Posttraumatic stress disorder (PTSD) is an anxiety disorder that may develop following severe psychological trauma. The person’s immediate response to the event must involve intense fear, helplessness, or horror (or in children, disorganized or agitated behavior).1 Three symptom clusters that characterize the emergence of PTSD are reexperiencing, avoidance and numbing, and hyperarousal. Specific symptoms include flashbacks, nightmares, and feeling detached or estranged following exposure to an extremely traumatic stressful event. These symptoms usually appear within the first 3 months after the trauma, although there may be a delay of months or even years.
Terrorist attacks, such as those occurring on September 11, 2001, and combat experiences in Afghanistan and Iraq, have put many Americans at risk for long-term psychological consequences and the development of PTSD. Instead of a gradual recovery from preoccupation with whatever serious life-threatening event a person has experienced, persons with PTSD have traumatic memories with daytime recollections, recurrent nightmares, repetitive flashbacks to the original stressor, and maladaptive avoidance patterns. PTSD will develop in about 25% of persons exposed to extreme trauma, but the likelihood that symptoms will develop in an individual depends on the intensity and kind of traumatic exposure as well as on individual resilience.2 In community studies, the reported lifetime prevalence rate is about 8% for PTSD.3
Ways to prevent PTSD include keeping civilian and military populations out of harm’s way and completely eliminating emotional traumas associated with rape, violent crime, or severe accidents. Unfortunately, neither goal is possible to achieve. Therefore, we need to focus on better therapies for sufferers of acute trauma so that longstanding PTSD will develop in fewer of these individuals.
It also turns out that certain persons run a higher risk of PTSD than others. Women have twice as high a risk as men,4 and sexual and physical abuse during childhood may sensitize the nervous system, which then overreacts and perseverates when exposed to traumatic events in adulthood.5 In a 2004 literature review and discussion article, Charney6 identified 11 possible neurochemical, neuropeptide, and hormonal mediators of the psychobiologic response to extreme stress and related them to either resilience or vulnerability. The list includes cortisol, dehydroepiandrosterone, corticotropin- releasing hormone, the locus caeruleus-norepinephrine system, estrogen, neuropeptide Y, dopamine(Drug information on dopamine), serotonin, benzodiazepine receptors, and several other systems.
How little we actually know about preventing PTSD after exposure to a traumatic emotional event is illustrated by recent research that found that critical incident stress debriefing (CISD), the major intervention following 9/11, was relatively ineffective. It may even turn out that CISD, which involves a single 1-hour to 3-hour individual or group session soon after the event, allowing people to vent their emotions and relive the traumatic experience, may be more harmful than helpful. A 2003 interdisciplinary task force assembled by the American College of Neuropsychopharmacology concluded that it is possible that reliving and rehearsing raw emotion leads to consolidation of traumatic memories.7
That conclusion is supported by a 2002 meta-analysis of 7 controlled trials measuring clinical outcomes after various interventions within 1 month of various kinds of psychological trauma. This analysis found no benefit from CISD and suggested a detrimental effect when it was compared with no intervention or minimal help (30-minute counseling, education, and historical group debriefing).8 A just-updated Cochrane Review concluded: “There is no evidence that single session individual psychological debriefing is a useful treatment for the prevention of posttraumatic stress disorder after traumatic incidents. Compulsory debriefing of victims of trauma should cease. A more appropriate response could involve a 'screen and treat' model.”9
In contrast to (but theoretically consistent with) the disappointing findings from CISD, findings from a pilot study show that early intervention with an adrenergic blocking agent within a few hours after a catastrophic event is helpful.10 The logic behind this approach is based on previous research showing that epinephrine(Drug information on epinephrine), either exogenously administered or endogenously released, strengthens memory consolidation and fear conditioning. Therefore, Pitman and colleagues10 decided to try a placebo-controlled trial of the β-blocker propranolol(Drug information on propranolol) administered in an emergency department setting just after a traumatic event. They gave 40 mg orally within 6 hours of the event and then had patients continue taking 40 mg qid for the next 10 days. At 1 month, the rate of PTSD among those who took placebo was 6 (30%) of 20 compared with 2 (18%) of 11 among those who took propranolol.