Medical School · Year 2 · Neuroscience · includes a discussion video

Lecture 19: Stroke and Cerebrovascular Disease

Unit 2.5: Neuroscience

Learning Objectives

By the end of this lecture, students will be able to:

1. Describe the epidemiology and risk factors for stroke
2. Explain the pathophysiology of ischemic and hemorrhagic stroke
3. Describe the clinical presentations of stroke by vascular territory
4. Explain the acute management of ischemic stroke
5. Describe the approach to hemorrhagic stroke
6. Explain secondary stroke prevention strategies

Lecture Outline

I. Stroke Overview

Stroke is defined as a neurological deficit caused by a vascular etiology, either ischemic (from blood vessel occlusion) or hemorrhagic (from blood vessel rupture). The modern tissue-based definition requires symptoms lasting more than 24 hours or imaging evidence of infarction regardless of symptom duration. Transient ischemic attack (TIA) is now defined as transient neurological symptoms without evidence of infarction on imaging. The term "brain attack" emphasizes the emergency nature of stroke, analogous to "heart attack" for myocardial infarction.

Stroke is a major public health problem. Approximately 800,000 strokes occur in the United States annually, making it the fifth leading cause of death and the leading cause of adult disability. Ischemic stroke accounts for approximately 87% of all strokes, while hemorrhagic strokes comprise the remainder (intracerebral hemorrhage 10%, subarachnoid hemorrhage 3%). The economic burden includes direct medical costs and lost productivity, with many survivors requiring long-term care.

Risk factors for stroke are classified as modifiable and non-modifiable. Hypertension is the most important modifiable risk factor, present in approximately 70% of stroke patients and increasing risk 3-4 fold. Other major modifiable risk factors include atrial fibrillation (5-fold increased risk), diabetes mellitus, dyslipidemia, smoking, obesity, physical inactivity, and excessive alcohol consumption. Non-modifiable risk factors include age (risk doubles each decade after 55), sex (males have higher incidence until advanced age), race (Black and Hispanic populations have higher stroke rates), family history, and prior stroke or TIA (which confers 10-fold increased risk).

<image>Stroke overview: Panel 1 - Pie chart showing stroke subtypes: ischemic 87% (broken down by mechanism), intracerebral hemorrhage 10%, subarachnoid hemorrhage 3%. Panel 2 - Risk factor hierarchy diagram showing modifiable factors (hypertension at top with relative risk, then AF, diabetes, smoking, dyslipidemia) and non-modifiable factors (age, sex, race, family history). Panel 3 - Epidemiological data showing incidence by age, sex, and race with geographic distribution in US. Panel 4 - Timeline showing stroke as medical emergency with "time is brain" concept: 1.9 million neurons lost per minute of ischemia.</image>

II. Ischemic Stroke Pathophysiology

Ischemic stroke results from occlusion of a cerebral blood vessel, causing downstream tissue infarction. The TOAST classification categorizes ischemic stroke by mechanism. Large artery atherosclerosis (approximately 20%) involves stenosis greater than 50% of a major extracranial or intracranial artery, typically from atherosclerotic plaque with superimposed thrombosis or artery-to-artery embolism. Cardioembolism (approximately 25%) involves emboli from cardiac sources, most commonly atrial fibrillation, but also including mechanical valves, recent myocardial infarction, left ventricular thrombus, or infective endocarditis. Small vessel disease (lacunar, approximately 25%) causes small deep infarcts from lipohyalinosis of penetrating arteries, typically associated with hypertension. Other determined causes (approximately 5%) include dissection, hypercoagulable states, and vasculitis. Cryptogenic stroke (approximately 25%) has no identified cause after complete workup.

The ischemic cascade describes the molecular events following ischemia. Within seconds, energy failure occurs as ATP depletion leads to failure of ion pumps and membrane depolarization. Within minutes, excessive glutamate release causes excitotoxicity through NMDA and AMPA receptor overactivation, leading to calcium influx and activation of destructive enzymes. Over hours, inflammatory cascades amplify injury with microglial activation, cytokine release, and blood-brain barrier breakdown. Over days, apoptotic pathways are activated in the penumbral tissue.

The ischemic penumbra is the tissue surrounding the irreversibly damaged core that is functionally impaired but potentially salvageable. The core experiences severe ischemia (cerebral blood flow less than 10 mL/100g/min) and infarcts rapidly. The penumbra has reduced but present blood flow (10-25 mL/100g/min) and may survive for hours depending on collateral circulation. The therapeutic goal is to reperfuse the penumbra before it converts to infarct core. The phrase "time is brain" emphasizes urgency: approximately 1.9 million neurons die per minute of untreated ischemia. However, penumbral survival varies considerably depending on collateral blood supply, explaining why some patients benefit from treatment beyond traditional time windows.

<image>Ischemic stroke pathophysiology: Panel 1 - TOAST classification diagram showing the five categories with typical imaging findings and percentage breakdown for each. Panel 2 - Ischemic cascade timeline: seconds (energy failure, ion pump failure), minutes (glutamate release, excitotoxicity), hours (inflammation, BBB breakdown), days (apoptosis). Panel 3 - Core and penumbra concept showing central irreversibly damaged core (CBF <10) surrounded by at-risk penumbra (CBF 10-25) and benign oligemia (CBF >25). Panel 4 - CT perfusion imaging demonstrating core (CBV reduced) vs penumbra (MTT prolonged, CBV preserved) mismatch as therapeutic target.</image>

III. Stroke Syndromes by Vascular Territory

Middle cerebral artery (MCA) territory stroke is the most common and clinically recognizable stroke syndrome. The MCA supplies the lateral cerebral convexity, including the motor and sensory cortices for the face and arm, language areas in the dominant hemisphere, and attention networks in the non-dominant hemisphere. Proximal MCA occlusion causes the classic triad of contralateral hemiparesis affecting the face and arm more than the leg, contralateral hemisensory loss in the same distribution, and homonymous hemianopia from optic radiation involvement. The eyes deviate toward the lesion side. In the dominant (usually left) hemisphere, global aphasia occurs with both expression and comprehension affected. In the non-dominant (usually right) hemisphere, hemispatial neglect and anosognosia (unawareness of deficit) develop.

Anterior cerebral artery (ACA) territory stroke causes a different clinical picture. The ACA supplies the medial surfaces of the frontal and parietal lobes, including the motor and sensory cortices for the leg on the paracentral lobule. ACA stroke causes contralateral leg weakness greater than arm weakness, the opposite pattern from MCA stroke. Sensory loss follows the same leg-predominant distribution. Behavioral changes may occur, including abulia (lack of will or initiative), personality changes, and urinary incontinence. Bilateral ACA infarction (from anterior communicating artery aneurysm rupture with vasospasm) can cause akinetic mutism.

Posterior cerebral artery (PCA) territory stroke primarily causes visual deficits. The PCA supplies the occipital lobe (including primary visual cortex) and the medial temporal lobe. PCA occlusion causes contralateral homonymous hemianopia, often with macular sparing because the macular cortex at the occipital pole may have dual blood supply from MCA branches. If the medial temporal lobe is involved, memory impairment may occur. Proximal PCA occlusion can affect thalamoperforating branches, causing thalamic sensory loss and thalamic pain syndrome (Dejerine-Roussy syndrome). Basilar artery occlusion is a neurological emergency causing quadriplegia, bilateral cranial nerve palsies, and potentially locked-in syndrome (consciousness preserved but only able to communicate through vertical eye movements and blinking).

<image>Stroke syndromes by territory: Panel 1 - MCA syndrome: lateral convexity diagram showing affected regions, clinical features (face/arm > leg weakness, aphasia or neglect, hemianopia), eye deviation toward lesion, with motor homunculus correlation. Panel 2 - ACA syndrome: medial surface showing leg motor cortex, clinical features (leg > arm weakness, abulia, incontinence). Panel 3 - PCA syndrome: occipital and medial temporal involvement, visual field defect diagram showing homonymous hemianopia with macular sparing. Panel 4 - Basilar artery syndrome: locked-in syndrome illustration showing awake patient with only vertical eye movement, compared to complete basilar occlusion with quadriplegia and cranial nerve signs.</image>

IV. Lacunar Syndromes

Lacunar infarcts result from small vessel disease affecting penetrating arteries, causing small (less than 15 mm) deep infarcts in the basal ganglia, thalamus, internal capsule, pons, and corona radiata. The underlying pathology is lipohyalinosis, a degenerative process of small arteries strongly associated with chronic hypertension. Lacunar strokes cause pure deficits without cortical signs such as aphasia, neglect, or visual field cuts.

Five classic lacunar syndromes are recognized. Pure motor hemiparesis, the most common, results from infarction of the posterior limb of the internal capsule or basis pontis, causing contralateral face, arm, and leg weakness without sensory loss or cortical signs. Pure sensory stroke results from thalamic (specifically ventral posterolateral nucleus) infarction, causing contralateral hemibody numbness without weakness. Ataxic hemiparesis combines weakness with ipsilateral cerebellar-type ataxia, typically from pontine or internal capsule lesions. Dysarthria-clumsy hand syndrome presents with facial weakness, dysarthria, dysphagia, and clumsiness of one hand, usually from pontine infarction. Sensorimotor stroke results from thalamocapsular lesions affecting both sensory and motor fibers.

The key clinical feature of lacunar syndromes is the absence of cortical signs. There is no aphasia, neglect, hemianopia, or altered level of consciousness. This is because the infarcts are subcortical and do not affect the cortex directly. Recognition of lacunar syndromes is important because the underlying mechanism (small vessel disease) differs from large artery atherosclerosis or cardioembolism, which has implications for diagnostic workup and prevention. However, small deep infarcts can occasionally result from emboli rather than small vessel disease, so the clinical syndrome alone does not definitively establish the mechanism.

<image>Lacunar syndromes: Panel 1 - Anatomical locations of lacunar infarcts: internal capsule (anterior limb, genu, posterior limb), thalamus, pons, and corona radiata with typical sizes (<15mm). Panel 2 - Classic lacunar syndromes with lesion location and clinical features: pure motor (posterior limb IC/pons), pure sensory (thalamus VPL), ataxic hemiparesis (pons/IC), dysarthria-clumsy hand (pons), sensorimotor (thalamocapsular). Panel 3 - MRI appearance of lacunar infarcts showing T2 hyperintensity and DWI restriction in typical locations. Panel 4 - Comparison emphasizing no cortical signs: lacunar (no aphasia, no neglect, no hemianopia, no visual symptoms) vs cortical stroke.</image>

V. Acute Stroke Assessment

The initial evaluation of suspected stroke focuses on rapid stabilization, confirmation of diagnosis, and determination of treatment eligibility. The phrase "time is brain" drives the urgency: every minute of ischemia causes additional irreversible damage. Stroke protocols aim for door-to-needle time (thrombolysis initiation) of less than 60 minutes and door-to-groin puncture time (for thrombectomy) of less than 90 minutes.

Initial assessment follows ABCs (airway, breathing, circulation) and includes immediate point-of-care glucose testing because hypoglycemia can mimic stroke and is rapidly correctable. The most critical piece of history is the time of symptom onset or "last known well"—the last time the patient was definitely normal. This determines eligibility for time-sensitive treatments. The NIH Stroke Scale (NIHSS) provides standardized severity assessment, scoring consciousness, gaze, visual fields, facial palsy, motor strength in each limb, limb ataxia, sensory loss, language, dysarthria, and extinction/inattention on a scale from 0 (normal) to 42 (most severe).

Neuroimaging is essential for acute stroke evaluation. Non-contrast CT of the head is the initial study, primarily to exclude hemorrhage before considering thrombolysis. Early ischemic changes on CT may be subtle (loss of gray-white differentiation, insular ribbon sign, sulcal effacement) or absent within the first few hours. CT angiography (CTA) rapidly identifies large vessel occlusions amenable to thrombectomy. CT perfusion (CTP) distinguishes ischemic core (irreversibly damaged) from penumbra (salvageable) by measuring cerebral blood flow and volume; a large penumbra with small core ("mismatch") identifies patients who may benefit from intervention even beyond standard time windows. MRI with diffusion-weighted imaging (DWI) is highly sensitive for acute ischemia within minutes of onset, showing restricted diffusion as hyperintensity on DWI with corresponding dark signal on the apparent diffusion coefficient (ADC) map.

<image>Acute stroke assessment: Panel 1 - Stroke code protocol flowchart: EMS notification → ED arrival → immediate glucose, neuro exam, NIHSS → CT head (exclude hemorrhage) → CTA (identify occlusion) → treatment decision → door-to-needle goal <60 min. Panel 2 - NIH Stroke Scale domains with scoring examples for each: consciousness, gaze, visual, facial, motor arms and legs, ataxia, sensory, language, dysarthria, extinction. Panel 3 - Early CT signs of ischemia: hyperdense MCA sign (thrombus in artery), loss of insular ribbon, loss of basal ganglia gray-white differentiation, with ASPECTS scoring regions. Panel 4 - Imaging comparison: CT (hemorrhage exclusion), CTA (vessel occlusion), CTP (core vs penumbra mismatch), DWI (acute infarct).</image>

VI. Acute Ischemic Stroke Treatment

Intravenous thrombolysis with alteplase or tenecteplase aims to dissolve the occluding thrombus and restore blood flow. The standard time window is within 4.5 hours of symptom onset or last known well. Alteplase is dosed at 0.9 mg/kg (maximum 90 mg), with 10% given as bolus and the remainder infused over 60 minutes. Tenecteplase, given as a single bolus, appears at least equivalent and is increasingly used. The efficacy of thrombolysis is time-dependent: the number needed to treat for good outcome is approximately 4.5 at 0-90 minutes, 9 at 90-180 minutes, and 14 at 180-270 minutes. Patients who wake with stroke symptoms may be treated if MRI shows small or no DWI lesion with significant perfusion deficit (DWI-perfusion mismatch).

Absolute contraindications to thrombolysis include active internal bleeding, recent intracranial hemorrhage, intracranial neoplasm or AVM, severe uncontrolled hypertension (above 185/110 despite treatment), and known bleeding diathesis. Relative contraindications include recent major surgery, recent lumbar puncture, recent arterial puncture at non-compressible site, and current anticoagulation (depending on specific agent and levels). Blood pressure must be controlled below 185/110 before and maintained below 180/105 for 24 hours after thrombolysis.

Mechanical thrombectomy has revolutionized treatment of large vessel occlusion (LVO) stroke affecting the internal carotid artery or proximal MCA (M1, sometimes M2). Stent retrievers or aspiration catheters remove the clot endovascularly. The standard time window is within 6 hours for most patients, but DAWN and DEFUSE-3 trials demonstrated benefit up to 24 hours in patients with favorable imaging (small core, large penumbra). The number needed to treat for reduced disability is remarkably low: approximately 2-4 depending on time and imaging selection. Thrombectomy is typically performed in addition to IV thrombolysis when eligible, though may be used alone when thrombolysis is contraindicated.

<image>Acute ischemic stroke treatment: Panel 1 - Thrombolysis eligibility flowchart with time windows, contraindications checklist, and dosing (alteplase 0.9 mg/kg, 10% bolus, 90% over 1 hour). Panel 2 - Thrombectomy procedure illustration showing catheter access from femoral artery through ICA to occlusion site, stent retriever deployment, and clot retrieval. Panel 3 - Time windows diagram: thrombolysis (0-4.5 hours standard, extended with perfusion mismatch), thrombectomy (0-6 hours standard, up to 24 hours with favorable imaging). Panel 4 - Number needed to treat by time: thrombolysis efficacy declining with time, thrombectomy efficacy by NIHSS and time to treatment.</image>

VII. Secondary Prevention

Antiplatelet therapy is the cornerstone of secondary prevention for non-cardioembolic ischemic stroke. Aspirin 81-325 mg daily reduces recurrent stroke risk by approximately 20-25%. Clopidogrel 75 mg daily is an alternative, particularly in patients with aspirin intolerance or failure. Aspirin plus extended-release dipyridamole is another option. Dual antiplatelet therapy with aspirin plus clopidogrel for 21-30 days, followed by single antiplatelet therapy, is recommended for minor stroke (NIHSS ≤3) or high-risk TIA, based on CHANCE and POINT trials showing reduced early recurrence.

Anticoagulation is indicated for cardioembolic stroke, most commonly atrial fibrillation. Direct oral anticoagulants (DOACs) including apixaban, rivaroxaban, edoxaban, and dabigatran are generally preferred over warfarin for non-valvular atrial fibrillation due to better efficacy, safety, and convenience. Warfarin remains indicated for mechanical heart valves and certain other conditions. The timing of anticoagulation initiation after stroke is guided by infarct size and hemorrhagic transformation risk: typically 4-14 days after stroke, with earlier initiation for TIA or small infarcts and delayed initiation for large infarcts.

Risk factor management is crucial for long-term prevention. Blood pressure should be lowered to below 130/80 mmHg in most patients after the acute phase, as each 10 mmHg reduction decreases recurrence by approximately 30%. High-intensity statin therapy targeting LDL below 70 mg/dL reduces recurrence by 16-20%. Diabetes management, smoking cessation, and lifestyle modifications (diet, exercise, weight management) are all important. For symptomatic carotid stenosis of 70-99%, carotid endarterectomy or stenting substantially reduces stroke risk, with surgery preferred for most patients; 50-69% stenosis offers moderate benefit; and less than 50% stenosis is managed medically.

<image>Secondary prevention: Panel 1 - Antiplatelet therapy decision tree based on stroke mechanism: non-cardioembolic (aspirin, clopidogrel, or combination short-term), and relative efficacy of each agent. Panel 2 - Anticoagulation for atrial fibrillation: CHA2DS2-VASc score calculation, DOAC comparison table, timing of initiation based on infarct size (4-14 day window). Panel 3 - Risk factor modification targets: blood pressure (<130/80), LDL (<70), HbA1c (individualized), with expected relative risk reduction for each. Panel 4 - Carotid disease management by stenosis severity: symptomatic 70-99% (CEA/CAS), 50-69% (consider CEA), <50% (medical management), with NASCET criteria illustration.</image>

VIII. Intracerebral Hemorrhage

Intracerebral hemorrhage (ICH) results from rupture of a blood vessel within the brain parenchyma, causing a hematoma that expands and damages surrounding tissue. It accounts for approximately 10% of all strokes but has higher mortality than ischemic stroke (30-50% at 30 days). The presentation depends on hematoma location and size: headache, focal neurological deficits (contralateral weakness, sensory loss), and decreased level of consciousness are common.

Hypertension is the most common cause, responsible for approximately 50-70% of ICH. Hypertensive hemorrhages typically occur in deep locations: the putamen (35%), thalamus (15%), cerebellum (10%), and pons (5%). The underlying pathology is chronic hypertensive damage to small penetrating arteries (lipohyalinosis) with eventual rupture. Cerebral amyloid angiopathy (CAA) causes lobar hemorrhages in elderly patients due to amyloid deposition in cortical and leptomeningeal vessels; it is the most common cause of lobar ICH in patients over 70 and carries high risk of recurrence. Other causes include anticoagulation (which increases ICH risk 7-10 fold and leads to larger hematomas), vascular malformations (arteriovenous malformations, cavernous malformations), hemorrhagic transformation of ischemic stroke, tumors, and recreational drug use (cocaine, amphetamines cause vasospasm and hypertensive surges).

Medical management of ICH focuses on preventing hematoma expansion, managing blood pressure, and reversing anticoagulation. The INTERACT2 trial supports aggressive blood pressure lowering to systolic below 140 mmHg within the first few hours to reduce hematoma expansion. Anticoagulation reversal should be immediate: for warfarin, four-factor prothrombin complex concentrate (4F-PCC) and vitamin K; for dabigatran, idarucizumab; for factor Xa inhibitors (apixaban, rivaroxaban), andexanet alfa or 4F-PCC. Surgical evacuation is considered for cerebellar hemorrhages (risk of brainstem compression), large lobar hemorrhages in accessible locations in deteriorating patients, and cases with obstructive hydrocephalus requiring ventricular drainage. Deep hemorrhages are generally managed medically.

<image>Intracerebral hemorrhage: Panel 1 - CT appearance of ICH: acute hyperdensity with surrounding hypodense edema, showing typical locations for hypertensive (putamen, thalamus, pons, cerebellum) vs amyloid angiopathy (lobar). Panel 2 - Causes by location: deep structures (hypertension), lobar (CAA in elderly, other in young), with imaging features distinguishing each. Panel 3 - Acute management algorithm: BP target <140 systolic, anticoagulation reversal agents by drug (warfarin→4F-PCC+vitK, dabigatran→idarucizumab, Xa inhibitors→andexanet), ICP management. Panel 4 - Surgical indications: cerebellar hemorrhage >3cm or with brainstem compression, accessible lobar hemorrhage with deterioration, hydrocephalus requiring EVD.</image>

IX. Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) results from bleeding into the subarachnoid space, most commonly from rupture of a saccular (berry) aneurysm (approximately 85% of cases). Aneurysms typically occur at arterial bifurcations, with the most common locations being the anterior communicating artery (30%), posterior communicating artery (25%), and MCA bifurcation (20%). Risk factors for aneurysm formation and rupture include hypertension, smoking, excessive alcohol use, family history, and certain connective tissue disorders (autosomal dominant polycystic kidney disease, Ehlers-Danlos syndrome).

The classic presentation is sudden onset of severe headache, often described as the "worst headache of life" or "thunderclap headache." Patients may report a "sentinel headache" from a minor leak in the days preceding major rupture in up to 40% of cases. Associated symptoms include nausea and vomiting, neck stiffness (from meningeal irritation by blood), transient or sustained loss of consciousness, and focal neurological deficits depending on the aneurysm location. The Hunt-Hess scale grades clinical severity from I (mild headache) to V (comatose), which correlates with outcome.

Diagnosis begins with non-contrast CT, which is over 95% sensitive within 6 hours of symptom onset but sensitivity decreases over subsequent days. If CT is negative but clinical suspicion is high, lumbar puncture is required to look for xanthochromia (yellow discoloration from hemoglobin breakdown, present after 12 hours and persisting for 2 weeks) and red blood cells that do not clear between tubes. CT angiography or conventional angiography identifies the source aneurysm.

Management priorities include securing the aneurysm (endovascular coiling is preferred over surgical clipping for most aneurysms), preventing vasospasm (nimodipine 60 mg every 4 hours for 21 days reduces poor outcomes from delayed cerebral ischemia), monitoring for delayed cerebral ischemia (days 4-14, detected by transcranial Doppler, clinical decline, or imaging), managing hydrocephalus (external ventricular drainage if needed), and preventing systemic complications. Blood pressure management balances preventing rebleeding (lower pressure) against maintaining cerebral perfusion (higher pressure).

<image>Subarachnoid hemorrhage: Panel 1 - CT appearance showing blood in basal cisterns and Sylvian fissures with pattern suggesting aneurysm location (anterior communicating, posterior communicating, MCA bifurcation). Panel 2 - Common aneurysm locations on Circle of Willis diagram with approximate percentages at each site. Panel 3 - Hunt-Hess grading scale (I-V) with associated mortality at each grade. Panel 4 - Management timeline: immediate (stabilize, CT, CTA) → secure aneurysm (coiling vs clipping) → vasospasm prevention and monitoring (nimodipine, TCD days 4-14) → rehabilitation.</image>

X. TIA and Stroke Mimics

Transient ischemic attack (TIA) is now defined by tissue rather than time: transient neurological symptoms due to focal brain ischemia without infarction on imaging. Most TIAs last less than one hour. TIA is a medical emergency because it indicates high risk of subsequent stroke: 10-15% of TIA patients will have a stroke within 90 days, with half of those occurring within 48 hours. The ABCD2 score estimates short-term stroke risk: Age ≥60 (1 point), Blood pressure ≥140/90 (1 point), Clinical features (speech impairment without weakness 1 point, unilateral weakness 2 points), Duration (10-59 minutes 1 point, ≥60 minutes 2 points), and Diabetes (1 point). Scores of 4 or higher indicate high risk requiring hospitalization or urgent outpatient evaluation.

The workup for TIA mirrors that for stroke and should be completed urgently. Brain imaging with MRI (preferred) or CT evaluates for infarction (approximately 30-50% of clinical TIAs show diffusion restriction on MRI, meaning they are actually small strokes). Vascular imaging with CTA, MRA, or carotid ultrasound identifies large artery stenosis. Cardiac evaluation includes ECG (for atrial fibrillation) and echocardiography. Extended cardiac monitoring (Holter or event monitor for 30 days) increases detection of paroxysmal atrial fibrillation. Treatment follows secondary prevention principles, with dual antiplatelet therapy (aspirin plus clopidogrel) recommended for 21-30 days following high-risk TIA.

Stroke mimics are conditions that present with sudden focal neurological symptoms but are not vascular in etiology. Distinguishing mimics from true stroke is important because thrombolysis carries risks that are not justified for non-ischemic conditions. Common mimics include seizure with postictal (Todd's) paralysis (often with witnessed seizure, positive symptoms like jerking), migraine with aura (gradual symptom spread over minutes, often with headache and prior similar episodes), hypoglycemia (check glucose immediately; symptoms resolve with glucose correction), conversion disorder (inconsistent examination, psychiatric history, but diagnosis of exclusion), brain tumor (usually slower onset, may have headache and other signs), and multiple sclerosis (young patient, prior episodes, characteristic MRI findings). Clinical assessment and imaging help distinguish mimics, but when uncertain, the risks of untreated stroke generally outweigh the risks of thrombolysis in borderline cases.

<image>TIA and stroke mimics: Panel 1 - TIA tissue-based definition diagram: transient symptoms + no infarction on DWI = TIA; transient symptoms + DWI lesion = stroke. Panel 2 - ABCD2 score components and risk stratification: low risk (0-3), high risk (4-7), with corresponding 7-day stroke risk percentages. Panel 3 - Urgent TIA workup checklist: brain MRI/CT, vascular imaging (CTA/MRA/duplex), ECG, echo, extended cardiac monitoring, labs. Panel 4 - Stroke mimics comparison table: seizure (postictal, witnessed event), migraine (gradual spread, headache), hypoglycemia (low glucose, rapid reversal), conversion (inconsistent exam), with key distinguishing features for each.</image>

Summary

• Stroke is a vascular neurological emergency: 87% ischemic, 10% intracerebral hemorrhage, 3% subarachnoid hemorrhage
• Ischemic stroke mechanisms (TOAST): large artery atherosclerosis 20%, cardioembolism 25%, small vessel 25%, other 5%, cryptogenic 25%
• MCA stroke: contralateral face/arm > leg weakness, aphasia (dominant) or neglect (non-dominant), homonymous hemianopia
• ACA stroke: contralateral leg > arm weakness; PCA stroke: contralateral homonymous hemianopia with macular sparing
• Lacunar strokes cause pure motor, pure sensory, ataxic hemiparesis, dysarthria-clumsy hand, or sensorimotor syndromes without cortical signs
• IV thrombolysis: within 4.5 hours (extended with perfusion mismatch); mechanical thrombectomy: up to 24 hours for LVO with favorable imaging
• ICH: BP target <140 systolic; reverse anticoagulation immediately; consider surgery for cerebellar hemorrhage
• SAH: thunderclap headache; CT then LP if negative; secure aneurysm; nimodipine for vasospasm prevention
• Secondary prevention: antiplatelets for non-cardioembolic stroke; anticoagulation for AF; BP <130/80, LDL <70
• TIA is a medical emergency with high short-term stroke risk; urgent workup and dual antiplatelet therapy for 21-30 days

Key Terms

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