acute disseminated encephalomyelitis (ADEM), neuromyelitis optica spectrum disorder (NMOSD) and to a lesser degree multiple sclerosis). Imaging presentation of MOGAD is variable and with no pathognomonic imaging features, with patients having an imaging phenotype often indistinguishable from other inflammatory white matter diseases of the central nervous system (e.g. Myelin oligodendrocyte glycoprotein (MOG) is expressed on oligodendrocytes and the outer lamellae of myelin sheaths 6. 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. 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.
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