Dr. Belzer is research fellow and Dr. Liebowitz is director of the Anxiety Disorders Clinic at New York State Psychiatric Institute in New York City. Dr. McKee is clinical assistant professor of psychology in psychiatry at the Weill Medical College of Cornell University and research scientist at the Anxiety Disorders Clinic at the New York State Psychiatric Institute in New York City.
Disclosure: Drs. Belzer and McKee receive research support from the National Institute of Mental Health. Dr. Liebowitz is a consultant to Eli Lilly, Forest, and GlaxoSmithKline; is on the speaker’s bureaus of Bristol-Myers Squibb, Pfizer, and Wyeth; and receives grant support from Eli Lilly, Forest, GlaxoSmithKline, Pfizer, and Wyeth.
Please direct all correspondence to Kenneth D. Belzer, PhD, New York State Psychiatric Institute, 1051 Riverside Drive, Unit 69, New York, NY 10032; Tel: 212-543-5132; Fax: 212-543-6515; E-mail: firstname.lastname@example.org.
This article provides a clinically relevant overview of issues related to social anxiety disorder (SAD), with particular emphasis on its diagnosis and treatment. The history and evolution of SAD as a clinical syndrome are briefly reviewed, and the phenomenology and clinical presentation of SAD are discussed. Data on prevalence, onset, course, comorbidity, and functional impairment associated with SAD in clinical and epidemiological samples are reviewed. An overview of assessment and treatment via pharmacotherapy and cognitive-behavioral therapy, with a focus on practical clinical applications, is also presented. Finally, research aimed at integrating pharmacologic and psychotherapeutic interventions to maximize long-term treatment effectiveness is considered.
Subjective distress and discomfort in particular social situations are to some degree both natural and expected. It is reasonable to assume that all people, at one time or another, have experienced embarrassment or stage fright, or perhaps have become tongue-tied in the midst of conversation. When such experiences become ubiquitous in everyday life, however, and ordinary social interactions elicit fear and/or anxiety severe enough to foster significant and maladaptive avoidance behavior, a threshold has been crossed into the province of pathological social anxiety. This condition is known clinically as social anxiety disorder (SAD), an impairing and often chronic anxiety disorder that has profoundly adverse consequences on the quality of life and adaptive functioning of the afflicted individual.1-5 The syndrome is strongly associated with, and appears to serve as a vulnerability factor for, several other debilitating psychiatric conditions.6-7 Moreover, SAD has been found to be the most common anxiety disorder and third most common psychiatric disorder in the United States, exceeded only by major depressive disorder (MDD) and substance use disorders.8-9
Given the scope of the problem, its robust association with other forms of psychopathology, and the overwhelming human burden of this illness, clinicians should be proficient in detecting and diagnosing SAD, and should be knowledgeable about evidence-based treatment modalities. The purpose of this article is to provide a clinically relevant overview of some of the more substantive issues concerning the diagnosis and treatment of SAD. The article begins with a brief account of the evolution of SAD from its early beginnings as an undifferentiated phobic disorder to its present status as an independent diagnosis, as detailed in the current Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Revised (DSM-IV-TR).10 A discussion of the nature, core features, and phenomenology of SAD follows. Issues concerning the assessment of SAD in the clinical and research settings are reviewed, and an overview of current empirically supported psychopharmacologic and psychotherapeutic treatments is provided. Finally, the article underscores the necessity of integrating biologically based and psychosocial therapies to maximize long-term treatment effectiveness of SAD.
History: From a Neglected Anxiety Disorder to a Social Anxiety Spectrum
Descriptions of social phobic states appeared in the empirical psychiatric literature nearly 4 decades ago. Marks and Gelder1 reported that in a subgroup of patients in their series of phobic adults, social anxiety manifested variably as “shyness, fears of blushing in public, of eating meals in restaurants, of meeting men or women, of going to dances or parties, or of shaking when the center of attention.” Of note, these symptoms could be distinguished from other phobic disorders including agoraphobia, specific animate phobias, and situational phobia, on the basis of both the nature of the phobic stimulus (ie, social situations), and a consistent age of onset, primarily in the late adolescent years. Marks2 later described a variety of social phobias, including “fears of eating, drinking, shaking, blushing, speaking, writing, or vomiting in the presence of other people.” Central to these phobic states were excessive concerns over one’s appearance or performance being judged, scrutinized, or negatively evaluated by others.3
As the boundaries and core features of the syndrome were being discerned, behaviorally oriented clinicians were simultaneously laying the groundwork for both reliable measurement and behavioral and cognitive treatments of social anxiety-related difficulties. Techniques including social skills training, relaxation training, systematic desensitization, and rational/cognitive restructuring were being applied to problems that were variably referred to as social phobia, social-evaluative anxiety, performance anxiety, interpersonal anxiety, heterosexual anxiety, social failure, and social inadequacy.11-17 An apparent strength of the behavioral approaches was the targeting of discrete patterns of socially anxious experience and/or maladaptive avoidance behavior, rather than a specific diagnostic entity. In contrast, early pharmacologic treatment approaches may have been somewhat hindered, as SAD had yet to be formally recognized as an autonomous syndrome requiring independent investigation. Thus, much of the early psychopharmacologic work was conducted with heterogeneous diagnostic groups and analogue samples.18 Nonetheless, preliminary evidence suggested the potential efficacy of monoamine oxidase inhibitors (MAOIs) and β-adrenergic blockers.18
With the publication of the DSM–III,19 SAD was formally acknowledged as an independent diagnosis in its own right. It was viewed as distinct, along with agoraphobia and simple phobias, from the former diffuse class of phobic reactions or phobic neuroses in earlier versions of the DSM as illustrated in the Figure.20-23 Research clearly supported the validity of the distinction, indicating that persons with social phobia could be empirically differentiated from other phobic disorders on the basis of several sociodemographic, clinical, and psychobiological correlates.1-3,18 Despite these advances, however, some argued that social phobia remained under-recognized and understudied relative to other anxiety disorders.18 In their seminal paper, Liebowitz and colleagues18 comprehensively surveyed the literature on SAD, advocated for increased systematic efforts in clinical and psychobiological investigation, and laid the groundwork for a research agenda that has largely guided subsequent empirical inquiry into SAD for nearly 20 years.
As a consequence of these key developments, the past 2 decades have been characterized by substantial progress in understanding the origins, nature, and treatment of SAD. Nearly 3,000 empirical studies, review papers, and book chapters, and more than 30 scientific and self-help books on SAD have been published. Importantly, as the empirical knowledge base continues to expand, new and alternative theoretical conceptualizations of SAD have emerged. For example, Schneier and colleagues24 have cogently argued for the recognition and study of a social anxiety spectrum, which would encompass clinical social phobic states, as well as subsyndromal manifestations, associated symptoms, behaviors, and underlying variations in temperament and personality traits, (eg, shyness, behavioral inhibition). Among the advantages of a dimensional approach, Schneier and colleagues24 suggest that a social anxiety spectrum has utility in understanding the associations among SAD and diverse comorbid clinical syndromes, identifying underlying trait-like psychological constructs, and candidate neurobiological and neurochemical substrates. Similarly, McNeil25 has proposed a continuum model of social anxiety and its disorders in which these anxieties and fears exist along a continuum, normally distributed in the general population. The most severe manifestations reside at the high end, labeled variably as social phobia, SAD, and/or avoidant personality disorder.
Diagnosis and Definition
While spectrum or continuum approaches hold promise and can guide further systematic investigation, the current and most widely accepted definition of SAD derives from the DSM-IV-TR.10
To qualify for the diagnosis of SAD, an individual must have a marked or persistent fear of one or more social situations wherein there is exposure to unfamiliar people or possible scrutiny by others. The core fears center on behaving in a way or showing symptoms of anxious arousal (eg, blushing, sweating, trembling, stuttering, etc.) that would be humiliating or embarrassing (Criterion A). Exposure to these phobic situations consistently evokes an anxiety response, which in some cases may be in the form of a panic attack (Criterion B). The individual has some insight that the fear is excessive or unreasonable, though this is not necessarily true in children (Criterion C). There must also be prominent avoidance of the phobic performance or situation and, if not, it is typically endured with great anxiety or distress (Criterion D). The criteria also require clinically significant social and/or occupational functional impairment, or the individual experiences marked distress over having the phobia (Criterion E). If the person is <18 years of age, the anxiety and/or avoidance must have endured for at least 6 months at the time of diagnosis (Criterion F). Finally, the effects of a substance, general medical condition, or the presence of other psychiatric disorders must be ruled out as causative (Criterion G), or in the case of comorbid disorders, the fear, anxiety and avoidance of SAD are not better accounted for by the co-occurring condition (Criterion H).10
The Generalized Subtype
When the diagnostic criteria for SAD were first published in the DSM-III,19 it was noted that generally, an individual has only one social phobia. Moreover, the criteria stated that unless the disorder is severe, it is rarely incapacitating. Subsequent research has provided evidence quite contrary to this early view. A significant and consequential revision of the DSM-III-R22 was the inclusion of a generalized subtype specifier, which has been retained in subsequent revisions (Figure).10,22,23 The generalized subtype encompasses a variant of SAD in which there is fear of most if not all social situations.10 Research has shown that the generalized subtype is far more common than previously thought and significantly more impairing than a more specific or circumscribed SAD (eg, a public speaking phobia). Up to two thirds of the community appears to represent the generalized subtype.26
It is widely acknowledged that generalized SAD bears close resemblance to avoidant personality disorder (APD), which is diagnosed as an Axis II disorder in the DSM-IV-TR.10 The two conditions frequently co-occur, with an average comorbidity rate of 56% based on one quantitative review of 13 studies reporting overlap.27 At present, the DSM-IV-TR allows for the diagnosis of the generalized SAD subtype on Axis I, and APD on Axis II.10 However, definitive conclusions on the nature of the underlying relationship between generalized SAD and APD have yet to be reached. One possible interpretation of the available empirical evidence is that generalized SAD and APD are not actually qualitatively independent disorders.27 An alternative conceptualization holds that APD represents the most severe form of the generalized subtype of SAD, thus suggesting a quantitative distinction.25 Whether this matter will be resolved with the publication of the DSM-V remains to be seen.
As currently defined, SAD encompasses excessive fears and resultant avoidance of one or more social or performance situations in which there is the potential for scrutiny by others and the possibility of embarrassment or humiliation.
One of the most common forms this fear takes is that of public speaking in both large and small groups. Public speaking may be an unpleasant and somewhat distressing prospect for a significant proportion of the general population. Individuals with SAD experience such incapacitating anxiety that it can actually have the untoward effect of undermining their public speaking performance, consequently reinforcing many of the fearful and maladaptive core beliefs driving the anxiety. Public speaking situations may be avoided to the extent that one’s social success and occupational advancement are compromised, (eg, turning down a promotion for fear of conducting presentations, or speaking to and managing subordinates). Interestingly, research has shown that persons with SAD consistently overestimate the anxiety that audiences perceive, and appraise their own performances as significantly poorer than observers do.28
Excessive anxiety over interacting with strangers, such as approaching someone and engaging in “small talk” at a social gathering, or speaking over the telephone, is quite common for people with SAD. These individuals will frequently complain of worries that they “won’t be able to think of anything to say.” They may also have substantial difficulty in engaging with people who are attractive to them (eg, approaching or asking someone for a date). This likely leads to lower marriage rates among people with SAD patients. Communicating with authority figures such as supervisors or managers can be problematic, as well.
Socially phobic people may also fear situations such as eating or drinking in public, as one may spill a drink, make an awkward movement, drop a utensil, or perhaps even choke or vomit. Writing in public or signing one’s name may be problematic due to the fear that one’s hand may tremble. People with SAD often fear that their symptoms of anxiety, (eg, blushing, perspiration, trembling, or a quivering voice) will be noticeable to others. For men in particular, using public lavatories to urinate may be avoided, as they may “freeze-up,” a problem known as paruresis, or “shy bladder syndrome.” What is universal among these diverse manifestations of SAD is that each occurs in a social milieu, wherein the potential for negative evaluation by others exists. In sharp contrast, these behaviors are typically performed quite effectively in private, with no distress or impairment.29
It should be noted that much of what is described above are predominantly modes of expression of SAD in Western-oriented societies. However, clinicians should be mindful of cultural variations in the presentation of SAD, or of social anxiety phenomena more generally. A notable example of a culturally dependent manifestation of social anxiety is a condition known as taijin kyofusho, which has been reported in some Asian cultures including Japan and Korea, and is categorized as a culturally bound syndrome in the DSM-IV-TR.10 Whereas the primary focus of fear and anxiety in SAD is the prospect of embarrassing or humiliating oneself, in taijin kyofusho the individual is exquisitely sensitive to interpersonal relations, and may be preoccupied with concerns over doing something, or presenting oneself in a manner, that would be embarrassing or offensive to others in a social context (the offensive subtype). Clinical presentations include excessive concerns about offending others by emitting an unpleasant bodily odor, staring inappropriately so as to make others feel uncomfortable, blushing, not presenting the appropriate facial expression, or having some real or perceived physical deformity.30
The exact nature of the relationship between taijin kyofusho and the DSM-IV-TR10 SAD is not fully clear at present. One plausible hypothesis is that there may be a common underlying core trait of social anxiety, the expression of which varies as a function of cultural idioms. More specifically, Western societies have historically emphasized the value of independence, individualism, and the importance of the construct of self. This is in contrast to traditional Eastern societies where greater importance is allocated to social interdependence, community, and/or the construct of other. Thus, clinicians (especially those serving diverse populations) should be cognizant of this and other potential culturally variable expressions of social anxiety.
SAD is a common disorder in both community and clinical populations. Estimates from large epidemiological studies of representative community samples indicate that 12.1% to 13.2% of the US population will experience diagnosable SAD during their lifetime, with 12-month prevalence rates of 6.8% to 7.4%.8-9 A recent cohort analysis conducted by Heimberg and colleagues31 demonstrated that the prevalence of SAD has increased over the past 4 decades. The disorder appears to be slightly more prevalent in females, with a female to male ratio of 3:2. Lifetime prevalence estimates from the National Comorbidity Survey (NCS) were 15.5% and 11.1%, for females and males, respectively.8 In most clinical settings, however, the genders are equally represented, or more males are seen.10 This ascertainment bias may be due to increased social demands resulting from traditional societal gender roles. For example, historically, men have been more likely to enter the workforce and to be the initiators of romantic relationships. Difficulties in these significant roles presumably lead to greater salience and recognition of personal functional impairment in men, and to subsequent treatment seeking.
Prevalence estimates in clinical samples range from 10% to 20%, but tend to vary widely.10 Estimates of prevalence in clinical settings should also be qualified by evidence showing that individuals with SAD have much lower rates of treatment seeking than people with other psychiatric illnesses of comparable severity.32 Specifically, findings from the NCS revealed that only 22.6% of people with the generalized subtype, and only 12.7% of people with nongeneralized SAD, ever sought treatment by a physician in their lifetime.26 Interestingly, in a recent survey of callers to the Anxiety Disorders Association of America, 1,000 participants were screened for the presence of diagnosable or subthreshold SAD. A current prevalence rate of 29.5% was found for diagnosable SAD, while another 4.1% met subthreshold criteria.33 These data speak both to the very high rates of SAD among anxiety disorder populations, and quite possibly to the means by which people with the disorder may initiate contact with the mental health specialty sector.
Onset and Course
Clinicians and epidemiologists in the research community generally agree that SAD has an early onset, often in childhood or adolescence. Onsets later in life, after a peak between the second and third decades, are relatively rare and are more likely to be cases of SAD occurring secondarily to, or as sequellae of, another mental disorder (eg, depression, psychotic disorders, eating disorders).34 Though onset is characteristically early, individuals with SAD may not recognize the fears and anxieties they experience in social situations as legitimate emotional problems in need of treatment. Rather, the symptoms may be construed or dismissed as excessive shyness, or merely as a character flaw. Equally problematic, the very nature of the core pathology in SAD, fear and avoidance of embarrassment and humiliation, leads to reduced treatment seeking. Thus, it is not surprising that analysis of NCS data revealed a median interval of 15 years between the age of first onset of SAD and the age at which people with SAD first sought professional help.26 It is arguable that the primary reason the vast majority of individuals seek mental health services is not because of their SAD per se; rather, it is the impairment resulting from secondary comorbid conditions including panic, substance abuse, depression, and suicidal ideation.26,32
Research clearly suggests a largely chronic and unremitting course, which can last for decades if left untreated. Untreated SAD, especially the generalized subtype, will almost invariably lead to increasing levels of functional impairment as major role transitions occur. Specifically, as the person with SAD attempts to progress through stages of life with increasing social demands, and requiring greater social facility, (eg, high school to college, college to employment, marriage), one’s failure to thrive and master these social challenges may lead to feelings of hopelessness and despair. In turn, such feelings may lead to attempts to self medicate. These periods are fertile grounds for secondary psychiatric illnesses to emerge (eg, depression, substance abuse).26,32
In virtually all major studies of representative community and clinical samples, SAD has shown elevated rates of comorbidity (both as a primary and secondary disorder). Among the most frequent co-occurring Axis I disorders in primary SAD are depressive illnesses (eg, MDD, dysthymia),6,35 other anxiety disorders (eg, panic disorder with or without agoraphobia, generalized anxiety disorder)35,36 and substance use/abuse disorders (eg, alcohol abuse or dependence).32,35 As already noted, among the Axis II disorders, APD is highly comorbid with SAD, especially the generalized subtype.27
While impairments in occupational and social functioning, including inability to work, attend school, socialize, or marry, are significant in SAD, these problems are compounded by the presence of comorbid psychopathology.37-40 For example, in a prospective community study, young adults with comorbid SAD and MDD who were followed for approximately 4 years were significantly more likely than those with only MDD to experience more depressive symptoms, a longer duration of major depressive disorder, more intense suicidal ideation, and greater odds of having attempted suicide during the follow-up period.41
Important in this regard, data from both cross-sectional (using retrospective report) and prospective longitudinal studies have consistently demonstrated temporal precedence of anxiety disorders in cases of comorbidity with MDD.42,43 For example, analysis of data from the Epidemiological Catchment Area Program Surveys (waves 1 and 2) revealed that individual anxiety disorders (assessed at wave 1) each appear to confer an independent risk for the onset of adult MDD within 12 months (wave 2).44 Anxiety disorders have been found to be the most common primary disorders associated with MDD, and to predict the greatest risk of subsequent MDD. Of note, secondary cases of MDD were found to be more persistent and severe than pure or primary MDD.42
Thorough assessment of SAD and social anxiety symptoms is a key part of the treatment process. Clinical observations, focused interviewing, and the use of appropriate measures can help to facilitate accurate diagnosis and effective treatment planning. Several comprehensive reviews of the methodological issues and available assessment instruments for SAD have been presented elsewhere.45-47 The authors of this article provide a brief summary of strategies and tools that have been particularly useful in the assessment of SAD and social anxiety.
The clinical interview typically serves as the point of departure in assessing for SAD and social-evaluative anxieties. A detailed inquiry concerning a range of anxiety-provoking and/or avoided social situations is requisite (see phenomenology above). Careful observation of in-session behavior and patient report of physiological reactivity is also helpful. Poor eye contact, restlessness, hand tremor, brief answers to questions, late arrival to appointments, and requests to leave early, may all be evidence of the individual’s discomfort with the interview, which itself is a type of social interaction. The individual may also have trouble tracking the course of the conversation due to the interference of anxiety with sustained attention over time.
Identification of comorbid psychopathology is an especially important part of the diagnostic process, as people with co-occurring conditions pose a more significant treatment challenge. In this regard, clinicians should be particularly vigilant for the presence of other anxiety disorders, substance use or abuse, depressive symptoms, and possible suicidal ideation. Likewise, when these frequently co-occurring conditions are the presenting complaint, accompanying symptoms of social anxiety should be carefully probed for.
Clinician Administered Instruments
A variety of structured interviews and clinician-administered measures are also valuable in the assessment process. The Structured Clinical Interview for DSM-IV (SCID-IV) is a comprehensive clinician-administered diagnostic interview, with both clinical and research versions available.48 It has been designed to be consistent with the classification of psychiatric diagnoses published in DSM-IV,24 and is organized into separate modules which evaluate classes of disorders (eg, psychotic, affective, anxiety, etc). Social phobia and its generalized subtype are assessed in the anxiety disorders module.
The SCID-IV is broad and comprehensive in its coverage and has become an industry standard for clinical research requiring thorough diagnostic evaluations. However, it can also be time-consuming to administer, especially in more complex clinical presentations. The instrument requires adequate training and instruction to ensure appropriate administration and interpretation. Thus, it is most commonly employed in academic and/or research settings, where there is likely to be adequate staff and resources available for its use.
Another structured interview that focuses more precisely on the diagnosis of anxiety disorders is the Anxiety Disorders Interview Schedule for the DSM-IV (ADIS-IV).49 This interview is also administered by a clinical examiner in a semi-structured format, and identifies the presence of SAD, its generalized subtype, and the various other anxiety syndromes. There are modules to detect common co-occurring disorders, (eg, affective, substance use, and somatoform disorders), as well. The ADIS-IV is also equipped with a psychotic screening module. Much like the SCID-IV, the ADIS-IV requires training and is more typically employed in clinical research settings and anxiety disorder specialty clinics.
The frequently used, 24-item, clinician-administered Liebowitz Social Anxiety Scale (LSAS) provides ratings of fear and avoidance among a wide range of social situations.50 Patients’ levels of fear and avoidance are rated separately for each of the specified social situations on a four-point Likert scale. A total score is obtained by summing the two subscales. The LSAS is both valid and reliable, and has become the standard primary outcome measure for social anxiety symptoms in clinical trials research. When readministered at later points in the treatment process, the LSAS has shown a high degree of sensitivity to change in the severity of social anxiety symptoms.51 Though not designed to be an instrument for the diagnosis of SAD per se, scoring ranges of the LSAS roughly correspond to the following diagnostic levels: With total scores of ≤30, a diagnosis of SAD is less likely; however, patients may still meet criteria for SAD in a specific circumstance, such as giving a presentation in front of others. Total scores in the range of 30–60 are more typical of those with social anxiety in a specific circumstance, such as public speaking, eating in front of others, or other performance anxiety. Total scores in the range of 60–90 commonly occur in patients with the generalized subtype of SAD. Total scores of ≥90 occur in those patients with the generalized subtype of SAD experiencing very severe social anxiety and avoidance in a variety of situations.
The Brief Fear of Negative Evaluation Scale (BFNE)52 is a useful 12-item self-report measure based on the original 30-item scale developed by Watson and Friend.13 Whereas the LSAS focuses on the dimensions of fear and avoidance in various social situations, the BFNE assesses the degree to which patients have core components of social-evaluative anxiety, including thoughts, expectations, and associated distress over possible negative social judgments and embarrassing behaviors. Representative statements include “I am afraid that others will not approve of me,” and “I often worry that I will say or do the wrong things.” Statements are rated as true or false with endorsed items summed for a total score. The scale has been found to be reliable and valid in nonclinical samples, and was recently validated in a sample of clinically anxious individuals.53 The BFNE has also been found to be a sensitive measure of change over the course of treatment.
Historically, treatments for social-evaluative anxieties and SAD have included both psychopharmacologic and psychotherapeutic strategies. Although these two modalities have largely developed independent of one another and are reviewed individually here, good clinical practice often necessitates a judicious combination of both medication and psychosocial therapy. This is particularly important in more complex presentations, including the generalized subtype of SAD and the presence of co-occurring psychopathology.54
Although pharmacotherapy of SAD was relatively neglected early on,18 recent years have witnessed a dramatic increase in progress of medication-based treatment. Several factors have likely contributed to this shift in priorities. Foremost among these was the recognition of SAD as a formal diagnosis, one that is both highly prevalent and substantially impairing. Equally important has been the demonstrated effectiveness of specific pharmacologic agents in treating SAD as well as the recent ascendance of biological psychiatry and psychopharmacology as a clinical specialization. Widely increased research efforts have been sponsored and/or conducted by the pharmaceutical industry in efforts to obtain specific indications in the treatment of SAD for various drug products.
Several comprehensive narrative and quantitative reviews of the pharmacotherapy literature in SAD have been presented elsewhere.18,55-60 This article emphasizes fundamentally practical medication treatments that have received the greatest attention and been subjected to rigorous empirical investigation (typically through randomized, double-blinded, placebo-controlled clinical trials), and that are generally viewed by a consensus of the research community as first- or second-line treatments for SAD. These medications include MAOIs and reversible MAOIs (RIMAs), selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), benzodiazepines, β-adrenergic blockers, and novel therapeutic agents (eg, anticonvulsants).
As a group, these studies have been characterized by some degree of methodological heterogeneity, such as varying research designs, number and nature of comparison conditions, sample composition, duration of acute treatment, medication dosage, and follow-up intervals. However, a useful thread of continuity within the extant literature has been the relatively consistent use of specific outcome measures, namely the LSAS (as described above)50 and the Clinical Global Impressions–Improvement (CGI-I) rating scale. The CGI-I is a clinician-rated measure of improvement in which a rating of 2 equals a global judgment of “much improved,” and a rating of 1 equals “very much improved.”61 Reductions in pretreatment to posttreatment LSAS scores and specific thresholds, or cutoff scores, are also reflective of varying degrees of improvement including treatment response (sometimes arbitrarily set at a 20% to 30% reduction from baseline LSAS), and remission (LSAS <30).62 Similarly, global ratings of 1 or 2 on the CGI-I are often used as an index of treatment response. Because of their common usage in the pharmacotherapy literature, these instruments provide useful metrics for inter-study comparisons.
Irreversible Monoamine Oxidase Inhibitors
The MAOIs were one of the first groups of medications to receive intensive systematic evaluation in the treatment of SAD via controlled clinical trials. Among this class, the irreversible MAOI phenelzine has consistently demonstrated its effectiveness in treating SAD, with supporting evidence coming from four published double-blind, placebo-controlled trials (Table 1).63-67 Rates of improvement have ranged from 64% to 91%,64,65 generally far exceeding rates of response in placebo-controlled conditions, as well as surpassing rates of improvement seen with alprazolam,63 cognitive-behavioral group therapy (on some measures),63,66 atenolol,64 and moclomebide (on the social avoidance subscale of LSAS).65 Essentially, these studies have established the methodological groundwork for subsequent pharmacotherapy studies in SAD, and phenelzine has largely set the standard of comparison for treatment efficacy in SAD.
Two other MAOIs have been examined in the treatment of SAD (Table 1). Positive results were reported in two open clinical trials of tranylcypromine.68,69 In a study by Versiani and colleagues,68 patients were followed openly for 52 weeks with 62% of patients showing marked improvement, and another 17% showing moderate improvement. In comparison, modest levels of improvement were found in a 6-week, open clinical trial of the MAOI selegilene in 16 SAD patients (12 with generalized SAD) using a fixed dose regimen of 5 mg bid. In this trial, 9 of 16 patients (56%) completed treatment with 3 of those 9 (33%) classified as markedly or moderately improved on the CGI-I.70
Despite the proven effectiveness of the irreversible MAOIs in the treatment of SAD, and of phenelzine in particular, their use has been limited by an adverse side-effect profile, including the potential danger of hypertensive crisis if dietary restrictions on tyramine-rich foods are not carefully followed. This has lead to the development and examination of RIMAs as an alternative.56
Reversible Monoamine Oxidase Inhibitors
Moclobemide was the first RIMA to be developed, showing moderate efficacy in the treatment of MDD.56 In the treatment of SAD, four randomized, double-blind, placebo-controlled trials have been published, each reporting varying degrees of efficacy (Table 1).65,71-73 In a study by Versiani and colleagues,65 14 of 17 (82%) patients (remaining out of an initial 26) treated with moclobemide were classified as treatment responders. Additionally, moclobemide was better tolerated than phenelzine. In another study, by Katschnig and colleagues,73 a dose-response relationship was observed; patients receiving 600 mg/day achieved more improvement than those receiving 300 mg/day. Response rates were 47%, 41%, and 34% for the 600 mg/day, 300 mg/day, and placebo groups, respectively. In sharp contrast, null findings were reported in the other two controlled trials of moclobemide. Specifically, no evidence of superior clinical efficacy over placebo was found for moclobemide in an 8-week flexible-dose design,71 or in a 12-week fixed-dose design.72
A second RIMA, brofaromine, which is similar to the SSRIs in that it inhibits reuptake of serotonin, has been subjected to three controlled trials in the treatment of SAD (Table 1).74-76 Each of these studies produced generally positive results indicating superior clinical efficacy of brofaromine over placebo on primary outcome measures, as well as superiority on secondary outcome measures in studies by van Vliet and colleagues74 and Fahlen and colleagues.75 Among completers across studies, improvement rates ranged from 50% to 78%75,76 for the groups treated with brofaromine as compared to 14% to 23% in the groups treated with placebo. In all three trials, the medication was generally well tolerated.
Selective Serotonin and Serotonin Norepinephrine Reuptake Inhibitors
SSRIs are also well tolerated and are highly efficacious for both depressive and other anxiety disorders, which are often comorbid with SAD. SSRIs are easily managed compared to other drug classes, and have therefore been investigated extensively in the treatment of SAD and its generalized subtype. Virtually all SSRIs, including citalopram,77-79 escitalopram,80-81 fluoxetine,82-88 fluvoxamine,89-91 paroxetine,92-98 paroxetine controlled release,99 and sertraline100-104 have been subjected to randomized, double-blind, placebo-controlled clinical trials, typically demonstrating superior treatment efficacy to placebo control conditions on primary efficacy parameters (Table 1). While paroxetine was the first drug in this class to receive Food and Drug Administration approval in the US for the treatment of SAD, sertraline and the SNRI venlafaxine extended release (XR) have also secured FDA approval.
Given the preponderance of evidence in support of the SSRIs, at present these medications are widely accepted and strongly recommended as first-line treatments for SAD and its generalized subtype. Additionally, recent placebo and comparator-controlled studies of venlafaxine XR have demonstrated superior treatment efficacy over placebo-controlled conditions, as well as comparable efficacy to paroxetine in head-to-head comparisons (Table 1).105-109 Hence, venlafaxine XR should now be considered a first-line treatment for generalized SAD.
Despite demonstrated efficacy in treating other anxiety disorders (eg, panic disorder, obsessive-compulsive disorder [OCD]), there is little existing data to support the efficacy of tricyclic antidepressants in the treatment of SAD. Imipramine and clomipramine have been evaluated. One investigation using a randomized, placebo-controlled, flexible dose design found that only 11.1% (2 of 18) patients treated with imipramine versus 4.35% (1 of 23) patients receiving placebo, improved.110 Similarly, in a case series of 15 patients treated with a mean dose of 176.4 mg/day of imipramine, Simpson and colleagues111 reported that only 20% of patients were rated as improved or very much improved. Open clinical trials of clomipramine have generally produced mixed results.56
Gelernter and colleagues63 compared alprazolam (on average 4.2 mg/day) to phenelzine, placebo, and Heimberg’s cognitive behavioral group therapy (CBGT).66 Only 38% of patients receiving alprazolam were classified as treatment responders compared to 69% of patients receiving phenelzine. Moreover, only 2 months after drug discontinuation, most patients reported a return to baseline levels of social anxiety symptoms. In contrast, the efficacy of the longer acting benzodiazepine, clonazepam, was tested in a 10-week, double-blind, placebo-controlled trial, revealing a treatment response rate of 78% compared to only 20% of patients receiving placebo.112 The effectiveness of clonazepam in treating SAD has also been supported by several open clinical trials, and has recently been examined in a placebo-controlled clinical trial as augmentation for partial and nonresponse to SSRI therapy. Some benefit was observed suggesting the need for further controlled investigation.113
Interestingly, Jefferson114 points out that there has been a general reluctance among clinicians to utilize benzodiazepines, especially in longer-term treatment of SAD, despite evidence suggesting long-term effectiveness and safety of agents such as clonazepam. In fact, medications such as clonazepam possess a number of desirable qualities, including its established efficacy in treating SAD, relatively rapid onset of action, good tolerability, overdose safety, and dose flexibility. On the downside, however, there are several undesirable side effects such as sedation, impairment of coordination and cognition, and possible sexual dysfunction. However, these side effects are not specific to benzodiazepines. There is also greater abuse potential, discontinuation difficulties, adverse interactions with alcohol and other substances of abuse, and ineffectiveness for comorbid conditions, particularly depression.114 At present, there are no established guidelines suggesting the use of clonazepam over SSRIs as a first-line treatment for SAD. Rather, clinicians will need to assess potential benefits and liabilities on a case-by-case basis, remaining vigilant throughout the course of therapy.
The appeal of β-adrenergic blockers has historically been the ability of these drugs to reduce the increased autonomic arousal that commonly accompanies discrete performance situations (eg, public speaking engagements, musical performances). Thus, much of the early research with these agents focused on performance-related anxiety.18 In the controlled study by Liebowitz and colleagues,64 however, only 30% of SAD patients receiving atenolol (≥50 mg/day) were rated as improved compared to 23% of patients receiving placebo.
Generally speaking, β-adrenergic blockers (eg, propranolol) should be reserved for treating the prominent physiological arousal characteristic of discrete public performance situations. When a clinical presentation suggests a circumscribed or situation-specific case of performance anxiety, a standing dose of an SSRI/SNRI or other medication is unnecessary. Clinicians should consider prescribing agents such as propranolol.
Novel Therapeutic Agents
Recent interest in the use of novel anticonvulsants as antianxiety agents has prompted investigation of these medications in the treatment of generalized SAD. One randomized, double-blind, placebo-controlled study of the novel anticonvulsant gabapentin, reported superior efficacy of this medication over placebo in generalized SAD.115 Another recent controlled investigation of the closely related compound pregabalin has reportedly shown superior clinical efficacy of over a placebo control group of generalized SAD patients.116 These medications warrant further investigation.
Patients with generalized SAD who are going to receive medication treatment should first be given one of the established SSRIs or SNRIs.90-109 Treating generalized SAD effectively usually requires 8–12-week trials, and dosages tend to be on the higher side of the therapeutic range for each drug. In this regard, treating generalized SAD is more like treating OCD than MDD. Discontinuation trials suggest that ≥6 months of maintenance treatment is helpful to preserve acute treatment gains. Nonresponders should be tried on alternative drugs of proven efficacy, including drugs of a different class (eg, MAOIs63-66 or RIMAs).65,71-76
Partial responders can be maintained on their original drug, augmented by benzodiazepines such as clonazepam.113 Medication augmentation with an established psychosocial treatment seems helpful in clinical practice, and is currently under study in our lab and others.87,88
Patients with nongeneralized SAD often do well with PRN β-blocker administration used acutely before a speech or performance.18 However, β-blockers seem more helpful for symptoms such as tremor, palpitations, tachycardia, and a catch in one’s throat than for the anticipatory anxiety that often plagues such patients for days (and nights) before an important speech or performance. Benzodiazepines appear helpful for this anticipatory anxiety, and can be used in conjunction with β-blockers. In such a situation, the benzodiazepine would be used for several days before the event, and the β-blockers would be taken approximately 1 hour before the speech or performance. Whether MAOIs, SSRIs, or SNRIs used on a maintenance basis are helpful in patients who only suffer performance anxiety is not clear. However, they do seem to help the performance anxiety that is a component of generalized SAD.
SAD and social-evaluative anxiety states have been treated with a variety of behavioral, cognitive, and combined cognitive-behavioral therapies (CBT). Briefly reviewed are some methods employed to treat SAD via cognitive and behavioral therapies. The authors of this article focus on the CBT protocol developed by Heimberg and colleagues, which is currently being used in conjunction with pharmacotherapy in a collaborative research program between the Anxiety Disorders Clinic of New York State Psychiatric Institute and the Adult Anxiety Clinic of Temple University. A more comprehensive examination of the CBT literature can be found in articles by Heimberg and Juster,117 Hoffman and Barlow,29 and Turk and colleagues.118
Behavior therapies used for SAD have been relatively problem focused, addressing the most prominent features associated with the disorder. These have included social skills training to address functional skill deficits, physiological retraining to address the physical symptoms of anxious arousal occurring in social contexts, and systematic exposure to actual anxiety-provoking social situations.117
If skill deficits are present, social skills training focuses primarily on helping patients acquire skills necessary to relate to others more naturally and competently in social situations. These skills include developing topics for conversation and maintaining appropriate eye contact and bodily orientation. In essence, this training instructs patients in knowing what to say and how to say it. Such skills are typically rehearsed in session with the therapist and then practiced in real-life situations as homework assignments between therapy sessions.
Physiological retraining, or applied relaxation, involves teaching patients to use breathing techniques and progressive muscle relaxation when anxiety-provoking social situations are encountered. Patients are taught to identify the earliest physiological cues of anxious arousal upon entering socially anxious situations, and then to counter these sensations via rapid deployment of learned anxiety reduction skills.
Systematic exposure, either real or imagined, to a hierarchy of progressively more anxiety-provoking stimuli has been found to be a powerful component of treatment for several anxiety disorders. These disorders include panic disorder (eg, physical sensations), OCD (eg, perceived contaminants, intrusive thoughts) and posttraumatic stress disorder (eg, traumatic memories and associated environmental cues). In systematic exposure for SAD, patients engage in a feared social activity such as making small talk, public speaking, and dating, and remain in the feared situation until the anxious arousal subsides. In the continued presence of the anxiety-provoking social stimulus, the central nervous system gradually habituates, so that the stimulus situation no longer has the capacity to evoke anxious arousal. Treatments that have focused on social skills acquisition and physiological retraining have likely contained similar habituation-related mechanisms that are believed to operate in exposure-based treatments.
Individuals with SAD typically have persistent negative thoughts and maladaptive beliefs regarding how others perceive and evaluate them socially. These distorted cognitions generate significant anxiety and form the psychological core of the disorder. Cognitive therapy, also known as cognitive restructuring, has been used to help individuals with SAD alter or “restructure” these distorted views of their social world, in turn reducing their experience of anxiety.119
The essential components of cognitive therapy for SAD involve learning to pay attention to the thoughts that occur automatically in anxiety-provoking social situations (eg, “They will think I am weird”), and challenging or disputing these negative cognitions. Patients are taught to treat each negative automatic thought as a hypothesis, much like a scientist, and to evaluate the available evidence via systematic logical analysis. If the hypothesis does not hold up after a careful review of available data (eg, “What is the evidence?”), then the capacity of the thought to generate further anxiety should weaken.
A set of common beliefs and errors in logic that socially anxious persons habitually make has been discerned,118 and the patient is taught to self-monitor and identify these errors in his or her automatic thoughts. For example, an anxiety provoking thought that others will think the individual is “weird” is dependent in part on the capacity of the individual to read another’s mind or to predict the future. Once these erroneous beliefs are identified, alternative interpretations of the situation are sought by structured disputing questions (eg, “Do I have a crystal ball?” or “What is another way of looking at it?”), as well as considering means to moderate the impact of negative outcomes (eg, “So what if it happens?”). This type of hypothesis testing proceeds through a Socratic-like dialogue between therapist and patient in session. Patients are trained to internalize and utilize this dialogue when working to challenge maladaptive anxiety-provoking thoughts on their own between sessions.
Combined Cognitive-Behavioral Therapy
The authors of this article use CBT treatment protocol in their clinic, which combines psychoeducation, cognitive therapy, and in-session systematic exposures to feared social situations using planned and structure role-play techniques. Cognitive restructuring exercises and in vivo exposures are assigned for between session homework, as well. For a complete presentation of the components of the treatment, including in-session exercises and homework assignments, one may refer to the Social Anxiety Client Manual by Hope and colleagues.120
Briefly, individuals with SAD are educated about social anxiety in both its normal and pathological manifestations. The therapist works to create an atmosphere of collaboration in which data acquired through careful assessment (as discussed above) are used to create a hierarchy of feared and avoided social situations. A rating of fear is established for each item in the hierarchy using the Subjective Units of Distress Scale, a 0–100 rating scale in which higher numbers indicate increasing levels of distress and anxiety. The degree of avoidance of each situation is also estimated using a similar 0–100 rating scale. A typical fear and avoidance hierarchy is shown in Table 2.
Clients are taught to employ cognitive restructuring techniques, as discussed above, which help them to cope with anxiety experienced during in-session role-plays with the therapist. A “rational response” to the negative content of the automatic thoughts is eventually derived from the Socratic-like dialogue between patient and therapist (eg, “Being friendly does not equal being weird”). Importantly, the rational response is not seen merely as positive thinking superimposed on the negative thoughts. Rather, it is the powerful end result of a logical and scientific disputation process.
Role plays within session proceed by involving the patient, therapist and/or one or more therapeutic confederates, depending on the parameters of the anxiety-provoking social situation (eg, age, gender, size of group). This provides both in-session practice of cognitive restructuring skills and exposure to the distressing social situation, so that the patient can experience the process of habituation. Role plays may also provide practice with situations the patient may have very little experience with given their previous patterns of avoidance. The therapist and patient gradually work through the hierarchy beginning with situations that prompt moderate amounts of anxiety, and working up to more distressing situations as therapy progresses. Much of the critical work is also done between sessions by assigning homework in which patients practice using these skills to cope with challenging and phobic situations in their natural social environment.
Group Cognitive-Behavioral Therapy for Social Anxiety
CBT for the treatment of SAD has frequently been conducted in a group format. This approach provides a therapeutic context in which members of the group enact and replicate some of the problematic or anxiety-provoking social situations that individuals encounter in daily life. For example, patients can practice presentations or public speaking in front of the group, role-play social encounters with members of either sex, and receive constructive feedback from co-members. This also enables group therapists to evaluate the accuracy patients have in assessing their own social behavior, as well as the degree to which their anxiety is visible to others.120
Thus far, several comprehensive meta-analytic reviews have evaluated the extant literature on controlled studies of the behavioral therapy and CBT described above.121-124 Reviewers have consistently reached the same broad conclusions. Namely, systematic exposure by itself, or combined with cognitive therapy, results in superior effect sizes (eg, mean Cohen’s d=.74)123 when compared to control conditions. Equally impressive has been the durability of therapeutic benefit achieved with these treatment modalities, and the propensity toward increasing gains over follow-up periods.122
Monotherapy Versus Combined Therapy
Effective treatment of complex presentations of SAD, including the generalized subtype and/or co-occurring psychopathology, often require a multimodal treatment approach, utilizing both evidence-based pharmacotherapy and psychosocial therapies. This assertion is predicated more on clinical experience than on existent empirical literature, which has yet to unequivocally demonstrate the superiority of combination therapy over monotherapy.
Early studies contrasted pharmacotherapy and psychotherapy, implicitly seeking the answer to the question of which therapy is superior.63,66 Findings have been mixed, demonstrating for example, that pharmacotherapy with phenelzine is superior to CBGT in the acute phase of illness.66 However, when patients are followed-up, it appears that gains obtained from psychosocial therapy may catch up to gains achieved via pharmacotherapy, or may exceed those gains on some efficacy parameters.67 The picture may be more complex, however. Specifically, it is not clear at present that superiority of CBT in long-term follow-up is due solely to continuing accrual or consolidation of gains with CBT. Rather, differences favoring CBT may be due in part to relapse of some patients when medication is discontinued. If this were determined to be the case, it would only serve to bolster support for the conduct of sequencing and augmentation studies.
Recently, investigators have questioned whether the combination of pharmacotherapy and psychosocial therapy is superior to either therapy alone.86,87 Results have generally been equivocal. Studies by Kobak and colleagues86 and Clark and colleagues87 demonstrated that both combinations of active treatments and monotherapy are superior to placebo-controlled conditions. However, thus far there is little evidence suggesting superiority of the combined treatments over either individual treatment. It should be noted that both of these studies used fluoxetine, which generally has less support in the literature as a treatment for SAD. A recently completed study conducted by Liebowitz and Heimberg (unpublished data, 2005), however, has combined two of the most efficacious treatments known for SAD, phenelzine and Heimberg’s CBGT, contrasting their combination with each therapy individually. Data are presently being analyzed and results are forthcoming.
Equally promising, current work in the authors’ clinic, in collaboration with Heimberg and colleagues at the Adult Anxiety Disorders Clinic of Temple University (unpublished data, 2005), has taken the next logical step in this line of investigation by examining whether the “sequencing” or “augmentation” of pharmacotherapy with individual CBT provides superior treatment outcome as compared to pharmacotherapy alone. To our knowledge this is the first study of its kind. Large scale, multicenter, clinical trial research of this nature is by necessity painstaking and somewhat lengthy. However, designs employing sequencing and augmentation strategies for partial and/or nonresponders should help discern optimal combinations and/or sequences of treatment, thus informing clinical practice and maximizing long-term treatment effectiveness.
SAD has clearly evolved from a once neglected anxiety disorder to an increasingly recognized, highly prevalent, and impairing psychiatric condition with considerable public health significance. The distinguishing of a generalized subtype, which bears close resemblance to APD, has had important implications for assessment and treatment of SAD. Optimal assessment of SAD can be achieved via careful clinical interviewing and in-session behavioral observation, the use of semi-structured interview procedures, and/or symptom-specific clinician-administered and self-report questionnaires. Probing for co-occurring conditions, especially other anxiety, affective, and substance use disorders, is equally critical in evaluating patients with suspected or probable SAD. Several medications including MAOIs, RIMAs, SSRIs, benzodiazepines, and b-blockers have shown acute phase treatment efficacy in randomized, double-blind, placebo-controlled trials. CBT, combining cognitive restructuring techniques and systematic graded exposure, has also shown treatment efficacy, typically with maintenance of gains enduring beyond the acute phase of therapy. As of yet, the combination of pharmacotherapy and psychotherapy has not been established empirically to be more effective than either therapy alone. However, clinical experience continues to suggest the utility of multimodal treatment approaches in maximizing long-term effectiveness. Systematic research efforts are presently underway to discern optimal treatment strategies and to provide a solid empirical foundation for current clinical practice. PP
1. Marks IM, Gelder MG. Different ages of onset in varieties of phobia. Am J Psychiatry. 1966;123(2):218-221.
2. Marks IM. The classification of phobic disorders. Br J Psychiatry. 1970;116(533):377-386.
3. Amies PL, Gelder MG, Shaw PM. Social phobia: a comparative clinical study. Br J Psychiatry. 1983;142:174-179.
4. Schneier FR, Johnson J, Hornig CD, Liebowitz MR, Weissman MM. Social phobia. Comorbidity and morbidity in an epidemiologic sample. Arch Gen Psychiatry. 1992;49(4):282-288.
5. Schneier FR, Heckelman LR, Garfinkel R, et al. Functional impairment in social phobia. J Clin Psychiatry. 1994;55(8):322-331.
6. Kessler RC, Stang P, Wittchen HU, Stein M, Walters EE. Lifetime co-morbidities between social phobia and mood disorders in the U.S National Comorbidity Survey. Psychol Med. 1999;29(3):555-567.
7. Stein MB, Fuetsch M, Müller N, Höfler M, Lieb R, Wittchen HU. Social anxiety disorder and the risk of depression: a prospective community study of adolescents and young adults. Arch Gen Psychiatry. 2001;58(3):251-256.
8. Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month prevalence of DSM III-R psychiatric disorders in the United States. Results from the National Comorbidity Survey. Arch Gen Psychiatry. 1994;51(1):8-19.
9. Kessler RC, Berglund P, Demler O, Jin R, et al. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62(6):593-602.
10. Diagnostic and Statistical Manual of Mental Disorders. 4th ed text rev. Washington, DC: American Psychiatric Association; 2000.
11. Paul G. Insight Versus Desensitization in Psychotherapy: An Experiment in Anxiety Reduction. Stanford, CA: Stanford University Press; 1966.
12. D’Zurilla TJ. Reducing heterosexual anxiety. In: Krumboltz JD, Thoresen CE, eds. Behavioral Counseling: Cases and Techniques. New York, NY: Holt, Rinehart and Winston; 1969.
13. Watson D, Friend R. Measurement of social-evaluative anxiety. J Consult Clin Psychol. 1969;33(4):448-457.
14. Marzillier JS, Lambert C, Kellett J. A controlled evaluation of systematic desensitization and social skills training for socially inadequate psychiatric patients. Behav Res Ther.1976;14(3):225-238.
15. Trower P, Yardley K, Bryant B, Shaw P. The treatment of social failure: A comparison of anxiety-reduction and skills acquisition procedures on two social problems. Behav Mod. 1978;2(1):41-60.
16. Kanter NJ, Goldfried MR. Relative effectiveness of rational restructuring and self-control desensitization in the reduction of interpersonal anxiety. Behav Res Ther. 1979;14(4):472-490.
17. Öst LG, Jerremalm A, Johansson J. Individual response patterns and the effects of different behavioral methods in the treatment of social phobia. Behav Res Ther. 1981;19(1):1-16.
18. Liebowitz MR, Gorman JM, Fyer AJ, Klein DF. Social phobia: Review of a neglected anxiety disorder. Arch Gen Psychiatry. 1985;42(7):729-736.
19. Diagnostic and Statistical Manual of Mental Disorders. 3rd ed. Washington, DC: American Psychiatric Association; 1980.
20. Diagnostic and Statistical Manual of Mental Disorders. Washington, DC: American Psychiatric Association; 1952.
21. Diagnostic and Statistical Manual of Mental Disorders. 2nd ed. Washington, DC: American Psychiatric Association; 1968.
22. Diagnostic and Statistical Manual of Mental Disorders. 3rd ed rev. Washington, DC: American Psychiatric Association; 1987.
23. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994.
24. Schneier FR, Blanco C, Antia SX, Liebowitz MR. The social anxiety spectrum. Psych Clin North Am. 2002;25(4):757-774.
25. McNeil DW. Terminology and evolution of the constructs. In: Hofmann SG, DiBartolo PM, eds. From Social Anxiety to Social Phobia: Multiple Perspectives. Needham Heights, MA: Allyn & Bacon; 2000.
26. Kessler RC, Stein MB, Berglund P. Social phobia subtypes in the national comorbidity survey. Am J Psychiatry. 1998;155(5):613-619.
27. Reich J. The relationship of social phobia to avoidant personality disorder. In: Hoffman SG, DiBartolo PM, eds. From Social Anxiety to Social Phobia: Multiple Perspectives. Needham Heights, MA: Allyn & Bacon; 2000:148-161.
28. Rapee RM, Lim L. Discrepancy between self- and observer ratings of performance in social phobics. J Abnorm Psychol. 1992;101(4):728-731.
29. Hoffman SG, Barlow DH. Social phobia (Social Anxiety Disorder). In: Barlow DH, ed. Anxiety and Its Disorders: The Nature and Treatment of Anxiety and Panic. New York, NY: Guilford Press; 2002:454-476.
30. Clarvit SR, Schneier FR, Liebowitz MR. The offensive subtype of Taijin-kyofu-sho in New York City: The phenomenology and treatment of a social anxiety disorder. J Clin Psychiatry. 1996;57(11):523-527.
31. Heimberg RG, Stein MB, Hiripi E, Kessler RC. Trends in the prevalence of social phobia in the United States: a synthetic cohort analysis of changes over four decades. Eur Psychiatry. 2000;15(1):29-37.
32. Kessler RC. The impairments caused by social phobia in the general population: Implications for intervention. Acta Psychiatr Scand Suppl. 2003;(417):19-27.
33. Zhang W, Ross J, Davidson JR. Social anxiety disorder in callers to the Anxiety Disorders Association of America. Depress Anxiety. 2004;20(3):101-106.
34. Wittchen HU, Fehm L. Epidemiology and natural course of social fears and social phobia. Acta Psychiatr Scand Suppl. 2003;( 417):4-18.
35. Brown TA, Campbell LA, Lehman CL, Grisham JR, Mancill RB. Current and lifetime comorbidity of the DSM-IV anxiety and mood disorders in a large clinical sample. J Abnorm Psychol. 2001;110(4):585-599.
36. Wittchen HU, Zhao S, Kessler RC, Eaton WW. DSM-III-R generalized anxiety disorder in the national comorbidity survey. Arch Gen Psychiatry. 1994;51(5):355-365.
37. Schneier FR, Johnson J, Hornig CD, Liebowitz MR, Weissman MM. Social phobia. Comorbidity and morbidity in an epidemiologic sample. Arch Gen Psychiatry. 1992;49(4):282–8.
38. Davidson JR, Hughes DL, George LK, Blazer DG. The epidemiology of social phobia: Findings from the Duke Epidemiological Catchment Area study. Psychol Med. 1993;23(3):709-718.
39. Schneier FR, Heckelman LR, Garfinkel R, et al. Functional impairment in social phobia. J Clin Psychiatry. 1994;55(8):322-331.
40. Wittchen HU, Beloch E. The impact of social phobia on quality of life. Int Clin Psychopharmacol. 1996;11(suppl 3):15-23.
41. Stein MB, Fuetsch M, Muller N, Hofler M, Lieb R, Wittchen HU. Social anxiety disorder and the risk of depression: A prospective community study of adolescents and young adults. Arch Gen Psychiatry. 2001;58(3):251-256.
42. Kessler RC, Nelson CB, McGonagle KA, Liu J, Swartz M, Blazer DG. Comorbidity of DSM-III-R major depressive disorder in the general population: results from the US National Comorbidity Survey. Br J Psychiatry Suppl. 1996;(30):17-30.
43. Wittchen HU, Beesdo K, Bittner A, Goodwin RD. Depressive episodes—evidence for a causal role of primary anxiety disorders? Eur Psychiatry. 2004;18(8):384-393.
44. Goodwin RD. Anxiety disorders and the onset of depression among adults in the community. Psychol Med. 2002;32(6):1121–1124.
45. Orsillo SM, Hammond C. Social phobia: A brief overview and guide to assessment. In: Antony MM, Orsillo SM, Roemer L, eds. AABT Clinical Assessment Series: Practitioner’s Guide to Empirically Based Measures of Anxiety. New York, NY: Kluwer Academic/Plenum Publishers; 2001:159-164.
46. Orsillo SM. Measures for social phobia. In: Antony MM, Orsillo SM, Roemer L, eds. AABT Clinical Assessment Series: Practitioner’s Guide to Empirically Based Measures of Anxiety. New York, NY: Kluwer Academic/Plenum Publishers; 2001:165-187.
47. Herbert, JD, Rheingold AA, Brandsma, LL. Assessment of social anxiety and social phobia. In: Hofmann SG, DiBartolo PM, eds. From Social Anxiety to Social Phobia: Multiple Perspectives. Needham Heights, MA: Allyn & Bacon, 2001:20-45.
48. First MB, Spitzer RL, Gibbon M. Structured Clinical Interview for DSM-IV Axis I Disorders. New York, NY: New York State Psychiatric Institute, Biometrics Research Unit, 1995.
49. Dinardo PA, Brown TA, Barlow DH. Anxiety Disorders Interview Schedule for DSM-IV: Lifetime Version. San Antonio, TX: Psychological Corp; 1994.
50. Liebowitz MR. Social phobia. Mod Probl Pharmacopsychiatry. 1987;22:141-173.
51. Heimberg RG, Horner KJ, Juster HR, et al. Psychometric properties of the Liebowitz Social Anxiety Scale. Psychol Med. 1999;29(1):199-211.
52. Leary MR. A brief version of the Fear of Negative Evaluation Scale. Pers Soc Psychol Bull. 1983;9(3):371-375.
53. Collins KA, Westra HA, Dozois DJ, Stewart SH. The validity of the brief version of the Fear of Negative Evaluation Scale. J Anxiety Disord. 2005;19(3):345-359.
54. Belzer K, Schneier FR. Comorbidity of anxiety and depressive disorders: issues in conceptualization, assessment and treatment. J Psychiatr Pract. 2004;10(5):296–306.
55. van der Linden GJ, Stein DJ, van Balkom AJ. The efficacy of selective serotonin reuptake inhibitors for social anxiety disorder (social phobia): A meta-analysis of randomized controlled trials. Int Clin Psychopharmacol. 2000;15(suppl 2):S15-S23.
56. Blanco, C, Schneier, FR, Liebowitz, MR. Psychopharmacology. In: SG Hoffman SG, DiBartolo PM, eds. From Social Anxiety to Social Phobia: Multiple Perspectives. Needham Heights, MA: Allyn & Bacon, 2001:335-353.
57. Fedoroff IC, Taylor S. Psychological and pharmacological treatments of social phobia: A meta-analysis. J Clin Psychopharmacol. 2001;21(3):311-324.
58. Blanco C, Raza MS, Schneier FR, Liebowitz MR. The evidence-based pharmacological treatment of social anxiety disorder. Intl J Neoropsychopharmacol. 2003;6(4):427-442.
59. Davidson, JR. Pharmacotherapy of social phobia. Acta Psychiatr Scand Suppl. 2003;(417):65-71.
60. Blanco C, Schneier FR, Schmidt A, et al. Pharmacological treatment of social anxiety disorder: A meta-analysis. Depress Anxiety. 2003;18(1):29-40
61. Guy W. 1976. ECDEU assessment manual for psychopharmacology: Publication adm 76-338. Washington, DC: US Department of Health, Education, and Welfare; 1976.
62. Liebowitz MR. Medications: Achieving remission in the anxiety disorders. Symposium presented at the 25th Annual Meeting of the Anxiety Disorders Association of America. March 17-20, 2005. Seattle, Washington.
63. Gelernter CS, Uhde TW, Cimbolic P, et al. Cognitive-behavioral and pharmacological treatments of social phobia: a controlled study. Arch Gen Psychiatry. 1991;48(10):938-945.
64. Liebowitz MR Schneier F, Campeas R, et al. Phenelzine vs atenolol in social phobia. A placebo-controlled comparison. Arch Gen Psychiatry. 1992. 49(4):290-300.
65. Versiani M, Nardi AE, Mundim FD, Alves AB, Liebowitz MR, Amrein R. Pharmacotherapy of social phoba: a controlled study with moclobemide and phenelzine. Br J Psychiatry. 1992. 161:353–360.
66. Heimberg RG, Liebowitz MR, Hope DA, et al. Cognitive behavioral group therapy vs phenelzine therapy for social phobia: 12-week outcome. Arch Gen Psychiatry. 1998;55(12):1133-1141.
67. Liebowitz MR, Heimberg RG, Schneier FR, Hope DA, et al. Cognitive-behavioral group therapy versus phenelzine in social phobia: long-term outcome. Depress Anxiety.1999:10(3):89-98.
68. Versiani M, Mundim FD, Nardi AE, Liebowitz MR. Tranylcypromine in social phobia. J Clin Psychopharmacol. 1988;8(4):279–283.
69. Versiani M, Nardi AE, Mundim FD. Fobia social. J Brasileiro dePsiquiatria. 1989;38(5):251-256.
70. Simpson HB, Schneier FR, Marshall RD. et al. Low dose selegilene (L-Deprenyl) in social phobia. Depress Anxiety.1998;7(3):126–129.
71. Schneier FR, Goetz D, Campeas R, Fallon B, Marshall R, Liebowitz MR. Placebo-controlled trial of moclobemide in social phobia. Br J Psychiatry. 1998;172:70-77.
72. Noyes R Jr, Moroz G, Davidson JR, et al. Moclobemide in social phobia: A controlled dose-response trial. J Clin Psychopharmacol. 1997;17(4):247-254.
73. Katschnig H, Stein MB, Buller R. The International Multicenter Clinical Trial Group on Moclobemide in Social Phobia.Moclobemide in social phobia: a double-blind, placebo-controlled clinical study. Eur Arch Psychiatry Clin Neurosci. 1997;247(2):71-80.
74. van Vliet IM, den Boer JA, Westenberg HJM. Psychopharmacological treatment of social phobia: clinical and biochemical effects of brofaromine, a selective MAO-A inhibitor. Eur Neuropsychopharmacol. 1992;2(1):21-29
75. Fahlen T, Nilsson HL, Borg K, Humble M, Pauli U. Social phobia: the clinical efficacy of and tolerability of the monoamine oxidase-A and serotonin uptake inhibitor brofaromine: A double-blind placebo-controlled study. Acta Psychiatr Scand. 1995;92(5):351–58.
76. Lott M, Greist JH, Jefferson JW, et al. Brofaromine for social phobia: a multicenter, placebo-controlled, double-blind study. J Clin Psychopharmacol. 1997;17(4):255-260.
77. Furmark T, Tillfors M, Marteinsdottir I, et al. Common changes in cerebral blood flow in patients with social phobia treated with citalopram or cognitive-behavioral therapy. Arch Gen Psychiatry. 2002;59(5):425-433.
78. Atmaca M. Kuloglu M. Tezcan E, Unal A. Efficacy of citalopram and moclobemide in patients with social phobia: some preliminary findings. Hum Psychopharmacol. 2002;17(8):401-405.
79. Schneier FR, Blanco C, Campeas R, et al. Citalopram treatment of social anxiety disorder with comorbid major depression. Depress Anxiety. 2003;17(4):191-196.
80. Lader M, Stender K, Burger V, Nil R. Efficacy and tolerability of escitalopram in 12- and 24-week treatment of social anxiety disorder: randomised, double-blind, placebo-controlled, fixed-dose study. Depress Anxiety. 2004;19(4):241-248.
81. Kasper S, Stein DJ, Loft H, Nil R. Escitalopram in the treatment of social anxiety disorder: randomised, placebo-controlled, flexible-dosage study. Br J Psychiatry. 2005;186:222-226.
82. Sternbach H. Fluoxetine treatment of social phobia. J Clin Psychopharmacol. 1990;10(3):230-231.
83. Schneier FR, Chin SJ, Hollander E, Liebowitz MR. Fluoxetine in social phobia. J Clin Psychopharmacol. 1992;12(1):62-64.
84. Black B, Uhde TW, Tancer ME. Fluoxetine for the treatment of social phobia. J Clin Psychopharmacol. 1992;12(4):293-295.
85. Van Ameringen M, Mancini C, Streiner DL. Fluoxetine efficacy in social phobia. J Clin Psychiatry.1993;54(1):27-32.
86. Kobak KA, Griest JH, Jefferson JW, Katzelnick DJ. Fluoxetine in social phobia: a double-blind, placebo-controlled pilot study. J Clin Psychopharmacol. 2002;22(3):257-262.
87. Clark DM, Ehlers A, McManus F, et al. Cognitive therapy versus fluoxetine in generalized social phobia: a randomized placebo-controlled trial. J Consult Clin Psychol. 2003;71(6):1058-1067.
88. Davidson JR, Foa EB, Huppert JD, et al. Fluoxetine, comprehensive cognitive behavioral therapy, and placebo in generalized social phobia. Arch Gen Psychiatry. 2004;61(10):1005-1013.
89. van Vliet IM, den Boer JA, Westenberg HG. Psychopharmacological treatment of social phobia; a double blind placebo controlled study with fluvoxamine. Psychopharmacology (Berl). 1994;115(1-2):128-134.
90. Stein MB, Fyer AJ, Davidson JR, Pollack MH, Wiita B. Fluvoxamine treatment of social phobia (social anxiety disorder): a double-blind, placebo-controlled study. Am J Psychiatry. 1999;156(5):756-760.
91. Stein DJ, Westenberg HG, Yang H, et al. Fluvoxamine CR in the long-term treatment of social anxiety disorder: the 12- to 24-week extension phase of a multicentre, randomized, placebo-controlled trial. Int J Neuropsychopharmacol. 2003;6(4):317-323.
92. Stein DJ, Westenberg HG, Yang H, Li D, Barbato LM. Paroxetine treatment of generalized social phobia (social anxiety disorder): a randomized controlled trial. JAMA. 1998;26;280(8):708-713.
93. Baldwin D, Bobes J, Stein DJ, Scharwachter I, Faure M. Paroxetine in social phobia/social anxiety disorder. Randomised, double-blind, placebo-controlled study. Paroxetine Study Group. Br J Psychiatry. 1999;175:120-126.
94. Allgulander C. Paroxetine in social anxiety disorder: a randomized placebo-controlled study. Acta Psychiatr Scand. 1999;100(3):193-198.
95. Stein DJ, Berk M, Els C, et al. A double-blind placebo-controlled trial of paroxetine in the management of social phobia (social anxiety disorder) in South Africa. S Afr Med J. 1999;89(4):402-406.
96. Allgulander C, Nilsson B. A prospective study of 86 new patients with social anxiety disorder. Acta Psychiatr Scand. 2001;103(6):447-452.
97. Stein DJ, Versiani M, Hair T, Kumar R. Efficacy of paroxetine for relapse prevention in social anxiety disorder: a 24-week study. Arch Gen Psychiatry. 2002;59(12):1111-1118.
98. Wagner KD, Berard R, Stein MB, et al. A multicenter, randomized, double-blind, placebo-controlled trial of paroxetine in children and adolescents with social anxiety disorder. Arch Gen Psychiatry. 2004;61(11):1153-1162.
99. Lepola U, Bergtholdt B, St Lambert J, Davy KL, Ruggiero L. Controlled-release paroxetine in the treatment of patients with social anxiety disorder. J Clin Psychiatry. 2004;65(2):222-229.
100. Katzelnick DJ, Kobak KA, Greist JH, et al. Sertraline for social phobia: a double-blind, placebo-controlled crossover study. Am J Psychiatry. 1995;152(9):1368-1371.
101. Blomhoff S, Haug TT, Hellstrom K, et al. Randomised controlled general practice trial of sertraline, exposure therapy and combined treatment in generalised social phobia. Br J Psychiatry. 2001;179:23-30.
102. Haug TT, Blomhoff S, Hellstrom K, et al. Exposure therapy and sertraline in social phobia: I-year follow-up of a randomised controlled trial. Br J Psychiatry. 2003;182:312-318
103. Van Ameringen M, Oakman J, Mancini C, Pipe B, Chung H. Predictors of response in generalized social phobia: effect of age of onset. J Clin Psychopharmacol. 2004;24(1):42-48.
104. Liebowitz MR, DeMartinis NA, Weihs K, et al. Efficacy of sertraline in severe generalized social anxiety disorder: results of a double-blind, placebo-controlled study. J Clin Psychiatry. 2003;64(7):785-792.
105. Rickels K, Mangano R, Khan A. A double-blind, placebo-controlled study of a flexible dose of venlafaxine ER in adult outpatients with generalized social anxiety disorder. J Clin Psychopharmacol. 2004;24(5):488-496.
106. Allgulander C, Mangano R, Zhang J, et al. Efficacy of venlafaxine ER in patients with social anxiety disorder: a double-blind, placebo-controlled, parallel-group comparison with paroxetine. Hum Psychopharmacol. 2004;19(6):387-396.
107. Stein MB, Pollack MH, Bystritsky A, et al. Efficacy of low and higher dose extended-release venlafaxine in generalized social anxiety disorder: a 6-month randomized controlled trial. Psychopharmacology (Berl). 2005;177(3):280-288.
108. Liebowitz MR, Gelenberg AJ, Munjack D. Venlafaxine extended release vs placebo and paroxetine in social anxiety disorder. Arch Gen Psychiatry. 2005;62(2):190-198.
109. Liebowitz MR, Mangano RM, Bradwejn J, Asnis G. A randomized controlled trial of venlafaxine extended release in generalized social anxiety disorder. J Clin Psychiatry. 2005;66(2):238-247.
110. Emmanuel NP, Johnson M, Villareal G. Imipramine in the treatment of social phobia A double blind study. Poster presented at: the 37th Annual Meeting of the American College of Neuropsychopharmacology. December 1998; Puerto Rico.
111. Simpson HB, Schneier FR, Campeas R, et al. Imipramine in the treatment of social phobia. J Clin Psychopharmacol. 1998;18(2):132-135.
112. Davidson JR, Potts N, Richichi E, et al. Treatment of social phobia with clonazepam and placebo. J Clin Psychopharmacol. 1993;13(6):423-428.
113. Seedat S, Stein MB. Double-blind, placebo-controlled assessment of combined clonazepam with paroxetine compared with paroxetine monotherapy for generalized social anxiety disorder. J Clin Psychiatry. 2004;65(2):244-248.
114. Jefferson JW. Benzodiazepines and anticonvulsants for social phobia (social anxiety disorder). J Clin Psychiatry. 2001;62(suppl 1):50-53.
115. Pande AC, Davidson JR, Jefferson JW, et al. Treatment of social phobia with gabapentin: a placebo-controlled study. J Clin Psychopharmacol. 1999;19(4):341-348.
116. Pande AC, Feltner DE, Jefferson JW, et al. Efficacy of the novel anxiolytic pregabalin in social anxiety disorder: a placebo-controlled, multicenter study. J Clin Psychopharmacol. 2004;24(2):141-149.
117. Heimberg RG, Juster HR. Cognitive-behavioral treatments: literature review. In: Heimberg RG, Liebowitz MR, Hope DA, Schneier FR, eds. Social Phobia: Diagnosis, Assessment and Treatment. New York, NY: Guilford Press; 1995:261-309.
118. Turk C, Heimberg R, Hope D. Social anxiety disorder. In: Barlow DH, ed. Clinical Handbook of Psychological Disorders. 3rd ed. New York, NY: The Guilford Press; 2001:114-153.
119. Beck AT, Emery G, Greenberg RL. Anxiety Disorders and Phobias: A Cognitive Perspective. New York, NY: Basic Books; 1985.
120. Hope DA, Heimberg RG, Juster HA, Turk CL. Managing Social Anxiety: A Cognitive Behavioral Therapy Approach (Client Manual). New York, NY: Oxford University Press; 2000.
121. Feske U, Chambless D. Cognitve behavioral versus exposure only treatment for social phobia: A meta-analysis. Behav Ther. 1995;26(4)695-720.
122. Taylor S. Meta-analysis of cognitive-behavioral treatments for social phobia. J Behav Ther Exp Psychiatry. 1996;27(1):1-9.
123. Gould RA, Buckminster S, Pollack MH, et al. Cognitive-behavioral and pharmacological treatment for social phobia: A meta-analysis. Clin Psychol Science Prac. 1997;4(4):291-306.
124. Fedoroff IC, Taylor S. Psychological and pharmacological treatments of social phobia: a meta-analysis. J Clin Psychopharmacol. 2001;21(3):311-324.