title: Antibodies to voltage-gated potassium and calcium channels in epilepsy.
abstract: OBJECTIVE
  To determine the prevalence of antibodies to ion channels in patients with long standing epilepsy.
  
  
  BACKGROUND
  Although the CNS is thought to be protected from circulating antibodies by the blood brain barrier, glutamate receptor antibodies have been reported in Rasmussen's encephalitis, glutamic acid decarboxylase (GAD) antibodies have been found in a few patients with epilepsy, and antibodies to voltage-gated potassium channels (VGKC) have been found in a non-paraneoplastic form of limbic encephalitis (with amnesia and seizures) that responds to immunosuppressive therapy.
  
  
  METHODS
  We retrospectively screened sera from female epilepsy patients (n=106) for autoantibodies to VGKC (Kv 1.1, 1.2 or 1.6), voltage-gated calcium channels (VGCC) (P/Q-type), and GAD. All positive results, based on the values of control data [McKnight, K., Jiang, Y., et al. (2005). Serum antibodies in epilepsy and seizure-associated disorders. Neurology 65, 1730-1735], were retested at lower serum concentrations, and results compared with previously published control data. Demographics, medical history, and epilepsy related information was gathered.
  
  
  RESULTS
  The studied group consisted predominantly of patients with long standing drug resistant epilepsy. VGKC antibodies were raised (>100 pM) in six patients. VGCC antibodies (>45 pM) were slightly raised in only one patient. GAD antibodies were <3 U/ml in all patients. The clinical features of the patients with VGKC antibodies differed from previously described patients with limbic encephalitis-like syndrome, and were not different with respect to seizure type, age at first seizure, duration of epilepsy, or use of anti-epileptic drugs from the VGKC antibody negative patients.
  
  
  CONCLUSIONS
  The results demonstrate that antibodies to VGKC are present in 6% of patients with typical long-standing epilepsy, but whether these antibodies are pathogenic or secondary to the primary disease process needs to be determined.
authors.affiliation: Epilepsy Centre Kempenhaeghe, Heeze, The Netherlands. majoiem@kempenhaeghe.nl
authors.forename: H J Marian
authors.initials: HJ
authors.lastname: Majoie
authors.forename: Mark
authors.initials: M
authors.lastname: de Baets
authors.forename: Willy
authors.initials: W
authors.lastname: Renier
authors.forename: Bethan
authors.initials: B
authors.lastname: Lang
authors.forename: Angela
authors.initials: A
authors.lastname: Vincent
mesh_terms: D000293:Adolescent; D000328:Adult; D001323:Autoantibodies / Q000097:blood*; D015220:Calcium Channels / Q000276:immunology*; D004827:Epilepsy / Q000276:immunology* / Q000473:pathology; D005260:Female; D006801:Humans; D008875:Middle Aged; D024642:Potassium Channels, Voltage-Gated / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D015220:Calcium Channels; D024642:Potassium Channels, Voltage-Gated