PURPOSE: The presence of anti-ganglioside (GM1) or anti-glutamic acid decarboxylase (GAD) antibodies has been reported in association with therapy-resistant epilepsy mostly of focal origin. Our aim was to detect GM1 and GAD autoantibodies in patients with juvenile myoclonic epilepsy (JME) and to evaluate their association with rarely encountered therapy-resistant cases in this idiopathic generalised epilepsy syndrome. METHODS: Ninety-six consecutive JME patients and 25 healthy normal control subjects were included to the study. We investigated anti-GM1 and anti-GAD antibodies with enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA), respectively. RESULTS: We found anti-GM1 antibodies in one of 96 (1.04%) JME patients and in one out of 25 (4%) healthy controls, without reaching a significant difference between the titres. Anti-GAD antibodies were detected in 5.8% of the patients and in 4% of the healthy controls. Both antibodies did not have any association with therapy-resistant cases and with any other relevant parameters. CONCLUSIONS: The results of our pilot study suggested that anti-GM1 and anti-GAD antibodies are rare and they did not associate with therapy-resistance and other parameters in JME syndrome.
PURPOSE: The presence of anti-ganglioside (GM1) or anti-glutamic acid decarboxylase (GAD) antibodies has been reported in association with therapy-resistant epilepsy mostly of focal origin. Our aim was to detect GM1 and GAD autoantibodies in patients with juvenile myoclonic epilepsy (JME) and to evaluate their association with rarely encountered therapy-resistant cases in this idiopathic generalised epilepsy syndrome. METHODS: Ninety-six consecutive JME patients and 25 healthy normal control subjects were included to the study. We investigated anti-GM1 and anti-GAD antibodies with enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA), respectively. RESULTS: We found anti-GM1 antibodies in one of 96 (1.04%) JME patients and in one out of 25 (4%) healthy controls, without reaching a significant difference between the titres. Anti-GAD antibodies were detected in 5.8% of the patients and in 4% of the healthy controls. Both antibodies did not have any association with therapy-resistant cases and with any other relevant parameters. CONCLUSIONS: The results of our pilot study suggested that anti-GM1 and anti-GAD antibodies are rare and they did not associate with therapy-resistance and other parameters in JME syndrome.