| Paul Bohn, MD, PsyD, and Harvey Sternbach, MD |
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Educational Objectives:
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Physical complaints associated with social phobia may only partially respond to behavioral and/or psychopharmacologic treatments, leaving patients with residual symptoms and impairment. Yet problems such as blushing, sweating, tachycardia, tremors, dry mouth, paruresis, and nausea may respond to specific pharmacologic augmentation strategies.
This article reviews the literature on available pharmacologic approaches that target these physical symptoms to maximize overall treatment response for the individual patient.
Social phobia has a 2% to 13% lifetime prevalence,1,2 can significantly interfere with occupational, academic, and relationship functioning,3 and can be complicated by depression, substance abuse, and other anxiety disorders.1 Social phobia syndrome can be divided into three interacting symptom domains: cognitive, eg, fears of evaluation, humiliation, or embarrassment; behavioral, eg, gaze aversion or avoidance; and physical, eg, blushing and sweating (Table 1; PP6:14).4
Controlled studies of monoamine oxidase (MAO) inhibitors, serotonin reuptake inhibitors, and benzodiazepines have shown statistically significant reduction in social phobic symptoms.5-10 The majority of these studies indicate, however, that social phobic symptoms are reduced, on average, only 35% to 50%. Although this does not separate out complete responders, it nevertheless indicates that a partial response is common.11 There are no controlled studies, and only a few case reports, on treatment augmentation strategies in social phobia.11,12
The DSM-IV states, "Individuals with social phobia almost always experience [physical] symptoms of anxiety (eg, palpitations, tremors, sweating, gastrointestinal discomfort, diarrhea, muscle tension, blushing...)."13 We have found that several of these associated physical symptoms are particularly treatment-resistant. Based on our own clinical experience and a modest, primarily anecdotal literature, we offer suggestions for pharmacologic augmentation strategies that target specific physical symptoms when other pharmacologic or behavioral treatments are insufficient.
Blushing, or flushing -- as well as a fear of blushing -- has been noted to be a prevalent and psychologically debilitating condition.14 Charles Darwin was the pioneer who related blushing to social anxiety: "The thinking of others thinking of us . . . excites a blush. Most persons, while blushing intensely, have their mental powers confused. They lose their presence of mind and utter singularly inappropriate remarks."15
Goldstein16 reported that clonidine was successfully used to treat a patient with social phobia and blushing, when treatment with alprazolam, phenelzine, and propranolol failed. Clonidine has also been used to treat the vasomotor instability associated with menopause,17 with variable results, in a dosage range of 0.05-0.15 mg/day. Goldstein's patient with social phobia16 took 0.1 mg bid with continued benefit at 4-month follow-up. Limiting side effects can include orthostatic hypotension, sedation, depression, fatigue, and gastrointestinal upset.
Table
1 Slide
#PP6:14
Social Phobia Symptom Domains4,13 | |
|---|---|
| Symptom Domain | Typical Symptoms |
| Cognitive | Fear of evaluation, humiliation, or embarrassment |
| Behavioral | Gaze aversion Avoidance Slumping of shoulders |
| Physical | Blushing Sweating Nausea Tachycardia Tremor Dry Mouth Paruresis |
| Bohn P, Sternbach H. Primary Psychology. Vol. 5 No. 6. 1998. | |
Excessive sweating, or hyperhidrosis, is a common symptom in social phobia.18 Topical aluminum chloride 20% in anhydrous ethyl alcohol 93% (Drysol) applied to dry skin has been reported to be an effective treatment for hyperhidrosis,19,20 including social phobia-related hyperhidrosis.21 Alternatively, clonidine can be used. This agent has been reported to be effective for reducing sweating secondary to menopause,17,22,23 and secondary to tricyclic antidepressants, whereas beta blockers have not been effective for treatment of tricyclic-induced sweating.24 Lofexidine, an alpha-2 adrenergic agonist, has also been effective for menopausal sweating.25 Guanfacine may also be effective, and causes less sedation than clonidine.
Nausea and the fear of vomiting are infrequent but previously reported symptoms of social phobia.18 Cisapride, a 5-HT3 antagonist/5-HT4 agonist, has been reported effective in the treatment of selective serotonin reuptake inhibitor (SSRI)-related nausea26 and social phobia-related nausea.27 Caution is necessary, however, when prescribing cisapride concomitantly with agents that inhibit P450 3A4, which metabolizes cisapride, (eg, nefazodone, erythromycin, and ketoconazole), as these drugs may raise cisapride to cardiotoxic levels.28,29 Ondansetron, an antiemetic with anxiolytic properties, has been shown to be effective for treatment of social phobia in a double-blind, placebo-controlled study.30 Although Ondansetron might be ideal in social phobia-related nausea, its cost is prohibitive.
Public speaking performance anxiety is the most commonly feared of the discrete social phobia situations,31 with tachycardia in discrete social phobics exceeding the tachycardia of generalized social phobics immediately before and during speeches.32,33 A proposed feedback mechanism in social phobic public speaking anxiety hypothesizes that anxiety produces tachycardia and tremulousness, and the awareness of this tachycardia and tremulousness results in further anxiety.34
Beta-adrenergic antagonists have been shown to lower heart rate, tremor, and anxiety and improve fine-motor performance in placebo-controlled, single-dose crossover trials in nonclinical populations of musicians (mostly string players).35-37 Of note, however, is a study comparing three different doses of nadolol (20 mg, 40 mg, and 80 mg) measuring performance anxiety and performance quality in vocalists.38 No clear anxiolytic effect was demonstrated; in fact, the higher doses impaired performance quality. It was hypothesized that the beta blockade-induced heart rate suppression in the vocalists impeded the accomplishment of the proper level of physical exertion required for optimal performance. This study demonstrates the need to carefully assess the specific needs of the performer before prescribing, especially in those whose performance demands athletic prowess.39
In another nonclinical population, propranolol (40 mg) was demonstrated to be superior to placebo for lowering public speaking performance anxiety in 16 "normally anxious volunteers"40; and in a clinical population, a small open study of 10 social phobics (both discrete and generalized), using a standing dose of atenolol 50-100 mg qid, reported significantly diminished symptoms.41 However, the only controlled trials using beta blockers in a pure discrete social phobia sample were inconclusive due to small sample sizes.42,43
Despite the lack of definitive controlled trials, the anecdotal and nonclinical population evidence supports the use of beta blockers for the tachycardia and tremulousness of social phobia, although the inhibitory effect of beta blockade on extreme physical exertion must be considered. The mechanism of action is most likely peripheral rather than central, since atenolol‹a hydrophilic beta blocker with poorer entry to the central nervous system‹appears as effective as the lipophilic beta blockers (eg, propranolol), although comparison trials have not been conducted.39
Dry mouth causes great difficulty in public speaking, and is prevalent in social phobia.44 Though cholinergic agents such as pilocarpine can stimulate the flow of saliva, they may also produce undesirable associated effects such as sweating or increased gastrointestinal motility. One report36 notes that propranolol increases the volume of saliva produced when administered for performance anxiety. Another report indicates that yohimbine reverses tricyclic-induced dry mouth.45 We have found Optimoist‹a nonprescription, artificial saliva spray‹to be helpful and convenient for our own patients.
Paruresis‹psychogenic urinary hesitation or retention‹typically occurs acutely in public restrooms where the social phobic may be observed or heard by others.46 The point prevalence of paruresis was found to be 14% in a survey of 1,419 college students (1,008 men, 411 women).46 Paruresis also differs from other emotionally influenced forms of urinary retention, which are more chronic, seen mostly in children, and often leading to structural damage and incontinence. These chronic forms have variously been called nonneurogenic neurogenic bladder, Hinman syndrome, and vesical-sphincter dyssynergia.47
The mechanism of paruresis is unknown.48-50 One hypothesis is that anxiety-related sympathetic nervous system arousal results in simultaneous alpha-receptormediated contraction of the internal urethral sphincter and beta-receptormediated relaxation of the detrusor muscle‹which act, in concert, to prevent urination.49 Other explanations include dyssynergia between the bladder's sympathetic, parasympathetic, and somatic innervation leading to voiding incoordination.49 Feelings of embarrassment, through as yet unexplained mechanisms, may delay the overcoming of the "holding" reflex, a reflex whose function is to maintain urinary continence when the bladder is full by contracting the external urethral sphincter.49
Paruresis may present as an inability to void in public restrooms, and may lead to a generalized avoidance response. One case report noted the development of bladder atony and urosepsis in a paruretic.51
Anecdotal reports have shown a benefit in the treatment of paruresis with in vivo exposure paired with relaxation training.52 The addition of either adjunctive furosemide to ensure adequate quantity and flow of urine53 or bethanechol to increase urinary urgency and contract the bladder54 may be useful, since in vivo exposure alone can otherwise be complicated by a long period of waiting between voidings.
Alternative approaches to treatment of paruresis with
medication have been disappointing. The benzodiazepine diazepam (20 mg bid) was
ineffective in one case report,55 as were beta blockers (propranolol
and atenolol),56-59 comporting with urologic literature that
indicates beta-adrenergic stimulation, rather than blockade, results in urethral
sphincter relaxation.48 MAO inhibitors were likewise ineffective in
three patients.59 Though alpha-adrenergic blockers (eg, prazosin,
terazosin) are used to decrease intraluminal urethral pressure and ease urinary
flow,55,60 there are no reports on their use in paruresis. Alpha
blockers, however, may be poorly tolerated due to hypotension and tachycardia,
while use of beta-agonists would be limited by their propensity to cause
subjective nervousness. Therefore, effective pharmacologic management of
paruresis remains elusive at this time.
Discussion
The central cognitive theme in social phobia concerns the fear of being the center of attention and of being negatively evaluated.61 Physical symptoms exacerbate this fear by increasing the social phobic's fear that the anxiety will be noticed, fueling an upward spiral of anxiety which may result in diminished performance. Marshall62 states, "Once the socially phobic person blushes (or shakes, stammers, or trembles), he considers the response a trigger for more harsh judgments‹and thus there is no way out." Because the social phobic is preoccupied by his symptoms and distracted from the task at hand, he may not perform at his peak.34 This suboptimal performance may elicit negative evaluation from observers, thus confirming the social phobic's worst fear.61
Attenuating or eliminating the development of physical symptoms
may help prevent this social phobic anxiety spiral. When first-line behavioral
and medication treatment options are insufficient, we suggest the augmentation
strategy of targeting residual physical symptoms with specific pharmacologic
agents (Table 2; PP6:15).
Conclusion
The definitive pharmacologic treatment of social phobia may require augmentation strategies. Although MAO inhibitors, SSRIs, and benzodiazepines have demonstrated efficacy in controlled studies, a partial response appears common. The reports summarized above‹mostly anecdotal‹suggest that additional pharmacologic interventions for specific physical symptoms such as blushing, sweating, nausea, dry mouth, tremor, and tachycardia may enhance treatment response, while an effective pharmacologic strategy for paruresis remains to be determined.
Table
2 Slide
#PP6:15
Pharmacologic Augmentation Strateges Targeting Physical Symptoms Associated With Social Phobia | ||
|---|---|---|
| Specific Physical Symptom | Common Phobic Situation | Pharmacologic Treatment Recommendations |
| Blushing | Generalized | Clonidine16 |
| Sweating | Speaking | Topical Aluminum Chloride
(Drysol)21 Clonidine, guanfacine* |
| Tremor | Writing, Eating | Beta Blocker41 |
| Tachycardia | Speaking | Beta Blocker41 |
| Parusesis | Voiding | Benzodiazepines* Bronchodilators* Alpha agonists* |
| Nausea | Eating | Cisapride27 Ondansetron30 |
| Dry Mouth | Speaking | Propranolol36 Optimoist* |
| *Theoretical rationale | ||
| Bohn P, Sternbach H. Primary Psychology. Vol. 5 No. 6. 1998. | ||
No financial, academic, or other support of this work was acknowledged by the authors.
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