Cerebral infarction

1. Definition

• Cerebral infarction = ischemic stroke; the brain undergoes liquefactive necrosis — first anemic, later may become hemorrhagic.

2. Causes

• Thrombus: atherosclerosis at the carotid bifurcation, middle cerebral artery, or basilar tip.
• Embolus: more common than thrombi; usually cardiac origin (e.g. mural thrombus, AF).

3. Morphology

• Around the softening (emollition) → whitish pale perifocal edema with BBB damage; demarcated by edema (not neutrophils); tissue “disappears.”
• Encephalomalacia = localized brain softening; stages 1–3 anemic, 4 hemorrhagic.

Encephalomalacia stages

1. Alba — first 36–48 h: swollen, soft; macrophages by day 3 → pale/white.
2. Flava — liquefactive digestion → yellow.
3. Cysta post-encephalomalacia — fluid-filled cyst lined by gray tissue; marginal gliosis (astrocyte proliferation/hypertrophy + new capillaries/CT fibres).
4. Rubra (hemorrhagic) — red, due to:
   • Reperfusion (plaque dissolution attempt)
   • Venous thrombosis (impaired drainage)
   • Border-zone (watershed) necrosis — e.g. circle of Willis; anastomotic regions with less robust supply, ischemia-prone.

💡 High-yield: The brain is the exception to coagulative necrosis — infarction → liquefactive necrosis → fluid-filled cyst with surrounding gliosis. Emboli (often cardiac) are the most common cause; MCA territory is most frequently involved.