Abstract

The triple network model provides a common framework for understanding affective and neurocognitive dysfunctions across multiple disorders, including central executive network (CEN), default mode network (DMN), and salience network (SN). Considering the effect of traumatic experience on post-traumatic stress disorder (PTSD), this study aims to explore the alteration of triple network connectivity in a specific PTSD induced by a single prolonged trauma exposure. With an arterial spin labeling sequence, three networks were first identified using independent component analysis among 10 PTSD patients and 10 healthy survivors, who experienced the same coal mining flood disaster. Then, the triple network connectivity was analyzed and compared between PTSD and non-PTSD groups. In PTSD patients, decreased connectivity was identified in left middle frontal gyrus of CEN, left precuneus and bilateral superior frontal gyrus of DMN, and right anterior insula of SN. The decreased connectivity in left middle frontal gyrus of CEN was associated with clinical severity. Furthermore, no significant connection of SN with CEN and DMN was found in PTSD patients. The decreased triple network connectivity was found in this study, which not only supports the triple network model, but also suggests a possible neurobiological mechanism for cognitive dysfunction of this type of PTSD.

Highlights

  • Increasing evidence has proved the dysfunction within CEN9, DMN10, and SN11 in post-traumatic stress disorder (PTSD)

  • In contrast to most PTSD studies focusing on subjects who experienced repeated and short-duration traumas[1], such as earthquake or abuse experience, few studies have investigated the effect of recent onset PTSD induced by a single prolonged trauma exposure

  • The present study investigated alteration of the triple network connectivity between survivors with and without recent onset PTSD from a coal mining flood disaster, using the pulsed arterial spin labeling (ASL) sequence

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Summary

Introduction

Increasing evidence has proved the dysfunction within CEN9, DMN10, and SN11 in PTSD. In our previous studies, which used structural and perfusion MRI data acquired from survivors experiencing a mining flood disaster, a series of structural and functional alterations were identified at nodes of the three ICNs, including volume deficits in left hippocampus and parahippocampal gyrus[3], cortical thinning in the left precuneus and right parahippocampal gyrus[1], and cerebral blood flow (CBF) deficits in bilateral frontal lobes and right superior frontal gyrus[16] The integration of these findings suggests possibly decreased connectivity within these ICNs, due to volume, cortical thickness, and CBF deficits. The relationship between connectivity changes and clinical symptoms was investigated

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