Disrupted architecture of large-scale brain functional connectivity networks in patients with generalized tonic–clonic seizure

Disrupted architecture of large-scale brain functional connectivity networks in patients with... Generalized tonic–clonic seizure (GTCS) is characterized by the abnormal functional organization among distant brain regions. Previous studies in GTCS that have comprehensively examined connectivity abnormalities across the complete range of large-scale brain networks remain relatively rare. Here, we employed an amount of regions of interest to investigate the intra- and inter-connections among seven large-scale brain networks in GTCS and healthy controls. Network contingency analysis revealed that patients with GTCS exhibit significantly increased connectivity between default mode network (DMN) and frontoparietal network (FPN), between DMN and dorsal attention network, and between somatomotor network and limbic network, and decreased functional connectivity within FPN (all p values were Bonferroni corrected). Consistent with existing evidence, the disrupted functional architecture of the DMN and task-positive network may be related to self-related processes and deficits in cognitive control and attention in patients. These findings support the notion that GTCS is associated with disrupted architecture in large-scale brain networks, providing information for better understanding of the pathophysiological mechanisms of GTCS. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Applied Informatics Springer Journals

Disrupted architecture of large-scale brain functional connectivity networks in patients with generalized tonic–clonic seizure

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by The Author(s)
Subject
Computer Science; Computing Methodologies; Bioinformatics; Health Informatics; Computer Imaging, Vision, Pattern Recognition and Graphics; Computer Applications; Statistics for Life Sciences, Medicine, Health Sciences
eISSN
2196-0089
D.O.I.
10.1186/s40535-017-0045-2
Publisher site
See Article on Publisher Site

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