Acute Stress Disorder (ASD)

Introduction and Clinical Features of ASD

an individual suffering from acute-stress-disorder
Image courtesy of Spacious Therapy Opens in new window

In recognition of the severe distress and psychological dysfunction that often occur immediately after a trauma Opens in new window, a new diagnostic classification labeled Acute Stress Disorder (ASD) was adopted in the DSM-IV Opens in new window in 1994.

Acute stress disorder (ASD) is a number of physical and psychological reactions occurring immediately after a traumatic experience, lasts between two days and a month (if symptoms last longer than that, the diagnosis is PTSD Opens in new window), and causes symptoms so severe that they interfere with a person’s ability to handle normal, day-to-day activities.

Many trauma victims report being disoriented and anxious after a trauma and have difficulty sleeping and concentrating. Victims are often reluctant to talk about the trauma or deliberately contemplate it; nevertheless the traumatic memory intrudes on their thoughts quite frequently instead of fading away in a few days or weeks.

DSM-IV Diagnostic Criteria for ASD

In DSM-IV the ASD diagnosis required that the individual needed to be exposed to a traumatic event in which there was actual or threatened death or serious injury and they experienced fear, helplessness, or horror.

Four additional symptom clusters needed to be satisfied. Three of these clusters were similar to the PTSD criteria, insofar as the person needed to exhibit one or more re-experiencing symptoms, marked avoidance of stimuli that remind the individual of the trauma, and marked anxiety or arousal symptoms.

These symptoms also had to cause significant distress or impairment and last for a minimum of two days and a maximum of four weeks.

The distinctive symptom cluster of ASD involved dissociative features, and consequently, the diagnostic criteria required at least three of the following dissociative symptoms:

  1. a subjective sense of numbing, detachment, or absence of emotional responsiveness;
  2. reduced awareness of surroundings (e.g., being a daze);
  3. derealization;
  4. depersonalization; and
  5. dissociative amnesia.

The historical roots of this emphasis on dissociation in ASD can be traced to the work of Janet in the early 20th century (Janet, 1907), who proposed that some trauma survivors respond to traumatic experiences by splitting awareness of their distressed state from consciousness.

Janet posited that this reaction placed demands on one’s psychological resources, which led to subsequent psychopathological states. This perspective became popular in the years prior to DSM-IV, and this led to the notion that dissociative symptoms in the aftermath of trauma were pivotal in moderating subsequent PTSD (van der Kolk & van der Hart, 1989). Accordingly, it was proposed that dissociative responses to the trauma in the acute phase resulted in limited access to trauma memories, which would limit processing of emotional experiences and lead to ongoing PTSD (Spiegel, Koopman, & Classen, 1994).

Supporting this idea was early evidence that dissociation in the acute phase was associated with subsequent PTSD (Cardeňa & Spiegel, 1993; Holen, 1993), and which has been replicated numerous times.

ASD in DSM-5

The evidence reviewed above was important in laying the foundation for changes in the ASD diagnosis in the fifth edition of the DSM (DSM-5; American Psychiatric Association, 2013).

On the basis of the ASD having poor predictive capacity, one of the most important changes in DSM-5 was that the ASD diagnosis was no longer intended to predict subsequent PTSD (Bryant, Friedman, Spiegel, Ursano, & Strain, 2011).

The emphasis of the diagnosis was shifted solely to identifying people who are experiencing severe stress reactions and may require mental health assistance.

In DSM-IV the diagnosis of ASD required satisfaction of four different symptom clusters. Whereas several factor analytic studies of ASD symptoms have supported the DSM-IV conceptualization of the four factors (Brooks et al., 2008; Cardena, Koopman, Classen, Waelde, & Spiegel, 2000; Wang et al., 2000), others have found that the four-factor structure does not accommodate ASD responses (Armour, Elklit, & Shevlin, 2013; Bryant, Moulds, & Guthrie, 2000).

As a result, in DSM-5 the diagnosis of ASD was restructured such that it did not require specific symptom clusters to be present. Instead, it was decided that a minimum of 9 out of a possible 14 symptoms should be present. This was deemed to reflect people who suffered severe stress reactions that may warrant mental health intervention.

Other changes were introduced in the wake of increasing evidence. The number of dissociative symptoms were reduced from the five to two:

  1. reduced awareness of one’s surroundings was deleted on the grounds that it pertained predominantly to response occurring during the trauma,
  2. symptoms of derealization and depersonalization were combined into a single item because of the documented overlap between these two responses (Harvey & Bryant, 1999c); and
  3. dissociative amnesia was retained.

There were also a minor shift in the time frame of when ASD can be diagnosed. There is evidence that many people who will experience stress reactions in the initial days after trauma will subsequently report fewer reactions in the following weeks (Solomon, Laor, & McFarlane, 1996), and so the change was extended from two to three days.

Incidence of ASD

In contrast to most psychiatric disorders, there is an absence of epidemiological studies of ASD.

Because it is not chronic disorder, it is unusual for population studies to index this disorder in the context of traumatic events that occurred in the previous month.

Hence, knowledge of the incidence of ASD is restricted to studies that are conducted on trauma-exposed populations within one month of exposure.

These studies have led to quite varied rates of ASD. For example, ASD has been reported following motor vehicle accidents (13% to 21%), mild traumatic brain injury (14%), assault (16% to 19%), burns (10%), industrial accidents (6%), and witnessing a mass shooting (33%).

It is worth noting that these studies employed the DSM-IV criteria for ASD diagnosis, and there is limited evidence regarding the incidence of ASD using the DSM-5 criteria. Using DSM-5 criteria, ASD has been noted in 10% of bank robbery victims and 14% of traumatic injury patients; however, further studies are needed to establish a robust evidence base of the incidence of ASD using the DSM-5 definition.

Biological Models of ASD

Arguably the major model of acute traumatic stress involves biological process. This perspective typically involves fear conditioning models, which posit that psychological trauma triggers noradrenergic and glucocorticoid activation, which fosters consolidation of trauma memories.

Fear conditioning models propose that the fear experienced at the time of trauma causes strong associative conditioning between the fear and many stimuli associated with the trauma and that when one is confronted with trauma reminders, conditioned responses are triggered; these responses may include re-experiencing symptoms, such as intrusive memories and physiological reactivity (Pitman, 1989).

In support of this model is much evidence that psychophysiological reactivity is activated in PTSD patients when exposed to trauma reminders (Blanchard, Kolb, Gerardi, Ryan, & Pallmeyer, 1986).

It is proposed that most people adapt to a traumatic experience by virtue of extinction learning, in which trauma survivors are exposed to trauma reminders without any harmful consequences and thereby new learning occurs that the previously conditioned reminders now signal safety (Milad, Rauch, Pitman, & Quirk, 2006). In this sense, PTSD can be regarded as an example of failed extinction learning (Myers & Davis, 2007).

Consistent with fear conditioning models, studies have examined resting heart rate immediately after trauma exposure because sympathetic arousal may reflect the level of fear conditioning. These studies have noted that higher resting heart rates in adults and children in the days after trauma exposure predict subsequent PTSD (Shalev et al., 1998). This pattern is also reflected in the finding that elevated respiration rate in the first 48 hours predicts PTSD (Bryant et al., 2008b).

More direct support for the process of fear conditioning is a finding that phasic increases in heart rate in response to trauma reminders are a stronger predictor of PTSD than resting state heart rate (O’Donnell, Creamer, Elliott, & Bryant, 2007). It is also worth noting that nearly all people with ASD reported having panic symptoms during the trauma, and most of these persist in the weeks after the event (Nixon & Bryant, 2003).

Several studies have shown that only a minority of people develop PTSD, and there is evidence that one of the key risk factors for PTSD is if they are predisposed to enhanced conditioning or impaired extinction before the trauma exposure. For example, one study assessed newly recruited fire-fighters, who at the time of assessment were in class-based training and had not commenced active duty, on conditioning paradigms. This study found that recruits’ skin conductance and eyeblink startle reactions in response to startling tones predicted their level of acute stress symptoms within a month of subsequently being exposed to a traumatic event as a fire-fighter (Guthrie & Bryant, 2005).

This observation may suggest that the tendency to be reactive to stressors increases vulnerability to fear conditioning. In a more direct study of conditioning, this study also assessed extinction learning on an experimental task before trauma exposure and found that the level of PTSD two years after commencing firefighting duties was predicted by impoverished extinction learning as a recruit (Guthrie & Bryant, 2006).

This finding has been replicated in both first responders and military personnel who were assessed prior to exposure to traumatic events (Lommen, Engelhard, Sijbrandij, van den Hout, & Hermans, 2013; Orr et al., 2012). These findings strongly indicate that individual differences in extinction learning are pivotal in the risk for PTSD.

Cognitive Models of ASD

The other influential model focuses on cognitive mechanisms. This model proposes that traumatic stress is moderated by

  1. the manner in which the trauma is encoded in memory and
  2. excessively negative appraisals about the traumatic experience and the aftermath (Ehlers & Clark, 2000).

In terms of appraisals, cognitive models posit that trauma response is influenced by how the survivor interprets trauma experiences, especially regarding one’s role in the trauma, one’s vulnerability for future harm, and one’s worth as a person.

Specifically, the appraisals of vulnerability (e.g., “I can never feel safe again”), one’s role in the trauma (e.g., “the attack was my fault”), one’s role in the trauma (e.g., “the attack was my fault”), or one’s worth (e.g., “I am a terrible mother for not coping better”) can contribute substantially to the acute and chronic stress response.

Much evidence supports this model, with people with chronic PTSD displaying distorted appraisals (Dunmore, Clark, & Ehlers, 1997). In terms of acute stress, people with ASD exaggerate both the probability of negative events happening to them and also the severity of how adverse those events would be (Smith & Bryant, 2000; Warda & Bryant, 1998).

Further, negative appraisals in the acute phase are predictive of later PTSD (Dunmore, Clark, & Ehlers, 2001). Relatedly, cognitive styles that are characterized by ruminating after a traumatic event are also predictive of later PTSD (Ehlers, Mayou, & Bryant, 2003).

Cognitive models also emphasize the importance of how memories are encoded and consolidated. The strong arousal at the time of trauma purportedly results in details of the trauma being encoded in a predominantly sensory (and often visual) manner. That is, a motor vehicle accident survivor may have recurring images of the grill of the truck he smashed into but have patchy recall of other events as they occurred.

According to this model, this form of encoding (“data-driven processing”) leads to fragmented memories of the trauma that foster a sense of “newness” in which person re-experiences the memory as if it is still in the present.

Consistent with this perspective, data-driven processing has been associated with intrusive memories and PTSD (Ehring, Ehlers, & Glucksman, 2008).

Moreover, data-driven processing in the acute phase is linked with heart rate increase in response to trauma-related stimuli (Ehlers et al., 2010). Similarly, children with ASD report more sensory-laden memories of their trauma, which in turn mediates the relationship between perceived threat of a trauma and severity of ASD (Meiser-Stedman, Dalgleish, Smith, Yule, & Glucksman, 2007). Also people with ASD have fragmented memories (Harvey & Bryant, 1999a), which accords with the proposal that acute stress is associated with memory disorganization.

Treating ASD

  1. Psychotherapy Approaches

Similar to the status of treatment of PTSD Opens in new window, the evidence indicates that the treatment of choice for ASD is trauma-focuses cognitive behavior therapy (CBT). Treatment guidelines around the world recommend this approach for the treatment of ASD and prevention of PTSD (Foa, Keane, Friedman, & Cohen, 2009).

This therapy typically begins with education about psychological trauma and then focuses on anxiety management, exposure therapy, and cognitive restructuring.

Education intends to normalize the trauma response, explains basic mechanisms for ASD symptoms, and discusses how core symptoms will be treated during therapy. Anxiety management techniques intend to reduce arousal through breathing retraining, relaxation skills, and self-talk.

Arguably the most central technique of CBT is exposure therapy, which can involve both imaginal and in vivo exposure. Imaginal exposure (also called prolonged exposure) directs patients to “relive” their trauma for prolonged periods (often for at least 30 minutes; Foa, 2011). This involves people providing a detailed narrative of their experience with the goal of accessing emotional engagement and relevant details.

This technique is often combined with in vivo exposure, which involves graded exposure to stimuli that causes distress (the patient initially remains in proximity to mildly distressing trauma reminders) and then repeating this exercise with increasingly distressing scenarios situations. Most programs also include cognitive restructuring, which teaches patients to identify and evaluate the evidence for negative automatic thoughts and develop more realistic appraisals of these factors.

  1. Pharmacological Approaches

In contrast to the evidence on psychotherapeutic approaches, there is a paucity of evidence for pharmacological interventions. In a Jerusalem study that randomized patients to either prolonged exposure, cognitive restructuring, wait-list (who were then randomized to exposure or cognitive restructuring after 12 weeks), escitalopram (SSRI), or placebo (Shalev et al., 2012), nine months after treatment, rates of PTSD in exposure (21%) and restructuring (22%) conditions were lower than rates in the SSRI (42%) and placebo (47%) conditions.

Another study of ASD patients also found no greater benefit of escitalopram relative to placebo (Suliman et al., 2015).

In terms of pharmacological interventions with children, one randomized trial reported that seven days of treatment with imipramine was more effective in treating symptoms of ASD in 25 child and adolescent burns victims than chloral hydrate (Robert, Blakeney, Villarreal, Rosenberg, & Meyer, 1999), although another study with burnt children found no effect for imipramine (Robert et al., 2008).

Several small and uncontrolled trials have used benzodiazepines to address the acute anxiety, agitation, or sleep problems that commonly occur in the immediate aftermath of trauma exposure, with mixed results suggesting that benzodiazepines can reduce stress symptoms (Gelpin, Bonne, Peri, & Brandes, 1996); it should be noted, however, that persistent use may lead to exacerbation of PTSD symptoms.

Although no randomized controlled trials have been conducted, there is reason to believe that morphine in the acute phase after trauma may reduce later PTSD.

Morphine can serve to reduce noradrenergic release, and animal work indicates that morphine injections into the amygdala impairs acquisition of fear conditioning and impairs memory for fear conditioning.

Several studies have demonstrated that greater morphine dose in the initial days after trauma exposure is associated with reduced subsequent PTSD in both adults and children. It is important to note that none of these studies represent controlled trials, and so one needs to be cautious about interpreting any causal relationship.

    Adapted from: Trauma- and Stressor-Related Disorders, edited by Frederick J. Stoddard, David M. Benedek, Mohammed R. Milad, Robert J. Ursano. References as cited include:
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