The majority of the injured trauma sample demonstrated resiliency, with those exhibiting distress doing so as a delayed, chronic, or recovered trajectory. Coping self efficacy, education, assaultive trauma type, and anger were important covariates of depression and PTSD trajectories. These results are similar to studies of individuals who experienced a major health threat and with survivors from the World Trade Center attacks in the U.S.
There is a growing interest in the effectiveness of mindfulness meditation for sleep disturbed populations. Our study sought to evaluate the effect of mindfulness meditation interventions on sleep quality. To assess for relative efficacy, comparator groups were restricted to specific active controls (such as evidenced‐based sleep treatments) and nonspecific active controls (such as time/attention‐matched interventions to control for placebo effects), which were analyzed separately. From 3303 total records, 18 trials with 1654 participants were included. We determined the strength of evidence using four domains (risk of bias, directness of outcome measures, consistency of results, and precision of results). At posttreatment and follow‐up, there was low strength of evidence that mindfulness meditation interventions had no effect on sleep quality compared with specific active controls (ES 0.03 (95% CI –0.43 to 0.49)) and (ES –0.14 (95% CI –0.62 to 0.34)), respectively. Additionally, there was moderate strength of evidence that mindfulness meditation interventions significantly improved sleep quality compared with nonspecific active controls at postintervention (ES 0.33 (95% CI 0.17–0.48)) and at follow‐up (ES 0.54 (95% CI 0.24–0.84)). These preliminary findings suggest that mindfulness meditation may be effective in treating some aspects of sleep disturbance. Further research is warranted.
As presently defined, post-traumatic stress disorder (PTSD) is an amalgam of symptoms falling into: re-experiencing of the trauma, avoidance of reminders of it, emotional numbing and hyperarousal. PTSD has a well-known proximate cause, commonly occurring after a life-threatening event that induces a response of intense fear, horror, and helplessness. Much of the advancement in understanding of the neurobiology of PTSD has emerged from conceptualizing the disorder as one that involves substantial dysfunction in fear processing. This article reviews recent knowledge of fear processing markers in PTSD. A systematic search was performed of reports within the specific three-year publication time period of January 2010 to December 2012. We identified a total of 31 studies reporting fear processing markers in PTSD. We further categorized them according to the following classification: (1) neural-activation markers (n=10), (2) psychophysiological markers (n=14), and (3) behavioral markers (n=7). Across most studies reviewed here, significant differences between individuals with PTSD and healthy controls were shown. Methodological, theoretical and clinical implications were discussed.
Key Points Question Is a brief mindfulness-based program effective and feasible in reducing stress among health care professionals during work hours? Findings In this randomized clinical trial including 78 participants randomized to a 5-session (7.5-hour total) mindfulness program or a life-as-usual control, participants in the mindfulness program reported reduced stress and anxiety compared with life-as-usual controls at the end of the intervention. Meaning This randomized clinical trial found that this brief mindfulness intervention was an effective way of reducing stress in a health care setting.
Symptoms of post-traumatic stress disorder (PTSD) are common in military populations, and frequently associated with a history of combat-related mild traumatic brain injury (mTBI). In this study, we examined relationships between severity of PTSD symptoms and levels of extracellular vesicle (EV) proteins and miRNAs measured in the peripheral blood in a cohort of military service members and Veterans (SMs/Vs) with chronic mTBI(s). Participants (n = 144) were divided into groups according to mTBI history and severity of PTSD symptoms on the PTSD Checklist for DSM-5 (PCL-5). We analyzed EV levels of 798 miRNAs (miRNAs) as well as EV and plasma levels of neurofilament light chain (NfL), Tau, Amyloid beta (Aβ) 42, Aβ40, interleukin (IL)-10, IL-6, tumor necrosis factor-alpha (TNFα), and vascular endothelial growth factor (VEGF). We observed that EV levels of neurofilament light chain (NfL) were elevated in participants with more severe PTSD symptoms (PCL-5 ≥ 38) and positive mTBI history, when compared to TBI negative controls (p = 0.024) and mTBI participants with less severe PTSD symptoms (p = 0.006). Levels of EV NfL, plasma NfL, and hsa-miR-139–5p were linked to PCL-5 scores in regression models. Our results suggest that levels of NfL, a marker of axonal damage, are associated with PTSD symptom severity in participants with remote mTBI. Specific miRNAs previously linked to neurodegenerative and inflammatory processes, and glucocorticoid receptor signaling pathways, among others, were also associated with the severity of PTSD symptoms. Our findings provide insights into possible signaling pathways linked to the development of persistent PTSD symptoms after TBI and biological mechanisms underlying susceptibility to PTSD.
predict depression reoccurrence, 7 which highlights the critical importance of treating underlying sleep disturbances in patients with mood and anxiety disorders to maintain psychiatric recovery, especially in the often stressful period of deployment readjustment. Although sleep disturbance represents a strong risk factor for depression and PTSD, less is known regarding the impact of targeting sleep disturbances directly to improve BRIEF SUMMARY Current Knowledge/Study Rationale: Previous studies recognized a relationship between sleep disturbance and psychiatric morbidity; however, limited work has examined this link in military personnel, a cohort at elevated risk for both insomnia and psychopathology. The current study examines the relation between improved sleep and attenuation of depression and posttraumatic symptoms in military personnel, as well as changes in trophic factors that likely modulate these conditions. Study Impact: Results indicate a strong association between improved sleep and reduced psychiatric symptoms, as well as enriched healthrelated quality of life. Sleep-focused treatments may be an effective means to facilitate psychiatric recovery. Findings highlight the importance of conducting sleep assessments in military personnel with mood and anxiety disorders.Study Objectives: One-third of deployed military personnel will be diagnosed with insomnia, placing them at high risk for comorbid depression, posttraumatic stress disorder (PTSD), and medical conditions. The disruption of trophic factors has been implicated in these comorbid conditions, which can impede postdeployment recovery. This study determined if improved sleep quality is associated with (1) reductions in depression and posttraumatic symptoms, as well as enrichments in health-related quality of life (HRQOL), and (2) changes in plasma concentrations of brain derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1). Methods: Forty-four military personnel diagnosed with insomnia underwent clinical evaluations and blood draws at pretreatment and at posttreatment following cognitive behavioral therapy for insomnia and automatic positive airway pressure treatment. Participants were classifi ed as sleep improved (n = 28) or sleep declined (n = 16) based on their change in pretreatment to posttreatment Pittsburgh Sleep Quality Index (PSQI) score. Both groups were compared on outcomes of depression, PTSD, HRQOL, BDNF, and IGF-1. Results: Paired t-tests of the sleep improved group revealed signifi cant declines in depression (p = 0.005) and posttraumatic arousal (p = 0.006) symptoms, and a signifi cant increase in concentrations of IGF-1 (p = 0.009). The sleep declined group had no relevant change in psychiatric symptoms or trophic factors, and had further declines on fi ve of eight dimensions of HRQOL. Between-group change score differences were signifi cant at p < 0.05. Conclusions: These fi ndings suggest that interventions, which successfully improve sleep quality, are an effective means to reduce the depression and ...
Study objectivesSleep disturbances are common in military personnel and are associated with increased risk for psychiatric morbidity, including posttraumatic stress disorder (PTSD) and depression, as well as inflammation. Improved sleep quality is linked to reductions in inflammatory bio-markers; however, the underlying mechanisms remain elusive.MethodsIn this study, we examine whole genome expression changes related to improved sleep in 68 military personnel diagnosed with insomnia. Subjects were classified into the following groups and then compared: improved sleep (n = 46), or non-improved sleep (n = 22) following three months of standard of care treatment for insomnia. Within subject differential expression was determined from microarray data using the Partek Genomics Suite analysis program and the ingenuity pathway analysis (IPA) was used to determine key regulators of observed expression changes. Changes in symptoms of depression and PTSD were also compared.ResultsAt baseline, both groups were similar in demographics, clinical characteristics, and gene-expression profiles. The microarray data revealed that 217 coding genes were differentially expressed at the follow-up-period compared to baseline in the participants with improved sleep. Expression of inflammatory cytokines were reduced including IL-1β, IL-6, IL-8, and IL-13, with fold changes ranging from −3.19 to −2.1, and there were increases in the expression of inflammatory regulatory genes including toll-like receptors 1, 4, 7, and 8 in the improved sleep group. IPA revealed six gene networks, including ubiquitin, which was a major regulator in these gene-expression changes. The improved sleep group also had a significant reduction in the severity of depressive symptoms.ConclusionInterventions that restore sleep likely reduce the expression of inflammatory genes, which relate to ubiquitin genes and relate to reductions in depressive symptoms.
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