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Different patterns of brainstem and cerebellar MRI abnormalities in demyelinating disorders with MOG and aquaporin-4 antibodies
  1. Akiyuki Uzawa,
  2. Masahiro Mori,
  3. Satoshi Kuwabara
  1. Neurology, Chiba University Graduate School of Medicine School of Medicine, Chiba, Japan
  1. Correspondence to Dr Akiyuki Uzawa, Neurology, Chiba University Graduate School of Medicine School of Medicine, Chiba, Chiba, Japan; auzawa{at}chiba-u.jp

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MRI findings may reflect differences in target molecules in myelin-associated glycoprotein-IgG-associated disorder when compared with aquaporin-4-IgG-positive neuromyelitis optica spectrum disorders

The central nervous system (CNS) demyelinating disorder linked with myelin-associated glycoprotein (MOG)-IgG, termed MOG antibody-associated neurological disorder (MOGAD), is becoming increasingly recognised worldwide.1 MOGAD displays a number of clinical phenotypes, including optic neuritis, transverse myelitis and acute demyelinating encephalomyelitis. If the optic nerves and spinal cord are predominantly involved, the disorder appears similar to seronegative neuromyelitis optica spectrum disorders (NMOSD), another CNS inflammatory disease associated with autoantibodies against aquaporin-4 (AQP4) expressed on astrocytes.1 The two disorders share a common profile: (1) recurrent optic neuritis and myelitis, (2) presence of disease-specific antibodies and (3) immunological characteristics, such as cytokine or T cell profiles and the rare presence of oligoclonal bands.2 3 However, pathological studies have …

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Footnotes

  • Contributors AU wrote the draft, and MM and SK supervised and made revisions.

  • Funding This work was supported in part by the Health and Labour Sciences Research Grant on Intractable Diseases (Neuroimmunological Diseases) from the Ministry of Health, Labour and Welfare of Japan (20FC1030).

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; internally peer reviewed.

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