Girls born weighing less than 2,500 grams (about 5.5 pounds) may be more likely to develop depression between ages 13 to 16 than those born at a normal weight, while the same does not appear to be true for boys, according to a report in the March issue of Archives of General Psychiatry, one of the JAMA/Archives journals.
Several previous studies have linked low birth weight with depression in adolescence and adulthood, according to background information in the article. Some suggest that, like adult-onset diabetes or cardiovascular disease, the potential for depression may lie dormant in individuals born with low birth weight, emerging under stressful conditions. However, previous research has not considered differences in rates of depression by age and sex, the authors note.
Elizabeth Jane Costello, Ph.D., Duke University Medical School, Durham, N.C., and colleagues examined the association between low birth weight and depression in 1,420 participants between the ages of 9 and 16 years, 49 percent of whom were female. Children from 11 North Carolina counties were enrolled in the Great Smoky Mountains Study in 1993 and assessed yearly for depression and other psychiatric disorders during childhood (age 9 to 12) and adolescence (age 13 to 16 years). The children's mothers gave information about birth weight and other indicators of adversity, such as having a mother younger than age 18 at birth or having a parent who left school before the 11th grade.
A total of 5.7 percent of the girls in the study were born weighing less than 2,500 grams. Of those, 38.1 percent experienced at least one episode of depression between ages 13 and 16, compared with 8.4 percent of those born at a normal weight. The risk of depression attributable to low birth weight was 18 percent - in other words, if all female babies were born at a normal weight, 18 percent fewer teen girls would have episodes of depression. On average, 23.5 percent of teen girls with low birth weight were depressed each year, compared with 3.4 percent of those with normal birth weight.
The same effect was not observed in boys - throughout childhood and adolescence, no more than 4.9 percent of boys experienced depression, regardless of birth weight. Low birth weight was not associated with an increased risk of any other psychiatric condition, including anxiety disorders, in either boys or girls.
"The findings need replication in larger samples that include prospective data from birth to adulthood. Important next steps will include separate examination of the many different hormonal, morphological, psychological and social aspects of puberty that might best explain the increase in risk seen in adolescence, herein indexed by age," the authors conclude. "For the present, the findings suggest that pediatricians and parents of girls who were of low birth weight should pay close attention to their mental health as they enter puberty."
(Arch Gen Psychiatry. 2007;64:338-344. Available pre-embargo to the media at jamamedia.)
This study was supported by grants from the National Institute of Mental Health, the National Institute on Drug Abuse and the William T. Grant Foundation. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
Contact: Tracey Koepke
JAMA and Archives Journals
вторник, 30 августа 2011 г.
воскресенье, 28 августа 2011 г.
Postpartum Mood Disturbances In Healthy New Mothers May Be Predicted By Their Perception Of Poor Sleep
A study of healthy new mothers in the April 1 issue of the journal Sleep found that the perception of poor sleep and the conscious awareness of its impact on daytime functioning might be stronger predictors of immediate postpartum mood disturbances than actual sleep quality and quantity.
Results indicate that both objective and subjective nighttime sleep significantly worsened with decreased total sleep time and sleep efficiency after giving birth. However, variables related to the subjective perception of sleep and sleep-related daytime dysfunction were stronger predictors of postpartum mood. After giving birth, subjective total sleep time at night fell from 437 minutes to 348 minutes, and mean subjective sleep efficiency decreased from 79 percent to 66 percent. Seventeen participants (46 percent) experienced some deterioration of mood after delivery.
Lead author Bei Bei, DPsych, clinical psychologist at the University of Melbourne in Victoria, Australia, said that while pregnancy is a joyous and exciting time, it also exposes women to many stressors, including disturbed sleep.
"We were surprised that while objective sleep was not irrelevant, subjective perception of sleep shared a much stronger relationship with mood," said Bei. "Women who are concerned about their sleep and/or mood should speak to health care professionals about cognitive-behavioral therapy, which is effective for improving both sleep and mood."
The two-stage longitudinal study measured sleep and mood during the third trimester and one week postpartum in 44 healthy women at low risk for postpartum depression. The average age of participants was 30 years, with a range from 18 to 41 years. The sample included 20 first-time mothers (45.5 percent) and 24 mothers with multiple children (54.5 percent). The majority of participants (91 percent) were married or in a stable relationship.
Objective sleep was measured by actigraphy, and subjective sleep by the Pittsburgh Sleep Quality Index. Mood was assessed by the Depression Anxiety Stress Scale, the Hospital Anxiety Depression Scale, and the Positive and Negative Affect Schedule. Subjective sleep and mood scales were administered during both phases of the study, and objective sleep measures were recorded continuously for seven days during the third trimester and seven days after delivery.
Poorer subjective nighttime sleep both during the third trimester and after delivery was associated with worse postpartum mood. As women's nighttime sleep worsened following delivery, their perceived sleep-related daytime dysfunction and napping behavior became relevant to their mood changes: higher sleep-related daytime dysfunction and more frequent naps were associated with higher reported distress. Sleep obtained in a daytime nap did not appear to provide the same restorative value as sleep obtained at night.
Objective sleep deteriorated after delivery as the mean total sleep time at night fell from 428 minutes during the third trimester to 373 minutes postpartum, and average sleep efficiency dropped from 77 percent to 63 percent. The average amount of time spent awake in bed after initially falling asleep at night increased from 77 minutes to 150 minutes, and mean daily nap time increased from 32 minutes to 101 minutes.
However, evidence supporting a relationship between objective nighttime sleep and mood was weak. Lower positive affect after delivery was related to poorer overall objective sleep during the third trimester but was unrelated to objective postpartum sleep. A series of analyses also found no significant difference in postpartum mood between women who had daytime labor and those who had nighttime labor.
The authors noted that the study was unable to determine if it was poor sleep that led to emotional distress, or if poor mood caused sleep complaints. However, they proposed that women with higher levels of psychological distress might perceive their sleep to be poorer; this perception of disturbed sleep at night might exacerbate subjective stress and frustration, thus creating a potentially vicious cycle.
The study: "Subjective Perception of Sleep, but not its Objective Quality, is Associated with Immediate Postpartum Mood Disturbances in Healthy Women"
Results indicate that both objective and subjective nighttime sleep significantly worsened with decreased total sleep time and sleep efficiency after giving birth. However, variables related to the subjective perception of sleep and sleep-related daytime dysfunction were stronger predictors of postpartum mood. After giving birth, subjective total sleep time at night fell from 437 minutes to 348 minutes, and mean subjective sleep efficiency decreased from 79 percent to 66 percent. Seventeen participants (46 percent) experienced some deterioration of mood after delivery.
Lead author Bei Bei, DPsych, clinical psychologist at the University of Melbourne in Victoria, Australia, said that while pregnancy is a joyous and exciting time, it also exposes women to many stressors, including disturbed sleep.
"We were surprised that while objective sleep was not irrelevant, subjective perception of sleep shared a much stronger relationship with mood," said Bei. "Women who are concerned about their sleep and/or mood should speak to health care professionals about cognitive-behavioral therapy, which is effective for improving both sleep and mood."
The two-stage longitudinal study measured sleep and mood during the third trimester and one week postpartum in 44 healthy women at low risk for postpartum depression. The average age of participants was 30 years, with a range from 18 to 41 years. The sample included 20 first-time mothers (45.5 percent) and 24 mothers with multiple children (54.5 percent). The majority of participants (91 percent) were married or in a stable relationship.
Objective sleep was measured by actigraphy, and subjective sleep by the Pittsburgh Sleep Quality Index. Mood was assessed by the Depression Anxiety Stress Scale, the Hospital Anxiety Depression Scale, and the Positive and Negative Affect Schedule. Subjective sleep and mood scales were administered during both phases of the study, and objective sleep measures were recorded continuously for seven days during the third trimester and seven days after delivery.
Poorer subjective nighttime sleep both during the third trimester and after delivery was associated with worse postpartum mood. As women's nighttime sleep worsened following delivery, their perceived sleep-related daytime dysfunction and napping behavior became relevant to their mood changes: higher sleep-related daytime dysfunction and more frequent naps were associated with higher reported distress. Sleep obtained in a daytime nap did not appear to provide the same restorative value as sleep obtained at night.
Objective sleep deteriorated after delivery as the mean total sleep time at night fell from 428 minutes during the third trimester to 373 minutes postpartum, and average sleep efficiency dropped from 77 percent to 63 percent. The average amount of time spent awake in bed after initially falling asleep at night increased from 77 minutes to 150 minutes, and mean daily nap time increased from 32 minutes to 101 minutes.
However, evidence supporting a relationship between objective nighttime sleep and mood was weak. Lower positive affect after delivery was related to poorer overall objective sleep during the third trimester but was unrelated to objective postpartum sleep. A series of analyses also found no significant difference in postpartum mood between women who had daytime labor and those who had nighttime labor.
The authors noted that the study was unable to determine if it was poor sleep that led to emotional distress, or if poor mood caused sleep complaints. However, they proposed that women with higher levels of psychological distress might perceive their sleep to be poorer; this perception of disturbed sleep at night might exacerbate subjective stress and frustration, thus creating a potentially vicious cycle.
The study: "Subjective Perception of Sleep, but not its Objective Quality, is Associated with Immediate Postpartum Mood Disturbances in Healthy Women"
пятница, 26 августа 2011 г.
Low Cholesterol, Depression Linked To Early Death
New Geisinger research shows that men with a combination of low total cholesterol and depression were seven times more likely to die prematurely from unnatural causes, such as suicide and accidents.
The study, which was published recently in Journal of Psychiatric Research, found that men with low total cholesterol (165 milligrams of cholesterol per deciliter or less) and depression were at very high risk for premature death from "external causes" including suicide, drug overdose, accidental poisoning and unintended injuries.
"While it's generally understood that having low cholesterol is a good health sign, combined with other factors, it could actually put a person at risk," said Geisinger senior investigator Joseph Boscarino, PhD, MPH.
Low cholesterol levels in a person's blood may lead to decreased serotonin, which is a neurotransmitter that helps relay signals to various parts of the brain. Decreased serotonin is linked to depression, anger, sleep loss and other problems, Dr. Boscarino said.
Those with anti-social personality disorder, which is associated with high risk-taking and thrill-seeking, were twice as likely to die prematurely, according to the study. Men with morbid depression had a similar risk.
Cholesterol is important because it serves as a key component or "constituent" of nerve cells in the body, said Geisinger neurologist and study co-author Stuart Hoffman, DO.
"A certain amount of cholesterol needs to be present for neurons to function normally," Dr. Hoffman said. "Our study shows that if a person's cholesterol is too low, nervous system problems could develop."
For the study, Dr. Boscarino reviewed medical histories and medical exams performed on nearly 4,500 Vietnam veterans in 1985/86. These reports included comprehensive mental health assessments, physical exams and assessment of lipid levels, including total cholesterol. Dr. Boscarino also reviewed death certificate data for the veterans that were available in 2000.
The research was funded, in part, with a National Institute of Mental Health Training Grant to Dr. Boscarino.
About Geisinger Health System
Founded in 1915, Geisinger Health System is one of the nations largest integrated health services organizations. Serving more than 2.6 million residents throughout central and northeastern Pennsylvania, the physician-led organization is a nationally recognized leader in the use of electronic health records, patient access and engagement in their healthcare, and in medical education for the next generation. Geisinger is comprised of three medical center campuses, a 740-member group practice, a not-for-profit health insurance company and research that extends across our large system- all dedicated to creating new models for scientific discovery, quality patient care, and successful clinical outcomes. Geisinger's Weis Center, Center for Health Research and Center for Clinical Studies include basic science, population-based and clinical trials research, complemented by collaborative relationships with top academic centers. Geisinger Ventures, the system's for profit entrepreneurial arm, seeks and promotes opportunities to speed the delivery of medical innovation to benefit patients. For more information, visit geisinger.
Geisinger Health System
100 N Academy Ave.
Danville
PA
United States
geisinger
The study, which was published recently in Journal of Psychiatric Research, found that men with low total cholesterol (165 milligrams of cholesterol per deciliter or less) and depression were at very high risk for premature death from "external causes" including suicide, drug overdose, accidental poisoning and unintended injuries.
"While it's generally understood that having low cholesterol is a good health sign, combined with other factors, it could actually put a person at risk," said Geisinger senior investigator Joseph Boscarino, PhD, MPH.
Low cholesterol levels in a person's blood may lead to decreased serotonin, which is a neurotransmitter that helps relay signals to various parts of the brain. Decreased serotonin is linked to depression, anger, sleep loss and other problems, Dr. Boscarino said.
Those with anti-social personality disorder, which is associated with high risk-taking and thrill-seeking, were twice as likely to die prematurely, according to the study. Men with morbid depression had a similar risk.
Cholesterol is important because it serves as a key component or "constituent" of nerve cells in the body, said Geisinger neurologist and study co-author Stuart Hoffman, DO.
"A certain amount of cholesterol needs to be present for neurons to function normally," Dr. Hoffman said. "Our study shows that if a person's cholesterol is too low, nervous system problems could develop."
For the study, Dr. Boscarino reviewed medical histories and medical exams performed on nearly 4,500 Vietnam veterans in 1985/86. These reports included comprehensive mental health assessments, physical exams and assessment of lipid levels, including total cholesterol. Dr. Boscarino also reviewed death certificate data for the veterans that were available in 2000.
The research was funded, in part, with a National Institute of Mental Health Training Grant to Dr. Boscarino.
About Geisinger Health System
Founded in 1915, Geisinger Health System is one of the nations largest integrated health services organizations. Serving more than 2.6 million residents throughout central and northeastern Pennsylvania, the physician-led organization is a nationally recognized leader in the use of electronic health records, patient access and engagement in their healthcare, and in medical education for the next generation. Geisinger is comprised of three medical center campuses, a 740-member group practice, a not-for-profit health insurance company and research that extends across our large system- all dedicated to creating new models for scientific discovery, quality patient care, and successful clinical outcomes. Geisinger's Weis Center, Center for Health Research and Center for Clinical Studies include basic science, population-based and clinical trials research, complemented by collaborative relationships with top academic centers. Geisinger Ventures, the system's for profit entrepreneurial arm, seeks and promotes opportunities to speed the delivery of medical innovation to benefit patients. For more information, visit geisinger.
Geisinger Health System
100 N Academy Ave.
Danville
PA
United States
geisinger
среда, 24 августа 2011 г.
New 'Smart' Materials For The Brain
Research done by scientists in Italy and Switzerland has shown that carbon nanotubes may be the ideal "smart" brain material. Their results, published in the advance online edition of the journal Nature Nanotechnology, are a promising step forward in the search to find ways to "bypass" faulty brain wiring.
The research shows that carbon nanotubes, which, like neurons, are highly electrically conductive, form extremely tight contacts with neuronal cell membranes. Unlike the metal electrodes that are currently used in research and clinical applications, the nanotubes can create shortcuts between the distal and proximal compartments of the neuron, resulting in enhanced neuronal excitability.
The study was conducted in the Laboratory of Neural Microcircuitry at EPFL in Switzerland and led by Michel Giugliano (now an assistant professor at the University of Antwerp) and University of Trieste professor Laura Ballerini. "This result is extremely relevant for the emerging field of neuro-engineering and neuroprosthetics," explains Giugliano, who hypothesizes that the nanotubes could be used as a new building block of novel "electrical bypass" systems for treating traumatic injury of the central nervous system. Carbon nano-electrodes could also be used to replace metal parts in clinical applications such as deep brain stimulation for the treatment of Parkinson's disease or severe depression. And they show promise as a whole new class of "smart" materials for use in a wide range of potential neuroprosthetic applications.
Henry Markram, head of the Laboratory of Neural Microcircuitry and an author on the paper, adds: "There are three fundamental obstacles to developing reliable neuroprosthetics:
stable interfacing of electromechanical devices with neural tissue,
understanding how to stimulate the neural tissue, and
understanding what signals to record from the neurons in order for the device to make an automatic and appropriate decision to stimulate.
The new carbon nanotube-based interface technology discovered together with state of the art simulations of brain-machine interfaces is the key to developing all types of neuroprosthetics -- sight, sound, smell, motion, vetoing epileptic attacks, spinal bypasses, as well as repairing and even enhancing cognitive functions."
Contact information:
Michele Giugliano, Department of Biomedical Sciences, University of Antwerp
Laura Ballerini, MD, Life Sciences Department, Center for Neuroscience B.R.A.I.N. University of Trieste
Henry Markram, professor, EPFL Laboratory of Neural Microcircuitry
The research shows that carbon nanotubes, which, like neurons, are highly electrically conductive, form extremely tight contacts with neuronal cell membranes. Unlike the metal electrodes that are currently used in research and clinical applications, the nanotubes can create shortcuts between the distal and proximal compartments of the neuron, resulting in enhanced neuronal excitability.
The study was conducted in the Laboratory of Neural Microcircuitry at EPFL in Switzerland and led by Michel Giugliano (now an assistant professor at the University of Antwerp) and University of Trieste professor Laura Ballerini. "This result is extremely relevant for the emerging field of neuro-engineering and neuroprosthetics," explains Giugliano, who hypothesizes that the nanotubes could be used as a new building block of novel "electrical bypass" systems for treating traumatic injury of the central nervous system. Carbon nano-electrodes could also be used to replace metal parts in clinical applications such as deep brain stimulation for the treatment of Parkinson's disease or severe depression. And they show promise as a whole new class of "smart" materials for use in a wide range of potential neuroprosthetic applications.
Henry Markram, head of the Laboratory of Neural Microcircuitry and an author on the paper, adds: "There are three fundamental obstacles to developing reliable neuroprosthetics:
stable interfacing of electromechanical devices with neural tissue,
understanding how to stimulate the neural tissue, and
understanding what signals to record from the neurons in order for the device to make an automatic and appropriate decision to stimulate.
The new carbon nanotube-based interface technology discovered together with state of the art simulations of brain-machine interfaces is the key to developing all types of neuroprosthetics -- sight, sound, smell, motion, vetoing epileptic attacks, spinal bypasses, as well as repairing and even enhancing cognitive functions."
Contact information:
Michele Giugliano, Department of Biomedical Sciences, University of Antwerp
Laura Ballerini, MD, Life Sciences Department, Center for Neuroscience B.R.A.I.N. University of Trieste
Henry Markram, professor, EPFL Laboratory of Neural Microcircuitry
понедельник, 22 августа 2011 г.
Two Years Later: DIAMOND Program Continues To Get Nearly 50% Of Patients With Depression Into Remission Within Six Months
The DIAMOND program (Depression Improvement Across Minnesota, Offering a New Direction) continues to get at least five times as many patients into remission by six months than patients receiving typical primary care treatment, according to two-year findings reported by the Institute for Clinical Systems Improvement.
Of the 1,752 patients contacted six months after entering into the DIAMOND program to date, 45% were in remission and another 16% had at least a 50% reduction in the severity of their depression. An additional 1,285 DIAMOND patients unable to be reached at six months to determine their progress are presumed to be still depressed, although they could have gotten better. Using this measurement, 26% of DIAMOND clinic patients were in remission at six months, compared to only 5.8% of patients treated in 184 primary care and behavioral health clinics reporting in 2009 to MN Community Measurement, a nonprofit organization that publicly reports on medical group's quality results in Minnesota.
"Among the clinics reporting on patient outcomes stemming from their treatment plans, seven offering the DIAMOND program were in the top 10," said Jim Chase, president of MN Community Measurement. "Mayo Clinic had two of the state's top performing clinics, and clinics run by Family HealthServices Minnesota, HealthPartners Medical Group and Allina Medical Clinic that also offered the DIAMOND program all posted top 10 results."
"What's exciting about our latest data is that we continue to see significant positive patient response to DIAMOND treatment after two years of implementation and across metro and rural clinics," says Nancy Jaeckels, ICSI vice president of member relations and strategic initiatives. "DIAMOND was modeled on a concept proven in almost 40 research studies; now our consistent results across thousands of patients demonstrate that this program is replicable in virtually any 'real world' setting."
The DIAMOND Program
Medical groups, health plans, employers, patients and the Minnesota Department of Human Services, under the auspices of ICSI, collaborated to develop the DIAMOND program. Launched in March 2008 through 10 clinics and now offered through a total of 83 primary care clinics, it is the first depression treatment program in the nation to integrate a collaborative care model with a reimbursement structure that enables medical groups to provide enhanced care support to patients with depression.
Key elements of the program, based on the IMPACT model created by Dr. Jurgen Unutzer, University of Washington, include: use of a standard assessment tool to improve the diagnosis and management of depression, the addition of a care manager and consulting psychiatrist to the patient's primary care treatment team, an evidence-based stepped-care approach to treatment, a tracking system to monitor follow-up care and treatment effectiveness, and tools to prevent the patient from relapsing back into depression. This extra bundle of care means the patient with depression is more frequently contacted, educated, encouraged and supported.
"Our two-year data also show that the DIAMOND program's approach to treatment including involving patients in their own recovery and giving them tools to avoid falling back into depressio works. Among 735 patients contacted a year after entering DIAMOND, 50% are in remission and another 17% have had at least a 50% reduction in the severity of their depression," says Jaeckels.
Payment Model
A key to the program's success has been a new payment model whereby medical groups receive a monthly fee from health plans to cover the costs of these additional care services. Without changes to the payment structure, medical groups would not be able to provide the care manager and consulting psychiatrist services to patients.
Health plans currently reimbursing clinics for delivering DIAMOND services include Blue Cross Blue Shield of Minnesota, HealthPartners, Mayo Clinic MMSI, Medica, Metropolitan Health Plan, PreferredOne, PrimeWest Health and UCare.
HealthPartners Research Foundation is nearing the halfway point of a five-year study on the DIAMOND program that is funded by a $3 million grant from the National Institute of Mental Health. That study is evaluating all aspects of the initiative, including changes in care delivery, patient outcomes (including productivity effects), and health care cost-effectiveness. The findings of that study will help determine the full value of the DIAMOND program.
"Our mission at ICSI is to improve the quality and lower the cost of care," said Kent Bottles, MD, president of ICSI. "DIAMOND is an excellent example of how collaboration among medical groups, health plans, employers and patients enables us to deliver on that mission."
The Institute for Clinical Systems Improvement (icsi) is a non-profit health care improvement organization that brings diverse stakeholders together to find solutions to complex health care problems. Sponsored by six health plans in Minnesota and Wisconsin, ICSI helps its 56 medical group and hospital members deliver higher quality and lower cost health care.
Of the 1,752 patients contacted six months after entering into the DIAMOND program to date, 45% were in remission and another 16% had at least a 50% reduction in the severity of their depression. An additional 1,285 DIAMOND patients unable to be reached at six months to determine their progress are presumed to be still depressed, although they could have gotten better. Using this measurement, 26% of DIAMOND clinic patients were in remission at six months, compared to only 5.8% of patients treated in 184 primary care and behavioral health clinics reporting in 2009 to MN Community Measurement, a nonprofit organization that publicly reports on medical group's quality results in Minnesota.
"Among the clinics reporting on patient outcomes stemming from their treatment plans, seven offering the DIAMOND program were in the top 10," said Jim Chase, president of MN Community Measurement. "Mayo Clinic had two of the state's top performing clinics, and clinics run by Family HealthServices Minnesota, HealthPartners Medical Group and Allina Medical Clinic that also offered the DIAMOND program all posted top 10 results."
"What's exciting about our latest data is that we continue to see significant positive patient response to DIAMOND treatment after two years of implementation and across metro and rural clinics," says Nancy Jaeckels, ICSI vice president of member relations and strategic initiatives. "DIAMOND was modeled on a concept proven in almost 40 research studies; now our consistent results across thousands of patients demonstrate that this program is replicable in virtually any 'real world' setting."
The DIAMOND Program
Medical groups, health plans, employers, patients and the Minnesota Department of Human Services, under the auspices of ICSI, collaborated to develop the DIAMOND program. Launched in March 2008 through 10 clinics and now offered through a total of 83 primary care clinics, it is the first depression treatment program in the nation to integrate a collaborative care model with a reimbursement structure that enables medical groups to provide enhanced care support to patients with depression.
Key elements of the program, based on the IMPACT model created by Dr. Jurgen Unutzer, University of Washington, include: use of a standard assessment tool to improve the diagnosis and management of depression, the addition of a care manager and consulting psychiatrist to the patient's primary care treatment team, an evidence-based stepped-care approach to treatment, a tracking system to monitor follow-up care and treatment effectiveness, and tools to prevent the patient from relapsing back into depression. This extra bundle of care means the patient with depression is more frequently contacted, educated, encouraged and supported.
"Our two-year data also show that the DIAMOND program's approach to treatment including involving patients in their own recovery and giving them tools to avoid falling back into depressio works. Among 735 patients contacted a year after entering DIAMOND, 50% are in remission and another 17% have had at least a 50% reduction in the severity of their depression," says Jaeckels.
Payment Model
A key to the program's success has been a new payment model whereby medical groups receive a monthly fee from health plans to cover the costs of these additional care services. Without changes to the payment structure, medical groups would not be able to provide the care manager and consulting psychiatrist services to patients.
Health plans currently reimbursing clinics for delivering DIAMOND services include Blue Cross Blue Shield of Minnesota, HealthPartners, Mayo Clinic MMSI, Medica, Metropolitan Health Plan, PreferredOne, PrimeWest Health and UCare.
HealthPartners Research Foundation is nearing the halfway point of a five-year study on the DIAMOND program that is funded by a $3 million grant from the National Institute of Mental Health. That study is evaluating all aspects of the initiative, including changes in care delivery, patient outcomes (including productivity effects), and health care cost-effectiveness. The findings of that study will help determine the full value of the DIAMOND program.
"Our mission at ICSI is to improve the quality and lower the cost of care," said Kent Bottles, MD, president of ICSI. "DIAMOND is an excellent example of how collaboration among medical groups, health plans, employers and patients enables us to deliver on that mission."
The Institute for Clinical Systems Improvement (icsi) is a non-profit health care improvement organization that brings diverse stakeholders together to find solutions to complex health care problems. Sponsored by six health plans in Minnesota and Wisconsin, ICSI helps its 56 medical group and hospital members deliver higher quality and lower cost health care.
суббота, 20 августа 2011 г.
A new culprit in depression?
The brains of people with severe depression have lower levels of several related molecules that are key to the
development, organization, growth and repair of the brain than the brains of people without the disease, or those with the
bipolar form of depression, a new study finds.
The discovery, which surprised researchers in the multi-university consortium that made it, suggests a whole new direction
for understanding depression and developing new depression treatments. It may even help scientists understand how some
antidepressant medications work in the brain to ease symptoms, and why there is wide variation in how depressed people
respond to different antidepressants.
The finding was made in two specific areas of the brain known to be important to depression. The study relied on microarray
analysis of 32 post-mortem brain samples -- the microarray method can simultaneously measure the level of activity of tens of
thousands of genes that are functional in a given tissue.
The researchers found that levels of molecules called fibroblast growth factors (FGFs), and two of the receptors that bind to
them, were significantly lower among people who had been diagnosed with severe clinical depression and had died in a
depressed state. There was also some indication that those depressed people who had been taking antidepressants before their
deaths had levels of FGF and FGF receptors that were closer to normal.
The results are published online this week in the early edition of the Proceedings of the National Academy of Sciences by
researchers from the Pritzker Neuropsychiatric Disorders Research Consortium, which is supported by the Pritzker Family
Philanthropic Fund and by the National Institute of Mental Health. The research team consisted of scientists from the
University of Michigan's Mental Health Research Institute and Department of Psychiatry, working in close collaboration with
researchers from the University of California's Davis and Irvine campuses and from Stanford University.
"This finding comes from a completely unbiased search that began with no hypothesis, to find what genes best differentiate
major depression brains from normal and bipolar brains," says senior author Huda Akil, Ph.D., the Gardner C. Quarton
Distinguished Professor of Neurosciences in Psychiatry at U-M. "A wide set of individual genes came up as different between
the depressed and control individuals, but the family of genes that was most different and showed the highest significance as
a coherent group was the FGF family. This suggests a more profound change in an entire system of communication and control
within the brain."
No previous studies have directly examined the role of FGFs or their receptors in psychiatric illnesses. Another growth
factor, called Brain Derived Neurotrophic Factor, has been hypothesized to play a role in the effects of stress on the brain
and in the mode of action of antidepressants.
FGFs are a family of molecules that stimulate cell growth in many areas of the body, and are involved in the growth of
multiple tissues and in growth that takes place at various stages of life. They have potent effects during embryonic, fetal
and child development, and can modify the size and structure of particular brain regions. They are also involved in the
repair of adult tissues after injury and may mediate the cross-talk between different cell types in the brain.
As a result, they can be seen as mediators of the property that neuroscientists call "neural plasticity" -- the ability of
the brain to adapt to stress, experience, disease and the effects of drugs.
The research group started their study by measuring levels of approximately 20,000 different kinds of messenger RNA in
dissected brain samples from people who died from suicide, accidents and sudden medical causes. Messenger RNA levels are a
measure of how active different genes are, and the researchers took care only to study brains that had no complicating
factors that would have changed their mRNA levels at death.
The analysis was conducted on samples from two areas of the brain involved in the coordination of thinking and emotion: the
dorsolateral prefrontal cortex and the anterior cingulate cortex. Both are located toward the front of the brain behind the
forehead. Previously, brain scan studies have found differences in brain activity levels and size in these areas in people
with psychiatric illnesses.
In the current paper, the researchers report what they found when they zeroed in on a group of six kinds of related mRNA that
had the most coordinated differences between the samples from depressed brains, the non-depressed brains and the bipolar
brains.
These turned out to be mRNAs for four different FGF molecules and two receptors that bind to FGF and are key to their
function. Levels of all of the mRNAs encoding these proteins were lower in the brains of people with major depression. Lower
mRNA levels mean the brain may not produce enough protein to carry out normal function.
The team confirmed its finding using another genetic technique called PCR analysis, which revealed that the most significant
differences were in levels of mRNA for one of the FGFs, called FGF1, and for the two receptors, FGFR2 and FGFR3.
The researchers emphasize that they do not yet know whether the depressed people were born with lower levels of these
molecules, or whether the lower levels were brought on by the effects of depression on the brain or by external factors such
as stressful events. Other studies have shown that genes involved in brain chemistry and stress response are expressed
differently in the brains of depressed people and non-depressed people.
"We can't say whether these FGF gene expression changes are a predisposing factor for depression, or a consequence of the
disease process itself," says lead author and U-M research investigator Simon Evans, Ph.D. "There may be totally normal
people out there with compromised FGF systems, but if they don't experience stressful life events they may never develop
major depression. We need to study this system further to unravel this question."
Even as they made their discovery, the researchers grasped the potential significance of the FGF finding. "It's a new
direction for depression research to go," says Evans. "Given the known roles of this FGF family in neural development and
maintenance, it's not a huge leap to see how compromising the system could lead to changes in neural circuitry and contribute
to mood disorders."
"The bottom line is, the FGF system is less active in depressed individuals and presumably, correcting that would be part of
how you can make them better," says Akil, who is co-director of the U-M Mental Health Research Institute. "This finding gives
us a new target and a new set of ideas for pursuing better treatment."
Akil notes that the brains of bipolar people in the study did not show the decreased FGF gene activity. "This was all the
more remarkable since both groups of individuals were severely depressed at the time of death," she says. "This is yet
another indication that bipolar illness, though classified with depression as a mood disorder, is biologically a very
different disease.
The Pritzker Neuropsychiatric Disorders Research Fund L.L.C. has filed a patent application related to this research, but the
research team has made all of its data on mRNA levels for all types of growth factors available on the Internet. These can be
found with the paper on the PNAS web site, pnas.
With these results in hand, the research team hopes now to look at FGF levels in other areas of the brain including the
hippocampus, and to look for differences in levels of other families of growth factors. They also hope to look at the
different layers of the brain's cortex to see if there are any differences by layer. And, they hope to look at the genes that
encode FGFs and their receptors, to see if slight differences in gene sequence could modify the activity level of these genes
in the brain and contribute to the observed differences.
Akil also says it might be possible someday to study FGF differences in living people, if scientists can develop tools to
measure levels of the FGF receptors using brain imaging such as positron emission tomography, or PET.
In addition to Evans and Akil, the study's authors are: from the University of Michigan, Stanley J. Watson, Juan F. Lopez,
Robert C. Thompson, J. D. Stead, C.R. Neal and F. Meng; from UC Davis, P.V. Choudary and E.G. Jones, who communicated the
article to PNAS; from Stanford's Human Genome Center, J.Z. Li and R.M. Myers; and from UC Irvine, M.P. Vawter, H. Tomita,
D.M. Walsh, and W.E. Bunney. Several authors are members of the U-M Depression Center, the nation's first comprehensive
center devoted to research, treatment, education and public policy on depressive disorders.
Reference: Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0406788101 (open access paper)
Contact: Sally Pobojewski
poboumich
734-764-2220
University of Michigan Health System
development, organization, growth and repair of the brain than the brains of people without the disease, or those with the
bipolar form of depression, a new study finds.
The discovery, which surprised researchers in the multi-university consortium that made it, suggests a whole new direction
for understanding depression and developing new depression treatments. It may even help scientists understand how some
antidepressant medications work in the brain to ease symptoms, and why there is wide variation in how depressed people
respond to different antidepressants.
The finding was made in two specific areas of the brain known to be important to depression. The study relied on microarray
analysis of 32 post-mortem brain samples -- the microarray method can simultaneously measure the level of activity of tens of
thousands of genes that are functional in a given tissue.
The researchers found that levels of molecules called fibroblast growth factors (FGFs), and two of the receptors that bind to
them, were significantly lower among people who had been diagnosed with severe clinical depression and had died in a
depressed state. There was also some indication that those depressed people who had been taking antidepressants before their
deaths had levels of FGF and FGF receptors that were closer to normal.
The results are published online this week in the early edition of the Proceedings of the National Academy of Sciences by
researchers from the Pritzker Neuropsychiatric Disorders Research Consortium, which is supported by the Pritzker Family
Philanthropic Fund and by the National Institute of Mental Health. The research team consisted of scientists from the
University of Michigan's Mental Health Research Institute and Department of Psychiatry, working in close collaboration with
researchers from the University of California's Davis and Irvine campuses and from Stanford University.
"This finding comes from a completely unbiased search that began with no hypothesis, to find what genes best differentiate
major depression brains from normal and bipolar brains," says senior author Huda Akil, Ph.D., the Gardner C. Quarton
Distinguished Professor of Neurosciences in Psychiatry at U-M. "A wide set of individual genes came up as different between
the depressed and control individuals, but the family of genes that was most different and showed the highest significance as
a coherent group was the FGF family. This suggests a more profound change in an entire system of communication and control
within the brain."
No previous studies have directly examined the role of FGFs or their receptors in psychiatric illnesses. Another growth
factor, called Brain Derived Neurotrophic Factor, has been hypothesized to play a role in the effects of stress on the brain
and in the mode of action of antidepressants.
FGFs are a family of molecules that stimulate cell growth in many areas of the body, and are involved in the growth of
multiple tissues and in growth that takes place at various stages of life. They have potent effects during embryonic, fetal
and child development, and can modify the size and structure of particular brain regions. They are also involved in the
repair of adult tissues after injury and may mediate the cross-talk between different cell types in the brain.
As a result, they can be seen as mediators of the property that neuroscientists call "neural plasticity" -- the ability of
the brain to adapt to stress, experience, disease and the effects of drugs.
The research group started their study by measuring levels of approximately 20,000 different kinds of messenger RNA in
dissected brain samples from people who died from suicide, accidents and sudden medical causes. Messenger RNA levels are a
measure of how active different genes are, and the researchers took care only to study brains that had no complicating
factors that would have changed their mRNA levels at death.
The analysis was conducted on samples from two areas of the brain involved in the coordination of thinking and emotion: the
dorsolateral prefrontal cortex and the anterior cingulate cortex. Both are located toward the front of the brain behind the
forehead. Previously, brain scan studies have found differences in brain activity levels and size in these areas in people
with psychiatric illnesses.
In the current paper, the researchers report what they found when they zeroed in on a group of six kinds of related mRNA that
had the most coordinated differences between the samples from depressed brains, the non-depressed brains and the bipolar
brains.
These turned out to be mRNAs for four different FGF molecules and two receptors that bind to FGF and are key to their
function. Levels of all of the mRNAs encoding these proteins were lower in the brains of people with major depression. Lower
mRNA levels mean the brain may not produce enough protein to carry out normal function.
The team confirmed its finding using another genetic technique called PCR analysis, which revealed that the most significant
differences were in levels of mRNA for one of the FGFs, called FGF1, and for the two receptors, FGFR2 and FGFR3.
The researchers emphasize that they do not yet know whether the depressed people were born with lower levels of these
molecules, or whether the lower levels were brought on by the effects of depression on the brain or by external factors such
as stressful events. Other studies have shown that genes involved in brain chemistry and stress response are expressed
differently in the brains of depressed people and non-depressed people.
"We can't say whether these FGF gene expression changes are a predisposing factor for depression, or a consequence of the
disease process itself," says lead author and U-M research investigator Simon Evans, Ph.D. "There may be totally normal
people out there with compromised FGF systems, but if they don't experience stressful life events they may never develop
major depression. We need to study this system further to unravel this question."
Even as they made their discovery, the researchers grasped the potential significance of the FGF finding. "It's a new
direction for depression research to go," says Evans. "Given the known roles of this FGF family in neural development and
maintenance, it's not a huge leap to see how compromising the system could lead to changes in neural circuitry and contribute
to mood disorders."
"The bottom line is, the FGF system is less active in depressed individuals and presumably, correcting that would be part of
how you can make them better," says Akil, who is co-director of the U-M Mental Health Research Institute. "This finding gives
us a new target and a new set of ideas for pursuing better treatment."
Akil notes that the brains of bipolar people in the study did not show the decreased FGF gene activity. "This was all the
more remarkable since both groups of individuals were severely depressed at the time of death," she says. "This is yet
another indication that bipolar illness, though classified with depression as a mood disorder, is biologically a very
different disease.
The Pritzker Neuropsychiatric Disorders Research Fund L.L.C. has filed a patent application related to this research, but the
research team has made all of its data on mRNA levels for all types of growth factors available on the Internet. These can be
found with the paper on the PNAS web site, pnas.
With these results in hand, the research team hopes now to look at FGF levels in other areas of the brain including the
hippocampus, and to look for differences in levels of other families of growth factors. They also hope to look at the
different layers of the brain's cortex to see if there are any differences by layer. And, they hope to look at the genes that
encode FGFs and their receptors, to see if slight differences in gene sequence could modify the activity level of these genes
in the brain and contribute to the observed differences.
Akil also says it might be possible someday to study FGF differences in living people, if scientists can develop tools to
measure levels of the FGF receptors using brain imaging such as positron emission tomography, or PET.
In addition to Evans and Akil, the study's authors are: from the University of Michigan, Stanley J. Watson, Juan F. Lopez,
Robert C. Thompson, J. D. Stead, C.R. Neal and F. Meng; from UC Davis, P.V. Choudary and E.G. Jones, who communicated the
article to PNAS; from Stanford's Human Genome Center, J.Z. Li and R.M. Myers; and from UC Irvine, M.P. Vawter, H. Tomita,
D.M. Walsh, and W.E. Bunney. Several authors are members of the U-M Depression Center, the nation's first comprehensive
center devoted to research, treatment, education and public policy on depressive disorders.
Reference: Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0406788101 (open access paper)
Contact: Sally Pobojewski
poboumich
734-764-2220
University of Michigan Health System
четверг, 18 августа 2011 г.
Brain Changes Linked To Depression Caused By Light At Night
Exposure to even dim light at night is enough to cause physical changes in the brains of hamsters that may be associated with depression, a new study shows.
Researchers found that female Siberian hamsters exposed to dim light every night for eight weeks showed significant changes in a part of the brain called the hippocampus.
This is the first time researchers have found that light at night, by itself, may be linked to changes in the hippocampus.
These alterations may be a key reason why the researchers also found that the hamsters exposed to dim light at night showed more depressive symptoms when compared to hamsters in a standard light-dark cycle.
"Even dim light at night is sufficient to provoke depressive-like behaviors in hamsters, which may be explained by the changes we saw in their brains after eight weeks of exposure," said Tracy Bedrosian, co-author of the study and doctoral student in neuroscience at Ohio State University.
Bedrosian and her colleagues presented the result in San Diego at the annual meeting of the Society for Neuroscience.
The results are significant because the night-time light used in the study was not bright: 5 lux, or the equivalent of having a television on in a darkened room, said Randy Nelson, co-author of the study and professor of neuroscience and psychology at Ohio State.
"You would expect to see an impact if we were blasting these hamsters with bright lights, but this was a very low level, something that most people could easily encounter every night," said Nelson, who is also a member of Ohio State's Institute for Behavioral Medicine Research.
The study involved female Siberian hamsters, which had their ovaries removed to ensure that hormones produced in the ovary would not interfere with the results.
Half were housed in a standard light-dark cycle of 16 hours of light (at 150 lux) and eight hours of total darkness. The other half were housed in 16 hours of daylight (150 lux) and eight hours of dim light (5 lux).
After eight weeks in their lighting condition, they were tested for depressive-like behaviors. These tests are the same ones used by pharmaceutical companies to test anti-depressive and anti-anxiety drugs in animals before they are used in humans.
One depression test, for example, measured how much sugar water the mice drank. Mice generally like the drink, but those with depressive-like symptoms will not drink as much, presumably because they don't get as much pleasure from activities they usually enjoy.
Results showed that hamsters that lived in the dim light at night showed more symptoms of depression compared to the hamsters in the standard light-dark cycle.
At the end of the experiment, the researchers examined the hippocampus area of the hamsters' brains.
Results showed that mice that lived in the dim light had a significantly reduced density of dendritic spines - hairlike growths on brain cells, which are used to send chemical messages from one cell to another.
"The hippocampus plays a key role in depressive disorders, so finding changes there is significant," Bedrosian said.
The researchers found no difference between the two groups of hamsters in terms of concentrations of the stress hormone cortisol. That's important because hormones like cortisol have been linked to changes in the hippocampus.
"To the best of our knowledge, this is the first study to document that light at night is a sufficient stimulus to induce changes in the hippocampus, without changes in cortisol levels," Nelson said.
How is light at night causing the changes in the hippocampus? The researchers believe it is related to production of the hormone melatonin. Light at night suppresses secretion of melatonin, which is involved in how the body knows it is nighttime.
The lower levels of melatonin at night may be the cause of the lower density of dendritic spines in the hippocampus, Bedrosian said.
The researchers are continuing this work by investigating the exact role of melatonin in the findings of this study.
These results are consistent with an earlier study by Nelson and his colleagues which found that constant bright light at night is linked to depressive symptoms in male mice. In another recent study, they found that light at night is also linked to weight gain in mice.
Other co-authors of the current study were Laura Fonken and James Walton, both graduate students at Ohio State.
Researchers found that female Siberian hamsters exposed to dim light every night for eight weeks showed significant changes in a part of the brain called the hippocampus.
This is the first time researchers have found that light at night, by itself, may be linked to changes in the hippocampus.
These alterations may be a key reason why the researchers also found that the hamsters exposed to dim light at night showed more depressive symptoms when compared to hamsters in a standard light-dark cycle.
"Even dim light at night is sufficient to provoke depressive-like behaviors in hamsters, which may be explained by the changes we saw in their brains after eight weeks of exposure," said Tracy Bedrosian, co-author of the study and doctoral student in neuroscience at Ohio State University.
Bedrosian and her colleagues presented the result in San Diego at the annual meeting of the Society for Neuroscience.
The results are significant because the night-time light used in the study was not bright: 5 lux, or the equivalent of having a television on in a darkened room, said Randy Nelson, co-author of the study and professor of neuroscience and psychology at Ohio State.
"You would expect to see an impact if we were blasting these hamsters with bright lights, but this was a very low level, something that most people could easily encounter every night," said Nelson, who is also a member of Ohio State's Institute for Behavioral Medicine Research.
The study involved female Siberian hamsters, which had their ovaries removed to ensure that hormones produced in the ovary would not interfere with the results.
Half were housed in a standard light-dark cycle of 16 hours of light (at 150 lux) and eight hours of total darkness. The other half were housed in 16 hours of daylight (150 lux) and eight hours of dim light (5 lux).
After eight weeks in their lighting condition, they were tested for depressive-like behaviors. These tests are the same ones used by pharmaceutical companies to test anti-depressive and anti-anxiety drugs in animals before they are used in humans.
One depression test, for example, measured how much sugar water the mice drank. Mice generally like the drink, but those with depressive-like symptoms will not drink as much, presumably because they don't get as much pleasure from activities they usually enjoy.
Results showed that hamsters that lived in the dim light at night showed more symptoms of depression compared to the hamsters in the standard light-dark cycle.
At the end of the experiment, the researchers examined the hippocampus area of the hamsters' brains.
Results showed that mice that lived in the dim light had a significantly reduced density of dendritic spines - hairlike growths on brain cells, which are used to send chemical messages from one cell to another.
"The hippocampus plays a key role in depressive disorders, so finding changes there is significant," Bedrosian said.
The researchers found no difference between the two groups of hamsters in terms of concentrations of the stress hormone cortisol. That's important because hormones like cortisol have been linked to changes in the hippocampus.
"To the best of our knowledge, this is the first study to document that light at night is a sufficient stimulus to induce changes in the hippocampus, without changes in cortisol levels," Nelson said.
How is light at night causing the changes in the hippocampus? The researchers believe it is related to production of the hormone melatonin. Light at night suppresses secretion of melatonin, which is involved in how the body knows it is nighttime.
The lower levels of melatonin at night may be the cause of the lower density of dendritic spines in the hippocampus, Bedrosian said.
The researchers are continuing this work by investigating the exact role of melatonin in the findings of this study.
These results are consistent with an earlier study by Nelson and his colleagues which found that constant bright light at night is linked to depressive symptoms in male mice. In another recent study, they found that light at night is also linked to weight gain in mice.
Other co-authors of the current study were Laura Fonken and James Walton, both graduate students at Ohio State.
вторник, 16 августа 2011 г.
Study: Diabetes Affects Patients' Well-Being And Also Impacts Spouses
Older patients with diabetes who are not dealing well with the disease are likely to have symptoms of depression, and spouses of older patients also suffer distress related to diabetes and its management, according to research from Purdue University.
"Responsibilities and anxieties can differ for patients with diabetes and their spouses, but each may experience stress, frustration and sadness at times related to the demands of living with this disease," said Melissa M. Franks, an assistant professor of child development and family studies. "We know spouses often support their partners, but in our work we want to know what form their involvement takes and how the disease and its management affect both the patient and spouse."
Franks and her team found that the distress spouses feel is similar to what patients feel, and this could contribute to their own depressive symptoms such as irritability or sadness. These depressive symptoms come from their own anxieties about living with the disease or caring for someone with the disease and not necessarily because the other person is struggling.
Researchers also found that when male patients were concerned about the management of their diabetes, their depressive symptoms were elevated more than those for female patients with similar levels of concerns.
"This gender difference is consistent with prior work showing that male patients who are not managing their disease well tend to experience greater depressive symptoms," Franks said. "And while we saw this difference between male and female patients, we did not see the same pattern of distress between their respective spouses. This is surprising, because one might assume that the spouse would be as worried, or, according to family roles, that wives might worry more. However, more research, especially long-term observations, is needed."
The findings, based on statistical models with 185 couples older than 50, appeared in the December issue of the Family Relations journal. The patients and spouses completed individual surveys that measured distress related to diabetes, such as adherence to treatment recommendations, as well as depressive symptoms. The gender effects were measured by comparing the couples' responses. There were 67 female patients and 118 male patients, and each couple was screened to make sure only one person had diabetes.
"Because spouses' distress is not always directly linked to feelings of their partner, it tells us that we need to pay more attention to the spouse as well as the patient," she said. "Understanding the triggers for depressive symptoms can help practitioners and experts better care for patients and spouses as individuals and as a unit.
"We also found that many people reported some depressive symptoms, and some reported levels indicative of risk for clinical depression. It's important to consider depressive symptoms because they may signal concerns and problems that could be alleviated with treatment."
Diabetes affects about one in five Americans over the age of 60, and the majority of those people have Type 2 diabetes, which is a disease of the endocrine system. Type 2 diabetes, also referred to as adult-onset diabetes, is caused by insufficient secretion of insulin and resistance to insulin, which is problematic because it lessens the ability of cells to absorb glucose from the bloodstream. The incidence of the disease, which is considered a leading cause of death, is increasing as more people are overweight and sedentary.
The disease is managed daily through diet, exercise and medications. Complications, such as poor blood circulation, vision impairment, heart disease and stroke, are possible if the disease is not managed. In this study, spouses often reported that the disease's daily management as well as the fear of their loved one's living with diabetes were common concerns.
Franks co-authored the study with Todd Lucas from Wayne State University, Mary Ann Parris Stephens from Kent State University, Karen S. Rook from the University of California at Irvine and Richard Gonzalez at University of Michigan.
This work was funded by the National Institute on Aging and the Kent State University-Summa Health System Center for the Treatment and Study of Traumatic Stress. Franks' future studies will look at diet management in the context of distress and depression for patients and their spouses.
"Responsibilities and anxieties can differ for patients with diabetes and their spouses, but each may experience stress, frustration and sadness at times related to the demands of living with this disease," said Melissa M. Franks, an assistant professor of child development and family studies. "We know spouses often support their partners, but in our work we want to know what form their involvement takes and how the disease and its management affect both the patient and spouse."
Franks and her team found that the distress spouses feel is similar to what patients feel, and this could contribute to their own depressive symptoms such as irritability or sadness. These depressive symptoms come from their own anxieties about living with the disease or caring for someone with the disease and not necessarily because the other person is struggling.
Researchers also found that when male patients were concerned about the management of their diabetes, their depressive symptoms were elevated more than those for female patients with similar levels of concerns.
"This gender difference is consistent with prior work showing that male patients who are not managing their disease well tend to experience greater depressive symptoms," Franks said. "And while we saw this difference between male and female patients, we did not see the same pattern of distress between their respective spouses. This is surprising, because one might assume that the spouse would be as worried, or, according to family roles, that wives might worry more. However, more research, especially long-term observations, is needed."
The findings, based on statistical models with 185 couples older than 50, appeared in the December issue of the Family Relations journal. The patients and spouses completed individual surveys that measured distress related to diabetes, such as adherence to treatment recommendations, as well as depressive symptoms. The gender effects were measured by comparing the couples' responses. There were 67 female patients and 118 male patients, and each couple was screened to make sure only one person had diabetes.
"Because spouses' distress is not always directly linked to feelings of their partner, it tells us that we need to pay more attention to the spouse as well as the patient," she said. "Understanding the triggers for depressive symptoms can help practitioners and experts better care for patients and spouses as individuals and as a unit.
"We also found that many people reported some depressive symptoms, and some reported levels indicative of risk for clinical depression. It's important to consider depressive symptoms because they may signal concerns and problems that could be alleviated with treatment."
Diabetes affects about one in five Americans over the age of 60, and the majority of those people have Type 2 diabetes, which is a disease of the endocrine system. Type 2 diabetes, also referred to as adult-onset diabetes, is caused by insufficient secretion of insulin and resistance to insulin, which is problematic because it lessens the ability of cells to absorb glucose from the bloodstream. The incidence of the disease, which is considered a leading cause of death, is increasing as more people are overweight and sedentary.
The disease is managed daily through diet, exercise and medications. Complications, such as poor blood circulation, vision impairment, heart disease and stroke, are possible if the disease is not managed. In this study, spouses often reported that the disease's daily management as well as the fear of their loved one's living with diabetes were common concerns.
Franks co-authored the study with Todd Lucas from Wayne State University, Mary Ann Parris Stephens from Kent State University, Karen S. Rook from the University of California at Irvine and Richard Gonzalez at University of Michigan.
This work was funded by the National Institute on Aging and the Kent State University-Summa Health System Center for the Treatment and Study of Traumatic Stress. Franks' future studies will look at diet management in the context of distress and depression for patients and their spouses.
воскресенье, 14 августа 2011 г.
In Workplace, Bipolar Disorder Exacts Twice Depression's Toll
Bipolar disorder costs twice as much in lost productivity as major depressive disorder, a study funded by the National Institutes of Health's (NIH) National Institute of Mental Health (NIMH) has found. Each U.S. worker with bipolar disorder averaged 65.5 lost workdays in a year, compared to 27.2 for major depression. Even though major depression is more than six times as prevalent, bipolar disorder costs the U.S. workplace nearly half as much - a disproportionately high $14.1 billion annually. Researchers traced the higher toll mostly to bipolar disorder's more severe depressive episodes rather than to its agitated manic periods. The study by Drs. Ronald Kessler, Philip Wang, Harvard University, and colleagues, is among two on mood disorders in the workplace published in the September 2006 issue of the American Journal of Psychiatry.
Their study is the first to distinguish the impact of depressive episodes due to bipolar disorder from those due to major depressive disorder on the workplace. It is based on one-year data from 3378 employed respondents to the National Co-morbidity Survey Replication, a nationally representative household survey of 9,282 U.S. adults, conducted in 2001-2003.
The researchers measured the persistence of the disorders by asking respondents how many days during the past year they experienced an episode of mood disorder. They judged the severity based on symptoms during a worst month. Lost work days due to absence or poor functioning on the job, combined with salary data, yielded an estimate of lost productivity due to the disorders.
Poor functioning while at work accounted for more lost days than absenteeism. Although only about 1 percent of workers have bipolar disorder in a year, compared to 6.4 percent with major depression, the researchers projected that bipolar disorder accounts for 96.2 million lost workdays and $14.1 billion in lost salary-equivalent productivity, compared to 225 million workdays and $36.6 billion for major depression annually in the United States.
About three-fourths of bipolar respondents had experienced depressive episodes over the past year, with about 63 percent also having agitated manic or hypomanic episodes. The bipolar-associated depressive episodes were much more persistent - affecting 134-164 days - compared to only 98 days for major depression. The bipolar-associated depressive episodes were also more severe. All measures of lost work performance were consistently higher among workers with bipolar disorder who had major depressive episodes than those who reported only manic or hypomanic episodes. The latter workers' lost performance was on a par with workers who had major depressive disorder.
"Major depressive episodes due to bipolar disorder are sometimes incorrectly treated as major depressive disorder," noted Wang. "Since antidepressants can trigger the onset of mania, workplace programs should first rule out the possibility that a depressive episode may be due to bipolar disorder."
Future effectiveness trials could gauge the return on investment for employers offering coordinated evaluations and treatment for both mood disorders, he said.
Also participating in the study were: Dr. Kathleen Merikangas, NIMH; Dr. Minnie Ames and Robert Jin, Harvard University; Dr. Howard Birnbaum, Paul Greenberg, Analysis Group Inc.; Dr. Robert Hirschfeld, University of Texas; Dr. Hagop Akiskal, University of California San Diego.
In a related NIMH-funded study in the same issue of the American Journal of Psychiatry, Drs. Debra Lerner, David Adler, and colleagues, Tufts University School of Medicine and Tufts-New England Medical Center, found that many aspects of job performance are impaired by depression and that the effects linger even after symptoms have improved.
The researchers tracked the job performance and productivity of 286 employed patients with depression and dysthymia, 93 with rheumatoid arthritis and 193 healthy controls recruited from primary care physician practices for 18 months. While job performance improved as depression symptoms waned, even "clinically improved" depressed patients performed worse than healthy controls on mental, interpersonal, time management, output and physical tasks. The arthritis patients showed greater impairment, compared to healthy controls, only for physical job demands.
Noting that 44 percent of the depressed patients were already taking antidepressants when they began the study and still met clinical criteria for depression - and that job performance continued to suffer despite some clinical improvement - the researchers recommended that the goal of depression treatment should be remission. They also suggest that health professionals pay more attention to recovery of work function and that workplace supports be developed, perhaps through employee assistance programs and worksite occupational health clinics, to help depressed patients better manage job demands.
Also participating in the study were: Dr. William Rogers, Dr. Hong Chang, Leueen Lapitsky, Tufts-New England Medical Center; Dr. Thomas McLaughlin, University of Massachusetts Medical School.
The National Institute on Drug Abuse (NIDA), Substance Abuse and Mental Health Services Administration (SAMHSA), Robert Wood Johnson Foundation and John W. Alden Trust provided supplemental funding.
The Tufts-New England Medical Center General Clinical Research Center is funded by the NIH's National Center for Research Resources.
The National Institute of Mental Health (NIMH) mission is to reduce the burden of mental and behavioral disorders through research on mind, brain, and behavior. More information is available at the NIMH website, nimh.nih/.
The National Institute on Drug Abuse is a component of the National Institutes of Health, U.S. Department of Health and Human Services. NIDA supports more than 85 percent of the world's research on the health aspects of drug abuse and addiction. The Institute carries out a large variety of programs to ensure the rapid dissemination of research information and its implementation in policy and practice. Fact sheets on the health effects of drugs of abuse and information on NIDA research and other activities can be found on the NIDA home page at drugabuse/.
NCRR provides laboratory scientists and clinical researchers with the environments and tools they need to understand, detect, treat, and prevent a wide range of diseases. With this support, scientists make biomedical discoveries, translate these findings to animal-based studies, and then apply them to patient-oriented research. Ultimately, these advances result in cures and treatments for both common and rare diseases. NCRR also connects researchers with one another, and with patients and communities across the nation. These connections bring together innovative research teams and the power of shared resources, multiplying the opportunities to improve human health. For more information, visit ncrr.nih/.
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit nih/.
Contact: Jules Asher
NIH/National Institute of Mental Health
Their study is the first to distinguish the impact of depressive episodes due to bipolar disorder from those due to major depressive disorder on the workplace. It is based on one-year data from 3378 employed respondents to the National Co-morbidity Survey Replication, a nationally representative household survey of 9,282 U.S. adults, conducted in 2001-2003.
The researchers measured the persistence of the disorders by asking respondents how many days during the past year they experienced an episode of mood disorder. They judged the severity based on symptoms during a worst month. Lost work days due to absence or poor functioning on the job, combined with salary data, yielded an estimate of lost productivity due to the disorders.
Poor functioning while at work accounted for more lost days than absenteeism. Although only about 1 percent of workers have bipolar disorder in a year, compared to 6.4 percent with major depression, the researchers projected that bipolar disorder accounts for 96.2 million lost workdays and $14.1 billion in lost salary-equivalent productivity, compared to 225 million workdays and $36.6 billion for major depression annually in the United States.
About three-fourths of bipolar respondents had experienced depressive episodes over the past year, with about 63 percent also having agitated manic or hypomanic episodes. The bipolar-associated depressive episodes were much more persistent - affecting 134-164 days - compared to only 98 days for major depression. The bipolar-associated depressive episodes were also more severe. All measures of lost work performance were consistently higher among workers with bipolar disorder who had major depressive episodes than those who reported only manic or hypomanic episodes. The latter workers' lost performance was on a par with workers who had major depressive disorder.
"Major depressive episodes due to bipolar disorder are sometimes incorrectly treated as major depressive disorder," noted Wang. "Since antidepressants can trigger the onset of mania, workplace programs should first rule out the possibility that a depressive episode may be due to bipolar disorder."
Future effectiveness trials could gauge the return on investment for employers offering coordinated evaluations and treatment for both mood disorders, he said.
Also participating in the study were: Dr. Kathleen Merikangas, NIMH; Dr. Minnie Ames and Robert Jin, Harvard University; Dr. Howard Birnbaum, Paul Greenberg, Analysis Group Inc.; Dr. Robert Hirschfeld, University of Texas; Dr. Hagop Akiskal, University of California San Diego.
In a related NIMH-funded study in the same issue of the American Journal of Psychiatry, Drs. Debra Lerner, David Adler, and colleagues, Tufts University School of Medicine and Tufts-New England Medical Center, found that many aspects of job performance are impaired by depression and that the effects linger even after symptoms have improved.
The researchers tracked the job performance and productivity of 286 employed patients with depression and dysthymia, 93 with rheumatoid arthritis and 193 healthy controls recruited from primary care physician practices for 18 months. While job performance improved as depression symptoms waned, even "clinically improved" depressed patients performed worse than healthy controls on mental, interpersonal, time management, output and physical tasks. The arthritis patients showed greater impairment, compared to healthy controls, only for physical job demands.
Noting that 44 percent of the depressed patients were already taking antidepressants when they began the study and still met clinical criteria for depression - and that job performance continued to suffer despite some clinical improvement - the researchers recommended that the goal of depression treatment should be remission. They also suggest that health professionals pay more attention to recovery of work function and that workplace supports be developed, perhaps through employee assistance programs and worksite occupational health clinics, to help depressed patients better manage job demands.
Also participating in the study were: Dr. William Rogers, Dr. Hong Chang, Leueen Lapitsky, Tufts-New England Medical Center; Dr. Thomas McLaughlin, University of Massachusetts Medical School.
The National Institute on Drug Abuse (NIDA), Substance Abuse and Mental Health Services Administration (SAMHSA), Robert Wood Johnson Foundation and John W. Alden Trust provided supplemental funding.
The Tufts-New England Medical Center General Clinical Research Center is funded by the NIH's National Center for Research Resources.
The National Institute of Mental Health (NIMH) mission is to reduce the burden of mental and behavioral disorders through research on mind, brain, and behavior. More information is available at the NIMH website, nimh.nih/.
The National Institute on Drug Abuse is a component of the National Institutes of Health, U.S. Department of Health and Human Services. NIDA supports more than 85 percent of the world's research on the health aspects of drug abuse and addiction. The Institute carries out a large variety of programs to ensure the rapid dissemination of research information and its implementation in policy and practice. Fact sheets on the health effects of drugs of abuse and information on NIDA research and other activities can be found on the NIDA home page at drugabuse/.
NCRR provides laboratory scientists and clinical researchers with the environments and tools they need to understand, detect, treat, and prevent a wide range of diseases. With this support, scientists make biomedical discoveries, translate these findings to animal-based studies, and then apply them to patient-oriented research. Ultimately, these advances result in cures and treatments for both common and rare diseases. NCRR also connects researchers with one another, and with patients and communities across the nation. These connections bring together innovative research teams and the power of shared resources, multiplying the opportunities to improve human health. For more information, visit ncrr.nih/.
The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit nih/.
Contact: Jules Asher
NIH/National Institute of Mental Health
пятница, 12 августа 2011 г.
Depressed College Students Benefit From Study
A pilot program called the College Screening Project, a suicide prevention outreach program, was successful in identifying and treating college students with severe depression and feelings of desperation that may have led to suicide. The study, supported by the American Foundation for Suicide Prevention (AFSP), was conducted with Emory University students over six college semesters from 2002-2005.
Depression is a significant risk factor for suicide, and according to the Centers for Disease Control and Prevention (CDC) suicide is the third leading cause of death for teenagers and young adults, behind accidents and homicides.
"A profound percentage of the students who participated in AFSP's College Screening Project reported current (past four weeks) suicide ideation and were subsequently treated," says Charles B. Nemeroff, MD, PhD, Reunette W. Harris Professor and chair of the Department of Psychiatry and Behavioral Sciences at Emory University. "That represents a large number of lives that were improved, and possibly saved, because of this program."
The study, which began as simply an outreach program, revealed some startling statistics about suicide risk and depression in college students:
11 percent of the participants in the screening project reported current suicidal ideation
16.5 percent of the participants in the screening project had made at least one lifetime suicide attempt
More than half had clinically significant depression
Suicide ideation was related not just to depression, but also to feelings of desperation and feeling overwhelmed or out of control.
"These are important emotions to look for in at risk students," says Nemeroff.
From 2002-2005, approximately 8,000 students were invited to participate in the AFSP program and asked to complete a brief questionnaire that covered depression and related problems. The invitations were distributed on a secure, project-developed website. During the three-year study interval, a total of 729 Emory students participated by completing the questionnaire.
An experienced clinician reviewed the responses and a detailed personalized assessment was returned to each student's secured email address. Students whose questionnaire results suggested significant problems were urged to come in for a face-to-face evaluation. In addition, a dialogue feature on the website gave the students the option to exchange follow-up messages with the clinician while remaining anonymous.
Study data showed that 91 percent of the students who filled out the questionnaire viewed the counselor's assessment; 34 percent engaged in dialogues and 20 percent came in for an evaluation. More than 80 students characterized as high-risk entered psychotherapy after the in-person evaluation.
The study also found that among students designated to be at-risk, the rates of those coming for in-person evaluation and entering treatment were three times higher for those who engaged in online dialogues than for those who did not. In addition, for some students who dialogued with the counselor the online relationship appeared to have had a therapeutic effect.
Steve Garlow, MD, PhD, a study co-author, believes that college students are particularly vulnerable when it comes to feelings of depression, but don't seek treatment because of concerns about the stigma attached to mental illness. "The students responded to this program because it was readily available and they were using technology that they could relate to and trusted to keep their identity anonymous."
David Moore, MD, study investigator and psychiatrist at Emory University's Student Health Center says, "We have always tended to be proactive, but this project was so effective that we continued to use the AFSP program at Emory. We believe it is a very effective tool for supporting our students."
Dr. Charles Nemeroff was principal investigator for the study, and currently serves as President of the American Foundation for Suicide Prevention.
Drs. Moore and Garlow are assistant professors in Emory's Department of Psychiatry and Behavioral Sciences. Jill Rosenberg, LCSW, project counselor, was with the department when the study was implemented.
The University of North Carolina, Chapel Hill (UNC) was included in the project for the last three of the six semesters.
In addition to Emory faculty, study authors included, Ann Haas, PhD, and J. John Mann, MD, with the AFSP; Bethany Koestner, BS, with the AFSP at the time the project was implemented; Jan Sedway, PhD, and Linda Nicholas, MD, with the Department of Psychiatry at the University of North Carolina School of Medicine, Chapel Hill and Herbert Hendin, MD, with New York Medical College in Valhalla.
The research was supported by unrestricted grants to the American Foundation for Suicide Prevention from Eli Lilly and Company, Wyeth Pharmaceuticals, Janssen Pharmaceuticals and Solvay Pharmaceuticals, Inc.
An article describing key findings of the initial implementation of the program recently appeared in the journal Depression and Anxiety (Vol 25: 482-488) 2008 and a second article summarizing the combined results of the pilot test that included both Emory University and UNC was published in the Journal of American College Health (Vol 57 (1): 15-22 (2008).
Depression is a significant risk factor for suicide, and according to the Centers for Disease Control and Prevention (CDC) suicide is the third leading cause of death for teenagers and young adults, behind accidents and homicides.
"A profound percentage of the students who participated in AFSP's College Screening Project reported current (past four weeks) suicide ideation and were subsequently treated," says Charles B. Nemeroff, MD, PhD, Reunette W. Harris Professor and chair of the Department of Psychiatry and Behavioral Sciences at Emory University. "That represents a large number of lives that were improved, and possibly saved, because of this program."
The study, which began as simply an outreach program, revealed some startling statistics about suicide risk and depression in college students:
11 percent of the participants in the screening project reported current suicidal ideation
16.5 percent of the participants in the screening project had made at least one lifetime suicide attempt
More than half had clinically significant depression
Suicide ideation was related not just to depression, but also to feelings of desperation and feeling overwhelmed or out of control.
"These are important emotions to look for in at risk students," says Nemeroff.
From 2002-2005, approximately 8,000 students were invited to participate in the AFSP program and asked to complete a brief questionnaire that covered depression and related problems. The invitations were distributed on a secure, project-developed website. During the three-year study interval, a total of 729 Emory students participated by completing the questionnaire.
An experienced clinician reviewed the responses and a detailed personalized assessment was returned to each student's secured email address. Students whose questionnaire results suggested significant problems were urged to come in for a face-to-face evaluation. In addition, a dialogue feature on the website gave the students the option to exchange follow-up messages with the clinician while remaining anonymous.
Study data showed that 91 percent of the students who filled out the questionnaire viewed the counselor's assessment; 34 percent engaged in dialogues and 20 percent came in for an evaluation. More than 80 students characterized as high-risk entered psychotherapy after the in-person evaluation.
The study also found that among students designated to be at-risk, the rates of those coming for in-person evaluation and entering treatment were three times higher for those who engaged in online dialogues than for those who did not. In addition, for some students who dialogued with the counselor the online relationship appeared to have had a therapeutic effect.
Steve Garlow, MD, PhD, a study co-author, believes that college students are particularly vulnerable when it comes to feelings of depression, but don't seek treatment because of concerns about the stigma attached to mental illness. "The students responded to this program because it was readily available and they were using technology that they could relate to and trusted to keep their identity anonymous."
David Moore, MD, study investigator and psychiatrist at Emory University's Student Health Center says, "We have always tended to be proactive, but this project was so effective that we continued to use the AFSP program at Emory. We believe it is a very effective tool for supporting our students."
Dr. Charles Nemeroff was principal investigator for the study, and currently serves as President of the American Foundation for Suicide Prevention.
Drs. Moore and Garlow are assistant professors in Emory's Department of Psychiatry and Behavioral Sciences. Jill Rosenberg, LCSW, project counselor, was with the department when the study was implemented.
The University of North Carolina, Chapel Hill (UNC) was included in the project for the last three of the six semesters.
In addition to Emory faculty, study authors included, Ann Haas, PhD, and J. John Mann, MD, with the AFSP; Bethany Koestner, BS, with the AFSP at the time the project was implemented; Jan Sedway, PhD, and Linda Nicholas, MD, with the Department of Psychiatry at the University of North Carolina School of Medicine, Chapel Hill and Herbert Hendin, MD, with New York Medical College in Valhalla.
The research was supported by unrestricted grants to the American Foundation for Suicide Prevention from Eli Lilly and Company, Wyeth Pharmaceuticals, Janssen Pharmaceuticals and Solvay Pharmaceuticals, Inc.
An article describing key findings of the initial implementation of the program recently appeared in the journal Depression and Anxiety (Vol 25: 482-488) 2008 and a second article summarizing the combined results of the pilot test that included both Emory University and UNC was published in the Journal of American College Health (Vol 57 (1): 15-22 (2008).
среда, 10 августа 2011 г.
European Medicines Agency Concludes New Advice To Doctors And Patientsfor Champix Needed
The European Medicines Agency (EMEA) has concluded that updated warnings
to doctors and patients are needed to increase awareness of cases of
suicidal ideation and suicide attempts reported in patients using
Champix (varenicline), a medicine indicated for smoking cessation in
adults.
The Committee for Medicinal Products for Human Use (CHMP) has been
closely monitoring the safety of Champix since it was first authorised
in the European Union (EU) in September 2006. As part of the routine
pharmacovigilance activities, all adverse reactions for Champix are
analysed on a regular basis. Cases of suicidal ideation and suicide were
reviewed in July, October and November 2007.
At its December 2007 meeting, the CHMP concluded that there is a need to
update the product information for Champix to warn doctors and patients
that depression has been reported in patients who are trying to stop
smoking using Champix. The symptoms of this depression may include
suicidal ideation and suicide attempt.
The CHMP has requested that the marketing authorisation holder, Pfizer,
submits a variation to the marketing authorisation for Champix before 19
December 2007 to implement these changes to the product information.
The EMEA will continue to keep this issue under close scrutiny and take
appropriate actions if further concerns arise.
Notes:
1. More information is available in a question-and-answer document here.
2. More information about Champix is available here.
emea.europa.eu
to doctors and patients are needed to increase awareness of cases of
suicidal ideation and suicide attempts reported in patients using
Champix (varenicline), a medicine indicated for smoking cessation in
adults.
The Committee for Medicinal Products for Human Use (CHMP) has been
closely monitoring the safety of Champix since it was first authorised
in the European Union (EU) in September 2006. As part of the routine
pharmacovigilance activities, all adverse reactions for Champix are
analysed on a regular basis. Cases of suicidal ideation and suicide were
reviewed in July, October and November 2007.
At its December 2007 meeting, the CHMP concluded that there is a need to
update the product information for Champix to warn doctors and patients
that depression has been reported in patients who are trying to stop
smoking using Champix. The symptoms of this depression may include
suicidal ideation and suicide attempt.
The CHMP has requested that the marketing authorisation holder, Pfizer,
submits a variation to the marketing authorisation for Champix before 19
December 2007 to implement these changes to the product information.
The EMEA will continue to keep this issue under close scrutiny and take
appropriate actions if further concerns arise.
Notes:
1. More information is available in a question-and-answer document here.
2. More information about Champix is available here.
emea.europa.eu
понедельник, 8 августа 2011 г.
Largest Gathering Of Neuromodulation Experts Explores Breaking Developments In Neurodevice Technologies
Leading researchers and clinicians from the field of neuromodulation assembled today at the 12th annual meeting of the North American Neuromodulation Society (NANS), continuing until December 7 in Las Vegas, NV. Through scientific oral and poster presentations, as well as tradeshow exhibits, participants in the NANS Conference will explore the latest research in new, reversible technologies that modulate brain and nerve cell activity to treat diseases and medical conditions including chronic pain, Alzheimer's disease, depression, obesity, epilepsy and Parkinson's disease.
"Neuromodulation has made impressive advances in the last year, including new medical technologies serving an increasing number of patients and scientific understanding to help unlock the secrets of the brain," noted Dr. Jaimie Henderson, NANS President and Stanford Medical School neurosurgeon. "This conference is a unique opportunity to bring together experts in the state-of-the-art practice and emerging applications of neuromodulation."
Highlights from the conference include:
Major Depressive Disorder. This year's meeting focuses special emphasis on the use of neuromodulation for the treatment of depression. Only two months ago, the FDA approved the first use of transcranial magnetic stimulation (TMS) for a central brain disorder - depression. For the many sufferers of intractable depression who have exhausted other treatment avenues, deep brain stimulation (DBS) holds similar hope.
In separate presentations, Dr. Clement Hamani of the Toronto Western Hospital will report promising results from a multicenter study of 20 patients treated with DBS for major depressive order, and Helen Mayberg, Professor of Psychiatry and Neurology Emory University Atlanta, will describe recent advances in our understanding of the brain circuits involved in depression and which areas should be targeted for neuromodulation therapies.
Pain. Several presentations at this year's conference describe advances in the use of neuromodulation to treat debilitating pain, ranging from lower back pain to migraines and cluster headaches. In addition, Dr. Lisa Stearns of the Center for Pain & Supportive Care in Scottsdale, AZ, will report a new cost analysis of the use of intrathecal drug delivery (sending drugs directly into the cerebral spinal fluid to reach pain-sensitive neurons) which supports its use in the treatment of pain associated with cancer. And Stanford University anesthesiologist Dr. Sean Mackey will provide an overview of recent work imaging the neural circuits involved in the perception of pain.
Stroke Rehabilitation. The idea that the adult brain can reorganize to restore normal function after sustaining trauma is well accepted, but the means to achieving such rehabilitation is still a work-in-progress. A recent clinical trial - EVEREST - tested the idea that directly stimulating the brain with electrical signals coupled with classical rehabilitation techniques may speed the recovery of movement. Dr. Robert Levy, a neurosurgeon at Northwestern University in Chicago, will report new analyses of the trial data which suggest that this approach may be successful in some, but not all, stroke victims.
New Technologies. A special session on novel neuromodulation therapies will explore the cutting edge of electrical and optical technologies for studying and altering pathological brain activity. These include advances in the use of light as a tool to alter neural activity, new uses of transcranial magnetic stimulation and the use of oscillating electric fields to regrow spinal nerves after injury. Dr Karl Deisseroth, a neuroscientist at Stanford University, will deliver the keynote address, reporting on his work to engineer light-reactive molecules into neural circuits to manipulate and study patterns of activity in model organisms.
About Neuromodulation
Neuromodulation employs advanced medical device technologies to enhance or suppress activity of the nervous system for the treatment of disease. These technologies include implantable as well as non-implantable devices that deliver electrical, chemical or other agents to reversibly modify brain and nerve cell activity.
Neuromodulation therapies are:
- Highly targeted to specific areas of the brain or spinal cord, rather than systemic throughout the body such as pharmaceutical treatments
- Highly reversible, allowing physicians to immediately cease treatment with the removal of the device
- Continuous, improving therapeutic compliance over techniques that rely on fixed intermittent dosing
The most common neuromodulation therapy is spinal cord stimulation to treat chronic neuropathic pain. In addition to chronic pain relief, some examples of neuromodulation therapies employed around the world include deep brain stimulation for the treatment of numerous disorders including essential tremor, Parkinson's Disease, dystonia, epilepsy and psychiatric disorders such as depression, obsessive compulsive disorder and Tourette's Syndrome; sacral nerve stimulation for pelvic disorders and incontinence; gastric and colonic stimulation for gastrointestinal disorders such as dysmotility or obesity; vagal nerve stimulation for epilepsy, obesity or depression; and spinal cord stimulation for ischemic disorders such as angina and peripheral vascular disease.
About the North American Neuromodulation Society
The North American Neuromodulation Society (NANS) is the largest chapter of the International Neuromodulation Society (INS). These non-profit organizations connect researchers, clinicians, companies and institutions worldwide that are focused on research, development and implementation of neuromodulation therapies.
INS and NANS provide a forum for communication and interaction among clinicians, basic scientists and bioengineers engaged in neuromodulation research and therapeutic development through a combination of scientific meetings, scientific publications and an interactive website.
North American Neuromodulation Society
"Neuromodulation has made impressive advances in the last year, including new medical technologies serving an increasing number of patients and scientific understanding to help unlock the secrets of the brain," noted Dr. Jaimie Henderson, NANS President and Stanford Medical School neurosurgeon. "This conference is a unique opportunity to bring together experts in the state-of-the-art practice and emerging applications of neuromodulation."
Highlights from the conference include:
Major Depressive Disorder. This year's meeting focuses special emphasis on the use of neuromodulation for the treatment of depression. Only two months ago, the FDA approved the first use of transcranial magnetic stimulation (TMS) for a central brain disorder - depression. For the many sufferers of intractable depression who have exhausted other treatment avenues, deep brain stimulation (DBS) holds similar hope.
In separate presentations, Dr. Clement Hamani of the Toronto Western Hospital will report promising results from a multicenter study of 20 patients treated with DBS for major depressive order, and Helen Mayberg, Professor of Psychiatry and Neurology Emory University Atlanta, will describe recent advances in our understanding of the brain circuits involved in depression and which areas should be targeted for neuromodulation therapies.
Pain. Several presentations at this year's conference describe advances in the use of neuromodulation to treat debilitating pain, ranging from lower back pain to migraines and cluster headaches. In addition, Dr. Lisa Stearns of the Center for Pain & Supportive Care in Scottsdale, AZ, will report a new cost analysis of the use of intrathecal drug delivery (sending drugs directly into the cerebral spinal fluid to reach pain-sensitive neurons) which supports its use in the treatment of pain associated with cancer. And Stanford University anesthesiologist Dr. Sean Mackey will provide an overview of recent work imaging the neural circuits involved in the perception of pain.
Stroke Rehabilitation. The idea that the adult brain can reorganize to restore normal function after sustaining trauma is well accepted, but the means to achieving such rehabilitation is still a work-in-progress. A recent clinical trial - EVEREST - tested the idea that directly stimulating the brain with electrical signals coupled with classical rehabilitation techniques may speed the recovery of movement. Dr. Robert Levy, a neurosurgeon at Northwestern University in Chicago, will report new analyses of the trial data which suggest that this approach may be successful in some, but not all, stroke victims.
New Technologies. A special session on novel neuromodulation therapies will explore the cutting edge of electrical and optical technologies for studying and altering pathological brain activity. These include advances in the use of light as a tool to alter neural activity, new uses of transcranial magnetic stimulation and the use of oscillating electric fields to regrow spinal nerves after injury. Dr Karl Deisseroth, a neuroscientist at Stanford University, will deliver the keynote address, reporting on his work to engineer light-reactive molecules into neural circuits to manipulate and study patterns of activity in model organisms.
About Neuromodulation
Neuromodulation employs advanced medical device technologies to enhance or suppress activity of the nervous system for the treatment of disease. These technologies include implantable as well as non-implantable devices that deliver electrical, chemical or other agents to reversibly modify brain and nerve cell activity.
Neuromodulation therapies are:
- Highly targeted to specific areas of the brain or spinal cord, rather than systemic throughout the body such as pharmaceutical treatments
- Highly reversible, allowing physicians to immediately cease treatment with the removal of the device
- Continuous, improving therapeutic compliance over techniques that rely on fixed intermittent dosing
The most common neuromodulation therapy is spinal cord stimulation to treat chronic neuropathic pain. In addition to chronic pain relief, some examples of neuromodulation therapies employed around the world include deep brain stimulation for the treatment of numerous disorders including essential tremor, Parkinson's Disease, dystonia, epilepsy and psychiatric disorders such as depression, obsessive compulsive disorder and Tourette's Syndrome; sacral nerve stimulation for pelvic disorders and incontinence; gastric and colonic stimulation for gastrointestinal disorders such as dysmotility or obesity; vagal nerve stimulation for epilepsy, obesity or depression; and spinal cord stimulation for ischemic disorders such as angina and peripheral vascular disease.
About the North American Neuromodulation Society
The North American Neuromodulation Society (NANS) is the largest chapter of the International Neuromodulation Society (INS). These non-profit organizations connect researchers, clinicians, companies and institutions worldwide that are focused on research, development and implementation of neuromodulation therapies.
INS and NANS provide a forum for communication and interaction among clinicians, basic scientists and bioengineers engaged in neuromodulation research and therapeutic development through a combination of scientific meetings, scientific publications and an interactive website.
North American Neuromodulation Society
суббота, 6 августа 2011 г.
Depression May Increase The Risk Of Kidney Failure
Depression is associated with an increased risk of developing kidney failure in the future, according to a study appearing in an upcoming issue of the Clinical Journal of the American Society Nephrology (CJASN). Approximately 10% of the US population will suffer from depression at some point during their lifetime.
Lead investigator, Dr. Willem Kop (Department of Medical Psychology and Neuropsychology at the University of Tilburg, the Netherlands) and colleagues studied 5,785 people from four counties across the United States for 10 years. The participants were 65 years and older and not yet on dialysis. They completed a questionnaire measuring depressive symptoms and a broad range of medical measurements, including estimated glomerular filtration rate (eGFR) and risk factors for kidney and heart diseases. The investigators examined whether depression predicted the onset of kidney disease or other medical problems in which the kidneys play a critical role.
According to the results, depression coincided with the presence of chronic kidney disease (CKD) and was 20% more common in individuals with kidney disease than those without kidney disease. The study shows that depression predicted subsequent rapid decline in kidney function, new onset clinically severe kidney disease (or end-stage renal disease), and hospitalizations that were complicated by acute kidney injury. When the investigators corrected for the long-term effects of other medical measures, the predictive value of depression for hospitalizations with acute kidney injury remained high.
Take home message: "People with elevated depressive symptoms have a higher risk of subsequent adverse kidney disease outcomes. This is partially explained by other medical factors related to depression and kidney disease. But, the association with depression was stronger in patients who were otherwise healthy compared to those who had co-existing medical disorders such as diabetes or heart disease," explains Kop.
The investigators are currently analyzing which factors may explain the association with depression, which could include delayed seeking of medical care and miscommunications between patient and physicians and important biological processes associated with depression, such as the immune and nervous systems.
Study co-authors include Stephen Seliger (University of Maryland, Nephrology); Jeffrey Fink (University of Maryland Medical System, Department of Medicine, Division of Nephrology); Ronit Katz (University of Washington, Biostatistics); Michelle Odden (University of California, Berkeley, Department of Epidemiology); Linda Fried (Veterans Affairs Pittsburgh Health System); Dena Rifkin (UCSD and VASDHS, Medicine); Mark Sarnak (Tufts-New England Medical Center, Medicine); and John Gottdiener (University of Maryland, School of Medicine, Medicine).
Disclosures: The project is based on the Cardiovascular Health Study, in collaboration with the Department of Medicine of the University of Maryland at Baltimore and other institutions throughout the United States and funded by the National Heart Lung and Blood Institute of the National Institutes of Health. The authors reported no financial disclosures.
Lead investigator, Dr. Willem Kop (Department of Medical Psychology and Neuropsychology at the University of Tilburg, the Netherlands) and colleagues studied 5,785 people from four counties across the United States for 10 years. The participants were 65 years and older and not yet on dialysis. They completed a questionnaire measuring depressive symptoms and a broad range of medical measurements, including estimated glomerular filtration rate (eGFR) and risk factors for kidney and heart diseases. The investigators examined whether depression predicted the onset of kidney disease or other medical problems in which the kidneys play a critical role.
According to the results, depression coincided with the presence of chronic kidney disease (CKD) and was 20% more common in individuals with kidney disease than those without kidney disease. The study shows that depression predicted subsequent rapid decline in kidney function, new onset clinically severe kidney disease (or end-stage renal disease), and hospitalizations that were complicated by acute kidney injury. When the investigators corrected for the long-term effects of other medical measures, the predictive value of depression for hospitalizations with acute kidney injury remained high.
Take home message: "People with elevated depressive symptoms have a higher risk of subsequent adverse kidney disease outcomes. This is partially explained by other medical factors related to depression and kidney disease. But, the association with depression was stronger in patients who were otherwise healthy compared to those who had co-existing medical disorders such as diabetes or heart disease," explains Kop.
The investigators are currently analyzing which factors may explain the association with depression, which could include delayed seeking of medical care and miscommunications between patient and physicians and important biological processes associated with depression, such as the immune and nervous systems.
Study co-authors include Stephen Seliger (University of Maryland, Nephrology); Jeffrey Fink (University of Maryland Medical System, Department of Medicine, Division of Nephrology); Ronit Katz (University of Washington, Biostatistics); Michelle Odden (University of California, Berkeley, Department of Epidemiology); Linda Fried (Veterans Affairs Pittsburgh Health System); Dena Rifkin (UCSD and VASDHS, Medicine); Mark Sarnak (Tufts-New England Medical Center, Medicine); and John Gottdiener (University of Maryland, School of Medicine, Medicine).
Disclosures: The project is based on the Cardiovascular Health Study, in collaboration with the Department of Medicine of the University of Maryland at Baltimore and other institutions throughout the United States and funded by the National Heart Lung and Blood Institute of the National Institutes of Health. The authors reported no financial disclosures.
четверг, 4 августа 2011 г.
SEROQUEL Exhibits Distinct Mechanism Of Action And Reduces The Risk Of A Mood Event In Bipolar I Disorder
New long-term clinical trial data presented recently at the European Congress of Neuropsychopharmacology (ECNP) in Vienna showed that SEROQUEL® (quetiapine fumarate) in combination with lithium or divalproex significantly increases the time to recurrence of any mood event in patients with bipolar I disorder.1 Further pre-clinical data demonstrated that three neurotransmitter pathways are targeted by SEROQUEL in the brain - this may contribute to its unique clinical profile.2 This data also showed that dosing with SEROQUEL causes occupancy of NET - transporter for norepinephrine, a neurotransmitter which is known to have a role in depression.
A large-scale, international, double-blind study (Study 126) investigated the time to recurrence of a mood event (manic, mixed, or depressed) in 1461 patients with bipolar I disorder initially stabilised with SEROQUEL (400-800 mg/day) plus lithium or divalproex.1 After stabilisation for a minimum of 12 weeks, 703 patients were randomised to maintenance treatment with SEROQUEL in combination with lithium or divalproex, or placebo in combination with lithium or divalproex for up to 104 weeks. Compared with placebo, fewer patients in the SEROQUEL group had a mood event, defined as a manic, mixed or depressed episode (49.0% versus 18.5%). SEROQUEL combination treatment also significantly reduced the risk of recurrence of a mood event in comparison with placebo plus lithium or divalproex (hazard ratio 0.28; p
A large-scale, international, double-blind study (Study 126) investigated the time to recurrence of a mood event (manic, mixed, or depressed) in 1461 patients with bipolar I disorder initially stabilised with SEROQUEL (400-800 mg/day) plus lithium or divalproex.1 After stabilisation for a minimum of 12 weeks, 703 patients were randomised to maintenance treatment with SEROQUEL in combination with lithium or divalproex, or placebo in combination with lithium or divalproex for up to 104 weeks. Compared with placebo, fewer patients in the SEROQUEL group had a mood event, defined as a manic, mixed or depressed episode (49.0% versus 18.5%). SEROQUEL combination treatment also significantly reduced the risk of recurrence of a mood event in comparison with placebo plus lithium or divalproex (hazard ratio 0.28; p
вторник, 2 августа 2011 г.
Patients Need Continuing Access To Life-Saving Treatment
The American Psychiatric Association is pleased that patients will continue to have access to life-saving Electroconvulsive Therapy (ECT) following an FDA advisory panel's two-day discussion about a possible reclassification of ECT devices.
"We're optimistic that this life-saving procedure will continue to be available as a treatment option for patients with debilitating illnesses," said APA President Carol Bernstein, M.D. "ECT is appropriate for a small percentage of patients, generally those with severe mental illnesses that have not responded to other treatments. When used properly, under the appropriate guidelines and by a well-trained psychiatrist, ECT is extremely safe and effective."
The panel was asked to advise the FDA whether to reclassify ECT devices from Class III to the less restrictive Class II for medical devices. Under Class III, makers of the devices would be required to go through the extensive premarket approval process.
Sarah H. Lisanby, M.D., Chair of the APA Task Force to Revise the Practice of Electroconvulsive Therapy, said the panel hearing discussions highlighted the high prevalence of Major Depressive Disorder in the country and the suffering that this condition can cause, including the risk of suicide.
"There was a general consensus that ECT is effective for severe major depression when other treatments fail, which is consistent with recently published randomized large-scale NIMH-sponsored studies," Dr. Lisanby said. "The continued availability for this life-saving treatment is of great importance to the patients who are suffering from severe depression that has not responded to other treatments.
"There was an acknowledgement that there are difficulties in performing controlled trials in acute and life-threatening conditions, such as catatonia. I am pleased that the FDA has undertaken a process to evaluate the evidence, and has sought the input of experts and consumer representatives on an issue of such high public health importance."
Bernstein said the use of ECT should be a decision between the fully informed patient and the physician.
"As with any medical procedure, the risks and benefits for the patient should be carefully weighed."
"We're optimistic that this life-saving procedure will continue to be available as a treatment option for patients with debilitating illnesses," said APA President Carol Bernstein, M.D. "ECT is appropriate for a small percentage of patients, generally those with severe mental illnesses that have not responded to other treatments. When used properly, under the appropriate guidelines and by a well-trained psychiatrist, ECT is extremely safe and effective."
The panel was asked to advise the FDA whether to reclassify ECT devices from Class III to the less restrictive Class II for medical devices. Under Class III, makers of the devices would be required to go through the extensive premarket approval process.
Sarah H. Lisanby, M.D., Chair of the APA Task Force to Revise the Practice of Electroconvulsive Therapy, said the panel hearing discussions highlighted the high prevalence of Major Depressive Disorder in the country and the suffering that this condition can cause, including the risk of suicide.
"There was a general consensus that ECT is effective for severe major depression when other treatments fail, which is consistent with recently published randomized large-scale NIMH-sponsored studies," Dr. Lisanby said. "The continued availability for this life-saving treatment is of great importance to the patients who are suffering from severe depression that has not responded to other treatments.
"There was an acknowledgement that there are difficulties in performing controlled trials in acute and life-threatening conditions, such as catatonia. I am pleased that the FDA has undertaken a process to evaluate the evidence, and has sought the input of experts and consumer representatives on an issue of such high public health importance."
Bernstein said the use of ECT should be a decision between the fully informed patient and the physician.
"As with any medical procedure, the risks and benefits for the patient should be carefully weighed."
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