期刊
FRONTIERS IN NEUROLOGY
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fneur.2021.810186
关键词
gray matter density; thalamus; anterior thalamic nucleus; hippocampal-thalamic-cortical network; temporal lobe epilepsy
资金
- Ministry of Science and Technology, Taiwan [MOST 110-2221-E-038-008]
High-resolution brain MRI was used to study the disruption of the prefrontal-thalamo-hippocampal network in patients with temporal lobe epilepsy (TLE). Thalamic subfield atrophy was found to be related to changes in gray matter density in the ipsilateral inferior frontal gyrus, and this association differed between left-TLE and right-TLE.
IntroductionBrain cortico-subcortical connectivity has been investigated in epilepsy using the functional MRI (MRI). Although structural images cannot demonstrate dynamic changes, they provide higher spatial resolution, which allows exploration of the organization of brain in greater detail. MethodsWe used high-resolution brain MRI to study the hippocampal-thalamic-cortical networks in temporal lobe epilepsy (TLE) using a volume-based morphometric method. We enrolled 22 right-TLE, 33 left-TLE, and 28 age/gender-matched controls retrospectively. FreeSurfer software was used for the thalamus segmentation. ResultsAmong the 50 subfields, ipsilateral anterior, lateral, and parts of the intralaminar and medial nuclei, as well as the contralateral parts of lateral nuclei had significant volume loss in both TLE. The anteroventral nucleus was most vulnerable. Most thalamic subfields were susceptible to seizure burden, especially the left-TLE. SPM12 was used to conduct an analysis of the gray matter density (GMD) maps. Decreased extratemporal GMD occurred bilaterally. Both TLE demonstrated significant GMD loss over the ipsilateral inferior frontal gyrus, precentral gyrus, and medial orbital cortices. SignificanceThalamic subfield atrophy was related to the ipsilateral inferior frontal GMD changes, which presented positively in left-TLE and negatively in right-TLE. These findings suggest prefrontal-thalamo-hippocampal network disruption in TLE.
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