This study examined the power of theory-derived models to account for the development of PTSD, Complex PTSD (CPTSD), depression, and anxiety in children and adolescents who had experienced a single-event trauma.

Children (n = 234, aged 8–17 years) recruited from local Emergency Departments were assessed at two and nine weeks post-trauma. Data obtained from self-report questionnaires completed by the child, telephone interviews with parents, and hospital data were used to develop four predictive models of risk factors for PTSD, CPTSD, depression, and Generalized Anxiety Disorder (GAD). ICD-11 proposed diagnostic criteria were used to generate measures for CPTSD and PTSD to assess for risk factors and identify the sample prevalence of these disorders.

At nine weeks post-trauma, 64% did not meet criteria for any disorder, 23.5% met criteria for PTSD, and 5.2% met criteria for CPTSD. 23.9% and 10.7% had developed clinically significant symptoms of depression and GAD, respectively. A cognitive model was the most powerful predictive model, a psychosocial model was weak, and subjective markers of event severity were more powerful than objective measures.

Youth exposed to single-incident trauma may develop different forms of psychopathology, and PTSD and CPTSD are frequently experienced alongside other conditions. The cognitive model of PTSD shows utility in identifying predictors of PTSD, CPTSD, depression, and GAD, particularly the role of trauma-related negative appraisals. This supports the application of cognitive interventions which focus upon re-appraising trauma-related beliefs in youth.

Post-traumatic stress disorder (PTSD) has been shown to predict psychotic symptomology. However, few studies have examined the relative contribution of PTSD compared to broader post-traumatic sequelae in maintaining psychosis. Complex PTSD (cPTSD), operationalized using ICD-11 criteria, includes core PTSD (intrusions, avoidance, hyperarousal) as well as additional “disturbances of self-organisation” (DSO; emotional dysregulation, interpersonal difficulties, negative self-concept) symptoms, more likely to be associated with complex trauma histories. It was hypothesized that DSOs would be associated with positive psychotic symptoms (paranoia, voices, and visions) in daily life, over and above core PTSD symptoms.

This study (N = 153) employed a baseline subsample of the Study of Trauma And Recovery (STAR), a clinical sample of participants with comorbid post-traumatic stress and psychosis symptoms. Core PTSD, DSO and psychosis symptoms were assessed up to 10 times per day at quasi-random intervals over six consecutive days using Experience Sampling Methodology.

DSOs within the preceding 90 min predicted paranoia, voices, and visions at subsequent moments. These relationships persisted when controlling for core PTSD symptoms within this timeframe, which were themselves significant. The associations between DSOs and paranoia but not voices or visions, were significantly stronger than those between psychosis and core PTSD symptoms.

Consistent with an affective pathway to psychosis, the findings suggest that DSOs may be more important than core PTSD symptoms in maintaining psychotic experiences in daily life among people with comorbid psychosis and cPTSD, and indicate the potential importance of addressing broad post-traumatic sequelae in trauma-focused psychosis interventions.

Major depressive disorder (MDD) is the leading cause of disability globally, with moderate heritability and well-established socio-environmental risk factors. Genetic studies have been mostly restricted to European settings, with polygenic scores (PGS) demonstrating low portability across diverse global populations.

This study examines genetic architecture, polygenic prediction, and socio-environmental correlates of MDD in a family-based sample of 10 032 individuals from Nepal with array genotyping data. We used genome-based restricted maximum likelihood to estimate heritability, applied S-LDXR to estimate the cross-ancestry genetic correlation between Nepalese and European samples, and modeled PGS trained on a GWAS meta-analysis of European and East Asian ancestry samples.

We estimated the narrow-sense heritability of lifetime MDD in Nepal to be 0.26 (95% CI 0.18–0.34, p = 8.5 × 10−6). Our analysis was underpowered to estimate the cross-ancestry genetic correlation (rg = 0.26, 95% CI −0.29 to 0.81). MDD risk was associated with higher age (beta = 0.071, 95% CI 0.06–0.08), female sex (beta = 0.160, 95% CI 0.15–0.17), and childhood exposure to potentially traumatic events (beta = 0.050, 95% CI 0.03–0.07), while neither the depression PGS (beta = 0.004, 95% CI −0.004 to 0.01) or its interaction with childhood trauma (beta = 0.007, 95% CI −0.01 to 0.03) were strongly associated with MDD.

Estimates of lifetime MDD heritability in this Nepalese sample were similar to previous European ancestry samples, but PGS trained on European data did not predict MDD in this sample. This may be due to differences in ancestry-linked causal variants, differences in depression phenotyping between the training and target data, or setting-specific environmental factors that modulate genetic effects. Additional research among under-represented global populations will ensure equitable translation of genomic findings.

Fear learning is a core component of conceptual models of how adverse experiences may influence psychopathology. Specifically, existing theories posit that childhood experiences involving childhood trauma are associated with altered fear learning processes, while experiences involving deprivation are not. Several studies have found altered fear acquisition in youth exposed to trauma, but not deprivation, although the specific patterns have varied across studies. The present study utilizes a longitudinal sample of children with variability in adversity experiences to examine associations among childhood trauma, fear learning, and psychopathology in youth.

The sample includes 170 youths aged 10–13 years (M = 11.56, s.d. = 0.47, 48.24% female). Children completed a fear conditioning task while skin conductance responses (SCR) were obtained, which included both acquisition and extinction. Childhood trauma and deprivation severity were measured using both parent and youth report. Symptoms of anxiety, externalizing problems, and post-traumatic stress disorder (PTSD) were assessed at baseline and again two-years later.

Greater trauma-related experiences were associated with greater SCR to the threat cue (CS+) relative to the safety cue (CS−) in early fear acquisition, controlling for deprivation, age, and sex. Deprivation was unrelated to fear learning. Greater SCR to the threat cue during early acquisition was associated with increased PTSD symptoms over time controlling for baseline symptoms and mediated the relationship between trauma and prospective changes in PTSD symptoms.

Childhood trauma is associated with altered fear learning in youth, which may be one mechanism linking exposure to violence with the emergence of PTSD symptoms in adolescence.

Although several evidence-based trauma-focused treatments have been developed for post-traumatic stress disorder (PTSD), a high proportion of treatment completers fail to show total symptom or disorder-level remission. Trauma-focused treatments are predicated on the ability of one to emotionally engage with a trauma memory in order to process the traumatic experience and facilitate safety learning in the post-trauma ‘here and now’. Alexithymia, a difficulty in identifying, describing and tending to one’s emotions, occurs in approximately 40% of those who experience PTSD. This article investigates the role of emotional mechanisms in the effectiveness of trauma-focused treatments for PTSD, particularly prolonged exposure and trauma-focused cognitive behaviour therapy. Second, it explores how alexithymia poses challenges to emotion processing, undermining the effectiveness of trauma-focused treatments. The article concludes with a discussion of the clinical implications and possible treatment augmentation for those presenting with alexithymia and PTSD.

1. (1) To recognise the important affective mechanisms that can undermine trauma-focused CBT interventions.

2. (2) To widen the understanding and recognition of those who may be at risk of treatment non-response.

3. (3) To increase knowledge of available strategies and approaches in treating those who may have difficulties engaging with frontline exposure-based interventions.

Knowledge of sex differences in risk factors for posttraumatic stress disorder (PTSD) can contribute to the development of refined preventive interventions. Therefore, the aim of this study was to examine if women and men differ in their vulnerability to risk factors for PTSD.

As part of the longitudinal AURORA study, 2924 patients seeking emergency department (ED) treatment in the acute aftermath of trauma provided self-report assessments of pre- peri- and post-traumatic risk factors, as well as 3-month PTSD severity. We systematically examined sex-dependent effects of 16 risk factors that have previously been hypothesized to show different associations with PTSD severity in women and men.

Women reported higher PTSD severity at 3-months post-trauma. Z-score comparisons indicated that for five of the 16 examined risk factors the association with 3-month PTSD severity was stronger in men than in women. In multivariable models, interaction effects with sex were observed for pre-traumatic anxiety symptoms, and acute dissociative symptoms; both showed stronger associations with PTSD in men than in women. Subgroup analyses suggested trauma type-conditional effects.

Our findings indicate mechanisms to which men might be particularly vulnerable, demonstrating that known PTSD risk factors might behave differently in women and men. Analyses did not identify any risk factors to which women were more vulnerable than men, pointing toward further mechanisms to explain women's higher PTSD risk. Our study illustrates the need for a more systematic examination of sex differences in contributors to PTSD severity after trauma, which may inform refined preventive interventions.

Hemodynamic collapse in multi-trauma patients with severe traumatic brain injury (TBI) poses both a diagnostic and therapeutic challenge for prehospital clinicians. Brain injury associated shock (BIAS), likely resulting from catecholamine storm, can cause both ventricular dysfunction and vasoplegia but may present clinically in a manner similar to hemorrhagic shock. Despite different treatment strategies, few studies exist describing this phenomenon in the early post-injury phase. This retrospective observational study aimed to describe the frequency of shock in isolated TBI in prehospital trauma patients and to compare their clinical characteristics to those patients with hemorrhagic shock and TBI without shock.

All prehospital trauma patients intubated by prehospital medical teams from New South Wales Ambulance Aeromedical Operations (NSWA-AO) with an initial Glasgow Coma Scale (GCS) of 12 or less were investigated. Shock was defined as a pre-intubation systolic blood pressure under 90mmHg and the administration of blood products or vasopressors. Injuries were classified from in-hospital computed tomography (CT) reports. From this, three study groups were derived: BIAS, hemorrhagic shock, and isolated TBI without shock. Descriptive statistics were then produced for clinical and treatment variables.

Of 1,292 intubated patients, 423 had an initial GCS of 12 or less, 24 patients (5.7% of the original cohort) had shock with an isolated TBI, and 39 patients had hemorrhagic shock. The hemodynamic parameters were similar amongst these groups, including values of tachycardia, hypotension, and elevated shock index. Prehospital clinical interventions including blood transfusion and total fluids administered were also similar, suggesting they were indistinguishable to prehospital clinicians.

Hemodynamic compromise in the setting of isolated severe TBI is a rare clinical entity. Current prehospital physiological data available to clinicians do not allow for easy delineation between these patients from those with hemorrhagic shock.