Social Buffering of Posttraumatic Stress Disorder: Longitudinal Effects and Neural Mediators

Posttraumatic stress disorder (PTSD) is a well-characterized psychiatric disorder that features changes in mood and arousal following traumatic events. Previous animal and human studies of social support during the peritraumatic window have demonstrated a buffering effect with regard to acute biological and psychological stress symptoms. Fewer studies have explored the magnitude of and mechanism through which early posttrauma social support can reduce longitudinal PTSD severity.

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 multisite AURORA study, 315 participants reported PTSD symptoms (PTSD Checklist for DSM-5) and perceived emotional support (Patient-Reported Outcomes Measurement Information System) at 2 weeks, 8 weeks, 3 months, and 6 months post emergency department visit. Additionally, neuroimaging data were collected at 2 weeks posttrauma.

We hypothesized that early posttrauma social support would be linked with greater fractional anisotropic 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 fractional anisotropy in the bilateral cingulum and bilateral uncinate fasciculus as a function of early posttrauma emotional support, we also identified greater threat reactivity in the precuneus/posterior cingulate, a component of the default mode network.

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