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X44 Neurology Toronto Notes 2023

•central: abnormal CNS activity

• phantom limb, postspinal cord injury, poststroke, MS

Treatment

•identify/treat underlying cause

•pharmacotherapy

stepwise approach (Canadian Pain Society, 2014)

. 1st line:gabapentinoids.TCA.SNRI

2nd line: tramadol, opioid analgesics

3rd line:cannabinoids

4th line:methadone, anticonvulsants(lamotrigine,lacosamide),tapentadol, botulinum toxin

•common non-pharmacologic therapies

neuropsychiatry:CBT,psychotherapy

rehabilitation:physiotherapy

•surgical therapies:dorsal column neurostimulator, DBS (thalamus)

Trigeminal Neuralgia

Clinical Features

• recurrent episodes ofsudden onset, excruciating, unilateral, paroxysmal,shooting “electric"

pain in

trigeminal root territory (V3>V2»V1)

• may have normalsensory exam (if abnormal,think ofsecondary orstructural cause)

• pain lastsseconds/minutes over davs/weeks, may remit for weeks/months

• triggers: touching face, eating, talking, cold wind,shaving, applying make-up

Etiology

• dassicTN: compression of CN V by tortuous blood vessel (usually superior cerebellar artery)

• 2° TN:cerebellopontine angle tumour (5%),MS (5%)

• idiopathic TN

Epidemiology

• F>M;usually middle-aged and elderly

Diagnosis

• dinical diagnosis

• investigate for secondary7

causes, which are more likely if bilateral TN or associated sensory loss

MR1 to rule outstructural lesion,MS,or vascular lesion

Treatment

• first line: carbamazepine or oxcarbazepine

• second line: baclofen orlamotrigine

• for medically-refractory classic TN, consider microvascular decompression

• other neurosurgical optionsfor medically refractory7

TN:trigeminal ganglion percutaneous

technique,gamma knife radiosurgery, invasive percutaneous denervation (radiofrequeney/glycerol),

percutaneous balloon microcompression,microvascular decompression

• narcotics not generally recommended

Postherpetic Neuralgia

Clinical Features

• pain persisting in the region of a cutaneous outbreak of herpes zoster

• constant deep ache or burning, intermittent spontaneous lancinating/ jabbing pain, allodvnia

• distribution: thoracic,trigeminal, cervical,lumbar,sacral

• associated symptoms:impaired sleep, decreased appetite, decreased libido

Etiology and Pathogenesis

• destruction of the sensory7

ganglion neurons(e.g.dorsal root,trigeminal,or geniculate ganglia)

secondary to reactivation of herpes zoster infection

Epidemiology

• incidence in those with zoster increases with age (2% in <60 yr, 19% in >70 yr)

• risk factors: older age,greater acute pain,greater rash severity

Prevention

• varicella zoster vaccine (Varivax*) in childhood reduces incidence of varicella zoster

• herpes zoster vaccine (Zostavax* or Shingrix*) reducesincidences ofshingles, PHN, and other

herpetic sequelae

Zostavax* is a live vaccine, recommended for patients >60 yr

• Shingrix*

is a recombinant vaccine, recommended for patients >50 yr (more efficacious than

Zostavax*)

Herpes Zoster of Trigeminal Nerve

Typically involves VI (ophthalmic

division)

Hutchinson'

sSign

Tip of nose involvement predicts comeal

involvement

n\

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Treatment

• medical:TCA (e.g. amitriptyline), anticonvulsants(e.g. pregabalin, gabapentin),analgesia (e.g.

opiates, lidocaine patch),intrathecal methylprednisolone, topical capsaicin

early treatment of acute herpes zoster with antivirals (longer-acting famciclovir and valacydovir

more effective)

treatment of herpes zoster with corticosteroids does not decrease PHN

- surgical:spinal tractotomy, dorsal root entry zone lesion, DBS of thalamus

Painful Diabetic Neuropathy

•see hndocrinologv. h16

Approach

•determine if pain is neuropathic or vascular

•more likely neuropathic if pain is present at rest and improves with walking,pain issharp/tingling,

more in feet -» calves

Treatment

•level A:pregabalin

•level B: venlafaxine, duloxetine, amitriptyline,gabapentin, valproate, rarely opioids, capsaicin

Complex Regional Pain Syndromes

Definition

• regional pain disproportionate to an inciting event (e.g.fracture,stroke), typically lasting 4-6 rvk

Diagnosis

• clinical diagnosis consistent with the Budapest Criteria:

1.continuing regional pain disproportionate to an inciting event

2.patient must have symptoms in 3 of the 4 categories, and must have signs in 2 of the 4 categories

(a sign must be observed at the time of diagnosis):

sensory: hyperesthesia and/or allodynia

vasomotor:temperature and/orskin colour asymmetry

sudomotor/edema:edema,sweating changes,and/orsweating asymmetry

motor/trophic:decreased range of motion, motor dysfunction (weakness, tremor, dystonia)

and/or trophic changes (hair,skin, nail)

3.absence of any other diagnosisthat would better explain the signs orsymptoms

• bone scintigraphy <5 mo ofsymptom onset may support diagnosis (negative test does not rule it out)

• MRI may help rule out other causes of regional pain if indicated

Classification

• CRPS type1 (reflex sympathetic dystrophy):minor injuries oflimb or lesions in remote body areas

precede onset ofsymptoms

• CRPS type II (causalgia):injury of peripheral nerves precedes the onset ofsymptoms

Prevention

• early mobilization after injury/infarction

Treatment

• goal of treatment isto facilitate function

• conservative treatment education,support groups,PT,OT,smoking cessation

• medical:topical capsaicin; ICA;NSAID;tender point injections with corticosteroid/lidocaine;

gabapentin/pregabalin /lamotrigine; calcitonin or bisphosphonates; oral corticosteroids

• surgical:paravertebralsympathetic ganglion blockade

• refer to pain management clinic

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Headache

•see Emergency Medicine. ER23 and lamiiy Medicine. EM36

Clinical Approach

•history

pain characteristics:onset,frequency, duration, intensity,location, radiation, other specific features

(e.g. worse in AM, worse with bending/coughing/Valsalva)

associated symptoms:visual changes, change in mental status, N/V, fever, meningismus, photophobia,

phonophobia, temporomandibular popping/clicking, jaw claudication, neurological symptoms

• precipitating/alleviating factors (triggering factors, analgesics), medications (especially nitrates,

calcium channel blockers, NSAlDs, anticoagulants), PMHx, l-

'

Hx

• red Hags (possible indicationsfor CT scan/further investigation) “SNOOP4”:Systemic symptoms or 2"

risk factors (fever, weight change, immunocompromised); Any focal neurological symptoms on history

or exam;; Onset sudden (

'

thunderclap'); Older age ( new-onset headache >50 yr); Pattern change;

Positional; Progressive;Precipitated by Valsalva; Pregnancy-CSVT/llH/Preeclampsia

• physical exam

• vitals (including BP and temperature), Jolt accentuation/Kernig’s/Krudzinski'

s, MSK examination of

head and neck

• HEEN'

l:fundi (papilledema, retinal hemorrhages), red eye, temporal artery tenderness,sinus

palpation, IM|

full neurological exam (including LOG, orientation, pupils (symmetry), and focal neurological deficits)

red Hags: papilledema, altered IOC, fever, meningismus, focal neurological deficits,signs of head

trauma

If CT is negative but clinically there is

suspicion of SAH or meningitis,perform

an LP

Headache DDx

ER VISIT

Ey e (acute angle closure glaucoma,

sinusitis)

Recurrent/Chronic (migraine,tension,

cluster,temporomandibular joint

disease, cervical 0A)

Vascular (SAH.ICH. temporal arteritis)

Infectious (meningitis,encephalitis)

Systemic (anemia, anoxia.CO. preeclampsia)

ICP (mass/abscess.HTN

encephalopathy.IIH)

Trauma (concussion.SOH. epidural

headache)

Classification

•primary

tension, migraine, cluster, autonomic cephalgias, short-lasting unilateral neuralgiform headache

with conjunctival injection and tearing (SUNCT)

Trialof Gakaneiumabin Prevention ol Episodic

Cluster Headache

HE JM 2019:381:132 41

Purpose Toinvestigate the efticacy and safety ol

galcanetumab at preventive treatment lor cluster

headache.

Methods 106 patients who had m n. oneattacX

every other dry.mm. four total attacks, and mac

eight attacks

'd. pi us a history of cluster headache

cdildlti-i)

- '

6 *

re « S. r«e lfd3M 11

galcanerumabor placebo, administered SC al

baseline and1month.

Results: Alter 3 weeks,the mean reduction m the

weekly frequency ol duster headache attacks was

8.2 attacks in the galcanetumab group is.S.2 m the

placebo group (difference. 3.5/wk:95% Cl.0.2-6.7:

P-0.04), and the proportion ol patients who had

a reduction of >60% in headache frequency was

71% and 53%.respecting (P-0.046|.Incidence of

adverse events were similarin both groups.

Conclusion: Galcanetumab reducedthe weekly

frequency of attacks ol episodic cluster headache.

•.secondary

• cervical OA,TM|syndrome, SAH, ICH , stroke, venous sinus thrombosis, meningitis/encephalitis,

trauma, increased ICP (space-occupying lesion, malignant HTN, or IIH ), temporal arteritis,

sinusitis, acute-angle closure glaucoma, pre-eclampsia, post LP, drugs/toxins (e.g. nitroglycerin

use and analgesia withdrawal ); all can be associated with serious morbidity or mortality

Table 22. Headaches - Selected Primary Types

Tension-Type Migraine Cluster

Prevalence 30 40% -10- 20% «n

Age of Onset

Sex Bias

Family Histoiy

location

15- 40 10 30 20 40

f >M f -M M»f

None

Bilateral frontal

Nuchal- occipital

Unilateral > bilateral (in adults

especially)

Frontotemporal

Hours days

Gradual,worse in PM; can also

be acute

Pulsating, throbbing

Moderate-severe

Retro orbital

Supraorbital

temporal

10 min-2 h

Oaily attacks lor weeks lo months;

mote common early AM or lale PM

Constant, aching,stabbing

Severe (wakes Irom sleep)

Duration

Onset/Course

Minutes days

Gradual, worse in PM

Episodic or chronic

Band-like, constant

Mild-moderate (doesnotwakeyouup

from sleep)

Depression

Anxiety

Noise

Hunger

Sleep deprivation

Ouality

Severity

Triggers/Provoking Noise/lighl light

Calfe in e/alcohol

Hunger

Stress

Sleep deprivation

Antiepileptics in Migraine Prophylaxis:An

Updated Cochrane Review

C ephalag a 2015:35:51-62

Purpose: lo review the evidence for anticonvulsants

in migraine propItylacbts.

Study:Systematic meta-analysis ol 32 published and

3 unpublished prospective,controlled trials of regular

use of anticonvulsantsto prevent migranes and/or

improve quality of life related to migraines.

Results:Sodium valproate and toprramate were

associated with a reduction of 4 d and1d of headache

per month, respecbveiy.and patentstaking either

drug were more than 2 times aslikely to experience

greater than 50% reducton in headache frequency,

vs.placebo. Neither drag was associated with undue

rates of adverse events,though higher dosesof

topiramate were associated with increased adverse

events.There is insufficient evidence of efficacy with

other antiepileptic drags,including ga'

oapentin.for

migraine prophylaxis.

Conclusions: Daily sodium valproate 400 mgand

topiramate 50 mgare well tolerated and effective

in prnpbyf actic treatment nf migraine headache

in adults.

fclOrt

Palliating

Associated Symptoms

Rest Rest Walking around

Red watery eye

Eyelid, forehead swelling

Nasal congestion or rhinorrhea

Unilateral Horner's

Acute Rx

No vomiting

No photophobia

N/V

Photo/phonophobia/osmophobia

t Aura

Management Non pharmacological:

Eliminating known triggers

Healthy lifestyle:sleep, diet (protein

for breakfast),exercise, hydration,

be aware of technology use, vitamin/

minerals

Psychological counseling

Physical modalities(e.g. heat,massage)

Pharmacological

Vitamins/minerals - Magnesium citrate. TCA

Riboflavin (Vitamin B2),Coenzyme 010, CCB

Melatonin ifinsomnia or difficulty falling Anticonvulsants

asleep

Simple analgesics:Tylenol, NSAlDs

Acute Rxi'Abortive:

NSAlDs

Triplans

Ergotamine

Valproate

Anti-emetics

CGRP Antagonists

02

Sumatriptan (nasal or injection)

Prophylaxis

Verapamil

Lithium

Methysergide

Prednisolone

Valproate

CGRP antibody

r n

L J

Prophylaxis/Prevenlive:

(3 -Blockers +

Botox

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N‘I7 Neurology Toronto Notes 2023

Table 23. Prophylactic Management of Migraine Headaches

Class Drug Evidence Contraindications Side Effects

p-blockcrs Propranolol

Timolol

Metoprolol

Amitriptyline

Nortriptyline

A Asthma. DM (mask

hypoglycemia)

Fatigue

Depression

lightheadedness A

CHF

B

Sedation

Dry mouth

Weight gain

lighlheadcdness

Weight gain,depression, PD (rare)

Weight gam (4.5-9 kg),constipation

Weight gain,elevated liver enzymes/

hyperammonemia, tremor,alopecia,

teratogenic:neural tube defect

Paresthesia,acute angle-closure

glaucoma,weight loss,cognitive:memory

loss,difficulty concentrating,renal stone

(rare)

TCA A Heart disease,glaucoma

Avoid inelderly C

CCDs Flunariiine

Verapamil

Valproate

Depression,obesity

Heart disease

Liver,,pancreatic disease

A

B

AED A

Topiramate A Renal disease

Table 24. Headaches - Selected Serious but Rare Secondary Types

Meningeal Irritation Increased ICP Temporal Arteritis

Any age

Generalized

Meningitis:houis-days

SAH:thunderclap onset

Severe

Head movement

Any age

Any location

Gradual; worse nocturnal and AM

»60 yr

Temporal

Variable

AgcolOnset

location

Onset/Course

Severe Variable, can be severe

Jawdaudication

Severity

Provoking lying down

Valsalva

Head low

Exertion

Associated Symptoms N/V Polymyalgia rheumatica

Visual loss

Heck stiffness

Photophobia

Focal deficits (e g. CN palsies)

Kernig’ssign

Brudzlnskl'sslgn

Meningismus

CT/MRI with gadolinium.

IP. antibiotics for bacterial

meningitis

Meningitis. SAH

Focal neurologicalsymptoms

Decreased LOC

Focal neurological symptoms

Papilledema

PhysicalSigns Temporal aitery changes:firm,

nodular. Incompressible,tender

CT/MRI and treatment to reduce pressure Prednisone

See Neurosurgery.IIS6 and NS8

Management

See Rheumatology,RH22

Etiology Tumour Vasculitis (GCA)

. CSVT, IIH,malignant HTN

Migraine Headaches

Definition (Common Migraine)

• >5 attacks fulfilling each of the following criteria

• 4-72 h in duration

• 2 of the following:unilateral, pulsating, moderate-severe (interferes with daily activity),

aggravated by routine physical activity

• 1 of the following: N/ V, photophobia/phonophobia/osmophobia

• not better accounted for by another diagnosis

Epidemiology

• 18nu females,6% males;frequency decreases with age (especially at menopause)

• in pre-pubertal children, more commonly seen in males; post-pubertal, more commonly seen in

females

Etiology and Pathophysiology

• theories of migraine etiology

depolarizing wave of "cortical spreading depression"

across the cerebral cortex that may cause an

aura (e.g. visual symptoms due to wave through occipital cortex) and activate trigeminal nerve

afferent fibres

• possible association with vasoconstriction/dilation

• significant genetic contribution

• triggers:stress,sleep excess/deprivation, drugs (estrogen, nitroglycerin), hormonal changes, caffeine

withdrawal, chocolate, tyramines (e.g. red wine), nitrites(e.g. processed meats)

Migraine auras can mimic other causes

of transient neurological deficits (e.g.

TIAs and seizures)

‘‘Menstrual Migraine" Subtype

Migraine headache that is associated

with the onset of menstruation - usually

2 d before to 3 d after the onset of

menstrual bleeding

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Signs and Symptoms

• stages of uncomplicated migraine

1. prodrome (hours to days before headache onset)

2. aura

3. headache

4. postdrome

• aura

self-resolving symptom of focal cerebral dysfunction lasting <60 min

e.g.:visual disturbance (fortification spectra - zigzags;scintillating scotomata -spots), unilateral

paresthesia and numbness or weakness, aphasia

• prodrome/postdrome: appetite change, autonomic symptoms,altered mood, psvehomotor agitation

retardation

• classification of migraines

• common migraine: no aura

• classic migraine: with aura (headache follows reversible aura within 60 min)

complicated migraine: with severe/persistent sensorimotor deficits

examples:basilar-type migraine (occipital headache with diplopia, vertigo, ataxia, and altered

LOC), hemiplegic/hemisensory migraine,ophthalmoplegic migraine

acephalgic migraine (i.e. migraine equivalent):aura without headache

status migrainosus:single attack lasting longer than 72 h

Treatment

• avoid triggers

• mild to moderate migraine

• 1st line:NSAlDs(ibuprofen, naproxen)

• moderate to severe migraine

• triptans(most effective), ergots (dihydroergotamine, dihydroergotamine mesylate (DHH))

• migraine prophylaxis: anticonvulsants (valproate, topiramate,),TCA (amitriptyline, nortriptyline),

propranolol,calcium channel blocker (verapamil)

• medication overuse (use of triptans/opioids/combination analgesics for >10 d/mo, or use of NSAlDs

for >15 d/mo) can lead to medication-overuse headaches

The oral contraceptive pill is

contraindicated with complicated

migraine due to risk of stroke

• Can still use non-estrogen based

forms of birth control (e.g.copper

IUD, Depo-provera shot

If patient presents to ED with severe

migraine and NA/- consider treating

with IV fluids and anti emetics

(chlorpromazine . prochlorperazine)

Sleep Disorders s

Overview of Sleep Elements of Sleep History

Initiation of sleep

Events prior to bed

Lights

latency (estimated)

Restless legs

Hallucinations

Maintaining sleep

Number of nighttime awakenings

Sleep walking/talking

Snoring/gasping

Drearm/nightmares

Consequences of sleep

Restorative

Morning headache

Falling asleep In inappropriate setting

Recommendations

• newborn: 18 h sleep (50% REM ), adolescents:10 h, adults: 7-9 h but most get insufficient amounts

• many older patients have reduced sleep as a consequence of underlying sleep disorders

Sleep Architecture

• PSG measures: EEG, eye movements (electro-oculogram - EOG), EMG, respiratory effort,

oxygenation,ECG

Table 25.Sleep Stage Characteristics

EEG EOG Muscle Tone Other Characteristics

Waking State Alpha waves:high

frequency (8-12 Hz),

moderate amplitude

Beta waves:frequency >13

Hz.low amplitude

*50% Alpha waves (see Slow,roving eye

above),mixed with slow movements

wave activity (theta.

4-7 Hz)

K complexes (high voltage Still

negative and positive

discharges) with sleep

spindles (12-14 Hz) are

central and midline

Delta waves:low

frequency (<2 Hz),high

voltage (>75 pV)

Rapid,blinking High

Marker for very light

quality sleep or sleep

disruption

Stage N1(~5%) Drug Effects on Wakefulness and Sleep

• Antihistamines increase sleepiness

• Stimulants increase arousal

• Caffeine (an adenosine antagonist)

increas wakefulness

• Benzodiazepines reduce amount

of slow wave sleep and cause

sleepiness

• Antidepressants (TCAMAOISSRI)

reduce amount of REM sleep and

prolong REM latency

• Alcohol may hasten sleep onset but

is associated with increased nightime

arousals and poorsleep efficency

High,but gradually

dropping

Stage M2 (

-50%) High

Homeostatic sleep

Reduced BP. HR.cardiac

output,RR

Growth hormonerelease

Irregular respiration

HR variation

Classical dreaming state

Stage N3 (previously 3 Still

and 4) SJow Wave.Delta

Sleep (

-20%)

Low

r

^

Sawtooth waves, mixed Rapid eye movements

frequency,low voltage

Rapid Eye Movement

Sleep (~2S%)

Very low

+

Avoid sleep medications (especially in

elderly patients) due to increased risk

of falls, pseudodepression,and memory

loss

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I9 Neurology Toronto Notes 2023

Coma

• see Neurosurgery, NS40

Insomnia

Definition

• difficulty initiating or maintaining sleep, or waking up earlier than desired (leading to sleep that is

chronically non-restorative/poor quality) despite adequate opportunity and circumstances for sleep

Types

• sleep state misperception, psychophysiologic insomnia (learned sleep-preventing associationsi.e. clock watching),idiopathic (lifelong difficulty)

secondary causes

psychiatric disorders(80% of psychiatric patients):i.e.depression and anxiety (see Psychiatry,

PS12 and PS15)

neurologic disorders: i.e. neurodegenerative disease, epilepsy, neuromuscular disorders

sleep disorders: i.e. RLS (sleep initiation difficulties),sleep apnea (sleep maintenance

difficulties)

medical conditions:i.e. pregnancy, cardiorespiratory (COPD/heart failure), gastroesophageal

reflux disease, pain (arthritis,fibromyalgia, cancer)

drugs/toxins:i.e. caffeine, alcohol,stimulants, antidepressants,steroids,sedative withdrawal

fatal familial insomnia:i.e.rare genetic prion protein mutation causing autonomic

dysfunction

Treatment

sleep log,sleep hygiene,stimulus control,sleep restriction,relaxation response,CBT, melatonin

Sleep Apnea

• see Respirology. R29

Definition

• disorder of breathing in sleep associated with sleep disruption and consequent excessive somnolence

(or drowsiness)

Epidemiology

• >6% of the Canadian population

• correlated with obesity

• significant morbidity: HTN,stroke, heart failure, sleepiness, mortality (accidents)

Types

• obstructive sleep apnea;etiology:collapse of airway due to low muscle tone in deep and REM sleep

• centralsleep apnea:no effort to breath >10 s;etiology:heart failure,opiates, brainstem pathology,

myotonic dystrophy

• mixed apnea: combination of both central and obstructive sleep apnea

Diagnosis

• PS(i or ambulatory sleep monitoring device-apnea hypopnea index (AHI) or respiratory disturbance

index (RDI) 5

Treatment

• weight loss, positional therapy, dental devices, CPAP (common),surgery (rare), ensure driving safety

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Restless Legs Syndrome and Periodic Limb Movement in

Sleep

•RLS:urge to move legs accompanied by uncomfortable sensationsthat begin or worsen with rest, is

partially or totally relieved with movement, and is worse in evening/night;these features cannot be

accounted forby another medical/behavioural condition

•PLMS: involuntary, jerking movements of the legs during sleep, diagnosed with PSG

•epidemiology: 10% North Americans, 90% of RLS have PLMS, 50% of patients with PLMS have RLS

•associated conditions: peripheral nervous system (radiculopathy, neuropathy), pregnancy, iron

deficiency, alcohol use, PD,uremia/renal failure

Treatment

•underlying contributors (iron and B 12 supplementation), dopaminergic agonists (first line),

clonazepam (causes tachyphylaxis), gabapentin, opioids (only exceptional circumstances)

•NOT recommended: levodopa/carbidopa (Sinemet*) which causes augmentation

Narcolepsy

Definition

• excessive daytime sleepiness (all narcolepsy), cataplexy (loss of muscle tone with emotionalstimuli,

pathognomonic),sleep paralysis (unable to move upon wakening), hypnagogic and hvpnopompic

hallucinations (vivid hallucinations while falling asleep or waking up, respectively)

Epidemiology

• prevalence 1 in 2000, onset in adolescence/early'adulthood; life-long disorder

Etiology

• presumed autoimmune attack on orexin/hypocretin system, post head injur)', MS, hypothalamic

tumours; rarely familial

Diagnosis

• based on clinical history and multiple sleep latency test findings ofshort sleep latency <8 min and

REM within 15 min ofsleep onset on 2/4 naps

Treatment

• sleep hygiene and scheduled brief naps, restricted driving

• alerting agents: modafinil (non-amphetamine stimulant),stimulant (i.e. methylphenidate)

• anticataplectic:TCAs,SSRls,sodium oxybate

Parasomnias

Definition

• unusual behaviours in sleep with clinical features appropriate to stageofsleep

Etiology

• in elderly, REM sleep behaviour disorder may be associated with PD;in children,slow wave sleep

arousals (sleep walking) may be associated with sleep-disordered breathing

Diagnosis

• dinical history in children, polysomnography in adults to exclude nocturnal seizures

Treatment

• behavioural management (safety, adequate sleep), clonazepam for REM sleep behaviour,tonsillectomy

if appropriate in children

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Central Nervous System Infections

• see Infectious Diseases. 1D17 Hypertension Encephalopathy

Acute severe HTN (typically d8P >130

or sBP >200) can cause hypertensive

encephalopathy. Abnormal fundoscopic

exam (papilledema, hemorrhages,

exudates, cotton wool spots), focal

neurologic symptoms. N/V, visual

disturbances, seizures, and change

in IOC

Spinal Cord Syndromes

• sec Neurosurgery. NS34

Stroke

Terminology Consider transfer of acute stroke

patient to a designated stroke centre for

neuroprotective or thrombolytic therapy,

and endovascular therapy (EVT) if the

patient isseen in first few hours

• stroke:focal cerebral,spinal, or retinal infarction in a defined vascular distribution

infarction is permanent tissue injury (confirmed by neuroimaging)

•

'

11A: transient (<24 h), episode of neurological dysfunction caused by focal brain,spinal cord or

retinal ischemia without acute infarction on CT or MR!

may present with amaurosis fugax (transient monocular painless vision loss)

Early seizure activity occurs In 5-25% of

Pathophysiology patients after ICH

•two major types:ischemic (~80%) and hemorrhagic (~20%)

1. ischemic

arterial thrombosis: thrombus formation in artery (local//n situ)

large vessel:stenosis or occlusion of the internal carotid artery, vertebral artery, basilar

artery, or middle/anterior/posterior cerebral arteries

- mechanism: insufficient blood flow beyond lesion (hemodynamic stroke)

- underlying processes: atherosclerosis (most common cause), dissection, and

vasculitis

small vessel/lacunar

- mechanism: chronic HTN and DM cause vessel wall thickening and decreased

luminal diameter

- affects mainly small penetrating arteries (primarily basal ganglia, internal capsule,

and thalamus)

• cardioembolic:blockage of cerebral arterial blood flow due to thrombus originating from a

cardiac source

atrial fibrillation (most common), rheumatic valve disease, prosthetic heart valves, recent Ml,

fibrous and infectious endocarditis

systemic hypoperfusion (global cerebral ischemia)

Cerebral venoussinusthrombosis

should be considered in the differential

diagnosis of stroke and headache.It

is an uncommon cause of either, but

is associated with high morbidity and

mortality. Patients often present with

headache alone, but can have seizures,

focal neurological deficits, or cranial

nerve palsies. This is diagnosed with

MRV or CTV.Treatment is typically

anticoagulation with heparin initially,

then warfarin eventually

20-40% of patients with ischemic

stroke may develop hemorrhagic

transformation within 1 wk after the

initial infarction

Can be exacerbated by reperfusion

injury (distal migration of clot as

it dissolves) naturally or by use of

thrombolytic therapy, endovascular

therapy or anticoagulation

• inadequate blood flow to brain, usually secondary to cardiac pump failure (e.g. cardiac arrest,

arrhythmia, or Ml )

primarily affects watershed areas ( between the major cerebral arterial territories)

2. hemorrhagic

intracerebral hemorrhage

hypertensive (most common): due to chronic arteriosclerosis which predisposes vessels

to focal necrosis and pseudoaneurysm formation eventually leading to intraparenchymal

hemorrhage; most common sites are putamen, caudate nucleus, thalamus, cerebellum, and

pons

other: trauma, amyloid angiopathy (associated with lobar hemorrhage),

malformations, aneurysms, vasculitis, drug use (cocaine or amphetamines)

• SAH,see Ncurosuruerv. NS22

Stroke Syndromes According to Vascular Territory

•ACA:contralateral leg paresis,sensory loss, cognitive deficits (e.g. apathy, confusion, and poor

judgment)

•MCA:proximal occlusion involves

contralateral weakness and sensory loss of face and arm

cortical sensory loss

may have contralateral homonymous hemianopia or quadrantanopia

if dominant (usually left ) hemisphere: aphasia

• if non-dominant (usually right) hemisphere: neglect

eye deviation towards the side of the lesion (away from the weak side)

$