Amygdala-related electroencephalogram neurofeedback as add-on therapy for treatment-resistant childhood sexual abuse posttraumatic stress disorder: feasibility study.

AIM: Childhood sexual abuse (CSA) among women is an alarmingly prevalent traumatic experience that often leads to debilitating and treatment-refractory posttraumatic stress disorder (PTSD), raising the need for novel adjunctive therapies. Neuroimaging investigations systematically report that amygdala hyperactivity is the most consistent and reliable neural abnormality in PTSD and following childhood abuse, raising the potential of implementing volitional neural modulation using neurofeedback (NF) aimed at down-regulating amygdala activity. This study aimed to reliably probe limbic activity but overcome the limited applicability of functional magnetic resonance imaging (fMRI) NF by using a scalable electroencephalogram NF probe of amygdala-related activity, termed amygdala electrical-finger-print (amyg-EFP) in a randomized controlled trial. METHOD: Fifty-five women with CSA-PTSD who were in ongoing intensive trauma-focused psychotherapy for a minimum of 1 year but still met Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) PTSD criteria were randomized to either 10 add-on sessions of amyg-EFP-NF training (test group) or continuing psychotherapy (control group). Participants were blindly assessed for PTSD symptoms before and after the NF training period, followed by self-reported clinical follow-up at 1, 3, and 6 months, as well as one session of amygdala real-time fMRI-NF before and after NF training period. RESULTS: Participants in the test group compared with the control group demonstrated a marginally significant immediate reduction in PTSD symptoms, which progressively improved during the follow-up period. In addition, successful neuromodulation during NF training was demonstrated. CONCLUSION: This feasibility study for patients with treatment-resistant CSA-PTSD indicates that amyg-EFP-NF is a viable and efficient intervention.

Reduced emotion regulatory selection flexibility in post-traumatic stress disorder: converging performance-based evidence from two PTSD populations.

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, ŋ²â‚š= 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, ŋ²â‚š= 0.114). CONCLUSIONS: Two studies provide converging evidence for reduced emotion regulatory selection flexibility in two PTSD populations.

Limbic self-neuromodulation as a novel treatment option for emotional dysregulation in premenstrual dysphoric disorder (PMDD); a proof-of-concept study.

AIM: To assess the efficacy of a novel neurofeedback (NF) method, targeting limbic activity, to treat emotional dysregulation related to premenstrual dysphoric disorder (PMDD). METHODS: We applied a NF probe targeting limbic activity using a functional magnetic resonance imaging-inspired electroencephalogram model (termed Amyg-EFP-NF) in a double-blind randomized controlled trial. A frontal alpha asymmetry probe (AAS-NF), served as active control. Twenty-seven participants diagnosed with PMDD (mean age = 33.57 years, SD = 5.67) were randomly assigned to Amyg-EFP-NF or AAS-NF interventions with a 2:1 ratio, respectively. The treatment protocol consisted of 11 NF sessions through three menstrual cycles, and a follow-up assessment 3 months thereafter. The primary outcome measure was improvement in the Revised Observer Version of the Premenstrual Tension Syndrome Rating Scale (PMTS-OR). RESULTS: A significant group by time effect was observed for the core symptom subscale of the PMTS-OR, with significant improvement observed at follow-up for the Amyg-EFP group compared with the AAS group [F(1, 15)=4.968, P = 0.042]. This finding was specifically robust for reduction in anger [F(1, 15) = 22.254, P < 0.001]. A significant correlation was found between learning scores and overall improvement in core symptoms (r = 0.514, P = 0.042) suggesting an association between mechanism of change and clinical improvement. CONCLUSION: Our preliminary findings suggest that Amyg-EFP-NF may serve as an affordable and accessible non-invasive treatment option for emotional dysregulation in women suffering from PMDD. Our main limitations were the relatively small number of participants and the lack of a sham-NF placebo arm.

Structural brain features signaling trauma, PTSD, or resilience? A systematic exploration.

BACKGROUND: 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. AIMS: 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. MATERIALS & METHODS: 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. RESULTS: 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. DISCUSSION & CONCLUSION: Findings support the existence of structural brain markers of resilience.

Cognitive processing of emotional information during menstrual phases in women with and without postpartum depression: differential sensitivity to changes in gonadal steroids.

Gonadal steroids (GSs) have been repeatedly shown to play a central role in the onset of postpartum depression (PPD). The underlying mechanisms, however, are only partially understood. We investigated the relationship between cognitive processing of emotional information and naturally occurring hormonal fluctuations in women with and without previous PPD. Euthymic, parous women, with a history (hPPD, n=32) and without a history (nhPPD, n=43) of PPD, were assessed during late-follicular and late-luteal phases. Participants were administered cognitive tasks assessing attention (dot-probe; emotional Stroop), evaluation (self-referential encoding) and incidental recall, and self-report measures. Menstrual-phase-specific differences were found between late-follicular vs. late-luteal phases among hPPD only, with depression-associated patterns observed in the late-luteal phase on the self-referential encoding and incidental recall task and emotional Stroop task, but not on the dot-probe task. No main effect for menstrual phase was found on any of the tasks or questionnaires, apart from the brooding component of rumination. Women with hPPD demonstrate a differential bias in cognitive processing of emotional information that is menstrual phase dependent, and did not correspond to similar difference in mood symptoms. These biases may reflect sensitivity to gonadal steroid fluctuations that are associated with PPD.

Why place and space matter for intimate partner violence survivors' mental wellbeing and communities in Northeastern Uganda.

The context of place matters for mental health. Employing a feminist framework, this study used key informant interviews and focus group discussions in May 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.

Bias-contingent attention bias modification and attention control training in treatment of PTSD: a randomized control trial.

BACKGROUND: Randomized 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. METHODS: Fifty 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. RESULTS: ACT 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. CONCLUSIONS: The 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.

Exposure-based therapy changes amygdala and hippocampus resting-state functional connectivity in patients with posttraumatic stress disorder.

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: A total of 24 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 pretreatment 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.

Altered resting state functional connectivity of fear and reward circuitry in comorbid PTSD and major depression.

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.

Sex Differences in Trauma-Related Psychopathology: a Critical Review of Neuroimaging Literature (2014-2017).

PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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.

Challenges and Opportunities in Global Mental Health: a Research-to-Practice Perspective.

PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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.

PTSD REMISSION AFTER PROLONGED EXPOSURE TREATMENT IS ASSOCIATED WITH ANTERIOR CINGULATE CORTEX THINNING AND VOLUME REDUCTION.

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.

Posttraumatic symptom structure across age groups.

The applicability of diagnostic criteria of Posttraumatic Stress Disorder to the pediatric population has been a focus of much debate (e.g., Carrion, Weems, Ray, & Reiss, 2002 ), informing changes in the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5). The current study examined the factor structure of posttraumatic distress among adult versus pediatric samples using confirmatory factor analysis. The analysis was performed on the DSM-IV-adherent Posttraumatic Diagnostic Scale (Foa, Cashman, Jaycox, & Perry, 1997 ) and Child Posttraumatic Symptom Scale (Foa, Johnson, Feeny, & Treadwell, 2001 ). The sample included 378 adult and 204 child and adolescent victims of diverse single-event traumas. A series of models based on previous findings and DSM-IV specification were evaluated. A 4-factor model (Intrusions, Avoidance, Dysphoria, and Hyperarousal), similar to the DSM-5 model, best fit the data among adults, and a different 4-factor model (Intrusion, Avodiance, Numbing, and Hyperarousal) best fit the data among children and adolescents. Despite some similarity, the posttraumatic symptom profiles of pediatric and adult samples may differ. These differences are not fully incorporated into the DSM-5, and warrant further examination.

Integration of limbic self-neuromodulation with psychotherapy for complex post-traumatic stress disorder: treatment rationale and case study.

Treatment Rationale: Exposure to repeated sexual trauma, particularly during childhood, often leads to protracted mental health problems. Childhood adversity is specifically associated with complex posttraumatic stress disorder (PTSD) presentation, which is particularly tenacious and treatment refractory, and features severe emotion dysregulation. Augmentation approaches have been suggested to enhance treatment efficacy in PTSD thus integrating first-line psychotherapy with mechanistically informed self-neuromodulation procedures (i.e. neurofeedback) may pave the way to enhanced clinical outcomes. A central neural mechanism of PTSD and emotion dysregulation involves amygdala hyperactivity that can be volitionally regulated by neurofeedback. We outline a treatment rationale that includes a detailed justification for the potential of combining psychotherapy and NF and delineate mechanisms of change. We illustrate key processes of reciprocal interactions between neurofeedback engagement and therapeutic goals.Case Study: We describe a clinical case of a woman with complex PTSD due to early and repetitive childhood sexual abuse using adjunctive neurofeedback as an augmentation to an ongoing, stable, traditional treatment plan. The woman participated in (a) ten sessions of neurofeedback by the use of an fMRI-inspired EEG model of limbic related activity (Amygdala Electrical-Finger-Print; AmygEFP-NF), (b) traditional weekly individual psychotherapy, (c) skills group. Before and after NF training period patient was blindly assessed for PTSD symptoms, followed by a 1, 3- and 6-months self-report follow-up. We demonstrate mechanisms of change as well as the clinical effectiveness of adjunctive treatment as indicated by reduced PTSD symptoms and improved daily functioning within this single case.Conclusions: We outline an integrative neuropsychological framework for understanding the unique mechanisms of change conferring value to conjoining NF applications with trauma-focused psychotherapy in complex PTSD.

Self-neuromodulation procedures that regulates limbic-related activity in adjunction to therapy show clinical effectivity in complex PTSD.We present an integrative perspective of neurofeedback embedded in psychotherapy, illustrated by a single case report.A single case provides an illustration of the potential utility of multifaced treatment including psychotherapy with adjunctive neurofeedback.

On the stress of being a woman: The synergistic contribution of sex as a biological variable and gender as a psychosocial one to risk of stress-related disorders.

Stress-related disorders (SRD) disproportionately affect women. Cortisol blunting, a failure to demonstrate a typical rise and fall of cortisol in response to stress, is associated with SRDs and has been found to be more pronounced among women. Cortisol blunting relates to both sex as a biological variable (SABV; e.g., estrogens and their fluctuations, impact on neural circuits) and gender as a psychosocial variable (GAPSV; e.g., discrimination, harassment, gender roles). I suggest a theoretical model linking experience, sex- and gender-related factors, and neuroendocrine substrates of SRD to the heightened risk among women. The model thus bridges multiple gaps in the literature to create a synergistic conceptual framework with which to understand the stress of being a woman. Utilizing such a framework in research may allow identifying targeted, sex-and gender-dependent risk factors, informing psychological treatment, medical advice, educational and community programming, and policy.

Underlying Hippocampal Mechanism of Posttraumatic Stress Disorder Treatment Outcome: Evidence From Two Clinical Trials.

Background: The hippocampus plays an important role in the pathophysiology of posttraumatic stress disorder (PTSD) and its prognosis. Accumulating findings suggest that individuals with larger pretreatment hippocampal volume are more likely to benefit from PTSD treatment, but the mechanism underlying this effect is unknown. We investigated whether further increase in hippocampal volume during treatment explains the better prognosis of individuals with greater pretreatment hippocampal volume. Methods: We collected structural magnetic resonance imagesfrom patients with PTSD before and after treatment. We examined whether larger hippocampal volume moderates the effect of increased hippocampal volume during treatment on symptom reduction. Given the relatively small sample sizes of treatment studies with pre- and posttreatment magnetic resonance imaging, we focused on effect sizes and sought to replicate findings in an external sample. We tested our hypothesis in study 1 (N = 38; prolonged exposure therapy) and then tested whether the results could be externally replicated in study 2 (N = 20; ketamine infusion followed by exposure therapy). Results: Findings from study 1 revealed that increased right hippocampal volume during treatment was associated with greater PTSD symptom reduction only in patients with greater pretreatment right hippocampal volume (p = .03; η2 = 0.13, a large effect). Findings were partially replicated in study 2 for depressive symptoms (p = .034; η2 = 0.25, a very large effect) and for PTSD symptoms (p = .15; η2 = 0.15, a large effect). Conclusions: Elucidating increased hippocampal volume as one of the neural mechanisms predictive of therapeutic outcome for individuals with larger pretreatment hippocampal volume may help identify clinical targets for this subgroup.

Postpartum post-traumatic stress symptoms during the COVID-19 period: exposure and fear as mediating factors.

Background: Post-traumatic stress symptoms (PTSS) following childbirth are common within a stressful environment and are mitigated by social support. During the COVID-19 pandemic, an increase in such symptoms has been reported. The current study aims to longitudinally model the influence of general and pandemic-specific risk and protective factors on the temporal unfolding of symptoms among postpartum women.Methods: Participants were 226 women following a liveborn, term birth during the first lockdown in Israel. Participants completed questionnaires 10 weeks (T1) and 6 months (T2) after delivery. PATH analyses included predictors of symptoms in T1: demographics, exposure to traumatic events, medical complications during delivery or pregnancy, exposure to COVID-19-related events and their subjective impact, fear of COVID-19, and social support. Predictors of symptoms in T2 were: T1 predictors, both as direct effects and mediated by T1 PTSS, as well as predictors measured again in T2.Results: Results showed the suggested model fit the data. The effect of COVID-19-related fear and subjective impact at T1 on symptoms at T2 were fully mediated by PTSS in T1, as were the effects of marriage and high social support at T1. COVID-19-related fear at T2 positively predicted symptoms at T2, while social support at T2 had the opposite effect. Medical complications during pregnancy negatively predicted symptoms in T2 only.Discussion: Persistent fear appears to be a risk factor and supports a consistent buffer in postpartum PTSS during the COVID-19 pandemic. Medical complications during pregnancy served as a protective factor, possibly due to habituation to medical settings.

Post-traumatic stress symptoms (PTSS) following childbirth during the COVID-19 pandemic may unfold in a unique manner, relating to pandemic-related stressors and fears.Women who experience stressful pandemic-related events are not at heightened risk of developing PTSS within the six months following birth, but those reporting COVID-19 related fears are.Women who had medical complications during pregnancy, but not delivery, are at lower risk of developing subsequent PTSS, perhaps due to their ongoing contact with medical facilities despite the pandemic.

Neurobiological Alterations in Females With PTSD: A Systematic Review.

Most females experience at least one traumatic event in their lives, but not all develop PTSD. Despite considerable research, our understanding of the key factors that constitute risk for PTSD among females is limited. Previous research has largely focused on sex differences, neglecting within group comparisons, thereby obviating differences between females who do and do not develop PTSD following exposure to trauma. In this systematic review, we conducted a search for the extent of existing research utilizing magnetic resonance imaging (MRI) to examine neurobiological differences among females of all ages, with and without PTSD. Only studies of females who met full diagnostic criteria for PTSD were included. Fifty-six studies were selected and reviewed. We synthesized here findings from structural MRI (sMRI), functional MRI (fMRI), diffusion tensor imaging (DTI), and resting state functional connectivity (rs-FC MRI) studies, comparing females with and without PTSD. A range of biopsychosocial constructs that may leave females vulnerable to PTSD were discussed. First, the ways timing and type of exposure to trauma may impact PTSD risk were discussed. Second, the key role that cognitive and behavioral mechanisms may play in PTSD was described, including rumination, and deficient fear extinction. Third, the role of specific symptom patterns and common comorbidities in female-specific PTSD was described, as well as sex-specific implications on treatment and parenting outcomes. We concluded by identifying areas for future research, to address the need to better understand developmental aspects of brain alterations, the differential impact of trauma types and timing, the putative role of neuroendocrine system in neurobiology of PTSD among females, and the impact of social and cultural factors on neurobiology in females with PTSD.

Postpartum Depression in COVID-19 Days: Longitudinal Study of Risk and Protective Factors.

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.