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Posttraumatic stress disorder (PTSD) is a chronic, often debilitating mental health disorder that may develop after a traumatic life event. Fortunately, effective psychological treatments for PTSD exist. In 2017, the Veterans Health Administration and Department of Defense (VA/DoD) and the American Psychological Association (APA) each published treatment guidelines for PTSD, which are a set of recommendations for providers who treat individuals with PTSD. The purpose of the current review article is to briefly review the methodology used in each set of 2017 guidelines and then discuss the psychological treatments of PTSD for adults that were strongly recommended by both sets of guidelines. Both guidelines strongly recommended use of Prolonged Exposure (PE), Cognitive Processing Therapy (CPT) and trauma-focused Cognitive Behavioral Therapy (CBT). Each of these treatments has a large evidence base and is trauma-focused, which means they directly address memories of the traumatic event or thoughts and feelings related to the traumatic event. Finally, we will discuss implications and future directions.

Background Increased psychophysiological reactivity is a hallmark intermediate phenotype of posttraumatic stress disorder (PTSD). Individuals with PTSD exhibit greater skin conductance (SC) responses to trauma scripts than trauma survivors without PTSD. However, trauma scripts require time for development and cannot be easily used in a single visit. Thus, there is a need for a low‐cost, easy‐to‐use, SC recording protocol for PTSD assessment. Methods Using a mobile device (eSense) connected to a portable tablet computer, we assessed SC reactivity to a standard trauma interview (STI) in 63 participants recruited from Grady Memorial Hospital in Atlanta, GA, approximately 1 year after trauma exposure. SC response (SCR) was calculated by subtracting the SC level (SCL) at the end of the baseline recording from the maximum SCL during the STI. Results SCL was significantly higher during the STI compared to baseline (P < .001), and individuals with PTSD showed significantly greater SCR than individuals without PTSD (P = .006). Logistic regression using SCR with PTSD diagnosis as the outcome showed an odds ratio of 1.76 (95% CI: 1.11–2.78). Lastly, higher SCR during the STI was also significantly associated with PTSD symptom total score controlling for demographics and trauma severity (b = 0.42, P = .001). Conclusions The current study demonstrated feasibility of the use of a mobile device for assessing psychophysiological reactivity in those with PTSD. The use of this low‐cost, easy‐to‐use mobile device to collect objective physiological data in concert with a STI can be easily disseminated in clinical and research settings.

Annually, approximately 30 million patients are discharged from the emergency department (ED) after a traumatic event 1 . These patients are at substantial psychiatric risk, with approximately 10–20% developing one or more disorders, including anxiety, depression or post-traumatic stress disorder (PTSD) 2 – 4 . At present, no accurate method exists to predict the development of PTSD symptoms upon ED admission after trauma 5 . Accurate risk identification at the point of treatment by ED services is necessary to inform the targeted deployment of existing treatment 6 – 9 to mitigate subsequent psychopathology in high-risk populations 10 , 11 . This work reports the development and validation of an algorithm for prediction of post-traumatic stress course over 12 months using two independently collected prospective cohorts of trauma survivors from two level 1 emergency trauma centers, which uses routinely collectible data from electronic medical records, along with brief clinical assessments of the patient’s immediate stress reaction. Results demonstrate externally validated accuracy to discriminate PTSD risk with high precision. While the predictive algorithm yields useful reproducible results on two independent prospective cohorts of ED patients, future research should extend the generalizability to the broad, clinically heterogeneous ED population under conditions of routine medical care. A machine-learning algorithm using electronic medical records and self-reported measures of stress at admission to the emergency department due to trauma can predict the risk and long-term trajectories of post-traumatic stress disorder in two independent cohorts.

Posttraumatic stress disorder (PTSD) is a significant public health issue. Yet, there are limited treatment options and no data to suggest which treatment will work for whom. We tested the efficacy of virtual reality exposure (VRE) or prolonged imaginal exposure (PE), augmented with D-cycloserine (DCS) for combat-related PTSD. As an exploratory aim, we examined whether brain-derived neurotrophic factor (BDNF) and fatty acid amide hydrolase (FAAH) moderated treatment response. Military personnel with PTSD ( n  = 192) were recruited into a multisite double-blind randomized controlled trial to receive nine weeks of VRE or PE, with DCS or placebo. Primary outcome was the improvement in symptom severity. Randomization was stratified by comorbid depression (MDD) and site. Participants in both VRE and PE showed similar meaningful clinical improvement with no difference between the treatment groups. A significant interaction ( p  = 0.45) suggested VRE was more effective for depressed participants (CAPS difference M = 3.51 [95% CI 1.17–5.86], p  = 0.004, ES = 0.14) while PE was more effective for nondepressed participants (M = −8.87 [95% CI −11.33 to −6.40], p  < 0.001, ES = −0.44). The main effect of DCS vs. placebo was not significant. Augmentation by MDD interaction ( p  = 0.073) suggested that depressed participants improved more on placebo (M = −8.43 [95% CI −10.98 to −5.88], p  < 0.001, ES = −0.42); DCS and placebo were equally effective for nondepressed participants. There was an apparent moderating effect of BDNF Val66Met polymorphism on DCS augmentation (ES = 0.67). Met66 allele carriers improved more on DCS (ES = −0.25). FAAH 385 A carriers improved more than non-carriers (ES = 0.33), particularly those with MDD (ES = 0.62). This study provides a step toward precision therapeutics for PTSD by demonstrating that comorbid MDD and genetic markers may help guide treatment selection. ClinicalTrials.gov Identifier: NCT01352637.

Background Exposure to a traumatic event leads to posttraumatic stress disorder in 10% to 20% of exposed individuals. Predictors of risk are needed to target early interventions to those who are most vulnerable. The objective of the study was to test whether a noninvasive mobile device that measures a physiological biomarker of autonomic nervous system activation could predict future posttraumatic stress disorder symptoms. Methods Skin conductance response was collected during a trauma interview in the emergency department within hours of exposure to trauma in 95 individuals. Trajectories of posttraumatic stress disorder symptoms over 12-month posttrauma were identified using latent growth mixture modeling. Results Skin conductance response was significantly correlated with the probability of being in the chronic posttraumatic stress disorder trajectory following trauma exposure in the emergency department (r = 0.489, p < 0.000001). Lasso regression with elastic net was performed with demographic and clinical measures obtained in the emergency department, demonstrating that skin conductance response was the most significant predictor of the chronic posttraumatic stress disorder trajectory (p < 0.00001). Conclusions This study is the first prospective study of posttraumatic stress disorder showing skin conductance response in the immediate aftermath of trauma predicts subsequent development of chronic posttraumatic stress disorder. This finding points to an easily obtained, and neurobiologically informative, biomarker in emergency departments that can be disseminated to predict the development of posttraumatic stress disorder.

Intensive care unit (ICU) nurses work in a demanding environment where they are repetitively exposed to traumatic situations and stressful events. The psychological effects on nurses as a result of working in the ICU are relatively unknown. To determine whether there is an increased prevalence of psychological symptoms in ICU nurses when compared with general nurses. We surveyed ICU and general nurses from three different hospitals (n=351) and then surveyed ICU nurses throughout the metropolitan area (n=140). In both cohorts of nurses, we determined the prevalence of symptoms of post-traumatic stress disorder (PTSD), anxiety, and depression using validated survey instruments. Within our hospital system, 24% (54/230) of the ICU nurses tested positive for symptoms of PTSD related to their work environment, compared with 14% (17/121) of the general nurses (p=0.03). ICU nurses did not report a greater amount of stress in their life outside of the hospital than general nurses. There was no difference in symptoms of depression or anxiety between ICU and general nurses. In the second survey of ICU nurses from our metropolitan area, 29% (41/140) of the respondents reported symptoms of PTSD, similar to our first cohort of ICU nurses. ICU nurses have an increased prevalence of PTSD symptoms when compared with other general nurses. These results may increase awareness of these symptoms in nurses and lead to future interventions that improve their mental health and job satisfaction and help retain ICU nurses in their profession.

Female individuals are more likely to be diagnosed with PTSD following trauma exposure than males, potentially due, in part, to underlying neurobiological factors. Several brain regions underlying fear learning and expression have previously been associated with PTSD, with the hippocampus, amygdala, dorsal anterior cingulate cortex (dACC), and rostral ACC (rACC) showing altered volume and function in those with PTSD. However, few studies have examined how sex impacts the predictive value of subcortical volumes and cortical thickness in longitudinal PTSD studies. As part of an emergency department study completed at the Grady Trauma Project in Atlanta, GA, N = 93 (40 Female) participants were enrolled within 24 h following a traumatic event. Multi-echo T1-weighted MRI images were collected one-month post-trauma exposure. Bilateral amygdala and hippocampal volumes and rACC and dACC cortical thickness were segmented. To assess the longitudinal course of PTSD, the PTSD Symptom Scale (PSS) was collected 6 months post-trauma. We investigated whether regional volume/thickness interacted with sex to predict later PTSD symptom severity, controlling for PSS score at time of scan, age, race, and trauma type, as well as intracranial volume (ICV) for subcortical volumes. There was a significant interaction between sex and rACC for 6-month PSS, such that right rACC thickness was positively correlated with 6-month PSS scores in females, but not in males. In examining PTSD symptom subtypes and depression symptoms, greater rACC thickness in females predicted greater avoidance symptoms, while smaller rACC thickness in males predicted greater depression symptoms. Amygdala and hippocampus volume and dACC thickness showed no main effect or interaction with sex. The current findings provide evidence for sex-based differences in how brain volume predicts future PTSD severity and symptoms and supports the rACC as being a vital region regarding PTSD. Gender differences should be assessed in future longitudinal PTSD MRI studies for more accurate identification of future PTSD risk following trauma.

Posttraumatic stress disorder (PTSD) is a debilitating syndrome with substantial morbidity and mortality that occurs in the aftermath of trauma. Symptoms of major depressive disorder (MDD) are also a frequent consequence of trauma exposure. Identifying novel risk markers in the immediate aftermath of trauma is a critical step for the identification of novel biological targets to understand mechanisms of pathophysiology and prevention, as well as the determination of patients most at risk who may benefit from immediate intervention. Our study utilizes a novel approach to computationally integrate blood-based transcriptomics, genomics, and interactomics to understand the development of risk vs. resilience in the months following trauma exposure. In a two-site longitudinal, observational prospective study, we assessed over 10,000 individuals and enrolled >700 subjects in the immediate aftermath of trauma (average 5.3 h post-trauma (range 0.5–12 h)) in the Grady Memorial Hospital (Atlanta) and Jackson Memorial Hospital (Miami) emergency departments. RNA expression data and 6-month follow-up data were available for 366 individuals, while genotype, transcriptome, and phenotype data were available for 297 patients. To maximize our power and understanding of genes and pathways that predict risk vs. resilience, we utilized a set-cover approach to capture fluctuations of gene expression of PTSD or depression-converting patients and non-converting trauma-exposed controls to find representative sets of disease-relevant dysregulated genes. We annotated such genes with their corresponding expression quantitative trait loci and applied a variant of a current flow algorithm to identify genes that potentially were causal for the observed dysregulation of disease genes involved in the development of depression and PTSD symptoms after trauma exposure. We obtained a final list of 11 driver causal genes related to MDD symptoms, 13 genes for PTSD symptoms, and 22 genes in PTSD and/or MDD. We observed that these individual or combined disorders shared ESR1, RUNX1, PPARA, and WWOX as driver causal genes, while other genes appeared to be causal driver in the PTSD only or MDD only cases. A number of these identified causal pathways have been previously implicated in the biology or genetics of PTSD and MDD, as well as in preclinical models of amygdala function and fear regulation. Our work provides a promising set of initial pathways that may underlie causal mechanisms in the development of PTSD or MDD in the aftermath of trauma.