Immediate Aftermath Of Trauma Research Articles

Acceptability of a smartphone-based intervention targeting anxiety sensitivity among women receiving emergency care after sexual assault: A pilot uncontrolled trial.

Anxiety sensitivity (AS), defined as the fear of anxious arousal, is a promising therapeutic target to reduce posttraumatic stress disorder (PTSD) symptom development after trauma exposure. Computerized AS interventions have been shown to be acceptable to individuals with PTSD symptoms and effective in achieving symptom reduction; however, to our knowledge, no research has examined AS interventions initiated in the immediate aftermath of trauma. We evaluated the feasibility, acceptability, and credibility of a brief (i.e., ∼75 min of psychoeducation, ∼2 hr of ecological momentary intervention) smartphone-based AS intervention in a pilot study. Participants were 12 women who presented for emergency care after sexual assault with high levels of peritraumatic PTSD symptoms. Most women who started the intervention completed the majority of it and reported using the techniques provided. Results indicated that participants perceived the intervention as logical and believed it would help in reducing their symptoms. Qualitative feedback was mostly positive but also indicated concern regarding intervention length. Although not the purpose of the study, results indicated medium-to-large, statistically significant decreases in AS, g = 0.74, and PTSD symptoms, g = 1.20. Overall, these preliminary findings suggest that this novel smartphone-based intervention targeting AS was feasible, acceptable, and credible in this small sample of women receiving emergency care following sexual assault. Treatment outcome data must be considered in the context of natural recovery; however, these promising preliminary feasibility, acceptability, and credibility data support continuing to pilot the feasibility and potential efficacy of the intervention to reduce AS and prolonged PTSD symptoms.

A network analysis investigating the associations between posttraumatic stress symptoms, markers of inflammation and metabolic syndrome

Chronic systemic inflammation has been implicated in trauma exposure, independent of a psychiatric diagnosis, and in posttraumatic stress disorder (PTSD) and its highly comorbid conditions, such as metabolic syndrome (MetS). The present study used network analysis to examine the interacting associations between pro-inflammatory cytokines, posttraumatic stress (PTS) symptoms and symptom clusters, and individual components of MetS, in a cohort of 312 participants (n = 139 PTSD cases, n = 173 trauma-exposed controls). Pro-inflammatory cytokines were measured in serum samples using immunoturbidimetric and multiplex assays. Three network models were assessed, and the decision on which model to use was guided by network stability estimates and denseness. Weak negative associations were observed between interleukin one beta (IL-1β) and detachment (D6) and irritability (E1); tumour necrosis factor alpha (TNFα) and hypervigilance (E3); and C-reactive protein (CRP) and emotional cue reactivity (B4), which could be due to high cortisol levels present in a female-majority cohort. Network models also identified positive associations between CRP and waist circumference, blood pressure, and high-density lipoprotein cholesterol (HDL-C). The strongest association was observed between CRP and waist circumference, providing evidence that central obesity is an important inflammatory component of MetS. Some networks displayed high instability, which could be due to the small pool of participants with viable cytokine data. Overall, this study provides evidence for associations between inflammation, PTS symptoms and components of MetS. Future longitudinal studies measuring pro-inflammatory cytokines in the immediate aftermath of trauma are required to gain better insight into the role of inflammation in trauma-exposure and PTSD.

0660 Identifying Patients at Risk of Acute Sleep Disturbances Within the Immediate Aftermath of Trauma

Abstract Introduction Acute sleep disturbances are a common, modifiable consequence of trauma that, if left untreated, increase risk of PTSD by nearly two-fold. This suggests acute sleep disturbances after trauma are an important contributor to the etiology of PTSD that could be targeted early to prevent the disorder. Yet, effective strategies to prevent PTSD cannot currently be implemented because we cannot identify who is most at risk of acute sleep disturbances after trauma, thus obstructing the ability to identify high-risk groups in need of early intervention. This study will test sleep reactivity – a trait predisposition to experience sleep disturbances after stress – as a predictor of posttraumatic sleep disturbances within one month following trauma exposure. Methods We recruited patients admitted to Henry Ford Hospital’s intensive care unit in Detroit for traumatic injury (e.g., gunshot wound) (N = 88, M age = 39.53, SD = 14.31). While hospitalized, patients reported their pre-trauma sleep reactivity (Ford Insomnia Response to Stress Test; FIRST) and insomnia symptoms from the past two weeks (Insomnia Severity Index; ISI). Patients then completed the ISI again one month later (n = 48). We tested high sleep reactivity (FIRST > 21) as a prospective predictor of clinically significant posttraumatic sleep disturbances (ISI > 10). Results Patients were mostly black men (67%), and nearly half reported an annual income < $20,000 (47.7%). Motor vehicle collisions were the most common trauma that precipitated patients’ hospital admission (42%), followed by assaults with a weapon (30.7%). While adjusting for age and pre-trauma sleep disturbance, high sleep reactivity predicted increased odds of sleep disturbances one month after trauma (b = 2.08, SE = .98, p = .033, OR = 8.01, CI = 1.19 – 54.15). Conclusion Individuals with high sleep reactivity are at increased susceptibility of clinically significant sleep disturbances after trauma. The 9-item FIRST is a brief and clinically useful indicator that offers providers the ability to predict the onset of acute sleep disturbances after trauma, which are novel targets for early intervention. This might enable the early identification of potentially vulnerable individuals who might develop PTSD, toward whom sleep-focused preventive efforts can be targeted. Support (if any)

Epigenetic aging and PTSD outcomes in the immediate aftermath of trauma.

Psychological trauma exposure and posttraumatic stress disorder (PTSD) have been associated with advanced epigenetic age. However, whether epigenetic aging measured at the time of trauma predicts the subsequent development of PTSD outcomes is unknown. Moreover, the neural substrates underlying posttraumatic outcomes associated with epigenetic aging are unclear. We examined a multi-ancestry cohort of women and men (n = 289) who presented to the emergency department (ED) after trauma. Blood DNA was collected at ED presentation, and EPIC DNA methylation arrays were used to assess four widely used metrics of epigenetic aging (HorvathAge, HannumAge, PhenoAge, and GrimAge). PTSD symptoms were evaluated longitudinally at the time of ED presentation and over the ensuing 6 months. Structural and functional neuroimaging was performed 2 weeks after trauma. After covariate adjustment and correction for multiple comparisons, advanced ED GrimAge predicted increased risk for 6-month probable PTSD diagnosis. Secondary analyses suggested that the prediction of PTSD by GrimAge was driven by worse trajectories for intrusive memories and nightmares. Advanced ED GrimAge was also associated with reduced volume of the whole amygdala and specific amygdala subregions, including the cortico-amygdaloid transition and the cortical and accessory basal nuclei. Our findings shed new light on the relation between biological aging and trauma-related phenotypes, suggesting that GrimAge measured at the time of trauma predicts PTSD trajectories and is associated with relevant brain alterations. Furthering these findings has the potential to enhance early prevention and treatment of posttraumatic psychiatric sequelae.

Promoter methylation of the glucocorticoid receptor following trauma may be associated with subsequent development of PTSD

Objectives The ability to identify persons at elevated risk for post-traumatic stress disorder (PTSD) soon after exposure to trauma, could aid clinical decision-making and treatment. In this study, we explored whether cytosine methylation of the 1 F promoter of the NR3C1 (glucocorticoid receptor [GR]) gene obtained immediately following a trauma could predict PTSD. Methods Our sample comprised 52 trauma survivors (28 women, 24 men), presenting to the Emergency Department (ED) within six hours of a traumatic event and followed for 13 months. Blood samples were taken at intake (n = 42) and again at the end of the study (13 months later, n = 27) to determine NR3C1-1F promoter methylation as well as plasma levels of cortisol, adrenocorticotropic-hormone (ACTH), and neuropeptide-Y (NPY). Results At the 13-month follow-up, participants who met the PTSD criteria (n = 4) showed significantly lower NR3C1-1F promoter sum percent methylation compared to the non-PTSD group (n = 38). Further, NR3C1-1F methylation at ED intake was inversely correlated with PTSD severity 13 months later, indicating that lower NR3C1-1F promoter methylation in the immediate aftermath of trauma was associated with the development of PTSD. Conclusion To the extent that reduced promoter methylation is associated with greater GR expression and responsivity, this finding is consistent with the hypothalamic-pituitary-adrenal dysregulation previously described for PTSD.

Use of serial smartphone-based assessments to characterize diverse neuropsychiatric symptom trajectories in a large trauma survivor cohort

The authors sought to characterize adverse posttraumatic neuropsychiatric sequelae (APNS) symptom trajectories across ten symptom domains (pain, depression, sleep, nightmares, avoidance, re-experiencing, anxiety, hyperarousal, somatic, and mental/fatigue symptoms) in a large, diverse, understudied sample of motor vehicle collision (MVC) survivors. More than two thousand MVC survivors were enrolled in the emergency department (ED) and completed a rotating battery of brief smartphone-based surveys over a 2-month period. Measurement models developed from survey item responses were used in latent growth curve/mixture modeling to characterize homogeneous symptom trajectories. Associations between individual trajectories and pre-trauma and peritraumatic characteristics and traditional outcomes were compared, along with associations within and between trajectories. APNS across all ten symptom domains were common in the first two months after trauma. Many risk factors and associations with high symptom burden trajectories were shared across domains. Both across and within traditional diagnostic boundaries, APNS trajectory intercepts, and slopes were substantially correlated. Across all domains, symptom severity in the immediate aftermath of trauma (trajectory intercepts) had the greatest influence on the outcome. An interactive data visualization tool was developed to allow readers to explore relationships of interest between individual characteristics, symptom trajectories, and traditional outcomes (http://itr.med.unc.edu/aurora/parcoord/). Individuals presenting to the ED after MVC commonly experience a broad constellation of adverse posttraumatic symptoms. Many risk factors for diverse APNS are shared. Individuals diagnosed with a single traditional outcome should be screened for others. The utility of multidimensional categorizations that characterize individuals across traditional diagnostic domains should be explored.

Hotspots in the immediate aftermath of trauma – Mental imagery of worst moments highlighting time, space and motion

Intrusive memories of trauma (memories that enter consciousness involuntarily) highjack cognitive processing, cause emotional distress, and represent a core symptom of posttraumatic stress disorder. Intrusive memories often contain the worst moment/s (‘hotspots’) of the trauma memory. Little is known about hotspots shortly after they are formed, i.e., in the first hours after trauma. We investigated the features of hotspots in trauma-exposed individuals (n = 21) within 72 h post-trauma, using linguistic analysis and qualitative coding. On average, participants reported three hotspots per traumatic event (M = 7.8 words/hotspot). Hotspots primarily contained words related to time, space, motion, and sensory processing. Most hotspots contained sensory features (97%) and motion (59%). Few cognitions and no emotion words were identified. Results indicate that hotspots collected shortly post-trauma are expressed as motion-rich sensory-perceptual experiences (mental imagery) with little detail about emotion/cognition. Findings are discussed in terms of the function of hotspots (e.g., preparedness for action) and clinical implications.

Integration of peripheral transcriptomics, genomics, and interactomics following trauma identifies causal genes for symptoms of post-traumatic stress and major depression.

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 traitloci 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.

Dynamics and determinants of cortisol and alpha-amylase responses to repeated stressors in recent interpersonal trauma survivors

BackgroundAlterations in major stress response systems are present during the immediate aftermath of trauma and may play a role in determining risk for developing posttraumatic stress disorder (PTSD). However, the dynamics and determinants of stress responses during this acute recovery phase, and their relevance for longitudinal clinical course and prognosis, have yet to be fully examined. The objectives of the present study were to characterize stress response and habituation patterns to repeated social stressors in women who recently experienced interpersonal trauma and to determine the extent to which these stress responses were associated with PTSD during prospective follow-up. MethodThis longitudinal study examined salivary cortisol and alpha-amylase and heart rate (HR) responses to repeated stressors in 98 young women (ages 18–30). Participants included women who had experienced an incident of interpersonal trauma (i.e., physical and/or sexual assault) in the three months prior to their baseline assessment (n = 58) and a comparison group of healthy, non-traumatized women (n = 40). Women completed the Trier Social Stress Test (TSST), clinical interviews to evaluate posttraumatic stress symptom severity at the baseline assessment and again at 1-, 3-, and 6-month follow-ups. ResultsMultilevel models revealed a pattern of robust initial cortisol TSST responses and habituation across successive TSSTs; alpha-amylase and HR responses showed no evidence of habituation across TSSTs. Among interpersonal trauma survivors, current PTSD status was associated with more pronounced cortisol responses to the first TSST. Survivors exhibited similarly blunted cortisol responses across follow-up TSSTs regardless of PTSD status, suggesting habituation of cortisol responses among survivors who developed PTSD. PTSD re-experiencing symptoms were uniquely associated with blunting of cortisol TSST responses. ConclusionFindings suggest that PTSD as a diagnostic entity is meaningfully associated with cortisol responses to repeated social stressors. Social-evaluative threat is a salient form of danger for interpersonal trauma survivors. Identifying the determinants of cortisol (non)habituation to repeated social-evaluative threat among interpersonal trauma survivors could inform the development of early interventions for PTSD.

Investigation of optimal dose of early intervention to prevent posttraumatic stress disorder: A multiarm randomized trial of one and three sessions of modified prolonged exposure.

Posttraumatic stress disorder (PTSD) is linked to a specific event, providing the opportunity to intervene in the immediate aftermath of trauma to prevent the development of this disorder. A previous trial demonstrated that trauma survivors who received three sessions of modified prolonged exposure therapy demonstrated decreased PTSD and depression prospectively compared to assessment only. The present study investigated the optimal dosing of this early intervention to test one versus three sessions of exposure therapy in the immediate aftermath of trauma. Participants (n = 95) recruited from a Level 1 Trauma Center were randomly assigned in a 1.5:1.5:1 ratio in a parallel-group design to the three conditions: one-session exposure therapy, three-session exposure therapy, and assessment only. Follow-up assessments were conducted by study assessors blind to study condition. Mixed-effects model results found no significant differences in PTSD or depression symptoms between the control condition and those who received one or three exposure therapy sessions across 1-12-month follow-up assessment. Results indicate that the intervention did not interfere with natural recovery. Receiver operating characteristic curve analyses on the screening measure used for study inclusion (Predicting PTSD Questionnaire; PPQ) in the larger sample from which the treatment sample was drawn (n = 481) found that the PPQ was a poor predictor of likely PTSD at all follow-up time points (Area under the curve's = 0.55-0.62). This likely impacted study results as many participants demonstrated natural recovery. Recommendations for future early intervention research are reviewed, including strategies to identify more accurately those at risk for PTSD and oversampling more severe trauma types.

Literature review and methodological considerations for understanding circulating risk biomarkers following trauma exposure.

Exposure to traumatic events is common. While many individuals recover following trauma exposure, a substantial subset develop adverse posttraumatic neuropsychiatric sequelae (APNS) such as posttraumatic stress, major depression, and regional or widespread chronic musculoskeletal pain. APNS cause substantial burden to the individual and to society, causing functional impairment and physical disability, risk for suicide, lost workdays, and increased health care costs. Contemporary treatment is limited by an inability to identify individuals at high risk of APNS in the immediate aftermath of trauma, and an inability to identify optimal treatments for individual patients. Our purpose is to provide a comprehensive review describing candidate blood-based biomarkers that may help to identify those at high risk of APNS and/or guide individual intervention decision-making. Such blood-based biomarkers include circulating biological factors such as hormones, proteins, immune molecules, neuropeptides, neurotransmitters, mRNA and noncoding RNA expression signatures, while we do not review genetic and epigenetic biomarkers due to other recent reviews of this topic. The current state of the literature on circulating risk biomarkers of APNS is summarized, and key considerations and challenges for their discovery and translation are discussed. We also describe the AURORA study, a specific example of current scientific efforts to identify such circulating risk biomarkers and the largest study to date focused on identifying risk and prognostic factors in the aftermath of trauma exposure.

338 Improved Trauma Survivor Phenotypes Are Critical for Better Biomarkers, Prediction Tools, and Treatments: Initial Results From the AURORA study

Adverse posttraumatic neuropsychiatric sequelae (APNS) are common among civilian trauma survivors and military veterans. APNS, as traditionally classified, include posttraumatic stress, post-concussion syndrome, depression, and regional or widespread pain. These traditional classifications artificially fragment APNS into siloed, syndromic diagnoses unmoored to discrete components of brain functioning. These traditional classifications are typically studied in isolation, and do not accurately reflect actual posttraumatic neuropsychiatric phenotypes. Most trauma survivors experience complex patterns of overlapping/co-occurring symptoms across multiple traditional classifications, and increasing evidence indicates that co-occurring symptoms can share an interwoven neurobiological substrate. Determining more discrete, homogenous APNS outcomes over time may improve the ability to index APNS to brain function, and categorizing individuals across these outcomes may provide more holistic, accurate phenotyping. Developing such phenotypes is a goal of the ongoing AURORA study, a ∼40 million dollar effort funded by NIH, the DoD, and foundation and industry partners. 5,000 trauma survivors presenting to 29 EDs for care are enrolled. Core self-report posttraumatic phenotype trajectories are developed using data obtained via serial administration of brief smartphone-based self-report surveys. Biomarkers for these outcomes are identified via serial assessments of neurocognitive, physiologic, digital phenotyping, psychophysical, neuroimaging, and genomic domains. After derivation and validation, these biomarkers will be integrated into outcome phenotype definitions. In the present abstract, the development of core self-report outcomes in the immediate aftermath of trauma is described. The Mindstrong™ App is used to assess symptom indicators for homogenous outcomes across the APNS spectrum (sleep, pain, loss, nightmares, avoidance, re-experiencing, anxiety, hyperarousal, cognition, and somatic). Each indicator group is assessed 6 times during the initial 8 weeks after trauma. Data from an initial study subsample experiencing a common trauma exposure (MVC, n=837) were used to develop measurement models and latent growth curves across timepoints for each outcome. Initial multidimensional outcome groups were developed using latent profile analyses. Construct measurement models provided a good fit to the data (eg, pain CFI 0.99, Loss CFI 0.97). Latent growth curves were developed and mixture model classes created for display purposes (Figure 1). Multidimensional outcomes were identified/selected based on relative model fit and clinical utility; non-recovered groups had markedly different inter-construct profiles. New phenotyping categorizations such as those resulting from the AURORA study have the potential to advance the evaluation and treatment of trauma survivors.

Increased Skin Conductance Response in the Immediate Aftermath of Trauma Predicts PTSD Risk

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.

F187. Hippocampal Activation During Inhibition Predicts PTSD: A Prospective Emergency Department Study

Impaired inhibition of fear or behavioral responses is thought to be central to PTSD symptomatology. Recent studies have shown the significance of hippocampal functioning in this context; however, prospective studies are needed to understand its role in resilience versus the development of PTSD in the immediate aftermath of trauma.

Psychological and psychobiological responses to immediate early intervention in the emergency department: Case report of one-session exposure therapy for the prevention of PTSD.

Research suggests that exposure therapy provided in the hours immediately following trauma exposure may prevent PTSD development. This case report presents data on an at-risk for PTSD participant involved in a motor-vehicle crash that caused her severe distress. She received one session of exposure therapy in the emergency department (ED) as part of an ongoing randomized controlled study examining the optimal dose of exposure therapy in the immediate aftermath of trauma. PTSD and depression measures were collected at pre-treatment assessment and one- and three-month follow-up. Potential PTSD biomarkers were also examined. Psychophysiological reactions were measured using skin conductance data measured on an iPad during the exposure therapy session and the follow-up assessments. A fear-potentiated startle paradigm and an functional magnetic resonance imaging (fMRI) behavioral inhibition task were used at follow-up. The participant demonstrated subjective and psychophysiological extinction from pre- to post-imaginal exposure. At follow-up, she did not meet DSM-IV criteria for PTSD or demonstrate hyperarousal to trauma reminders and showed robust fear extinction and the ability to inhibit responses in an fMRI behavioral inhibition task. In line with previous early intervention for the prevention of PTSD studies, this case report supports the need for ongoing empirical research investigating the possibility that one session of exposure therapy in the ED may attenuate risk for PTSD. Furthermore, the current findings demonstrate psychophysiological extinction serving as a prognostic indicator of treatment response for PTSD early intervention to be an exciting avenue to explore in future systematic research.

Sleep Deprivation Disrupts Recall of Conditioned Fear Extinction

BackgroundLearned fear is crucial in the development and maintenance of posttraumatic stress disorder and other anxiety disorders, and extinction of learned fear is necessary for response to exposure-based treatments. In humans, research suggests that disrupted sleep impairs consolidation of extinction, though no studies have examined this experimentally using total sleep deprivation. MethodsSeventy-one healthy control subjects underwent a paradigm to acquire conditioned fear to a visual cue. Twenty-four hours after fear conditioning, participants underwent extinction learning. Twenty-four hours after extinction learning, participants underwent extinction recall. Participants were randomized to three groups: 1) well-rested throughout testing (“normal sleep”; n = 21); 2) 36 hours’ total sleep deprivation before extinction learning (“pre-extinction deprivation”; n = 25); or 3) 36 hours’ total sleep deprivation after extinction learning and before extinction recall (“post-extinction deprivation”; n = 25). The groups were compared on blink electromyography reactivity to the condition stimulus during extinction learning and recall. ResultsThere were no differences among the three groups during extinction learning. During extinction recall, the pre-extinction deprivation group demonstrated significantly less extinction recall than the normal sleep group did. There was no significant difference between the normal sleep and post-extinction deprivation group during extinction recall. Results indicated sleep deprivation before extinction training significantly disrupts extinction recall. ConclusionsThese findings suggest that 1) sleep deprivation in the immediate aftermath of trauma could be a potential contributor to posttraumatic stress disorder development and maintenance via interference with natural extinction processes and 2) management of sleep symptoms should be considered during extinction-based therapy.

Early Intervention May Prevent the Development of Posttraumatic Stress Disorder: A Randomized Pilot Civilian Study with Modified Prolonged Exposure

Posttraumatic stress disorder (PTSD) is a major public health concern with long-term sequelae. There are no accepted interventions delivered in the immediate aftermath of trauma. This study tested an early intervention aimed at modifying the memory to prevent the development of PTSD before memory consolidation. Patients (n = 137) were randomly assigned to receive three sessions of an early intervention beginning in the emergency department compared with an assessment only control group. Posttraumatic stress reactions (PTSR) were assessed at 4 and 12 weeks postinjury and depression at baseline and week 4. The intervention consisted of modified prolonged exposure including imaginal exposure to the trauma memory, processing of traumatic material, and in vivo and imaginal exposure homework. Patients were assessed an average of 11.79 hours posttrauma. Intervention participants reported significantly lower PTSR than the assessment group at 4 weeks postinjury, p < .01, and at 12 weeks postinjury, p < .05, and significantly lower depressive symptoms at week 4 than the assessment group, p < .05. In a subgroup analysis, the intervention was the most effective at reducing PTSD in rape victims at week 4 (p = .004) and week 12 (p = .05). These findings suggest that the modified prolonged exposure intervention initiated within hours of the trauma in the emergency department is successful at reducing PTSR and depression symptoms 1 and 3 months after trauma exposure and is safe and feasible. This is the first behavioral intervention delivered immediately posttrauma that has been shown to be effective at reducing PTSR.

Startle reactivity in acute stress disorder and posttraumatic stress disorder.

The aim of this study is to prospectively examine electromyographic (EMG) responses in patients diagnosed with acute stress disorder (ASD) after experiencing a traffic accident or violent attack, within one month after the traumatic event and six months later. Half of the participants met criteria for posttraumatic stress disorder (PTSD) after six months. Psychophysiological parameters can provide a better clarification between ASD and PTSD patients. Heightened startle magnitude in the immediate aftermath of trauma may be a good predictor of PTSD; moreover, a lack of startle habituation appears to be a more stable marker of PTSD, which persists for six months after trauma exposure.

Duration of Exposure and the Dose-Response Model of PTSD

A dose-response model underlies posttraumatic stress disorder (PTSD) and posits a relationship between event magnitude and clinical outcome. The present study examines whether one index of event magnitude--duration of exposure--contributes to risk of PTSD among female victims of sexual assault. Findings support a small but significant contribution of event duration to clinical status in the immediate aftermath of trauma but not at 3-month follow-up. The opposite pattern is obtained for subjective appraisals of threat. These findings add to a growing literature that suggests that a simple application of the dose-response model to objective event characteristics may be insufficient to explain the risk of PTSD.

Collective memory: A perspective from (experimental) clinical psychology

This paper considers the concept of collective memory from an experimental clinical psychology perspective. Exploration of the term collective reveals a broad distinction between literatures that view collective memories as a property of groups (collectivistic memory) and those that regard these memories as a property of individuals who are, to a greater or lesser extent, an integral part of their social environment (social memory). First, we argue that the understanding of collectivistic memory phenomena may benefit from drawing parallels with current psychological models such as the self-memory system theory of individualistic autobiographical memory. Second, we suggest that the social memory literature may inform the study of trauma-related disorders. We argue that a factual focus induced by collaborative remembering may be beneficial to natural recovery in the immediate aftermath of trauma, and propose that shared remembering techniques may provide a useful addition to the treatment of post-traumatic stress disorder.