Current Psychiatry

What do you tell your patients who are self-medicating with herbal remedies? Can dietary supplements safely improve mood disorders, insomnia, and other psychiatric complaints?

Evidence is limited on complementary and alternative medicines (CAMs), their active components, pharmacokinetics/dynamics, adverse effects, drug interactions, and therapeutic outcomes. Based on our review of trial data, case reports, and an NIH National Center for Complementary and Alternative Medicine (NCCAM) survey,¹ we offer information to help you:

• identify patients using dietary supplements
• avoid serious interactions with common psychotropics
• counsel patients on the efficacy and safety of ginkgo biloba, St. John’s wort, kava kava, and valerian (Table 1).

DON’T BE AFRAID TO ASK

One-third of Americans who took part in the NCCAM survey reported using CAM. After prayer—the number-one CAM—respondents said they most often used natural products such as herbals, botanicals, nutraceuticals, phytomedicinals, and dietary supplements (Figure).¹

Table 1

4 herbal supplements with purported psychotropic effects

Patients tend to use CAM to treat chronic medical conditions such as back pain, depression, and anxiety.¹ Although CAM use is common, only 38% of patients say they disclose using CAM to their physicians.² These use and disclosure patterns are similar in psychiatry.³

Herbal products may produce symptoms that mimic those of mental illnesses, such as psychosis and mania, complicating diagnosis and treatment. Abruptly stopping some herbs can produce withdrawal symptoms similar to those seen with benzodiazepine and antidepressant cessation. Supplements also can inhibit or augment prescribed psychotropics’ effects, and notable consequences include the potential for serotonin syndrome with use of St. John’s wort.

The key to learning about a patient’s use of dietary supplements is to ask. Patients commonly say they do not tell their doctors about using dietary supplements because “it wasn’t important for the doctor to know” or “the doctor never asked.”^4,5 Ten tips for discussing nutritional supplements with patients are shown in the Box.

Buyer—and psychiatrist—beware. Because of dietary supplements’ regulatory status, physicians and patients need to learn as much as they can about these products’ documented safety and efficacy. The Dietary Supplement Health and Education Act passed by Congress in 1994 does not require manufacturers to prove their products are safe or effective before marketing them. They also can make claims that suggest uses in physical/emotional structure and function, such as “helps maintain a healthy emotional outlook.”

The FDA bears the burden of proof regarding safety and can remove a dietary supplement from the market only after receiving documented adverse event information from the public.⁶ The FDA has confiscated herbal products containing prescription drugs and misidentified herbal components.

GINKGO BILOBA FOR DEMENTIA

Ginkgo biloba was the third most commonly used herbal product (21%) in the NCCAM survey. Ginkgo is promoted primarily for dementia, cerebrovascular dysfunction, and memory enhancement. The standardized ginkgo extract (EGb 761) contains several components to which its pharmacologic activity has been attributed. Its constituents are thought to act primarily through anticoagulant effects by inhibiting platelet-activating factor and cyclic GMP phosphodiesterase. They also act through membrane stabilization, antioxidant properties, free-radical scavenging, and inhibition of beta-amyloid deposition.⁷

Efficacy. In patients with dementia, clinical trials using EGb 761 have shown small improvements in or maintenance of cognitive and social functioning, compared with placebo.^8,9 The clinical significance of these findings is unclear, however. Ginkgo’s usefulness in enhancing memory is less certain. Controlled clinical trials are evaluating ginkgo’s efficacy in various conditions.¹⁰

Adverse effects. Bleeding complications are the primary concern with ginkgo biloba use, and caution is urged when it is taken concomitantly with aspirin or other antithrombotic drugs. Patients receiving warfarin should not take ginkgo because of the combined antiplatelet effects and ginkgo’s inhibition of warfarin metabolism and elimination.

Drug-herb interactions. One report showed that EGb 761 is a strong inhibitor of the cytochrome P-450 2C9 enzyme system (CYP 2C9).¹¹ Other identified inhibitors of CYP 2C9 are fluvoxamine (strong inhibitor), amiodarone, cimetidine, fluoxetine, and omeprazole. Drugs that serve as substrates for that system and can have decreased clearance include phenytoin, warfarin, amitriptyline, and diazepam;¹² use caution, therefore, when you co-administer these drugs with ginkgo.

Figure 10 CAM therapies patients report using most often

CAM: Complimentary and alternative medicines

Source: Barnes T, Powell-Griner E, McFann K, Nahin R. Complementary and alternative medicine use among adults: United States, 2002. Atlanta: Centers for Disease Control and Prevention, May 27, 2004: Advance Data Report #343 (available at http://www.cdc.gov/nchs/data/ad/ad343.pdf) Dosage. The usual dosage for standardized ginkgo extract is 120 to 240 mg/d, given in divided doses. Improvements associated with ginkgo use usually are seen within 4 to 12 weeks after starting therapy.⁷ Consider discontinuing therapy if you see no results after that time. Little is known about ginkgo’s effect after 1 year of use.

Recommendation. Limited data show a slight benefit in treating dementia by slowing cognitive and behavioral decline, but ginkgo biloba cannot be recommended as a first-line treatment until further controlled trials are available.

Box

ST. JOHN’S WORT FOR DEPRESSION

St. John’s wort (Hypericum perforatum), used to treat mild-to-moderate depression and anxiety,¹³ is one of the most-recognized herbal remedies. It accounted for 12% of the natural products used in the NCCAM survey. Several clinical trials assessing St. John’s wort are in progress and include placebo-controlled evaluations in obsessive-compulsive disorder and social phobia.¹⁴

As with ginkgo, St. John’s wort has many proposed active constituents; most preparations are standardized based on a hypericin content of 0.3%. Its mechanism of action in depression is unclear but laboratory models hint that it may be related to very mild inhibition of:

• monoamine oxidase (MAO)
• catechol-O-methyltransferase(COMT)
• selective serotonin reuptake
• interleukin-6 release (thereby increasing corticotropin-releasing hormone levels)
• norepinephrine uptake.¹⁵

Efficacy. St. John’s wort has been studied in mild, moderate, and major depression and compared with placebo and prescription therapies. In treating mild and moderate depression, St. John’s wort has been more effective than placebo and equivalent to tricyclic antidepressants.^16,17 Criticisms of these trials include lack of product standardization, lack of comparison with standard antidepressants at appropriate dosages, and small sample sizes. Larger trials comparing St. John’s wort with placebo and sertraline in treating major depression showed no difference in effect among the three.^18,19

Adverse effects are generally infrequent and include insomnia, anxiety, GI upset, and photosensitivity reactions.²⁰ St. John’s wort can induce hypomania and mania in patients with bipolar disorder and cause psychosis in schizophrenic patients.¹³

Drug-herb interactions. Of greatest concern with St. John’s wort use is the remarkable number of drug-herb interactions that have been identified (Table 2 and Table 3).^13,21 The primary mechanisms appear to be substantial induction of CYP 3A4, induction of P-glycoprotein mediated drug elimination, and—to a lesser extent—induction of other CYP isoenzymes.²² Interactions resulting in serotonin syndrome have been documented, with restlessness, sweating, and agitation.²³

The 3A4 isoenzyme metabolizes most drugs processed via the CYP system.¹² Severe interactions seen with St. John’s wort include:

• reduced cyclosporine levels, resulting in heart transplant rejection in two patients
• reduced antiretroviral levels in HIV patients
• pregnancy in women taking oral contraceptives.

Enzyme induction may persist for as long as 14 days after patients stop taking St. John’s wort.

Dosage. The recommended St. John’s wort dosage (using standardized 0.3% hypericin content) is 300 mg 2 or 3 times daily. Dosages of 1,200 to 1,800 mg/d have been used.^13,18 Benefits may not be seen for 2 to 3 weeks, and experience with use beyond 8 weeks in mild-to-moderate depression is very limited.

Recommendation. Advise patients to taper off St. John’s wort when stopping therapy to decrease the risk of withdrawal symptoms such as confusion, headache, nausea, insomnia, and fatigue.²¹ Given the high risk for drug interactions associated with St. John’s wort, we do not recommend its use in patients receiving any other medications.

KAVA KAVA AND LIVER TOXICITY

Kava kava (Piper methysticum) is used by some patients to treat anxiety and insomnia. Compared with other nutritional supplements, kava is less commonly used—by only 6.6% of adults using nutritional supplements,¹—and it is not being evaluated in NIH-sponsored trials.

The active-ingredient content varies considerably in kava root, so extracts are standardized to contain 70% kava-lactones (WS 1490). Although its exact mechanism is unclear, kava appears to:

• alter the limbic system
• inhibit monoamine oxidase type B (MAO-B)
• increase the number of gamma-aminobutyric acid (GABA) binding sites
• relax skeletal muscle
• produce anesthesia.²⁴

Table 2

Documented interactions with St. John’s wort

Table 3

Select potential interactions with St. John’s wort

Efficacy. A meta-analysis of studies found kava more effective than placebo in treating anxiety,²⁵ although most studies suffer from poor design and/or small sample size.

Adverse effects. Reports have associated kava use with hepatic toxicity, liver failure requiring liver transplantation, and death. The European Union and Canada have banned kava sales, and the FDA issued a consumer advisory noting kava’s risks. Emerging information indicates that kava inhibits virtually all CYP-450 enzymes, which would increase levels of and potential adverse effects from any medications taken with kava.²⁶

Other common adverse effects include GI upset, enlarged pupils, extrapyramidal side effects, and dizziness.^24,27

Dosage. Kava is usually given at 100 mg (70 mg of kavalactones) three times daily. Urge patients to avoid driving when taking kava because of its side effects. Anxiety symptoms may improve with 1 to 8 weeks of therapy, but adverse hepatic effects can occur within 3 to 4 weeks of starting kava use.

Recommendation. Avoid kava kava use because of substantial risk of hepatotoxicity and drug interactions.

VALERIAN FOR INSOMNIA, ANXIETY

Valerian (Valeriana officinalis) is promoted as a sedative/hypnotic and anxiolytic. The prevalence of valerian use (5.9%) mirrors that of kava.¹ An NCCAM study is enrolling patients to evaluate valerian’s effectiveness in treating Parkinson’s disease-related sleep disturbances.

Efficacy. Information on valerian’s mechanism of action and clinical effectiveness is quite limited. In animal studies, its components produced direct sedative effects and inhibited CNS catabolism of GABA.²⁸ Results are mixed in humans with insomnia; some studies have found reduced sleep latency and improved sleep quality with valerian use, whereas others found no improvements.²⁹ Limited, small evaluations suggest that valerian may be useful in treating anxiety.

Adverse effects. The FDA categorizes valerian as an approved food additive, so it is considered safe in usual amounts found in food. FDA lists no amount that it considers safe in food, however, and the federal code covering valerian states that only enough needed to impart the desired flavor should be used.

When taken in therapeutic amounts, valerian’s most common adverse effects are headache and residual morning drowsiness. Because of the herb’s sedative effects, urge caution if patients drive while using it. On discontinuation, withdrawal symptoms similar to those seen with benzodiazepine withdrawal—anxiety, headache, emotional lability—have been reported.

Dosage. For insomnia, valerian is taken 2 hours to 30 minutes before bedtime; doses start at 300 to 400 mg and increase to 600 to 900 mg. Recommended doses vary, as standardization is less common with valerian than with other herbals. Continuous treatment seems more effective than as-needed dosing, as valerian may take up to 4 weeks to improve insomnia.

Recommendation. Well-controlled trials are lacking, and safety data at therapeutic doses are limited. Monitor patients using valerian for adverse effects and drug interactions.

Related resources

• Natural Medicines Comprehensive Database.www.naturaldatabase.com
• National Center for Complementary and Alternative Medicine. http://nccam.nih.gov
• FDA MedWatch Adverse Event Reporting Program. www.fda.gov/medwatch/how.htm
• ConsumerLab.com. Independent testing of dietary supplements. www.consumerlab.com

Drug brand names

• Alprazolam • Xanax
• Amiodarone • Cordarone, Pacerone
• Amitriptyline • Elavil
• Buspirone • BuSpar
• Cimetidine • Tagamet
• Cyclosporine • various
• Diazepam • Valium
• Digoxin • Lanoxin
• Donepezil • Aricept
• Fentanyl • Duragesic
• Fexofenadine • Allegra
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Indinavir • Crixivan
• Irinotecan • Camptosar
• Methadone • various
• Midazolam • Versed
• Nefazodone • Serzone
• Nevirapine • Viramune
• Omeprazole • Prilosec
• Paroxetine • Paxil
• Phenytoin • Dilantin
• Sertraline • Zoloft
• Simvastatin • Zocor
• Tacrolimus • Prograf
• Temazepam • Restoril
• Theophylline • various
• Triazolam • Halcion
• Venlafaxine • Effexor
• Warfarin • Coumadin

Disclosures

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

What do you tell your patients who are self-medicating with herbal remedies? Can dietary supplements safely improve mood disorders, insomnia, and other psychiatric complaints?

Evidence is limited on complementary and alternative medicines (CAMs), their active components, pharmacokinetics/dynamics, adverse effects, drug interactions, and therapeutic outcomes. Based on our review of trial data, case reports, and an NIH National Center for Complementary and Alternative Medicine (NCCAM) survey,¹ we offer information to help you:

• identify patients using dietary supplements
• avoid serious interactions with common psychotropics
• counsel patients on the efficacy and safety of ginkgo biloba, St. John’s wort, kava kava, and valerian (Table 1).

DON’T BE AFRAID TO ASK

One-third of Americans who took part in the NCCAM survey reported using CAM. After prayer—the number-one CAM—respondents said they most often used natural products such as herbals, botanicals, nutraceuticals, phytomedicinals, and dietary supplements (Figure).¹

Table 1

4 herbal supplements with purported psychotropic effects

Patients tend to use CAM to treat chronic medical conditions such as back pain, depression, and anxiety.¹ Although CAM use is common, only 38% of patients say they disclose using CAM to their physicians.² These use and disclosure patterns are similar in psychiatry.³

Herbal products may produce symptoms that mimic those of mental illnesses, such as psychosis and mania, complicating diagnosis and treatment. Abruptly stopping some herbs can produce withdrawal symptoms similar to those seen with benzodiazepine and antidepressant cessation. Supplements also can inhibit or augment prescribed psychotropics’ effects, and notable consequences include the potential for serotonin syndrome with use of St. John’s wort.

The key to learning about a patient’s use of dietary supplements is to ask. Patients commonly say they do not tell their doctors about using dietary supplements because “it wasn’t important for the doctor to know” or “the doctor never asked.”^4,5 Ten tips for discussing nutritional supplements with patients are shown in the Box.

Buyer—and psychiatrist—beware. Because of dietary supplements’ regulatory status, physicians and patients need to learn as much as they can about these products’ documented safety and efficacy. The Dietary Supplement Health and Education Act passed by Congress in 1994 does not require manufacturers to prove their products are safe or effective before marketing them. They also can make claims that suggest uses in physical/emotional structure and function, such as “helps maintain a healthy emotional outlook.”

The FDA bears the burden of proof regarding safety and can remove a dietary supplement from the market only after receiving documented adverse event information from the public.⁶ The FDA has confiscated herbal products containing prescription drugs and misidentified herbal components.

GINKGO BILOBA FOR DEMENTIA

Ginkgo biloba was the third most commonly used herbal product (21%) in the NCCAM survey. Ginkgo is promoted primarily for dementia, cerebrovascular dysfunction, and memory enhancement. The standardized ginkgo extract (EGb 761) contains several components to which its pharmacologic activity has been attributed. Its constituents are thought to act primarily through anticoagulant effects by inhibiting platelet-activating factor and cyclic GMP phosphodiesterase. They also act through membrane stabilization, antioxidant properties, free-radical scavenging, and inhibition of beta-amyloid deposition.⁷

Efficacy. In patients with dementia, clinical trials using EGb 761 have shown small improvements in or maintenance of cognitive and social functioning, compared with placebo.^8,9 The clinical significance of these findings is unclear, however. Ginkgo’s usefulness in enhancing memory is less certain. Controlled clinical trials are evaluating ginkgo’s efficacy in various conditions.¹⁰

Adverse effects. Bleeding complications are the primary concern with ginkgo biloba use, and caution is urged when it is taken concomitantly with aspirin or other antithrombotic drugs. Patients receiving warfarin should not take ginkgo because of the combined antiplatelet effects and ginkgo’s inhibition of warfarin metabolism and elimination.

Drug-herb interactions. One report showed that EGb 761 is a strong inhibitor of the cytochrome P-450 2C9 enzyme system (CYP 2C9).¹¹ Other identified inhibitors of CYP 2C9 are fluvoxamine (strong inhibitor), amiodarone, cimetidine, fluoxetine, and omeprazole. Drugs that serve as substrates for that system and can have decreased clearance include phenytoin, warfarin, amitriptyline, and diazepam;¹² use caution, therefore, when you co-administer these drugs with ginkgo.

Figure 10 CAM therapies patients report using most often

CAM: Complimentary and alternative medicines

Source: Barnes T, Powell-Griner E, McFann K, Nahin R. Complementary and alternative medicine use among adults: United States, 2002. Atlanta: Centers for Disease Control and Prevention, May 27, 2004: Advance Data Report #343 (available at http://www.cdc.gov/nchs/data/ad/ad343.pdf) Dosage. The usual dosage for standardized ginkgo extract is 120 to 240 mg/d, given in divided doses. Improvements associated with ginkgo use usually are seen within 4 to 12 weeks after starting therapy.⁷ Consider discontinuing therapy if you see no results after that time. Little is known about ginkgo’s effect after 1 year of use.

Recommendation. Limited data show a slight benefit in treating dementia by slowing cognitive and behavioral decline, but ginkgo biloba cannot be recommended as a first-line treatment until further controlled trials are available.

Box

ST. JOHN’S WORT FOR DEPRESSION

St. John’s wort (Hypericum perforatum), used to treat mild-to-moderate depression and anxiety,¹³ is one of the most-recognized herbal remedies. It accounted for 12% of the natural products used in the NCCAM survey. Several clinical trials assessing St. John’s wort are in progress and include placebo-controlled evaluations in obsessive-compulsive disorder and social phobia.¹⁴

As with ginkgo, St. John’s wort has many proposed active constituents; most preparations are standardized based on a hypericin content of 0.3%. Its mechanism of action in depression is unclear but laboratory models hint that it may be related to very mild inhibition of:

• monoamine oxidase (MAO)
• catechol-O-methyltransferase(COMT)
• selective serotonin reuptake
• interleukin-6 release (thereby increasing corticotropin-releasing hormone levels)
• norepinephrine uptake.¹⁵

Efficacy. St. John’s wort has been studied in mild, moderate, and major depression and compared with placebo and prescription therapies. In treating mild and moderate depression, St. John’s wort has been more effective than placebo and equivalent to tricyclic antidepressants.^16,17 Criticisms of these trials include lack of product standardization, lack of comparison with standard antidepressants at appropriate dosages, and small sample sizes. Larger trials comparing St. John’s wort with placebo and sertraline in treating major depression showed no difference in effect among the three.^18,19

Adverse effects are generally infrequent and include insomnia, anxiety, GI upset, and photosensitivity reactions.²⁰ St. John’s wort can induce hypomania and mania in patients with bipolar disorder and cause psychosis in schizophrenic patients.¹³

Drug-herb interactions. Of greatest concern with St. John’s wort use is the remarkable number of drug-herb interactions that have been identified (Table 2 and Table 3).^13,21 The primary mechanisms appear to be substantial induction of CYP 3A4, induction of P-glycoprotein mediated drug elimination, and—to a lesser extent—induction of other CYP isoenzymes.²² Interactions resulting in serotonin syndrome have been documented, with restlessness, sweating, and agitation.²³

The 3A4 isoenzyme metabolizes most drugs processed via the CYP system.¹² Severe interactions seen with St. John’s wort include:

• reduced cyclosporine levels, resulting in heart transplant rejection in two patients
• reduced antiretroviral levels in HIV patients
• pregnancy in women taking oral contraceptives.

Enzyme induction may persist for as long as 14 days after patients stop taking St. John’s wort.

Dosage. The recommended St. John’s wort dosage (using standardized 0.3% hypericin content) is 300 mg 2 or 3 times daily. Dosages of 1,200 to 1,800 mg/d have been used.^13,18 Benefits may not be seen for 2 to 3 weeks, and experience with use beyond 8 weeks in mild-to-moderate depression is very limited.

Recommendation. Advise patients to taper off St. John’s wort when stopping therapy to decrease the risk of withdrawal symptoms such as confusion, headache, nausea, insomnia, and fatigue.²¹ Given the high risk for drug interactions associated with St. John’s wort, we do not recommend its use in patients receiving any other medications.

KAVA KAVA AND LIVER TOXICITY

Kava kava (Piper methysticum) is used by some patients to treat anxiety and insomnia. Compared with other nutritional supplements, kava is less commonly used—by only 6.6% of adults using nutritional supplements,¹—and it is not being evaluated in NIH-sponsored trials.

The active-ingredient content varies considerably in kava root, so extracts are standardized to contain 70% kava-lactones (WS 1490). Although its exact mechanism is unclear, kava appears to:

• alter the limbic system
• inhibit monoamine oxidase type B (MAO-B)
• increase the number of gamma-aminobutyric acid (GABA) binding sites
• relax skeletal muscle
• produce anesthesia.²⁴

Table 2

Documented interactions with St. John’s wort

Table 3

Select potential interactions with St. John’s wort

Efficacy. A meta-analysis of studies found kava more effective than placebo in treating anxiety,²⁵ although most studies suffer from poor design and/or small sample size.

Adverse effects. Reports have associated kava use with hepatic toxicity, liver failure requiring liver transplantation, and death. The European Union and Canada have banned kava sales, and the FDA issued a consumer advisory noting kava’s risks. Emerging information indicates that kava inhibits virtually all CYP-450 enzymes, which would increase levels of and potential adverse effects from any medications taken with kava.²⁶

Other common adverse effects include GI upset, enlarged pupils, extrapyramidal side effects, and dizziness.^24,27

Dosage. Kava is usually given at 100 mg (70 mg of kavalactones) three times daily. Urge patients to avoid driving when taking kava because of its side effects. Anxiety symptoms may improve with 1 to 8 weeks of therapy, but adverse hepatic effects can occur within 3 to 4 weeks of starting kava use.

Recommendation. Avoid kava kava use because of substantial risk of hepatotoxicity and drug interactions.

VALERIAN FOR INSOMNIA, ANXIETY

Valerian (Valeriana officinalis) is promoted as a sedative/hypnotic and anxiolytic. The prevalence of valerian use (5.9%) mirrors that of kava.¹ An NCCAM study is enrolling patients to evaluate valerian’s effectiveness in treating Parkinson’s disease-related sleep disturbances.

Efficacy. Information on valerian’s mechanism of action and clinical effectiveness is quite limited. In animal studies, its components produced direct sedative effects and inhibited CNS catabolism of GABA.²⁸ Results are mixed in humans with insomnia; some studies have found reduced sleep latency and improved sleep quality with valerian use, whereas others found no improvements.²⁹ Limited, small evaluations suggest that valerian may be useful in treating anxiety.

Adverse effects. The FDA categorizes valerian as an approved food additive, so it is considered safe in usual amounts found in food. FDA lists no amount that it considers safe in food, however, and the federal code covering valerian states that only enough needed to impart the desired flavor should be used.

When taken in therapeutic amounts, valerian’s most common adverse effects are headache and residual morning drowsiness. Because of the herb’s sedative effects, urge caution if patients drive while using it. On discontinuation, withdrawal symptoms similar to those seen with benzodiazepine withdrawal—anxiety, headache, emotional lability—have been reported.

Dosage. For insomnia, valerian is taken 2 hours to 30 minutes before bedtime; doses start at 300 to 400 mg and increase to 600 to 900 mg. Recommended doses vary, as standardization is less common with valerian than with other herbals. Continuous treatment seems more effective than as-needed dosing, as valerian may take up to 4 weeks to improve insomnia.

Recommendation. Well-controlled trials are lacking, and safety data at therapeutic doses are limited. Monitor patients using valerian for adverse effects and drug interactions.

Related resources

• Natural Medicines Comprehensive Database.www.naturaldatabase.com
• National Center for Complementary and Alternative Medicine. http://nccam.nih.gov
• FDA MedWatch Adverse Event Reporting Program. www.fda.gov/medwatch/how.htm
• ConsumerLab.com. Independent testing of dietary supplements. www.consumerlab.com

Drug brand names

• Alprazolam • Xanax
• Amiodarone • Cordarone, Pacerone
• Amitriptyline • Elavil
• Buspirone • BuSpar
• Cimetidine • Tagamet
• Cyclosporine • various
• Diazepam • Valium
• Digoxin • Lanoxin
• Donepezil • Aricept
• Fentanyl • Duragesic
• Fexofenadine • Allegra
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Indinavir • Crixivan
• Irinotecan • Camptosar
• Methadone • various
• Midazolam • Versed
• Nefazodone • Serzone
• Nevirapine • Viramune
• Omeprazole • Prilosec
• Paroxetine • Paxil
• Phenytoin • Dilantin
• Sertraline • Zoloft
• Simvastatin • Zocor
• Tacrolimus • Prograf
• Temazepam • Restoril
• Theophylline • various
• Triazolam • Halcion
• Venlafaxine • Effexor
• Warfarin • Coumadin

Disclosures

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

What do you tell your patients who are self-medicating with herbal remedies? Can dietary supplements safely improve mood disorders, insomnia, and other psychiatric complaints?

Evidence is limited on complementary and alternative medicines (CAMs), their active components, pharmacokinetics/dynamics, adverse effects, drug interactions, and therapeutic outcomes. Based on our review of trial data, case reports, and an NIH National Center for Complementary and Alternative Medicine (NCCAM) survey,¹ we offer information to help you:

• identify patients using dietary supplements
• avoid serious interactions with common psychotropics
• counsel patients on the efficacy and safety of ginkgo biloba, St. John’s wort, kava kava, and valerian (Table 1).

DON’T BE AFRAID TO ASK

One-third of Americans who took part in the NCCAM survey reported using CAM. After prayer—the number-one CAM—respondents said they most often used natural products such as herbals, botanicals, nutraceuticals, phytomedicinals, and dietary supplements (Figure).¹

Table 1

4 herbal supplements with purported psychotropic effects

Patients tend to use CAM to treat chronic medical conditions such as back pain, depression, and anxiety.¹ Although CAM use is common, only 38% of patients say they disclose using CAM to their physicians.² These use and disclosure patterns are similar in psychiatry.³

Herbal products may produce symptoms that mimic those of mental illnesses, such as psychosis and mania, complicating diagnosis and treatment. Abruptly stopping some herbs can produce withdrawal symptoms similar to those seen with benzodiazepine and antidepressant cessation. Supplements also can inhibit or augment prescribed psychotropics’ effects, and notable consequences include the potential for serotonin syndrome with use of St. John’s wort.

The key to learning about a patient’s use of dietary supplements is to ask. Patients commonly say they do not tell their doctors about using dietary supplements because “it wasn’t important for the doctor to know” or “the doctor never asked.”^4,5 Ten tips for discussing nutritional supplements with patients are shown in the Box.

Buyer—and psychiatrist—beware. Because of dietary supplements’ regulatory status, physicians and patients need to learn as much as they can about these products’ documented safety and efficacy. The Dietary Supplement Health and Education Act passed by Congress in 1994 does not require manufacturers to prove their products are safe or effective before marketing them. They also can make claims that suggest uses in physical/emotional structure and function, such as “helps maintain a healthy emotional outlook.”

The FDA bears the burden of proof regarding safety and can remove a dietary supplement from the market only after receiving documented adverse event information from the public.⁶ The FDA has confiscated herbal products containing prescription drugs and misidentified herbal components.

GINKGO BILOBA FOR DEMENTIA

Ginkgo biloba was the third most commonly used herbal product (21%) in the NCCAM survey. Ginkgo is promoted primarily for dementia, cerebrovascular dysfunction, and memory enhancement. The standardized ginkgo extract (EGb 761) contains several components to which its pharmacologic activity has been attributed. Its constituents are thought to act primarily through anticoagulant effects by inhibiting platelet-activating factor and cyclic GMP phosphodiesterase. They also act through membrane stabilization, antioxidant properties, free-radical scavenging, and inhibition of beta-amyloid deposition.⁷

Efficacy. In patients with dementia, clinical trials using EGb 761 have shown small improvements in or maintenance of cognitive and social functioning, compared with placebo.^8,9 The clinical significance of these findings is unclear, however. Ginkgo’s usefulness in enhancing memory is less certain. Controlled clinical trials are evaluating ginkgo’s efficacy in various conditions.¹⁰

Adverse effects. Bleeding complications are the primary concern with ginkgo biloba use, and caution is urged when it is taken concomitantly with aspirin or other antithrombotic drugs. Patients receiving warfarin should not take ginkgo because of the combined antiplatelet effects and ginkgo’s inhibition of warfarin metabolism and elimination.

Drug-herb interactions. One report showed that EGb 761 is a strong inhibitor of the cytochrome P-450 2C9 enzyme system (CYP 2C9).¹¹ Other identified inhibitors of CYP 2C9 are fluvoxamine (strong inhibitor), amiodarone, cimetidine, fluoxetine, and omeprazole. Drugs that serve as substrates for that system and can have decreased clearance include phenytoin, warfarin, amitriptyline, and diazepam;¹² use caution, therefore, when you co-administer these drugs with ginkgo.

Figure 10 CAM therapies patients report using most often

CAM: Complimentary and alternative medicines

Source: Barnes T, Powell-Griner E, McFann K, Nahin R. Complementary and alternative medicine use among adults: United States, 2002. Atlanta: Centers for Disease Control and Prevention, May 27, 2004: Advance Data Report #343 (available at http://www.cdc.gov/nchs/data/ad/ad343.pdf) Dosage. The usual dosage for standardized ginkgo extract is 120 to 240 mg/d, given in divided doses. Improvements associated with ginkgo use usually are seen within 4 to 12 weeks after starting therapy.⁷ Consider discontinuing therapy if you see no results after that time. Little is known about ginkgo’s effect after 1 year of use.

Recommendation. Limited data show a slight benefit in treating dementia by slowing cognitive and behavioral decline, but ginkgo biloba cannot be recommended as a first-line treatment until further controlled trials are available.

Box

ST. JOHN’S WORT FOR DEPRESSION

St. John’s wort (Hypericum perforatum), used to treat mild-to-moderate depression and anxiety,¹³ is one of the most-recognized herbal remedies. It accounted for 12% of the natural products used in the NCCAM survey. Several clinical trials assessing St. John’s wort are in progress and include placebo-controlled evaluations in obsessive-compulsive disorder and social phobia.¹⁴

As with ginkgo, St. John’s wort has many proposed active constituents; most preparations are standardized based on a hypericin content of 0.3%. Its mechanism of action in depression is unclear but laboratory models hint that it may be related to very mild inhibition of:

• monoamine oxidase (MAO)
• catechol-O-methyltransferase(COMT)
• selective serotonin reuptake
• interleukin-6 release (thereby increasing corticotropin-releasing hormone levels)
• norepinephrine uptake.¹⁵

Efficacy. St. John’s wort has been studied in mild, moderate, and major depression and compared with placebo and prescription therapies. In treating mild and moderate depression, St. John’s wort has been more effective than placebo and equivalent to tricyclic antidepressants.^16,17 Criticisms of these trials include lack of product standardization, lack of comparison with standard antidepressants at appropriate dosages, and small sample sizes. Larger trials comparing St. John’s wort with placebo and sertraline in treating major depression showed no difference in effect among the three.^18,19

Adverse effects are generally infrequent and include insomnia, anxiety, GI upset, and photosensitivity reactions.²⁰ St. John’s wort can induce hypomania and mania in patients with bipolar disorder and cause psychosis in schizophrenic patients.¹³

Drug-herb interactions. Of greatest concern with St. John’s wort use is the remarkable number of drug-herb interactions that have been identified (Table 2 and Table 3).^13,21 The primary mechanisms appear to be substantial induction of CYP 3A4, induction of P-glycoprotein mediated drug elimination, and—to a lesser extent—induction of other CYP isoenzymes.²² Interactions resulting in serotonin syndrome have been documented, with restlessness, sweating, and agitation.²³

The 3A4 isoenzyme metabolizes most drugs processed via the CYP system.¹² Severe interactions seen with St. John’s wort include:

• reduced cyclosporine levels, resulting in heart transplant rejection in two patients
• reduced antiretroviral levels in HIV patients
• pregnancy in women taking oral contraceptives.

Enzyme induction may persist for as long as 14 days after patients stop taking St. John’s wort.

Dosage. The recommended St. John’s wort dosage (using standardized 0.3% hypericin content) is 300 mg 2 or 3 times daily. Dosages of 1,200 to 1,800 mg/d have been used.^13,18 Benefits may not be seen for 2 to 3 weeks, and experience with use beyond 8 weeks in mild-to-moderate depression is very limited.

Recommendation. Advise patients to taper off St. John’s wort when stopping therapy to decrease the risk of withdrawal symptoms such as confusion, headache, nausea, insomnia, and fatigue.²¹ Given the high risk for drug interactions associated with St. John’s wort, we do not recommend its use in patients receiving any other medications.

KAVA KAVA AND LIVER TOXICITY

Kava kava (Piper methysticum) is used by some patients to treat anxiety and insomnia. Compared with other nutritional supplements, kava is less commonly used—by only 6.6% of adults using nutritional supplements,¹—and it is not being evaluated in NIH-sponsored trials.

The active-ingredient content varies considerably in kava root, so extracts are standardized to contain 70% kava-lactones (WS 1490). Although its exact mechanism is unclear, kava appears to:

• alter the limbic system
• inhibit monoamine oxidase type B (MAO-B)
• increase the number of gamma-aminobutyric acid (GABA) binding sites
• relax skeletal muscle
• produce anesthesia.²⁴

Table 2

Documented interactions with St. John’s wort

Table 3

Select potential interactions with St. John’s wort

Efficacy. A meta-analysis of studies found kava more effective than placebo in treating anxiety,²⁵ although most studies suffer from poor design and/or small sample size.

Adverse effects. Reports have associated kava use with hepatic toxicity, liver failure requiring liver transplantation, and death. The European Union and Canada have banned kava sales, and the FDA issued a consumer advisory noting kava’s risks. Emerging information indicates that kava inhibits virtually all CYP-450 enzymes, which would increase levels of and potential adverse effects from any medications taken with kava.²⁶

Other common adverse effects include GI upset, enlarged pupils, extrapyramidal side effects, and dizziness.^24,27

Dosage. Kava is usually given at 100 mg (70 mg of kavalactones) three times daily. Urge patients to avoid driving when taking kava because of its side effects. Anxiety symptoms may improve with 1 to 8 weeks of therapy, but adverse hepatic effects can occur within 3 to 4 weeks of starting kava use.

Recommendation. Avoid kava kava use because of substantial risk of hepatotoxicity and drug interactions.

VALERIAN FOR INSOMNIA, ANXIETY

Valerian (Valeriana officinalis) is promoted as a sedative/hypnotic and anxiolytic. The prevalence of valerian use (5.9%) mirrors that of kava.¹ An NCCAM study is enrolling patients to evaluate valerian’s effectiveness in treating Parkinson’s disease-related sleep disturbances.

Efficacy. Information on valerian’s mechanism of action and clinical effectiveness is quite limited. In animal studies, its components produced direct sedative effects and inhibited CNS catabolism of GABA.²⁸ Results are mixed in humans with insomnia; some studies have found reduced sleep latency and improved sleep quality with valerian use, whereas others found no improvements.²⁹ Limited, small evaluations suggest that valerian may be useful in treating anxiety.

Adverse effects. The FDA categorizes valerian as an approved food additive, so it is considered safe in usual amounts found in food. FDA lists no amount that it considers safe in food, however, and the federal code covering valerian states that only enough needed to impart the desired flavor should be used.

When taken in therapeutic amounts, valerian’s most common adverse effects are headache and residual morning drowsiness. Because of the herb’s sedative effects, urge caution if patients drive while using it. On discontinuation, withdrawal symptoms similar to those seen with benzodiazepine withdrawal—anxiety, headache, emotional lability—have been reported.

Dosage. For insomnia, valerian is taken 2 hours to 30 minutes before bedtime; doses start at 300 to 400 mg and increase to 600 to 900 mg. Recommended doses vary, as standardization is less common with valerian than with other herbals. Continuous treatment seems more effective than as-needed dosing, as valerian may take up to 4 weeks to improve insomnia.

Recommendation. Well-controlled trials are lacking, and safety data at therapeutic doses are limited. Monitor patients using valerian for adverse effects and drug interactions.

Related resources

• Natural Medicines Comprehensive Database.www.naturaldatabase.com
• National Center for Complementary and Alternative Medicine. http://nccam.nih.gov
• FDA MedWatch Adverse Event Reporting Program. www.fda.gov/medwatch/how.htm
• ConsumerLab.com. Independent testing of dietary supplements. www.consumerlab.com

Drug brand names

• Alprazolam • Xanax
• Amiodarone • Cordarone, Pacerone
• Amitriptyline • Elavil
• Buspirone • BuSpar
• Cimetidine • Tagamet
• Cyclosporine • various
• Diazepam • Valium
• Digoxin • Lanoxin
• Donepezil • Aricept
• Fentanyl • Duragesic
• Fexofenadine • Allegra
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Indinavir • Crixivan
• Irinotecan • Camptosar
• Methadone • various
• Midazolam • Versed
• Nefazodone • Serzone
• Nevirapine • Viramune
• Omeprazole • Prilosec
• Paroxetine • Paxil
• Phenytoin • Dilantin
• Sertraline • Zoloft
• Simvastatin • Zocor
• Tacrolimus • Prograf
• Temazepam • Restoril
• Theophylline • various
• Triazolam • Halcion
• Venlafaxine • Effexor
• Warfarin • Coumadin

Disclosures

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

Many physicians communicate with patients or colleagues via e-mail but lose this connectivity when they travel. If you find traditional home and office e-mail accounts are no longer enough, several e-mail access options can help you stay connected anytime.

How e-mail works

Typical home e-mail accounts-known as post office protocol (POP) accounts-use a client-server access method. The client-such as Outlook Express, Eudora, or Netscape Mail-checks the server for mail, which is then downloaded onto the home computer. Once downloaded, the message is gone from the server.

By contrast, an Internet message access protocol (IMAP) account offers more capabilities, such as allowing users to store e-mail on the server and organize mail into folders.^{December 2003). Also, some public locations such as New York’s Bryant Park offer free wireless Internet as a public service.2 Personal digital assistants or notebook computers with wireless capability, such as the Tungsten TC or the Toshiba e800, are best suited to this type of access.}

Dial-up Internet service is possible over your cell phone. Most mobile phone carriers charge extra for data transmission, and you will need a specific cable to connect your phone to your computer. Bluetooth wireless technology can eliminate the need for cables but beware: Data transfer is much slower with Bluetooth than with other methods.

Third-generation networks (3G)-higher-speed protocols that allow faster data transmission for multimedia-have been touted as the next best service from mobile phone providers. Wireless devices such as the Palm Treo or the Research in Motion BlackBerry are specifically designed for this type of access. Monthly data service costs approximately $30 for unlimited downloads or less when bundled with a voice plan. Access is limited to the cellular coverage area, however.

Wireless access protocol, an alternative to 3G, lets you access e-mail via your mobile phone. This service, available from mobile service providers for an additional monthly fee (about $10), lets you read mail on the phone screen, but there are several drawbacks:

• Some people may find the text too small to read.
• Text entry via the telephone keypad can be difficult. You either tap a key multiple times to select letters or use word prediction based on letters entered.
• Not all phones available for each carrier can perform this function.

Wireless access protocol is well suited to reading e-mails. To compose an e-mail, however, you need to choose letters by clicking on numbers, which can be very difficult.

Many physicians communicate with patients or colleagues via e-mail but lose this connectivity when they travel. If you find traditional home and office e-mail accounts are no longer enough, several e-mail access options can help you stay connected anytime.

How e-mail works

Typical home e-mail accounts-known as post office protocol (POP) accounts-use a client-server access method. The client-such as Outlook Express, Eudora, or Netscape Mail-checks the server for mail, which is then downloaded onto the home computer. Once downloaded, the message is gone from the server.

By contrast, an Internet message access protocol (IMAP) account offers more capabilities, such as allowing users to store e-mail on the server and organize mail into folders.^{December 2003). Also, some public locations such as New York’s Bryant Park offer free wireless Internet as a public service.2 Personal digital assistants or notebook computers with wireless capability, such as the Tungsten TC or the Toshiba e800, are best suited to this type of access.}

Dial-up Internet service is possible over your cell phone. Most mobile phone carriers charge extra for data transmission, and you will need a specific cable to connect your phone to your computer. Bluetooth wireless technology can eliminate the need for cables but beware: Data transfer is much slower with Bluetooth than with other methods.

Third-generation networks (3G)-higher-speed protocols that allow faster data transmission for multimedia-have been touted as the next best service from mobile phone providers. Wireless devices such as the Palm Treo or the Research in Motion BlackBerry are specifically designed for this type of access. Monthly data service costs approximately $30 for unlimited downloads or less when bundled with a voice plan. Access is limited to the cellular coverage area, however.

Wireless access protocol, an alternative to 3G, lets you access e-mail via your mobile phone. This service, available from mobile service providers for an additional monthly fee (about $10), lets you read mail on the phone screen, but there are several drawbacks:

• Some people may find the text too small to read.
• Text entry via the telephone keypad can be difficult. You either tap a key multiple times to select letters or use word prediction based on letters entered.
• Not all phones available for each carrier can perform this function.

Wireless access protocol is well suited to reading e-mails. To compose an e-mail, however, you need to choose letters by clicking on numbers, which can be very difficult.

Many physicians communicate with patients or colleagues via e-mail but lose this connectivity when they travel. If you find traditional home and office e-mail accounts are no longer enough, several e-mail access options can help you stay connected anytime.

How e-mail works

Typical home e-mail accounts-known as post office protocol (POP) accounts-use a client-server access method. The client-such as Outlook Express, Eudora, or Netscape Mail-checks the server for mail, which is then downloaded onto the home computer. Once downloaded, the message is gone from the server.

By contrast, an Internet message access protocol (IMAP) account offers more capabilities, such as allowing users to store e-mail on the server and organize mail into folders.^{December 2003). Also, some public locations such as New York’s Bryant Park offer free wireless Internet as a public service.2 Personal digital assistants or notebook computers with wireless capability, such as the Tungsten TC or the Toshiba e800, are best suited to this type of access.}

Dial-up Internet service is possible over your cell phone. Most mobile phone carriers charge extra for data transmission, and you will need a specific cable to connect your phone to your computer. Bluetooth wireless technology can eliminate the need for cables but beware: Data transfer is much slower with Bluetooth than with other methods.

Third-generation networks (3G)-higher-speed protocols that allow faster data transmission for multimedia-have been touted as the next best service from mobile phone providers. Wireless devices such as the Palm Treo or the Research in Motion BlackBerry are specifically designed for this type of access. Monthly data service costs approximately $30 for unlimited downloads or less when bundled with a voice plan. Access is limited to the cellular coverage area, however.

Wireless access protocol, an alternative to 3G, lets you access e-mail via your mobile phone. This service, available from mobile service providers for an additional monthly fee (about $10), lets you read mail on the phone screen, but there are several drawbacks:

• Some people may find the text too small to read.
• Text entry via the telephone keypad can be difficult. You either tap a key multiple times to select letters or use word prediction based on letters entered.
• Not all phones available for each carrier can perform this function.

Wireless access protocol is well suited to reading e-mails. To compose an e-mail, however, you need to choose letters by clicking on numbers, which can be very difficult.

Pediatric overweight and obesity can cause serious health problems later on. Use of psychotropics associated with potential weight gain compounds this risk.

Convincing youths to exercise and eat healthier foods can help them maintain a normal weight for their age and gender (see “Choose precise BMI charts to track youths’ weight gain,” (Current Psychiatry, October 2004,).

Cutting calories

Discuss the fat and calorie content of popular high-fat foods with the parents, who can then encourage their child to make more-informed dietary choices. Explain, for example, that it takes all day to burn the calories in two doughnuts, one fast-food bacon cheeseburger, or one extra-large serving of fast-food french fries.

A table listing portions of high-fat foods equaling 500 Kcal—the amount of energy a typical youth burns in 1 day through brisk walking—accompanies this article at www.currentpsychiatry.com.

Increasing exercise

Physical activity declines substantially during adolescence.¹ In youths with chronic mental illness, reduced activity may contribute more than increased caloric intake to overweight/obesity.

Tell youths that they can lose 1 lb of body fat per week with normal walking and can lose more weight by simply taking a 30-minute walk each day. Alternately, each of the following activities burns as many Kcal as a 30-minute walk:

• jumping rope 11 minutes
  
• jogging 13 minutes
  
• swimming 19 minutes
  
• moderate cycling 24 minutes
  
• mowing lawn 30 minutes.
  

The pedometer is attached to the belt near the buckle and records a step every time the hip drops. Pedometers measure activity by steps per day; they cannot gauge activity on a bicycle.

Assuming that a youth burns 40 Kcal per 1,000 steps, a child will burn 480 to 640 Kcal and an adolescent will burn 440 to 480 Kcal per day through brisk walking. Burning 500 Kcal/day translates to 3,500 Kcal—the equivalent of 1 lb of body fat—across 1 week.

Encouraging exercise. It is harder to promote exercise to a chronically mentally ill youth than to a youth who is not mentally ill. Work with the patient’s family, case manager, school system, teacher, nurse, and/or family doctor or pediatrician to plan an exercise regimen.

Pediatric overweight and obesity can cause serious health problems later on. Use of psychotropics associated with potential weight gain compounds this risk.

Convincing youths to exercise and eat healthier foods can help them maintain a normal weight for their age and gender (see “Choose precise BMI charts to track youths’ weight gain,” (Current Psychiatry, October 2004,).

Cutting calories

Discuss the fat and calorie content of popular high-fat foods with the parents, who can then encourage their child to make more-informed dietary choices. Explain, for example, that it takes all day to burn the calories in two doughnuts, one fast-food bacon cheeseburger, or one extra-large serving of fast-food french fries.

A table listing portions of high-fat foods equaling 500 Kcal—the amount of energy a typical youth burns in 1 day through brisk walking—accompanies this article at www.currentpsychiatry.com.

Increasing exercise

Physical activity declines substantially during adolescence.¹ In youths with chronic mental illness, reduced activity may contribute more than increased caloric intake to overweight/obesity.

Tell youths that they can lose 1 lb of body fat per week with normal walking and can lose more weight by simply taking a 30-minute walk each day. Alternately, each of the following activities burns as many Kcal as a 30-minute walk:

• jumping rope 11 minutes
  
• jogging 13 minutes
  
• swimming 19 minutes
  
• moderate cycling 24 minutes
  
• mowing lawn 30 minutes.
  

The pedometer is attached to the belt near the buckle and records a step every time the hip drops. Pedometers measure activity by steps per day; they cannot gauge activity on a bicycle.

Assuming that a youth burns 40 Kcal per 1,000 steps, a child will burn 480 to 640 Kcal and an adolescent will burn 440 to 480 Kcal per day through brisk walking. Burning 500 Kcal/day translates to 3,500 Kcal—the equivalent of 1 lb of body fat—across 1 week.

Encouraging exercise. It is harder to promote exercise to a chronically mentally ill youth than to a youth who is not mentally ill. Work with the patient’s family, case manager, school system, teacher, nurse, and/or family doctor or pediatrician to plan an exercise regimen.

Pediatric overweight and obesity can cause serious health problems later on. Use of psychotropics associated with potential weight gain compounds this risk.

Convincing youths to exercise and eat healthier foods can help them maintain a normal weight for their age and gender (see “Choose precise BMI charts to track youths’ weight gain,” (Current Psychiatry, October 2004,).

Cutting calories

Discuss the fat and calorie content of popular high-fat foods with the parents, who can then encourage their child to make more-informed dietary choices. Explain, for example, that it takes all day to burn the calories in two doughnuts, one fast-food bacon cheeseburger, or one extra-large serving of fast-food french fries.

A table listing portions of high-fat foods equaling 500 Kcal—the amount of energy a typical youth burns in 1 day through brisk walking—accompanies this article at www.currentpsychiatry.com.

Increasing exercise

Physical activity declines substantially during adolescence.¹ In youths with chronic mental illness, reduced activity may contribute more than increased caloric intake to overweight/obesity.

Tell youths that they can lose 1 lb of body fat per week with normal walking and can lose more weight by simply taking a 30-minute walk each day. Alternately, each of the following activities burns as many Kcal as a 30-minute walk:

• jumping rope 11 minutes
  
• jogging 13 minutes
  
• swimming 19 minutes
  
• moderate cycling 24 minutes
  
• mowing lawn 30 minutes.
  

The pedometer is attached to the belt near the buckle and records a step every time the hip drops. Pedometers measure activity by steps per day; they cannot gauge activity on a bicycle.

Assuming that a youth burns 40 Kcal per 1,000 steps, a child will burn 480 to 640 Kcal and an adolescent will burn 440 to 480 Kcal per day through brisk walking. Burning 500 Kcal/day translates to 3,500 Kcal—the equivalent of 1 lb of body fat—across 1 week.

Encouraging exercise. It is harder to promote exercise to a chronically mentally ill youth than to a youth who is not mentally ill. Work with the patient’s family, case manager, school system, teacher, nurse, and/or family doctor or pediatrician to plan an exercise regimen.

Starting with this issue, Current Psychiatry is being sent to more than 3,000 advanced practice psychiatric nurses, who join the 37,000 psychiatrists who already receive it. The same “news you can use” that has made Current Psychiatry the most highly read journal among psychiatrists should help psychiatric nurses as well.

Advanced practice nurses have prescriptive authority in 49 states, and many prescribe on their own signatures. Laws governing their prescribing vary from state to state, as do their titles, including nurse practitioner (NP), clinical nurse specialist (CNS), advanced practitioner of nursing (APN), and perhaps a dozen others. All are registered nurses who have completed the additional graduate-level education and training required to diagnose and treat psychiatric disorders. [For more information, see the special report, “The Role of Advanced Practice Psychiatric Nurses,” at www.currentpsychiatry.com.]

In the past, organized psychiatry has systematically opposed nurses prescribing, and I believe that opposition was a bad thing. Nurses and physicians have been partners in caring for patients with mental illness for more than a century. We are members of distinct health professions but share the same goal: to ensure that our patients receive the best care.

Both professional groups have the necessary biologically-based training to appropriately prescribe the wonderful—and potentially dangerous—medications used in psychiatric practice. Both groups are committed to a program of lifelong learning, and both need unbiased, clinically relevant sources of therapeutic information—such as Current Psychiatry.

We are all in this together. Welcome, welcome.

Starting with this issue, Current Psychiatry is being sent to more than 3,000 advanced practice psychiatric nurses, who join the 37,000 psychiatrists who already receive it. The same “news you can use” that has made Current Psychiatry the most highly read journal among psychiatrists should help psychiatric nurses as well.

Advanced practice nurses have prescriptive authority in 49 states, and many prescribe on their own signatures. Laws governing their prescribing vary from state to state, as do their titles, including nurse practitioner (NP), clinical nurse specialist (CNS), advanced practitioner of nursing (APN), and perhaps a dozen others. All are registered nurses who have completed the additional graduate-level education and training required to diagnose and treat psychiatric disorders. [For more information, see the special report, “The Role of Advanced Practice Psychiatric Nurses,” at www.currentpsychiatry.com.]

In the past, organized psychiatry has systematically opposed nurses prescribing, and I believe that opposition was a bad thing. Nurses and physicians have been partners in caring for patients with mental illness for more than a century. We are members of distinct health professions but share the same goal: to ensure that our patients receive the best care.

Both professional groups have the necessary biologically-based training to appropriately prescribe the wonderful—and potentially dangerous—medications used in psychiatric practice. Both groups are committed to a program of lifelong learning, and both need unbiased, clinically relevant sources of therapeutic information—such as Current Psychiatry.

We are all in this together. Welcome, welcome.

Starting with this issue, Current Psychiatry is being sent to more than 3,000 advanced practice psychiatric nurses, who join the 37,000 psychiatrists who already receive it. The same “news you can use” that has made Current Psychiatry the most highly read journal among psychiatrists should help psychiatric nurses as well.

Advanced practice nurses have prescriptive authority in 49 states, and many prescribe on their own signatures. Laws governing their prescribing vary from state to state, as do their titles, including nurse practitioner (NP), clinical nurse specialist (CNS), advanced practitioner of nursing (APN), and perhaps a dozen others. All are registered nurses who have completed the additional graduate-level education and training required to diagnose and treat psychiatric disorders. [For more information, see the special report, “The Role of Advanced Practice Psychiatric Nurses,” at www.currentpsychiatry.com.]

In the past, organized psychiatry has systematically opposed nurses prescribing, and I believe that opposition was a bad thing. Nurses and physicians have been partners in caring for patients with mental illness for more than a century. We are members of distinct health professions but share the same goal: to ensure that our patients receive the best care.

Both professional groups have the necessary biologically-based training to appropriately prescribe the wonderful—and potentially dangerous—medications used in psychiatric practice. Both groups are committed to a program of lifelong learning, and both need unbiased, clinically relevant sources of therapeutic information—such as Current Psychiatry.

We are all in this together. Welcome, welcome.

Adding just 5 to 10 minutes of psychotherapy to medication monitoring visits can help patients overcome hallucinations, delusions, and other psychotic symptoms. Targeted cognitive-behavioral therapy (CBT) can:

• prevent crisis visits and hospitalizations
  
• improve long-term medication and treatment adherence
  
• enhance the therapeutic alliance.
  

Treatment goals for patients with chronic mental illness are changing as clinicians, patients, and families aspire for more than improved symptoms ( Box ).^1-14 This article describes brief interventions to target medication nonadherence and positive and negative symptoms in patients with schizophrenia, schizoaffective disorder, bipolar disorder, major depressive disorder, and other chronic disorders.

CASE: VOICES FROM THE PAST

Ms. W, age 45, is seen every 6 to 8 weeks in an outpatient medication management clinic for symptoms of schizoaffective disorder, depressed type; posttraumatic stress disorder; and generalized anxiety disorder. She has a history of severe abuse by her father, self-mutilation in response to anxiety and stress, and repeated hospitalizations following visits to her mother.

She recently visited her mother again and saw her father as well. The trip led to increased symptoms of intrusive traumatic memories, thoughts of suicide with plans to overdose, visual hallucinations of her father, and increased auditory hallucinations with derogatory content.

Goals of the first therapy session after Ms. W’s trip home were to reduce her suicidal thoughts and prevent hospitalization. We encouraged her to list her positive qualities, accomplishments, important relationships, religious beliefs, goals, and dreams. She then wrote all these reasons to live on a cue card. Reading the card twice in the session stopped her suicidal thoughts, and she expressed some hope.

We encouraged her to read the card whenever suicidal ideas became strong. We scheduled her next visit 1 week later, and she contracted not to attempt suicide during that time.

DEVELOPING AN ALLIANCE

To develop an alliance with psychotic patients such as Ms. W, the first task is to help them leave each session feeling understood, validated, and enjoying the therapist’s company. This alone provides a powerful counterbalance to the isolation, demoralization, and hopelessness they bring to therapy.

Box

5 steps in effective cognitive-behavioral interventions

In normalization, the stress vulnerability model is used to explain psychosis to the patient. Psychotic symptoms are emphasized as something normal people can experience in extreme situations, such as:

• hallucinations in states of sleep deprivation or medical and drug-induced states
  
• paranoia as error in thinking in states of heightened vigilance and perceived threat.¹⁵
  

In a collaborative therapeutic alliance, the patient is not a passive recipient but an active collaborator in therapy. He or she contributes to decisions—such as the length of therapy and topics to be discussed—and gives feedback on interventions and therapist style.

Focusing on life goals makes therapy meaningful to the patient.

Set priorities. Because only one or two therapeutic interventions can be tried during a medication-monitoring visit, problems need to be prioritized. As with Ms. W, the first visit’s goal was crisis intervention: to reduce suicidal thoughts and prevent hospitalization. Table 1 offers a framework for effective therapeutic interventions.

Save time by giving patients out-of-session assignments, which:

• collect important information to review with patients during the next monitoring session
  
• help empower patients to manage their symptoms.
  

IMPROVING ADHERENCE

Medication nonadherence and partial adherence can result from:

• illness-related factors such as lack of insight
  
• patient-related factors such as attitudes and beliefs about medication
  
• treatment factors such as side effects
  
• physician-related factors such as showing an authoritarian attitude toward patients
  
• system-related factors such as treatment access problems.
  

Table 2

Interventions to improve patient medication adherence

CASE: NOT REALLY HER FATHER

By the second session 1 week later, Ms. W’s suicidal thoughts had become infrequent and mild, and she was using the coping card as needed. This visit focused on visual hallucinations associated with anxiety about facing her father. We encouraged her to describe the hallucinations in great detail, and she realized that she visualized her father as he had looked 20 years ago, not as he looks today. Her anxiety decreased as she considered that she might be seeing not him but an image. Her homework assignment was to closely observe the hallucinations. Because she was more stable, the next visit was scheduled in 2 weeks.

By the third session, she reported that the visual hallucinations had disappeared, and the focusing technique had helped her. She continued to hear voices, however, particularly in the evening when she was alone and anxious or depressed. With prompting, she identified activities she could engage in at night, such as calling her mother and praying with her mother on the phone. This reduced her loneliness and helped her relax.

Table 3

Interventions to manage auditory and visual hallucinations

MANAGING POSITIVE SYMPTOMS

In serious mental illnesses such as schizophrenia, the most common hallucinations are auditory ( Table 3 ),¹⁹ followed by visual and other types.²⁰ Sometimes patients view hallucinations as helpful, providing reassurance, advice, or companionship. The content may be an expression of the patient’s own beliefs.

Table 4

Interventions to help patients examine common delusions

• Are the hallucinations distressing, and does the patient want them to stop?
  
• What triggers them (usually depressed mood, anxiety, anger, or boredom)?
  
• What coping mechanisms has the patient used, and how effective have they been?
  
• What is the source of the patient’s distress?
  

Table 5

Interventions for managing schizophrenia’s negative symptoms

Never dispute a patient’s delusional beliefs. Maintain an attitude of benevolent curiosity to elicit the reasoning processes by which he or she came to believe the delusions. By encouraging the patient to become curious about the experience, you can create a chink of insight and help the him or her achieve important goals despite disturbing sensory experiences and beliefs.

Thought disorder can be addressed by gently pointing out that you are having trouble understanding the patient’s speech. Ask if other people whom the patient trusts have commented on his or her speech.

Because thought disorder worsens the longer a patient talks, suggest a 5-sentence rule during sessions. You and the patient try to speak no more than 5 sentences at a time before pausing to let the other person speak. Encourage the patient to monitor your speech and to indicate when you violate the rule. Monitoring your speech helps patients start monitoring their own.

Thought disorder worsens when patients experience negative emotions such as anxiety. When this occurs, move the discussion to a neutral topic or encourage deep regular breathing for 2 minutes to reduce anxiety.

MANAGING NEGATIVE SYMPTOMS

Negative symptoms of schizophrenia ( Table 5 ) overlap with depression and with medication side effects. Anhedonia and social withdrawal, for example, may reflect a patient’s depression and demoralization, rather than just schizophrenia’s biological core symptoms.

Similarly, limited facial expression may be caused by drug side effects, rather than absence of affect. Negative symptoms also can occur in the absence of depression or side effects, such as when a patient’s automatic thoughts related to expectations of failure lead to lack of motivation.

Negative symptoms usually bother patients much less than positive symptoms do. Thus, enlisting family members to help patients monitor and deal with negative symptoms can be very useful.

CASE SUMMARY

Ms. W’s stress-related psychotic symptoms resolved to baseline with cognitive therapy done in a regular medication management clinic. Throughout this episode, her medication dosages remained unchanged. The interventions added about 10 minutes to sessions, effectively dealt with her symptom exacerbation, and prevented hospitalization.

Psychotropics remain a critical component of treating psychotic disorders, and psychotherapy can also be very helpful. But in the many situations when psychotherapy is not available, brief psychotherapeutic techniques can:

• increase patient and family satisfaction
  
• enhance the therapeutic alliance
  
• improve medication adherence
  
• promote recovery.
  

Adding just 5 to 10 minutes of psychotherapy to medication monitoring visits can help patients overcome hallucinations, delusions, and other psychotic symptoms. Targeted cognitive-behavioral therapy (CBT) can:

• prevent crisis visits and hospitalizations
  
• improve long-term medication and treatment adherence
  
• enhance the therapeutic alliance.
  

Treatment goals for patients with chronic mental illness are changing as clinicians, patients, and families aspire for more than improved symptoms ( Box ).^1-14 This article describes brief interventions to target medication nonadherence and positive and negative symptoms in patients with schizophrenia, schizoaffective disorder, bipolar disorder, major depressive disorder, and other chronic disorders.

CASE: VOICES FROM THE PAST

Ms. W, age 45, is seen every 6 to 8 weeks in an outpatient medication management clinic for symptoms of schizoaffective disorder, depressed type; posttraumatic stress disorder; and generalized anxiety disorder. She has a history of severe abuse by her father, self-mutilation in response to anxiety and stress, and repeated hospitalizations following visits to her mother.

She recently visited her mother again and saw her father as well. The trip led to increased symptoms of intrusive traumatic memories, thoughts of suicide with plans to overdose, visual hallucinations of her father, and increased auditory hallucinations with derogatory content.

Goals of the first therapy session after Ms. W’s trip home were to reduce her suicidal thoughts and prevent hospitalization. We encouraged her to list her positive qualities, accomplishments, important relationships, religious beliefs, goals, and dreams. She then wrote all these reasons to live on a cue card. Reading the card twice in the session stopped her suicidal thoughts, and she expressed some hope.

We encouraged her to read the card whenever suicidal ideas became strong. We scheduled her next visit 1 week later, and she contracted not to attempt suicide during that time.

DEVELOPING AN ALLIANCE

To develop an alliance with psychotic patients such as Ms. W, the first task is to help them leave each session feeling understood, validated, and enjoying the therapist’s company. This alone provides a powerful counterbalance to the isolation, demoralization, and hopelessness they bring to therapy.

Box

5 steps in effective cognitive-behavioral interventions

In normalization, the stress vulnerability model is used to explain psychosis to the patient. Psychotic symptoms are emphasized as something normal people can experience in extreme situations, such as:

• hallucinations in states of sleep deprivation or medical and drug-induced states
  
• paranoia as error in thinking in states of heightened vigilance and perceived threat.¹⁵
  

In a collaborative therapeutic alliance, the patient is not a passive recipient but an active collaborator in therapy. He or she contributes to decisions—such as the length of therapy and topics to be discussed—and gives feedback on interventions and therapist style.

Focusing on life goals makes therapy meaningful to the patient.

Set priorities. Because only one or two therapeutic interventions can be tried during a medication-monitoring visit, problems need to be prioritized. As with Ms. W, the first visit’s goal was crisis intervention: to reduce suicidal thoughts and prevent hospitalization. Table 1 offers a framework for effective therapeutic interventions.

Save time by giving patients out-of-session assignments, which:

• collect important information to review with patients during the next monitoring session
  
• help empower patients to manage their symptoms.
  

IMPROVING ADHERENCE

Medication nonadherence and partial adherence can result from:

• illness-related factors such as lack of insight
  
• patient-related factors such as attitudes and beliefs about medication
  
• treatment factors such as side effects
  
• physician-related factors such as showing an authoritarian attitude toward patients
  
• system-related factors such as treatment access problems.
  

Table 2

Interventions to improve patient medication adherence

CASE: NOT REALLY HER FATHER

By the second session 1 week later, Ms. W’s suicidal thoughts had become infrequent and mild, and she was using the coping card as needed. This visit focused on visual hallucinations associated with anxiety about facing her father. We encouraged her to describe the hallucinations in great detail, and she realized that she visualized her father as he had looked 20 years ago, not as he looks today. Her anxiety decreased as she considered that she might be seeing not him but an image. Her homework assignment was to closely observe the hallucinations. Because she was more stable, the next visit was scheduled in 2 weeks.

By the third session, she reported that the visual hallucinations had disappeared, and the focusing technique had helped her. She continued to hear voices, however, particularly in the evening when she was alone and anxious or depressed. With prompting, she identified activities she could engage in at night, such as calling her mother and praying with her mother on the phone. This reduced her loneliness and helped her relax.

Table 3

Interventions to manage auditory and visual hallucinations

MANAGING POSITIVE SYMPTOMS

In serious mental illnesses such as schizophrenia, the most common hallucinations are auditory ( Table 3 ),¹⁹ followed by visual and other types.²⁰ Sometimes patients view hallucinations as helpful, providing reassurance, advice, or companionship. The content may be an expression of the patient’s own beliefs.

Table 4

Interventions to help patients examine common delusions

• Are the hallucinations distressing, and does the patient want them to stop?
  
• What triggers them (usually depressed mood, anxiety, anger, or boredom)?
  
• What coping mechanisms has the patient used, and how effective have they been?
  
• What is the source of the patient’s distress?
  

Table 5

Interventions for managing schizophrenia’s negative symptoms

Never dispute a patient’s delusional beliefs. Maintain an attitude of benevolent curiosity to elicit the reasoning processes by which he or she came to believe the delusions. By encouraging the patient to become curious about the experience, you can create a chink of insight and help the him or her achieve important goals despite disturbing sensory experiences and beliefs.

Thought disorder can be addressed by gently pointing out that you are having trouble understanding the patient’s speech. Ask if other people whom the patient trusts have commented on his or her speech.

Because thought disorder worsens the longer a patient talks, suggest a 5-sentence rule during sessions. You and the patient try to speak no more than 5 sentences at a time before pausing to let the other person speak. Encourage the patient to monitor your speech and to indicate when you violate the rule. Monitoring your speech helps patients start monitoring their own.

Thought disorder worsens when patients experience negative emotions such as anxiety. When this occurs, move the discussion to a neutral topic or encourage deep regular breathing for 2 minutes to reduce anxiety.

MANAGING NEGATIVE SYMPTOMS

Negative symptoms of schizophrenia ( Table 5 ) overlap with depression and with medication side effects. Anhedonia and social withdrawal, for example, may reflect a patient’s depression and demoralization, rather than just schizophrenia’s biological core symptoms.

Similarly, limited facial expression may be caused by drug side effects, rather than absence of affect. Negative symptoms also can occur in the absence of depression or side effects, such as when a patient’s automatic thoughts related to expectations of failure lead to lack of motivation.

Negative symptoms usually bother patients much less than positive symptoms do. Thus, enlisting family members to help patients monitor and deal with negative symptoms can be very useful.

CASE SUMMARY

Ms. W’s stress-related psychotic symptoms resolved to baseline with cognitive therapy done in a regular medication management clinic. Throughout this episode, her medication dosages remained unchanged. The interventions added about 10 minutes to sessions, effectively dealt with her symptom exacerbation, and prevented hospitalization.

Psychotropics remain a critical component of treating psychotic disorders, and psychotherapy can also be very helpful. But in the many situations when psychotherapy is not available, brief psychotherapeutic techniques can:

• increase patient and family satisfaction
  
• enhance the therapeutic alliance
  
• improve medication adherence
  
• promote recovery.
  

Adding just 5 to 10 minutes of psychotherapy to medication monitoring visits can help patients overcome hallucinations, delusions, and other psychotic symptoms. Targeted cognitive-behavioral therapy (CBT) can:

• prevent crisis visits and hospitalizations
  
• improve long-term medication and treatment adherence
  
• enhance the therapeutic alliance.
  

Treatment goals for patients with chronic mental illness are changing as clinicians, patients, and families aspire for more than improved symptoms ( Box ).^1-14 This article describes brief interventions to target medication nonadherence and positive and negative symptoms in patients with schizophrenia, schizoaffective disorder, bipolar disorder, major depressive disorder, and other chronic disorders.

CASE: VOICES FROM THE PAST

Ms. W, age 45, is seen every 6 to 8 weeks in an outpatient medication management clinic for symptoms of schizoaffective disorder, depressed type; posttraumatic stress disorder; and generalized anxiety disorder. She has a history of severe abuse by her father, self-mutilation in response to anxiety and stress, and repeated hospitalizations following visits to her mother.

She recently visited her mother again and saw her father as well. The trip led to increased symptoms of intrusive traumatic memories, thoughts of suicide with plans to overdose, visual hallucinations of her father, and increased auditory hallucinations with derogatory content.

Goals of the first therapy session after Ms. W’s trip home were to reduce her suicidal thoughts and prevent hospitalization. We encouraged her to list her positive qualities, accomplishments, important relationships, religious beliefs, goals, and dreams. She then wrote all these reasons to live on a cue card. Reading the card twice in the session stopped her suicidal thoughts, and she expressed some hope.

We encouraged her to read the card whenever suicidal ideas became strong. We scheduled her next visit 1 week later, and she contracted not to attempt suicide during that time.

DEVELOPING AN ALLIANCE

To develop an alliance with psychotic patients such as Ms. W, the first task is to help them leave each session feeling understood, validated, and enjoying the therapist’s company. This alone provides a powerful counterbalance to the isolation, demoralization, and hopelessness they bring to therapy.

Box

5 steps in effective cognitive-behavioral interventions

In normalization, the stress vulnerability model is used to explain psychosis to the patient. Psychotic symptoms are emphasized as something normal people can experience in extreme situations, such as:

• hallucinations in states of sleep deprivation or medical and drug-induced states
  
• paranoia as error in thinking in states of heightened vigilance and perceived threat.¹⁵
  

In a collaborative therapeutic alliance, the patient is not a passive recipient but an active collaborator in therapy. He or she contributes to decisions—such as the length of therapy and topics to be discussed—and gives feedback on interventions and therapist style.

Focusing on life goals makes therapy meaningful to the patient.

Set priorities. Because only one or two therapeutic interventions can be tried during a medication-monitoring visit, problems need to be prioritized. As with Ms. W, the first visit’s goal was crisis intervention: to reduce suicidal thoughts and prevent hospitalization. Table 1 offers a framework for effective therapeutic interventions.

Save time by giving patients out-of-session assignments, which:

• collect important information to review with patients during the next monitoring session
  
• help empower patients to manage their symptoms.
  

IMPROVING ADHERENCE

Medication nonadherence and partial adherence can result from:

• illness-related factors such as lack of insight
  
• patient-related factors such as attitudes and beliefs about medication
  
• treatment factors such as side effects
  
• physician-related factors such as showing an authoritarian attitude toward patients
  
• system-related factors such as treatment access problems.
  

Table 2

Interventions to improve patient medication adherence

CASE: NOT REALLY HER FATHER

By the second session 1 week later, Ms. W’s suicidal thoughts had become infrequent and mild, and she was using the coping card as needed. This visit focused on visual hallucinations associated with anxiety about facing her father. We encouraged her to describe the hallucinations in great detail, and she realized that she visualized her father as he had looked 20 years ago, not as he looks today. Her anxiety decreased as she considered that she might be seeing not him but an image. Her homework assignment was to closely observe the hallucinations. Because she was more stable, the next visit was scheduled in 2 weeks.

By the third session, she reported that the visual hallucinations had disappeared, and the focusing technique had helped her. She continued to hear voices, however, particularly in the evening when she was alone and anxious or depressed. With prompting, she identified activities she could engage in at night, such as calling her mother and praying with her mother on the phone. This reduced her loneliness and helped her relax.

Table 3

Interventions to manage auditory and visual hallucinations

MANAGING POSITIVE SYMPTOMS

In serious mental illnesses such as schizophrenia, the most common hallucinations are auditory ( Table 3 ),¹⁹ followed by visual and other types.²⁰ Sometimes patients view hallucinations as helpful, providing reassurance, advice, or companionship. The content may be an expression of the patient’s own beliefs.

Table 4

Interventions to help patients examine common delusions

• Are the hallucinations distressing, and does the patient want them to stop?
  
• What triggers them (usually depressed mood, anxiety, anger, or boredom)?
  
• What coping mechanisms has the patient used, and how effective have they been?
  
• What is the source of the patient’s distress?
  

Table 5

Interventions for managing schizophrenia’s negative symptoms

Never dispute a patient’s delusional beliefs. Maintain an attitude of benevolent curiosity to elicit the reasoning processes by which he or she came to believe the delusions. By encouraging the patient to become curious about the experience, you can create a chink of insight and help the him or her achieve important goals despite disturbing sensory experiences and beliefs.

Thought disorder can be addressed by gently pointing out that you are having trouble understanding the patient’s speech. Ask if other people whom the patient trusts have commented on his or her speech.

Because thought disorder worsens the longer a patient talks, suggest a 5-sentence rule during sessions. You and the patient try to speak no more than 5 sentences at a time before pausing to let the other person speak. Encourage the patient to monitor your speech and to indicate when you violate the rule. Monitoring your speech helps patients start monitoring their own.

Thought disorder worsens when patients experience negative emotions such as anxiety. When this occurs, move the discussion to a neutral topic or encourage deep regular breathing for 2 minutes to reduce anxiety.

MANAGING NEGATIVE SYMPTOMS

Negative symptoms of schizophrenia ( Table 5 ) overlap with depression and with medication side effects. Anhedonia and social withdrawal, for example, may reflect a patient’s depression and demoralization, rather than just schizophrenia’s biological core symptoms.

Similarly, limited facial expression may be caused by drug side effects, rather than absence of affect. Negative symptoms also can occur in the absence of depression or side effects, such as when a patient’s automatic thoughts related to expectations of failure lead to lack of motivation.

Negative symptoms usually bother patients much less than positive symptoms do. Thus, enlisting family members to help patients monitor and deal with negative symptoms can be very useful.

CASE SUMMARY

Ms. W’s stress-related psychotic symptoms resolved to baseline with cognitive therapy done in a regular medication management clinic. Throughout this episode, her medication dosages remained unchanged. The interventions added about 10 minutes to sessions, effectively dealt with her symptom exacerbation, and prevented hospitalization.

Psychotropics remain a critical component of treating psychotic disorders, and psychotherapy can also be very helpful. But in the many situations when psychotherapy is not available, brief psychotherapeutic techniques can:

• increase patient and family satisfaction
  
• enhance the therapeutic alliance
  
• improve medication adherence
  
• promote recovery.
  

HISTORY: WINTER WOES

Mrs. A, age 64, lives alone in an old farmhouse. For approximately 8 months, she had complained of depressed mood, decreased interest, difficulty sleeping, low energy, decreased concentration, and feelings of hopelessness. She met DSM-IV-TR criteria for major depressive disorder with underlying anxiety.

Mrs. A also reported having sinus headaches throughout the fall and winter. Blood chemistry, CBC with differential, thyroid profile including T₄& TSH, urine drug screen, urine analysis, and ECG results were normal.

In April, Mrs. A was enrolled in an outpatient study of depression relapse prevention treatment. After taking the active study drug for 2 months, she reported continued low mood, low energy, difficulty concentrating, poor sleep and worsening headaches. Because her depression did not improve sufficiently, she was dropped from the study.

In July, Mrs. A saw a psychiatrist and was started on sertraline, 50 mg/d. By November, the dosage had been increased to 150 mg/d. At this time, she reported unsteadiness, dizziness, frequent falls, and intolerable headaches in addition to her depressive symptoms. She was referred to a neurologist to rule out a neurologic disorder.

Table 1

Symptoms that suggest major depression and/or chronic CO poisoning

The authors’ observations

Chronic fatigue syndrome is characterized by severe unexplained fatigue that persists for >6 months. The new-onset fatigue is not abated with rest. Other symptoms include impaired memory or concentration, sore throat, tender lymph nodes, muscle pain, headaches, pain in several joints, and disturbed sleep.¹

Mrs. A, however, never complained of sore throat or joint or muscle pain, and her laboratory findings were normal.

Seasonal affective disorder (SAD) is characterized by a temporal relationship between onset of depressive symptoms and a particular time of year (eg, symptoms emerge each winter) for at least 2 years. Full remission also occurs at a characteristic time (eg, each summer).²

Mrs. A’s headaches, frequent falls, dizziness, and difficulties with balance do not suggest SAD. Also, these symptoms have not persisted long enough for an SAD diagnosis.

Thyroid disorder. Hypothyroidism symptoms—particularly low mood, decreased energy, fatigue, psychomotor retardation, and lack of motivation—can mimic depression. Mrs. A’s T₄ and TSH readings were normal, however.

Metabolic dysfunction. Symptoms secondary to decreased serum concentrations of sodium, potassium, magnesium, or calcium can mimic depression, but blood tests showed Mrs. A has normal electrolyte levels.

Brain tumor. Patients with a brain tumor can present with mood symptoms, psychosis, headaches, mania, cognitive impairments, seizure problems, and other symptoms depending on the tumor’s size and location.

FURTHER TREATMENT: SUDDEN RELIEF

By late November Mrs. A’s fatigue, once present only mornings, plagued her throughout the day. We considered changing antidepressants because of her complaints and sertraline’s lack of efficacy.

The following month, however, Mrs. A told us that her fatigue and headaches were gone. Mood, sleep, and concentration were also improved. Her Hamilton Rating Scale for Depression score had improved from 21 when she entered the study—indicating moderate severity—to 6, indicating remission. Her neurologic referral was cancelled.

Mrs. A then mentioned that her home’s water heater had been malfunctioning for several months. She said she could not afford to get it repaired during the summer but finally hired plumbers to fix it in late November.

After working all day in Mrs. A’s basement, two workers suffered acute headaches and nausea. The symptoms prompted the workers to search the basement for a carbon monoxide leak; they found a small leak in the water heater, which they replaced.

The next morning, Mrs. A said, her headache disappeared. Her other symptoms were gone within 4 days.

The authors’ observations

The sudden disappearance of Mrs. A’s symptoms after her water heater was replaced and emergence of severe physical symptoms in the two plumbers suggest carbon monoxide (CO) poisoning, a common and potentially lethal medical problem.

Low-level CO poisoning usually results from repeated exposure to incomplete combustion in a defective heating appliance, such as a water heater (Box 1).^3,4 Symptoms usually surface in the winter, when heating appliance use peaks and windows are left closed, allowing indoor CO to accumulate in high concentrations.⁷

Box 1

Whereas severe, acute CO poisoning typically is detected immediately after exposure, symptoms of chronic low-level CO exposure are easily mistaken for a primary depressive (Table 1) or other neuropsychiatric disorder—or overlooked altogether. Some cases persist for months before CO exposure is diagnosed. Clinicians often give unnecessary—sometimes costly—medical treatment while ignoring the underlying poisoning.

Mechanism of action. CO binds with hemoglobin (with an affinity >200 times that of oxygen) to form carboxyhemoglobin (COHb), which causes cellular anoxia by blocking transport of oxygen to the tissues, including the brain.^4,6,8

CO poisoning symptoms vary depending on COHb concentration (Table 2). COHb >5% in a symptomatic nonsmoker may indicate chronic low-level CO poisoning and require further evaluation.⁹ Levels >10% are common in heavy smokers (2 to 4 packs/day). It should be noted that Mrs. A does not smoke.

Presentation. Patients with chronic low-level CO poisoning often present with vague, nonspecific symptoms, such as weakness and fatigue, abdominal pain, nausea, vomiting, diarrhea, decreased concentration, diminished cognitive abilities, persistent headaches, and trouble sleeping.^4,8,10,11 Patients age >65 especially may present with multiple cognitive and somatic complaints that suggest Parkinson’s disease, chronic fatigue syndrome, dementia, or—in Mrs. A’s case—depression.^5,10,12

Table 2

Signs, symptoms of CO poisoning that emerge at different carboxyhemoglobin levels

Health effects of CO exposure range from subtle cardiovascular and neurobehavioral sequelae at low concentrations to loss of consciousness and death after acute exposure to higher concentrations.^3,5

Hypoxia of the brain and other organs resulting from low-level CO poisoning can cause a range of physiologic effects, including mental status changes.^10,11 Low-level CO exposure is particularly dangerous to pregnant women and to patients with a pre-existing ischemic illness.

Pregnancy. Chronic low-level CO exposure during pregnancy can harm the fetus, leading to low birth weight, short neonatal length, prematurity, perinatal death, and increased risk of developmental dysfunction.¹³

Ischemic illnesses. Because COHb cannot transport oxygen, the tissues that demand the most oxygen—such as the brain, heart, and skeletal muscles—are most affected. Because cardiac muscles extract approximately 75% of available oxygen from blood, patients with cardiac and pulmonary ischemic illnesses face a high risk for tissue injury with CO poisoning. At COHb levels >10%, patients with pre-existing cardiac disease experience increased severity and duration of angina; concentrations >15% place them at risk of myocardial infarction.⁶

Length of recovery from chronic CO exposure varies widely depending on severity of exposure and the patient’s general health.^3,5 CO has a 4- to 6-hour half-life and is excreted via the lungs fairly rapidly, so recovery can be swift once CO exposure is stopped. Emergency room referral depends upon severity of symptoms and CO exposure duration and nature (accidental or intentional).

The authors’ observations

CO poisoning can lead to long-term mental status changes. In a 3-year follow-up of patients repeatedly exposed to low CO levels:

• 43% developed neurologic sequelae including memory impairment
• 33% experienced personality changes including irritability, verbal aggression, violence and impulsivity, moodiness, distractibility, and sexual promiscuity
• 11% suffered gross neuropsychological effects, including psychosis, disorientation, and blindness.⁴

Primary care physicians and psychiatrists should monitor patients who have recovered from CO poisoning for symptoms of these disorders.

DETECTING CHRONIC CO EXPOSURE

Mrs. A’s case illustrates the seriousness and diagnostic complexity of chronic low-level CO exposure in older patients, especially during the fall and winter with increased home heating appliance use.⁷ CO exposure was not considered as a cause of Mrs. A’s symptoms until heating contractors found the water heater leak.

Watch for patients whose neuropsychiatric symptoms do not respond to treatment. Ask them about possible environmental, seasonal, or diurnal variations in symptoms. Also ask if the patient’s home heating system or water heater is ≥10 years old or has been malfunctioning (Box 2).

Checking COHb blood levels is the simplest way to confirm CO poisoning.^6,14

Box 2

FOLLOW-UP: ANXIOUS MOMENTS

Mrs. A’s depressive symptoms, headaches, dizziness, and balance problems have not returned. Her underlying anxiety symptoms worsened, however, when the psychiatrist tried to taper sertraline. She was diagnosed with generalized anxiety disorder and continued on sertraline, 100 mg/d.

The psychiatrist sees her every 4 to 6 weeks, and she routinely sees her primary care physician. No long-term effects of CO poisoning have been found.

Related resources

• U.S. Centers for Disease Control and Prevention. Enter “carbon monoxide poisoning” in search field. http://www.cdc.gov.
• Kao LW, Nanagas KA. Carbon monoxide poisoning. Emerg Med Clin North America 2004;22:985-1018.

Drug brand names

• Sertraline • Zoloft

Disclosure

Drs. Khan and D’Empaire report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Preskorn has been a speaker for, consultant to, or principal investigator for several antidepressant manufacturers, including Pfizer Inc.

HISTORY: WINTER WOES

Mrs. A, age 64, lives alone in an old farmhouse. For approximately 8 months, she had complained of depressed mood, decreased interest, difficulty sleeping, low energy, decreased concentration, and feelings of hopelessness. She met DSM-IV-TR criteria for major depressive disorder with underlying anxiety.

Mrs. A also reported having sinus headaches throughout the fall and winter. Blood chemistry, CBC with differential, thyroid profile including T₄& TSH, urine drug screen, urine analysis, and ECG results were normal.

In April, Mrs. A was enrolled in an outpatient study of depression relapse prevention treatment. After taking the active study drug for 2 months, she reported continued low mood, low energy, difficulty concentrating, poor sleep and worsening headaches. Because her depression did not improve sufficiently, she was dropped from the study.

In July, Mrs. A saw a psychiatrist and was started on sertraline, 50 mg/d. By November, the dosage had been increased to 150 mg/d. At this time, she reported unsteadiness, dizziness, frequent falls, and intolerable headaches in addition to her depressive symptoms. She was referred to a neurologist to rule out a neurologic disorder.

Table 1

Symptoms that suggest major depression and/or chronic CO poisoning

The authors’ observations

Chronic fatigue syndrome is characterized by severe unexplained fatigue that persists for >6 months. The new-onset fatigue is not abated with rest. Other symptoms include impaired memory or concentration, sore throat, tender lymph nodes, muscle pain, headaches, pain in several joints, and disturbed sleep.¹

Mrs. A, however, never complained of sore throat or joint or muscle pain, and her laboratory findings were normal.

Seasonal affective disorder (SAD) is characterized by a temporal relationship between onset of depressive symptoms and a particular time of year (eg, symptoms emerge each winter) for at least 2 years. Full remission also occurs at a characteristic time (eg, each summer).²

Mrs. A’s headaches, frequent falls, dizziness, and difficulties with balance do not suggest SAD. Also, these symptoms have not persisted long enough for an SAD diagnosis.

Thyroid disorder. Hypothyroidism symptoms—particularly low mood, decreased energy, fatigue, psychomotor retardation, and lack of motivation—can mimic depression. Mrs. A’s T₄ and TSH readings were normal, however.

Metabolic dysfunction. Symptoms secondary to decreased serum concentrations of sodium, potassium, magnesium, or calcium can mimic depression, but blood tests showed Mrs. A has normal electrolyte levels.

Brain tumor. Patients with a brain tumor can present with mood symptoms, psychosis, headaches, mania, cognitive impairments, seizure problems, and other symptoms depending on the tumor’s size and location.

FURTHER TREATMENT: SUDDEN RELIEF

By late November Mrs. A’s fatigue, once present only mornings, plagued her throughout the day. We considered changing antidepressants because of her complaints and sertraline’s lack of efficacy.

The following month, however, Mrs. A told us that her fatigue and headaches were gone. Mood, sleep, and concentration were also improved. Her Hamilton Rating Scale for Depression score had improved from 21 when she entered the study—indicating moderate severity—to 6, indicating remission. Her neurologic referral was cancelled.

Mrs. A then mentioned that her home’s water heater had been malfunctioning for several months. She said she could not afford to get it repaired during the summer but finally hired plumbers to fix it in late November.

After working all day in Mrs. A’s basement, two workers suffered acute headaches and nausea. The symptoms prompted the workers to search the basement for a carbon monoxide leak; they found a small leak in the water heater, which they replaced.

The next morning, Mrs. A said, her headache disappeared. Her other symptoms were gone within 4 days.

The authors’ observations

The sudden disappearance of Mrs. A’s symptoms after her water heater was replaced and emergence of severe physical symptoms in the two plumbers suggest carbon monoxide (CO) poisoning, a common and potentially lethal medical problem.

Low-level CO poisoning usually results from repeated exposure to incomplete combustion in a defective heating appliance, such as a water heater (Box 1).^3,4 Symptoms usually surface in the winter, when heating appliance use peaks and windows are left closed, allowing indoor CO to accumulate in high concentrations.⁷

Box 1

Whereas severe, acute CO poisoning typically is detected immediately after exposure, symptoms of chronic low-level CO exposure are easily mistaken for a primary depressive (Table 1) or other neuropsychiatric disorder—or overlooked altogether. Some cases persist for months before CO exposure is diagnosed. Clinicians often give unnecessary—sometimes costly—medical treatment while ignoring the underlying poisoning.

Mechanism of action. CO binds with hemoglobin (with an affinity >200 times that of oxygen) to form carboxyhemoglobin (COHb), which causes cellular anoxia by blocking transport of oxygen to the tissues, including the brain.^4,6,8

CO poisoning symptoms vary depending on COHb concentration (Table 2). COHb >5% in a symptomatic nonsmoker may indicate chronic low-level CO poisoning and require further evaluation.⁹ Levels >10% are common in heavy smokers (2 to 4 packs/day). It should be noted that Mrs. A does not smoke.

Presentation. Patients with chronic low-level CO poisoning often present with vague, nonspecific symptoms, such as weakness and fatigue, abdominal pain, nausea, vomiting, diarrhea, decreased concentration, diminished cognitive abilities, persistent headaches, and trouble sleeping.^4,8,10,11 Patients age >65 especially may present with multiple cognitive and somatic complaints that suggest Parkinson’s disease, chronic fatigue syndrome, dementia, or—in Mrs. A’s case—depression.^5,10,12

Table 2

Signs, symptoms of CO poisoning that emerge at different carboxyhemoglobin levels

Health effects of CO exposure range from subtle cardiovascular and neurobehavioral sequelae at low concentrations to loss of consciousness and death after acute exposure to higher concentrations.^3,5

Hypoxia of the brain and other organs resulting from low-level CO poisoning can cause a range of physiologic effects, including mental status changes.^10,11 Low-level CO exposure is particularly dangerous to pregnant women and to patients with a pre-existing ischemic illness.

Pregnancy. Chronic low-level CO exposure during pregnancy can harm the fetus, leading to low birth weight, short neonatal length, prematurity, perinatal death, and increased risk of developmental dysfunction.¹³

Ischemic illnesses. Because COHb cannot transport oxygen, the tissues that demand the most oxygen—such as the brain, heart, and skeletal muscles—are most affected. Because cardiac muscles extract approximately 75% of available oxygen from blood, patients with cardiac and pulmonary ischemic illnesses face a high risk for tissue injury with CO poisoning. At COHb levels >10%, patients with pre-existing cardiac disease experience increased severity and duration of angina; concentrations >15% place them at risk of myocardial infarction.⁶

Length of recovery from chronic CO exposure varies widely depending on severity of exposure and the patient’s general health.^3,5 CO has a 4- to 6-hour half-life and is excreted via the lungs fairly rapidly, so recovery can be swift once CO exposure is stopped. Emergency room referral depends upon severity of symptoms and CO exposure duration and nature (accidental or intentional).

The authors’ observations

CO poisoning can lead to long-term mental status changes. In a 3-year follow-up of patients repeatedly exposed to low CO levels:

• 43% developed neurologic sequelae including memory impairment
• 33% experienced personality changes including irritability, verbal aggression, violence and impulsivity, moodiness, distractibility, and sexual promiscuity
• 11% suffered gross neuropsychological effects, including psychosis, disorientation, and blindness.⁴

Primary care physicians and psychiatrists should monitor patients who have recovered from CO poisoning for symptoms of these disorders.

DETECTING CHRONIC CO EXPOSURE

Mrs. A’s case illustrates the seriousness and diagnostic complexity of chronic low-level CO exposure in older patients, especially during the fall and winter with increased home heating appliance use.⁷ CO exposure was not considered as a cause of Mrs. A’s symptoms until heating contractors found the water heater leak.

Watch for patients whose neuropsychiatric symptoms do not respond to treatment. Ask them about possible environmental, seasonal, or diurnal variations in symptoms. Also ask if the patient’s home heating system or water heater is ≥10 years old or has been malfunctioning (Box 2).

Checking COHb blood levels is the simplest way to confirm CO poisoning.^6,14

Box 2

FOLLOW-UP: ANXIOUS MOMENTS

Mrs. A’s depressive symptoms, headaches, dizziness, and balance problems have not returned. Her underlying anxiety symptoms worsened, however, when the psychiatrist tried to taper sertraline. She was diagnosed with generalized anxiety disorder and continued on sertraline, 100 mg/d.

The psychiatrist sees her every 4 to 6 weeks, and she routinely sees her primary care physician. No long-term effects of CO poisoning have been found.

Related resources

• U.S. Centers for Disease Control and Prevention. Enter “carbon monoxide poisoning” in search field. http://www.cdc.gov.
• Kao LW, Nanagas KA. Carbon monoxide poisoning. Emerg Med Clin North America 2004;22:985-1018.

Drug brand names

• Sertraline • Zoloft

Disclosure

Drs. Khan and D’Empaire report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Preskorn has been a speaker for, consultant to, or principal investigator for several antidepressant manufacturers, including Pfizer Inc.

HISTORY: WINTER WOES

Mrs. A, age 64, lives alone in an old farmhouse. For approximately 8 months, she had complained of depressed mood, decreased interest, difficulty sleeping, low energy, decreased concentration, and feelings of hopelessness. She met DSM-IV-TR criteria for major depressive disorder with underlying anxiety.

Mrs. A also reported having sinus headaches throughout the fall and winter. Blood chemistry, CBC with differential, thyroid profile including T₄& TSH, urine drug screen, urine analysis, and ECG results were normal.

In April, Mrs. A was enrolled in an outpatient study of depression relapse prevention treatment. After taking the active study drug for 2 months, she reported continued low mood, low energy, difficulty concentrating, poor sleep and worsening headaches. Because her depression did not improve sufficiently, she was dropped from the study.

In July, Mrs. A saw a psychiatrist and was started on sertraline, 50 mg/d. By November, the dosage had been increased to 150 mg/d. At this time, she reported unsteadiness, dizziness, frequent falls, and intolerable headaches in addition to her depressive symptoms. She was referred to a neurologist to rule out a neurologic disorder.

Table 1

Symptoms that suggest major depression and/or chronic CO poisoning

The authors’ observations

Chronic fatigue syndrome is characterized by severe unexplained fatigue that persists for >6 months. The new-onset fatigue is not abated with rest. Other symptoms include impaired memory or concentration, sore throat, tender lymph nodes, muscle pain, headaches, pain in several joints, and disturbed sleep.¹

Mrs. A, however, never complained of sore throat or joint or muscle pain, and her laboratory findings were normal.

Seasonal affective disorder (SAD) is characterized by a temporal relationship between onset of depressive symptoms and a particular time of year (eg, symptoms emerge each winter) for at least 2 years. Full remission also occurs at a characteristic time (eg, each summer).²

Mrs. A’s headaches, frequent falls, dizziness, and difficulties with balance do not suggest SAD. Also, these symptoms have not persisted long enough for an SAD diagnosis.

Thyroid disorder. Hypothyroidism symptoms—particularly low mood, decreased energy, fatigue, psychomotor retardation, and lack of motivation—can mimic depression. Mrs. A’s T₄ and TSH readings were normal, however.

Metabolic dysfunction. Symptoms secondary to decreased serum concentrations of sodium, potassium, magnesium, or calcium can mimic depression, but blood tests showed Mrs. A has normal electrolyte levels.

Brain tumor. Patients with a brain tumor can present with mood symptoms, psychosis, headaches, mania, cognitive impairments, seizure problems, and other symptoms depending on the tumor’s size and location.

FURTHER TREATMENT: SUDDEN RELIEF

By late November Mrs. A’s fatigue, once present only mornings, plagued her throughout the day. We considered changing antidepressants because of her complaints and sertraline’s lack of efficacy.

The following month, however, Mrs. A told us that her fatigue and headaches were gone. Mood, sleep, and concentration were also improved. Her Hamilton Rating Scale for Depression score had improved from 21 when she entered the study—indicating moderate severity—to 6, indicating remission. Her neurologic referral was cancelled.

Mrs. A then mentioned that her home’s water heater had been malfunctioning for several months. She said she could not afford to get it repaired during the summer but finally hired plumbers to fix it in late November.

After working all day in Mrs. A’s basement, two workers suffered acute headaches and nausea. The symptoms prompted the workers to search the basement for a carbon monoxide leak; they found a small leak in the water heater, which they replaced.

The next morning, Mrs. A said, her headache disappeared. Her other symptoms were gone within 4 days.

The authors’ observations

The sudden disappearance of Mrs. A’s symptoms after her water heater was replaced and emergence of severe physical symptoms in the two plumbers suggest carbon monoxide (CO) poisoning, a common and potentially lethal medical problem.

Low-level CO poisoning usually results from repeated exposure to incomplete combustion in a defective heating appliance, such as a water heater (Box 1).^3,4 Symptoms usually surface in the winter, when heating appliance use peaks and windows are left closed, allowing indoor CO to accumulate in high concentrations.⁷

Box 1

Whereas severe, acute CO poisoning typically is detected immediately after exposure, symptoms of chronic low-level CO exposure are easily mistaken for a primary depressive (Table 1) or other neuropsychiatric disorder—or overlooked altogether. Some cases persist for months before CO exposure is diagnosed. Clinicians often give unnecessary—sometimes costly—medical treatment while ignoring the underlying poisoning.

Mechanism of action. CO binds with hemoglobin (with an affinity >200 times that of oxygen) to form carboxyhemoglobin (COHb), which causes cellular anoxia by blocking transport of oxygen to the tissues, including the brain.^4,6,8

CO poisoning symptoms vary depending on COHb concentration (Table 2). COHb >5% in a symptomatic nonsmoker may indicate chronic low-level CO poisoning and require further evaluation.⁹ Levels >10% are common in heavy smokers (2 to 4 packs/day). It should be noted that Mrs. A does not smoke.

Presentation. Patients with chronic low-level CO poisoning often present with vague, nonspecific symptoms, such as weakness and fatigue, abdominal pain, nausea, vomiting, diarrhea, decreased concentration, diminished cognitive abilities, persistent headaches, and trouble sleeping.^4,8,10,11 Patients age >65 especially may present with multiple cognitive and somatic complaints that suggest Parkinson’s disease, chronic fatigue syndrome, dementia, or—in Mrs. A’s case—depression.^5,10,12

Table 2

Signs, symptoms of CO poisoning that emerge at different carboxyhemoglobin levels

Health effects of CO exposure range from subtle cardiovascular and neurobehavioral sequelae at low concentrations to loss of consciousness and death after acute exposure to higher concentrations.^3,5

Hypoxia of the brain and other organs resulting from low-level CO poisoning can cause a range of physiologic effects, including mental status changes.^10,11 Low-level CO exposure is particularly dangerous to pregnant women and to patients with a pre-existing ischemic illness.

Pregnancy. Chronic low-level CO exposure during pregnancy can harm the fetus, leading to low birth weight, short neonatal length, prematurity, perinatal death, and increased risk of developmental dysfunction.¹³

Ischemic illnesses. Because COHb cannot transport oxygen, the tissues that demand the most oxygen—such as the brain, heart, and skeletal muscles—are most affected. Because cardiac muscles extract approximately 75% of available oxygen from blood, patients with cardiac and pulmonary ischemic illnesses face a high risk for tissue injury with CO poisoning. At COHb levels >10%, patients with pre-existing cardiac disease experience increased severity and duration of angina; concentrations >15% place them at risk of myocardial infarction.⁶

Length of recovery from chronic CO exposure varies widely depending on severity of exposure and the patient’s general health.^3,5 CO has a 4- to 6-hour half-life and is excreted via the lungs fairly rapidly, so recovery can be swift once CO exposure is stopped. Emergency room referral depends upon severity of symptoms and CO exposure duration and nature (accidental or intentional).

The authors’ observations

CO poisoning can lead to long-term mental status changes. In a 3-year follow-up of patients repeatedly exposed to low CO levels:

• 43% developed neurologic sequelae including memory impairment
• 33% experienced personality changes including irritability, verbal aggression, violence and impulsivity, moodiness, distractibility, and sexual promiscuity
• 11% suffered gross neuropsychological effects, including psychosis, disorientation, and blindness.⁴

Primary care physicians and psychiatrists should monitor patients who have recovered from CO poisoning for symptoms of these disorders.

DETECTING CHRONIC CO EXPOSURE

Mrs. A’s case illustrates the seriousness and diagnostic complexity of chronic low-level CO exposure in older patients, especially during the fall and winter with increased home heating appliance use.⁷ CO exposure was not considered as a cause of Mrs. A’s symptoms until heating contractors found the water heater leak.

Watch for patients whose neuropsychiatric symptoms do not respond to treatment. Ask them about possible environmental, seasonal, or diurnal variations in symptoms. Also ask if the patient’s home heating system or water heater is ≥10 years old or has been malfunctioning (Box 2).

Checking COHb blood levels is the simplest way to confirm CO poisoning.^6,14

Box 2

FOLLOW-UP: ANXIOUS MOMENTS

Mrs. A’s depressive symptoms, headaches, dizziness, and balance problems have not returned. Her underlying anxiety symptoms worsened, however, when the psychiatrist tried to taper sertraline. She was diagnosed with generalized anxiety disorder and continued on sertraline, 100 mg/d.

The psychiatrist sees her every 4 to 6 weeks, and she routinely sees her primary care physician. No long-term effects of CO poisoning have been found.

Related resources

• U.S. Centers for Disease Control and Prevention. Enter “carbon monoxide poisoning” in search field. http://www.cdc.gov.
• Kao LW, Nanagas KA. Carbon monoxide poisoning. Emerg Med Clin North America 2004;22:985-1018.

Drug brand names

• Sertraline • Zoloft

Disclosure

Drs. Khan and D’Empaire report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Preskorn has been a speaker for, consultant to, or principal investigator for several antidepressant manufacturers, including Pfizer Inc.