Stroke is the second leading cause of death worldwide. A majority of patients survive stroke, however, making this disorder a major source of human disability. Although most patients have some spontaneous behavioral improvements after a stroke, the recovery is generally incomplete. Compounding this burden of disability is the fact that one in four patients who have a stroke is under 65 years of age.
An emerging approach to reducing the degree of disability after a stroke focuses on brain repair. Repair therapies aim to restore the brain, a goal that differs from that of neuroprotection therapies, in which the aim is to limit acute stroke injury. A number of repair-related therapies have been defined in preclinical studies. Such therapies can produce enduring behavioral gains when introduced days to months after the onset of stroke. Several classes of therapy are under study for brain repair, including the use of stem cells, growth factors, small molecules, electromagnetic stimulation, and intensive physiotherapy.1 Many of these therapies, including robot-based physiotherapy,2 are already in human trials.
It is in this context that Lo et al.3 describe a multicenter, randomized, controlled trial to evaluate the effect of robotic therapy on motor status in people with long-term disability after stroke. As reported in this issue of the Journal, the primary study hypothesis was that robotic therapy, when compared with intensive comparison therapy or usual care, would lead to greater improvements in upper-limb function at 12 weeks, as measured by the change in score on the Fugl-Meyer scale. Patients were randomly assigned to one of three types of treatment: robot-assisted therapy, which consisted of high-intensity, repetitive movements of the proximal and distal arm; intensive comparison therapy, which matched the robotic therapy in schedule, form, and intensity but did so with the use of conventional rehabilitation techniques; or usual care, which may have included various types of physical and occupational therapy. Subjects in the two intensive-therapy groups received three sessions (each approximately 1 hour in duration) per week over 12 weeks. Patients in the trial varied widely in the time since the onset of stroke (6 months to 24 years), had multiple coexisting illnesses (including mental health conditions and previous strokes), and were receiving multiple medications.
The investigators' results did not support their study hypothesis. When robot-assisted therapy was compared with either intensive comparison therapy or usual care, no significant differences in the change in the Fugl-Meyer score were seen. There were no safety concerns. In secondary analyses extending to 24 weeks after treatment, robot-based therapy was better than usual care but was not better than intensive comparison therapy. However, since function had improved in patients in the two active treatment groups, these findings reaffirm the idea that motor status can be improved in patients with long-term disability after stroke.
Lo et al. successfully completed a difficult study and achieved a high rate of compliance, a low dropout rate, an extended follow-up period, and careful matching of therapy details across the two active treatment groups. But some basic facts of the chronic phase of stroke can frustrate hypothesis testing in clinical trials. Behavioral gains in the active-treatment groups were smaller than anticipated in power calculations, possibly because the average baseline motor deficits in patients were severe, and severe deficits are harder to improve. Finding a treatment difference between groups also might have been hampered by recruitment of highly motivated patients in all three study groups, since patients who had had a stroke sometimes many years earlier had to agree to leave home for 36 visits to a research laboratory.
Other features of the patients also may have influenced study outcomes. Patients had a substantial number of coexisting illnesses in multiple domains. For example, depression might have influenced results, given that 38% of patients were taking antidepressants. In addition, 73% of all study enrollees were receiving some form of rehabilitation therapy at baseline — a very high rate for patients with long-term disability after stroke4 — and this proportion changed little throughout the study. The high rate of rehabilitation therapy outside study protocol but concomitant with study interventions, as observed by Lo et al., is similar to previous experience in patients months or years after stroke5 and complicates hypothesis testing. What else did subjects practice during the other 165 hours per week? The experience of Lo et al. reminds us that many factors can have a substantial effect on studies involving patients after stroke and prompts conservative power calculations for future repair-based trials.
In the bigger picture, the potential for robotic therapy after stroke remains enormous. Robotic devices can provide therapy in different functional modes, a point that was not examined by Lo et al. Robots work in a consistent and precise manner and over long periods without fatigue.6 They can modulate timing, content, and intensity of training in reproducible ways, with a reduced need for human oversight.2 Robotic devices can also measure the performance of patients during therapy. In addition, robot-based therapy can interface with computers in brain-stimulation treatment or to provide simultaneous cognitive training.
The findings of Lo et al. are of broad value to planning repair-based trials. Movement training, at the heart of the current study, stands on its own as a means of improving behavior in the stroke-injured brain, as shown by Wolf et al. in a phase 3 trial.7 But movement training will also be of critical value as an adjunctive therapy to other treatments that target brain repair, such as the use of growth factors or stimulants. Repair-based therapies drive maximum brain plasticity and achieve best behavioral gains when they are shaped by training and experience.8 Thus, the findings in the active treatment groups in the study by Lo et al. will be instructive in future trials.
These results challenge us to better stratify patients with long-term disabilities after stroke. Such patients are generally selected on the basis of behavioral status. Functional neuroimaging studies have clearly shown that a single behavioral phenotype can arise on the basis of many different brain states. Anatomical and physiological testing might assist in the identification of patients whose brains have sufficient biologic substrate to improve in response to therapy. Toward this end, recent studies suggest that measures of injury to the central nervous system9 or of brain function10 can help predict a patient's capacity for treatment gains after stroke. Many different neurobiologic states can produce a particular behavioral picture, but only some of these states are likely to yield improved behavior in response to a repair-based therapy.
Studies such as that by Lo et al. reinforce the theory that the adult brain has the capacity for clinically relevant plasticity even in the chronic phase after a stroke. The future holds great hope for the development of brain-repair protocols to greatly reduce the degree of disability after stroke.
Source Information
From the Departments of Neurology and Anatomy and Neurobiology, University of California, Irvine. This article (10.1056/NEJMe1003399) was published on April 16, 2010, at NEJM.org.
Wednesday, April 21, 2010
Psychotropic Medications Overprescribed to Children: Study Suggests
ScienceDaily (Apr. 20, 2010) — A new study from the Journal of Marital & Family Therapy warns of the dramatic rise in the use of psychotropic medications for children. One in every fifty Americans is now considered permanently disabled by mental illness, and up to eight million children take one or more psychotropic drugs.
The authors, James P. Morris, Ph.D. and George Stone, LCSW, state that there is little evidence available to warrant the widespread use of psychotropic drugs for children, and little long term data regarding its long term impact on development.
According to the authors the mental health field is currently designed to treat adults with psychotropic medications, but they are often misused in the case of children and adolescents, "This presents an ethical challenge to marriage and family therapists, who should be very cautious about these medications as an option for children. The long-term research on their safety for children is uncertain."
As an example, the diagnosis of early onset bipolar disorder and attention deficit hyperactivity disorder has climbed drastically in the past decade. Drugs designed to treat the above two disorders show a fair short term risk-benefit ratio, but a poor long-term benefit. Morris and Stone indicate, "If the psychiatric community has been misled by pharmaceutical companies in thinking that these drugs are safe for their children, the parents of these children have been in turn deluded into putting their children in harm's way."
The authors continue that the pharmaceutical industry is largely influenced by the desire for economic profit, and the marketing muscle behind the industry, and leniency of institutions such as the FDA, tout benefits that are not yet properly evaluated for pediatric use. Between 1994 and 2001, psychotropic prescriptions for adolescents rose more than sixty percent; the rise post-1999 was connected to the development and marketing of several new psychotropic drugs and the rebranding of several older ones.
Morris and Stone claim that family health professionals are put in the line of fire when children begin to experience the negative consequences of long-term use of these medications. They are left with the challenge of evaluating the quality of evidence-based care offered to their pediatric clients by the psychiatric community, and the negative effects of the medications without sufficient empirical evidence or information
The authors, James P. Morris, Ph.D. and George Stone, LCSW, state that there is little evidence available to warrant the widespread use of psychotropic drugs for children, and little long term data regarding its long term impact on development.
According to the authors the mental health field is currently designed to treat adults with psychotropic medications, but they are often misused in the case of children and adolescents, "This presents an ethical challenge to marriage and family therapists, who should be very cautious about these medications as an option for children. The long-term research on their safety for children is uncertain."
As an example, the diagnosis of early onset bipolar disorder and attention deficit hyperactivity disorder has climbed drastically in the past decade. Drugs designed to treat the above two disorders show a fair short term risk-benefit ratio, but a poor long-term benefit. Morris and Stone indicate, "If the psychiatric community has been misled by pharmaceutical companies in thinking that these drugs are safe for their children, the parents of these children have been in turn deluded into putting their children in harm's way."
The authors continue that the pharmaceutical industry is largely influenced by the desire for economic profit, and the marketing muscle behind the industry, and leniency of institutions such as the FDA, tout benefits that are not yet properly evaluated for pediatric use. Between 1994 and 2001, psychotropic prescriptions for adolescents rose more than sixty percent; the rise post-1999 was connected to the development and marketing of several new psychotropic drugs and the rebranding of several older ones.
Morris and Stone claim that family health professionals are put in the line of fire when children begin to experience the negative consequences of long-term use of these medications. They are left with the challenge of evaluating the quality of evidence-based care offered to their pediatric clients by the psychiatric community, and the negative effects of the medications without sufficient empirical evidence or information
Tuesday, March 30, 2010
When Memory-Related Neurons Fire in Sinc With Certain Brain Waves, Memories Last
ScienceDaily (Mar. 28, 2010) — They say there's only one chance to make a first impression, but what makes that memory last?
Research scientists at Cedars-Sinai Medical Center and the California Institute of Technology suggest in an article in the March 24, 2010, journal Nature (online) that when memory-related neurons in the brain fire in sync with certain brain waves, the resulting image recognition and memories are stronger than if this synchronization does not occur.
Synchronization is influenced by "theta waves," which are associated with relaxation, daydreaming and drowsiness, but also with learning and memory formation. While it has long been understood that a relaxed mind is one that is ready to receive new information, this study pinpoints a mechanism by which this state of mind allows neurons to work together to improve memory retention. Further exploration of these events could have implications for developing new therapies to treat learning disabilities and some types of dementia, according to the authors.
Brain waves oscillate, with rhythmic highs and lows, and can be measured with electroencephalograms, which use electrodes to record electrical activity. One measure of waves is the frequency of peaks per second, but two waves of the same frequency may not be locked in "phase." Like the sound waves of two musical instruments that are slightly out of tune, two out-of-phase brain waves of the same frequency would be similar but slightly out of sync.
"Theta oscillations are known to be involved in memory formation, and previous studies have identified correlations between memory strength and the activity of certain neurons, but the relationships between these events have not been understood. Our research shows that when memory-related neurons are well coordinated to theta waves during the learning process, memories are stronger," said Adam N. Mamelak, M.D., a neurosurgeon at Cedars-Sinai Medical Center whose areas of expertise include treatment of seizure disorders. Mamelak is one of the article's senior authors, with Erin M. Schuman, Ph.D., professor of biology at the California Institute of Technology.
"We have yet to discover all factors that influence theta oscillations and the coordination of spike timing, but this study establishes a direct relationship between events at the circuit level of the brain -- individual neuron spike timing relative to the local brain wave environment -- and their effects on human behavior," said Ueli Rutishauser, Ph.D., a postdoctoral scholar at the California Institute of Technology, and the article's first author. He noted that the study also found that while the predictability of memory strength was determined by spike timing relative to theta oscillations, it was not influenced by other related factors, such as the neuron firing rate or the amplitude of the theta oscillations.
Subjects in the study were presented with novel stimuli that they had not previously seen. These were in the form of 100 photographs of a wide range of objects, each viewed for one second. Fifteen to 30 minutes later, they were shown a set of 100 photos, 50 that were new and 50 that had been in the first set. They were asked to recall which ones they had seen before and to estimate how confident they were in their answers.
While these activities were in progress, the researchers recorded the activity of single neurons -- 296 in all -- and the "background" local electrical signals in regions of the brain where memories are encoded (the hippocampus and the amygdala). According to the results, image recognition was stronger when learning occurred while neuronal spikes were in sync with local theta waves.
Most studies of theta waves have been conducted in rats, with only a few studies in humans, in part because EEG electrodes need to be placed directly on the brain's surface for highly precise measurements. This study was conducted with eight volunteers who suffer from epilepsy and were undergoing intracranial EEGs. These are often used to pinpoint the source of epileptic seizure activity. The authors note that steps were taken to ensure that the patients' underlying medical condition did not affect the outcome of the study.
Brain wave frequency is measured per second and quantified in hertz (Hz). A wave that cycles 10 times per second is considered a 10 Hz wave. Most brain waves recorded in humans range up to about 40 Hz, although they also go much higher. Theta waves oscillate toward the lower end of the scale, in about the four Hz to seven Hz range.
Neurosurgeon Ian B. Ross, M.D., and the Huntington Memorial Hospital Epilepsy & Brain Mapping Unit also participated in this study.
Funding for the study was provided by the Gordon and Betty Moore Foundation, the William T. Gimbel Discovery Fund, and the Howard Hughes Medical Institute.
Research scientists at Cedars-Sinai Medical Center and the California Institute of Technology suggest in an article in the March 24, 2010, journal Nature (online) that when memory-related neurons in the brain fire in sync with certain brain waves, the resulting image recognition and memories are stronger than if this synchronization does not occur.
Synchronization is influenced by "theta waves," which are associated with relaxation, daydreaming and drowsiness, but also with learning and memory formation. While it has long been understood that a relaxed mind is one that is ready to receive new information, this study pinpoints a mechanism by which this state of mind allows neurons to work together to improve memory retention. Further exploration of these events could have implications for developing new therapies to treat learning disabilities and some types of dementia, according to the authors.
Brain waves oscillate, with rhythmic highs and lows, and can be measured with electroencephalograms, which use electrodes to record electrical activity. One measure of waves is the frequency of peaks per second, but two waves of the same frequency may not be locked in "phase." Like the sound waves of two musical instruments that are slightly out of tune, two out-of-phase brain waves of the same frequency would be similar but slightly out of sync.
"Theta oscillations are known to be involved in memory formation, and previous studies have identified correlations between memory strength and the activity of certain neurons, but the relationships between these events have not been understood. Our research shows that when memory-related neurons are well coordinated to theta waves during the learning process, memories are stronger," said Adam N. Mamelak, M.D., a neurosurgeon at Cedars-Sinai Medical Center whose areas of expertise include treatment of seizure disorders. Mamelak is one of the article's senior authors, with Erin M. Schuman, Ph.D., professor of biology at the California Institute of Technology.
"We have yet to discover all factors that influence theta oscillations and the coordination of spike timing, but this study establishes a direct relationship between events at the circuit level of the brain -- individual neuron spike timing relative to the local brain wave environment -- and their effects on human behavior," said Ueli Rutishauser, Ph.D., a postdoctoral scholar at the California Institute of Technology, and the article's first author. He noted that the study also found that while the predictability of memory strength was determined by spike timing relative to theta oscillations, it was not influenced by other related factors, such as the neuron firing rate or the amplitude of the theta oscillations.
Subjects in the study were presented with novel stimuli that they had not previously seen. These were in the form of 100 photographs of a wide range of objects, each viewed for one second. Fifteen to 30 minutes later, they were shown a set of 100 photos, 50 that were new and 50 that had been in the first set. They were asked to recall which ones they had seen before and to estimate how confident they were in their answers.
While these activities were in progress, the researchers recorded the activity of single neurons -- 296 in all -- and the "background" local electrical signals in regions of the brain where memories are encoded (the hippocampus and the amygdala). According to the results, image recognition was stronger when learning occurred while neuronal spikes were in sync with local theta waves.
Most studies of theta waves have been conducted in rats, with only a few studies in humans, in part because EEG electrodes need to be placed directly on the brain's surface for highly precise measurements. This study was conducted with eight volunteers who suffer from epilepsy and were undergoing intracranial EEGs. These are often used to pinpoint the source of epileptic seizure activity. The authors note that steps were taken to ensure that the patients' underlying medical condition did not affect the outcome of the study.
Brain wave frequency is measured per second and quantified in hertz (Hz). A wave that cycles 10 times per second is considered a 10 Hz wave. Most brain waves recorded in humans range up to about 40 Hz, although they also go much higher. Theta waves oscillate toward the lower end of the scale, in about the four Hz to seven Hz range.
Neurosurgeon Ian B. Ross, M.D., and the Huntington Memorial Hospital Epilepsy & Brain Mapping Unit also participated in this study.
Funding for the study was provided by the Gordon and Betty Moore Foundation, the William T. Gimbel Discovery Fund, and the Howard Hughes Medical Institute.
Thursday, February 11, 2010
Evidence-Based Steps To Reduce Risk of Dementia by 20%
Your guide to reducing the risk of dementia
The jury is unfortunately still out on whether the crossword can help. You cannot alter your age or the genes you are born with, but there are lifestyle changes you can adopt which may reduce your chance of developing dementia by as much as 20%.
The BBC convened a panel of independent experts, chaired by the Alzheimer's Society, which evaluated more than 70 research papers and articles to come up with a series of tips for reducing your risk.
It may sound young, but the age of 35, they suggest, is high time to start thinking about these recommendations. If more of us acted on these, thousands of cases of dementia could be prevented in the future.
There is very strong evidence for the following:
EXERCISE
Prof Clive Ballard gives his top tips on how to cheat dementia
What is good for the heart is good for the brain. Exercise can have a beneficial effect at any age to help protect against dementia. To help reduce the risk at least 30 minutes of exercise, five times a week is suggested. It does not have to be the gym - a brisk walk is a perfectly acceptable alternative. Whatever form of exercise gets your heart pumping and leaves you somewhat out of breath is doing the trick. Exercise helps maintain a healthy weight and blood pressure, and so is indirectly thought to reduce the risk of dementia.
There is also growing evidence that regular exercise has other health effects such as promoting cell and tissue repair mechanisms including growth of new cells in the brain.
NOT BEING OBESE
Being seriously overweight is deemed a risk factor for developing dementia. This really matters in mid-life - between the ages of 35 and 65. Obesity increases the likelihood of developing Type 2 diabetes - believed to be a risk factor - but whether this causes the disease, or is simply more likely to develop in those who are also more prone to dementia is unclear. Obesity is also associated with higher cholesterol and blood pressure - again, known to be risk factors. You are deemed clinically obese - very overweight - if you have a BMI of 30 and above.
BRING DOWN HIGH BLOOD PRESSURE
The panel evaluated more than 70 research papers
Again, the key here is having consistently raised blood pressure in mid-life - anything above 140/90mmHg. It is thought that this increases the chance of dementia by causing damage to the brain. This may happen as a result of a stroke - in which blood supply to part or all of the brain is cut off - or due to microvascular disease, a condition which slows the flow of blood through the body thereby damaging cells and nerves in the brain. If you are over 40, or have a history of dementia or cardiovascular disease in your family, then get your blood pressure checked regularly.
REDUCE CHOLESTEROL
It is mid-life levels once more which appear to pose the greatest problem. Like high blood pressure, high levels of cholesterol raise the risk of stroke and microvascular disease. But cholesterol is also thought to be involved in the mechanism which causes amyloid protein plaques - the protein deposits that characterise Alzheimer's disease - to build up. Again if you are over 40 or have a family history, get your cholesterol checked. The Department of Health recommends a total cholesterol level of less than 5.0mmol/l.
NOT SMOKING
This had been an area of confusion, as some studies had suggested nicotine could have a protective effect - with the chemical reducing plaques when administered to animals in water. But the way in which we smoke tobacco, and the other chemicals inhaled in the process, negates this benefit. As well as raising the risk of vascular disease - a risk factor for dementia - smoking can result in low oxygen levels in the brain which in turn can promote the production of the protein found in brain plaques.
It is possible the following may have an impact:
ALCOHOL
There is no need to start drinking if you do not already
In fact the studies are quite clear that drinking a modest amount appears to protect against cognitive decline. Moderate drinking is defined as keeping within the recommended daily limits - up to two small glasses of wine for a woman, and three for a man. The problem is that these studies compare drinkers with non-drinkers - and people who abstain may do so for health reasons, which in turn may affect their chances of developing dementia. The message is if you are drinking within your weekly guidelines there is no need to stop, but there is no need to take up drinking or increase the amount you consume, as heavy drinking may in fact increase your risk.
FOLLOWING A MEDITERRANEAN DIET
Several recent studies have highlighted the potential for this diet to reduce the risk of Alzheimer's Disease. It involves eating lots of fruit and vegetables, whole grain foods, fish and plenty of olive oil, but it is relatively low in dairy products and processed foods. Further long term research is needed to confirm the effects of eating this way.
BEING SOCIALLY ACTIVE
Some evidence suggests that an active social life throughout life can be protective, with both the social ties one enjoys with others and non-physical leisure time deemed important. However, examining these factors and designing studies which can separate their effects is very difficult - consequently the conclusions which can be drawn from results are limited. One particular study has found that being single and living alone is a risk factor for dementia: social isolation is thought to have negative effects on health generally, increasing depression and cardiovascular disease.
Studies have also suggested that engaging in non-physical leisure activities such as gardening, and knitting may have a protective effect, a benefit that is likely to accumulate gradually over decades.
But the jury is out on:
BRAIN TRAINING
It sounds both attractive and plausible that giving your brain a "workout" could guard against dementia, and there is some evidence that very intensive brain training under strict conditions can improve specific functions like reasoning and problem solving. But there is no evidence as yet that doing a crossword a day or a number puzzle - or even learning a new language at 50 - will protect against dementia. That does mean they do not - simply that the proof that they do is presently lacking.
VITAMIN SUPPLEMENTS
There is no consistent evidence either way as to whether B vitamin supplements - folic acid, vitamin B12 or B6 - are effective in reducing the incidence of dementia. Research continues. However vitamin E supplements, which it was once hoped could prevent and even reverse early neurodegenerative changes, have not appeared to be effective in trials.
The jury is unfortunately still out on whether the crossword can help. You cannot alter your age or the genes you are born with, but there are lifestyle changes you can adopt which may reduce your chance of developing dementia by as much as 20%.
The BBC convened a panel of independent experts, chaired by the Alzheimer's Society, which evaluated more than 70 research papers and articles to come up with a series of tips for reducing your risk.
It may sound young, but the age of 35, they suggest, is high time to start thinking about these recommendations. If more of us acted on these, thousands of cases of dementia could be prevented in the future.
There is very strong evidence for the following:
EXERCISE
Prof Clive Ballard gives his top tips on how to cheat dementia
What is good for the heart is good for the brain. Exercise can have a beneficial effect at any age to help protect against dementia. To help reduce the risk at least 30 minutes of exercise, five times a week is suggested. It does not have to be the gym - a brisk walk is a perfectly acceptable alternative. Whatever form of exercise gets your heart pumping and leaves you somewhat out of breath is doing the trick. Exercise helps maintain a healthy weight and blood pressure, and so is indirectly thought to reduce the risk of dementia.
There is also growing evidence that regular exercise has other health effects such as promoting cell and tissue repair mechanisms including growth of new cells in the brain.
NOT BEING OBESE
Being seriously overweight is deemed a risk factor for developing dementia. This really matters in mid-life - between the ages of 35 and 65. Obesity increases the likelihood of developing Type 2 diabetes - believed to be a risk factor - but whether this causes the disease, or is simply more likely to develop in those who are also more prone to dementia is unclear. Obesity is also associated with higher cholesterol and blood pressure - again, known to be risk factors. You are deemed clinically obese - very overweight - if you have a BMI of 30 and above.
BRING DOWN HIGH BLOOD PRESSURE
The panel evaluated more than 70 research papers
Again, the key here is having consistently raised blood pressure in mid-life - anything above 140/90mmHg. It is thought that this increases the chance of dementia by causing damage to the brain. This may happen as a result of a stroke - in which blood supply to part or all of the brain is cut off - or due to microvascular disease, a condition which slows the flow of blood through the body thereby damaging cells and nerves in the brain. If you are over 40, or have a history of dementia or cardiovascular disease in your family, then get your blood pressure checked regularly.
REDUCE CHOLESTEROL
It is mid-life levels once more which appear to pose the greatest problem. Like high blood pressure, high levels of cholesterol raise the risk of stroke and microvascular disease. But cholesterol is also thought to be involved in the mechanism which causes amyloid protein plaques - the protein deposits that characterise Alzheimer's disease - to build up. Again if you are over 40 or have a family history, get your cholesterol checked. The Department of Health recommends a total cholesterol level of less than 5.0mmol/l.
NOT SMOKING
This had been an area of confusion, as some studies had suggested nicotine could have a protective effect - with the chemical reducing plaques when administered to animals in water. But the way in which we smoke tobacco, and the other chemicals inhaled in the process, negates this benefit. As well as raising the risk of vascular disease - a risk factor for dementia - smoking can result in low oxygen levels in the brain which in turn can promote the production of the protein found in brain plaques.
It is possible the following may have an impact:
ALCOHOL
There is no need to start drinking if you do not already
In fact the studies are quite clear that drinking a modest amount appears to protect against cognitive decline. Moderate drinking is defined as keeping within the recommended daily limits - up to two small glasses of wine for a woman, and three for a man. The problem is that these studies compare drinkers with non-drinkers - and people who abstain may do so for health reasons, which in turn may affect their chances of developing dementia. The message is if you are drinking within your weekly guidelines there is no need to stop, but there is no need to take up drinking or increase the amount you consume, as heavy drinking may in fact increase your risk.
FOLLOWING A MEDITERRANEAN DIET
Several recent studies have highlighted the potential for this diet to reduce the risk of Alzheimer's Disease. It involves eating lots of fruit and vegetables, whole grain foods, fish and plenty of olive oil, but it is relatively low in dairy products and processed foods. Further long term research is needed to confirm the effects of eating this way.
BEING SOCIALLY ACTIVE
Some evidence suggests that an active social life throughout life can be protective, with both the social ties one enjoys with others and non-physical leisure time deemed important. However, examining these factors and designing studies which can separate their effects is very difficult - consequently the conclusions which can be drawn from results are limited. One particular study has found that being single and living alone is a risk factor for dementia: social isolation is thought to have negative effects on health generally, increasing depression and cardiovascular disease.
Studies have also suggested that engaging in non-physical leisure activities such as gardening, and knitting may have a protective effect, a benefit that is likely to accumulate gradually over decades.
But the jury is out on:
BRAIN TRAINING
It sounds both attractive and plausible that giving your brain a "workout" could guard against dementia, and there is some evidence that very intensive brain training under strict conditions can improve specific functions like reasoning and problem solving. But there is no evidence as yet that doing a crossword a day or a number puzzle - or even learning a new language at 50 - will protect against dementia. That does mean they do not - simply that the proof that they do is presently lacking.
VITAMIN SUPPLEMENTS
There is no consistent evidence either way as to whether B vitamin supplements - folic acid, vitamin B12 or B6 - are effective in reducing the incidence of dementia. Research continues. However vitamin E supplements, which it was once hoped could prevent and even reverse early neurodegenerative changes, have not appeared to be effective in trials.
Wednesday, February 3, 2010
Escitalopram and Enhancement of Cognitive Recovery Following Stroke
The new issue of *Archives of General Psychiatry* (Vol. 67 No. 2)includes a study: "Escitalopram and Enhancement of Cognitive RecoveryFollowing Stroke."The authors are Ricardo E. Jorge, MD; Laura Acion, MS; David Moser, PhD;Harold P. Adams Jr, MD; & Robert G. Robinson, MD.
ContextAdjunctive restorative therapies administered during the first fewmonths after stroke, the period with the greatest degree of spontaneousrecovery, reduce the number of stroke patients with significant disability.
Objective: To examine the effect of escitalopram on cognitive outcome. Wehypothesized that patients who received escitalopram would show improvedperformance in neuropsychological tests assessing memory and executivefunctions than patients who received placebo or underwent ProblemSolving Therapy.DesignRandomized trial.SettingStroke center.
Participants: One hundred twenty-nine patients were treated within 3 months followingstroke. The 12-month trial included 3 arms: a double-blind placebo-controlled comparison of escitalopram (n = 43) with placebo (n = 45),and a nonblinded arm of Problem Solving Therapy (n = 41).Outcome MeasuresChange in scores from baseline to the end of treatment for theRepeatable Battery for the Assessment of Neuropsychological Status(RBANS) and Trail-Making, Controlled Oral Word Association, WechslerAdult Intelligence Scale-III Similarities, and Stroop tests.
Result: sWe found a difference among the 3 treatment groups in change in RBANStotal score (P < .01) and RBANS delayed memory score (P < .01). Afteradjusting for possible confounders, there was a significant effect ofescitalopram treatment on the change in RBANS total score (P < .01,adjusted mean change in score: escitalopram group, 10.0; nonescitalopramgroup, 3.1) and the change in RBANS delayed memory score (P < .01,adjusted mean change in score: escitalopram group, 11.3; nonescitalopramgroup, 2.5). We did not observe treatment effects in otherneuropsychological measures.
Conclusions: When compared with patients who received placebo or underwent ProblemSolving Therapy, stroke patients who received escitalopram showedimprovement in global cognitive functioning, specifically in verbal andvisual memory functions. This beneficial effect of escitalopram wasindependent of its effect on depression. The utility of antidepressantsin the process of poststroke recovery should be further investigated.
ContextAdjunctive restorative therapies administered during the first fewmonths after stroke, the period with the greatest degree of spontaneousrecovery, reduce the number of stroke patients with significant disability.
Objective: To examine the effect of escitalopram on cognitive outcome. Wehypothesized that patients who received escitalopram would show improvedperformance in neuropsychological tests assessing memory and executivefunctions than patients who received placebo or underwent ProblemSolving Therapy.DesignRandomized trial.SettingStroke center.
Participants: One hundred twenty-nine patients were treated within 3 months followingstroke. The 12-month trial included 3 arms: a double-blind placebo-controlled comparison of escitalopram (n = 43) with placebo (n = 45),and a nonblinded arm of Problem Solving Therapy (n = 41).Outcome MeasuresChange in scores from baseline to the end of treatment for theRepeatable Battery for the Assessment of Neuropsychological Status(RBANS) and Trail-Making, Controlled Oral Word Association, WechslerAdult Intelligence Scale-III Similarities, and Stroop tests.
Result: sWe found a difference among the 3 treatment groups in change in RBANStotal score (P < .01) and RBANS delayed memory score (P < .01). Afteradjusting for possible confounders, there was a significant effect ofescitalopram treatment on the change in RBANS total score (P < .01,adjusted mean change in score: escitalopram group, 10.0; nonescitalopramgroup, 3.1) and the change in RBANS delayed memory score (P < .01,adjusted mean change in score: escitalopram group, 11.3; nonescitalopramgroup, 2.5). We did not observe treatment effects in otherneuropsychological measures.
Conclusions: When compared with patients who received placebo or underwent ProblemSolving Therapy, stroke patients who received escitalopram showedimprovement in global cognitive functioning, specifically in verbal andvisual memory functions. This beneficial effect of escitalopram wasindependent of its effect on depression. The utility of antidepressantsin the process of poststroke recovery should be further investigated.
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