Pharmacotherapy for social anxiety disorder (SAnD).
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ABSTRACT:
SUBMITTER: Williams T
PROVIDER: S-EPMC6360927 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Social anxiety disorder (SAD) is highly prevalent and associated with high levels of impairment and distress. Therapies for SAD leave many patients symptomatic at the end of treatment, and little is known about predictors or mechanisms of treatment outcome. Given the interpersonal dysfunction fundamental to SAD, this study investigated whether prominent interpersonal features of SAD (submissive behavior, childhood maltreatment, suppression of anger, and depression) predicted attrition and response to pharmacotherapy and whether the working alliance mediated these relationships. This is the first study to examine the role of the working alliance in pharmacotherapy for SAD. One hundred thirty-eight treatment-seeking individuals with a primary diagnosis of SAD received 12 weeks of open treatment with paroxetine. Higher levels of depression predicted greater severity of SAD at the end of treatment, and higher levels of submissive behavior and childhood emotional maltreatment predicted a greater probability of attrition from treatment. The psychiatrist-assessed working alliance mediated response to pharmacotherapy for individuals who reported a history of emotional maltreatment. These results identify variables that predict pharmacotherapy outcome and emphasize the importance of the working alliance as a mechanism of treatment response for those with a history of emotional maltreatment. Implications for person-specific treatment selection are discussed.
| S-EPMC5689479 | biostudies-literature
Project description:Social anxiety disorder (SAD) is a psychiatric disorder characterized by extensive fear in social situations. Multiple genetic and environmental factors are known to contribute to its pathogenesis. One of the main environmental risk factors is early life adversity (ELA). Evidence is emerging that epigenetic mechanisms such as DNA methylation might play an important role in the biological mechanisms underlying SAD and ELA. To investigate the relationship between ELA, DNA methylation, and SAD, we performed an epigenome-wide association study for SAD and ELA examining DNA from whole blood of a cohort of 143 individuals using DNA methylation arrays. We identified two differentially methylated regions (DMRs) associated with SAD located within the genes SLC43A2 and TNXB. As this was the first epigenome-wide association study for SAD, it is worth noting that both genes have previously been associated with panic disorder. Further, we identified two DMRs associated with ELA within the SLC17A3 promoter region and the SIAH3 gene and several DMRs that were associated with the interaction of SAD and ELA. Of these, the regions within C2CD2L and MRPL28 showed the largest difference in DNA methylation. Lastly, we found that two DMRs were associated with both the severity of social anxiety and ELA, however, neither of them was found to mediate the contribution of ELA to SAD later in life. Future studies are needed to replicate our findings in independent cohorts and to investigate the biological pathways underlying these effects.
2021-01-31 | GSE164056 | GEO
Project description:BackgroundDespite considerable effort, the neurobiological underpinnings of hyper-responsive threat processing specific to patients suffering from generalized anxiety disorder (GAD) remain poorly understood. The current functional magnetic resonance imaging (fMRI) study aims to delineate GAD-specific brain activity during immediate threat processing by comparing GAD patients to healthy controls (HC), to social anxiety disorder (SAD) and to panic disorder (PD) patients.MethodBrain activation and functional connectivity patterns to threat vs. neutral pictures were investigated using event-related fMRI. The sample consisted of 21 GAD, 21 PD, 21 SAD and 21 HC.ResultsGAD-specific elevated activity to threat vs. neutral pictures was found in cingulate cortex, dorsal anterior insula/frontal operculum (daI/FO) and posterior dorsolateral prefrontal cortex (dlPFC). Defining these effects as seed regions, we detected GAD-specific increased functional connectivity to threat vs. neutral pictures between posterior dlPFC and ventrolateral prefrontal cortex, between cingulate cortex and amygdala, between cingulate cortex and anterior insula, as well as decreased functional connectivity between daI/FO and mid-dlPFC.ConclusionThe findings present the first evidence for GAD-specific neural correlates of hyper-responsive threat processing, possibly reflecting exaggerated threat sensitivity, maladaptive appraisal and attention-allocation processes.
| S-EPMC5065042 | biostudies-literature
Project description:Conventional cognitive-behavioral therapy for social anxiety disorder, which is closely based on the treatment for depression, has been shown to be effective in numerous randomized placebo-controlled trials. Although this intervention is more effective than waitlist control group and placebo conditions, a considerable number of clients do not respond to this approach. Newer approaches include techniques specifically tailored to this particular population. One of these techniques, social mishap exposure practice, is associated with significant improvement in treatment gains. We will describe here the theoretical framework for social mishap exposures that addresses the client's exaggerated estimation of social cost. We will then present clinical observations and outcome data of a client who underwent treatment that included such social mishap exposures. Findings are discussed in the context of treatment implications and directions for future research.
| S-EPMC4238930 | biostudies-literature
Project description:Social anxiety disorder symptoms are generally proposed to be related to broad temperamental vulnerabilities (e.g., a low level of approach and high level of avoidance temperament), specific psychological vulnerabilities (e.g., fears of negative and positive evaluation), and additional disorders (e.g., major depressive disorder). However, existing tests of such a model have either not considered depressive symptoms or relied on samples of undergraduates. We examined these and related questions via a latent variable model in a large dataset (N=2253) that combined participants across a variety of studies. The model had adequate fit in the whole sample, and good fit in a subsample in which more participants completed the depression measure. The model indicated that low level of approach and high level of avoidance temperament contributed to fears of evaluation and social anxiety symptoms, and that fears of evaluation additionally contributed independently to social anxiety symptoms. The relationship between social anxiety and depressive symptoms was entirely accounted for by these vulnerabilities: Depressive symptoms were only predicted by avoidance temperament.
| S-EPMC5346047 | biostudies-literature
Project description:Attention bias to threat (selective attention toward threatening stimuli) has been frequently found in anxiety disorder samples, but its distribution both within and beyond this category is unclear. Attention bias has been studied extensively in social anxiety disorder (SAD) but relatively little in obsessive compulsive disorder (OCD), historically considered an anxiety disorder, or anorexia nervosa (AN), which is often characterized by interpersonal as well as body image/eating fears.Medication-free adults with SAD (n = 43), OCD (n = 50), or AN (n = 30), and healthy control volunteers (HC, n = 74) were evaluated for attention bias with an established dot probe task presenting images of angry and neutral faces. Additional outcomes included attention bias variability (ABV), which summarizes fluctuation in attention between vigilance and avoidance, and has been reported to have superior reliability. We hypothesized that attention bias would be elevated in SAD and associated with SAD severity.Attention bias in each disorder did not differ from HC, but within the SAD group attention bias correlated significantly with severity of social avoidance. ABV was significantly lower in OCD versus HC, and it correlated positively with severity of OCD symptoms within the OCD group.Findings do not support differences from HC in attention bias to threat faces for SAD, OCD, or AN. Within the SAD sample, the association of attention bias with severity of social avoidance is consistent with evidence that attention bias moderates development of social withdrawal. The association of ABV with OCD diagnosis and severity is novel and deserves further study.
| S-EPMC4891283 | biostudies-other
Project description:Social anxiety disorder (SAD) is a major health concern with high lifetime prevalence. The current medication is rather unspecific and, despite considerable efforts, its efficacy is still unsatisfactory. However, there are no appropriate and specific animal models available to study the underlying etiology of the disorder. Therefore, we aimed to establish a model of specific social fear in mice and use this social fear conditioning (SFC) model to assess the therapeutic efficacy of the benzodiazepine diazepam and of the antidepressant paroxetine; treatments currently used for SAD patients. We show that by administering electric foot shocks (2-5, 1?s, 0.7?mA) during the investigation of a con-specific, the investigation of unfamiliar con-specifics was reduced for both the short- and long-term, indicating lasting social fear. The induced fear was specific to social stimuli and did not lead to other behavioral alterations, such as fear of novelty, general anxiety, depression, and impaired locomotion. We show that social fear was dose-dependently reversed by acute diazepam, at doses that were not anxiolytic in a non-social context, such as the elevated plus maze. Finally, we show that chronic paroxetine treatment reversed social fear. All in all, we demonstrated robust social fear after exposure to SFC in mice, which was reversed with both acute benzodiazepine and chronic antidepressant treatment. We propose the SFC model as an appropriate animal model to identify the underlying etiology of SAD and possible novel treatment approaches.
| S-EPMC3327848 | biostudies-other
Project description:Cognitive-behavioral therapy (CBT) for social anxiety disorder (SAD) may decrease social anxiety by training emotion regulation skills. This randomized controlled trial of CBT for SAD examined changes in weekly frequency and success of cognitive reappraisal and expressive suppression, as well as weekly intensity of social anxiety among patients receiving 16 weekly sessions of individual CBT. We expected these variables to (1) differ from pre-to-post-CBT vs. Waitlist, (2) have differential trajectories during CBT, and (3) covary during CBT. We also expected that weekly changes in emotion regulation would predict (4) subsequent weekly changes in social anxiety, and (5) changes in social anxiety both during and post-CBT. Compared to Waitlist, CBT increased cognitive reappraisal frequency and success, decreased social anxiety, but had no impact on expressive suppression. During CBT, weekly cognitive reappraisal frequency and success increased, whereas weekly expressive suppression frequency and social anxiety decreased. Weekly decreases in social anxiety were associated with concurrent increases in reappraisal success and decreases in suppression frequency. Granger causality analysis showed that only reappraisal success increases predicted decreases in subsequent social anxiety during CBT. Reappraisal success increases pre-to-post-CBT predicted reductions in social anxiety symptom severity post-CBT. The trajectory of weekly changes in emotion regulation strategies may help clinicians understand whether CBT is effective and predict decreases in social anxiety.NCT00380731; http://www.clinicaltrials.gov/ct2/show/NCT00380731?term=social+anxiety+cognitive+behavioral+therapy+Stanford&rank=1.
| S-EPMC4136443 | biostudies-literature
Project description:An imbalance in the neural motivational system may underlie Social Anxiety Disorder (SAD). This study examines social reward and punishment anticipation in SAD, predicting a valence-specific effect: increased striatal activity for punishment avoidance compared to obtaining a reward. Individuals with SAD (n = 20) and age, gender, and education case-matched controls (n = 20) participated in a functional magnetic resonance imaging (fMRI) study. During fMRI scanning, participants performed a Social Incentive Delay (SID) task to measure the anticipation of social reward and punishment. The left putamen (part of the striatum) showed a valence-specific interaction with group after correcting for medication use and comorbidity. The control group showed a relatively stronger activation for reward vs. punishment trials, compared to the social anxiety group. However, post-hoc pairwise comparisons were not significant, indicating that the effect is driven by a relative difference. A connectivity analysis (Psychophysiological interaction) further revealed a general salience effect: SAD patients showed decreased putamen-ACC connectivity compared to controls for both reward and punishment trials. Together these results suggest that the usual motivational preference for social reward is absent in SAD. In addition, cortical control processes during social incentive anticipation may be disrupted in SAD. These results provide initial evidence for altered striatal involvement in both valence-specific and valence-nonspecific processing of social incentives, and stress the relevance of taking motivational processes into account when studying social anxiety.
| S-EPMC4283602 | biostudies-literature
Project description:BACKGROUND:We used network analyses to examine symptoms that may play a role in the co-occurrence of social anxiety disorder (SAD) and major depressive disorder (MDD). Whereas latent variable models examine relations among latent constructs, network analyses have the advantage of characterizing direct relations among the symptoms themselves. METHOD:We conducted network modeling on symptoms of social anxiety and depression in a clinical sample of 130 women who met criteria for SAD, MDD, both disorders, or had no lifetime history of mental illness. RESULTS:In the resulting network, the core symptoms of social fear and depressed mood appeared at opposite ends of the network and were weakly related; so-called "bridges" between these symptoms appeared to occur via intervening variables. In particular, the worthless variable appeared to play a central role in the network. LIMITATIONS:Because our data were cross-sectional, we are unable to draw conclusions about the direction of these effects or whether these variables are related to each other prospectively. CONCLUSIONS:Continued testing of these pathways using longitudinal data will help facilitate the development of more effective clinical interventions for these disorders.
| S-EPMC6202058 | biostudies-literature