Activity

CSA was linked to greater disorganization scores that were associated with higher scores of emotion dysregulation. Emotion dysregulation was in turn associated with increased severity of dissociation symptoms in preschool children one year later. LIMITATIONS Given that attachment and emotion dysregulation were both assessed at T1, the temporal sequencing of mediators remains to be validated in a longitudinal design. CONCLUSIONS Findings highlight the relevance of fostering healthy parent-child relationships, as well as the development of optimal emotion regulation skills in young CSA victims to prevent the emergence of dissociation symptoms in this vulnerable population. BACKGROUND Current brain-based theoretical models of generalized anxiety disorder (GAD) suggest a dysfunction of amygdala-ventromedial prefrontal cortex emotional regulatory mechanisms. These alterations might be reflected by an altered resting state functional connectivity between both areas and could extend to vulnerable non-clinical samples such as high worriers without a GAD diagnosis. However, there is a lack of information in this regard. METHODS We investigated differences in resting state functional connectivity between the basolateral amygdala and the ventromedial prefrontal cortex (amygdala-vmPFC) in 28 unmedicated participants with GAD, 28 high-worriers and 28 low-worriers. We additionally explored selected clinical variables as predictors of amygdala-vmPFC connectivity, including anxiety sensitivity. RESULTS GAD participants presented higher left amygdala-vmPFC connectivity compared to both groups of non-GAD participants, and there were no differences between the latter two groups. In our exploratory analyses, concerns about the cognitive consequences of anxiety (the cognitive dimension of anxiety sensitivity) were found to be a significant predictor of the left amygdala-vmPFC connectivity. LIMITATIONS The cross-sectional nature of our study preclude us from assessing if functional connectivity measures and anxiety sensitivity scores entail an increased risk of GAD. CONCLUSIONS These results suggest a neurobiological qualitative distinction at the level of the amygdala-vmPFC emotional-regulatory system in GAD compared to non-GAD participants, either high- or low-worriers. At this neural level, they question previous hypotheses of continuity between high worries and GAD development. Instead, other anxiety traits such as anxiety sensitivity might confer a greater proneness to the amygdala-vmPFC connectivity alterations observed in GAD. V.BACKGROUND Recent research has linked emotion dysregulation with increases in subjective ratings of negative affect (NA reactivity) to trauma reminders, a central symptom of posttraumatic stress disorder (PTSD). The current study adds to this burgeoning line of research by exploring elicited PTSD symptoms as a mechanism explicating the relation between emotion dysregulation and NA reactivity following trauma cue exposure. METHODS Participants were 60 treatment-seeking marijuana users with insomnia symptoms who reported exposure to a traumatic event. Participants were administered questionnaires assessing emotion dysregulation, PTSD symptoms, and NA prior to and/or after listening to a personalized trauma script, and subsequently completed a diagnostic interview. RESULTS Results demonstrated that greater emotion dysregulation was associated with heightened NA reactivity through re-experiencing symptoms, but not avoidance or dissociation symptoms, even after accounting for past 30-day PTSD symptom severity and pre-trauma script NA. These effects were driven by the dimensions of emotion dysregulation characterized by nonacceptance of negative emotions and limited access to effective emotion regulation strategies. LIMITATIONS This study requires replication among other clinical samples, and is limited by use of self-report measures. CONCLUSIONS Findings provide novel empirical support for one mechanism through which emotion dysregulation may confer vulnerability to PTSD symptomology, and offer implications for refining PTSD treatments. BACKGROUND Positive reappraisal and distancing are two distinct cognitive reappraisal strategies for emotion regulation. Critically however, research examining the impact of elevated trait anxiety on cognitive reappraisal has often conflated these strategies. FPSZM1 Thus, the present study investigated whether high-trait-anxious (HTA) women can effectively utilize positive reappraisal and distancing to regulate emotional responses to negative stimuli. METHODS Twenty-six HTA women and twenty-seven low-trait-anxious (LTA) women were investigated in a self-generated reappraisal paradigm. Subjective measures of emotional regulation and event-related potentials (ERPs) were recorded while participants were instructed to passively view neutral or negative pictures, or to reinterpret negative pictures in a positive way (positive reappraisal) or a detached and unemotional way (distancing). RESULTS HTA women, as compared to LTA women, reported smaller reductions in negative affect after positive reappraisal and smaller reductions in emotional arousal after distancing. Though ERP data did not reveal corresponding differences in the centro-parietal late positive potential during emotion regulation, data did reveal HTA women exhibited enhanced recruitment of cognitive control during positive reappraisal and greater preparatory processing before engaging in distancing. LIMITATIONS Future research should examine the generalizability of the present results in clinical anxiety individuals, male sample and other reappraisal strategies. CONCLUSIONS Overall, HTA women appeared to recruit more cortical resources, suggestive of compensatory mechanisms, to achieve a similar performance as LTA women when engaging in positive reappraisal and distancing strategies to regulate negative emotions. Therefore, the findings demonstrate that HTA women are characterized by the inefficient implementation of positive reappraisal and distancing strategies. BACKGROUND Adverse events (AEs) are known to occur while patients are treated with placebos, part of the so-called nocebo effect. Yet evidence is limited regarding the likelihood that specific AEs occurring with antidepressant treatment are or are not due to nocebo effects. METHODS This study identified 56 placebo-controlled, randomized controlled trials (RCTs) of antidepressant monotherapy for adults with major depressive disorder that reported AE rates in sufficient detail for comparison. Poisson regression analyses compared rates of AEs according to antidepressant class weighted by study population to determine which separated from placebo. A “nocebo index” was also calculated (with 0 defined as the lowest rate and 1 or higher indicating the same or greater rate of an AE in the placebo group). RESULTS Numerous AEs did not differ statistically between antidepressant classes and placebo including worsening psychiatric symptoms, all forms of pain, weight gain and respiratory symptoms. Nevertheless, a number of AEs were significantly more common in antidepressants than placebos across multiple antidepressant classes.