Objective: Dissociation, a disruption or discontinuity in psychological functioning, is often linked with worse psychiatric symptoms; however, the prognostic value of dissociation after trauma is inconsistent. Determining whether trauma-related dissociation is uniquely predictive of later outcomes would enable early identification of at-risk trauma populations. We completed the largest prospective, longitudinal, biomarker study of persistent dissociation to date to determine its predictive capacity for adverse psychiatric outcomes following acute trauma. Methods: All data were part of the Freeze 2 data release from the AURORA study. Individuals provided self-report data about persistent derealization (N=1,464), a severe type of dissociation, and completed a functional magnetic resonance imaging (fMRI) emotion reactivity task and resting-state scan 2-weeks post-trauma (N=145). We collected 3-month follow-up reports of posttraumatic stress, depression, pain, anxiety symptoms and functional impairment. Results: Derealization was associated with increased ventromedial prefrontal cortex (vmPFC) activation in the emotion reactivity task and decreased resting-state vmPFC connectivity with cerebellum and orbitofrontal cortex. Furthermore, in separate analyses, brain-based and self-report measures of persistent derealization at 2-weeks predicted worse 3-month posttraumatic stress symptoms, distinct from childhood maltreatment and current posttraumatic stress symptoms. Conclusions: Our work suggests persistent derealization is both an early psychological and biological marker of worse later psychiatric outcomes. The neural correlates of trauma-related dissociation may serve as potential targets for treatment engagement to prevent PTSD. These results underscore dissociation assessment as crucial following trauma exposure to identify at-risk individuals and highlight an unmet clinical need for tailored early interventions.

In this study, we considered connections between the content of immediate trauma narratives and longitudinal trajectories of negative symptoms to address questions about the timing and predictive value of collected trauma narratives. Participants (N = 68) were individuals who were admitted to the emergency department of a metropolitan hospital and provided narrative recollections of the traumatic event that brought them into the hospital that day. They were then assessed at intervals over the next 12 months for depressive and posttraumatic symptom severity. Linguistic analysis identified words involving affect (positive and negative emotions), sensory input (sight, sound, taste, touch, and smell), cognitive processing (thoughts, insights, and reasons), and temporal focus (past, present, and future) within the narrative content. In participants’ same-day narratives of the trauma, past-focused utterances predicted greater decreases in depressive symptom severity over the next year, d = −0.13, whereas cognitive process utterances predicted more severe posttraumatic symptom severity across time points, d = 0.32. Interaction analyses suggested that individuals who used fewer past-focused and more cognitive process utterances within their narratives tended to report more severe depressive and posttraumatic symptom severity across time, ds = 0.31 to 0.34. Overall, these findings suggest that, in addition to other demographics and baseline symptom severity, early narrative content can serve as an informative marker for longitudinal psychological symptoms, even before extensive narrative processing and phenomenological meaning-making have occurred.

Background Studies suggest that exaggerated amygdala reactivity is a vulnerability factor for posttraumatic stress disorder (PTSD); however, our understanding is limited by a paucity of prospective, longitudinal studies. Recent studies in healthy samples indicate that, relative to reactivity, habituation is a more reliable biomarker of individual differences in amygdala function. We investigated reactivity of the amygdala and cortical areas to repeated threat presentations in a prospective study of PTSD. Methods Participants were recruited from the emergency department of a large level I trauma center within 24 hours of trauma. PTSD symptoms were assessed at baseline and approximately 1, 3, 6, and 12 months after trauma. Growth curve modeling was used to estimate symptom recovery trajectories. Thirty-one individuals participated in functional magnetic resonance imaging around the 1-month assessment, passively viewing fearful and neutral face stimuli. Reactivity (fearful > neutral) and habituation to fearful faces was examined. Results Amygdala reactivity, but not habituation, 5 to 12 weeks after trauma was positively associated with the PTSD symptom intercept and predicted symptoms at 12 months after trauma. Habituation in the ventral anterior cingulate cortex was positively associated with the slope of PTSD symptoms, such that decreases in ventral anterior cingulate cortex activation over repeated presentations of fearful stimuli predicted increasing symptoms. Conclusions Findings point to neural signatures of risk for maintaining PTSD symptoms after trauma exposure. Specifically, chronic symptoms were predicted by amygdala hyperreactivity, and poor recovery was predicted by a failure to maintain ventral anterior cingulate cortex activation in response to fearful stimuli. The importance of identifying patients at risk after trauma exposure is discussed.

Introduction: Firearm injury prevention discussions with emergency department (ED) patients provide a unique opportunity to prevent death and injury in high-risk patient groups. Building mutual understanding of safe firearm practices between patients and providers will aid the development of effective interventions. Examining ED patient baseline characteristics, perspectives on healthcare-based safety discussions, and experience with and access to firearms, will allow practitioners to craft more effective messaging and interventions. Methods: Using an institutional review board-approved cross-sectional survey modified from a validated national instrument, we recruited 625 patients from three large, urban, academically affiliated EDs in the South to assess patient baseline characteristics, perspectives regarding firearms and firearm safety discussions, and prior violence history, as well as firearm access and safety habits. We compared the degree to which patients were open to discussions regarding firearms across a variety of provider types and clinical scenarios between those with and without gun access. Results: Of the 625 patients consented and eligible for the study, 306 had access to firearms. The patients with firearm access were predominantly male, were more likely to have military experience, live in an urban or suburban region, and have experienced prior violence when compared to those without firearm access. Patients with and without gun access view firearm safety discussions with their healthcare provider as acceptable and analogous to other behavioral health interventions (i.e., helmet/seat belt use, alcohol/cigarette use). Patients were also accepting of these firearm safety discussions in many clinical contexts and led by multiple provider types. Of the patients with gun access, storage of each type of firearm was reviewed and the primary reason for ownership was for personal protection across all firearm types. Conclusion: Patients in the ED indicate openness to firearm safety discussions delivered by a variety of providers and in diverse clinical scenarios. Healthcare providers engaging firearm owners in appropriate risk-benefit discussions using a trauma-informed approach is a critical next step in research and intervention.

Safety policy for e-scooters in the United States tends to vary by municipality, and the effects of safety interventions have not been well studied. We reviewed medical records at a large, urban tertiary care and trauma center in Atlanta, Georgia with the goal of identifying trends in e-scooter injury and the effects of Atlanta’s nighttime ban on e-scooter rentals on injuries treated in the emergency department (ED). Records from all ED visits occurring between June 2018 through August 2020 were reviewed. To account for ambiguity in medical records, confidence levels of either “certain” or “possible” were assigned using a set of predefined criteria to categorize patient injuries as being associated with an e-scooter. A total of 380 patients categorized as having certain e-scooter related injuries were identified. The average age of these patients was 31 years old, 65% were male, 41% had head injuries, 20% of injuries were associated with the built environment, and approximately 20% were admitted to the hospital. Approximately 19% of patients with injuries associated with e-scooters noted to be clinically intoxicated or have a serum ethanol level exceeding 80 mg/dL. The implementation of a nighttime rental ban on e-scooter rentals reduced the proportion of patients with e-scooter injuries with times of arrival during the hours of the ban from 32% to 22%, however this effect was not significant (p = 0.16). More research is needed to understand how e-scooter use patterns are affected by the nighttime rental ban.

Adverse posttraumatic neuropsychiatric sequelae (APNS) are common among civilian trauma survivors and military veterans. These APNS, as traditionally classified, include posttraumatic stress, post-concussion syndrome, depression, and regional or widespread pain. Traditional classifications have come to hamper scientific progress because they artificially fragment APNS into siloed, syndromic diagnoses unmoored to discrete components of brain functioning and studied in isolation. These limitations in classification and ontology slow the discovery of pathophysiologic mechanisms, biobehavioral markers, risk prediction tools, and preventive/treatment interventions. Progress in overcoming these limitations has been challenging, because such progress would require studies that both evaluate a broad spectrum of posttraumatic sequelae (to overcome fragmentation) and also perform in-depth biobehavioral evaluation (to index sequelae to domains of brain function). This article summarizes the methods of the Advancing Understanding of RecOvery afteR traumA (AURORA) Study. AURORA conducts a large scale (n = 5,000 target sample) in-depth assessment of APNS development using a state-of-the-art battery of self-report, neurocognitive, physiologic, digital phenotyping, psychophysical, neuroimaging, and genomic assessments, beginning in the early aftermath of trauma and continuing for one year. The goals of AURORA are to achieve improved phenotypes, prediction tools, and understanding of molecular mechanisms to inform the future development and testing of preventive and treatment interventions.

Background: Understanding the neurobiological mechanisms that predict posttraumatic stress disorder (PTSD) in recent trauma survivors is important for early interventions. Impaired inhibition of fear or behavioral responses is thought to be central to PTSD symptomatology, but its role in predicting PTSD is unknown. Here we examine whether brain function during response inhibition early after a civilian trauma can predict future PTSD symptoms. Methods: Participants (original sample, n = 27; replication sample, n = 31) were recruited in the emergency department within 24 hours of trauma exposure. PTSD symptoms were assessed in the emergency department and 1, 3, and 6 months posttrauma. A Go/NoGo procedure in a 3T magnetic resonance imaging scanner was used to measure neural correlates of response inhibition 1 to 2 months posttrauma. Elastic net regression was used to define the most optimal model to predict PTSD symptoms at 3 and 6 months among demographic, clinical, and imaging measures. Results: Less hippocampal activation was a significant predictor in the model predicting PTSD symptoms at 3 months (F11,22 = 4.33, p =.01) and 6 months (F9,19 = 4.96, p =.01). Other significant predictors in the model were race and pain level in the emergency department (3 months), and race and baseline depression symptoms (6 months). Using these predictors in a linear regression in the replication sample again resulted in significant models (3 months [F3,23 = 3.03, p =.05], 6 months [F3,20 = 5.74, p =.007]) with hippocampal activation predicting PTSD symptoms at 3 and 6 months. Conclusions: Decreased inhibition-related hippocampal activation soon after trauma predicted future PTSD symptom severity. This finding may contribute to early identification of at-risk individuals and reveals potential targets for intervention or symptom prevention in the aftermath of trauma.

Hippocampal impairments are reliably associated with post-traumatic stress disorder (PTSD); however, little research has characterized how increased threat-sensitivity may interact with arousal responses to alter hippocampal reactivity, and further how these interactions relate to the sequelae of trauma-related symptoms. In a sample of individuals recently exposed to trauma (N=116, 76 Female), we found that PTSD symptoms at 2-weeks were associated with decreased hippocampal responses to threat as assessed with functional magnetic resonance imaging (fMRI). Further, the relationship between hippocampal threat sensitivity and PTSD symptomology only emerged in individuals who showed transient, high threat-related arousal, as assayed by an independently collected measure of Fear Potentiated Startle. Collectively, our finding suggests that development of PTSD is associated with threat-related decreases in hippocampal function, due to increases in fear-potentiated arousal.Significance StatementAlterations in hippocampal function linked to threat-related arousal are reliably associated with post-traumatic stress disorder (PTSD); however, how these alterations relate to the sequelae of trauma-related symptoms is unknown. Prior models based on non-trauma samples suggest that arousal may impact hippocampal neurophysiology leading to maladaptive behavior. Here we show that decreased hippocampal threat sensitivity interacts with fear-potentiated startle to predict PTSD symptoms. Specifically, individuals with high fear-potentiated startle and low, transient hippocampal threat sensitivity showed the greatest PTSD symptomology. These findings bridge literatures of threat-related arousal and hippocampal function to better understand PTSD risk.

Aims Childhood adversities (CAs) predict heightened risks of posttraumatic stress disorder (PTSD) and major depressive episode (MDE) among people exposed to adult traumatic events. Identifying which CAs put individuals at greatest risk for these adverse posttraumatic neuropsychiatric sequelae (APNS) is important for targeting prevention interventions. Methods Data came from n = 999 patients ages 18-75 presenting to 29 U.S. emergency departments after a motor vehicle collision (MVC) and followed for 3 months, the amount of time traditionally used to define chronic PTSD, in the Advancing Understanding of Recovery After Trauma (AURORA) study. Six CA types were self-reported at baseline: physical abuse, sexual abuse, emotional abuse, physical neglect, emotional neglect and bullying. Both dichotomous measures of ever experiencing each CA type and numeric measures of exposure frequency were included in the analysis. Risk ratios (RRs) of these CA measures as well as complex interactions among these measures were examined as predictors of APNS 3 months post-MVC. APNS was defined as meeting self-reported criteria for either PTSD based on the PTSD Checklist for DSM-5 and/or MDE based on the PROMIS Depression Short-Form 8b. We controlled for pre-MVC lifetime histories of PTSD and MDE. We also examined mediating effects through peritraumatic symptoms assessed in the emergency department and PTSD and MDE assessed in 2-week and 8-week follow-up surveys. Analyses were carried out with robust Poisson regression models. Results Most participants (90.9%) reported at least rarely having experienced some CA. Ever experiencing each CA other than emotional neglect was univariably associated with 3-month APNS (RRs = 1.31-1.60). Each CA frequency was also univariably associated with 3-month APNS (RRs = 1.65-2.45). In multivariable models, joint associations of CAs with 3-month APNS were additive, with frequency of emotional abuse (RR = 2.03; 95% CI = 1.43-2.87) and bullying (RR = 1.44; 95% CI = 0.99-2.10) being the strongest predictors. Control variable analyses found that these associations were largely explained by pre-MVC histories of PTSD and MDE. Conclusions Although individuals who experience frequent emotional abuse and bullying in childhood have a heightened risk of experiencing APNS after an adult MVC, these associations are largely mediated by prior histories of PTSD and MDE.

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.