Medicine:Acute stress reaction

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Acute stress reaction

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, or witnessing a traumatic event that induces a strong emotional response within the individual. It should not be confused with the unrelated circulatory condition of shock/hypoperfusion. Acute stress reaction (ASR) may develop into delayed stress reaction (better known as Posttraumatic stress disorder, or PTSD) if stress is not correctly managed. ASR is characterized by re-living and avoiding reminders of an aversive event, as well as generalized hypervigilance after initial exposure to a traumatic event. ASR is differentiated from PTSD as a disorder that precedes it, and if symptoms last for more than one month, it will develop into PTSD. It can thus be thought of as the acute phase of PTSD.[1]

Signs and symptoms

The DSM-IV specifies that ASD must be accompanied by the presence of dissociative symptoms, which largely differentiates it from PTSD.

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).[2]

In addition to the characteristic dissociative symptoms, Acute Stress Disorder from the DSM-5 can present from four other distinct symptom clusters such as[3]:

  • Intrusion Symptom Cluster
    • 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 said distressing memories, thoughts, and feelings of, or closely associated to traumatic event.
  • Arousal Symptom Cluster
    • Sleep disturbances, hypervigilance, difficulties with concentration, easy to startle, and irritability/anger/aggression.[3]


There are several theoretical perspectives on trauma response, including cognitive, biological, and psychobiological. While the theories are PTSD-specific, they are still useful in understanding ASD, as both share many symptoms.[2]

Acute stress disorder (abbreviated ASD, and not to be confused with autism spectrum 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. A study of rescue personnel after exposure to a traumatic event showed no gender difference in acute stress reaction.[4] Acute stress reaction is a variation of post-traumatic stress disorder (PTSD).

A recent study found that a single stressful event may cause long-term consequences in the brain. This result calls the traditional distinction between the effects of acute vs chronic stress into question.[5]


Stress is characterized by specific physiological responses to aversive or noxious stimuli.

Hans Selye was the first to coin the term “general adaptation syndrome”, to suggest that stress induced physiological responses proceed through the stages of alarm, resistance, and exhaustion.[6]

The sympathetic branch of the autonomic nervous system gives rise to a specific set of physiological responses in response to physical or psychological stress. The body’s response to stress is also termed “fight-or-flight response”, and it is characterized by an increase in blood flow to skeletal muscles, the heart and brain, a rise in heart rate and blood pressure, as well as dilation of pupils, and an increase in the amount of glucose released by the liver.[7]

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 behaviors often related to combat or escape.[citation needed]

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.[citation needed]

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 norepinephrine 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. Stress activates this axis and produces neurobiological changes. These chemical changes increase the chances of survival by bringing the physiological system back to homeostasis. [8]

The autonomic nervous system controls all automatic functions in the body and contains two subsections within it that aids in 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 sympathetic nerve fibers in order 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 in an effort 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 in order to optimize blood flow to the heart, lungs, and skeletal muscles. This plays a role in the alarm reaction stage. The para-sympathetic 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 in order to send more blood to those systems to increase the process of digestion. In order to do this, it must inhibit the cardiovascular system and respiratory system in an effort to optimize blood flow to the digestive tract causing low heart and respiratory rates. Parasympathetic plays no role in acute stress response (VanPutte Regan Russo 2014).[9]

Studies have shown that patients with ASD have overactive right amygdalae and pre-frontal cortices, both structures that are involved in the fear-processing pathway.[1]


According to the DSM 5, symptom presentation must last for 3 days in order for a diagnosis of ASD to be made. If symptoms persist past 1 month, the diagnosis of PSTD is explored.[3] 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. 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; the symptoms usually resolve rapidly 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.[10]

The DSM-5 specifies there is a higher prevalence rate of ASD in females compared to males due to higher risk of experiencing traumatic events and neurobiological gender differences in stress response that increase the risk of ASD.[11]


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. did find that re-experiences of the traumatic event and arousal were better predictors of PTSD.[12] Early pharmacotherapy may prevent the development of posttraumtic symptoms.[13] Additionally, early trauma-focused cognitive-behavioral therapy (TFCBT) for those with a diagnosis of ASD can protect an individual from chronic PTSD.[14]

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 counseling.[15] Mindfulness based stress reduction programs also appear to be effective for stress management.[16]

In a wilderness context where counseling, psychotherapy, and cognitive behavioral therapy is unlikely to be available, the treatment for acute stress reaction is very similar for the treatment of cardiogenic shock, vascular shock, and hypovolemic shock; that is, allowing the patient to lie down, providing reassurance, and removing the stimulus for the occurrence of the reaction. In traditional shock cases, this is generally the relieving of pain from injuries or the stopping of blood loss. In an acute stress reaction, this may be pulling a rescuer away from the emergency to calm down, or blocking the sight of an injured friend from a patient.[9]


The term ASR 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, and 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.[2]

The APA officially included the term ASD in the DSM-IV in 1994, and prior to that, symptomatic individuals within the first month of trauma were diagnosed with adjustment disorder. According to the DSM IV, ASR refers to the symptoms experienced right after exposure to a traumatic event, up until 48 hours after it. In contrast, ASD is defined by symptoms experienced after 48 hours of the event, up until one month past the event. Symptoms experienced for longer than one month are consistent with a diagnosis of PTSD.[2]


  1. 1.0 1.1 Reynaud, Emmanuelle; Guedj, Eric; Trousselard, Marion; El Khoury-Malhame, Myriam; Zendjidjian, Xavier; Fakra, Eric; Souville, Marc; Nazarian, Bruno et al. (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. 
  2. 2.0 2.1 2.2 2.3 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. 
  3. 3.0 3.1 3.2 American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders (5 ed.). Arlington, VA: American Psychiatric Publishing. 
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  5. 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. Lay summary – Neuroscience News (November 23, 2016). 
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  7. 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. 
  8. 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. 
  9. 9.0 9.1 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. 
  10. "Acute Stress Disorder". 
  11. American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders (5 ed.). Arlington, VA: American Psychiatric Publishing. 
  12. 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. 
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  14. 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. 
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