Abstract
This report describes a 7‐year‐old boy with MOGAD presenting as severe ADEM with fever, encephalopathy, seizures, markedly elevated intracranial pressure, diffuse multifocal MRI abnormalities, and serum MOG‐IgG positivity. He required intravenous corticosteroids, plasma exchange, IVIG, and tocilizumab, followed by rehabilitation and maintenance IVIG. Persistent sequelae included dysarthria, memory and learning difficulties, and ADHD diagnosed after the acute illness. Approximately 3 years later, he developed frequent hyperkinetic seizures with bifrontal‐predominant multifocal epileptiform abnormalities and subsequently achieved seizure freedom on combination therapy. Follow‐up contrast‐enhanced MRI after epilepsy onset demonstrated multifocal encephalomalacia/gliosis and diffuse cerebral volume loss, without acute infarct, hemorrhage, mass effect, hydrocephalus, abnormal enhancement, or hippocampal abnormality. Prior inflammatory brain injury is therefore a plausible acquired substrate, but an independent genetic, traumatic, or other epilepsy predisposition cannot be excluded. The case emphasizes long‐term neurodevelopmental follow‐up after severe pediatric MOGAD‐ADEM and careful etiologic evaluation when remote epilepsy emerges. Severe pediatric MOGAD‐associated ADEM may leave persistent neurocognitive morbidity despite aggressive immunotherapy. When epilepsy emerges years later, prior inflammatory injury is one possible substrate but should not be assumed causal; contemporaneous neuroimaging and epilepsy‐focused genetic evaluation are important to assess alternative structural and genetic etiologies.