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Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease: practical considerations
  1. Maciej Juryńczyk1,2,
  2. Anu Jacob3,
  3. Kazuo Fujihara4,
  4. Jacqueline Palace5
  1. 1Department of Neurology, Royal Hampshire County Hospital, Winchester, UK
  2. 2Department of Neurology, University Hospital Southampton, Southampton, UK
  3. 3Department of Neurology, Walton Centre, Liverpool, UK
  4. 4Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan
  5. 5Department of Clinical Neurology, John Radcliffe University Hospital, Oxford, UK
  1. Correspondence to Dr Jacqueline Palace, John Radcliffe University Hospital, Oxford OX3 9DU, UK; jacqueline.palace{at}


The field of central nervous system (CNS) inflammatory diseases has recently broadened to include a new condition associated with pathogenic serum antibodies against myelin oligodendrocyte glycoprotein (MOG). This is distinct from multiple sclerosis (MS) and aquaporin-4 (AQP4) antibody neuromyelitis optica spectrum disorders (NMOSD). MOG antibody-associated disease phenotypes are varied and range from classical neuromyelitis optica to acute demyelinating encephalomyelitis and cortical encephalitis. The diagnosis depends on using a reliable, specific and sensitive assay of the antibody. Clinical and imaging features of MOG-associated syndromes overlap with AQP4 antibody NMOSD but can be usually distinguished from MS: in particular, the silent lesions typical of MS that progressively increase lesion volume are rare in MOG antibody disease. The disease can relapse but medium-term immunosuppression appears to be protective. Permanent disability, particularly severe ambulatory and visual disability, is less frequent than in AQP4 antibody NMOSD and usually results from the onset attack. However, sphincter and sexual dysfunction after a transverse myelitis is common. Here we review the practical aspects of diagnosing and managing a patient with MOG antibody-associated disease.


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  • Contributors All contributors meet the criteria for authorship.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent Not required.

  • Provenance and peer review Commissioned. Externally peer reviewed by Neil Robertson, Cardiff, UK.

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