PATHOPHYSIOLOGICAL MECHANISM OF SLOW WAVE ACTIVITY IN FRONTAL LOBE EPILEPSY
Abstract number :
1.138
Submission category :
Year :
2003
Submission ID :
1806
Source :
www.aesnet.org
Presentation date :
12/6/2003 12:00:00 AM
Published date :
Dec 1, 2003, 06:00 AM
Authors :
Alberto Fern[aacute]ndez, Felipe Quesney, Marta Garc[iacute]a-Fern[aacute]ndez, Carlos Amo, Fernando Maest[uacute], M[ordf] Carmen D[iacute]az-Obreg[oacute]n Centro MEG, Universidad Complutense de Madrid, Madrid, Spain; Montreal Neurological Institute, Mc
A post-traumatic etiology which is commonly associated with bifrontal damage, is a frequent etiopathological factor in frontal lobe epilepsy (FLE). A priori, this would suggest a correlation between the slow wave activity and the structural lesion. In order to assess this, we studied the correlation between slow wave activity, MEG spiking and MRI in FLE.
Simultaneous MEG-EEG recordings were performed in12 patients with FLE (5 females, mean age: 24 years). We performed dipole density analysis (DDA) of the MEG delta and theta activity (method of Fehr et al. 2001) and correlated it with the distribution of the interictal EEG spiking as well as with the dipole source localization of MEG spikes and with the MRI.
A subgroup of 5/12 patients (42%) presented with bifrontal EEG epileptiform activity. The dipoles corresponding to MEG spikes lateralized 5/5 of patients (100%) and slow wave activity DDA correctly lateralized 4/5 (80%). In 1/12 patients (8%) without EEG or MEG spikes, DDA provided a correct lateralization.
The 6 remaining patients of this series (50%), presented either with diffuse unilateral EEG findings (3 patients, 25%), questionable lateralized EEG findings (1 patient, 8%) or correctly lateralized EEG findings (2 patients, 17%). Slow wave activity DDA agreed with the EEG lateralization in 6/6 patients (100%). MEG spikes equivalent dipole agreed with the EEG localization only in 5/6 patients (83%).
A perfect concordance between MEG spikes equivalent dipole and structural lesions was seen in 6/6 patients (100%) with positive MRI findings. Interestingly, slow wave activity DDA agreed with the MEG spike dipole in 9/11 patients (81%) and with the MRI findings in 4/6 (67%).
Our findings show a better correlation of the slow wave activity with the MEG spike dipole localization than with the MRI structural lesion in FLE, thus indicating a preferential relationship of this activity with frontal lobe epileptogenesis. The pathophysiological explanation for this finding remains unclear but it is very likely related to MEG [acute]s higher sensitivity to localize the epileptic generator and its concurrent inhibition, which is probably the main source of slow wave activity.