Somatic Disorders

WASHINGTON – Insomnia is a disorder of hyperarousal rather than one of sleep deprivation, Thomas Roth, Ph.D., said at the annual meeting of the American Academy of Clinical Psychiatrists.

“Mothers of newborn babies don't have insomnia; they simply don't have adequate opportunities for sleep,” said Dr. Roth, director of research and chief of sleep medicine at the Henry Ford Hospital in Detroit.

Because 90% of people with insomnia have other comorbid conditions, insomnia was seen as a symptom rather than an independent disorder until 2005. That's when the National Institute of Mental Health declared that insomnia met the criteria for a disorder, which include impairment in function and quality of life that is associated with specific symptoms and rooted in physiology.

To meet the diagnostic criteria for insomnia, a person must report one or more of the following symptoms: difficulty falling asleep, difficulty staying asleep, or nonrestorative sleep.

When treating a patient who complains of chronic sleep problems, be sure to ask these several key questions, Dr. Roth said in an interview:

▸ What is the nature of the nighttime sleep problems (difficulty falling asleep, difficulty staying asleep)?

▸ What is the nature of daytime consequences (daytime sleepiness, impaired function)?

▸ What are the frequency and duration of symptoms?

▸ Does the patient have any comorbid medical or psychiatric conditions?

Prevalence data are limited, but about 30% of the general population has some type of disturbed sleep, Dr. Roth said.

Many patients with insomnia report that the daytime impairment and distress resulting from insomnia are more frustrating for them than their difficulty sleeping at night.

Chronic pain is a common comorbidity in insomnia patients. In addition, people with insomnia are significantly more likely to develop comorbid psychiatric disorders.

Dr. Roth cited a recent study from his laboratory in which the researchers evaluated 1,000 people who had never had a psychiatric disease and found that 240 met criteria for insomnia. At a follow-up 3.5 years later, the people with insomnia had 4.5 times the risk of developing a psychiatric disorder.

Treatment of insomnia remains a challenge, but recognition of the role of hyperarousal and the frequency of comorbidities allows for new therapeutic targets, including some sedating antidepressants.

WASHINGTON – Insomnia is a disorder of hyperarousal rather than one of sleep deprivation, Thomas Roth, Ph.D., said at the annual meeting of the American Academy of Clinical Psychiatrists.

“Mothers of newborn babies don't have insomnia; they simply don't have adequate opportunities for sleep,” said Dr. Roth, director of research and chief of sleep medicine at the Henry Ford Hospital in Detroit.

Because 90% of people with insomnia have other comorbid conditions, insomnia was seen as a symptom rather than an independent disorder until 2005. That's when the National Institute of Mental Health declared that insomnia met the criteria for a disorder, which include impairment in function and quality of life that is associated with specific symptoms and rooted in physiology.

To meet the diagnostic criteria for insomnia, a person must report one or more of the following symptoms: difficulty falling asleep, difficulty staying asleep, or nonrestorative sleep.

When treating a patient who complains of chronic sleep problems, be sure to ask these several key questions, Dr. Roth said in an interview:

▸ What is the nature of the nighttime sleep problems (difficulty falling asleep, difficulty staying asleep)?

▸ What is the nature of daytime consequences (daytime sleepiness, impaired function)?

▸ What are the frequency and duration of symptoms?

▸ Does the patient have any comorbid medical or psychiatric conditions?

Prevalence data are limited, but about 30% of the general population has some type of disturbed sleep, Dr. Roth said.

Many patients with insomnia report that the daytime impairment and distress resulting from insomnia are more frustrating for them than their difficulty sleeping at night.

Chronic pain is a common comorbidity in insomnia patients. In addition, people with insomnia are significantly more likely to develop comorbid psychiatric disorders.

Dr. Roth cited a recent study from his laboratory in which the researchers evaluated 1,000 people who had never had a psychiatric disease and found that 240 met criteria for insomnia. At a follow-up 3.5 years later, the people with insomnia had 4.5 times the risk of developing a psychiatric disorder.

Treatment of insomnia remains a challenge, but recognition of the role of hyperarousal and the frequency of comorbidities allows for new therapeutic targets, including some sedating antidepressants.

WASHINGTON – Insomnia is a disorder of hyperarousal rather than one of sleep deprivation, Thomas Roth, Ph.D., said at the annual meeting of the American Academy of Clinical Psychiatrists.

“Mothers of newborn babies don't have insomnia; they simply don't have adequate opportunities for sleep,” said Dr. Roth, director of research and chief of sleep medicine at the Henry Ford Hospital in Detroit.

Because 90% of people with insomnia have other comorbid conditions, insomnia was seen as a symptom rather than an independent disorder until 2005. That's when the National Institute of Mental Health declared that insomnia met the criteria for a disorder, which include impairment in function and quality of life that is associated with specific symptoms and rooted in physiology.

To meet the diagnostic criteria for insomnia, a person must report one or more of the following symptoms: difficulty falling asleep, difficulty staying asleep, or nonrestorative sleep.

When treating a patient who complains of chronic sleep problems, be sure to ask these several key questions, Dr. Roth said in an interview:

▸ What is the nature of the nighttime sleep problems (difficulty falling asleep, difficulty staying asleep)?

▸ What is the nature of daytime consequences (daytime sleepiness, impaired function)?

▸ What are the frequency and duration of symptoms?

▸ Does the patient have any comorbid medical or psychiatric conditions?

Prevalence data are limited, but about 30% of the general population has some type of disturbed sleep, Dr. Roth said.

Many patients with insomnia report that the daytime impairment and distress resulting from insomnia are more frustrating for them than their difficulty sleeping at night.

Chronic pain is a common comorbidity in insomnia patients. In addition, people with insomnia are significantly more likely to develop comorbid psychiatric disorders.

Dr. Roth cited a recent study from his laboratory in which the researchers evaluated 1,000 people who had never had a psychiatric disease and found that 240 met criteria for insomnia. At a follow-up 3.5 years later, the people with insomnia had 4.5 times the risk of developing a psychiatric disorder.

Treatment of insomnia remains a challenge, but recognition of the role of hyperarousal and the frequency of comorbidities allows for new therapeutic targets, including some sedating antidepressants.

Depressive symptoms appear to correlate with the development of coronary artery disease, but hostility and anxiety may not, Jesse C. Stewart, Ph.D., and his associates reported.

Several studies have linked various negative emotions with the development of coronary artery disease in initially healthy subjects. But teasing out the relative contributions of depression, anxiety, and hostility has been difficult because they tend to overlap. Dr. Stewart and his associates of the University of Pittsburgh assessed a wide range of such symptoms in a prospective cohort study of subclinical atherosclerosis in healthy subjects aged 50–70 years.

The 324 subjects underwent ultrasonographic assessment of carotid intimal medial thickness (IMT), a noninvasive measure of subclinical atherosclerosis, as well as tests evaluating emotional factors, including the Beck Depression Inventory, the Beck Anxiety Inventory, the Cooke-Medley Hostility Scale, and the State-Trait Anger Expression Inventory.

During 3-year follow-up, only mild to moderate depressive symptoms correlated with the decreasing carotid IMT that signals progression of subclinical atherosclerosis. Hostility symptoms of anxiety, the experience of anger, and the expression of anger showed no correlation with carotid IMT change.

This study is the first ever to report an association between depressive symptoms and carotid IMT change, the investigators said (Arch. Gen. Psychiatry 2007;64:225–33).

The exact mechanism underlying this association is unclear, but depression is known to affect physiologic pathways also involved in atherosclerosis, such as autonomic nervous system dysfunction, hypothalamic-pituitary-adrenal axis dysregulation, inflammatory processes, and altered platelet function, they said.

A post hoc analysis of the data showed that IMT worsening was associated with somatic-vegetative symptoms of depression such as fatigue, sleep disturbance, loss of appetite, and anhedonia, but not associated with more cognitive-affective depressive symptoms such as sadness, pessimism, discontent, or indecisiveness.

Depressive symptoms appear to correlate with the development of coronary artery disease, but hostility and anxiety may not, Jesse C. Stewart, Ph.D., and his associates reported.

Several studies have linked various negative emotions with the development of coronary artery disease in initially healthy subjects. But teasing out the relative contributions of depression, anxiety, and hostility has been difficult because they tend to overlap. Dr. Stewart and his associates of the University of Pittsburgh assessed a wide range of such symptoms in a prospective cohort study of subclinical atherosclerosis in healthy subjects aged 50–70 years.

The 324 subjects underwent ultrasonographic assessment of carotid intimal medial thickness (IMT), a noninvasive measure of subclinical atherosclerosis, as well as tests evaluating emotional factors, including the Beck Depression Inventory, the Beck Anxiety Inventory, the Cooke-Medley Hostility Scale, and the State-Trait Anger Expression Inventory.

During 3-year follow-up, only mild to moderate depressive symptoms correlated with the decreasing carotid IMT that signals progression of subclinical atherosclerosis. Hostility symptoms of anxiety, the experience of anger, and the expression of anger showed no correlation with carotid IMT change.

This study is the first ever to report an association between depressive symptoms and carotid IMT change, the investigators said (Arch. Gen. Psychiatry 2007;64:225–33).

The exact mechanism underlying this association is unclear, but depression is known to affect physiologic pathways also involved in atherosclerosis, such as autonomic nervous system dysfunction, hypothalamic-pituitary-adrenal axis dysregulation, inflammatory processes, and altered platelet function, they said.

A post hoc analysis of the data showed that IMT worsening was associated with somatic-vegetative symptoms of depression such as fatigue, sleep disturbance, loss of appetite, and anhedonia, but not associated with more cognitive-affective depressive symptoms such as sadness, pessimism, discontent, or indecisiveness.

Depressive symptoms appear to correlate with the development of coronary artery disease, but hostility and anxiety may not, Jesse C. Stewart, Ph.D., and his associates reported.

Several studies have linked various negative emotions with the development of coronary artery disease in initially healthy subjects. But teasing out the relative contributions of depression, anxiety, and hostility has been difficult because they tend to overlap. Dr. Stewart and his associates of the University of Pittsburgh assessed a wide range of such symptoms in a prospective cohort study of subclinical atherosclerosis in healthy subjects aged 50–70 years.

The 324 subjects underwent ultrasonographic assessment of carotid intimal medial thickness (IMT), a noninvasive measure of subclinical atherosclerosis, as well as tests evaluating emotional factors, including the Beck Depression Inventory, the Beck Anxiety Inventory, the Cooke-Medley Hostility Scale, and the State-Trait Anger Expression Inventory.

During 3-year follow-up, only mild to moderate depressive symptoms correlated with the decreasing carotid IMT that signals progression of subclinical atherosclerosis. Hostility symptoms of anxiety, the experience of anger, and the expression of anger showed no correlation with carotid IMT change.

This study is the first ever to report an association between depressive symptoms and carotid IMT change, the investigators said (Arch. Gen. Psychiatry 2007;64:225–33).

The exact mechanism underlying this association is unclear, but depression is known to affect physiologic pathways also involved in atherosclerosis, such as autonomic nervous system dysfunction, hypothalamic-pituitary-adrenal axis dysregulation, inflammatory processes, and altered platelet function, they said.

A post hoc analysis of the data showed that IMT worsening was associated with somatic-vegetative symptoms of depression such as fatigue, sleep disturbance, loss of appetite, and anhedonia, but not associated with more cognitive-affective depressive symptoms such as sadness, pessimism, discontent, or indecisiveness.

BOSTON – Sleep strengthens declarative memory, a finding that could one day be exploited to combat cognitive declines associated with dementia and neurologic disorders, Dr. Jeffrey M. Ellenbogen reported at the annual meeting of the American Academy of Neurology.

Sleep previously has been shown to improve motor, visual, and perceptual memories in humans, but this study is one of the first to substantiate a role for sleep in protecting declarative or consciously discussed memories from associative interference, said Dr. Ellenbogen of Harvard Medical School, Boston.

For the study, 48 healthy individuals, aged 18–30 years, were evaluated. No participants took any medications, and all had normal sleep patterns. Subjects were placed in one of four groups, and all were asked to remember 20 words, each of which was paired with an associated word cue.

All groups were tested for their abilities to remember the associated words 12 hours after learning the list. No one in the study was sleep deprived, but the subjects in two groups slept before testing and those in the other two groups did not.

The individuals who slept remembered 94% of the associations; those who did not sleep remembered 82% of the words. Those differences fell just short of statistical significance (P = .06).

The differences were marked, however, in the remaining two groups subjected to associative interference. For this part of the study, both groups also learned the same list of 20 word associations.

Again, one group slept and the other did not, and both groups were tested at 12 hours. But 12 minutes before they were tested on the list of words, both groups were subjected to associative interference. They were asked to learn a second list of 20 additional words related to the same word cues. Subjects who had slept and were introduced to the second list of words were able to recall 76% of the word associations from the first list. The subjects who had not slept were able to remember just 32% of the words. The difference in performance was highly significant (P less than .0001).

Sleep is ultimately a brain state that may hold the keys to understanding the neurobiology of memory consolidation, he said. The next step in his research will be to look at the relationships between sleep disorders, cognitive impairment, and neurologic disorders. Dr. Ellenbogen's research was supported by the National Institutes of Health and the University of Pennsylvania's Nassau Undergraduate Research Fund.

BOSTON – Sleep strengthens declarative memory, a finding that could one day be exploited to combat cognitive declines associated with dementia and neurologic disorders, Dr. Jeffrey M. Ellenbogen reported at the annual meeting of the American Academy of Neurology.

Sleep previously has been shown to improve motor, visual, and perceptual memories in humans, but this study is one of the first to substantiate a role for sleep in protecting declarative or consciously discussed memories from associative interference, said Dr. Ellenbogen of Harvard Medical School, Boston.

For the study, 48 healthy individuals, aged 18–30 years, were evaluated. No participants took any medications, and all had normal sleep patterns. Subjects were placed in one of four groups, and all were asked to remember 20 words, each of which was paired with an associated word cue.

All groups were tested for their abilities to remember the associated words 12 hours after learning the list. No one in the study was sleep deprived, but the subjects in two groups slept before testing and those in the other two groups did not.

The individuals who slept remembered 94% of the associations; those who did not sleep remembered 82% of the words. Those differences fell just short of statistical significance (P = .06).

The differences were marked, however, in the remaining two groups subjected to associative interference. For this part of the study, both groups also learned the same list of 20 word associations.

Again, one group slept and the other did not, and both groups were tested at 12 hours. But 12 minutes before they were tested on the list of words, both groups were subjected to associative interference. They were asked to learn a second list of 20 additional words related to the same word cues. Subjects who had slept and were introduced to the second list of words were able to recall 76% of the word associations from the first list. The subjects who had not slept were able to remember just 32% of the words. The difference in performance was highly significant (P less than .0001).

Sleep is ultimately a brain state that may hold the keys to understanding the neurobiology of memory consolidation, he said. The next step in his research will be to look at the relationships between sleep disorders, cognitive impairment, and neurologic disorders. Dr. Ellenbogen's research was supported by the National Institutes of Health and the University of Pennsylvania's Nassau Undergraduate Research Fund.

BOSTON – Sleep strengthens declarative memory, a finding that could one day be exploited to combat cognitive declines associated with dementia and neurologic disorders, Dr. Jeffrey M. Ellenbogen reported at the annual meeting of the American Academy of Neurology.

Sleep previously has been shown to improve motor, visual, and perceptual memories in humans, but this study is one of the first to substantiate a role for sleep in protecting declarative or consciously discussed memories from associative interference, said Dr. Ellenbogen of Harvard Medical School, Boston.

For the study, 48 healthy individuals, aged 18–30 years, were evaluated. No participants took any medications, and all had normal sleep patterns. Subjects were placed in one of four groups, and all were asked to remember 20 words, each of which was paired with an associated word cue.

All groups were tested for their abilities to remember the associated words 12 hours after learning the list. No one in the study was sleep deprived, but the subjects in two groups slept before testing and those in the other two groups did not.

The individuals who slept remembered 94% of the associations; those who did not sleep remembered 82% of the words. Those differences fell just short of statistical significance (P = .06).

The differences were marked, however, in the remaining two groups subjected to associative interference. For this part of the study, both groups also learned the same list of 20 word associations.

Again, one group slept and the other did not, and both groups were tested at 12 hours. But 12 minutes before they were tested on the list of words, both groups were subjected to associative interference. They were asked to learn a second list of 20 additional words related to the same word cues. Subjects who had slept and were introduced to the second list of words were able to recall 76% of the word associations from the first list. The subjects who had not slept were able to remember just 32% of the words. The difference in performance was highly significant (P less than .0001).

Sleep is ultimately a brain state that may hold the keys to understanding the neurobiology of memory consolidation, he said. The next step in his research will be to look at the relationships between sleep disorders, cognitive impairment, and neurologic disorders. Dr. Ellenbogen's research was supported by the National Institutes of Health and the University of Pennsylvania's Nassau Undergraduate Research Fund.

WASHINGTON – Prompt, short-term treatment with antidepressants is associated with significantly improved physical, cognitive, and survival outcomes in stroke patients–regardless of whether they have symptoms of depression, Dr. Robert Robinson said at the annual meeting of the American Academy of Clinical Psychiatrists.

“Perhaps all patients who suffer a stroke should be evaluated by a psychiatrist and treated with antidepressants, because [these drugs] appear to improve their recovery,” said Dr. Robinson, who serves on the speakers' bureau for Forest Laboratories Inc. He also serves as a consultant for Hamilton Pharmaceuticals Inc. and Avanir Pharmaceuticals.

Data from recent studies have shown that antidepressants have beneficial effects on physical and cognitive recovery (as well as on mortality) after a stroke and that these effects may last for several years, said Dr. Robinson, professor and head of the department of psychiatry at the University of Iowa, Iowa City.

Dr. Robinson shared data that he collected in collaboration with his colleague at the university, Dr. Kenji Narushima, on 34 stroke patients who were treated with nortriptyline, fluoxetine, or a placebo starting within a month of having a stroke (average of 19 days after the stroke) and 28 patients who began treatment more than a month after the stroke (J. Nerv. Ment. Dis. 2003;191:645–52).

The nortriptyline doses were 25 mg/day for the first week, which then was increased to 50 mg/day for weeks 2–3, 75 mg/day for weeks 4–6, and 100 mg/day for the final 6 weeks.

The fluoxetine dosage started at 10 mg/day for the first 3 weeks, which then was increased to 20 mg/day for weeks 4–6, 30 mg/day for weeks 7–9, and 40 mg/day for the final 3 weeks, the investigators reported.

The patients who were treated early had a significantly better recovery in activities of daily living than did those who were treated later, even after a logistic regression analysis controlled for several factors, including existing depression, motor impairment, and psychiatric history. The finding suggests that patients who are given antidepressants–whether they are depressed or not–within the first month after a stroke recover better than if they are given antidepressants at a later date, Dr. Robinson said.

Similarly, a study of cognitive outcomes based on executive function tests showed that patients who were treated with antidepressants within a month of a stroke scored significantly higher at 21 months' follow-up, compared with patients who received a placebo.

The improvements were independent of any diagnosis of depression at the start of treatment.

Not all patients respond to antidepressant medication, but those who do seem to gain a cognitive effect that lasts, Dr. Robinson said.

Stroke patients who receive antidepressants also tend to live longer.

Dr. Robinson cited results from a randomized study of 104 stroke patients on which he was a coinvestigator. The patients received 12 weeks of either nortriptyline or a placebo, and 68% of the nortriptyline patients were alive after 9 years, compared with 36% of placebo patients.

Interestingly, the placebo patients were significantly more likely to have died of cardiovascular events, while the patients who took antidepressants were more likely to have died from other causes (Am. J. Psychiatry 2003;160:1823–9).

The long-term benefits from only 12 weeks of antidepressant therapy are remarkable, Dr. Robinson said, although the mechanism of action that drives the benefits remains uncertain.

One possible explanation for the long-term effect is that the antidepressants foster nerve growth, and the growth of new nerves may protect against a future stroke. “But where the neurogenesis is occurring is something that is a particularly intriguing question,” Dr. Robinson said. Neurogenesis may be involved in a neurophysiologic mechanism that turns on or off for extended periods of time in response to antidepressants, but more research is needed, he said.

“A major goal of clinical psychiatry is to see how our treatments affect outcome,” he added.

Antidepressants foster nerve growth, and growth of new nerves may protect against a future stroke. DR. ROBINSON

ELSEVIER GLOBAL MEDICAL NEWS

WASHINGTON – Prompt, short-term treatment with antidepressants is associated with significantly improved physical, cognitive, and survival outcomes in stroke patients–regardless of whether they have symptoms of depression, Dr. Robert Robinson said at the annual meeting of the American Academy of Clinical Psychiatrists.

“Perhaps all patients who suffer a stroke should be evaluated by a psychiatrist and treated with antidepressants, because [these drugs] appear to improve their recovery,” said Dr. Robinson, who serves on the speakers' bureau for Forest Laboratories Inc. He also serves as a consultant for Hamilton Pharmaceuticals Inc. and Avanir Pharmaceuticals.

Data from recent studies have shown that antidepressants have beneficial effects on physical and cognitive recovery (as well as on mortality) after a stroke and that these effects may last for several years, said Dr. Robinson, professor and head of the department of psychiatry at the University of Iowa, Iowa City.

Dr. Robinson shared data that he collected in collaboration with his colleague at the university, Dr. Kenji Narushima, on 34 stroke patients who were treated with nortriptyline, fluoxetine, or a placebo starting within a month of having a stroke (average of 19 days after the stroke) and 28 patients who began treatment more than a month after the stroke (J. Nerv. Ment. Dis. 2003;191:645–52).

The nortriptyline doses were 25 mg/day for the first week, which then was increased to 50 mg/day for weeks 2–3, 75 mg/day for weeks 4–6, and 100 mg/day for the final 6 weeks.

The fluoxetine dosage started at 10 mg/day for the first 3 weeks, which then was increased to 20 mg/day for weeks 4–6, 30 mg/day for weeks 7–9, and 40 mg/day for the final 3 weeks, the investigators reported.

The patients who were treated early had a significantly better recovery in activities of daily living than did those who were treated later, even after a logistic regression analysis controlled for several factors, including existing depression, motor impairment, and psychiatric history. The finding suggests that patients who are given antidepressants–whether they are depressed or not–within the first month after a stroke recover better than if they are given antidepressants at a later date, Dr. Robinson said.

Similarly, a study of cognitive outcomes based on executive function tests showed that patients who were treated with antidepressants within a month of a stroke scored significantly higher at 21 months' follow-up, compared with patients who received a placebo.

The improvements were independent of any diagnosis of depression at the start of treatment.

Not all patients respond to antidepressant medication, but those who do seem to gain a cognitive effect that lasts, Dr. Robinson said.

Stroke patients who receive antidepressants also tend to live longer.

Dr. Robinson cited results from a randomized study of 104 stroke patients on which he was a coinvestigator. The patients received 12 weeks of either nortriptyline or a placebo, and 68% of the nortriptyline patients were alive after 9 years, compared with 36% of placebo patients.

Interestingly, the placebo patients were significantly more likely to have died of cardiovascular events, while the patients who took antidepressants were more likely to have died from other causes (Am. J. Psychiatry 2003;160:1823–9).

The long-term benefits from only 12 weeks of antidepressant therapy are remarkable, Dr. Robinson said, although the mechanism of action that drives the benefits remains uncertain.

One possible explanation for the long-term effect is that the antidepressants foster nerve growth, and the growth of new nerves may protect against a future stroke. “But where the neurogenesis is occurring is something that is a particularly intriguing question,” Dr. Robinson said. Neurogenesis may be involved in a neurophysiologic mechanism that turns on or off for extended periods of time in response to antidepressants, but more research is needed, he said.

“A major goal of clinical psychiatry is to see how our treatments affect outcome,” he added.

Antidepressants foster nerve growth, and growth of new nerves may protect against a future stroke. DR. ROBINSON

ELSEVIER GLOBAL MEDICAL NEWS

WASHINGTON – Prompt, short-term treatment with antidepressants is associated with significantly improved physical, cognitive, and survival outcomes in stroke patients–regardless of whether they have symptoms of depression, Dr. Robert Robinson said at the annual meeting of the American Academy of Clinical Psychiatrists.

“Perhaps all patients who suffer a stroke should be evaluated by a psychiatrist and treated with antidepressants, because [these drugs] appear to improve their recovery,” said Dr. Robinson, who serves on the speakers' bureau for Forest Laboratories Inc. He also serves as a consultant for Hamilton Pharmaceuticals Inc. and Avanir Pharmaceuticals.

Data from recent studies have shown that antidepressants have beneficial effects on physical and cognitive recovery (as well as on mortality) after a stroke and that these effects may last for several years, said Dr. Robinson, professor and head of the department of psychiatry at the University of Iowa, Iowa City.

Dr. Robinson shared data that he collected in collaboration with his colleague at the university, Dr. Kenji Narushima, on 34 stroke patients who were treated with nortriptyline, fluoxetine, or a placebo starting within a month of having a stroke (average of 19 days after the stroke) and 28 patients who began treatment more than a month after the stroke (J. Nerv. Ment. Dis. 2003;191:645–52).

The nortriptyline doses were 25 mg/day for the first week, which then was increased to 50 mg/day for weeks 2–3, 75 mg/day for weeks 4–6, and 100 mg/day for the final 6 weeks.

The fluoxetine dosage started at 10 mg/day for the first 3 weeks, which then was increased to 20 mg/day for weeks 4–6, 30 mg/day for weeks 7–9, and 40 mg/day for the final 3 weeks, the investigators reported.

The patients who were treated early had a significantly better recovery in activities of daily living than did those who were treated later, even after a logistic regression analysis controlled for several factors, including existing depression, motor impairment, and psychiatric history. The finding suggests that patients who are given antidepressants–whether they are depressed or not–within the first month after a stroke recover better than if they are given antidepressants at a later date, Dr. Robinson said.

Similarly, a study of cognitive outcomes based on executive function tests showed that patients who were treated with antidepressants within a month of a stroke scored significantly higher at 21 months' follow-up, compared with patients who received a placebo.

The improvements were independent of any diagnosis of depression at the start of treatment.

Not all patients respond to antidepressant medication, but those who do seem to gain a cognitive effect that lasts, Dr. Robinson said.

Stroke patients who receive antidepressants also tend to live longer.

Dr. Robinson cited results from a randomized study of 104 stroke patients on which he was a coinvestigator. The patients received 12 weeks of either nortriptyline or a placebo, and 68% of the nortriptyline patients were alive after 9 years, compared with 36% of placebo patients.

Interestingly, the placebo patients were significantly more likely to have died of cardiovascular events, while the patients who took antidepressants were more likely to have died from other causes (Am. J. Psychiatry 2003;160:1823–9).

The long-term benefits from only 12 weeks of antidepressant therapy are remarkable, Dr. Robinson said, although the mechanism of action that drives the benefits remains uncertain.

One possible explanation for the long-term effect is that the antidepressants foster nerve growth, and the growth of new nerves may protect against a future stroke. “But where the neurogenesis is occurring is something that is a particularly intriguing question,” Dr. Robinson said. Neurogenesis may be involved in a neurophysiologic mechanism that turns on or off for extended periods of time in response to antidepressants, but more research is needed, he said.

“A major goal of clinical psychiatry is to see how our treatments affect outcome,” he added.

Antidepressants foster nerve growth, and growth of new nerves may protect against a future stroke. DR. ROBINSON

ELSEVIER GLOBAL MEDICAL NEWS

MIAMI BEACH – Comorbid psychiatric conditions are common in patients with headache disorders, and can adversely affect the prognosis in patients with such disorders, Alvin E. Lake III, Ph.D., said at a symposium sponsored by the American Headache Society.

However, combined behavioral and drug therapy as well as patient education have been shown to improve outcomes, said Dr. Lake, director of the behavioral medicine division at the Michigan Headache and Neurological Institute, Ann Arbor.

Studies suggest that close to 50% of patients with chronic daily headache have an anxiety and/or mood disorder. In those with medication overuse headaches, the prevalence of mood and anxiety disorders appears to be even higher at 68%, according to one study.

Headache patients with psychiatric disorders also appear to have poorer long-term outcomes than do those with no psychiatric disorder. In one study, 57% of patients with multiple psychiatric disorders had worsening of their headaches over an 8-year period, compared with 7% of those with no psychiatric disorder. In addition, 29% of those with multiple psychiatric disorders experienced improvement, compared with 53% of those with no psychiatric disorder.

It appears that in most cases, the psychiatric disorders preceded the headache disorders. In a study of 41 patients with medication overuse headaches and comorbid psychiatric disorders, the psychiatric disorder preceded the headaches in 76% of those with a major depressive episode, 79% of those with panic disorder, 80% of those with generalized anxiety disorder, 89% of those with substance abuse disorder, and 100% of those with social phobia, Dr. Lake noted.

In addition to mood disorders, which have a genetic component, psychological factors, such as anticipatory fear of pain, and psychosocial factors, such as family and work pressures and a need to function, can drive excessive use of preemptive treatment, which in turn can lead to headache chronicity, he explained.

In one study of headache patients, the use of analgesics at initial assessment was associated with a relative risk of 19.6 for chronic daily headaches at 11-year follow-up, compared with a relative risk of 3.1 in those without analgesic overuse. Daily or weekly analgesic use also elevated the risk for chronic pain; in those who used analgesics more than 15 days per month, the relative risk of chronic migraine was 13.3 and the relative risk of nonmigraine headache was 6.2, compared with those without analgesic overuse.

Differential attention to the headache pain has been shown to modulate the subjective experience of pain, Dr. Lake said.

For example, attention to pain location increases responses in the somatosensory cortex, while attention to the unpleasantness of the pain increases responses in the limbic system.

Distraction, such as activities that divert attention away from the pain, can lower pain intensity and increase brain stem periaqueductal gray activation, which has been shown to predict changes in perceived pain intensity.

Thus, behavioral therapy is useful in this patient population. Several studies demonstrate improved outcomes with combined treatment.

For example, in one study of patients with chronic tension headaches, 64% of patients who received tricyclic antidepressants as well as stress management training had improvement at 8 months, compared with 29% of placebo patients, 38% of those on tricyclic antidepressants alone, and 35% who received stress management training alone.

In another study of patients with medication overuse headaches, headache days per month were reduced at 3 years' follow-up from 30 to 11 days in patients who received inpatient pharmacologic therapy and biofeedback-assisted relaxation training, compared with a reduction from 30 to 18 days in those who received only inpatient pharmacologic therapy.

Analgesic doses per month were reduced from 59 to 4 doses in the combination treatment group, compared with a reduction from 59 to 20 doses in those with preventive medication treatment alone. The relapse rate to medication overuse headaches was 13% in the combination treatment group, compared with 42% in the medication-only group.

Patient education has also been shown to be of benefit, Dr. Lake said.

A study published in May 2006 showed that patients who attended three 90-minute educational sessions taught by intensively trained lay migraineurs was useful for improving outcomes and reducing analgesic overuse (Headache 2006;46:726–31).

Of 100 consecutive migraine patients who received routine medical management and were randomly assigned to attend or not attend the classes–which offered information on migraine pathogenesis, management, and risks of rebound–those who attended had a significantly greater reduction in mean migraine disability assessment scores (reduction of 24 vs. 14 points) at 6 months.

They also had fewer headache days per month, less headache-related dysfunction, less abortive medication use, less analgesic overuse, and fewer headache-related phone calls and unscheduled visits to doctors, Dr. Lake said.

MIAMI BEACH – Comorbid psychiatric conditions are common in patients with headache disorders, and can adversely affect the prognosis in patients with such disorders, Alvin E. Lake III, Ph.D., said at a symposium sponsored by the American Headache Society.

However, combined behavioral and drug therapy as well as patient education have been shown to improve outcomes, said Dr. Lake, director of the behavioral medicine division at the Michigan Headache and Neurological Institute, Ann Arbor.

Studies suggest that close to 50% of patients with chronic daily headache have an anxiety and/or mood disorder. In those with medication overuse headaches, the prevalence of mood and anxiety disorders appears to be even higher at 68%, according to one study.

Headache patients with psychiatric disorders also appear to have poorer long-term outcomes than do those with no psychiatric disorder. In one study, 57% of patients with multiple psychiatric disorders had worsening of their headaches over an 8-year period, compared with 7% of those with no psychiatric disorder. In addition, 29% of those with multiple psychiatric disorders experienced improvement, compared with 53% of those with no psychiatric disorder.

It appears that in most cases, the psychiatric disorders preceded the headache disorders. In a study of 41 patients with medication overuse headaches and comorbid psychiatric disorders, the psychiatric disorder preceded the headaches in 76% of those with a major depressive episode, 79% of those with panic disorder, 80% of those with generalized anxiety disorder, 89% of those with substance abuse disorder, and 100% of those with social phobia, Dr. Lake noted.

In addition to mood disorders, which have a genetic component, psychological factors, such as anticipatory fear of pain, and psychosocial factors, such as family and work pressures and a need to function, can drive excessive use of preemptive treatment, which in turn can lead to headache chronicity, he explained.

In one study of headache patients, the use of analgesics at initial assessment was associated with a relative risk of 19.6 for chronic daily headaches at 11-year follow-up, compared with a relative risk of 3.1 in those without analgesic overuse. Daily or weekly analgesic use also elevated the risk for chronic pain; in those who used analgesics more than 15 days per month, the relative risk of chronic migraine was 13.3 and the relative risk of nonmigraine headache was 6.2, compared with those without analgesic overuse.

Differential attention to the headache pain has been shown to modulate the subjective experience of pain, Dr. Lake said.

For example, attention to pain location increases responses in the somatosensory cortex, while attention to the unpleasantness of the pain increases responses in the limbic system.

Distraction, such as activities that divert attention away from the pain, can lower pain intensity and increase brain stem periaqueductal gray activation, which has been shown to predict changes in perceived pain intensity.

Thus, behavioral therapy is useful in this patient population. Several studies demonstrate improved outcomes with combined treatment.

For example, in one study of patients with chronic tension headaches, 64% of patients who received tricyclic antidepressants as well as stress management training had improvement at 8 months, compared with 29% of placebo patients, 38% of those on tricyclic antidepressants alone, and 35% who received stress management training alone.

In another study of patients with medication overuse headaches, headache days per month were reduced at 3 years' follow-up from 30 to 11 days in patients who received inpatient pharmacologic therapy and biofeedback-assisted relaxation training, compared with a reduction from 30 to 18 days in those who received only inpatient pharmacologic therapy.

Analgesic doses per month were reduced from 59 to 4 doses in the combination treatment group, compared with a reduction from 59 to 20 doses in those with preventive medication treatment alone. The relapse rate to medication overuse headaches was 13% in the combination treatment group, compared with 42% in the medication-only group.

Patient education has also been shown to be of benefit, Dr. Lake said.

A study published in May 2006 showed that patients who attended three 90-minute educational sessions taught by intensively trained lay migraineurs was useful for improving outcomes and reducing analgesic overuse (Headache 2006;46:726–31).

Of 100 consecutive migraine patients who received routine medical management and were randomly assigned to attend or not attend the classes–which offered information on migraine pathogenesis, management, and risks of rebound–those who attended had a significantly greater reduction in mean migraine disability assessment scores (reduction of 24 vs. 14 points) at 6 months.

They also had fewer headache days per month, less headache-related dysfunction, less abortive medication use, less analgesic overuse, and fewer headache-related phone calls and unscheduled visits to doctors, Dr. Lake said.

MIAMI BEACH – Comorbid psychiatric conditions are common in patients with headache disorders, and can adversely affect the prognosis in patients with such disorders, Alvin E. Lake III, Ph.D., said at a symposium sponsored by the American Headache Society.

However, combined behavioral and drug therapy as well as patient education have been shown to improve outcomes, said Dr. Lake, director of the behavioral medicine division at the Michigan Headache and Neurological Institute, Ann Arbor.

Studies suggest that close to 50% of patients with chronic daily headache have an anxiety and/or mood disorder. In those with medication overuse headaches, the prevalence of mood and anxiety disorders appears to be even higher at 68%, according to one study.

Headache patients with psychiatric disorders also appear to have poorer long-term outcomes than do those with no psychiatric disorder. In one study, 57% of patients with multiple psychiatric disorders had worsening of their headaches over an 8-year period, compared with 7% of those with no psychiatric disorder. In addition, 29% of those with multiple psychiatric disorders experienced improvement, compared with 53% of those with no psychiatric disorder.

It appears that in most cases, the psychiatric disorders preceded the headache disorders. In a study of 41 patients with medication overuse headaches and comorbid psychiatric disorders, the psychiatric disorder preceded the headaches in 76% of those with a major depressive episode, 79% of those with panic disorder, 80% of those with generalized anxiety disorder, 89% of those with substance abuse disorder, and 100% of those with social phobia, Dr. Lake noted.

In addition to mood disorders, which have a genetic component, psychological factors, such as anticipatory fear of pain, and psychosocial factors, such as family and work pressures and a need to function, can drive excessive use of preemptive treatment, which in turn can lead to headache chronicity, he explained.

In one study of headache patients, the use of analgesics at initial assessment was associated with a relative risk of 19.6 for chronic daily headaches at 11-year follow-up, compared with a relative risk of 3.1 in those without analgesic overuse. Daily or weekly analgesic use also elevated the risk for chronic pain; in those who used analgesics more than 15 days per month, the relative risk of chronic migraine was 13.3 and the relative risk of nonmigraine headache was 6.2, compared with those without analgesic overuse.

Differential attention to the headache pain has been shown to modulate the subjective experience of pain, Dr. Lake said.

For example, attention to pain location increases responses in the somatosensory cortex, while attention to the unpleasantness of the pain increases responses in the limbic system.

Distraction, such as activities that divert attention away from the pain, can lower pain intensity and increase brain stem periaqueductal gray activation, which has been shown to predict changes in perceived pain intensity.

Thus, behavioral therapy is useful in this patient population. Several studies demonstrate improved outcomes with combined treatment.

For example, in one study of patients with chronic tension headaches, 64% of patients who received tricyclic antidepressants as well as stress management training had improvement at 8 months, compared with 29% of placebo patients, 38% of those on tricyclic antidepressants alone, and 35% who received stress management training alone.

In another study of patients with medication overuse headaches, headache days per month were reduced at 3 years' follow-up from 30 to 11 days in patients who received inpatient pharmacologic therapy and biofeedback-assisted relaxation training, compared with a reduction from 30 to 18 days in those who received only inpatient pharmacologic therapy.

Analgesic doses per month were reduced from 59 to 4 doses in the combination treatment group, compared with a reduction from 59 to 20 doses in those with preventive medication treatment alone. The relapse rate to medication overuse headaches was 13% in the combination treatment group, compared with 42% in the medication-only group.

Patient education has also been shown to be of benefit, Dr. Lake said.

A study published in May 2006 showed that patients who attended three 90-minute educational sessions taught by intensively trained lay migraineurs was useful for improving outcomes and reducing analgesic overuse (Headache 2006;46:726–31).

Of 100 consecutive migraine patients who received routine medical management and were randomly assigned to attend or not attend the classes–which offered information on migraine pathogenesis, management, and risks of rebound–those who attended had a significantly greater reduction in mean migraine disability assessment scores (reduction of 24 vs. 14 points) at 6 months.

They also had fewer headache days per month, less headache-related dysfunction, less abortive medication use, less analgesic overuse, and fewer headache-related phone calls and unscheduled visits to doctors, Dr. Lake said.

TAMPA – Anorexia nervosa reduces bone mass and puts young women at risk for early onset of osteoporosis, just at the time when they should be building peak bone mass, Dr. Steven Crawford said at the annual meeting of the International Society for Clinical Densitometry.

Anorexia nervosa is one of the most common psychiatric diagnoses in adolescent women, with the age of onset showing bimodal peaks at age 14 and 18 years.

Health consequences can be severe. In addition to loss of bone density, patients can suffer cardiovascular problems, muscle loss and weakness, severe dehydration, anemia, and leukopenia. Female patients with anorexia nervosa are amenorrheic. Anorexia nervosa leads to a sevenfold increase in fracture risk. Of adult women with anorexia nervosa, 38% have osteoporosis, and 50% have a bone mineral density (BMD) level below the fracture threshold.

The extent of bone damage is directly affected by the severity of malnutrition and the disease duration. Consequences are more severe when disease onset occurs during the time of peak bone development. Approximately 60% of total bone mass is attained in the growth spurt that normally occurs in adolescence, and skeletal growth essentially is complete by age 18.

“Bone mineral density is lower when anorexia nervosa begins in adolescence than when it occurs in adult life, even when the duration of illness is comparable,” said Dr. Crawford, a clinical psychiatrist at the Center for Eating Disorders, Sheppard Pratt Health System, Baltimore.

Pathophysiology of low bone density in anorexia nervosa results from multiple factors, including undernutrition, hypogonadism, altered levels of bone-essential hormones and growth factors, excessive exercise, and hypercortisolism, among others. Undernutrition in anorexia nervosa leads to decreased levels of the sex hormones critical for bone development.

Low BMD occurs at all skeletal sites in patients with anorexia nervosa, affecting both trabecular and cortical bone. The spine is more likely to be affected than the hip, said Dr. Crawford.

In addition to decreased BMD, another factor that contributes to bone fragility in patients with anorexia nervosa is decreased bone size. Patients with anorexia nervosa develop smaller bones in the vertebral body and femoral neck, compared with normal patients. Consequences of osteoporosis in anorexic patients are stress fractures in weight-bearing bones, and vertebral fractures leading to chronic back pain and reduced height.

Dr. Crawford recommends a routine bone density scan in all patients with anorexia nervosa at disease onset and at least every 2 years thereafter. Restoration of normal weight can improve BMD in anorexic patients, but bone loss may continue, with bone restoration taking at least 21 months. “Overall, data [suggest] despite improvement there are permanent deficits in BMD, underscoring the importance of timely diagnosis and treatment,” she said.

Bisphosphonates are not approved for treatment of premenopausal women. Moreover, the increased bone turnover that occurs normally during adolescence makes the use of bisphosphonates especially controversial for patients in that age group.

Although adequate calcium and vitamin D intake should be provided to patients with anorexia nervosa, supplementation with calcium and vitamin does not increase BMD in anorexic patients. Some evidence suggests that a combination of twice-daily IGF-I administration and estrogen-progesterone treatment may be effective in increasing BMD in anorexic women. Androgen replacement studies have shown conflicting results.

Normally, patients with osteoporosis are advised to engage in weight-bearing exercise such as walking, stair climbing, and weight lifting. However, for patients with anorexia nervosa, the potential benefits of exercise might be offset by the risk of fractures, delayed weight gain, and exercise-induced amenorrhea.

'Bone mineral density is lower when anorexia nervosa begins in adolescence than when it occurs in adult life.' DR. CRAWFORD

TAMPA – Anorexia nervosa reduces bone mass and puts young women at risk for early onset of osteoporosis, just at the time when they should be building peak bone mass, Dr. Steven Crawford said at the annual meeting of the International Society for Clinical Densitometry.

Anorexia nervosa is one of the most common psychiatric diagnoses in adolescent women, with the age of onset showing bimodal peaks at age 14 and 18 years.

Health consequences can be severe. In addition to loss of bone density, patients can suffer cardiovascular problems, muscle loss and weakness, severe dehydration, anemia, and leukopenia. Female patients with anorexia nervosa are amenorrheic. Anorexia nervosa leads to a sevenfold increase in fracture risk. Of adult women with anorexia nervosa, 38% have osteoporosis, and 50% have a bone mineral density (BMD) level below the fracture threshold.

The extent of bone damage is directly affected by the severity of malnutrition and the disease duration. Consequences are more severe when disease onset occurs during the time of peak bone development. Approximately 60% of total bone mass is attained in the growth spurt that normally occurs in adolescence, and skeletal growth essentially is complete by age 18.

“Bone mineral density is lower when anorexia nervosa begins in adolescence than when it occurs in adult life, even when the duration of illness is comparable,” said Dr. Crawford, a clinical psychiatrist at the Center for Eating Disorders, Sheppard Pratt Health System, Baltimore.

Pathophysiology of low bone density in anorexia nervosa results from multiple factors, including undernutrition, hypogonadism, altered levels of bone-essential hormones and growth factors, excessive exercise, and hypercortisolism, among others. Undernutrition in anorexia nervosa leads to decreased levels of the sex hormones critical for bone development.

Low BMD occurs at all skeletal sites in patients with anorexia nervosa, affecting both trabecular and cortical bone. The spine is more likely to be affected than the hip, said Dr. Crawford.

In addition to decreased BMD, another factor that contributes to bone fragility in patients with anorexia nervosa is decreased bone size. Patients with anorexia nervosa develop smaller bones in the vertebral body and femoral neck, compared with normal patients. Consequences of osteoporosis in anorexic patients are stress fractures in weight-bearing bones, and vertebral fractures leading to chronic back pain and reduced height.

Dr. Crawford recommends a routine bone density scan in all patients with anorexia nervosa at disease onset and at least every 2 years thereafter. Restoration of normal weight can improve BMD in anorexic patients, but bone loss may continue, with bone restoration taking at least 21 months. “Overall, data [suggest] despite improvement there are permanent deficits in BMD, underscoring the importance of timely diagnosis and treatment,” she said.

Bisphosphonates are not approved for treatment of premenopausal women. Moreover, the increased bone turnover that occurs normally during adolescence makes the use of bisphosphonates especially controversial for patients in that age group.

Although adequate calcium and vitamin D intake should be provided to patients with anorexia nervosa, supplementation with calcium and vitamin does not increase BMD in anorexic patients. Some evidence suggests that a combination of twice-daily IGF-I administration and estrogen-progesterone treatment may be effective in increasing BMD in anorexic women. Androgen replacement studies have shown conflicting results.

Normally, patients with osteoporosis are advised to engage in weight-bearing exercise such as walking, stair climbing, and weight lifting. However, for patients with anorexia nervosa, the potential benefits of exercise might be offset by the risk of fractures, delayed weight gain, and exercise-induced amenorrhea.

'Bone mineral density is lower when anorexia nervosa begins in adolescence than when it occurs in adult life.' DR. CRAWFORD

TAMPA – Anorexia nervosa reduces bone mass and puts young women at risk for early onset of osteoporosis, just at the time when they should be building peak bone mass, Dr. Steven Crawford said at the annual meeting of the International Society for Clinical Densitometry.

Anorexia nervosa is one of the most common psychiatric diagnoses in adolescent women, with the age of onset showing bimodal peaks at age 14 and 18 years.

Health consequences can be severe. In addition to loss of bone density, patients can suffer cardiovascular problems, muscle loss and weakness, severe dehydration, anemia, and leukopenia. Female patients with anorexia nervosa are amenorrheic. Anorexia nervosa leads to a sevenfold increase in fracture risk. Of adult women with anorexia nervosa, 38% have osteoporosis, and 50% have a bone mineral density (BMD) level below the fracture threshold.

The extent of bone damage is directly affected by the severity of malnutrition and the disease duration. Consequences are more severe when disease onset occurs during the time of peak bone development. Approximately 60% of total bone mass is attained in the growth spurt that normally occurs in adolescence, and skeletal growth essentially is complete by age 18.

“Bone mineral density is lower when anorexia nervosa begins in adolescence than when it occurs in adult life, even when the duration of illness is comparable,” said Dr. Crawford, a clinical psychiatrist at the Center for Eating Disorders, Sheppard Pratt Health System, Baltimore.

Pathophysiology of low bone density in anorexia nervosa results from multiple factors, including undernutrition, hypogonadism, altered levels of bone-essential hormones and growth factors, excessive exercise, and hypercortisolism, among others. Undernutrition in anorexia nervosa leads to decreased levels of the sex hormones critical for bone development.

Low BMD occurs at all skeletal sites in patients with anorexia nervosa, affecting both trabecular and cortical bone. The spine is more likely to be affected than the hip, said Dr. Crawford.

In addition to decreased BMD, another factor that contributes to bone fragility in patients with anorexia nervosa is decreased bone size. Patients with anorexia nervosa develop smaller bones in the vertebral body and femoral neck, compared with normal patients. Consequences of osteoporosis in anorexic patients are stress fractures in weight-bearing bones, and vertebral fractures leading to chronic back pain and reduced height.

Dr. Crawford recommends a routine bone density scan in all patients with anorexia nervosa at disease onset and at least every 2 years thereafter. Restoration of normal weight can improve BMD in anorexic patients, but bone loss may continue, with bone restoration taking at least 21 months. “Overall, data [suggest] despite improvement there are permanent deficits in BMD, underscoring the importance of timely diagnosis and treatment,” she said.

Bisphosphonates are not approved for treatment of premenopausal women. Moreover, the increased bone turnover that occurs normally during adolescence makes the use of bisphosphonates especially controversial for patients in that age group.

Although adequate calcium and vitamin D intake should be provided to patients with anorexia nervosa, supplementation with calcium and vitamin does not increase BMD in anorexic patients. Some evidence suggests that a combination of twice-daily IGF-I administration and estrogen-progesterone treatment may be effective in increasing BMD in anorexic women. Androgen replacement studies have shown conflicting results.

Normally, patients with osteoporosis are advised to engage in weight-bearing exercise such as walking, stair climbing, and weight lifting. However, for patients with anorexia nervosa, the potential benefits of exercise might be offset by the risk of fractures, delayed weight gain, and exercise-induced amenorrhea.

'Bone mineral density is lower when anorexia nervosa begins in adolescence than when it occurs in adult life.' DR. CRAWFORD

WASHINGTON – Many fibromyalgia patients could benefit from the care and expertise provided by psychiatrists, Dr. Lesley M. Arnold said at the annual meeting of the American Academy of Clinical Psychiatrists.

Psychiatrists are in a position to evaluate fibromyalgia patients for psychiatric comorbidities and consider prescribing antidepressants as part of a treatment plan, said Dr. Arnold, associate professor of psychiatry at the University of Cincinnati.

Tricyclics have been shown to reduce chronic pain independent of any effects on the patient's mood, which suggests a common neurochemical channel for persistent pain and psychiatric conditions that remains unexplored, she said.

Consequently, fibromyalgia patients might benefit from a multidisciplinary approach, said Dr. Arnold, who has received grants and research support from several pharmaceutical companies, including Eli Lilly, Pfizer, and Cypress Bioscience. She also has served as a consultant for these and other pharmaceutical companies.

The American College of Rheumatology criteria for fibromyalgia include chronic widespread pain of more than 3 months' duration and pain in at least 11 of 18 pressure point areas of the body. Patients must report pain with about 4 kg of pressure (enough to blanch your thumb when you press on the area).

But the muscular criteria are only part of the disorder. Patients with fibromyalgia may have hyperalgesia throughout the body rather than at specific points, and patients who do not report pressure on at least 11 of the 18 tender points will often report other symptoms of fibromyalgia, including debilitating fatigue, Dr. Arnold said.

“Fatigue really knocks people out, and that impairs their function more than the pain,” she commented. Fibromyalgia patients also report difficulty falling asleep, difficulty staying asleep, and unrefreshing sleep.

Patients with fibromyalgia report depression and anxiety symptoms, too. The fibromyalgia literature suggests that about one-third of patients with a fibromyalgia diagnosis have a comorbid psychiatric condition, which contributes to the rationale for treating fibromyalgia patients with antidepressants, Dr. Arnold said.

To further assess the relationship between psychiatric comorbidity and fibromyalgia, Dr. Arnold and colleagues conducted a family study. They recruited 78 patients with fibromyalgia and 533 of their relatives, and compared the prevalence of mood disorders between this population and 40 patients with rheumatoid arthritis and 272 of their relatives (Arthritis Rheum. 2004;50;944–52).

“Mood disorders were much more common in the relatives of the fibromyalgia patients than the RA patients,” she said. Overall, 32% of relatives of fibromyalgia patients had any mood disorder versus 19% of relatives of rheumatoid arthritis patients. On further analysis, the odds ratio for bipolar disorder was much higher in patients with fibromyalgia, compared with those who didn't have fibromyalgia, she added.

When prescribing antidepressants off label to fibromyalgia patients with comorbid mood disorders, be sure to titrate the medication to a high enough dose for a long enough time to allow a response, Dr. Arnold said.

“There is a tendency to use low doses when treating chronic pain, but I encourage people to use the full standard dose,” she said. Also consider combining a tricyclic antidepressant with a selective serotonin reuptake inhibitor, but be aware of drug interactions. “Sometimes you need to do two treatments–one for mood and one for pain,” she added.

Dr. Arnold and her colleagues conducted two randomized trials to assess the effectiveness of duloxetine (Cymbalta) on reducing pain in fibromyalgia patients with and without major depressive disorder. Overall, duloxetine was associated with significantly less pain than a placebo, whether or not the patients had major depressive disorder (Arthritis Rheum. 2004;50:2974–84).

Similarly, pregabalin and gabapentin are approved by the Food and Drug Administration for treating some types of neuropathic pain and neuralgia, and they are being studied as treatments for anxiety disorders and fibromyalgia.

WASHINGTON – Many fibromyalgia patients could benefit from the care and expertise provided by psychiatrists, Dr. Lesley M. Arnold said at the annual meeting of the American Academy of Clinical Psychiatrists.

Psychiatrists are in a position to evaluate fibromyalgia patients for psychiatric comorbidities and consider prescribing antidepressants as part of a treatment plan, said Dr. Arnold, associate professor of psychiatry at the University of Cincinnati.

Tricyclics have been shown to reduce chronic pain independent of any effects on the patient's mood, which suggests a common neurochemical channel for persistent pain and psychiatric conditions that remains unexplored, she said.

Consequently, fibromyalgia patients might benefit from a multidisciplinary approach, said Dr. Arnold, who has received grants and research support from several pharmaceutical companies, including Eli Lilly, Pfizer, and Cypress Bioscience. She also has served as a consultant for these and other pharmaceutical companies.

The American College of Rheumatology criteria for fibromyalgia include chronic widespread pain of more than 3 months' duration and pain in at least 11 of 18 pressure point areas of the body. Patients must report pain with about 4 kg of pressure (enough to blanch your thumb when you press on the area).

But the muscular criteria are only part of the disorder. Patients with fibromyalgia may have hyperalgesia throughout the body rather than at specific points, and patients who do not report pressure on at least 11 of the 18 tender points will often report other symptoms of fibromyalgia, including debilitating fatigue, Dr. Arnold said.

“Fatigue really knocks people out, and that impairs their function more than the pain,” she commented. Fibromyalgia patients also report difficulty falling asleep, difficulty staying asleep, and unrefreshing sleep.

Patients with fibromyalgia report depression and anxiety symptoms, too. The fibromyalgia literature suggests that about one-third of patients with a fibromyalgia diagnosis have a comorbid psychiatric condition, which contributes to the rationale for treating fibromyalgia patients with antidepressants, Dr. Arnold said.

To further assess the relationship between psychiatric comorbidity and fibromyalgia, Dr. Arnold and colleagues conducted a family study. They recruited 78 patients with fibromyalgia and 533 of their relatives, and compared the prevalence of mood disorders between this population and 40 patients with rheumatoid arthritis and 272 of their relatives (Arthritis Rheum. 2004;50;944–52).

“Mood disorders were much more common in the relatives of the fibromyalgia patients than the RA patients,” she said. Overall, 32% of relatives of fibromyalgia patients had any mood disorder versus 19% of relatives of rheumatoid arthritis patients. On further analysis, the odds ratio for bipolar disorder was much higher in patients with fibromyalgia, compared with those who didn't have fibromyalgia, she added.

When prescribing antidepressants off label to fibromyalgia patients with comorbid mood disorders, be sure to titrate the medication to a high enough dose for a long enough time to allow a response, Dr. Arnold said.

“There is a tendency to use low doses when treating chronic pain, but I encourage people to use the full standard dose,” she said. Also consider combining a tricyclic antidepressant with a selective serotonin reuptake inhibitor, but be aware of drug interactions. “Sometimes you need to do two treatments–one for mood and one for pain,” she added.

Dr. Arnold and her colleagues conducted two randomized trials to assess the effectiveness of duloxetine (Cymbalta) on reducing pain in fibromyalgia patients with and without major depressive disorder. Overall, duloxetine was associated with significantly less pain than a placebo, whether or not the patients had major depressive disorder (Arthritis Rheum. 2004;50:2974–84).

Similarly, pregabalin and gabapentin are approved by the Food and Drug Administration for treating some types of neuropathic pain and neuralgia, and they are being studied as treatments for anxiety disorders and fibromyalgia.

WASHINGTON – Many fibromyalgia patients could benefit from the care and expertise provided by psychiatrists, Dr. Lesley M. Arnold said at the annual meeting of the American Academy of Clinical Psychiatrists.

Psychiatrists are in a position to evaluate fibromyalgia patients for psychiatric comorbidities and consider prescribing antidepressants as part of a treatment plan, said Dr. Arnold, associate professor of psychiatry at the University of Cincinnati.

Tricyclics have been shown to reduce chronic pain independent of any effects on the patient's mood, which suggests a common neurochemical channel for persistent pain and psychiatric conditions that remains unexplored, she said.

Consequently, fibromyalgia patients might benefit from a multidisciplinary approach, said Dr. Arnold, who has received grants and research support from several pharmaceutical companies, including Eli Lilly, Pfizer, and Cypress Bioscience. She also has served as a consultant for these and other pharmaceutical companies.

The American College of Rheumatology criteria for fibromyalgia include chronic widespread pain of more than 3 months' duration and pain in at least 11 of 18 pressure point areas of the body. Patients must report pain with about 4 kg of pressure (enough to blanch your thumb when you press on the area).

But the muscular criteria are only part of the disorder. Patients with fibromyalgia may have hyperalgesia throughout the body rather than at specific points, and patients who do not report pressure on at least 11 of the 18 tender points will often report other symptoms of fibromyalgia, including debilitating fatigue, Dr. Arnold said.

“Fatigue really knocks people out, and that impairs their function more than the pain,” she commented. Fibromyalgia patients also report difficulty falling asleep, difficulty staying asleep, and unrefreshing sleep.

Patients with fibromyalgia report depression and anxiety symptoms, too. The fibromyalgia literature suggests that about one-third of patients with a fibromyalgia diagnosis have a comorbid psychiatric condition, which contributes to the rationale for treating fibromyalgia patients with antidepressants, Dr. Arnold said.

To further assess the relationship between psychiatric comorbidity and fibromyalgia, Dr. Arnold and colleagues conducted a family study. They recruited 78 patients with fibromyalgia and 533 of their relatives, and compared the prevalence of mood disorders between this population and 40 patients with rheumatoid arthritis and 272 of their relatives (Arthritis Rheum. 2004;50;944–52).

“Mood disorders were much more common in the relatives of the fibromyalgia patients than the RA patients,” she said. Overall, 32% of relatives of fibromyalgia patients had any mood disorder versus 19% of relatives of rheumatoid arthritis patients. On further analysis, the odds ratio for bipolar disorder was much higher in patients with fibromyalgia, compared with those who didn't have fibromyalgia, she added.

When prescribing antidepressants off label to fibromyalgia patients with comorbid mood disorders, be sure to titrate the medication to a high enough dose for a long enough time to allow a response, Dr. Arnold said.

“There is a tendency to use low doses when treating chronic pain, but I encourage people to use the full standard dose,” she said. Also consider combining a tricyclic antidepressant with a selective serotonin reuptake inhibitor, but be aware of drug interactions. “Sometimes you need to do two treatments–one for mood and one for pain,” she added.

Dr. Arnold and her colleagues conducted two randomized trials to assess the effectiveness of duloxetine (Cymbalta) on reducing pain in fibromyalgia patients with and without major depressive disorder. Overall, duloxetine was associated with significantly less pain than a placebo, whether or not the patients had major depressive disorder (Arthritis Rheum. 2004;50:2974–84).

Similarly, pregabalin and gabapentin are approved by the Food and Drug Administration for treating some types of neuropathic pain and neuralgia, and they are being studied as treatments for anxiety disorders and fibromyalgia.

ORLANDO – Patients who were depressed after coronary artery bypass surgery were significantly more likely to have atherosclerotic-disease progression within their grafted vessels during follow-up, in a post hoc analysis of data collected from more than 1,300 patients.

This suggestive finding should prompt a prospective study to definitely assess whether depression plays a causal role in atherosclerosis, Dr. Ambar Kulshreshtha said while presenting a poster at a conference on cardiovascular disease epidemiology and prevention sponsored by the American Heart Association.

The new analysis used data collected in the Post Coronary Artery Bypass Graft trial, which was designed to test whether treatment with an aggressive lipid-lowering regimen and low-dose warfarin could slow the progression of atherosclerosis within saphenous-vein bypass grafts. The study used patients who had undergone coronary bypass surgery 1–11 years prior to their enrollment. The primary findings of the trial were that aggressive lowering of LDL cholesterol was effective in significantly reducing the progression of atherosclerosis within grafted veins, but low-dose warfarin had no benefit (N. Engl. J. Med. 1997;336:153–63).

Almost 98% of the enrolled patients, a total of 1,319, were evaluated for depression at the time they entered the study using the Centers for Epidemiologic Studies depression (CES-D) scale. Patients were considered to have depression if their score on the CES-D was at least 16. According to the way the CES-D is scaled, a score of 16–27 is considered to represent mild depression, and a score greater than 27 indicates moderate to severe depression.

When they underwent evaluation, 127 of the post-bypass patients scored 16 or greater on the CES-D, and the remaining 1,192 patients had scores of 15 or less.

All patients also had a baseline coronary angiogram when they entered the study, and a follow-up examination at an average of 4.2 years later.

In an analysis that adjusted for several baseline differences, patients who were diagnosed with depression at entry had a 40% increased risk of having substantial atherosclerosis progression in their saphenous vein grafts, compared with patients who were not depressed at baseline, said Dr. Kulshreshtha, a cardiovascular research physician at Beth Israel Deaconess Medical Center in Boston. This difference in the progression of atherosclerosis was statistically significant.

Among the many potential confounders that were used for adjustment in the analysis were gender, race, years since bypass surgery, systolic blood pressure, kidney function, diabetes, body mass index, and physical activity.

ORLANDO – Patients who were depressed after coronary artery bypass surgery were significantly more likely to have atherosclerotic-disease progression within their grafted vessels during follow-up, in a post hoc analysis of data collected from more than 1,300 patients.

This suggestive finding should prompt a prospective study to definitely assess whether depression plays a causal role in atherosclerosis, Dr. Ambar Kulshreshtha said while presenting a poster at a conference on cardiovascular disease epidemiology and prevention sponsored by the American Heart Association.

The new analysis used data collected in the Post Coronary Artery Bypass Graft trial, which was designed to test whether treatment with an aggressive lipid-lowering regimen and low-dose warfarin could slow the progression of atherosclerosis within saphenous-vein bypass grafts. The study used patients who had undergone coronary bypass surgery 1–11 years prior to their enrollment. The primary findings of the trial were that aggressive lowering of LDL cholesterol was effective in significantly reducing the progression of atherosclerosis within grafted veins, but low-dose warfarin had no benefit (N. Engl. J. Med. 1997;336:153–63).

Almost 98% of the enrolled patients, a total of 1,319, were evaluated for depression at the time they entered the study using the Centers for Epidemiologic Studies depression (CES-D) scale. Patients were considered to have depression if their score on the CES-D was at least 16. According to the way the CES-D is scaled, a score of 16–27 is considered to represent mild depression, and a score greater than 27 indicates moderate to severe depression.

When they underwent evaluation, 127 of the post-bypass patients scored 16 or greater on the CES-D, and the remaining 1,192 patients had scores of 15 or less.

All patients also had a baseline coronary angiogram when they entered the study, and a follow-up examination at an average of 4.2 years later.

In an analysis that adjusted for several baseline differences, patients who were diagnosed with depression at entry had a 40% increased risk of having substantial atherosclerosis progression in their saphenous vein grafts, compared with patients who were not depressed at baseline, said Dr. Kulshreshtha, a cardiovascular research physician at Beth Israel Deaconess Medical Center in Boston. This difference in the progression of atherosclerosis was statistically significant.

Among the many potential confounders that were used for adjustment in the analysis were gender, race, years since bypass surgery, systolic blood pressure, kidney function, diabetes, body mass index, and physical activity.

ORLANDO – Patients who were depressed after coronary artery bypass surgery were significantly more likely to have atherosclerotic-disease progression within their grafted vessels during follow-up, in a post hoc analysis of data collected from more than 1,300 patients.

This suggestive finding should prompt a prospective study to definitely assess whether depression plays a causal role in atherosclerosis, Dr. Ambar Kulshreshtha said while presenting a poster at a conference on cardiovascular disease epidemiology and prevention sponsored by the American Heart Association.

The new analysis used data collected in the Post Coronary Artery Bypass Graft trial, which was designed to test whether treatment with an aggressive lipid-lowering regimen and low-dose warfarin could slow the progression of atherosclerosis within saphenous-vein bypass grafts. The study used patients who had undergone coronary bypass surgery 1–11 years prior to their enrollment. The primary findings of the trial were that aggressive lowering of LDL cholesterol was effective in significantly reducing the progression of atherosclerosis within grafted veins, but low-dose warfarin had no benefit (N. Engl. J. Med. 1997;336:153–63).

Almost 98% of the enrolled patients, a total of 1,319, were evaluated for depression at the time they entered the study using the Centers for Epidemiologic Studies depression (CES-D) scale. Patients were considered to have depression if their score on the CES-D was at least 16. According to the way the CES-D is scaled, a score of 16–27 is considered to represent mild depression, and a score greater than 27 indicates moderate to severe depression.

When they underwent evaluation, 127 of the post-bypass patients scored 16 or greater on the CES-D, and the remaining 1,192 patients had scores of 15 or less.

All patients also had a baseline coronary angiogram when they entered the study, and a follow-up examination at an average of 4.2 years later.

In an analysis that adjusted for several baseline differences, patients who were diagnosed with depression at entry had a 40% increased risk of having substantial atherosclerosis progression in their saphenous vein grafts, compared with patients who were not depressed at baseline, said Dr. Kulshreshtha, a cardiovascular research physician at Beth Israel Deaconess Medical Center in Boston. This difference in the progression of atherosclerosis was statistically significant.

Among the many potential confounders that were used for adjustment in the analysis were gender, race, years since bypass surgery, systolic blood pressure, kidney function, diabetes, body mass index, and physical activity.

ORLANDO – Alterations in brain circuitry and chemistry mediated through the dorsolateral prefrontal cortex can cause executive dysfunction in multiple disorders, according to a presentation at a psychopharmacology congress sponsored by the Neuroscience Education Institute.

“Executive dysfunction is there. It hits you in the face if you are dealing with schizophrenia,” said Dr. Thomas L. Schwartz. “But in depression you may have to look for it. I was always looking for that in the background–insomnia, fatigue, and executive dysfunction–the key residual symptoms of depression treatment.”

Decreased metabolism in the dorsal and medial prefrontal cortex and the anterior cingulate are neurobiologic factors that might contribute to executive dysfunction in depression, Dr. Schwartz said. A decrease in N-acetyl aspartate, a marker or neuronal function, also may play a role. “It's another way to look at the brain, and in depressed folks you can show the brain is not doing what it is supposed to,” said Dr. Schwartz, director of the depression and anxiety disorders research program at the State University of New York, Syracuse.

Executive dysfunction is associated with noradrenergic, dopaminergic, and histaminergic projections to the dorsolateral prefrontal cortex. One tactic to get more norepinephrine to flow in that circuitry is to manipulate the serotonin levels, Dr. Schwartz said.

“Too much serotonin can be a bad thing in the frontal lobes. If you inhibit the inhibitor you can get more norepinephrine up there and help return executive functioning,” he added.

Pharmacologic agents that might increase norepinephrine, dopamine, and/or histamine and help improve executive function include drugs such as bupropion, atomoxetine (Straterra), and modafinil (Provigil), and drug classes such as stimulants and atypical antipsychotics, Dr. Schwartz said.

“Use of atomoxetine for executive dysfunction in depression makes biological sense and circuitry sense,” he said. “But there are no controlled studies [of atomoxetine] in executive dysfunction in depression.”

Executive dysfunction also is associated with sleep disorders. “Your brain wants you to have a homeostatic amount of sleep. If you get sleep deprived, no matter what the cause, you function poorly and make errors in omission and commission,” Dr. Schwartz said. Again, “there is poor metabolism in the prefrontal cortex.”

Addition of a sleep aid can have positive effects on next-day functioning. Stimulants, modafinil, or armodafinil can improve attention and concentration during the day, Dr. Schwartz said. “If you can keep people more awake during the day, and they avoid napping, they may not need a sleeping pill at night.”

Insomnia is comorbid with depression in around 85% of people (J. Clin. Psychiatry 2004;65:27–32). “That is a lot of people,” Dr. Schwartz said. Some antidepressant medications can have a direct effect on sleep, he added. For example, bupropion increases REM sleep and sleep latency, but reduces sleep continuity. Trazodone decreases REM sleep time and may cause daytime sedation. In contrast, nefazodone increases REM sleep time and is associated with minimal daytime sedation.

Sleep aids are a treatment option. Examples include zolpidem (Ambien), eszopiclone (Lunesta), and zaleplon (Sonata). “I don't think one is better than the other, so choose based on half-life,” Dr. Schwartz suggested. Sonata has the shorter half life; Ambien is in the middle; Lunesta has the longest. “Which one can you take at 3 a.m, if you need to work at 9 in the morning? Sonata.”

Modafinil is another pharmacologic option in patients with executive dysfunction and other adverse effects of impaired sleep. “This will not save every one of your patients but you can try it,” Dr. Schwartz said. “It's the only product that raises histamine that I know of, and histamine going up to the cortex is good for executive function.”

Dr. Schwartz said, “Modafinil is a funny drug–doses above 300 mg backfire in certain populations. Lower doses may be better for treatment of executive dysfunction.”

ORLANDO – Alterations in brain circuitry and chemistry mediated through the dorsolateral prefrontal cortex can cause executive dysfunction in multiple disorders, according to a presentation at a psychopharmacology congress sponsored by the Neuroscience Education Institute.

“Executive dysfunction is there. It hits you in the face if you are dealing with schizophrenia,” said Dr. Thomas L. Schwartz. “But in depression you may have to look for it. I was always looking for that in the background–insomnia, fatigue, and executive dysfunction–the key residual symptoms of depression treatment.”

Decreased metabolism in the dorsal and medial prefrontal cortex and the anterior cingulate are neurobiologic factors that might contribute to executive dysfunction in depression, Dr. Schwartz said. A decrease in N-acetyl aspartate, a marker or neuronal function, also may play a role. “It's another way to look at the brain, and in depressed folks you can show the brain is not doing what it is supposed to,” said Dr. Schwartz, director of the depression and anxiety disorders research program at the State University of New York, Syracuse.

Executive dysfunction is associated with noradrenergic, dopaminergic, and histaminergic projections to the dorsolateral prefrontal cortex. One tactic to get more norepinephrine to flow in that circuitry is to manipulate the serotonin levels, Dr. Schwartz said.

“Too much serotonin can be a bad thing in the frontal lobes. If you inhibit the inhibitor you can get more norepinephrine up there and help return executive functioning,” he added.

Pharmacologic agents that might increase norepinephrine, dopamine, and/or histamine and help improve executive function include drugs such as bupropion, atomoxetine (Straterra), and modafinil (Provigil), and drug classes such as stimulants and atypical antipsychotics, Dr. Schwartz said.

“Use of atomoxetine for executive dysfunction in depression makes biological sense and circuitry sense,” he said. “But there are no controlled studies [of atomoxetine] in executive dysfunction in depression.”

Executive dysfunction also is associated with sleep disorders. “Your brain wants you to have a homeostatic amount of sleep. If you get sleep deprived, no matter what the cause, you function poorly and make errors in omission and commission,” Dr. Schwartz said. Again, “there is poor metabolism in the prefrontal cortex.”

Addition of a sleep aid can have positive effects on next-day functioning. Stimulants, modafinil, or armodafinil can improve attention and concentration during the day, Dr. Schwartz said. “If you can keep people more awake during the day, and they avoid napping, they may not need a sleeping pill at night.”

Insomnia is comorbid with depression in around 85% of people (J. Clin. Psychiatry 2004;65:27–32). “That is a lot of people,” Dr. Schwartz said. Some antidepressant medications can have a direct effect on sleep, he added. For example, bupropion increases REM sleep and sleep latency, but reduces sleep continuity. Trazodone decreases REM sleep time and may cause daytime sedation. In contrast, nefazodone increases REM sleep time and is associated with minimal daytime sedation.

Sleep aids are a treatment option. Examples include zolpidem (Ambien), eszopiclone (Lunesta), and zaleplon (Sonata). “I don't think one is better than the other, so choose based on half-life,” Dr. Schwartz suggested. Sonata has the shorter half life; Ambien is in the middle; Lunesta has the longest. “Which one can you take at 3 a.m, if you need to work at 9 in the morning? Sonata.”

Modafinil is another pharmacologic option in patients with executive dysfunction and other adverse effects of impaired sleep. “This will not save every one of your patients but you can try it,” Dr. Schwartz said. “It's the only product that raises histamine that I know of, and histamine going up to the cortex is good for executive function.”

Dr. Schwartz said, “Modafinil is a funny drug–doses above 300 mg backfire in certain populations. Lower doses may be better for treatment of executive dysfunction.”

ORLANDO – Alterations in brain circuitry and chemistry mediated through the dorsolateral prefrontal cortex can cause executive dysfunction in multiple disorders, according to a presentation at a psychopharmacology congress sponsored by the Neuroscience Education Institute.

“Executive dysfunction is there. It hits you in the face if you are dealing with schizophrenia,” said Dr. Thomas L. Schwartz. “But in depression you may have to look for it. I was always looking for that in the background–insomnia, fatigue, and executive dysfunction–the key residual symptoms of depression treatment.”

Decreased metabolism in the dorsal and medial prefrontal cortex and the anterior cingulate are neurobiologic factors that might contribute to executive dysfunction in depression, Dr. Schwartz said. A decrease in N-acetyl aspartate, a marker or neuronal function, also may play a role. “It's another way to look at the brain, and in depressed folks you can show the brain is not doing what it is supposed to,” said Dr. Schwartz, director of the depression and anxiety disorders research program at the State University of New York, Syracuse.

Executive dysfunction is associated with noradrenergic, dopaminergic, and histaminergic projections to the dorsolateral prefrontal cortex. One tactic to get more norepinephrine to flow in that circuitry is to manipulate the serotonin levels, Dr. Schwartz said.

“Too much serotonin can be a bad thing in the frontal lobes. If you inhibit the inhibitor you can get more norepinephrine up there and help return executive functioning,” he added.

Pharmacologic agents that might increase norepinephrine, dopamine, and/or histamine and help improve executive function include drugs such as bupropion, atomoxetine (Straterra), and modafinil (Provigil), and drug classes such as stimulants and atypical antipsychotics, Dr. Schwartz said.

“Use of atomoxetine for executive dysfunction in depression makes biological sense and circuitry sense,” he said. “But there are no controlled studies [of atomoxetine] in executive dysfunction in depression.”

Executive dysfunction also is associated with sleep disorders. “Your brain wants you to have a homeostatic amount of sleep. If you get sleep deprived, no matter what the cause, you function poorly and make errors in omission and commission,” Dr. Schwartz said. Again, “there is poor metabolism in the prefrontal cortex.”

Addition of a sleep aid can have positive effects on next-day functioning. Stimulants, modafinil, or armodafinil can improve attention and concentration during the day, Dr. Schwartz said. “If you can keep people more awake during the day, and they avoid napping, they may not need a sleeping pill at night.”

Insomnia is comorbid with depression in around 85% of people (J. Clin. Psychiatry 2004;65:27–32). “That is a lot of people,” Dr. Schwartz said. Some antidepressant medications can have a direct effect on sleep, he added. For example, bupropion increases REM sleep and sleep latency, but reduces sleep continuity. Trazodone decreases REM sleep time and may cause daytime sedation. In contrast, nefazodone increases REM sleep time and is associated with minimal daytime sedation.

Sleep aids are a treatment option. Examples include zolpidem (Ambien), eszopiclone (Lunesta), and zaleplon (Sonata). “I don't think one is better than the other, so choose based on half-life,” Dr. Schwartz suggested. Sonata has the shorter half life; Ambien is in the middle; Lunesta has the longest. “Which one can you take at 3 a.m, if you need to work at 9 in the morning? Sonata.”

Modafinil is another pharmacologic option in patients with executive dysfunction and other adverse effects of impaired sleep. “This will not save every one of your patients but you can try it,” Dr. Schwartz said. “It's the only product that raises histamine that I know of, and histamine going up to the cortex is good for executive function.”

Dr. Schwartz said, “Modafinil is a funny drug–doses above 300 mg backfire in certain populations. Lower doses may be better for treatment of executive dysfunction.”

Having both type 2 diabetes and depression puts patients with coronary artery disease at greater risk of death over a 4.5-year period than does either condition alone.

That finding emerged from a study presented at the American Psychosomatic Society meeting in Budapest, Hungary.

The more severe the depressive symptoms were in those patients with both coronary artery disease and diabetes, the greater their risk of death in the follow-up period.

Having high scores on the Beck Depression Inventory increased the risk of dying during the follow-up period by 20%–30%, compared with patients with similar depression scores but without type 2 diabetes, according to investigators from Duke University, Durham, N.C.

These findings suggest that physicians should screen for and treat depression in patients with diabetes and heart disease.

“There is some sort of synergistic effect between type 2 diabetes and depression that we don't fully understand,” lead researcher Anastasia Georgiades, Ph.D., said in a written statement. “In our analysis, we controlled for factors that could influence mortality, such as heart disease severity and age. For whatever reasons, these patients were still at higher risk of dying, and future research will aim to investigate the mechanisms for this association.”

The study compared 325 patients with type 2 diabetes and 582 patients without the disease during hospitalization for a coronary angiography. Their depression symptoms were rated using the Beck Depression Inventory (BDI). Approximately 25% scored at least 10 on the BDI, indicating depression, Lana Watkins, Ph.D., an investigator in the study, noted in an interview.

During the follow-up period of 4.5 years (median, 3 years), the researchers documented 135 deaths among the study participants. Among the depressed patients, 19% died, compared with 12% of those patients without depression, Dr. Watkins said.

The researchers found statistically significant associations between depressive symptoms and increased mortality and, separately, diabetes and increased mortality. The highest mortality was among patients with both diabetes and elevated BDI scores. The researchers did not publicize hazard ratios, however, because they said those statistics would overestimate the risk and create anxiety among patients.

“Patients with type 2 diabetes typically have an extensive self-care regimen involving special diet, medications, exercise, and numerous appointments with their doctor,” Dr. Georgiades said in the statement. “It may be that such patients who are depressed might not be as motivated to carry out all these activities, thereby putting them at higher risk.”

Physicians treating patients with heart disease and diabetes need to screen them for depression and treat as needed.

“Regular exercise has been shown to improve depression, too, so that might be an option,” Dr. Watkins noted in an interview. “This could potentially improve depression and diabetes, and might be a good first choice for diabetics who would prefer not having to take additional medications.”

Having both type 2 diabetes and depression puts patients with coronary artery disease at greater risk of death over a 4.5-year period than does either condition alone.

That finding emerged from a study presented at the American Psychosomatic Society meeting in Budapest, Hungary.

The more severe the depressive symptoms were in those patients with both coronary artery disease and diabetes, the greater their risk of death in the follow-up period.

Having high scores on the Beck Depression Inventory increased the risk of dying during the follow-up period by 20%–30%, compared with patients with similar depression scores but without type 2 diabetes, according to investigators from Duke University, Durham, N.C.

These findings suggest that physicians should screen for and treat depression in patients with diabetes and heart disease.

“There is some sort of synergistic effect between type 2 diabetes and depression that we don't fully understand,” lead researcher Anastasia Georgiades, Ph.D., said in a written statement. “In our analysis, we controlled for factors that could influence mortality, such as heart disease severity and age. For whatever reasons, these patients were still at higher risk of dying, and future research will aim to investigate the mechanisms for this association.”

The study compared 325 patients with type 2 diabetes and 582 patients without the disease during hospitalization for a coronary angiography. Their depression symptoms were rated using the Beck Depression Inventory (BDI). Approximately 25% scored at least 10 on the BDI, indicating depression, Lana Watkins, Ph.D., an investigator in the study, noted in an interview.

During the follow-up period of 4.5 years (median, 3 years), the researchers documented 135 deaths among the study participants. Among the depressed patients, 19% died, compared with 12% of those patients without depression, Dr. Watkins said.

The researchers found statistically significant associations between depressive symptoms and increased mortality and, separately, diabetes and increased mortality. The highest mortality was among patients with both diabetes and elevated BDI scores. The researchers did not publicize hazard ratios, however, because they said those statistics would overestimate the risk and create anxiety among patients.

“Patients with type 2 diabetes typically have an extensive self-care regimen involving special diet, medications, exercise, and numerous appointments with their doctor,” Dr. Georgiades said in the statement. “It may be that such patients who are depressed might not be as motivated to carry out all these activities, thereby putting them at higher risk.”

Physicians treating patients with heart disease and diabetes need to screen them for depression and treat as needed.

“Regular exercise has been shown to improve depression, too, so that might be an option,” Dr. Watkins noted in an interview. “This could potentially improve depression and diabetes, and might be a good first choice for diabetics who would prefer not having to take additional medications.”

Having both type 2 diabetes and depression puts patients with coronary artery disease at greater risk of death over a 4.5-year period than does either condition alone.

That finding emerged from a study presented at the American Psychosomatic Society meeting in Budapest, Hungary.

The more severe the depressive symptoms were in those patients with both coronary artery disease and diabetes, the greater their risk of death in the follow-up period.

Having high scores on the Beck Depression Inventory increased the risk of dying during the follow-up period by 20%–30%, compared with patients with similar depression scores but without type 2 diabetes, according to investigators from Duke University, Durham, N.C.

These findings suggest that physicians should screen for and treat depression in patients with diabetes and heart disease.

“There is some sort of synergistic effect between type 2 diabetes and depression that we don't fully understand,” lead researcher Anastasia Georgiades, Ph.D., said in a written statement. “In our analysis, we controlled for factors that could influence mortality, such as heart disease severity and age. For whatever reasons, these patients were still at higher risk of dying, and future research will aim to investigate the mechanisms for this association.”

The study compared 325 patients with type 2 diabetes and 582 patients without the disease during hospitalization for a coronary angiography. Their depression symptoms were rated using the Beck Depression Inventory (BDI). Approximately 25% scored at least 10 on the BDI, indicating depression, Lana Watkins, Ph.D., an investigator in the study, noted in an interview.

During the follow-up period of 4.5 years (median, 3 years), the researchers documented 135 deaths among the study participants. Among the depressed patients, 19% died, compared with 12% of those patients without depression, Dr. Watkins said.

The researchers found statistically significant associations between depressive symptoms and increased mortality and, separately, diabetes and increased mortality. The highest mortality was among patients with both diabetes and elevated BDI scores. The researchers did not publicize hazard ratios, however, because they said those statistics would overestimate the risk and create anxiety among patients.

“Patients with type 2 diabetes typically have an extensive self-care regimen involving special diet, medications, exercise, and numerous appointments with their doctor,” Dr. Georgiades said in the statement. “It may be that such patients who are depressed might not be as motivated to carry out all these activities, thereby putting them at higher risk.”

Physicians treating patients with heart disease and diabetes need to screen them for depression and treat as needed.

“Regular exercise has been shown to improve depression, too, so that might be an option,” Dr. Watkins noted in an interview. “This could potentially improve depression and diabetes, and might be a good first choice for diabetics who would prefer not having to take additional medications.”