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Table 2: Conditions with reversible/transient white matter diffusion restriction and their pathophysiology
Condition Proposed Pathophysiology Relevance to Cerebral Malaria
Acute toxic leukoencephalopathy Intramyelinic edema, myelin vacuolization Endothelial injury is a pathophysiologic mechanism in CM³⁸
Capillary endothelial injury
Direct toxic demyelination¹⁶
Hypoglycemia Energy failure leading to excitatory edema²¹ Hypoglycemia is a frequent complication in children with severe falciform malaria³⁹; local/focal hypoglycemia may occur due to sludging even in the absence of systemic hypoglycemia
Peri-/postictal state Increased metabolic demand leading to energy failure and resultant cytotoxic and vasogenic edema⁴⁰ Seizures, often recurrent, are a frequent manifestation of CM and associated with worse outcome²⁹
Penumbra of ischemic infarct Early white matter ischemic injury with axonal swelling and intramyelinic edema¹³ Sequestration in postcapillary venules of the brain and venous congestion are central to CM pathogenesis²⁵
Demyelination Immune-mediated perivenular inflammation and demyelination⁴¹ Vascular inflammatory markers are associated with CM, and perivenular inflammation is thought to contribute to CM pathogenesis³⁸