Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease Presenting as Acute Cerebellitis: A Case Report of Diagnostic Challenges in an Elderly Patient
Andres Ricaurte-Fajardo1, Carmela Fawcett1, Diana Riaño1, Lina Lancheros1, Diego Rivera2, Luis Zarco1
1Neuroscience, 2Radiology, Pontificia Universidad Javeriana
Objective:
To describe a rare presentation of Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) manifesting as acute cerebellitis in an elderly patient and to highlight the diagnostic challenges distinguishing it from other demyelinating disorders.
Background:
Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) is an inflammatory demyelinating disorder of the central nervous system (CNS) that typically presents with optic neuritis, transverse myelitis, or acute disseminated encephalomyelitis (ADEM). Cerebellar involvement in MOGAD is rare and poorly described.
Design/Methods:
A 70-year-old female presented with a 15-day history of vertigo, dysarthria, and gait instability. Initial imaging at a low-complexity center showed no structural lesions. On admission, neurological examination revealed left hemispheric cerebellar and paravermian syndrome with left pyramidal signs. MRI demonstrated hyperintense T2/FLAIR lesions in both superior cerebellar peduncles and the pons, consistent with an inflammatory or demyelinating process. Serological testing was positive for anti-MOG antibodies, confirming MOGAD. She was treated with intravenous methylprednisolone and plasmapheresis followed by oral steroid tapering, achieving marked clinical improvement.
Results:
This case expands the clinical spectrum of MOGAD, illustrating isolated cerebellar involvement. Differentiation from multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) is crucial due to distinct management strategies. Unlike MS, MOGAD lesions rarely exhibit T1 “black holes,” and unlike NMOSD, MOGAD lacks AQP4 antibodies and may involve more extensive brain regions. Anti-MOG antibody testing was essential for diagnosis and treatment guidance.
Conclusions:
MOGAD should be considered in acute cerebellar syndromes without alternative etiologies. Early recognition and targeted immunotherapy can lead to favorable outcomes even in atypical presentations.
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