Major depression and PTSD are independent sequelae of traumatic events, have similar prognoses, and interact to increase distress and dysfunction. Both should be targeted by early treatment interventions and by neurobiological research.

No abstract

Differences in physiological response to startling tones develop along with PTSD in the months that follow a traumatic event. This pattern supports the theories that associate PTSD with progressive neuronal sensitization.

The use of psychometrics and clinical interviews to predict PTSD should be guided by clinical relevance and by the availability of resources.

No abstract

Early symptoms are reliable risk indicators of PTSD across events and circumstances. Converging effects of terror-induced fear, adjustment, and resiliency might explain the lack of effect of intense terrorism on the course of PTSD symptoms.

The occurrence of depression during the months that follow a traumatic event is an important mediator of chronicity in PTSD.

Prolonged exposure, CT, and delayed PE effectively prevent chronic PTSD in recent survivors. The lack of improvement from treatment with escitalopram requires further evaluation. Trauma-focused clinical interventions have no added benefit to survivors with subthreshold PTSD symptoms. Trial Registration clinicaltrials.gov Identifier: NCT00146900.