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.

Smaller hippocampal volume is not a necessary risk factor for developing PTSD and does not occur within 6 months of expressing the disorder. This brain abnormality might occur in individuals with chronic or complicated PTSD.

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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.

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

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