Cerebral infarction (ischemic stroke) is the most frequent cause of liquefactive necrosis because the brain contains abundant lipid-rich myelin and high enzymatic activity. Ischemic injury leads to rapid enzymatic digestion of dead cells, resulting in a liquid viscous mass. In contrast, myocardial infarction typically causes coagulative necrosis, and tuberculous lymphadenitis causes caseous necrosis. Fat necrosis is a distinct form involving enzymatic fat digestion, not liquefactive. Thus, the brain's unique structure and metabolism explain why cerebral infarction predominantly leads to liquefactive necrosis.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th Edition, Volume 1, Chapter 5: Cell Injury, Cell Death, and Adaptations / Pages 53-55