Core Feature Of Posttraumatic Stress Disorder Research Articles

Pre-trauma memory contextualization as predictor for PTSD-like behavior in male rats

While many people experience potentially threatening events during their life, only a minority develops posttraumatic stress disorder (PTSD). The identification of individuals at risk among those exposed to trauma is crucial for PTSD prevention in the future. Since re-experiencing trauma elements outside of the original trauma-context is a core feature of PTSD, we investigate if the ability to bind memories to their original encoding context (i.e. memory contextualization) predicts PTSD vulnerability. We hypothesize that pre-trauma neutral memory contextualization (under stress) negatively relates to PTSD-like behavior, in a prospective design using the cut-off behavioral criteria rat model for PTSD. 72 male Sprague Dawley rats were divided in two experimental groups to assess the predictive value of 1) memory contextualization without acute stress (NS-group) and 2) memory contextualization during the recovery phase of the acute stress-response (S-group) for susceptibility to PTSD-like behavior. A powerful extension to regression analysis -path analysis-was used to test this specific hypothesis, together with secondary research questions. Following traumatic predator scent stress, 19.4% of the rats displayed PTSD-like behavior. Results showed a negative relation between pre-trauma memory contextualization and PTSD-like behavior, but only in the NS-group. Pre-trauma memory contextualization was positively related to fear association in the trauma environment, again only in the NS group. If the predictive value of pre-trauma contextualization of neutral information under non-stressful conditions for PTSD susceptibility is replicated in prospective studies in humans, this factor would supplement already known vulnerability factors for PTSD and improve the identification of individuals at risk among the trauma exposed, especially those at high trauma risk such as soldiers deployed on a mission.

Shame as a Mediator in the Association Between Emotion Dysregulation and Posttraumatic Stress Disorder Symptom Reductions Among Combat Veterans in a Residential Treatment Program.

Emotion dysregulation (ED) can be defined as one's inability to effectively respond to and manage internal experiences and the expression of emotion. ED has been linked to the development and maintenance of posttraumatic stress disorder (PTSD), with recent research suggesting that reductions in ED may predict improved treatment outcomes among both civilian and veteran populations. However, few studies have examined how changes in ED may predict treatment outcomes among veterans with PTSD and whether certain core features of PTSD, such as shame, may act as potential mediators in the association between ED and PTSD symptom reductions. The present study sought to explore facets of ED, feelings of shame, and PTSD symptoms among 43 combat veterans upon their admission and discharge to a residential PTSD program. The results demonstrated that all variables of interest significantly decreased from admission to discharge, ds = 0.75-1.84. Correlations indicated that reductions in ED, R2 = .184, and shame, R2 = .228, were associated with reductions in PTSD symptoms. However, the association between reductions in ED and PTSD was significantly mediated by reductions in shame. Overall, these results suggest that higher levels of emotion regulation may partially affect PTSD symptoms through reductions in shame. This may explain the efficacy of frontline PTSD treatments, as they explicitly focus on the processing of one's traumatic experience by reducing PTSD symptoms through regulation techniques that target emotional-behavioral cycles, which may include the shame-withdraw cycle.

High prevalence of somatisation in ICD-11 complex PTSD: A cross sectional cohort study

BackgroundWhile research demonstrates that somatisation is highly correlated with post-traumatic stress disorder (PTSD), the relationship between International Classification of Diseases 11th edition (ICD-11) PTSD, complex PTSD (CPTSD) and somatisation has not previously been determined. ObjectiveTo determine the relationship between frequency and severity of somatisation and ICD-11 PTSD/CPTSD. MethodThis cross-sectional study included 222 individuals recruited to the National Centre for Mental Health (NCMH) PTSD cohort. We assessed rates of Patient Health Questionnaire 15 (PHQ-15) somatisation stratified by ICD-11 PTSD/CPTSD status. Path analysis was used to explore the relationship between PTSD/CPTSD and somatisation, including number of traumatic events, age, and gender as controls. Results70% (58/83) of individuals with CPTSD had high PHQ-15 somatisation symptom severity compared with 48% (12/25) of those with PTSD (chi-square: 95.1, p value <0.001). Path analysis demonstrated that core PTSD symptoms and not disturbances in self organisation (DSO) symptoms were associated with somatisation (unstandardised coefficients: 0.616 (p-value 0.017) and − 0.012 (p-value 0.962) respectively. ConclusionsIndividuals with CPTSD have higher somatisation than those with PTSD. The core features of PTSD, not the DSO, characteristic of CPTSD, were associated with somatisation.

DSM-5 posttraumatic stress disorder: Factor structure and rates of diagnosis

Posttraumatic stress disorder (PTSD) is a significant problem among Iraq/Afghanistan-era veterans. To date, however, there has been only limited research on how the recent changes in DSM-5 influence the prevalence and factor structure of PTSD. To address this key issue, the present research used a modified version of a gold-standard clinical interview to assess PTSD among a large sample of Iraq/Afghanistan-era veterans (N = 414). Thirty-seven percent of the sample met DSM-5 criteria for PTSD compared to a rate of 38% when DSM-IV diagnostic criteria were used. Differences in rates of diagnosis between DSM-IV and DSM-5 were primarily attributable to changes to Criterion A and the separation of the “avoidance” and “numbing” symptoms into separate clusters. Confirmatory factor analysis (CFA) was used to compare the fit of the previous 3-factor DSM-IV model of PTSD to the 4-factor model specified in DSM-5, a 4-factor “dysphoria” model, and a 5-factor model. CFA demonstrated that the 5-factor model (re-experiencing, active avoidance, emotional numbing, dysphoric arousal, anxious arousal) provided the best overall fit to the data, although substantial support was also found for the 4-factor DSM-5 model. Low factor loadings were noted for two of the symptoms in the DSM-5 model (psychogenic amnesia and reckless/self-destructive behavior), raising questions regarding the adequacy of fit between these symptoms and the other core features of PTSD. Overall, findings suggest the DSM-5 model of PTSD is an improvement over the previous DSM-IV model of PTSD, but still may not represent the true underlying factor structure of PTSD.

Following the development of ICD-11 through World Psychiatry (and other sources).

Following the development of ICD-11 through World Psychiatry (and other sources).

Sleeping Patterns of Afghan Unaccompanied Asylum-Seeking Adolescents: A Large Observational Study

Unaccompanied asylum-seeking children (UASC) have experienced multiple traumas and are a high-risk group for posttraumatic stress disorder (PTSD). The effects of trauma are known to be associated with sleep problems; indeed sleeping problems are core features of PTSD. However, there has been no systematic research examining the sleep of this high risk group of children. This study presents the first evidence on the sleeping patterns of Afghan UASC living in the UK. A total of 222 male Afghan children, aged 13–18, were interviewed using validated self-report questionnaires measuring sleeping patterns and PTSD. Overall, UASC patterns for bed time and rise time appear acculturated to the country of asylum. Mean UASC sleep onset latency scores were approximately 20 minutes greater compared with normative scores, which may be a reflection of UASC pre-migration and post-migration experiences. As expected, UASC who screened above the clinical cut-off for PTSD reported significantly greater sleep onset latency, increased nightmares, and less total sleep time compared to the non-PTSD group. The results may be of particular interest to clinicians given that, compared to screening for PTSD, screening for sleep problems may be a less culturally disputed form of initial assessment indicating distress in UASC. Similarly, the field of UASC and refugee child interventions is largely focused on trauma, yet sleep may provide a novel avenue for equally or more effective treatment.

Chronic idiopathic urticaria and post-traumatic stress disorder (PTSD): An under-recognized comorbidity

A large body of literature supports the role of psychologic stress in urticaria; however, the comorbidity between chronic idiopathic urticaria (CIU) and post-traumatic stress disorder (PTSD), a classic stress-mediated syndrome, has received little attention. The underlying etiology of urticaria is not identifiable in about 70% of patients, possibly because of difficulties with identification of a direct cause-and-effect relationship between a potential causative factor and the onset of urticaria. The core features of PTSD (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision [DSMIV-TR]) that are important in urticaria include (1) autonomic nervous system reactivity and state of sympathetic hyperarousal that can manifest as CIU, and (2) the persistent re-experiencing of the traumatic events in PTSD, which can manifest as urticaria or angioedema, or both, affecting a previously traumatized body region (eg, urticarial wheals affecting the body region where the patient had been stabbed years earlier). The following features of PTSD make it difficult to use the cause-and-effect model for the determination of causation: (1) PTSD may first emerge years after the initial trauma and is classified as PTSD with Delayed Onset (DSMIV-TR); and (2) the traumatic triggers that precipitate the PTSD symptoms may be unique and idiosyncratic to the patient and not even qualify as stressful or traumatic by standard criteria (eg, precipitating events for the PTSD may include smell of a certain cologne that was used by the perpetrator or witnessing a scene in a movie that was reminiscent of the location where the abuse occurred). Finally, in PTSD with Delayed Onset, patients may not make a conscious association between their recurrent urticaria and their earlier traumas because they can develop classically conditioned associations between stimuli that are reminiscent of the original abuse situation and their somatic reactions such as urticaria. The clinician needs to be aware of these factors, because satisfactory resolution of the CIU may not occur without treatment of the PTSD. If the clinician suspects underlying PTSD, it is best to refer the patient to a qualified mental health professional, because detailed history taking about traumatic experiences alone can have an acute destabilizing effect and heighten PTSD symptoms in some patients.

Predictors of susceptibility and resilience in an animal model of posttraumatic stress disorder.

Animal models of posttraumatic stress disorder (PTSD) are based on fear conditioning where innocuous cues elicit reactions that originally occur to traumatic events--a core feature of PTSD. Another core feature is hyperarousal--exaggerated reactions to stressful events. One limitation of animal models of PTSD is that group effects do not model the sporadic incidence of PTSD. We developed an animal model of PTSD in which rabbit nictitating membrane responses become exaggerated as a function of classical conditioning to a tone conditioned stimulus (CS) paired with a shock unconditioned stimulus (US). Exaggerated responses to the US are a form of hyperarousal termed conditioning-specific reflex modification (CRM) and occur in the absence of the CS. Inspecting data across several experiments, we determined 25% of our rabbits exhibit strong CRM despite all subjects having high levels of conditioning. To determine how prone rabbits were to CRM (susceptibility) or how resistant (resilience), we examined data from 135 rabbits analyzing for factors during CS-US pairings and during US prescreening that would predict CRM. We found the magnitude of CRM was correlated with the onset latency and area of conditioned responding during CS-US pairings and with the peak latency of a response during US pretesting. In an animal model of PTSD that more accurately reflects clinical prevalence, we can begin to predict susceptibility not only during responding to a stressful conditioning situation but also during a screening process before the stressful situation takes place. The results suggest relatively innocuous testing may help detect PTSD after trauma and screen for it before trauma occurs.

Will Reconsolidation Blockade Offer a Novel Treatment for Posttraumatic Stress Disorder?

OPINION article Front. Behav. Neurosci., 04 March 2011Sec. Learning and Memory https://doi.org/10.3389/fnbeh.2011.00011

Sleep-specific mechanisms underlying posttraumatic stress disorder: Integrative review and neurobiological hypotheses

Posttraumatic stress disorder (PTSD) is a prevalent disorder that is associated with poor clinical and health outcomes, and considerable health care utilization and costs. Recent estimates suggest that 5-20% of military personnel who serve in current conflicts in Iraq and Afghanistan meet diagnostic criteria for PTSD. Clinically, sleep disturbances are core features of PTSD that are often resistant to first-line treatments, independently contribute to poor daytime functioning, and often require sleep-focused treatments. Physiologically, these observations suggest that PTSD is partially mediated by sleep disruption and its neurobiological correlates that are not adequately addressed by first-line treatments. However, polysomnographic studies have provided limited insights into the neurobiological underpinnings of PTSD during sleep. There is an urgent need to apply state-of-the-science sleep measurement methods to bridge the apparent gap between the clinical significance of sleep disturbances in PTSD and the limited understanding of their neurobiological underpinnings. Here, we propose an integrative review of findings derived from neurobiological models of fear conditioning and fear extinction, PTSD, and sleep-wake regulation, suggesting that the amygdala and medial prefrontal cortex can directly contribute to sleep disturbances in PTSD. Testable hypotheses regarding the neurobiological underpinnings of PTSD across the sleep-wake cycle are offered.