Acute Aftermath Of Trauma Research Articles

Understanding nightmares after traumatic events in Detroit (UNiTED): prospective associations with interpersonal violence and posttraumatic stress disorder symptoms

ABSTRACT Background: Research suggests trauma-related nightmares (TRNs) during the acute aftermath of trauma may contribute to posttraumatic stress disorder (PTSD). However, it is unknown who is most vulnerable to TRNs, which is critical to identify at-risk patients toward whom early nightmare-focused treatments can be targeted to prevent PTSD. Objective: We tested trauma type (interpersonal violence [e.g. assault] vs non-interpersonal trauma [e.g. motor vehicle collision]) as a risk factor for TRNs in a predominantly low-income, Black, urban sample in Detroit, MI, USA. Method: We recruited patients from the intensive care unit following traumatic injury (N = 88; M age = 39.53 ± SD 14.31 years, 67.0% male, 67.0% Black, 47.7% annual income ≤ $20,000) and administered surveys at three post trauma timepoints: one week (T1), one month (T2; n = 61), and two months (T3; n = 59). Trauma type was assessed at T1 via electronic medical records. Participants reported the extent to which their dreams’ content was similar to the trauma for which they were hospitalized across T1-T3. Participants then completed the PTSD Checklist for DSM-5 at T3. Results: TRNs were more prevalent over time among patients exposed to interpersonal violence (80%) vs non-interpersonal trauma (48.7%, p = .005). Patients hospitalized for interpersonal violence faced greater odds for TRNs across timepoints relative to non-interpersonal trauma patients (Odds Ratio = 4.95, p = .021). TRNs, in turn, prospectively predicted PTSD symptoms such that TRNs at T2 presaged more severe PTSD at T3 (p = .040, η p 2 = .31), above and beyond T1 PTSD status. Conclusions: This prospective study provides first evidence that interpersonal violence exposure is a robust risk factor for TRNs, which prospectively contribute to PTSD symptom development. Early intervention on TRNs after interpersonal violence exposure may decrease PTSD risk. Future studies are encouraged to use ambulatory methods to capture nightmares sooner after they occur.

Prior Sexual Trauma Exposure Impacts Posttraumatic Dysfunction and Neural Circuitry Following a Recent Traumatic Event in the AURORA Study

BackgroundPrior sexual trauma (ST) is associated with greater risk for posttraumatic stress disorder after a subsequent traumatic event; however, the underlying neurobiological mechanisms remain opaque. We investigated longitudinal posttraumatic dysfunction and amygdala functional dynamics following admission to an emergency department for new primarily nonsexual trauma in participants with and without previous ST. MethodsParticipants (N = 2178) were recruited following acute trauma exposure (primarily motor vehicle collision). A subset (n = 242) completed magnetic resonance imaging that included a fearful faces task and a resting-state scan 2 weeks after the trauma. We investigated associations between prior ST and several dimensions of posttraumatic symptoms over 6 months. We further assessed amygdala activation and connectivity differences between groups with or without prior ST. ResultsPrior ST was associated with greater posttraumatic depression (F1,1120 = 28.35, p = 1.22 × 10−7, ηp2 = 0.06), anxiety (F1,1113 = 17.43, p = 3.21 × 10−5, ηp2 = 0.05), and posttraumatic stress disorder (F1,1027 = 11.34, p = 7.85 × 10−4, ηp2 = 0.04) severity and more maladaptive beliefs about pain (F1,1113 = 8.51, p = .004, ηp2 = 0.02) but was not related to amygdala reactivity to fearful versus neutral faces (all ps > .05). A secondary analysis revealed an interaction between ST and lifetime trauma load on the left amygdala to visual cortex connectivity (peak Z value: −4.41, corrected p < .02). ConclusionsFindings suggest that prior ST is associated with heightened posttraumatic dysfunction following a new trauma exposure but not increased amygdala activity. In addition, ST may interact with lifetime trauma load to alter neural circuitry in visual processing regions following acute trauma exposure. Further research should probe the relationship between trauma type and visual circuitry in the acute aftermath of trauma.

Evaluating the Evidence for Brain-Based Biotypes of Psychiatric Vulnerability in the Acute Aftermath of Trauma.

The weak link between subjective symptom-based diagnostic methods for posttraumatic psychopathology and objectively measured neurobiological indices forms a barrier to the development of effective personalized treatments. To overcome this problem, recent studies have aimed to stratify psychiatric disorders by identifying consistent subgroups based on objective neural markers. Along these lines, a promising 2021 study by Stevens et al. identified distinct brain-based biotypes associated with different longitudinal patterns of posttraumatic symptoms. Here, the authors conducted a conceptual nonexact replication of that study using a comparable data set from a multimodal longitudinal study of recent trauma survivors. A total of 130 participants (mean age, 33.61 years, SD=11.21; 48% women) admitted to a general hospital emergency department following trauma exposure underwent demographic, clinical, and neuroimaging assessments 1, 6, and 14 months after trauma. All analyses followed the pipeline outlined in the original study and were conducted in collaboration with its authors. Task-based functional MRI conducted 1 month posttrauma was used to identify four clusters of individuals based on profiles of neural activity reflecting threat and reward reactivity. These clusters were not identical to the previously identified brain-based biotypes and were not associated with prospective symptoms of posttraumatic psychopathology. Overall, these findings suggest that the original brain-based biotypes of trauma resilience and psychopathology may not generalize to other populations. Thus, caution is warranted when attempting to define subtypes of psychiatric vulnerability using neural indices before treatment implications can be fully realized. Additional replication studies are needed to identify more stable and generalizable neuroimaging-based biotypes of posttraumatic psychopathology.

Brain-Based Biotypes of Psychiatric Vulnerability in the Acute Aftermath of Trauma.

Major negative life events, such as trauma exposure, can play a key role in igniting or exacerbating psychopathology. However, few disorders are diagnosed with respect to precipitating events, and the role of these events in the unfolding of new psychopathology is not well understood. The authors conducted a multisite transdiagnostic longitudinal study of trauma exposure and related mental health outcomes to identify neurobiological predictors of risk, resilience, and different symptom presentations. A total of 146 participants (discovery cohort: N=69; internal replication cohort: N=77) were recruited from emergency departments within 72 hours of a trauma and followed for the next 6 months with a survey, MRI, and physiological assessments. Task-based functional MRI 2 weeks after a motor vehicle collision identified four clusters of individuals based on profiles of neural activity reflecting threat reactivity, reward reactivity, and inhibitory engagement. Three clusters were replicated in an independent sample with a variety of trauma types. The clusters showed different longitudinal patterns of posttrauma symptoms. These findings provide a novel characterization of heterogeneous stress responses shortly after trauma exposure, identifying potential neuroimaging-based biotypes of trauma resilience and psychopathology.

Dynamics of diurnal cortisol and alpha-amylase secretion and their associations with PTSD onset in recent interpersonal trauma survivors.

Dysfunction in major stress response systems during the acute aftermath of trauma may contribute to risk for developing posttraumatic stress disorder (PTSD). The current study investigated how PTSD diagnosis and symptom severity, depressive symptoms, and childhood trauma uniquely relate to diurnal neuroendocrine secretion (cortisol and alpha-amylase rhythms) in women who recently experienced interpersonal trauma compared to non-traumatized controls (NTCs). Using a longitudinal design, we examined diurnal cortisol and alpha-amylase rhythms in 98 young women (n = 57 exposed to recent interpersonal trauma, n = 41 NTCs). Participants provided saliva samples and completed symptom measures at baseline and 1-, 3-, and 6-month follow-up. Multilevel models (MLMs) revealed lower waking cortisol predicted the development of PTSD in trauma survivors and distinguished at-risk women from NTCs. Women with greater childhood trauma exposure exhibited flatter diurnal cortisol slopes. Among trauma-exposed individuals, lower waking cortisol levels were associated with higher concurrent PTSD symptom severity. Regarding alpha-amylase, MLMs revealed women with greater childhood trauma exposure exhibited higher waking alpha-amylase and slower diurnal alpha-amylase increase. Results suggest lower waking cortisol in the acute aftermath of trauma may be implicated in PTSD onset and maintenance. Findings also suggest childhood trauma may predict a different pattern of dysfunction in stress response systems following subsequent trauma exposure than the stress system dynamics associated with PTSD risk; childhood trauma appears to be associated with flattened diurnal cortisol and alpha-amylase slopes, as well as higher waking alpha-amylase.

Neural Activation During Fear Extinction Acutely Post-Trauma Predicts Chronic PTSD Severity

Deficits in extinction of conditioned fear have been proposed as a translational mechanism to understand exaggerated fear responding characteristic of posttraumatic stress disorder (PTSD). Aberrant activation of diffuse neural circuitry critical to fear expression and inhibition has been observed during extinction learning and recall in PTSD; however, it is unclear whether differences in neural activation during these processes may actually predict chronic symptoms in the acute aftermath of trauma.

The emergence of ketamine as a novel treatment for posttraumatic stress disorder.

A serious lack of effective pharmacotherapeutic interventions for posttraumatic stress disorder (PTSD) raises the urgent need for the development of novel treatments. Ketamine-a noncompetitive glutamate N-methyl-d-aspartate (NMDA) receptor antagonist in use for decades as an anesthetic and analgesic agent-has more recently been demonstrated to have rapid-onset antidepressant effects in patients with treatment-resistant depression (TRD). In the present review of ketamine as an emerging novel pharmacotherapeutic intervention for chronic PTSD, we discuss findings from the first proof-of-concept, randomized clinical trial (RCT) of single-dose intravenous ketamine in patients with chronic PTSD, as well as open-label studies and current practice. We introduce ongoing RCTs investigating the efficacy of repeated ketamine infusions in rapidly reducing symptoms and maintaining improvement in samples of individuals with PTSD stemming from civilian and military traumas. Additionally, we discuss mixed findings from published reports on ketamine administration in the acute aftermath of trauma. Studies in animal models of chronic stress have investigated molecular mechanisms underlying ketamine's effects, generating a shift in the conceptualization of PTSD as a disorder of impaired neural connectivity. We review animal studies examining the potential of ketamine to modify the expression of fear by altering memory reconsolidation or enhancing fear extinction, as well as others investigating ketamine administration prophylactically prior to stress exposure. We introduce the need for additional study in humans to evaluate whether ketamine might enhance the efficacy of psychotherapeutic interventions in individuals with chronic PTSD, harnessing a window of ketamine-induced neuroplasticity. While research on ketamine for PTSD is still in its early stages, it brings about the promise of novel and more effective treatments for this disabling condition.

Coping strategies as mediators in relation to resilience and posttraumatic stress disorder

BackgroundResilience has been shown to protect against the development of posttraumatic stress disorder (PTSD) in the aftermath of trauma. However, it remains unclear how coping strategies influence resilience and PTSD development in the acute aftermath of trauma. The current prospective, longitudinal study investigated the relationship between resilience, coping strategies, and the development of chronic PTSD symptoms. MethodsA sample of patients was recruited from an emergency department following a Criterion A trauma. Follow-up assessments were completed at 1-, 3-, and 6-months post-trauma to assess PTSD symptom development (N = 164). RESULTS: Resilience at 1-month positively correlated with the majority of active coping strategies (all p < .05) and negatively correlated with the majority of avoidant coping strategies (all p < .05), as well as future PTSD symptoms (p < .001). Additionally, all avoidant coping strategies, including social withdrawal, positively correlated with future PTSD symptoms (all p < .01). After controlling for demographic and clinical variables, social withdrawal at 3-months fully mediated the relationship between resilience at 1-month and PTSD symptoms at 6-months. LimitationsLimitations include participant drop out and the conceptual overlap between avoidant coping and PTSD. ConclusionsThese data suggest that resilience and social withdrawal may be possible therapeutic targets for mitigating the development of chronic PTSD in the aftermath of trauma.

The temporal relationship between mental health and disability after injury.

This longitudinal study investigated the temporal relationship patterns between disability and mental health after injury, with a focus on posttraumatic stress disorder (PTSD), depression, and anxiety. We conducted a multi-sited longitudinal cohort study with a large sample of hospital patients admitted after injury (N = 1,149, mean age = 37.9, 73.6% male). Data were collected prior to discharge from hospital, and follow-up assessments took place 3 and 12 months postinjury. A cross-lagged structural equation model (SEM) was used to assess the prospective relationship between posttraumatic stress, anxiety, and depression symptoms and disability while controlling for demographic characteristics and objective measures of injury severity. Acute depression significantly predicted 3-month disability, and 3-month PTSD severity significantly predicted 12-month disability. Premorbid disability had a significant effect on acute anxiety, depression, and posttraumatic stress symptoms, and 3-month depression but disability after the injury did not predict 12-month psychopathology. We did not find a reciprocal relationship between disability and psychopathology. Rather we found that depression played a role in early disability while PTSD played a role in contributing to long-term delays in the recovery process. The results of this study highlight the need for mental health screening for symptoms of PTSD and depression in the acute aftermath of trauma, combined with early intervention programs in injury populations.

Disease markers: molecular biology of PTSD.

There have been significant advances in understanding the phenomenology and biology of PTSD in the more than thirty years since the disorder first appeared in the DSM-III. However, as we stand in the crossroads towards DSM-V, it is clear that scientific efforts in the examination of PTSD have yielded more questions than they have answered. PTSD was initially described as a condition in which “the essential feature is the development of characteristic symptoms following a psychologically traumatic event that is generally outside the range of usual human experience” (APA, 1980). It was not only implied, but made explicit in the DSM-III, that the symptoms result from the trauma exposure. Thus, the one question that investigators did not feel they had to attend to in the early years of research on this disorder was what causes PTSD. Rather, initial investigations focused on demonstrating that persons who experience extreme trauma showed alterations in biological systems that have also been implicated in chronic stress and/or identified as correlates of fear. A variety of converging findings have now provided a scientific mandate to answer the question of what causes PTSD. First and foremost are results from epidemiologic studies demonstrating that only a proportion of trauma exposed persons develop PTSD. These studies have led to the conclusion that trauma exposure alone is not a sufficient causal agent. Furthermore, it has become clear that the findings related to stress or fear neurobiology may not be fully or completely applicable to the PTSD phenotype. It is true that the two major stress-responsive biological systems – the hypothalamic pituitary adrenal (HPA) axis and sympathetic nervous system (SNS) – seem to be dysregulated in PTSD. However, it has not been possible to conclude from extant findings that the PTSD neurobiology is analogous to the classical neurobiology of chronic stress or fear. While stress neurobiology arguably explains the emergence of some symptoms in the acute aftermath of trauma, it has not been able to explain either the persistence of those symptoms in the subset of trauma survivors who do not recover, or why such persons do not undergo what is arguably the defining hallmark of the stress response – the recalibration of biological systems towards homeostasis. Given these existing questions, the next generation of biological studies in PTSD must evaluate a broader range of biological mechanisms, and this examination must include molecular biology. It is for this reason that we have compiled a volume that puts together a series of conceptually related papers on the emerging molecular biology of PTSD. In that this is a new field, a volume that summarizes various methodological and theoretical approaches may have value in creating a scaffolding for future studies. Molecular biology is an approach that focuses on integrating information about the functioning of different cellular components. This includes how information travels from DNA to RNA, from RNA to protein synthesis, and ultimately from protein synthesis to function and behavior. Molecular biology is not only interested in the regulation of transcription and translation, but also in other processes of gene regulation including epigenetic regulation or genomic imprinting. The latter mechanisms are particularly interesting to examine in PTSD because they may reflect enduring consequences of environmental perturbations. In turn, epigenetic alterations can influence other molecular processes such as transcriptional and post-transcriptional regulation (e.g., sequestration, alternative splicing, trans-

Heart rate measured in the acute aftermath of trauma can predict post-traumatic stress disorder: A prospective study in motor vehicle accident survivors

Objective To determine whether increased physiological arousal immediately after trauma or at emergency admission can predict post-traumatic stress disorder (PTSD) in motor vehicle accident (MVA) survivors with physical injuries. Methods We included 119 MVA survivors with physical injuries. In this prospective cohort study, heart rate (HR) and blood pressure (BP) were assessed during ambulance transport (T1) and at hospital admission (T2). One and four months after the accident, we assessed patients for PTSD (Davidson trauma scale, confirmed with the structured clinical interview for DSM-IV axis I disorders). Multivariate logistic regression models assessed the relationship between HR or BP and PTSD. Results PTSD was diagnosed in 54 (45.4%) patients at 1 month and in 39 (32.8%) at 4 months. In the multivariate analysis, HR at T1 or at T2 predicted PTSD at 1 month (OR=1.156, 95% CI [1.094;1.221] p < 0.0001). Only HR at T1 (not at T2) predicted PTSD at 4 months (OR=1.059, 95% CI [1.013; 1.108] p = 0.012). Injury severity predicted PTSD at 4 months (OR=1.207, 95% CI [1.085; 1.342] p = 0.001). A cut-off of 84 beats per minute yielded a sensitivity of 62.5% and a specificity of 75.0% for PTSD. Conclusions HR measured at the scene of MVA and severity of injury predicted PTSD 4 months later.

Predictors of acute stress symptoms in rape victims.

Victims of traumatic experiences such as rape often report a variety of symptoms in the acute aftermath of trauma. Reactions to trauma may take the shape of acute stress disorder (ASD), which may later develop into posttraumatic stress disorder, or they may be symptoms of more general distress. The purpose of the present cross-sectional study was to test the hypothesis that symptoms of ASD and general stress, though correlated, represent two independent ways of reacting to trauma. Acute reactions to trauma were examined in a population of 150 female victims of sexual assault. Respondents were interviewed about demographic data and peritraumatic factors and filled out self-administered questionnaires concerning pretraumatic and posttraumatic factors including two dissociative items, ASD symptoms measured by the Acute Stress Disorder Scale and symptoms of general distress measured by a modified version of the Trauma Symptom Checklist. Two separate regression analyses were carried out to examine whether ASD ...

PTSD plus depression are comorbid conditions but depression can occur independently in the acute aftermath of trauma

O’Donnell ML, Creamer M, Pattison P. Posttraurnatic stress disorder and depression following trauma: understanding comorbidity. Am J Psychiatr 2004;161:1390–6.[OpenUrl][1][CrossRef][2][PubMed][3][Web of Science][4] Q Following trauma, are depression and post-traumatic stress disorder...

Hypnosis and Traumatic Dissociation: Therapeutic Opportunities

ABSTRACT Hypnosis and the related phenomenon of dissociation have long been linked to trauma. Evidence is reviewed regarding the relationship between trauma and dissociation, the prevalence of these dissociative symptoms in the acute aftermath of trauma, and their salience in predicting the development of later PTSD symptoms. The evidence reviewed regarding the prevalence of dissociative and other symptoms in the immediate aftermath of trauma formed the basis for including Acute Stress Disorder (ASD) as a new diagnosis in the DSM-IV. Dissociative amnesia is described as the key commonality between formally induced hypnosis and dissociative symptomatology, and controversy regarding traumatic amnesia is discussed. Finally principles of psychotherapy involving hypnosis and related techniques for dissociative and other post-traumatic symptoms are reviewed.

Dreams in the acute aftermath of trauma and their relationship to PTSD

AbstractDreams following trauma have been suggested to aid emotional adaptation, yet trauma‐related nightmares are a diagnostic symptom of Posttraumatic Stress Disorder (PTSD). There is little published data relating dreams to PTSD soon after trauma. We assessed dreams and PTSD in 60 injured patients after life‐threatening events and obtained follow‐up assessments in 39 of these participants 6 weeks later. Ten of 21 dream reports from morning diaries were rated and described as similar to the recent traumatic event. The participants reporting these distressing “trauma dreams” had more severe concurrent PTSD symptoms than those reporting other categories of dreams and had more severe initial and follow‐up PTSD than those without dream recall. These findings along with our preliminary longitudinal observations relating changes in dream patterns to outcome, suggest a relationship of dream characteristics and early adaptive versus maladaptive patterns of processing traumatic memory.