![]() ![]() Many patients with NMOSD are misdiagnosed as having MS. Some patients may present with acute disseminated encephalomyelitis (ADEM). Neuromyelitis optica (NMO), sometimes called Devic disease or opticospinal multiple sclerosis (MS) is a severe, relapsing, autoimmune, inflammatory and demyelinating central nervous system disease (IDD) that predominantly affects optic nerves and spinal cord.(1) The disorder is now recognized as a spectrum of autoimmunity (termed NMO spectrum disorders: NMOSD).(1-3) Brain lesions are observed in more than 60% of patients with NMOSD and approximately 10% will be MS-like.(4) Children tend to have greater brain involvement than adults, and brain lesions are more symptomatic than is typical for adult patients.(3) The clinical course is characterized by relapses of optic neuritis or transverse myelitis or both. Seropositivity for MOG-IgG in the setting of a severe relapse of central nervous system demyelination warrants aggressive therapy with intravenous methylprednisolone or plasmapheresis. Seropositivity for MOG-IgG in NMOSD-like disorders, including optic neuritis, transverse myelitis, and acute disseminated encephalomyelitis, predicts relapse and warrants consideration for maintenance immunosuppression. MS therapies may worsen MOG-IgG associated IDD, so correct diagnosis is important. Detection of MOG-IgG implies an inflammatory demyelinating disorder distinct from MS. Patients seropositive for MOG-IgG are commonly misdiagnosed as MS. There is currently no biomarker specific for MS (multiple sclerosis). Patients only rarely harbor both antibodies. Seropositivity predicts a relapsing phenotype and warrants immunosuppressive therapy. Of the remaining 20%, one-third harbor MOG-IgG. Epub 2017 Dec 30.Myelin oligodendrocyte glycoprotein (MOG)-IgG with neuromyelitis optica (NMO) spectrum disorder (SD)-like phenotype is now recognized as a sensitive and specific diagnostic antibody biomarker of inflammatory demyelinating disorders (IDD).Īpproximately 80% of patients fulfilling 2006 Wingerchuk criteria for NMO are seropositive for aquaporin-4 (AQP4)-IgG. ‘Leukodystrophy-like’ phenotype in children with myelin oligodendrocyte glycoprotein antibody-associated disease. (10) Hacohen Y, Rossor T, Mankad K, et al. ![]() Anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in patients with optic neuritis and seizures. (9) Gutman JM, Kupersmith M, Galetta S, Kister I. Clinical spectrum and prognostic value of CNS MOG autoimmunity in adults: The MOGADOR study. (8) Cobo-Calvo A, Ruiz A, Maillart E, et al. Antibodies to MOG and AQP4 in children with neuromyelitis optica and limited forms of the disease. (5) Lechner C, Baumann M, Hennes EM, et al. Defining distinct features of anti-MOG antibody associated central nervous system demyelination. (4) Weber MS, Derfuss T, Metz I, Brück W. 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. 10 Leukodystrophies are genetic rare diseases that affect the central nervous system by disrupting myelination. One study described symptoms and MRI findings of MOG antibody disease in children under the age of 7 that were similar to leukodystrophies. 1 NMDA receptor encephalitis is an autoimmune encephalitis that can cause psychosis, issues with memory and language, and seizures. ![]() MOG antibody disease can also occur in relation to another condition called anti-N-methyl-D-aspartate (NMDA) receptor encephalitis. When a relapse occurs, the diagnosis of MOGAD is confirmed. In some, the MOG antibody persists, and relapses may occur. In many kids, the MOG antibody disappears within 1 year, and relapses do not occur. 4Ĭhildren can be found to have the MOG antibody in the setting of ADEM however, a positive MOG antibody test in the setting of ADEM does not necessarily imply a course of MOGAD. Those with MOG antibody disease are more likely to have both optic nerves affected at the same time, and if the symptoms are in only one eye, the other optic nerve may show subclinical atrophy.
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