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Social Anxiety Disorder Case Study

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Published: 10th Dec 2019

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Tags: Mental Health

 Social Anxiety Disorder

Introduction and Overview

Description

Social anxiety disorder (SAD), formerly known as social phobia, is characterized by an excessive and disproportionate fear of social and/or performance situations in which the individual fears they might exhibit anxiety symptoms (e.g., sweating, blushing, shaking, etc.) or behave in a manner that will expose them to scrutiny, embarrassment, humiliation, rejection, or otherwise negative evaluation by others (American Psychiatric Association, 2013). Individuals with SAD either actively avoid these feared social situations or suffer through them with intense fear or anxiety (American Psychiatric Association, 2013). SAD causes a great degree of distress and impairment in many important areas of functioning, including social, occupational, or academic deficits (American Psychiatric Association, 2013).

To better illustrate a typical presentation of SAD, the following case example from Clinical Handbook of Psychological Disorders: A Step-by-Step Treatment Manual, Chapter 3: Social Anxiety Disorder (Turk, Heimberg, & Hope, 2001) is presented.

Josie, a 22-year-old woman, presented with significant anxiety concerning both social interaction and performance situations. She was studying music at a local college and living with a roommate. At the time she entered treatment, Josie was a full-time student. She was not employed despite significant financial need. Josie described herself as shy and having trouble connecting with others. Josie reported that she socialized with her roommate and her boyfriend, but she often turned down opportunities to socialize with their friends because of anxiety. Josie reported that she had no close friends of her own and that her anxiety kept her from forming close friendships, especially with women her age. Josie’s social anxiety had also resulted in occupational and academic impairment. For example, although Josie had gone on numerous job interviews and had even been offered positions, she was currently unemployed because she had difficulty accepting job offers because of fears that she would get fired. She reported great anxiety in her classes and did not participate unless directly asked a question, even if participation was a significant part of her grade. She often declined to enroll in classes that interested her because of participation requirements. In addition, Josie was required to do recitals and in-class critiques of her music compositions several times a semester. Although she never avoided any of these recitals, she worried about them for weeks in advance and suffered through them with great anxiety. Josie feared that her social anxiety would cause her even greater difficulty after graduation, when she would need to go on job interviews and auditions. (p. 144-145)

Epidemiology

Prevalence and incidence. According to the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), the estimated 12-month prevalence rate of SAD in the United States is approximately 7% (American Psychiatric Association, 2013). Earlier research using the diagnostic criteria from previous revisions of the DSM reported much lower prevalence rates; Somers and colleagues (2006) reported a 12-month prevalence rate of 4.5% and a lifetime prevalence rate of 3.6%, Faravelli and colleagues (2000) reported a lifetime prevalence rate of 3.27%, and den Boer (2000) estimated the lifetime prevalence to be between 2% and 5%. This discrepancy could potentially be explained by the omission of DSM-IV criterion C from the DSM-5 diagnostic criteria for SAD; criterion C required that the person recognize that their fears were unreasonable and excessive (American Psychiatric Association, 2000). The removal of criterion C, and the resulting shift of the assessment of fears as unreasonable from the individual to the assessor, may have resulted in an increase in prevalence rates. Indeed, Karlsson and colleagues (2016) compared 1-month prevalence rates of SAD in a non-clinical population of older adults based on both DSM-IV and DSM-5 diagnostic criteria and reported a 2.5% prevalence rate based on DSM-IV criteria and a 5.1% prevalence rate based on the DSM-5 criteria. This finding suggests that within the general population, the removal of criterion C from the DSM-5 diagnostic criteria may result in an increase in the estimated prevalence rates of SAD in older adults (Karlsson et al., 2016).

Estimated prevalence rates of SAD as reported in the DSM-5 are comparable for children, adolescents, and adults, but tend to decrease with old age, with older adults having 12-month prevalence rates ranging from 2% to 5% (American Psychiatric Association, 2013). This is consistent with the research literature, where many researchers have found the prevalence rates of SAD to be significantly lower for older adults than for younger adults (Chou, 2009; Gretarsdottir & Woodruff-Borden, 2004; Karlsson et al., 2016; Kessler et al., 2005).

Gender differences. In the general population, there is generally a higher prevalence of SAD in females than in males, especially for adolescents and young adults (American Psychiatric Association, 2013). In clinical samples, however, the prevalence rate of SAD tends to be equivalent or slightly higher for males than for females (American Psychiatric Association, 2013). However, this statement is not supported by much of the available literature. Somers and colleagues (2006) reported the 12-month prevalence rate of SAD to be 3.0% in males and 4.6% in females, and the lifetime prevalence rate to be 1.8% in males and 2.9% in females. Likewise, McLean and colleagues (2011) reported the 12-month prevalence of SAD (when controlled for racial group, age, education, and SES) as 6.5% in females and 4.8% in males; however, they found no significant differences in the lifetime prevalence rates of SAD based on gender.

Race and cultural differences. The DSM-5 reports that compared to non-Hispanic white individuals within the United States, the prevalence of SAD is higher for American Indians and lower for individuals of Asian, African American, Latino, and Afro-Caribbean descent (American Psychiatric Association, 2013). Consistent with this data, Kisely and colleagues (2017) reported that the lifetime prevalence rate of SAD was significantly higher in Indigenous persons than in non-Indigenous persons; however, no significant differences were found in 12-month prevalence rates (Kisely et al., 2017). When using the same diagnostic measures, the DSM-5 reports that most other parts of the world generally have lower prevalence estimates, with a 2.3% median prevalence rate in Europe and prevalence rates between 0.5% and 2.0% in the rest of the world (American Psychiatric Association, 2013).

Course

Age of onset. Unlike most other anxiety disorders that tend to have an onset during adulthood, the onset of SAD typically occurs during early adolescence, with an average age of onset between 8 and 15 years (American Psychiatric Association, 2013; Heimberg et al., 1995; Keller, 2003; Wittchen & Fehm, 2003). Initial onset of SAD after the age of approximately 25 is rare, and typically only occurs following a humiliating life event or a major life change that involves a new social role, such as receiving a promotion or marrying an individual from a higher social class (American Psychiatric Association, 2013; Wittchen & Fehm, 2003). However, a fear of public speaking that develops in isolation of any other fears tends to have an onset that is slightly later on average than other social fears (Wittchen & Fehm, 2003). The onset of SAD during earlier childhood is relatively rare, but the recovery rate tends to be especially low when the onset of SAD occurs before the age of 11 (Wittchen & Fehm, 2003). No gender differences have been found in the average age of onset of SAD (McLean et al., 2011).

Typical course. SAD typically has a chronic and unremitting course, and is commonly considered to be a lifelong illness (Keller, 2003; Wittchen & Fehm, 2003). With an average duration of illness between 10 and 29 years, SAD is much more chronic than both panic disorder and MDD (Keller, 2003; Wittchen & Fehm, 2003). Further, progressive worsening of symptoms is frequently established by the time the affected individual reaches 19 years of age (Wittchen & Fehm, 2003). In many individuals, the severity of SAD symptoms can wax and wane alongside various challenges and stressful situations in life (Wittchen & Fehm, 2003), and recurrences are common (Keller, 2003). Again, no significant gender differences have been reported regarding the chronicity or duration of SAD (McLean et al., 2011; Yonkers et al., 2003).

Prognosis. SAD comes with a remarkably high level of disability and functional impairment which tends to increase at a steady rate across the lifespan, and the level of functional impairment associated with the generalized subtype of SAD is higher than that of the performance-only subtype (Keller, 2003; Wittchen & Fehm, 2003). Individuals with SAD are significantly more likely to drop out of school early, be unemployed or experience other negative impacts on their career, and never marry compared to non-SAD individuals (American Psychiatric Association, 2013; Keller, 2003; Wittchen & Fehm, 2003). Those who do marry have an increased likelihood of divorce (Keller, 2003; Wittchen & Fehm, 2003). In addition, SAD is associated with an increased risk of suicide attempts; Keller (2003) reports that an estimated 20% of SAD patients have had at least one past suicide attempt, compared to approximately 8% of non-SAD patients.

Outcome. The probability of experiencing complete or partial remission from SAD is very low, with only approximately 36% of patients no longer meeting full diagnostic criteria for SAD 8 years after initial onset and less than 30% attaining complete remission (Keller, 2003; Yonkers et al., 2003). The 5-year relapse rate for SAD is lower on average than that seen in panic disorder or MDD; however, it is still fairly likely and tends to steadily increase over time (Keller, 2003).

SAD patients with comorbid depression, personality disorders, or other anxiety disorders usually have an even poorer outcome than those with uncomplicated SAD (Keller, 2003). The findings of Keller (2003) indicate that SAD patients with comorbid MDD have more past suicide attempts, an increased likelihood of additional comorbid anxiety disorders, and are more likely to have had psychiatric hospitalizations during their lifetime. However, comorbid MDD was not demonstrated to decrease the remission rate of SAD compared to uncomplicated SAD. Individuals with both SAD and APD, on the other hand, have both a poorer outcome and are estimated to be approximately 39% less likely than those without APD to achieve full remission from SAD symptoms, with an even lower remission rate associated with generalized SAD (rather than performance-only SAD) with comorbid APD (Brown et al., 1995; Huppert et al., 2008; Keller, 2003).

Comorbidity

Mood disorders. SAD is highly comorbid with mood disorders, particularly depressive disorders (Beesdo et al., 2007; Van Ameringen et al., 1991). Erwin et al. (2002) reported MDD to be the most common mood disorder comorbid with SAD (53.85%), followed by dysthymic disorder (27.27%) and depressive disorder NOS (27.27%). Research literature examining the comorbidity rates between SAD and mood disorders dates back to over 25 years ago; Van Ameringen and colleagues (1991) reported that the most common comorbid diagnosis in individuals with SAD was a mood disorder, with comorbid MDD being particularly common (70.2%). Consistent with these early findings, researchers in Munich (Beesdo et al., 2007) found that individuals with SAD were twice as likely to develop subsequent depression than individuals without SAD, and almost three times as likely to develop subsequent depression compared to individuals with no anxiety disorders.

Several individual characteristics have been identified as potential risk factors for the subsequent onset of depressive disorders in individuals with SAD. Findings by Beesdo and colleagues (2007) suggest that the largest distal risk factor for the onset of a depressive disorder in socially anxious individuals is a behavioral inhibition (BI) temperament in childhood, which is characterized by consistent restraint in response to situations of both a social and nonsocial nature (Beesdo et al., 2007). Disorder-specific characteristics associated with a greater risk of subsequent depression include a greater occurrence of panic attacks, as well as the fear of having a panic attack in social situations (Beesdo et al., 2007), and a greater number of feared social situations (Beesdo et al., 2007; Kessler et al., 1999).

In the vast majority of individuals with comorbid SAD and mood disorders, the reported age of onset of SAD precedes the age of onset of the mood disorder (Kessler et al., 1999; Van Ameringen et al., 1991), which indicates that SAD itself could be considered to be a major risk factor for the development of subsequent mood disorders, particularly MDD (Kessler et al., 1999; Regier et al., 1998; Van Ameringen et al., 1991). This supposition is supported by the finding of Kessler and colleagues (1999) that SAD is associated not only with a greater risk of the onset of a subsequent mood disorder, but also with increased measures of their severity and course of illness (Kessler et al., 1999). In addition, socially anxious individuals with comorbid depression tend to have more frequent depressive episodes, a greater number of depressive symptoms during these episodes, increased suicidal ideation and suicide attempts, and an overall poorer prognosis in regards to both their SAD symptoms and depressive symptoms (Beesdo et al., 2007). Likewise, Erwin and colleagues (2002) found that individuals with SAD and comorbid depressive disorders had significantly higher symptom severity and impairment ratings both pre- and post-treatment than individuals with uncomplicated SAD.

Other anxiety disorders. In addition to mood disorders, evidence of an extraordinarily high rate of comorbidity between SAD and other anxiety disorders has been well established in the literature. Van Ameringen et al. (1991) reported that 70.2% of individuals with SAD had at least one other comorbid anxiety disorder during their lifetime. There are inconsistencies in the available research literature as to which comorbid anxiety disorder is most common, but significantly high rates of comorbidity have been demonstrated between SAD and generalized anxiety disorder (GAD), specific phobia, panic disorder, and agoraphobia (American Psychiatric Association, 2013; Erwin et al., 2002; Heimberg et al., 1995; Van Ameringen et al., 1991).

Like comorbid mood disorders, the onset of comorbid anxiety disorders is typically preceded by the onset of SAD in the vast majority of cases (American Psychiatric Association, 2013; Schneier et al., 1992; Van Ameringen et al., 1991). Thus, as is the case for mood disorders, SAD could be viewed as a potential risk factor for the subsequent onset of other anxiety disorders.

Addictive disorders. SAD is also frequently comorbid with alcohol and substance use disorders (American Psychiatric Association, 2013; Heimberg et al., 1995; Regier et al., 1998; Schneier et al., 1992; Van Ameringen et al., 1991). Like with mood disorders and other anxiety disorders, is largely considered to be a risk factor for the development of addictive disorders (Regier et al., 1998), as many socially anxious individuals may attempt to alleviate their social fears by self-medicating with alcohol or drugs (American Psychiatric Association, 2013). However, some intoxication or withdrawal symptoms (e.g., sweating, tremors) may actually function as an additional source of social fear (American Psychiatric Association, 2013).

Personality disorders. Because SAD most frequently has an onset during childhood or adolescence and tends to persist through adulthood, it can often resemble a personality disorder (American Psychiatric Association, 2013). In particular, there is a substantial degree of overlap between the generalized subtype of SAD and avoidant personality disorder (APD), with up to 89% of individuals with generalized SAD having comorbid APD, as well as a vast majority of individuals with APD also meeting the diagnostic criteria for generalized SAD (Dalrymple, 2012; Heimberg et al., 1995). The notably large degree of overlap in the diagnostic criteria for these two disorders has prompted a substantial amount of criticism in the available research literature, which will be discussed in further detail below.

Current Issues

The remarkably high rate of comorbidity between SAD and APD has led many researchers to question the validity of the diagnostic boundaries between these two disorders. The similarities between the diagnostic criteria for each disorder in the DSM-5 are undeniable; for example, criterion A of SAD describes a “marked fear or anxiety about one or more social situations in which the individual is exposed to possible scrutiny by others” (American Psychiatric Association, 2013), which bears a striking resemblance to criterion 4 of APD, which describes the affected individual as being “preoccupied with being criticized or rejected in social situations” (American Psychiatric Association, 2013). For the diagnostic criteria of SAD and APD in the DSM-5, refer to Appendices A and B, respectively.

The controversial degree of overlap between generalized SAD and APD has been examined by researchers since the original inclusion of the generalized subtype of SAD in the DSM-III-R. Indeed, based on the degree of overlap in diagnoses of generalized SAD and APD, Turner, Beidel, and Townsley (1992) suggested that these two diagnoses have a greater number of similarities than differences. Currently, the available research literature lacks a clear consensus as to whether the additional diagnosis of APD in individuals with generalized SAD provides any additional, clinically useful information beyond simply greater SAD symptom severity and depression among individuals with generalized SAD. Many researchers argue that APD is simply a more severe presentation of SAD, and assert that there are no substantial qualitative differences in the psychopathology of these two disorders that would justify the need for two distinct categorical diagnoses (Dalrymple, 2012; Heimberg et al., 1995). On the other hand, some researchers have cited studies that identify a significant number of individuals diagnosed with APD but not SAD as evidence toward their being two distinct disorders (Dalrymple, 2012; Lampe & Sunderland, 2015). Findings from a study by Marques and colleagues (2012) suggest that although a comorbid diagnosis APD appears to offer relatively little additional information beyond what could be attributed simply to a more severe presentation of SAD with depressive features, APD may encompass certain interpersonal aspects (e.g., emotional guardedness, impairments in interpersonal functioning) that are absent in generalized SAD. Although there currently exists no definitive solution to this debate, the available literature does appear to offer support towards a more dimensional approach towards classifying social anxiety rather than the use of discrete categorical distinctions (Dalrymple, 2012; Marques et al., 2012; Rettew, 2000). Such a dimensional approach could conceptualize SAD and APD as points along a broader spectrum that encompasses varying severities of social anxiety (Dalrymple, 2012). To facilitate the development of a more representative classification system and clarify the distinction (or lack thereof) between SAD and APD, future studies could examine whether the differences in psychopathological in psychopathological features between individuals diagnosed with SAD with and without comorbid APD remain after controlling for SAD symptom severity, as empirical research addressing this issue is both scarce and inconsistent (Marques et al., 2012).

In addition to the ambiguous distinction between SAD and APD, the available literature includes a great deal of debate over the distinction between SAD and the normal temperament of shyness, and its implications for the potential overdiagnosis of SAD (Dalrymple, 2012; Heimberg et al., 1995). The steady increase in the lifetime prevalence rates of SAD since its original inclusion in the DSM-III has prompted researchers to debate whether SAD was underdiagnosed in the past, or if it is overdiagnosed at present (Dalrymple, 2012). Many researchers have voiced concern over whether the current diagnostic criteria and rate of SAD diagnosis represents an over-pathologization of normal shyness, which may have consequences including the over-prescription of antidepressants and anxiolytics as well as the financial burden of unnecessary treatment (Dalrymple, 2012). The DSM-5 (nor its previous revisions) does not contain a clear and objective method for determining whether an individual experiences a level of distress or impairment that is sufficient enough to warrant a diagnosis of SAD; until such guidelines are uniformly included in the diagnostic criteria, the distinction between normal shyness and psychopathology will remain subjective and arbitrary (Dalrymple, 2012). Once again, this issue lends support towards the development of a more dimensional approach towards the classification of social anxiety, with both normal shyness and SAD (along with APD) existing along a broad continuum representing social anxiety and social functioning.

History

The concept of social phobia was first described by French psychologist Pierre Janet in 1903, who used this term to describe patients that exhibited excessive fear of being observed when speaking, writing, or performing (Heimberg et al., 1995). Until its first inclusion as a distinct disorder in the DSM-III, social phobia was grouped together with all other phobias, a classification that reflected the dominant psychoanalytic perspective of that time period in which phobic symptoms were thought to be a consequence of unacceptable unconscious desires (Heimberg et al., 1995). The eventual separation of social phobia from other types of phobias was spearheaded by the 1966 works of Marks and Gelder, who described phobic disorders as falling into four distinct categories: specific animal phobias, specific situational phobias, agoraphobias, and social phobias. Individuals with specific animal phobias, as the name implies, typically had isolated fears of specific animals or insects, whereas individuals with specific situational phobias had isolated fears related to certain situations not involving animate objects, such as a fear of heights or thunderstorms (Marks & Gelder, 1966). Individuals with agoraphobias were described as having an excessive fear of being trapped in open or closed spaces, of traveling via public transportation or walking along public streets, of being in large crowds, or other situations from which they feel they may not be able to easily escape (Marks & Gelder, 1966). Finally, individuals with social phobias exhibited fears of social situations such as blushing, eating, speaking, or performing in front of other people (Marks & Gelder, 1966).

Nomenclature. The name “Social Anxiety Disorder” (SAD) was introduced initially as an alternative name for social phobia in the DSM-IV (American Psychiatric Association, 1994), and officially replaced social phobia as the primary name of the disorder in the DSM-5 (American Psychiatric Association, 2013; Heimberg et al., 2014). This change in nomenclature was adopted in response to concerns over the connotations associated with social phobia; many researchers argued that this term downplayed the both the prevalence and degree of impairment caused by the disorder, and trivialized the often more widespread nature of social phobia by equating it to specific phobias in which the fear is typically limited to a single object or situation (Heimberg et al., 2014; Liebowitz et al., 2000). Social Anxiety Disorder, on the other hand, was deemed to have more appropriate and realistic connotations regarding the pervasive and disabling nature of the disorder, as well as a more appropriate degree of separation from specific phobias (Liebowitz et al., 2000). Although this change in nomenclature may seem semantic in nature, it has been shown to have a significant impact on the perceived importance of seeking treatment for the disorder. In a demonstration of the stigma associated with the name social phobia as opposed to SAD, Bruce and colleagues (2012) presented an identical vignette describing an individual with symptoms characteristic of the disorder, and labeled these symptoms as representing either social phobia or social anxiety disorder (SAD). Indeed, respondents were significantly more likely to recommend that the individual described in the vignette seek treatment for their symptoms when they were labeled as SAD than when they were labeled as social phobia. Thus, the renaming of social phobia to SAD may positively influence the percentage of affected individuals who seek treatment for their symptoms, as well as encourage clinicians to more thoroughly screen for the disorder and recognize its severity (Heimberg et al., 2014).

Diagnosis and Classification

Current and Recent Diagnostic Criteria

DSM-III and DSM-III-R. Social phobia was first included as a disorder in the DSM-III in 1980 (American Psychiatric Association, 1980). The preliminary diagnostic criteria were catered primarily towards individuals who had only a small number of feared social situations or events. The exclusion of individuals who also met the diagnostic criteria of APD effectively disqualified individuals with more general social fears, only allowing those with specific and isolated fears such as performance anxiety or test anxiety to be eligible for the diagnosis (Heimberg et al., 2014). The DSM-III text also asserted that social phobia was fairly rare and did not typically cause a great deal of disability or impairment, a statement that sparked a great deal of criticism by researchers who argued that the disorder was much more common and disabling than suggested by the DSM-III (American Psychiatric Association, 1980; Heimberg et al., 2014; Liebowitz et al., 1985).

The revised version of the DSM-III (DSM-III-R), published 7 years later, addressed these concerns by removing the APD exclusion from the diagnostic criteria of social phobia, allowing individuals to be diagnosed with both social phobia and APD (American Psychiatric Association, 1987; Heimberg et al., 2014). In addition, the DSM-III-R introduced the “generalized subtype” of social phobia to include individuals who had a more widespread array of fears across “most social situations” (Heimberg et al., 2014). However, a new exclusionary criterion was also added that prevented individuals whose social fears were attributable to an unrelated medical condition (e.g., Parkinson’s, stuttering, hyperhidrosis, obesity, essential tremors, etc.) from receiving a diagnosis of social phobia (Heimberg et al., 2014).

DSM-IV. As stated previously, the fourth revision of the DSM (DSM-IV) was the first to introduce “Social Anxiety Disorder” (SAD) as an alternative name for social phobia (American Psychiatric Association, 1994). Otherwise, the only changes made to the diagnostic criteria of SAD between the DSM-III-R and the DSM-IV regarded its use in the diagnosis of children with social anxiety (Heimberg et al., 2014). Although adults were still required to acknowledge that their social fears were unreasonable or excessive in order to receive a diagnosis of SAD, this was no longer required for children in the DSM-IV (Heimberg et al., 2014). The diagnostic category of “avoidant disorder of childhood or adolescence,” a diagnosis that was frequently given to children with symptoms of social anxiety, was eliminated from the DSM-III-R because it was judged to have an excessively high overlap with SAD (Heimberg et al., 2014). In addition, in order for children to receive a diagnosis of SAD according to the DSM-IV diagnostic criteria, they were required to exhibit anxiety in social interactions with their peers, rather than only having symptoms of anxiety in interactions with adults (Heimberg et al., 2014).

DSM-5. In addition to the official retirement of the term “social phobia” in favor of SAD, several major changes were made to the diagnostic criteria of SAD in the DSM-5 (American Psychiatric Association, 2013). The DSM-5 Anxiety Sub-Workgroup broadened the criterion describing the main fear of SAD to emphasize the role of fear of being negatively evaluated by others, rather than limiting that fear simply to embarrassment or humiliation (Heimberg et al., 2014). This important shift allowed the diagnosis to incorporate other means of negative evaluation by others, such as the fear of rejection or of offending others, which are common interpersonal fears in SAD patients in addition to fears of embarrassment or humiliation (Heimberg et al., 2014). In addition, although the DSM-5 retained the exclusionary criterion that prevents individuals whose social anxiety symptoms could be attributed to another medical condition, it does allow such comorbid diagnoses if the individual’s social fears, anxiety, or avoidance behaviors are not strictly related to the medical disorder or are deemed to be “excessive” (Heimberg et al., 2014).

In another significant update to the diagnostic criteria of SAD, the DSM-5 Anxiety Sub-Workgroup decided to remove the diagnostic criterion that required the affected individual to recognize that their fear or anxiety was unreasonable or excessive, and instead transferred the responsibility of making that judgment from the patient to the clinician (Heimberg et al., 2014). This requirement was originally included in the diagnostic criteria as a means of distinguishing between SAD and psychotic disorders such as paranoia. However, the researchers in the DSM-5 Anxiety Sub-Workgroup ultimately decided that it was unnecessary to make SAD and paranoia/other psychotic disorders mutually exclusive diagnoses due to empirical evidence suggesting that individuals with psychotic disorders and comorbid SAD may still benefit from treatment of their SAD symptoms (Heimberg et al., 2014). The removal of this criterion was also based on research findings indicating that individuals with social anxieties are likely to overestimate the probability of social situations resulting in a negative outcome, as well as underestimate their own ability to behave in an appropriate manner in such situations (Heimberg et al., 2014). However, the DSM-5 Anxiety Sub-Workgroup warned clinicians to exercise extreme caution when making these judgments, stressing the importance of taking into account the individual’s sociocultural context when determining whether their fears are unreasonable or excessive, as behaviors that may be appropriate in one culture may be unreasonable in another (Heimberg et al., 2014).

Regarding the diagnosis of SAD in children, the DSM-5 Anxiety Sub-Workgroup asserted that children as young as 6 years can be reliably diagnosed with SAD, and that the diagnostic criteria can be used interchangeably across age groups without requiring separate criteria for different age groups. They also deemed a minimum duration of SAD of 6 months to be considered an appropriate guideline of diagnosis, regardless of the age of the affected individual (Heimberg et al., 2014).

Subtypes

As stated previously, the “generalized” subtype of SAD was first introduced by the DSM-III-R to incorporate individuals who had more widespread fears that applied to “most social situations” (American Psychiatric Association, 1987); this classification remained in the diagnostic criteria through the DSM-IV-TR (American Psychiatric Association, 2000). Proponents of this change argued that labeling socially anxious individuals with widespread social fears as having APD carried potentially severe ramifications, as the diagnosis of a personality disorder may result in clinicians refusing to even consider the use of potentially efficacious pharmacological interventions (Liebowitz et al., 1985). Indeed, the findings of Turner, Beidel, and Townsley (1992) supported the use of the generalized subtype for providing valuable information regarding the symptom severity, chronicity, and pervasiveness of distress for patients with generalized or non-generalized (specific) SAD. The results of this study indicated that individuals who met the criteria for the generalized subtype generally had higher symptom severity and a greater level of general distress, as well as a less favorable treatment response than the specific subtype. In addition, the authors asserted that the distinction between the generalized and specific subtypes of SAD was not simply attributable to the generalized subtype’s diagnostic overlap with APD (Turner, Beidel, & Townsley, 1992).

The DSM-5 replaced the generalized subtype with a “performance only” specifier, which was added to the diagnosis of SAD if the affected individual’s fears only involve performing or speaking in front of others, as opposed to more widespread social fears (American Psychiatric Association, 2015; Heimberg et al., 2014). This change effectively shifted the primary characterization of SAD by essentially redefining generalized SAD as the trunk of the tree rather than a branch; the shift meant that individuals who would previously have been diagnosed using the “generalized subtype” specifier would now simply be diagnosed with SAD, and those who previously were diagnosed simply with SAD would now be described using the “performance-only” specifier. Many researchers argue that the heterogeneity of “generalized” SAD would be better represented by a dimensional scale measuring severity, improved operationalized descriptions regarding the types or inherent qualities of certain feared situations, or even simply counting the number of feared social situations, rather than the categorical separation of generalized vs. performance-only (Bögels et al., 2010). The shift from conceptualizing generalized SAD as a subtype to defining it as the diagnostic norm (and, in turn, shifting the conceptualization of strictly performance-related SAD from the normative presentation to a more limited specifier/subgroup) was introduced in the DSM-5 as a function of diagnostic ease; many of the researchers in the DSM-5 Anxiety Sub-Workgroup argued that reliably deciding what would classify a more limited expression of SAD would be easier than a more generalized and universal expression of SAD (Heimberg et al., 2014).

 

Differential Diagnosis

The line between normal shyness and SAD can be difficult to distinguish at times, but generally a diagnosis of SAD should only be considered if the individual experiences serious impairment in daily activities, including negative impacts in social and occupational areas of functioning (American Psychiatric Association, 2013; Heimberg et al., 1995). In addition, whereas “shyness” is typically conceptualized as a transitory temperament, SAD has a chronic and unremitting course that causes significant impairment and distress (Dalrymple, 2012).

SAD is often confused with agoraphobia, as persons with agoraphobia may also fear and/or avoid certain social situations. However, the fears associated with agoraphobia are in relation to being in a situation from which escape might be difficult, whereas individuals with SAD are more afraid of scrutiny or negative evaluation by others (American Psychiatric Association, 2013). In addition, individuals with agoraphobia often fear being left alone, typically associated with fears of being trapped in a space in which they may not be able to escape, whereas individuals with SAD typically prefer being alone because being around others prompts their fears of being scrutinized and negatively evaluated by others (American Psychiatric Association, 2013; Heimberg et al., 1995). A similar distinction can be applied to GAD, in that the anxiety experienced by individuals with SAD are solely in relation to potential negative evaluation by others in social situations, whereas individuals with GAD experience anxiety over situations of a nonsocial nature as well (American Psychiatric Association, 2013; Heimberg et al., 1995).

Individuals suffering from major depression often present with avoidance behaviors and withdrawal from social situations; however, the motivation behind their avoidance of such social situations typically stems from a lack of energy or anhedonia, in addition to feelings of low self-worth (American Psychiatric Association, 2013; Heimberg et al., 1995). In contrast, individuals with SAD avoid social situations due to fears of being negatively evaluated or scrutinized, and may fear humiliation or embarrassment as a result of others’ negative evaluations of their social behaviors (American Psychiatric Association, 2013).

Although individuals with SAD can experience panic attacks, they can be distinguished from individuals with panic disorder because these individuals’ fears are centered around the panic attacks themselves, rather than fear of being negatively evaluated by others (American Psychiatric Association, 2013; Brown et al., 2016). In addition, when individuals with panic disorder experience panic attacks, they frequently fear that they will die or “lose control” as a result of the physiological symptoms experienced during the panic attack, whereas individuals with SAD rarely experience fears of dying or losing control during panic attacks (Heimberg et al., 1995). The situations surrounding the onset of panic attacks are often different for individuals with panic disorder and SAD as well, with panic attacks often occurring without any specific situational triggers and sometimes while sleeping for individuals with panic disorder, whereas individuals with social anxiety typically only experience panic attacks in response to socially relevant situational triggers (Brown et al., 2016; Heimberg et al., 1995).

Like individuals with SAD, individuals with separation anxiety disorder may fear and avoid social situations; however, their fear only stems from being separated from a trusted attachment figure, such as a parent (in children) or significant other (in adults), and they typically are perfectly comfortable in those social situations when their attachment figure is present (American Psychiatric Association, 2013). Children with selective mutism may avoid speaking in front of others for fear of negative evaluation, but the distinction between selective mutism and SAD lies in the fact that individuals with selective mutism do not experience distress or fear in relation to social situations that do not involve speaking, such as nonverbal play (American Psychiatric Association, 2013; Bögels et al., 2010). In addition, selective mutism typically has a much earlier age of onset than SAD, usually developing between the ages of 2 and 4 (Bögels et al., 2010). Children with ODD also may refuse to speak as well, but their avoidance of speaking generally stems from an opposition towards authority figures rather than fear of being negatively evaluated (American Psychiatric Association, 2013).

Certain medical conditions may cause an individual to develop social anxiety symptoms as a reactionary phobic avoidance mechanism, in that a medical condition unrelated to SAD may cause an individual to avoid social situations in which exposure of their medical condition may result in humiliation or ridicule at the hands of others. Common medical conditions that have been reported to provoke social anxiety symptoms include stuttering, benign essential tremor, Parkinson’s disease, obesity, and disfigurement resulting from burns or other physical trauma (Heimberg et al., 1995). Secondary social anxiety resulting from an unrelated medical condition, however, is excluded from the diagnostic criteria for SAD unless the anxiety is clearly excessive (American Psychiatric Association, 2013), and the affected individuals instead receive a diagnosis of “anxiety disorder due to another medical condition” in the DSM-5.

Assessment

Thorough assessment of SAD involves comprehensive evaluation of several important characteristics through the use of diagnostic clinical interviews (both structured and unstructured), self-monitoring techniques (such as behavioral diaries), self-report scales, and behavioral assessment procedures, such as behavioral observations and clinician’s assessments of skills deficits (Beidel & Turner, 2007). Structured and unstructured interviews can help clinicians assess the presence of avoidance behaviors, cognitive cues related to feared social situations/events or their anticipated negative outcomes, presence and magnitudes of social skills deficits, general levels of distress and impairment in important areas of functioning, and areas of the patient’s background history that could have relevant implications for treatment planning, such as the patient’s treatment history, environmental and familial factors, comorbid diagnoses, and other significant medical and mental health issues (Antony & Rowa, 2005). Even when an individual appears to clearly meet the diagnostic criteria for SAD (or any other disorder), it is of extreme importance to obtain information from the patient regarding all of these areas, as they can have important implications for treatment planning and outcome (Antony & Rowa, 2005; Heimberg et al., 1995). In addition to the broad range of clinical interview techniques used in the diagnostic assessment of mental disorders as a whole, the Emotion Regulation Interview (ERI) has garnered some empirical support for its use in measuring both the frequency and the patient’s self-efficacy of five empirically established emotion regulation strategies suggested to be relevant in SAD, with data indicating that individuals with SAD tend to have deficits in specific emotion regulation strategies and areas of emotion regulation, including deficits in cognitive reappraisal and increased levels of avoidance and suppression of emotional expression (Werner et al., 2011).

In addition to clinical interviews, self-monitoring techniques such as the use of diaries can be used to assess the cognitive cues for SAD mentioned above (i.e., feared social situations/events or their anticipated negative outcomes), and assess and monitor situational triggers of social anxiety and their associated avoidance behaviors; however, such self-monitoring techniques have yet to be empirically examined to establish reliability and support for validity (Antony & Rowa, 2005).

Many self-report scales have been introduced for the assessment of SAD; however, several of these scales are somewhat dated, as they are based on diagnostic criteria from earlier editions of the DSM. With this in mind, however, the self-report scales with the greatest psychometric support in the available literature for the assessment of SAD in adults include the Social Interaction Anxiety Scale (SIAS) and the Social Phobia Scale (SPS) (Heimberg et al., 1993). The SIAS was designed to measure the level of anxiety an individual experiences in a more general array of “contingent interactions,” or social situations that involve social interactions with others, such as conversations and meeting new people (Heimberg et al., 1993). The SPS, on the other hand, was designed to measure anxiety levels in “noncontingent interactions,” or social situations in which the individual might be scrutinized or observed by others, such as public speaking and performance (Heimberg et al., 1993). Both the SIAS and SPS have empirically demonstrated validity, clinical utility, and ease in scoring, and although it is advised that clinicians keep in mind their basis of DSM-III-R diagnostic criteria, the available literature supports the use of both these self-report instruments in clinical and nonclinical populations (Brown et al., 1997; Heimberg et al., 1993; Mattick & Clarke, 1998). The Social Phobia Inventory (SPIN; Connor et al., 2000) has also been demonstrated to have good support of its psychometric properties, and empirical evidence suggests that it is an effective measure of clinically important domains of avoidance, fear, and physiological symptoms related to SAD (Connor et al., 2000). In addition, the Social Phobia and Anxiety Inventory for Children (SPAI-C) has been successfully shown to distinguish between socially anxious children and children who were not socially anxious, and the available data demonstrated excellent psychometric properties for measuring fear and social anxiety in childhood (Beidel, Turner, & Morris, 1995).

Self-report measures can be used to assess interoceptive cues that can trigger anxiety in individuals with SAD (Antony & Rowa, 2005), such as the Anxiety Sensitivity Index (Peterson & Reiss, 1993) and the Body Sensations Questionnaire (Chambless et al., 1984), both of which measure anxiety levels in relation to the experience of particular physiological sensations (Antony & Rowa, 2005). Although these measures are most often used for panic disorder, interoceptive anxiety triggers can also occur in individuals with SAD, and these measures can help inform the clinician if there is a need to implement treatment strategies (such as interoceptive exposure interventions) that specifically target the fear of experiencing those physiological symptoms (Antony & Rowa, 2005).

Arguably the most commonly used clinician-administered assessment tool for SAD is the Liebowitz Social Anxiety Scale (LSAS; Liebowitz, 1987). The LSAS is an empirically validated social anxiety rating scale that was designed to measure the level of distress and anxiety that an individual experiences in a variety of common social and performance situations, as well as assess the extent to which they actively avoid such situations (Mennin et al., 2002). The validity and other psychometric properties of the LSAS has been widely supported by the available data, as well as its sensitivity to change reflecting positive response to treatment (Fresco et al., 2001; Heimberg et al., 1999). Findings by Mennin and colleagues (2002) indicated that the optimum diagnostic cutoff scores on the clinician-administered LSAS that best represented the balance between sensitivity and specificity were 60 for generalized SAD and 30 for performance-only SAD, and that the LSAS reliably demonstrated the ability to identify the presence of the disorder with exceptional accuracy. However, the diagnostic accuracy of the clinician-administered LSAS was found to be slightly stronger for discrete (i.e., performance-only) SAD than for generalized SAD, and the LSAS was demonstrated to be considerably better at classifying the presence of the disorder than the subtype of the disorder (Mennin et al., 2002).

Etiology

Biological Theories

Genetic. The available research literature supports a strong familial link in SAD, with empirical data suggesting that SAD, like many other anxiety disorders, tends to cluster within families (Dalrymple, 2012; Heimberg et al., 1995; Spence & Rapee, 2016). An early twin study by Kendler and colleagues (1992) demonstrated a higher concordance of SAD in monozygotic twins (24.4%) than in dizygotic twins (15.3%), which suggests a genetic contribution to the development of SAD; however, there exists a significant lack of similar twin studies in more recent literature that can replicate these findings using more up-to-date diagnostic criteria for SAD (this study uses criteria from the DSM-III), and the concordance rates found by Kendler and colleagues (1992) only indicate a heritability estimate of approximately 30% for SAD (Detweiler et al., 2014; Heimberg et al., 1995). Recent heritability estimates of SAD fall between approximately 20% and 40%, with the remaining variability purported to be attributable to environmental factors (Fox & Kalin, 2014). To date, there exists a gap in the literature in regards to the implication of specific genes associated with the development of SAD that show a sufficient degree of separation from those associated with anxiety disorders in general (Spence & Rapee, 2016). However, there has been a wide array of findings (discussed below) examining the involvement of specific brain structures and neural pathways, along with considerable support of the role of the behaviorally inhibited (BI) temperament, which lends significant support to the existence of biologically intrinsic risk factors contributing to the development of SAD (Spence & Rapee, 2016).

Temperament. A majority of the available research literature concerning the etiology of SAD acknowledges the role of Behavioral Inhibition (BI), a dimension of temperament that can be identified beginning in infancy and that reflects heightened sensitivity and distress in response to unfamiliar stimuli, and avoidance or withdrawal from unfamiliar situations, environments, or people (Clauss & Blackford, 2012; Dalrymple, 2012; Fox & Kalin, 2014; Rosenbaum et al., 1991; Spence & Rapee, 2016). Children with the BI temperament tend to be shy and fearful, and have higher levels of physiological arousal at rest than their uninhibited counterparts, including higher levels of cortisol and a faster stable heart rate (Clauss & Blackford, 2012). The general defining feature of BI is the avoidance and withdrawal behaviors in response to novel stimuli, with high BI children tending to make little eye contact and few verbal utterances, preferring to stay in close proximity to trusted attachment figures such as parents and primary caregivers, and avoiding perceived threat stimuli (Spence & Rapee, 2016). BI has also been reported to be associated with functional and structural differences in brain activity, including amygdala response to novel faces and differences in the structure of the ventral prefrontal cortex (Clauss & Blackford, 2012). In addition to the unmistakable overlap in the behavioral characteristics of BI and SAD, many of these same physiological characteristics of individuals with the BI temperament have also been observed in individuals with SAD (i.e., higher stable heart rate at rest, amygdala hyperactivity in response to novel faces), which is highly suggestive of a biological link between BI and the development of SAD (Clauss & Blackford, 2012; Spence & Rapee, 2016).

Thus, the BI temperament has been widely recognized in the available research literature as an important pathway that indicates genetic involvement in the development of SAD. Empirical studies and meta-analyses dating as far back as the early 1990s (Rosenbaum et al., 1991) have demonstrated that a BI temperament is associated with a significantly increased risk of future development of SAD; a meta-analysis by Clauss and Blackford (2012) estimated that BI children were over seven times more likely to develop SAD than were uninhibited children. In addition, empirical data has sufficiently demonstrated that BI predicts a significantly higher risk for the development of SAD in particular than it does for other anxiety disorders (Spence & Rapee, 2016; Rapee, 2014). In fact, many researchers have identified BI as the single greatest risk factor for SAD, based on evidence that nearly half of children with extreme BI temperament later develop SAD (Clauss & Blackford, 2012; Fox & Kalin, 2014).

Brain structures and neural pathways. One of the strongest findings to date that indicates differences in brain functioning between individuals with SAD and normal individuals (without SAD) concerns bilateral hyperactivation of the amygdala, a structure within the limbic system that is involved in the processing of visual, emotionally salient stimuli, particularly emotional expression, fear, aversion, and other related social cues (Detweiler et al., 2014; Hattingh et al., 2012). When normal individuals are presented with facial cues, the level of activation of the amygdala increases alongside the perceived social threat (Morris et al., 1996). Because individuals with SAD tend to overestimate the probability of negative outcomes in social situations (Heimberg et al., 2014), along with evidence indicating that they show an attentional bias towards negative social cues (Amir et al., 2003), it is fairly unsurprising that empirical research has indicated that individuals with SAD have significantly higher levels of amygdala activity in response to both explicit and subliminal social threat cues and socially emotive stimuli (particularly in facial cues) than observed in normal individuals (Hattingh et al., 2012; Phan et al., 2006). The exaggerated amygdala activity in individuals with SAD has been observed to occur in response to visual emotional stimuli including both neutral and negative facial expressions, as well as in response to both the anticipation and experience of public speaking (Freitas-Ferrari et al., 2010). Furthermore, Amiel and colleagues (2009) reported that compared to individuals without SAD, individuals with SAD had elevated levels of cerebral blood flow (CBF) in the amygdala, but had decreased levels of CBF in the insular cortex, orbitofrontal cortex, and temporal pole when speaking in public. This imbalance is suggested to be related to a lack of cortical inhibition, which may offer an explanation for the exaggerated fear response seen in individuals with SAD (Amiel et al., 2009).

In addition to increased amygdala activation, the findings of Hattingh and colleagues (2012) indicated that individuals with SAD demonstrated significantly higher levels of activation of the anterior cingulate cortex (ACC) than normal individuals. The ACC is involved in the regulation of cognitive and emotional processes associated with error detection in relation to inconsistencies between anticipated and actual outcomes, and also experiences increased activation when an individual anticipates social/emotional pain (Bush, Luu, & Posner, 2000; Eisenberger, Lieberman, & Williams, 2003; Hattingh et al., 2012). Increased levels of ACC activation in individuals with SAD in response to threat may represent a deficit in their ability to regulate discordant predictions of potential outcomes of social situations or events, and may reflect a greater level of anticipation that a social event will result in a socially painful experience (Duval, Javanbakht, & Loberzon, 2015; Hattingh et al., 2012).

The available research data have also implicated the hippocampus and hippocampal complex as regions of interest in the study of SAD (Freitas-Ferrari et al., 2010). The hippocampus has been recognized for its role in fear conditioning; in particular, it appears to be involved in the processing of context relevant to conditioned fears (Freitas-Ferrari et al., 2010). However, the available literature regarding the specific mechanism of hippocampal involvement in SAD is somewhat conflicting at the present time, with some findings suggesting decreased hippocampal volume in individuals with SAD, some findings suggesting increased hippocampal volume in individuals with SAD, and some findings reporting no differences in hippocampal volume (Duval, Javanbakht, & Loberzon, 2015). Thus, further examination of the specific role of the hippocampus in SAD is warranted.

The insula, another brain structure within the limbic system, has been suggested to be involved in “interoceptive awareness,” or the awareness and interpretation of particular bodily sensations and internal states (Freitas-Ferrari et al., 2010). In particular, the insular cortex is involved in the ability to recognize and experience fear, disgust, and pain (Peyron et al., 2002). Individuals with SAD have been shown to experience significantly increased activity in the insula (compared to normal individuals) in response to visual stimuli depicting disgusted and angry facial expressions, images containing negative emotional content, and when anticipating having to speak in front of an audience (Duval, Javanbakht, & Loberzon, 2015; Freitas-Ferrari et al., 2010).

Neurotransmitters. The available research literature regarding the involvement of specific neurotransmitters in the etiology of SAD appears to be in its preliminary stage at the present time, but based on the wide array of pharmacological treatments that have shown at least a moderate degree of effectiveness in treating SAD (see treatment section below), it can be assumed that no single neurotransmitter system can fully explain the neurobiological mechanisms of SAD (Feldman & Rivas-Vasquez, 2003; Heimberg et al., 1995). The range of empirical evidence regarding the role of amygdala hyperactivity in SAD implicates the potential involvement of the neurotransmitters involved in the activity of the amygdala and other structures of the limbic system, particularly serotonin and dopamine (Feldman & Rivas-Vasquez, 2003). However, empirical research describing the specific mechanisms of individual neurotransmitters and their involvement in the development and maintenance of SAD is scarce, and further investigation of the neurobiological mechanisms of SAD is warranted.

Psychological Theories

Psychodynamic. Although research literature describing etiological theories of the development of SAD from a psychodynamic perspective appears to be relatively scarce and have garnered little support in more recent literature, early psychodynamic theories emphasize the involvement of shame and separation anxiety in the development of SAD symptoms. Gabbard (1992) describes the central role of shame experiences in SAD, suggesting that individuals with SAD have an unconscious desire to obtain positive affirmations from others and be the center of attention in social situations. Chastisement or expressions of disapproval from parental figures (or other respected individuals) in response to behavioral expressions of this unconscious desire elicits feelings of shame and imagined humiliation in the individual, which then prompts them to avoid social situations that they believe carry the risk of similar shame-inducing disapproving responses from others (Gabbard, 1992).

In regards to separation anxiety, Gabbard (1992) suggests that socially anxious individuals are afraid to make efforts to achieve autonomy and expand their social connections because they fear that such efforts may result in the loss of the love and intimate connection they have with their parents, caregivers, or other primary attachment figures. This principle is rooted in attachment theory, and references findings of mother-infant attachment studies in which infants exhibited immediate anxious and fearful reactions when they were separated (or when they simply believed they were separated) from their mothers, as well as irritable reactions from the mothers in response to their infants’ attempts to achieve autonomy (Mahler, Pine, & Bergman, 1975). This finding is alleged to support the psychodynamic theory that individuals with SAD have exaggerated fears of losing the love and care of their parents or primary attachment figures and attempt to prevent this devastating loss by avoiding making connections with other people outside that primary connection with their caregiver (Gabbard, 1992). However, as previously stated, evidence supporting this theory is relatively lacking, and the majority of the available theories of the psychological etiology of SAD in the literature provide support for cognitive and behavioral underpinnings of SAD.

Cognitive. Earlier cognitive models of SAD were mainly concerned with the proposed maintenance mechanisms of SAD, rather than theories of its initial development (Spence & Rapee, 2016). A cognitive model proposed by Clark and Wells (1995) attempted to explain why the fears of individuals with SAD do not undergo extinction even after being repeatedly exposed to feared social situations without experiencing negative outcomes. They proposed that individuals with SAD have a particularly intense desire to be favorably evaluated by others and make a positive impression, and believe that others hold unreasonably high standards of the individual’s behaviors or performance in social situations (Clark & Wells, 1995; Rapee & Heimberg, 1997). In turn, socially anxious individuals hold an excessive fear that they might behave in an inappropriate manner during social or performance situations, which they predict will result in extreme humiliation and catastrophically negative evaluation by others, irreparably violating those high expectations they feel others have for them (Ollendick & Hirshfeld-Becker, 2002). Social and performance situations are thus perceived to be extremely threatening and elicit behavioral and physiological symptoms of anxiety (e.g., blushing, sweating), which may then intensify the SAD individual’s anxiety by introducing the fear that others will notice these symptoms and judge them harshly. This cycle continues as the SAD individual begins to obsess over these physiological anxiety symptoms and becomes distracted from the actual social situation, and their anxious behaviors may even result in actual negative evaluation by others, effectively confirming their fears (Clark & Wells, 1995; Ollendick & Hirshfeld-Becker, 2002; Spence & Rapee, 2016).

Similar cycles have been proposed for children and adolescents in relation to actual deficits in social performance, which also often result in aversive outcomes in social situations and consequently leads to increased social anxiety, further social skills deficits, and increased social avoidance behaviors (Alfano, Beidel, & Turner, 2006; Spence, Donovan, & Brechman Toussaint, 1999; Spence & Rapee, 2016). These cognitive models also emphasize the influence of maladaptive safety behaviors in children and adolescents that are meant to reduce the likelihood of negative outcomes (e.g., avoiding eye contact, refraining from speaking, avoiding calling attention to themselves; Kley, Tuschen-Caffier, & Heinrichs, 2012) on the maintenance of social anxiety even in the absence of actual negative outcomes, by proposing that individuals with SAD may believe that any successful social interactions were only successful because the individual engaged in those safety behaviors (Clark & Wells, 1995; Rapee & Heimberg, 1997; Spence & Rapee, 2016). As a result, the high anticipated threat of social situations is maintained regardless of actual outcome (Spence & Rapee, 2016).

Other cognitive theories regarding the development and maintenance mechanisms of social avoidance behaviors in SAD have suggested that socially anxious individuals tend to be particularly likely to engage in excessive post-event rumination (Heimberg, Brozovich, & Rapee, 2010). Many researchers have contended that high levels of post-event rumination may be a significant predictor of social avoidance behaviors in individuals with SAD; constantly recalling and ruminating over past perceived failures in social interactions may lead to a cognitive bias toward threat, and cause the individual to overgeneralize the negative outcomes experienced in past social interactions and develop pervasively negative outcome expectancies for all subsequent social situations (Beck, Emery, & Greenberg, 2005; Heimberg, Brozovich, & Rapee, 2010; Miers et al., 2014; Spence & Rapee, 2016). In addition, Beck, Emery, and Greenberg (2005) argued that the cognitive bias individuals with SAD have towards threat results in hypervigilance and overreactiveness in social contexts; such individuals are always on the lookout for threats of danger in social situations and their hypervigilance makes them more likely to magnify the gravity of minor threats and interpret neutral situations as threatening (Beck et al., 2005). Indeed, this theory is corroborated by the findings of Amir and colleagues (2003) as well as by Heinrichs and Hoffman (2001), both reporting evidence that individuals with SAD have an attentional bias toward threatening cues in social contexts.

Behavioral. Many etiological theories of SAD emphasize the role of fear conditioning, and a great deal of research has examined the possible contributing factors to the exaggerated fear response to socially relevant unconditioned stimuli observed in individuals with SAD. Fear conditioning is a learning process in which a neutral conditioned stimulus is repeatedly paired with an aversive unconditioned stimulus until the neutral conditioned stimulus elicits a fearful response, even in the absence of the aversive unconditioned stimulus, and this process is thought to potentially play a role in the onset and course of SAD (Lissek et al., 2008; Mineka & Zinbarg, 1995). In fear conditioning theories of SAD, the aversive unconditioned stimulus is considered to be the experience of humiliation, whereas the conditioned stimuli are the people and social situations that elicited the humiliating experience (Lissek et al., 2008). Results of a study by Lissek and colleagues (2008) examining whether individuals with SAD would develop a more fearful response than individuals without SAD to socially relevant stimuli consisting of disapproving facial expressions and negative feedback found that compared with non-SAD individuals, individuals with SAD indeed demonstrated increased conditioned fear-potentiated startle responses and reported more unpleasant reactions to the socially aversive stimuli (Lissek et al., 2008).

The role of conditioning in the development of SAD is supported by reports that a significant proportion of adults with SAD, particularly those with performance-only SAD, can identify a particular humiliating event that they associate with the origin or exacerbation of their social anxiety (Ollendick & Hirshfeld-Becker, 2002). However, such findings must be interpreted with caution for several reasons. It is important to consider these findings within the context of the attentional bias described previously, in which individuals with SAD tend to disproportionally allocate their attention toward negative or threatening social cues, which indicates that individuals with SAD may also have a memory bias for past traumatic social experiences (Amir et al., 2003; Heinrichs & Hoffman, 2001; Ollendick & Hirshfeld-Becker, 2002). Furthermore, retrospective reports of early traumatic experiences many years later may often reflect an inaccurate recall of events in which the individual unintentionally exaggerates the subjective humiliation they experienced during the event (Ollendick & Hirshfeld-Becker, 2002). In addition, these reported early humiliating events may in actuality represent a preliminary manifestation of SAD rather than a causal precipitant of the disorder (Lissek et al., 2008). Finally, it is important to note that a significant proportion of individuals without SAD report having early traumatic or humiliating social experiences as well (Stemberger et al., 1995). Taken together, these findings suggest that conditioning in the form of traumatic social experiences may only lead to the development of SAD in individuals who also have other factors (e.g., of a genetic, temperamental, or biological nature as discussed above) contributing to a multifaceted vulnerability toward developing the disorder (Mineka & Zinbarg, 1995; Ollendick & Hirshfeld-Becker, 2002).

Treatment

Pharmacological Treatments

SSRIs. The available research literature indicates that selective serotonin reuptake inhibitors (SSRIs) have been widely regarded as the first choice for treatment of SAD (Davidson, 2003; Nardi, 2001). As reported in a 2003 meta-analysis (Davidson, 2003), double-blind placebo-controlled studies examining the efficacy of the SSRI fluvoxamine in the treatment of SAD have demonstrated that fluvoxamine has a significantly higher efficacy than placebo in the reduction of core symptoms of SAD, including physiological arousal, fear, and avoidance behaviors.

Based on data from Davidson’s 2003 meta-analysis of pharmacological treatments for SAD, SSRIs such as fluvoxamine and paroxetine have been demonstrated to have high rates of success compared to placebo. However, the majority of SAD patients in the empirical studies investigated in the meta-analysis continued to have residual symptoms after completion of 12 weeks of treatment, and some patients simply did not respond to SSRI treatment at all. Although SSRIs can produce significant improvements in the symptomatology of a large percentage of patients with SAD, they are far from a one-size-fits-all approach, and some SAD patients may respond more favorably to other pharmacological treatments (Davidson, 2003).

Benzodiazepines. In a double-blind, placebo-controlled study of 75 patients with SAD using a maximum dose of 3mg of clonazepam per day, clonazepam began producing benefits within the first week of treatment and continued to provide benefits for the 10-week duration of the study (Davidson et al., 1993). 78% of SAD patients in this study responded positively to clonazepam, which was significantly higher than the 20% of patients who showed improvement with the placebo (Davidson et al., 1993). However, withdrawal symptoms were a common experience in the 2 weeks following termination of clonazepam treatment, and withdrawal also resulted in higher rates of relapse compared with placebo (Davidson et al., 1993; Davidson, 2003).

Another relatively early study has examined the use of another benzodiazepine, alprazolam, in the treatment of SAD. Results from a double-blind, placebo-controlled study by Gelernter and colleagues (1991) indicated that treatment with alprazolam produced significantly higher response rates in SAD patients compared with those in the placebo group; however, the response rate for alprazolam was still much lower than the response rates seen in studies of clonazepam (as well as other pharmacological treatments, such as phenelzine and certain SSRIs), and the magnitude of the difference in response rates for alprazolam and placebo (38% and 20%, respectively) was relatively small (Gelernter et al., 1991). Overall, little evidence exists that suggests the use of alprazolam as a primary or major treatment for SAD, as its effectiveness in managing the symptoms of SAD is minor at best, and withdrawal following the termination of treatment can have potentially severe consequences (Davidson, 2003).

In general, the findings from Davidson’s (2003) meta-analysis concerning the use of benzodiazepines in the treatment of SAD suggest that these drugs, particularly clonazepam, can provide valuable benefits for the management of SAD symptoms. Benzodiazepines may be particularly useful as secondary approaches to pharmacological treatment of SAD, or as a first-line treatment for SAD patients who are not able to tolerate SSRIs (Davidson, 2003).

MAOIs and RIMAs. The monoamine oxidase inhibitor (MAOI) phenelzine is the most widely studied MAOI treatment for individuals with SAD. Results of one of the earliest studies (Liebowitz et al., 1992) examining the efficacy of phenelzine treatment of individuals with both generalized and performance-only SAD demonstrated phenelzine to be significantly more effective than placebo for the treatment of generalized SAD. In contrast, the magnitude of difference in treatment response rates to phenelzine and placebo in this study were much smaller for individuals with performance-only SAD (Liebowitz et al., 1992). Indeed, findings of a 2003 meta-analysis (Davidson, 2003) indicated that phenelzine has been demonstrated to be significantly more effective than placebo in a multitude of double-blind drug comparison studies. However, the magnitude of differences in positive response rates of phenelzine versus placebo is much larger and more stable across the available empirical studies for generalized SAD than for performance-only SAD, although some studies have found it to be significantly effective for the treatment of performance-only SAD as well (Davidson, 2003; Heimberg, Liebowitz, & Hope, 1998; Liebowitz et al., 1992).

Despite the abundant empirical data demonstrating the benefits and effectiveness of phenelzine in the treatment of SAD, it is generally not recommended as a first-line of treatment due to its potentially serious risks and side effects, such as hypertensive crisis and hepatitis (Davidson, 2003; Goldberg, 1964). In addition, MAOIs in general are well-known for having potentially dangerous interactions with food and other drugs, which can complicate its use for managing symptoms (Goldberg, 1964). Although phenelzine has been shown to significantly reduce social anxiety symptoms and avoidance behaviors in individuals with generalized SAD compared to placebo, they tend to have a higher risk of serious side effects and potentially harmful interactions with other drugs and food (Nardi, 2001).

Preliminary results of a double-blind, placebo-controlled study using the reversible inhibitor of monoamine oxidase (RIMA) moclobemide appeared promising, with one early study reporting a response rate that was nearly as high as those found in studies of phenelzine such as those discussed above (Versiani et al., 1992). However, many subsequent similar studies have shown the difference in response rates between moclobemide and placebo to be negligible (Davidson, 2003). On the other hand, a small handful of early studies using brofaromine (another RIMA) have demonstrated positive results, with response rates that were significantly higher than placebo response (Davidson, 2003; Fahlén et al., 1992; van Vliet, den Boer, & Westenberg, 1992). However, the commercial manufacturing of brofaromine was discontinued for several years until its recent re-licensure, so further investigation of brofaromine once the drug is more readily available may have important implications for the future directions of treatment of SAD (Davidson, 2003). Regardless, the presently available empirical data concerning the treatment of SAD using RIMAs remains somewhat lacking and generally unpromising. This is unfortunate, given that RIMAs are generally safer and more easily tolerated than standard MAOIs such as phenelzine (Davidson, 2003).

Cognitive-Behavioral-Based Treatments

Exposure and cognitive restructuring. A search of the available research literature yielded several meta-analyses evaluating and comparing the effectiveness of exposure interventions and cognitive restructuring (CR) interventions in the treatment of individuals with SAD. Although the authors of nearly all of these meta-analyses hypothesized that CR would be more effective than exposure alone, none produced results that indicated any superiority of CR over exposure therapy in short-term treatment of SAD; rather, the two treatment techniques were widely demonstrated to have equally favorable outcomes (Federoff & Taylor, 2001; Feske & Chambless, 1995; Hope, Heimberg, & Bruch, 1995), and one study demonstrated an advantage of exposure alone over CR alone in producing cognitive change (Gould et al., 1997). In addition, studies examining the combined use of exposure techniques and CR found it to have equal, if not slightly reduced, effectiveness compared to exposure alone in producing cognitive change (Federoff & Taylor, 2001; Gould et al., 1997). Given that the available empirical data indicates exposure therapy, CR therapy, and combined exposure + CR therapy to all be significantly more effective in the treatment of SAD compared to controls, these findings suggest that CR interventions are not necessary for producing cognitive change in individuals with SAD, as exposure therapy alone can produce equivalent (or even slightly superior) levels of cognitive change (Feske & Chambless, 1995; Gould et al., 1997; Hope, Heimberg, & Bruch, 1995).

Relaxation training. Relaxation training is a subset of cognitive-behavioral therapy in which individuals with SAD learn to mindfully recognize and control the level of physiological anxiety symptoms that they experience when anticipating or experiencing a feared social or performance situation (Heimberg, 2002). This treatment approach involves the use of relaxation techniques such as progressive muscle relaxation (PMR), in which the individual briefly tightens one particular muscle group at a time, pausing for several seconds before releasing the tension, mindfully observing the difference in the physical sensations between tension and relaxation (Bernstein & Borkovec, 1973). Relaxation training for individuals with SAD is typically implemented by first teaching the patient to recognize the physiological symptoms of anxiety (including muscle tension), training the patient to quickly relax and relieve these symptoms in session, and helping the patient learn to apply these relaxation skills outside of therapy to the social or performance situations that typically elicit anxiety (Heimberg, 2002). By nature, this sequence, commonly referred to as “applied relaxation,” incorporates elements of exposure therapy into relaxation training with the intention of helping individuals with SAD develop a set of relaxation skills that they can use to cope with their physiological anxiety symptoms during feared situations or events (Öst, 1987). However, research investigating the efficacy of relaxation training in the treatment of SAD is relatively unpromising, and it has generally been outperformed by exposure therapies and CR interventions, as well as by pharmacological treatments including SSRIs, benzodiazepines, and MAOIs (Donohue, Van Hasselt, & Hersen, 1994; Federoff & Taylor, 2001).

Recommendations

Overall, the available research literature regarding the treatment of SAD suggests that pharmacological treatments, particularly SSRIs and benzodiazepines, are more effective than psychological treatments for the short-term treatment of SAD (Bögels et al., 2010; Davidson, 2003; Davidson et al., 1993; Federoff & Taylor, 2001; Gelernter et al., 1991; Nardi, 2001). However, pharmacological treatments were frequently associated with higher rates of relapse at follow-up than non-pharmacological treatments (Gould et al., 1997), with cognitive-behavioral techniques (particularly exposure interventions) having a longer-lasting treatment effect than pharmacological treatments (Federoff & Taylor, 2001). Taken together, these findings can be used to propose a potentially more favorable integrative approach to treatment that combines the short-term advantages of pharmacological treatments and the long-lasting effects of cognitive-behavioral therapy techniques, in which individuals with SAD are acutely treated using pharmacological treatments such as SSRIs, followed by cognitive-behavioral therapy (particularly exposure interventions) during the drug tapering stage and the period that follows (Federoff & Taylor, 2001; Gould et al., 1997).

Implications

Social anxiety disorder has had an interesting history of simultaneously being known as one of the most common anxiety disorders and one of the most neglected anxiety disorders. Since its first inclusion as a distinct disorder in the DSM-III (American Psychiatric Association, 1980), SAD has undergone several diagnostic changes that have helped to raise awareness of the commonness and level of impairment associated with the disorder. Arguably, the most impactful changes in the diagnostic criteria in this regard have been the distinction between generalized and performance-specific forms of SAD, and the retirement of the previous name of social phobia in favor of social anxiety disorder, a term which more adequately conveys the weight of the diagnosis and thus may result in a higher likelihood that clinicians will screen for SAD as well as a higher likelihood that affected individuals will seek treatment for their symptoms (Heimberg et al., 2014).

However, the current diagnostic criteria for SAD is not devoid of controversy. The diagnostic overlap and corresponding high comorbidity rates between SAD and APD raises questions regarding the validity of the categorical classification system itself. The lines that separate normal shyness, SAD, and APD are blurry, which indicates that the diagnostic boundaries as they currently exist do not sufficiently describe the comprehensive range of symptoms and traits exhibited by individuals in this domain. Future editions of the DSM could address this issue by adopting a more dimensional model of classification that conceptualizes social anxiety as existing on a spectrum, with normal shyness on one end and the more severe and pervasive features of APD on the other end.

In addition, there are many gaps in the literature regarding the biological underpinnings of SAD, particularly in regards to the roles of specific genes and neurotransmitters, which opens many possible directions for future research examining the etiology of SAD. The identification of specific neurobiological pathways that predispose an individual toward the future development of SAD and/or exacerbate the existing symptoms of SAD would have profound implications for the pharmacological treatment of the disorder by facilitating the development of disorder-specific drugs that directly target the neurobiological mechanisms involved in SAD. Such findings would represent a monumental breakthrough, as the current research regarding the most effective pharmacological treatment of SAD has yet to discover a treatment that can reliably produce total remission of the disorder.

 

Appendix A: DSM-5 Criteria:

Social Anxiety Disorder (Social Phobia)

 

Diagnostic Criteria        300.23 (F40.10)

  1. Marked fear or anxiety about one or more social situations in which the individual is exposed to possible scrutiny by others. Examples include social interactions (e.g., having a conversation, meeting unfamiliar people), being observed (e.g., eating or drinking), and performing in front of others (e.g., giving a speech).

Note: In children, the anxiety must occur in peer settings and not just during interactions with adults.

  1. The individual fears that he or she will act in a way or show anxiety symptoms that will be negatively evaluated (i.e., will be humiliating or embarrassing; will lead to rejection or offend others).
  1. The social situations almost always provoke fear or anxiety.

Note: In children, the fear or anxiety may be expressed by crying, tantrums, freezing, clinging, shrinking, or failing to speak in social situations.

  1. The social situations are avoided or endured with intense fear or anxiety.
  1. The fear or anxiety is out of proportion to the actual threat posed by the social situation and to the sociocultural context.
  1. The fear, anxiety, or avoidance is persistent, typically lasting for 6 months or more.
  1. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
  1. The fear, anxiety, or avoidance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition.
  1. The fear, anxiety, or avoidance is not better explained by the symptoms of another mental disorder, such as panic disorder, body dysmorphic disorder, or autism spectrum disorder.
  1. If another medical condition (e.g., Parkinson’s disease, obesity, disfigurement from burns or injury) is present, the fear, anxiety, or avoidance is clearly unrelated or is excessive.

Specify if:

Performance only: If the fear is restricted to speaking or performing in public.

Note: American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders: DSM-5. Washington,

D.C: American Psychiatric Association. p. 202-203.

Appendix B: DSM-5 Criteria:

Avoidant Personality Disorder

 

Diagnostic Criteria                    301.82 (F60.6)

A pervasive pattern of social inhibition, feelings of inadequacy, and hypersensitivity to negative evaluation, beginning by early adulthood and present in a variety of contexts, as indicated by four (or more) of the following:

  1. Avoids occupational activities that involve significant interpersonal contact because of fears of criticism, disapproval, or rejection.
  2. Is unwilling to get involved with people unless certain of being liked.
  3. Shows restraint within intimate relationships because of the fear of being shamed or ridiculed.
  4. Is preoccupied with being criticized or rejected in social situations.
  5. Is inhibited in new interpersonal situations because of feelings of inadequacy.
  6. Views self as socially inept, personally unappealing, or inferior to others.
  7. Is unusually reluctant to take personal risks or to engage in any new activities because they may prove embarrassing.

Note: American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders: DSM-5. Washington,

D.C: American Psychiatric Association. p. 672-673.

References

Alfano, C. A., Beidel, D. C., & Turner, S. M. (2006). Cognitive correlates of social phobia among children and adolescents. Journal of Abnormal Child Psychology, 34(2), 182–194.

American Psychiatric Association. (1980). Diagnostic and statistical manual (DSM-III). Washington, DC: American Psychiatric Association.

American Psychiatric Association. (1987). Diagnostic and Statistical Manual of Mental Health Disorders (DSM-III-R). American Psychiatric Association.

American Psychiatric Association. (1994). DSM-IV: Diagnostic and statistic manual of mental disorders. American Psychiatric Association, Washington DC.

American Psychiatric Association. (2000). Diagnostic and statistical manual, 4th edition, Text Revision (DSM-IV-TR). American Psychiatric Association, Washington.

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (DSM-5®). American Psychiatric Pub.

Amiel, J. M., Mathew, S. J., Garakani, A., Neumeister, A., & Charney, D. S. (2009). Neurobiology of Anxiety Disorders. In The American Psychiatric Publishing Textbook of         Psychopharmacology (Vols. 1–0). American Psychiatric Publishing. https://doi.org/10.1176/appi.books.9781585623860.as47

Amir, N., Elias, J., Klumpp, H., & Przeworski, A. (2003). Attentional bias to threat in social phobia: facilitated processing of threat or difficulty disengaging attention from threat? Behaviour Research and Therapy, 41(11), 1325–1335.

Antony, M. M., & Rowa, K. (2005). Evidence-based assessment of anxiety disorders in adults. Psychological Assessment, 17(3), 256.

Beck, A. T., Emery, G., & Greenberg, R. L. (2005). Anxiety disorders and phobias: A cognitive perspective. Basic Books.

Beesdo, K., Bittner, A., Pine, D. S., Stein, M. B., Höfler, M., Lieb, R., & Wittchen, H.-U. (2007). Incidence of social anxiety disorder and the consistent risk for secondary depression in the first three decades of life. Archives of General Psychiatry, 64(8), 903–912.

Beidel, D. C., & Turner, S. M. (2007). Shy children, phobic adults: Nature and treatment of social anxiety disorder. American Psychological Association Washington, DC.

Beidel, D. C., Turner, S. M., & Morris, T. L. (1995). A new inventory to assess childhood social anxiety and phobia: The Social Phobia and Anxiety Inventory for Children. Psychological Assessment, 7(1), 73.

Bernstein, D., & Borkovec, T. (1973). Progressive muscle relaxation: A manual for the helping professions.

Bögels, S. M., Alden, L., Beidel, D. C., Clark, L. A., Pine, D. S., Stein, M. B., & Voncken, M. (2010). Social anxiety disorder: questions and answers for the DSM‐V. Depression and Anxiety, 27(2), 168–189.

Brown, E. J., Heimberg, R. G., & Juster, H. R. (1995). Social phobia subtype and avoidant personality disorder: Effect on severity of social phobia, impairment, and outcome of cognitive behavioral treatment. Behavior Therapy, 26(3), 467–486. https://doi.org/10.1016/S0005-7894(05)80095-4

Brown, E. J., Turovsky, J., Heimberg, R. G., Juster, H. R., Brown, T. A., & Barlow, D. H. (1997). Validation of the Social Interaction Anxiety Scale and the Social Phobia Scale across the anxiety disorders. Psychological Assessment, 9(1), 21.

Brown, L. A., LeBeau, R., Liao, B., Niles, A. N., Glenn, D., & Craske, M. G. (2016). A comparison of the nature and correlates of panic attacks in the context of panic disorder and social anxiety disorder. Psychiatry Research, 235, 69–76.

Bruce, L. C., Heimberg, R. G., & Coles, M. E. (2012). Social phobia and social anxiety disorder: effect of disorder name on recommendation for treatment. American Journal of Psychiatry, 169(5), 538–538.

Bush, G., Luu, P., & Posner, M. I. (2000). Cognitive and emotional influences in anterior cingulate cortex. Trends in Cognitive Sciences, 4(6), 215–222.

Chambless, D. L., Caputo, G. C., Bright, P., & Gallagher, R. (1984). Assessment of fear of fear in agoraphobics: The Body Sensations Questionnaire and the Agoraphobic Cognitions Questionnaire. Journal of Consulting and Clinical Psychology, 52(6), 1090.

Chartier, M. J., Hazen, A. L., & Stein, M. B. (1998). Lifetime patterns of social phobia: a retrospective study of the course of social phobia in a nonclinical population. Depression and Anxiety, 7(3), 113–121.

Chou, K.-L. (2009). Social anxiety disorder in older adults: evidence from the National Epidemiologic Survey on alcohol and related conditions. Journal of Affective Disorders, 119(1), 76–83.

Clark, D. M., & Wells, A. (1995). A cognitive model of social phobia. Social Phobia: Diagnosis, Assessment, and Treatment, 41(68), 22–3.

Clauss, J. A., & Blackford, J. U. (2012). Behavioral inhibition and risk for developing social anxiety disorder: a meta-analytic study. Journal of the American Academy of Child & Adolescent Psychiatry, 51(10), 1066–1075.

Connor, K. M., Davidson, J. R., Churchill, L. E., Sherwood, A., Weisler, R. H., & FOA, E. (2000). Psychometric properties of the social phobia inventory (SPIN). The British Journal of Psychiatry, 176(4), 379–386.

Dalrymple, K. L. (2012). Issues and controversies surrounding the diagnosis and treatment of social anxiety disorder. Expert Rev Neurother, 12(8), 993–1008.

Davidson, J. (2003). Pharmacotherapy of social phobia. Acta Psychiatrica Scandinavica, 108(s417), 65–71.

Davidson, J. R., Potts, N., Richichi, E., Krishnan, R., Ford, S. M., Smith, R., & Wilson, W. H. (1993). Treatment of social phobia with clonazepam and placebo. Journal of Clinical Psychopharmacology, 13(6), 423–428.

Den Boer, J. A. (2000). Social anxiety disorder/social phobia: epidemiology, diagnosis, neurobiology, and treatment. Comprehensive Psychiatry, 41(6), 405–415.

Detweiler, M. F., Comer, J. S., Crum, K. I., & Albano, A. M. (2014). Social Anxiety in Children and Adolescents: Biological, Developmental, and Social Considerations. In Social anxiety: Clinical, developmental, and social perspectives (3rd ed)(pp 253–309) xxvi, 818 pp San Diego, CA, US (pp. 253–309). Elsevier Academic Press US.

Donohue, B. C., Van Hasselt, V. B., & Hersen, M. (1994). Behavioral assessment and treatment of social phobia: An evaluative review. Behavior Modification, 18(3), 262–288.

Duval, E. R., Javanbakht, A., & Liberzon, I. (2015). Neural circuits in anxiety and stress disorders: a focused review. Therapeutics & Clinical Risk Management, 11.

Eisenberger, N. I., Lieberman, M. D., & Williams, K. D. (2003). Does rejection hurt? An fMRI study of social exclusion. Science, 302(5643), 290–292.

Erwin, B. A., Heimberg, R. G., Juster, H., & Mindlin, M. (2002). Comorbid anxiety and mood disorders among persons with social anxiety disorder. Behaviour Research and Therapy, 40(1), 19–35.

Fahlén, T., Humble, M., Koczkas, C., & Nilsson, H. (1992). Social Phobia And Its Treatment With Brofaromine. Efficacy Regarding Social Phobia Symptoms And Personality Traits. Clinical Neuropharmacology, 15, 64B.

Faravelli, C., Zucchi, T., Viviani, B., Salmoria, R., Perone, A., Paionni, A., … D’adamo, D. (2000). Epidemiology of social phobia: a clinical approach. European Psychiatry, 15(1), 17–24.

Fedoroff, I. C., & Taylor, S. (2001). Psychological and pharmacological treatments of social phobia: a meta-analysis. Journal of Clinical Psychopharmacology, 21(3), 311–324.

Feldman, L. B., & Rivas-Vazquez, R. A. (2003). Assessment and treatment of social anxiety disorder. Professional Psychology: Research and Practice, 34(4), 396.

Feske, U., & Chambless, D. L. (1995). Cognitive behavioral versus exposure only treatment for social phobia: A meta-analysis. Behavior Therapy, 26(4), 695–720.

Fox, A. S., & Kalin, N. H. (2014). A translational neuroscience approach to understanding the development of social anxiety disorder and its pathophysiology. American Journal of Psychiatry, 171(11), 1162–1173.

Freitas-Ferrari, M. C., Hallak, J. E., Trzesniak, C., Santos Filho, A., Machado-de-Sousa, J. P., Chagas, M. H. N., … Crippa, J. A. S. (2010). Neuroimaging in social anxiety disorder: a systematic review of the literature. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 34(4), 565–580.

Fresco, D., Coles, M., Heimberg, R. G., Liebowitz, M., Hami, S., Stein, M., & Goetz, D. (2001). The Liebowitz Social Anxiety Scale: a comparison of the psychometric properties of self-report and clinician-administered formats. Psychological Medicine, 31(6), 1025–1035.

GABBARD, G. (1992). Psychodynamics of panic disorder and social phobia. Bulletin of the Menninger Clinic, 56(2), A3–A13.

Gelernter, C. S., Uhde, T. W., Cimbolic, P., Arnkoff, D. B., Vittone, B. J., Tancer, M. E., & Bartko, J. J. (1991). Cognitive-behavioral and pharmacological treatments of social phobia: a controlled study. Archives of General Psychiatry, 48(10), 938–945.

Goldberg, L. I. (1964). Monoamine oxidase inhibitors: adverse reactions and possible mechanisms. Jama, 190(5), 456–462.

Gould, R. A., Buckminster, S., Pollack, M. H., & Otto, M. W. (1997). Cognitive‐behavioral and pharmacological treatment for social phobia: A meta‐analysis. Clinical Psychology: Science and Practice, 4(4), 291–306.

Gretarsdottir, E., Woodruff-Borden, J., Meeks, S., & Depp, C. A. (2004). Social anxiety in older adults: phenomenology, prevalence, and measurement. Behaviour Research and Therapy, 42(4), 459–475.

Hattingh, C. J., Ipser, J., Tromp, S., Syal, S., Lochner, C., Brooks, S., & Stein, D. J. (2012). Functional magnetic resonance imaging during emotion recognition in social anxiety disorder: an activation likelihood meta-analysis. Frontiers in Human Neuroscience, 6.

Heimberg, R. G. (2002). Cognitive-behavioral therapy for social anxiety disorder: current status and future directions. Biological Psychiatry, 51(1), 101–108.

Heimberg, R. G., Horner, K., Juster, H., Safren, S., Brown, E., Schneier, F., & Liebowitz, M. (1999). Psychometric properties of the Liebowitz social anxiety scale. Psychological Medicine, 29(1), 199–212.

Heimberg, R. G., Liebowitz, M., Hope, D., & Schneier, F. (1995). Social phobia. Guilford, New York.

Heimberg, R. G., Mueller, G. P., Holt, C. S., Hope, D. A., & Liebowitz, M. R. (1993). Assessment of anxiety in social interaction and being observed by others: The Social Interaction Anxiety Scale and the Social Phobia Scale. Behavior Therapy, 23(1), 53–73.

Heinrichs, N., & Hofmann, S. G. (2001). Information processing in social phobia: a critical review. Clinical Psychology Review, 21(5), 751–770. https://doi.org/10.1016/S0272-7358(00)00067-2

Huppert, J. D., Strunk, D. R., Ledley, D. R., Davidson, J. R. T., & Foa, E. B. (2008). Generalized social anxiety disorder and avoidant personality disorder: structural analysis and treatment outcome. Depression and Anxiety, 25(5), 441–448. https://doi.org/10.1002/da.20349

Janet, P., & Raymond, F. (1903). Les obsessions et la psychasthénie (Vol. 2). Félix Alcan.

Karlsson, B., Sigström, R., Östling, S., Waern, M., Börjesson-Hanson, A., & Skoog, I. (2016). DSM-IV and DSM-5 Prevalence of Social Anxiety Disorder in a Population Sample of Older People. The American Journal of Geriatric Psychiatry, 24(12), 1237–1245. https://doi.org/10.1016/j.jagp.2016.07.023

Keller, M. (2003). The lifelong course of social anxiety disorder: a clinical perspective. Acta Psychiatrica Scandinavica, 108(s417), 85–94.

Kendler, K. S., Neale, M. C., Kessler, R. C., Heath, A. C., & Eaves, L. J. (1992). The genetic epidemiology of phobias in women: The interrelationship of agoraphobia, social phobia, situational phobia, and simple phobia. Archives of General Psychiatry, 49(4), 273–281.

Kessler, R. C., Berglund, P., Demler, O., Jin, R., Merikangas, K. R., & Walters, E. E. (2005). Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry, 62(6), 593–602.

Kessler, R. C., Stang, P., Wittchen, H.-U., Stein, M., & Walters, E. E. (1999). Lifetime co-morbidities between social phobia and mood disorders in the US National Comorbidity Survey. Psychological Medicine, 29(3), 555–567.

Kessler, R. C., Stein, M. B., & Berglund, P. (1998). Social phobia subtypes in the National Comorbidity Survey. American Journal of Psychiatry, 155(5), 613–619.

Kisely, S., Alichniewicz, K. K., Black, E. B., Siskind, D., Spurling, G., & Toombs, M. (2017). The prevalence of depression and anxiety disorders in indigenous people of the Americas: A systematic review and meta-analysis. Journal of Psychiatric Research, 84, 137–152.

Kley, H., Tuschen-Caffier, B., & Heinrichs, N. (2012). Safety behaviors, self-focused attention and negative thinking in children with social anxiety disorder, socially anxious and non-anxious children. Journal of Behavior Therapy and Experimental Psychiatry, 43(1), 548–555.

Lampe, L., & Sunderland, M. (2015). Social phobia and avoidant personality disorder: similar but different? Journal of Personality Disorders, 29(1), 115–130.

Liebowitz, M. R. (1987). Social phobia. Karger Publishers.

Liebowitz, M. R., Gorman, J. M., Fyer, A. J., & Klein, D. F. (1985). Social phobia: Review of a neglected anxiety disorder. Archives of General Psychiatry, 42(7), 729–736.

Liebowitz, M. R., Heimberg, R. G., Fresco, D. M., Travers, J., & Stein, M. B. (2000). Social phobia or social anxiety disorder: what’s in a name? Archives of General Psychiatry, 57(2), 191–192.

Liebowitz, M. R., Schneier, F., Campeas, R., Hollander, E., Hatterer, J., Fyer, A., … Gully, R. (1992). Phenelzine vs atenolol in social phobia: a placebo-controlled comparison. Archives of General Psychiatry, 49(4), 290–300.

Lissek, S., Levenson, J., Biggs, A. L., Johnson, L. L., Ameli, R., Pine, D. S., & Grillon, C. (2008). Elevated Fear Conditioning to Socially Relevant Unconditioned Stimuli in Social Anxiety Disorder. American Journal of Psychiatry, 165(1), 124–132. https://doi.org/10.1176/appi.ajp.2007.06091513

Mahler, M. S., Pine, F., & Bergman, A. (1975). The Psychological Birth of the Human Infant. Symbiosis and Individuation. New York (Basic Books) 1975.

Marks, I. M., & Gelder, M. (1966). Different ages of onset in varieties of phobia. American Journal of Psychiatry, 123(2), 218–221.

Marques, L., Porter, E., Keshaviah, A., Pollack, M. H., Van Ameringen, M., Stein, M. B., & Simon, N. M. (2012). Avoidant personality disorder in individuals with generalized social anxiety disorder: What does it add? Journal of Anxiety Disorders, 26(6), 665–672.

Mattick, R. P., & Clarke, J. C. (1998). Development and validation of measures of social phobia scrutiny fear and social interaction anxiety. Behaviour Research and Therapy, 36(4), 455–470.

McLean, C. P., Asnaani, A., Litz, B. T., & Hofmann, S. G. (2011). Gender differences in anxiety disorders: prevalence, course of illness, comorbidity and burden of illness. Journal of Psychiatric Research, 45(8), 1027–1035.

Mennin, D. S., Fresco, D. M., Heimberg, R. G., Schneier, F. R., Davies, S. O., & Liebowitz, M. R. (2002). Screening for social anxiety disorder in the clinical setting: using the Liebowitz Social Anxiety Scale. Journal of Anxiety Disorders, 16(6), 661–673.

Miers, A. C., Blöte, A. W., Heyne, D. A., & Westenberg, P. M. (2014). Developmental pathways of social avoidance across adolescence: The role of social anxiety and negative cognition. Journal of Anxiety Disorders, 28(8), 787–794.

Mineka, S., & Zinbarg, R. (1995). Conditioning and ethological models of social phobia. Social Phobia: Diagnosis, Assessment, and Treatment, 134–162.

Morris, J. S., Frith, C. D., Perrett, D. I., & Rowland, D. (1996). A differential neural response in the human amygdala to fearful and happy facial expressions. Nature, 383(6603), 812.

Nardi, A. E. (2001). Antidepressants in social anxiety disorder. Arquivos de Neuro-Psiquiatria, 59(3A), 637–642.

Ollendick, T. H., & Hirshfeld-Becker, D. R. (2002). The developmental psychopathology of social anxiety disorder. Biological Psychiatry, 51(1), 44–58.

Öst, L.-G. (1987). Applied relaxation: description of a coping technique and review of controlled studies. Behaviour Research and Therapy, 25(5), 397–409.

Peterson, R. A., & Reiss, S. (1993). Anxiety sensitivity index revised test manual. IDS Publ.

Peyron, R., Frot, M., Schneider, F., Garcia-Larrea, L., Mertens, P., Barral, F., … Mauguiere, F. (2002). Role of operculoinsular cortices in human pain processing: converging evidence from PET, fMRI, dipole modeling, and intracerebral recordings of evoked potentials. Neuroimage, 17(3), 1336–1346.

Phan, K. L., Fitzgerald, D. A., Nathan, P. J., & Tancer, M. E. (2006). Association between amygdala hyperactivity to harsh faces and severity of social anxiety in generalized social phobia. Biological Psychiatry, 59(5), 424–429.

Rapee, R. M. (2014). Preschool environment and temperament as predictors of social and nonsocial anxiety disorders in middle adolescence. Journal of the American Academy of Child & Adolescent Psychiatry, 53(3), 320–328.

Rapee, R. M., & Heimberg, R. G. (1997). A cognitive-behavioral model of anxiety in social phobia. Behaviour Research and Therapy, 35(8), 741–756. https://doi.org/10.1016/S0005-7967(97)00022-3

Regier, D. A., Rae, D. S., Narrow, W. E., Kaelber, C. T., & Schatzberg, A. F. (1998). Prevalence of anxiety disorders and their comorbidity with mood and addictive disorders. The British Journal of Psychiatry.

Rettew, D. C. (2000). Avoidant personality disorder, generalized social phobia, and shyness: Putting the personality back into personality disorders. Harvard Review of Psychiatry, 8(6), 283–297.

Rosenbaum, J. F., Biederman, J., Hirshfeld, D. R., Bolduc, E. A., Faraone, S. V., Kagan, J., … Reznick, J. S. (1991). Further evidence of an association between behavioral inhibition and anxiety disorders: results from a family study of children from a non-clinical sample. Journal of Psychiatric Research, 25(1), 49–65.

Schneier, F. R., Johnson, J., Hornig, C. D., Liebowitz, M. R., & Weissman, M. M. (1992). Social phobia: comorbidity and morbidity in an epidemiologic sample. Archives of General Psychiatry, 49(4), 282–288.

Somers, J. M., Goldner, E. M., Waraich, P., & Hsu, L. (2006). Prevalence and incidence studies of anxiety disorders: a systematic review of the literature. The Canadian Journal of Psychiatry, 51(2), 100–113.

Spence, S. H., & Rapee, R. M. (2016). The etiology of social anxiety disorder: an evidence-based model. Behaviour Research and Therapy, 86, 50–67.

Stemberger, R. T., Turner, S. M., Beidel, D. C., & Calhoun, K. S. (1995). Social phobia: An analysis of possible developmental factors. Journal of Abnormal Psychology, 104(3), 526.

Turk, C. L., Heimberg, R. G., & Hope, D. A. (2001). Social anxiety disorder. Clinical Handbook of Psychological Disorders: A Step-by-Step Treatment Manual, 3, 114–153.

Turner, S. M., Beidel, D. C., & Townsley, R. M. (1992). Social phobia: A comparison of specific and generalized subtypes and avoidant personality disorder. Journal of Abnormal Psychology, 101(2), 326–331.

Van Ameringen, M., Mancini, C., Styan, G., & Donison, D. (1991). Relationship of social phobia with other psychiatric illness. Journal of Affective Disorders, 21(2), 93–99.

Van Vliet, I. M., den Boer, J. A., & Westenberg, H. G. (1992). Psychopharmacological treatment of social phobia: clinical and biochemical effects of brofaromine, a selective MAO-A inhibitor. European Neuropsychopharmacology, 2(1), 21–29.

Versiani, M., Nardi, A., Mundim, F., Alves, A., Liebowitz, M., & Amrein, R. (1992). Pharmacotherapy of social phobia. A controlled study with moclobemide and phenelzine. The British Journal of Psychiatry, 161(3), 353–360.

Werner, K. H., Goldin, P. R., Ball, T. M., Heimberg, R. G., & Gross, J. J. (2011). Assessing emotion regulation in social anxiety disorder: The emotion regulation interview. Journal of Psychopathology and Behavioral Assessment, 33(3), 346–354.

Wittchen, H., & Fehm, L. (2003). Epidemiology and natural course of social fears and social phobia. Acta Psychiatrica Scandinavica, 108(s417), 4–18.

Yonkers, K. A., Bruce, S. E., Dyck, I. R., & Keller, M. B. (2003). Chronicity, relapse, and illness—course of panic disorder, social phobia, and generalized anxiety disorder: findings in men and women from 8 years of follow‐up. Depression and Anxiety, 17(3), 173–179.

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