Abstracts

Rationale: The temporal lobe epilepsy (TLE) is associated with hippocampal atrophy. However, the brain damage is not limited to limbic structures. The mechanisms underlying extrahippocampal brain damage in TLE are unknown. Seizures or medicines may lead to neuronal damage, but another possible explanation is deafferentation from loss of hippocampal connections. This study we combined the use of Fracional anisotropy (FA), mean diffusibility (D), parallel diffusibility (D//), perpendicular diffusibility (D?), and Magnetization Transfer Ratio (MTR) to localize the regions where occur axonal lesion and demyelization. Methods: Two different MRI sequences were performed involving 33 patients with unilateral TLE (15 left and 18 right) and 20 healthy controls (age matched): (1) Magnetization transfer and (2) diffusion tensor imaging (DTI). Tract-based spatial statistics (TBSS) was applied to analyze the FA data. After, the regions with alteration were studied with D, D//, D? and MTR maps. When compare with controls, the decrease of MTR values and/or increase of D? indicate demyelization and decrease of D? can indicate axonal lesion. Results: Both patients with left- as well as right-sided mesial sclerosis exhibited widespread degradation of fractional anisotropy (FA). With D, D//, D? and MTR maps analysis we found demyelization evidences in corpus callosum (all the parts), left corticospinal tract, fornix, right Anterior limb of internal capsule (in patients with right-sided mesial sclerosis), Retrolenticular part of internal capsule, corona radiate, Sagittal stratum (include inferior longitidinal fasciculus and inferior fronto-occipital fasciculus), cingulum, fronto-occipital fasciculus and uncinate fasciculus. Evidences of Axonal lesion was found in Anterior limb of internal capsule, Posterior thalamic radiation (include optic radiation), right Sagittal stratum, cingulum and Uncinate fasciculus left (in in patients with left-sided mesial sclerosis). Conclusions: DTI and MTR measures demonstrate widespread clusters of abnormal in prominent white matter tracts linking mesial temporal lobe structures with other brain areas. Our results are consistent with the hypothesis that exist demyelization and axonal damage in patients with temporal lobe epilepsy.