Department of Neurology, Philipps-University, Marburg, Germany, MGH/MIT/HMS Athinoula A. Martinos Center for Biomedical Imaging, Charlestown MA, USA, Departments of Radiology and Neuroscience, University at California, San Diego, USA, Department of Psychology, Boston University, Boston, USA
- Mots-clés : epilepsy, MRI, temporal lobe, seizure propagation, white matter microstructures, diffusion tensor imaging
- DOI : 10.1684/epd.2009.0272
- Page(s) : 244-50
- Année de parution : 2009
Objective. Patients with mesial temporal lobe epilepsy (TLE) due to hippocampal sclerosis (HS) often show ictal and interictal propagation of epileptiform EEG activity to the ipsilateral temporal neocortex, the ipsilateral frontal lobe or the contralateral hippocampus, although structural MRI only shows unilateral involvement of the hippocampal formation. We used whole-head diffusion Tensor Imaging (DTI) to delineate a network that facilitates propagation of interictal epileptiform and seizure activity in this patient group. Methods. Isotropic 2 mm DTI was performed at 3 Tesla in 12 patients with medically intractable left TLE due to HS and compared to 12 controls. Whole-brain maps of fractional anisotropy (FA) were compared using a voxel based t-test to search for regions affected in patients with HS. This preliminary analysis was complementary to a set of anatomically guided region of interest (ROI) analyses that were manually defined on each individual’s FA map. Results. Left HS patients showed FA decreases in the temporal lobe white matter bilaterally, the ipsilateral frontal lobe white matter (WM) and in the genu and trunk of the corpus callosum. ROI analysis identified a significant FA decrease in left HS subjects in the affected hippocampus, WM of the ipsilateral parahippocampal gyrus and the genu and trunk of the corpus callosum. Conclusion. WM alterations occur bilaterally in the temporal lobe and in the ipsilateral superior frontal gyrus in left HS. The etiology and significance of these changes are unclear but the role of these regions in epileptogenesis and for pathways of epileptic spread should be further investigated.