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Epilepsy and cerebellar ataxia associated with anti-glutamic acid decarboxylase antibodies
  1. S Vulliemoz1,
  2. G Vanini2,
  3. A Truffert1,
  4. C Chizzolini2,
  5. M Seeck1
  1. 1Department of Neurology, University Hospital of Geneva, Geneva, Switzerland
  2. 2Immunology and Allergy, Department of Internal Medicine, University Hospital of Geneva
  1. Correspondence to:
 M Seeck
 Department of Neurology, University Hospital of Geneva, Micheli-du-Crest 24, 1211 Geneva 14, Switzerland; margitta.seeck{at}hcuge.ch

Abstract

Anti-glutamic acid decarboxylase (GAD) antibodies are described in stiff-person syndrome and also in other neurological syndromes, including cerebellar ataxia and epilepsy. This paper reports the case of a patient who had chronic focal epilepsy, upbeat nystagmus and cerebellar ataxia, associated with a polyautoimmune response including anti-GAD antibodies. Both gait and nystagmus improved markedly after immunosuppressive treatment with corticosteroids and azathioprine. After the introduction of benzodiazepines, previously refractory seizures were completely controlled. Anti-GAD antibodies should be actively sought out in pharmacoresistant epilepsy, particularly if other neurological abnormalities are present. Combined treatment with immunosuppressants and γhydroxybutyric acidergic agents may be highly effective.

  • CAPA, cerebellar ataxia with polyendocrine autoimmunity
  • GABA, γhydroxybutyric acid
  • GAD, glutamic acid decarboxylase
  • GAD-Ab, autoantibodies against GAD
  • IDDM, insulin-dependent diabetes mellitus
  • MRI, magnetic resonance imaging
  • PET, positron emission tomography
  • SPS, stiff-person syndrome

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Footnotes

  • Funding: This study was supported by SNF grants IB74B0-111086, 3200B0-104146, 3200-068105 and 3200-113766.

  • Competing interests: None declared.

  • Informed consent was obtained for publication of the patient’s details described in this report.

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