Myelin oligodendrocyte glycoprotein (MOG) is a glycoprotein located on the myelin surface and found exclusively in the central nervous system (CNS). Randomised control trials are limited, but observational open-label experience suggests a role for high-dose steroids and plasma exchange in the treatment of acute attacks, and for immunosuppressive therapies, such as steroids, oral immunosuppressants and rituximab as maintenance treatment. Cerebrospinal fluid oligoclonal bands are uncommon. MRI characteristics can help in differentiating MOG-AD from other neuroinflammatory disorders, including multiple sclerosis and neuromyelitis optica. To avoid misdiagnosis, MOG antibody testing should be undertaken in selected cases presenting clinical and paraclinical features that are felt to be in keeping with MOG-AD, using a validated cell-based assay. Recent advances in MOG antibody testing offer improved sensitivity and specificity. Residual disability develops in 50–80% of patients, with transverse myelitis at onset being the most significant predictor of long-term outcome. Disease course can be either monophasic or relapsing, with subsequent relapses most commonly involving the optic nerve. Although no age group is exempt, median age of onset is within the fourth decade of life, with optic neuritis being the most frequent presenting phenotype. eCollection 2018.Myelin oligodendrocyte glycoprotein (MOG) antibody disease (MOG-AD) is now recognised as a nosological entity with specific clinical and paraclinical features to aid early diagnosis. Defining distinct features of anti-MOG antibody associated central nervous system demyelination. (4) Weber MS, Derfuss T, Metz I, Brück W. MOG-IgG-Associated Optic Neuritis, Encephalitis, and Myelitis: Lessons Learned From Neuromyelitis Optica Spectrum Disorder. (3) Dos Passos GR, Oliveira LM, da Costa BK, et al. Diagnosis and treatment of anti-myelin oligodendrocyte glycoprotein antibody positive optic neuritis. Comparison of myelin oligodendrocyte glycoprotein (MOG)-antibody disease and AQP4-IgG-positive neuromyelitis optica spectrum disorder (NMOSD) when they co-exist with anti-NMDA (N-methyl-D-aspartate) receptor encephalitis. 4 Furthermore, those with MOG antibody disease seem to be less likely to have other autoimmune disorders (such as rheumatoid arthritis, Hashimoto’s thyroiditis, etc.) than those with AQP-4 positive NMOSD. MOG antibody disease and AQP-4 positive NMOSD are thought to have distinct immunological mechanisms. Those with MOG antibody disease do not test positive for the NMO antibody called aquaporin 4 (AQP-4). Patients with persistently positive antibodies are at risk for recurrent events.
Those with MOG Antibody Disease may previously have been diagnosed with Neuromyelitis Optica Spectrum Disorder (NMOSD), Transverse Myelitis (TM), Acute Disseminated Encephalomyelitis (ADEM), Optic Neuritis (ON), or multiple sclerosis (MS) because of the pattern of inflammation it causes including brain, spinal cord and optic nerve damage. 3 The diagnosis is confirmed when MOG antibodies in the blood are found in patients who have repeated inflammatory attacks of the central nervous system.
1,2 While the function of this glycoprotein is not exactly known, MOG is a target of the immune system in this disease. Myelin oligodendrocyte glycoprotein (MOG) is a protein that is located on the surface of myelin sheaths in the central nervous system. MOG antibody disease (MOGAD) is a recently coined neuro-inflammatory condition that preferentially causes inflammation in the optic nerve but can also cause inflammation in the spinal cord and brain. This information sheet has been reviewed and approved by members of SRNA’s Medical and Scientific Council.
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