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What are effective treatments for panic disorder?
Selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), benzodiazepines (BDZs), and cognitive behavioral therapy (CBT) are effective for panic disorder (PD) with or without agoraphobia (NNT5 for complete remission). SSRIs may be most effective, but BDZs work faster. Clomipramine is more effective than other TCAs. CBT improves response and decreases relapse rates when used with medication. Severe symptoms may warrant short-term use of a BDZ until other therapies take effect (Grade of recommendation: A, based on systematic reviews of randomized clinical trials (RCTs); high quality RCTs).
Evidence summary
SSRIs were more effective than imipramine or alprazolam in a meta-analysis,1 but equivalent to these drugs in an effect-size analysis.2 The absolute difference in efficacy is difficult to determine; few studies directly compare SSRIs with other drugs. In 2 randomized head-to-head trials,3,4 remission rates (eliminating symptoms) were 50%-65% for paroxetine, 37%-53% for clomipramine, and 32%-34% for placebo after 9-12 weeks of therapy; differences between the 2 active drugs were not significant. Clomipramine is serotoninergic and was more effective than other tricyclics in an RCT.5 Adding a BDZ to an SSRI for the first 3 weeks can rapidly stabilize symptoms6 (Table).
Two meta-analyses concluded that CBT is as effective as antidepressants or BDZs during acute treatment7 and during long-term follow-up (31-121 weeks).8 CBT and imipramine each reduce symptoms in 45%-48% of patients; combining them reduces symptoms in 60%.9 Imipramine is more effective initially; CBT is more durable9 but effects may be therapist-dependent. When used in conjunction with medication, graded exposure to panicinducing situations reduces agoraphobia7 but does not improve relapse rates.8 Behavioral therapy with exposure homework has good long-term results.10
An adequate trial of medication requires 6-8 weeks.11 Before treating, evaluate patients for comorbid mood, anxiety, personality, substance use, or medical disorders, which affect 40%-50% of patients with panic disorder, and may influence the choice of treatment.12 Current practice is to slowly taper and discontinue medication after 12-18 months of maintenance treatment12 if there are no significant residual symptoms, no increased psychosocial stressors, and no history of severe or recurrent relapse.
TABLE
Drugs used to treat panic disorder
| Drug Class | Side Effects | Other Considerations |
|---|---|---|
| Selective serotonin reuptake inhibitors | Nausea (10-30%), drowsiness (7-20%), insomnia (< 10%), nervousness(< 10%), sexual dysfunction (< 10% but underreported). | All equivalently effective. Some patients may respond to lower than usual doses. Start at half the usual dose. |
| Tricyclic antidepressants | Dry mouth (> 45%), dizziness (2%), constipation (15%), sweating (15%), tremors (15%), fatigue (< 10%) | Requires more time to titrate to treatment dose. Clomipramine more effective. Some patients with panic disorder are extremely sensitive both to the therapeutic and adverse effects of TCAs. Start at very low doses. |
| Benzodiazepines | Somnolence (15-34%) and impaired coordination (6-22%). Potential for physical dependence and withdrawal symptoms, but psychological addiction has not been a significant problem in clinical trials. | Faster onset of action than antidepressants, but do not treat comorbid depression and are more difficult to discontinue. |
Recommendations from others
The American Psychiatric Association Guideline states that CBT and pharmacotherapy are equivalently effective, and that SSRIs, TCAs, BDZs, and MAOIs are equivalently effective.12 The International Consensus Group on Depression and Anxiety concludes that SSRIs, TCAs, and BDZs are effective. SSRIs and BDZs are tolerated better than TCAs, and BDZs act faster (1 week vs. 4-8 weeks).11
Read a Clinical Commentary by William A. Hensel, MD, at www.fpin.org.
1. Boyer W. Int Clin Psychopharmacol 1995;10:45-9.
2. Otto MW, Tuby KS, Gould RA, et al. Am J Psychiatry 2001;158:1989-92.
3. Lecrubier Y, Bakker A, Dunbar G, et al. Acta Psychiatrica Scand 1997;95:145-52.
4. Bakker A, van Dyck R, Spinhoven P, et al. J Clin Psychiatry 1999;60:831-8.
5. Modigh K, Westberg P, Eriksson E. J Clin Psychopharmacol 1992;12:251-61.
6. Goddard AW, Brouette T, Almai A, et al. Arch Gen Psychiatry 2001;58:681-6.
7. van Balkom A, Bakker A, Spinhoven P, et al. J Nerv Ment Dis 1997;185:510-6.
8. Bakker A, van Balkom A, Spinhoven P, et al. J Nerv Ment Dis 1998;186:414-9.
9. Barlow D, Gorman J, Shear M, et al. JAMA 2000;283:2529-36.
10. Fava GA, Rafanelli C, Grandi S, et al. Psychol Med 2001;31(5):891-8.
11. Ballenger J, Davidson J, Lecrubier Y, et al. J Clin Psychiatry 1998;59(suppl 8):47-54.
12. American Psychiatric Association. Am J Psychiatry 1998;155(5 Suppl):1S-34S.
Selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), benzodiazepines (BDZs), and cognitive behavioral therapy (CBT) are effective for panic disorder (PD) with or without agoraphobia (NNT5 for complete remission). SSRIs may be most effective, but BDZs work faster. Clomipramine is more effective than other TCAs. CBT improves response and decreases relapse rates when used with medication. Severe symptoms may warrant short-term use of a BDZ until other therapies take effect (Grade of recommendation: A, based on systematic reviews of randomized clinical trials (RCTs); high quality RCTs).
Evidence summary
SSRIs were more effective than imipramine or alprazolam in a meta-analysis,1 but equivalent to these drugs in an effect-size analysis.2 The absolute difference in efficacy is difficult to determine; few studies directly compare SSRIs with other drugs. In 2 randomized head-to-head trials,3,4 remission rates (eliminating symptoms) were 50%-65% for paroxetine, 37%-53% for clomipramine, and 32%-34% for placebo after 9-12 weeks of therapy; differences between the 2 active drugs were not significant. Clomipramine is serotoninergic and was more effective than other tricyclics in an RCT.5 Adding a BDZ to an SSRI for the first 3 weeks can rapidly stabilize symptoms6 (Table).
Two meta-analyses concluded that CBT is as effective as antidepressants or BDZs during acute treatment7 and during long-term follow-up (31-121 weeks).8 CBT and imipramine each reduce symptoms in 45%-48% of patients; combining them reduces symptoms in 60%.9 Imipramine is more effective initially; CBT is more durable9 but effects may be therapist-dependent. When used in conjunction with medication, graded exposure to panicinducing situations reduces agoraphobia7 but does not improve relapse rates.8 Behavioral therapy with exposure homework has good long-term results.10
An adequate trial of medication requires 6-8 weeks.11 Before treating, evaluate patients for comorbid mood, anxiety, personality, substance use, or medical disorders, which affect 40%-50% of patients with panic disorder, and may influence the choice of treatment.12 Current practice is to slowly taper and discontinue medication after 12-18 months of maintenance treatment12 if there are no significant residual symptoms, no increased psychosocial stressors, and no history of severe or recurrent relapse.
TABLE
Drugs used to treat panic disorder
| Drug Class | Side Effects | Other Considerations |
|---|---|---|
| Selective serotonin reuptake inhibitors | Nausea (10-30%), drowsiness (7-20%), insomnia (< 10%), nervousness(< 10%), sexual dysfunction (< 10% but underreported). | All equivalently effective. Some patients may respond to lower than usual doses. Start at half the usual dose. |
| Tricyclic antidepressants | Dry mouth (> 45%), dizziness (2%), constipation (15%), sweating (15%), tremors (15%), fatigue (< 10%) | Requires more time to titrate to treatment dose. Clomipramine more effective. Some patients with panic disorder are extremely sensitive both to the therapeutic and adverse effects of TCAs. Start at very low doses. |
| Benzodiazepines | Somnolence (15-34%) and impaired coordination (6-22%). Potential for physical dependence and withdrawal symptoms, but psychological addiction has not been a significant problem in clinical trials. | Faster onset of action than antidepressants, but do not treat comorbid depression and are more difficult to discontinue. |
Recommendations from others
The American Psychiatric Association Guideline states that CBT and pharmacotherapy are equivalently effective, and that SSRIs, TCAs, BDZs, and MAOIs are equivalently effective.12 The International Consensus Group on Depression and Anxiety concludes that SSRIs, TCAs, and BDZs are effective. SSRIs and BDZs are tolerated better than TCAs, and BDZs act faster (1 week vs. 4-8 weeks).11
Read a Clinical Commentary by William A. Hensel, MD, at www.fpin.org.
Selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), benzodiazepines (BDZs), and cognitive behavioral therapy (CBT) are effective for panic disorder (PD) with or without agoraphobia (NNT5 for complete remission). SSRIs may be most effective, but BDZs work faster. Clomipramine is more effective than other TCAs. CBT improves response and decreases relapse rates when used with medication. Severe symptoms may warrant short-term use of a BDZ until other therapies take effect (Grade of recommendation: A, based on systematic reviews of randomized clinical trials (RCTs); high quality RCTs).
Evidence summary
SSRIs were more effective than imipramine or alprazolam in a meta-analysis,1 but equivalent to these drugs in an effect-size analysis.2 The absolute difference in efficacy is difficult to determine; few studies directly compare SSRIs with other drugs. In 2 randomized head-to-head trials,3,4 remission rates (eliminating symptoms) were 50%-65% for paroxetine, 37%-53% for clomipramine, and 32%-34% for placebo after 9-12 weeks of therapy; differences between the 2 active drugs were not significant. Clomipramine is serotoninergic and was more effective than other tricyclics in an RCT.5 Adding a BDZ to an SSRI for the first 3 weeks can rapidly stabilize symptoms6 (Table).
Two meta-analyses concluded that CBT is as effective as antidepressants or BDZs during acute treatment7 and during long-term follow-up (31-121 weeks).8 CBT and imipramine each reduce symptoms in 45%-48% of patients; combining them reduces symptoms in 60%.9 Imipramine is more effective initially; CBT is more durable9 but effects may be therapist-dependent. When used in conjunction with medication, graded exposure to panicinducing situations reduces agoraphobia7 but does not improve relapse rates.8 Behavioral therapy with exposure homework has good long-term results.10
An adequate trial of medication requires 6-8 weeks.11 Before treating, evaluate patients for comorbid mood, anxiety, personality, substance use, or medical disorders, which affect 40%-50% of patients with panic disorder, and may influence the choice of treatment.12 Current practice is to slowly taper and discontinue medication after 12-18 months of maintenance treatment12 if there are no significant residual symptoms, no increased psychosocial stressors, and no history of severe or recurrent relapse.
TABLE
Drugs used to treat panic disorder
| Drug Class | Side Effects | Other Considerations |
|---|---|---|
| Selective serotonin reuptake inhibitors | Nausea (10-30%), drowsiness (7-20%), insomnia (< 10%), nervousness(< 10%), sexual dysfunction (< 10% but underreported). | All equivalently effective. Some patients may respond to lower than usual doses. Start at half the usual dose. |
| Tricyclic antidepressants | Dry mouth (> 45%), dizziness (2%), constipation (15%), sweating (15%), tremors (15%), fatigue (< 10%) | Requires more time to titrate to treatment dose. Clomipramine more effective. Some patients with panic disorder are extremely sensitive both to the therapeutic and adverse effects of TCAs. Start at very low doses. |
| Benzodiazepines | Somnolence (15-34%) and impaired coordination (6-22%). Potential for physical dependence and withdrawal symptoms, but psychological addiction has not been a significant problem in clinical trials. | Faster onset of action than antidepressants, but do not treat comorbid depression and are more difficult to discontinue. |
Recommendations from others
The American Psychiatric Association Guideline states that CBT and pharmacotherapy are equivalently effective, and that SSRIs, TCAs, BDZs, and MAOIs are equivalently effective.12 The International Consensus Group on Depression and Anxiety concludes that SSRIs, TCAs, and BDZs are effective. SSRIs and BDZs are tolerated better than TCAs, and BDZs act faster (1 week vs. 4-8 weeks).11
Read a Clinical Commentary by William A. Hensel, MD, at www.fpin.org.
1. Boyer W. Int Clin Psychopharmacol 1995;10:45-9.
2. Otto MW, Tuby KS, Gould RA, et al. Am J Psychiatry 2001;158:1989-92.
3. Lecrubier Y, Bakker A, Dunbar G, et al. Acta Psychiatrica Scand 1997;95:145-52.
4. Bakker A, van Dyck R, Spinhoven P, et al. J Clin Psychiatry 1999;60:831-8.
5. Modigh K, Westberg P, Eriksson E. J Clin Psychopharmacol 1992;12:251-61.
6. Goddard AW, Brouette T, Almai A, et al. Arch Gen Psychiatry 2001;58:681-6.
7. van Balkom A, Bakker A, Spinhoven P, et al. J Nerv Ment Dis 1997;185:510-6.
8. Bakker A, van Balkom A, Spinhoven P, et al. J Nerv Ment Dis 1998;186:414-9.
9. Barlow D, Gorman J, Shear M, et al. JAMA 2000;283:2529-36.
10. Fava GA, Rafanelli C, Grandi S, et al. Psychol Med 2001;31(5):891-8.
11. Ballenger J, Davidson J, Lecrubier Y, et al. J Clin Psychiatry 1998;59(suppl 8):47-54.
12. American Psychiatric Association. Am J Psychiatry 1998;155(5 Suppl):1S-34S.
1. Boyer W. Int Clin Psychopharmacol 1995;10:45-9.
2. Otto MW, Tuby KS, Gould RA, et al. Am J Psychiatry 2001;158:1989-92.
3. Lecrubier Y, Bakker A, Dunbar G, et al. Acta Psychiatrica Scand 1997;95:145-52.
4. Bakker A, van Dyck R, Spinhoven P, et al. J Clin Psychiatry 1999;60:831-8.
5. Modigh K, Westberg P, Eriksson E. J Clin Psychopharmacol 1992;12:251-61.
6. Goddard AW, Brouette T, Almai A, et al. Arch Gen Psychiatry 2001;58:681-6.
7. van Balkom A, Bakker A, Spinhoven P, et al. J Nerv Ment Dis 1997;185:510-6.
8. Bakker A, van Balkom A, Spinhoven P, et al. J Nerv Ment Dis 1998;186:414-9.
9. Barlow D, Gorman J, Shear M, et al. JAMA 2000;283:2529-36.
10. Fava GA, Rafanelli C, Grandi S, et al. Psychol Med 2001;31(5):891-8.
11. Ballenger J, Davidson J, Lecrubier Y, et al. J Clin Psychiatry 1998;59(suppl 8):47-54.
12. American Psychiatric Association. Am J Psychiatry 1998;155(5 Suppl):1S-34S.
Evidence-based answers from the Family Physicians Inquiries Network
What are the treatment options for SSRI-related sexual dysfunction?
Substituting bupropion, nefazodone, or mirtazapine is beneficial. (Grade of recommendation: B, randomized controlled trials [RCTs].) Augmentation therapy with amantadine, bupropion, and buspirone is no better than placebo. (Grade of recommendation: B, RCTs.) Augmentation therapy with multiple other agents may be beneficial. (Grade of recommendation: D, open-label nonrandomized studies, case series, and case reports.) SSRI “drug holidays” may also be effective (Table 1). (Grade of recommendation: D, open-label nonrandomized studies.)
TABLE
Summary of treatment options for SSRI-induced sexual dysfunction
| Strategy | Drugs considered | RCT data | Other data |
|---|---|---|---|
| Switch therapy | Bupropion SR, bupropion, mirtazapine, nefazodone | Nefazodone effective | All agents effective in nonrandomized open-label trials |
| Augmentation | Buspirone, amantadine, bupropion, cyproheptadine, dextroamphetamine, granisetron, ginkgo biloba, methylphenidate, mirtazapine, nefazodone, pemoline, sildenafil, yohimbine | Small, transient effect with high-dose buspirone. | Other RCT with buspirone, amantadine, and bupropion showed no difference vs placebo. Most agents effective in nonrandomized open-label trials, case-series, or case reports. Placebo effect unknown |
| Drug holiday | Fluoxetine, paroxetine, sertraline | None available | Improvement in 2 of 4 weekends for sertraline and paroxetine only |
Evidence summary
SSRI-related sexual dysfunction may be dose dependent and diminish with time, but these aspects have not been evaluated prospectively. Data suggest that bupropion, nefazodone, and mirtazapine have little to no effect on sexual functioning.1 Changing from SSRIs to one of these agents may alleviate SSRI-induced sexual dysfunction. In a randomized double-blind study, patients experiencing sexual dysfunction on sertraline improved when switched to nefazodone 400 mg daily.2 Additional open-label nonrandomized studies of all 3 agents suggest improved sexual functioning in 60% to 85% of patients with little to no loss of antidepressant efficacy.1,3,6 The potential for placebo effects makes interpreting these open-label trials more difficult.
Three augmentation therapies have been tested in double-blind placebo-controlled trials. In the first, buspirone augmentation resulted in a statistical improvement in sexual functioning at weeks 2 and 3 of therapy, but not at weeks 1 and 4 (mean dose 48.5 mg per day).7 In the second, adding buspirone 20 to 30 mg per day, amantadine 50 to 100 mg per day, or placebo resulted in equal improvement in women’s sexual function.8 Finally, in a third trial, adding bupropion or placebo showed equal improvement in sexual function.9 Multiple other agents have been tested in open-label nonrandomized studies, case series, and case reports. Most showed a beneficial effect, but results must be interpreted with caution. One open-label nonrandomized study of weekend “drug holidays” showed no benefit for fluoxetine and inconsistent results for paroxetine and sertraline.10
Recommendations from others
Tertiary literature sources recommend the strategies described above.11
Clinical Commentary by Michael Fisher, MD, additional references, search strategy, and detailed evidence table at http://www.fpin.org.
1. Zajecka J, Drouin MA, Yang WH, Horak F, et al. J Clin Psychiatry 2001;62(suppl 3):35-43.2.Allergy 1992;12(suppl):173.-
2. Ferguson JM, Shrivastava RK, Stahl SM, et al. J Clin Psychiatry. 2001;62:24-9.
3. Rosen RC, Lane RM, Menza M. J Clin Psychopharmacol 1999;19:67-85.
4. Gelenberg AJ, Laukes C, McGahuey C, et al. J Clin Psychiatry 2000;61:356-60.
5. Clayton AH, McGarvey EL, Abouesh AI, et al. J Clin Psychiatry 2001;62:185-90.
6. Walker PW, Cole JO, Gardner EA, et al. J Clin Psychiatry 1993;54:459-65.
7. Landen M, Eriksson E, Agren H, et al. J Clin Psychopharmacol 1999;19:268-71
8. Michelson D, Bancroft J, Targum S, et al. Am J Psychiatry 2000;157:239-43.
9. Masand PS, Ashton AK, Gupta S, et al. Am J Psychiatry 2001;158:805-7.
10. Rothschild AJ. Am J Psychiatry 1995;152:1514-6.
11. Marangell LB, Yudofsky SC, Silver JM. Psychopharmacology and electroconvulsive therapy. In: Hales RE, Yudofsky SC, Talbott JA, eds. Textbook of Psychiatry. 3rd ed. Washington, DC: American Psychiatric Press; 1999;1025-132.
Substituting bupropion, nefazodone, or mirtazapine is beneficial. (Grade of recommendation: B, randomized controlled trials [RCTs].) Augmentation therapy with amantadine, bupropion, and buspirone is no better than placebo. (Grade of recommendation: B, RCTs.) Augmentation therapy with multiple other agents may be beneficial. (Grade of recommendation: D, open-label nonrandomized studies, case series, and case reports.) SSRI “drug holidays” may also be effective (Table 1). (Grade of recommendation: D, open-label nonrandomized studies.)
TABLE
Summary of treatment options for SSRI-induced sexual dysfunction
| Strategy | Drugs considered | RCT data | Other data |
|---|---|---|---|
| Switch therapy | Bupropion SR, bupropion, mirtazapine, nefazodone | Nefazodone effective | All agents effective in nonrandomized open-label trials |
| Augmentation | Buspirone, amantadine, bupropion, cyproheptadine, dextroamphetamine, granisetron, ginkgo biloba, methylphenidate, mirtazapine, nefazodone, pemoline, sildenafil, yohimbine | Small, transient effect with high-dose buspirone. | Other RCT with buspirone, amantadine, and bupropion showed no difference vs placebo. Most agents effective in nonrandomized open-label trials, case-series, or case reports. Placebo effect unknown |
| Drug holiday | Fluoxetine, paroxetine, sertraline | None available | Improvement in 2 of 4 weekends for sertraline and paroxetine only |
Evidence summary
SSRI-related sexual dysfunction may be dose dependent and diminish with time, but these aspects have not been evaluated prospectively. Data suggest that bupropion, nefazodone, and mirtazapine have little to no effect on sexual functioning.1 Changing from SSRIs to one of these agents may alleviate SSRI-induced sexual dysfunction. In a randomized double-blind study, patients experiencing sexual dysfunction on sertraline improved when switched to nefazodone 400 mg daily.2 Additional open-label nonrandomized studies of all 3 agents suggest improved sexual functioning in 60% to 85% of patients with little to no loss of antidepressant efficacy.1,3,6 The potential for placebo effects makes interpreting these open-label trials more difficult.
Three augmentation therapies have been tested in double-blind placebo-controlled trials. In the first, buspirone augmentation resulted in a statistical improvement in sexual functioning at weeks 2 and 3 of therapy, but not at weeks 1 and 4 (mean dose 48.5 mg per day).7 In the second, adding buspirone 20 to 30 mg per day, amantadine 50 to 100 mg per day, or placebo resulted in equal improvement in women’s sexual function.8 Finally, in a third trial, adding bupropion or placebo showed equal improvement in sexual function.9 Multiple other agents have been tested in open-label nonrandomized studies, case series, and case reports. Most showed a beneficial effect, but results must be interpreted with caution. One open-label nonrandomized study of weekend “drug holidays” showed no benefit for fluoxetine and inconsistent results for paroxetine and sertraline.10
Recommendations from others
Tertiary literature sources recommend the strategies described above.11
Clinical Commentary by Michael Fisher, MD, additional references, search strategy, and detailed evidence table at http://www.fpin.org.
Substituting bupropion, nefazodone, or mirtazapine is beneficial. (Grade of recommendation: B, randomized controlled trials [RCTs].) Augmentation therapy with amantadine, bupropion, and buspirone is no better than placebo. (Grade of recommendation: B, RCTs.) Augmentation therapy with multiple other agents may be beneficial. (Grade of recommendation: D, open-label nonrandomized studies, case series, and case reports.) SSRI “drug holidays” may also be effective (Table 1). (Grade of recommendation: D, open-label nonrandomized studies.)
TABLE
Summary of treatment options for SSRI-induced sexual dysfunction
| Strategy | Drugs considered | RCT data | Other data |
|---|---|---|---|
| Switch therapy | Bupropion SR, bupropion, mirtazapine, nefazodone | Nefazodone effective | All agents effective in nonrandomized open-label trials |
| Augmentation | Buspirone, amantadine, bupropion, cyproheptadine, dextroamphetamine, granisetron, ginkgo biloba, methylphenidate, mirtazapine, nefazodone, pemoline, sildenafil, yohimbine | Small, transient effect with high-dose buspirone. | Other RCT with buspirone, amantadine, and bupropion showed no difference vs placebo. Most agents effective in nonrandomized open-label trials, case-series, or case reports. Placebo effect unknown |
| Drug holiday | Fluoxetine, paroxetine, sertraline | None available | Improvement in 2 of 4 weekends for sertraline and paroxetine only |
Evidence summary
SSRI-related sexual dysfunction may be dose dependent and diminish with time, but these aspects have not been evaluated prospectively. Data suggest that bupropion, nefazodone, and mirtazapine have little to no effect on sexual functioning.1 Changing from SSRIs to one of these agents may alleviate SSRI-induced sexual dysfunction. In a randomized double-blind study, patients experiencing sexual dysfunction on sertraline improved when switched to nefazodone 400 mg daily.2 Additional open-label nonrandomized studies of all 3 agents suggest improved sexual functioning in 60% to 85% of patients with little to no loss of antidepressant efficacy.1,3,6 The potential for placebo effects makes interpreting these open-label trials more difficult.
Three augmentation therapies have been tested in double-blind placebo-controlled trials. In the first, buspirone augmentation resulted in a statistical improvement in sexual functioning at weeks 2 and 3 of therapy, but not at weeks 1 and 4 (mean dose 48.5 mg per day).7 In the second, adding buspirone 20 to 30 mg per day, amantadine 50 to 100 mg per day, or placebo resulted in equal improvement in women’s sexual function.8 Finally, in a third trial, adding bupropion or placebo showed equal improvement in sexual function.9 Multiple other agents have been tested in open-label nonrandomized studies, case series, and case reports. Most showed a beneficial effect, but results must be interpreted with caution. One open-label nonrandomized study of weekend “drug holidays” showed no benefit for fluoxetine and inconsistent results for paroxetine and sertraline.10
Recommendations from others
Tertiary literature sources recommend the strategies described above.11
Clinical Commentary by Michael Fisher, MD, additional references, search strategy, and detailed evidence table at http://www.fpin.org.
1. Zajecka J, Drouin MA, Yang WH, Horak F, et al. J Clin Psychiatry 2001;62(suppl 3):35-43.2.Allergy 1992;12(suppl):173.-
2. Ferguson JM, Shrivastava RK, Stahl SM, et al. J Clin Psychiatry. 2001;62:24-9.
3. Rosen RC, Lane RM, Menza M. J Clin Psychopharmacol 1999;19:67-85.
4. Gelenberg AJ, Laukes C, McGahuey C, et al. J Clin Psychiatry 2000;61:356-60.
5. Clayton AH, McGarvey EL, Abouesh AI, et al. J Clin Psychiatry 2001;62:185-90.
6. Walker PW, Cole JO, Gardner EA, et al. J Clin Psychiatry 1993;54:459-65.
7. Landen M, Eriksson E, Agren H, et al. J Clin Psychopharmacol 1999;19:268-71
8. Michelson D, Bancroft J, Targum S, et al. Am J Psychiatry 2000;157:239-43.
9. Masand PS, Ashton AK, Gupta S, et al. Am J Psychiatry 2001;158:805-7.
10. Rothschild AJ. Am J Psychiatry 1995;152:1514-6.
11. Marangell LB, Yudofsky SC, Silver JM. Psychopharmacology and electroconvulsive therapy. In: Hales RE, Yudofsky SC, Talbott JA, eds. Textbook of Psychiatry. 3rd ed. Washington, DC: American Psychiatric Press; 1999;1025-132.
1. Zajecka J, Drouin MA, Yang WH, Horak F, et al. J Clin Psychiatry 2001;62(suppl 3):35-43.2.Allergy 1992;12(suppl):173.-
2. Ferguson JM, Shrivastava RK, Stahl SM, et al. J Clin Psychiatry. 2001;62:24-9.
3. Rosen RC, Lane RM, Menza M. J Clin Psychopharmacol 1999;19:67-85.
4. Gelenberg AJ, Laukes C, McGahuey C, et al. J Clin Psychiatry 2000;61:356-60.
5. Clayton AH, McGarvey EL, Abouesh AI, et al. J Clin Psychiatry 2001;62:185-90.
6. Walker PW, Cole JO, Gardner EA, et al. J Clin Psychiatry 1993;54:459-65.
7. Landen M, Eriksson E, Agren H, et al. J Clin Psychopharmacol 1999;19:268-71
8. Michelson D, Bancroft J, Targum S, et al. Am J Psychiatry 2000;157:239-43.
9. Masand PS, Ashton AK, Gupta S, et al. Am J Psychiatry 2001;158:805-7.
10. Rothschild AJ. Am J Psychiatry 1995;152:1514-6.
11. Marangell LB, Yudofsky SC, Silver JM. Psychopharmacology and electroconvulsive therapy. In: Hales RE, Yudofsky SC, Talbott JA, eds. Textbook of Psychiatry. 3rd ed. Washington, DC: American Psychiatric Press; 1999;1025-132.
Evidence-based answers from the Family Physicians Inquiries Network