Abstracts

Rationale: Increasing evidence supports the central role of overnight sleep in day-to-day down-regulation of cortical excitability. We hypothesized that patients with refractory epilepsy would display abnormal sleep EEG patterns, possibly linked with their abnormally high cortical excitability. We took advantage of the high spatial resolution of 256 electrodes high density EEG to compare sleep slow wave activity (SWA) topography in normal subjects and patients with drug-refractory focal epilepsy.Methods: 15 drug-refractory epileptic patients (mean age 43 ± SD 14, 9 females) were recruited at the Epilepsy Monitoring Unit of the University of Wisconsin. The localization of patients focal epileptic scalp EEG activity was determined on 10-20 clinical EEG montages by certified Epileptologists. In a second step, the patients’ high-density EEG overnight recordings were analyzed and compared to those of 9 healthy subjects (mean age 42 ± SD 15, 7 females) who also underwent high-density EEG overnight recordings at the University of Wisconsin. High-density EEG data were filtered between 0.5 and 40 Hz. Artifact rejection was then performed using semi-automated in-house Matlab software to select clean non REM sleep epochs and EEG channels. Individual sleep SWA topographies (delta frequency, 0.5 to 4Hz) were then computed using a Fourier transform and averaged across all night in all subjects. Statistical comparisons between controls and patients EEG SWA scalp topographies were performed using Statistical Parametric Mapping (SPM) using a random effects approach to take into account between-subject variability. Statistics were performed both on absolute differences in SWA as well as on relative topographical differences (data normalized to the within-subject mean SWA). All results were corrected for multiple comparisons using SPM family wise error cluster-corrected p value < 0.05.Results: Individual patients presented variable localization of focal epileptic activity on 10-20 EEG clinical readings: left temporal (n = 5), right temporal (n=3), left frontal (n=2), bilateral frontal (n=2), bilateral occipital (n=1), right occipital (n=1). In comparison to controls, group analyses however revealed that patients with refractory focal epilepsy displayed consistently greater absolute SWA power over bilateral fronto-temporal scalp regions. Patients also displayed consistently lower relative SWA over medial scalp regions. In individual patients, lateralized areas with maximal relative SWA corresponded to the origins of interictal epileptic activity determined on independent reading of clinical 10-20 EEG.Conclusions: These results suggest widespread abnormalities in sleep EEG SWA in patients with refractory focal epilepsy, suggesting a link between epileptic foci, cortical excitability, and its regulation through sleep SWA.