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Updated: Jul 10, 2026

Myelin Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune Encephalomyelitis (EAE) in C57BL/6 Mice
Published on: April 15, 2014
Acute MOG-IgG-Associated Myelitis in a Patient with Long-Standing Multiple Sclerosis: A Case Report
José Luis Sánchez-Menoyo1,2, Miriam Cortés-Rubiales1, Iñigo Vicente-Olabarría3
1Department of Neurology, Galdakao-Usansolo University Hospital, Osakidetza (Basque Health Service), Usansolo, Spain.
Introduction:
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and multiple sclerosis (MS) are distinct inflammatory demyelinating disorders that may share overlapping clinical and imaging features, creating important diagnostic challenges.
Case Presentation:
We describe a 58-year-old woman with unequivocal long-standing relapsing-remitting MS fulfilling established diagnostic criteria, including typical periventricular and deep white matter lesions on magnetic resonance imaging (MRI) and clear dissemination in space and time, with characteristic brain and spinal MRI findings and more than a decade of clinical and MRI stability under extended-interval natalizumab therapy. Following a febrile prodrome, she developed acute severe myelitis with rapid progression from baseline paraparesis (Expanded Disability Status Scale [EDSS] 6.0) to near-complete paraplegia (EDSS 8.0) within 7 days. Cerebrospinal fluid analysis revealed marked pleocytosis, elevated protein levels, and absence of oligoclonal bands, findings atypical for MS relapse. Serum testing demonstrated high-titre MOG immunoglobulin G antibodies, which progressively declined and became negative during follow-up. Retrospective spinal cord MRI revealed transient central grey matter involvement with a characteristic H-sign on axial T2-weighted sequences, consistent with MOGAD-associated myelitis. The patient responded to high-dose intravenous corticosteroids and returned to baseline disability within 3 months.
Conclusion:
This case highlights that acute neurological deterioration in patients with established MS should not automatically be attributed to disease reactivation and supports careful consideration of alternative inflammatory demyelinating processes such as MOGAD when clinical, cerebrospinal fluid, and imaging features are atypical. Integration of clinical findings, cerebrospinal fluid analysis, MRI features, and antibody testing is essential to avoid diagnostic anchoring and ensure appropriate management.
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