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(Drug information on 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(Drug information on 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(Drug information on 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