Deena A Tajfirouz1, M Tariq Bhatti1,2, John J Chen3,4. 1. Department of Neurology, Mayo Clinic, 200 First Street, SW, Rochester, MN, 55905, USA. 2. Department of Ophthalmology, Mayo Clinic, 200 First Street, SW, Rochester, MN, 55905, USA. 3. Department of Neurology, Mayo Clinic, 200 First Street, SW, Rochester, MN, 55905, USA. Chen.john@mayo.edu. 4. Department of Ophthalmology, Mayo Clinic, 200 First Street, SW, Rochester, MN, 55905, USA. Chen.john@mayo.edu.
Abstract
PURPOSE OF REVIEW: Antibodies against myelin oligodendrocyte glycoprotein (MOG) are associated with a unique acquired central nervous system demyelinating disease-termed MOG-IgG-associated disorder (MOGAD)-which has a variety of clinical manifestations, including optic neuritis, transverse myelitis, acute disseminating encephalomyelitis, and brainstem encephalitis. In this review, we summarize the current knowledge of the clinical characteristics, neuroimaging, treatments, and outcomes of MOGAD, with a focus on optic neuritis. RECENT FINDINGS: The recent development of a reproducible, live cell-based assay for MOG-IgG, has improved our ability to identify and study this disease. Based on contemporary studies, it has become increasingly evident that MOGAD is distinct from multiple sclerosis and aquaporin-4-positive neuromyelitis optica spectrum disorder with different clinical features and treatment outcomes. There is now sufficient evidence to separate MOGAD from other inflammatory central nervous system demyelinating disorders, which will allow focused research on understanding the pathophysiology of the disease. Prospective treatment trials are needed to determine the best course of treatment, and until then, treatment plans must be individualized to the clinical manifestations and severity of disease.
PURPOSE OF REVIEW: Antibodies against myelin oligodendrocyte glycoprotein (MOG) are associated with a unique acquired central nervous system demyelinating disease-termed MOG-IgG-associated disorder (MOGAD)-which has a variety of clinical manifestations, including optic neuritis, transverse myelitis, acute disseminating encephalomyelitis, and brainstem encephalitis. In this review, we summarize the current knowledge of the clinical characteristics, neuroimaging, treatments, and outcomes of MOGAD, with a focus on optic neuritis. RECENT FINDINGS: The recent development of a reproducible, live cell-based assay for MOG-IgG, has improved our ability to identify and study this disease. Based on contemporary studies, it has become increasingly evident that MOGAD is distinct from multiple sclerosis and aquaporin-4-positive neuromyelitis optica spectrum disorder with different clinical features and treatment outcomes. There is now sufficient evidence to separate MOGAD from other inflammatory central nervous system demyelinating disorders, which will allow focused research on understanding the pathophysiology of the disease. Prospective treatment trials are needed to determine the best course of treatment, and until then, treatment plans must be individualized to the clinical manifestations and severity of disease.
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Authors: John J Chen; Elias S Sotirchos; Amanda D Henderson; Eleni S Vasileiou; Eoin P Flanagan; M Tariq Bhatti; Sepideh Jamali; Eric R Eggenberger; Marie Dinome; Larry P Frohman; Anthony C Arnold; Laura Bonelli; Nicolas Seleme; Alvaro J Mejia-Vergara; Heather E Moss; Tanyatuth Padungkiatsagul; Hadas Stiebel-Kalish; Itay Lotan; Mark A Hellmann; Dave Hodge; Frederike Cosima Oertel; Friedemann Paul; Shiv Saidha; Peter A Calabresi; Sean J Pittock Journal: Mult Scler Relat Disord Date: 2022-01-11 Impact factor: 4.339
Authors: Alexander U Brandt; Hanna G Zimmermann; Norman K Gigengack; Frederike C Oertel; Seyedamirhosein Motamedi; Charlotte Bereuter; Ankelien Duchow; Rebekka Rust; Judith Bellmann-Strobl; Klemens Ruprecht; Tanja Schmitz-Hübsch; Friedemann Paul Journal: Sci Rep Date: 2022-10-20 Impact factor: 4.996
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