Acute Stress Reactions

Article about acute stress reactions.

Topics covered: 

  • Introduction
  • Clinical features
  • Classification
  • Diagnosis and differential diagnosis
    • Stressor criterion
    • Symptom patterns
    • Time course of symptoms
    • Assessment instruments
    • Acute stress disorder interview
    • Structured clinical interview for DSM-IV dissociative disorders
    • Structured clinical interview for DSM-IV (SCID)
    • Stanford acute stress reaction questionnaire
    • Differential diagnoses
    • Post-traumatic stress disorder
    • Adjustment disorder
    • Brain injury
    • Brief psychotic disorder
    • Dissociative disorders
  • Epidemiology
    • Incidence
    • Comorbidity
  • Aetiology
    • Psychological theories
    • Psychological explanations of re-experiencing symptoms
    • Dissociation and other processes that impede recovery
    • Biological theories
  • Course and prognosis
    • Time course of symptoms
    • Predictors of acute stress disorder
  • Treatment
    • Psychological treatments
    • Debriefing
    • Cognitive–behaviour therapy
    • Psychopharmacological treatment  
    • Advice about management
    • Possibilities for prevention
  • References


Exceptionally stressful life events can cause severe psychological symptoms, including anxiety, feelings of derealization and depersonalization, and hyperarousal. In one of the first studies to comprehensively document acute reactions to extreme stress, Lindemann (1) observed that the symptoms reported by survivors of the Coconut Grove Fire included avoidance, re-experiencing scenes from the fire, reports of derealization, and the experience of anxiety when exposed to reminders of the event. Similarly, acute responses reported by soldiers who fought in the First and Second World Wars included re-experiencing symptoms and dissociative responses such as numbing, amnesia, and depersonalization. (2)

The International Classification of Diseases has recognized acute stress reactions since 1948 (ICD-6). (3) In the most recent edition (ICD-10), (4) early reactions to exceptionally stressful life events are diagnosed as acute stress reaction, one of the diagnoses in the section headed ‘Reactions to severe stress, and adjustment disorders'.

In contrast, the Diagnostic and Statistical Manual of Mental Disorders did not formally recognize that exceptionally stressful life events are a sufficient cause of psychological symptoms until 1980 when its third edition (DSM-III) (5) introduced the diagnosis of post-traumatic stress disorder (PTSD). DSM-III did not stipulate a duration for the symptoms, but the revised third version (DSM-III-R) (6) required that the symptoms of PTSD must be present for more than 1 month after the traumatic event. This stipulation precluded the inclusion of acutely traumatized individuals who instead were diagnosed with adjustment disorder. (7) In 1994 the fourth edition of DSM (DSM-IV) (8) formally recognized acute trauma reactions by introducing the new diagnosis of acute stress disorder into the anxiety disorders section.

The diagnoses of acute stress reactions in ICD-10 and of acute stress disorder in DSM-IV have similarities in that they are caused by extreme stress and have some overlap in symptom patterns. They can be considered as two separate points on a continuum from transient to more enduring symptoms. However, there are also differences in the underlying concepts, as we will discuss in this chapter.

Clinical features 

Acute stress reactions, as defined in ICD-10, are transient reactions to exceptional physical and/or mental stress. There is an initial stage of a ‘daze', including narrowing of attention, inability to comprehend stimuli, and disorientation. This is followed by a rapidly changing picture of symptoms that may include withdrawal from the surrounding situation, flight reactions, panic anxiety and autonomic hyperarousal, depression, anger, or despair. Symptoms usually begin to diminish after 24 to 48 h and should be minimal after about 3 days.

In contrast, acute stress disorder, as defined in DSM-IV, is only diagnosed if the psychological symptoms persist for more than 2 days. Dissociative symptoms dominate the symptom pattern. Dissociation refers to a disruption of the usually integrated feelings of consciousness, memory, identity, or perception of the environment. Symptoms include a subjective sense of numbing or detachment, reduced awareness of surroundings, derealization, depersonalization, or dissociative amnesia. In addition, patients with acute stress disorder experience symptoms that are typical of PTSD, namely re-experiencing aspects of the event, avoidance of reminders of the event, and hyperarousal symptoms. Acute stress disorder is seen in DSM-IV as a precursor of PTSD. If the re-experiencing, avoidance, and hyperarousal symptoms persist for more than 4 weeks, PTSD is diagnosed.


ICD-10 classifies acute stress reactions (F43.0) among the reactions to severe stress and adjustment disorders (F43) that are primarily caused by stressful events. DSM-IV classifies acute stress disorder (308.3) among the anxiety disorders, like Post Traumatic Stress Disorder.

Diagnosis and differential diagnosis

The main diagnostic criteria for acute stress reactions DSM-IV are shown in Table 1.

Table 1. DSM-IV-TR diagnostic criteria for ASD

A1. Exposure to catastrophic stressor

A2. Intense emotional reaction to stressor

B. During or after experiencing the distressing event, the individual has three (or more) of the following dissociative symptoms

  1. Sense of numbing, detachment, or absence of emotional responsiveness
  2. Reduction in awareness of surroundings (e.g., ‘‘being in a daze’’)
  3. Derealization
  4. Depersonalization
  5. Dissociative amnesia

C. The traumatic event is persistently reexperienced in at least one of the following ways: recurrent images, thoughts, dreams, illusions, flashback episodes, or a sense of reliving the experience; or distress on exposure to reminders of the traumatic event

D. Marked avoidance of stimuli that arouse recollections of the trauma (e.g., thoughts, feelings, conversations, activities, places, people)

E. Marked symptoms of anxiety or increased arousal (e.g., difficulty sleeping, irritability, poor concentration, hypervigilence, exaggerated startle response, motor restlessness)

F. The disturbance causes significant distress or impairment

G. The disturbance lasts for a minimum of 2 days and a maximum of 4 weeks and occurs within 4 weeks of the traumatic event

H. Disturbance is not due to the effects of substance use or medical condition or is not better accounted for by brief psychotic disorder, and is not merely an exacerbation of a preexisting Axis I or II disorder

Stressor criterion

Both ICD-10 and DSM-IV require that acute stress responses must occur in the immediate aftermath of an exceptionally stressful event. ICD-10 uses a broad concept of what qualifies as an ‘exceptional mental or physical stressor'. This includes stressors that would be regarded as traumatic (e.g. rape, criminal assault, natural catastrophe) as well as unusually sudden changes in the social position and/or network of the individual (e.g. domestic fire or multiple bereavement). In contrast, DSM-IV uses a narrow definition of stressors that lead to acute stress disorder, which is identical to the stressor criterion of PTSD. It requires (1) that the traumatic event must have involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others, and (2) that the person's response to the traumatic event must have involved intense fear, helplessness, or horror (or disorganized or agitated behaviour in children).

Symptom patterns

The diagnostic criteria for acute stress reactions (ICD-10) and acute stress disorder (DSM-IV) overlap, in that they include symptoms of dissociation, anxiety, and hyperarousal. DSM-IV puts a much greater emphasis on dissociation, requiring a minimum of three of the dissociative symptoms specified in Table 1 (Criterion B). According to ICD-10, any combination of a minimum of four symptoms of generalized anxiety disorder would be sufficient to establish the diagnosis of acute stress reaction. In addition, DSM-IV, but not ICD-10, requires the individual to have at least one re-experiencing symptom, to show marked avoidance of reminders of the trauma, and to experience significant distress or impairment of functioning. In contrast to DSM-IV, ICD-10 distinguishes between mild, moderate, and severe forms of acute stress reactions on the basis of additional symptoms (Criterion C, additional symptoms, Table 1) such as social withdrawal, hopelessness, or excessive grief. A mild severity is stipulated when none of these symptoms are present, moderate when two are reported, and s evere when four are reported or when there is dissociative stupor.

Time course of symptoms

The two diagnoses cover distinct periods on a continuum from transient to more persistent symptoms. Specifically, to meet the criteria for acute stress reaction (ICD-10), symptoms must be manifest within 1 h of the stressor (Criterion B) and begin to diminish after no more than 8 h for a transient stressor and after no more than 48 h for an enduring stressor (Criterion D). The diagnostic criteria for acute stress disorder (DSM-IV) require that the disturbance must last for a minimum of 2 days and a maximum of 4 weeks post-trauma, after which a diagnosis of PTSD can be considered.

Assessment instruments 

There are three clinician-administered and one self-report measure of acute stress disorder (DSM-IV) available. As yet, there are no established standardized assessment instruments for transient acute stress reactions (ICD-10).

Acute stress disorder interview

This structured clinical interview establishes the presence or ab sence of 19 symptoms of acute stress disorder. (9) The sum of the symptoms scored as being present indicates acute stress disorder severity. This measure has very good internal consistency (r = 0.90), and, with clinician-based diagnoses as the criterion, very good sensitivity (91 per cent) and specificity (93 per cent). Test–retest reliability is strong ( r = 0.88).

Structured clinical interview for DSM-IV dissociative disorders

This instrument has also been offered as a structured interview for acute stress disorder. (10) It provides a comprehensive assessment of five core dissociative symptoms: amnesia, depersonalization, derealization, identity confusion, and identity alteration. However, it does not fully assess the re-experiencing, avoidance, and arousal symptoms that also constitute the acute stress disorder diagnosis.

Structured clinical interview for DSM-IV (SCID (11))

The SCID interview indexes the presence, absence, or subthreshold presence of each acute stress disorder symptom specified in DSM-IV. An advantage of employing this interview is that it provides a comprehensive assessment of the differential diagnoses and comorbid disorders that can be present in trauma populations.

Stanford acute stress reaction questionnaire

This self-report inventory asks patients to rate the frequency of a range of dissociative, intrusive, somatic anxiety, hyperarousal, attention disturbance, and sleep disturbance symptoms. (12) The questionnaire has very good internal consistency (Cronbach's alpha = 0.90 and 0.91 for dissociative and anxiety symptoms, respectively) and concurrent validity with scores on the Impact of Event Scale ( r = 0.52 to 0.69).(13,14). It can be employed as a measure of the severity of symptoms, but does not allow the diagnosis of acute stress disorder to be established as it has not yet been validated against clinician diagnoses.

Differential diagnoses

Both ICD-10 and DSM-IV require that the symptoms are not merely an exacerbation of a pre-existing disorder. In addition, a number of alternative diagnoses need to be considered.

Post-traumatic stress disorder

In ICD-10, PTSD is conceptualized as an alternative diagnosis of acute stress reactions. The definitions of acute stress reaction and PTSD differ in terms of the stressor criterion (exceptionally stressful life event vs. exceptionally threatening or catastrophic event), the time course (symptoms start to diminish within 48 h versus no time limit), and symptom pattern (PTSD, but not acute stress reaction, includes involuntary re-experiencing the traumatic event). In DSM-IV, acute stress disorder can be distinguished from PTSD by the time-frame covered by the diagnoses. Acute stress disorder refers to the period from 2 days to 1 month post-trauma, after which a diagnosis of PTSD can be considered. The primary difference between the symptom criteria for acute stress disorder and PTSD in DSM-IV is the former's emphasis on dissociative reactions.

Adjustment disorder

This diagnosis covers a wide range of emotional or behavioural symptoms indicative of distress, which are judged to be out of proportion to the stressor experienced. This broad coverage can be contrasted with (1) the specific set of symptoms described by the acute stress disorder and acute stress reaction criteria, and (2) the stipulation that the stressor involves both a threat to life and a subjective response of fear for the acute stress disorder and an exceptional stressor in the case of acute stress reaction.

Brain injury

A number of acute stress disorder symptoms overlap with symptoms of brain injury including reduced awareness, depersonalization, derealization, irritability, and concentration difficulties. (15) While results from neuropsychological and neurological investigations may assist in the differential diagnosis, there appear to be a group of individuals with a mild head injury for whom there are no known tools to differentiate whether the disturbance is due to brain injury or acute stress disorder, or whether both are present.

Brief psychotic disorder 

When there is one or more psychotic symptoms present after experiencing an extreme stressor, the brief psychotic disorder diagnosis should be considered.

Dissociative disorders

Given the emphasis on dissociative symptoms in acute stress disorder, it needs to be distinguished from dissociative amnesia and depersonalization disorder. The criteria for these diagnoses stipulate that if the amnesia or depersonalization can be accounted for by acute stress disorder then a dissociative disorder cannot be diagnosed.



There is little research into what proportion of people develop acute stress reactions to severe stress. In a study of accident survivors, 14 per cent experienced a response pattern characterized by derealization, and a further 17 per cent exhibited strong anxiety or dysphoria. (16) The incidence of acute stress disorder is 13 to 14 per cent in motor vehicle accident survivors, (15,17) 19 per cent in assault victims, (18) and 33 per cent in witnesses of a mass shooting.(19) Given the variable procedures and assessment tools employed across studies, it is difficult to determine whether the different rates of acute stress disorder detected are attributable to differences in method or in the type of trauma.


Data on comorbidity are sparse. Given the similarities between acute stress disorder and PTSD it is likely that the conditions found to be comorbid with PTSD, in particular depression and substance abuse, will be applicable to acute stress disorder.


Both psychological and biological theories have attempted to explain the symptoms of acute stress disorder. They overlap largely with theories of PTSD. Given that acute stress reaction describes a transient disturbance, there are no specific theories of acute stress reactions as defined in ICD-10.

Psychological theories

Psychological explanations of re-experiencing symptoms

Psychological theories have offered two major explanations for the re-experiencing symptoms following traumatic stress, characteristics of the trauma memory, and the effect of trauma on basic beliefs about the self and the world. Foa and colleagues (20,21) suggested that PTSD is characterized by a pathological network in memory that is particularly large and easily triggered. It contains many stimulus propositions erroneously linked to danger, causing fear responses to harmless stimuli associated with the traumatic event in memory. Ehlers and Clark (22) suggest that re-experiencing occurs because the trauma memory is inadequately linked to its context in time, place, and other autobiographical memories. Stimuli resembling those present during the traumatic event can thus trigger vivid memories and strong emotional responses that are experienced as if the event was happening right now. Brewin et al. (23) postulated that dual representations of the trauma are formed in memory. The first, termed verbally accessible memory, contains the conscious recollection of the trauma. The second memory representation, termed situationally accessible memory, which cannot be deliberately accessed, comprises sensory, physiological, and motor aspects of the trauma in the form of codes that enable the re-experiencing of the original experience.

Horowitz (24) explained re-experiencing symptoms as the result of a slow process that helps the traumatized person to adjust their inner models (schemas) of the self and the world to the traumatic experience. Until this process is completed, the information related to the traumatic event is thought to be held in active memory and thus intrudes into consciousness. Similarly, Janoff-Bulman (25) proposed that traumatic events ‘shatter' previously held beliefs (for instance, ‘The world is a safe place'), and that post-trauma adjustment requires rebuilding basic beliefs about the self and the world. Traumatic events can not only shatter basic beliefs, but also confirm pre-existing negative beliefs. (20,26)

Dissociation and other processes that impede recovery

Psychological models of post-trauma reactions concur that recovery is thought to require ‘working through' the trauma memory—in other words, going through the experience again in one's own mind, understanding the meaning of the event, distinguishing which of the stimuli that were present at the time the trauma are dangerous and which are innocuous, and readjusting basic beliefs about the self and the world.

Horowitz(24) suggested that the normal process of recovery involves working through the traumatic experience in a graduated manner, i.e. the individual uses protective cognitive mechanisms such as denial to prevent becoming overwhelmed by the experience. Psychological models concur in that the excessive use of such avoidant strategies (e.g. trying not to think about the trauma, efforts to push intrusive memories out of one's mind, ruminating about how the trauma could have been avoided) prevents recovery. (20,22,24) There is preliminary empirical evidence supporting this hypothesis. (27,28 and 29)

The cognitive mechanism that has received the most attention in relation to acute stress disorder is dissociation, as reflected in the DSM-IV criteria. It has been argued that dissociation minimizes the adverse emotional consequences of trauma by restricting awareness of the experience to avoid overwhelming fear and loss of control. (14) Dissociation is thought to prevent recovery because it prevents the integration f the traumatic experience into existing schemas (30) and it prevents the full activation of the trauma memory which is thought to be necessary for its modification. (31) In line with these hypotheses, dissociation during or immediately after a

Biological theories

Biological theories propose that extreme stress affects neuronal functions, and that the resulting changes are responsible for the symptoms of acute stress disorder and PTSD. Specifically, there is considerable theoretical speculation concerning the neurotransmitters involved in the responses to traumatic stressors. Catecholamines, glucocorticoids, serotonin, and endogenous opioids have been studied as potential mediators of post-traumatic stress responses. In one of the few studies of biological correlates of acute stress, Resnick et al. (33) found that lower cortisol levels in the acute phase after rape predicted the presence of PTSD 3 months later. These findings are in line with other research showing abnormally low levels of cortisol in PTSD, suggesting that the hypothalamic–pituitary–adrenal axis is set to produce large responses to further stressors in PTSD.

Although some theorists, such as Kolb, (34) have proposed that excessive stimulation of the central nervous system at the time of the traumatic experience can result in permanent neuronal changes, most theories implicate prolonged stress, or the repeated stress of intrusive re-experiencing symptoms, as the major reason for neurophysiological changes. (35)

The degree of acute arousal during the traumatic stressor may be one of the factors that determine longer term trauma reactions. Acute arousal may have direct biological effects, or may reflect levels of distress that mediate persistent intrusive and avoidance patterns. (36)

Course and prognosis

Time course of symptoms

Whereas the ICD-10 criteria define acute stress reactions as a disorder that remits within a few days, DSM-IV conceptualizes acute stress disorder as a marker of those vulnerable to the development of PTSD. (30) Evidence relating to these different assumptions was sparse at the time the diagnoses were established.

Recent evidence supports the assumption that acute stress disorder is a precursor to PTSD. (17,18 and 19,37,38) In general, people who have more severe symptoms of PTSD in the weeks following trauma have a poorer prognosis than those with less severe symptoms. (39,40) Nevertheless, there is a substantial rate of spontaneous remission of about 50 per cent in the first year after a traumatic event. (39,40) Whether or not initial dissociative symptoms predict PTSD over and above what can be predicted from the initial PTSD symptoms remains unclear, and a recent prospective study reported negative findings. (18)

Predictors of acute stress disorder

Little is known about predictors of acute stress reactions. A history of psychiatric disorder, depressive and dissociative symptoms prior to the traumatic event, and previous trauma predict acute stress disorder. (38,41,42)


Psychological treatments


Critical incident stress debriefing is a widely practised intervention that has the goal of promoting adaptation to traumatic events. Debriefing is generally conducted in a group within 24 to 72 h of the trauma. However, these parameters have been modified to permit more flexible interventions. Mitchell (43) proposes that debriefing comprises seven phases:

  1. an initial outline of the purpose and benefits of debriefing;
  2. the fact phase, in which participants relate what happened to them;
  3. a thought phase, in which participants relate their initial thoughts after the critical incident;
  4. a feeling phase, which requires participants to focus on the worst aspects of the incident and engage in their emotional reactions to the incident;
  5. an assessment phase, in which participants are trained to note their physical, cognitive, emotional, and behavioural symptoms;
  6. an education phase, which provides information about stress responses and ways to manage them;
  7. the re-entry phase, in which the information given is summarized and referral information offered.

These phases may take 1 to 5 h, and are usually co-ordinated by a trained mental health professional.

Anecdotal evidence and clinical reports attest to the efficacy of debriefing. However, despite its widespread use, very few controlled trials have been conducted. A Cochrane review of randomized controlled studies of individual debriefing (44) found that although participants usually found the intervention useful, debriefing had no overall positive effect on psychological symptoms. Out of six studies included in the review, two actually found that the debriefing group had a worse outcome than the control group. (45,46 and 47) A recent randomized controlled study confirmed the conclusion that individual debriefing has no beneficial effect on post-trauma symptoms. (48)

In line with these results on individual debriefing, the first two non-randomized controlled studies of the efficacy of group debriefing found that the intervention had no beneficial effects on post-trauma symptoms. (49,50) One of the studies found negative effects of the intervention after 18 months. (50)

Cognitive–behaviour therapy

Cognitive–behavioural interventions are effective in treating PTSD. The results of two randomized controlled studies of rape victims and road traffic accident survivors suggest that a brief four-session version of this treatment is effective in acute stress disorder and prevents the development of chronic post-trauma reactions. (51,52) Treatment involved the following: 1. education about trauma reactions; 2. progressive muscle relaxation; 3. prolonged exposure; 4. cognitive restructuring of fear-related beliefs; 5. graded in vivo exposure. However, the results remain preliminary as other studies have shown a significant rate of spontaneous recovery within the first year after trauma. (39,40)

Psychopharmacological treatment

Case studies report on the utility of tricyclic antidepressants, (53) benzodiazepine anxiolytics, (54) and benzodiazepine hypnotics (55) in acutely traumatized individuals. However, no randomized controlled trials have been completed. Research on PTSD suggests that selective serotonin-reuptake inhibitors are, to date, the best pharmacological treatment for persistent reactions to traumatic stress.

Advice about management

Given the transient nature of acute stress reactions (ICD-10) and the doubtful effectiveness of early psychological debriefing, no psychological intervention that focuses on working through the traumatic experience appears to be indicated for this condition. However, clinicians who see acutely traumatized individuals are faced practical help in resuming one's life, and, if possible, facilitation of social support may be helpful. Furthermore, patients may benefit from practical advice about issues such as hospital procedures, police questioning, insurance claims, legal procedures, and media pressure to tell one's story.

If patients with acute stress reactions appear unable to tolerate the anxiety and arousal symptoms, single doses (or a few days) of benzodiazepine treatment may be considered. (54) Hypnotic medication may be considered if the patient is unable to sleep. (55) However, it remains unclear whether these medications have positive or negative effects on long-term recovery. Benzodiazepines are ineffective in treating persistent post-traumatic symptoms.

For more persistent reactions to extreme stress, treatment may be indicated. However, patients with acute stress disorder who have low symptom severity have a good chance of recovering without intervention. For those with more severe acute stress disorder symptoms, a course of cognitive–behavioural treatment may be considered. If the patient is offered cognitive–behavioural treatment, therapists need to be aware that avoidance is a hallmark symptom of acute stress disorder and may reduce the likelihood that an individual will attend treatment sessions regularly. Flexible treatment procedures (e.g. initial contacts by telephone, scheduling sessions around the patient's preferences) and discussions about the ambivalence towards treatment may be helpful. Therapists need to be knowledgeable about the conditions surrounding the traumatic event and be sensitive to the particular sociocultural background of the patient, which will affect the personal meaning of the event. If anger is a major problem, the use of specialized cognitive–behavioural techniques is recommended. (56) This treatment involves the following: 

  1. devising an anger-provocation hierarchy based on a period of self-monitoring;
  2. relaxation, breathing, and guided-imagery training to reduce physiological arousal; 
  3. restructuring of anger-related cognitions;
  4. training in communication, problem-solving, and assertiveness training.

The lack of randomized controlled trials suggests that pharmacological treatment cannot be considered a front-line treatment for acute stress disorder, but research on PTSD suggests that selective serotonin reuptake inhibitors may be helpful.

Possibilities for prevention

Identifying highly symptomatic individuals with acute stress disorder and providing a cognitive–behavioural intervention from approximately 2 weeks post-trauma may reduce the risk of later PTSD. Additional preventive methods have been explored that prepare individuals ‘at risk' (e.g. emergency services and military personnel) for experiencing trauma so as to enhance their coping strategies and reduce the risk of them developing longer term symptomatology. For those individuals at high risk of experiencing a trauma, providing them with training to remain calm, evaluate the situation objectively, (57) to not identify with victims, to utilize social supports, and to express emotional reactions (58) have all been found to be associated with better coping after the trauma. However, evidence remains preliminary.


1. Lindemann, E. (1944). Symptomatology and management of acute grief. American Journal of Psychiatry, 101, 141–8.

2. Sargent, W. and Slater, E. (1941). Amnesic syndromes in war. Proceedings of the Royal Society for Social Medicine, 34, 757–74.

3. World Health Organization (1948). International statistical classification of diseases, injuries, and causes of death (6th revision). World Health Organization, Geneva.

4. World Health Organization (1992). The ICD-10 classification of mental and behavioural disorder: diagnostic criteria for research (10th revision). World Health Organization, Geneva.

5. American Psychiatric Association (1980). Diagnostic and statistical manual of mental disorders (3rd edn). American Psychiatric Association, Washington, DC.

6. American Psychiatric Association (1989). Diagnostic and statistical manual of mental disorders (3rd edn, revised). American Psychiatric Association, Washington, DC.

7. Pincus, H.A., Frances, A., Davis, W.W., First, M.B., and Widiger, T.A. (1992). DSM-IV and new diagnostic categories: holding the line on proliferation. American Journal of Psychiatry, 149, 112–17.

8. American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders (4th edn). American Psychiatric Association, Washington, DC.

9. Bryant, R.A., Harvey, A.G., Dang, S., and Sackville, T. (1998). Assessing acute stress disorder: psychometric properties of a structured clinical interview. Psychological Assessment,

10, 215–20. 10. Steinberg, M. (1993). Structured clinical interview for DSM-IV dissociative disorders (SCID-D). American Psychiatric Press, Washington, DC.

11. First, M.B., Spitzer, R.L., Gibbon, M., and Williams, J.B.W. (1995). Structured clinical interview for DSM-IV Axis I disorders—patient version (SCID-I/P, Version 2.0). Biometrics Research Department of the New York State Psychiatric Institute, New York.

12. Cardeña, E., Classen, C., and Spiegel, D. (1991). Stanford acute stress reaction questionnaire. Stanford University Medical School, Stanford, CA.

13. Koopman, C., Classen, C., and Spiegel, D. (1994). Predictors of post-traumatic stress symptoms among survivors of the Oakland/Berkeley, Calif. firestorm. American Journal of Psychiatry, 151, 888–94.

14. Spiegel, D. (1991). Dissociation and trauma. In American psychiatric press review of psychiatry, Vol. 10 (ed. A. Tasman and S.M. Goldfinger), pp. 261–75. American Psychiatric Press, Washington, DC.

15. Harvey, A.G. and Bryant, R.A. (1998). Acute stress disorder following mild traumatic brain injury. Journal of Nervous and Mental Disease, 186, 333–7.

16. Schnyder, U. and Malt, U.F. (1998). Acute stress response patterns to accidental injuries. Journal of Psychosomatic Research, 45, 419–24.

17. Harvey, A.G. and Bryant, R.A. (1998). The relationship between acute stress disorder and post-traumatic stress disorder: a prospective evaluation of motor vehicle accident survivors. Journal of Consulting and Clinical Psychology, 66, 507–12.

18. Brewin, C.R., Andrews, B., Rose, S., and Kirk, M. (1999). Acute stress disorder and post-traumatic stress disorder in victims of violent crime. American Journal of Psychiatry, 156, 360–6.

19. Classen, C., Koopman, C., Hales, R., and Spiegel, D. (1998). Acute stress disorder as a predictor of post-traumatic stress symptoms. American Journal of Psychiatry, 155, 620–4.

20. Foa, E.B. and Riggs, D.S. (1993). Post-traumatic stress disorder in rape victims. In Annual review of psychiatry, Vol. 12 (ed. J. Oldham, M.B. Riba, and A. Tasman), pp. 273–303. American Psychiatric Association, Washington, DC.

21. Foa, E.B., Steketee, G., and Rothbaum, B.O. (1989). Behavioral/cognitive conceptualizations of post-traumatic stress disorder. Behavior Therapy, 20, 155–76.

22. Ehlers, A. and Clark, D.M. A cognitive model of persistent post-traumatic stress disorder. Behaviour Research and Therapy, in press.

23. Brewin, C.R., Dalgleish, T., and Joseph, S. (1996). A dual representation theory of post-traumatic stress disorder. Psychological Review, 103, 670–86.

24. Horowitz, M.J. (1997). Stress response syndromes. PTSD, grief and adjustment disorders. Jason Aronson, Northvale, NJ.

25. Janoff-Bulman, R. (1992). Shattered assumptions: toward a new psychology of trauma. Free Press, New York.

26. Resick, P.A. and Schnicke, M.K. (1993). Cognitive processing therapy for rape victims. Sage, Newbury Park, CA.

27. Ehlers, A. and Steil, R. (1995). Maintenance of intrusive memories in post-traumatic stress disorder: a cognitive approach. Behavioural and Cognitive Psychotherapy, 23, 217–49.

28. Ehlers, A., Mayou, R.A., and Bryant, B. (1998). Psychological predictors of chronic post-traumatic stress disorder after motor vehicle accidents. Journal of Abnormal Psychology, 107, 508–19.

29. Harvey, A.G. and Bryant, R.A. (1998). The effect of attempted thought suppression in acute stress disorder. Behaviour Research and Therapy, 36, 583–90.

30. Koopman, C., Classen, C., Cardena, E., and Spiegel, D. (1995). When disaster strikes, acute stress disorder may follow. Journal of Traumatic Stress, 8, 29–46.

31. Foa, E.B. and Hearst-Ikeda, D. (1996). Emotional dissociation in response to trauma: an information-processing approach. In Handbook of dissociation: theoretical and clinical perspectives (ed. L.K. Michelson and W.J. Ray), pp. 207–22. Plenum Press, New York.

32. Shalev, A.Y., Peri, T., Canetti, L., and Schreiber, S. (1996). Predictors of PTSD in injured trauma survivors: a prospective study. American Journal of Psychiatry, 153, 219–25.

33. Resnick, H., Yehuda, R., Pitman, R.K., and Foy, D.W. (1995). Effect of previous trauma on acute plasma cortisol level following rape. American Journal of Psychiatry, 152, 1675–7.

34. Kolb, L.C. (1987). Neurophysiological hypothesis explaining post-traumatic stress disorder. American Journal of Psychiatry, 144, 989–95.

35. van der Kolk, B.A. (1996). The psychobiology of PTSD. In Traumatic stress: the effects of overwhelming experience on mind, body, and society (ed. B.A. van der Kolk, A.C. McFarlane, and L. Weisaeth), pp. 214–41. Guilford Press, New York.

36. Shalev, A.Y. (1992). Post-traumatic stress disorder among injured survivors of a terrorist attack. Journal of Nervous and Mental Disease, 180, 505–9.

37. Bryant, R.A. and Harvey, A.G. (1998). The relationship between acute stress disorder and post-traumatic stress disorder following mild traumatic brain injury. American Journal of Psychiatry, 155, 625–9.

38. Murray, J., Ehlers, A., and Mayou, R.A. Predictors of acute stress disorder and post-traumatic stress disorder after motor vehicle accidents. Results from two prospective studies, in preparation.

39. Blanchard, E.B., Hickling, E.J., Barton, K.A., Taylor, A.E., Loos, W.R., and Jones-Alexander, J. (1996). One-year prospective follow-up of motor vehicle accident victims. Behaviour Research and Therapy, 34, 775–86.

40. Rothbaum, B.O., Foa, E.B., Riggs, D.S., Murdock, T., and Walsh, W. (1992). A prospective examination of post-traumatic stress disorder in rape victims. Journal of Traumatic Stress, 5, 455–75.

41. Barton, K.A., Blanchard, E.B., and Hickling, E.J. (1996). Antecedents and consequences of acute stress disorder among motor vehicle accident victims. Behaviour Research and Therapy, 34, 805–13.

42. Harvey, A.G. and Bryant, R.A. (1999). Predictors of acute stress following motor vehicle accidents. Journal of Traumatic Stress, 12, 519–26.

43. Mitchell, J. (1983). When disaster strikes. The critical incident stress debriefing process. Journal of Emergency Medical Services, 8, 36–9.

44. Rose, S. and Bisson, J. (1998). Brief early psychological interventions following trauma: a systematic review of the literature. Journal of Traumatic Stress, 11, 697–710.

45. Bisson, J.I., Jenkins, P.L., Alexander, J., and Bannister, C. (1997). Randomised controlled trial of psychological debriefing for victims of acute burn trauma. British Journal of Psychiatry, 171, 78–81.

46. Hobbs, M., Mayou, R., Harrison, B., and Worlock, P. (1996). A randomised controlled trial of psychological debriefing for victims of road traffic accidents. British Medical Journal, 7, 1438–9.

47. Mayou, R.A., Ehlers, A., and Hobbs, M. A three year follow-up of a randomised controlled trial of psychological debriefing for road traffic accident victims. Submitted for publication.

48. Rose, S., Brewin, C., Andrews, B., and Kirk, M. A randomised trial of psychological debriefing for victims of violent crime. Submitted for publication.

49. Kenardy, J.A., Webster, R.A., Lewin, T.J., Carr, V. J., Hazell, P.L., and Carter, G.L. (1996). Stress debriefing and patterns of recovery following a natural disaster. Journal of Traumatic Stress, 9, 37–49.

50. Carlier, I.V.E., Lamberts, R.D., van Uchelen, A.J., and Gersons, B.P.R. (1998). Disaster-related post-traumatic stress in police officers: a field study of the impact of debriefing. Stress Medicine, 14, 143–8.

51. Foa, E.B., Hearst-Ikeda, D., and Perry, K.J. (1995). Evaluation of a brief cognitive–behavioural program for the prevention of chronic PTSD in recent assault victims. Journal of Consulting and Clinical Psychology, 63, 948–55.

52. Bryant, R.A., Harvey, A.G., Dang, S.T., Sackville, T., and Basten, C. (1998). Treatment of acute stress disorder: a comparison of cognitive behaviour therapy and supportive counselling. Journal of Consulting and Clinical Psychology, 66, 862–6.

53. Blake, D.J. (1986). Treatment of acute postraumatic stress disorder with tricyclic antidepressants. Southern Medical Journal, 79, 201–4.

54. Ashton, H. (1994). Guidelines for the rational use of benzodiazepines. Drugs, 48, 25–40.

55. Mellman, T.A., Byers, P.M., and Augenstein, J.S. (1998). Pilot evaluation of hypnotic medication during acute traumatic stress response. Journal of Traumatic Stress, 11, 563–9.

56. Chemtob, C.M., Novaco, R.W., Hamada, R.S., and Gross, D.M. (1997). Anger regulation deficits in combat-related posttraumatic stress disorder. Journal of Traumatic Stress, 10, 17–36.

57. Hytten, K. (1989). Helicopter crash in water: effects of simulator escape training. Acta Psychiatrica Scandinavica, 80 (Supplement), 73–8.

58. Fullerton, C.S., McCarroll, J.E., Ursano, R.J., and Wright, K.M. (1992). Psychological responses of rescue workers: fire fighters and trauma. American Journal of Orthopsychiatry, 62, 371–8.