Kaiqing Xue1, Cheng Luo1, Dan Zhang1, Tianhua Yang2, Jianfu Li1, Diankun Gong1, Long Chen1, Yasser Iturria Medina3, Jean Gotman4, Dong Zhou2, Dezhong Yao5. 1. Key Laboratory for NeuroInformation of Ministry of Education, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China. 2. Department of Neurology, West China Hospital of Sichuan University, Chengdu, China. 3. Neuroimaging Department, Cuban Neuroscience Center, La Habana, Cuba. 4. Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada. 5. Key Laboratory for NeuroInformation of Ministry of Education, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China. Electronic address: dyao@uestc.edu.cn.
Abstract
PURPOSE: The structural connection patterns of the human brain are the underlying bases for functional connectivity. Although abnormal functional connectivity has been uncovered in childhood absence epilepsy (CAE) in previous electroencephalography and functional magnetic resonance imaging studies, little is known regarding the structural connectivity in CAE. We hypothesized that the structural connectivity would be disrupted in response to the decreased brain function in CAE. METHODS: Diffusion tensor imaging tractography was utilized to map the white matter (WM) structural network, composed of 90 cortical and sub-cortical regions, in 18 CAE and 18 age- and gender-matched healthy controls. Graph theoretical methods were applied to investigate the alterations in the topological and nodal properties of the networks in these patients. RESULTS: Both the CAE and the controls showed small-world properties in their WM networks. However, the network connection strength, absolute clustering coefficient, and global/local efficiency were significantly decreased, but characteristic path length was significantly increased in the CAE compared with the controls. Significantly decreased WM connections, nodal properties, and impaired sub-networks were found in the sub-cortical structures, orbitofrontal area, and limbic cortex in the CAE. Moreover, network connection strength, local efficiency, and nodal features in some regions were significantly negatively correlated with the duration of epilepsy. CONCLUSIONS: The present study demonstrated, for the first time, the disrupted topological organization of WM networks in CAE. The decreased connectivity and efficiency in the orbitofrontal and sub-cortical regions may serve as anatomical evidence to support the functional abnormalities related to the epileptic discharges observed in CAE. Moreover, the orbitofrontal sub-network may play a key role in CAE. These findings open up new avenues toward the understanding of absence epilepsy.
PURPOSE: The structural connection patterns of the human brain are the underlying bases for functional connectivity. Although abnormal functional connectivity has been uncovered in childhood absence epilepsy (CAE) in previous electroencephalography and functional magnetic resonance imaging studies, little is known regarding the structural connectivity in CAE. We hypothesized that the structural connectivity would be disrupted in response to the decreased brain function in CAE. METHODS: Diffusion tensor imaging tractography was utilized to map the white matter (WM) structural network, composed of 90 cortical and sub-cortical regions, in 18 CAE and 18 age- and gender-matched healthy controls. Graph theoretical methods were applied to investigate the alterations in the topological and nodal properties of the networks in these patients. RESULTS: Both the CAE and the controls showed small-world properties in their WM networks. However, the network connection strength, absolute clustering coefficient, and global/local efficiency were significantly decreased, but characteristic path length was significantly increased in the CAE compared with the controls. Significantly decreased WM connections, nodal properties, and impaired sub-networks were found in the sub-cortical structures, orbitofrontal area, and limbic cortex in the CAE. Moreover, network connection strength, local efficiency, and nodal features in some regions were significantly negatively correlated with the duration of epilepsy. CONCLUSIONS: The present study demonstrated, for the first time, the disrupted topological organization of WM networks in CAE. The decreased connectivity and efficiency in the orbitofrontal and sub-cortical regions may serve as anatomical evidence to support the functional abnormalities related to the epileptic discharges observed in CAE. Moreover, the orbitofrontal sub-network may play a key role in CAE. These findings open up new avenues toward the understanding of absence epilepsy.
Authors: Maarten J Vaessen; Jacobus F A Jansen; Hilde M H Braakman; Paul A M Hofman; Anton De Louw; Albert P Aldenkamp; Walter H Backes Journal: PLoS One Date: 2014-03-04 Impact factor: 3.240