2022) no single set of diagnostic criteria are universally accepted 5. No specific presentation distinguishes individuals with anti-MOG antibodies from those presenting with similar clinical manifestation but without the antibodies and at the time of writing (c. Transverse myelitis (30%) including conus medullaris syndromeĪssociated with longitudinally extensive spinal cord lesionsĪssociated with FLAIR-hyperintense lesions in anti-MOG associated encephalitis with seizures (FLAMES) 7 This may encompass cases previously termed chronic relapsing inflammatory optic neuropathy (CRION) Not all presentations are equally prevalent: In approximately half of cases there is viral prodrome 2. Clinical presentationĬlinical presentation is similar to that of other acquired demyelinating conditions and varies from individual to individual. In children with acquired demyelination syndrome, MOG-IgGs are more commonly detected than aquaporin 4 antibodies 5.Īdditionally, children with MOGAD are more likely to present with an ADEM-like clinical picture, whereas adults are more likely to present with an NMO-like syndrome 5. MOGAD is primarily encountered in children and young adults 1. Epub 2017 Dec 30.As research was undergoing into MOGAD, many alternate terms were used in the literature, including MOG-IgG-associated optic neuritis, encephalitis, and myelitis (MONEM), anti-MOG associated encephalomyelitis, anti-MOG encephalitis and other variations on this theme 1-4. ‘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. Paraparesis (weakness) of a limb or limbs.Paralysis (no motor function) of a limb or limbs.Loss or blurring of vision in one or both eyes.MOG antibody disease preferentially causes inflammation in the optic nerve, 8 but can also cause inflammation in the spinal cord, brain, and brainstem. COVID-19 and Rare Neuroimmune Disorders.
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