Stroke

Etiologies

• Embolic (- 75%): artery — artery, cardioembolic, paradoxical, or cryptogenic s • Thrombotic (- 25%): lacunar (arteriolar, seen in HTN & DM) or large vessel

• Other, dissection, vasculitis, vasospasm, hyperviscosity, watershed

Clinical Manifestations

Embolic rapid onset, sx maximum at onset Thrombotic progression of sx over h to days with stuttering course

Artery

Deficits

ICA Ophth

Amaurosis fugax (transient monocular blindness)

Confusion, abulia, urinary incontinence, primitive reflexes

MCA

Hemiplegia (arm & face > leg); hemianesthesia; homonymous hemianopia Aphasia if dom. hemisphere: sup. div. expressive; inf. receptive Apraxia and neglect if nondominant hemisphere Drowsiness & stupor seen later (due to brain swelling)

PCA

Thalamic syndromes with contralateral hemisensory disturbance, aphasia Macular-sparing homonymous hemianopia

Vertebral

Wallenberg's syndrome = numbness of ipsilateral face and contralateral limbs, diplopia, dysarthria, ipsilateral Horner's

Basilar

Pinpoint pupils, long tract signs (quadriplegia and sensory loss), cranial nerve abnormalities, cerebellar dysfunction

Cerebellar

Vertigo, nausea vomiting, diplopia, nystagmus, ipsilateral limb ataxia

Lacunar

Pure hemiplegia, pure hemianesthesia, ataxic hemiparesis. or dysarthria + clumsy hand

Transient ischemia attacks (TIAs) are sudden neurologic deficits caused by cerebral ischemia that resolve w in 24 h (usually w in 1 h) and are a harbinger of stroke. Ddx: seizure, migraine, syncope, anxiety.

Physical examination

• General including rhythm, murmurs, carotid & subclavian bruits, signs of peripheral emboli

• Neurologic including NIH stroke scale (NIHSS) Diagnostic studies

• Laboratory: electrolytes. Cr. glc. CBC. PT. PTT. LFTs. tox screen;

hypercoagulable w u (consider in young Pts; send once stable & ideally before anticoag)

. • Urgent CT is usually the initial imaging study because of its rapidity and availability first, noncontrast CT tor o hemorrhage (Se for ischemic As is «-20% w in 12 h) then, CT angio to evaluate cerebrovascular anatomy & patency consider CT perfusion for areas of reversible ischemia

• MRI offers superior imaging but may not identify acute hemorrhage (although recent data suggests may be equivalent; jama 2004:292.1823) and may be falsely -> for small brainstem strokes w in 1st 3 h; should be avoided if Pt is unstable or will delay therapy

• Carotid Doppler U S. transcranial Doppler (TCD) s • Holter monitoring to assess for paroxysmal AF

• Echocardiography w bubble study to r o PFO or atrial septal aneurysm (confer -4x t risk of stroke; nejm 2001:34S:1740). cardiac thrombus, valvular vegetations Treatment of TIA (NEJM 2002:347 1 687)

• Heparin IV -> warfarin for known or presumptive cardioembolicTlAs; use as bridge to mechanical intervention (CEA. stenting) for large vessel atherothrombotic disease

• Antiplatelet therapy with ASA. clopidogrel, or ASA - dipyridamole k • Carotid revascularization if sx >70% ipsilateral stenosis (see below)

Risk of progression of TIA to stroke (lonctt 2007:369:283)

• ABCD': Age ^60 y 1): BP ^140 90 (+1);Clinical features: unilateral weakness (+2).

speech impairment w o weakness (+1); [Duration .-60 min (+2) or 10-59 min (+1); Diabetes (+1)

• Risk of stroke at 2 d: low risk (0-3) = 1.0%; moderate (4-5) =4.1%; high (6-7) =8.1%

Treatment of ischemic stroke (lancet 2003:362.1211)

• Thrombolysis (IV): 0.9 mg kg (max 90 mg). w 10% as bolus over 1 min. rest over 1 h consider if onset w in 3 h. large deficit, 0 hemorrhage, and 0 contraindicauon to lysis 12% absolute 1 in excellent functional outcome. 5.8% absolute T ICH, 4% absolute i mortality (p NS) (NINDS rt-PA Stroke Stu4y.NE)M 199S;333:1381)

• Intra-arterial therapy with thrombolysis (PROACTII./MM 1999;282:2003) or catheter-based techniques promising (66% rate of recanalization) but still experimental currently reserved for occlusion of a major vessel (ICA. MCA. basilar)

• Anticoagulation with UFH of no proven benefit with t risk of hemorrhagic transformation consider infusion w o bolus if Pt not thrombolysed and having progressive sx long-term warfarin if embolic stroke: no role in nonembolic stroke (Nejm 2001:345:1444)

• Antiplatelet therapy

ASA i death & recurrent stroke (Stroke 2000.31:1240) and is superior to warfarin alone (NEJM 200S:352 1305)

dipyridamole + ASA superior to ASA alone (J Neurol So 1996:143:1; Lflncet 2006:367:1665) clopidogrel • ASA not more effective than ASA alone and ! bleeding (Lancet 2004.364:331)

• BP should not be lowered unless severe (SBP 200) or evidence of Ml or CHF

if considering thrombolysis, then lower to <180 110 with nitrates or labetalol

• DVT prophylaxis: enoxaprin 40 mg SC qd more efficacious than UFH 5000 U SC ql2h

(Lancet 2007:369:1347)

• Cerebral edema peaks at 3-4 d poststroke — I ICP requiring elevated head of bed >30°

intubation and hyperventilation to P.COi -30 (transient benefit) osmotherapy with mannitol IV 1 gm kg -* 0.25 g kg q6h; • hypertonic saline surgical decompression

• Statin i in recurrent stroke & I MACE (HPS, Lancet 2002:360:7; SPARCL. NEJM 2006:355:549)

Carotid revascularization

• Carotid endarterectomy (if institutional morbidity & mortality ^6%) indicated for:

symptomatic stenosis ^70% (? 50-69% if male, age >75 y. or recent sx) 65% i

Stroke (NASCET.NQM 1991:325:445: lancet 2004:363:915) asx stenosis -70% & <75 y - -50% . Stroke (ACST.lancet 2004 363:1491)

• Superiority and even noninferiority of carotid stenting remains controversial (NEJM

2004:351:1493: Lancet 2006:368:1239; NEJM 2006:355:1660)

Hemorrhagic (-30%)

Etiologies

• Intracerebral (ICH. 90%): HTN. AVM, amyloid angiopathy, anticoagulation thrombolysis.

venous thrombosis

• Subarachnoid (SAH, -10%: Loncet 2007:369:306): ruptured aneurysm, trauma

Clinical manifestations

• ICH: sudden impairment in level of consciousness vomiting ~ headache may cause progressive focal neurologic deficit depending on site of hemorrhage

• SAH: severe headache, nausea. & vomiting nuchal rigidity and other signs of meningeal irritation impairment in level of consciousness

Diagnostic studies

• Angiography (CT or conventional) to determine the source of bleeding (aneurysm, AVM)

• LP to ✓ for xanthochromia if no evidence of hemorrhage on CT and suspicious for SAH

Treatment

• Reverse any coagulopathies

• Recombinant activated Factor VII is currently investigational, but may 1 hematoma expansion and mortality at the expense of t risk of adverse thromboembolic events (NEJM 2005:351777)

• Strict BP control w goal SBP 140. unless risk for hypoperfusion b c critical carotid sten.

• ICH: surgical decompression for large hemorrhage with clinical deterioration

• SAH: nimodipine to A risk of vasospasm, phenytoin for seizure prophylaxis, endovascular

(Lane« 2005:366:783) or surgical correction of aneurysm AVM to prevent rebleeding

• Cerebral venous thrombosis: paradoxically, requires anticoagulation with IV heparin

WEAKNESS & NEUROMUSCULAR DYSFUNCTION

Feature

Upper Motor

Lower Motor

Myopathy

Neuron

Neuron

Distribution of

Regional

Distal,

Proximal

weakness

segmental

Atrophy

None

Severe

Mild

Fasciculations

None

Common

None

Tone

t

I

Normal or 1

DTRs

4- +• ♦ ♦

of*

+ / + +

Babinski

Present

Absent

Absent

Peripheral Neuropathies

Etiologies

• Mononeuropathy (one nerve): entrapment, compression, trauma, DM. Lyme

• Mononeuropathy multiplex (multiple, noncontiguous, separate nerves)

Axonal: vasculitis, sarcoidosis, diabetes, hereditary neuropathy with pressure palsies

• Polyneuropathy (multiple symmetric nerves)

DemyelinatJng acute: acute inflammatory demyelinating polyneuropathy (AIDP) = Guillain-Barre subacute: CI DP. meds (taxol)

chronic diabetes, hypothyroidism, toxins, paraneoplastic, paraproteinemia, hereditary Axonal acute: porphyria, vasculitis subacute: meds (cisplatin. taxol. vincristine. INH. ddl). alcohol. Bu defic.. sepsis chronic: diabetes, uremia, lead, arsenic. Lyme. HIV. paraneoplastic, paraproteinemia

Clinical manifestations

• Motor and or sensory dysfunction with weakness and or dysesthesias

• Depressed or absent DTRs

Diagnostic studies

• Electrolytes. BUN. Cr. Glc. HbAic. CBC. TSH. LFTs, ANA. ESR. SPEP

• HIV. Lyme titers, heavy metal screening as indicated by clinical history

• EMG. NCS. nerve biopsy; MRI if possible radiculopathy or plexopathy

Guillain-Barré Syndrome (GBS)

Definition and epidemiology

• Acute inflammatory demyelinating polyneuropathy (AIDP)

• Précipitants: viral illness (EBV. CMV. HSV. HIV), URI (Mycoplasma). gastroenteritis

(Campylobacter). surgery, older immunizations

Clinical manifestations

• Ascending paralysis over hours to days

• Hypoactive or absent reflexes

• Sensory dysesthesias are often first symptoms, back pain is also common

• Respiratory compromise requiring ventilatory assistance occurs in 30%;

autonomic instability and arrhythmias occur in 50%

Diagnostic studies

• Lumbar puncture: albuminocytologic dissociation - î protein w o pleocytosis (<20

lymphs)

• EMG & NCS: 1 nerve conduction velocity and conduction block

• FVC & NIF: to assess for risk of respiratory failure

Treatment

• Plasma exchange (Neurology 198S;3S 1096) or IVIg (NifM 1992:3261123)

no additional benefit with both (Lancet 1997:349:225)

• Supportive care with monitoring in ICU setting if rapid progression or resp. failure

• Watch for autonomic dysfunction: labile BP. dysrhythmias (telemetry)

Myasthenia Gravis

Definition and epidemiology

• Autoimmune disorder with Ab directed against acetylcholine receptor (AChR) in NMJ

• Prevalence 1 in 7500

• Occurs at all ages; peak for women in 20s-30s; peak for men in 60s-70s Clinical manifestations

• Weakness and fatigability with weakness worse with repetitive use, relieved by rest

• Cranial muscles involved early — ocular (ptosis, diplopia) in 50%; bulbar (difficulty chewing, dysarthria, dysphagia) in 15%

• Limb weakness proximal > distal; DTRs preserved

• Exacerbations triggered by stressors such as URI. surgery, pregnancy, meds (eg.

aminoglycosides, procainamide, phenytoin); prednisone can worsen acutely

• Myasthenic crisis ■ exacerbation need for respiratory assistance

• Cholinergic crisis weakness due to overtreatment with anticholinesterase medications;

may have excessive salivation, abdominal cramping and diarrhea; rare at normal doses Diagnostic studies

• Bedside tests: timing of sustained upgaze. forced mouth closure on tongue blade, etc.

• Edrophonium (Tensilon) tesc temporary t strength; false © & © occur; atropine at bedside

• EMG: i response with repetitive nerve stimulation (vs. i response in Lambert-Eaton)

• Anti-AChR Ab: Se 80%. 50% if ocular disease only; Sp >90%; muscle specific receptor tyrosine Kinase (MuSK) may account for some AchR Ab-negative cases

• CT or MRI of thorax to evaluate thymus (65% hyperplasia. 10% thymoma) Treatment

• Anticholinesterase medications (eg. pyridostigmine)

• Thymectomy: mandatory if thymoma; also leads to improvement in 85% Pes w o thymoma

• Immunosuppression: prednisone, azathioprine. cyclophosphamide

• Myasthenic crisis: treat precipitant consider d c anticholinesterase if suspect cholinergic crisis aggressive immunosuppression with glucocorticoids (but watch for initial worsening) IVIg. plasmapheresis

ICU if rapid or severe (follow FVC. NIF)

Myopathies (also see Rheumatology)

Etiologies

• Hereditary: Duchenne. Becker, limb-girdle, myotonic

• Endocrine: hypothyroidism, hyperparathyroidism. Cushing syndrome

• Toxic: statins, fibrates. glucocorticoids, zidovudine, alcohol, cocaine, antimalarials.

colchicine

• Polymyositis and dermatomyositis Clinical manifestations

I • Progressive weakness, proximal > distal

• Eventual muscle atrophy Diagnostic studies

• Muscle biopsy

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