Subsequent Development Of Posttraumatic Stress Disorder Research Articles

Compassion buffers the association between trauma exposure and PTSD symptom severity: Findings of a cross-sectional study

To advance intervention science dedicated to improve refugees’ mental health, a better understanding of factors of risk and resilience involved in the etiology and maintenance of post-traumatic stress disorder (PTSD) is needed. In the present study, we tested whether empathy and compassion, two trainable aspects of social cognition related to health, would modulate risk for PTSD after war-related trauma. Fifty-six refugees and 42 migrants from Arabic-speaking countries reported on their trauma experiences, PTSD symptoms, and perceived trait empathy and compassion. They further completed the EmpaToM, a naturalistic computer task measuring behavioral empathy and compassion. Moderation analyses revealed that behavioral, but not self-reported compassion was a significant moderator of the trauma-PTSD link. Trauma was more strongly related to PTSD symptoms when individuals had low (β =.59, t = 4.27, p <.001) as compared to high levels of behavioral compassion. Neither self-reported nor behavioral empathy moderated the trauma-PTSD link (β =.24, t = 1.57, p =.120). Findings indicate that the ability to go beyond the sharing of others’ suffering and generate the positive feeling of compassion may support resilience in the context of trauma and subsequent development of PTSD. Hence, compassion may be a suitable target for prevention and intervention approaches reducing PTSD symptoms after trauma.

Promoter methylation of the glucocorticoid receptor following trauma may be associated with subsequent development of PTSD

Objectives The ability to identify persons at elevated risk for post-traumatic stress disorder (PTSD) soon after exposure to trauma, could aid clinical decision-making and treatment. In this study, we explored whether cytosine methylation of the 1 F promoter of the NR3C1 (glucocorticoid receptor [GR]) gene obtained immediately following a trauma could predict PTSD. Methods Our sample comprised 52 trauma survivors (28 women, 24 men), presenting to the Emergency Department (ED) within six hours of a traumatic event and followed for 13 months. Blood samples were taken at intake (n = 42) and again at the end of the study (13 months later, n = 27) to determine NR3C1-1F promoter methylation as well as plasma levels of cortisol, adrenocorticotropic-hormone (ACTH), and neuropeptide-Y (NPY). Results At the 13-month follow-up, participants who met the PTSD criteria (n = 4) showed significantly lower NR3C1-1F promoter sum percent methylation compared to the non-PTSD group (n = 38). Further, NR3C1-1F methylation at ED intake was inversely correlated with PTSD severity 13 months later, indicating that lower NR3C1-1F promoter methylation in the immediate aftermath of trauma was associated with the development of PTSD. Conclusion To the extent that reduced promoter methylation is associated with greater GR expression and responsivity, this finding is consistent with the hypothalamic-pituitary-adrenal dysregulation previously described for PTSD.

The impact of sleep quality on the incidence of PTSD: Results from a 7-Year, Nationally Representative, Prospective Cohort of U.S. Military Veterans

Sleep and posttraumatic stress disorder (PTSD) have a complex relationship, with some studies showing that disrupted sleep is associated with subsequent development of PTSD. The purpose of the current study was to examine the relationship between sleep quality and the development of probable PTSD in U.S. veterans surveyed as part of the National Health and Resilience in Veterans Study, a 7-year, nationally representative, prospective cohort study with four waves of data collection. Sociodemographic, military, trauma, and clinical variables were entered into a multivariate analysis to examine independent determinants of new-onset PTSD. A total of 142 (7.3 %) veterans developed PTSD over the 7-year study period. Poor/fair sleep quality at Wave 1 was associated with 60 % greater likelihood of developing PTSD, with more than twice as many veterans who developed PTSD reporting poor sleep quality at Wave 1 (47.8 % vs. 20.7 %). Younger age, using the VA as a primary source of healthcare, greater traumas since Wave, and lifetime depression were additionally associated with this outcome. Results of this study underscore the importance of self-reported sleep quality as a potential risk factor for the development of PTSD in the U.S. veteran population.

Longitudinal mental health outcomes of combat-injured service members.

BackgroundThe relationship between traumatic injury and subsequent mental health diagnoses is not well understood and may have significant implications for patient screening and clinical intervention. We sought to determine the adjusted association between traumatic injury and the subsequent development of post‐traumatic stress disorder (PTSD), depression, and anxiety.MethodsUsing Department of Defense and Veterans Affairs datasets between February 2002 and June 2016, we conducted a retrospective cohort study of 7,787 combat‐injured United States service members matched 1:1 to combat‐deployed, uninjured service members. The primary exposure was combat injury versus no combat injury. Outcomes were diagnoses of PTSD, depression, and anxiety, defined by International Classification of Diseases 9th and 10th Revision Clinical Modification codes.ResultsCompared to noninjured service members, injured service members had higher observed incidence rates per 100 person‐years for PTSD (17.1 vs. 5.8), depression (10.4 vs. 5.7), and anxiety (9.1 vs. 4.9). After adjustment, combat‐injured patients were at increased risk of development of PTSD (HR 2.92, 95%CI 2.68–3.17), depression (HR 1.47, 95%CI 1.36–1.58), and anxiety (HR 1.34, 95%CI 1.24–1.45).ConclusionsTraumatic injury is associated with subsequent development of PTSD, depression, and anxiety. These findings highlight the importance of increased screening, prevention, and intervention in patients with exposure to physical trauma.

A double-hit of stress and low-grade inflammation on functional brain network mediates posttraumatic stress symptoms

Growing evidence indicates a reciprocal relationship between low-grade systemic inflammation and stress exposure towards increased vulnerability to neuropsychiatric disorders, including posttraumatic stress disorder (PTSD). However, the neural correlates of this reciprocity and their influence on the subsequent development of PTSD are largely unknown. Here we investigated alterations in functional connectivity among brain networks related to low-grade inflammation and stress exposure using two large independent data sets. Functional couplings among the higher-order cognitive network system including the salience, default mode, and central executive networks were reduced in association with low-grade inflammation and stress exposure. This reduced functional coupling may also be related to subsequent posttraumatic stress symptom severity. The current findings propose functional couplings among the higher-order cognitive network system as neural correlates of low-grade inflammation and stress exposure, and suggest that low-grade inflammation, alongside with stress, may render individuals more vulnerable to PTSD.

Alcohol Use Disorder and Posttraumatic Stress Disorder: An Introduction.

Alcohol use disorder (AUD) and posttraumatic stress disorder (PTSD) are two of the most common, chronic and debilitating mental health disorders in our society. Epidemiologic data indicate that lifetime rates of AUD and PTSD in the general population are 29.1% and 7.8%, respectively (Grant et al., 2015; Kessler et al., 1995). These two disorders frequently co-occur and are associated with substantial suffering and functional impairment. This paper introduces a virtual issue of Alcoholism: Clinical and Experimental Research (ACER) which is focused on the co- occurrence of AUD and PTSD. This introduction is not a comprehensive review of the topic, but rather a focused review of recent papers published in ACER that address treatments for comorbid AUD and PTSD, and discuss special populations at increased risk of developing AUD and PTSD. To begin, two systematic reviews discuss the current state of behavioral (Simpson et al., 2017) and pharmacological (Petrakis & Simpson, 2017) treatments for comorbid AUD/PTSD. The Simpson et al. (2017) article extends prior reviews of behavioral treatments for AUD/PTSD by considering whether comparison treatment conditions are matched to the experimental treatment condition on time and attention, and by reporting on alcohol and drug use outcomes separately when possible. The Petrakis and Simpson (2017) review of pharmacological treatments is specific to the comorbidity of PTSD and AUD, as compared to other substance use disorders, and it includes several more recently published randomized controlled trials that are not included in prior reviews on this topic. In the next section, two studies focus on the prevalence and correlates of AUD and PTSD in racial and ethnic minority communities. Werner and colleagues (2016) report on the increased rates of trauma exposure and PTSD among African American (AA) women as compared to European American (EA) women, and examine differences in the relationship between PTSD and AUD among AA and EA women. This study extends prior work by examining the unique contributions of specific types of trauma and PTSD on alcohol involvement in AA and EA women, and identifying racial/ethnic disparities in the prevalence and timing of first alcohol use, AUD symptoms and AUD diagnostic progression. The Emerson et al. (2017) study is the first to examine the association between AUD and PTSD in American Indian and Alaskan Natives (AIAN) as compared to non-Hispanic Whites. High rates of PTSD among AIAN women and high rates of comorbid AUD/PTSD among AIAN men, in particular, are highlighted and discussed in terms of the need for targeted screening and intervention among AIAN communities. Finally, two studies in this virtual issue focus on military personnel and veterans. The first study by Stein and colleagues (2017) reports on alcohol misuse and AUD prior to enlistment in the Army, and highlights the strong association between prior AUD and subsequent development of PTSD among newly enlisted soldiers. The second study is a laboratory study (Ralevski et al., 2016) among military veterans with AUD and PTSD. It is among the first studies to examine the effects of trauma cues and stress (non-trauma) cues on alcohol craving, mood, physiological and neuroendocrine responses, and demonstrates the powerful effects of trauma cues on alcohol craving and consumption. Together, the six papers included in this virtual issue raise important considerations for future research and may help to inform best practices in the treatment of comorbid AUD and PTSD.

A longitudinal examination of peritraumatic emotional responses and their association with posttraumatic stress disorder and major depressive disorder among veterans

ABSTRACTResearch has revealed a significant association between several peritraumatic emotional responses and posttraumatic stress disorder (PTSD). Preliminary research has also linked peritraumatic emotional responses with a diagnosis of major depressive disorder (MDD). The majority of this research has been cross-sectional, thereby making it difficult to determine the extent to which the various peritraumatic emotional responses may increase risk for, or serve as a premorbid marker of, PTSD and MDD. This study examined the longitudinal role of peritraumatic emotional responses on the subsequent development of PTSD and MDD in a sample of US military veterans. Whereas a number of peritraumatic emotional responses were concurrently associated with PTSD, only peritraumatic numbness maintained the association with this diagnosis longitudinally. For MDD, peritraumatic numbness was the only emotional response related to the diagnosis both concurrently and longitudinally. Study findings are a preliminary proof of concept that peritraumatic numbness may serve as a premorbid marker for the development of PTSD and MDD following a traumatic event. Implications of these findings for the diagnosis, assessment, and treatment of both PTSD and MDD are discussed.

Awake/sleep cortisol levels and the development of posttraumatic stress disorder in injury patients with peritraumatic dissociation.

Differences in the time of day that cortisol is sampled and failure to consider the impact of peritraumatic dissociation have been hypothesized as factors possibly contributing to the inconsistent findings in research examining associations between cortisol levels soon after trauma exposure and the subsequent development of posttraumatic stress disorder (PTSD). The present study examined associations between urinary cortisol levels during wake and sleep times soon after a serious injury and the subsequent development of PTSD in adult patients reporting low or high peritraumatic dissociative (PD) symptoms. Thirty-nine injury patients (20 with high and 19 with low PD symptoms) provided a 15-hour (6 PM to 9 AM) urine sample at 3-weeks post-injury and completed the Clinician Administered PTSD Scale at a 7-week follow-up. Participants collected their urine during wake and sleep times separately. Results showed that in the total sample and in the high PD group, wake, but not sleep, cortisol levels were lower in patients who developed PTSD compared to those who did not. A multiple linear regression analysis revealed a significant main effect of PD and a non-significant interaction between wake cortisol and PD in predicting PTSD symptom severity. In addition, results showed that PD was a better predictor of PTSD symptom severity than wake cortisol levels. These results were consistent with prior research indicating lower afternoon/evening cortisol levels in PTSD and strong associations between PD and PTSD, but did not support the existence of subgroups of PTSD patients (dissociators versus non-dissociators) who may differ in basal cortisol levels.

The importance of the peritraumatic experience in defining traumatic stress.

In the Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev., DSM-IV-TR; American Psychiatric Association, 2000), posttraumatic stress disorder (PTSD) Criterion A2 stipulates that an individual must experience intense fear, helplessness, or horror during an event that threatened the life or physical integrity of oneself or others to be eligible for the PTSD diagnosis. In considering this criterion, we describe its origins, review studies that have examined its predictive validity, and reflect on the intended purpose of the criterion and how it complements the mission of the DSM. We then assert that the predictive validity of Criterion A2 may not be an appropriate metric for evaluating its worth. We also note that the current Criterion A2 may not fully capture all the salient aspects of the traumatic stress response. To support this claim, we review empirical research showing that individuals adapt to extreme environmental events by responding in a complex and coordinated manner. This complex response set involves an individual's appraisal regarding the degree to which the event taxes his or her resources, as well as a range of other cognitions (e.g., dissociation), felt emotions (e.g., fear), physiological reactions (e.g., heart rate increase), and behaviors (e.g., tonic immobility). We provide evidence that these response components may be associated with the subsequent development of PTSD. We then describe the challenges associated with accurately assessing an individual's traumatic stress response. We conclude with a discussion of the need to consider the individual's immediate response when defining a traumatic stressor.

Putative biological mechanisms for the association between early life adversity and the subsequent development of PTSD

Early Life Stress (ELS) increases risk for both adult traumatization and posttraumatic stress disorder (PTSD). Adult PTSD may also reflect a continuation of a response to an earlier exposure to adversity. Given similarities between neuroendocrine aspects of PTSD and ELS, such as in reduced cortisol signaling and glucocorticoid receptor (GR) responsiveness, some aspects of the biology of PTSD may reflect biological correlates of risk. This paper will examine how empirical findings regarding the biological basis of ELS can inform our understanding of the neuroendocrinology of PTSD. This paper will also propose a hypothetical model to guide future research that integrates genetic, epigenetic, neuroendocrine, and psychological observations to understand the contribution of ELS neurobiology to PTSD. Recent genetic findings demonstrate heritable aspects of at least some of these cortisol-related disturbances. Furthermore, ELS may produce at least some of the PTSD-associated changes in glucocorticoid responsiveness through epigenetic mechanisms such as developmental programming. These, then, may contribute to enduring changes in stress responsiveness as well as enhanced risk for adult exposure and PTSD. Molecular mechanisms associated with gene x environment interactions or GR programming are essential in explaining current observations in the neuroendocrinology of PTSD that have been difficult to understand through the lens of contemporary stress theory.

Cognitive difficulties and posttraumatic stress disorder in female victims of intimate partner violence.

Subjective cognitive complaints of women exposed to intimate partner violence (IPV) and nonabused women were examined using the Cognitive Difficulties Scale (CDS). Cognitive complaints were compared among victims of IPV with a lifetime diagnosis of posttraumatic stress disorder (PTSD) (PTSD+; n=20), victims of IPV without lifetime PTSD (PTSD-; n=21), and a nonabused comparison group (n=22). The results indicated that both the PTSD+ and PTSD- groups had significantly higher levels of self-perceived cognitive difficulties than nonabused women. Furthermore, PTSD symptom severity was found to be positively correlated with self-perceived cognitive difficulties (r=.47). Further research is needed to determine whether cognitive complaints are associated with exposure to IPV, with the subsequent development of PTSD, or with other not yet understood factors. Furthermore, additional work is needed to resolve whether cognitive complaints are accompanied by objective evidence of cognitive dysfunction in victims of IPV.

Posttraumatic stress disorder: a sensitization reaction.

This article discusses past research bearing on the question of the etiology of Posttraumatic Stress Disorder (PTSD). It argues that PTSD can be adequately accounted for by a process of emotional sensitization and that this is a more parsimonious explanation than the two-factor learning theory of Mowrer, now postulated by several writers. In brief, the etiology and subsequent development of PTSD is viewed as the result of the sensitization of fear/anxiety which is linked to a variety of to be conditional stimuli by both backward and forward association: these become conditional stimuli (CSi) once paired with the instigating circumstances. It is furthermore assumed that PTSD will not occur in the absence of a genetic susceptibility that may vary from zero to absolute certainty. Thus far, our evidence is limited to a sensitivity to loud sounds, but it is highly probable that touch and other sensory systems are involved (not necessarily in parallel). The fact that abuse often leads to behavioral disorders, including sexually seductive behaviors in children sexually abused, requires a recognition that emotional reactions other than fear may be sensitized. Fear in combination with pleasure or pleasure alone coupled with a loss of self-esteem may explain these acting-out behaviors.