Post-dengue acute disseminated encephalomyelitis evolving into multiple sclerosis: a case report

Abstract

Case Presentation: A 32-year-old male with Dengue infection confirmed by IgM serology 24 days earlier presented with acute psychotic changes, including complex visual hallucinations and affective blunting. Symptoms rapidly progressed to acute encephalopathy with a decreased level of consciousness and divergent strabismus, requiring intensive care admission. Initial brain and spinal magnetic resonance imaging revealed multiple non-enhancing T2/FLAIR hyperintense lesions with diffusion restriction across supratentorial, infratentorial (midbrain, middle cerebellar peduncle), and spinal cord parenchyma (C7, T1, T4). Cerebrospinal fluid analysis demonstrated lymphocytic pleocytosis (85 cells/mm³), elevated protein (71 mg/dL), and pattern-3 oligoclonal bands. Workup was negative for systemic and infectious causes, as well as anti-aquaporin-4, anti-glutamic acid decarboxylase, and anti-myelin oligodendrocyte glycoprotein antibodies. Given the acute severe encephalopathy, marked CSF pleocytosis, and recent viral infection, an initial diagnosis of post-Dengue acute disseminated encephalomyelitis (ADEM) was established. Treatment with high-dose intravenous methylprednisolone and seven plasmapheresis sessions led to rapid recovery of consciousness and resolution of hallucinations, though marked cognitive impairment persisted (MoCA: 9/30). Two months post-discharge, he was readmitted with ataxia, internuclear ophthalmoplegia, and spatial disorientation. Repeat neuroimaging revealed new active, gadolinium-enhancing lesions in the brainstem, frontal cortex, and thoracic spinal cord (T9-T10). Fulfilling spatial and temporal dissemination criteria, the diagnosis evolved to Multiple Sclerosis following post-Dengue ADEM. He received high-dose intravenous methylprednisolone, rescue plasmapheresis, and high-efficacy induction with Natalizumab, achieving disease stability with partial recovery of neurological deficits. Discussion: In adults, acute disseminated encephalomyelitis can occasionally serve as the initial presentation or trigger for Multiple Sclerosis. In this case, the acute encephalopathy and prominent CSF pleocytosis — atypical for an initial Multiple Sclerosis presentation — strongly supported the initial diagnosis of post-Dengue ADEM. The negative autoantibody panel ruled out MOGAD and NMOSD. The subsequent appearance of new active lesions on follow-up imaging, alongside intrathecal pattern-3 oligoclonal bands, fulfilled the McDonald criteria for spatial and temporal dissemination, establishing the evolution to Multiple Sclerosis. This case highlights that post-viral ADEM in adults warrants close longitudinal monitoring, as non-monophasic disease progression may unmask underlying Multiple Sclerosis. Final Comments: Post-Dengue ADEM in adults can act as a trigger or initial manifestation of Multiple Sclerosis. Recognizing a non-monophasic course through serial neuroimaging allows for timely reevaluation and early transition to high-efficacy disease-modifying therapy to halt disease activity and promote clinical stabilization.