Abstract

AbstractIn Asia, prior to the discovery of aquaporin 4 (AQP4) antibody, many cases of neuromyelitis optica spectrum disorder (NMOSD) were misdiagnosed as multiple sclerosis (MS) or the so‐called opticospinal multiple sclerosis (OSMS). The AQP4 antibody discovery was an important milestone in the field of NMOSD, leading to correct diagnosis and reclassification of NMOSD cases, and the subsequent appropriate therapy. This is especially pertinent in Asia where the prevalence of MS is generally much lower than the Caucasian populations. East Asians have a higher NMOSD prevalence rate (~4/100 000) than Caucasians (~1‐1.5/100 000) and other Asian racial groups (Austronesians: 1.2‐1.5/100 000; South Asians: ~1/100 000; Arabs: ~1‐1.5/100 000). Myelin oligodendrocyte glycoprotein (MOG) antibody‐associated disease (MOGAD) comprises cases of AQP4‐antibody‐negative NMOSD, optic neuritis, myelitis, and certain unique phenotypes such as cases with acute disseminated encephalomyelitis (ADEM)‐like presentation, and cerebral cortical encephalitis. MOGAD appears not too uncommon among Japanese, Chinese, Sri Lankans and Indians, but data in different Asian populations and geographical locations are needed. There exist some differences in clinical features of NMOSD and MOGAD between Asians and other populations. As for risk factors, genetic studies have identified certain HLA associations with NMOSD among Asians that were different from other populations. North‐South latitudinal gradient as seen in MS was not observed in NMOSD in Japan and China. Seasonal variation and preceding infection are among some risk factors worth further investigations. Population‐based MOGAD study in Asia, and further genetic and environmental studies are useful to further inform the epidemiology and potential pathogenetic mechanism of this unique neuroinflammatory disease.

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