Abstracts

We investigated optimaized VBM in TLE patients to identify gray matter (GM) and white matter (WM) abnormalities beyond the hippocampus in TLE with HS (TLE-H) and TLE without HS (TLE-NH), and to determine whether extratemporal GM abnormalities differ between the two groups., Optimized VBM of GM and WM with modulation was performed in 16 left TLE (5 TLE-H [amp] 11 TLE-NH: mean age, 34.1[plusmn]5.7 years), 12 right TLE patients (7 TLE-H [amp] 6 TLE-NH: mean age, 31.4[plusmn]9.6 years) and 17 age and sex matched normal subjects (mean age, 26.6[plusmn]7.6 years)., In left TLE-H group, GM volume reduction was found in the ipsilateral hippocampus, contralateral thalamus, cerebellum and WM volume reduction was seen in the ipsilateral internal capsule and bilateral parieto-occipital areas. In right TLE-H group, GM volume reduction was shown to be confined to the bilateral medial temporal areas, more definite in the ipsilateral side. In contrast, TLE-NH group showed GM volume reduction in ipsilateral posterior fusiform and lingual cortex and its extent of GM volume reduction in TLE-NH group was much smaller than that observed in TLE-H group. WM volume reduction was widely scattered in bilateral cerebral deep white matters in all TLE-H groups (predominantly distributed in central to posterior areas). But, in TLE-NH group, WM volume loss was obvious in ipsilateral posterior temporal WM (right TLE-NH group) or adjacent corticospinal tract near the ipsilateral temporal stem (left TLE-NH group). Also the extent of WM volume reduction in TLE-NH group was much smaller than that observed in TLE-H group., In not only TLE-H but TLE-NH, optimized VBM showed discrete volume reduction of GM in the ipsilateral hippocampus and temporal area. The WM change of TLE-NH group may represent the early changes which cannot be detected by gross inspection and the possibility of lateralizing capacity of epileptogenicity of TLE-NH. This further supports the hypothesis that TLE-NH is an early stage of the disease progressing to TLE-H rather than a different clinicopathologic entity from TLE-H.,