Current Psychiatry

Over 2 decades, carbamazepine has become a well-established, off-label alternative to lithium for treating acute mania. In December, the FDA approved an extended-release form of the anticonvulsant to treat type I bipolar disorder (Table 1).

This article addresses clinical use of extended-release capsules of carbamazepine (ERC-CBZ) and their safety, tolerability, and potential to interact with other medications.

Table 1

Extended-release capsules
of carbamazepine:
Fast facts

PHARMACOKINETICS

Because ERC-CBZ and carbamazepine yield similar molecules, the extended- and immediate-release forms have similar pharmacodynamic properties. There are notable pharmacokinetic differences, however.

With chronic use, carbamazepine autoinduces cytochrome P-450 (CYP) 3A4 hepatic enzymes. These enzymes rapidly break down carbamazepine to its active 10, 11-epoxide metabolite and the epoxide to the inactive diol. Because this sequence shortens carbamazepine’s half-life considerably—from 35 to 40 hours to 12 to 17 hours after 2 to 3 weeks of use—multiple daily dosing and minor dosage increases often are needed to maintain carbamazepine blood levels. Also, with immediate-release carbamazepine’s peak/trough variations, transient side effects such as ataxia, dizziness, or diplopia may emerge 2 to 3 hours after dosing once steady state is reached.

By contrast, ERC-CBZ should be more tolerable and easier to use because it smooths out these variations. Although studies of ERC-CBZ in mania have examined twice-daily dosing, using once-nightly dosing instead (starting at 200 mg) will harness carbamazepine’s sedative and other side effects to promote sleep onset, and lower levels throughout the day will further increase its tolerability.¹ Patients who experience breakthrough afternoon or evening manic symptoms with once-nightly dosing can be returned to twice-daily dosing.

EFFICACY IN BIPOLAR DISORDER

ERC-CBZ has shown efficacy for treating bipolar disorder in three studies,^2,3,4 including two large double-blind, placebo-controlled, multi-center trials that followed patients with type I bipolar disorder with current manic or mixed episodes.

In the first trial,² 204 patients received ERC-CBZ, 400 to 1,600 mg/d (mean±SD daily dosage 756.4±413.4 mg/d, mean plasma level 8.9 μg/mL), or placebo for 3 weeks. Young Mania Rating Scale (YMRS) scores decreased 50% in 41.5% of the treatment group and in 22.4% of the placebo group. Hamilton Rating Scale for Depression (HAM-D) scores decreased more in the ERC-CBZ group, but the difference was not clinically significant.

In a second trial of 239 patients,³ YMRS scores fell 50% across 3 weeks in 60.8% of those taking ERC-CBZ, 400 to 1,600 mg/d (mean±SD dosage 642±369.2 mg/d), compared with 28.7% of placebotreated patients. HAM-D total scores also improved significantly in ERC-CBZ-treated patients compared with the placebo group in a subanalysis of 188 intent-to-treat patients with a manic episode.

In a 6-month extension following 92 patients from two double-blind trials,⁴ mean total YMRS scores decreased among former placebo group patients switched to open-label ERC-CBZ, 200 to 1,600 mg/d (mean dosage 938 mg, mean serum level 6.6 μg/mL). Patients who had taken ERC-CBZ during the acute trial saw little change in YMRS scores during continued ERC-CBZ treatment, except in the second month. At end point, however, YMRS scores fell further for both treatment groups. HAM-D total scores differed little across 6 months, but 54 patients with mixed states maintained significant reductions.

Maintenance therapy. In many studies, carbamazepine has compared favorably with lithium for long-term bipolar maintenance in some patients. Consider patients who respond well to acute carbamazepine therapy for continuation treatment with ERC-CBZ. Patients who may be most likely to respond to carbamazepine therapy include those with:

• type II bipolar disorder
• substance abuse comorbidity
• mood-incongruent delusions
• no family history of bipolar illness among first-degree relatives.⁵

Contraindications (such as use during pregnancy or breast-feeding) are the same for extended- and immediate-release carbamazepine.

TOLERABILITY

Carbamazepine in any form can cause a range of common to rare side effects (Table 2), which have been reviewed elsewhere.^4-6

Side effects of ERC-CBZ most commonly reported during the double-blind, placebo-controlled studies include dizziness, nausea, somnolence, headache, vomiting, dyspepsia, dry mouth, pruritus, and benign rash. Slower upward titration of single nighttime doses—instead of the twice-daily dosing used in these studies—could prevent most of these effects.

Only one patient in either study developed a serious side effect possibly related to ERC-CBZ (fever with rash); the rash resolved 6 days after the drug was stopped.

Total cholesterol in patients taking ERC-CBZ also rose 12% to 13% in the double-blind studies.^2,3 Consider dietary and/or cholesterol-lowering medications in patients taking ERC-CBZ who are at high risk for cardiovascular events.

In the 6-month open-label study, headache, dizziness, and benign rash were most frequently reported. No serious adverse events related to the study drug were reported.

Table 2

Carbamazepine’s common to rare side effects

INTERACTIONS WITH OTHER MEDICATIONS

Because of its potent induction of CYP 3A4 enzymes,⁶ carbamazepine in any form may substantially lower blood levels of several compounds metabolized principally by CYP 3A4 isoenzymes (Table 3), including typical antipsychotics such as haloperidol and the atypical antipsychotic aripiprazole. Even so, patients often improve with combination carbamazepine/haloperidol therapy despite lower haloperidol blood levels.

If a patient is taking oral contraceptives, inform her primary care physician or OB/GYN when prescribing carbamazepine. Because the anticonvulsant lowers circulating estrogen, a higher contraceptive dosage or alternate birth-control method should be considered to prevent unwanted pregnancy.

Most other drug-drug interactions have been well-delineated and can be avoided. Inform the patient and his or her primary care physician when giving carbamazepine concomitantly with any drug.

Numerous medications can also increase serum carbamazepine levels, causing problems in a patient already near his or her side-effect threshold (Table 4). Reduce the carbamazepine dosage to avoid these adverse effects.

Table 3

Carbamazepine decreases serum concentrations of these drugs

Table 4

These drugs increase serum carbamazepine and may cause toxicity

CLINICAL IMPLICATIONS

Long-acting carbamazepine suitable for single nighttime dosing should facilitate adherence and reduce daytime side effects. Consider ERC-CBZ for patients not responding adequately to lithium or valproate, as individual response to any of these three drugs can vary greatly. Sideeffect tolerability (such as less weight gain with carbamazepine than with valproate) also could help guide drug choice. In patients with rapid cycling, carbamazepine plus lithium may be more effective than either drug alone.

New data suggest that carbamazepine offers acute antidepressant effects in some individuals and in long-term depression treatment.⁵ More research is needed to identify depressed patients most likely to respond to this agent.

For now, when using ERC-CBZ, we can draw from the larger experience with immediate-release carbamazepine to treat epilepsy, bipolar disorder, and related mood disorders. Once you master carbamazepine’s pharmacokinetic interactions with other commonly used agents, ERC-CBZ in slowly titrated, single nighttime dosages should simplify the compound’s administration and tolerability.

Related resources

• Carbamazepine (extended-release) Web site. www.equetro.com.
• Post RM, Speer AM, Obrocea GV, Leverich GS. Acute and prophylactic effects of anticonvulsants in bipolar depression. Clin Neurosci Res 2002;2:228-51.
• Denicoff KD, Smith-Jackson EE, Disney ER, et al. Comparative prophylactic efficacy of lithium, carbamazepine, and the combination in bipolar disorder. J Clin Psychiatry 1997;58:470-8.

Drug brand names

• Aripiprazole • Abilify
• Carbamazepine (extended-release) • Equetro
• Carbamazepine (immediate-release) • Tegretol, others
• Haloperidol • Haldol
• Lithium • Eskalith, others
• Valproate • Depakote

Disclosure

Dr. Post reports no current financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Over 2 decades, carbamazepine has become a well-established, off-label alternative to lithium for treating acute mania. In December, the FDA approved an extended-release form of the anticonvulsant to treat type I bipolar disorder (Table 1).

This article addresses clinical use of extended-release capsules of carbamazepine (ERC-CBZ) and their safety, tolerability, and potential to interact with other medications.

Table 1

Extended-release capsules
of carbamazepine:
Fast facts

PHARMACOKINETICS

Because ERC-CBZ and carbamazepine yield similar molecules, the extended- and immediate-release forms have similar pharmacodynamic properties. There are notable pharmacokinetic differences, however.

With chronic use, carbamazepine autoinduces cytochrome P-450 (CYP) 3A4 hepatic enzymes. These enzymes rapidly break down carbamazepine to its active 10, 11-epoxide metabolite and the epoxide to the inactive diol. Because this sequence shortens carbamazepine’s half-life considerably—from 35 to 40 hours to 12 to 17 hours after 2 to 3 weeks of use—multiple daily dosing and minor dosage increases often are needed to maintain carbamazepine blood levels. Also, with immediate-release carbamazepine’s peak/trough variations, transient side effects such as ataxia, dizziness, or diplopia may emerge 2 to 3 hours after dosing once steady state is reached.

By contrast, ERC-CBZ should be more tolerable and easier to use because it smooths out these variations. Although studies of ERC-CBZ in mania have examined twice-daily dosing, using once-nightly dosing instead (starting at 200 mg) will harness carbamazepine’s sedative and other side effects to promote sleep onset, and lower levels throughout the day will further increase its tolerability.¹ Patients who experience breakthrough afternoon or evening manic symptoms with once-nightly dosing can be returned to twice-daily dosing.

EFFICACY IN BIPOLAR DISORDER

ERC-CBZ has shown efficacy for treating bipolar disorder in three studies,^2,3,4 including two large double-blind, placebo-controlled, multi-center trials that followed patients with type I bipolar disorder with current manic or mixed episodes.

In the first trial,² 204 patients received ERC-CBZ, 400 to 1,600 mg/d (mean±SD daily dosage 756.4±413.4 mg/d, mean plasma level 8.9 μg/mL), or placebo for 3 weeks. Young Mania Rating Scale (YMRS) scores decreased 50% in 41.5% of the treatment group and in 22.4% of the placebo group. Hamilton Rating Scale for Depression (HAM-D) scores decreased more in the ERC-CBZ group, but the difference was not clinically significant.

In a second trial of 239 patients,³ YMRS scores fell 50% across 3 weeks in 60.8% of those taking ERC-CBZ, 400 to 1,600 mg/d (mean±SD dosage 642±369.2 mg/d), compared with 28.7% of placebotreated patients. HAM-D total scores also improved significantly in ERC-CBZ-treated patients compared with the placebo group in a subanalysis of 188 intent-to-treat patients with a manic episode.

In a 6-month extension following 92 patients from two double-blind trials,⁴ mean total YMRS scores decreased among former placebo group patients switched to open-label ERC-CBZ, 200 to 1,600 mg/d (mean dosage 938 mg, mean serum level 6.6 μg/mL). Patients who had taken ERC-CBZ during the acute trial saw little change in YMRS scores during continued ERC-CBZ treatment, except in the second month. At end point, however, YMRS scores fell further for both treatment groups. HAM-D total scores differed little across 6 months, but 54 patients with mixed states maintained significant reductions.

Maintenance therapy. In many studies, carbamazepine has compared favorably with lithium for long-term bipolar maintenance in some patients. Consider patients who respond well to acute carbamazepine therapy for continuation treatment with ERC-CBZ. Patients who may be most likely to respond to carbamazepine therapy include those with:

• type II bipolar disorder
• substance abuse comorbidity
• mood-incongruent delusions
• no family history of bipolar illness among first-degree relatives.⁵

Contraindications (such as use during pregnancy or breast-feeding) are the same for extended- and immediate-release carbamazepine.

TOLERABILITY

Carbamazepine in any form can cause a range of common to rare side effects (Table 2), which have been reviewed elsewhere.^4-6

Side effects of ERC-CBZ most commonly reported during the double-blind, placebo-controlled studies include dizziness, nausea, somnolence, headache, vomiting, dyspepsia, dry mouth, pruritus, and benign rash. Slower upward titration of single nighttime doses—instead of the twice-daily dosing used in these studies—could prevent most of these effects.

Only one patient in either study developed a serious side effect possibly related to ERC-CBZ (fever with rash); the rash resolved 6 days after the drug was stopped.

Total cholesterol in patients taking ERC-CBZ also rose 12% to 13% in the double-blind studies.^2,3 Consider dietary and/or cholesterol-lowering medications in patients taking ERC-CBZ who are at high risk for cardiovascular events.

In the 6-month open-label study, headache, dizziness, and benign rash were most frequently reported. No serious adverse events related to the study drug were reported.

Table 2

Carbamazepine’s common to rare side effects

INTERACTIONS WITH OTHER MEDICATIONS

Because of its potent induction of CYP 3A4 enzymes,⁶ carbamazepine in any form may substantially lower blood levels of several compounds metabolized principally by CYP 3A4 isoenzymes (Table 3), including typical antipsychotics such as haloperidol and the atypical antipsychotic aripiprazole. Even so, patients often improve with combination carbamazepine/haloperidol therapy despite lower haloperidol blood levels.

If a patient is taking oral contraceptives, inform her primary care physician or OB/GYN when prescribing carbamazepine. Because the anticonvulsant lowers circulating estrogen, a higher contraceptive dosage or alternate birth-control method should be considered to prevent unwanted pregnancy.

Most other drug-drug interactions have been well-delineated and can be avoided. Inform the patient and his or her primary care physician when giving carbamazepine concomitantly with any drug.

Numerous medications can also increase serum carbamazepine levels, causing problems in a patient already near his or her side-effect threshold (Table 4). Reduce the carbamazepine dosage to avoid these adverse effects.

Table 3

Carbamazepine decreases serum concentrations of these drugs

Table 4

These drugs increase serum carbamazepine and may cause toxicity

CLINICAL IMPLICATIONS

Long-acting carbamazepine suitable for single nighttime dosing should facilitate adherence and reduce daytime side effects. Consider ERC-CBZ for patients not responding adequately to lithium or valproate, as individual response to any of these three drugs can vary greatly. Sideeffect tolerability (such as less weight gain with carbamazepine than with valproate) also could help guide drug choice. In patients with rapid cycling, carbamazepine plus lithium may be more effective than either drug alone.

New data suggest that carbamazepine offers acute antidepressant effects in some individuals and in long-term depression treatment.⁵ More research is needed to identify depressed patients most likely to respond to this agent.

For now, when using ERC-CBZ, we can draw from the larger experience with immediate-release carbamazepine to treat epilepsy, bipolar disorder, and related mood disorders. Once you master carbamazepine’s pharmacokinetic interactions with other commonly used agents, ERC-CBZ in slowly titrated, single nighttime dosages should simplify the compound’s administration and tolerability.

Related resources

• Carbamazepine (extended-release) Web site. www.equetro.com.
• Post RM, Speer AM, Obrocea GV, Leverich GS. Acute and prophylactic effects of anticonvulsants in bipolar depression. Clin Neurosci Res 2002;2:228-51.
• Denicoff KD, Smith-Jackson EE, Disney ER, et al. Comparative prophylactic efficacy of lithium, carbamazepine, and the combination in bipolar disorder. J Clin Psychiatry 1997;58:470-8.

Drug brand names

• Aripiprazole • Abilify
• Carbamazepine (extended-release) • Equetro
• Carbamazepine (immediate-release) • Tegretol, others
• Haloperidol • Haldol
• Lithium • Eskalith, others
• Valproate • Depakote

Disclosure

Dr. Post reports no current financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

Over 2 decades, carbamazepine has become a well-established, off-label alternative to lithium for treating acute mania. In December, the FDA approved an extended-release form of the anticonvulsant to treat type I bipolar disorder (Table 1).

This article addresses clinical use of extended-release capsules of carbamazepine (ERC-CBZ) and their safety, tolerability, and potential to interact with other medications.

Table 1

Extended-release capsules
of carbamazepine:
Fast facts

PHARMACOKINETICS

Because ERC-CBZ and carbamazepine yield similar molecules, the extended- and immediate-release forms have similar pharmacodynamic properties. There are notable pharmacokinetic differences, however.

With chronic use, carbamazepine autoinduces cytochrome P-450 (CYP) 3A4 hepatic enzymes. These enzymes rapidly break down carbamazepine to its active 10, 11-epoxide metabolite and the epoxide to the inactive diol. Because this sequence shortens carbamazepine’s half-life considerably—from 35 to 40 hours to 12 to 17 hours after 2 to 3 weeks of use—multiple daily dosing and minor dosage increases often are needed to maintain carbamazepine blood levels. Also, with immediate-release carbamazepine’s peak/trough variations, transient side effects such as ataxia, dizziness, or diplopia may emerge 2 to 3 hours after dosing once steady state is reached.

By contrast, ERC-CBZ should be more tolerable and easier to use because it smooths out these variations. Although studies of ERC-CBZ in mania have examined twice-daily dosing, using once-nightly dosing instead (starting at 200 mg) will harness carbamazepine’s sedative and other side effects to promote sleep onset, and lower levels throughout the day will further increase its tolerability.¹ Patients who experience breakthrough afternoon or evening manic symptoms with once-nightly dosing can be returned to twice-daily dosing.

EFFICACY IN BIPOLAR DISORDER

ERC-CBZ has shown efficacy for treating bipolar disorder in three studies,^2,3,4 including two large double-blind, placebo-controlled, multi-center trials that followed patients with type I bipolar disorder with current manic or mixed episodes.

In the first trial,² 204 patients received ERC-CBZ, 400 to 1,600 mg/d (mean±SD daily dosage 756.4±413.4 mg/d, mean plasma level 8.9 μg/mL), or placebo for 3 weeks. Young Mania Rating Scale (YMRS) scores decreased 50% in 41.5% of the treatment group and in 22.4% of the placebo group. Hamilton Rating Scale for Depression (HAM-D) scores decreased more in the ERC-CBZ group, but the difference was not clinically significant.

In a second trial of 239 patients,³ YMRS scores fell 50% across 3 weeks in 60.8% of those taking ERC-CBZ, 400 to 1,600 mg/d (mean±SD dosage 642±369.2 mg/d), compared with 28.7% of placebotreated patients. HAM-D total scores also improved significantly in ERC-CBZ-treated patients compared with the placebo group in a subanalysis of 188 intent-to-treat patients with a manic episode.

In a 6-month extension following 92 patients from two double-blind trials,⁴ mean total YMRS scores decreased among former placebo group patients switched to open-label ERC-CBZ, 200 to 1,600 mg/d (mean dosage 938 mg, mean serum level 6.6 μg/mL). Patients who had taken ERC-CBZ during the acute trial saw little change in YMRS scores during continued ERC-CBZ treatment, except in the second month. At end point, however, YMRS scores fell further for both treatment groups. HAM-D total scores differed little across 6 months, but 54 patients with mixed states maintained significant reductions.

Maintenance therapy. In many studies, carbamazepine has compared favorably with lithium for long-term bipolar maintenance in some patients. Consider patients who respond well to acute carbamazepine therapy for continuation treatment with ERC-CBZ. Patients who may be most likely to respond to carbamazepine therapy include those with:

• type II bipolar disorder
• substance abuse comorbidity
• mood-incongruent delusions
• no family history of bipolar illness among first-degree relatives.⁵

Contraindications (such as use during pregnancy or breast-feeding) are the same for extended- and immediate-release carbamazepine.

TOLERABILITY

Carbamazepine in any form can cause a range of common to rare side effects (Table 2), which have been reviewed elsewhere.^4-6

Side effects of ERC-CBZ most commonly reported during the double-blind, placebo-controlled studies include dizziness, nausea, somnolence, headache, vomiting, dyspepsia, dry mouth, pruritus, and benign rash. Slower upward titration of single nighttime doses—instead of the twice-daily dosing used in these studies—could prevent most of these effects.

Only one patient in either study developed a serious side effect possibly related to ERC-CBZ (fever with rash); the rash resolved 6 days after the drug was stopped.

Total cholesterol in patients taking ERC-CBZ also rose 12% to 13% in the double-blind studies.^2,3 Consider dietary and/or cholesterol-lowering medications in patients taking ERC-CBZ who are at high risk for cardiovascular events.

In the 6-month open-label study, headache, dizziness, and benign rash were most frequently reported. No serious adverse events related to the study drug were reported.

Table 2

Carbamazepine’s common to rare side effects

INTERACTIONS WITH OTHER MEDICATIONS

Because of its potent induction of CYP 3A4 enzymes,⁶ carbamazepine in any form may substantially lower blood levels of several compounds metabolized principally by CYP 3A4 isoenzymes (Table 3), including typical antipsychotics such as haloperidol and the atypical antipsychotic aripiprazole. Even so, patients often improve with combination carbamazepine/haloperidol therapy despite lower haloperidol blood levels.

If a patient is taking oral contraceptives, inform her primary care physician or OB/GYN when prescribing carbamazepine. Because the anticonvulsant lowers circulating estrogen, a higher contraceptive dosage or alternate birth-control method should be considered to prevent unwanted pregnancy.

Most other drug-drug interactions have been well-delineated and can be avoided. Inform the patient and his or her primary care physician when giving carbamazepine concomitantly with any drug.

Numerous medications can also increase serum carbamazepine levels, causing problems in a patient already near his or her side-effect threshold (Table 4). Reduce the carbamazepine dosage to avoid these adverse effects.

Table 3

Carbamazepine decreases serum concentrations of these drugs

Table 4

These drugs increase serum carbamazepine and may cause toxicity

CLINICAL IMPLICATIONS

Long-acting carbamazepine suitable for single nighttime dosing should facilitate adherence and reduce daytime side effects. Consider ERC-CBZ for patients not responding adequately to lithium or valproate, as individual response to any of these three drugs can vary greatly. Sideeffect tolerability (such as less weight gain with carbamazepine than with valproate) also could help guide drug choice. In patients with rapid cycling, carbamazepine plus lithium may be more effective than either drug alone.

New data suggest that carbamazepine offers acute antidepressant effects in some individuals and in long-term depression treatment.⁵ More research is needed to identify depressed patients most likely to respond to this agent.

For now, when using ERC-CBZ, we can draw from the larger experience with immediate-release carbamazepine to treat epilepsy, bipolar disorder, and related mood disorders. Once you master carbamazepine’s pharmacokinetic interactions with other commonly used agents, ERC-CBZ in slowly titrated, single nighttime dosages should simplify the compound’s administration and tolerability.

Related resources

• Carbamazepine (extended-release) Web site. www.equetro.com.
• Post RM, Speer AM, Obrocea GV, Leverich GS. Acute and prophylactic effects of anticonvulsants in bipolar depression. Clin Neurosci Res 2002;2:228-51.
• Denicoff KD, Smith-Jackson EE, Disney ER, et al. Comparative prophylactic efficacy of lithium, carbamazepine, and the combination in bipolar disorder. J Clin Psychiatry 1997;58:470-8.

Drug brand names

• Aripiprazole • Abilify
• Carbamazepine (extended-release) • Equetro
• Carbamazepine (immediate-release) • Tegretol, others
• Haloperidol • Haldol
• Lithium • Eskalith, others
• Valproate • Depakote

Disclosure

Dr. Post reports no current financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.

When evaluating a patient diagnosed as having a “refractory” mental disorder, ask yourself:

• Is the working diagnosis correct?
  
• Could another undiagnosed condition be hindering response to treatment?
  
• Is the patient adhering to his or her prescribed treatment?
  
• Have prior medication trials used adequate dosages and durations?
  

For example, in a patient diagnosed with “refractory depression,” undiagnosed bipolar depression may explain the lack of response to antidepressant monotherapy. An undiagnosed general medical condition, such as hypothyroidism, would also explain the lack of response.

Also consider the effects of a comorbid psychiatric disorder. Anxiety, substance use, and personality disorders are common in patients with “refractory” depression.

Addressing nonadherence

Always suspect nonadherence—a frequent problem among patients with mental disorders—when assessing a “refractory” condition.^1,2 Collateral sources of information such as family, friends, and previous inpatient and outpatient psychiatrists can help clarify this issue when the patient’s account seems unreliable.

If the patient is not adhering to prescribed medication, re-evaluate your therapeutic alliance by considering these questions:

• Has the patient seemed comfortable and open during recent sessions?
  
• Has he or she been able to discuss emotionally laden material that might lead to shame or guilt?
  
• Did the patient maintain eye contact and respond appropriately to questions and observations?
  

If the patient has been following the treatment plan but complains of persistent symptoms, verify that an adequate dosage (often the maximum recommended) and duration (at least 4 to 6 weeks for major depression) of medication have been prescribed. Also assess the adequacy of any psychotherapy.³

When evaluating a patient diagnosed as having a “refractory” mental disorder, ask yourself:

• Is the working diagnosis correct?
  
• Could another undiagnosed condition be hindering response to treatment?
  
• Is the patient adhering to his or her prescribed treatment?
  
• Have prior medication trials used adequate dosages and durations?
  

For example, in a patient diagnosed with “refractory depression,” undiagnosed bipolar depression may explain the lack of response to antidepressant monotherapy. An undiagnosed general medical condition, such as hypothyroidism, would also explain the lack of response.

Also consider the effects of a comorbid psychiatric disorder. Anxiety, substance use, and personality disorders are common in patients with “refractory” depression.

Addressing nonadherence

Always suspect nonadherence—a frequent problem among patients with mental disorders—when assessing a “refractory” condition.^1,2 Collateral sources of information such as family, friends, and previous inpatient and outpatient psychiatrists can help clarify this issue when the patient’s account seems unreliable.

If the patient is not adhering to prescribed medication, re-evaluate your therapeutic alliance by considering these questions:

• Has the patient seemed comfortable and open during recent sessions?
  
• Has he or she been able to discuss emotionally laden material that might lead to shame or guilt?
  
• Did the patient maintain eye contact and respond appropriately to questions and observations?
  

If the patient has been following the treatment plan but complains of persistent symptoms, verify that an adequate dosage (often the maximum recommended) and duration (at least 4 to 6 weeks for major depression) of medication have been prescribed. Also assess the adequacy of any psychotherapy.³

When evaluating a patient diagnosed as having a “refractory” mental disorder, ask yourself:

• Is the working diagnosis correct?
  
• Could another undiagnosed condition be hindering response to treatment?
  
• Is the patient adhering to his or her prescribed treatment?
  
• Have prior medication trials used adequate dosages and durations?
  

For example, in a patient diagnosed with “refractory depression,” undiagnosed bipolar depression may explain the lack of response to antidepressant monotherapy. An undiagnosed general medical condition, such as hypothyroidism, would also explain the lack of response.

Also consider the effects of a comorbid psychiatric disorder. Anxiety, substance use, and personality disorders are common in patients with “refractory” depression.

Addressing nonadherence

Always suspect nonadherence—a frequent problem among patients with mental disorders—when assessing a “refractory” condition.^1,2 Collateral sources of information such as family, friends, and previous inpatient and outpatient psychiatrists can help clarify this issue when the patient’s account seems unreliable.

If the patient is not adhering to prescribed medication, re-evaluate your therapeutic alliance by considering these questions:

• Has the patient seemed comfortable and open during recent sessions?
  
• Has he or she been able to discuss emotionally laden material that might lead to shame or guilt?
  
• Did the patient maintain eye contact and respond appropriately to questions and observations?
  

If the patient has been following the treatment plan but complains of persistent symptoms, verify that an adequate dosage (often the maximum recommended) and duration (at least 4 to 6 weeks for major depression) of medication have been prescribed. Also assess the adequacy of any psychotherapy.³

Many thanks for your warm welcome to me and my advanced practice nurse colleagues (Current Psychiatry, January 2005).

Nurses and physicians have long been partnering to care for patients with mental illness. Old habits die hard, however, and much needs to be done professionally and collegially to address boundary issues and physicians’ concerns regarding nurses with diagnostic and prescriptive authority.

Cathy Phillips MS, CS, APRN-BC
Lanning Center for Behavioral Services
Hastings, NE

Many thanks for your warm welcome to me and my advanced practice nurse colleagues (Current Psychiatry, January 2005).

Nurses and physicians have long been partnering to care for patients with mental illness. Old habits die hard, however, and much needs to be done professionally and collegially to address boundary issues and physicians’ concerns regarding nurses with diagnostic and prescriptive authority.

Cathy Phillips MS, CS, APRN-BC
Lanning Center for Behavioral Services
Hastings, NE

Many thanks for your warm welcome to me and my advanced practice nurse colleagues (Current Psychiatry, January 2005).

Nurses and physicians have long been partnering to care for patients with mental illness. Old habits die hard, however, and much needs to be done professionally and collegially to address boundary issues and physicians’ concerns regarding nurses with diagnostic and prescriptive authority.

Cathy Phillips MS, CS, APRN-BC
Lanning Center for Behavioral Services
Hastings, NE

“Prudent Prescribing” by Drs. Richard Rosse and Stephen Deutsch (Current Psychiatry, October 2004) offers valuable advice about when psychiatrists should start medical workups. I have some additional thoughts.

Indications for a medical workup. The authors illuminated the need for medical testing for patients with clozapine complications, long-term complications of atypical antipsychotics, and health problems secondary to substance abuse. Psychiatrists also might be called upon to initiate or arrange for a medical evaluation in other situations, such as when:

• the patient presents in compromised health and has no primary care doctor
  
• the patient presents with a seemingly acute medical condition or reports such a problem over the phone
  
• the patient is acutely medically ill and his or her primary care doctor cannot be reached
  
• an acutely ill patient has no health insurance
  
• the patient fears going to the emergency room.
  

Psychiatry is ‘primary care.’ The National Health Service Corps considers psychiatry a primary care specialty. At times, we perform a “physician extender” role when collaborating with medical colleagues. Whereas in large multispecialty groups our role may be more narrowly defined, we may need to employ a far broader range of medical skills in private practice and even more so in treating underserved populations.

We are fully licensed physicians with the same training in basic clinical diagnosis as our colleagues in other specialties. It is our duty to distinguish organic from functional causes of psychiatric presentations to move our patients toward definitive care.

Medical screening tests. The authors listed several medical tests psychiatrists might order. That list should also include:

• antinuclear antibody and erythrocyte sedimentation rate tests, because autoimmune conditions often have psychiatric presentations
  
• hormone level testing for women, as perimenopause and menopause can have an enormous emotional impact
  
• mononucleosis spot test/Epstein-Barr virus titers, because mononucleosis can present with depression.
  

‘Turf’ issues. Because we see many patients more frequently than do our medical colleagues, we might be the first to spot a medical problem. A psychiatrist might be the only clinician with whom the patient is willing to discuss fears about the symptom—or the only clinician a paranoid patient will agree to see, period.

We must retain the right to start basic diagnostic workup and convey findings promptly to our medical colleagues without “turf” issues or threats of peer review for “overstepping our bounds.”

Sara Epstein, MD
Los Angeles, CA

“Prudent Prescribing” by Drs. Richard Rosse and Stephen Deutsch (Current Psychiatry, October 2004) offers valuable advice about when psychiatrists should start medical workups. I have some additional thoughts.

Indications for a medical workup. The authors illuminated the need for medical testing for patients with clozapine complications, long-term complications of atypical antipsychotics, and health problems secondary to substance abuse. Psychiatrists also might be called upon to initiate or arrange for a medical evaluation in other situations, such as when:

• the patient presents in compromised health and has no primary care doctor
  
• the patient presents with a seemingly acute medical condition or reports such a problem over the phone
  
• the patient is acutely medically ill and his or her primary care doctor cannot be reached
  
• an acutely ill patient has no health insurance
  
• the patient fears going to the emergency room.
  

Psychiatry is ‘primary care.’ The National Health Service Corps considers psychiatry a primary care specialty. At times, we perform a “physician extender” role when collaborating with medical colleagues. Whereas in large multispecialty groups our role may be more narrowly defined, we may need to employ a far broader range of medical skills in private practice and even more so in treating underserved populations.

We are fully licensed physicians with the same training in basic clinical diagnosis as our colleagues in other specialties. It is our duty to distinguish organic from functional causes of psychiatric presentations to move our patients toward definitive care.

Medical screening tests. The authors listed several medical tests psychiatrists might order. That list should also include:

• antinuclear antibody and erythrocyte sedimentation rate tests, because autoimmune conditions often have psychiatric presentations
  
• hormone level testing for women, as perimenopause and menopause can have an enormous emotional impact
  
• mononucleosis spot test/Epstein-Barr virus titers, because mononucleosis can present with depression.
  

‘Turf’ issues. Because we see many patients more frequently than do our medical colleagues, we might be the first to spot a medical problem. A psychiatrist might be the only clinician with whom the patient is willing to discuss fears about the symptom—or the only clinician a paranoid patient will agree to see, period.

We must retain the right to start basic diagnostic workup and convey findings promptly to our medical colleagues without “turf” issues or threats of peer review for “overstepping our bounds.”

Sara Epstein, MD
Los Angeles, CA

“Prudent Prescribing” by Drs. Richard Rosse and Stephen Deutsch (Current Psychiatry, October 2004) offers valuable advice about when psychiatrists should start medical workups. I have some additional thoughts.

Indications for a medical workup. The authors illuminated the need for medical testing for patients with clozapine complications, long-term complications of atypical antipsychotics, and health problems secondary to substance abuse. Psychiatrists also might be called upon to initiate or arrange for a medical evaluation in other situations, such as when:

• the patient presents in compromised health and has no primary care doctor
  
• the patient presents with a seemingly acute medical condition or reports such a problem over the phone
  
• the patient is acutely medically ill and his or her primary care doctor cannot be reached
  
• an acutely ill patient has no health insurance
  
• the patient fears going to the emergency room.
  

Psychiatry is ‘primary care.’ The National Health Service Corps considers psychiatry a primary care specialty. At times, we perform a “physician extender” role when collaborating with medical colleagues. Whereas in large multispecialty groups our role may be more narrowly defined, we may need to employ a far broader range of medical skills in private practice and even more so in treating underserved populations.

We are fully licensed physicians with the same training in basic clinical diagnosis as our colleagues in other specialties. It is our duty to distinguish organic from functional causes of psychiatric presentations to move our patients toward definitive care.

Medical screening tests. The authors listed several medical tests psychiatrists might order. That list should also include:

• antinuclear antibody and erythrocyte sedimentation rate tests, because autoimmune conditions often have psychiatric presentations
  
• hormone level testing for women, as perimenopause and menopause can have an enormous emotional impact
  
• mononucleosis spot test/Epstein-Barr virus titers, because mononucleosis can present with depression.
  

‘Turf’ issues. Because we see many patients more frequently than do our medical colleagues, we might be the first to spot a medical problem. A psychiatrist might be the only clinician with whom the patient is willing to discuss fears about the symptom—or the only clinician a paranoid patient will agree to see, period.

We must retain the right to start basic diagnostic workup and convey findings promptly to our medical colleagues without “turf” issues or threats of peer review for “overstepping our bounds.”

Sara Epstein, MD
Los Angeles, CA

Dr. Susan Stern’s comments on the role of psychotherapy in her psychiatric practice may have inadvertently foreshadowed psychiatry’s demise as a profession (“Pearls: Treatment resistance? Try psychotherapy,” Current Psychiatry, February 2005).

Dr. Stern shared the story of Mrs. H, who has had depression nearly half her life. The patient’s condition persisted despite numerous antidepressants across several classes. Dr. Stern then tried “several medication augmentation strategies” to alleviate the depression, but nothing worked.

“Finally,” Dr. Stern explained, as if she had exhausted all obvious and reasonable options, “I left her medications alone and listened to her story.”

Excuse me, but had Dr. Stern not realized that Mrs. H’s story might be relevant—even central—to her 20-year battle with depression and to her recovery? If this is a revelation, then psychiatry is on life support.

Too many psychiatrists have stopped listening to their patients and have become obsessed with finding the right drug augmentation strategy. Yet as Dr. Stern’s piece amply demonstrates, a prescribe-first-and-ask-questions-later approach spells almost certain failure—if not disaster—for both the patient and profession.

Although psychotropics have their place, psychiatry’s greatest legacy—the healing power of the doctor-patient relationship—has been allowed to slip silently beneath the waves. Your patients are hurting and they need you, not just your drugs. Put down your pens, close your mouths, and open your ears and hearts. Listen with your “third ear,” as Theodor Reik implored. The results will amaze you.

Barry D. Berger, PhD
Clinical psychologist and president
Mission Psychological Center, Mission, TX

Dr. Stern responds

Dr. Berger’s response to my Pearls article indicates a growing view that psychiatrists in general use medications first to treat depression, with psychotherapy as a mere afterthought. Most psychiatrists I know, however, are interested in doing what they feel is right for the patient, whatever the treatment modality.

A desire to institute or change medications early in the therapeutic process may stem from various sources, including the acuity of the patient’s clinical situation (in which not addressing a patient’s medications would be considered negligent).

Patients often expect psychopharmacologic intervention when they see a psychiatrist. Whether this attitude stems from a fantasy of “instant cure” or is simply a resistance to self-exploration, we should use every means available to address their suffering. The purpose of my article was to illustrate that patients who are considered “refractory” or “resistant” to medications can still be responsive to psychotherapy.

Susan Stern, MD
Instructor in psychiatry
Columbia University College of Physicians and Surgeons
New York, NY

Dr. Susan Stern’s comments on the role of psychotherapy in her psychiatric practice may have inadvertently foreshadowed psychiatry’s demise as a profession (“Pearls: Treatment resistance? Try psychotherapy,” Current Psychiatry, February 2005).

Dr. Stern shared the story of Mrs. H, who has had depression nearly half her life. The patient’s condition persisted despite numerous antidepressants across several classes. Dr. Stern then tried “several medication augmentation strategies” to alleviate the depression, but nothing worked.

“Finally,” Dr. Stern explained, as if she had exhausted all obvious and reasonable options, “I left her medications alone and listened to her story.”

Excuse me, but had Dr. Stern not realized that Mrs. H’s story might be relevant—even central—to her 20-year battle with depression and to her recovery? If this is a revelation, then psychiatry is on life support.

Too many psychiatrists have stopped listening to their patients and have become obsessed with finding the right drug augmentation strategy. Yet as Dr. Stern’s piece amply demonstrates, a prescribe-first-and-ask-questions-later approach spells almost certain failure—if not disaster—for both the patient and profession.

Although psychotropics have their place, psychiatry’s greatest legacy—the healing power of the doctor-patient relationship—has been allowed to slip silently beneath the waves. Your patients are hurting and they need you, not just your drugs. Put down your pens, close your mouths, and open your ears and hearts. Listen with your “third ear,” as Theodor Reik implored. The results will amaze you.

Barry D. Berger, PhD
Clinical psychologist and president
Mission Psychological Center, Mission, TX

Dr. Stern responds

Dr. Berger’s response to my Pearls article indicates a growing view that psychiatrists in general use medications first to treat depression, with psychotherapy as a mere afterthought. Most psychiatrists I know, however, are interested in doing what they feel is right for the patient, whatever the treatment modality.

A desire to institute or change medications early in the therapeutic process may stem from various sources, including the acuity of the patient’s clinical situation (in which not addressing a patient’s medications would be considered negligent).

Patients often expect psychopharmacologic intervention when they see a psychiatrist. Whether this attitude stems from a fantasy of “instant cure” or is simply a resistance to self-exploration, we should use every means available to address their suffering. The purpose of my article was to illustrate that patients who are considered “refractory” or “resistant” to medications can still be responsive to psychotherapy.

Susan Stern, MD
Instructor in psychiatry
Columbia University College of Physicians and Surgeons
New York, NY

Dr. Susan Stern’s comments on the role of psychotherapy in her psychiatric practice may have inadvertently foreshadowed psychiatry’s demise as a profession (“Pearls: Treatment resistance? Try psychotherapy,” Current Psychiatry, February 2005).

Dr. Stern shared the story of Mrs. H, who has had depression nearly half her life. The patient’s condition persisted despite numerous antidepressants across several classes. Dr. Stern then tried “several medication augmentation strategies” to alleviate the depression, but nothing worked.

“Finally,” Dr. Stern explained, as if she had exhausted all obvious and reasonable options, “I left her medications alone and listened to her story.”

Excuse me, but had Dr. Stern not realized that Mrs. H’s story might be relevant—even central—to her 20-year battle with depression and to her recovery? If this is a revelation, then psychiatry is on life support.

Too many psychiatrists have stopped listening to their patients and have become obsessed with finding the right drug augmentation strategy. Yet as Dr. Stern’s piece amply demonstrates, a prescribe-first-and-ask-questions-later approach spells almost certain failure—if not disaster—for both the patient and profession.

Although psychotropics have their place, psychiatry’s greatest legacy—the healing power of the doctor-patient relationship—has been allowed to slip silently beneath the waves. Your patients are hurting and they need you, not just your drugs. Put down your pens, close your mouths, and open your ears and hearts. Listen with your “third ear,” as Theodor Reik implored. The results will amaze you.

Barry D. Berger, PhD
Clinical psychologist and president
Mission Psychological Center, Mission, TX

Dr. Stern responds

Dr. Berger’s response to my Pearls article indicates a growing view that psychiatrists in general use medications first to treat depression, with psychotherapy as a mere afterthought. Most psychiatrists I know, however, are interested in doing what they feel is right for the patient, whatever the treatment modality.

A desire to institute or change medications early in the therapeutic process may stem from various sources, including the acuity of the patient’s clinical situation (in which not addressing a patient’s medications would be considered negligent).

Patients often expect psychopharmacologic intervention when they see a psychiatrist. Whether this attitude stems from a fantasy of “instant cure” or is simply a resistance to self-exploration, we should use every means available to address their suffering. The purpose of my article was to illustrate that patients who are considered “refractory” or “resistant” to medications can still be responsive to psychotherapy.

Susan Stern, MD
Instructor in psychiatry
Columbia University College of Physicians and Surgeons
New York, NY

Pressed for time? Then discover the time-saving resources available at www.currentpsychiatry.com. Our Web site now has full-text HTML and PDF versions of any article we have ever published. You can search by title, subject, or author; read Web-only content such as Dr. John Luo’s “Psyber Psychiatry;” earn CME credits online, and much more.

I have used currentpsychiatry.com twice recently to solve real clinical problems:

• One weekend, an 80-year-old patient was concerned about medication interactions. I got the information I needed on cytochrome P-450 isoenzymes without having to search the whole Internet or evaluate a hundred different sites’ reliability. Even more important, I didn’t have to make a special trip to my office or the library.
• Another time, a patient asked me what I knew about omega-3 fatty acids and ADHD. She and I visited the site and discussed the data on the spot.

Having this information online makes it difficult to justify keeping old journals for years. I found my March 2005 editorial on this topic in seconds by entering “hoarding” in the site’s search field. I never would have found that issue in my messy office. It also makes it difficult to justify using books as reference sources because they quickly become outdated, whereas our Web site remains forever current.

f

Pressed for time? Then discover the time-saving resources available at www.currentpsychiatry.com. Our Web site now has full-text HTML and PDF versions of any article we have ever published. You can search by title, subject, or author; read Web-only content such as Dr. John Luo’s “Psyber Psychiatry;” earn CME credits online, and much more.

I have used currentpsychiatry.com twice recently to solve real clinical problems:

• One weekend, an 80-year-old patient was concerned about medication interactions. I got the information I needed on cytochrome P-450 isoenzymes without having to search the whole Internet or evaluate a hundred different sites’ reliability. Even more important, I didn’t have to make a special trip to my office or the library.
• Another time, a patient asked me what I knew about omega-3 fatty acids and ADHD. She and I visited the site and discussed the data on the spot.

Having this information online makes it difficult to justify keeping old journals for years. I found my March 2005 editorial on this topic in seconds by entering “hoarding” in the site’s search field. I never would have found that issue in my messy office. It also makes it difficult to justify using books as reference sources because they quickly become outdated, whereas our Web site remains forever current.

f

Pressed for time? Then discover the time-saving resources available at www.currentpsychiatry.com. Our Web site now has full-text HTML and PDF versions of any article we have ever published. You can search by title, subject, or author; read Web-only content such as Dr. John Luo’s “Psyber Psychiatry;” earn CME credits online, and much more.

I have used currentpsychiatry.com twice recently to solve real clinical problems:

• One weekend, an 80-year-old patient was concerned about medication interactions. I got the information I needed on cytochrome P-450 isoenzymes without having to search the whole Internet or evaluate a hundred different sites’ reliability. Even more important, I didn’t have to make a special trip to my office or the library.
• Another time, a patient asked me what I knew about omega-3 fatty acids and ADHD. She and I visited the site and discussed the data on the spot.

Having this information online makes it difficult to justify keeping old journals for years. I found my March 2005 editorial on this topic in seconds by entering “hoarding” in the site’s search field. I never would have found that issue in my messy office. It also makes it difficult to justify using books as reference sources because they quickly become outdated, whereas our Web site remains forever current.

f

HISTORY: THREE DIAGNOSES BY AGE 15

Matthew, age 17, has been hospitalized twice for psychiatric treatment. At school, he has no friends, is extremely energetic and volatile, and has paranoid delusional thoughts. At night, he becomes depressed over his inability to “fit in.”

Brilliant and deeply spiritual, Matthew obsesses over sins he believes he committed, yet he is angry with God over his illness, its impact on his life, and his apparently dimmed prospects for the future.

His troubles started early. While in preschool, a teacher said he had “autistic tendencies.” He was shy and larger than most children (>90th percentile in height and weight). He acquired language slowly, beginning at 18 months, and slept poorly, waking several times nightly.

Throughout grade school, Matthew was both bright and eccentric. His Wechsler Intelligence Scale for Children-III scores, taken at age 9, were 133 (full scale), 143 (verbal), and 111 (performance). By the third grade, he struggled with the meaning of the universe and other existential issues. In sixth grade, he believed his mouth stank and frequently used mouthwash, even at school. He also had periods of excessive hand-washing.

In fifth grade, a pediatrician diagnosed Matthew as having attention-deficit/hyperactivity disorder after his teacher complained about his behavior in class (blurting out answers, correcting the teacher, restlessness, questioning authority). The doctor prescribed methylphenidate and dextroamphetamine, but the combination made Matthew feel both “drugged and wired.” He stopped taking the agents after 8 weeks.

At age 15, Matthew saw a psychiatrist. His parents said he was depressed and obsessively afraid of being abandoned. Every day, they said, he kissed both parents twice on each cheek.

The psychiatrist diagnosed Matthew with obsessive-compulsive disorder. A trial of paroxetine, 20 mg/d, caused mild irritability with no symptom improvement. After 2 months, Matthew was switched to fluoxetine, initially 10 mg/d and increased to 20 mg/d, but after 6 weeks he suffered an acute manic episode. He claimed he was one with the universe and reported auditory hallucinations, intense suicidal thoughts, and sleeplessness for days on end.

Matthew was hospitalized for 7 days. Haloperidol, dosage unknown, decreased his psychosis but did not return him to baseline. The psychiatrist stopped fluoxetine because Matthew’s parents feared the antidepressant was causing his suicidality. No other agent was tried at this time.

The authors’ observations

Soon after Matthew began taking fluoxetine for apparent OCD and depressive symptoms, profound psychotic symptoms surfaced. These included command hallucinations, delusions, disordered and disorganized thought, high suicidality, motoric hyperarousal, and marked anxiety.

Although positive schizophrenia symptoms were predominant, mood and affect instability were also pronounced. The admitting psychiatrist diagnosed Matthew with schizoaffective disorder but did not include in the record the basis for this diagnosis.

Matthew’s OCD symptoms did not appear to derive from a delusional system or impaired reality testing. These symptoms were often associated with guilt and were consistent with other excessive behaviors.

HOSPITALIZATION: NEW DIAGNOSIS

Out of the hospital, Matthew’s ability to function declined over several months and he began to look disheveled and dirty. He was acutely suicidal, excessively guilty, isolative, and slept 1 to 2 hours nightly.

Matthew was again hospitalized, this time for 2 months. The psychiatrist revised the diagnosis to schizoaffective disorder, bipolar type, based on Matthew’s psychotic episodes, emerging positive symptoms, social withdrawal, and family history. (A male maternal cousin has paranoid schizophrenia.)

Risperidone, initially 0.5 mg nightly and titrated to 0.5 mg each morning and 1.5 mg nightly, gradually improved Matthew’s psychotic symptoms. The psychiatrist added divalproex, 250 mg bid titrated to 250 mg each morning, 250 mg at noon and 500 mg nightly, to address Matthew’s affective lability. After another 2 months of partial hospitalization, he was discharged. Thought disorder symptoms persisted, but reality testing was intact.

Back in high school, Matthew has gotten into a screaming match with the principal and heated political arguments with his teachers. He shows bursts of energy, agitation, and euphoria and is at times overdramatic and grandiose. His rapid-fire creativity easily shifts to irritability and paranoid delusional thinking punctuated by rage.

Almost nightly, Matthew sinks into depression. He also compulsively washes his hands, binge eats, has difficulty reading social cues and making conversation, and believes he is a “misfit.” He views Internet pornography to relieve sexual obsessions, but this habit leads to guilt-ridden ruminations that trigger suicidal thoughts.

For Matthew, high school’s pattern of alternating regimentation and intellectual stimulation constantly provokes mania. He sometimes disguises these episodes by playing “class clown,” only to sink into despair at night over his dyscontrol. His desperation causes frequent anxiety attacks. Searching for answers, Matthew changes psychiatrists and turns to us for help.

The authors’ observations

Matthew’s positive symptoms, bipolar presentation, and the severity and duration of his psychotic episodes supported the schizoaffective disorder diagnosis,¹ yet his cardinal type I bipolar disorder features were striking. His severe thought disorder and perceptual distortions improved, but rapid cycles between euphoria, rage, and depression persisted, as did shifts from hypersomnia to insomnia.

Matthew’s lack of negative symptoms prompted me (Dr. Lundt) to rethink the diagnosis. Though isolated from peers, Matthew remained affable throughout treatment and was emotionally attached to his parents and treating psychiatrist. He rarely appeared flat or blunted and showed no hostility or other signs of resistance typical of a patient with schizophrenia. He cooperated with treatment and showed insight into his illness, even at the height of his acute psychosis. His language was never significantly disorganized but his depression and obsessive guilt were chronic, dominant, and treatment-resistant. I learn over time that Matthew finds certain events highly stressful, and these exacerbate his psychotic features.

Matthew’s diagnosis—and how to address it—came down to two issues:

• Treatment would be similar for schizoaffective disorder or type I bipolar disorder with severe psychotic features.
  
• Matthew viewed schizoaffective disorder as a life sentence of insanity. Changing the diagnosis to type I bipolar disorder would allow him and his family to see a more manageable and hopeful prognosis.
  

In managing Matthew’s care, I refer him to a psychologist (Dr. Brownsmith) whose psychotherapeutic approach will depart significantly from traditional medical-model psychotherapy. Because bipolar and psychotic symptoms have stalled Matthew’s development, the psychologist will combine cognitive-behavioral therapy (CBT) with psychoeducation that emphasizes skills acquisition and coping techniques (Table 1). The goal is to convince Matthew that he can learn to manage his life.²

Table 1

Why psychoeducation can help
patients with bipolar disorder

TREATMENT: TEAM MEETINGS

Matthew begins individual psychotherapy with periodic family therapy and continued medication. Risperidone, 0.5 mg each morning and 1.5 mg nightly, and divalproex, 500 mg bid, have minimized Matthew’s psychosis and stabilized his mood but caused a 45-lb weight gain across 6 months. Matthew alternately joined professional weight-loss programs and worked with a personal trainer to stabilize his weight.

Because day-to-day intervention is critical to keeping Matthew’s anger from derailing his progress, we meet regularly—sometimes weekly—with him, his parents, and his school social worker to plan treatment and provide psychoeducation (Table 2).³

Throughout his senior year, Matthew’s sexual obsessions cause severe guilt, and he begs to be “chemically castrated.” Clomipramine, started at 25 mg nightly and titrated to 300 mg nightly over 2 years, diminishes his obsessions. ECGs are performed and clomipramine plasma levels are checked quarterly to guard against cardiotoxicity. Risperidone is continued and divalproex is gradually increased to 1,000 mg bid, ultimately reaching valproic acid levels of 79 μg/mL.

Through our therapeutic alliance and the change in diagnosis, we help Matthew gradually overcome his initial anger, resistance, despair, and suicidality. Drawing from research data while offering emotional support, we engage Matthew in a team therapy approach.

Matthew acknowledges his grief and anger at having a severe mental illness and agrees to learn to regulate his moods and participate in CBT. Responding with humor to his rapid-fire, manic discussions and animation helps solidify the alliance. We stay highly involved with his parents, often responding to their after-hours phone calls.

After approximately 9 months of CBT, Matthew sees his disordered thoughts and perceived loss of control as symptoms to be overcome.⁴ He adapts some of his fantasy life to replace his obsessive fear and anger. He develops highly creative, embellished visual imagery of a “safe place” in which he feels nurtured and protected. This imagery, coupled with relaxation exercises, is audiotaped so that he can practice at home.⁵ Psychoeducation and problem-solving help him dress appropriately and improve his hygiene.

Matthew’s intelligence and social awareness underlie strongly held values and opinions that fuel his anger. Media coverage of politicians, political debates in school, extreme religious views, and judgmental statements about sexuality frequently provoke rage. (Matthew once battered a street preacher who was decrying homosexuality.) By acquiring anger management strategies, he learns to avoid potentially volatile situations.⁶

Frequent crisis intervention keeps Matthew stable, while family therapy helps him follow his psychologist’s plan to maintain medication adherence and manage his circadian rhythms, activities of daily living, and CBT. His parents prompt him to use therapeutic techniques, support him during crises, and make sure he has the structure and support to participate in treatment, school, and social activities.⁷

Thanks to this team effort, Matthew graduates high school and is accepted at a small coastal college 1,500 miles from home.

Table 2

Keys to successful psychotherapy
for bipolar disorder

The authors’ observations

We continue to work with Matthew’s parents to help him handle college life. His parents identify prospective mental health professionals near the college; we interview them and provide Matthew’s history and treatment information. We communicate during school holidays, home visits, and by phone as needed with Matthew, his new therapist and psychiatrist, and his parents.

CONTINUED TREATMENT: THE ‘AWAY TEAM’

Together, Matthew’s home- and college-based treatment teams ensure treatment continuity. During school breaks, Matthew’s “home team” continues medication management and psychotherapy. Thanks to such persistent monitoring, Matthew finishes college in 4 years.

Medications and careless eating habits, however, have taken a severe metabolic toll. To help Matthew confront the added pressures of college, risperidone was gradually increased to 1 mg bid, divalproex to 1,000 mg each morning and 1,500 mg nightly, and clomipramine to 350 mg/d. By graduation day, he weighs 330 lbs with a body mass index of 40 kg². His triglycerides have more than doubled (141 mg/dL before college, 307 mg/dL after), and he has developed hypothyroidism. Total cholesterol is 247 mg/dL. His family doctor prescribes thyroid supplementation and atorvastatin, titrated to 40 mg/d.

To stem Matthew’s weight gain, we taper him off divalproex and switch him to topiramate, 100 mg nightly, but topiramate alone does not control his mood. Subsequent trials of quetiapine, 200 mg nightly, olanzapine, 20 mg nightly, and ziprasidone, 80 mg bid, are ineffective.

The authors’ observations

Matthew’s problem is common. He responded well to risperidone and divalproex, but these agents contributed to significant weight gain. Topiramate augmentation and trials of other atypical antipsychotics were unsuccessful. The atypical antipsychotic aripiprazole or anticonvulsant lamotrigine might have stabilized Matthew’s mood and weight, but these drugs were not available while he was in college. Dietary interventions were tried but are difficult to enforce on a college student living away from home.

CONCLUSION: A LEARNING EXPERIENCE

We stop divalproex and restart topiramate, 200 mg nightly. Matthew continues to take risperidone, 2 mg each morning and 5 mg at night; clomipramine, 150 mg each morning; thyroid supplementation, 0.2 mg/d; and atorvastatin, 40 mg/d. He loses 10 lbs over 3 months; his weight eventually drops to 290 lbs and remains stable.

Matthew enters another university to pursue a master’s degree. He shifts to a new college-based mental health team and moves into an apartment.

There are setbacks. Missed therapy appointments cause treatment lapses, and a teaching assistantship leads to problems managing schoolwork. Working with Matthew’s treatment team and his parents, we intervene to resolve crises, re-establish treatment, and help him resolve issues of identity, confidence, coping, and routine. With this persistent follow-up, he earns his master’s degree.

Now age 26, Matthew is pursuing a doctorate. He is taking more responsibility for his appointments and medication and is undertaking bill-paying and travel arrangements. With ongoing psychotherapy and mediation, Matthew regulates his mood and is learning to recognize prodromal symptoms and anticipate stress.⁸ He is more comfortable in social settings and has some friends and study partners, although he continues to deeply ponder philosophical and spiritual issues.

Related resources

• Miklowitz D. The bipolar disorder survival guide. New York: Guilford Press, 2002.
  
• Averill PM, Reas DL, Shack A, et al. Is schizoaffective disorder a stable diagnostic category: A retrospective examination. Psychiatr Q 2004;75:215-27.
  
• Bipolar focus (information, chat room for families and patients). www.moodswing.org.
  

• Atorvastatin • Lipitor
  
• Clomipramine • Anafranil
  
• Dextroamphetamine • Dexedrine
  
• Divalproex • Depakote
  
• Fluoxetine • Prozac
  
• Methylphenidate • Concerta, Ritalin
  
• Olanzapine • Zyprexa
  
• Paroxetine • Paxil
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Topiramate • Topamax
  
• Ziprasidone • Geodon
  

Dr. Brownsmith receives research support from Pfizer Inc.

Dr. Lundt receives research support from and is a speaker for Eli Lilly and Co., Pfizer Inc., and GlaxoSmithKline, and receives research support from Ortho-McNeil Pharmaceutical.

HISTORY: THREE DIAGNOSES BY AGE 15

Matthew, age 17, has been hospitalized twice for psychiatric treatment. At school, he has no friends, is extremely energetic and volatile, and has paranoid delusional thoughts. At night, he becomes depressed over his inability to “fit in.”

Brilliant and deeply spiritual, Matthew obsesses over sins he believes he committed, yet he is angry with God over his illness, its impact on his life, and his apparently dimmed prospects for the future.

His troubles started early. While in preschool, a teacher said he had “autistic tendencies.” He was shy and larger than most children (>90th percentile in height and weight). He acquired language slowly, beginning at 18 months, and slept poorly, waking several times nightly.

Throughout grade school, Matthew was both bright and eccentric. His Wechsler Intelligence Scale for Children-III scores, taken at age 9, were 133 (full scale), 143 (verbal), and 111 (performance). By the third grade, he struggled with the meaning of the universe and other existential issues. In sixth grade, he believed his mouth stank and frequently used mouthwash, even at school. He also had periods of excessive hand-washing.

In fifth grade, a pediatrician diagnosed Matthew as having attention-deficit/hyperactivity disorder after his teacher complained about his behavior in class (blurting out answers, correcting the teacher, restlessness, questioning authority). The doctor prescribed methylphenidate and dextroamphetamine, but the combination made Matthew feel both “drugged and wired.” He stopped taking the agents after 8 weeks.

At age 15, Matthew saw a psychiatrist. His parents said he was depressed and obsessively afraid of being abandoned. Every day, they said, he kissed both parents twice on each cheek.

The psychiatrist diagnosed Matthew with obsessive-compulsive disorder. A trial of paroxetine, 20 mg/d, caused mild irritability with no symptom improvement. After 2 months, Matthew was switched to fluoxetine, initially 10 mg/d and increased to 20 mg/d, but after 6 weeks he suffered an acute manic episode. He claimed he was one with the universe and reported auditory hallucinations, intense suicidal thoughts, and sleeplessness for days on end.

Matthew was hospitalized for 7 days. Haloperidol, dosage unknown, decreased his psychosis but did not return him to baseline. The psychiatrist stopped fluoxetine because Matthew’s parents feared the antidepressant was causing his suicidality. No other agent was tried at this time.

The authors’ observations

Soon after Matthew began taking fluoxetine for apparent OCD and depressive symptoms, profound psychotic symptoms surfaced. These included command hallucinations, delusions, disordered and disorganized thought, high suicidality, motoric hyperarousal, and marked anxiety.

Although positive schizophrenia symptoms were predominant, mood and affect instability were also pronounced. The admitting psychiatrist diagnosed Matthew with schizoaffective disorder but did not include in the record the basis for this diagnosis.

Matthew’s OCD symptoms did not appear to derive from a delusional system or impaired reality testing. These symptoms were often associated with guilt and were consistent with other excessive behaviors.

HOSPITALIZATION: NEW DIAGNOSIS

Out of the hospital, Matthew’s ability to function declined over several months and he began to look disheveled and dirty. He was acutely suicidal, excessively guilty, isolative, and slept 1 to 2 hours nightly.

Matthew was again hospitalized, this time for 2 months. The psychiatrist revised the diagnosis to schizoaffective disorder, bipolar type, based on Matthew’s psychotic episodes, emerging positive symptoms, social withdrawal, and family history. (A male maternal cousin has paranoid schizophrenia.)

Risperidone, initially 0.5 mg nightly and titrated to 0.5 mg each morning and 1.5 mg nightly, gradually improved Matthew’s psychotic symptoms. The psychiatrist added divalproex, 250 mg bid titrated to 250 mg each morning, 250 mg at noon and 500 mg nightly, to address Matthew’s affective lability. After another 2 months of partial hospitalization, he was discharged. Thought disorder symptoms persisted, but reality testing was intact.

Back in high school, Matthew has gotten into a screaming match with the principal and heated political arguments with his teachers. He shows bursts of energy, agitation, and euphoria and is at times overdramatic and grandiose. His rapid-fire creativity easily shifts to irritability and paranoid delusional thinking punctuated by rage.

Almost nightly, Matthew sinks into depression. He also compulsively washes his hands, binge eats, has difficulty reading social cues and making conversation, and believes he is a “misfit.” He views Internet pornography to relieve sexual obsessions, but this habit leads to guilt-ridden ruminations that trigger suicidal thoughts.

For Matthew, high school’s pattern of alternating regimentation and intellectual stimulation constantly provokes mania. He sometimes disguises these episodes by playing “class clown,” only to sink into despair at night over his dyscontrol. His desperation causes frequent anxiety attacks. Searching for answers, Matthew changes psychiatrists and turns to us for help.

The authors’ observations

Matthew’s positive symptoms, bipolar presentation, and the severity and duration of his psychotic episodes supported the schizoaffective disorder diagnosis,¹ yet his cardinal type I bipolar disorder features were striking. His severe thought disorder and perceptual distortions improved, but rapid cycles between euphoria, rage, and depression persisted, as did shifts from hypersomnia to insomnia.

Matthew’s lack of negative symptoms prompted me (Dr. Lundt) to rethink the diagnosis. Though isolated from peers, Matthew remained affable throughout treatment and was emotionally attached to his parents and treating psychiatrist. He rarely appeared flat or blunted and showed no hostility or other signs of resistance typical of a patient with schizophrenia. He cooperated with treatment and showed insight into his illness, even at the height of his acute psychosis. His language was never significantly disorganized but his depression and obsessive guilt were chronic, dominant, and treatment-resistant. I learn over time that Matthew finds certain events highly stressful, and these exacerbate his psychotic features.

Matthew’s diagnosis—and how to address it—came down to two issues:

• Treatment would be similar for schizoaffective disorder or type I bipolar disorder with severe psychotic features.
  
• Matthew viewed schizoaffective disorder as a life sentence of insanity. Changing the diagnosis to type I bipolar disorder would allow him and his family to see a more manageable and hopeful prognosis.
  

In managing Matthew’s care, I refer him to a psychologist (Dr. Brownsmith) whose psychotherapeutic approach will depart significantly from traditional medical-model psychotherapy. Because bipolar and psychotic symptoms have stalled Matthew’s development, the psychologist will combine cognitive-behavioral therapy (CBT) with psychoeducation that emphasizes skills acquisition and coping techniques (Table 1). The goal is to convince Matthew that he can learn to manage his life.²

Table 1

Why psychoeducation can help
patients with bipolar disorder

TREATMENT: TEAM MEETINGS

Matthew begins individual psychotherapy with periodic family therapy and continued medication. Risperidone, 0.5 mg each morning and 1.5 mg nightly, and divalproex, 500 mg bid, have minimized Matthew’s psychosis and stabilized his mood but caused a 45-lb weight gain across 6 months. Matthew alternately joined professional weight-loss programs and worked with a personal trainer to stabilize his weight.

Because day-to-day intervention is critical to keeping Matthew’s anger from derailing his progress, we meet regularly—sometimes weekly—with him, his parents, and his school social worker to plan treatment and provide psychoeducation (Table 2).³

Throughout his senior year, Matthew’s sexual obsessions cause severe guilt, and he begs to be “chemically castrated.” Clomipramine, started at 25 mg nightly and titrated to 300 mg nightly over 2 years, diminishes his obsessions. ECGs are performed and clomipramine plasma levels are checked quarterly to guard against cardiotoxicity. Risperidone is continued and divalproex is gradually increased to 1,000 mg bid, ultimately reaching valproic acid levels of 79 μg/mL.

Through our therapeutic alliance and the change in diagnosis, we help Matthew gradually overcome his initial anger, resistance, despair, and suicidality. Drawing from research data while offering emotional support, we engage Matthew in a team therapy approach.

Matthew acknowledges his grief and anger at having a severe mental illness and agrees to learn to regulate his moods and participate in CBT. Responding with humor to his rapid-fire, manic discussions and animation helps solidify the alliance. We stay highly involved with his parents, often responding to their after-hours phone calls.

After approximately 9 months of CBT, Matthew sees his disordered thoughts and perceived loss of control as symptoms to be overcome.⁴ He adapts some of his fantasy life to replace his obsessive fear and anger. He develops highly creative, embellished visual imagery of a “safe place” in which he feels nurtured and protected. This imagery, coupled with relaxation exercises, is audiotaped so that he can practice at home.⁵ Psychoeducation and problem-solving help him dress appropriately and improve his hygiene.

Matthew’s intelligence and social awareness underlie strongly held values and opinions that fuel his anger. Media coverage of politicians, political debates in school, extreme religious views, and judgmental statements about sexuality frequently provoke rage. (Matthew once battered a street preacher who was decrying homosexuality.) By acquiring anger management strategies, he learns to avoid potentially volatile situations.⁶

Frequent crisis intervention keeps Matthew stable, while family therapy helps him follow his psychologist’s plan to maintain medication adherence and manage his circadian rhythms, activities of daily living, and CBT. His parents prompt him to use therapeutic techniques, support him during crises, and make sure he has the structure and support to participate in treatment, school, and social activities.⁷

Thanks to this team effort, Matthew graduates high school and is accepted at a small coastal college 1,500 miles from home.

Table 2

Keys to successful psychotherapy
for bipolar disorder

The authors’ observations

We continue to work with Matthew’s parents to help him handle college life. His parents identify prospective mental health professionals near the college; we interview them and provide Matthew’s history and treatment information. We communicate during school holidays, home visits, and by phone as needed with Matthew, his new therapist and psychiatrist, and his parents.

CONTINUED TREATMENT: THE ‘AWAY TEAM’

Together, Matthew’s home- and college-based treatment teams ensure treatment continuity. During school breaks, Matthew’s “home team” continues medication management and psychotherapy. Thanks to such persistent monitoring, Matthew finishes college in 4 years.

Medications and careless eating habits, however, have taken a severe metabolic toll. To help Matthew confront the added pressures of college, risperidone was gradually increased to 1 mg bid, divalproex to 1,000 mg each morning and 1,500 mg nightly, and clomipramine to 350 mg/d. By graduation day, he weighs 330 lbs with a body mass index of 40 kg². His triglycerides have more than doubled (141 mg/dL before college, 307 mg/dL after), and he has developed hypothyroidism. Total cholesterol is 247 mg/dL. His family doctor prescribes thyroid supplementation and atorvastatin, titrated to 40 mg/d.

To stem Matthew’s weight gain, we taper him off divalproex and switch him to topiramate, 100 mg nightly, but topiramate alone does not control his mood. Subsequent trials of quetiapine, 200 mg nightly, olanzapine, 20 mg nightly, and ziprasidone, 80 mg bid, are ineffective.

The authors’ observations

Matthew’s problem is common. He responded well to risperidone and divalproex, but these agents contributed to significant weight gain. Topiramate augmentation and trials of other atypical antipsychotics were unsuccessful. The atypical antipsychotic aripiprazole or anticonvulsant lamotrigine might have stabilized Matthew’s mood and weight, but these drugs were not available while he was in college. Dietary interventions were tried but are difficult to enforce on a college student living away from home.

CONCLUSION: A LEARNING EXPERIENCE

We stop divalproex and restart topiramate, 200 mg nightly. Matthew continues to take risperidone, 2 mg each morning and 5 mg at night; clomipramine, 150 mg each morning; thyroid supplementation, 0.2 mg/d; and atorvastatin, 40 mg/d. He loses 10 lbs over 3 months; his weight eventually drops to 290 lbs and remains stable.

Matthew enters another university to pursue a master’s degree. He shifts to a new college-based mental health team and moves into an apartment.

There are setbacks. Missed therapy appointments cause treatment lapses, and a teaching assistantship leads to problems managing schoolwork. Working with Matthew’s treatment team and his parents, we intervene to resolve crises, re-establish treatment, and help him resolve issues of identity, confidence, coping, and routine. With this persistent follow-up, he earns his master’s degree.

Now age 26, Matthew is pursuing a doctorate. He is taking more responsibility for his appointments and medication and is undertaking bill-paying and travel arrangements. With ongoing psychotherapy and mediation, Matthew regulates his mood and is learning to recognize prodromal symptoms and anticipate stress.⁸ He is more comfortable in social settings and has some friends and study partners, although he continues to deeply ponder philosophical and spiritual issues.

Related resources

• Miklowitz D. The bipolar disorder survival guide. New York: Guilford Press, 2002.
  
• Averill PM, Reas DL, Shack A, et al. Is schizoaffective disorder a stable diagnostic category: A retrospective examination. Psychiatr Q 2004;75:215-27.
  
• Bipolar focus (information, chat room for families and patients). www.moodswing.org.
  

• Atorvastatin • Lipitor
  
• Clomipramine • Anafranil
  
• Dextroamphetamine • Dexedrine
  
• Divalproex • Depakote
  
• Fluoxetine • Prozac
  
• Methylphenidate • Concerta, Ritalin
  
• Olanzapine • Zyprexa
  
• Paroxetine • Paxil
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Topiramate • Topamax
  
• Ziprasidone • Geodon
  

Dr. Brownsmith receives research support from Pfizer Inc.

Dr. Lundt receives research support from and is a speaker for Eli Lilly and Co., Pfizer Inc., and GlaxoSmithKline, and receives research support from Ortho-McNeil Pharmaceutical.

HISTORY: THREE DIAGNOSES BY AGE 15

Matthew, age 17, has been hospitalized twice for psychiatric treatment. At school, he has no friends, is extremely energetic and volatile, and has paranoid delusional thoughts. At night, he becomes depressed over his inability to “fit in.”

Brilliant and deeply spiritual, Matthew obsesses over sins he believes he committed, yet he is angry with God over his illness, its impact on his life, and his apparently dimmed prospects for the future.

His troubles started early. While in preschool, a teacher said he had “autistic tendencies.” He was shy and larger than most children (>90th percentile in height and weight). He acquired language slowly, beginning at 18 months, and slept poorly, waking several times nightly.

Throughout grade school, Matthew was both bright and eccentric. His Wechsler Intelligence Scale for Children-III scores, taken at age 9, were 133 (full scale), 143 (verbal), and 111 (performance). By the third grade, he struggled with the meaning of the universe and other existential issues. In sixth grade, he believed his mouth stank and frequently used mouthwash, even at school. He also had periods of excessive hand-washing.

In fifth grade, a pediatrician diagnosed Matthew as having attention-deficit/hyperactivity disorder after his teacher complained about his behavior in class (blurting out answers, correcting the teacher, restlessness, questioning authority). The doctor prescribed methylphenidate and dextroamphetamine, but the combination made Matthew feel both “drugged and wired.” He stopped taking the agents after 8 weeks.

At age 15, Matthew saw a psychiatrist. His parents said he was depressed and obsessively afraid of being abandoned. Every day, they said, he kissed both parents twice on each cheek.

The psychiatrist diagnosed Matthew with obsessive-compulsive disorder. A trial of paroxetine, 20 mg/d, caused mild irritability with no symptom improvement. After 2 months, Matthew was switched to fluoxetine, initially 10 mg/d and increased to 20 mg/d, but after 6 weeks he suffered an acute manic episode. He claimed he was one with the universe and reported auditory hallucinations, intense suicidal thoughts, and sleeplessness for days on end.

Matthew was hospitalized for 7 days. Haloperidol, dosage unknown, decreased his psychosis but did not return him to baseline. The psychiatrist stopped fluoxetine because Matthew’s parents feared the antidepressant was causing his suicidality. No other agent was tried at this time.

The authors’ observations

Soon after Matthew began taking fluoxetine for apparent OCD and depressive symptoms, profound psychotic symptoms surfaced. These included command hallucinations, delusions, disordered and disorganized thought, high suicidality, motoric hyperarousal, and marked anxiety.

Although positive schizophrenia symptoms were predominant, mood and affect instability were also pronounced. The admitting psychiatrist diagnosed Matthew with schizoaffective disorder but did not include in the record the basis for this diagnosis.

Matthew’s OCD symptoms did not appear to derive from a delusional system or impaired reality testing. These symptoms were often associated with guilt and were consistent with other excessive behaviors.

HOSPITALIZATION: NEW DIAGNOSIS

Out of the hospital, Matthew’s ability to function declined over several months and he began to look disheveled and dirty. He was acutely suicidal, excessively guilty, isolative, and slept 1 to 2 hours nightly.

Matthew was again hospitalized, this time for 2 months. The psychiatrist revised the diagnosis to schizoaffective disorder, bipolar type, based on Matthew’s psychotic episodes, emerging positive symptoms, social withdrawal, and family history. (A male maternal cousin has paranoid schizophrenia.)

Risperidone, initially 0.5 mg nightly and titrated to 0.5 mg each morning and 1.5 mg nightly, gradually improved Matthew’s psychotic symptoms. The psychiatrist added divalproex, 250 mg bid titrated to 250 mg each morning, 250 mg at noon and 500 mg nightly, to address Matthew’s affective lability. After another 2 months of partial hospitalization, he was discharged. Thought disorder symptoms persisted, but reality testing was intact.

Back in high school, Matthew has gotten into a screaming match with the principal and heated political arguments with his teachers. He shows bursts of energy, agitation, and euphoria and is at times overdramatic and grandiose. His rapid-fire creativity easily shifts to irritability and paranoid delusional thinking punctuated by rage.

Almost nightly, Matthew sinks into depression. He also compulsively washes his hands, binge eats, has difficulty reading social cues and making conversation, and believes he is a “misfit.” He views Internet pornography to relieve sexual obsessions, but this habit leads to guilt-ridden ruminations that trigger suicidal thoughts.

For Matthew, high school’s pattern of alternating regimentation and intellectual stimulation constantly provokes mania. He sometimes disguises these episodes by playing “class clown,” only to sink into despair at night over his dyscontrol. His desperation causes frequent anxiety attacks. Searching for answers, Matthew changes psychiatrists and turns to us for help.

The authors’ observations

Matthew’s positive symptoms, bipolar presentation, and the severity and duration of his psychotic episodes supported the schizoaffective disorder diagnosis,¹ yet his cardinal type I bipolar disorder features were striking. His severe thought disorder and perceptual distortions improved, but rapid cycles between euphoria, rage, and depression persisted, as did shifts from hypersomnia to insomnia.

Matthew’s lack of negative symptoms prompted me (Dr. Lundt) to rethink the diagnosis. Though isolated from peers, Matthew remained affable throughout treatment and was emotionally attached to his parents and treating psychiatrist. He rarely appeared flat or blunted and showed no hostility or other signs of resistance typical of a patient with schizophrenia. He cooperated with treatment and showed insight into his illness, even at the height of his acute psychosis. His language was never significantly disorganized but his depression and obsessive guilt were chronic, dominant, and treatment-resistant. I learn over time that Matthew finds certain events highly stressful, and these exacerbate his psychotic features.

Matthew’s diagnosis—and how to address it—came down to two issues:

• Treatment would be similar for schizoaffective disorder or type I bipolar disorder with severe psychotic features.
  
• Matthew viewed schizoaffective disorder as a life sentence of insanity. Changing the diagnosis to type I bipolar disorder would allow him and his family to see a more manageable and hopeful prognosis.
  

In managing Matthew’s care, I refer him to a psychologist (Dr. Brownsmith) whose psychotherapeutic approach will depart significantly from traditional medical-model psychotherapy. Because bipolar and psychotic symptoms have stalled Matthew’s development, the psychologist will combine cognitive-behavioral therapy (CBT) with psychoeducation that emphasizes skills acquisition and coping techniques (Table 1). The goal is to convince Matthew that he can learn to manage his life.²

Table 1

Why psychoeducation can help
patients with bipolar disorder

TREATMENT: TEAM MEETINGS

Matthew begins individual psychotherapy with periodic family therapy and continued medication. Risperidone, 0.5 mg each morning and 1.5 mg nightly, and divalproex, 500 mg bid, have minimized Matthew’s psychosis and stabilized his mood but caused a 45-lb weight gain across 6 months. Matthew alternately joined professional weight-loss programs and worked with a personal trainer to stabilize his weight.

Because day-to-day intervention is critical to keeping Matthew’s anger from derailing his progress, we meet regularly—sometimes weekly—with him, his parents, and his school social worker to plan treatment and provide psychoeducation (Table 2).³

Throughout his senior year, Matthew’s sexual obsessions cause severe guilt, and he begs to be “chemically castrated.” Clomipramine, started at 25 mg nightly and titrated to 300 mg nightly over 2 years, diminishes his obsessions. ECGs are performed and clomipramine plasma levels are checked quarterly to guard against cardiotoxicity. Risperidone is continued and divalproex is gradually increased to 1,000 mg bid, ultimately reaching valproic acid levels of 79 μg/mL.

Through our therapeutic alliance and the change in diagnosis, we help Matthew gradually overcome his initial anger, resistance, despair, and suicidality. Drawing from research data while offering emotional support, we engage Matthew in a team therapy approach.

Matthew acknowledges his grief and anger at having a severe mental illness and agrees to learn to regulate his moods and participate in CBT. Responding with humor to his rapid-fire, manic discussions and animation helps solidify the alliance. We stay highly involved with his parents, often responding to their after-hours phone calls.

After approximately 9 months of CBT, Matthew sees his disordered thoughts and perceived loss of control as symptoms to be overcome.⁴ He adapts some of his fantasy life to replace his obsessive fear and anger. He develops highly creative, embellished visual imagery of a “safe place” in which he feels nurtured and protected. This imagery, coupled with relaxation exercises, is audiotaped so that he can practice at home.⁵ Psychoeducation and problem-solving help him dress appropriately and improve his hygiene.

Matthew’s intelligence and social awareness underlie strongly held values and opinions that fuel his anger. Media coverage of politicians, political debates in school, extreme religious views, and judgmental statements about sexuality frequently provoke rage. (Matthew once battered a street preacher who was decrying homosexuality.) By acquiring anger management strategies, he learns to avoid potentially volatile situations.⁶

Frequent crisis intervention keeps Matthew stable, while family therapy helps him follow his psychologist’s plan to maintain medication adherence and manage his circadian rhythms, activities of daily living, and CBT. His parents prompt him to use therapeutic techniques, support him during crises, and make sure he has the structure and support to participate in treatment, school, and social activities.⁷

Thanks to this team effort, Matthew graduates high school and is accepted at a small coastal college 1,500 miles from home.

Table 2

Keys to successful psychotherapy
for bipolar disorder

The authors’ observations

We continue to work with Matthew’s parents to help him handle college life. His parents identify prospective mental health professionals near the college; we interview them and provide Matthew’s history and treatment information. We communicate during school holidays, home visits, and by phone as needed with Matthew, his new therapist and psychiatrist, and his parents.

CONTINUED TREATMENT: THE ‘AWAY TEAM’

Together, Matthew’s home- and college-based treatment teams ensure treatment continuity. During school breaks, Matthew’s “home team” continues medication management and psychotherapy. Thanks to such persistent monitoring, Matthew finishes college in 4 years.

Medications and careless eating habits, however, have taken a severe metabolic toll. To help Matthew confront the added pressures of college, risperidone was gradually increased to 1 mg bid, divalproex to 1,000 mg each morning and 1,500 mg nightly, and clomipramine to 350 mg/d. By graduation day, he weighs 330 lbs with a body mass index of 40 kg². His triglycerides have more than doubled (141 mg/dL before college, 307 mg/dL after), and he has developed hypothyroidism. Total cholesterol is 247 mg/dL. His family doctor prescribes thyroid supplementation and atorvastatin, titrated to 40 mg/d.

To stem Matthew’s weight gain, we taper him off divalproex and switch him to topiramate, 100 mg nightly, but topiramate alone does not control his mood. Subsequent trials of quetiapine, 200 mg nightly, olanzapine, 20 mg nightly, and ziprasidone, 80 mg bid, are ineffective.

The authors’ observations

Matthew’s problem is common. He responded well to risperidone and divalproex, but these agents contributed to significant weight gain. Topiramate augmentation and trials of other atypical antipsychotics were unsuccessful. The atypical antipsychotic aripiprazole or anticonvulsant lamotrigine might have stabilized Matthew’s mood and weight, but these drugs were not available while he was in college. Dietary interventions were tried but are difficult to enforce on a college student living away from home.

CONCLUSION: A LEARNING EXPERIENCE

We stop divalproex and restart topiramate, 200 mg nightly. Matthew continues to take risperidone, 2 mg each morning and 5 mg at night; clomipramine, 150 mg each morning; thyroid supplementation, 0.2 mg/d; and atorvastatin, 40 mg/d. He loses 10 lbs over 3 months; his weight eventually drops to 290 lbs and remains stable.

Matthew enters another university to pursue a master’s degree. He shifts to a new college-based mental health team and moves into an apartment.

There are setbacks. Missed therapy appointments cause treatment lapses, and a teaching assistantship leads to problems managing schoolwork. Working with Matthew’s treatment team and his parents, we intervene to resolve crises, re-establish treatment, and help him resolve issues of identity, confidence, coping, and routine. With this persistent follow-up, he earns his master’s degree.

Now age 26, Matthew is pursuing a doctorate. He is taking more responsibility for his appointments and medication and is undertaking bill-paying and travel arrangements. With ongoing psychotherapy and mediation, Matthew regulates his mood and is learning to recognize prodromal symptoms and anticipate stress.⁸ He is more comfortable in social settings and has some friends and study partners, although he continues to deeply ponder philosophical and spiritual issues.

Related resources

• Miklowitz D. The bipolar disorder survival guide. New York: Guilford Press, 2002.
  
• Averill PM, Reas DL, Shack A, et al. Is schizoaffective disorder a stable diagnostic category: A retrospective examination. Psychiatr Q 2004;75:215-27.
  
• Bipolar focus (information, chat room for families and patients). www.moodswing.org.
  

• Atorvastatin • Lipitor
  
• Clomipramine • Anafranil
  
• Dextroamphetamine • Dexedrine
  
• Divalproex • Depakote
  
• Fluoxetine • Prozac
  
• Methylphenidate • Concerta, Ritalin
  
• Olanzapine • Zyprexa
  
• Paroxetine • Paxil
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Topiramate • Topamax
  
• Ziprasidone • Geodon
  

Dr. Brownsmith receives research support from Pfizer Inc.

Dr. Lundt receives research support from and is a speaker for Eli Lilly and Co., Pfizer Inc., and GlaxoSmithKline, and receives research support from Ortho-McNeil Pharmaceutical.

Many clinicians refer alcohol-dependent patients to Alcoholics Anonymous, but how effective is AA in reducing drinking? Evidence is elusive—partly because of AA’s tradition of anonymity—but clinician encouragement is among three variables that appear essential to successful AA use.

The pioneer of twelve-step programs (Box 1),^1,2 AA is a widely accessible, free adjunct to professional alcohol abuse treatment. This article describes the evidence supporting AA’s efficacy for reducing drinking among persons with alcohol use disorders. We also recommend referral strategies that increase AA participation and discuss special needs of alcohol-dependent patients with comorbid psychiatric disorders.

Box 1

KEYS TO AA SUCCESS

Besides clinician encouragement, two patient variables—severity of alcohol dependence and self-efficacy—have been associated with successful AA use.

Clinician encouragement. When psychiatrists and other clinicians encourage alcohol-dependent patients to attend AA, the rate of AA use increases and drinking decreases.^3-7 When clinicians remain interested in alcohol-dependent patients’ AA use—rather than simply recommending AA—patients are more likely to follow through with a referral and to participate long enough to obtain benefit.

Clinicians play an important role in helping patients benefit from AA referral (Box 2).⁶ Patients who are personally helped to an AA group will rapidly attend, whereas those only given referral information are unlikely to follow up.⁷ Moreover, clinicians who encourage patients to attend AA and follow up on that attendance have more patients who attend and participate in AA than do less proactive clinicians.⁸

Box 2

Self-efficacy. Believing that one can abstain from drinking is associated with being able to reduce one’s drinking. Alcohol-dependent patients with self-efficacy are more likely to use AA, and this trait is believed to be a component of the change process associated with reduced drinking.^11,12

HOW EFFECTIVE IS AA?

Randomized, controlled trials (RCTs) may be the “gold standard” for determining any treatment’s efficacy, but constructing an RCT of AA use is complicated. AA does not engage in or support research, which makes AA use difficult to administer as a controlled variable in clinical trials. Also, the variability of AA groups and environments confounds the interpretation of study results and limits their application to populations at large.¹³

Even so, AA can be effective as an adjunct to professional treatments—such as detoxification—and as aftercare to maintain reduced drinking:

• Kelly’s¹⁴ comprehensive review and critical analysis of the main studies through 2003 showed a correlation between professional treatment plus AA attendance and improved outcomes.
  
• Project MATCH-—a large RCT—also supports AA’s benefits, as reported in smaller, less rigorously controlled studies.^4,5
  

• Kownacki and Shadish¹⁵ found poorer 12-month drinking outcomes with AA alone, compared with other treatments or no treatment. Their review assessed attendance as a predictor of alcohol use outcomes, and most subjects were attending AA under court orders. Because AA’s philosophy stresses that members must desire to stop drinking (Table 1), these study results may not apply to the voluntary, motivated individuals who usually use AA.
  
• Two other meta-analyses^9,10 that included nonrandomized studies and RCTs showed that attending AA has modest, favorable effects in reducing drinking and improving psychosocial functioning.
  

Outpatient studies showed positive correlations between AA attendance/involvement and:

• reduced drinking
  
• improved psychological adjustment and improved family relationships.
  

All three meta-analyses excluded studies of alcohol-dependent individuals with co-occurring drug use disorders, leaving unaddressed the effect of adjunctive AA in that population.

Table 1

AA’s Twelve Steps of personal recovery

• 12 sessions of cognitive-behavioral coping skills (CBT)
  
• 4 sessions of motivational enhancement therapy (MET).
  

Project MATCH thus found that a twelve-step individual therapy was at least as effective as CBT and MET in reducing post-treatment drinking and maintaining abstinence.

Real-world efficacy. A naturalistic study that resembled Project MATCH enrolled 3,018 male military veterans with substance use disorders across 15 program sites.¹⁸ Drug dependence was not excluded, and 51% of the men had co-occurring alcohol and drug dependence.

Participants received inpatient detoxification, followed by 21 to 28 days of intensive twelve-step treatment, CBT, or both. Alcohol and drug abuse declined equally in all three groups, and subjects were referred for outpatient aftercare and self-help groups. After 1 year, involvement in a self-help group predicted better outcome, regardless of the initial treatment.¹⁹

Unlike earlier studies,^15,20,21 this trial found that individuals with co-occurring psychiatric disorders and those legally mandated to get treatment did as well at 1-year follow-up as those without these variables. It provides additional evidence that twelve-step treatments can reduce substance use across varied populations, including patients with co-occurring alcohol and drug dependence.

AA ATTENDANCE VS. PARTICIPATION

Twelve-step programs appear most effective for individuals who actively participate. This may seem obvious, but most studies of 12-step treatments have monitored meeting attendance rather than engagement. Most studies that separate these variables report that active participation—not passive attendance—correlates with reduced substance use.

Montgomery et al²² followed 66 alcohol-dependent individuals in a 12-step oriented, 28-day residential treatment program and investigated:

• relationships between AA attendance and participation
  
• drinking outcomes over 31 weeks after treatment.
  

Similarly, Project MATCH participants involved in AA during the first 6 months after treatment had more-frequent abstinent days in the 7 to 12 months after treatment. AA “involvement” included identifying oneself as an AA member, working the steps, having an AA sponsor, and celebrating sobriety milestones.¹²

The National Drug Abuse Collaborative Cocaine Treatment Study is the most detailed analysis of self-help use. This multi-site RCT by Weiss and colleagues enrolled 487 individuals for behavioral treatment of cocaine dependence.²³

Twelve-step attendance did not predict substance use outcomes, but active participation (such as making coffee for a meeting or reading AA literature) in a given month predicted decreased substance use in the following month. Subjects whose participation increased over the first 3 months showed reduced drug use in the following 3 months. Interestingly, those who participated without attending meetings regularly (such as by reading AA literature or calling a sponsor) benefited as much as those who attended meetings more regularly.

Summary. Actively engaging in 12-step treatment—as measured by identifying with the fellowship and following the steps—appears more important to success than simply attending meetings.

EFFECTIVE AA REFERRALS

To encourage engagement when referring, try to match patients to AA groups attended by persons with whom they feel comfortable (Table 2).²⁴ Adolescents, for example, tend to have more difficulty engaging and remaining in AA than do adults.²⁵ One remedy may be to recommend a Young Person’s AA group composed primarily of adolescents and young adults.

Although AA embraces a spiritual approach to recovery, a person can benefit from participating without having a specific religious affiliation or spiritual beliefs.^12,26 The emphasis on spirituality and a “higher power” varies from one AA group to another as well as from region to region. For patients who are uncomfortable with AA’s religiosity, other self-help options for alcohol dependence include SMART Recovery (a CBT-based treatment) and Secular Organization for Sobriety (see Related resources).

Table 2

Matching patients to AA groups:
6 variables to consider

Some studies^20,21—but not all²⁷—suggest that individuals with co-occurring psychiatric disorders have more difficulty participating fully in AA than those without such comorbidity.

Kelly et al²⁰ examined the influence of major depressive disorder (MDD) on AA participation and treatment outcomes in 2,161 men with substance use disorders. During the first year after discharge from inpatient substance-abuse treatment, MDD appeared to have no effect on AA attendance rates or substance abuse outcomes. However, the 110 men with co-occurring MDD showed significantly less social participation in AA—with fewer friends, contacts/calls, and sponsors—and they continued to suffer substantial depression.

This suggests that clinicians could help patients with MDD engage in AA by addressing social anxiety symptoms (how to ask for a sponsor, the importance of establishing and using the AA social network). Carefully monitoring and treating acute depressive symptoms also may enhance AA social participation, especially for patients new to AA.

Impaired social relating is common to many psychiatric disorders—such as psychotic disorders, anxiety disorders, trauma and personality disorders—and social skills training may help other dual-diagnosis patients entering AA. Those with impaired self-control—as with mania or overt psychosis—or inability to maintain interpersonal boundaries are best referred to AA after you stabilize symptoms that would disrupt the group setting.

Related resources

• Alcoholics Anonymous. General Services Office, PO Box 459, Grand Central Station, New York, NY 10163. Phone (212) 870-3400. www.aa.org
  
• AA Grapevine: International Journal of Alcoholics Anonymous. http://www.aagrapevine.org.
  
• National Institute on Alcohol Abuse and Alcoholism. http://www.niaaa.nih.gov
  
• National Institute on Drug Abuse. http://www.nida.nih.gov/NIDAHome.html
  
• Cocaine Anonymous. http://www.ca.org
  
• Narcotics Anonymous. http://www.na.org
  
• Secular Organizations for Sobriety. http://www.sossobriety.org
  
• SMART Recovery. http://www.smartrecovery.org
  

Many clinicians refer alcohol-dependent patients to Alcoholics Anonymous, but how effective is AA in reducing drinking? Evidence is elusive—partly because of AA’s tradition of anonymity—but clinician encouragement is among three variables that appear essential to successful AA use.

The pioneer of twelve-step programs (Box 1),^1,2 AA is a widely accessible, free adjunct to professional alcohol abuse treatment. This article describes the evidence supporting AA’s efficacy for reducing drinking among persons with alcohol use disorders. We also recommend referral strategies that increase AA participation and discuss special needs of alcohol-dependent patients with comorbid psychiatric disorders.

Box 1

KEYS TO AA SUCCESS

Besides clinician encouragement, two patient variables—severity of alcohol dependence and self-efficacy—have been associated with successful AA use.

Clinician encouragement. When psychiatrists and other clinicians encourage alcohol-dependent patients to attend AA, the rate of AA use increases and drinking decreases.^3-7 When clinicians remain interested in alcohol-dependent patients’ AA use—rather than simply recommending AA—patients are more likely to follow through with a referral and to participate long enough to obtain benefit.

Clinicians play an important role in helping patients benefit from AA referral (Box 2).⁶ Patients who are personally helped to an AA group will rapidly attend, whereas those only given referral information are unlikely to follow up.⁷ Moreover, clinicians who encourage patients to attend AA and follow up on that attendance have more patients who attend and participate in AA than do less proactive clinicians.⁸

Box 2

Self-efficacy. Believing that one can abstain from drinking is associated with being able to reduce one’s drinking. Alcohol-dependent patients with self-efficacy are more likely to use AA, and this trait is believed to be a component of the change process associated with reduced drinking.^11,12

HOW EFFECTIVE IS AA?

Randomized, controlled trials (RCTs) may be the “gold standard” for determining any treatment’s efficacy, but constructing an RCT of AA use is complicated. AA does not engage in or support research, which makes AA use difficult to administer as a controlled variable in clinical trials. Also, the variability of AA groups and environments confounds the interpretation of study results and limits their application to populations at large.¹³

Even so, AA can be effective as an adjunct to professional treatments—such as detoxification—and as aftercare to maintain reduced drinking:

• Kelly’s¹⁴ comprehensive review and critical analysis of the main studies through 2003 showed a correlation between professional treatment plus AA attendance and improved outcomes.
  
• Project MATCH-—a large RCT—also supports AA’s benefits, as reported in smaller, less rigorously controlled studies.^4,5
  

• Kownacki and Shadish¹⁵ found poorer 12-month drinking outcomes with AA alone, compared with other treatments or no treatment. Their review assessed attendance as a predictor of alcohol use outcomes, and most subjects were attending AA under court orders. Because AA’s philosophy stresses that members must desire to stop drinking (Table 1), these study results may not apply to the voluntary, motivated individuals who usually use AA.
  
• Two other meta-analyses^9,10 that included nonrandomized studies and RCTs showed that attending AA has modest, favorable effects in reducing drinking and improving psychosocial functioning.
  

Outpatient studies showed positive correlations between AA attendance/involvement and:

• reduced drinking
  
• improved psychological adjustment and improved family relationships.
  

All three meta-analyses excluded studies of alcohol-dependent individuals with co-occurring drug use disorders, leaving unaddressed the effect of adjunctive AA in that population.

Table 1

AA’s Twelve Steps of personal recovery

• 12 sessions of cognitive-behavioral coping skills (CBT)
  
• 4 sessions of motivational enhancement therapy (MET).
  

Project MATCH thus found that a twelve-step individual therapy was at least as effective as CBT and MET in reducing post-treatment drinking and maintaining abstinence.

Real-world efficacy. A naturalistic study that resembled Project MATCH enrolled 3,018 male military veterans with substance use disorders across 15 program sites.¹⁸ Drug dependence was not excluded, and 51% of the men had co-occurring alcohol and drug dependence.

Participants received inpatient detoxification, followed by 21 to 28 days of intensive twelve-step treatment, CBT, or both. Alcohol and drug abuse declined equally in all three groups, and subjects were referred for outpatient aftercare and self-help groups. After 1 year, involvement in a self-help group predicted better outcome, regardless of the initial treatment.¹⁹

Unlike earlier studies,^15,20,21 this trial found that individuals with co-occurring psychiatric disorders and those legally mandated to get treatment did as well at 1-year follow-up as those without these variables. It provides additional evidence that twelve-step treatments can reduce substance use across varied populations, including patients with co-occurring alcohol and drug dependence.

AA ATTENDANCE VS. PARTICIPATION

Twelve-step programs appear most effective for individuals who actively participate. This may seem obvious, but most studies of 12-step treatments have monitored meeting attendance rather than engagement. Most studies that separate these variables report that active participation—not passive attendance—correlates with reduced substance use.

Montgomery et al²² followed 66 alcohol-dependent individuals in a 12-step oriented, 28-day residential treatment program and investigated:

• relationships between AA attendance and participation
  
• drinking outcomes over 31 weeks after treatment.
  

Similarly, Project MATCH participants involved in AA during the first 6 months after treatment had more-frequent abstinent days in the 7 to 12 months after treatment. AA “involvement” included identifying oneself as an AA member, working the steps, having an AA sponsor, and celebrating sobriety milestones.¹²

The National Drug Abuse Collaborative Cocaine Treatment Study is the most detailed analysis of self-help use. This multi-site RCT by Weiss and colleagues enrolled 487 individuals for behavioral treatment of cocaine dependence.²³

Twelve-step attendance did not predict substance use outcomes, but active participation (such as making coffee for a meeting or reading AA literature) in a given month predicted decreased substance use in the following month. Subjects whose participation increased over the first 3 months showed reduced drug use in the following 3 months. Interestingly, those who participated without attending meetings regularly (such as by reading AA literature or calling a sponsor) benefited as much as those who attended meetings more regularly.

Summary. Actively engaging in 12-step treatment—as measured by identifying with the fellowship and following the steps—appears more important to success than simply attending meetings.

EFFECTIVE AA REFERRALS

To encourage engagement when referring, try to match patients to AA groups attended by persons with whom they feel comfortable (Table 2).²⁴ Adolescents, for example, tend to have more difficulty engaging and remaining in AA than do adults.²⁵ One remedy may be to recommend a Young Person’s AA group composed primarily of adolescents and young adults.

Although AA embraces a spiritual approach to recovery, a person can benefit from participating without having a specific religious affiliation or spiritual beliefs.^12,26 The emphasis on spirituality and a “higher power” varies from one AA group to another as well as from region to region. For patients who are uncomfortable with AA’s religiosity, other self-help options for alcohol dependence include SMART Recovery (a CBT-based treatment) and Secular Organization for Sobriety (see Related resources).

Table 2

Matching patients to AA groups:
6 variables to consider

Some studies^20,21—but not all²⁷—suggest that individuals with co-occurring psychiatric disorders have more difficulty participating fully in AA than those without such comorbidity.

Kelly et al²⁰ examined the influence of major depressive disorder (MDD) on AA participation and treatment outcomes in 2,161 men with substance use disorders. During the first year after discharge from inpatient substance-abuse treatment, MDD appeared to have no effect on AA attendance rates or substance abuse outcomes. However, the 110 men with co-occurring MDD showed significantly less social participation in AA—with fewer friends, contacts/calls, and sponsors—and they continued to suffer substantial depression.

This suggests that clinicians could help patients with MDD engage in AA by addressing social anxiety symptoms (how to ask for a sponsor, the importance of establishing and using the AA social network). Carefully monitoring and treating acute depressive symptoms also may enhance AA social participation, especially for patients new to AA.

Impaired social relating is common to many psychiatric disorders—such as psychotic disorders, anxiety disorders, trauma and personality disorders—and social skills training may help other dual-diagnosis patients entering AA. Those with impaired self-control—as with mania or overt psychosis—or inability to maintain interpersonal boundaries are best referred to AA after you stabilize symptoms that would disrupt the group setting.

Related resources

• Alcoholics Anonymous. General Services Office, PO Box 459, Grand Central Station, New York, NY 10163. Phone (212) 870-3400. www.aa.org
  
• AA Grapevine: International Journal of Alcoholics Anonymous. http://www.aagrapevine.org.
  
• National Institute on Alcohol Abuse and Alcoholism. http://www.niaaa.nih.gov
  
• National Institute on Drug Abuse. http://www.nida.nih.gov/NIDAHome.html
  
• Cocaine Anonymous. http://www.ca.org
  
• Narcotics Anonymous. http://www.na.org
  
• Secular Organizations for Sobriety. http://www.sossobriety.org
  
• SMART Recovery. http://www.smartrecovery.org
  

Many clinicians refer alcohol-dependent patients to Alcoholics Anonymous, but how effective is AA in reducing drinking? Evidence is elusive—partly because of AA’s tradition of anonymity—but clinician encouragement is among three variables that appear essential to successful AA use.

The pioneer of twelve-step programs (Box 1),^1,2 AA is a widely accessible, free adjunct to professional alcohol abuse treatment. This article describes the evidence supporting AA’s efficacy for reducing drinking among persons with alcohol use disorders. We also recommend referral strategies that increase AA participation and discuss special needs of alcohol-dependent patients with comorbid psychiatric disorders.

Box 1

KEYS TO AA SUCCESS

Besides clinician encouragement, two patient variables—severity of alcohol dependence and self-efficacy—have been associated with successful AA use.

Clinician encouragement. When psychiatrists and other clinicians encourage alcohol-dependent patients to attend AA, the rate of AA use increases and drinking decreases.^3-7 When clinicians remain interested in alcohol-dependent patients’ AA use—rather than simply recommending AA—patients are more likely to follow through with a referral and to participate long enough to obtain benefit.

Clinicians play an important role in helping patients benefit from AA referral (Box 2).⁶ Patients who are personally helped to an AA group will rapidly attend, whereas those only given referral information are unlikely to follow up.⁷ Moreover, clinicians who encourage patients to attend AA and follow up on that attendance have more patients who attend and participate in AA than do less proactive clinicians.⁸

Box 2

Self-efficacy. Believing that one can abstain from drinking is associated with being able to reduce one’s drinking. Alcohol-dependent patients with self-efficacy are more likely to use AA, and this trait is believed to be a component of the change process associated with reduced drinking.^11,12

HOW EFFECTIVE IS AA?

Randomized, controlled trials (RCTs) may be the “gold standard” for determining any treatment’s efficacy, but constructing an RCT of AA use is complicated. AA does not engage in or support research, which makes AA use difficult to administer as a controlled variable in clinical trials. Also, the variability of AA groups and environments confounds the interpretation of study results and limits their application to populations at large.¹³

Even so, AA can be effective as an adjunct to professional treatments—such as detoxification—and as aftercare to maintain reduced drinking:

• Kelly’s¹⁴ comprehensive review and critical analysis of the main studies through 2003 showed a correlation between professional treatment plus AA attendance and improved outcomes.
  
• Project MATCH-—a large RCT—also supports AA’s benefits, as reported in smaller, less rigorously controlled studies.^4,5
  

• Kownacki and Shadish¹⁵ found poorer 12-month drinking outcomes with AA alone, compared with other treatments or no treatment. Their review assessed attendance as a predictor of alcohol use outcomes, and most subjects were attending AA under court orders. Because AA’s philosophy stresses that members must desire to stop drinking (Table 1), these study results may not apply to the voluntary, motivated individuals who usually use AA.
  
• Two other meta-analyses^9,10 that included nonrandomized studies and RCTs showed that attending AA has modest, favorable effects in reducing drinking and improving psychosocial functioning.
  

Outpatient studies showed positive correlations between AA attendance/involvement and:

• reduced drinking
  
• improved psychological adjustment and improved family relationships.
  

All three meta-analyses excluded studies of alcohol-dependent individuals with co-occurring drug use disorders, leaving unaddressed the effect of adjunctive AA in that population.

Table 1

AA’s Twelve Steps of personal recovery

• 12 sessions of cognitive-behavioral coping skills (CBT)
  
• 4 sessions of motivational enhancement therapy (MET).
  

Project MATCH thus found that a twelve-step individual therapy was at least as effective as CBT and MET in reducing post-treatment drinking and maintaining abstinence.

Real-world efficacy. A naturalistic study that resembled Project MATCH enrolled 3,018 male military veterans with substance use disorders across 15 program sites.¹⁸ Drug dependence was not excluded, and 51% of the men had co-occurring alcohol and drug dependence.

Participants received inpatient detoxification, followed by 21 to 28 days of intensive twelve-step treatment, CBT, or both. Alcohol and drug abuse declined equally in all three groups, and subjects were referred for outpatient aftercare and self-help groups. After 1 year, involvement in a self-help group predicted better outcome, regardless of the initial treatment.¹⁹

Unlike earlier studies,^15,20,21 this trial found that individuals with co-occurring psychiatric disorders and those legally mandated to get treatment did as well at 1-year follow-up as those without these variables. It provides additional evidence that twelve-step treatments can reduce substance use across varied populations, including patients with co-occurring alcohol and drug dependence.

AA ATTENDANCE VS. PARTICIPATION

Twelve-step programs appear most effective for individuals who actively participate. This may seem obvious, but most studies of 12-step treatments have monitored meeting attendance rather than engagement. Most studies that separate these variables report that active participation—not passive attendance—correlates with reduced substance use.

Montgomery et al²² followed 66 alcohol-dependent individuals in a 12-step oriented, 28-day residential treatment program and investigated:

• relationships between AA attendance and participation
  
• drinking outcomes over 31 weeks after treatment.
  

Similarly, Project MATCH participants involved in AA during the first 6 months after treatment had more-frequent abstinent days in the 7 to 12 months after treatment. AA “involvement” included identifying oneself as an AA member, working the steps, having an AA sponsor, and celebrating sobriety milestones.¹²

The National Drug Abuse Collaborative Cocaine Treatment Study is the most detailed analysis of self-help use. This multi-site RCT by Weiss and colleagues enrolled 487 individuals for behavioral treatment of cocaine dependence.²³

Twelve-step attendance did not predict substance use outcomes, but active participation (such as making coffee for a meeting or reading AA literature) in a given month predicted decreased substance use in the following month. Subjects whose participation increased over the first 3 months showed reduced drug use in the following 3 months. Interestingly, those who participated without attending meetings regularly (such as by reading AA literature or calling a sponsor) benefited as much as those who attended meetings more regularly.

Summary. Actively engaging in 12-step treatment—as measured by identifying with the fellowship and following the steps—appears more important to success than simply attending meetings.

EFFECTIVE AA REFERRALS

To encourage engagement when referring, try to match patients to AA groups attended by persons with whom they feel comfortable (Table 2).²⁴ Adolescents, for example, tend to have more difficulty engaging and remaining in AA than do adults.²⁵ One remedy may be to recommend a Young Person’s AA group composed primarily of adolescents and young adults.

Although AA embraces a spiritual approach to recovery, a person can benefit from participating without having a specific religious affiliation or spiritual beliefs.^12,26 The emphasis on spirituality and a “higher power” varies from one AA group to another as well as from region to region. For patients who are uncomfortable with AA’s religiosity, other self-help options for alcohol dependence include SMART Recovery (a CBT-based treatment) and Secular Organization for Sobriety (see Related resources).

Table 2

Matching patients to AA groups:
6 variables to consider

Some studies^20,21—but not all²⁷—suggest that individuals with co-occurring psychiatric disorders have more difficulty participating fully in AA than those without such comorbidity.

Kelly et al²⁰ examined the influence of major depressive disorder (MDD) on AA participation and treatment outcomes in 2,161 men with substance use disorders. During the first year after discharge from inpatient substance-abuse treatment, MDD appeared to have no effect on AA attendance rates or substance abuse outcomes. However, the 110 men with co-occurring MDD showed significantly less social participation in AA—with fewer friends, contacts/calls, and sponsors—and they continued to suffer substantial depression.

This suggests that clinicians could help patients with MDD engage in AA by addressing social anxiety symptoms (how to ask for a sponsor, the importance of establishing and using the AA social network). Carefully monitoring and treating acute depressive symptoms also may enhance AA social participation, especially for patients new to AA.

Impaired social relating is common to many psychiatric disorders—such as psychotic disorders, anxiety disorders, trauma and personality disorders—and social skills training may help other dual-diagnosis patients entering AA. Those with impaired self-control—as with mania or overt psychosis—or inability to maintain interpersonal boundaries are best referred to AA after you stabilize symptoms that would disrupt the group setting.

Related resources

• Alcoholics Anonymous. General Services Office, PO Box 459, Grand Central Station, New York, NY 10163. Phone (212) 870-3400. www.aa.org
  
• AA Grapevine: International Journal of Alcoholics Anonymous. http://www.aagrapevine.org.
  
• National Institute on Alcohol Abuse and Alcoholism. http://www.niaaa.nih.gov
  
• National Institute on Drug Abuse. http://www.nida.nih.gov/NIDAHome.html
  
• Cocaine Anonymous. http://www.ca.org
  
• Narcotics Anonymous. http://www.na.org
  
• Secular Organizations for Sobriety. http://www.sossobriety.org
  
• SMART Recovery. http://www.smartrecovery.org