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The exact pathogenesis of acute stress disorder is not fully understood. It is thought that acute stress disorder is caused by either 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]], or [[hypothalamic-pituitary-adrenal axis]].<ref name="wiki">Acute stress disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Acute_stress_reaction Accessed on january 4, 2016</ref >
The exact pathogenesis of acute stress disorder is not fully understood. It is thought that acute stress disorder is caused by either 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]], or [[hypothalamic-pituitary-adrenal axis]].<ref name="wiki">Acute stress disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Acute_stress_reaction Accessed on january 4, 2016</ref >
==Pathophysiology==
==Pathophysiology==
*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 breathing and heart rate, constricting blood vessels. An abundance of catecholamines at neuroreceptor sites facilitates reliance on spontaneous or instinctive behaviors often related to combat or escape.
*When triggered by a stimuli, the body has a natural "fight-or-flight" response
*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.
*In response to such stimuli, the body can release either adrenaline or noradrenaline, which result in physiological responses such as increased heart rate, constricted blood vessels, and increased breathing
*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, respiratory centers, [[blood vessels]], 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]].<ref name="wiki">Acute stress disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Acute_stress_reaction Accessed on january 4, 2016</ref >
*The locus ceruleus "fires" neurons in a very minimal manner when an individual is in a calm state
*It is not known why some people develop acute stress disorder (ASD) following a traumatic event. Nor is it fully understood why some people with acute stress disorder develop subsequent [[posttraumatic stress disorder]] (PTSD) and others do not. However, research studies and conceptual models suggest the following underlying factors.<ref name="pmid16919525">{{cite journal| author=Rauch SL, Shin LM, Phelps EA| title=Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research--past, present, and future. | journal=Biol Psychiatry | year= 2006 | volume= 60 | issue= 4 | pages= 376-82 | pmid=16919525 | doi=10.1016/j.biopsych.2006.06.004 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16919525  }} </ref><ref name="pmid8466391">{{cite journal| author=Charney DS, Deutch AY, Krystal JH, Southwick SM, Davis M| title=Psychobiologic mechanisms of posttraumatic stress disorder. | journal=Arch Gen Psychiatry | year= 1993 | volume= 50 | issue= 4 | pages= 295-305 | pmid=8466391 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8466391  }} </ref><ref name="pmid19014750">{{cite journal| author=Bryant RA, Creamer M, O'Donnell M, Silove D, McFarlane AC| title=A multisite study of initial respiration rate and heart rate as predictors of posttraumatic stress disorder. | journal=J Clin Psychiatry | year= 2008 | volume= 69 | issue= 11 | pages= 1694-701 | pmid=19014750 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19014750  }} </ref><ref name="pmid10895573">{{cite journal| author=Bryant RA, Harvey AG, Guthrie RM, Moulds ML| title=A prospective study of psychophysiological arousal, acute stress disorder, and posttraumatic stress disorder. | journal=J Abnorm Psychol | year= 2000 | volume= 109 | issue= 2 | pages= 341-4 | pmid=10895573 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10895573  }} </ref><ref name="pmid15385703">{{cite journal| author=Bryant RA, Marosszeky JE, Crooks J, Gurka JA| title=Elevated resting heart rate as a predictor of posttraumatic stress disorder after severe traumatic brain injury. | journal=Psychosom Med | year= 2004 | volume= 66 | issue= 5 | pages= 760-1 | pmid=15385703 | doi=10.1097/01.psy.0000138121.13198.84 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15385703  }} </ref><ref name="pmid17189749">{{cite journal| author=Bryant RA, Salmon K, Sinclair E, Davidson P| title=Heart rate as a predictor of posttraumatic stress disorder in children. | journal=Gen Hosp Psychiatry | year= 2007 | volume= 29 | issue= 1 | pages= 66-8 | pmid=17189749 | doi=10.1016/j.genhosppsych.2006.10.002 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17189749  }} </ref><ref name="pmid15753247">{{cite journal| author=Kassam-Adams N, Garcia-España JF, Fein JA, Winston FK| title=Heart rate and posttraumatic stress in injured children. | journal=Arch Gen Psychiatry | year= 2005 | volume= 62 | issue= 3 | pages= 335-40 | pmid=15753247 | doi=10.1001/archpsyc.62.3.335 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15753247  }} </ref><ref name="pmid9633675">{{cite journal| author=Shalev AY, Sahar T, Freedman S, Peri T, Glick N, Brandes D et al.| title=A prospective study of heart rate response following trauma and the subsequent development of posttraumatic stress disorder. | journal=Arch Gen Psychiatry | year= 1998 | volume= 55 | issue= 6 | pages= 553-9 | pmid=9633675 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9633675  }} </ref><ref name="pmid10761279">{{cite journal| author=Ehlers A, Clark DM| title=A cognitive model of posttraumatic stress disorder. | journal=Behav Res Ther | year= 2000 | volume= 38 | issue= 4 | pages= 319-45 | pmid=10761279 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10761279  }} </ref><ref name="pmid9745802">{{cite journal| author=Warda G, Bryant RA| title=Cognitive bias in acute stress disorder. | journal=Behav Res Ther | year= 1998 | volume= 36 | issue= 12 | pages= 1177-83 | pmid=9745802 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9745802  }} </ref><ref name="pmid10875192">{{cite journal| author=Smith K, Bryant RA| title=The generality of cognitive bias in acute stress disorder. | journal=Behav Res Ther | year= 2000 | volume= 38 | issue= 7 | pages= 709-15 | pmid=10875192 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10875192  }} </ref><ref name="pmid9715585">{{cite journal| author=Ehlers A, Mayou RA, Bryant B| title=Psychological predictors of chronic posttraumatic stress disorder after motor vehicle accidents. | journal=J Abnorm Psychol | year= 1998 | volume= 107 | issue= 3 | pages= 508-19 | pmid=9715585 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9715585  }} </ref><ref name="pmid11520012">{{cite journal| author=Dunmore E, Clark DM, Ehlers A| title=A prospective investigation of the role of cognitive factors in persistent posttraumatic stress disorder (PTSD) after physical or sexual assault. | journal=Behav Res Ther | year= 2001 | volume= 39 | issue= 9 | pages= 1063-84 | pmid=11520012 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11520012  }} </ref><ref name="pmid17560541">{{cite journal| author=Bryant RA, Salmon K, Sinclair E, Davidson P| title=A prospective study of appraisals in childhood posttraumatic stress disorder. | journal=Behav Res Ther | year= 2007 | volume= 45 | issue= 10 | pages= 2502-7 | pmid=17560541 | doi=10.1016/j.brat.2007.04.009 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17560541  }} </ref><ref name="pmid12495267">{{cite journal| author=Meiser-Stedman R| title=Towards a cognitive-behavioral model of PTSD in children and adolescents. | journal=Clin Child Fam Psychol Rev | year= 2002 | volume= 5 | issue= 4 | pages= 217-32 | pmid=12495267 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12495267  }} </ref>
*The locus ceruleus "fires" neurons at a much faster and more intense rate if a stimulus seems threatening
**The finding that panic plays a role in the etiology of acute stress disorder is consistent with the prevailing model of acute stress disorder and post traumatic stress disorder. Fear conditioning models hypothesize that the fear elicited during a traumatic event results in conditioning in which subsequent reminders of the trauma elicit anxiety in response to trauma reminders. This model postulates that extreme sympathetic arousal at the time of a traumatic event may result in the release of stress neurochemicals which include [[norepinephrine]] and [[epinephrine]] that results in overconsolidation of trauma memories.
*The "fight-or-flight" response we feel is a result of our sympathetic nervous system, which raises our pulse and causes anxiety
**According to this model, most trauma survivors successfully engage in extinction learning in the days and weeks after trauma as they learn that the reminders are not signaling further threat. In terms of responses in the acute phase, there is much evidence that people who eventually develop post traumatic stress disorder display elevated heart rate in the days after the trauma. There is also an evidence that people with elevated respiration rate after trauma are more likely to develop [[post traumatic stress disorder]]. These findings suggest that elevated arousal in the acute phase is important in the etiology of acute stress disorder and post traumatic stress disorder.
*Another response, called the "rest-and-digest" response, is a result of the parasympathetic nervous system, which reduces heart rate, and can potentially cause loss of consciousness
**The other major conceptual model for acute stress disorder involves cognitive processes, which postulates that extremely negative and unrealistic estimation about the traumatic event, stronger beliefs about likelihood of future harm, and greater levels of [[symptomatic]] response will increase the extent to which PTSD develops.
*The parasympathetic nervous system increases digestion by stimulating the digestive system and urinary system


==References==
==References==

Revision as of 19:32, 2 January 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

The exact pathogenesis of acute stress disorder is not fully understood. It is thought that acute stress disorder is caused by either 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, or hypothalamic-pituitary-adrenal axis.[1]

Pathophysiology

  • When triggered by a stimuli, the body has a natural "fight-or-flight" response
  • In response to such stimuli, the body can release either adrenaline or noradrenaline, which result in physiological responses such as increased heart rate, constricted blood vessels, and increased breathing
  • The locus ceruleus "fires" neurons in a very minimal manner when an individual is in a calm state
  • The locus ceruleus "fires" neurons at a much faster and more intense rate if a stimulus seems threatening
  • The "fight-or-flight" response we feel is a result of our sympathetic nervous system, which raises our pulse and causes anxiety
  • Another response, called the "rest-and-digest" response, is a result of the parasympathetic nervous system, which reduces heart rate, and can potentially cause loss of consciousness
  • The parasympathetic nervous system increases digestion by stimulating the digestive system and urinary system

References

  1. Acute stress disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Acute_stress_reaction Accessed on january 4, 2016

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