Event centrality in trauma and PTSD: relations between event relevance and posttraumatic symptoms

The purpose of this study was to determine whether anterior limbic and paralimbic regions of the brain are differentially activated during the recollection and imagery of traumatic events in trauma-exposed individuals with and without posttraumatic stress disorder (PTSD). Positron emission tomography (PET) was used to measure normalized regional cerebral blood flow (CBF) in 16 women with histories of childhood sexual abuse: eight with current PTSD and eight without current PTSD. In separate script-driven imagery conditions, participants recalled and imagined traumatic and neutral autobiographical events. Psychophysiologic responses and subjective ratings of emotional state were measured for each condition. In the traumatic condition versus the neutral control conditions, both groups exhibited regional CBF increases in orbitofrontal cortex and anterior temporal poles; however, these increases were greater in the PTSD group than in the comparison group. The comparison group exhibited regional CBF increases in insular cortex and anterior cingulate gyrus; increases in anterior cingulate gyrus were greater in the comparison group than in the PTSD group. Regional CBF decreases in bilateral anterior frontal regions were greater in the PTSD group than in the comparison group, and only the PTSD group exhibited regional CBF decreases in left inferior frontal gyrus. The recollection and imagery of traumatic events versus neutral events was accompanied by regional CBF increases in anterior paralimbic regions of the brain in trauma-exposed individuals with and without PTSD. However, the PTSD group had greater increases in orbitofrontal cortex and anterior temporal pole, whereas the comparison group had greater increases in anterior cingulate gyrus.

This study examined the prevalence of lifetime traumatic events and current symptoms of posttraumatic stress disorder (PTSD) among treatment-seeking cocaine-dependent outpatients and compared patients with and without PTSD on current substance use, psychopathology, and sociodemographic characteristics. The subjects were 122 adult cocaine-dependent outpatients participating in a treatment outcome study of psychosocial therapy. In addition to standard self-report and interview measures of psychopathology and substance use, the subjects completed the Trauma History Questionnaire and the PTSD Checklist before entering treatment. These patients experienced a large number of lifetime traumatic events (mean = 5.7); men experienced more general disasters and crime-related traumas than women, and women experienced more physical and sexual abuse than men. According to self-report measures, 20.5% of the subjects currently met the DSM-III-R criteria for PTSD; the rate of PTSD was 30.2% among women and 15.2% among men. Patients with PTSD had significantly higher rates of co-occurring axis I and axis II disorders, interpersonal problems, medical problems, resistance to treatment, and psychopathology symptoms than patients without PTSD. Psychopathology symptoms represented the most consistent difference between the two groups and provided the best prediction of PTSD status in a logistic regression. However, the groups did not differ significantly in current substance use or sociodemographic characteristics. These findings underscore the value of screening substance abusers for PTSD, because it can identify a small but substantial number who might require additional treatment. Further studies of the relationship between PTSD and substance abuse appear warranted.

Posttraumatic stress disorder (PTSD) is one of the few psychiatric conditions in which a subjective decrease in emotional range serves as a diagnostic criterion. In order to investigate whether veterans with chronic PTSD also experienced objective limitations in emotional perception, the authors administered the Aprosodia Battery to a group of 11 veterans with chronic PTSD, nine subjects with right hemisphere damage, seven subjects with left hemisphere damage, and 12 comparison subjects. The patients with PTSD displayed significant deficiencies in the comprehension and discriminative components of affective speech, similar in severity and performance profile on the Aprosodia Battery to the individuals with focal right hemisphere damage due to ischemic infarction.

The authors aim to delineate cognitive dysfunction associated with posttraumatic stress disorder (PTSD) by evaluating a well-defined cohort of former World War II prisoners of war (POWs) with documented trauma and minimal comorbidities. The authors studied a cross-sectional assessment of neuropsychological performance in former POWs with PTSD, PTSD with other psychiatric comorbidities, and those with no PTSD or psychiatric diagnoses. Participants who developed PTSD had average IQ, while those who did not develop PTSD after similar traumatic experiences had higher IQs than average (approximately 116). Those with PTSD performed significantly less well in tests of selective frontal lobe functions and psychomotor speed. In addition, PTSD patients with co-occurring psychiatric conditions experienced impairment in recognition memory for faces. Higher IQ appears to protect individuals who undergo a traumatic experience from developing long-term PTSD, while cognitive dysfunctions appear to develop with or subsequent to PTSD. These distinctions were supported by the negative and positive correlations of these cognitive dysfunctions with quantitative markers of trauma, respectively. There is a suggestion that some cognitive decrements occur in PTSD patients only when they have comorbid psychiatric diagnoses.

Objective Post-traumatic stress disorder (PTSD) is a mental disorder that manifests after exposure to a stressful traumatic event, such as combat experience. Accumulated evidence indicates an important genetic influence in the development of PTSD. The serotonin transporter (5-HTT) gene has been identified as a candidate for PTSD and a polymorphism of the serotonin transporter-linked promoter region (5-HTTLPR) is associated with the disorder in the general population. However, whether it is associated with PTSD in active military service members has not been investigated. This study aimed to investigate the relationship between 5-HTTLPR and PTSD in service members. Methods Leucocyte genomic DNA was extracted from service members, including those with PTSD (n = 134) or without PTSD (n = 639). The 5-HTTLPR polymorphism was detected by means of 2 stages of TaqMan fluorescent PCR assay. PTSD symptoms and symptom severity were assessed using the PTSD Checklist (PCL), a 17-item, DSM-based, self-report questionnaire with well-established validity and reliability. PTSD was determined based on endorsement of DSM-IV criteria and a PCL total score ≥ 44. Results Significant differences in biallele distribution were observed between PTSD and controls (χ2 = 7.497, P = .024). The frequency of SS, SL, and LL genotypes in the PTSD group was 0.17, 0.56, and 0.27 respectively, compared to the frequencies of 0.27, 0.43, and 0.29 in non-PTSD controls. Carriers of the L allele had higher scores for reexperiencing and arousal symptoms on the PCL, compared to SS homozygote carriers (P < .05). The triallele genotypes showed no significant differences in distribution between the PTSD and control groups (P > .05) and no relationship with PTSD symptom severity. The interaction of triallelic genotypes of 5-HTTLPR and traumatic life events was associated with re-experiencing, avoidance, and arousal (P < .05 for all). Multiple regression analysis revealed significant correlations between both biallelic and triallelic genotypes of 5-HTTLPR, the interaction of the number of stressful lifetime events, and 5-HTTLPR genotypes with PCL total score (P < .001). Conclusion Our findings suggested that 5-HTT might play a minor role in PTSD, and the interaction between 5-HTTLPR and the environment had effects on PCL score, complementing and emphasizing 5-HTT for PTSD, especially in the military population.

Post-traumatic stress disorder (PTSD) is a heterogeneous mental health condition, characterized by diverse symptom profiles and biological underpinnings. A dissociative subtype of PTSD has been identified, though the potential risk factors and underlying neurobiology are yet to be understood. The current study comprised Canadian Armed Forces (CAF) members and Veterans with a history of deployment, and with diagnoses of non-dissociative (n = 31) and dissociative subtypes of PTSD (n = 19), in addition to non-deployed healthy controls (n = 14). Participants completed questionnaires assessing clinical symptoms and experiences of trauma, and provided saliva and blood samples for cortisol and inflammatory marker assessments. Individuals with dissociative PTSD displayed elevated PTSD and depression symptom severity, and greater reports of specific forms of childhood trauma compared to individuals with non-dissociative PTSD and controls. Morning cortisol was elevated in both PTSD groups compared to controls, however the PTSD groups did not differ from one another. Evening cortisol concentrations were elevated in both PTSD groups compared to controls, and in the dissociative PTSD subtype compared to the non-dissociative PTSD subtype when controlling for depression symptoms. PTSD diagnostic group moderated the relationship between awakening cortisol levels and PTSD symptom severity, such that the non-dissociative PTSD group displayed a negative correlation between awakening cortisol levels and PTSD symptom severity, while no significant relation was identified in the dissociative PTSD group. C-reactive protein (CRP) levels did not differ across diagnostic groups when accounting for body mass index (BMI). However, CRP positively correlated with depressive symptoms only among individuals with dissociative PTSD. Together, examining PTSD subtypes may help inform more effective and personalized treatment strategies in the future.

Toward the Predeployment Detection of Risk for PTSD

Event centrality, defined as the extent to which a traumatic event becomes a core component of a person's identity (Berntsen & Rubin, 2006), is both a correlate and predictor of posttraumatic stress disorder (PTSD) symptoms, over and above event severity. These findings suggest that decreasing the perceived centrality of a traumatic event to one's identity might result in decreases in PTSD symptom severity. To date, few studies have examined how centrality is affected by PTSD treatment. The present study tested the hypotheses that change in centrality would be associated with both change in PTSD symptom severity and discharge PTSD symptom severity in an exposure-based PTSD partial hospitalization program (N = 132; 86.0% White; 85.2% female; M age = 36 years). At discharge (i.e., after approximately 6 weeks of treatment), both PTSD symptoms and centrality had significantly decreased, ds = .70 and .98, respectively, with large effect sizes. Decreases in Centrality of Events Scale (CES) scores at posttreatment, baseline CES scores, and baseline PTSD Checklist for DSM-5 (PCL-5) scores were associated with change (i.e., decrease) in PCL-5 scores, p < .001, as well as with posttreatment PCL-5 scores, p < .001. Decreases in CES scores over time, baseline CES scores, and baseline PCL-5 scores explained 31% of the variance in PCL-5 change and 34% of the variance in posttreatment PCL-5 scores. The results indicate the potential importance of decreasing the centrality of a traumatic event in PTSD treatment and recovery.

Exposure-based therapy, an effective treatment for posttraumatic stress disorder (PTSD), relies on extinction learning principles. In PTSD patients, dysfunctional patterns in the neural circuitry underlying fear extinction have been observed using resting-state or functional activation measures. It remains undetermined whether resting activity predicts activations during extinction recall or PTSD symptom severity. Moreover, it remains unclear whether trauma exposure per se affects resting activity in this circuitry. The authors employed a multimodal approach to examine the relationships among resting metabolism, clinical symptoms, and activations during extinction recall. Three cohorts were recruited: PTSD patients (N=24), trauma-exposed individuals with no PTSD (TENP) (N=20), and trauma-unexposed healthy comparison subjects (N=21). Participants underwent a resting positron emission tomography scan 4 days before a functional MRI fear conditioning and extinction paradigm. Amygdala resting metabolism negatively correlated with clinical functioning (as measured by the Global Assessment of Functioning Scale) in the TENP group, and hippocampal resting metabolism negatively correlated with clinical functioning in the PTSD group. In the PTSD group, dorsal anterior cingulate cortex (dACC) resting metabolism positively correlated with PTSD symptom severity, and it predicted increased dACC activations but decreased hippocampal and ventromedial prefrontal cortex activations during extinction recall. The TENP group had lower amygdala resting metabolism compared with the PTSD and healthy comparison groups, and it exhibited lower hippocampus resting metabolism relative to the healthy comparison group. Resting metabolism in the fear circuitry correlated with functioning, PTSD symptoms, and extinction recall activations, further supporting the relevance of this network to the pathophysiology of PTSD. The study findings also highlight the fact that chronic dysfunction in the amygdala and hippocampus is demonstrable in PTSD and other trauma-exposed individuals, even without exposure to an evocative stimulus.

ABSTRACTObjectives: There is substantial evidence regarding the role of event centrality (EC) in posttraumatic stress disorder (PTSD) symptoms, but little research has examined the explanatory pathways linking EC with PTSD symptoms severity. The present study examined whether core beliefs (CB) mediates the relationship between EC and PTSD symptoms in internally displaced older adults.Method: Internally displaced older adults (N = 279; mean age = 62 years) sheltered in two camps located in north-central Nigeria, completed Tiv language versions of self-report measures, namely, the Harvard Trauma Questionnaire, the Centrality of Event Scale, Core Beliefs Inventory, and provided relevant demographic information.Results: Analysis indicated that EC and CB were linked to greater PTSD symptoms as well as re-experiencing/intrusion, avoidance and hyperarousal symptoms severity. The mediator path was significant which implies that CB was a pathway through which EC influences PTSD symptoms clusters and overall PTSD symptomatology.Conclusion: A traumatic event becoming more central in a person's identity and life story distorts entrenched beliefs about oneself, others and the world, thereby resulting in greater PTSD symptoms. Our findings suggest that considerations of disrupted world assumptions may be a salient target for prevention and treatment efforts.

Serum brain-derived neurotrophic factor remains elevated after long term follow-up of combat veterans with chronic post-traumatic stress disorder

Sustained Elevation of Serum Interleukin-6 and Relative Insensitivity to Hydrocortisone Differentiates Posttraumatic Stress Disorder with and Without Depression

Research suggests autistic people experience greater post-traumatic stress disorder symptom severity than non-autistic people following traumatic events. Post-trauma appraisals are fundamental in cognitive models of post-traumatic stress disorder, but have not been explored in autistic people. We aimed to explore whether we could replicate effects of heightened trauma exposure and post-traumatic stress disorder symptom severity in autistic adults, and examine how post-traumatic appraisals affect the association between autism and post-traumatic stress disorder symptom severity. Two hundred forty-two autistic (n = 148) and non-autistic adults (n = 94) completed a survey measuring trauma exposure, post-traumatic stress disorder symptom severity and post-trauma appraisals. Exposure to types of traumatic events did not differ significantly between the groups, but the autistic group endorsed more events that 'happened to me' directly. Post-traumatic stress disorder symptom severity and endorsement of negative post-traumatic appraisals were significantly higher in the autistic group, specifically alienation, shame and fear appraisals. These appraisals mediated the association between autism and post-traumatic stress disorder symptom severity. Therefore, as in the general population, greater endorsement of negative post-traumatic appraisals may be a risk factor for post-traumatic stress disorder symptom development in autistic adults, particularly appraisals of shame, fear and alienation. Longitudinal designs are required to confirm the direction of these effects and to elucidate factors underlying these negative appraisals in autistic people.Lay SummaryMany people experience intrusive memories and anxiety after a traumatic event. However, for some, these symptoms last longer and they might be diagnosed with post-traumatic stress disorder. Research suggests that autistic people might be more likely to develop post-traumatic stress disorder and experience more severe symptoms compared to non-autistic people after traumatic events. One factor that is important in post-traumatic stress disorder development is how people think about the trauma. These might be thoughts like 'It was my fault', 'I'm not safe', 'I'm disconnected from other people'. There has not been research into how autistic people think about traumatic events compared to non-autistic people, and this could be important for making post-traumatic stress disorder treatments more effective for them, as many of these focus on thoughts. In this study, we asked 148 autistic people and 94 non-autistic people in the United Kingdom to complete an online survey about their trauma history, post-traumatic stress disorder symptoms and thoughts about a traumatic event. We found that autistic people experienced more types of traumatic events directly (it happened to them), but they did not experience more types of traumatic events overall. Interestingly, both groups reported events like bullying or the death of a loved one as traumatic, but these events would not meet the official diagnostic criteria for post-traumatic stress disorder. As expected, autistic people reported worse post-traumatic stress disorder symptoms than non-autistic people and were more likely to meet the cut-off for post-traumatic stress disorder diagnosis. Autistic people also reported more negative thoughts about the trauma, especially feeling unsafe, disconnected, ashamed or that the trauma was their fault. Having more thoughts like this was associated with being autistic and experiencing more severe post-traumatic stress disorder symptoms. Our findings suggest that therapies focusing on these negative thoughts could be helpful for autistic people with post-traumatic stress disorder. Future research should explore why autistic people have more of these thoughts after traumatic events and should use longitudinal or experimental designs to explore how these factors influence one another over time. Efforts to prevent negative experiences, challenge negative attitudes in society towards autism and support positive autistic identity and well-being will be helpful for changing this in the future. It is also important that mental health services offer support for post-traumatic stress disorder even when events do not meet the current diagnostic criteria, as this might prevent autistic and non-autistic people who need support with post-traumatic stress disorder getting help.

Objectives: The present study examined the impact of cumulative trauma exposure on current posttraumatic stress disorder (PTSD) symptom severity in a nonclinical sample of adults in their 60s. The predictive utility of cumulative trauma exposure was compared to other known predictors of PTSD, including trauma severity, personality traits, social support, and event centrality.Method: Community-dwelling adults (n = 2515) from the crest of the Baby Boom generation completed the Traumatic Life Events Questionnaire, the PTSD Checklist, the NEO Personality Inventory, the Centrality of Event Scale, and rated their current social support.Results: Cumulative trauma exposure predicted greater PTSD symptom severity in hierarchical regression analyses consistent with a dose–response model. Neuroticism and event centrality also emerged as robust predictors of PTSD symptom severity. In contrast, the severity of individuals’ single most distressing life event, as measured by self-report ratings of the A1 PTSD diagnostic criterion, did not add explanatory variance to the model. Analyses concerning event categories revealed that cumulative exposure to childhood violence and adulthood physical assaults were most strongly associated with PTSD symptom severity in older adulthood. Moreover, cumulative self-oriented events accounted for a larger percentage of variance in symptom severity compared to events directed at others.Conclusion: Our findings suggest that the cumulative impact of exposure to traumatic events throughout the life course contributes significantly to posttraumatic stress in older adulthood above and beyond other known predictors of PTSD.

Evidence from animal and human studies suggests glutamatergic dysfunction in posttraumatic stress disorder (PTSD). The purpose of this study was to investigate glutamate abnormalities in the dorsolateral prefrontal cortex (DLFPC) of individuals with PTSD using 7T MRS, which has better spectral resolution and signal-to-noise ratio than lower field strengths, thus allowing for better spectral quality and higher sensitivity. We hypothesized that individuals with PTSD would have lower glutamate levels compared to trauma-exposed individuals without PTSD and individuals without trauma exposure. Additionally, we explored potential alterations in other neurometabolites and the relationship between glutamate and psychiatric symptoms. Individuals with PTSD (n=27), trauma-exposed individuals without PTSD (n=27), and individuals without trauma exposure (n=26) underwent 7T MRS to measure glutamate and other neurometabolites in the left DLPFC. The severities of PTSD, depression, anxiety, and dissociation symptoms were assessed. We found that glutamate was lower in the PTSD and trauma-exposed groups compared to the group without trauma exposure. Furthermore, N-acetylaspartate (NAA) was lower and lactate was higher in the PTSD group compared to the group without trauma exposure. Glutamate was negatively correlated with depression symptom severity in the PTSD group. Glutamate was not correlated with PTSD symptom severity. In this first 7T MRS study of PTSD, we observed altered concentrations of glutamate, NAA, and lactate. Our findings provide evidence for multiple possible pathological processes in individuals with PTSD. High-field MRS offers insight into the neurometabolic alterations associated with PTSD and is a powerful tool to probe trauma- and stress-related neurotransmission and metabolism in vivo.