Neuro Handbook (SUNY)

CONTAINS
COPYRIGHTED
MATERIAL.
PLEASE DO NOT
DISTRIBUTE.
CONTAINS
COPYRIGHTED
MATERIAL.
PLEASE DO NOT
DISTRIBUTE.
Designed and edited by Igor Rybinnik M.D., with contributions
from Yasir El-Sherif M.D. and Pedro Torrico M.D.
The authors of this book thank Downstate neurology attendings

for their support, input and proof-reading. Special thanks to Drs.
Gropin and Janjua for reviewing the vascular neurology section.
No attendings, residents or patients were harmed in the making

of this guide.
This book contains copyrighted material. Please do not reproduce

without express permission of the authors.
Image References:
Blumenfeld H. Neuroanatomy Through Clinical Cases. Massachusetts: Sinauer Associ-
ates, 2002
Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology, 5th Edition. Phila-
delphia: Lippincott Williams & Wilkins, 2007
Posner JB, Saper CB, Plum F, N Schiff. Diagnosis of Stupor and Coma. Oxford Universi-
ty Press, 2007
OBrien MD. Aids to the Examination of the Peripheral Nervous System, 4th Edition.
Britain: Elsevier, 2000.
Netter FH, Craig JA, Perkins J. Atlast of Neuroanatomy and Neurophysiology. New
Jersey: Icon, 2002
Rohkamm R. Color Atlas of Neurology. New York: Thieme.
Resident, Attending Pagers 1 Status Epilepticus 68
PHONES
and Phone Numbers

Hypertensive Encephalo- 69
UHB Extensions 3 pathies (PRES, Eclampsia)
KCH Extensions 4 Cerebral Venous Throm- 71
bosis
Arterial Anatomy 7
Cord Compression, Cauda 74
Venous Anatomy 17
Equina
Thalamus 19
Myasthenia Gravis Crisis 75
Basal Ganglia 20
Guillain-Barre Syndromes 76
EMERGENCIES
Brainstem And Cranial 21
Nerves Botulism, Critical Illness 77
NEUROANATOMY
Neuropathy / Myopathy
Visual System 29
Neuroleptic Malignant, 78
Aphasias 30 Serotonin Syndromes
Spinal Cord 31 Intracranial Infections 79
Cerebrospinal Fluid Circu- 37
Acute Dystonic Reaction 81
lation
Peripheral Nerves 38 Epilepsies, Seizure Types, 83
AEDs
Major Tracts 49
Approach to Electroen- 89
Ischemic Stroke 53 cephalography
APPENDIX
Hemorrhagic Stroke 59 Neuropathies, Myopa- 92

thies, NCS/EMG
Increased Intracranial 61
Pressure Movement Disorders 95
Stupor, Coma, Brain Death 63 Minimental Exam 96
NEUROLOGY INTERNS: PGY 1 FELLOWS
Ariel Antezana 917-219-1752 Florence Chum 917-219-1987
ELECTROPHYSIOLOGY
Sebina Bulic 917-219-1762
Shefali Gandhi 917-219-4152
Cindy Jadoo 917-219-1767 ELECTROPHYSIOLOGY
Bryan Long 917-219-1773 Kessarin Panichpisal 917-219-1238

NEUROVASCULAR
Johanne Personna- Bilal Saulat
917-219-1776 917-219-1433
Policard ELECROPHYSIOLOGY
Volodymyr Vulkanov 917-219-1778 Maja Ilic 917-219-1833

PEDIATRIC NEUROLOGY, CHIEF
Paige Kalika 917-219-1835
PEDIATRIC NEUROLOGY
NEUROLOGY RESIDENTS: PGY 2 Kathleen Jalandoni 917-219-1805
PEDIATRIC NEUROLOGY
Darwin Abreu 917-219-1901
Christopher Dardis 917-219-1904 Basanagoud Mudigoudar 917-219-1808
PEDIATRIC NEUROLOGY
Susan Law 917-219-1920
Eghosa Omoregie 917-219-1928
Andres Rodriguez 917-219-1936
OTHER
Diana Soto 917-219-1945
UHB Consult 917-219-1705
Harini Sarva 917-219-1953
Arya Kapil 917-219-1960 UHB Ward 917-219-1791
Sumit Verma 917-219-1968 KCH Consult 917-219-1702
KCH Ward 917-219-1797

NEUROLOGY RESIDENTS: PGY 3 Peds Neuro Consult 917-219-1267
Yasir El-Sherif 917-219-1811 EEG Tech On-Call 917-219-2987
Ali Emami 917-219-1881
Epilepsy Fellow On-Call 917-219-1092
Samit Malhotra 917-219-1884
Stroke Fellow On-Call 917-219-1238
Mahsa Mehrazin 917-219-1887
Claude Nguyen 917-219-1890
(718) 780-2000,
Nurkia Peguero 917-219-1899 LICH Call Room
x8931
LICH Ward 23005
NEUROLOGY RESIDENTS: PGY 4 LICH Consult 23003
Jason Freeman CHIEF 917-219-1878 UHB Neuro Office 270-2051
UHB Call Room 270-8971

Igor Rybinnik CHIEF 917-219-1868
Sylvana Gonzalez 917-219-1874 KCH Neuro Office 245-5403, 5404
Steven Lin 917-219-1877 Suite C Neuro Clinic 270-1491
Eduard Rozner 917-219-1873 8th Fl Neuro Clinic 245-3480, 3477
Pedro Torrico 917-219-1867 5th Fl Peds Neuro Clinic 245-3612
Ellen Edgar 917-219-1080 MDA Clinic 270-3215
1 CONTACT INFORMATION
NEUROLOGY ATTENDINGS
NAME PAGER / OFFICE MOBILE / HOME
Abrams, Charles NEUROMUSCULAR (917) 218-1047 (914) 965-9435
Anziska, Brian GENERAL NEUROLOGY (917) 760-0879 (914) 633-0818
Anziska, Yaacov NEUROMUSCULAR, IM (917) 218-4313 (914) 656-9038
Baird, Alison STROKE (347) 422-0369 (917) 218-2963
Bhagavati, Satyakam GENERAL NEURO (917) 218-5747 (212) 598-0311
Bodis-Wollner, Ivan PARKINSON, N-OPHTH. (917) 760-0880 (718) 522-3068
Chari, Geetha PEDIATRIC EPILEPSY (917) 760-0741
Cherian, Sheba (917) 218-4205
Cracco, Joan PEDIATRIC EPILEPSY (917) 761-1497
Crystal, Howard NEUROBEHAVIORAL (917) 760-1780 (201) 433-4310
Eggers, Arnold GENERAL NEUROLOGY (917) 760-0908 (914) 965-8435
Giridharan, Radha PEDIATRIC EPILEPSY (917) 760-0896
Grant, Arthur ADULT EPILEPSY (917) 218-6283
Gropen, Toby STROKE 24143 (718) 596-5354 (h)
Janjua, Nazli NEURO-INTERVENTIONAL 24294 (917) 841-0172 (m)
Maccabee, Paul NEUROMUSCULAR (917) 760-0885 (914) 478-0087
Mangla, Sundeep NEUROINTERVENTIONAL (917) 760-1305
Maus, Douglas ADULT EPILEPSY (917) 218-5896
Memon, Zaitoon GENERAL NEUROLOGY (917) 760-0918 (718) 672-0743
Merlin, Lisa GENERAL NEUROLOGY (917) 760-0919 (718) 758-9022
Mesh, Alla GENERAL NEUROLOGY (917) 359-8378 (m)
McSween, Tresa PEDIATRIC EPILEPSY (917) 761-1066
Morales, Ximena STROKE, ADULT EPILEPSY 24126 (215) 806-1420 (m)
Moreno, Herman NEUROBEHAVIORAL (917) 218-6582 (212) 544-8218
Mortati, Katherine ADULT EPILEPSY (917) 219-8312
Reznikov, Alexandra PEDIATRIC NEURO (917) 218-8447
Roohi, Fereydoon NEUROMUSCULAR 24053 (718) 667-1022 (h)
Rose, Arthur NEURO DEVELOPMENTAL (917) 760-0898
Rosenbaum, Daniel STROKE (917) 218-9077
Seliger, Marion ADULT EPILEPSY 24344 (516) 507-8740 (m)
Sharfstein, Sophia STROKE (917) 218-8132 (516) 364-5355
Slyker, Jonathan NEUROPSYCH (845) 987-0471
Somasundaram, Mahendra GEN NEURO (917) 760-0915 (516) 627-5331
Valsamis, Helen ADULT EPILEPSY (917) 760-0888 (718) 403-9151
Vas, George GENERAL NEUROLOGY (917) 760-0891 (718) 596-0717
Yu, Hua NEUROSONOGRAPHY (718) 270-7108 (o)
CONTACT INFORMATION 2
UHB EXTENSIONS (718) 270-1000
Page Operator 2121 Microbiology 1655
Admitting 2862-4 Microscopy Urinalysis 2977
Benefits Office 3014, 3015 Neurology 2051, 2945
Blood Bank 4630 Nuclear Medicine 1632, 1633
Bookstore 2486 NS 61 2816
Cardiac Cath Observation 4276, 2717 NS 62 2850
Cardiac Recovery 4278 NS 71 2887
Cardiac Stress Test Lab 2607 NS 72 5562
Cardiology Appt 1081, 8251 NS 73 2887
Cath Lab 8631, 4282 NS 74 (Rehab) 3785, 3786
Cath Lab - Holding 4278 NS 81 2822, 2823
Cardiothoracic Surgery 1981 NS 82 2824, 2890
CCU 2436-7 NS 83 8681
Chemistry - Result 2921-2 Parking 1363
Chest Pain Unit 8171, 8178 Pathology 1668
Coumadin Clinic 1491 Payroll 1139
Diabetes Treatment Center 2812-3 Pharmacy 2854, 2856, 6143
Diabetes Nurse Educator 1068 Physical Therapy 2811
(Outpt)
Diabetes Nurse Educator 1548
(Inpt) PA Team Beepers
Computer Assistance 4902 Team 1 (917) 218-6416
(Residents)
Computer Help Desk 4357 Team 2 (917) 218-6436
CAT Scan 7393 Team 3 (917) 218-6363
CT Scheduling 2916 Team 4 (917) 218-0006
Cytology 1666 Team 5 (917) 218-0426
Dialysis Inpatient 2510 Pulm Critical Care 1770
EEG 2430, 2734 Pulmonary Func Lab 1771
EMG 2430 Radiation Oncology 1886
Echo Lab 1587, 2708, 4687 Radiology 3125, 3122
Emergency Room 4580, 4575 Radiology Reading Rm 4134
Employee Health 195 Radiology Senior (917) 760-1124
Family Practice Office 2560 Rehab 2047
Gastro/Hepatology 1113 Respiratory 3149
Endoscopy Center 718-282-7234 Security 2626
Gynecology 2460 Serology 1837
Heme/Onc 2785 Smoking Cessation 7673
HIVCounseling 4099, 4121 Social Work 2005-6
GME Office 4220 Sonogram 1730, 2552, 2515
Infectious Disease 1432 Speech Therapy 2049, (917) 760-
1688
Internal Medicine 1531 Stroke Unit 1644
Interventional Rad 1996, 8292, 8293 Surgery 1973
Linens 1881 Surgical Pathology 1669
MICU 2701-3 V/Q Scan 1633
MRI 3383, 1343 Vascular Office 1035
Medical Records 2499 Vascular Lab 2515
Purchase Requisitions 3188, (347) 578-
(William Stewart) 1371
3 CONTACT INFORMATION
KCH EXTENSIONS (718) 245-3131
Main operator 3135 Medical records 4200, 4233
Page operator 3141-2 Methadone program 2639
ACLS office 4790 MISys computing 4000
Admitting 7403-4 MRI 5585
AIDS team 2800 D7N 7038-42
BCLS office 3111 D7S 7043-4
Bronchoscopy 3952 D4N 7008-12
Cardiology 3477 D4S 7013-17
CCU 7580-1 D2S 7156-60
Chemotherapy 2851 D2N 7153
Clinic appointment 3391 Obstetrics floor 4570
Computer help desk 4054 Patient escort 3994
Dialysis inpatient 8175, 3723 Pharmacy, B building 4313, 4318
Dialysis outpatient 5005, 5029 Pharmacy, D building 7129-31
Dietary 3699 Controlled substances 3010, 4313
ECHO 3736, 3765, Psych consult (917) 205-4735
4802
EEG 4715 Psych Followup Appt 2727
EMG 4538 Pulmonary Func Lab 3685-6
ER (CCT) 4601 Radiology Inpatient 4424
ER (Suite B) 4620 Interventional 4442-3
Employee health 3536 CAT Scan 4463
GI suite 3840, 3836 CAT Scan (ER) 4739
Gyn-Onc 2057 CT Scheduling 3312
Hematology 5373 ER 4380-1
Holter 3767, 3524 Sonogram 4698-9
Home care 5222 Radiation Oncology 2836
Housekeeping 4321 Reading Room 4461
ICU 7584, 7583 Rehab 7147, 7299
Labor and delivery 4571 Security 4300
Laboratories Sickle Cell Clinic 613-8188
AFB 5354, 5350 Social Workers 4113
Blood bank 4897 Urinalysis 5348
Blood gases 4632 XR 4424
Chemistry 5342 XR - STAT Portables 4654
Hematology 5348, 5373
Micro 5355, 5357
Pathology 5374
Serology 5363
CONTACT INFORMATION 4
7 ARTERIAL ANATOMY
LENTICULOSTRIATE
ARTERIES
Coronal section show-

ing the lenticulostriate
arteries arising from
the proximal middle
cerebral artery and
supplying the basal
ganglia and internal
capsule. The recurrent
artery of Heubner
arises from the anteri-
or cerebral artery.
Note: Vertebral
arteries enter
transverse fo-
ramina at C6,
ascend to C2,
turn laterally
and exit the
vertebral foram-
ina at C1.
ARTERIAL ANATOMY 8
BLOOD SUPPLY TO THE CEREBRUM ACA: Anterior Cerebral Artery, PCA: Posterior Cerebral Artery,
MCA: Middle Cerebral Artery
9 ARTERIAL ANATOMY
BLOOD VESSELS SUPPLYING BASAL GANGLIA AND THALAMUS
BLOOD SUPPLY TO INTERNAL CAPSULE AND GLOBUS PALLIDUS
ARTERIAL ANATOMY 10
MAJOR VASCULAR SYNDROMES
Middle cerebral, anterior cerebral, posterior cerebral arteries
LOCATION OF AFFECTED
DEFICITS
INFARCT TERRITORY
LEFT MCA Right face and arm weakness

SUPERIOR Nonfluent or Brocas aphasia
DIVISION Some right face and arm cortical-type sensory loss
Fluent, or Wernickes, aphasia

LEFT MCA Right visual field deficit
INFERIOR Some right face and arm cortical-type sensory loss
DIVISION Some mild right-sided weakness
Patients may seem confused
Right pure motor hemiparesis

LEFT MCA
Cortical deficits, such as aphasia, may be produced by
DEEP TERRITORY
larger infarcts
Combination of the above:

LEFT MCA
Right hemiplegia, right hemianesthesia, right homonymous
STEM
hemianopia, global aphasia, left gaze preference
RIGHT MCA Left face and arm weakness

SUPERIOR Left hemineglect
DIVISION Some left face and arm cortical-type sensory loss
Profound left hemineglect

RIGHT MCA Left visual field and somatosensory deficits
INFERIOR Motor neglectdecreased voluntary or spontaneous initia-
DIVISION tion of movements on left side despite brisk withdrawal to
pain
Left pure motor hemiparesis

RIGHT MCA
Cortical deficits, such as hemineglect, may be produced
DEEP TERRITORY
by larger infarcts
Combination of the above:

RIGHT MCA Left hemiplegia, left hemianesthesia, left homonymous
STEM hemianopia, profound left hemineglect, right gaze prefer-
ence
Contralateral leg weakness and cortical-type sensory loss

Grasp reflex, frontal lobe behavioral abnormalities
ACA
Transcortical aphasia (left ACA)
Left hemineglect (right ACA)
Contralateral homonymous hemianopia

Contralateral hemiparesis, hemianesthesia (with larger
infarcts involving thalamus, internal capsule)
PCA
Alexia without agraphia (damage to splenium of corpus
callosum, left PCA)
Aphasia (large left PCA infarcts)
11 ARTERIAL ANATOMY
WATERSHED INFARCTIONS
ARTERIAL SYNDROME ANATOMICAL
CLINICAL FEATURES
TERRITORIES NAME(S) STRUCTURES
MCA-PCA- Balint Bilateral parieto- Simultagnosia (inability to perceive parts of
ACA Syndrome occipital associa- visual scene as a whole)
tion cortex Optic ataxia (impaired hand eye coordination)
Ocular apraxia (difficulty in voluntarily di-
recting gaze through saccades)
ACA-MCA Man-in-the- Pre-rolandic and Brachial diplegia with normal findings of the
barrel subcortical area legs
Syndrome
MCA-PCA Gerstmann Dominant inferior Agraphia

Syndrome parietal lobule Acalculia
(angular gyrus) Finger agnosia
Left-right disorientation
Anton Bilateral parieto- Cortical blindness with denial of blindness
Syndrome occipital cortex
IMAGING A and B demonstrate

appearance of acute watershed
infarcts on diffusion-weighted
imaging. C. Absence of right
internal carotid artery signal on
MRA (indicating severe carotid
stenosis or occlusion) predis-
A B C
poses to such infarcts.
ARTERIAL ANATOMY 12
13 ARTERIAL ANATOMY
D
ARTERIAL ANATOMY 14
MAJOR VASCULAR SYNDROMES OF THE PONS
SYNDROME VASCULAR ANATOMICAL
REGION CLINICAL FEATURES
NAME(S) SUPPLY STRUCTURES
MEDIAL Dysarthria Paramedian Corticospinal and Contralateral face, arm and leg
PONTINE hemiparesis branches of corticobulbar tracts weakness, dysarthria
BASIS (pure motor basilar artery,
hemiparesis) ventral territory
Ataxic Same as above Corticospinal and Contralateral face, arm and leg
Hemiparesis corticobulbar tracts weakness, dysarthria
Pontine nuclei and Contralateral ataxia
pontocerebellar (occasionally ipsilateral ataxia)
fibers
MEDIAL Foville Paramedian Corticospinal tract Contralateral face, arm and leg
PONTINE Syndrome branches of weakness, dysarthria
BASIS AND basilar artery, Fascicles of facial Ipsilateral peripheral-type
TEGMENTUM ventral and nerve facial paralysis
dorsal territories Pontine paramedi- Paralysis of horizontal gaze to
an reticular for- the side of the lesion
mation
Pontine Same as above Corticospinal and Contralateral face, arm and leg
wrong-way corticobulbar tracts weakness
eyes Dysarthria
Aducens nucleus or Ipsilateral horizontal gaze
paramedian pon- palsy
tine reticular for-
mation
Millard-Gubler Paramedian Corticospinal and Contralateral hemiplegia
Syndrome branches of corticobulbar tracts
basilar artery, Fascicles of facial Ipsilateral peripheral-type
ventral territo- nerve facial paralysis
ries Fascicles of abdu- Ipsilateral lateral rectus paraly-
cens nerve sis (diplopia with failure to
abduct the ipsilateral eye)
Other regions Medial lemniscus Contralateral decreased posi-
variably in- tion and vibration sense
volved Medial longitudinal Internuclear ophthalmoplegia
fasciculus (INO)
LATERAL AICA AICA Middle cerebellar Ipsilateral ataxia
CAUDAL Syndrome peduncle
PONS Vestibular nuclei Vertigo, nystagmus
Trigeminal nucleus Ipsilateral facial decreased
and tract pain and temperature sense
Spinothalamic tract Contralateral body decreased
pain and temperature sense
Descending sympa- Ipsilateral Horners syndrome
thetic fibers
Labyrinthine Inner ear Ipsilateral hearing loss
artery (usually a
branch of AICA)
DORSOLAT- SCA Syndrome SCA Superior cerebellar Ipsilateral ataxia
ERAL peduncle and cere-
ROSTRAL bellum
PONS Other lateral teg- Variable features of lateral
mental structures tegmental involvement (see
(variable) AICA syndrome)
15 ARTERIAL ANATOMY
MAJOR VASCULAR SYNDROMES OF THE MIDBRAIN
MIDBRAIN Webers Branches of PCA Oculomotor nerve Ipsilateral third-nerve palsy
BASIS Syndrome and top of basi- fascicles
lar artery Cerebral peduncle Contralateral hemiparesis
(corticospinal,
corticobulbar fi-
bers)
MIDBRAIN Claudes Branches of PCA Oculomotor nerve Ipsilateral third-nerve palsy
TEGMENTUM Syndrome and top of basi- fascicles
lar artery Red nucleus, supe- Contralateral ataxia (more
rior cerebellar prominent than in Benedikts
peduncle syndrome
MIDBRAIN Benedikts Branches of PCA Oculomotor nerve Ipsilateral third-nerve palsy
BASIS AND Syndrome and top of basi- fascicles
TEGMENTUM lar artery Cerebral peduncle Contralateral hemiparesis
Red nucleus, sub- Contralateral ataxia, hemi-
stantia nigra, supe- tremor, and involuntary move-
rior cerebellar ments (hemiathetosis, hemi-
peduncle fibers chorea)
Note: Peduncular hallucinosis is syndrome where complex, vivid, non-threatening hallucinations may be asso-
ciated with quadriparesis (lesions were described in cerebral peduncles, bilateral medial substantia nigra pars
reticulata as well as thalamus and lateral geniculate body)
MAJOR VASCULAR SYNDROMES OF THE MEDULLA

MEDIAL Medial Paramedian Pyramidal tract Contralateral hemiparesis
MEDULLA medullary branches of Medial lemniscus Contralateral decreased posi-
syndrome vertebral and tion and vibration sense
anterior spinal Hypoglossal nucle- Ipsilateral tongue weakness
arteries us and exiting CN
XII fascicles
LATERAL Lateral Vertebral artery Inferior cerebellar Ipsilateral ataxia, vertigo,
MEDULLA medullary (more common- peduncle, vestibu- nystagmus, nausea
syndrome ly than PICA) lar nuclei
(Wallenberg) Trigeminal nucleus Ipsilateral facial decreased
and tract pain and temperature sense
Spinothalamic tract Contralateral body decreased
pain and temperature sense
Descending sympa- Ipsilateral Horners syndrome
thetic fibers
Nucleus ambiguus Hoarness, dysphagia
Nucleus solitaries Ipsilateral decreased taste
Note: There is minimal motor involvement in lateral medullary syndrome, and prognosis is generally good.
Also, ipsilateral facial weakness is possible as CN VI fibers may be affected as they loop caudally into the me-
dulla before exiting at ponto-medullary junction.
ARTERIAL ANATOMY 16
MAGNETIC RESONANCE VENOGRAPHY
Superficial saggital sinus

Sigmoid sinus
Transverse sinus
Straight sinus
Confluence of sinuses
17 VENOUS SYSTEM
CEREBRAL VENOUS DRAINAGE TERRITORIES
Superficial cortical veins

Sylvian veins (peri-insular region)
into the basal dural sinuses
Transverse sinus and vein of
Labbe (drainage from temporal,
parietal, occipital lobes)
Deep cerebral veins (Internal
cerebral vein, vein of Galen
VENOUS SYSTEM 18
THALAMIC NUCLEI, INPUTS AND OUTPUTS VPL: Ventral posterior lateral, VPM: Ventral posterior medial,
LGN: Lateral geniculate body, MGN: Medial geniculate body, VL: ventral lateral, VA: ventral anterior, MD:
Mediodorsal, In: Intralaminar nuclei
19 THALAMUS
INPUTS arrive OUTPUTS
at the striatum arise from the
GPi and SNPr
BASAL GANGLIA INTERNAL CONNECTIONS
BASAL GANGLIA 20
FUNCTIONAL COLUMNS OF BRAINSTEM SENSORY AND MOTOR CRANIAL NERVE NUCLEI
OCULOMOTOR (CN III) NUCLEAR COMPLEX Edinger-Westphal parasympathetic innervation is bilateral.

Thus, unilateral weakness of levator superior or unilateral pupillary dilatation cannot result from unilateral
CN III nucleus lesion
21 CRANIAL NERVES AND NUCLEI

OCULOMOTOR FASCICULAR ORGANIZATION IN VENTRAL MIDBRAIN TEGMENTUM From lateral to me-
dial as follows: inferior oblique (IO), superior rectus (SR), medial rectus (MR), levator palpebri (LP), inferior
rectus (IR), and pupillary fibers (most medial).
COURSE OF THIRD
CRANIAL NERVE
Note the close
proximity of CN III
to posterior cere-
bral artery
CAVERNOUS SINUS Note that

CN III, CN IV, CN IV, CN V1 and
V2 all traverse this sinus and
that CN VI is closest to the
carotid artery
CRANIAL NERVES AND NUCLEI 22

TROCHLEAR NERVE (CN IV) COURSE Nerve fascicles course posteroinferiorly around the aqueduct to
decussate in the dorsal midbrain in the anterior medullary velum; they then emerge from the brainstem
near the dorsal midline, immediately below the inferior colliculi. The cisternal segment then runs anteriorly
over the lateral aspect of the brainstem, successively traversing the quadrigeminal, ambient, crural, and
pontomesencephalic cisterns; the cisternal part of the nerve is closely related to the tentorium cerebelli.
After traveling on the undersurface of the tentorial edge, it pierces the dura at a point slightly below the
oculomotor nerve into the cavernous sinus.

ABDUCENS NERVE (CN VI) COURSE Axons emerge in the horizontal sulcus between the pons and medulla,
lateral to the corticospinal bundles. The nerve then ascends along the base of the pons in the prepontine
cistern and enters Dorello's canal beneath petroclinoid ligament. It travels in the lateral wall of the cavernous
sinus. In its course from the pericarotid plexus to the ophthalmic branch of the trigeminal nerve, the pupil's
sympathetic fibers join the abducens nerve for a few millimeters. After passing through the superior orbital
fissure, the abducens nerve innervates the lateral rectus muscle.
PONTINE HORIZONTAL GAZE CENTER AND GAZE ABNORMALITIES

C3, C4
TRIGEMINAL NERVE (CN V) NUCLEI From the gasserian (semilunar) ganglion, the fibers of CN V
enter the pons, course dorsomedially, and terminate in three major nuclear complexes: nucleus of the spinal
tract of trigeminal nerve, main (or principal) sensory nucleus, and mesencephalic nucleus. In the pons, many
of the sensory fibers descend as the spinal tract of trigeminal nucleus through the caudal end of the medulla
and into the spinal cord (as far as C3-4).
SOMATOTOPIC ARRANGEMENT OF TRIGEMINAL NUCLEI Onion skin pattern: midline facial areas
(nose and mouth) are represented rostrally in the spinal nucleus, whereas the more lateral facial sensation
fibers terminate in more caudal spinal nucleus regions

FACIAL NERVE Nerve root
sweeps over the dorsal
surface of abducens nucle-
us (genu of facial n.), then
emerges on lateral aspect
of brainstem at cerebel-
lopontine angle.
CN VII then enters internal

auditory meatus (temporal
bone) with CN VIII, internal
auditory artery and vein.
CN VII along with nervus

intermedius (sensory and
parasympathetic fibers)
then travels through the
facial canal.
In the mastoid segment,

CN VII branches off to
nerve to stapedius and
chorda tympani
(parasympathetics and
taste from anterior two-
thirds of tongue)

VESTIBULO-COCHLEAR NERVE (CN VIII) AND VESTIBULAR PATHWAYS

CRANIAL NERVES

VISUAL PATHWAYS, LESIONS AND CORRESPONDING VISUAL
FIELD DEFECTS Bitemporal hemianopia occurs with chias-
matic lesions. Pie in the sky (superior quadrantanopia)
occurs with temporal lobe (Meyers loop) lesions. Pie on the
floor (inferior quadrantanopia) occurs with parietal lobe
(upper optic radiations) lesions.
Monocular concentric
vision loss due to chronic
increased intracranial
pressure
Left homonymous hemiano-

pia with macular sparing
caused by right PCA infarct
preserving occipital pole
Left superior quadrantanopia

with macular sparing caused
by inferior right calcarine
fissure lesion sparing occipital
pole
MACULAR SPARING Fovea has large cortical repre-

sentation. Partial lesions of visual pathway and exter-
nal compression of optic nerve may spare the macula.
29 VISUAL PATHWAYS
CLASSIFICATION OF APHASIAS
APHASIAS
30
Crossed at this level
Partially crossed at this level
Uncrossed at this level
ASCENDING AND DESCENDING PATHWAYS GF: Gracile Fasciculus, CF: Cuneate Fasciculus, PLT: Posterol-
ateral, PSCT: Posterior Spinocerebellar, RSCT: Rostral Spinocerebellar, LSTT: Lateral Spinothalamic, ASCT:
Anterior Spinothalamic, SOT: Spinoolivary Tract, ASTT: Anterior Spinothalamic, ST: Spinotectal Tract, SRT:
Spinoreticular Tract
SOMATOTOPIC ORGANIZATION OF ANTERIOR HORN CELLS
31 SPINAL CORD
SPINOTHALAMIC PATHWAYS Sensory modalities, upper cervical level
TRACT LAMINATION IN SPINAL CORD S: Sacral, L: Lumbar, Th: Thoracic, C: Cervical
SPINAL CORD 32
VASCULAR SUPPLY OF SPINAL CORD Watershed zones (C4, T3-T4, T8-T9)
33 SPINAL CORD
ARTERIAL SUPPLY OF A SPINAL
CORD SEGMENT
WATERSHED REGION OF BLOOD

SUPPLY TO CERVICAL CORD C: Cer-
vical, T: Thoracic, L: Lumbar, S: Sacral
SPINAL CORD 34
ANTERIOR CORD SYNDROME e.g. aortic dissection, vasculitis, atherosclerosis of aorta, post-op (spine,
aortic, thoracic surgery, AVM, and decompressive surgeries), cervical spondylosis
Bilateral posterior column and

upper motor neuron signs
POSTEROLATERAL COLUMN (COMBINED SYSTEM DEGENERATION) e.g. HIV, HTLV-1 associated myelop-
athy, Nitrous Oxide Myeloneuropathy, B12 Deficiency (pictured), copper deficiency, cervical spondylosis,
tabes dorsales
ANTERIOR HORN AND PYRAMIDAL e.g. ALS, HTLV-1
35 SPINAL CORD
BROWN SEQUARD
e.g. traumatic,
intramedullary
tumors
ANTERIOR HORN ONLY e.g. COMPLETE CORD TRANSECTION

Poliomyelitis, West Nile virus, e.g. post-infectious, multiple scle-
post-radiation, hexosaminidase rosis, post-vaccinal, traumatic,
deficiency, spinal muscular atro- epidural hematoma, tumor, para-
phies (hereditary motor neurop- neoplastic
athies)
Early lesion
(Crossing spinotha-
lamic fibers are in-
volved)
(Crossing CENTRAL CORD

spinothalamic LESION e.g. in-
fibers and tramedullary spi-
motor neurons nal cord tumors,
syringomyelia
are involved)
(traumatic or with
Late lesion Chiari malfor-
mation pictured Chiari I malformation with syrin-
on MRI). gomyelia
SPINAL CORD 36
Epidural space
Subdural space
Subarachnoid space
Perivascular space
CEREBROSPINAL FLUID CIRCULATION Cerebrospinal fluid produced by choroid plexus flows from the
lateral ventricles, through the foramen on Monro, into the third ventricle, through the Sylvian aqueduct,
into the fourth ventricle, out through the lateral foramina of Luschka and medial foramen of Magendie,
into the subarachoid space, and up to the arachnoid granulations to be reabsorbed into the bloodstream.
37 CEREBROSPINAL FLUID SYSTEM

DERMATOMES AND CUTANOUS NERVES
PERIPHERAL NERVOUS SYSTEM

38
BRACHIAL PLEXUS
COMPLETE PLEXUS LESIONS UPPER ROOT LESIONS LOWER ROOT LESIONS

(C5-T1) (C5-6) (C8, T1)
39 PERIPHERAL NERVOUS SYSTEM

TESTING FOR BRACHIAL PLEXUS LESIONS
RHOMBOIDS SUPRASPINATUS
Dorsal Scapular Nerve (C4, C5) Suprascapular Nerve (C5, C6)
Pressing palm of hand backwards Abducting upper arm against resist-
against examiners hand ance.
SERRATUS ANTERIOR INFRASPINATUS

Long Thoracic Nerve (C5-7) Suprascapular Nerve (C5, C6)
Patient pushing against wall. Left Externally rotating upper arm and
serratus paralyzed (winging of scapula) shoulder against resistance.
PECTORALIS MAJOR: CLAVIC. HEAD LATISSIMUS DORSI

Lateral Pectoral Nerve (C5, C6) Thoracodorsal Nerve (C6, C7, C8)
Arm above horizontal and patient push- Upper arm is horizontal and patient is
ing forward. adducting against resistance. Lower
arrow: muscle belly.
PECT. MAJOR: STERNOCOSTAL HEAD TERES MAJOR

Lat/Med Pectoral Nerves (C6, C7, C8) Subscapular Nerve (C5, C6, C7)
Adducting upper arm against resistance. Adducting elevated upper arm against
resistance.
PERIPHERAL NERVOUS SYSTEM 40

AXILLARY NERVE
SENSORY CHANGES
DELTOID
Axillary Nerve
(C5, C6)
Retracting abducted
upper arm against
resistance

RADIAL NERVE
SENSORY CHANGES
ABDUCTOR POLLICIS LONGUS EXTENSOR CARPI ULNARIS, EX- TRICEPS

Post Interosseous Nerve TENSOR DIGITORUM Radial Nerve (C6, C7, C8)
(C7, C8) Post Interosseous Nerve (C7, C8) Extending forearm at elbow
Abducting thumb at carpo- Extension and adduction of wrist against resistance (arrow point
metacarpal joint in plane at against resistance to long and lateral heads)
right angle to palm (arrow Extension at metacarpophalangeal
points to tendon) joints against resistance
MEDIAN NERVE
FLEXOR CARPI RADIALIS FLEXOR DIGITTORUM PROFUNDUS OPPONENS POLLICIS

Median Nerve Ant. Interosseous Nerve Median Nerve
(C6, C7) (C7, C8) (C8, T1)
Flexing and abducting wrist Flexing distal phalanx of index finger Touching base of little finger
against resistance against resistance with middle phal- with thumb against resistance
anx fixed

ULNAR NERVE
ADDUCTOR POLLICIS
Ulnar Nerve
(C8, T1)
Adducting thumb at right
angle to palm against re-
sistance
FLEXOR CARPI ULNARIS 1ST DORSAL INTEROSSEOUS 2ND PALMAR INTEROSSE-

Ulnar Nerve Ulnar Nerve OUS
(C7, C8, T1) (C8, T1) Ulnar Nerve (C8, T1)
Flexing and adducting wrist Abducting index finger against Adducting index finger
against resistance resistance (arrow points to mus- against resistance
cle belly)
LUMBOSACRAL PLEXUS

NERVES OF THE LOWER LIMB AND SENSORY DISTRIBUTIONS

NERVES OF THE LOWER LIMB AND SENSORY DISTRIBUTIONS

MOTOR EXAM OF THE LOWER LIMBS
ILIOPSOAS QUADRICEPS FEMORIS HAMSTRING MUSCLES

Branches from L1, 2, 3 spinal Femoral Nerve Sciatic Nerve
nerves and Femoral Nerve (L2, L3, L4) (L5, S1, S2)
(L1, L2, L3) Extending leg against resistance Patient lies on back with limb
Flexing thigh at hip against with limb flexed at hip and knee flexed at hip and knee and is
resistance with leg flexed at (arrow points to rectus femoris flexing leg at knee against resist-
knee and hip. muscle belly) ance
GLUTEUS MAXIMUS GASTROCNEMIUS EXTENSOR

Inferior Gluteal Nerve Tibial Nerve DIGITORUM
(L5, S1, S2) (S1, S2) LONGUS
Patient lies on back with leg extended at Plantar-flexing foot against resistance Deep Perone-
knee and is extending limb at the hip against (arrow points to muscle belly) al Nerve
resistance. (L5, S1)
TIBIALIS ANTERIOR TIBIALIS POSTERIOR PERONEUS BREVIS AND

Deep Peroneal Nerve Tibial Nerve LONGUS
(L4, L5) (L4, L5) Superficial Peroneal N.
Dorsiflexing foot against resistance (arrows Inverting foot against (L5, S1)
point to muscle belly and tendon) resistance (arrow points Everting foot against
to tendon) resistance (arrows point
to respective tendons)

49
MAJOR TRACTS
LATERAL CORTICOSPINAL TRACT
POSTERIOR COLUMN
MEDIAL LEMNISCAL
PATHWAY
SPINOCEREBELLAR TRACT
MAJOR TRACTS 50
ISCHEMIC STROKE ALGORITHM
Acute focal neurologic deficit
Vitals, Glucose
Establish onset time
NIHSS
CT head
BMP, CBC, Coags
IV Access (18-20 gauge)
ECG
Onset < 4.5 hours? Onset between 4.5 and 12

hours?
*Consider non-invasive
Yes
vascular imaging (CTA,
Yes
MRA or TCD) for patients
IV t-PA exclusions present? where presence of major
vascular syndrome is
Does the patient have
unclear. If vascular occlu-
No significant non-lacunar
sion is documented, con-
syndrome?
sider endovascular treat-
IV t-PA as per protocol ment.
Yes
Does patient have significant

Interventional treatment
non-lacunar syndrome and Yes
available at UHB?
does not improve?
No
Call 718-780-BEST to arrange for transfer for
endovascular treatment Yes
IF ACCEPTED FOR TRANSFER:

1. Call 718-780-1961 for LICH ED to give report Consider endovascular
2. Insert Foley catheter treatment at UHB
3. Send ED notes, labs, radiology reports (for both UHB and KCH
4. One family member should go with patient
patients)
EXCLUSION CRITERIA (3 hours) EXCLUSION CRITERIA (3-4.5 hours)

Intracranial hemorrhage on CT Non-compressible arterial puncture <7 Age >80
Suspected SAH days Previous stroke + Diabetes (together)
Rapidly improving or minor symptoms Platelet count <100,000 NIHSS >25
Seizure at onset Warfarin use with INR >1.7 or PT >15 sec Large >1/3 of MCA territory infarct
Stroke, serious head trauma, intracranial Heparin use <48 hours with elevated PTT Using Coumadin
or intraspinal surgery < 3 months Serum glucose <50 mg/dl or > 400 mg/dl
History of intracranial neoplasm, AVM, Persistent SBP <185 or DBP <110
aneurysm
History of ICH Relative Contraindications:
GI or GU hemorrhage <21 days Large stroke (NIHSS >22)
Major surgery <14 days Large >1/3 of MCA territory infarct
TISSUE PLASMINOGEN ACTIVATOR (ALTEPLACE) DOSING
Dosing is in milligrams, weight is in kilograms or pounds. Maximum total dose is 90 mg.
WEIGHT TOTAL BOLUS INFUSION WEIGHT TOTAL BOLUS INFUSION
(kg) (Lb) DOSE DOSE DOSE (kg) (Lb) DOSE DOSE DOSE
50 110 45 4 41 76 168 68 7 61
51 112 46 5 41 77 170 69 7 62
52 115 47 5 42 78 172 70 7 63
53 117 48 5 43 79 174 71 7 64
54 119 49 5 44 80 176 72 7 65
55 121 50 5 45 81 179 73 7 66
56 123 50 5 45 82 181 74 7 67
57 126 51 5 46 83 183 75 8 67
58 128 52 5 47 84 185 76 8 68
59 130 53 5 48 85 187 77 8 69
60 132 54 5 49 86 190 77 8 69
61 134 55 6 49 87 192 78 8 70
62 137 56 6 50 88 194 79 8 71
63 139 57 6 51 89 196 80 8 72
64 141 58 6 52 90 198 81 8 73
65 143 59 6 53 91 201 82 8 74
66 146 60 6 54 92 203 83 8 75
67 148 60 6 54 93 205 84 8 76
68 150 61 6 55 94 207 85 9 76
69 152 62 6 56 95 209 86 9 77
70 154 63 6 57 96 212 86 9 77
71 157 64 6 58 97 214 87 9 78
72 159 65 7 58 98 216 88 9 79
73 161 66 7 59 99 218 89 9 80
74 163 67 7 60 100 221 90 9 91
75 165 68 7 61 >100 90 9 91
SUSPECT BLEEDING COMPLICATION POST t-PA MONITORING PROTOCOL

DURING t-PA INFUSION? 1. NIHSS on completion of infusion
1. Stop infusion immediately 2. Vital signs:
2. STAT head CT to rule out hemor- q15 min x2 hours - BP <185/110
rhage q30 min x6 hours - BP <185/110
3. CBC, Platelet count, INR, PT, PTT, No hemorrhage q1 hour x 16 hours - BP <180/105
Fibrinogen, D-Dimer, Glucose 3. Avoid venipuncture, line place-
4. Manage intracranial hemorrhage ment x24 hours
(page 59) 4. Maintain glucose <150 mg/dL
5. Maintain IV hydration with nor-
mal saline fluids
ABCD2 SCORE 6. Keep temperature <98 F
Risk stratification for 48 hours after minor stroke or TIA 7. Repeat head CT in 24 hours to
CRITERIA SCORE assess for intracranial bleeding
Age 1: Age 60
Blood Pressure 1: SBP >140, DBP >90

1: Speech disturbance without weakness Rapidly resolving symptoms, not
Clinical Features
2: Unilateral weakness a candidate for t-PA?
0: <10 minutes
6-7 points (8.1% two-day risk)
Duration 1: 10-59 minutes
2: 60 minutes 4-5 points (4.1% two-day risk)
Diabetes Mellitus 1: Present 0-3 points (1% two-day risk)
ISCHEMIC STROKE 54
NIH STROKE SCALE
FUNCTION SCORE EFFECTS OF IV t-PA (NINDS,
1a. Level of Consciousness 0 = Alert ECASS III TRIALS)
1 = Drowsy (arousable by minor
stimulation to obey, answer or
respond) 24 Hour 4 Point Improvement
2 = Stuporous (requires repeated in NIHSS:
stimuli or strong painful stimula-
tion) 47% (vs 39% placebo)
3 = Comatose (reflex responses only) at 0-180min
1b. LOC Questions 0 = Both Correct
Month, Age 1 = One Correct
90 Day Global Outcome
2 = Incorrect
1c. LOC Commands 0 = Obeys both Correctly Modified Ranking Scale,
Open close eyes make 1 = Obeys one Correctly Barthel Index, NIHSS (Odds
fist 2 = Incorrect Ratio):
2. Best Gaze 0 = Normal
Eyes open, patient fol- 1 = Partial gaze palsy 1.9 (0-90, 91-180min)
lows object 2 = Forced deviation 1.3 (180-270 min)
3. Visual Fields 0 = No Loss
Finger counting or visual 1 = Partial hemianopia
threat 2 = Complete hemianopia Symptomatic ICH:
3 = Forced deviation
4. Facial Palsy 0 = Normal 6.4% (vs 0.6% placebo)
Score symmetry of gri- 1 = Minor Asymmetry at 0-180min
mace in comatose 2 = Partial (lower face paralysis) 7.9% (vs 3.5% placebo)
3 = Complete at 180-270min
5a/b. Motor Arm 0 = No drift
Elevate extremity 90 1 = Drift
and score drift/ 2 = Some effort against gravity
movement 3 = No effort against gravity
4 = No movement EFFECTS OF IA t-PA (PROACT
UN = Amputation, joint fusion II TRIAL)
6a/b. Motor Leg 0 = No drift
Elevate extremity 30 1 = Drift
Recanalization rates
and score drift/ 2 = Some effort against gravity
movement 3 = No effort against gravity 66% (vs 18% placebo)
4 = No movement
UN = Amputation, joint fusion Hemorrhagic transformation
7. Limb Ataxia 0 = Absent 10% (vs 2% placebo)
Finger-nose, Heel-Shin 1 = Present in upper or lower
2 = Present in both
Favorable outcome (mRS 2
8. Sensory 0 = Normal
at 90 days)
Pinprick Face/Arm/Leg 1 = Partial Loss
2 = Dense Loss 40% (vs 25% placebo)
9. Best Language 0 = No aphasia
Name items, describe a 1 = Mild-Moderate aphasia
picture read a sentence 2 = Severe Aphasia
3 = Mute, Global Aphasia
10. Dysarthria 0 = Normal articulation
Evaluate speech clarity 1 = Mild-Moderate slurring
2 = Severe, nearly unintelligible
11. Extinction and Inattention 0 = No neglect
Check sensory neglect or 1 = Partial neglect (extinction to a
double simultaneous sensory modality)
stimuli 2 = Profound neglect (orients to only
one side of space)
55 ISCHEMIC STROKE
NIH STROKE SCALE
ISCHEMIC STROKE 56
NIH STROKE SCALE
You know how.
Down to earth.
I got home from work.
Near the table in the dining room.
They heard him speak on the radio

last night.
MAMA
TIP - TOP
FIFTYFIFTY
THANKS
HUCKLEBERRY
BASEBALL PLAYER
57 ISCHEMIC STROKE
NIH STROKE SCALE
ISCHEMIC STROKE 58
HEMORRHAGIC STROKE ALGORITHM
Acute focal neurologic deficit REVERSAL OF COAGULOPATHY

+ severe headache, LOC, nuchal rigidity, Warfarin:
FFP 10ml/kg over 90 minutes
seizure, nausea, vomiting
Repeat INR in 4 hours
If INR >1.3, administer second
dose of FFP
Vitals, Glucose Heparin:
Establish onset time Protamine 10mg to 50mg IV
NIHSS over 1-3 min
CT head Aspirin or Clopidogrel:
BMP, CBC, Coags, UCG Platelets 1 unit
IV Access (> 20 gauge)
ECG
If suspecting SAH, is
Hemorrhage present on CT? No xanthochromia present
on CSF sampling?
Yes
1. Hold anticoagulation (reverse if indicated)

2. Hold anti-platelet agents (reverse if indicated)
3. Maintain SBP 140-160, DBP 70-90, MAP 100-120
Labetalol 10-20mg IVP q10 min to max 300mg
or Nicardipine IVPB 25mg/250cc NS @ 5-15mg/hr
Yes
4. Maintain normoglycemia (120-150 mg/dl)
5. Maintain normothermia (97F)
6. Seizure prophylaxis (Fosphenytoin 20mg/kg
bolus followed by 5mg/kg q8h maintenance )
7. STAT Neurosurg., Neuro-Interventional Consults
Signs of increased intracranial Airway, Breathing, Circulation

pressure (obtundation, nausea, Intubation if indicated
Yes
vomiting, hypertension with Manage increased intracranial
bradycardia)? pressure (see page 61)
No
SUBARACHNOID (NON-TRAUMATIC) INTRACEREBRAL

1. Obtain CT Angiogram prior to intervention 1. Management as above.
2. Consider Aminocaproic Acid 5gm/250cc NS over 60 min x1 dose 2. Bedrest (head of bed >30 degrees)
3. Nimodipine 60mg po q4hr (hold for SBP<120) 3. Neuro checks q2 hours
4. Seizure prophylaxis: Phenytoin, or status epilepticus protocol if 4. Repeat head CT within 24 hours, or STAT
seizing if neurologic deterioration is noted.
Hematoma growth occurs largely within
Complications: first 3 hours, and rarely beyond 20 hours.
Rebleeding (24-48 hours) - Prevent with aneurysmal clipping (surgical) or 5. Resume DVT prophylaxis in 48-72 hours if
coilning (endovascular); 48% mortality patient remains neurologically stable
Vasospasm (day 5-10) - Prevent with Nimodipine and Triple-H therapy
(hemodilution, induced hypertension, and hypervolemia). Monitor Complications:
patient with neuro exams and daily TCD. If neurologic deterioration Mass effect, Increased ICP - See page 561
noted, take measures to increase cerebral perfusion and consult Hydrocephalus - More common with intra-
Neuro-Interventional immediately for angiogram. ventricular extension of bleed. EVD place-
Hydrocephalus - External ventricular drainage (EVD) is indicated if deteri- ment if IVH, GCS <8, posturing, or declin-
orating level of consciousness, GCS<8, IVH, posturing or no improve- ing obtundation. Additional possibility of
ment in hydrocephalus in 24 hours follow-up imaging. intraventricular t-PA.
HEMORRHAGIC STROKE GRADING SCALES / REVERSAL OF ANTICOAGULATION
HUNT AND HESS SCALE GLASGOW COMA SCALE
Non-traumatic subarachnoid hemorrhage
DESCRIPTION GRADE 1 = Does not open
2 = Opens to pain
Asymptomatic, mild headache, slight 1 EYES
3 = Opens to voice
nuchal rigidity 4 = Opens spontaneously
Moderate to severe headache, nuchal 2 1 = Makes no sounds
rigidity, no neurologic deficits other than
VERBAL 2 = Incomprehensible sounds
cranial nerve palsy
3 = Inappropriate words
Drowsiness, confusion, mild focal neuro- 3 4 = Confused, disoriented
logic deficit
5 = Oriented, converses
Stupor, moderate-severe hemiparesis 4 1 = No movements
Coma, decerebrate posturing 5 2 = Extension to painful stimu-
li
MOTOR 3 = Abnormal flexion to pain
MODIFIED FISHER SCALE 4 = Flexion, withdrawal to
Prediction of vasospasm in patients with SAH pain
APPEARANCE OF HEMORRHAGE 5 = Localizes to pain
GRADE RISK 6 = Obeys commands
ON CT
None or minimal blood in cisterns 1 10%
DOSING OF FRESH FROZEN PLASMA
Thin (<1mm) basal blood + bilateral 2 20%
IVH DECIDE ON TARGET INR
Thick blood (> 1 mm) in cisterns 3 30% Moderate bleeding,

2.0-2.1
high risk of thrombosis
Thick blood + intraventricular hem- 4 40% Serious bleeding, mod-
orrhage (IVH) 1.5
erate risk of thrombosis
Serious or life-
MANAGEMENT SUPRATHERAPEUTIC INR 1.0 threatening bleeding,
TARGET low risk of thrombosis
BLEEDING ACTION
INR CONVERT INR TO PROTHROMBIN COM-
Lower warfarin dose or PLEX
> thera-
omit a dose and resume >5 5%
peutic, No
warfarin when INR is in 4.0-4.9 10%
< 5.0
therapeutic range 2.6-3.2 15%
Omit 1-2 doses of warfarin 2.2-2.5 20%
> 5.0, and monitor until INR is 1.9-2.1 25%
No
< 9.0 therapeutic, or administer 1.7-1.8 30%
1 to 2mg oral Vitamin K 1.4-1.6 40%
Hold warfarin, give 5 to 1.0 100%
> 9.0 No 10mg Vitamin K and more CALCULATE DOSE
in needed, monitor INR (target level as percentage - present
Hold warfarin, administer level as percentage) x body weight
Serious or 10mg Vitamin K by slow (kg) = mL of fresh frozen plasma
life- IV infusion, supplement
Any
threaten- with fresh frozen plasma,
Factors associated with increased 30-
ing prothrombin complex
concentrate day mortality:
Age
VOLUME OF BLEED may be estimated by using the GCS score at admission 8
formula (A x B x C)/2, where A is the longest diame- ICH volume >30cc
ter, B is a diameter perpendicular to A, and C is Intraventricular extension
depth (the number of CT slices multiplied by slice Glucose level at admission
thickness). Previous antiplatelet use
HEMORRHAGIC STROKE 60
INTRACEREBRAL EDEMA POST CVA (CYTOTOXIC EDEMA)
TIME COURSE Edema starts to develop within hours of
stroke onset, peaks at 2 to 5 days, and then gradually resolves
PREDICTORS OF INCREASED RISK

Malignant MCA infarcts
Posterior fossa infarcts (whole PICA, SCA)
Early nausea, vomiting, obtundation, respiratory distress
NIHSS score 15
12-hour systolic BP > 180 mmHg
Early hypodensity > 50% of MCA territory on CT
Diffusion lesion volume > 82 mL within 6 hours of onset
History of HTN or CHF
Acute involvement of multiple vascular territories
EDEMA ON CT Large hypodensity
with mass effect on lateral ventricle
ACUTE MANAGEMENT and midline shift
1. Intubation, hyperventilation, sedation
Keep pCO2 26-35 mmHg
Lowers ICP within minutes, but effect does not last more than 24-36 hours
Use rapidly reversible sedation agent (e.g. Propofol) if needed, but examine frequently off sedation.
2. Hyperosmolar therapy
Mannitol 25%
Dosing: 0.5-1.0 gm/kg (max 100g) IVPB bolus over 30 min, then 0.25g/kg every 4 hours
Monitoring: check serum osmolarity q6h, and target 300-310
Side-effects: hypotension, rebound intracranial hypertension, renal failure
Hypertonic saline
Dosing: 23.4% NaCl 30mL IV over 20 min into central line or switch IVF to 3% NaCl / Na Acetate (1:1)
Monitoring: target Na 145-155 mmol/dL
3. Decompressive Therapy
Hemicraniectomy Eligibility:
Procedure: Removing large frontotemporal- Age 60
parietal bone flap and opening the dura ipsilat- NIHSS 15
eral to side of infarction to allow outward her- Decrease in level of consciousness to
niation of the brain, thus lowering ICP a score 1 on Item 1a of NIHSS
Benefits: If done within 48 hours, lowers mortal- CT hypodensity involving 50% of the
ity in patients with non-dominant malignant non-dominant MCA territory
MCA infarction and increases chances of favor- Absence of bilaterally fixed, dilated
able outcome from 24% to 75% without in- pupils
creasing number of severely disabled survivors Inclusion within 45 hours of stroke
(DECIMAL, DESTINY, HAMLET trials) onset.
External Ventricular Drain, Suboccipital Craniectomy
Indications: Large posterior fossa infarcts (whole PICA, SCA) with signs of medullary compression
with tonsilar herniation (rapidly progressive bradycardia, obtundation, respiratory arrest)
Acute Hematoma Evacuation of Supratentorial Spontaneous ICH (STICH Trial)
Inclusion: >2cm diameter of clot on CT, spontaneous ICH <72hrs (hemorrhagic CVA), GCS 5
Outcome: if IVH present, surgery had more favorable outcome than conservative management,
but otherwise non-beneficial.
61 INCREASED INTRACRANIAL PRESSURE

ICP / MANAGEMENT OF VASOGENIC INTRACEREBRAL EDEMA
DEFINITIONS
Elevated ICP 20mmHg in adults
CPP (Cerebral perfusion pressure) = MAP
(Mean Arterial Pressure) - ICP (Intracranial
Pressure)
SIGNS / SYMPTOMS OF ELEVATED ICP

Headache
Depressed consciousness
Vomiting
CN VI palsies
Papilledema
Cushings reflex: bradycardia, hypertension
and respiratory depression)
Symptomatic plateau waves: with increased ICP, normal sustained intracranial pressure waves can
temporarily cut off cerebral perfusion, leading to loss of consciousness
ICP MONITORING
Target ICP <20 mmHg
Target CPP = 60-75 mmHg
CPP < 110mmHg may be tolerated without increase in ICP
Indications:
GCS 3-8 + abnormal head CT
or normal head CT + 2 or more factors: Age >40, posturing, SBP <90mmHg
MANAGEMENT:
1. Corticosteroids
Temporizing measure
Dexamethasone
Advantages: Has relative lack of mineralocorticoid activity, and reduces fluid retention
Associated with a lower risk of infection and cognitive impairment
Dosing: 10 mg loading dose, followed by 4mg q6h or 8 mg bid (half life is sufficiently
long for bid maintenance); may be increased up to 100 mg/day
Complications: Gastrointestinal (gastritis, peptic ulcer disease, perforation)
Steroid myopathy (20%, proximal weakness, after 9-12 weeks treatment re-
covery after discontinuation of steroids occurs within 2-3 months
Pneumocystis carinii pneumonia (PCP)
2. Treat Underlying Cause

E.g. tumor, infection, demyelination
CORTICOSTEROID ACTION
ACTION TIME
Decrease in capillary permeability Within 6 hours
Changes on diffusion-weighted MRI
48-72 hours
indicating decreased edema
Maximal symptomatic improvement 24-72 hours
May take sever-
Adequate reduction of elevated ICP
al days
PAPILLEDEMA
INCREASED INTRACRANIAL PRESSURE 62
APPROACH TO UNCONSCIOUS PATIENT
AIRWAY Intubate if GCS 8 and pCO2 > 45 torr

BREATHING Maintain SaO2 > 90%, pCO2 < 40 torr
CIRCULATION Maintain MAP > 70 mmHg
Glucose
Electrolytes
Arterial blood gas
Liver, thyroid function tests
Complete blood count
Toxicology screen
EKG
NEUROLOGICAL ASSESSMENT
Hyperventialtion, mannitol 0.5-1.0 g/kg (or 30 mL 23.4% NaCl) if clinical evidence of increased ICP/
herniation
Thiamine (100mg IV) followed by glucose (if < 40 mg/dL, 10 mL aliquots of 50% solution until blood
glucose > 60 mg/dL
Naloxone if opiod overdose is suspected (0.4-2.0 mg IV q3 min or continuous IV infusion 0.8 mg/kg/hr)
Flumazenil if benzodiazepine overdose suspected (0.2 mg/min, maximum dose 1 mg IV)
After intubation, gastic lavage with activated charcoal if drug intoxication is suspected
HEAD CT, CERVICAL SPINE CT if structural cause suspected

CONSIDER EEG, LUMBAR PUNCTURE, MRI after detailed
history and physical exam
DIFFERENTIAL CHARACTERISTICS OF STATES CAUSING SUSTAINED UNRESPONSIVENESS

SUPRATENTORIAL SUBTENTORIAL MASSES METABOLIC, DIFFUSE, PSYCHIATRIC UNRE-
MASS LESIONS OR DESTRUCTION MULTIFOCAL COMA SPONSIVENESS
Lids close actively
Signs of focal cere- History of preceding Pupils reactive or dilated
Confusion and stupor
bral dysfunction brainstem dysfunction (cycloplegics)
commonly precede
present at onset or sudden onset of Oculocephalic responses
motor signs
Signs of dysfunction coma are unpredictable;
Motor signs are usual-
proceed rostral to Localizing brainstem oculovestibular re-
ly symmetric
caudal signs precede or sponses physiologic
Pupillary reactions are
Neurologic signs at accompany onset of for wakefulness (i.e.
usually preserved
any given time coma nystagmus is present)
Asterixis, myoclonus,
point to one ana- Pupillary and oculomo- Motor tone is inconsist-
tremor, and sei-
tomic area (e.g. tor abnormal findings ent or normal
zures are common
diencephalon, usually present Eupnea or hypoventila-
Acid-base imbalance
midbrain-pons, Abnormal respiratory tion is usual
with hyper or
medulla) patterns common and No pathologic reflexes
hypoventilation is
Motor Signs are usually appear at are present
frequent
often asymmetric onset Electroencephalogram is
normal
63 STUPOR, COMA, BRAIN DEATH
UNCAL HERNIATION, UNCAL HERNIATION, CENTRAL TRANSTENTORIAL HERNIATION,
EARLY THIRD NERVE STAGE LATE THIRD NERVE STAGE EARLY DIENCEPHALIC STAGE
STAGES OF BRAIN HERNIATION
STUPOR, COMA, BRAIN DEATH

64
65
STAGES OF BRAIN HERNIATION (CONTINUED)
CENTRAL TRANSTENTORIAL HERNIATION, TRANSTENTORIAL HERNIATION, TRANSTENTORIAL HERNIATION,

LATE DIENCEPHALIC STAGE MIDBRAIN-UPPER PONS STAGE LOWER PONS-MEDULLA STAGE
DORSAL MIDBRAIN COMPRESSION HERNIATION SYNDROMES (1) Subfalcine, (2) Central, (3) Transtentorial, (4) Tonsillar
STAGES OF BRAIN HERNIATION (CONTINUED)

66
BRAIN DEATH PROTOCOL
DEFINITION Brain
death is the absence of
clinical brain function when
the proximate cause is
known and demonstrably
irreversible.
PREREQUISITES
1. Clinical or neuroimag-
ing evidence of an
acute CNS catastrophe
compatible with diag-
nosis of brain death
2. No severe electrolyte,
acid-base, or endo-
crine disturbance
3. No drug intoxication or
poisoning
4. Core temperature 32
C (90F), 36.5C (97
F) for apnea testing
5. Systolic blood pressure
90 mmHg
6. Euvolemia. Optional: positive fluid balance in the previous 6 hours
7. Arterial PCO2 40 mmHg, and preoxygenation to obtain arterial PO2 200 mmHg
CRITERIA
1. Coma: no cerebral motor response to deep pain
2. Absence of brainstem reflexes: fixed, unresponsive, 4-9 mm pupils; absent oculocephalic reflex; no
cold caloric response; no corneal reflex; no cough response to bronchial suctioning; no gag
3. Apnea testing:
Deliver 100% O2 6L/min into the trachea
Disconnect ventilator
Look closely for respiratory movements (abdominal or chest excursions that produce adequate
tidal volumes
Measure arterial pO2, pCO2, and pH after 8 minutes
Result supporting brain death: absent respiratory movements, pCO2 is 60 mm Hg or 20 mm Hg
increase in pCO2 over a baseline
4. Repeat neurologic exam 6 hours after initial exam
CONFIRMATORY TESTS (OPTIONAL)

1. Conventional angiography: No intracerebral filling at level of carotid bifurcation or circle of Willis.
2. EEG: No electrical activity during 30 minutes of recording.
3. Transcranial Doppler: Small systolic peaks in early systole without diastolic flow or reverberating
flow, indicating very high vascular resistance associated with greatly increased intracranial pressure.
4. Technetium-99m brain scan: No uptake of isotope in brain parenchyma
5. Somatosensory evoked potentials: Bilateral absence of N20-P22 response with median nerve stim.
67 STUPOR, COMA, BRAIN DEATH
1.
1. Airway, breathing, circulation, Operational Definition
Lorazepam 0.1 mg/kg IV at 2mg/min) vitals Seizure persisting for > 5 min, or 2
2. Establish type and duration of seizures without return to baseline
Additional emergency drug therapy may not be required if seizures seizure(s), history of exacer- between each
stop and the cause of status epilepticus is rapidly corrected bating factors
Seizures continuing 3. Glucose, Metabolic panel, Mg, Causes
LFTs, CBC, Coags AED noncompliance
2.
4. IV Access Withdrawal syndrome (alcohol,
5. CT head barbiturate, baclofen, benzodiaze-
Fosphenytoin (20 mg/kg PE IV at 150 mg/min) 6. UTox, EtOH Level, UCG pines)
(while labs are being drawn, Structural injury (acute or chronic)
Seizures continuing proceed with status protocol) Metabolic abnormalities
Infections (exacerbate seizures in
3. patients with underlying structural
Fosphenytoin lesion; meningitis, encephalitis)
(additional 5-10 mg/kg IV PE) Over dose of drugs which lower
seizure threshold
Seizures continuing Chronic intractable epilepsy
4. Note: Protocol also applies in

Phenobarbital (20mg/kg IV at 50-75 mg/min) eclamptic seizures during pregnan-
or Valproic Acid (20-30 mg/kg IV at 20 mg/min) cy if magnesium sulfate fails
Seizures continuing
Proceed immediately to anesthesia with midazolam
or propofol if the patient develops status epilepti- 5.
cus while in the intensive care unit, has severe Phenobarbital
systemic disturbances (e.g. extreme hyperthermia), (additional 5-10 mg/kg)
or has seizures that have continued for more than
60 to 90 minutes. Seizures continuing
6.
Midazolam 0.2 mg/kg IV bolus, 0.1-0.4 mg/kg/hr maintenance
or Propofol 3-5 mg/kg IV bolus, 5-10 mg/kg/hr maintenance
or Pentobarbital 3-5 mg/kg IV bolus, 1 mg/kg/hr maintenance
STATUS EPILEPTICUS ALGORITHM
STATUS EPILEPTICUS
0 10 20 30 40 50 60 70 80 Time (minutes)
68
ECLAMPSIA
ONSET 20 weeks gestation to 4 weeks post partum DIAGNOSTIC CRITERIA FOR ECLAMPSIA
Acute proteinuria ( 5 grams/24 hrs)
TREATMENT Hypertension (> 160/110)
1. Control blood pressure CNS dysfunction:
Target BP: 140-155/90-105 severe persistent headache, gener-
Labetalol 10-20 mg IV, then double dose alized tonic clonic seizures (up to
q10min up to 80mg (max total dose 220 2%, self-limiting <2 min), visual
mg) disturbances (59%: blurred vision,
or Hydralazine 5 mg IV q20 min prn scotomata, hemianopsias, diplopia,
amaurosis), altered mental status,
2. Seizure Management CVA (15-20%)
seizures usually self limited Hepatocellular injury (transaminitis
Magnesium Sulfate 6 g IV bolus over 15 2x normal)
min, 2-3 g/hour IVPB Thrombocytopenia (<100,000 plate-
Target: cessation of seizures (guideline Mg lets/mm3)
level 4.8-8.4 mg/dL) Oliguria (<500 mL in 24 hours)
Advantages: reduces seizure recurrence by Pulmonary edema or cyanosis
33-50% as compared to Diazepam,
Phenytoin; reduces maternal death by
30% (Eclampsia Trial Collaborative Group)
Adverse effects: can precipitate myasthenic crisis, hypotension if used with calcium channel
blockers
Monitoring: presence of patellar reflex (loss of DTRs is the first manifestation of symptomatic
hypermagnesemia), respirations >12/min, urine output >100 mL in 4 hours
If continues to seize: Mg Sulfate 2g IV bolus over 15-20 minutes x2, then status epilepticus
protocol
3. Delivery within 24 hours
4. Post-partum
discontinue AED after 24-48 hours if improved (seizure recurrence risk is 2%)
diuresis >100 cc/hr x2 consecutive hours, >4L/day most accurate clinical indicators of resolution
69 HYPERTENSIVE ENCEPHALOPATHIES
POSTERIOR REVERSIBLE LEUKOENCEPHALOPATHY
PATHOGENESIS: Acute, severe hypertension beyond
limits of cerebral autoregulation leading to vasogenic PRECIPITATING FACTORS
edema Mean blood pressure >25% of base-
line
SIGNS AND SYMPTOMS Significant fluid overload (>10% of
Headaches: constant, non-localized, unrespon- baseline weight)
sive to analgesia Renal disease: Creatinine >1.8 mg/dL
Altered consciousness: mild somnolence to coma (160 mol/L)
Visual disturbances: hemianopia, visual neglect, Immunosuppressive therapies
visual hallucinations, cortical blindness (cyclosporine, cisplatin), even after
Seizures several months of exposure to drug
Papilledema with accompanying flame-shaped
retinal hemorrhages and exudates
NEUROIMAGING (MRI) FEATURES

Symmetric white matter edema in parieto-occipital regions
(posterior circulation has less sympathetic innervation and thus less protected from hypertension)
Calcarine and paramedian parts of occipital lobe are spared (unlike in bilateral PCA infarctions)
Involvement of the cerebellum and brainstem is common
Lesions of anterior cortex occur in more severe cases
Lesions cross vascular territories
Gyriform signal enhancement (with Gadolinium), reflecting disruption of the blood-brain barrier
Parenchymal hemorrhages
Hypo, iso-intense on diffusion-weighted imaging (DWI), and hyperintense on apparent diffusion coeffi-
cient (ADC) maps (unlike CVA, which is hyperintense on DWI and hypointense on ADC)
TREATMENT
1. Hypertension: lower diastolic pressure to about 100-105 mmHg within 2-6 hours (maximum initial fall
<25% of presenting value)
2. Seizures: start Phenytoin, and continue for 1-3 months as clinical and imaging findings resolve
A B C
MAGNETIC RESONANCE IMAGING demonstrates extensive signal changes on (A) T2-weighted imaging and (B)
fluid attenuation inversion recovery, that are diffusion negative (C).
HYPERTENSIVE ENCEPHALOPATHIES 70
CEREBRAL VENOUS THROMBOSIS
CLINICAL FEARURES
Isolated Intracranial Focal Syndrome Encephalopathy

Hypertension Syndrome Focal neurologic deficits (mono-, Altered sensorium
Headache (89%) hemiparesis in 37%) Coma
Vomiting Fluent aphasia (left transverse si-
Papilledema nus)
Visual problems Focal, generalized seizures (39-58%,
depending on presence of cortical
venous infarcts, hemorrhages)
NATURAL COURSE
79% recover completely
23% deteriorate PRO-COAGULANT WORK-UP
3% die (acutely) Antithrombin III
2-6% risk of recurrence Protein C
Protein S
PRECIPITATING FACTORS
Factor V Leiden mutation
Pregnancy and purperium
Lupus Anticoagulant and Anti-
Oral contraceptives Cardiolipin Antibodies
Malignancy Prothrombin G20210A mutation
Infections Homocysteine
Head injury, lumbar puncture
Pro-coagulant state
DIAGNOSIS
1. Head CT
MRI, MRV A. Venous infarct (DWI positive), B.
Normal in up to 30%, with usually non-specific
Isodense superior saggital sinus, C. MR venogram
findings
showing occluded superior sagittal sinus
Empty delta sign (lack of filling of confluence
of sinuses on contrast CT
Cord sign (liner hyperdensity over cortex repre-
senting thrombosed cortical vein)
2. MR Venography
<5 days: isointense on T1, hypointense on T2
>5 days, <1 month: hyperintense on T1 and T2
> 1 month: variable signal, can be isointense
A B
Cord Sign Hyperdense Straight Sinus Empty Delta

CEREBRAL VENOUS THROMBOSIS
Suspected Cerebral Venous Thrombosis
Acute neuro deficits + headache (89%), focal or general-
ized seizures (8-58%), altered sensorium / coma,
papilledema, visual loss, intracranial hemorrhage (39%)
Acute: MICU admission and

Signs of increased intracranial
Yes emergent management of
pressure? elevated ICP (see page 61)
1. Head CT to evaluate for venous

infarction, hemorrhage once
2. MR Venography or CT Venography stabilized
shows cerebral venous thrombosis
PREDICTORS OF 30-DAY MORTALITY IN

1. ANTICOAGULANT TREATMENT INTERNATIONAL STUDY OF CEREBRAL
Start Heparin IV drip (see protocol on VEIN AND DURAL THROMBOSIS (ISCVT)
page 69) and titrate to PTT 45-60
or Low Molecular Weight Heparin Depressed consciousness
180 anti-factor Xa international units/kg Altered mental status
day div bid Thrombosis of the deep venous
system
Note: presence of hemorrhagic venous
infarction is NOT contraindication for
Right hemisphere hemorrhage
anticoagulant treatment in CVT Posterior fossa lesions
2. SEIZURE PROPHYLAXIS PREDICTORS OF LONG-TERM POOR

Start AED in patients with supratentorial PROGNOSIS (ISCVT)
lesion (e.g. hemorrhage) with seizure at
presentation Central nervous system infection
Note: AED is not indicated otherwise. Any malignancy
Seizure recurrence is low (8%) after single Deep venous system thrombosis
seizure without cortical lesion, or cortical Hemorrhage on CT or MRI
lesion without seizures
GSC <9 on admission
Choose AED that is not hepatically cleared
to avoid interference with anticoagulants
Altered sensorium
(e.g. Keppra) Age >37 years
Male gender
Patient worsening despite anticoagu-

No
lation and supportive care?
Yes
CHRONIC ANTICOAGULATION Warfarin for

3. ENDOVASCULAR THROMBOLYSIS
3-6 months, target INR 2.0-3.0
Indicated for severe CVT, critically ill pa-
Continue AED treatment for up to 1 year if
tients. Risk of death with procedure ~38%
seizure at onset with cortical lesion
(ISCVT Trial)
(otherwise risk of epilepsy 5-11%)
CEREBRAL VENOUS THROMBOSIS 72

HEPARIN USE GUIDELINES
1. PRIOR TO HEPARIN THERAPY

Heparin is used only with attending approval
Verify initial PT/PTT, CBC
Verify absence of intracerebral hemorrhage with non-contrast head CT (contraindication to Hepa-
rin with the exception of venous sinus thrombosis)
Check for contraindications (active bleeding, infective endocarditis, BP >180/105, thrombocytope-
nia, heparin allergy)
Verify guaiac negative
2. INITIATING THERAPY
NO BOLUS
Most patients: 12 units/kg/hr, see
attached table (Note: maximum initial HEPARIN HEPARIN RATE FOR
WEIGHT
dose is 1000units/hour) DOSE 2,500 units/25ccNS
Adjust initial dose based on clinical fac- lbs kg units/kg/hr cc/hr
tors (renal failure, poor nutrition etc.) 88 40 480 4.8
Monitor PTT 6 hours after dose initiation 99 45 540 5.4
or dose change (except as noted in #3).
110 50 600 6.0
If no change, monitor PTT each morning
121 55 660 6.6
and CBC every day.
132 60 720 7.2
Look for dropping platelets and hemato-
143 65 780 7.8
crit etc.
154 70 840 8.4
165 75 900 9.0
3. ADJUSTING THERAPY
176 80 960 9.6
Target PTT is 1.5 times control
187 85 1000 10.0
45-60 s: usually acceptable
198 90 1000 10.0
60-70 s: gray zone, and should be dis- 209 95 1000 10.0
cussed with your attending
220 100 1000 10.0
70-90 s: hold for 2 hours, restart at 231 105 1000 10.0
least 200 u/hr lower.
242 110 1000 10.0
>90 s: hold infusion, check PTT every 2h
253 115 1000 10.0
until 60 s, restart at lower dose based
on observations.
4. CAUTIONS
If a patient deteriorates neurologically or has a possible source of bleeding, STOP the heparin be-
fore initiation of the workup (head CT etc.) and restart only after intracranial or systemic hemor-
rhage has been ruled out.
For PTT >90 s, Do NOT RESTART until PTT is 60 s.
PTTs are drawn by the Neurology team. All PTTs are STAT.
If a patient leaves the floor, STOP the heparin until the patient returns unless the patient is accom-
panied by a resident.
73 CEREBRAL VENOUS THROMBOSIS

Signs, Symptoms Of Acute Cord / Cauda Compression
back pain (90%), weakness and sensory level (77%), gait problems (31%),
bladder and bowel dysregulation (38%)
NEOPLASTIC TRAUMATIC
CAUSES CRITERIA FOR STEROID USE:

Metastatic: breast, prostate, 1. Spinal cord injury (no in-
lung, renal cell carcinoma, mye- volvement of cauda
equina)
loma, colon cancer
2. Exclude penetrating in-
Intradural, Extramedullary: juries, such as stabbing
nerve sheath (neurofibromas of gunshot wounds
and schwannomas), meningio- 3. <8 hours from time of
injury
mas
Intramedullary: ependymomas,
TREATMENT
Vertebral break on CT astrocytomas
of spine with cord
1. Methylprednisolone
transection Bolus: 30-mg/kg IV over 15
TREATMENT min
1. Corticosteroids Maintenance:
Severe neurologic deficitshigh- If <3 hours from injury 5.4
mg/kg/h IV x23 hours
dose corticosteroids: Dexametha-
If 3-8 hours from injury
sone 96mg IV bolus, followed by 5.4 mg/kg/h IV x47 hours
24 mg q6h x3 days, then tapered
over 10 days 2. Blood Pressure
Pain, minimal neurologic deficits Maintain MAP >85 x7 days
(improves neuro outcome)
moderate-dose corticosteroids:
Dexamethasone 10mg IV bolus,
followed by 4mg q6h po
Acute trauma and cord 2. Surgery +/- Radiotherapy

signal change (T2 hyperin-
tensity) indicating edema. Radioresistant tumors, limited
disease burden, favorable prog-
nosis: Radical decompressive
resection followed by radiation
therapy 14 days after surgery (30
Gy in 10 fractions) 30% of
paraparetics and 3-6% of para-
plegics regain ability to walk; 20- FAVORABLE PROGNOSTIC
40% regain bladder control FACTORS
Extensive systemic disease, se- Radiosensitive tumors
vere fixed neurologic deficits: (e.g. lymphoma, myelo-
Radiation therapy alone for ma, breast)
symptom paliation
Slowly developing motor
3. Supportive Care deficit (>1-2 weeks)
Pain management Absence of visceral metas-
DVT prophylaxis tases
Extramedullary mass Aggressive bowel regimen Ambulatory status
compressing the cord.
CORD, CAUDA EQUINA COMPRESSION 74

MYASTHETIC CRISIS
DEFINITION Weakness from acquired myasthenia DIAGNOSIS OF MYASTHENIA
gravis that is severe enough to necessitate intubation, or delay Ice Pack Test: Used in awake pa-
extubation following surgery
tients with ptosis. Place ice pack
on closed eyelid for 2 minutes
PRECIPITATING FACTORS
then look for improvement in
Infection
ptosis. Sensitivity 80%
Surgery
Ach-Receptor Antibodies: sensitivity
Tapering immunosuppressants
up to 93%, specificity 95%
Drugs
MuSK Antibodies: in 38-50% of
MANAGEMENT AChR-Ab negative myasthenia
1. Admit to Intensive care unit Repetitive Nerve Stimulation shows
2. Measure FVC q2 hours if respiratory status is deteriorating progressive decrement (>10%) in
3. Indications for intubation: compound muscle action potential
FVC < 15 mL/kg body weight
(CMAP)
Single-fiber EMG shows increased
Declining forced vital capacity (FVC) approaching 15
jitter (variability in time be-
mL/kg
tween action potentials); 95%
Declining negative inspiratory force (NIF)
sensitive
approaching 25 cm H2O
Respiratory distress
Difficulty handling oral secretions, swallowing, or speaking
4. Withdraw anticholinesterase medications to reduce airway secretions in patients who are intubated
5. Begin rapid therapy: Plasmapheresis or IVIG
6. Begin immunomodulating therapy: High dose corticosteroids (eg, Prednisone 60-80 mg/day). Note that
glucocorticoids can cause serious (in 50%), transient (lasting 5 days) worsening 5-10 days after initiation.
Consider azathioprine, mycophenolate mofetil, or cyclosporine if steroids are contraindicated.
COMPARISON OF IVIG AND PLASMAPHERESIS

FEATURE PLASMAPHERESIS IVIG
Removes acetylcholine receptor antibodies Anti-diotypic antibodies modulating
Mechanism
from the circulation, works more quickly expression, function of Fc receptors
5 exchange treatments of 3 to 5 liters over
Usual adult dose 400 mg/kg daily for five days
10-14 days
Onset of effect 1-7 days 1-2 weeks
Maximal effect 1-3 weeks 1-3 weeks
Efficacy No difference between treatments (Myasthenia Gr. Clinical Study Group Trial)
Headache, fluid overload, aseptic
Line infection, hypotension, thromboembo-
Adverse reactions meningitis, rash, acute renal failure,
lism, sepsis
hyperviscosity leading to stroke (rare)
COMMONLY USED THERAPIES FOR MYASTHENIA DRUGS EXACERBATING MYASTHE-

THERAPY ONSET MAXIMAL EFFECT NIA anticholinergics, aminogly-
Symptomatic cosides, fluoroquinolones, anticon-
Pyridostigmine 10-15 min 2 hours vulsants (phenytoin, carbamaze-
Chronic Immunotherapies pine, lithium), neuroleptics (phe-
Prednisone 2-3 weeks 5-6 months
nothiazines, clozapine), cardiovas-
Azathioprine 4- 10 months 1-2 years
Mycophenolate mofetil 2-4 months 5-6 months cular agents (-blockers, quinidine,
Cyclosporine 2-4 months 7 months procainamide, calcium channel
Surgery blockers), neuromuscular blockers
Thymectomy 1-10 years 1-10 years
75 MYASTHENIA GRAVIS
MANAGEMENT OF GUILLAIN BARRE SYNDROMES
DIAGNOSTIC CRITERIA CLINICAL COURSE

Clinical: Weakness in >1 limb, Progression: 74% progress for up to 2 weeks
progressing over days4 weeks Plateau phase: lasting 2-4 weeks
to involve all limbs, trunk, bulbar/ Recovery of function
facial muscles (50%), and external Relapse: occurs in 10%, and 2% develop chronic inflam-
opthalmoplegia (15%) matory demyelinating polyradiculoneuropathy (CIDP)
Factors associated with poor prognosis: older age,
Supporting features: symmetry,
rapid onset (<7 days), need for ventilatory support,
mild sensory, no fever at onset,
average distal motor response amplitude reduction to
autonomic dysfunction (30%),
<20% of normal, preceding diarrheal illness
albuminocytologic dissociation
normal WBC count in CSF but
high protein (90%, after 1 week)
1. SUPPORTIVE CARE
Consider admission to MICU
Respiratory Failure (30%)
Monitor Vital Capacity (VC) and Negative Inspiratory Force (NIF)
Predictors of necessity mechanical ventilation:
Time of onset to admission <7 days Impending respiratory failure criteria:
Inability to cough, stand Forced vital capacity <20 mL/kg
Inability to lift the elbows, head Maximum inspiratory pressure <30 cm H2O
Liver enzyme increases Maximum expiratory pressure <40 cm H2O
Autonomic Dysfunction (70%)
Symptoms: Sinus tachycardia (37%)
Paroxysmal hypertension alternating with hypotension (24%)
Orthostatic hypotension (19%)
Bradycardia, asystole (4%) and other cardiac arrhythmias
Urinary retention and adynamic ileus
Loss of sweating
Close cardiorespiratory monitoring
Check for orthostatic hypotension
Maintain intravascular volume
Avoid drugs with hypotensive side effects
Neuropathic Pain (40-50%)
May start Neurontin 300mg q8h and titrate to a max of 3600mg/day
Carbamazepine and NSAIDs may also be tried
Use opiods with care in patients with autonomic dysfunction (monitor for ileus)
2. DISEASE MODIFYING TREATMENT

IVIG is equivalent to Plasmapheresis
Treatment with IVIG or plasma exchange shortens period to recovery by 40-50%
Combining the two treatments is not beneficial
No role for steroids (glucocorticoids have been found ineffective)
Check IgA levels before starting IVIG as IgA deficiency (although rare) can lead to anaphylaxis.
3. REHABILITATION
GUILLAIN-BARRE SYNDROMES 76
BOTULISM
SOURCES OF ORGANISM
Wound: injection drug users
Food-borne: home canned foods (12 to 36 hours after ingestion)
Infant botulism: ingestion of raw honey and soil containing C. botulinum spores
SIGNS AND SYMPTOMS
acute bilateral cranial neuropathies (fixed pupillary dilation and palsies of cranial nerves III, IV,
and VI)
symmetric descending weakness
absence of fever
autonomic synapses are unaffected
no sensory deficits
urinary retention and constipation (smooth muscle paralysis)
diaphragmatic paralysis, upper airway compromise
normal CSF
DIAGNOSIS
serum analysis for toxin
EMG
TREATMENT
1. Admit to MICU
2. Intubate if indicated
3. Administer antitoxin
CRITICAL ILLNESS POLYNEUROPATHY, MYOPATHY
CRITICAL ILLNESS MYOPATHY VS NEUROPATHY

FEATURE NEUROPATHY MYOPATHY
Limb weakness and atrophy, decreased
Flaccid quadriparesis, proximal > distal
Clinical reflexes, loss of peripheral sensation, pre-
Failure to wean from ventilator
served cranial nerve function
Glucocorticoid use, paralytic agents,
Neurologic manifestation of systemic in-
Risk Factors higher illness severity index, hypergly-
flammatory response syndrome (SIRS)
cemia, hyperthyroidism, sepsis
Elevated CK: 1500-7400 U/L, peaks 4
Normal CSF protein
Lab Results days after steroid treatment and per-
Normal CK
sists for 16 days
Sensory and motor amplitudes >80%
Sensory and motor amplitudes <80% of
of normal in 2 nerves
NCS/EMG normal in 2 nerves
Muscle inexcitability on direct muscle
Direct muscle stim.
stimulation
Muscle Biopsy Neurogenic atrophy Myopathy with myosin loss
Reversible in weeks to months

Treatment
Discontinuation of glucocorticoids and treatment of medical conditions
77 CRITICAL ILLNESS MYOPATHY / NEUROPATHY AND BOTULISM

NEUROLEPTIC MALIGNANT SYNDROME SEROTONIN SYNDROME
SIGNS AND SYMPTOMS PROGNOSIS (NMS) SIGNS AND SYMPTOMS

1. Mental status change: 1. Mental status change: agi-
Resolution: within 2 weeks
agitated delirium, confu- tated delirium, restlessness,
sion, encephalopathy (82%) Mortality: 10-20% (50% disorientation
2. Muscular rigidity: lead with myoglobinuria and 2. Neuromuscular hyperreactivi-
pipe, tremor (up to 92%) renal failure) ty: tremor, rigidity, myoclo-
3. Hyperthermia: >38C Recurrence: 10-90%, in- nus, rigidity, hyperreflexia
(87%), >40C (40%) (+Babinski and clonus), dilat-
creased by early (<2 weeks)
4. Autonomic instability: ed pupils
tachycardia (88%), labile BP resumption of neuroleptics, 3. Autonomic instability: di-
(77%), tachypnea (73%), lithium use aphoresis, hypertension,
diaphoresis PROGNOSIS (SS) diarrhea, vomiting
Resolves within 24 hours
DIAGNOSTIS HUNTER TOXICITY DIAGNOSTIC
Serum CK: >1,000 IU/L CRITERIA
(as high as 100,000 IU/L) 80% sensitive, 97% specific
Leukocytosis: 10,000 - 40,000/mm3
Myoglobinuric acute renal failure from Serotonergic use and at least one of following:
rhabdomyolysis Spontaneous clonus
Lumbar puncture: usually normal, but can Inducible clonus plus agitation or diaphore-
show elevated protein (37%) sis
Imaging (MRI, CT), EEG to exclude other Ocular clonus plus agitation or diaphoresis
pathologies Tremor and hyperreflexia
Hypertonia
TREATMENT Temp >38C plus ocular clonus or inducible
1. Admit to MICU clonus
2. Discontinue neuroleptic agent or precipi-
tating drug TREATMENT
3. Dantrolene 0.25-2 mg/kg IV q6-12 hours 1. Admit to MICU
(max dose 10 mg/kg/day) 2. Discontinue serotonergic agent or precipi-
Advantages: reduction of heat produc- tating drug (e.g. MAOIs)
tion, rigidity; effects within minutes 3. Sedation with benzodiazepines
Adverse effects: hepatotoxicity 4. Supportive care (including management of
Duration: 10 days, followed by slow autonomic instability, cooling)
taper 5. Cyptoheptadine 12 mg PO, then 2mg q2 hours
4. Bromocriptine 2.5mg PO q6-8 hours (max until clinical response
dose 40mg/day) Indication: sedation and supportive care
or Amantidine 100mg PO q12 hours (max failed
200mg q12 hours)
Advantages: restores lost dopaminergic
tone
Duration: 10 days, followed by slow
taper
5. Supportive care (avoid lasting sedatives; use
cooling blankets and ice for fever; control
agitation with small doses of short-active
benzodiazepines, eg. Lorezepam 0.5-1.0mg
prn)
NEUROLEPTIC MALIGNANT AND SEROTONIN SYNDROMES 78

APPROACH TO MENINGITIS, ENCEPHALITIS
Headache, Nuchal Ridigity, Fever
79 INTRACRANIAL INFECTIONS
APPROACH TO MENINGITIS, ENCEPHALITIS (CONTINUED)
CSF ANALYSIS
GLUCOSE (mg/dL)
PROTEIN (mg/dL) WBC COUNT (cells/L)
Normal is 2/3 plasma gluc
> 1000
Bacterial
<10 > 250 (neutrophilic
meningitis
predominance)
5-100
Fungal meningitis
<40 > 250 (lymphocytic
(including TB)
predominance)
< 100
Viral meningitis
10-45 50-250 (lymphocytic
encephalitis
predominance)
INTRACRANIAL INFECTIONS 80
ACUTE DYSTONIC REACTION
DEFINITION adverse extrapyramidal effects manifesting as sustained or intermittent, painful

muscular spasms and producing twisting abnormal postures
RISK FACTORS
Family history of dystonia
Recent cocaine or alcohol use
Use of potent dopamine D2 receptor antagonist (e.g. fluphenazine, haloperidol)
Use of antiemetics (e.g. Reglan)
CLINICAL MANIFESTATION
Location: Neck dystonia (30%)
Tongue dystonia (17%)
Jaw dystonia (15%)
Oculogyric crisis (eyes rolling back and neck arching) (6%)
Opisthotonus (body arching) (5%)
Duration: minutes to hours
Onset: within 48 hours of neuroleptic use (50%), within 5 days (90%)
DIFFERENTIAL DIAGNOSIS
Hypomagnesemia
Hypocalcemia
Stroke
Toxicity (Phenytoin, Valproate, Carbamazepine, Anticholinergic)
Tetanus
Seizure
Catatonia
TREATMENT
1. Discontinue offending agent
2. Secure airway (rarely needed with laryngeal and pharyngeal dystonia)
3. Benztropine 2 mg IV/IM, repeat prn (IV has most rapid onset, within 10 min)
or Diphenhydramine 50-100 mg IV/IM, repeat prn (reduce dose in the elderly and monitor for
excessive sedation)
4. If dystonic reaction persist or anticholinergics are contraindicated:
Diazepam 2.5-10 mg IV slow push (or other benzodiazepines)
4. Continue x24-48 hours to prevent relapse (depending on half-life of neuroleptic)
Benztropine 1-2 mg PO bid
Diphenhydramine 25-50 mg PO qid
Trihexyphenidyl 2 mg PO bid
81 DYSTONIA
SEIZURE TYPES AND LOCALIZATION
SEIZURE TYPES AND FEATURES
SEIZURE APPROX. ALTERATION OF TYPICAL CLINICAL POST-ICTAL TYPICAL ICTAL EEG
TYPE DURATION CONSCIOUSNESS FEATURES CONFUSION
Simple 5-30 sec No Motor; somatosen- No Normal in most;
partial sory; special senso- focal spikes or rhyth-
ry; psychic; auto- mic waveforms
nomic
Complex 1-3 min Yes Often preceded by Yes Focal rhythmic activ-
partial simple partial; star- ity spreading to
ing; loss of aware- involve one or both
ness; automatisms hemispheres
Secondari- 1-2 min Yes Simple or complex Yes (severe) Focal rhythmic activ-
ly general- partial onset; head ity, spreading to
ized tonic- version; asymmetric involve both hemi-
clonic tonic posture; gen- spheres symmetri-
eralized clonus cally
Primary 1-2 min Yes Sudden loss of con- Yes (severe) Low-voltage rhyth-
general- sciousness; ictal cry; mic activity pro-
ized tonic- tonic phase; clonic gressing to general-
clonic phase ized high amplitude
spikes
Typical 5-20 sec Yes Staring; eyelid No Generalized 3-Hz
Absence fluttering spike-and-wave
Atypical 15-45 sec Yes Staring, clonus, Yes Generalized <2.5-Hz
absence myoclonus, atonic spike-and-wave
Myoclonic 100-200 No Generalized rapid No Generalized pol-
ms jerks of limbs yspikes and wave
Tonic 5-20 sec Yes Sustained posture of No Low-voltage paroxys-
limbs or minimal mal fast activity
Atonic 5-10 sec Maybe Sudden loss of tone No Variable
or minimal
LOCALIZATION OF SEIZURE FOCUS
ICTAL FEATURE LATERALITY LOCALIZATION
Contralat. in frontal seizures; contrala-
Eye deviation Frontal or occipital
teral or ipsilateral in occipital seizures
Early nonforced head turn Ipsilateral Temporal
Late forced head turn Contralateral Frontal
Focal clonus Contralateral Frontal
Temporal (spread to basal gan-
Dystonic limb Contralateral
glia)
Tonic limb Contralateral Frontal
Motionless limb Contralateral Temporal or frontal
Asymmetric tonic, fencing
Contralateral Frontal, supplementary motor
postures
Figure 4 sign Contralateral to extended limb
Oroalimentary Automatisms Temporal
Limb automatisms (unilateral) Ipsilateral Temporal
Hyperkinetic automatisms,
Frontal
pedaling, bicycling
Speech arrest Dominant hemisphere Temporal or frontal
POST-ICTAL FEATURES
Todds paresis Contralateral
Nose wiping Ipsilateral Temporal
Aphasia Dominant hemisphere
Confusion Temporal greater than frontal
83 EPILEPSY
CLASSIFICATION OF EPILEPSIES
Localization-
Generalized Other Syndromes
Related
IDIOPATHIC IDIOPATHIC Neonatal seizures

Benign childhood Benign neonatal Severe myoclonic
epilepsy with cen- familial convulsions epilepsy of child-
trotemporal spikes Benign neonatal hood
Childhood epilepsy convulsions Epilepsy with con-
with occipital parox- Benign myoclonic tinuous spike-waves
ysms epilepsy in infancy during slow-wave
Primary reading Childhood absence sleep
epilepsy Juvenile absence Acquired epileptic
Juvenile myoclonic aphasia (Landau-
epilepsy Kleffner syndrome)
Epilepsies with grand
SYMPTOMATIC
mal seizures on
Mesial temporal lobe awakening
epilepsy with hippo- Generalized epilepsy
campal sclerosis with febrile seizures
Autosomal dominant plus
nocturnal frontal
lobe epilepsy
Autosomal dominant
temporal lobe epilep- SYMPTOMATIC
sy with auditory West syndrome
features (infantile spasms)
Temporal, parietal, Lennox-Gastaut
frontal, occipital Epilepsy with myo-
epilepsies clonic-astatic seizures
Chronic progressive Epilepsy with myo-
epilepsia partialis clonic absences
continua of child-
Progressive myoclon-
hood
ic epilepsies
A B
MAGNETIC RESONANCE IMAGING IN EPILEPSY T1-weighted images showing (A) abnormal double cortex
(subcortical band heterotopia), (B) right mesial temporal sclerosis (atrophy and signal changes in
hippocampus and atrophy of temporal lobe)
EPILEPSY 84
85
NAME MECHANISM INDICATIONS DOSING HALF-LIFE, METAB. ADVERSE PREG.
LEVEL
PHENYTOIN Narrow spec- Focal and unclassifia- Load: 15-20mg/kg PO div 12-29h Hepatic Serious: Cardiac con- Class D
(Dilantin) trum ble seizures in 3 doses 2-4h apart Level: 10-20 Enzyme in- duction abnormalities, Lactation:
Blocks neu- Aggravates: general- Maintenance: 300-400 (correct for ducer Stevens-Johnson or toxic probably
ronal voltage- ized epilepsies mg per day PO div qd-tid Albumin) epidermal necrolysis safe
gated sodium (myoclonus, absence) Max: 400 mg/dose (4/10k), hepatotoxicity,
channels drug-induced lupus,
osteopenia
Common: Dizziness,
ataxia, gingival hyper-
plasia
ANTIEPILEPTIC MEDICATIONS
FOSPHENYTOIN Same as Pheny- Status epilepticus, Load: 15-20 mg PE/kg IV Prodrug, Same as Phenytoin Same as
(Cerebyx) toin short term treatment @ <150 mg/min infusion converted to Lesser incidence of mus- phenytoin
of focal seizures Maintenance: 4-6 mg Phenytoin cle necrosis (purple glove
PE/kg/day IV div qd-tid syndrome)
CARBAMAZEPINE Narrow spec- Focal seizures, sec- Start: 200mg po bid, 25-65h Hepatic Serious: Agranulo- Class D
(Tegretol, Tegretol trum ondary generalized incr. 200 mg/day qwk (initial dos- Enzyme in- cytosis (1/200k), aplastic Lactation:
XR, Carbatrol) Bind voltage- seizures Max: 1600mg day es) ducer anemia (1/500k), hepatic probably
gated Na chan- Aggravates: general- 12-17h Autoinduction failure, Stevens-Johnson, safe
nels and pro- ized seizures, myoclo- Monitoring: Sodium, (repeat Active metab- hyponatremia, leukope-
longs their nus, absence seizures LFTs, CBC doses) olite nia (7%)
inactivated Common: Dizziness,
phase Level: 8-12 diplopia, ataxia, weight
mcg/mL gain, sedation
OXCARBAZEPINE Narrow spec- Focal seizures, sec- Start: 300mg PO bid, 2h (9h active Hepatic Serious: Hyponatremia Class C
(Trileptal) trum ondary generalized increase by max 600mg/ metabolite Only mild (SIADH, 23%), leukope- Lactation:
Similar to seizures day qweek monohy- enzyme in- nia, cardiac arrhythmias, safety
Cabamazepine Aggravates: general- Max: 2400 mg/day droxy- duction hepatitis unknown
ized seizures, myoclo- carbamaze- Common: same as Car-
nus, absence seizures pine) bamazepine
LAMOTRIGINE Broad spectrum Focal and primarily or Start: 25mg PO bid, 25-28h Hepatic (90%) Serious: Stevens- Class C
(Lamictal) Blocks voltage- secondary generalized increase by 25-50 mg/ 14h (+ en- Clearance Johnson (1/1000), hyper- Lactation:
gated Na chan- seizures; add-on in day q1-2wk zyme- increases sensitivity, multiorgan unsafe
nels, selective Lennox-Gastaut syn- Max: 250 mg PO bid inducers) during preg- failure
for glutamate , drome 59h (+ nancy Common: tremor, in-
aspartate neu- Aggravates: myoclo- Valproate) somnia, headache
rons nus
LEVETIRACETAM Broad spectrum Add-on therapy for Start: 500mg PO q12, 6-8h Excreted un- Serious: Depression, Class C
(Keppra) Binds specifical- focal and secondarily incr by 1000mg/day changed in psychosis (3%) Lactation:
ly with synaptic generalized seizures; q2wk urine Common: Sedation probably
vesicle protein idiopathic generalized Max: 3000 mg/day (10%), confusion, asthe- safe
SVA2 implicated tonic-clonic convul- Renal: CrCl 50-80: 500- nia
in epileptogen- sions, juvenile myo- 1000 mg q12h; CrCl 30-
icity, alters clonic epilepsy 50: 250-750 mg q12h;
vesicle fusion CrCl <30: 250-500 mg
q12h; HD: 500-1000 mg
q24h, give 250-500 mg
supplement
TOPIRAMATE Broad spectrum Add-on therapy for Start: 25 mg PO bid 15-20h Hepatic, mini- Serious: metabolic acido- Class C
(Topamax) Blocks voltage- focal and secondarily x1wk, incr. 50 mg/day mally sis (44%, due to renal Lactation:
gated Na chan- generalized seizures, qwk until 100 mg PO bid, Excreted in bicarbonate loss), neph- safety
nels, enhances Lennox-Gastaut syn- then incr. 100 mg/day urine largely rolithiasis (1.5%), acute unknown
GABA inhibition drome qwk until 200 mg PO bid unchanged glaucoma, hypohidrosis
via GABA (A) Max: 400 mg/day (60%) Common: paresthesias,
receptors, an- Weak carbonic psychomotor slowing,
tagonizes anhydrase weight loss
NMDA gluta- inhibitor
mate receptor
VALPROIC ACID Broad spectrum All types Start: 15 mg/kg/day PO 16h Hepatic Serious: Hepatotoxicity Class D
(Depakene = Blocks voltage- div qd-tid, incr. 5-10 mg/ Level: 50- Weak enzyme (1/20,000), hyperammo- Lactation:
capsule and sy- gated sodium kg/day q7 days; decr. 100 mg/dL inhibitor nemic encephalopathy, probably
rop, Depacon = channels, in- start dose in elderly pts; Protein-bound pancreatitis (1/3000), safe
IV, Depakote ER = creases presyn- Max: 60 mg/kg/day and displaces pancytopenia, reversible
qd, Depakote = aptic GABA Phenytoin parkinsonism (5%)
bid) levels, blocks T- from its bind- Common: weight gain,
type calcium ing sites alopecia, thrombocy-
channels top.enia
PHENOBARBITAL Broad spectrum All types, except Start: 300-800 mg IV or 79h Hepatic (75%) Serious: TTP, respiratory Class D
(Lumital) Binds GABA (A) absence 15-20 mg/kg Level: 15-45 Renal (25%) depression, megalo- Lactation:
receptor, ex- Max: 60 mg PO bid-tid mcg/mL blastic anemia safety
tending GABA- Renal: CrCl <10: give q12- Common: drowsiness unknown
mediated chlo- 16h; HD: give dose after
ride opening, dialysis
causing neu-
ronal hyperpo-
86
larization
87
LEVEL
GABAPENTIN Narrow spectrum Add-on therapy Start: 300 mg PO qd day 1, 5-7h Excreted in Serious: none known Class C
(Neurontin) Binds to auxillary for partial sei- bid day 2, then tid; urine largely Common: sedation, Lactation:
alpha-2-delta zures Max: 3600 mg/day; unchanged drowsiness, dizziness safety
subunit of voltage Renal: CrCl 10-50: give qd- unknown
-dependent Ca Aggravates: bid; CrCl <10: give q48h; HD:
channel generalized give supplement
seizures, myoclo-
nus
ZONISAMIDE Broad spectrum Add-on therapy Start: 50 mg PO qd, increase 60-70h Hepatic Serious: Aplastic ane- Class C
(Zonegran) Blocks voltage- for partial, tonic by 50mg/day q2wk 27-36h (with Weak car- mia, renal calculi (4%),
gated Na channels clonic, myoclonic Max: 600 mg/day enzyme bonic anhy- rash (2%), Stevens-
and vaoltage- seizures Renal: CrCl 50-80: caution inducers) drase inhibi- Johnson, hypohidrosis
gated T type advised, titrate slowly; CrCl Level: 10-40 tor Common: Drowsiness,
calcium channels <50: contraindicated mcg/L cognitive slowing,
weight loss
FELBAMATE Broad spectrum Partial seizures, Start: 1200mg/day PO div tid- 20-23h Hepatic Serious: Aplastic ane- Class C
(Felbatrol) Blocks NMDA Lennox-Gastaut qid, incr. 600 mg/day q2wk (50%) mia (1/3000), hepato- Lactation:
glutamate chan- syndrome Max: 3600 mg/day Unchanged toxicity (1/10000) possibly
nels, augments Renal: 50% of dose excretion in Common: weight loss, unsafe
GABA function urine GI disturbance, insom-
Inhibits nia
Phenytoin,
induces
Carbamaze-
pine
LACOSAMIDE Narrow spectrum Add-on in partial Start: 50 mg PO/IV bid, incr. 13h Hepatic Serious: Hypersensitivi- Class C
(Vimpat) Enhances slow seizures by 100 mg/day qwk; ty reaction, multi-organ Lactation:
inactivation of Max: 400 mg/day (300 mg/ failure, cardiac conduc- safety
voltage-gated Na day with mild-mod hepatic tion abnormalities unknown
channels, stabiliz- impairment)
es memebranes, Renal: CrCl <30: max 300
binds CRMP2 mg/day; HD: give 50% usual
involved in dose as supplement
epilleptogenensis
LEVEL
TIAGABIN Narrow spectrum Add-on therapy Start: 4 mg PO qd, increase 7-9h Hepatic Serious: Pro-convulsive Class C
(Gabitril) Inhibits GABA for partial sei- by 4-8 mg/day qweek (2-5h with effect, non-convulsive Lactation:
reuptake into zures Max: 56 mg/day, div bid-qid hepatic status epilepticus (5%) safety
presynaptic termi- enzyme- Common: Drowsiness, unknown
nal and glia inducing dizziness, nausea, trem-
agents) or
CLONAZEPAM Broad spectrum Clonazepam: Start: 0.5-1.0 mg PO tid, in- 20-50h Hepatic Serious: Withdrawal Class D
(Klonopin) Bind GABA (B), add-on in myo- crease 0.5-1.0 mg/day q3d seizures, tachyphylaxis, Lactation:
enhance inhibition clonic, atonic Max: 20 mg/day, div tid rapid tolerance, hepa- safety
by increasing seizures totoxicity, respiratory unknown
frequency of depression
GABA-mediated Common: drowsiness,
chloride channel irritability, ataxia, de-
openings pression
PREGABALIN Narrow spectrum Add-on therapy Start: 150 mg/day PO (div bid- 6h Unchanged Serious: none known Class C
(Lyrica) Binds to alpha-2- for partial sei- tid), double dose qweek excretion in Common: sedation, Lactation:
delta subunit of zures Max: 600 mg/day, div bid-tid urine drowsiness, dizziness, safety
voltage-gated Ca weight gait, peripheral unknown
channel; modu- edema, euphoria
lates glutamate,
norepinephrine,
substance P trans-
mission
RUFINAMIDE Broad spectrum Adjunctive thera- Start: 200-400 mg PO bid, 6-10h Hepatic Serious: QT shortening, Class C
(Banzel) Prolongation of py for partial incr. by 400-800 mg/day qod suicidality, leukopenia, Lactation:
inactivation of seizures and in to 1600 mg PO bid hypersensitivity rxn safety
sodium channels Lennox-Gastaut Max: 3200 mg/day Common: somnolence, unknown
syndrome headache, dizziness,
tremor
88
LOCALIZATION IN EEG a-b Phase reversal: Imagine a negative dis-
b-c charge coming from c (e.g. -100 uV). As it
A disperses, both b and d are less negative in
relation to c (e.g. -80 uV).
c-d b - c = -80 - (-100) = +20 (downward)
d-e c - d = -100 - (-80) = -20 (upward)
B
Where phase reverses, discharge originates
from a common electrode (in this case c)
a-b Phase cancellation: Now imagine a nega-

EEG measures difference in
tive discharge coming from midway be-
potential between two elec-
b-c tween b and c. Both electrodes register the
trodes. By convention, nega-
same potential and when subtracted, yield 0
tive difference in potential c-d
(straight line). Thus, the phase cancellation
registers as upward deflec-
d-e principle allows localization of discharge
tion (A), and positive as
originating between two electrodes.
downward (B).
Monopolar montages com- End-of-chain: Now imagine a negative

pare each electrode to a a-b discharge coming from a (-100 uV). Hypo-
reference. Bipolar montages thetically, b registers -60 uV, c -30 uV, d -10
b-c
compare each electrode to an uV, e -10 uV. When subtracting the elec-
c-d trodes as above, the last line is isoelectric (d
adjacent electrode (see page
87 for examples). d-e - e = 0). Note: same tracing will correspond
to a positive discharge coming from e. So,
both a and e are ends of chain.
Alpha frequency (8-13 Hz)
Beta frequency (>13 Hz)
Theta frequency (4-7 Hz)
Delta frequency (<4 Hz)
EEG FREQUENCIES (1) Alpha rhythm is posterior (occipital lobes) in awake individuals and attenuates with
eye opening. Age of patient = alpha frequency + 2, and should be at least 3 in a 3 month old. (2) Beta fre-
quency is frontocentral and normal in awake individuals. It may be accentuated with certain medications.
Together alpha and beta make up normal anterior-to-posterior gradient. (3), (4) Theta, delta waves indicate
slowing of EEG frequencies, which may be normal during sleep, but abnormal if consistently asymmetric
(possibly indicative of structural lesion).
89 APPROACH TO EEG
EEG MONTAGES, WAVE MORPHOLOGY
Long (Saggital) Bipolar

includes several anterior-
to-posterior lines of elec-
trodes. This montage
accentuates discharges
that disperse in rostra-
caudal direction (e.g.
seizure focus at F4 send-
ing discharges to the
occiput).
Transverse Bipolar in-

cludes several transverse
ipsilateral-to-contralateral
arrangements of elec-
trodes. This montage
accentuates discharges
that disperse mostly in
ipsilateral to contralateral
direction (e.g. seizure
focus at F7 sending dis-
charges across corpus
callosum).
Spike (<70 ms)
Slow wave
Spike-and-wave
Polyspike-and-wave
INTERICTAL EPILEPTIFORM DISCHARGES are charac-

terized as paroxysmal, distinct from background, hav-
ing abrupt change in polarity, duration of <200 ms, and
physiologic field.
APPROACH TO EEG 90
ONSET OF LOCALIZATION-RELATED SEIZURE Notice a low-voltage rhythm developing in the right hemisphere.
The discharge gradually increases in amplitude and declines in frequency. Left hemisphere begins to partici-
pate during the seventh second.
NON-CONVULSIVE STATUS EPILEPTICUS Periodic pattern of generalized bi and even triphasic sharp wave
discharges with a bifrontal preponderance.
91 APPROACH TO EEG
PARTIAL CONDUCTION BLOCK COMPLETE CONDUCTION BLOCK
H REFLEX represents activation of sensory muscle

spindles and subsequent signal traveling to spinal
cord and synapsing with anterior horn cells and
stimulating contraction of muscle. The H-relfex is
the electrical representation of the tendon reflex
circuit.
F WAVE Impulse travels back through motor
fibers to anterior horn cells, which activates a small
number of them and causes the signal to go back
down to the muscle. Signal only traverses the ven-
tral root.
Normal F-wave and absent H-reflex is found in
diseases of the sensory nerves and roots.
APPROACH TO EMG 92
CLASSIFICATION OF NEUROPATHIES
ACUTE AIDP, Porphyria, Diphtheria, Drugs (dapsone, nitrofuranto-

in, vincristine), Toxins (arsenic, thalium), Tick paralysis, Vasculitis
TEMPORAL
COURSE SUBACUTE
CHRONIC Hereditary or acquired
LARGE FIBER (MOTOR, SENSORY) Decreased vibration, touch,

proprioception; hyporeflexia, fasciculations, myokymia, parasthesias
SMALL FIBER (PAIN, TEMP) Diabetes, Amyloidosis, drugs (DDI,

FIBER TYPE DDC), hypertriglyceridemia, HSN, Tangiers, Fabrys, HIV, idiopathic.
NCS/EMG not helpful
AUTONOMIC (UNMYELINATED) Arrhythmias, pressure changes,

impotence, urinary retention, perspiration changes
SYMMETRIC
ASYMMETRIC
Asymmetric and proximal > distal Indicates non-length depend-
ent pattern
PATTERN Mononeuropathy multiplex
Radiculopathy
Entrapment neuropathy (e.g. carpal tunnel)
CIDP variant
Porphyria
AXONAL
Mostly large fiber, symmetric, distal
Toxic, metabolic (e.g. diabetes), drug induced, nutritional, con-
nective tissue disorders, endocrine-associated
DEMYELINATING
Hereditary: HMSN Type 1 (CMT), HMSN Type 1 (Dejerine-Sottas),
SMSN Type IV (Refsum), HNPP, Congenital Hypomyelinating Neu-
PATHOLOGY
ropathy, Metachromatic Leukodystrophy, Krabbes Disease, Adre-
noleukodystrophy, Cockayne Syndrome, Niemann-Pick, Cere-
brotendinous xanthomatosis
Acquired: AIDP, CIDP, HIV, MGUS, anti-myelin associated glyco-
protein antibody, Waldenstroms macroglobulonemia, osteoscle-
rotic myeloma, multifocal motor neuropathy with conduction
block (+/- anti-GM antibodies), diphtheria, toxic (e.g. amioda-
rone, perhexilline, arcenic, glue sniffing)
93 NEUROPATHIES, MYOPATHIES
NEUROPATHIES: DEMYELINATING vs AXONAL
FEATURE DEMYELINATING AXONAL
Mechanism of weakness Conduction block Axonal loss
Atrophy No or late (disuse atrophy) Yes
Fasciculations No Yes
Mechanism of recovery Remyelination Axonal sprouting (reinnervation)
Nerve conduction velocities Slow Normal or slightly decreased
Motor action potential Normal or smaller distally than
Equally small distally and proximally
amplitudes proximally, with temporal dispersion
Fibrillation potentials No Yes
Recruitment Poor Poor
Motor unit potentials Normal Large, long duration, polyphasic
COMPARISON OF NEUROPATHIES AND MYOPATHIES
MYOPATHIES vs NEUROPATHIES
FEATURE NEUROPATHY MYOPATHY
Distribution of weakness Distal more than proximal Proximal more than distal
Atrophy Yes (mostly distal) Yes (generally proximal)
Fasciculations Yes No
Reflexes Decreased Normal or decreased (late)
Sensory loss Yes No
Autonomic dysfunction Sometimes No
Creatinine kinase Normal Increased levels (in most cases)
Electromyography
Conduction velocity Decreased Normal
Sensory action potential
Decreased Normal
amplitude
Fibrillation potentials Yes Occasionally
Recruitment Decreased Increased
Long duration, large amplitude, Short duration, low amplitude, poly-
Motor unit panel
polyphasic phasic
Muscle biopsy Group atrophy, fiber-type grouping Variable muscle fiber size, inclusions
NORMAL NEUROPATHY MYOPATHY
Condition
Motor Unit
Potential
Recruitment
Biopsy
NEUROPATHIES, MYOPATHIES 94
CLASSIFICATION OF MOVEMENT DISORDERS
HYPOKINETIC HYPERKINETIC
Delayed, slow, low- Involuntary movements that
amplitude voluntary occur spontaneously or superim-
movements with rigidity posed on volitional movement.
and impairments in gait
and postural reflexes.
RHYTHMIC NON-RHYTHMIC
(TREMORS)
PARKINSONS DISEASE CHOREA Brief, quasi-
Sporadic purposeful, irregular, non-
Genetic rhythmic (e.g. Sydenhams
RESTING
Parkinsonian, 3-5Hz chorea, Huntingtons
Dopamine receptor disease)
blockers
PARKINSONISM PLUS
Progressive supranuclear DYSTONIA Sustained
palsy muscle contractions cause
Multiple system atrophy twisting and repetitive
Dementia with Lewy bod- INTENTION
movements or abnormal
postures (Sporadic, inherit-
ies Cerebellar
ed, drug-induced)
Corticobasal degeneration
Alzheimers disease
Frontotemporal dementia
MYOCLONUS Brief,
involuntary jerk-like move-
RUBRAL ment that is not suppressi-
At resting, at posture ble. (e.g. Cortical myoclo-
SECONDARY PARKINSONSISM and with intention nus, epilepsia partialis
Coarse, slow
Medication (dopamine continua, metabolic, etc.)
Lesion in red nucleus
receptor agonists, Reglan,
psychotropics) ATHETOSIS Slow, sinu-
Heredodegenerative dis- ous writhing, twisting
eases movements
Vascular disease
POSTURAL
Infectious disease
Essential tremor
Metabolic disease TIC Sudden, repetitive,
Endocrine disease non-rhythmic, stereotyped
Toxins motor movement or vocal-
Head trauma ization (e.g. Tourette Syn-
drome)
Normal pressure hydro-
cephalus OCULOPALATAL MYO-
CLONUS
HEMIBALLISMUS Se-
1-2Hz rhythmic involun-
vere chorea, thrashing
tary jerks of palate,
motions, lesion in contrala-
pendular nystagmus
teral subthalamic nucleus
95 MOVEMENT DISORDERS
MINIMENTAL STATUS EXAM
SCORE TASK
ORIENTATION
5 What is the (year) (season) (date) (day) (month)?
5 Where are we (state) (country) (town) (hospital) (floor)?
REGISTRATION
3 Name 3 objects: 1 second to say each. Then ask the patient all 3 after you have said
them. Give 1 point for each correct answer. Then repeat until patient learns all 3.
Count trials and record.
ATTENTION AND CALCULATION
5 Serial 7s. 1 point for each correct answer. Stop after 5 answers. Alternatively, spell
world backwards.
RECALL
3 Ask for the 3 objects repeated above. Give 1 point for each correct answer.
LANGUAGE
2 Name a pencil and watch
1 Repeat the following: No ifs, ands, or buts
3 Follow a 3-stage command: Take a paper in your hand, fold it in half, and put it on the
floor
1 Read and obey the following: CLOSE YOUR EYES
1 Write a sentence
1 Copy the design shown.
SCORES
30 Maximum
>27 Normal
20-26 Mild to moderate cognitive impairment
10-19 Moderate to severe cognitive impairment
<10 Very severe cognitive impairment
Note that exam scores need to be interpreted in the

context of patients education level. For instance,
a score of 27-30 is abnormal for a person with
high level of education.
MINIMENTAL STATUS EXAM 96

Neuro Handbook (SUNY)

Uploaded by

Copyright:

Available Formats

Neuro Handbook (SUNY)

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Neuro Handbook (SUNY)

Uploaded by

Copyright:

Available Formats

CONTAINS

The authors of this book thank Downstate neurology attendings

No attendings, residents or patients were harmed in the making

This book contains copyrighted material. Please do not reproduce

and Phone Numbers

Hemorrhagic Stroke 59 Neuropathies, Myopa- 92

Bryan Long 917-219-1773 Kessarin Panichpisal 917-219-1238

Volodymyr Vulkanov 917-219-1778 Maja Ilic 917-219-1833

Sumit Verma 917-219-1968 KCH Consult 917-219-1702

KCH Ward 917-219-1797

NEUROLOGY RESIDENTS: PGY 4 LICH Consult 23003

Jason Freeman CHIEF 917-219-1878 UHB Neuro Office 270-2051

UHB Call Room 270-8971

Sylvana Gonzalez 917-219-1874 KCH Neuro Office 245-5403, 5404

Steven Lin 917-219-1877 Suite C Neuro Clinic 270-1491

Eduard Rozner 917-219-1873 8th Fl Neuro Clinic 245-3480, 3477

Pedro Torrico 917-219-1867 5th Fl Peds Neuro Clinic 245-3612

Ellen Edgar 917-219-1080 MDA Clinic 270-3215

Coronal section show-

BLOOD SUPPLY TO INTERNAL CAPSULE AND GLOBUS PALLIDUS

LEFT MCA Right face and arm weakness

Fluent, or Wernickes, aphasia

Right pure motor hemiparesis

Combination of the above:

RIGHT MCA Left face and arm weakness

Profound left hemineglect

Left pure motor hemiparesis

Combination of the above:

Contralateral leg weakness and cortical-type sensory loss

Contralateral homonymous hemianopia

MCA-PCA Gerstmann Dominant inferior Agraphia

IMAGING A and B demonstrate

MAJOR VASCULAR SYNDROMES OF THE MEDULLA

Superficial saggital sinus

Superficial cortical veins

BASAL GANGLIA INTERNAL CONNECTIONS

OCULOMOTOR (CN III) NUCLEAR COMPLEX Edinger-Westphal parasympathetic innervation is bilateral.

21 CRANIAL NERVES AND NUCLEI

CAVERNOUS SINUS Note that

CRANIAL NERVES AND NUCLEI 22

23 CRANIAL NERVES AND NUCLEI

PONTINE HORIZONTAL GAZE CENTER AND GAZE ABNORMALITIES

CRANIAL NERVES AND NUCLEI 24

25 CRANIAL NERVES AND NUCLEI

CN VII then enters internal

CN VII along with nervus

In the mastoid segment,

CRANIAL NERVES AND NUCLEI 26

27 CRANIAL NERVES AND NUCLEI

CRANIAL NERVES AND NUCLEI 28

Left homonymous hemiano-

Left superior quadrantanopia

MACULAR SPARING Fovea has large cortical repre-

Partially crossed at this level

Uncrossed at this level

SOMATOTOPIC ORGANIZATION OF ANTERIOR HORN CELLS

TRACT LAMINATION IN SPINAL CORD S: Sacral, L: Lumbar, Th: Thoracic, C: Cervical

WATERSHED REGION OF BLOOD

Bilateral posterior column and

ANTERIOR HORN AND PYRAMIDAL e.g. ALS, HTLV-1