Altered Structural Network in Newly Onset Childhood Absence Epilepsy
10.3988/jcn.2020.16.4.573
- Author:
Eun-Hee KIM
1
;
Woo-Hyun SHIM
;
Jin-Seong LEE
;
Hee-Mang YOON
;
Tae-Sung KO
;
Mi-Sun YUM
Author Information
1. Department of Pediatrics, Sejong Chungnam National University Hospital, Chungnam National University College of Medicine, Sejong, Korea
- Publication Type:ORIGINAL ARTICLE
- From:Journal of Clinical Neurology
2020;16(4):573-580
- CountryRepublic of Korea
- Language:0
-
Abstract:
Background:and Purpose: Recent quantitative neuroimaging studies of childhood absence epilepsy (CAE) have identified various structural abnormalities that might be involved in the onset of absence seizure and associated cognitive and behavioral functions. However, the neuroanatomical alterations specific to CAE remain unclear, and so this study investigated the regional alterations of brain structures associated with newly diagnosed CAE.
Methods:Surface and volumetric magnetic resonance imaging data of patients with newly diagnosed CAE (n=18) and age-matched healthy controls (n=18) were analyzed using FreeSurfer software. A group comparison using analysis of covariance was performed with significance criteria of p<0.05 andp<0.01 in global and regional analyses, respectively.
Results:Compared with control subjects, the patients with CAE had smaller total and regional volumes of cortical gray-matter (GM) in the right rostral middle frontal, right lateral orbitofrontal, and left rostral middle frontal regions, as well as in the right precentral, right superior, middle, left middle, and inferior temporal gyri. The cortex in the right posterior cingulate gyrus and left medial occipital region was significantly thicker in patients with CAE than in controls.
Conclusions:Patients with CAE showed a reduced bilateral frontotemporal cortical GM volume and an increased posterior medial cortical thickness, which are associated with the default mode network. These structural changes can be suggested as the neural basis of the absence seizures and neuropsychiatric comorbidities in CAE.
