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Can Posttraumatic Stress Disorder Be Prevented?

Can Posttraumatic Stress Disorder Be Prevented?

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, 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, 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 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.

Results of this small study suggest that the hypothesis that a β-blocker may interrupt the cycle of extreme emotional arousal deserves further study. Positive findings of a subsequent study by other investigators using a slightly different protocol—40 mg of propranolol tid for 7 days followed by a taper period of 8 to 12 days—also suggested that propranolol may be useful for mitigating the development of PTSD symptoms after an initial traumatic event.11

Another possible pharmacologic approach to preventing PTSD is hinted at by the report of using low-dose cortisol to successfully treat established PTSD.12 During a 3-month observational period, 10 mg/d of cortisol was administered orally for 1 month to 3 patients with chronic PTSD in a double-blind, placebo-controlled, crossover design. In each patient, there was a significant cortisol-related reduction of at least 38% in one of the daily rated symptoms of traumatic memories, as assessed by self-administered rating scales. Clinician-administered rating scales also showed cortisol-related improvement for reexperiencing symptoms and (in 1 patient) for avoidance symptoms. Investigators demonstrated in previous work that an elevation of glucocorticoid levels inhibits memory retrieval in animals and healthy human subjects.13 As Aerni and coauthors12 point out in the more recent study, it is known that patients with chronic PTSD often have low basal cortisol levels, and the risk of subsequent PTSD is higher in persons with reduced cortisol excretion in response to a traumatic event.14

Instead of a single intervention strategy, investigators from the University of Washington School of Medicine and Harborview Injury Prevention and Research Center achieved modest success with a multifaceted disease-management, collaborativecare approach to acutely injured trauma survivors recruited from the surgical inpatient unit of a level I trauma center.15 One hundred twenty patients at high risk for PTSD were randomly assigned to the collaborative-care intervention or to a usual-care group. The collaborative-care patients received stepped care that consisted of continuous postinjury case management, motivational interviews targeting alcohol abuse/dependence, and evidence-based pharmacotherapy and/or cognitive-behavioral therapy for patients with persistent PTSD at 3 months after injury. Such early interventions resulted in significantly less symptomatic outcomes for the collaborative- care patients than the usual-care patients both in the rate of alcohol abuse/dependence (-24.2% in the collaborative-care vs +12.9% in usualcare) and in adjusted rates of change in PTSD symptoms (-4.2% for collaborative care vs +6% for usual care) 12 months after initial injury.

I conclude from these intriguing pilot studies that preventing PTSD after vulnerable persons are exposed to extreme life-threatening trauma is possible, although we are in the very early stages of knowing exactly what to do. The National Institute of Mental Health has funded at least 3 new trials, currently recruiting patients, which may provide some answers:

  • Effect of Propranolol on Preventing Post-Traumatic Stress Disorder.16
  • Behavioral Treatments for Acute Stress Disorder in Firefighters.17
  • A School Program for Children Exposed to Violence.18

Stahl19 has some interesting ideas about what else to experiment with. He suggests trying benzodiazepines or early use of selective serotonin reuptake inhibitors or serotonin-norepinephrine reuptake inhibitors to prevent the march of acute symptoms to PTSD. Corticotropin- releasing hormone blockers, or even mood stabilizers such as pregabalin (Lyrica), are other suggestions he makes for possibly calming excessively activated fear circuits. The key may be very early use, soon after the traumatic experience.

It may be that letting go of traumatic memories is sometimes better than focusing on them. To prevent the emergence of PTSD after a traumatic stressor, it may be necessary to interrupt the neuronal events that establish and perpetuate the symptoms of PTSD. Following a powerful acute stressor, the nervous system not only mediates acute symptoms of peritraumatic distress, but in vulnerable persons it seems to “over learn” and become hypervigilant and overly sensitive. Is this a place not only to try medications, but also novel forms of “desensitizing” psychotherapy and/or behavior therapy?

None of the above is to say that psychotherapy (eg, exposure treatment combined with stress inoculation; cognitive-behavioral therapy) and pharmacotherapy (eg, antidepressants, antianxiety agents, atypical antipsychotics) do not work for PTSD. These approaches often are helpful, but treatment usually is given only after PTSD is firmly established and quite difficult to treat and already causing much distress to the patient.20

Disclosures

Dr Pomerantz practices psychiatry in Longmeadow, Mass, and is assistant clinical professor of psychiatry at Harvard Medical School in Boston. He has no conflicts to report regarding the subject matter of this article.

References

References
1. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Text Revision. Washington, DC: American Psychiatric Association; 2000.
2. O’Donnell DA, Schwab-Stone ME, Muyeed AZ. Multidimensional resilience in urban children exposed to community violence. Child Dev. 2002; 73:1265-1282.
3. Kessler RC, Sonnega A, Bromet E, et al. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry. 1995; 52:1048-1060.
4. Yonkers KA, Ellison JM. Anxiety disorders in women and their pharmacological treatment. In: Jensvold MF, Halbreich U, Hamilton JA, eds. Psychopharmacology and Women. Washington DC: American Psychiatric Press; 1996:261-285.
5. Heim C, Newport DJ, Heit S, et al. Pituitary-adrenal and autonomic responses to stress in women after sexual and physical abuse in childhood. JAMA. 2000;284:592-597.
6. Charney DS. Psychobiological mechanisms of resilience and vulnerability: implications for successful adaptation to extreme stress. Am J Psychiatry. 2004;161:195-216.
7. American College of Neuropharmacology. Executive Summary. The impact of terrorism on brain and behavior: what we know and what we need to know. Available at: http://www.acnp.org/Docs/TaskForceReports/ impact_of_terrorism.pdf. Accessed February 27, 2006.
8. van Emmerik AA, Kamphuis JH, Hulsbosch AM, Emmelkamp PM. Single session debriefing after psychological trauma: a meta-analysis. Lancet. 2002; 360:766-771.
9. Rose S, Bisson J, Churchill R, Wessely S. Psychological debriefing for preventing post traumatic stress disorder (PTSD). Cochrane Database Syst Rev. 2002;(2):CD000560. Abstract available at: www.update-software.com/abstracts/ab000560.htm
10. Pitman RK, Sanders KM, Zusman RM, et al. Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biol Psychiatry. 2002;51:189-192.
11. Vaiva G, Ducrocq F, Jezequel K, et al. Immediate treatment with propranolol decreases posttraumatic stress disorder two months after trauma [published correction appears in Biol Psychiatry. 2003;54:1471]. Biol Psychiatry. 2003;54:947-949.
12. Aerni A, Traber R, Hock C, et al. Low-dose cortisol for symptoms of posttraumatic stress disorder. Am J Psychiatry. 2004;161:1488-1490.
13. de Quervain DJ, Roozendaal B, Nitsch RM, et al. Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nat Neurosci. 2000;3:313-314.
14. Yehuda R. Post-traumatic stress disorder. N Engl J Med. 2002;346:108-114.
15. Zatzick D, Roy-Byrne P, Russo J, et al. A randomized effectiveness trial of stepped collaborative care for acutely injured trauma survivors. Arch Gen Psychiatry. 2004;61:498-506.
16. Effect of propranolol on preventing posttraumatic stress disorder. Available at: http://www.clinicaltrials.gov/ct/show/NCt00158262. Accessed February 27, 2006.
17. Behavioral treatments for acute stress disorder in firefighters. Available at: http://www.clinicaltrials.gov/ct/show/ NCt00183508. Accessed February 27, 2006
18. A school program for children exposed to violence. Available at: http://www.clinicaltrials.gov/ct/show/NCt00260195. Accessed February 27, 2006.
19. Stahl SM. Is psychopharmacologic “inoculation” effective in preventing posttraumatic stress disorder? J Clin Psychiatry. 2005;66:5-6
20. Hamner MB, Robert S, Frueh BC. Treatment resistant posttraumatic stress disorder: strategies for intervention. CNS Spectr. 2004;9:740-752.

 

 
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