Contrasting diagnostic challenges of headache before and after acute disseminated encephalomyelitis in children: Two case reports and review of literature

BACKGROUNDAcute disseminated encephalomyelitis (ADEM) is an acute inflammatory demyelinating disorder of the central nervous system (CNS) where headache can occur at different clinical stages, creating diagnostic challenges when it precedes the neurological syndrome or persists during recovery. CASE SUMMARYWe report two children with contrasting headache presentations in ADEM.Case 1 involved a 6-year-old boy who presented with isolated severe headache that evolved into encephalopathy and ataxia; brain magnetic resonance imaging (MRI) demonstrated multifocal bilateral cerebral lesions consistent with ADEM.After corticosteroid and intravenous immunoglobulin (IVIG) therapy, he fully recovered.Case 2 involved a 10year-old girl presenting with acute ADEM (headache, confusion, ataxia) who initially received high-dose intravenous corticosteroids followed by IVIG with partial neurological recovery.She subsequently developed a persistent, unremitting daily frontal headache for approximately 3 months, unresponsive to lifestyle modifications and preventive agents (amitriptyline, propranolol, topiramate).Pre-retreatment MRI at 3 months and cerebrospinal fluid examination showed no new demyelinating lesions or abnormalities.Despite a second course of intravenous methylprednisolone and an oral taper, and near-complete radiological resolution of prior lesions, the clinical course did not establish an inflammatory cause for the persistent headache. CONCLUSIONHeadache significance in pediatric ADEM depends on its temporal relationship to neurological disease.Evolving encephalopathy or multifocal signs accompanying headache warrant evaluation for secondary CNS pathology.Conversely, persistent 4 / 39 headache following ADEM-absent new encephalopathy, polyfocal events, or new MRI lesions-should not be interpreted as recurrent or multiphasic ADEM.Persistent headache resolved after corticosteroid retreatment, independent of new demyelinating lesions, and this temporal sequence does not establish a causal therapeutic or inflammatory mechanism.