Early intervention for post‐traumatic stress disorder

Early Intervention in Psychiatry 2007; 1: 19–26 doi:10.1111/j.1751-7893.2007.00006.x Review Article Early intervention for post-traumatic stress disorder Richard A. Bryant Abstract Aims: The potentially debilitating effect of posttraumatic stress disorder (PTSD) has created much interest in early intervention strategies that can reduce PTSD. This review critiques the evidence for psychological debriefing approaches and alternate early intervention strategies. School of Psychology, University of New South Wales, Sydney, New South Wales, Australia Corresponding author: Dr Richard A. Bryant, School of Psychology, University of New South Wales, NSW 2052, Australia. Email: r.bryant@unsw.edu.au Received 1 November 2006; accepted 30 November 2006 Methods: The review critiques the randomized controlled trials of psychological debriefing, and early provision of cognitive behavior therapy. The latter approach involves therapy attention on acutely traumatized individuals who are high risk for PTSD Results: Psychological debriefing does not prevent PTSD. Cognitive behaviour therapy strategies have proven efficacy in reducing subsequent PTSD in ASD populations. Conclusions: Despite the promising evidence for early provision of CBT, many people do not benefit from CBT. This review concludes with consideration of major challenges facing early intervention approaches in the context of terrorist attacks and mass disasters. Key words: acute stress disorder, posttraumatic stress disorder, anxiety, trauma. INTRODUCTION Post-traumatic stress disorder (PTSD) is the major psychiatric disorder that can occur in the aftermath of exposure to a traumatic event. PTSD is characterized by re-experiencing symptoms (e.g. intrusive memories, nightmares), avoidance (e.g. avoiding reminders of the trauma) and hyperarousal (e.g. insomnia, startle response). Epidemiological studies indicate that between 60% and 90% of community populations will experience a traumatic stressor and that between 10% and 20% will develop chronic PTSD.1,2 The potential for PTSD to contribute functional impairment and adverse health outcomes has led to considerable attention on early intervention programmes that may reduce the likelihood of PTSD.3 PSYCHOLOGICAL DEBRIEFING Over the past 20 years, the most common form of early psychological intervention following trau© 2007 The Author Journal compilation © 2007 Blackwell Publishing Asia Pty Ltd development, and particularly in people with acute stress disorder (ASD). matic incidents has been psychological debriefing. The most common form of debriefing has been adaptations of critical incident stress debriefing (CISD), which was designed to reduce the adverse psychological consequences of traumatic events by limiting the intensity of acute symptoms of stress, thereby reducing the risk of subsequent psychiatric morbidity.4 According to this approach, a single debriefing session ‘will generally alleviate the acute stress responses which appear at the scene and immediately afterwards and will eliminate, or at least inhibit, delayed stress reactions’ (p. 36).4 Originally developed for emergency service personnel, it is now deemed helpful for primary victims of trauma as well.5 Debriefings now occur in businesses, schools, hospitals and in the military.6 A debriefing session ‘entails either an individual or group meeting between the rescue worker and a caring individual (facilitator) who is able to help the person talk about his feelings and reactions to the critical incident’ (p. 37).4 The session typically involves education about stress reactions, a review of the traumatic event, as well as one’s thoughts and emotional responses. 19 Early intervention for PTSD Although most people who receive debriefing report it to be helpful,5,6 there is convergent evidence that debriefing does not prevent PTSD. Rose and colleagues randomly assigned 157 adult crime victims (118 men) to either psychological debriefing, an educational intervention, or assessment only.7 The debriefing occurred for 1 h and required the participant to describe his or her traumatic experience in detail, including specifying the facts of the crime and the thoughts and feelings that occurred during it. By the 11-month assessment, all groups exhibited significant improvement over time on measures of PTSD and depression but the groups did not differ. Similar findings have been reported in other randomized controlled trials.8,9 Two studies have suggested that debriefing may impede natural recovery from trauma. Another study randomly assigned burn victims to either debriefing (n = 57) or to an assessment only control condition (n = 46).10 The debriefing session followed the CISD model and occurred between 2 and 19 days after the accident. At the 13-month assessment, however, the rate of PTSD was significantly higher among debriefed subjects than among control subjects (26% vs. 9%). Moreover, the debriefed group had significantly higher scores on self-report measures of PTSD, anxiety and depression than did the control group. In another study, victims of road traffic accidents were randomly assigned to either a single debriefing session (n = 54) or to an assessment only control condition (n = 52).11 The 1-h debriefing occurred between 24 and 48 h after the accident, involved provision of information about common emotional reactions, a review of the trauma, encouragement of emotional expression, and suggestions for gradual return to normal travel. A 3-year follow up to this study found that relative to the control group, the debriefing group was significantly more impaired on selfreported PTSD symptoms, general psychiatric symptoms, fear of travelling as a passenger, pain, physical problems and financial problems.12 Further analyses indicated that those who had initially scored high on the measure of PTSD and who were not debriefed improved markedly by the 3year follow up. However, those who had originally scored high on the PTSD measure and who were debriefed remained highly symptomatic at follow up. Therefore, debriefing appeared to impede natural recovery from acute PTSD symptoms. A major meta-analysis concluded that ‘There is no current evidence that psychological debriefing is a useful treatment for the prevention of post traumatic stress disorder after traumatic incidents. Compulsory debriefing of victims of trauma should 20 cease’ (pp. 1–2).13 Another meta-analysis indicated that trauma-exposed individuals who had not received CISD experienced reductions in PTSD symptoms, whereas those who had received CISD did not.14 THE COURSE OF POST-TRAUMATIC STRESS REACTIONS One of the problems inherent in the debriefing approach is that it presumes that all trauma survivors require assistance. There is much evidence of a broad array of stress reactions in the initial weeks after trauma exposure, including dissociative, reexperiencing, avoidance and hyperarousal symptoms.15–19 Despite the prevalence of acute stress reactions, the majority of these stress responses are transient. For example, one study has reported that whereas 94% of rape victims displayed sufficient PTSD symptoms 2 weeks post trauma to meet criteria (excluding the 1 month time requirement), this rate dropped to 47% 11 weeks later.20 Comparable patterns have been found following non-sexual,21 motor vehicle accidents,22 the September 11 terrorist attacks23,24 and the Asian tsunami.25 It appears that most people who are initially distressed gradually recover in the following months. This pattern raises issues for early intervention after trauma because there is no need for uniform interventions for all trauma survivors if the majority are progressing towards recovery. ACUTE STRESS DISORDER In recognition of the common transient stress reactions that occur after trauma exposure, DSM-IV stipulated that PTSD could only be diagnosed at least 1 month after a trauma. DSM-IV introduced the acute stress disorder (ASD) diagnosis to describe stress reactions that occur in the initial month after trauma exposure.26 One goal of the diagnosis was to describe initial traumatic stress reactions because post-traumatic stress reactions occurring in this period were not encompassed in PTSD criteria.27 A second goal was to identify people who, shortly after trauma exposure, would subsequently develop PTSD. DSM-IV stipulates that ASD can occur after a fearful response to experiencing or witnessing a threatening event (cluster A). The requisite symptoms to meet criteria for ASD include three dissociative symptoms (cluster B), one re-experiencing symptom (cluster C), marked avoidance (cluster D), marked anxiety or increased arousal (cluster E) and evidence of significant distress or impairment © 2007 The Author Journal compilation © 2007 Blackwell Publishing Asia Pty Ltd R. A. Bryant (cluster F). The disturbance must last for a minimum of 2 days and a maximum of 4 weeks (cluster G) after which time a diagnosis of PTSD should be considered. The primary difference between the criteria for ASD and PTSD is the time frame and the former’s emphasis on dissociative reactions to the trauma. ASD refers to symptoms manifested during the period from 2 days to 4 weeks post trauma, whereas PTSD can only be diagnosed from 4 weeks. A series of prospective studies of adults have prospectively assessed the relationship between ASD in the initial month after trauma, and development of subsequent PTSD.28–39 In terms of people who meet criteria for ASD, a number of studies have found that approximately three quarters of trauma survivors who display ASD subsequently develop PTSD.28–32 Compared with the expected remission of most people who display initial post-traumatic stress reactions, these studies indicate that the ASD diagnosis is performing reasonably well in predicting people who will develop PTSD. The predictive utility of the ASD diagnosis is less encouraging when one considers the proportion of people who eventually developed PTSD and who initially displayed ASD. In most studies, the minority of people who eventually developed PTSD initially met criteria for ASD.29,30,32,33,35,37–39 That is, whereas the majority of people who develop ASD are at high risk for developing subsequent PTSD, there are many other people who will develop PTSD who do not initially meet ASD criteria. It appears that a major reason for people who are at high risk for PTSD not meeting ASD criteria is the requirement that three dissociative symptoms be displayed.40 This pattern has been recently replicated in studies of children, which have also shown that the dissociative symptoms do not assist prediction of subsequent PTSD development in children.41,42 These patterns suggest that focusing early intervention strategies on people with ASD (or ASD but lacking dissociative responses) is a worthwhile goal because they are likely to develop chronic PTSD. COGNITIVE BEHAVIOUR THERAPY The major alternative approach to debriefing all trauma survivors is focusing on those individuals who are at high risk for developing PTSD. In this context, recent studies have focused on people with ASD. This approach provides treatment only after assessment and high risk is determined, and treatment does not commence until several weeks after trauma exposure. This approach is adopted because of evidence that much adaptation occurs in the © 2007 The Author Journal compilation © 2007 Blackwell Publishing Asia Pty Ltd initial weeks after exposure, and identification of high risk is more accurate when the initial distress has subsided.26 Adapting cognitive behaviour therapy (CBT) techniques with proven efficacy in treating chronic PTSD,43 recent studies have abridged these treatments to provide five sessions of therapy. The treatment components that typically constitute CBT are psychoeducation, exposure, cognitive restructuring and anxiety management. Psychoeducation involves providing information about common symptoms following a traumatic event is given during the initial treatment session. The aim is to legitimize the trauma reactions, to help the patient develop a formulation of their symptoms, and to establish a rationale for treatment. CBT may involve anxiety management techniques that aim to provide individuals with coping skills to assist them to gain a sense of mastery over their fear, to reduce arousal levels, and to assist the individual when engaging in exposure to the traumatic memories. Anxiety management approaches often include relaxation skills and breathing retraining. Prolonged imaginal exposure requires the individual to vividly imagine the trauma for prolonged periods (50 min), during which the patient provides a narrative of their traumatic experience in a way that emphasizes all relevant details, including sensory cues and affective responses. Most exposure treatments supplement imaginal exposure with in vivo exposure that involves live graded exposure to the feared trauma-related stimuli. Cognitive restructuring, which is based on considerable evidence that catastrophic appraisals contribute to the maintenance of PTSD,44 teaches patients to evaluate the evidence for negative automatic thoughts, as well as helps patients to evaluate their beliefs about the trauma, the self, the world and the future. WHAT IS THE EVIDENCE FOR CBT? In one of the early attempts at early intervention, Foa and colleagues provided brief CBT to sexual and non-sexual assault victims shortly after the assault.45 This study compared CBT (including exposure, anxiety management, in vivo exposure and cognitive restructuring) with matched participants who had received repeated assessments. Each participant received four treatment sessions, and then received assessment by blind assessors at 2 months post treatment and 5 months follow up. Whereas 10% of the CBT group met criteria for PTSD at 2 months, 70% of the control group met criteria; there were no differences between groups at 5 months, although the CBT group was less 21 Early intervention for PTSD depressed. This study suggests that CBT may accelerate natural recovery from trauma. Inferences from this study were limited, however, by the lack of random assignment. A potential limitation of these studies is that the inclusion of all recently distressed trauma survivors raises the possibility that treatment effects may overlap with natural recovery in the initial months after trauma exposure. In an attempt to overcome this problem, other studies have focused on people who meet criteria for ASD because of evidence that most people who do display ASD are at high risk for subsequent PTSD.40 In an initial study of ASD participants, Bryant and colleagues randomly allocated motor vehicle accident or non-sexual assault survivors with ASD to either CBT or Supportive Counseling.46 Both interventions consisted of five 1.5-h weekly individual therapy sessions. CBT included education about post-traumatic reactions, relaxation training, cognitive restructuring and imaginal and in vivo exposure to the traumatic event. The supportive counselling condition included trauma education and more general problem-solving skills training in the context of an unconditionally supportive relationship. At the 6month follow up, there were fewer participants in the CBT group (20%) who met diagnostic criteria for PTSD compared with supportive counselling control participants (67%). In a subsequent study that dismantled the components of CBT, 45 civilian trauma survivors with ASD were randomly allocated to five sessions of either (i) CBT (prolonged exposure, cognitive therapy, anxiety management), (ii) prolonged exposure combined with cognitive therapy, or (iii) supportive counselling.47 This study found that at 6 months follow up, PTSD was observed in approximately 20% of both active treatment groups compared with 67% of those receiving supportive counselling. A follow up of participants who completed these two treatment studies indicated that the treatment gains of those who received CBT were maintained 4 years after treatment.48 Two recent studies by the same research group have supported the utility of CBT for people with ASD. One study randomly allocated civilian trauma survivors (n = 89) with ASD to either CBT, CBT associated with hypnosis, or supportive counselling.49 This study added hypnosis to CBT because some commentators have argued that hypnosis may breach dissociative symptoms that characterize ASD.50 Furthermore, people who develop ASD are particularly adept at hypnosis.51 To this end, the hypnosis component was provided immediately prior to imaginal exposure in an attempt to facilitate emotional processing of the trauma memories. In terms 22 of treatment completers, more participants in the supportive counselling condition (57%) met PTSD criteria at 6-month follow up than those in the CBT (21%) or CBT + hypnosis (22%) condition. Interestingly, participants in the CBT + hypnosis condition reported greater reduction of re-experiencing symptoms at post-treatment than those in the CBT condition. This finding suggests that hypnosis may facilitate treatment gains in ASD participants. A follow up of this study also reported that these treatment gains were maintained 3 years after treatment.52 Finally, a recent study replicated the original Bryant et al.’s46 study with a sample of ASD participants (n = 24) who sustained mild traumatic brain injury following motor vehicle accidents.53 This study investigated the efficacy of CBT in people who lost consciousness during the trauma as a result of their traumatic injury. Consistent with the previous studies, fewer participants receiving CBT (8%) met criteria for PTSD at 6-month follow up than those receiving supportive counselling (58%). A recent adaptation of this approach was used with 152 patients attending emergency rooms who indicated elevated anxiety, depression, or post-traumatic stress with 3 weeks of injury.54 Patients were administered either 4 × 1-h sessions of CBT between 5 and 10 weeks after trauma, or a no-intervention control condition. Independent assessments conducted 13 months later found that those in the CBT condition had significantly less post-traumatic stress than those in the no-intervention condition. Another team provided a two-session CBT intervention that was intended to promote memory reconstruction in 17 survivors of accidents.55 This approach was based on the premise that facilitating people’s organization of trauma memories would assist processing of these memories about thereby assist recovery. Using an entry criterion of a heart rate higher than 94 beats per minute at admission to the emergency room,56,57 this study provided a telephone-administered protocol 1–3 days after the accident. Patients who received this intervention had greater reductions in severity of PTSD symptoms 3–4 months after the trauma than did those who received two sessions of supportive listening over the telephone. PHARMACOLOGICAL APPROACHES Biological perspectives of early intervention have focused on fear conditioning and progressive neural sensitization in the weeks after trauma as possible explanations of the genesis of PTSD.58,59 These models posit that exposure to a traumatic event © 2007 The Author Journal compilation © 2007 Blackwell Publishing Asia Pty Ltd R. A. Bryant (unconditioned stimulus) leads to a strong fear reaction (unconditioned response), which is experienced by most trauma survivors. In the following weeks and months, however, most people engage in extinction learning in which they learn that the many stimuli that were associated with trauma are no longer dangerous, and accordingly their fear reaction subside. In contrast, a minority of people develop strong conditioned responses such that when they are exposed to reminders of the trauma (conditioned stimuli), they experience strong fear reactions (conditioned response).60 It has been hypothesized that extreme sympathetic arousal at the time of a traumatic event may result in the release of stress neurochemicals (including noradrenalin and adrenalin) into the cortex, mediating an overconsolidation of trauma memories.61 Furthermore, it is possible that sensitization occurs as a result of repetitive activation by trauma reminders elevating sensitivity of limbic networks,62 and that as time progresses these responses become increasingly conditioned to trauma-related stimuli.63 In this way, PTSD responses can be regarded as failed extinction learning after the initial fear conditioning that occurs at the time of the trauma.64 Recent work has explored the possibility of preventing PTSD by limiting the consolidation of trauma memories via reduction of noradrenalin in the immediate aftermath of exposure. Pitman and colleagues have reported a pilot study that attempted to prevent PTSD by administering propranolol (a β-adrenergic blocker) within 6 h of trauma exposure;65 there is evidence that propanolol abolishes the adrenalin enhancement of conditioning.61 Although propanolol did not result in reduced PTSD relative to a placebo condition, patients receiving propanolol displayed less reactivity to trauma reminders 3 months later. A subsequent uncontrolled study found that propanolol administered shortly after trauma exposure led to reduced PTSD severity 3 months later.66 Although preliminary at this stage, these initial data point to potentially exciting pharmacological means of limiting the initial biological reactions that may contribute to PTSD development. FUTURE DIRECTIONS The modest predictive power of the ASD diagnosis has led researchers to look beyond diagnostic categories to identify acutely trauma-exposed individuals who at high risk for subsequent PTSD. For example, there is evidence that people with depression immediately after trauma exposure are more © 2007 The Author Journal compilation © 2007 Blackwell Publishing Asia Pty Ltd likely to develop subsequent PTSD.67 There have also been attempts to identify biological markers of high risk that have emerged from models that involve fear conditioning65 or sensitization of the hypothalamic-pituitary-axis in which reduced cortisol fails to contain sympathetic activity.68 In support of these proposals, there is evidence that people who eventually develop PTSD display elevated resting heart rates in the initial week after trauma.69,70 The importance of increased arousal in the acute phase is also indicated by the prevalence of panic attacks in people with ASD.71,72 There is also some evidence that lower cortisol levels are predictive of subsequent PTSD development.73,74 Despite the statistically predictive power of these biological markers, they have little practical utility because the sensitivity and specificity of these indices are very weak in correctly identifying people at high risk.75 Recent cognitive models of trauma response have proposed that the transition from acute stress reaction to chronic PTSD is mediated by people’s cognitive styles and in the ways that they manage their memories of a trauma.44 These models primarily suggest that PTSD can be explained in terms of excessively negative appraisals of the trauma and its aftermath. Consistent with this approach there is evidence that people with ASD exaggerate both the probability of future negative events occurring and the adverse effects of these events.76,77 There is also evidence that catastrophic appraisals about oneself in the immediate period after trauma exposure predict subsequent PTSD.78,79 There is also initial evidence that the attributions of responsibility for a trauma that trauma survivors make in the acute post-trauma phase influences subsequent PTSD.80,81 It should be recognized that depression is also common following trauma.82,83 Less is known about predicting depression in traumatized individuals. One prospective study has found that development of post-traumatic depression was strongly associated with a pretrauma history of depression.84 There is also evidence that post-traumatic depression is associated with psychiatric history, prior alcohol use and negative predictions about the effects of trauma.83 Finally, depressive rumination after trauma predicts longer-term depression.85 Although it is likely that many cases of depression, and particularly comorbid depression/PTSD will be detected by measures that aim to identify high risk for PTSD, there is still an important need for further prospective studies to identify early markers of those who will develop depression, as distinct from PTSD, after trauma. Although available evidence indicates that early provision of CBT facilitates adaptation after trauma 23 Early intervention for PTSD exposure, many people do not respond to treatment. Across studies, approximately 20% of participants drop out of therapy and 20% do not respond to treatment. There is a need to develop better early interventions that acutely traumatized people can tolerate and respond to. Evidence from CBT studies indicates that treatment type does not influence drop-out rates.86 Instead, individual factors appear to be the major predictors of treatment dropout, including excessive avoidance and a tendency to engage in catastrophic thinking.87 There is a need to tailor early interventions for those individuals who cannot adhere to current CBT practices.88 Furthermore, current interventions are labour-intensive and few agencies have the capacity to provide early intervention in the context of mass violence or natural disaster. In the context of terrorist threats and massive disasters, there is a need to adapt the change mechanisms that we observe in CBT to delivery modes that can meet the early intervention needs of thousands of people who may be at high risk for PTSD development. REFERENCES 1. Breslau N, Davis GC, Andreski P et al. Traumatic events and posttraumatic stress disorder in an urban population of young adults. Arch Gen Psychiatry 1991; 48: 216–22. 2. Kessler RC, Sonnega A, Bromet E et al. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995; 52: 1048–60. 3. Rapaport MH, Clary C, Fayyad R et al. Quality-of-life impairment in depressive and anxiety disorders. Am J Psychiatry 2005; 162: 1171–8. 4. Mitchell JT. When disaster strikes . . . the critical incident stress debriefing process. J Emerg Med Serv 1983; 8: 36–9. 5. Everly GS Jr, Mitchell JT. Critical Incident Stress Management (CISM): A New Era and Standard of Care in Crisis Intervention, 2nd edn. 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