MEG of interictal spike activity: correlation with BOLD responses in EEG-fMRI studies
Abstract number :
2.221;
Submission category :
3. Clinical Neurophysiology
Year :
2007
Submission ID :
7670
Source :
www.aesnet.org
Presentation date :
11/30/2007 12:00:00 AM
Published date :
Nov 29, 2007, 06:00 AM
Authors :
C. Grova1, 2, E. Kobayashi1, L. Tyvaert1, J. M. Lina2, 3, F. Dubeau1, P. Jolicoeur2, J. Gotman1
Rationale: Combined recording of EEG and fMRI allows us to identify changes in the blood oxygenation level dependent (BOLD) signal at the time of the spikes. The significance of BOLD responses in regions with no clear EEG abnormalities is not well understood. MEG can provide additional information about epileptic activity, since magnetic fields are less attenuated by the skull than electric fields. Our goal was to evaluate concordance of MEG source localization and spike-related BOLD responses.Methods: 3 patients underwent EEG-fMRI recording (19 MR compatible electrodes, 1.5T or 3T MRI scanner) and EEG-MEG recording (271 MEG sensors, 64 EEG electrodes). EEGs acquired in both sessions were visually inspected. Spikes were marked at their largest peak and classified according to spatial distribution/morphology. FMRI data were analyzed using a linear model combining several hemodynamic responses after each spike. BOLD responses were identified in t-maps superimposed on the anatomical MRI. MEG spikes were averaged and used for source localization using the Maximum Entropy on the Mean to estimate a current density distributed on the cortical surface. We compared MEG sources and BOLD responses to similar EEG spikes using Anatomist software, which allows 3D synchronization between BOLD maps and MEG sources.Results: Patient 1 (no MRI lesion) had left centro-temporo-parietal (CTP) EEG spikes. Left superior T MEG activity extending to temporo-occipital (TO) areas was concordant with BOLD activation. No MEG activity could be identified close to the bi-O deactivation. Patient 2 (left P lesion) had left CP EEG spikes and polyspikes. For left CP spikes, left P MEG activity (in the lesion) was concordant with BOLD activation, while left T MEG activity had no correspondent BOLD response. The MEG source at the first peak of the polyspike was in the lesion, concordant with the left P activation, whereas the second peak showed MEG sources distributed in areas surrounding the lesion (CTO), with no clear concordance with fMRI. Patient 3 (left F lesion) had left FC spikes, left CP spikes and left CP polyspikes. Left FC spikes showed concordance of activation and MEG sources, within the lesion and perilesional area. No MEG sources were found in the left and right C deactivations. Left CP spikes MEG source was located in the left C sulcus, concordant with deactivation in the posterior perilesional area. A smaller left F source within the lesion was concordant with the main activation. There was no MEG source in the right C deactivation. MEG sources at the first peak of left CP polyspikes were within the left F lesion, inferior to the main activation, wheras the MEG sources at the main peak were far from the lesion in the left PO area.Conclusions: MEG activity can help understand the significance of BOLD responses that are more widespread than the spike seen in the EEG. This was more apparent for activations than for deactivations. MEG analysis demonstrated propagating fields during polyspikes and could explain remote BOLD activity. MEG and EEG-fMRI can complement each other in the understanding of epileptogenicity.
Neurophysiology