Acute stress disorder describes posttraumatic stress reactions that occur between 2 days and 4 weeks following a trauma +(1). A major use of this diagnosis is that it can identify many individuals in the acute phase who will subsequently develop chronic posttraumatic stress disorder (PTSD). For example, between 78% and 82% of motor vehicle accident survivors who satisfy the criteria for acute stress disorder suffer PTSD 6 months posttrauma +(2, +3). These patterns contrast with evidence that whereas 94% of rape victims meet the symptomatic criteria shortly after their assaults, only 47% still meet these criteria 3 months after the trauma +(4). It appears that the particular diagnostic criteria in acute stress disorder permit a more accurate identification of those individuals who will not naturally recover from the adverse effects of their traumatic experience.

The capacity to identify in the acute trauma phase those individuals who are at risk of developing chronic PTSD provides an opportunity to prevent the development of chronic PTSD through early intervention. Numerous studies have evaluated early treatment programs for posttraumatic stress. One early study +(5) reported that recent rape victims demonstrated comparable symptom reduction following either behavioral intervention, repeated assessment, or delayed assessment. Another study +(6) provided recent assault victims with either four sessions of cognitive behavior therapy or repeated assessments. Whereas 10% of the cognitive behavior therapy group and 70% of the repeated assessment group met the criteria for PTSD 2 months after the trauma, 6 months after the assault, the rates of PTSD were comparable (cognitive behavior therapy group=11%, assessment comparison group=22%). These studies did not treat people with acute stress disorder, however, and accordingly, it is possible that these earlier studies employed samples that may have experienced transient posttraumatic stress reactions that did not develop into persistent PTSD. In the only treatment study to date of acute stress disorder +(7), five sessions of either cognitive behavior therapy or supportive counseling were provided to civilian trauma survivors who met the criteria for acute stress disorder. Cognitive behavior therapy involved prolonged imaginal exposure, cognitive therapy, and anxiety management, and supportive counseling included nondirective counseling and general problem solving. This study found that 17% and 67% of the cognitive behavior therapy and supportive counseling groups, respectively, met the criteria for PTSD 6 months after the trauma. This finding indicated that cognitive behavior therapy was an effective technique for resolving acute trauma responses that would otherwise lead to chronic PTSD.

The current study aimed to replicate and extend these previous findings by identifying the critical ingredients of cognitive behavior therapy that can prevent PTSD in people with acute stress disorder. Specifically, previous studies have argued that the therapeutic gains achieved by cognitive behavior therapy are primarily mediated by the activation of fear networks as a result of prolonged exposure +(6, +7). It is proposed that resolution of a traumatic experience requires prolonged activation of trauma-related mental representations in order to allow habituation of anxiety and modification of maladaptive trauma-related beliefs +(8). This interpretation is consistent with finding that chronic PTSD is mediated by deficits in accessing trauma memories during the acute trauma phase +(9). It is also supported by evidence that prolonged exposure leads to long-standing gains in the treatment of chronic PTSD +(8).

The other active component of cognitive behavior therapy is anxiety management, which is included to reduce the arousal symptoms associated with acute stress disorder. There is increasing evidence that acute stress reactions are mediated by elevated arousal. Biological models of PTSD propose that excessive arousal at the time of the traumatic experience results in strong fear conditioning that results in PTSD +(10). This notion is supported by recent findings that people who subsequently develop PTSD show higher levels of heart rates in the acute phase after a traumatic event than those who do not develop PTSD +(11, +12). This evidence suggests that the reduction of arousal in the acute phase may prevent the development of PTSD. There is evidence that anxiety management techniques can lead to significant reductions in PTSD symptoms +(8, +13). Accordingly, this study indexed the extent to which the benefits of prolonged exposure can be enhanced by also providing anxiety management to recent trauma survivors who suffer acute stress disorder. Additionally, we compared these treatments to supportive counseling to provide an index of the benefits of active treatments relative to nonspecific therapy. On the premise that the combined treatment program would have an additive benefit in treating acute stress disorder, we predicted that prolonged exposure plus anxiety management would result in fewer PTSD symptoms than prolonged exposure and that both treatments would be more effective than supportive counseling.

Patients were survivors of either motor vehicle accidents or nonsexual assault who were referred to the PTSD Unit at Westmead Hospital, Sydney, New South Wales, Australia. The referral sources included hospital staff, local community mental health centers, and police. Inclusion criteria included 1) having been involved in either a motor vehicle accident or a nonsexual assault within the past 2 weeks, 2) satisfying the criteria for acute stress disorder, 3) proficiency in English, and 4) aged 18–60 years. Exclusion criteria ­included 1) current suicidal ideation (N=4), 2) a diagnosis of ­psychosis, organic mental disorder, or substance abuse (N=8), and 3) evidence of brain injury sustained in the trauma (N=3).

There were initially 66 patients in the study but 11 (four in prolonged exposure plus anxiety management, four in prolonged exposure, and three in supportive counseling) dropped out of treatment before completion of all treatment sessions. In terms of completed treatment, there were 15 (seven women and eight men) patients in the prolonged exposure plus anxiety management condition, 14 (seven women and seven men) in the prolonged exposure condition, and 16 (nine women and seven men) in the supportive counseling condition. There were seven motor vehicle accident survivors in each group, and eight, seven, and nine nonsexual assault victims in the prolonged exposure plus anxiety management, prolonged exposure, and supportive counseling groups, respectively. Each group included several patients who did not fully satisfy the criteria for acute stress disorder because they reported only two, rather than three, dissociative symptoms (two in prolonged exposure plus anxiety management, two in prolonged exposure, and three in supportive counseling). +table 1 presents the mean participant characteristics. One-way analyses of variance (ANOVAs) indicated no significant differences between groups in terms of age, intervals between trauma and assessment, intervals before posttreatment follow-up, or pretreatment acute stress disorder severity.

The Acute Stress Disorder Interview +(14) is a structured clinical interview that is based on the DSM-IV criteria for acute stress disorder, contains 19 dichotomously scored items that relate to the symptoms of acute stress disorder, and provides a total score of acute stress severity (range=1–19). The Acute Stress Disorder Interview possesses sound test-retest reliability (r=0.95), sensitivity (91%), and specificity (93%).

The Clinician Administered PTSD Scale, Form 2 +(15), was employed for posttreatment and follow-up diagnostic assessments because the time frame of these assessments required PTSD, rather than acute stress disorder, diagnostic decisions. The Clinician Administered PTSD Scale, Form 2, assesses the frequency and severity of each PTSD symptom in the context of the last week and possesses sound test-retest reliability and strong convergent validity with standard measures of PTSD +(15).

The Impact of Event Scale +(16) is a 15-item, self-report inventory that indexes intrusive and avoidance symptoms of posttraumatic stress.

The Beck Depression Inventory +(17) is a 21-item inventory that indexes depression and correlates soundly (0.62–0.66) with clinician ratings of depression.

The State-Trait Anxiety Inventory +(18) state anxiety scale contains 20 items that index state anxiety and possesses sound test-retest reliability (0.73–0.86) and strong internal consistency (0.83–0.92).

After explanation of the treatment rationale, patients were asked to rate their confidence in the expected efficacy of their treatment by completing a 10-point Likert scale (1=not at all confident, 10=extremely confident).

After complete description of the study to the patients, written informed consent was obtained. Patients were assessed before treatment (time 1), after treatment (time 2), and at 6-month follow-up (time 3). All posttreatment and follow-up assessments were conducted by a clinical psychologist (T.S., S.T.D., M.M., or R.G.) who was blind to treatment group status. All measures were administered at each assessment, except that the Acute Stress Disorder Interview was administered at time 1 and the Clinician Administered PTSD Scale, Form 2, was administered at times 2 and 3. Patients who met the criteria for acute stress disorder were randomly allocated to one treatment program. Each group received five 1.5-hour individually administered sessions conducted by one of the four clinical psychologists. Each therapist was trained in the therapy protocols by the first author (R.A.B.). Sessions occurred once weekly. Treatment adherence was facilitated by strict compliance with therapy manuals and was monitored by the first author (R.A.B.), who reviewed case notes and monitoring records of each participant on a weekly basis.

The first session comprised education about trauma reactions, breathing retraining, training in progressive muscle relaxation, and learning self-talk exercises to manage anxiety-producing situations. Subsequent to the initial session, patients completed each of these techniques on a daily basis as homework, and patients’ progress was monitored at each session. The second session involved the rationale for exposure and commencement of prolonged imaginal exposure to traumatic memories. Fifty minutes of each of the final four sessions were devoted to patients reliving their traumas by focusing attention on their memories and engaging with their affective responses. These narratives were not audiotaped, but patients were instructed to complete this exposure in the same manner as in therapy as daily homework. Following each exposure session, cognitive restructuring of fear-related beliefs that were identified during the exposure was conducted. Cognitive restructuring involved teaching patients to identify irrational, threat-related beliefs and to enhance realistic thinking by evaluating thoughts against the available evidence. Cognitive restructuring was combined with exposure in this study because of the reported utility of modifying trauma-related cognitions that are elicited by exposure +(19). Sessions 4 and 5 also included in vivo exposure and relapse-prevention exercises.

The first session involved education about trauma reactions and an explanation of prolonged exposure. The second session focused on prolonged exposure, in the same manner as described in the prolonged exposure plus anxiety management condition. Each prolonged exposure session was followed by cognitive restructuring. Care was taken to ensure that equivalent time was allocated to imaginal exposure in both the prolonged exposure plus anxiety management and prolonged exposure conditions because previous work has indicated that the efficacy of combined treatments may be reduced by restricting the time available to exposure +(20). Accordingly, the prolonged exposure condition was supplemented with supportive counseling to ensure that the active treatment components were controlled across the prolonged exposure plus anxiety management and the prolonged exposure conditions. Prolonged exposure and cognitive restructuring were continued in each session. Sessions 4 and 5 included in vivo exposure and relapse-prevention exercises.

The first session involved education about trauma and an explanation of the nature of supportive counseling. The following sessions included general problem-solving skills and the provision of an unconditionally supportive role for the therapist. Homework involved diary keeping of current problems and mood states. Supportive counseling specifically avoided exposure or anxiety management techniques.

The seven patients who displayed two acute dissociative symptoms of stress disorder did not differ from patients who displayed the required three dissociative symptoms on any pretreatment measures, including the Impact of Event Scale, the State-Trait Anxiety Inventory, and the Beck Depression Inventory. That is, these patients displayed comparable levels of acute psychopathology as those who met the full criteria. The 11 patients who dropped out of treatment differed from those who completed treatment in terms of the severity of their acute stress disorder (F=2.48, df=2, 54, p<0.05) and their State-Trait Anxiety Inventory scores for state anxiety (F=3.55, df=2, 64, p<0.01). That is, those who dropped out of treatment reported more severe acute stress disorder and higher scores for state anxiety than those who completed therapy. Of the 45 patients who completed treatment, four (two in prolonged exposure plus anxiety management, one in prolonged exposure, and one in supportive counseling) were not included in the follow-up assessment because two could not be contacted and two were instructed by legal counsel not to participate.

McNemar’s chi-square tests indicated that at posttreatment, fewer patients in the prolonged exposure plus anxiety management group (20%, N=3 of 15) and the prolonged exposure group (14%, N=2 of 14) met the criteria for PTSD than in the supportive counseling group (56%, N=9 of 16) (χ²=7.43, N=45, df=2, p<0.05, with Yates’s correction +[21]). Paired chi-square comparisons indicated that more patients in the supportive counseling group met the criteria for PTSD than in the prolonged exposure plus anxiety management group (χ²=4.27, N=31, df=1, p<0.05, with Yates’s correction) and in the prolonged exposure group (χ²=5.54, N=30, df=1, p<0.02, with Yates’s correction). Similarly, at the 6-month follow-up, fewer patients in the prolonged exposure plus anxiety management (23%, N=3 of 13) and prolonged exposure (15%, N=2 of 13) groups met the criteria for PTSD than in the supportive counseling group (67%, N=10 of 15) (χ²=9.39, N=41, df=2, p<0.01, with Yates’s correction). Paired chi-square comparisons indicated that more patients in the supportive counseling group met the criteria for PTSD than in the prolonged exposure plus anxiety management group (χ²=5.36, N=28, df=1, p<0.05, with Yates’s correction) and in the prolonged exposure group (χ²=7.59, N=28, df=1, p<0.01, with Yates’s correction).

A series of three-(group) by-three (assessment), repeated-measures ANOVAs were conducted on Impact of Event Scale, State-Trait Anxiety Inventory, and Beck Depression Inventory scores (+table 2). Post hoc Tukey comparisons were conducted with an adjusted alpha rate of 0.01 to provide an overall significance level of 0.05. A three-by-three, repeated-measures ANOVA on Impact of Event Scale scores for instruction indicated a significant main effect for time (F=56.05, df=2, 37, p<0.001) and a significant group-by-time interaction effect (F=5.03, df=4, 76, p<0.001). Post hoc Tukey comparisons indicated that patients reported higher Impact of Event Scale scores for intrusion at time 1 than at times 2 and 3. When we used post hoc t tests, patients in supportive counseling reported higher Impact of Event Scale scores for intrusion at posttreatment than did patients with prolonged exposure (t=4.08, df=28, p<0.001).

A three-by-three, repeated-measures ANOVA on Impact of Event Scale avoidance scores indicated a significant main effect for time (F=26.78, df=2, 37, p<0.001) and a significant group-by-time interaction effect (F=2.98, df=4, 76, p<0.05). Post hoc comparisons indicated that patients reported higher Impact of Event Scale avoidance scores at time 1 than at times 2 and 3. Further, supportive counseling patients displayed higher Impact of Event Scale scores for avoidance at the 6-month follow-up than both the patients with prolonged exposure plus anxiety management (t=3.91, df=26, p<0.01) and the patients with prolonged exposure (t=11.75, df=26, p<0.001).

A three-by-three, repeated-measures ANOVA on State-Trait Anxiety Inventory scores for state anxiety indicated a significant main effect for time (F=29.45, df=2, 37, p<0.001) and a significant group-by-time interaction effect (F=2.58, df=4, 76, p<0.05). Post hoc comparisons indicated that patients reported higher State-Trait Anxiety Inventory scores for state anxiety at time 1 than at times 2 and 3. The supportive counseling patients displayed only marginally higher State-Trait Anxiety Inventory scores for state anxiety at the 6-month follow-up than both the patients with prolonged exposure plus anxiety management (t=2.50, df=26, p<0.02) and the patients with prolonged exposure (t=2.08, df=26, p<0.05).

A three-by-three, repeated-measures ANOVA on Beck Depression Inventory scores indicated a significant main effect for time (F=19.95, df=2, 37, p<0.001). Post hoc comparisons indicated that patients reported higher Beck Depression Inventory scores at time 1 than at times 2 and 3.

Separate three-by-two, repeated-measures ANOVAs were also conducted on Clinician Administered PTSD Scale, Form 2, scores for intensity and frequency; the Clinician Administered PTSD Scale, Form 2, scores were obtained only after treatment and at follow-up. A three-by-two, repeated-measures ANOVA of Clinician Administered PTSD Scale, Form 2, scores for intensity indicated significant main effects for time (F=8.26, df=1, 38, p<0.01) and group (F=8.07, df=2, 38, p<0.001). Patients reported lower scores for intensity after treatment than at follow-up. The supportive counseling patients reported higher scores for intensity than did the patients with prolonged exposure (t=4.09, df=26, p<0.001) and the patients with prolonged exposure plus anxiety management (t=3.13, df=26, p<0.01). A three-by-two, repeated-measures ANOVA of Clinician Administered PTSD Scale, Form 2, scores for frequency indicated a significant main effect for group (F=4.18, df=2, 38, p<0.05). Post hoc comparisons indicated that supportive counseling patients reported higher scores for frequency than did the patients with prolonged exposure (t=3.48, df=26, p<0.01) and the patients with prolonged exposure plus anxiety management (t=3.13, df=26, p<0.01).

To index the clinical significance of therapy gains, we followed Jacobson and Truax’s +(22) suggested technique for when population norms are unavailable. That is, because of the lack of normative data on acute stress disorder populations, we defined clinical improvement as a reduction of at least 2 standard deviations below the pretreatment mean of our study group. +Table 3 presents the summary data of treatment effects. At posttreatment, more patients with prolonged exposure plus anxiety management and more patients with prolonged exposure than patients with supportive counseling improved in terms of the Impact of Event Scale scores for intrusion and avoidance and State-Trait Anxiety Inventory scores for state anxiety. The groups did not differ on Beck Depression Inventory scores. At the follow-up assessment, more patients with prolonged exposure plus anxiety management and more patients with prolonged exposure than patients with supportive counseling improved in terms of Impact of Event Scale scores for avoidance.

These findings replicate a previous report that acute stress disorder can be effectively treated, and PTSD prevented, with a brief intervention of cognitive behavior therapy in the acute posttrauma phase +(7). In contrast to previous reports that approximately 80% of individuals who initially meet the criteria for acute stress disorder will suffer chronic PTSD 6 months after the trauma +(2, +3), this study found that relatively few individuals met the criteria for PTSD after either prolonged exposure plus anxiety management (23%, N=3 of 13) or prolonged exposure (15%, N=2 of 13).

Contrary to our expectations, there were no differences in outcomes between the prolonged exposure and prolonged exposure plus anxiety management groups. This pattern suggests that anxiety management did not add to the treatment gains obtained by prolonged exposure. It may be argued that habituation of anxiety through prolonged exposure and modification of maladaptive beliefs through cognitive therapy were the critical therapeutic processes that mediated adaptation. This interpretation is consistent with evidence that whereas anxiety management can result in immediate symptom reduction in chronic PTSD, prolonged exposure leads to a more effective long-term reduction of PTSD symptoms +(8). This finding may be interpreted in terms of information-processing theory, which holds that recovery from trauma requires 1) activation of traumatic memories and 2) modification of threat-based beliefs to correct the fear networks that perpetuate PTSD symptoms +(23).

An unexpected finding in this study was that whereas prolonged exposure plus anxiety management and prolonged exposure produced greater reductions in avoidance behavior at follow-up, there were comparable reductions in intrusive and arousal symptoms across all groups. This finding may be understood, in part, in the context of evidence that whereas intrusions can decline with time, avoidance behaviors can develop as time passes +(24). It appears that a significant benefit for patients who received prolonged exposure plus anxiety management and prolonged exposure was that they did not develop avoidance behaviors that were evident in those who received supportive counseling. The active treatments may have resulted in reductions in acute symptoms that would otherwise have elicited avoidance behavior.

The rate of PTSD in those who received supportive counseling (67%, N=10 of 15) was comparable to previous reports of treating acute stress disorder with supportive counseling +(7). Although the rate of PTSD following supportive counseling was significantly higher than the rates following the active treatments, the rate of PTSD 6 months after supportive counseling was less than the incidence of 80% that has been reported in prospective studies of acute stress disorder +(2, +3). This finding suggests that therapeutic support may play some helpful role in ameliorating the symptoms of acute stress disorder. These benefits appear to be marginal, however, in comparison to the positive effects of cognitive behavior therapy.

Conclusions from this study need to be interpreted in the context of several methodological issues. First, these results are applicable only to motor vehicle accident and nonsexual assault victims and should not be generalized to other trauma populations. Second, we did not index comorbidity issues. The influence of early intervention on long-term depression, substance abuse, and other comorbid conditions commonly associated with PTSD would strengthen our conclusions concerning the use of treating acute stress disorder. Third, the diagnosis of acute stress disorder is a recent development, and its validity has yet to be firmly established. Although the Acute Stress Disorder Interview has strong psychometric properties, our initial assessments could have been stronger by including interrater reliability checks. Fourth, we did not include the Clinician Administered PTSD Scale at the initial assessment because of patients’ acute stress disorder status. Completion of the Clinician Administered PTSD Scale at each assessment would have permitted a stronger measurement of the effects of treatment on PTSD symptoms. Fifth, this study’s use of combined prolonged ­exposure and cognitive therapy did not permit delineation of the relative effects of imaginal exposure and cognitive therapy. Although information-processing theories posit that prolonged exposure can facilitate cognitive restructuring +(25), recent commentaries have questioned this assumption +(26). Future treatment studies of acute stress disorder could usefully compare the efficacy of prolonged exposure and prolonged exposure combined with cognitive therapy. Finally, we recognize that our group size was modest, and it is possible that increased power may have resulted in a more stringent comparison of prolonged exposure and prolonged exposure plus anxiety management. Relatedly, we recognize that we included seven patients who displayed two, rather than the required three, dissociative symptoms. We concluded that these patients should be included in the study because 1) they reported comparable psychopathology levels to those who reported three dissociative symptoms, 2) there is no empirical justification for the stipulation of three dissociative symptoms in the acute stress disorder criteria +(1), and 3) there is evidence that these patients are as likely to suffer chronic PTSD as those who meet the full criteria for acute stress disorder +(3, +27).

We recognize that patients who dropped out of treatment were characterized by more severe acute stress disorder and higher levels of anxiety. This pattern suggests that whereas early intervention has a strong potential to prevent PTSD, those individuals who are most distressed may not be amenable to early intervention. Alternatively, different strategies may need to be developed to meet the particular needs of more severely distressed individuals in the acute phase. Considering the prominence of acute dissociative symptoms in patients with acute stress disorder, future treatment studies should investigate strategies that may facilitate exposure in patients with dissociative disorder. Techniques such as hypnotherapy may be useful for acute dissociative symptoms and should be evaluated through controlled outcome studies +(28). Empirically determining the optimal components of acute stress disorder treatments will facilitate our ability to prevent PTSD in acutely traumatized patients who are most at risk of long-term disorder.

Received Dec. 3, 1998; revision received April 15, 1999; accepted April 30, 1999. From the School of Psychology, University of New South Wales. Address reprint requests to Dr. Bryant, School of Psychology, University of New South Wales, Sydney NSW 2052, Australia; r.bryant@unsw.edu.au (e-mail). Supported by a grant from the National Health and Medical Research Council.