Current Psychiatry

After 10 years of heroin dependence, Mr. T, age 36, calls your office and says, “I want to get off heroin.” For 8 months, he’s been using IV heroin 2 to 3 times daily. He says he has tried methadone treatment but found daily dosing cumbersome.

He found your office number on the Substance Abuse and Mental Health Services Administration Web site, which lists physicians qualified to prescribe buprenorphine for opiate detoxification. He has heard about “bup” on the street and wants to know if he is eligible and what he can expect from treatment.

Like Mr. T, 1 million Americans are addicted to opiates.¹ As qualified physicians gain experience with using buprenorphine, this agent could revolutionize how opiate-dependent patients are routinely treated. Instead of receiving methadone only in specialized clinics, they can now choose to be treated in physicians’ offices.

Several obstacles, however, are preventing widespread buprenorphine use:

• Too few physicians are trained to offer this office-based treatment.
• Many of the 2,000 doctors who are trained remain uncertain about using buprenorphine.

This article is intended to help overcome obstacles to opiate-dependence treatment by familiarizing psychiatrists—whether trained or not in using buprenorphine—with evidence of this agent’s efficacy and its advantages compared with other treatments.

Efficacy and obstacles

Buprenorphine is a partial opioid agonist that binds to the mu receptor (Box 1).^2-5 It is a controlled substance (schedule-III narcotic). Outpatient trials have shown that buprenorphine is more effective than placebo and as effective as methadone for opiate detoxification.^6-10

In one of the largest trials, 326 opiate-dependent outpatients were randomly assigned to buprenorphine, buprenorphine/naloxone combination, or placebo for 4 weeks. Both buprenorphine forms were more effective than placebo, as measured by clean urine samples and patient reports of reduced opiate cravings.⁷

In maintenance treatment, buprenorphine has been shown to be more effective than placebo and as effective as methadone, 60 mg/d, in preventing relapse. In a randomized comparison study, 220 opiate-dependent patients received levomethadyl acetate (LAAM), 75 to 115 mg three times a week; buprenorphine, 16 to 32 mg three times a week; high-dose methadone (60 to 100 mg/d); or low-dose methadone (20 mg/d). Subjects reported using opiates 20 to 30 times in the week before study enrollment. After 17 weeks, treatment retention rates were 58% for buprenorphine, 73% for high-dose methadone, and 20% for low-dose methadone. At the same point, urine samples were negative for opiate use in 40% of patients receiving buprenorphine compared with 39% of those receiving high-dose methadone.¹⁰

Box 1

Table

Buprenorphine: A typical dosing strategy

Slow adoption. Opiate-dependence treatments such as methadone are prescribed in highly regulated environments, which is one reason only 25% of opiate addicts in the United States ever receive treatment.¹ Unfortunately, little has changed in the 20 months since the FDA approved buprenorphine for office-based detoxification and maintenance treatment of opiate dependence. More than 2,000 physicians have been trained to use buprenorphine, yet only 20% of them report prescribing it.¹¹

Reasons for this slow introduction include:

• difficulty in obtaining the medication
• lack of appropriate support staff and facilities
• uncertainty about prescribing the medication, despite special training.

Availability. When buprenorphine came to market in late 2003, most commercial pharmacies were not stocking it and it had to be special-ordered. As a result, patients receiving prescriptions had to wait 2 to 3 days for their first dose—a substantial deterrent to prescribing or taking this type of medication. Also, some private physicians and clinics do not keep buprenorphine samples to dispense on-site.

More pharmacies are stocking the medication now, but it remains the physician’s responsibility to ensure that a supply can be dispensed the day it is prescribed.

Support staff and facilities. To prescribe buprenorphine effectively, the physician needs resources for urine testing, physical exams, lab testing, and storing and dispensing buprenorphine. An integrated treatment clinic for opiate-dependent patients, complete with nursing and administrative staff, is ideal. If this support is not available, however, clinicians in private practice can safely prescribe buprenorphine from the office.

Uncertainty. Physicians often adopt new prescription products without hesitation, but buprenorphine’s administration and patient population are unusual. Even some physicians who have taken the special training course remain anxious about using this agent because it may precipitate opiate withdrawal. Also, the training requirement creates a sense that specialist-level knowledge is needed to safely prescribe buprenorphine.

Treatment requirements

For clinicians. The Drug Addiction Treatment Act of 2000 allows physicians to apply for a waiver from the Controlled Substances Act to prescribe buprenorphine for detoxification. A waiver is not required to prescribe buprenorphine for pain.¹²

To qualify for the waiver, physicians must be board-certified in addiction psychiatry or have completed a buprenorphine training course. Training is offered online and as a 1-day conference by the American Society of Addiction Medicine, American Academy of Addiction Psychiatry, American Medical Association, and American Psychiatric Association.

For patients. Like Mr. T, opiate users who ask about buprenorphine will want to know what to expect from treatment. To be eligible for buprenorphine treatment, a patient must:

• meet criteria for opiate dependence
• commit to keeping regular appointments—at least 3 times a week for the first 2 weeks then usually once weekly until detoxification is complete
• undergo random urine testing
• participate in psychosocial treatments.

So far, patients’ awareness of buprenorphine is highly variable. Asking an opiate user who presents for treatment what he or she knows about buprenorphine can be a useful screening tool. Highly motivated patients will have read about buprenorphine on the Internet, where they probably obtained your office phone number.

When a patient is accepted into treatment, detoxification with buprenorphine includes three phases: induction, stabilization/mainte-nance, and discontinuation.¹³ After stabilization, some patients remain in maintenance indefinitely and choose not to discontinue buprenorphine. The choice of who to discontinue and who to maintain on buprenorphine is a clinical decision made by the patient and practitioner. Success rates of detoxification with buprenorphine are similar to rates achieved with methadone and clonidine, although most studies have been conducted during buprenorphine maintenance.⁵

Case continued: Surprised to feel ‘normal’

Mr. T qualified for buprenorphine and came to the office feeling fairly ill. During withdrawal, his usual first symptom is rhinorrhea, followed by malaise, myalgia, restlessness, and intense cravings. His score of 24 on the Clinical Opiate Withdrawal Scale (COWS), indicated moderate withdrawal.

He felt better but not completely well 1 hour after taking buprenorphine/naloxone, 4 mg. He was given a 4-mg tablet to take at home 2 hours later. The next day his COWS score was 8, indicating mild withdrawal. He said he was surprised at how “normal” he was feeling.

Induction: Getting started

Buprenorphine induction is usually done during mild to moderate opiate withdrawal. Starting buprenorphine too soon—while the patient is relatively comfortable—may precipitate withdrawal because the agent will rapidly displace opiate bound to the receptors. In most cases, the first dose is given in the office so that the patient’s response can be monitored.

Two formulations. Buprenorphine comes alone (in 2- or 8-mg tablets) or in combination with naloxone (in 2 mg/0.5 mg and 8 mg/2 mg tablets). Both forms are given sublingually. Contrary to popular belief, IM buprenorphine is not approved for treating opiate addiction.

Naloxone is not absorbed in sublingual form and serves only to deter IV diversion of buprenorphine. Induction with buprenorphine alone is reserved for patients with documented allergy to naloxone or who are being detoxified from long-acting opiates such as methadone.

Dosing strategies are identical for both formulations. The usual starting dosage is 4 mg once daily, with a maximum dosage of 32 mg/d (Table). Withdrawal symptoms are typically controlled with 12 to 24 mg/d.¹⁴

If the patient is in active opiate withdrawal, the starting dose usually relieves symptoms in 30 to 45 minutes. If not, a second 4-mg dose can be given. Most patients do not require >8 mg the first day, but some may require 16 to 24 mg to suppress withdrawal symptoms.¹⁵

Some clinicians—such as solo practitioners who lack the resources of an outpatient clinic—prefer to have the patient take the first dose at home. Patients are instructed to take the first dose after withdrawal symptoms begin and to repeat the dose in 1 hour if symptoms persist. Thus, patients titrate their own dosages, but the clinician must be immediately available to handle complications. Induction continues until withdrawal symptoms are controlled.

The next day, patients return for evaluation. An objective scale such as the 11-item COWS can quantify withdrawal symptom severity.¹⁶ For each symptom—heart rate, nausea, diaphoresis, or restlessness—the COWS assigns a number corresponding to its severity. A total score >25 indicates moderately severe withdrawal.

After withdrawal symptoms are controlled, follow-up visits are scheduled every 2 to 3 days the first week and then weekly. Some physicians maintain daily contact with patients via e-mail or telephone to track symptoms.

Case continued: Steady improvement

By day 3, Mr. T gradually increased his buprenorphine/naloxone dosage to 16 mg once daily. He continued that dosage for 10 days before his next visit. At that point, he was slightly anxious but physically comfortable. He came into the office on days 2, 5, and 10 and his COWS scores decreased each time.

Stabilization and maintenance

When withdrawal symptoms are stabilized, patients begin maintenance therapy at the dosage that stabilized their symptoms. During maintenance therapy, the average buprenorphine dosage is 16 to 24 mg/d. Because of its long half-life, buprenorphine can be taken once daily, though some patients prefer twice-daily dosing for psychological comfort. Several studies comparing buprenorphine with methadone have found that buprenorphine, 8 to 16 mg/d, is similar in effect to approximately 60 mg/d of methadone.⁵

During the maintenance phase, it is important to have a policy for patients who relapse to substance abuse while taking buprenorphine (Box 2). During buprenorphine maintenance treatment, the estimated relapse rate to opiate use (chance of one positive test for opiates) ranges from 20% to 60%, compared with a relapse rate of 80% to 90% seen with placebo during clinical trials.⁵

Case continued: Time to taper?

After taking buprenorphine 2 months, Mr. T wants to taper off. He has been seen weekly and receives individual psychotherapy and group counseling. All urine drug screens have been negative for opiates.

With the psychiatrist’s observation, Mr. T. begins to taper his dosage of 16 mg/d by 4 mg a week. He is comfortable when he reaches 4 mg/d, but notices increased anxiety and general achiness when he reduces buprenorphine to 2 mg/d. He elects to remain at 4 mg/d for another 2 months.

Discontinuation

After the patient has reached a stable dose of buprenorphine, the clinician and patient together consider two treatment options:

• sustain the dose as maintenance therapy
• or taper and discontinue buprenorphine.

Box 2

Patients who have had multiple relapses and endured severe opiate withdrawal might consider remaining on buprenorphine for several months before tapering. Mild opiate withdrawal may occur if buprenorphine is tapered too rapidly, though this is not as severe or distressing as a full agonist withdrawal.

Tapering recommendations. To taper buprenorphine, reduce by 2 to 4 mg every 3 to 5 days until the patient is taking 2 mg/d. Most patients remain on this dosage at least 1 week and then discontinue. Those who experience side effects when dropping from 2 mg to 0 mg can take 2 mg every other day for 1 week and then discontinue.

After patients are tapered completely off buprenorphine, encourage them to follow up with the treating physician for at least another month. Opiate withdrawal symptoms have been reported to linger 2 to 3 weeks after the last dose of buprenorphine, but these symptoms—usually anxiety or insomnia—tend to be self-limiting.⁵

Case continued: Time to taper?

Mr. T has been free from heroin use for 4 months and has returned to work. He is rebuilding his life and continues with psychotherapy. He follows up at the buprenorphine clinic monthly for medication management. At each visit, he repeats the COWS test and undergoes a urine drug screen and vital signs check.

Related resources

• Substance Abuse and Mental Health Services Administration. Physician locator for buprenorphine providers.
• American Academy of Addiction Psychiatry. Information about buprenorphine training course. www.aaap.org/buprenorphine/buprenorphine.html
• Buprenorphine manufacturer’s Web site. Answers to frequently-asked questions. www.suboxone.com

Drug brand names

• Buprenorphine • Subutex
• Buprenorphine/naloxone • Suboxone
• Buprenorphine (IM) • Buprenex
• Clonidine • Catapres

After 10 years of heroin dependence, Mr. T, age 36, calls your office and says, “I want to get off heroin.” For 8 months, he’s been using IV heroin 2 to 3 times daily. He says he has tried methadone treatment but found daily dosing cumbersome.

He found your office number on the Substance Abuse and Mental Health Services Administration Web site, which lists physicians qualified to prescribe buprenorphine for opiate detoxification. He has heard about “bup” on the street and wants to know if he is eligible and what he can expect from treatment.

Like Mr. T, 1 million Americans are addicted to opiates.¹ As qualified physicians gain experience with using buprenorphine, this agent could revolutionize how opiate-dependent patients are routinely treated. Instead of receiving methadone only in specialized clinics, they can now choose to be treated in physicians’ offices.

Several obstacles, however, are preventing widespread buprenorphine use:

• Too few physicians are trained to offer this office-based treatment.
• Many of the 2,000 doctors who are trained remain uncertain about using buprenorphine.

This article is intended to help overcome obstacles to opiate-dependence treatment by familiarizing psychiatrists—whether trained or not in using buprenorphine—with evidence of this agent’s efficacy and its advantages compared with other treatments.

Efficacy and obstacles

Buprenorphine is a partial opioid agonist that binds to the mu receptor (Box 1).^2-5 It is a controlled substance (schedule-III narcotic). Outpatient trials have shown that buprenorphine is more effective than placebo and as effective as methadone for opiate detoxification.^6-10

In one of the largest trials, 326 opiate-dependent outpatients were randomly assigned to buprenorphine, buprenorphine/naloxone combination, or placebo for 4 weeks. Both buprenorphine forms were more effective than placebo, as measured by clean urine samples and patient reports of reduced opiate cravings.⁷

In maintenance treatment, buprenorphine has been shown to be more effective than placebo and as effective as methadone, 60 mg/d, in preventing relapse. In a randomized comparison study, 220 opiate-dependent patients received levomethadyl acetate (LAAM), 75 to 115 mg three times a week; buprenorphine, 16 to 32 mg three times a week; high-dose methadone (60 to 100 mg/d); or low-dose methadone (20 mg/d). Subjects reported using opiates 20 to 30 times in the week before study enrollment. After 17 weeks, treatment retention rates were 58% for buprenorphine, 73% for high-dose methadone, and 20% for low-dose methadone. At the same point, urine samples were negative for opiate use in 40% of patients receiving buprenorphine compared with 39% of those receiving high-dose methadone.¹⁰

Box 1

Table

Buprenorphine: A typical dosing strategy

Slow adoption. Opiate-dependence treatments such as methadone are prescribed in highly regulated environments, which is one reason only 25% of opiate addicts in the United States ever receive treatment.¹ Unfortunately, little has changed in the 20 months since the FDA approved buprenorphine for office-based detoxification and maintenance treatment of opiate dependence. More than 2,000 physicians have been trained to use buprenorphine, yet only 20% of them report prescribing it.¹¹

Reasons for this slow introduction include:

• difficulty in obtaining the medication
• lack of appropriate support staff and facilities
• uncertainty about prescribing the medication, despite special training.

Availability. When buprenorphine came to market in late 2003, most commercial pharmacies were not stocking it and it had to be special-ordered. As a result, patients receiving prescriptions had to wait 2 to 3 days for their first dose—a substantial deterrent to prescribing or taking this type of medication. Also, some private physicians and clinics do not keep buprenorphine samples to dispense on-site.

More pharmacies are stocking the medication now, but it remains the physician’s responsibility to ensure that a supply can be dispensed the day it is prescribed.

Support staff and facilities. To prescribe buprenorphine effectively, the physician needs resources for urine testing, physical exams, lab testing, and storing and dispensing buprenorphine. An integrated treatment clinic for opiate-dependent patients, complete with nursing and administrative staff, is ideal. If this support is not available, however, clinicians in private practice can safely prescribe buprenorphine from the office.

Uncertainty. Physicians often adopt new prescription products without hesitation, but buprenorphine’s administration and patient population are unusual. Even some physicians who have taken the special training course remain anxious about using this agent because it may precipitate opiate withdrawal. Also, the training requirement creates a sense that specialist-level knowledge is needed to safely prescribe buprenorphine.

Treatment requirements

For clinicians. The Drug Addiction Treatment Act of 2000 allows physicians to apply for a waiver from the Controlled Substances Act to prescribe buprenorphine for detoxification. A waiver is not required to prescribe buprenorphine for pain.¹²

To qualify for the waiver, physicians must be board-certified in addiction psychiatry or have completed a buprenorphine training course. Training is offered online and as a 1-day conference by the American Society of Addiction Medicine, American Academy of Addiction Psychiatry, American Medical Association, and American Psychiatric Association.

For patients. Like Mr. T, opiate users who ask about buprenorphine will want to know what to expect from treatment. To be eligible for buprenorphine treatment, a patient must:

• meet criteria for opiate dependence
• commit to keeping regular appointments—at least 3 times a week for the first 2 weeks then usually once weekly until detoxification is complete
• undergo random urine testing
• participate in psychosocial treatments.

So far, patients’ awareness of buprenorphine is highly variable. Asking an opiate user who presents for treatment what he or she knows about buprenorphine can be a useful screening tool. Highly motivated patients will have read about buprenorphine on the Internet, where they probably obtained your office phone number.

When a patient is accepted into treatment, detoxification with buprenorphine includes three phases: induction, stabilization/mainte-nance, and discontinuation.¹³ After stabilization, some patients remain in maintenance indefinitely and choose not to discontinue buprenorphine. The choice of who to discontinue and who to maintain on buprenorphine is a clinical decision made by the patient and practitioner. Success rates of detoxification with buprenorphine are similar to rates achieved with methadone and clonidine, although most studies have been conducted during buprenorphine maintenance.⁵

Case continued: Surprised to feel ‘normal’

Mr. T qualified for buprenorphine and came to the office feeling fairly ill. During withdrawal, his usual first symptom is rhinorrhea, followed by malaise, myalgia, restlessness, and intense cravings. His score of 24 on the Clinical Opiate Withdrawal Scale (COWS), indicated moderate withdrawal.

He felt better but not completely well 1 hour after taking buprenorphine/naloxone, 4 mg. He was given a 4-mg tablet to take at home 2 hours later. The next day his COWS score was 8, indicating mild withdrawal. He said he was surprised at how “normal” he was feeling.

Induction: Getting started

Buprenorphine induction is usually done during mild to moderate opiate withdrawal. Starting buprenorphine too soon—while the patient is relatively comfortable—may precipitate withdrawal because the agent will rapidly displace opiate bound to the receptors. In most cases, the first dose is given in the office so that the patient’s response can be monitored.

Two formulations. Buprenorphine comes alone (in 2- or 8-mg tablets) or in combination with naloxone (in 2 mg/0.5 mg and 8 mg/2 mg tablets). Both forms are given sublingually. Contrary to popular belief, IM buprenorphine is not approved for treating opiate addiction.

Naloxone is not absorbed in sublingual form and serves only to deter IV diversion of buprenorphine. Induction with buprenorphine alone is reserved for patients with documented allergy to naloxone or who are being detoxified from long-acting opiates such as methadone.

Dosing strategies are identical for both formulations. The usual starting dosage is 4 mg once daily, with a maximum dosage of 32 mg/d (Table). Withdrawal symptoms are typically controlled with 12 to 24 mg/d.¹⁴

If the patient is in active opiate withdrawal, the starting dose usually relieves symptoms in 30 to 45 minutes. If not, a second 4-mg dose can be given. Most patients do not require >8 mg the first day, but some may require 16 to 24 mg to suppress withdrawal symptoms.¹⁵

Some clinicians—such as solo practitioners who lack the resources of an outpatient clinic—prefer to have the patient take the first dose at home. Patients are instructed to take the first dose after withdrawal symptoms begin and to repeat the dose in 1 hour if symptoms persist. Thus, patients titrate their own dosages, but the clinician must be immediately available to handle complications. Induction continues until withdrawal symptoms are controlled.

The next day, patients return for evaluation. An objective scale such as the 11-item COWS can quantify withdrawal symptom severity.¹⁶ For each symptom—heart rate, nausea, diaphoresis, or restlessness—the COWS assigns a number corresponding to its severity. A total score >25 indicates moderately severe withdrawal.

After withdrawal symptoms are controlled, follow-up visits are scheduled every 2 to 3 days the first week and then weekly. Some physicians maintain daily contact with patients via e-mail or telephone to track symptoms.

Case continued: Steady improvement

By day 3, Mr. T gradually increased his buprenorphine/naloxone dosage to 16 mg once daily. He continued that dosage for 10 days before his next visit. At that point, he was slightly anxious but physically comfortable. He came into the office on days 2, 5, and 10 and his COWS scores decreased each time.

Stabilization and maintenance

When withdrawal symptoms are stabilized, patients begin maintenance therapy at the dosage that stabilized their symptoms. During maintenance therapy, the average buprenorphine dosage is 16 to 24 mg/d. Because of its long half-life, buprenorphine can be taken once daily, though some patients prefer twice-daily dosing for psychological comfort. Several studies comparing buprenorphine with methadone have found that buprenorphine, 8 to 16 mg/d, is similar in effect to approximately 60 mg/d of methadone.⁵

During the maintenance phase, it is important to have a policy for patients who relapse to substance abuse while taking buprenorphine (Box 2). During buprenorphine maintenance treatment, the estimated relapse rate to opiate use (chance of one positive test for opiates) ranges from 20% to 60%, compared with a relapse rate of 80% to 90% seen with placebo during clinical trials.⁵

Case continued: Time to taper?

After taking buprenorphine 2 months, Mr. T wants to taper off. He has been seen weekly and receives individual psychotherapy and group counseling. All urine drug screens have been negative for opiates.

With the psychiatrist’s observation, Mr. T. begins to taper his dosage of 16 mg/d by 4 mg a week. He is comfortable when he reaches 4 mg/d, but notices increased anxiety and general achiness when he reduces buprenorphine to 2 mg/d. He elects to remain at 4 mg/d for another 2 months.

Discontinuation

After the patient has reached a stable dose of buprenorphine, the clinician and patient together consider two treatment options:

• sustain the dose as maintenance therapy
• or taper and discontinue buprenorphine.

Box 2

Patients who have had multiple relapses and endured severe opiate withdrawal might consider remaining on buprenorphine for several months before tapering. Mild opiate withdrawal may occur if buprenorphine is tapered too rapidly, though this is not as severe or distressing as a full agonist withdrawal.

Tapering recommendations. To taper buprenorphine, reduce by 2 to 4 mg every 3 to 5 days until the patient is taking 2 mg/d. Most patients remain on this dosage at least 1 week and then discontinue. Those who experience side effects when dropping from 2 mg to 0 mg can take 2 mg every other day for 1 week and then discontinue.

After patients are tapered completely off buprenorphine, encourage them to follow up with the treating physician for at least another month. Opiate withdrawal symptoms have been reported to linger 2 to 3 weeks after the last dose of buprenorphine, but these symptoms—usually anxiety or insomnia—tend to be self-limiting.⁵

Case continued: Time to taper?

Mr. T has been free from heroin use for 4 months and has returned to work. He is rebuilding his life and continues with psychotherapy. He follows up at the buprenorphine clinic monthly for medication management. At each visit, he repeats the COWS test and undergoes a urine drug screen and vital signs check.

Related resources

• Substance Abuse and Mental Health Services Administration. Physician locator for buprenorphine providers.
• American Academy of Addiction Psychiatry. Information about buprenorphine training course. www.aaap.org/buprenorphine/buprenorphine.html
• Buprenorphine manufacturer’s Web site. Answers to frequently-asked questions. www.suboxone.com

Drug brand names

• Buprenorphine • Subutex
• Buprenorphine/naloxone • Suboxone
• Buprenorphine (IM) • Buprenex
• Clonidine • Catapres

After 10 years of heroin dependence, Mr. T, age 36, calls your office and says, “I want to get off heroin.” For 8 months, he’s been using IV heroin 2 to 3 times daily. He says he has tried methadone treatment but found daily dosing cumbersome.

He found your office number on the Substance Abuse and Mental Health Services Administration Web site, which lists physicians qualified to prescribe buprenorphine for opiate detoxification. He has heard about “bup” on the street and wants to know if he is eligible and what he can expect from treatment.

Like Mr. T, 1 million Americans are addicted to opiates.¹ As qualified physicians gain experience with using buprenorphine, this agent could revolutionize how opiate-dependent patients are routinely treated. Instead of receiving methadone only in specialized clinics, they can now choose to be treated in physicians’ offices.

Several obstacles, however, are preventing widespread buprenorphine use:

• Too few physicians are trained to offer this office-based treatment.
• Many of the 2,000 doctors who are trained remain uncertain about using buprenorphine.

This article is intended to help overcome obstacles to opiate-dependence treatment by familiarizing psychiatrists—whether trained or not in using buprenorphine—with evidence of this agent’s efficacy and its advantages compared with other treatments.

Efficacy and obstacles

Buprenorphine is a partial opioid agonist that binds to the mu receptor (Box 1).^2-5 It is a controlled substance (schedule-III narcotic). Outpatient trials have shown that buprenorphine is more effective than placebo and as effective as methadone for opiate detoxification.^6-10

In one of the largest trials, 326 opiate-dependent outpatients were randomly assigned to buprenorphine, buprenorphine/naloxone combination, or placebo for 4 weeks. Both buprenorphine forms were more effective than placebo, as measured by clean urine samples and patient reports of reduced opiate cravings.⁷

In maintenance treatment, buprenorphine has been shown to be more effective than placebo and as effective as methadone, 60 mg/d, in preventing relapse. In a randomized comparison study, 220 opiate-dependent patients received levomethadyl acetate (LAAM), 75 to 115 mg three times a week; buprenorphine, 16 to 32 mg three times a week; high-dose methadone (60 to 100 mg/d); or low-dose methadone (20 mg/d). Subjects reported using opiates 20 to 30 times in the week before study enrollment. After 17 weeks, treatment retention rates were 58% for buprenorphine, 73% for high-dose methadone, and 20% for low-dose methadone. At the same point, urine samples were negative for opiate use in 40% of patients receiving buprenorphine compared with 39% of those receiving high-dose methadone.¹⁰

Box 1

Table

Buprenorphine: A typical dosing strategy

Slow adoption. Opiate-dependence treatments such as methadone are prescribed in highly regulated environments, which is one reason only 25% of opiate addicts in the United States ever receive treatment.¹ Unfortunately, little has changed in the 20 months since the FDA approved buprenorphine for office-based detoxification and maintenance treatment of opiate dependence. More than 2,000 physicians have been trained to use buprenorphine, yet only 20% of them report prescribing it.¹¹

Reasons for this slow introduction include:

• difficulty in obtaining the medication
• lack of appropriate support staff and facilities
• uncertainty about prescribing the medication, despite special training.

Availability. When buprenorphine came to market in late 2003, most commercial pharmacies were not stocking it and it had to be special-ordered. As a result, patients receiving prescriptions had to wait 2 to 3 days for their first dose—a substantial deterrent to prescribing or taking this type of medication. Also, some private physicians and clinics do not keep buprenorphine samples to dispense on-site.

More pharmacies are stocking the medication now, but it remains the physician’s responsibility to ensure that a supply can be dispensed the day it is prescribed.

Support staff and facilities. To prescribe buprenorphine effectively, the physician needs resources for urine testing, physical exams, lab testing, and storing and dispensing buprenorphine. An integrated treatment clinic for opiate-dependent patients, complete with nursing and administrative staff, is ideal. If this support is not available, however, clinicians in private practice can safely prescribe buprenorphine from the office.

Uncertainty. Physicians often adopt new prescription products without hesitation, but buprenorphine’s administration and patient population are unusual. Even some physicians who have taken the special training course remain anxious about using this agent because it may precipitate opiate withdrawal. Also, the training requirement creates a sense that specialist-level knowledge is needed to safely prescribe buprenorphine.

Treatment requirements

For clinicians. The Drug Addiction Treatment Act of 2000 allows physicians to apply for a waiver from the Controlled Substances Act to prescribe buprenorphine for detoxification. A waiver is not required to prescribe buprenorphine for pain.¹²

To qualify for the waiver, physicians must be board-certified in addiction psychiatry or have completed a buprenorphine training course. Training is offered online and as a 1-day conference by the American Society of Addiction Medicine, American Academy of Addiction Psychiatry, American Medical Association, and American Psychiatric Association.

For patients. Like Mr. T, opiate users who ask about buprenorphine will want to know what to expect from treatment. To be eligible for buprenorphine treatment, a patient must:

• meet criteria for opiate dependence
• commit to keeping regular appointments—at least 3 times a week for the first 2 weeks then usually once weekly until detoxification is complete
• undergo random urine testing
• participate in psychosocial treatments.

So far, patients’ awareness of buprenorphine is highly variable. Asking an opiate user who presents for treatment what he or she knows about buprenorphine can be a useful screening tool. Highly motivated patients will have read about buprenorphine on the Internet, where they probably obtained your office phone number.

When a patient is accepted into treatment, detoxification with buprenorphine includes three phases: induction, stabilization/mainte-nance, and discontinuation.¹³ After stabilization, some patients remain in maintenance indefinitely and choose not to discontinue buprenorphine. The choice of who to discontinue and who to maintain on buprenorphine is a clinical decision made by the patient and practitioner. Success rates of detoxification with buprenorphine are similar to rates achieved with methadone and clonidine, although most studies have been conducted during buprenorphine maintenance.⁵

Case continued: Surprised to feel ‘normal’

Mr. T qualified for buprenorphine and came to the office feeling fairly ill. During withdrawal, his usual first symptom is rhinorrhea, followed by malaise, myalgia, restlessness, and intense cravings. His score of 24 on the Clinical Opiate Withdrawal Scale (COWS), indicated moderate withdrawal.

He felt better but not completely well 1 hour after taking buprenorphine/naloxone, 4 mg. He was given a 4-mg tablet to take at home 2 hours later. The next day his COWS score was 8, indicating mild withdrawal. He said he was surprised at how “normal” he was feeling.

Induction: Getting started

Buprenorphine induction is usually done during mild to moderate opiate withdrawal. Starting buprenorphine too soon—while the patient is relatively comfortable—may precipitate withdrawal because the agent will rapidly displace opiate bound to the receptors. In most cases, the first dose is given in the office so that the patient’s response can be monitored.

Two formulations. Buprenorphine comes alone (in 2- or 8-mg tablets) or in combination with naloxone (in 2 mg/0.5 mg and 8 mg/2 mg tablets). Both forms are given sublingually. Contrary to popular belief, IM buprenorphine is not approved for treating opiate addiction.

Naloxone is not absorbed in sublingual form and serves only to deter IV diversion of buprenorphine. Induction with buprenorphine alone is reserved for patients with documented allergy to naloxone or who are being detoxified from long-acting opiates such as methadone.

Dosing strategies are identical for both formulations. The usual starting dosage is 4 mg once daily, with a maximum dosage of 32 mg/d (Table). Withdrawal symptoms are typically controlled with 12 to 24 mg/d.¹⁴

If the patient is in active opiate withdrawal, the starting dose usually relieves symptoms in 30 to 45 minutes. If not, a second 4-mg dose can be given. Most patients do not require >8 mg the first day, but some may require 16 to 24 mg to suppress withdrawal symptoms.¹⁵

Some clinicians—such as solo practitioners who lack the resources of an outpatient clinic—prefer to have the patient take the first dose at home. Patients are instructed to take the first dose after withdrawal symptoms begin and to repeat the dose in 1 hour if symptoms persist. Thus, patients titrate their own dosages, but the clinician must be immediately available to handle complications. Induction continues until withdrawal symptoms are controlled.

The next day, patients return for evaluation. An objective scale such as the 11-item COWS can quantify withdrawal symptom severity.¹⁶ For each symptom—heart rate, nausea, diaphoresis, or restlessness—the COWS assigns a number corresponding to its severity. A total score >25 indicates moderately severe withdrawal.

After withdrawal symptoms are controlled, follow-up visits are scheduled every 2 to 3 days the first week and then weekly. Some physicians maintain daily contact with patients via e-mail or telephone to track symptoms.

Case continued: Steady improvement

By day 3, Mr. T gradually increased his buprenorphine/naloxone dosage to 16 mg once daily. He continued that dosage for 10 days before his next visit. At that point, he was slightly anxious but physically comfortable. He came into the office on days 2, 5, and 10 and his COWS scores decreased each time.

Stabilization and maintenance

When withdrawal symptoms are stabilized, patients begin maintenance therapy at the dosage that stabilized their symptoms. During maintenance therapy, the average buprenorphine dosage is 16 to 24 mg/d. Because of its long half-life, buprenorphine can be taken once daily, though some patients prefer twice-daily dosing for psychological comfort. Several studies comparing buprenorphine with methadone have found that buprenorphine, 8 to 16 mg/d, is similar in effect to approximately 60 mg/d of methadone.⁵

During the maintenance phase, it is important to have a policy for patients who relapse to substance abuse while taking buprenorphine (Box 2). During buprenorphine maintenance treatment, the estimated relapse rate to opiate use (chance of one positive test for opiates) ranges from 20% to 60%, compared with a relapse rate of 80% to 90% seen with placebo during clinical trials.⁵

Case continued: Time to taper?

After taking buprenorphine 2 months, Mr. T wants to taper off. He has been seen weekly and receives individual psychotherapy and group counseling. All urine drug screens have been negative for opiates.

With the psychiatrist’s observation, Mr. T. begins to taper his dosage of 16 mg/d by 4 mg a week. He is comfortable when he reaches 4 mg/d, but notices increased anxiety and general achiness when he reduces buprenorphine to 2 mg/d. He elects to remain at 4 mg/d for another 2 months.

Discontinuation

After the patient has reached a stable dose of buprenorphine, the clinician and patient together consider two treatment options:

• sustain the dose as maintenance therapy
• or taper and discontinue buprenorphine.

Box 2

Patients who have had multiple relapses and endured severe opiate withdrawal might consider remaining on buprenorphine for several months before tapering. Mild opiate withdrawal may occur if buprenorphine is tapered too rapidly, though this is not as severe or distressing as a full agonist withdrawal.

Tapering recommendations. To taper buprenorphine, reduce by 2 to 4 mg every 3 to 5 days until the patient is taking 2 mg/d. Most patients remain on this dosage at least 1 week and then discontinue. Those who experience side effects when dropping from 2 mg to 0 mg can take 2 mg every other day for 1 week and then discontinue.

After patients are tapered completely off buprenorphine, encourage them to follow up with the treating physician for at least another month. Opiate withdrawal symptoms have been reported to linger 2 to 3 weeks after the last dose of buprenorphine, but these symptoms—usually anxiety or insomnia—tend to be self-limiting.⁵

Case continued: Time to taper?

Mr. T has been free from heroin use for 4 months and has returned to work. He is rebuilding his life and continues with psychotherapy. He follows up at the buprenorphine clinic monthly for medication management. At each visit, he repeats the COWS test and undergoes a urine drug screen and vital signs check.

Related resources

• Substance Abuse and Mental Health Services Administration. Physician locator for buprenorphine providers.
• American Academy of Addiction Psychiatry. Information about buprenorphine training course. www.aaap.org/buprenorphine/buprenorphine.html
• Buprenorphine manufacturer’s Web site. Answers to frequently-asked questions. www.suboxone.com

Drug brand names

• Buprenorphine • Subutex
• Buprenorphine/naloxone • Suboxone
• Buprenorphine (IM) • Buprenex
• Clonidine • Catapres

Ms. H, age 26, is being evaluated for moderate to severe depressive symptoms, including oversleeping and overeating. She has had difficulty adhering to medication in the past and is ambivalent about taking antidepressants. She takes a passive approach to managing her depression, preferring to “wait for it to pass.”

Her psychiatrist prescribes fluoxetine, 20 mg in the morning, and recommends that Ms. H change her coping strategies from napping and snacking to increased physical activity. She encourages Ms. H to think about what activities interest her and to set exercise goals.

Ms. H says she has considered buying exercise equipment (an elliptical machine) and increasing her walking outside. She sets a goal to walk 20 minutes most days and to spend 10 to 15 minutes using the elliptical machine while watching television.

Physical activity’s mental health benefits are less well-known than its well-documented medical benefits—reduced risk of heart disease, hypertension, and diabetes; weight control; bone mass preservation; better sleep, and improved cholesterol levels.¹ By encouraging exercise, you can improve patients’ mood, well-being, and quality of life, independent of medication and psychotherapy. In this article, we:

• explore the relationship between physical activity and mental health
• compare exercise with medication and psychotherapies for easing depression
• discuss counseling strategies shown to be effective in helping sedentary patients become more physically active.

Table 1

Why physical activity may improve mental health

Mental benefits of exercise

Adults who exercise regularly report lower levels of depressive and anxiety disorders than the overall U.S. population.² As a therapeutic intervention, exercise has been studied primarily in depressed individuals, although some data also support its efficacy in:

• reducing anxiety symptoms in panic disorder³
• reducing disruptive behavior in developmentally disabled patients⁴
• alleviating chronic fatigue symptoms⁵
• improving body esteem in patients with body image disturbance⁶
• increasing function in chronic pain⁷
• reducing urges to smoke and improving smoking abstinence among nicotine-dependent individuals.⁸

Why exercise helps. Mechanisms that would explain exercise’s positive effect on mood are not well understood.⁹ Physiologic and psychological hypotheses have been suggested (Table 1),^10,11 and researchers are attempting to elucidate them by using animal models.¹³

Case report: Feeling more energetic

At follow-up 6 weeks later, Ms. H. reported a substantial reduction in depressive symptoms. She noted increased energy, improved sleep, decreased overeating, higher self-esteem, and greater confidence in her ability to manage her depression.

Exercising also helped structure her day. She noticed that on days she did not exercise she was more likely to take a nap, miss her medication, or feel pessimistic about her depression.

Exercise as an antidepressant

Exercise vs psychotherapy. Exercise has been shown to be more effective at reducing depressive symptoms than no treatment, occupational therapy, cognitive therapy, health seminars, routine care, or meditation. Interventions used in these meta-analyses ranged from nonaerobic exercise training several times a week to 1 hour of supervised running 4 times a week.¹² Literature reviews also have concluded that exercise training compares favorably with individual or group psychotherapy and with cognitive therapy for treating depression.⁷

Exercise vs medication. Exercise training has also been compared with drug therapy in treating depression.

In a randomized, controlled trial, 156 men and women over age 50 with major depression received exercise training, sertraline, or exercise plus sertraline. Subjects in the exercise groups completed 40 minutes of aerobic exercise (biking or brisk walking/ jogging) 3 times a week. Subjects treated with sertraline received 50 to 200 mg/d, depending on response.

After 16 weeks, all three groups were significantly improved, with no clinically or statistically significant differences in depressive symptoms, as measured with the Hamilton Rating Scale for Depression (HRSD) and Beck Depression Inventory.¹³

In a follow-up study 6 months later,¹⁴ the exercise group had significantly lower rates of relapse (defined as HRSD scores >15 and meeting diagnostic criteria) than did the medication group. Combining exercise with medication did not provide an added benefit in preventing relapse.

Exercise as monotherapy. Some studies have investigated using exercise instead of medication and psychotherapy. Many of these trials, however, were limited by methodologic weaknesses such as nonrandomized samples or lack of appropriate control groups.¹²

To address the need for higher-quality evidence, the Depression Outcomes Study of Exercise (DOSE) is investigating the dose-continued from page 12 response effects of exercise as monotherapy for major depressive disorder (MDD).⁵ The 12-week trial included 80 men and women ages 20 to 45 diagnosed with mild-to-moderate MDD using the Structured Clinical Interview for Depression. They were randomly assigned to one of five supervised exercise regimens:

• 7.0 kcal/kg/week in 3 days/week
• 7.0 kcal/kg/week in 5 days/week
• 17.5 kcal/kg/week in 3 days/week
• 17.5 kcal/kg/week in 5 days/week
• 3 days/week of stretching and flexibility exercises for 15 to 20 min/session.

Table 2

How much physical activity is recommended for adults?

Depressive symptoms were measured with the HRSD and Inventory of Depressive Symptoms (clinician and self-report). Other outcome measures included cardiorespiratory fitness, self-efficacy, and quality of life. Results are being prepared for publication and will likely help clarify the role of physical activity in treating patients with MDD.

Table 3

Why patients don’t exercise: Common barriers they perceive

How much exercise is therapeutic?

In the absence of physical activity guidelines specific to mental health, we suggest using standard public health guidelines (Table 2):

• 30 minutes or more of moderate-intensity physical activity (brisk walking, swimming, dancing, cycling) most days of the week (recommended by the Centers for Disease Control and Prevention and American College of Sports Medicine)¹
• 60 minutes of moderate-intensity physical activity daily for weight loss and maintenance (recommended by the Institute of Medicine).¹⁶

A recent study investigated the effects of exercise duration and intensity on weight loss in overweight, sedentary women. These researchers recommended setting the initial intervention target at 150 minutes or more of moderate-intensity exercise per week and progressing to 60 minutes per day as appropriate.¹⁶

Increasing the number of steps taken per day, as measured by a pedometer, also can be beneficial. Encourage patients to obtain a baseline measure of daily steps and to gradually increase toward a moderate goal of 10,000 steps per day.¹⁷

Case report: Accentuating the positive

On follow-up, Ms. H was quick to report the many barriers to exercise she had experienced and the times she did not meet her goal. Rather than dwell on shortcomings, the psychiatrist redirected her to examine the many positive actions she had taken to manage her depression.

As she considered how to overcome barriers to exercise, she reported increased confidence that she could stick with her medication and exercise regimen. She continues to exercise regularly and adheres to her fluoxetine. Her depressive symptoms remain well-controlled.

Overcoming barriers to exercise

Patient obstacles. Many patients acknowledge that regular exercise makes them feel physically and emotionally healthier but have difficulty exercising long term. Less than one-half of those who start an exercise program stick with it beyond 6 months.¹⁸ Drop-out reasons include injuries, lack of time, and low motivation (Table 3).^19,20

Depressive symptoms—fatigue, loss of interest, low self-esteem, feelings of helplessness, and psychomotor retardation—make exercise adherence even more difficult.

Physician obstacles. The U.S. Preventive Services Task Force recommends that physicians advise all patients to increase physical activity, but the national rate of physician counseling about exercise is low. In a population-based survey of more than 9,000 patients, 34% said their physicians counseled them about exercise at their most recent visit within the past year.²¹

Physician-reported barriers to exercise counseling include:

• competing demands for limited clinical time
• perceived ineffectiveness of advice to exercise
• lack of training and knowledge about exercise counseling and prescription.^22,23

Patients are more likely to become active and continue exercising when their physicians help them set achievable goals.

Project PACE. Physicians can overcome barriers to counseling patients about exercise. Those who participated in Project PACE (Physician-based Assessment and Counseling for Exercise)²⁴ said they felt more confident that they could counsel patients about physical activity in 1 to 5 minutes.

In a controlled study of 212 sedentary adults, patients who received PACE counseling from their physicians significantly increased their minutes of weekly walking compared with a control group. Also, 52% of patients who received PACE counseling adopted some physical activity, compared with 12% of controls.²⁵

Though modest initial goals are not sufficient for achieving the full benefits of exercise, success with a small goal is a powerful motivator. Rather than giving up, patients feel encouraged and are more likely to set a subsequent, more ambitious goal.

Recommendations. To help patients start exercising, determine how motivated and ready they are. Start by asking them to describe their current activities. Ask if they were ever more active and what they liked about it. Did they experience any benefits? Establish which of increased activity’s benefits—improved sleep, reduced depression, increased energy—would most benefit the patient, based on his or her symptoms.

Discuss barriers to physical activity and encourage problem-solving to overcome them and incorporate physical activity into their lives. Encourage patients to seek support from family, friends, coworkers, and exercise groups.

Help them set realistic, achievable goals. Even a modest 10 minutes of activity has been shown to enhance mood,²⁶ and a 10-minute brisk walk is one-third of the day’s public health guideline. Suggest that patients choose a variety of activities they enjoy.

During follow-up visits, reinforce any progress toward change. When patients’ exercise efforts fall short, explain that the process of becoming more active often includes setbacks. Advise them to seek support and to consider adopting more-achievable goals.

Related resources

• Getting started. Resources on nutrition and physical activity from the National Center for Chronic Disease Prevention and Health Promotion. http://www.cdc.gov/nccdphp/dnpa/physical/starting/index.htm
• Marcus B, Forsyth L. Motivating people to be physically active. Champaign, IL: Human Kinetics, 2002.

Drug brand names

• Fluoxetine • Prozac
• Sertraline • Zoloft

Disclosure

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

Ms. H, age 26, is being evaluated for moderate to severe depressive symptoms, including oversleeping and overeating. She has had difficulty adhering to medication in the past and is ambivalent about taking antidepressants. She takes a passive approach to managing her depression, preferring to “wait for it to pass.”

Her psychiatrist prescribes fluoxetine, 20 mg in the morning, and recommends that Ms. H change her coping strategies from napping and snacking to increased physical activity. She encourages Ms. H to think about what activities interest her and to set exercise goals.

Ms. H says she has considered buying exercise equipment (an elliptical machine) and increasing her walking outside. She sets a goal to walk 20 minutes most days and to spend 10 to 15 minutes using the elliptical machine while watching television.

Physical activity’s mental health benefits are less well-known than its well-documented medical benefits—reduced risk of heart disease, hypertension, and diabetes; weight control; bone mass preservation; better sleep, and improved cholesterol levels.¹ By encouraging exercise, you can improve patients’ mood, well-being, and quality of life, independent of medication and psychotherapy. In this article, we:

• explore the relationship between physical activity and mental health
• compare exercise with medication and psychotherapies for easing depression
• discuss counseling strategies shown to be effective in helping sedentary patients become more physically active.

Table 1

Why physical activity may improve mental health

Mental benefits of exercise

Adults who exercise regularly report lower levels of depressive and anxiety disorders than the overall U.S. population.² As a therapeutic intervention, exercise has been studied primarily in depressed individuals, although some data also support its efficacy in:

• reducing anxiety symptoms in panic disorder³
• reducing disruptive behavior in developmentally disabled patients⁴
• alleviating chronic fatigue symptoms⁵
• improving body esteem in patients with body image disturbance⁶
• increasing function in chronic pain⁷
• reducing urges to smoke and improving smoking abstinence among nicotine-dependent individuals.⁸

Why exercise helps. Mechanisms that would explain exercise’s positive effect on mood are not well understood.⁹ Physiologic and psychological hypotheses have been suggested (Table 1),^10,11 and researchers are attempting to elucidate them by using animal models.¹³

Case report: Feeling more energetic

At follow-up 6 weeks later, Ms. H. reported a substantial reduction in depressive symptoms. She noted increased energy, improved sleep, decreased overeating, higher self-esteem, and greater confidence in her ability to manage her depression.

Exercising also helped structure her day. She noticed that on days she did not exercise she was more likely to take a nap, miss her medication, or feel pessimistic about her depression.

Exercise as an antidepressant

Exercise vs psychotherapy. Exercise has been shown to be more effective at reducing depressive symptoms than no treatment, occupational therapy, cognitive therapy, health seminars, routine care, or meditation. Interventions used in these meta-analyses ranged from nonaerobic exercise training several times a week to 1 hour of supervised running 4 times a week.¹² Literature reviews also have concluded that exercise training compares favorably with individual or group psychotherapy and with cognitive therapy for treating depression.⁷

Exercise vs medication. Exercise training has also been compared with drug therapy in treating depression.

In a randomized, controlled trial, 156 men and women over age 50 with major depression received exercise training, sertraline, or exercise plus sertraline. Subjects in the exercise groups completed 40 minutes of aerobic exercise (biking or brisk walking/ jogging) 3 times a week. Subjects treated with sertraline received 50 to 200 mg/d, depending on response.

After 16 weeks, all three groups were significantly improved, with no clinically or statistically significant differences in depressive symptoms, as measured with the Hamilton Rating Scale for Depression (HRSD) and Beck Depression Inventory.¹³

In a follow-up study 6 months later,¹⁴ the exercise group had significantly lower rates of relapse (defined as HRSD scores >15 and meeting diagnostic criteria) than did the medication group. Combining exercise with medication did not provide an added benefit in preventing relapse.

Exercise as monotherapy. Some studies have investigated using exercise instead of medication and psychotherapy. Many of these trials, however, were limited by methodologic weaknesses such as nonrandomized samples or lack of appropriate control groups.¹²

To address the need for higher-quality evidence, the Depression Outcomes Study of Exercise (DOSE) is investigating the dose-continued from page 12 response effects of exercise as monotherapy for major depressive disorder (MDD).⁵ The 12-week trial included 80 men and women ages 20 to 45 diagnosed with mild-to-moderate MDD using the Structured Clinical Interview for Depression. They were randomly assigned to one of five supervised exercise regimens:

• 7.0 kcal/kg/week in 3 days/week
• 7.0 kcal/kg/week in 5 days/week
• 17.5 kcal/kg/week in 3 days/week
• 17.5 kcal/kg/week in 5 days/week
• 3 days/week of stretching and flexibility exercises for 15 to 20 min/session.

Table 2

How much physical activity is recommended for adults?

Depressive symptoms were measured with the HRSD and Inventory of Depressive Symptoms (clinician and self-report). Other outcome measures included cardiorespiratory fitness, self-efficacy, and quality of life. Results are being prepared for publication and will likely help clarify the role of physical activity in treating patients with MDD.

Table 3

Why patients don’t exercise: Common barriers they perceive

How much exercise is therapeutic?

In the absence of physical activity guidelines specific to mental health, we suggest using standard public health guidelines (Table 2):

• 30 minutes or more of moderate-intensity physical activity (brisk walking, swimming, dancing, cycling) most days of the week (recommended by the Centers for Disease Control and Prevention and American College of Sports Medicine)¹
• 60 minutes of moderate-intensity physical activity daily for weight loss and maintenance (recommended by the Institute of Medicine).¹⁶

A recent study investigated the effects of exercise duration and intensity on weight loss in overweight, sedentary women. These researchers recommended setting the initial intervention target at 150 minutes or more of moderate-intensity exercise per week and progressing to 60 minutes per day as appropriate.¹⁶

Increasing the number of steps taken per day, as measured by a pedometer, also can be beneficial. Encourage patients to obtain a baseline measure of daily steps and to gradually increase toward a moderate goal of 10,000 steps per day.¹⁷

Case report: Accentuating the positive

On follow-up, Ms. H was quick to report the many barriers to exercise she had experienced and the times she did not meet her goal. Rather than dwell on shortcomings, the psychiatrist redirected her to examine the many positive actions she had taken to manage her depression.

As she considered how to overcome barriers to exercise, she reported increased confidence that she could stick with her medication and exercise regimen. She continues to exercise regularly and adheres to her fluoxetine. Her depressive symptoms remain well-controlled.

Overcoming barriers to exercise

Patient obstacles. Many patients acknowledge that regular exercise makes them feel physically and emotionally healthier but have difficulty exercising long term. Less than one-half of those who start an exercise program stick with it beyond 6 months.¹⁸ Drop-out reasons include injuries, lack of time, and low motivation (Table 3).^19,20

Depressive symptoms—fatigue, loss of interest, low self-esteem, feelings of helplessness, and psychomotor retardation—make exercise adherence even more difficult.

Physician obstacles. The U.S. Preventive Services Task Force recommends that physicians advise all patients to increase physical activity, but the national rate of physician counseling about exercise is low. In a population-based survey of more than 9,000 patients, 34% said their physicians counseled them about exercise at their most recent visit within the past year.²¹

Physician-reported barriers to exercise counseling include:

• competing demands for limited clinical time
• perceived ineffectiveness of advice to exercise
• lack of training and knowledge about exercise counseling and prescription.^22,23

Patients are more likely to become active and continue exercising when their physicians help them set achievable goals.

Project PACE. Physicians can overcome barriers to counseling patients about exercise. Those who participated in Project PACE (Physician-based Assessment and Counseling for Exercise)²⁴ said they felt more confident that they could counsel patients about physical activity in 1 to 5 minutes.

In a controlled study of 212 sedentary adults, patients who received PACE counseling from their physicians significantly increased their minutes of weekly walking compared with a control group. Also, 52% of patients who received PACE counseling adopted some physical activity, compared with 12% of controls.²⁵

Though modest initial goals are not sufficient for achieving the full benefits of exercise, success with a small goal is a powerful motivator. Rather than giving up, patients feel encouraged and are more likely to set a subsequent, more ambitious goal.

Recommendations. To help patients start exercising, determine how motivated and ready they are. Start by asking them to describe their current activities. Ask if they were ever more active and what they liked about it. Did they experience any benefits? Establish which of increased activity’s benefits—improved sleep, reduced depression, increased energy—would most benefit the patient, based on his or her symptoms.

Discuss barriers to physical activity and encourage problem-solving to overcome them and incorporate physical activity into their lives. Encourage patients to seek support from family, friends, coworkers, and exercise groups.

Help them set realistic, achievable goals. Even a modest 10 minutes of activity has been shown to enhance mood,²⁶ and a 10-minute brisk walk is one-third of the day’s public health guideline. Suggest that patients choose a variety of activities they enjoy.

During follow-up visits, reinforce any progress toward change. When patients’ exercise efforts fall short, explain that the process of becoming more active often includes setbacks. Advise them to seek support and to consider adopting more-achievable goals.

Related resources

• Getting started. Resources on nutrition and physical activity from the National Center for Chronic Disease Prevention and Health Promotion. http://www.cdc.gov/nccdphp/dnpa/physical/starting/index.htm
• Marcus B, Forsyth L. Motivating people to be physically active. Champaign, IL: Human Kinetics, 2002.

Drug brand names

• Fluoxetine • Prozac
• Sertraline • Zoloft

Disclosure

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

Ms. H, age 26, is being evaluated for moderate to severe depressive symptoms, including oversleeping and overeating. She has had difficulty adhering to medication in the past and is ambivalent about taking antidepressants. She takes a passive approach to managing her depression, preferring to “wait for it to pass.”

Her psychiatrist prescribes fluoxetine, 20 mg in the morning, and recommends that Ms. H change her coping strategies from napping and snacking to increased physical activity. She encourages Ms. H to think about what activities interest her and to set exercise goals.

Ms. H says she has considered buying exercise equipment (an elliptical machine) and increasing her walking outside. She sets a goal to walk 20 minutes most days and to spend 10 to 15 minutes using the elliptical machine while watching television.

Physical activity’s mental health benefits are less well-known than its well-documented medical benefits—reduced risk of heart disease, hypertension, and diabetes; weight control; bone mass preservation; better sleep, and improved cholesterol levels.¹ By encouraging exercise, you can improve patients’ mood, well-being, and quality of life, independent of medication and psychotherapy. In this article, we:

• explore the relationship between physical activity and mental health
• compare exercise with medication and psychotherapies for easing depression
• discuss counseling strategies shown to be effective in helping sedentary patients become more physically active.

Table 1

Why physical activity may improve mental health

Mental benefits of exercise

Adults who exercise regularly report lower levels of depressive and anxiety disorders than the overall U.S. population.² As a therapeutic intervention, exercise has been studied primarily in depressed individuals, although some data also support its efficacy in:

• reducing anxiety symptoms in panic disorder³
• reducing disruptive behavior in developmentally disabled patients⁴
• alleviating chronic fatigue symptoms⁵
• improving body esteem in patients with body image disturbance⁶
• increasing function in chronic pain⁷
• reducing urges to smoke and improving smoking abstinence among nicotine-dependent individuals.⁸

Why exercise helps. Mechanisms that would explain exercise’s positive effect on mood are not well understood.⁹ Physiologic and psychological hypotheses have been suggested (Table 1),^10,11 and researchers are attempting to elucidate them by using animal models.¹³

Case report: Feeling more energetic

At follow-up 6 weeks later, Ms. H. reported a substantial reduction in depressive symptoms. She noted increased energy, improved sleep, decreased overeating, higher self-esteem, and greater confidence in her ability to manage her depression.

Exercising also helped structure her day. She noticed that on days she did not exercise she was more likely to take a nap, miss her medication, or feel pessimistic about her depression.

Exercise as an antidepressant

Exercise vs psychotherapy. Exercise has been shown to be more effective at reducing depressive symptoms than no treatment, occupational therapy, cognitive therapy, health seminars, routine care, or meditation. Interventions used in these meta-analyses ranged from nonaerobic exercise training several times a week to 1 hour of supervised running 4 times a week.¹² Literature reviews also have concluded that exercise training compares favorably with individual or group psychotherapy and with cognitive therapy for treating depression.⁷

Exercise vs medication. Exercise training has also been compared with drug therapy in treating depression.

In a randomized, controlled trial, 156 men and women over age 50 with major depression received exercise training, sertraline, or exercise plus sertraline. Subjects in the exercise groups completed 40 minutes of aerobic exercise (biking or brisk walking/ jogging) 3 times a week. Subjects treated with sertraline received 50 to 200 mg/d, depending on response.

After 16 weeks, all three groups were significantly improved, with no clinically or statistically significant differences in depressive symptoms, as measured with the Hamilton Rating Scale for Depression (HRSD) and Beck Depression Inventory.¹³

In a follow-up study 6 months later,¹⁴ the exercise group had significantly lower rates of relapse (defined as HRSD scores >15 and meeting diagnostic criteria) than did the medication group. Combining exercise with medication did not provide an added benefit in preventing relapse.

Exercise as monotherapy. Some studies have investigated using exercise instead of medication and psychotherapy. Many of these trials, however, were limited by methodologic weaknesses such as nonrandomized samples or lack of appropriate control groups.¹²

To address the need for higher-quality evidence, the Depression Outcomes Study of Exercise (DOSE) is investigating the dose-continued from page 12 response effects of exercise as monotherapy for major depressive disorder (MDD).⁵ The 12-week trial included 80 men and women ages 20 to 45 diagnosed with mild-to-moderate MDD using the Structured Clinical Interview for Depression. They were randomly assigned to one of five supervised exercise regimens:

• 7.0 kcal/kg/week in 3 days/week
• 7.0 kcal/kg/week in 5 days/week
• 17.5 kcal/kg/week in 3 days/week
• 17.5 kcal/kg/week in 5 days/week
• 3 days/week of stretching and flexibility exercises for 15 to 20 min/session.

Table 2

How much physical activity is recommended for adults?

Depressive symptoms were measured with the HRSD and Inventory of Depressive Symptoms (clinician and self-report). Other outcome measures included cardiorespiratory fitness, self-efficacy, and quality of life. Results are being prepared for publication and will likely help clarify the role of physical activity in treating patients with MDD.

Table 3

Why patients don’t exercise: Common barriers they perceive

How much exercise is therapeutic?

In the absence of physical activity guidelines specific to mental health, we suggest using standard public health guidelines (Table 2):

• 30 minutes or more of moderate-intensity physical activity (brisk walking, swimming, dancing, cycling) most days of the week (recommended by the Centers for Disease Control and Prevention and American College of Sports Medicine)¹
• 60 minutes of moderate-intensity physical activity daily for weight loss and maintenance (recommended by the Institute of Medicine).¹⁶

A recent study investigated the effects of exercise duration and intensity on weight loss in overweight, sedentary women. These researchers recommended setting the initial intervention target at 150 minutes or more of moderate-intensity exercise per week and progressing to 60 minutes per day as appropriate.¹⁶

Increasing the number of steps taken per day, as measured by a pedometer, also can be beneficial. Encourage patients to obtain a baseline measure of daily steps and to gradually increase toward a moderate goal of 10,000 steps per day.¹⁷

Case report: Accentuating the positive

On follow-up, Ms. H was quick to report the many barriers to exercise she had experienced and the times she did not meet her goal. Rather than dwell on shortcomings, the psychiatrist redirected her to examine the many positive actions she had taken to manage her depression.

As she considered how to overcome barriers to exercise, she reported increased confidence that she could stick with her medication and exercise regimen. She continues to exercise regularly and adheres to her fluoxetine. Her depressive symptoms remain well-controlled.

Overcoming barriers to exercise

Patient obstacles. Many patients acknowledge that regular exercise makes them feel physically and emotionally healthier but have difficulty exercising long term. Less than one-half of those who start an exercise program stick with it beyond 6 months.¹⁸ Drop-out reasons include injuries, lack of time, and low motivation (Table 3).^19,20

Depressive symptoms—fatigue, loss of interest, low self-esteem, feelings of helplessness, and psychomotor retardation—make exercise adherence even more difficult.

Physician obstacles. The U.S. Preventive Services Task Force recommends that physicians advise all patients to increase physical activity, but the national rate of physician counseling about exercise is low. In a population-based survey of more than 9,000 patients, 34% said their physicians counseled them about exercise at their most recent visit within the past year.²¹

Physician-reported barriers to exercise counseling include:

• competing demands for limited clinical time
• perceived ineffectiveness of advice to exercise
• lack of training and knowledge about exercise counseling and prescription.^22,23

Patients are more likely to become active and continue exercising when their physicians help them set achievable goals.

Project PACE. Physicians can overcome barriers to counseling patients about exercise. Those who participated in Project PACE (Physician-based Assessment and Counseling for Exercise)²⁴ said they felt more confident that they could counsel patients about physical activity in 1 to 5 minutes.

In a controlled study of 212 sedentary adults, patients who received PACE counseling from their physicians significantly increased their minutes of weekly walking compared with a control group. Also, 52% of patients who received PACE counseling adopted some physical activity, compared with 12% of controls.²⁵

Though modest initial goals are not sufficient for achieving the full benefits of exercise, success with a small goal is a powerful motivator. Rather than giving up, patients feel encouraged and are more likely to set a subsequent, more ambitious goal.

Recommendations. To help patients start exercising, determine how motivated and ready they are. Start by asking them to describe their current activities. Ask if they were ever more active and what they liked about it. Did they experience any benefits? Establish which of increased activity’s benefits—improved sleep, reduced depression, increased energy—would most benefit the patient, based on his or her symptoms.

Discuss barriers to physical activity and encourage problem-solving to overcome them and incorporate physical activity into their lives. Encourage patients to seek support from family, friends, coworkers, and exercise groups.

Help them set realistic, achievable goals. Even a modest 10 minutes of activity has been shown to enhance mood,²⁶ and a 10-minute brisk walk is one-third of the day’s public health guideline. Suggest that patients choose a variety of activities they enjoy.

During follow-up visits, reinforce any progress toward change. When patients’ exercise efforts fall short, explain that the process of becoming more active often includes setbacks. Advise them to seek support and to consider adopting more-achievable goals.

Related resources

• Getting started. Resources on nutrition and physical activity from the National Center for Chronic Disease Prevention and Health Promotion. http://www.cdc.gov/nccdphp/dnpa/physical/starting/index.htm
• Marcus B, Forsyth L. Motivating people to be physically active. Champaign, IL: Human Kinetics, 2002.

Drug brand names

• Fluoxetine • Prozac
• Sertraline • Zoloft

Disclosure

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

Just three words—“My tummy hurts”—can mobilize a child’s parents into a high state of worry, especially on school days. They wonder: Is our child sick? Should he or she stay home? Why is this happening so often?

Although recurrent abdominal pain (RAP) is real, it usually is not caused by tissue damage or serious physical disease. When children with RAP are referred for psychiatric evaluation—often after extensive medical workups—we can help them and their parents manage the problem and function more normally. This article:

• describes physiologic mechanisms that may underlie recurrent GI distress
• discusses the high correlation of psychiatric comorbidities with RAP
• recommends judicious laboratory testing
• reviews evidence on medications and psychotherapies to improve RAP symptoms
• offers advice on building a therapeutic alliance with the patient and family.

Figure Comorbid anxiety and depressive disorders in children with RAP

Children with functional RAP are much more likely to be anxious or depressed than similar pain-free children. A recent blinded study followed 80 children ages 8 to 15 (42 with RAP and 38 controls) identified through screening at primary care pediatric offices. Each was assessed using the Schedule for Affective Disorders and Schizophrenia for School Age Children, Present and Lifetime version (K-SADS-PL). Percentage meeting diagnostic criteria

Source: Reference 5.

RAP: A ‘Functional’ disorder

RAP is a somatoform (or “functional”) disorder, defined as physical symptoms not fully explained by a medical condition, effects of a substance, or another mental disorder. Symptoms cause distress and/or functional impairment and are not intentionally produced.¹

A patient with RAP experiences at least three episodes of abdominal pain over 3 months that interfere with daily activities.² RAP affects 7% to 25% of school-aged children and adolescents,³ most of whom have a functional disorder.⁴

RAP is equally common among prepubertal boys and girls but more common among girls during adolescence.³ RAP can impair school attendance and performance and stigmatize a child as “sickly.”

Common comorbid symptoms

Physical. Besides stomach pain, children with RAP often experience headaches (including migraines), other GI symptoms, general aches and pains, dizziness, and fatigue.

Patients with RAP who do not experience GI bleeding, anemia, fever, weight loss, growth failure, or persistent vomiting most likely do not have a serious underlying disease.

Psychiatric. Children with RAP have much higher rates of anxiety (80%) and depressive (40%) disorders than do their unaffected peers (Figure).⁵ We have also seen higher levels of suicidal thinking in children with RAP in primary care settings compared with pain-free controls (14% vs. 4%, P = 0.04; unpublished data).

In most cases, psychiatric comorbidities appear to precede or coincide with RAP onset. Separation fears, generalized anxiety, and social anxiety in particular are common in patients with RAP yet are seldom recognized in medical settings.

Having childhood RAP increases the risk of anxiety, depression, and hypochondriacal fears in adulthood.⁶ We do not know whether early intervention prevents later disability.

Use of medical services. Abdominal pain accounts for 2% to 4% of all pediatric office visits.⁷ In one study, 8% of middle school and high school students said they had visited a physician for evaluation of stomach pain during the previous year.⁸ Children with RAP make more ambulatory health and mental health visits than peers⁹ and are at risk for unnecessary and potentially dangerous medical tests, procedures, and treatments, including abdominal surgery.¹⁰

Four functional GI disorders

To better characterize youths with functional RAP, symptom-based criteria have been developed and applied for functional GI disorders, defined as chronic or recurrent GI symptoms without explanatory structural or biochemical abnormalities.¹¹ Four such disorders are relevant in children with RAP.

Irritable bowel syndrome (IBS): RAP with at least two of the following symptoms: relief with defecation, change in stool frequency, and change in stool form or appearance (occurs in approximately 50% of RAP cases).

Functional dyspepsia: RAP centered in the upper abdomen that is not associated with changes in bowel habits.

Abdominal migraine: Paroxysmal midline abdominal pain lasting 2 hours to several days with symptom-free intervals of weeks to months and at least two of the following: headache during episodes, photophobia during episodes, unilateral headache, aura, and a family history of migraine.

Functional abdominal pain: Continuous or nearly continuous abdominal pain for 6 months or more.

The reliability, validity, and clinical relevance of these criteria have not been demonstrated. Some children with RAP do not meet any criteria for a specific functional GI disorder.

Gut-brain connections. RAP may be associated with a heightened sensitivity to visceral sensations (visceral hyperalgesia) and a low pressure-pain threshold, leading to speculation that these children are hypersensitive to pain.

High rates of anxiety disorders and temperamental harm avoidance also are seen in patients with RAP, along with a tendency to develop pain when faced with unexpected events. Whether these children are more likely than others to perceive novel internal or external perceptions as threatening is open to debate.

Table 1

Recurrent abdominal pain: 8 steps to assessment and diagnosis

Serotonin communicates nociceptive information between the gut and brain and may mediate visceral hyperalgesia. Gut enterochromaffin cells contain more than 90% of the body’s total serotonin. They act as sensory transducers, releasing serotonin in response to increased intraluminal pressure or inflammation.

The released serotonin can cause abdominal discomfort by stimulating 5-HT 3 receptors on vagal afferents and can influence gut peristaltic activity by stimulating enteric afferents. The same serotonin transporter responsible for CNS serotonin reuptake is expressed throughout the gut.

A constellation of clues

The ideal RAP evaluation includes information from the child, parents, educators, and other health care professionals (Table 1).

Begin by acknowledging the patient’s suffering and the parent’s concerns; do not challenge the pain’s subjective reality. Rather than prejudging its cause, document the pain’s timing, context, and characteristics, and review the patient’s history. A constellation of clues is most suggestive of RAP (Table 2); single clues are not definitive.^12,13

Table 2

Clues that suggest functional pain*

Diagnostic testing. Be judicious in selecting diagnostic tests and procedures. Continuing to order studies in a haphazard effort to rule out disease can generate concerns that “the doctor doesn’t know what’s wrong” and heighten the family’s fear that a disease has been missed.

The process of “ruling out” physical disease may have no apparent end. Unless you are reasonably comfortable that a serious physical disease has not been missed, it is difficult to explain RAP to the patient and family and lay the foundation for intervention.

On the other hand, you must balance the importance of minimizing your own and the family’s anxiety about unrecognized disease against the physical and psychological risks and costs associated with medical tests and procedures.

Social assessment. Assess social and familial reinforcement (secondary gain) of the pain. Parents sometimes inadvertently encourage their children’s sick-role behaviors by providing excessive attention, rewards, or opportunities to avoid uncomfortable situations. RAP can become an excuse for poor performance (self-handicapping), particularly in children with a learning disorder.

How to deliver the diagnosis

Functional abdominal pain is essentially a clinical diagnosis that relies on presentation, course, and findings. As mentioned, a constellation of “clues” is most supportive, as is having typical IBS symptoms.

Before declaring the diagnosis, discuss with the family the patient’s physical, emotional, and behavioral symptoms and the context in which RAP developed. Doing so can help maintain your credibility and establish a consensus.

Once you declare the diagnosis, discuss it clearly and frankly. Families are not likely to be reassured if you do not offer a plausible explanation for the lack of physical findings.

Precautions. When a definitive diagnosis is not possible, acknowledge that uncertainty. Although you must discuss any recognized psychiatric comorbidity, attempting to “explain” that the disorder is causing the pain is usually impractical and intellectually dishonest.

Also, given the pervasive nature of stigma, do not convey embarrassment or unease about diagnosing functional RAP or any comorbid psychiatric disorder.

Follow-up testing. Once you diagnose functional RAP, further testing is generally not necessary. Tests might be indicated if you:

• receive new information
• observe a change in clinical status
• or are convinced that treatment will not work unless the family is reassured by further investigation.

Collaborative treatment

Reassurance and education. Reassurance that the patient does not have a serious physical disease is necessary but rarely sufficient. Explain that the child’s pain does not appear to reflect tissue damage and is not threatening. On the other hand, avoid giving excessive reassurance, particularly when obsessional illness worry and hypochondriacal fears are prominent. Address illness worry as a problem to be solved together.

Discuss with the patient and family what is known and not known about functional RAP, and encourage them to ask questions. This is an opportunity for you to instill hope and cultivate positive expectations, but avoid promising cure. Discuss the gut-brain connection and relevance of visceral hyperalgesia, including serotonin’s potential roles in RAP pathogenesis.

Partners in care. Collaborative treatment increases the likelihood of success. Discuss the importance of a therapeutic partnership, and clarify any areas of disagreement with the diagnosis or treatment plan.

Clearly delineate your roles and responsibilities and those of the patient, family, and other health care team members. Poor communication is pediatricians’ most common complaint about psychiatrists.¹⁴ Good interdisciplinary communication decreases the chance that treatment strategies will be duplicated, diluted, or misinterpreted.

Consolidate medical care with a single clinician—often the primary care physician—based on discussions with the patient, family, and health care team. The coordinating clinician can mediate between the school and family when tensions develop over poor attendance or requests for special treatment. It is often useful for this clinician to spell out:

• what constitutes a legitimate medical excuse for school absence
• who will legitimize excuses.

All parties should understand that the school will view an unexcused absence as truancy and act appropriately.

Diet and lifestyle. Encourage the patient to maintain a regular schedule and a healthy diet. Specific dietary interventions have not been proven effective, despite speculation that lack of dietary fiber or lactose intolerance might cause RAP.^15,16 Also encourage adequate sleep and regular exercise.

Medication and psychotherapy

Because no strong evidence-based guidelines address pediatric RAP intervention, family preferences usually guide initial treatment decisions. This highlights the importance of good communication and a therapeutic partnership among the clinician, family, and patient.

Antispasmodics, acid reducers, and antidepressants are commonly prescribed for RAP, though none are well-supported in the literature and no controlled studies have gauged medication’s impact on psychiatric comorbidity.¹⁶

Antidepressants. Selective serotonin reuptake inhibitors (SSRIs) might help relieve RAP symptoms, but the evidence is inconclusive. SSRIs are considered potentially beneficial in RAP because they may help communicate nociceptive information between the gut and brain and mediate visceral hyperalgesia.

SSRIs at first may increase serotonin at the synapse, which one might assume would to worsen abdominal symptoms. However, ongoing SSRI use could “down-regulate” postsynaptic 5-HT₃ receptors and desensitize postsynaptic cells to the effects of local serotonin.

Our group recently conducted a 12-week open trial of citalopram for functional pediatric RAP.¹⁷ The 25 participants received 10 mg/d the first week, then 20 mg/d thereafter if tolerated. At week 4, nonresponders and partial responders who were tolerating the medication began receiving 40 mg/d.

Table 3

SSRI daily dosing for pediatric RAP

At trial’s end, more than two-thirds of participants were taking 40 mg/d. We rated 21 of 25 patients (84%) as “much improved” or “very much improved,” using the Clinical Global Impression-Improvement scale. Abdominal pain, anxiety, depression, other somatic symptoms, and functional impairment all improved significantly during treatment. Suicidal thoughts diminished progressively from baseline, and no patient reported suicidal thinking at study’s end. Citalopram was generally well tolerated.

With SSRI treatment, start at a low dosage for 3 to 7 days (Table 3). If tolerated, increase to a typical therapeutic dosage. If symptoms fail to respond after 2 or 3 weeks, consider a higher dosage. A short course of an oral benzodiazepine (such as clonazepam, 0.25 mg bid) during the first weeks of SSRI treatment sometimes helps particularly anxious patients or those whose pain appears closely associated with anxiety or “stress.”

Pediatric gastroenterologists often prescribe a low-dose tricyclic antidepressant as first-line therapy, but we discourage this. TCAs lack efficacy in pediatric depression and pose a greater risk of side effects and safety concerns than SSRIs.¹⁸

Other agents have been tried for RAP-associated conditions:

Famotidine, a histamine type 2 receptor blocker, may reduce pain in children with dyspepsia and RAP.¹⁹

Peppermint oil reduced abdominal pain in one study of children with IBS but had little effect on other symptoms.²⁰

Medications such as alosetron and tegaserod that interrupt serotonergic neurotransmission in the gut have shown benefit in adults with IBS but have not been studied in children.

Psychotherapy. A few small studies suggest that cognitive-behavioral therapies (CBT) are helpful in RAP, but CBT may be difficult to deliver in medical settings.^21,22 A simplified “rehabilitative” approach that incorporates CBT principles involves having the clinician and patient view RAP as a challenge to be overcome, rather than a burden to be endured. Such an approach emphasizes the child’s fundamental strength and adaptability rather than vulnerabilities.

The goal of therapy is redirected from finding a cure to coping with and overcoming the problem. This approach challenges the notion that the child cannot resume normal function until the pain is completely gone. It encourages active, problem-focused coping, and discourages passive acceptance—which is associated with greater symptom burden and functional impairment.

Work with parents to reinforce the child’s health-promoting behaviors and minimize negative and social reinforcements (secondary gain) associated with RAP. Advise parents to:

• encourage and reward full school attendance
• avoid home-bound instruction
• expect the child to function despite physical distress
• insist that the child perform age-appropriate household chores and other responsibilities.

Self-management skills—such as relaxation training, hypnosis, biofeedback, and guided imagery—may help reduce pain and manage physiologic arousal.¹⁶ Deception strategies such as placebo or sham interventions are unethical and impractical.

Related resources

• Campo JV. Functional recurrent abdominal pain in children and adolescents. Digestive Health Matters 2003;12(3):15-7.
• International Foundation for Functional Gastrointestinal Disorders. www.iffgd.org
• University of Pittsburgh. Advanced Center for Interventions and Services Research on Early Onset Mood and Anxiety Disorders. www.moodykids.org

Drug brand names

• Alosetron • Lotronex
• Citalopram • Celexa
• Clonazepam • Klonopin
• Escitalopram • Lexapro
• Famotidine • Pepcid
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Sertraline • Zoloft
• Tegaserod • Zelnorm

Disclosure

Dr. Campo’s work has been supported by the National Institute of Mental Health (grant MH01780) and in part by the Advanced Center for Interventions and Services Research on Early Onset Mood and Anxiety Disorders (grant MH66371). He also receives grants from Forest Pharmaceuticals and is a consultant to Eli Lilly and Co.

Just three words—“My tummy hurts”—can mobilize a child’s parents into a high state of worry, especially on school days. They wonder: Is our child sick? Should he or she stay home? Why is this happening so often?

Although recurrent abdominal pain (RAP) is real, it usually is not caused by tissue damage or serious physical disease. When children with RAP are referred for psychiatric evaluation—often after extensive medical workups—we can help them and their parents manage the problem and function more normally. This article:

• describes physiologic mechanisms that may underlie recurrent GI distress
• discusses the high correlation of psychiatric comorbidities with RAP
• recommends judicious laboratory testing
• reviews evidence on medications and psychotherapies to improve RAP symptoms
• offers advice on building a therapeutic alliance with the patient and family.

Figure Comorbid anxiety and depressive disorders in children with RAP

Children with functional RAP are much more likely to be anxious or depressed than similar pain-free children. A recent blinded study followed 80 children ages 8 to 15 (42 with RAP and 38 controls) identified through screening at primary care pediatric offices. Each was assessed using the Schedule for Affective Disorders and Schizophrenia for School Age Children, Present and Lifetime version (K-SADS-PL). Percentage meeting diagnostic criteria

Source: Reference 5.

RAP: A ‘Functional’ disorder

RAP is a somatoform (or “functional”) disorder, defined as physical symptoms not fully explained by a medical condition, effects of a substance, or another mental disorder. Symptoms cause distress and/or functional impairment and are not intentionally produced.¹

A patient with RAP experiences at least three episodes of abdominal pain over 3 months that interfere with daily activities.² RAP affects 7% to 25% of school-aged children and adolescents,³ most of whom have a functional disorder.⁴

RAP is equally common among prepubertal boys and girls but more common among girls during adolescence.³ RAP can impair school attendance and performance and stigmatize a child as “sickly.”

Common comorbid symptoms

Physical. Besides stomach pain, children with RAP often experience headaches (including migraines), other GI symptoms, general aches and pains, dizziness, and fatigue.

Patients with RAP who do not experience GI bleeding, anemia, fever, weight loss, growth failure, or persistent vomiting most likely do not have a serious underlying disease.

Psychiatric. Children with RAP have much higher rates of anxiety (80%) and depressive (40%) disorders than do their unaffected peers (Figure).⁵ We have also seen higher levels of suicidal thinking in children with RAP in primary care settings compared with pain-free controls (14% vs. 4%, P = 0.04; unpublished data).

In most cases, psychiatric comorbidities appear to precede or coincide with RAP onset. Separation fears, generalized anxiety, and social anxiety in particular are common in patients with RAP yet are seldom recognized in medical settings.

Having childhood RAP increases the risk of anxiety, depression, and hypochondriacal fears in adulthood.⁶ We do not know whether early intervention prevents later disability.

Use of medical services. Abdominal pain accounts for 2% to 4% of all pediatric office visits.⁷ In one study, 8% of middle school and high school students said they had visited a physician for evaluation of stomach pain during the previous year.⁸ Children with RAP make more ambulatory health and mental health visits than peers⁹ and are at risk for unnecessary and potentially dangerous medical tests, procedures, and treatments, including abdominal surgery.¹⁰

Four functional GI disorders

To better characterize youths with functional RAP, symptom-based criteria have been developed and applied for functional GI disorders, defined as chronic or recurrent GI symptoms without explanatory structural or biochemical abnormalities.¹¹ Four such disorders are relevant in children with RAP.

Irritable bowel syndrome (IBS): RAP with at least two of the following symptoms: relief with defecation, change in stool frequency, and change in stool form or appearance (occurs in approximately 50% of RAP cases).

Functional dyspepsia: RAP centered in the upper abdomen that is not associated with changes in bowel habits.

Abdominal migraine: Paroxysmal midline abdominal pain lasting 2 hours to several days with symptom-free intervals of weeks to months and at least two of the following: headache during episodes, photophobia during episodes, unilateral headache, aura, and a family history of migraine.

Functional abdominal pain: Continuous or nearly continuous abdominal pain for 6 months or more.

The reliability, validity, and clinical relevance of these criteria have not been demonstrated. Some children with RAP do not meet any criteria for a specific functional GI disorder.

Gut-brain connections. RAP may be associated with a heightened sensitivity to visceral sensations (visceral hyperalgesia) and a low pressure-pain threshold, leading to speculation that these children are hypersensitive to pain.

High rates of anxiety disorders and temperamental harm avoidance also are seen in patients with RAP, along with a tendency to develop pain when faced with unexpected events. Whether these children are more likely than others to perceive novel internal or external perceptions as threatening is open to debate.

Table 1

Recurrent abdominal pain: 8 steps to assessment and diagnosis

Serotonin communicates nociceptive information between the gut and brain and may mediate visceral hyperalgesia. Gut enterochromaffin cells contain more than 90% of the body’s total serotonin. They act as sensory transducers, releasing serotonin in response to increased intraluminal pressure or inflammation.

The released serotonin can cause abdominal discomfort by stimulating 5-HT 3 receptors on vagal afferents and can influence gut peristaltic activity by stimulating enteric afferents. The same serotonin transporter responsible for CNS serotonin reuptake is expressed throughout the gut.

A constellation of clues

The ideal RAP evaluation includes information from the child, parents, educators, and other health care professionals (Table 1).

Begin by acknowledging the patient’s suffering and the parent’s concerns; do not challenge the pain’s subjective reality. Rather than prejudging its cause, document the pain’s timing, context, and characteristics, and review the patient’s history. A constellation of clues is most suggestive of RAP (Table 2); single clues are not definitive.^12,13

Table 2

Clues that suggest functional pain*

Diagnostic testing. Be judicious in selecting diagnostic tests and procedures. Continuing to order studies in a haphazard effort to rule out disease can generate concerns that “the doctor doesn’t know what’s wrong” and heighten the family’s fear that a disease has been missed.

The process of “ruling out” physical disease may have no apparent end. Unless you are reasonably comfortable that a serious physical disease has not been missed, it is difficult to explain RAP to the patient and family and lay the foundation for intervention.

On the other hand, you must balance the importance of minimizing your own and the family’s anxiety about unrecognized disease against the physical and psychological risks and costs associated with medical tests and procedures.

Social assessment. Assess social and familial reinforcement (secondary gain) of the pain. Parents sometimes inadvertently encourage their children’s sick-role behaviors by providing excessive attention, rewards, or opportunities to avoid uncomfortable situations. RAP can become an excuse for poor performance (self-handicapping), particularly in children with a learning disorder.

How to deliver the diagnosis

Functional abdominal pain is essentially a clinical diagnosis that relies on presentation, course, and findings. As mentioned, a constellation of “clues” is most supportive, as is having typical IBS symptoms.

Before declaring the diagnosis, discuss with the family the patient’s physical, emotional, and behavioral symptoms and the context in which RAP developed. Doing so can help maintain your credibility and establish a consensus.

Once you declare the diagnosis, discuss it clearly and frankly. Families are not likely to be reassured if you do not offer a plausible explanation for the lack of physical findings.

Precautions. When a definitive diagnosis is not possible, acknowledge that uncertainty. Although you must discuss any recognized psychiatric comorbidity, attempting to “explain” that the disorder is causing the pain is usually impractical and intellectually dishonest.

Also, given the pervasive nature of stigma, do not convey embarrassment or unease about diagnosing functional RAP or any comorbid psychiatric disorder.

Follow-up testing. Once you diagnose functional RAP, further testing is generally not necessary. Tests might be indicated if you:

• receive new information
• observe a change in clinical status
• or are convinced that treatment will not work unless the family is reassured by further investigation.

Collaborative treatment

Reassurance and education. Reassurance that the patient does not have a serious physical disease is necessary but rarely sufficient. Explain that the child’s pain does not appear to reflect tissue damage and is not threatening. On the other hand, avoid giving excessive reassurance, particularly when obsessional illness worry and hypochondriacal fears are prominent. Address illness worry as a problem to be solved together.

Discuss with the patient and family what is known and not known about functional RAP, and encourage them to ask questions. This is an opportunity for you to instill hope and cultivate positive expectations, but avoid promising cure. Discuss the gut-brain connection and relevance of visceral hyperalgesia, including serotonin’s potential roles in RAP pathogenesis.

Partners in care. Collaborative treatment increases the likelihood of success. Discuss the importance of a therapeutic partnership, and clarify any areas of disagreement with the diagnosis or treatment plan.

Clearly delineate your roles and responsibilities and those of the patient, family, and other health care team members. Poor communication is pediatricians’ most common complaint about psychiatrists.¹⁴ Good interdisciplinary communication decreases the chance that treatment strategies will be duplicated, diluted, or misinterpreted.

Consolidate medical care with a single clinician—often the primary care physician—based on discussions with the patient, family, and health care team. The coordinating clinician can mediate between the school and family when tensions develop over poor attendance or requests for special treatment. It is often useful for this clinician to spell out:

• what constitutes a legitimate medical excuse for school absence
• who will legitimize excuses.

All parties should understand that the school will view an unexcused absence as truancy and act appropriately.

Diet and lifestyle. Encourage the patient to maintain a regular schedule and a healthy diet. Specific dietary interventions have not been proven effective, despite speculation that lack of dietary fiber or lactose intolerance might cause RAP.^15,16 Also encourage adequate sleep and regular exercise.

Medication and psychotherapy

Because no strong evidence-based guidelines address pediatric RAP intervention, family preferences usually guide initial treatment decisions. This highlights the importance of good communication and a therapeutic partnership among the clinician, family, and patient.

Antispasmodics, acid reducers, and antidepressants are commonly prescribed for RAP, though none are well-supported in the literature and no controlled studies have gauged medication’s impact on psychiatric comorbidity.¹⁶

Antidepressants. Selective serotonin reuptake inhibitors (SSRIs) might help relieve RAP symptoms, but the evidence is inconclusive. SSRIs are considered potentially beneficial in RAP because they may help communicate nociceptive information between the gut and brain and mediate visceral hyperalgesia.

SSRIs at first may increase serotonin at the synapse, which one might assume would to worsen abdominal symptoms. However, ongoing SSRI use could “down-regulate” postsynaptic 5-HT₃ receptors and desensitize postsynaptic cells to the effects of local serotonin.

Our group recently conducted a 12-week open trial of citalopram for functional pediatric RAP.¹⁷ The 25 participants received 10 mg/d the first week, then 20 mg/d thereafter if tolerated. At week 4, nonresponders and partial responders who were tolerating the medication began receiving 40 mg/d.

Table 3

SSRI daily dosing for pediatric RAP

At trial’s end, more than two-thirds of participants were taking 40 mg/d. We rated 21 of 25 patients (84%) as “much improved” or “very much improved,” using the Clinical Global Impression-Improvement scale. Abdominal pain, anxiety, depression, other somatic symptoms, and functional impairment all improved significantly during treatment. Suicidal thoughts diminished progressively from baseline, and no patient reported suicidal thinking at study’s end. Citalopram was generally well tolerated.

With SSRI treatment, start at a low dosage for 3 to 7 days (Table 3). If tolerated, increase to a typical therapeutic dosage. If symptoms fail to respond after 2 or 3 weeks, consider a higher dosage. A short course of an oral benzodiazepine (such as clonazepam, 0.25 mg bid) during the first weeks of SSRI treatment sometimes helps particularly anxious patients or those whose pain appears closely associated with anxiety or “stress.”

Pediatric gastroenterologists often prescribe a low-dose tricyclic antidepressant as first-line therapy, but we discourage this. TCAs lack efficacy in pediatric depression and pose a greater risk of side effects and safety concerns than SSRIs.¹⁸

Other agents have been tried for RAP-associated conditions:

Famotidine, a histamine type 2 receptor blocker, may reduce pain in children with dyspepsia and RAP.¹⁹

Peppermint oil reduced abdominal pain in one study of children with IBS but had little effect on other symptoms.²⁰

Medications such as alosetron and tegaserod that interrupt serotonergic neurotransmission in the gut have shown benefit in adults with IBS but have not been studied in children.

Psychotherapy. A few small studies suggest that cognitive-behavioral therapies (CBT) are helpful in RAP, but CBT may be difficult to deliver in medical settings.^21,22 A simplified “rehabilitative” approach that incorporates CBT principles involves having the clinician and patient view RAP as a challenge to be overcome, rather than a burden to be endured. Such an approach emphasizes the child’s fundamental strength and adaptability rather than vulnerabilities.

The goal of therapy is redirected from finding a cure to coping with and overcoming the problem. This approach challenges the notion that the child cannot resume normal function until the pain is completely gone. It encourages active, problem-focused coping, and discourages passive acceptance—which is associated with greater symptom burden and functional impairment.

Work with parents to reinforce the child’s health-promoting behaviors and minimize negative and social reinforcements (secondary gain) associated with RAP. Advise parents to:

• encourage and reward full school attendance
• avoid home-bound instruction
• expect the child to function despite physical distress
• insist that the child perform age-appropriate household chores and other responsibilities.

Self-management skills—such as relaxation training, hypnosis, biofeedback, and guided imagery—may help reduce pain and manage physiologic arousal.¹⁶ Deception strategies such as placebo or sham interventions are unethical and impractical.

Related resources

• Campo JV. Functional recurrent abdominal pain in children and adolescents. Digestive Health Matters 2003;12(3):15-7.
• International Foundation for Functional Gastrointestinal Disorders. www.iffgd.org
• University of Pittsburgh. Advanced Center for Interventions and Services Research on Early Onset Mood and Anxiety Disorders. www.moodykids.org

Drug brand names

• Alosetron • Lotronex
• Citalopram • Celexa
• Clonazepam • Klonopin
• Escitalopram • Lexapro
• Famotidine • Pepcid
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Sertraline • Zoloft
• Tegaserod • Zelnorm

Disclosure

Dr. Campo’s work has been supported by the National Institute of Mental Health (grant MH01780) and in part by the Advanced Center for Interventions and Services Research on Early Onset Mood and Anxiety Disorders (grant MH66371). He also receives grants from Forest Pharmaceuticals and is a consultant to Eli Lilly and Co.

Just three words—“My tummy hurts”—can mobilize a child’s parents into a high state of worry, especially on school days. They wonder: Is our child sick? Should he or she stay home? Why is this happening so often?

Although recurrent abdominal pain (RAP) is real, it usually is not caused by tissue damage or serious physical disease. When children with RAP are referred for psychiatric evaluation—often after extensive medical workups—we can help them and their parents manage the problem and function more normally. This article:

• describes physiologic mechanisms that may underlie recurrent GI distress
• discusses the high correlation of psychiatric comorbidities with RAP
• recommends judicious laboratory testing
• reviews evidence on medications and psychotherapies to improve RAP symptoms
• offers advice on building a therapeutic alliance with the patient and family.

Figure Comorbid anxiety and depressive disorders in children with RAP

Children with functional RAP are much more likely to be anxious or depressed than similar pain-free children. A recent blinded study followed 80 children ages 8 to 15 (42 with RAP and 38 controls) identified through screening at primary care pediatric offices. Each was assessed using the Schedule for Affective Disorders and Schizophrenia for School Age Children, Present and Lifetime version (K-SADS-PL). Percentage meeting diagnostic criteria

Source: Reference 5.

RAP: A ‘Functional’ disorder

RAP is a somatoform (or “functional”) disorder, defined as physical symptoms not fully explained by a medical condition, effects of a substance, or another mental disorder. Symptoms cause distress and/or functional impairment and are not intentionally produced.¹

A patient with RAP experiences at least three episodes of abdominal pain over 3 months that interfere with daily activities.² RAP affects 7% to 25% of school-aged children and adolescents,³ most of whom have a functional disorder.⁴

RAP is equally common among prepubertal boys and girls but more common among girls during adolescence.³ RAP can impair school attendance and performance and stigmatize a child as “sickly.”

Common comorbid symptoms

Physical. Besides stomach pain, children with RAP often experience headaches (including migraines), other GI symptoms, general aches and pains, dizziness, and fatigue.

Patients with RAP who do not experience GI bleeding, anemia, fever, weight loss, growth failure, or persistent vomiting most likely do not have a serious underlying disease.

Psychiatric. Children with RAP have much higher rates of anxiety (80%) and depressive (40%) disorders than do their unaffected peers (Figure).⁵ We have also seen higher levels of suicidal thinking in children with RAP in primary care settings compared with pain-free controls (14% vs. 4%, P = 0.04; unpublished data).

In most cases, psychiatric comorbidities appear to precede or coincide with RAP onset. Separation fears, generalized anxiety, and social anxiety in particular are common in patients with RAP yet are seldom recognized in medical settings.

Having childhood RAP increases the risk of anxiety, depression, and hypochondriacal fears in adulthood.⁶ We do not know whether early intervention prevents later disability.

Use of medical services. Abdominal pain accounts for 2% to 4% of all pediatric office visits.⁷ In one study, 8% of middle school and high school students said they had visited a physician for evaluation of stomach pain during the previous year.⁸ Children with RAP make more ambulatory health and mental health visits than peers⁹ and are at risk for unnecessary and potentially dangerous medical tests, procedures, and treatments, including abdominal surgery.¹⁰

Four functional GI disorders

To better characterize youths with functional RAP, symptom-based criteria have been developed and applied for functional GI disorders, defined as chronic or recurrent GI symptoms without explanatory structural or biochemical abnormalities.¹¹ Four such disorders are relevant in children with RAP.

Irritable bowel syndrome (IBS): RAP with at least two of the following symptoms: relief with defecation, change in stool frequency, and change in stool form or appearance (occurs in approximately 50% of RAP cases).

Functional dyspepsia: RAP centered in the upper abdomen that is not associated with changes in bowel habits.

Abdominal migraine: Paroxysmal midline abdominal pain lasting 2 hours to several days with symptom-free intervals of weeks to months and at least two of the following: headache during episodes, photophobia during episodes, unilateral headache, aura, and a family history of migraine.

Functional abdominal pain: Continuous or nearly continuous abdominal pain for 6 months or more.

The reliability, validity, and clinical relevance of these criteria have not been demonstrated. Some children with RAP do not meet any criteria for a specific functional GI disorder.

Gut-brain connections. RAP may be associated with a heightened sensitivity to visceral sensations (visceral hyperalgesia) and a low pressure-pain threshold, leading to speculation that these children are hypersensitive to pain.

High rates of anxiety disorders and temperamental harm avoidance also are seen in patients with RAP, along with a tendency to develop pain when faced with unexpected events. Whether these children are more likely than others to perceive novel internal or external perceptions as threatening is open to debate.

Table 1

Recurrent abdominal pain: 8 steps to assessment and diagnosis

Serotonin communicates nociceptive information between the gut and brain and may mediate visceral hyperalgesia. Gut enterochromaffin cells contain more than 90% of the body’s total serotonin. They act as sensory transducers, releasing serotonin in response to increased intraluminal pressure or inflammation.

The released serotonin can cause abdominal discomfort by stimulating 5-HT 3 receptors on vagal afferents and can influence gut peristaltic activity by stimulating enteric afferents. The same serotonin transporter responsible for CNS serotonin reuptake is expressed throughout the gut.

A constellation of clues

The ideal RAP evaluation includes information from the child, parents, educators, and other health care professionals (Table 1).

Begin by acknowledging the patient’s suffering and the parent’s concerns; do not challenge the pain’s subjective reality. Rather than prejudging its cause, document the pain’s timing, context, and characteristics, and review the patient’s history. A constellation of clues is most suggestive of RAP (Table 2); single clues are not definitive.^12,13

Table 2

Clues that suggest functional pain*

Diagnostic testing. Be judicious in selecting diagnostic tests and procedures. Continuing to order studies in a haphazard effort to rule out disease can generate concerns that “the doctor doesn’t know what’s wrong” and heighten the family’s fear that a disease has been missed.

The process of “ruling out” physical disease may have no apparent end. Unless you are reasonably comfortable that a serious physical disease has not been missed, it is difficult to explain RAP to the patient and family and lay the foundation for intervention.

On the other hand, you must balance the importance of minimizing your own and the family’s anxiety about unrecognized disease against the physical and psychological risks and costs associated with medical tests and procedures.

Social assessment. Assess social and familial reinforcement (secondary gain) of the pain. Parents sometimes inadvertently encourage their children’s sick-role behaviors by providing excessive attention, rewards, or opportunities to avoid uncomfortable situations. RAP can become an excuse for poor performance (self-handicapping), particularly in children with a learning disorder.

How to deliver the diagnosis

Functional abdominal pain is essentially a clinical diagnosis that relies on presentation, course, and findings. As mentioned, a constellation of “clues” is most supportive, as is having typical IBS symptoms.

Before declaring the diagnosis, discuss with the family the patient’s physical, emotional, and behavioral symptoms and the context in which RAP developed. Doing so can help maintain your credibility and establish a consensus.

Once you declare the diagnosis, discuss it clearly and frankly. Families are not likely to be reassured if you do not offer a plausible explanation for the lack of physical findings.

Precautions. When a definitive diagnosis is not possible, acknowledge that uncertainty. Although you must discuss any recognized psychiatric comorbidity, attempting to “explain” that the disorder is causing the pain is usually impractical and intellectually dishonest.

Also, given the pervasive nature of stigma, do not convey embarrassment or unease about diagnosing functional RAP or any comorbid psychiatric disorder.

Follow-up testing. Once you diagnose functional RAP, further testing is generally not necessary. Tests might be indicated if you:

• receive new information
• observe a change in clinical status
• or are convinced that treatment will not work unless the family is reassured by further investigation.

Collaborative treatment

Reassurance and education. Reassurance that the patient does not have a serious physical disease is necessary but rarely sufficient. Explain that the child’s pain does not appear to reflect tissue damage and is not threatening. On the other hand, avoid giving excessive reassurance, particularly when obsessional illness worry and hypochondriacal fears are prominent. Address illness worry as a problem to be solved together.

Discuss with the patient and family what is known and not known about functional RAP, and encourage them to ask questions. This is an opportunity for you to instill hope and cultivate positive expectations, but avoid promising cure. Discuss the gut-brain connection and relevance of visceral hyperalgesia, including serotonin’s potential roles in RAP pathogenesis.

Partners in care. Collaborative treatment increases the likelihood of success. Discuss the importance of a therapeutic partnership, and clarify any areas of disagreement with the diagnosis or treatment plan.

Clearly delineate your roles and responsibilities and those of the patient, family, and other health care team members. Poor communication is pediatricians’ most common complaint about psychiatrists.¹⁴ Good interdisciplinary communication decreases the chance that treatment strategies will be duplicated, diluted, or misinterpreted.

Consolidate medical care with a single clinician—often the primary care physician—based on discussions with the patient, family, and health care team. The coordinating clinician can mediate between the school and family when tensions develop over poor attendance or requests for special treatment. It is often useful for this clinician to spell out:

• what constitutes a legitimate medical excuse for school absence
• who will legitimize excuses.

All parties should understand that the school will view an unexcused absence as truancy and act appropriately.

Diet and lifestyle. Encourage the patient to maintain a regular schedule and a healthy diet. Specific dietary interventions have not been proven effective, despite speculation that lack of dietary fiber or lactose intolerance might cause RAP.^15,16 Also encourage adequate sleep and regular exercise.

Medication and psychotherapy

Because no strong evidence-based guidelines address pediatric RAP intervention, family preferences usually guide initial treatment decisions. This highlights the importance of good communication and a therapeutic partnership among the clinician, family, and patient.

Antispasmodics, acid reducers, and antidepressants are commonly prescribed for RAP, though none are well-supported in the literature and no controlled studies have gauged medication’s impact on psychiatric comorbidity.¹⁶

Antidepressants. Selective serotonin reuptake inhibitors (SSRIs) might help relieve RAP symptoms, but the evidence is inconclusive. SSRIs are considered potentially beneficial in RAP because they may help communicate nociceptive information between the gut and brain and mediate visceral hyperalgesia.

SSRIs at first may increase serotonin at the synapse, which one might assume would to worsen abdominal symptoms. However, ongoing SSRI use could “down-regulate” postsynaptic 5-HT₃ receptors and desensitize postsynaptic cells to the effects of local serotonin.

Our group recently conducted a 12-week open trial of citalopram for functional pediatric RAP.¹⁷ The 25 participants received 10 mg/d the first week, then 20 mg/d thereafter if tolerated. At week 4, nonresponders and partial responders who were tolerating the medication began receiving 40 mg/d.

Table 3

SSRI daily dosing for pediatric RAP

At trial’s end, more than two-thirds of participants were taking 40 mg/d. We rated 21 of 25 patients (84%) as “much improved” or “very much improved,” using the Clinical Global Impression-Improvement scale. Abdominal pain, anxiety, depression, other somatic symptoms, and functional impairment all improved significantly during treatment. Suicidal thoughts diminished progressively from baseline, and no patient reported suicidal thinking at study’s end. Citalopram was generally well tolerated.

With SSRI treatment, start at a low dosage for 3 to 7 days (Table 3). If tolerated, increase to a typical therapeutic dosage. If symptoms fail to respond after 2 or 3 weeks, consider a higher dosage. A short course of an oral benzodiazepine (such as clonazepam, 0.25 mg bid) during the first weeks of SSRI treatment sometimes helps particularly anxious patients or those whose pain appears closely associated with anxiety or “stress.”

Pediatric gastroenterologists often prescribe a low-dose tricyclic antidepressant as first-line therapy, but we discourage this. TCAs lack efficacy in pediatric depression and pose a greater risk of side effects and safety concerns than SSRIs.¹⁸

Other agents have been tried for RAP-associated conditions:

Famotidine, a histamine type 2 receptor blocker, may reduce pain in children with dyspepsia and RAP.¹⁹

Peppermint oil reduced abdominal pain in one study of children with IBS but had little effect on other symptoms.²⁰

Medications such as alosetron and tegaserod that interrupt serotonergic neurotransmission in the gut have shown benefit in adults with IBS but have not been studied in children.

Psychotherapy. A few small studies suggest that cognitive-behavioral therapies (CBT) are helpful in RAP, but CBT may be difficult to deliver in medical settings.^21,22 A simplified “rehabilitative” approach that incorporates CBT principles involves having the clinician and patient view RAP as a challenge to be overcome, rather than a burden to be endured. Such an approach emphasizes the child’s fundamental strength and adaptability rather than vulnerabilities.

The goal of therapy is redirected from finding a cure to coping with and overcoming the problem. This approach challenges the notion that the child cannot resume normal function until the pain is completely gone. It encourages active, problem-focused coping, and discourages passive acceptance—which is associated with greater symptom burden and functional impairment.

Work with parents to reinforce the child’s health-promoting behaviors and minimize negative and social reinforcements (secondary gain) associated with RAP. Advise parents to:

• encourage and reward full school attendance
• avoid home-bound instruction
• expect the child to function despite physical distress
• insist that the child perform age-appropriate household chores and other responsibilities.

Self-management skills—such as relaxation training, hypnosis, biofeedback, and guided imagery—may help reduce pain and manage physiologic arousal.¹⁶ Deception strategies such as placebo or sham interventions are unethical and impractical.

Related resources

• Campo JV. Functional recurrent abdominal pain in children and adolescents. Digestive Health Matters 2003;12(3):15-7.
• International Foundation for Functional Gastrointestinal Disorders. www.iffgd.org
• University of Pittsburgh. Advanced Center for Interventions and Services Research on Early Onset Mood and Anxiety Disorders. www.moodykids.org

Drug brand names

• Alosetron • Lotronex
• Citalopram • Celexa
• Clonazepam • Klonopin
• Escitalopram • Lexapro
• Famotidine • Pepcid
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Sertraline • Zoloft
• Tegaserod • Zelnorm

Disclosure

Dr. Campo’s work has been supported by the National Institute of Mental Health (grant MH01780) and in part by the Advanced Center for Interventions and Services Research on Early Onset Mood and Anxiety Disorders (grant MH66371). He also receives grants from Forest Pharmaceuticals and is a consultant to Eli Lilly and Co.

Dr. Timothy Fong’s article on self-mutilation (Current Psychiatry, February 2003) was practical and on target.

As a professional counselor who frequently deals with such behaviors, these data were appreciated. The article also reinforced observations I have seen in the therapeutic setting.

Randy Tungate, M.MFT
Covenant Counseling Center
Lubbock, TX

Dr. Timothy Fong’s article on self-mutilation (Current Psychiatry, February 2003) was practical and on target.

As a professional counselor who frequently deals with such behaviors, these data were appreciated. The article also reinforced observations I have seen in the therapeutic setting.

Randy Tungate, M.MFT
Covenant Counseling Center
Lubbock, TX

Dr. Timothy Fong’s article on self-mutilation (Current Psychiatry, February 2003) was practical and on target.

As a professional counselor who frequently deals with such behaviors, these data were appreciated. The article also reinforced observations I have seen in the therapeutic setting.

Randy Tungate, M.MFT
Covenant Counseling Center
Lubbock, TX

I read with interest Dr. Stanley Caroff’s excellent article on neuroleptic malignant syndrome (Current Psychiatry, December 2003).

As an instructor of psychiatry residents and clinical staff, I have utilized an acronym that helps raise the index of suspicion for NMS. Coming from the northland, it isn’t difficult for me to correlate shaking and stiffness with “FARGO:”

Fever

Autonomic dysregulation

Rigidity

Granulocytosis

Orientation changes

Andrew McLean, MD
Clinical professor of neuroscience
University of North Dakota School of Medicine
and Health Sciences
Fargo, ND

I read with interest Dr. Stanley Caroff’s excellent article on neuroleptic malignant syndrome (Current Psychiatry, December 2003).

As an instructor of psychiatry residents and clinical staff, I have utilized an acronym that helps raise the index of suspicion for NMS. Coming from the northland, it isn’t difficult for me to correlate shaking and stiffness with “FARGO:”

Fever

Autonomic dysregulation

Rigidity

Granulocytosis

Orientation changes

Andrew McLean, MD
Clinical professor of neuroscience
University of North Dakota School of Medicine
and Health Sciences
Fargo, ND

I read with interest Dr. Stanley Caroff’s excellent article on neuroleptic malignant syndrome (Current Psychiatry, December 2003).

As an instructor of psychiatry residents and clinical staff, I have utilized an acronym that helps raise the index of suspicion for NMS. Coming from the northland, it isn’t difficult for me to correlate shaking and stiffness with “FARGO:”

Fever

Autonomic dysregulation

Rigidity

Granulocytosis

Orientation changes

Andrew McLean, MD
Clinical professor of neuroscience
University of North Dakota School of Medicine
and Health Sciences
Fargo, ND

Dr. Martinez’ and Dr. Marangell’s review on use of omega-3 fatty acids (Current Psychiatry, January 2004) was excellent.

Please clarify how these agents have been dosed. More specifically, when a study specifies a milligram dose amount of eicosapentaenoic acid (EPA) and/or docosahexaenoic acid (DHA), does that include only the “active” ingredient or the total milligrams of the capsule? In a commercial preparation, for example, a 2-gram fish oil capsule might contain 360 mg of EPA.

Robert L. Murdock, MD
Roanoke, VA

Dr. Martinez responds

The studies that Dr. Lauren Marangell and I reviewed reported the total daily amount of either EPA or DHA (or both, if combination treatment was being studied) that a study participant would receive.

For example, in studies investigating 2 grams/d of EPA versus placebo, the treatment group received 2 grams/d total of EPA, with no DHA in the study compound. If the study drug contained 200 mg of EPA per capsule, patents would take 10 capsules per day.

Also, only studies looking at combination EPA/DHA treatment used study medications that contained both fatty acids. Again, these studies specified the total daily dosages of both the EPA and DHA portions.

James M. Martinez MD
Department of psychiatry
Baylor College of Medicine, Houston, TX

Dr. Martinez’ and Dr. Marangell’s review on use of omega-3 fatty acids (Current Psychiatry, January 2004) was excellent.

Please clarify how these agents have been dosed. More specifically, when a study specifies a milligram dose amount of eicosapentaenoic acid (EPA) and/or docosahexaenoic acid (DHA), does that include only the “active” ingredient or the total milligrams of the capsule? In a commercial preparation, for example, a 2-gram fish oil capsule might contain 360 mg of EPA.

Robert L. Murdock, MD
Roanoke, VA

Dr. Martinez responds

The studies that Dr. Lauren Marangell and I reviewed reported the total daily amount of either EPA or DHA (or both, if combination treatment was being studied) that a study participant would receive.

For example, in studies investigating 2 grams/d of EPA versus placebo, the treatment group received 2 grams/d total of EPA, with no DHA in the study compound. If the study drug contained 200 mg of EPA per capsule, patents would take 10 capsules per day.

Also, only studies looking at combination EPA/DHA treatment used study medications that contained both fatty acids. Again, these studies specified the total daily dosages of both the EPA and DHA portions.

James M. Martinez MD
Department of psychiatry
Baylor College of Medicine, Houston, TX

Dr. Martinez’ and Dr. Marangell’s review on use of omega-3 fatty acids (Current Psychiatry, January 2004) was excellent.

Please clarify how these agents have been dosed. More specifically, when a study specifies a milligram dose amount of eicosapentaenoic acid (EPA) and/or docosahexaenoic acid (DHA), does that include only the “active” ingredient or the total milligrams of the capsule? In a commercial preparation, for example, a 2-gram fish oil capsule might contain 360 mg of EPA.

Robert L. Murdock, MD
Roanoke, VA

Dr. Martinez responds

The studies that Dr. Lauren Marangell and I reviewed reported the total daily amount of either EPA or DHA (or both, if combination treatment was being studied) that a study participant would receive.

For example, in studies investigating 2 grams/d of EPA versus placebo, the treatment group received 2 grams/d total of EPA, with no DHA in the study compound. If the study drug contained 200 mg of EPA per capsule, patents would take 10 capsules per day.

Also, only studies looking at combination EPA/DHA treatment used study medications that contained both fatty acids. Again, these studies specified the total daily dosages of both the EPA and DHA portions.

James M. Martinez MD
Department of psychiatry
Baylor College of Medicine, Houston, TX

The Texas Medication Algorithms (Current Psychiatry, February 2004) have been most useful to our practice.

When the algorithms arrived in 2000, our peer reviewer (not a physician) tried to classify them under “treatment rules.” We had some difficulty getting everyone to understand that these are “guidelines,” which encourage individual patient decisions, rather than “rules,” which mandate treatment based on “cookbook recipes.”

With this understanding, though, the algorithms have been beneficial and we look forward to the revisions.

Y.Scott Moore, MD
Lincoln, NE

The Texas Medication Algorithms (Current Psychiatry, February 2004) have been most useful to our practice.

When the algorithms arrived in 2000, our peer reviewer (not a physician) tried to classify them under “treatment rules.” We had some difficulty getting everyone to understand that these are “guidelines,” which encourage individual patient decisions, rather than “rules,” which mandate treatment based on “cookbook recipes.”

With this understanding, though, the algorithms have been beneficial and we look forward to the revisions.

Y.Scott Moore, MD
Lincoln, NE

The Texas Medication Algorithms (Current Psychiatry, February 2004) have been most useful to our practice.

When the algorithms arrived in 2000, our peer reviewer (not a physician) tried to classify them under “treatment rules.” We had some difficulty getting everyone to understand that these are “guidelines,” which encourage individual patient decisions, rather than “rules,” which mandate treatment based on “cookbook recipes.”

With this understanding, though, the algorithms have been beneficial and we look forward to the revisions.

Y.Scott Moore, MD
Lincoln, NE

Want to take an online audio CME course or view educational film clips while traveling? Don’t forget your handheld.

Once limited to text-based information, today’s more powerful personal digital assistants (PDAs) can also play audio and video files. Innovations in capture and conversion technology allow you to store media-rich online files on your PDA, letting you access multimedia Internet content while you are offline.

File portability

PEG-audio layer 3 (MP3) is a compression algorithm used to decrease an audio file’s size, allowing numerous audio files to be stored onto an MP3 player.

Other formats-including WAV, Real Audio, and Ogg-Vorbis-can be used to compress files, but MP3 is the most popular and has become the standard.

Video files usually contain massive amounts of data-including synchronized audio-and are quite large. Files created via advanced systems format (ASF) typically are uncompressed general video files. Windows Media and Real Media are other common online video formats.

Several compression algorithms exist for online video, including MPEG-1, MPEG-2, and MPEG-4. Each compression type is geared towards a specific media delivery mechanism.

Playing online audio on PDAs

Pocket PC devices come with Windows Media Player, which enables users to play MP3s. Alternate programs-such as RealOne Player, Pocket Mind, Pocket Player, and withMP3 (Table 1)-offer features such as an equalizer and can handle streaming audio and play audio books.

To store an MP3 file onto your PDA, simply download the file and store it in the “My Pocket PC” folder on your computer desktop. Storing the file this way, however, consumes much of the PDA’s main memory. To preserve PDA memory:

• Store the file in the PDA’s compact flash or secure digital card by enter your Pocket PC via the “Activesync” window, then store the file in the device’s secure digital card
• Or use a separate USB memory card reader to transfer the file to the memory card, then place the card into the Pocket PC. This is the fastest option.

Palm OS devices can play MP3 files with RealOne Player, Aero Player, and Pocket Tunes. Audio files are easily installed using Palm Quick Install.

Drag a copy of the file into the expansion card, and it will be transferred at the next HotSync (synchronization of information from PDA to desktop). However, this process takes about 10 minutes depending on the file’s size because the file must go through the Palm memory. To save time, place the file on a separate USB memory card reader, then transfer the file directly.

Playing video files

Older PDAs could not display video data quickly enough, making images appear jerky and blotchy. Today’s Palm OS and Pocket PC PDAs have faster processors, more memory, and can display video at decent quality.

Pocket PC devices can play Windows Media Video and ASF video files with the Pocket PC version of Windows Media Player. Other third-party video players include Project Mayo, Pocket MVP, Pocket TV, and RealOne Player.

Because these video players are not compatible with older Palm OS devices, vendors have created converters that can convert video files for use with the vendors’ proprietary video formats (Table 2). All video files must be converted via the desktop and then installed onto the PDA or memory card.

By contrast, newer Palm OS devices (such as OS 5) have enough processing power to display MPEG-4 files using software such as MMPlayer.

Portability issues

Video. Online grand rounds or other lectures are designed for viewing online. “Streaming” allows a Web site to distribute the video to many users at once. 1 Web casts typically are created in Real Media or Windows Media format, but the streaming is not stored on the computer hard drive for later use. More importantly, the link from the Web site does not contain the media when accessed, but actually is a command to the streaming server.

To capture the video stream, try WM Recorder or HiDownload.

Audio files cannot be heard on PDAs without headphones, making them difficult to listen to while driving. FM radio broadcast devices such as the iRock 400 or Belkin Tunecast solve this problem by transmitting a low-strength signal that can be picked up on a car radio.

Other devices

Aside from PDAs, other portable devices are made for viewing audio and video, and others are being invented.

Many MP3 players are smaller and more portable than PDAs. Video “jukeboxes” such as the Archos AV320 and TightSystems TAZ are also available.

Tiquit, OQO, and FlipStart plan later this year to release fully capable computers. They contain hard drives, central processing units and other necessities of full-sized computers, but are only the size of a PDA. These innovations could make the aforementioned devices and programs obsolete by year’s end. (For information on these developing technologies, watch for future installments of Psyber Psychiatry.)

Table 1

Audio player programs for PDA

Table 2

Video conversion programs for Palm OS devices

If you have any questions about these products or comments about Psyber Psychiatry, click here to contact Dr. Luo or send an e-mail to [email protected].

Related Resources

• NPI Webcasting. UCLA grand rounds, Department of Psychiatry and Behavioral Sciences. http://www.mentalhealth.ucla.edu/opce/gr.html
• Prelinger Archives. Movie archives of patients with schizophrenia. http://www.archive.org/movies/movieslisting-browse.php?collection=prelinger (Click on “schizophrenia” in subject index)
• Luo J. Psyber Psychiatry: A world of information in your pocket. Current Psychiatry April online edition. http://www.currentpsychiatry.com/psyber_psy.asp.

Disclosure

Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions expressed by Dr. Luo in this column are his own and do not necessarily reflect those of Current Psychiatry.

Want to take an online audio CME course or view educational film clips while traveling? Don’t forget your handheld.

Once limited to text-based information, today’s more powerful personal digital assistants (PDAs) can also play audio and video files. Innovations in capture and conversion technology allow you to store media-rich online files on your PDA, letting you access multimedia Internet content while you are offline.

File portability

PEG-audio layer 3 (MP3) is a compression algorithm used to decrease an audio file’s size, allowing numerous audio files to be stored onto an MP3 player.

Other formats-including WAV, Real Audio, and Ogg-Vorbis-can be used to compress files, but MP3 is the most popular and has become the standard.

Video files usually contain massive amounts of data-including synchronized audio-and are quite large. Files created via advanced systems format (ASF) typically are uncompressed general video files. Windows Media and Real Media are other common online video formats.

Several compression algorithms exist for online video, including MPEG-1, MPEG-2, and MPEG-4. Each compression type is geared towards a specific media delivery mechanism.

Playing online audio on PDAs

Pocket PC devices come with Windows Media Player, which enables users to play MP3s. Alternate programs-such as RealOne Player, Pocket Mind, Pocket Player, and withMP3 (Table 1)-offer features such as an equalizer and can handle streaming audio and play audio books.

To store an MP3 file onto your PDA, simply download the file and store it in the “My Pocket PC” folder on your computer desktop. Storing the file this way, however, consumes much of the PDA’s main memory. To preserve PDA memory:

• Store the file in the PDA’s compact flash or secure digital card by enter your Pocket PC via the “Activesync” window, then store the file in the device’s secure digital card
• Or use a separate USB memory card reader to transfer the file to the memory card, then place the card into the Pocket PC. This is the fastest option.

Palm OS devices can play MP3 files with RealOne Player, Aero Player, and Pocket Tunes. Audio files are easily installed using Palm Quick Install.

Drag a copy of the file into the expansion card, and it will be transferred at the next HotSync (synchronization of information from PDA to desktop). However, this process takes about 10 minutes depending on the file’s size because the file must go through the Palm memory. To save time, place the file on a separate USB memory card reader, then transfer the file directly.

Playing video files

Older PDAs could not display video data quickly enough, making images appear jerky and blotchy. Today’s Palm OS and Pocket PC PDAs have faster processors, more memory, and can display video at decent quality.

Pocket PC devices can play Windows Media Video and ASF video files with the Pocket PC version of Windows Media Player. Other third-party video players include Project Mayo, Pocket MVP, Pocket TV, and RealOne Player.

Because these video players are not compatible with older Palm OS devices, vendors have created converters that can convert video files for use with the vendors’ proprietary video formats (Table 2). All video files must be converted via the desktop and then installed onto the PDA or memory card.

By contrast, newer Palm OS devices (such as OS 5) have enough processing power to display MPEG-4 files using software such as MMPlayer.

Portability issues

Video. Online grand rounds or other lectures are designed for viewing online. “Streaming” allows a Web site to distribute the video to many users at once. 1 Web casts typically are created in Real Media or Windows Media format, but the streaming is not stored on the computer hard drive for later use. More importantly, the link from the Web site does not contain the media when accessed, but actually is a command to the streaming server.

To capture the video stream, try WM Recorder or HiDownload.

Audio files cannot be heard on PDAs without headphones, making them difficult to listen to while driving. FM radio broadcast devices such as the iRock 400 or Belkin Tunecast solve this problem by transmitting a low-strength signal that can be picked up on a car radio.

Other devices

Aside from PDAs, other portable devices are made for viewing audio and video, and others are being invented.

Many MP3 players are smaller and more portable than PDAs. Video “jukeboxes” such as the Archos AV320 and TightSystems TAZ are also available.

Tiquit, OQO, and FlipStart plan later this year to release fully capable computers. They contain hard drives, central processing units and other necessities of full-sized computers, but are only the size of a PDA. These innovations could make the aforementioned devices and programs obsolete by year’s end. (For information on these developing technologies, watch for future installments of Psyber Psychiatry.)

Table 1

Audio player programs for PDA

Table 2

Video conversion programs for Palm OS devices

If you have any questions about these products or comments about Psyber Psychiatry, click here to contact Dr. Luo or send an e-mail to [email protected].

Related Resources

• NPI Webcasting. UCLA grand rounds, Department of Psychiatry and Behavioral Sciences. http://www.mentalhealth.ucla.edu/opce/gr.html
• Prelinger Archives. Movie archives of patients with schizophrenia. http://www.archive.org/movies/movieslisting-browse.php?collection=prelinger (Click on “schizophrenia” in subject index)
• Luo J. Psyber Psychiatry: A world of information in your pocket. Current Psychiatry April online edition. http://www.currentpsychiatry.com/psyber_psy.asp.

Disclosure

Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions expressed by Dr. Luo in this column are his own and do not necessarily reflect those of Current Psychiatry.

Want to take an online audio CME course or view educational film clips while traveling? Don’t forget your handheld.

Once limited to text-based information, today’s more powerful personal digital assistants (PDAs) can also play audio and video files. Innovations in capture and conversion technology allow you to store media-rich online files on your PDA, letting you access multimedia Internet content while you are offline.

File portability

PEG-audio layer 3 (MP3) is a compression algorithm used to decrease an audio file’s size, allowing numerous audio files to be stored onto an MP3 player.

Other formats-including WAV, Real Audio, and Ogg-Vorbis-can be used to compress files, but MP3 is the most popular and has become the standard.

Video files usually contain massive amounts of data-including synchronized audio-and are quite large. Files created via advanced systems format (ASF) typically are uncompressed general video files. Windows Media and Real Media are other common online video formats.

Several compression algorithms exist for online video, including MPEG-1, MPEG-2, and MPEG-4. Each compression type is geared towards a specific media delivery mechanism.

Playing online audio on PDAs

Pocket PC devices come with Windows Media Player, which enables users to play MP3s. Alternate programs-such as RealOne Player, Pocket Mind, Pocket Player, and withMP3 (Table 1)-offer features such as an equalizer and can handle streaming audio and play audio books.

To store an MP3 file onto your PDA, simply download the file and store it in the “My Pocket PC” folder on your computer desktop. Storing the file this way, however, consumes much of the PDA’s main memory. To preserve PDA memory:

• Store the file in the PDA’s compact flash or secure digital card by enter your Pocket PC via the “Activesync” window, then store the file in the device’s secure digital card
• Or use a separate USB memory card reader to transfer the file to the memory card, then place the card into the Pocket PC. This is the fastest option.

Palm OS devices can play MP3 files with RealOne Player, Aero Player, and Pocket Tunes. Audio files are easily installed using Palm Quick Install.

Drag a copy of the file into the expansion card, and it will be transferred at the next HotSync (synchronization of information from PDA to desktop). However, this process takes about 10 minutes depending on the file’s size because the file must go through the Palm memory. To save time, place the file on a separate USB memory card reader, then transfer the file directly.

Playing video files

Older PDAs could not display video data quickly enough, making images appear jerky and blotchy. Today’s Palm OS and Pocket PC PDAs have faster processors, more memory, and can display video at decent quality.

Pocket PC devices can play Windows Media Video and ASF video files with the Pocket PC version of Windows Media Player. Other third-party video players include Project Mayo, Pocket MVP, Pocket TV, and RealOne Player.

Because these video players are not compatible with older Palm OS devices, vendors have created converters that can convert video files for use with the vendors’ proprietary video formats (Table 2). All video files must be converted via the desktop and then installed onto the PDA or memory card.

By contrast, newer Palm OS devices (such as OS 5) have enough processing power to display MPEG-4 files using software such as MMPlayer.

Portability issues

Video. Online grand rounds or other lectures are designed for viewing online. “Streaming” allows a Web site to distribute the video to many users at once. 1 Web casts typically are created in Real Media or Windows Media format, but the streaming is not stored on the computer hard drive for later use. More importantly, the link from the Web site does not contain the media when accessed, but actually is a command to the streaming server.

To capture the video stream, try WM Recorder or HiDownload.

Audio files cannot be heard on PDAs without headphones, making them difficult to listen to while driving. FM radio broadcast devices such as the iRock 400 or Belkin Tunecast solve this problem by transmitting a low-strength signal that can be picked up on a car radio.

Other devices

Aside from PDAs, other portable devices are made for viewing audio and video, and others are being invented.

Many MP3 players are smaller and more portable than PDAs. Video “jukeboxes” such as the Archos AV320 and TightSystems TAZ are also available.

Tiquit, OQO, and FlipStart plan later this year to release fully capable computers. They contain hard drives, central processing units and other necessities of full-sized computers, but are only the size of a PDA. These innovations could make the aforementioned devices and programs obsolete by year’s end. (For information on these developing technologies, watch for future installments of Psyber Psychiatry.)

Table 1

Audio player programs for PDA

Table 2

Video conversion programs for Palm OS devices

If you have any questions about these products or comments about Psyber Psychiatry, click here to contact Dr. Luo or send an e-mail to [email protected].

Related Resources

• NPI Webcasting. UCLA grand rounds, Department of Psychiatry and Behavioral Sciences. http://www.mentalhealth.ucla.edu/opce/gr.html
• Prelinger Archives. Movie archives of patients with schizophrenia. http://www.archive.org/movies/movieslisting-browse.php?collection=prelinger (Click on “schizophrenia” in subject index)
• Luo J. Psyber Psychiatry: A world of information in your pocket. Current Psychiatry April online edition. http://www.currentpsychiatry.com/psyber_psy.asp.

Disclosure

Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions expressed by Dr. Luo in this column are his own and do not necessarily reflect those of Current Psychiatry.