Acute stress disorder pathophysiology: Difference between revisions
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{{Acute stress disorder}} | {{Acute stress disorder}} | ||
{{CMG}}{{AE}}{{Simrat}} | {{CMG}}{{AE}}{{Simrat}} | ||
==Overview== | ==Overview== | ||
==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. | |||
*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. | |||
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 heart rate | *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. | ||
*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. | |||
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. | **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. | |||
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 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 finding that panic plays a role in the etiology of | |||
The other major conceptual model for | |||
Revision as of 07:19, 4 January 2016
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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
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.
- 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.
- 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.