Abstracts

Rationale: The concept of deep brain stimulation (DBS) of the anterior thalamic nuclei (ANT) for pharmacoresistant focal epilepsies originates from animal studies, examining the connectivity of these nuclei [Mirski et al., Science 1984 ]. According to the SANTE-study [Fisher et al., Epilepsia 2010] patients with seizure origin in one or both temporal regions benefitted from ANT-DBS. Stereotactic insertion of the electrodes into the ATN allows electrophysiological activity to be recorded directly from the ATN in the first few days post-operatively, before the electrodes were connected to the stimulator. Stability of the electrodes was achieved by deeper insertion, and as a result, it was additionally possible to record activity from the dorsomedial thalamic nuclei (DMTN). A recent animal study [Zhang et al., Epilepsia 2015] showed that low-frequency stimulation of the DMTN reduces seizure occurrence . We therefore examined activity recorded before commencement of stimulation therapy from the DMTN as well as the ATN, in order to investigate whether spontaneous epileptiform discharges were detectable in these nuclei.Methods: Methods: Nose-referenced intracranial EEG-data were recorded from 4 patients suffering from temporal lobe epilepsy. The data were re-referenced to a bipolar montage by subtracting the deeper neighbour from each electrode on each side. They were then visually inspected at 10 s intervals for a total of 15 minutes, at a resolution of 25 microvolts per centimeter in order to identify epileptiform spikes and slow waves. These were categorized as having a narrow or a wide field and localized to the ATN, DMTN, or not localized.Results: While only 2 of the patients had spikes or slow waves localized to the ANT, three patients had spikes or slow waves localized in a narrow field in the DMTN (Table 1). Patient 1 moreover had both narrow field and wide field epileptiform activity identifiable in both the ATN and DMTN. In patient 2, although no spikes were localized in the ATN, non-localized epileptifom activity was detected in the thalamus in addition to that localized to the DMTN. Patient 3 exhibited localized spikes or slow waves only in the ANT. The one patient(patient 4) who had a temporal lobectomy exhibited an exceedingly high number of spikes / slow waves only in a narrow field of the DMTN.Conclusions: Stimulation of the ATN for the treatment of pharmacoresistant focal epilepsy has thus far yielded mixed outcomes. The present results suggest that the DMTN is involved in interictal activity, which is independent from the interictal activity of the ANT. Further data has to be collected to substantiate these preliminary findings. It can be speculated that the DMTN-stimulation could potentially disrupt epileptiform activity. Provided a tranventricular approach for electrode insertion has been used, stimulation of the DMTN might be an additional treatment possibility, especially for non-responders to ATN-stimulation.