Altered whole-brain resting-state functional connectivity and brain network topology in typhoon-related post-traumatic stress disorder

Background: Altered resting-state functional connectivity has been found in patients with post-traumatic stress disorder (PTSD). However, the alteration of resting-state functional connectivity at whole-brain level in typhoon-traumatized individuals with PTSD remains largely unknown. Objectives: To investigate changes in whole-brain resting-state functional connectivity and brain network topology in typhoon-traumatized subjects with and without PTSD. Design: Cross-sectional study. Methods: Twenty-seven patients with typhoon-related PTSD, 33 trauma-exposed controls (TEC), and 30 healthy controls (HC) underwent resting-state functional MRI scanning. The whole brain resting-state functional connectivity network was constructed based on the automated anatomical labeling atlas. The graph theory method was used to analyze the topological properties of the large-scale resting-state functional connectivity network. Whole-brain resting-state functional connectivity and the topological network property were compared by analyzing the variance. Results: There was no significant difference in the area under the curve of γ, λ, σ, global efficiency, and local efficiency among the three groups. The PTSD group showed increased dorsal cingulate cortex (dACC) resting-state functional connectivity with the postcentral gyrus (PoCG) and paracentral lobe and increased nodal betweenness centrality in the precuneus relative to both control groups. Compared with the PTSD and HC groups, the TEC group showed increased resting-state functional connectivity between the hippocampus and PoCG and increased connectivity strength in the putamen. In addition, compared with the HC group, both the PTSD and TEC groups showed increased connectivity strength and nodal efficiency in the insula. Conclusion: Aberrant resting-state functional connectivity and topology were found in all trauma-exposed individuals. These findings broaden our knowledge of the neuropathological mechanisms of PTSD.

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