Social Anxiety Disorder: An Update on Evidence-Based Treatment Options

May 13, 2009
Sy Atezaz Saeed, MD, MS

Volume 26, Issue 5

Social anxiety disorder (SAD), also referred to as social phobia, is a chronic and potentially disabling anxiety disorder characterized by the intense and persistent fear of being scrutinized or negatively evaluated by others. At its core, people with this disorder fear and/or avoid the scrutiny of others. Symptoms may occur only in circumscribed situations, such as a fear of speaking in formal or informal situations, or eating or drinking in front of others.

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Educational Objectives

After reading this article, you will be familiar with:

• Strategies used in cognitive behavioral therapy (CBT) for the treatment of severe mental illness
• Treatment approaches
• The benefits and challenges of using CBT

Who will benefit from reading this article?
Psychiatrists, psychologists, primary care physicians, nurse practitioners, and other health care professionals. To determine whether this article meets the continuing education requirements of your specialty, please contact your state licensing and certification boards.

Social anxiety disorder (SAD), also referred to as social phobia, is a chronic and potentially disabling anxiety disorder characterized by the intense and persistent fear of being scrutinized or negatively evaluated by others. At its core, people with this disorder fear and/or avoid the scrutiny of others. Symptoms may occur only in circumscribed situations, such as a fear of speaking in formal or informal situations, or eating or drinking in front of others. More commonly, in the most severe form of SAD, symptoms arise in a variety of social situations.1

A large-scale US epidemiological study, the National Comorbidity Survey, reported a lifetime prevalence for SAD of 13.3%, with a 1-year rate of 7.9% in community samples. These rates make SAD the third most common psychiatric disorder, following substance abuse and depression.2 The more recent National Comorbidity Survey Replication estimated 12-month and lifetime prevalences to be 7.1% and 12.1%, respectively, with higher prevalence in females.3,4

In both clinical and community samples, SAD is commonly associated with other psychiatric disorders. Merikangas and Angst5 reported that an average of 80% of persons with SAD who were identified in community samples also met the diagnostic criteria for another lifetime psychiatric disorder. The lifetime risk of depression is reported to be about 2 to 4 times higher in persons who have SAD.6,7 An earlier study reported that up to 16% of patients with SAD may also have alcohol abuse problems.8

More recently, there has been an increasing realization that alcohol use disorders are commonly comorbid with SAD.9-12 The National Epidemiologic Survey on Alcohol and Related Conditions showed that 48% of those with a lifetime diagnosis of SAD also met diagnostic criteria for an alcohol use disorder.11

Furthermore, the 12-month prevalence of alcohol use disorder among those with SAD was 13.1% compared with 8.5% in the general population.11,12 Kessler and colleagues9 reported that women with SAD appeared to show higher rates of alcohol use disorder than men.

An average of 50% of people with SAD in the community samples also report another anxiety disorder, such as panic disorder, generalized anxiety disorder, or another phobic disorder.5 Which came first is always a question with comorbidity. Schneier and colleagues6 reported that SAD preceded approximately 75% of comorbid mental disorders and 85% of comorbid substance abuse problems, which suggests that most comorbidity was a consequence of SAD.

Clearly, comorbidity has implications for treatment selection. The presence of comorbidity in SAD has also been reported to be associated with an increased lifetime prevalence of suicide ideation and attempts.6

Evidence-based treatment options
There is a robust body of evidence, based on large randomized controlled trials, to support the efficacy of both medications and cognitive-behavioral therapy (CBT) for the treatment of SAD.13,14

Both pharmacotherapy and CBT are empirically supported choices for first-line management of SAD. Studies that have compared CBT and pharmacotherapy for SAD suggest that while effects of CBT may be more enduring than those of medication, it takes longer to produce those results with CBT.15,16 Anecdotally, combined treatment has been recommended often, but there is no established evidence to suggest that combined treatment (CBT plus medications) is more effective than either treatment alone.

Two landmark studies examined the question of whether combining CBT with pharmacotherapy enhances the overall outcome.17,18 In the first study, 387 patients with generalized SAD were randomly selected to receive sertraline, sertraline plus exposure therapy, exposure therapy plus placebo, or placebo alone for 24 weeks. Response rates for both sertraline groups were significantly greater than for placebo; there was a trend toward enhanced efficacy in the sertraline plus placebo group.17

In the second study, 295 patients with generalized SAD were randomized to receive fluoxetine, comprehensive group CBT, fluoxetine plus comprehensive group CBT plus placebo, or placebo for 14 weeks. All active treatments outperformed placebo and were comparable to each other. No advantage was seen with combination therapy.18

Pharmacological interventions
Before choosing a pharmacological intervention, it is important first to determine whether the patient has generalized or circumscribed SAD. Those with circumscribed SAD, which is limited to such settings as public speaking or artistic performance, usually respond well to medications on an as-needed basis. Patients with generalized SAD usually require standing-dose schedules of medications.

Selective serotonin reuptake inhibitors
SSRIs are currently considered appropriate first-line treatment for SAD. Their efficacy in this setting is supported by several randomized controlled trials and by systematic reviews and meta-analyses.19-31 The number of head-to-head comparisons of various SSRIs is limited. Currently available comparisons fail to show superiority of one SSRI over another, and the selection of an individual SSRI is typically based on matching specific patient parameters with the SSRI (eg, adverse-effect profile, previous history, comorbid general medical conditions, drug interactions).32,33

It may take as long as 8 to 12 weeks of treatment with an SSRI before a favorable response is manifested. Treatment for 12 months or longer is generally advised, once a favorable response is achieved, to prevent relapse. Some patients may require maintenance therapy to sustain benefits.33,34 Relapse rates are relatively high once medication is discontinued-up to 60% at 3- to 6-month follow-up after a 5- to 12-month course and even higher after shorter courses of treatment.33

SSRIs are generally well tolerated. Common adverse effects include sleep problems, fatigue, sexual dysfunction (eg, decreased sex drive, delayed or absent orgasm, erectile dysfunction), restlessness, agitation, and GI symptoms. It is advisable to start with a dosage that is lower than the conventional starting dose for depression and gradually to titrate upward.

In 2004, the FDA released an advisory concerning SSRIs and risk of suicidal ideation. Although rare, it is possible for symptoms to worsen initially. Hence, it is important to monitor symptoms during this time.

When it is time to discontinue, it is advisable to taper an SSRI gradually because abrupt discontinuation can result in a relapse of anxiety symptoms. In some cases, abrupt withdrawal can trigger serotonin discontinuation syndrome, which presents with flu-like symptoms, anxiety, difficulty with coordination, tingly sensations, vivid dreams, and depressed mood.

Serotonin norepinephrine reuptake inhibitors
The serotonin norepinephrine reuptake inhibitors (SNRIs) include venlafaxine and duloxetine. Several controlled studies have reported efficacy of venlafaxine in the treatment of SAD.32,35-38 In a controlled study of 440 patients who were randomized to venlafaxine extended release (ER), paroxetine, or placebo for 12 weeks, a similar response rate was reported for venlafaxine and paroxetine; both were superior to placebo.32

In a second trial that compared venlafaxine with paroxetine, no significant differences in primary or secondary efficacy variables were observed between the 2 active treatments.35 The primary efficacy variable was the Liebowitz Social Anxiety Scale total score. Secondary efficacy variables included the patient-rated social phobia inventory and the proportion of responders in each group (a responder was defined as having a clinical global impression improvement score of 1 or 2). At week 12 the response rates were 69%, 66%, and 36% for the venlafaxine ER, paroxetine, and placebo groups, respectively. Both active treatments were generally well tolerated and were associated with a similar incidence of adverse events.

Monoamine oxidase inhibitors
Phenelzine has been considered the best studied and perhaps the most efficacious pharmacological treatment for SAD until quite recently.15,39-41 Evidence that supports the efficacy of monoamine oxidase inhibitors (MAOIs) is well summarized by Blanco and colleagues.42

MAOIs require dietary restrictions (a low tyramine diet), and they can be associated with substantial adverse events. A potentially fatal hypertensive reaction can occur if users of MAOIs do not comply with the diet. The MAOIs cannot be used in conjunction with some common over-the-counter medications; these include cold and cough formulas.

Reversible MAOIs, such as moclobemide, which do not require dietary restrictions and have fewer adverse effects than traditional MAOIs, showed promise in early trials but provided mixed results in more recent ones.13,43-45

Given the availability of safer medications with similar efficacy, the use of MAOIs should probably be limited to those patients who have not responded to other first-line treatments.

Beta-adrenergic blockers
b-Blockers are currently used on an as-needed basis for circumscribed social anxiety, mostly based on anecdotal evidence of utility for performance anxiety (eg, propranolol in low doses [10 to 40 mg] taken an hour before a performance that is the focus of anxiety).

Studies of b-blockers as SAD therapy have reported mixed results. Standing doses, ie, regular daily doses, of b-blockers for generalized SAD have performed poorly in clinical trials.39,46 These controlled trials have involved patients with generalized as well as circumscribed SAD. Results suggest that b-blockers are not effective in generalized SAD, and samples of patients with the nongeneralized subtype have been too small for meaningful analysis.42

b-Blockers have minimal adverse effects but should be avoided in patients with asthma, diabetes, and certain heart diseases. To minimize the risk of long-term psychological dependence, patients are encouraged to use the medication intermittently until their confidence in performance situations is restored. Thus, except for use in specific social performance situations, b-blockers are not recommended as a treatment for SAD.

Benzodiazepines
Benzodiazepines are the fastest-acting and perhaps the best-tolerated agents for the acute treatment of SAD. There is evidence that supports the use of benzodiazepines in SAD patients who are resistant to or unable to tolerate SSRIs.47 Controlled studies of alprazolam and clonazepam have reported acute treatment improvement rates ranging from 40% to 80%.15,48 While the improvement rates are impressive, benzodiazepines also have significant drawbacks. Patients often struggle to taper or discontinue benzodiazepines because of symptomatic worsening and acute relapse.15

Many clinicians use benzodiazepines in combination with an SSRI when starting treatment with the goal of discontinuing the benzodiazepine once the response to the SSRI is manifested. While this appears to be a reasonable practical approach, a small, 10-week randomized controlled trial of open-label paroxetine given in combination with clonazepam or placebo for SAD showed no significant differences between the 2 groups early or later in treatment.49

Benzodiazepines must also be cautiously used in patients who have a history of substance abuse. When benzodiazepines are used as needed for circumscribed SAD, sedation and psychological dependence can be a problem. In general, benzodiazepines are best reserved for patients at low risk for substance abuse in whom first-line treatments have failed. Benzodiazepines can also be useful for initial severe symptom relief in conjunction with an antidepressant, psychotherapy, or both.

Other agents
Two anticonvulsants, gabapentin and pregabalin, have demonstrated moderate effectiveness for generalized SAD. One randomized controlled trial of 600 mg/d of pregabalin in patients with SAD demonstrated efficacy.50 In another randomized controlled trial, gabapentin led to significant reductions in social anxiety after 14 weeks.51

Results of trials of the efficacy of buspirone as monotherapy for SAD have been mixed. This drug was found to be modestly effective in 2 open trials.52,53 In a subsequent double-blind, placebo-controlled study of patients with SAD, buspirone was found to be no different from placebo.54

However, buspirone may be useful in augmenting a partial response to an SSRI. The results of an 8-week study of 10 patients with SAD who were partially responsive to an SSRI suggest that the addition of buspirone to an SSRI as an augmentation strategy may be useful in enhancing treatment response.55

The tricyclic antidepressants have not been studied extensively in clinical trials of patients with SAD, but some case reports suggest that they may be effective. Findings from a large open-label study with clomipramine indicate that this agent may be effective for patients who have SAD. Another open trial of imipramine indicated a lack of efficacy.56,57

Agents such as bupropion, mirtazapine, nefazodone, olanzapine, and clonidine have not been investigated outside of case reports and clinical anecdotes.57

Psychosocial treatments
Nondirective or nonspecific psychotherapies are not as effective for treating SAD as the more directive behavioral therapy and CBT that are specifically targeted toward reducing social fears and avoidance.58 CBT can have several components, including psychoeducation, social skills training, symptom management skills, progressive muscle relaxation, exposure (imaginal and in vivo), and cognitive restructuring.59 CBT focuses on the present rather than the past, and it involves working collaboratively with patients and teaching them cognitive and behavioral skills.

While it is not at all clear yet which component of CBT is the most effective, evidence suggests that it is important to include both exposure and cognitive components.60 A recent qualitative review of 30 randomized controlled trials that evaluated the efficacy of social skills training, exposure therapy, and cognitive treatments for social phobia in adults concluded that CBT was the psychological intervention of choice for SAD.61 The Table provides a brief description of the empirically supported components of CBT for treatment of SAD.

CBT can be conducted in individual or group formats. It typically lasts 16 to 24 sessions. It is considered an appropriate first-line option for treating SAD. However, it requires specialized training, which limits its availability. The evidence that supports the efficacy of various components of CBT interventions for treatment of SAD is quite extensive, and results suggest that as many as 75% of patients can benefit from it.60-62 There are also emerging data for its efficacy in older children and adolescents.63,64

The treatment gains from CBT are generally more enduring over the long term than those from pharmacotherapy. Also, relapse rates after discontinuation of CBT are significantly lower.65,66

Regarding efficacy, randomized studies that compared the use of medications with CBT have not demonstrated superiority of one treatment over the other.67,68 However, the onset of symptom response tends to be faster with pharmacotherapy, while CBT appears to result in a more durable response.67

Treatment selection
The empirical evidence reviewed above suggests that a variety of effective psychosocial and pharmacological options are available to treat SAD. In this respect, the field has advanced significantly since the diagnosis of SAD (social phobia) was introduced. However, we still do not have a very clear understanding about:

• Which treatments work best for which individuals

• What factors lead to better treatment outcomes

• The best clinical approach for those who do not respond to treatment

Patients with SAD often need sensitive clinical management. Many have had the disorder for years and tend to have a history of varied, ineffective, and failed treatments. Patients should be educated about the disorder and reassured of a realistic hope for recovery. A therapeutic alliance with patients is an important part of any selected treatment and includes establishing a relationship that provides respectful attention to the patient’s concerns and worries, realistic reassurance and instillation of hope, and a willingness to be available in case of unexpected problems. It includes exploring and discussing the patient’s concerns about medications and explaining treatment options.

Treatment planning begins by discussing the benefits and risks of treatment options. Both clinician and patient must consider several factors that go beyond acute treatment success rates when selecting an approach. These decisions involve weighing the advantages and disadvantages of each treatment to see how well it matches a patient’s presentation, severity of symptoms, degree of functional impairment, psychiatric and substance-related comorbidities, personal and financial resources, and preferences.

There is no empirically derived algorithm for treating SAD, although global options include pharmacotherapy, CBT, or both. As mentioned earlier, studies suggest that pharmacological treatment may result in faster response than CBT, while the effects of CBT may last longer. Even when formal CBT is not used, to facilitate long-term gains, some form of gradual reentry into feared situations should be a part of every treatment plan for SAD.

Regarding the choice of pharmacological treatment, empirical evidence suggests that the SSRIs are an appropriate first consideration. Benzodiazepines, at minimum therapeutic dosage, may be a useful adjunct to an SSRI (or CBT), if prompt relief is indicated. If a benzodiazepine is used initially, the treatment plan should include its discontinuation when the effects of the SSRI are expected (ie, approximately 4 to 6 weeks). This approach will help minimize the risks of discontinuation difficulties. Although benzodiazepines are an appropriate intervention after SSRIs and other medications have failed, they should not be prescribed if comorbid substance abuse or a history of such abuse is suspected. Benzodiazepines should not be prescribed as monotherapy if the patient has comorbid depression.

When treatment consists of medication only, it is advisable to continue it for at least 12 months. Earlier discontinuation may result in symptom rebound and relapse. Many patients respond to acute treatment and maintain those gains over the long term; those who do not may need some form of continuation pharmacotherapy and/or CBT to restore or maintain gains. While not empirically tested, one possible strategy to help increase the response to maintenance therapy may be to ini­ti­ate treatment with medication and provide CBT subsequently.

As mentioned above, b-blockers are currently used on an as-needed basis for circumscribed SAD (eg, 10 to 40 mg of propranolol taken an hour before the situation that is the focus of anxiety). Exposure-based CBT, with or without initial as-needed b-blockers, is also an appropriate first-line treatment for those with circumscribed SAD.

Once treatment is selected, the patient should be monitored approximately weekly. When stabilized, patients should be encouraged to reenter previously avoided situations gradually-regardless of the treatment approach being used. Alternatives should be considered if the treatment response is inadequate after approximately 8 weeks.

Treatment of SAD with comorbidity
As noted, SAD is commonly associated with other psychiatric disorders.5-12 Clearly, comorbidity has implications for treatment selection. An important question is whether the first-line treatments for SAD with comorbidity are still safe and effective in this patient population.

We are beginning to see an emerging literature on treating SAD comorbid with alcohol use disorders and depression. Unfortunately, evidence on how to treat SAD in the context of a current comorbid psychiatric condition still remains scarce. One reason is that clinical trials usually exclude persons with comorbid disorders.

The scarcity of evidence on how to treat SAD with comorbidities was highlighted in a relatively recent review of pharmacotherapy for SAD and in another recent review of treatment recommendations for persons with a co-occurring affective or anxiety and substance use disorder.14,69 Both these reviews called for more research on comorbid samples.

SAD comorbid with depression tends to be associated with more impairment and more severe social anxiety symptoms than SAD alone.70 Higher rates of attempted suicide have been reported in this comorbid group.71 The treatment of comorbid depression or anxiety is challenging, and unfortunately there is a scarcity of data to inform treatment.

An open-label study of citalopram in a group of 21 patients with generalized SAD comorbid with major depression demonstrated improvement in both mood and anxiety symptoms after 12 weeks of treatment. Improvement in depressive symptoms occurred earlier than improvement in SAD symptoms.72 In another placebo-controlled study, moclobemide was both effective and well tolerated in the short- and long-term treatment of a sample of 390 patients with comorbid anxiety.73

A robust literature indicates that alcohol use disorders are commonly comorbid with SAD.9-12 While there is compelling evidence that supports the first-line use of SSRIs in the treatment of SAD, the efficacy of SSRIs has been determined in studies that typically excluded persons with alcohol use disorder.

To investigate whether an SSRI is safe and effective treatment for social anxiety in patients with alcohol use disorders, Randall and colleagues74 undertook a small 8-week pilot study. Findings from this study indicate that paroxetine is an effective treatment for SAD in persons with comorbid alcohol problems. However, the investigators recommend that further study is warranted. Book and colleagues75 subsequently conducted a 16-week, double-blind, placebo-controlled clinical trial of paroxetine that included 42 patients with SAD and comorbid alcohol use disorder. Paroxetine was superior to placebo in reducing social anxiety.75

The same group of investigators studied whether effective treatment of social anxiety will also reduce drinking in patients with a dual diagnosis who report using alcohol to cope with their anxiety symptoms.76 All of the 42 participants who sought treatment for social anxiety and not for the alcohol problem met DSM-IV diagnostic criteria for SAD and alcohol abuse or dependence. Paroxetine reduced self-reported reliance on alcohol for self-medication purposes but did not effect a change relative to placebo in the quantity and frequency of drinking or the proportion of drinking days that were identified as coping-related.76

rugs Mentioned in This Article
Alprazolam (Xanax)
Bupropion (Wellbutrin, Zyban)
Buspirone (BuSpar)
Citalopram (Celexa)
Clomipramine (Anafranil)
Clonazepam (Klonopin, Rivotril)
Clonidine (Catapres)
Duloxetine (Cymbalta)
Fluoxetine (Prozac, Sarafem, Symbyax)
Gabapentin (Neurontin, Gabarone)
Imipramine (Tofranil)
Mirtazapine (Remeron)
Moclobemide (Manerix)
Nefazodone (Serzone)
Olanzapine (Zyprexa)
Paroxetine (Paxil)
Phenelzine (Nardil)
Pregabalin (Lyrica)
Propranolol (Inderal)
Sertraline (Zoloft)
Venlafaxine (Effexor)

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Evidence-Based References
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Stein MB, Stein DJ. Social anxiety disorder. Lancet. 2008;371:1115-1125.