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==Overview== | ==Overview== | ||
==Pathophysiology== | |||
Acute stress 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. [1] Acute stress reaction is a variation of post-traumatic stress disorder (PTSD). | |||
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 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. | |||
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 (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. | |||
The finding that panic plays a role in the etiology of ASD is consistent with the prevailing model of ASD and PTSD. Fear conditioning models posit 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 [21]. This model proposes that extreme sympathetic arousal at the time of a traumatic event may result in the release of stress neurochemicals (including norepinephrine and epinephrine) that results in overconsolidation of trauma memories [22]. 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 PTSD display elevated heart rate in the days after the trauma [23-28]. Further, there is evidence that people with elevated respiration rate after trauma are more likely to develop PTSD [23]. These findings underscore the proposal that elevated arousal in the acute phase is important in the etiology of ASD and PTSD. | |||
The other major conceptual model for ASD involves cognitive processes, which posit that extremely negative and unrealistic appraisals about the traumatic event, greater levels of symptomatic response, and stronger beliefs about the likelihood of future harm will increase the extent to which PTSD develops [29]. Supporting this model is evidence that people with ASD exaggerate the probability of future negative events [30,31]. Catastrophic appraisals in the initial period after trauma exposure predict subsequent PTSD in adults [32,33] and children [34,35]. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 20:46, 2 January 2016
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Acute stress disorder Microchapters |
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Acute stress disorder pathophysiology On the Web |
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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
Acute stress 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. [1] Acute stress reaction is a variation of post-traumatic stress disorder (PTSD).
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 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.
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 (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.
The finding that panic plays a role in the etiology of ASD is consistent with the prevailing model of ASD and PTSD. Fear conditioning models posit 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 [21]. This model proposes that extreme sympathetic arousal at the time of a traumatic event may result in the release of stress neurochemicals (including norepinephrine and epinephrine) that results in overconsolidation of trauma memories [22]. 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 PTSD display elevated heart rate in the days after the trauma [23-28]. Further, there is evidence that people with elevated respiration rate after trauma are more likely to develop PTSD [23]. These findings underscore the proposal that elevated arousal in the acute phase is important in the etiology of ASD and PTSD.
The other major conceptual model for ASD involves cognitive processes, which posit that extremely negative and unrealistic appraisals about the traumatic event, greater levels of symptomatic response, and stronger beliefs about the likelihood of future harm will increase the extent to which PTSD develops [29]. Supporting this model is evidence that people with ASD exaggerate the probability of future negative events [30,31]. Catastrophic appraisals in the initial period after trauma exposure predict subsequent PTSD in adults [32,33] and children [34,35].