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Neurology

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Question
Answer
Ischemic stroke pathogenesis   atheroembolic (50%); cardioembolic (30%)  
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Venous infarction RFs and presentation   OCP/SMK. HA; aphasia, weakness  
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Atheroembolic Stroke is characterized by:   Single vascular territory; Warning signs; Stepwise progression  
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Atheroembolic presentation   Hx HTN, CAD; transient language disturbance; transient weakness; Normal head CT; Doppler US: high grade stenosis (e.g., L ICA)  
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Ant cerebral art infarct: likely fx:   contralateral leg (motor > sensory)  
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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  
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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  
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Subcortical infarct fx:   face = arms = legs  
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Cortical infarct fx:   gradation btw face, arms, & legs  
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Lacunar syndromes   Pure Motor Stroke; Pure Sensory Stroke; Ataxic Hemiparesis; Clumsy Hand Dysarthria  
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Atheroembolic stroke: additional eval   Neuroimaging; Carotid US; MRA; CTA; Catheter angiography  
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Cardioembolic stroke presentation   Aphasia; hemiparesis/hemisensory deficit affecting face and arm; Carotid US normal (no brain lg vessel prob)  
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Cardioembolic: dx   Maximal deficit at onset; Multiple vascular territories; Cardioembolic source; Hemorrhagic infarction (Wedge shaped infarct towards cortical surface)  
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Cardioembolic: possible sources   A-fib; cardiomyopathy; acute MI; mural thrombus; valvular heart dz; bacterial endocarditis; atrial myxoma  
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Cardioembolic stroke: additional eval   pulse; EKG; 24-48 hr EKG; TTE (microcavitation); TEE  
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TIA   Acute focal neuro deficits; ischemic, usually embolic (carotid / vertebrobasilar) etiology; Sx/Sx resolve within 24 hr; no radiological evidence of infarct  
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Modifiable RF for first stroke   *HTN*; A fib; carotid stenosis; DM; hyperlipidemia; prior stroke/TIA  
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Lifestyle mods affecting BP   wt reduction; DASH diet; sodium reduction; exercise; moderate EtOH consumption  
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Stroke comorbid RF’s   CHD, CHF, DM, stroke  
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Prevention of A fib RF:   Low risk (0-1) ASA; mod (2) ASA or warfarin (but AE/bleed risks); high risk (>2) warfarin  
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Asx carotid stenosis: eval   Carotid bruit; Doppler US; MRA, CTA  
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Stroke prevention DM pts   glucose ctrl: no fx on stroke/macrovascular comp; tight BP ctrl (<130/80) effective; statins  
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Stroke prevention: hyperlipidemia   chol reduction w/statins  
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ASA recommended for 10-yr stroke risk of:   6-10%  
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Ischemic stroke: Tx   tPA (within 4.5 hrs of sx onset); head CT w/o evidence of hemorrhage/complicating lesion  
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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  
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tPA CI (3-4.5 hr)   >85 yo; NIH-SS >25; h/o both stroke/DM  
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If pt not tPA candidate: Tx:   poss endovascular tx; MERCI clot retriever?  
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Acute stroke mgmt   Temperature; Fluids/Glucose; BP; Antithrombotic agents  
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Acute ischemic stroke: tx BP?   No (drop in MAP can drop CBF, make things worse)  
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Secondary stroke prevention   Platelet antiaggregants (ASA vs Aggrenox / Plavix); Anticoagulants; BP; Lipid lowering; Endarterectomy  
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Antihypertensives & stroke risk   each 10 mmHg drop in BP = 28% decrease stroke risk  
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Stroke w/L paresis and R facial droop =   Right pons infarct  
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Hemiplegia (leg>arm), abulia, urinary incontinence, primitive reflexes: site of lesion =   ACA  
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Hemiplegia (arm/face > leg), hemianesthesia, homonymous hemianopia, aphasia, apraxia/neglect of nondominant side, drowsiness: site of lesion =   MCA  
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MCA: characteristic aphasia =   aphasia of dominant hemisphere (superior division: expressive; inferior division: receptive)  
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Thalamic syndromes (allodynia) with contralateral hemisensory disturbance & aphasia; macular-sparing homonymous hemianopia: site of lesion =   posterior cerebral artery  
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Wallenberg syndrome: numb in ipsilateral face & contralateral limbs; diplopia, dysarthria, ipsilateral Horner syndrome: site of lesion =   vertebral artery  
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Pinpoint pupils, long tract sxs (quadriplegia & sensory loss), CN abnormalities, cerebellar dysfunction: site of lesion =   basilar artery  
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Vertigo, N/V, diplopia, nystagmus, ipsilateral limb ataxia: site of lesion =   cerebellar artery  
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Sxs: (pure hemiplegia, pure hemianesthesia, ataxic hemiparesis) OR (clumsy hand & dysarthria): site of lesion =   lacunar CVA  
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Definition Apraxia   inability to do learned purposeful movements, including apraxia of speech  
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Definition Ataxia   incoordination of muscular movements  
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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  
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Definition Dysarthria   poor verbal articulation due to neuro injury  
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CVA labs (Acute)   CMP (lytes, glucose, BUN/Cr, LFT), CBC, PTT/INR, ESR, tox screen. If suspect endocarditis, get blood cultures  
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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)  
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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  
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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  
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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)  
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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)  
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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  
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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  
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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  
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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.  
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If PFO and stroke/TIA: tx   No evidence of warfarin > ASA. If pt is at increased risk or hx of DVT/PE, consider anticoagulation  
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Amaurosis fugax (transient monocular blindness): site of lesion =   Internal carotid artery / ophthalmic artery  
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Types of lacunar stroke (physiologically):   small vessel, penetrating arteries, atheroma, lipohyalinosis  
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Types of large vessel thrombosis:   atherosclerosis, dissection  
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Lacunar infarct (stroke):   15-20% of strokes; small vessel ischemia; HTN; usually pure sensory OR motor  
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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  
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Crescendo TIA =   increasing number & frequency of TIAs, highly likely to evolve to CVA (esp if 2 or more attacks within 24 hr)  
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Ischemic stroke pathophysiology   atheroembolic (50%); cardioembolic (30%); OR 2/3 thrombotic & 1/3 embolic  
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Stroke pathophysiology   80% ischemic, 20% hemorrhagic  
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Hemorrhagic stroke pathophysiology   parenchymal ICH (10-15%); subarachnoid (5-10%)  
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Anterior circulation consists of:   Ant choroidal, ant cerebral, MCA  
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Anterior circulation supplies:   Cortex, subcortical white matter, basal ganglia, internal capsule  
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Anterior circulation stroke   Hemispheric s/s: aphasia, apraxia, hemiparesis, hemisensory loss, visual field defects  
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Posterior circulation consists of:   Verterbral & basilar arteries  
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Posterior circulation supplies:   Brain stem, cerebellum, thalamus, parts of temporal & occipital lobes  
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Posterior circulation stroke   Sxs of brainstem dysfn: coma, drop attacks, vertigo, N/V, ataxia  
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Thrombotic vs embolic stroke sx progression   Thrombotic: stepwise progression, often preceded by TIA; Embolic: abrupt & without warning  
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Amyloid angiopathy stroke: patho   Blood vessel degeneration; Dementia; Lobar hemorrhage  
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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  
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Venous infarction presentation   h/o OCP/SMK; HA; aphasia, weakness  
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Atheroembolic stroke characterized by:   Single vascular territory; Warning signs; Stepwise progression  
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Atheroembolic stroke presentation   Hx HTN, CAD; transient language disturbance; transient weakness  
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Ant cerebral art infarct: likely fx:   contralateral leg (motor > sensory)  
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Subcortical infarct effects by body area:   face = arms = legs  
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Cortical infarct fx by body area:   gradation btw face, arms, & legs  
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Cardioembolic stroke presentation   h/o A fib; aphasia; hemiparesis/hemisensory deficit affecting face and arm  
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Cardioembolic CVA: dx   Maximal deficit at onset; Multiple vascular territories; Cardioembolic source; Hemorrhagic infarction (Wedge shaped infarct towards cortical surface)  
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Cardioembolic CVA: possible etiology   A fib; Cardiomyopathy; Acute MI; Valvular heart dz  
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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  
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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  
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Modifiable RF for first stroke   *HTN*; A fib; carotid stenosis; DM; hyperlipidemia; prior stroke/TIA  
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Prevention of A fib RF:   Low risk (0-1) ASA; mod (2) ASA or warfarin (but AE/bleed risks); high risk (>2) warfarin  
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Stroke prevention DM pts   glucose ctrl: no fx on stroke/macrovascular comp; tight BP ctrl (<130/80) effective; statins  
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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)  
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TIA vertebrobasilar S/S   diplopia, ataxia, vertigo, dysarthria, CN palsies, LE weak, blurred vision, perioral numbness, poss drop attacks  
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TIA DDx   Sz, migraine, syncope, hypoglycemia, mass lesion  
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2/3 of all cerebral infarcts are:   MCA stroke  
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Cause of Amaurosis Fugax   embolization of retinal arteries  
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Hollenhorst plaque   cholesterol emboli from carotid  
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Diplopia, dysphagia, dysarthria =   vertebrobasilar insufficiency  
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Types of stroke   ischemic (thrombotic, embolic 20%, hypoperfusion); hemorrhagic (intracerebral, subarachnoid)  
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Contralateral weakness (lower > upper), AMS, incontinence; likely source of stroke =   anterior cerebral artery  
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Contralateral weakness (face/arm > lower), contra sensory deficits, poss dysphasia; likely source of stroke =   MCA  
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Contralateral visual field deficits, AMS, cortical blindness; likely source of stroke =   posterior cerebral artery  
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vertigo/nystagmus, syncope, dysarthria, dysphagia, contralat pain/temp deficits; likely source of stroke =   vertebrobasilar arteries  
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stroke PE   neuro, CV (carotid bruit), EKG (A-fib, AMI/hypoperfusion)  
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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  
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Capsular warning syndrome =   deep lacunar infarcts (eg, hemiplegic TIAs) with a fluctuating sx course that may predict an acute internal capsule infarct  
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smaller deep lacunar infarcts that often fluctuate, sometimes over the course of days, are known as the:   capsular warning syndrome  
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Lacunar stroke: 5 types of clinical presentation   Pure motor hemiparesis, pure sensory stroke, ataxic hemiparesis, dysarthria-clumsy hand syndrome, multiple subcortical infarcts & dementia  
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contralateral hemiplegia, hemisensory loss, & homonymous hemianopia (& global aphasia if dominant hemisphere is affected) =   MCA stroke  
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MCA stroke: anterior main div occlusion vs posterior   anterior occlusion: expressive dysphasia; posterior: receptive/ Wernicke  
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posterior cerebral artery occlusion leads to:   thalamic syndrome: contralateral hemisensory deficit, spont pain & hyperpathia  
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anterior comm artery occlusion causes:   weakness & cortical sensory loss in contralateral leg, poss arm weakness  
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ischemic stroke tx   ASA, some get thrombolytics (dipyridamole, heparin for cardioembolic)  
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hemorrhagic stroke tx   supportive; poss surg (stroke/AVM); aneurysm clipping/coil embolization  
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MCA stroke: anterior main div occlusion vs posterior   anterior occlusion: expressive dysphasia; posterior: receptive/ Wernicke  
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