Abnormalities of Cortical Thickness in Pediatric Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis

Abstract

Objective: Mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) is the most common intractable seizure type of pediatric epilepsy, with alterations in the cortex across the whole brain. The aim of this study is to investigate the abnormalities of cortical thickness in pediatric MTLE-HS. Methods: Subjects were recruited from Shenzhen Children’s Hospital between September 2015 and December 2016. MTLE was confirmed by the experienced neurological physician based on International League Against Epilepsy (ILAE) diagnosis criteria, and structural magnetic resonance imaging (MRI) was performed at 3T for quantitative assessment of cortical thickness. A general linear model with age and gender as covariates was used to examine the vertex-wise differences in cortical thickness between: 1) left MTLE-HS (LMTLE-HS) and healthy controls (HC), and 2) right MTLE-HS (RMTLE-HS) and HC. The family-wise error corrected significance threshold was set at P<0.05. Through a combination of probability and cluster-size thresholding, cluster-wise P values were obtained for the resulted clusters. Results: 13 LMTLE-HS, 6 RMTLE-HS, and 20 age-matched HC were finally enrolled into the study. No significant difference in the mean age (LMTLE-HS vs. HC, p=0.57; RMTLE-HS vs. HC, p=0.39) and gender ratio (LMTLE-HS vs. HC, p=0.24; RMTLE-HS vs. HC, p=0.72) were found between MTLE-HS and HC. In LMTLE-HS, cortical thickness was found significantly decreased in the ipsilateral caudal middle frontal gyrus (p=0.012), increased in the contralateral inferior temporal gyrus (p=0.020). In RMTLE-HS, cortical thickness significantly decreased in the ipsilateral posterior parietal lobe (superior, p<0.001 and inferior parietal gyrus, p=0.03), the anterior parietal lobe (postcentral gyrus, p=0.006), the posterior frontal lobe (precentral gyrus, p=0.04 and the lateral occipital gryus, p<0.001), and the contralateral lateral occipital gyrus, middle frontal (p<0.0001) and superior frontal gyrus (p<0.001), and pericalcarine cortex (p=0.020). Conclusion: We detected significant cortical abnormalities in pediatric MTLE-HS patients compared with HC. These cortical abnormalities could be explained by specific pathogenesis in MTLE-HS, and may finally contribute to understanding the intrinsic mechanism of MTLE-HS.