Somatic Disorders

BALTIMORE – Depression frequently co-occurs with eating disorders, making treatment challenging, Dr. Graham W. Redgrave said at a symposium on mood disorders sponsored by Johns Hopkins University.

“There are high rates of concurrent major depressive disorder in anorexia,” said Dr. Redgrave of the Johns Hopkins University in Baltimore. Among patients with the restricting type of anorexia, 15%–50% also have major depressive disorder (MDD). The rates among patients with the binge-eating/purging type of anorexia are even higher at 46%–80%. The rates are higher still when these patients are asked whether they have ever had depression.

Numbers like these suggest that anorexia might simply be a behavioral manifestation of an underlying mood disorder. However, controlled family studies have provided good evidence that these disorders are different and independent, Dr. Redgrave said.

One reason so much overlap exists between anorexia and MDD is that starvation produces a host of psychiatric conditions in the body, such as mood lability, irritability, anxiety, apathy, obsessiveness, poor concentration, social withdrawal, and decreased libido.

Patients with anorexia aren't the only ones suffering from comorbid depression. Among patients with bulimia, 30%–60% have concurrent MDD and 50%–65% have had a lifetime occurrence of depression.

In patients with bulimia, starvation can magnify feelings of guilt, shame, and hopelessness, Dr. Redgrave said. Increased frequency in the binge and purge cycles decreases the ability to concentrate, because the fear of being overweight increases in importance.

Depression also is high among patients with binge-eating disorder, with 36%–60% of these patients also having MDD. In addition, 48% of obese women who binge also have MDD, compared with only 26% of obese women who do not binge. “It's not just the obesity. There's something about the psychopathology of depression and the binge eating that seems to be related,” Dr. Redgrave said.

Treatment of patients with eating disorders and depression can be a challenge because “when you are treating an eating disorder, you are asking your patient to give up something that is very rewarding,” he said. Patients can recognize that what they're doing is problematic but have a hard time giving it up.

“Imagine if you have a parallel mood disorder that is making your thoughts about yourself more hopeless and self-deprecating. … How much harder would it be to give up behavior that is rewarding?”, Dr. Redgrave said at the symposium, also sponsored by the Depression and Related Affective Disorders Association.

Treatment for an eating disorder focuses first on behaviors and then on thoughts and feelings. Underlying connections and associations are addressed only when the patient is stabilized. When the patient's health is in jeopardy, “you can't be worried about why this happened, you just have to fix it, and then worry about the why,” he said.

Pharmacotherapy is primarily an adjunctive treatment for patients with anorexia. Antidepressants are of modest but important benefit in bulimia nervosa, Dr. Redgrave said. Fluoxetine at high doses is especially useful, though most antidepressants can be useful in this population. Bupropion is contraindicated because of the risk of seizures.

BALTIMORE – Depression frequently co-occurs with eating disorders, making treatment challenging, Dr. Graham W. Redgrave said at a symposium on mood disorders sponsored by Johns Hopkins University.

“There are high rates of concurrent major depressive disorder in anorexia,” said Dr. Redgrave of the Johns Hopkins University in Baltimore. Among patients with the restricting type of anorexia, 15%–50% also have major depressive disorder (MDD). The rates among patients with the binge-eating/purging type of anorexia are even higher at 46%–80%. The rates are higher still when these patients are asked whether they have ever had depression.

Numbers like these suggest that anorexia might simply be a behavioral manifestation of an underlying mood disorder. However, controlled family studies have provided good evidence that these disorders are different and independent, Dr. Redgrave said.

One reason so much overlap exists between anorexia and MDD is that starvation produces a host of psychiatric conditions in the body, such as mood lability, irritability, anxiety, apathy, obsessiveness, poor concentration, social withdrawal, and decreased libido.

Patients with anorexia aren't the only ones suffering from comorbid depression. Among patients with bulimia, 30%–60% have concurrent MDD and 50%–65% have had a lifetime occurrence of depression.

In patients with bulimia, starvation can magnify feelings of guilt, shame, and hopelessness, Dr. Redgrave said. Increased frequency in the binge and purge cycles decreases the ability to concentrate, because the fear of being overweight increases in importance.

Depression also is high among patients with binge-eating disorder, with 36%–60% of these patients also having MDD. In addition, 48% of obese women who binge also have MDD, compared with only 26% of obese women who do not binge. “It's not just the obesity. There's something about the psychopathology of depression and the binge eating that seems to be related,” Dr. Redgrave said.

Treatment of patients with eating disorders and depression can be a challenge because “when you are treating an eating disorder, you are asking your patient to give up something that is very rewarding,” he said. Patients can recognize that what they're doing is problematic but have a hard time giving it up.

“Imagine if you have a parallel mood disorder that is making your thoughts about yourself more hopeless and self-deprecating. … How much harder would it be to give up behavior that is rewarding?”, Dr. Redgrave said at the symposium, also sponsored by the Depression and Related Affective Disorders Association.

Treatment for an eating disorder focuses first on behaviors and then on thoughts and feelings. Underlying connections and associations are addressed only when the patient is stabilized. When the patient's health is in jeopardy, “you can't be worried about why this happened, you just have to fix it, and then worry about the why,” he said.

Pharmacotherapy is primarily an adjunctive treatment for patients with anorexia. Antidepressants are of modest but important benefit in bulimia nervosa, Dr. Redgrave said. Fluoxetine at high doses is especially useful, though most antidepressants can be useful in this population. Bupropion is contraindicated because of the risk of seizures.

BALTIMORE – Depression frequently co-occurs with eating disorders, making treatment challenging, Dr. Graham W. Redgrave said at a symposium on mood disorders sponsored by Johns Hopkins University.

“There are high rates of concurrent major depressive disorder in anorexia,” said Dr. Redgrave of the Johns Hopkins University in Baltimore. Among patients with the restricting type of anorexia, 15%–50% also have major depressive disorder (MDD). The rates among patients with the binge-eating/purging type of anorexia are even higher at 46%–80%. The rates are higher still when these patients are asked whether they have ever had depression.

Numbers like these suggest that anorexia might simply be a behavioral manifestation of an underlying mood disorder. However, controlled family studies have provided good evidence that these disorders are different and independent, Dr. Redgrave said.

One reason so much overlap exists between anorexia and MDD is that starvation produces a host of psychiatric conditions in the body, such as mood lability, irritability, anxiety, apathy, obsessiveness, poor concentration, social withdrawal, and decreased libido.

Patients with anorexia aren't the only ones suffering from comorbid depression. Among patients with bulimia, 30%–60% have concurrent MDD and 50%–65% have had a lifetime occurrence of depression.

In patients with bulimia, starvation can magnify feelings of guilt, shame, and hopelessness, Dr. Redgrave said. Increased frequency in the binge and purge cycles decreases the ability to concentrate, because the fear of being overweight increases in importance.

Depression also is high among patients with binge-eating disorder, with 36%–60% of these patients also having MDD. In addition, 48% of obese women who binge also have MDD, compared with only 26% of obese women who do not binge. “It's not just the obesity. There's something about the psychopathology of depression and the binge eating that seems to be related,” Dr. Redgrave said.

Treatment of patients with eating disorders and depression can be a challenge because “when you are treating an eating disorder, you are asking your patient to give up something that is very rewarding,” he said. Patients can recognize that what they're doing is problematic but have a hard time giving it up.

“Imagine if you have a parallel mood disorder that is making your thoughts about yourself more hopeless and self-deprecating. … How much harder would it be to give up behavior that is rewarding?”, Dr. Redgrave said at the symposium, also sponsored by the Depression and Related Affective Disorders Association.

Treatment for an eating disorder focuses first on behaviors and then on thoughts and feelings. Underlying connections and associations are addressed only when the patient is stabilized. When the patient's health is in jeopardy, “you can't be worried about why this happened, you just have to fix it, and then worry about the why,” he said.

Pharmacotherapy is primarily an adjunctive treatment for patients with anorexia. Antidepressants are of modest but important benefit in bulimia nervosa, Dr. Redgrave said. Fluoxetine at high doses is especially useful, though most antidepressants can be useful in this population. Bupropion is contraindicated because of the risk of seizures.

HONOLULU – Biofeedback proved superior to standard therapy for long-term management of patients with the most common cause of chronic constipation in the first-ever randomized trial featuring a full year of follow-up.

Previous short-term randomized trials have demonstrated that biofeedback is effective in patients with dyssynergic defecation. But this form of constipation is a long-term problem–and although uncontrolled studies have suggested good long-term maintenance of efficacy with biofeedback, it was important to establish in a more rigorous randomized trial setting whether this nonpharmacologic therapy maintains its effectiveness over time.

The answer–at least through 1 year of formal follow-up–is clearly yes, Dr. Satish S.C. Rao said at the annual meeting of the American College of Gastroenterology.

The clinical relevance of this finding lies in the fact that recent surveys indicate that up to 50% of patients with chronic constipation are dissatisfied with their current treatment. This is largely because conventional therapies focus primarily on reducing stool hardness rather than addressing the underlying physiologic dysfunction. In the setting of dyssynergic defecation, which accounts for roughly half of all cases of chronic constipation, the pathophysiology involves a lack of coordination between the pelvic floor muscles and anal sphincter, explained Dr. Rao, a gastroenterologist at the University of Iowa, Iowa City.

He reported on 52 patients, 47 of whom were women, who were randomized to a 3-month biofeedback program or standard therapy. All met strict manometric diagnostic criteria for dyssynergic defecation. Patients with the other two common types of chronic constipation–irritable bowel syndrome and slow-transit constipation–were excluded.

The biofeedback program entailed biweekly hour-long treatment sessions in which participants learned techniques aimed at increasing their pushing effort through improved anorectal coordination and sensory conditioning. They also practiced expelling a simulated stool made of silicone.

The standard-therapy control arm involved three monthly visits with a gastroenterologist, dietician, and nurse for instruction in dietary modification, exercise, toilet habits, and appropriate use of laxatives. “That's a lot more than the usual standard therapy in clinical practice,” Dr. Rao noted.

Of the 52 patients, 44 completed the 3-month active treatment phase. Since no single end point adequately defines the outcome of constipation therapy, follow-up with a variety of objective and subjective measures of improvement was conducted at 3, 6, and 12 months. The 1-year intent-to-treat analysis involved 13 patients from each arm.

Only 1 of 13 patients in the biofeedback arm still met diagnostic criteria for dyssynergia at 1 year, in contrast to all 13 in the control group. Mean balloon expulsion time fell from a baseline of 143 seconds in the biofeedback group to 13 seconds at 3 months and 18 seconds at 1 year, compared with 87 seconds at 1 year in controls.

The number of complete, spontaneous bowel movements per week increased significantly in the biofeedback group, as did objective measures of anorectal and colonic function and patient satisfaction with bowel function; none of these end points improved over the course of a year in the controls.

In response to audience questions, Dr. Rao said that it has been his clinical experience outside the randomized trial setting that at least two-thirds of patients who have undergone a course of biofeedback for dyssynergic defecation maintain the benefits in multiyear follow-up, while the effects wane beyond 1 year in about one-third, who benefit from a refresher.

Dr. Rao's study, for which he received the 2005 ACG Auxiliary Award, was funded by the National Institutes of Health.

HONOLULU – Biofeedback proved superior to standard therapy for long-term management of patients with the most common cause of chronic constipation in the first-ever randomized trial featuring a full year of follow-up.

Previous short-term randomized trials have demonstrated that biofeedback is effective in patients with dyssynergic defecation. But this form of constipation is a long-term problem–and although uncontrolled studies have suggested good long-term maintenance of efficacy with biofeedback, it was important to establish in a more rigorous randomized trial setting whether this nonpharmacologic therapy maintains its effectiveness over time.

The answer–at least through 1 year of formal follow-up–is clearly yes, Dr. Satish S.C. Rao said at the annual meeting of the American College of Gastroenterology.

The clinical relevance of this finding lies in the fact that recent surveys indicate that up to 50% of patients with chronic constipation are dissatisfied with their current treatment. This is largely because conventional therapies focus primarily on reducing stool hardness rather than addressing the underlying physiologic dysfunction. In the setting of dyssynergic defecation, which accounts for roughly half of all cases of chronic constipation, the pathophysiology involves a lack of coordination between the pelvic floor muscles and anal sphincter, explained Dr. Rao, a gastroenterologist at the University of Iowa, Iowa City.

He reported on 52 patients, 47 of whom were women, who were randomized to a 3-month biofeedback program or standard therapy. All met strict manometric diagnostic criteria for dyssynergic defecation. Patients with the other two common types of chronic constipation–irritable bowel syndrome and slow-transit constipation–were excluded.

The biofeedback program entailed biweekly hour-long treatment sessions in which participants learned techniques aimed at increasing their pushing effort through improved anorectal coordination and sensory conditioning. They also practiced expelling a simulated stool made of silicone.

The standard-therapy control arm involved three monthly visits with a gastroenterologist, dietician, and nurse for instruction in dietary modification, exercise, toilet habits, and appropriate use of laxatives. “That's a lot more than the usual standard therapy in clinical practice,” Dr. Rao noted.

Of the 52 patients, 44 completed the 3-month active treatment phase. Since no single end point adequately defines the outcome of constipation therapy, follow-up with a variety of objective and subjective measures of improvement was conducted at 3, 6, and 12 months. The 1-year intent-to-treat analysis involved 13 patients from each arm.

Only 1 of 13 patients in the biofeedback arm still met diagnostic criteria for dyssynergia at 1 year, in contrast to all 13 in the control group. Mean balloon expulsion time fell from a baseline of 143 seconds in the biofeedback group to 13 seconds at 3 months and 18 seconds at 1 year, compared with 87 seconds at 1 year in controls.

The number of complete, spontaneous bowel movements per week increased significantly in the biofeedback group, as did objective measures of anorectal and colonic function and patient satisfaction with bowel function; none of these end points improved over the course of a year in the controls.

In response to audience questions, Dr. Rao said that it has been his clinical experience outside the randomized trial setting that at least two-thirds of patients who have undergone a course of biofeedback for dyssynergic defecation maintain the benefits in multiyear follow-up, while the effects wane beyond 1 year in about one-third, who benefit from a refresher.

Dr. Rao's study, for which he received the 2005 ACG Auxiliary Award, was funded by the National Institutes of Health.

HONOLULU – Biofeedback proved superior to standard therapy for long-term management of patients with the most common cause of chronic constipation in the first-ever randomized trial featuring a full year of follow-up.

Previous short-term randomized trials have demonstrated that biofeedback is effective in patients with dyssynergic defecation. But this form of constipation is a long-term problem–and although uncontrolled studies have suggested good long-term maintenance of efficacy with biofeedback, it was important to establish in a more rigorous randomized trial setting whether this nonpharmacologic therapy maintains its effectiveness over time.

The answer–at least through 1 year of formal follow-up–is clearly yes, Dr. Satish S.C. Rao said at the annual meeting of the American College of Gastroenterology.

The clinical relevance of this finding lies in the fact that recent surveys indicate that up to 50% of patients with chronic constipation are dissatisfied with their current treatment. This is largely because conventional therapies focus primarily on reducing stool hardness rather than addressing the underlying physiologic dysfunction. In the setting of dyssynergic defecation, which accounts for roughly half of all cases of chronic constipation, the pathophysiology involves a lack of coordination between the pelvic floor muscles and anal sphincter, explained Dr. Rao, a gastroenterologist at the University of Iowa, Iowa City.

He reported on 52 patients, 47 of whom were women, who were randomized to a 3-month biofeedback program or standard therapy. All met strict manometric diagnostic criteria for dyssynergic defecation. Patients with the other two common types of chronic constipation–irritable bowel syndrome and slow-transit constipation–were excluded.

The biofeedback program entailed biweekly hour-long treatment sessions in which participants learned techniques aimed at increasing their pushing effort through improved anorectal coordination and sensory conditioning. They also practiced expelling a simulated stool made of silicone.

The standard-therapy control arm involved three monthly visits with a gastroenterologist, dietician, and nurse for instruction in dietary modification, exercise, toilet habits, and appropriate use of laxatives. “That's a lot more than the usual standard therapy in clinical practice,” Dr. Rao noted.

Of the 52 patients, 44 completed the 3-month active treatment phase. Since no single end point adequately defines the outcome of constipation therapy, follow-up with a variety of objective and subjective measures of improvement was conducted at 3, 6, and 12 months. The 1-year intent-to-treat analysis involved 13 patients from each arm.

Only 1 of 13 patients in the biofeedback arm still met diagnostic criteria for dyssynergia at 1 year, in contrast to all 13 in the control group. Mean balloon expulsion time fell from a baseline of 143 seconds in the biofeedback group to 13 seconds at 3 months and 18 seconds at 1 year, compared with 87 seconds at 1 year in controls.

The number of complete, spontaneous bowel movements per week increased significantly in the biofeedback group, as did objective measures of anorectal and colonic function and patient satisfaction with bowel function; none of these end points improved over the course of a year in the controls.

In response to audience questions, Dr. Rao said that it has been his clinical experience outside the randomized trial setting that at least two-thirds of patients who have undergone a course of biofeedback for dyssynergic defecation maintain the benefits in multiyear follow-up, while the effects wane beyond 1 year in about one-third, who benefit from a refresher.

Dr. Rao's study, for which he received the 2005 ACG Auxiliary Award, was funded by the National Institutes of Health.

SAN DIEGO – When choosing a therapy for physical fatigue in patients being treated for depression, it is important to consider the presence or absence of residual sadness, Dr. Stephen C. Ellen said at a psychopharmacology congress sponsored by the Neuroscience Education Institute.

Two strategies exist for treating patients on antidepressants who complain that activities make them feel more physically tired, winded, or older than they felt before depression set in, despite getting help for the depression. Both bupropion and stimulants will boost dopamine and norepinephrine in the cortex, striatum, and spinal cord. Modafinil will boost histamine in the cortex, he said.

Dr. Ellen is a speaker for GlaxoSmithKline, which makes Wellbutrin (bupropion). He also serves as a consultant and speaker for Cephalon Inc., which makes Provigil (modafinil).

If the patient's antidepressant therapy has virtually eliminated the sadness and mood issues, choose modafinil or methylphenidate (for example, Ritalin) or another stimulant to treat the residual physical fatigue. If some sadness still remains, however, bupropion may boost antidepressant effects and reduce fatigue, said Dr. Ellen of the University of Massachusetts, Worcester.

Modafinil or stimulants work much better at “waking somebody up” from residual symptoms of depression than does bupropion, he said. Bupropion “is brightening, but I don't think it is particularly wake promoting.”

Physical fatigue is common in patients with depression or obstructive sleep apnea, and the two problems overlap. One in six depressed people has obstructive sleep apnea, and one in five people with obstructive sleep apnea is depressed, he noted. A 2003 study of 60 patients found that the more severe the depression in a patient with sleep apnea, the greater the level of fatigue.

In patients with both depression and obstructive sleep apnea, the fatigue usually derives from the depression. “So if you're still getting words that sound like fatigue” after treatment, consider switching to a stronger antidepressant or increasing the dose, Dr. Ellen advised.

Bupropion is widely used to treat fatigue in patients with depression but it “takes a while to kick in,” typically 4–6 weeks, he said. Some reports suggest that bupropion may be less likely than other antidepressants to destabilize a patient with bipolar disorder, but other reports suggest that the risk is no different with bupropion.

A case series of 42 patients treated for depression with selective serotonin reuptake inhibitors found that energy levels stayed the same or improved in patients who received adjuvant bupropion but worsened in nearly half of patients who remained on monotherapy, Dr. Ellen said.

Stimulants are not commonly used to treat fatigue in depressed patients, but they can quickly provide a boost in alertness with short-term use. Most studies of stimulants for fatigue focus on patients with HIV or AIDS. There are no controlled trials of stimulants for fatigue associated with depression, “but that shouldn't throw you off, because there's not a single controlled study of [bupropion for this indication] either, and we use that like crazy,” he said.

Stimulants, however, can cause cardiovascular or CNS side effects and have a high risk for abuse with long-term use. Patients may develop psychological or physical dependence on them, and tolerance to the drug develops rapidly, Dr. Ellen said.

Adding modafinil to antidepressant therapy appears to significantly reduce patients' fatigue scores if the drug is given in proper doses. The best effects are seen with 100–200 mg/day. Less benefit comes from a dosage of 300 mg/day, and a dosage of 400 mg/day can increase fatigue, he said.

Modafinil's effects on fatigue in depression appear to be independent of mood, and the onset of action usually is immediate, he noted.

SAN DIEGO – When choosing a therapy for physical fatigue in patients being treated for depression, it is important to consider the presence or absence of residual sadness, Dr. Stephen C. Ellen said at a psychopharmacology congress sponsored by the Neuroscience Education Institute.

Two strategies exist for treating patients on antidepressants who complain that activities make them feel more physically tired, winded, or older than they felt before depression set in, despite getting help for the depression. Both bupropion and stimulants will boost dopamine and norepinephrine in the cortex, striatum, and spinal cord. Modafinil will boost histamine in the cortex, he said.

Dr. Ellen is a speaker for GlaxoSmithKline, which makes Wellbutrin (bupropion). He also serves as a consultant and speaker for Cephalon Inc., which makes Provigil (modafinil).

If the patient's antidepressant therapy has virtually eliminated the sadness and mood issues, choose modafinil or methylphenidate (for example, Ritalin) or another stimulant to treat the residual physical fatigue. If some sadness still remains, however, bupropion may boost antidepressant effects and reduce fatigue, said Dr. Ellen of the University of Massachusetts, Worcester.

Modafinil or stimulants work much better at “waking somebody up” from residual symptoms of depression than does bupropion, he said. Bupropion “is brightening, but I don't think it is particularly wake promoting.”

Physical fatigue is common in patients with depression or obstructive sleep apnea, and the two problems overlap. One in six depressed people has obstructive sleep apnea, and one in five people with obstructive sleep apnea is depressed, he noted. A 2003 study of 60 patients found that the more severe the depression in a patient with sleep apnea, the greater the level of fatigue.

In patients with both depression and obstructive sleep apnea, the fatigue usually derives from the depression. “So if you're still getting words that sound like fatigue” after treatment, consider switching to a stronger antidepressant or increasing the dose, Dr. Ellen advised.

Bupropion is widely used to treat fatigue in patients with depression but it “takes a while to kick in,” typically 4–6 weeks, he said. Some reports suggest that bupropion may be less likely than other antidepressants to destabilize a patient with bipolar disorder, but other reports suggest that the risk is no different with bupropion.

A case series of 42 patients treated for depression with selective serotonin reuptake inhibitors found that energy levels stayed the same or improved in patients who received adjuvant bupropion but worsened in nearly half of patients who remained on monotherapy, Dr. Ellen said.

Stimulants are not commonly used to treat fatigue in depressed patients, but they can quickly provide a boost in alertness with short-term use. Most studies of stimulants for fatigue focus on patients with HIV or AIDS. There are no controlled trials of stimulants for fatigue associated with depression, “but that shouldn't throw you off, because there's not a single controlled study of [bupropion for this indication] either, and we use that like crazy,” he said.

Stimulants, however, can cause cardiovascular or CNS side effects and have a high risk for abuse with long-term use. Patients may develop psychological or physical dependence on them, and tolerance to the drug develops rapidly, Dr. Ellen said.

Adding modafinil to antidepressant therapy appears to significantly reduce patients' fatigue scores if the drug is given in proper doses. The best effects are seen with 100–200 mg/day. Less benefit comes from a dosage of 300 mg/day, and a dosage of 400 mg/day can increase fatigue, he said.

Modafinil's effects on fatigue in depression appear to be independent of mood, and the onset of action usually is immediate, he noted.

SAN DIEGO – When choosing a therapy for physical fatigue in patients being treated for depression, it is important to consider the presence or absence of residual sadness, Dr. Stephen C. Ellen said at a psychopharmacology congress sponsored by the Neuroscience Education Institute.

Two strategies exist for treating patients on antidepressants who complain that activities make them feel more physically tired, winded, or older than they felt before depression set in, despite getting help for the depression. Both bupropion and stimulants will boost dopamine and norepinephrine in the cortex, striatum, and spinal cord. Modafinil will boost histamine in the cortex, he said.

Dr. Ellen is a speaker for GlaxoSmithKline, which makes Wellbutrin (bupropion). He also serves as a consultant and speaker for Cephalon Inc., which makes Provigil (modafinil).

If the patient's antidepressant therapy has virtually eliminated the sadness and mood issues, choose modafinil or methylphenidate (for example, Ritalin) or another stimulant to treat the residual physical fatigue. If some sadness still remains, however, bupropion may boost antidepressant effects and reduce fatigue, said Dr. Ellen of the University of Massachusetts, Worcester.

Modafinil or stimulants work much better at “waking somebody up” from residual symptoms of depression than does bupropion, he said. Bupropion “is brightening, but I don't think it is particularly wake promoting.”

Physical fatigue is common in patients with depression or obstructive sleep apnea, and the two problems overlap. One in six depressed people has obstructive sleep apnea, and one in five people with obstructive sleep apnea is depressed, he noted. A 2003 study of 60 patients found that the more severe the depression in a patient with sleep apnea, the greater the level of fatigue.

In patients with both depression and obstructive sleep apnea, the fatigue usually derives from the depression. “So if you're still getting words that sound like fatigue” after treatment, consider switching to a stronger antidepressant or increasing the dose, Dr. Ellen advised.

Bupropion is widely used to treat fatigue in patients with depression but it “takes a while to kick in,” typically 4–6 weeks, he said. Some reports suggest that bupropion may be less likely than other antidepressants to destabilize a patient with bipolar disorder, but other reports suggest that the risk is no different with bupropion.

A case series of 42 patients treated for depression with selective serotonin reuptake inhibitors found that energy levels stayed the same or improved in patients who received adjuvant bupropion but worsened in nearly half of patients who remained on monotherapy, Dr. Ellen said.

Stimulants are not commonly used to treat fatigue in depressed patients, but they can quickly provide a boost in alertness with short-term use. Most studies of stimulants for fatigue focus on patients with HIV or AIDS. There are no controlled trials of stimulants for fatigue associated with depression, “but that shouldn't throw you off, because there's not a single controlled study of [bupropion for this indication] either, and we use that like crazy,” he said.

Stimulants, however, can cause cardiovascular or CNS side effects and have a high risk for abuse with long-term use. Patients may develop psychological or physical dependence on them, and tolerance to the drug develops rapidly, Dr. Ellen said.

Adding modafinil to antidepressant therapy appears to significantly reduce patients' fatigue scores if the drug is given in proper doses. The best effects are seen with 100–200 mg/day. Less benefit comes from a dosage of 300 mg/day, and a dosage of 400 mg/day can increase fatigue, he said.

Modafinil's effects on fatigue in depression appear to be independent of mood, and the onset of action usually is immediate, he noted.

Depression strikes one in five patients hospitalized for myocardial infarction, with severe consequences, including a threefold increased risk of cardiac mortality and significantly elevated mortality from all causes, a comprehensive evidence review has concluded.

The review, conducted by the federal Agency for Healthcare Research and Quality at the behest of the American Academy of Family Physicians, is destined to become the framework for evidence-based clinical practice guidelines, according to the AAFP.

Highlights of the review coordinated by the Johns Hopkins Evidence-Based Practice Center in Baltimore include:

▸ Evidence from 25 trials pointing to a prevalence of depression in one in five patients hospitalized for an MI.

▸ Data from three studies that depression during the initial MI hospitalization persists from 1–4 months in 60%–70% of patients.

▸ “Strikingly consistent” evidence that post-MI depression puts patients at an increased risk for death by cardiac causes (a threefold increased risk) and other causes.

▸ Conclusions from three studies showing that depressed post-MI patients are less likely than are others to take their prescribed medications or to comply with lifestyle modification.

▸ Findings that suggest psychosocial intervention and selective serotonin reuptake inhibitors (SSRIs) improve depression in post-MI patients, but not necessarily other outcomes.

The lengthy analysis pointed out a number of important gaps in scientific knowledge about depression and MI, such as the best way to measure depression in hospitalized MI patients and the true impact of interventions.

For example, SSRIs were found to improve some surrogate markers of cardiac risk, “but no studies of sufficient power address the question of whether this treatment improves survival,” the analysis said.

The Johns Hopkins team, led by Dr. David E. Bush and Dr. Roy C. Ziegelstein, included clinicians and researchers from cardiology, psychiatry, general internal medicine, and cardiac rehabilitation, as well as representatives from the AAFP, the nursing community, and private and government payers.

Six key questions were compiled, several with important subcategories. A literature review was conducted electronically and by hand of 16 specific journals and the electronic databases Medline, Cochrane Central Register of Controlled Trials, the Cochrane Database of Methodology Reviews, the Cumulative Index to Nursing and Allied Health Literature, the Psychological Abstracts, and Embase.

The intensive review unveiled the magnitude of evidence pointing to depression as an important impedance to a full recovery and a return to productive life in many MI patients.

Its conclusions suggest a pivotal role for family physicians, who may be in the best position to oversee “the whole patient” as he or she embarks on the long course of recovery, Dr. Lee A. Green, the AAFP representative to the review panel and a member of the family medicine faculty at the University of Michigan in Ann Arbor, said in a telephone interview.

Patients can survive heart attacks and their hearts can be fine, but they can be disabled by their depression, he said.

The severity of an MI may overshadow less evident aspects of health that should be identified early and managed with the best tools available.

Although the literature review shows that more research is needed to illuminate the best approaches to post-MI depression, it provides ample evidence of the worth of such research.

In the immediate future, the stark findings about the importance of depression following MI may lead to more communication among specialists, including psychiatrists, family physicians, and cardiologists, Dr. Green said.

Depression strikes one in five patients hospitalized for myocardial infarction, with severe consequences, including a threefold increased risk of cardiac mortality and significantly elevated mortality from all causes, a comprehensive evidence review has concluded.

The review, conducted by the federal Agency for Healthcare Research and Quality at the behest of the American Academy of Family Physicians, is destined to become the framework for evidence-based clinical practice guidelines, according to the AAFP.

Highlights of the review coordinated by the Johns Hopkins Evidence-Based Practice Center in Baltimore include:

▸ Evidence from 25 trials pointing to a prevalence of depression in one in five patients hospitalized for an MI.

▸ Data from three studies that depression during the initial MI hospitalization persists from 1–4 months in 60%–70% of patients.

▸ “Strikingly consistent” evidence that post-MI depression puts patients at an increased risk for death by cardiac causes (a threefold increased risk) and other causes.

▸ Conclusions from three studies showing that depressed post-MI patients are less likely than are others to take their prescribed medications or to comply with lifestyle modification.

▸ Findings that suggest psychosocial intervention and selective serotonin reuptake inhibitors (SSRIs) improve depression in post-MI patients, but not necessarily other outcomes.

The lengthy analysis pointed out a number of important gaps in scientific knowledge about depression and MI, such as the best way to measure depression in hospitalized MI patients and the true impact of interventions.

For example, SSRIs were found to improve some surrogate markers of cardiac risk, “but no studies of sufficient power address the question of whether this treatment improves survival,” the analysis said.

The Johns Hopkins team, led by Dr. David E. Bush and Dr. Roy C. Ziegelstein, included clinicians and researchers from cardiology, psychiatry, general internal medicine, and cardiac rehabilitation, as well as representatives from the AAFP, the nursing community, and private and government payers.

Six key questions were compiled, several with important subcategories. A literature review was conducted electronically and by hand of 16 specific journals and the electronic databases Medline, Cochrane Central Register of Controlled Trials, the Cochrane Database of Methodology Reviews, the Cumulative Index to Nursing and Allied Health Literature, the Psychological Abstracts, and Embase.

The intensive review unveiled the magnitude of evidence pointing to depression as an important impedance to a full recovery and a return to productive life in many MI patients.

Its conclusions suggest a pivotal role for family physicians, who may be in the best position to oversee “the whole patient” as he or she embarks on the long course of recovery, Dr. Lee A. Green, the AAFP representative to the review panel and a member of the family medicine faculty at the University of Michigan in Ann Arbor, said in a telephone interview.

Patients can survive heart attacks and their hearts can be fine, but they can be disabled by their depression, he said.

The severity of an MI may overshadow less evident aspects of health that should be identified early and managed with the best tools available.

Although the literature review shows that more research is needed to illuminate the best approaches to post-MI depression, it provides ample evidence of the worth of such research.

In the immediate future, the stark findings about the importance of depression following MI may lead to more communication among specialists, including psychiatrists, family physicians, and cardiologists, Dr. Green said.

Depression strikes one in five patients hospitalized for myocardial infarction, with severe consequences, including a threefold increased risk of cardiac mortality and significantly elevated mortality from all causes, a comprehensive evidence review has concluded.

The review, conducted by the federal Agency for Healthcare Research and Quality at the behest of the American Academy of Family Physicians, is destined to become the framework for evidence-based clinical practice guidelines, according to the AAFP.

Highlights of the review coordinated by the Johns Hopkins Evidence-Based Practice Center in Baltimore include:

▸ Evidence from 25 trials pointing to a prevalence of depression in one in five patients hospitalized for an MI.

▸ Data from three studies that depression during the initial MI hospitalization persists from 1–4 months in 60%–70% of patients.

▸ “Strikingly consistent” evidence that post-MI depression puts patients at an increased risk for death by cardiac causes (a threefold increased risk) and other causes.

▸ Conclusions from three studies showing that depressed post-MI patients are less likely than are others to take their prescribed medications or to comply with lifestyle modification.

▸ Findings that suggest psychosocial intervention and selective serotonin reuptake inhibitors (SSRIs) improve depression in post-MI patients, but not necessarily other outcomes.

The lengthy analysis pointed out a number of important gaps in scientific knowledge about depression and MI, such as the best way to measure depression in hospitalized MI patients and the true impact of interventions.

For example, SSRIs were found to improve some surrogate markers of cardiac risk, “but no studies of sufficient power address the question of whether this treatment improves survival,” the analysis said.

The Johns Hopkins team, led by Dr. David E. Bush and Dr. Roy C. Ziegelstein, included clinicians and researchers from cardiology, psychiatry, general internal medicine, and cardiac rehabilitation, as well as representatives from the AAFP, the nursing community, and private and government payers.

Six key questions were compiled, several with important subcategories. A literature review was conducted electronically and by hand of 16 specific journals and the electronic databases Medline, Cochrane Central Register of Controlled Trials, the Cochrane Database of Methodology Reviews, the Cumulative Index to Nursing and Allied Health Literature, the Psychological Abstracts, and Embase.

The intensive review unveiled the magnitude of evidence pointing to depression as an important impedance to a full recovery and a return to productive life in many MI patients.

Its conclusions suggest a pivotal role for family physicians, who may be in the best position to oversee “the whole patient” as he or she embarks on the long course of recovery, Dr. Lee A. Green, the AAFP representative to the review panel and a member of the family medicine faculty at the University of Michigan in Ann Arbor, said in a telephone interview.

Patients can survive heart attacks and their hearts can be fine, but they can be disabled by their depression, he said.

The severity of an MI may overshadow less evident aspects of health that should be identified early and managed with the best tools available.

Although the literature review shows that more research is needed to illuminate the best approaches to post-MI depression, it provides ample evidence of the worth of such research.

In the immediate future, the stark findings about the importance of depression following MI may lead to more communication among specialists, including psychiatrists, family physicians, and cardiologists, Dr. Green said.

ATLANTA – Women with postpartum depression are more likely than are nondepressed women to have urge urinary incontinence, according to findings presented in a poster at the annual meeting of the American Urogynecologic Society.

Of 146 women who participated in the cross-sectional study, 12% had postpartum depression at their 6-week visit as measured by the Edinburgh Postnatal Depression Scale. At that time, those with depression had a fourfold increase in overall and subscale scores on the Urge-Incontinence Impact Questionnaire (UIIQ), compared with nondepressed women.

This finding suggests that depressed patients have more symptoms and a greater impact on their lives from urge urinary incontinence, Dr. Dee Fenner reported during a press briefing at the meeting.

Depressed and nondepressed patients were similar in age, race, parity, and body mass index. On multivariate analysis, depression scores were shown to be affected by UIIQ score, smoking, and infant feeding mode (bottle vs. breast). But urge incontinence symptoms had the greatest effect on depression scores. In addition, depressed patients were more than twice as likely as nondepressed patients to have had a cesarean delivery, Dr. Fenner said.

That finding amplifies the association between urinary incontinence and postpartum depression because studies have shown that women who have a C-section generally are less likely to develop urge urinary incontinence than are those who deliver vaginally, she noted.

The findings have several implications. “We hope this will serve for future studies as a model to predict the onset of depression and to actually work out whether or not this is the depression causing the incontinence or the incontinence causing the depression,” Dr. Fenner said.

ATLANTA – Women with postpartum depression are more likely than are nondepressed women to have urge urinary incontinence, according to findings presented in a poster at the annual meeting of the American Urogynecologic Society.

Of 146 women who participated in the cross-sectional study, 12% had postpartum depression at their 6-week visit as measured by the Edinburgh Postnatal Depression Scale. At that time, those with depression had a fourfold increase in overall and subscale scores on the Urge-Incontinence Impact Questionnaire (UIIQ), compared with nondepressed women.

This finding suggests that depressed patients have more symptoms and a greater impact on their lives from urge urinary incontinence, Dr. Dee Fenner reported during a press briefing at the meeting.

Depressed and nondepressed patients were similar in age, race, parity, and body mass index. On multivariate analysis, depression scores were shown to be affected by UIIQ score, smoking, and infant feeding mode (bottle vs. breast). But urge incontinence symptoms had the greatest effect on depression scores. In addition, depressed patients were more than twice as likely as nondepressed patients to have had a cesarean delivery, Dr. Fenner said.

That finding amplifies the association between urinary incontinence and postpartum depression because studies have shown that women who have a C-section generally are less likely to develop urge urinary incontinence than are those who deliver vaginally, she noted.

The findings have several implications. “We hope this will serve for future studies as a model to predict the onset of depression and to actually work out whether or not this is the depression causing the incontinence or the incontinence causing the depression,” Dr. Fenner said.

ATLANTA – Women with postpartum depression are more likely than are nondepressed women to have urge urinary incontinence, according to findings presented in a poster at the annual meeting of the American Urogynecologic Society.

Of 146 women who participated in the cross-sectional study, 12% had postpartum depression at their 6-week visit as measured by the Edinburgh Postnatal Depression Scale. At that time, those with depression had a fourfold increase in overall and subscale scores on the Urge-Incontinence Impact Questionnaire (UIIQ), compared with nondepressed women.

This finding suggests that depressed patients have more symptoms and a greater impact on their lives from urge urinary incontinence, Dr. Dee Fenner reported during a press briefing at the meeting.

Depressed and nondepressed patients were similar in age, race, parity, and body mass index. On multivariate analysis, depression scores were shown to be affected by UIIQ score, smoking, and infant feeding mode (bottle vs. breast). But urge incontinence symptoms had the greatest effect on depression scores. In addition, depressed patients were more than twice as likely as nondepressed patients to have had a cesarean delivery, Dr. Fenner said.

That finding amplifies the association between urinary incontinence and postpartum depression because studies have shown that women who have a C-section generally are less likely to develop urge urinary incontinence than are those who deliver vaginally, she noted.

The findings have several implications. “We hope this will serve for future studies as a model to predict the onset of depression and to actually work out whether or not this is the depression causing the incontinence or the incontinence causing the depression,” Dr. Fenner said.

SANTA ANA PUEBLO, N.M. – Elderly people with depression and arthritis experienced significant pain relief with duloxetine in a placebo-controlled trial reported at the annual meeting of the Academy of Psychosomatic Medicine.

Conducted by investigators from Eli Lilly & Co., the research findings also documented significant improvement in cognitive functions, primarily verbal learning and memory, for depressed patients treated with duloxetine (Cymbalta) in the 8-week, multicenter study.

“I think (these findings are) very encouraging,” investigator Dr. Michael J. Robinson, a clinical research physician at Lilly's medical division in Indianapolis, said in an interview. “Duloxetine may be advantageous for those specific cognitive symptoms.”

The results suggest duloxetine can alleviate arthritis pain, a common comorbidity in depressed elderly patients. An inhibitor of serotonin and norepinephrine reuptake, duloxetine is known to have analgesic properties and is approved for treatment of peripheral neuropathic pain in patients with diabetes.

Cognition was a primary outcome in the trial, which randomized 207 depressed elderly patients to 60 mg daily of duloxetine and 104 to placebo. The two cohorts were similar, with an average age of 73 years, slightly more women than men, and more than three-fourths the population being white. All patients were at least 65 years old and had previous episodes of depression.

Similar proportions of patients withdrew because of adverse events. The most common in the duloxetine group were dry mouth, nausea, and constipation.

As could be expected, duloxetine produced faster and more significant reductions than placebo on the Geriatric Depression Scale (GDS) and the Hamilton Rating Scale for Depression (HAMD 17). On average, the GDS fell −4.07 in patients on duloxetine vs. -1.34 in the placebo cohort. HAMD 17 scores declined −6.49 with duloxetine and −3.72 with placebo.

The duloxetine cohort also demonstrated significantly greater improvement in a composite cognitive score based on four cognitive tests: a mean change of +1.95 vs. +0.76 for the placebo group. At baseline, the mean composite cognitive scores were 22.70 for the duloxetine group and 23.17 for the placebo group. Most of the improvement could be attributed to changes in scores on verbal learning and recall tests.

Visual analog scale scores for all 311 patients in the trial demonstrated greater improvement in back pain and “time in pain while awake” for the duloxetine cohort. In a subgroup analysis limited to patients with comorbid arthritis, 117 patients on duloxetine had significantly greater improvement in four of six pain measures, compared with scores of 55 patients on placebo.

At the outset, all patients with arthritis had significantly higher baseline scores on five of six pain categories assessed with visual analog scales. Overall severity was 38.3 for patients with arthritis vs. 22.5 in patients who did not have arthritis.

Over the course of the trial, arthritis patients in the duloxetine cohort had significantly greater improvements in overall pain, back pain, time in pain while awake, and interference with daily activities. Arthritis patients in the placebo group had more headache and shoulder pain, but the difference was not significant.

The mean change in overall pain scores was −6.70 for arthritis patients on duloxetine vs. −1.89 for arthritis patients on placebo. The most dramatic effect was for back pain, which fell by a mean of more than 20% with duloxetine while increasing more than 10% with placebo.

“We don't know if this is their pain due to arthritis or their pain due to depression,” Dr. Robinson said. “This is just looking at general pain outcomes.” Baseline scores for depression and improvements in mood were similar for arthritis patients in the two arms of the trial.

SANTA ANA PUEBLO, N.M. – Elderly people with depression and arthritis experienced significant pain relief with duloxetine in a placebo-controlled trial reported at the annual meeting of the Academy of Psychosomatic Medicine.

Conducted by investigators from Eli Lilly & Co., the research findings also documented significant improvement in cognitive functions, primarily verbal learning and memory, for depressed patients treated with duloxetine (Cymbalta) in the 8-week, multicenter study.

“I think (these findings are) very encouraging,” investigator Dr. Michael J. Robinson, a clinical research physician at Lilly's medical division in Indianapolis, said in an interview. “Duloxetine may be advantageous for those specific cognitive symptoms.”

The results suggest duloxetine can alleviate arthritis pain, a common comorbidity in depressed elderly patients. An inhibitor of serotonin and norepinephrine reuptake, duloxetine is known to have analgesic properties and is approved for treatment of peripheral neuropathic pain in patients with diabetes.

Cognition was a primary outcome in the trial, which randomized 207 depressed elderly patients to 60 mg daily of duloxetine and 104 to placebo. The two cohorts were similar, with an average age of 73 years, slightly more women than men, and more than three-fourths the population being white. All patients were at least 65 years old and had previous episodes of depression.

Similar proportions of patients withdrew because of adverse events. The most common in the duloxetine group were dry mouth, nausea, and constipation.

As could be expected, duloxetine produced faster and more significant reductions than placebo on the Geriatric Depression Scale (GDS) and the Hamilton Rating Scale for Depression (HAMD 17). On average, the GDS fell −4.07 in patients on duloxetine vs. -1.34 in the placebo cohort. HAMD 17 scores declined −6.49 with duloxetine and −3.72 with placebo.

The duloxetine cohort also demonstrated significantly greater improvement in a composite cognitive score based on four cognitive tests: a mean change of +1.95 vs. +0.76 for the placebo group. At baseline, the mean composite cognitive scores were 22.70 for the duloxetine group and 23.17 for the placebo group. Most of the improvement could be attributed to changes in scores on verbal learning and recall tests.

Visual analog scale scores for all 311 patients in the trial demonstrated greater improvement in back pain and “time in pain while awake” for the duloxetine cohort. In a subgroup analysis limited to patients with comorbid arthritis, 117 patients on duloxetine had significantly greater improvement in four of six pain measures, compared with scores of 55 patients on placebo.

At the outset, all patients with arthritis had significantly higher baseline scores on five of six pain categories assessed with visual analog scales. Overall severity was 38.3 for patients with arthritis vs. 22.5 in patients who did not have arthritis.

Over the course of the trial, arthritis patients in the duloxetine cohort had significantly greater improvements in overall pain, back pain, time in pain while awake, and interference with daily activities. Arthritis patients in the placebo group had more headache and shoulder pain, but the difference was not significant.

The mean change in overall pain scores was −6.70 for arthritis patients on duloxetine vs. −1.89 for arthritis patients on placebo. The most dramatic effect was for back pain, which fell by a mean of more than 20% with duloxetine while increasing more than 10% with placebo.

“We don't know if this is their pain due to arthritis or their pain due to depression,” Dr. Robinson said. “This is just looking at general pain outcomes.” Baseline scores for depression and improvements in mood were similar for arthritis patients in the two arms of the trial.

SANTA ANA PUEBLO, N.M. – Elderly people with depression and arthritis experienced significant pain relief with duloxetine in a placebo-controlled trial reported at the annual meeting of the Academy of Psychosomatic Medicine.

Conducted by investigators from Eli Lilly & Co., the research findings also documented significant improvement in cognitive functions, primarily verbal learning and memory, for depressed patients treated with duloxetine (Cymbalta) in the 8-week, multicenter study.

“I think (these findings are) very encouraging,” investigator Dr. Michael J. Robinson, a clinical research physician at Lilly's medical division in Indianapolis, said in an interview. “Duloxetine may be advantageous for those specific cognitive symptoms.”

The results suggest duloxetine can alleviate arthritis pain, a common comorbidity in depressed elderly patients. An inhibitor of serotonin and norepinephrine reuptake, duloxetine is known to have analgesic properties and is approved for treatment of peripheral neuropathic pain in patients with diabetes.

Cognition was a primary outcome in the trial, which randomized 207 depressed elderly patients to 60 mg daily of duloxetine and 104 to placebo. The two cohorts were similar, with an average age of 73 years, slightly more women than men, and more than three-fourths the population being white. All patients were at least 65 years old and had previous episodes of depression.

Similar proportions of patients withdrew because of adverse events. The most common in the duloxetine group were dry mouth, nausea, and constipation.

As could be expected, duloxetine produced faster and more significant reductions than placebo on the Geriatric Depression Scale (GDS) and the Hamilton Rating Scale for Depression (HAMD 17). On average, the GDS fell −4.07 in patients on duloxetine vs. -1.34 in the placebo cohort. HAMD 17 scores declined −6.49 with duloxetine and −3.72 with placebo.

The duloxetine cohort also demonstrated significantly greater improvement in a composite cognitive score based on four cognitive tests: a mean change of +1.95 vs. +0.76 for the placebo group. At baseline, the mean composite cognitive scores were 22.70 for the duloxetine group and 23.17 for the placebo group. Most of the improvement could be attributed to changes in scores on verbal learning and recall tests.

Visual analog scale scores for all 311 patients in the trial demonstrated greater improvement in back pain and “time in pain while awake” for the duloxetine cohort. In a subgroup analysis limited to patients with comorbid arthritis, 117 patients on duloxetine had significantly greater improvement in four of six pain measures, compared with scores of 55 patients on placebo.

At the outset, all patients with arthritis had significantly higher baseline scores on five of six pain categories assessed with visual analog scales. Overall severity was 38.3 for patients with arthritis vs. 22.5 in patients who did not have arthritis.

Over the course of the trial, arthritis patients in the duloxetine cohort had significantly greater improvements in overall pain, back pain, time in pain while awake, and interference with daily activities. Arthritis patients in the placebo group had more headache and shoulder pain, but the difference was not significant.

The mean change in overall pain scores was −6.70 for arthritis patients on duloxetine vs. −1.89 for arthritis patients on placebo. The most dramatic effect was for back pain, which fell by a mean of more than 20% with duloxetine while increasing more than 10% with placebo.

“We don't know if this is their pain due to arthritis or their pain due to depression,” Dr. Robinson said. “This is just looking at general pain outcomes.” Baseline scores for depression and improvements in mood were similar for arthritis patients in the two arms of the trial.

Chronic pain—particularly lower back pain—is frustrating to both patient and clinician. Because most cases lack an obvious physical explanation, the doctor may wonder if the patient is faking or exaggerating—that the pain is “in the patient’s head.” Studies suggest this cerebral component may exist—but not in ways you might expect.

How the brain processes pain

According to traditional belief, the brain passively receives noxious signals from injured tissue (nociceptive) or damaged nerve (neuropathic). Extensive—some would say excessive—tests are often conducted in search of a bone or muscle injury that might explain the pain.

Functional imaging studies across 15 years have shown activity in various brain regions when subjects feel pain. In addition to the somatosensory cortex, pain also activates brain areas involved with mood, attention, and anxiety. More important, the brain does not passively receive signals from the periphery but can inhibit ascending signals with endogenous opioids, such as endorphins and enkephalins.

Apkarian et al^{Posttraumatic stress disorder: Nature and nurture?, May 2004.)}

Drugs. Medications and other substances taken to alleviate pain might also reduce gray matter. Excessive alcohol and opioid use have long-term adverse effects on the CNS.³ Is treatment or self-medication mildly toxic to the brain?

Overuse atrophy. Apkarian et al¹ propose that cortical loss may be secondary to overuse. They suggest that persistent pain perception— and the resultant negative affect and stress—causes an excitotoxic and inflammatory state that wears out portions of the brain circuitry. If this is true, then chronic pain itself causes cerebral atrophy.

Whatever the explanation, this study indicates that chronic lower back pain pathology extends beyond the lower back.

Related resources

• Deyo RA, Weinstein JN. Low back pain. N Engl J Med 2001;344:363-70.
• International Association for the Study of Pain. www.iasp-pain.org.

Chronic pain—particularly lower back pain—is frustrating to both patient and clinician. Because most cases lack an obvious physical explanation, the doctor may wonder if the patient is faking or exaggerating—that the pain is “in the patient’s head.” Studies suggest this cerebral component may exist—but not in ways you might expect.

How the brain processes pain

According to traditional belief, the brain passively receives noxious signals from injured tissue (nociceptive) or damaged nerve (neuropathic). Extensive—some would say excessive—tests are often conducted in search of a bone or muscle injury that might explain the pain.

Functional imaging studies across 15 years have shown activity in various brain regions when subjects feel pain. In addition to the somatosensory cortex, pain also activates brain areas involved with mood, attention, and anxiety. More important, the brain does not passively receive signals from the periphery but can inhibit ascending signals with endogenous opioids, such as endorphins and enkephalins.

Apkarian et al^{Posttraumatic stress disorder: Nature and nurture?, May 2004.)}

Drugs. Medications and other substances taken to alleviate pain might also reduce gray matter. Excessive alcohol and opioid use have long-term adverse effects on the CNS.³ Is treatment or self-medication mildly toxic to the brain?

Overuse atrophy. Apkarian et al¹ propose that cortical loss may be secondary to overuse. They suggest that persistent pain perception— and the resultant negative affect and stress—causes an excitotoxic and inflammatory state that wears out portions of the brain circuitry. If this is true, then chronic pain itself causes cerebral atrophy.

Whatever the explanation, this study indicates that chronic lower back pain pathology extends beyond the lower back.

Related resources

• Deyo RA, Weinstein JN. Low back pain. N Engl J Med 2001;344:363-70.
• International Association for the Study of Pain. www.iasp-pain.org.

Chronic pain—particularly lower back pain—is frustrating to both patient and clinician. Because most cases lack an obvious physical explanation, the doctor may wonder if the patient is faking or exaggerating—that the pain is “in the patient’s head.” Studies suggest this cerebral component may exist—but not in ways you might expect.

How the brain processes pain

According to traditional belief, the brain passively receives noxious signals from injured tissue (nociceptive) or damaged nerve (neuropathic). Extensive—some would say excessive—tests are often conducted in search of a bone or muscle injury that might explain the pain.

Functional imaging studies across 15 years have shown activity in various brain regions when subjects feel pain. In addition to the somatosensory cortex, pain also activates brain areas involved with mood, attention, and anxiety. More important, the brain does not passively receive signals from the periphery but can inhibit ascending signals with endogenous opioids, such as endorphins and enkephalins.

Apkarian et al^{Posttraumatic stress disorder: Nature and nurture?, May 2004.)}

Drugs. Medications and other substances taken to alleviate pain might also reduce gray matter. Excessive alcohol and opioid use have long-term adverse effects on the CNS.³ Is treatment or self-medication mildly toxic to the brain?

Overuse atrophy. Apkarian et al¹ propose that cortical loss may be secondary to overuse. They suggest that persistent pain perception— and the resultant negative affect and stress—causes an excitotoxic and inflammatory state that wears out portions of the brain circuitry. If this is true, then chronic pain itself causes cerebral atrophy.

Whatever the explanation, this study indicates that chronic lower back pain pathology extends beyond the lower back.

Related resources

• Deyo RA, Weinstein JN. Low back pain. N Engl J Med 2001;344:363-70.
• International Association for the Study of Pain. www.iasp-pain.org.

MONTREAL – Refeeding syndrome is a potential problem for all eating-disordered patients who are reintroducing fluids and food, but it is difficult to predict which patients are at greatest risk, Ovidio Bermudez, M.D., said at an international conference sponsored by the Academy for Eating Disorders.

“There is something about the reintroduction of nutrients to someone who has suffered a significant nutritional insult that can cause severe metabolic imbalances, resulting in cardiovascular, pulmonary, neurological, hepatic, and even bone marrow dysfunction,” he said in an interview.

Once the body has adjusted to a state of malnourishment, refeeding will signal the body to switch off its compensatory mechanisms, thus unmasking many nutritional deficiencies, said Dr. Bermudez, medical director of the eating disorders program at Laureate Psychiatric Clinic and Hospital in Tulsa, Okla. The result is electrolyte and fluid imbalances, glucose intolerance, liver dysfunction, and thiamine deficiency.

“All patients who are refed will develop some degree of refeeding syndrome, but there is great variability in terms of the severity of the readjustment. Most patients fare well without any apparent clinical challenges, some patients have a moderate challenge, and a few patients have very severe or even fatal consequences,” he said.

Although there are few predictive factors to identify patients most at risk for refeeding syndrome, they tend to be those who are the most underweight (less than 70% of their ideal body weight) and have low prealbumin levels. But these predictors should not be relied on too heavily, Dr. Bermudez warned. “The idea that a person who has had only a moderate metabolic insult is not going to develop some of these problems would be a false reassurance. The best approach we should have as physicians is to know the literature and know the group of patients at highest risk,” but to be alert for any trouble, he said.

By screening for problems prior to refeeding and then monitoring patients carefully during the refeeding, Dr. Bermudez noted, most serious consequences can be avoided.

He recommended that a comprehensive metabolic panel (including liver and renal function tests), calcium, phosphorous and magnesium levels, CBC, and a prealbumin test should be performed prior to refeeding. Any vitamin and trace mineral deficiencies, as well as electrolyte and glucose imbalances, should also be corrected at that time. During refeeding, fluids and caloric intake should be increased gradually by 200–250 kcal every 2–3 days, and weight gain should not exceed 2–3 pounds per week, Dr. Bermudez said. Initially, patients should have their vital signs, weight, and fluid intake and output monitored daily, with weekly assessments of CBC, electrolytes and glucose, calcium, phosphorus, magnesium, and liver and renal function, he said.

“How long to do this is not quite clear. In our setting, it is usually 2–3 weeks, but in others it can be up to 6 weeks,” he said. “Sometimes patients are ambulatory, but I think the sicker patients should be refed in the hospital. Then you can relax the surveillance and be more guided by symptoms.”

MONTREAL – Refeeding syndrome is a potential problem for all eating-disordered patients who are reintroducing fluids and food, but it is difficult to predict which patients are at greatest risk, Ovidio Bermudez, M.D., said at an international conference sponsored by the Academy for Eating Disorders.

“There is something about the reintroduction of nutrients to someone who has suffered a significant nutritional insult that can cause severe metabolic imbalances, resulting in cardiovascular, pulmonary, neurological, hepatic, and even bone marrow dysfunction,” he said in an interview.

Once the body has adjusted to a state of malnourishment, refeeding will signal the body to switch off its compensatory mechanisms, thus unmasking many nutritional deficiencies, said Dr. Bermudez, medical director of the eating disorders program at Laureate Psychiatric Clinic and Hospital in Tulsa, Okla. The result is electrolyte and fluid imbalances, glucose intolerance, liver dysfunction, and thiamine deficiency.

“All patients who are refed will develop some degree of refeeding syndrome, but there is great variability in terms of the severity of the readjustment. Most patients fare well without any apparent clinical challenges, some patients have a moderate challenge, and a few patients have very severe or even fatal consequences,” he said.

Although there are few predictive factors to identify patients most at risk for refeeding syndrome, they tend to be those who are the most underweight (less than 70% of their ideal body weight) and have low prealbumin levels. But these predictors should not be relied on too heavily, Dr. Bermudez warned. “The idea that a person who has had only a moderate metabolic insult is not going to develop some of these problems would be a false reassurance. The best approach we should have as physicians is to know the literature and know the group of patients at highest risk,” but to be alert for any trouble, he said.

By screening for problems prior to refeeding and then monitoring patients carefully during the refeeding, Dr. Bermudez noted, most serious consequences can be avoided.

He recommended that a comprehensive metabolic panel (including liver and renal function tests), calcium, phosphorous and magnesium levels, CBC, and a prealbumin test should be performed prior to refeeding. Any vitamin and trace mineral deficiencies, as well as electrolyte and glucose imbalances, should also be corrected at that time. During refeeding, fluids and caloric intake should be increased gradually by 200–250 kcal every 2–3 days, and weight gain should not exceed 2–3 pounds per week, Dr. Bermudez said. Initially, patients should have their vital signs, weight, and fluid intake and output monitored daily, with weekly assessments of CBC, electrolytes and glucose, calcium, phosphorus, magnesium, and liver and renal function, he said.

“How long to do this is not quite clear. In our setting, it is usually 2–3 weeks, but in others it can be up to 6 weeks,” he said. “Sometimes patients are ambulatory, but I think the sicker patients should be refed in the hospital. Then you can relax the surveillance and be more guided by symptoms.”

MONTREAL – Refeeding syndrome is a potential problem for all eating-disordered patients who are reintroducing fluids and food, but it is difficult to predict which patients are at greatest risk, Ovidio Bermudez, M.D., said at an international conference sponsored by the Academy for Eating Disorders.

“There is something about the reintroduction of nutrients to someone who has suffered a significant nutritional insult that can cause severe metabolic imbalances, resulting in cardiovascular, pulmonary, neurological, hepatic, and even bone marrow dysfunction,” he said in an interview.

Once the body has adjusted to a state of malnourishment, refeeding will signal the body to switch off its compensatory mechanisms, thus unmasking many nutritional deficiencies, said Dr. Bermudez, medical director of the eating disorders program at Laureate Psychiatric Clinic and Hospital in Tulsa, Okla. The result is electrolyte and fluid imbalances, glucose intolerance, liver dysfunction, and thiamine deficiency.

“All patients who are refed will develop some degree of refeeding syndrome, but there is great variability in terms of the severity of the readjustment. Most patients fare well without any apparent clinical challenges, some patients have a moderate challenge, and a few patients have very severe or even fatal consequences,” he said.

Although there are few predictive factors to identify patients most at risk for refeeding syndrome, they tend to be those who are the most underweight (less than 70% of their ideal body weight) and have low prealbumin levels. But these predictors should not be relied on too heavily, Dr. Bermudez warned. “The idea that a person who has had only a moderate metabolic insult is not going to develop some of these problems would be a false reassurance. The best approach we should have as physicians is to know the literature and know the group of patients at highest risk,” but to be alert for any trouble, he said.

By screening for problems prior to refeeding and then monitoring patients carefully during the refeeding, Dr. Bermudez noted, most serious consequences can be avoided.

He recommended that a comprehensive metabolic panel (including liver and renal function tests), calcium, phosphorous and magnesium levels, CBC, and a prealbumin test should be performed prior to refeeding. Any vitamin and trace mineral deficiencies, as well as electrolyte and glucose imbalances, should also be corrected at that time. During refeeding, fluids and caloric intake should be increased gradually by 200–250 kcal every 2–3 days, and weight gain should not exceed 2–3 pounds per week, Dr. Bermudez said. Initially, patients should have their vital signs, weight, and fluid intake and output monitored daily, with weekly assessments of CBC, electrolytes and glucose, calcium, phosphorus, magnesium, and liver and renal function, he said.

“How long to do this is not quite clear. In our setting, it is usually 2–3 weeks, but in others it can be up to 6 weeks,” he said. “Sometimes patients are ambulatory, but I think the sicker patients should be refed in the hospital. Then you can relax the surveillance and be more guided by symptoms.”

MONTREAL – When young patients with eating disorders transfer from the pediatric to the adult care setting, they literally take their lives into their own hands–which sometimes leaves their families and health care professionals empty handed.

Parents and the health care team play a central decision-making role in the pediatric setting, but the adult system transfers full responsibility to the patient. Some adolescents are ready for this new empowerment. For others, the freedom to refuse treatment or to exclude family members can create many bumps along the road, noted experts at an international conference sponsored by the Academy for Eating Disorders.

“Everyone's fear is that the child will enter the adult system, get less attention, and eventually die,” said D. Blake Woodside, M.D., director of the inpatient eating disorders program at Toronto General Hospital. Indeed, the harsh reality is that, unlike pediatric programs, most adult eating disorder programs have no resources and often no legal jurisdiction to treat involuntary patients, he said.

But although many patients drift away from treatment at this time, the natural course of anorexia nervosa (AN), is such that the risk of death during this middle phase of the illness tends to be low, he said.

“There is a period of instability and risk of death in the early phase of the disease [around puberty] and the late phase after fifteen or more years, but through the middle phase it stabilizes and there are few deaths,” he said. “We have had hundreds of patients who have had a Body Mass Index of 14 for years. Sure, they are very sick, but they probably will not die.”

Many adolescents with eating disorders do not recognize or acknowledge their need to continue treatment as adults, said Debra K. Katzman, M.D., of the department of pediatrics at the University of Toronto's Hospital for Sick Children. In a recent survey of adolescents under age 18 with AN, only 14% anticipated that they would need treatment in the adult system and only 33% said they would participate in such a transfer.

She said it is useful for parents and pediatric caregivers to remember that aggressive treatment early in the course of the illness can have a positive outcome on child and adolescent growth and development and eventual long-term outcome.

“What we struggle with as pediatricians is the worry, knowing that we can make a significant impact on the patient's growth and development if we intervene. But once these patients are adults, intervention is less likely to make significant change.”

Dr. Katzman recommends that the transition from pediatric to adult care should be an extended and gradual one, starting as early as age 10. “The transition may take years. It's a process through which patients and their families are empowered to become active participants in their own care.”

The first step is actually a step back on the part of parents, said Leora Pinhas, M.D., psychiatric director of the eating disorders program at the University of Toronto's Hospital for Sick Children. Although the adolescent may be 18 years old, many teens with eating disorders are developmentally delayed–which makes this process particularly difficult. “We try to encourage them to accept help from those who have their best interests at heart,” she said.

But family dynamics can be very fragile, added Dr. Woodside. “If parents are sufficiently anxious and can't back off, the patient can cut off contact with them completely,” he explained.

MONTREAL – When young patients with eating disorders transfer from the pediatric to the adult care setting, they literally take their lives into their own hands–which sometimes leaves their families and health care professionals empty handed.

Parents and the health care team play a central decision-making role in the pediatric setting, but the adult system transfers full responsibility to the patient. Some adolescents are ready for this new empowerment. For others, the freedom to refuse treatment or to exclude family members can create many bumps along the road, noted experts at an international conference sponsored by the Academy for Eating Disorders.

“Everyone's fear is that the child will enter the adult system, get less attention, and eventually die,” said D. Blake Woodside, M.D., director of the inpatient eating disorders program at Toronto General Hospital. Indeed, the harsh reality is that, unlike pediatric programs, most adult eating disorder programs have no resources and often no legal jurisdiction to treat involuntary patients, he said.

But although many patients drift away from treatment at this time, the natural course of anorexia nervosa (AN), is such that the risk of death during this middle phase of the illness tends to be low, he said.

“There is a period of instability and risk of death in the early phase of the disease [around puberty] and the late phase after fifteen or more years, but through the middle phase it stabilizes and there are few deaths,” he said. “We have had hundreds of patients who have had a Body Mass Index of 14 for years. Sure, they are very sick, but they probably will not die.”

Many adolescents with eating disorders do not recognize or acknowledge their need to continue treatment as adults, said Debra K. Katzman, M.D., of the department of pediatrics at the University of Toronto's Hospital for Sick Children. In a recent survey of adolescents under age 18 with AN, only 14% anticipated that they would need treatment in the adult system and only 33% said they would participate in such a transfer.

She said it is useful for parents and pediatric caregivers to remember that aggressive treatment early in the course of the illness can have a positive outcome on child and adolescent growth and development and eventual long-term outcome.

“What we struggle with as pediatricians is the worry, knowing that we can make a significant impact on the patient's growth and development if we intervene. But once these patients are adults, intervention is less likely to make significant change.”

Dr. Katzman recommends that the transition from pediatric to adult care should be an extended and gradual one, starting as early as age 10. “The transition may take years. It's a process through which patients and their families are empowered to become active participants in their own care.”

The first step is actually a step back on the part of parents, said Leora Pinhas, M.D., psychiatric director of the eating disorders program at the University of Toronto's Hospital for Sick Children. Although the adolescent may be 18 years old, many teens with eating disorders are developmentally delayed–which makes this process particularly difficult. “We try to encourage them to accept help from those who have their best interests at heart,” she said.

But family dynamics can be very fragile, added Dr. Woodside. “If parents are sufficiently anxious and can't back off, the patient can cut off contact with them completely,” he explained.

MONTREAL – When young patients with eating disorders transfer from the pediatric to the adult care setting, they literally take their lives into their own hands–which sometimes leaves their families and health care professionals empty handed.

Parents and the health care team play a central decision-making role in the pediatric setting, but the adult system transfers full responsibility to the patient. Some adolescents are ready for this new empowerment. For others, the freedom to refuse treatment or to exclude family members can create many bumps along the road, noted experts at an international conference sponsored by the Academy for Eating Disorders.

“Everyone's fear is that the child will enter the adult system, get less attention, and eventually die,” said D. Blake Woodside, M.D., director of the inpatient eating disorders program at Toronto General Hospital. Indeed, the harsh reality is that, unlike pediatric programs, most adult eating disorder programs have no resources and often no legal jurisdiction to treat involuntary patients, he said.

But although many patients drift away from treatment at this time, the natural course of anorexia nervosa (AN), is such that the risk of death during this middle phase of the illness tends to be low, he said.

“There is a period of instability and risk of death in the early phase of the disease [around puberty] and the late phase after fifteen or more years, but through the middle phase it stabilizes and there are few deaths,” he said. “We have had hundreds of patients who have had a Body Mass Index of 14 for years. Sure, they are very sick, but they probably will not die.”

Many adolescents with eating disorders do not recognize or acknowledge their need to continue treatment as adults, said Debra K. Katzman, M.D., of the department of pediatrics at the University of Toronto's Hospital for Sick Children. In a recent survey of adolescents under age 18 with AN, only 14% anticipated that they would need treatment in the adult system and only 33% said they would participate in such a transfer.

She said it is useful for parents and pediatric caregivers to remember that aggressive treatment early in the course of the illness can have a positive outcome on child and adolescent growth and development and eventual long-term outcome.

“What we struggle with as pediatricians is the worry, knowing that we can make a significant impact on the patient's growth and development if we intervene. But once these patients are adults, intervention is less likely to make significant change.”

Dr. Katzman recommends that the transition from pediatric to adult care should be an extended and gradual one, starting as early as age 10. “The transition may take years. It's a process through which patients and their families are empowered to become active participants in their own care.”

The first step is actually a step back on the part of parents, said Leora Pinhas, M.D., psychiatric director of the eating disorders program at the University of Toronto's Hospital for Sick Children. Although the adolescent may be 18 years old, many teens with eating disorders are developmentally delayed–which makes this process particularly difficult. “We try to encourage them to accept help from those who have their best interests at heart,” she said.

But family dynamics can be very fragile, added Dr. Woodside. “If parents are sufficiently anxious and can't back off, the patient can cut off contact with them completely,” he explained.

PITTSBURGH – Patients with bipolar disorder have an unexpectedly high prevalence of medical comorbidities, based on findings from a study of 175 patients.

These 175 patients, with an average age of 35, had a high prevalence of gastrointestinal, musculoskeletal, genitourinary, and other medical comorbidities, Ellen Frank, Ph.D., said at the Sixth International Conference on Bipolar Disorder.

The rates were “very high for such a young population. It stunned us,” said Dr. Frank, professor of psychiatry and psychology at the University of Pittsburgh, which sponsored the conference.

If physicians focus only on the psychiatric symptoms of patients with bipolar disorder, they “do their patients a disservice because they also have a lot of medical illness … associated with poor psychiatric outcomes,” she told this newspaper.

The Pittsburgh Study of Maintenance Therapies in Bipolar Disorders was designed to assess the efficacy of a psychosocial therapy as an adjunct to pharmacotherapy. But as part of the study, the participants underwent a thorough medical work-up at baseline.

The initial assessment found large numbers of patients with an active medical illness. For example, 59 of the 175 patients (34%) had active gastrointestinal disease; a total of 97 (55%) had a history of gastrointestinal disease, but the condition was not active in all patients.

Active musculoskeletal or joint disease was found in 56 patients (32%), and a total of 131 (75%) had a history of this comorbidity. A substantial fraction also had active genitourinary disease (43 patients, 25%), headaches or migraines (42 patients, 24%), asthma or respiratory disease (41 patients, 23%), and cardiovascular disease (32 patients, 18%). In addition, 58 patients (33%) were obese.

One analysis of the findings compared the efficacy of maintenance treatment in patients with four or more active comorbidities with those with fewer comorbidities. The analysis showed that, during 2 years of follow-up, patients with four or more active comorbidities were about twice as likely to have a recurrence of bipolar symptoms as were patients with fewer comorbidities, reported Dr. Frank, who is also director of the depression and manic-depression prevention program at the Western Psychiatric Institute and Clinic in Pittsburgh.

In the subgroup of patients with a high number of active, medical comorbidities, intensive clinical management was the superior maintenance therapy. The second psychosocial treatment tested–interpersonal and social rhythm therapy–was more effective for patients with fewer medical comorbidities. The high prevalence of medical comorbidities seen in this study leads to two additional messages on how to best manage patients: First, “some treatments for bipolar disorder may exacerbate medical symptoms,” Dr. Frank said. “We need to be careful when treating patients who are at risk” for obesity, cardiovascular disease, and other conditions. “Many bipolar disorder drugs have cardiac effects, so physicians have to be aware of these risk factors.”

Also, because bipolar patients are frequently depressed, they often find it hard to adhere to a healthy diet and exercise. Patients with bipolar disorder must be given tools for improving their physical health-related behavior, Dr. Frank said.

PITTSBURGH – Patients with bipolar disorder have an unexpectedly high prevalence of medical comorbidities, based on findings from a study of 175 patients.

These 175 patients, with an average age of 35, had a high prevalence of gastrointestinal, musculoskeletal, genitourinary, and other medical comorbidities, Ellen Frank, Ph.D., said at the Sixth International Conference on Bipolar Disorder.

The rates were “very high for such a young population. It stunned us,” said Dr. Frank, professor of psychiatry and psychology at the University of Pittsburgh, which sponsored the conference.

If physicians focus only on the psychiatric symptoms of patients with bipolar disorder, they “do their patients a disservice because they also have a lot of medical illness … associated with poor psychiatric outcomes,” she told this newspaper.

The Pittsburgh Study of Maintenance Therapies in Bipolar Disorders was designed to assess the efficacy of a psychosocial therapy as an adjunct to pharmacotherapy. But as part of the study, the participants underwent a thorough medical work-up at baseline.

The initial assessment found large numbers of patients with an active medical illness. For example, 59 of the 175 patients (34%) had active gastrointestinal disease; a total of 97 (55%) had a history of gastrointestinal disease, but the condition was not active in all patients.

Active musculoskeletal or joint disease was found in 56 patients (32%), and a total of 131 (75%) had a history of this comorbidity. A substantial fraction also had active genitourinary disease (43 patients, 25%), headaches or migraines (42 patients, 24%), asthma or respiratory disease (41 patients, 23%), and cardiovascular disease (32 patients, 18%). In addition, 58 patients (33%) were obese.

One analysis of the findings compared the efficacy of maintenance treatment in patients with four or more active comorbidities with those with fewer comorbidities. The analysis showed that, during 2 years of follow-up, patients with four or more active comorbidities were about twice as likely to have a recurrence of bipolar symptoms as were patients with fewer comorbidities, reported Dr. Frank, who is also director of the depression and manic-depression prevention program at the Western Psychiatric Institute and Clinic in Pittsburgh.

In the subgroup of patients with a high number of active, medical comorbidities, intensive clinical management was the superior maintenance therapy. The second psychosocial treatment tested–interpersonal and social rhythm therapy–was more effective for patients with fewer medical comorbidities. The high prevalence of medical comorbidities seen in this study leads to two additional messages on how to best manage patients: First, “some treatments for bipolar disorder may exacerbate medical symptoms,” Dr. Frank said. “We need to be careful when treating patients who are at risk” for obesity, cardiovascular disease, and other conditions. “Many bipolar disorder drugs have cardiac effects, so physicians have to be aware of these risk factors.”

Also, because bipolar patients are frequently depressed, they often find it hard to adhere to a healthy diet and exercise. Patients with bipolar disorder must be given tools for improving their physical health-related behavior, Dr. Frank said.

PITTSBURGH – Patients with bipolar disorder have an unexpectedly high prevalence of medical comorbidities, based on findings from a study of 175 patients.

These 175 patients, with an average age of 35, had a high prevalence of gastrointestinal, musculoskeletal, genitourinary, and other medical comorbidities, Ellen Frank, Ph.D., said at the Sixth International Conference on Bipolar Disorder.

The rates were “very high for such a young population. It stunned us,” said Dr. Frank, professor of psychiatry and psychology at the University of Pittsburgh, which sponsored the conference.

If physicians focus only on the psychiatric symptoms of patients with bipolar disorder, they “do their patients a disservice because they also have a lot of medical illness … associated with poor psychiatric outcomes,” she told this newspaper.

The Pittsburgh Study of Maintenance Therapies in Bipolar Disorders was designed to assess the efficacy of a psychosocial therapy as an adjunct to pharmacotherapy. But as part of the study, the participants underwent a thorough medical work-up at baseline.

The initial assessment found large numbers of patients with an active medical illness. For example, 59 of the 175 patients (34%) had active gastrointestinal disease; a total of 97 (55%) had a history of gastrointestinal disease, but the condition was not active in all patients.

Active musculoskeletal or joint disease was found in 56 patients (32%), and a total of 131 (75%) had a history of this comorbidity. A substantial fraction also had active genitourinary disease (43 patients, 25%), headaches or migraines (42 patients, 24%), asthma or respiratory disease (41 patients, 23%), and cardiovascular disease (32 patients, 18%). In addition, 58 patients (33%) were obese.

One analysis of the findings compared the efficacy of maintenance treatment in patients with four or more active comorbidities with those with fewer comorbidities. The analysis showed that, during 2 years of follow-up, patients with four or more active comorbidities were about twice as likely to have a recurrence of bipolar symptoms as were patients with fewer comorbidities, reported Dr. Frank, who is also director of the depression and manic-depression prevention program at the Western Psychiatric Institute and Clinic in Pittsburgh.

In the subgroup of patients with a high number of active, medical comorbidities, intensive clinical management was the superior maintenance therapy. The second psychosocial treatment tested–interpersonal and social rhythm therapy–was more effective for patients with fewer medical comorbidities. The high prevalence of medical comorbidities seen in this study leads to two additional messages on how to best manage patients: First, “some treatments for bipolar disorder may exacerbate medical symptoms,” Dr. Frank said. “We need to be careful when treating patients who are at risk” for obesity, cardiovascular disease, and other conditions. “Many bipolar disorder drugs have cardiac effects, so physicians have to be aware of these risk factors.”

Also, because bipolar patients are frequently depressed, they often find it hard to adhere to a healthy diet and exercise. Patients with bipolar disorder must be given tools for improving their physical health-related behavior, Dr. Frank said.