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Stroke

Neurology

QuestionAnswer
Ischemic stroke pathogenesis atheroembolic (50%); cardioembolic (30%)
Venous infarction RFs and presentation OCP/SMK. HA; aphasia, weakness
Atheroembolic Stroke is characterized by: Single vascular territory; Warning signs; Stepwise progression
Atheroembolic presentation Hx HTN, CAD; transient language disturbance; transient weakness; Normal head CT; Doppler US: high grade stenosis (e.g., L ICA)
Ant cerebral art infarct: likely fx: contralateral leg (motor > sensory)
MCA infarct: likely fx: face/arm more than leg/vision; gaze preference to affected side. If left side affected, possible aphasia. If right side, apraxia, hemi-neglect
Vertebrobasilar art infarct: fx: Midbrain: 3d nerve nuclei; ipsilateral ptosis; eye deviated outward (bc CN VI is fine, but III is affected); crossed signs: pt has CNIII probs on one side and sensory probs on opp side of body
Subcortical infarct fx: face = arms = legs
Cortical infarct fx: gradation btw face, arms, & legs
Lacunar syndromes Pure Motor Stroke; Pure Sensory Stroke; Ataxic Hemiparesis; Clumsy Hand Dysarthria
Atheroembolic stroke: additional eval Neuroimaging; Carotid US; MRA; CTA; Catheter angiography
Cardioembolic stroke presentation Aphasia; hemiparesis/hemisensory deficit affecting face and arm; Carotid US normal (no brain lg vessel prob)
Cardioembolic: dx Maximal deficit at onset; Multiple vascular territories; Cardioembolic source; Hemorrhagic infarction (Wedge shaped infarct towards cortical surface)
Cardioembolic: possible sources A-fib; cardiomyopathy; acute MI; mural thrombus; valvular heart dz; bacterial endocarditis; atrial myxoma
Cardioembolic stroke: additional eval pulse; EKG; 24-48 hr EKG; TTE (microcavitation); TEE
TIA Acute focal neuro deficits; ischemic, usually embolic (carotid / vertebrobasilar) etiology; Sx/Sx resolve within 24 hr; no radiological evidence of infarct
Modifiable RF for first stroke *HTN*; A fib; carotid stenosis; DM; hyperlipidemia; prior stroke/TIA
Lifestyle mods affecting BP wt reduction; DASH diet; sodium reduction; exercise; moderate EtOH consumption
Stroke comorbid RF’s CHD, CHF, DM, stroke
Prevention of A fib RF: Low risk (0-1) ASA; mod (2) ASA or warfarin (but AE/bleed risks); high risk (>2) warfarin
Asx carotid stenosis: eval Carotid bruit; Doppler US; MRA, CTA
Stroke prevention DM pts glucose ctrl: no fx on stroke/macrovascular comp; tight BP ctrl (<130/80) effective; statins
Stroke prevention: hyperlipidemia chol reduction w/statins
ASA recommended for 10-yr stroke risk of: 6-10%
Ischemic stroke: Tx tPA (within 4.5 hrs of sx onset); head CT w/o evidence of hemorrhage/complicating lesion
tPA absolute CI (<3 hr) CT: bleed/comp (AVM); SBP >185 or DBP >110; recent stroke/ICH; bleed elsewhere; anticoag use; plt <100K; h/o seizure preceding stroke
tPA CI (3-4.5 hr) >85 yo; NIH-SS >25; h/o both stroke/DM
If pt not tPA candidate: Tx: poss endovascular tx; MERCI clot retriever?
Acute stroke mgmt Temperature; Fluids/Glucose; BP; Antithrombotic agents
Acute ischemic stroke: tx BP? No (drop in MAP can drop CBF, make things worse)
Secondary stroke prevention Platelet antiaggregants (ASA vs Aggrenox / Plavix); Anticoagulants; BP; Lipid lowering; Endarterectomy
Antihypertensives & stroke risk each 10 mmHg drop in BP = 28% decrease stroke risk
Stroke w/L paresis and R facial droop = Right pons infarct
Hemiplegia (leg>arm), abulia, urinary incontinence, primitive reflexes: site of lesion = ACA
Hemiplegia (arm/face > leg), hemianesthesia, homonymous hemianopia, aphasia, apraxia/neglect of nondominant side, drowsiness: site of lesion = MCA
MCA: characteristic aphasia = aphasia of dominant hemisphere (superior division: expressive; inferior division: receptive)
Thalamic syndromes (allodynia) with contralateral hemisensory disturbance & aphasia; macular-sparing homonymous hemianopia: site of lesion = posterior cerebral artery
Wallenberg syndrome: numb in ipsilateral face & contralateral limbs; diplopia, dysarthria, ipsilateral Horner syndrome: site of lesion = vertebral artery
Pinpoint pupils, long tract sxs (quadriplegia & sensory loss), CN abnormalities, cerebellar dysfunction: site of lesion = basilar artery
Vertigo, N/V, diplopia, nystagmus, ipsilateral limb ataxia: site of lesion = cerebellar artery
Sxs: (pure hemiplegia, pure hemianesthesia, ataxic hemiparesis) OR (clumsy hand & dysarthria): site of lesion = lacunar CVA
Definition Apraxia inability to do learned purposeful movements, including apraxia of speech
Definition Ataxia incoordination of muscular movements
Definition Aphasia: (1) Broca; (2) Wernicke (1) expressive: few words/written or spoken; difficulty producing words; may comprehend others. (2) receptive: word salad; decreased comprehension
Definition Dysarthria poor verbal articulation due to neuro injury
CVA labs (Acute) CMP (lytes, glucose, BUN/Cr, LFT), CBC, PTT/INR, ESR, tox screen. If suspect endocarditis, get blood cultures
CVA labs (when pt is stable) Lipids, HbA1c, TSH, homocysteine, lipoprotein (a). If pt <65 yo or cryptogenic stroke: hypercoagulability workup (before anticoagulant tx is initiated)
CVA: diagnostic studies Labs, ECG, noncontrast head CT acutely (then CTA / perfusion to eval CV patency & areas of reversible ischemia (if considering intra-arterial/catheter interventions), carotid US, Holter monitor, TTE
TIA tx 1) ? heparin IV -> warfarin IF: presumed cardioembolic TIA; or bridging to mech intervention (CEA, stent) for Lg vessel atherothrombotic dz (2) Antiplatelet tx: ASA, Plavix, or ASA+Aggrenox. (3) carotid revascularization if sx >70% ipsilateral stenosis
ABCD2 score criteria: Age>/=60 (1 point); BP>/=140/90 (1); Clinical: unilateral weakness (+2); speech impaired w/o weakness (1); Duration >60min (2) or 10-59min (1); DM (1)
ABCD2 stroke risk scoring: CVA risk at 2 days: 0-3 pts: low (1%); 4-5 pts: moderate (4.1%); 6-7 pts: high (8.1%). Risk of progression higher in TIA due to large artery / lacunar disease (vs cardioembolic)
Ischemic stroke Tx IV thrombolysis; antiplatelet; permissive HTN (lower acutely only if SBP>200) or MI/CHF. BP to <180/110 with nitrate/labetolol pre-tPA. Cerebral edema mgmt; DVT Ppx; statin
Ischemic stroke tx: cerebral edema mgmt: (edema peaks at 3-4 days post-CVA) Increased ICP requires elevate HOB 30degrees, intubate / hyperventilation to PaCO2 = 30. Osmotherapy: mannitol IV 1gm/kg ->0.25g/kg Q6h. +/-hypertonic saline. ?Surgical decompression
Ischemic stroke tx: carotid revascularization Carotid endarterectomy (if hospital M&M <6%). CEA indicated for: (1) Sx Stenosis >/=70% (?50-69% if female, >75yo or recent sxs): 65% decrease in CVA; (2) Asx stenosis >/=70% & >75yo: 50% decrease in CVA
PFO & CVA risk 27% of popn. 0.1% annual CVA risk in healthy popn. Inc CVA risk if >4mm separation, R->L shunt at rest, inc septal mobility.
If PFO and stroke/TIA: tx No evidence of warfarin > ASA. If pt is at increased risk or hx of DVT/PE, consider anticoagulation
Amaurosis fugax (transient monocular blindness): site of lesion = Internal carotid artery / ophthalmic artery
Types of lacunar stroke (physiologically): small vessel, penetrating arteries, atheroma, lipohyalinosis
Types of large vessel thrombosis: atherosclerosis, dissection
Lacunar infarct (stroke): 15-20% of strokes; small vessel ischemia; HTN; usually pure sensory OR motor
Risk of progression of TIA to CVA: 11% risk of stroke within 3 mo; 63% of strokes occur within the first week, 85% within first month; higher risk of CVA in DM / HTN
Crescendo TIA = increasing number & frequency of TIAs, highly likely to evolve to CVA (esp if 2 or more attacks within 24 hr)
Ischemic stroke pathophysiology atheroembolic (50%); cardioembolic (30%); OR 2/3 thrombotic & 1/3 embolic
Stroke pathophysiology 80% ischemic, 20% hemorrhagic
Hemorrhagic stroke pathophysiology parenchymal ICH (10-15%); subarachnoid (5-10%)
Anterior circulation consists of: Ant choroidal, ant cerebral, MCA
Anterior circulation supplies: Cortex, subcortical white matter, basal ganglia, internal capsule
Anterior circulation stroke Hemispheric s/s: aphasia, apraxia, hemiparesis, hemisensory loss, visual field defects
Posterior circulation consists of: Verterbral & basilar arteries
Posterior circulation supplies: Brain stem, cerebellum, thalamus, parts of temporal & occipital lobes
Posterior circulation stroke Sxs of brainstem dysfn: coma, drop attacks, vertigo, N/V, ataxia
Thrombotic vs embolic stroke sx progression Thrombotic: stepwise progression, often preceded by TIA; Embolic: abrupt & without warning
Amyloid angiopathy stroke: patho Blood vessel degeneration; Dementia; Lobar hemorrhage
Amyloid angiopathy: presentation Dementia; Episodic worsening; No h/ o HTN; poss acute limb weakness; BP less severe than in ICH; stroke d/t cerebral microhemorrhages
Venous infarction presentation h/o OCP/SMK; HA; aphasia, weakness
Atheroembolic stroke characterized by: Single vascular territory; Warning signs; Stepwise progression
Atheroembolic stroke presentation Hx HTN, CAD; transient language disturbance; transient weakness
Ant cerebral art infarct: likely fx: contralateral leg (motor > sensory)
Subcortical infarct effects by body area: face = arms = legs
Cortical infarct fx by body area: gradation btw face, arms, & legs
Cardioembolic stroke presentation h/o A fib; aphasia; hemiparesis/hemisensory deficit affecting face and arm
Cardioembolic CVA: dx Maximal deficit at onset; Multiple vascular territories; Cardioembolic source; Hemorrhagic infarction (Wedge shaped infarct towards cortical surface)
Cardioembolic CVA: possible etiology A fib; Cardiomyopathy; Acute MI; Valvular heart dz
TIA S/S Acute focal neuro def; S/S resolve within 24 hr; No rad evidence of infarction; Ischemic etiology, usu carotid or vertebral vascular distn
TIA: risk of subsequent stroke: 11% risk of stroke within 3 mo; 1/3 of TIAs have stroke within 5 yrs; 63% of strokes occur within the first wk, 85% within first month
Modifiable RF for first stroke *HTN*; A fib; carotid stenosis; DM; hyperlipidemia; prior stroke/TIA
Prevention of A fib RF: Low risk (0-1) ASA; mod (2) ASA or warfarin (but AE/bleed risks); high risk (>2) warfarin
Stroke prevention DM pts glucose ctrl: no fx on stroke/macrovascular comp; tight BP ctrl (<130/80) effective; statins
TIA carotid: S/S contralat hand-arm weak & sensory def; ipsilateral visual sx & aphasia or amaurosis fugax; poss carotid bruit (absent in high grade stenosis)
TIA vertebrobasilar S/S diplopia, ataxia, vertigo, dysarthria, CN palsies, LE weak, blurred vision, perioral numbness, poss drop attacks
TIA DDx Sz, migraine, syncope, hypoglycemia, mass lesion
2/3 of all cerebral infarcts are: MCA stroke
Cause of Amaurosis Fugax embolization of retinal arteries
Hollenhorst plaque cholesterol emboli from carotid
Diplopia, dysphagia, dysarthria = vertebrobasilar insufficiency
Types of stroke ischemic (thrombotic, embolic 20%, hypoperfusion); hemorrhagic (intracerebral, subarachnoid)
Contralateral weakness (lower > upper), AMS, incontinence; likely source of stroke = anterior cerebral artery
Contralateral weakness (face/arm > lower), contra sensory deficits, poss dysphasia; likely source of stroke = MCA
Contralateral visual field deficits, AMS, cortical blindness; likely source of stroke = posterior cerebral artery
vertigo/nystagmus, syncope, dysarthria, dysphagia, contralat pain/temp deficits; likely source of stroke = vertebrobasilar arteries
stroke PE neuro, CV (carotid bruit), EKG (A-fib, AMI/hypoperfusion)
Elevated troponins and ECG changes c/w MI can be seen in pt with acute stroke because of: an imbalance of the autonomic nervous system, with resulting excess of sympathetic activity and increased catecholamine effect on myocardial cells
Capsular warning syndrome = deep lacunar infarcts (eg, hemiplegic TIAs) with a fluctuating sx course that may predict an acute internal capsule infarct
smaller deep lacunar infarcts that often fluctuate, sometimes over the course of days, are known as the: capsular warning syndrome
Lacunar stroke: 5 types of clinical presentation Pure motor hemiparesis, pure sensory stroke, ataxic hemiparesis, dysarthria-clumsy hand syndrome, multiple subcortical infarcts & dementia
contralateral hemiplegia, hemisensory loss, & homonymous hemianopia (& global aphasia if dominant hemisphere is affected) = MCA stroke
MCA stroke: anterior main div occlusion vs posterior anterior occlusion: expressive dysphasia; posterior: receptive/ Wernicke
posterior cerebral artery occlusion leads to: thalamic syndrome: contralateral hemisensory deficit, spont pain & hyperpathia
anterior comm artery occlusion causes: weakness & cortical sensory loss in contralateral leg, poss arm weakness
ischemic stroke tx ASA, some get thrombolytics (dipyridamole, heparin for cardioembolic)
hemorrhagic stroke tx supportive; poss surg (stroke/AVM); aneurysm clipping/coil embolization
MCA stroke: anterior main div occlusion vs posterior anterior occlusion: expressive dysphasia; posterior: receptive/ Wernicke
Created by: Abarnard
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