Abstract
Posttraumatic stress disorder (PTSD) is a relatively common anxiety spectrum syndrome, in which memory of a triggering trauma becomes aberrantly linked to autonomic and emotional arousal. The recurrent, internally generated stress response can produce enduring behavioral and brain changes. Mechanistically, this may involve both dysregulation of the hypothalamo-pituitaryadrenal axis as well as degradation of the capacity of supramodal cortical areas to process and manage trauma-related emotional content. The optimal balance of information processing and hence behavioral reactivity shifts from the refl ective prefrontal cortex in favor of the more emotionally reactive amygdala. Trauma-focused therapies exploit adaptive neuroplasticity to decouple the memory of the trauma from the aberrant emotional and behavioral responses, in effect reconfi guring brain networks. The effect-size of such psychological therapies is generally larger than that for pharmacological treatments which are currently limited to drugs repurposed for PTSD. Nonetheless, in a signifi cant number of patients, some symptoms can be at least partially attenuated by selective serotonin reuptake inhibitors. In addition, the frequency and intensity of trauma-related nightmares can usually be lowered by adrenergic alpha-1 receptor agonists. Even as novel modalities continue to be developed, the judicious implementation of currently available evidence-based treatments for PTSD can target the underlying neurobiology, provide symptomatic relief, and promote psychosocial recovery.