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Myasthenia Gravis during the Course of Neuromyelitis Optica

Published: October 2011

Myasthenia Gravis during the Course of Neuromyelitis Optica
Masoud Etemadifara–d, Seyed-Hossein Abtahia–c, Alireza Dehghania,e, Mohammad-Ali Abtahia,e, Mojtaba Akbaria,f, Nasim Tabrizia,d, Tannaz Goodarzig

aMedical School, Isfahan University of Medical Sciences,
bIsfahan Medical Students Research Committee (IMSRC),
cIsfahan Research Committee of Multiple Sclerosis,
dDepartment of Neurology, Medical School, Isfahan University of Medical Sciences,
eOphthalmology Ward, Feiz Hospital, Isfahan University of Medical Sciences,
fDepartment of Epidemiology and Statistics, Isfahan University of Medical Sciences, Isfahan, and
gNational Institute of Genetic Engineering and Biotechnology, Department of Plant Biotechnology, Canker Group, Tehran, Iran

Address of Corresponding Author

Case Rep Neurol 2011;3:268-273 (DOI: 10.1159/000334128)

??Key Words

  • Neuromyelitis optica
  • Devic’s syndrome
  • Myasthenia gravis
  • Multiple sclerosis
  • Aquaporin-4
  • Interferon
  • Thymectomy


Neuromyelitis optica (NMO) is an inflammatory demyelinating disorder of the central nervous system that has been thought to be a severe subtype of multiple sclerosis for a long time. The discovery of aquaporin-4 (AQP4) antibody as a highly specific marker responsible for the pathogenesis of NMO, not only has made a revolutionary pace in establishing a serologic distinction between the two diseases, but it has also classified NMO as an antibody-mediated disorder. Similarly, myasthenia gravis (MG) is a well-known antibody-mediated disorder. In this report, we describe the case of a middle-aged female patient who experienced definite MG with an unclear clinical picture of chronic demyelinating disease that initially reflected the diagnosis of MS, but further imaging and paraclinical workup (e.g. positive AQP4 antibody test) revealed NMO. The coexistence of NMO and MG is previously described. However, this is the first case with NMO symptoms preceding the onset of MG. Of note, the development of MG occurred after a 2-year period of interferon ?-1b (IFN ?-1b) administration. This calls the question to mind of whether in our case MG is induced by the administration of interferon, instead of an original pathogenic link between MG and NMO. In other words, immunomodulatory treatments can slip the immunity towards T-helper II predominant pathways that can trigger MG. However, if we assume that such an explanation (i.e. increased susceptibility to autoantibody-mediated disorders) is true, our case can be considered the first case of NMO who developed MG following IFN ?-1b treatment.

Copyright ? 2011 S. Karger AG, Basel

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