Abstracts

Rationale: Centro-medium thalamic nucleus stimulation has been investigated in the treatment of both focal and generalized refractory epilepsy. We have targeted this nucleus only in patients with generalized refractory epilepsy taking into consideration the non-specific nature of its relays. We report on the seizure outcome in four patients with refractory generalized epilepsy who have already been previously submitted to callosal section. Methods: Four adult patients (aged 17-33 years) with refractory generalized epilepsy (2 Lennox-Gastaut, 2 refractory idiopathic generalized epilepsy) who had been previously submitted to extended (90%) callosotomy were studied. All patients benefit from their primary surgery (callosal section), with a mean 80% reduction in generalized seizure frequency. All patients were submitted to bilateral alternated thalamic centro-medium stimulation using Kinetra electrodes. Patients were submitted to electrode implantation under general anesthesia targeting the centro-medium nucleus 10 mm off the midline at the posterior commissural plane. Final parameters were 2V, 300usec and 130 Hz. Results: The first three patients had at least one year of follow-up (mean 15 months) and the fourth one is still reaching the final parameters. An 80% mean reduction in seizure frequency was noted in the first 3 patients (70-90%). A decrease in seizure frequency was initially noted when stimulation reached 1.6V (130Hz, 300 usec), and appeared to be maximal at 2V. We did not stimulate above 2V yet. In one patient, somato-sensitive side effects were obtained while stimulating at 2.2V; the other 2 patients tolerated further increase but were kept under 2V stimulation so far. Conclusions: Bilateral stimulation of the centro-medium thalamic nuclei was effective in reducing the generalized seizure frequency in patients with Lennox-Gastaut or refractory idiopathic generalized epilepsy previously submitted to callosotomy. These results were similar to those obtained in patients not submitted to callosal section; interhemispheric pathways seem not to be involved in the anticonvulsant effect of thalamic stimulation.