Hippocampal DBS affects disease development in the kainic acid rat model for temporal lobe epilepsy

Abstract

Event Abstract Back to Event Hippocampal DBS affects disease development in the kainic acid rat model for temporal lobe epilepsy Bregt Van Nieuwenhuyse1*, Robrecht Raedt1, Mathieu Sprengers1, Ine Dauwe1, Stefanie Gadeyne1, Jean Delbeke1, Wytse Wadman1, 2, Paul Boon1 and Kristl Vonck1 1 Ghent University, Neurology, Belgium 2 Amsterdan University, Department of Neurobiology, Netherlands Rationale: There is increasing evidence that the effect of deep brain stimulation (DBS) on seizures increases with prolonged treatment suggesting a disease modifying potential for DBS. To further investigate this, we studied the effect of hippocampal DBS on seizure development in the kainic acid (KA)-induced status epilepticus (SE) model for temporal lobe epilepsy (TLE). Methods: Rats were implanted with a quadripolar DBS/EEG-recording electrode in the right hippocampus and a bipolar EEG-recording electrode in the left hippocampus. 24 hours after kainic acid (KA) induced status epilepticus (SE), one group (n=10) was subjected to long-term DBS (LT-DBS) (Poisson Distributed Stimulation, 130 PPS, 100µs PW, 100µA) during 23 weeks. A control group (n=8) received sham stimulation (SHAM). Video-EEG was recorded continuously during 30 weeks in both groups. Results: During stimulation, the gradual increase in seizure frequency is lower in the DBS group compared to the SHAM group, resulting in significant lower seizure frequencies from week 22 to 25 after SE (p<0.05). In the LT-DBS group 5/10 (50%) of the treated rats showed no gradual increase in daily seizure frequency seizure frequency during 23 weeks of stimulation and were defined as responders. In the SHAM group all rats experienced a gradual increase in seizure frequency during the first 23 weeks after SE. This results in a significantly lower seizure rate in the responder rats compared to the SHAM rats from week 16 to 24 after SE (p<0.01). When stimulation was stopped after 23 weeks, an increase in daily seizure frequency occurred in all responder rats within one week. This resulted in similar seizure rates from week 25 to week 30 in the responder rats and SHAM group (fig.1). No significant differences in seizure rate were observed between the non-responder group and SHAM group during DBS. For all rats, a sigmoid curve could be fitted to the seizure rate data. Statistical analysis of the fitted sigmoid curve’s equation parameters show that only the time after SE at which the EEG seizure frequency in disease development reached half-maximum was significantly retarded from 13.5 weeks post SE in the SHAM group to 24.7 weeks post SE in the responder group (p<0.01)(fig.2A&B). Conclusion: Starting treatment with hippocampal DBS 24h after SE in the post-SE KA model retards normal disease progression in 5/10 (50%) of all treated rats by efficiently suppressing seizures. We show that DBS started 24 hours after the start of SE suppresses the gradual increase in daily seizure frequency that is typically observed in the post-SE KA model. Figure 1 Figure 2 Keywords: deep brain stimulation (DBS), Hippocampus, Epilepsy, Seizures, disease progression, Kainic Acid, neurostimulation Conference: Belgian Brain Council 2014 MODULATING THE BRAIN: FACTS, FICTION, FUTURE, Ghent, Belgium, 4 Oct - 4 Oct, 2014. Presentation Type: Oral Presentation Topic: Basic Neuroscience Citation: Van Nieuwenhuyse B, Raedt R, Sprengers M, Dauwe I, Gadeyne S, Delbeke J, Wadman W, Boon P and Vonck K (2014). Hippocampal DBS affects disease development in the kainic acid rat model for temporal lobe epilepsy. Conference Abstract: Belgian Brain Council 2014 MODULATING THE BRAIN: FACTS, FICTION, FUTURE. doi: 10.3389/conf.fnhum.2014.214.00013 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 19 Jun 2014; Published Online: 25 Jun 2014. * Correspondence: Mr. Bregt Van Nieuwenhuyse, Ghent University, Neurology, Ghent, Belgium, bregt.vannieuwenhuyse@ugent.be Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Bregt Van Nieuwenhuyse Robrecht Raedt Mathieu Sprengers Ine Dauwe Stefanie Gadeyne Jean Delbeke Wytse Wadman Paul Boon Kristl Vonck Google Bregt Van Nieuwenhuyse Robrecht Raedt Mathieu Sprengers Ine Dauwe Stefanie Gadeyne Jean Delbeke Wytse Wadman Paul Boon Kristl Vonck Google Scholar Bregt Van Nieuwenhuyse Robrecht Raedt Mathieu Sprengers Ine Dauwe Stefanie Gadeyne Jean Delbeke Wytse Wadman Paul Boon Kristl Vonck PubMed Bregt Van Nieuwenhuyse Robrecht Raedt Mathieu Sprengers Ine Dauwe Stefanie Gadeyne Jean Delbeke Wytse Wadman Paul Boon Kristl Vonck Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.