![]() ![]() Nonetheless, certain imaging features are increasingly recognized as being more typical of MOGAD, allowing the diagnosis to be suspected on the basis of imaging. 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. They are especially looking for participants with recurrent clinical events of optic neuritis and/or transverse myelitis with either a negative anti-AQP4 antibody test or a positive anti-MOG antibody test from another lab.Clinical presentation is similar to that of other acquired demyelinating conditions and varies from individual to individual. Michael Levy and the NMO lab at Johns Hopkins University are developing tests for Anti-MOG (myelin oligodendrocyte glycoprotein) disease. They found that their study participants had reduced relapse rates when they were on maintenance steroids, intravenous immunoglobulin (IVIg), or immunosuppression with rituximab or mycophenolate.ĭr. They found that the individuals in the study responded well to steroids, but relapsed when steroids were stopped. Researchers from the Kids Research Institute at the Children’s Hospital at Westmead in Sydney, Australia, found that 54% of all patients developed optic neuritis as their first disease sign. His argument was that patients with anti-MOG and patients with anti-AQP4 disease have similar cerebrospinal fluid characteristics, clinical characteristics, MRI characteristics, and the same acute and long-term treatment options.Īnother presentation at ECTRIMS described a study that followed 33 children and 26 adults who were anti-MOG-positive over an average of five years. Roman Marignier of the Hospital Pierre Wertheimer of Lyon University Hospital in France argued that anti-MOG disease is a variant of NMOSD that occurs without antibodies to AQP4. Douglas Sato of the Brain Institute of the Rio Grande do Sul in Porte Allegre, Brazil, argued that there are enough differences between anti-MOG disease and NMOSD, and proposed that it be called MONEM, an acronym for “anti-MOG associated optic neuritis, encephalitis and myelitis (MONEM).” In contrast, Dr. Recently at The European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) annual meeting, there was a discussion about anti-MOG and whether it should be its own diagnostic category or another variant of NMOSD. Those with anti-MOG NMOSD tend to have attacks most often in the optic nerve, or optic neuritis (ON), but can also present with inflammation in the spinal cord (transverse myelitis) and brainstem. Anti-MOG antibodies have been found in individuals diagnosed with NMOSD who do not have antibodies to AQP4, in acute disseminated encephalomyelitis, transverse myelitis, and optic neuritis. Although MOG’s exact function is not fully known, it is thought to be an important glycoprotein that influences the myelination of nerves in the central nervous system. There has recently been more discussion about Myelin Oligodendrocyte Glycoprotein or MOG, and its relationship to NMOSD. For example, demyelination from MS is thought to be caused by the activation of white blood cells called T cells (and maybe B cells), while most cases of NMOSD involve antibodies to aquaporin-4 (anti-AQP4 or NMO-IgG). Siegel Eclipse Fund for ResearchĪs researchers continue to study disorders like neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS), we are learning more and more about factors that contribute to the disease processes seen in these conditions. COVID-19 and Rare Neuroimmune Disorders. ![]()
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