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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.

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.

There is growing evidence that cognitive-behavioral therapy (CBT) is an effective method for treating posttraumatic stress in toddlers and preschoolers. However, implementing CBT in this population requires cognitive case conceptualization (CCC) that incorporates evidence-based methods to assess factors contributing to onset and maintenance of presenting problems and to guide treatment selection in a developmentally appropriate manner. The present article presents a developmentally focused model of CCC (DCCC) for the assessment and treatment of toddlers and preschoolers. The model elaborates on the relational context of posttraumatic symptomatology, and emphasizes the cognitive mechanisms within the toddler–parent relations matrix. A case conceptualization example illustrates the use of DCCC with a toddler who experienced a medical trauma followed by a brief description of the treatment and its outcomes. Therapists working with toddlers and preschoolers may find the DCCC model an appropriate guiding map t...

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

Traumatic events have potentially debilitating long-lasting effects on the child's normal development and, therefore, should be effectively treated. Prolonged Exposure (PE) therapy has been found to be effective in reducing posttraumatic stress disorder symptoms in adults and in adolescents (e.g., Gilboa-Schechtman et al., 2010; Nacasch et al., 2011). It has not yet been tested in toddlers. This paper presents a detailed description of four cases of PE therapy adapted to toddlers and their parents whose posttraumatic stress symptoms developed following invasive medical procedures. Treatment consisted of several active components that were tailored specifically for the treatment of toddlers: psychoeducation about trauma, recounting scenes from the traumatic events, and in-vivo exposures to associated feared stimuli and triggers. The treatments resulted in substantial improvement in the toddlers and in their parents. At the time of treatment termination all toddlers had lost the posttraumatic stress disorder diagnosis and resumed normal functioning. These case studies provide preliminary clinical evidence for the efficacy of PE in toddlers. Conclusions, limitations, and suggestions for future research regarding the treatment of toddlers with PTSD and their parents following medical procedures are discussed.

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.

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.

We examined implicit and explicit self-evaluations (SEs) and their relation to social anxiety. So far, research indicated that individuals high in social anxiety consistently report low explicit SE, while concurrently exhibiting high implicit SE. To understand this pattern, we highlight the distinctions between the domains of social rank and of affiliation. In Study 1, participants (N = 113) completed a self-report measure of global SE, as well as self-ratings of social rank and affiliation measures. In Study 2 (N = 84), implicit measures (based on self-IAT, Implicit Association Task, Greenwald & Farnham, 2000) versions of social rank and affiliation SE were added. In both Study 1 and Study 2, severity of social anxiety was negatively associated with social rank, but not affiliation SEs, over and above the association with depression and global SE. In Study 2, social anxiety severity was negatively associated with explicit and implicit measures of social rank above and beyond the influence of general SE, ...

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.

We evaluated the psychometric properties of the Hebrew version of the Child Posttraumatic Symptom Scale (CPSS), a self-report measure assessing the severity of posttraumatic distress in youth. Participants (N= 156, ages 8-18) were treatment-seeking victims of diverse traumas. Internal consistency of the Hebrew version in these data was .91 for the total score, .77 for intrusion, .67 for avoidance, and .72 for arousal, similar to the original version. Test-retest reliability over 1 week in a subsample of 45 was r = .81. The point biserial correlation with a clinician-based diagnosis of PTSD was .54. Other convergent and divergent relationships expand the existing literature on the measure and support it as a valuable assessment tool for children exposed to traumatic events.

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.

Two evolutionarily designed systems govern the way we navigate the vagaries of the social world: the affiliation biobehavioral system and the social rank biobehavioral system. We suggest that social anxiety is characterized by (1) a thin-skinned disposition to matters of social rank; (2) a propensity to respond to social rank changes by lowering one’s social profile; and (3) an enhanced coupling of the affiliation and the social rank systems. We review a diverse set of findings suggesting that social rank sensitivity, reactivity, and coupling are evident in the perception and expression of emotional signals, impression formation, self-presentations in virtual social networks, reactions to changes in social rank (subjective, hormonal), and reactions to changes in belongingness. We argue that the evolutionary conceptual framework is uniquely positioned to seamlessly integrate findings from diverse disciplines and to inform and direct empirical research on social anxiety.