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The autoantibody against myelin oligodendrocyte glycoprotein (MOG) is present in patients with several inflammatory diseases such as neuromyelitis optica spectrum disorder (NMOSD), acute disseminated encephalomyelitis (ADEM), optic neuritis and transverse myelitis. Differential diagnosis is difficult because of overlapping clinical and radiological features.1
In adult patients with MOG-Ab-associated disease (MOGAD), the highest occurrence of lesions was in the thalamus and pons in MOGADOR study,1 but the other study showed that MOGAD lesion was more often found in subcortical white matter and the internal capsule, but the pontine lesion was not revealed as distinct.2 In paediatric patients, the cerebellar peduncle was dominant in MOGAD, but there were no statistically significant differences in the pons, thalamus and cortical lesions.3 Such discrepancies might suggest a wide diversity in lesion configuration and extraction, range of diseases and various age of disease onsets.
In our large-scale study, we divided the brain regions of interest into 21 defined sections and analysed lesion distributions for both MOGAD and NMOSD.
Inclusion criteria is as followed: (1) CNS (central nervous system) demyelinating disease referred to the Department of Neurology at Tohoku University in 2018, (2) aquaporin-4 or MOG antibody positivity by in-house cell-based assay, (3) the availability of brain MRI data, and (4) the detected MRI lesions taken within 1 month in clinically acute stage. We finally enrolled 134 patients with MOGAD and 70 patients with NMOSD (online supplement file - Patients).
Brain MRI analysis
Clinical brain MRI scans, including T2-weighted and fluid-attenuated inversion recovery sequences, had been acquired using 3.0/1.5 T scanners. An independent neurologist and a blinded neuroradiologist (YM and SM, respectively) performed MRI assessments by brain lesion division (21 areas; online supplement file - MRI). In cases of disagreement, final decisions were based on a consensus between the two evaluators.
To better visualise the prevalence and …
Contributors YM: design and conceptualised study; analysed the data; drafted the manuscript for intellectual content. TM: design and conceptualised study; drafting and revision of manuscript. SM: data collection and analysis for MRI images. YT, SN, HK, JF and IN: data collection and analysis. TT: data collection and analysis for antibody testing. KF: design and conceptualised study; drafting and revision for intellectual content. MA: drafting and revision for intellectual content.
Funding This work was supported by JSPS KAKENHI Grant Numbers 19K07953 and 17H04192.
Competing interests YM reports no disclosure. TM received speaker honoraria from Tanabe Mitsubishi Pharma, Novartis Pharma., Alexion Pharma., Viela Bio., and Biogen Idec Japan, and received research support from Cosmic Corporation; and received grant-in-aid for scientific research from Ministry of Education, Culture, Sports, Science and Technology. SM reports no disclosure. YT reports no disclosure. SN reports no disclosure. HK reports no disclosure. TT received speaker honoraria from Biogen Idec and Cosmic Corporation and received research support from Cosmic Corporation. JF reports no disclosure. IN received travel funding and speaker honoraria from Biogen Japan, Tanabe Mitsubishi, and Novartis Pharma; is on the editorial board for Multiple Sclerosis International; and received research support from LSI Medience Corporation. KF serves on the advisory boards for Bayer Schering Pharma, Biogen Idec, Mitsubishi Tanabe Pharma Corporation, Novartis Pharma, Chugai Pharmaceutical, Ono Pharmaceutical, Nihon Pharmaceutical, Alexion Pharmaceuticals, and Medimmune; has received travel funding and speaker honoraria from Bayer Schering Pharma, Biogen Idec, Eisai, Mitsubishi Tanabe Pharma Corporation, Novartis Pharma, Astellas Pharma, Takeda Pharmaceutical Company Limited, Asahi Kasei Medical Co., Daiichi Sankyo, and Nihon Pharmaceutical; is on the editorial board for Clinical and Experimental Neuroimmunology; is an advisory board member for Sri Lanka Journal of Neurology; and received research support from Bayer Schering Pharma, Biogen Idec Japan, Asahi Kasei Medical, The Chemo-Sero-Therapeutic Research Institute, Teva Pharmaceutical, Mitsubishi Tanabe Pharma, Teijin Pharma, Chugai Pharmaceutical, Ono Pharmaceutical, Nihon Pharmaceutical, Genzyme Japan, Ministry of Education, Science and Technology of Japan, and Ministry of Health, Welfare and Labor of Japan. MA received research support from Japanese Ministry of Health Labor and Welfare, Japanese Ministry of Education, Culture, Sports, Science and Technology.
Provenance and peer review Not commissioned; externally peer reviewed.
Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.
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