Acute stress reaction | |
---|---|
Classification and external resources | |
After being attacked and stabbed, Austrian empress Elisabeth of Bavaria boarded a ship, unaware of the severity of her condition as a consequence of an acute stress reaction. Bleeding to death from a puncture wound to the heart, Elisabeth's last words were, "What happened to me?" |
|
ICD-10 | F43.0 |
ICD-9 | 308 |
MeSH | D040701 |
Acute stress reaction (also called acute stress disorder, psychological shock, mental shock, or simply shock) is a psychological condition arising in response to a terrifying or traumatic event. It should not be confused with the unrelated circulatory condition of shock.
"Acute stress response" was first described by Walter Cannon in the 1920s as a theory that animals react to threats with a general discharge of the sympathetic nervous system. The response was later recognized as the first stage of a general adaptation syndrome that regulates stress responses among vertebrates and other organisms.
The onset of a stress response is associated with specific physiological actions in the sympathetic nervous system, both directly and indirectly through the release of adrenaline and to a lesser extent noradrenaline from the medulla of the adrenal glands. These catecholamine hormones facilitate immediate physical reactions by triggering increases in heart rate and breathing, constricting blood vessels. An abundance of catecholamines at neuroreceptor sites facilitates reliance on spontaneous or intuitive behaviors often related to combat or escape.
Normally, when a person is in a serene, unstimulated state, the "firing" of neurons in the locus ceruleus is minimal. A novel stimulus, once perceived, is relayed from the sensory cortex of the brain through the thalamus to the brain stem. That route of signaling increases the rate of noradrenergic activity in the locus ceruleus, and the person becomes alert and attentive to the environment.
If a stimulus is perceived as a threat, a more intense and prolonged discharge of the locus ceruleus activates the sympathetic division of the autonomic nervous system (Thase & Howland, 1995). The activation of the sympathetic nervous system leads to the release of noradrenaline from nerve endings acting on the heart, blood vessels, respiratory centers, and other sites. The ensuing physiological changes constitute a major part of the acute stress response. The other major player in the acute stress response is the hypothalamic-pituitary-adrenal axis.
Contents |
By definition, acute stress disorder is the result of a traumatic event in which the person experiences or witnesses an event that causes the victim/witness to experience extreme, disturbing or unexpected fear, stress or pain, and that involves or threatens serious injury, perceived serious injury or death to themselves or someone else. Acute stress reaction is a variation of Post-Traumatic Stress Disorder (PTSD) and is the mind's and body's response to feelings (both perceived and real) of intense helplessness.
The symptoms show great variation but typically include an initial state of "daze", with some constriction of the field of consciousness and narrowing of attention, inability to comprehend stimuli, and disorientation.
This state may be quickly followed by either further withdrawal from the surrounding situation (to the extent of a dissociative stupor), or by agitation and overactivity, anxiety, impaired judgement, confusion, detachment, and depression. Autonomic signs of panic anxiety (tachycardia, sweating, flushing) are also commonly present.
The symptoms usually appear within minutes of the impact of the stressful stimulus or event, and disappear within 2–3 days (often within hours). Partial or complete amnesia for the episode may be present.
Common symptoms that sufferers of acute stress disorder experience are: numbing; detachment; derealization; depersonalization or dissociative amnesia; continued re-experiencing of the event by such ways as thoughts, dreams, and flashbacks; and avoidance of any stimulation that reminds them of the event. During this time, they must have symptoms of anxiety, and significant impairment in at least one essential area of functioning. Symptoms last for a minimum of 2 days, and a maximum of 4 weeks, and occur within 4 weeks of the event.[1]
There must be an immediate and clear temporal connection between the impact of an exceptional stressor and the onset of symptoms; onset is usually within a few minutes, if not immediate. In addition, the symptoms show a mixed and usually changing picture; in addition to the initial state of "daze", depression, anxiety, anger, despair, overactivity, and withdrawal may all be seen, but no one type of symptom predominates for long; resolve rapidly (within a few hours at the most) in those cases where removal from the stressful environment is possible; in cases where the stress continues or cannot by its nature be reversed, the symptoms usually begin to diminish after 24–48 hours and are usually minimal after about 3 days.[1]
If symptoms last for more than a month, then the patient might be instead diagnosed with PTSD.
This disorder may resolve itself with time or may develop into a more severe disorder such as PTSD. However, results of Creamer, O'Donnell, and Pattison's (2004) study of 363 patients suggests that a diagnoses of Acute Stress Disorder had only limited predictive validity for PTSD. Creamer et al. did however find that re-experiences of the traumatic event and arousal were better predictors of PTSD.[2] Medication can be used for a very short duration (up to four weeks).
A number of studies have been conducted to assess the efficacy of counselling and psychotherapy for people with ASD. Cognitive behavioral therapy which included exposure and cognitive restructuring was found to be effective in preventing PTSD in patients diagnosed with ASD with clinically significant results at 6 months follow-up. A combination of relaxation, cognitive restructuring, imaginal exposure, and in vivo exposure was superior to supportive counselling.[3]
|