Acute stress reaction

Last updated
Acute stress reaction
Other namesAcute stress disorder, psychological shock, mental shock, shock
Specialty Psychiatry
Symptoms
Duration< 1 month
CausesExposure to a traumatic event
Differential diagnosis Post-traumatic stress disorder, adjustment disorder

Acute stress reaction (ASR), also known as psychological shock, mental shock, or simply shock, [lower-alpha 1] and acute stress disorder (ASD), is a psychological response to a terrifying, traumatic, or surprising experience. Combat stress reaction (CSR) is a similar response to the trauma of war. The reactions may include but are not limited to intrusive or dissociative symptoms, and reactivity symptoms such as avoidance or arousal. It may be exhibited for days or weeks after the traumatic event. [1] If the condition is not correctly addressed, it may develop into post-traumatic stress disorder (PTSD). [2] [3]

Contents

Diagnostic criteria

The International Classification of Diseases (ICD) treats this condition differently from the Diagnostic and Statistical Manual of Mental Disorders (DSM). According to the ICD-11, acute stress reaction refers to the symptoms experienced a few hours to a few days after exposure to a traumatic event. In contrast, DSM-5 defines acute stress disorder 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 per both classifications.

Acute stress reaction per ICD

The ICD-11 MMS gives the following description:

Acute stress reaction refers to the development of transient emotional, somatic, cognitive, or behavioural symptoms as a result of exposure to an event or situation (either short- or long-lasting) of an extremely threatening or horrific nature (e.g., natural or human-made disasters, combat, serious accidents, sexual violence, assault). Symptoms may include autonomic signs of anxiety (e.g., tachycardia, sweating, flushing), being in a daze, confusion, sadness, anxiety, anger, despair, overactivity, inactivity, social withdrawal, or stupor. The response to the stressor is considered to be normal given the severity of the stressor.

Symptoms typically appear within hours to days following the stressful event, and usually begin to subside within a few days after the event or following removal from the threatening situation, when this is possible. In cases where the stressor is ongoing or removal is not possible, symptoms may persist but are usually greatly reduced within approximately 1 month as the person adapts to the changed situation.

Acute Stress Reaction in help-seeking individuals is usually, but not necessarily, accompanied by substantial subjective distress and/or interference with personal functioning.

In children, responses to stressful events can include somatic symptoms (e.g., stomachaches or headaches), disruptive or oppositional behaviour, regression, hyperactivity, tantrums, concentration problems, irritability, withdrawal, excessive daydreaming, increased clinginess, bedwetting, and sleep disturbances. In adolescents, responses can include substance use and various forms of acting out or risk-taking.

Acute stress disorder per DSM

According to the DSM-5, acute stress disorder requires the exposure to actual or threatened death, serious injury, or sexual violation by either directly experiencing it, witnessing it in person, learning it occurred to a close family or friend, or experiencing repeated exposure to aversive details of a traumatic event. [4] In addition to the initial exposure, individuals may also present with a variety of different symptoms that fall within several clusters including intrusion, negative mood, dissociation, avoidance of distressing memories and emotional arousal. Intrusion symptoms include recurring and distressing dreams, flashbacks, or memories related to the traumatic event and related somatic symptoms. [4] Negative mood refers to ones inability to experience positive emotions such as happiness or satisfaction. [4] Dissociative symptoms include a sense of numbing or detachment from emotional reactions, a sense of physical detachment, 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). [5] Emotional arousal symptoms include sleep disturbances, hypervigilance, difficulties with concentration, more common startle response, and irritability. [4] Symptom presentation must last for at least three consecutive days after trauma exposure to be classified as acute stress disorder. If symptoms persist past one month, the diagnosis of PTSD should be assessed for. [4] The presenting symptoms must also cause significant impairment in multiple domains of one's life to be diagnosed. [4]

Additional diagnoses that may develop from acute stress disorder include depression, anxiety, mood disorders, and substance abuse problems. Untreated acute stress disorder can also lead to the development of post-traumatic stress disorder. [6]

Diagnostic assessment

Evaluation of patients is done through close examination of emotional response. Using self-report from patients is a large part of diagnosing acute stress disorder, as acute stress is the result of reactions to stressful situations. [6]

Development and course

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. [5] 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. [7]

Risk factors

Risk factors for developing acute stress disorder include a previously existing mental health diagnosis, avoidant coping mechanisms, and exaggerated appraisals of events. [4] Additional factors also include prior trauma history and heightened emotional reactivity. [4] The DSM-5 specifies that there is a higher prevalence of acute stress disorder among females compared to males due to neurobiological gender differences in stress response, as well as an alleged higher risk of experiencing traumatic events (a now defunct assumption originating from the continued prevalence of the Duluth Model in the legal cultures of relevant demographics, despite its having been soundly discredited in modern times by an overwhelming body of combined research and clinical experience); even though this specification has since been demonstrated to be erroneous, no official updates to the DSM have been committed to reflect as much. As a consequence of this oversight combined with the multitude of pervasive social stigmas and double-standards currently surrounding male mental health in many areas of the world, acute stress disorder and PTSD are both under-reported and under-diagnosed in a majority of male populations to date. A substantially increased realization of risk factors followed by a corresponding surge in diagnoses for males over the next several decades should be expected. [4]

Types

Sympathetic

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 ASR 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 ASR masks the pain and other vital signs that would otherwise be symptomatic. [2]

Parasympathetic

Parasympathetic acute stress disorder is characterized by feeling faint and nauseated. 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. [2]

Pathophysiology

Stress is characterised by specific physiological responses to adverse 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. [8]

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. [9]

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. [10]

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. [11]

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. [12] 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 neuro-biological changes. These chemical changes increase the chances of survival by bringing the physiological system back to homeostasis. [13]

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 optimize 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. [14] [15]

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. [3]

Treatment

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. [16] Early pharmacotherapy may prevent the development of post-traumatic symptoms. [17] Additionally, early trauma-focused cognitive behavioural therapy (TF-CBT) for those with a diagnosis of ASD can protect an individual from developing chronic PTSD. [18]

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. [19] Mindfulness-based stress reduction programmes also appear to be effective for stress management. [20]

The pharmacological approach has made some progress in lessening the effects of acute stress disorder. To relax patients and allow for better sleep, prazosin can be given to patients, which regulates their sympathetic response. [6] Hydrocortisone has shown some success as an early preventative measure following a traumatic event, typically in the treatment of PTSD. [21]

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 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. [14]

History

The term "acute stress disorder" (ASD) 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. [5]

The American Psychiatric Association officially included ASD in the DSM-IV in 1994. Before that, symptomatic individuals within the first month of trauma were diagnosed with adjustment disorder. [5]

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. [22]

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. [23] Also, the terms ASD and ASR have been criticized for not fully covering the range of stress reactions. [24]

In animals

Notes

  1. ↑ Not to be confused with circulatory shock.

Related Research Articles

Neurosis is a term mainly used today by followers of Freudian thinking to describe mental disorders caused by past anxiety, often that has been repressed. In recent history, the term has been used to refer to anxiety-related conditions more generally.

Post-traumatic stress disorder (PTSD) is a mental and behavioral disorder that develops from experiencing a traumatic event, such as sexual assault, warfare, traffic collisions, child abuse, domestic violence, or other threats on a person's life or well-being. Symptoms may include disturbing thoughts, feelings, or dreams related to the events, mental or physical distress to trauma-related cues, attempts to avoid trauma-related cues, alterations in the way a person thinks and feels, and an increase in the fight-or-flight response. These symptoms last for more than a month after the event and can include triggers such as misophonia. Young children are less likely to show distress, but instead may express their memories through play. A person with PTSD is at a higher risk of suicide and intentional self-harm.

<span class="mw-page-title-main">Fight-or-flight response</span> Physiological reaction to a perceived threat or harmful event

The fight-or-flight or the fight-flight-freeze-or-fawn is a physiological reaction that occurs in response to a perceived harmful event, attack, or threat to survival. It was first described by Walter Bradford Cannon in 1915. His theory states that animals react to threats with a general discharge of the sympathetic nervous system, preparing the animal for fighting or fleeing. More specifically, the adrenal medulla produces a hormonal cascade that results in the secretion of catecholamines, especially norepinephrine and epinephrine. The hormones estrogen, testosterone, and cortisol, as well as the neurotransmitters dopamine and serotonin, also affect how organisms react to stress. The hormone osteocalcin might also play a part.

Psychological trauma is an emotional response caused by severe distressing events that are outside the normal range of human experiences. It must be understood by the affected person as directly threatening the affected person or their loved ones generally with death, severe bodily injury, or sexual violence; indirect exposure, such as from watching television news, may be extremely distressing and can produce an involuntary and possibly overwhelming physiological stress response, but does not produce trauma per se. Examples of distressing events include violence, rape, or a terrorist attack.

Adjustment disorder is a maladaptive response to a psychosocial stressor. It is classified as a mental disorder. The maladaptive response usually involves otherwise normal emotional and behavioral reactions that manifest more intensely than usual, causing marked distress, preoccupation with the stressor and its consequences, and functional impairment.

Dissociative disorders (DDs) are a range of conditions characterized by significant disruptions or fragmentation "in the normal integration of consciousness, memory, identity, emotion, perception, body representation, motor control, and behavior." Dissociative disorders involve involuntary dissociation as an unconscious defense mechanism, wherein the individual with a dissociative disorder experiences separation in these areas as a means to protect against traumatic stress. Some dissociative disorders are caused by major psychological trauma, though the onset of depersonalization-derealization disorder may be preceded by less severe stress, by the influence of psychoactive substances, or occur without any discernible trigger.

<span class="mw-page-title-main">Complex post-traumatic stress disorder</span> Psychological disorder

Complex post-traumatic stress disorder is a stress-related mental disorder generally occurring in response to complex traumas, i.e., commonly prolonged or repetitive exposures to a series of traumatic events, within which individuals perceive little or no chance to escape.

Somatic psychology or, more precisely, "somatic clinical psychotherapy" is a form of psychotherapy that focuses on somatic experience, including therapeutic and holistic approaches to the body. It seeks to explore and heal mental and physical injury and trauma through body awareness and movement. Wilhelm Reich was first to try to develop a clear psychodynamic approach that included the body.

Memory and trauma is the deleterious effects that physical or psychological trauma has on memory.

<span class="mw-page-title-main">Effects of stress on memory</span> Overview of the effects of stress on memory

The effects of stress on memory include interference with a person's capacity to encode memory and the ability to retrieve information. Stimuli, like stress, improved memory when it was related to learning the subject. During times of stress, the body reacts by secreting stress hormones into the bloodstream. Stress can cause acute and chronic changes in certain brain areas which can cause long-term damage. Over-secretion of stress hormones most frequently impairs long-term delayed recall memory, but can enhance short-term, immediate recall memory. This enhancement is particularly relative in emotional memory. In particular, the hippocampus, prefrontal cortex and the amygdala are affected. One class of stress hormone responsible for negatively affecting long-term, delayed recall memory is the glucocorticoids (GCs), the most notable of which is cortisol. Glucocorticoids facilitate and impair the actions of stress in the brain memory process. Cortisol is a known biomarker for stress. Under normal circumstances, the hippocampus regulates the production of cortisol through negative feedback because it has many receptors that are sensitive to these stress hormones. However, an excess of cortisol can impair the ability of the hippocampus to both encode and recall memories. These stress hormones are also hindering the hippocampus from receiving enough energy by diverting glucose levels to surrounding muscles.

PTSD or post-traumatic stress disorder, is a psychiatric disorder characterised by intrusive thoughts and memories, dreams or flashbacks of the event; avoidance of people, places and activities that remind the individual of the event; ongoing negative beliefs about oneself or the world, mood changes and persistent feelings of anger, guilt or fear; alterations in arousal such as increased irritability, angry outbursts, being hypervigilant, or having difficulty with concentration and sleep.

Caffeine-induced anxiety disorder is a subclass of the DSM-5 diagnosis of substance/medication-induced anxiety disorder.

<span class="mw-page-title-main">Post-traumatic stress disorder among athletes</span> Prevalence of PTSD among athletes

Posttraumatic stress disorder (PTSD) is a cognitive disorder, which may occur after a traumatic event. It is a psychiatric disorder, which may occur across athletes at all levels of sport participation.

<span class="mw-page-title-main">Richard Bryant (psychologist)</span> Australian psychologist

Richard Allan Bryant is an Australian medical scientist. He is Scientia Professor of Psychology at the University of New South Wales (UNSW) and director of the UNSW Traumatic Stress Clinic, based at UNSW and Westmead Institute for Medical Research. His main areas of research are posttraumatic stress disorder (PTSD) and prolonged grief disorder. On 13 June 2016 he was appointed a Companion of the Order of Australia (AC), for eminent service to medical research in the field of psychotraumatology, as a psychologist and author, to the study of Indigenous mental health, as an advisor to a range of government and international organisations, and to professional societies.

Operational stress injury or OSI is a non-clinical, non-medical term referring to a persistent psychological difficulty caused by traumatic experiences or prolonged high stress or fatigue during service as a military member or first responder. The term does not replace any individual diagnoses or disorders, but rather describes a category of mental health concerns linked to the particular challenges that these military members or first responders encounter in their service. There is not yet a single fixed definition. The term was first conceptualized within the Canadian Armed Forces to help foster understanding of the broader mental health challenges faced by military members who have been impacted by traumatic experiences and who face difficulty as a result. OSI encompasses a number of the diagnoses found in the Diagnostic and Statistical Manual of Mental Disorders (DSM) classification system, with the common thread being a linkage to the operational experiences of the afflicted. The term has gained traction outside of the military community as an appropriate way to describe similar challenges suffered by those whose work regularly exposes them to trauma, particularly front line emergency first responders such as but not limited to police, firefighters, paramedics, correctional officers, and emergency dispatchers. The term, at present mostly used within Canada, is increasingly significant in the development of legislation, policy, treatments and benefits in the military and first responder communities.

The term functional somatic syndrome (FSS) refers to a group of chronic diagnoses with no identifiable organic cause. This term was coined by Hemanth Samkumar. It encompasses disorders such as fibromyalgia, chronic widespread pain, temporomandibular disorder, irritable bowel syndrome, lower back pain, tension headache, atypical face pain, non-cardiac chest pain, insomnia, palpitation, dyspepsia and dizziness. General overlap exists between this term, somatization and somatoform. The status of ME/CFS as a functional somatic syndrome is contested. Although the aetiology remains unclear, there are consistent findings of biological abnormalities, and major health bodies such as the NAM, WHO, and NIH, classify it as an organic disease.

<span class="mw-page-title-main">Post-traumatic stress disorder and substance use disorders</span> Association of PTSD and substance dependencies

Post-traumatic stress disorder (PTSD) can affect about 3.6% of the U.S. population each year, and 6.8% of the U.S. population over a lifetime. 8.4% of people in the U.S. are diagnosed with substance use disorders (SUD). Of those with a diagnosis of PTSD, a co-occurring, or comorbid diagnosis of a SUD is present in 20–35% of that clinical population.

Disaster psychiatry is a field of psychiatry which focuses on responding to natural disasters, climate change, school shootings, large accidents, public health emergencies, and their associated community-wide disruptions and mental health implications. All disasters, regardless of exact type, are characterized by disruption: disruption of family and community support structures, threats to personal safety, and an overwhelming of available support resources. Disaster psychiatry is a crucial component of disaster preparedness, aiming to mitigate both immediate and prolonged psychiatric challenges. Its primary objective is to diminish acute symptoms and long-term psychiatric morbidity by minimizing exposure to stressors, offering education to normalize responses to trauma, and identifying individuals vulnerable to future psychiatric illness.

<span class="mw-page-title-main">Post-traumatic stress disorder after World War II</span>

WWII lasted from September 1st, 1939 until September 2nd, 1945. The death toll during WWII has been estimated to be between 35,000,000 and 60,000,000. However, the exact number is unknown. With all those fatalities, it should not be surprising that it left so many lasting effects on the survivors. There have been many terms for these lasting effects over the decades. These terms include, but are not limited to, shell shock and combat fatigue. In 1980, the diagnosis of PTSD was added to the newly published DSM 3.

Borderline personality disorder (BPD) is a personality disorder characterized by a pervasive, long-term pattern of significant interpersonal relationship instability, a distorted sense of self, and intense emotional responses, which can be misdiagnosed. Misdiagnosis may involve erroneously assigning a BPD diagnosis to individuals not meeting the specific criteria or attributing an incorrect alternate diagnosis in cases where BPD is the accurate condition.

References

  1. ↑ Friedman, Matthew J. (2015). Posttraumatic and acute stress disorders (Sixth ed.). Cham: Springer International Publishing Switzerland. p. 118. ISBN   978-3-319-15066-6. OCLC   904253583.
  2. 1 2 3 Isaac, Jeff. (2013). Wilderness and rescue medicine. Jones & Bartlett Learning. ISBN   9780763789206. OCLC   785442005.
  3. 1 2 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.
  4. 1 2 3 4 5 6 7 8 9 American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders (5 ed.). Arlington, VA: American Psychiatric Publishing.
  5. 1 2 3 4 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.
  6. 1 2 3 Fanai, Mehdi; Khan, Moien AB (2021), "Acute Stress Disorder", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   32809650 , retrieved 2021-03-14
  7. ↑ 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.
  8. ↑ Butler, G (1993). "Definitions of stress". Occasional Paper (Royal College of General Practitioners) (61): 1–5. PMC   2560943 . PMID   8199583.
  9. ↑ 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.
  10. ↑ Eiden, Lee E. (2013). "Neuropeptide–Catecholamine Interactions in Stress". A New Era of Catecholamines in the Laboratory and Clinic. Advances in Pharmacology. Vol. 68. pp. 399–404. doi:10.1016/B978-0-12-411512-5.00018-X. ISBN   9780124115125. ISSN   1054-3589. PMC   3928117 . PMID   24054154.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ 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.
  14. 1 2 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.
  15. ↑ 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.
  16. ↑ 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.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ Lambert, M.J., ed. (2004). Bergin and Garfield's Handbook of Psychotherapy and Behavioral Change. New York: Wiley.[ page needed ]
  20. ↑ 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.
  21. ↑ 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.
  22. ↑ 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.
  23. ↑ 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.
  24. ↑ 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.
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