Acute loss of brain function due to disrupted blood flow—usually from an arterial blockage (ischemic stroke, ~85% of cases) or a ruptured vessel causing bleeding (hemorrhagic stroke, ~15%).
Very common (≈800k strokes/year in US) and a leading cause of adult disability and death (5th leading cause of death). Rapid recognition and treatment ("time is brain") can save brain tissue, so stroke is a high-yield emergency topic on boards.
Typically a sudden onset of focal neurologic deficits: one-sided weakness or numbness, facial droop, speech difficulty (aphasia or slurred speech), vision loss, or imbalance. The mnemonic FAST (Face drooping, Arm weakness, Speech difficulty, Time) highlights common signs and urgency.
Ischemic strokes usually cause painless loss of function (e.g., hemiparesis, hemisensory loss, aphasia). Hemorrhagic strokes are more likely to present with headache, vomiting, or altered consciousness due to increased intracranial pressure. (e.g., intracerebral hemorrhage often causes sudden severe headache and stupor; subarachnoid hemorrhage classically causes a "thunderclap" headache with neck stiffness.)
Risk factors: Hypertension is the single most important risk factor (accounts for ~48% of stroke risk). Other major contributors are smoking, diabetes, dyslipidemia, and atrial fibrillation (a key cause of cardioembolic ischemic strokes). Older age and vascular disease history also increase risk.
Subtypes: TIA (transient ischemic attack) – brief stroke-like deficit that resolves within 24 hours by definition (often <1 hour) with no permanent damage. Lacunar strokes – small deep infarcts from chronic HTN (lipohyalinosis) in penetrating arteries, causing isolated syndromes (e.g., pure motor hemiparesis) without cortical signs. Large-vessel strokes – occlusion of a major artery (e.g., MCA) leading to extensive deficits (contralateral hemiplegia, hemisensory loss, gaze deviation, and aphasia if dominant hemisphere or neglect if non-dominant).
Stabilize ABCs and immediately check fingerstick glucose (hypoglycemia can mimic stroke).
Perform a focused neurologic exam with NIH Stroke Scale (NIHSS) scoring (0–42 scale, higher = more severe deficit) to quantify stroke severity.
Obtain emergent noncontrast head CT (within minutes) to distinguish ischemic vs hemorrhagic stroke. If no hemorrhage (ischemic stroke), consider urgent vascular imaging (CT or MR angiography) to detect large vessel occlusion (for potential thrombectomy).
If ischemic stroke confirmed: assess eligibility for reperfusion therapy – IV alteplase (tPA) if within 3–4.5 hour window (no contraindications), and for a large occlusion, add mechanical thrombectomy (endovascular clot retrieval, within 6–24 h for select patients). Begin supportive measures (e.g., keep patient NPO until swallowing is evaluated; permissive hypertension is allowed in ischemic stroke to promote perfusion, unless above tPA limits).
If hemorrhagic stroke: manage airway and blood pressure (usually target SBP ~140 mmHg to limit bleeding), reverse any anticoagulation, and obtain neurosurgery consult early (for possible hematoma evacuation or aneurysm treatment).
After initial stabilization, work up the cause: e.g., carotid imaging (Doppler ultrasound, CTA) for carotid stenosis, cardiac evaluation (ECG/telemetry for atrial fibrillation, echocardiogram for clots), and labs (e.g., lipids, HbA1c, hypercoagulability tests in young patients).
Condition
Distinguishing Feature
Hypoglycemia
low blood sugar can cause focal deficits or confusion; always check glucose first
Seizure (Todd paralysis)
postictal transient paralysis after a seizure; look for preceding convulsions or tongue bite
Migraine with aura
hemiplegic migraine can mimic stroke with transient neurologic deficits, usually gradual onset and with headache
Ischemic stroke (acute): If within 4.5 hours of symptom onset and meets criteria, give IV thrombolytic (alteplase/tPA) to dissolve the clot. For a large artery occlusion (especially proximal anterior circulation), perform urgent mechanical thrombectomy (endovascular clot removal), ideally within 6 hours (up to 24 h in select cases). Control blood pressure (must be <185/110 mmHg before tPA; if no tPA, do not lower BP unless >220/120).
Hemorrhagic stroke (acute): Reverse anticoagulation (if applicable), lower blood pressure (target ~140 mmHg systolic) to reduce bleeding, and manage intracranial pressure (head elevation, mannitol, or hyperventilation for signs of herniation). Consult neurosurgery; urgent surgical evacuation is considered for cerebellar hemorrhages or large hematomas causing mass effect. For aneurysmal subarachnoid hemorrhage, secure the aneurysm (coiling or clipping) and give nimodipine to prevent vasospasm.
Aftercare & prevention: Start aspirin within 24–48 hours for ischemic stroke (typically after 24 h repeat CT if tPA was given). Long-term, use antiplatelet therapy (aspirin ± dipyridamole, or clopidogrel) for non-cardioembolic stroke, or anticoagulation for cardioembolic stroke (e.g., warfarin or DOAC in atrial fibrillation), usually starting about 1–2 weeks after stroke. Implement secondary prevention: high-intensity statin for atherosclerotic stroke, blood pressure control, diabetes management, smoking cessation. Early mobilization and comprehensive stroke rehabilitation (physical, occupational, speech therapy) are crucial for functional recovery.
Always check glucose in acute neuro deficits – stroke mimics like hypoglycemia are easily ruled out with a fingerstick.
Time is brain: an untreated large stroke can destroy ~2 million neurons per minute, so every minute of delay in reperfusion worsens outcome.
Blood pressure management differs by stroke type: in ischemic stroke, allow permissive hypertension (don't lower BP acutely unless >185/110 mmHg when giving tPA) to maintain perfusion, whereas in hemorrhagic stroke, aggressive BP control (≈140s) is needed to prevent hematoma expansion.
Lacunar infarcts (small vessel strokes) cause pure motor or pure sensory strokes and notably lack cortical signs like aphasia or neglect – a clue that the lesion is subcortical (e.g., internal capsule).
Declining level of consciousness or new coma in a stroke patient → suspect massive stroke with edema or an expanding hemorrhage causing increased intracranial pressure and possible herniation (urgent intervention needed, e.g., decompressive craniectomy).
After thrombolytic therapy, watch for acute neurologic worsening with headache or vomiting → sign of possible intracerebral hemorrhage (tPA complication). Stop infusion and get emergent CT scan if this is suspected.
Within 10 min of arrival: perform a quick exam (vitals, NIHSS) and obtain emergent noncontrast CT of the head to differentiate ischemic vs hemorrhagic stroke.
If no hemorrhage on CT (→ ischemic stroke): assess tPA eligibility (≤4.5 h since onset, BP <185/110, no major contraindications) and begin thrombolysis if appropriate. Simultaneously, if large vessel occlusion is suspected (severe deficits, cortical signs), get CT or MR angiography to confirm and arrange thrombectomy (can be done up to 24 h in select cases).
If intracerebral hemorrhage on CT: focus on airway protection (intubate if decreased LOC) and blood pressure reduction (often target ~140 mmHg) to prevent expansion. Reverse any anticoagulants and consult neurosurgery urgently (for possible hematoma evacuation or intracranial pressure relief). Treat complications (e.g., seizures, elevated ICP) as needed.
Admit to a stroke unit for monitoring. After acute treatment, initiate rehabilitation early and evaluate stroke etiology to guide secondary prevention (e.g., carotid imaging for endarterectomy if stenosis, start antithrombotics, manage risk factors).
Right-handed 70‑year‑old with atrial fibrillation (off anticoagulation) suddenly develops right facial droop, right arm weakness, and aphasia → left (dominant) MCA ischemic stroke (likely cardioembolic from AF).
Middle-aged patient with long-standing hypertension complains of the "worst headache of my life," then rapidly becomes obtunded with vomiting and left-sided weakness → intracerebral hemorrhage (e.g., hypertensive basal ganglia hemorrhage).
A patient reports a 10-minute episode of blurry vision and left hand weakness that self-resolved, exam now normal → transient ischemic attack (TIA) (warning sign for future stroke).
Case 1
A 68‑year‑old man with hypertension and poorly controlled atrial fibrillation suddenly develops slurred speech and right-sided weakness.
Diagram of cerebral arterial territories: anterior cerebral artery (yellow), middle cerebral artery (red), and posterior cerebral artery (blue).