Bilateral structural brain alterations are commonly identified in TLE, and not necessarily related to seizure frequency. Newly, studies have investigated the heritability as an important factor in structural alterations in TLE. There has been a search for a biomarker that proves the familial role in the TLE; therefore, quantitative MRI studies have been used to evaluate cortical alterations in their asymptomatic relatives.

We aimed to examine the heritability as a factor by analyzing cortical and subcortical measurements of first-degree asymptomatic relatives of non-familial Temporal Lobe Epilepsy (TLE) patients.

We invited fifty-eight asymptomatic first-degree relatives of sporadic TLE patients (free from neurologic diseaseand never presented seizures). Relatives were compared to sixty-nine healthy volunteers (paired for age(p=0.13) and sex (p= 0.9)). High-resolution 3D-T1 weighted images (isotropic voxels of 1 mm3) were segmented according to standard SPM12/CAT 12( protocol which included: spatial normalization [MNI-152], tissue segmentation, smoothing, and quality control of image segmentation.  Subcortical volumes (hippocampus, amygdala, caudate, pallidum, thalamus and putamen) were extracted with Freesurfer 5.3 (. Statistical comparisons of cortical maps were performed with SPM/CAT12, while clinical and subcortical data were analyzed with multivariate analyses on SPSS 23.

No differences in subcortical structures were observed between groups for any of the six structures evaluated in both hemispheres [F(5,106)=0.56; p=0.74; partial eta-squared (η2)=0.03]. However, we identified a significant reduction of cortical thickness on asymptomatic relatives compared to healthy controls in the left postcentral gyrus, bilateral parietal superior gyrus and precuneus (p<0.05, corrected with FDR).

 Areas of atrophy identified in first-degree relatives of TLE patients strongly suggest a heritable condition/trait. Further studies of brain connectivity with functional MRI and white matter with Diffusion Tensor Images may reveal subtle alterations to corroborate this hypothesis and further understanding the extension of heritability of brain abnormalities in TLE.