Posttraumatic stress disorder, trauma exposure, and the current health of Canadian bus drivers.

OBJECTIVE: Previous studies of veterans have linked posttraumatic stress disorder (PTSD) after combat-related trauma to increased reports of health problems. It is unclear whether this association between PTSD and increased health problems generalizes to civilians who are exposed to a broader array of traumatic events. We also do not know whether trauma exposure is associated with increased health problems in individuals who do not develop PTSD. Using a non-treatment-seeking civilian sample, we examined whether lifetime PTSD or trauma exposure by itself was associated with current health problems. METHODS: Using a cross-sectional design and self-report measures, we evaluated urban Canadian bus drivers (n = 342) on trauma exposure, lifetime PTSD, and current health problems. Based on their responses, we divided our sample into individuals who had never experienced trauma (n = 91), trauma-exposed individuals who had never developed PTSD (n = 218), and persons who developed PTSD at some point after trauma (n = 33). We compared these groups on health problems, treatment service use, and health assessment measures. RESULTS: The PTSD group reported increased health complaints, more frequent use of health treatments, and poorer health self-ratings compared with the exposed non-PTSD and nonexposed groups. Trauma-exposed drivers without PTSD did not differ from unexposed drivers on any health measure. Controlling for sex and trauma frequency did not alter our findings. CONCLUSIONS: Trauma exposure that leads to PTSD is associated with increased health problems, while trauma exposure alone is not. Our results extend previous findings to a broader civilian context and clarify associations between trauma exposure and health.     

Salivary cortisol and posttraumatic stress disorder in a low-income community sample of women.

BACKGROUND: Studies of male combat veterans with posttraumatic stress disorder have demonstrated a profile of low cortisol. Studies with women with posttraumatic stress disorder (PTSD) have focused on childhood sexual abuse and holocaust survivors, both of whom experienced trauma during development, which could be different than adult trauma exposure. METHODS: Using an epidemiologic sample of low-income women from an urban area in Michigan, we conducted structured psychiatric interviews and saliva cortisol collection on a subsample of women with exposure to trauma but never PTSD (n = 72), recent PTSD (n = 29), and past PTSD (n = 70). Saliva cortisol was collected at awakening, 30 minutes later, at bedtime, and during a clinic visit. RESULTS: Recent trauma exposure but not past trauma exposure led to an increase in saliva cortisol. Neither recent PTSD nor past PTSD resulted in any saliva cortisol changes compared with the trauma exposed, never PTSD group. Recent major depression (past 12 months) demonstrated a weak effect (p =.08) on bedtime saliva cortisol. CONCLUSIONS: While recent trauma exposure can increase saliva cortisol, neither recent nor past PTSD affected saliva cortisol in our community sample of women. Our data do not support saliva cortisol changes associated with PTSD.     

Persistent posttraumatic stress disorder following September 11 in patients with bipolar disorder

OBJECTIVE: We examined the development of posttraumatic stress disorder (PTSD) following indirect exposure to the September 11, 2001, terrorist attacks in a cohort at high risk for adverse trauma-related sequelae as a result of having bipolar disorder. METHOD: Subjects (N = 137) were participants in the ongoing, naturalistic, longitudinal study Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) prior to September 11, 2001. The present study examined prospectively collected pre-event information about bipolar disorder and other potential predictors of PTSD, along with assessment of the level of indirect trauma exposure (i.e., via media) and peritraumatic distress in the aftermath of September 11, and their association with 9/11-related, new-onset PTSD as assessed by a self-report measure, the Posttraumatic Stress Diagnostic Scale. RESULTS: Posttrauma assessments were completed a mean +/- SD of 430.6 +/- 78.7 days (range, 0.5-1.5 years) after September 11. Twenty percent (N = 27) of patients reported development of new-onset PTSD in response to the September 11 attacks. Rates of PTSD were significantly associated with the presence of a hypomanic, manic, or mixed mood state at the time of trauma (chi(2) = 4.25; p < .05); 62% of patients in these states developed PTSD. Mania/hypomania remained a significant predictor of PTSD in response to the September 11 attacks after controlling for peritraumatic exposure and distress variables, suggestive of a substantial increase in risk compared with those in recovery (OR = 17; 95% CI = 2.6 to 115.6; p = .0034). CONCLUSIONS: Rates of persistent new-onset PTSD among bipolar patients were elevated in the aftermath of the September 11 attacks. Our findings suggest that the presence of a manic state may be the most critical risk factor for adverse sequelae following indirect traumatic exposure in bipolar individuals.     

Elevated plasma arginine vasopressin levels in veterans with posttraumatic stress disorder

BACKGROUND: Posttraumatic stress disorder (PTSD) is associated with altered hypothalamic-pituitary-adrenal (HPA) axis functioning. Arginine vasopressin (AVP), in conjunction with corticotrophin releasing hormone, has shown to be an important modulator of the HPA axis. In order to evaluate the effect of trauma and PTSD on central AVP secretion we assessed plasma AVP levels in equally trauma exposed veterans with and without PTSD and a non-traumatized healthy control group. METHODS: Assessment of plasma AVP in 29 male veterans with PTSD, 29 traumatized veterans without PTSD, matched for age, gender, year and region of deployment (trauma controls), and 26 age matched healthy controls. RESULTS: Plasma AVP levels were higher in PTSD patients compared to both healthy controls (p = 0.004) and trauma controls (p < 0.001). In PTSD patients without a comorbid MDD a significant correlation was observed between plasma AVP levels and symptoms of avoidance measured with the Clinician Administered PTSD Scale (CAPS). CONCLUSION: Elevated plasma AVP levels are specifically related to PTSD and not to exposure to traumatic stress during deployment. Our results indicate that AVP may play a role as an anxiogenic factor, but they do not support a role for AVP in the altered response to dexamethasone in PTSD.     

Anxiety sensitivity and PTSD among female victims of intimate partner violence

The purpose of this study was to evaluate the relationship between anxiety sensitivity (AS) and posttraumatic stress disorder (PTSD) in women. The study involved three groups: women with no history of exposure to serious trauma (n = 30), women who had been exposed to intimate partner violence (IPV) but never developed PTSD (n = 23), and women with IPV exposure and current PTSD (n = 19). As a part of a larger study, they completed measures of AS, PTSD symptomatology, and depression. Women with PTSD reported the highest levels of AS, although traumatized women with PTSD reported more AS than did women with no trauma history. AS-related psychological concerns were a statistical predictor of PTSD symptoms when the entire sample of women was considered but not among the subset with a trauma history. Nonetheless, AS may be an important factor to consider in treatment of individuals with PTSD.     

Limitations to the Psychotherapy of Schizophrenics

Objective: Diathesis-stress models of posttraumatic stress disorder (PTSD) hypothesize that exposure to trauma may interact with individual differences in the development of PTSD. Previous studies have not assessed immediate responses to a proximate stressor, but the current “natural laboratory” study was designed to empirically test the role that individual differences in pathological narcissism may play in the development of acute anxiety symptoms among civilians facing rocket and missile fire. Method: We assessed demographic features, trauma exposure severity, narcissistic personality features, and acute anxiety symptoms (PTSD and General Anxiety Disorder [GAD]) among 342 Israeli female adults during the November 2012 eruption of violence in the Middle East. Results: Results demonstrate an association between exposure severity and acute anxiety symptoms (both PTSD and GAD) for individuals with high levels of pathological narcissism but not for those with low levels of pathological narcissism. These results suggest that individuals with narcissistic personality features are at high risk for the development of acute anxiety symptoms following exposure to uncontrollable and life-threatening mass trauma. Conclusion: The findings underscore the role of intra-personal resources in the immediate psychological aftermath of war by highlighting the increased risk associated with narcissistic personality features. Theoretical and clinical implications of the findings are discussed.     

Sensory filtering phenomenology in PTSD

Disrupted sensory filtering, or problems with suppressing irrelevant environmental sensory stimuli, has been reported in individuals with posttraumatic stress disorder (PTSD). However, the relationship of sensory filtering deficits to specific PTSD symptoms versus an association with general trauma exposure is unclear. These relationships were examined by administering self-report measures of trauma exposure, PTSD, and sensory gating phenomenology to undergraduate participants with PTSD (n=32), with trauma history but without PTSD (n=144), and with minimal trauma history (n=153). Subjects with PTSD reported greater filtering disruption than individuals in the trauma only and low trauma groups, who did not differ. Individuals endorsing reexperiencing and numbing symptoms, and females endorsing hypervigilance, reported disrupted sensory filtering phenomenology. These results suggest that impaired filtering differentiates between individuals with PTSD symptoms and asymptomatic individuals exposed to multiple traumas and low-trauma controls.     

Enhanced sensitivity to glucocorticoids in peripheral mononuclear leukocytes in posttraumatic stress disorder.

BACKGROUND: The aim of this study was to determine whether there is increased responsiveness to corticosteroids in posttraumatic stress disorder (PTSD) by examining the differential effects of dexamethasone (DEX) on the inhibition of lysozyme activity. METHODS: 60 mL of blood was withdrawn at 8:00 am, and mononuclear leukocytes were isolated from the blood of 26 men with, and 18 men without, PTSD. An aliquot of live cells was incubated with a series of concentrations of DEX to determine the rate of inhibition of lysozyme activity; a portion of cells was frozen for the determination of glucocorticoid receptors (GR). RESULTS: Subjects with PTSD showed evidence of a greater sensitivity to glucocorticoids as reflected by a significantly lower mean concentration (nmol/L) of dexamethasone at which 50% of lysozyme activity is inhibited (IC(50-DEX)) (PTSD+ = 4.9 +/-.53; PTSD- group = 7.2 +/-.64). The lysozyme IC(50-DEX) was significantly correlated with age at exposure to the first traumatic event in subjects with PTSD (r =.44, n = 26, p =.025). The number of cytosolic glucocorticoid receptors was also correlated with age at exposure to the focal traumatic event (r = -.44, n = 25, p =.03) in PTSD. CONCLUSIONS: This is the first in vitro demonstration of an alteration in target tissue sensitivity to glucocorticoids in PTSD. The lower lysozyme IC(50-DEX) might be related to the risk factor of prior exposure to trauma.     

Biology of post-traumatic stress disorder in childhood and adolescence

Diverse patterns of cortisol secretion with consistently high circulating catecholamines have been reported in post-traumatic stress disorder (PTSD), an anxiety state that develops after exposure to traumatic life events. Indeed, peripheral cortisol levels have been reported to be low or normal in the majority of adult chronic PTSD studies, whereas, in most paediatric studies, high cortisol values have been documented. Longitudinal studies on PTSD biology, including the transition from childhood to adulthood, may shed light on these discrepancies. In children, elevated evening salivary cortisol in the aftermath of the trauma was predictive of PTSD development 6 months later, whereas plasma interleukin-6 correlated positively with evening cortisol and was equally predictive of later PTSD. Longitudinal assessment of PTSD children 1 and 6 months later revealed progressive normalisation of cortisol levels, whereas noradrenaline concentrations became gradually higher. We hypothesise that, in adults with chronic PTSD, low cortisol levels, together with high catecholamines, may reflect a late event in the natural history of the disorder, months or years after the trauma. The progressive divergence of cortisol and noradrenaline concentrations over time may be responsible for PTSD maintenance in children and explain the differences between the child and adult PTSD endophenotypes. In adults studied immediately after the trauma, and by contrast to children, low cortisol levels are predictive of later PTSD development. Our hypothesis that low cortisol levels may reflect a previous trauma, earlier in development, is supported by the well established observation that prior trauma is a risk factor for a new PTSD diagnosis. The developmental stage of an individual in relation to previous exposure to trauma and PTSD vulnerability are crucial variables that may determine clinical and biological PTSD phenotypes and explain the discrepancies between adults and children in reported cortisol levels.     

Cortisol and catecholamines in posttraumatic stress disorder: an epidemiologic community study

BACKGROUND: Prior research has connected posttraumatic stress disorder (PTSD) to increased levels of catecholamines. However, studies of cortisol levels have produced mixed results. OBJECTIVE: To examine urinary catecholamine and cortisol levels in individuals with PTSD in a community sample. DESIGN: A representative cohort of young adult community residents, assessed periodically during a 10-year period for exposure to trauma and PTSD, was used to select a subset for urine collection studies conducted in a sleep laboratory across 2 consecutive nights and the intermediate day. SETTING: The sample of young adults was randomly selected from a large health maintenance organization and is representative of the geographic area except for the extremes of the socioeconomic status range. PARTICIPANTS: A subsample was selected from the 10-year follow-up cohort (n = 913; 91.1% of the initial sample). Eligibility criteria were: (1) persons exposed to trauma during the preceding 5 years, (2) other individuals who met PTSD criteria, and (3) a random preselected subsample. Of 439 eligible individuals, 292 (66.5%) participated, including 69 with lifetime PTSD. MAIN OUTCOME MEASURES: Measures of cortisol and catecholamine levels in urine. RESULTS: The lifetime PTSD group demonstrated significantly higher catecholamine levels than the group exposed to trauma without PTSD and the nonexposed group. Individuals exposed to trauma without PTSD demonstrated significantly lower urine catecholamine levels than the nonexposed and the PTSD groups. Mean cortisol levels did not differ across groups. When analyzed by comorbidity with major depressive disorder (MDD), the PTSD-only group did not differ in cortisol levels from the groups with neither PTSD nor MDD. Women with MDD plus PTSD demonstrated significantly higher cortisol levels than women with neither disorder or with either disorder alone. CONCLUSIONS: Trauma per se does not lead to sustained increases in cortisol or catecholamine levels. Posttraumatic stress disorder is associated with higher catecholamine levels. In contrast, persons with PTSD had neither an increase nor a decrease in mean urinary cortisol levels. Women with PTSD and comorbid MDD had higher cortisol levels.     

Psychological resilience and neurocognitive performance in a traumatized community sample

Background: Whether psychological resilience correlates with neurocognitive performance is largely unknown. Therefore, we assessed association between neurocognitive performance and resilience in individuals with a history of childhood abuse or trauma exposure. Methods: In this cross‐sectional study of 226 highly traumatized civilians, we assessed neurocognitive performance, history of childhood abuse and other trauma exposure, and current depressive and PTSD symptoms. Resilience was defined as having ≥1 trauma and no current depressive or PTSD symptoms; non‐resilience as having ≥1 trauma and current moderate/severe depressive or PTSD symptoms. Results: The non‐resilient group had a higher percentage of unemployment (P=.006) and previous suicide attempts (P<.0001) than the resilient group. Both groups had comparable education and performance on verbal reasoning, nonverbal reasoning, and verbal memory. However, the resilient group performed better on nonverbal memory (P=.016) with an effect size of .35. Additionally, more severe childhood abuse or other trauma exposure was significantly associated with non‐resilience. Better nonverbal memory was significantly associated with resilience even after adjusting for severity of childhood abuse, other trauma exposure, sex, and race using multiple logistic regression (adjusted OR=1.2; P=.017). Conclusions: We examined resilience as absence of psychopathology despite trauma exposure in a highly traumatized, low socioeconomic, urban population. Resilience was significantly associated with better nonverbal memory, a measure of ability to code, store, and visually recognize concrete and abstract pictorial stimuli. Nonverbal memory may be a proxy for emotional learning, which is often dysregulated in stress‐related psychopathology, and may contribute to our understanding of resilience. Depression and Anxiety, 2010. © 2010 Wiley‐Liss, Inc.     

Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder.

BACKGROUND: Alterations in the gamma-amino-butyric acid (GABA) neurotransmitter system have been identified in some populations with posttraumatic stress disorder (PTSD). METHODS: To further investigate factors of relevance to GABAergic neurotransmission in PTSD, we measured cerebrospinal fluid (CSF) levels of allopregnanolone and pregnanolone combined (ALLO: congeners that potently and positively modulate effects of GABA at the GABA(A) receptor), 5alpha-dihydroprogesterone (5alpha-DHP: the immediate precursor for allopregnanolone), dehydroepiandrosterone (DHEA: a negative modulator of GABA(A) receptor function), and progesterone with gas chromatography, mass spectrometry in premenopausal women with (n = 9) and without (n = 10) PTSD. Subjects were free of psychotropic medications, alcohol, and illicit drugs; all were in the follicular phase of the menstrual cycle except three healthy and four PTSD subjects receiving oral contraceptives. RESULTS: There were no group differences in progesterone, 5alpha-DHP, or DHEA levels. The PTSD group ALLO levels were < 39% of healthy group levels. The ALLO/DHEA ratio correlated negatively with PTSD re-experiencing symptoms (n = -.82, p < 008; trend) and with Profile of Mood State depression/dejection scores (n = -0.70, p < 0008). CONCLUSION: Low CSF ALLO levels in premenopausal women with PTSD might contribute to an imbalance in inhibitory versus excitatory neurotransmission, resulting in increased PTSD re-experiencing and depressive symptoms.     

PTSD and the HPA axis: differences in response to the cold pressor task among individuals with child vs. adult trauma

Hypothalamic pituitary adrenal (HPA) axis and subjective stress response to a cold-water immersion task, the cold pressor task (CPT), in individuals (N=89) with post-traumatic stress disorder (PTSD) were examined. All tests were conducted at 08:00h after an overnight hospital stay. Plasma adrenocorticotrophin hormone (ACTH), cortisol, and subjective stress were examined at baseline and five post-task time points in controls (n=31), subjects with PTSD as a result of an index trauma during childhood (i.e. before age 18; n=25), and subjects with PTSD as a result of an index trauma as an adult (n=33). Approximately, 50% of individuals in both trauma groups were alcohol dependent, and the impact of this comorbidity was also examined. Subjects with PTSD, regardless of age of index trauma, had a less robust ACTH response as compared to controls. Regardless of the presence or absence of comorbid alcohol dependence, subjects with childhood trauma had lower cortisol at baseline and at all post-task measurement points and did not demonstrate the decrease in cortisol over the course of the 2h monitoring period seen in subjects with adult index trauma and controls. The findings reveal differences in the neuroendocrine response to the CPT in individuals with PTSD compared to control subjects, and differences in PTSD subjects when examined by age of index trauma.     

Full and partial PTSD among earthquake survivors in rural Taiwan

In 1999, a major earthquake struck central Taiwan. Ten months after the earthquake, survivors were surveyed to examine the background factors of demographics and exposure that are associated with posttraumatic stress disorder (PTSD) and subthreshold posttraumatic stress disorder (PTSS) and to investigate the relationships between other psychiatric problems and PTSD and PTSS following the earthquake. Subjects (n=252) randomly selected from two rural communities near the epicenter of the earthquake were interviewed to obtain the following information: demographic characteristics; extent of earthquake exposure; severity of posttraumatic stress symptoms; other psychiatric morbidity; and other morbidity-related factors, including general mental health, disability, stress vulnerability, social support, and wellbeing. Three diagnostic groups were identified with regard to trauma-related symptoms: full PTSD, partial PTSD (PTSS), and non-PTSD. Prevalence rates were calculated and bivariate and multivariate comparisons adjusted for age, sex and education were performed. The prevalence rates for PTSD (n=26) and PTSS (n=48) were 10.3% and 19.0%, respectively. The PTSD and PTSS groups differed significantly from non-PTSD on most variables, with greater likelihood of the following: female gender; total trauma exposure; generalized anxiety disorder; suicidality; any other axis I disorder; general psychopathology, disability; and impaired wellbeing. Few differences were observed between the PTSD and PTSS groups, although greater likelihood for major depression, trauma-related loss of life, and impaired stress vulnerability were noted in the PTSD group. In conclusion, PTSD and PTSS are commonly observed following earthquake exposure and are associated with similarly high levels of psychosocial impairment.     

Dissociation and posttraumatic stress disorder in Vietnam combat veterans.

OBJECTIVE: This study compared current dissociative symptoms and dissociation at the time of specific traumatic events in Vietnam combat veterans with posttraumatic stress disorder (PTSD) and Vietnam combat veterans without PTSD. METHOD: Vietnam combat veterans who sought treatment for PTSD (N = 53) were compared to Vietnam combat veterans without PTSD (N = 32) who sought treatment for medical problems. Dissociative symptoms were evaluated with the Dissociative Experiences Scale. Dissociation at the time of a combat-related traumatic event was evaluated retrospectively with the modified Dissociative Experiences Questionnaire. The Combat Exposure Scale was used to measure level of combat exposure. RESULTS: There was a significantly higher level of dissociative symptoms, as measured by the Dissociative Experiences Scale, in patients with PTSD (mean = 27.0, SD = 18.0) than in patients without PTSD (mean = 13.7, SD = 16.0). This difference persisted when the difference in level of combat exposure was controlled with analysis of covariance. PTSD patients also reported more dissociative symptoms at the time of combat trauma, as measured retrospectively by the Dissociative Experiences Questionnaire (mean = 11.5, SD = 1.6) than non-PTSD patients (mean = 1.8, SD = 2.1). CONCLUSIONS: Dissociative symptoms are an important element of the long-term psychopathological response to trauma.     

SLC6A4 methylation modifies the effect of the number of traumatic events on risk for posttraumatic stress disorder

Background: Posttraumatic stress disorder (PTSD) is a common and debilitating mental disorder that occurs following exposure to a traumatic event. However, most individuals do not develop PTSD following even a severe trauma, leading to a search for new variables, such as genetic and other molecular variation, associated with vulnerability and resilience in the face of trauma exposure. Method: We examined whether serotonin transporter (SLC6A4) promoter genotype and methylation status modified the association between number of traumatic events experienced and PTSD in a subset of 100 individuals from the Detroit Neighborhood Health Study. Results: Number of traumatic events was strongly associated with risk of PTSD. Neither SLC6A4 genotype nor methylation status was associated with PTSD in main effects models. However, SLC6A4 methylation levels modified the effect of the number of traumatic events on PTSD after controlling for SLC6A4 genotype. Persons with more traumatic events were at increased risk for PTSD, but only at lower methylation levels. At higher methylation levels, individuals with more traumatic events were protected from this disorder. This interaction was observed whether the outcome was PTSD diagnosis, symptom severity, or number of symptoms. Conclusions: Gene‐specific methylation patterns may offer potential molecular signatures of increased risk for and resilience to PTSD. Depression and Anxiety, 2011. © 2011 Wiley‐Liss, Inc.     

Immediate treatment with propranolol decreases posttraumatic stress disorder two months after trauma.

BACKGROUND: This study investigated the efficacy of propranolol prescribed shortly after trauma exposure in the prevention of posttraumatic stress disorder (PTSD) symptoms and diagnosis. METHODS: Eleven patients received 40 mg of propranolol 3 times daily for 7 days, followed by a taper period of 8-12 days. They were compared with eight patients who refused propranolol but agreed to participate in the study. Though nonrandomized, the two groups did not differ on demographics, exposure characteristics, physical injury severity, or peritraumatic emotional responses. RESULTS: Posttraumatic stress disorder rates were higher in the group who refused propranolol (3/8) compared with those who received the medication (1/11), as were the levels of PTSD symptoms (U = 85, p =.037). CONCLUSIONS: Our results are consistent with earlier findings and suggest that propranolol may be useful for mitigating PTSD symptoms or perhaps even preventing the development of PTSD.     

Enhanced cortisol suppression in response to dexamethasone administration in traumatized veterans with and without posttraumatic stress disorder

BACKGROUND: While enhanced cortisol suppression in response to dexamethasone is one of the most consistent biological findings in posttraumatic stress disorder (PTSD), the relative contribution of trauma exposure to this finding remains unclear. METHODS: Assessment of diurnal salivary cortisol levels and 1600 h salivary cortisol before and after oral administration of 0.5mg dexamethasone in veterans with PTSD, veterans without PTSD (trauma controls) and healthy controls. Assessment of 1600 h plasma cortisol, ACTH and corticotrophin binding globulin (CBG) in response to dexamethasone in PTSD patients and trauma controls. RESULTS: Both PTSD patients and trauma controls demonstrated significantly more salivary cortisol suppression compared to healthy controls. Salivary cortisol, plasma cortisol and ACTH suppression as well as CBG levels did not differ between PTSD patients and trauma controls. PTSD patients showed a reduced awakening cortisol response (ACR) compared to healthy controls that correlated significantly with PTSD symptoms. No significant differences were observed in ACR between PTSD patients and trauma controls. CONCLUSIONS: These data suggest that enhanced cortisol suppression to dexamethasone is related to trauma exposure and not specifically to PTSD. The correlation between the ACR and PTSD severity suggests that a flattened ACR may be a result of clinical symptoms.     

Vagal modulation of responses to mental challenge in posttraumatic stress disorder.

BACKGROUND: Studies of the autonomic nervous system in posttraumatic stress syndrome (PTSD) have focused on the sympathetic modulation of arousal and have neglected the parasympathetic contribution. This study addresses the parasympathetic control of heart rate in individuals who have survived traumatic events. METHODS: Twenty-nine survivors, 14 with current PTSD and 15 without, participated in the study. The groups were comparable with regard to age, type of trauma, time since the latest traumatic event, and lifetime exposure to traumatic events. Electrocardiograms were recorded during rest and an arithmetic task. Heart period, respiratory sinus arrhythmia (RSA), and the amplitude of the Traube-Hering-Mayer wave were quantified. RESULTS: The groups did not differ on resting measures. During the arithmetic task, the past trauma group showed a significant increase in RSA (p <.007), whereas the PTSD group did not. In the past trauma group only, RSA and heart period were highly correlated (r =.75), thereby suggesting that the response to challenge was under vagal control. CONCLUSIONS: Trauma survivors who develop PTSD differ from those who do not in the extent to which their heart rate response to challenge is controlled by vagal activity. Responses to challenge in PTSD may be mediated by nonvagal, possibly sympathetic mechanisms.     

Posttraumatic stress disorder and depression following trauma: understanding comorbidity

OBJECTIVE: Posttraumatic stress disorder (PTSD) and major depression occur frequently following traumatic exposure, both as separate disorders and concurrently. This raises the question of whether PTSD and depression are separate disorders in the aftermath of trauma or part of a single general traumatic stress construct. This study aimed to explore the relationships among PTSD, depression, and comorbid PTSD/depression following traumatic injury. METHOD: A group of 363 injury survivors was assessed just prior to discharge from hospital and 3 and 12 months postinjury. Canonical correlations were used to examine the relationship between PTSD and depression symptom severity and a set of predictor variables. Multinomial logistic regression was used to identify whether the diagnostic categories of PTSD, depression, and comorbid PTSD/depression were associated with different groups of predictors. RESULTS: The majority of psychopathology in the aftermath of trauma was best conceptualized as a general traumatic stress factor, suggesting that when PTSD and depression occur together, they reflect a shared vulnerability with similar predictive variables. However, there was also evidence that in a minority of cases at 3 months, depression occurs independently from PTSD and was predicted by a different combination of variables. CONCLUSIONS: While PTSD and comorbid PTSD/depression are indistinguishable, the findings support the existence of depression as a separate construct in the acute, but not the chronic, aftermath of trauma.