Influenza-associated acute necrotizing encephalopathy (ANE) is a rare, fulminant neurologic complication of influenza infection.
It predominantly affects children.
Associated with rapid onset of altered consciousness, seizures, and multifocal neurologic deficits following a viral prodrome.
Neuroimaging typically reveals symmetric, bilateral thalamic lesions with evidence of necrosis and/or hemorrhage.
Lesions often extend to the basal ganglia, brainstem, and cerebellum.
Involves a hyperinflammatory response and cytokine storm rather than direct viral invasion.
ANE has a genetic susceptibility (notably RANBP2 mutations) contributing to risk in some cases.
Laboratory findings may include elevated serum transaminases, creatine kinase, procalcitonin, and cerebrospinal fluid (CSF) protein, with low CSF white cell count; high procalcitonin (>4.25 ng/mL) and CSF protein (>0.48 g/L) may help differentiate ANE from other influenza-associated encephalopathies.
Management is primarily supportive, including early antiviral therapy and critical care interventions. Immunomodulatory therapies such as intravenous methylprednisolone and intravenous immunoglobulin (IVIG) are frequently used, but evidence for efficacy is limited and optimal regimens are not established.
Mortality is high, up to 50%, and survivors often have significant neurologic sequelae.
Early recognition and prompt neuroimaging are essential for diagnosis.
Prevention through annual influenza vaccination is recommended for all eligible children, as most fatal cases occur in previously healthy, unvaccinated individuals.