Volume of subcortical brain regions in social anxiety disorder: mega-analytic results from 37 samples in the ENIGMA-Anxiety Working Group.

There is limited convergence in neuroimaging investigations into volumes of subcortical brain regions in social anxiety disorder (SAD). The inconsistent findings may arise from variations in methodological approaches across studies, including sample selection based on age and clinical characteristics. The ENIGMA-Anxiety Working Group initiated a global mega-analysis to determine whether differences in subcortical volumes can be detected in adults and adolescents with SAD relative to healthy controls. Volumetric data from 37 international samples with 1115 SAD patients and 2775 controls were obtained from ENIGMA-standardized protocols for image segmentation and quality assurance. Linear mixed-effects analyses were adjusted for comparisons across seven subcortical regions in each hemisphere using family-wise error (FWE)-correction. Mixed-effects d effect sizes were calculated. In the full sample, SAD patients showed smaller bilateral putamen volume than controls (left: d = -0.077, pFWE = 0.037; right: d = -0.104, pFWE = 0.001), and a significant interaction between SAD and age was found for the left putamen (r = -0.034, pFWE = 0.045). Smaller bilateral putamen volumes (left: d = -0.141, pFWE < 0.001; right: d = -0.158, pFWE < 0.001) and larger bilateral pallidum volumes (left: d = 0.129, pFWE = 0.006; right: d = 0.099, pFWE = 0.046) were detected in adult SAD patients relative to controls, but no volumetric differences were apparent in adolescent SAD patients relative to controls. Comorbid anxiety disorders and age of SAD onset were additional determinants of SAD-related volumetric differences in subcortical regions. To conclude, subtle volumetric alterations in subcortical regions in SAD were detected. Heterogeneity in age and clinical characteristics may partly explain inconsistencies in previous findings. The association between alterations in subcortical volumes and SAD illness progression deserves further investigation, especially from adolescence into adulthood.

Baseline reward processing and ventrostriatal dopamine function are associated with pramipexole response in depression.

The efficacy of dopamine agonists in treating major depressive disorder has been hypothesized to stem from effects on ventrostriatal dopamine and reward function. However, an important question is whether dopamine agonists are most beneficial for patients with reward-based deficits. This study evaluated whether measures of reward processing and ventrostriatal dopamine function predicted response to the dopamine agonist, pramipexole (ClinicalTrials.gov Identifier: NCT02033369). Individuals with major depressive disorder (n = 26) and healthy controls (n = 26) (mean ± SD age = 26.5 ± 5.9; 50% female) first underwent assessments of reward learning behaviour and ventrostriatal prediction error signalling (measured using functional MRI). 11C-(+)-PHNO PET before and after oral amphetamine was used to assess ventrostriatal dopamine release. The depressed group then received open-label pramipexole treatment for 6 weeks (0.5 mg/day titrated to a maximum daily dose of 2.5 mg). Symptoms were assessed weekly, and reward learning was reassessed post-treatment. At baseline, relative to controls, the depressed group showed lower reward learning (P = 0.02), a trend towards blunted reward-related prediction error signals (P = 0.07), and a trend towards increased amphetamine-induced dopamine release (P = 0.07). Despite symptom improvements following pramipexole (Cohen's d ranging from 0.51 to 2.16 across symptom subscales), reward learning did not change after treatment. At a group level, baseline reward learning (P = 0.001) and prediction error signalling (P = 0.004) were both associated with symptom improvement, albeit in a direction opposite to initial predictions: patients with stronger pretreatment reward learning and reward-related prediction error signalling improved most. Baseline D2/3 receptor availability (P = 0.02) and dopamine release (P = 0.05) also predicted improvements in clinical functioning, with lower D2/3 receptor availability and lower dopamine release predicting greater improvements. Although these findings await replication, they suggest that measures of reward-related mesolimbic dopamine function may hold promise for identifying depressed individuals likely to respond favourably to dopaminergic pharmacotherapy.

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.

Impaired generalization of reward but not loss in obsessive-compulsive disorder.

BACKGROUND: Generalizing from past experiences can be adaptive by allowing those experiences to guide behavior in new situations. Generalizing too much, however, can be maladaptive. For example, individuals with pathological anxiety are believed to overgeneralize emotional responses from past threats, broadening their scope of fears. Whether individuals with pathological anxiety overgeneralize in other situations remains unclear. METHODS: The present study (N = 57) used a monetary sensory preconditioning paradigm with rewards and losses to address this question in individuals with obsessive-compulsive disorder (OCD) and social anxiety disorder (SAD), comparing them to healthy comparison subjects (HC). In all groups, we tested direct learning of associations between cues and reward vs. loss outcomes, as well as generalization of learning to novel choice options. RESULTS: We found no differences between the three groups in the direct learning of stimuli with their outcomes: all subjects demonstrated intact stimulus-response learning by choosing rewarding options and avoiding negative ones. However, OCD subjects were less likely to generalize from rewards than either the SAD or HC groups, and this impairment was not found for losses. Additionally, greater deficits in reward generalization were correlated with severity of threat estimation, as measured by a subscale of the Obsessive Beliefs Questionnaire, both within OCD and across all groups. CONCLUSIONS: These findings suggest that a compromised ability to generalize from rewarding events may impede adaptive behavior in OCD and in those susceptible to high estimation of threat.

A randomized controlled pilot trial of vilazodone for adult separation anxiety disorder.

BACKGROUND: Separation anxiety disorder was recently recognized by fifth edition of the Diagnostic and Statistical Manual of Mental Disorders as a diagnosis in adults, but no publications to date have characterized a sample of patients seeking treatment for adult separation anxiety disorder (ASAD) or assessed treatment efficacy. We hypothesized that vilazodone, a selective serotonin reuptake inhibitor (SSRI) and serotonin 1a (5HT1a ) receptor partial agonist, would have efficacy in ASAD, because SSRIs have appeared efficacious in children with mixed diagnoses including separation anxiety disorder and in animal models of separation anxiety. METHODS: In this pilot study, 24 adults (ages 18-60) with a principal diagnosis of ASAD were randomized to 12 weeks of double-blind treatment with vilazodone (n = 13) or placebo (n = 11). Outcome was assessed by an independent evaluator and self-ratings, and analyzed with mixed effect models. RESULTS: This sample was predominantly female (67%), with comorbid psychiatric disorders (58%), and adult onset of separation anxiety disorder (62%). Response rates at week 12 did not differ significantly between groups. Across all time points, the vilazodone group evidenced greater improvement on the Structured Clinical Interview for Separation Anxiety Symptoms (P = .026) and the Quality of Life Enjoyment and Satisfaction Questionnaire (P = .011), and trends toward greater improvement on the Adult Separation Anxiety Questionnaire (P = .054) and the Clinical Global Impression-Change Scale (P = .086), all with large between-group effect sizes. CONCLUSIONS: Findings demonstrate feasibility of a clinical trial in ASAD, and they suggest that vilazodone may have efficacy in the treatment of ASAD and warrants further study.

The Role of Response Inhibition in Medicated and Unmedicated Obsessive-Compulsive Disorder Patients: Evidence from the Stop-Signal Task.

BACKGROUND: Numerous studies have investigated response inhibition (RI) in obsessive-compulsive disorder (OCD), with many reporting that OCD patients demonstrate deficits in RI as compared to controls. However, reported effect sizes tend to be modest and results have been inconsistent, with some studies finding intact RI in OCD. To date, no study has examined the effect of medications on RI in OCD patients. METHODS: We analyzed results from a stop-signal task to probe RI in 65 OCD patients (32 of whom were medicated) and 58 healthy controls (HCs). RESULTS: There was no statistically significant difference in stop-signal reaction time between the OCD group and the HC group, or between the medicated and unmedicated OCD patients. However, variability was significantly greater in the medicated OCD group compared to the unmedicated group. CONCLUSIONS: These results indicate that some samples of OCD patients do not have deficits in RI, making it unlikely that deficient RI underlies repetitive behaviors in all OCD patients. Future research is needed to fully elucidate the impact of medication use on stop-signal performance. Implications for future research on the cognitive processes underlying repetitive thoughts and behaviors are discussed.

Temporal discounting across three psychiatric disorders: Anorexia nervosa, obsessive compulsive disorder, and social anxiety disorder.

BACKGROUND: Temporal discounting refers to the tendency for rewards to lose value as the expected delay to receipt increases. Individuals with anorexia nervosa (AN) have been found to show reduced temporal discounting rates, indicating a greater preference for delayed rewards compared to healthy peers. Obsessive-compulsive disorder (OCD) and social anxiety disorder (SAD) commonly co-occur with AN, and anxiety has been related to development and prognosis of AN. We examined whether reduced temporal discounting is present across these potentially related disorders, and explored the relationship between temporal discounting and anxiety transdiagnostically. METHODS: One hundred ninety six individuals (75 healthy controls (HC); 50 OCD; 27 AN; 44 SAD) completed two temporal discounting tasks in which they chose between smaller-sooner and larger-later monetary rewards. Two measures of discounting-discount rate and discount factor-were compared between diagnostic groups, and associations with anxious traits were examined. RESULTS: Individuals with AN showed decreased temporal discounting compared to HC. OCD and SAD groups did not differ significantly from HC. Across the sample, anxiety was associated with decreased discounting; more anxious individuals showed a greater preference for delayed reward. CONCLUSIONS: We replicated the findings that individuals with AN show an increased preference for delayed reward relative to HC and that individuals with OCD do not differ from HC. We also showed that individuals with SAD do not differ from HC in discounting. Across this large sample, two measures of anxious temperament were associated with temporal discounting. These data raise new questions about the relationship between this dimensional trait and psychopathology.

PREPULSE INHIBITION DEFICITS ONLY IN FEMALES WITH OBSESSIVE-COMPULSIVE DISORDER.

BACKGROUND: Deficits in sensorimotor gating have been hypothesized to underlie the inability to inhibit repetitive thoughts and behaviors. To test this hypothesis, this study assessed prepulse inhibition (PPI), a measure of sensorimotor gating, across three psychiatric disorders (obsessive-compulsive disorder [OCD], social anxiety disorder [SAD], and anorexia nervosa [AN]) whose clinical presentations include repetitive thoughts and behaviors METHODS: We tested acoustic PPI in unmedicated individuals with OCD (n = 45), SAD (n = 37), and AN (n = 26), and compared their results to matched healthy volunteers (n = 62). All participants completed a structured clinical interview and a clinical assessment of psychiatric symptom severity. RESULTS: Percent PPI was significantly diminished in females with OCD compared to healthy female volunteers (P = .039). No other differences between healthy volunteers and participants with disorders (male or female) were observed. Percent PPI was not correlated with severity of obsessions and compulsions, as measured by the Yale-Brown Obsessive Compulsive Scale. CONCLUSIONS: This is the first study to assess PPI in participants with SAD or AN, and the largest study to assess PPI in participants with OCD. We found PPI deficits only in females with OCD, which suggests that the cortico-striato-pallido-thalamic and pontine circuitry (believed to underlie PPI) differs between males and females with OCD. Given that PPI deficits were only present in females with OCD and not related to repetitive thoughts and behaviors, our results do not support the hypothesis that sensorimotor gating deficits, as measured by PPI, underlie the inability to inhibit repetitive thoughts and behaviors in individuals with OCD, SAD, and AN.

INFLUENCE OF STUDY DESIGN ON TREATMENT RESPONSE IN ANXIETY DISORDER CLINICAL TRIALS.

OBJECTIVE: The influence of study design variables and publication year on response to medication and placebo was investigated in clinical trials for social anxiety disorder (SAD), generalized anxiety disorder (GAD), and panic disorder (PD). METHOD: Hierarchical linear modeling determined whether publication year, treatment assignment (medication vs. placebo), study type (placebo-controlled or active comparator), study duration, and the number of study visits affected the mean change associated with medication and placebo. RESULTS: In the 66 trials examined, the change associated with both medication and placebo increased over time (t = 4.23, df = 39, P < .001), but average drug-placebo differences decreased over time (t = -2.04, df = 46, P = .047). More severe baseline illness was associated with greater drug-placebo differences for serotonin norepinephrine reuptake inhibitors (SNRIs, t = 3.46, df = 106, P = .001) and selective serotonin reuptake inhibitors (SSRI, t = 10.37, df = 106, P < .001). Improvement with medication was significantly greater in active-comparator studies compared to placebo-controlled trials (t = 3.41, df = 39, P = .002). A greater number of study visits was associated with greater symptom improvement in PD trials relative to SAD (t = 2.83, df = 39, P = .008) and GAD (t = 2.16, df = 39, P = .037). CONCLUSIONS: Placebo response is substantial in SAD, GAD, and PD trials, and its rise over time has been associated with diminished drug-placebo differences. Study design features that influence treatment response in anxiety disorder trials include patient expectancy, frequency of follow-up visits, and baseline illness severity.

COMBINED MIRTAZAPINE AND SSRI TREATMENT OF PTSD: A PLACEBO-CONTROLLED TRIAL.

BACKGROUND: Combined treatment with a selective serotonin reuptake inhibitor (SSRI) plus mirtazapine has shown superior efficacy in some studies of depression, but has not been studied in posttraumatic stress disorder (PTSD). This study aimed to assess acceptability of combined sertraline plus mirtazapine treatment for PTSD and to estimate its effect size relative to sertraline plus placebo. METHODS: Thirty-six adults with PTSD were randomized to 24 weeks of double-blind treatment with sertraline plus mirtazapine or sertraline plus placebo. Outcomes were analyzed with mixed effects models. RESULTS: The combined treatment group showed a significantly greater remission rate (P = .042) and improvement in depressive symptoms (P = .023) than the sertraline plus placebo group. There were no significant group differences in the two primary outcomes of treatment retention and PTSD severity, or in other secondary outcomes (sleep impairment, sexual functioning, quality of life, and physical and mental functioning), but the combined treatment group showed numerical advantages on all of these outcomes, and effect sizes relative to sertraline plus placebo ranged from small to moderate (d = .26-.63). Both treatments were well-tolerated, with significantly increased appetite but not weight gain in the combined treatment group. CONCLUSION: Findings suggest that combined treatment of PTSD with sertraline plus mirtazapine may have clinically meaningful advantages in symptomatic improvement, relative to SSRI treatment alone, and acceptable tolerability. Combined treatment with an SSRI plus mirtazapine in PTSD deserves additional study as initial treatment or as an augmentation strategy for nonresponders to an SSRI.

Social anxiety disorder in DSM-5.

With the publication of DSM-5, the diagnostic criteria for social anxiety disorder (SAD, also known as social phobia) have undergone several changes, which have important conceptual and clinical implications. In this paper, we first provide a brief history of the diagnosis. We then review a number of these changes, including (1) the primary name of the disorder, (2) the increased emphasis on fear of negative evaluation, (3) the importance of sociocultural context in determining whether an anxious response to a social situation is out of proportion to the actual threat, (4) the diagnosis of SAD in the context of a medical condition, and (5) the way in which we think about variations in the presentation of SAD (the specifier issue). We then consider the clinical implications of changes in DSM-5 related to these issues.

Psychometric properties of the gaze anxiety rating scale: convergent, discriminant, and factorial validity.

Fear and avoidance of gaze are two features thought to be associated with problematic social anxiety. Avoidance of eye contact has been linked with such undesirable traits as deceptiveness, insincerity, and lower self-esteem. The Gaze Anxiety Rating Scale (GARS) is a self-report measure designed to assess gaze anxiety and avoidance, but its psychometric properties have only been assessed in one preliminary study. We further investigated psychometric properties of the GARS by assessing convergent and factorial validity. We obtained a two-factor solution: gaze anxiety and avoidance across situations (1) in general (GARS-General) and (2) related to dominance communication (GARS-Dominance). The GARS-General factor related more strongly to social anxiety than the GARS-Dominance, and convergent validity of the factors was supported by expected relationships with personality and social anxiety variables. Our results indicate that the GARS subscales are psychometrically valid measures of gaze aversion, supporting their use in future study of the relationship between social anxiety and eye contact behavior.

Vulnerabilities in social anxiety: Integrating intra- and interpersonal perspectives.

What are the major vulnerabilities in people with social anxiety? What are the most promising directions for translational research pertaining to this condition? The present paper provides an integrative summary of basic and applied translational research on social anxiety, emphasizing vulnerability factors. It is divided into two subsections: intrapersonal and interpersonal. The intrapersonal section synthesizes research relating to (a) self-representations and self-referential processes; (b) emotions and their regulation; and (c) cognitive biases: attention, interpretation and judgment, and memory. The interpersonal section summarizes findings regarding the systems of (a) approach and avoidance, (b) affiliation and social rank, and their implications for interpersonal impairments. Our review suggests that the science of social anxiety and, more generally, psychopathology may be advanced by examining processes and their underlying content within broad psychological systems. Increased interaction between basic and applied researchers to diversify and elaborate different perspectives on social anxiety is necessary for progress.

The evidence-based pharmacotherapy of social anxiety disorder.

Social anxiety disorder (SAD) is a highly prevalent and often disabling disorder. This paper reviews the pharmacological treatment of SAD based on published placebo-controlled studies and published meta-analyses. It addresses three specific questions: What is the first-line pharmacological treatment of SAD? How long should treatment last? What should be the management of treatment-resistant cases? Based on their efficacy for SAD and common co-morbid disorders, tolerability and safety, selective serotonin reuptake inhibitors (SSRIs) and venlafaxine should be considered the first-line treatment for most patients. Less information is available regarding the optimal length of treatment, although individuals who discontinue treatment after 12-20 wk appear more likely to relapse than those who continue on medication. Even less empirical evidence is available to support strategies for treatment-resistant cases. Clinical experience suggests that SSRI non-responders may benefit from augmentation with benzodiazepines or gabapentin or from switching to monoamine oxidase inhibitors, reversible inhibitors of monoamine oxidase A, benzodiazepines or gabapentin. Cognitive-behavioural is a well-established alternative first line therapy that may also be a helpful adjunct in non-responders to pharmacological treatment of SAD.

Pilot study of single-dose psilocybin for serotonin reuptake inhibitor-resistant body dysmorphic disorder.

OBJECTIVE: Body dysmorphic disorder (BDD) is an often-severe condition in which individuals are preoccupied by misperceptions of their appearance as defective or ugly. Only serotonin reuptake inhibitors and cognitive-behavioral therapy have been demonstrated efficacious in randomized controlled trials. Psilocybin is a psychedelic drug with growing evidence for safety and efficacy in treatment of depression. This study aimed to pilot test the feasibility, tolerability, safety, and efficacy of psilocybin treatment of adults with BDD. METHODS: In this open-label trial, 12 adults (8 women, 4 men) with moderate-to-severe non-delusional BDD that had been unresponsive to at least one serotonin reuptake inhibitor trial received a single oral dose of psilocybin 25 mg. There was no control group. Psychological support was provided before, during, and after the dosing session. The primary outcome measure for efficacy was the Yale-Brown Obsessive Compulsive Disorder Scale Modified for BDD (BDD-YBOCS) score during 12 weeks of assessments after dosing. RESULTS: All participants completed dosing and all follow-up assessments. BDD-YBOCS scores decreased significantly over 12 weeks of follow-up (p < .001) with a large effect size (partial eta squared = 0.54), and significant changes from baseline were present at week 1 and persisted through week 12. Secondary efficacy measures of BDD symptoms, conviction of belief, negative affect, and disability also improved significantly, and no serious adverse events occurred. At week 12, seven participants (58%) were rated responders, based on ≥30% decrease in BDD-YBOCS. CONCLUSION: This study provides promising preliminary support for psilocybin as a treatment of BDD, warranting future controlled studies.

Childhood maltreatment and social anxiety disorder: implications for symptom severity and response to pharmacotherapy.

BACKGROUND: Childhood maltreatment has been associated with symptom severity, reduced quality of life, and impaired functioning in adults with social anxiety disorder (SAD). No study has investigated how childhood maltreatment impacts pharmacotherapy outcomes in this population, despite evidence for such a link in depression. The current study replicates previous work on childhood maltreatment within SAD and examines its impact on response to pharmacotherapy. METHODS: One hundred and fifty six individuals seeking treatment for SAD completed the Childhood Trauma Questionnaire, which measures various types of abuse and neglect, along with the measures of symptom severity, quality of life, and disability. Data from a subset of patients enrolled in a paroxetine trial (N = 127) were analyzed to gauge the impact of childhood maltreatment on attrition and treatment response. RESULTS: All types of maltreatment except for sexual abuse and physical abuse were related to greater symptom severity. Emotional abuse and neglect were related to greater disability, and emotional abuse, emotional neglect, and physical abuse were related to decreased quality of life. Emotional abuse significantly predicted attrition. A time by emotional abuse interaction suggests that for those who stayed the course, the impact of emotional abuse on severity of social anxiety weakened significantly over time. CONCLUSIONS: Emotional maltreatment was most strongly linked to dysfunction in SAD, despite a tendency in the anxiety literature to focus on the effects of sexual and physical abuse. Additionally, individuals reporting emotional abuse were more likely to dropout from pharmacotherapy, but those who stayed the course displayed similar outcomes to those without such a history.

Personality disorders in hypochondriasis: prevalence and comparison with two anxiety disorders.

OBJECTIVE: Symptoms of hypochondriasis are sometimes attributed to personality psychopathology by health care providers. The goals of this study were to assess the prevalence of personality disorder (PD) comorbidity in hypochondriasis (HYP) and to compare the PD comorbidity profile of patients with HYP with that found among patients with other disorders characterized by intrusive thoughts and fears. METHODS: Structured Clinical Interview for DSM-IV Axis I and Axis II Disorders (SCID-I and SCID-II) were administered to 179 individuals: 62 with HYP, 46 with obsessive-compulsive disorder (OCD), and 71 with social anxiety disorder (SAD). For group contrasts, the samples were "purified" of the comparison comorbid disorders. General linear models were used to test the combined effect of group (HYP, OCD, SAD), age, and gender on the PD outcome variables. RESULTS: 59.7% of HYP subjects had no Axis II comorbidity. The most common PDs in HYP were paranoid (19.4%), avoidant (17.7%), and obsessive-compulsive (14.5%). HYP significantly differed from SAD in the likelihood of a cluster C disorder, whereas no significant difference was noted for HYP vs. OCD. The proportion of subjects having at least two PDs was not significantly different for HYP vs. OCD or for HYP vs. SAD. CONCLUSION: Although 40% of patients with hypochondriasis have PD comorbidity as assessed by the SCID-II, the amount of PD comorbidity is not significantly different than found among individuals with two comparison anxiety disorders. Therefore, health providers should be aware that PD may complicate the clinical profile of HYP, but they should avoid assuming that PD psychopathology is the primary source of hypochondriacal distress.

Social anxiety and functional impairment in patients seeking surgical evaluation for hyperhidrosis.

Primary hyperhidrosis is characterized by excessive sweating and often accompanied by social avoidance. Social anxiety disorder (SAD) is characterized by fear and avoidance of social situations, often partly related to fears of showing signs of excessive autonomic nervous system activation, such as sweating. To clarify the relationship of hyperhidrosis and SAD, this study assessed severity of sweating, overall social anxiety and social anxiety due to sweating, and disability in 2 groups: patients seeking surgical treatment for hyperhidrosis (n = 40) and patients seeking treatment for SAD (n = 64). Hyperhidrosis and SAD patients overlapped in severity of overall social anxiety and social anxiety related to sweating. Hyperhidrosis patients reported elevated levels of social anxiety, with mean severity near the threshold for the generalized subtype of SAD, but significantly lower social anxiety than in the SAD patients. Significantly more hyperhidrosis patients than SAD patients attributed most of their social anxiety to sweating (76% vs 20%). Among hyperhidrosis patients, the pattern of correlations of sweating, social anxiety, and disability was consistent with a model of social anxiety as a mediator of sweating-related disability. The overlap of symptoms in patients presenting for treatment of SAD or hyperhidrosis suggests that both social anxiety and sweating should be assessed in these patients and considered as potential targets of treatment.

Development and initial validation of the Visual Social Anxiety Scale (VSAS): Could a picture be worth a thousand words?

Accurate assessment is crucial for determining appropriate therapeutic interventions for social anxiety and conducting sound clinical research. While self-report measures of social anxiety are widely used in both research and clinical settings, they have several drawbacks inherent to their textual nature. Here, we describe the development and initial validation of the Visual Social Anxiety Scale (VSAS), a novel picture-based self-report measure of social anxiety, based on the well-established widely-used Liebowitz Social Anxiety Scale (LSAS). Specifically, the 24 items of the LSAS were used as the basis for social situations to be included in the VSAS. First, pictures to serve as VSAS items were selected using a rigorous two-phase process (four pilot studies; n = 225). Next, reliability (internal consistency, test-retest) and validity (convergent, discriminant) were explored with new participants (n = 304) who completed the VSAS and a battery of additional self-report questionnaires, delivered in a random order. The VSAS was completed again a month later (n = 260/304). The VSAS showed high internal consistency and test-retest reliability, and good convergent and discriminant validities. VSAS correlations with convergent measures were significantly greater than its correlations with discriminant measures. Thus, the VSAS shows initial promise as a novel picture-based self-report measure of social anxiety.

Fast evidence accumulation in social anxiety disorder enhances decision making in a probabilistic reward task.

Choices and response times in two-alternative decision-making tasks can be modeled by assuming that individuals steadily accrue evidence in favor of each alternative until a response boundary for one of them is crossed, at which point that alternative is chosen. Prior studies have reported that evidence accumulation during decision-making tasks takes longer in adults with psychopathology than in healthy controls, indicating that slow evidence accumulation may be transdiagnostic. However, few studies have examined perceptual decision making in anxiety disorders, where hypervigilance might enhance performance. Therefore, this study used the Hierarchical Drift Diffusion model to investigate evidence accumulation in adults with social anxiety disorder (SAD) and healthy controls as they performed a probabilistic reward task (PRT), in which social rewards were delivered for correct perceptual judgments. Adults with SAD completed the PRT before and after gaze-contingent music reward therapy (GCMRT), which trains attention allocation and has shown efficacy for SAD. Healthy controls also completed the PRT twice. Results revealed excellent performance in adults with SAD, especially after GCMRT: relative to controls, they showed faster evidence accumulation, better discriminability, and earned more rewards. These data highlight a positive effect of attention training on performance in anxious adults and show how a behavioral trait that is typically problematic-hypervigilance in SAD-can nevertheless confer advantages in certain contexts. The data also indicate that, in contrast to other forms of psychopathology, SAD is not characterized by slow evidence accumulation, at least in the context of the social PRT. (PsycInfo Database Record (c) 2022 APA, all rights reserved).