Abstract
The presentation and distribution of gray matter (GM) and white matter (WM) abnormalities in temporal lobe epilepsy (TLE) have been widely studied. Here, we investigated the GM and WM abnormalities in TLE patients with and without hippocampal sclerosis (HS) in five groups of participants: healthy controls (HCs) (n = 28), right TLE patients with HS (n = 26), right TLE patients without HS (n = 30), left TLE patients with HS (n = 25), and left TLE patients without HS (n = 27). We performed a flexible factorial statistical test in a whole-brain voxel-based morphometry analysis to identify significant GM and WM abnormalities and analysis of variance of hippocampal and amygdala regions among the five groups using the FreeSurfer procedure. Furthermore, we conducted multiple regression analysis to assess regional GM and WM changes with disease duration. We observed significant ipsilateral mesiotemporal GM and WM volume reductions in TLE patients with HS compared with HCs. We also observed a slight GM amygdala swelling in right TLE patients without HS. The regression analysis revealed significant negative GM and WM changes with disease duration specifically in left TLE patients with HS. The observed GM and WM abnormalities may contribute to our understanding of the root of epilepsy mechanisms.
Highlights
Temporal lobe epilepsy (TLE) is a common form of epilepsy that originates in the temporal lobes and is usually characterized by unpredictable seizures
The voxel-based morphometry (VBM) analysis revealed a significant increase in the gray matter (GM) in the right amygdala in the right TLE with no HS (RTLE-no) subjects compared with the healthy controls (HCs) (Figure 1D)
The VBM analysis showed no significant GM volume alterations in the LTLE-no group compared with the HCs or in the reverse contrast
Summary
Temporal lobe epilepsy (TLE) is a common form of epilepsy that originates in the temporal lobes and is usually characterized by unpredictable seizures. Hippocampal sclerosis (HS), as one of the most common pathological findings in TLE, is identified by neuronal cell loss in some hippocampal regions, such as the cornu ammonis 1 area (CA1) [1]. TLE patients with HS (TLE-HS) account for about 65% of TLE patients and suffer from significant neuronal cell loss and gliosis in hippocampal regions [2]. Individuals with TLE-HS experience focal seizures with impaired awareness. TLE patients without an abnormal brain structure (TLE-no) account for about 35% of all TLE patients. These individuals have very mild or absent neuronal atrophy in hippocampal regions [2]
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