<p class="first" id="d3349569e906">Neurobiological markers of future susceptibility
to posttraumatic stress disorder
(PTSD) may facilitate identification of vulnerable individuals in the early aftermath
of trauma. Variability in resting-state networks (RSNs), patterns of intrinsic functional
connectivity across the brain, has previously been linked to PTSD, and may thus be
informative of PTSD susceptibility. The present data are part of an initial analysis
from the AURORA study, a longitudinal, multisite study of adverse neuropsychiatric
sequalae. Magnetic resonance imaging (MRI) data from 109 recently (i.e., ~2 weeks)
traumatized individuals were collected and PTSD and depression symptoms were assessed
at 3 months post trauma. We assessed commonly reported RSNs including the default
mode network (DMN), central executive network (CEN), and salience network (SN). We
also identified a proposed arousal network (AN) composed of a priori brain regions
important for PTSD: the amygdala, hippocampus, mamillary bodies, midbrain, and pons.
Primary analyses assessed whether variability in functional connectivity at the 2-week
imaging timepoint predicted 3-month PTSD symptom severity. Left dorsolateral prefrontal
cortex (DLPFC) to AN connectivity at 2 weeks post trauma was negatively related to
3-month PTSD symptoms. Further, right inferior temporal gyrus (ITG) to DMN connectivity
was positively related to 3-month PTSD symptoms. Both DLPFC-AN and ITG-DMN connectivity
also predicted depression symptoms at 3 months. Our results suggest that, following
trauma exposure, acutely assessed variability in RSN connectivity was associated with
PTSD symptom severity approximately two and a half months later. However, these patterns
may reflect general susceptibility to posttraumatic dysfunction as the imaging patterns
were not linked to specific disorder symptoms, at least in the subacute/early chronic
phase. The present data suggest that assessment of RSNs in the early aftermath of
trauma may be informative of susceptibility to posttraumatic dysfunction, with future
work needed to understand neural markers of long-term (e.g., 12 months post trauma)
dysfunction. Furthermore, these findings are consistent with neural models suggesting
that decreased top-down cortico-limbic regulation and increased network-mediated fear
generalization may contribute to ongoing dysfunction in the aftermath of trauma.
</p>