Combat-related posttraumatic stress disorder among Israeli soldiers. A two-year follow-up.
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This study tested the hypothesis that combat veterans with posttraumatic stress disorder (PTSD) experience sympathetic nervous system activation in response to war-related laboratory stimuli. Circulating plasma catecholamines, vital signs, and affect ratings were measured in 10 Vietnam combat veterans with PTSD and 11 control subjects, during and after viewing combat and noncombat stress films. PTSD subjects responded more strongly than controls to the combat film, with greater increases in plasma epinephrine, pulse, blood pressure, and subjective distress. The increases in autonomic activity of PTSD subjects was more pronounced and long lasting in response to the combat film than to the noncombat film, but type of film had no systematic effect on control subjects' responses. These findings are consistent with biological models that posit sympathoadrenal activation in response to memory-evoking cues of traumatic events in PTSD.
The current study provides a portrait of emotional-behavioral functioning within a small sample of Vietnam veterans with combat-related posttraumatic stress disorder (PTSD), their partners, and older adolescent and adult children. Veterans, their partners and children reported moderate-low to moderate-high levels of violent behavior. In addition, partner and veteran hostility scores were elevated relative to gender and age matched norms. Partners also reported heightened levels of psychological maltreatment by veterans. Veterans' combat exposure was positively correlated with hostility and violent behavior among children but unrelated to partner variables. Veterans' reports of PTSD symptoms were positively associated with reports of hostility and violence among children, and hostility and general psychological distress among partners. Veterans' violent behavior was also positively correlated with children's violent behavior, but did not yield significant correlations with other child or partner variables. Findings are discussed in relation to prior work and directions for future research are addressed.
There is a need for family therapy interventions that are specific to the conditions found in families of traumatized people such as combat veterans. In these families, the historically "real" event of the trauma often continues to exert influence on the family system despite collusive arrangements that serve to keep it hidden. In families of combat veterans, a situation develops whereby the veteran becomes triangulated with a dead buddy without the spouse's knowledge. The discrepancy between past and present emerges in what we call the critical interaction between the spouses. This article outlines a method of couples therapy that attempts to demystify this critical interaction, and begins to integrate the discrepant narratives of each spouse. The establishment of a nascent mutuality of perspective within the couple releases energies that can be directed toward support rather than symptom-formation in the family system.
We used path analysis to model the effects of combat exposure, posttraumatic stress disorder (PTSD) symptoms, and health behaviors on physical health. Participants were 921 male military veterans from the Normative Aging Study. Their mean age at time of study was 65. Measures of combat exposure, PTSD symptoms, smoking, and alcohol problems were used to predict subsequent self-reported physical health status. Both combat exposure and PTSD were correlated with poorer health. In path analysis, combat exposure had only an indirect effect on health status, through PTSD, whereas PTSD had a direct effect. Smoking had a small effect on health status but did not mediate the effects of PTSD, and alcohol was unrelated to health status. We conclude that PTSD is an important predictor of physical health and encourage further investigation of health behaviors and other possible mediators of this relationship.
Since the diagnosis of posttraumatic stress disorder (PTSD) first appeared in the psychiatric nomenclature in 1980, considerable debate has revolved around the nature of the condition. Specifically, is PTSD best conceptualized as one end of a continuum of human response to traumatic stress or does it represent a discontinuous latent category? Two taxometric procedures were used to investigate this issue in a random community sample of 692 Australian combat veterans, using structured interview and self-report instruments to assess PTSD symptomatology. Findings favored a dimensional model of PTSD, consistent with previous taxometric work on treatment-seeking samples (A. Ruscio, Ruscio, & Keane, 2002). Implications are drawn for the conceptualization, etiology, and assessment of PTSD.
This study used an analog approach to the perceptions of tour of duty, combat and noncombat, and levels of social support, high and low. Their influence was assessed in the symptomatology of Posttraumatic Stress Disorder. 80 subjects were randomly assigned to read one of four vignettes depicting levels of combat and social support as main effects. Results were congruent with recent research indicating significant main effects for combat and social support in the symptomatology of Posttraumatic Stress Disorder.
This study adopted a quasi-experimental design to compare the treatment outcomes of inpatient-outpatient programs and day hospital programs for chronic, combat-related posttraumatic stress disorder. Data were drawn from 202 Vietnam veterans who had completed treatment at four programs across Australia. The veterans were assessed on a range of psychological and social variables at intake to the programs and followed up at 3 and 9 months after discharge. A significant main effect was found for time, with veterans from both program models demonstrating improvements that were maintained over the 9-month follow-up period. Group by time effects were not significant, which suggests that inpatient-outpatient programs are not more efficacious than the less expensive day hospital alternatives. In line with current mental health policy directions, the current study lends broad support to the recommendation that treatment services for veterans with posttraumatic stress disorder be delivered in the least restrictive environment.
OBJECTIVE: The purpose of the study was to search for the intrapsychic correlates of individual differences in cortisol levels in male Vietnam combat veterans with posttraumatic stress disorder. METHODS: The study involved measurement of urinary cortisol levels and clinical assessment with a broad profile of psychometric tests during a single 48-hour period in 30 inpatients. RESULTS: The main finding by both correlation and t test analyses was a significant inverse relationship between urinary cortisol levels and a symptom complex composed of two closely interrelated clinical subgroupings, "disengagement" (principally involving emotional numbing) and "shame-laden depression." CONCLUSIONS: The findings support the concept that cortisol levels reflect the ongoing balance between the undifferentiated emotional arousal state of engagement (associated with higher cortisol levels) and opposing antiarousal disengagement defense mechanisms (associated with lower cortisol levels). It appears that the low cortisol levels often seen in patients with posttraumatic stress disorder are psychogenic and reflect a dominating effect of disengagement coping strategies, which represent secondary compensatory adaptations during the chronic course of this disorder to counteract primary arousal symptoms, especially those related to an intractable shame-laden depressive syndrome. The psychoendocrine findings suggest that the relatively inconspicuous clinical feature of shame resulting from both the primary and secondary traumatizations is a particularly powerful, preoccupying, and overwhelming source of emotional engagement. Shame may represent a "sleeper" that is worthy of greater attention in both research and clinical efforts to understand the pathogenesis and psychopathology of this devastating stress-related disorder.
Levels of serum interleukin-1 beta (IL-1 beta) and soluble interleukin-2 receptor (sIL-2R) were assessed in 19 male patients with combat-related posttraumatic stress disorder (PTSD) in comparison to 19 age- and sex-matched healthy volunteers. Serum IL-1 beta levels (but not sIL-2R) were significantly higher (p < .001) in the PTSD patients than in the controls. IL-1 beta levels did not correlate with cortisol levels, severity of PTSD, anxiety, depressive symptoms, or alexithymia score; however, they did correlate significantly (r = .54, p < .005) with the duration of PTSD symptoms. It is possible that desensitization of the hypothalamic-pituitary-adrenal axis in chronic PTSD patients counteracts the stimulatory effect of IL-1 beta on cortisol secretion.
OBJECTIVE: Studies in nonhuman primates suggest that high levels of cortisol associated with stress have neurotoxic effects on the hippocampus, a brain structure involved in memory. The authors previously showed that patients with combat-related posttraumatic stress disorder (PTSD) had deficits in short-term memory. The purpose of this study was to compare the hippocampal volume of patients with PTSD to that of subjects without psychiatric disorder. METHOD: Magnetic resonance imaging was used to measure the volume of the hippocampus in 26 Vietnam combat veterans with PTSD and 22 comparison subjects selected to be similar to the patients in age, sex, race, years of education, socioeconomic status, body size, and years of alcohol abuse. RESULTS: The PTSD patients had a statistically significant 8% smaller right hippocampal volume relative to that of the comparison subjects, but there was no difference in the volume of other brain regions (caudate and temporal lobe). Deficits in short-term verbal memory as measured with the Wechsler Memory Scale were associated with smaller right hippocampal volume in the PTSD patients only. CONCLUSIONS: These findings are consistent with a smaller right hippocampal volume in PTSD that is associated with functional deficits in verbal memory.
The aim of our study was to assess concentrations of serum cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides in soldiers with combat-related posttraumatic stress disorder (PTSD), in comparison with combat-experienced soldiers without PTSD. The second aim of our study was to explore the relationship between PTSD symptoms such as re-experiencing, avoidance, increased arousal, and serum lipid levels. In 53 soldiers with combat-related PTSD and 49 with combat experiences without PTSD, serum cholesterol, LDL-C, HDL-C, and triglycerides were assayed by an enzyme-assay method. Soldiers with combat-related PTSD were found to have significantly higher concentrations of cholesterol (P = 0.001), LDL-C (P = 0.002), and triglycerides (P = 0.001) than soldiers without current PTSD. HDL-C was statistically lower (P < 0.001) in soldiers with combat-related PTSD than in those without PTSD. A positive correlation was found between increased arousal and cholesterol (r = 0.464; P = 0.039), or LDL-C (r = 0.479; P = 0.021) concentrations.
A 10-week open-label trial of fluvoxamine was conducted for male Vietnam combat veterans with chronic PTSD. Subjects were excluded if they met full current criteria for panic disorder or agoraphobia, and lifetime criteria for psychosis, bipolar disorder, or organic mental syndrome. Repeated MANOVA was performed to determine change over time. Fluvoxamine was well tolerated; side effects were observed primarily early in treatment with headache, insomnia, sedation, and gastrointestinal distress being most frequent. Fluvoxamine was effective for treating the core intrusion, avoidance, and arousal symptoms of PTSD. Large treatment effects were seen by 4-6 weeks, and maintained at 10 weeks. The magnitude of change was greater than has been previously reported for antidepressant treatment of male Vietnam combat veterans with PTSD.
BACKGROUND: We examined the effects of nefazodone on polysomnographic sleep measures and subjective reports of sleep quality and nightmares. as well as other symptoms, in patients with chronic combat-related posttraumatic stress disorder (PTSD) during a 12-week, open-label clinical trial. To our knowledge, this is the first polysomnographic study of treatment in patients with PTSD. METHOD: The subjects were 12 male veterans (mean age = 54 years) who met DSM-IV diagnostic criteria for PTSD (mean duration = 30 years). All but I patient also met DSM-IV criteria for major depressive disorder. Patients were evaluated weekly with clinical ratings in an open-label clinical trial. Polysomnographic recordings for 2 consecutive nights were obtained before treatment and at 2, 4, 8, and 12 weeks. The dose of nefazodone was adjusted according to individual clinical needs. Final mean daily dose was 441 mg. RESULTS: The patients reported significantly fewer nightmares and sleep problems during treatment. Nevertheless, contrary to studies in depressed patients, nefazodone did not significantly affect polysomnographic sleep measures compared with baseline. In addition, the patients showed significant improvement in the Clinical Global Impressions of PTSD symptoms (global score, hyperarousals and intrusions subscales), the Clinician-Administered PTSD Scale (global, hyperarousal, and intrusions subscales), the Hamilton Rating Scale for Depression (HAM-D). and the Beck Depression Inventory (BDI). CONCLUSION: These patients with chronic, treatment-resistant, combat-related PTSD showed significant improvement of subjective symptoms of nightmares and sleep disturbance, as well as depression and PTSD symptoms. in this 12-week open-label clinical trial. Nevertheless, objective polysomnographic sleep measures did not change. Further studies, including double-blind. placebo-controlled trials, are needed to extend these findings and to understand the relationships between the physiology of sleep and symptoms of poor sleep and nightmares.
OBJECTIVE: Animals exposed to stress exhibit a decrease in benzodiazepine receptor binding in the frontal cortex. No studies have examined central benzodiazepine receptor binding in patients with posttraumatic stress disorder (PTSD). The purpose of this study was to examine measures of benzodiazepine receptor binding in PTSD. METHOD: From 13 patients with Vietnam combat-related PTSD and 13 case-matched healthy comparison subjects, a quantitative measure related to benzodiazepine receptor binding (distribution volume) was obtained with single photon emission computed tomography (SPECT) imaging of [(123)I]iomazenil binding and measurement of radioligand concentration in plasma. Distribution volume image data were analyzed by means of statistical parametric mapping. RESULTS: Lower distribution volumes were found in the prefrontal cortex (Brodmann's area 9) of PTSD patients than in comparison subjects. CONCLUSIONS: These findings of lower values for the benzodiazepine receptor binding measure of distribution volume are consistent with fewer benzodiazepine receptors and/or reduced affinity of receptor binding in the medial prefrontal cortex in patients with PTSD. Alterations in benzodiazepine receptor function in this area may underlie many of the symptoms of PTSD.
Given the association of injury and posttraumatic stress disorder (PTSD), we examined whether head injury might be associated with increased frequency and severity of PTSD. Using a mail survey, we queried 143 male combat veterans with and without PTSD, who had previously participated in PTSD research in our laboratory, about their history of head injury. Respondents with a PTSD diagnosis were significantly more likely to report a history of head injury than those without. Patients with a history of head injury also reported more severe symptoms of PTSD compared with PTSD patients without head injury. The association of head injury and PTSD was not due to greater combat exposure in the head-injured group. Head injury is associated with a greater likelihood of developing combat-related PTSD and with more severe PTSD symptoms. This retrospective study did not address mechanisms that could account for this finding. The results indicate head injury should be systematically assessed by both nonpsychiatric and psychiatric physicians concerned with the psychological sequelae of exposure to victimizing experiences.
We examined the relations between coping, locus of control, and social support and combat-related posttraumatic stress disorder (PTSD). The sample consisted of 262 Israeli soldiers who suffered a combat stress reaction episode during the 1982 Lebanon war and were followed 2 and 3 years after their participation in combat. Cross-sectional analyses revealed significant relations between locus of control, coping, and social support and PTSD at the two points of assessment. Changes in PTSD from Time 1 to Time 2 were also associated with changes in coping. We discuss theoretical and methodological implications of the findings.
OBJECTIVE: Central nervous system norepinephrine (NE) is normally involved in blood pressure regulation, but it is pathophysiologically elevated in posttraumatic stress disorder (PTSD). METHODS: We monitored blood pressure while performing serial cerebrospinal fluid (CSF) sampling for 6 hours to determine CSF NE concentrations in men with combat-related PTSD (n = 11) and in healthy men (n = 8). RESULTS: CSF NE concentrations strongly and positively correlated with mean diastolic blood pressure in the healthy men (R = 0.93, p <.002) but not in the patients (R = 0.10, p =.77). Within individuals, mean arterial pressure, systolic blood pressure, diastolic blood pressure and pulse pressure were poorly correlated over time in patients with PTSD but highly correlated over time in the healthy men, indicating that measurement of these hemodynamic parameters are poorly prognostic of subsequent measurements of the same parameter in patients with PTSD. CONCLUSION: These data demonstrate the loss of the normal direct relationship between CSF NE and blood pressure in combat veterans with PTSD. Whether this dysynchrony mechanistically relates to the hemodynamic abnormalities in PTSD or, like some of the psychobehavioral symptoms, can be corrected with anti-noradrenergic pharmacotherapy remains to be determined.