Mental Health Nursing Journal
Content
Electroconvulsive therapy
Stuart Carney, associate director Centre for Evidence Based Mental Health John Geddes, professor of epidemiological psychiatry
Electroconvulsive therapy is one of the most controversial treatments in medicine. Opinions are often polarised; some consider electroconvulsive therapy to be effective and potentially lifesaving whereas others regard it as unhelpful and harmful and campaign energetically for it to be banned. In response to comments on a mental health white paper, “Reforming the Mental Health Act,” the UK Department of Health commissioned two systematic reviews of electroconvulsive therapy in 2001. One assessed its efficacy and safety in the treatment of depression,1 mania, and schizophrenia and the other reviewed surveys of patients' experiences and is published in this issue of the BMJ (p 1363).2 So what is the current status of our knowledge about electroconvulsive therapy? Both reviews reveal the limitations of the primary studies and the need for genuinely collaborative high quality research—rather than research done by consumers for consumers and by clinicians for clinicians resulting in research with limited general credibility. Nonetheless both reviews produced some useful results. The systematic review of patients' experiences found that approximately a third describe persistent loss of memory following electroconvulsive therapy.2 Rose et al report that there were substantial variations between studies in the perception of benefit from electroconvulsive therapy. The finding that surveys conducted by clinicians tend to report higher rates of perceived benefit whereas those performed by consumers' organisations tend to find lower rates is of particular interest. Of course this may be explained by differences in the selection of the populations sampled or, as the authors suggest, by differences in the focus of the questions and the way they were asked. The review of randomised trials found a reasonable body of evidence on the effects of electroconvulsive therapy in depressive disorder, but less on mania and schizophrenia.1,4 Electroconvulsive therapy produces more improvement on scales of depressive symptoms than simulated electroconvulsive therapy (in which the patient receives all the procedures including anaesthetic but not the electric current). Treatment with electroconvulsive therapy was more effective than drug treatment in the short term, bilateral stimulation was more effective than unilateral, and high dose more effective than low dose. Most of the trials, however, were old and small. Cognitive functioning was not measured consistently across the trials and pooled analyses were not possible. Very few trials investigated the possibility of long term cognitive impairment but those that did suggested that this was not a substantial problem. In view of the limited reliable long term evidence it is
understandable that there should be residual concern about the possible long term adverse effects of electroconvulsive therapy, and this should be reflected in the information given to patients.
Reaction In recent years, the technique of ECT has been much improved. The treatment is given in the hospital under anesthesia so that people receiving ECT do not feel pain. Most patients undergo 6 to 10 treatments. An electrical current is passed through the brain to cause a controlled seizure, which typically lasts for 20 to 90 seconds. The patient is awake in 5 to 10 minutes. The most common side effect is short-term memory loss, which resolves quickly. After the initial course of treatment, ECT can be safely done as an outpatient procedure.
Depression Linked to Heart Disease in Young Adults
Deborah Brauser November 10, 2011 — Depression and previous suicide attempts may be significant predictors of heart disease mortality in young adults, according to new research. A large survey of more than 7000 participants younger than age 40 years found that those with a history of depression or attempted suicide were at a significantly increased risk for ischemic heart disease (IHD) death compared with those without. Although both sexes with these factors also had a higher risk for cardiovascular disease (CVD) mortality, the risk for IHD death was 14 times higher in the women with than in those without the factors. "Our study found a profound role of psychological risk factors on premature heart disease deaths in a young population, which is a group that hasn't really been looked at before in this way," coinvestigator Viola Vaccarino, MD, PhD, professor of epidemiology and medicine at Emory University in Atlanta, Georgia, and chair of the epidemiology department at the Rollins School of Public Health at Emory, told Medscape Medical News. "Most of the data out there on cardiovascular risk are based on middle-aged or older people. That's just the way the field has gone so far, because traditionally it's considered a disease that mostly affects older age groups." Dr. Vaccarino noted that although that is usually true, there are often competing risks for CVD mortality in an older population — but not as much in a younger age group. "Highlighting risk factors for young people may give us important information on things that may be prevented early on. And I think our results call for additional studies that look specifically at this younger age group." The study is published in the November issue of the Archives of General Psychiatry. Novel Focus on the Young
According to the investigators, many previous studies have shown major depressive disorder is associated with increased risk for heart disease. Almost all of these have focused on older populations, but IHD actually begins in youth, write the researchers. For this study, the investigators evaluated data on 7641 adults aged 17 to 39 years (mean age, 28.1 years; 54.5% female) from the 1988-1994 Third National Health and Nutrition Examination Survey (NHANES III), with linkage to the National Death Index. The Diagnostic Interview Schedule was used to assess both unipolar/bipolar depression and history of attempted suicides. Results showed that, after a median follow-up of 14.9 years, 51 of all participants died of CVD; 28 of these deaths were from IHD. In addition, 538 of all patients were found to have a lifetime history of unipolar or bipolar depression and 419 had reported previous suicide attempts. A total of 136 had a history of both. The adjusted hazard ratio (HR) for risk for CVD death was 2.38 for patients with depression (95% confidence interval [CI], 0.93 - 6.08) and 3.21 for those with past suicide attempts (95% CI, 1.36 - 7.56). For IHD mortality, the adjusted HR was 3.70 for the study participants with depression (95% CI, 1.32 - 10.35) and 7.12 for participants with previous suicide attempts (95% CI, 2.67 - 18.98).
Reaction
There is considerable debate about the consequences of depression and cardiovascular disease mortality in women as compared to men. I think the evidence from this study is strong but future studies are obviously warranted.
New Suicide Scale a Reliable Method of Risk Assessment
Megan Brooks November 10, 2011 — The Columbia-Suicide Severity Rating Scale (C-SSRS) is a reliable, user-friendly tool for assessment of suicidal ideation and behavior in adolescents and adults, according to a report published online November 8 in the American Journal of Psychiatry. "Research on suicide prevention and interventions requires a standard method for assessing both suicidal ideation and behavior to identify those at risk and to track treatment response," Kelly Posner, PhD, director of the Center for Suicide Risk Assessment at Columbia University in New York City, and colleagues note in the report. "However, to date, the field has lacked a single standard measure that assesses both suicidal ideation and behavior," they point out. Dr. Posner and colleagues developed the C-SSRS to fill this need. In contrast to other assessment tools, the C-SSRS assesses suicidal ideation and behavior and more precisely identifies the severity and intensity, or lethality, of suicidal thoughts and behaviors, its developers say. It is also the only scale that provides definitions of suicidal behavior, which have been adopted by the Centers for Disease Control and Prevention. Validated in 3 Studies Dr. Posner's team tested the validity of the C-SSRS in 3 separate studies that used it along with other established assessment tools, including the Columbia Suicide History Form (which assesses behavior) and the Beck Scale for Suicide Ideation (which assesses ideation). One study involved 237 adults presenting to an emergency department for psychiatric problems, a second involved 124 adolescent suicide attempters participating in a treatment study, and the third was a medication efficacy trial of 312 depressed adolescents without current ideation or a history of suicide attempt. The C-SSRS showed "good convergent and divergent validity" with the established ideation and behavior scales, the investigators say. It also had "high sensitivity and specificity" for suicidal
behavior, was sensitive to change in behavior over time, and could accurately pinpoint those at greatest risk for suicide attempt. These findings, they say, support its use in the clinical and research settings. Suicide remains a major preventable public health problem, according to the National Institute of Mental Health's Web site. In 2007, it was the tenth leading cause of death in the United States, accounting for 34,598 deaths.
Reaction
Prevention depends on appropriate identification of phenomena, If we can't identify something, it limits our ability to understand, manage, and treat illness. That limits our confidence in drug trials and epidemiological findings.
Autism Likely Begins Before Birth, Postmortem Study Suggests
Excess Neurons May Be Behind Brain Overgrowth in Autism Megan Brooks
November 8, 2011 — An excess of neurons in the prefrontal cortex (PFC) may be a key contributor to brain overgrowth in autism, results of a new study suggest. In a postmortem study, researchers found significantly more neurons in the PFC tissue in 7 of 7 autistic boys, in addition to larger than average brain weight, relative to 6 typically developing boys. "To our knowledge, this study is the first direct quantitative test and confirmation of the theory that a pathological overabundance of neurons in critical brain regions is present at a young age in autism," the authors note. "Because cortical neurons are generated in prenatal, not postnatal life, pathological overabundance of neurons indicates early developmental disturbances in molecular and genetic mechanisms that govern proliferation, cell cycle regulation, and apoptosis," they write.
The study was published November 9 in JAMA.
Reaction
This study, tells us that in autism, things begin to go wrong very early on; this helps rule out things like measles/mumps/rubella vaccine. It also points to possible causes and that's why it's very exciting.
Dementia Pathology Linked to Late-Life Major Depression
Caroline Cassels November 9, 2011 — Amyloid plaques and tau tangles in the brains of older individuals may indicate not only Alzheimer's disease (AD) and other dementias but also major depression, a new imaging study suggests. Using FDDNP, a novel chemical marker, investigators at the University of California, Los Angeles, showed that patients with late-life major depressive disorder (MDD) had a greater burden of amyloid beta (Aβ) plaques and tau tangles in critical brain regions including the posterior cingulate (PC) and lateral temporal areas. "These findings suggest that the higher protein load in critical brain regions may contribute to the development of severe depression in late life," principal investigator Gary Small, MD, said in a release. The study appears in the November issue of the Archives of General Psychiatry. Precursor to Dementia One of the most common mental disorders in the elderly population, MDD is responsible for significant adverse medical, psychosocial, and economic outcomes. Although the biological underpinnings of major depression remain unclear, possible culprits include neurodegeneration and/or vascular mechanisms. Previous imaging studies show that compared with control patients, patients with MDD have smaller brain volumes, which is widely considered a marker of neurodegeneration. The investigators note that vascular mechanisms are also relevant to the pathogenesis of MDD and state that neurodegeneration and vascular injury may work in tandem in the manifestation of the disorder. Preliminary evidence from plasma data indicate that in addition to being an early biomarker of AD, the ratio of Aβ-42 to Aβ-40 may also be a biomarker for MDD. Furthermore, depression in the elderly has been identified as a risk factor and a precursor for AD.
Higher Protein Load Using FDDNP positron emission tomography (PET), the researchers examined and compared amyloid and tau protein binding in 20 patients with late-life MDD with that found in 19 healthy control patients matched for age, sex, and education level. The study's primary outcome measure was the relative distribution volume of the proteins in regions of interest including the PC gyrus and mesial temporal, lateral temporal, frontal, and parietal lobes in all study participants. Investigators found that patients with late-life MDD had significantly higher FDDNP binding globally, with a particular concentration found in the lateral temporal and PC regions compared with in the healthy counterparts. Other regions including the anterior cingulated and mesial temporal also showed higher FDDNP binding compared with control patients, but the difference did not reach significance. "These findings suggest that neuronal injury associated with higher protein load in critical brain regions might provide a mechanism in the pathophysiologic manifestation of MDD in late life and have implications for the therapeutics of depression in elderly individuals," the authors write. Larger, longitudinal studies are needed to determine whether higher FDDNP binding at baseline leads to AD over time. PET imaging with FDDNP before and after treatment with antidepressants and/or antiamyloid agents may provide useful information about whether such agents can change the course of amyloid deposition, and if so, whether this has a positive effect on clinical outcomes.
Reaction
We may find that depression in the elderly may be an initial manifestation of progressive neurodegenerative disease. Brain scans using FDDNP allow us to take a closer look at the different types of protein deposits and track them to see how clinical symptoms develop.
Stuart Carney, associate director Centre for Evidence Based Mental Health John Geddes, professor of epidemiological psychiatry
Electroconvulsive therapy is one of the most controversial treatments in medicine. Opinions are often polarised; some consider electroconvulsive therapy to be effective and potentially lifesaving whereas others regard it as unhelpful and harmful and campaign energetically for it to be banned. In response to comments on a mental health white paper, “Reforming the Mental Health Act,” the UK Department of Health commissioned two systematic reviews of electroconvulsive therapy in 2001. One assessed its efficacy and safety in the treatment of depression,1 mania, and schizophrenia and the other reviewed surveys of patients' experiences and is published in this issue of the BMJ (p 1363).2 So what is the current status of our knowledge about electroconvulsive therapy? Both reviews reveal the limitations of the primary studies and the need for genuinely collaborative high quality research—rather than research done by consumers for consumers and by clinicians for clinicians resulting in research with limited general credibility. Nonetheless both reviews produced some useful results. The systematic review of patients' experiences found that approximately a third describe persistent loss of memory following electroconvulsive therapy.2 Rose et al report that there were substantial variations between studies in the perception of benefit from electroconvulsive therapy. The finding that surveys conducted by clinicians tend to report higher rates of perceived benefit whereas those performed by consumers' organisations tend to find lower rates is of particular interest. Of course this may be explained by differences in the selection of the populations sampled or, as the authors suggest, by differences in the focus of the questions and the way they were asked. The review of randomised trials found a reasonable body of evidence on the effects of electroconvulsive therapy in depressive disorder, but less on mania and schizophrenia.1,4 Electroconvulsive therapy produces more improvement on scales of depressive symptoms than simulated electroconvulsive therapy (in which the patient receives all the procedures including anaesthetic but not the electric current). Treatment with electroconvulsive therapy was more effective than drug treatment in the short term, bilateral stimulation was more effective than unilateral, and high dose more effective than low dose. Most of the trials, however, were old and small. Cognitive functioning was not measured consistently across the trials and pooled analyses were not possible. Very few trials investigated the possibility of long term cognitive impairment but those that did suggested that this was not a substantial problem. In view of the limited reliable long term evidence it is
understandable that there should be residual concern about the possible long term adverse effects of electroconvulsive therapy, and this should be reflected in the information given to patients.
Reaction In recent years, the technique of ECT has been much improved. The treatment is given in the hospital under anesthesia so that people receiving ECT do not feel pain. Most patients undergo 6 to 10 treatments. An electrical current is passed through the brain to cause a controlled seizure, which typically lasts for 20 to 90 seconds. The patient is awake in 5 to 10 minutes. The most common side effect is short-term memory loss, which resolves quickly. After the initial course of treatment, ECT can be safely done as an outpatient procedure.
Depression Linked to Heart Disease in Young Adults
Deborah Brauser November 10, 2011 — Depression and previous suicide attempts may be significant predictors of heart disease mortality in young adults, according to new research. A large survey of more than 7000 participants younger than age 40 years found that those with a history of depression or attempted suicide were at a significantly increased risk for ischemic heart disease (IHD) death compared with those without. Although both sexes with these factors also had a higher risk for cardiovascular disease (CVD) mortality, the risk for IHD death was 14 times higher in the women with than in those without the factors. "Our study found a profound role of psychological risk factors on premature heart disease deaths in a young population, which is a group that hasn't really been looked at before in this way," coinvestigator Viola Vaccarino, MD, PhD, professor of epidemiology and medicine at Emory University in Atlanta, Georgia, and chair of the epidemiology department at the Rollins School of Public Health at Emory, told Medscape Medical News. "Most of the data out there on cardiovascular risk are based on middle-aged or older people. That's just the way the field has gone so far, because traditionally it's considered a disease that mostly affects older age groups." Dr. Vaccarino noted that although that is usually true, there are often competing risks for CVD mortality in an older population — but not as much in a younger age group. "Highlighting risk factors for young people may give us important information on things that may be prevented early on. And I think our results call for additional studies that look specifically at this younger age group." The study is published in the November issue of the Archives of General Psychiatry. Novel Focus on the Young
According to the investigators, many previous studies have shown major depressive disorder is associated with increased risk for heart disease. Almost all of these have focused on older populations, but IHD actually begins in youth, write the researchers. For this study, the investigators evaluated data on 7641 adults aged 17 to 39 years (mean age, 28.1 years; 54.5% female) from the 1988-1994 Third National Health and Nutrition Examination Survey (NHANES III), with linkage to the National Death Index. The Diagnostic Interview Schedule was used to assess both unipolar/bipolar depression and history of attempted suicides. Results showed that, after a median follow-up of 14.9 years, 51 of all participants died of CVD; 28 of these deaths were from IHD. In addition, 538 of all patients were found to have a lifetime history of unipolar or bipolar depression and 419 had reported previous suicide attempts. A total of 136 had a history of both. The adjusted hazard ratio (HR) for risk for CVD death was 2.38 for patients with depression (95% confidence interval [CI], 0.93 - 6.08) and 3.21 for those with past suicide attempts (95% CI, 1.36 - 7.56). For IHD mortality, the adjusted HR was 3.70 for the study participants with depression (95% CI, 1.32 - 10.35) and 7.12 for participants with previous suicide attempts (95% CI, 2.67 - 18.98).
Reaction
There is considerable debate about the consequences of depression and cardiovascular disease mortality in women as compared to men. I think the evidence from this study is strong but future studies are obviously warranted.
New Suicide Scale a Reliable Method of Risk Assessment
Megan Brooks November 10, 2011 — The Columbia-Suicide Severity Rating Scale (C-SSRS) is a reliable, user-friendly tool for assessment of suicidal ideation and behavior in adolescents and adults, according to a report published online November 8 in the American Journal of Psychiatry. "Research on suicide prevention and interventions requires a standard method for assessing both suicidal ideation and behavior to identify those at risk and to track treatment response," Kelly Posner, PhD, director of the Center for Suicide Risk Assessment at Columbia University in New York City, and colleagues note in the report. "However, to date, the field has lacked a single standard measure that assesses both suicidal ideation and behavior," they point out. Dr. Posner and colleagues developed the C-SSRS to fill this need. In contrast to other assessment tools, the C-SSRS assesses suicidal ideation and behavior and more precisely identifies the severity and intensity, or lethality, of suicidal thoughts and behaviors, its developers say. It is also the only scale that provides definitions of suicidal behavior, which have been adopted by the Centers for Disease Control and Prevention. Validated in 3 Studies Dr. Posner's team tested the validity of the C-SSRS in 3 separate studies that used it along with other established assessment tools, including the Columbia Suicide History Form (which assesses behavior) and the Beck Scale for Suicide Ideation (which assesses ideation). One study involved 237 adults presenting to an emergency department for psychiatric problems, a second involved 124 adolescent suicide attempters participating in a treatment study, and the third was a medication efficacy trial of 312 depressed adolescents without current ideation or a history of suicide attempt. The C-SSRS showed "good convergent and divergent validity" with the established ideation and behavior scales, the investigators say. It also had "high sensitivity and specificity" for suicidal
behavior, was sensitive to change in behavior over time, and could accurately pinpoint those at greatest risk for suicide attempt. These findings, they say, support its use in the clinical and research settings. Suicide remains a major preventable public health problem, according to the National Institute of Mental Health's Web site. In 2007, it was the tenth leading cause of death in the United States, accounting for 34,598 deaths.
Reaction
Prevention depends on appropriate identification of phenomena, If we can't identify something, it limits our ability to understand, manage, and treat illness. That limits our confidence in drug trials and epidemiological findings.
Autism Likely Begins Before Birth, Postmortem Study Suggests
Excess Neurons May Be Behind Brain Overgrowth in Autism Megan Brooks
November 8, 2011 — An excess of neurons in the prefrontal cortex (PFC) may be a key contributor to brain overgrowth in autism, results of a new study suggest. In a postmortem study, researchers found significantly more neurons in the PFC tissue in 7 of 7 autistic boys, in addition to larger than average brain weight, relative to 6 typically developing boys. "To our knowledge, this study is the first direct quantitative test and confirmation of the theory that a pathological overabundance of neurons in critical brain regions is present at a young age in autism," the authors note. "Because cortical neurons are generated in prenatal, not postnatal life, pathological overabundance of neurons indicates early developmental disturbances in molecular and genetic mechanisms that govern proliferation, cell cycle regulation, and apoptosis," they write.
The study was published November 9 in JAMA.
Reaction
This study, tells us that in autism, things begin to go wrong very early on; this helps rule out things like measles/mumps/rubella vaccine. It also points to possible causes and that's why it's very exciting.
Dementia Pathology Linked to Late-Life Major Depression
Caroline Cassels November 9, 2011 — Amyloid plaques and tau tangles in the brains of older individuals may indicate not only Alzheimer's disease (AD) and other dementias but also major depression, a new imaging study suggests. Using FDDNP, a novel chemical marker, investigators at the University of California, Los Angeles, showed that patients with late-life major depressive disorder (MDD) had a greater burden of amyloid beta (Aβ) plaques and tau tangles in critical brain regions including the posterior cingulate (PC) and lateral temporal areas. "These findings suggest that the higher protein load in critical brain regions may contribute to the development of severe depression in late life," principal investigator Gary Small, MD, said in a release. The study appears in the November issue of the Archives of General Psychiatry. Precursor to Dementia One of the most common mental disorders in the elderly population, MDD is responsible for significant adverse medical, psychosocial, and economic outcomes. Although the biological underpinnings of major depression remain unclear, possible culprits include neurodegeneration and/or vascular mechanisms. Previous imaging studies show that compared with control patients, patients with MDD have smaller brain volumes, which is widely considered a marker of neurodegeneration. The investigators note that vascular mechanisms are also relevant to the pathogenesis of MDD and state that neurodegeneration and vascular injury may work in tandem in the manifestation of the disorder. Preliminary evidence from plasma data indicate that in addition to being an early biomarker of AD, the ratio of Aβ-42 to Aβ-40 may also be a biomarker for MDD. Furthermore, depression in the elderly has been identified as a risk factor and a precursor for AD.
Higher Protein Load Using FDDNP positron emission tomography (PET), the researchers examined and compared amyloid and tau protein binding in 20 patients with late-life MDD with that found in 19 healthy control patients matched for age, sex, and education level. The study's primary outcome measure was the relative distribution volume of the proteins in regions of interest including the PC gyrus and mesial temporal, lateral temporal, frontal, and parietal lobes in all study participants. Investigators found that patients with late-life MDD had significantly higher FDDNP binding globally, with a particular concentration found in the lateral temporal and PC regions compared with in the healthy counterparts. Other regions including the anterior cingulated and mesial temporal also showed higher FDDNP binding compared with control patients, but the difference did not reach significance. "These findings suggest that neuronal injury associated with higher protein load in critical brain regions might provide a mechanism in the pathophysiologic manifestation of MDD in late life and have implications for the therapeutics of depression in elderly individuals," the authors write. Larger, longitudinal studies are needed to determine whether higher FDDNP binding at baseline leads to AD over time. PET imaging with FDDNP before and after treatment with antidepressants and/or antiamyloid agents may provide useful information about whether such agents can change the course of amyloid deposition, and if so, whether this has a positive effect on clinical outcomes.
Reaction
We may find that depression in the elderly may be an initial manifestation of progressive neurodegenerative disease. Brain scans using FDDNP allow us to take a closer look at the different types of protein deposits and track them to see how clinical symptoms develop.
