3% and 0.7% in the general pop- Section (11MHPS), Detroit, MI, USA C
ulation and as high as 3% in individuals with
development disabilities. Agenesis of the corpus
callosum results in symptoms ranging from asymp- Synonyms
tomatic with normal intelligence to intellectual
retardation, seizures, hydrocephalus, and spasticity. Pearson r; r; rho
In individuals suffering from severe epilepsy, a
surgical procedure known as corpus callostomy
may be performed, which involves the partial or Definition
complete transaction of the corpus callosum. This
procedure is only performed in patients who are at A measure of the strength of the relationship
risk of accidental injury resulting from severe sei- between two variables, x and y.
zures. The layman’s term for this condition is split
brain due to the loss of interhemispheric commu-
nication. Much of the original research detailing Historical Background
the consequence of corpus callostomy was
conducted by Dr. Roger Wolcott Sperry. The correlation, or co-relation, coefficient is typi-
cally attributed to Karl Pearson who developed the
formalized idea of correlation during the mid- to
Cross-References late 1800s. However, the beginning of the idea of
correlation may have come from Sir Francis Galton,
▶ Ganglion cousin of Charles Darwin. Galton worked on
▶ Gazzaniga, M. S. (1939–) genetic heritability of sweet peas. Through his
▶ Sperry, Roger Wolcott (1913–1994) work on heritability, he developed the beginnings
▶ Split-Brain of regression and correlation. Pearson, who worked
in Galton’s lab and was later his biographer, attrib-
uted the development of the regression slope to
References and Readings Galton. Pearson then generalized Galton’s work
into the Pearson product-moment correlation
Barr, M., & Kiernan, J. (1983). The human nervous (PPMC) or “moment” meaning the mean of a set
system – An anatomical viewpoint (4th ed.). Philadel- of products. The PPMC is often identified as “r,”
phia: Harper and Row.
which Galton originally used to denote “regres-
Gazzaniga, M. S. (2005). Forty-five years of split-brain
research and still going strong. Nature Reviews Neuro- sion” and Pearson later used as notation for corre-
science, 6(8), 653–659. lation. In 1896, Pearson published an article in
Haines, D. (2006). Fundamental neuroscience for basic which he credited Bravais for developing the rudi-
and clinical applications (3rd ed.). Philadelphia: Chur-
chill Livingstone Elsevier.
ments of the correlation formula. In this work,
Kandel, E., Schwartz, J. H., & Jessel, T. M. Principles of published in the Philosophical Transactions of the
neural science (4th ed.). New York: McGraw-Hill. Royal Society of London, Pearson showed that the
Paul, L. K., Brown, W. S., Adolphs, R., Tyszka, J. M., optimum values for the regression line and correla-
Richards, L. J., Mukherjee, P., et al. (2007). Agenesis of
tion could be derived from the product moment or
the corpus callosum: Genetic, developmental and func-
tional aspects of connectivity. Nature Reviews Neuro- xy/n, where x and y are derivations from their
science, 8(4), 287–299. respective means and n is the number of pairs.
968 Correlation Coefficients

Correlation Coefficients, 10
Fig. 1

y
4

0
0 2 4 6 8 10
x

Correlation Coefficients, 30
Fig. 2

25

20
y

15

10
0 5 10 15 20
x

Correlation Coefficients, 10
Fig. 3
8

6
y

0
0 2 4 6 8 10
x

Current Knowledge correlation can range between +1 and 1 with

these two extremes representing perfect relation-
A correlation, or co-relation, of two variables can ships, which rarely if ever occur in research, and a
be visually scanned initially by simply looking at correlation coefficient of 0 would represent no
a scatter plot of the data. The values of a relationship given certain assumptions are made.
Correlation Coefficients 969

Correlation Coefficients,
Fig. 4
8

6
C

y
4

2
0 2 4 x 6 8 10

Correlation Coefficients, 25
Fig. 5
20

15
y

10

0
0 5 10 15 20
x

A line can be drawn through data that are related There may also be negative associations, such
that generally approximates a regression line, that for every unit that x goes up, y goes down, or
which is how Galton identified the first regression a  1 relationship, such as the below idealized
line in his heritability studies with peas. Correla- example.
tion is a measure of the strength of the relationship However, typically, a scatter plot will not be as
between two variables. Thus, if data in a scatter obvious, and the data will look more like an
plot are randomly scattered, such as in the below ellipse like the below example, which still illus-
example, then there is no relationship, as no single trates a strong correlation of over 0.8.
line adequately represents the data and the corre- The above examples show linear relationships
lation would be roughly 0. between variables, which is an assumption of
If data are positively related, such that as one most correlation coefficients. An examination of
variable increases in value so does the other, then scatter plots can also show nonlinear relation-
one would be able to draw a line that would ships, which are not well represented by standard
approximately represent the data. The below exam- correlation coefficients, such as the PPMC, but
ple illustrates an ideal relationship that rarely can be shown with other methods, such as eta.
occurs in research of a + 1 correlation such that The below example has a near 0 Pearson r, but the
for every one unit that x goes up, y goes up one unit. variables are clearly related nonlinearly.
970 Correlation Coefficients

There are several forms of correlation that need degree that the distributions of the different
to be addressed including those for continuous variables differ, the correlation will attenuate
variables, categorical variables, and correlations the relationship between them, for example, if
that are more robust to nonlinear and skewed correlating a variable that is normally distrib-
relationships. The scope of this article is to cover uted, like height, with one that is highly skewed
the basic foundations of correlation coefficients. like ability to walk. This is done when corre-
The use of correlation ranges far and wide, and a lating a continuous variable with a dichoto-
thorough examination of this subject is the subject mous variable or when correlating interval
of chapters and entire texts referenced below. data with ordinal. If this assumption is violated
Thus, it is not the object of this entry to go in to a significant degree, then rank-order corre-
depth, but to cover foundational issues related to lation may be used, such as Spearman’s rho or
correlation coefficients. There are more correla- other nonparametric correlations.
tion coefficients than those presented below, 4. The data must have homoscedasticity: the error,
though several different forms of correlation and or random variance in X and Y, contained in the
their properties are considered. It is important to data is assumed to be equal along the entire
note that correlation, even a strong correlation, distribution. If, for example, one portion of the
does not infer causation. In other words, simply distribution has a much larger random variance,
because two variables are related does not mean then the correlation may overrepresent the rela-
that one causes the other. For example, you need tionship because it would underrepresent the
light to read this text. Simply because the light is amount of variance that is attributable to error.
on while you are reading does not mean that light If data are heteroscedastic, then the distribution
is causing you to read; they are certainly related, will not be normal and the correlation may mis-
as there will always be some light source when represent the data.
you read, but one does not cause the other. 5. The data has no or limited outliers: correlation
A determination of causation has more to do is sensitive to outliers. Some forms of correla-
with the experimental design. tion are more robust to a violation of this
First, there are certain important components assumption than others, but normally correla-
that underlie most correlations. Correlations are tion is a representation of deviations of mean
most meaningful when certain criteria are met. values. Thus, to the degree that the mean is
These include: affected by outliers, then the correlation will be
also. If there are many outliers, or few that are
1. The data are interval: the level of measurement large, this problem can be managed through
must at least be interval as opposed to nominal use of a Spearman’s rho, which ranks data.
or ordinal, though this can be managed if it is 6. There is limited measurement error present in
violated. the sample: it is assumed that the measurement
2. The data must have a linear relationship: most is relatively free from or has limited error. In
correlations assume that the data are linearly other words, if one has an invalid test that only
related, as opposed to nonlinear. To the degree measures error, then the correlation will be near
which the data are better explained by a non- zero, as the data will be random and show little
linear relationship correlation coefficients will relationship. It is rare in behavioral research to
underestimate the relationship. Prior to com- be free from error, but limiting it is an important
pleting a correlation analysis, this can be exam- aspect of experimental control.
ined by looking at a scatter plot, as discussed 7. The data have adequate variance: in order to
above. adequately assess relationships among vari-
3. The variables have similar and normal under- ables, there must be variance among the vari-
lying distributions (more formally in a bivari- ables. In general, the more variance, the higher
ate correlation, such as the Pearson r): to the the correlation will be.
Correlation Coefficients 971

To the extent that these criteria are violated, nominal variable, such as gender. The point-
which they often are, the correlation coefficient is biserial correlation is for naturally dichotomous
more or less impacted depending on the type of variables, such as gender, not artificially dichot-
correlation. omized variables, such as taking a naturally
There are several different methods calculating continuous distribution, such as intelligence,
basic correlation coefficients depending on the type and making it into high and low intelligence.
and characteristics of the data being analyzed. (C) Phi: This is a special case of the PPMC for C
There are several different types of correlation that use when both variables are dichotomous and
depend on the level of measurement (nominal, ordi- nominal. Note that as with rpb this is for
nal, interval, ratio) being made. Most are special naturally dichotomous variables, such as gen-
cases of the Pearson r. There are also other methods der, not artificially dichotomized variables.
that are more robust to violations of the above (D) Biserial or rb: This is for use when there is one
assumptions, such as Spearman’s rho or eta in the continuous variable, such as height, and a
case of a nonlinear relationship. The correlation dichotomized variable, such as high and low
coefficient is considered a measure of effect size, intelligence. So, the biserial correlation mea-
which is a measure of how different two distribu- sures the relationship between X and Y as if
tions are. By convention, a correlation of 0.1 is Y were not artificially dichotomized. This is
small, 0.3 moderate, and 0.5 large (Cohen1988), similar to the point-biserial, but the formula is
at least in the behavioral sciences that can expect designed to replace some of the variance that
weaker relationships in general due to the complex- is lost. One of the important components
ity of the subject matter. For example, the correla- listed above is that the data have adequate
tion between IQ and academic achievement is variance. However, when a variable is dichot-
approximately 0.55 (Griffenstein and Baker 2003), omized, much of the variance is lost. Thus,
but one would expect no effect for a correlation the biserial formula replaces some of that
between IQ and height. The correlation coefficient variance, which always yields a higher corre-
can also be squared to give the coefficient of deter- lation than a point-biserial correlation.
mination, which is the amount of variance in one (E) Tetrachoric: This is similar to the phi, except
variable that is accounted for by another. For exam- that it is assumed that there is a continuous
ple, if one had a correlation of 0.55 between IQ and distribution underlying the dichotomized var-
academic achievement, then the coefficient of deter- iables, and it thusly replaces some of that
mination (r2) would be 0.30, which means that variance, as opposed to phi that assumes that
approximately 30% of the variance in academic the two variables are naturally dichotomous,
achievement is accounted for by IQ: such as gender and employment status.
(F) Spearman’s rho or rs or r: Spearman’s rho is a
(A) Pearson product moment correlation (PPMC) nonparametric statistic. In other words, it
or r: The PPMS is an association of two makes no assumptions about the underlying
continuous variables that shows the degree distribution of the variables. One of the pri-
of linear relationship between them. It can be mary components of the typical PPMC is that
calculated using raw scores and deviation there is a normal or bell-shaped distribution
scores or by using a covariance formula. underlying the variable. However, in many
A common method is to calculate the stan- cases, distributions are highly skewed. For
dard score (or z score) and sum the products example, if one were to look at a distribution
of the two variables and divide them by the of people who live into adulthood in the USA,
degrees of freedom (n-1) or xy/n  1. the distribution would likely be very skewed to
(B) Point-biserial or rpb: This is a special case of the the left, meaning that the vast majority of peo-
PPMC for use when there is a continuous var- ple live at least until they are of adult age.
iable, such as height, and a dichotomous Relate that distribution to the number of people
972 Cortical Blindness

who vote, which would be positively skewed,

meaning that few people of adult age vote Cortical Blindness
proportionally, and a PPMC would not yield
an inaccurate representation, as this distribu- Steven Z. Rapcsak, G. Alex Hishaw and
tion significantly violates the assumptions of Tanya P. Lin
the PPMC. Thus, one could convert raw scores Neurology Section, Southern Arizona VA
into ranks and complete the correlation. This is Healthcare System, Tucson, AZ, USA
more robust to violations of some of the under- Department of Neurology, University of Arizona,
lying components of correlation. Tucson, AZ, USA
(G) Measures of nonlinear relationships: Eta is a
measure of association that can be used if the
data are nonlinear, as in the final scatter plot Synonyms
above. It is a measure of the strength of the
effect and is always positive. Eta is always Anton’s syndrome; Blindsight
higher than |r| and is therefore a biased esti-
mate of the effect.
Short Description or Definition
In practical usage, many of the different corre-
lation coefficients are calculated using the same Cortical blindness refers to severe visual loss pro-
method, such as the PPMC and the point-biserial, duced by bilateral damage to the geniculostriate
given the ubiquity of computer statistical packages. visual pathways. The underlying pathophysiologi-
What is important to note with any correlation cal mechanism involves direct destruction and/or
being used are the number and degree of the com- deafferentation of primary visual cortex (striate cor-
ponents that are violated and what impact that has tex, Brodmann area 17, or V1). The term Anton’s
on the relationship between the variables. For syndrome is applied to patients with cortical blind-
example, if one is using a PPMC to assess highly ness who demonstrate explicit denial or unaware-
skewed data, then the relationship may be very low, ness (anosognosia) of their visual impairment. Some
where actually, if a nonparametric method is used, patients with cortical blindness retain the ability to
such as the Spearman’s rho, then the relationship process visual stimuli without conscious awareness,
may be significant. Conversely, if a PPMC is used a phenomenon that has been coined “blindsight.”
on data that have many large outliers, the relation-
ship may look strong and be significant, but in
reality, it is the impact of those large outliers that Categorization
are falsely raising the strength of the associations.
Although no universally agreed upon classifica-
tion system exists, patients with cortical blindness
See Also differ in terms of the severity of the visual loss, the
presence/absence of spared visual abilities (con-
▶ Statistical Significance scious or unconscious), the degree of awareness
▶ Z Scores of the deficit, and the extent of functional recov-
ery. There are also variations across cases with
respect to the capacity to generate internal visual
Further Reading representations using mental imagery and the sus-
ceptibility to experience abnormal visual sensa-
Chen, P., & Popovich, P. (2002). Correlation: Parametric
tions/hallucinations. The precise neurobiological
and nonparametric measures. Thousand Oaks: Sage.
Cohen, J. (1988). Statistical power analysis for the behav- mechanisms underlying these individual differ-
ioral sciences (2nd ed.). Hoboken: Lawrence Erlbaum. ences remain to be determined.
Cortical Blindness 973

Epidemiology Neuropsychology and Psychology of

Cortical Blindness
Cortical blindness is a relatively rare condition,
typically caused by bilateral occipital strokes in In severe cases of cortical blindness, all forms of
the territory of the posterior cerebral arteries. conscious visual perception may be abolished.
Other less common etiologies include anoxic However, this type of total visual loss is relatively
brain damage, carbon monoxide poisoning, head uncommon, and many patients retain at least some C
trauma, and occipital lobe tumors. Transient cor- rudimentary visual awareness of motion or light.
tical blindness can be seen in the context of the Visual form discrimination is profoundly
reversible posterior leukoencephalopathy syn- impaired and objects, faces, or written words can-
drome (RPLS) related to hypertensive encepha- not be identified. Visuospatial orientation is also
lopathy, the use of chemotherapeutic and severely compromised, and patients may repeat-
immunosuppressant drugs, or the injection of edly bump into objects when attempting to navi-
radiological contrast agents during cerebral gate in their environment. Patients with cortical
angiography. blindness may experience visual hallucinations,
and the capacity to generate visual mental images
may be preserved.
Although individuals with cortical blindness
Natural History, Prognostic Factors, and do not have normal conscious awareness of visual
Outcomes events, they can sometimes demonstrate surpris-
ing ability to respond to stimuli presented within
Although some recovery of visual function is the blind portions of their visual fields. Specifi-
observed in most cases of cortical blindness, cally, patients may be able to detect, locate, and
patients with neuroimaging evidence of exten- discriminate visual stimuli that they claim not to
sive structural damage to occipital cortex typi- see. Residual visual capacity within the cortically
cally do not regain fully normal vision. Residual blind field in the absence of conscious awareness
visual field defects are common, and cortical has been referred to as “blindsight” (Weiskrantz
blindness may evolve into visual agnosia char- 1986; Stoerig and Cowey 1997, 2007; Stoerig
acterized by a persistent inability to recognize 2006; Cowey 2010). The fact that blindsight can
objects, faces, or words despite the return of be observed in patients with extensive destruction
more elementary visual functions. It is currently or deafferentation of primary visual cortex or V1
unclear whether recovery of visual capacity in suggests that the preserved visual abilities of these
cortical blindness is mediated by spared neural individuals are mediated by neural pathways from
tissue within primary visual cortex, or whether it the retina to extrastriate visual cortex that bypass
reflects the strengthening and increasing utiliza- the damaged geniculostriate system. In fact, neu-
tion of alternative visual pathways to extrastriate roimaging studies in humans have demonstrated
cortical regions that bypass the damaged several non-striate subcortical-cortical pathways
geniculostriate system, or both. Anosognosia capable of transmitting visual information to tem-
for visual loss in patients with Anton’s syndrome poral and parietal extrastriate areas that constitute
also tends to diminish over time, often parallel the ventral and dorsal visual streams critical for
to the resolution of the visual impairment, object recognition and visually guided motor
but partial defects of awareness are not uncom- behaviors. The specific visual functions retained
mon. In cases of transient cortical blindness in blindsight may depend on which of these mul-
due to RPLS, full recovery of vision can tiple parallel visual pathways are available to
occur within a few days along with complete patients. For instance, accurate hand (pointing/
resolution of the characteristic neuroradiological grasping) or eye movements toward targets
abnormalities. presented in the blind field (“action blindsight”)
974 Cortical Blindness

and successful navigation around obstacles during being blind and produce confabulatory responses
locomotion may depend on retinotectal projec- when questioned about their visual abilities. Other
tions to parietal cortex/dorsal visual pathway via patients acknowledge a change in their vision, but
superior colliculus and pulvinar (Danckert and they typically offer a variety of excuses to explain
Rossetti 2005; de Gelder et al. 2008; Tamietto the difficulty, attributing it to poor lighting condi-
et al. 2010; Buetti et al. 2013). Other dorsal stream tions or to a problem with their eyeglasses.
functions, such as preserved motion perception, A number of theories have been advanced to
may primarily utilize pathways directly linking explain anosognosia for blindness (Bisiach and
lateral geniculate nucleus (LGN) to the human Geminiani 1991; Heilman 1991; Celesia
middle temporal motion area (MT/V5), although et al. 1997; Adair et al. 2003). For instance, it
retinotectal projections to this extrastriate region has been proposed that normal visual awareness
have also been implicated (Bridge et al. 2008, depends on a hypothetical monitor located in
2010; Goebel et al. 2001; Ajina et al. 2015a, b; extrastriate visual association areas that receives
Hervais-Adelman et al. 2015). By contrast, afferent input from primary visual cortex
geniculo-extrastriate connections to category-spe- (Heilman 1991). In addition to evaluating activity
cific regions within inferior temporal cortex/ven- within the visual areas of the brain, the monitor
tral visual pathway are likely to be involved in also sends efferent information to cortical lan-
mediating unconscious discrimination of colors, guage areas enabling subjects to verbally com-
objects, faces, and body shapes (Trevethan ment on their visual experiences. Lesions that
et al. 2007; Goebel et al. 2001; Solca et al. 2015; disrupt the input and/or output connections of
Van den Stock et al. 2014), whereas subcortical the visual monitor, or produce damage to the
retinotectal/colliculo-pulvinar pathways targeting monitor itself, result in anosognosia for visual
the amygdala may play a dominant role in implicit impairment that may include verbal denial of the
visual processing of emotionally salient stimuli deficit and the production of confabulatory
including facial expressions, eye contact, and responses by the disconnected language areas. It
body language (“affective blindsight”) (Morris has also been suggested that in cases of cortical
et al. 2001; Pegna et al. 2005; Van den Stock blindness, internally generated visual experiences
et al. 2011; Burra et al. 2013; Tamietto et al. in the form of hallucinations or imagery may
2012). Functional imaging studies in patients provide faulty input to an otherwise intact moni-
with blindsight are consistent with the notion tor. The loss of normal visual input following
that unconscious processing of visual information damage to primary visual cortex may in fact give
depends on non-striate visual pathways. Specifi- rise to frequent “release” hallucinations in patients
cally, these investigations have demonstrated acti- with cortical blindness due to increased cortical
vation in subcortical visual nuclei, extrastriate excitability in deafferented extrastriate areas. Fur-
cortex, and the amygdala in the absence of con- thermore, since visual perception and imagery are
comitant activity in the lesioned primary visual mutually inhibitory under normal circumstances,
cortex during visual stimulation of the blind field the absence of bottom-up activation by
(Sahraie et al. 1997; Stoerig 2006; Morris geniculostriate afferent signals may be accompa-
et al. 2001; Pegna et al. 2005; Bridge et al. 2010; nied by a relative enhancement of visual imagery
Tamietto et al. 2010; Van den Stock et al. 2011; mediated by unopposed top-down activation of
Goebel et al. 2001; Ajina et al. 2015a; Hervais- sensory representations in extrastriate cortex.
Adelman et al. 2015). Consistent with this hypothesis, it has been dem-
Patients with cortical blindness may demon- onstrated that preserved visual imagery following
strate unawareness of their profound visual destruction of primary visual cortex is associated
impairment. This striking clinical condition is with activation of category-specific extrastriate
referred to as Anton’s syndrome. Anosognosia visual areas presumably mediated by top-down
for visual loss can take several different forms. influences from frontoparietal cortical networks
In extreme cases, patients emphatically deny (Bridge et al. 2012; de Gelder et al. 2015).
Cortical Blindness 975

Furthermore, unlike in normal individuals, extra- to visual field defects and/or domain-specific
striate neural responses during visual imagery in impairments in processing distinct visual stimulus
patients with cortical blindness may be stronger attributes (e.g., form, color, motion). If the same
than the activations elicited in the same cortical lesions also interfere with the bottom-up activation
areas by external visual stimulation (Bridge of the frontoparietal cortical network that normally
et al. 2012). Taken together, these results suggest enables conscious awareness and introspective
that patients with cortical blindness may deny report about visual experiences, anosognosia for C
their visual loss because they continue to experi- the visual impairment ensues. Defective awareness
ence internally generated visual sensations in the of visual function may also result from direct dam-
form of hallucinations or imagery and may mis- age to the putative frontoparietal network that pro-
take these for veridical perceptions resulting from vides the critical top-down attentional amplification
retinal stimulation by external visual events. required for perceptual information processed
To understand anosognosia for visual loss, it is within visual cortical modules to enter conscious-
useful to briefly consider what is currently known ness, or it may be produced by lesions that disrupt
about the neural correlates of normal visual feedforward/feedback connections between
awareness. In this context, it is important to frontoparietal cortex and visual processing areas.
emphasize that conscious awareness of visual In summary, conscious awareness of both normal
events normally entails the capacity to acknowl- and abnormal vision requires dynamic reciprocal
edge, describe, reflect upon, and make appropriate interactions between cortical visual areas and spe-
cognitive judgments about ongoing visual experi- cialized regions within frontal and parietal cortex.
ences (Weiskrantz 1997; Block 2005; Dehaene Lesions that disrupt the spatial distribution, inten-
et al. 2006). Thus, awareness and the ability to sity, or timing of activation across the different
provide introspective report or commentary about functional components of this large-scale neural
the quality, content, and veridicality of visual per- system may give rise to a variety of clinical condi-
ceptions are closely related functions. Although tions characterized by unawareness of preserved or
localized neural activity in cortical visual areas impaired visual processing, including blindsight,
(striate and extrastriate cortex) is obviously nec- visual neglect, and anosognosia for blindness.
essary for visual information to reach this “com-
mentary stage” of conscious awareness, it is by
itself not sufficient (Weiskrantz 1997; Rees et Evaluation
al. 2002; Dehaene et al. 2006). In particular, evi-
dence from neuroimaging studies suggests that Neuro-ophthalmological examination in cortical
conscious vision requires the additional recruit- blindness confirms the normal fundoscopic
ment of dorsolateral prefrontal and parietal corti- appearance of the retinas and optic nerves. The
cal regions implicated in visual attention and pupillary light response is characteristically pre-
working memory (Rees et al. 2002; Dehaene served, as the retinal fibers that mediate this reflex
et al. 2006; Dehaene and Changeux 2011). Pre- leave the optic tract prior to the origin of the
frontal cortex may also be involved in strategic geniculostriate pathways. Reflexive blinking to
cognitive operations necessary for evaluating and threatening visual gestures is usually absent, and
interpreting visual experiences, including reason- in the majority of cases, optokinetic nystagmus
ing, problem-solving, the use of contextual cues cannot be elicited by moving a striped object in
and other relevant information, criterion setting, front of the patient’s eyes. The dissociation
and decision-making. between preserved pupillary light response and
Activation of frontal and parietal regions by absent optokinetic nystagmus can have diagnostic
input from cortical visual areas is also likely to utility in distinguishing patients with cortical
play an essential role in awareness of abnormal blindness from patients with severe peripheral
visual function. Specifically, damage to primary visual loss due to bilateral eye or optic nerve
visual cortex and extrastriate areas may give rise pathology in whom both responses are lost and
976 Cortical Blindness

also from individuals with psychogenic blindness should be questioned about abnormal visual per-
in whom both responses are retained. ceptions and hallucinations. Unawareness of deficit
Clinical evaluation of visual function in patients may be revealed by spontaneous comments or
with cortical blindness should include tests of behavior, but patients should also be specifically
visual acuity, determination of light and motion asked to describe the quality and content of their
perception in different sectors of the visual field, visual experiences. The severity of anosognosia can
tests of spatial localization, as well as assessments be quantified by simple rating scales (Bisiach and
of color perception, object and face recognition, Geminiani 1991; Celesia et al. 1997).
and reading ability. Studying blindsight usually Structural neuroimaging (CT/MRI) studies in
requires the use of specialized testing equipment patients with cortical blindness due to stroke typ-
in an experimental laboratory environment. How- ically reveal extensive bilateral infarctions involv-
ever, in the clinical setting, blindsight can be tested ing primary visual cortex and underlying white
by requiring patients to guess the presence/absence, matter, often with evidence of lesion extension
location, movement, or identity of objects pre- into adjacent extrastriate visual association areas
sented in their blind field using a forced-choice (Brodmann areas 18/19, 37) (Fig. 1). SPECT/PET
response method (e.g., was it a key or a coin?). scans frequently demonstrate blood flow/meta-
Above chance performance on these tasks is taken bolic abnormalities that extend beyond the bound-
to be indicative of blindsight. Alternatively, patients aries of the lesions seen on CT/MRI, providing
can be asked to try to reach for and grasp objects in evidence that the cortical visual areas that appear
their blind field. Regardless of the testing method spared by structural imaging studies are in fact
used, it is important to establish after each trial functionally compromised. In patients with tran-
whether the patient had any conscious awareness sient cortical blindness due to RPLS, neuroimag-
of the visual stimulus. Visual imagery can be tested ing studies have demonstrated reversible bilateral
by asking subjects to answer questions about the subcortical white matter abnormalities in poste-
visual attributes of familiar objects or animals (e.g., rior occipito-temporo-parietal regions attributable
do polar bears have long or short tails?). Patients to vasogenic edema.

Cortical Blindness, Fig. 1 Diffusion-weighted MRI extension into ventral extrastriate visual association areas
scan in a patient with cortical blindness following bilateral (Brodmann areas 18, 19, 37). This individual demonstrated
posterior cerebral artery strokes. Note massive destruction complete denial of blindness (anosognosia), consistent
of primary visual cortex (Brodmann area 17), with lesion with Anton’s syndrome
Cortical Blindness 977

Treatment absence of the primary visual cortex. Journal of Neu-

roscience, 259, 1062–1070.
Buetti, S., Tamietto, M., Hervais-Adelman, A., Kerzel, D.,
A number of behavioral approaches have been de Gelder, B., & Pegna, A. J. (2013). Dissociation
tried with varying degrees of success to restore between goal-directed and discrete response localiza-
visual function in the cortically blind field and/or tion in a patient with bilateral cortical blindness. Jour-
help patients learn alternative strategies to nal of Cognitive Neuroscience, 25, 1769–1775.
compensate for their visual impairment (Kerkhoff
Burra, N., Hervais-Adelman, A., Kerzel, D., Tamietto, M.,
de Gelder, B., & Pegna, A. J. (2013). Amygdala acti-
C
2000). Attempts to increase awareness of the vation for eye contact despite complete cortical blind-
visual deficit in patients with anosognosia consti- ness. Journal of Neuroscience, 33, 10483–10489.
tute an important component of the treatment Celesia, G. G., Brigell, M. G., & Vaphiades, M. S. (1997).
Hemianopic anosognosia. Neurology, 49, 88–97.
program. It has been shown that blindsight perfor- Cowey, A. (2010). The blindsight saga. Experimental
mance can be improved by training, and the use of Brain Research, 200, 3–24.
these techniques may aid the recovery of vision in Danckert, J., & Rossetti, Y. (2005). Blindsight in action:
individuals with cortical blindness (Stoerig 2006; What can the different sub-types of blindsight tell us
about the control of visually guided actions? Neurosci-
Sahraie et al. 2006, 2013). ence and Biobehavioral Reviews, 29, 1035–1046.
Dehaene, S., & Changeux, J.-P. (2011). Experimental and
Cross-References theoretical approaches to conscious processing. Neu-
ron, 70, 200–227.
Dehaene, S., Changeux, J.-P., Naccache, L., Sackur, J., &
▶ Anosognosia Sergent, C. (2006). Conscious, preconscious, and sub-
▶ Visual Hallucinations liminal processing: A testable taxonomy. Trends in
Cognitive Sciences, 10, 204–211.
de Gelder, B., Tamietto, M., van Boxtel, G., Goebel, R.,
Sahraie, A., Van den Stock, J., Stienen, B. M. C.,
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Motion area V5/MTþ response to global motion in the Goebel, R., Muckli, L., Zanella, F. E., Singer, W., &
absence of V1 resembles early visual cortex. Brain, Stoerig, P. (2001). Sustained extrastriate cortical acti-
138, 164–178. vation without visual awareness revealed by fMRI
Ajina, S., Pestilli, F., Rokem, A., Kennard, C., & Bridge, studies of hemianopic patients. Vision Research, 41,
H. (2015b). Human blindsight is mediated by an intact 1459–1474.
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Bisiach, E., & Geminiani, G. (1991). Anosognosia related chological mechanisms. In G. P. Prigatano & D.
to hemiplegia and hemianopia. In G. P. Prigatano & D. L. Schacter (Eds.), Awareness of deficit after brain
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Block, N. (2005). Two neural correlates of consciousness. Tamietto, M., de Gelder, B., & Pegna, A. J. (2015).
Trends in Cognitive Sciences, 9, 46–52. Looming sensitive cortical regions without V1 input:
Bridge, H., Thomas, O., Jbabdi, S., & Cowey, A. (2008). evidence from a patient with bilateral cortical blind-
Changes in connectivity after visual cortical brain dam- ness. Frontiers in Integrative Neuroscience, 9, 51.
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1433–1444. Kerkhoff, G. (2000). Neurovisual rehabilitation:
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absence of V1 activation. Neuropsychologia, 48, Morris, J. S., DeGelder, B., Weiskrantz, L., & Dolan, R.
4148–4154. J. (2001). Differential extrageniculostriate and amyg-
Bridge, H., Harrold, S., Holmes, E. A., Stokes, M. S., & dala responses to presentation of emotional faces in a
Kennard, C. (2012). Vivid visual mental imagery in the cortically blind field. Brain, 124, 1241–1252.
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Pegna, A. J., Khateb, A., Lazeyras, F., & Seghier, M.

L. (2005). Discriminating emotional faces without pri- Cortical Contusion
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Sahraie, A., Trevethan, C. T., McLeod, M.-J., Weiskrantz,
L., & Hunt, A. R. (2013). The continuum of detection Cortical contusions are bruises on the brain tissue
and awareness of visual stimuli within the blindfield:
that form from the small blood vessel leaks (veins
from blindsight to sighted-sight. Investigative Ophthal-
mology and Visual Science, 54, 3579–3585. and arteries covering the parenchymal tissue) or a
Solca, M., Guggisberg, A. G., Schnider, A., & Leemann, B. series of microhemorrhages following trauma.
(2015). Facial blindsight. Frontiers in Human Neurosci- Trauma is usually the result of physical blows to
ence., 9, 522. https://doi.org/10.3389/fnhum.2015.00522.
the head such as those sustained in a motor vehicle
Stoerig, P. (2006). Blindsight, conscious vision, and the
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Research, 155, 217–234. significant sports-related injuries. Veins and arter-
Stoerig, P., & Cowey, A. (1997). Blindsight in man and ies on the surface of the brain are damaged, which
monkey. Brain, 120, 535–559.
results in bleeding and bruising. When the blood
Stoerig, P., & Cowey, A. (2007). Blindsight. Current Biol-
ogy, 17, R822–R824. vessel is torn, blood escapes from the vessel at a
Tamietto, M., Cauda, F., Corazzini, L. L., Savazzi, S., Marzi, rate that is faster than the blood that can be
C. A., Goebel, R., Weiskrantz, L., & de Gelder, B. absorbed by the brain. Consequently, cortical con-
(2010). Collicular vision guides nonconscious behavior.
tusions commonly result in edema and increased
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Tamietto, M., Pullens, P., de Gelder, B., Weiskrantz, L., & intracranial pressure.
Goebel, R. (2012). Subcortical connections to human
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Trevethan, C. T., Sahraie, A., & Weiskrantz, L. (2007).
Current Knowledge
Form discrimination in a case of blindsight. Neuropsy-
chologia, 45, 2092–2103. Second to diffuse axonal injury, cortical contusion
Van den Stock, J., Tamietto, M., Sorger, B., Pichon, S., is the most common type of intra-axial lesion
Grezes, J., & de Gelder, B. (2011). Cortico-subcortical
following brain trauma. By radiologic definition,
visual, somatosensory, and motor activations for per-
ceiving dynamic whole-body emotional expressions a cortical contusion must involve some portion of
with and without striate cortex (V1). Proceedings of the superficial gray matter. Because gray matter
the National Academy of Science, 108, 16188–16193. has more vasculature than white matter, most cor-
Van den Stock, J., Tamietto, M., Zhan, M., Heinecke, A.,
tical contusions are hemorrhagic, whereas diffuse
Hervais-Adelman, A., Legrand, L. B., Pegna, A. J., & de
Gelder, B. (2014). Neural correlates of body and face axonal injuries are rarely hemorrhagic. The frontal
perception following bilateral destruction of the primary and temporal lobes are the most common sites of
visual cortices. Frontiers in Behavioral Neuroscience, 8, cortical contusions. When present, cortical contu-
30. https://doi.org/10.3389/fnbeh.2014.00030.
sions are usually found bilaterally. Compared to
Weiskrantz, L. (1986). Blindsight: A case study and impli-
cations. Oxford: Clarendon Press. diffuse axonal injury lesions, cortical contusions
Weiskrantz, L. (1997). Consciousness lost and found. are much less likely to involve an initial presenta-
Oxford: Oxford University Press. tion of coma or altered loss of consciousness.
Cortical Magnification 979

Cross-References Current Knowledge

▶ Contrecoup Injury Cortical magnification reflects an important con-

▶ Edema cept in the field of cognitive neuroscience; the
▶ Focal Lesion, Contusion cortical volume, and ultimately the number of
▶ Intracranial Pressure neurons allocated to a particular function, typi-
cally varies as a function of the significance of C
the function. For example, since the sense of touch
References and Readings is particularly important for the hands, there are
many more nerve receptors in the fingertips than
Bigler, E. D. (2001). The lesions in traumatic brain injury: in the trunk of the body. Similarly, the volume of
Implications for clinical neurophysiology. Archives of
motor cortex dedicated to controlling the hands
Clinical Neuropsychology, 16, 95–131.
Graham, D. I., Saatman, K. E., Marklund, N., Conte, V., and mouth in humans is much greater than the
Morales, D., Royo, N., & McIntosh, T. K. (2006). The volume dedicated to large muscle groups with
neuropathology of trauma. In R. W. Evans (Ed.), Neurol- more limited action. Given the critical role that
ogy and trauma (2nd ed., pp. 45–94). New York: Oxford
vision plays in human cognition, a tremendous
University Press.
magnification of neurons is dedicated to visual
processing, with this magnification occurring at
various processing stages along the visual path-
ways beginning in the retina. The extent of corti-
cal magnification is often expressed as a ratio of
Cortical Magnification millimeters of cortical surface per degree of visual
angle. This ratio varies across visual areas.
Ronald A. Cohen Among primates, neurons devoted to processing
Department of Clinical and Health Psychology, foveal input from the retina are about 100 times
College of Public Health and Health Professions, more prevalent than neurons devoted to peripheral
University of Florida, Gainesville, FL, USA stimuli in the primary visual cortex (Daniel and
Center for Cognitive Aging and Memory, Whitteridge 1961).
McKnight Brain Institute, University of Florida, The principle of cortical magnification indi-
Gainesville, FL, USA cates an important relationship between the num-
ber of neurons dedicated to big or small visual
angles and the receptive field of those neurons.
Definition When a large number of neurons are involved in
a small visual angle, there is inherently a large
Cortical magnification refers to the fact that the processing capacity being assigned to a smaller
number of neurons in the visual cortex responsi- area of visual focus. Conversely, a smaller num-
ble for processing the visual stimulus of a given ber of neurons handling a visual angle are indic-
size varies as a function of the location of the ative of a larger receptive field, as each neuron
stimulus in the visual field. Stimuli occurring in must be sensitive to changes occurring across a
the center of the visual field that have been larger area of space. This creates an inherent
detected in the fovea of the retina are processed relationship between the spatial frequency of
by a very large number of neurons in the primary the visual information being processed and the
visual cortex of the occipital lobe, though these size of the receptive field that is essential for
neurons handle only a very small region of the considering how neurons across different visual
central visual field. Conversely, stimuli detected cortical areas are tuned to respond to the featural
in the peripheral visual field tend to be processed and spatial characteristics of visual input.
by a much smaller number of neurons in the A consequence of this organization for the pri-
primary visual cortex. mary visual cortex is that visual acuity and the
980 Cortical Mapping

ability to detect small features of stimuli are best areas critical for sensory, motor, or language func-
in the center of the visual field and poorest in the tion. This procedure is utilized when brain surgery
periphery. Yet broad spatial changes with move- involves the removal or disruption of potentially
ment are easily detected at the periphery. Since functional cortical areas. Sites identified via
visual cortical areas differ in their emphasis on cortical mapping are typically spared from resec-
specific informational characteristics (e.g., tion, with the goal of preserving function
shape, color, texture, position, movement), neu- postoperatively.
rons with greatest sensitivity to these dimensions Stimulation is applied using a bipolar stimula-
vary as a function of cortical magnification fac- tor, usually via pairs of adjacent subdural elec-
tors and a trade-off of size of the receptive field trodes. The procedure can be conducted intra-
and the number of neurons dedicated to each part operatively in a conscious patient before resection
of the field. of brain tissue, or extra-operatively, if subdural
electrodes have been implanted, most commonly
in pharmacologically resistant epilepsy patients
Cross-References who require intracranial EEG monitoring to delin-
eate the region of seizure onset and spread (Fig.
▶ Magnocellular Neurons 1). The identification of sensory and motor sites is
▶ Parvocellular Neurons based on stimulation-evoked “positive”
▶ Spatial Frequency Analysis responses, such as a subjective sensation (e.g.,
▶ Spatial Processing tingling) or an observable movement (e.g., muscle
twitch). In contrast, the stimulation of language
cortex elicits no experiential or observable
References and Readings response in an inactive patient. Rather, cortical
language mapping relies on “negative” responses,
Daniel, P. M., & Whitteridge, D. (1961). The representa- in that the patient must be engaged in a language
tion of the visual field on the cerebral cortex in mon-
task and stimulation of language cortex will dis-
keys. Journal of Physiology, 159, 203–221.
rupt task performance. Thus, for language map-
ping, stimulation produces a discrete, reversible
lesion, theoretically enabling the examiner to
observe the functional consequences of damage
Cortical Mapping to the site(s) stimulated. The stimulation of frontal
language cortex typically produces speech arrest,
Marla J. Hamberger whereas the stimulation of posterior (temporal/
Department of Neurology, Columbia University parietal) language cortex typically elicits compre-
Medical Center, New York, NY, USA hension, naming or reading difficulties. Because
cortical language mapping is based on negative
responses, thorough mapping of language cortex
Synonyms requires an administration of tasks assessing a
range of language functions.
Direct stimulation mapping; Electrical stimulation Depending on the location of the area identi-
mapping (ESM); Functional mapping fied and the nature of the response elicited by
stimulation, it is generally held that the removal
of a positive sensory, motor, or language site
Description identified by stimulation will result in impaired
function postoperatively. Of the few clinical series
Cortical mapping is an invasive procedure in published, results suggest that postoperative func-
which electrical stimulation is applied briefly to tion is best preserved when the resection margin
the cortical surface for the purpose of identifying exceeds 1 cm from the functional site. On the
Cortical Mapping 981

Cortical Mapping,
Fig. 1 Implanted subdural
electrode grid used for EEG
recording and electrical
stimulation mapping

other hand, there is some evidence that certain It should be noted that despite decades of
sites identified by stimulation can be removed widespread clinical use, cortical mapping is
without concern of postoperative decline. These unstandardized, with few empirical studies of
include motor sites identified in the supplemen- procedural parameters and no published guide-
tary motor area, tongue, and lower face areas (due lines. Across surgery programs, variations can be
to their bilateral representation) and, possibly, found with regard to electrical stimulation
language sites identified in the basal temporal parameters, language tasks utilized, and medical
region, although this is controversial. management.
For motor and sensory mapping, the duration
of electrical stimulation is typically 2 s, whereas
language mapping typically requires 4–8 s of Historical Background
stimulation, depending on the particular task
under assessment. The level of stimulation admin- The alteration of function via cortical stimulation
istered ranges from 1 mA to a maximum of in both animals and humans dates back to the mid-
17 mA, with motor and sensory cortex typically 1800s. The procedure came into clinical use in the
utilizing <10 mA and language cortex typically early twentieth century in association with surgi-
requiring >10 mA. Under normal circumstances, cal resection of epileptogenic cortex in patients
cortical stimulation causes neither pain nor dis- with pharmacologically refractory epilepsy. Ini-
comfort. One risk of stimulation, however, is the tially used to identify sensory and motor cortex,
evocation of a seizure, particularly in patients with Wilder Penfield and colleagues pioneered the
epilepsy, due to a likely lower seizure threshold in technique in the 1950s for use in the identification
epileptogenic areas. To minimize the probability of language cortex. Stimulation-based language
of a stimulation-induced seizure, cortical mapping mapping was further refined by George Ojemann
is usually conducted, while patients are on anti- and colleagues who essentially established the
seizure medication. Additionally, EEG is moni- current clinical standards. In addition to its clini-
tored on an ongoing basis, and the stimulation cal utility, investigators have used the opportunity
intensity is lowered when abnormal discharges provided by clinical stimulation to investigate
are associated with stimulation. Nevertheless, structure-function relations. These studies build
benzodiazepines are typically kept close at hand upon the lesion model, contributing more precise
for IV administration, for instance, when a seizure information regarding functional localization due
occurs and fails to resolve rapidly on its own. to both the controlled setting and the smaller,
982 Cortical Motor Pathways

more discrete “lesions” induced temporarily by impinge upon or possibly overlap with cortical
stimulation than that typically found with natu- regions necessary for function.
rally occurring lesions.

Cross-References
Psychometric Data
▶ Epilepsy
As noted, cortical mapping procedures remain ▶ Functional Imaging
unstandardized. Due to its highly invasive nature, ▶ Localization
data from cortical mapping are based on clinical
rather than normal populations, and therefore,
classic psychometric data are unavailable. It has References and Readings
also been difficult to assess reliability, as cortical
mapping is rarely performed more than once in Hamberger, M. (2007). Cortical language mapping in epi-
lepsy: A critical review. Neuropsychology Review, 4,
the same patient. Nevertheless, patients with
477–489.
indwelling subdural grids who undergo mapping Hamberger, M. J., Williams, A. C., & Schevon, C. A.
over 2 or more days and patients who require a (2014). Extraopeartive neurostimulation mapping:
second surgery involving adjacent brain regions Results from an international survey of epilepsy sur-
gery programs. Epilepsia, 55(6), 933–939.
provide opportunities for repeat mapping,
Ojemann, G. A. (1983). Electrical stimulation and the
although these circumstances are relatively infre- neurobiology of language. The Behavioral and Brain
quent. In the absence of published studies Sciences, 2, 221–230.
addressing this issue, anecdotal reports suggest a
reasonable level of consistency in the location of
simulation-identified sites within individuals.
Across individuals, consistency is relatively high
for the location of motor and sensory cortex. Cortical Motor Pathways
Frontal language cortex is slightly more variable,
with most positive sites clustered in the frontal Christina R. Marmarou
opercular region, anterior to the tongue area. The Neurosurgery, Virginia Commonwealth
location of posterior temporal and parietal lan- University, Richmond, VA, USA
guage sites appears to vary more among individ-
uals, although this might merely reflect alterations
in the distribution of language sites in patients Synonyms
with epileptogenic cortex in the temporal region.
Corticospinal tract; Pyramidal tract; Voluntary
motor tract
Clinical Uses

One of the main challenges with brain surgery Definition

involving cortical regions is to remove a sufficient
amount of pathological tissue without removing The cortical motor pathway consists of four
areas critical for function. Cortical mapping is regions of the cerebral cortex (primary motor cor-
used to identify cortical regions critical for func- tex, posterior parietal cortex, premotor cortex, and
tion, in order to spare these areas from resection or supplementary motor cortex) whose neuronal cell
protect them from damage during surgical pro- bodies are located in layer V (five) and whose
cedures. Cortical mapping is typically performed projections are involved with the execution of
when there is concern that resective brain surgery muscle contraction largely on the contralateral
(e.g., tumor resection, epilepsy surgery) might side of the body.
Cortical Motor Pathways 983

Current Knowledge basal ganglia) – to execute planning and control of

voluntary motor activity. Other projections from
The cortical motor pathway describes a trajectory layer V of M1 include the corticostriatal fibers to
of fibers whose cells of origin are located in layer the striatum (caudate and putamen), corticorubral
Vof the cerebral motor cortex. The cerebral motor fibers to the red nucleus, and projections that ter-
cortex is a term that describes the four main areas minate in the reticular formations with the medulla
of the cerebral cortex that contribute to the plan- and pons of the brain stem. M1 projections also C
ning, control, and execution of voluntary motor modulate other motor areas within the cortex and
fibers: the primary motor cortex (M1), secondary include reciprocal connections with the supple-
motor cortices, premotor cortex, and the supple- mentary motor area, the premotor and posterior
mentary motor area (SMA). parietal motor areas. These fibers are part of a
vast reciprocal network that cross via the corpus
callosum and are referred to as callosal connec-
Cortical Location and Overall Function tions. The SMA contributes to the corticospinal
tract and has reciprocal callosal projections to con-
The primary motor cortex (M1) is located in the tralateral areas of the motor cortex. The premotor
frontal lobe of the brain and the cells of origin, in cortex (PMC) contributes to the corticospinal tract
layer V, are found within the precentral gyrus. and also has extensive reciprocal connections to
These cells generate neural impulses that control both SMA and M1.
the execution of movement directed to skeletal
muscles on the contralateral side of the body.
Other regions of the cortex that contribute to the Cross-References
cortical motor pathway – termed secondary motor
cortices – include the posterior parietal area
▶ Cerebral Cortex
(PMA), the premotor cortex (PMC), and the sup- ▶ Decerebrate Posturing
plementary motor area (SMA). The posterior pari-
▶ Decorticate Posturing
etal cortex is responsible for transforming visual
▶ Hemiplegia
information into motor commands relayed via the ▶ Homunculus
premotor and supplementary motor area. The pre-
▶ Internal Capsule
motor cortex is involved in sensory guidance of
▶ Periventricular White Matter
movement and control of proximal and trunk ▶ Precentral Gyrus
muscles of the body. The supplementary motor
▶ Pyramidal System
area is involved in the planning and coordination ▶ Sensorimotor Assessment
of complex movements, such as those requiring ▶ Supplementary Motor Area (SMA)
coordination of two-handed movement.
Multiple pathways arise from the efferent pro-
jections of the motor cortices. Neuronal cell bodies References and Readings
located in layer V of the M1, SMA, and premotor
cortex send vast projections that collectively give Berne, R. M., & Levy, M. N. (2000). Principles of physi-
rise to the largest single pathway, the pyramidal or ology. St. Louis: Mosby.
corticospinal tract. The tract descends through the Fix, J. (1995). Neuroanatomy. Baltimore: Williams &
Wilkins.
internal capsule and forms the pyramids of the Haines, D. E. (2000). Neuroanatomy. Philadelphia:
medulla, crossing midline at the pyramidal decus- Lippincott Williams & Wilkins.
sation, ultimately terminating in the ventral horn of Haines, D. E. (2004). Neuroanatomy: An atlas of struc-
the cervical-through-lumbar spinal cord. These tures, sections, and systems. Philadelphia: Lippincott
Williams & Wilkens.
cortical motor pathways work in tandem with
Kandel, E. R., Schwartz, J. H., & Jessel, T. M. (1991).
other cortical motor areas of the brain – notably Principles of neuroscience. Norwalk: Appleton and
the cerebellum and subcortical motor nuclei (the Lange.
984 Cortical Thickness

Current Knowledge
Cortical Thickness
Cortical thickness is often calculated using auto-
Shawn Gale and Trevor Huff mated software packages such as the Advanced
Department of Psychology and Neuroscience Normalization Tools (ANTs) (see http://stnava.
Center, Brigham Young University, Provo, UT, github.io/ANTs/) software suite or FreeSurfer
USA (Fischl 2012) and subsequently used to compare
and contrast different groups of interest either in a
cross-sectional or longitudinal fashion.
Synonyms
Differences in regional cortical thickness
between groups may reflect atrophic changes
Brain development; Common measure; Cortical
(e.g., cell loss) or pruning, while increases in
atrophy; Cortical gray matter; Cortical thickness;
thickness may reflect increased synaptic density
Global gray matter; Magnetic resonance imaging,
within a cortical region. In addition, areas of
MRI; Neuroimaging; Pruning; Region of interest;
decreased or increased cortical thickness can be
Surface of brain
correlated with measures of cognitive function or
important covariates such as sociodemographic
Definition variables, clinical symptoms, etc. Prior studies
have measured cortical thickness as it relates to
Cortical thickness in neuroimaging is a common typical brain development including gene and
measure used to describe the distance between the environmental interactions (Giedd et al. 2010),
innermost and outermost edges of the cerebral cor- traumatic brain injury (Turken et al. 2009), atten-
tical gray matter (see Fig. 1). This can then be used tion-deficit/hyperactivity disorder (Narr et al.
to describe an average thickness for the entire brain 2009), aging and sleep quality (Sexton et al.
(i.e., global), or it can be localized (i.e., local) to 2014), autism (Hardan et al. 2006), Alzheimer’s
different regions of interest (e.g., dorsolateral pre- disease (Lerch et al. 2005), and schizophrenia
frontal cortex, temporal pole, motor cortex etc.). (Narr et al. 2005).

Cortical Volume
Pial Cortical Volume
Surface
Pial Surface
Gray Matter Cortical Thickness

White Matter
Gray Matter

White Matter
Cortical Thickness

Cortical Thickness, Fig. 1 A graphical representation and enhanced coronal section of a T1 MP-RAGE
that compares cortical thickness with other related mea- sequence (Image by Trevor J. Huff, 2015) (NOTE: T1
sures. On the left is a drawing of one sulcus in-between T1-weighted, MP-RAGE magnetization prepared rapid
two gyri and is meant as a simplified representation of the acquisition gradient echo)
surface of the brain. The image on the right is an amplified
Cortical-Subcortical Loop 985

See Also
Cortical-Subcortical Loop
▶ Alzheimer’s Disease
▶ Attention Deficit Hyperactivity Disorder Janna L. Harris
▶ FreeSurfer Department of Anatomy and Cell Biology,
▶ Neuroimaging University of Kansas Medical Center, Kansas
▶ Schizophrenia City, KS, USA C
▶ Severe Brain Injury Hoglund Brain Imaging Center, University of
Kansas Medical Center, Kansas City, KS, USA

References and Readings

Synonyms
Fischl, B. (2012). FreeSurfer. Neuro Image, 62(2), 774–781.
https://doi.org/10.1016/j.neuroimage.2012.01.021.
Basal ganglia-thalamocortical circuit; Cortico-
Giedd, J. N., Stockman, M., Weddle, C., Liverpool, M.,
Alexander-Bloch, A., Wallace, G. L., . . ., & Lenroot, basal ganglia loop
R. K. (2010). Anatomic magnetic resonance
imaging of the developing child and adolescent brain
and effects of genetic variation. Neuropsychology
Review, 20(4), 349–361. https://doi.org/10.1007/
Definition
s11065-010-9151-9.
Hardan, A. Y., Muddasani, S., Vemulapalli, M., Keshavan, The cortical-subcortical loop describes a class of
M. S., & Minshew, N. J. (2006). An MRI study of distinct, parallel circuits that connect specific
increased cortical thickness in autism. American Jour-
regions of cerebral cortex with the basal ganglia
nal of Psychiatry, 163(7), 1290–1292. https://doi.org/
10.1176/appi.ajp.163.7.1290. and specific thalamic nuclei. The thalamic nuclei
Lerch, J. P., Pruessner, J. C., Zijdenbos, A., Hampel, H., complete the loop by projecting back to the same
Teipel, S. J., & Evans, A. C. (2005). Focal decline regions of cortex from which the circuits originate.
of cortical thickness in Alzheimer’s disease
identified by computational neuroanatomy. Cerebral
Cortex, 15(7), 995–1001. https://doi.org/10.1093/
cercor/bhh200. Current Knowledge
Narr, K. L., Bilder, R. M., Toga, A. W., Woods, R. P., Rex,
D. E., Szeszko, P. R., . . ., & Thompson, P. M. (2005).
Mapping cortical thickness and gray matter concentra- Several distinct, anatomically segregated cortical-
tion in first episode schizophrenia. Cerebral Cortex, subcortical loops may be characterized based on
15(6), 708–719. https://doi.org/10.1093/cercor/bhh172. the functional role of the cortical regions
Narr, K. L., Woods, R. P., Lin, J., Kim, J., Phillips, O. R.,
Del’Homme, M., . . ., & Levitt, J. G. (2009). Wide- involved.
spread cortical thinning is a robust anatomical marker
for attention-deficit/hyperactivity disorder. Journal of Motor Loop The motor loop plays a role in the
the American Academy of Child and Adolescent Psy-
preparation and execution of movement. Primary
chiatry, 48(10), 1014–1022. https://doi.org/10.1097/
CHI.0b013e3181b395c0. motor cortex and associated premotor areas pro-
Sexton, C. E., Storsve, A. B., Walhovd, K. B., Johansen- ject via the putamen to the ventral tier nuclei of the
Berg, H., & Fjell, A. M. (2014). Poor sleep quality is thalamus, which then complete the loop with pro-
associated with increased cortical atrophy in commu-
jections back to motor cortex. Somatotopic orga-
nity-dwelling adults. Neurology, 83(11), 967–973.
https://doi.org/10.1212/wnl.0000000000000774. nization is maintained through all stages of this
Turken, A. U., Herron, T. J., Kang, X., O’Connor, L. E., circuit.
Sorenson, D. J., Baldo, J. V., & Woods, D. L. (2009).
Multimodal surface-based morphometry reveals dif-
Oculomotor Loop The oculomotor loop is
fuse cortical atrophy in traumatic brain injury. BMC
Medical Imaging, 9, 20. https://doi.org/10.1186/1471- involved in the control of eye movements. The
2342-9-20. frontal eye fields (FEF) and supplementary eye
986 Corticobasal Degeneration

fields (SEF) project via the body of the caudate loops may be associated with disorders as diverse
nucleus to the ventral anterior (VA) and as obsessive-compulsive disorder, schizophrenia,
mediodorsal (MD) thalamic nuclei, which com- and Tourette syndrome. Recently, interventions
plete the loop by projecting back to FEF and SEF. that surgically remove or modify (e.g., with deep
brain stimulation) the dysfunctional component of
Prefrontal Associative Loops The prefrontal the cortical-subcortical loop have met with con-
associative loops describe two distinct components, siderable success. These promising treatment
which subserve different aspects of higher cogni- approaches are the subject of intensive ongoing
tive processing. The “dorsolateral prefrontal loop” research.
plays a role in cognitive processes including spatial
memory and working memory. In this circuit, the
dorsolateral prefrontal cortex (PFC) projects via the Cross-References
dorsolateral head of the caudate to VA and MD
thalamic nuclei, which then project back to dorso- ▶ Basal Ganglia
lateral PFC. The “lateral orbitofrontal loop” plays a ▶ Deep Brain Stimulator (Parkinson’s)
role in cognitive processes including the ability to ▶ Parkinson’s Disease
select and shift behavioral sets, and response inhi-
bition related to social context or emotional subject
matter. In this loop, the lateral orbitofrontal cortex References and Readings
(OFC) projects via the ventromedial caudate
nucleus to VA and MD thalamic nuclei, which in Alexander, G. E., Crutcher, M. D., & DeLong, M. R. (1990).
Basal ganglia-thalamocortical circuits: Parallel sub-
turn send projections back to lateral OFC. strates for motor, oculomotor, “prefrontal” and “limbic”
functions. Progress in Brain Research, 85, 119–146.
Affective-Motivational Loop This loop is also DeLong, M. R., & Wichmann, T. (2007). Circuits and
called the “Limbic loop.” This circuit plays a role circuit disorders of the basal ganglia. Archives of Neu-
rology, 64(1), 20–24.
in emotional and motivational behaviors. Wide-
spread areas of “limbic cortex” including the ante-
rior cingulate gyrus, medial OFC, and portions of
the temporal lobe all send projections via the
nucleus accumbens to MD thalamus. The circuit Corticobasal Degeneration
is completed by thalamocortical projections from
MD to the anterior cingulate and medial OFC. Alexander I. Tröster
Department of Clinical Neuropsychology and
Center for Neuromodulation, Barrow
Clinical Disorders and Treatment Neurological Institute, Phoenix, AZ, USA
Approaches

An understanding of the architecture of cortical- Synonyms

subcortical loops has given rise to a prevailing
view of numerous clinical disorders as essentially Corticobasal syndrome; Corticodentatonigral
circuit disorders, arising from abnormal neuronal degeneration with neuronal achromasia
activity at some stage of the finely tuned circuit.
The best-studied examples involve the motor
loop, where disturbances within the circuit can Short Description or Definition
result in either hypokinetic movement disorders
(e.g., Parkinson’s disease) or hyperkinetic disor- First described as corticodentatonigral degenera-
ders (e.g., chorea, ballismus, and dystonia). In tion with neuronal achromasia by Rebeiz et al. in
addition, abnormal activity within the non-motor 1968, corticobasal degeneration (CBD) was long
Corticobasal Degeneration 987

thought to be predominantly a motor disorder. The human tau gene (MAPT), containing
Indeed, the original description of the disorder 16 exons, is located on the long arm of chromosome
emphasized the relative preservation of mental 17 and encodes for the six isoforms of tau found in
faculties. More recently, emphasis has been the central nervous system. The isoforms differ by
placed on the neurobehavioral features of CBD, the presence or absence of amino acid inserts
and the overlapping clinical and neuropathologi- encoded by exons 2, 3, and 10. Whether the tran-
cal features of CBD with frontotemporal lobar script of exon 10 is spliced in or out of the final tau C
degenerations continue to generate debate about protein product determines whether the isoform has
the classification and nosology of the disorder. three or four repeated microtubule-binding
The motor presentation of CBD most often domains (three isoforms have three repeats and
involves an asymmetric, progressive, akinetic- three isoforms have four repeats). The four repeat
rigid parkinsonism of gradual onset that responds isoforms of tau (4R tau) promote microtubule
minimally if at all to levodopa and is sometimes assembly at more than twice the rate of the three
accompanied by dystonia or myoclonus. Cortical repeat (3R tau) isoforms. Although the expression
signs that are common in CBD include asymmet- of 3R and 4R tau is cell-type specific, the 3R tau
ric apraxia, cortical sensory signs (e.g., expression in normal human brain is 1-1.5-fold
astereognosis, graphesthesia), and alien hand higher than the 4R expression level. In spontaneous
sign. The latter may involve a sense of lack of and genetic CBD, 4R tau represents the main path-
ownership of the limb in the absence of visual ological inclusion. Recent findings that mutations
cues, involuntary purposeful movements, or associated with parkinsonism (in LRRK2) and
frank interference of one limb with the other’s frontotemporal lobar degeneration (in progranulin)
execution of purposeful movement. These motor can be seen in some cases presenting with
and cortical signs are core features of CBD. corticobasal syndrome further highlight the hetero-
geneity of corticobasal syndrome (CBS).
Autopsy in CBD cases reveals asymmetric
Categorization frontal and parietal atrophy, depigmentation of
the substantia nigra without Lewy bodies, and
The neurobehavioral expression of CBD is quite often the presence of ballooned cells in cortex.
variable, and cases with confirmed CBD neuropa- Tau-positive astrocytic plaques, oligodendroglial
thology have presented with features suggestive of coiled bodies, and threadlike lesions are seen in
primary progressive aphasia and frontotemporal white and gray matter, especially the superior
dementia. Recent diagnostic criteria (2013) recog- frontal and parietal gyri and the pre- and post-
nize this heterogeneity of CBD and identify four central gyri, and in the striatum.
phenotypes: corticobasal syndrome, frontal-
behavioral-spatial syndrome, nonfluent/agrammatic
variant of primary progressive aphasia (PPA), and Epidemiology
progressive supranuclear palsy syndrome. Given
the heterogeneous presentation of CBD, current Prevalence and incidence of CBD are poorly stud-
convention holds that the term corticobasal syn- ied, but incidence in the USA has been estimated
drome (CBS) is applied to the core clinical features at 0.62–0.92 per 100,000 and accounts for about
of CBD regardless of etiology. In contrast, the term 1% of parkinsonian patients seen in movement
corticobasal degeneration (CBD) is reserved for the disorder clinics. Although the H1/H1 tau haplo-
distinctive neuropathological condition of CBD. type has been identified as heightening suscepti-
From a neuropathologic standpoint, CBD, like bility to both CBD and progressive supranuclear
frontotemporal lobar degeneration, has been cate- palsy, no clear genetic etiology has been identi-
gorized as a tauopathy. Tau is a microtubule- fied. Dementia and other cognitive and behavioral
associated protein that promotes the polymeriza- abnormalities were thought to be rare in CBD
tion of tubulin and thus microtubule assembly. until the last decade, but it is now appreciated
988 Corticobasal Degeneration

that the frequency of neurobehavioral abnormali- disproportionate benefit is derived from cuing
ties observed as a presenting problem (in about suggesting a retrieval rather than semantic mem-
half of patients) or during the course of the con- ory deficit. Comprehension is typically preserved
dition is quite high. It might be that the inconsis- early, but comprehension of grammatically com-
tent incidence and prevalence estimates of plex material declines with disease progression.
cognitive impairment in CBD are a function of Executive dysfunction, as indicated by poor
whether patients were drawn from movement dis- performance on tasks such as the card sorting
order, dementia, or psychiatry clinics. tasks and the Trail Making Test, is common. Epi-
sodic memory impairments in CBD are relatively
mild early in the course of the condition and appear
Natural History, Prognostic Factors, and to involve both encoding and retrieval deficits.
Outcomes Remote memory has been little studied in CBD,
but the pattern of poor recall but intact recognition
Disease onset is usually in the sixth decade of life, on remote memory tasks suggests a retrieval defi-
and mean time to death from diagnosis is about cit. Visuospatial impairments have been observed,
7–8 years. Men and women seem equally and one study observed these to be among pre-
affected. Shorter survival may be associated with senting complaints in 20% of cases. Rarely, CBD
bilateral bradykinesia, two of three parkinsonian presents as posterior cortical atrophy.
signs (tremor, rigidity, bradykinesia), and frontal With respect to emotional and neuropsychiat-
syndrome. ric issues, depression is common in CBD (73% of
patients), though apathy (40%), irritability (20%),
and agitation (20%) also occur with frequency.
Neuropsychology and Psychology of
Corticobasal Degeneration
Evaluation
CBD involves an asymmetric apraxia, most often
of the ideomotor type, but ideational and limb The selection of specific neuropsychological tests
kinetic apraxias also occur. Thus, patients most in CBD, like any other condition, should be guided
often have difficulty demonstrating the use of by the referral questions and the patient’s ability to
tools. Poor drawing (constructional apraxia) is cooperate and meet task demands. However, tests
also commonly seen. Language disturbance of executive function (e.g., planning, abstraction,
occurs early or during progression of the syn- and cognitive flexibility), praxis, visuospatial func-
drome, and the aphasia is most often nonfluent tions, attention, learning and memory, and word
(about 56% of cases) or anomic (30%). The pat- retrieval should be employed. Short screening mea-
tern of performance on language tests in patients sures such as the Frontal Assessment Battery may
with the traditional CBD presentation is some- be helpful. Symptom inventories relating to apathy,
what inconsistent across studies, but phonological depression, and “frontal” behavior syndromes,
impairments may be an important feature. Perfor- such as the Neuropsychiatric Inventory, Hamilton
mance on verbal fluency tests, especially lexical Depression Scale, and Frontal Systems Behavior
or phonemic fluency tests, is usually impaired Scale, can be helpful in characterizing neuropsy-
either due to the executive demands of those chiatric features of CBD.
tasks or aphasia. Performance on semantic mem-
ory tasks such as conceptual matching and visual
confrontation naming and expressive vocabulary Treatment
is relatively preserved and impaired in a minority
of patients, although some studies have reported Treatment remains symptomatic. Some cases may
considerable impairment on semantic tasks early show transient improvement in parkinsonian fea-
in the disease. When naming is impaired, tures with levodopa treatment; dopamine agonists
Corticotropin-Releasing Hormone 989

are generally even less helpful than levodopa. Litvan, I., Cummings, J. L., & Mega, M. (1998). Neuro-
Tremor, if present, may be alleviated by benzodi- psychiatric features of corticobasal degeneration. Jour-
nal of Neurology, Neurosurgery, and Psychiatry, 65,
azepines. Dystonia may be helped by botulinum 717–721.
toxin. Antidepressants with anticholinergic profiles Marsili, L., Suppa, A., Berardelli, A., & Colosimo,
are to be avoided given possible adverse cognitive C. (2016). Therapeutic interventions in parkinsonism:
side effects, but selective serotonin reuptake inhib- Corticobasal degeneration. Parkinsonism and Related
itors may be helpful in treating depression. Speech
Disorders, 22(Suppl. 1), S96–S100.
Murray, R., Neumann, M., Forman, M. S., Farmer, J.,
C
therapy is helpful in treating dysphagia. Recent Massimo, L., Rice, A., et al. (2007). Cognitive and
trials with glycogen synthase kinase 3-beta inhibi- motor assessment in autopsy-proven corticobasal
tors (decreasing the kinase’s contribution to tau degeneration. Neurology, 68, 1274–1283.
Sha, S., Hou, C., Viskontas, I. V., & Miller, B. L. (2006).
hyperphosphorylation) were discontinued due to Are frontotemporal lobar degeneration, progressive
poor tolerance. There is no evidence to support supranuclear palsy and corticobasal degeneration dis-
the use of cholinesterase inhibitors or memantine tinct diseases? Nature Clinical Practice Neurology, 2,
to treat cognition in CBD. 658–665.
Stamelou, M., & Bhatia, K. P. (2015). Atypical parkinson-
ism. Neurologic Clinics, 33, 39–56.
Tröster, A. I., & Garrett, R. (2018). Parkinson’s disease and
other movement disorders. In J. E. Morgan & J. H.
Cross-References Ricker (Eds.), Textbook of clinical neuropsychology
(2nd ed.) (pp. 507–559). New York: Psychology Press.
▶ Basal Ganglia Tröster, A. I. (Ed.). (2015). Clinical neuropsychology and
▶ Corticobasal Degeneration cognitive neurology of Parkinson’s disease and other
movement disorders. New York: Oxford University
▶ Frontal Lobe Press.
▶ Frontal Temporal Dementia
▶ Frontotemporal Lobar Degenerations
▶ Gait Disorders
▶ Movement Disorders
▶ Parkinson Plus Syndromes
Corticotropin-Releasing
▶ Parkinson’s Disease
Hormone
▶ Parkinsonism
Chava Creque1 and Stephanie A. Kolakowsky-
▶ Striatum
Hayner2
▶ Tauopathy 1
Department of Psychology and Neuroscience,
University of Colorado Boulder, Boulder, CO,
USA
References and Readings 2
Department of Rehabilitation Medicine, Icahn
Armstrong, M. J., Litvan, I., Lang, A. E., Bak, T. H., School of Medicine at Mount Sinai, New York,
Bhatia, K. P., Borroni, B., Boxer, A. L., Dickson, NY, USA
D. W., Grossman, M., Hallett, M., Josephs, K. A.,
Kertesz, A., Lee, S. E., Miller, B. L., Reich, S. G.,
Riley, D. E., Tolosa, E., Tröster, A. I., Vidailhet, M.,
& Weiner, W. J. (2013). Criteria for the diagnosis of Synonyms
corticobasal degeneration. Neurology, 80, 496–503.
Boeve, B. F. (2007). Parkinson-related dementias. Neuro- Corticoliberin; Corticotropin-releasing factor
logic Clinics, 25, 761–781.
Geda, Y. E., Boeve, B. F., Negash, S., Graff-Radford, N. R.,
(CRF)
Knopman, D. S., Parisi, J. E., et al. (2007). Neuropsy-
chiatric features in 36 pathologically confirmed cases of
corticobasal degeneration. Journal of Neuropsychiatry Definition
and Clinical Neurosciences, 19, 77–80.
Graham, N. L., Bak, T. H., & Hodges, J. R. (2003).
Corticobasal degeneration as a cognitive disorder. Corticotropin-releasing hormone (CRH) is a
Movement Disorders, 18, 1224–1232. hormone that is primarily produced by the
990 Craig Handicap Assessment and Reporting Technique

hypothalamus and is involved in the stress drinking hypertonic saline. Behavioral Neuroscience,
response. Stress increases levels of corticotropin- 109(6), 1146–1157.
Weber, M., & Richardson, R. (2001). Centrally adminis-
releasing hormone, which activates the hypotha- tered corticotropin-releasing hormone and peripheral
lamic-pituitary-adrenal (HPA) axis. Elevated injections of strychnine hydrochloride potentiate the
CRH levels have been implicated in conditions acoustic startle response in pre-weanling rats. Behav-
like depression and post-traumatic stress disorder. ioral Neuroscience, 115(6), 1273–1282.
It is released from the paraventricular nucleus of
the hypothalamus with the primary action within
the anterior lobe of the pituitary to initiate the Craig Handicap Assessment
release of adrenocorticotropic hormone (ACTH). and Reporting Technique
CRH (41 amino acids long) is derived from a
191 amino acid preprohormone. Other areas of Angela M. Philippus and Gale G. Whiteneck
CRH synthesis include peripheral tissues, and it Craig Hospital, Englewood, CO, USA
is highly expressed in the placenta.

Synonyms
Cross-References
CHART; CHART-SF
▶ Hormones

Description
References and Readings
The Craig Handicap Assessment and Reporting
Bennett, M. (2008). Stress and anxiety in schizophrenia Technique (CHART) is a 32-item instrument
and depression: Glucocorticoids, corticotropin-releas- designed to provide a simple, objective measure
ing hormone and synapse regression. The Australian
of the degree to which impairments and disabil-
and New Zealand Journal of Psychiatry, 42(12),
995–1002. ities result in handicaps (societal participation
Cole, R. D., Kawasumi, Y., Parikh, V., & Bangasser, D. A. limitations) for adolescents and adults (15 years
(2016). Corticotropin releasing factor impairs sustained and older) in the years after initial rehabilitation.
attention in male and female rats. Behavioural Brain
The CHART includes six subscales (physical
Research, 296, 30–34.
Dunlop, B. W., Rothbaum, B. O., Binder, E. B., Duncan, independence, cognitive independence, mobility,
E., Harvey, P. D., Jovanovic, T., Kelley, M. E., occupation, social integration, and economic
Kinkead, B., Kutner, M., Iosifescu, D. V., Mathew, independence), which closely reflect the disable-
S. J., Neylan, T. C., Kilts, C. D., Nemeroff, C. B., &
Mayberg, H. S. (2014). Evaluation of a corticotropin
ment model developed by the World Health Orga-
releasing hormone type 1 receptor antagonist in women nization (WHO 1980, 2001). Each subscale
with posttraumatic stress disorder: Study protocol for a contains 3–7 questions, which together quantify
randomized controlled trial. Trials, 15(1), 240. the extent to which individuals fulfill various
Fabricio, A., Tringali, G., Pozzoli, G., & Navarra,
social roles. CHART focuses on objective,
P. (2005). Mirtazapine acutely inhibits basal and Kþ-
stimulated release of corticotropin-releasing hormone observable criteria that are easily quantifiable
from the rat hypothalamus via a non-genomic mecha- and unlikely to be open to subjective interpreta-
nism. Psychopharmacology, 178(1), 78–82. tion. Each of the domains or subscales of the
Guendelman, S., Lang Kosa, J., Pearl, M., Graham, S., &
Kharrazi, M. (2008). Exploring the relationship of sec-
CHART has a maximum score of 100 points,
ond-trimester corticotropin releasing hormone, chronic which is considered to be the level of performance
stress and preterm delivery. The Journal of Maternal- typical of the average nondisabled person. High
Fetal & Neonatal Medicine, 21(11), 788–795. subscale scores indicate less handicap or higher
Watts, A., Kelly, A., & Sanchez-Watts, G. (1995). Neuro-
peptides and thirst: The temporal response of cortico-
social and community participation.
tropin-releasing hormone and neurotensin/neuromedin The CHART was developed in 1992 for use
N gene expression in rat limbic forebrain neurons to with persons with spinal cord injury (SCI) and
Craig Handicap Assessment and Reporting Technique 991

originally did not address the WHO handicap psychosocial adjustment is clearly regarded as the
dimension described as “orientation” (Whiteneck ultimate outcome of rehabilitation. The CHART
et al. 1992). The current CHART was revised in was specifically developed to help fill this gap –
1995 with the addition of a “Cognitive Indepen- to assess the WHO dimensions of handicap and to
dence” subscale (to assess orientation) and has provide a simple, objective measure of the degree
proven to be an appropriate measure of societal to which impairments and disabilities result in par-
participation that can be used with individuals ticipation limitations in the years after initial C
having a range of physical or cognitive impair- rehabilitation.
ments (Mellick et al. 1999). A 19-item short form The model of disablement suggested by the
with subscales closely approximating the subscale WHO provides useful conceptual distinctions for
scores for the CHART long form is recommended impairment, disability, and handicap (WHO
for those applications or populations in which 1980). In practical terms, impairment occurs at
time is at a minimum (Whiteneck et al. 1998). the organ level, representing any loss or abnor-
CHART has been translated into seven different mality of psychological, physiological, or ana-
languages and has been validated cross-culturally tomical structure or function. Disability occurs at
as a useful tool in populations outside of the the person level, demonstrated as any restriction
United States. or lack of ability (resulting from impairment) to
The CHART was designed to be administered perform any activity in the manner or within the
by interview, either in person or by telephone, and range considered normal for a human being.
takes approximately 15 minutes to administer. Handicap occurs at the societal level. It is a dis-
Participant-proxy agreement across disability advantage for a given individual, resulting from
groups on the CHART has provided evidence in an impairment or a disability that limits or pre-
support of the use of proxy data for persons with vents the fulfillment of a role that is normal
various types of disabilities (Cusick et al. 2001). (depending on age, sex, and social and cultural
There is no set time period for administering factors) for that individual. The initial disablement
the CHART; however, it is recommended that model, the “International Classification of Impair-
multiple measurements be taken over the course ment, Disability and Health (ICIDH)” (WHO
of a person’s lifetime to assess changes with 1980), was later revised as the “International Clas-
adaptation to the disability and to gain insight sification of Functioning, Disability and Health
into changes in participation, which may occur (ICF)” (WHO 2001). The domain of “handicap”
over time. was reconceptualized and changed to “participa-
tion.” The migration away from the use of “hand-
icap” toward the more widespread use of
Historical Background “participation” is evident in literature published
since 2001. According to the WHO, handicap
WHO describes a conceptual model of disablement (participation) describes the total effects and inter-
that includes impairment at the organ level, disabil- play of all the consequences of disability: social,
ity describing functional status, and “handicap,” or economic, cultural, and environmental.
more recently, “participation,” encompassing the Each CHART dimension of handicap is charac-
roles one plays in the world and society. Despite terized by directly observable qualities which lend
its importance as a rehabilitation goal, handicap themselves to easy quantification. While an infinite
(absence of social participation) is the least often number of factors might have been included, to
measured of all rehabilitation outcomes. A great keep the instrument to a practical length, the fol-
deal of work has been done in developing tools to lowing dimensions have been operationalized
measure and document impairment and disability; based on the WHO definitions.
however, limited attempts have focused on the Physical independence is the individual’s abil-
measurement and assessment of long-term partici- ity to sustain a customarily effective independent
pation limitations (handicap), despite the fact that existence. The major component of this subscale
992 Craig Handicap Assessment and Reporting Technique

is the number of hours per day someone is needed as the remaining disposable household family
to provide routine or occasional assistance income after nonreimbursed medical expenses
(whether paid or unpaid). Individuals are viewed have been excluded.
as somewhat less handicapped if they take pri-
mary responsibility for instructing and directing
people who are providing assistance to them. Psychometric Data
Cognitive independence is the individual’s
ability to sustain a customary level of indepen- Initial calibration of the CHART scoring system
dence without the need for supervision. The fac- was based on the administration of the instrument
tors included in this subscale reflect the amount of to 88 able-bodied individuals and 100 persons with
hours that a person needs supervision both inside SCI. Once the norms had been established, two
and outside the home, as well as the amount of studies were conducted to assess the psychometric
difficulty an individual has in remembering, com- properties. CHART showed high test-retest
municating, and managing money. reliability – 0.93 for the total score and from 0.80
Mobility is the individual’s ability to move to 0.95 for the subscales. The correlation of subject-
about effectively in his/her surroundings and is proxy scores was 0.83 for the total CHART score.
demonstrated by the hours per day out of bed, Rasch analysis established that CHART is a well-
days per week out of the house, nights per year calibrated linear scale, with a good fit of both items
spent away from home, accessibility of the home, and persons to its data (Whiteneck et al. 1992).
and transportation utilization. These studies established the CHART as a reliable
Occupation is the individual’s ability to and valid instrument, as well as a well-calibrated
occupy time in the manner customary to that linear scale (Whiteneck et al. 1997b; Dijkers 1991).
person’s sex, age, and culture. The time spent in A decade later, subsequent testing on a group of
various activities is used to measure this dimen- 236 persons with SCI reported similar results – test-
sion. The relative value society places on different retest correlations of 0.87 and subject-proxy corre-
activities is used to weight the time in each cate- lations of 0.85 were reported (Whiteneck et al.
gory. Although there was a potential for subjective 1997a).
bias based on value judgments in developing the The Revised CHART which included the “Cog-
scale in this dimension, priority has been given to nitive Independence” subscale was tested on 1110
gainful employment, schooling, and active home- persons in six impairment categories – SCI, trau-
making and maintenance, and this prioritization matic brain injury, stroke, multiple sclerosis, ampu-
has been supported by validity and reliability test- tation, and burn (Whiteneck et al. 1997a). Results
ing. Other elements documented include volun- indicated that the cognitive subscale of the CHART
teer work, recreational pursuits, and self- was reliable and enhanced the appropriateness of
improvement activities. the CHART in assessing handicap among persons
Social integration is the individual’s ability to having cognitive impairments (Mellick et al.
participate in and maintain customary social rela- 1999). Participant-proxy agreement across the six
tionships. The factors in this subscale include disability groups provided evidence in support of
household composition; romantic involvement; the inclusion of proxy data for persons with various
the number of relatives, business associates, and types of disabilities (Cusick et al. 2001).
friends with whom regular written or oral contract In an effort to reduce the number of items in
is maintained; and the frequency of initiating con- the CHART, a short form was developed.
versations with strangers. A multidimensional analysis was performed
Economic self-sufficiency is the individual’s which showed that fewer variables were needed
ability to sustain customary socioeconomic activ- to obtain CHART scores. Regression analyses
ity and independence. This dimension is defined were performed on each subscale with the
Craig Handicap Assessment and Reporting Technique 993

dependent measure being the scale score and the Cross-cultural validation studies of CHART and
variables contributing to the subscale acting as the CHART-SF reported adequate psychometric
predictor variables. All CHART subscale properties of the measure and demonstrated its
scores could be reduced by fewer questions to usefulness in populations outside of the United
reach 90% explained variance except Economic States (Tozato et al. 2005; Golhasani-Keshtan
Self-Sufficiency, which using the main variables et al. 2013).
could only explain 45%. C
For additional information about the develop-
ment, testing, and scoring procedures for the Cross-References
CHART and CHART-SF, please consult the Guide
for use of the CHART: Craig Handicap Assessment ▶ CHART Short Form
and Reporting Technique at https://craighospital.
org/programs/research/research-instruments.
References and Readings

Cusick, C. P., Gerhart, K. A., & Mellick, D. C. (2000).

Clinical Uses Participant-proxy reliability in traumatic brain injury
outcome research. Journal of Head Trauma Rehabili-
The CHART is a useful tool to measure handicap tation, 15(1), 739–749.
(participation limitations) in populations with Cusick, C. P., Brooks, C. A., & Whiteneck, G. G. (2001).
The use of proxies in community integration research.
injury or chronic illness with or without rehabili- Archives of Physical Medicine and Rehabilitation,
tation intervention. The CHART is designed as an 82(8), 1018–1024.
interview tool, which can be administered face-to- Dijkers, M. (1991). Scoring CHART: Survey and sensitiv-
face or by telephone. Each item on the instrument ity analysis. Journal of the American Paraplegia Soci-
ety, 14, 85–86.
has been carefully and concisely worded to min- Golhasani-Keshtan, F., Ebrahimzadeh, M. H., Fattahi,
imize ambiguity of interpretation. It is possible to A. S., Soltani-Moghaddas, S. H., & Omidi-Kashani,
use the instrument as a mailed questionnaire, F. (2013). Validation and cross-cultural adaptation of
although some valuable data potentially would the Persian version of Craig handicap assessment and
reporting technique (CHART) short form. Disability
be lost in the absence of interaction with an inter- and Rehabilitation, 35(22), 1909–1914.
viewer providing consistent prompts. There is no Hall, K. M., Dijkers, M., Whiteneck, G., Brooks, C. A., &
set time period for administering the CHART; Krause, J. S. (1998). The Craig handicap assessment
however, it is recommended that multiple mea- and reporting technique (CHART): Metric properties
and scoring. Topics in Spinal Cord Injury Rehabilita-
surements be taken over the course of a person’s tion, 4(1), 16–30.
lifetime to assess changes with adaptation to the Mellick, D., Walker, N., Brooks, C. A., & Whiteneck,
disability and to gain insight into changes in par- G. (1999). Incorporating the cognitive independence
ticipation which may occur over time. CHART domain into CHART. Journal of Rehabilitation Out-
come Measures, 3(3), 12–21.
has been demonstrated to be a reliable measure of Segal, M. E., & Schall, R. R. (1995). Assessing handicap of
societal participation limitations in a variety of stroke survivors. A validation study of the Craig hand-
populations including people with physical icap assessment and reporting technique. American
and/or cognitive functional limitations. CHART Journal of Physical Medicine & Rehabilitation, 74,
276–286.
is the most widely used tool to quantify handicap Tozato, F., Tobimatsu, Y., Wang, C., Iwaya, T., Kumamoto,
among persons with SCI but has also been used to K., & Ushiyama, Y. (2005). Reliability and validity of
assess persons with traumatic brain injury, stroke, the Craig handicap assessment and reporting technique
multiple sclerosis, burn, amputations, Parkinson for Japanese individuals with spinal cord injury. The
Tohoku Journal of Experimental Medicine, 205(4),
disease, and spina bifida. The questionnaire has 357–366.
been translated into Spanish, Japanese, Chinese, Walker, N., Mellick, D., Brooks, C. A., & Whiteneck, G. G.
Korean, Italian, Turkish, and Persian languages. (2003). Measuring participation across impairment
994 Cranial Nerves

groups using the Craig handicap assessment and Historical Background

reporting technique. American Journal of Physical Med-
icine and Rehabilitation, 82(12), 936–941.
Whiteneck, G. G., Charlifue, S. W., Gerhart, K. A., Over- The enumeration of the cranial nerves can be traced
hosler, J. D., & Richardson, G. N. (1992). Quantifying back to the second-century Greek physician-philos-
handicap: A new measure of long-term rehabilitation opher Galen, whose initial description included 7 of
outcomes. Archives of Physical Medicine and Rehabil- the 12 currently accepted pairs. English physician
itation, 73, 519–526.
Whiteneck, G. G., Brooks, C. A., & Mellick, D. C. and neuroanatomist Thomas Willis’ reclassification
(1997a). Handicap assessment – Final report. Rehabil- of the cranial nerves in the seventeenth century
itation research and training center on functional consisted of nine pairs and superseded Galen’s
assessment and evaluation of rehabilitation outcomes. previous description. German anatomist Samuel
Buffalo: State University of New York.
Whiteneck, G. G., Fougeyrolles, P., & Gerhart, K. A. Thomas von Soemmerring introduced the contem-
(1997b). Elaborating the model of disablement. In porary classification system, comprising 12 pairs of
M. Fuhrer (Ed.), Assessing medical rehabilitation prac- cranial nerves, in the late eighteenth century.
tices: The promise of outcomes research. Baltimore:
Paul H. Brooks Publishing Co.
Whiteneck, G., Brooks, C. A., Charlifue, S., Gerhart,
K. A., Mellick, D., Overholser, D., et al. (1998). Current Knowledge
Guide for use of the CHART: Craig handicap assess-
ment and reporting technique. www.craighospital.org/ Cranial Nerve Nuclei
Research/CHART. Accessed 29 Dec 2009.
World Health Organization. (1980). International classifi- The majority of cranial nerves (CNs) either orig-
cation of impairments, disabilities and handicaps: inate from or project to collections of neurons
A manual of classification relating to the consequences (nuclei) located within the brainstem (exceptions
of disease. Geneva: World Health Organization. to this rule are CNs I and II, which are associated
World Health Organization. (2001). International classifi-
cation of functioning, disability and health. Geneva: with the forebrain and diencephalon, respec-
World Health Organization. tively). CNs III and IV emerge from the midbrain
portion of the brainstem, CNs V–VIII arise from
the pons, and the remaining cranial nerves (CNs
IX–XII) emerge from the medulla. Taken
Cranial Nerves together, the cranial nerves convey both motor
and sensory innervation. However, individual cra-
Melissa J. McGinn nial nerves may transmit sensory information only
Anatomy and Neurobiology, Virginia (CNs I, II, and VIII), motor innervation only (CNs
Commonwealth University School of Medicine, III, IV, VI, XI, and XII), or may be considered
Richmond, VA, USA mixed nerves, meaning that they convey a com-
bination of motor and sensory fibers (CNs V, VII,
IX, and X). Motor neurons located within
Definition brainstem motor nuclei send axonal projections,
via cranial nerves, to mediate the contraction of
Cranial nerves serve as conduits for communica- various types of muscle (skeletal, smooth, and
tion between the brain and the body, providing cardiac muscle) and to regulate glandular tissue
motor and sensory innervation to structures in the secretions. Conversely, neuronal cell bodies that
head and neck as well as the thoracic and abdom- give rise to sensory cranial nerve fibers typically
inal viscera. There are 12 pairs of cranial nerves, reside within peripheral sensory ganglia (collec-
each of which is designated by both a Roman tions of sensory neurons residing outside of the
numeral and a name (see Table 1). Roman brain) and function to convey sensation from var-
numerals I–XII indicate the rostrocaudal order in ious types of sensory receptors (i.e., somatosen-
which cranial nerves emerge from the brain, while sory receptors on the skin, taste receptors on the
the name designated to each pair of cranial nerves tongue, etc.) to neurons housed within sensory
denotes either its function or distribution. nuclei of the brainstem. As a general rule, the
Cranial Nerves 995

Cranial Nerves, Table 1 Cranial Nerves Overview

Associated
Functional Cells of origin/ cranial
Cranial nerve component(s)a termination opening Function/distribution
I – OLFACTORY Special sensory Olfactory Cribriform Olfaction
(SVA) epithelium/ plate (of
olfactory bulb ethmoid)
II – OPTIC Special sensory Retina (retinal Optic Vision C
(SSA) ganglion cells)/ foramen
lateral geniculate
nucleus
III – OCULOMOTOR Visceral motor Edinger-Westphal Superior Sphincter pupillae m. (pupil
(GVE) nucleus (ganglion: orbital constriction)
ciliary) fissure Ciliary body/muscle (lens
accommodation)
Somatic motor Oculomotor Superior rectus m.
(GSE) nucleus Inferior rectus m.
Medial rectus m.
Inferior oblique m.
Levator palpebrae superioris m.
IV – TROCHLEAR Somatic motor Trochlear nucleus Superior oblique m.
(GSE)
VI – ABDUCENS Somatic motor Abducens nucleus Lateral rectus m.
(GSE)
V – TRIGEMINAL Somatic sensory Trigeminal Superior Sensation from the meninges,
V1 – OPHTHALMIC div. (GSA) ganglion/ orbital cornea, skin of the forehead,
trigeminal sensory fissure scalp, eyelids, nose, and mucosa
nuclei lining the nasal cavity and
paranasal sinuses
V – TRIGEMINAL Foramen Sensation from the meninges,
V2 – MAXILLARY div. rotundum skin of the face overlying the
maxilla (cheek, upper lip), the
maxillary teeth, mucosa lining
the nasal cavity, paranasal
sinuses, and palate
V – TRIGEMINAL Foramen Sensation from the meninges,
V3 – MANDIBULAR div. ovale skin of the face overlying the
mandible (lower lip, side of
head), mandibular teeth, TMJ,
anterior two third of tongue, the
lingual/sublingual mucosa
Branchial motor Trigeminal motor Motor to muscles of mastication
(SVE) nucleus (+ a few other small muscles)
VII – FACIAL Branchial motor Facial motor Internal Muscles of facial expression,
(SVE) nucleus auditory stapedius m. (+ a few others)
Visceral motor Superior salivatory meatus Glands – lacrimal, nasal, palatal,
(GVE) nucleus (ganglia: (+others) sublingual, and submandibular
pterygopalatine
submandibular)
Special visceral Geniculate Taste (anterior two third of
sensory (SVA) ganglion/solitary tongue)
nucleus
General somatic Geniculate Sensation from skin of external
sensory (GSA) ganglion/ auditory meatus and auricle
trigeminal sensory
nuclei
VIII – VESTIBULOCOCHLEAR Special sensory Vestibular Internal Vestibulation
(SSA) ganglion/vestibular auditory
nuclei meatus
Cochlear ganglion/ Hearing
cochlear nuclei
(continued)
996 Cranial Nerves

Cranial Nerves, Table 1 (continued)

Associated
Functional Cells of origin/ cranial
Cranial nerve component(s)a termination opening Function/distribution
IX – GLOSSOPHARYNGEAL Branchial motor Nucleus ambiguus Jugular Stylopharyngeus m.
(SVE) foramen
Visceral motor Inferior salivatory Parotid gland
(GVE) nucleus (ganglion:
otic)
General visceral Petrosal (inferior) Carotid body (chemoreceptors),
sensory (GVA) ganglion/solitary carotid sinus (baroreceptors)
nucleus
Special visceral Petrosal (inferior) Taste (posterior one third of the
sensory (SVA) ganglion/solitary tongue)
nucleus
General somatic Superior (jugular) Sensation from the posterior one
sensory (GSA) ganglion/ third of tongue, pharynx, tonsils,
trigeminal sensory tympanic cavity, auditory tube
nuclei
X – VAGUS Branchial motor Nucleus ambiguus Jugular Muscles of the palate, pharynx,
(SVE) foramen and (intrinsic) larynx
Visceral motor Dorsal motor Cervical, thoracic, and
(GVE) nucleus of X or abdominal viscera
nucleus ambiguus
(ganglia: in or
near viscera)
General visceral Nodose (inferior) Sensation from pharynx, larynx,
sensory (GVA) ganglion/solitary pulmonary, cardiac, and GI
nucleus viscera
Special visceral Nodose (inferior) Taste (epiglottis)
sensory (SVA) ganglion/solitary
nucleus
Somatic sensory Superior (jugular) Sensation from skin of external
(GSA) ganglion/ ear, external acoustic meatus,
trigeminal sensory meninges
nuclei
XI – SPINAL ACCESSORY Somatic motor Accessory nucleus Jugular Sternocleidomastoid and
(GSE) foramen trapezius muscles
XII – HYPOGLOSSAL Somatic motor Hypoglossal Hypoglossal Muscles of the tongue (intrinsic
(GSE) nucleus canal and extrinsic)
a
Alternative names for the functional components include following: general somatic efferent (GSE), somatic motor;
general visceral efferent (GVE), visceral motor; special visceral efferent (SVE), branchial motor; general somatic afferent
(GSA), somatic sensory; general visceral afferent (GVA), visceral sensory; special somatic afferent (SSA) and special
visceral afferent (SVA), special sensory

sensory brainstem nuclei to which sensory cranial Functional Components

nerve fibers project are situated more laterally in In addition to the generalized classification of cra-
the brainstem, while the motor nuclei are posi- nial nerves as sensory, motor, or mixed nerves, the
tioned more medially. The sulcus limitans is the fibers that comprise each CN can be further cate-
landmark that demarcates the boundary between gorized according to the specific nature of the
these efferent (motor) and afferent (sensory) afferent or efferent information being transmitted
nuclear zones in the brainstem, which are typi- and the types of structures innervated. These fiber
cally arranged in a longitudinal columnar manner classifications, which are referred to as functional
according to functional components (see Func- components, include somatic motor, visceral
tional Components below). motor, branchial motor, somatic sensory, visceral
Cranial Nerves 997

sensory, and special sensory fibers. A cranial nerve brainstem to peripheral parasympathetic ganglia
can convey just one or several of these functional located in the head, neck, thoracic, and abdominal
components. regions to mediate glandular secretions and
smooth and cardiac muscle contraction. The
Motor Cranial Nerves motor neurons that regulate parasympathetic vis-
Three of the six functional classifications of cra- ceral motor processes are typically positioned
nial nerve fibers convey motor innervation: immediately lateral to the branchial motor nuclei C
somatic motor, branchial motor, and visceral column in the brainstem. Visceral motor fibers in
motor fibers. Somatic motor fibers (aka general CN III convey parasympathetic innervation from
somatic efferents) arise from collections of motor the Edinger-Westphal nucleus to mediate the pro-
neurons (motor nuclei) located in the medial- cesses of pupil constriction and lens accommoda-
most cell column of the brainstem and function tion. The superior and inferior salivatory nuclei
to transmit motor impulses to voluntary skeletal send projections, via CNs VII and IX, respec-
muscle (of developmental somatic myotome ori- tively, that regulate the secretory activity of vari-
gin) in the head and neck. CNs III, IV, and VI ous glands throughout the head and neck (i.e.
convey somatic motor fibers from their respec- salivary, lacrimal and mucosal glands). CN X
tive extraocular motor nuclei (the oculomotor, has the most extensive distribution of the cranial
trochlear, and abducens nuclei) to the extraocular nerves, with its innervation extending from vis-
muscles of the eye to mediate eye movements, ceral structures of the head and neck down to
CNXI arises from the accessory nucleus (located those located in the thoracic and abdominal
in the cervical spinal cord) and transmits somatic regions. CN X conveys visceral motor innervation
motor innervation to the sternocleidomastoid and from the dorsal motor nucleus of the vagus and
trapezius muscles of the neck/shoulder region, nucleus ambiguus to mediate glandular secretion
and CN XII conveys somatic motor information and smooth and cardiac muscle contraction
from the hypoglossal nucleus to the tongue within the gastrointestinal, pulmonary, and car-
musculature. diovascular viscera.
Branchial motor fibers (aka special visceral
efferents) are similar to somatic motor fibers in Sensory Cranial Nerves
that they convey motor innervation to voluntary The remaining three functional classifications of
striated muscles located within the head and neck cranial nerve fibers convey sensory information
region. However, branchial motor fibers and the and include somatic sensory, visceral sensory, and
muscles that they innervate are afforded a separate special sensory fibers. As previously mentioned,
classification based on their embryologic deriva- the neuronal cell bodies that give rise to the major-
tion from branchial/pharyngeal arches and the fact ity of sensory cranial nerve fibers reside within
that branchial motor nuclei are located in a distinct peripheral sensory ganglia, and the brainstem
brainstem column (situated immediately lateral to nuclei that receive input from these sensory fibers
the somatic motor nuclei). Muscles of branchial are located more laterally in the brainstem relative
origin include the muscles of facial expression to motor nuclei and are arranged in longitudinal
(innervated by motor neurons in the facial columns according to functional components
nucleus, via CN VII), the pharyngeal and laryn- (from lateral to medial: special sensory, somatic
geal musculature (innervated by motor neurons in sensory, and visceral sensory nuclei). Somatic
the nucleus ambiguus by way of CNs IX and X), sensory fibers (aka general somatic afferents)
and the muscles of mastication (innervated by the transmit information from exteroreceptors and
trigeminal motor nucleus, via CN V). proprioceptors in the skin, muscles, tendons, and
Visceral motor fibers (aka general visceral joints of the head and neck to mediate the percep-
efferents) convey autonomic innervation from tion of pain, temperature, touch, and propriocep-
parasympathetic motor nuclei located in the tion. CN V, which is comprised of three divisions
998 Cranial Nerves

(ophthalmic, maxillary, and mandibular divi- from sensory receptors in the inner ear to the
sions), is the major somatic sensory nerve of the cochlear and vestibular nuclei of the brainstem,
head, mediating cutaneous and proprioceptive respectively.
sensation from the skin, muscles, and joints in
the face, mouth, and jaw as well as sensory inner- Intracranial Courses
vation of the teeth, oral and nasal mucosa, para- Cranial nerves must traverse foramina (small open-
nasal sinuses, and meninges. The sensory fibers of ings) within the skull in order to navigate the path
CNV arise from neurons residing within the tri- between the brain and the various structures to
geminal ganglion and project to the trigeminal which they provide innervation. Often, cranial
sensory nuclei located in the brainstem. CNs nerves will travel through these foramina together
VII, IX and X also convey somatic sensory in groups as they exit the cranium. For example,
input from various regions within the head to the CNs IX, X, and XI pass through the jugular fora-
trigeminal sensory nuclei of the brainstem. men on their descent to structures in the neck,
In contrast to somatic sensory fibers, visceral thoracic, and abdominal cavities, while CNs III,
sensory fibers (aka general visceral afferents) IV, V (ophthalmic division), and VI all traverse
receive sensory input from receptive endings in the superior orbital fissure to enter into the orbit to
visceral structures, such as walls of blood vessels target the extraocular muscles, among other struc-
or of the digestive tract. Congruent with its expan- tures. Knowledge of the associated brainstem
sive distribution, CN X conveys visceral input nuclei and location of emergence from the
from a variety of visceral structures, including brainstem, intracranial course, and the cranial
those within the pharynx, larynx, thoracic, and foramina through which cranial nerves pass is cru-
abdominal cavities. CN IX transmits visceral sen- cial to any neurological exam, as the diagnosis of
sory information from the carotid sinus and dysfunction of specific nerves can help to pinpoint
carotid body, which are important structures in the site of and provide valuable information about
the regulation of blood pressure and respiration. damage or injury to the brain. For example, one of
Visceral sensory fibers coursing within both CNs the early symptoms of a pituitary adenoma is
IX and X project to the solitary nucleus of the impaired vision, which results from the close prox-
brainstem. imity between the pituitary gland and fibers of CN
The final category of sensory cranial nerve II (crossing in the optic chiasm), which can become
fibers is the special sensory fibers (aka special compressed as a result of the tumor bulk. Similarly,
somatic afferents and special visceral afferents), CN VI has a very long intracranial course, and, due
which convey sensory information relating to the to its emergence near the base of the brain and its
senses of olfaction (CN I), vision (CN II), audition course through the cavernous sinus, it is often the
(CN VIII), balance (CN VIII), and taste (CNs VII, first cranial nerve to be affected in the case of
IX, and X). Recall that CNs I and II differ from the elevated intracranial pressure, common symptoms
remaining cranial nerves in that they neither orig- of which include painful eye movement and blurred
inate from nor project to nuclei located within the or double vision (diplopia). Unlike the majority of
brainstem. CN I conveys olfactory information cranial nerves, which exit from the ventral surface
from olfactory receptor neurons (located in the of the brainstem, CN IVexits the midbrain dorsally
roof of the nasal cavity) to the olfactory bulb of and wraps around the lateral surface of the
the forebrain, while CN II conveys visual sensory brainstem to enter the orbit. Due to this long periph-
input from the retinal ganglion cell layer of the eye eral course around the brainstem, CN IV is partic-
to the thalamus (by way of the optic nerve, chiasm ularly susceptible to head trauma, where damage to
and tract). Cranial nerves VII, IX, and X transmit this nerve is manifested by diplopia or blurred
taste input from taste receptors in the oral cavity to vision. Such examples demonstrate the manner in
the solitary nucleus of the brainstem, and CN VIII which cranial nerve dysfunction can provide insight
conveys both auditory and vestibular input into pathological events occurring within the brain.
Cranial Nerves 999

Cranial Nerve Dysfunction trigeminal neuralgia (CN V), Bell’s palsy (CN
Cranial nerve dysfunction is not uncommon and VII), Ramsay Hunt syndrome (CN VII), vestibu-
can result from a variety of underlying patholo- lar schwannoma (CN VIII), glossopharyngeal
gies, ranging from brain trauma to various forms neuralgia (CN IX), eye movement-related cranial
of neurological disease (see Table 2). Common nerve palsies (CNs III, IV, and VI), hyposmia/
cranial nerve dysfunctions/disorders include anosmia (CN I), and various anopias (CN II),
among others. Due to its expansive innervation, C
Cranial Nerves, Table 2 Indicators of Cranial Nerve CN X damage/dysfunction can result in a variety
Lesion/Dysfunction of deficits relating to visceral processes in the
CN DEFICIT heart, lungs, and abdomen. Interestingly, CN X
I Anosmia, hyposmia nerve stimulation is an emerging adjunctive treat-
II Blindness of ipsilateral eye; impaired pupillary ment for certain types of intractable epilepsy and
light reflex (afferent limb) treatment-resistant depression; however, the man-
III Eye deviation inferiorly and laterally (down and ner in which CN X stimulation exerts its thera-
out); ptosis; dilated pupil; diplopia; impaired peutic effects is yet to be fully established.
pupillary light reflex (efferent limb), impaired
lens accommodation
IV Weakness in depression of adducted eye;
diplopia
V Loss of sensation from the face, meninges, oral/
Cross-References
nasal/paranasal mucosa, teeth, etc.; impaired
corneal blink reflex (V1 = afferent limb); (V3 only ▶ Acoustic Neuroma
= hemiparalysis of masticatory muscles; jaw ▶ Anosmia
weakness, deviation TOWARD the lesion in
▶ Auditory Pathway
opened jaw; impaired jaw jerk reflex)
VI Inability to abduct the eye, medial deviation of
▶ Auditory System
the eye at rest, diplopia ▶ Autonomic Nervous System
VII Facial muscle hemiparalysis, hyperacusis (due to ▶ Bell’s Palsy
loss of stapedius m. function); impaired corneal ▶ Deaf/Hearing Impairment
blink reflex (efferent limb); loss of taste on ▶ Diplopia
anterior two third of tongue; loss of tearing/
lacrimation; dry mouth/diminished saliva ▶ Dysphagia
production ▶ Dysphonia
VIII Deafness in the ipsilateral ear; tinnitus; ▶ Medulla
disequilibrium; spontaneous nystagmus; vertigo; ▶ Midbrain
impaired vestibular reflexes,i.e., vestibuloocular, ▶ Neurologic Examination
vestibulospinal, and vestibulocollic reflexes
(afferent limb) ▶ Olfaction
IX Loss of sensation from the tonsillar region, ▶ Olfactory Bulb
posterior one third of tongue, oropharynx; loss of ▶ Optic Nerve
gag reflex (afferent limb); loss of taste on ▶ Optic Neuropathy
posterior one third of tongue; (slight) dysphagia;
▶ Pons
(partial) dry mouth
X Dysphagia; hoarseness (due to vocal cord
▶ Ptosis
paralysis); sagging palatal arch with deviation of ▶ Pupillary Light Response, Pupillary Response
the uvula to the CONTRALATERAL side; loss ▶ Taste
of sensation from the pharynx/larynx; impaired ▶ Tinnitus
gag reflex (efferent limb)
▶ Trochlear Nerve
XI Weakness in shrugging ipsilateral shoulder and
turning head to the CONTRALATERAL side ▶ Vertigo
XII Tongue hemiparalysis with LMN signs (atrophy, ▶ Vestibulocochlear Nerve
fasciculations, etc.); protruded tongue deviates ▶ Visual Field Deficit
TOWARD the lesion ▶ Visual System
1000 Craniectomy

References and Readings pressure and pressure on the brain stem. Although
the section of the skull that is removed in a
Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2000). craniectomy is not immediately replaced, the
Principles of neural science (4th ed.). New York:
bone removed may be stored and replaced at a
McGraw-Hill.
Shaw, J. P. (1992). A history of the enumeration of cranial later date when brain swelling is reduced and
nerves by European and British Anatomists from the stable. Artificial materials may also be used to
time of Galen to 1895, with comments on nomencla- replace the removed skull. In a craniotomy, a
ture. Clinical Anatomy, 5(6), 466–484.
section of the skull is removed and replaced as
part of the initial surgical procedure. Craniotomy
is more frequently performed as part of surgical
intervention for disorders such as brain tumor or
arteriovenous malformation. However, a
Craniectomy craniectomy may be preferred in such cases if
the condition appears to be associated with brain
James F. Malec swelling. Craniectomy may have no advantage
Department of Physical Medicine and over craniotomy in long-term outcome after
Rehabilitation, Indiana University School of severe brain injury (Woertgen et al. 2006). How-
Medicine and the Rehabilitation Hospital of ever, standard craniectomy appears to result in
Indiana, Indianapolis, IN, USA better outcomes than limited craniectomy (Jiang
et al. 2005).

Synonyms

Decompressive craniectomy Cross-References

▶ Brain Swelling
▶ Craniotomy
Definition

Craniectomy or decompressive craniectomy is a

surgical procedure in which a section of the skull References and Readings
is removed and not immediately replaced (Aarabi
Aarabi, B., Hesdorffer, D., Ahn, E., Aresco, C., Scalea,
et al. 2006). This procedure is most frequently T. M., & Eisenberg, H. M. (2006). Outcome following
used when increased intracranial pressure follow- decompressive craniectomy for malignant swelling due
ing traumatic brain injury does not respond to to severe head injury. Journal of Neurosurgery, 104,
other less aggressive interventions. However, its 469–479.
Jiang, J. Y., Xu, W., Li, W. P., Xu, W. H., Zhang, J., Bao,
use and benefits remain controversial (Kolias et al. Y. H., et al. (2005). Efficacy of standard trauma
2013). Following brain trauma, the brain may craniectomy for refractory intracranial hypertension
expand within the skull. The resulting increased with severe traumatic brain injury: A multicenter, pro-
intracranial pressure can compromise brain func- spective, randomized controlled study. Journal of
Neurotrauma, 22(6), 623–628.
tion, particularly in the brain stem. Compression Kolias, A. G., Kirkpatrick, P. J., & Hutchinson, P. J. (2013).
of the brain stem can compromise its basic life Decompressive craniectomy: Past, present and future.
support functions, that is, cardiac and respiratory Nature Reviews Neurology, 9(7), 405–415.
regulation, creating a life-threatening situation. Woertgen, C., Rothoerl, R. D., Schebesch, K. M., & Albert,
R. (2006). Comparison of craniotomy and craniectomy
By removing part of the skull, the swelling brain in patients with acute subdural haematoma. Journal of
is provided room to expand, reducing intracranial Clinical Neuroscience, 13(7), 718–721.
Cranioplasty 1001

References and Readings

Craniopharyngioma
Fahlbusch, R., Honegger, J., Paulus, W., Huk, W., &
Buchfelder, M. (1999). Surgical treatment of
Ethan Moitra
craniopharyngiomas: Experience with 168 patients.
Department of Psychiatry and Human Behavior, Journal of Neurosurgery, 90, 237–250.
Brown University, Providence, RI, USA
C

Definition Cranioplasty

Craniopharyngioma is a slow-growing, extra- Jacinta McElligott

axial, epithelial-squamous, calcified cystic tumor Rehabilitation Medicine, National Rehabilitation
that develops near the pituitary gland. It occupies Hospital, Dun Laoghaire Co Dublin, Ireland
the suprasellar/sellar region and shows benign
histology but malignant behavior, as it may invade
surrounding areas and recur after treatment Definition
(Fahlbusch et al. 1999). Craniopharyngiomas
may develop embryogenetically, arising from Cranioplasty or replacement of bone flap or pros-
remnants of the craniopharyngeal duct and/or thesis is a surgical procedure usually performed to
Rathke cleft, or metaplastically because of resid- fill in or replace a defect in the skull following a
ual squamous epithelium. The most common pre- craniectomy or removal of a bone flap (Fig. 1).
senting symptoms are endocrine dysfunction,
headache, and visual disturbances. Craniophar-
yngiomas are treated with surgical excision or Further Reading
surgery followed by radiotherapy (Fig. 1).
Craniectomy is currently performed acutely in
patients with traumatic or acute brain injury in
the management of raised intracranial pressure,
in hemorrhages, or in the context of infected or
contaminated wounds. The decision to perform

Craniopharyngioma, Fig. 1 (Courtesy Michael Fisher,

MD, Peter C. Phillips, MD. The Children’s Hospital of
Philadelphia) Cranioplasty, Fig. 1 Source: Winder et al. (1999)
1002 Craniospinal Radiotherapy

and the timing of the cranioplasty to replace the Long, D. F. (2013). Diagnosis and management of late
skull defect, following craniectomy, can be vari- Complications of traumatic brain injury. In N. D.
Zasler, D. I. Katz, & R. D. Zafonte (Eds.), Brain injury
able, and this decision is not taken lightly as the medicine (2nd ed., p. 731). New York: Demo’s Medical
risk of complications can be high (Long 2013). Publishing.
There has been recent interest in performing Waziri, A., Fusco, D., Mayer, S. A., McKhann, G. M., &
cranioplasty much earlier than in the past when Connolly Jr., E. S. (2007). Postoperative hydrocephalus
in patients undergoing decompressive hemicraniectomy
cranioplasty may have been delayed and consid- for ischemic or hemorrhagic stroke. Neurosurgery,
ered to be largely a cosmetic procedure. 61(3), 489–493.
Cranioplasty may be performed to prevent or Winder, R. J., Cooke, R. S., Gray, J., Fannin, T., & Fegan,
treat potential late neurological complications of T. (1999). Medical rapid prototyping and 3D CT in the
manufacture of custom made cranial titanium plates.
craniectomy such as hydrocephalus (Waziri et al. Journal of Medical Engineering and Technology,
2007) and the “syndrome of trephined” (Dujovny 23(1), 26–28.
et al. 1999; Long 2007). Characteristics of
the syndrome of trephined include a marked inden-
tation or sunken appearance to the skin overlying
the skull defect. Neurological symptoms including Craniospinal Radiotherapy
headache, dizziness, irritability, epilepsy, discom-
fort, and ocular and psychiatric symptoms Jacqueline L. Cunningham
(Dujovny et al. 1997). Neurological and functional Department of Psychology, Children’s
improvements have been shown to improve fol- Hospital of Philadelphia, Philadelphia,
lowing cranioplasty in this syndrome (Long 2013; PA, USA
Dujovny et al. 1997; Gardner 1945).
Cranioplasty can be performed with the
patient’s own bone flap, which can be frozen or Synonyms
stored in the patient’s abdomen. Where the
patient’s own bone flap is not available, comput- Craniospinal irradiation; CSI
erized techniques can be used to generate a
custom-made cranioplasty prosthesis; multiple
materials can be used; however some studies Definition
have indicated that lower rates of postoperative
infection are being reported with titanium or tita- Craniospinal radiotherapy is an irradiation that is
nium mesh (Long 2013). directed at the whole brain and length of the spinal
axis, including the meninges, as part of the cancer
treatment to control malignant cells. It serves as a
radical (curative) antineoplastic therapy, as a
References and Readings prophylaxis against a neoplasm’s involvement
with the central nervous system, or as a palliative
Dujovny, M., Aviles, A., Fernandez, P., & Charbel, F. T.
recourse when cure is impossible. Craniospinal
(1997). Cranioplasty: Cosmetic or therapeutic? Surgi-
cal Neurology, 47, 238–241. irradiation (CSI) is technically challenging, and is
Dujovny, M., Agner, C., & Aviles, A. (1999). Syndrome of used with computed tomography (CT) simulation
the trephined: Theory and facts. Critical Reviews in and multimodality MRI registration to define a
Neurosurgery: CR, 9(5), 271–278.
Gardner, W. J. (1945). Closure of defects of the skull with
large target volume, which spares healthy tissues,
tantalum. Surgery, Gynaecology Obstetrics, 80, and assures exact reproducibility of treatment from
303–312. day-to-day. Intensity-modulated radiation therapy,
Long, D. F. (2007). Diagnosis and management of proton radiotherapy, and other new methods are
late intracranial complications of TBI. In N. D.
Zasler, D. L. Katz, & R. D. Zafonte (Eds.), Brain
new techniques for craniospinal treatment in order
injury medicine. Principles and practice. New York: to reduce side effects and preserve sensitive neural
Demos. and other tissue, such as cardiac, near the spine.
Craniotomy 1003

MRI evidence of the craniospinal radiation Mahajan, A. (2014). Proton craniospinal radiation therapy:
injury to the brain has been seen in l’Hermitte’s Rationale and clinical evidence. International Journal
of Particle Therapy, 1(2), 299–407.
sign (a side effect of radiotherapy on the spinal Sharma, D. S., Gupta, T., Jalali, R., Master, Z.,
cord, experienced as shock sensations), telangiecta- Phurailatpam, R. D., & Sarin, R. (2009). High-
sia (dilated capillaries), white matter changes, basal precision radiotherapy for craniospinal irradiation:
ganglia change, necrosis, and cerebral atrophy. Evaluation of three-dimensional conformal radiother-
Although the differential sensitivity of specific
apy, intensity-modulated radiation therapy and helical
TomoTherapy. The British Journal of Radiology, 82,
C
brain regions to radiotherapy has not been deter- 1000–1009.
mined, factors relating to total dose, dose per frac-
tion, and interval between fractions have been
identified as important variables influencing the
brain’s response to radiation. Present research
focuses on the development of treatment protocols Craniotomy
based on the efficacy in tumor control while
using the least dose of craniospinal radiotherapy Eduardo Lopez
(1,800 cGy), often in conjunction with chemother- Rehabilitation Medicine, New York Medical
apy, as the efficacy of CSI dose reduction in ame- College, Metropolitan Hospital, New York, NY,
liorating neuroendocrine and neurocognitive USA
sequelae remains unclear. Today, in contrast to the
much higher doses used in the past decades, CSI
doses of 2,400 and 3,600 cGy (with daily fractions Synonyms
of 150 or 180 cGy) are standard. Studies continue to
evaluate how low a dose will remain effective in a Craniectomy; Trephination
risk-adapted setting. Controversy also exists on
the expression of radiation effects on specific
neurocognitive domains. Attention and memory
Definition
are known to bear a vulnerability to neurotoxicity,
but issues of individual differences, including pre-
Neurosurgical procedure involving the opening of
morbid and disease-related risk factors, are expected
the skull as a means of decreasing intracranial
to influence neuropsychological outcomes.
pressure (ICP) and/or for purposes of removal of
a mass lesion.

Cross-References
Current Knowledge
▶ Radiation Injury
▶ Radiation Oncology
Craniotomy as a treatment for increased ICP
▶ Radiotherapy
from a mass lesion has its foundation early in
the history of neurosurgery. Decompressive cra-
niotomy (DC) initially was introduced to lower
References and Readings the intracranial pressure (ICP) in patients with
Armstrong, C. L., Gyato, K., Awadalla, A. W., Lustig, R.,
inoperable tumors and in managing
& Tochner, Z. A. (2004). A critical review of the uncontrolled ICP after traumatic brain injury
clinical effects of therapeutic irradiation damage to (Brit and Hamilton 1978). DC has been
the brain: The roots of controversy. Neuropsychology recommended as an alternative treatment for
Review, 14, 65–86.
Brady, L. W., Heilmann, H. P., Molls, M., & Schlegel,
space occupying acute hemispheric infarction
W. (2006). New techniques in radiation oncology. with or without massive medically uncontrolled
New York: Springer. brain edema (Schwab 1998). A scientific
1004 Craniotomy

statement addressing the early approach to a thrombosis, encephalitis, intracerebral hema-

patient with a swollen ischemic stroke in a toma, and metabolic encephalopathies. In a
cerebral or cerebellar hemisphere has been recent publication, the RESCUEicp tri-
produced (Wijdicks et al. 2014). During the alcomparing DC to best medical therapy in
acute period following cerebral infarction, neu- patients with severe TBI and medically refrac-
rologic decline is often attributed to surrounding tory ICP’s. Results show a definite survival ben-
edema. Apart from relieving the mass effect, efit but worse functional outcome with DC than
restoration of the microcirculation around the those treated medically for refractory elevated
infarcted area is the target of DC. The manage- ICP (Hutchinson et al. 2016). Previous DECRA
ment of increased intracranial pressure is a trial resulted in no difference in death found
common clinical scenario in neurosurgery. between groups but an associated worse func-
Strategies for the management of ICP fall into tional outcome with DC (Cooper et al.
two general categories: to reduce the volume of 2011). Results were thought to be secondary to
the intracranial compartment (medical manage- earlier time of surgery with associated complica-
ment) and to remove the mechanical constraints tions and patient selection process.
imposed by the cranial vault (surgical).
In patients who sustain a severe non-penetrat-
ing head injury, overall 25–45% require a crani-
otomy for evacuation of a hemorrhagic mass Cross-References
lesion, including epidural, subdural, and intrace-
rebral hematomas (Miller 1981). There is little ▶ Temporal Lobectomy
debate in the surgical management of a rapidly
deteriorating patient with a focal neurological
deficit and neuroimaging findings of an References and Readings
expanding intracranial hematoma associated
with significant mass effect and midline shift. Aldrich, E. F., Eisenberg, H. M., Saydhari, C., et al. (1992).
For less obvious situations, controversy remains Diffuse brain swelling in head-injured children. Jour-
nal of Neurosurgery, 76(3), 450–454.
given the lack of class I and II data to support any
Brit, R., & Hamilton, R. (1978). Large decompressive
treatment standard. Level III recommendation craniotomy in the treatment of acute subdural hema-
exists for pediatric patients with severe TBI, toma. Neurosurgery, 2(3), 195–200.
thought to be more prone than adults in develop- Bullock, R., Chestnut, R., Ghajar, J., et al. (2006). Surgical
management of subdural hematoma. Neurosurgery, 58
ing diffuse severe cerebral edema (Aldrich et al.
(3), S2-16–S2-24.
1992). Complete removal of a brain tumor with- Chen, C., Smith, E., Ogilvy, C., & Carter, B. S. (2006).
out inflicting neurological deficits is a desirable Decompressive craniectomy: Physiological rationale,
end result in neurosurgical practice. Craniotomy clinical indications, and surgical considerations. 5,
70–80.
was tailored to encompass tumor plus adjacent
Cooper, D. J., et al. (2011). Decompressive craniectomy in
areas presumed to contain eloquent cortex. Mag- diffuse traumatic brain injury. New England Journal of
netic brain stimulation or intraoperative cortical Medicine, 364(16), 1493–1502.
stimulation can be used to guide resection of Hutchinson, P. J., Kolias, A. G., Timofeev, I. S., et al. (2016)
Trial of decompressive craniectomy for traumatic intra-
functional cortex.
cranial hypertension. New England Journal of Medicine,
DC remains a controversial procedure in 375(12):1119–1130.
spite of a number of studies published in the Wijdicks, E. F., Sheth, K. N., Carter, B. S., et al. (2014).
literature on its use in the treatment of intracra- Recommendations for the management of cerebral and
cerebellar infarction with selling: A statement for
nial hypertension secondary to malignant
healthcare professionals from the American Heart
cerebral edema, traumatic brain injury, aneurys- Association/American Stroke Association. Stroke,
mal subarachnoid hemorrhage, central venous 45(4), 1222–1238.
Creutzfeldt-Jakob Disease 1005

geographical clustering (although there are

Creutzfeldt-Jakob Disease regions with an increased incidence of familial
cases). The gender incidence is equal.
Kari Hawkins1, Robert G. Will2 and
Narinder Kapur3
1
Neuropsychology Department, Addenbrooke’s Natural History, Prognostic Factors, and
Hospital, Cambridge, UK Outcomes C
2
University of Edinburgh, Edinburgh, UK
3
Research Department of Clinical, Educational Historical Background
and Health Psychology, University College Sporadic and familial CJDs have been recognized
London, London, UK as prion diseases for many years, showing wide
geographical spread; however, variant CJD has
been confined largely to the UK, with the first
Synonyms cases reported in 1996. It is thought that meat
products intended for human consumption
CJD; Prion disease; Transmissible spongiform contained contaminated brain and spinal cord
encephalopathy (TSE from animals affected by the epidemic of a prion
disease in cattle (bovine spongiform encephalopa-
thy) in the 1980s (Hilton 2006). Initial fears of a
Short Description or Definition catastrophic epidemic of vCJD among humans
have been partially quelled, with a peak in new
Creutzfeldt-Jakob Disease (CJD) is a rare, fatal neu- cases during 2000 reducing steadily to only one
rodegenerative disease, which is one of the trans- new case in 2013 (http://www.cjd.ed.ac.uk). How-
missible spongiform encephalopathies or prion ever, all vCJD cases to date have shared a common
diseases. These conditions are characterized patho- genotype (methionine/methionine) raising the pos-
logically by neuronal loss, spongiform change, and sibility of subsequent peaks, which occur due to
astrocytic gliosis. Cell loss can be seen microscop- lengthened incubation times among other geno-
ically as multiple perforations to the brain tissue typic groups. In addition, evidence from Kuru, an
creating the characteristic “spongelike” appearance. acquired prion disease arising from cannibalistic
Prion diseases are caused by infectious agents, funeral practices among the Fore people of Papua
which are abnormal self-replicating forms of a nor- New Guinea carried out until 1950s, suggests that
mal brain protein, prion protein. incubation times for acquired prion disease may
stretch to several decades (Collinge et al. 2006). It
is also possible for a person-to-person spread to
Categorization and Epidemiology occur, as has been seen in four cases of blood
transfusion-associated vCJD infection (most recent
Creutzfeldt-Jakob disease (CJD) may be sporadic incidence figures are available from http://www.
(that is develop spontaneously without apparent cjd.ed.ac.uk).
cause), familial (inherited), or acquired (transmitted
by infection). Natural History and Prognosis
CJD occurs worldwide with a mean annual Different CJD phenotypes develop and progress
incidence of approximately one to two cases per at different rates, although all subtypes develop
million population (Ladogana et al. 2005). Except profound dementia and multiple neurological fea-
for variant and iatrogenic CJDs, which are in tures progressing to loss of awareness and death.
decline, the disease has a relatively stable A summary of clinical presenting features is given
incidence with no convincing evidence of in Table 1.
1006 Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob Disease, Table 1 Forms, causes, and incidence of CJD

Form Phenotype Cause Incidence
Sporadic Sporadic Creutzfeldt- Unknown Approximately one case per million
Jakob disease (sCJD) population. Accounts for around
85% of CJD cases
Familial Familial Creutzfeldt- Inheritance of mutation in the PrP gene Approximately 10–15% of CJD
Jakob disease (fCJD) cases are familial
Acquired Iatrogenic Case-to-case transmission via Less than 1% of CJD cases arise
contaminated neurosurgical through acquired infection
instruments, human dura mater grafts,
or exposure to human pituitary
hormones. The variant form of CJD
can also be transmitted via blood
transfusion.
Variant CJD (vCJD) Ingestion of contaminated meat 177 cases in total in the UK,
products from cattle infected with 27 cases in France, and a total of
bovine spongiform encephalopathy 25 cases elsewhere in the world
(as of Jan 2016)

sCJD presents with cumulative multifocal neu- Neuropsychology and Psychology of

rological deficits in association with a rapidly Creutzfeldt-Jakob Disease
progressive dementia. The cardinal clinical signs
are dementia and myoclonus, with a significant The Presentation of the CJD Patient
proportion of cases exhibiting ataxia and para- The differential diagnosis is often the question at
tonic rigidity of the limbs. The mean survival referral, in particular, the distinction between a
from onset to death is only 4 months, although psychiatric or neurological basis for the pre-
patients in the younger age groups often survive senting symptoms or to distinguish CJD from
for more than a year. sCJD affects predominantly other neurological conditions. A thorough history,
the older age groups with the mean age being as always, is essential in establishing both the
65 years at death. profile of the presenting symptoms and the course
The clinical presentation in familial CJD is of the illness, and care should be taken to obtain
often similar to sCJD, but the age of onset is corroborative reporting from relatives given the
about 10 years earlier, and in some forms, there difficulties of accurate history taking in individ-
may be early ataxia and/or slow progression. uals with cognitive decline. Sporadic CJD can
Iatrogenic CJD may present as in sCJD, but often be distinguished from other disorders by
human pituitary hormone recipients typically the speed and degree of cognitive decline, the
develop progressive ataxia and cognitive impair- short duration of illness, and the associated neu-
ment develops late, if at all. rological signs. Concentration and memory symp-
Variant CJD presents with a psychiatric syn- toms may often be the presenting cognitive
drome, including depression and anxiety, for difficulties, but more atypical cognitive presenta-
about 6 months before there is a progressive neu- tions may also be found, including disorders of
rological and cognitive decline as in sCJD, language (Martory et al. 2012; Nakamura et al.
although chorea and dystonia occur as well as 2014) and visual symptoms (Verma et al. 2013;
myoclonus. The mean survival is 14 months, and Wong et al. 2015). Some cases of fCJD present
vCJD affects a younger age group, with the mean very similarly to sCJD; however, in fCJD, there
age being 29 years at death. is often a younger age of onset, a longer disease
Creutzfeldt-Jakob Disease 1007

Creutzfeldt-Jakob Disease, Table 2 Clinical presentation of CJD

Approximate
duration of Early clinical Neuropsychological
Form Age at onset illness features findings Exceptions
Sporadic 90% of cases 4 months Neurological Areas of early Rare cases occur
between 50 and (65% of cases signs including cognitive deficit younger than 50.
80 years, mean survive cerebellar ataxia, vary in this Young cases may
65 years <6 months cognitive heterogeneous present with C
from impairment group, but there is some psychiatric
symptom (global dementia often marked symptoms
onset) or specific deficits impairment by the initially, similar
in earlier stages), time of a referral for to the vCJD
followed by testing. Most cases presentation, and
myoclonus, show rapid may have longer
rigidity, and rapid progression to a disease duration
deterioration to wide-ranging
loss of speech, dementia including
voluntary verbal and nonverbal
movement, and memory, executive
awareness dysfunction, and
nominal skills. Poor
memory and/or
attention are often
early features, but
there may be
occasional cases
where initial deficits
reflect dysphasia or
visual disturbance
Look for: rapid 19% sCJD cases
cognitive decline have a disease
over multiple test duration
sessions >12 months
Fluctuations in Heidenhain form:
responsiveness and very focal visual
distractibility difficulties for
weeks/months
before other
cognitive
symptoms
Intrusion errors Brownell-
Verbal and motor Oppenheimer
perseveration form: pure
cerebellar
syndrome for
several weeks or
months before
cognitive decline
(continued)
1008 Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob Disease, Table 2 (continued)

Approximate
duration of Early clinical Neuropsychological
Form Age at onset illness features findings Exceptions
Familial Dependent on the Dependent on Dependent on fCJD cases may Some cases can
specific mutation the specific mutation, may demonstrate less have an illness
of the prion mutation, but present in a severe/rapid duration of years
protein gene, but on average similar fashion to cognitive decline at Fatal familial
most often 2–5 years sCJD or with the early stages of a insomnia: early
between the ages predominant sleep longer disease sleep disturbance
of 30 and 50 years and autonomic course than sCJD or and autonomic
disturbance or vCJD cases. A single dysfunction are
cerebellar ataxia case in 2000 showed prominent
(see Exceptions, specific isolated Gerstmann
right). deficits in delayed Straussler
Deterioration is verbal memory and syndrome:
usually slower word finding prior to progressive
than in vCJD or global involvement. cerebellar ataxia
sCJD with a One study suggests
longer disease that naming ability
course may be preserved in
some cases in
comparison to sCJD
and vCJD. Look for:
family history of
CJD or other
(possibly
misclassified)
neurological disease
Iatrogenic Dependent on age Following Human growth Dependent on mode
at exposure. dura mater hormone of transmission;
Incubation period graft similar infection: human growth
following to sCJD, with progressive hormone patients
intracerebral human cerebellar present with ataxia
exposure is pituitary syndrome, with relatively
19–46 months, hormones delayed onset of preserved cognitive
extending to 12–18 months dementia Human function until later
many years or dura mater stages, while
decades with infection: rapidly intracerebral cases
peripheral progressive present with broad-
exposure dementia, similar ranging dementia
to sCJD with rapid
deterioration as seen
in sCJD. Look for:
rapid cognitive
decline over
multiple test
sessions for
intracerebral
exposure cases.
History of relevant
exposure to
differentiate from
sCJD
(continued)
Creutzfeldt-Jakob Disease 1009

Creutzfeldt-Jakob Disease, Table 2 (continued)

Approximate
duration of Early clinical Neuropsychological
Form Age at onset illness features findings Exceptions
Variant Median age Median Most commonly, Measurable In 15%,
28 (range 12–74) 14 months initial impairments on tests neurological
presentation is of both verbal and symptoms
psychiatric nonverbal memory, precede C
disturbance executive function, psychiatric
including speed of attention,
depression, and nominal skills
agitation, and have characterized
behavioral descriptions of
changes, although published cases.
in some cases, Language, verbal
cognitive changes reasoning, and
may be the first visuoperceptual
sign of skills may be less
abnormality. frequently impaired,
A delay of months although this may
is possible before reflect an earlier
distinct disease stage at the
neurological time of testing. One
signs, although study suggests
cognitive changes possible preserved
may be found ability in some
earlier in the components of
disease course. visuoperception in
Sensory comparison to
symptoms such as patients suffering
pain or odd from sCJD or fCJD.
sensation in limbs Global involvement
or face may be follows with rapid
reported. Ataxia, disease progression.
myoclonus, and Look for: fluctuating
significant attention and effort
cognitive during testing.
impairment (such Cognitive
as memory) impairment more
develop as the profound than
disease expected for
progresses depression or
including areas of
deficit unusual for
psychiatric disorders
Significant cognitive
decline over follow-
up assessment
sessions
Sources of information for this table are referenced under “References and Readings”

duration, and a family history of either CJD or early psychiatric symptoms (including mood,
another neurological disorder. In iatrogenic delusion, and agitation) and may also reveal cog-
cases, there should be a clear history of a relevant nitive decline in everyday activities, of the type
exposure. The history in vCJD cases includes that might typically be attributed to depression.
1010 Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob Disease, Table 3 Investigations used in the diagnosis of CJD

Phenotype MRI EEG CSF 14-3-3 Tonsil biopsy Blood test History
Sporadic Important in In 60–80% of A positive Negative At codon
(sCJD) excluding cases, 14-3-3 CSF 129 of the
other generalized bi- immunoassay prion protein
conditions. or triphasic is strongly gene: 70%
High signal on periodic sharp supportive of methionine
FLAIR or wave a diagnosis of homozygous
DWI complexes at sCJD in the
sequences in 1/s. May not appropriate
the caudate appear until clinical
and putamen later stages of context, i.e.,
in about 70% the disease rapidly
of cases progressive
dementia.
Positive in
90% of cases
of sCJD
Familial Some cases Characteristic Positive less Negative Analysis of Positive
(fCJD) similar to periodic pattern frequently the prion family
sCJD is less than sCJD protein gene history of
frequently seen for mutations CJD in
than in sCJD about 30%
of cases
Iatrogenic Similar to Characteristic Positive in a Negative Mainly Relevant
sporadic CJD periodic pattern proportion of homozygous exposure
is less cases methionine risk such
frequently seen or valine as
than in sCJD treatment
with
cadaveric-
derived
human
growth
hormone
or human
dura mater
graft
Variant Characteristic Normal or Positive in As vCJD, unlike All tested
(vCJD) high signal in nonspecifically 50% of cases, the other CJD cases
the posterior abnormal. but does not phenotypes, methionine
thalamic Characteristic distinguish involves the homozygous
region (the periodic pattern from sCJD lymphoreticular
“pulvinar in two cases system,
sign”) in over late in clinical abnormal
90% of cases course protein may be
on FLAIR or found in the
DWI biopsy of tonsil
sequences tissue in about
90% of cases
Adapted from the National Creutzfeldt-Jakob Disease Surveillance Unit website (http://www.cjd.ed.ac.uk/investigations.htm)
Creutzfeldt-Jakob Disease 1011

In some cases, neuropsychological symptoms progresses, the management of issues such as feed-
may precede psychiatric or neurological indica- ing or continence. Intervention may be needed for
tors that develop as the disease progresses. The the management of mood or psychotic symptoms.
early presenting features in all CJD subtypes are Since a high level of care will inevitably become
summarized in Table 2. necessary, planning for the provision of this should
begin early, in consultation with the family. In the
Neuropsychological Testing case of a diagnosis of familial CJD, the family will C
Patients with CJD often present at too late a stage face difficult decisions regarding genetic screening
for formal testing with a full neuropsychological and should be guided through such a process by an
battery. This is reflected in the literature, in which appropriately qualified professional.
reports focus on small cohorts and case studies. It is often the case that the cognitive symptoms
Efforts should be made to obtain sufficient of CJD show extremely rapid deterioration, and,
breadth across cognitive domains when testing in view of this, cognitive rehabilitative efforts are
to aid diagnosis and enable repeat testing if appro- unlikely to produce helpful returns. However, in
priate. Observations of test behavior will also be cases with early referral or a longer disease
helpful. A study is currently underway to establish course, supportive aids (such as a calendar for
whether a brief bedside screening test might be orientation) or environmental adaptations may
sufficient to give an indication of whether the produce improvements in activities of daily liv-
degree or pattern of impairment seen in a patient ing, self-efficacy, and mood, at least in the early
could indicate CJD. days, as is the case in other dementias (Clare
2007; Smith-Bathgate 2005).
While the patients themselves are likely to lose
Evaluation awareness of their predicament as their cognitive
ability declines, their families observe a devastat-
Neuropsychological testing may occur prior to, in ing deterioration in their loved ones. There is a
parallel with, or following medical investigations role for the clinical psychologist, nurse practi-
and may provide support for a diagnosis of CJD or tioner, or other qualified healthcare professionals
prompt the clinician to instigate more extensive in supporting individuals and their families
investigation than would usually be undertaken in through a period of acceptance, adjustment, loss,
patients presenting, for example, with primarily and ultimately grief. Provision might also be made
psychiatric complaints as in vCJD. A number of for the counselling of healthcare staff involved in
further investigations may be used in the diagno- these distressing cases.
sis of CJD (Table 3).

Treatment Cross-References

CJD is fatal. There is currently no effective treat- ▶ Encephalopathy

ment for the disease itself, despite ongoing trials of ▶ Prion Disease
quinacrine, pentosan polysulfate, and flupirtine
(Stewart et al. 2008; see the MRC New Therapies
Scrutiny Group for Prion Disease website for up-to- References and Readings
date information concerning recent treatment stud-
Clare, L. (2007). Neuropsychological rehabilitation and
ies). Medical management should focus on allevi-
people with dementia. Hove: Psychology Press.
ating discomfort, including the use of medication to Collinge, J., Whitfield, J., McKintosh, E., Beck, J., Mead, S.,
manage myoclonic jerks or pain and, as the disease Thomas, D. J., et al. (2006). Kuru in the 21st century –
1012 Criminal Forensics

An acquired human prion disease with very long incu- Wong, A., Matheos, K., & Danesh-Meyer, H. (2015). Visual
bation periods. Lancet, 367(9528), 2068–2074. symptoms in the presentation of Creutzfeldt-Jakob dis-
Cordery, R. J., Alner, K., Cipolotti, L., Ron, M., Kennedy, ease. Journal of Clinical Neuroscience, 22, 1688–1689.
A., Collinge, J., et al. (2005). The neuropsychology of
variant CJD: A comparative study with inherited and
sporadic forms of prion disease. Journal of Neurology,
Neurosurgery and Psychiatry, 76, 330–336. Criminal Forensics
Creutzfeldt-Jakob Disease Foundation website. (2015).
http://www.cjdfoundation.org
Gass, C. S., Luis, C. A., Meyers, T. L., & Kuljis, R. O. Moira C. Dux
(2000). Familial Creutzfeldt-Jakob disease: A neuropsy- US Department of Veteran Affairs, Baltimore,
chological case study. Archives of Clinical Neuropsy- MD, USA
chology, 15(2), 165–175.
Hilton, D. A. (2006). Pathogenesis and prevalence of var-
iant Creutzfeldt-Jakob disease. Journal of Pathology,
208(2), 134–141. Definition
Kapur, N., Abbott, P., Lowman, A., & Will, R. G. (2003).
The neuropsychological profile associated with variant
Creutzfeldt-Jakob disease. Brain, 126, 2693–2702.
Within the field of forensic psychology, the utiliza-
Ladogana, A., Puopolo, M., Croes, E. A., Budka, H., Jarius, tion of clinical neuropsychological expertise for
C., Collins, S., et al. (2005). Mortality from Creutzfeldt- criminal forensic cases can be considered a sub-
Jakob disease and related disorders in Europe, Australia, specialty of the field. Denney and Wynkoop (2000)
and Canada. Neurology, 64, 1586–1591.
Martory, M., Roth, S., Lovblad, K., et al. (2012).
modified Mrad’s (1996) multiple data source
Creutzfeldt-Jakob disease revealed by a logopenic var- model (MDSM) to the practice of criminal forensic
iant of primary progressive aphasia. European Neurol- neuropsychology. The purpose of the model is to
ogy, 67, 360–362. provide a framework for clinicians to evaluate all
Medical Research Council New Therapies Scrutiny Group
for Prion Disease website. (2015). http://www.mrc.ac.
relevant sources of information, most notably
uk/PolicyGuidance/PolicyDevelopment/NewTherapies information relevant to the defendant’s mental
ScrutinyGroupforPrionDisease state at the time of the offense. The model covers
Nakamura, K., Sakai, K., Samuraki, M., et al. (2014). three time points of analysis: present, time of
Agraphia of Kanji (Chinese characters): An early
symptom of sporadic Creutzfeldt-Jakob disease in a
offense, and prior history. Moreover, the model
Japanese patient: A case report. Journal of Medical assesses symptoms/behaviors, explanations, etc.,
Case Reports, 8, 269. via the self-report of the defendant as well as via
National Creutzfeldt-Jakob Disease Surveillance Unit other sources of data (e.g., neuropsychological
(NCJDSU) website. (2015). http://www.cjd.ed.ac.uk
National Prion Clinic website. (2015). http://www.national
tests, mental status exam, medical/neurological
prionclinic.org exam, arrest reports, witness statements, physical
Smith-Bathgate, B. (2005). Creutzfeldt-Jakob disease: Diag- evidence, hospital/psychiatric records, employ-
nosis and nursing care issues. Nursing Times, 101, 52–53. ment records, family/friend reports, etc.). Once all
Snowden, J. S., Mann, D. M. A., & Neary, D. (2002).
Distinct neuropsychological characteristics in
of the relevant pieces of information are gathered,
Creutzfeldt-Jakob disease. Journal of Neurology, Neu- spanning the three time points, it is the role of the
rosurgery and Psychiatry, 73, 686–694. forensic neuropsychologist to consolidate the
Spencer, M. D., Knight, R. S. G., & Will, R. G. (2002). information and formulate opinions. Evaluators
First hundred cases of variant Creutzfeldt-Jakob dis-
ease: Retrospective case note review of early psychiat-
involved in criminal forensics typically have very
ric and neurological features. British Medical Journal, different roles compared to general practitioners.
324, 1479–1482. Specifically, in forensic evaluations, the client is
Stewart, L. A., Rydzewska, L. H. M., Keogh, G. F., & typically not the person being examined, and the
Knight, R. S. G. (2008). Systematic review of thera-
peutic interventions in human prion disease. Neurol-
ultimate goal is to evaluate the facts, not to main-
ogy, 70, 1272–1281. tain an alliance with the examinee as is the case in a
Verma, R., Junewar, V., & Sahu, R. (2013). Creutzfeldt- clinical context. Moreover, forensic criminal eval-
Jakob disease presenting with visual symptoms: A case uations typically involve much more extensive
of the ‘Heidenhain variant’. BMJ Case Reports. https://
doi.org/10.1136/bcr-2012-008006.
application of corroborative information as well
Criminal Responsibility 1013

as validated assessments of negative response bias, having committed a crime. However, if a defendant
symptom validity, and malingering. claims insanity (e.g., cannot appreciate the wrong-
fulness of the act nor conform their conduct to the
requirements of the law), then the burden of proof in
proving one’s insanity falls on the defendant. Under
Cross-References
criminal litigation, the state must demonstrate that
the accused satisfied each element of the statutory C
▶ Criminal Litigation
definition of the crime and prove the defendant’s
involvement beyond a reasonable doubt. In the
context of criminal litigation, forensic neuropsy-
References and Readings
chologists often provide determinations regarding
Denney, R. L. (2005). Criminal responsibility and other “mens rea” (e.g., guilty mind) or not guilty by
criminal forensic issues. In G. Larrabee (Ed.), Forensic reason of insanity (NGRI), competent waiver of
neuropsychology: A scientific approach. New York: Miranda rights, and/or competence to proceed
Oxford University Press.
(e.g., stand trial, to be sentenced, etc.).
Denney, R. L., & Sullivan, J. P. (2008). Clinical neuropsy-
chology in the criminal forensic setting. New York:
Guilford.
Denney, R. L., & Wynkoop, T. F. (2000). Clinical neuro- Cross-References
psychology in the criminal forensic setting. Journal of
Head Trauma Rehabilitation, 15, 804–828.
Mrad, D. (1996). Criminal responsibility evaluations. ▶ Actus Reus
Paper presented at issues in forensic assessment sym- ▶ Criminal Forensics
posium. Atlanta: Federal Bureau of Prisons. ▶ Insanity
▶ Mens Rea

Criminal Litigation References and Readings

Moira C. Dux Denney, R. L., & Sullivan, J. P. (2008). Clinical neuropsy-

US Department of Veteran Affairs, Baltimore, chology in the criminal forensic setting. New York:
Guilford.
MD, USA
Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychol-
ogy and the law: Principles of productive attorney-
neuropsychologist relations. In G. Larrabee (Ed.),
Definition Forensic neuropsychology: A scientific approach.
New York: Oxford University Press.

In civil litigation, a lawsuit is filed by a private party,

seeking damages from another party as a result of
some type of injury, negligence, or malpractice. In Criminal Responsibility
criminal litigation, the case is filed by the govern-
ment against a defendant whom the government Robert L. Heilbronner
believes has committed a crime. Crimes are classi- Chicago Neuropsychology Group, Chicago, IL,
fied into one of two categories: misdemeanors or USA
felonies. Punishment for misdemeanors involve a
maximum possible sentence of less than 1 year of
incarceration; felonies carry a maximum possible Definition
sentence of more than 1 year of incarceration. The
burden of proof in criminal litigation is always Criminal responsibility, or the conclusion of guilt
assumed by the state. Thus, it is the state’s respon- for a criminal offense, centers on four elements:
sibility to prove that the defendant is guilty of (1) The defendant must have committed the act
1014 Crisis Intervention

(actus reus). (2) The defendant’s actions must have Denney, R. L. (2005). Criminal responsibility and other
caused the crime. (3) The defendant must have criminal forensic issues. In G. Larrabee (Ed.), Forensic
neuropsychology: A scientific approach. New York:
committed the crime with a guilty state of mind Oxford University Press.
(mens rea). (4) There must be no circumstance Heilbronner, R. L., & Waller, D. (2008). Neuropsycholog-
constituting a legal defense for the charged crime ical consultation in the sentencing phase of capital
(e.g., self-defense). In short, there must be the crim- cases. In R. Denney & J. Sullivan (Eds.), Clinical
neuropsychology in the criminal forensic setting.
inal act and the criminal intent and both must be New York: Guilford.
proven, beyond a reasonable doubt. Mental health Shapiro, D. L. (1999). Criminal responsibility evaluations:
professionals are typically involved with A manual for practice. Sarasota: Professional Resource
establishing intent and mens rea, which involves Press.
Wrightsman, L. S., Greene, E., Nietzel, M. T., & Fortune,
the assessment and professional opinions related to W. H. (2002). Psychology and the legal system
a defendant’s sanity and/or diminished capacity (5th ed.). Belmont: Wadsworth, Thompson Learning.
(which includes a decreased level of intent). Yates, K. F., & Denney, R. L. (2008). Neuropsychology in
Criminal responsibility evaluations are also the assessment of mental state at the time of the offense.
In R. Denney & J. Sullivan (Eds.), Clinical neuropsy-
called sanity evaluations or assessment of mental chology in the criminal forensic setting. New York:
state at the time of the offense evaluations. Deter- Guilford.
mining whether or not a defendant was sane at the
time of the offense is one of the most controversial
questions forensic examiners are asked to address
given that the purpose of the exam is to identify
individuals who should not be held morally respon- Crisis Intervention
sible (“not guilty by reason of insanity”) for their
acts (Yates and Denney 2008). An insanity plea is Paul B. Perrin
pursued in about 9 out of 1000 cases, and it is Department of Psychology, Virginia
successful approximately 25% of the time Commonwealth University, Richmond, VA, USA
(Wrightsman et al. 2002). It is very rare when a
defendant is acquitted secondary to insanity caused
by a brain-injury-related issue. Nonetheless, neu- Synonyms
ropsychologists are increasingly being called
upon to determine whether or not brain pathology Emotional de-escalation; Suicide intervention
may contribute to criminal behavior (Barr 2008).

Cross-References Short Description or Definition

▶ Actus Reus A crisis occurs during the clinical encounter in

▶ Diminished Capacity neuropsychology when a patient’s stressors out-
▶ Diminished Responsibility weigh his or her assets, which include coping
▶ Insanity strategies, personal strengths, and resources. In
▶ Intent, General v. Specific this situation, the clinician is called upon to
▶ Mens Rea intervene.

References and Readings Current Knowledge

Barr, W. B. (2008). Neuropsychological approaches to
criminality and violence. In R. Denney & J. Sullivan
Because stressors can be infinite and assets are
(Eds.), Clinical neuropsychology in the criminal foren- finite, everyone is vulnerable to encountering a
sic setting. New York: Guilford. state of crisis at various points in one’s life,
Crossed Aphasia 1015

perhaps particularly so in the context of the devel- crises are not fixable by the clinician. It is quite
opment of a neurological condition. Common cri- easy for a clinician to take on the same urgency the
sis behavioral responses in patients include altered patient feels in the crisis, which unfortunately can
sleeping and eating patterns, altered activity cause the clinician to omit important interventions
levels, and emotional lability. The basics of crisis and assessments or redirect a session away
intervention in the context of neuropsychology from the session’s purpose. Unhelpful responses
involve two overlapping components: empathy on the part of the clinician during crisis interven- C
and assessment/referral. tion include superficial reassurance, avoidance
To show empathy, the clinician must commu- of strong feelings, inadequate assessment of sui-
nicate understanding through both listening and cidal or homicidal intent, failure to identify a
paraphrasing what the patient is presenting and precipitating event, insufficient directedness,
describing. The clinician can use content para- advice giving, and defensiveness (Neimeyer and
phrases, which involve rephrasing and repeating Pfeiffer 1994).
back to the patient what the patient has said, a
process that shows the patient that the clinician is
listening and understands. In an emotional para-
References and Readings
phrase, the clinician takes content paraphrasing
deeper and identifies and validates the emotions Joiner, T., Kalafat, J., Draper, J., Stokes, H., Knudson, M.,
the patient feels but perhaps is not directly Berman, A. L., & McKeon, R. (2007). Establishing
expressing. The fundamental premise of crisis standards for the assessment of suicide risk among
intervention is that emotional identification and callers to the National Suicide Prevention Lifeline.
Suicide and Life-Threatening Behavior, 37, 353–365.
validation help de-escalate a patient in crisis and Neimeyer, R. A., & Pfeiffer, A. M. (1994). Evaluation of
build therapeutic rapport. suicide intervention effectiveness. Death Studies, 18,
When engaging in assessment/referral, the cli- 131–166.
nician should alternate assessment questions with
content or emotional paraphrases in order to main-
tain rapport throughout the session yet still obtain
the necessary information in order to take more
concrete action, if needed. The clinician’s princi- Crossed Aphasia
ple priority should be the patient’s safety
and security. If possible, the clinician should Patrick Coppens
respond to the patient’s needs, helping to locate Communication Sciences and Disorders, SUNY
resources when available such as additional Plattsburgh, Plattsburgh, NY, USA
services or agencies. If clinically indicated, the
clinician should perform a proper suicidality or
homicidality assessment and consider hospitaliza- Definition
tion if the patient is at high risk for harming
him/herself or others. The clinician should finally Crossed aphasia is an acquired language impair-
predict and prepare, helping the patient to identify ment following a lesion in the right hemisphere in
alternative choices for handling the crisis, even if a right-handed individual.
no immediate solutions are available. The clini-
cian can help the patient plan for future crisis
situations, set additional appointments if appro- Current Knowledge
priate, and develop a concrete plan for follow-up
care (Joiner et al. 2007). The term “crossed aphasia” (CA) was coined by
Despite these clinical tasks, it is important Byrom Bramwell (1899) to indicate an aphasia
much of the time for the clinician not to get caught caused by a cerebral lesion ipsilateral to the dom-
up in trying to fix the patient’s problem, as most inant hand regardless of handedness. Currently,
1016 Cross-Examination

CA only refers to right-handed individuals. obscure these right-hemisphere signs, but these
The frequency of CA among stroke survivors is represent a major difference in symptomatology
rare (1–3%). between CA and LHA.
Although some earlier authors considered CA
to be the consequence of a weaker language
lateralization, it appears that individuals with Cross-References
CA have language as strongly lateralized as
those with left-hemisphere aphasia (LHA), ▶ Aphasia
mainly because both populations show a similar ▶ Handedness
prognosis.
CA can be mirror image or anomalous (Alex-
ander et al. 1989). Mirror-image CA denotes the References and Readings
expected correspondence between symptomatol-
ogy and lesion location within the language-dom- Alexander, M. P., Fischette, M. R., & Fischer, R. S. (1989).
Crossed aphasias can be mirror image or anomalous.
inant hemisphere, whereas anomalous CA
Brain, 112, 953–973.
implies the presence of unexpected language Basso, A., Capitani, E., Laiacona, M., & Zanobio, M. E.
symptoms given the lesion location (e.g., (1985). Crossed aphasia: One or more syndromes?
Wernicke’s aphasia following a frontal lesion Cortex, 21, 25–45.
Bramwell, B. (1899). On “crossed” aphasia. Lancet, 1,
(Basso et al. 1985), a mixed transcortical aphasia
1473–1479.
with preserved naming (Fujii et al. 1997). Close to Coppens, P., Hungerford, S., Yamaguchi, S., & Yamadori,
two thirds of CA cases are mirror image. The CA A. (2002). Crossed aphasia: An analysis of the symp-
language symptomatology is virtually indistin- toms, their frequency, and a comparison with left-hemi-
sphere aphasia symptomatology. Brain and Language,
guishable from LHA, and all aphasia types have
83, 425–463.
been reported in CA. Falchook, A. D., Brandon Burtis, D., Acosta, L. M., Sala-
The cause of CA is essentially unknown, but zar, L., Hedna, V. S., Anna, Y., Khanna, A. Y., &
the influence of left-handedness in the family has Heilman, K. M. (2014). Praxis and writing in a right-
hander with crossed aphasia. Neurocase, 20(3),
long been considered an important causal factor, a
317–327.
hypothesis called familial sinistrality. However, Fujii, T., Yamadori, A., Fukatsu, R., Ogawa, T., & Suzuki,
familial sinistrality is absent in the majority K. (1997). Crossed mixed transcortical aphasia with
(63%) of reported CA cases (Coppens et al. hypernomia. European Neurology, 37, 193–194.
2002). Further, there does not seem to be any
difference in CA symptomatology when compar-
ing patients with and without familial sinistrality,
and the presence of familial sinistrality does not
increase the number of anomalous cases, as could Cross-Examination
be expected if language laterality was weak
(Coppens et al. 2002). Interestingly, oral praxis Moira C. Dux
seems to lateralize with language and limb praxis US Department of Veteran Affairs, Baltimore,
with handedness (Coppens et al. 2002; Falchook MD, USA
et al. 2014).
Individuals with CA also often display typical
right-hemisphere symptoms (e.g., left-side
neglect, visuospatial/visuoconstruction problems, Definition
affective dysprosody, and spatial agraphia) which
indicate that those skills may lateralize indepen- A deposition or actual trial testimony consists
dent of language. The aphasic difficulties may of two parts: the direct examination and the
Cue 1017

cross-examination. Direct examination precedes

the cross-examination and involves testimony Cue
brought forth by the retaining attorney. Cross-
examination occurs immediately after the direct Janet Patterson
examination and is carried out by the opposing Audiology and Speech-Language Pathology
attorney. The main purpose of cross-examination Service, VA Northern California Health Care
is to test the “reliability, accuracy, and credibil- System, Martinez, CA, USA C
ity” of witnesses’ testimony produced during the
direct examination. Questions posed during
cross-examination typically fall into two catego- Synonyms
ries: those intended to expose weaknesses or
errors in the expert witnesses’ data acquisition Discriminative stimulus; Prime; Prompt
or interpretations and those related to expose
biases in the testimony. During cross-
examination, expert witnesses are expected to Definition
give responsive answers. That is, they are to
provide relevant answers, but the answers need A cue is a verbal or nonverbal instruction to
not be those implicitly desired by the opposing induce behavior change (Papathanasiou et al.
attorney. The opposing attorney may use several 2016). Cues are internal or self-generated or exter-
tactics during cross examination including: nal coming from the environment (e.g., an exam-
challenging credibility, establishing doubt, lead- iner, a sight, or a sound). Examples of self-
ing questions, feigned ignorance, the cut-off generated, internal cues are reminders for future
(e.g., testimony of witness terminated to stop action (e.g., remember to walk the dog), mental
the witness from providing further information sequences used in the tip-of-the-tongue state (e.g.,
that could be detrimental to the opposing telling oneself that the name rhymes with sock), or
attorney’s position), intentional ambiguity, teaching/treatment strategies (e.g., using an asso-
implying impropriety, rattling the witness, and ciation strategy for naming, such as reciting the
many others. alphabet to cue the name) (Tompkins et al. 2006).
Examples of external cues are environmental
signs (e.g., walk/do not walk signals), pre-
programmed reminders (e.g., alarm clock), or
Cross-References
teaching/treatment techniques (e.g., semantic-
phonological cueing hierarchy). A cueing hierar-
▶ Direct Examination
chy is a set of cues progressing from weak cues
providing little information about the target
response to strong cues providing much informa-
References and Readings tion (Linebaugh et al. 2005; Wambaugh et al.
2002). Figure 1 shows an example of a cueing
(1975). Federal rules of evidence for United States courts hierarchy used in treatment to assist a person in
and magistrates. St. Paul: West Publishing.
naming a target item. Cues may appear spontane-
Brodsky, S. L. (2004). Coping with cross-examination and
other pathways to effective testimony. Washington, DC: ously as a behavior is unfolding in order to effect
American Psychological Association. immediate change. For example, when one sees
Greiffenstein, M. F., & Cohen, L. (2005). Neuropsychol- the cue of a deer running into the road, one veers
ogy and the law: Principles of productive attorney
away to avoid a collision, or when one is engaged
neuropsychologist relations. In G. Larrabee (Ed.),
Forensic neuropsychology: A scientific approach. in conversation and hears the cue of his or her
New York: Oxford University Press. sentence that does not adequately express the
1018 Cue

Present Cue # 1 Present Cue # 4

Present a picture and say, "Say the name of this," or Say "It starts with "and say the first sound
"What's this" or "Tell me the name of this"
If correct response
If correct response (a) Say "correct" or "right"
(a) Say "correct" or "right" (b) Present Cue #3
(b) Ask for five repetitions
(c) Move to next picture item If correct response
(a) Present Cue #5
If incorrect response
(a) Present Cue #2
Present Cue # 5
Present Cue # 2 Say "The word is "and say the name of the item
Say "It goes with "and give the semantic cue
If correct response
If correct response (a) Say "correct" or "right"
(1) Say "correct" or "right" (b) Present Cue #4
(2) Present Cue #1
If incorrect response
If incorrect response (a) Repeat cue and ask for repetition
(a) Present Cue #3 (b) If unable to repeat item name after three
consecutive presentations of Cue #5
Present Cue # 3 move to next picture item
Say "It sounds like "and give the rhyme cue

If correct response
(a) Say "correct" or "right"
(b) Present Cue #2

If incorrect response
(a) Present Cue #4

Cue, Fig. 1 An example of a cueing hierarchy for oral naming using semantic and phonological cues

intended meaning, one immediately changes the ▶ Semantic Cue

sentence. Cues may also appear as a learned strat- ▶ Semantics
egy and be repeated in a consistent format. For ▶ Verbal Fluency
example, drivers know that when the cue of a
yellow traffic light appears, they should slow the
car in preparation to stop when the red traffic light References and Readings
appears, or in a communication interaction when
another individual offers the cue of a greeting, one Linebaugh, C. W., Shishler, R. J., & Lehner, L. (2005).
Cueing hierarchies and word retrieval: A therapy pro-
should respond in kind.
gram. Aphasiology, 19(1), 77–92.
Papathanasiou, I. & Coppens, P.C. (2016). Aphasia and
related neurogenic communication disorders (2nd ed.).
Burlington: Jones & Bartlett Learning.
Cross-References
Tompkins, C. A., Scharp, V. L., & Marshall, R. S. (2006).
Communicative value of self cues in aphasia: A re-
▶ Cue Dominance evaluation. Aphasiology, 20(7), 684–704.
▶ Cued Recall Wambaugh, J. L., Doyle, P. J., Martinez, A. L., &
Kalinyak-Fliszar, M. (2002). Effects of two lexical
▶ Free Recall
retrieval cueing treatments on action naming in aphasia.
▶ Phonemic Cue Journal of Rehabilitation Research and Development,
▶ Recency Effect 39(4), 455–466.
Cue Dominance 1019

dominance. For example, studies examining

Cue Dominance intrinsic cue dominance demonstrated that mon-
keys have a natural preference for response to
Ronald A. Cohen color over other perceptual dimensions, such as
Department of Clinical and Health Psychology, size and shape (Draper 1965). Experiments with
College of Public Health and Health Professions, human infants demonstrated cue dominance for
University of Florida, Gainesville, FL, USA certain shapes over others based on whether they C
Center for Cognitive Aging and Memory, resembled the shape of a human face (Fantz and
McKnight Brain Institute, University of Florida, Miranda 1975). While certain stimulus features
Gainesville, FL, USA have intrinsic cue dominance across many animal
species, the ability to form complex cues based on
the association of simple cues appears greatest
Synonyms among humans, as is the ability to exhibit reversal
learning in order to shift response from one cue to
Cue salience; Orienting stimulus; Stimulus strength another (Kendler and Ward 1972; Kendler 1971).
In neuropsychological studies and assessment
methods, cues are often used to either facilitate
Definition attention to particular spatial locations, semantic
information, or response demands. Alternatively,
Cue dominance refers to the tendency to perceive cues are used to create interference to test the
or respond to a particular stimulus or class of effects of distraction or the redirection of attention
stimuli over others in the environment. Stimuli away from the primary demands of a task. This is
may either have intrinsic properties that give them a fundamental element of the spatial selective
strength or “dominance” based on physical attri- attention paradigms that involve cueing to spatial
butes (e.g., loudness, color) or may acquire domi- locations (Posner et al. 1980). Furthermore, the
nance (i.e., propensity to elicit a response) as a tendency of the semantic value associated with a
function of associative learning and task demands. word to be dominant over color and to interfere
with attention to and naming of the actual color
that is being presented underlies the Stroop effect.
Current Knowledge Researchers and clinicians studying or assessing
attentional processes need to account for both the
Cue dominance is an important principle derived inherent and acquired cue dominance of stimuli
from behavioral studies of animal conditioning being used in the context of particular tasks.
and learning theories. It provides a theoretical
foundation for the neuroscience of selective atten- Cross-References
tion, linking basic behavioral and learning pro-
cesses with higher-order information processing. ▶ Enhancement
In the context of behavioral conditioning, cues ▶ Selective Attention Models
refer to stimuli that have the capacity to elicit an ▶ Visual Form Discrimination
orienting response, anticipation, subsequent atten-
tion, and response intention and preparation. Cues
lack the inherent biological salience of uncondi- References and Readings
tioned stimuli and do not elicit unconditioned
Pavlovian responses but can become conditioned Draper, W. A. (1965). Cue dominance in oddity discrimi-
stimuli through associative learning. Studies of nations by rhesus monkeys. Journal of Comparative
and Physiological Psychology, 60(1), 140–141.
discrimination learning conducted in the middle
Fantz, R. L., & Miranda, S. B. (1975). Newborn infant
of the twentieth century established many of attention to form of contour. Child Development, 46(1),
the operational characteristics underlying cue 224–228.
1020 Cued Recall

Kendler, T. S. (1971). Continuity theory and cue-dominance. Clinical Uses of Cued Recall Testing
In H. H. Kendler & J. T. Spence (Eds.), Essays in In addition to the use of free recall tests, tests of
neobehaviorism: A memorial volume to Kenneth
W. Spence. East Norwalk: Appleton-Century-Crofts. cued recall may be used in identifying memory
Kendler, H. H., & Ward, J. W. (1972). Reversal learning: impairments in a wide array of disorders including
The effects of conceptual and perceptual training in the mild cognitive impairment and Alzheimer’s dis-
absence of differential observing responses. ease. In some instances, tests of cued recall may
Psychonomic Science, 28(6), 346–348.
Posner, M. I., Snyder, C. R., & Davidson, B. J. (1980). be more accurate than free recall tests in detecting
Attention and the detection of signals. Journal of cognitive changes. For example, Ivanoiu et al.
Experimental Psychology: General, 109(2), 160–174. (2005) found that a cued recall test is more reliable
in testing memory impairment in Alzheimer’s dis-
ease than free recall testing. This has been further
supported by the work of Dierckx et al. (2009)
Cued Recall who found that a verbal cued recall test was the
best predictor of conversion of mild cognitive
Margaret Moult impairment to Alzheimer’s disease. While both
Olin Neuropsychiatry Research Center, Institute tests of memory are impaired in such individuals,
of Living, Hartford, CT, USA cued recall may be a more accurate measure of
cognitive decline. This is because deficits other
than pure memory deficits, such as impaired atten-
Definition tion or depression, may account for a decreased
performance in free recall. Conversely, cued recall
Cued recall is the retrieval of memory with the help tests may be used to more directly measure the
of cues. Such cues are often semantic although they encoding and retrieval that takes place in memory
can also be visual. Cued recall differs from free tasks.
recall in that a cue or word is presented that is
related to the information being remembered
which aids in the process of memory retrieval. Cross-References
Some examples of cued recall are the names of
the categories in which words were originally ▶ California Verbal Learning Test (California
grouped or the presentation of related words. For Verbal Learning Test-II)
instance, in remembering the word feather, the ▶ Cue
word bird may be used as a cued recall. ▶ Free Recall
▶ Hopkins Verbal Learning Test
▶ Memory Impairment
Current Knowledge

Tests of Cued Recall References and Readings

There are many tests of cued recall. One of the
most commonly used tests of cued recall is the Buschke, H., Kuslansky, G., Katz, M., et al. (1999).
California Verbal Learning Test (CVLT) devel- Screening for dementia with the memory impairment
screen. Neurology, 52, 231–238.
oped by Delis et al. This semantic test, like
Carpenter, S. K., Pashler, H., & Vul, E. (2006). What types
many other tests of memory, utilizes both free of learning are enhanced by a cued recall test?
and cued recall. Other tests of cued recall include Psychonomic Bulletin & Review, 13, 826–830.
the Memory Impairment Screen plus (MIS plus) Dierckx, E., Engelborghs, S., Raedt, R., et al. (2009).
Verbal cued recall as a predictor of conversion to
developed by Buschke et al. in 1999 and the
Alzheimer’s disease in mild cognitive impairment.
Visual Association Test (VAT) developed by International Journal of Geriatric Psychiatric, 24,
Lindeboom et al. in 2002. 1094–1100.
Cultural Diversity in Neuropsychology 1021

Ivanoiu, A., Adam, S., Van der Linden, M., Salmon, E., Current Knowledge
Juillerat, A. C., Mulligan, R., et al. (2005). Memory
evaluation with a new cued recall test in patients with
mild cognitive impairment and Alzheimer’s disease. Multicultural competency is a challenging but
Journal of Neurology, 252, 47–55. essential area of focus within the field of neuro-
Lindeboom, J., Schmand, B., Tulern, L., et al. (2002). psychology. Factors supporting an increased need
Visual association test to detect early dementia of the for neuropsychological services to ethnic minori-
Alzheimer type. Journal of Neurology, Neurosurgery &
Psychiatry, 24, 1094–1100. ties include demographic shifts in the US popula- C
Vogel, A., Morentsen, L., Gade, A., & Waldemar, G. tion, ethics of psychology, and construct validity
(2007). The category cued recall tests in very mild requirements for neuropsychological instruments
Alzheimer’s disease: Discriminative validity and cor- (Rivera Mindt et al. 2010). While efforts to pro-
relation with semantic memory functions. European
Journal of Neurology, 14, 102–108. vide competent neuropsychological services to
ethnic minorities are ongoing, these efforts con-
tinue to lag behind the needs of the rapidly chang-
ing ethnic and racial diversity of the US. Readers
Cultural Diversity in are encouraged to review current guidelines,
Neuropsychology including the American Psychological Associa-
tion’s (APA) Ethical Principles (2002) and Multi-
Sarah K. Lageman cultural Guidelines (2002) and the American
Parkinson’s and Movement Disorders Center, Academy of Clinical Neuropsychology’s Practice
Department of Neurology, School Of Medicine, Guidelines for Neuropsychological Assessment
Virginia Commonwealth University, Richmond, and Consultation, which provide some discussion
VA, USA regarding “underserved populations/cultural
issues” (Board of Directors 2007). A call to action
publication (Rivera Mindt et al. 2010) provides
Definition additional discussion of issues and recommenda-
tions for improving neuropsychological services
The term “cultural diversity” generally refers to to ethnic minorities.
the differences in defining cultural features that To date, clinical and research studies have
exist between people (or within a given popula- examined how cultural variables influence perfor-
tion), such as “belief systems and value orienta- mance on neuropsychological measures and pub-
tions that influence customs, norms, practices, lications have provided test norms for specific
and social institutions, including psychological racial and ethnic groups. However, no compre-
processes (language, care taking practices) and hensive norms exist for ethnic minorities and the
organizations (media, educational systems)” use of racial and ethnic norms for neuropsycho-
(retrieved October 16, 2015, from apa.org/pi/ logical measures remains a contentious issue.
oema/resources/policy/multicultural-guidelines. Highlights of the 2008 Diversity Summit and
aspx). With respect to neuropsychology, the term recent literature follow and readers are encour-
encompasses racial and ethnic diversity, and aged to review summary of the summit (Romero
other dimensions of diversity, including lan- et al. 2009) for further details.
guage, sexual orientation, gender, age, disability, Recent studies emphasize that the deconstruc-
class status, education, religion/spiritual orienta- tion of race is critical for improved clinical care of
tion, and other cultural dimensions, among neu- ethnically diverse populations. The construct has
ropsychologists themselves and the populations been identified as a “proxy for more meaningful
they interact with, as well as issues related to the but complex variables” such as acculturation and
influences of race, ethnicity, and other aspects of indicators of quality of education, which account
diversity on neuropsychological evaluations and for significant proportions of racial and ethnic
interventions. differences in neuropsychological test scores
1022 Cultural Diversity in Neuropsychology

(Romero et al. 2009, p. 765). However, increasing the normative sample, (5) to predict future perfor-
emphasis has been placed on the importance of the mance in employment or academic settings, and
clinician knowing when to apply race- and ethnic- (6) for employment selection decisions. In addi-
based norms, as their use can actually reduce tion to these clinical guidelines, emphasis is being
detection of neuropsychological impairment. increasingly placed on correctly using probabilis-
The complexity of this issue was demonstrated tic statistics to predict group membership (i.e.,
in one of the Mayo’s Older African American diagnosis) for individuals. Readers are encour-
Normative Studies in which adjustment of test aged to review recent publications regarding like-
scores for reading level surprisingly reduced lihood ratios, which express the risk associated
detection of cognitive impairment in African with certain test scores (Smith et al. 2008).
Americans. Lucas et al. (2005) suggested this While additional study of the deconstruction of
may have occurred due to restricted range of edu- race is needed, development of ethnic group
cation quality in their cohort, which resulted in norms itself is a challenging and complex task.
reading level being more reflective of individual Test publishers increasingly make efforts to
differences in cognitive ability rather than contex- include important background variables in norma-
tual differences such as educational backgrounds. tive samples. However, the cost of recruiting and
While race may be a very efficient and parsimo- assessing large cohorts is prohibitive for individ-
nious variable for clinicians to use at times, the ual centers and researchers and is often even a
confounding of causes and effects of these vari- challenge for larger test publishing companies.
ables presents significant challenges. While inclusion of demographic variables in
In an effort to initiate the development of prac- research articles is an important piece to further
tical guidelines regarding the use of demographic develop this area, federal and foundation-funded
corrections, Diversity Summit participants devel- grants may be necessary to support multicenter
oped clinical criteria. As detailed in the Diversity partnerships, ideally suited to study large, diverse
Summit proceedings, demographic corrections cohorts.
are useful to identify and characterize acquired Despite the development of racially and ethni-
neurocognitive impairments in adults who (1) are cally diverse norms, including the widely used
natives of the country of assessment, (2) devel- Heaton norms for African American and Cauca-
oped normally, (3) received mainstream educa- sian adults, the almost endless variety possible
tion, and (4) speak English as their first language with regard to individuals’ language, culture,
(for the US norms). Demographic corrections are and education backgrounds limits the application
sometimes useful to identify and characterize of demographically corrected norms for every
acquired neurocognitive impairments in (1) teen- possible clinical situation (Heaton et al. 2004).
agers or young adults who have not completed Local norms may be helpful for clinicians work-
their education, (2) adults who may have had a ing with population groups with less common
mild developmental disorder, or (3) anyone with a background variables; however, integration of
linguistic, cultural, or educational background not test scores with a person’s individual context is
well represented in the normative subject sample. ultimately critical for formulation of an accurate
Demographic corrections are not recommended diagnosis. In clinical practice, other issues regard-
when the clinician is asked (1) to characterize ing assessment of ethnic, linguistic, and cultural
“absolute” levels of functioning, (2) to identify minorities are also present. The use of translated
or characterize possible acquired impairment in tests, interpreters, and bilingual psychometrists
capital punishment cases or when determining are all current methods for evaluating non-
qualifications for special services, or (3) in cases English-speaking patients. However, the shear
of possible acquired impairment in individuals complexity of language fluency is important to
who have developmental disability, (4) to charac- consider. Language fluency of an individual can
terize acquired cognitive impairment in individ- vary widely with regard to (1) age of acquisition,
uals who have major background differences from (2) proficiency, (3) manner of learning, (4)
Cultural Diversity in Neuropsychology 1023

amount of language exposure, (5) predominant speaking patients. Access to care and other factors
mode of bilingual interaction, and (6) language affecting ethnic minority patient outcomes have
structure variables (i.e., alphabetic versus logo- increasingly been examined in the field of neuro-
graphic languages and phonemic versus non- psychology. Readers are encouraged to review
phonemic status). Currently, the use of translated two issues of the Journal of Head Trauma Reha-
tests and official interpreters or bilingual bilitation, dedicated to US and international cul-
psychometrists are preferred over using family tural issues in the rehabilitation of survivors of C
members as interpreters and site translation, traumatic head injury (Arango-Lasprilla and
which refers to the practice of quickly translating Niemeier 2007; Mayer 2007). Articles in these
a test with no standardization procedures. Readers issues highlight complex relationships between
are encouraged to review the National Academy functional outcomes, disability severity, return to
of Neuropsychology (NAN) Position Paper that work, and utilization of professional psychologi-
discusses professional considerations for improv- cal services in ethnic minority groups as well as
ing neuropsychological evaluation of Hispanics models of care used in different health care sys-
(Judd et al. 2009). tems and international perspectives on research
In keeping with the demographic changes in and development in the field of traumatic brain
the USA, training programs and national organi- injury rehabilitation.
zations are brainstorming ways to promote The study of health disparities among ethnic
recruitment and retention of students with diverse minority populations is a complex but critical field
racial and ethnic backgrounds in the study of of research. Multiple dimensions of disparity
neuropsychology. Emphasis has been placed on exist, including many of the variables discussed
student exposure to neuropsychology earlier in regarding the deconstruction of race such as
academic careers, mentoring with minority and ethnicity, education, income, occupation, and
nonminority faculty who are sensitive to diversity geography. Continuous study of these variables
issues and financial support of minority students. is critical to improve clinical care for ethnic
Active recruitment and retention of ethnic minor- minorities.
ity faculty has also been recommended, given
assertion that low representation of ethnic minor-
ity individuals in the faculty, student bodies, and
communities of universities significantly contrib- Cross-References
utes to the trend for minorities to not pursue
advanced neuropsychological training (Rivera ▶ AACN Practice Guidelines
Mindt et al. 2010). The study of cultural diversity ▶ Clinical Practice Guidelines
itself has gained support and many licensing ▶ Cultural Sensitivity
bureaus require documentation of diversity train- ▶ Culture Fair Test
ing in graduate school for licensure. Numerous ▶ Ethics in the Practice of Clinical Neuropsychol-
organizations, including the APA Division 40, ogy: Foundations and New Horizons
AACN, the International Neuropsychological
Society (INS), and NAN, promote awareness of
diversity issues and foster collaborations among References and Readings
clinicians and researchers interested in diversity
American Academy of Clinical Neuropsychology (AACN).
issues. (2015). Multicultural references. Retrieved 16 Oct 2015,
Diversity in neuropsychology has become of from the AACN website: https://www.theaacn.org/
increasing interest and importance; however, userdocuments/aacn_multicultural_references.pdf.
measures to improve diagnostic assessment of American Psychological Association. (2002). Guidelines on
multicultural education, training, research, practice,
ethnic minorities may not fully address the issue
and organizational change for psychologists. Retrieved
of improving clinical care of ethnic minorities, 16 Oct 2015, from apa.org/pi/oema/resources/policy/
given limited health care access of non-English- multicultural-guidelines.aspx.
1024 Cultural Sensitivity

American Psychological Association’s Division 45, Soci- Romero, H. R., Lageman, S. K., Kamath, V., Irani, F., Sim,
ety for the Psychological Study of Culture, Ethnicity A., Suarez, P., . . . the Summit Participants. (2009).
and Race (apa.org/about/division/div45.aspx). Challenges in the neuropsychological assessment of
American Psychological Association’s Ethical Principles ethnic minorities: Summit proceedings. The Clinical
of Psychologists and Code of Conduct with the 2010 Neuropsychologist, 23, 761–779.
Amendments (apa.org/ethics/code/index.aspx). Smith, G. E., Ivnik, R. J., & Lucas, J. (2008). Assessment
American Psychological Association’s Ethnic Minority techniques: Tests, test batteries, norms, and methodo-
Affairs Office (apa.org/pi/oema/about/index.aspx). logical approaches. In J. E. Morgan & J. H. Ricker
American Psychological Association’s Ethnic Minority (Eds.), Textbook of clinical neuropsychology (pp.
Affairs Office Multicultural Training Resources (apa. 38–57). New York: Taylor & Francis.
org/pi/oema/resources/multicultural-training.aspx). Uzzell, B. P., Pontón, M., & Ardila, A. (Eds.). (2007).
American Psychological Association’s Minority Fellow- International handbook of cross-cultural neuropsy-
ship Program (apa.org/pi/mfp/index.aspx). chology. Mahwah: Lawrence Erlbaum Associates.
Arango-Lasprilla, J. C., & Niemeier, J. (Eds.). (2007).
Cultural issues related to TBI: Recent research and
new frontiers. Journal of Head Trauma Rehabilitation,
22(2), 73–139.
Board of Directors. (2007). American Academy of clinical
neuropsychology (AACN) practice guidelines for neu- Cultural Sensitivity
ropsychological assessment and consultation. The Clin-
ical Neuropsychologist, 21(2), 209–231. Retrieved 16 Christian Schutte1,2 and Bradley N. Axelrod2
Oct 2015, from the AACN website: http://www. 1
tandfonline.com/doi/pdf/10.1080/13825580601025932. Henry Ford Allegiance, Jackson, MI, USA
2
Ferraro, F. R. (Ed.). (2002). Minority and cross-cultural John D. Dingell VA Medical Center, Psychology
aspects of neuropsychological assessment. Lisse: Section (11MHPS), Detroit, MI, USA
Swets & Zeitlinger.
Fletcher-Janzen, E., Strickland, T. L., & Reynolds, C. R.
(Eds.). (2000). Handbook of cross-cultural neuropsy-
chology. New York: Kluwer/Plenum Publishers. Synonyms
Heaton, R. K., Miller, S. W., Taylor, M. J., & Grant, I.
(2004). Revised comprehensive norms for an expanded Multicultural
Halstead-Reitan battery: Demographically adjusted
neuropsychological norms for African American and
Caucasian adults. Lutz: Psychological Assessment
Resources. Definition
Mayer, N. H. (Ed.) (2007). International Programs and Per-
spectives on Traumatic Brain Injury Rehabilitation. Jour-
nal of Head Trauma Rehabilitation, 22(4), 209–256. There are a couple of pertinent definitions, or
Judd, T., Capetillo, D., Carrión-Baralt, J., Mármol, L. M., applications, of cultural sensitivity to the field of
San Miguel-Montes, L., Navarrete M. G., . . . the NAN neuropsychology. First is the position of the
Policy and Planning Committee. (2009). Professional American Psychological Association (APA),
considerations for improving the neuropsychological
evaluation of Hispanics: A national academy of neuro- which is reflected in the 2002 APA Ethical Prin-
psychology education paper. Archives of Clinical Neu- ciples of Psychologists and Code of Conduct. The
ropsychology, 24(2), 127–135. ethical principles state “Psychologists are aware
Lucas, J. A., Ivnik, R. J., Willis, F. B., Ferman, T. J., Smith, of and respect cultural, individual, and role differ-
G. E., Parfitt, F. C., . . . Graff-Radford, N. R. (2005).
Mayo’s older African American normative studies: ences, including those based on age, gender, gen-
Normative data for commonly used clinical neuropsy- der identity, race, ethnicity, culture, national
chological measures. The Clinical Neuropsychologist, origin, religion, sexual orientation, disability, lan-
19(2), 162–183. guage, and socioeconomic status and consider
Nell, V. (1999). Cross-cultural neuropsychological assess-
ment: Theory and practice. Mahwah: Lawrence these factors when working with members of
Erlbaum Associates. such groups. Psychologists try to eliminate the
Rivera Mindt, M., Byrd, D., Saez, P., & Manly, J. (2010). effect on their work of biases based on those
Increasing culturally competent neuropsychological ser- factors, and they do not knowingly participate in
vices for ethnic minority populations: A call to action.
The Clinical Neuropsychologist, 24(3), 429–453. https:// or condone activities of others based upon such
doi.org/10.1080/13854040903058960. prejudices.” Cultural sensitivity is also reflected
Culture Fair Test 1025

in the 2002 APA Guidelines on multicultural edu- See Also

cation, training, research, practice, and organiza-
tional change for psychologists. The APA defines ▶ Normative Data
“multicultural” specifically as referring to interac-
tions with “individuals from minority ethnic and
racial groups in the United States and the domi- References
nant European-American culture.” This document C
states that all individuals are in a social, political, American Psychological Association. (2002a). Ethical
principles of psychologists and code of conduct.
and economic context and that it is increasingly
American Psychological Association. (2002b). Guidelines
important for psychologists to be aware of the on multicultural education, training, research, practice
specific needs of individuals based on their eth- and organizational change for psychologists.
nic/racial heritage and social group identity. Heaton, R. K., Walden Miller, S., Taylor, M. J., & Grant, I.
(2004). Revised comprehensive norms for an expanded
Guideline number four in this document regarding
Halstead-Reitan battery: Demographically adjusted
research directs psychologists to “recognize the neuropsychological norms for African American and
importance of conducting culture-centered and Caucasian adults. Lutz: Psychological Assessment
ethical psychological research among persons Resources Inc.
Nagra, A., Skeel, R. L., & Sbrage, T. P. (2007). A pilot
from ethnic, linguistic and racial minority
investigation on the effects of stress on neuropsycho-
backgrounds.” logical performance in Asian-Indians in the United
A second area of cultural sensitivity that States. Cultural Diversity & Ethnic Minority Issues,
directly relates to neuropsychology is the impact 13, 54–63.
Smith, G. E., Ivnik, R. J., & Jucan, J. (2008). Assessment
of culture on testing and on normative data. It is
techniques: Tests, test batteries, norms and methodo-
important that an individual examinee’s test per- logical approaches. In J. E. Morgan & J. H. Ricker
formance be related to individuals of similar back- (Eds.), Textbook of clinical neuropsychology
grounds, for example, the normative group that an (pp. 38–57). New York: Taylor Francis.
elderly, well-educated African American man
should closely match his background. Without
close matching of cultural, demographic, and edu-
cational background, unacceptable problems with Culture Fair Test
misclassification of normal test results as abnor-
mal can be made and thusly misdiagnose the Glen E. Getz
patient. There is evidence that examiners of a Department of Psychiatry, Allegheny General
different culture than the examinee can illicit Hospital, Pittsburgh, PA, USA
some anxiety, which may have a deleterious effect Neuropsychology Specialty Care, LLC,
on test scores on more demanding cognitive tasks Pittsburgh, PA, USA
(Nagra et al. 2007). Additionally, cultural back-
ground, demographics, and educational history
can have a sizeable impact on normative data. Synonyms
Smith et al. (2008) discuss the development of
norms specifically for older adults on commonly Culturally reduced test; Culture free test
used neuropsychological tests. They subsequently
developed more specific norms for older African
Americans, as it was found that culture had a Definition
significant impact on normative data. Heaton
et al. (2004) have published norms that take into Culture fair test is a test that is equally fair to all
account age, education, and cultural background. cultural groups. Fairness is related to a lack of bias
This area of cultural sensitivity plays an important in the interpretation or use of a test to classify or
role in neuropsychology in terms of diagnosis and diagnose. In a culture fair test, the validity of the
test evaluation. interpretation is similar across different cultural
1026 Cuneus

groups. It is unlikely that any test can entirely brain area. The cuneus is a wedge-shaped cortical
eliminate the influence of learning and cultural area located in the medial occipital gyri, superior
experience, given that the test content, language, to the calcarine fissure and posterior to the
directions, and validity criteria are culturally parietal-occipital fissure. The cuneus is part of
bound. However, avoiding culturally loaded the occipital lobe, corresponding to Brodmann
items, items that are found to be unfair to certain area 17. Pyramidal cells in the cuneus (striate
groups of people, increases the likelihood of it cortex) project to extrastriate cortices
being a culturally fair test. Culturally loaded (Brodmann areas 18 and 19). The cuneus consists
items, such as those that utilize pictures or general of both striatal and extrastriatal visual cortex
information that are differentially prevalent for consisting of five layers. The striatal areas are
certain cultures, decrease the likelihood of a cul- largely posterior and are idiotypic homomodal
turally fair test. (Mesulam’s classification), while the extrastriatal
areas contain heterotypic cell types that respond to
more complex visual information. The cuneus
Cross-References
receives input from the contralateral superior ret-
ina corresponding to the lower visual field. From
▶ Cultural Sensitivity
the extrastriatal areas of the cuneus, information is
▶ Raven’s Progressive Matrices
processed through both ventral and dorsal path-
ways. The dorsal pathway is particularly impor-
tant for higher spatial analysis and visual
References and Readings
integration (Fig. 1).
Jensen, A. R. (1974). How biased are culture-loaded tests?
Genetic Psychology Monographs, 90, 185–244.
Scarr, S. (1994). Culture fair and culture free test. In R. J.
Sternberg (Ed.), Encyclopedia of human intelligence. Function
New York: Macmillan.

The cuneus plays as essential role in primary

visual processing. The striatal regions that contain
Cuneus primary visual processing areas contain neurons
with small receptive fields that are sensitive to
Ronald A. Cohen very basic visual frequency information related
Department of Clinical and Health Psychology, to position, local orientation, spatial frequency,
College of Public Health and Health Professions, and color (Beason-Held et al. 1998; Jeannerod
University of Florida, Gainesville, FL, USA 2004; Ulbert et al. 2001; Ungerleider and Pribram
Center for Cognitive Aging and Memory, 1977). However, more anterior to the primary
McKnight Brain Institute, University of Florida, visual areas are neurons that respond to more
Gainesville, FL, USA complex information contained in the visual infor-
mation processed by the primary receptors
(Ungerleider and Haxby 1994). Accordingly, the
Synonyms cuneus plays a role in both primary and secondary
visual processing. Extrastriatal areas of the cuneus
Brodmann area 17 are known to respond to reward, anticipatory,
attention, and working memory manipulations,
and there is even evidence that posterior striatal
Structure areas respond to attentional signals, providing
evidence that this cortical plays some role in
The term cuneus comes from the Latin term for higher cognitive function involving basic visual
wedge, which reflects the shape of this occipital information.
Cuneus 1027

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Cingulate gyrus sul
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Cuneus, Fig. 1 Sagittal illustration showing the cuneus in the posterior cortex

Illness Another study found that compulsive gamblers

had increased activity in dorsal visual processing
Damage to the cuneus would typically occur pathways, including the cuneus when compared
among patients experiencing focal brain lesions. with controls (Crockford et al. 2005). Whether
Most often such lesions occur secondary to cere- such findings reflect a specific role of the cuneus
bral infarction (stroke) typically involving the in these psychiatric disorders versus more inci-
posterior cerebral circulation, though neurosur- dental findings needs to be determined in future
gery to remove neoplasm may result in focal dam- investigations.
age to the cuneus as well. Some atypical
neurodegenerative diseases are also known to
cause tissue loss in this occipital area. The effects Cross-References
of focal damage to the cuneus are known primar-
ily from experimental ablation in primate studies ▶ Spatial Frequency Analysis
and to some extent from single-case studies of
stroke. Posterior cuneus lesions tend to disrupt
primary visual perception, particularly response References and Readings
to stimuli occurring in the lower visual fields.
Damage to more anterior areas of the cuneus Beason-Held, L. L., Purpura, K. P., Krasuski, J. S., Maisog,
J. M., Daly, E. M., Mangot, D. J., et al. (1998). Cortical
also affects visual functions (e.g., movement per-
regions involved in visual texture perception: A fMRI
ception), though often for higher level operations study. Brain Research Cognitive Brain Research, 7(2),
involved in object perception and spatial analysis, 111–118.
including attention (De Weerd et al. 1999). Crockford, D. N., Goodyear, B., Edwards, J., Quickfall, J.,
& el -Guebaly, N. (2005). Cue-induced brain activity in
Interestingly, there is also evidence that cuneus pathological gamblers. Biological Psychiatry, 58(10),
volume is related to other behavioral processes 787–795.
not obviously tied in a direct way to visual pro- De Weerd, P., Peralta III, M. R., Desimone, R., &
cessing. For example, one recent study found Ungerleider, L. G. (1999). Loss of attentional stimulus
selection after extrastriate cortical lesions in macaques.
greater cuneus volume to be associated with
Nature Neuroscience, 2(8), 753–758.
greater inhibitory control among patients with Haldane, M., Cunningham, G., Androutsos, C., &
bipolar affective disorder (Haldane et al. 2008). Frangou, S. (2008). Structural brain correlates of
1028 Cushing’s Syndrome

response inhibition in Bipolar Disorder I. Journal of as well as cognitive impairment – are highly prev-
Psychopharmacology, 22(2), 138–143. alent in CS patients (Bourdeau et al. 2005).
Jeannerod, M. (2004). Visual and action cues contribute to
the self-other distinction. Nature Neuroscience, 7(5), The principal aim of this chapter is to present
422–423. psychiatric and cognitive data on adult patients
Ulbert, I., Karmos, G., Heit, G., & Halgren, E. (2001). with CS. The recognition of psychoneurological
Early discrimination of coherent versus incoherent abnormalities associated with hypercortisolism is
motion by multiunit and synaptic activity in human
putative MT +. Human Brain Mapping, 13(4), of clinical importance in the management of
226–238. patients affected by CS.
Ungerleider, L. G., & Haxby, J. V. (1994). “What” and
“where” in the human brain. Current Opinion in Neu-
robiology, 4(2), 157–165.
Ungerleider, L. G., & Pribram, K. H. (1977). Aetiology
Inferotemporal versus combined pulvinar-prestriate
lesions in the rhesus monkey: Effects on color, object Exogenous CS refers to iatrogenic CS resulting
and pattern discrimination. Neuropsychologia, 15(4-5), from chronic GC therapy. GC, which have potent
481–498.
anti-inflammatory and immunologic actions, are
widely used for the treatment of various diseases
such as inflammatory bowel disease, asthma,
rheumatoid arthritis, and organ transplantation.
Cushing’s Syndrome Thus, exogenous CS is the most common form
of CS. Endogenous CS may be caused by
Isabelle Bourdeau1 and Hélène Forget2 dysregulation at various levels of the hypo-
1
Division of Endocrinology, Department of thalamic–pituitary–adrenal axis (HPA), resulting
Medicine, Research Centre, Centre hospitalier de in cortisol overproduction. The regulation of cor-
l’université de Montréal (CHUM), Montreal, QC, tisol synthesis and secretion is mediated by the
Canada hypothalamus, pituitary, and adrenal glands. Cor-
2
Département de psychoéducation et de ticotropin (ACTH) is synthesized and secreted by
psychologie, Université du Québec en Outaouais, corticotrophs of the pituitary, which are mainly
Gatineau, QC, Canada regulated by two hypothalamic hormones,
corticotropin-releasing hormone (CRH) and argi-
nine vasopressin. Pituitary ACTH is secreted in
Short Description or Definition the peripheral circulation and reaches cells in the
cortex of the adrenal gland where cortisol biosyn-
Endogenous Cushing’s syndrome (CS) is a rare thesis is initiated. Cortisol itself exerts negative
disorder occurring in about 0.2–5.0 individuals feedback control on ACTH and CRH secretion,
per million population per year and a prevalence maintaining a normal secretion rate in case of
of 39–79 per million in various populations HPA activation, in stress, for example (Fig. 1).
(Lacroix et al. 2015). CS comprises symptoms ACTH is released physiologically in a series of
and signs resulting from chronic supra- secretory episodes, followed by an equal number
physiological exposure to glucocorticoids (GC). of cortisol bursts in plasma. Thus, plasma cortisol
The classical clinical features of CS are centripetal levels are at their maximum in the early morning
obesity with abnormal fat distribution, mainly hours around awakening, gradually decline
affecting the face, neck, trunk, and abdomen and throughout the morning, and reach nadir values
sparing the extremities. Other findings are facial late in the evening. Variations in ACTH and cor-
plethora, easy bruisability, purple abdominal striae, tisol values constitute the normal circadian
hirsutism, musc