Abstracts

RESPONSIVE NEUROSTIMULATION IN PATIENTS WITH PERIVENTRICULAR NODULAR HETEROTOPIA (PNH)

Abstract number : 2.209
Submission category : 4. Clinical Epilepsy
Year : 2014
Submission ID : 1868291
Source : www.aesnet.org
Presentation date : 12/6/2014 12:00:00 AM
Published date : Sep 29, 2014, 05:33 AM

Authors :
Paul Rutecki, Aamr Herekar, Paul Van Ness, Gregory Bergey, Carl Bazil, David King-Stephens, Felice Sun, Ritu Kapur and Martha Morrell

Rationale: Opportunities for resective surgery may be limited in patients with intractable partial onset epilepsy and periventricular nodular heterotopias (PNH) due to PNH's location deep in the brain and underneath eloquent cortex. Temporal lobe resection in patients with PNH has had mixed results with respect to seizure reduction. It is also not always clear whether seizures arise from the PNH or from other cortical regions, or both. Data from the RNS® System trials represent the first experience with responsive neurostimulation to treat seizures in these patients as well as the first chronic ambulatory recordings from depth leads placed in PNH. Methods: The RNS System is approved as an adjunctive therapy in reducing the frequency of frequent and disabling seizures in individuals ≥18 years old with medically refractory partial onset seizures arising from 1 or 2 seizure foci. A cranially implanted programmable responsive neurostimulator is connected to 2 depth and/or subdural leads placed at the seizure focus. The neurostimulator is programmed to detect specific epileptiform electrocorticographic activity (ECoG) and to provide responsive stimulation. Data were analyzed for subjects with a documented PNH who were participating in an RNS System trial with ≥ 3 months of seizure diary data in the open label period and who were treated with responsive neurostimulation. The percent change from baseline seizure rate was calculated for the most recent 3 months (last observation carried forward). Results: Eight of 256 subjects in the trials had a confirmed PNH. The median percent reduction in seizures for the PNH subjects was 69%, with a range of 30-100%. Six of 8 subjects were implanted with a depth lead in the PNH as well as either a depth lead in the ipsilateral hippocampus (n=4), or a subdural strip lead placed where seizure onsets were observed (including frontal and temporal lobes; n=2). Two of the 8 subjects did not have leads placed in the PNH. One of these subjects was implanted bilaterally with depth leads in the hippocampi, and the other subject was implanted with one hippocampal depth lead and one strip lead in cortex overlying the PNH. All 6 subjects with leads placed in the PNH received stimulation on the lead in the PNH. Conclusions: There is not sufficient power to provide statistical conclusions about the clinical response of patients with PNH to treatment with the RNS System. However, descriptive analyses suggest that the clinical response in these patients is not different than the response in other patients in the clinical trials. The experience in patients with PNH indicates that treatment with responsive neurostimulation may provide seizure reduction. Chronic ambulatory ECoG recordings from depth leads placed in the PNH suggest that seizures may not always arise in the PNH and that patients should be evaluated for other seizure foci.
Clinical Epilepsy