title: Prevalence of Autoantibodies and the Efficacy of Immunotherapy for Autoimmune Cerebellar Ataxia.
abstract: OBJECTIVE
  Autoimmune cerebellar ataxias were recently reported to be treatable. However, the proportion of patients with cortical cerebellar atrophy of unknown etiology with autoimmune-associated cerebellar ataxia and the actual effectiveness of immunotherapy in these diseases remain unknown.
  
  
  METHODS
  We measured the level of autoantibodies (including anti-gliadin antibody, anti-glutamic acid decarboxylase (GAD) antibody, and anti-thyroid antibody) in 58 Japanese patients with cerebellar ataxia, excluding those with multiple system atrophy, hereditary spinocerebellar ataxia, cancer, or those who were receiving phenytoin, and the efficacy of immunotherapy was assessed.
  
  
  RESULTS
  Thirty-one of 58 (53%) patients were positive for anti-GAD antibody, anti-gliadin antibody, or anti-thyroid antibody. Seven of the 12 anti-gliadin antibody-positive patients, three of the four anti-GAD antibody-positive patients, and three of the six anti-thyroid antibody-positive patients responded well to immunotherapy, indicating that 59% of patients with ataxia-associated antibody-positive cerebellar ataxia undergoing immunotherapy responded well.
  
  
  CONCLUSIONS
  Some patients with cerebellar ataxia have autoimmune conditions and diagnosing autoimmune cerebellar ataxia is therefore an important component in the care of patients with this disease entity.
authors.affiliation: Department of Neurology, Tokyo Medical University Hachioji Medical Center, Japan.
authors.forename: Kazunori
authors.initials: K
authors.lastname: Nanri
authors.forename: Misaki
authors.initials: M
authors.lastname: Okuma
authors.forename: Saki
authors.initials: S
authors.lastname: Sato
authors.forename: Makoto
authors.initials: M
authors.lastname: Yoneda
authors.forename: Takeshi
authors.initials: T
authors.lastname: Taguchi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Mitoma
authors.forename: Junji
authors.initials: J
authors.lastname: Yamada
authors.forename: Sakae
authors.initials: S
authors.lastname: Unezaki
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Nagatani
authors.forename: Shiho
authors.initials: S
authors.lastname: Otsubo
authors.forename: Mayumi
authors.initials: M
authors.lastname: Sugawara
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Tanaka
authors.forename: Hidehiro
authors.initials: H
authors.lastname: Mizusawa
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001323:Autoantibodies / Q000097:blood*; D001327:Autoimmune Diseases / Q000453:epidemiology / Q000276:immunology* / Q000628:therapy; D002524:Cerebellar Ataxia / Q000453:epidemiology / Q000276:immunology* / Q000628:therapy; D005260:Female; D005903:Gliadin / Q000097:blood*; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use*; D007167:Immunotherapy; D007564:Japan / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D016896:Treatment Outcome
chemical_list: D001323:Autoantibodies; D016756:Immunoglobulins, Intravenous; D005903:Gliadin