Social Buffering of PTSD: Longitudinal Effects and Neural Mediators.

Abstract

Background: Post-traumatic stress disorder (PTSD) is a well characterized psychiatric disorder featuring changes in mood and arousal following traumatic events. Prior animal and human studies on social support in the peri-traumatic window demonstrate a buffering effect with regards to acute biological and psychological stress symptoms. Fewer studies have explored the magnitude and mechanism on how early, post-trauma social support can reduce longitudinal PTSD severity.

Methods: In this study we investigated the beneficial impact of social support on longitudinal PTSD symptoms, and probed brain regions sensitive to this buffering phenomenon, such as the amygdala and ventromedial prefrontal cortex. In the multi-site AURORA study, n=315 participants reported PTSD symptoms (PCL-5) and perceived emotional support (PROMIS) at 2-weeks, 8-weeks, 3-months, and 6-months post-ED visit. Additionally, neuroimaging data was collected at 2 weeks post trauma.

Results: We hypothesized that early, post-trauma social support would be linked with greater fractional anisotropic (FA) values in white matter tracts that have known connectivity between the amygdala and prefrontal cortex and would predict reduced neural reactivity to social threat cues in the amygdala. Interestingly, while we observed greater FA in the bilateral cingulum and bilateral uncinate fasciculus as a function of early post-trauma emotional support, we also identified greater threat reactivity in the precuneus/posterior cingulate, a component of the default mode network.

Conclusion: Our findings suggest that the neurocircuitry underlying the response to social threat cues are facilitated through broader pathways that involve the posterior hub of the default mode network.