ENCEPHALOMALACIA: PATHOLOGICAL PROGRESSION, RADIOLOGIC CLASSIFICATION, AND THE CLINICAL IMPACT OF CORTICAL SOFTENING

Abstract

Background: Encephalomalacia is a descriptive term for the localized softening or loss of brain parenchyma resulting from irreversible tissue injury. It represents the final macroscopic stage of various neuropathological insults, characterized by the replacement of functional neural tissue with fluid-filled cavities or glial scars. Unlike most systemic tissues that undergo coagulative necrosis, the central nervous system (CNS) is uniquely prone to liquefactive necrosis, leading to the distinct "softened" texture of the brain following injury. Pathophysiology: The progression of encephalomalacia typically follows an evolutionary sequence from initial cellular death to chronic cavitation. This process begins with an acute inflammatory response, followed by the enzymatic digestion of necrotic tissue by macrophages and microglia. As the liquid debris is resorbed, the brain undergoes "white softening," where the resulting void is surrounded by a dense network of hypertrophic astrocytes—a process known as gliosis. Etiology and Classification: The condition is most commonly triggered by vascular events (ischemic or hemorrhagic stroke), mechanical trauma (traumatic brain injury), or severe inflammatory processes (encephalitis). In neonatal populations, it often presents as "multicystic encephalomalacia," a severe consequence of global hypoxic-ischemic injury. Conclusion: Although encephalomalacia is a permanent and non-progressive finding once the initial insult has stabilized, it acts as a significant focus for secondary complications, most notably post-traumatic or post-stroke epilepsy. Accurate characterization via neuroimaging is essential for differentiating simple volume loss from active pathological processes and for guiding long-term rehabilitative strategies. 

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