Cerebrovascular Accident (Stroke): A High-Yield USMLE Review

A cerebrovascular accident is the sudden onset of focal neurological deficits from disrupted cerebral blood flow, either ischemic (vessel occlusion) or hemorrhagic (vessel rupture). It is a time-critical emergency where 'time is brain'—every minute of ischemia kills neurons—so the exam tests rapid recognition, distinguishing ischemia from hemorrhage, localizing the vascular territory, and identifying candidates for reperfusion therapy.

Presentation

• Sudden onset of focal deficits: MCA strokes cause contralateral face and arm weakness/sensory loss (leg relatively spared) and, in the dominant hemisphere, aphasia—Broca's (non-fluent, effortful, comprehension intact, frustration) with superior division, Wernicke's (fluent nonsense, impaired comprehension) with inferior division.
• Non-dominant hemisphere MCA strokes cause hemispatial neglect and anosognosia; complete MCA syndrome adds contralateral homonymous hemianopia.
• ACA strokes produce contralateral leg weakness predominating over arm and face, with abulia and (in bilateral damage) urinary incontinence; PCA strokes cause visual field cuts and brainstem strokes cause crossed findings.
• UMN facial pattern: lower face droops while the forehead is spared (bilateral cortical innervation)—distinguishing stroke from a Bell's palsy that weakens the entire hemiface.
• Lacunar strokes from deep penetrating vessels give pure motor or pure sensory deficits without cortical signs such as aphasia or neglect.
• Posterior circulation strokes may present with 'non-specific' dizziness and ataxia and are frequently under-diagnosed.

Diagnosis

• Non-contrast CT head immediately—the first priority is to rule out hemorrhage; a normal CT in the hyperacute phase is expected in ischemic stroke and does NOT exclude it (means 'ischemic stroke,' not 'no stroke').
• CT angiography to evaluate for large vessel occlusion (ICA, M1, sometimes M2), especially when thrombectomy is being considered.
• Bedside glucose check and NIHSS scoring during initial assessment to gauge deficit severity and exclude mimics.
• For TIA and mechanism workup: brain imaging (MRI may show infarct even after clinical resolution), vascular imaging (carotid ultrasound, CTA, or MRA), and cardiac evaluation (ECG, echocardiogram, prolonged monitoring for atrial fibrillation).

Management

• Rapid reperfusion for ischemic stroke: IV thrombolysis with alteplase (tPA) in eligible patients within 4.5 hours, targeting door-to-needle under 60 minutes; hemorrhage on CT is an absolute contraindication.
• Mechanical thrombectomy for large vessel occlusion, generally within 6 hours—or up to 24 hours in selected patients with favorable perfusion imaging (small core, large penumbra), as established by the DAWN and DEFUSE-3 trials.
• Secondary prevention tailored to mechanism: anticoagulation for cardioembolic stroke (warfarin INR 2–3 or a DOAC), antiplatelet therapy plus high-intensity statin for atherosclerotic stroke, and blood pressure control for small-vessel disease.
• Carotid revascularization (endarterectomy or stenting) for symptomatic carotid stenosis ≥70%, with greatest benefit within 2 weeks of symptoms; anticoagulate atrial fibrillation guided by CHA₂DS₂-VASc score.
• In the acute phase (first 48–72 hours) allow permissive hypertension; treat TIA as an emergency with urgent workup because stroke risk is highest in the first 48–72 hours.

High-yield

• 'Time is brain'—the goal is rapid reperfusion via IV thrombolysis and/or thrombectomy.
• CT rules out hemorrhage, not ischemia; a normal early CT with acute focal deficits still means stroke.
• Lipohyalinosis of small penetrating arteries → lacunar (ischemic) infarcts, whereas rupture of Charcot-Bouchard microaneurysms → hypertensive intracerebral hemorrhage (putamen, thalamus, pons, cerebellum).
• Vascular territory patterns: MCA = face/arm weakness + aphasia (dominant) or neglect (non-dominant); ACA = leg weakness; PCA = visual field cut; brainstem = crossed findings.
• Stroke mechanism dictates secondary prevention: cardioembolic → anticoagulation, atherosclerotic → statin + antiplatelet, small vessel → BP control.
• UMN facial weakness spares the forehead (bilateral innervation), unlike the full-face weakness of Bell's palsy.
• Young strokes: think dissection (especially with neck pain), cardioembolism, hypercoagulable states, and paradoxical embolism.
• Subarachnoid hemorrhage presents with thunderclap headache and CT may be normal—do an LP if suspicion is high.

Pitfalls

• Do not let a normal CT reassure you that there is no stroke—CT is done to detect hemorrhage, and ischemic stroke looks normal early.
• Don't confuse the mechanisms of small-vessel disease: lipohyalinosis causes lacunar ischemic infarcts, while Charcot-Bouchard microaneurysm rupture causes hypertensive hemorrhage.
• Do not withhold thrombolysis just because a patient takes daily aspirin; aspirin alone is not a contraindication.
• Don't miss posterior circulation strokes: dizziness and ataxia are easily dismissed—perform a complete neurological exam on every dizzy patient.
• Don't assume patients arriving 'too late' for tPA cannot be helped—always obtain vascular imaging, since the extended thrombectomy window reaches 24 hours with favorable imaging.
• Don't dismiss a TIA as resolved; stroke risk peaks in the first 48–72 hours, so urgent workup is mandatory.