Posttraumatic Stress Disorder

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25 Posttraumatic Stress Disorder

Kenneth Lakritz

Clinical Vignette

Friends say that John W. was never the same after he returned from the war in Iraq. He had been wounded, but seemed to recover uneventfully, was sent back for a second tour of duty, and was finally granted an honorable discharge.

His troubles began after returning home to find out that his previous civilian job had been permanently filled with no opportunity for him to return to that company. Subsequently, he was uncharacteristically passive about finding a new position. His family found him distant, preoccupied, and jittery; they joked that he would dive under the kitchen table if a car backfired. They were unaware that John’s sleep was chronically disrupted by vivid nightmares, replaying the worst of his combat experiences.

After being home a year, John had developed a chronic dependence on alcohol. Eventually, he was hospitalized for detoxification after his second arrest for drunk driving. Although Alcoholics Anonymous helped him to successfully cease drinking, his anxiety and social withdrawal proved unresponsive to treatment and he was eventually granted a disability pension.

Posttraumatic Stress Disorder is a syndrome of chronic maladaptation following unusual stress or trauma. It is characterized by persistent reexperiencing of the trauma (flashbacks and nightmares), avoidance of trauma-related stimuli, hyperarousal (excessive vigilance and insomnia), and impaired social and vocational functioning, all lasting for more than 1 month.

PTSD—initially described as “shell-shock” or “combat fatigue” —was first recognized in military veterans at least as early as World War I, when it was referred to as neurasthenia, a term that previously had a broader definition encompassing civilian as well as military experiences. In earlier versions of the Diagnostic and Statistical Manual of Mental Disorders (DSM), one could only diagnose PTSD in individuals who had suffered trauma “outside the range of usual human experience” (Fig. 25-1). However, as lesser traumas can trigger the syndrome in susceptible individuals, PTSD is relatively common, with a lifetime prevalence in the United States of 8%.

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Figure 25-1 Posttraumatic Stress Syndrome.

Clinical Presentation

Patients with PTSD often look depressed, but their neuroendocrine profile is distinct from, and in some ways nearly opposite to, that seen in depression. Typically these patients have three groups of symptoms: (1) flashbacks, which are often very fearful, frightening thoughts often occurring as night terrors or dreams; (2) withdrawal from social interactions or “avoidance,” especially of any setting that reminds one of their inciting experiences—a tendency to being emotionally numb, guilty, and anhedonic, thus losing interest in previously enjoyable activities as well as an inability to recall the precise precipitating events; (3) a constant state of hyperarousal characterized by inability to sleep well, perpetually being edgy or tense, easily startled, and prone to angry inappropriate outbursts. All of these symptoms prevent the PTSD patient from reentering society in a productive fashion after the inciting traumatic event.

Although such symptoms are normally found in any healthy individual after an acute stressful traumatic life experience, it is the chronicity of these signs that leads to a virtual emotional paralysis manifested as PTSD. Interestingly, there may be a period of normal behavior immediately following the severe trauma with the individual initially seeming to cope very well with their experiences. There may be a latency of months before the PTSD begins to take its toll on the individual’s activities of daily living.

PTSD patients typically have low serum cortisol, an enhanced response to the Dexamethasone Suppression Test, and elevated levels of corticotropin-releasing hormone. An initial response combining high catecholamine levels and low cortisol is postulated to lead to overlearning and consolidation of traumatic memories. Low baseline cortisol levels may also be a risk factor for developing PTSD. Childhood trauma, preexisting mood and anxiety disorders, dissociation after trauma, and lack of social supports are also predisposing factors.

Treatment

Most patients with PTSD require intensive, sustained, multimodal therapy. Cognitive therapy is effective, as is exposure or reimagining, and some element of exposure may be necessary.

Selective serotonin reuptake inhibitor antidepressants are a cornerstone of the pharmacotherapy of PTSD, but rarely if ever produce full remission. Commonly used adjunctive treatments include atypical antipsychotics and mood stabilizers. Low-dose cortisol, a rational attempt to remediate the typical endocrine disturbance, may also be helpful. The antiadrenergic agent prazosin appears to be especially effective in treating the nightmares and disordered sleep architecture characteristic of the disorder.

Once established, PTSD is stubborn and difficult to treat; thus effective prevention would be worthwhile. However, the previously intuitive idea of requiring trauma victims to “talk out” their experience by providing Critical Incident Debriefing or Critical Incident Stress Management after trauma exposure has not proved useful and may even increase the odds of developing PTSD. There is now some suggestive evidence that prophylactic administration of modest doses of propranolol in the days following traumatic exposure decreases the risk of developing PTSD. Therefore, the use of propranolol should be considered in emergency departments and trauma centers.

Additional Resources

Aerni A, Traber R, Hock C, et al. Low-dose cortisol for symptoms of posttraumatic stress disorder. Am J Psychiatry. 2004 Aug;161(8):1488-1490.

Davidson JRT, Rothbaum BO, van der Kolk BA, et al. Multicenter, double-blind comparison of sertraline and placebo in the treatment of posttraumatic stress disorder. Arch Gen Psychiatry. 2001;58:485-492.

Kessler RC, Sonnega A, Bromet E, et al. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry. 1995;52:1048-1060.

Koenen KC, Moffitt TE, Poulton R, et al. Early childhood factors associated with the development of post-traumatic stress disorder: results from a longitudinal birth cohort. Psychol Med. 2007;37:181-192.

McNally RJ. Psychological debriefing does not prevent posttraumatic stress disorder. Psychiatric Times. April 1, 2004. Vol. 21 No. 4

Ozer EJ, Best SR, Lipsey TL, et al. Predictors of posttraumatic stress disorder and symptoms in adults: a meta-analysis. Psychol Bull. 2003;129:52-73.

Pitman RK, Sanders KM, Zusman RM, et al. Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Am J Psychiatry. 2004 Aug;161(8):1488-1490.

Raskind MA, Peskind ER, Hoff DJ, et al. A parallel group placebo controlled study of prazosin for trauma nightmares and sleep disturbance in combat veterans with post-traumatic stress disorder. Biol Psychiatry. 2007 Apr 15;61(8):928-934.

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