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Armed conflict is associated with significant long-term psychiatric morbidity. Interventions to reduce the incidence of psychiatric disorder following psychological trauma may be classified into three categories. Primary prevention includes the selection, preparation and training of individuals likely to be exposed to potentially traumatizing events. Secondary prevention comprises a variety of brief psychological techniques immediately or shortly after traumatizing life events, the best known of which is Psychological Debriefing. Tertiary interventions comprise the treatment of established PTSD and others. Psychiatric morbidity was studied in 106 British soldiers returning from UN peace-keeping duties in the former Republic of Yugoslavia. All 106 soldiers received an Operational Stress Training Package prior to their deployment and a randomly selected group also received a post-operational PD. Very low rates of PTSD and other psychopathology were found overall and the Operational Stress Training Package may have contributed to this. Elevated CAGE scores suggestive of significant alcohol misuse were observed in both groups and chemical avoidance behaviours arising from this may have masked psychopathology. CAGE scores diminished significantly in the debriefed group by the end of the follow-up period suggesting that PD may have been of benefit despite the apparent absence of PTSD. This study also demonstrates that a high incidence of psychiatric morbidity is not an inevitable consequence of military conflict.
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PMID:Preventing psychological trauma in soldiers: the role of operational stress training and psychological debriefing. 1075 52

There is some evidence that a traumatic life event can induce long-term alterations in corticotropin-releasing hormone (CRH) producing neurons in humans, which may play a role in the pathophysiology of anxiety disorders, including post-traumatic stress disorder (PTSD). To study the long-term effects of a traumatic event on brain CRH-immunoreactivity (CRH-ir) and phospho-cAMP response element binding protein-immunoreactivity (P-CREB-ir), rats were exposed to a single session of foot shocks (preshocked) or no shocks (control). Two weeks later half of the control rats and half of the preshocked rats received an electrified prod in the home cage for 15 min and behavior was recorded. Fifteen minutes after the removal of the prod rats were perfused and brain sections were stained for CRH-ir and P-CREB-ir. There was no basal difference between preshocked and control rats in brain CRH-ir and P-CREB-ir. Exposure to the electrified prod induced a significant increase in CRH-ir in the paraventricular nucleus of the hypothalamus, the median eminence and the central amygdala in preshocked rats, but not in control rats. The electrified prod increased the number of P-CREB-ir neurons in the paraventricular nucleus of the hypothalamus and the locus coeruleus, but the preshock experience did not affect this response. In an additional experiment with a similar design plasma hormone levels were measured 14 days after the foot shocks. The preshock experience sensitized the shock prod-induced ACTH and corticosterone response. No behavioral differences between preshocked and control rats were found during the shock prod tests. We suggest that long-term stress-induced changes in neuropeptide dynamics of CRH-ir neurons may play a role in long-term stress-induced neuroendocrine sensitization.
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PMID:Stress-induced sensitization of CRH-ir but not P-CREB-ir responsivity in the rat central nervous system. 1145 29

The aim of this study was to compare aggressive behavior in soldiers with combat-related post-traumatic stress disorder (PTSD), PTSD comorbid with alcohol addiction and alcohol addiction only. Three groups of male combat experienced soldiers with PTSD (n=43), PTSD comorbid with alcohol addiction (n=41) and alcohol addiction (n=39) were compared by Aggression rating scale A-87. PTSD was diagnosed according to DSM-IV criteria and Watson's PTSD rating scale. Alcohol addiction was diagnosed according to DSM-IV criteria and CAGE Questionnaire. Combat-experienced soldiers with alcohol addiction as well as soldiers with combat-related PTSD comorbid with alcohol addiction have a high level of verbal latent aggression (VLA), (F=26.65; P<0.001), physically latent aggression (PLA), (F=37.86; P<0.001), indirect aggression (INA), (F=56.94; P<0.001), verbal manifest aggression (VMA), (F=18.35; P<0.001), and physically manifest aggression (PMA), (F=43.22; P<0.001), vs. soldiers with combat-related PTSD without comorbid conditions. Alcohol addiction is a severe factor in increasing aggression levels in soldiers with PTSD.
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PMID:Comorbid alcohol addiction increases aggression level in soldiers with combat-related post-traumatic stress disorder. 1277 94

In this article, the authors examine patterns of medical services use among the Department of Veterans Affairs (VA) ambulatory care patients who screened positive for posttraumatic stress, depression, or alcohol-related disorders. On the basis of research linking mental disorders with increased use of medical services, the authors hypothesize that even after controlling for age and medical disease comorbidity, patients in VA ambulatory care who screen positive for targeted mental disorders would be more likely to use VA medical services and have higher rates of such use than those who did not screen positive. Baseline data were obtained from the Veterans Health Study, a longitudinal investigation of veterans' health. Four Boston-area VA ambulatory care facilities were used as study sites. A random sample of 2425 participants (mean age = 62) was drawn from male VA ambulatory care patients screened for eligibility during specified periods. Screening measures were Center for Epidemiological Studies-Depression Scale for depression, Posttraumatic Stress Disorder Checklist for posttraumatic stress disorder, and CAGE Questionnaire for alcohol-related disorders with endorsement of prior year consumption for alcohol-related disorders. Prior medical services use was assessed by self-report. Although unadjusted analyses of medical services use revealed clear effects of the screening presence of mental disorders on most outcomes, after adjusting for age and medical comorbidity, almost all these effects were reduced, and some previously nonsignificant results became significant. Findings suggest that healthcare policy and risk adjustment predicated upon the presumed relationship between mental disorders in the aggregate and medical services use should reconsider the important contributions of age, comorbid medical disorders, and specific mental disorder diagnoses.
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PMID:Mental disorders and medical care utilization of VA ambulatory care patients: the veterans health study. 1634 Jun 19

Posttraumatic stress disorder (PTSD) is the fourth most common psychiatric disorder. It is associated with somatic complaints like pain problems. Only a proportion of persons exposed to traumatic events develop PTSD. Several factors, like genetic predisposition, stressor intensity, cognitive appraisal mechanisms and coping processes influence the likelihood of developing PTSD after exposure to a trauma. We used a single session of footshocks in rats, an animal model with a high degree of validity for PTSD, to study whether individual behavioural traits predict long-term stress-induced sensitisation of behavioural responsivity and somatic pain sensitivity and therefore can act as a vulnerability factor. Rats were selected for low (LA) and high (HA) open-field locomotor reactivity and then underwent a single session of footshocks. Two to 5 weeks after footshocks, behavioural sensitisation was investigated using a noise challenge, an electrified prod challenge and a forced swim test. Somatic pain sensitivity was measured using a tail-immersion test. During exposure to noise in a novel cage, footshocked rats showed increased immobility compared to controls, which was significantly greater in LA than in HA rats. Footshocked rats showed increased burying in the electrified prod challenge and no effect was found in the forced swim test. Footshocks caused hyperalgesia in LA rats, but hypoalgesia in HA rats. We conclude that low open-field locomotor reactivity predicts the degree of stress-induced behavioural sensitisation and the direction of altered somatic pain sensitivity, suggesting that an anxiety-prone personality or passive coping style may increase the risk of developing stress-related psychosomatic disorders.
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PMID:Individual reactivity to the open-field predicts the expression of stress-induced behavioural and somatic pain sensitisation. 1692 Feb 5

Electric shocks lead to lasting behavioral deficits in rodents, and as such are often used to model post-traumatic stress disorder (PTSD) in the laboratory. Here we show that a single exposure of rats to 3 mA-strong shocks results in a marked social avoidance that lasts at least 28 days; moreover, the response intensifies over time. In an attempt to study the impact of cue reminders on the behavior of shocked rats, we administered shocks in the presence of a highly conspicuous, 10 cm-large object. This object was introduced into the home cage of rats 28 days after shock exposure. Shocked rats manipulated the object considerably less than controls. More importantly, however, the object was buried by shocked rats. This behavior was virtually absent in controls. The response strongly depended on the intensity of shocks, and was robust. Rats shocked with 3 mA currents spent 40% of time burying the object, which was often hardly visible at the end of the 5 min test. Subsequent experiments demonstrated that the response was not cue-specific as unfamiliar objects were also buried. Rats are well known to bury dangerous objects; the shock-prod burying test of anxiety is based on this response. Behavioral similarities with this test and the differences from the marble-burying behavior of mice suggest that traumatized rats bury unfamiliar objects in defense, and the response can be interpreted as a sign of hyper-vigilance. We further suggest that object burying can be used as a sign of hyper-vigilance in models of PTSD.
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PMID:Rats exposed to traumatic stress bury unfamiliar objects--a novel measure of hyper-vigilance in PTSD models? 1833 10

A single session of footshocks in rats causes long-lasting sensitisation of behavioural, hormonal and autonomic responses to subsequent novel stressful challenges as well as altered pain sensitivity. These changes mimic aspects of post-traumatic stress disorder in humans. Our aim was to identify neuropeptide substrates in the central nervous system involved in stress sensitisation. Male Wistar rats were exposed to ten footshocks in 15 min (preshocked) or placed in the same cage without shocks (control). Two weeks later, rats were placed in a novel cage, subjected to 5 min of 85 dB noise, and returned to their home cage. Rats were killed either before or 1 h after noise and their brains processed for in situ hybridization for neuropeptide Y (NPY) and beta-preprotachykinin-I (PPT) mRNA. Additional groups of rats were killed under basal conditions and brains processed for NPY and neurokinin receptor binding with radiolabelled ligands. Two weeks after footshock treatment NPY mRNA expression was increased in the basolateral amygdala and showed preshockxnoise interaction in the locus coeruleus (down after noise in controls, lower basal and unchanged after noise in preshocked). PPT expression in the lateral parabrachial nucleus also showed preshockxnoise interaction (up after noise in controls, higher basal and down after noise in preshocked), and was increased after noise in the periaquaeductal grey. NK1 receptor binding in the agranular insular cortex and arcuate nucleus of the hypothalamus and NK2 receptor binding in the amygdala was lower in preshocked rats than in controls. Altered expression of NPY in the basolateral amygdala and locus coeruleus could contribute to or compensate for behavioural and autonomic sensitisation in preshocked rats. Altered PPT expression in the parabrachial nucleus may be involved in the altered pain processing seen in this model. Lower NK1 and NK2 receptor numbers in cortex, hypothalamus and amygdala may reflect secondary adaptations to altered neuropeptide release. These long-term changes in brain neuropeptide systems could offer novel leads for pharmacological modulation of long-term stress-induced sensitisation.
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PMID:Altered neuropeptide Y and neurokinin messenger RNA expression and receptor binding in stress-sensitised rats. 1844 Apr 96

One prominent symptom of post-traumatic stress disorder (PTSD) is avoidance of stimuli reminiscent of the traumatic event. We attempted to study this aspect of PTSD in two experiments. Groups of rats received forty 3-s tailshocks, or served as home cage controls (HCC). Twenty-four hours later, all subjects received a 4-h session of leverpress escape/avoidance conditioning. In Experiment 1, shock periods in the absence of a response were 1 s; in Experiment 2 they were 30 s. No group differences were observed in Experiment 1. In Experiment 2, previously shocked animals made more avoidance responses and had a higher percent avoidance during the fourth hour of the session than controls. Further, previously shocked animals had a higher efficiency ratio (the percent of responses that were avoidances). No group differences were observed in leverpresses during the safety period (an index of anxiety) in either study. Results are discussed in terms of the effects of stress on avoidance behavior as a potential model for this important feature of PTSD.
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PMID:Stress-induced increases in avoidance responding: an animal model of post-traumatic stress disorder behavior? 1856 26

We have previously reported that prior exposure to inescapable tailshock stress increased avoidance responding 24 hours later. We argued previously that this might model the avoidance behavior characteristic of post-traumatic stress disorder (PTSD). The current experiment was conducted to determine whether a more ethologically relevant stressor would produce similar effects on avoidance responding. Therefore, rats were restrained for 2 hours and exposed to trimethylthiazoline (TMT), a component of fox feces, restrained only, or served as home cage controls. Twenty-four hours later, subjects received a 4-hour escape-avoidance session. Animals exposed to TMT made more escape responses overall, and made more avoidance responses than the other two groups by the 4th hour of the session. Differences between the TMT-exposed animals and restraint alone could not be explained by differences in corticosterone (CORT) levels. Results are discussed in terms of the possible neural changes induced by TMT exposure and the relationship to the behavioral aspects of PTSD or acute stress.
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PMID:Predator odor exposure facilitates acquisition of a leverpress avoidance response in rats. 1941 47

Environmental stress produces adverse affects on memory in humans and rodents. Increased noradrenergic neurotransmission is a major component of the response to stress and noradrenaline (NA) plays an important role in modulating processes involved in learning and memory. The present study investigated the effect of NA depletion on stress-induced changes on memory performance in the mouse. Central NA depletion was induced using the selective neurotoxin N-(2-chloroethyl)-N-ethyl-2 bromobenzylamine (DSP-4) and verified by high performance liquid chromatography (HPLC). A novel cage stress procedure involving exposure to a new clean cage for 1 h per day, 4 days per week for 4 weeks, was used to produce stress-induced memory deficits measured using the object recognition task. 50 mg/kg DSP-4 produced large and sustained reductions in NA levels in the frontal cortex and hippocampus measured 24 h, 1 week and 5 weeks after treatment. Four weeks of exposure to novel cage stress induced a memory deficit in the object recognition task which was prevented by DSP-4 pre-treatment (50 mg/kg 1 week before the commencement of stress).These findings indicate that chronic environmental stress adversely affects recognition memory and that this effect is, in part, mediated by the noradrenergic stress response. The implication of these findings is that drugs targeting the noradrenergic system to reduce over-activity may be beneficial in the treatment of stress-related mental disorders such as post-traumatic stress disorder or anxiety in which memory is affected.
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PMID:Central noradrenergic depletion by DSP-4 prevents stress-induced memory impairments in the object recognition task. 1972 Jan 15


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