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Background Understanding cognitive and biological mechanisms of PTSD treatment can help refine treatments and increase rates of response. Methods Thirty‐six veterans with PTSD were randomly assigned to receive Prolonged exposure therapy (PE) or Present‐Centered therapy (PCT). We examined symptoms, trauma‐related cognitions, and two indices of HPA axis function (cortisol awakening response and cortisol response to a script‐driven imagery task). Results Thirty veterans started treatment and 26 completed. PE resulted in significantly more symptom reduction than PCT (P = .008). High treatment responders collapsed across treatments showed nominally higher cortisol levels measured at pretreatment 30 min after trauma script exposure compared to low responders (P = .08). At midtreatment, high treatment responders showed higher cortisol levels throughout the imagery task (Ps = .03–.04). There were no differences between high and low treatment responders at posttreatment. Thoughts of incompetence (F (1.6, 35.8) = 16.8, P = .000) and a dangerous world (F (1.3, 29.9) = 8.2, P = .004) significantly improved over time in high treatment responders but showed no change in low responders. Script‐associated cortisol response prior to treatment and reductions in thoughts of incompetence accounted for 83% of the variance in reductions in PTSD severity with PE. Conclusions Both increased cortisol response to personal trauma script prior to PTSD therapy and reductions in cognitive symptoms of PTSD were significantly and uniquely related to reductions in the core symptoms of PTSD in PE. However, contrary to our hypotheses, cortisol measures were not related to cognitive changes.

Steroid hormone dysregulations have frequently been implicated in posttraumatic stress disorder (PTSD) pathogenesis. However, the translation into naturalistic clinical settings as markers of symptomatology and treatment success remains complex. Particularly, there is little longitudinal data on steroid secretion over the course of interventions. This study examined the potential of long-term steroid hormone secretion assessed in hair as diagnostic and intervention-related biomarkers among medicated, multimorbid inpatients with PTSD. As part of a secondary analysis of a randomised controlled trial, 54 female inpatients with a primary diagnosis of PTSD received standardised treatment and provided hair samples at pre-treatment, post-treatment, and 3-month follow-up. Cortisol, cortisone, and dehydroepiandrosterone (DHEA) were determined, alongside clinical assessments. Cross-sectional results showed a negative association of pre-treatment DHEA with anxiety symptoms and a trend-level association with lifetime trauma exposure. While inpatients improved in PTSD symptomatology during treatment, neither pre-treatment steroids, nor treatment-induced steroid changes predicted PTSD symptoms at post-treatment or 3-month follow-up. The study highlights the challenges of establishing biomarkers in naturalistic clinical populations. While the association of attenuated DHEA with anxiety symptoms warrants further exploration, our data points towards the potential necessity of patient sub-sample selection to understand, and in the long run clinically target, the endocrine mechanisms in PTSD.

While psychotherapeutic treatments for posttraumatic stress disorder (PTSD) show in general good responses in affected individuals, 30–40% of patients show limited improvement. On a biological level, the endocannabinoid system of the body may play a role in the aftermath of trauma, in PTSD, and in extinction processes. This study is a secondary analysis of a randomized-controlled trial including patients with PTSD over the course of trauma-focused inpatient treatment. It aimed to investigate whether endocannabinoid system alterations are associated with symptom severity and treatment response. Fifty-four female inpatients with PTSD provided hair samples and completed psychometric questionnaires at pre-treatment, post-treatment, and 3-month follow-up. Endocannabinoid (EC: AEA, 1-AG/2-AG) and N -acylethanolamine (NAE: SEA, PEA, OEA) concentrations were measured in scalp-near 3-cm hair segments, reflecting cumulative concentrations in the 3 months prior to sampling. At pre-treatment, higher depressive and anxiety symptoms were significantly associated with lower hair AEA levels, whereas higher PTSD symptoms (when controlling for depressive symptoms) and more traumatic experiences were significantly associated with higher hair AEA and NAE levels respectively. PTSD symptoms improved across treatment, remaining stable at 3-month follow-up, but were predicted neither by pre-treatment hair ECs/NAEs nor their changes across treatment and follow-up, which was confirmed in subgroup analyses. Our findings suggest that hair ECs/NAEs may be distinctly linked with trauma-related and affective and anxiety symptoms, however, do not predict treatment response in PTSD. This challenges expectations and highlights the complexity of endocannabinoid system alterations in stress-related psychopathology. Given the study’s limitations, including a female-only sample and lack of a control group, larger studies with control groups and multiple biomarkers are needed to identify intervention-related biomarkers in PTSD. Highlights Hair endocannabinoids and N -acylethanolamines at pre-treatment and their change were unrelated to PTSD symptoms across treatment and follow-up At pre-treatment, hair AEA associated negatively with pre-treatment depressive and anxiety symptoms At pre-treatment, hair AEA associated positively with PTSD symptoms after controlling for depressive symptoms At pre-treatment, more traumatic experiences were related to higher hair SEA, PEA, and OEA levels in female inpatients with PTSD

Background Meta-analyses of studies on psychological treatment of refugees describe highly varying outcomes, and research on multi-facetted and personalized treatment of refugees with post-traumatic stress disorder (PTSD) is needed. Music therapy has been found to affect arousal regulation and emotional processing, and a pilot study on the music therapy method Trauma-focused Music and Imagery (TMI) with traumatized refugees resulted in significant changes of trauma symptoms, well-being and sleep quality. The aim of the trial is to test the efficacy of TMI compared to verbal psychotherapy. Methods A randomized controlled study with a non-inferiority design is carried out in three locations of a regional outpatient psychiatric clinic for refugees. Seventy Arabic-, English- or Danish-speaking adult refugees (aged 18–67 years) diagnosed with PTSD are randomized to 16 sessions of either music therapy or verbal therapy (standard treatment). All participants are offered medical treatment, psychoeducation by nurses, physiotherapy or body therapy and social counseling as needed. Outcome measures are performed at baseline, post therapy and at 6 months’ follow-up. A blind assessor measures outcomes post treatment and at follow-up. Questionnaires measuring trauma symptoms (HTQ), quality of life (WHO-5), dissociative symptoms (SDQ-20, DSS-20) and adult attachment (RAAS) are applied, as well as physiological measures (salivary oxytocin, beta-endorphin and substance P) and participant evaluation of each session. Discussion The effect of music therapy can be explained by theories on affect regulation and social engagement, and the impact of music on brain regions affected by PTSD. The study will shed light on the role of therapy for the attainment of a safe attachment style, which recently has been shown to be impaired in traumatized refugees. The inclusion of music and imagery in the treatment of traumatized refugees hopefully will inform the choice of treatment method and expand the possibilities for improving refugee health and integration. Trial registration ClinicalTrials.gov ID number NCT03574228, registered retrospectively on 28 June 2016.

Background Pharmacologic treatment options for posttraumatic stress disorder (PTSD) are limited in number and effectiveness. Medications currently in use to treat PTSD were originally approved based on their efficacy in other disorders, such as major depression. Substantial research in PTSD suggests that increased activity of corticotropin releasing hormone (CRH)-containing circuits are involved in the pathophysiology of the disease. This Phase II trial aims to evaluate the efficacy of a CRH type 1 receptor (CRHR1) antagonist in the treatment of PTSD. Methods/design Currently untreated adult women, ages 18 to 65 years, with a primary psychiatric diagnosis of PTSD of at least 3 months’ duration, are being enrolled in a parallel-group, double-blind, placebo-controlled, randomized clinical trial evaluating the efficacy and safety of GSK561679, a novel CRHR1 receptor antagonist. GSK561679 (or matching placebo) is prescribed at a fixed dose of 350 mg nightly for six weeks. The primary trial hypothesis is that GSK561679 will reduce symptoms of PTSD, as measured by the Clinician-Administered PTSD Scale (CAPS), significantly more than placebo after six weeks of treatment. Putative biological markers of PTSD which may influence treatment response are measured prior to randomization and after five weeks’ exposure to the study medication, including: fear conditioning and extinction using psychophysiological measures; variants of stress-related genes and gene expression profiles; and indices of HPA axis reactivity. In addition, the impact of PTSD and treatment on neuropsychological performance and functional capacity are assessed at baseline and after the fifth week of study medication. After completion of the six-week double blind treatment period, subjects enter a one-month follow-up period to monitor for sustained response and resolution of any adverse effects. Discussion Considerable preclinical and human research supports the hypothesis that alterations in central nervous system CRH neuronal activity are a potential mediator of PTSD symptoms. This study is the first to assess the efficacy of a specific antagonist of a CRH receptor in the treatment of PTSD. Furthermore, the biological and neuropsychological measures included in this trial will substantially inform our understanding of the mechanisms of PTSD. Trial registration Clinicaltrials.gov Identifier: NCT01018992 . Registered 6 November 2009. First patient randomized 14 January 2010.

Horticultural therapy (HT) is a subgroup of occupational therapy (OT). Both HT and OT have been successful as adjunctive treatment modalities in substance abuse treatment. Studies have indicated that gardening promotes neuroendocrine and affective restoration from stress. The study intended to assess the effect of HT versus nonhorticultural OT on cortisol levels, depression, symptoms of posttraumatic stress disorder (PTSD), alcohol cravings, and quality of life. The research team designed a randomized pilot study. The study was open for participation from July 2012-October 2012. It took place during multiple occurrences of a 28-d treatment programs for substance use disorder at a Veterans Affairs medical center. Participants • Participants were 49 veterans, averaging 46.4 y old (SD = 11.9); the dropout rate was 37%. Participants were randomly assigned to the HT or the OT group. They attended supervised HT and OT groups 5 h/d for 3 wk. Outcome Measures • Pre- and posttreatment, participants completed the Quality of Life Enjoyment and Satisfaction Questionnaire-Short Form (Q-LES-Q-SF), the Alcohol Craving Questionnaire (ACQ-NOW), the Posttraumatic Stress Disorder Checklist Civilian Version (PCLC), and the Center for Epidemiologic Studies Depression Scale (CES-D). Salivary cortisol samples were taken at wk 1, 2, and 3. A repeated measures analysis of variance (ANOVA) (F2,20 = 0.878) revealed that the HT performed was associated with a 12% reduction in salivary cortisol levels from wk 1 to wk 3, but the difference was not statistically significant (P = .43). Separate 1-way analyses of covariance (ANCOVAs) revealed no statistically significant differences in the self-administered tests, although both the Q-LES-Q-SF and CES-D showed a trend toward improving quality of life and depressive symptoms in the HT group compared with the OT group. Additional analysis of the nonbiologic tests suggests that most participants in the HT and OT had some benefit from the programmed activities. The trends suggest that HT may modulate stress in veterans, as evidenced by decreased cortisol levels and depressive symptoms, and may improve quality of life more than the programs in which the OT group participated. Further investigation with larger samples, including a nontreatment control group, is needed to determine whether the observed trends are treatment effects or due to abstinence.

Introduction: There has long been an interest in the effects of diet on mental health, and the interaction of the two with stress; however, the nature of these relationships is not well understood. Although associations between diet, obesity and the related metabolic syndrome (MetS), stress, and mental disorders exist, causal pathways have not been established. Methods: We reviewed the literature on the relationship between diet, stress, obesity and psychiatric disorders related to stress. Results: Diet and obesity can affect mood through direct effects, or stress-related mental disorders could lead to changes in diet habits that affect weight. Alternatively, common factors such as stress or predisposition could lead to both obesity and stress-related mental disorders, such as depression and posttraumatic stress disorder (PTSD). Specific aspects of diet can lead to acute changes in mood as well as stimulate inflammation, which has led to efforts to assess polyunsaturated fats (PUFA) as a treatment for depression. Bidirectional relationships between these different factors are also likely. Finally, there has been increased attention recently on the relationship between the gut and the brain, with the realization that the gut microbiome has an influence on brain function and probably also mood and behavior, introducing another way diet can influence mental health and disorders. Brain areas and neurotransmitters and neuropeptides that are involved in both mood and appetite likely play a role in mediating this relationship. Conclusions: Understanding the relationship between diet, stress and mood and behavior could have important implications for the treatment of both stress-related mental disorders and obesity.

Background Posttraumatic stress disorder (PTSD) is associated with abnormal functioning of the hypothalamic–pituitary–adrenal (HPA) axis; however, limited research has examined whether cortisol levels change following successful PTSD treatment. The current study examined the impact of successful PTSD treatment on the cortisol awakening response (CAR). Method Twenty‐nine adults participating in a treatment trial for chronic PTSD provided saliva samples (upon waking, and 30‐, 45‐, and 60 min postwaking) before and after receiving either prolonged exposure therapy or sertraline. PTSD responder status (i.e., loss or retention of a PTSD diagnosis) served as the predictor variable. Outcome measures included area under the curve with respect to ground and increase, reflecting total cortisol output and HPA axis reactivity, respectively. Results A series of hierarchical regressions revealed no significant main effects of PTSD responder status for either CAR outcome. However, a significant gender by treatment response interaction for cortisol reactivity revealed that female treatment nonresponders displayed higher cortisol reactivity following treatment than female responders, whereas cortisol reactivity did not change pre‐ to posttreatment for male responders. Findings remained after controlling for age, trauma history, baseline medication status, baseline PTSD, and baseline depressive symptoms. Conclusion Loss of a PTSD diagnosis may contribute to decreased cortisol reactivity in females. Neuroendocrine changes following treatment may emerge only for specific subgroups, highlighting the importance of exploring treatment moderators.

Post-traumatic stress disorder (PTSD) is a common, debilitating condition with limited treatment options. Extinction of fear memories through prolonged exposure therapy, the primary evidence-based behavioral treatment for PTSD, has only partial efficacy. In mice, pharmacological inhibition of fatty acid amide hydrolase (FAAH) produces elevated levels of anandamide (AEA) and promotes fear extinction, suggesting that FAAH inhibitors may aid fear extinction-based treatments. A human FAAH 385C->A substitution encodes an FAAH enzyme with reduced catabolic efficacy. Individuals homozygous for the FAAH 385A allele may therefore offer a genetic model to evaluate the impact of elevations in AEA signaling in humans, helping to inform whether FAAH inhibitors have the potential to facilitate fear extinction therapy for PTSD. To overcome the challenge posed by low frequency of the AA genotype (appr. 5%), we prospectively genotyped 423 individuals to examine the balanced groups of CC, AC, and AA individuals (n = 25/group). Consistent with its loss-of-function nature, the A allele was dose dependently associated with elevated basal AEA levels, facilitated fear extinction, and enhanced the extinction recall. Moreover, the A-allele homozygotes were protected against stress-induced decreases in AEA and negative emotional consequences of stress. In a humanized mouse model, AA homozygous mice were similarly protected against stress-induced decreases in AEA, both in the periphery, and also in the amygdala and prefrontal cortex, brain structures critically involved in fear extinction and regulation of stress responses. Collectively, these data suggest that AEA signaling can temper aspects of the stress response and that FAAH inhibition may aid the treatment for stress-related psychiatric disorders, such as PTSD.

The current report provides an updated review of sleep disturbance in posttraumatic stress disorder and anxiety-related disorders. First, this review provides a summary description of the unique and overlapping clinical characteristics and physiological features of sleep disturbance in specific DSM anxiety-related disorders. Second, this review presents evidence of a bidirectional relationship between sleep disturbance and anxiety-related disorders, and provides a model to explain this relationship by integrating research on psychological and neurocognitive processes with a current understanding of neurobiological pathways. A heuristic neurobiological framework for understanding the bidirectional relationship between abnormalities in sleep and anxiety-related brain pathways is presented. Directions for future research are suggested.