A Network-Based Neurobiological Model of PTSD: Evidence From Structural and Functional Neuroimaging Studies

Abstract

Purpose of review: Although a fine-grained understanding of the neurobiology of posttraumatic stress disorder (PTSD) is yet to be elucidated, the last two decades have seen a rapid growth in the study of PTSD using neuroimaging techniques. The current review summarizes important findings from functional and structural neuroimaging studies of PTSD, by primarily focusing on their relevance towards an emerging network-based neurobiological model of the disorder.

Recent findings: PTSD may be characterized by a weakly connected and hypoactive default mode network (DMN) and central executive network (CEN) that are putatively destabilized by an overactive and hyperconnected salience network (SN), which appears to have a low threshold for perceived saliency, and inefficient DMN-CEN modulation. There is considerable evidence for large-scale functional and structural network dysfunction in PTSD. Nevertheless, several limitations and gaps in the literature need to be addressed in future research.

Keywords: Central executive network; Default mode network; Functional magnetic resonance imaging; Posttraumatic stress disorder; Salience network; Structural MRI.

Figure 1. Network-based neurobiological model of PTSD

The figure shows the cortical representations of the salience network (SN; orange), default mode network (DMN; red), and central executive network (CEN; blue) in healthy individuals [16]; notable region-of-interests (ROIs) within these networks; the changes in PTSD predicted by the model; and the putative resulting phenotypic abnormalities. Alterations within and between the SN, CEN, and DMN may underlie the psychopathology of PTSD. According to this model, the SN is hyperconnected and hyperactive and has a low threshold for perceived saliency (underlying symptoms of hyperarousal), and is incapable of efficient DMN-CEN modulation (i.e. switching between task-relevant and task-irrelevant behavior); the CEN is a weakly interconnected and hypoactive (paralleling impaired cognition), and is incapable of top-down SN regulation; finally, the DMN is a weakly interconnected and hypoactive resulting in disrupted ability to maintain a calm inner state (intrusive symptoms), altered sense of self/world (dissociation), and fear generalization (avoidance; mediated by the hippocampus). * Denotes altered between-network connectivity.