Acute stress disorder
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|Acute stress reaction|
Acute stress disorder (ASD, also known as acute stress reaction, psychological shock, mental shock, or simply shock) is a psychological response to a terrifying, traumatic, or surprising experience. Acute stress disorder is not fatal, but it may bring about delayed stress reactions (better known as posttraumatic stress disorder, or PTSD) if not correctly addressed.
Types of ASD
Sympathetic (also known as "fight or flight" response)
Sympathetic acute stress disorder is caused by the release of excessive adrenaline and norepinephrine into the nervous system. These hormones may speed up a person's pulse and respiratory rate, dilate pupils, or temporarily mask pain. This type of ASD developed as an evolutionary advantage to help humans survive dangerous situations. The "fight or flight" response may allow for temporarily-enhanced physical output, even in the face of severe injury. However, other physical illnesses become more difficult to diagnose, as ASD masks the pain and other vital signs that would otherwise be symptomatic.
Parasympathetic acute stress disorder is characterised by feeling faint and nauseous. This response is fairly often triggered by the sight of blood. In this stress response, the body releases acetylcholine. In many ways, this reaction is the opposite of the sympathetic response, in that it slows the heart rate and can cause the patient to either regurgitate or temporarily lose consciousness. The evolutionary value of this is unclear, although it may have allowed for prey to appear dead to avoid being eaten.
Signs and symptoms
Dissociative symptoms include a sense of numbing or detachment from emotional reactions, a sense of physical detachment – such as seeing oneself from another perspective – decreased awareness of one's surroundings, the perception that one's environment is unreal or dreamlike, and the inability to recall critical aspects of the traumatic event (dissociative amnesia).
In addition to these characteristics, ASD can be present in the following four distinct symptom clusters;
Recurring and distressing dreams, flashbacks, and/or memories related to the traumatic event.
Intense/prolonged psychological distress or somatic reactions to internal or external traumatic cues.
- Negative mood cluster
A persistent inability to experience positive emotions such as happiness, loving feelings, or satisfaction.
- Avoidance symptom cluster
The avoidance of distressing memories, thoughts, feelings (or external reminders of them) that are closely associated with the traumatic event.
- Arousal symptom cluster
Sleep disturbances, hyper-vigilance, difficulties with concentration, easily startled, and irritability/anger/aggression.
There are a number of issues that can arise from acute stress. Depression, anxiety, mood disorders, and substance abuse problems can develop from acute stress. Untreated ASD can also lead to the development of Post-Traumatic Stress Disorder.
There are several theoretical perspectives on trauma response, including cognitive, biological, and psycho-biological. While PTSD-specific, these theories are still useful in understanding acute stress disorder, as the two disorders share many symptoms. A recent study found that even a single stressful event may have long-term consequences on cognitive function. This result calls the traditional distinction between the effects of acute and chronic stress into question.
Stress is characterised by specific physiological responses to adverse or noxious stimuli.
The sympathetic branch of the autonomic nervous system gives rise to a specific set of physiological responses to physical or psychological stress. The body's response to stress is also termed a "fight or flight" response, and it is characterised by an increase in blood flow to the skeletal muscles, heart, and brain, a rise in heart rate and blood pressure, dilation of pupils, and an increase in the amount of glucose released by the liver.
The onset of an acute 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 behaviours often related to combat or escape.
Normally, when a person is in a serene, non-stimulated 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 signalling increases the rate of noradrenergic activity in the locus ceruleus, and the person becomes more alert and attentive to their 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. The activation of the sympathetic nervous system leads to the release of norepinephrine from nerve endings acting on the heart, blood vessels, respiratory centres, 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. Stress activates this axis and produces neuro-biological changes. These chemical changes increase the chances of survival by bringing the physiological system back to homeostasis.
The autonomic nervous system controls all automatic functions in the body and contains two subsections within it that aid the response to an acute stress reaction. These two subunits are the sympathetic nervous system and the parasympathetic nervous system. The sympathetic response is colloquially known as the "fight or flight" response, indicated by accelerated pulse and respiration rates, pupil dilation, and a general feeling of anxiety and hyper-awareness. This is caused by the release of epinephrine and norepinephrine from the adrenal glands. The epinephrine and norepinephrine strike the beta receptors of the heart, which feeds the heart's sympathetic nerve fibres to increase the strength of heart muscle contraction; as a result, more blood gets circulated, increasing the heart rate and respiratory rate. The sympathetic nervous system also stimulates the skeletal system and muscular system to pump more blood to those areas to handle the acute stress. Simultaneously, the sympathetic nervous system inhibits the digestive system and the urinary system to optimise blood flow to the heart, lungs, and skeletal muscles. This plays a role in the alarm reaction stage. The parasympathetic response is colloquially known as the "rest and digest" response, indicated by reduced heart and respiration rates, and, more obviously, by a temporary loss of consciousness if the system is fired at a rapid rate. The parasympathetic nervous system stimulates the digestive system and urinary system to send more blood to those systems to increase the process of digestion. To do this, it must inhibit the cardiovascular system and respiratory system to optimise blood flow to the digestive tract, causing low heart and respiratory rates. The parasympathetic nervous system plays no role in acute stress response.
Studies have shown that patients with acute stress disorder have overactive right amygdalae and prefrontal cortices; both structures are involved in the fear-processing pathway.
According to the DSM-V, symptom presentation must last for three consecutive days to be classified as acute stress disorder. If symptoms persist past one month, the diagnosis of PTSD is explored. There must be a clear temporal connection between the impact of an exceptional stressor and the onset of symptoms; onset is usually within a few minutes or days but may occur up to one month after the stressor. Also, the symptoms show a mixed and rapidly changing picture; although "daze" depression, anxiety, anger, despair, hyper-activity, and withdrawal may all be seen, no one symptom dominates for long. The symptoms usually resolve rapidly where removal from the stressful environment is possible. In cases where the stress continues, the symptoms usually begin to diminish after 24–48 hours and are usually minimal after about three days.
Evaluation of patients is done through close examination of emotional response. Using self-report from patients is a large part of diagnosing ASD, as acute stress is the result of reactions to stressful situations.
The DSM-V specifies that there is a higher prevalence rate of ASD among females compared to males due to higher risk of experiencing traumatic events and neurobiological gender differences in stress response.
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 diagnosis of acute stress disorder had only limited predictive validity for PTSD. Creamer et al. found that re-experiences of the traumatic event and arousal were better predictors of PTSD. Early pharmacotherapy may prevent the development of post-traumatic symptoms. Additionally, early trauma-focused cognitive behavioural therapy (TF-CBT) for those with a diagnosis of ASD can protect an individual from developing chronic PTSD.
Studies have been conducted to assess the efficacy of counselling and psychotherapy for people with acute stress disorder. Cognitive behavioural therapy, which includes exposure and cognitive restructuring, was found to be effective in preventing PTSD in patients diagnosed with acute stress disorder with clinically significant results at six-month follow-up appointments. A combination of relaxation, cognitive restructuring, imaginal exposure, and in-vivo exposure was superior to supportive counselling. Mindfulness-based stress reduction programmes also appear to be effective for stress management.
The pharmacological approach has made some progress in lessening the effects of ASD. To relax patients and allow for better sleep, Prazosin can be given to patients, which regulates their sympathetic response. Hydrocortisone has shown some success as an early preventative measure following a traumatic event, typically in the treatment of PTSD.
In a wilderness context where counselling, psychotherapy, and cognitive behavioural therapy is unlikely to be available, the treatment for acute stress reaction is very similar to the treatment of cardiogenic shock, vascular shock, and hypovolemic shock; that is, allowing the patient to lie down, providing reassurance, and removing the stimulus that prompted the reaction. In traditional shock cases, this generally means relieving injury pain or stopping blood loss. In an acute stress reaction, this may mean pulling a rescuer away from the emergency to calm down or blocking the sight of an injured friend from a patient.
The term "acute stress disorder" was first used to describe the symptoms of soldiers during World War I and II, and it was therefore also termed "combat stress reaction" (CSR). Approximately 20% of U.S. troops displayed symptoms of CSR during WWII. It was assumed to be a temporary response of healthy individuals to witnessing or experiencing traumatic events. Symptoms include depression, anxiety, withdrawal, confusion, paranoia, and sympathetic hyperactivity.
The APA officially included the term ASD in the DSM-IV in 1994. Before that, symptomatic individuals within the first month of trauma were diagnosed with adjustment disorder. According to the DSM-IV, acute stress reaction refers to the symptoms experienced immediately to 48 hours after exposure to a traumatic event. In contrast, acute stress disorder is defined by symptoms experienced 48 hours to one month following the event. Symptoms experienced for longer than one month are consistent with a diagnosis of PTSD.
Initially, being able to describe different ASRs was one of the goals of introducing ASD. Some criticisms surrounding ASD's focal point include issues with ASD recognising other distressing emotional reactions, like depression and shame. Emotional reactions similar to these may then be diagnosed as adjustment disorder under the current system of trying to diagnose ASD.
Since its addition to the DSM-IV, questions about the efficacy and purpose of the ASD diagnosis have been raised. The diagnosis of ASD was criticized as an unnecessary addition to the progress of diagnosing PTSD, as some considered it more akin to a sign of PTSD than an independent issue requiring diagnosis. Also, the terms ASD and ASR have been criticized for not fully covering the range of stress reactions.
- Isaac, Jeff. (2013). Wilderness and rescue medicine. Jones & Bartlett Learning. ISBN 9780763789206. OCLC 785442005.
- Reynaud, Emmanuelle; Guedj, Eric; Trousselard, Marion; El Khoury-Malhame, Myriam; Zendjidjian, Xavier; Fakra, Eric; Souville, Marc; Nazarian, Bruno; Blin, Olivier; Canini, Frédéric; Khalfa, Stephanie (2015). "Acute stress disorder modifies cerebral activity of amygdala and prefrontal cortex". Cognitive Neuroscience. 6 (1): 39–43. doi:10.1080/17588928.2014.996212. PMID 25599382. S2CID 12378221.
- Bryant, R.; Harvey, A. (2000). Acute Stress Disorder: A Handbook Of Theory, Assessment, And Treatment. Washington, D.C.: American Psychological Association. pp. 3–40, 87–134.
- American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders (5 ed.). Arlington, VA: American Psychiatric Publishing.
- Fanai, Mehdi; Khan, Moien AB (2021), "Acute Stress Disorder", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 32809650, retrieved 2021-03-14
- Musazzi, L; Tornese, P; Sala, N; Popoli, M (2016). "Acute stress is not acute: Sustained enhancement of glutamate release after acute stress involves readily releasable pool size and synapsin I activation". Molecular Psychiatry. 22 (9): 1226–1227. doi:10.1038/mp.2016.175. PMID 27698433. S2CID 7077097. Lay summary – Neuroscience News (November 23, 2016).
- Butler, G (1993). "Definitions of stress". Occasional Paper (Royal College of General Practitioners) (61): 1–5. PMC 2560943. PMID 8199583.
- Widmaier, Eric P. (2015). Vander's Human Physiology: The Mechanisms Of Body Function. Boston: McGraw-Hill Education. p. 182. ISBN 978-1-259-60779-0.
- Eiden, Lee E. (2013). "Neuropeptide–Catecholamine Interactions in Stress". A New Era of Catecholamines in the Laboratory and Clinic. Advances in Pharmacology. 68. pp. 399–404. doi:10.1016/B978-0-12-411512-5.00018-X. ISBN 9780124115125. ISSN 1054-3589. PMC 3928117. PMID 24054154.
- McEwen, Bruce S.; Bowles, Nicole P.; Gray, Jason D.; Hill, Matthew N.; Hunter, Richard G.; Karatsoreos, Ilia N.; Nasca, Carla (2015). "Mechanisms of stress in the brain". Nature Neuroscience. 18 (10): 1353–1363. doi:10.1038/nn.4086. ISSN 1097-6256. PMC 4933289. PMID 26404710.
- Robins, Clive J. (1993). "Cognitive therapy with inpatients. J. Wright, M. Thase, A. Beck, J. Ludgate (eds). Guilford Press, New York, 1993. 445 pp., $36.95". Depression. 1 (6): 329–330. doi:10.1002/depr.3050010609. ISSN 1062-6417.
- Tsigos, Constantine; Chrousos, George P (October 2002). "Hypothalamic–pituitary-adrenal axis, neuroendocrine factors and stress". Journal of Psychosomatic Research. 53 (4): 865–871. doi:10.1016/s0022-3999(02)00429-4. ISSN 0022-3999. PMID 12377295.
- Isaac, Jeffrey E.; Johnson, David E. (2013). Wilderness and Rescue Medicine. Burlington, MA: Jones & Bartlett Learning. pp. 27–8. ISBN 978-0-7637-8920-6.
- VanPutte, C. L., Regan, J., Russo, A., Seeley, R. R., Stephens, T. D., Tate, P., & Seeley, R. R. (2014). Seeley's anatomy & physiology. New York, NY: McGraw-Hill.
- Creamer, Mark; o'Donnell, Meaghan L; Pattison, Phillipa (2004). "The relationship between acute stress disorder and posttraumatic stress disorder in severely injured trauma survivors". Behaviour Research and Therapy. 42 (3): 315–28. doi:10.1016/s0005-7967(03)00141-4. PMID 14975772.
- Vaiva, G; Ducrocq, F; Jezequel, K; Averland, B; Lestavel, P; Brunet, A; Marmar, C. R (2003). "Immediate treatment with propranolol decreases posttraumatic stress disorder two months after trauma". Biological Psychiatry. 54 (9): 947–9. doi:10.1016/s0006-3223(03)00412-8. PMID 14573324. S2CID 3064619.
- Kornør, Hege; Winje, Dagfinn; Ekeberg, Øivind; Weisæth, Lars; Kirkehei, Ingvild; Johansen, Kjell; Steiro, Asbjørn (September 2008). "Early trauma-focused cognitive-behavioural therapy to prevent chronic post-traumatic stress disorder and related symptoms: A systematic review and meta-analysis". BMC Psychiatry. 8: 8. doi:10.1186/1471-244x-8-81. PMC 2559832. PMID 18801204.
- Lambert, M.J., ed. (2004). Bergin and Garfield's Handbook of Psychotherapy and Behavioral Change. New York: Wiley.[page needed]
- Sharma, Manoj; Rush, Sarah E (2014). "Mindfulness-Based Stress Reduction as a Stress Management Intervention for Healthy Individuals". Journal of Evidence-Based Complementary & Alternative Medicine. 19 (4): 271–86. doi:10.1177/2156587214543143. PMID 25053754.
- Astill Wright, Laurence; Sijbrandij, Marit; Sinnerton, Rob; Lewis, Catrin; Roberts, Neil P.; Bisson, Jonathan I. (December 2019). "Pharmacological prevention and early treatment of post-traumatic stress disorder and acute stress disorder: a systematic review and meta-analysis". Translational Psychiatry. 9 (1): 334. doi:10.1038/s41398-019-0673-5. ISSN 2158-3188. PMC 6901463. PMID 31819037.
- Bryant, Richard A.; Friedman, Matthew J.; Spiegel, David; Ursano, Robert; Strain, James (September 2011). "A review of acute stress disorder in DSM-5". Depression and Anxiety. 28 (9): 802–817. doi:10.1002/da.20737. PMID 21910186. S2CID 46689852.
- Harvey, Allison G.; Bryant, Richard A. (2002). "Acute stress disorder: A synthesis and critique". Psychological Bulletin. 128 (6): 886–902. doi:10.1037/0033-2909.128.6.886. ISSN 1939-1455. PMID 12405136.
- Isserlin, Leanna; Zerach, Gadi; Solomon, Zahava (2008). "Acute stress responses: A review and synthesis of ASD, ASR, and CSR". American Journal of Orthopsychiatry. 78 (4): 423–429. doi:10.1037/a0014304. ISSN 1939-0025. PMID 19123763.