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 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Technology for psychiatric prevention is poorly developed, and knowledge about the causes of mental illness is difficult to apply to practical preventive work. As it would take many years before the effects of primary preventive efforts would be visible, secondary and tertiary prevention are essential to reducing the prevalence of mental illness. Recent studies on reducing the negative health consequences of acute stress seem to justify some optimism that psychosocially-oriented prevention is possible. Experience with the preventive benefits of social support at times of crisis suggests that active social support can prevent social disintegration at the community level and mental health problems for individuals.
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PMID:Psychiatric interventions for prevention of mental disorders. A psychosocial perspective. 913 70

The majority of persons exposed to a disaster do well and have only mild, transitory symptoms. However, some individuals develop psychiatric illness postdisaster. Such illnesses include those that are secondary to physical injury and sickenss as well as specific trauma-related psychiatric disorders such as acute stress disorder. The extent of the psychiatric morbidity and mortality that develops in individuals in the community depends on the type of disaster, the degree of injury sustained, the amount of life threat, and the duration of community disruption. In this paper we examine the posttraumatic responses of direct concern to psychiatrists working in a community exposed to a disaster. We review the epidemiology of posttraumatic responses, the interface of psychiatry and traumatic stress, the psychiatric disorders associated with trauma, and psychiatric consultation to the disaster community. Overall, psychiatric intervention after a disaster is based on the principles of preventive medicine and includes community consultation and outreach programs with the goals of identifying high-risk groups, promoting community recovery, and minimizing social disruption.
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PMID:Psychiatric dimensions of disaster: patient care, community consultation, and preventive medicine. 938 48

The Acute Stress Disorder Scale (ASDS) is a self-report inventory that (a) indexes acute stress disorder (ASD) and (b) predicts posttraumatic stress disorder (PTSD). The ASDS is a 19-item inventory that is based on Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV, American Psychiatric Association, 1994) criteria. The ASDS possessed good sensitivity (95%) and specificity (83%) for identifying ASD against the ASD Interview on 99 civilian trauma survivors. Test-retest reliability of the ASDS scores between 2 and 7 days was strong (r = .94). The ASDS predicted 91% of bushfire survivors who developed PTSD and 93% of those who did not; one third of those identified by the ASDS as being at risk did not develop PTSD, however. The ASDS shows promise as a screening instrument to identify acutely traumatized individuals who warrant more thorough assessment for risk of PTSD.
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PMID:Acute Stress Disorder Scale: a self-report measure of acute stress disorder. 1075 64

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.
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PMID:Evaluation of post-traumatic stress disorders. 1177 35

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.
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PMID:Psychobiology of the acute stress response and its relationship to the psychobiology of post-traumatic stress disorder. 1213 6

An understanding of PTSD and stress-related conditions is in its infancy. This is not surprising given the fact PTSD was not recognized as a distinct diagnostic entity until 1980. Since that time, the diagnostic classification has undergone continuous change as our understanding of PTSD is refined. The authors believe that PTSD can be best understood through a dimensional conceptualization viewed along at least three spectra: (1) symptom severity, (2) the nature of the stressor, and (3) responses to trauma. Along the severity spectrum, studies that review diagnostic thresholds reveal significant prevalence of PTSD symptoms and impairment that results from subthreshold conditions. Comorbidity patterns suggest that when PTSD is associated with other psychiatric illness, diagnosis is more difficult and the overall severity of PTSD is considerably greater. With regard to a stressor criteria spectrum, the diagnostic nomenclature initially only recognized severe forms of trauma personally experienced. More recently, however, the person's subjective response and events occurring to loved ones were included. This has greatly broadened the stressor criteria by leading to an appreciation of the range of precipitating stressors and the potential impact of "low-magnitude" events. Given that responses to trauma vary considerably, another possible spectrum includes trauma-related conditions. Traumatic grief, somatization, acute stress disorder and dissociation, personality disorders, depressive disorders, and other anxiety disorders all have significant associations with PTSD. Further research is needed to clarify and expand the current understanding of PTSD and other trauma-related conditions. Consideration of the severity of symptoms and the range of stressors coupled with the various disorders precipitated by trauma should greatly influence scientific research. The future undoubtedly will bring a refinement of the current understanding of PTSD and improved treatments.
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PMID:Rationale for a posttraumatic stress spectrum disorder. 1246 60

Many psychiatric disorders, including depression, post-traumatic stress disorder and other anxiety disorders, result from an interaction between genetic factors and exposure to a sufficiently sensitizing environmental stressor. The inbred Wistar Kyoto (WKY) rat strain has been proposed as a model of stress vulnerability, exhibiting an exaggerated hypothalamic-pituitary-adrenal (HPA) response to stress and susceptibility to gastric ulceration. Previously, we showed that stress-activation of the brain noradrenergic system was deficient in WKY rats, and they lacked noradrenergic facilitation of the HPA response in the lateral bed nucleus of the stria terminalis (BSTL), compared to outbred Sprague-Dawley (SD) controls. Deficient modulatory function of the noradrenergic system may contribute to the stress susceptibility of WKY rats. Thus, we investigated the influence of a sensitizing stimulus, chronic intermittent cold exposure, on neuroendocrine and noradrenergic stress reactivity, and on noradrenergic facilitation of the HPA response in these two strains. Chronic cold exposure (7 days, 4 h/day, 4 degrees C) potentiated activation of the HPA axis by acute immobilization stress, assessed by measuring plasma adrenocorticotropic hormone (ACTH), in both strains, although to a greater extent in WKY rats, and enhanced stress-induced norepinephrine (NE) release in BSTL of WKY but not SD rats. We then compared the influence of chronic cold exposure on noradrenergic modulation of the HPA stress response in BSTL, by measuring changes in acute stress-induced elevation of plasma ACTH after microinjecting the alpha(1)-adrenoreceptor antagonist benoxathian into the BSTL. As shown previously, benoxathian attenuated stress-induced ACTH secretion in control SD but not control WKY rats. After chronic cold, the ACTH response to acute stress was attenuated by benoxathian administration into BSTL of both strains, such that the WKY response was not different from that of SD rats. Thus, chronic cold not only sensitized the release of NE in BSTL of WKY rats, but also restored noradrenergic facilitation of their already-elevated HPA response. Such functional sensitization of a previously-deficient facilitatory system may be one mechanism whereby exposure to repeated or severe stress may induce pathologic dysregulation of the stress response in susceptible individuals, resulting in psychiatric illness.
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PMID:Chronic cold stress sensitizes brain noradrenergic reactivity and noradrenergic facilitation of the HPA stress response in Wistar Kyoto rats. 1269 37

Dissociative disorders have a lifetime prevalence of about 10%. Dissociative symptoms may occur in acute stress disorder, posttraumatic stress disorder, somatization disorder, substance abuse, trance and possession trance, Ganser's syndrome, and dissociative identity disorder, as well as in mood disorders, psychoses, and personality disorders. Dissociative symptoms and disorders are observed frequently among patients attending our rural South Carolina community mental health center. Given the prevalence of mental illness in primary care settings and the diagnostic difficulties encountered with dissociative disorders, such illness may be undiagnosed or misdiagnosed in primary care settings. We developed an intervention model that may be applicable to primary care settings or helpful to primary care physicians. Key points of the intervention are identification of dissociative symptoms, patient and family education, review of the origin of the symptoms as a method of coping with trauma, and supportive reinforcement of cognitive and relaxation skills during follow-up visits. Symptom recognition, Education of the family, Learning new skills, and Follow-up may be remembered by the mnemonic device SELF. We present several cases to illustrate dissociative symptoms and our intervention. Physicians and other professionals using the 4 steps and behavioral approaches will be able to better recognize and triage patients with dissociative symptoms. Behaviors previously thought to be secondary to psychosis or personality disorders may be seen in a new frame of reference, strengthening the therapeutic alliance while reducing distress and acting-out behaviors.
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PMID:Dissociative Spectrum Disorders in the Primary Care Setting. 1501 80

This article reviews the existing evolutionary perspectives on the acute stress response habitual faintness and blood-injection-injury type-specific phobia (BIITS phobia). In this article, an alternative evolutionary perspective, based on recent advances in evolutionary psychology, is proposed. Specifically, that fear-induced faintness (eg, fainting following the sight of a syringe, blood, or following a trivial skin injury) is a distinct Homo sapiens-specific extreme-stress survival response to an inescapable threat. The article suggests that faintness evolved in response to middle paleolithic intra-group and inter-group violence (of con-specifics) rather than as a pan-mammalian defense response, as is presently assumed. Based on recent literature, freeze, flight, fight, fright, faint provides a more complete description of the human acute stress response sequence than current descriptions. Faintness, one of three primary physiological reactions involved in BIITS phobia, is extremely rare in other phobias. Since heritability estimates are higher for faintness than for fears or phobias, the author suggests that trait-faintness may be a useful complement to trait-anxiety as an endophenotype in research on the human fear circuitry. Some implications for the forthcoming Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition as well as for clinical, health services, and transcriptomic research are briefly discussed.
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PMID:Freeze, flight, fight, fright, faint: adaptationist perspectives on the acute stress response spectrum. 1533 64

Research has suggested that rescue workers are at increased risk for psychological distress. To determine whether 9/11 deployment was a significant risk factor for canine search and rescue handlers, 82 deployed handlers were compared to 32 nondeployed handlers on measures of posttraumatic stress disorder (PTSD), depression, anxiety, acute stress, and clinical diagnoses. Deployed handlers reported more PTSD and general psychological distress 6 months after 9/11. Among deployed handlers, prior diagnoses and peritraumatic reactions were associated with psychological distress whereas social support and training were protective. Results suggest that more extensive screening and prophylactic interventions for individuals with a history of mental illness could be beneficial. Future research should examine identified risk/resilience factors prospectively, and training and intervention should be designed accordingly.
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PMID:Risk and resilience in canine search and rescue handlers after 9/11. 1628 Dec 48


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