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Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Presenting as Intracranial Hypertension: A Case Report

The production of autoantibodies against myelin oligodendrocyte glycoprotein (MOG) can cause a spectrum of autoimmune disorders, including optic neuritis, transverse myelitis, brainstem encephalitis, and acute disseminated encephalomyelitis. In this study, we present the case of a 19-year-old woman...

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Detalles Bibliográficos
Autores principales: Chaudhuri, Jaydip Ray, Bagul, Jui Jade, Swathi, Alluri, Singhal, Bhim Sen, Reddy, N. Chakradhar, Vallam, Kiran Kumar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9581460/
https://www.ncbi.nlm.nih.gov/pubmed/36261298
http://dx.doi.org/10.1212/NXI.0000000000200020
Descripción
Sumario:The production of autoantibodies against myelin oligodendrocyte glycoprotein (MOG) can cause a spectrum of autoimmune disorders, including optic neuritis, transverse myelitis, brainstem encephalitis, and acute disseminated encephalomyelitis. In this study, we present the case of a 19-year-old woman with an unusual clinical presentation of intracranial hypertension (IH) and bilateral papilledema. The patient presented with symptoms of increased intracranial pressure, which followed a relapsing, remitting course over several months. Serial CSF studies showed an increased opening pressure during clinical relapses. The CSF and serum tested positive for MOG immunoglobulin G antibodies. Contrast-enhanced MRI of the brain showed mild meningeal enhancement in the left parietal region with subtle underlying cortical hyperintensities, indicating possible fluid-attenuated inversion recovery variable unilateral enhancement of the leptomeninges. The patient responded well to immunosuppressive therapy using rituximab. The presentation of MOG antibody-associated disease (MOGAD) as IH without optic neuritis is rare. This report presents the first description of a relapsing remitting course presenting each time with only symptoms of raised intracranial pressure, without developing any typical clinical manifestations of MOGAD.