Grey and white matter abnormalities in temporal lobe epilepsy with and without mesial temporal sclerosis

Abstract

Temporal lobe epilepsy with (TLE-mts) and without (TLE-no) mesial temporal sclerosis display different patterns of cortical neuronal loss, suggesting that the distribution of white matter damage may also differ between the sub-groups. The purpose of this study was to examine patterns of white matter damage in TLE-mts and TLE-no and to determine if identified changes are related to neuronal loss at the presumed seizure focus. The 4 T diffusion tensor imaging (DTI) and T1-weighted data were acquired for 22 TLE-mts, 21 TLE-no and 31 healthy controls. Tract-based spatial statistics (TBSS) was used to compare fractional anisotropy (FA) maps and voxel-based morphometry (VBM) was used to identify grey matter (GM) volume atrophy. Correlation analysis was conducted between the FA maps and neuronal loss at the presumed seizure focus. In TLE-mts, reduced FA was identified in the genu, body and splenium of the corpus callosum, bilateral corona radiata, cingulum, external capsule, ipsilateral internal capsule and uncinate fasciculus. In TLE-no, FA decreases were identified in the genu, the body of the corpus callosum and ipsilateral anterior corona radiata. The FA positively correlated with ipsilateral hippocampal volume. Widespread extra-focal GM atrophy was associated with both sub-groups. Despite widespread and extensive GM atrophy displaying different anatomical patterns in both sub-groups, TLE-mts demonstrated more extensive FA abnormalities than TLE-no. The microstructural organization in the corpus callosum was related to hippocampal volume in both patients and healthy subjects demonstrating the association of these distal regions.

Conflict of interest statement

Conflicts of interest The authors declare that they have no conflict of interest.

Figures

Fig. 1

Regions of interests (ROI) defined using the JHU white matter probabilistic tractography atlas. IFO inferior fronto-occipital fasciculus, ILF inferior longitudinal fasciculus, SLF superior longitudinal fasciculus, UNC uncinate fasciculus. The mean FA skeleton is represented in green, the ROI in blue

Fig. 2

Clusters of voxels (p < 0.05, TFCE) with significantly reduced FA in a TLE-mts and b TLE-no compared with controls. The mean FA skeleton where analysis was carried out is represented in green. Significant FA differences after correction for multiple comparisons are presented in yellow/red. SLF superior longitudinal fasciculus, CC corpus callosum

Fig. 3

Clusters of voxels (p < 0.05, TFCE) with significant positive correlations between ipsilateral hippocampal volume and FA in a TLE-mts and controls b TLE-no and controls. The mean FA skeleton where analysis was carried out is represented in green. Significant FA differences after correction for multiple comparisons are presented in yellow/red. Graphs show correlation between hippocampal volume and FA in the genu of the corpus callosum

Fig. 4

Reduction of GM volume (GMV) in TLE-mts and TLE-no compared to controls (p < 0.05, FDR), corrected (top) and uncorrected (bottom) t-statistic maps. Ipsilateral hemisphere is located on the right hand side