![]() In this review, we summarize available clinical, immunological and histopathological data on patients with MOG + CNS demyelinating disease. Using pathophysiologically meaningful cell-based assays, this humoral response is extremely rare in adult MS and absent in classical AQP-4 + NMO, sharply differentiating the evolving group from both established disorders. Recent investigations discovered that a subgroup of these AQP-4 – NMOSD patients produce an ab response against myelin oligodendrocyte glycoprotein (MOG), a molecule expressed on the outer lamella of the myelin sheath. Delineating these patients concomitantly revealed that not all patients presenting with clinically NMO-suggestive disease phenotype express AQP-4 ab, which created the pathogenetically undefined category of NMO spectrum disorders (NMOSD). Nowadays, AQP-4 + NMO is considered an autoimmune astrocytopathy, in which CNS demyelination occurs only as a consequence of a primary destruction of astrocytes. Indeed, the greatest success so far in deciphering the pathogenesis of a CNS demyelinating disorder resulted from the discovery of anti-aquaporin (AQP)-4 antibodies (ab), which allowed progressive delineation of neuromyelitis optica (NMO), formerly considered a variant of the most common CNS demyelinating disorder, multiple sclerosis (MS), as a distinct disease. To a great extent, this may reflect that the group of inflammatory CNS demyelinating disorders likely contains multiple pathogenetically distinct disease entities. Marignier R.Extensive research over the last decades basically failed to identify a common cause of noninfectious inflammatory central nervous system (CNS) demyelinating disease. Treatment of neuromyelitis optica: state-of-the-art and emerging Anti-MOG + neuromyelitis optica spectrum disorder treated with Oshiro A, Nakamura S, Tamashiro K, Fujihara K. Neurological update: MOG antibody disease. ![]() MRI features of demyelinating disease associated Deneve M, Biotti D, Patsoura S, Ferrier M, Meluchova Z, et al. MOG encephalomyelitis: international recommendations onĭiagnosis and antibody testing. Jarius S, Paul F, Aktas O, Asgari N, Dale RC, et al. Optica and multiple sclerosis: difference in repeated cerebrospinal fluid examination. 2016 13:279.ġ1.ěergamaschi R, Tonietti S, Franciotta D, Candeloro E, Tavazzi E, et al. Part 1: frequency, syndrome specificity, influence of disease acitivity, long term courseĪssociation with AQP4-IgG, and origin. MOG-IgG in NMO and related disorder: a muylticenter Jarius S, Ruprecht K, Kleiter I, Borisow N, Asgarin N, et al. Neuritis, encephalitis and myelitis: Lessons learned from neuromyelitis optica spectrum disorder Front Neurol.ġ0. dos Passos GR, Oliveira LM, da Costa BK, Apostolos-Pereira SL, Callegaro D, et al. Structural insights into antigenicity of myelin Breithaupt C, Schubart A, Zander H, Skerra A, Huber R. The structure and function of myelin oligodendrocyte glycoprotein. Subgroup of patients with neuromyelitis optica phenotype. Probstel A, Rudolf G, Dornmair K, Collongues N, Chanson J, et al. Persisting myelin oligodendrocyte glycoproteinĪntibodies in aquaporin-4 antibody negative pediatric neuromyelitis optica. Rostasy K, Mader S, Hennes EM, Schanda K, Gredler V, et al. Anti–Myelin Oligodendrocyte GlycoproteinAntibodies in Rostasy K, Mader S, Schanda K, Huppke P, Gartner J. A serum autoantibody marker of neuromyelitisoptica: distinctionįrom multiple sclerosis. Lennon VA, Wingerchuk DM, Kryzer TJ, et al. The case of the Marquis de Causan (1804): an early account of visual lossassociated with Patient was treated with intravenous pulse methylprednisolone for five days and partially recovered.Ĭonclusion : Anti-MOG antibody may be suspected in patient who clinically presented with NMO-SD but negative for aquaporin-4 antibody and oligoclonal band.ġ. Serology studies were negative for oligoclonal band and anti-aquaporin-4 but positive for anti-MOG. Magnetic resonance imaging of spine revealed intramedullary hypersignal intensity of spinal cord from C5 to T11 level with skipped lesion at T12 to conus medullaris. We present a pediatric patient with clinically diagnosed with long segments transverse myelitis with positive anti-MOG antibody.įindings : An eleven-year-old patient presented with weakness on both legs and decreased sensation below T6 level. Background : Antibody against myelin oligodendrocyte glycoprotein is associated with various central nervous system demyelination especially patient with clinical diagnosis of neuromyelitis optica spectrum disorder (NMO-SD) or certain CNS demyelinating disease but negative for anti-aquaporin-4.
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