Abstracts

Rationale: Recent quantitative neuroimaging studies of idiopathic generalized epilepsies (IGE) have identified diverse cortical and subcortical abnormalities. The importance of these findings is underscored by involvement of these brain regions in the onset and spread of seizures, as well as the associated cognitive and behavioral problems. However, the underlying neuroanatomical alteration specific to childhood absence epilepsy (CAE) remains unclear. This study aimed to investigate the regional alteration of cortical thickness as well as cortical and subcortical volumes associated with new onset CAE.Methods: Surface and volumetric magnetic resonance (MR) imaging data of children with newly diagnosed CAE (n = 18, 12 females) at Asan Medical Center Children’s Hospital (2007-2014) and age-matched healthy controls (n = 18) were analyzed using FreeSurfer (version 5.3.0, https://surfer.nmr.mgh.harvard.edu). A group comparison was carried out using an analysis of covariance with a value of significance set as p < 0.01.Results: Regional analysis of cortical thickness revealed significantly greater thickness of the right posterior cingulate gyrus (p = 0.004) and the left medial occipital region (p = 0.008) in CAE patients than in control. Compared to control subjects, CAE subjects had smaller volumes of cortical gray matter in the right middle frontal (p = 0.001), lateral orbitofrontal (p = 0.004), the precentral gyrus (p = 0.001), the superior (p = 0.001) and middle (p < 0.001) temporal gyri, and the left middle frontal (p = 0.009), middle (p = 0.001) and inferior (p = 0.003) temporal gyri. The regional gray matter volumes of subcortical structures and the regional white matter volumes showed no significant differences between subjects with CAE and healthy controls.Conclusions: Children with CAE demonstrated the increased thickness of the posterior medial cortices and reduced cortical gray matter volume of the bilateral frontotemporal regions. These findings can support the cortical focus theory of CAE and suggest a possible biologic basis of cognitive comorbidity in CAE.