A 70-year-old hypertensive man suddenly develops right-sided hemiplegia and aphasia. He dies 5 days later. Autopsy reveals a 4 cm softened, pale yellow, gelatinous area in the left middle cerebral artery territory. Microscopically, the area shows liquefactive necrosis with numerous lipid-laden macrophages (gitter cells). What is the mechanism of this infarct pattern?

• A Coagulative necrosis due to direct neuronal ischemia
• B Caseous necrosis from mycobacterial infection
• C Fat necrosis from release of myelin lipases
• D Liquefactive necrosis because CNS tissue has high lipid content and lacks structural protein scaffolding ✓

Explanation

Unlike most organs where ischemic infarcts produce coagulative necrosis (preserved architectural ghost outlines), the brain undergoes liquefactive necrosis. This is because CNS tissue has a high lipid content and is rich in proteolytic enzymes but poor in structural proteins, resulting in rapid autodigestion and liquefaction. The lipid-laden macrophages (gitter cells or foam cells) are recruited microglia/monocytes that phagocytose myelin breakdown products during the subacute phase.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.