Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study investigated the role of acute arousal in the development of posttraumatic stress disorder (PTSD). Hospitalized motor-vehicle-accident survivors (n = 146) were assessed for acute stress disorder (ASD) within 1 month of the trauma and were reassessed (n = 113) for PTSD 6 months posttrauma. Heart rate (HR) and blood pressure (BP) were assessed on the day of hospital discharge. Participants with subclinical ASD had higher HR than those with ASD and no ASD. Participants who developed PTSD had higher HR in the acute posttrauma phase than those without PTSD. Diagnosis of ASD and resting HR accounted for 36% of the variance of the number of PTSD symptoms. A formula composed of a diagnosis of ASD or a resting HR of > 90 beats per minute possessed strong sensitivity (88%) and specificity (85%) in predicting PTSD. These findings are discussed in terms of acute arousal and longer term adaptation to trauma.
 ...
PMID:A prospective study of psychophysiological arousal, acute stress disorder, and posttraumatic stress disorder. 1089 73

Although symptoms of acute stress disorder or PTSD in the aftermath of physical trauma may be a reason for psychiatric referral, little has been written on the management of patients in this context. We report the possible benefit of risperidone, an atypical antipsychotic, in 4 cases where flashbacks were reported in patients hospitalized for the treatment of physical trauma.
 ...
PMID:Risperidone in the treatment of acute stress disorder in physically traumatized in-patients. 1094 42

The impact of the mental stress on the human functioning and health has been evidenced in numerous studies. The majority of these studies focus on adverse effects of a long-term stress. Recently, a growing attention has been paid to the relationship between health and acute stress induced by sudden and short-lasting events or experiences characterised by particular intensity. A traumatic stress is one of the forms of the acute stress. It is some kind of reaction to an event in which life of an individual is directly threatened (serious injury, endangered physical integrity, etc.) or he/she witnesses sudden death, serious injury or life-threatening situation of other people. Traumatic experiences may lead among others to post-traumatic stress disorder (PTSD). The review of the studies, presented in this paper, indicates that the proportion of people with traumatic experiences ranges between 40 and 90% depending on the population. There are professions (rescue services, the police, etc.) with inherent traumatic experiences. About 10% of people with traumatic experiences develop PTSD. The author indicates factors responsible for the development of PTSD. The society, particularly people whose professions involve traumatic experiences, and those employed in various institutions responsible for health care should be aware of health problems related to this kind of experiences.
 ...
PMID:[Post-traumatic stress disorder: a problem for occupational medicine]. 1100 73

The present study aimed to index the accuracy of memory for acute trauma symptoms by comparing the symptoms reported by motor vehicle accident (MVA) victims within 1 month posttrauma with the recall of these symptoms at 2 years posttrauma. Ninety-two consecutive MVA admissions were assessed for the presence of acute stress disorder (ASD) within 1 month posttrauma. At 2 years posttrauma, 61% (N = 56) of the sample were reassessed for posttraumatic stress disorder (PTSD) and for accuracy of recall of the symptoms reported during the first assessment. At least one of the four ASD diagnostic clusters was recalled inaccurately by 75% of patients. High levels of posttraumatic stress severity and high subjective ratings of injury severity at 2 years posttrauma were associated with errors of addition (i.e., recalling the presence of acute symptoms 2 years posttrauma that were not reported during the first assessment). Low levels of posttraumatic stress severity and low subjective ratings of injury severity at 2 years posttrauma were associated with errors of omission (i.e., omitting to recall acute symptoms 2 years posttrauma that were reported during the first assessment). These results suggest that retrospective reports of acute stress symptoms should be interpreted cautiously because of the influence of current symptoms on recall of acute symptoms.
 ...
PMID:Memory for acute stress disorder symptoms: a two-year prospective study. 1100 34

The hormones and other physiological agents that mediate the effects of stress on the body have protective and adaptive effects in the short run and yet can accelerate pathophysiology when they are over-produced or mismanaged. Here we consider the protective and damaging effects of these mediators as they relate to the immune system and brain. 'Stress' is a principle focus, but this term is rather imprecise. Therefore, the article begins by noting two new terms, allostasis and allostatic load that are intended to supplement and clarify the meanings of 'stress' and 'homeostasis'. For the immune system, acute stress enhances immune function whereas chronic stress suppresses it. These effects can be beneficial for some types of immune responses and deleterious for others. A key mechanism involves the stress-hormone dependent translocation of immune cells in the blood to tissues and organs where an immune defense is needed. For the brain, acute stress enhances the memory of events that are potentially threatening to the organism. Chronic stress, on the other hand, causes adaptive plasticity in the brain, in which local neurotransmitters as well as systemic hormones interact to produce structural as well as functional changes, involving the suppression of ongoing neurogenesis in the dentate gyrus and remodelling of dendrites in the Ammon's horn. Under extreme conditions only does permanent damage ensue. Adrenal steroids tell only part of the story as far as how the brain adapts, or shows damage, and local tissue modulators - cytokines for the immune response and excitatory amino acid neurotransmitters for the hippocampus. Moreover, comparison of the effects of experimenter-applied stressors and psychosocial stressors show that what animals do to each other is often more potent than what experimenters do to them. And yet, even then, the brain is resilient and capable of adaptive plasticity. Stress-induced structural changes in brain regions such as the hippocampus have clinical ramifications for disorders such as depression, post-traumatic stress disorder and individual differences in the aging process.
 ...
PMID:The neurobiology of stress: from serendipity to clinical relevance. 1111 95

1. To distinguish GAD from panic disorder is not difficult if a patient has frequent, spontaneous panic attacks and agoraphobic symptoms, but many patients with GAD have occasional anxiety attacks or panic attacks. Such patients should be considered as having GAD. An even closer overlap probably exists between GAD and social phobia. Patients with clear-cut phobic avoidant behavior may be distinguished easily from patients with GAD, but patients with social anxiety without clear-cut phobic avoidant behavior may overlap with patients with GAD and possibly should be diagnosed as having GAD and not social phobia. The cardinal symptoms of GAD commonly overlap with those of social phobia, particularly if the social phobia is more general and not focused on a phobic situation. For example, free-floating anxiety may cause the hands to perspire and may cause a person to be shy in dealing with people in public, and thus many patients with subthreshold social phobic symptoms have, in the authors' opinion, GAD and not generalized social phobia. The distinction between GAD and obsessive-compulsive disorder, acute stress disorder, and posttraumatic stress disorder should not be difficult by definition. At times, however, it may be difficult to distinguish between adjustment disorder with anxious mood from GAD or anxiety not otherwise specified, particularly if the adjustment disorder occurs in a patient with a high level of neuroticism or trait anxiety or type C personality disorder. Table 2 presents features distinguishing GAD from other psychiatric disorders. 2. Lifetime comorbid diagnoses of other anxiety or depression disorders, not active for 1 year or more and not necessitating treatment during that time period, should not effect a diagnosis of current GAD. On the other hand, if concomitant depressive symptoms are present and if these are subthreshold, a diagnosis of GAD should be made, and if these are full threshold, a diagnosis of MDD should be made. 3. If GAD is primary and if no such current comorbid diagnosis, such as other anxiety disorders or MDD, is present, except for minor depression and dysthymia, or if only subthreshold symptoms of other anxiety disorders are present, GAD should be considered primary and treated as GAD; however, patients with concurrent threshold anxiety or mood disorders should be diagnosed according to the definitions of these disorders in the DSM-IV and ICD-10 and treated as such. 4. Somatization disorders are now classified separately from anxiety disorders. Some of these, particularly undifferentiated somatization disorder, may overlap with GAD and be diagnostically difficult to distinguish. The authors believe that, as long as psychic symptoms of anxiety are present and predominant, patients should be given a primary diagnosis of GAD. 5. Two major shifts in the DSM diagnostic criteria for GAD have markedly redefined the definition of this disorder. One shift involves the duration criterion from 1 to 6 months, and the other, the increased emphasis on worry and secondary psychic [table: see text] symptoms accompanied by the elimination of most somatic symptoms. This decision has had the consequence of orphaning a large population of patients suffering from GAD that is more transient and somatic in its focus and who typically present not to psychiatrists but to primary care physicians. Therefore, clinicians should consider using the ICD-10 qualification of illness duration of "several months" to replace the more rigid DSM-IV criterion of 6 months and to move away from the DSM-IV focus on excessive worry as the cardinal symptom of anxiety and demote it to only another important anxiety symptom, similar to free-floating anxiety. One also might consider supplementing this ICD-10 criterion with an increased symptom severity criterion as, for example, a Hamilton Anxiety Scale of 18. Finally, the adjective excessive, not used in the definition of other primary diagnostic criteria, such as depressed mood for MDD, should be omitted (Table 3). 6. One may want to consider the distinction of trait (chronic) from state (acute) anxiety, but whether the presence of some personality characteristics, particularly anxious personality or Cluster C personality and increased neuroticism, as an indicator of trait [table: see text] anxiety is a prerequisite for anxiety disorders; occurs independently of anxiety disorders; or is a vulnerability factor that, in some patients, leads to anxiety symptoms and, in others, does not, is unknown. 7. Symptoms that some clinicians consider cardinal for a diagnosis of GAD, such as extreme worry, obsessive rumination, and somatization, also are present in other disorders, such as MDD. (ABSTRACT TRUNCATED)
 ...
PMID:Overview and clinical presentation of generalized anxiety disorder. 1122 2

Thought Field Therapy (TFT) is a self-administered treatment developed by psychologist Roger Callahan. TFT uses energy meridian treatment points and bilateral optical-cortical stimulation while focusing on the targeted symptoms or problem being addressed. The clinical applications of TFT summarized included anxiety, adjustment disorder with anxiety and depression, anxiety due to medical condition, anger, acute stress, bereavement, chronic pain, cravings, depression, fatigue, nausea, neurodermatitis, obsessive traits, panic disorder without agoraphobia, parent-child stress, phobia, posttraumatic stress disorder, relationship stress, trichotillomania, tremor, and work stress. This uncontrolled study reports on changes in self-reported Subjective Units of Distress (SUD; Wolpe, 1969) in 1,594 applications of TFT, treating 714 patients. Paired t-tests of pre- and posttreatment SUD were statistically significant in 31 categories reviewed. These within-session decreases of SUD are preliminary data that call for controlled studies to examine validity, reliability, and maintenance of effects over time. Illustrative case and heart rate variability data are presented.
 ...
PMID:Thought Field Therapy clinical applications: utilization in an HMO in behavioral medicine and behavioral health services. 1152 9

This paper introduces important considerations in the evaluation of psychological reactions to traumatic events. Proper assessment should include consideration of psychometric, cultural, and ethical issues. Mental disorders frequently observed in the aftermath of trauma (acute stress disorder and post-traumatic stress disorder) and stress (adjustment disorders) are defined, and the reader is provided with information on both general and specific resources for their evaluation.
 ...
PMID:Evaluation of post-traumatic stress disorders. 1177 35

The mediating effect of coping self-efficacy (CSE) perceptions between acute stress responses (ASR) and 1-year distress following two disasters was tested. Between 3 and 8 weeks after the second disaster and again at 1 year, 46 residents completed questionnaires. Posttraumatic Stress Disorder (PTSD) symptoms and global distress served as outcomes. Multiple regression demonstrated that ASR and Time I CSE were significant predictors of both Time 1 outcomes. Time 1 PTSD symptoms and Time 2 CSE were significant factors for Time 2 PTSD symptoms. Gender was significant for Time 2 PTSD symptoms, but not for Time 2 global distress. Longitudinally, Time 1 CSE predicted Time 2 PTSD symptoms, but not general distress. CSE mediated between ASR and both psychological outcomes at Time 2. Coping self-efficacy perceptions provide a possible intervention target.
 ...
PMID:Coping self-efficacy perceptions as a mediator between acute stress response and long-term distress following natural disasters. 1209 9

The literature to date that examines the biology of the acute stress reactions suggests that relatively lower baseline cortisol is associated with the development of PTSD. This is particularly informative because of the ongoing controversy surrounding baseline cortisol in PTSD. Studies have found low baseline cortisol, normal range, and elevated baseline cortisol in chronic PTSD, and it has been unclear whether this reflects methodologic differences across studies or true heterogeneity within the disorder. Thus, the few studies to date support the finding of low-normal baseline cortisol in chronic PTSD and suggest that it is a pre-existing functional trait. Whether it plays an etiologic role or is an epiphenomenon of some other process is unclear. What does seem clear, however, is that this characteristic is relatively nonspecific to PTSD, given the fact that low cortisol has been observed in multiple subject populations, including normal individuals under chronic stress as well as chronic medical conditions (for review see [23]). For example, it is possible that reduced baseline cortisol reflects the net result of input to the hypothalamus from cortical and subcortical regions of the brain linked to increased vigilance, sensitization to trauma because of prior traumatic experiences, or genetic factors. For example, primate studies have demonstrated persistent alterations in HPA axis functioning in animals reared by mothers living in moderately stressful conditions [24]. The development of PTSD is associated with sensitization of the startle response. Because the neurobiology of startle is well characterized, this finding implicates a role for specific neurocircuitry in PTSD [25]. Non-habituation of the startle response in PTSD appears related to sensitization specifically to contextual cues (i.e., the environment) that signal the presence of potential threat of danger-related fears [26]. This may be the neurobiological correlate to the over-generalization seen in PTSD that distinguishes the disorder from a simple trauma-induced phobia. The bed nucleus of the stria terminalis (BNST) is specifically implicated from preclinical research in the mediation of context-dependent cues [1]. Treatments that result in down-regulation of the BNST are therefore of particular interest in therapeutic models of prevention after trauma. The fact that a number of vulnerability factors associated with increased risk for developing PTSD are also likely to be biologically based (e.g., a genetic component, prior psychiatric history, prior family of history of psychiatric disorder), provides further evidence in support of a role for psychobiological factors in producing PTSD. Nevertheless, the considerable overlap on these measures between those who will develop PTSD, and those who eventually recover spontaneously, belies any attempt to identify any single or pathognomonic biological marker for risk. For now, the standard of care in predicting level of symptomatology and prognosis in the acute setting continues to be based on careful, informed, serial assessments of symptoms and functioning. Because the capacity to learn from and adapt to adverse conditions are essential to the survival of any species, understanding the neurobiological pathways that mediate learning from traumatic experiences in an adaptive way is as important as understanding the etiology of PTSD and other trauma-related maladaptive consequences. Biological models that trace the causal cascade of post-traumatic events in the brain and neuroendocrine systems may offer a multiplicity of possibilities for intervention. It is well established that conditioned responses are robust and persistent. Moreover, the primary mechanism of habituation is overlearning rather than extinction. Interventions that promote overlearning may therefore prove to be the most powerful and efficient preventative treatments. The therapeutics literature supports this hypothesis, in that brief psychosocial interventions based on sophisticated cognitive-behavioral models have proven effective in reducing suffering, symptom severity, and chronicity in individuals presenting with acute PTSD symptoms [27-29]. No acutely administered pharmacologic treatment to date has been shown effective in accelerating the process of recovery or in preventing the development of chronic PTSD. However, pharmacologic interventions that would prevent sensitization of circuits related to context-dependent threat perception, dysregulation of affect, and/or dysregulation of normal circadian rhythms are of theoretical interest and deserve further study.
 ...
PMID:Psychobiology of the acute stress response and its relationship to the psychobiology of post-traumatic stress disorder. 1213 6


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>