1. Anti-MOG-associated demyelinating disorders: two sides of the same coin
- Author
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Marianna Pezzella, Valentino Manzo, Sergio Ferrari, Elisa Capone, Michele Spiniello, Massimo Napolitano, Lia Allegorico, Giorgia Teresa Maniscalco, Sara Mariotto, Lidia Altomare, Gennaro Alfieri, Giovanna Servillo, Rosaria Renna, and Angelo Ranieri
- Subjects
medicine.medical_specialty ,Optic Neuritis ,Neurology ,Dermatology ,Disease ,Antibodies ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Plasma exchange ,Humans ,Optic neuritis ,030212 general & internal medicine ,Demyelinating Disorder ,Autoantibodies ,Anti-myelin oligodendrocyte glycoprotein (MOG) antibodies ,business.industry ,Anti-MOG-associated disorders (MOGAD) ,General Medicine ,medicine.disease ,Oligodendrocyte ,Psychiatry and Mental health ,medicine.anatomical_structure ,Immunology ,Encephalitis ,Myelin-Oligodendrocyte Glycoprotein ,Rituximab ,Neurology (clinical) ,Neurosurgery ,business ,030217 neurology & neurosurgery ,Demyelinating Diseases ,medicine.drug - Abstract
Anti-myelin oligodendrocyte glycoprotein antibody-associated disorders (MOGAD) are new emerging diseases with heterogeneous course, treatment, response, and prognosis. We herein present 2 cases with antibodies to MOG, one with a cerebellar/brainstem monophasic syndrome which partially improved after treatment, and the other with an optic neuritis onset then relapsed with cortical encephalitis and presented a subsequent complete recovery. We further discuss elements possibly associated with disease heterogeneity and influencing treatment choices. MOGAD is an extremely variable disease which can relapse and accumulate disability over time. An early diagnosis and correct timely treatment is fundamental to improve clinical outcome.
- Published
- 2020
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