BACKGROUND A common feature of complex posttraumatic stress disorder (CPTSD) is impulsivity. Despite the importance of this characteristic in functional difficulties in CPTSD, little is known about its mechanisms. The… Click to show full abstract
BACKGROUND A common feature of complex posttraumatic stress disorder (CPTSD) is impulsivity. Despite the importance of this characteristic in functional difficulties in CPTSD, little is known about its mechanisms. The aim of this study was to identify the distinctive neural profile of CPTSD during attempted inhibition. METHODS The present study examined functional alterations in neural networks involved in inhibitory control across functional magnetic resonance imaging (fMRI) and electroencephalogram (EEG) paradigms in CPTSD (n = 30), PTSD (n = 40), and healthy control (n = 40) participants who completed a Go/NoGo response inhibition task during separate fMRI and EEG sessions. Brain activations were calculated during the NoGo trials relative to the baseline to evaluate response inhibition functioning. RESULTS There was reduced bilateral thalamic activation in participants with CPTSD relative to PTSD and controls during inhibition trials, but no activation differences between PTSD and controls for this brain region. There were no differences in functional connectivity between the thalamus and other regions involved in cognitive control between groups. No differences were observed between groups on EEG responses. CONCLUSIONS These findings provide initial evidence of aberrant functioning in the neurocircuitry of inhibitory control, involving the thalamus, in CPTSD. This evidence suggests that CPTSD is distinguished from PTSD by impaired neural processes implicated in response inhibition.
               
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