social phobia: Epidemiology, diagnosis, neurobiology, and treatment

Comprehensive Psychiatry (Official Journal of the American Psychopathological Association)

VOL. 41, NO. 6

NOVEMBER/DECEMBER

Social Anxiety Disorder/Social Phobia: Epidemiology, Diagnosis, Neurobiology, and Treatment Johan A. den Boer Some anticipatory anxiety is expected on specific occasions such as giving a speech. However, some individuals have an excessive fear of such situations when they are under scrutiny, believing that their performance will cause them embarrassment or humiliation, frequently leading to deliberate avoidance of these situations. This disabling condition has been termed social anxiety disorder. Social anxiety disorder is common, with a lifetime prevalence of 2% to 5%, but is probably underreported. The sufferer often avoids seeking assistance, leading to comorbid mental disorders, greater disability, and an increased risk of suicide. Consequently, a high burden is placed on the patient’s caregivers and on society. The diagnosis of social anxiety disorder is aided by the patient’s history

together with DSM-IV criteria. Research into the neurobiology of social anxiety disorder suggests a dysfunction of postsynaptic serotonin receptors and a hypersensitivity to challenge with caffeine, CO2, and pentagastrin. Neuroimaging studies suggest a dysfunction of the striatal presynaptic dopamine transporter in social anxiety disorder. Clear guidelines for the management of social anxiety disorder, including both pharmacotherapy and psychotherapy, are yet to be established. Selective serotonin reuptake inhibitors (SSRIs) show the most promise for the future, while cognitive-behavioral therapy may also be helpful. In the meantime, physicians should treat social anxiety disorder promptly and aggressively. Copyright r 2000 by W.B. Saunders Company

T

of socioeconomic status, and approximately 22% were receiving welfare payments, suggesting that they were unable to work.3 This level of functional disability imposes an economic burden on society not only because of the sufferers’ financial dependency and lack of gainful productivity but also because of the increased risk of suicide attempts, particularly if there is a comorbid disorder.3 This disabling condition therefore necessitates early recognition and treatment. This review examines the current status of investigations into the epidemiology, diagnosis, neurobiology, and treatment of this prevalent and debilitating condition.

HE MAJORITY of individuals will admit to recognizing an element of anticipatory anxiety on specific occasions when they are under public scrutiny, such as prior to giving a speech or playing a musical instrument; this has been called ‘‘normal’’ social discomfort.1 However, social anxiety disorder is the excessive fear harbored by some people that their performance or social interaction will be viewed as inadequate, to the point of causing them embarrassment or humiliation. These people experience extreme distress in or will completely avoid the feared social setting. Social anxiety disorder is a common mental disorder, yet it is one of the least investigated and most misunderstood.2 The avoidance of everyday social situations by patients with social anxiety disorder can cause considerable disruption to patients’ work, relationships, and normal functioning.3-5 Many patients with social anxiety disorder are single, divorced, or separated.6 In addition, they may have a lower educational attainment and a lower socioeconomic status. In an epidemiologic study, over 50% of patients with social anxiety disorder did not complete secondary school, more than 70% were in the lowest two quartiles in terms

From the Department of Biological Psychiatry, Academic Hospital Groningen, Groningen, The Netherlands. A short review from this article appeared in BMJ 1997;315: 796-800. Address reprint requests to Johan A. den Boer, M.D., Ph.D., Department of Biological Psychiatry, Academic Hospital Groningen, Hanzeplein 1, PO Box 30.001, 9700 RB Groningen, The Netherlands. Copyright r 2000 by W.B. Saunders Company 0010-440X/00/4106-0007$10.00/0 doi:10.1053/comp.2000.16564

Comprehensive Psychiatry, Vol. 41, No. 6 (November/December), 2000: pp 405-415

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EPIDEMIOLOGY

Social anxiety disorder is common in the general population. A review of epidemiologic studies found that the lifetime prevalence of social anxiety disorder in adults tended to be about 2% to 5%,5 with a female to male ratio of 2.5 to 1.2 However, a wide range of lifetime prevalence rates have been reported, from 0.4% in a rural Taiwanese village7 to 16% in the Basel epidemiologic study.8 Differences in patient selection, age range, culture, or survey methodology may explain some of the wide variation observed. Both of the surveys that found the highest rates in adults (Basel and the American National Comorbidity Survey [NCS]) 9 used the criteria of the Composite International Diagnostic Interview and the DSM-III-R. When ICD-10 criteria were applied in the Basel study, 9.6% of subjects were diagnosed as having social anxiety disorder, compared with 16% using DSM-III-R criteria.8 This difference was mainly accounted for by individuals who did not meet the ICD-10 criterion stating that subjects have sought help or used medication to relieve symptoms and that the symptoms interfere significantly with social life, but who did meet the corresponding DSM-III-R criterion in reporting autonomic symptoms of anxiety in the feared situations which interfere significantly with social life. It is not known why the prevalence rates were lower in the surveys conducted in Southeast Asia (0.4% to 0.6%), but this may reflect a cultural difference.7-10 In the few small studies that have investigated the prevalence of social anxiety disorder in children and adolescents, the prevalence rate of social anxiety disorder was about 1%.5 More recently, the lifetime prevalence of simple phobia and social anxiety disorder in young adults (mean age, 18 years) was shown to be 23%, with about half meeting the criteria for social anxiety disorder only.11 This survey found no gender difference in prevalence. As social anxiety disorder is more common in young people, the inclusion of younger subjects, that is, ages 15 to 54 years in the NCS9 and 18 to 65 years in the Basel study,8 may have increased the prevalence rate found in these studies. The prevalence of social anxiety disorder may be underestimated by general physicians because, by its very nature, patients feel inhibited about social interaction and are thus unwilling to consult their family doctor. This increases the risk of developing

comorbid conditions. Approximately 80% of patients with social anxiety disorder from community samples meet diagnostic criteria for a comorbid condition,12 frequently anxiety or depression, and the comorbid condition is preceded by the social anxiety disorder in about 77% of cases.3 It may only be the subsequent comorbid condition that prompts the patient to present for treatment, many years after the social anxiety disorder developed.2 DEFINING AND DIAGNOSING SOCIAL ANXIETY DISORDER

The updated DSM (DSM-IV)13 and ICD-10 criteria can be used to define social anxiety disorder. Both criteria state that social anxiety disorder is a distinct disorder involving a marked fear or anxiety of behaving in an embarrassing or humiliating manner while under the gaze of other people, which then leads to avoidance of the situations that stimulate this fear.4,5 Two distinct subtypes of social anxiety disorder are recognized, nongeneralized and generalized. Nongeneralized social anxiety disorder involves one or two social or performance situations such as public speaking, whereas individuals with generalized social anxiety disorder fear a multitude of social and performance situations.14 Typical precipitating situations of generalized social anxiety disorder include conversing or speaking in small social groups, speaking to strangers or meeting new people, particularly those in authority, and eating in public places.2 The symptoms experienced by patients with social anxiety disorder when they anticipate or are placed in such a stressful social situation are appropriate to a fear response, i.e., palpitations, trembling, and sweating.15 Social anxiety disorder and agoraphobia have a feature in common, namely avoidance of specific social situations, but careful questioning, such as ‘‘Could you go to a busy shopping complex without talking to anyone?’’, will help to clarify the diagnosis. The patient with social anxiety disorder will reply affirmatively to this question, while the patient with agoraphobia will reply negatively and be fearful about becoming stranded or forced to make a speedy and embarrassing exit.2-4 Other conditions from which social anxiety disorder should be distinguished are panic disorder, separation anxiety (in children), and atypical depression, although fear or avoidance of social or performance situations in a public setting should

SOCIAL ANXIETY DISORDER: AN UPDATE

identify the patient with social anxiety disorder. Diagnoses of social anxiety disorder and avoidant personality disorder (APD) have arisen from different historical sources; however, the difference between these conditions has become indistinct with the introduction of DSM-III-R criteria. Schneier et al.16 found that most (89%) of the patients with generalized social anxiety disorder were also diagnosed with APD. This co-occurrence of social anxiety disorder and APD may indicate a more severe form of social anxiety disorder.17 Most commonly, the onset of social anxiety disorder is in childhood (median age, 10 to 13 years), with a high-risk period at puberty.4 The onset may abruptly follow a stressful or humiliating experience or may be insidious.4-11 The course of the condition is often lifelong and unremitting unless treated, as it is unlikely to remit spontaneously. There may be a family history of social anxiety disorder observed, as evidence from family studies shows that a tendency to social anxiety disorder can be inherited, with a threefold increase in the rate of social anxiety disorder in the relatives of patients.12 Furthermore, studies in twins indicated that shared genetic factors explain a substantial proportion of the comorbidity between social anxiety disorder and depression.12

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Comorbidity In clinical and community populations, social anxiety disorder is strongly associated with other anxiety disorders, substance abuse, and affective disorders. On average, 80% of patients with social anxiety disorder identified in community samples met diagnostic criteria for another lifetime condition, demonstrating that comorbidity tends to be the rule rather than the exception.12 Anxiety disorders were most often associated with social anxiety disorder (about 50% of subjects), followed by major depressive disorder (20%) and alcohol abuse (15%).12 These figures agree with data from an analysis of four US Epidemiologic Catchment Area sites involving 361 patients with social anxiety disorder diagnosed by DSM-III-R criteria (Fig 1).3 There is a need for the recognition and treatment of social anxiety disorder, preferably before a comorbid condition develops. Social anxiety disorder precedes the comorbid disorder in 77% of cases,3 suggesting that the presence of social anxiety disorder may predispose the patient to a second psychiatric disorder. Once a comorbid condition is present, the patient is more likely to seek psychiatric help but the social anxiety disorder itself may be more difficult to recognize. In the Epidemiological Catchment Area study, only 5.4% of patients with

Fig 1. Lifetime comorbidity prevalence in social anxiety disorder.3 MDD, major depressive disorder; OCD, obsessive-compulsive disorder.

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uncomplicated social anxiety disorder had sought psychiatric outpatient help, compared with 37.8% of those with a comorbid condition. However, as social anxiety disorder is generally underdiagnosed,18 only the comorbid condition may be identified and treated. NEUROBIOLOGIC FEATURES

Various models have been used to study the neurobiology of social anxiety disorder, including assessments of central neurotransmitter function, response to chemical challenge, and neuroendocrine function and neuroimaging.19-21 However, all of these studies have involved a limited number of patients, and there is still no clearly defined biologic dysfunction in patients with social anxiety disorder. Serotonergic Function The effectiveness of serotonin-selective reuptake inhibitors (SSRIs) in the treatment of patients with social anxiety disorder (discussed later) suggests that serotonergic function has a role in the etiology of social anxiety disorder. The benzodiazepine clonazepam also has demonstrable efficacy in social anxiety disorder,22 an effect which may be mediated by its effect on 5-hydroxytryptamine (5-HT) utilization in the brain.23 Studies investigating the specific 5-HT1A agonist, buspirone,24 and ondansetron, a 5-HT3 antagonist,25 have not yet demonstrated efficacy in patients with social anxiety disorder. The role of serotonergic function in the etiology of social anxiety disorder has also been studied using pharmacologic tools. Fenfluramine, a serotonin-releasing agent, produced a significantly greater increase in cortisol in patients with social anxiety disorder compared with control subjects, but had no effect on prolactin in patients or controls.26 The findings from this small study were interpreted as evidence of the supersensitivity of postsynaptic 5-HT2 receptors associated with the anxiogenic response in patients with social anxiety disorder, but normal 5-HT1 receptors responsible for the prolactin response. However, the results of this small study require replication and confirmation. Noradrenergic and Dopaminergic Function The fear response of social anxiety disorder provokes symptoms that may be adrenergically mediated (e.g., sweating, palpitations, and tremor).

Therefore, Tancer et al.26 also assessed the noradrenergic and dopaminergic systems for dysfunction in patients with social anxiety disorder. A blunted growth hormone response to clonidine, an ␣2antagonist, but unchanged prolactin or eye-blink responses to levodopa were observed in patients with social anxiety disorder compared with normal subjects. This indicates that a disturbance of noradrenergic, but not dopaminergic, function is present in patients with social anxiety disorder. However, there is limited evidence to suggest involvement of the dopaminergic system in the etiology of social anxiety disorder. Anxiety disorders such as social anxiety disorder occur at a higher rate than normal in patients with Parkinson’s disease, which may be due to the neurobiologic processes accompanying Parkinson’s disease,27 although the development of anxiety disorders could also be due to psychological factors. In addition, a small neuroimaging study showed evidence that the density of striatal dopamine reuptake sites was considerably lower in patients with social anxiety disorder compared with healthy controls.28 Neuroendocrine Function To date, neuroendocrine studies have shown no definite dysfunction in the hypothalamic-pituitaryadrenal and hypothalamic-pituitary-thyroid axes in individuals with social anxiety disorder.21,29 Response to Chemical Provocation The administration of specific substances to provoke experimental panic or anxiety symptoms is an accepted technique in anxiety research and has been reviewed by Miner and Davidson.21 However, the role of these agents requires further investigation. Adrenaline caused an increase in catecholamine levels in patients with social anxiety disorder but did not increase anxiety; however, as adrenaline does not penetrate the blood-brain barrier, these results are open to interpretation. Although lactate induced panic attacks in patients with panic disorder, it had no effect in individuals with social anxiety disorder. Caffeine induced panic attacks in patients with panic disorder and in those with social anxiety disorder. Inhalation of 5% CO2 produced panic attacks in 12 of 31 patients (39%) with panic disorder and agoraphobia, but not in patients with social anxiety disorder. However, a higher concentration of CO2 (35%) precipitated panic attacks in a similar proportion of patients

SOCIAL ANXIETY DISORDER: AN UPDATE

with panic disorder or social anxiety disorder.30 Furthermore, the pentapeptide pentagastrin, an analog of cholecystokinin-4, has been shown to induce panic attacks in patients with social anxiety disorder,24,25 as well as patients with obsessive-compulsive disorder31 and panic disorder.32 Thus, patients with panic disorder and social anxiety disorder have a common sensitivity to caffeine, carbon dioxide, and pentagastrin suggesting a biological similarity. Neuroimaging Magnetic resonance spectroscopy revealed that patients with social anxiety disorder (n ⫽ 20) demonstrated significantly lower choline (Cho) and creatinine (Cr) signal to noise ratios in subcortical, thalamic, and caudate areas compared with ageand gender-matched controls (n ⫽ 20).33 N-Acetylaspartate (NAA) and the ratio of NAA to other metabolites were significantly lower in cortical and subcortical regions in patients with social anxiety disorder. Furthermore, the most severe cases of social anxiety disorder showed the lowest levels of metabolic activity. In addition, another study found that patients with social anxiety disorder (n ⫽ 19) had significantly lower NAA/Cho and higher Cho/ Cr, myo-inositol (mI)/Cr, and mI/NAA amplitudes in cortical gray matter than control subjects (n ⫽ 10).34 Neuroimaging has also recently been used to implicate a possible dysfunction of the dopaminergic system in patients with social anxiety disorder. Using a 123I-labeled cocaine analog, 2␤-carboxymethoxy-3␤-(4-iodophenyl)tropane (␤-CIT), with single photon emission computed tomography, Tiihonen et al.28 showed that striatal dopamine reuptake site densities were markedly lower in patients with social anxiety disorder (n ⫽ 11) versus control subjects (n ⫽ 28). This suggests that dopamine reuptake inhibitors or monoamine oxidase type B (MAO-B) inhibitors could be of therapeutic benefit to patients with social anxiety disorder. MANAGEMENT OPTIONS

As the need for the treatment of social anxiety disorder has been recognized only recently, optimum treatment strategies have not yet been defined. The SSRIs have been recommended as the pharmacologic treatment of choice,35 but the role of combined or sequential psychotherapeutic and pharmacologic treatment is yet to be clarified.36 Drug treatment may relieve the symptoms of social

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anxiety disorder, but habitual patterns of avoidant behavior may take longer to respond; therefore, a combined strategy may be more effective than either alone.37 Pharmacologic Approaches Pharmacologic treatment of social anxiety disorder has become established only in the past decade. The most recently investigated drug class is the SSRIs, for which there is growing support.38,39 Other explored drug classes include tricyclic antidepressants, monoamine oxidase inhibitors (MAOIs), benzodiazepines, and ␤-blockers.40 SSRIs Two large double-blind, placebo-controlled trials have recently reported a significant improvement of patients with social anxiety disorder who received paroxetine compared with those given placebo,41,42 and a double-blind placebo-controlled trial of fluvoxamine has also demonstrated the efficacy of this SSRI against the symptoms of social anxiety disorder.43 Data for other SSRIs are limited to mainly open and small-scale trials.44-52 The results of open and double-blind studies using SSRIs to treat patients with social anxiety disorder are shown in Table 1. SSRIs also provide effective and well-tolerated treatment for depression and panic disorder,53 both of which may be comorbid with social anxiety disorder. Tricyclic Agents Studies published more than 20 years ago reported positive results for clomipramine in the treatment of phobic disorders.54,55 However, these were open studies and the patient population was not well defined. A further small study found that clomipramine significantly improved some aspects of social anxiety disorder and agoraphobia as compared with diazepam, but the patient population was again ill-defined.56 A recent small open trial of imipramine did not support its efficacy as a treatment for social anxiety disorder.57 MAOIs Double-blind, placebo-controlled trials have shown that patients with social anxiety disorder respond better to phenelzine, an irreversible MAOI, than to alprazolam,58 atenolol,59 or placebo.58,59 Earlier studies also suggested that phenelzine was more effective than placebo, but these studies suffered from methodologic problems, making in-

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Table 1. Summary of Studies of SSRIs in Patients With Social Anxiety Disorder Drug

Paroxetine

Sertraline

Type of Study

No. of Patients

Outcome

12-week, doubleblind, placebocontrolled study

187

12-week, doubleblind, placebocontrolled study

290

Relative to baseline, paroxetine produced significantly greater improvements than placebo in endpoint Liebowitz Social Anxiety Scale (LSAS) total scores (P ⬍ .001), subscale scores (P ⬍ .001), Social and Anxiety Distress Scale scores (SADS; P ⬍ .001), and Sheehan Disability Inventory scores (SDI; P ⬍ .05). The proportion of responders with paroxetine (55%) was significantly higher than with placebo (24%; P ⬍ .001). Patients receiving paroxetine experienced a significantly greater reduction in the LSAS total score compared with placebo (P ⱕ .001). The proportion of responders in the paroxetine group was significantly greater versus the placebo group (65.7% v 32.4%; P ⬍ .001). Paroxetine also produced significant improvements in social avoidance as measured by the SADS (P ⬍ .032) and in patients’ family (P ⬍ .001), social (P ⬍ .05), and work (P ⬍ .001) lives as measured by the SDI compared with placebo. At week 12, 70.5% of paroxetine-treated patients and 8.3% of placebo-treated patients were responders (P ⫽ .0001). Paroxetine produced significantly greater improvements than placebo in endpoint LSAS total scores (P ⫽ .0001). Paroxetine was also significantly superior to placebo in terms of improvements in the Brief Social Phobia Scale (P ⫽ .0001), Fear of Negative Evaluation Scale (P ⫽ .0003), and SDI work (P ⫽ .0065), social (P ⫽ .0048), and family life (P ⫽ .0092) scores. Twenty-three of 30 patients (77%) were ‘‘much’’ or ‘‘very much’’ improved on the Clinical Global Impression scale. Baseline/week 11 reductions on the Duke Social Phobia Scale and Liebowitz Social Phobia Scale were 36 to 20 (P ⬍ .0005) and 75 to 37 (P ⬍ .0005), respectively. Paroxetine produced an 83% response assessed by a moderate to marked symptomatic improvement on the Liebowitz Social Phobia Scale. After 4 and 6 weeks, sertraline produced significant improvements compared with baseline (P ⬍ .05) on the Davidson Brief Social Phobia Rating Scale and Clinical Global Impression Severity and Change scales. 58% responded to treatment Sixteen of 20 responded to treatment. All measures of social anxiety and functioning and depression significantly improved compared with baseline.

Randomized, doubleblind, placebocontrolled, 12-week trial

99

11-week, open study

36

12-week, open study

18

6-week, open study

24

12-week, open study

22

Reference

Stein et al., 199841

Baldwin et al., 199942

Allgulander 199944

Stein et al., 199645

Mancini and van Ameringen, 199646

Martins et al., 1994/9547

van Ameringen et al., 199448

SOCIAL ANXIETY DISORDER: AN UPDATE

411

Table 1. Summary of Studies of SSRIs in Patients With Social Anxiety Disorder (Cont’d) Drug

No. of Patients

Outcome

20-week, randomized, double-blind, crossover study

12

12-week, open study

11

Fluoxetine

12-week, open study

13

Fluvoxamine

12-week, doubleblind, placebo-controlled study with 12-week follow-up

30

Double-blind, randomized, placebocontrolled, 12-week trial

92

Scores on the Liebowitz Social Anxiety Scale significantly improved with sertraline (P ⫽ .001) but not with placebo. Six of 12 moderately or markedly improved while taking sertraline, compared with 1 of 12 on placebo. Five of 7 completers substantially responded to treatment. Ten patients had a moderate to marked improvement independent of changes on the Beck Depression Inventory. Fluvoxamine was significantly better than placebo on Symptom Checklist 90 (P ⬍ .05) and superior to placebo on the social anxiety item of the Social Phobia Scale. Further improvements were observed during the follow-up period. At week 12, 53.3% of the fluvoxamine group and 23.5% of the placebo group were responders (P ⫽ .01). Compared with placebo, fluvoxamine produced significantly greater improvements on the BSPS (P ⬍ .05), Social Phobia Inventory (P ⬍ .05), LSAS (P ⬍ .05), and work and family life items of the SDI (P ⬍ .05).

Sertraline (cont’d)

Type of Study

terpretation of the results difficult.60 However, the use of phenelzine is limited due to the potentiation of the tyramine pressor effect, which can lead to hypertensive crises. Conflicting results have been obtained with reversible MAOIs such as brofaromine and moclobemide, which do not exhibit the tyramine pressor effect. Brofaromine appeared to significantly improve the symptoms of social anxiety disorder compared with placebo,61,62 but is now no longer in development. Moclobemide also appeared to be statistically significantly more effective than placebo after 8 weeks’ treatment in a small double-blind study63 and a large (N ⫽ 578) 12week trial in patients with social anxiety disorder.64 However, a further large (N ⫽ 583) 12-week double-blind, placebo-controlled trial in patients with social anxiety disorder failed to find a significant difference between moclobemide and placebo.65 Benzodiazepines Clonazepam and alprazolam have been evaluated in a few open studies and were found to be effective in social anxiety disorder.66 Bronazepam was significantly superior to placebo in a 12-week

Reference

Katzelnick et al., 199549

Munjack et al., 1994/9550 van Ameringen et al., 199351 van Vliet et al., 199452

Stein et al., 199943

double-blind study.67 In small controlled trials, clonazepam was significantly superior to placebo,68 while alprazolam was also superior to placebo but inferior to phenelzine.58 However, the putative efficacy of phenelzine in social anxiety disorder may be due to its strong sedative effect rather than true anxiolysis. Furthermore, since alcohol abuse is a common comorbid condition in social anxiety disorder, benzodiazepines should be avoided due to the risk of excessive sedation. Long-term use may also lead to dependency. ␤-Blockers ␤-Blockers may alleviate anxiety as a secondary consequence of the reduction in autonomic symptoms (tremors and palpitations). These drugs have been effective in the short-term for performance anxiety.69-71 Despite promising early studies with atenolol,72 subsequent investigations have not established efficacy for ␤-blockers in generalized social anxiety disorder.69 Other Drugs A recent randomized placebo-controlled trial involving 69 patients demonstrated the efficacy of the anticonvulsant gabapentin in the treatment of

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social anxiety disorder.73 After 14 weeks of treatment, patients receiving gabapentin experienced a significant (P ⬍ .05) reduction in the symptoms of social anxiety disorder compared with those receiving placebo. In an open trial of nefazodone, 69% of patients (n ⫽ 23) showed moderate or marked improvement after 12 weeks of treatment.74 Venlafaxine also produced improvements in social anxiety disorder symptoms in a small open study involving 12 patients.75 Larger placebo-controlled trials are required to fully determine the efficacy of these agents. Nonpharmacologic Approaches The biologic and psychologic factors underlying social anxiety disorder may be interdependent. Recognizing the psychodynamic themes (feelings of shame and guilt and separation anxiety) underlying patients’ social anxiety can be an aid to tailoring treatment.76 An integrated treatment strategy might include drug therapy, behavioral techniques, and dynamic psychotherapy.77 Some management guidelines have been suggested and include the following: identifying the underlying cause (to eradicate the ‘‘cause’’ of the symptoms), addressing the problem of comorbidity, providing symptomatic relief before beginning psychologic therapy, and asking the patient to accept the condition as a psychiatric illness (to encourage compliance with drug treatment).77 Cognitive-Behavioral Therapy Cognitive-behavioral treatment aims to help people overcome anxiety reactions in social and performance situations and to alter the beliefs and responses that maintain this behavior. One type of treatment, cognitive-behavioral group therapy, is given in 12 weekly sessions, each lasting about 2.5 hours. It has six elements: cognitive-behavioral explanation of social anxiety disorder; structured exercises to recognize maladaptive thinking; exposure to simulations of situations that provoke anxiety; cognitive restructuring sessions to teach patients to control maladaptive thoughts; homework assignments in preparation for real social situations; and a self-administered cognitive restructuring routine.78 A comprehensive critique of cognitive-behavioral therapy found that cognitive techniques seemed to enhance behavioral procedures; cognitivebehavioral group therapy was associated with long-

JOHAN A. DEN BOER

term benefit in moderately impaired patients and compared well with pharmacologic treatment (phenelzine and alprazolam).36 Group therapy has been shown to be an effective treatment for social anxiety disorder in comparison to control groups or pill placebo.78,79 Other Techniques Social skills training and relaxation training also have been used in the treatment of social anxiety disorder. However, the reported outcomes do not provide convincing evidence of a specific anxiolytic effect in social situations.79 Impact of Comorbidity on Treatment Strategies Comorbidity may reflect a more severe psychopathology, with more disability and impaired functioning than in the absence of comorbidity. This may create the expectation of a more difficult treatment course and a less favorable outcome, resistance to treatment, the need to treat each disorder effectively, and extended or long-term maintenance treatment to prevent relapse.80 Empirically, there are four general principles for dealing with comorbid disorders: (1) tailor treatment to individual patients; (2) use monotherapy in preference to polypharmacy, provided that the chosen drug is effective in both disorders and the comorbid disorder is secondary to the social anxiety disorder; (3) consider compatible drugs for some patients; and (4) administer a combination of psychotherapy and pharmacotherapy.80 Social anxiety disorder comorbid with alcoholism is a special case because of the risk of excessive sedation with concomitant medication (benzodiazepines, for example), and patients should be carefully questioned about their use of alcohol, as well as the amount and pattern of intake.81 Comorbidity affects the choice of treatment, as well as its efficacy. A treatment scheme for comorbid conditions is outlined in Table 2.38 CONCLUSIONS

Social anxiety disorder was recognized as a condition separate from other phobias and panic disorders as recently as the 1960s.82 Three decades later, there is still much to learn about the causes and treatment of the disorder. While social anxiety disorder is common in the general population, it is probably underreported in

SOCIAL ANXIETY DISORDER: AN UPDATE

413

Table 2. Treatment Scheme for Comorbid Conditions Disorder

Social anxiety disorder and major depression Social anxiety disorder and panic disorder

Suggested Treatment

SSRI or MAOI SSRI, MAOI, or benzodiazepine One Drug/ Both Disorders

Social anxiety disorder and obsessive-compulsive disorder (OCD) Social anxiety disorder and alcoholism Social anxiety disorder with no comorbidity

SSRI or MAOI

— —

One Drug per Disorder

Clonazepam for social anxiety disorder, clomipramine for OCD SSRI for social anxiety disorder, disulfiram for alcohol abuse —

Combined Approach

SSRI, clomipramine, or MAOI and behavior therapy SSRI, disulfiram, and Alcoholics Anonymous SSRI, MAOI, or benzodiazepine (with or without cognitivebehavioral therapy)

Based on Rosenbaum and Pollock (1994),80 and Jefferson (1995).38

general practice because, by its very nature, patients are reluctant to seek treatment. The delay in seeking help for social anxiety disorder may lead to the development of other psychiatric disorders such as major depression, and a consequent greater disability and risk of suicide. In addition, the inability of the patient to function as a normal, productive member of the community places an economic burden on the sufferer and on society. Early diagnosis and treatment of social anxiety disorder may help to alleviate the burdens imposed by the condition. The causes of social anxiety disorder are still to

be fully elucidated, but evidence suggests that a combination of biologic and psychologic factors contribute to its development. One current focus of research is the role of subtypes of serotonin receptor in the etiology of social anxiety disorder. Optimum treatment strategies for social anxiety disorder have not been clearly defined. However, no one would disagree that treatment should be aggressive in view of the potential disability caused by the disorder. SSRIs show the most promise for the treatment of social anxiety disorder. Perhaps now is the time to look social anxiety disorder straight in the eye and treat it accordingly.

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