Future randomized trials will determine the optimal treatment for MOGAD. Recognition of the clinical and radiologic features allow for the correct diagnosis. The optimal treatment for reducing relapses is unknown. ![]() The purpose of this article is to describe MRI features of MOG-AD. Objective Myelin oligodendrocyte glycoproteinimmunoglobulin G (MOG-IgG) associated disorder (MOGAD) often manifests with recurrent CNS demyelinating attacks. ![]() MOGAD is a unique entity that is separate from both MS and AQP4-IgG-positive NMOSD. with antibodies against MOG predominantly involving the optic nerve and spinal cord. MOG-AD is an inflammatory demyelinating condition of the CNS characterised by a monophasic or relapsing course of neurological dysfunction, which does not meet the typical criteria for MS or other known neuroinflammatory conditions and occurs in the presence of serum MOG antibodies detected using specific cell-based assays 16. Rituximab, azathioprine, mycophenolate mofetil, and monthly intravenous immune globulin are the most commonly utilized treatments. Patients with relapsing disease will often need chronic immunotherapy. Although the nadir of vision loss is severe with MOG-IgG optic neuritis, the recovery is typically better than AQP4-IgG optic neuritis and therefore has a favorable overall prognosis. Patients with clinical-MRI phenotypes typically recognized to be associated with MOGAD (see also Clinical-MRI attributes above) are considered to have a high pre-test probability and a low risk of false positive results. Clinical characteristics suggestive of MOG-IgG optic neuritis include recurrent optic neuritis, prominent disc edema, and perineural enhancement of the optic nerve on magnetic resonance imaging. When MOG-IgG testing is ordered, a thorough phenotypical assessment is mandatory to determine the pre-test probability. Myelin oligodendrocyte glycoprotein (MOG) immunlglobulin (Ig)G antibody-associated disorders (MOGAD) describe a new entity of demyelinating neurological syndromes defined by the presence of serum IgG autoantibodies against MOG detected by cell-based assays. Optic neuritis is the most common presentation in adults, whereas ADEM is the most common presentation in children. The phenotype of MOGAD is broad and includes optic neuritis, transverse myelitis, and acute demyelinating encephalomyelitis (ADEM). Serum antibodies to MOG have recently been found to be a biomarker of MOG-IgG-associated disorder (MOGAD), a demyelinating disease distinct from both multiple sclerosis (MS) and aquaporin-4-IgG neuromyelitis optica spectrum disorder (AQP4-IgG-positive NMOSD). 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.Īcute disseminating encephalomyelitis (ADEM) Aquaporin-4 (AQP4) Multiple sclerosis Myelin oligodendrocyte glycoprotein (MOG) Neuromyelitis optica spectrum disorder (NMOSD) Optic neuritis.To review the clinical characteristics, radiological manifestations and treatment of myelin oligodendrocyte glycoprotein (MOG)-immunoglobulin G (IgG) optic neuritis. 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. 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. The recent development of a reproducible, live cell-based assay for MOG-IgG, has improved our ability to identify and study this disease. Background and objectives: Rituximab is used widely for relapse prevention in neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein (MOG)-IgG-associated disease (MOGAD) however, data regarding the effectiveness and safety of long-term rituximab use in these conditions are limited. In this review, we summarize the current knowledge of the clinical characteristics, neuroimaging, treatments, and outcomes of MOGAD, with a focus on optic neuritis. 3 The diagnosis is confirmed when MOG antibodies in the blood are found in patients who have. 1,2 While the function of this glycoprotein is not exactly known, MOG is a target of the immune system in this disease. ![]() ![]() 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. Myelin oligodendrocyte glycoprotein (MOG) is a protein that is located on the surface of myelin sheaths in the central nervous system.
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