Childhood Maltreatment and Amygdala-Mediated Anxiety and Posttraumatic Stress Following Adult Trauma.

Background: Childhood abuse (physical, emotional, and sexual) is associated with aberrant connectivity of the amygdala, a key threat-processing region. Heightened amygdala activity also predicts adult anxiety and posttraumatic stress disorder (PTSD) symptoms, as do experiences of childhood abuse. The current study explored whether amygdala resting-state functional connectivity may explain the relationship between childhood abuse and anxiety and PTSD symptoms following trauma exposure in adults. Methods: Two weeks posttrauma, adult trauma survivors (n = 152, mean age [SD] = 32.61 [10.35] years; women = 57.2%) completed the Childhood Trauma Questionnaire and underwent resting-state functional magnetic resonance imaging. PTSD and anxiety symptoms were assessed 6 months posttrauma. Seed-to-voxel analyses evaluated the association between childhood abuse and amygdala resting-state functional connectivity. A mediation model evaluated the potential mediating role of amygdala connectivity in the relationship between childhood abuse and posttrauma anxiety and PTSD. Results: Childhood abuse was associated with increased amygdala connectivity with the precuneus while covarying for age, gender, childhood neglect, and baseline PTSD symptoms. Amygdala-precuneus resting-state functional connectivity was a significant mediator of the effect of childhood abuse on anxiety symptoms 6 months posttrauma (B = 0.065; 95% CI, 0.013-0.130; SE = 0.030), but not PTSD. A secondary mediation analysis investigating depression as an outcome was not significant. Conclusions: Amygdala-precuneus connectivity may be an underlying neural mechanism by which childhood abuse increases risk for anxiety following adult trauma. Specifically, this heightened connectivity may reflect attentional vigilance for threat or a tendency toward negative self-referential thoughts. Findings suggest that childhood abuse may contribute to longstanding upregulation of attentional vigilance circuits, which makes one vulnerable to anxiety-related symptoms in adulthood.

Experiences of childhood abuse are related to long-term mental health outcomes, but the mechanisms of this relationship have been unclear. In this study of adult trauma survivors, Harb et al. found that experiences of childhood abuse are related to abnormal connectivity patterns of the amygdala, a key region for fear and threat processing, and precuneus. These connectivity patterns were identified as a mechanism through which experiences of child abuse are related to adult anxiety symptoms posttrauma. These findings advance our understanding of the specific downstream impacts of experiencing childhood abuse and can inform targeted assessment and intervention methods, especially in an adult trauma sample.

Subtypes of childhood maltreatment and posttraumatic stress disorder symptoms in an adult trauma sample: The mechanistic role of sleep.

OBJECTIVE: Childhood maltreatment is indisputably linked to adverse mental health outcomes, including an increased risk to develop posttraumatic stress disorder (PTSD) in adulthood. The role of childhood maltreatment in the context of recovery from a trauma later in adulthood is not well understood. A variable related to both childhood maltreatment and PTSD symptoms, and a potential link between the two, is sleep. The current study aimed to understand how sleep disturbances may play a mechanistic role in the effect of subtypes of childhood maltreatment on PTSD symptom severity in an adult trauma sample. METHOD: 160 adults (90 women; Mage = 33.73, SD = 10.86) were recruited from the emergency department at a Level-1 trauma center in southeastern Wisconsin after experiencing a traumatic injury. Experiences of childhood maltreatment and sleep were self-reported at 2-week and 3-month posttrauma, respectively. PTSD symptoms were clinically assessed 6 months later. RESULTS: Sleep disturbances 3-month posttrauma mediated the effect of emotional abuse, physical neglect, and emotional neglect on PTSD symptom 6 months after the traumatic injury. The effect of sexual and physical abuse on PTSD symptoms was not significantly mediated by sleep disturbances. CONCLUSIONS: These findings highlight the differential impact of subtypes of childhood maltreatment on PTSD symptoms, the mechanistic role of sleep, and the need to consider early life adversity when assessing adult posttrauma experiences. These results also suggest that interventions aimed at improving sleep quality might improve PTSD symptoms in those who have experienced childhood maltreatment and a subsequent traumatic injury in adulthood. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Childhood adversity is associated with reduced BOLD response in inhibitory control regions amongst preadolescents from the ABCD study.

Adolescence is characterized by dynamic neurodevelopment, which poses opportunities for risk and resilience. Adverse childhood experiences (ACEs) confer additional risk to the developing brain, where ACEs have been associated with alterations in functional magnetic resonance imaging (fMRI) BOLD signaling in brain regions underlying inhibitory control. Socioenvironmental factors like the family environment may amplify or buffer against the neurodevelopmental risks associated with ACEs. Using baseline to Year 2 follow-up data from the Adolescent Brain Cognitive Development (ABCD) Study, the current study examined how ACEs relate to fMRI BOLD signaling during successful inhibition on the Stop Signal Task in regions associated with inhibitory control and examined whether family conflict levels moderated that relationship. Results showed that greater ACEs were associated with reduced BOLD response in the right opercular region of the inferior frontal gyrus and bilaterally in the pre-supplementary motor area, which are key regions underlying inhibitory control. Further, greater BOLD response was correlated with less impulsivity behaviorally, suggesting reduced activation may not be behaviorally adaptive at this age. No significant two or three-way interactions with family conflict levels or time were found. Findings highlight the continued utility of examining the relationship between ACEs and neurodevelopmental outcomes and the importance of intervention/prevention of ACES.

Racial discrimination increases the risk for nonremitting posttraumatic stress disorder symptoms in traumatically injured Black individuals living in the United States.

Traumatic, life-threatening events are experienced commonly among the general U.S. population, yet Black individuals in the United States (i.e., Black Americans) exhibit higher prevalence rates of posttraumatic stress disorder (PTSD) and more severe symptoms than other populations. Although empirical research has noted a range of symptom patterns that follow traumatic injury, minimal work has examined the role of racial discrimination in relation to PTSD symptom trajectories. The current study assessed racial discrimination and PTSD symptom trajectories at 6 months postinjury across two separate samples of traumatically injured Black Americans (i.e. emergency department (ED)-discharged and hospitalized). Identified PTSD symptom trajectories largely reflect those previously reported (i.e., ED: nonremitting, moderate, remitting, and resilient; hospitalized: nonremitting, delayed, and resilient), although the resilient trajectory was less represented than expected given past research (ED: 55.8%, n = 62; hospitalized: 46.9%, n = 38). Finally, higher racial discrimination was associated with nonremitting, ED: relative risk ratio (RR) = 1.32, hospitalized: RR = 1.23; moderate, ED: RR = 1.18; and delayed, hospitalized: RR = 1.26, PTSD symptom trajectories. Overall, the current findings not only emphasize the inimical effects of racial discrimination but also demonstrate the unique ways in which race-related negative events can impact PTSD symptom levels and recovery across time.

Intrusive Traumatic Re-Experiencing Domain: Functional Connectivity Feature Classification by the ENIGMA PTSD Consortium.

Background: Intrusive traumatic re-experiencing domain (ITRED) was recently introduced as a novel perspective on posttraumatic psychopathology, proposing to focus research of posttraumatic stress disorder (PTSD) on the unique symptoms of intrusive and involuntary re-experiencing of the trauma, namely, intrusive memories, nightmares, and flashbacks. The aim of the present study was to explore ITRED from a neural network connectivity perspective. Methods: Data were collected from 9 sites taking part in the ENIGMA (Enhancing Neuro Imaging Genetics through Meta Analysis) PTSD Consortium (n= 584) and included itemized PTSD symptom scores and resting-state functional connectivity (rsFC) data. We assessed the utility of rsFC in classifying PTSD, ITRED-only (no PTSD diagnosis), and trauma-exposed (TE)-only (no PTSD or ITRED) groups using a machine learning approach, examining well-known networks implicated in PTSD. A random forest classification model was built on a training set using cross-validation, and the averaged cross-validation model performance for classification was evaluated using the area under the curve. The model was tested using a fully independent portion of the data (test dataset), and the test area under the curve was evaluated. Results: rsFC signatures differentiated TE-only participants from PTSD and ITRED-only participants at about 60% accuracy. Conversely, rsFC signatures did not differentiate PTSD from ITRED-only individuals (45% accuracy). Common features differentiating TE-only participants from PTSD and ITRED-only participants mainly involved default mode network-related pathways. Some unique features, such as connectivity within the frontoparietal network, differentiated TE-only participants from one group (PTSD or ITRED-only) but to a lesser extent from the other group. Conclusions: Neural network connectivity supports ITRED as a novel neurobiologically based approach to classifying posttrauma psychopathology.

Experiences of racial discrimination and adverse gene expression among black individuals in a level 1 trauma center sample.

Up to 40 % of individuals who sustain traumatic injuries are at risk for posttraumatic stress disorder (PTSD) and the conditional risk for developing PTSD is even higher for Black individuals. Exposure to racial discrimination, including at both interpersonal and structural levels, helps explain this health inequity. Yet, the relationship between racial discrimination and biological processes in the context of traumatic injury has yet to be fully explored. The current study examined whether racial discrimination is associated with a cumulative measure of biological stress, the gene expression profile conserved transcriptional response to adversity (CTRA), in Black trauma survivors. Two-weeks (T1) and six-months (T2) post-injury, Black participants (N = 94) provided a blood specimen and completed assessments of lifetime racial discrimination and PTSD symptoms. Mixed effect linear models evaluated the relationship between change in CTRA gene expression and racial discrimination while adjusting for age, gender, body mass index (BMI), smoking history, heavy alcohol use history, and trauma-related variables (mechanism of injury, lifetime trauma). Results revealed that for individuals exposed to higher levels of lifetime racial discrimination, CTRA significantly increased between T1 and T2. Conversely, CTRA did not increase significantly over time in individuals exposed to lower levels of lifetime racial discrimination. Thus, racial discrimination appeared to lead to a more sensitized biological profile which was further amplified by the effects of a recent traumatic injury. These findings replicate and extend previous research elucidating the processes by which racial discrimination targets biological systems.

The Dichotomy of Threat and Deprivation as Subtypes of Childhood Maltreatment: Differential Functional Connectivity Patterns of Threat and Reward Circuits in an Adult Trauma Sample.

BACKGROUND: Childhood maltreatment is associated with reduced activation of the nucleus accumbens, a central region in the reward network, and overactivity in the amygdala, a key region in threat processing. However, the long-lasting impact of these associations in the context of later-life stress is not well understood. The current study explored the association between childhood threat and deprivation and functional connectivity of threat and reward regions in an adult trauma sample. METHODS: Trauma survivors (N = 169; mean age [SD] = 32.2 [10.3] years; female = 55.6%) were recruited from a level I trauma center. Two weeks after injury, participants completed the Childhood Trauma Questionnaire (measuring experiences of threat and deprivation) and underwent resting-state functional magnetic resonance imaging. Seed-to-voxel analyses evaluated the effect of childhood threat and deprivation on amygdala and nucleus accumbens resting-state connectivity. RESULTS: Higher levels of threat were associated with increased connectivity between the right nucleus accumbens with temporal fusiform gyrus/parahippocampal gyrus and the left amygdala and the precuneus (false discovery rate-corrected p < .05). After controlling for posttraumatic symptoms 2 weeks posttrauma and lifetime trauma exposure, only the nucleus accumbens findings survived. There were no significant relationships between experiences of childhood deprivation and amygdala or nucleus accumbens connectivity. CONCLUSIONS: Experiences of threat are associated with increased nucleus accumbens and amygdala connectivity, which may reflect a preparedness to detect salient and visual stimuli. This may also reflect a propensity toward dysregulated reward processing. Overall, these results suggest that childhood threat may be contributing to aberrant neural baseline reward and threat sensitivity later in life in an adult trauma sample.

Differences in parent and youth perceived neighborhood threat on nucleus accumbens-frontoparietal network resting state connectivity and alcohol sipping in children enrolled in the ABCD study.

Purpose: Evidence has shown neighborhood threat (NT) as a social driver of emotional and brain development. Few studies have examined the relationship between NT and neural function. Altered functional connectivity in the nucleus accumbens (NAcc) with the frontoparietal network (FPN) has been implicated in the development of substance use, however, little is known about perceived NT-related brain function or downstream alcohol sipping during early adolescence. This study examined the longitudinal relationship between youth and combined youth/parent perceived NT, resting state functional connectivity (RSFC) of the NAcc-FPN, and alcohol sipping behavior during late childhood and preadolescence. Methods: This study used data (N = 7,744) from baseline to 2-year follow-up (FU) of the Adolescent Brain Cognitive Development Study (ABCD; Release 4.0). Relationships between youth and combined youth/parent perceive NT, alcohol sipping (baseline to two-year FU), and NAcc-FPN (left/right) connectivity, adjusting for demographics, family/peer history of alcohol use, parental monitoring and warmth, externalizing symptoms, and site, were examined in a mediation model via PROCESS in R. Results: Greater youth-reported NT at baseline was significantly associated with lower RSFC between the right (but not left) NAcc-FPN holding covariates constant (R2 = 0.01, B = -0.0019 (unstandardized), F (12, 7,731) = 8.649, p = 0.0087) and increased odds of alcohol sipping at baseline up to the two-year FU (direct effect = 0.0731, 95% CI = 0.0196, 0.1267). RSFC between the right NAcc-FPN did not significantly predict alcohol sipping at the two-year FU (b = -0.0213, SE = 0.42349, p = 0.9599; 95% CI = -0.8086, 0.8512). No significant relationships were observed for combined youth/parent report predicting alcohol sipping or NAcc-FPN connectivity. Conclusion: Findings suggest notable reporting differences in NT. Combined youth/parent report did not reveal significant findings; youth perceived NT was related to increased likelihood of alcohol sipping and lower neural connectivity between the right NAcc-FPN during late childhood and early adolescence. NT context - and source of reporting - may be crucial in examining links with downstream neuronal function and health behaviors. Future research should investigate reward processing and threat as the cohort ages into later adolescence.

Neural processes of emotional conflict detection and prediction of posttraumatic stress disorder symptom clusters in traumatic injury survivors.

OBJECTIVE: Given the prevalence and significant burden of posttraumatic stress disorder (PTSD), identifying early predictors of symptom development following trauma is critical. PTSD is a heterogeneous disorder comprised of distinct symptom clusters-reexperiencing, avoidance, negative mood, and hyperarousal-that contribute to the broad range of possible symptom profiles. Affective and attentional regulation processes, such as emotional conflict detection, are impaired in individuals with PTSD; however, the neural mechanisms underlying these alterations and their predictive utility for the development of PTSD symptoms remain unclear. METHOD: Traumatic injury survivors (N = 49) without traumatic brain injury were recruited from the emergency department of an urban, Level-1 trauma center. Within 1 month of trauma exposure, participants completed a well-characterized emotional conflict task during a functional magnetic resonance imaging scan. Participants returned 6-month later for a clinical assessment of PTSD symptoms. Using a region-of-interest mask derived from whole-brain voxelwise analyses during emotional conflict detection (vs. no emotional conflict detection) we examined whether differential neural activity predicted 6-month PTSD symptom cluster severity. RESULTS: Greater activation of the right middle frontal gyrus during emotional conflict detection prospectively predicted lower PTSD avoidance symptom severity 6 months later (above and beyond the effects of self-reported baseline PTSD and depressive symptoms, previous traumatic life events, racial discrimination, age, sex, and injury severity). CONCLUSIONS: Neural processes of emotion conflict detection measured in the early aftermath of a potentially traumatic event are useful as predictors for the development of PTSD symptoms. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Gray space and default mode network-amygdala connectivity.

Introduction: Aspects of the built environment relate to health factors and equity in living conditions, and may contribute to racial, ethnic, or economic health disparities. For example, urbanicity is linked with negative factors including exposure to gray space (e.g., impervious surfaces such as concrete, streets, or rooftops). While there is existing research on access to green space and urbanicity on some mental health and cognitive outcomes, there is limited research on the presence of gray space linked with cognitive functioning in youth. The goal of this study was to investigate the link between gray space and amygdala-default mode network (DMN) connectivity. Methods: This study used data from the ABCD Study. Participants (n = 10,144; age M = 119.11 months, female = 47.62%) underwent resting-state fMRI acquisition at baseline. Impervious surfaces (gray space) were measured via the Child Opportunity Index (COI). To examine the relationship between presence of gray space and -amygdala-DMN (left/right) connectivity, we employed linear mixed effects models. Correlations were run between amygdala-DMN connectivity and internalizing and externalizing symptoms. Finally, post hoc sensitivity analyses were run to assess the impact of race. Results: More gray space, adjusting for age, sex, and neighborhood-level variables, was significantly associated with increased left amygdala-DMN connectivity (p = 0.0001). This association remained significant after sensitivity analyses for race were completed (p = 0.01). No significant correlations were observed between amygdala-DMN and internalizing or externalizing symptoms. Discussion: Findings suggest gray space was linked with increased left amygdala-DMN connectivity, circuits that have been implicated in affective processing, emotion regulation, and psychopathology. Thus gray space may be related to alterations in connectivity that may enhance risk for emotion dysregulation. Future investigation of these relationships is needed, as neuroimaging findings may represent early dysregulation not yet observed in the behavioral analyses at this age (i.e., the present study did not find significant relationships with parent-reported behavioral outcomes). These findings can help to inform future public policy on improving lived and built environments.

Attributional negativity bias and acute stress disorder symptoms mediate the association between trauma history and future posttraumatic stress disorder.

Individuals who have experienced more trauma throughout their life have a heightened risk of developing posttraumatic stress disorder (PTSD) following injury. Although trauma history cannot be retroactively modified, identifying the mechanism(s) by which preinjury life events influence future PTSD symptoms may help clinicians mitigate the detrimental effects of past adversity. The current study proposed attributional negativity bias, the tendency to perceive stimuli/events as negative, as a potential intermediary in PTSD development. We hypothesized an association between trauma history and PTSD symptom severity following a new index trauma via heightened negativity bias and acute stress disorder (ASD) symptoms. Recent trauma survivors (N =189, 55.5% women, 58.7% African American/Black) completed assessments of ASD, negativity bias, and lifetime trauma 2-weeks postinjury; PTSD symptoms were assessed 6 months later. A parallel mediation model was tested with bootstrapping (10,000 resamples). Both negativity bias, Path b1 : ß = -.24, t(187) = -2.88, p = .004, and ASD symptoms, Path b2 : ß = .30, t(187) = 3.71, p < .001, fully mediated the association between trauma history and 6-month PTSD symptoms, full model: F(6, 182) = 10.95, p < .001, R 2 = .27; Path c': ß = .04, t(187) = 0.54, p = .587. These results suggest that negativity bias may reflect an individual cognitive difference that can be further activated by acute trauma. Moreover, negativity bias may be an important, modifiable treatment target, and interventions addressing both acute symptoms and negativity bias in the early posttrauma period may weaken the link between trauma history and new-onset PTSD.

Experiencing racial discrimination increases vulnerability to PTSD after trauma via peritraumatic dissociation.

Background: Racial discrimination is a traumatic stressor that increases the risk for posttraumatic stress disorder (PTSD), but mechanisms to explain this relationship remain unclear. Peritraumatic dissociation, the complex process of disorientation, depersonalization, and derealization during a trauma, has been a consistent predictor of PTSD. Experiences of frequent racial discrimination may increase the propensity for peritraumatic dissociation in the context of new traumatic experiences and contribute to PTSD symptoms. However, the role of peritraumatic dissociation in the relationship between experiences of discrimination and PTSD has not been specifically explored.Objective: The current study investigated the role of peritraumatic dissociation in the impact of racial discrimination on PTSD symptoms after a traumatic injury, and the moderating role of gender.Method: One hundred and thirteen Black/African American individuals were recruited from the Emergency Department at a Level I Trauma Center. Two weeks after the trauma, participants self-reported their experiences with racial discrimination and peritraumatic dissociation. At the six-month follow-up appointment, individuals underwent a clinical assessment of their PTSD symptoms.Results: Results of longitudinal mediation analyses showed that peritraumatic dissociation significantly mediated the effect of racial discrimination on PTSD symptoms, after controlling for age and lifetime trauma exposure. A secondary analysis was conducted to examine the moderating role of gender. Gender was not a significant moderator in the model.Conclusions: Findings show that racial discrimination functions as a stressor that impacts how individuals respond to other traumatic events. The novel results suggest a mechanism that explains the relationship between racial discrimination and PTSD symptoms. These findings highlight the need for community spaces where Black Americans can process racial trauma and reduce the propensity to detach from daily, painful realities. Results also show that clinical intervention post-trauma must consider Black Americans' experiences with racial discrimination.

Peritraumatic dissociation operates as a mechanism through which racial discrimination predicts posttraumatic symptoms in an adult trauma sample.Racial discrimination functions as a stressor that increases the risk for trauma-related symptoms.The lived experiences of Black Americans elicit the use of emotional detachment strategies that may mitigate effects of racial discrimination but increase the risk for peritraumatic dissociation.

Facets of emotion dysregulation differentially predict depression and PTSD symptom severity following traumatic injury.

Background: Emotion dysregulation is a hallmark characteristic of psychopathology following trauma. Yet, emotion dysregulation is multifaceted, and little is known about which aspects of emotion dysregulation predict depression and posttraumatic stress disorder (PTSD) symptom severity following traumatic injury.Objective: The aim of this longitudinal study was to evaluate how facets of dysregulation differentially predicted the severity of PTSD symptom clusters and depressive symptoms six months after a traumatic injury requiring medical treatment.Methods: Traumatically injured adults (N = 99) presenting to a Level 1 trauma centre completed a measure of emotion dysregulation 2 weeks post-injury, and PTSD and depression were assessed at 2-weeks and 6 months later.Results: Using stepwise regressions controlling for baseline symptoms, age, gender, race, and injury severity, results showed baseline emotion dysregulation significantly predicted the four symptom clusters of PTSD 6 months post-injury. Notably, hyperarousal symptoms and negative alterations in mood and cognition were predicted by a lack of clarity. On the other hand, depressive symptoms were significantly predicted by difficulty accessing emotion regulation strategies.Conclusion: Results highlight that specific facets of emotion dysregulation predict PTSD and depression symptom severity differentially after injury. Indeed, lack of emotional clarity appears to predict PTSD symptomatology, suggesting a potential mechanism driving worsening symptoms. Lack of clarity could also be detrimental to engagement in PTSD treatment. Conversely, lack of regulation strategies may represent a sense of helplessness in managing depression after trauma. As such, future research should elucidate whether interventions targeting aspects of emotion dysregulation based on symptom presentations are useful in treating PTSD and depression following injury.

Specific facets of emotion dysregulation are differentially associated with PTSD symptom clusters and depression symptom severity after injury.Findings suggest that targeting lack of emotional clarity may be critical for patients with prominent hyperarousal and trauma-related changes in mood and cognitions (i.e. two PTSD symptom clusters).Patients with depressive symptoms following trauma may especially benefit from the development of emotion regulation strategies.

Harmonizing PTSD severity scales across instruments and sites.

OBJECTIVE: The variety of instruments used to assess posttraumatic stress disorder (PTSD) allows for flexibility, but also creates challenges for data synthesis. The objective of this work was to use a multisite mega analysis to derive quantitative recommendations for equating scores across measures of PTSD severity. METHOD: Empirical Bayes harmonization and linear models were used to describe and mitigate site and covariate effects. Quadratic models for converting scores across PTSD assessments were constructed using bootstrapping and tested on hold out data. RESULTS: We aggregated 17 data sources and compiled an n = 5,634 sample of individuals who were assessed for PTSD symptoms. We confirmed our hypothesis that harmonization and covariate adjustments would significantly improve inference of scores across instruments. Harmonization significantly reduced cross-dataset variance (28%, p < .001), and models for converting scores across instruments were well fit (median R² = 0.985) with an average root mean squared error of 1.46 on sum scores. CONCLUSIONS: These methods allow PTSD symptom severity to be placed on multiple scales and offers interesting empirical perspectives on the role of harmonization in the behavioral sciences. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Event centrality and posttraumatic stress symptoms after traumatic injury: A longitudinal investigation.

The development of posttraumatic stress symptoms (PTSS) can occur following a traumatic injury, which may include an increase in negative cognitions. One cognitive construct shown to be associated with the development of PTSS is event centrality, or the degree to which an individual views a traumatic experience as central to their life story. Although cross-sectional work has demonstrated a robust connection between event centrality and PTSS, the directionality of this association remains unclear. Most previous work has investigated centrality as a predictor of PTSS, although one recent study suggests that PTSS may, in fact, predict event centrality. The current longitudinal study enrolled adult civilian participants (N = 191) from a Level 1 trauma center following a traumatic injury and assessed both event centrality and PTSS at three points posttrauma (3, 12, and 18 months). A time-constrained random intercept cross-lagged panel analysis showed that PTSS predicted event centrality over the 18-month follow-up period, B = 0.16, p = .021, but event centrality did not predict PTSS, B = -0.27, p = .340. These findings suggest that the development of PTSS following trauma exposure may lead to the perception of the traumatic event as central to an individual's story over time. Further longitudinal research is necessary to determine what variables may influence the connection between PTSS and event centrality.

Machine learning prediction of posttraumatic stress disorder trajectories following traumatic injury: Identification and validation in two independent samples.

Due to its heterogeneity, the prediction of posttraumatic stress disorder (PTSD) development after traumtic injury is difficult. Recent machine learning approaches have yielded insight into predicting PTSD symptom trajectories. Using data collected within 1 month of traumatic injury, we applied eXtreme Gradient Boosting (XGB) to classify admitted and discharged patients (hospitalized, n = 192; nonhospitalized, n = 214), recruited from a Level 1 trauma center, according to PTSD symptom trajectories. Trajectories were identified using latent class mixed models on PCL-5 scores collected at baseline, 1-3 months posttrauma, and 6 months posttrauma. In both samples, nonremitting, remitting, and resilient PTSD symptom trajectories were identified. In the admitted patient sample, a unique delayed trajectory emerged. Machine learning classifiers (i.e., XGB) were developed and tested on the admitted patient sample and externally validated on the discharged sample with biological and clinical self-report baseline variables as predictors. For external validation sets, prediction was fair for nonremitting versus other trajectories, areas under the curve (AUC = .70); good for nonremitting versus resilient trajectories, AUCs = .73-.76; and prediction failed for nonremitting versus remitting trajectories, AUCs = .46-.48. However, poor precision (< .57) across all models suggests limited generalizability of nonremitting symptom trajectory prediction from admitted to discharged patient samples. Consistency in symptom trajectory identification across samples supports prior studies on the stability of PTSD symptom trajectories following trauma exposure; however, continued work and replication with larger samples are warranted to understand overlapping and unique predictive features of PTSD in different traumatic injury populations.

Neighborhood Socioeconomic Disadvantage and the Neurobiology of Uncertainty in Traumatically Injured Adults.

BACKGROUND: Individuals residing in more socioeconomically disadvantaged neighborhoods experience greater uncertainty through insecurity of basic needs such as food, employment, and housing, compared with more advantaged neighborhoods. Although the neurobiology of uncertainty has been less frequently examined in relation to neighborhood disadvantage, there is evidence that neighborhood disadvantage is associated with widespread neural alterations. METHODS: Recently traumatically injured participants (n = 90) completed a picture anticipation task in the magnetic resonance imaging scanner, in which they viewed images presented in a temporally predictable or unpredictable manner. We investigated how neighborhood disadvantage (via area deprivation index [ADI]) was related to neural activation during anticipation and presentation of negative and neutral images after accounting for individual factors (i.e., age, gender, income, acute posttraumatic stress symptoms). RESULTS: There was a significant interaction during the anticipation period such that higher ADI rankings were related to greater activation of the right anterior cingulate cortex to predictable versus unpredictable neutral stimuli. Although no other robust interactions emerged related to ADI, we note several novel simple effects of ADI during anticipation and presentation periods in the hippocampus and prefrontal, cingulate, and occipital cortices. CONCLUSIONS: Together, these results may represent an adaptive response to predictable and/or negative stimuli, stemming from chronic exposure to socioeconomic-based uncertainties. Although effects were modest, future work should continue to examine pretrauma context on posttrauma outcomes. To better understand trauma outcomes, it is imperative that researchers consider the broader context in which trauma survivors reside.

The role of pain and socioenvironmental factors on posttraumatic stress disorder symptoms in traumatically injured adults: A 1-year prospective study.

Approximately 20% of individuals who experience a traumatic injury will subsequently develop posttraumatic stress disorder (PTSD). Physical pain following traumatic injury has received increasing attention as both a distinct, functionally debilitating disorder and a comorbid symptom related to PTSD. Studies have demonstrated that both clinician-assessed injury severity and patient pain ratings can be important predictors of nonremitting PTSD; however, few have examined pain and PTSD alongside socioenvironmental factors. We postulated that both area- and individual-level socioeconomic circumstances and lifetime trauma history would be uniquely associated with PTSD symptoms and interact with the pain-PTSD association. To test these effects, pain and PTSD symptoms were assessed at four visits across a 1-year period in a sample of 219 traumatically injured participants recruited from a Level 1 trauma center. We used a hierarchal linear modeling approach to evaluate whether (a) patient-reported pain ratings were a better predictor of PTSD than clinician-assessed injury severity scores and (b) socioenvironmental factors, specifically neighborhood socioeconomic disadvantage, individual income, and lifetime trauma history, influenced the pain-PTSD association. Results demonstrated associations between patient-reported pain ratings, but not clinician-assessed injury severity scores, and PTSD symptoms, R2( fvm ) = .65. There was a significant interaction between neighborhood socioeconomic disadvantage and pain such that higher disadvantage decreased the strength of the pain-PTSD association but only among White participants, R2( fvm ) = .69. Future directions include testing this question in a larger, more diverse sample of trauma survivors (e.g., geographically diverse) and examining factors that may alleviate both pain and PTSD symptoms.

Racial Discrimination and Resting-State Functional Connectivity of Salience Network Nodes in Trauma-Exposed Black Adults in the United States.

Importance: For Black US residents, experiences of racial discrimination are still pervasive and frequent. Recent empirical work has amplified the lived experiences and narratives of Black people and further documented the detrimental effects of racial discrimination on both mental and physical health; however, there is still a need for further research to uncover the mechanisms connecting experiences of racial discrimination with adverse health outcomes. Objective: To examine neurobiological mechanisms that may offer novel insight into the association of racial discrimination with adverse health outcomes. Design, Setting, and Participants: This cross-sectional study included 102 Black adults who had recently experienced a traumatic injury. In the acute aftermath of the trauma, participants underwent a resting-state functional magnetic resonance imaging scan. Individuals were recruited from the emergency department at a Midwestern level 1 trauma center in the United States between March 2016 and July 2020. Data were analyzed from February to May 2021. Exposures: Self-reported lifetime exposure to racial discrimination, lifetime trauma exposure, annual household income, and current posttraumatic stress disorder (PTSD) symptoms were evaluated. Main Outcomes and Measures: Seed-to-voxel analyses were conducted to examine the association of racial discrimination with connectivity of salience network nodes (ie, amygdala and anterior insula). Results: A total of 102 individuals were included, with a mean (SD) age of 33 (10) years and 58 (57%) women. After adjusting for acute PTSD symptoms, annual household income, and lifetime trauma exposure, greater connectivity between the amygdala and thalamus was associated with greater exposure to discrimination (t(97) = 6.05; false discovery rate (FDR)-corrected P = .03). Similarly, racial discrimination was associated with greater connectivity between the insula and precuneus (t(97) = 4.32; FDR-corrected P = .02). Conclusions and Relevance: These results add to the mounting literature that racial discrimination is associated with neural correlates of vigilance and hyperarousal. The study findings extend this theory by showing that this association is apparent even when accounting for socioeconomic position, lifetime trauma, and symptoms of psychological distress related to an acute trauma.