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Diffusion tensor tractography reveals disrupted structural connectivity in childhood absence epilepsy
Kaiqing Xue1, Cheng Luo1, Dan Zhang1
1Key Laboratory for NeuroInformation of Ministry of Education, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China.
Epilepsy Research
|November 20, 2013
Summary
Childhood absence epilepsy (CAE) shows disrupted white matter (WM) networks, with reduced connectivity and efficiency, particularly in the orbitofrontal and sub-cortical regions. These structural changes may explain functional abnormalities in CAE.
Area of Science:
- Neuroscience
- Neurology
- Medical Imaging
Background:
- Brain structural connectivity underpins functional connectivity.
- Previous studies noted functional connectivity abnormalities in childhood absence epilepsy (CAE).
- Structural connectivity in CAE remains largely unexplored.
Purpose of the Study:
- To investigate white matter (WM) structural network organization in CAE.
- To test the hypothesis of disrupted structural connectivity in CAE.
- To identify specific brain regions affected by structural alterations in CAE.
Main Methods:
- Diffusion tensor imaging (DTI) tractography to map WM networks.
- Analysis of 90 cortical and sub-cortical brain regions.
- Application of graph theoretical methods to assess network topology and nodal properties in 18 CAE patients and 18 controls.
Main Results:
- CAE patients exhibited significantly decreased network connection strength, clustering coefficient, and global/local efficiency compared to controls.
- Characteristic path length was significantly increased in CAE.
- Reduced WM connections and impaired sub-networks were observed in sub-cortical, orbitofrontal, and limbic regions, correlating with epilepsy duration.
Conclusions:
- This study reveals disrupted topological organization of WM networks in CAE for the first time.
- Decreased connectivity and efficiency in specific regions provide anatomical evidence for functional abnormalities in CAE.
- The orbitofrontal sub-network may be crucial in the pathophysiology of CAE, offering new insights into absence epilepsy.
