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The Social Phobia Inventory (SPIN; Connor et al., 2000) is a well-validated instrument for assessing severity of social anxiety disorder (SAD). However, evaluations of its factor structure have produced inconsistent results and this aspect of the scale requires further study. Primary care patients with SAD (N=397) completed the SPIN as part of baseline assessment for the Coordinated Anxiety Learning and Management study (Roy-Byrne et al., 2010). These data were used for exploratory and confirmatory factor analysis of the SPIN. A 3-factor model provided the best fit for the data and factors were interpreted as Fear of Negative Evaluation, Fear of Physical Symptoms, and Fear of Uncertainty in Social Situations. Tests of a second-order model showed that the three factors loaded strongly on a single higher-order factor that was labeled Social Anxiety. Findings are consistent with theories identifying Fear of Negative Evaluation as the core feature of SAD, and with evidence that anxiety sensitivity and intolerance of uncertainty further contribute to SAD severity., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Importance: Exposure to trauma increases the risk for developing threat (ie, fear) symptoms, such as reexperiencing and hyperarousal symptoms, and loss (ie, dysphoria) symptoms, such as emotional numbing and depressive symptoms. While preclinical data have implicated the activated dynorphin/κ-opioid receptor (KOR) system in relation to these symptoms, the role of the KOR system in mediating these phenotypes in humans is unknown. Elucidation of molecular targets implicated in threat and loss symptoms is important because it can help inform the development of novel, mechanism-based treatments for trauma-related psychopathology., Objective: To use the newly developed [11C]LY2795050 radiotracer and high-resolution positron emission tomography to evaluate the relation between in vivo KOR availability in an amygdala-anterior cingulate cortex-ventral striatal neural circuit and the severity of threat and loss symptoms. We additionally evaluated the role of 24-hour urinary cortisol levels in mediating this association., Design, Setting, and Participants: This cross-sectional positron emission tomography study under resting conditions was conducted at an academic medical center. Thirty-five individuals representing a broad transdiagnostic and dimensional spectrum of trauma-related psychopathology, ranging from nontrauma-exposed psychiatrically healthy adults to trauma-exposed adults with severe trauma-related psychopathology (ie, posttraumatic stress disorder, major depressive disorder, and/or generalized anxiety disorder)., Main Outcomes and Measures: [11C]LY2795050 volume of distribution values in amygdala-anterior cingulate cortex-ventral striatal neural circuit; composite measures of threat (ie, reexperiencing, avoidance, and hyperarousal symptoms) and loss (ie, emotional numbing, major depressive disorder, and generalized anxiety disorder symptoms) symptoms as assessed using the Clinician-Administered PTSD Scale, Hamilton Depression Rating Scale, and Hamilton Rating Scale for Anxiety; and 24-hour urinary cortisol levels., Results: [11C]LY2795050 volume of distribution values in an amygdala-anterior cingulate cortex-ventral striatal neural circuit were negatively associated with severity of loss (r = -0.39; 95% CI, -0.08 to -0.66), but not threat (r = -0.03; 95% CI, -0.30 to 0.27), symptoms; this association was most pronounced for dysphoria symptoms (r = -0.45; 95% CI, -0.10 to -0.70). Path analysis revealed that lower [11C]LY2795050 volume of distribution values in this circuit was directly associated with greater severity of loss symptoms and indirectly mediated by 24-hour urinary cortisol levels., Conclusions and Relevance: Results of this study suggest that KOR availability in an amygdala-anterior cingulate cortex-ventral striatal neural circuit mediates the phenotypic expression of trauma-related loss (ie, dysphoria) symptoms. They further suggest that an activated corticotropin-releasing factor/hypothalamic-pituitary-adrenal axis system, as assessed by 24-hour urinary cortisol levels, may indirectly mediate this association. These results may help inform the development of more targeted, mechanism-based transdiagnostic treatments for loss (ie, dysphoric) symptoms.

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., (© 2014 Wiley Periodicals, Inc.)

Unbiased genome-wide approaches can provide novel insights into the biological pathways that are important for human behavior and psychiatric disorder risk. The association of α-endomannosidase gene (MANEA) variants and cocaine-induced paranoia (CIP) was initially described in a study that used a whole-genome approach. Behavioral effects have been reported for other mannosidase genes, but MANEA function in humans and the clinical potential of the previous findings remain unclear. We hypothesized that MANEA would be associated with psychiatric phenotypes unrelated to cocaine use. We used a multi-stage association study approach starting with four psychiatric disorders to show an association between a MANEA single-nucleotide polymorphism (SNP; rs1133503) and anxiety disorders. In the first study of 2073 European American (EA) and 2459 African American subjects mostly with comorbid drug or alcohol dependence, we observed an association in EAs of rs1133503 with panic disorder (PD) (191 PD cases, odds ratio (OR)=1.7 (95% confidence interval (CI): 1.22-2.41), P=0.002). We replicated this finding in an independent sample of 142 PD cases (OR =1.53 (95% CI: 1.00-2.31), P=0.043) and extended it in an independent sample of 131 generalized social anxiety disorder cases (OR=2.15 (95% CI: 1.27-3.64), P=0.004). MANEA alleles and genotypes were also associated with gene expression differences in whole blood cells. Using publically available data, we observed a consistent effect on expression in brain tissue. We conclude that pathways involving α-endomannosidase warrant further investigation in relation to anxiety disorders.

Objective: Most patients remain symptomatic after an initial intervention with approved treatments for generalized social anxiety disorder. This randomized controlled trial provides systematic, prospectively derived data on the relative benefits of "next-step" pharmacotherapies to improve outcomes for individuals with generalized social anxiety disorder who remain symptomatic after initial treatment., Method: This three site, 12-week, double-blind randomized controlled trial compared the relative benefits of three strategies for patients remaining symptomatic (Liebowitz Social Anxiety Scale [LSAS] score >50) after a 10-week trial of sertraline alone: the addition of up to 3.0 mg/day of clonazepam (sertraline plus clonazepam), a switch to up to 225 mg/day of venlafaxine, or prolonged sertraline treatment with placebo (sertraline plus placebo)., Results: A total of 397 participants received at least one dose of sertraline; 181 nonresponders (LSAS score >50) at week 10 were randomly assigned to sertraline plus clonazepam, switch to venlafaxine, or sertraline plus placebo. Overall, 21% of patients achieved remission (LSAS score ≤30) at the endpoint, and 27% of patients assigned to sertraline plus clonazepam achieved remission compared with patients assigned to sertraline plus placebo (17%) or venlafaxine (19%), but the differences did not reach significance. Sertraline plus clonazepam was associated with a significantly greater drop in LSAS severity (p=0.020) and disability (p=0.0028) compared with sertraline plus placebo; no significant differences were observed on these parameters between venlafaxine and either sertraline plus placebo or sertraline plus clonazepam. In supplemental analysis, the overall response rate (LSAS score ≤50) was 46%, including a significantly greater proportion of patients in the sertraline plus clonazepam group (56%) compared with the sertraline plus placebo group responding (36%; p=0.027); differences did not reach significance between venlafaxine and sertraline plus placebo or sertraline plus clonazepam., Conclusions: The findings suggest that the clonazepam augmentation strategy provides relative benefits for sertraline nonresponders in social anxiety disorder.

The Social Phobia Inventory (SPIN) is a widely used measure in mental health settings and a 3-item version (mini-SPIN) has been developed as a screening instrument for social anxiety disorder. In the present study, we examined the psychometric properties of the SPIN and developed a brief version (mini-SPIN-R) designed to assess social anxiety severity using item response theory. Our sample included 569 individuals with social anxiety disorder who participated in 2 clinical trials and filled out a battery of self-report measures. Using a nonparametric kernel smoothing method we identified the most sensitive items of the SPIN. These 3 items comprised the mini-SPIN-R, which was found to have greater internal consistency, and to capture a greater range of symptoms compared to the mini-SPIN. The mini-SPIN-R evidenced superior convergent validity compared to the mini-SPIN and both measures had similar divergent validity. Thus, the mini-SPIN-R is a promising brief measure of social anxiety severity., (Copyright © 2013. Published by Elsevier Ltd.)

Background: Generalized social phobia (gSP), also known as generalized social anxiety disorder, is characterized by excessive fear of scrutiny by others and pervasive avoidance of social interactions. Pathophysiologic models of gSP implicate exaggerated reactivity of the amygdala and insula in response to social evaluative threat, making them plausible targets for treatment. Although selective serotonin reuptake inhibitor (SSRI) treatment is known to be an effective treatment, little is known about the mechanism through which these agents exert their anxiolytic effects at a brain level in gSP., Methods: We acquired functional magnetic resonance imaging data of brain response to social signals of threat (fearful/angry faces) in 21 gSP patients before and after they completed 12 weeks of open-label treatment with the SSRI sertraline. For comparison, 19 healthy control (HC) subjects also underwent two functional magnetic resonance imaging scans, 12 weeks apart., Results: Whole-brain voxelwise analysis of variance revealed significant Group×Time interactions in the amygdala and the ventral medial prefrontal cortex. Follow-up analyses showed that treatment in gSP subjects reduced amygdala reactivity to fearful faces (which was exaggerated relative to HCs before treatment) and enhanced ventral medial prefrontal cortex activation to angry faces (which was attenuated relative to HCs before treatment). However, these brain changes were not significantly related to social anxiety symptom improvement., Conclusions: SSRI treatment response in gSP is associated with changes in a discrete limbic-paralimbic brain network, representing a neural mechanism through which SSRIs may exert their actions., (Published by Elsevier Inc.)

Objective: Co-occurring depression is common in patients seeking treatment for anxiety; however, the literature on the effects of depression on anxiety treatment outcomes is inconclusive. The current study evaluated prescriptive and prognostic effects of depression on anxiety treatment outcomes in a large primary care sample., Method: Data were analyzed from a randomized controlled effectiveness trial that compared coordinated anxiety learning and management (CALM) to usual care. The study enrolled 1,004 patients between June 2006 and April 2008. Patients were referred by their primary care provider and met DSM-IV criteria for generalized anxiety disorder, panic disorder, posttraumatic stress disorder, and/or social anxiety disorder. They were treated for approximately 3 to 12 months with CALM (computer-assisted cognitive-behavioral therapy, medication management, or their combination) or usual care. Outcomes were evaluated by blinded assessment at 6, 12, and 18 months. Effects of baseline major depressive disorder (MDD) on anxiety symptoms, anxiety-related disability, and response/remission rates were evaluated using statistical models accounting for baseline anxiety and patient demographics., Results: MDD did not moderate the effects of CALM (relative to usual care) on anxiety symptoms, anxiety-related disability, or response/remission rates. Greater improvements in anxiety symptoms and anxiety-related disability were observed in depressed patients, regardless of treatment assignment (P values < .005). However, cross-sectionally depressed patients displayed higher anxiety symptom and anxiety-related disability scores at baseline and all subsequent assessments (P values < .001). Depressed patients also displayed lower remission rates at each follow-up (P values < .001)., Conclusions: CALM had comparable advantages over usual care for patients with and without MDD. Depressed patients displayed more severe anxiety symptoms and anxiety-related disability at baseline, but their clinical improvement was substantial and larger in magnitude than that observed in the nondepressed patients. Results support the use of empirically supported interventions for anxiety disorders in patients with co-occurring depression., Trial Registration: ClinicalTrials.gov identifier: NCT00347269., (© Copyright 2012 Physicians Postgraduate Press, Inc.)

Avoidant personality disorder (AvPD) has a high level of symptom overlap and comorbidity with generalized social anxiety disorder (GSAD). We examined whether the presence of comorbid AvPD adds significant clinically relevant information for individuals seeking treatment for GSAD. Results suggested that AvPD was significantly associated with poorer quality of life and greater disability in univariate, but not multivariate analyses. Endorsement of more AvPD symptoms was associated with increased disability, increased risk of intimacy, and lower social support, even after covariate adjustment. Specifically, AvPD item 3, hard to be "open" even with people you are close to, was most strongly correlated with quality of life and disability. A binary diagnosis of AvPD alone adds little beyond a marker of greater GSAD severity and depression among patients with GSAD, while a specific feature of AvPD not captured by the GSAD diagnosis, namely emotional guardedness, may be associated with greater impairment., (Published by Elsevier Ltd.)

Background: Selective mutism (SM), considered an early-onset variant of social anxiety disorder, shares features of impaired social interaction and communication with autism spectrum disorders (ASDs) suggesting a possible shared pathophysiology. We examined association of a susceptibility gene, contactin-associated protein-like 2 (CNTNAP2), for ASDs and specific language impairment with SM and social anxiety-related traits., Methods: Sample 1 subjects were 99 nuclear families including 106 children with SM. Sample 2 subjects were young adults who completed measures of social interactional anxiety (n = 1028) and childhood behavioral inhibition (n = 920). Five single nucleotide polymorphisms in CNTNAP2 (including rs7794745 and rs2710102, previously associated with ASDs) were genotyped., Results: Analyses revealed nominal significance (p = .018) for association of SM with rs2710102, which, with rs6944808, was part of a common haplotype associated with SM (permutation p = .022). Adjusting for sex and ancestral proportion, each copy of the rs2710102*a risk allele in the young adults was associated with increased odds of being >1 SD above the mean on the Social Interactional Anxiety Scale (odds ratio = 1.33, p = .015) and Retrospective Self-Report of Inhibition (odds ratio = 1.40, p = .010)., Conclusions: Although association was found with rs2710102, the risk allele (a) for the traits studied here is the nonrisk allele for ASD and specific language impairment. These findings suggest a partially shared etiology between ASDs and SM and raise questions about which aspects of these syndromes are potentially influenced by CNTNAP2 and mechanism(s) by which these influences may be conveyed., (Copyright © 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Objective: To compare different social fears and social phobia subtypes with regard to clinical (age of onset, avoidance, impairment, comorbidities) and vulnerability factors (behavioural inhibition (BI), parental psychopathology and parental rearing) among community youth., Methods: Fears of 6 social situations and Social Phobia (SP), along with their clinical features, were assessed using the Munich-Composite International Diagnostic Interview (DIA-X/M-CIDI) in a population-based sample of N = 3021 14-24 year olds that were followed up for 10 years. BI and parental rearing were assessed using self-report questionnaires. Parental psychopathology was assessed directly in parents via DIA-X/M-CIDI, supplemented by offsprings' family history reports., Results: In the total sample, 20.0%, 11.6%, 11.7% reported fear of 1, 2, 3 or more social situations, respectively; rates were 24.2%, 18.7%, and 57.1% in SP-cases (6.6% of the total sample). Exploring the factorial structure indicated rather unidimensionality of social fears than mutual distinction of social fears by interaction vs. performance situations. Except for fear of taking tests and public speaking, social fears rarely occurred in isolation. Social fears of both interaction and performance situations were associated with severe avoidance (vs. fear of either situation; Odds Ratios, OR = 1.5, 95%CI: 1.1-1.9) and impairment (OR = 3.6, 95%CI: 2.6-4.9), and more comorbid anxiety and depressive disorders (OR range 3.2-5.8, p > .001). Fear of interaction situations was associated with higher BI (vs. performance-related fears, OR range 1.2-2.1, p < .05). Associations with parental psychopathology and unfavourable parental rearing were less consistent, albeit stronger for fear of interaction situations (vs. performance-related fears). Interactions with time indicated an earlier onset of SP for higher BI, but not for parental psychopathology or unfavourable parental rearing., Conclusions: Interaction-related social fears differ in their clinical and vulnerability factors from performance-related social fears. The current DSM-IV specifier of "generalized" SP may fall short of adequately denoting these differences. Fear of taking tests appears to be conceptually and, possibly, etiologically distinct from other social fears, and may be better placed in another category (e.g., as a type of specific phobia)., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

A growing evidence base on the management of social anxiety disorder has yielded many meta-analyses and guidelines on the pharmacotherapy of this clinically important condition. We aimed to update a pharmacotherapy algorithm for the treatment of social anxiety disorder that was developed to be concise and user friendly and that was addressed to the primary care practitioner in particular. The updated algorithm attempts to summarize succinctly the recent literature in this area, as well as to include the views of an international panel of experts with diverse experience. The algorithm comprises eight sequential steps, beginning with those focused on diagnosis and initiating treatment and ending with the management of the treatment-refractory patient.

Background: This review evaluates the DSM-IV criteria of social anxiety disorder (SAD), with a focus on the generalized specifier and alternative specifiers, the considerable overlap between the DSM-IV diagnostic criteria for SAD and avoidant personality disorder, and developmental issues., Method: A literature review was conducted, using the validators provided by the DSM-V Spectrum Study Group. This review presents a number of options and preliminary recommendations to be considered for DSM-V., Results/conclusions: Little supporting evidence was found for the current specifier, generalized SAD. Rather, the symptoms of individuals with SAD appear to fall along a continuum of severity based on the number of fears. Available evidence suggested the utility of a specifier indicating a "predominantly performance" variety of SAD. A specifier based on "fear of showing anxiety symptoms" (e.g., blushing) was considered. However, a tendency to show anxiety symptoms is a core fear in SAD, similar to acting or appearing in a certain way. More research is needed before considering subtyping SAD based on core fears. SAD was found to be a valid diagnosis in children and adolescents. Selective mutism could be considered in part as a young child's avoidance response to social fears. Pervasive test anxiety may belong not only to SAD, but also to generalized anxiety disorder. The data are equivocal regarding whether to consider avoidant personality disorder simply a severe form of SAD. Secondary data analyses, field trials, and validity tests are needed to investigate the recommendations and options.

The current mainstays of social anxiety disorder pharmacotherapy are serotonergic agents, with less known about the efficacy of more noradrenergic drugs. Atomoxetine (ATM), a highly selective norepinephrine reuptake inhibitor, is currently approved for the treatment of attention-deficit/hyperactivity disorder (ADHD). We describe the first controlled trial of ATM with respect to efficacy and tolerability in adults with the generalized subtype of social anxiety disorder (GSAD) without comorbid ADHD. Twenty-seven outpatients with clinically prevailing diagnoses of GSAD by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition were randomized in a 1:1 ratio to 10 weeks of double-blind flexible-dose treatment with either ATM 40-100 mg per day (n = 14) or placebo (n = 13). Primary efficacy outcome was score at end point on the Liebowitz Social Anxiety Scale in the intention-to-treat sample. There were no significant group differences in patients completing the study (ATM, 79%; placebo, 77%). Whereas ATM was well tolerated, there were no significant differences in clinical efficacy between ATM and placebo for GSAD. There were few responders overall (ATM, 21%; placebo, 33%), but proportions were similar in each group (chi [1, 26] = 0.47; P = 0.67). Analysis of variance with repeated measures on the Liebowitz Social Anxiety Scale was performed to detect any differential change in social anxiety symptoms between groups. A significant time effect was found (F = 8.71; P = 0.007), but the time-by-treatment interaction was nonsignificant (F = 0.013; P = 0.91). Although the small sample size limits confidence in the reported results, the comparable, and low, response rates for ATM and placebo suggest that in the absence of comorbid ADHD, ATM is unlikely to be an effective agent for the treatment of GSAD.

Little is understood about generalized and non-generalized social anxiety disorder (SAD) and their associations with co-occurring internalizing and externalizing problems in adolescence. In the present study, we investigated adolescent boys with SAD symptoms and considered depressive symptoms as well as antisocial behaviors when looking for patterns during two developmental time periods; junior high and high school. Participants in the analyses were part of a longitudinal study. No patterns were found linking antisocial problems and non-generalized SAD in either junior high or high school. Furthermore, it was uncommon for youths in the non-generalized SAD subgroup to develop comorbidity over time. The generalized SAD subgroup of boys, however, was likely to develop comorbidity either with depressive symptoms only or with depressive symptoms and antisocial tendencies. Our findings suggest that developmental pathways for SAD subgroups may differ.

Objective: There has been ongoing clinical controversy dating back to the revised third edition of the Diagnostic and Statistical Manual of Mental Disorders concerning the boundaries and extent of overlap between Axis I generalized social phobia (GSP) and Axis II avoidant personality disorder (APD). This study sought to examine the relationship between the fourth edition of Diagnostic and Statistical Manual of Mental Disorders GSP and APD in a large nationally representative sample of the United States population., Method: We used the National Epidemiologic Survey on Alcohol and Related Conditions (n=43,093; age 18+; response rate=81%) to study fourth edition of Diagnostic and Statistical Manual of Mental Disorders Axes I and II psychiatric disorders, assessed by a reliable semi-structured in-person interview., Results: The lifetime prevalence was 2.8% for GSP and 2.4% for APD. The overlap between GSP and APD varied according to the number of GSP social situations feared. Although 36.4% of individuals with GSP were diagnosed with APD, the majority (57.3%) of individuals with GSP who feared all 13 social situations assessed were diagnosed with APD. Nearly 40% of individuals with APD also had GSP. Compared to individuals with GSP alone, individuals with comorbid GSP and APD showed significantly lower mental health-related quality of life on the Medical Outcomes Study Short Form, more interaction and observation fears, and an increased likelihood of having other psychiatric disorders such as major depression., Conclusions: APD and GSP show a high degree of overlap (16-57%), depending on the number of social situations feared. Overall, results suggest that APD and GSP appear to be highly related, but potentially separable constructs. Further research is needed to identify the determinants and consequences of having either or both diagnoses.

Objective: This study examined whether the self-report version of the Liebowitz Social Anxiety Scale (LSAS-SR) could accurately identify individuals with social anxiety disorder and individuals with the generalized subtype of social anxiety disorder. Furthermore, the study sought to determine the optimal cutoffs for the LSAS-SR for identifying patients with social anxiety disorder and its generalized subtype., Methods: Two hundred and ninety-one patients with clinician-assessed social anxiety disorder (240 with generalized social anxiety disorder) and 53 control participants who were free from current Axis-1 disorders completed the LSAS-SR., Results: Receiver Operating Characteristic analyses revealed that the LSAS-SR performed well in identifying participants with social anxiety disorder and generalized social anxiety disorder. Consistent with Mennin et al.'s [2002: J Anxiety Disord 16:661-673] research on the clinician-administered version of the LSAS, cutoffs of 30 and 60 on the LSAS-SR provided the best balance of sensitivity and specificity for classifying participants with social anxiety and generalized social anxiety disorder, respectively., Conclusions: The LSAS-SR may be an accurate and cost-effective way to identify and subtype patients with social anxiety disorder, which could help increase the percentage of people who receive appropriate treatment for this debilitating disorder., ((c) 2008 Wiley-Liss, Inc.)

Since the emergence of social phobia in DSM nomenclature, the mental health community has witnessed an expansion in standardized methods for the screening, diagnosis and measurement of the disorder. This article reviews formal assessment methods for social phobia, including diagnostic interview, clinician-administered instruments, and self report questionnaires. Frequently used tools for assessing constructs related to social phobia, such as disability and quality of life, are also briefly presented. This review evaluates each method by highlighting the assessment features recommended in social phobia literature, including method of administration, item content, coverage, length of scale, type of scores generated, and time frame.

Background: We examined social approachability judgments in a psychiatric population that frequently experiences interpersonal difficulties and reduced social satisfaction, individuals with generalized social phobia (gSP)., Methods: Our objective was to broaden the understanding of the social cognitive tendencies of individuals with gSP by systematically investigating their interpretation of positive facial expressions. We hypothesized that approachability ratings would be lower for positive as well as negative emotional faces in the gSP group compared to the healthy comparison group. Each participant evaluated 24 emotional faces presented on a computer screen. Participants first labeled the faces as either happy, disgust, or angry in emotional expression, and then they rated each face's approachability. Analysis of variance and post hoc analyses were used to identify group, emotion, and group by emotion rating differences., Results: Happy face approachability ratings were higher than disgust and anger in both groups. The central finding was that individuals with gSP rated happy faces as less approachable than the healthy participants and that degree of social anxiety was associated with lower approachability ratings within the gSP sample. Explicit approachability judgments of negative faces did not differ as predicted., Conclusions: Consistent with earlier indirect evidence of interpretation biases of positive social emotional information, this study reveals that individuals with gSP demonstrate explicit, subjective social interpretation biases of overtly positive social feedback. The therapeutic relevance of these results is discussed.

Background: There is a paucity of data examining the prevalence and impact of childhood maltreatment in patients presenting with a primary diagnosis of social anxiety disorder (SAD). We thus examined the presence of a broad spectrum of childhood maltreatment, including physical, sexual, and emotional abuse and neglect, in treatment-seeking individuals with the generalized subtype of SAD (GSAD). We hypothesized that a history of childhood maltreatment would be associated with greater SAD symptom severity and poorer associated function., Methods: One hundred and three participants with a primary diagnosis of GSAD (mean age 37+/-14; 70% male) completed the well-validated, self-rated Childhood Trauma Questionnaire (CTQ), as well as measures of SAD symptom severity and quality of life., Results: Fully 70% (n=72) of the GSAD sample met severity criteria for at least one type of childhood abuse or neglect as measured by the CTQ subscales using previously established thresholds. CTQ total score adjusted for age and gender was associated with greater SAD severity, and poorer quality of life, function, and resilience. Further, the number of types of maltreatment present had an additive effect, with specific associations for emotional abuse and neglect with SAD severity., Conclusions: Despite the use of validated assessments, our findings are limited by the retrospective and subjective nature of self-report measures used to assess childhood maltreatment. Nonetheless, these data suggest a high rate of childhood maltreatment in individuals seeking treatment for GSAD, and the association of maltreatment with greater disorder severity suggests that screening is clinically prudent.

Childhood social phobia (SP) is common and associated with varying forms of impairment. The cause of social anxiety disorder is often complex, involving both genetic and environmental factors. Shyness in young children may be a possible precursor to social anxiety later in life, although not the sole antecedent. Current assessment of childhood social anxiety includes psychometrically sound self report and clinician administered measures either specifically targeting SP disorder or including the construct as a subscale of a broader measure. The type of measure that is used most often depends on the purpose of the assessment, the setting, time constraints, and required training. Extant data support the efficacy of both psychosocial and pharmacological interventions, with response rates ranging from 50-80%. Further research is needed to clarify the developmental stages of SP, the psychometric properties of brief measures, as well as the efficacy of combined interventions.

The goal of this study was to develop an empirically derived classification system for selective mutism (SM) using parent-report measures of social anxiety, behavior problems, and communication delays. The sample consisted of parents of 130 children (ages 5-12) with SM. Results from latent profile analysis supported a 3-class solution made up of an anxious-mildly oppositional group, an anxious-communication delayed group, and an exclusively anxious group. Follow-up tests indicated significant group differences on measures of SM symptom severity, externalizing problems, and expressive/receptive language abilities. These results suggest that, although social anxiety is typically a prominent feature of SM, children with the disorder are also likely to present with communication delays and/or mild behavior problems.

Our understanding of social anxiety disorder (also known as social phobia) has moved from rudimentary awareness that it is not merely shyness to a much more sophisticated appreciation of its prevalence, its chronic and pernicious nature, and its neurobiological underpinnings. Social anxiety disorder is the most common anxiety disorder; it has an early age of onset--by age 11 years in about 50% and by age 20 years in about 80% of individuals--and it is a risk factor for subsequent depressive illness and substance abuse. Functional neuroimaging studies point to increased activity in amygdala and insula in patients with social anxiety disorder, and genetic studies are increasingly focusing on this and other (eg, personality trait neuroticism) core phenotypes to identify risk loci. A range of effective cognitive behavioural and pharmacological treatments for children and adults now exists; the challenges lie in optimum integration and dissemination of these treatments, and learning how to help the 30-40% of patients for whom treatment does not work.

Background: Despite heightened awareness of the clinical significance of social phobia, information is still lacking about putative subtypes, functional impairment, and treatment-seeking. New epidemiologic data on these topics are presented from the National Comorbidity Survey Replication (NCS-R)., Method: The NCS-R is a nationally representative household survey fielded in 2001-2003. The World Health Organization (WHO) Composite International Diagnostic Interview Version 3.0 (CIDI 3.0) was used to assess 14 performance and interactional fears and DSM-IV social phobia., Results: The estimated lifetime and 12-month prevalence of social phobia are 12.1% and 7.1% respectively. Performance and interactional fears load onto a single latent factor, and there is little evidence for distinct subtypes based either on the content or the number of fears. Social phobia is associated with significant psychiatric co-morbidity, role impairment, and treatment-seeking, all of which have a dose-response relationship with number of social fears. However, social phobia is the focus of clinical attention in only about half of cases where treatment is obtained. Among non-co-morbid cases, those with the most fears were least likely to receive social phobia treatment., Conclusions: Social phobia is a common, under-treated disorder that leads to significant functional impairment. Increasing numbers of social fears are associated with increasingly severe manifestations of the disorder.

Objective: To examine the history of lifetime psychiatric disorders in the parents of children with selective mutism (SM) compared to parents of children in a control group., Method: Seventy parent dyads (n = 140) of children with lifetime SM and 31 parent dyads (n = 62) of children without SM were interviewed with the Structured Clinical Interview for DSM-IV (IV and II) anxiety disorders, mood disorders, avoidant personality disorder, and schizoid personality disorder modules via telephone. Interviewers were blind to proband status. The NEO Personality Inventory was also administered., Results: Lifetime generalized social phobia was present in 37.0% of SM parents compared to 14.1% of control parents (chi2 = 10.98; p < .001; odds ratio 3.6, 95% confidence interval 1.6-7.9). Avoidant personality disorder was present in 17.5% of the SM parents compared to 4.7% of control parents (chi2 = 6.18; p < .05; odds ratio 4.3, 95% confidence interval 1.3-14.9). The proportion of parents with other psychiatric disorders was not different between groups. SM parents had higher neuroticism and lower openness scores on the NEO Personality Inventory than control parents., Conclusions: These results support earlier uncontrolled findings of a familial relationship between generalized social phobia and SM.

Background: Individuals with social phobia (SP) have altered behavioral and neural responses to emotional faces and are hypothesized to have deficits in inhibiting emotion-related amygdala responses. We tested for such amygdala deficits to emotional faces in a sample of individuals with SP., Method: We used functional magnetic resonance imaging (fMRI) to examine the neural substrates of emotional face processing in 14 generalized SP (gSP) and 14 healthy comparison (HC) participants. Analyses focused on the temporal dynamics of the amygdala, prefrontal cortex (PFC), and fusiform face area (FFA) across blocks of neutral, fear, contempt, anger, and happy faces in gSP versus HC participants., Results: Amygdala responses in participants with gSP occurred later than the HC participants to fear, angry, and happy faces. Parallel PFC responses were found for happy and fear faces. There were no group differences in temporal response patterns in the FFA., Conclusions: This finding might reflect a neural correlate of atypical orienting responses among individuals with gSP. Commonly reported SP deficits in habituation might reflect neural regions associated with emotional self-evaluations rather than the amygdala. This study highlights the importance of considering time-varying modulation when examining emotion-related processing in individuals with gSP.

Context: Epidemiological findings demonstrating an increased risk for individuals with social anxiety disorder (SAD) to develop depression have been challenged by discrepant findings from prospective longitudinal examinations in childhood and early adolescence., Objectives: To examine patterns of SAD incidence, the consistency of associations of SAD with subsequent depression, and distal and proximal predictors for subsequent depression., Design: Face-to-face, 10-year prospective longitudinal and family study of up to 4 waves. The DSM-IV Munich-Composite International Diagnostic Interview was administered by clinically trained interviewers., Setting: Community sample in Munich., Participants: Three thousand twenty-one individuals aged 14 to 24 years at baseline and 21 to 34 years at follow-up., Main Outcome Measures: Cumulative incidence of SAD and depression (major depressive episode or dysthymia)., Results: Cumulative incidence for SAD was 11.0%; for depression, 27.0%. Standardized person-years of incidence for SAD were highest for those aged 10 to 19 years (0.72%) and were low before (0.20%) and after (0.19%) that age range. Depression incidence was different, characterized by delayed and continued high rates. Social anxiety disorder was consistently associated with subsequent depression, independent of age at onset for SAD (relative risk range, 1.49-1.85, controlling for age and sex). Crude Cox regressions showed significant distal (eg, parental anxiety or depression, behavioral inhibition) and proximal SAD characteristics (eg, severity measures, persistence) as predictors. Most associations were attenuated in multiple models, leaving behavioral inhibition (hazard ratio, 1.30 [95% confidence interval, 1.04-1.62; P = .02]) and, less consistently, panic (hazard ratio, 1.85 [95% confidence interval, 1.08-3.18; P = .03]) as the remaining significant predictors., Conclusions: Social anxiety disorder is an early, adolescent-onset disorder related to a substantially and consistently increased risk for subsequent depression. The demonstration of proximal and particularly distal predictors for increased depression risks requires further exploration to identify their moderator or mediator role. Along with previous evidence that comorbid SAD is associated with a more malignant course and character of depression, these results call for targeted prevention with the aim of reducing the burden of SAD and its consequences.

Background: Although evidence suggests the involvement of the amygdala in generalized social phobia (GSP), few studies have examined other neural regions. Clinical, preclinical, and dopamine receptor imaging studies demonstrating altered dopaminergic functioning in GSP suggest an association with striatal dysfunction. This is the first functional magnetic resonance imaging (fMRI) study to use a cognitive task known to involve the striatum to examine the neural correlates of GSP. We examined whether subjects with GSP had differential activation in striatal regions compared with healthy control subjects while engaged in a cognitive task that has been shown to activate striatal regions reliably., Methods: Ten adult, unmedicated subjects with a primary DSM-IV diagnosis of GSP and 10 age-, gender-, and education-matched healthy comparison subjects underwent fMRI while performing the implicit sequence learning task., Results: The GSP and healthy comparison subjects did not differ significantly on the behavioral performance of the task. Subjects with GSP, however, had significantly reduced neural activation related to implicit learning compared with healthy comparison subjects in the left caudate head, left inferior parietal lobe, and bilateral insula., Conclusions: These findings support the hypothesis that GSP is associated with striatal dysfunction and further the neurobiological understanding of this complex anxiety disorder.

This study investigated the extent to which occasional cannabis use moderated anxiety and depression outcomes in the Collaborative Care for Anxiety and Panic (CCAP) study, a combined cognitive-behavioral therapy (CBT) and pharmacotherapy randomized effectiveness trial. Participants were 232 adults from six university-based primary care outpatient clinics in three West Coast cities randomized to receive either the CCAP intervention or the usual care condition. Results showed significant (P<.01) evidence of an interaction between treatment group (CCAP vs. usual care) and cannabis use status (monthly vs. less than monthly) for depressive symptoms, but not for panic disorder or social phobia symptoms (all P>.05). Monthly cannabis users' depressive symptoms improved in the CCAP intervention just as much as those who used cannabis less than monthly, whereas monthly users receiving usual care had significantly more depressive symptoms than those using less than monthly. A combined CBT and medication treatment intervention may be a promising approach for the treatment of depression among occasional cannabis users., ((c) 2006 Wiley-Liss, Inc.)

Objective: To evaluate the usefulness of screening measures to detect social phobia among youth in a primary care setting., Methods: Families recruited from a pediatric primary care setting completed by mail the Social Anxiety Scale (SAS), the Social Worries Questionnaire (SWQ), and the social phobia subscale of the Screen for Child Related Anxiety Disorders (SCARED). Diagnoses were obtained from 190 parent interviews. Receiver operating characteristic (ROC) analyses were used to determine the utility of the measures as screening instruments., Results: Most of the parent report measures, including the single item ("My child is shy") from the SCARED, were at least moderately accurate screeners and performed best for the generalized subtype of social phobia., Conclusion: The use of valid, brief screening instruments can significantly improve the feasibility of detecting social phobia among youth in primary care pediatric settings.

Social anxiety disorder (SAD) is among the most common mental disorders on a lifetime basis, ranging from 12% to 14%. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, categorizes SAD as either generalized (fear/avoidance of multiple social situations) or nongeneralized (fearing only a limited number of social situations), with some overlap between the 2 subtypes. Generalized SAD is associated with more comorbid mental disorders, greater functional impairment, and lower health-related quality of life. Half of SAD patients have onset by age 13 years and 90% by age 23 years; however, SAD is rarely diagnosed or treated by the pediatrician, highlighting the low awareness level of SAD and the need to increase attention among physicians. Social anxiety disorder is associated with an increased risk for depression and a more malignant course, characterized by increased likelihood of suicide attempts and greater disease chronicity. SAD has an adverse impact on outcomes in patients with other comorbid mental conditions such as bipolar disorder, eating disorders, and personality disorders.

Childhood social anxiety disorder is a condition of complex origins. Longitudinal studies of shyness and behavioral inhibition, and twin and family history studies, support a genetic component, but experiences such as family environment, parenting, and traumatic conditioning also are observed. Many children with significant shyness and behavioral inhibition do not develop social anxiety disorder, reinforcing the need for longitudinal studies exploring resiliency and risk factors that can be incorporated into diathesis stress models. Efficacy data regarding cognitive and behavioral therapies and pharmacotherapy are promising, and their effectiveness awaits further research. These studies will need to incorporate a multiplicity of perspectives to ensure the long-term sustainability of interventions for social anxiety disorder in children and adolescents.

We believe that the harmful dysfunction model is important to consider when defining disorders. However, we question whether, when used in isolation, it provides an adequate basis for discriminating disorders from normal variations of temperament. We believe that it is important to consider the interaction between the individual's temperament and the demands of present-day society. We also assert that, when taken in the aggregate, the DSM-IV criteria for social phobia adequately establish the presence of harmful dysfunctions, particularly when significant impairment in one or more important domains of functioning is present. Finally, we argue that practical issues must be considered when we classify conditions as disorders. The fact that social phobia is classified as a legitimate disorder has undoubtedly spurred research efforts and encouraged countless individuals to seek relief for their suffering.

Rationale: There is a need for new pharmacological treatments for generalized social anxiety disorder (GSAD), which is a common, often disabling condition., Objective: To compare the efficacy and safety over 6 months duration of two dose ranges of venlafaxine extended-release (ER) with placebo in patients with GSAD., Method: Twenty-eight-week, double-blind, multi-center study in 386 adult outpatients with DSM-IV GSAD. Patients were randomized to placebo, venlafaxine ER fixed low dose (75 mg/day), or venlafaxine ER flexible higher dose (150-225 mg/day). Primary efficacy variable was change on the Liebowitz Social Anxiety Scale (LSAS). Secondary efficacy variables included, among others, the proportion of responders on the CGI Global Improvement Item (score 1 or 2), and the proportion of remitters (defined as an LSAS score of

Background: Social anxiety disorder is a debilitating, highly prevalent disorder in children and adolescents. If left untreated, it can interfere with emotional, social, and school functioning., Objective: To evaluate the efficacy and tolerability of paroxetine in children and adolescents with social anxiety disorder., Design and Setting: Multicenter, 16-week, randomized, double-blind, placebo-controlled, flexible-dose, parallel-group, outpatient study. Patients A total of 322 children (8-11 years of age) and adolescents (12-17 years of age) with social anxiety disorder as their predominant psychiatric illness. Intervention Eligible patients were randomized (1:1) to receive paroxetine (10-50 mg/d) or placebo., Results: Four hundred twenty-five patients were screened, and 322 were randomized to treatment. Of these, 319 were included in the intention-to-treat population (paroxetine, n = 163; placebo, n = 156). At the week 16 last observation carried forward end point, the odds of responding (Clinical Global Impression-Improvement score of 1 or 2) were statistically significantly greater for paroxetine (77.6% response [125/161]) than for placebo (38.3% response [59/154]) (adjusted odds ratio, 7.02; 95% confidence interval, 4.07 to 12.11; P<.001). The proportion of patients who were "very much" improved (Clinical Global Impression-Improvement score of 1) was 47.8% (77/161) for paroxetine compared with 14.9% (23/154) for placebo. Adverse events occurring at an incidence of 5% or greater for paroxetine and twice that for placebo were insomnia (14.1% vs 5.8%), decreased appetite (8.0% vs 3.2%), and vomiting (6.7% vs 1.9%). Withdrawals due to adverse events were infrequent (5.5% [9/163] for paroxetine and 1.3% [2/156] for placebo)., Conclusion: Paroxetine is an effective, generally well-tolerated treatment for pediatric social anxiety disorder.

Background: This study sought to extend findings from a preliminary clinical investigation [J. Affect. Disord. 57 (2000) 223] by examining relations between the personality dimension of self-criticism and diagnostic prevalence of social phobia in a large nationally representative sample., Methods: Participants were from the national comorbidity survey Part II [n=5877; Arch. Gen. Psychiatry 51 (1994) 8]. Psychiatric diagnoses were made using a modified version of the composite international psychiatric interview. Personality dimensions and distress were assessed using brief self-report measures with strong psychometric properties., Results: Self-criticism was elevated in NCS respondents with a diagnosis of social phobia, even in cases of only past history of social phobia (i.e. >1 year ago), compared to individuals with no psychiatric disorder. The highest levels of self-criticism were reported by people with the complex subtype of social phobia, both with and without comorbid major depression. These levels were significantly greater compared to those observed in another anxiety disorder (panic disorder), the pure speaking subtype of social phobia, and cases of major depression alone. In a regression analysis that controlled for current emotional distress, the broad personality trait of neuroticism, and lifetime histories of mood, anxiety, and substance use disorders, self-criticism remained significantly associated with lifetime prevalence of social phobia., Limitations: The cross-sectional design of the study does not permit causal inferences., Conclusions: Findings from this general population mental health survey demonstrated that self-criticism is robustly associated with social phobia. It may represent an important core psychological process in the complex subtype of this anxiety disorder.

Background: Comorbidity between adult social anxiety disorder and major depression is extensive. Considerably less information about this relationship is available among youth., Methods: A randomly selected (from enrollees in a pediatric primary care clinic) sample of 190 families with children between the ages of 8 and 17 responded by mail to questionnaires assessing social anxiety, depression, and social functioning. Parents also completed a semi-structured telephone diagnostic interview about their child., Results: The generalized type of social anxiety disorder was highly comorbid with major depression, generalized anxiety disorder, specific phobias, and ADHD, while little comorbidity was present for the nongeneralized subtype of social anxiety disorder. Logistic regression analyses indicated that generalized social anxiety disorder was the only anxiety disorder associated with an increased likelihood of major depression (OR=5.1). In all cases, social anxiety disorder had a significantly earlier age of onset than major depression., Limitations: This study relies on cross-sectional data and diagnoses are based on parent reporting of child behavior., Conclusions: Generalized social anxiety disorder is strongly associated with depressive illness in youth. Screening and treatment approaches that consider both social anxiety and depressive symptoms are necessary. Early intervention to treat social anxiety disorder may prevent later depressive disorders., (Copyright 2003 Elsevier B.V.)

Background: Generalized social anxiety disorder (GSAD) is a pervasive form of social anxiety that affects approximately 5% of persons in the community. Among evidence-based pharmacologic treatments for the disorder, selective serotonin reuptake inhibitors (SSRIs) have become widely used and are known to be efficacious. Monotherapy with the benzodiazepine clonazepam is also efficacious for GSAD, but the adjunctive use of clonazepam with an SSRI to potentially improve outcomes has not been studied to date., Method: Twenty-eight patients (22 men and 6 women) with DSM-IV-defined GSAD were randomly assigned to receive double-blind clonazepam (or placebo), 1.0 to 2.0 mg/day (divided b.i.d.) along with open-label paroxetine, 20 to 40 mg/day, for 10 weeks. A 2-week taper of double-blind medication was followed by an additional 8 weeks of open-label paroxetine treatment (during which the dose of paroxetine could be increased to a maximum of 50 mg/day). Twenty-three patients (82%) met DSM-IV criteria for avoidant personality disorder. The patients' mean +/- SD age was 31.2 +/- 7.7 years, and their mean duration of illness was 12.1 +/- 5.8 years. Data were gathered from August 2001 to April 2002., Results: Nineteen (68%) of 28 patients completed treatment. At the end of the 10-week double-blind treatment, there was a trend (p <.06) favoring the paroxetine/clonazepam group, who had a 79% response rate (Clinical Global Impressions-Global Improvement scale [CGI-I] score of 1 or 2) compared with a 43% response rate for the paroxetine/placebo group. However, no significant differences on other outcome measures were noted between the 2 groups in an intent-to-treat analysis, in terms of either very early (2-4 weeks) or not as early (5-10 weeks) responses during treatment. Dropout rates due to adverse events were rare (1 patient in each group), indicating that the paroxetine/clonazepam combination was well tolerated., Conclusion: Coadministration of clonazepam with an SSRI, in contrast to findings in panic disorder, did not lead to more rapid resolution of symptoms in GSAD. On the other hand, there is some evidence that the clonazepam-added group had superior global outcomes (e.g., as measured on the CGI-I), although power to detect such differences in this study was small. These observations suggest that a role for adjunctive benzodiazepines in patients with GSAD (e.g., for augmenting SSRI partial response or nonresponse) is deserving of further controlled investigation.

We present prevalence and treatment utilization rates for child anxiety disorders in a university-affiliated primary care clinic. Families were recruited from a pediatric patient list and 714 families participated in an initial study wherein they completed child anxiety questionnaires. According to parent and child self-report questionnaires (n=714), 22% and 20% of children, respectively, were above a suggested clinical cutoff on a brief anxiety screen; 19% and 14% of children exceeded clinical cutoffs on a separate social anxiety questionnaire. All families were invited to participate in a second study that included the Anxiety Disorders Interview Schedule for Children-Parent Version and questions about treatment utilization; telephone interviews with 190 parents showed 1-year prevalence rates of DSM-IV child disorders to be 10.0% (se=2.2%) for specific phobia, 6.8% (se=1.8%) for social phobia, 3.2% (se=1.3%) for generalized anxiety disorder, 0.5% (se=.7%) for selective mutism, 1.6% (se=.9%) for major depressive disorder, 1.1% (se=.7%) for dysthymia, and 12.6% (se=2.4%) for attention deficit-hyperactivity disorder (ADHD). Among children with a current anxiety disorder, 31% had received counseling or medication treatment during their lifetime, compared to 40% of children with depression and 79% with ADHD. Adolescent age and being Caucasian were predictors of psychotherapy use; having an ADHD diagnosis was a predictor of both psychotherapy and medication use. The high prevalence of impairing anxiety disorders, in concert with the very low extent of treatment utilization, suggests a need for methods to identify and disseminate empirically validated treatments for these disorders in the primary care setting., ((c) 2005 Wiley-Liss, Inc.)

Objective: Social phobia is a common, sometimes disabling, fear of situations that might entail scrutiny by others. Several anxiety disorders, including social phobia, are genetically influenced. Genetic linkage analysis can provide the means to identify genomic locations harboring susceptibility loci for genetically influenced disorders. Identifying loci for social phobia was the goal of this study., Method: The authors conducted a genome-wide linkage scan, i.e., tested enough genetic markers to query the entire genome, in 17 American pedigrees (163 subjects) ascertained through probands with panic disorder. Several anxiety disorders segregate in these families; diagnoses were based on structured interviews. A total of 422 markers (404 autosomal, 18 on the X chromosome) with an average spacing of less than 10 centimorgans were genotyped. Multipoint lod score and nonparametric (Zlr score) linkage analyses for social phobia were completed with Allegro and Genehunter X software., Results: Evidence for linkage to social phobia for chromosome 16 markers was identified. A Zlr score of 3.41 was observed for chromosome 16 near marker D16S415. The maximum observed lod score was 2.22, also for chromosome 16, between D16S415 and D16S503 (under a model of recessive inheritance). Additional areas of interest were identified on chromosomes 9, 14, and 18., Conclusions: These findings meet conservative criteria for "suggestive" linkage. The gene encoding the norepinephrine transporter protein (SLC6A2) maps to this broad region, making SLC6A2 both a positional and physiological candidate for influencing social phobia risk. To the authors' knowledge, this is the first complete linkage genome scan for this disorder.

Background: Considering comorbidity in social phobia contributes to our understanding of causal pathways and improved classifications for psychiatric disorders. Comorbidity also has important clinical implications. While a number of studies have investigated comorbidity in social phobia, only one other study has used the Composite International Diagnostic Interview (CIDI) and considered comorbidity in subtypes of social phobia. This study evaluated lifetime social phobia comorbidity with other common mental disorders as well as comorbidity in subtypes of social phobia. We also considered whether social fears, reported by respondents with social phobia, had an earlier or later age of onset than other disorders., Methods: Data came from the Mental Health Supplement to the Ontario Health Survey, a survey of 8,116 Canadian respondents, ages 15-64. Psychiatric diagnoses were determined using the CIDI. This instrument is considered more sensitive than earlier instruments for diagnosing social phobia., Results: Fifty-two percent of respondents with lifetime social phobia reported at least one other lifetime mental disorder and 27% reported three or more lifetime mental disorders. Social phobia, in this sample, is strongly comorbid with anxiety and affective disorders, and moderately comorbid with substance abuse disorders. When two social phobia subgroups were considered, the largest odds ratios were found among the not-exclusively-speaking social phobia group. This subgroup would include most of the respondents with a generalized form of social phobia. Age of onset of social fears, in respondents with social phobia, preceded age of onset of the comorbid disorder in 32% of cases with comorbid anxiety disorder, 71% of cases with comorbid affective disorder and 80% of cases with comorbid substance dependence/abuse disorder., Conclusions: Comorbidity and relative age of onset among respondents with social phobia in this study are generally consistent with previous epidemiologic studies. Clinicians should be vigilant for comorbidity in social phobia and should select treatments that target the full range of comorbid disorders. Early intervention or prevention of social fears or social phobia has the potential to reduce the risk of comorbid disorders.

Cognitive models of social phobia posit that an individual's negative beliefs about the way he or she is perceived by others (metaperceptions) are a core feature of the disorder. The social relations model () was used to analyze interpersonal perception data collected following unstructured social interactions in 62 socially anxious (SA) and 62 not socially anxious (NSA) individuals. Using this model, the interpersonal perceptions were analyzed to evaluate whether pathological levels of social anxiety are associated with self-perceptions, metaperceptions, and perceptions from others. SA participants saw themselves negatively and believed others saw them negatively. Although seen as more nervous by others, SA participants were not seen as less likeable. A mediational model demonstrated that the negative metaperceptions of SA individuals were more a function of their own self-perceptions than the negative perceptions of others. These findings were not attributable to depressive symptoms. Implications for theory and treatment of social phobia are discussed.

This study surveyed parents' opinions about treatment for childhood social anxiety disorder and assessed variables that may affect treatment acceptability. A 20-item survey assessing treatment attitudes and a semistructured interview were administered to 190 parents of children (8-17 years) who were randomly selected from a pediatric primary care setting. An exploratory factor analysis of the treatment attitudes survey yielded four factors: medication acceptability, counseling acceptability, counseling feasibility, and general beliefs about social anxiety treatment. Findings revealed that parents endorsed favorable attitudes toward counseling and somewhat neutral beliefs about medication. White parents were more accepting of medication and counseling and also perceived counseling as more feasible than nonwhite parents. Treatment acceptance was associated with past mental health utilization but not with severity of social anxiety. Further research is necessary to determine if clinical interventions for child anxiety disorders may be more efficacious if parents' attitudes and beliefs about prescribed treatments are addressed.

Social anxiety disorder frequently begins in early life and is associated with the subsequent development of comorbid conditions such as depressive and substance use disorders. Social anxiety disorder, particularly the generalized subtype, is characterized by marked impairment in numerous functional domains, including education and social relations. Paroxetine, the first medication to receive an indication in the United States for the treatment of social anxiety disorder, has been shown to be effective in 50% to 60% of patients. The mechanism of action of paroxetine in the treatment of social anxiety disorder is at present unclear. A possible role for early treatment to prevent complications of social anxiety disorder should be explored.

This study addressed the paucity of research on the covariation and hierarchic structure of fears in nationally representative or "real world" samples. Using data from the U.S. National Comorbidity Survey (N=8098), exploratory and confirmatory factor analyses were employed with split-half samples to delineate the multidimensional structure and hierarchic organization of 19 feared situations assessed by structured interview. On a first-order level, support was obtained for a five-factor model of fears: (1). agoraphobia, (2). speaking fears, (3). fears of being observed, (4). fears of heights or water, and (5). threat fears. The four latter fear dimensions in turn loaded on to two second-order fear factors: social fears and specific fears. A hierarchic model with a single, general fear factor at a third-order level provided good fit to the data. Results are discussed in the context of Taylor's [Behav. Res. Ther. 36 (1998) 205-214] proposed hierarchic framework of fears. Implications of these general population findings for the composition and classification of phobias in recent editions of the DSM are also highlighted.

The existence of subtypes of social phobia has been questioned. Although cluster analytic methods have been used to support various subtype models, a continuous model based on total number of feared social situations seems equally plausible. In a community sample, we calculated mean similarity measures for combinations of item pairs of feared social situations. Speaking fear items were significantly more similar to each other than to other items. There was also a trend for interaction fear items to be more similar to each other than to other items. These findings suggest that fear of speaking and interactional situations may represent distinct domains of socially feared situations. They should be considered separately in delineation of treatment response and may, if replicated in clinical samples, help identify meaningful subtypes of social phobia., (Copyright 2003 Wiley-Liss, Inc.)

In a recent study of treatment for panic disorder in primary care, the Composite International Diagnostic Interview (CIDI-Auto) was used to provide psychiatric diagnoses. However, during and after data collection, it was discovered that the CIDI appeared to place, or fail to place, a substantial number of people into diagnostic categories in ways that conflicted with the investigators' clinical experience. The wording of questions in the panic module, coupled with a lack of structured follow-up probes, resulted in apparent false negatives for panic disorder. Moreover, patients who would otherwise meet criteria for panic disorder or social phobia did not receive a diagnosis based on rules that may be discordant with clinical practice and, at times, the design of the DSM-IV. For this study, changes were made to the interview, including additional probes for the panic disorder module and modification of the decision rules used to assign or rule out diagnoses of panic disorder and social phobia. The changes resulted in greater inclusion of patients in the panic disorder and social phobia diagnostic categories and we argue that these changes to the CIDI-Auto increase the clinical validity of this instrument. We did not examine the false positive rate for the unmodified or modified CIDI, but this is an important issue that needs to be evaluated in future research.

Background: Generalized social phobia (GSP) is characterized by fear of social interactions and sensitivity to disapproval by others. Given the established role of the amygdala as part of a distributed neural system for the processing of emotional cues, we hypothesized that subjects with GSP would exhibit greater amygdala activation in response to harsh (angry, fearful, and contemptous) vs accepting (happy) facial emotional expressions compared with healthy control subjects (HCs)., Methods: Fifteen subjects with DSM-IV GSP and 15 age-, sex-, handedness-, and education-matched HCs, free of psychotropic medication for at least 12 weeks, viewed 60 color photographs from a standardized set of human facial stimuli, during which the task was to identify the sex of the person in the photograph. Data were collected across 3 functional (echo-planar) runs using a Siemens 1.5-T magnet, and analyzed using Analysis of Functional Neuroimaging software (Medical College of Wisconsin, Milwaukee)., Results: In the left allocortex (including the amygdala, uncus, and parahippocampal gyrus), subjects with GSP produced a significantly greater percent blood oxygen level-dependent signal change than did HCs for contemptous compared with happy faces (GSP: 0.72% vs HC: -0.01%; F(1,29) = 9.56, P =.004, Cohen d = 1.15) and for angry compared with happy faces (GSP: 0.45% vs HC: -0.09%; F(1,29) = 6.78, P =.02, Cohen d = 1.00). Subjects with GSP and HCs did not produce a statistically different percent signal change for fearful or nonexpressive faces compared with the happy faces in this region., Conclusions: These findings are consistent with a role for differential amygdala (and associated limbic) functioning in GSP. The pronounced response to contemptuous and angry facial expressions suggests that the amygdala in GSP may be particularly active in the processing of disorder-salient stimuli.