Abstracts

C15O2-Positron Emission Tomography Activation Study in Patients Treated with Vagus Nerve Stimulation for Refractory Epilepsy.

Abstract number : 1.131
Submission category :
Year : 2000
Submission ID : 2633
Source : www.aesnet.org
Presentation date : 12/2/2000 12:00:00 AM
Published date : Dec 1, 2000, 06:00 AM

Authors :
Tom Vandekerckhove, Paul A J M Boon, Koen Van Laere, Kristl Je Vonck, Rudy Dierckx, Jacques De Reuck, Ghent Univ Hosp, Ghent, Belgium.

RATIONALE: The mode of action of vagus nerve stimulation (VNS) for refractory epilepsy remains to be elucidated. This study aims to investigate regional cerebral blood flow (rCBF) changes during initial VNS with C15O2-positron emission tomography (PET). Previous reports showed an increased rCBF in bilateral thalami and the right-sided fusiform gyrus that correlated with seizure control. METHODS: Between 1/1999 and 2/2000, 6 patients (3M/3F) treated with VNS at Ghent University Hospital underwent C15O2-PET at the time of initial stimulation of 0.25 mA. Mean age was 35 years, mean duration of refractory epilepsy 22 years and mean follow-up 8 months. 5/6 patients were responders (>50% reduction in seizure frequency). The activation PET study (Siemens ECAT 951/31) was performed with dynamic scanning over two one-minute intervals starting from the onset of stimulation. Per patient 8 sequential scans were performed, 4 scans with VNS in the ?on?-mode, 4 scans in the ?off? -mode. RESULTS: Significantly increased rCBF was found in the right-sided thalamus and somatosensory cortex and left-sided inferior cerebellum. Significantly decreased rCBF was found in the left-sided fusiform gyrus and in bilateral dorsolateral parietal cortex. We were not able to find time-related rCBF differences. CONCLUSIONS: Acute and initial VNS induces rCBF changes that can be measured using C15O2-PET. Compared to previously published PET studies, fewer areas of rCBF changes were identified. Right-sided rCBF activation is likely to reflect somatosensory processing. Left-sided deactivation of the fusiform gyrus may be involved in the mode of action of VNS. (Supported by Grants BOZF 01105399, 01104495, 011A0996, 01104699, 011A099 from Ghent University; Grant 1.5.236.99 from the Fund for Scientific Research-Flanders and Clinical Epilepsy Grant 1998-2000