Regional Atrophy in Temporal Lobe Epilepsy: Correlations with Cognitive Impairment

Purpose: Cognitive impairment is commonly observed in patients with Temporal Lobe Epilepsy (TLE). Recently, volumetric analysis showed widespread cortical and subcortical atrophy in patients with TLE. In this study, we hypothesized that the diffuse atrophy in TLE with and without Mesial Temporal Sclerosis (MTS) was associated with cognitive impairment. Methods: To investigate atrophy patterns in TLE, we studied 40 patients with TLE and MTS and 34 patients with TLE without MTS determined by gross visual inspection of structural Magnetic Resonance Imaging (MRI). Volumetric analysis was performed using Free Surfer software. The relationship between volume/cortical thickness and performance on neuropsychological tests was evaluated in 33 patients. Results: Whole brain volume loss and widespread sub-cortical regional atrophy was noted in both TLE with and without MTS regardless of lateralization of seizure onset. Bilateral hippocampus atrophy was seen in both TLE with and without MTS. However, hippocampal volume loss was asymmetrical with more prominent ipsilateral atrophy in the TLE patients with MTS and symmetrical bilaterally in these without MTS. Widespread neocortical thinning was noted in all TLE patients. In TLE without MTS, the cortical thinning pattern was similar in patients with left and right seizure onset. In TLE with MTS, patients with left MTS had more diffused contralateral cortical involvement compared to these with right MTS. One-to-one structural-functional association was only found in immediate and delayed memory performance in all groups. In addition to left hippocampal volume, the cortical thickness in the inferior frontal gyrus and bilateral amygdala also had additional predictive value to performance in memory tests. Conclusions: The results of this study confirmed widespread regional atrophy in the TLE patients with and without MTS. It also provided evidence that extrahippocampal atrophy (i.e., in prefrontal regions and amygdala) contributes to memory impairment in medically intractable TLE.