Psychiatric treatment and psychosocial support may make a significant difference to survival and quality of life in women with cancer, a patient population with high rates of depression and anxiety, according to 2 studies presented here at the American Psychiatric Association 2011 Annual Meeting.
In the first study, a secondary analysis of a randomized controlled trial (RCT) of 125 women with metastatic breast cancer, investigators found that the median survival time for those who had decreasing depression symptom scores during a 1-year period was double that of those with increasing scores (53.6 vs 25.1 months).
"We were surprised at how big this difference was. It shows that treatment of depression, both psychotherapeutic and pharmacologic, is feasible and effective even in advanced cancer," David Spiegel, MD, Department of Psychiatry and Behavioral Sciences at Stanford University School of Medicine, California, and Stanford's Center on Stress and Health, told Medscape Medical News.
"Although the intervention we used wasn't associated with increased survival, we were able to show that decreasing depression may improve not only the quality but also the quantity of life for these women," added Dr. Spiegel.
In the second study, which was published online March 2 in Psycho-Oncology, researchers found that women who receive a cancer diagnosis during pregnancy were at particular risk of experiencing high levels of distress.
"Physicians should pay particular attention to several early markers of distress suggesting a need for referral to psychological supports. This may lead to improved long-term quality of life for both the women and for their children," Melissa Henry, PhD, from McGill University in Montreal, Quebec, Canada, told Medscape Medical News.
Monday, May 30, 2011
Thursday, May 26, 2011
Heavy Smoking Accompanies Postpartum Depression
Cigarette smoking should be a tip-off for the possibility of postpartum depression, according to a survey from the Pregnancy Risk Assessment Monitoring System. Results of a study suggesting this were presented here at American Congress of Obstetricians and Gynecologists 59th Annual Clinical Meeting.
The large survey showed that nearly 1 of every 3 mothers who reported smoking more than 10 cigarettes per day also had symptoms of clinical depression. Depression was more likely among heavier smokers who were younger, who were non-Hispanic black, and who had low levels of education.
"Our study suggests that screening and treatment of depression should be considered in all smoking-cessation programs that target new mothers," lead author Diana Cheng, MD, from the Maryland Department of Health and Mental Hygiene in Baltimore, told meeting attendees. The findings also suggest that healthcare workers should be alert to the possibility of postpartum depression in new mothers who are heavy smokers, and prescribe treatment accordingly, she added.
The study was based on a survey of a random sample of 8074 new mothers in Maryland who delivered babies between 2004 and 2008. Participants completed the survey between 2 and 9 months after delivery.
Fourteen percent of respondents reported smoking. Women were considered to have depression if they answered questions about depressive symptoms (mood and lack of interest) with "often" or "always". Compared with nonsmoking, heavier smoking was associated with 2 to 3 times the prevalence of depression (P < .05). Depression was strongly associated with the number of cigarettes smoked; it was found in 13% of nonsmokers, 22% of light smokers (10 or fewer cigarettes per day), and 29% of those who smoked more than 10 cigarettes per day.
The prevalence of depression was highest among heavier smokers who were younger than 20 years of age (41%) and were non-Hispanic blacks (39%). Depression was also strongly associated with education level: it was found in 46% of women who did not finish high school and in 9% of college graduates.
Postpartum depression is of great concern because it increases the risk of developing bipolar disorder and other psychosis, said Kristie Baisden, DO, chief resident at Georgetown University School of Medicine in Washington, DC. At the meeting, Dr. Baisden presented a poster on risk factors for postpartum depression. Her research on more than 900 women found that unemployment, being older than 35 years of age, and having any history of anxiety or depression increased the risk for postpartum depression.
"It is important to recognize and treat postpartum depression to avoid worsening mental health and subsequent problems," she stated.
The large survey showed that nearly 1 of every 3 mothers who reported smoking more than 10 cigarettes per day also had symptoms of clinical depression. Depression was more likely among heavier smokers who were younger, who were non-Hispanic black, and who had low levels of education.
"Our study suggests that screening and treatment of depression should be considered in all smoking-cessation programs that target new mothers," lead author Diana Cheng, MD, from the Maryland Department of Health and Mental Hygiene in Baltimore, told meeting attendees. The findings also suggest that healthcare workers should be alert to the possibility of postpartum depression in new mothers who are heavy smokers, and prescribe treatment accordingly, she added.
The study was based on a survey of a random sample of 8074 new mothers in Maryland who delivered babies between 2004 and 2008. Participants completed the survey between 2 and 9 months after delivery.
Fourteen percent of respondents reported smoking. Women were considered to have depression if they answered questions about depressive symptoms (mood and lack of interest) with "often" or "always". Compared with nonsmoking, heavier smoking was associated with 2 to 3 times the prevalence of depression (P < .05). Depression was strongly associated with the number of cigarettes smoked; it was found in 13% of nonsmokers, 22% of light smokers (10 or fewer cigarettes per day), and 29% of those who smoked more than 10 cigarettes per day.
The prevalence of depression was highest among heavier smokers who were younger than 20 years of age (41%) and were non-Hispanic blacks (39%). Depression was also strongly associated with education level: it was found in 46% of women who did not finish high school and in 9% of college graduates.
Postpartum depression is of great concern because it increases the risk of developing bipolar disorder and other psychosis, said Kristie Baisden, DO, chief resident at Georgetown University School of Medicine in Washington, DC. At the meeting, Dr. Baisden presented a poster on risk factors for postpartum depression. Her research on more than 900 women found that unemployment, being older than 35 years of age, and having any history of anxiety or depression increased the risk for postpartum depression.
"It is important to recognize and treat postpartum depression to avoid worsening mental health and subsequent problems," she stated.
Wednesday, May 25, 2011
Many Adults Report Troubled Childhood Experiences
Dec. 16, 2010 -- More than half of adults surveyed reported experiencing one or more difficult childhood experiences, such as domestic violence or verbal abuse, indicating that troubled childhood experiences could be common, according to a CDC study.
Adverse childhood experiences, such as physical abuse, sexual abuse, parents going through a divorce, a family member being in jail, and being mentally ill or abusing drugs, have been associated with an increased risk for several health problems, including heart disease, depression, cancer, and diabetes. By identifying and documenting the prevalence of adverse childhood experiences (ACEs), health care providers can boost their efforts in child abuse prevention and other parenting programs as a means to reduce ACEs.
Health Risks From Childhood
In this study, researchers from five state departments of health analyzed data from 26,229 adults living in Arkansas, Louisiana, New Mexico, Tennessee, and Washington State. The survey participants were asked about their childhood experiences involving eight categories of ACEs: verbal, physical, or sexual abuse, household mental illness, household substance abuse, witnessed domestic violence, parental separation or divorce, and incarcerated household member. Fifty-nine percent of the group reported experiencing at least one of these eight ACEs. Among the researchers' other findings:
8.7% of survey respondents reported experiencing five or more ACEs. Women were more likely than men to report more than five ACEs, 10.3% vs. 6.7%.
41% reported no ACEs.
Substance abuse was reported by 29.1% of the group, whereas an incarcerated family member was the least common response at 7.2%.
More than a quarter of respondents reported being verbally abused as a child; 14.8% reported physical abuse, and 12.2% reported sexual abuse.
Sexual abuse was more common among females than males, 17.2% vs. 6.7%.
26.6% of the group reported parental separation/divorce.
19.4% reported a history of living with someone mentally ill.
16.3% reported witnessing domestic violence.
Younger adults reported higher levels of physical abuse during their childhood compared with older adults, 16.9% among those aged 18 to 24 vs. 9.6% for those aged 55 and up.
Education was a major factor in ACEs, whereas race was not as significant. People with the least education were far more likely to report five or more ACEs compared with those who had higher levels of education; 14.9% among those who didn't complete high school vs. 8.7% among high school graduates vs. 7.7% among those with more than a high school education.
The findings are published in the Dec. 17 issue of Morbidity and Mortality Weekly Report (MMWR), a publication of the CDC.
"State-based surveillance of ACEs can provide guidance for the allocation of maltreatment prevention strategies and trauma-related intervention services," the authors write in MMWR. "In addition, more research is needed to disentangle the specific role each ACE plays in the development of health problems later in life."
Adverse childhood experiences, such as physical abuse, sexual abuse, parents going through a divorce, a family member being in jail, and being mentally ill or abusing drugs, have been associated with an increased risk for several health problems, including heart disease, depression, cancer, and diabetes. By identifying and documenting the prevalence of adverse childhood experiences (ACEs), health care providers can boost their efforts in child abuse prevention and other parenting programs as a means to reduce ACEs.
Health Risks From Childhood
In this study, researchers from five state departments of health analyzed data from 26,229 adults living in Arkansas, Louisiana, New Mexico, Tennessee, and Washington State. The survey participants were asked about their childhood experiences involving eight categories of ACEs: verbal, physical, or sexual abuse, household mental illness, household substance abuse, witnessed domestic violence, parental separation or divorce, and incarcerated household member. Fifty-nine percent of the group reported experiencing at least one of these eight ACEs. Among the researchers' other findings:
8.7% of survey respondents reported experiencing five or more ACEs. Women were more likely than men to report more than five ACEs, 10.3% vs. 6.7%.
41% reported no ACEs.
Substance abuse was reported by 29.1% of the group, whereas an incarcerated family member was the least common response at 7.2%.
More than a quarter of respondents reported being verbally abused as a child; 14.8% reported physical abuse, and 12.2% reported sexual abuse.
Sexual abuse was more common among females than males, 17.2% vs. 6.7%.
26.6% of the group reported parental separation/divorce.
19.4% reported a history of living with someone mentally ill.
16.3% reported witnessing domestic violence.
Younger adults reported higher levels of physical abuse during their childhood compared with older adults, 16.9% among those aged 18 to 24 vs. 9.6% for those aged 55 and up.
Education was a major factor in ACEs, whereas race was not as significant. People with the least education were far more likely to report five or more ACEs compared with those who had higher levels of education; 14.9% among those who didn't complete high school vs. 8.7% among high school graduates vs. 7.7% among those with more than a high school education.
The findings are published in the Dec. 17 issue of Morbidity and Mortality Weekly Report (MMWR), a publication of the CDC.
"State-based surveillance of ACEs can provide guidance for the allocation of maltreatment prevention strategies and trauma-related intervention services," the authors write in MMWR. "In addition, more research is needed to disentangle the specific role each ACE plays in the development of health problems later in life."
Psychiatry Deemed a Religion in New Study
Researchers at Jakarta's renowned Hebrew University recently published a study conclusively proving that Psychiatry should be classified as a religion. The study consisted of a study of Psychiatric textbooks and journals (which will now be known as scriptures) and interviews with Psychiatrists (better classified as priests) and patients (hereafter known as "the flock").
This work brings a logical answer to many nagging questions, like how Psychiatry could be considered the "authority" in matters of the mind when their results in the field have been poor, and are known to cause more damage than benefit. It may also shed some light on the tendency of Psychiatrists to molest children in a much higher percentage than the general populace.
"Psychiatry is portrayed alternately as a scientific study or branch of medicine but either of these is rapidly disproved," says Moshe Sapere of Hebrew University. "The science of Psychiatry is flawed. Their studies are mainly funded by drug companies and they publish illogical conclusions which - Surprise! - make the drug companies look good. Psychiatry claims similarity to medicine but this is in reality only marketing; the only real similarities to actual medicine are clothing and terminology. If you dressed up a parrot in a doctor's smock and taught it some Latin phrases, it wouldn't be a doctor. It's the same with Psychiatrists."
Some of the researchers were reluctant to agree with the "religion" moniker for a group known to be profit-based and harmful, but a study of religions of the past shows that many have been used for profit and have done harm to others. The matter of faith in a deity was also a sticking point but a study of Psychiatric scriptures reveals that Psychiatrists believe in an invisible entity known as "chemical imbalance". The existence of Chemical Imbalance is stated as fact in the texts though there is no proof of his existence, analogous to a Christian's belief in God or a Muslim's belief in Allah.
The key answer that led the researchers to declare Psychiatry as a religion is that their High Priests demand complete belief in unobservable phenomena and continue to forward their beliefs despite no obvious benefit. They are also known to vehemently attack anyone who points out the lack of proof to their claims. Most religions promise salvation in a future existence. Psychiatry does not specifically make those claims but clearly provides dubious benefit in this existence. The researchers are pleased that they have been able to finally clarify this subject and would like to pass the following message to Psychiatrists worldwide, "may Chemical Imbalance bless you".
This work brings a logical answer to many nagging questions, like how Psychiatry could be considered the "authority" in matters of the mind when their results in the field have been poor, and are known to cause more damage than benefit. It may also shed some light on the tendency of Psychiatrists to molest children in a much higher percentage than the general populace.
"Psychiatry is portrayed alternately as a scientific study or branch of medicine but either of these is rapidly disproved," says Moshe Sapere of Hebrew University. "The science of Psychiatry is flawed. Their studies are mainly funded by drug companies and they publish illogical conclusions which - Surprise! - make the drug companies look good. Psychiatry claims similarity to medicine but this is in reality only marketing; the only real similarities to actual medicine are clothing and terminology. If you dressed up a parrot in a doctor's smock and taught it some Latin phrases, it wouldn't be a doctor. It's the same with Psychiatrists."
Some of the researchers were reluctant to agree with the "religion" moniker for a group known to be profit-based and harmful, but a study of religions of the past shows that many have been used for profit and have done harm to others. The matter of faith in a deity was also a sticking point but a study of Psychiatric scriptures reveals that Psychiatrists believe in an invisible entity known as "chemical imbalance". The existence of Chemical Imbalance is stated as fact in the texts though there is no proof of his existence, analogous to a Christian's belief in God or a Muslim's belief in Allah.
The key answer that led the researchers to declare Psychiatry as a religion is that their High Priests demand complete belief in unobservable phenomena and continue to forward their beliefs despite no obvious benefit. They are also known to vehemently attack anyone who points out the lack of proof to their claims. Most religions promise salvation in a future existence. Psychiatry does not specifically make those claims but clearly provides dubious benefit in this existence. The researchers are pleased that they have been able to finally clarify this subject and would like to pass the following message to Psychiatrists worldwide, "may Chemical Imbalance bless you".
Tuesday, May 24, 2011
Chromosome 3 Area Linked to Depression- this heading will be posted in both blog , facebook and twitter, and the content below will be posted in blog only
May 19, 2011 — A study led by scientists at the Washington University School of Medicine, Saint Louis, Missouri, shows genomewide significant linkage between a region on chromosome 3 and major depressive disorder in individuals with a history of heavy smoking.
An independent study at King's College London, United Kingdom, has also identified this region — 3p25–3p26 — as being linked to severe depression. Both reports were published online May 15 in the American Journal of Psychiatry.
Replicated findings in separate studies of depression are unusual in the genetic linkage literature and in genomewide association studies (GWAS). The new studies provide "one of the strongest replicated genetic findings in studies for depression," said the British paper.
The US study stemmed from an interest in the high incidence of depression among cigarette smokers. Genetic factors are widely acknowledged in depression, but major depression is estimated to occur at some time in the lives of more than 60% of smokers who try to quit. Smokers with this history often experience more difficult nicotine withdrawal and are more likely to resume smoking.
Study participants were selected from families with a history of cigarette smoking and at least 1 pair of siblings having a history of major depression. Both depressive disorder, based on the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, and tobacco use and dependency were evaluated by telephone interviews.
Participants (91 Australian families, 187 participants; and 25 Finnish families, 33 participants) were genotyped, and analysis of "affected sibling pair nonparametric linkage" generated logarithmic odds ratio (LOD) scores. Typically, a LOD score greater than 3.0 is evidence of linkage. If LOD equals 3, the odds are 1000 to 1 (ie, 103 to 1) that the linkage is not caused by chance.
"I don't think linkage necessarily provides an advantage over association studies [GWAS], they are just different approaches," explained first author Michele L. Pergadia, PhD, from the Department of Psychiatry, Washington University School of Medicine, in an email to Medscape Medical News.
"Linkage is a classic way to map very broad genomic regions in families that are characterized by specific traits," said Dr. Pergadia. "[I]t highlights an area that may be of interest to study further, in order to identify the actual genes, but it is not a method for identification of the specific genes yet, just a first step in that process."
Analysis of the Australian cohort found a "multipoint LOD score" equaling 4.14 for major depressive disorder in a region on chromosome 3, a result that has genomewide significance (P = .004).
The highest LOD score for a single-point marker was 3.7 for a location within GRM7, the gene for the metabotropic glutamate receptor 7.
The Finnish sample showed no regions with this level of significance, and major linkage signals did not overlap between the Australian and Finnish samples. However, when the US scientists sought to replicate their results, the British researchers contacted them to report the same significant finding, says the Washington University press release.
Authors of the US study note that previous investigators have found evidence of associations between GRM7 variants and depressive disorder, but none of this evidence has reached genomewide significance.
"GRM7 is an interesting gene," observed Douglas F. Levinson, MD, professor of psychiatry, Stanford University School of Medicine, California, in an email to Medscape Medical News. "If you search in PubMed for GRM7 and mood or depression, you will find a large animal pharmacological literature that suggests a role in mood regulation and interest in this gene as a possible antidepressant target."
Dr. Levinson had coauthored a study that suggested a possible GWAS signal in GRM7, but after genomewide correction, the results were not statistically significant. In fact, he is unaware of any significant evidence of associations for GRM7 after correction.
"Our linkage findings highlight a broad area, which spans many genes (>90) that could potentially be contributing to our findings," said Dr. Pergadia. "There are many interesting candidate genes in this region, including, for example, those that code for proteins related to the oxytocin receptor gene (OXTR) [or] GABA transporters (eg, SLC6A11), in addition to those associated with glutamate receptors (eg, GRM7 and GRIP2), but again we did not find any that met genomewide significance.
"So far as I know, while suggestive association has been reported, none of these genes has been associated with depression at the level which would meet genomewide significance (eg, ~5 × 10−8)," Dr. Pergadia added.
The King's College London study investigated recurrent depression, rather than nicotine use, studying sibling pairs with recurrent unipolar depression from clinics in several countries. Their study involved genomewide linkage analysis of 839 families, including 971 pairs of siblings affected with recurrent severe depression.
Their highest LOD scores found were 4.01, for "severe recurrent and very severe recurrent" depression, which identified a linkage signal with genomewide significance in the 3p25-3p26 region. However, when this region was mapped in a depression GWAS sample, the association did not achieve significance. Among potential candidate genes within the region are GRM7 and OXTR, as well as ITPR1 — encoding a receptor for inositol triphosphate, which influences calcium channels and serves as a second messenger in the nervous system.
Despite the replicated findings of these 2 studies, a gene or genes responsible for severe depression are still not identified. Dr. Pergadia summarized the current situation: "I think we're just beginning to make our way through the maze of influences on depression."
The Pergadia study was supported by the European Union and a Center for Inherited Disease Research grant. Various authors in the Pergadia study report receiving an Academy of Finland postdoctoral fellowship, an Australian National Health and Medical Research Council fellowship, the National Health and Medical Research Council (Australia) Sidney Sax Fellowship, and an Australian National Health and Medical Research Council fellowship, as well as funding from the Doctoral Programs of Public Health, University of Helsinki; National Institutes of Health; US Department of Defense; Netherlands Organisation for Scientific Research; Australian National Health and Medical Research Council; AstraZeneca; Genentech; Pfizer; and the Academy of Finland Center of Excellence for Complex Disease Genetics, in addition to receiving an advisory panel payment from AstraZeneca, consultation fees and an unrestricted grant from Pfizer. The Breen study was supported by GlaxoSmithKline Research and Development. Authors in the Breen study report having been employed by GlaxoSmithKline, being a shareholder with GlaxoSmithKline, being an employee and a shareholder with F. Hoffman-La Roche, being affiliated with Medical Genetics, being employed by NeuroSearch A/S, and having received travel and subsistence from GlaxoSmithKline. Dr. Levinson has disclosed no relevant financial relationships.
An independent study at King's College London, United Kingdom, has also identified this region — 3p25–3p26 — as being linked to severe depression. Both reports were published online May 15 in the American Journal of Psychiatry.
Replicated findings in separate studies of depression are unusual in the genetic linkage literature and in genomewide association studies (GWAS). The new studies provide "one of the strongest replicated genetic findings in studies for depression," said the British paper.
The US study stemmed from an interest in the high incidence of depression among cigarette smokers. Genetic factors are widely acknowledged in depression, but major depression is estimated to occur at some time in the lives of more than 60% of smokers who try to quit. Smokers with this history often experience more difficult nicotine withdrawal and are more likely to resume smoking.
Study participants were selected from families with a history of cigarette smoking and at least 1 pair of siblings having a history of major depression. Both depressive disorder, based on the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, and tobacco use and dependency were evaluated by telephone interviews.
Participants (91 Australian families, 187 participants; and 25 Finnish families, 33 participants) were genotyped, and analysis of "affected sibling pair nonparametric linkage" generated logarithmic odds ratio (LOD) scores. Typically, a LOD score greater than 3.0 is evidence of linkage. If LOD equals 3, the odds are 1000 to 1 (ie, 103 to 1) that the linkage is not caused by chance.
"I don't think linkage necessarily provides an advantage over association studies [GWAS], they are just different approaches," explained first author Michele L. Pergadia, PhD, from the Department of Psychiatry, Washington University School of Medicine, in an email to Medscape Medical News.
"Linkage is a classic way to map very broad genomic regions in families that are characterized by specific traits," said Dr. Pergadia. "[I]t highlights an area that may be of interest to study further, in order to identify the actual genes, but it is not a method for identification of the specific genes yet, just a first step in that process."
Analysis of the Australian cohort found a "multipoint LOD score" equaling 4.14 for major depressive disorder in a region on chromosome 3, a result that has genomewide significance (P = .004).
The highest LOD score for a single-point marker was 3.7 for a location within GRM7, the gene for the metabotropic glutamate receptor 7.
The Finnish sample showed no regions with this level of significance, and major linkage signals did not overlap between the Australian and Finnish samples. However, when the US scientists sought to replicate their results, the British researchers contacted them to report the same significant finding, says the Washington University press release.
Authors of the US study note that previous investigators have found evidence of associations between GRM7 variants and depressive disorder, but none of this evidence has reached genomewide significance.
"GRM7 is an interesting gene," observed Douglas F. Levinson, MD, professor of psychiatry, Stanford University School of Medicine, California, in an email to Medscape Medical News. "If you search in PubMed for GRM7 and mood or depression, you will find a large animal pharmacological literature that suggests a role in mood regulation and interest in this gene as a possible antidepressant target."
Dr. Levinson had coauthored a study that suggested a possible GWAS signal in GRM7, but after genomewide correction, the results were not statistically significant. In fact, he is unaware of any significant evidence of associations for GRM7 after correction.
"Our linkage findings highlight a broad area, which spans many genes (>90) that could potentially be contributing to our findings," said Dr. Pergadia. "There are many interesting candidate genes in this region, including, for example, those that code for proteins related to the oxytocin receptor gene (OXTR) [or] GABA transporters (eg, SLC6A11), in addition to those associated with glutamate receptors (eg, GRM7 and GRIP2), but again we did not find any that met genomewide significance.
"So far as I know, while suggestive association has been reported, none of these genes has been associated with depression at the level which would meet genomewide significance (eg, ~5 × 10−8)," Dr. Pergadia added.
The King's College London study investigated recurrent depression, rather than nicotine use, studying sibling pairs with recurrent unipolar depression from clinics in several countries. Their study involved genomewide linkage analysis of 839 families, including 971 pairs of siblings affected with recurrent severe depression.
Their highest LOD scores found were 4.01, for "severe recurrent and very severe recurrent" depression, which identified a linkage signal with genomewide significance in the 3p25-3p26 region. However, when this region was mapped in a depression GWAS sample, the association did not achieve significance. Among potential candidate genes within the region are GRM7 and OXTR, as well as ITPR1 — encoding a receptor for inositol triphosphate, which influences calcium channels and serves as a second messenger in the nervous system.
Despite the replicated findings of these 2 studies, a gene or genes responsible for severe depression are still not identified. Dr. Pergadia summarized the current situation: "I think we're just beginning to make our way through the maze of influences on depression."
The Pergadia study was supported by the European Union and a Center for Inherited Disease Research grant. Various authors in the Pergadia study report receiving an Academy of Finland postdoctoral fellowship, an Australian National Health and Medical Research Council fellowship, the National Health and Medical Research Council (Australia) Sidney Sax Fellowship, and an Australian National Health and Medical Research Council fellowship, as well as funding from the Doctoral Programs of Public Health, University of Helsinki; National Institutes of Health; US Department of Defense; Netherlands Organisation for Scientific Research; Australian National Health and Medical Research Council; AstraZeneca; Genentech; Pfizer; and the Academy of Finland Center of Excellence for Complex Disease Genetics, in addition to receiving an advisory panel payment from AstraZeneca, consultation fees and an unrestricted grant from Pfizer. The Breen study was supported by GlaxoSmithKline Research and Development. Authors in the Breen study report having been employed by GlaxoSmithKline, being a shareholder with GlaxoSmithKline, being an employee and a shareholder with F. Hoffman-La Roche, being affiliated with Medical Genetics, being employed by NeuroSearch A/S, and having received travel and subsistence from GlaxoSmithKline. Dr. Levinson has disclosed no relevant financial relationships.
AN EXAMPLE OF PHYSICAL PROBLEMS DUE TO MANIFESTATION OF INNER PSYCHIC CONFLICTS
"A MAN CAME WITH COMPLAINTS OF BURNING SENSATION AND GENERALIZED BODY ACHE,HIS ALL INVESTIGATION REPORTS WERE NORMAL ON ENQUIRING IT WAS FOUND THAT HE HAS RELATIONSHIP PROBLEMS WITH HIS WIFE,WHICH CAUSED HIM MASKED DEPRESSION , AFTER DOING COUNSELING AND PRESCRIBING ANTIDEPRESSANTS .HE IS DOING WELL NOW 1 MONTH LATER"
THIS IS AN EXAMPLE OF PHYSICAL PROBLEMS DUE TO MANIFESTATION OF INNER PSYCHIC CONFLICTS - Dr.Tirthankar Dasgupta.
THIS IS AN EXAMPLE OF PHYSICAL PROBLEMS DUE TO MANIFESTATION OF INNER PSYCHIC CONFLICTS - Dr.Tirthankar Dasgupta.
Wednesday, May 18, 2011
Experiencing trauma and/or witnessing traumatic events may significantly increase the risk of developing physical disease, including diabetes, obesity, and cardiovascular disease (CVD), new research suggests.
A national study presented here at the American Psychiatric Association 2011 Annual Meeting shows undergoing injurious or psychological trauma or directly witnessing a traumatic event were all associated with a significant unadjusted risk for CVD, arteriosclerosis or hypertension, gastrointestinal (GI) disease, diabetes, arthritis, and obesity.
In addition, experiencing a natural disaster or terrorism was associated with all these conditions except for obesity, whereas combat trauma was associated with cardiovascular and GI disease only.
"We found that a variety of events were significantly associated with a number of physical conditions, which, based on past research, was expected," principal investigator Natalie Husarewycz, MD, told Medscape Medical News.
Injurious (or direct) trauma included accidents or physical attacks; psychological trauma included neglect, being stalked, or threatened with a weapon; and combat-related trauma included events experienced by active military personnel, peacekeepers, unarmed civilians in war time, and refugees.
Clinical Implications
Although the study could not establish causation, Dr. Husarewycz said the findings have important clinical implications.
"Even in individuals with a trauma history that don't fulfill Axis I or II disorder criteria, we should perhaps consider screening for physical health conditions. And there may be reason for primary care physicians seeing people with multiple somatic conditions to consider screening for past traumatic events."
Dr. Husarewycz reported that patients with peptic ulcer disease, CVD, asthma, or diabetes have increased odds of having a mood or anxiety disorder.
According to the presentation, past research has suggested an association between posttraumatic stress disorder (PTSD) and chronic pain conditions, CVD, GI disease, and cancer. Other findings have suggested that physical and sexual abuse is significantly associated with health conditions that include neurologic, musculoskeletal, and GI disorders.
"However, there has been a dearth of population-based research examining whether the nature of trauma experienced may be related to physical health conditions," the study authors report.
"Our questions were: is there a cumulative effect of multiple traumatic events that would predict these physical conditions? And is it the nature of the trauma that was experienced or a mental disorder that would drive the relationship to physical health conditions?" added Dr. Husarewycz.
The researchers evaluated data on 34,653 patients older than 20 years from the US National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) Wave II.
Lifetime trauma experiences and past-year physician-diagnosed medical conditions were reported by all NESARC participants in a face-to-face interview.
Significant Physical Conditions
Results showed substantial overlap between the groups, with 30.68% of the participants experiencing an injurious trauma, 17.32% a psychological trauma, 16.10% a natural disaster or terrorism-related trauma, and 7.53% a combat-related trauma. A total of 71.57 reported witnessing a traumatic event.
Overall, there was "an increased likelihood of suffering from physical health conditions with increased exposure to traumatic events, in a linear pattern," reported Dr. Husarewycz.
After adjusting for sociodemographic factors only, the odds ratios (ORs) were significant for experiencing all physical health conditions by those who underwent injurious (ORs ranging from 1.24 to 1.89) or psychological trauma (ORs, 1.17 – 1.77) or witnessed trauma (ORs, 1.30 – 1.78); were significant for experiencing all but obesity by those who underwent trauma involving natural disaster or terrorism (ORs, 1.20 – 1.55); and were significant for experiencing CVD (OR, 1.36) and GI disease (OR, 1.39) for those with combat trauma.
After also adjusting for any Axis I or Axis II mental disorders in a second model, the findings were similar except that combat trauma was negatively associated with obesity and actually offered a protective effect (OR, 0.87).
In a third study model that adjusted also for all other trauma groups to account for event overlap, the findings were similar to the second model except that psychological trauma was no longer associated with arteriosclerosis/hypertension or obesity and natural disaster/terrorism was no longer associated with arteriosclerosis/hypertension or diabetes.
In addition, in this model, combat trauma lost association with all physical health conditions except for offering a protective effect for obesity.
Biological Changes
When discussing possible reasons for the various associations found, Dr. Husarewycz explained that alterations in hormones and other mediators are commonly seen in patients with PTSD, including cortisol levels. However, some research has found that even without PTSD, survivors of trauma have increased autonomic reactivity.
"It's likely that trauma itself is associated with biological changes," said Dr. Husarewycz.
She noted that "the main reason" why the association between the physical conditions and combat-related trauma disappeared in the last adjustments was because "the other types of trauma, which were controlled for only in the final model, likely mediated the relationship."
She also voiced the possibility of a "healthy warrior" effect. "This is the idea that perhaps chronically ill soldiers are selectively withheld from deployment while physically healthier soldiers may be deployed and would then experience the trauma."
Study limitations cited included its retrospective design and that participants self-reported their physical conditions, which may have led to some recall bias.
During a question and answer session following the presentation, session moderator Jerald Block, MD, asked Dr. Husarewycz if perhaps the investigators were "measuring a somatic preoccupation in patients exposed to trauma" — and therefore getting more medical diagnoses.
"As with anything that is self-reported, there is certainly that potential. In these data, it's supposedly physician diagnosed, but there wasn't any way to know that for sure," replied Dr. Husarewycz.
"Traumatic events related to physical conditions is a finding that's been talked about for years and years and goes back to psychoanalytic theory about PTSD and such. So I think it's helpful and good to see confirmation in these sorts of findings," Dr. Block, clinical director for the Rural Mental Health Program for the Portland VA in Oregon, later told Medscape Medical News.
"It's certainly an important area of study but at this early phase I'd be cautious about drawing too much from the specifics in this research. Still, I think it's very worthwhile to pursue it more," concluded Dr. Block.
The study authors and Dr. Block have disclosed no relevant financial relationships.
American Psychiatric Association (APA) 2011 Annual Meeting: Scientific and Clinical Report Session 6, No. 3. Presented May 14, 2011.
In addition, experiencing a natural disaster or terrorism was associated with all these conditions except for obesity, whereas combat trauma was associated with cardiovascular and GI disease only.
"We found that a variety of events were significantly associated with a number of physical conditions, which, based on past research, was expected," principal investigator Natalie Husarewycz, MD, told Medscape Medical News.
Injurious (or direct) trauma included accidents or physical attacks; psychological trauma included neglect, being stalked, or threatened with a weapon; and combat-related trauma included events experienced by active military personnel, peacekeepers, unarmed civilians in war time, and refugees.
Clinical Implications
Although the study could not establish causation, Dr. Husarewycz said the findings have important clinical implications.
"Even in individuals with a trauma history that don't fulfill Axis I or II disorder criteria, we should perhaps consider screening for physical health conditions. And there may be reason for primary care physicians seeing people with multiple somatic conditions to consider screening for past traumatic events."
Dr. Husarewycz reported that patients with peptic ulcer disease, CVD, asthma, or diabetes have increased odds of having a mood or anxiety disorder.
According to the presentation, past research has suggested an association between posttraumatic stress disorder (PTSD) and chronic pain conditions, CVD, GI disease, and cancer. Other findings have suggested that physical and sexual abuse is significantly associated with health conditions that include neurologic, musculoskeletal, and GI disorders.
"However, there has been a dearth of population-based research examining whether the nature of trauma experienced may be related to physical health conditions," the study authors report.
"Our questions were: is there a cumulative effect of multiple traumatic events that would predict these physical conditions? And is it the nature of the trauma that was experienced or a mental disorder that would drive the relationship to physical health conditions?" added Dr. Husarewycz.
The researchers evaluated data on 34,653 patients older than 20 years from the US National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) Wave II.
Lifetime trauma experiences and past-year physician-diagnosed medical conditions were reported by all NESARC participants in a face-to-face interview.
Significant Physical Conditions
Results showed substantial overlap between the groups, with 30.68% of the participants experiencing an injurious trauma, 17.32% a psychological trauma, 16.10% a natural disaster or terrorism-related trauma, and 7.53% a combat-related trauma. A total of 71.57 reported witnessing a traumatic event.
Overall, there was "an increased likelihood of suffering from physical health conditions with increased exposure to traumatic events, in a linear pattern," reported Dr. Husarewycz.
After adjusting for sociodemographic factors only, the odds ratios (ORs) were significant for experiencing all physical health conditions by those who underwent injurious (ORs ranging from 1.24 to 1.89) or psychological trauma (ORs, 1.17 – 1.77) or witnessed trauma (ORs, 1.30 – 1.78); were significant for experiencing all but obesity by those who underwent trauma involving natural disaster or terrorism (ORs, 1.20 – 1.55); and were significant for experiencing CVD (OR, 1.36) and GI disease (OR, 1.39) for those with combat trauma.
After also adjusting for any Axis I or Axis II mental disorders in a second model, the findings were similar except that combat trauma was negatively associated with obesity and actually offered a protective effect (OR, 0.87).
In a third study model that adjusted also for all other trauma groups to account for event overlap, the findings were similar to the second model except that psychological trauma was no longer associated with arteriosclerosis/hypertension or obesity and natural disaster/terrorism was no longer associated with arteriosclerosis/hypertension or diabetes.
In addition, in this model, combat trauma lost association with all physical health conditions except for offering a protective effect for obesity.
Biological Changes
When discussing possible reasons for the various associations found, Dr. Husarewycz explained that alterations in hormones and other mediators are commonly seen in patients with PTSD, including cortisol levels. However, some research has found that even without PTSD, survivors of trauma have increased autonomic reactivity.
"It's likely that trauma itself is associated with biological changes," said Dr. Husarewycz.
She noted that "the main reason" why the association between the physical conditions and combat-related trauma disappeared in the last adjustments was because "the other types of trauma, which were controlled for only in the final model, likely mediated the relationship."
She also voiced the possibility of a "healthy warrior" effect. "This is the idea that perhaps chronically ill soldiers are selectively withheld from deployment while physically healthier soldiers may be deployed and would then experience the trauma."
Study limitations cited included its retrospective design and that participants self-reported their physical conditions, which may have led to some recall bias.
During a question and answer session following the presentation, session moderator Jerald Block, MD, asked Dr. Husarewycz if perhaps the investigators were "measuring a somatic preoccupation in patients exposed to trauma" — and therefore getting more medical diagnoses.
"As with anything that is self-reported, there is certainly that potential. In these data, it's supposedly physician diagnosed, but there wasn't any way to know that for sure," replied Dr. Husarewycz.
"Traumatic events related to physical conditions is a finding that's been talked about for years and years and goes back to psychoanalytic theory about PTSD and such. So I think it's helpful and good to see confirmation in these sorts of findings," Dr. Block, clinical director for the Rural Mental Health Program for the Portland VA in Oregon, later told Medscape Medical News.
"It's certainly an important area of study but at this early phase I'd be cautious about drawing too much from the specifics in this research. Still, I think it's very worthwhile to pursue it more," concluded Dr. Block.
The study authors and Dr. Block have disclosed no relevant financial relationships.
American Psychiatric Association (APA) 2011 Annual Meeting: Scientific and Clinical Report Session 6, No. 3. Presented May 14, 2011.
Tuesday, May 17, 2011
ANNOUNCEMENT
"PROJECTIVE PSYCHOMETRIC TEST IS REGULARLY NOW DONE AT MONER ALO, BARASAT , MM MEDICAL BALLYGUNJE , AND CHARRING CROSS NURSING HOME , KANKURGACHI, PRIOR APPOINTMENT IS REQUIRED"
Monday, May 16, 2011
New Announcement
PATIENTS SUFFERING FROM BEHAVIORAL DISTURBANCES IF DOESN'T WANT TO COME TO CLINIC,NEED ADMISSION IN A PSYCHIATRY HOME.WE HAVE PICK UP FACILITY ALSO.
DEPRESSION CAN PRESENT IN THIS WAY ALSO
A PATIENT CAME IN MY CLINIC 1 MONTH BEFORE WITH COMPLAINTS OF PAIN AND BURNING SENSATION ON BOTH LOWER LIMBS,HIS ALL INVESTIGATION REPORTS INCLUDING MRI LS SPINE AND NCV STUDY ARE NORMAL , I GAVE HIM ANTIDEPRESANT, HE RESPONDEND WELL , TODAY HE CAME IN FOLLO UP AND DOING WELL , DEPRESSION CAN PRESENT IN THIS WAY ALSO .
Friday, May 6, 2011
Narcolepsy Presenting as Schizophrenia: A Literature Review and Two Case Reports
April 2011
by Farid Ramzi Talih, MD
Dr. Talih is the Director of Psychiatry and Co-Director of Sleep Medicine at the Ashtabula County Medical Center (an affiliate hospital of the Cleveland Clinic), Diplomat of the American Board of Psychiatry and Neurology in Psychiatry and Diplomat of the American Board of Psychiatry and Neurology in Sleep Medicine in Ashtabula, Ohio.
Innov Clin Neurosci. 2011;8(4):30–34
Funding: There was no funding for this article.
Financial disclosures: The author lists no conflicts of interest relevant to the content of this article.
Key words: narcolepsy, schizophrenia, hypersomnia, visual hallucinations, mean sleep latency testing (MSLT)
Abstract. Schizophrenia is a psychiatric disorder that causes significant disability and morbidity. Narcolepsy is a disorder, less prevalent than schizophrenia, but a disorder in which symptoms overlap with schizophrenia. This overlap in symptoms can cause narcolepsy to be confused with schizophrenia. The differences and similarities between narcolepsy and schizophrenia are discussed in the context of two cases. The first case describes an adolescent and the second case describes a refractory case of narcolepsy that did not respond to stimulants. Both cases were previously diagnosed as schizophrenia and did not respond to trials of antipsychotics and other psychotropics. The patients were reevaluated and referred to sleep testing at our facility for clinical suspicion of narcolepsy. Both patients underwent polysomnography with subsequent multiple sleep latency testing. The sleep testing results and multiple sleep latency testing criteria for narcolepsy are also discussed. The patients were treated for narcolepsy resulting in remission of the psychotic symptoms with significant behavioral improvement. We recommend that psychiatrists consider narcolepsy in the differential diagnosis when faced with refractory psychosis.
Introduction
Schizophrenia and narcolepsy share common symptoms and can be difficult to differentiate clinically. The spectrum of symptoms in both conditions can overlap leading to the misdiagnosis of narcolepsy as schizophrenia.[1]
Brief overview of schizophrenia. Schizophrenia is usually chronic and causes lifelong morbidity and significant disability. The prevalence of schizophrenia is approximately one percent in the general population, and there are no significant race or gender differences in the prevalence of the disease.[2] Significant advances in identifying genetic abnormalities and marker have occurred.[3] There is a strong hereditary link in schizophrenia, and having one parent with schizophrenia significantly increases the risk of the disease in children.[4] Brain imaging studies have detected differences between the schizophrenic brain and healthy controls.[5,6] However, the exact pathophysiology of the disease remains elusive. The hallmarks of schizophrenia are a disorganized behavior and speech and the presence of psychosis.[7] Psychosis in schizophrenia includes hallucinations and delusions. Delusions are usually paranoid in nature but can also be religious, somatic, or bizarre. The most common type of hallucinations is auditory; however, visual and other sensory hallucinations can occur. Schizophrenia usually manifests in late adolescence in male individuals and in female individuals in the early to mid-20s.[2] Treatment of schizophrenia is usually with antipsychotics. This class of medications mainly antagonizes dopamine receptors as well as modulating other neurotransmitters in the brain. In addition to dopamine antagonism, serotonergic, histaminergic, adrenergic, and cholinergic pathways are affected by antipsychotics.[8] Antipsychotics and other psychotropics frequently used to control the symptoms of schizophrenia can cause sedation and somnolence. The disorganized thought process and behaviors of schizophrenia can lead to disruption of the sleep-wake cycle and frequently manifests as daytime somnolence. Schizophrenia is diagnosed by a formal psychiatric evaluation; currently, there are no specific objective diagnostic tests.[2,7]
Brief overview of narcolepsy. Narcolepsy causes unstable sleep and wake states. The sudden intrusion of sleep into wakefulness causes excessive sleepiness and introduces rapid eye movement (REM) sleep-related phenomena into wakefulness.[9] REM-related phenomena include skeletal muscle atonia, autonomic instability, hypnogogic hallucinations, somnolence, and autonomic instability. Narcolepsy also causes the fragmentation of nocturnal sleep, and sleep becomes fragmented from frequent awakenings interrupting sleep.[10] The prevalence of narcolepsy in the general population is 0.01 to 0.18 percent. Narcolepsy is more prevalent in Japan and less common in Israel and has a slight male preponderance. Narcolepsy usually manifests in the second decade of life.[11] The underlying pathophysiology in narcolepsy is a loss of hypocretin-producing cells in the posterior hypothalamus. Narcolepsy is strongly associated with the human leukocyte antigen (HLA) DQB1*0602.[12] A pentad of symptoms characterizes narcolepsy: hypersomnia, hypnogogic/ hypnopompic hallucinations, sleep paralysis, cataplexy, and disturbed nocturnal sleep. Cataplexy occurs in the context of strong emotions, usually laughter, and can be subtle (a slight sagging of the jaw) or dramatic (generalized loss of muscle tone leading to falling). Consciousness is maintained during cataplexy. The hallucinations are vivid visual hallucinations from the intrusion of REM into wakefulness. They can be brief and startling or they can be complex and elaborate.[13] However, other hallucinations can also occur in the context of narcolepsy. The hypersomnia and disrupted sleep-wake cycle in narcolepsy can lead to unusual behaviors and significant disability, which can be similar to the disorganized behaviors of schizophrenia. Unlike schizophrenia, there are specific tests available for narcolepsy. These include mean sleep latency testing (MSLT), HLA typing, and measuring hypocretin levels in cerebrospinal fluid.[11–13]
Testing. MSLT, a common diagnostic test for narcoleps, is an electrophysiological test to objectively evaluate hypersomnia. The test is performed after an overnight polysomnography (PSG). If the PSG does not show sleep-disordered breathing or a movement disorder that can account for the hypersomnia, then the MSLT is performed. MSLT is a series of five naps, two hours apart. The first nap is two hours after awakening. A nap is terminated after 20 minutes if no sleep occurs. If sleep occurs, the nap is terminated after 15 minutes. In between naps, patients are not allowed to use caffeine, stimulants, sedatives, or exercise. The diagnostic criteria for narcolepsy, as per the International Classification of Sleep Disorders, Second Edition (ICSD-2), are a mean sleep latency (MSL) of less than eight minutes in the five naps and at least two of the naps having sleep onset REM periods (SOREMPS).[12] The Epworth Sleepiness Scale (ESS) measures hypersomnia, has a range from 0 to 24, and a score greater than 10 indicates excessive daytime sleepiness.[14] The ESS can measure the degree of patient-reported hypersomnia and is a helpful tool for evaluating response to treatment. Central nervous system stimulants and wake-promoting agents are the main therapy for narcolepsy.[15] Adjunct treatment, especially for cataplexy, includes selective serotonin reuptake inhibitors and serotonin norepinephrine reuptake inhibitors.[16] Sodium oxybate (gamma aminobutyric acid [GABA] agonist) is indicated for narcolepsy with fragmented nocturnal sleep or refractory cataplexy.[16,17]
Case presentations
We present two cases that reflect the clinical implications of the above discussion. Both patients were being treated for refractory schizophrenia. PSG and MSLT results from both cases are also discussed.
Case 1. An 18-year-old African American woman with schizophrenia and pervasive developmental disorder presented to our clinic for persistent hypersomnia. She reported sleeping 14 to 16 hours a day (nocturnal sleep was approximately 10–12 hours with 2–3 daytime naps 1–2 hours each). The hypersomnia caused significant impairment academically and socially. She was diagnosed two years previously with schizophrenia. The patient reported vivid visual hallucinations for at least two years. She did not report any auditory or other hallucinations. Paranoid or bizarre delusions were not present. No evidence of disorganized behavior or speech was noted. Visual hallucinations consisted of human figures in dark cloaks. The hallucinations were almost exclusively hypnogogic.
The patient was obese, had a history of a corrected congenital cardiac malformation (ventricular septum defect), and was on digitalis. She was previously treated for almost one year with risperidone. The visual hallucinations did not remit, and she developed galactorrhea from the risperidone. She was subsequently switched to haloperidol. The galactorrhea resolved but the hallucinations persisted. Due to concerns about snoring and obesity, a PSG was ordered. MSLT was ordered for clinical suspicion of narcolepsy due to the severe hypersomnia, visual hallucination, and episodes of mild cataplexy. Cataplexy in this patient presented as transient sagging of the jaw and, occasionally, as head drooping due to neck muscle weakness. PSG findings were suggestive of possible narcolepsy. Those findings were decreased sleep onset latency (SOL) of nine minutes and sleep onset REM of one minute (Figure 1). Total sleep time (TST) of 473 minutes was within normal limits. Sleep architecture was not fragmented with a sleep efficiency index of 97 percent, an arousal index (AI) of 0.5/hour, and decreased REM at 6.7 percent of TST (Figure 1). The apnea hypopnea index (AHI), which measures the degree of sleep-disordered breathing, was 0.1 (AHI<5 is normal). There were no periodic leg movements detected. The MSLT confirmed the diagnosis of narcolepsy with mean sleep latency (MSL) of one minute and 12 seconds and five naps with SOREMPS. The patient was considered for centrally acting stimulants and wake-promoting agents. Modafanil was our first choice due to its favorable side effect profile, efficacy, and tolerability.[14] Because of the cardiac history in this patient, a consultation and clearance to use stimulants was obtained from her cardiologist. Consent from the patient and her guardian was obtained after risks and benefits were explained. She was started on modafanil 200mg daily. At the two-week follow up, the hallucinations had resolved and the hypersomnia improved. Night time sleep became consolidated, and the patient maintained wakefulness in the daytime. The ESS improved from 21 (severe) pre-treatment to 8 (normal) post-treatment. No adverse effects were reported. The patient at the two-month follow up was doing well. Haloperidol reduction in this patient was well tolerated, and the long-term goal is to discontinue antipsychotics. Case 2. A 41-year-old Caucasian woman with a diagnosis of schizophrenia was referred to our clinic to be evaluated for hypersomnia. She reported chronic depression and visual hallucinations. There were no auditory hallucinations reported by this patient and no delusions. She reported sleepiness since she was a child. Routinely, she slept 7 to 8 hours per night and complained of severe daytime hypersomnia. The patient frequently napped 1 to 2 hours during the day. She was unable to maintain a job and would frequently fall asleep during the work day. She subsequently became very depressed and developed suicidal ideation. This patient had no history of substance abuse. The visual hallucinations did not respond to multiple trials of typical and atypical antipsychotics. She reported snoring and unrefreshing sleep. There was no history suggestive of cataplexy. Her medical history included diabetes, hypertension, hypothyroidism, and headaches. Medications included thyroxine, carbamazepine, diazepam, haloperidol, quetiapine, metoprolol, venlafaxine, eletriptan, metformin, and glipizide. PSG and MSLT were ordered. PSG was suggestive of narcolepsy with a decreased SOL of five minutes and an increased arousal index (AI) of 40 arousals per hour, indicative of fragmented sleep (AI<10 is normal). TST of 498 minutes was within normal limits. The AHI was 1.2 (normal), and moderate snoring was reported. No periodic leg movements were detected. MSLT confirmed the diagnosis of narcolepsy with MSL of five minutes and 54 seconds and three SOREMPS. After narcolepsy was confirmed, modafanil 200mg daily was started. There was only a minimal improvement reported. After two weeks, she was switched to amphetamine salt 20mg daily. She was unable to tolerate the side effects of anxiety and agitation. Due to the high degree of sleep fragmentation noted on her PSG (Figure 2) and the severity of the hypersomnia, she was started on sodium oxybate. Sodium oxybate was initiated at a nightly dose of 4.5g orally (supplied in a 0.5g/mL solution). The dose was divided equally with 2.25g at bedtime and 2.25g three hours after bedtime. She reported improvement in daytime hypersomnia and a resolution of the visual hallucinations. Nausea was reported as a side effect that improved after one week. ESS improved from 15 (severe) pre-treatment to 9 (normal) post-treatment. The long-term goal is to taper and reduce psychotropic medications. Discussion
Both cases had findings on PSG (which preceded the MSLT) suggestive of narcolepsy. The first case had decreased SOL and sleep onset REM (Figure 1), and the second case had decreased SOL and increased sleep fragmentation (Figure 2). In both hypnograms, sleep architecture indicates reduced REM sleep. In Case 1, REM was 6.7 percent of TST and in Case 2, REM was 12 percent of TST. Decreased REM sleep in both cases was most likely multifactorial due to the REM-reducing effects of the psychotropics both patients were receiving and from REM fragmentation of narcolepsy. Complicating psychiatric factors were present in both patients. The disorganized behavior from hypersomnia and visual hallucinations likely facilitated the diagnosis of schizophrenia. A large review that compared psychotic symptoms in schizophrenia and narcolepsy found that the most useful distinguishing features are visual hallucinations in narcolepsy versus mainly auditory hallucinations in schizophrenia, and the delusional component is absent in psychosis of narcolepsy.[18] There are reports in the literature of narcolepsy misdiagnosed as schizophrenia.[19–22] These cases were refractory to standard schizophrenia therapies and when reevaluated led to a diagnosis of narcolepsy. The adolescent case presented here was similar to reports on childhood narcolepsy.[23] These reports are a reflection of the increasing awareness among physicians that narcolepsy can present as schizophrenia.
Conclusion
The treating physician should consider narcolepsy in the differential of unusual or refractory schizophrenia. Narcolepsy can be confirmed by safe and noninvasive testing, mainly the MSLT. Treatment for narcolepsy is safe and effective. In certain cases, when hypersomnia or symptoms of narcolepsy recur or are exacerbated, a repeat MSLT or maintenance of wakefulness test can be considered to reevaluate the efficacy of treatment or the need for adjusting or modifying the stimulant and waking-promoting agents. However, as in the cases discussed here, there are cases that do not respond to standard stimulant or wake-promoting agent therapy. Some patients can have comorbidities that require special attention when using stimulants. The co-occurrence of narcolepsy and schizophrenia in the same patient is unlikely.24
by Farid Ramzi Talih, MD
Dr. Talih is the Director of Psychiatry and Co-Director of Sleep Medicine at the Ashtabula County Medical Center (an affiliate hospital of the Cleveland Clinic), Diplomat of the American Board of Psychiatry and Neurology in Psychiatry and Diplomat of the American Board of Psychiatry and Neurology in Sleep Medicine in Ashtabula, Ohio.
Innov Clin Neurosci. 2011;8(4):30–34
Funding: There was no funding for this article.
Financial disclosures: The author lists no conflicts of interest relevant to the content of this article.
Key words: narcolepsy, schizophrenia, hypersomnia, visual hallucinations, mean sleep latency testing (MSLT)
Abstract. Schizophrenia is a psychiatric disorder that causes significant disability and morbidity. Narcolepsy is a disorder, less prevalent than schizophrenia, but a disorder in which symptoms overlap with schizophrenia. This overlap in symptoms can cause narcolepsy to be confused with schizophrenia. The differences and similarities between narcolepsy and schizophrenia are discussed in the context of two cases. The first case describes an adolescent and the second case describes a refractory case of narcolepsy that did not respond to stimulants. Both cases were previously diagnosed as schizophrenia and did not respond to trials of antipsychotics and other psychotropics. The patients were reevaluated and referred to sleep testing at our facility for clinical suspicion of narcolepsy. Both patients underwent polysomnography with subsequent multiple sleep latency testing. The sleep testing results and multiple sleep latency testing criteria for narcolepsy are also discussed. The patients were treated for narcolepsy resulting in remission of the psychotic symptoms with significant behavioral improvement. We recommend that psychiatrists consider narcolepsy in the differential diagnosis when faced with refractory psychosis.
Introduction
Schizophrenia and narcolepsy share common symptoms and can be difficult to differentiate clinically. The spectrum of symptoms in both conditions can overlap leading to the misdiagnosis of narcolepsy as schizophrenia.[1]
Brief overview of schizophrenia. Schizophrenia is usually chronic and causes lifelong morbidity and significant disability. The prevalence of schizophrenia is approximately one percent in the general population, and there are no significant race or gender differences in the prevalence of the disease.[2] Significant advances in identifying genetic abnormalities and marker have occurred.[3] There is a strong hereditary link in schizophrenia, and having one parent with schizophrenia significantly increases the risk of the disease in children.[4] Brain imaging studies have detected differences between the schizophrenic brain and healthy controls.[5,6] However, the exact pathophysiology of the disease remains elusive. The hallmarks of schizophrenia are a disorganized behavior and speech and the presence of psychosis.[7] Psychosis in schizophrenia includes hallucinations and delusions. Delusions are usually paranoid in nature but can also be religious, somatic, or bizarre. The most common type of hallucinations is auditory; however, visual and other sensory hallucinations can occur. Schizophrenia usually manifests in late adolescence in male individuals and in female individuals in the early to mid-20s.[2] Treatment of schizophrenia is usually with antipsychotics. This class of medications mainly antagonizes dopamine receptors as well as modulating other neurotransmitters in the brain. In addition to dopamine antagonism, serotonergic, histaminergic, adrenergic, and cholinergic pathways are affected by antipsychotics.[8] Antipsychotics and other psychotropics frequently used to control the symptoms of schizophrenia can cause sedation and somnolence. The disorganized thought process and behaviors of schizophrenia can lead to disruption of the sleep-wake cycle and frequently manifests as daytime somnolence. Schizophrenia is diagnosed by a formal psychiatric evaluation; currently, there are no specific objective diagnostic tests.[2,7]
Brief overview of narcolepsy. Narcolepsy causes unstable sleep and wake states. The sudden intrusion of sleep into wakefulness causes excessive sleepiness and introduces rapid eye movement (REM) sleep-related phenomena into wakefulness.[9] REM-related phenomena include skeletal muscle atonia, autonomic instability, hypnogogic hallucinations, somnolence, and autonomic instability. Narcolepsy also causes the fragmentation of nocturnal sleep, and sleep becomes fragmented from frequent awakenings interrupting sleep.[10] The prevalence of narcolepsy in the general population is 0.01 to 0.18 percent. Narcolepsy is more prevalent in Japan and less common in Israel and has a slight male preponderance. Narcolepsy usually manifests in the second decade of life.[11] The underlying pathophysiology in narcolepsy is a loss of hypocretin-producing cells in the posterior hypothalamus. Narcolepsy is strongly associated with the human leukocyte antigen (HLA) DQB1*0602.[12] A pentad of symptoms characterizes narcolepsy: hypersomnia, hypnogogic/ hypnopompic hallucinations, sleep paralysis, cataplexy, and disturbed nocturnal sleep. Cataplexy occurs in the context of strong emotions, usually laughter, and can be subtle (a slight sagging of the jaw) or dramatic (generalized loss of muscle tone leading to falling). Consciousness is maintained during cataplexy. The hallucinations are vivid visual hallucinations from the intrusion of REM into wakefulness. They can be brief and startling or they can be complex and elaborate.[13] However, other hallucinations can also occur in the context of narcolepsy. The hypersomnia and disrupted sleep-wake cycle in narcolepsy can lead to unusual behaviors and significant disability, which can be similar to the disorganized behaviors of schizophrenia. Unlike schizophrenia, there are specific tests available for narcolepsy. These include mean sleep latency testing (MSLT), HLA typing, and measuring hypocretin levels in cerebrospinal fluid.[11–13]
Testing. MSLT, a common diagnostic test for narcoleps, is an electrophysiological test to objectively evaluate hypersomnia. The test is performed after an overnight polysomnography (PSG). If the PSG does not show sleep-disordered breathing or a movement disorder that can account for the hypersomnia, then the MSLT is performed. MSLT is a series of five naps, two hours apart. The first nap is two hours after awakening. A nap is terminated after 20 minutes if no sleep occurs. If sleep occurs, the nap is terminated after 15 minutes. In between naps, patients are not allowed to use caffeine, stimulants, sedatives, or exercise. The diagnostic criteria for narcolepsy, as per the International Classification of Sleep Disorders, Second Edition (ICSD-2), are a mean sleep latency (MSL) of less than eight minutes in the five naps and at least two of the naps having sleep onset REM periods (SOREMPS).[12] The Epworth Sleepiness Scale (ESS) measures hypersomnia, has a range from 0 to 24, and a score greater than 10 indicates excessive daytime sleepiness.[14] The ESS can measure the degree of patient-reported hypersomnia and is a helpful tool for evaluating response to treatment. Central nervous system stimulants and wake-promoting agents are the main therapy for narcolepsy.[15] Adjunct treatment, especially for cataplexy, includes selective serotonin reuptake inhibitors and serotonin norepinephrine reuptake inhibitors.[16] Sodium oxybate (gamma aminobutyric acid [GABA] agonist) is indicated for narcolepsy with fragmented nocturnal sleep or refractory cataplexy.[16,17]
Case presentations
We present two cases that reflect the clinical implications of the above discussion. Both patients were being treated for refractory schizophrenia. PSG and MSLT results from both cases are also discussed.
Case 1. An 18-year-old African American woman with schizophrenia and pervasive developmental disorder presented to our clinic for persistent hypersomnia. She reported sleeping 14 to 16 hours a day (nocturnal sleep was approximately 10–12 hours with 2–3 daytime naps 1–2 hours each). The hypersomnia caused significant impairment academically and socially. She was diagnosed two years previously with schizophrenia. The patient reported vivid visual hallucinations for at least two years. She did not report any auditory or other hallucinations. Paranoid or bizarre delusions were not present. No evidence of disorganized behavior or speech was noted. Visual hallucinations consisted of human figures in dark cloaks. The hallucinations were almost exclusively hypnogogic.
The patient was obese, had a history of a corrected congenital cardiac malformation (ventricular septum defect), and was on digitalis. She was previously treated for almost one year with risperidone. The visual hallucinations did not remit, and she developed galactorrhea from the risperidone. She was subsequently switched to haloperidol. The galactorrhea resolved but the hallucinations persisted. Due to concerns about snoring and obesity, a PSG was ordered. MSLT was ordered for clinical suspicion of narcolepsy due to the severe hypersomnia, visual hallucination, and episodes of mild cataplexy. Cataplexy in this patient presented as transient sagging of the jaw and, occasionally, as head drooping due to neck muscle weakness. PSG findings were suggestive of possible narcolepsy. Those findings were decreased sleep onset latency (SOL) of nine minutes and sleep onset REM of one minute (Figure 1). Total sleep time (TST) of 473 minutes was within normal limits. Sleep architecture was not fragmented with a sleep efficiency index of 97 percent, an arousal index (AI) of 0.5/hour, and decreased REM at 6.7 percent of TST (Figure 1). The apnea hypopnea index (AHI), which measures the degree of sleep-disordered breathing, was 0.1 (AHI<5 is normal). There were no periodic leg movements detected. The MSLT confirmed the diagnosis of narcolepsy with mean sleep latency (MSL) of one minute and 12 seconds and five naps with SOREMPS. The patient was considered for centrally acting stimulants and wake-promoting agents. Modafanil was our first choice due to its favorable side effect profile, efficacy, and tolerability.[14] Because of the cardiac history in this patient, a consultation and clearance to use stimulants was obtained from her cardiologist. Consent from the patient and her guardian was obtained after risks and benefits were explained. She was started on modafanil 200mg daily. At the two-week follow up, the hallucinations had resolved and the hypersomnia improved. Night time sleep became consolidated, and the patient maintained wakefulness in the daytime. The ESS improved from 21 (severe) pre-treatment to 8 (normal) post-treatment. No adverse effects were reported. The patient at the two-month follow up was doing well. Haloperidol reduction in this patient was well tolerated, and the long-term goal is to discontinue antipsychotics. Case 2. A 41-year-old Caucasian woman with a diagnosis of schizophrenia was referred to our clinic to be evaluated for hypersomnia. She reported chronic depression and visual hallucinations. There were no auditory hallucinations reported by this patient and no delusions. She reported sleepiness since she was a child. Routinely, she slept 7 to 8 hours per night and complained of severe daytime hypersomnia. The patient frequently napped 1 to 2 hours during the day. She was unable to maintain a job and would frequently fall asleep during the work day. She subsequently became very depressed and developed suicidal ideation. This patient had no history of substance abuse. The visual hallucinations did not respond to multiple trials of typical and atypical antipsychotics. She reported snoring and unrefreshing sleep. There was no history suggestive of cataplexy. Her medical history included diabetes, hypertension, hypothyroidism, and headaches. Medications included thyroxine, carbamazepine, diazepam, haloperidol, quetiapine, metoprolol, venlafaxine, eletriptan, metformin, and glipizide. PSG and MSLT were ordered. PSG was suggestive of narcolepsy with a decreased SOL of five minutes and an increased arousal index (AI) of 40 arousals per hour, indicative of fragmented sleep (AI<10 is normal). TST of 498 minutes was within normal limits. The AHI was 1.2 (normal), and moderate snoring was reported. No periodic leg movements were detected. MSLT confirmed the diagnosis of narcolepsy with MSL of five minutes and 54 seconds and three SOREMPS. After narcolepsy was confirmed, modafanil 200mg daily was started. There was only a minimal improvement reported. After two weeks, she was switched to amphetamine salt 20mg daily. She was unable to tolerate the side effects of anxiety and agitation. Due to the high degree of sleep fragmentation noted on her PSG (Figure 2) and the severity of the hypersomnia, she was started on sodium oxybate. Sodium oxybate was initiated at a nightly dose of 4.5g orally (supplied in a 0.5g/mL solution). The dose was divided equally with 2.25g at bedtime and 2.25g three hours after bedtime. She reported improvement in daytime hypersomnia and a resolution of the visual hallucinations. Nausea was reported as a side effect that improved after one week. ESS improved from 15 (severe) pre-treatment to 9 (normal) post-treatment. The long-term goal is to taper and reduce psychotropic medications. Discussion
Both cases had findings on PSG (which preceded the MSLT) suggestive of narcolepsy. The first case had decreased SOL and sleep onset REM (Figure 1), and the second case had decreased SOL and increased sleep fragmentation (Figure 2). In both hypnograms, sleep architecture indicates reduced REM sleep. In Case 1, REM was 6.7 percent of TST and in Case 2, REM was 12 percent of TST. Decreased REM sleep in both cases was most likely multifactorial due to the REM-reducing effects of the psychotropics both patients were receiving and from REM fragmentation of narcolepsy. Complicating psychiatric factors were present in both patients. The disorganized behavior from hypersomnia and visual hallucinations likely facilitated the diagnosis of schizophrenia. A large review that compared psychotic symptoms in schizophrenia and narcolepsy found that the most useful distinguishing features are visual hallucinations in narcolepsy versus mainly auditory hallucinations in schizophrenia, and the delusional component is absent in psychosis of narcolepsy.[18] There are reports in the literature of narcolepsy misdiagnosed as schizophrenia.[19–22] These cases were refractory to standard schizophrenia therapies and when reevaluated led to a diagnosis of narcolepsy. The adolescent case presented here was similar to reports on childhood narcolepsy.[23] These reports are a reflection of the increasing awareness among physicians that narcolepsy can present as schizophrenia.
Conclusion
The treating physician should consider narcolepsy in the differential of unusual or refractory schizophrenia. Narcolepsy can be confirmed by safe and noninvasive testing, mainly the MSLT. Treatment for narcolepsy is safe and effective. In certain cases, when hypersomnia or symptoms of narcolepsy recur or are exacerbated, a repeat MSLT or maintenance of wakefulness test can be considered to reevaluate the efficacy of treatment or the need for adjusting or modifying the stimulant and waking-promoting agents. However, as in the cases discussed here, there are cases that do not respond to standard stimulant or wake-promoting agent therapy. Some patients can have comorbidities that require special attention when using stimulants. The co-occurrence of narcolepsy and schizophrenia in the same patient is unlikely.24
Thursday, May 5, 2011
Partners Who Don't Pull Their Weight: Here's the Solution
It's a common complaint: One physician is slacking off while everyone else runs between patients, fields calls after hours, and squeezes in staff meetings. Do you have a colleague who isn't working as hard as everyone else? Who either doesn't bring in enough revenue, or refuses to be on call as often as they should? Or perhaps he or she doesn't take part in your practice's community outreach efforts.
Introduction
Exasperated group members are frequently reticent about confronting the offender, especially if the doctor is a venerable senior partner who is decelerating toward retirement.
"They are loath to take steps," says Judy Bee, a partner in the Practice Performance Group in La Jolla, California. "I don't know how many times we've started working with a medical practice and we are given a clear agenda, but we get there and they say, 'It's about Harry. You have to get him to behave.'"
Younger physicians can be a source of ire, too. Perceptions of indolence, it turns out, are generational. You can have a 65-year-old doctor "who has worked his practice from dawn until dusk, and he gets angry when younger doctors don't like to do that," says Judy Capko, the founder of Capko & Company, in Thousand Oaks, California. However, she points out, the attitudes and goals of younger physicians tend to be entirely different, and expecting the same single-minded devotion from them is "totally unrealistic."
Solving the problem means addressing 2 areas: figuring out an appropriate solution, and dealing with the recalcitrant physician.
What's Causing the Problem?
To handle the dilemma successfully, you have to identify the problem you're trying to solve, says Bee. For example, is practice income suffering because a physician's limited hours make it impossible to expand the patient base? "If you have someone who isn't taking the volume and the rest of the doctors can't handle any more, there won't be enough business to hire another doctor," Bee says. Or, maybe patients are complaining because they can't get an appointment. "That's a killer," she adds. "It's going to hurt the practice."
In the best scenarios, the practice already uses a compensation formula based on productivity, fixed expenses, and variable expenses, both experts agree. This indirectly -- and objectively -- addresses work ethic. Part of the physician's pay is determined by patient visits or a comparable measure, such as relative value units. Doctors who see more patients earn more money.
Fixed expenses represent the portion of operating costs that are shared equally, regardless of how much the physician works. "That penalizes the doctor who isn't really serious about a big practice," Bee says. A physician who is not earning enough to comfortably cover fixed expenses might question the wisdom of maintaining unprofitable work habits. Variable expenses are also determined by productivity -- busier physicians pay a bigger share because more staff time, office space, and supplies went into the care of their patients.
Younger members of a group practice that had been founded in the 1960s may be frustrated if the practice relies on an outdated compensation formula. Back when the practice was "awash in money," the bills were paid, and profits were distributed equally, even though the founding physician was working harder than everyone else, Bee comments. "Then managed care comes into view, and you may be working hard, but the amount you're paid for each case is smaller. Also, the senior guy has aged, and he wants to slow down." Younger physicians, who never experienced the boom days, resented the older physician's percentage, and they kept leaving. "If you don't change the mechanism, you have serial turnover, and that is expensive," Bee notes.
Even so, a carefully crafted formula does not offer a total solution. Another staff member might be necessary, whether that is a midlevel provider, a part-time physician, or a full-time physician. "Aside from an adequate supply of patients, that new employee requires compensation, and the money needs to come from somewhere," Capko says.
However, you cannot simply offset underperformance with a salary adjustment because that could violate the physician agreement, and that agreement, which must be examined before action is taken, might go back decades.
Develop a Cohesive Approach
Though a daunting prospect, you must have a frank discussion with the physician who is dodging a share of the duties, regardless of seniority. "The senior doctor shouldn't carry more weight than the other partners. We should all be even stakeholders who are looking out for the common good of the practice," Capko says.
Advance preparation is essential. "There's a certain baseline cost for carrying a doctor, whether 10 or 20 patients are being seen. You need to gather a lot of data to see what the financial impact of this physician's routine is on the practice," Capko says. Determine what you need the underperforming physician to do, discuss the best way to lay out your position, and present it as a united group.
The group spokesman should be someone this physician greatly respects. Although some practices engage a management consultant as a facilitator, "You have a much better chance of succeeding if a physician expresses the group's viewpoint than if the consultant is given the role of dealing with this. Otherwise, the doctor who feels challenged is just going to attack the consultant. He or she is not going to see that the doctors agree with that consultant unless that's voiced," Capko says.
Don't Make It Personal
Steer the discussion away from the physician's behavior and focus on the long-term health of the practice. Capko recommends something like, "You have been the foundation of this practice. We owe you a lot. But this practice -- your practice -- is struggling with some issues, and we need to address these for the future." Then you can delineate your concerns. If, for example, the compensation formula does not adjust for productivity, the group should press for a change. Or, if rooms are standing empty and support staff is marking time due to the physician's erratic schedule, talk about what that unpredictability costs the practice. Suggest that the doctor's appointments be compressed into specific periods so the facility can be used most efficiently.
It's not unusual for a contract to say that physicians decrease or drop call once they have been with a practice for a specified time and reach a certain age. Still, taking on more help is sensible because everyone else is "tap-dancing as fast as they can," Bee observes. She offers the following proposal: "We would like to buy you out so that you get the profit you helped generate, and we're going to enter into an employment contract where we can agree on so many sessions a week or a month. Let's come to terms that allow you to be around, see patients, and help us with your wisdom."
Explain that the practice needs a system in place as each physician heads toward retirement. "Bring the conversation around to the best way you can be productive as a group. It's a way of doing it without offending the doctor. You want that doctor to be involved in the decision. That's the only way you have the best outcome," Capko says.
What if the doctor is a newer addition? "One of the reasons we get into this situation is we don't set up expectations in the first place," Capko says. "We don't say, 'we expect you to be seeing 20 patients per day or generating this much revenue.'" Every new agreement should include the physician's standard schedule, and if the practice has more than 1 site, whether he or she will move between them.
However, if that information wasn't in the agreement and a physician is not as industrious as you had hoped, you have to renegotiate the schedule. Note that you can work together to define what must be done and make the blueprint fair to all parties. "Your goal is to get a commitment from that doctor," Capko says. "Usually, they're earning the right to partnership, so this is like a trial period." Make it clear that partnership is not going to happen if the practice's needs are not met.
Sometimes a physician will be unwilling to change and will quit, possibly without notice. "Then you have to go back and say, 'Wait a minute; let's develop a plan that works for both of us,'" Capko concludes. "You have to prepare for that and make sure you aren't violating the contract."
Introduction
Exasperated group members are frequently reticent about confronting the offender, especially if the doctor is a venerable senior partner who is decelerating toward retirement.
"They are loath to take steps," says Judy Bee, a partner in the Practice Performance Group in La Jolla, California. "I don't know how many times we've started working with a medical practice and we are given a clear agenda, but we get there and they say, 'It's about Harry. You have to get him to behave.'"
Younger physicians can be a source of ire, too. Perceptions of indolence, it turns out, are generational. You can have a 65-year-old doctor "who has worked his practice from dawn until dusk, and he gets angry when younger doctors don't like to do that," says Judy Capko, the founder of Capko & Company, in Thousand Oaks, California. However, she points out, the attitudes and goals of younger physicians tend to be entirely different, and expecting the same single-minded devotion from them is "totally unrealistic."
Solving the problem means addressing 2 areas: figuring out an appropriate solution, and dealing with the recalcitrant physician.
What's Causing the Problem?
To handle the dilemma successfully, you have to identify the problem you're trying to solve, says Bee. For example, is practice income suffering because a physician's limited hours make it impossible to expand the patient base? "If you have someone who isn't taking the volume and the rest of the doctors can't handle any more, there won't be enough business to hire another doctor," Bee says. Or, maybe patients are complaining because they can't get an appointment. "That's a killer," she adds. "It's going to hurt the practice."
In the best scenarios, the practice already uses a compensation formula based on productivity, fixed expenses, and variable expenses, both experts agree. This indirectly -- and objectively -- addresses work ethic. Part of the physician's pay is determined by patient visits or a comparable measure, such as relative value units. Doctors who see more patients earn more money.
Fixed expenses represent the portion of operating costs that are shared equally, regardless of how much the physician works. "That penalizes the doctor who isn't really serious about a big practice," Bee says. A physician who is not earning enough to comfortably cover fixed expenses might question the wisdom of maintaining unprofitable work habits. Variable expenses are also determined by productivity -- busier physicians pay a bigger share because more staff time, office space, and supplies went into the care of their patients.
Younger members of a group practice that had been founded in the 1960s may be frustrated if the practice relies on an outdated compensation formula. Back when the practice was "awash in money," the bills were paid, and profits were distributed equally, even though the founding physician was working harder than everyone else, Bee comments. "Then managed care comes into view, and you may be working hard, but the amount you're paid for each case is smaller. Also, the senior guy has aged, and he wants to slow down." Younger physicians, who never experienced the boom days, resented the older physician's percentage, and they kept leaving. "If you don't change the mechanism, you have serial turnover, and that is expensive," Bee notes.
Even so, a carefully crafted formula does not offer a total solution. Another staff member might be necessary, whether that is a midlevel provider, a part-time physician, or a full-time physician. "Aside from an adequate supply of patients, that new employee requires compensation, and the money needs to come from somewhere," Capko says.
However, you cannot simply offset underperformance with a salary adjustment because that could violate the physician agreement, and that agreement, which must be examined before action is taken, might go back decades.
Develop a Cohesive Approach
Though a daunting prospect, you must have a frank discussion with the physician who is dodging a share of the duties, regardless of seniority. "The senior doctor shouldn't carry more weight than the other partners. We should all be even stakeholders who are looking out for the common good of the practice," Capko says.
Advance preparation is essential. "There's a certain baseline cost for carrying a doctor, whether 10 or 20 patients are being seen. You need to gather a lot of data to see what the financial impact of this physician's routine is on the practice," Capko says. Determine what you need the underperforming physician to do, discuss the best way to lay out your position, and present it as a united group.
The group spokesman should be someone this physician greatly respects. Although some practices engage a management consultant as a facilitator, "You have a much better chance of succeeding if a physician expresses the group's viewpoint than if the consultant is given the role of dealing with this. Otherwise, the doctor who feels challenged is just going to attack the consultant. He or she is not going to see that the doctors agree with that consultant unless that's voiced," Capko says.
Don't Make It Personal
Steer the discussion away from the physician's behavior and focus on the long-term health of the practice. Capko recommends something like, "You have been the foundation of this practice. We owe you a lot. But this practice -- your practice -- is struggling with some issues, and we need to address these for the future." Then you can delineate your concerns. If, for example, the compensation formula does not adjust for productivity, the group should press for a change. Or, if rooms are standing empty and support staff is marking time due to the physician's erratic schedule, talk about what that unpredictability costs the practice. Suggest that the doctor's appointments be compressed into specific periods so the facility can be used most efficiently.
It's not unusual for a contract to say that physicians decrease or drop call once they have been with a practice for a specified time and reach a certain age. Still, taking on more help is sensible because everyone else is "tap-dancing as fast as they can," Bee observes. She offers the following proposal: "We would like to buy you out so that you get the profit you helped generate, and we're going to enter into an employment contract where we can agree on so many sessions a week or a month. Let's come to terms that allow you to be around, see patients, and help us with your wisdom."
Explain that the practice needs a system in place as each physician heads toward retirement. "Bring the conversation around to the best way you can be productive as a group. It's a way of doing it without offending the doctor. You want that doctor to be involved in the decision. That's the only way you have the best outcome," Capko says.
What if the doctor is a newer addition? "One of the reasons we get into this situation is we don't set up expectations in the first place," Capko says. "We don't say, 'we expect you to be seeing 20 patients per day or generating this much revenue.'" Every new agreement should include the physician's standard schedule, and if the practice has more than 1 site, whether he or she will move between them.
However, if that information wasn't in the agreement and a physician is not as industrious as you had hoped, you have to renegotiate the schedule. Note that you can work together to define what must be done and make the blueprint fair to all parties. "Your goal is to get a commitment from that doctor," Capko says. "Usually, they're earning the right to partnership, so this is like a trial period." Make it clear that partnership is not going to happen if the practice's needs are not met.
Sometimes a physician will be unwilling to change and will quit, possibly without notice. "Then you have to go back and say, 'Wait a minute; let's develop a plan that works for both of us,'" Capko concludes. "You have to prepare for that and make sure you aren't violating the contract."
NIDA'S Top Doc Honored for Leading-Edge Addiction Research
Nora Volkow Receives Baylor's Alexander Award in Psychiatry
— Nora Volkow, MD, director of the National Institute on Drug Abuse (NIDA), who was one of the first scientists to demonstrate that addiction is a disease, is the recipient of the Joan and Stanford Alexander Award in Psychiatry by Baylor College of Medicine, Houston, Texas.
The award was established in honor of Stuart C. Yudofsky, MD, who is professor and chair of the Menninger Department of Psychiatry and Behavioral Sciences at Baylor College of Medicine. Dr. Yudofsky was also the first recipient of the Alexander Award.
The award is given annually. Last year's recipient was Nobel Laureate Eric R. Kandel, MD, of Columbia University in New York City, who received the 2000 Nobel Prize in Physiology and Medicine for his research into basic molecular mechanisms underlying learning and memory in the brain.
Dr. Volkow shares Dr. Kandel's interest in how the brain works. She told Medscape Medical News that she has always been intrigued by the human brain and the complexity about what makes us human.
"Since I was a child, I wanted to understand how the brain works and how diseases of the brain affect behavior and emotions," she explained. "That is why I went to medical school."
Born in Mexico, where she still has family, Dr. Volkow received her medical degree from the National University of Mexico in Mexico City and then went to New York University in New York City to complete her residency in psychiatry.
Addiction a Personal Interest
She became interested in drug addiction for scientific and personal reasons.
"On my mother's side of the family there is a history of alcoholism. My uncle was an alcoholic. He was an extraordinary person, but when he was intoxicated his behavior was so profoundly disrupted, and I wanted to understand that.
"So I had that scientific curiosity about the brain, and then I had this person I loved very much, so I wanted to figure out how to help someone overcome the overpowering drive to drink alcohol. That's why I ended up in the whole area of drug addiction," said Dr. Volkow.
One of the first scientists to show that brain circuitry is altered in cocaine addicts, Dr. Volkow used positron emission tomography (PET) imaging to demonstrate that the prefrontal cortex is involved in the reward circuitry of the brain and that it modulated cognition and motivation.
"My work solidly established that addiction is a disease of the brain, and it identified circuits that are pathologically involved in drug addiction, giving us a much more complex picture than was originally believed about the addiction process," she said.
Dr. Volkow has also made discoveries about attention-deficit/hyperactivity disorder (ADHD). One important finding is that ADHD is associated with a deficit in the reward circuitry of the brain, and as a result, people with the disorder are unable to function because they have a deficit in motivation and interest.
"We've turned the whole concept of ADHD upside down. Everybody has been concentrating on inattention, but we are showing that ADHD patients have a deficit in their reward circuitry and lack motivation and interest," she said. "In fact, I'd like to propose that we change the name of attention-deficit/hyperactivity disorder to attention and motivation deficit disorder."
Cell Phone Use Good or Bad?
More recently, Dr. Volkow was in the news for her study on cell phones, which was published in February in the Journal of the American Medical Association. Using PET imaging, she demonstrated that brain glucose metabolism, an indicator of brain function, was significantly increased when subjects were using their cell phone.
"I don't know if this is bad or good, but we did find that we could change excitability of brain tissue, make it more responsive and more reactive. So there is no evidence that cell phones produce damage at this point, but we need to explore whether this has therapeutic uses. If you can increase excitability then perhaps you could stimulate a part of the brain when it starts to atrophy," she said.
Dr. Volkow admits that her own brain is very active.
"My brain jumps around a lot. I am very curious. They say curiosity killed the cat, but I'm still alive. I must have many lives."
She also admits that she is a very determined person who likes challenges.
"To me, the greatest challenge of all — the greatest challenge — is to understand how the brain works. Why are we so different from animals? Why do we get attached to one another to form families? Why is the brain so powerful? Why does someone become schizophrenic and then their reality is so different from mine? Why does someone get depressed, and then everything gets so dark, and they lose their enjoyment and desire for life? I have always been curious about it all."
Addiction Is a Disease
"Nora has done some major, seminal research in the addiction field that really has pushed the field into thinking about drug addiction as a brain disease," David Shurtleff, MD, acting deputy director of NIDA, told Medscape Medical News.
"She was one of the first people to use positron emission tomography imaging to show changes in the brain of drug addicts, particularly, cocaine addicts. When it was first presented people didn't actually believe it, but she kept persisting," Dr. Shurtleff said.
People used to think of addiction as a moral failing or lack of will power, he said.
"What Nora Volkow has done is show, both with her leadership at NIDA and through her research, that the drugs do affect the brain in fundamental, profound ways that lead to this compulsive taking that we call drug addiction. She has definitely been a leader in this area."
Dr. Shurtleff also praised Dr. Volkow's leadership of NIDA.
"Nora is voracious in reading and learning about all the research that goes on in the addiction field and related areas, and she's very good at connecting the dots and formulating hypotheses that the field can latch onto to develop further.
"She is also very much translational in the sense that she looks at the epidemiological data, the clinical data, and then thinks about what that means in terms of underlying basic mechanisms of the brain," he said. "She identifies the problem and then she looks for solutions and that is a real strength of a leader in this field," he said.
— Nora Volkow, MD, director of the National Institute on Drug Abuse (NIDA), who was one of the first scientists to demonstrate that addiction is a disease, is the recipient of the Joan and Stanford Alexander Award in Psychiatry by Baylor College of Medicine, Houston, Texas.
The award was established in honor of Stuart C. Yudofsky, MD, who is professor and chair of the Menninger Department of Psychiatry and Behavioral Sciences at Baylor College of Medicine. Dr. Yudofsky was also the first recipient of the Alexander Award.
The award is given annually. Last year's recipient was Nobel Laureate Eric R. Kandel, MD, of Columbia University in New York City, who received the 2000 Nobel Prize in Physiology and Medicine for his research into basic molecular mechanisms underlying learning and memory in the brain.
Dr. Volkow shares Dr. Kandel's interest in how the brain works. She told Medscape Medical News that she has always been intrigued by the human brain and the complexity about what makes us human.
"Since I was a child, I wanted to understand how the brain works and how diseases of the brain affect behavior and emotions," she explained. "That is why I went to medical school."
Born in Mexico, where she still has family, Dr. Volkow received her medical degree from the National University of Mexico in Mexico City and then went to New York University in New York City to complete her residency in psychiatry.
Addiction a Personal Interest
She became interested in drug addiction for scientific and personal reasons.
"On my mother's side of the family there is a history of alcoholism. My uncle was an alcoholic. He was an extraordinary person, but when he was intoxicated his behavior was so profoundly disrupted, and I wanted to understand that.
"So I had that scientific curiosity about the brain, and then I had this person I loved very much, so I wanted to figure out how to help someone overcome the overpowering drive to drink alcohol. That's why I ended up in the whole area of drug addiction," said Dr. Volkow.
One of the first scientists to show that brain circuitry is altered in cocaine addicts, Dr. Volkow used positron emission tomography (PET) imaging to demonstrate that the prefrontal cortex is involved in the reward circuitry of the brain and that it modulated cognition and motivation.
"My work solidly established that addiction is a disease of the brain, and it identified circuits that are pathologically involved in drug addiction, giving us a much more complex picture than was originally believed about the addiction process," she said.
Dr. Volkow has also made discoveries about attention-deficit/hyperactivity disorder (ADHD). One important finding is that ADHD is associated with a deficit in the reward circuitry of the brain, and as a result, people with the disorder are unable to function because they have a deficit in motivation and interest.
"We've turned the whole concept of ADHD upside down. Everybody has been concentrating on inattention, but we are showing that ADHD patients have a deficit in their reward circuitry and lack motivation and interest," she said. "In fact, I'd like to propose that we change the name of attention-deficit/hyperactivity disorder to attention and motivation deficit disorder."
Cell Phone Use Good or Bad?
More recently, Dr. Volkow was in the news for her study on cell phones, which was published in February in the Journal of the American Medical Association. Using PET imaging, she demonstrated that brain glucose metabolism, an indicator of brain function, was significantly increased when subjects were using their cell phone.
"I don't know if this is bad or good, but we did find that we could change excitability of brain tissue, make it more responsive and more reactive. So there is no evidence that cell phones produce damage at this point, but we need to explore whether this has therapeutic uses. If you can increase excitability then perhaps you could stimulate a part of the brain when it starts to atrophy," she said.
Dr. Volkow admits that her own brain is very active.
"My brain jumps around a lot. I am very curious. They say curiosity killed the cat, but I'm still alive. I must have many lives."
She also admits that she is a very determined person who likes challenges.
"To me, the greatest challenge of all — the greatest challenge — is to understand how the brain works. Why are we so different from animals? Why do we get attached to one another to form families? Why is the brain so powerful? Why does someone become schizophrenic and then their reality is so different from mine? Why does someone get depressed, and then everything gets so dark, and they lose their enjoyment and desire for life? I have always been curious about it all."
Addiction Is a Disease
"Nora has done some major, seminal research in the addiction field that really has pushed the field into thinking about drug addiction as a brain disease," David Shurtleff, MD, acting deputy director of NIDA, told Medscape Medical News.
"She was one of the first people to use positron emission tomography imaging to show changes in the brain of drug addicts, particularly, cocaine addicts. When it was first presented people didn't actually believe it, but she kept persisting," Dr. Shurtleff said.
People used to think of addiction as a moral failing or lack of will power, he said.
"What Nora Volkow has done is show, both with her leadership at NIDA and through her research, that the drugs do affect the brain in fundamental, profound ways that lead to this compulsive taking that we call drug addiction. She has definitely been a leader in this area."
Dr. Shurtleff also praised Dr. Volkow's leadership of NIDA.
"Nora is voracious in reading and learning about all the research that goes on in the addiction field and related areas, and she's very good at connecting the dots and formulating hypotheses that the field can latch onto to develop further.
"She is also very much translational in the sense that she looks at the epidemiological data, the clinical data, and then thinks about what that means in terms of underlying basic mechanisms of the brain," he said. "She identifies the problem and then she looks for solutions and that is a real strength of a leader in this field," he said.
Earlier Initiation of Smoking Cessation Drug Before Quitting Improves Outcomes
"The use of varenicline tartrate alleviates postquit withdrawal discomfort, but it also seems to reduce the 'reward' associated with smoking," write Peter Hajek, PhD, from United Kingdom Centre for Tobacco Control Studies, Wolfson Institute of Preventive Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary, University of London, United Kingdom, and colleagues. "The current treatment schedule, which commences 1 week before quitting, relies primarily on the first mechanism. We set out to determine whether increasing the prequit medication period renders cigarettes less satisfying and facilitates quitting."
Participants consisted of 101 smokers attending a stop-smoking clinic in London, United Kingdom. These were randomly assigned to receive varenicline for 4 weeks before the target quit date (TQD) or to receive placebo for 3 weeks before the TQD, followed by varenicline for 1 week before the TQD. For 3 months after the TQD, both groups also received standard varenicline treatment. Study outcomes included smoking satisfaction and smoke intake before quitting, urges to smoke and withdrawal discomfort after quitting, and sustained abstinence from the TQD to 3 months.
In the group that received varenicline preloading, prequit enjoyment of smoking (P = .004) and smoke intake (P < .001) were less vs the group that did not receive varenicline preloading, and cotinine concentrations decreased by at least 50% in more than one third (36.7%) of participants (reducers).
Varenicline preloading was associated with improved 12-week abstinence rates (47.2% in the varenicline group vs 20.8% in the placebo group; P = .005), although postquit withdrawal symptoms did not differ between the groups.
For reducers in the varenicline group, the 12-week abstinence rate was 66.7% vs 22.6% in nonreducers (P = .002). Varenicline preloading was well tolerated.
"Although several issues remain to be clarified, varenicline preloading can generate a substantial reduction in ad lib smoking and enhance 12-week quit rates," the study authors write. "Current treatment schedules may lead to suboptimal treatment results. Trials with longer follow-up periods are needed to corroborate these findings."
Limitations of this study include insufficient power for long-term follow-up and lack of data on abstinence rates beyond 3 months. In addition, the study was designed to examine only 1 possible mediating mechanism (the effect of varenicline preloading on withdrawal discomfort), and it did not include measures of cue reactivity, which could also be another possible explanatory factor.
An accompanying Invited Commentary by Joel A. Simon, MD, MPH, from the San Francisco VA Medical Center, University of California School of Medicine, discusses various smoking cessation interventions.
"Additional pharmacotherapies are in the pipeline (eg, the nicotine vaccine), and innovative nonpharmacologic approaches continue to be investigated (eg, Web-based interventions, hypnosis, and text messaging)," Dr. Simon writes. "However, there already exists a sufficient evidence base for counseling and drug interventions that if broadly, wholeheartedly, and effectively implemented would likely result in decreased tobacco-related misery."
Participants consisted of 101 smokers attending a stop-smoking clinic in London, United Kingdom. These were randomly assigned to receive varenicline for 4 weeks before the target quit date (TQD) or to receive placebo for 3 weeks before the TQD, followed by varenicline for 1 week before the TQD. For 3 months after the TQD, both groups also received standard varenicline treatment. Study outcomes included smoking satisfaction and smoke intake before quitting, urges to smoke and withdrawal discomfort after quitting, and sustained abstinence from the TQD to 3 months.
In the group that received varenicline preloading, prequit enjoyment of smoking (P = .004) and smoke intake (P < .001) were less vs the group that did not receive varenicline preloading, and cotinine concentrations decreased by at least 50% in more than one third (36.7%) of participants (reducers).
Varenicline preloading was associated with improved 12-week abstinence rates (47.2% in the varenicline group vs 20.8% in the placebo group; P = .005), although postquit withdrawal symptoms did not differ between the groups.
For reducers in the varenicline group, the 12-week abstinence rate was 66.7% vs 22.6% in nonreducers (P = .002). Varenicline preloading was well tolerated.
"Although several issues remain to be clarified, varenicline preloading can generate a substantial reduction in ad lib smoking and enhance 12-week quit rates," the study authors write. "Current treatment schedules may lead to suboptimal treatment results. Trials with longer follow-up periods are needed to corroborate these findings."
Limitations of this study include insufficient power for long-term follow-up and lack of data on abstinence rates beyond 3 months. In addition, the study was designed to examine only 1 possible mediating mechanism (the effect of varenicline preloading on withdrawal discomfort), and it did not include measures of cue reactivity, which could also be another possible explanatory factor.
An accompanying Invited Commentary by Joel A. Simon, MD, MPH, from the San Francisco VA Medical Center, University of California School of Medicine, discusses various smoking cessation interventions.
"Additional pharmacotherapies are in the pipeline (eg, the nicotine vaccine), and innovative nonpharmacologic approaches continue to be investigated (eg, Web-based interventions, hypnosis, and text messaging)," Dr. Simon writes. "However, there already exists a sufficient evidence base for counseling and drug interventions that if broadly, wholeheartedly, and effectively implemented would likely result in decreased tobacco-related misery."
Depression makes more tougher and resilient
London, May 3: Depression has become something of a modern-day epidemic, with some experts arguing that it can be a positive life-changing experience that leaves people tougher, more resilient and more creative.
Some even argue that depression may not be an illness at all, but an evolutionary survival mechanism that helps us cope with life's crises by forcing us to reassess our priorities.
Eleven years ago, Helen McNallen suffered an episode of depression so severe she attempted to take her own life.
So it may seem extraordinary that the 43-year-old former city trader now devotes most of her time to running a website she has started up calledwww.depressioncanbefun.com, reports the Daily Mail.
She set it up because she is convinced that her mental health crisis, which was triggered by the pressures of her job, has, in the long run, transformed her life for the better.
"I'm glad I had depression," says Helen, from Sheffield in South Yorkshire.
"Now, I feel very lucky to be able to spend my time helping other people. It was a turning point in my life," she added.
The controversial idea, that depression might do some of us good in the long run, is backed up by a recent study carried out in the Netherlands.
It analysed the effects of depression on 165 people by looking at how well they coped with life's stresses and strains before and after their mental breakdown.
The study found that the majority had more vitality, improved social lives and were performing better at work.
But if suffering mental health problems really can be beneficial, experts agree it's only likely to apply to those with mild to moderate depression - the majority of cases.
Some even argue that depression may not be an illness at all, but an evolutionary survival mechanism that helps us cope with life's crises by forcing us to reassess our priorities.
Eleven years ago, Helen McNallen suffered an episode of depression so severe she attempted to take her own life.
So it may seem extraordinary that the 43-year-old former city trader now devotes most of her time to running a website she has started up calledwww.depressioncanbefun.com, reports the Daily Mail.
She set it up because she is convinced that her mental health crisis, which was triggered by the pressures of her job, has, in the long run, transformed her life for the better.
"I'm glad I had depression," says Helen, from Sheffield in South Yorkshire.
"Now, I feel very lucky to be able to spend my time helping other people. It was a turning point in my life," she added.
The controversial idea, that depression might do some of us good in the long run, is backed up by a recent study carried out in the Netherlands.
It analysed the effects of depression on 165 people by looking at how well they coped with life's stresses and strains before and after their mental breakdown.
The study found that the majority had more vitality, improved social lives and were performing better at work.
But if suffering mental health problems really can be beneficial, experts agree it's only likely to apply to those with mild to moderate depression - the majority of cases.
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