Abstracts

Rationale: Simultaneous recording of ElectroEncephaloGraphy EEG and functional Magnetic Resonance Imaging fMRI allows us to identify changes in the blood oxygenation level dependent (BOLD) signal at the time of epileptic discharges. Studying spatial concordance between EEG sources and BOLD responses to epileptic discharges, we previously showed that part of the BOLD response was highly concordant with EEG sources, whereas other fMRI clusters were found distant or discordant with EEG sources. MEG can provide additional information about epileptic activity, since magnetic fields are less attenuated by the skull than electric fields and MEG is only sensitive to tangential sources. Our objective was to study the complementarities between sources of epileptic activity localized either from EEG or MEG data and their correspondance with BOLD responses. Methods: 6 patients underwent EEG-fMRI recording (19 MR compatible electrodes) and EEG-MEG recording (271 MEG sensors, 56 EEG electrodes). EEG acquired in both sessions were visually inspected to detect spikes and marked at their largest peak according to similar spatial distribution/morphology. FMRI data were analyzed using a linear model combining several hemodynamic responses after each spike. MEG and EEG spikes were averaged and used for source localization using the Maximum Entropy on the Mean to estimate a sources distributed on the cortical surface. Results: Patient 1 (no lesion) had left centro-temporo-parietal (CTP) EEG discharges. Left superior T MEG activity extending to temporo-occipital (TO) areas was concordant with BOLD activation, but non concordant with the left inferior T EEG source. Patient 2 (left P focal cortical dysplasia FCD) had left CP EEG polyspikes. Both MEG and EEG sources at the first peak of the polyspikes were located in the lesion, concordant with a left parietal BOLD activation. At the second peak of the polyspikes, only MEG sources showed an additional left frontal (F) source concordant with a left F BOLD activation. Patient 3 (left F FCD) had left CP polyspikes. At the first peak of the polyspikes, both MEG and EEG sources were localized in the lesion, in concordance with the main BOLD activation. At the second peak of the polyspikes, left P MEG and EEG sources were concordant with a BOLD activation, whereas only MEG data found activity in the perilesional area (concordant with a BOLD activation) and in bilateral central regions (concordant with BOLD deactivations) (Fig 1). Patients 4, 5 and 6 were patients with temporal lobe epilepsy (TLE). For all of them, EEG and MEG showed concordant sources in the lateral side ot the spiking T lobe. Only for Patient 5, fMRI data showed a main left mesial T BOLD activation. Conclusions: In TLE, EEG and MEG are mainly sensitive to lateral T genarators whereas fMRI results are usually more extended and less localizing. EEG, MEG and EEG-fMRI can complement each other in the understanding of epileptogenicity for extra-temporal epilepsy and notably for focal cortical dysplasia.