Assessment Issues in Child Neuropsychology
Assessment Issues in Child Neuropsychology
Assessment Issues in Child Neuropsychology
Child Neuropsychology
Critical Issues in Neuropsychology
Series Editors:
Cecil R. Reynolds Antonio E. Puente
Texas A&M University University of North Carolina, Wilmington
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Assessment Issues in
Child Neuropsychology
Edited by
Michael G. Tramontana
Bradley Hospital
East Providence, Rhode Island
and Brown University
Providence, Rhode Island
and
Stephen R. Hooper
Clinical Center for the Study of Development and Learning
University of North Carolina School of Medicine
Chapel Hill, North Carolina
DNLM/DLC 88-22399
for Library of Congress CIP
ISBN 978-1-4757-9303-1 ISBN 978-1-4757-9301-7 (eBook)
DOI 10.1007/978-1-4757-9301-7
To my family
S.R.H.
Contributors
vii
viii CONTRIBUTORS
ix
x FOREWORD
framework has been attempted for individual topics during the last twen-
ty years and as integrated overviews only in recent years.
I think it is important to remember and acknowledge, as well as to
integrate existing knowledge into deve-Iopmental neuropsychology rather
than treat this field as terra nova. This book is a first criticall!Ppraisal of
the clinical application of child neuropsychology focusing on assess-
ment issues. It is to the credit of the editors and authors that they present
assessment issues not in isolation, but in the context of basic knowledge
about developmental neuropsychology, its history, and its neighbor disci-
plines. The book is not restricted to the critical evaluation of traditional
assessment methods, but includes a coverage of basic neurodevelopmen-
tal considerations, a comparison with pediatric, radiologic and elec-
trodiagnostic sources of information, different models of neuro-
psychological inference, and the implications of assessment for treatment.
It then moves on to the major topics of assessment of attention, memory,
functional laterality, language, and to more specific areas such as infancy,
early childhood, and learning disabilities. The successful integration of
these diverse areas is a major accomplishment of this book.
One recurrent problem is, of course, the practice of drawing on as-
sessment techniques developed for the adult patient, and extending these
methods downward. Within certain age limits and for some areas of func-
tion, this may be satisfactory. However, most techniques "bottom out" at
age 5 or 6, Le., at an age before the child becomes aquainted with the test-
taking attitude required in school. The preschool child has not yet ac-
quired these attitudes, and does not deliver a consistent performance.
More serious yet is the problem of developmental changes. To expect
the same tests to measure the changing component skills in the young
child which gradually develop into complex adult performance is haz-
ardous and disregards the accumulated knowledge of child development.
Hence, new and age-appropriate measuring instruments need to be devel-
oped and linked to neuropsychological theory. Most of the authors in this
book consider these problems carefully for their area of assessment and
suggest ways in which existing methods can be used in a neuro-
psychological framework; others find areas which are not covered suffi-
ciently and recommend a new design and a drastic re-development of
assessment methodology.
Finally, the limited behavioral repertoire of the infant, toddler, or
young child, allows fewer and fewer standardized psychological measure-
ments compared to what can be used with the adolescent and adult.
Observations of "baby holds rattle" or responses to light, sound,and touch
stimuli take the place of tests. Yet, observing the richness of the Brazelton
examination in newborns gives us an inkling of what is to come as the
child grows up. As Aylward describes in this book, the expansion of this
FOREWORD xi
Otfried Spreen
Victoria, B. C., Canada
Preface
xiii
xiv PREFACE
Michael G. Tramontana
Stephen R. Hooper
Contents
Part I: INTRODUCTION
Chapter 1
Child Neuropsychological Assessment:
Overview of Current Status .................................... 3
Michael G. Tramontana and Stephen R. Hooper
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
Historical Trends in Assessment ............................... 5
Current Approaches in Child Neuropsychological Assessment ... . 9
Fixed-Battery Approaches ................................... 9
Other General Approaches. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16
Special-Purpose Measures ................................... 20
Applications ................................................. 21
Neurological Disorders ...................................... 21
Systemic Illness ............................................ 23
Psychiatric Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
Learning Disabilities ........................................ 26
Rehabilitation and Assessing Recovery of Function. . . . . . . . . . . . 27
Conceptual and Practical Issues ..................... . . . . . . . . . . . 28
Summary.................................................... 32
References ................................................... 32
Chapter 2
Neuropsychology of the Developing Brain: Implications for
Neuropsychological Assessment ............................... 41
Anthony H. Risser and Dorothy Edgell
Introduction .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41
xvii
xviii CONTENTS
Chapter 3
The Role of Neuropsychological Assessment in Relation to Other
Types of Assessment with Children ............................ 67
Erin D. Bigler
Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67
Pediatric Neurological Exam (PNE) ............................. 68
Basic Components .......................................... 68
The Nature of Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70
Mental Status Characteristics of Neurologically Impaired
Children ............................................... 74
Relationship between Pediatric Neurological Exam and
Neuropsychological Assessment ......................... 75
Neuroradiological Tests ....................................... 75
Electrodiagnostic Tests ........................................ 80
Relationship between Electrodiagnostic Findings and
Neuropsychological Assessment ......................... 82
Psychological Assessment........................... .......... 84
Intellectual Assessment versus Neuropsychological Assessment
with Children: What's the Difference? .................... 86
Conclusions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87
References ................................................... 88
Chapter 4
Neuropsychological Diagnosis with Children: Actuarial and
Clinical Models . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
W. Grant Willis
Diagnostic Models ............................................ 94
Data-Diagnosis Contingency. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
Consideration of Data ....................................... 95
Relative Importance of Data ................................. 96
Actuarial Models ............................................. 97
Methods ................................................... 97
CONTENTS xix
Chapter 5
From Assessment to Treatment: Linkage to Interventions with
Children ..................................................... 113
G. Reid Lyon, Louisa Moats, and Jane M. Flynn
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 113
Neuropsychological Assessment: Purposes and Measurement
Characteristics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 115
Relating Assessment to Treatment: Models and Studies .......... 119
Standardized Assessment Batteries: Implications for Treatment. .. 119
The Halstead-Reitan: Linkages to Treatment ............ '" . . .. 119
The Luria-Nebraska: Linkages to Treatment ................... 122
The K-ABC: Linkages to Treatment . . . . . . . . . . . . . . . . . . . . . . . . . .. 122
Selected Assessment Batteries: Linkages to Treatment ........... 123
Empirical Subtype Intervention Studies: The Lyon Research
Program. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 125
Clinical Subtype Intervention Studies: The Bakker Research
Program. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 131
Direct Assessment Intervention Studies: The Flynn Research
Program. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 132
Some Final Thoughts, Conclusions, and Directions .............. 135
Professional Preparation and Experience. . . . . . . . . . . . . . . . . . . . .. 135
Developmental Issues in Assessment ......................... 136
The Need for Dynamic Assessment. . . . . . . . . . . . . . . . . . . . . .. . . .. 137
The Need for Continued Classification Research. . . . . . . . . . . . . .. 138
References ................................................... 139
Chapter 6
Attention .................................................... 145
Russell A. Barkley
Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 145
xx CONTENTS
Chapter 7
Clinical Assessment of Memory in Children: A Developmental
Framework for Practice. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 177
Thomas A. Boyd
Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 177
Current Status of Memory Assessment with Children ............ 179
Models of Memory Development in Childhood ... . . . . . . . . . . . . . .. 185
Information-Processing Models .............................. 186
Interactionist Models of Memory . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 188
Suggestions for a Children's Memory Battery: General Format .... 195
Suggestions for a Children's Memory Battery: Types of Tasks. . . .. 196
Clinical Relevance of the Models. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 199
Conclusions .................................................. 200
References ................................................... 201
Chapter 8
Assessing Functional Laterality ................................ 205
Jeffrey W. Gray and Raymond S. Dean
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 205
Methods of Laterality Assessment .............................. 206
Perceptual Asymmetry Techniques ........................... 207
Electrophysiological Measures ............................... 210
Lateral Preference Measures ................................. 211
Unimanual Performance Measures ........................... 214
Applications with Learning-Disabled/Language-Impaired
Children .............................................. 215
Clinical Implications .......................................... 218
References ................................................... 219
CONTENTS xxi
Chapter 9
Infant and Early Childhood Assessment ........................ 225
Glen P. Aylward
The Status of Neuropsychological Assessment in Infancy and
Early Childhood ........................................ 225
Conceptual Issues in Early Neuropsychological Assessment ...... 227
Differences in Assessing School-Age versus Younger
Children ............................................... 227
Consistency of Dysfunction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 229
Classification of Early Neuropsychological Findings ........... 231
Assessment Instruments ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 234
Newborn/Neonatal. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 235
Infancy .................................................... 235
Early Childhood ............................................ 235
Useful Findings ............................................ 239
Directions .................................................... 239
Appendix .................................................... 245
References ................................................... 246
Chapter 10
Questions of Developmental Neurolinguistic Assessment. . . . . . . .. 249
Michael A. Crary, Kyjta K. S. Voeller, and Nancy J. Haak
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 249
Basics of Language Development ............................... 250
Prelinguistic Communication ................................ 251
Lexical Expansion Stage. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 252
Grammatical Expansion Stage. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 253
A Comment on Styles of Language Processing. . . . . . . . . . . . . . . .. 254
Relation of Neurological Maturation to Acquisition of Language
Skills ................................................. 254
Neuroanatomic Maturation .................................. 254
Hemispheric Functions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 256
Language Assessment at Present-What's Covered,
What's Not? ........................................... 261
Prelinguistic Assessment (0 to 12+ Months) .................. 262
Lexical Expansion Assessment (12 to 24+ Months) ............ 263
Grammatical Expansion Assessment (2 to 4+ Years) ........... 264
Summary of Present Assessment Capabilities ................. 269
Guidelines and Questions Regarding Developmental
Neurolinguistic Assessment ........ . . . . . . . . . . . . . . . . . . . .. 269
xxii CONTENTS
Chapter 11
Learning Disabilities Subtypes: Perspectives and Methodological
Issues in Clinical Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 281
George W. Hynd, Robert T. Connor, and Naomi Nieves
Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 281
Early Conceptualizations of Learning Disabilities ................ 282
Clinical Case Reports and Observations . . . . . . . . . . . . . . . . . . . . . .. 282
What's in a Name? .......................................... 283
Defining Learning Disabilities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 284
The Public Forum and PL 94-142 ............................ 284
Acknowledging the Neurological Etiology. . . . . . . . . . . . . . . . . . . .. 284
Multifactor Research .......................................... 285
Perspectives on the Single Factor Research ................... 285
Early Subtyping Studies ..................................... 286
Some Directions in Subtyping Research: Multivariate
Classification Approaches ............................... 287
Neurolinguistic Subtyping . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 300
Neuroanatomical-Linguistic Perspectives. . . . . . . . . . . . . . . . . . . . . .. 301
The Wernicke-Geschwind Model. .. . . .. .. . . . . . . . . . . . . .. . . . .. 301
Clinical Implications for Process-Based Assessment ........... 304
Conceptual Framework for Clinical Evaluation .................. 305
Conclusions .................................................. 307
References ................................................... 308
Chapter 12
The Prediction of Learning Disabilities in the Preschool Child: A
Neuropsychological Perspective. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 313
Stephen R. Hooper
Introduction.. . . .. . . .. . . .. . . .. . . .. . . .. . . . . . . . . . . .. . . .. . . . . . . .. 313
The Importance of Early Prediction of Learning Disabilities ...... 314
Extent of the Problem ....................................... 315
Minimizing Educational Failure. . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 316
Minimizing Social-Emotional Difficulties .................... 316
Effects of Environmental Influences .......................... 317
Summary .................................................. 318
The Prediction of Learning Disabilities: Current Status. . . . . . . . . .. 318
Recent Reviews of the Literature ............................. 318
Exemplary Studies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 321
CONTENTS xxiii
Chapter 13
Electrophysiological Assessment in Learning Disabilities. . . . . . . .. 337
Grant 1. Morris, Joel Levy, and Francis J. Pirozzolo
Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 337
Anatomical Correlates of Learning Disorders .................. 338
Neuroimaging Methods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 340
Electrophysiological Techniques and Findings .................. 343
Electroencephalography ..................................... 343
Evoked Potentials. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 352
Conclusions .................................................. 362
References ................................................... 363
Chapter 14
Problems and Prospects in Child Neuropsychological
Assessment .................................................. 369
Michael G. Tramontana
Introduction
1
Child Neuropsychological
Assessment
Overview of Current Status
MICHAEL G. TRAMONTANA and STEPHEN R. HOOPER
INTRODUCTION
3
4 MICHAEL G. TRAMONTANA and STEPHEN R. HOOPER
important. The first had to do with the passage of the Education for All
Handicapped Children Act (Public Law 94-142, Federal Register, 1976)
and, among other things, its calling national attention to the fact that a
significant percentage of children suffer from learning disabilities and
other developmental handicaps presumed to have a neurodevelopmental
etiology. This, in turn, served to accentuate an important role for neuro-
psychological assessment both in the identification of specific neuro-
developmental disorders and in helping to devise appropriate educa-
tional plans. Another factor cited by Hynd et 01. concerns the increased
prevalence of children surviving neurological trauma. Advances in medi-
cal care have brought about a dramatic increase in the survival of children
whose conditions (or their treatment) have a potentially adverse impact
on the developing brain (e.g., very low birthweight associated with pre-
maturity, iatrogenic effects of childhood cancer treatment). Thus, whereas
mortality has decreased, there has been a relative increase in morbidity.
This has created a greater need for the careful assessment of the extent,
pattern, and developmental significance of possible neuropsychological
sequelae in these survivors of serious childhood illness.
Along with this increased demand for child neuropsychological as-
sessment has come the growing realization of important differences in
brain-behavior relationships between children and adults. Not only do
children differ in the types of brain insult commonly experienced, they
also differ with respect to the specificity of behavioral effects manifested,
the pattern and course of (re)acquisition of function after injury, the modi-
fying effects of ongoing developmental change, and the extent to which
deficits sometimes can be delayed or "silent" until later developmental
periods (Almli & Finger, 1984; Boll & Barth, 1981; Chadwick & Rutter,
1983; Rourke et 01., 1983). Developmentalists argue that a child should
never be viewed as simply a scaled-down version of an adult. Likewise,
an appropriate assessment of brain-behavior relationships in children
cannot be based simply on scaled-down versions of assessment methods
used with adults.
Unfortunately, many of the available assessment tools in child neuro-
psychology largely represent downward extensions of adult neuro-
psychological models and methods, many of which lack any clear linkage
with the neuropsychology of the developing brain. There is more to the
development of appropriate assessment procedures for children than sim-
ply gathering norms on adult tests for children of different ages (although
even this would be welcome in many instances). It also means more than
simply reducing the length or complexity of test procedures to make them
more practical for use with children. The measures themselves, as well as
their organization within an overall assessment strategy, must be tailored
to elucidate brain-behavior relationships as they unfold at different
points in a child's development. It is important that the field does not
OVERVIEW OF CURRENT STATUS 5
rush to meet the increased demand and new challenges it now faces
armed only with assessment tools borrowed from work with adults. New
challenges will require new approaches if the field of child neuropsychol-
ogy is to prosper and continue to grow.
This volume is devoted to underscoring important assessment issues
in child neuropsychology. In this chapter we will provide a general over-
view of historical trends within the field, the current approaches to as-
sessment, their clinical applications, and some of the key conceptual and
practical issues involved in the neuropsychological assessment of chil-
dren. We hope thus to set the stage for selected issues and topics to be
pursued at greater depth in subsequent chapters in this volume.
Fixed-Battery Approaches
A fixed-battery approach in neuropsychological assessment is one
that aims to provide a comprehensive assessment of brain function using
an invariant set of validated test procedures. The composition of the
battery is not tailored to the presenting characteristics of the individual
patient being assessed nor to the specific clinical hypotheses to be ad-
dressed. Rather, the emphasis is on administering as many of the desig-
nated procedures as the patient's condition will permit. Individual
variability is thought to be captured reasonably well so long as the battery
has been designed to tap a broad range of human capabilities. Moreover,
the use of a fixed battery across patients provides a standard data base on
which different clinical groups can be compared.
To date, fixed batteries such as the Halstead-Reitan Neuropsycho-
logical Battery (HRNB) and the Luria-Nebraska Neuropsychological Bat-
tery (LNNB) have represented the most commonly used approaches in
neuropsychological assessment (Hynd et aI., 1986). A detailed review of
these batteries is beyond the scope of this chapter, but some of the more
pertinent features of each are discussed below. The reader may wish to
refer to other available sources for a more thorough description of the
composition and validation of the HRNB (Boll, 1981; Reitan & Davison,
1974) and the children's revision of the LNNB (Golden, 1981, 1987). Also,
Hynd et al. (1986) have provided an excellent critical review of the valid-
ity and utility of both of these batteries in child neuropsychological
assessment.
strongly to Factor I, whereas the Vocabulary subtest had the highest rank
of the variables loading on Factor III.
Several studies have examined the interdependence between intel-
ligence, as assessed on the Wechsler Intelligence Scale for Children-Re-
vised (WISC-R), and performance on the older children's version of the
HRNB (Klesges, 1983; Seidenberg, Giordani, Berent, & Boll, 1983; Tra-
montana, Klee, & Boyd, 1984). Taken together, the results of these studies
have indicated substantial overlap between general intelligence and over-
all performance on the HRNB (e.g., r = .59 in the Tramontana et al. study).
The greatest influence of IQ has been found on the tests tapping more
complex skills and problem-solving abilities, language functions, and au-
ditory-perceptual analysis. In contrast, measures of basic tactile percep-
tion, motor strength and speed, and right-left hand differences have not
been found to be affected by IQ and thus appear to represent the more
distinctive and nonredundant aspects of functioning assessed by the
HRNB. Moreover, there is some indication that the overlap between gen-
eral intelligence and performance on the HRNB is greater in brain-
damaged children than among normals (Boll & Reitan, 1972).
Critique. The HRNB clearly has been the dominant approach to child
neuropsychological assessment for over the last 20 years. It has been used
in research on childhood brain dysfunction not only by Reitan and his
colleagues but also in some fashion by many other investigators. Reitan
certainly must be credited for pioneering a rigorous clinical approach to
neuropsychological diagnosis through the use of a standard battery of
tests. The strict emphasis on standardization has had the benefit of pro-
moting replicability and comparability of findings across clinicians and
researchers alike. It also has provided a standard data base on which
different clinical groups can be compared.
The HRNB provides a reasonably accurate means of distinguishing
brain-damaged, learning-disabled, and normal children. To date, howev-
er. there is little evidence to support its validity in localizing early brain
lesions or in specifying other lesion characteristics in brain-damaged chil-
dren. Its discriminative power appears to be limited to fairly broad diag-
nostic categories that, to some degree, can be differentiated on the basis of
intelligence testing alone. It has been shown to overlap substantially with
IQ, with its nonredundant contributions to assessment mainly involving
measures of basic motor and sensory-perceptual abilities. Given this,
comparable accuracy probably could be achieved in discriminating brain-
damaged, learning-disabled, and normal children simply through the use
of standard measures of intelligence and academic achievement supple-
mented by selected tests of motor and sensory-perceptual abilities.
Consistent with the goals of neuropsychological assessment at the
time of its development, the composition of the HRNB was based heavily
OVERVIEW OF CURRENT STATUS 13
Qualitative Approaches
Rather than an emphasis on quantifying the extent of deficit, qualita-
tive approaches are concerned more with determining how the individual
passes or fails a particular task. For example, although a child may recall a
memory item accurately, it is extremely important from a qualitative per-
spective to understand what strategies the child used to remember. Did
the child utilize cues based on the verbal, visual, or multimodal aspects of
the task? Were contextual ones (e.g., main themes or key words) em-
ployed? Perhaps rehearsal, chunking, verbal labeling, or other mnemonic
18 MICHAEL G. TRAMONTANA and STEPHEN R. HOOPER
strategies were utilized to some degree. These kinds of data are extremely
important not only in distinguishing the precise nature of underlying
neuropsychological dysfunction but also in identifying effective treat-
ment strategies that can be used in helping the child to compensate for
deficits in particular skills.
Qualitative approaches are less concerned with test standardization
or in comparing an individual's performance against general norms than
with conducting a careful idiographic analysis of performance for each
case. Almost any task may be used or modified in such a way as to
facilitate an in-depth analysis of where and how a particular individual's
performance breaks down. Informal testing procedures typically are used,
but even standardized tests can be utilized from a qualitative perspective
so long as the emphasis is on observing how the individual performs
instead of focusing only on the test scores that are obtained.
Probably the most recognized approach to qualitative assessment is
exemplified in the work of Luria (1966,1973) as described by Christensen
(1975). There are three major parts to Luria's Neuropsychological Investi-
gation. The first part consists of an initial evaluation of the individual's
functioning utilizing a hypothesis-testing approach. Based on the pa-
tient's initial performance, the second part employs a more individual-
ized set of tasks to explore suspected deficits more fully. Finally, once the
qualitative information is obtained, the results are formulated according
to Luria's theory of functional systems. Christensen organized the various
examination tasks used by Luria into 11 major areas of function. Golden et
a1. (1980) later used these as the original pool of items from which the
summary scales of the LNNB were developed.
Process-Oriented Approaches
These approaches represent a hybrid of quantitative and qualitative
methods in neuropsychological assessment. For example, in the Boston
Process Approach (Milberg, Hebben, & Kaplan, 1986) the emphasis is on
understanding the qualitative nature of the behavior assessed by psycho-
metric tests. It draws selectively from a core set of standardized tests for
the purpose of gaining a quantified overview of the patient's general pat-
tern of spared and impaired functions. Depending on the initial results,
the examination thereafter is guided by clinical hypothesis-testing aimed
at pinpointing the precise nature of the individual's deficits. This is
achieved through the use of various "satellite tests," which may consist of
standardized tests, the addition of new components to published tests, or
a set of tasks designed specifically for each patient. The possibilities are
limited only by the examiner's knowledge of available tests and his/her
creativity in designing new tasks for assessing particular deficit areas.
Using a similar logic, Wilson (1986) has presented a branching hy-
OVERVIEW OF CURRENT STATUS 19
General Critique
There are distinct advantages associated with each of the approaches
to neuropsychological assessment considered in this section. Eclectic bat-
teries preserve the quantitative nature of neuropsychological assessment
but are not bound to any particular tests or measures in achieving that
end. Rather, the emphasis is on selecting tests that are best suited to assess
particular abilities, which, taken together, span a broad range of function.
Tests may be substituted as better ones become available, and specific
tests may be added or deleted in adapting the battery to different applica-
tions. Moreover, the approach lends itself nicely to neuropsychological
description if tests are selected deliberately so that they are aligned with
well-defined areas of ability. Qualitative approaches offer maximum flexi-
bility and a richness of clinical data that surpasses what possibly could be
obtained through the use of standardized tests alone. The emphasis on
identifying the cognitive strategies available to the patient provides an
obvious linkage between assessment and treatment planning. Of all the
approaches considered, it is the one that is most dependent on the skills
and conceptual framework of the individual examiner. Process-oriented
approaches attempt to integrate quantitative and qualitative methods of
assessment, taking the best from both worlds so to speak. Also, as in
qualitative approaches, the emphasis in process-oriented approaches on
careful case study serves to play an important role in theory building.
However, a major problem with each of these approaches is that there
has been insufficient validation research on which to judge their ade-
quacy. The absence of standardization in qualitative approaches is incom-
patible with conducting independent appraisals of reliability and valid-
ity. Many American neuropsychologists would argue that standardization
and quantification are defining features of neuropsychological assess-
ment, and that qualitative approaches are more characteristic of methods
in behavioral neurology. An eclectic battery may utilize well-validated
20 MICHAEL G. TRAMONTANA and STEPHEN R. HOOPER
individual tests, but little is known about the validity and utility of the
battery as a whole. Indeed, this would be difficult to assess if the composi-
tion of the battery were subjected to constant change. There also is the
problem of making comparisons among the measures within a battery that
may differ in terms of their normative base, test construction, and other
factors. Even if they were more carefully researched, it is doubtful that the
present examples of eclectic batteries would not share some of the prob-
lems identified with the HRNB and LNNB-CR. The flexible nature of test
selection in process-oriented approaches is thought to result in greater
diagnostic efficiency, but this is yet to be demonstrated. As Rourke et a1.
(1983) have pointed out, a flexible or individualized approach would be
at least as time-consuming as a fixed battery if an assessment of compara-
ble breadth is to be achieved. Also, a fixed-battery approach serves to
assure a consistently comprehensive assessment that is not biased by
either referral complaints or the child's initial presentation.
The differences among the various approaches to neuropsychological
assessment seem to have gotten overstated sometimes for the sake of aca-
demic argument. In practice, there probably are relatively few neuropsy-
chologists who are purists with respect to one approach or another, and a
melding of approaches probably is quite common. This makes good sense
because the different perspectives can be combined in a complementary
fashion in an effort to maximize both breadth and depth of assessment. A
fixed battery of procedures that is brief, but nonetheless spans a broad
range of abilities, helps to assure a consistently comprehensive assess-
ment that can produce comparable results across times, patient groups,
and different research settings. It provides a horizontal analysis of general
functioning that, along with qualitative observation, can be used in tailor-
ing an in-depth or vertical analysis of specific functional areas based on a
more flexible selection of tests. Process-oriented approaches achieve this
to some extent, but the validity of initial screening decisions may be
compromised by the absence of a fixed set of procedures that could assure
a consistently broad-based assessment for all cases.
Special-Purpose Measures
In addition to the general, all-purpose approaches to neuropsycholog-
ical assessment that we have discussed, there are a host of individual
measures and specialized test batteries available to assess more specific
aspects of neuropsychological functioning in children. Examples include
Benton's Motor Impersistence Battery and other special-purpose tests
(Benton, Hamsher, Varney, & Spreen, 1983), the Goldman, Fristoe, and
Woodcock (1974) Auditory Skills Battery, the children's version of the
California Verbal Learning Test (Delis, Kramer, Kaplan, & Ober, 1986),
and the Wisconsin Card Sorting Test (Heaton, 1981), to name only a few.
OVERVIEW OF CURRENT STATUS 21
APPLICATIONS
Neurological Disorders
There are literally dozens of neurological disorders in childhood that
may require a careful neuropsychological assessment. These include ge-
22 MICHAEL G. TRAMONTANA and STEPHEN R. HOOPER
Systemic Illness
Interest in the neuropsychological functioning of children with sys-
temic illness has shown considerable growth recently (e.g., Hynd &
Willis, 1988). There are a variety of pediatric illnesses that can impact
negatively on the developing nervous system, including defects in specif-
ic organ systems (e.g., pulmonary disease, congenital heart disease, renal
dysfunction), metabolic disorders (e.g., elevated blood phenylalanine,
defects in amino acid metabolism, lipid storage diseases, and mucopoly-
saccharidosis), autoimmune disorders, and infections (e.g., meningitis,
cytomegalovirus, Reye's syndrome). Evidence regarding the neuropsycho-
logical sequelae of such childhood illnesses has begun to emerge.
For example, Holmes and Richman (1985) examined the cognitive
profiles of children with insulin-dependent diabetes and found that chil-
dren with early disease onset (7 years of age or younger) and a chronic
course (5 years or more) were more likely to show reading and memory
difficulties. They also tended to have a lower Performance IQ on the
24 MICHAEL G. TRAMONTANA and STEPHEN R. HOOPER
WISC-R, but this appeared to be due largely to slow response time rather
than to a specific deficit in visual-spatial abilities. Similar findings have
been obtained by other researchers (Ryan, Vega, & Drash, 1985; Ryan,
Vega, Longstreet, & Drash, 1984). However, interacting factors apparently
must be considered as well; i.e., Rovet, Gore, and Ehrlich (1983) found
that whereas females with diabetes onset prior to 3 years of age tended to
experience deficits in visual-motor functioning, their male counterparts
did not.
A major area in which neuropsychological assessment can play a
crucial role is in pediatric oncology. For example, acute lymphocytic
leukemia (ALL) accounts for 35% of all malignancies of childhood, with
approximately 40% of these cases becoming disease-free survivors (George,
Aur, Mauer, & Simone, 1979). An important question concerns the possible
iatrogenic effects of the various treatments required to stabilize these
children medically. The evidence is inconclusive, but there is some indica-
tion that children with ALL who receive intracranial radiation and chemo-
therapy (Methotrexate) may suffer a variety of posttreatment neuropsycho-
logical deficits (Goff, 1982; Waber, Sollee, Wills, & Fischer, 1986) and are
more likely to be later diagnosed as having learning disabilities (Elbert,
Culbertson, Gerrity, Guthrie, & Bayles, 1985).
As was noted before, advances in medical care have brought about a
dramatic increase in the survival of children with serious illnesses. This
has created a greater need for the careful assessment of possible neuropsy-
chological sequelae associated with these diseases or their treatment. On-
going neuropsychological assessment may contribute effectively to
monitoring improvement, stability, or deterioration in the child's func-
tioning, and may indicate the need for other kinds of intervention (e.g.,
special education). Its utility in assessing children with various pediatric
illnesses is only beginning to be realized.
Psychiatric Disorders
There is strong evidence that brain dysfunction in childhood is associ-
ated with an increased risk for psychiatric disorder. The risk is much
greater than for children with other types of physical handicap (Seidel,
Chadwick, & Rutter, 1975), and the relationship appears to hold both for
children with documented brain damage (e.g., Brown et aI., 1981; Rutter et
aI., 1970) and for those with so-called soft neurological signs (e.g., Shaffer
et aI., 1985). Among children with accidental head injuries, the risk is
compounded by factors such as psychosocial adversity and any pre-exist-
ing tendencies toward behavioral or emotional disturbance (Brown et a1.,
1981). The relationship is not trivial, given that the effects appear to persist
and influence the child's long-range behavioral adjustment (Breslau &
Marshall, 1985; Shaffer et aI., 1985).
OVERVIEW OF CURRENT STATUS 25
Learning Disabilities
As was noted before, the study of learning disabilities has been one of
the most intensive areas of investigation in child neuropsychology. The
explicit presumption of central nervous system dysfunction in current
definitions of learning disability (Hammill, Leigh, McNutt, & Larsen, 1981)
has served to underscore the important role of neuropsychological assess-
ment in this field. Neuropsychological assessment can contribute effective-
ly both in the identification of specific underlying dimensions of dysfunc-
tion in particular learning handicaps and in the formulation and evaluation
of specific educational plans. The work in learning disabilities-which has
dealt with the child's adaptive capacity (and future potential) in the real-
life context of school-has taken an exemplary lead in relating neuropsy-
chological assessment to questions of ecological validity. Much remains to
be learned, but major advances have been achieved in the area of syndrome
definition and subtype analysis, and in the identification of developmental
precursors of learning disabilities, possible neuroanatomical and neu-
OVERVIEW OF CURRENT STATUS 27
We have seen that the effects of brain damage tend to be less specific
in children than in adults (Chadwick & Rutter, 1983). Because brain
damage primarily seems to impair new learning and achievement, decre-
ments in general intelligence often are among the chief manifestations of
early childhood brain injury (Boll & Barth, 1981; Rourke et a1., 1983).
Hynd et a1. (1986) have suggested that the effects of brain damage begin to
take on a more specific character, resembling those seen in adults, when
injuries are sustained after the functional organization of the cerebral
hemispheres has become fairly well established, at about 5 to 7 years of
age. Nonetheless, there is considerable overlap or redundancy between
standard measures of intelligence and current test batteries used for as-
OVERVIEW OF CURRENT STATUS 29
above issues may apply in the evaluation of adults, they are far more
likely to arise as complicating factors in the neuropsychological assess-
ment of children.
Nowhere are the age-specific constraints on assessment more appar-
ent than in the evaluation of children during the first 3 or 4 years of life.
Perhaps this is why, with few exceptions, the bulk of research and prac-
tice in child neuropsychology has dealt almost exclusively with children
5 years of age and older. The relatively limited response repertoire of
infants or toddlers that can be used in assessing their abilities, together
with the degree to which performance is state-dependent, places major
constraints on formal neuropsychological assessment (see Chapter 9, this
volume). This is largely an uncharted territory for neuropsychologists
that, up to this point, mainly has involved the work of developmental
psychologists and pediatric neurologists. At present, there is little re-
semblance between what is done in assessing brain function in infancy or
early childhood (which tends to rely heavily on the evaluation of reflexes,
sensorimotor development, and other developmental milestones) and
what ordinarily would constitute a neuropsychological assessment in
later years. The extent to which there is continuity in the neuropsycholog-
ical meaning of the assessment data obtained over these developmental
periods is an open question.
Finally, consideration must be given to the unique challenges that
arise in the assessment of children with special handicapping conditions
such as sensory loss, physical deformities, motor disabilities, and lan-
guage impairment. The nature of the handicap as well as its impact on the
child's general functioning must be assessed, but care must be taken to
devise an appropriate assessment strategy that will yield a balanced pic-
ture of the child's overall abilities. It would be inappropriate to utilize
tasks that unduly tax the child's specific handicap, and then go on and
use these results to draw conclusions about the child's more general func-
tioning. For example, the assessment of nonverbal abilities in a language-
impaired child would be biased if this were based on tasks that depended
heavily on the comprehension of spoken instructions. Conducting a com-
prehensive assessment that effectively works around the child's handicap
and maintains his or her motivation to perform requires a great deal of
skill, ingenuity, and patience on the part of the examiner. It also requires a
knowledge of any unique neurodevelopmental features associated with
specific handicaps. For example, a blind child is likely to show delays in
sensorimotor development, and may use different cognitive strategies in
performing certain tasks than a sighted child. Although inconclusive,
there also is evidence to suggest that children with a specific sensory loss
in early life may develop an atypical pattern of cerebral organization of
function (e.g., Gibson & Bryden, 1984). Differential neuropsychological
features may be associated with other types of handicap as well. This is an
32 MICHAEL G. TRAMONTANA and STEPHEN R. HOOPER
SUMMARY
REFERENCES
Adamovich, B. B., Henderson, J. A., & Auerbach, S. (1985). Cognitive rehabilitation of closed
head injured patients. San Diego, CA: College-Hill Press.
Almli, C. R., & Finger, S. (1984). Early brain damage. Orlando, FL: Academic Press.
Aylward, G. P., Gustafson, N., Verhulst, S. J., & Colliver, J. A. (1987). Consistency in the
diagnosis of cognitive, motor, and neurologic function over the first three years. Journal
of Pediatric Psychology, 12, 77-98.
Bender, 1. (1938). A visual motor gestalt test and its clinical use (Research Monograph No.
3). New York: American Orthopsychiatric Association.
Benton, A. 1. (1963). The Revised Visual Retention Test: Clinical and experimental applica-
tions. New York: Psychological Corporation.
OVERVIEW OF CURRENT STATUS 33
Benton, A. 1., Hamsher, K., Varney, N. R., & Spreen, O. (1983). Contributions to neuropsy-
chological assessment: A clinical manual. New York: Oxford University Press.
Berg, R A., Bolter, J. F., Ch'ien, 1. T., Williams, S. J., Lancaster, W., & Cummins, J. (1984).
Comparative diagnostic accuracy of the Halstead-Reitan and the Luria-Nebraska Neuro-
psychological Adult and Children's Batteries. Clinical Neuropsychology. 6(3), 200-204.
Boll, T. J. (1974). Behavioral correlates of cerebral damage in children aged 9-14. In R M.
Reitan & 1. A. Davison (Eds.), Clinical neuropsychology: Current status and applica-
tions (pp. 91-120). New York: Wiley.
Boll, T. J. (1981). The Halstead-Reitan Neuropsychology Battery. In S. B. Filskov & T. J. Boll
(Eds.), Handbook of clinical neuropsychology (pp. 577-607). New York: Wiley.
Boll, T. J., & Barth, J. T. (1981). Neuropsychology of brain damage in children. In S. B.
Filskov & T. J. Boll (Eds.)' Handbook of clinical neuropsychology (pp. 418-452). New
York: Wiley.
Boll, T. J., & Reitan, R M. (1972). Comparative ability interrelationships in normal and brain-
damaged children. Journal of Clinical Psychology, 28, 152-156.
Bolter, J. F. (1984). Neuropsychological impairment and behavioral dysfunction in children
with chronic epilepsy. Unpublished doctoral dissertation, Memphis State University.
Boyd, T. A., Tramontana, M. G., & Hooper, S. R (1986). Cross-validation of a psychometric
system for screening neuropsychological abnormality in older children. Archives of
Clinical Neuropsychology, 1, 387-391.
Breslau, N., & Marshall, 1. A. (1985). Psychological disturbance in children with physical
disabilities: Continuity and change in a 5-year follow-up. Journal of Abnormal Child
Psychology, 13, 199-216.
Brink, J., Garrett, A., Hale, W., Woo Sam, J., & Nickel, V. (1970). Recovery of motor and
intellectual function in children sustaining severe head injuries. Developmental Medi-
cine and Child Neurology, 12, 565-571.
Brown, G., Chadwick, 0., Shaffer, D., Rutter, M., & Traub, M. (1981). A prospective study of
children with head injuries: III. Psychiatric sequelae. Psychological Medicine, 11,63-
78.
Chadwick, 0., & Rutter, M. (1983). Neuropsychological assessment. In M. Rutter (Ed.), Devel-
opmental neuropsychiatry (pp. 181-212). New York: Guilford Press.
Chadwick, 0., Rutter, M., Brown, G., Shaffer, D., & Traub, M. (1981). A prospective study of
children with head injuries: II. Cognitive sequelae. Psychological Medicine, 11, 49-
61.
Chelune, G. J., & Edwards, P. (1981). Early brain lesions: Ontogenetic-environmental consid-
erations. Journal of Consulting and Clinical Psychology, 49, 777-790.
Chelune, G., Ferguson, W., Koon, R, & Dickey, T. (1986). Frontal lobe dysinhibition in
attention deficit disorder. Child Psychiatry and Human Development, 16, 221-234.
Christensen, A. 1. (1975). Luria's neuropsychological investigation. New York: Spectrum.
Craft, A., Shaw, D., & Cartlidge, N. (1972). Head injuries in children. British Medical Journal,
4, 200-203.
Crockett, D., Klonoff, H., & Bjerring, J. (1969). Factor analysis of neuropsychological tests.
Perceptual and Motor Skills, 29, 791-802.
Cull, c., & Wyke, M. A. (1984). Memory function of children with spina bifida and shunted
hydrocephalus. Developmental Medicine and Child Neurology, 26, 177-183.
Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (1986). The California Verbal Learning
Test: Children's Version. New York: Psychological Corporation.
Dennis, M. (1985a). Intelligence after early brain injury: I. Predicting IQ scores from medical
variables. Journal of Clinical and Experimental Neuropsychology, 7, 526-554.
Dennis, M. (1985b). Intelligence after early brain injury: II. IQ scores of subjects classified on
the basis of medical history variables. Journal of Clinical and Experimental Neuropsy-
chology, 7, 555-576.
Dreisbach, M., Ballard, M., Russo, D. c., & Schain, R J. (1982). Educational intervention for
34 MICHAEL G. TRAMONTANA and STEPHEN R HOOPER
children with epilepsy: A challenge for collaborative service delivery. Journal of Special
Education. 16,111-121.
Elbert, J. c., Culbertson, J. 1., Gerrity, K. M., Guthrie, 1. J., & Bayles, R (1985, February).
Neuropsychological and electrophysiologic follow-up of children surviving acute lym-
phocytic leukemia. Paper presented at the annual meeting of the International Neuro-
psychological Society, San Diego.
Emhart, C. B., Graham, F. K., Eichman, P. L., Marshall, J. M., & Thurston, D. (1963). Brain
injury in the preschool child: Some developmental considerations. II. Comparison of
brain-injured and normal children. Psychological Monographs, 77(Whole No. 574), 17-
33.
Fein, D., Waterhouse, 1., Lucci, D., & Snyder, D. (1985). Cognitive subtypes in developmen-
tally disabled children: A pilot study. Journal of Autism and Developmental Disorders,
15, 77-95.
Fennell, E. B., Eisenstadt, T., Bodiford, C., Rediess, S., de Bijl, M., & Mickle, J. (1987,
February). The assessment of neuropsychological dysfunction in children shunted for
hydrocephalus. Paper presented at the Fifteenth Annual Meeting of the International
Neuropsychological Society, Washington, D.C.
Filskov, S. B., & Boll, T. J. (Eds.). (1981). Handbook of clinical neuropsychology. New York:
Wiley.
Filskov, S. B., & Goldstein, S. G. (1974). Diagnostic validity of the Halstead-Reitan Neuropsy-
chological Battery. Journal of Consulting and Clinical Psychology, 42, 383-388.
Gaddes, W. H. (1985). Learning disabilities and brain function: A neuropsychological ap-
proach (2nd ed.). New York: Springer-Verlag.
Geary, D. c., & Gilger, J. W. (1984). The Luria-Nebraska Neuropsychological Battery-Chil-
dren's Revision: Comparison of learning disabled and normal children matched on full
scale IQ. Perceptual and Motor Skills, 58, 115-118.
Geary, D. C., Jennings, S. M., Schultz, D. D., & Alper, T. G. (1984). The diagnostic accuracy of
the Luria-Nebraska Neuropsychological Battery-Children's Revision for 9 to 12 year old
learning disabled children. School Psychology Review, 13, 375-380.
George, S. 1., Aur, R J. A., Mauer, A. M., & Simone, J. V. (1979). A reappraisal of the results
of stopping therapy in childhood leukemia. New England Journal of Medicine, 300,
269-273.
Gibson, C. J., & Bryden, M. P. (1984). Cerebral laterality in deaf and hearing children. Brain
and Language, 23, 1-12.
Goff, J. R (1982). Memory deficits and distractibility in survivors of childhood leukemia.
Paper presented at the annual meeting of the American Psychological Association.
Golden, C. J. (1981). The Luria-Nebraska Children's Battery: Theory and formulation. In G.
W. Hynd & J. E. Obrzut (Eds.), Neuropsychological assessment and the school-age child:
Issues and perspectives (pp. 277-302). New York: Grune and Stratton.
Golden, C. J. (1987). Manual for the Luria-Nebraska Neuropsychological Battery-Children's
Revision. Los Angeles, CA: Western Psychological Services.
Golden, C. J., Hammeke, T. A., & Purisch, A. D. (1980). Manual for the Luria-Nebraska
Neuropsychological Battery. Los Angeles: Western Psychological Services.
Goldman, R, Fristoe, M., & Woodcock, R W. (1974). Manual for the Goldman-Fristoe-
Woodcock Auditory Skills Test Battery. Circle Pines, MN: American Guidance Service.
Graham, F. K., Emhart, C. B., Craft, M., & Berman, P. W. (1963). Brain injury in the preschool
child: Some developmental considerations: I: Performance of normal children. Psycho-
logical Monographs, 77(Whole No. 573), 1-16.
Graham, F. K., & Kendall, B. S. (1960). Memory-for-Designs-Test: Revised general manual.
Perceptual and Motor Skills Monograph (Supplement, No.2-VII), 11, 147-188.
Gustavson, J. 1., Golden, C. J., Wilkening, G. N., Hermann, B. P., Plaisted, J. R, MacInnes, W.
D., & Leark, R A. (1984). The Luria-Nebraska Neuropsychological Battery-Children's
Revision: Validation with brain-damaged and normal children. Journal of Psychoeduca-
tional Assessment, 2, 199-208.
OVERVIEW OF CURRENT STATUS 35
Gustavson, J. 1., Wilkening, G. N., Hermann, B. P., & Plaisted, J. R. (1982). Factor analysis of
the children's revision of the Luria-Nebraska Neuropsychological Battery. Unpublished
manuscript.
Hagen, C. (1981). Language disorders secondary to closed head injury: Diagnosis and treat-
ment. Topics in Language Disorders, 1, 73-87.
Hammill, D. D., Leigh, J. E., McNutt, G., & Larsen, S. C. (1981). A new definition of learning
disabilities. Learning Disability Quarterly, 4, 336-342.
Heaton, R K. (1981). Manual for the Wisconsin Card Sorting Test. Odessa, FL: Psychological
Assessment Resources.
Herbert, M. (1964). The concept and testing of brain damage in children: A review. Journal of
Child Psychology and Psychiatry,S, 197-216.
Holmes, C. S., & Richman, 1. C. (1985). Cognitive profiles of children with insulin-depen-
dent diabetes. Journal of Developmental and Behavioral Pediatrics, 6, 323-326.
Hooper, S. R, & Tramontana, M. G. (1987). The relationship between neuropsychological
variables and academic achievement in child psychiatric patients. Paper presented at
the 95th Annual Convention of the American Psychological Association, New York.
Hurley, A. D., Laatsch, 1. K., & Dorman, C. (1983). Comparison of spina bifida, hydro-
cephalic patients, and matched controls on neuropsychological tests. Zeitschrift fUr
Kinderchir, 17, 65-70.
Hynd, G. W., & Obrzut, J. E. (Eds.). (1981). Neuropsychological assessment and the school-
age child: Issues and procedures. New York: Grune and Stratton.
Hynd, G. W., Snow, J., & Becker, M. G. (1986). Neuropsychological assessment in clinical
child psychology. In B. Lahey & A. Kazdin (Eds.). Advances in clinical child psychology
(Vol. 9). New York: Plenum.
Hynd, G. W., & Willis, W. G. (1988). Pediatric neuropsychology. New York: Grune and
Stratton.
Incagnoli, T., & Newman, B. (1985). Cognitive and behavioral interventions. International
Journal of Clinical Neuropsychology, 7, 173-182.
Ivan, L. P. (Ed.). (1984). Pediatric neuropsychology. St. Louis: Warren H. Green.
Karras, D., Newlin, D. B., Franzen, M. D., Golden, C. J., Wilkening, G. N., Rothermel, RD., &
Tramontana, M. G. (1987). Development of factor scales for the Luria-Nebraska Neuro-
psychological Battery-Children's Revision. Journal of Clinical Child Psychology, 16,
19-28.
Kaufman, A. S., & Kaufman, N. 1. (1983). Manual for the Kaufman Assessment Battery for
Children. Circle Pines, MN: American Guidance Service.
Kay, G. G., Becker, B., Bleiberg, J., & Long, C. J. (1986, August). Cognitive rehabilitation
software: Therapy or adjunct? A call for standards. Paper presented at the Annual
Meeting of the American Psychological Association, Washington, D.C.
Klesges, R C. (1983). The relationship between neuropsychological, cognitive, and behav-
ioral assessments of brain functioning in children. Clinical Neuropsychology, 1, 28-32.
Klonoff, H., Low, M. D., & Clark, C. (1977). Head injuries in children with a prospective 5-
year follow-up. Journal of Neurology, Neurosurgery and Psychiatry, 40, 1211-1219.
Klonoff, H., Robinson, G. C., & Thompson, G. (1969). Acute and chronic brain syndromes in
children. Developmental Medicine in Child Neurology, 11, 198-213.
Knights, R M. (1966). Normative data on tests for evaluating brain damage in children from 5
to 14 years of age (Research Bulletin No. 20). London, Ontario: University of Western
Ontario.
Kolb, B., & Wishaw, I. Q. (1980). Fundamentals of human neuropsychology. San Francisco:
W. H. Freeman.
Koppitz, E. M. (1964). The Bender Gestalt Test for Young Children. New York: Grune and
Stratton.
Levin, H. S., & Eisenberg, H. M. (1979). Neuropsychological impairment after closed head
injury in children and adolescents. Journal of Pediatric Psychology, 4, 389-402.
Luria, A. R. (1966). Higher cortical functions in man. New York: Basic Books.
36 MICHAEL G. TRAMONTANA and STEPHEN R. HOOPER
nomonic, left sensorimotor, and right sensorimotor scales for the Luria-Nebraska Neuro-
psychological Battery-Children's Revision. Journal of Clinical Child Psychology, 13(2),
165-169.
Seidel. U. P., Chadwick, 0., & Rutter, M. (1975). Psychological disorders in crippled chil-
dren: A comparative study of children with and without brain damage. Developmental
Medicine and Child Neurology, 17, 563-573.
Seidenberg, M., Giordani, B., Berent, S., & Boll, T. J. (1983). IQ level and performance on the
Halstead-Reitan Neuropsychological Test Battery for Older Children. Journal of Con-
sulting and Clinical Psychology, 51, 406-413.
Selz, M., & Reitan, R. M. (1979). Rules for neuropsychological diagnosis: Classification of
brain function in older children. Journal of Consulting and Clinical Psychology, 47(2).
258-264.
Shaffer, D., Schonfeld, 1., O'Connor, P. A., Stokman, C., Trautman, P., Shafer, S., & Ng, S.
(1985). Neurological soft signs. Archives of General Psychiatry, 42, 342-351.
Smith, A. (1975). Neuropsychological testing in neurological disorders. In W. J. Friedlander
(Ed.). Advances in neurology (Vol. 7). New York: Raven Press.
Snow, J. H., & Hynd, G. W. (1985). Factor structure of the Luria-Nebraska Neuropsychologi-
cal Battery-Children's Revision. Journal of School Psychology, 23, 271-275.
Snow, J. H., Hynd, G. W., & Hartlage, 1. C. (1984). Difference between mildly and more
severely learning-disabled children on the Luria-Nebraska Neuropsychological Battery-
Children's Revision. Journal of Psychoeducational Assessment, 2, 23-28.
Soare, P. 1., & Raimondi, A. J. (1977). Intellectual and perceptual-motor characteristics of
treated myelomeningocele children. American Journal of Diseases of Children, 131,
199-204.
Spreen, O. J., & Gaddes, W. H. (1969). Development norms for 15 neuropsychological tests
age 6-15. Cortex, 5, 171-191.
Spreen, O. J., Tupper, D., Risser, A., Tuokko, H., & Edgell, D. (1984). Human developmental
neuropsychology. New York: Oxford University Press.
Sweet, J. J., Carr, M. A., Rossini. E., & Kaspar, C. (1986). Relationship between the Luria-
Nebraska Neuropsychological Battery-Children's Revision and the WISC-R: Further ex-
amination using Kaufman's factors. International Journal of Clinical Neuropsychology,
8, 177-180.
Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness. Lancet,
11,81-84.
Tramontana, M. G. (1983). Neuropsychological evaluation of children and adolescents with
psychopathological disorders. In C. J. Golden & P. J. Vicente (Eds.). Foundations of
clinical neuropsychology (pp. 309-340). New York: Plenum.
Tramontana, M. G., & Boyd, T. A. (1986). Psychometric screening of neuropsychological
abnormality in older children. International Journal of Clinical Neuropsychology, 8,
53-59.
Tramontana, M. G., Hooper, S. R., & Nardolillo, E. M. (in press). Behavioral manifestations of
neuropsychological impairment in children with psychiatric disorders. Archives of
Clinical Neuropsychology
Tramontana, M. G., & Hooper, S. R. (1987). Discriminating the presence and pattern of
neuropsychological impairment in child psychiatric disorders. International Journal of
Clinical Neuropsychology, 9, 111-119.
Tramontana, M. G., & Hooper, S. R. (in press). Neuropsychology of child psychopathology.
In C. R. Reynolds (Ed.). Handbook of child clinical neuropsychology. New York:
Plenum.
Tramontana, M. G., Hooper, S. R., Curley, A. D., & Nardolillo, E. M. (1988, January). Determi-
nants of academic achievement in children with psychiatric disorders. Paper presented
at the Annual National Conference of the International Neuropsychological Society,
New Orleans.
38 MICHAEL G. TRAMONTANA and STEPHEN R. HOOPER
Tramontana, M. G., Klee, S. H., & Boyd, T. A. (1984). WISC-R interrelationships with the
Halstead-Reitan and Children's Luria Neuropsychological Batteries. International Jour-
nal of Clinical Neuropsychology, 6, 1-8.
Tramontana, M. G., & Sherrets, S. D. (1985). Brain impairment in child psychiatric disorders:
Correspondencies between neuropsychological and CT scan results. Journal of the
American Academy of Child Psychiatry, 24, 590-596.
Tramontana, M. G., Sherrets, S. D., & Golden, C. J. (1980). Brain dysfunction in youngsters
with psychiatric disorders: Application of Selz-Reitan rules for neuropsychological di-
agnosis. Clinical Neuropsychology, 2, 118-123.
Tramontana, M. G., Sherrets, S. D., & Wolf, B. A. (1983). Comparability of the Luria-Nebraska
and Halstead-Reitan Neuropsychological Batteries for older children. Clinical Neuro-
psychology,S, 186-190.
Waber, D., Sollee, N., Wills, K., & Fischer, R (1986, February). Neuropsychological effects of
two levels of cranial radiation in children with acute lymphoblastic leukemia (ALL).
Paper presented at the Fourteenth Annual Meeting of the International Neuropsycholog-
ical Society, Denver, Colorado.
Wender, P. (1971). Minimal brain dysfunction in children. New York: Wiley.
Wilkening, G. N., Golden, C. J., Macinnes, W. D., Plaisted, J. R, & Hermann, B. P. (1981,
August). The Luria-Nebraska Neuropsychological Battery-Children's Revision: A pre-
liminary report. Paper presented at the meeting of the American Psychological Associa-
tion, Los Angeles.
Wilson, B. C. (1986). An approach to the neuropsychological assessment of the preschool
child with developmental deficits. In S. B. Filskov & T. J. Boll (Eds.), Handbook of
clinical neuropsychology (Vol. 2). New York: Wiley.
Wilson, H., & Staton, R D. (1984). Neuropsychological changes in children associated with
tricyclic antidepressant therapy. International Journal of Neuroscience, 24, 307-312.
Wolf, B. A., & Tramontana, M. G. (1982). Aphasia Screening Test interrelationships with
complete Halstead-Reitan test results for older children. Clinical Neuropsychology, 4,
179-186.
Yule, W. (1980). Educational achievement. In B. M. Kulig, M. Meinhardi, & G. Stores (Eds.),
Epilepsy and behavior. Lisse, The Netherlands: Swets & Zeitlinger.
II
INTRODUCTION
41
42 ANTHONY H. RISSER and DOROTHY EDGELL
within brain areas. Brain-cell proliferation slows by the end of the first
trimester of pregnancy; most neurons have been created by the beginning of
the final trimester.
Once a population of neuroblasts has stopped multiplying, its con-
stituents migrate as true neurons outward from their birth sites. Young
neurons migrate in sheets (laminae) of similar cells created at similar
times toward specific zones of the outer layer of the neural tube, which
eventually will become the multilayered cortical "gray matter" and the
various subcortical nuclei. Axons that will enter or leave this outer layer
on route to their target synaptic zones form an intermediate layer destined
to become "white matter." Rakic (1981) has provided a detailed descrip-
tion of migratory mechanisms and their roles in configuring the cortex.
The goal of migration is to emplace neurons at their mature functional
sites, creating the gridwork for subsequent cellular differentiation and
synapse formation.
Characteristic physical changes in the fetal brain during this time
involve its regional distinctiveness: the rapid growth of the cerebral hemi-
spheres, the initial appearance of sulcal and gyral landmarks, and cere-
bellar development. As early as the sixth gestational week, features such
as the cortex and the internal capsule are evident. By the 23rd week, major
sulcal and gyrallandmarks on the cortical surface are evident (Chi, Dool-
ing, & Gilles, 1977). Figure 1 presents sulcal development in relation to
brain weight over the course of prenatal development.
Differentiation
Differentiation is a multifactorial growth period during which maturation
of the structure of existing cells is accomplished. Differentiation permits
cells to function as committed constituents of specific neural systems.
The major components of differentiation include (1) formation of the den-
dritic field and distal axonal growth, (2) maturation of cell-body struc-
tures that are required for proper metabolic functioning, (3) creation and
maturation of synaptic architecture and the establishment of functional
transmission links, (4) maturation of enzyme and neurotransmitter syn-
thesis and storage, and (5) selective retrogressive processes (e.g., neuronal
death) to streamline the neural substrate. Differentiation of neuronal pop-
ulations begins in earnest once they have migrated to their mature place-
ment sites. Differentiation is a characteristic feature of fetal brain develop-
ment, but it also continues beyond birth. Some elements of differentiation
become life-span features of neurological maintenance. For example, syn-
aptic differentiation is extensive during fetal development when synaptic
turnover (i.e., creation and elimination) is great, but it also may continue
as a modulating mechanism in response to change throughout the life-
span (Cotman & Nieto-Sampedro, 1982, 1984).
NEUROPSYCHOLOGY OF THE DEVELOPING BRAIN 45
400
360
320
280
(i)
E
~ 240
!!J
~
J:
S? 200
w
~
Z
160
a:
CD
120
80
40
0
110 150 190 270
BIRTH
GESTATIONAL AGE (days)
FIGURE 1. The relation between brain weight and the development of cerebral sulci. (Adapt-
ed from Lemire, Loeser, Leech, & Alvord, 1975,)
trimester. Other areas, such as the cerebellum and the vast regions of
microneuron-composed association cortex, continue to differentiate well
beyond birth, concurrent with the substantial functional acquisitions in
language and motor control that the infant achieves during the first 2
years of life. The neural differentiation that occurs in the context of medi-
ating normal psychological learning remains an enigma, addressed spec-
ulatively in classic works such as that by Hebb (1949) and more recently
by Bakker (1984).
Birth occurs while the majority of neuronal populations are still dif-
ferentiating. As the sine qua non for further brain-behavior development,
birth provides the evolving brain with the environmental context to guide
subsequent maturation. The full-term newborn's brain is a functioning
organ, although historically it was considered to be quiescent. A cardinal
change in all developmental disciplines has been the relatively recent
understanding of the functioning of the neonatal brain. This has entailed
its recognition as more than the modest precursor to the adult brain. The
neonatal brain has matured by birth to encounter the real-time ontogenet-
ic adaptations it must make to ensure continued normative development,
albeit predominantly through relatively more mature reflexive subcortical
systems. These adaptations have been described by Oppenheim (1981)
and Turkewitz and Kenny (1982). Examples of these adaptations are neo-
natal reflexes and modal sensory abilities. Many observed neonatal reflex-
es, once considered to be the primitive features of mature behavior, are
now considered to be prenatal neurobehavioral adaptations to increase
the probability that the fetus will be in the lower-risk, normal vertex birth
position. Likewise, sensory abilities at any given time during develop-
ment are attuned to adaptive ontogenetic requirements for different com-
binations of intramodal and intermodal performances, and are not simply
the immature versions of adult sensory capabilities.
Myelination
Prior to myelination, neuronal communication is characterized by
slow transmission rates and long refractory periods (Bronson, 1982). Al-
though many neuronal populations are structurally mature prior to their
myelination, true functional maturity occurs only after this process of
exogenous axonal sheathing has occurred. The relative rates of myelina-
tion in different brain regions do serve as a rough index of the sequence in
which components of the eNS reach functional adult levels (Yakovlev &
Lecours, 1967), although a myelin sheath is not necessary for conduction
of action potentials and some neuronal populations do not require mye-
lination at all (Bronson, 1982; Purpura & Reaser, 1974). The population of
glial cells that produce myelin have late proliferation periods and mature
postnatally. The bulk of axonal myelination, therefore, occurs during in-
48 ANTHONY H. RISSER and DOROTHY EDGELL
fancy and early childhood. New glia and their myelin product are the
prime factors (along with continued structural differentiation of neuron
populations) that account for the dramatic postnatal growth in the size of
the brain (Bronson, 1982). Brain weight at birth is approximately 350 g,
about one-quarter of approximate adult weight. However, by age 2, brain
weight is approximately 1300 g-close to the adult range of 1400-1500 g.
Myelination, like other dimensions of brain development, proceeds
in a general temporal-spatial pattern. This was noted as early as 1901 by
Flechsig. Yakovlev and LeCours (1967) and LeCours (1975) have provided
a detailed description of human myelogenetic development (Figure 2).
Beginning with the sensory and motor roots of the spinal cord and pro-
ceeding to axons of neurons in "primordial zones," such as the primary
sensorimotor cortical areas, myelination starts prenatally and continues
through early infancy. In the pyramidal tract, for example, the major
efferents from the motor cortex begin to undergo myelination 1 month
prior to birth and are essentially completed by the end of the first year of
life. The slower, postnatal myelination of cortical-subcortical pathways,
callosal fibers, and association cortex Golgi class II interneurons is related
to the gradual emergence of language, cognitive, and motor skills from late
infancy through middle childhood.
Better clinical appreciation of normal (and aberrant) patterns of mye-
FIGURE 2. Myelogenetic cycles of regional maturation in the human brain. (Adapted from
Yakovlev & LeCours, 1967.)
NEUROPSYCHOLOGY OF THE DEVELOPING BRAIN 49
Functional Organization
Postnatally, during periods of continued differentiation and myelina-
tion, brain development is paralleled by elaboration of the organism's
adaptive behavioral repertoire. Exactly how structure and function are
related is unclear, but it appears that the two are mutually dependent.
Structural changes appear in many ways to produce modifications in
behavior, whereas various dimensions of brain structure are shaped, to
some degree, by behavioral experiences that may contribute to individual
differences in brain-behavior patterns (e.g., Greenough & Juraska, 1979).
The traditional topograpical representation of different structural areas on
the lateral and medial surfaces of the brain and their related functions are
illustrated by Brodmann's map of the cytoarchitecture of the cortex (Fig-
ure 3), which defines areas by cell structure and cellular layers. To the
neuropsychologist, units of interest are composed by the functional inte-
gration of these regions. Components of functionally integrated units at-
tain maturity at different rates and at different times during early develop-
ment. As a result, assessment of children depends upon measures that
take into account the pattern of structural and functional maturation at
any given time in a changing, maturing brain.
The "behavioral geography of the brain" (Lezak, 1983, p. 41) reflects
the discipline of adult behavioral neurology and is well presented in
many neuropsychological resources (e.g., Walsh, 1978). One of several
ways to approach this behavioral geography, which incorporates develop-
ment, was presented by Luria (1973). As part of Luria's neuropsychologi-
cal model of three functional units delineating the CNS (Le., arousal,
informational interaction, and programming units), three functional cor-
tical zones may be distinguished and described ontogenetically. These are
the primary, secondary, and tertiary zones.
Primary zones are modality specific and receive input from the
senses or control motor activity. These zones are somatotopically ar-
ranged and possess an abundance of neurons in afferent cell layer IV.
Their characteristic topographical organization and modality specificity
50 ANTHONY H. RISSER and DOROTHY EDGELL
Function
VISION
primary 17
secondary 18.19
AUDITORY
pnmary 41
secondary 22.24
BODY SENSES
prImary 1.2.3
secondary 5.7
SENSORY. TERTIARY 7.21.22.37.39.40
MOTOR
primary 4
secondary 6
eye movement 8
speech 44
MOTOR, TERTIARY 9.10. 11 .45.46.47
Summary
If made more elaborate, this selective overview of the most rapid and
critical periods of growth observed in the developing brain would fall far
afield of the overall focus of this volume. Yet it is during this period of
normal brain development that the bulk of the neural framework for sub-
sequent neuropsychological functioning is created. It is also here, per-
haps, that a subclinical anoxic-ischemic episode or some microstructural
or neurochemical anomaly may set the stage for a neuropsychological
disorder, such as a specific learning disability or an attentional deficit,
that may not be evident until later in childhood.
Proposals of the sort described above have a notable history (Kno-
bloch & Pasamanick, 1966) and have been presented on the basis of selec-
tive neuropathological findings (Fuller, Guthrie, & Alvord, 1983; Towbin,
1971), but they remain speculative. Speculative relations of this type,
tested on a case-study postmortem basis, have gained an invaluable docu-
mentational aid in Galaburda's cytoarchitectonic studies of the
postmortem brains of dyslexic individuals (Galaburda & Eidelberg, 1982;
Galaburda & Kemper, 1979; Galaburda, Sherman, Rosen, Aboitiz, &
Geschwind, 1985). In group analyses, however, such speculative relations
are usually found to account for only a very small portion of outcome
variability. Naeye and Peters (1987), for example, found that the presence
of fetal and perinatal hypoxia accounted for only 2% of IQ variation on the
Wechsler Intelligence Scale for Children (WISC) at age 7. In sum, although
at a tangent to the practical concerns of the clinician, explorations of the
neural side of normal brain-behavior development do, and shall continue
to, contribute to a fuller understanding of normal cognitive and behav-
ioral development and provide a firmer basis for appreciating the signifi-
cance of deviations from normal development.
adult eNS. Although the bulk of the literature addressing this issue has
been delineated in terms of age, it is now recognized that reference to the
age of the eNS may be more confusing than helpful in seeking to under-
stand those eNS mechanisms that account for differences in the develop-
ing versus the mature brain's response to injury. More precisely, damage
to the functionally uncommitted brain may not be the same as damage to
the committed brain (Goldman-Rakic et 01.,1983). Relevant experimental
evidence about the traditional role of age dates back to Stoltmann in 1876
(cited by Goldman-Rakic et 01., 1983) and has generated two heuristic
guidelines about the timing of a brain insult. It also has created an arena
for critical debate about recovery of function following a brain insult
(Isaacson, 1975; Schneider, 1979; St. James-Roberts, 1979).
The two guidelines that have emerged from this literature are the
Kennard principle (Kennard, 1940, 1942) and the Dobbing hypothesis
(Dobbing & Smart, 1974). The ablation studies in monkeys by Kennard
(1942) led to the general conclusion that brain lesions early in life pro-
duced fewer deficits than similar lesions in later life. The Kennard princi-
ple states, therefore, that the degree of impaired function subsequent to
brain damage is proportional to the age at which the injury occurred. The
Dobbing hypothesis, tested extensively upon rat models of adult brain-
behavior consequences of early-life malnutrition or irradiation (Dobbing
& Sands, 1971), states that brain damage during development has its great-
est impact upon those cell populations and/or individual growth param-
eters that show the greatest rate of development at the time of the insult.
Insults occurring during cell proliferation limit the number of cells in the
mature brain; insults during differentiation do not necessarily alter the
number of cells in the brain but do influence cell size-a gross index of
altered cellular architecture (Winick & Rosso, 1969).
Euphemistically, Kennard's principle suggests that earlier rather than
later brain damage would be preferable in sparing function, whereas Dob-
bing's hypothesis suggests the opposite-later, rather than earlier, brain
damage would be preferable to avoid permanent impairment. The fact
that either may have relevance at different levels of analysis (e.g., cellular,
systemic, behavioral) and in different contexts (e.g., language develop-
ment, electrophysiology) points toward an underlying complexity that
evades a simple explanation. The behavioral consequences of brain
damage are made more complex by findings that suggest that plasticity at
a structural level is not necessarily associated with improved function
(Isaacson, 1975).
Perhaps the simplest statement that can be made from an integration
of both rules is that brain damage during infancy and early childhood may
prove less devastating in outcome than damage either during fetal devel-
opment or in the mature brain. The timing of an insult to the developing
brain will influence the nature and extent of any resultant deficit and the
NEUROPSYCHOLOGY OF THE DEVELOPING BRAIN 53
Neuropsychological
Etiologic agent Neural abnormality consequence
"Categories are not meant to be exhaustive in delineation or representative of any classification system.
NEUROPSYCHOLOGY OF THE DEVELOPING BRAIN 55
ical and intellectual features (e.g., Down's and Turner's syndromes) char-
acterize many of the survivable genetic diseases (Robinson & Robinson,
1976). Although the predominant worldwide cause of acquired defective
brain development and neurobehavioral morbidity is protein-calorie mal-
nutrition and its attendant milieu of deprivation and infection (Pollitt &
Thomson, 1977), the most frequent identifiable cause in industrialized
societies is traumatic brain damage. Traumatic brain damage in late infan-
cy and childhood is typically the result of head injuries caused by falls
and motor vehicle or recreational accidents (Annegers, Grabow, Kurland,
& Laws, 1980).
In an earlier era, perinatal brain trauma was a fairly frequent phe-
nomenon. Although medical advances have resulted in a significant de-
crease in birth-related mechanical injury, other frequent perinatal causes
of neural abnormalities usually result from the spectrum of risks associ-
ated with preterm and postterm births. This is particularly true for the
very-Iow-birth-weight (VLBW; defined as a birth weight at or under 1500
g) premature newborn (Levene & Dubowitz, 1982). The VLBW neonate is
at particular risk for periventricular and intraventricular hemorrhages
from the germinal matrix and the choroid plexus (Goddard-Finegold,
1984). Other risks for the premature newborn include anoxic-ischemia,
seizures, infections, and systemic disease. Generally, however, single fac-
tors are less important than combinations of complications in determin-
ing outcome. Although survival rates have improved, neurobehavioral
morbidity is a frequent outcome. Performances of VLBW infants usually
are poorer than normal-birthweight infants on neurobehavioral measures
at follow-up (Kitchen et a1., 1986).
as to suggest that these phenomena are of only limited clinical value for
screening and prediction. Although these are associated with learning
and behavior problems, even on a long-term basis in certain children, they
also are observed frequently in normal children without being correlated
with cognitive deficits or maladaptive outcomes.
Assessing whether the term dysfunctional actually can be employed to
implicate covert aberrant brain function, which can only be detected upon
proper and sensitive (typically neuropsychological) evaluation, has a legit-
imate basis, despite its various controversies (Benton, 1975). Among the
many available works, Taylor et al. (1984) provide a concise review of the
concept of dysfunction in the evolution of developmental neuropsychol-
ogy; a thoughtful paper by Denckla (1978), which addresses key conceptual
concerns, is also of value. One realm of developmental neuropsychological
research has been directed at determining the existence of brain-behavior
relations in the absence of both overt brain damage and a recognized
neurological etiology. Examples of this research include the search for
biochemical explanations of minimal brain damage (Wender, 1971), struc-
tural hemispheric deviations from the range of normative findings in
computed tomography (CT) (Haslam, Dalby, Johns, & Rademaker, 1981;
Hier, LeMay, Rosenberger, & Perla, 1978; LeMay, 1981) and in MRI imaging
data of the brains of dyslexic children (Rumsey et a1., 1986), and the
detailed cytoarchitectonic study of the brains of dyslexics at autopsy (e.g.,
Galaburda & Kemper, 1979).
Another aspect of concern is whether observed dysfunctions are truly
evidence of neurological defects or instead are indicators of a develop-
mental delay. The concept of delayed development infers that there is a
slower rate of maturation of otherwise normal brain regions and behav-
ioral manifestations of brain functioning (Satz, Taylor, Friel, & Fletcher,
1978). Mental retardation in the absence of a genetic or acquired struc-
tural etiology might be considered an example of delayed maturation in
its most severe form. A maturational lag is based on the assumption that
structure and function normally mature according to an identifiable pat-
tern, are hierarchically organized, and develop sequentially by a system of
associated and interrelated components. According to Rodier (1984),
there is little evidence of a genuine delay (Le., a retardation) in brain
morphology. A brain that has sustained injury during development does
not appear immature or "unfinished." Rather, the regions forming during
the injury appear abnormal. The implication of a delay (Le., that at some
point in the future, development will eventually be finished) appears
inappropriate to describe morphologically based dysfunctions.
The concept of delayed maturation has been questioned on the
grounds that if a delay in function is due to a maturational lag, then
psychological development should otherwise be normal, except for the
fact that its timing is off (Knights & Bakker, 1976). However, a 12-year-old
NEUROPSYCHOLOGY OF THE DEVELOPING BRAIN 59
with a reading problem does not read as if he or she were 7 years old.
Research with reading-disabled children suggests that learning strategies
used by these children are not merely delayed but are truly aberrant, thus
suggesting a deficit in skills rather than skill slowness. An early work by
Witelson (1976), for example, posited an association between reading
problems and inadequate hemispheric specialization for both linguistic
and spatial functioning. The same finding appears true for children with
language delays. In addition to a delay in language function, these chil-
dren often are found to show deviant aspects of language function (Men-
yuk, 1978).
A key aspect in the debate about developmental delays is found in the
learning disability follow-up literature. Studies have demonstrated that
although learning-disabled readers may improve their skills somewhat
over time, they continue to be disabled readers, never "catching up" to
their peers in reading skills (Rutter, Tizard, Yule, Graham, & Whitmore,
1976; Satz & Sparrow, 1970; Satz, et al., 1978; Spreen, 1978). In fact, it is
likely that the presence of delay itself may act as an influence upon the
child, thus altering the form and quality of continued growth (Zigler,
1969). Conceivably, a developmental delay could result in faulty organi-
zation of cognitive skills, causing defective and aberrant levels of perfor-
mance. On the other hand, the presence of a frank deficit does not imply
that some gains cannot be anticipated over time or that aggressive inter-
vention may not prove a significant aid in improving the child's abilities
to approximate better adaptive functioning. Validation of an acceptable
construct of delay will await the development of direct measures of in
vivo brain maturation, and a clearer understanding of the relation be-
tween function and brain maturation.
CONCLUSIONS
REFERENCES
Adams, R. D. & Victor, M. (1985). Principles of neurology (3rd ed.). New York: McGraw-Hill.
Annegers, J. F., Grabow, J. D., Kurland, 1. T., & Laws, E. R. (1980). The incidence, causes, and
secular trends of head trauma in Olmsted County, Minnesota, 1935-1974. Neurology,
30, 912-919.
Bakker, D. J. (1984). The brain as a dependent variable. Journal of Clinical Neuropsychology,
6, 1-16.
Barkley, R. A. (1981). Hyperactive children: A handbook for diagnosis and treatment. New
York: Guilford Press.
Benton, A. (1975). Developmental dyslexia: Neurological aspects. Advances in Neurology, 7,
1-27.
Benton, A. (1982). Child neuropsychology: Retrospect and prospect. In J. de Wit & A. Benton
(Eds.), Perspectives in child study: Integration of theory and practice (pp. 41-61). Lisse:
Swets and Zeitlinger.
Boll, T. J., & Barth, J. T. (1981). Neuropsychology of brain damage in children. In S. B.
Filskov & T. J. Boll (Eds.)' Handbook of clinical neuropsychology (pp. 418-452). New
York: Wiley Press.
Bronson, G. (1982). Structure, status and characteristics of the nervous system at birth. In P.
Stratton (Ed.), Psychobiology of the human newborn (pp. 99-114). New York: Wiley
Press.
Bryden, M. P. (1982). Laterality: Functional asymmetry in the intact brain. New York:
Academic Press.
Chelune, G. J., & Edwards, P. (1981). Early brain lesions: Ontogenetic environmental consid-
erations. Journal of Consulting and Clinical Psychology, 49, 777-790.
Chi, J. G., Dooling, E. C., & Gilles, F. H. (1977). Gyral development of the human brain.
Annals of Neurology, 1, 86-93.
Corballis, M. C., & Morgan, M. J. (1978). On the biological basis of human laterality: 1.
Evidence for a maturational left-right gradient. Behavioral and Brain Sciences, 2, 261-
336.
Cotman, C. W., & Nieto-Sampedro, M. (1982). Brain function, synapse renewal, and plas-
ticity. Annual Review of Psychology, 33, 371-401.
Cotman, C. W., & Nietro-Sampedro, M. (1984). Cell biology of synaptic plasticity. Science,
225, 1287-1294.
Cowan, W. M., Fawcett, J. W., O'Leary, D. D. M., & Stanfield, B. B. (1984). Regressive events
in neurogenesis. Science, 225, 1258-1265.
Denckla, M. B. (1978). Minimal brain dysfunction. In J. S. ChaJl & A. F. Mirsky (Eds.),
Education and the brain, 77th yearbook of the National Society for the Study of Educa-
tion (pp. 223-268). Chicago: University of Chicago Press.
DiSimoni, F. (1978). The Token Test for Children, manual. Hingham, MA: Teaching Re-
sources Corp.
Dobbing, J., & Sands, J. (1971). Vulnerability of developing brain: IX. The effect of nutritional
growth retardation on the timing of the brain growth spurt. Biology of the Neonate, 19,
363-378.
NEUROPSYCHOLOGY OF THE DEVELOPING BRAIN 61
Dobbing, J., & Smart, J. L. (1974). Vulnerability of developing brain and behavior. British
Medical Journal, 30, 164-168.
Elliott, H. (1969). Textbook of anatomy. Philadelphia: Lippincott.
Flechsig, P. (1901). Developmental (myelogenetic) localization in the cerebral cortex of the
human subject. Lancet, 2, 1027-1029.
Fuller, P. W., Guthrie, R. D., & Alvord, E. C. (1983). A proposed neuropathological basis for
learning disabilities in children born prematurely. Developmental Medicine and Child
Neurology, 25, 214-231.
Gaddes, W. H. (1985). Learning disabilities and brain function: A neuropsychological ap-
proach (2nd ed.). New York: Springer-Verlag.
Gaddes, W. H., & Crockett, D. J. (1973). The Spreen-Benton aphasia tests, normative data as
a measure of normal language development (Research Monograph No. 25). Victoria, BC:
University of Victoria.
Galaburda, A. M., & Eidelberg, D. (1982). Symmetry and asymmetry in the human posterior
thalamus. II. Thalamic lesions in a case of developmental dyslexia. Archives of Neu-
rology, 39, 333-336.
Galaburda, A. M., & Kemper, T. L. (1979). Cytoarchitectonic abnormalities in developmental
dyslexia: A case study. Annals of Neurology, 6, 94-100.
Galaburda, A. M., Sherman, G. F., Rosen, G. D., Aboitiz, F., & Geschwind, N. (1985). Devel-
opmental dyslexia: Four consecutive patients with cortical anomalies. Annals of Neu-
rology, 18, 222-233.
Gazzaniga, M. S., Stein, D., & Volpe, E. T. (1979). Functional neuroscience. New York:
Harper & Row.
Geschwind, N., & Galaburda, A. M. (1985a). Cerebrallateralization: Biological mechanisms,
associations, and pathology. A hypothesis and a program for research. Archives of
Neurology, 42, 428-459.
Geschwind, N., & Galaburda, A. M. (1985b). Cerebrallateralization: Biological mechanisms,
associations, and pathology. A hypothesis and a program for research. Archives of
Neurology, 42, 521-552.
Geschwind, N., & Galaburda, A. M. (1985c). Cerebrallateralization: Biological mechanisms,
associations, and pathology. A hypothesis and a program for research. Archives of
Neurology, 42, 634-654.
Goddard-Finegold, J. (1984). Periventricular, intraventricular hemorrhages in the premature
newborn: Update on pathologic features, pathogenesis, and possible means of preven-
tion. Archives of Neurology, 41, 766-771.
Goldman, P. S. (1979). Development and plasticity of frontal association cortex in the in-
frahuman primate. In C. L. Ludlow & M. E. Doran-Quine (Eds.). The neurological bases
of language disorders in children: Methods and directions for research (NIH Publication
No. 79-440) (pp. 1-16). Washington, DC: U.S. Government Printing Office.
Goldman, P. S., & Galkin, T. W. (1978). Prenatal removal of frontal association cortex in the
fetal rhesus monkey: Anatomical and functional consequences in postnatal life. Brain
Research, 152, 451-485.
Goldman-Rakic, P., Isserhoff, A., Schwartz, M. L., & Bugbee, N. M. (1983). The neurobiology
of cognitive development. In M. M. Haith & J. J. Campos (Eds.). Infancy and develop-
mental psychobiology; Vol. 2 of P. H. Mussen (Ed.). Handbook of child psychology (4th
ed., pp. 281-344). New York: Wiley Press.
Greenough, W. T., & Juraska, J. M. (1979). Experience-induced changes in brain fine struc-
ture: Their behavioral implications. In M. E. Hahn, C. Jensen, & B. C. Dudek (Eds.).
Development and evolution of brain size (pp. 295-320). New York: Academic Press.
Haslam, R. H. A., Dalby, J. T., Johns, R. D., & Rademaker, A. W. (1981). Cerebral asymmetry
in developmental dyslexia. Archives of Neurology, 38, 679-682.
Hebb, D. O. (1949). Organization of behavior. New York: Wiley Press.
62 ANTHONY H. RISSER and DOROTHY EDGELL
Hier, D. B., LeMay, M., Rosenberger, P. B., & Perlo, V. P. (1978). Developmental dyslexia:
Evidence for a subgroup with a reversal of cerebral asymmetry. Archives of Neurology,
35, 90-92.
Isaacson, R. L. (1975). The myth of recovery from early brain damage. In N. R. Ellis (Ed.),
Aberrant development in infancy (pp. 1-25). Potomac: Erlbaum.
Jacobsen, c. F. (1936). Studies of cerebral function in primates. Comparative Psychological
Monographs, 13, 1-68.
Jacobson, M. (1978). Developmental neurobiology (2nd ed.). New York: Plenum Press.
Johnson, M. A., Pennock, J. M., Bydder, G. M., Dubowitz, L. M. S., Thomas, D. J., & Young,l.
R. (1987). Serial MR imaging in neonatal cerebral injury. American Journal of Neu-
roradiology, 8, 83-92.
Kandel, E. R. & Schwartz, J. H. (1981). Principles of neural science. New York: Else-
vier/North-Holland.
Kennard, M. A. (1940). Relation of age to motor impairment in man and subhuman primates.
Archives of Neurology and Psychiatry, 44, 377-397.
Kennard, M. A. (1942). Cortical reorganization of motor function: Studies on series of
monkeys of different ages from infancy to maturity. Archives of Neurology and Psychia-
try, 47, 227-240.
Kitchen, W. H., Rickards, W. H., Ryan, M. M., Ford, G. W., Lissenden, J. V., & Boyle, L. W.
(1986). Improved outcome to two years of very low birthweight infants: Fact or artifact.
Developmental Medicine and Child Neurology, 28, 579-588.
Knights, R. M., & Bakker, D. J. (Eds.). (1976). The neuropsychology of learning disorders:
Theoretical approaches. Baltimore: University Park Press.
Knobloch, H., & Pasamanick, B. (1966). Prospective studies on the epidemiology of re-
productive casualty: Methods, findings, and some implications. Merrill-Palmer Quar-
terly of Behaviour and Development, 12, 27-43.
Kopp, C. B. (1983). Risk factors in development. In M. M. Haith & J. J. Campos (Eds.), Infancy
and developmental psychobiology; Vol. 2 of P. H. Mussen (Ed.), Handbook of child
psychology (4th ed., pp. 1081-1188). New York: Wiley Press.
Kopp, C. B., & Parmelee, A. H. (1979). Prenatal and perinatal influences on infant behavior.
In J. Osofsky (Ed.), Handbook on infant behavior (pp. 29-74). New York: Wiley-
Interscience.
LeCours, A. R. (1975). Myelogenetic correlates of the development of speech and language.
In E. H. Lenneberg & E. Lenneberg (Eds.), Foundations of language development: A
multidisciplinary approach (Vol. 1, pp. 121-135). New York: Academic Press.
Lee, B. C. P., Lipper, E., Nass, R., Ehrlich, M. E., deCiccio-Bloom, E., & Auld, P. A. M. (1986).
MRI of the central nervous system in neonates and young children. American Journal of
Neuroradiology, 7, 605-616.
LeMay, M. (1981). Are there radiological changes in the brains of individuals with dyslexia?
Bulletin of the Orton Society, 31, 135-141.
Lemire, R. J., Loeser, J. D., Leech, R. W., & Alvord, E. C. (1975). Normal and abnormal
development of the human nervous system. New York: Harper & Row.
Levene, M. I., & Dubowitz, L. M. S. (1982). Low-birth-weight babies long-term follow-up.
British Journal of Hospital Medicine, 24, 487-491.
Lezak, M. (1983). Neuropsychological assessment (2nd ed.). New York: Oxford Press.
Lund, R. D. (1978). Development and plasticity of the brain: An introduction. New York:
Oxford Press.
Luria, A. R. (1973). The working brain: An introduction to neuropsychology. Middlesex:
Penguin Press.
McArdle, C. B., Richardson, C. J., Nicholas, D. A., Mirfakhree, M., Hayden, C. K., & Amparo,
E. G. (1987). Developmental features of the neonatal brain: MR imaging: Part I. Gray-
white matter differentiation and myelination. Radiology, 162, 223-229.
NEUROPSYCHOLOGY OF THE DEVELOPING BRAIN 63
Tarter & G. Goldstein (Eds.), Advances in clinical neuropsychology (Vol. 2, pp. 1-62).
New York: Plenum Press.
Winick, M., & Rosso, P. (1969). The effect of severe early malnutrition on cellular growth of
human brain. Pediatric Research, 3, 181-187.
Witelson, S. F. (1976). Abnormal right hemisphere specialization in developmental dyslexia.
In R. M. Knights & D. J. Bakker (Eds.), The neuropsychology of learning disorders:
Theoretical approaches (pp. 233-256). Baltimore: University Park Press.
Witelson, S. F. (1977). Early hemisphere specialization and interhemisphere plasticity: An
empirical and theoretical review. In S. J. Segalowitz & F. A. Gruber (Eds.), Language
development and neurological theory (pp. 213-287). New York: Academic Press.
Yakovlev, P. 1., & LeCours, A. R. (1967). The myelogenetic cycles of regional maturation of
the brain. In A. Minkowski (Ed.), Regional development of the brain in early life (pp. 3-
69). Oxford: Blackwell Scientific.
Zigler, E. (1969). Development versus difference theories of mental retardation and the
problem of motivation. American Journal of Mental Deficiency, 73, 536-556.
3
INTRODUCTION
ERIN D. BIGLER Austin Neurological Clinic, Austin, Texas, and Department of Psychol-
ogy, University of Texas at Austin, Austin, Texas.
67
68 ERIN D. BIGLER
Basic Components
The pediatric neurological exam (PNE) naturally varies with the age
of the child. For the purpose of this chapter, the neurological exam out-
lined will be based on the child 4 years of age and older since it is at this
age that the exam begins to take on the characteristics of the more formal,
systematic exam of the adolescent or adult patient (Hartlage & Krawiecki,
1984). In general, the components of the exam include an evaluation of
gait and station, motor and sensory function, reflex integrity, and physical
development, along with a brief overview of mental status. These topic
areas will be briefly reviewed below.
Motor Function
Muscle tone and strength are tested by the child's strength of grip and
limb strength resistence in various positions of the extremities. Muscle
NEUROPSYCHOLOGICAL AND OTHER TYPES OF ASSESSMENT 69
Sensory-Perceptual Function
Simple touch usually is tested by the child's ability to report light
touch. Two-point tactile discrimination is another test of simple tactile
perception. By the time a child is 6 years of age, formal testing of stereog-
nosis (tactile perception of a coin, paper clip, or key placed in the palm of
the hand) also can be undertaken. By 8 years of age, formal graphesthesic
perception can be tested using letters or numbers "written" on the palm
or fingertips (Herskowitz & Rosman, 1982). These tests, along with the
perception of double simultaneous tactile stimulation, constitute the as-
70 ERIN D. BIGLER
~
en
~
t""
'-l
....
TABLE 2. Anomaly Grading Scale of the Yale
Neuropsychoeducational Assessment Scales
Hair: Frontal bossing:
Whorls: (1) lor a line '3 1" long)
Electric hair: (Normal) (Fine: soon awry) (Very
fine; will not comb)
Coarse, brittle:
Eyes: Strabismus:
Ptosis:
Crusting of lid:
Epicanthus: (absent) (partial) (deep)
Ears: Malformed
Asymmetric:
Pits or tags:
Soft and pliable:
Low set (above) (';;0.5 cm below) (>0.5 cm below)
line through nosebridge and eye
Lobe extension: (below attachment) (straight back)
(toward crown)
Nose: Antiverted nostrils:
Hypoplastic tip:
Hypoplastic philtrum:
Mouth: Palate: (normal arch) (flat steeple ri,) (high
steeplerl)
Cleft palate-soft or hard:
Tongue furrowed:
Tongue with smooth-rough spots:
Teeth-enamel hypoplasia; carious:
Teeth small:
Upper vermillion thin:
Jaw: Prominent maxilla:
Micrognathia:
Prognathia:
Midfacial hypoplasia:
Torso: Webbed neck:
Pectus excavatum:
Pectus carinatum:
Nipples widely spaced:
Heart murmur:
Vertebral defects:
Hernia-umbilical, diaphragm, groin;
diastasis recti
Hypospadias:
Skin: Thin skin-visible vascular pattern:
Dry, coarse, rough:
Cafe-au-lail:
Hemangiomata:
Nails-hypoplastic or dysplastic:
Hands: Palm-coarse skin:
Palm-single transverse crease:
Small, broad hands:
Thin, tapering hands:
Joint limitation:
Clinodactyly:
Broad first toe or thumb:
Feet: Gap between first and second toes:
Partial syndactylia of 2nd and 3rd toes:
Length of 2nd and third toes:
(2nd> 3rd) (2nd = 3rd) (2nd < 3rd)
NEURORADIOLOGICAL TESTS
FIGURE 1. MRI and CT depictions of neuroanatomy. The MRI scan on top is taken in the
sagittal plane and depicts normal brain anatomy. Major anatomic structures are labeled
numerically (l-corpus callosum. 2-fornix. 3-thalamus, 4-hypothalamus, 5-mamillary bodies,
6-tegmentum, 7-tectum, 8-aqueduct of Sylvius, 9-fourth ventricle, 10-pons, ll-cerebellum,
12-frontal lobe, 13-parietal lobe, 14-occipitallobe, 15-temporallobe). Note the clarity and
resolution that can be obtained with MRI imaging. The CT scan on the bottom is in the
horizontal plane. This patient was an 18-year-old male who had suffered a severe head
injury 1 year prior to the CT. This scan was selected because it demonstrates frontal atrophy
and ventricular enlargement, which permits better visualization of some of the major ana-
tomi~ structures that are labeled numerically in the adjacent drawing (l-frontal lobe, 2-
interhemispheric fissure, 3-anterior horn, lateral ventricle, 4-caudate nucleus, 5-internal
capsule, 6-thalamus, 7-putamen/globus pallidus complex, 8-third ventricle, 9-posterior
horn, lateral ventricle, 10-Sylvian fissure, ll-temporallobe, 12-occipitallobe.
genital porencephaly (see Figure 6), and a host of other childhood disor-
ders (see Bigler, 1984).
With the advent of these techniques, there was a period of great
optimism concerning the advancement of "lesion-localization" work ex-
amining specific functions of specific brain regions (Kertesz, 1983). Prior
ELECTRODIAGNOSTIC TESTS
ished. For example, a focal abnormality may alter the EEG in such a
fashion as to produce predominantly delta waves in that region, with
other recording sites displaying relatively normal activity. This would be
contrasted with diffuse slowing of the EEG, which would be seen in
generalized disorders (see Figure 8; Kiloh, McComas, & Osselton, 1979).
The clinical parameters of pediatric EEG have been well established
for over two decades (Kiloh et al. 1979). However, despite numerous
studies examining the relationship between EEG variables and neuropsy-
chological features, the results have generally lacked specificity (Brandeis
& Lehmann, 1986; Capute, Niedermeyer, & Richardson, 1968; Hughes,
1971; Hughes & Denckla, 1978). Although there is a greater incidence of
EEG abnormalities in children with learning disability, hyperactivity, psy-
chiatric disorder, and developmental deficits (Golden, 1982), there are no
distinctive EEG findings that are diagnostic of such conditions. The case
illustrated in Figure 8 is representative of this problem.
Evoked potential (EP) testing may reveal the intactness of visual,
auditory, and somatosensory pathways, and such findings may be useful
in cerebral localization studies (Luders, Dinner, Lesser, & Morris, 1986).
FIGURE 8. EEG in a 12-year-old right-handed male patient with a history of learning disor-
der. Asynchronous slow-wave (underlined) activity in the fight parietal region is noted. This
type of irregularity is seen with greater frequency in children with minor neurological
abnormalities. It does not indicate any specific abnormality and is not epileptogenic. Such
abnormalities frequently do not relate to any specific neurological or neuropsychological
pattern. In this child his neuropsychological studies suggested language-based deficits that
would implicate posterior left hemisphere dysfunction, but, as indicated, the EEG abnormal-
ity was in the right parietal region. Thus, such EEG abnormalities are a variant from normal
but do not necessarily correlate with the type of neuropsychological impairment present,
only with the presence of such impairment.
82 ERIN D. BIGLER
PATIENT
PSYCHOLOGICAL ASSESSMENT
usually spared at the expense of nonverbal skills (see also Bigler & Naugle,
1984).
Accordingly, some neuropsychological inferences can and should be
made from WISC-R results. However, the WISC-R is incomplete from the
neuropsychological perspective because it does not provide a direct as-
sessment of specific motor or sensory abilities, only incompletely assesses
language, and provides no in-depth assessment of memory. Thus, al-
though the WISC-R (like other measures of intelligence) is extremely valu-
able and worthwhile in the assessment of the child, it can be viewed only
as an adjunct to a comprehensive neuropsychological test battery. Such a
battery should assess cortical function in a thorough fashion, fully exam-
ining motor, sensory-perceptual, spatial-perceptual, memory (both verbal
and nonverbal), graphomotor, language, and cognitive functions.
Recently, the Kaufman Assessment Battery for Children (K-ABC) was
developed to overcome some of these problems (Kaufman & Kaufman,
1983). Instead of the Verbal-Performance schema, the K-ABC used the
dichotomy of simultaneous versus sequential/successive processing. This
differentiation is based, in part, on Luria's (1973) research that suggested
sequential processing to be primarily a frontotemporal activity and simul-
taneous processing to be more related to parietoccipital functioning. How-
ever, in preliminary studies (Morris & Bigler, 1987) the results are equiv-
ocal at this point in terms of the advantages of this measure over the
WISC-R in children with neurological disorders. Morris and Bigler found
that the K-ABC Simultaneous Processing score demonstrated greater sen-
sitivity for a variety of nonverbal, spatial-perceptual-motor deficits than
did the PIQ measure from the WISC-R. However, this did not hold up for
the Sequential score, with the WISC-R VIQ measures demonstrating a
greater sensitivity for verbal-language deficits in neurologically impaired
children.
Thus, traditional intellectual assessment methods yield only partial
neuropsychological information. Accordingly, these methods should be
considered as only a subset and not a substitute for the more complete
neuropsychological assessment. This is certainly well demonstrated by
the case illustrated in Figure 6. In this case, the child had shown average
intellectual ability over a span of 4 years, with no significant VIQ-PIQ
difference, despite the absence of two-thirds of her left cerebral hemi-
sphere. However, she did have a moderate right-sided spastic hemiplegia
and tactile sensory loss.
CONCLUSIONS
sitive (or more sensitive) and less invasive than other techniques for as-
sessing "organic" dysfunction (Small, 1980). However, with the diag-
nostic improvements in neuroradiology and electrophysiology, as well as
the better understanding of minor neurological abnormalities in relation
to a variety of neurobehavioral disorders, neuropsychology must continue
to integrate its clinical findings in relation to these other areas. To that
end, this chapter has attempted to integrate neuropsychological test find-
ings in children with other assessment techniques. Despite certain limita-
tions, particularly with respect to children, neuropsychological assess-
ment techniques remain the best functional assessment tools for the
evaluation of higher cortical functioning. They provide a crucial perspec-
tive that should be integrated with other neurodiagnostic and psychologi-
cal procedures in gaining a comprehensive understanding of the neu-
rologically impaired child.
REFERENCES
Beery, K. E. (1967). Developmental Test of Visual-Motor Integration. Chicago: Follett Educa-
tional Corporation.
Bender, 1. A. (1938). A visual motor gestalt test and its clinical use (Research Monographs,
3). New York: American Orthopsychiatric Association.
Bigler, E. D. (1980). Neuropsychological assessment and brain scan results: A case study
approach. Clinical Neuropsychology, 2, 13-24.
Bigler, E. D. (1984). Diagnostic clinical neuropsychology. Austin: University of Texas Press.
Bigler, E. D., & Ehrfurth, J. W. (1981). The continued inappropriate singular use of the Bender
Visual Motor Gestalt Test. Professional Psychology, 12, 562-569.
Bigler, E. D., Hubler, D. W., Cullum, C. M., & Turkheimer, E. (1985). Intellectual and memory
impairment in dementia: CT volume correlations. Journal of Nervous and Mental Dis-
ease, 173. 347-352.
Bigler, E. D., & Naugle, R. I. (1984). Case studies in cerebral plasticity. International Journal
of Clinical Neuropsychology, 7, 12-23.
Boll, T., & Barth, J. T. (1981). Neuropsychology of brain damage in children. In S. B. Filskov
& T. J. Boll (Eds.)' Handbook of clinical neuropsychology (pp. 418-452). New York:
Wiley.
Brandeis, D., & Lehmann, D. (1986). Event-related potentials of the brain and cognitive
processes: Approaches and applications. Neuropsychologia, 24, 151-168.
Brown, S. B. (1982). Neurologic examination of the older child. In K. F. Swaiman & F. S.
Wright (Eds.), The practice of pediatric neurology (pp. 110-129). St. Louis: C. V. Mosby.
Capute, A. J., Neidermeyer, E. F. 1., & Richardson, F. (1968). The EEG in children with
minimal cerebral dysfunction. Pediatrics, 41,1104-1114.
Carr, A. C. (1985). Psychological testing of personality. In H. I. Kaplan & B. J. Sadock (Eds.),
Comprehensive textbook of psychiatry (4th ed., pp. 514-535). New York: Williams &
Wilkins.
Courchesne, E., Kilman, B. A., Galambos, R., & Lincoln, A. J. (1984). Autism: Processing of
novel auditory information assessed by event-related potentials. Electroencephalogra-
phy and Clinical Neurophysiology: Evoked Potentials, 59, 238-248.
Cullum, C. M., & Bigler, E. D. (1986). Ventricle size, cortical atrophy and the relationship
with neuropsychological status in closed head injury: A quantitative analysis. Journal of
Clinical and Experimental Neuropsychology, 8, 437-452.
NEUROPSYCHOLOGICAL AND OTHER TYPES OF ASSESSMENT 89
Delis, D. C., Kramer, J. H., Kaplan, E., & Ober, B. A. (1986). The California Verbal Learning
Test. Orlando, FL: Harcourt Brace Jovanovich.
Dileo, J. H. (1983). Interpreting children's drawings. New York: Brunner/Maze!'
Duckett, S. (1981). Neuropathological aspects: I. Congenital malformations. In P. Black (Ed.),
Brain dysfunction in children: Etiology. diagnosis and management (pp. 17-46). New
York: Raven Press.
Duffy, F. H., Denckla, M. B., Bartels, D. H., & Sandini, G. (1980). Dyslexia: Regional dif-
ferences in brain electrical activity by topographic mapping. Annals of Neurology, 7,
412-420.
Duffy, F. H., & McAnulty, G. B. (1985). Brain electrical activity mapping (BEAM): The search
for a physiological signature of dyslexia. In F. H. Duffy & N. Geschwind (Eds.), Dyslexia:
A neuroscientific approach to clinical evaluation (pp. 105-122). Boston: Little, Brown.
Dworkin, P. H. (1985). Learning and behavioral problems of schoolchildren. Philadelphia:
W. B. Saunders.
Gaddes, W. H. (1985). Learning disabilities and brain function (2nd ed.). New York: Spring-
er-Verlag.
Galaburda, A. M. (1984). Anatomical asymmetries. In N. Geschwind & A. M. Galaburda
(Eds.), Cerebral dominance (pp. 11-25). Cambridge, MA: Harvard University Press.
Golden, G. S. (1982). Neurobiological correlates of learning disabilities. Annals of Neu-
rology, 12,409-418.
Harris, D. B. (1963). Children's drawings as a measure of intellect. New York: Harcourt Brace
& World.
Hartlage, P. L., & Krawiecki, N. S. (1984). The neurological assessment of children. In R. E.
Tarter & G. Goldstein (Eds.), Advances in clinical neuropsychology (Vol. 2, pp. 63-77).
New York: Plenum Press.
Heiss, W. D., Herholz, K., Pawlik, G., Wagner, R., & Wienhard, K. (1986). Positron emission
tomography in neuropsychology. Neuropsychologia, 24, 141-149.
Herskowitz, J., & Rosman, N. P. (1982). Pediatrics, neurology and psychiatry-Common
ground. New York: Macmillan.
Hughes, J. R. (1971). EEG and learning disabilities. In H. R. Myckleburst (Ed.), Progress in
learning disabilities (Vo!. 2, pp. 196-223). New York: Grune and Stratton.
Hughes, J. R., & Denckla, M. B. (1978). Outline of a pilot study of electroencephalographic
correlates of dyslexia. In A. L. Benton & D. Pearl (Eds.), Dyslexia: An appraisal of
current knowledge (pp. 217-245). New York: Oxford University Press.
John, E. R., Karmel, B. Z., Corning, W. D., Easton, P., Brown, D., Ahn, H., John, M., Harmony,
T., Prichep, L., Toro, A., Garson, I., Bartlett, F., Thatcher, R.,Kaye, H., Valdes, P. &
Schwartz, E. (1977). Neurometrics. Science, 196. 1393-1410.
Kaufman, A. S., & Kaufman, N. L. (1983). Kaufman Assessment Battery for Children. Circle
Pines. MN: American Guidance Service.
Kaufman, A. S., Long, S. W., & O'Neal, M. R. (1986). Topical review of the WISC-R for
pediatric neuroclinicians. Journal of Child Neurology. 1,89-98.
Kaufman, D. M. (1981). Clinical neurology for psychiatrists. New York: Grune and Stratton.
Kemper, T. L. (1984). Asymmetrical lesions in dyslexia. In N. Geschwind & A. M. Galaburda
(Eds.), Cerebral dominance (pp. 75-89). Cambridge, MA: Harvard University Press.
Kertesz, A. (1983). Localization in neuropsychology. New York: Academic Press.
Kiloh, L. G., McComas, A. J., & Osselton, J. W. (1979). Clinical electroencephalography.
London: Butterworths.
Klorman, R., Salzman, L. F., Bauer, L. 0., Coons, H. W., Borgstedt, A. D., & Halpern, W. I.
(1983). Effects of two doses of methylphenidate on cross-situational and borderline
hyperactive children's evoked potentials. Electroencephalography and Clinical Neu-
rophysiology, 56, 169-185.
Krahn, G. L. (1985). The use of projective assessment techniques in pediatric settings. Jour-
nal of Pediatric Psychology, 10. 179-193.
90 ERIN D. BIGLER
Lacks, P. (1984). Bender Gestalt screening for brain dysfunction. New York: Wiley-Inter-
science.
Lezak, M. D. (1983). Neuropsychological assessment. New York: Oxford University Press.
Luders, H., Dinner, D. S., Lesser, R P., & Morris, H. H. (1986). Evoked potentials in cortical
localization. Journal of Clinical Neurophysiology, 3, 75-84.
Luria, A. R (1973). The working brain. London: Penguin Press.
Morris, J. M., & Bigler, E. D. (1987). Hemispheric functioning and the K-ABC: Results in
neurologically impaired children. Developmental Neuropsychology, 3, 67-79.
Nauta, W. J. H., & Feirtag, M. (1986). Fundamental neuroanatomy. New York: W. H.
Freeman.
Nussbaum, N. L., & Bigler, E. D. (1986). Neuropsychological and behavioral profiles of
empirically derived subgroups of learning disabled children. International Journal of
Clinical Neuropsychology, 7, 82-89.
Nussbaum, N. L., Bigler, E. D., & Koch, W. (1986). Neuropsychologically derived subgroups
of learning disabled children: Personality/behavioral dimensions. Journal of Research
and Development in Education, 19, 57-67.
O'Donohoe, N. V. (1981). Epilepsies of childhood. London: Butterworths.
Oldendorf, W. H. (1980). The quest for an image of brain. New York: Raven Press.
PassIer, M. A., Isaac, W., & Hynd, G. W. (1985). Neuropsychological development of behav-
ior attributed to frontal lobe functioning in children. Developmental Neuropsychology,
1, 349-370.
Raven, J. C. (1965). The Coloured Progressive Matrices Test. London: H. K. Lewis.
Rie, H. E., & Rie, E. D. (1980). Handbook of minimal brain dysfunction. New York: Wiley.
Risberg, J. (1986). Regional cerebral blood flow in neuropsychology. Neuropsychologia, 24,
135-140.
Riva, D., & Cazzaniga, L. (1986). Late effects of unilateral brain lesions sustained before and
after age one. Neuropsychologia, 24, 423-428.
Rourke, B. P., Bakker, D. J., Fisk, J. L., & Strang, J. D. (1983). Child neuropsychology. New
York: Guilford Press.
Schimschock, J. R, Milford-Cooley, M., & Cooley, N. (1984). Practical management of chil-
dren with apparent learning disabilities. Neurologic clinics. Philadelphia: W. B.
Saunders.
Scott, L. H. (1981). Measuring intelligence with the Goodenough-Harris Test. Psychological
Bulletin, 89, 483-505.
Shafer, S. Q., Shaffer, D., O'Connor, P. A., & Stokman, C. J. (1983). Hard thoughts on neu-
rological "soft signs." In M. Rutter (Ed.), Developmental neuropsychiatry (pp. 133-
143). New York: Guilford Press.
Shaffer, D., O'Connor, P. A., Shafer, S. Q., & Propis, S. (1983). Neurological "soft signs":
Their origins and significance for behavior. In M. Rutter (Ed.), Developmental neurop-
sychiatry (pp. 144-163). New York: Guilford Press.
Shaffer, D., Schonfeld, 1., O'Connor, P. A., Stokman, C., Trautman, P., Shafer, S., & Ng, S.
(1985). Neurological soft signs, their relationship to psychiatric disorder and intel-
ligence in childhood and adolescence. Archives of General Psychiatry, 42, 342-352.
Shaywitz, S. E. (1982). The Yale Neuropsychoeducational Assessment Scales. Schizo-
phrenia Bulletin, 8, 360-424.
Small, L. (1980). Neuropsychodiagnosis in psychotherapy (2nd ed.). New York: Brun-
ner/Mazel.
Touwen, B. C. L. (1979). Examination of the child with minor neurological dysfunction (2nd
ed.). Philadelphia: J. B. Lippincott.
Van Allen, M. W. (1969). Pictorial manual of neurologic tests. Chicago: Year Book Medical
Publishers.
Visser, S. L., Njiokiktjien, Ch. J., & De Rijke, W. (1982). Neurological condition at birth in
NEUROPSYCHOLOGICAL AND OTHER TYPES OF ASSESSMENT 91
relation to the electroencephalogram (EEG) and visual evoked potential (VEP) at the age
of 5. Electroencephalography and Clinical Neurophysiology, 54, 458-468.
Wechsler, D. (1949). Wechsler Intelligence Scale for Children. New York: Psychological
Corporation.
Wechsler, D. (1974). Wechsler Intelligence Scale for Children-Revised. New York: Psycho-
logical Corporation.
Whelihan, W. M., & Lesher, E. L. (1985). Neuropsychological changes in frontal functions
with aging. Developmental Neuropsychology, 1, 371-380.
Williams, R., & Caviness, V. S. (1984). Normal and abnormal development of the brain. In R.
E. Tartar & G. Goldstein (Eds.), Advances in clinical neuropsychology (Vol. 2, pp. 1-62).
New York: Plenum Press.
4
93
94 W. GRANT WILLIS
DIAGNOSTIC MODELS
Data-Diagnosis Contingency
In order to know how useful a particular source of assessment data is
in terms of arriving at some diagnosis, clinicians must first understand the
relationship (Le., contingency) between those data and the diagnosis. For
actuarial models, the contingency between assessment data and the diag-
nostic decision is estimated through statistical techniques. These tech-
niques are typically multivariate in nature and may include, for example,
discriminant analysis, multiple regression, and cluster analysis. Because
data-diagnosis contingencies are established empirically, the probability
of making an accurate diagnostic prediction can be determined and subse-
quently evaluated by the clinician. In contrast, for clinical models, the
contingency between assessment data and the diagnostic decision is esti-
NEUROPSYCHOLOGICAL DIAGNOSIS WITH CHILDREN 95
Consideration of Data
A second distinction between the models concerns the ways in which
different sources of assessment data are considered. For actuarial models,
data are considered simultaneously whereas in clinical models, data are
typically considered independently. Because different sources of assess-
ment data are usually interrelated (i.e., they are not truly independent),
each source does not contribute entirely unique information to the diag-
nostic prediction. Thus, independent consideration of data frequently
leads to diagnostic errors.
For example, if the degree of contingency between a particular neuro-
psychological sign (e.g., a test result) and a diagnosis is 0.7, then, in the
absence of any other information about the patient, the clinician knows
0.7 2 x 100% or 49% of the total amount of information that is necessary in
order to make a completely accurate diagnosis. It does not follow, howev-
er, that given another neuropsychological sign (e.g., age-inappropriate
gait), for which the contingency with the diagnosis is say 0.4, that the
clinician now knows 49% + 0.4 2 X 100%, or 65%, of the information
required for certainty with respect to the diagnosis. Rather, the actual
proportion of diagnostic information that the clinician has obtained is
reduced by an amount that corresponds to the degree that the neuropsy-
chological signs are themselves interrelated. These intercorrelations are
accounted for when data integration is accomplished statistically. When
data integration is accomplished clinically, however, the intercorrelations
among neuropsychodiagnostic signs must be estimated. The difficulty of
these estimations, of course, increases dramatically with the number of
signs considered and is rarely undertaken in clinical practice.
96 W. GRANT WILLIS
ACTUARIAL MODELS
Methods
There are numerous statistical methods that can be used to derive
actuarial diagnostic rules, but three of the most popular methods are
discriminant analysis, multiple regression, and cluster analysis (see
Huberty, 1975, 1984; McDermott, 1982; Pedhazur, 1982; Tryon & Bailey,
1970). In all of these statistical methods, the variability among multiple
sources of assessment data is analyzed.
In order to use discriminant analysis and multiple regression meth-
ods to derive an actuarial diagnostic rule, particular diagnostic outcomes
must be specified prior to the analysis. For discriminant analysis meth-
ods, these outcomes are scaled in nominal units (e.g., diagnostic classifi-
cations), and the result of the analysis is an equation that indicates how
the various sources of assessment data should be weighted and combined
in order to discriminate maximally among the outcomes. Subsequently,
clinicians can evaluate an empirically derived probability that suggests
how closely a particular pattern of assessment data collected from a pa-
tient corresponds to similar data collected from some previously diag-
nosed group. For multiple regression methods, outcomes may be scaled in
metric units; consequently, degrees of some criterion (e.g., level of impair-
ment or prognostic information) can be predicted from the combined
assessment data. The result of a multiple regression analysis is an equa-
tion that indicates how the various sources of assessment data should be
weighted and combined in order to best predict the degree of some out-
come of interest.
98 W. GRANT WILLIS
Base-Rate Considerations
When an actuarial diagnostic rule is published, the hit rate is usually
presented as an index of that rule's accuracy. For example, Selz and
Reitan (1979; see also Reitan, 1984) developed an actuarial rule to classify
children aged 9 through 14 as normal, learning-disabled, or brain-dam-
aged; their data are presented in Table 1. There were 25 children in each
group who had been diagnosed independently according to the criteria for
these categories. Using only the actuarial rule, 24 of the 25 normal chil-
dren were correctly classified, 14 of the 25 learning-diasbled children
were correctly classified, and 17 of the 25 brain-damaged children were
correctly classified. Thus, from a total of 75 children, 24 + 14 + 17, or
55/75, were correctly classified; the hit rate in this case was 73.3%.
In order to evaluate a particular hit rate appropriately, it must be
compared to a base rate. In the example, the base rates for each of the three
diagnostic classifications were 25/75, or approximately 33.3%. This
NEUROPSYCHOLOGICAL DIAGNOSIS WITH CHILDREN 99
Actual diagnosis
Normal 24 8 4
Learning-disabled 1 14 4
Brain-damaged 0 3 17
aFrom Selz and Reitan (1979). Copyright 1979 by the American Psychological
Association. Adapted by permission.
(o-e)VN
z= (1)
VerN - e)
where 0 is the observed number of hits (ef. hit rate), e is the expected
number of hits (i.e., the number of cases in the largest diagnostic group; d.
base rate), and N is the total number of cases in the sample. Substituting
values in the example taken from Selz and Reitan for variables in Equa-
tion 1, z = 7.35 (p < .001). Thus, the hit rate obtained from using the
actuarial rule significantly improved on the chance assignment of patients
to diagnostic classifications.
Huberty (1984) also proposed a different kind of comparison that is
useful when clinicians are interested in classification accuracy for a par-
ticular diagnostic group. For example, one might be interested in how
100 W. GRANT WILLIS
where ngg is the number of correctly identified patients within the diag-
nostic group of interest (d. 0, hit rate), e" is the number of patients within
that group expected to be diagnosed correctly by chance (calculated as
ng2!N; d. e, base rate), and ng is the number of patients within the diag-
nostic group of interest (d. N). Substituting values from Selz and Reitan
for variables in Equation 2, z = 3.69 (p < .001). Thus, the accuracy associ-
ated with identifying brain-damaged children was significantly better
than chance.
Finally, Huberty (1984) further proposed an index that is useful in
determining the degree to which an actuarial rule can improve diagnostic
accuracy over chance levels. This index is
(3)
where Ho is the observed hit rate, and He is the hit rate expected by chance
(i.e., base rate). This improvement-over-chance index (I) can be used in
the context of either Equation 1 or 2. For example, Is = 0.60 and 0.52, for
the overall and the brain-damaged classification comparisons, respec-
tively. Thus, the use of the actuarial rule proposed by Selz and Reitan
(1979) improved diagnostic accuracy overall by 60% and within the brain-
damaged group by 52%.
Although comparisons between base rates and hit rates are relatively
straightforward and were, in fact, proposed by Meehl and Rosen (1955)
over three decades ago, they are frequently absent from current reports of
neuropsychological actuarial rules. For example, when evaluated in this
context, published neuropsychological actuarial rules often do not signifi-
cantly improve on chance levels of diagnostic accuracy; worse yet, many
yield a level of diagnostic accuracy that is significantly poorer than
chance (see Willis, 1984). Thus, it is important for clinicians to evaluate
actuarial rules in terms of hit-rate to base-rate comparisons in order to
make informed decisions about the utility of those rules.
were used to establish the actuarial rule. The validity of any actuarial rule
is necessarily limited by the validities of the criteria used to establish that
rule. Moreover, the validities of those criteria are necessarily limited by
their associated reliabilities. The problem is compounded in the case of
children because of the often invasive nature of definitive diagnostic cri-
teria for neuropsychological disorders, in addition to the limited data base
describing the course and sequelae of particular disorders. Further, given
the special circumstance that child (versus adult) psychological symp-
toms are usually pathological only in the context of developmental de-
lays, diagnostic criteria used to establish actuarial rules for children
should be referenced against particular age-level expectations.
The level of inference adopted by researchers who develop actuarial
rules is another consideration of some importance with reference to valid-
ity. For example, particular subtypes of specific developmental disorders
(SDD, d. specific learning disabilities, SLD) are often assumed to be
organically (neuropsychologically) based. This assumption may be at
least partially predicated on the (perhaps erroneous) idea that if a particu-
lar form of observable neurological impairment can cause severe forms of
a disorder such as epilepsy or cerebral palsy, then milder forms of such
impairment may result in milder forms of disorders such as hyperactivity
or SDDISLD (Fletcher & Taylor, 1984; however, see Rosen, Sherman, &
Galaburda, 1986). It is often the case that groups of children of varying
ages are diagnosed as SDDISLD according to DSM-III-R (American Psychi-
atric Association, 1987) or federal, state, and local educational agency
criteria (primarily on the basis of psychoeducational assessment), and
that such children are subsequently subtyped or differentiated from oth-
ers on the basis of patterns of neuropsychological assessment data (Fisk &
Rourke, 1979, 1983; Fletcher, Smidt, & Satz, 1979; Lyon, Stewart, & Freed-
man, 1982; Selz & Reitan, 1979). Two limitations inherent in these ap-
proaches are that (a) the validity of the external SDDISLD diagnosis may
be, in itself, questionable (see Shepard, Smith, & Vojir, 1983) and (b)
because the diagnosis of these disorders is contingent on developmental
comparisons, merging diagnosed children of greatly different chronologi-
cal ages for the purpose of statistical analysis is probably inappropriate.
CLINICAL JUDGMENT
these rules are free from the methodological problems described. The
second is that actuarial rules are readily available for clinical evaluation.
The third is that when diagnostic errors are made (as they inevitably will
be), the costs associated with different kinds of error are constant both
across cases and for an individual patient (or at least match those esti-
mated by the developer of the rule). In reality, certain kinds of error are
much more costly (Le., serious) than others in terms of a variety of criteria.
Moreover, the current state of the field is such that, with children, the first
two assumptions would often be violated as well.
In situations where these assumptions are violated, child neuro-
psychologists cannot depend on actuarial rules to guide diagnostic deci-
sion making. Instead, assessment data must be aggregated clinically, and,
as such, without thoughtful consideration of the cognitive processes in-
volved, decisions are subject to a high degree of error. Moreover, even
when methodologically sound actuarial rules are available, clinicians ide-
ally will use these models of data integration as guides to help clarify the
diagnostic or prognostic decision-making process, as opposed to an ex-
clusive dependence on the application of rules per se. In the final analy-
sis, of course, clinicians diagnose patients; rules and assessment data do
not. The ultimate responsibility for accurate decisions lies with clinicians
rather than with the tools they choose to help them think. As already
noted, however, thoughtful clinical judgment demands systematically or-
ganized thinking. An examination of how interpretive strategies, debias-
ing techniques, assessment design, and decision rules can be useful in
this respect follows.
Interpretive Strategies
Clinical decisions are often biased (and therefore erroneous) owing to
the inconsistent use of particular strategies for interpreting assessment
data (see also McDermott, 1981). Two major interpretive strategies are
normative and ipsative. For normative strategies, each source of assess-
ment data collected from a patient is compared with a reference group,
and marked discrepancies from this normative distribution are consid-
ered as abnormal. In contrast, for ipsative strategies, the patient's own
baseline (or average) level of functioning is taken as the reference point
against which specific areas of functioning are compared. The latter in-
terpretive strategy has become increasingly more widespread in recent
years, especially in the pediatric literature (e.g., Kaufman & Kaufman,
1983; Reynolds, 1982; Reynolds & Clark, 1983; Reynolds & Gutkin, 1981;
Reynolds & Kaufman, 1985).
These two interpretive strategies are well illustrated by Reitan's (e.g.,
Reitan & Davison, 1974) approach to neuropsychological test interpreta-
tion, which comprises four methods of inference (see also Selz, 1981).
104 W. GRANT WILLIS
Two of these methods are distinctly normative whereas the other two are
ipsative. The two normative strategies concern level of performance and
pathognomonic signs. Level-of-performance measures (e.g., numbers of
errors on the Category Test) are compared against norms established for
children of similar age levels in order to determine deficiencies in perfor-
mance abilities. Although useful in that context, these measures are simi-
larly limited, as are other kinds of normative data in child neuropsycho-
logical evaluations, because of difficulties in distinguishing developmen-
tal delays from deficits. Such distinctions are important in terms of diag-
nosis and prognosis as well as treatment planning. Additionally, premor-
bid levels of functioning are neglected sources of information when as-
sessment data are considered primarily in a normative sense. Thus, an
average level of performance may be interpreted mistakenly as asymptom-
atic in those cases where a premorbid level was actually superior. Pathog-
nomonic signs (e.g., errors on Imperception Tests) are also normative
sources of data in the sense that their presence is compared with that of
some reference group. They are less susceptible to interpretive errors,
however, because such signs can be (but are not always) symptomatic
independent of developmental considerations. The two ipsative strategies
concern pattern-of-performance measures (e.g., a particular configuration
of test scores) and right-left differences (e.g., differences in finger-tapping
rates between the hands). Both of these strategies involve intraindividual
as opposed to normative group comparisons.
Most ipsative strategies are predicated on the assumption that each
source of assessment data possesses an adequate degree of specificity for
individual interpretation. In this context, specificity refers to that propor-
tion of the variance of a particular source of assessment data that is reli-
able and unique (i.e., is independent of other sources). If a particular
source of assessment data lacks specificity, then it should not ordinarily
be interpreted in the typical ipsative sense as representing a unique func-
tion. Ipsative interpretations of most subtests from the Kaufman Assess-
ment Battery for Children (Kaufman & Kaufman, 1983) and the Wechsler
Intelligence Scale for Children-Revised (Wechsler, 1974), for example, are
well established strategies because adequate degrees of subtest specificity,
for the most part, have been documented (Kaufman & Kaufman, 1983;
Reynolds & Kaufman, 1985).
When clinicians are consistent in applying interpretive strategies
(whether normative, ipsative, or both) to assessment data, they are less
likely to bias diagnostic and prognostic decisions. For example, an initial
prejudicial choice of a particular approach (either for an individual pa-
tient or for a particular source of assessment data) can help to determine
the outcome of a case. In these instances, diagnostic decisions may be
inappropriately influenced by methodological rather than more important
substantive issues.
NEUROPSYCHOLOGICAL DIAGNOSIS WITH CHILDREN 105
Debiasing Techniques
Research investigating judgmental heuristics has delineated several
cognitive biases associated with diagnostic inaccuracy as well as several
possible debiasing techniques (Achenbach, 1985; Arkes, 1981). As noted
previously, one common source of bias is an inappropriate conceptualiza-
tion or assessment of symptom-diagnosis covariation. Table 2 is a pro-
totypical contingency table of the relationship between a particular symp-
tom (25-point discrepancy between the Verbal and Performance IQs on
the WISe) and neurologic insult (presence vs. absence of brain damage).
Entries in the table are estimated calculations based on data presented by
Holroyd and Wright (1965), assuming a total of 100 cases and a liberal
incidence estimate for childhood brain damage of 10%. These hypo-
thetical data show that 30% of a sample of non brain-damaged children
demonstrated a discrepancy of 25 or more points between Verbal and
Performance IQ scores and 80% of a sample of brain-damaged children
demonstrated this same symptom. Similar data (e.g., Black, 1976) are
often misinterpreted as evidence that this size of discrepancy may be
symptomatic of brain damage in children (e.g., Sattler, 1982, p. 460; how-
ever, d. Sattler, 1988, pp. 705-706).
These kinds of interpretations of symptom-diagnosis contingencies
are often made when some of the available data (e.g., the proportion of
cases in which the symptom is absent but the diagnosis is present) are
considered to be less important than others (e.g., the proportion of cases
in which both the symptom and the diagnosis are present; see Arkes &
Harkness, 1983; Nisbett & Ross, 1980). In fact, all data are equally impor-
tant in determining the degree of relationship between the symptom and
the diagnosis. An accurate assessment of this relationship for the data
presented in Table 2 indicates that the interpretation noted is perhaps not
as clear as it may seem.
Several pieces of information are required in order to determine the
probability that the diagnosis of brain damage is correct or even if this
symptom is likely to be from a brain-damaged child. This information
includes (a) prior odds, (b) likelihood ratio, and (c) posterior odds (see
Arkes, 1981). The ratio representing prior odds is simply the likelihood
Diagnosis
that the diagnosis is correct divided by the likelihood that the diagnosis is
incorrect and is thus comparable to a base-rate index. Prior odds are
subsequently modified when information concerning a symptom is ob-
tained. Such information can be expressed as a likelihood ratio, which is
the probability of obtaining that symptom if the diagnosis were correct
divided by the probability of obtaining that symptom if the diagnosis were
incorrect. Finally, the ratio representing posterior odds is the probability
that the diagnosis is correct given the symptom and it is determined by
the product of the prior odds and the likelihood ratio.
Substituting values from Table 2, the prior odds are (8 + 2)/(27 + 63)
or 10/90. The likelihood ratio is (8/[8 + 2])/(27/[27 + 63]) or 0.8/0.3.
Consequently, the posterior odds are (10/90)(0.8/0.3) or 8/27 (Le.,0.3).
Thus, the probability that a diagnosis of brain damage is correct when
based on the 25-point VIQ-PIQ discrepancy is only 30%; the probability
that a 25-point VIQ-PIQ discrepancy is from a brain-damaged child is
only 8/(8 + 27) or 23%. Results fare even worse given more conservative
incidence estimates for childhood brain damage. When all data in con-
tingency tables are given proper consideration, symptom-diagnosis rela-
tionships can be perceived much more accurately.
In addition to this kind of Bayesian analysis of symptom-diagnosis
covariation, clinicians should entertain alternative diagnostic or prog-
nostic possibilities until all have been actively considered. This is be-
cause another source of error in clinical decision making is that, once a
decision is made, the processing of subsequent assessment data may be
biased. In this respect, clinicians should also endeavor to decrease the
degree to which they rely on memory when assessment data are being
aggregated. For example, biased decisions may result because unpre-
sented symptoms that are consistent with a particular diagnosis tend to be
remembered as having been presented, whereas symptoms that are actu-
ally presented, yet are inconsistent with the diagnosis, tend to be forgot-
ten (Arkes & Harkness, 1980). Thus, it is not surprising that the most
accurate clinicians are those who arrive at diagnostic decisions relatively
later than less accurate clinicians (Elstein, Shulman, & Sprafka, 1978).
tion. It is the multiaxial process that is perhaps more useful (especially for
childhood disorders) than the DSM-III-R diagnostic codes per se.
Consider the assessment situation that, from the point of view of
accuracy, would be ideal: use of multiple techniques such as tests, observa-
tions, and interviews to collect information in each of the five DSM-III-R
domains (i.e., clinical syndromes, developmental disorders, physical con-
ditions, psychosocial stressors, global adaptive functioning). Further, a
variety of assesssors would be used in the multiple settings in which the
child interacts (e.g., home, school, clinic). This kind of design, in which
technique, domain, assessor, and setting are crossed, would serve to mini-
mize biased diagnostic and prognostic decisions by eliminating confound-
ing influences inherent in more typical assessment situations. In a more
typical situation, for example, a child suspected of being learning-disabled
might be examined by a neuropsychologist in a clinic where the focus of
that examination is primarily related to DSM-III-R Axis II domains. Infor-
mation also might be solicited from the teacher at school via rating scales
and work samples regarding academic performance, and from the mother
via an interview regarding home-related and parental concerns. Here,
potential differences among these three major sources of assessment infor-
mation could be a function of technique, domain, assessor (or informant),
setting, or some combination of factors. The confounding influences can
only be reduced to the extent that multiple techniques, domains, assessors,
and settings are used. Given a variety of constraints, idealized assessment
designs are impractical, of course, but it is incumbent that clinicians be
sensitive to the ways in which their diagnostic and prognostic decisions are
influenced by deviations from such designs.
Finally, when child neuropsychologists are able to approach evalua-
tions from a multidimensional perspective, they can expect that the large
amount of assessment data collected often will be difficult to aggregate
without the guidance of actuarial rules. Applying decision rules can be a
useful strategy in such circumstances. Decision rules help to reduce bias
by specifying a prescribed sequence of decisions that should be made, as
well as the criteria (usually empirically derived) upon which those deci-
sions should be based. McDermott and Watkins (1985) developed a com-
prehensive set of these rules for the diagnosis of childhood psychological
disorders (see also Aaron, 1981; Spitzer, Skodol, Gibbon, & Williams,
1981). Similar to multivariate actuarial rules, however, decision rules
should be carefully evaluated prior to their use because associated relia-
bility and validity issues will limit the utility of the clinician's diagnostic
prediction.
SUMMARY
REFERENCES
Aaron, P. G. (1981). Diagnosis and remediation of learning disabilities in children-A neuro-
psychological key approach. In G. W. Hynd & J. E. Obrzut (Eds.), Neuropsychological
assessment and the school-age child (pp. 303-333). New York: Grune and Stratton.
Achenbach, T. M. (1985). Assessment and taxonomy of child and adolescent psycho-
pathology. Beverly Hills, CA: Sage.
Achenbach, T. M., & Edelbrock, C. S. (1978). The classification of child psychopathology: A
review and analysis of empirical efforts. Psychological Bulletin, 85, 1275-1301.
American Psychiatric Association. (1987). Diagnostic and statistical manual of mental dis-
orders (3rd ed., rev.). Washington, DC: Author.
Arkes, H. R (1981). Impediments to accurate clinical judgment and possible ways to mini-
mize their impact. Journal of Consulting and Clinical Psychology, 49, 323-330.
Arkes, H. R, & Harkness, A. R (1980). The effect of making a diagnosis on subsequent
recognition of symptoms. Journal of Experimental Psychology: Human Learning and
Memory, 6, 568-575.
Arkes, H. R, & Harkness, A. R (1983). Estimates of contingency between two dichotomous
variables. Journal of Experimental Psychology: General, 112, 117-135.
Black, F. W. (1976). Cognitive, academic, and behavioral findings in children with suspected
and documented neurological dysfunction. Journal of Learning Disabilities, 9, 182-187.
Cattin, P. (1980). Note on the estimation of the squared cross-validated multiple correlation
of a regression model. Psychological Bulletin, 87, 63-65.
Chapman, 1. (1967). Illusory correlation in observational report. Journal of Verbal Learning
and Verbal Behavior, 6, 151-155.
Chapman, L., & Chapman, J. (1967). Genis of popular but erroneous psychodiagnostic obser-
vations. Journal of Abnormal Psychology, 72, 193-204.
Chapman, L., & Chapman, J. (1969). Illusory correlation as an obstacle to the use of valid
psychodiagnostic signs. Journal of Abnormal Psychology, 74, 271-280.
Elstein, A. S., Shulman, A. S., & Sprafka, S. A. (1978). Medical problem solving: An analysis
of clinical reasoning. Cambridge, MA: Harvard University Press.
Fisk, J. 1., & Rourke, B. P. (1979). Identification of subtypes of learning-disabled children at
three age levels: A neuropsychological, multivariate approach. Journal of Clinical Neu-
ropsychology, 1, 289-310.
NEUROPSYCHOLOGICAL DIAGNOSIS WITH CHILDREN 109
Mitchell, B. (1967). Predictive validity of the Metropolitan Readiness Test and the Murphy-
Durrell Reading Readiness Analysis for white and negro pupils. Educational and Psy-
chological Measurement, 27, 1047-1054.
Mosier, C. I. (1951). Problems and designs of cross-validation. Educational and Psychologi-
cal Measurement, 11, 5-11.
Nisbett, R. E., & Ross, L. (1980). Human inference: Strategies and shortcomings of social
judgment. Englewood Cliffs, NJ: Prentice-Hall.
Obrzut, J. E., Hynd, G. W., & Obrzut, A. (1983). Neuropsychological assessment of learning
disabilities: A discriminant analysis. Journal of Experimental Child Psychology, 35, 46-
55.
Pedhazur, E. J. (1982). Multiple regression in behavioral research (2nd ed.). New York: Holt,
Rinehart & Winston.
Phelan, J. G. (1964). Rationale employed by clinical psychologists in diagnostic judgment.
Journal of Clinical Psychology, 20, 454-458.
Rapoport, J. L., & Ismond, D. R. (1984). DSM-III training guide for diagnosis of childhood
disorders. New York: Brunner/Mazel.
Reitan, R. M. (1984). An impairment index of brain functions in children. Perceptual and
Motor Skills, 58, 875-881.
Reitan, R. M., & Davison, L. A. (Eds.). (1974). Clinical neuropsychology: Current status and
applications. Washington, DC: V. H. Winston.
Reynolds, C. R. (1982). Determining statistically reliable strengths and weaknesses in the
performance of single individuals on the Luria-Nebraska Neuropsychological Battery.
Journal of Consulting and Clinical Psychology, 50, 525-529.
Reynolds, C. R., & Clark, J. H. (1983). Assessment of cognitive abilities. In K. D. Paget & B.
Bracken (Eds.), The psychoeducational assessment of preschool children (pp. 163-
189). New York: Grune and Stratton.
Reynolds, C. R., & Gutkin, T. B. (1981). Statistics for the interpretation of Bannatyne re-
organization of WPPSI subtests. Journal of Learning Disabilities, 14,446-467.
Reynolds, C. R., & Kaufman, A. S. (1985). Clinical assessment of children's intelligence with
the Wechsler scales. In B. B. Wolman (Ed.), Handbook of intelligence: Theories, mea-
surements, and applications (pp. 601-661). New York: Wiley.
Rosen, G. D., Sherman, G. F., & Galaburda, A. M. (1986). Biological interactions in dyslexia
(pp. 155-173). In J. E. Obrzut & G. W. Hynd (Eds.), Child neuropsychology: Vol. 1.
Theory and research. Orlando, FL: Academic Press.
Sattler, J. M. (1982). Assessment of children's intelligence and special abilities (2nd ed.).
Boston: Allyn & Bacon.
Sattler, J. M. (1988). Assessment of children (3rd ed.). San Diego, CA: Jerome M. Sattler.
Scarr-Salapatek, S. (1971). Race, social class, and IQ. Science, 174, 1285-1295.
Selz, M. (1981). Halstead-Reitan neuropsychological test batteries for children. In G. W.
Hynd & J. E. Obrzut (Eds.), Neuropsychological assessment and the school-age child
(pp. 195-235). New York: Grune and Stratton.
Selz, M., & Reitan, R. M. (1979). Rules for neuropsychological diagnosis: Classification of
brain function in older children. Journal of Consulting and Clinical Psychology, 47,
258-264.
Shepard, L. A., Smith, M. L., & Vojir, C. P. (1983). Characteristics of pupils identified as
learning disabled. American Educational Research Journal, 20, 309-331.
Spitzer, R. L., Skodol, A. E., Gibbon, M., & Williams, J. B. W. (1981). DSM-III case book.
Washington. DC: American Psychiatric Association.
Starr, J. G., & Katkin, E. (1969). The clinician as an aberrant actuary: Illusory correlation and
the Incomplete Sentences Blank. Journal of Abnormal Psychology, 74, 670-675.
Thorndike, R. L. (1982). Applied psychometrics. Boston: Houghton Mifflin.
Tryon, R. c., & Bailey, D. E. (1970). Cluster analysis. New York: McGraw-Hill.
NEUROPSYCHOLOGICAL DIAGNOSIS WITH CHILDREN 111
Tversky, A., & Kahneman, D. (1973). Availability: A heuristic for judging frequency and
probability. Cognitive Psychology,S, 207-232.
Wallach, M. S., & Schoof, K. (1965). Reliability of degree of disturbance rating. Journal of
Clinical Psychology, 21, 273-275.
Wechsler, D. (1974). Wechsler Intelligence Scale for Children-Revised. New York: Psycho-
logical Corporation.
Willis, W. G. (1984). Reanalysis of an actuarial approach to neuropsychological diagnosis in
consideration of base rates. Journal of Consulting and Clinical Psychology, 52, 567 -569.
Willson, V. 1., & Reynolds, C. R. (1982). Methodological and statistical problems in deter-
mining membership in clinical populations. Clinical Neuropsychology, 4, 134-138.
5
INTRODUCTION
113
114 G. REID LYON et a1.
& Knights, 1986). Less documentable, but equally influential, are the so-
cial, political, and educational trends that have created and fostered a
major role for neuropsychological treatment approaches in the fields of
learning disabilities and cognitive rehabilitation. Models for treatment
that claim to derive validity from biological science are appealing in the
field of learning disabilities (LD), in particular, where previously em-
ployed aptitude-treatment interaction models have failed to generate the
foundations of a clinical science (Lyon, 1987; Lyon & Moats, in press).
The heterogeneity of the LD population, although now recognized, con-
tinues to beg classification and validation (Lyon & Risucci, 1988). Thus,
treatment models that invoke biological explanations for intellectual and
behavioral differences are welcome in the void. A focus on intrinsic bio-
logic variables permits us to minimize the importance of educational,
cultural-familial, and societal causes for individual differences (Chall &
Mirsky, 1978) and, thus, to empower ourselves by defining treatment
problems in terms of simple, often dichotomous neurobehavioral con-
structs (e.g., right vs. left brain learners, sequential vs. simultaneous
processing).
Taken at face value and for whatever reasons, the shift in emphasis
from neuropsychological assessment for classification purposes (i.e.,
presence or absence of brain damage) to assessment for prescriptive pur-
poses (i.e., treatment) reflects a possibly productive transition toward
enhanced clinical relevance. Indeed, Alfano and Finlayson (1987) and
others (Lyon & Moats, in press; Newcomb, 1985) have pointed out re-
cently that the power of the clinical contributions that evolve from neuro-
psychological practice ultimately depends upon the field's capacity to (1)
delineate neuropsychological strengths and weaknesses in a reliable and
valid fashion, (2) predict the extent to which these information-process-
ing characteristics influence recovery of function and/or learning, and (3)
generate testable hypotheses concerned with remedial methodologies for
individuals who either lost or did not acquire information because of
known or suspected neural insult.
Perusal of the current literature in both child and adult clinical neu-
ropsychology reveals significant support for the concept of establishing
valid linkages between the information generated from neuropsychologi-
cal assessment practices and the development of management, rehabilita-
tion, and remediation programs (Rourke, Fisk, & Strang, 1986). However,
such support is generally given in the form of rhetorical and testimonial
presentation, case study information, or anecdotal reports. Although
these particular forums underscore the value of attempting to develop
valid neuropsychologically based treatment programs, we feel that popu-
lar views regarding the clinical benefits of such practices go beyond the
data. Given this observation, it should be made clear that our purpose in
this chapter is not to advocate dismissal of the concept of neuropsycho-
FROM ASSESSMENT TO TREATMENT 115
and clinical efficacy of Rourke's (Rourke et aI., 1983, 1986) model. Clearly,
however, the model does offer well-reasoned and comprehensive guide-
lines for intervention that can serve as clinical frames of reference.
Lyon and his associates (Lyon, 1983, 1985a, 1985b; Lyon, Stewart, &
Freedman, 1982; Lyon & Watson, 1981) have questioned the appropri-
ateness of a single-deficit classification model for reading disability and
hypothesized that LD readers (dyslexics) constitute a population that is
composed of a number of subtypes, each of which is defined by its own
particular array of linguistic, perceptual, and reading characteristics. The
theoretical background underlying Lyon's research can be viewed as a
logical extension of Luria's (1966, 1973) clinical neuropsychological theo-
ry and Benson and Geschwind's (1975) multiple syndrome model of alex-
ia. For example, Lyon (1983) proposed that reading development is a
complex process that requires the concerted participation of cognitive,
linguistic, and perceptual subskills. As such, deficiencies in anyone sub-
skill can limit the acquisition of fluent decoding and/or comprehension
abilities.
Within this theoretical context, an initial series of studies was con-
ducted (Lyon, Rietta, Watson, Porch, & Rhodes, 1981; Lyon & Watson,
1981) in which a battery of tasks designed to assess linguistic and percep-
tual skills related to reading development was administered to 100 LD
readers and 50 normal readers matched for age (11-12 years) and IQ (M =
104). The data were submitted to a series of cluster analyses to test the
hypothesis that subtypes could be identified. Six distinct subtypes were
delineated and characterized by significantly different patterns of lin-
guistic and perceptual deficits. The six-subtype solution remained stable
across internal validation studies employing different variable subsets
and clustering algorithms. Further, 94% of subjects were recovered into
similar subtypes in a cross-validation study using a new subject sample
(Lyon, 1983). A brief description of each of the subtypes' information-
processing characteristics is provided here, followed by an overview of
the intervention program. Readers are referred to cited references for spe-
cific details.
Children who were assigned empirically to subtype 1 (n = 10) exhib-
ited significant deficits in language comprehension, the ability to blend
phonemes, visual-motor integration, visual-spatial skills, and visual
memory skills, with strengths in naming and auditory discrimination
skills. Analysis of the reading and spelling errors made by members of
subtype 1 indicated significant deficits in the development of both a sight
word vocabulary and word attack skills.
Children in subtype 2 (n = 12) also exhibited a pattern of mixed
deficits but in a milder form than observed in subtype 1. Specifically,
significant problems in language comprehension, auditory memory, and
visual-motor integration were observed and may have been related to the
126 G. REID LYON et a1.
the Peabody Individual Achievement Test (PlAT) ranged from 3.0 to 3.3,
with percentile ranks ranging from 4 to 8. It was not possible to control for
the amount and type of previous reading instruction experienced by the
children, their present curriculum, and the amount of time spent in class-
rooms for learning-disabled youngsters. Thus, the results obtained from
this study must be evaluated in light of these confounding features.
The teaching method selected for the study was a synthetic phonics
program (Traub & Bloom, 1975). This program was chosen because of its
sequenced format, its coverage of major phonics concepts, and its famil-
iarity to the teachers in training who were providing the instruction. All
subjects were provided 1 hour of reading instruction per week (in addi-
tion to their special and regular classroom instruction) for 26 weeks.
Following the 26 hours of phonics instruction, the 30 children were
posttested with the PlAT Reading Recognition subtest, and gain scores
employing percentile ranks and grade equivalents were computed. A one-
way analysis of variance indicated significant differences among the six
subtypes for both types of gain scores achieved from preintervention to
posttesting. An analysis of subtype gain scores and subsequent pairwise
comparisons indicated that members of subtype 6 made the most progress
(mean percentile rank gain = 18.0)' followed by members of subtype 4
(mean percentile rank gain = 8.2). On the other hand, subtypes 1, 2, 3, and
5 made minimal gains in percentile ranks and were not significantly dif-
ferent from one another in terms of gains achieved. Subtypes 6 and 4 were
both significantly different from one another and from all other subtypes
with respect to their improvement in the oral reading of single words.
The data obtained in this subtype remediation study indicate that, for
some subtypes, a synthetic phonics teaching intervention appeared to
enhance significantly the ability to read single words accurately. Clearly,
members of subtypes 6 and 4 demonstrated robust improvements in their
decoding capabilities. Whether or not the absence of auditory-verbal defi-
cits in these two subtypes was associated with their good response to
instruction cannot be answered clearly at this time, but one could hypoth-
esize that this might be the case. This hypothesis is made more tenable by
the observation that those subtypes with the most severe auditory recep-
tive and auditory expressive language deficits made either minimal gains
(e.g., subtypes 2 and 3) or no gains (e.g., subtypes 1 and 5) in the ability to
pronounce single words accurately and efficiently.
In a related program of research carried out with younger disabled
readers (Lyon, 1985a; Lyon et a1., 1982), five LD subtypes were identifed
and validated internally and externally by using different variable sub-
tests, clustering algorithms, and subtype-teaching method interaction
studies. Again, a brief description of each of the subtypes' information-
processing characteristics is provided, followed by an overview of the
external validation intervention program.
128 G. REID LYON et a1.
and sequence presented in the Traub and Bloom (1975) reading program.
A brief description of the instructional format for this approach was pre-
sented earlier. The combined remediation group learned to label whole
words (three nouns, three verbs) rapidly by first pairing the word with
pictures, then recognizing the names of the words (by a pointing re-
sponse), and then finally reading the words in isolation. Following the
development of rapid reading ability for these six words, function words
(the, is, was, are) were introduced and taught. Following stable reading of
these words, short sentences using combinations of the sight and function
words were constructed and read in order to introduce the concept of
contextual analysis and to develop metalinguistic awareness of reading as
a meaningful language skill. Following contextual reading drills, the com-
bined group received instruction in structural analysis and the reading
and comprehension of the morpho syntactical markers -ed, -s, and -ing.
These morphemes were written on anagrams and introduced into context
so that the children could readily grasp their effect on syntax and mean-
ing. Finally, analytic phonics drills were initiated to develop letter-
sound correspondences with the context of whole words. Specifically,
phonetically regular words that could be read rapidly by sight were pre-
sented, and children were first asked to recognize a particular letter-
sound correspondence ("Point to the letter that makes the /a/ sound") and
then to give a recall response ("What sound(s) does this letter make?"). As
children became more adept at recalling grapheme-phoneme relations,
drills in auditory analysis and blending were initiated.
Following the 30 hours of remediation, children in both groups were
posttested with an alternate form of the Woodcock Reading Mastery Word
Identification subtest. Significant differences were found between the two
remediation groups with respect to postintervention reading percentile
rank scores (Mann-Whitney Z < .0003). Children within the combined
remediation group gained, on the average, 11 percentile rank points,
whereas members of the synthetic phonics group gained approximately 1
percentile rank point.
There is little doubt that subtype 2 members responded significantly
differently to two forms of reading instruction. Apparently, the auditory
receptive and auditory expressive language deficits that characterized
each member of the subtype 2 impeded their response to a reading in-
structional method that required learning letter-sound correspondences
in isolation followed by blending and contextual reading components. A
tentative hypothesis might be that subtype 2 children did not have the
auditory language subskills necessary for success with this approach but
could deploy their relatively robust visual-perceptual and memory skills
more effectively with whole words, as seen within the combined remedia-
tion. A more tenable hypothesis is that whole-word reading placed far less
linguistic demands on these readers than alphabetic approaches that re-
quire a phonological awareness of sound structure and acoustic bound-
FROM ASSESSMENT TO TREATMENT 131
aries and the relationship of these units to letter sequences. Thus, whereas
subtype 2 members learned to read whole words in structured, isolated
context, their ability to generalize phonological and orthographic con-
cepts to read new words is most likely to remain limited.
In general, the data derived from this series of subtype identification
and remediation studies support a model of dyslexia that presumes that a
number of diverse information-processing deficits can have specific read-
ing disability as a common correlate. Although the results from these
basic research endeavors are interesting, the findings have limited clinical
utility for a number of reasons. First, the kinds of subtypes identified and
their descriptions are limited by the range and quality of the tests that
provide the data for cluster analysis. For example, the tasks selected for
use in Lyon's assessment batteries did not provide adequate coverage of
some linguistic factors (particularly phonology) implicated in the devel-
opmental reading process. Second, the specific nature of the relationship
between subtype assessment characteristics and response to reading in-
struction is difficult to determine because the assessment tasks are indi-
rect measures of associated symptomatology. Third, it is not well under-
stood if the correlated information-processing deficits constitute
necessary and/or sufficient conditions for reading disability. Fourth,
methodological limitations in sample size and the number and type of
dependent reading measures preclude adequate interpretations and confi-
dent generalization of the subtype-teaching method interaction studies.
Finally, even though particular teaching (treatment) approaches had dif-
ferential effects for some subtypes, it is difficult to determine if the effects
should be attributed to subtype characteristics, the instructional program,
the interaction between the two, the teacher, time spent in remediation, or
previous or concomitant educational experiences.
cluded multiple oral reading samples using the reading model to classify
errors and the Boder Test of Reading-Spelling patterns (BTRSP; Boder &
Jarrico, 1982). Thus, test content was directly related to the tasks that
children face on a daily basis.
The BTRSP was chosen as a direct measurement of word-recognition
skills involving phonology, memory, and perception. Dyslexic children
were classified as dysphonetic (deficient in sequential auditory pro-
cesses), dyseidetic (deficient in visual-spatial skills), or mixed (deficient
in both processes), according to an adaptation of the Boder procedures
(Boder & Jarriso, 1982). The initial thrust of this research was to investi-
gate the construct validity of the BTRSP through external validation stud-
ies involving quantitative neurophysiology and subtype-treatment re-
mediation programs. As the reader will note, results of the studies
indicate that a reconceptualization of the dyslexic subtypes originally
proposed by Boder may offer greater explanatory power and lead more
directly to testable reading remediation hypotheses.
With this direct assessment model, subtypes of children who demon-
strated distinct profiles of reading behaviors were identified. One sub-
type, described as deficient in phonetic development, demonstrated diffi-
culty with syntactical and alphabetic skills. Generally, semantics and
sight word recognition skills were areas of strength. Oral reading was
characterized by global substitutions, difficulty with sound-symbol rela-
tionships, and semantic substitutions. Often, comprehension was rela-
tively intact despite numerous reading inaccuracies. Conversely, children
with presumed deficits in whole word recognition skills displayed excel-
lent phonetic analysis skills. Characteristically slow but accurate readers,
they often failed to understand the meaning of a passage.
The question of whether these clinical description of reading profiles
represent reliable, replicable subtypes that have ecological and predictive
validity (i.e., lead to testable remediation hypotheses and prognoses) was
investigated through external validation studies, including quantitative
neurophysiology studies and a subtype-treatment remediation project. In
the first neurophysiology study (Flynn & Deering, 1987),44 children (ages
7-10) were assessed using direct measures of reading and spelling behav-
iors, a neurological evaluation, and spectral analysis of theta and alpha
brain waves during cognitive tasks. The results suggested that distinct
subtypes of reading-disabled children could be formed using direct mea-
sures of word recognition skills. The data also suggested that reading
disability in the subtype of children identified variously as dyseidetic
(Boder, 1971, 1973), L-type dyslexics (Bakker & Vinke, 1985), visual or
visual-spatial (Johnson & Myklebust, 1967; Mattis, French, & Rapin, 1975;
Pirozzolo, 1981) may be attributable to overutilization of early-developing
linguistic skills (phonological decoding) rather than deficient visual per-
ceptual processes.
Although this study clearly differentiated the dyseidetic dyslexics
134 G. REID LYON et al.
from other groups on three of the six cognitive tasks, the direction and
location of neurophysiologic difference was initially quite surprising
given previous reports of this subtype's characteristics. For example, dys-
eidetic children's reading disabilities have been attributed to deficient
visual-spatial abilities referable to atypical, right hemisphere develop-
ment with concomitant strength in phonetic skills (Boder, 1971, 1973;
Boder & Jarrico, 1982). In the Flynn and Deering (1987) investigation,
however, dyseidetic children demonstrated significant increases from
resting baseline in left temporal-parietal theta compared with the other
groups. That this difference occurred in the area of the angular gyrus,
presumed to be important in phonetic decoding (Hynd & Hynd, 1984),
suggested that the reportedly normal phonetic skills of dyseidetic chil-
dren may, in fact, indicate overutilization of a processing strategy that
results in, or is caused by, relative inefficiency of right hemisphere visual
gestalt abilities.
A second study of 64 children (ages 8-9), subtyped according to
modified Boder procedures (Boder & Jarrico, 1982) and oral reading pat-
terns, provided replicated evidence of increased left theta activity in dys-
eidetic children during task engagement (Flynn & Deering, 1987). Further
external validation studies investigated the efficacy of the classification
system for prescribing remediation (Flynn, 1987). Using the neuropsycho-
logical principle of teaching to intact or compensatory processes, a sub-
type-treatment research program was initiated. The study involved 22
first-, second-, and third-graders classified as dysphonetic or dyseidetic.
Children were randomly assigned to a treatment group and received a full
year of remediation, three sessions per week. The reading approaches
included (1) a language experience, analytic phonetic approach using the
Initial Teaching Alphabet; (2) Distar, a synthetic phonics approach; and
(3) a multisensory, analytic phonetic approach using regular orthography.
Data derived from the reading remediation project provided addi-
tional validation of ecologically based assessment procedures for subtyp-
ing dyslexic children (Flynn, 1987). However, the data also demonstrated
the inadequacy of a design that implies a simple match between reading
subtype and remediation system. Specifically, within each treatment con-
dition, there were some children who benefited whereas others with the
same reading profile made less than average gains.
Data from the neurophysiology and remediation studies suggest that
not all children fail to develop fluent reading behaviors for the same
reason, that distinct subtypes of dyslexic children can be identified on the
basis of direct measurements of reading and spelling behaviors, and that,
to some degree, responses of subtyped children to specific reading ap-
proaches can be predicted. The data also suggest that more dynamic,
interactive models of the teaching-learning situation must be developed
in order to describe and predict adequately how the child's processing
FROM ASSESSMENT TO TREATMENT 135
deficits covary with instructional variables (e.g., the reading system and
the learning context).
REFERENCES
Alfano, D. P., & Finlayson, M. A. J. (1987). Clinical neuropsychology in rehabilitation.
Clinical Neuropsychologist, 1, 105-123.
Ayres, R R, & Cooley, E. J. (1986). Sequential versus simultaneous processing on the K-ABC:
Validity in predicting learning success. Journal of Psychoeducational Assessment, 4,
211-220.
Bakker, D. (1983). Hemispheric specialization and specific reading retardation. In M. Rutter
(Ed.), Developmental neuropsychiatry (pp. 203-232). New York: Guilford Press.
Bakker, D., & Vinke, J. (1985). Effects of hemisphere specific stimulation on brain activity
and reading in dyslexics. Journal of Clinical and Experimental Neuropsychology, 7,
505-525.
Bakker, D. J., Moerland, R, GoeKoop-Hoefkens, M. (1981). nlltcts of hemisphere-specific
stimulation on the reading performance of dyslexic boys: A pilot study. Journal of
Clinical Neuropsychology 3, 155-159.
Beaumont, J. G. (1983). Introduction to neuropsychology. New York: Guilford Press.
Benson, D. F., & Geschwind, N. (1975). The alexias. In D. J. Vinkis & G. W. Bruyn (Eds.),
Handbook of clinical neurology (Vol. 4). New York: American Elsevier.
Boder, E. (1971). Developmental dyslexia: Prevailing diagnostic concepts and a new diag-
nostic approach. In H. Mykelbust (Ed.), Progress in learning disabilities (Vol. 2). New
York: Grune and Stratton.
Boder, E. (1973). Developmental dyslexia: A diagnostic approach based on three atypical
reading-spelling patterns. Developmental Medicine and Child Neurology, 15,663-687.
Boder, E. D., & Jarrieo, S. (1982). The Boder Test of Reading-Spelling Patterns. A diagnostic
screening test for subtypes of reading disability. Orlando, FL: Grune and Stratton.
Boll, T. J. (1981). The Halstead-Reitan Neuropsychological Test Battery. In S. B. Filskov & T.
J. Boll (Eds.), Handbook of clinical neuropsychology (pp. 577-607). New York: Wiley.
Boll, T. J., & Reitan, R M. (1972). Comparative ability interrelationships in normal and brain-
damaged children. Journal of Clinical Psychology, 28, 152-156.
Bornstein, R A., King, G., & Carroll, A. (1983). Neuropsychological abnormalities in Gilles
de la Tourette's syndrome. Journal of Nervous and Mental Disease, 171,497-502.
Brown, A. 1., & Campione, J. C. (1986). Psychological theory and the study of learning
disabilities. American Psychologist, 14, 1059-1068.
Chall, J. S., & Mirsky, A. F. (1978). The implications for education. In J. S. Chall & A. F.
Mirsky (Eds.), Education and the brain: The seventy-seventh yearbook of the National
Society for the Study of Education. Chicago: University of Chicago Press.
Cook, 1. (1981). Misspelling analysis in dyslexia. Observation of developmental strategy
shifts. Bulletin of the Orton Society, 31, 123-134.
Craig, D. 1. (1979). Neuropsychological assessment in public psychiatric hospHals: The
current state of practice. Clinical Neuropsychology, 1, 1-7.
Dawson, G. (1983). Lateralized brain dysfunction in autism: Evidence from the Halstead-
Reitan Neuropsychological Battery. Journal of Autism and Developmental Disorders,
13, 269-286.
Diller, 1., & Gordon, W. A. (1981a). Intervention for cognitive deficits in brain-injured adults.
Journal of Consulting and Clinical Psychology, 49, 822-839.
Diller, L., & Gordon, W. A. (1981b). Rehabilitation and clinical neuropsychology. In S. B.
Filskov & T. J. Boll (Eds.), Handbook of clinical neuropsychology (pp. 702-7330). New
York: Wiley.
Diller, 1., & Weinberg, J. (1977). Hemi-inattention in rehabilitation: The evolution of a
140 G. REID LYON et al.
Luria, A. R, & Tzetkova, L. S. (1968). The re-education of brain-damaged patients and its
psychopedagogical application. In J. Hellmuth (Ed.), Learning disorders (pp. 139-154).
Seattle: Special Child Publications.
Lyon, G. R (1983). Subgroups of learning disabled readers: Clinical and empirical identifica-
tion. In H. R Mykelbust (Ed.), Progress in learning disabilities (Vol. 5, pp. 103-134).
New York: Grune and Stratton.
Lyon, G. R (1985a). Educational validation of learning disability subtypes: In B. P. Rourke
(Ed.), Neuropsychology of learning disabilities: Essentials of subtype analysis (pp. 228-
256). New York: Guilford Press.
Lyon, G. R (1985b). Identification and remediation of learning disability subtypes: Prelimi-
nary findings. Learning Disabilities Focus, 1, 21-35.
Lyon, G. R (1987). Learning disabilities research: False starts and broken promises. In S.
Vaughn & C. Bos (Eds.), Research in learning disabilities: Issues and future directions
(pp. 69-85). San Diego: College Hill Press.
Lyon, G. R, & Moats, L. C. (in press). Critical issues in the instruction of the learning
disabled. Journal of Consulting and Clinical Psychology.
Lyon, G. R, Rietta, S., Watson, B., Porch, B., & Rhodes, J. (1981). Selected linguistic and
perceptual abilities of empirically derived subgroups of learning disabled readers. Jour-
nal of School Psychology, 19, 152-166.
Lyon, G. R, & Risucci, D. (1988). Classification issues in learning disabilities. In K. A. Kavale
(Ed.), Learning disabilities: State of the art and practice. San Diego: College Hill Press.
Lyon, G. R, Stewart, N., & Freedman, D. (1982). Neuropsychological characteristics of em-
pirically derived subgroups of learning disabled readers. Journal of Clinical Neuropsy-
chology, 4, 343-365.
Lyon, G. R, & Toomey, F. (1985). Neurological, neuropsychological, and cognitive-develop-
mental approaches to learning disabilities. Topics in Learning Disabilities, 2, 1-15.
Lyon, G. R, & Watson, B. (1981). Empirically derived subgroups of learning disabled readers:
Diagnostic characteristics. Journal of Learning Disabilities, 14, 256-261.
Mann, 1. (1979). On the trail of process. New York: Grune and Stratton.
Mann, 1., & Sabatino, D. A. (1985). Foundations of cognitive process in remedial and special
education. Rockville, MD: Aspen.
Mattis, S., French, J., & Rapin, I. (1975). Dyslexia in children and young adults. Three
independent neuropsychological syndromes. Developmental Medicine and Child Neu-
rology, 17, 150-163.
Moats, 1. (1983). A comparison of the spelling errors of older dyslexic and normal second
grade children. Annals of Dyslexia, 33, 121-140.
Newcomb, F. (1985). Neuropsychological qua interface. Journal of Clinical and Experimen-
tal Neuropsychology, 7. 663-681.
Nolan. D. R, Hammeke. T. A., & Barkley, R A. (1983). A comparison of the neuropsychologi-
cal performance in two groups of learning disabled children. Journal of Clinical Child
Psychology, 12, 13-21.
Obrzut. J. E., & Hynd. G. W. (1986). Child neuropsychology (Vol. 2). Orlando. FL: Academic
Press.
Pirozzolo. F. (1981). Language and brain: Neuropsychological aspects of developmental
reading disability. School Psychology Review. 10. 350-355.
Plaisted, J. R, Gustavson, J. 1., Wilkening, G. N., & Golden, C. J. (1983). The Luria-Nebraska
Neuropsychological Battery-Children's Revision: Theory and current research findings.
Journal of Clinical Child Psychology, 12, 13-21.
Rao. S. M., & Bieliauskas, 1. A. (1983). Cognitive rehabilitation two and one-half years post
right temporal lobectomy. Journal of Clinical Neuropsychology. 5. 313-320.
Reed. H. B. C., Reitan, R M., & Klove, H. (1965). Influence of cerebral lesions in psychologi-
cal test performance of older children. Journal of Consulting Psychology, 29. 247-251.
Reitan, R. M. (1966). A research program on the psychological effects of brain lesions in
142 G. REID LYON et a1.
Attention
RUSSELL A. BARKLEY
INTRODUCTION
145
146 RUSSELL A. BARKLEY
why relatively simple measures of attention typically have not been in-
cluded in the test batteries frequently given by either clinical child psy-
chologists (Rosenberg & Beck, 1986) or child neuropsychologists (Plai-
sted, Gustavson, Wilkening, & Golden, 1983; Rourke, 1981). What types of
attention should be assessed and how to do so conveniently in routine
clinical practice remain unresolved issues in clinical child neuropsychol-
ogy. Yet much of the research literature on attention has been conducted
with children, and a considerable amount of this with children having a
quasi-neuropsychological disorder known as attention deficit disorder
(ADD), with or without hyperactivity (American Psychiatric Association,
1980). In fact, ADD is probably the most well studied of childhood psy-
chological disorders (Barkley, 1988; Ross & Ross, 1982; Weiss &
Hechtman, 1979).
It is the purpose of this chapter to draw upon this wealth of research
to provide (1) an appreciation for the importance of attention in child
neuropsychological assessment, (2) an understanding of its components,
(3) a brief survey of currently available methods of clinical assessment,
and (4) awareness of some of the critical issues that remain to be ad-
dressed in each of these domains. Psychophysiological measures or corre-
lates of attention will not be reviewed in this chapter owing to their rare
inclusion in neuropsychological assessments of children and their indi-
rectness as indices of attention as a cognitive or behavioral construct.
Instead, the focus of this chapter is upon behavioral measures of attention
and its components.
Components of Attention
Numerous attempts have been made to define attention, many of
which are lacking in precision and operational terms (Gibson & Rader,
1979). Early philosophers viewed attention as a mental faculty dispensed
by organisms from a limited pool or capacity. In such conceptualizations,
attention is "paid" or deployed by the organism as if it were withdrawn
from a limited cognitive bank account or staging area that could be de-
pleted (Mackworth, 1976). Other theorists speculate that there is not just a
limited reservoir of attention but also a limited range of stimuli or ac-
tivities to which an organism can optimally attend simultaneously. What
determines these limits is not clear in these formulations.
Current conceptualizations as well as experimental research with
children suggest that attention may be best understood as a multidimen-
sional construct having numerous components (Piontrowski & Calfee,
1979). There exists at least some consensus for the following dimensions:
Alertness or arousal appears to refer to the degree of general sensitivity of
the child to the environment. Alertness seems to mean a generalized
wakefulness or state of responsivity, but to nothing in particular. Selec-
tive or focused attention most commonly refers to the child's ability to
focus on critical stimuli, or those essential to the task, while ignoring
unessential elements. Deficits in this component may be thought of as
inattention. It is closely linked to distractibility, which refers to the extent
to which a child responds to the unessential or irrelevant aspects of a task.
Although it is not typically considered a component of attention, exten-
sive research of ADD children (Douglas & Peters, 1979; Milich & Kramer,
1984) suggests that impulsivity closely overlaps with these aspects of
attention. It often means the speed and accuracy with which a child reacts
to an event or task. Rapid, inaccurate responding is defined as impulsivity
(Milich & Kramer, 1984). Sustained attention means the duration of a
child's responding to a task or stimulus and is sometimes referred to as
vigilance. It seems more accurate, however, to view vigilance as an aspect
of sustained attention in which the child persists in directing his sensory
ATTENTION 149
Developmental Considerations
Because children's mental and physical abilities seem almost in a
constant state of change and maturation, attention and its components
should be found to vary considerably with development. Ample research
documents an increase in the specificity of perception or focus of atten-
tion with increasing age (Gibson & Rader, 1979). This progressive differ-
entiation of selective attention with experience and maturation results in
greater economy of effort as children learn to distinguish "signal" from
"noise" more efficiently, or relevance from irrelevance in stimulus dis-
plays. Also with maturation comes a lengthening of children's attention
span, such that more time is spent looking at, exploring, manipulating,
and generally interacting with an object than occurred in prior stages of
development (Milich, 1984). Children demonstrate increased vigilance or
duration of sustained perception to a signal detection task as well as a
commensurate decrease in impulsivity with increased maturation (Gor-
don, McClure, & Post, 1983; Salkind & Nelson, 1980). After age 12 years,
response time remains relatively unchanged whereas accuracy continues
to improve, implying an ongoing development in efficiency of attentional
search strategies at these later ages.
Seemingly at odds with the progressive specificity of attention with
age, children also display greater breadth of attention or span of ap-
prehension with development. In other words, they are able to attend to a
far larger array of stimuli simultaneously as they mature (Gibson & Rader,
1979). This should not be surprising, however, given that greater specific-
ity or sharpness of attention may permit older children to monitor and
respond simultaneously to larger and more complex stimulus arrays with
heightened efficiency. Along with these changes appears to come a de-
cline in their proneness to distraction by task-irrelevant stimuli (Wood-
cock, 1976). Condry, McMahon, and Levy (1979) have shown that older
children also seem better able to effectively utilize warning stimuli, or
information preceding a task or activity, than do younger children. This
suggests a greater preparedness to attend with increasing age in children
(Gibson & Rader, 1979). Perhaps related to this, children acquire and
utilize progressively more efficient, complex, and effective search strat-
egies over time so as to expend attention more economically during prob-
lem-solving activities (Salkind & Nelson. 1980).
With these changes in attention, particularly those related to greater
sustained attention, the duration of children's compliance with parental
commands and requests increases (Barkley, Karlsson, & Pollard, 1985).
This is accompanied by a corresponding decline in the amount of direc-
tion, commands, and control exerted by caregivers over the children's
play and task performance activities. Such findings underscore the impor-
tance of attention in social functioning. Deficits in the components of
ATTENTION 151
ASSESSMENT OF ATTENTION
Rating N of Ages
scale a Rater items Norms (years) Relevant scales
"CPRS = Conners Parent Rating Scale. CPRS-R = Conners Parent Rating Scale-Revised. CTRS = Conners
Teacher Rating Scale. CTRS-R = Conners Teacher Rating Scale-Revised. CBCL = Child Behavior Check-
list. CBCL-TRF = Child Behavior Checklist-Techer Report Form. CAP = Child Assessment Profile. RBPC
= Revised Behavior Problem Profile. PBQ = Preschool Behavior Questionnaire. ACTeRS = Add-H
Comprehensive Teacher Rating Scale.
Below is a list of items that describes pupils. For each item that describes the pupil now or
within the past week, check whether the item is Not True, Somewhat or Sometimes True, or
Very or Often True. Please check all items as well as you can, even if some do not seem to
apply to this pupil.
Somewhat Very
or or
Not Sometimes Often
True True True
1. Fails to finish things he/she starts ............ . [I [I [I
2. Can't concentrate, can't pay attention for long .. [I [I [I
3. Can't sit still, restless, or hyperactive ......... . [I [I [I
4. Fidgets ..................................... . [I [I [I
5. Daydreams or gets lost in his/her thoughts .... . [I [I [I
6. Impulsive or acts without thinking ........... . [I [I [I
7. Difficulty following directions ............... . [I [I [I
8. Talks out of turn ............................ . [I [I [I
9. Messy work ................................ . [I [I [I
10. Inattentive, easily distracted ................. . [I [I [I
11. Talks too much ............................. . [I [I [I
12. Fails to carry out assigned tasks .............. . [I [I [I
Please feel free to write any comments about the pupil's work or behavior in the last week.
FIGURE 1. CAP rating scale. (cl Copyright 1986 Craig Edelbrock, Psychiatry,
UMMS, Worcester, MA 01605.
Inattention b
Median 1 2 0
69th percentile 3 4 2
84th percentile 6 7 5
93rd percentile 8 9 7
98th percentile 11 12 10
Overactivity
Median 0 1 0
69th percentile 1 2 1
84th percentile 4 4 2
93rd percentile 6 6 5
98th percentile 8 8 7
Total score
Median 2 4 1
69th percentile 6 7 4
84th percentile 10 11 8
93rd percentile 14 15 11
98th percentile 19 20 16
oNumbers in parentheses are sample sizes.
blnattention score is the sum of items 1, 2, 5, 7, 9, 10, and 12.
The Overactivity score is the sum of items 3, 4, 6, 8, and 11.
Table entries are raw scores that fall at or below the desig-
nated percentile range. The 93rd percentile is the recom-
mended upper limit of the normal range. Scores exceeding
this cutoff are in the clinical range. All scores are based on
teacher reports.
Cancellation Tasks
Several paper-and-pencil versions of CPT tasks have been used as
methods of assessing attention, primarily vigilance and impulsivity.
These tasks typically involve having the subject scan a series of symbols
(i.e., letters, numbers, shapes) in rows on paper. The subject is typically
required to draw a line through or under the target stimulus using a
pencil. One such task is the Children's Checking Task (CCT), developed
by Margolis (1971). The task consists of a series of 15 numerals per row
printed in 16 rows on a page. There are seven pages to the task. A tape
recorder reads off the numbers in each row, and the child is required to
draw a line through each number as it is read. Discrepancies between the
tape and the printed page are to be circled. There are seven discrepancies
between the tape and the printed pages. The task takes about 30 minutes.
Scores are derived for errors of omission (missed discrepancies) and er-
rors of commission (numbers circled when no discrepancy exists). The
task discriminates educationally handicapped from normally achieving
students (Keough & Margolis, 1976) and ADD from reading-disabled chil-
dren (Brown & Wynne, 1982). It also appears to correlate to a modest but
significant degree with other measures of attention (Keough & Margolis,
1976).
Another cancellation task is the Underlining Test developed by
Doehring and used extensively in neuropsychological studies by Rourke
and his colleagues (Rourke & Gates, 1980; Rourke & Orr, 1977). The task
consists of 14 subtests. Each subtest varies as to whether it involves num-
bers, geometric shapes, letters or letter combinations, or words. In each
subscale, the child is required to scan rows of these symbols on a page and
to underline a particular one that matches a sample provided at the top of
164 RUSSELL A. BARKLEY
the page. The child's speed and accuracy in performing the task are re-
corded. The subtests range in degree of difficulty, with subtests 1 and 13
being identical to assess practice effects, and another subtest (14) involving
stimuli (rectangles) that are all identical, and all of which the child must
underline. This is designed to control for motor speed. Normative data are
available (Rourke & Gates, 1980), and impairments on the tests have some
relationship to reading and spelling deficits in children (Rourke & Orr,
1977). The test would seem to require adequate visual perception, spatial
discrimination, number and letter facility, and adequate motor speed and
coordination. Where these are intact but performance on the task is im-
paired, deficits in selective attention may be hypothesized.
Mazes
Maze performance has frequently been used in child neuropsycho-
logical research as a measure of motor planning, speed, and execution, as
well as impulsivity and sustained attention (Reitan & Davison, 1974; Rou-
rke, Bakker, Fisk, & Strang, 1983). Poor maze performances have been
noted in ADD children (Milich & Kramer, 1984), children surviving
closed head injury (Klonoff, Low, & Clark, 1977), and epileptic children
undergoing treatments with anticonvulsants (Schain et 01., 1977). Such
tests also have proven sensitive to stimulant drug effects in ADD children
(Barkley, 1977a, 1977b).
ATTENTION 165
Probably the most commonly used maze test is the Porteus Mazes
(1965). Although originally intended as a measure of intelligence, the test
has been most typically used to assess impulsivity, sustained attention,
and the motor parameters noted above. In this paper-and-pencil task, the
printed mazes progress across a range of increasingly difficult configura-
tions. A year level, test quotient, and Q score are obtained, the latter
believed to assess impulsivity. Another paper-and-pencil maze test is an
optional subtest of the Wechsler Intelligence Scale for Children-Revised
(1974), for which normative data are available. A maze test often used in
neuropsychological evaluations is part of the Wisconsin version of the
Halstead-Reitan Neuropsychological Test Battery (Matthews & Klove,
1965). It involves the child's using a metal stylus to traverse a raised metal
maze. The child's speed of performance, number of contacts with the
sides of the maze, and time in contact with the sides is recorded.
to press a button, wait a while, and press it again. If the child has waited
long enough, a point is earned. Cumulative points are recorded on a
display screen. The child is not informed of the delay interval (6 seconds)
but is reinforced with points on each trial that exceeds the standard inter-
val. The test is brief (8 minutes), and normative data are available for more
than 1400 children. The test discriminates ADD from non-ADD clinic-
referred children, and it correlates moderately and significantly with the
MFFT, the Conners parent and teacher rating scales, and the Child Behav-
ior Checklist Teacher Report Form (Gordon e1 01., 1983). Although prom-
ising, the task has not proven sensitive to stimulant drug effects with ADD
children (Barkley e1 01., 1988).
pecially if clinic analogue settings are used. They also are particularly
sensitive to treatment manipulations. However, their main drawback at
present remains the lack of normative data for use in establishing de-
viance of attention during initial clinic evaluations. This is less of an issue
in child neuropsychological research, but it is a major problem for clinical
practice. Nevertheless, such recordings may still prove useful in measur-
ing within-subject changes in behavior due to stimulant medication or
other interventions in clinical practice.
DISCUSSION
SUMMARY
REFERENCES
Abikoff, H., Gittelman-Klein, R., & Klein, D. (1977). Validation of a classroom observation
code for hyperactive children. Journal of Consulting and Clinical Psychology, 45, 772-
783.
Achenbach, T. M., & Edelbrock, C. (1983). Manual for the Child Behavior Checklist and
Revised Child Behavior Profile. Burlington, VT: Thomas Achenbach.
American Psychiatric Association. (1980). Diagnostic and statistical manual of mental dis-
orders (3rd ed.). Washington, D.C.
Barkley, R. (1977a). A review of stimulant drug research with hyperactive children. Journal
of Child Psychology and Psychiatry, 18, 137-165.
Barkley, R. (1977b). The effects of methylphenidate on various measures of activity level and
attention in hyperkinetic children. Journal of Abnormal Child Psychology, 5, 351-369.
172 RUSSELL A. BARKLEY
Barkley, R. A. (1981). Hyperactive children: A handbook for diagnosis and treatment. New
York: Guilford Press.
Barkley, R. A. (1985). Family interaction patterns in hyperactive children: Precursors to
aggressive behavior? In M. Wolraich & D. Routh (Eds.), Advances in behavioral pedi-
atrics (pp. 117-150). Greenwich, CT: JAI Press.
Barkley, R. A. (1987). A review of child behavior checklists and rating scales for research in
child psychopathology. In M. Rutter, A. H. Tuma, & 1. S. Lann (Eds.), Assessment and
diagnosis in child psychopathology. New York: Guilford Press.
Barkley, R. A. (1988a). Attention deficit disorders. In E. Mash & 1. Terdal (Eds.), Behavioral
assessment of childhood disorders (2nd ed.). New York: Guilford Press.
Barkley, R. A. (1988b). Tic disorders and Tourette's syndrome. In E. Mash & 1. Terdal (Eds.),
Behavioral assessment of childhood disorders (2nd ed.). New York: Guilford Press.
Barkley, R. A. (in press). The problem of stimulus control and rule-governed behavior in
attention deficit disorder with hyperactivity. In 1. Bloomingdale & J. Swanson (Eds.),
Attention deficit disorders (vol. 3). New York: Pergamon.
Barkley, R., Fischer, M., Newby, R. F., & Breen, M. J. (1988). Development of a multi-method
clinical protocol for assessing stimulant drug responding in ADD children. Journal of
Clinical Child Psychology, 17,14-24.
Barkley, R., Karlsson, J., & Pollard, S. (1985). Effects of age on the mother-child interactions
of hyperactive boys. Journal of Abnormal Child Psychology, 13,631-637.
Behar, L., & Stringfield, S. (1974). A behavior rating scale for the preschool child. Develop-
mental Psychology, 10, 601-610.
Boll, T. J. (1981). The Halstead-Reitan Neuropsychological Test Battery. In S. Filskov & T.
Boll (Eds.), Handbook of clinical neuropsychology (Vol. 1, pp. 577-607). New York:
Wiley.
Boll, T. J. (1983). Minor head injury in children-Out of sight but not out of mind. Journal of
Clinical Child Psychology, 12, 74-80.
Bremer, D. A., & Stern, J. A. (1976). Attention and distractibility during reading in hyperac-
tive boys. Journal of Abnormal Child Psychology, 4, 381-387.
Brouwers, P., Riccardi, R., Poplack, D., & Fedio, P. (1984). Attentional deficits in long term
survivors of childhood acute lymphoblastic leukemia (ALL). Journal of Clinical Neuro-
psychology, 6, 325-336.
Brown, R. T., & Quay, 1. C. (1977). Reflection-impulsivity in normal and behavior-disor-
dered children. Journal of Abnormal Child Psychology,S, 457-462.
Brown, R. T., & Wynne, M. E. (1982). Correlates of teacher ratings, sustained attention, and
impulsivity in hyperactive and normal boys. Journal of Clinical Child Psychology, 11,
262-267.
Buchsbaum, M. S. & Sostek, A. J. (1980). An adaptive continuous performance test: Vigilance
characteristics and reliability for 400 male students. Perceptual and Motor Skills, 51,
707-713.
Cantwell, D. P., & Carlson, G. (1978). Stimulants. In J. Werry (Ed.), Pediatric psychophar-
macology (pp. 171-207). New York: Brunner/Mazel.
Condry, S., McMahon, M., & Levy, A. (1979). A developmental investigation of selective
attention to graphic, phonetic, and semantic information in words. Perception and
Psychophysics, 25, 88-94.
Conners, C. K. (1969). A teacher rating scale for use in drug studies with children. American
Journal of Psychiatry, 126, 884.
Conners, C. K. (1970). Symptom patterns in hyperkinetic, neurotic, and normal children.
Child Development, 41, 667-682.
Czudner, G., & Rourke, B. P. (1972). Age differences in visual reaction time of "brain-
damaged" and normal children under regular and irregular preparatory interval condi-
tions. Journal of Experimental Child Psychology, 13, 516-526.
ATTENTION 173
Denton, C. 1., & Mcintyre, C. W. (1978). Span of apprehension in hyperactive boys. Journal
of Abnormal Child Psychology, 6, 19-24.
Douglas, V. I. (1983). Attention and cognitive problems. In M. Rutter (Ed.), Developmental
neuropsychiatry (pp. 280-329). New York: Guilford Press.
Douglas, V. 1., & Peters, K. G. (1979). Toward a clearer definition of the attentional deficit of
hyperactive children. In G. A. Hale & M. Lewis (Eds.), Attention and cognitive develop-
ment (pp. 173-248). New York: Plenum.
Draeger, S., Prior, M., & Sanson, A. (1986). Visual and auditory attention performance in
hyperactive children: Competence or compliance Journal of Abnormal Child Psychol-
ogy, 14,411-424.
Edelbrock, C., & Achenbach, T. A. (1984). The Teacher Version of the Child Behavior Profile:
I. Boys aged 6-11. Journal of Consulting and Clinical Psychology, 52, 207-217.
Egeth, H., & Bevan, W. (1973). Attention. In B. B. Wolman (Ed.), Handbook of general
psychology. Englewood Cliffs, NJ: Prentice-Hall.
Foch, T. T., & Plomin. R (1980). Specific cognitive abilities in 5- to 11-year-old twins.
Behavior Genetics, 10, 507-520.
Gibson, E., & Rader, N. (1979). Attention: Perceiver as performer. In G. Hale & M. Lewis
(Eds.), Attention and cognitive development (pp. 1-22). New York: Plenum.
Goff, J. R, Anderson, H. R, & Cooper, P. F. (1980). Distractibility and memory deficits in
long-term survivors of acute lymphoblastic leukemia. Developmental and Behavioral
Pediatrics, 1, 158-163.
Gordon, M. (1979). The assessment of impulsivity and mediating behaviors in hyperactive
and nonhyperactive children. Journal of Abnormal Child Psychology, 7, 317-326.
Gordon, M., McClure, F. D., & Post, E. M. (1983). Interpretive guide to the Gordon Diagnostic
System. DeWitt, NY: Gordon Systems.
Gosling, H., & Jenness, D. (1974). Temporal variables in simple reaction times of mentally
retarded boys. American Journal of MentaI' Deficiency, 79, 214-224.
Goyette, C. H., Conners, C. K., & Ulrich, R F. (1978). Normative data for Revised Conners
Parent and Teacher Rating Scales. Journal of Abnormal Child Psychology, 6, 221-236.
Gray, J. A. (1972). Learning theory, the conceptual nervous system, and personality. In V. D.
Neblitsin & J. A. Gray (Eds.), Biological bases of individual behavior (pp. 370-398).
New York: Academic Press.
Gray, J. A. (1982). The neuropsychology of anxiety: An enquiry into the functions of the
septo-hippocampal system. New York: Oxford University Press.
Hale, G., & Lewis, M. (1979). Attention and cognitive development. New York: Plenum.
Heilman, K., & Valenstein, F. (1985) Clinical neuropsychology (2nd ed.). New York: Oxford
University Press.
Holdsworth, 1., & Whitmore, K. (1974). A study of children with epilepsy attending ordinary
schools. I: Their seizure patterns, progress, and behaviour in school. Developmental and
Child Neurology, 16, 746-758.
James, W. (1890). The principles of psychology. New York: Holt.
Kagan, J., Rosman, B., Day, D., Albert, J., & Phillips, W. (1964). Information processing in the
child: Significance of analytic and reflective attitudes. Psychological Monographs,
78,(1, Whole No. 578).
Kaufman, A. S. (1975). Factor analysis of the WISC-R at eleven age levels between 6V, and
16V, years. Journal of Consulting and Clinical Psychology, 43, 135-147.
Kaufman, A. S. (1980). Issues in psychological assessment: Interpreting the WISC-R intel-
ligently. In B. Lahey & A. Kazdin (Eds.), Advances in clinical child psychology (Vol. 3,
pp. 177-214). New York: Plenum.
Kazdin, A. E., Esveldt-Dawson, K. & Loar, 1. 1. (1983). Correspondence of teacher ratings and
direct observations of classroom behavior of psychiatric inpatient children. Journal of
Abnormal Child Psychology, 11, 549-564.
174 RUSSELL A. BARKLEY
Quay, H. C., & Peterson, D. R. (1983). Interim manual for the Revised Behavior Problem
Checklist. Unpublished manuscript, University of Miami.
Rapport, M. D., Stoner, G., DuPaul, G. J., Birmingham, B. K, & Tucker, S. (1985). Meth-
ylyphenidate in hyperactive children: Differential effects of dose on academic learning,
and social behavior. Journal of Abnormal Child Psychology, 13, 227-244.
Reitan, R. & Davison, L. (1974). Clinical Neuropsychology: current status and applications.
New York: Wiley.
Rosenbert, R. P., & Beck, S. (1986). Preferred assessment methods and treatment modalities
for hyperactive children among clinical child and school psychologists. Journal of
Clinical Child Psychology, 15, 142-147.
Ross, D. M., & Ross, S. A. (1982). Hyperactivity: Current issues, research, and theory (2nd
ed.). New York: Wiley.
Rosvold, H. E., Mirsky, A. F., Sarason, I., Bransome, E. D., & Beck, 1. H. (1956). A continuous
performance test of brain damage. Journal of Consulting Psychology, 20, 343-350.
Rourke, B. P. (1981). Neuropsychological assessment of children with learning disabilities.
In S. Filskov & T. Boll (Eds.), Handbook of clinical neuropsychology (Vol. 1, pp. 453-
480). New York: Wiley.
Rourke, B. P., Bakker D. J., Fisk, J. L., & Strang, J. D. (1983). Child neuropsychology. New York:
Guilford Press.
Rourke, B. P., & Gates, R. D. (1980). Underlining test: Preliminary norms. Windsor, Ontario:
Authors.
Rourke, B. P., & Orr, R. R. (1977). Prediction of the reading and spelling performances of
normal and retarded readers: Four-year follow-up. Journal of Abnormal Child Psychol-
ogy, 5, 9-20.
Routh, D. K., & Schroeder, C. S. (1976). Standardized playroom measures as indices of
hyperactivity. Journal of Abnormal Child Psychology, 4, 199-207.
Salkind, N. J., & Nelson, C. F. (1980). A note on the developmental nature of reflection-
impulsivity. Developmental Psychology, 16, 237-238.
Schain, R. J., Ward, J. W., & Guthrie, D. (1977). Carbamazine as an anticonvulsant in chil-
dren. Neurology, 27, 476-480.
Skinner, B. F. (1953). Science and human behavior. New York: Macmillan.
Skinner, B. F. (1969). Contingencies of reinforcement: A theoretical analysis. New York:
Appleton-Century-Crofts.
Stein, L. (1985, October). Methylphenidate and the effects of reinforcement. Paper presented
at the Hogg Foundation Conference on Attention Deficit Disorders, San Antonio, TX.
Stewart, K J., & Moely, B. E. (1983). The WISC-R third factor: What does it mean? Journal of
Consulting and Clinical Psychology, 51, 940-941.
Swanson, J., & Kinsbourne, M. (1979). The cognitive effects of stimulant drugs on hyperac-
tive children. In G. Hale & M. Lewis (Eds.), Attention and cognitive development (pp.
249-274). New York: Plenum.
Titchener, E. B. (1924). A textbook of psychology. New York: Macmillan.
Trites, R. L., Blouin, A. G. A., & LaPrade, K. (1982). Factor analysis of the Conners Teacher
Rating Scale based on a large normative sample. Journal of Consulting and Clinical
Psychology, 50, 615-623.
Ullmann, R. K, Sleator, E. K., & Sprague, R. L. (1984). A new rating scale for diagnosis and
monitoring of ADD children. Psychopharmacology Bulletin, 20, 160-164.
Wechsler, D. (1974). The Wechsler Intelligence Scale for Children-Revised. New York: Psy-
chological Corp.
Weiss, G., & Hechtman, L. (1979). The hyperactive child syndrome. Science, 205, 1348-
1354.
Werry, J., & Quay, H. (1971). The prevalence of behavior symptoms in younger elementary
school children. American Journal of Orthopsychiatry, 41, 136-143.
176 RUSSELL A. BARKLEY
Whalen, C., & Henker, B. (1980). Hyperactive children: The social ecology of identification
and treatment. New York: Academic Press.
Whalen, C., Henker, B., & Dotemoto, S. (1980). Methylphenidate and hyperactivity: Effects
on teacher behaviors. Science, 208, 1280-1282.
Witkin, H. A., Oltman, P., Raskin, E., & Karp, S. (1971). Manual for the Children's Embedded
Figures Test. Palo Alto, CA: Consulting Psychologists Press.
Wolf, S. M., & Forsythe, A. (1978). Behavior disturbance, phenobarbital, and febrile seizures.
Pediatrics, 61, 728-731.
Woodcock, R. W. (1976). Goldman-Fristoe-Woodcock Auditory Skills Test Battery Tech-
nical Manual. Circle Pines, MN: American Guidance Service.
7
THOMAS A. BOYD
INTRODUCTION
THOMAS A. BOYD Cleveland Metropolitan General Hospital, and Case Western Reserve
University School of Medicine, Cleveland, Ohio.
177
178 THOMAS A. BOYD
Wechsler Intelligence
Scale for Children-Re-
vised (Wechsler, 1974)
Information Long-term verbal recall of general Verbal Verbal 6-0 to 16-11 Based on Guilford's (1967)
information Structure of Intellect
Digit Span Short-term memory span for digits Verbal Verbal! Model.
pointing Vocabulary also may be a
Arithmetic Numerical reasoning, long-term Verbal Verbal measure of long-term ver-
memory bal memory.
Digit Span can be adapted to
pointing (Smith, 1975).
Cooper (1982) has developed
a Post-Wechsler Memory
Scale.
Stanford-Binet Intelligence
Scale (Thorndike,
Hagen, & Sattler, 1986)
Bead Memory Replication of bead sequences Visual Motor 2-0 to 18 Short-term memory com-
from memory prises one of three broad-
Memory for Sentences Sentence repetition Verbal Verbal band factors in the tests'
Memory for Digits Short-term memory span for digits Verbal Verbal hierarchical model of cog-
Memory for Objects Sequential pointing to objects pre- Visual Motor nitive abilities. A standard
viously displayed Age Score is derived for
short-term memory. Over-
comes limitations of the
1960 Stanford-Binet (Her-
man & Merrill, 1960/1973)
owing to discontinuous
presentation of memory
tasks across age levels.
McCarthy Scales of Chil-
dren's Abilities (McCar-
thy, 1972)
Pictorial Memory Short-term memory for objects Visual! Verbal 2-6 to 8-6 Difficult to make com-
verbal parisons between subtest
Tapping Sequence Short-term nonverbal sequential Visual! Motor scores.
Verbal Memory I and memory auditory
II Word and sentence repetition; Verbal Verbal
Numerical Memory I short-term story recall
and II Short-term memory span for digits Verbal Verbal
Kaufman Assessment Bat-
tery for Children (Kauf-
man & Kaufman, 1983a,
1983b)
Face Recognition Short-term memory for faces Visual Motor 2-6 to 4-11 All of the achievement sub-
Hand Movements Visual Motor 2-6 to 12-5 tests are considered to in-
Short-term recall of sequential volve long-term memory
Number Recall hand movements Verbal Verbal 2-6 to 12-5 (Kaufman & Kaufman,
Word Order Short-term recall of sequential Verbal Verbal! 4-0 to 12-5 1983b).
hand movements motor
Spatial Memory Short-term memory span for digits Visual Motor 5-0 to 12-5
Sequential touching of previously
named objects
Recall locations of pictures ar-
ranged randomly on a page
Detroit Tests of Learning
Aptitude (2nd ed.)
DTLA-2 (Hammill,
1985)
Sentence Imitation Sentence repetition Verbal Verbal 6-0 to 17-11 Revision of the DTLA (Baker
Oral Directions Perform orally directed series of Verbal Motor & Leland, 1967).
actions Poor subtest reliability (Ra-
(continued)
TABLE 1. (Continued)
Word Sequences Repeat string of unrelated words Verbal Verbal dencich, 1986).
Design Reproduction Draw geometric form from Visual Motor
Object Sentences memory Visual Motor/
Written recall of series of pictured verbal
Letter Sequences objects Visual Motor/
Written recall of sequence of let- verbal
ters
Halstead-Reitan Neuropsy-
chological Batteries (Re-
itan & Davison, 1974)
Target Test Reproduction of visual-spatial Visual Visual- 5 to 8 No specific measures of ver-
configurations motor bal memory appear in the
Tactual Performance Draw shapes and location of stim- Tactile Visual- 5 to 14 battery other than those
Test ulus blocks from memory motor associated with WISC-R.
Category Test Recall of previously learned deci- Visual Motor/ 9 to 14
sion principles nonverbal
Luria-Nebraska Neuropsy-
chological Battery
(Golden, Hammeke, &
Purisch, 1980)
Memory Scale Eleven memory tasks (13 test Verbal Verbal 13 to adult Test is normed on an adult
items) assessing short-term ver- sample but frequently ap-
bal and nonverbal memory with Visual Verbal! plied to adolescents.
and without interference motor
Luria-Nebraska Neuropsy-
chological Battery Chil-
dren's Revision (Golden,
1981)
Memory Scale Eight memory tasks (8 items) as- Verbal Verbal 8 to 12 Test items are based on
sessing short-term verbal and adult version of the
nonverbal memory with and Visual Verbal! LNNB.
without interference motor
Denman Neuropsychologi- 11 subtests measuring immediate Verbal Verbal 10 to adult Format of battery highly
cal Memory Scale (Den- recall, short-term memory, and similar to Wechsler Intelli-
man, 1984) memory for remotely stored in- Visual- Visual- gence Scales.
formation across verbal (6 sub- motor motor Major weaknesses apparent
tests) and nonverbal (5 subtests) in test construction. Poor
domains Auditory Verbal norms and validity.
Benton Revised Visual Re-
tention Test (Benton,
1974)
Administration A 10-second exposure to geometric Visual Motor 8 to adult Norms for age 8 to 14 for
shapes with immediate recall Administration A and C
reproduction only.
Administration B 5second exposure with immedi- 15 to adult Norms take into account age
ate recall and intelligence level. No
Administration C Copy shapes; no recall norms for Administration
Administration D 10-second exposure with recall af- D.
ter 15-second delay 3 alternate forms.
Memory for Designs Test 15 geometric designs, exposed one Visual Motor 8-6 to 60 Corrections for age and in-
(Graham & Kendall, at a time for 5 seconds followed telligence are recom-
1960) by immediate recall! mended for children.
reproduction Scoring system of question-
able reliability.
Auditory-Verbal Learning Immediate recall of 15-word list Verbal Verbal 5 to 15 Limited norms available.
Test (Rey, 1964) wi th repeated trials Adults
184 THOMAS A. BOYD
The Benton Visual Retention Test (Benton, 1974), the Memory for
Designs Test (Graham & Kendall, 1960), the Auditory Verbal Learning Test
(Rey, 1964), and other similar single-task procedures represent the main-
stay of specific memory assessment in clinical practice. Beyond re-
strictions in their task composition and complexity, most of these pro-
cedures possess distinct psychometric weaknesses, such as poor
reliability, as well as inadequacies in their standardization and limitations
in age-based norms. Further, systematic comparison across these various
measures is invalidated by the differences in their standardization and
psychometric properties.
The Denman Neuropsychology Memory Scale (DNMS; Denman,
1984), to date, does not appear to be a frequently employed test in clinical
practice. Nevertheless, it has been included in Table 1 because it repre-
sents a contemporary effort to address some of the deficiencies cited in
the preceding paragraph regarding single-task procedures. The DNMS
comprises six Verbal subtests and five Nonverbal subtests packaged in a
format similar to the Wechsler intelligence scales. Scores are derived for
each subtest (M = 10, SD = 3) and for Verbal, Nonverbal, and Full Scale
Memory Quotients (M = 100, SD = 15). The subtests of the DNMS have
been based on existing assessment methods drawn from clinical tradition,
and their combined standardization within a single battery ostensibly
permits valid systematic comparisons across the various subtests and be-
tween broad domains of memory (i.e., Verbal and Nonverbal). Unfortu-
nately, the DNMS is a seriously flawed psychometric instrument that,
even upon casual review, is severely limited in its clinical utility (Hooper
& Boyd, 1987). The subtests of the DNMS provide solely a quantitative
assessment of memory functions to the exclusion of important qualitative
factors (e.g., there are no cross-modal pairings of stimulus materials). The
normative base for the battery is extraordinarily weak at present and not
representative of the general population. In general, it does not appear
that appropriate standards for test construction (i.e., the establishment of
reliability and validity) were followed. Aslo, it represents a rather am-
bitious attempt to assess memory functions across nearly a 60-year age
span (age 10 and older) without recourse to a theoretical model of memory
development.
Although the DNMS is not by any means unique in the kind and
seriousness of its deficiencies, it amply illustrates the fallacy inherent to
any modern effort to develop a battery of memory tests simply by collect-
ing new norms for a set of unimodal traditional methods. Memory pro-
cesses are not simple, and measurement tools consisting of a variety of
separate unimodal measures, no matter how venerated, will only con-
tinue the tradition of piecemeal assessment and will not adequately eval-
uate the complexities of memory performance and its dysfunctions.
The foregoing caveats regarding memory tests and their construction
CHILDREN'S MEMORY 185
Information-Processing Models
Although no universally accepted model of memory development
has appeared to date, information-processing models of memory are ex-
tant. These embrace the concept of memory as a dynamic phenomenon
that undergoes predictable changes with development. To be discussed
are the multistore model of memory proposed by Atkinson and Shiffrin
(1968) and the levels-of-processing model proposed by Craik and Lock-
hart (1972).
ty, can maintain information by rehearsal, and (3) a long-term store with
unlimited capacity. Changes in memory ability that occur during infancy
and early childhood are usually attributed to changes in the child's struc-
tural features that possibly reflect developments in neural structure (Kail
& Hagen, 1982). Age-related improvements in school-age children are
attributed to increasing sophistication in the child's available control pro-
cesses. These self-directed processes control the flow of information
among the three structural components and are described as "transient
phenomena under the control of the subject; their appearance depends on
such factors as instructional set, the experimental task, and the past histo-
ry of the subject" (Atkinson & Shiffrin, 1968, p. 106). This latter point has
important clinical significance because it anticipates the model proposed
by Jenkins (1979), which will be discussed later in this section.
Kail, 1979; Ornstein, 1978; Paris & Lindauer, 1982) have used these and
other general models of memory as frameworks for organizing the devel-
opmentalliterature on memory, the models possess few specific develop-
mental implications and do not furnish any particular insights to the task
of constructing a clinically relevant battery of memory tests.
CHARACTERISTICS OF
THE LEARNER
Skills
Knowledge
Intent
MotivatIOn
Strategic competence
Metamemory
Cognitive level
Memory capacity
etc.
CRITERIAL TASKS
LEARNING ACTIVITIES
Recognition
Orienting task Recall
Task instructions Problem solving
Strategies Transfer of skills
etc, etc.
STIMULUS MATERIALS
Sensory modality
Physical structure
Psychological structure
Conceptual difficulty
Sequence of materials
Number of stimuli
Cues
etc.
of stimulus material (learner variable) may affect the child's selection and
the relative success of particular strategic approaches (activity variable).
Also, although recognition memory is generally assumed to be less
difficult than verbatim recall (task variables), the difference may depend
considerably on whether the material is familiar (e.g., words) or not (e.g.,
nonsense syllables) (Jenkins, 1979). Likewise, changing the structure of
the material while holding the type of material constant can alter a child's
success on a memory task (Moley, 1977; Ornstein & Corsale, 1980; Perl-
mutter & Myers, 1979). Accordingly, the speed of identifying the second
word of a pair is greater if the words are drawn from the same categories
(e.g., dog-lion) as opposed to different ones (e.g., dog-piano) (Sperber,
McCauley, Ragin, & Weil, 1979). Further, compared with younger and/or
impaired learners, older and/or efficient learners show a preference for
taxonomic (e.g., horse-cow) groupings over thematic (e.g., horse-saddle)
190 THOMAS A. BOYD
groupings of materials that enhance both their learning rate (Smiley &
Brown, 1979) and memory performance (Overcast, Murphy, Smiley, &
Brown, 1975).
Criteria1 Tasks. The second point of the pyramid, the criterial task, is
the dependent measure in memory investigations. As noted above,
whether the criterial task requires recognition or recall may impact signif-
icantly on a child's relative success. The interaction between the criterial
task and the learner's activities is at the heart of the levels-of-processing
paradigm in memory research (Jenkins, 1979). If the learner's activities are
focused toward deeper, semantic levels of processing, then superior recall
will be expected. However, it is possible to construct memory tasks in a
manner that precludes particular strategies, such as using materials that
are not semantically related or introducing activities that intervene be-
tween learning and recall as a means of circumventing rehearsal strat-
egies. The degree of mastery over the material to be learned also can be
assessed by using criterial tasks that require inferential problem solving,
or transferring acquired knowledge to new contexts.
evidence for his theory (Burtis, 1982). Case, Kurland and Goldberg (1982),
however, have proposed that the total processing space required for short-
term memory operations remains constant throughout development. The
increments in functional memory capacity result from reductions in the
space required for executing memory operations. This is made possible by
the growing speed, efficiency, and automaticity of these basic processes.
Chi (1976) suggested that restrictions in the young child's knowledge
base, which may limit the richness of associations of various memory
chunks in the system, may underlie these basic processing inefficiencies.
Brown et 01. (1983) consider the capacity-development issue as moot
and conclude that there is insufficient evidence to support the contention
that total processing capacity increases with age. Rather, they propose
that the interaction of developmental changes in the child's knowledge
base, efficiency of basic processes, and the use of strategies accounts for
the observed increments in memory span. These, in turn, are dependent
on the factorial interactions of the tetrahedral model.
The importance of strategic competence to developmental models of
memory has been stressed throughout this section and will not be further
elaborated here. However, one final characteristic of the learner listed in
Figure 1 remains to be discussed. The concept of metamemory (Flavell,
1970; Flavell & Wellman, 1977; Kreutzer, Leonard, & Flavell, 1975)-that
is, knowing about knowing-is an important developmental variable in-
fluencing interactions involving all factors of the tetrahedral model. The
model serves to remind clinical and experimental investigators that
knowledge of interactions within the tetrahedron are essential to an effec-
tive understanding of memory abilities. Similarly, the maturing child also
needs to know something about his or her own characteristics as a learner,
the significance of various learning activities, the demand characteristics
of various tasks, and the inherent nature of various materials in order to
become an effective learner, or to "learn how to learn" (Brown et 01.,
1983).
The multifactorial nature of the tetrahedral model cannot be over-
emphasized in its importance, although the sheer number of possible
interactions places a cumbersome burden on the practical limitations of
time and needs for efficiency in clinical practice. In addition to six 2-
factor interactions, the model allows for three 3-factor interactions and
one 4-factor interaction; each of these would be subject to systematic
variation across the several characteristics of each factor in order to ex-
haust all the possibilities permitted by the model. A set of guidelines is
required that would assist the clinician in selecting which permutations
of the tetrahedral interactions are likely to be most sensitive to develop-
mental changes in memory, or in discriminating competent from incom-
petent memory abilities. Fortunately, a second model, to be described
below, provides just such a set of guidelines.
CHILDREN'S MEMORY 193
Episodic Differences in
> ~ levels, not patterns
Possible dif-
Semantic ferences, pri-
L - - - - - - - - - t.... marily in
(Mediation deficiency)
difference in leve Is patterns
and patterns
Task
FIGURE 2. A model for selecting developmentally sensitive memory tasks. (From Brown,1975.]
CHILDREN'S MEMORY 195
Turning now to the four ideal tasks outlined by Brown (1975), atten-
tion must be paid to the sequence of their presentation so as to minimize
the potential contamination effects between tasks. In general, for reasons
elaborated below, the sequence of presentation should proceed through a
continuum from nonstrategic to strategic tasks, first with semantic mate-
rials followed by an examination of episodic memory abilities.
Nonstrategic-semantic tasks should reflect learning that arises as the
automatic results of meaningful activity. Essentially, these tasks assess
incidental memory, and because the orienting instructions would not
direct the child toward intentional learning, these tasks must precede
those that would induce specific learning sets. If the material of these
tasks matches the child's level of cognitive development, then memory for
CHILDREN'S MEMORY 197
CONCLUSIONS
REFERENCES
Anastasi, A. (1982). Psychological testing. New York: Macmillan.
Appel, 1., Cooper, R., McCarrell, N., Sims-Knight, J., Yussen, S., & Flavell, J. (1972). The
development of the distinction between perceiving and memorizing. Child Develop-
ment, 43, 1365-1381.
Atkinson, R., & Shiffrin, R. (1968). Human memory: A proposed system and its control
processes. In K. W. Spence & J. T. Spence (Eds.), The psychology of learning and
motivation (Vol. 2). New York: Academic Press.
Bach, M., & Underwood, B. (1970). Developmental changes in memory attributes. Journal of
Educational Psychology, 61, 292-296.
Baker, H., & Leland, B. (1967). Detroit Tests of Learning Aptitude. Indianapolis: Bobbs-
Merrill.
Benton, A. L. (1974). Revised Visual Retention Test: Clinical and experimental applications
(4th ed.). New York: Psychological Corporation.
CHILDREN'S MEMORY 201
Golden, c., Hammeke, T., & Purisch, A. (1980). The Luria-Nebraska Neuropsychological
Battery manual. Los Angeles: Western Psychological Services.
Graham, F., & Kendall, B. (1960). Memory for Designs Test: Revised general manual. Percep-
tual and Motor Skills, Monograph Supplement No. 2-VIU, 11, 147-188.
Guilford, J. P. (1967). The nature of human intelligence. New York: McGraw-Hill.
Hagen, J., Jongeward, R, & Kail, R (1975). Cognitive perspectives on the development of
memory. In H. W. Reese (Ed.). Advances in child development and behavior (Vol. 10,
pp. 57-101). New York: Academic Press.
Hagen, J., & Kingsley, P. (1968). Labeling efforts in short-term memory. Child Development,
39, 113-121.
Hammill, D. (1985). Detroit Tests of Learning Aptitude-DTLA-2. Austin, TX: PRO-ED.
Hooper, S. R, & Boyd, T. A. (1986). Neurodevelopmentallearning disorders. In J. E. Obrzut &
G. W. Hynd (Eds.). Child neuropsychology, Volume 2: Clinical Practice. New York:
Academic Press.
Hooper, S., & Boyd, T. (1987). Test review: The Denman Neuropsychology Memory Scale.
International Journal of Clinical Neuropsychology, 9, 141-144.
Horton, D. L., & Mills, C. B. (1984). Human learning and memory. Annual Review of Psychol-
ogy, 35, 361-394.
Howe, M., Brainerd, C., & Kingman, J. (1985). Storage-retrieval processes of normal and
learning-disabled children: A stages-of-learning analysis of picture-word effects. Child
Development, 56, 1120-1133.
Hulicka, 1. M. (1966). Age differences in Wechsler Memory Scale scores. Journal of Generic
Psychology, 109, 135-145.
Hynd, G. W., & Obrzut, J. E. (Eds.). (1981). Neuropsychological assessment and the school-
age child: Issues and procedures. New York: Grune and Stratton.
Istomina, Z. (1975). The development of voluntary memory in preschool-age children. Sovi-
et Psychology. 13, 5-64.
Ivison, D. J. (1977). The Wechsler Memory Scale: Preliminary findings toward an Australian
standardization. Australian Psychologist, 12, 303-312.
Jenkins, J. J. (1979). Four points to remember: A tetrahedral model of memory experiments.
In 1. S. Cermak & F. 1. M. Craik (Eds.). Levels of processing in human memory (pp. 429-
446). Hillsdale, NJ: Erlbaum.
Kagan. J., Klein. R. Finley, G.. Rogoff. B., & Nolan, E. (1979). A cross-cultural study of
cognitive development. Monographs of the Society for Research in Child Development,
44(5. Serial No. 180).
Kail, R (1975). Interrelations in children's use of mnemonic strategies. Unpublished doc-
toral dissertation, University of Michigan.
Kail, R (1979). Use of strategies and individual differences in children's memory. Develop-
mental Psychology, 15, 251-255.
Kail, R. & Hagen. J. W. (1982). Memory in childhood. In B. Wolman, G. Stricker. S. Ellman,
P. Keith-Spiegel, & D. Palermo (Eds.). Handbook of developmental psychology (pp.
350-366). Englewood Cliffs, NJ: Prentice-Hall.
Kaufman, A. & Kaufman. N. (1983a). Administration and scoring manual for the Kaufman
Assessment Battery for Children. Circle Pines, MN: American Guidance Service.
Kaufman, A., & Kaufman, N. (1983b). Interpretive manual for the Kaufman Assessment
Battery for Children. Circle Pines, MN: American Guidance Service.
Klonoff. H., & Kennedy, M. A. (1966). A comparative study of cognitive functioning in old
age. Journal of Gerontology, 21, 239-243.
Kreutzer, M., Leonard, C., & Flavell, J. (1975). An interview study of children's knowledge
about memory. Monographs of the Society for Research in Child Development, 40.{1,
Whole No. 159).
Lezak. M. D. (1983). Neuropsychological assessment (2nd ed.). New York: Oxford University
Press.
CHILDREN'S MEMORY 203
Smiley, S. S., & Brown, A. L. (1979). Conceptual preference for thematic and taxonomic
relations: A nonmonotonic age trend from preschool to old age. Journal of Experimental
Child Psychology, 28, 249-257
Smith, A. (1975). Neuropsychological testing in neurological disorders. In W. J. Friedlander
(Ed.), Advances in neurology (Vol. 7). New York: Raven Press.
Sperber, R. D., McCauley, C., Ragin, R., & Weil, C. (1979). Semantic priming effects on
picture and word processing. Memory and Cognition, 7, 339-345.
Spreen, 0., Tupper, D., Risser, A., Tuokko, H., & Edgell, D. (1984). Human developmental
neuropsychology. New York: Oxford University Press.
Stevenson, H., Parker, T., & Wilkinson, A. (1975). Ratings and measures of memory pro-
cesses in young children. Unpublished manuscript, University of Michigan.
Stone, C. P., & Wechsler, D. A. (1945). Wechsler Memory Scale Form II. New York: Psycho-
logical Corporation.
Stones, M. J. (1979). Rekitting the Wechsler paired-associate task: The Waterford Index.
Journal of Clinical Psychology, 35, 626-630.
Tarter. R. E., & Goldstein, G. (1984). Advances in clinical neuropsychology (Vol. 2). New
York: Plenum Press.
Terman, L., & Merrill, M. (1973). Stanford-Binet Intelligence Scale. Boston: Houghton
Mifflin. (Original work published 1960)
Thorndike, R., Hagen, E., & Sattler, J. (1986). Guide for administering and scoring the Stan-
ford-Binet Intelligence Scale: Fourth Edition. Chicago: Riverside.
Wechsler, D. A. (1945). A standardized memory scale for clinical use. Journal of Psychology,
19, 87-95.
Wechsler, D. A. (1974). Manual for the Wechsler Intelligence Scale for Children-Revised.
New York: Psychological Corporation.
Wedding, D., Horton, A. M., & Webster, J. (Eds.). (1986). The neuropsychology handbook:
Behavioral and clinical perspectives. New York: Springer.
Wickens, D. (1972). Characteristics of word encoding. In A. W. Melton & E. Martin (Eds.),
Coding processes in human memory. Washington, D.C.: D. H. Winston.
8
INTRODUCTION
205
206 JEFFREY W. GRAY and RAYMOND S. DEAN
Dichotic Listening
Considered to be one of the most widely used methods of investigat-
ing cerebral laterality, the dichotic listening technique was originally in-
troduced by Broadbent in 1954 and subsequently refined by Kimura
(1961a, 1961b, 1963). This technique involves presenting two different
auditory stimuli to each ear simultaneously. Because contralateral audito-
ry pathways have a greater number of ear-to-hemisphere nerve fibers than
do the ipsilateral connections (Majkowski, Bochenck, Bochenck, Knapik-
Fijalkowska, & Kopec, 1971), and the contralateral input "blocks" or oc-
cludes information passing along the ipsilateral path (Gruber & Segalo-
witz, 1977), the dominant hemisphere for a particular stimulus should
produce more correct recall for input to the contralateral ear. Thus, infor-
mation from the right ear would reach the left hemisphere more quickly
than it would the right hemisphere, whereas the opposite would be true
for a left ear input. This being the case, if a subject is consistently faster
and more accurate in identifying information presented to a particular
ear, it is concluded that the cerebral hemisphere opposite the more profi-
cient ear has a specialized function with regard to that type of stimulus.
The dichotic listening task has proven to be a reliable clinical pro-
cedure in assessing cerebral laterality in children (e.g., Hynd & Obrzut,
1977). Easily administered, this method simply involves presenting the
child with pairs of auditory stimuli (e.g., digits, nonsense words, sen-
tences, consonant-vowel-consonant syllables) to each ear simultaneously,
and asking the subject to recall or recognize the stimulus perceived. Stim-
uli are presented by means of a dual-channel tape recorder equipped with
stereophonic headphones. Thus, the dichotic listening task may be ad-
ministered in most clinical settings. However, portability may be prob-
lematic.
As may be expected, early research in the area of dichotic listening
was conducted with brain-damaged subjects (Kimura, 1961a). Along these
lines, Kimura (1961a) found that patients who had undergone temporal
lobe excision showed a depressed performance on the ear contralateral to
the damaged area. More important, she also found that patients with
documented left hemispheric speech lateralization (from sodium amytal
tests) showed a right ear advantage (REA). However, those subjects with
208 JEFFREY W. GRAY and RAYMOND S. DEAN
right hemisphere specialization for language were found to have a left ear
superiority, regardless of their hand preference. Similarily, Kimura
(1961b) examined the dichotic listening performances of normal right-
handed subjects and again found a significant right ear superiority. On the
basis of these findings, she concluded that the ear contralateral to the
hemisphere specialized for language was more efficient at processing ver-
bal stimuli.
In support of Kimura's (1961a, 1961b) earlier findings, more recent
evidence from dichotic listening studies has indicated that normal adults
(e.g., Dean & Hua, 1982) and children (e.g., Hynd & Obrzut, 1977) show an
REA for verbal material. Among the most robust and replicated findings
in contemporary experimental psychology, these data are often used to
support the inference of left hemisphere specialization for language. In-
deed, numerous authors have argued that the dichotic listening paradigm
is the most valid noninvasive method of inferring hemisperic lateraliza-
tion for language (Witelson, 1977). At the same time, however, this pro-
cedure is not without methodological problems (Satz, 1976). Factors such
as attentional bias, perceptual set, and memory (Bryden, 1982), acoustic
variables (i.e., signal intensity, signal-to-noise ratio; Berlin & Cullen,
1977), and response distortions (e.g., Birkett, 1977) all have been impli-
cated as contributing to major methodological deficiencies.
In response to such methodological problems, a number of pro-
cedural improvements have been suggested (e.g., Studdert-Kennedy &
Shankweiler, 1970). One such alteration involves the presentation of sin-
gle pairs of consonant-vowel-consonant (CVC) nonsense syllables rather
than whole stimulus lists. The use of single pairs is seen as "reducing the
memory load on the subject ... and eliminating many of the response
organization factors that complicate the interpretation of list data"
(Bryden, 1982, pp. 46-47). In a different approach, Geffen, Traub, and
Stierman (1978) introduced large word-pair lists in which a target word
was randomly presented to one ear or the other. The subject was in-
structed to respond via a button-press upon perception of the predeter-
mined target word. Under these conditions, the collection of both ac-
curacy and latency data was possible. Importantly, normal subjects have
been shown to have a right ear advantage with regard to both accuracy and
speed of responding.
Perhaps the most important methodological refinement, the atten-
tional monitoring procedure differs from those previously discussed in
that subjects are required to attend and respond to dichotic stimuli only in
one prespecified ear. This directed dichotic task eliminates the possibility
of order effects because stimulus items are presented in counterbalanced
fashion. It has been argued that when used in conjunction with single-pair
stimulus material, this procedure may overcome the majority of the most
frequently cited methodological problems (Bryden, 1982). Thus, this may
be the most clinically useful dichotic listening procedure. More recently,
LATERALITY ASSESSMENT 209
Electrophysiological Measures
As a result of the inherent methodological difficulties in perceptual
asymmetry paradigms, a number of researchers and clinicians have opted
to use more direct measures of hemispheric lateralization. For various
reasons, most have relied upon measures of the electrical activity in the
brain. Two of the most common indices include the ongoing electroen-
cephalogram (EEG) and the average evoked potential (AEP). Both pro-
cedures involve the examination of electrical activity in a general area of
the cerebral cortex as measured from EEG leads. An alpha wave pattern
(8-13 Hz) has most often been associated with a relaxed, resting state and
is seen as reflecting a decrease in electrical activity in a particular area of
the brain. Beta waves (greater than 13 Hz), on the otcer hand, are found
with an alert or aroused state (e.g., attending to a stimulus). Given these
assumptions, one would expect differential alpha activity in the two cere-
bral hemispheres depending upon the task at hand.
Whereas early research involving these procedures focused on lateral
differences in electrical activity when the subject was at rest, recent em-
phasis has been upon the examination of brain wave activity of subjects
performing various tasks (Bryden, 1982). These investigations have
shown less activity (Le., a predominance of alpha) in postcentral areas of
the right hemisphere when normal right-handed subjects are involved in
verbal analytic tasks (Doyle, Ornstein, & Galin, 1974; Galin & Ornstein,
1972; Morgan, McDonald, & McDonald, 1971). In contrast, a predomi-
nance of alpha waves has been found in the left hemisphere of normal
individuals when they are required to perform more spatially oriented
tasks (Doyle et a1., 1974; Galin & Ornstein, 1972; Morgan et a1., 1971). The
combined results of these investigations support the existence of a verbal-
analytic versus spatial-holistic processing difference between the two
hemispheres. However, in an investigation that examined subjects' block
design performance, Galin, Johnstone, and Herron (1978) found increased
beta activity in the left hemisphere concomitant with increased task com-
plexity. Interestingly, it appeared that as this predominantly right hemi-
spheric task became more difficult, the analytical, sequential mode of
processing most often attributed to the left hemisphere was activated. It is
important to note that this also may apply to dichotic listening and visual
half-field paradigms. Thus, the clinician must pay close attention to the
particular stimuli and task demands used with such techniques, and
should interpret the data with caution.
Consistent with EEG findings, the majority of investigations using the
evoked potential paradigm have shown a significantly larger AEP in the
left hemisphere for verbal stimuli and an increased right hemisphere AEP
for nonverbal musical stimuli (e.g., Shucard, Shucard, & Thomas, 1977).
Of particular interest, Molfese and his colleagues (Molfese & Hess, 1978;
LATERALITY ASSESSMENT 211
showed that only 30% of all left-handed individuals have right hemi-
sphere or inconsistent hemispheric specialization for language.
Consistent with Milner's (1974) findings, Satz (1972, 1976) has sug-
gested that differences between left-handed persons in language later-
alization may be attributed to the differences in the etiology of the left-
hand preference. He has argued in favor of both a genetically or environ-
mentally predisposed left-handedness and a form of left-handedness that
arises out of early brain damage and/or a developmental anomaly in the
left hemisphere. In light of more recent findings (see Satz, 1976), the early
hypotheses (e.g., Orton, 1937) that offered handedness as a definitive
indicator of language lateralization now seem rather simplistic.
With this in mind, it is not surprising to find that investigations
examining the relationship between left/mixed handedness and chil-
dren's learning problems have produced inconsistent results. Indeed,
such findings have led a number of authors to conclude that the rela-
tionship between hand preference and language or scholastic achieve-
ment is minimal at best (Beaumont & Rugg, 1978; Benton, 1975; Hardyck,
Petrinovich, & Goldman, 1977). Supporting this argument, Dunlop, Dun-
lop, and Fenelon (1973) found that simple hand preference accounted for
little of the total variance associated with language lateralization as mea-
sured by dichotic listening. In contrast, these authors showed a clear
relationship between eye/hand use and chronic learning problems.
Although measures of lateral preference (e.g., handedness) have been
used most often to classify subjects in a nominal fashion (left, right,
mixed), it has been argued that lateral preference data may be more
clinically useful if they are treated in a continuous manner (see Dean,
1978,1981,1982,1984; Shankweiler & Studdert-Kennedy, 1975). Similar-
ly, it seems reasonable that whereas simple handedness may not reliably
reflect cerebral organization, coherently lateralized cerebral systems (e.g.,
visually guided fine motor performance) may offer more clinical utility in
the examination of cerebrallateralization (Dean, 1982). Indeed, a number
of investigations have shown preference for visually guided motor tasks
(e.g., picking up a penny) to be most sensitive to other measures of neuro-
psychological impairment (Dean, Schwartz, & Smith, 1981; Gray, Dean, &
Seretny, in press). This point of view tends to support Luria's (1966)
position that lateral dominance of the hemispheres varies as a function of
the cerebral system under investigation. Thus, lateral preference patterns
differ not only between individuals but within individuals as a function
of the task variable under investigation.
Dean (1978) developed a multifactorial measure of lateral preference
that treats lateral preference in a continuous fashion (Laterality Preference
Schedule; LPS). This 49-item self-report measure requires respondents to
indicate their lateral preference for unimanual tasks on a 5-point Likert
scale. All items produced both stability and predictive validity estimates
214 JEFFREY W. GRAY and RAYMOND S. DEAN
However, like Zurif and Carson (1970), they failed to find an REA for good
readers.
As a result of the popular conceptualization that linguistically dis-
abled children may suffer delayed cerebrallateralization (e.g., Critchley,
1970), numerous investigations have attempted to examine the develop-
mental implications of ear asymmetry for a number of clinical popula-
tions when compared with normal controls (Bakker, 1973; Hynd et al.,
1979; Satz, 1976; Satz, Rardin, & Ross, 1971; Sparrow & Satz, 1970). Over-
all, few studies have reported the expected ear-by-age interaction for
groups. Thus, it appears that there is little evidence to support the devel-
opmentallag hypothesis of cerebrallateralization in children with learn-
ing disorders.
In contrast, the majority of investigations have shown a less pro-
nounced right VHF dominance for linguistic material in language-dis-
abled children when compared with normal controls (Kershner, 1977;
Marcel, Katz, & Smith, 1974; Marcel & Rajan, 1975; McKeever & Van
Deventer, 1975). Using both a bilateral and a unilateral presentation,
McKeever and Van Deventer (1975) compared the VHF performance of
dyslexic and normal controls. As a control for eye movements, subjects in
this investigation were required to focus on and subsequently identify a
"fixation number" prior to their reporting any experimental stimuli. Al-
though both groups showed an overall right visual half-field advantage
under the unilateral presentation, dyslexic subjects performed much
more poorly on the word recognition task than did the normal controls. Of
particular interest, dyslexic subjects differed more from their normal co-
horts on RVF than on LVF presentations. Under the bilateral presentation,
however, dyslexic children showed a normal right VHF advantage. Al-
though McKeever and Van Deventer acknowledged the inconsistency of
these findings, they interpreted the results as indicating an impaired "left
hemisphere functioning" for dyslexic subjects in this study. Clearly,
whereas this interpretation was consistent with the unilateral presenta-
tion, it was not supported by the results under the bilateral condition.
These findings suggest that the use of bilateral versus unilateral presenta-
tion can make a difference in measurement.
In a second experiment, these investigators presented subjects with
verbal stimuli via a visual half-field procedure as well as a dichotic listen-
ing paradigm. Interestingly, their dyslexic subjects showed a normal left
hemispheric superiority for the auditory presentation (REA) but a reduc-
tion in asymmetry for stimuli presented visually. Moreover, there was
little correspondence between the ear advantage and VHF performance of
the dyslexic subjects. In a related investigation, Tomlinson-Keasey and
Kelly (1979) found a significant relationship between right hemispheric
specialization for words and linguistic disabilities in third-grade chil-
dren. Conversely, as a left VHF advantage (right hemisphere) for pictures
218 JEFFREY W. GRAY and RAYMOND S. DEAN
CLINICAL IMPLICATIONS
siderable clinical appeal. However, this procedure may not offer the por-
tability necessary for some clinical settings. Similarly, the visual half-
field procedure is both bulky and costly. Although seen as a more direct
measure of laterality, EEG techniques lack the data necessary for large-
scale clinical use. Measures of handedness may be the most widely used
index of laterality; however, in light of the interaction between hand
preference and both social learning and environmental effects, the rela-
tionship between simple handedness and cerebrallateralization is equiv-
ocal. Problems with inventory techniques notwithstanding, multifactorial
inventories of laterality may offer the single most economical and psycho-
metrically sound method of evaluating lateral preference patterns in most
clinical settings. However, as noted before, these may not be appropriate
for use with reading-disabled or younger children. Regardless of the pro-
cedure used, it is important to interpret the data obtained from such
measures in light of other clinical and psychometric findings. Perhaps the
most reliable method of laterality assessment involves the use of multiple
measures. With the agreement of multiple measures comes the clinical
assurance that generalizations concerning the patient's functional later-
alization are warranted. Conversely, important implications may be
drawn on the basis of the pattern of findings and how they vary according
to the procedure, mode of input, and type of task used.
REFERENCES
Bryden, M. P. (1982). Laterality: Functional asymmetry in the intact brain. New York:
Academic Press.
Critchley, M. (1970). The dyslexic child (2nd ed.). London: Heinemann.
Crovitz, H. F., & Zener, K. (1962). A group-test for assessing hand and eye dominance.
American Journal of Psychology, 75, 271-276.
Davidson, R. J., & Schwartz, G. (1977). The influence of musical training on patterns of EEG
asymmetry during musical and non-musical self-generalization tasks. Psycho-
physiology, 14, 58-63.
Dean, R. S. (1978). Cerebral laterality and reading comprehension. Neuropsychologia, 16,
633-636.
Dean, R. S. (1979). Cerebral laterality and verbal-performance discrepancies in intelligence.
Journal of School Psychology, 17, 145-150.
Dean, R. S. (1981). Cerebral dominance and childhood learning disorders: Theoretical per-
spectives. School Psychology Review, 10, 373-378.
Dean, R. S. (1982). Assessing patterns of lateral preference. Journal of Clinical Neuropsy-
chology, 4, 124-128.
Dean, R. S. (1984). Functionallateralization of the brain. Journal of Special Education, 18,
240-256.
Dean, R. S., & Hua, M. S. (1982). Laterality effects in cued auditory asymmetries. Neuropsy-
chologia, 20. 685-690.
Dean, R. S., Schwartz, N. H., & Hua, M. (in press). Lateral preference patterns in schizo-
phrenia and affective disorders, Journal of Abnormal Psychology.
Dean, R. S., Schwartz, N. H., & Smith, 1. S. (1981). Lateral reference patterns as a discrimi-
nator of learning disabilities. Journal of Consulting and Clinical Psychology, 49, 227-
235.
Doyle, J. C., Ornstein, R., & Galin, D. (1974). Lateral specialization of cognitive mode: II. EEG
frequency analysis. Psychophysiology, 11, 567-578.
Dunlop, D. B., Dunlop, P., & Fenelon, B. (1973). Vision laterality analysis in children with
reading disability: The results of new techniques of examination. Cortex, 9, 227-236.
Galin, D., Johnstone, J., & Herron, J. (1978). Effects of task difficulty on EEG measures of
cerebral engagement. Neuropsychologia, 16, 461-472.
Galin, D., & Ornstein, R. (1972). Lateral specialization of cognitive mode: An EEG study.
Psychophysiology, 9, 412-418.
Gazzaniga, M. S. (1970). The bisected brain. New York: Appleton-Century-Crofts.
Geffen, G., Traub, E., & Stierman, I. (1978). Language laterality assessed by unilateral ECT
and dichotic monitoring. Journal of Neurology, Neurosurgery, and Psychiatry, 41, 354-
360.
Geschwind, N. (1974). Selected papers on language and the brain. The Netherlands: D.
Reidal.
Gray, J. W., Dean, R. S., & Seretny M. 1. (1986). Lateral preference as a predictor of cognitive
rigidity, Journal of Clinical Psychology, 42, 956-960.
Gruber, F. A., & Segalowitz, S. J. (1977). Some issues and methods in the neuropsychology of
language. In S. J. Segalowitz & F. A. Gruber (Eds.)' Language development and neu-
rological theory (pp. 3-19). New York: Academic Press.
Hardyck, C., Petrinovich, 1. F., & Goldman, R. D. (1977). Left-handedness and cognitive
deficit. Cortex, 17, 266-279.
Heron, W. (1957). Perception as a function of retinal locus and attention. American Journal
of Psychology, 70, 38-48.
Hines, D., & Satz, P. (1977). Cross-model asymmetries in perception related to asymmetry in
cerebral function. Neuropsychologia, 12, 239-247.
Humphrey, M. (1951). Handedness and cerebral dominance. Bachelor of Science thesis,
Oxford University.
Hynd, G. W., & Obrzut, J. E. (1977). Effects of grade level and sex on the magnitude of the
dichotic ear advantage. Neuropsychologia, 15, 689-692.
LATERALITY ASSESSMENT 221
Hynd, G. W., Obrzut,]. E., Weed, W., & Hynd, C. R. (1979). Development of cerebral domi-
nance: Dichotic lstening asymmetry in normal and learning-disabled children. Journal
of Experimental Child Psychology, 2B, 445-454.
]ackson,]. H. (lB74). On the duality of the brain. Medical Press, 1, 19. Reprinted in]. Taylor
(Ed.), Selected writings of John Hughlings Jackson (Vol. 2). London: Hodder and
Stoughton, 1932.
Kershner, ]. B. (1977). Cerebral dominance in disabled readers, good readers, and gifted
children: Search for a valid model. Child Development, 4B, 61-67.
Kimura, D. (1961a). Cerebral dominance and the perception of verbal stimuli. Canadian
Journal of Psychology, 15, 166-171.
Kimura, D. (1961b). Some effects of temporal lobe damage on auditory perception. Canadian
Journal of Psychology, 15, 156-165.
Kimura, D. (1963). Right temporal lobe damage. Archives of Neurology, B, 264-271.
Kimura, D., & Durnford, M. (1974). Normal studies on the function of the right hemisphere in
vision. In S. ]. Dimond & ]. G. Beaumont (Eds.), Hemisphere functions in the human
brain (pp. 159-175). London: Elek Scientific Books.
Kinsbourne, M., & Hiscock, M. (1977). Does cerebral dominance develop? In S.]. Segalowitz
& F. A. Gruber (Eds.), Language development and neurological theory (pp. 171-191).
New York: Academic Press.
Lake, D., & Bryden, M. (1976). Handedness and sex differences in hemispheric asymmetry.
Brain and Language. 3, 266-282.
Levy,]. (1969). Possible basis for the evaluation of lateral specialization of the human brain.
Nature, 224, 614-615.
Luria, A. R. (1966). Human brain and psychological processes. New York: Harper & Row.
MacKinnon, G. E., Forde, ]., & Piggens, D. ]. (1969). Stabilized images, steadily fixated
figures, and prolonged after images. Canadian Journal of Psychology, 23, 184-195.
Majkowski, ]., Bochenck, Z., Bochenck, W., Knapik-Fijalkowska, D., & Kopec, ]. (1971).
Latency of average evoked potentials to contralateral and i psalateral auditory stimula-
tion in normal subjects. Brain Research, 25, 416-419.
Marcel, T., Katz, 1., & Smith, M. (1974). Laterality and reading proficiency. Neuropsycho-
logia, 12, 131-139.
Marcel, T., & Rajan, P. (1975). Lateral specialization for recognition of words and faces in
good and poor readers. Neuropsychologia, 13,489-497.
McKeever, W F., & Van Deventer, A. D. (1975). Dyslexic adolescents: Evidence of impaired
visual and auditory language processing associated with normallateralization and visu-
al responsivity. Cortex, 11, 361-378.
Milner, B. (1971). Interhemispheric differences and psychological processes. British Medical
Bulletin, 27, 272-277.
Milner, B. (1974). Hemispheric specialization: Scope and limits. In F. O. Schmitt & F. G.
Warden (Eds.), The neurosciences: Third study programme (pp. 75-89). Cambridge,
MA: M.LT. Press.
Milner, B., Branch, c., & Rasmussen, T. (1964). Observations on cerebral dominance. In A. V.
S. DeRenck & M. O'Connor (Eds.), Disorders of language (CIBA Foundation Sym-
posium) (pp. 200-241). London: Churchill.
Molfese, D. 1., Freeman, R. B., & Palermo, D. (1975). The ontogeny of brain lateralization for
speech and nonspeech stimuli. Brain and Language, 2, 356-368.
Molfese, D. 1., & Hess, T. M. (1978). Hemispheric specialization for VOT perception in the
preschool child. Journal of Experimental Child Psychology, 26, 71-84.
Molfese, D. 1., & Molfese, V.]. (1979a). Hemisphere and stimulus differences as reflected in
the cortical responses of newborn infants to speech stimuli. Developmental Psychology,
15,505-511.
Molfese, D. 1., & Molfese, V.]. (1979b). VOT distinctions in infants: Learned or innate. In H.
A. Whitaker & H. Whitaker (Eds.), Studies in neurolinguistics (Vol. 4, pp. 21-35). New
York: Academic Press.
222 JEFFREY W. GRAY and RAYMOND S. DEAN
Morgan, A., McDonald, P. J., & McDonald, H. (1971). Differences in bilateral alpha activity as
a function of experimental tasks, with a note on lateral eye movements and hypno-
tizability. Neuropsychologia, 9, 459-469.
Oldfield, R. C. (1971). The assessment and analysis of handedness: The Edinburgh invento-
ry. Neuropsychologia, 9, 94-113.
Orton, S. T. (1937). Specific reading disability-strephosymbolia. Journal of the American
Medical Association, 90, 1095-1099.
Peters, M., & Durding, B. (1978). Handedness as continuous variable. Canadian Journal of
Psychology, 32, 257-261.
Pizzamiglio, L. (1976). Cognitive approach to hemispheric dominance. In R. M. Knights & D.
Bakker (Eds.), The neuropsychology of learning disorders (pp. 265-272). Baltimore:
University Park Press.
Pritchard, R. M., Heron, W., & Hebb, D. O. (1960). Visual perception approached by the
method of stabilized images. Canadian Journal of Psychology, 14, 66-77.
Provins, K. A., & Cunliffe, P. (1972). Motor performance tests of handedness and motivation.
Perceptual and Motor Skills, 35, 143-150.
Raczkowski, D., Kalat, J. W., & Nebes, R. (1974). Reliability and validity of some handedness
questionnaire items. Neuropsychologia, 12, 43-47.
Reitan, R. M. (1969). Manual for administration of neuropsychological test batteries for
adults and children. Indianapolis: Author.
Reynolds, C. R., Hartlage, L. C., & Haak, R. (1981). The relationship between lateral prefer-
ence, as determined by neuropsychological test performance, and aptitude-achieve-
ment discrepancies. Clinical Neuropsychology, 3, 19-21.
Sappington, J. T. (1980). Measures of lateral dominance: Interrelationships and temporal
stability. Perceptual and Motor Skills, 50, 783-790.
Satz, P. (1972). Pathological left-handedness: An explanatory model. Cortex, 8, 121-135.
Satz, P. (1976). Cerebral dominance and reading disability: An old problem revisited. In R.
M. Knights & D. Bakker (Eds.), The neuropsychology of learning disorders (pp. 273-
294). Baltimore: University Park Press.
Satz, P., Bakker, D. J., Teunissen, J., Goebel, R., & van der Vlugt, H. (1975). Developmental
parameters of the ear asymmetry. A multivariate approach. Brain and Language, 2, 71-
85.
Satz, P., Rardin, D., & Ross, J. (1971). An evaluation of a theory of specific developmental
dyslexia. Child Development, 42, 2009-2021.
Shankweiler, D., & Studdert-Kennedy, M. (1975). A continuum of lateralization for speech
perception. Brain and Language, 2, 212-225.
Shucard, D. W., Shucard, J. L., & Thomas, D. G. (1977). Auditory evoked potentials as probes
of hemispheric differences in cognitive processing. Science, 197, 1295-1297.
Sparrow, S., & Satz, P. (1970). Dyslexia, laterality, and neuropsychological development. In
D. J. Bakker & P. Satz (Eds.). Specific reading disability: Advances in theory and method
(pp. 41-60). Rotterdam: Rotterdam University Press.
Sperry, R. W., Gazzaniga, M. S., & Bogen, J. H. (1969). Interhemispheric relationships: The
neocortical commissures: Syndromes of hemispheric disconnection. In P. Vinken & G.
W. Bruyn (Eds.), Handbook of clinical neurology (Vol. 4, pp. 273-290). New York:
Wiley.
Studdert-Kennedy, M., & Shankweiler, D. (1970). Hemispheric specialization for speech
perception. Journal of the Acoustical Society of America, 48, 579-594.
Summers, R. K., & Taylor, M. L. (1972). Cerebral speech dominance in language-disordered
and normal children. Cortex, 8, 224-232.
Tjossem, T. D., Hansen, T. J., & Ripley, H. S. (1961). An investigation of reading difficulty in
young children. Paper presented at the 117th annual meeting of the American Psycho-
logical Association, Chicago.
Tomlinson-Keasey, C., & Kelly, R. R. (1979). Is hemispheric specialization important to
scholastic achievement? Cortex, 15, 97-107.
LATERALITY ASSESSMENT 223
Wada, J., Clark, R., & Hamm, A. (1975). Cerebral hemispheric asymmetry in humans. Ar-
chives of Neurology. 32, 239-246.
Walker, H. A., & Birch, H. G. (1970). Lateral preference and right-left awareness in schizo-
phrenic children. Journal of Nervous and Mental Disease, 15, 341-351.
Witelson, S. F. (1976). Early hemispheric specialization and interhemisphere plasticity: An
empirical and theoretical review. In S. Segalowitz & F. Gruber (Eds.)' Language and
development and neurologic theory (pp. 213-286). New York: Academic Press.
Witelson, S. F. (1977). Developmental dyslexia: Two right hemispheres and none left. Sci-
ence, 195,309-311.
Witelson, S. F., & Rabinovitch, M. S. (1972). Children's recall strategies in dichotic listening.
Journal of Experimental Child Psychology, 12, 106-113.
Woo, T. L., & Pearson, K. (1927). Dextrality and sinistrality. Biometrika, 19, 192-198.
Zangwill, O. C. (1960). Cerebral dominance and its relationship to psychological function.
London: Oliver & Boyd.
Zangwill, O. C. (1962). Dyslexia in relation to cerebral dominance. In J. Money (Ed.), Reading
disability (pp. 103-113). Baltimore: Johns Hopkins.
Zurif, E. F., & Carson, G. (1970). Dyslexia in relation to cerebral dominance and temporal
analysis. Neuropsychologia, 8, 351-361.
9
225
226 GLEN P. AYLWARD
Behavioral State
The behavioral state of the neonate is defined as the level of nervous
system arousal (Prechtl, 1977). States, originally developed by correlating
observed behavior with measures of physiological function, are generally
classified as quiet sleep, rapid eye movement sleep, quiet wakefulness,
active wakefulness, and crying. Behavioral states are critical because the
quality of elicited reflexes often varies as a function of state (Lenard, von
Bernuth, & Prechtl, 1968; Prechtl, Vlach, Lenard, & Grant, 1967). State
also influences habituation to external stimuli, muscle tone, and deep
tendon reflexes. Many neurobehavioral items are best administered in
specific behavioral states. States also afford insight into an infant's reac-
tivity and therefore can aid in assessment. Prechtl has included states in
the criteria for the diagnosis of several abnormal syndromes (Prechtl,
1977; Prechtl & Beintema, 1964). A predominance of certain states (e.g.,
crying) has been associated with subtle central nervous system dysfunc-
tion (Parmelee & Michaelis, 1971).
The influence of these behavioral states on assessment becomes less
important with increasing age. However, problems in physical discomfort
such as hunger, thirst, sleepiness, crying, and bowel and bladder disten-
tion continue to be important (Ulrey, 1982). Therefore, more flexibility in
neuropsychological testing is needed at these younger ages.
Temperament
Temperament is analogous to behavioral style, a biologically based
behavioral predisposition in spontaneous and reactive behavior (Chess &
Thomas, 1983). There are three major classifications of temperament. The
difficult child, estimated to comprise 10% of the general population, is
characterized by irregularity in biological function, negative withdrawal
responses to new situations, negative mood and intensity, and nonadap-
tability or slow adaptability to change. The slow-to-warm-up infant (15%)
typically displays negative responses of a mild intensity to new stimuli
and slow adaptability after repeated contact. In contrast, the easy child,
(40% of the population) adopts a positive response to new stimuli, adapts
quickly and easily to change, and has a predominantly positive mood.
These behavioral styles persist and can affect test scores of infants and
young children in various ways (see Hertzig, 1983).
ble. This is especially true among infants with severe motor impairment
because our current infant assessment instruments rely heavily on motor
responses. In neuropsychological assessment of young infants, the pres-
ence or absence of a behavior, and the qualitative manner in which a task
is carried out should be evaluated, with emphasis on the inclusion of
incidental observations. Many have argued that systematic assessment of
test-taking behavior should be included in the general evaluation of in-
fants and young children. This is evident in the development of the Bay-
ley (1969) Infant Behavior Record, which is used in addition to the Mental
and Psychomotor Developmental Indices.
There are other limitations as well. Hanson, Smith, and Hume (1984),
using the Griffiths Scales of Mental Development, question the reliability
of maternal report, the administration of certain items, and scoring crite-
ria. Discrepancies in scoring were found to be greatest at younger ages.
Disagreement in the scoring of what is observed may not be the issue; the
potential problem is in deciding whether to accept a behavior as the
child's optimum performance. The examiner's judgment of response qual-
ity (i.e., whether the response is the best of which the infant is capable) is
difficult to quantify, and traditional reliability measures do not take this
into account.
Noncompliance
This problem is reflected in the "nontestable" classification on the
Denver Developmental Screening Test (Frankenburg & Dodds, 1967).
Ounsted, Cockburn, and Moar (1983) reported lower global developmen-
tal scores in infants who were not cooperative, and noncompliant behav-
ior in 18% of their 4-year-olds precluded computation of a developmental
score. Many infants refused gross motor tasks, whereas those who were
minimally cooperative (enough for completion of a score) frequently dis-
played compromised visual-motor function. These investigators also re-
port an increased probability of subsequent problems in the noncoopera-
tive infants. It is possible that an unwillingness to attempt certain tasks
reflects an inability to perform these tasks, and this needs to be differenti-
ated in early neuropsychological assessment. There also is evidence that
abnormal infants behave differently on tests (Oski & Honig, 1978), and
behavior that is poorly adaptive and observed infrequently may indicate
abnormality and thus have diagnostic utility (Wolf & Lozoff, 1985).
Consistency of Dysfunction
Prediction
Early neurobehavioral diagnosis in severely impaired infants is fairly
straightforward (Davies, 1984). Prediction, however, is less certain. Pre-
230 GLEN P. AYLWARD
diction rates may account for as much as 49% of the variance between
early and later measures in significantly damaged infants, usually those
with developmental quotients less than 80 (Aylward & Kenny, 1979).
Similar predictive accuracy is reported in newborn infants who manifest
Prechtl's (1977) neurological syndromes (hyperexcitability, apathy, hemi-
syndrome). However, these prediction rates are for groups, not indi-
viduals, and there is much individual variability in cognitive, motor, and
neurological diagnoses over the first 3 years (Aylward, Gustafson, Ver-
hulst, & Colliver, 1987).
Diagnosis and longitudinal prediction are difficult in those infants
who are not overtly abnormal at an early age but whose performance is
suspect. Coolman et a1. (1985) found a 50% incidence of mild neuromotor
dysfunction in their high-risk nursery population, 75% of whom were
normal by age 2. Seven percent of the babies displayed moderate dysfunc-
tion, and half of these were normal by 2. In another investigation (Ayl-
ward et a1., 1987), using approximately 275 infants followed to age 3,
function was divided into cognitive, motor, and neurological spheres.
Seventy-one percent of the babies who were cognitively suspect at 40
weeks were normal by 3 years of age, 88% of the babies suspected to have
motor defects improved by age 3 whereas 93% of the infants defined as
neurologically suspect at 40 weeks had improved. Certain neu-
robehavioral conditions, such as hypotonia or head lag, are less persistent
over time than other neurological conditions (Bierman-van Eendenburg,
Jurgens-van der Zee, Olinga, Huisjes, & Touwen, 1981; Dubowitz et a1.,
1984; Hack, Caron, Rivers, & Fanaroff, 1983).
Psychometric Concerns
Several methodological problems that may affect the reliability of
early neuropsychological assessment have been delineated (Aylward &
Kenny, 1979): the criterion measure used, the age at which testing is
administered (i.e., the keyage or the age of acquisition of new behaviors),
maturity, and strongly canalized sensory-motor development. Correction
for prematurity (Hunt, 1981; Siegel, 1983) may obscure subtle neuropsy-
chological findings by overcorrecting for gestational age. Any of these
factors could significantly affect neuropsychological status and therefore
must be considered.
Receptive Functions
Receptive functions involve the entry of information into the central
processing system, utilizing sensation and perception. This class of func-
tion becomes more complex with age. Visual, auditory, and tactile abili-
ties are involved, but owing to testing instruments, visual and auditory
functions are emphasized more than tactile processes in early assessment.
Tactile function is assessed in the first several months of life in the form of
proprioceptive reflexes, grasping, and mouthing objects. Auditory dis-
crimination and verbal receptive skills also are involved in this functional
grouping.
Expressive Functions
Expressive functions refer to behaviors produced by the child and
observed by the examiner. The repertoire of behavior reflecting expressive
functions increases with age. Fine motor abilities include eye-hand coor-
dination, manipulating with the fingers, constructional abilities, and psy-
chomotor speed. Oral motor and language functions consist of what is
said and how it is articulated. Gross motor function involves motility,
coordination, ambulation, and gait. Deficits in this area are often defined
as apraxias, dysphasias, anomias, or dyskinesias.
Processing
Processing includes two components: memory/learning and think-
ing/reasoning. Memory/learning involves visual and auditory short-term
memory (registration and immediate memory) and long-term memory.
234 GLEN P. AYLWARD
Mental Activity
This class of function consists of two components: attentional ac-
tivities/level of consciousness, and activity. Attentional activities are
heavily dependent upon developmental age since such skills are poorly
developed in younger infants and children. These functions can therefore
be diagnostically useful when attentional behavior is compared with what
is expected at a specific age. Many of these functions also determine how
an infant approaches test taking. Behavioral states are important early;
later, alertness becomes more crucial. Activity, whether characterized as
hypo- or hyperactivity, will affect test-taking behavior, but it is also of
diagnostic utility because diffuse neuropsychological dysfunction can be
reflected in either excessively high or low activity levels.
In summary, it is important to emphasize that the classes of function
in Table 1 are interrelated, and that the divisions are provided to form a
conceptual framework. For example, when an infant follows commands,
receptive functions (temporal-sequential) as well as expressive abilities
are involved. Similarly, on form boards, receptive functions (visual per-
ceptual), processing (thinking/reasoning), and mental activities (attention
and concentration) are employed. Nonetheless, careful analysis of data
obtained in early neuropsychological assessment enables the progressive
discrimination of areas of adequate function and those of deficit.
ASSESSMENT INSTRUMENTS
There are few, if any, tests that are designed specifically to provide
neuropsychological data for infants and young children. However, many
tests yield neuropsychological information but simply have not been
EARLY ASSESSMENT 235
Newborn/N eonatal
Neuropsychological functions measured by assessment instruments
in this age range cluster in the neurological function/intactness, ex-
pressive (gross motor), and mental activity groupings (level of con-
sciousness, activity). All examinations are adequate to assess intactness,
although the examiner's additional observations are necessary in some.
Infancy
At this age, assessments cluster in the receptive, expressive, and pro-
cessing groupings. Sensorimotor skills are generally emphasized; these
include visual/motor integrative, fine motor-constructive, and gross
motor functions. Visual/perceptual abilities are also heavily weighted.
Inclusion of more neurological function items in assessment at this age is
necessary. The other major deficiency is found in the mental activity
grouping. In both cases, additional items and observations could be in-
cluded. Reflexes are evaluated only with the Milani-Comparetti exam at
this age; this suggests the advisability of incorporating this assessment
instrument with other more developmentally oriented techniques.
Early Childhood
As in the infancy age range, little emphasis is placed on the neu-
rological function and mental activity groupings. Gross motor skills are
TABLE 2. Assessment Instruments Used in Early Neuropsychological Testing
Age: Newborn
Brazelton Neonatal Behav- 27 behavioral items (9-point How infant responds to ( +) Clinical instrument, provides good re-
ioral Assessment Scale scale), 20 elicited re- caretakers and environ- search information, recovery from stress;
(Brazelton, 1973) sponses (3-point scale) ment; states, habituation, ( -) some problems with data interpreta-
orientation (visual, audi- tion and scaling, poor long-range predic-
tory), muscle tone, ac- tion
tivity; "best performance"
Prechtl Neurological Ex- Approximatley 52 items + Gross state of CNS reactivity (+) Extensivley studied, good standardiza-
amination (Prechtl, 1977; states, postures, spon- (motor activity, states) + tion, provides immediate diagnosis, prog-
Prechtl & Beintema, 1964) taneous activity specific lesional approach; nosis, those needing follow-up,
syndromes identified behavioral response descriptions; (-)
lengthy, perhaps too detailed
Brief Infant Neu- Reduced version of Revised Screen of CNS intactness (+) Easily administered, less time-consum-
robehavioral Optimality Prechtl Neurological Ex- (tonus, tendon reflexes, ing, similar sensitivity and specificity
Scale (Aylward, Verhulst, amination, 15 items scored spontaneous activity, some values as Prechtl, summary score; (-) not
& Colliver, 1985) in optimal/nonoptimal primitive reflexes) as much data on states, not as extensive
manner as Prechtl
Parmelee's Neurological Divided into two sections- Active and reflexive muscle (+) Brief-takes 10 minutes to administer,
Examination (Parmelee, Section I: state observa- tone, primary reflexes, summary score; (-) not as extensive as
Michaelis, Kopp, & Sig- tions, 20 items; Section II: arousal, and spontaneous Prechtl
man, 1974) crying, activity, tremor, behavior
etc.
Graham Behavior Test for Five scales: pain threshold, Originally designed to differ- ( +) Correlations between neonatal data and
Neonates (Graham, maturational level, visual entiate normal and brain- early infant data, revision had large sam-
Matarazzo, & Caldwell, responsiveness, irritability, injured newborns; motor ple; (-) long-range predictability fair,
1956; Rosenblith, 1974) and muscle tension rat- function (head control, used infrequently
ings; pain threshold crawl) tactile-adaptive
deleted in revision (cotton over nose), visual
tracking, auditory respon-
siveness, irritability rating
Age: Infancy
Gesell Developmental Items provided at each of Key ages: 4, 16, 28, and 40 ( +) Basis for most examinations of infancy,
Schedules (Knobloch & key ages, under five weeks; 12, 18, 36, and 48 good screening inventory; (-) not as well
Pasmanick, 1974; groups; can be scored by months; gross motor, fine standardized as other infant examina-
Knobloch, Stevens, & Mal- observation or history motor, adaptive, language, tions, ratio developmental quotient
one, 1980). personal-social
Bayley Scales of Infant De- Mental Developmental Index Sensorimotor skills, problem (+) Well standardized, good overall assess-
velopment (Bayley, 1969) (163 items), Psychomotor solving, verbal skills, and ment of child's strengths and weaknesses,
Developmental Index (81 areas outlined previously most widely used; (-) questionable pre-
items), Infant Behavior in Gesell dictability, very dependent on motor
Record function
Griffiths Mental Develop- Derived from Gesell, 498 Locomotor, personal-social, (+) Used predominantly in Great Britain,
mental Scale (Griffiths, items, most detailed in hearing and speech, eye rigorous training; (-) many unreliable
1954, 1970) first 2 years; five areas and hand coordination, items
with several items for each performance; designed to
month of age enable examiner to distin-
guish normal and abnor-
mal children
Cattell Infant Intelligence Items arranged on an age Many motor items at early (+) Smooth transition from infant to early
Scale (1940) scale, drawing from Gesell ages; later ages include childhood examination, good for testing
at early ages and Stanford- more cognitive and lan- older children who function at lower lev-
Binet from 22 months up- guage items; provides an els; (-) small standardization sample
wards; 2-36 months IQ score (294), IQ concept questionable, not used
frequently
Milani-Comparetti Neuro- Assesses spontaneous be- Neuromotor abnormalities- (+) Administered in 5-10 minutes, good
Developmental Screening havior, postural control, head and body control, screening device that can be used with
Examination (Milani-Com- evoked responses; chart movement, evoked primi- other examinations; (-) tilting reactions
paretti & Gidoni, 1967) provided with age norms tive reflexes, righting, par- need tilt board, which is often not readily
in terms of onset and dis- achute, and tilting available
appearance of responses reactions; enables detec-
0-24 months tion of cerebral palsy, de-
velopmental delay
(continued)
TABLE 2. (Continued)
Useful Findings
Neuropsychological indicators in the newborn period that are partic-
ularly useful as indicators of dysfunction include Prechtl's syndromes,
hypertonicity of the axial musculature and lower extremities, high ampli-
tude-low frequency tremors, nystagmus, clonus, reflex overflow, and ab-
errant state regulation. Isolated abnormal findings are generally not help-
ful. In addition, early hypotonia and head lag, subtle asymmetries,
mediocre visual tracking, and suspected motor or neurological diagnoses
are often transient. During infancy, persistence of primitive reflexes, cor-
tical thumb sign, consistent irritability, persistent dystonia, a very pre-
dominant hand preference, stereotyped, repetitive movements, and devel-
opmental quotients that are 2 or more standard deviations below average
indicate significant problems. Suspect motor or neurological diagnoses
are often variable, and most infants tend to improve. In early childhood,
many of the functions seen in older children become more apparent.
Neuropsychological assessment should focus particularly on emerging
temporal-sequential skills (but not digits backwards), concentration, word
retrieval difficulties, perseverative tendencies (motor and cognitive), ac-
tivity levels, and gross motor function. Visual-motor skills may be over-
emphasized during infancy and at this later time period.
DIRECTIONS
Assessment instrument
I. Neurologic functions
Reflexes + + + + + +
Asymmetries + + +
Stereotyped/lateralized postures + + + + + + + +
Muscle tone + + + + + + + + + +
Visual tracking/intactness + + + + + + +
LlR discrepancy + + + + +
Motor inhibition +
Protective reflexes + + + + +
Auditory orientation + + + + + + +
II. Receptive functions
Visual perception + + + + + + + + + +
Auditory /language + + + + + + + +
Spatial relations + + + + + + + +
Tactile processing + + + + + + + +
III. Expressive functions
A. Fine motor/oral motor
Visual/motor integrative + + + + + + + +
Language/ speech + + + + + + + +
Fine motor constructive + + + + + + + +
Visual/spatial + + + + + + + +
Articulation + + + +
B. Gross motor
Motility + + + + + + + + + + + +
Coordination + + + + + + + + + + + +
IV. Processing
A. Memory
Temporal-sequential organization + + + + + + + + + +
(auditory)
Anticipatory behaviors + + + +
Visual memory + + + + + + + +
Visual sequencing + +
Word retrieval + + + + + + + +
B. Thinking/reasoning
Cognitive/adaptive problem + + + + + + + +
solving
Abstracting + + + + +
Seriation/classification + + + + +
Number concepts + + + + + + +
Imitation + + + + + + +
Judgment + + + + + + + +
V. Mental activity
A. Attentional/level of consciousness
Conceptual tracking/concentration + + +
Perseveration
Attention/ distractabili ty +
Behavioral states + + + +
Alertness + + + + +
B. Activity
Arousal + + +
Cognitive + + +
Motor + + + + + + + +
Irritability + + + + +
aA "+" indicates function is assessed by evaluation instrument; a "-" indicates function is not assessed directly; a "*,, means observations of this function can be made
but are not scored formally.
242 GLEN P. AYLWARD
pass at a given age. Better methods are needed to help in scoring behaviors
that have not been scored previously. It may be more informative to focus
on how an infant or a young child achieves a criterion measure rather than
if the item is passed or not. Further, many functions are linked with test
items in a post hoc method (e.g., Stanford-Binet), rather than defining a
function and devising a task to assess it.
Selection of combinations of items, drawn from existing tests but
based on a conceptual framework of functions, is suggested as the best
approach. It is advisable to implement the basics of Prechtl's (1980) op-
timality concept in early neuropsychological assessment. Rather than
focusing on the normality or abnormality of a response, the optimality
concept provides a measure of deviation (or lack of deviation) from a
known optimal neuropsychological response. The problem of weighting
different items is circumvented because the optimal responses are
summed and divided by the total number of neuropsychological items
administered. Cutoff scores (e.g., 75% of the responses were optimal)
could be devised to assist in diagnosis. This technique has been used by
investigators during the neonatal and earl infancy period with good re-
sults (Aylward, Verhulst & Colliver, 1985; Stave & Ruvalo, 1980). This
method would be particularly helpful in infancy and early childhood
assessment, where combinations of examination instruments and tech-
niques need to be employed. The optimal response for each item could be
determined from previous data, and these criteria could then be as-
sembled into a workable assessment battery.
The need for an instrument that would identify infants and young
children who have abnormalities of posture, tone, and movement, as well
as those with developmental delays, has recently been emphasized. This
is because categorical results of developmental assessment instruments
often yield low sensitivity (Sciarillo, Brown, Robinson, Bennett, & Sells,
1986). We are currently applying this methodology with the Early Neuro-
psychological Optimality Rating Scales (ENORS). Different scales have
been developed in an a priori manner to reflect major developmental
acquisitions at several key ages (6, 12, 18, and 24 months). As an example,
the 12-month ENORS is found in the Appendix.
The scales are a synthesis of information outlined previously in Ta-
bles 1 and 3 and are designed to provide a more thorough assessment by
covering functions that would ordinarily be missed with the administra-
tion of a developmental or neurological examination in isolation. The
scales utilize components of the Bayley, the Milani-Comparetti, and neu-
rological indicators, as well as developmental milestones. Individual
items included in the ENORS are not necessarily new; basic reflexes and
many expressive and receptive functions are emphasized in pediatric
postgraduate training. Similarly, developmental milestones and the Bay-
ley developmental quotients are used by developmental psychologists.
244 GLEN P. AYLWARD
I. Basic Reflexes
Persistence of primitive reflexes (Moro, asymmetric No Yes
tonic neck, palmar/plantar grasps, etc.)
Asymmetries/marked L-R discrepancy (mirroring, ob- No Yes
vious hand preference)
Presence of protective reactions (parachute reactions) Yes No
Good head control Yes No
Hypotonia/hypertonia-extremities No Yes
Absence of stereotyped, repetitive movements and/or Yes No
cortical thumb sign
II. Receptive Functions
Appropriate responses to auditory stimuli (orients, Yes No
turns head)
Appropriate responses to visual stimuli (tracking, lack Yes No
of nystagmus, etc.)
Follows simple commands Yes No
III. Expressive Functions
A. Fine motor/oral motor
Neat pincer grasp Yes No
Presence of midline behaviors (hands together, trans- Yes No
fers, holds two objects simultaneously)
Radial-digital grasp Yes No
Babbles/appropriate sounds for age (dada/mama spe- Yes No
cifically, etc.)
Good eye-hand coordination Yes No
B. Gross motor
Age-appropriate gait/ambulation (no tiptoe walking, Yes No
no dragging of an extremity)
Uncoordinated movements No Yes
Psychomotor Developmental Yes No
Index 2: 90
IV. Processing
Appreciation of object permanency Yes No
Imitative abilities Yes No
Simple problem-solving skills Yes No
V. Mental Activity
Goal-directed behaviors Yes No
Attentive to procedures Yes No
Average level of activity for age Yes No
Persistant crying/irritability No Yes
Mental Developmental Index 2: 90 Yes No
Total Optimal
Total Nonoptimal
Total Optimal ( )
Neuropsychological Optimality Score =
Optimal ( ) + Nonoptimal (
246 GLEN P. AYLWARD
REFERENCES
Amiel-Tison, C. (1982). Neurologic signs, aetiology, and implications. In P. Stratton (Ed.),
Psychobiology of the human newborn (pp. 75-94). New York: Wiley.
Aylward, G. P., Dunteman, G., Hatcher, R. P., Gustafson, N. F., & Widemayer, S. (1985). The
SES-Composite Index: A tool for developmental outcome studies. Psychological Docu-
ments, 15(Ms. No. 2683).
Aylward, G. P., Gustafson, N., Verhulst, S. J., & Colliver, J. A. (1987). Consistency in the
diagnosis of cognitive, motor and neurologic function over the first three years. Journal
of Pediatric Psychology, 12, 77-98.
Aylward, G. P., & Kenny, T. J. (1979). Developmental follow-up: Inherent problems and a
conceptual model. Journal of Pediatric Psychology, 4, 331-343.
Aylward, G. P., Verhulst, S. J., & Colliver, J. A. (1985). Development of a brief infant neu-
robehavioral optimality scale: Longitudinal sensitivity and specificity. Developmental
Neuropsychology, 1, 265-276.
Bayley, N. (1969). Bayley Scales of Infant Development. New York: Psychological Corpora-
tion.
Bierman-van Eendenburg, M. E. C., Jurgens-van der Zee, A. D., Olinga, A. A., Huisjes, H. H.,
& Touwen, B. C. L. (1981). Predictive value of neonatal neurological examination. A
follow-up study at 18 months. Developmental Medicine and Child Neurology, 23, 296-
305.
Brazelton, T. B. (1973). Neonatal behavioral assessment scale. Clinics in Developmental
Medicine, No. 50. Philadelphia: Lippincott.
Cattell, P. (1940). The measurement of intelligence of infants and young children. New York:
Psychological Corp.
Chess, S., & Thomas, A. (1983). Dynamics of individual behavioral development. In M. D.
Levine, W. B. Carey, A. C. Crocker, & R. T. Gross. Developmental-behavioral pediatrics
(pp. 158-174). Philadelphia: W.B. Saunders.
Coolman, R. B., Bennett, F. C., Sells, C. J., Swanson, M. W., Andrews, M. S., & Robinson, N.
M. (1985). Neuromotor development of graduates of the neonatal intensive care unit:
Patterns encountered in the first two years of life. Journal of Developmental and Behav-
ioral Pediatrics, 6, 327-333.
Davies, P. A. (1984). Follow-up of low birthweight children. Archives of Disease in Child-
hood, 59, 794-797.
Dubowitz, L. M. S., Dubowitz, V., Palmer, P. G., Miller, G., Fawer, C. L., & Levine, M. l.
(1984). Correlation of neurologic assessment in the preterm newborn infant with out-
come at one year. Journal of Pediatrics, 105, 452-456.
Ellenberg, J. H., & Nelson, K. B. (1981). Early recognition of infants at high risk for cerebral
palsy: Examination at age four months. Developmental Medicine and Child Neurology,
14, 575-584.
Frankenburg, W. K. (1983). Infant and preschool developmental screening. In M. D. Levine,
W. B. Carey, A. C. Crocker, & R. T. Gross (Eds). Developmental-behavioral pediatrics
(pp. 927-937). Philadelphia: W. B. Saunders.
Frankenburg, W. K., & Dodds, J. B. (1967). The Denver Developmental Screening Test.
Journal of Pediatrics, 71, 181-191.
Freeman, J. (Ed). (1985). Prenatal and perinatal factors associated with brain disorders (NIH
Pub. No. 85-1149). Washington, DC: U.S. Department of Health and Human Services.
Gesell, A. (1928). Infancy and human growth. New York: Macmillan.
Gesell, A., & Amatruda, C. (1947). Developmental diagnosis (2nd ed.). New York: Hoeber.
Graham, F. K., Matarazzo, R. G., & Caldwell, B. M. (1956). Behavioral differences between
normal and traumatized newborns: II. Standardization, reliability and validity. Psycho-
logical Monographs, 70(21. Whole No. 428).
Griffiths, R. (1954). The abilities of babies. New York: McGraw-Hill.
EARLY ASSESSMENT 247
Prechtl, H. F. R., Vlach, V., Lenard, H. G., & Grant, D. (1967). Exteroceptive and tendon
reflexes in various behavioral states in the newborn infant. Biologia Neonatorum, 11,
159-175.
Public Law 94-142. (1975). Education for all handicapped children act. 94th Congress, S.6.
Rosenblith, J. F. (1974). Relations between neonatal behaviors and those at eight months.
Developmental Psychology, 10, 779-792.
Sameroff, A. J. (1975). Early influences on development: Fact or fancy? Merrill-Palmer Quar-
terly, 21, 267-294.
Sciarillo, W. G., Brown, M. M., Robinson, N. M., Bennett, F. c., & Sells, C. J. (1986). Effective-
ness of the Denver Developmental Screening Test with biologically vulnerable infants.
Journal of Developmental and Behavioral Pediatrics, 7, 77-83.
Siegel, L. S. (1983). Correction for prematurity and its consequences for the assessment of the
very low birth weight infant. Child Development, 54, 1176-1188.
Stave, V., & Ruvalo, C. (1980). Neurological development in very-low-birthweight infants:
Application of a standardized examination and Prechtl's optimality concept in routine
evaluations. Early Human Development, 4, 229-241.
Stutsman, R. (1948). Guide for administering the Merrill-Palmer Scale of mental tests. New
York: Harcourt Brace Jovanovich.
Taylor. D. j. (1984). Low birthweight and neurodevelopmental handicap. Clinics in Obstet-
rics and Gynecology, 11, 525-542.
Terman, 1., & Merrill, M. (1972). Stanford-Binet intelligence scale. Boston: Houghton
Mifflin.
Thorndike, R. 1., Hagen, E. P., & Sattler, J. M. (1986). Guide for administering and scoring the
fourth edition. Stanford-Binet intelligence scale. Chicago: Riverside.
Tjossem, T. (1976). Intervention strategies for high risk infants and young children. Bal-
timore: University Park Press.
Touwen, B. C. 1. (1973). The neurological development of the human infant. In D. Davis & j.
Dobbing (Eds.)' Scientific foundations of pediatrics. Leiden: University Press.
Touwen, B. C. 1. (1978). Variability and stereotyping in normal and deviant development. In
J. Apley (Ed.), Care of the handicapped child. Clinics in Developmental Medicine, No.
67 (pp. 99-110). London: Heinemannn.
Ulrey, G. (1981). Psychological evaluation. In W. K. Frankenburg, S. M. Thornton, & M. E.
Cohrs (Eds.), Pediatric developmental diagnosis (pp. 175-183). New York: Thieme-
Stratton.
Ulrey, G. (1982). Influences of infant behavior on assessment. In G. Ulrey & S. J. Rogers
(Eds.), Psychological assessment of handicapped infants and young children (pp. 14-
24). New York: Thieme-Stratton.
Ulrey, G., & Schnell, R. R. (1982). Introduction to assessing young children. In G. Ulrey & S. j.
Rogers (Eds.), Psychological assessment of handicapped infants and young children
(pp. 1-13). New York: Thieme-Stratton.
Vohr, B. R., & Hack, M. (1982). Developmental follow-up of low-birthweight infants. Pedi-
atric Clinics of North America, 29, 1441-1454.
Wolf, A. W., & Lozoff, B. (1985). A clinically interpretable method for analyzing the Bayley
Infant Behavior Record. Journal of Pediatric Psychology, 10, 199-214.
Yang, R. K. (1979). Early infant assessment: An overview. In J. D. Osofsky (Ed.), Handbook of
infant development (pp. 165-184). New York: Wiley.
10
Questions of Developmental
Neurolinguistic Assessment
MICHAEL A. CRARY, KY]TA K. S. VOELLER,
and NANCY]. HAAK
INTRODUCTION
It is obvious upon the most casual inspection that children develop lan-
guage gradually and that there is an apparent temporal sequence to the
acquisition of linguistic skills. A basic premise of this chapter is that the
order of events of language acquisition reflects, or more pointedly, is
dependent upon, a normal sequence of neurological maturation. This
seems to be an almost obvious supposition. Yet the clinical evaluation of
communicative abilities in children has not, to date, subscribed to a de-
velopmental neurolinguistic philosophy. In the following pages the ques-
tions of the utility of a developmental neurolinguistic approach to speech/
language assessment will be addressed. It would be preliminary to offer a
comprehensive model given present knowledge. Nonetheless, the major
purpose is to propose the possibility of such an approach and to identify
areas for additional study.
An oversimplified description of language development might in-
clude the sequence from babbling to single words, to word combinations,
to increasingly complex grammatic expressions. Additional descriptive
subdivisions might include the separation of comprehension of spoken
language from the ability to express verbal concepts. There are, however,
multiple skill areas that have potential influence upon a developing lan-
guage system. Included among these attributes are motor performance,
249
250 MICHAEL A. CRARY et 01.
Prelinguistic Communication
The prelinguistic stage extends from birth to approximately 12
months. It is during this time that the child is developing rapidly in a
variety of skill areas, with the most obvious being motor skills, social
development, and finally the emergence of spoken language. Early behav-
iors lack intention and might be characterized as reflexive. At this stage,
the infant is able to communicate basic biological and social needs via a
rudimentary system of movements and vocalizations. Language, as the
adult recognizes it, has not yet emerged. However, language foundations
are being constructed during this time. For example, there is increasing
evidence that infants have a remarkable ability to perceive certain aspects
of human communication. Neonates will show excitation to selective peo-
ple, voices, or objects (Alegria & Noirot, 1978). Also Lieberman (1967) has
pointed out that children as young as 3 months will change the pitch of
the voice during vocal play depending on the adult with whom they are
interacting. Voice pitch is higher if the adult is a female rather than a
male. This would indicate that the infant has recognition of certain para-
linguistic parameters and is able to exert some control over vocal produc-
tions at this early age.
The child's repertoire of preintentional behaviors expands until at
about 8 months of age, when the first signs of intentional behaviors are
recognized (Bates, 1975). At this time the infant becomes more persistent
in communicative signaling. Behaviors give the adult a clear indication of
whether responses are appropriate or not, and vocal patterns become
increasingly varied. During this stage the interactive system of gestures,
facial expressions, and vocalizations becomes so rich that it has been
called a "protolanguage" (Halliday, 1975). This pattern of complex behav-
iors expands and leads to the onset of first words early in the second year
of life. The emergence of productions recognized by adults as meaningful
words signals the beginning of the lexical stage of language development.
252 MICHAEL A. CRARY et 01.
Neuroanatomic Maturation
There are at least two perspectives regarding maturation of human
cortex and the development of functional systems. Traditionally, a hier-
archial model of cortical development has been proposed. On the basis of
indices such as brain weight, dendritic proliferation, and myelination
(Altman, 1967; Conel 1939-1963; Flechsig, 1901; Yakovlev & Lecours,
1967), this model has proposed that the primary sensory and motor pro-
QUESTIONS OF NEUROLINGUISTIC ASSESSMENT 255
tion ... " (p. 143). He contends that focal cortical areas develop out of
generalized neocortex. This phylogenetic approach proposed by Brown
appears to share points of agreement with the recent findings of Rakic et
a1. (1986). The resulting model appears to be the converse of the more
traditional hierarchical model. However, both views recognize the post-
natal development of cortical functional subsystems. In this respect, the
two views have similar implications for language development. Both
would predict that early behaviors would reflect more diffuse/nonfocal
processes and that development of more refined/analytic behaviors
would result from maturation of specific subsystems. Thus, although
there are questions concerning the precise nature of neurological matura-
tion relevant to language development, the functional interpretations may
be similar at a simplified behavioral level.
Hemispheric Functions
Another question concerns the role of the right versus the left hemi-
sphere in the development of neurolinguistic functions. One approach to
this topic is to evaluate the effects of early unilateral lesions on subse-
quent language development. Until the early 1970s, it was accepted wide-
ly that left hemisphere lesions early in development had little impact on
subsequent language acquisition. This position was based on the concept
of plasticity or the equipotentiality of the two cerebral hemispheres to
process language in the young child. It was assumed that if a child sus-
tained left hemisphere damage, the right hemisphere would take over
these functions. Lenneberg (1967) stated that lateralization of language to
the left hemisphere was a function of development and that plasticity
continued until adolescence. However, the concept of plasticity rested on
two assumptions and several clinical observations that have not weath-
ered the test of time.
The first premise was that the immature brain had a remarkable re-
silience to early lesions (Kennard, 1938). Acceptance of the fact that spe-
cific early lesions resulted in impaired functioning at maturity in experi-
mental animals did not occur until the 1970s, following the work of
Goldman and colleagues (Goldman, 1971, Miller, Goldman, & Rosvold,
1973). Working with macaques, these investigators demonstrated that the
timing and location of focal brain lesions was critical in determining the
extent of behavioral deficits. Early prenatal lesions resulted in little func-
tional impairment whereas later lesions (infancy) tended to create pro-
found deficits. Also, the appearance of some behavioral deficits was tem-
porally distant from the lesion. For example, lesions of dorsolateral
frontal cortex did not result in any immediate impairment in a delayed
response task. However, at approximately 16 months of age, the time at
which this cortical area is believed to become functionally active in the
QUESTIONS OF NEUROLINGUISTIC ASSESSMENT 257
the right hemisphere group, but they did find a significant age effect
among subjects in the left hemisphere group. Children who incurred
damage later in life presented more severe residual deficits than children
who sustained early damage. Yet, even in those cases of prenatal left
hemisphere lesions, subtle linguistic deficits persisted.
The collective impression from reports such as those reviewed here is
that a modified form of plasticity may apply to the developing neu-
rolinguistic system. Although it appears that the left hemisphere has a
special function in language processing from birth, the right hemisphere
also is capable of linguistic processing, albeit not as efficiently. With
development, the left hemisphere becomes more dominant in the control
of linguistic functions. Given these observations, a better understanding
of developmental neurolinguistic functions will require information re-
garding the role of the right hemisphere in language processing and the
development of subsystems within the left hemisphere to process differ-
ent types of language tasks.
children near the end of this stage used prosodic information to signal
grammatical distinctions in expressive language. Also, there has been
speculation that "normal" prosodic abilities in this age range are ex-
tremely important to subsequent grammatical growth (Crystal 1979; Shad-
den, Asp, Tonkovich, & Mason, 1980). However, there are no formal as-
sessment approaches for prosodic recognition or production at this stage
of development. Practitioners may be able to infer information regarding
prosodic abilities by evaluating how the child responds to different affec-
tive voices (happy, sad, angry) or by using linguistic prosody to signal
grammatical distinctions (questions, emphasis).
Another aspect of linguistic growth is the rapid expansion of pho-
nological abilities that occurs near the end of the stage of lexical expan-
sion. Although the child's sound inventory begins to expand during this
time, the majority of phonological growth coincides with syntactic devel-
opment during the stage of grammatic expansion.
Language Expression/Formulation
Expressive language functions would appear to be predominately
within the domain of the left hemisphere, even in the young child. As
discussed before, children with expressive language deficits in the pres-
ence of relatively good comprehension typically present with both pho-
nological and syntactic deficits. Again, there are multiple clinical pro-
cedures available to assess these language areas. Standardized
phonological assessments typically follow a developmental sound acquisi-
tion orientation, and test for the production of various speech sounds in
different positions within a word. Examples of common speech-articula-
tion tests include the Templin-Darley Tests of Articulation (Templin &
Darley, 1969) and the Goldman-Fristoe Test of Articulation (Goldman &
Fristoe, 1969). Recent application of linguistic theory has emphasized a
rule-governed or pattern analysis over the more traditional one-sound-at-a-
time approach. Although no standardized protocols exist for these analy-
ses, formal descriptive procedures are available (e.g., Hodson, 1980;
Shriberg & Kwiatkowski, 1980). Using both of these approaches permits the
practitioner to establish a developmental performance level for pho-
nological ability and to describe major error patterns.
There are numerous procedures available for the evaluation of syn-
266 MICHAEL A. CRARY et a1.
Repetition
Although many clinical protocols use repetition in one way or an-
other, the significance of strengths or deficits in this communicative func-
tion has not been explained fully. It would be tempting, for example, to
speculate that those children studied by Aram and Nation (1975) or
Denckla (1981) who demonstrated good repetition skills represented a
developmental transcortical neurolinguistic impairment. However, such
an assumption would be highly speculative. Use of repetition tasks has
been criticized from the perspective that such tasks overestimate (Marat-
sos & Kuczaj, 1974; Smith, 1970) or underestimate (Prutting, Gallagher, &
Mulac, 1975) language knowledge. It is possible that comparison of lan-
QUESTIONS OF NEUROLINGUISTIC ASSESSMENT 267
Naming
In both the child and the adult, naming is probably a bihemispheric
linguistic task. Thus, the identification of quantitative deficits on naming
tasks such as the Boston Naming Test (Kaplan, Goodglass, & Weintraub,
1983) or the Expressive One-Word Vocabulary Test (M. F. Gardner, 1979)
may not be useful in differentiating neurolinguistic deficits. Differential
patterns of naming impairment across tasks may be more informative in
identifying a pattern of selective neurolinguistic deficits.
Prosody
Assessment of prosodic abilities is an additional area that has re-
ceived limited attention in child populations. The Seashore Tests of Mu-
sical Ability (Seashore, Lewis, & Saetveit, 1960) evaluates the percep-
tion/discrimination of multiple prosodic features. This procedure is,
however, designed for children 9 years of age or older. There has been
268 MICHAEL A. CRARY et 01.
Paralanguage Measures
Three paralanguage areas that may affect a child's performance on
language tasks include motor ability, memory, and attending skill. Motor
speech ability may affect growth in the child's phonological system.
Motor speech performance may be assessed by visual inspection of the
speech mechanism and by tests of oral-facial praxis and speech di-
adochokinesis. There is no formal protocol for assessing facial praxis in
the child. Most practitioners use modifications of procedures recom-
mended for adult patients. Motor speech abilities are typically assessed
with speech diadochokinetic tasks. In this regard, Fletcher (1978) has
published performance data from 6 years to 13 years, and Riley (Riley &
Riley, 1985) has provided limited normative data down to 4 years of age.
The child with reduced short-term memory ability may present im-
paired repetition functions as well as deficient performance in other lan-
guage areas. There are several memory assessment procedures available.
For example, subtests of the Detroit Test of Learning Aptitude (Hammill,
1985) evaluate auditory retention of unrelated words and oral directions.
In addition, digit span memory may be assessed using the appropriate
subtest from the Illinois Test of Psycho linguistic Ability (Kirk, et 01.,
1968).
Impaired attending ability has been postulated to contribute to re-
duced comprehension performance in certain brain-damaged language-
impaired children (Campbell & McNeil, 1985). Yet mechanisms of atten-
tion, their clinical assessment, and their potential contributions to appar-
ent language dysfunction have received limited investigation. Aside from
skilled observations regarding a child's attending ability, there are few
available tests that attempt to estimate the potential influence of attention
deficits on language performance. Two procedures that evaluate aspects
of "auditory attention" are the Goldman-Fristoe-Woodcock Selective At-
tention Test (Goldman, Fristoe, & Woodcock, 1974) and the Flowers-Cos-
tello Tests of Central Auditory Abilities (Flowers, Costello, & Small,
1970). Additional aspects of attention such as concentration or sustained
attention may be inferred from tasks such as digit span (forward and
QUESTIONS OF NEUROLINGUISTIC ASSESSMENT 269
backward) or other counting and spelling tasks (e.g., Lezak, 1983). Can-
cellation tasks, visual closure tasks, and selected subtests from the
Wechsler Intelligence Scale for Children-Revised (Arithmetic, Coding,
Mazes) also have been suggested for the evaluation of concentration
(Gardner, 1979). Gardner (1979) further describes tasks of auditory or
visual vigilance (sustained attention) that might be useful for evaluation
of attention in language-impaired children. Barkley (Chapter 6, this vol-
ume) provides a superb overview of the assessment of attention in
children.
Paralanguage
Language performance
Language functions content factors
A Concluding Example
Crary (1984) has attempted an initial neurolinguistic interpretation of
one group of developmental communication deficits. In evaluating rela-
tionships between motor and speech-language limitations, he has pro-
posed a continuum of impairments under the label of developmental
verbal dyspraxia. Children with more "executive" dysfunctions would
present difficulties in most motor and speech tasks, whereas children
with deficits more toward the "planning" end of the continuum would
274 MICHAEL A. CRARY et a1.
REFERENCES
Alajouanine, T. H., & L'Hermitte, F. (1965). Acquired aphasia in children. Brain, BB, 635-
662.
Alegria, J., & Noirot, E. (197B). Neonate orientation behavior towards the human voice.
International Journal of Behavioral Development, 1, 291-312.
QUESTIONS OF NEUROLINGUISTIC ASSESSMENT 275
Altman, J. (1967). Postnatal growth and differentiation of the mammalian brain, with im-
plications for a morphological theory of memory. In C. Quarton, T. Melnechuk, & F.
Schmitt (Eds.), The neurosciences, New York: Rockefeller University Press.
Aram, D. M., & Nation, J. E. (1975). Patterns of language behavior in children with develop-
mental language disorders. Journal of Speech and Hearing Research, 18, 229-241.
Aram, D. M., Rose, D. F., Rekate, H. L., & Whitaker, H. A. (1983). Acquired capsular/striatal
aphasia in childhood. Archives of Neurology, 40, 614-617.
Basser, L. S. (1962). Hemiplegia of early onset and the faculty of speech with special refer-
ence to the effects of hemispherectomy. Brain, 85, 427-460.
Bates, E. (1975). Acquisition of performatives prior to speech. Merrill-Palmer Quarterly, 21,
205-226.
Bates, E. (1979). The biology of symbols: Some concluding thoughts. In E. Bates, L. Benigni,
I. Bretherton, L. Camaioni, & V. Volterra (Eds.), The emergence of symbols: Cognition
and communication in infancy. New York: Academic Press.
Bates, E., Benigni, L., Bretherton, I., Camaioni, L., & Volterra, V. (1979). The emergence of
symbols: Cognition and communication in infancy. New York: Academic Press.
Bloom, L. (1973). One word at a time: The use of single-word utterances before syntax. The
Hague: Mouton.
Brown, J. W. (1979). Language representation in the brain. In H. D. Steklis & M. J. Raliegh
(Eds.), Neurobiology of social communication in primates: An evolutionary perspective
(pp. 133-195). New York: Academic Press.
Brown, R (1973). A first language: The early stages. Cambridge: Harvard University Press.
Bzoch, K. R, & League, R (1971). Receptive-expressive emergent language scale. Gaines-
ville, FL: Tree of Life Press.
Campbell, T. F., & McNeil, M. R (1985). Effects of presentation rate and divided attention on
auditory comprehension in children with an acquired language disorder. Journal of
Speech and Hearing Research, 28, 513-520.
Cappa, S., Cavotti, G., & Vignolo, L. A. (1981). Phonemic and lexical errors in fluent aphasia:
Correlation with lesion site. Neuropsychologia, 19, 171-177.
Carrow, E. (1974). Carrow Elicited Language Inventory. Austin, TX: Learning Concepts.
Carrow, E. (1985). Test for Auditory Comprehension of Language-Revised. Boston: Teaching
Resources.
Chi, J. D., Dooling, E. C., & Gilles, F. H. (1977). Left-right asymmetries of the temporal speech
areas of the human fetus. Archives of Neurology, 34, 346-348.
Chomsky, C. (1969). The acquisition of syntax in children from 5 to 10. Cambridge, MA:
M.I.T. Press.
Clark, E. V. (1973). What's in a word: On the child's acquisition of semantics in his first
language. In T. Moore (Ed.), Cognitive development and the acquisition of language.
New York: Academic Press.
Conel, J. L. (1939-1963). Postnatal development of the human cerebral cortex (Vols. 1-6).
Cambridge: Harvard University Press.
Crary, M. A. (1984). A neurolinguistic perspective of developmental verbal dyspraxia. Com-
municative Disorders, 9, 33-49.
Crary, M. A., & Tallman, V. L. (1985, November). Production of propositional prosodic
features by speech-language normal and speech-language disordered children. Paper
presented at the American Speech-Language-Hearing Association Annual Convention,
Washington, DC.
Crystal, D. (1979). Prosodic development. In P. Fletcher & M. Garman (Eds.), Language
acquisition. Cambridge: Cambridge University Press.
Denckla, M. B. (1981). Minimal brain dysfunction and dyslexia: Beyond diagnosis by exclu-
sion. In M. E. Blair, I. Rapin, & M. Kinsbourne (Eds.), Child neurology. New York:
Spectrum.
Dennis, M., & Whitaker, H. (1975). Hemispheric equipotentiality and language acquisition.
276 MICHAEL A. CRARY et a1.
Woods, B. T., & Carey, S. (1979). Language deficits after apparent clinical recovery from
childhood aphasia. Annals of Neurology, 6, 405-409.
Yakovlev, P. 1., & Lecours, A. R. (1967). The myelogenetic cycles of regional maturation of
the brain. In A. Minkowski (Ed.), Regional development of the brain in early life (pp. 3-
70). Oxford: Blackwell.
Zaidel, E. (1979). The split and half brain as models of congenital language disability. In C. L.
Ludlow & M. E. Doran-Quine (Eds.), The neurological basis of language disorders in
children: Methods and directions for research (NINCDS Monograph 22, pp. 55-89).
Washington, DC: U.S. Government Printing Office.
Zaidel. E. (1985). Language in the right hemisphere. In D. F. Benson & E. Zaidel (Eds.), The
dual brain: Hemispheric specialization in humans. New York: Guilford Press.
11
INTRODUCTION
In a relatively young industrial society such as ours, only about 100 years
have elapsed since an inability to learn, retain, and use a symbolic means
of communication fluently has been viewed as a learning disability. Prior
to the end of the 19th century, the acquisition of reading, arithmetical,
and other more demanding cognitive skills was not viewed as essential for
a productive life. These abilities are clearly essential today.
Considerable evolution has taken place in how learning disabilities
are conceptualized. Approximately a century ago they were considered
only insofar as reading abilities were affected. Today, serious deficits
cutting across many different domains such as arithmetic or spelling may
result in a diagnosis of learning disability. Even in the historically impor-
tant domain of reading, a variety of studies suggest the existence of many
subtypes or subpopulations of disabled readers. Further articulation of
these subtypes, more well-controlled research studies, and technologi-
cally sophisticated investigations that relate deficient regions of brain
activity (e.g., metabolic) to disordered cognitive ability will probably im-
pact on new conceptualizations of learning disabilities and their
assessment.
GEORGE W. HYND Departments of Educational Psychology and Psychology, University
of Georgia, Athens, Georgia, and Department of Neurology, Medical College of Georgia,
Augusta, Georgia. ROBERT T. CONNOR and NAOMI NIEVES Kennedy Institute,
Johns Hopkins School of Medicine, Baltimore, Maryland.
281
282 GEORGE W. HYND et 01.
her letters, displayed poor arithmetic skills, and misnamed musical notes.
Family history revealed that her uncle had reading problems as a young-
ster and still experienced difficulty spelling as an adult. Fisher described
this case as evidence of a familial condition of impairment in the left
angular gyrus; "the visual memory centre for words." These notions con-
cerning the possible congenital or genetic etiology continued to attract
support, as evidenced by Stephenson's (1905) case of congenital word
blindness affecting three generations.
Thus, by 1905 it was already reasonably well established that (1)
severe learning disabilities were manifested in children of normal intel-
ligence (although no standardized measure of IQ was yet generally avail-
able), (2) they affected a greater number of boys than girls, (3) the deficits
were manifested variably, impacting differentially on each child's ability
to read or perform some cognitive task, (4) the disability was not generally
responsive to traditional learning opportunities, (5) it seemed to have a
genetic component that expressed itself variably, (6) it could be diagnosed
using many different informal and formal clinical assessment practices,
and (7) it might be related to some neurodevelopmental pathology in the
region of the angular gyrus in the left hemisphere. With the benefit of
hindsight, it is remarkable how sophisticated and accurate were the obser-
vations made by these early clinicians.
What's in a Name?
By the early part of this century, many different terms had been
suggested in attempts to define this syndrome accurately. A representa-
tive few include amblyopia, amnesia visualis verbalis, bradylexia, cogeni-
tal alexia, congenital word blindness, and later, primary reading retarda-
tion, strephosymbolia, and developmental dyslexia (Drew, 1956; Hynd &
Cohen, 1983; Pirozzolo, 1979). Each of the investigators who introduced
these terms offered his or her own rationale.
However, it was Orton (1928) and his ideas regarding mixed cerebral
dominance that seemed to capture the attention of psychologists and edu-
cators alike. Historically, he was important, not so much because his
theories were well accepted but because he stimulated some five decades
of research into the relationship involving laterality, language abilities,
and reading acquisition. Overall, Orton estimated that 2 to 4% of the
school population had a significant reading deficit that merited special
training. After decades of research in which the relationships between
laterality and academic or cognitive performance have been examined, it
can be concluded firmly that Orton's (1928) ideas have not stood the test
of time. Reviews by Benton (1975), Kinsbourne and Hiscock (1981), and
Zangwill (1960) support this conclusion. His ideas do, however, continue
to attract attention (Geschwind & Behan, 1982). More recent efforts to
284 GEORGE W. HYND et 01.
Kinsbourne and 13 Nonverbal> verbal by M = 62% N/R No 8 to 31 1. WISC-R or W AIS Clinical impressions Qualitative P > V clinical tesing
Warrington at least 20 points F ~ 38% 2. Schonell Reading revealed signifi-
(1963) Verbal> nonverbal by and Spelling language
at least 20 points 3. Tests of Finger impairment.
Differentiation V > P failed tests of
finger differentiation
and had difficulties
with arithmetic.
Called Group 1, the
language-retardation
group.
Called Group 2, the
Gerstmann Group.
Ingram, Mason, 82 Dyslexics M = 80% NIR No 7 to 15.11 1. Stanford-Binet Frequencies Chi-square Specifics had a signifi-
and Blackburn 1. Specific dyslexics F = 20% 2. Schonell Reading, cant higher propor-
(1970) = 62 Spelling, tion of boys than
2. General dyslexics Arithmetic girls.
= 20 3. Goodenough Generals had signifi-
Draw-a-Man cantly more neu-
4. Neuropsychologi- rological findings.
cal Assessment Specifics had signifi-
(EEG, lateral cantly more au-
dominance) diophonic reading
5. Physical exam errors.
Rourke, Young, 90 LD 3 groups M ~ 80% N/R No 9 to 14 1. PPVT Differential perfor- Multiple 1-way HV-LP group was sig-
and Flewelling 1. PIQ> VIQ F = 20% 2. WRAT mance of LD types ANOVAs nificantly better on
(1971) 2. PIQ = VIQ 3. Reitan's Category those tasks involv-
3. PIQ < VIQ Test ing verbal, language,
4. Aphasia Screening and auditory per-
Test ceptual skills.
5. Speech Perception LP-HV group signifi-
Test Rhythm Test cantly better on
Trails A and B tasks involving visu-
al-perceptual skills.
Naidoo (1972) 98 Dyslexics All males Middle class Age + type 8 to 12.11 1. WISC Differential perfor- Cluster analysis Dyslexics had a sig-
1. 56 reading of school 2. Reading, Spelling mance of LD types nificantly greater
deficits tests family history of
2. 42 spelling 3. Perceptual tasks reading problems
deficits (auditory, visual, than controls. No
motor) subtypes of dyslexia
4. Social Adjustment were identified. Evi-
Scales dence suggests that
sequencing dis-
ability may underlie
reading and spelling
retardation.
Bader (1973) 107 Children who met the M ~ 86% N/R 8 to 16 Boder Reading-Spell- Clinical impression Qualitative 3 subtypes
world federation F = 14% ing Pattern Test 1. Dysphonetic
definition of devel- (63%)
opmental dyslexia. 2. dyseidetic (9%)
3. Mixed (22%)
Undetermined (6%)
Nelson and War- Study 1 N/R No 8 to 14 1. WISe Error analysis Multiple Hests Degree of VIQ decre-
rington (1974) Reading and Spell- 2. Schonell Reading ment is much more
ing deficits~2 years and Spelling strongly associated
39 1. More general Yer- M ~ 85% with degree of read-
bal retardation by F:::: 15% ing retardation than
15 points (WISC) with spelling retaf-
82 2. No general verbal M = 76% dation.
retardation F ~ 24%
Study 2 N/R No Same as Same as above Error analysis Multiple t-tests Spelling and reading
17 1. Reading < 2 M ~ 88% above retardates had sig
years retarded, F = 12% nificantly lower VIQ
spelling> 2 than spelling-only
years retarded retardates.
"Abbreviations in this table include (N/R) not reported, WISC-R (Wechsler Intelligence Scale for Children-Revised), WAIS (Wechsler Adult Intelligence Scale), PPVT
(Peabody Picture Vocabulary Test), WRAT (Wide Range Achievement Test), PIQ (Performance IQ), VIQ (Verbal IQ), FSIQ (Full Scale IQ), LP (Low Performance IQ), SPA
(Spatial factor), CON (Conceptual factor), SEQ (Sequential factor), FTNW (Finger Tip Number Writing), LNNB-CR (Luria-Nebraska Neuropsychological Battery-Chil-
dren's Revsion), VMI (Developmental Test of Visual Motor Integration), PlAT (Peabody Individual Achievement Test), K-ABC (Kaufman Assessment Battery for
Children), P (WISC Performance IQ), V (WISC Verbal IQ), M (males), F (females), EEG (Electroencephalogram), ANOV A (Analysis of Variance), LD (Learning-Disabled), X
(Mean), NLD (Non-Learning-Disabled), R-L (Right-Left), WISC (Wechsler Intelligence Scale for Children), EMR (Educable Mentally Retarded), SES (Sociometric Status),
ANCOVA (Analysis of Covariance), MANOVA (Multivariate Analysis of Variance), CAT (California Achievement Test), SLDR (Specific Learning Disabled Resource), CBI
(Classroom Behavior Inventory), SCAN (Schedule of Classroom Activity Norms), SEARCH (Systematic Evaluation of Reading Criteria for High Risk).
bIt should be noted that subtypes (auditory, visual, auditory-visual, emotional, and pedagogic) of reading disability were proposed earlier than 1963. For example,
Gjessing (1953) noted those listed above a decade earlier than Kinsbourne and Warrington's (1963) report. However, the validating evidence for the existence of these
subtypes has only been the focus of researchers during the past 25 years.
(continued)
TABLE 1. (Continued)
Age range
Author(s) N Population Sex SES Matched (years) Tests Type of study Analysis General findings
(continued)
TABLE 1. (Continued)
Age range
Author(s) N Population Sex SES Matched (years) Tests Type of study Analysis General findings
Sweeney and 48 Groups (3) M = 63% Middle class Age + 4th grade 1. Auditory tests Differential perfor- Multiple Normals significantly
Rourke (1978) 4th- and 8th-graders F = 37% wIse 9.9 to 2. Verbal tests mance of LD types ANOVAs greater than pho-
1. Nonphonetic re- PIQ 10.1 3. Reading and control with New- netically inaccurate
tarded spellers 4. Visual Closure man-Keuls spellers only at
2. Phonetic retarded test comparison older age level on
spellers 8th grade all but the simplest
3. Control 13.3 to of auditory discrimi-
13.4 nation and immedi-
ate auditory~verbal
memory measures,
Doehring, 158 3 subtypes N/A N/R Age + Sex 8 to 17 31 Tests Differential perfor- 1. Q~factor Q factor analysis repli~
Hoshko. and Reading problems (n 9 Reading mance of LD and 2. Cluster anal- cated same 3 sub-
Bryans (1979) ~ 34) 8 Visual Scanning controls ysis types when original
Mixed problems (n 7 Visual Matching data pooled with
~ 31) 7 Auditory-Visual normal readers.
Combination of Matching Same subtypes re-
reading and mixed mained well defined
problems (n ~ 62) when reexamined
Controls (n ~ 31) using cluster analy-
sis approach.
Fisk and Rourke 264 Learning-disabled M = 81% N/R No 9 to 14.9 1. WRAT Differential perfor- Q~factor analy- 54% of subjects were
(1979) 3 groups F = 16% 2. Reitan's Neuro- mance of LD types sis classified into sub-
9-10 years (n ~ psychological Bat- on neuropsycho~ types that were
100) tery logical battery "replicated" across 2
11-12 years (n ~ or more age levels.
100) Type A-Poor auditory
13-14 years (n ~ verbal processing
64) and finger localiza-
tion deficit.
Type B-Linguistic
deficit.
Type C-Poor perfor-
mance in fingertip
number writing per-
ception (may be a
variant of Subtype
A).
Petrauskas and 160 2 groups M = 86% N/R No 7 to 8.9 1. WRAT Reading Differential perfor- Pearson Prod- 3 reliable subtypes
Rourke (1979) N = 133 retarded F = 14% 2. Reitan 6 skill mance of normal uct-Moment found. 50% of sub-
readers areas: Tactile, Mo- and retarded read- Correlations ject sample could be
N = 27 normal readers tor, Visual-Spatial, ers Factor analysis reliably classified.
Auditory-Verbal, using iterated Type I-Most lan-
Abstract-Concep- principal guage disturbances.
tua!, and Sequenc- axes solution Type 2-Sequencing
ing deficits. Finger
Agnosia.
Type 3-Conceptual,
motoric. and verbal
expressive deficits.
Pirozzolo (1979) 24 Right-handed All males N/R Age + Full X=ll.1 1. 16 three-letter Differential perfor- ANOVA with Auditory-linguistic
3 groups Scale IQ range stimulus words mance of LD and Newman- group showed no
1. Visual dyslexics not re- 2. Eye movement controls Keuls com- lateral asymmetries
2. Auditory-linguis- ported monitor parisons for word recognition
tic dyslexics 3. Gray Oral Reading when compared
3. Normal readers Test passages with normals.
Visual-spatial group
had significant
deficits recognizing
words presented
parafoveally, faster
saccadic leftward
eye movement, and
more return sweep
reading inaccuracies
when compared
with normals.
Lyon and Wat- 150 100 learning-disabled M = 90% Middle class Age + 11 to 12.5 10 tests Differential perfor- Multiple I-way 6 homogeneous sub-
son (1981) resource F = 10% WISC-R 1. Auditory tests mance of LD and ANOVA groups for raw and
50 controls FSIQ 2. Token tests controls Cluster Analy- standard scores, ac-
3. Raven's Col- sis *(only on counted for 94% of
oured Progres- LD subjects) SLDR subjects.
sive Matrices Multivariate Discriminant analysis
4. VMI discriminant between 6 sub-
5. PlAT (2) analysis groups yielded 2
6. Memory for ScheWi post discriminant
designs hoc pairwise functions.
7. Naming Test comparisons 1. Language and vi-
(continued)
TABLE 1. (Continued)
Age range
Author(s) N Population Sex SES Matched (years) Tests Type of study Analysis General findings
sual-motor inte-
gration function
2. An orthogonal vi-
sual-motor inte-
gration
dimension.
Satz and Morris 325 5th-grade white boys All males N/R No X=l1 WRAT Differential perlor- 2 cluster anaIy- 5 subtypes
(1981) in Florida Longitu- years PPVT mance of white ses-first one 1. Impaired on both
dinal Project (range Neuropsychological 5th-graders to identify language
not re- Battery learning dis- variables.
ported) SES ability group, 2. Impaired on ver-
second to bal fluency only.
subtype the 3. Impaired on lan-
learning-dis- guage and per-
abled group ceptual measures.
4. Impaired on per-
ceptual only.
5. No impairment.
Thompson 83 Spelling and reading- N/R N/R No 3 age 1. WISC-R Error analysis l-way 3 subgroups were de-
(1982) disabled groups: 2. Raven's ANaVAs fined as basis of
Average IQ 8 to 10.11 3. British Ability with Tukey reading and spelling
3 age groups (n = Scales multiple errors. A greater
29) 4. Neal's Analysis of comparisons number of children
11 to Reading Ability for a repeat~ with auditory~lin~
13.11 ed-measures guistic deficits than
(n = design visuo-spatial at all
29) ages. Visuo-spatial
14 to group scored less
16.11 well on speed of in~
(n = formation process~
24) ing, block design
level and block
design power.
Nolan, Ham- 36 a. Normal-WRAT ;::= M = 78% N/R No 7 to 13 WISC-R, FTNW, Fin- Determine if LD I-way ANaVA Partial evidence for
meke, and 40 percentile F = 22% ger Agnosia, subtypes would Scheff;; AN- notion of unique
Barkley (1983) b. Reading-Spelling s LNNB-CR, WRA T exhibit unique CaVA neuropsychological
20 percentile neuropsychologi~ profiles. The expres-
Math" 40 cal profiles sive speech, writing.
percentile and reading scales
c, Math s 20 percen- of LNNB-CR differ-
tile, Reading-Spell- entia ted the poor
ing 2: 40 percentile reading/spelling
group from the other
2 groups. Did not
differentiate the
math deficient
group.
Watson, Goldgar, 65 Children who were re- M = 77% N/R No 7 to 14.11 6 skill areas: Differential perfor- Cluster analysis 3 clusters
and Ryschon ferred for LD F = 23% Reading/ Spelling mance of children with a. visual processing
(1983) Visual Processing referred for LD K-means iter- deficit
Language ative parti- b. generalized
Memory tianing language disorder
Perceptual method c. minimal deficit
Organization, subtype
VMJlBehavior Clusters relatively het-
erogeneous and may
have limited clinical
utility.
Meacham and 50 4 groups CAT scores M = 54% N/R No 7.1 to 9.2 CAT Differential perfoT- t tests, Q factor, 4 subtypes for
Fisher (1984) Normal readers (n = F ~ 46% SEARCH mance of LD types discriminant kindergarten.
20) WRAT and controls analysis 3 subtypes for second
Reading-disabled in grade.
Special Ed. (n ~ 10) There was little sta-
Reading/Language dis- bility in the sub-
abled in self-con- types from
tained LD (n = 10) kindergarten to sec-
Scores < 35%ile on and grade.
CAT-No remedia-
tion [n ~ 10)
Fletcher (1985) 87 Controls (16), Reading- M = 58% N/R No 7.6 to 12 WISC-R, WRAT, Ver- Differential Perfor- MANOVA, Relative to controls,
Spelling LD (10), F = 42% (X ~ bal and Nonverbal mance of LD ANOVA, Arithmetic-Spelling
Reading-Spelling- 9.94) Selective Remind- achievement sub- post hoc LD subjects had dif-
Arithmetic LD (38), ing Task types on verbal comparisons ficulty on the non-
Spelling-Arithmetic and nonverbal se- (Tukey) verbal task, the
LD (10), and Arith- lective reminding reading, spelling
metic LD (13) task. Influence of children had diffi-
IQ also examined. culty on the verbal
(continued)
TABLE 1. (Continued)
Age range
Author(s) N Population Sex SES Matched (years) Tests Type of study Analysis General findings
(continued)
TABLE 1. (Continued)
Age range
Author(s) N Population Sex SES Matched (years) Tests Type of study Analysis General findings
Thus, many of the studies cited in Table 1 are by and large athe-
oretical (rarely is any specific rationale given for tests employed). A typ-
ical multivariate study (in Table 1) utilizes variables that are distantly
related to actual reading or achievement. These variables then are clus-
tered to yield "subtypes" that often have little significance in helping us
understand why these children cannot learn normally.
Satz and Morris (1981), Taylor, Fletcher, and Satz (1982), and others
(e.g., Coltheart, 1980) have argued cogently that subtypes should be de-
fined in terms of actual patterns of deficient learning or reading behaviors
and then studied neuropsychologically. This type of approach makes
sense for three reasons.
First and foremost, grouping or subtyping children by the actual pat-
terns of errors they make in learning should, through careful error analy-
sis, eventually reveal many of the potential subprocesses directly in-
volved in learning within any specific domain. Thus, neurocognitive
theory will be advanced. Second, it should seem obvious that by assessing
actual processes involved in fluent reading, the assessment achieves more
ecological validity. Thus, the derived subtypes may actually be observed
in the clinic setting. Third, and probably most important, if neuropsychol-
ogists can delineate competently the actual neurocognitive, especially
neurolinguistic, behaviors that characterize these subtypes, direct treat-
ment implications may result.
In fact, Fletcher (1985) provides an excellent example of how such
research efforts should be conducted, He examined verbal and nonverbal
memory (storage and retrieval) using a selective reminding procedure
among four groups of learning-disabled children. These groups were
those with (1) reading-spelling disabilities, (2) reading-spelling-arith-
metic disabilities, (3) spelling-arithmetic disabilities, and (4) arithmetic-
only disabilities. Consistent with his hypotheses, he found that arith-
metic- and spelling-arithmetic-disabled children did poorer on the non-
verbal tasks whereas the reading-spelling group did worse on the verbal
task. Those with the reading-spelling-arithmetic disabilities performed
poorly on the storage and retrieval tasks tapping both verbal and nonver-
bal memory. Thus, Fletcher concluded that there does seem to be validity
in subtyping disabled learners on the basis of patterns of academic
achievement. With this study in mind, let us now return our attention to
reading disorders where some initial progress along this dimension is
being made.
Neurolinguistic Subtyping
Frustration with the fact that decades of research on "subtypes" of
reading disorders have failed to increase significantly our theoretical un-
derstanidng of the linguistic processes by which children access printed
SUBTYPES OF LEARNING DISABILITIES 301
NEUROANATOMICAL-LINGUISTIC PERSPECTIVES
Left Right
(ANTERIOR)
Broca's
Area
Arcuate
Corpus
'Com,ph,,",;o" _-.~-----1- Callosum
Wernicke's
Area - - . "
Angular
Gyrus ---'~
Medial
Occipital
Area
(POSTERIOR)
CONCLUSIONS
There has indeed been a long history, first in neurology and more
recently in psychology, in attempting to describe the manifestations of
learning disabilities in children. What first struck the early clinicians was
the similarities between these children's performance and that of brain-
damaged adults. Clearly, these disorders have a neurodevelopmental ori-
gin remarkably consistent with what was originally proposed by neu-
rologists nearly 100 years ago. Currently accepted definitions reflect this
perspective.
Concurrent with the involvement of psychologists in research with
these children, there has been a move away from the benefits that careful
clinical-observational research provides (e.g., Boder, 1973; Kinsbourne &
Warrington, 1963) toward a largely atheoretical multivariate approach.
Tests are often included in neuropsychological batteries for no apparent
reason, existing populations previously diagnosed as being disabled are
often employed without any screening as to the validity of the initial
diagnosis, and the resulting subtypes are often characterized by profiles
308 GEORGE W. HYND et a1.
REFERENCES
Bannatyne, A. (1966). The etiology of dyslexia and the color phonics system. In J. Money
(Ed.), The disabled reader: Education of the dyslexic child. Baltimore: Johns Hopkins
Press.
Bastian, H. C. (1898). Aphasia and other speech defects. London: H. K. Lewis.
Bateman, B. (1968). Interpretation of the 1961 Illinois Test of Psycholinguistic abilities.
Seattle: Special Child Publications.
Benton, A. L. (1975). Developmental dyslexia: Neurological aspects. In W. J. Friedlander
(Ed.), Advances in neurology (Vol. 2). New York: Raven Press.
Boder, E. (1973). Developmental dyslexia: A diagnostic approach based on three atypical
reading patterns. Developmental Medicine and Child Neurology, 15,663-687.
Breen, M. J. (1986). Cognitive patterns of learning disability subtypes as measured by the
Woodcock-Johnson Psychoeducational Battery. Journal of Learning Disabilities, 19,86-
90.
Claiborne, J. H. (1906). Types of congenital symbol amblyopia. Journal of the American
Medical Association, 47, 1813-1816.
Coltheart, M. (1980). Deep dyslexia: A review of the syndrome. In M. Coltheart, K. Patterson,
& J. C. Marshall (Eds.), Deep dyslexia. Boston: Routledge & Kegan Paul.
Critchley, M. (1970). The dysexic child. London: William Heinemann Medical Books.
Crockett, D., Klonoff, H., & Bjerring, J. (1969). Factor analysis of neuropsychological tests.
Perceptual and Motor Skills, 29, 791-802.
Deloche, G., Andreewsky, E., & Desi, M. (1982). Surface dyslexia: A case report. Brain and
Language, 15, 12-31.
Denckla, M. B. (1973). Research needs in learning disabilities: A neurologist's point of view.
Journal of Learning Disabilities, 6, 44-50.
Doehring, D. G., & Hoshko, 1. M. (1977). Classification of reading problems by the Q-tech-
nique of factor analysis. Cortex, 13, 281-294.
Doehring, D. G., Hoshko, 1. M., & Bryans, B. N. (1979). Statistical classification of children
with reading problems. Journal of Clinical Neuropsychology, 1, 5-16.
Doris, J. (1986). Learning disabilities. In S. J. Ceci (Ed.), Handbook of cognitive, social, and
neuropsychological aspects of learning disabilities (pp. 3-54). Hillsdale, NJ: Erlbaum.
Drake, W. E. (1968). Clinical and pathological findings in a child with a developmental
learning disability. Journal of Learning Disabilities, 1,486-502.
Drew, A. L. (1956). A neurological appraisal of familial congenital word blindness. Brain, 79,
440-460.
SUBTYPES OF LEARNING DISABILITIES 309
Duffy, F. H., Denckla, M. B., Bartels, P. H., & Sandini, G. (1980). Dyslexia: Regional dif-
ferences in brain electrical activity by topographic mapping. Annals of Neurology, 7,
412-420.
Federal Register (1976). Education of handicapped children and incentive grants programs
(Vol. 41, p. 46977). Bethesda, MD: U.S. Department of Health, Education and Welfare.
Fisher, J. H. (1905). Case of congenital word-blindness (Inability to learn to read). Ophthal-
mic Review, 24, 315-318.
Fisher, W. F., Lieberman, 1. Y., & Shankeiler, D. (1978) Reading reversal and developmental
dyslexia: A further study. Cortex, 14, 496-510.
Fisk, J. 1., & Rourke, B. P. (1979). Identification of subtypes of learning disabled children at
three age levels: A neuropsychological, multivariate approach. Journal of Clinical
Neuropsychology, 1,289-310.
Fletcher, J. M. (1985). Memory for verbal and nonverbal stimuli in learning disability sub-
groups: Analysis by selective reminding. Journal of Experimental Child Psychology, 40,
244-259.
Friedman, R. B., & Perlman, M. B. (1982). Underlying causes of semantic paralexias in a
patient with deep dyslexia. Neuropsychologia, 20, 559-568.
Galaburda, A. M., & Kemper, T. 1. (1979). Cytoarchitectonic abnormalities in developmental
dyslexia: A case study. Annals of Neurology, 6, 94-100.
Galaburda, A. M., Sherman, G. F., Rosen, G. D., Aboitiz, F., & Geschwind, N. (1985). Devel-
opmental dyslexia: Four consecutive patients with cortical anomalies. Annals of Neu-
rology, 18, 222-233.
Geschwind, N. (1974). Anatomical foundations of language and dominance. In C. 1. Ludlow
& M. E. Doran-Quine (Eds.), The neurological basis of language disorders in children:
Methods and direction for research (NIH Publication No. 79-440). Bethesda, MD: U.S.
Department of Health, Education, and Welfare.
Geschwind, N., & Behan, P. O. (1982). Left handedness: Association with immune disease,
migraine, and developmental learning disorders. Proceedings of the National Academy
of Sciences, 79, 5097-5100.
Hammill, D. D., Leigh, J. E., McNutt, G., & Larsen, S. C. (1981). A new definition of learning
disabilities. Learning Disability Quarterly, 4, 336-342.
Harris, T. 1., & Hodges, R. E. (Eds.). (1981). A dictionary of reading and related terms.
Newark, NJ: International Reading Association.
Hayes, F. B., Hynd, G. W., & Wisenbaker, J. (1986). Learning disabled and normally achiev-
ing college students on reaction time and speeded classification tasks. Journal of Educa-
tional Psychology, 78, 39-43.
Hinshelwood, J. (1895). Word-blindness and visual memory. Lancet, 2, 1564-1570.
Hinshelwood, J. (1900). Congenital word-blindness. Lancet, 1, 1506-1508.
Hooper, S. R., & Hynd, G. W. (1985). Differential diagnosis of subtypes of developmental
dyslexia with the Kaufman Assessment Battery for Children (K-ABC). Journal of
Clinical Child Psychology, 14, 145-152.
Hynd, C. (1986). Educational intervention in children with developmental learning disor-
ders. In J. E. Obrzut & G. W. Hynd (Eds.)' Child neuropsychology: Clinical practice (pp.
265-297). New York: Academic Press.
Hynd, G. W., & Cohen, M. (1983). Dyslexia: Neuropsychological theory, research, and
clinical differentiation. New York: Grune and Stratton.
Hynd, G. W., & Hynd, C. R. (1984). Dyslexia: Neuroanatomicallneurolinguistic perspectives.
Reading Research Quarterly, 19,482-498.
Hynd, G. W., Obrzut, J. E., Weed, W., & Hynd, C. R. (1979). Development of cerebral domi-
nance: Dichotic listening asymmetry in normal and learning-disabled children. Journal
of Experimental Child Psychology, 28, 445-454.
Hynd, G. W., Snow, J. H., & Becker, M. G. (1986). Neuropsychological assessment in clinical
child psychology. In B. B. Lahey & A. Kazdin (Eds.), Advances in clinical child neuro-
psychology (Vol. 9). New York: Plenum.
310 GEORGE W. HYND et a1.
Hynd. G. W., & Willis, W. G. (1988). Pediatric neuropsychology. Orlando, FL: Grune and
Stratton.
Ingram, T. S., Mason, A. W., & Blackburn, I. (1970). A retrospective study of 82 children with
reading disability. Developmental Medicine and Child Neurology, 12, 271-281.
Jansky, J., & deHirsch, K. (1972). Preventing reading failure-Prediction, diagnosis, and
intervention. New York: Harper & Row.
Jackson, E. (1906). Developmental alexia (congenital word blindness). American Journal of
Medical Science, 131,843-849.
Johnson, D. J., & Myklebust, H. R (1967). Learning disabilities: Educational principles and
practices. New York: Grune and Stratton.
Kinsbroune, M., & Hiscock, M. (1981). Cerebrallateralization and cognitive development:
Conceptual and methodological issues. In G. W. Hynd & J. E. Obrzut (Eds.), Neuropsy-
chological assessment and the school-age child: Issues and procedures. New York:
Grune and Stratton.
Kinsbourne, M., & Warrington, E. K. (1963). Developmental factors in reading and writing
backwardness. British Journal of Psychology, 54, 145-156.
Kirk, S. A., & Bateman, B. (1962). Diagnosis and remediation of learning disabilities. Excep-
tional Children, 29(2), 73-78.
Kussmaul, A. (1877). Disturbance of speech. Cyclopedia of Practical Medicine, 14, 581.
Liberman, I. Y., & Shankweiler, D., Orlando, L. Harris, K. S., & Bertt, F. B. (1971). Letter
confusion and reversal of sequence in the beginning reader: Implications for Orton's
theory of developmental dyslexia, Cortex, 7, 127-142.
Liberman, I. Y., Shankweiler, D., Liberman, A. M., Fowler, C., & Fischer, W. F. (1977).
Phonetic segmentation and recoding in the beginning reader. In A. Reber & D. Scar-
borough (Eds.), Toward a psychology of reading. Hillsdale, NJ: Erlbaum.
Luria, A. R (1980). Higher cortical functions in man (2nd ed.). New York: Basic Books.
Lyle, J. G. (1969). Reading retardation and reversal tendency: A factorial study. Child Devel-
opment, 40, 833-843.
Lyle, J. G., & Goyen, J. (1968). Visual recognition developmental lag and stephosymbolia in
reading retardation. Journal of Abnormal Psychology, 73, 25-29.
Lyle, J. G., & Goyen, J. (1975). Effects of speed of exposure and difficulty of discrimination on
visual recognition of retarded readers. Journal of Abnormal Psychology, 8, 673-676.
Lyon, R, & Watson, B. (1981). Empirically derived subgroups of learning disabled readers:
Diagnostic characteristics. Journal of Learning Disabilities, 14, 256-261.
Marshall, J. 1., & Newcombe, F. (1973). Patterns of paralexia: A psycho linguistic approach.
Journal of Psycholinguistic Research, 2, 175-197.
Marshall, J. C., & Newcombe, F. (1980). The conceptual status of deep dyslexia: A historical
perspective. In M. Coltheart, K. Patterson, & J. C. Marshall (Eds.), Deep dyslexia (pp. 1-
21). Boston: Routledge & Kegan Paul.
Mattis, S., French, J. H.,& Rapin, I. (1975). Dyslexia in children and young adults: Three
independent neuropsychological syndromes. Developmental Medicine and Child Neu-
rology, 17, 150-163.
Mayeux, R, & Kandel, E. R (1985). Natural language, disorders of language, and other
localizable disorders of cognitive functioning. In E. R Kandel & J. H. Schwartz (Eds.),
Principles of neural science (2nd ed., pp. 688-703). New York: Elsevier.
McCarthy, J. M. (1975). Children with learning disabilities. In J. J. Galagher (Ed.), The
application of child development research to exceptional children. Reston: Council for
Exceptional Children.
McCarthy, J. J., & McCarthy, J. F. (1969). Learning disabilities. Boston: Allyn Bacon.
Meacham, M. 1., & Fisher, G. 1. (1984). The identification and stability of subtypes of
disabled readers. International Journal of Clinical Neuropsychology, 4, 269-274.
Morgan, W. P. (1896). A case of congenital word-blindness. British Medical Journal, 2, 1378.
Morris, R, Blashfield, R, & Satz, P. (1986). Developmental classification of reading-disabled
children. Journal of Clinical and Experimental Neuropsychology, 8, 371-392.
SUBTYPES OF LEARNING DISABILITIES 311
Snow, J. H., Cohen, M., & Holliman, W. B. (1985). Learning disability subgroups using
cluster analysis of the WISC-R Journal of Psychoeducational Assessment, 4, 391-397.
Snow, J. H., & Hynd, G. W. (1985). A multivariate investigation of the Luria-Nebraska Neuro-
psychological Battery-Children's Revision with learning disabled children. Journal of
Psychoeducational Assessment, 3, 101-109.
Speece, D. L., McKinney, J. D., & Appelbaum, M. 1. (1985). Classification and validation of
behavioral subtypes of learning disabled children. Journal of Educational Psychology,
77, 67-77.
Spreen, 0., & Haaf, R G. (1986). Empirically derived learning disability subtypes: A replica-
tion attempt and longitudinal patterns over 15 years. Journal of Learning Disabilities,
19, 170-180.
Stephenson, S. (1905). Six cases of congenital word blindness affecting three generations of
one family. Ophthalmoscope,S, 482-484.
Sternberg, R, & Wagner, R K. (1982). Automatization failure in learning disabilities. Topics
in Learning and Learning Disabilities, 2, 1-11.
Strauss, A. A., & Kephart, N. C. (1955). Psychopathology and education of the brain-injured
child (Vol. 2). New York: Grune and Stratton.
Strauss, A. A., & Lehtinen, 1. E. (1947). Psychopathology and education of the brain-injured
child (Vol. 1). New York: Grune and Stratton.
Sweeney, J. E., & Rourke, B. A. (1978). Neuropsychological significance of phonetically
accurate and phonetically inaccurate spelling errors in younger and older retarded
spellers. Brain and Language, 6, 212-225.
Taylor, H. G., Fletcher, J. M., & Satz, P. (1982). Component processes in reading disabilities:
Neuropsychological investigation of distinct subskill deficits. In R N. Malatesha & P. G.
Aaron (Eds.), Reading disorders: Varieties and treatments (pp. 121-147). New York:
Academic Press.
Thomson, M. E. (1982). The assessment of children with specific reading difficulties (dyslex-
ia) using the British Ability Scales. British Journal of Psychology, 73, 461-478.
U.S. Department of Education, Office of Special Education and Rehabilitative Services
(1983). Fifth annual report to Congress on the implementation of PL 94-142: The Educa-
tion of All Handicapped Children's Act.
Warrington, E. K. (1981). Concrete word dyslexia. British Journal of Psychology, 72, 175-
196.
Watson, B. U., & Goldgar, D. E., & Ryschon, K. 1. (1983). Subtypes of reading disability.
Journal of Clinical Neuropsychology,S, 377-399.
Wernicke, C. (1874). Der aphasiche symptemkomplex. Breslaw: Cohn and Weigert.
Whitaker, H. A. (1976). Neurobiology of language. In E. R Carterette & M. P. Friedman (Eds.),
Handbook of perception (Vol. 7). New York: Academic Press.
Zangwill, D. 1. (1960). Cerebral dominance and its relation to psychological function. Edin-
burgh: Oliver & Boyd.
12
STEPHEN R. HOOPER
INTRODUCTION
313
314 STEPHEN R. HOOPER
is no accident that this area has not been advanced sooner owing to its
significant complexity.
Further compounding the difficulties confronted in the preschool
population, some investigators have taken the stance that disability la-
bels, such as learning disability, should be used sparingly with young
children, if at all, owing to the negative expectations that can arise (Al-
gozzine, Mercer, & Countermine, 1977; Foster, Schmidt, & Sabatino, 1976;
Foster & Ysseldyke, 1976). For example, preschoolers experiencing only a
temporary developmental delay may be misdiagnosed, and those working
with the child may begin to hold negative expectations of the child's
potential. This could create secondary problems of adjustment for such
children, confusion in their families, and self-fulfilling prophecies in the
form of actual learning difficulties. Given these concerns, it will be impor-
tant for developmentally appropriate, reliable, and valid neuropsycholog-
ical measures to be developed for this population. Such tools will prove
useful for the early identification and prediction of learning problems,
and in obtaining accurate descriptive accounts of a preschool child's
strengths and weaknesses in academic readiness.
This chapter will discuss the prediction of learning problems in the
preschool child from a neuropsychological perspective. Initially, the im-
portance of this area to child neuropsychology is presented, and this is
followed by a review of the literature addressing this question. Given
Aylward's discussion of the application of a neuropsychological perspec-
tive in infancy and early childhood (Chapter 9, this volume), this chapter
will be confined to children from approximately age 3 to age 5. Finally,
the literature is integrated to underscore important directions for neuro-
psychologists working with preschool children and to shed some light on
issues relevant to the early prediction of learning disabilities.
There are several major reasons that make the early identification and
prediction of learning disabilities important to the field of child neuro-
psychology. First, the extent of the problem is such that it cannot be
ignored by professionals working with preschoolers. Second, these chil-
dren appear to be at greater risk for a continuing downward spiral of
learning and perhaps social-emotional difficulties. However, it is reason-
able to assume that early identification and intervention can contribute to
eliminating or lessening the severity of later learning, emotional, and
behavioral difficulties that might arise. In conjunction with this view-
point, evidence also has been presented that timely, early intervention
actually may capitalize on sensitive neurodevelopmental periods during
the preschool years, thus maximizing the possibilities for a child to devel-
PREDICTION 315
Summary
The above discussion highlighted the importance of learning dis-
ability prediction to the child neuropsychologist. The extent of the prob-
lem, the possibility of minimizing learning and emotional difficulties,
and the potential for making a valuable contribution to the treatment
programming of children at risk for learning disabilities all argue for more
active efforts with preschoolers on the part of child neuropsychologists.
The next section will provide a review of the current status of the field
with respect to research on the early prediction of learning problems.
There have been hundreds of studies that have addressed the predic-
tion of learning problems during the preschool years. For over two dec-
ades researchers have attempted to find the "best" predictor, or groups of
predictors, for identifying the preschool child with a learning problem.
Needless to say, this search has turned up a wide variety of "effective"
predictors, numerous assessment strategies and, characteristic of the
learning disability field in general, findings that are contradictory in
nature. These contradictory data have served to demonstrate the complex-
ity of the prediction process. This section will discuss several recent
literature reviews related to the preschool prediction of learning dis-
abilities. Several exemplary studies also will be presented that have made
major contributions to the early prediction efforts.
Horn and Packard were cautious to note that predicting school suc-
cess or failure is a complex process, and that it is unreasonable to think
that a single predictor could account for all of the variance in school
achievement. They noted that even the best early predictors accounted for
less than 36% of the variance in elementary school reading achievement.
Nonetheless, as with the two previous reviews, the focus of the meta-
analysis was on univariate prediction, with only token consideration
being given to how various measures might be combined effectively to
increase prediction of learning difficulties. Also, like many of the early
identification and prediction studies, the Horn and Packard review
focused solely on reading problems and did not address other academic
areas. Further, the studies included in their review were not limited to
pre-first-grade prediction efforts. Finally, although the meta-analysis was
well done, this procedure likely masked the vast heterogeneity across
studies due to the nature of the technique (i.e., the need to compare the
investigations on a common metric) (Wilson & Rachman, 1983).
More recently, Tramontana et a1. (1988) provided a comprehensive
examination of the preschool prediction of later academic achievement.
This review focused on 74 studies conducted since approximately the
inception of PL 94-142 and included only studies in which the predictor
measures were administered prior to first grade. In general, effective pre-
dictors spanned a wide range of variables, which included cognitive,
verbal, sensory-perceptual, perceptual-motor, behavioral, and demo-
graphic domains. Further, the authors noted that predictive relationships
tended to vary according to the specific criterion variable being assessed.
Measures of letter naming, general cognitive ability, language, visual-
motor skills, and finger localization were found to be accurate predictors
of reading in grades 1 through 3. However, these findings can only be
viewed as preliminary because very few of the studies examined reading
in terms of its component parts (e.g., recognition, comprehension). The
one study that did examine reading more precisely found a differential
predictive pattern, with IQ being the best predictor of reading vocabulary
and the Bender-Gestalt being the best predictor of reading comprehension
(Wallbrown, Engin, Wallbrown, & Blaha, 1975). To complicate matters,
developmental factors seemed to contribute to an apparent shift in the
predictive power of a set of predictors. Satz, Taylor, Friel, and Fletcher
(1978) demonstrated this by noting the importance of visual perceptual
factors in the prediction of early reading recognition, but the relatively
greater importance of verbal abilities as children progressed through ele-
mentary school.
The Tramontana et a1. review found that math was predicted about as
well as reading, although it was not studied as extensively. Effective pre-
dictors included IQ, visual-motor skills, memory, attention, and auditory
comprehension of language. As with the reading criterion, selective com-
PREDICTION 321
Exemplary Studies
Although the early identification literature extends back as far as the
1920s (Smith, 1928), the interest in this area exploded during the 1960s.
Despite the large number of studies in this area, there have been only a
few exemplary works that have set the stage for current endeavors, partic-
ularly from a neuropsychological vantage point.
One of the first longitudinal efforts in the early prediction of reading
problems was initiated by de Hirsch et al. (1966). These investigators
examined the effectiveness of a battery of tests containing linguistic and
perceptual measures in the prediction of later reading achievement. Chil-
dren were tested at the end of their kindergarten year and re-evaluated at
the end of second grade. Jansky and de Hirsch (1972) reported that their
Screening Index accurately identified 79% of children with reading prob-
lems, although there was a large number of false-positive prediction errors
(i.e., 25%). Specific variables that were most predictive of second-grade
reading problems included letter naming, picture naming, word match-
ing, copying, and sentence memory. Generally, these authors stressed the
importance of language factors (e.g., verbal retrieval) as major predictors
of reading success.
Silver and Hagin (1972) also presented data from one of the first
longitudinal investigations on early identification. As early as 1960, Sil-
ver and Hagin postulated that the perceptual dysfunction typically ob-
served in reading disability was an extension of deficits in spatial and
temporal organization (e.g., deficits in visual discrimination, auditory se-
quencing problems, right-left confusion, finger agnosia). These investiga-
tors speculated that these deficits were associated with a lack of cerebral
dominance for language and/or they resulted from poorly modulated in-
terhemispheric transfer of information.
Silver and Hagin evaluated beginning first-grade students with a bat-
tery measuring neurological, psychiatric, psychological, social, and
achievement areas. A factor analysis of their battery was performed, and
five factors emerged that accounted for approximately 61% of the total
prediction variance. These factors were Auditory Association, Visual-
322 STEPHEN R. HOOPER
Summary
There is an extensive literature dealing with studies that were de-
signed to obtain the best predictor, or set of predictors, for later learning
difficulties. However, it appears that this has been too simplistic a goal,
given the complexities of the learning process and its underlying neuro-
psychological mechanisms. The child neuropsychologist investigating
the early identification and prediction of learning disabilities during the
preschool years will need to address a more complicated series of ques-
tions. For example, a more sophisticated question might be: What com-
324 STEPHEN R. HOOPER
Neurodevelopmental Theory
It will be crucial for work in the area of early prediction to be guided
by theoretical conceptualizations. Knowing that a specific predictor-cri-
terion relationship exists is not enough; it also is necessary to know why
such a relationship exists. Although the efforts of Luria (1980), Rourke et a1.
(1983), Satz et a1. (1978), Silver and Hagin (1972) and, more recently,
Levine (Blackman, Levine, Markowitz, & Aufseeser, 1983; Levine &
Schneider, 1982) have set the stage for employing a neurodevelopmental
theoretical perspective, it is surprising that this has not been developed
more extensively. This is especially the case with learning disabilities,
given that current definitions of learning disabilities require at least the
suspicion of underlying neuropathology (Hammill et a1., 1981). Some work
already has been advanced noting neuroanatomical (Hier, LeMay, Rosen-
berger, & Perlo, 1978) and neurophysiological (Duffy, Denckla, Bartels, &
Sandini, 1980) anomalies as correlates of learning disabilities. These
anomalies have been implicated in contributing to the academic deficits in
learning-disabled children as well as underlying their deviant information
processing.
Despite the promise of these findings, certain aspects of neurodevel-
opment are better substantiated and should be incorporated into a neuro-
psychological perspective with this population. For example, it has been
argued that cerebral lateralization of function does not "develop," but
that it is present at birth (Kinsbourne & Hiscock, 1978). Indirect evidence
for this supposition has been provided by Gilbert and Climan (1974),
Ingram (1975), and Marcotte and LaBarba (1985) using dichotic listening
paradigms with preschoolers as young as 2% years of age. Anatomical
asymmetries, favoring the left hemisphere, also have been reported in the
neonate (Witelson & Pallie, 1973). These data suggest that left hemisphere
language lateralization exists from the outset, and thus set the stage for the
interpretation of hemispheric specialization and functional systems in the
preschooler.
At present there are at least two major neurodevelopmental concep-
tualizations that attempt to account, at least in part, for the later emer-
gence of a learning disability. The first model proposes a maturational lag
in cortical functioning (Satz & van Nostrand, 1973), and the other suggests
that the area of deficit is always present, but that deficiencies are man-
ifested only when specific demands challenge the processing capabilities
of the involved brain region (Rourke et a1., 1983). This latter position also
is consistent with the neurodevelopmental model espoused by Luria
(1980).
The model put forth by Satz (Satz & van Nostrand, 1973) provided
much of the theoretical guidance for the Florida Longitudinal Project
(Satz et a1., 1978), which investigated the precursors to later reading prob-
326 STEPHEN R. HOOPER
demands. It is at this time that the selective deficits associated with the
brain lesion or structural anomaly are manifested. This theory would
begin to account for the observation that a large percentage of "normal"
functioning preschoolers (about 26% in the Florida Longitudinal Project)
later show learning impediments. This theoretical position also would
not limit the identification of early deficits mainly to visual-perceptual
abilities and, consequently, would be more consistent with recent hetero-
geneous conceptualizations of learning disabilities than a neuromatura-
tional-delay model.
The implications for neuropsychological assessment based on this
theoretical model provide guidance in the search for neurodevelopmental
precursors to learning problems. It broadens the number of potential
neuropsychological constructs that may be relevant to the preschool child
and would provide an explanation for the large number of "effective"
predictors that have been asserted. It also would explain why a measure
seemingly unrelated to academics, such as finger localization, has been
consistently predictive of later reading difficulties (Lindgren, 1978; Satz
et 01., 1978).
Specifically, finger localization is felt to represent a measure of par-
ietallobe functioning (Reitan & Davison, 1974). Structures directlyassoci-
ated with the parietal lobe, such as the angular gyrus, have been directly
linked to reading skills (Gaddes, 1985). These tertiary cortical regions are
slower to mature and hierarchically are dependent upon intact function-
ing of the modality-specific primary and secondary cortical zones (Luria,
1980). Finger localization, which is a secondary-level parietal function,
may forecast a child's readiness to engage in tertiary-level functions, such
as reading, although little is known about its predictive value for specific
aspects of reading dysfunction or perhaps other kinds of academic deficits
(e.g., math).
Given the neurodevelopmental perspective offered by Rourke et a1.
(1983), it will be important for the field to begin to evolve new instrumen-
tation and procedures. This goes beyond establishing normative data for a
set of tasks and extends into describing more accurately the neurocog-
nitive underpinnings of learning and achievement precursors. Although
debates will continue regarding when a child's brain becomes fully func-
tional, it is clear that there is a developmental sequence in brain develop-
ment that can be tapped by behavioral tasks during the preschool years. It
is suspected that the more accurately these underlying neurodevelopmen-
tal processes can be assessed, the better the prediction of later learning
and behavioral outcomes will become.
For example, with respect to the development of behaviors associated
with the frontal lobes, Luria (1959) demonstrated that 3-year-old children
typically are unable to inhibit their behaviors using overt verbal media-
tion, but that by age 4 this would emerge and later evolve into internal
328 STEPHEN R. HOOPER
Taken together, the clinical and empirical studies support the devel-
opment of a predictive neuropsychological assessment model covering a
wide array of lower as well as higher cognitive functions. It is suggested
that such a battery include specific neurodevelopmental tasks (e.g., Pass-
Ier et al. 1986) that will provide behavioral indicators of brain develop-
ment and, ultimately, clues to better prediction of learning problems.
Needless to say, a preschool neuropsychological battery designed to pre-
dict later learning difficulties also should include a comprehensive medi-
cal, family, and developmental history. This will contribute to delineating
social-cultural difficulties as well as possible brain-based learning deficits
in the assessment and prediction of learning disabilities.
ogist to employ multiple points for follow-up testing. The work by Satz
and colleagues amply illustrates how many children could be missed if
multiple assessment points were not instituted. There are many children
who appear to "grow into" learning problems despite functioning within
a normal range on a kindergarten screening battery. It would be useful for
the child neuropsychologist to institute additional planned follow-up
points so as to monitor the children who fall in the middle ranges of
functioning during the preschool years. This would serve to identify chil-
dren who may be primed to become immersed in an insidious academic
decline secondary to neurodevelopmental anomalies, particularly if such
testing were designed to occur simultaneously with the shifting pattern of
academic demands. This type of ongoing assessment/screening process
recognizes the dynamic and complex aspects of learning. It would allow
for the incorporation of external variables into the assessment process,
such as teacher variables, classroom behaviors, psychosocial issues (e.g.,
family), and socioeconomic factors. With the development of more so-
phisticated methods for the neuropsychological assessment of the pre-
school child, it also may prove fruitful for tracking the topographical
continuity of various learner subtype patterns with respect to their
evolvement, prognosis, and treatment.
It is surprising, given the contradictory predictive findings currently
generated and the interactive complexities of the learning process itself,
that predictors of specific learning disability subtypes have not emerged.
Rourke (1983) noted that the subtyping of learning disabilities may be the
most pressing issue at this time in the learning disability field, and its
downward extension to preschoolers is only logical. This will surface
undoubtedly once assessment technology and neurodevelopmental un-
derpinnings are better integrated, and their predictive accuracy substanti-
ated.
CONCLUSIONS
REFERENCES
Algozzine. B., Mercer, C. D., & Countermine, T. (1977). The effects of labels and behavior on
teacher expectations Exceptional Children, 44, 131-132.
Aram, D. M., & Nation, J. E. (1975). Patterns of language behavior in children with develop-
mental language disorders. Journal of Speech and Hearing Research, 18, 229-241.
Bakker, D. J., Moerland, R, & Goekoop-Hoefkens, M. (1981). Effects of hemisphere-specific
stimulation on the reading performance of dyslexic boys: A pilot study. Journal of
Clinical Neuropsychology, 3, 155-159.
Barrett, T. C. (1965). Relationship between measures of prereading visual discrimination and
first grade reading achievement: Review of the literature. Reading Research Quarterly,
1, 51-76.
Becker, M. G., Isaac, W., & Hynd, G. W. (1988). Neuropsychological development of non-
verbal behaviors attributed to frontal lobe functioning. Developmental Neuropsy-
chology
Behr, S., & Gallagher, J. J. (1981). Alternative administrative strategies for young handi-
capped children: A policy analysis. Journal of the Division for Early Childhood, 2, 113-
122.
Bennett, E. R (1976). Cerebral effects of differential experience and training. In M. R. Rosen-
zweig & E. L. Bennett (Eds.), Neural mechanisms of learning and memory (pp. 279-
287). Cambridge, MA: M.l.T. Press.
Blackman, J. A., Levine, M. D., Markowitz, M. T., & Aufseeser, C. L. (1983). The pediatric
extended examination at three: A system for diagnostic clarification of problematic
three-year-olds. Developmental and Behavioral Pediatrics, 4, 143-150.
Bryan, T., & Bryan, J. (1986). Understanding learning disabilities (3rd ed.). Palo Alto:
Mayfield.
PREDICTION 333
Casto, G., & Mastropieri, M. A. (1986). The efficacy of early intervention programs: A meta-
analysis. Exceptional Children, 52, 417-424.
Coss, R. G., & Globus, A. (1978). Spine stems on tectal interneurons in jewel fish are short-
ened by social stimulation. Science, 200, 787-790.
de Hirsch, K., Jansky, J., & Langford, W. (1966). Predicting reading failure. New York: Harper
& Row.
Deysach, R. E. (1986). The role of neuropsychological assessment in the comprehensive
evaluation of preschool-age children. School Psychology Review, 15, 233-244.
Doris, J. (1986). Learning disabilities. In S. J. Ceci (Ed.), Handbook of cognitive, social, and
neuropsychological aspects of learning disabilities (pp. 3-54). Hillsdale, NJ: Erlbaum.
Duane, D. D. (1979). Toward a definition of dyslexia: A summary of views. Bulletin of the
Orton Society, 29, 56-64.
Duffy, F. H., Denckla, M. B., Bartels, P. H., & Sandini, G. (1980). Dyslexia: Regional dif-
ferences in brain electrical activity by topographical mapping. Annals of Neurology, 7,
412-420.
Foster, G., Schmidt, C., & Sabatino, D. (1976). Teachers' expectancies and the label "learning
disabilities." Journal of Learning Disabilities, 9, 58-61.
Foster, G., & Ysseldyke, J. (1976). Expectancy and halo effects as a result of artificially
induced teacher bias. Contemporary Educational Psychology, 1,37-45.
Gaddes, W. (1985). Learning disabilities and brain function: A neuropsychological approach
(2nd ed.). New York: Springer-Verlag .
Gilbert, J. H. V., & CHman, I. (1974). Dichotic studies in two and three year olds: A prelimi-
nary report. Speech Communication Seminar, Stockholm (Vol. 2). Upsala: Almquist &
Wiksell.
Hagin, R. A., Silver, A. A., & Kreeger, H. (1976). Teach. New York: Walker Educational Book
Corporation.
Hammill, D. D., Leigh, J. E., McNutt, G., & Larsen, L. C. (1981). A new definition of learning
disabilities. Learning Disability Quarterly, 4, 336-342.
Hartlage, L. C., & Telzrow, C. F. (1982). Neuropsychological assessment. In K. Paget & B.
Bracken (Eds.), Psychoeducational assessment of preschool children (pp. 295-320).
New York: Grune and Stratton.
Heverly, L. L., Isaac, W., & Hynd, G. W. (1986). Neurodevelopmental and racial differences
in tactile-visual (cross-modal) discrimination in normal black and white children. Ar-
chives of Clinical Neuropsychology, 1, 139-145.
Hier, D. B., LeMay, M., Rosenberger, P. B., & Perlo, V. P. (1978). Developmental dyslexia:
Evidence for a subgroup with a reversal of cerebral asymmetry. Archives of Neurology,
35, 90-92.
Horn, W. F., & Packard, T. (1985). Early identification of learning problems: A meta-analysis.
Journal of Educational Psychology, 77, 597-607.
Ingram, D. (1975). Cerebral speech lateralization in young children. Neuropsychologia, 13,
103-105.
Jansky, J. J. (1970). The contribution of certain kindergarten abilities to second grade reading
and spelling achievement. Unpublished doctoral dissertation, Columbia University,
New York.
Jansky, J. J. (1978). A critical review of "Some developmental and predictive precursors of
reading disabilities." In A. L. Benton & D. Pearl (Eds.), Dyslexia. An appraisal of current
knowledge (pp. 377-394). New York: Oxford University Press.
Jansky, J. J., & de Hirsch, K. (1972). Preventing reading failure-prediction, diagnosis, inter-
vention. New York: Harper & Row.
Kinsbourne, M., & Hiscock, M. (1977). Does cerebral dominance develop? In S. J. Segalowitz
& F. A. Gruber (Eds.), Language development and neurological theory (pp. 171-191).
New York: Academic Press.
Korkman, M. E. (1987, February). NEPSY-A neuropsychological test battery for children,
334 STEPHEN R. HOOPER
based on Luria's investigation. Paper presented at the Fifteenth Annual Meeting of the
International Neuropsychological Society, Washington, DC.
Levine, M. D., & Schneider, E. A. (1982). Pediatric Examination of Educational Readiness.
Examiner's manual. Cambridge, MA: Educators Publishing Service.
Lindgren, S. D. (1978). Finger localization and the prediction of reading disability. Cortex,
14, 87-101.
Luria, A. R. (1959). The directive function of speech in development and dissolution. Word,
15,341-352.
Luria, A. R. (1980). Higher cortical functions in man (2nd ed.). New York: Basic Books.
Marcotte, A. C., & LaBarba, R. C. (1985). Cerebrallateralization for speech in deaf and normal
children. Brain and Language, 26, 244-258.
Mercer, C. D., Algozzine, B., & Trifiletti, J. J. (1979). Early identification: Issues and consid-
erations. Exceptional Children, 46, 52-54.
National Joint Committee on Learning Disabilities, The. (1986, February). A position paper
of the National Joint Committee on Learning Disabilities. Baltimore, MD: Orton Dyslex-
ia Society.
Nussbaum, N. L., & Bigler, E. D. (1986). Neuropsychological and behavioral profiles of
empirically derived subgroups of learning disabled children. International Journal of
Clinical Neuropsychology, 8, 82-89.
Passier, M., Issac, W., & Hynd, G. W. (1986). Neuropsychological development of behavior
attributed to frontal lobe functioning in children. Developmental Neuropsychology, 1,
349-370.
Porter, J. E., & Rourke, B. P. (1985). Socioemotional functioning of learning-disabled chil-
dren: A subtypal analysis of personality patterns. In B. P. Rourke (Ed.), Neuropsychol-
ogy of learning disabilities: Essentials of subtype analysis (pp. 257-280). New York:
Guilford Press.
Reitan, R. M., & Davison, L. A. (1974). Clinical neuropsychology: Current status and applica-
tions. New York: Wiley.
Rourke, B. P. (1983). Outstanding issues in research on learning disabilities. In M. Rutter
(Ed.), Developmental neuropsychiatry (pp. 564-574). New York: Guilford Press.
Rourke, B. P., Bakker, D. J., Fisk, J. L., & Strang, J. D. (1983). Child neuropsychology. New
York: Guilford Press.
Rutter, M., Tizard, J., Yule, W., Graham, P., & Whitmore, K. (1976). Research report: Isle of
Wight studies, 1964-1974. Psychological Medicine, 6, 313-332.
Satz, P., & Fletcher, J. M. (1982). Florida Kindergarten Screening Battery. Odessa, FL: Psy-
chological Assessment Resources.
Satz, P., Taylor, H. G., Friel, J., & Fletcher, J. M. (1978). Some developmental and predictive
precursors of reading disabilities: A six year follow-up. In A. L. Benton & D. Pearl (Eds.),
Dyslexia: An appraisal of current knowledge (pp. 315-347). New York: Oxford Univer-
sity Press.
Satz, P., & van Nostrand, G. K. (1973). Developmental dyslexia: An evaluation of a theory. In
P. Satz & J. Ross (Eds.), The disabled learner: Early detection and intervention (pp. 121-
148). Rotterdam: Rotterdam University Press.
Schonhaut, S., & Satz, P. (1983). Prognosis for children with learning disabilities: A review
of follow-up studies. In M. Rutter (Ed.), Developmental neuropsychiatry (pp. 542-563).
New York: Guilford Press.
Silver, A. A., & Hagin, R. A. (1960). Specific reading disability: Delineation of the syndrome
and relationship to cerebral dominance. Comparative Psychiatry, 1, 126-134.
Silver, A. A., & Hagin, R. A. (1972). Profile of a first grade: A basis for preventive psychiatry.
Journal of the American Academy of Child Psychiatry, 11, 645-674.
Silver, A. A., & Hagin, R. A. (1976). Search. New York: Walker Educational Book Corpora-
tion.
PREDICTION 335
Simner, M. 1. (1983). The warning signs of school failure: An updated profile of the at-risk
kindergarten child. Topics in Early Childhood Special Education, 17, 17.
Smith, N. B. (1928). Matching ability as a factor in first grade reading. Journal of Educational
Psychology, 19, 560-571.
Speece, D. 1., McKinney, J. D., & Appelbaum, M. 1. (1985). Classification and validation of
behavioral subtypes of learning disabled children. Journal of Educational Psychology,
77, 67-77.
Spreen, O. (1978). Learning-disabled children growing up (Finale report to Health and
Welfare Canada, Health Programs Branch). Ottawa: Health and Welfare Canada.
Stevenson, H. W., & Newman, R. S. (1986). Long-term prediction of achievement and at-
titudes in mathematics and reading. Child Development, 57, 646-659.
Stevenson, H. W., Parker, T., Wilkinson, A., Hegion, A., & Fish, E. (1976). Longitudinal study
of individual differences in cognitive development and scholastic achievement. Journal
of Educational Psychology, 68, 377-400.
Strang, J. D., & Rourke, B. P. (1985). Adaptive behavior of children who exhibit specific
arithmetic disabilities and associated neuropsychological abilities and deficits. In B. P.
Rourke (Ed.), Neuropsychology of learning disabilities: Essentials of subtype analysis
(pp. 302-328). New York: Guilford Press.
Teeter, P. A. (1985). Neurodevelopmental investigation of academic achievement: A report
of years 1 and 2 of a longitudinal study. Journal of Consulting and Clinical Psychology,
53, 709-717.
Tinsley, V. S., & Waters, H. S. (1982). The development of verbal control over motor behav-
ior: A replication and extension of Luria's findings. Child Development, 53, 746-753.
Tramontana, M. G., Hooper, S. R., & Selzer, S. C. (1988). Research on the preschool predic-
tion of later academic achievement. Developmental Review, 8, 89-147.
U. S. Department of Education, Division of Educational Services. (1984). Sixth annual report
to Congress on the implementation of Public Law 94-142: The Education for All Handi-
capped Children Act. Washington, DC: Author.
Wallbrown, J. D., Engin, A. W., Wallbrown, F. H., & Blaha, J. (1975). The prediction of first
grade reading achievement with selected perceptual-cognitive tests. Psychology in the
Schools, 12, 140-149.
Walsh, R. (1981). Towards an ecology of brain. Lancaster, PA: MIP Press.
White, K. R. (1986). Efficacy of early intervention. Journal of Special Education, 19, 401-
416.
Wilson, B. C. (1986). An approach to the neuropsychological assessment of the preschool
child with developmental deficits. In S. B. Filskov & T. J. Boll (Eds.), Handbook of
clinical neuropsychology (Vol. 2, pp. 121-171). New York: Wiley.
Wilson, G. T., & Rachman, S. J. (1983). Meta-analysis and the evaluation of psychotherapy
outcome: Limitations and liabilities. Journal of Consulting and Clinical Psychology, 51,
54-64.
Witelson, S. F., & Pallie, W. (1973). Left hemisphere specialization for language in the
newborn: Neuroanatomical evidence of asymmetry. Brain, 96, 671-696.
Wolff, P. H. (1981). Normal variation in human maturation. In K. J. Connolly and H. F. R.
Prectl (eds.), Maturation and development: Biological and psychological perspectives.
Clinics in Developmental Medicine, 77-78. Philadelphia: Lippincott.
Zihl, J. (1981). Recovery of visual functions in patients with cerebral blindness. Experimen-
tal Brain Research, 44, 159-169.
13
Electrophysiological Assessment in
Learning Disabilities
GRANT L. MORRIS, JOEL LEVY,
and FRANCIS J. PIROZZOLO
INTRODUCTION
337
338 GRANT 1. MORRIS et 01.
Neuroimaging Methods
CAT Scans
The now conventional CAT or CT scan is an X-ray technique that
technically should be referred to as X-ray transmission tomography. This
is because CT only stands for computed tomography, and a tomographic
image can be derived from different sources, including X-ray absorption
by tissue, the emission of internally administered radioactive substances,
or magnetic resonance.
In X-ray transmission tomography, the patient's head is placed in a
large doughnut-shaped housing. Inside this housing, a movable X-ray
emitter is positioned, with a detector aligned to oppose it on the other side
of the ring housing. This configuration revolves around the patient's head
in small stepwise increments. It also moves up and down the long axis of
the patient's body to make images every centimeter from the top of the
head to the base of the skull. As the scanner moves around the head,
measurements of the amount of X-radiation absorbed by the tissue be-
tween emitter and detector are made and converted to numerical density
data. Each point in the head is scanned from at least two directions. The
image is based on the principle that the cerebrospinal fluid absorbs less
radiation than brain white matter, which absorbs less than gray matter,
which in turn absorbs about l/zoth of the amount that bone does. Flowing
blood absorbs an amount that overlaps both gray and white matter ranges;
therefore, to visualize intracranial circulation or defects in the venous
system (e.g., hemorrhage or thrombosis), a radiation-opaque contrast me-
dium is usually injected intravenously.
The radiation absorption values are stored in a computer, which re-
constructs an image of the brain and skull after the scans have been
completed. It is important to remember that the scan is not like a direct
visual X-ray film but is the trans axial absorption data translated into a TV-
type picture. The most recent scanners can resolve about a 1 mm X 1 mm
area of tissue. The technique involves approximately the same dose of
radiation as a standard skull radiograph. Inaccuracies or artifacts in the
image are sometimes produced by the beam hitting bony structures and
producing a shadow. However, these shadows actually may hide small
brain lesions. Other inaccuracies include failure to distinguish some
types of hemorrhages or tumors from normal brain tissue. However, this is
not typically a consideration in brain volumetric studies such as would be
proposed for an LD evaluation. Risks associated with this procedure in-
clude allergic reactions that some people experience to the contrast me-
dia. The exposure to radiation and the infusion of contrast material make
X-ray transmission tomography perhaps the most invasive neuroimaging
procedure.
ELECTRO PHYSIOLOGICAL ASSESSMENT 341
Like PET, blood flow studies remain at the investigational stage for
assessment of childhood cognitive disabilities. Normative studies on in-
ter- and intrahemispheric blood flow have been reported (Hynd, Hynd,
Sullivan, & Kingsbury, 1987), and limited data are now available on hemi-
spheric asymmetry. Despite the lower resolution for rCBF, increased left
hemisphere blood flow has been correlated with verbal test performance,
whereas performance on a nonverbal perceptual test was found to be
associated with increased right frontal and parietal flow. In one of the first
blood flow studies on dyslexic children, Hynd et a1. (1987) found that
there was less cerebral blood flow in the dyslexic groups, for both resting
and activation states, than for matched controls. Increased blood flow
during reading occurred in the left perisylvian and right parietooccipital
regions for the normal controls.
As the technology advances and resolution of structures becomes
more refined, this methodology offers the same promise as PET for diag-
nosis of subtypes of learning disabilities because it traces active function
and directly relates it to structure. Unlike PET, however, the ease of using
inhalable tracer compounds appears to be more comfortable and suitable
for young children.
Electroencephalography
Basic Description
Electroencephalography (EEG) is a technique for amplifying and re-
cording the variations in the electrical potentials detectable on the scalp.
Exclusive of artifact generated by muscle activity (electromyographic ar-
tifact) in the vicinity of scalp electrodes, these potentials have their ori-
344 GRANT 1. MORRIS et 01.
gins within the brain. This cortical activity is measured either as the
difference in potential seen at two scalp electrodes (bipolar recording) or
the activity at a single site referred to some other part of the body pre-
sumed to be electrically inactive insofar as EEG is concerned (referential
recording). Bipolar recordings are especially useful in localizing abnor-
mal EEG activity, e.g., associated with a tumor site. Referential recordings
are of less use in localizing abnormal EEG activity, but they are sensitive
to EEG activity whose origin lies at some distance from the active elec-
trode (so-called far-field recording). The signal itself is a complex wave
form that appears to have an unstable frequency and amplitude. However,
under constant conditions of recording site and arousal, a stable dominant
frequency can be seen. The dominant frequency of EEG may vary from 0.5
to more than 50 Hz. Most EEG amplitudes lie within a range of 5 to 50
microvolts. Much of the research employs a band-pass classification
scheme that labels specific frequency ranges. These typically include del-
ta (0.5-4 Hz), theta (5-7 Hz), alpha (8-12 Hz), beta (13-30 Hz), and
gamma (30-50 Hz).
A "montage" is a description of a specific set of electrode locations.
Until the establishment of the standard International 10/20 system of
electrode placement (Jasper, 1958), variations in electrode placements
confounded attempts at replications and comparisons among laboratories.
The letters of the 10/20 system refer to the major area of the brain over
Front
Al~
Lef:1J
Inion
Top of head
which the electrode is placed: occipital (0), parietal (P), central (C), front-
al (F), and temporal (T). The subscript associated with each letter denotes
laterality, with odd numbers indicating left hemisphere placements, and
even numbers placement over the right hemisphere. The magnitude of the
number indicates the degree of displacement from the midline of the
brain, which is designated as zero (z). Although this convention is widely
followed, particular experiments may use different placements. However,
these unique placements typically are described in terms of their relation
to the 10/20 system. Figure 1 illustrates the 10/20 system for electrode
placement.
EEG in LD Children
Results of Analysis of EEG through Visual Inspection. In 1978, John
Hughes summarized work over the preceding two decades that looked at
EEG in hospitalized nondyslexic children as well as dyslexic children.
These studies used visual inspection to detect significant anomalies in the
EEG records. Ten of the reviewed studies involved a total of over 900
non dyslexic subjects. Across all of these studies, nearly half of the non-
dyslexic subjects were identified as having significant EEG anomalies. In
another ten studies during the same time period, a slightly smaller pro-
portion of dyslexic children were identified as having abnormal EEGs.
Clearly, the probability of false negatives and false positives was high.
Conners (1978), critiquing the studies covered in the Hughes review,
noted that the diagnostic category of subjects was often known to the EEG
reader, and thus the reliability of the EEG evaluation was questionable.
Conners found that the definition of dyslexia varied across studies, and
rarely was any attempt made to screen out possible associated behavioral
or neurological conditions. He observed that experimental procedures,
such as matching control and experimental subjects, were often poor or
absent, especially in the earlier studies. As experimental method im-
proved in the more recently reviewed studies, significantly less abnormal-
ity tended to be reported. He found that there was no consistent rela-
tionship across studies in terms of the locus or type of EEG abnormality,
and that there was often an inverse relationship between the degree of
behavioral impairment and the degree of severity of EEG abnormality. In
those few studies that employed a follow-up, the EEG contributed nothing
to the prediction of outcome.
Until that time the studies analyzing EEG through visual inspection
seemed to offer little consistent evidence to support a general conclusion
of an association between EEG abnormality and dyslexia. Although many
of the problems raised in the Hughes review have not been systematically
addressed by more recent studies, the use of automatic data analysis has
at least begun to address the problems presented by the visual inspection
technique.
tinguished the two diagnostic groups. A complex task, power, and diag-
nostic group relationship (as reflected in right and left parietal theta) was
most pronounced at the angular gyrus. A significant interaction with
groups led to the conclusion that the dyslexics had more left than right
power during reading-by-child that became less marked during drawing.
A discriminant analysis on theta power correctly classified 20 of the 22
children. An abundance of left theta during eyes open-relaxed and a slight
decline of that frequency during reading is consistent with Witelson's
(1977) supposition that dyslexics have a dysfunctional left hemisphere.
Fein et a1. (1983) recorded resting eyes-closed and eyes-open EEG in
normal and dyslexic 10- to 12-year-old boys. The EEG was recorded bilat-
erally from the central, parietal, and midtemporal regions. Two segments
of EEG were recorded which were separated by approximately a 4- to 5-
hour interval. Test-retest reliabilities were computed for each band and
for the entire spectrum, and reliabilities were assessed separately for each
condition and for absolute power and relative power. High reliability was
observed in the normal reading group. Reliabilities for the dyslexic group
were slightly lower but still were judged acceptable. No systematic EEG
differences were reported between the two groups. However, the authors
concluded that excellent reliability of both absolute and relative power
for the passive eyes-closed and eyes-open conditions can be obtained
from dyslexic children, and that this supports the utility of EEG power
spectra as a reliable index of brain functioning in studies of normal and
learning-disabled children.
The BEAM recording technique has been used to study a group of
pure dyslexic subjects and their age-matched controls (Duffy, Denckla,
Bartels, & Sandini, 1980; Duffy, Denckla, Bartels, Sandini, & Kiessling,
1980). These researchers found significant differences in patterns of EEG
activity between the two groups. Discrete brain areas that have been clas-
sically associated with speech and reading were identified in the dyslex-
ics as being significantly different from the control subjects. The dyslexic
children exhibited EEG anomalies in Broca's area and in the region of
intersection of the left temporal and parietal lobes, including the angular
gyrus and Wernicke's area.
Kaye et a1. (1981), using the neurometrics battery, evaluated the dif-
ferences in EEG and average evoked potential (AEP) characteristics of 50
children who were of normal IQ but who were underachievers either in
verbal academic performance, in arithmetic performance, or in both
(mixed). These underachievers were compared with matched controls
who were adequately achieving. They built the EEG portion of their neu-
rometrics battery around electrode sites and eyes-closed EEG relative
power age-related norms published by Matousek and Petersen (1973). The
EEG was recorded from four bilateral, bipolar locations, which included
the central, temporal, parietooccipital, and frontotemporal regions. Rela-
350 GRANT L. MORRIS et 01.
tive spectral EEG densities were derived for the delta, theta, alpha, and
beta frequency bands while eyes were closed. Age-normed and Z-trans-
formed measures of delta, theta, alpha, and beta wave shape coherence
and amplitude symmetry were available for each region.
In comparison with the matched controls, the poor verbal achievers
showed significant deviations only in temporal coherence and symmetry.
The poor arithmetic achievers exhibited marked deviations in several
bilateral regions across several of the frequency bands. The mixed under-
achievers showed yet another pattern of differences in comparison with
the controls. Their pattern included a larger number of left hemisphere
frontotemporal, temporal, and parietooccipital differences, and marked
frontotemporal incoherence and asymmetry. Kaye et a1. were successful
at replicating these findings with a larger sample of 215 children. These
highly variable patterns of group-specific EEG anomalies support the pre-
sumption of multiple etiologies of learning disability. Further, they also
may form the basis for significant discrimination between LD and normal
subjects, and among the subcatagories of LD.
In an earlier presentation of LD data using this approach, John (1977)
discussed the problem of unreliable, anecdotal, or psychometric diag-
nosis of learning disability when attempting to determine the elec-
trophysiological correlates of this disorder. Based upon the presumption
of accurate anecdotal diagnosis, or "prediagnosis" made by the teacher or
referring clinician, discriminant analysis of LD and normal children was
conducted using either a battery of psychometric instruments or the EEG
data collected as part of the neurometrics battery. Instruments found to
contribute to the multiple discriminant function included subscales of the
Wechsler Intelligence Scale for Children, the Wide Range Intelligence
Test, and the Peabody Picture Vocabulary Test. Overall accuracy of classi-
fication of normal and LD children based on the psychometric battery was
71 %. Selected EEG measures from the ueurometric battery yielded a 77%
accuracy in classification.
At that point, John had classifications of all subjects into normal or
LD categories based upon three independent criteria: the original classifi-
cations or "prediagnoses," the assignment to group by the psychometric
battery, and the group assignment by the EEG discriminant function. By
comparing the concordance of classification by the three schemes for each
child, John proposed some details of various etiologies. Children who
were classified as normal by prediagnosis and EEG measures, but classi-
fied as LD by psychometric criteria, were presumed normal; in these
cases, the psychometric-based LD classification was viewed as the result
of cultural factors or bias in the psychometric instruments. These ac-
counted for 5% of his sample. An additional 6.5% of his sample were
classified as normal by prediagnosis and psychometrics but were classi-
fied as LD by the neurometrics EEG. Although none of the children in his
ELECTRO PHYSIOLOGICAL ASSESSMENT 351
Summary
Recent reanalysis of the Matousek and Petersen (1973) developmen-
tal EEG changes in normals further confirms that there is an age x cortical
area x frequency interaction, with the modal EEG frequency moving pro-
gressively upward with age. This frequency-shift process (Le., matura-
tion) occurs earliest and most rapidly in the occipital region, but it is
considerably delayed in the frontal-temporal region in normals. At all
electrode sites the pattern of change seen within the EEG frequency spec-
trum is a progressive decline of delta and theta power acco~panied by an
increase in alpha and beta between birth and age 19 to 20 years (W. H.
Hudspeth, personal communication, June 1987). Alpha is the dominant
frequency in more developmentally mature individuals when resting
with eyes closed. In normals, alpha has replaced delta-theta as the domi-
nant frequency band in the pareitooccipital region by age 8 years.
Much of the research reviewed in this section is consistent with the
concept of cortical immaturity in LD as revealed by a "slowing" of EEG
activity. This is most frequently seen as higher-than-normal theta band
power for a given age. This finding is most stable during the recording of
eyes-closed spontaneous EEG in the posterior region (Lubar et a1., 1985;
Rebert et a1., 1978; Sklar et a1., 1973). The Lubar et a1. (1985) findings also
suggested that, while engaged in an activity, the theta EEG from the front-
al region permits considerable classification accuracy of LDs.
Rebert et a1. (1978) and Duffy, Denckla, Bartels, and Sandini (1980)
reported specific lateralized differences in LDs in the areas of the left
temporal-parietal cortex associated with language and reading skills, par-
ticularly during tasks that would activate these areas. Although the fact of
general cortical EEG "slowing" seems established, the more intriguing
findings of lateralized temporoparietal anomalies in LD children await
replication and further definition.
Evoked Potentials
Basic Description
An evoked potential (EP) is the electrical indication of the brain's
reception of, and response to, an external stimulus. Typically, EPs are not
visible during the ongoing EEG recording. This is because of the relatively
low amplitudes of most EPs (0.1-20 microvolts) and their presence with-
in normal spontaneous EEG from throughout the brain and other artifacts
(such as electromyographic activity) that may be as much as several hun-
dred microvolts in amplitude. Separation of the buried EP wave forms
from these unwanted artifacts is accomplished by computer signal averag-
ing. It is assumed that the electrical response of the brain to the stimulus
(the EP) always comes at the same interval of time after the stimulus, and
thus has a constant latency. It also is assumed that the other electrical
ELECTROPHYSIOLOGICAL ASSESSMENT 353
activities present are not coupled to the stimulus and may be considered
random. Because these assumptions appear to be valid, computers (signal
averagers) can be used to isolate the evoked potential from the temporally
random background activity. Stimuli are given repetitively, and the com-
puter averages the new data acquired after each stimulus (random EEG
plus EP) with the averaged results from previous stimuli stored in its
memory. This averaging process is continued until the random EEG and
other artifacts have been reduced to an acceptably low level, and the
desired evoked potential has "grown" by virtue of the summation of its
constant temporal characteristics relative to the eliciting stimulus over
many trials (Chiappa, 1983). When averaged in this manner, visual, au-
ditory, and somatosensory stimuli are seen to evoke a series of discrete
electrophysiological responses or "peaks" of characteristic latency for a
given set of stimulus parameters. In their early (short latency) stages, these
peaks reflect the progress of the stimulus-evoked neural response through
the series of synaptic junctions within the anatomical pathway of the
stimulated modality. As the latency of these peaks extends past 100 msec,
and their loci shift from peripheral or brain stem sites to the cortex, the
peaks become more variable in latency and amplitude, more diffuse in
terms of anatomic origin, and more sensitive to cognitive state and
attention.
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(MEDULLA) cOVP. E)I (PO~S)
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,po S) / CORTICA L)
OUlEIit
sv".'"
01.1 ..... ""
CO UPLEJI
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t
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FIGURE 2. Far-field recording of auditory brain stern responses latencies measured in human
subjects. Proposed functional-anatomical correlations.
ELECTROPHYSIOLOGICAL ASSESSMENT 355
such as phonemes. This is amplified for each test run, with the response
to the auditory stimulus being averaged over trials. Stimuli may be pre-
sented either monaurally or binaurally.
BSERs are thought to be the far-field reflection of sequential electrical
events at successively higher levels in the brain stem auditory pathway.
Depth recordings and lesion experiments in the feline suggest that the
approximate neural generators of waves I, II, III, V, and VI of the BSER are
the acoustic nerve, cochlear nuclei, superior olives, inferior colliculi, and
medial geniculate nuclei, respectively (Picton, Hillyard, Krausz, & Galam-
bos, 1974). The origin of other components of the polyphasic BSER are
less clear, but some authors speculate that late components have their
origins in the thalamic nuclei and auditory cortex (Stockard & Rossiter,
1977). However, Chiappa (1983) concluded that the origins of peaks V, VI,
and VII are still very much in doubt, and because waves VI and VII are
unreliable in appearance, they are not used in clinical interpretation.
These proposed functional-anatomical associations are illustrated in Fig-
ure 2.
Until recently, BSERs were evoked by bilateral auditory stimulation.
This practice has been criticized on the clinical grounds that a lateralized
dysfunction might be masked through blending the abnormal BSER from
the affected side with the BSER from the unaffected side (Chiappa, 1983).
Consequently, it is now standard practice to elicit BSERs with monaural
stimulation. This practice also opens the door to tlie discovery of any
asymmetry, normal or anomalous, that may exist in an individual's mon-
aural BSERs. An asymmetry would be any significant difference in the
latency or amplitude of the corresponding peaks in the BSERs of the two
ears. To date, only a few attempts at specifically assessing BSER symmetry
have been made. These reveal a controversy over the existence of symmetry
in neurologically normal persons (Chiappa, Gladstone, & Young, 1979;
Levine & McGaffigan, 1983) and characteristic asymmetry in patients with
various neurological diseases (Chiappa & Norwood, 1977) and in stutterers
(Decker & Howe, 1981). The limited research looking at evoked response
symmetry in LD populations has focused upon abnormalities in lateral
asymmetry in the cerebral cortex rather than in the brain stem.
Latency
I
I
I
I
I
I
I
I Po
Stimulus
t _ - - - - - 400-600 msec. - - - - - - - 1
Summary. Exogenous BSERs have not yet provided any useful diag-
nostic schema for the various subtypes of LD, nor have they been shown
to be consistently useful in a broad pathognomic sense (i.e., being able to
separate normal from LD children). This may well reflect the lack of
consistent attention paid to the selection and classification of subjects in
these studies. Nevertheless, the occurrence of anomalous BSERs in this
population as reported in several studies should encourage further re-
search using this technique. Unlike middle- and late-latency evoked re-
sponses, BSERs are a mature clinical tecnhique in audiology and neu-
rology, and extensive norms across developmental periods and for
ELECTRO PHYSIOLOGICAL ASSESSMENT 359
and Zetusky (1983) stated that the evidence compiled during the last two
decades has rendered untenable the hypothesis that dyslexia represents a
single neuropsychological or educational entity. Further, contemporary
evidence overwhelmingly supports the existence of at least two subtypes
of developmental dyslexia. These findings are the result of several clinical
studies employing differential diagnosis of the cognitive deficits observed
in large populations of reading-disabled children (see Chapter 12, this
volume).
Fried et a1. (1981) concurred that treating the dyslexic population as
homogeneous has been a major problem. Their classification included a
subgroup composed of individuals having serious impairments in audito-
ry-verbal decoding, auditory sequencing, and symbol manipulation (Le.,
dysphonetic), whereas the other subgroup showed deficits in visuospatial
organization and visual-motor performance (Le., dyseidetic). Dysphonetic
dyslexics have great difficulty in reading and spelling words phonet-
ically, which may be conceptualized as a defect in auditory processing of
speech sounds. In contrast, dyseidetic children have good auditory per-
ception and memory. Their handicap is primarily deficient visual pro-
cessing. The alexic dyslexics are considered to be a mixture of both dys-
phonetic and dyseidetic types.
In their investigation Fried et al. (1981) applied ERP techniques to
study auditory information processing in the left and right hemispheres of
dyslexic subjects classified into subgroups. Dyslexic subjects were 2 or
more years delayed in reading and spelling as measured by the Wide
Range Achievement Test (Jastak, Bijiou, & Jastak, 1965). Through Boder's
(1973) Diagnostic Screening Test for Developmental Dyslexia, five of the
dyslexic subjects were classified as dysphonetic, six as dyseidetic, and
two as alexic. Dyslexic subjects were age- and sex-matched with normal
controls, all of whom were right-handed. Electrodes were placed at left
and right frontal locations (F 7' F8) and temporoparietal sites (midway
between T 5 and C3 , and midway between T 6 and C4 , and labeled W 1 and
W 2' respectively). Recording was referential. Auditory evoked potential
stimuli were voiced words Do and Go, and strummed chords A7 and D7.
The word and musical chord stimuli were delivered to each subject bin-
aurally at 70 dB.
The ERP wave form lying between 50 and 400 msec after stimulus
onset was chosen as the most likely time in which endogenous ERP ac-
tivity relating to stimulus processing would occur. The normal and dys-
eidetic subjects exhibited the expected larger ratio ERP wave form ampli-
tudes to words over chords in the left hemisphere and a differentially
smaller ratio in the right hemisphere. However, the dysphonetic subjects
did not exhibit this ERP asymmetry to stimulus type by hemisphere. "The
lack of greater word-musical-chord ERP waveform differences over the
ELECTRO PHYSIOLOGICAL ASSESSMENT 361
left hemisphere in the dysphonetic group suggests that the left hemi-
sphere of dysphonetic dyslexics may not have a fully developed capacity
to process auditory information in a normal manner" (Fried et aI., 1981, p.
20).
Auditory and visual evoked potential measures also were used in the
Kaye et al. (1981) Neurometrics study reported above with children who
were underachieving in verbal, arithmetic, or mixed areas. Auditory
evoked potentials were evaluated for signal-to-noise ratio, wave shape
coherence, and amplitude symmetry. They reported major differences
among the underachieving groups in comparison with the matched nor-
mals and, with respect to each other, on the grand averages of both audito-
ry and visual evoked responses. In comparison to the AEP peak latency
values observed in the controls, the poor verbal achievers showed pri-
marily scattered left hemisphere latency deviations, whereas the poor
arithmetic achievers showed scattered left but consistent right hemi-
spheric latency deviations. The mixed (arithmetic and verbal) under-
achievers showed almost no right hemisphere problems, but consistent
left hemisphere latency deviations. Although these diagnostic group x
cortical area deviations do not fit easily into conventional models of
hemispheric or regional functional specialization, they do support the
importance of these diagnostic subtypes by showing their linkage to func-
tional cortical anomalies.
An attempt has been reported to remediate dysphonetic and dys-
eidetic subgroup specific asymmetry differences. Training involved prac-
tice at a task designed to appeal to the hemisphere in which in ERP
anomalies occurred (Bakker & Vinke, 1985). They concluded that their
training reduced these hemisphere-specific asymmetry anomalies, and
that this reduction was correlated with changes in measures of reading
accuracy and speed.
CONCLUSIONS
Most studies have used only a small portion of the range of neu-
roimaging and electrophysiological techniques we have surveyed. Over-
all, the results of these studies are promising, with many of them finding
structural or electrophysiological anomalies in the parietooccipital region
ELECTRO PHYSIOLOGICAL ASSESSMENT 363
where receptive speech systems are involved. Several studies also have
reported global electro physiological anomalies, especially in modal EEG
frequency. Relatively few of these studies have been sensitive to the need
to distinguish among the various subtypes of learning disability. Those
that were seem to have found considerable accuracy of classification into
those subtypes based upon the functional and structural neurological
evidence.
The most successful efforts have been those using a battery of elec-
trophysiological measures combined with clear classification of subjects
according to useful subcatagories of learning disability, and involving a
healthy sample size (e.g., Kaye et aI., 1981). These desirable features of
method are not unique to this area of research, and they have long been
recognized as sine qua non in the establishment of the research founda-
tion for any useful clinical assessment tool.
Computerized methods of neuroimaging and electrophysiology are
easily able to generate massive quantities of data. It is a temptation, when
applying new methods, to employ an atheoretical or "shotgun" approach,
rather than restricting the sphere of observation. Over a decade of comput-
erized investigation of EEGs and EPs in learning-disabled children has
yielded a large body of provocative, but scattered and inconsistent, re-
sults. An effort at consolidation would be helpful. This consolidation
needs to take the form of systematic theory and model testing, simul-
taneously employing as many of the complementary methods as possible.
Researchers committing themselves to a well-defined-and therefore
risky-explanation of the neurological basis of learning disabilities may
be confident, along with Sir Francis Bacon, that truth arises more readily
from error than from confusion.
The techniques described in this chapter hold all of the allure and
fascination of a possible technological breakthrough for a difficult assess-
ment problem. To be significant, however, neuroimaging and electro-
physiological procedures must demonstrate that they offset their high cost
and demand for specialized training. They must yield useful diagnostic
information about learning disabilities beyond that more cheaply and
easily gathered by conventional psychometric and clinical methods.
REFERENCES
Bakker, D. J., & Vinke, J. (1985). Effects of hemisphere-specific stimulation on brain activity
and reading in dyslexics. Journal of Clinical and Experimental Neuropsychology, 7,
505-525.
Boder, E. (1973). Developmental dyslexia: A diagnostic approach based on three atypical
reading-spelling patterns. Developmental Medicine and Child Neurology, 15,663-687.
Broca, P. (1861). Remarques sur Ie siege de la factule du language articule, suivi d'un
364 GRANT L. MORRIS et aJ.
Hier, D. B., LeMay, M., Rosenberg, P. B., & Perlo, V. P. (1978). Developmental dyslexia:
Evidence for a subgroup with reverse asymmetry. Archives of Neurology, 35, 90-92.
Hillyard, S., & Woods, D. (1979). Electrophysiological analysis of human brain function. In
M. Gazzaniga (Ed.), Handbook of behavioral neurobiology (Vol. 2, pp. 345-378). New
York: Plenum Press.
Hinshelwood, J. (1895). Word-blindness and visual memory. Lancet, 2, 1564-1570.
Holcomb, P., Ackerman, P. T., & Dykman, R. A. (1985). ERPs: Attention and reading deficits.
Psychophysiology, 22, 656-667.
Hughes, J. R. (1978). Electroencephalographic and neurophysiological studies in dyslexia. In
A. L. Benton & D. Pearl (Eds.). Dyslexia-An appraisal of current knowledge (pp. 205-
240). New York: Oxford University Press.
Hynd, G., Hynd, C., Sullivan, H., & Kingsbury, T. (1987). Regional cerebral blood flow (rCBF)
in developmental dyslexia: Activation during reading in a surface and deep dyslexic.
Journal of Reading Disabilities, 20, 294-300.
Jasper, H. H. (1958). The ten-twenty electrode system of the International Federation. Elec-
troencephalography and Clinical Neurophysiology, 10, 371-375.
Jastak, J., Bijiou, S. W., & Jastak, S. R. (1965). Wide Range Achievement Test. Wilmington,
DE: Guidance Associates.
John, E. R. (1963). Neural mechanisms of decision making. In W. S. Fields & W. Abbott
(Eds.). Information storage and neural control (pp. 243-282). Springfield, IL: Charles C
Thomas.
John, E. R. (1977). Neurometrics: Clinical applications of quantitative neurophysiology.
Hillsdale, NJ: Erlbaum.
John, E. R., Karmel, B. Z., Corning, W. c., Easton, P., Brown, D., Ahn, H., John, M., Harmony,
T., Prichep, L., Toro, A., Gerson, I., Bartlett, F., Thatcher, R., Kaye, H., Valdes, P., &
Schwartz, E. (1977). Neurometrics. Science, 196, 1393-1410.
Johnston, J. (1982). Probe event-related potentials during language processing in children: A
comparison of resource allocation and stimulus set models of attention. Unpublished
doctoral dissertation, University of California, San Francisco.
Johnstone, J., Galin, D., Fein, G., Yingling, C., Herron, J., & Marcus, M. (1984). Regional brain
activity in dyslexic and control children during reading tasks: Visual probe event-
related potentials. Brain and Language, 21, 233-254.
Kaye, H., & John, E. R., Ahn, H., & Prichep, L. (1981). Neurometric evaluation of learning
disabled children. International Journal of Neuroscience, 13, 15-25.
Kertesz, A., Black, S. E., Polk, M., & Howell, J. (1986). Cerebral asymmetries on magnetic
resonance imaging. Cortex, 22, 117-127.
LeMay, M. (1982). Morphological aspects of human brain asymmetry: An evolutionary per-
spective. Trends in Neurosciences, 5, 273-275.
LeMay, M., & Kido, D. K. (1978). Asymmetries of the cerebral hemispheres on computed
tomograms. Journal of Computer Assisted Tomography, 2, 471-476.
Lenhardt, M. L. (1981). Childhood central auditory processing disorder with brain stem
evoked response verification. Archives of Otolaryngology, 107, 623-625.
Levine, R. A., & McGaffigan, P. M., (1983). Right-left asymmetries in the human brain stem:
Auditory evoked potentials. Electroencephalography and Clinical Neurophysiology,
55, 532-537.
Lubar,J. F., Bianchini, K. J., Calhoun, W. H., Lambert, E. W., Brody, Z. H., & Shabsin, H. S.
(1985). Spectral analysis of EEG differences between children with and without learning
disabilities. Journal of Learning Disabilities, 18, 403-408.
Matousek, M., & Petersen, I. (Eds.). (1973). Automation of clinical electroencephalography.
New York: Raven Press.
Molfese, D. L., & Molfese, V. J. (1986). Psychophysiological indices of early cognitive pro-
cesses and their relationship to language. In J. E. Obrzut & G. W. Hynd (Eds.). Child
neuropsychology (Vol. 1, pp. 95-115). New York: Academic Press.
366 GRANT L. MORRIS et a1.
Comment
14
369
370 MICHAEL G. TRAMONTANA
The overall impression from reports such as these is that the young
child who sustains brain injury may benefit to some extent from cerebral
plasticity. However, any compensatory organization of function is apt to
be ineffecient because it would tend to go against the grain of the intrinsic
avenues for neural specialization that normally would unfold. Conse-
quently, residual deficits of some significance generally should be ex-
pected. These sometimes can be missed unless the assessment strategy is
geared to revealing the more subtle features of neuropsychological func-
tioning normally mediated by the injured brain region(s).
Existing evidence also would call into question the purported role of
maturational delays in the manifestation of neurodevelopmental disor-
ders. The concept of maturational lag usually has been invoked to account
for the fact that some children, including those with learning disabilities,
may show significant difficulties in neuropsychological functioning in
the absence of a documented history of brain injury. Presumably, these
difficulties simply may reflect a slower rate of maturation of an otherwise
normal brain (Satz, Taylor, Friel, & Fletcher, 1978). One problem with this
idea is that there is no evidence that the brains of children with significant
performance lags are immature or "unfinished" with respect to mor-
phological features (Rodier, 1984). Rather, investigations such as the de-
tailed cytoarchitectonic studies of the brains of dyslexics at autopsy (e.g.,
Galaburda & Kemper, 1979) indicate that brain morphology is truly abnor-
mal. Hynd et a1. (Chapter 11) have interpreted this work to suggest that
abnormalities in cell migration during later periods of fetal development
(resulting in assorted defects of the left perisylvian region such as focal
dysplasias, disordered cortical layering, and polymicrogyria) constitute
the neurodevelopmental basis for many learning disabilities.
Another problem with the concept of maturational lag is that it im-
plies that the child with functional delays eventually will "catch up" and
exhibit normal abilities. However, this generally is not the case, as shown
in the follow-up literature on children with learning disabilities (Schon-
haut & Satz, 1983). Although disabled readers may improve over time,
they typically continue to show inefficiencies in their reading skills (Rut-
ter, Tizard, Yule, Graham, & Whitmore, 1976). Moreover, with the excep-
tion of the position taken by Boyd (Chapter 7), the general consensus
among the authors in this volume is that the processing strategies utilized
by disabled learners cannot be compared to those of a younger child.
Their functioning is not simply delayed but deviant. These children are
delayed in the sense that their inefficiencies result in lower performance
levels on age-normed tests, but the kinds of processing strategies that they
utilize are uncharacteristic of normal functioning at any age.
Thus, it appears that the concept of maturational lag has little mean-
ing in current conceptualizations of neurodevelopmental disorders. Use
of the term should be limited to those instances in which there is a genu-
374 MICHAEL G. TRAMONTANA
ine delay in the normal timing or rate of skill acquisition without parallel
evidence of aberrations in existing processing abilities. This requires the
differentiation of process and product in assessment, and also has impor-
tant implications for how developmental precursors to learning problems
are identified. If functions are not organized differently in learning-dis-
abled children but instead operate less efficiently (as suggested by Hynd
et 01.), then learning disabilities should be forecast by dysfunction involv-
ing the brain regions that normally are preordained to mediate academic
skills. Hooper (Chapter 12) has discussed the challenge that this perspec-
tive poses for early identification research, given that deficits of this type
ordinarily are considered to be "silent" until relatively late in the pre-
school period.
Some concepts in child neuropsychology, like neuromaturationallag,
grew out of an era when it generally was not possible to obtain precise
information regarding brain structure and physiology in children with
functional handicaps. Just as inadequacies in neuropsychological assess-
ment sometimes resulted in an overestimation of recovery of function or
cerebral plasticity in brain-injured children, so too inadequacies in diag-
nostic tools for assessing brain pathology may have led to false (or at least
premature) conclusions concerning the apparent absence of brain anoma-
lies in certain neurodevelopmental disorders. Earlier researchers did not
have the benefit of the powerful methods now available for brain imaging
and the in vivo study of dynamic neurophysiological processes, which
were discussed in detail by Bigler (Chapter 3) and Morris et 01. (Chapter
13). The availability of this new generation of neurodiagnostic tools prom-
ises to have an unprecedented impact on the advancement of knowledge
in child neuropsychology, especially with respect to the neural side of
brain-behavior relationships. Full advantage should be taken of the new
avenues for investigation that these methods have opened, but without
losing sight of the unique contributions that child neuropsychology can
make in assessing and conceptualizing the behavioral aspects of various
brain anomalies. A clearer understanding of developmental brain-behav-
ior relationships cannot be obtained solely through technical advances in
diagnosing brain pathology but will depend also on parallel advances in
the development of more precise and ecologically valid tools for assessing
neuropsychological functioning.
At this point, there are a number of serious limitations associated
with all-purpose or omnibus approaches to the neuropsychological as-
sessment of children. Neuropsychological assessment is becoming in-
creasingly specialized and geared more toward the evaluation of compo-
nent processes and their impact on a child's everyday functioning. There
is a growing appreciation for the need to tailor the assessment process, as
well as the constructs that are assessed, according to the clinical questions
and specific populations involved. An assessment strategy that is quite
useful in one context may be useless in another. Also, new knowledge in
PROBLEMS AND PROSPECTS 375
REFERENCES
Bigler, E. D., & Naugle, R. 1. (1984). Case studies in cerebral plasticity. International Journal
of Clinical Neuropsychology, 7, 12-23.
Chelune, G. J., & Edwards, P. (1981). Early brain lesions: Ontogenetic-environmental consid-
erations. Journal of Consulting and Clinical Psychology, 49, 777-790.
Curley, A. D., Delaney, R. C., Mattson, R. H., Holmes, G. 1., & O'Leary, K. D. (1987). Determi-
nants of behavioral disturbance in boys with seizures. Paper presented at the 95th
Annual Convention of the American Psychological Association, New York.
Dennis, M. (1985). Intelligence after early brain injury: 1. Predicting IQ scores from medical
variables. Journal of Clinical and Experimental Neuropsychology, 7, 526-554.
Galaburda, A. M., & Kemper, T. 1. (1979). Cytoarchitectonic abnormalities in developmental
dyslexia: A case study. Annals of Neurology, 6, 94-100.
Kennard, M. A. (1940). Relation of age to motor impairment in man and subhuman primates.
Archives of Neurology and Psychiatry, 44, 377-397.
Kiessling, 1. S., Denckla, M. B., & Carlton, M. (1983). Evidence for differential hemispheric
function in children with hemiplegic cerebral palsy. Developmental Medicine and
Child Neurology, 25, 727-734.
Rodier, P. M. (1984). Exogenous sources of malformations in development. In E. S. Gollin
(Ed.), Malformations of development: Biological and psychological sources and conse-
quences (pp. 287-313). New York: Academic Press.
Rourke, B. P., Fisk, J. 1., & Strang, J. D. (1986). Neuropsychological assessment of children: A
treatment-oriented approach. New York: Guilford Press.
Rutter, M., Tizard, J., Yule, W., Graham, P., & Whitmore, K. (1976). Research report: Isle of
Wight studies, 1964-1974. Psychological Medicine, 6, 313-332.
Satz, P., Taylor, H. G., Friel, J., & Fletcher, J. M. (1978). Some developmental and predictive
precursors of reading disabilities: A six year follow-up. In A. Benton & D. Pearl (Eds.),
Dyslexia: An appraisal of current knowledge (pp. 313-348). New York: Oxford Press.
Schonhaut, S., & Satz, P. (1983). Prognosis for children with learning disabilities: A review
of follow-up studies. In M. Rutter (Ed.), Developmental neuropsychiatry (pp. 542-563).
New York: Guilford Press.
Tramontana, M. G., Klee, S. H., & Boyd, T. A. (1984). WISC-R interrelationships with the
Halstead-Reitan and Children's Luria Neuropsychological Batteries. International Jour-
nal of Clinical Neuropsychology, 6, 1-8.
Index
377
378 INDEX