Early Intervention May Prevent the Development of Posttraumatic Stress Disorder: A Randomized Pilot Civilian Study with Modified Prolonged Exposure

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia.
Biological psychiatry (Impact Factor: 10.26). 07/2012; 72(11). DOI: 10.1016/j.biopsych.2012.06.002
Source: PubMed


Posttraumatic stress disorder (PTSD) is a major public health concern with long-term sequelae. There are no accepted interventions delivered in the immediate aftermath of trauma. This study tested an early intervention aimed at modifying the memory to prevent the development of PTSD before memory consolidation.

Patients (n = 137) were randomly assigned to receive three sessions of an early intervention beginning in the emergency department compared with an assessment only control group. Posttraumatic stress reactions (PTSR) were assessed at 4 and 12 weeks postinjury and depression at baseline and week 4. The intervention consisted of modified prolonged exposure including imaginal exposure to the trauma memory, processing of traumatic material, and in vivo and imaginal exposure homework.

Patients were assessed an average of 11.79 hours posttrauma. Intervention participants reported significantly lower PTSR than the assessment group at 4 weeks postinjury, p < .01, and at 12 weeks postinjury, p < .05, and significantly lower depressive symptoms at week 4 than the assessment group, p < .05. In a subgroup analysis, the intervention was the most effective at reducing PTSD in rape victims at week 4 (p = .004) and week 12 (p = .05).

These findings suggest that the modified prolonged exposure intervention initiated within hours of the trauma in the emergency department is successful at reducing PTSR and depression symptoms 1 and 3 months after trauma exposure and is safe and feasible. This is the first behavioral intervention delivered immediately posttrauma that has been shown to be effective at reducing PTSR.

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Available from: Kerry Ressler, Sep 16, 2014
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    • "Single-session psychological debriefing [7,8] as well as multiple sessions of preventive Behavioral Therapy [9] administered within 3 months following traumatic events do not reduce distress, or prevent PTSD. Recently, a pilot study found that 3 sessions of prolonged exposure therapy administered within 2 weeks after trauma reduced post-traumatic stress reactions at 1 and 3 months post-trauma [10]. Other secondary preventive psychological interventions, such as brief Cognitive Behavioral Therapy (CBT), have yielded promising results [11,12] but can be applied only several weeks after trauma, when trauma-exposed individuals may already have developed acute PTSD. "
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    ABSTRACT: Currently few evidence based interventions are available for the prevention of PTSD within the first weeks after trauma. Increased risk for PTSD development is associated with dysregulated fear and stress responses prior to and shortly after trauma, as well as with a lack of perceived social support early after trauma. Oxytocin is a potent regulator of these processes. Therefore, we propose that oxytocin may be important in reducing adverse consequences of trauma. The 'BONDS' study is conducted in order to assess the efficacy of an early intervention with intranasal oxytocin for the prevention of PTSD. In this multicenter double-blind randomized placebo-controlled trial we will recruit 220 Emergency Department patients at increased risk of PTSD. Trauma-exposed patients are screened for increased PTSD risk with questionnaires assessing peri-traumatic distress and acute PTSD symptoms within 7 days after trauma. Baseline PTSD symptom severity scores and neuroendocrine and psychophysiological measures will be collected within 10 days after trauma. Participants will be randomized to 7.5 days of intranasal oxytocin (40 IU) or placebo twice a day. Follow-up measurements at 1.5, 3 and 6 months post-trauma are collected to assess PTSD symptom severity (the primary outcome measure). Other measures of symptoms of psychopathology, and neuroendocrine and psychophysiological disorders are secondary outcome measures. We hypothesize that intranasal oxytocin administered early after trauma is an effective pharmacological strategy to prevent PTSD in individuals at increased risk, which is both safe and easily applicable. Interindividual and contextual factors that may influence the effects of oxytocin treatment will be considered in the analysis of the results.Trial registration: Netherlands Trial Registry: NTR3190.
    Full-text · Article · Mar 2014 · BMC Psychiatry
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    • "Although many experience steady emotional recovery, a sizable percentage of these individuals (15–25%) will continue to report symptoms and eventually meet formal diagnostic criteria for PTSD (Riggs et al., 1995; Rothbaum et al., 1992). Fortunately, treatment for PTSD is highly effective for most (85%) patients (Powers, Halpern, Ferenschak, Gillihan, & Foa, 2010) and there are now pilot data showing that acute intervention may also prevent chronic PTSD (PTSD for ≥3 months) (Rothbaum et al., 2012). However, delivering interventions to all trauma survivors is not cost-effective, considering that many individuals recover without intervention (Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995; Riggs et al., 1995; Rothbaum et al., 1992), and for some, early intervention interferes with natural recovery (van Emmerik, Kamphuis, Hulsbosch, & Emmelkamp, 2002). "
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    ABSTRACT: Trauma centers are an ideal point of intervention in efforts to prevent posttraumatic stress disorder (PTSD). In order to assist in the development of prevention efforts, this study sought to identify early predictors of PTSD symptoms among adults admitted to a Level I trauma center using a novel analytic strategy (Fournier et al., 2009). Upon admission, participants (N=327) were screened for PTSD symptoms and provided information on potential predictor variables. Their PTSD symptoms were assessed again 3 months later (N=227). Participants were classified as symptomatic (positive PTSD screen) or asymptomatic (negative PTSD screen) at the follow-up assessment. Multinomial logistic regression showed that age, depression, number of premorbid psychiatric disorders, gunshot wound, auto vs. pedestrian injury, and alcohol use predicted who had PTSD symptoms at FU with 76.3% accuracy. However, when controlling for PTSD severity at baseline, only age, number of premorbid psychiatric disorders, and gunshot wounds predicted PTSD symptoms at FU but with 78.5% accuracy. These findings suggest that psychological prevention efforts in trauma centers may be best directed toward adults who are young, have premorbid psychiatric disorders, and those admitted with gunshot wounds.
    Full-text · Article · Feb 2014 · Journal of anxiety disorders
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    • "Received 24 June 2013; revised 9 January 2014; accepted 10 January 2014; accepted article preview online 14 February 2014 (Medicine, 2012), Department of Defense (2012a) and the NIMH (2008). The ability to identify persons at high risk of developing PTSD would enable providers to target evidence-based interventions to high risk groups (Rothbaum et al, 2012; Shalev et al, 2012). The identification of robust predictive biomarkers may also improve our understanding of the pathophysiology of PTSD and lead to more effective pharmacological interventions. "
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    ABSTRACT: The genetic architecture of post-traumatic stress disorder (PTSD) remains poorly understood with the vast majority of genetic association studies reporting on single candidate genes. We conducted a large genetic study in trauma exposed European American women (N=2538; 845 PTSD cases, 1693 controls) by testing 3742 SNPs across more than 300 genes and conducting polygenic analyses using results from the Psychiatric GWAS Consortium. We tested the association between each SNP and two measures of PTSD, a severity score and diagnosis. We found a significant association between PTSD (diagnosis) and SNPs (top SNP: rs363276, OR=1.4, p=2.1E-05) in SLC18A2 (vesicular monoamine transporter 2). A haplotype analysis of 9 SNPs in SLC18A2, including rs363276, identified a risk haplotype (CGGCGGAAG, p=0.0046), and the same risk haplotype was associated with PTSD in an independent cohort of trauma-exposed African Americans (p=0.049; N=748, men and women). SLC18A2 is involved in transporting monoamines to synaptic vesicles and has been implicated in a number of neuropsychiatric disorders including major depression. Eight genes previously associated with PTSD had SNPs with nominally significant associations (p<0.05). The polygenic analyses suggested that there are SNPs in common between PTSD severity and bipolar disorder. Our data are consistent with a genetic architecture for PTSD that is highly polygenic, influenced by numerous SNPs with weak effects, and may overlap with mood disorders. Genome-wide studies with very large samples sizes are needed to detectthese types of effects.Neuropsychopharmacology accepted article preview online, 14 February 2014; doi:10.1038/npp.2014.34.
    Full-text · Article · Feb 2014 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
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