Acute stress disorder pathophysiology
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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
- 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.
- 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. 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.[1]
- 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.[2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]
- 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.
- 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.
- 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.
References
- ↑ 1.0 1.1 Acute stress disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Acute_stress_reaction Accessed on january 4, 2016
- ↑ Rauch SL, Shin LM, Phelps EA (2006). "Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research--past, present, and future". Biol Psychiatry. 60 (4): 376–82. doi:10.1016/j.biopsych.2006.06.004. PMID 16919525.
- ↑ Charney DS, Deutch AY, Krystal JH, Southwick SM, Davis M (1993). "Psychobiologic mechanisms of posttraumatic stress disorder". Arch Gen Psychiatry. 50 (4): 295–305. PMID 8466391.
- ↑ Bryant RA, Creamer M, O'Donnell M, Silove D, McFarlane AC (2008). "A multisite study of initial respiration rate and heart rate as predictors of posttraumatic stress disorder". J Clin Psychiatry. 69 (11): 1694–701. PMID 19014750.
- ↑ Bryant RA, Harvey AG, Guthrie RM, Moulds ML (2000). "A prospective study of psychophysiological arousal, acute stress disorder, and posttraumatic stress disorder". J Abnorm Psychol. 109 (2): 341–4. PMID 10895573.
- ↑ Bryant RA, Marosszeky JE, Crooks J, Gurka JA (2004). "Elevated resting heart rate as a predictor of posttraumatic stress disorder after severe traumatic brain injury". Psychosom Med. 66 (5): 760–1. doi:10.1097/01.psy.0000138121.13198.84. PMID 15385703.
- ↑ Bryant RA, Salmon K, Sinclair E, Davidson P (2007). "Heart rate as a predictor of posttraumatic stress disorder in children". Gen Hosp Psychiatry. 29 (1): 66–8. doi:10.1016/j.genhosppsych.2006.10.002. PMID 17189749.
- ↑ Kassam-Adams N, Garcia-España JF, Fein JA, Winston FK (2005). "Heart rate and posttraumatic stress in injured children". Arch Gen Psychiatry. 62 (3): 335–40. doi:10.1001/archpsyc.62.3.335. PMID 15753247.
- ↑ Shalev AY, Sahar T, Freedman S, Peri T, Glick N, Brandes D; et al. (1998). "A prospective study of heart rate response following trauma and the subsequent development of posttraumatic stress disorder". Arch Gen Psychiatry. 55 (6): 553–9. PMID 9633675.
- ↑ Ehlers A, Clark DM (2000). "A cognitive model of posttraumatic stress disorder". Behav Res Ther. 38 (4): 319–45. PMID 10761279.
- ↑ Warda G, Bryant RA (1998). "Cognitive bias in acute stress disorder". Behav Res Ther. 36 (12): 1177–83. PMID 9745802.
- ↑ Smith K, Bryant RA (2000). "The generality of cognitive bias in acute stress disorder". Behav Res Ther. 38 (7): 709–15. PMID 10875192.
- ↑ Ehlers A, Mayou RA, Bryant B (1998). "Psychological predictors of chronic posttraumatic stress disorder after motor vehicle accidents". J Abnorm Psychol. 107 (3): 508–19. PMID 9715585.
- ↑ Dunmore E, Clark DM, Ehlers A (2001). "A prospective investigation of the role of cognitive factors in persistent posttraumatic stress disorder (PTSD) after physical or sexual assault". Behav Res Ther. 39 (9): 1063–84. PMID 11520012.
- ↑ Bryant RA, Salmon K, Sinclair E, Davidson P (2007). "A prospective study of appraisals in childhood posttraumatic stress disorder". Behav Res Ther. 45 (10): 2502–7. doi:10.1016/j.brat.2007.04.009. PMID 17560541.
- ↑ Meiser-Stedman R (2002). "Towards a cognitive-behavioral model of PTSD in children and adolescents". Clin Child Fam Psychol Rev. 5 (4): 217–32. PMID 12495267.