For example, no mention was made of the lenght of optic neuritis, which is usually greater than that found in patients with MS and even with NMOSD aquaporin 4 positive, although it is not usual to reach the optic chiasm. could have added more information regarding MRI. Regarding the data presented, Costa et al. However, the authors included a positive anti-MOG patient (patient 2) whose clinical presentation was neuritis and myelitis, which is beyond the scope of the article. Due to the rarity of the disease, the number of anti-MOG positive patients analyzed is quite reasonable. MOG-igG associated optic neuritis is not multiple sclerosis. describe six patients (four men) with optic neuritis (five monophasic, four bilateral) and serum anti-MOG antibody in very high titers except in one case 6 6. In this issue of Arquivos de Neuropsiquiatria, Costa et al. However, we must keep in mind that it is a knowledge still under construction, a road to be paved, particularly regarding the recognition of the whole spectrum, its long-term behavior and the best therapeutic approach. MOG antibody-positive, benign, unilateral, cerebral cortical encephalitis with epilepsy. Ogawa R, Nakashima I, Takahashi T, Kaneko K, Akaishi T, Takai Y et al. described four young men with unilateral encephalitis and epileptic seizures of benign evolution and response to steroids in which the anti-MOG antibody was the only one detected. The spectrum of MOG autoantibody-associated demyelinating diseases. Reindl M, Di Pauli F, Rostásy K, Berger T. To date, once the presence of the antibody in the serum has been identified, it seems reasonable to include the following entities under the anti-MOG spectrum: recurrent or bilateral optic neuritis (ON), ADEM, neuromyelitis optica spectrum disorders anti-aquaporin-4 negative and longitudinal extensive transverse myelitis 4 4. The development of a more specific and sensitive laboratory methodology (cell based assay, CBA) allowed to revisit the anti-MOG antibody in demyelinating diseases and to establish it as a new biomarker. Recommended standard of cerebrospinal fluid analysis in the diagnosis of multiple sclerosis: a consensus statement. Freedman MS, Thompson EJ, Deisenhammer F, Giovannoni G, Grimsley G, Keir G et al. Although anti-MOG antibodies have been found in such prototypical situations, probably for laboratory methodological reasons, the clinical utility of antibody detection as a reliable biomarker was abandoned 3 3. Myelin oligodendrocyte glycoprotein antibodies are associated with a non-MS course in children. Thereafter, the presence of anti-MOG antibodies was investigated in those diseases that represented the clinical prototype of demyelinating conditions: acute disseminated encephalomyelitis (ADEM) in children and multiple sclerosis (MS) in adults 2 2. The better structural characterization of MOG as well as its location rapidly made it an antigen used successfully in the induction of experimental models of demyelination such as experimental autoimmune encephalomyelitis. Anti-MOG antibody: the history, clinical phenotype, and pathogenicity of a serum biomarker for demyelination. MOG represents less than 0.05% of total myelin proteins but despite its meager concentration, it is believed to be involved in important functions, such as being a surface marker of the mature oligodendrocyte and participating in the interactions between myelin and its players 1 1. This may include IVIG and medication, such as azathioprine, myucophenolate mofetil, or rituximab.Myelin oligodendrocyte glycoprotein (MOG) is a protein expressed only on the outermost lamellae of the myelin sheath and on the surface of oligodendrocytes in the central nervous system (CNS). However, some patients may experience recurrent attacks and need a long-term management plan. ![]() ![]() Many individuals with anti-MOG syndrome will recover fully after their first treatment and never relapse. In rare cases, if high-dose steroids are not effective, patients may undergo intravenous immunoglobulin (IVIG) treatment. Intravenous corticosteroids are the first line of treatment. Treatment for acute symptoms of demyelination involves reducing inflammation. Symptoms of acute disseminated encephalomyelitis may include: Individuals with anti-MOG syndrome may experience optic neuritis, transverse myelitis, and/or acute dissemination encephalomyelitis, depending on which parts of their nervous system are affected. Barrow-ASU Center for Preclinical Imaging.Department of Translational Neuroscience.Department of ENT and Skull Base Surgery.Bioskills & Neurosurgery Research Laboratory.For Providers & Researchers Show submenu.Parkinson’s Disease & Movement Disorders.Center for Transitional Neuro-Rehabilitation.
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