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Stroke — Overview for Medical Students

Definition

• Transient ischemic attack (TIA): all neurologic signs resolve within 24 h and no infarction on imaging
• Stroke: deficits persist >24 h or brain infarction is demonstrated

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Epidemiology

• Second leading cause of death worldwide — 7.1 million deaths from stroke in 2020
• ~7 million Americans ≥20 years old have had a stroke; prevalence projected to rise by 3.4 million in the next decade (→ 4% of all adults)
• Age-standardized death rate has fallen ~15% over the past decade due to improved prevention and treatment
• Stroke remains the #1 cause of adult disability in the US; number one cause of acquired neurologic disability globally

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Classification: Two Major Types

1. Ischemic Stroke (~80–85%)

• Large-vessel atherothrombosis — carotid/vertebral/intracranial atherosclerosis
• Cardioembolic — atrial fibrillation (most common), valvular disease, LV thrombus, dilated cardiomyopathy
• Small-vessel (lacunar) — occlusion of single penetrating arteries, usually from lipohyalinosis due to hypertension/diabetes
• Cryptogenic — no source identified after full workup (~30%)
• Other determined cause — vasculitis, dissection, hypercoagulable states, Moyamoya, drug use

2. Hemorrhagic Stroke (~15–20%)

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Pathophysiology of Ischemic Stroke

Ischemic Core vs. Penumbra

• Ischemic core: irreversibly infarcted tissue at the center
• Ischemic penumbra: surrounding hypoperfused but potentially salvageable tissue — the target of reperfusion therapy

Cellular Cascade

1. ↓ CBF → ↓ O₂/glucose → ↓ ATP → failure of Na⁺/K⁺-ATPase
2. Neuronal depolarization → Na⁺/Ca²⁺ influx
3. Glutamate release (excitotoxicity) → sustained NMDA receptor activation → ↑ intracellular Ca²⁺
4. Reactive oxygen species (ROS) damage DNA, lipid membranes
5. Microglial activation + peripheral immune cell infiltration → inflammatory injury
6. Fever and hyperglycemia (>200 mg/dL) dramatically worsen injury

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Pathophysiology of ICH

• Spontaneous ICH = bleeding directly into brain parenchyma
• Creates a mass effect on neural structures + direct neurotoxicity from blood breakdown products
• Most common cause: chronic hypertension → lipohyalinosis of small penetrating vessels (putamen, thalamus, cerebellum, pons most common sites)
• Second most common: cerebral amyloid angiopathy (lobar hemorrhages in elderly)
• Blood pressure management is key: AHA/ASA guidelines target SBP 130–150 mmHg acutely for spontaneous ICH with initial SBP 150–220 mmHg

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Vascular Territories & Stroke Syndromes

Anterior Circulation (Internal Carotid → MCA/ACA)

Posterior Circulation (Vertebrobasilar)

Small-Vessel (Lacunar) Syndromes

• Pure motor hemiplegia (posterior limb of internal capsule or pons)
• Pure sensory stroke (thalamus)
• Ataxic hemiparesis
• Dysarthria–clumsy hand

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Risk Factors

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Key Points to Remember

1. Time is brain — ~1.9 million neurons die per minute during a large-vessel occlusion
2. Always CT first to exclude hemorrhage before any thrombolysis
3. The ischemic penumbra is the therapeutic window — this is why door-to-needle time matters
4. Atrial fibrillation is the single most important modifiable cardioembolic risk factor
5. Lacunar infarcts are caused by small-vessel disease from HTN/DM, not emboli — so workup and treatment differ
6. SAH presents with thunderclap headache ("worst headache of my life") — a clinical emergency requiring immediate imaging

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