TRANSIENT OLIGOCLONAL BANDS AND COMPLETE BRAIN LESION RESOLUTION IN PEDIATRIC MOGAD INITIALLY DIAGNOSED AS MULTIPLE SCLEROSIS: A 30-MONTH CASE REPORT

Abstract

Background: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) can overlap clinically and radiologically with pediatric-onset multiple sclerosis (MS). Transient cerebrospinal fluid (CSF) oligoclonal bands (OCBs), which may substitute for dissemination in time under the 2017 McDonald criteria, can contribute to diagnostic misclassification when interpreted without disease-specific serology. Case Presentation: A 15-year-old girl presented with binocular diplopia, dysarthria, and balance impairment. Brain MRI showed multiple non-enhancing lesions, and spinal MRI demonstrated multilevel intramedullary lesions. CSF was acellular with CSF-restricted OCBs. The findings were interpreted as fulfilling the 2017 McDonald criteria, and interferon beta-1b was initiated. At month 9, serum MOG-IgG was positive by cell-based assay (titer 1:100), while AQP4-IgG was negative. At month 14, the cerebral lesions had resolved completely, repeat CSF OCB testing was negative, and MOG-IgG remained positive. The diagnosis was reclassified as MOGAD, interferon beta-1b was discontinued, and maintenance intravenous immunoglobulin was initiated at month 18. At month 30, the patient remained clinically stable with an EDSS score of 0; the last documented MOG-IgG result at month 25 remained positive. Discussion: The longitudinal combination of transient OCB positivity and complete radiological resolution of extensive brain lesions prompted diagnostic reassessment. The case illustrates why formal fulfillment of MS criteria should be integrated with the clinical phenotype, disease-specific antibody testing, and serial MRI findings in pediatric demyelinating disease. Conclusions: Early serum MOG-IgG testing should be considered in children with a first demyelinating event, particularly when the phenotype or subsequent MRI evolution is atypical for MS. CSF OCB positivity should not be regarded as disease-specific evidence of MS in isolation.