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Background Contemporary views of emotion dysregulation in post-traumatic stress disorder (PTSD) highlight reduced ability to flexibly select regulatory strategies according to differing situational demands. However, empirical evidence of reduced regulatory selection flexibility in PTSD is lacking. Multiple studies show that healthy individuals demonstrate regulatory selection flexibility manifested in selecting attentional disengagement regulatory strategies (e.g. distraction) in high-intensity emotional contexts and selecting engagement meaning change strategies (e.g. reappraisal) in low-intensity contexts. Accordingly, we hypothesized that PTSD populations will show reduced regulatory selection flexibility manifested in diminished increase in distraction (over reappraisal) preference as intensity increases from low to high intensity. Methods Study 1 compared student participants with high (N = 22) post-traumatic symptoms (PTS, meeting the clinical cutoff for PTSD) and participants with low (N = 22) post-traumatic symptoms. Study 2 compared PTSD diagnosed women (N = 31) due to childhood sexual abuse and matched non-clinical women (N = 31). In both studies, participants completed a well-established regulatory selection flexibility performance-based paradigm that involves selecting between distraction and reappraisal to regulate negative emotional words of low and high intensity. Results Beyond demonstrating adequate psychometric properties, Study 1 confirmed that relative to the low PTS group, the high PTS group presented reduced regulatory selection flexibility (p = 0.01, $\eta _{\rm p}^2$ = 0.14). Study 2 critically extended findings of Study 1, in showing similar reduced regulatory selection flexibility in a diagnosed PTSD population, relative to a non-clinical population (p = 0.002, $\eta _{\rm p}^2$ = 0.114). Conclusions Two studies provide converging evidence for reduced emotion regulatory selection flexibility in two PTSD populations.

Studies have searched for neurobiological markers of trauma exposure, posttraumatic stress disorder (PTSD) diagnosis, and resilience to trauma to identify therapeutic targets for PTSD. Despite some promising results, findings are inconsistent.The present study adopted a data-driven approach to systematically explore whether structural brain markers of trauma, PTSD, or resilience emerge when all are explored.Differences between clusters in the proportion of PTSD, healthy controls (HC), and trauma-exposed healthy controls (TEHC) served to indicate the presence of PTSD, trauma, and resilience markers, respectively. A total of 129 individuals, including 46 with PTSD, 49 TEHCs, and 34 HCs not exposed to trauma were scanned. Volumes, cortical thickness, and surface areas of interest were obtained from T1 structural MRI and used to identify data-driven clusters.Two clusters were identified, differing in the proportion of TEHCs but not of PTSDs or HCs. The cluster with the higher proportion of TEHCs, referred to as the resilience cluster, was characterized by higher volume in brain regions implicated in trauma exposure, especially the thalamus and rostral middle frontal gyrus. Cross-validation established the robustness and consistency of the identified clusters.Findings support the existence of structural brain markers of resilience.

Background Posttraumatic stress disorder (PTSD) is twice as prevalent among females as compared to males following potentially traumatic events. While there is evidence for aberrant functional connectivity between hubs of the central executive network (CEN), salience network (SN), and the default mode network (DMN) in PTSD, little is known regarding sex-specificity of this connectivity. The current study aims to directly examine sex-specific resting-state functional connectivity (rs-FC) in trauma exposed males and females, with and without PTSD. Methods One hundred and seventy-eight individuals underwent functional magnetic resonance imaging (fMRI) at rest, of them 85 females (45 with PTSD) and 93 males (57 with PTSD). We conducted whole-brain seed-based analysis using CEN (lateral prefrontal cortex [lPFC]), SN (anterior cingulate cortex [ACC], insula, amygdala [AMG]), and DMN (medial prefrontal cortex [mPFC], posterior parietal cortex [PCC], and hippocampus [HIP]) hubs as seed regions. Group-by-Sex ANOVA was conducted. Results The amygdala-precuneus, ACC-precuneus, and hippocampus-precuneus pathways exhibited significant group-by-sex interaction effects, with females with PTSD consistently differing in connectivity patterns from males with PTSD and from trauma-exposed healthy females. Conclusions Sex-specific neural connectivity patterns were found within and between key nodes of the CEN, DMN, and the SN, suggesting opposite patterns of connectivity in PTSD and trauma-exposed controls as a function of sex as a biological variable (SABV). This may point to mechanistic sex differences in adaptation following trauma and may inform differential neural targets for treatment of females and males with PTSD.

Background New recommendations regarding the use of personal protective equipment (PPE) during delivery have changed the maternal birth experience. In this study, we investigated the mental perceived impact of PPE use during delivery on the development of maternal postpartum depression (PPD) and post-traumatic stress symptoms (PTSS). Methods This was a multicenter, retrospective cohort study concerning women who delivered during the COVID-19 pandemic first lockdown period in Israel. Postpartum women were approached and asked to complete a comprehensive online questionnaire. Impact of PPE was graded on a scale of 1–5, and Impact of PPE ≥4 was considered high. PPD and PTSS were assessed using the EPDS and City BiTS questionnaires. Results Of 421 parturients, 36 (9%) reported high Impact of PPE. Parturients with high Impact of PPE had significantly higher PPD and PTSS scores)EPDS 8.4 ± 5.8 vs. 5.7 ± 5.3; City BiTS 9.2 ± 10.3 vs. 5.8 ± 7.8, p < 0.05 for both). Following adjustment for socio-demographic and delivery confounders and fear of COVID-19 (using Fear of COVID19 scale), Impact of PPE remained positively correlated with PPD symptoms (ß = 0.103, 95% confidence intervals [CI] 0.029–1.006, p = 0.038). Conclusion When examining the risk factors for developing postpartum PTSS—experiences during labor and PPE were found to be significant variables. As the use of PPE is crucial in this era of COVID-19 pandemic in order to protect both parturients and caregivers, creative measures should be taken in order to overcome the communication gap it poses.

COVID-19 impacted the childbirth experience and increased the rates of postpartum depression (PPD). We assessed the longitudinal effects of the pandemic on the rates of PPD and evaluated the PPD causes and symptoms among women who delivered during the first COVID-19 quarantine in Israel. The participants completed online questionnaires 3 (T1) and 6 months (T2) following delivery. We used the ‘COVID-19 exposure’ questionnaire, while PPD symptoms, situational anxiety, and social support were evaluated with the EPDS, STAI, and MSPSS questionnaires. The mean EPDS scores increased between T1 and T2 (6.31 ± 5.6 vs. 6.92 ± 5.9, mean difference −0.64 ± 4.59 (95% CI (−1.21)–(−0.06)); t (244) = −2.17, p = 0.031), and the STAI scores decreased (45.35 ± 16.4 vs. 41.47 ± 14.0, t(234) = 4.39, p = 0.000). Despite the exposure to an increased number of COVID-19 events (3.63 ± 1.8 vs. (6.34 ± 2.3)), the impact of exposure decreased between T1 and T2 (8.91 ± 4.6 vs. 7.47 ± 4.1), p < 0.001). In the MSPSS, significant differences were noted on the family scale between the T1 (6.10 ± 1.3) and T2 (5.91 ± 1.4) scores; t (216) = 2.68, p = 0.0008. A regression analysis showed three statistically significant variables that correlated with increased EPDS scores: the MSPSS family subscale (F (1212.00) = 4.308, p = 0.039), the STAI scores (F (1212.00) = 31.988, p = 0.000), and the impact of exposure to COVID-19 (F (1212.00) = 5.038, p = 0.026). The rates of PPD increased for women who delivered during the first COVID-19 lockdown. Further research is warranted to help reduce PPD among these women.

The context of place matters for mental health. Employing a feminist framework, this study used key informant interviews and focus group discussions in May of 2012 with 77 conflict-affected adults, children, and adolescents in Northeastern Uganda to understand the relation of place and the symbolic space of family to IPV survivors’ mental wellbeing to shape intervention possibilities. Using Grounded Theory methods, narratives identified numerous negative mental health experiences, such as having a disturbed mind, associated with inhabiting a violent domestic space. Place-associated qualities interacted with the symbolic space of the family to impede women’s ability to enhance the safety of their domestic space, discourage separation, and encourage reunification in the case of separation, all of which related to negative mental health experiences. Interventions should not assume that IPV survivors’ exposure to violence has terminated and look beyond mental health as an individual outcome.

BACKGROUND: Recent research suggests that posttraumatic stress disorder (PTSD) is associated with altered amygdala and hippocampal resting-state functional connectivity (rsFC). However, less research has examined whether Prolonged Exposure (PE), a first line exposure-based treatment for PTSD, has the potential to alter resting state neural networks. METHODS: Twenty-four patients with PTSD and 26 matched trauma-exposed healthy controls (TEHCs) underwent resting-state functional magnetic resonance imaging (fMRI) at baseline. PTSD patients were scanned a second time after completing 10-session PE in which patients narrated a detailed trauma account (imaginal exposure) and confronted trauma reminders (in vivo exposure) to extinguish trauma-related fear responses. TEHC were scanned again following a 10-week waiting period. Seed regions of interest (ROIs) included centromedial amygdala (CMA), basolateral amygdala (BLA), and the hippocampus. RESULTS: Post- versus pre-treatment comparisons indicated increased rsFC of the BLA and CMA with the orbitofrontal cortex (OFC), and hippocampus-medial prefrontal cortex (mPFC) among patients with PTSD, but not among TEHC participants. CONCLUSIONS: Enhanced amygdala and hippocampus rsFC with prefrontal cortical regions following PE could underlie improved capacity for inhibition and re-evaluation of threat, and heightened memory encoding and retrieval ability, respectively. These findings encourage further investigation of this circuitry as a therapeutic target in PTSD.

BackgroundThe 11 September 2001 (9/11) attacks were unprecedented in magnitude and mental health impact. While a large body of research has emerged since the attacks, published reviews are few, and are limited by an emphasis on cross-sectional research, short time frame, and exclusion of treatment studies. Additionally, to date, there has been no systematic review of available longitudinal information as a unique data set. Consequently, knowledge regarding long-term trajectories of 9/11-related post-traumatic stress disorder (PTSD) among highly exposed populations, and whether available treatment approaches effectively address PTSD within the context of mass, man-made disaster, remains limited.MethodsThe present review aimed to address these gaps using a systematic review of peer-reviewed reports from October 2001 to May 2016. Eligible reports were of longitudinal studies of PTSD among highly exposed populations. We identified 20 reports of 9/11-related PTSD, including 13 longitudinal prevalence studies and seven treatment studies.ResultsFindings suggest a substantial burden of 9/11-related PTSD among those highly exposed to the attack, associated with a range of sociodemographic and back-ground factors, and characteristics of peri-event exposure. While most longitudinal studies show declining rates of prevalence of PTSD, studies of rescue/recovery workers have documented an increase over time. Treatment studies were few, and generally limited by methodological shortcomings, but support exposure-based therapies.ConclusionFuture directions for research, treatment, and healthcare policy are discussed.

Background Neurobiological models of posttraumatic stress disorder (PTSD) implicate fear processing impairments in the maintenance of the disorder. Specific deficits in extinction recall, the retention of learned extinction, have been demonstrated. While deficient extinction recall, and the associated activation pattern of prefrontal and hippocampal regions, distinguishes individuals with PTSD from controls, research has not yet examined changes following treatment. We examined the behavioral and neural correlates of extinction recall before and after cognitive behavioral treatment of PTSD. Methods Fifty-eight participants (30 with PTSD, 28 trauma-exposed matched controls) underwent a 2-day behavioral fear conditioning, extinction, and recall paradigm during functional magnetic resonance imaging (fMRI). The same procedures were repeated 10 weeks later, after PTSD patients had completed prolonged exposure treatment. We analyzed fMRI data from 32 subjects (16 PTSD; 16 controls) and skin conductance response (SCR) data from 33 subjects (16 PTSD; 17 controls). Neural activity during extinction recall, SCR, and PTSD symptoms were compared across groups and over time. Results PTSD patients exhibited pre- to post-treatment reduction in rostral anterior cingulate cortex (rACC) activation during extinction recall, and increase in functional coherence between the rACC and the ventromedial prefrontal cortex (vmPFC) and subgenual anterior cingulate cortex (sgACC). Reduced PTSD symptom severity from pre- to post-treatment was significantly associated with reduced subgenual ACC and parahippocampal activation during this task. SCR during the extinction recall phase did not significantly change with treatment in the PTSD group, but change in SCR was associated with reduction in PTSD symptom severity. Conclusions Prolonged exposure treatment appears to alter neural activation in PTSD patients during recall of fear extinction, and change in extinction recall (measured by SCR) is associated with symptom reduction. We discuss results in the context of neural systems involved in response to affective stimuli., Highlights • Deficient recall of extinguished fear (extinction recall; ER) has been associated with PTSD. • Prolonged exposure (PE) is a first line treatment for PTSD which relies on extinction. • Changes in prefrontal activation and functional connectivity during ER appeared following PE. • Changes in ER following PE corresponded to changes in PTSD severity. • Taken together, these findings suggest normalization of ER deficits in PTSD following PE.

BACKGROUND: Brain structures underlying posttraumatic stress disorder (PTSD) have been a focus of imaging studies, but associations between treatment outcome and alterations in brain structures remain largely unexamined. We longitudinally examined the relation of structural changes in the rostral anterior cingulate cortex (rACC), a previously identified key region in the PTSD fear network, to outcome of prolonged exposure (PE) treatment. METHOD: The sample included 78 adults (53 women): 41 patients with PTSD and 37 trauma-exposed healthy volunteers (TE-HCs). Patients underwent a 10-week course of PE treatment and completed pre- and posttreatment assessments and magnetic resonance imaging (MRI) structural scans. TE-HCs also underwent assessment and MRI at baseline and 10 weeks later. PE remitters (n = 11), nonremitters (n = 14), and TE-HCs, were compared at baseline on demographic and clinical characteristics and ACC structure. Remitters, nonremitters, and TE-HCs were compared for pre- to posttreatment clinical and structural ACC change, controlling for potential confounding variables. RESULTS: There were no baseline differences in structure between PTSD and TE-HCs or remitters and nonremitters. Following treatment, PTSD remitters exhibited cortical thinning and volume decrease in the left rACC compared with PTSD nonremitters and TE-HCs. CONCLUSIONS: These results, while in need of replication, suggest that PE treatment for PTSD, by extinguishing maladaptive trauma associations, may promote synaptic plasticity and structure change in rACC. Future research should explore possible underlying mechanisms. Language: en

BackgroundRandomized control trials (RCTs) comparing attention control training (ACT) and attention bias modification (ABM) in posttraumatic stress disorder (PTSD) have shown mixed results. The current RCT extends the extant literature by comparing the efficacy of ACT and a novel bias-contingent-ABM (BC-ABM), in which direction of training is contingent upon the direction of pre-treatment attention bias (AB), in a sample of civilian patients with PTSD.MethodsFifty treatment-seeking civilian patients with PTSD were randomly assigned to either ACT or BC-ABM. Clinician and self-report measures of PTSD and depression, as well as AB and attention bias variability (ABV), were acquired pre- and post-treatment.ResultsACT yielded greater reductions in PTSD and depressive symptoms on both clinician-rated and self-reported measures compared with BC-ABM. The BC-ABM condition successfully shifted ABs in the intended training direction. In the ACT group, there was no significant change in ABV or AB from pre- to post-treatment.ConclusionsThe current RCT extends previous results in being the first to apply ABM that is contingent upon AB at pre-treatment. This personalized BC-ABM approach is associated with significant reductions in symptoms. However, ACT produces even greater reductions, thereby emerging as a promising treatment for PTSD.

Summary Although psychiatric disorders are classified as non-communicable diseases, we believe this classification is too rigid and limiting. We present evidence of the communicability of psychiatric disorders through three major pathways: infectious and ecological, familial, and sociocultural communicability. Successful strategies developed to control the spread of communicable infectious diseases are relevant to curtailing the communicability of psychiatric disorders, thereby reducing their burden. Current interventions and policies that conceptualise psychiatric illnesses as non-communicable mostly focus on the individual. By applying strategies from infectious disease and chronic illness prevention models within a socioecological framework, we posit a broad communicable chronic disease psychiatric illness control plan for effectively treating the patient with the psychiatric disorder (host) as early as possible, providing benefits to their family and the community, and preventing transmission to others.

Sex differences in the epidemiology and clinical presentation of trauma-related psychopathology have long been documented. Multiple underlying mechanisms have been examined, both psychosocial and biological. Among the most promising biological mechanisms are neural substrates of trauma-related psychopathology that have been uncovered in recent years. Neuroimaging studies of sex-related heterogeneity published over the past 3 years (2014–2017) demonstrate an interaction between sex and type, timing, and load of trauma exposure. These studies suggest that, for males, early trauma exposure may involve a loss of gray matter in the limbic system, including the prefrontal cortex (PFC), amygdala, and hippocampus, and an over-activity and increased connectivity of salience hubs, and particularly dorsal anterior cingulate cortex (dACC). For females, however, early trauma exposure may involve overactive and possibly an enlarged amygdala, as well as decreased connectivity of salience hubs such as the dACC. Underlying mechanisms may include interaction with several endocrine systems and result in differential neural response to naturally occurring and added endocrine ligands, as well as sex-specific genetic and epigenetic risk and resilience factors. This complex interaction between multiple biological systems may be associated with sex-specific behavioral patterns, in turn associated with trauma-related psychopathology. While substantial number of published studies present preliminary evidence for neural mechanisms of sex-specific posttraumatic responses, there is a paucity of research directly designed to examine sex as a biological factor in trauma-related psychopathology. Specific foci for future studies aiming to bridge current gaps in the literature are discussed.

Globally, the majority of those who need mental health care worldwide lack access to high-quality mental health services. Stigma, human resource shortages, fragmented service delivery models, and lack of research capacity for implementation and policy change contribute to the current mental health treatment gap. In this review, we describe how health systems in low- and middle-income countries (LMICs) are addressing the mental health gap and further identify challenges and priority areas for future research.Common mental disorders are responsible for the largest proportion of the global burden of disease; yet, there is sound evidence that these disorders, as well as severe mental disorders, can be successfully treated using evidence-based interventions delivered by trained lay health workers in low-resource community or primary care settings. Stigma is a barrier to service uptake. Prevention, though necessary to address the mental health gap, has not solidified as a research or programmatic focus. Research-to-practice implementation studies are required to inform policies and scale-up services. Four priority areas are identified for focused attention to diminish the mental health treatment gap and to improve access to high-quality mental health services globally: diminishing pervasive stigma, building mental health system treatment and research capacity, implementing prevention programs to decrease the incidence of mental disorders, and establishing sustainable scale up of public health systems to improve access to mental health treatment using evidence-based interventions.

Background Individuals with comorbid posttraumatic stress disorder and major depressive disorder (PTSD-MDD) often exhibit greater functional impairment and poorer treatment response than individuals with PTSD alone. Research has not determined whether PTSD-MDD is associated with different network connectivity abnormalities than PTSD alone. Methods We used functional magnetic resonance imaging (fMRI) to measure resting state functional connectivity (rs-FC) patterns of brain regions involved in fear and reward processing in three groups: patients with PTSD-alone (n = 27), PTSD-MDD (n = 21), and trauma-exposed healthy controls (TEHCs, n = 34). Based on previous research, seeds included basolateral amygdala (BLA), centromedial amygdala (CMA), and nucleus accumbens (NAcc). Results Regardless of MDD comorbidity, PTSD was associated with decreased connectivity of BLA-orbitalfrontal cortex (OFC) and CMA-thalamus pathways, key to fear processing, and fear expression, respectively. PTSD-MDD, compared to PTSD-alone and TEHC, was associated with decreased connectivity across multiple amygdala and striatal-subcortical pathways: BLA-OFC, NAcc-thalamus, and NAcc-hippocampus. Further, while both the BLA-OFC and the NAcc-thalamus pathways were correlated with MDD symptoms, PTSD symptoms correlated with the amygdala pathways (BLA-OFC; CMA-thalamus) only. Conclusions Comorbid PTSD-MDD may be associated with multifaceted functional connectivity alterations in both fear and reward systems. Clinical implications are discussed.

Social exclusion is ubiquitous and painful. Evolutionary models indicate sex differences in coping with social stress. Recent empirical data suggest different sex patterns in hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenal-medullary (SAM) reactivity. The present study sought to test this hypothesis.We examined differences in endocrine and emotional response to exclusion by using a virtual ball tossing paradigm (Cyberball). Saliva samples and mood ratings were collected to reflect levels before, and repeatedly following, exclusion.The sample included 21 women and 23 men. Cortisol and salivary alpha amylase (sAA), biomarkers of the HPA and SAM systems, respectively, were used as indices of two arms of stress response.Following exclusion, all participants experienced mood worsening followed by mood improvement, with men reporting less distress than women. Women evinced decline in cortisol following the Cyberball task, whereas men's cortisol levels showed a non-significant rise, and then decline, following exclusion.Our results concur with previous findings showing SAM reactivity to be gender-neutral and HPA reactivity to be gender-divergent. Additional studies are needed to examine sex-specific response to social exclusion. Implications for individual differences in recovery from stress are discussed.

Previous research associates smaller hippocampal volume with posttraumatic stress disorder (PTSD). It is unclear, however, whether treatment affects hippocampal volume or vice versa. Seventy-six subjects, 40 PTSD patients and 36 matched trauma-exposed healthy resilient controls, underwent clinical assessments and magnetic resonance imaging (MRI) at baseline, and 10 weeks later, during which PTSD patients completed ten weeks of Prolonged Exposure (PE) treatment. The resilient controls and treatment responders (n=23) had greater baseline hippocampal volume than treatment non-responders (n=17) (p=0.012 and p=0.050, respectively), perhaps due to more robust fear-extinction capacity in both the initial phase after exposure to trauma and during treatment.

Depressive symptoms cause major impairment and may accelerate HIV progression despite the use of antiretroviral medication. The somatic symptoms criteria for HIV infection and depression partially overlap, which can make differential diagnosis challenging. Because of chronic inflammation caused by HIV infection, HIV-positive patients may develop somatic and affective-cognitive symptoms of depression. Inflammation-related depression is primarily characterized with severe somatic symptoms such as fatigue and sleep disturbance. This study sought to explore the patterns of somatic and cognitive-affective depressive symptoms that characterize HIV-positive patients. Our specific aims were (1) to identify subtypes of depressive symptoms in a sample of HIV-positive patients; and (2) to test the subtypes’ difference on inflammatory and HIV disease progression biomarkers. HIV-positive men and women (N = 102) with and without depressive symptoms were randomly selected from an Italian HIV clinic. Depressive symptoms (PHQ-9), viral load (VL), CD4+, Il-6, TNF-α, and monocytes were assessed. The three subtypes formed using Latent Class Analysis (LCA) identified patients with (1) severe cognitive-affective and somatic depressive symptoms; (2) severe/moderate somatic symptoms; and (3) absent or low depressive symptoms. The subtype with severe/moderate somatic symptoms was characterized with elevated levels of Il-6 and monocytes. No difference on HIV progression biomarkers was found. The subtypes of depressive symptoms might help differentiating depressive symptoms from HIV- and inflammatory-related somatic symptoms. When present, cognitive-affective and/or somatic symptoms cause significant impairment to patients’ lives and thus warrant further assessment and treatment.

Posttraumatic stress (PTSS) and generalized anxiety symptoms (GAS) may ensue following trauma. While they are now thought to represent different psychopathological entities, it is not clear whether both GAS and PTSS show a dose-response to trauma exposure. The current study aimed to address this gap in knowledge and to investigate the moderating role of subjects' demographics in the exposure-outcome associations. The sample included 249 civilian adults, assessed during the 2014 Israel-Gaza military conflict. The survey probed demographic information, trauma exposure, and symptoms. PTSS but not GAS was associated with exposure severity. Women were at higher risk for both PTSS and GAS than men. In addition, several demographic variables were only associated with PTSS levels. PTSS dose-response effect was moderated by education. These findings are in line with emerging neurobiological and cognitive research, suggesting that although PTSS and GAS have shared risk factors they represent two different psychopathological entities. Clinical and theoretical implications are discussed.