Courtney Nemeth Wiseman, MD, MPH

Re-experiencing a previous life-threatening stress through nightmares or recurrent memories is a hallmark of posttraumatic stress disorder (PTSD). In the United States, the lifetime risk of PTSD is 10.1% and the 12-month prevalence is 3.7%.¹ The selective serotonin reuptake inhibitors (SSRIs) sertraline and paroxetine are FDA-approved for treating PTSD; clinicians commonly use any SSRI for this disorder. Although SSRIs can alleviate many PTSD symptoms, at times patients experience only a partial response, which necessitates other interventions.

Rationale for using topiramate

The anticonvulsant topiramate blocks voltage-sensitive sodium channels, augments γ-aminobutyric acid type A, antagonizes the glutamate receptor, and inhibits carbonic anhydrase. Researchers have hypothesized that limbic nuclei become sensitized and “kindled” after exposure to a traumatic event. Anticonvulsants such as topiramate may help mitigate stress-activated kindling in PTSD.^2,3

What does the evidence say?

Although less compelling than double-blind, placebo-controlled trials, small open-label studies and some case reports indicate a potential role for topiramate in PTSD for specific populations.^4,5 In an 8-week open- label study, Alderman et al⁶ found adjunctive topiramate led to a statistically significant reduction in Clinician-Administered PTSD Scale (CAPS) scores and nightmares in 43 male veterans with combat-related PTSD. There was a nonsignificant decrease in high-risk alcohol use.

In a 2002 retrospective case series, Berlant et al⁷ found topiramate as monotherapy or adjunctive therapy reduced nightmares in 35 patients with chronic, non-combat PTSD. Nightmares decreased in 79% of patients and flashbacks decreased in 86%, with symptom improvement in a median of 4 days. Limitations of this study included lack of placebo control, a low number of participants, and a high dropout rate (9/35).

Two years later, Berlant⁸ used the PTSD Checklist-Civilian version (PCL-C) to assess response to topiramate in an open-label study of 33 patients with chronic, non-hallucinatory PTSD. Twenty-eight patients used topiramate as add-on therapy. PCL-C scores decreased by ≥30% in 77% of patients in 4 weeks, with a median dose of 50 mg/d and a median response time of 9 days.

In a double-blind, placebo-controlled trial, Tucker et al⁹ assessed 38 civilian patients who took topiramate monotherapy for PTSD. Using the CAPS, researchers concluded that topiramate reduced re-experiencing symptoms, but the effect was not statistically significant.⁹

Lindley et al¹⁰ conducted a randomized, double-blind, placebo-controlled trial to study the effect of add-on topiramate in 40 patients with chronic, combat-related PTSD. Because many patients in this study had a history of depression and substance use disorders, topiramate was added to antidepressants; no anticonvulsants, antipsychotics, or benzodiazepines were used. Similar to previous studies, researchers found no statistically significant effect on PTSD symptom severity or global symptom improvement. However, the small number of participants and a high dropout rate limited this study.¹⁰

In a 12-week, double-blind, placebo-controlled study of 35 men and women age 18 to 62 with PTSD, Yeh et al¹¹ found that topiramate (mean dose: 102.94 mg/d) lead to a statistically significant overall CAPS score reduction, with significant improvements in re-experiencing symptoms, such as nightmares.

Our opinion

FDA-approved treatments such as SSRIs should be the first pharmacologic intervention for PTSD. If a patient’s response is partial or inadequate, consider additional treatment options. For patients with persistent re-experiencing symptoms, evidence and experience with prazosin and trazodone are more robust than that for topiramate.¹²

Using topiramate to reduce re-experiencing symptoms such as nightmares in PTSD is not supported by statistically significant evidence from double-blind, placebo- controlled trials. However, numerous open-label studies and case reports suggest that there may be a role for topiramate in PTSD patients who do not respond to other treatments. Data indicate that topiramate may be helpful for PTSD patients who have high-risk alcohol use⁶ or migraine headaches.¹³ Because some patients who take topiramate lose weight, the medication may be useful for PTSD patients who are overweight.¹³

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Related Resource

• U.S. Department of Veterans Affairs. Nightmares and PTSD. www.ptsd.va.gov/public/pages/nightmares.asp.

Drug Brand Names

• Paroxetine • Paxil
• Sertraline • Zoloft
• Prazosin • Minipress
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro

Re-experiencing a previous life-threatening stress through nightmares or recurrent memories is a hallmark of posttraumatic stress disorder (PTSD). In the United States, the lifetime risk of PTSD is 10.1% and the 12-month prevalence is 3.7%.¹ The selective serotonin reuptake inhibitors (SSRIs) sertraline and paroxetine are FDA-approved for treating PTSD; clinicians commonly use any SSRI for this disorder. Although SSRIs can alleviate many PTSD symptoms, at times patients experience only a partial response, which necessitates other interventions.

Rationale for using topiramate

The anticonvulsant topiramate blocks voltage-sensitive sodium channels, augments γ-aminobutyric acid type A, antagonizes the glutamate receptor, and inhibits carbonic anhydrase. Researchers have hypothesized that limbic nuclei become sensitized and “kindled” after exposure to a traumatic event. Anticonvulsants such as topiramate may help mitigate stress-activated kindling in PTSD.^2,3

What does the evidence say?

Although less compelling than double-blind, placebo-controlled trials, small open-label studies and some case reports indicate a potential role for topiramate in PTSD for specific populations.^4,5 In an 8-week open- label study, Alderman et al⁶ found adjunctive topiramate led to a statistically significant reduction in Clinician-Administered PTSD Scale (CAPS) scores and nightmares in 43 male veterans with combat-related PTSD. There was a nonsignificant decrease in high-risk alcohol use.

In a 2002 retrospective case series, Berlant et al⁷ found topiramate as monotherapy or adjunctive therapy reduced nightmares in 35 patients with chronic, non-combat PTSD. Nightmares decreased in 79% of patients and flashbacks decreased in 86%, with symptom improvement in a median of 4 days. Limitations of this study included lack of placebo control, a low number of participants, and a high dropout rate (9/35).

Two years later, Berlant⁸ used the PTSD Checklist-Civilian version (PCL-C) to assess response to topiramate in an open-label study of 33 patients with chronic, non-hallucinatory PTSD. Twenty-eight patients used topiramate as add-on therapy. PCL-C scores decreased by ≥30% in 77% of patients in 4 weeks, with a median dose of 50 mg/d and a median response time of 9 days.

In a double-blind, placebo-controlled trial, Tucker et al⁹ assessed 38 civilian patients who took topiramate monotherapy for PTSD. Using the CAPS, researchers concluded that topiramate reduced re-experiencing symptoms, but the effect was not statistically significant.⁹

Lindley et al¹⁰ conducted a randomized, double-blind, placebo-controlled trial to study the effect of add-on topiramate in 40 patients with chronic, combat-related PTSD. Because many patients in this study had a history of depression and substance use disorders, topiramate was added to antidepressants; no anticonvulsants, antipsychotics, or benzodiazepines were used. Similar to previous studies, researchers found no statistically significant effect on PTSD symptom severity or global symptom improvement. However, the small number of participants and a high dropout rate limited this study.¹⁰

In a 12-week, double-blind, placebo-controlled study of 35 men and women age 18 to 62 with PTSD, Yeh et al¹¹ found that topiramate (mean dose: 102.94 mg/d) lead to a statistically significant overall CAPS score reduction, with significant improvements in re-experiencing symptoms, such as nightmares.

Our opinion

FDA-approved treatments such as SSRIs should be the first pharmacologic intervention for PTSD. If a patient’s response is partial or inadequate, consider additional treatment options. For patients with persistent re-experiencing symptoms, evidence and experience with prazosin and trazodone are more robust than that for topiramate.¹²

Using topiramate to reduce re-experiencing symptoms such as nightmares in PTSD is not supported by statistically significant evidence from double-blind, placebo- controlled trials. However, numerous open-label studies and case reports suggest that there may be a role for topiramate in PTSD patients who do not respond to other treatments. Data indicate that topiramate may be helpful for PTSD patients who have high-risk alcohol use⁶ or migraine headaches.¹³ Because some patients who take topiramate lose weight, the medication may be useful for PTSD patients who are overweight.¹³

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Related Resource

• U.S. Department of Veterans Affairs. Nightmares and PTSD. www.ptsd.va.gov/public/pages/nightmares.asp.

Drug Brand Names

• Paroxetine • Paxil
• Sertraline • Zoloft
• Prazosin • Minipress
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro

Re-experiencing a previous life-threatening stress through nightmares or recurrent memories is a hallmark of posttraumatic stress disorder (PTSD). In the United States, the lifetime risk of PTSD is 10.1% and the 12-month prevalence is 3.7%.¹ The selective serotonin reuptake inhibitors (SSRIs) sertraline and paroxetine are FDA-approved for treating PTSD; clinicians commonly use any SSRI for this disorder. Although SSRIs can alleviate many PTSD symptoms, at times patients experience only a partial response, which necessitates other interventions.

Rationale for using topiramate

The anticonvulsant topiramate blocks voltage-sensitive sodium channels, augments γ-aminobutyric acid type A, antagonizes the glutamate receptor, and inhibits carbonic anhydrase. Researchers have hypothesized that limbic nuclei become sensitized and “kindled” after exposure to a traumatic event. Anticonvulsants such as topiramate may help mitigate stress-activated kindling in PTSD.^2,3

What does the evidence say?

Although less compelling than double-blind, placebo-controlled trials, small open-label studies and some case reports indicate a potential role for topiramate in PTSD for specific populations.^4,5 In an 8-week open- label study, Alderman et al⁶ found adjunctive topiramate led to a statistically significant reduction in Clinician-Administered PTSD Scale (CAPS) scores and nightmares in 43 male veterans with combat-related PTSD. There was a nonsignificant decrease in high-risk alcohol use.

In a 2002 retrospective case series, Berlant et al⁷ found topiramate as monotherapy or adjunctive therapy reduced nightmares in 35 patients with chronic, non-combat PTSD. Nightmares decreased in 79% of patients and flashbacks decreased in 86%, with symptom improvement in a median of 4 days. Limitations of this study included lack of placebo control, a low number of participants, and a high dropout rate (9/35).

Two years later, Berlant⁸ used the PTSD Checklist-Civilian version (PCL-C) to assess response to topiramate in an open-label study of 33 patients with chronic, non-hallucinatory PTSD. Twenty-eight patients used topiramate as add-on therapy. PCL-C scores decreased by ≥30% in 77% of patients in 4 weeks, with a median dose of 50 mg/d and a median response time of 9 days.

In a double-blind, placebo-controlled trial, Tucker et al⁹ assessed 38 civilian patients who took topiramate monotherapy for PTSD. Using the CAPS, researchers concluded that topiramate reduced re-experiencing symptoms, but the effect was not statistically significant.⁹

Lindley et al¹⁰ conducted a randomized, double-blind, placebo-controlled trial to study the effect of add-on topiramate in 40 patients with chronic, combat-related PTSD. Because many patients in this study had a history of depression and substance use disorders, topiramate was added to antidepressants; no anticonvulsants, antipsychotics, or benzodiazepines were used. Similar to previous studies, researchers found no statistically significant effect on PTSD symptom severity or global symptom improvement. However, the small number of participants and a high dropout rate limited this study.¹⁰

In a 12-week, double-blind, placebo-controlled study of 35 men and women age 18 to 62 with PTSD, Yeh et al¹¹ found that topiramate (mean dose: 102.94 mg/d) lead to a statistically significant overall CAPS score reduction, with significant improvements in re-experiencing symptoms, such as nightmares.

Our opinion

FDA-approved treatments such as SSRIs should be the first pharmacologic intervention for PTSD. If a patient’s response is partial or inadequate, consider additional treatment options. For patients with persistent re-experiencing symptoms, evidence and experience with prazosin and trazodone are more robust than that for topiramate.¹²

Using topiramate to reduce re-experiencing symptoms such as nightmares in PTSD is not supported by statistically significant evidence from double-blind, placebo- controlled trials. However, numerous open-label studies and case reports suggest that there may be a role for topiramate in PTSD patients who do not respond to other treatments. Data indicate that topiramate may be helpful for PTSD patients who have high-risk alcohol use⁶ or migraine headaches.¹³ Because some patients who take topiramate lose weight, the medication may be useful for PTSD patients who are overweight.¹³

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Related Resource

• U.S. Department of Veterans Affairs. Nightmares and PTSD. www.ptsd.va.gov/public/pages/nightmares.asp.

Drug Brand Names

• Paroxetine • Paxil
• Sertraline • Zoloft
• Prazosin • Minipress
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro

For many clinicians, bupropion is the “go-to” medication for treating depressed patients who smoke, have concerns about sexual dysfunction side effects, and/or worry about weight gain. Bupropion is FDA-approved for preventing seasonal major depressive episodes in patients with seasonal affective disorder and is indicated as a smoking cessation aid.

“Anxious depression”—defined as depression with high levels of anxiety—is associated with poorer outcomes than “non-anxious” depression.¹ Prescribing medications for these patients can be challenging. Some clinicians believe that bupropion exacerbates anxiety and should not be used to treat patients who experience both anxiety and depression.

Reports from our patients and our cumulative clinical experience are key factors in developing expertise in selecting appropriate medications. When informing our patients about what to expect from medications, however, it can be useful to combine anecdotal evidence with knowledge of the facts or lack thereof. Are there data to support or contradict the idea that bupropion can cause anxiety while treating depression?

What the research shows

The drug manufacturer reports a “substantial proportion of patients treated with Wellbutrin experience some degree of increased restlessness, agitation, anxiety, and insomnia, especially shortly after initiation of treatment.”²

In 2001, Rush et al³ published the results of a 16-week study (n=248) assessing pre-treatment anxiety levels and response to sertraline or bupropion. The authors concluded that anxious and depressed patients who received sertraline didn’t experience a superior anxiolytic or antidepressant response compared with bupropion.³ The same authors came to similar conclusions in a retrospective analysis of a pair of 8-week randomized, controlled, double-blind trials of selective serotonin reuptake inhibitors (SSRIs) and bupropion.⁴

In 2001, Nieuwstraten et al⁵ compared bupropion with SSRIs for treating depression by reviewing several randomized, double-blind, controlled trials. The relative risk of developing “anxiety/agitation” was 1.32 (95% confidence interval, 0.85 to 2.04), which was not statistically significant.

In a 2008 meta-analysis, Papakostas et al⁶ pooled individual patient data from 10 randomized, double-blind, placebo-controlled trials. Their aim was to compare the efficacy of bupropion to SSRIs in treating “anxious depression.” They found no difference in timing or degree of improvement in anxiety symptoms between groups based on Hamilton Anxiety Scale or Hamilton Depression Rating Scale—Anxiety-Somatization (HDRS-AS) scores. The authors recommended that antidepressant choice should not be based on concerns about worsening anxiety symptoms in depressed patients.⁶

Another meta-analysis by Papakostas et al⁷ of the same 10 randomized, double-blind, placebo-controlled trials suggested SSRIs may confer an advantage over bupropion in treating a subset of patients with “anxious depression,” which they defined as a HDRS-AS score ≥7. The authors noted the advantage was statistically significant, although “modest.”

Other smaller studies suggest that bupropion does not increase anxiety.^8,9 A pilot study (N = 24, no placebo control) concluded that bupropion XL was comparable to escitalopram in treating anxiety in outpatients with generalized anxiety disorder.⁸

Because designing and executing drug trials can be expensive, it is not surprising that most of the evidence cited above derives from pharmaceutical company-sponsored or industry-affiliated work. As such, we should evaluate available evidence within the context of what we hear from and observe in our patients.

Our opinion

When assessing patients with depression and anxiety, we must carefully evaluate symptoms to distinguish between depression with associated anxiety symptoms and depression with a comorbid anxiety disorder.

If a patient suffers from depression with associated anxiety symptoms (“anxious depression”), keep in mind that although some data demonstrate a superior response to SSRIs, other studies show no difference in effect. Some research—albeit smaller, less compelling studies—suggests that bupropion may decrease anxiety.

If your patient suffers from comorbid depression and an anxiety disorder, bupropion would not be a first-line choice because it is not FDA-approved to treat anxiety disorders. Although it is possible that anxiety/agitation could result from bupropion use, there is not sufficient data to support its reputation as ”anxiogenic.”

What is your experience?

Do you agree with the authors? Send comments to [email protected] or share your thoughts on http://www.facebook.com/CurrentPsychiatry.

Related Resource

• American Psychiatric Association. Mixed anxiety-depressive disorder. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000:780-781.

Drug Brand Names

• Bupropion • Wellbutrin, Zyban
• Escitalopram • Lexapro
• Sertraline • Zoloft

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

For many clinicians, bupropion is the “go-to” medication for treating depressed patients who smoke, have concerns about sexual dysfunction side effects, and/or worry about weight gain. Bupropion is FDA-approved for preventing seasonal major depressive episodes in patients with seasonal affective disorder and is indicated as a smoking cessation aid.

“Anxious depression”—defined as depression with high levels of anxiety—is associated with poorer outcomes than “non-anxious” depression.¹ Prescribing medications for these patients can be challenging. Some clinicians believe that bupropion exacerbates anxiety and should not be used to treat patients who experience both anxiety and depression.

Reports from our patients and our cumulative clinical experience are key factors in developing expertise in selecting appropriate medications. When informing our patients about what to expect from medications, however, it can be useful to combine anecdotal evidence with knowledge of the facts or lack thereof. Are there data to support or contradict the idea that bupropion can cause anxiety while treating depression?

What the research shows

The drug manufacturer reports a “substantial proportion of patients treated with Wellbutrin experience some degree of increased restlessness, agitation, anxiety, and insomnia, especially shortly after initiation of treatment.”²

In 2001, Rush et al³ published the results of a 16-week study (n=248) assessing pre-treatment anxiety levels and response to sertraline or bupropion. The authors concluded that anxious and depressed patients who received sertraline didn’t experience a superior anxiolytic or antidepressant response compared with bupropion.³ The same authors came to similar conclusions in a retrospective analysis of a pair of 8-week randomized, controlled, double-blind trials of selective serotonin reuptake inhibitors (SSRIs) and bupropion.⁴

In 2001, Nieuwstraten et al⁵ compared bupropion with SSRIs for treating depression by reviewing several randomized, double-blind, controlled trials. The relative risk of developing “anxiety/agitation” was 1.32 (95% confidence interval, 0.85 to 2.04), which was not statistically significant.

In a 2008 meta-analysis, Papakostas et al⁶ pooled individual patient data from 10 randomized, double-blind, placebo-controlled trials. Their aim was to compare the efficacy of bupropion to SSRIs in treating “anxious depression.” They found no difference in timing or degree of improvement in anxiety symptoms between groups based on Hamilton Anxiety Scale or Hamilton Depression Rating Scale—Anxiety-Somatization (HDRS-AS) scores. The authors recommended that antidepressant choice should not be based on concerns about worsening anxiety symptoms in depressed patients.⁶

Another meta-analysis by Papakostas et al⁷ of the same 10 randomized, double-blind, placebo-controlled trials suggested SSRIs may confer an advantage over bupropion in treating a subset of patients with “anxious depression,” which they defined as a HDRS-AS score ≥7. The authors noted the advantage was statistically significant, although “modest.”

Other smaller studies suggest that bupropion does not increase anxiety.^8,9 A pilot study (N = 24, no placebo control) concluded that bupropion XL was comparable to escitalopram in treating anxiety in outpatients with generalized anxiety disorder.⁸

Because designing and executing drug trials can be expensive, it is not surprising that most of the evidence cited above derives from pharmaceutical company-sponsored or industry-affiliated work. As such, we should evaluate available evidence within the context of what we hear from and observe in our patients.

Our opinion

When assessing patients with depression and anxiety, we must carefully evaluate symptoms to distinguish between depression with associated anxiety symptoms and depression with a comorbid anxiety disorder.

If a patient suffers from depression with associated anxiety symptoms (“anxious depression”), keep in mind that although some data demonstrate a superior response to SSRIs, other studies show no difference in effect. Some research—albeit smaller, less compelling studies—suggests that bupropion may decrease anxiety.

If your patient suffers from comorbid depression and an anxiety disorder, bupropion would not be a first-line choice because it is not FDA-approved to treat anxiety disorders. Although it is possible that anxiety/agitation could result from bupropion use, there is not sufficient data to support its reputation as ”anxiogenic.”

What is your experience?

Do you agree with the authors? Send comments to [email protected] or share your thoughts on http://www.facebook.com/CurrentPsychiatry.

Related Resource

• American Psychiatric Association. Mixed anxiety-depressive disorder. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000:780-781.

Drug Brand Names

• Bupropion • Wellbutrin, Zyban
• Escitalopram • Lexapro
• Sertraline • Zoloft

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

For many clinicians, bupropion is the “go-to” medication for treating depressed patients who smoke, have concerns about sexual dysfunction side effects, and/or worry about weight gain. Bupropion is FDA-approved for preventing seasonal major depressive episodes in patients with seasonal affective disorder and is indicated as a smoking cessation aid.

“Anxious depression”—defined as depression with high levels of anxiety—is associated with poorer outcomes than “non-anxious” depression.¹ Prescribing medications for these patients can be challenging. Some clinicians believe that bupropion exacerbates anxiety and should not be used to treat patients who experience both anxiety and depression.

Reports from our patients and our cumulative clinical experience are key factors in developing expertise in selecting appropriate medications. When informing our patients about what to expect from medications, however, it can be useful to combine anecdotal evidence with knowledge of the facts or lack thereof. Are there data to support or contradict the idea that bupropion can cause anxiety while treating depression?

What the research shows

The drug manufacturer reports a “substantial proportion of patients treated with Wellbutrin experience some degree of increased restlessness, agitation, anxiety, and insomnia, especially shortly after initiation of treatment.”²

In 2001, Rush et al³ published the results of a 16-week study (n=248) assessing pre-treatment anxiety levels and response to sertraline or bupropion. The authors concluded that anxious and depressed patients who received sertraline didn’t experience a superior anxiolytic or antidepressant response compared with bupropion.³ The same authors came to similar conclusions in a retrospective analysis of a pair of 8-week randomized, controlled, double-blind trials of selective serotonin reuptake inhibitors (SSRIs) and bupropion.⁴

In 2001, Nieuwstraten et al⁵ compared bupropion with SSRIs for treating depression by reviewing several randomized, double-blind, controlled trials. The relative risk of developing “anxiety/agitation” was 1.32 (95% confidence interval, 0.85 to 2.04), which was not statistically significant.

In a 2008 meta-analysis, Papakostas et al⁶ pooled individual patient data from 10 randomized, double-blind, placebo-controlled trials. Their aim was to compare the efficacy of bupropion to SSRIs in treating “anxious depression.” They found no difference in timing or degree of improvement in anxiety symptoms between groups based on Hamilton Anxiety Scale or Hamilton Depression Rating Scale—Anxiety-Somatization (HDRS-AS) scores. The authors recommended that antidepressant choice should not be based on concerns about worsening anxiety symptoms in depressed patients.⁶

Another meta-analysis by Papakostas et al⁷ of the same 10 randomized, double-blind, placebo-controlled trials suggested SSRIs may confer an advantage over bupropion in treating a subset of patients with “anxious depression,” which they defined as a HDRS-AS score ≥7. The authors noted the advantage was statistically significant, although “modest.”

Other smaller studies suggest that bupropion does not increase anxiety.^8,9 A pilot study (N = 24, no placebo control) concluded that bupropion XL was comparable to escitalopram in treating anxiety in outpatients with generalized anxiety disorder.⁸

Because designing and executing drug trials can be expensive, it is not surprising that most of the evidence cited above derives from pharmaceutical company-sponsored or industry-affiliated work. As such, we should evaluate available evidence within the context of what we hear from and observe in our patients.

Our opinion

When assessing patients with depression and anxiety, we must carefully evaluate symptoms to distinguish between depression with associated anxiety symptoms and depression with a comorbid anxiety disorder.

If a patient suffers from depression with associated anxiety symptoms (“anxious depression”), keep in mind that although some data demonstrate a superior response to SSRIs, other studies show no difference in effect. Some research—albeit smaller, less compelling studies—suggests that bupropion may decrease anxiety.

If your patient suffers from comorbid depression and an anxiety disorder, bupropion would not be a first-line choice because it is not FDA-approved to treat anxiety disorders. Although it is possible that anxiety/agitation could result from bupropion use, there is not sufficient data to support its reputation as ”anxiogenic.”

What is your experience?

Do you agree with the authors? Send comments to [email protected] or share your thoughts on http://www.facebook.com/CurrentPsychiatry.

Related Resource

• American Psychiatric Association. Mixed anxiety-depressive disorder. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000:780-781.

Drug Brand Names

• Bupropion • Wellbutrin, Zyban
• Escitalopram • Lexapro
• Sertraline • Zoloft

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.