Cerebrovascular Diseases

Stroke Fundamentals - Brain Attack Basics

• Definition: Sudden focal neurological deficit of vascular origin. "Brain Attack" = medical emergency. Time is Brain!
• Types:
  • Ischemic (~87%): Due to ↓ blood flow.
    • Thrombotic: Local clot (e.g., MCA atherosclerosis).
    • Embolic: Distant clot (e.g., AF, carotid plaque).
    • Systemic Hypoperfusion: Affects watershed zones.
  • Hemorrhagic (~13%): Due to vessel rupture.
    • Intracerebral (ICH): Bleeding into parenchyma.
    • Subarachnoid (SAH): Bleeding into subarachnoid space.
• Risk Factors:
  • Non-Modifiable: Age (>55), Male sex, Ethnicity, Family Hx.
  • Modifiable:
    • Hypertension (HTN): #1 factor.
    • Diabetes Mellitus (DM).
    • Hyperlipidemia.
    • Smoking.
    • Atrial Fibrillation (AF).
    • Carotid Stenosis.
    • Obesity.

⭐ Hypertension is the single most important modifiable risk factor for all stroke types.

Ischemic Stroke - Clots & Consequences

• Pathogenesis: ~85% of strokes; neuronal death from ↓ blood flow. Major types:

  • Thrombotic: Atherosclerotic plaque rupture in cerebral artery (e.g., MCA, basilar). Common sites: carotid bifurcation, MCA origin, basilar artery.
  • Embolic: Detached clot from distant site (e.g., heart in AFib, valvular disease; carotid atheroma) lodges in cerebral artery.

• Risk Factors: HTN, DM, hyperlipidemia, smoking, AFib.

• Core Pathophysiology: Occlusion → Ischemia (core: irreversible damage; penumbra: salvageable tissue) → Infarction.

  • Mechanisms: Excitotoxicity (glutamate), inflammation, free radicals, apoptosis.

• Timeline of Pathological Changes:

• 

⭐ Liquefactive necrosis is characteristic of CNS infarcts due to high lipid content and lack of significant supporting stroma, leading to a fluid-filled cystic cavity.

• Complications: Cerebral edema (can cause herniation), hemorrhagic transformation (especially in embolic strokes), seizures.
• 📌 MCA Territory: Most common site. Contralateral hemiparesis/sensory loss (face/arm > leg), aphasia (dominant hemisphere), hemineglect (non-dominant).

Hemorrhagic Stroke & Aneurysms - Bleeds & Blowouts

• Intracerebral Hemorrhage (ICH): Bleeding into brain parenchyma.
  • Etiology: Hypertension (Charcot-Bouchard), CAA (elderly, lobar), AVMs, tumors, coagulopathy.
  • Clinical: Abrupt focal deficits, headache, vomiting, ↓consciousness.
• Subarachnoid Hemorrhage (SAH): Bleeding into subarachnoid space.
  • Etiology: Ruptured saccular (berry) aneurysm (~85%), AVM, trauma.
  • Clinical: Sudden "worst headache of my life" (thunderclap), nuchal rigidity, photophobia, LOC.
  • Dx: Non-contrast CT. If negative, LP for xanthochromia (after 6-12 hrs).
  • Complications: Rebleeding (peak 24-48 hrs), vasospasm (days 3-14, nimodipine prophylaxis), hydrocephalus, seizures.
• Aneurysms: Localized arterial dilations.
  • Saccular (Berry): Most common. Arterial bifurcations (Circle of Willis: AComA, PComA, MCA). Assoc: ADPKD, Ehlers-Danlos. Risks: Smoking, HTN.
  • Charcot-Bouchard: Small penetrating arteries (lenticulostriate). Due to chronic HTN. Rupture causes ICH.
  • Mycotic: Infected emboli (e.g., endocarditis).

⭐ Nimodipine prevents SAH-associated vasospasm; not for initial bleed treatment.

High‑Yield Points - ⚡ Biggest Takeaways

• MCA (Middle Cerebral Artery) is the most frequent site for embolic strokes.
• Hypertensive hemorrhage often involves Charcot-Bouchard microaneurysms in the basal ganglia or pons.
• Lacunar infarcts are small, deep strokes linked to hypertension and diabetes mellitus.
• Watershed infarcts occur in arterial border zones due to systemic hypoperfusion.
• Berry aneurysms are the leading cause of non-traumatic Subarachnoid Hemorrhage (SAH), typically at ACA-ACoA junction.
• The ischemic penumbra represents at-risk, salvageable brain tissue surrounding an infarct core.
• Hemorrhagic transformation is a significant complication following reperfusion therapy for ischemic strokes.