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 2Resident Responsibilities 3Discharge Planning 4On call advice 6Death Declaration/Certification 7Screening Neurological Exam 8Neurological Differential Diagnosis 10Localization/Etiological Matrix 11Detailed Neurological Exam 14Investigations & Diagnostic Imaging 22Lumbar Puncture 24Changes in mental status 28Seizures 30Stroke 34Circle of Willis Diagram 33Headache 42Weakness & Neuromuscular pathologies 44Management of Neurological Emergencies 48Glossary of Neurological Terms 50 Appendix/Inserts Neurology Sample Scutsheet MOCA

This edition is based on the detailed work of Dr. Nathalie Jetté & 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.

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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/non-active 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 don’t 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 patient’s 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.

3Discharge Planning:

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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 don’t transfer patients to team B between Friday and Sunday. If a patient’s 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 pt’s 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 pt’s 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).

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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 patient’s discharge. If the patient’s 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 sub-specialty 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.

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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, don’t 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 don’t 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. Don’t 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

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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 A fib Clotting d/o HTN Dyslipidemia Cancer Arthritis • Surgeries • Trauma • Also: perinatal hx & developmental milestones (if applicable) • Immunizations (pediatrics) 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

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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 Kernig’s sign (Knee flexion); Brudzinski’s 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) Motor

Power R L

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

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

Na

K

Cl

CO 2

Urea Gluc

Cr

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

WBC

HgB Plt

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)

LOCALIZATION MATRIX

Mus

cle

Neu

ro-

msc

ular

Ju

nctio

n

Perip

hera

l N

erve

Spin

al C

ord

Bra

inst

em

Dee

p W

hite

M

atte

r/BG

Th

alam

us

Cor

tex

Cer

ebel

lum

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:

ETIOLOGY MATRIX

Dru

gs

Infla

mm

atio

n

Met

abol

ic

Vas

cula

r

Elec

trica

l

Trau

ma

Neo

plas

tic

Deg

ener

ativ

e

Acute Sub-Acute

Chronic Table reproduced with permission by Dr. Chris Skinner

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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 • Headache—usually diffuse • Somnolence and decreased LOC • Meningismus (Kernig, Brudzinski signs) • Cranial nerve signs—often 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

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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.

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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 Don’t forget about: Referred pain (i.e. left arm paresthesias with cardiac origin; Psychiatric (conversion disorder, depression) & other non-neurological (syncope 2° to cardiac arrhythmia)

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

3. Oriented to person, place, date, and situation (A&O x 4)

Glasgow Coma Scale (/15) Eye Opening 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

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.

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C. Cognitive 1. MMSE or MOCA (see ACC desk on 6NW for copies)

Mini-Mental Status Exam (Folstein)

Place-yr/mos/season/day/date /5Orientation Time-Can/prov/city/hosp/flr /53 Objects-i.e penny/brown/honesty Patient has to repeat all 3 (1 pt/each)

/3Registration/ Attention

Serial 7s Or WORLD backwards

/5

Recall 5 Minute recall /3Name-pencil/watch /2Repeat-“no if’s ands or buts” /1Reads command written on paper & follows (i.e. Close your eyes)

/1

3 step command-“Take paper in your right hand, fold it in ½, put it on the floor”

/3

Copy-2 intersecting Pentagons

/1

Language

Write-sentence /1 If < 24/30=cognitive impairment /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.

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2. Cranial Nerves I Olfactory Smell-not usually assessed II Optic Fundi: disc, cup, arteries, veins, maculae, retina

[papilledema, hemorrhages, exudates, atrophy] Pupils (size & reaction to light) Visual Acuity L_____ R______ Visual Fields (to confrontation)

III IV VI

Oculomotor Trochlear Abducens

PERLA EOM (pursuit & saccades) Convergence Diplopia present ___ Nystagmus present ___ Also: Gaze preference, optokinetic nystagmus, Doll’s eye (oculocephalic) reflex, cold calorics, lid lag

V Trigeminal Sensory: face • (V1-ophthalmic, V2 maxillary, V3 Mandibular) Motor: jaw opening/closing (masseters, pterygoids, temporalis); jaw jerk Corneal reflex (afferent)

VII Facial Forehead wrinkling (frontalis muscle) Eye closure (orbicularis oculi muscle) Wide smile, Whistling Blowing (buccinator/orbicularis oris/zygomatic muscles) Taste (anterior 2/3 of tongue)

VIII Acoustic/ Vestibular

Hearing Weber lateralization (if reduced hearing) Rinne: air conduction (< or > than bone conduction) Oculovestibular (caloric) testing (if applicable)

IX Glosso-pharangeal

X Vagus

Gag Dysphonia (“ga-ga-ga”), uvula (deviation opposite to lesion), soft palate (paresis), swallow, cough

XI Accessory Sternocleidomastoid (turn head to opposite side) Upper trapezius (shrug shoulders)

XII Hypoglossal Atrophy, fasciculations, Tongue in midline, deviation to R-L Strength, coordination, dysarthria (“ta-ta-ta”)

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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 -Selective muscle groups -Velocity dependent -Occurs with: o Weakness o Hyperreflexia o Babinski sign

Rigidity -Diffuse in affected limb -Velocity independent -Occurs with: o Parkinsonism (tremor,

bradykinesia, postural instability)

Patterns of Weakness LMN UMN * Paresis + + Atrophy ++ +/- (disuse)

DTR ↓ ↑ Tone ↓ ↑ (spasticity) Fasciculations + ∅ Babinski sign ∅ +

* Hypotonia and hyporeflexia acutely

17d. Power/Strength:

Power R /5 L /5 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)

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

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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 • shoulder abd * • triceps * • supinator * • finger ext * • hip flexors* &

abduct • knee flexors * • ankle dorsiflex *

Spasticity • shoulder add • biceps * • pronator * • finger flex • hip add • knee ext * • plantar flex*

* = commonly tested

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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

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Deep Tendon Reflexes DTRs R L 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

6. Coordination Tremor:

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

• Resting, pill rolling • Intentional • Postural: 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

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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, simple cysts)

low high

Bone/calculi nil nil Collagen tissue low low Fat high med-high Prot containing fluid (abscess, complex cyst

medium high

Hemorrhage • Hyperacute (<24 hrs) low low • Acute (1-6 days) low high • Chronic (>7 days)

o Intracellular o Extracellular

high high

low high

Neuropathology • Ischemia, edema, demyelination, most malignant tumours

low

high

• Meningioma (medium or iso=isointense) med/iso med/iso

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Additional Radiological Findings

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

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

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

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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 pt’s 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

• 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 1–14. (via Access Medicine)

25

26

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 22-gauge) 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. Post-lumbar 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

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 RBC

s Prot Gluc Immune

** Cytology

Normal Values

0 0-3 0-3 <.45 mg

60% of serum

0 N cells

SAH ↑* ↑* ↑↑↑ ↑* N N N Bacterial Meningitis

↑ ↑ N ↑ ↓ ?↑ N

Viral Meningitis

↑ sev days

↑ N→ ↑ HSV

↑ N→↓ N N

Neoplastic Meningitis

N ↑ N ↑ ↓ N (+)

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

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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: (doll’s 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

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Differential Diagnosis of Delirium 'I WATCH DEATH' Infection HIV, sepsis, Pneumonia, SBE, meningitis (elderly:

pneumonias, UTIs) Withdrawal ETOH, barbiturates, neuroleptics, anticholinergics Acute metabolic

Lytes (i.e. hyponatremia), acidosis, alkalosis, hypoglycemia, hepatic failure, renal failure, pancreatitis, CTD

Trauma Closed-head injury (SDH, SAH), heat stroke, postop, 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

Hypoxia Anemia, carbon monoxide poisoning, hypotension, Pulmonary (COPD) or cardiac failure CHF, PNA

Deficiencies Vit B12, folate, niacin, thiamine, protein, calories, water

Endocrino-pathies

Hyper/hypoadrenocorticism, hyper/hypoglycemia, Myxedema, hyperparathyroidism; (thyroid, cortisol, Ca, cytokines)

Acute vascular Hypertensive encephalopathy, stroke, arrhythmia, shock, intracerebral bleed

Toxins or drugs

Prescription drugs, illicit drugs, pesticides, solvents Really anything if elderly, but anti-cholinergics, long 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

Wernicke’s 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

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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 (Alzheimer’s Disease) Electrolyte (decreased Na, glucose), uremia, liver failure + Triggers (lack of sleep, flashing lights, music) Assessment of Seizure

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 (Todd’s paralysis) Sequelae: "Unprotected falling" with significant injury suggests epileptic seizure; tongue biting suggests GTC

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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; café-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.

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 Status Epilepticus Rx Typical dose 1 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

4 mg IV pushes usual max dose: 8 mg 5-10 mg IV pushes

2 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.

1-1.5 g IV over 20 mins

3 Phenobarbital 20 mg/kg at 50-75 mg/min + 5-10 mg/kg if still sz

1-1.5 IV, (max 100 mg/min)

4 General anesthesia with propofol, midazolam, phenobarbital

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

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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 ICA)

Amaurosis fugax (transient monocular blindness)

MCA 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

ACA Hemiplegia (leg> arm, face); confusion, urinary incontinence, primitive reflexes

PCA homonymous hemianopia (macular-sparing) Thalamic syndromes with contralateral hemisensory disturbance

Vertebral Wallenberg’s syndrome (numbness of ipsilat face and clat limbs; dysarthria, ipsilat Horner’s) (or PICA)

Basilar Pinpoint pupils, long tract signs (quadriplegia and sensory loss), CN abnormalities, cerebellar dysfunction

Lacunar Very small area of stroke with pure motor hemiplegia, pure hemianesthesia, ataxic hemiparesis, or dysarthria & clumsy hand

Adapted from Pocket Medicine, p 9-4

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

36

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%)

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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, Kernig’s, 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:

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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

Blumenfeld (2002)

NIH Scale

39

Level of consciousness Alert, responsive 0 Requires minor stimulation to respond 1 Requires repeated or painful stimulation to respond 2 Comatose or responds only with stereotyped movements

3

LOC Questions Both questions correct 0 One question correct 1 Neither question correct 2 LOC Commands Both responses correct 0 One response correct 1 Neither response correct 2 Best Gaze (in horizontal directions) Full gaze in all directions 0 Partial gaze palsy 1 Total gaze paresis or forced paresis not overcome by oculocephalics

2

Visual Fields to confrontation Fully intact 0 Partial hemianopia (i.e. asymmetric visual fields) 1 Complete Hemianopia 2 Bilateral Hemianopia (including cortical blindness) 3 Facial Palsy Normal & Symmetric 0 Minor-flattened nasolabial fold, asymmetry with smiling

1

Partial paralysis (e.g. of lower face only) 2 Complete paralysis (upper & lower) of one or both sides

3

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NIH Scale Part 2 Best Motor of arm & leg (holding limb at 90 degrees)

No drift for ≥ 10 seconds 0 Drift 1 Some movement against gravity, but falls by 5 secs 2 No movement against gravity 3 Limb Ataxia (finger-nose, heel-knee-shin) Absent 0 Present in 1 limb 1 Present in 2 limbs 2 Sensory (to pinprick, grimace/withdrawal counts if obtunded)

Normal 0 Mild/moderate loss (identifies prick but impaired discrimination)

1

Severe loss (can’t identify prick) 2 Best language (regarding standard set of pictures) No aphasia 0 Mild/moderate aphasia (impaired comprehension, word finding and naming difficulties, semantic or phonemic paraphasias)

1

Severe aphasia 2 Mute, global aphasia 3 Dysarthria None 0 Mild slurring, but intelligible 1 Severe, unintelligible 2 Extinction & inattention (double stimulus stimulation)

Normal 0 Hemi-inattention in one of the sensory modalities (visual, tactile, auditory, special)

1

Hemi-attention in more than one modality 2

Total /30

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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

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Red Flags in Acute Headaches Red flag Differential diagnosis Investigations Headache beginning after 50 years of age

Temporal arteritis (visual changes, TMJ pain), mass lesion

ESR, neuroimaging

Sudden onset of headache

SAH, dissection, pituitary apoplexy, hemorrhage into mass lesion, ruptured AVM

Neuroimaging; LP if neuroimaging negative*

Headaches increasing in frequency and severity

Mass lesion, subdural hematoma, medication overuse

Neuroimaging, drug screen

New-onset headache in a pt with risk factors for HIV or cancer

Meningitis (chronic or carcinomatous), brain abscess (including toxoplasmosis), metastasis

Neuroimaging; lumbar puncture if neuroimaging is negative*

Headache with signs of systemic illness (fever, stiff neck, rash)

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

Neuroimaging, lumbar puncture, serology

Focal neurologic signs & symptoms (other than typical aura)

Mass lesion, vascular malformation, stroke, collagen vascular disease

Neuroimaging, collagen vascular evaluation (including antiphospholipid antibodies)

Papilledema Mass lesion, pseudotumour cerebri, meningitis

Neuroimaging, lumbar puncture

Headache subsequent to head trauma

Intracranial hemorrhage, subdural hematoma, epidural hematoma, post-traumatic headache

Neuroimaging of brain, skull and, possibly, cervical spine

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

Weakness and Neuromuscular Dysfunction Feature UMN LMN Myopathy* Atrophy None Severe Mild Weakness Distribution

Pyramidal Distal, segmental

Proximal

Fasciculations None Common None Tone Increased Decreased [N]/decreased DTRs Increased Decreased [N]/increased Babinski Present Absent Absent *In some muscular dystrophies, atrophy can be focal and marked Adapted from Pocket Medicine, p 9-6

Up to Date, Weakness algorithm, 2007

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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-Barré Syndrome);

• Chronic: CIDP, paraproteinemia, rarely paraneoplastic, Charcot-Marie 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, Wegener’s), 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

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Guillan Barré 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:

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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

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MANAGEMENT OF NEUROLOGICAL EMERGENCIES Guillain Barré 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 µg (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

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 25–30 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

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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 one’s 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

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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, Broca’s 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.

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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 Harrison’s 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)

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