Abstracts

Rationale: Increase white-matter diffusivity and decreased anisotropy have been commonly found in patients with brain structural lesion including hippocampal atrophy, cortical dysplasia, et al. We used diffusion-tensor imaging to study the integrity of different neural pathways in patients with chronic partial epilepsy and without visible lesion in brain images. Our aims are not only to find whether there is same white matter change but also to explore the possible variables which are responsible for the microstructural abnormality. Methods: Twenty-nine healthy volunteers (16 males, mean age = 27±4) and 24 patients with neocortical epilepsy (9 males, mean age = 26±13) were included in this study. Diffusion tensor imaging (DTI) data were acquired on a 3T GE Sigma scanner High-resolution T1-weight fast spoiled gradient recalled echo images (FSPGR) were also acquired. Diffusion-weighted images were first corrected for eddy-current distortion and head motion using FMRIB's diffusion toolbox. Using Analyze 10.0 software, maps of apparent diffusion coefficient (ADC) and fractional anisotropy (FA) were produced. We further extracted ADC and FA and generated nerve fibers for white-matter regions of interest (WM ROIs) separately, each of which was defined in ICBM probabilistic atlas. By DARTEL tool in SPM8, we deformed each ROI from ICBM template to individual with reference to personal SPGR. We tested the difference of ADC and FA between the patient and health groups. Then we examined the contribution of seizure-onset age (early-onset group: 12 patients ≦ 10 years; and late-onset group :10 patients > 10 years), pharmacoresistance, and disease duration to the change of diffusivity and isotropy by comparing the ADC and FA to control group. Results: Diffusely increased ADC and reduced FA in different pathways were found in the individual analyses and group comparison. Many neural pathways (anterior corona radiate, posterior thalamic radiation, splenium of corpus callosum, sagittal stratum and uncinate fasciculus) were found to have statistical difference of ADC and significantly reduced FA in the sagittal stratum was showed in the early-onset group. No significant change in ADC and FA was found in later-onset group. More neural pathways were found to be different in the drug-resistant patient group (significantly high ADC in the anterior corona radiate, posterior thalamic radiation and sagittal stratum) rather than the drug-responsive patient group (only the sagittal stratum showing significant changes in ADC and FA). Conclusions: Our data suggest that patients with MRI-negative neocortical epilepsy showed a reduction in white matter integrity relative to healthy controls particularly in sagittal striatum that is a major corticosubcortical white matter bundle. In addition, we observed widespread structural abnormality in the group of early onset and the group with pharmacoresistance.