The following excerpt is from the

University of Ottawa Adult Neurology

Residency Program publication, The
Neurology Survival Guide 2nd edition,
edited by Dr. J. Warman. This document
displays the first ten pages of the Guide,
and the first page of ten selected topics.
The Guide, in its entirety, is copyrighted
and available only to house staff
rotating through the Ottawa Hospital
Neurology service.

The Neurology Survival Guide

2ND Edition (2007)

Table of Contents
Introduction to the Neurology Service
Resident Responsibilities
Discharge Planning
On call advice
Death Declaration/Certification
Screening Neurological Exam
Neurological Differential Diagnosis
Localization/Etiological Matrix
Detailed Neurological Exam
Investigations & Diagnostic Imaging
Lumbar Puncture
Changes in mental status
Seizures
Stroke
Circle of Willis Diagram
Headache
Weakness & Neuromuscular pathologies
Management of Neurological Emergencies
Glossary of Neurological Terms

2
3
4
6
7
8
10
11
14
22
24
28
30
34
33
42
44
48
50

Appendix/Inserts
Neurology Sample Scutsheet
MOCA
This edition is based on the detailed work of Dr. Nathalie Jett & Dr. Alan Guberman
(1st Edition, 2000) and the significant contribution by Dr. Pierre Bourque.
We appreciate the comments and the feedback provided by the residents and staff neurologists
involved in this project, including Dr. Christine DeMeulemeester and Dr. Mike Sharma.
Editor of 2nd edition: Dr. Jodi Warman

Disclaimer:
The information contained in this booklet should be used as a general outline, and other
sources should be consulted for current medical guidelines.

Welcome to the Neurology Service

We hope that you have a great learning experience during your
rotation.
Organization of Teams: The neurology service is divided into two
teams:
A & B services. The Neurology Team A (NLA) service consists of
inpatients that are actively being treated or undergoing diagnostic tests.
6NW is the main neurology floor; however, more critically ill patients
are admitted to the neurology-observation (NeuroObs) unit. Team B
(NLB) is the neurology consults service and also follows chronic/nonactive patients.
Allied Services:
Paramedical professionals are an invaluable part of the team and
include nursing staff, physical therapists (assess mobility, motor
function), occupational therapists (ADLs/cognitive/positioning), social
workers (d/c planning, financial issues, family support/conflict),
neuropsychology (cognitive assessment), speech-language pathology
(dysphagia, aphasia), pharmacy and nutrition services. Also, we are
fortunate to have a nurse liaison that works with the team. She helps
coordinate care and patient teaching and facilitates discharge planning.
Teaching Opportunities & Rounds:
Weekly rounds neurology case presentation (Thurs 8-9 am): a ward
resident presents a selected patient from Team A. Usually, the patient
is assessed by one of the neurology residents to demonstrate
interesting findings, and an off-service resident provides a 10 minute
presentation on the topic of the neurological condition.
(pathophysiology, etiology, dx, ddx, investigations, management).
Grand rounds (Friday am), 8:00-9:00 am: radiology topics;
9:00-10:00 am: adult/pediatric neurology, neurosciences and
neurosurgery topics.
Neurology Resident Half Day (Tuesday 2:00-5:00 pm): Rotating
residents are welcome to attend these rounds.
Stroke Journal Club: Every 2nd Tuesday at 4:30 pm. Stroke literature is
reviewed and residents are welcome to attend. Every other Tuesday is
Neurovascular rounds, where patient cases are discussed.

So you want to be a superstar

We understand that the neurology service is busy, but it provides a
fantastic opportunity to strengthen your neurological exam skills and to
develop a solid approach to manage common (and not so common!)
neurological disorders. Staff, neurology residents and the neurology
floor nurses are willing to help.
Overview of Staff Expectations
The team meets for handover on 6NW at 8:00 am, so that the patient
list can be divided. Things run a lot more smoothly when people are on
time, so please dont be late. Rounds with the neurology staff usually
start between 9 & 10 am daily.
The neurology staff will expect you to have the most up to date
information about your patients, including lab work, imaging study
results, as well as a preliminary discharge plan. Daily progress notes
can be written after (or during) rounds. It is really important to
document changes in neurological status, diagnosis and management
issues as they are evolving. The staff & senior neurology resident
should be notified immediately about acute and potentially serious
changes in your patients condition.
Residents/students will meet with nurses/paramedical professionals
once weekly to discuss discharge planning, social and rehabilitation
issues about each patient. These interdisciplinary rounds are usually
Thursday morning (approximately 9:00-10:15 am).
Residents are expected to attend the family meetings about their
patients. Taking time with families is an essential part of patient
management and learning experience about patient expectations.
Resident and Rotation Evaluations:
It is the responsibility of rotating residents to complete their
WebEval evaluations before the rotation is finished and schedule a
feedback session with the neurology staff. It is hard to get a
meaningful evaluation once you have left the service. Also, do not
hesitate to remind staff to complete your evaluations, several times if
necessary!
We also welcome any comments you have about your neurology
rotation experience, whether positive or as constructive feedback.
Discharge Planning:
3

The B Service: Patients may be transferred to the B service once they

are medically stable (e.g., awaiting INR to become therapeutic) and are
awaiting transfer to a rehabilitation centre or to long term care. Once
patients are ready for B service: a) a stat discharge summary (code 111)
must be dictated; b) follow-up arranged (i.e. with stroke clinic or staff
neurologist) and c) approval obtained from the consult service staff
neurologist before these patients can be transferred. The neurology
consult service staff/residents receive consults during the day and are
responsible for the B service ward patients (max 6 patients). Please
dont transfer patients to team B between Friday and Sunday. If a
patients discharge from hospital is planned within two days, do not
transfer the patient to the B service.
Daily Thoughts for all patients to facilitate D/C planning:
-Does your pt need to be in hospital?!
-Have all necessary tests been ordered (i.e. stroke work-up)?
-Can your pt get out of bed today? Are PT/OT involved?
-Does your pt still need DVT prophylaxis (i.e. walking)
-Has SLP assessed for dysphagia or improvement in swallowing?
-Can your pts diet be advanced?
-Can IV meds be made po & can I saline lock the IV? (if pt can swallow)
-How much is pt drinking/urine output?
-Can the foley/tubes be removed?
-When was the pts last BM?
-What is the d/c plan? Is SW involved (i.e. home/LTC/rehab)?
Discharge Planning options include:
Home, no services necessary or Home with homecare (CCAC)
Stroke Rehab (need PT/OT/SW consults)
Geriatric Assessment Unit (GAU-for patients over 65 that need a
shorter rehab time)
Geriatric Rehab (for slower, longer rehab process)
Neurospinal rehab (i.e., GBS, MS, transverse myelitis)
Head Injury Rehab (Acquired Brain Injury)
Awaiting placement Unit (APU) can be initiated: once the discharge
plan is established (accepted by rehab, placement papers completed
and signed), no acute treatment required & pt has stable medical
status. APU d/c summary needs be dictated and APU service
consulted. Patients transferred to APU/ALC need the following
information on the chart: MRSA/VRE swab if not been done, change
vitals to once daily).
4

Follow-up Appointments with the Staff Neurologist

If the patient requires follow-up by a neurologist once discharged from
neurology CTU, follow-ups should be arranged according to the
following principles:
1. Patients, who were not previously being followed on a regular
basis by one of the neurologists in the city, should be referred to
the neurology attending on the CTU at the time of the patients
discharge. If the patients stay overlaps between two months, then
the neurology attending who knew the patient best should be the
one to follow him/her up.
2. Patients previously being followed in a specialty neurology clinic
(e.g. multiple sclerosis, epilepsy, movement disorders), should be
referred back to the neurologist who was following them in that
clinic.
3. Patients with a new diagnosis who would be appropriate for follow
up in one of the sub-specialty clinics, could be referred to those
clinics for follow-up but only after the attending neurologist on the
CTU has personally contacted the attending neurologist in the subspecialty clinic to whom they wished to refer the patient.
The principle is that it is the obligation of each attending staff on the
CTU to follow-up unassigned patients who were under their care in the
hospital unless they have made other arrangements

Dictations
PLEASE DO YOUR DISCHARGE SUMMARIES
FOR ALL OF YOUR PATIENTS-WE WILL TRACK YOU DOWN
EVEN WHEN YOU ARE OFF SERVICE!!!
Dictation # at the General: 78783 (2 to begin, 1 to pause, 3 to rewind)
Please keep discharge summaries concise, never longer than 2 pages.
Ensure that you mark the job id of the dictation summary on the
written discharge note.

On Call Advice
Neurology call can be really, really busy despite being home call.
If at home, you have to be able to get to the hospital in less than 20
minutes. On call, you will cover the General site and the staff
neurologist sees consults at the Civic. You can always call the staff
neurologist for any questions or if you are overwhelmed. Staff will also
help you deal with the pressures from other services to admit. Many
rotating junior residents feel more comfortable on the first few days on
call to stay in house.
The patient will be admitted under the name of the neurologist on call.
Please write in the orders to Transfer to Dr. ____ in am (to the CTU
staff neurologist). On your call stipend form, dont forget to mark down
the hours that you were in house (vs at home).
Typical floor calls consist of decreased LOC, seizures, worsening
neurological deficits, heparin assays & coumadin orders, medications,
and the usual medicine floor calls (chest pain, SOB). Emergency
referrals vary.
When you are on call on the week-end, you round alone (or with a
neurology resident) and you go home the next day at 8-9 am (i.e., if you
are on call Saturday, you dont have to round on Sunday). The staff will
meet with you during the day to go over the new patients that were
admitted the previous night or to see any patients that have active
issues.

Dont forget: equipment required for your neurology rotation includes:

Reflex hammer
Visual Acuity card
Tuning fork (at least 128 hz)
Disposable pins/safety pins for sensory testing

Death Declaration/Certification
Before you go into the room:

Verify circumstances of death (expected or not)

Family present (grieving? angry?...)
Familiarize yourself with the background history and in-hospital events
If you think that you need help, ask for it
Calm yourself before you enter the room

Declaring death:

Identify the patient by wrist bracelet

Unresponsive to verbal & tactile stimuli?
Absent heart sounds and central pulse?
Absent spontaneous respirations?
Absent pupillary responses?
No response to noxious stimuli (e.g., bright lights for pupils, sternal rub for tactile
stimulus)?

Family present:

Identify yourself and your role

Gauge initial reaction (grieving, anxious)
Do NOT ask them to leave, exam as above
Clearly state that the patient has died, offer condolences
Pause for grief reaction, remain quiet yet available
Console as appropriate
Give permission to pause before addressing autopsy, doing notification
Model saying good-bye to patient

Document in the chart and notify senior/attending/family MD

JAMA (2005) 293 (18): 2265-71
Marshall SA, Reudy J (2004) On call principles and protocols. 4th edition

Death Certificate Terminology

-[a] immediate cause of death: final complication of underlying cause of death,
occurs closes to time of and direct cause of death
-[b] antecedent [intermediate] cause of death: condition the result of
underlying cause but not the final complication or immediate cause of death
-[c] underlying cause of death condition triggering the chain of events leading to
death; temporarily the most remote condition, etiologically specific, not a
mechanism (e.g. cardiac arrest)
-going from [c] to [a] timing moves towards the present
-[a] and [b] can be blank
CMAJ. 1998 158 1317-1323

Summary used with permission by Dr. Jim Nishikawa

Summary of Neurology Hx & Exam

Hx:
ID (& Handedness):
Chief Complaint:
HPI:
PMHx:
Major Illnesses:
CVA/TIA
Seizures
Thyroid Dz
MI/angina/PVD
Clotting d/o
HTN
Dyslipidemia
Cancer Arthritis
Surgeries
Trauma
Also: perinatal hx & developmental milestones (if applicable)
Immunizations (pediatrics)

A fib

Medications:
*Allergies*
FHx: (including health, consanguinity)
Social: Education,
Hobbies/Employment (occupational hazards, exposures, toxins)
Marital & family status, problems at work/home
Habits: smoking _____ppd x yrs, ETOH ______, illicit drugs _____
-> consider HIV risk factors
General Review of Systems
Constitutional/Gen: fever, chills, night sweats, fatigue,
weight gain/loss, appetite, change in sleep pattern, easy
bruising, transfusions, lymphadenopathy
Derm: rashes, skin discolourations/bruising, lumps,
pruritis
Mouth/Nose: epistaxis, discharge, sinus diseases
dental disease, hoarseness, throat pain
Respiratory: cough, SOB, sputum, hemoptysis
Cardiovascular: chest pain, orthopnea, PND, dypnea
with exertion, claudication, edema, palpitations
GI: abdominal pain, N & V, change in bowel habits,
diarrhea, constipation, melena/hematochezia
GU: dysuria, freq of urination, hesitancy, hematuria, d/c
Gynecological: GTPALM, dysmenorrhea, contraception,
painful bleeding, breast masses
Endocrine: polyuria, polydipsia, skin/hair changes, heat
intolerance
MSK: joint pain, swelling, arthritis, myalgias
Lymphatics: lymphadenopathy
Neuropsychiatric: mood (i.e. depression), tension, stress

Neuro
Headaches
Head injury
Confusion
Memory Problems
Fainting/Seizures/Light
headedness
Diplopia, Vision loss or
changes/field deficits
Dizziness
Hearing, Tinnitus
Vertigo
Balance problems
Dysarthria
Dysphagia/odynophagia
Speech difficulty
Paresthesia/sensory loss
Weakness (focal vs
general)
Back Pain
Incontinence

General Physical Exam:

General Appearance:
Vitals: T ___C B/P (R)____ (L) ____ HR____ RR____ O2____
H & N: ears
oropharynx
thyroid lymphadenopathy MMM
Bruits: carotid cranial supraclavicular
Temporal artery pulses, tenderness, and nodularity
Meningeal irritation: nuchal rigidity
Kernigs sign (Knee flexion); Brudzinskis sign (neck flexion)
CVS: S1 S2 S3 S4 murmurs________(& radiation) OS/EC
JVP_____cm ASA, Periph/sacral edema PPP
Resp: (G)AE(B), adventitious sounds
Abdomen: BS, abdomen soft/rigid, guarding, masses
MSK: including skull, vertebral column
Skin: bruising, integrity
Neuro Screen (see following pages)
1. Mental status: speech, affect, mood, cognition, thought process & content
MMSE _____/30 (if applicable)
2. CN: II-XII
3. Motor Exam:

Inspection, Pronator Drift, Tone

Power (table)
4. Sensory:

Primary: Lt touch, pin prick, vibration, proprioception

5. Reflexes
Deep Tendon Reflexes:
Plantar Responses
6. Coordination:
FNF, HKS, RAM, tremor

Motor
Power
Sh-Abd
Elbow flex
Elbow Extn
Wrist-flex
Wrist-ext
Fing-abd
Fing-flex
Fing-ext
Hip-Flex
Hip-Ext
Knee-Flex
Knee-Ext
Ankle-dflex
Ankle-pflex

7. Gait: natural, heel walking, toe walking, heel to toe (tandem), Romberg
Investigations:

WBC
HgB

Plt

Na

Cl

CO 2

Urea
Cr

Gluc

Imaging: CT/MRI/TEE/Doppler & EKG/CXR etc

Impression & Plan: (numbered, issues based list format)
Attempt to localize the lesion(s) and identify etiology of the process
if possible in your DDx (see following pages)

Differential Diagnosis
When developing your list of differential diagnoses,
First, generate a list of differential diagnoses based on the localization
of the lesion(s)

Cerebellum

Cortex

Deep White
Matter/BG
Thalamus

Brainstem

Spinal Cord

Peripheral
Nerve

Neuromscular
Junction

Muscle

LOCALIZATION MATRIX

Mental Status
Cranial Nerves
Motor
Sensory
Reflexes
Coordination
Gait
Table reproduced with permission by Dr. Chris Skinner

Second, focus your list of differential diagnoses based on possible

etiologies:

Degenerative

Neoplastic

Trauma

Electrical

Vascular

Metabolic

Inflammation

Drugs

ETIOLOGY MATRIX

Acute
Sub-Acute
Chronic
Table reproduced with permission by Dr. Chris Skinner

10

Localization: Common Clinical Features

by Neuroanatomic Site
Cerebral Cortex
Unilateral focal neurologic signs such as hemiparesis,
hemihypesthesia, homonymous hemianopia
Aphasia, agnosia, apraxia
Dementia
Delirium
Memory loss
Seizures
Meninges and Cerebrospinal Fluid
Headacheusually diffuse
Somnolence and decreased LOC
Meningismus (Kernig, Brudzinski signs)
Cranial nerve signsoften with multiple nerves involved
Basal Ganglia
Extrapyramidal signs (e.g., bradykinesia, shuffling gait, masked
facies, postural instability)
Movement disorders (chorea, athetosis, or tremor, which may be
unilateral or bilateral)
Thalamus
Contralateral sensory loss and mild contralateral hemiparesis, gaze
paresis, homonymous hemianopia, miosis, aphasia, or confusion
Cerebellum
Ataxia of limbs (dysmetria, dysrhythmia), intention tremor
Truncal ataxia and unsteady gait
Nystagmus, vertigo, nausea, vomiting,
Dysarthria (scanning speech)
Pendular reflexes
Brainstem
Coma or decreased level of consciousness
Changes in blood pressure, heart rate, and respiratory rate
Cranial nerve involvement (especially diplopia, facial sensory loss,
facial weakness, dysphagia, dysarthria, hoarseness)
Vertigo
Hemiparesis or tetraparesis and spasticity
11

Spinal Cord
Weakness that may commonly involve both legs or all limbs
Leg spasticity
Sensory level present
Loss of reflexes at the level of cord involvement with hyperreflexia
below that level
Upgoing toes
Bowel and bladder signs
Autonomic nervous system dysfunction
Nerve Root
Neck or back pain that may extend into limb
Weakness only in muscles supplied by that root
Dermatomal distribution of sensory loss
Loss of deep tendon reflex associated with that root
Peripheral Nerve
Mixture of motor and sensory findings, reflexes decreased
Distribution of signs either in a single nerve or in many nerves
Distal limb signs more pronounced than proximal signs
Trunk uncommonly involved
Muscle atrophy and occasionally fasciculations corresponding to
involved nerve
Pain in feet or along a single nerve distribution
Sensory loss due to pain and temperature, or vibration and position
sense, or to all modalities
Neuromuscular Junction
Ptosis with fatiguable diplopia
Fatigue (especially with chewing/masseter muscles and proximal
limb muscles)
Weakness without sensory loss
No muscle atrophy, reflexes intact
Muscle
Weakness without sensory loss
Proximal muscles usually weaker than distal muscles
Weakness that is often slowly progressive
Muscle atrophy
Normal or decreased reflexes
Adapted from Davis, L.E. (2005) Fundamentals of neurologic disease : an introductory text.
12

Etiology: Neurological DDx (by VINDICaTE mnemonic)

VASCULAR diseases are acute & often asymmetrical
-usually focal - but may be diffuse (e.g. SAH)
Stroke/cerebral infarction; SAH; intracerebral hematoma,
Vascular malformations (AVM; aneurysm)
Venous occlusion
Migraine
INFLAMMATORY diseases are usually subacute or chronic and tend to be
progressive. They tend to diffuse or multifocal (e.g. autoimmune disease like multiple
sclerosis).
NEOPLASTIC processes are progressive, may be subacute or chronic, and tend to be
focal or multifocal but may be diffuse (e.g. carcinomatous meningitis).
Consider brain (intra-axial and extra-axial); spine; skull base; metastases)
Adults (mainly cortex involved) vs children (mainly cerebellum & brainstem)
DEGENERATIVE processes are progressive and diffuse with symmetrical signs
(pain seldom prominent)
Family history of similar illness may be present
Clinical features vary -> including dementia, parkinsonism, and weakness
INFECTIOUS: processes may be focal (e.g. abscess) or diffuse (e.g. meningitis,
encephalitis), Meningoencephalitis; cerebral or cerebellar abscess
Fairly rapid onset and progression with fever common
Signs usually involving meninges or cerebral cortex
WBC & ESR
CONGENITAL-DEVELOPMENTAL diseases are chronic and typically diffuse,
and may be static or progressive (i.e. tuberous sclerosis)
TRAUMATIC (& Mechanical): processes are often acute, may be static and
improving or progressive, and may be diffuse, focal, or multifocal. (i.e. subdural
hematoma, herniated intervertebral disc)
TOXIC - METABOLIC processes are diffuse and may have any time course (drugs,
electrolytes, endocrine, nutrition, organ failure)
Gradual onset of symptoms over hours/weeks, hx of drug or substance usage
Altered mental activity (confusion, delirium, stupor, or coma)
Distal symmetrical polyneuropathy common (focal signs less common)
EPILEPTIC: Partial or Generalized Seizures
Dont forget about: Referred pain (i.e. left arm paresthesias with cardiac origin;
Psychiatric (conversion disorder, depression) & other non-neurological (syncope 2 to
cardiac arrhythmia)

13

NEUROLOGY EXAM IN DETAIL

1. Mental Status
A. Level of Consciousness & Orientation
1. LOC (however, longer description of stimuli required to rouse pt is best)
=> it is much better to just describe what you see
Alert
Drowsy - easily awakens, however, inability to sustain wakefulness
without external stimuli
Obtunded - difficult to awaken, & aroused by vigorous stimuli, interacts
briefly
Stupor - aroused only by vigorous and repeated stimuli, but not
Comatose does not wake up to voice or pain
2. GCS score if indicated

Glasgow Coma Scale (/15)

Best Verbal Response
Best Motor Response
Follows commands-6
Oriented-5
Localizes to pain-5
Spontaneous-4
Confused-4
Withdraws to pain-4
To voice-3
Inappropriate words-3
Flexor response-3
To painful stim-2 Unintelligible sounds-2
Extensor response-2
None-1
None-1
None-1
3. Oriented to person, place, date, and situation (A&O x 4)
Eye Opening

B. Language
Fluency of speech: speech is fluent (effortlessly produced at a normal
rate), and prosody is preserved
Comprehension. Simple comprehension is assessed asking the patient
to execute a simple command (e.g., "stick out your tongue"), or more
complicated tasks touch your right thumb to your left ear or (point
at the ceiling, close your eyes and stick out your tongue).
Naming. Pt asked to name common objects (i.e., watch and pen) parts
of the objects (e.g., watchband, tip of pen).
Repetition. Following object naming, the patient repeats phases (e.g.,
"No ifs, ands, or buts") (easier: Mary had a little lamb)
Reading. Patients are asked to read a short sentence, i.e."The car
backed over the curb" or "The rabbit hopped down the lane."
Writing. Ask the pt to write a short sentence.
Note: Dysarthria is a disturbance (slurring) of articulation, not of
language; it may coexist with aphasia, but they are separate disorders.
Patients with dysarthria have a normal ability to read and write.
14

C. Cognitive
1. MMSE or MOCA (see ACC desk on 6NW for copies)
Mini-Mental Status Exam (Folstein)
Orientation
Registration/
Attention

Recall
Language

Place-yr/mos/season/day/date
Time-Can/prov/city/hosp/flr
3 Objects-i.e penny/brown/honesty
Patient has to repeat all 3 (1 pt/each)
Serial 7s
Or WORLD backwards
5 Minute recall
Name-pencil/watch
Repeat-no ifs ands or buts
Reads command written on paper &
follows (i.e. Close your eyes)
3 step command-Take paper in your
right hand, fold it in , put it on the
floor
Copy-2 intersecting Pentagons

Write-sentence
If < 24/30=cognitive impairment

/5
/5
/3
/5
/3
/2
/1
/1
/3
/1

/1
/30

2. "Simple" Clock-Drawing Test

Directions: Draw a large circle; instruct the patient that the circle
represents a clock face. Ask the patient to add the numbers so that the
circle looks like a clock and then set the time to ten after eleven.

15

2. Cranial Nerves
Olfactory
I
Optic
II

III
IV
VI

Oculomotor
Trochlear
Abducens

Smell-not usually assessed

Fundi: disc, cup, arteries, veins, maculae, retina
[papilledema, hemorrhages, exudates, atrophy]
Pupils (size & reaction to light)
Visual Acuity L_____ R______
Visual Fields (to confrontation)
PERLA
EOM (pursuit & saccades)
Convergence

Trigeminal

VII

Facial

VIII

Acoustic/
Vestibular

IX
X
XI

Glossopharangeal
Vagus
Accessory

XII

Hypoglossal

Diplopia present ___

Nystagmus present ___
Also: Gaze preference, optokinetic nystagmus,
Dolls eye (oculocephalic) reflex, cold calorics, lid
lag
Sensory: face
(V1-ophthalmic, V2 maxillary, V3 Mandibular)
Motor: jaw opening/closing (masseters, pterygoids,
temporalis); jaw jerk
Corneal reflex (afferent)
Forehead wrinkling (frontalis muscle)
Eye closure (orbicularis oculi muscle)
Wide smile, Whistling
Blowing (buccinator/orbicularis oris/zygomatic
muscles)
Taste (anterior 2/3 of tongue)
Hearing
Weber lateralization (if reduced hearing)
Rinne: air conduction (< or > than bone conduction)
Oculovestibular (caloric) testing (if applicable)
Gag
Dysphonia (ga-ga-ga), uvula (deviation opposite
to lesion), soft palate (paresis), swallow, cough
Sternocleidomastoid (turn head to opposite side)
Upper trapezius (shrug shoulders)
Atrophy, fasciculations,
Tongue in midline, deviation to R-L
Strength, coordination, dysarthria (ta-ta-ta)
16

3. Motor Exam:
a. Inspection
Bulk (atrophy/hypertrophy/asymmetry)
Involuntary movements (fasciculations, tremor, myoclonus, asterixis,
dystonia, athetosis, chorea, ballismus, tics)
b. Pronator Drift
c. Tone: N, hypotonia, spasticity, rigidity (cogwheeling, lead-pipe,
paratonia, gegenhalten)
Increased Tone
Spasticity
Rigidity
-Selective muscle groups -Diffuse in affected limb
-Velocity dependent
-Velocity independent
-Occurs with:
-Occurs with:
o Weakness
o Parkinsonism (tremor,
o Hyperreflexia
bradykinesia, postural
o Babinski sign
instability)

Paresis

Patterns of Weakness
LMN
UMN *
+
+

Atrophy

++

+/- (disuse)

DTR

Tone

(spasticity)

Fasciculations

Babinski sign

* Hypotonia and hyporeflexia acutely

d. Power/Strength:
17

Power
Sh-Abd (deltoid, supraspinatus)
Elbow flex (brachialis, biceps,
brachioradialis)
Elbow Extn (triceps)
Wrist-flex (flexor carpi radialis/ulnaris)
Wrist-ext (extensor carpi radialis/ulnaris)
Fing-abd (dorsal interossei)
Fing-flex (flexor digitorum profundus &
superficialis)
Fing-ext (extensor digitorum)
Hip-Flex (iliopsoas, TFL, rectus femoris)
Knee-Flex (hamstrings, Gracilis,
sartorius)
Knee-Ext (quadriceps femoris)
Ankle-dflex (tibialis ant, EDL, EHL)
Ankle-pflex (gastrocnemius, soleus, tib
post)
Toe extensors (EDL, EDB, EHL)
Toe flexors (flexor digitorum brevis,
lumbricals, interossei)

R /5

L /5

Assessing Power/Strength: (/5)

0=no contraction/mvt
1=flicker of mvt
2=mvt only with gravity eliminated
3=mvt against gravity
4=Mvt against gravity & resistance
5=Full strength
Pyramidal Weakness:
U/E: abductors & extensors > flexors
L/E: abductors & flexors > extensors

18

Motor Homunculus: A=> The large area of cortex devoted to motor control of the
hand, lips, and face is evident. B in the smaller diagram represents the motor cortex; A is
the sensory cortex. Adams and Victor's Neurology (McGraw-Hill Companies, via
Access Medicine, 2006) Figure 3-4

Stereotyped patterns in UMN lesion

Weakness
Spasticity
shoulder abd *
shoulder add
triceps *
biceps *
supinator *
pronator *
finger ext *
finger flex
hip flexors* &
hip add
abduct
knee ext *
knee flexors *
plantar flex*
ankle dorsiflex *
* = commonly tested

19

4. Sensory Exam
Primary Sensory modalities
Light Touch ____ Vibration ____Joint Position ____ (dorsal columns)
Pinprick _____ Temp_____ (spinothalamic)
Cortical Sensory modalities:
Stereognosis______Graphesthesia______2 pt discrimination______
Stimulus localization_____ Extinction (with double stimulus)_____
5. Reflexes
Deep Tendon Reflexes
R
DTRs
Biceps (C5-C6)
Triceps (C6-C7-C8)
Brachioradialis (C5-C6)
Finger Flex (C8-T1)
Quadriceps (L2-L3-L4)
Gastrocs/Soleus (S1-S2
0=absent, even if reinforcement
1=reduced, poss N
2=Normal/average
3=increased, poss N
4=Increased-with clonus

Plantar Response: N response is downward contraction of toes

Abnormal response (Babinski sign) is characterized by an
upgoing big toe and fanning outward of the other toes
Chaddock sign: upgoing big toe by stimulating lateral aspect of
foot from heel to small toe
Oppenheim: upgoing big toe with application of heavy pressure
with the thumb and index finger to anterior surface of tibia with
downward stroking from the infrapatellar region to the ankle
Additional Reflexes
Frontal Release: grasp, snout, root, suck
Glabellar response ( in PD), Palmomental
Spinal cord lesion: abdominal cutaneous reflexes, cremasteric
reflex, bulbocavernous reflex, anal wink
20

6. Coordination
Tremor:
Resting, pill rolling
Intentional
Postural:

R
L
Coordination
Finger-nose-finger
Wrist RAM*
Finger-RAM*
Heel-shin
Ankle RAM*
Note: RAM=Rapid Alternating Mvts

7. Posture & Gait

Posture:
Sitting
Romberg
Gait:
Natural Gait
Tandem/Heel to toe____Heel walking____Toe walking____ Arm
swinging____
Wide base____Circumduction____Difficulty turning around____

8. Autonomic
Sweating, skin temperature, cyanosis or pallor;
Trophic changes of skin/nails
Postural changes in BP

21

Diagnostic Tests
CT Scan: usually a first diagnostic test if you are concerned about an
intracranial or spinal pathology. Check renal function (indicate
creatinine on requisition form) and that patient is not allergic to dye.
Attenuation: bone=bright>grey matter>white matter>CSF>air=dark
->excellent at delineating bones and blood acutely, good at delineating
soft tissues, good for acute stroke
-> disadvantages: IV contrast injection may be indicated, higher
radiation exposure
CTA less invasive than traditional angiography
MRI: shows brain anatomy in fine detail and easily distinguishes white
from grey matter
-> need to decide if plain or if need contrast (usually Gado).
Check renal function and that the patient is not allergic to dye, no
arterial clips/implants etc. (see Radiology requisition for exclusions)
Patients can become quite claustrophobic in the MRI
MRA & MRV used for evaluation of vascular lesions (aneurysm,
AVMs, atherosclerotic disease); Time of flight MRA can be done
without contrast, however, study is more limited.
Tissue or body fluid on MRI
T1
T2
High water-bound tissues(muscle)
low
Low-med
High free-water tissues (edema, CSF,
low
high
simple cysts)
Bone/calculi
nil
nil
Collagen tissue
low
low
Fat
high
med-high
Prot containing fluid (abscess, complex
medium high
cyst
Hemorrhage
Hyperacute (<24 hrs)
low
low
Acute (1-6 days)
low
high
Chronic (>7 days)
o Intracellular
high
low
o Extracellular
high
high
Neuropathology
Ischemia, edema, demyelination, most
low
high
malignant tumours
Meningioma (medium or iso=isointense)
med/iso med/iso

22

Additional Radiological Findings

RING ENHANCING LESION (CT)
Abscess ring is more smooth and
regular - thinner on medial (WM) side
1 brain tumor (glioblastoma)irregular thick ring
Metastasis (especially if on ChemTx)
Multiple sclerosis - in white matter
Resolving hematoma - 10-21 days usually has perilesional lucency
Radiation necrosis - 9 months-3 years
after Rtx > 4000 rads
Postop change (at edges of resection)
Aneurysm from intraluminal thrombus
HYPODENSE MASS LESION (CT)
Infarct (acute from edema, chronic
from encephalomalacia)
Lipoma, Epidermoid, Pilocytic
astrocytoma
Arachnoid cyst (cyst fluid)
Ventricle/cistern
Chronic subdural
HYPERDENSE Lesion w/o contrast
Hemorrhage (acute) / hemorrhagic
infarct
Meningioma
Lymphoma (small round blue-cell
tumor - densely cellular)
- primary is usually intraaxial
- secondary is often extraaxial
Metastasis - Melanoma/Renal cell
Ca/Choriocarcinoma/Thyroid
Medulloblastoma, Glioblastoma,
Ependymoma, Colloid cyst
Craniopharyngioma , Germinoma

HYDROCEPHALUS vs. ATROPHY

Hydrocephalus (ventricles >> sulci)
- Ballooned and tight frontal horns Dilated temporal horns
- Dilated 3rd (hourglass shape) with flow
void on MR
- Dilated 4th ventricle
- Periventricular abnormal signal/density
Atrophy (sulci and ventricles dilate
proportionately)
- Large cortical sulci
- Less 3rd ventricular dilatation (with
parallel sides NOT hourglass shape)
- Increased with age
CAUSES OF HYDROCEPHALUS
Communicating (decreased reabsorption)
- Normal pressure hydrocephalus
- Prominent temporal horns
- Etiology: infection (meningitis) or SAH
Non-communicating (mechanical
obstruction to flow)
- Aqueductal stenosis
- Postinflammatory or congenital
- Tumors - especially colloid cyst
- Congenital anomalies
- Dandy-Walker cyst of 4th ventricle
- Arnold-Chiari malformation
Overproduction (increased CSF
production)
- Choroid plexus papilloma
COMMENT: Mimicked by atrophy "hydrocephalus ex vacuo"

Adapted from: Neuroradiology Differential Diagnoses (Original Text from Spencer

Gay, MD, UVA) with editing by: James G. Smirniotopoulos, M.D. (2006)
Uniformed Services University of the Health Sciences in Bethesda, Maryland

23

Echocardiogram: transthoracic (TTE-standard) and transesophageal

(TEE-if suspect PFO, atrial septal aneurysm, bacterial endocarditis,
cardiac thrombus).
Doppler: screening test for carotid stenosis.
Conventional Angiogram: used less now due to CTA & MRA
MRA & MRV used for evaluation of vascular lesions (atherosclerotic
disease, aneurysm, AVMs)
Patient should be NPO after midnight the night before and an IV
started in the interim. You need to write on the requisition if the
patient is on IV heparin and write in the orders to stop IV heparin 4
hours prior to the angiogram. Heparin can usually be restarted 4 hours
after angio, with a repeat hep assay in 6 hours.
EEG (available during business hours): need to select plain EEG vs
video/EEG telemetry (about 4 hrs long).
Indications for EEG: seizure d/o classification, encephalopathy
confirmation, sleep d/o dx, confirmation of brain death, prognosis in
coma, localization of functional lesions if imaging studies negative
If EEG ordered, sometimes helpful to hold the pts antiepileptic meds
the day before to increase your yield of seeing something on the EEG.
Also, you can ask the nurse to sleep deprive patients the night prior to
their telemetry.
EMG/NCS
Electromyograms (EMGs) and nerve conduction velocities (NCVs) are
tests of nerve and muscle function. They are useful in determining
whether a patient has neuropathy or myopathy, MG, ALS.
Hypercoagulable workup: Some of the following can be ordered:
CBC, ANA, ESR, Protein C & S, activated prot C, anti-thrombin III,
prothrombin gene, Factor V Leiden, antiphospholipid, anticardiolipin,
lupus anticoagulant, RF, anti-DNA, ANCA, C3, C4, fasting lipids,
serum homocysteine, serum protein electrophoresis.
Evoked Potentials: visual, auditory and somatosensory; often used if
demyelinating lesion (i.e. MS/ADEM) suspected.

Common Indications for Lumbar Puncture

24

Infections (eg, bacterial, mycobacterial, fungal, viral, protozoan)

Inflammatory diseases (MS, GBS, vasculitis).
Subarachnoid hemorrhage
Leptomeningeal carcinomatosis
Therapeutic i.e. benign intracranial hypertension/pseudotumor
cerebri)

FLOW OF CSF

Lange Neurology (2006) McGraw-Hill Companies

Figure 114. (via Access Medicine)

25

Lumbar Puncture Technique

1- Positioning is everything!!!
The patient should be lying in a lateral decubitus position, at the edge
of the bed (facing away from you) in a knee-chest position with the
neck flexed. The patient's head should rest on a pillow, so that the
entire cranio-spinal axis is parallel to the bed.
2- Localize: Find the posterior iliac crest and palpate below the L4
spinous process, and mark the spot with a cap/pen. Put on sterile
gloves.
Prepare/sterilize the skin by starting at the puncture site and working
outward in concentric circles. Drape the patient.
3- Anesthetize the skin & between the spinous processes using the 1%
lidocaine in the 10 mL syringe with the 25-gauge needle.
4- Insert in the midline with the lumbar puncture needle (approx 22gauge) parallel to the floor and directed towards the patient's umbilicus.
Advance slowly until a "pop'' (piercing dural membrane) is felt then
withdraw the stylet every 2- to 3-mm to check for CSF return. If the
needle meets the bone or if blood returns, withdraw slightly and
redirect the needle. If CSF return cannot be obtained, repeat the
process one disk space down.
5- When CSF begins to flow from the needle, allow 1 to 2 cc of CSF
to flow into each of the sterile tubes (more if oligoclonal bands or
cytology required). Cytology specimens require a fixative solution.
6- Replace the stylet and withdraw the needle. Dress the puncture site
with a band-aid. Have the patient lie in bed for a few hours. Postlumbar puncture headaches occur in 10% to 30% of patients within 1 to
3 days and last 2 to 7 days. The pain is relieved by lying flat. Treatment
consists of bed rest and fluid with simple analgesics.
MAIN CONTRAINDICATIONS TO LP: Increased ICP from
mass lesion, coagulopathy (INR needs to be < 1.5, platelets
>40,000), infection over the area to be punctured.
Adapted from: University of Illinois College of Medicine (2007)
www.med.uiuc.edu/internalMed/residency/ICUhandbook/LumbarPuncture.php

26

Typical lumbar puncture tubes sent are:

Tube #1: glucose & protein (also need blood glucose at the same time)
+/-Oligoclonal bands (in suspected MS or demyelinating lesion, there is
a specific CSF study from you need to fill out with blood tests that have
to be taken concurrently
Tube # 2: cell count & differential
Tube # 3: gram stain & culture
Tube #4: viral, fungal and other infectious agents (AFB staining,
serology)
Tube #5: cell count & differential (in case it was traumatic, will see
RBC decrease from tube 2 to 5)
PRN tubes:
PCR for HSV (in suspected herpes encephalitis)
Cytology (need at least 4-5 mLs)
Common CSF Results
Condition

PMNs

Monos

Normal
Values
SAH
Bacterial
Meningitis
Viral
Meningitis

0-3

RBC
s
0-3

sev
days

HSV
N

Prot

Gluc

<.45
mg
*

60% of
serum
N

Immune
**
0

Cytology
N cells

N
?

N
N

Neoplastic
N

N
(+)
Meningitis
GBS
N
N
N

N
N
N
MS
N

N
Poss N

N
Root Dz
N
N
N

N
N
N
*=in proportion to RBCs (if traumatic tap- correct WBC value by subtracting 1
WBC for every 700 RBCs)
**Specific Immunology tests: i.e. gamma globulins, oligoclonal bands

27

CHANGES IN MENTAL STATUS:

Encephalopathy: non specific term indicating diffuse cortical/subcortical
process
Delirium: acute confusional state with agitation and hallucinations
Dementia: sustained, acquired disorder of memory & cognition
Initial Evaluation:
Hx: previous or recent illness, including psychiatric d/os, head trauma,
surgeries, dates of indwelling line/catheters, medications, drug, or
alcohol abuse/withdrawal
General P/E: signs of infection/pt looks toxic, nuchal rigidity (SAH,
meningitis) => do not test nuchal rigidity if problem cervical spine/
fracture; signs of trauma, goiter, cyanosis, stigmata of liver dz, embolic
phenomena, signs of drug use
Neuro Exam: MMSE if possible
Observation for spontaneous mvts, response to stimuli, papilledema
CNs: Pupils: size & reactivity: pinpoint (opiates); midposition &
fixed (midbrain lesion), fixed and dilated [severe anoxic
encephalopathy; eye position at rest, visual threat, corneal reflex,
cough/gag (with ET tube manipulation if necessary)], dysarthria;
intact oculocephalic: (dolls eyes: eyes move opposite to head
movement) imply brainstem intact
Noxious stimuli detects general sensation to pain and motor response
in extremities (ie. purposeful vs posturing)
DTR/clonus, Plantar responses/Babinski
Dx:
Labs: CBC, lytes, Ur, Cr, glucose ABGs, LFTs, PTT/INR,
TSH, B12, Calcium/albumin, +/-troponin, +/-tox screen
Infection workup: U/A, CXR, blood cultures
Head CT if focal signs; cervical xrays to r/o C-spine fracture
Consider: LP to r/o meningitis if hx/p/e suggests
Consider: EEG to r/o subclinical szs (non-emergent)

Patients with underlying brain disorders (i.e. dementia) & extremes of age
are more likely to become delirious.
Risk factors include multiple medical problems, history of alcohol abuse,
sleep deprivation, visual or hearing impairment

28

Differential Diagnosis of Delirium 'I WATCH DEATH'

HIV, sepsis, Pneumonia, SBE, meningitis (elderly:
Infection
pneumonias, UTIs)
ETOH, barbiturates, neuroleptics, anticholinergics
Withdrawal
Lytes (i.e. hyponatremia), acidosis, alkalosis,
Acute
hypoglycemia, hepatic failure, renal failure,
metabolic
pancreatitis, CTD
Closed-head injury (SDH, SAH), heat stroke, postop,
Trauma
severe burns, hip/vertebral #, concealed bleed, urinary
retention, fecal impaction
CNS pathology Abscess, tumour/mets, hemorrhage, hydrocephalus,
subdural hematoma, Infection, seizures, stroke,
vasculitis, Encephalitis, meningitis, syphilis, AVM
Anemia, carbon monoxide poisoning, hypotension,
Hypoxia
Pulmonary (COPD) or cardiac failure CHF, PNA
Vit B12, folate, niacin, thiamine, protein, calories,
Deficiencies
water
Hyper/hypoadrenocorticism, hyper/hypoglycemia,
EndocrinoMyxedema, hyperparathyroidism; (thyroid, cortisol,
pathies
Ca, cytokines)
Acute vascular Hypertensive encephalopathy, stroke, arrhythmia,
shock, intracerebral bleed
Prescription drugs, illicit drugs, pesticides, solvents
Toxins or
Really anything if elderly, but anti-cholinergics, long
drugs
acting benzos narcotics (meperidine) and other
psychotropics cause most problems
Heavy Metals Lead, manganese, mercury
Initial Rx: Identify underlying cause!
Control airway, monitor vital signs, IV access
Consider:
Immobilization of c-spine if concern for cervical trauma
Thiamine (100 mg IV) prior to glucose to prevent exacerbation of
Wernickes encephalopathy then Dextrose (50 g IV push)
Naloxone 0.01 mg/kg if opiates suspected;
Flumazenil 0.2 mg IV if benzos suspected
If concerned for ICP/herniation: head of bed +/-mannitol,
hyperventilation, +/-dexamethasone, consider emergent surgical
decompression
29

SEIZURES:
Seizure (sz): paroxysmal excessive discharge of CNS neurons
Epilepsy: recurrent szs due to an underlying cause
Partial or focal szs (involves discrete areas, implies a focal, structural
lesion)
Simple: without impairment of consciousness/memory, may be motor,
sensory, autonomic or psychic
Complex: with impairment of consciousness/memory, may have
automatisms [stereotypical behaviours manifested with simple
involuntary motor activities (i.e., chewing)] or psychogenic features
Partial with secondary generalization: starts focal, becomes diffuse
Generalized szs: (diffuse brain involvement)
Tonic-clonic (grand mal): tonic phase (10-20 secs) with contraction of
muscles (causing expiratory moan, cyanosis, pooling of secretions,
tongue biting) with clonic phase (~ 30 secs) with intermittent relaxing
and tensing of muscles
Absence (petit mal): transient lapse of consciousness w/o loss of
postural tone
Myoclonic (infantile spasms, juvenile myoclonic epilepsy): sudden
brief contraction
Also: atonic (epileptic drop attacks), atypical absence, infantile
spasms, tonic, clonic
DDx of seizure.
Syncope; Confusional migraine; Stroke or TIA, Vertigo
Sleep disorder (narcolepsy); Episodic movement disorder
Metabolic encephalopathy (asterixis and change in mental status)
Cardiac arrhythmia, Hyperventilation, Breath-holding spell (pediatric)
Hypoglycemia, Night-terrors (pediatric)
Psychogenic seizure (pseudoseizure)
Seizure Etiology
Alcohol & benzo withdrawal, medications (sub-therapeutic AEDs,
beta-lactams, Demerol, cyclosporine), illicit drugs
Brain: congenital, tumour (esp GBM), trauma
Cerebrovascular dz: including subdural hematoma
Degenerative d/o of the CNS (Alzheimers Disease)
Electrolyte (decreased Na, glucose), uremia, liver failure
+ Triggers (lack of sleep, flashing lights, music)
Assessment of Seizure
30

Hx
Prior Szs: AED treatment, recent compliance with AED
Prior szs are best predictor of subsequent seizures
Risk Factors: Developmental delay, remote CNS injury, FHX
PMHx: Systemic illness, CNS illness (prior meningitis/encephalitis),
head trauma or surgery, stroke, febrile; meds or changes in meds;
ETOH/drug use
Initiating Factors: Stress & sleep deprivation poss precipitants
Ictal onset -> Aura (sec to min): peculiar visual, auditory, olfactory, or
psychic prodrome (classic for focal szs)
Ictal (during sz) (sec to min)
Does the pt remember events of the seizure; did anyone witness sz for
collateral hx?
Sympt Sequence: Stereotypic sequence suggests epileptic sz or
syncope; a variable sequence suggests psychogenic pseudoseizures
(events)
Vocal: Gasp, cry, slurred words, or garbled speech? (esp scream of
GTC)
Motor features: Focal or generalized movements, automatisms, eye
deviation, or eye or head turning-> Even brief focal or lateralizing
features at onset indicate an initial partial seizure
Autonomic features: Drooling, pupillary dilation, vomiting, change in
heart or respiratory rate; urine or stool (uncommon) incontinence
strongly suggests GTC; any incontinence rare in syncope or
pseudoseizure
Cognition and awareness: Complete or partial loss of consciousness
Even limited ability to speak or understand excludes a GTC
Termination: Rapid, slow, obvious, subtle? Termination rapid with
absence seizures
Duration: Most seizures last less than 3 minutes; absence seizures last
less than 30 seconds
Postictal (mins to hrs)
Slowly resolving period of amnesia, confusion, lethargy, aches /pains;
+/- focal neurological deficits or residual weakness (Todds paralysis)
Sequelae: "Unprotected falling" with significant injury suggests
epileptic seizure; tongue biting suggests GTC

31

Sz P/E
General: Wastings (symptomatic epilepsy or comorbid disease)
Vital signs: Fever (Intra- or extracranial infection); Hypertension
(Hypertensive encephalopathy)
Skin: hepatic or renal failure, or illicit drug use
neurocutaneous syndrome: symptomatic seizure; caf-au-lait spots,
facial angioma, or axillary freckling
HEENT: Tongue bite marks, hematoma or laceration of the scalp, face,
or neck (consider: sz 2 to CNS trauma or trauma 2 to sz)
Abnormal visual fields: lesion of optic pathway
Nystagmus Drug toxicity, especially if associated with ataxia
Cardiovascular: Carotid artery bruit or signs of cardiac disease (Marker
for cerebrovascular disease, especially elderly)
Abd: organomegaly or mass lesion (also in other locations, eg, breast) > CNS metastasis-related seizure or a metabolic storage disease
GU: Urinary incontinence
Neurologic
Mental status: Abnormal memory, language function, abstract thinking
CN: nystagmus, papilledema (toxicity, ICP); eye deviation
Motor: lateralized upper motor neuron signs; lesion in the frontal lobe;
transient Todd paralysis suggests focal onset
Sensory: hemisensory loss
Coordination: ataxia, dysmetria (Drug toxicity)
Investigations:
Labs: CBC, lytes, Ur/Cr, gluc, LFTs, TSH, tox screen, AED levels
CT initially than consider MRI to r/o structural abnormalities
Consider LP (after r/o space occupying lesions): if suspect meningitis
or encephalitis and in all HIV (+) pts
EEG: to identify seizure focus
Instructions to Pts: The Ministry of Transport must be informed (ask
for forms at ACC desk). Pts with epilepsy must be adherent with
medications and seizure free for 1 year in Ontario in order to regain a
class G license. Pts should not be alone in water (bathtub, swimming);
risks with scuba diving, climbing, unprotected heights, & open
flames. Precautions are required with cooking.
=> These restrictions can be modified once effective treatment has been
established or it has been established that recurrence risk is low.

32

Status epilepticus
State of continuing szs (any type, although common usage refers to
tonic-clonic szs) so frequent as to produce "an enduring ictal state."
Common practice defines status epilepticus as > 30 min of continuous
seizing or frequent back-to-back szs without intervening recovery.
Complications: neuronal death, rhabdomyolysis, lactic acidosis
Rx for Status Epilepticus
ABCs: Stabilize patient oral airway/cannular or non-rebreather mask
and pulse oximetry, RR, HR, BP +/- ABGs
Establish 2 good i.v. access points
Labs: CBC, lytes, Ur/Cr, Gluc, Calcium/albumin, Mg, coagulation
tests, Toxic screens, AED levels
EKG and cardiac monitor.
Rule out treatable causes for status. Start NS
Consider i.v. glucose 50cc 50% + thiamine 100 mg IV
Consider naloxone 0.4-2.0 mg.
Step
1

3
4

Status Epilepticus Rx
Lorazepam (ativan)* I.V.: 4 mg/dose slowly
over 2-5 mins; may repeat in 10-15 mins;
If seizures continue, infuse lorazepam (up to a
cumulative dose of 0.1 mg/kg) at max rate of 2
mg/min, and start phenytoin in another IV
infusion.
Or Diazepam (valium) 0.2 mg/kg @ 5 mg/min
Phenytoin 20 mg/Kg at 50 mg/min
Even if seizures terminate after the initial
lorazepam dose, phenytoin is indicated to
prevent sz recurrence. Reduce rate if significant
adverse effects of the infusion are seen.
Phenobarbital 20 mg/kg at 50-75 mg/min + 510 mg/kg if still sz

Typical dose
4 mg IV
pushes
usual max
dose: 8 mg
5-10 mg IV
pushes
1-1.5 g IV
over 20 mins

1-1.5 IV,
(max 100
mg/min)
General anesthesia with propofol, midazolam, phenobarbital

When seizures controlled, then get history, CT or MRI scan, LP

33

STROKE
I. ISCHEMIC STROKE (70%)
Etiology:
Thrombotic (~ 25%): lacunar (arteriolar, seen in HTN/DM) or large
vessel
causes: intracranial/carotid artery atherosclerosis, carotid dissection,
non-inflammatory arteriopathies (fibromuscular dysplasia, lacunar
infarcts/small vessel disease, migraines, moya moya), vasculitis,
hereditary (CADASIL, homocystinuria), drugs (cocaine,
amphetamines), hematological [sickle cell, polycythemia,
hypergocaogulable states (cancer, pregnancy, OCP, anti-phospholipid
antibody, prot C deficiency, thromobocytosis)]
progression of symptoms of hrs to days with stuttering course
Embolic (~75%) artery-> artery, cardioembolic
causes: atrial fibrillation, valvular disease, MI/wall motion
abnormalities, septal aneurysms, PFOs, dilated cardiomyopathy)
rapid onset at maximum severity, +/- during activity
Cryptogenetic unknown etiology
Artery
Clinical Manifestations
Ophth (off Amaurosis fugax (transient monocular blindness)
ICA)

MCA

ACA
PCA
Vertebral
Basilar
Lacunar

Hemiplegia (face, arm> leg); hemianesthesia,

homonoymous hemianopia;
Aphasia if dominant hemisphere (ant-> expressive;
post -> receptive [check])
Apraxia & neglect if non-dominant hemisphere
Later: drowsiness & stupor seen later due to edema
Hemiplegia (leg> arm, face); confusion, urinary
incontinence, primitive reflexes
homonymous hemianopia (macular-sparing) Thalamic
syndromes with contralateral hemisensory disturbance
Wallenbergs syndrome (numbness of ipsilat face and
clat limbs; dysarthria, ipsilat Horners) (or PICA)
Pinpoint pupils, long tract signs (quadriplegia and
sensory loss), CN abnormalities, cerebellar dysfunction
Very small area of stroke with pure motor hemiplegia,
pure hemianesthesia, ataxic hemiparesis, or dysarthria
& clumsy hand

Adapted from Pocket Medicine, p 9-4

34

Circle of Willis
ACA = anterior cerebral artery; AICA = anterior inferior cerebellar artery;
ICA = internal carotid artery; MCA = middle cerebral artery; PCA = posterior cerebral artery;
PICA = posterior inferior cerebellar artery; SCA = superior cerebellar artery.
(Reproduced from Pritchard TC and Alloway KD. Medical Neuroscience.
Madison, Connecticut: Fence Creek Publishing, 1999: 78. Fence Creek Publishing, LLC.)

Localization:
Cortical strokes: more often caused by cardioembolic sources or
internal carotid atherosclerosis (clinical signs: aphasia, apraxia,
visuospatial deficits, neglect, or loss of cortical sensory modalities)
Small vessel subcortical strokes are more likely to be related to HTN
& DM
Attempt to localize to a particular vascular territory-> do not forget
that there may be multiple lesions (i.e., with embolic strokes)

35

Establish Stroke Risk Factors: previous stroke/TIA, MI, atrial

fibrillation, smoking/ETOH/drug use, DM, bleeding d/o or
coagulopathy, OCP
Initial Stroke Management:
Verify airway (GCS<8 or not protecting airway-> consider
intubation), vital signs (BP control < 200 systolic for approximately 72
hrs after ischemic stroke), ensure IV access
SEE STROKE CODE Package in Emergency Room
TO VERIFY IF YOUR PATIENT IS ELIGIBLE FOR TPA!!!
Labs: CBC, lytes, Cr/Ur, gluc, PTT/INR, fasting lipids, LFTs,
CK/TnT; if patient young, consider hypercoagulable w/u & BhCG
ECG & CXR as baseline
Urgent CT head: first: non-contrast CT to r/o hemorrhage +/- CTA to
evaluate cerebrovascular anatomy & patency & cerebral perfusion
Look for: minor effacement of sulci, loss of gray/white
differentiation, hyperdense vessel sign, blurring of internal
capsule/caudate nucleus; signs of larger infarcts that prohibits tPA
include +edema/mass effect, major sulcal effacement, intracerebral
hemorrhage
MRI: superior imaging but may not identify acute hemorrhage
without special sequences
For the following day: Carotid Doppler, TTE/TEE and repeat CT head
24 hrs post TPA if applicable
Rx:
Antiplatelet therapy: with ASA (81 mg) or clopidogrel (Plavix-300 mg
loading dose then 75 mg once daily) or ASA & dipyridamole
(Aggrenox 1 tab bid))
If you are worried about dissection/embolic etiology, consider Heparin
IV => Coumadin (for known/presumptive cardioembolic TIAs)
Carotid vascularization may be indicated if > 70% ipsilateral stenosis
(consider neurosurgery/interventional neuroradiology consult)

II. HEMORRHAGIC STROKE (30%)

36

Etiologies:
Intracerebral (ICH ~67%): HTN, AVM, amyloid angiopathy,
anticoagulation/thrombolysis, mass lesions (tumours, AVMs,
cavernous angiomas), ischemic stroke transformation
1 (no underlying lesion) vs 2 (underlying lesion identified)
sudden level of consciousness; N/V +/- h/a; -> progressive focal
neurological deficits depending on site of hemorrhage
Subarachnoid (SAH ~ 33%): ruptured AVMs, aneurysm (berry,
mycotic), trauma
sudden, severe h/a (worst h/a of life), N & V; meningeal irritation
(nuchal rigidity, Kernigs, Brudzinki); in level of consciousness
Dx: as per ischemic stroke
Rx:
Reversal of any coagulopathies
Recombinant factor VII is under review
Strict BP control with SBP goal < 180, unless risk for hypoperfusion
(i.e. critical carotid stenosis)
ICH: consider surgical decompression for large hemorrhage with
clinical deterioration
SAH: nimodipine to risk of vasospasm, phenytoin for sz prophylaxis,
endovascular/surgical correction of aneurysm/AVM to prevent
rebleeding

Stroke Codes:
37

There are binders in the ER with Stroke Code packages including NIH
scales, tPA guidelines and contraindications to tPA.
Contraindications to IV tPA (check Stroke Package in the ER for
most recent exclusion criteria)
Exclusion Criteria
Period from 1st symptoms to tPA >3 hours
Minor neurological deficits (i.e. ataxia, pure sensory, dysarthria,
mild motor), NIHSS <4
Symptoms suggestive of SAH, even with normal CT head
Ischemic stroke or head trauma in the past 3 mos
History of intracranial hemorrhages with ongoing risk of
reoccurrence
Bleeding of GI, GU in the past 3 weeks
Major surgery or serious trauma within previous 2 weeks
Known bleeding diathesis
Pregnant
Recent MI (within 3 weeks) or pericarditis (within 3 months)
Possibility of migraine, post-ictal, tumour, MS
Intracranial hemorrhage on CT (even small petechiae)
Prolonged PTT or INR > 1.4 (i.e., patient on Heparin/Coumadin)
Blood glucose < 3 mmol/L
Platelets < 100
BP > 185/110 in spite or treatment
Relative Exclusions
Arterial puncture over noncompressible site in previous 7 days
LP in previous 7 days
Liver failure
Blood glucose > 22 mmol/L
Ct shows tumour, AVM, aneurysm

38

NIH Scale

Blumenfeld (2002)

39

Level of consciousness
Alert, responsive
Requires minor stimulation to respond
Requires repeated or painful stimulation to respond
Comatose or responds only with stereotyped
movements
LOC Questions
Both questions correct
One question correct
Neither question correct
LOC Commands
Both responses correct
One response correct
Neither response correct
Best Gaze (in horizontal directions)
Full gaze in all directions
Partial gaze palsy
Total gaze paresis or forced paresis not overcome
by oculocephalics
Visual Fields to confrontation
Fully intact
Partial hemianopia (i.e. asymmetric visual fields)
Complete Hemianopia
Bilateral Hemianopia (including cortical blindness)
Facial Palsy
Normal & Symmetric
Minor-flattened nasolabial fold, asymmetry with
smiling
Partial paralysis (e.g. of lower face only)
Complete paralysis (upper & lower) of one or both
sides

0
1
2
3
0
1
2
0
1
2
0
1
2
0
1
2
3
0
1
2
3

40

NIH Scale Part 2

Best Motor of arm & leg (holding limb at 90
degrees)
No drift for 10 seconds
Drift
Some movement against gravity, but falls by 5 secs
No movement against gravity
Limb Ataxia (finger-nose, heel-knee-shin)
Absent
Present in 1 limb
Present in 2 limbs
Sensory (to pinprick, grimace/withdrawal counts if
obtunded)
Normal
Mild/moderate loss (identifies prick but impaired
discrimination)
Severe loss (cant identify prick)
Best language (regarding standard set of pictures)
No aphasia
Mild/moderate aphasia (impaired comprehension, word
finding and naming difficulties, semantic or phonemic
paraphasias)
Severe aphasia
Mute, global aphasia
Dysarthria
None
Mild slurring, but intelligible
Severe, unintelligible
Extinction & inattention (double stimulus
stimulation)
Normal
Hemi-inattention in one of the sensory modalities
(visual, tactile, auditory, special)
Hemi-attention in more than one modality
Total

0
1
2
3
0
1
2
0
1
2
0
1
2
3
0
1
2
0
1
2
/30

41

Headaches
H/a Assessment:
Onset: chronic h/as less likely serious disease, unless pt > 50
Frequency: characterize h/a pattern
how often do h/as occur, how long do they last
Pain: sharp vs dull, throbbing, scale 1-10
Migraine: throbbing/pulsatile most common, often hemicranial with
stereotyped triggers (fatigue, stress, anxiety, menstruation, alcohol),
photophobia, photophonia
Tension: tight band across forehead, or temples
Cluster: very intense sharp pains, mostly behind eyes (retroorbital) or
temple; usually unilateral; lacrimation or injection, rhinorrhea
Mass lesions: constant, dull, usually ipsilateral; symptoms of
increased ICP (N/V, blurry vision, decreased LOC), worse in morning
or with prolonged recumbency or vasalva
Meningitis: appears unwell, altered level of consciousness, fever,
hypotension, rash, nuchal rigitidy
Pseudotumour cerebri: symptoms of increased ICP, blurry vision, +/obesity, OCP use
Trigeminal neuralgia: shock-like pain (often V2-V3 distribution)
Temporal arteritis: temple pain and difficulty chewing, polymyalgia
rheumatica, scalp tenderness
Glaucoma: increased eye pressure
Associated neck pain: cervicogenic h/as, SAH, meningitis, dissection
Non Pharmacological Therapies:
Adequate nutrition & hydration, avoidance of known triggers, d/c
caffeine & nicotine

42

Red flag
Headache
beginning after
50 years of age
Sudden onset of
headache
Headaches
increasing in
frequency and
severity
New-onset
headache in a pt
with risk factors
for HIV or
cancer
Headache with
signs of
systemic illness
(fever, stiff
neck, rash)
Focal
neurologic signs
& symptoms
(other than
typical aura)
Papilledema
Headache
subsequent to
head trauma

Red Flags in Acute Headaches

Differential diagnosis
Investigations
Temporal arteritis (visual
ESR,
changes, TMJ pain), mass
neuroimaging
lesion
SAH, dissection, pituitary
Neuroimaging; LP
apoplexy, hemorrhage into
if neuroimaging
mass lesion, ruptured AVM negative*
Mass lesion, subdural
Neuroimaging,
hematoma, medication
drug screen
overuse
Meningitis (chronic or
carcinomatous), brain
abscess (including
toxoplasmosis), metastasis

Neuroimaging;
lumbar puncture if
neuroimaging is
negative*

Meningitis, encephalitis,
Lyme disease, systemic
infection, collagen vascular
disease

Neuroimaging,
lumbar puncture,
serology

Mass lesion, vascular

malformation, stroke,
collagen vascular disease

Neuroimaging,
collagen vascular
evaluation
(including
antiphospholipid
antibodies)
Neuroimaging,
lumbar puncture
Neuroimaging of
brain, skull and,
possibly, cervical
spine

Mass lesion, pseudotumour

cerebri, meningitis
Intracranial hemorrhage,
subdural hematoma,
epidural hematoma, posttraumatic headache

Adapted from Newman LC, Lipton RB. Emergency department evaluation of headache.
Neurol Clin 1998;16:285-303/ American Family Physician (2001) 63/No. 4

43

Weakness and Neuromuscular Dysfunction

Feature
Atrophy
Weakness
Distribution
Fasciculations
Tone
DTRs
Babinski

UMN
None
Pyramidal
None
Increased
Increased
Present

LMN
Severe
Distal,
segmental
Common
Decreased
Decreased
Absent

Myopathy*
Mild
Proximal
None
[N]/decreased
[N]/increased
Absent

*In some muscular dystrophies, atrophy can be focal and marked

Adapted from Pocket Medicine, p 9-6

Up to Date, Weakness algorithm, 2007

44

Peripheral Neuropathies
Clinical Manifestations:
Sensory: numbness (loss of light touch, vibration, proprioception),
tingling (paresthesias), burning/jabbing (dysesthesias), heat/cold
intolerance
Motor: muscle weakness, muscle atropy, cramping, fasciculations
Autonomic: dyshydrosis, sicca (dry eyes & mouth), GI & sexual
dysfunction
DDx:
1. Mononeuropathies (one nerve): trauma (compression, entrapment),
DM, Lyme disease
2. Polyneuropathy (symmetric nerves, usually length dependent)
a) Demyelinating:
Acute: acute idiopathic demyelinating polyneuropathy (AIDP) (i.e.
Guillan-Barr Syndrome);
Chronic: CIDP, paraproteinemia, rarely paraneoplastic, CharcotMarie Tooth type I
b) Axonal
Acute: axonal GBS, porphyria (acute intermittent, variegate);
Subacute; sepsis, critical illness polyneuropathy (after ICU admission),
B12 deficiency, alcohol, meds (statins, chemotherapy); Chronic: DM,
uremia, lead, arsenic, Lyme, HIV, paraneoplastic, paraproteinemia
3. Mononeuropathy multiplex (multiple, non-contiguous, separate
nerves) => vasculitis (SLE, PAN, RA, scleroderma); granulomatous
(sarcoidosis, Wegeners), DM, hereditary (neuropathy with pressure
palsies)
Diagnostic Studies
Initial: Labs [CBC, lytes, Ur/Cr/Glucose, HbA1C, B12, LFTs, TSH,
ANA, RF, ESR +/- SPEP/UPEP], followed by NCS & EMG
Secondary tests as indicated by clinical hx i.e.Hep B/C, HIV, Lyme
titers, Heavy metal, CXR (neoplasm), +/-muscle biopsy

45

Guillan Barr Syndrome (GBS)

GBS= Acute Idiopathic Demyelinating Myopathy
most common cause of acquired generalized paralysis
Etiology: predominantly after infection => immune reaction resulting
in cellular & humoral responses that attack myelin components
precipitated by gastroenteritis (esp Campylobacter jejuni), URTI
(Mycoplasma), viral illness (EBV, CMV, HSV)
Clinical Manifestations:
Initially: numbness & tingling in fingers, toes trunk with ascending,
symmetric paralysis over hours to days; facial involvement (50%)
Respiratory compromise requiring ventilatory assistance in 1/3 of
patients! Autonomic instability and arrhythmias may also occur.
Hypoactive or absent reflexes
Sensory dysesthesias: dull aching or burning pain in L/Es or low back
is common
Diagnostic Imaging:
LP; albuminocytologic dissociation (increased protein without
pleocytosis <20 lymphocytes); Anti GQ1B if Miller Fisher variant
EMG & NCS: decreased nerve conduction velocity and conduction
block
Rx:
Plasma Exchange or IVIG (no role for steroids)
Supportive care with monitoring in NeuroObs/ICU if any signs of
worsening; PT/OT, DVT prophylaxis, pulmonary care & tracheostomy
if prolonged intubation, +/-tube feedings
ICU admission if likely to need mechanical ventilation
Vital capacity <20 mL/kg [~ FVC <1]
Maximum inspiratory pressure <30 cmH2O
Maximum expiratory pressure <40 cmH2O
Rapid progression (<7 days) of weakness
Inability to raise the head against gravity
Bulbar dysfunction (e.g., dysphagia, dysphonia, aspiration)
Bilateral facial weakness
Significant autonomic dysfunction (eg, orthostatic hypotension/BP
lability, cardiac arrhythmias)
Myasthenia Gravis:
46

Autoimmune disorder caused antibodies directed against the

acetylcholine receptor protein (AChR) in NMJ of skeletal muscle;
=> Muscular weakness, aggravated by continuing activity, improved
with rest and anti-acetylcholinesterase medications
Incidence: women (2-3rd decades) vs men (6-7th decades)
Clinical Manifestations:
Cranial muscles involved early -> ptosis & diplopia most common
symptoms, +/- difficulty chewing, dysarthria, dysphagia
Weakness and especially fatiguability, worse with repetitive use
Limb weakness: fluxuating (best in morning), proximal>distal,
Reflexes usually preserved
Exacerbations triggered by stressors, such as URTI, surgery, meds
(e.g., aminoglycosides, procainamides)
Myasthenic crisis (diaphragm & chest muscles become weak)=> need
for respiratory assistance
Cholinergic crisis: ( salivation, abdominal cramping, diarrhea)
weakness due to overtreatment with anticholinesterase inhibitors
Investigations:
P/E: sustained upgaze, repetitive deltoid testing
Labs: Anti-Acetylcholine antibody receptor antibody screening (85% +
in systemic MG and 50%+ in ocular MG); TSH, T3, T4
Tensilon test (edrophonium): temporary increase in strength, many
false positive and negatives; need atropine at the bedside
EMG: response with repetitive nerve stimulation (vs response in
Lambert-Eaton)
CT/MRI of thorax to evaluation thymus (65% hyperplasia, 10%
thymoma)
Treatment:
Acetylcholinesterase Inhibitor medications (pyridostigmine-Mestinon)
Immunosuppression: prednisone, cyclosporine, azathioprine, cellcept
Thymectomy: mandatory if thymoma; also leads to improvement in
85% of patients without thymoma
Myasthenic crisis: IVIG or plasmapheresis; treat precipitant; aggressive
immunosuppression with glucocorticoids,
d/c anticholinesterase medications to r/o cholinergic crisis

47

MANAGEMENT OF NEUROLOGICAL EMERGENCIES

Guillain Barr Syndrome
Airway: incentive spirometry, assisted coughing
Intubation if vital capacity 15 ml/kg and max inspiratory pressure
20 mm Hg
Fluids: NS IV
Nutrition (depends on severity):
Full strength enteral nutrition, parenteral nutrition if ileus
Specific Rx
IVIG 0.4 g/kg for 5 days or plasmapheresis
Ranitidine if mechanically ventilated
Ted stockings, s/c heparin
Pain management
Coma: Always start with ABCs
Cardiac monitor, pulse oxymeter, BP cuff on
Glucoscan
Stat IV NS, CBC, lytes, glucose, Ur/Cr, LFTs and blood/urine
toxicology screen unless reason for coma known
After checking glucoscan, may need to give:
D50W 50 cc & Thiamine 100 mg IV
Consider Narcan 0.4 g (1 amp)
Get hx from relatives/friends
P/E
Vitals
GCS
General: ETOH smell, tongue bite, meningismus, signs of trauma,
infection, IV drug skin tracts
Eyes: fundi, PEARL, EOM if possible, oculovestibular reflex,
corneals, facial asymmetry, gag
Neuro exam -> look for localizing sings
CVS, Resp, Abdo etc
Investigations depend on P/E
CT (no contrast) for localizing CNS signs, LP if possible CNS
infection, metabolic screen (ABGs, Ca/Phosphorous/Mg, B12, TSH,
antiepileptic levels etc), CXR, EKG, U/A
Additional management will depend on findings-> discuss DNR status
if appropriate

48

Increased Intracranial pressure

Etiology of ICP
Intracranial HTN:
Intracranial Hemorrhage
TBI, ruptured aneurysm, AVM, other vascular anomalies
CNS infections, neoplasm, vasculitis, ischemic infarcts, hydrocephalus,
pseudotumour cerebri, idiopathic
Cushing Response due to ICP
Systolic pressure increases -> widened pulse pressure
Bradycardia (occurs as result of reflexive slowing in response to
increased systolic pressure)
Decreased respiration rate
Management
Elevate head of bed 15 degrees.
Osmotic Diuresis:
Mannitol, IV, 1 -1.5 g/kg over 1 hour. (Do not repeat.)
Hypertonic saline 3% 50 mL/10 minutes [controversial]
MONITOR: Plasma osmolality (310-320mOsml/L), Ur/Cr, lytes, urine
output
Hyperventilation:
Maintain PCO2 at 2530 mmHg; intubate/ventilate if necessary.
Increase respiratory rate to 20 breaths/minute (AC or IMV mode)
Monitor: PC02; daily CXR for poss pneumothorax
Diuretics
Furosemide, i.e. 40 mg IV bid
Consider steroids if vasogenic edema (i.e. steroids)

Evidence of ICP: h/a, vomiting, HTN, HR,

papilledema, unilateral dilated pupil

49

Neurology Terminology
Abulia: loss of initiative, willpower or drive
Acalculia: inability to calculate
Agnosia: inability to recognize one or more classes of environmental
stimuli, even though necessary intellectual and perceptual functions are
intact
Agraphia: inability to write
Alexia: inability to read for comprehension
Amnesia: inability to retain new information
Amaurosis fugax: transient loss of vision in one eye, often like a
"window shade", due to vascular disease of the retina: a TIA of the eye.
Anisocoria: unequal pupils (by more than 1 mm).
Anomia: inability to name objects or think of words; often used a
synonym for dysnomia
Anosognosia: inability to recognize ones own impairment
Aphasia: complete loss of language function, but often used as
synonym for dysphasia
Apraxia: inability to perform a previously learned set of coordinated
movements even though the necessary component skills (including
intellect, language function, strength, coordination and sensation)
remain intact
Beta activity: in EEG, 13-35/sec activity.
Blepharospasm: involuntary closure of the eyes. This is a form of
movement disorder related to dystonia.
Broca aphasia: acquired language disorder characterized by non-fluent
verbal output with omission of relational words (prepositions,
conjunctions, articles and minor modifiers) and abnormal prosody,
impaired repetition and relatively intact comprehension
Brown-Sequard syndrome: dysfunction of half of the spinal cord, with
line of dysfunction in the anteriorposterior direction.
Conduction aphasia: acquired language disorder characterized by
prominent impairment of repetition, relatively intact comprehension
and verbal output that is fluent but contains literal paraphasias
Delirium: acute confusional state characterized by clouded, reduced or
shifting attention, often associated with sensory misperception or
disturbed thinking
Dementia: acquired impairment of memory and at least one other
cognitive function, without clouding of the sensorium or underlying
psychiatric disease
Doll's eye maneuver: tests for functioning oculocephalic reflex, by
which eyes remain relatively stable when the head is quickly turned.
Dysnomia: difficulty naming objects or finding the desired words
50

Dysphasia: acquired disorder of language not due to generalized

intellectual impairment or psychiatric disturbance
Expressive aphasia: acquired language disorder in which verbal output
is nonfluent (motor, Brocas aphasia)
Glabellar reflex: blinking to a tap between the eyes. Doing so once or
twice as normal, but failure to inhibit is abnormal.
Hemianopia: loss of vision in 1/2 of a visual field.
Hemiballismus: violent flinging movements of a limb, classically
associated with injury to the contralateral subthalamic nucleus.
Homonymous hemianopsia: loss of half of the visual field in each eye,
matched to the same side.
Horner's syndrome: ptosis, meiosis and anhydrosis, due to injury to the
sympathetic nerves to the eye.
Internuclear ophthalmoplegia: ipsilateral eye does not cross midline
and contralateral eye has nystagmus, associated with MLF lesion.
Korsakoff's amnesia: profound short-term memory problems,
classically attributed to thiamine deficiency or mammary body injury.
Marcus-Gunn pupil: pupil with an afferent defect to light. It dilates in
the "swinging flashlight" test.
Meralgia paresthetica: numbness on the anterior thigh, due to injury
to the superficial femoral cutaneous nerve.
Mydriasis: dilation of the pupil, the opposite of miosis.
Neurofibroma: a benign tumor of nerve or nerve roots, sometimes in
association with neurofibromatosis.
Neurofibromatosis: hereditary condition with multiple neurofibromas
(type I) or bilateral acoustic neuromas (type II), and other findings.
Nonfluent aphasia: acquired language disorder with verbal output that
is sparse, with only one to four words per phrase
Palmomental reflex: a primitive release reflex in which scratching the
ulnar side of the hand causes twitching of the ipsilateral mouth
Paraphasia: a substitution error in which the word produced is similar
in sound or meaning to the intended word; a literal or phonemic
paraphasia is a sound substitution error, resulting in production of a
word that is phonemically related to the intended word (e.g., greed
instead or green); a semantic or verbal paraphasia is a word substitution
error in which the word produced is semantically related to the intended
word (e.g., blue instead of green)
Prosody: rhythm or tempo of speech
Prosopagnosia: inability to recognize faces
Pyramidal: part of the cortical spinal tract passing through the
pyramids in the basis of the pons.
Snout reflex: a primitive release reflex, in which tapping the snout
results in puckering of the lips.
51

Transcortical aphasia: acquired language disorder in which the ability

to repeat is intact.
Vestibular-ocular reflex: a normal reflex to stabilize the eyes in space
when the head moves.
Weber syndrome: A IIIrd nerve palsy and contralateral paralysis from a
midbrain lesion.
Weber test: a hearing test, by asking the patient to localize a tuning fork
in midline forehead.
Wernicke aphasia: acquired language disorder characterized by
markedly impaired comprehension and repetition, with verbal output
that is fluent, but contaminated by numerous paraphasias or in severe
cases, jargon
Wernicke encephalopahy: Eye movement abnormalities (or
nystagmus), ataxia, and memory problems, due to thiamine deficiency.

Bibliography
Blumenfeld, H (2002) Neuroanatomy through Clinical Cases. Sinauer. Mass

Davis, L.E. (2005) Fundamentals of neurologic disease : an introductory

text. Demos Medical Publishing, Inc.

Jette, N. (2000) The Ottawa Hospital Neurology Resident Manual, 1st Edition
Fisher, R., Leigh R.., Risinger, M., Stanford Neurology Core Clerkship Manual
Harrisons InternalMedicine (2007)
Merck Micromedex-Best Practice (2007)
Pritchard TC and Alloway KD. (1999) Medical Neuroscience. Madison, CT
Rengachary D., (2004) The Washington Manual Neurology Survival Guide .
Sabatine M. Pocket Medicine 2nd Edition Lippincott Williams & Wilkins
Up to Date (2007)

52

53