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Original Article |

Treatment of Acute Stress Disorder:  A Randomized Controlled Trial FREE

Richard A. Bryant, PhD; Julie Mastrodomenico, MPsychol; Kim L. Felmingham, PhD; Sally Hopwood, MPsychol; Lucy Kenny, PhD; Eva Kandris, MPsychol; Catherine Cahill, MPsychol; Mark Creamer, PhD
[+] Author Affiliations

Author Affiliations: School of Psychology, University of New South Wales (Drs Bryant, Felmingham, and Kenny and Mss Mastrodomenico, Hopwood, Kandris, and Cahill), Sydney; and Department of Psychiatry, University of Melbourne, Melbourne (Dr Creamer), Australia.


Arch Gen Psychiatry. 2008;65(6):659-667. doi:10.1001/archpsyc.65.6.659.
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Published online

Context  Recent trauma survivors with acute stress disorder (ASD) are likely to subsequently develop chronic posttraumatic stress disorder (PTSD). Cognitive behavioral therapy for ASD may prevent PTSD, but trauma survivors may not tolerate exposure-based therapy in the acute phase. There is a need to compare nonexposure therapy techniques with prolonged exposure for ASD.

Objective  To determine the efficacy of exposure therapy or trauma-focused cognitive restructuring in preventing chronic PTSD relative to a wait-list control group.

Design, Setting, and Participants  A randomized controlled trial of civilians who experienced trauma and who met the diagnostic criteria for ASD (N = 90) seen at an outpatient clinic between March 1, 2002, and June 30, 2006.

Intervention  Patients were randomly assigned to receive 5 weekly 90-minute sessions of either imaginal and in vivo exposure (n = 30) or cognitive restructuring (n = 30), or assessment at baseline and after 6 weeks (wait-list group; n = 30).

Main Outcome Measures  Measures of PTSD at the 6-month follow-up visit by clinical interview and self-report assessments of PTSD, depression, anxiety, and trauma-related cognition.

Results  Intent-to-treat analyses indicated that at posttreatment, fewer patients in the exposure group had PTSD than those in the cognitive restructuring or wait-list groups (33% vs 63% vs 77%; P = .002). At follow-up, patients who underwent exposure therapy were more likely to not meet diagnostic criteria for PTSD than those who underwent cognitive restructuring (37% vs 63%; odds ratio, 2.10; 95% confidence interval, 1.12-3.94; P = .05) and to achieve full remission (47% vs 13%; odds ratio, 2.78; 95% confidence interval, 1.14-6.83; P = .005). On assessments of PTSD, depression, and anxiety, exposure resulted in markedly larger effect sizes at posttreatment and follow-up than cognitive restructuring.

Conclusions  Exposure-based therapy leads to greater reduction in subsequent PTSD symptoms in patients with ASD when compared with cognitive restructuring. Exposure should be used in early intervention for people who are at high risk for developing PTSD.

Figures in this Article

Posttraumatic stress disorder (PTSD) is a potentially debilitating anxiety disorder that affects at least 10% of people who experience traumatic events.1 The disorder is associated with mental and physical comorbid conditions,2 reductions in quality of life,3 and economic burden.4 In recent years, there has been much attention paid to possible early intervention strategies to prevent PTSD. There is convergent evidence that trauma-focused cognitive behavioral therapy is an efficacious treatment for PTSD.5,6 Cognitive behavioral therapy has been adapted to prevent PTSD by providing brief forms of treatment in the initial month after trauma exposure. Studies that have provided abridged cognitive behavioral therapy to people with acute symptoms have found that it can accelerate recovery.79 Other articles have focused on patients with acute stress disorder (ASD) because prospective studies demonstrate that these individuals are most likely to develop chronic PTSD.10 A series of studies has found that 5 therapy sessions comprising prolonged exposure (PE) and cognitive restructuring (CR) are efficacious in preventing PTSD in patients with ASD in the initial month after trauma exposure,1114 and these treatment gains are maintained as long as 4 years after treatment.15,16

An outstanding issue for the field of early intervention is the type of key therapeutic intervention that should be provided. All previous early interventions have included PE and CR. Some commentators have suggested that PE may not be the optimal strategy because of the distress that it elicits.17 Furthermore, there is evidence that many mental health care providers do not use exposure therapy for trauma survivors because it causes distress.18 These factors point to the need for study of the relative efficacy of exposure-based and non-exposure–based therapy for patients with ASD. The major alternative to PE is CR, which involves identification and modification of maladaptive appraisals of the traumatic event, one's response to the experience, and the future. There is much evidence that maladaptive appraisals are characteristic of ASD19,20 and are strongly predictive of subsequent PTSD.21 Moreover, CR can be effective in treating chronic PTSD.22 Accordingly, it is logical to expect that CR could be beneficial in treating ASD.

The goal of this randomized controlled trial was to conduct the first evaluation of PE vs CR in the treatment of ASD. These 2 treatment conditions were compared with a wait-list control group, in which patients were assessed at baseline and again 6 weeks later, to determine the efficacy of PE and CR relative to no treatment. Patients in the wait-list group were then offered active treatment, and patients in the PE and CR groups were subsequently assessed 6 months after treatment. We focused on patients with ASD because, although this diagnosis fails to identify many people who will develop chronic PTSD,23 most studies indicate that people who do meet criteria for ASD are likely to develop persistent PTSD.2428

PATIENTS

Participants were consecutive civilian trauma survivors who were referred to the Westmead Hospital Traumatic Stress Clinic following a nonsexual assault or motor vehicle crash between March 1, 2002, and June 30, 2006. Patients who were involved in a motor vehicle crash or nonsexual assault in the previous month and had a primary diagnosis of ASD were included in the study. Exclusion criteria included history of psychosis, organic brain syndrome, current substance dependence, borderline personality disorder, suicidal risk, inability to converse in English, or age younger than 17 or older than 70 years. Participants were initially screened by telephone, and full assessments were conducted only for participants who did not report any exclusion criteria during the telephone screening. All participants provided written informed consent approved by the Westmead Hospital Human Research Ethics Committee. The characteristics of the sample are presented in Table 1.

Table Graphic Jump LocationTable 1. Participant Characteristics
MEASURES
Diagnostic Interview

Clinical psychologists diagnosed ASD using the Acute Stress Disorder Interview.29 This structured clinical interview is based on DSM-IV criteria for ASD and contains 19 dichotomously scored items that relate to ASD symptoms. The Acute Stress Disorder Interview has high test-retest reliability (r = 0.95), sensitivity (92%), and specificity (93%).29 To ensure initial ASD assessments were conducted reliably, 25 of 145 (17%) assessments were conducted by 2 independent master’s-degree–level clinical psychologists (J.M., K.L.F., S.H., L.K., E.K., and C.C.). The interrater reliability of the 2 assessments in terms of diagnostic decision was 100%. Symptoms of PTSD were assessed using the Clinician-Administered PTSD Scale 2 (CAPS-2).30 The CAPS-2 is a structured clinical interview that assesses the 17 symptoms described in the DSM-IV PTSD criteria. The severity and frequency of each symptom during the past week are rated on a 5-point scale. The CAPS-2 was used at the baseline assessment to provide consistency with posttreatment and follow-up assessments of PTSD. Comorbid Axis I disorders were assessed by the Structured Clinical Interview for DSM-IV.31

Self-Report Assessments

Additional psychopathological assessments included the Beck Anxiety Inventory (BAI),32 the Beck Depression Inventory 2 (BDI-2),33 the Impact of Event Scale (IES),34 and the Posttraumatic Cognitions Inventory (PTCI)35 to quantify cognitive responses to trauma. The PTCI is a 36-item self-report scale that yields 3 factors: negative cognitions about self (PTCI-Self), negative cognitions about the world (PTCI-World), and self-blame (PTCI–Self-Blame).35 At the completion of session 1 and after the rationale had been explained, patients completed the Credibility/Expectancy Questionnaire.36 Specifically, patients in the PE or CR groups rated their confidence in the treatment (1, not at all confident; 10, extremely confident) and the logic of the treatment (1, not at all logical; 10, extremely logical). To obtain an estimate of verbal intelligence, participants were also administered the National Adult Reading Test before treatment.37 All assessments were administered at each session, except for the Acute Stress Disorder Interview, therapy confidence and logic ratings, and the National Adult Reading Test, which were only administered at baseline. In addition, at the completion of each therapy session, participants in the PE and CR groups were required to rate their subjective level of distress on a 100-point scale (1, not at all distressed; 100, extremely distressed).

PROCEDURE

Participants were informed that they would be randomly allocated to 1 of 3 treatment conditions. Randomization was conducted by a process of minimization stratified by sex, trauma type, and Acute Stress Disorder Interview score. Participants were assigned to groups using a random numbers system administered by an individual who worked at a site that was distant from the treatment center and was not otherwise involved with the study. Every 6 months, allocation was amended by the independent assigner to ensure that sex, trauma type, and ASD severity were balanced across conditions. If patients began taking medication after commencing treatment, they were dropped from the study to ensure that observed changes could not be attributed to medication. A total of 90 patients were randomized into the study and were allocated to either the PE (n = 30), CR (n = 30), or wait-list control (n = 30) groups (Figure 1); 69 participants (77%) completed treatment, and 42 of 60 patients in the PE and CR groups (70%) completed the 6-month follow-up assessment.

Place holder to copy figure label and caption
Figure 1.

Patient enrollment, randomization, and treatment. ASD indicates acute stress disorder.

Graphic Jump Location

Initial assessments were conducted at the pretreatment session, before randomization. Posttreatment and 6-month follow-up assessments were conducted by independent clinical psychologists (J.M., K.L.F., S.H., L.K., E.K., and C.C.) who were unaware of the participants' treatment groups. Blindness was maintained by ensuring that clinicians who conducted assessments did not have access to participants’ medical records or group allocation.

TREATMENT CONDITIONS

Individual therapy was conducted by 1 of 6 experienced master’s-degree–level clinical psychologists (J.M., K.L.F., S.H., L.K., E.K., or C.C.) who were trained to use treatment manuals and who received weekly supervision (R.A.B.). All therapists provided each type of treatment. Treatment comprised 5 once-weekly 90-minute sessions with structured daily homework activities.

Prolonged Exposure

Session 1 focused on psychoeducation, training in breathing control, the rationale of exposure, and conducting the initial imaginal exposure. The exposure exercise occurred for 50 minutes, and patients were instructed to verbalize reliving the trauma experience in a vivid manner that involved all perceptual and emotional details. Imaginal exposure was not audiotaped, but participants were given explicit instructions on how to complete the exercise. Participants engaged in imaginal exposure on a daily basis for homework. Session 2 included review of homework, introduction of in vivo exposure, and a 50-minute session of imaginal exposure. Session 3 included review of homework and completion of hierarchy for in vivo exposure. Following this session, participants completed imaginal exposure and in vivo exposure for daily homework. Session 4 included review of homework, imaginal exposure, and review of in vivo exposure. Session 5 was identical to Session 4, with the addition of relapse prevention strategies that instructed participants to rehearse the strategies learned during therapy whenever they perceived increases in PTSD symptoms.

Cognitive Restructuring

Session 1 focused on psychoeducation and the introduction of CR. Session 2 comprised identification of maladaptive thoughts about the traumatic event and the person's responses to the event and to issues occurring in the posttrauma environment; at this point, patients began monitoring automatic thoughts as daily homework. Session 3 included review of homework and CR. Cognitive restructuring involved daily monitoring of thoughts and affective states, modifying thoughts by Socratic questioning, probabilistic reasoning, and evidence-based thinking.38 The common themes of CR involved addressing catastrophic appraisals of future harm, guilt about one's behavior during the trauma, and excessive appraisals about one's capacity to cope with the stress reactions. Following this session, patients engaged in CR as daily homework. Session 4 included review of homework and more CR. Session 5 was identical to session 4, with the addition of relapse prevention strategies.

Wait-list Group

Following initial assessment, patients were informed that they would be reassessed after 6 weeks and then offered active treatment. The second assessment for this group was timed to coincide with the posttreatment assessment of the PE and CR groups.

TREATMENT FIDELITY

Of 264 therapy sessions, audiotapes of 45 (17%) were randomly selected and rated by 3 clinical psychologists experienced in cognitive behavioral therapy who were not otherwise involved with the study. Raters listened to audiotapes and determined the presence or absence of each of 34 treatment components, without regard to treatment group or session number. Raters also indicated the quality of the therapy provided on a 7-point scale (1, unacceptable; 7, very good). No PE session included CR, and no CR session included PE. The mean (SD) quality rating for treatment components in all groups was 5.8 (1.8).

DATA ANALYSIS

To determine the relative effects of the 3 treatment conditions, we performed multivariate analyses of covariance (MANCOVAs) for each of the 2 sets of continuous assessments (PTSD symptoms and associated symptoms) using the pretreatment scores as covariates. If multivariate effects of condition were significant, we conducted univariate ANCOVAs and tested differences between groups using Tukey comparisons. We report completer analyses and intent-to-treat analyses, in which we used the last observation carried forward procedure. Treatment effect sizes were between treatment conditions at posttreatment and follow-up. We derived Cohen d effect size by calculating the mean difference between assessments of each treatment condition and dividing this by the pooled standard deviation.39 We used Hedges g effect sizes to correct for variations caused by small sample sizes.40 Finally, we calculated high end-state adjustment as being below specific cutoff scores for PTSD, depression, and anxiety scales at the follow-up assessment. We adopted a conservative estimate of good end-state adjustment for PTSD by following an established cutoff score of 19 on the CAPS-2 (combining frequency and intensity scores) to indicate the absence of PTSD,41 a cutoff of 10 on the BDI-2,42 and a cutoff of 12 on the BAI.43 To estimate the number of patients required in the PE group for 1 patient to achieve a response outcome that would not have been achieved with CR, we calculated the number of patients needed to treat as 1 divided by the proportion responding to PE. Efficacious treatments typically have a number needed to treat between 2 and 4.44

PRELIMINARY ANALYSES

Planned comparisons of treatment completers and treatment dropouts indicated no differences between those who did and did not drop out of treatment on any pretreatment psychopathological or demographic variables. There were 5 reported adverse effects; 3 patients became overly distressed during exposure therapy and 2 dropped out of treatment. In addition, 2 patients dropped out of CR because they became distressed during CR sessions.

TREATMENT COMPLETER ANALYSIS

Table 2 presents the mean psychopathological assessment scores for the completer sample. The MANCOVA for posttreatment scores of PTSD symptoms indicated a significant main effect (F6,122 = 6.00; P<.001). Follow-up ANCOVAs indicated main effects for CAPS-2 (F2,62 = 12.58; P<.001), IES-Intrusions (F2,62 = 13.54; P<.001), and IES-Avoidance (F2,62 = 10.29; P<.001). Post hoc Tukey comparisons indicated that patients in the PE group scored lower than patients in the wait-list group on CAPS-2 (P<.001), IES-Intrusions (P=.002), and IES-avoidance (P<.001). Furthermore, patients in the PE group scored lower than patients in the CR group on IES-Intrusions (P=.03). Patients in the CR group did not differ from the wait-list group on any variable. The MANCOVA for posttreatment scores of associated symptoms indicated a significant main effect (F10,116 = 2.76; P=.003). Follow-up ANCOVAs indicated main effects for the BDI-2 (F2,61 = 4.68; P=.02), BAI (F2,61 = 5.59; P=.003), PTCI-Self (F2,61 = 5.79; P=.002), PTCI-World (F2,61 = 3.53; P=.04), and PTCI–Self-Blame (F2,61 = 3.82; P=.04). Post hoc Tukey comparisons indicated that patients in the PE group–scored lower than patients in the wait-list group on the BDI-2 (P=.03), BAI (P=.03), PTCI-Self (P=.008), and PTCI–Self-Blame (P=.03). Furthermore, patients in the PE group scored lower than patients in the CR group on the BDI-2 (P=.03) and BAI (P=.007). Patients in the CR group did not differ from those in the wait-list group on any variable. In follow-up analyses, the MANCOVA for PTSD symptoms indicated a significant main effect (F3,34 = 2.88; P=.04). Follow-up ANCOVAs indicated main effects for CAPS-2 (F1,36 = 8.42; P=.006), IES-Intrusions (F1,36 = 6.56; P=.02), and IES-Avoidance (F1,36 = 6.51; P=.008). Post hoc Tukey comparisons indicated that patients in the PE group scored lower than patients in the CR group on CAPS-2 (P=.007), IES-Intrusions (P=.007), and IES-Avoidance (P=.009). The MANCOVA for follow-up scores of associated symptoms indicated a nonsignificant main effect (F5,49 = 1.22; P = .31).

Table Graphic Jump LocationTable 2. Psychopathological Assessments for Intent-to-Treat and Completer Analysesa

At posttreatment, fewer patients in the PE group (3 [12%]) met criteria for PTSD than patients in the CR (12 [52%]) (χ24 = 9.00; odds ratio [OR], 8.00; 95% confidence interval [CI], 1.86-34.36; P=.003) or wait-list (15 [71%]) (χ245 = 15.90; OR, 17.11; 95% CI, 3.67-76.76; P<.001) group. At follow-up, fewer participants in the PE group (3 [14%]) met criteria for PTSD than in the CR group (9 [47%]) (χ241 = 5.60; OR, 5.70; 95% CI, 1.25-25.91; P=.02). In terms of follow-up status, the number needed to treat was 2.96.

Table 3 shows effect sizes for PTSD and other psychopathological assessment scores between treatment groups. According to Cohen's descriptors of effect sizes, effect sizes where d is greater than 0.80 are large.39 Among completers, PE achieved large effect sizes and CR achieved moderate effect sizes relative to the wait-list group at posttreatment on most assessments. At follow-up, the PE group achieved large effect sizes relative to the CR group for PTSD symptoms. In addition, nearly 3 times as many participants in the PE group (14 [61%]) as in the CR group (4 [21%]) achieved high end-state functioning at follow-up (χ232 = 5.04; OR, 5.76; 95% CI, 1.17-8.25; P = .05).

Table Graphic Jump LocationTable 3. Effect Sizes on Outcome Measures for Intent-to-Treat and Completer Analyses
DISTRESS RATINGS

Figure 2 presents the mean distress ratings reported by participants in the PE and CR groups at the beginning of each therapy session. A 2 (treatment condition) × 5 (session) repeated-measures analysis of variance indicated significant main effects for treatment condition (F1,46 = 14.52; P<.001), session (F4,43 = 16.62; P<.001), and a significant interaction effect (F4,43 = 3.72; P=.04). Specifically, patients in the PE group reported lower distress ratings than patients in the CR group at the completion of session 3 (P=.002), session 4 (P<.001), and session 5 (P=.003).

Place holder to copy figure label and caption
Figure 2.

Changes in total scores on the Clinician-Administered Posttraumatic Stress Disorder Scale 2 (CAPS-2) for intent-to-treat analysis. Standard errors are displayed in error bars.

Graphic Jump Location
INTENT-TO-TREAT ANALYSES

Table 2 and Figure 3 also present the mean psychopathological scores for the intent-to-treat sample. The MANCOVA for posttreatment scores of PTSD symptoms indicated a significant main effect (F6,164 = 4.29; P<.001). Follow-up analyses of covariance indicated main effects for CAPS-2 (F2,83 = 12.62; P<.001), IES-Intrusions (F2,83 = 11.34; P<.001), and IES-Avoidance (F2,83 = 10.02; P<.001). Post hoc Tukey comparisons indicated that patients in the PE group scored lower than those in the wait-list group on CAPS-2 (P<.001), IES-Intrusions (P=.001), and IES-Avoidance (P<.001). Patients in the CR group did not differ from patients in the wait-list group on any variable. The MANCOVA for posttreatment scores of associated symptoms indicated a significant main effect (F10,158 = 2.53; P=.009). Follow-up ANCOVAs indicated main effects for the BDI-2 (F2,82 = 7.21; P<.001), BAI (F2,82 = 5.85; P=.003), PTCI-Self (F2,82 = 8.56, P<.001), PTCI-World (F2,82 = 4.09; P=.03), and PTCI–Self-Blame (F2,82 = 3.15; P=.04). Post hoc Tukey comparisons indicated that patients in the PE group scored lower than those in the wait-list group on the BDI-2 (P=.003), BAI (P=.004), PTCI-Self (P=.009), and PTCI–Self-Blame (P=.03). Furthermore, patients in the PE group scored lower than patients in the CR group on the BAI (P=.008). Patients in the CR group did not differ from patients in the wait-list group on any variable.

Place holder to copy figure label and caption
Figure 3.

Mean distress ratings for each session as a function of treatment group for treatment completers. Standard errors are displayed in error bars.

Graphic Jump Location

In terms of follow-up analyses, the MANCOVA for PTSD symptoms indicated a significant main effect (F3,34 = 2.88; P=.04). Follow-up ANCOVAs indicated main effects for CAPS-2 (F1,36 = 8.42; P=.006), IES-Intrusions (F1,36 = 6.56; P=.008), and IES-Avoidance (F1,36 = 6.51; P=.0081). Post hoc Tukey comparisons indicated that patients in the PE group scored lower than patients in the CR group on CAPS-2 (P=.03), IES-Intrusions (P=.02), and IES-Avoidance (P=.03). The MANCOVA for follow-up scores of associated symptoms indicated a nonsignificant main effect (F5,49 = 1.22; P = .31).

The last observation carried forward method presumes that participants who drop out remain unchanged and that their pretreatment values are relevant indicators of posttreatment symptom levels. This approach is potentially problematic with ASD because of the documented tendency for symptoms to abate over time.10 The tendency for more patients in the wait-list group to drop out vs other participants may provide an overestimation of the efficacy of the active treatments at posttreatment using the last observation carried forward method. Accordingly, we conducted an additional analysis that presumed all noncompleters in all groups improved as much as completers in the wait-list group and repeated the analyses in this subsection on CAPS-2 and IES scores. On the basis that wait-list completers improved 0.6 SD of their initial CAPS-2 scores and 0.09 SD of their initial IES scores, we calculated these rates of recovery for all noncompleters. The ANCOVAs for posttreatment scores indicated significant effects for CAPS-2 (F2,82 = 12.92; P<.001), IES-Intrusions (F2,86 = 11.84; P<.001), and IES-Avoidance (F2,86 = 17.06; P<.001). Post hoc Tukey comparisons indicated that patients in the PE group scored lower than patients in the wait-list group on CAPS-2 (P<.001), IES-Intrusions (P<.002), and IES-Avoidance (P<.001). Patients in the CR group scored lower than patients in the wait-list group on CAPS-2 (P=.03). These results confirm the finding that PE, and to a lesser extent CR, resulted in greater symptom reduction than in the wait-list group.

Intent-to-treat analyses indicated that at posttreatment fewer patients in the PE group (10 [33%]) met criteria for PTSD than patients in the CR (19 [63%]) (χ260 = 9.78; P = .002; OR, 2.52; 95% CI, 1.28-4.93] or wait list (23 [77%]) (χ260 = 18.49; OR, 3.40; 95% CI, 1.73-6.67; P<.001) group. At follow-up, fewer patients in the PE group (11 [37%]) met criteria for PTSD than patients in the CR group (19 [63%]) (χ260 = 6.78; OR, 2.10; 95% CI, 1.12-3.94); P=.007. In terms of follow-up status, the number needed to treat was 3.75.

Table 3 demonstrates that PE led to larger effect sizes than CR for intent-to-treat and analyses at posttreatment. It should be noted that CR achieved a moderate effect size for most assessments relative to the wait-list group. At follow-up, PE resulted in moderate effect sizes relative to CR on all measures for intent-to-treat analyses. Nearly 4 times as many participants in the PE group (14 [47%]) as in the CR group (4 [13%]) achieved high end-state functioning at follow-up (χ260 = 7.94; OR, 2.78; 95% CI, 1.14-6.83; P = .005).

This study demonstrates that PE is a more efficacious intervention to prevent chronic PTSD than CR in patients with ASD. Six months after treatment, PE led to greater reductions than CR across PTSD symptoms as measured by independent clinical interviews, as well as self-report assessments of intrusive and avoidance symptoms. Moreover, at follow-up, nearly 4 times as many patients who received PE achieved high end-state functioning compared with those who received CR. Effect sizes for the PE group typically were double those of the CR group relative to the wait-list group. The pattern persisted at follow-up, when PE resulted in moderate effect sizes relative to CR. This suggests that PE probably accounted for many of the therapy gains in previous studies of cognitive behavioral therapy for patients with ASD. We note, however, that the present study compared PE with CR and did not allow for a comparison against the additive effects of PE and CR.

Despite some concerns that patients may not be able to manage the distress elicited by PE,19 there was no difference in drop-out rates for the PE and CR groups (17% vs 23%). The average drop-out rate for PE in PTSD studies was 20.5%, compared with 22.1% for CR.45 Therefore, the drop-out rates in the present study were comparable to drop-out rates across chronic PTSD treatment studies.

Why would PE result in better outcomes than CR? It has been suggested that PE includes habituations of anxiety triggered by the memory, correction of the belief that anxiety only reduces through avoidance, integration of corrective information into the trauma memory, and self-mastery through management of the exposure exercise,46,47 whereas CR involves correction of maladaptive appraisals about the trauma and its aftermath, and it is proposed that adapting more appropriate interpretations about the traumatic experience will enhance recovery.48 The current findings suggest that direct activation of trauma memories is particularly useful for prevention of PTSD symptoms in patients with ASD. This interpretation is in accordance with network models of PTSD that posit that adaptation occurs when the individual repeatedly engages with trauma reminders and learns that there is no aversive outcome.49

The finding that distress ratings were more reduced in the PE group vs the CR group after session 3 supports the hypothesis that patients experienced a marked reduction in distress after PE began. Exposure exercises began in session 2, which is also when patients were first assigned homework exercises. It appears that this resulted in reduced distress at the following session; in contrast, patients in the CR group continued to experience significant distress. This pattern underscores the conclusion posited by network models of PTSD that successful treatment of PTSD requires activation of fear memories and that treatment response is reflected in between-session habituation of distress.50

We note several limitations to this study. First, our sample was limited to survivors of motor vehicle crashes and nonsexual assaults, and it is questionable whether the findings are generalizable to other traumatized populations. Second, we note that traumatic events can lead to a broad range of psychiatric disorders.51 We did not assess for Axis I disorders at posttreatment or follow-up assessments, and accordingly we did not examine the influence of therapy on other psychiatric disorders; we also did not record medication use in the period after treatment. Third, we note that using the last observation carried forward method for managing missing data at follow-up is problematic because it may bias the data in unpredictable ways.52 We note, however, that completer analysis replicated the findings observed in the intent-to-treat analyses. Fourth, we did not require participants to record time spent on homework, and it is difficult to determine whether differential amounts of homework time contributed to outcomes. Finally, we did not assess functioning, and so we were not able to test the influence of treatment of functional levels.

We also note that our use of PE and CR was specific to the current research study, and there are differences in how PE and CR are used in different centers. To maintain the integrity of the research design, we did not permit the CR condition to include any exposure-based activities. It is worth noting that although this approach is consistent with traditional CR,37 more recent adaptations of cognitive therapy for PTSD have explicitly integrated reliving of trauma memories into the cognitive therapy programs.53 We note that although our completion rate of 77% is comparable to numerous studies, it is lower than that reported by one previous study; this study used briefer exposure periods integrated with CR, which may have resulted in greater treatment adherence.53 Similarly, PE protocols often stipulate that exposure should be followed by a discussion of the thoughts that arose during the exposure.54 Although the present study dictated that the therapist should discuss the patient's reactions to the exposure exercises, the PE manual precluded therapists from explicitly discussing the relationship of thoughts to feelings because this would have diluted the distinction between PE and CR. This adherence to each strategy may have resulted in the treatment gains made by patients being reduced relative to other treatment programs that have included components of both PE and CR in the therapy program. In this context, it is worth noting that cognitive change as measured by the PTCI was no greater following CR than PE.

It should also be noted that CR was efficacious at posttreatment and follow-up assessments. This finding is expected because of evidence that CR does reduce chronic PTSD symptoms.24 Although CR was a less effective intervention than PE, we recognize that it does provide an alternate early intervention for patients who are unsuitable for PE or unwilling to participate. Considering that maladaptive appraisals in the acute phase have been shown to be pivotal in the development of ASD,19,20 and to maintaining chronic PTSD,21 it may be useful to provide CR to patients in the acute phase to prevent subsequent PTSD.

In summary, these data provide the first evidence that PE is the more efficacious intervention for ASD shortly after trauma. The present study suggests that although CR is a useful early intervention for preventing PTSD, exposure-based therapy is likely to lead to better outcomes. Surveys highlight that many mental health care providers do not use PE for patients who have experienced trauma, apparently because of concerns that they may elicit aversive reactions.18 This study demonstrates that PE does not lead to greater drop-out rates or aversive responses than CR. Accordingly, there is a need to better educate mental health care providers about the use of PE as a frontline intervention for ASD.

Correspondence: Richard A. Bryant, PhD, School of Psychology, University of New South Wales, Sydney, New South Wales 2052, Australia (R.Bryant@unsw.edu.au).

Submitted for Publication: August 21, 2007; final revision received December 9, 2007; accepted December 10, 2007.

Author Contributions: Dr Bryant has had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Funding/Support: This research was supported by grant 300304 from the National Health and Medical Research Council Program, Canberra, Australia (Drs Bryant and Creamer).

Role of the Sponsor: The study sponsor had no role in the design and conduct of the study; in the collection, analysis, and interpretation of the data; or in the preparation, review, or approval of the manuscript.

Financial Disclosure: None reported.

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Magruder  KMFrueh  BCKnapp  RGJohnson  MRVaughan  JA  IIICarson  TCPowell  DAHebert  R PTSD symptoms, demographic characteristics, and functional status among veterans treated in VA primary care clinics. J Trauma Stress 2004;17 (4) 293- 301
PubMed Link to Article
Greenberg  PESisitsky  TKessler  RCFinkelstein  SNBerndt  ERDavidson  JRBallenger  JCFyer  AJ The economic burden of anxiety disorders in the 1990s. J Clin Psychiatry 1999;60 (7) 427- 435
PubMed Link to Article
Harvey  AGBryant  RATarrier  N Cognitive behaviour therapy of posttraumatic stress disorder. Clin Psychol Rev 2003;23 (3) 501- 522
PubMed Link to Article
Foa  EBMeadows  EA Psychosocial treatments for posttraumatic stress disorder: a critical review. Annu Rev Psychol 1997;48449- 480
PubMed Link to Article
Foa  EBHearst-Ikeda  DPerry  KJ Evaluation of a brief cognitive-behavioral program for the prevention of chronic PTSD in recent assault victims. J Consult Clin Psychol 1995;63 (6) 948- 955
PubMed Link to Article
Foa  EBZoelner  LAFeeny  NC An evaluation of three brief programs for facilitating recovery after assault. J Trauma Stress 2006;19 (1) 29- 43
PubMed Link to Article
Bisson  JIShepherd  JPJoy  DProbert  RNewcombe  RG Early cognitive-behavioural therapy for post-traumatic stress symptoms after physical injury: randomised controlled trial. Br J Psychiatry 2004;18463- 69
PubMed Link to Article
Bryant  RA Early predictors of posttraumatic stress disorder. Biol Psychiatry 2003;53 (9) 789- 795
PubMed Link to Article
Bryant  RAHarvey  AGSackville  TDang  SBasten  C Treatment of acute stress disorder: a comparison of cognitive-behavioral therapy and supportive counseling. J Consult Clin Psychol 1998;66 (5) 862- 866
PubMed Link to Article
Bryant  RASackville  TDang  STMoulds  MGuthrie  R Treating acute stress disorder: an evaluation of cognitive behavior therapy and counseling techniques. Am J Psychiatry 1999;156 (11) 1780- 1786
PubMed
Bryant  RAMoulds  MLGuthrie  RNixon  RD Treating acute stress disorder after mild brain injury. Am J Psychiatry 2003;160 (3) 585- 587
PubMed Link to Article
Bryant  RAMoulds  MGuthrie  RMNixon  RD The additive benefit of hypnosis and cognitive behavior therapy in treating acute stress disorder. J Consult Clin Psychol 2005;73 (2) 334- 340
PubMed Link to Article
Bryant  RAMoulds  MANixon  R Cognitive behaviour therapy of acute stress disorder: a four-year follow-up. Behav Res Ther 2003;41 (4) 489- 494
PubMed Link to Article
Bryant  RAMoulds  MLNixon  RVMastrodomenico  JFelmingham  KHopwood  S Hypnotherapy and cognitive behaviour therapy of acute stress disorder: a three-year follow-up. Behav Res Ther 2006;44 (9) 1331- 1335
PubMed Link to Article
Kilpatrick  DGBest  CL Some cautionary remarks on treating sexual assault victims with implosion. Behav Ther 1984;15421- 423
Link to Article
Rosen  CSChow  HCFinney  JFGreenbaum  MAMoos  RHSheikh  JIYesavage  JA Practice guidelines and VA practice patterns for treating posttraumatic stress disorder. J Trauma Stress 2004;17 (3) 213- 222
PubMed Link to Article
Warda  GBryant  RA Cognitive bias in acute stress disorder. Behav Res Ther 1998;36 (12) 1177- 1183
PubMed Link to Article
Smith  KBryant  RA The generality of cognitive bias in acute stress disorder. Behav Res Ther 2000;38 (7) 709- 715
PubMed Link to Article
Ehlers  AMayou  RABryant  B Psychological predictors of chronic PTSD after motor vehicle accidents. J Abnorm Psychol 1998;107 (3) 508- 519
PubMed Link to Article
Tarrier  NPilgrim  HSommerfield  CFaragher  BReynolds  MGraham  EBarrowclough  C A randomized trial of cognitive therapy and imaginal exposure in the treatment of chronic posttraumatic stress disorder. J Consult Clin Psychol 1999;67 (1) 13- 18
PubMed Link to Article
Harvey  AGBryant  RA Acute stress disorder: a synthesis and critique. Psychol Bull 2002;128 (6) 886- 902
PubMed Link to Article
Harvey  AGBryant  RA Relationship of acute stress disorder and posttraumatic stress disorder following motor vehicle accidents. J Consult Clin Psychol 1998;66 (3) 507- 512
PubMed Link to Article
Bryant  RAHarvey  AG Relationship of acute stress disorder and posttraumatic stress disorder following mild traumatic brain injury. Am J Psychiatry 1998;155 (5) 625- 629
PubMed
Brewin  CRAndrews  BRose  SKirk  M Acute stress disorder and posttraumatic stress disorder in victims of violent crime. Am J Psychiatry 1999;156 (3) 360- 365
PubMed
Harvey  AGBryant  RA Relationship of acute stress disorder and posttraumatic stress disorder: a two-year prospective study. J Consult Clin Psychol 1999;67 (6) 985- 988
PubMed Link to Article
Harvey  AGBryant  RA A two-year prospective evaluation of the relationship between acute stress disorder and posttraumatic stress disorder following mild traumatic brain injury. Am J Psychiatry 2000;157 (4) 626- 628
PubMed Link to Article
Bryant  RAHarvey  AGDang  SSackville  T Assessing acute stress disorder: psychometric properties of a structured clinical interview. Psychol Assess 1998;10215- 220
Link to Article
Blake  DDWeathers  FWNagy  LMKaloupek  DGGusman  FDCharney  DSKeane  TM The development of a Clinician-Administered PTSD scale. J Trauma Stress 1995;8 (1) 75- 90
PubMed Link to Article
Spitzer  RLGibbon  MWilliams  JBW Structured Clinical Interview for DSM-IV Axis I Disorders.  New York NY State Psychiatric Institute, Biometrics Research Department1996;
Beck  ATSteer  RA Beck Anxiety Inventory Manual.  San Antonio, TX Psychological Corporation1990;
Beck  ATSteer  RABrown  GK Beck Anxiety Inventory Manual. 2nd ed.  San Antonio, TX Psychological Corporation1996;
Horowitz  MWilner  NAlvarez  W The Impact of Event Scale: a measure of subjective stress. Psychosom Med 1979;41 (3) 209- 218
PubMed Link to Article
Foa  EBEhlers  AClark  DMTolin  DFOrsillo  SM The Posttraumatic Cognitions Inventory (PTCI): development and validation. Psychol Assess 1999;11303- 314
Link to Article
Deviliya  GJBorkovecb  TD Psychometric properties of the credibility/expectancy questionnaire. J Behav Ther Exp Psychiatry 2000;31 (2) 73- 86
PubMed Link to Article
Nelson  HE National Adult Reading Test (NART): Test Manual.  Windsor, England NFER-Nelson1982;
Beck  ATRush  AJShaw  BFEmery  G Cognitive Therapy of Depression.  New York, NY Guilford Press1979;
Cohen  J Statistical Power Analysis for the Behavioral Sciences.  New York, NY Academic Press1988;
Hedges  LV Estimation of effect size from a series of independent experiments. Psychol Bull 1982;92490- 499
Link to Article
Weathers  FWKeane  TMDavidson  JRT Clinician-Administered PTSD Scale: a review of the first ten years of research. Depress Anxiety 2001;13 (3) 132- 156
PubMed Link to Article
Kendall  PCHollon  SDBeck  ATHammen  CLIngram  RE Issues and recommendations regarding use of the Beck Depression Inventory. Cognit Ther Res 1987;11 (3) 289- 299
Link to Article
Foa  EBDancu  CVHembree  EAJaycox  LHMeadows  EAStreet  GP A comparison of exposure therapy, stress inoculation training, and their combination for reducing posttraumatic stress disorder in female assault victims. J Consult Clin Psychol 1999;67 (2) 194- 200
PubMed Link to Article
Chatellier  GZapletal  ELemaitre  DMenard  JGoulet  P The number needed to treat: a clinically useful monogram in its proper context. BMJ 1996;312 (7028) 426- 429
PubMed Link to Article
Hembree  EAFoa  EBDorfan  NMStreet  GPLowalski  JTu  X Do patients drop out prematurely from exposure therapy for PTSD? J Trauma Stress 2003;16 (6) 555- 562
PubMed Link to Article
Jaycox  LHFoa  EB Obstacles in implementing exposure therapy for PTSD: case discussions and practical solutions. Clin Psychol Psychother 1998;3 (3) 176- 184
Link to Article
Rothbaum  BOSchwartz  AC Exposure therapy for posttraumatic stress disorder. Am J Psychother 2002;56 (1) 59- 75
PubMed
Ehlers  AClark  D A cognitive model of posttraumatic stress disorder. Behav Res Ther 2000;38 (4) 319- 345
PubMed Link to Article
Foa  EBKozak  MJ Emotional processing of fear: exposure to corrective information. Psychol Bull 1986;99 (1) 20- 35
PubMed Link to Article
van Minnen  AFoa  EB The effect of imaginal exposure length on outcome of treatment for PTSD. J Trauma Stress 2006;19 (4) 427- 438
PubMed Link to Article
North  CSNixon  SJShariat  SMallonee  S McMillen  JCSpitznagel  ELSmith  EM Psychiatric disorders among survivors of the Oklahoma City bombing. JAMA 1999;282 (8) 755- 762
PubMed Link to Article
Mazumdar  SLiu  KSHouck  PRReynolds  CF Intent-to-treat analysis for longitudinal clinical trials: coping with the challenge of missing values. J Psychiatr Res 1999;33 (2) 87- 95
PubMed Link to Article
Ehlers  AClark  DMHackmann  A McManus  FFennell  MHerbert  CMayou  RA A randomized controlled trial of cognitive therapy, self-help, and repeated assessment as early interventions for PTSD. Arch Gen Psychiatry 2003;60 (10) 1024- 1032
PubMed Link to Article
Riggs  DSCahill  SPFoa  EB Prolonged exposure treatment of posttraumatic stress disorder. Follette  VMRuzek  JICognitive-Behavioral Therapies for Trauma. New York, NY Guilford2006;65- 95

Figures

Place holder to copy figure label and caption
Figure 1.

Patient enrollment, randomization, and treatment. ASD indicates acute stress disorder.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

Changes in total scores on the Clinician-Administered Posttraumatic Stress Disorder Scale 2 (CAPS-2) for intent-to-treat analysis. Standard errors are displayed in error bars.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 3.

Mean distress ratings for each session as a function of treatment group for treatment completers. Standard errors are displayed in error bars.

Graphic Jump Location

Tables

Table Graphic Jump LocationTable 1. Participant Characteristics
Table Graphic Jump LocationTable 2. Psychopathological Assessments for Intent-to-Treat and Completer Analysesa
Table Graphic Jump LocationTable 3. Effect Sizes on Outcome Measures for Intent-to-Treat and Completer Analyses

References

Kessler  RCSonnega  ABromet  EHughes  MNelson  CB Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995;52 (12) 1048- 1060
PubMed Link to Article
Brunello  NDavidson  JRDeahl  MKessler  RCMendlewicz  JRacagni  GShalev  AYZohar  J Posttraumatic stress disorder: diagnosis and epidemiology, comorbidity and social consequences, biology, and treatment. Neuropsychobiology 2001;43 (3) 150- 162
PubMed Link to Article
Magruder  KMFrueh  BCKnapp  RGJohnson  MRVaughan  JA  IIICarson  TCPowell  DAHebert  R PTSD symptoms, demographic characteristics, and functional status among veterans treated in VA primary care clinics. J Trauma Stress 2004;17 (4) 293- 301
PubMed Link to Article
Greenberg  PESisitsky  TKessler  RCFinkelstein  SNBerndt  ERDavidson  JRBallenger  JCFyer  AJ The economic burden of anxiety disorders in the 1990s. J Clin Psychiatry 1999;60 (7) 427- 435
PubMed Link to Article
Harvey  AGBryant  RATarrier  N Cognitive behaviour therapy of posttraumatic stress disorder. Clin Psychol Rev 2003;23 (3) 501- 522
PubMed Link to Article
Foa  EBMeadows  EA Psychosocial treatments for posttraumatic stress disorder: a critical review. Annu Rev Psychol 1997;48449- 480
PubMed Link to Article
Foa  EBHearst-Ikeda  DPerry  KJ Evaluation of a brief cognitive-behavioral program for the prevention of chronic PTSD in recent assault victims. J Consult Clin Psychol 1995;63 (6) 948- 955
PubMed Link to Article
Foa  EBZoelner  LAFeeny  NC An evaluation of three brief programs for facilitating recovery after assault. J Trauma Stress 2006;19 (1) 29- 43
PubMed Link to Article
Bisson  JIShepherd  JPJoy  DProbert  RNewcombe  RG Early cognitive-behavioural therapy for post-traumatic stress symptoms after physical injury: randomised controlled trial. Br J Psychiatry 2004;18463- 69
PubMed Link to Article
Bryant  RA Early predictors of posttraumatic stress disorder. Biol Psychiatry 2003;53 (9) 789- 795
PubMed Link to Article
Bryant  RAHarvey  AGSackville  TDang  SBasten  C Treatment of acute stress disorder: a comparison of cognitive-behavioral therapy and supportive counseling. J Consult Clin Psychol 1998;66 (5) 862- 866
PubMed Link to Article
Bryant  RASackville  TDang  STMoulds  MGuthrie  R Treating acute stress disorder: an evaluation of cognitive behavior therapy and counseling techniques. Am J Psychiatry 1999;156 (11) 1780- 1786
PubMed
Bryant  RAMoulds  MLGuthrie  RNixon  RD Treating acute stress disorder after mild brain injury. Am J Psychiatry 2003;160 (3) 585- 587
PubMed Link to Article
Bryant  RAMoulds  MGuthrie  RMNixon  RD The additive benefit of hypnosis and cognitive behavior therapy in treating acute stress disorder. J Consult Clin Psychol 2005;73 (2) 334- 340
PubMed Link to Article
Bryant  RAMoulds  MANixon  R Cognitive behaviour therapy of acute stress disorder: a four-year follow-up. Behav Res Ther 2003;41 (4) 489- 494
PubMed Link to Article
Bryant  RAMoulds  MLNixon  RVMastrodomenico  JFelmingham  KHopwood  S Hypnotherapy and cognitive behaviour therapy of acute stress disorder: a three-year follow-up. Behav Res Ther 2006;44 (9) 1331- 1335
PubMed Link to Article
Kilpatrick  DGBest  CL Some cautionary remarks on treating sexual assault victims with implosion. Behav Ther 1984;15421- 423
Link to Article
Rosen  CSChow  HCFinney  JFGreenbaum  MAMoos  RHSheikh  JIYesavage  JA Practice guidelines and VA practice patterns for treating posttraumatic stress disorder. J Trauma Stress 2004;17 (3) 213- 222
PubMed Link to Article
Warda  GBryant  RA Cognitive bias in acute stress disorder. Behav Res Ther 1998;36 (12) 1177- 1183
PubMed Link to Article
Smith  KBryant  RA The generality of cognitive bias in acute stress disorder. Behav Res Ther 2000;38 (7) 709- 715
PubMed Link to Article
Ehlers  AMayou  RABryant  B Psychological predictors of chronic PTSD after motor vehicle accidents. J Abnorm Psychol 1998;107 (3) 508- 519
PubMed Link to Article
Tarrier  NPilgrim  HSommerfield  CFaragher  BReynolds  MGraham  EBarrowclough  C A randomized trial of cognitive therapy and imaginal exposure in the treatment of chronic posttraumatic stress disorder. J Consult Clin Psychol 1999;67 (1) 13- 18
PubMed Link to Article
Harvey  AGBryant  RA Acute stress disorder: a synthesis and critique. Psychol Bull 2002;128 (6) 886- 902
PubMed Link to Article
Harvey  AGBryant  RA Relationship of acute stress disorder and posttraumatic stress disorder following motor vehicle accidents. J Consult Clin Psychol 1998;66 (3) 507- 512
PubMed Link to Article
Bryant  RAHarvey  AG Relationship of acute stress disorder and posttraumatic stress disorder following mild traumatic brain injury. Am J Psychiatry 1998;155 (5) 625- 629
PubMed
Brewin  CRAndrews  BRose  SKirk  M Acute stress disorder and posttraumatic stress disorder in victims of violent crime. Am J Psychiatry 1999;156 (3) 360- 365
PubMed
Harvey  AGBryant  RA Relationship of acute stress disorder and posttraumatic stress disorder: a two-year prospective study. J Consult Clin Psychol 1999;67 (6) 985- 988
PubMed Link to Article
Harvey  AGBryant  RA A two-year prospective evaluation of the relationship between acute stress disorder and posttraumatic stress disorder following mild traumatic brain injury. Am J Psychiatry 2000;157 (4) 626- 628
PubMed Link to Article
Bryant  RAHarvey  AGDang  SSackville  T Assessing acute stress disorder: psychometric properties of a structured clinical interview. Psychol Assess 1998;10215- 220
Link to Article
Blake  DDWeathers  FWNagy  LMKaloupek  DGGusman  FDCharney  DSKeane  TM The development of a Clinician-Administered PTSD scale. J Trauma Stress 1995;8 (1) 75- 90
PubMed Link to Article
Spitzer  RLGibbon  MWilliams  JBW Structured Clinical Interview for DSM-IV Axis I Disorders.  New York NY State Psychiatric Institute, Biometrics Research Department1996;
Beck  ATSteer  RA Beck Anxiety Inventory Manual.  San Antonio, TX Psychological Corporation1990;
Beck  ATSteer  RABrown  GK Beck Anxiety Inventory Manual. 2nd ed.  San Antonio, TX Psychological Corporation1996;
Horowitz  MWilner  NAlvarez  W The Impact of Event Scale: a measure of subjective stress. Psychosom Med 1979;41 (3) 209- 218
PubMed Link to Article
Foa  EBEhlers  AClark  DMTolin  DFOrsillo  SM The Posttraumatic Cognitions Inventory (PTCI): development and validation. Psychol Assess 1999;11303- 314
Link to Article
Deviliya  GJBorkovecb  TD Psychometric properties of the credibility/expectancy questionnaire. J Behav Ther Exp Psychiatry 2000;31 (2) 73- 86
PubMed Link to Article
Nelson  HE National Adult Reading Test (NART): Test Manual.  Windsor, England NFER-Nelson1982;
Beck  ATRush  AJShaw  BFEmery  G Cognitive Therapy of Depression.  New York, NY Guilford Press1979;
Cohen  J Statistical Power Analysis for the Behavioral Sciences.  New York, NY Academic Press1988;
Hedges  LV Estimation of effect size from a series of independent experiments. Psychol Bull 1982;92490- 499
Link to Article
Weathers  FWKeane  TMDavidson  JRT Clinician-Administered PTSD Scale: a review of the first ten years of research. Depress Anxiety 2001;13 (3) 132- 156
PubMed Link to Article
Kendall  PCHollon  SDBeck  ATHammen  CLIngram  RE Issues and recommendations regarding use of the Beck Depression Inventory. Cognit Ther Res 1987;11 (3) 289- 299
Link to Article
Foa  EBDancu  CVHembree  EAJaycox  LHMeadows  EAStreet  GP A comparison of exposure therapy, stress inoculation training, and their combination for reducing posttraumatic stress disorder in female assault victims. J Consult Clin Psychol 1999;67 (2) 194- 200
PubMed Link to Article
Chatellier  GZapletal  ELemaitre  DMenard  JGoulet  P The number needed to treat: a clinically useful monogram in its proper context. BMJ 1996;312 (7028) 426- 429
PubMed Link to Article
Hembree  EAFoa  EBDorfan  NMStreet  GPLowalski  JTu  X Do patients drop out prematurely from exposure therapy for PTSD? J Trauma Stress 2003;16 (6) 555- 562
PubMed Link to Article
Jaycox  LHFoa  EB Obstacles in implementing exposure therapy for PTSD: case discussions and practical solutions. Clin Psychol Psychother 1998;3 (3) 176- 184
Link to Article
Rothbaum  BOSchwartz  AC Exposure therapy for posttraumatic stress disorder. Am J Psychother 2002;56 (1) 59- 75
PubMed
Ehlers  AClark  D A cognitive model of posttraumatic stress disorder. Behav Res Ther 2000;38 (4) 319- 345
PubMed Link to Article
Foa  EBKozak  MJ Emotional processing of fear: exposure to corrective information. Psychol Bull 1986;99 (1) 20- 35
PubMed Link to Article
van Minnen  AFoa  EB The effect of imaginal exposure length on outcome of treatment for PTSD. J Trauma Stress 2006;19 (4) 427- 438
PubMed Link to Article
North  CSNixon  SJShariat  SMallonee  S McMillen  JCSpitznagel  ELSmith  EM Psychiatric disorders among survivors of the Oklahoma City bombing. JAMA 1999;282 (8) 755- 762
PubMed Link to Article
Mazumdar  SLiu  KSHouck  PRReynolds  CF Intent-to-treat analysis for longitudinal clinical trials: coping with the challenge of missing values. J Psychiatr Res 1999;33 (2) 87- 95
PubMed Link to Article
Ehlers  AClark  DMHackmann  A McManus  FFennell  MHerbert  CMayou  RA A randomized controlled trial of cognitive therapy, self-help, and repeated assessment as early interventions for PTSD. Arch Gen Psychiatry 2003;60 (10) 1024- 1032
PubMed Link to Article
Riggs  DSCahill  SPFoa  EB Prolonged exposure treatment of posttraumatic stress disorder. Follette  VMRuzek  JICognitive-Behavioral Therapies for Trauma. New York, NY Guilford2006;65- 95

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