The correctional officer in the preceding vignette displays many of the signs and symptoms consistent with Acute Stress Disorder (ASD). She was clearly having a difficult time adjusting after her exposure to the traumatic stressor of witnessing her colleague being murdered. She was not returning to a normal level of functioning, and her levels of stress were problematic enough to cause significant functional impairment. Acute Stress Disorder is sometimes considered the precursor to PTSD. Both of these disorders share a great many symptoms, although ASD includes more dissociative symptoms than PTSD. The main difference between the two is that ASD can only be diagnosed within the first 2 days to 4 weeks after a traumatic stressor, and PTSD can only be diagnosed after 4 weeks following exposure to a traumatic stressor. In essence, ASD is PTSD for 4 weeks; after that, if symptoms persist, it becomes PTSD. The main symptom clusters of ASD are the same as for PTSD: reexperiencing, avoidance, and hyperarousal. Acute Stress Disorder has the additional symptom cluster of dissociation as separate, and an individual has to exhibit three symptoms in order to meet criteria for this cluster. Examples of dissociative symptoms are numbing, reduced awareness of one's surroundings, depersonalization, derealization, and amnesia.
An important question regarding ASD is what distinguishes a normal or expected reaction to a traumatic stressor and a more pathological one such as ASD? After all, aren't people entitled to emotional turmoil, shock, and distress after a traumatic event? With the existence of the diagnosis of ASD, it would seem that we are all expected to get back to business after only 2 days and return to our baseline level of functioning. This is why PTSD is not diagnosed until after 4 weeks, in order not to "pathologize transient and normative stress reactions" (Harvey & Bryant, 2002, p. 86). One way to answer this question is to rely on the criterion for all DSM-IV-TR disorders that symptoms must be significant enough to cause significant impairment. This, however, is not a perfect remedy. Ultimately, the issue of whether the existence of ASD pathologizes normal and transient stress reactions is to know that its existence as a diagnosis is considered controversial within the field of mental health for this very reason. Acute Stress Disorder perhaps represents the prototypical example of what critics of the mental health field consider the pathologizing of all variation in human behavior and mental processes. This is one disorder where clinical judgment should be exercised with extreme care, carefully analyzing the nature of the exposure, the symptoms being displayed, and the severity of the functional impairment when considering giving an individual the diagnosis. Ultimately, professionals should be keenly aware of the purposes of diagnosis as a practice to aid in treatment. If an individual is exhibiting ASD-symptoms posttrauma, would a diagnosis of a formal mental disorder aid this person and help them be helped.
Rates of ASD collected in research range from 6 percent to 33 percent. In returning to the issue of the controversy for a moment, these rates should at least partially answer the question of whether normative stress reactions are being pathologized. Taking these rates as indicators, the answer to that question would be no because even in the case of the 33 percent, the large majority, 67 percent of people exposed to traumatic stressors, will not develop ASD symptoms, and 67 percent certainly represents a normative sample size. Individuals that have been found to be at risk for ASD include those with previous PTSD, premorbid psychological problems, previous depression, previous mental health treatment, and those who are prone to dissociate in the face of extreme stress (Barton, Blanchard, & Hickling, 1996; Bryant, Guthrie, & Moulds, 2001; Bryant & Harvey, 2000).
Theoretical models of ASD include dissociative, cognitive, and biological explanations (Harvey & Bryant, 2002). From the dissociative perspective, ASD develops as a consequence of dissociation interfering with the integration and resolution of traumatic memories and affect (Koopman, Classen, Cardeña, & Spiegel, 1995). From the cognitive perspective, ASD may be the consequence of individuals having difficulties in accessing and resolving trauma memories due to retrieval breakdown or schematic disorganization (Harvey & Bryant, 2002). Also, from the cognitive perspective, ASD is considered linked to an individual's cognitive distortion of the probability of future negative events (Warda & Bryant, 1998). Finally, from the biological perspective, ASD is related to disrupted catecholamine functioning and hypothalamic-pituitary-adrenal axis (HPA-Axis) dysfunction.
Finally, ASD treatment can be approached from either a cognitive-behavioral approach or with earlier interventions such as crisis intervention, psychological first aid, critical incident stress debriefing, and other forms of secondary prevention.
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