Abstracts

Rationale: In order to investigate whether autoimmune mechanisms against ion channels or receptors could be the pathogenic basis in some epilepsy patients, sera were collected from patients with preexisting autoimmune disease or a suspected autoimmune basis (immune cohort IC), consecutive newly-diagnosed epilepsy patients (NDE), patients with long-standing temporal lobe epilepsy (TLE), and patients with drug-resistant epilepsy (DRE). Methods: All sera were screened for antibodies against voltage-gated potassium channels (VGKC), voltage-gated calcium channels (VGCC), glutamic acid decarboxylase (GAD), N-methyl-D-aspartate receptor (NMDAR), and glycine receptor (GlyR) using radioimmunoassays and cell-based assays. The results were compared to healthy and disease controls. Results: Increased VGKC antibody titres (> 100 pM) were found in ~ 16 % of IC patients (half of whom had acute or subacute onsets), compared to 6.5 % in NDE and ~ 3 % in the DRE and TLE patient groups (Table 1). VGCC antibodies were rare in all cohorts, whereas high titre GAD antibodies (> 100 U/ml) were found in 1.5 - 3 % of patients. Interestingly, while NMDAR antibodies were found in all cohorts in the range of 1.5 - 5.9 %, GlyR antibodies seemed to be more frequent in patients with long-standing TLE. Conclusions: The results suggest an immune-mediated component in some forms of epilepsy, although further studies will be required to establish whether the antibodies are directly pathogenic or merely markers of a secondary immune response.