Jan. 14, 2013 — Parkinson's experts across the world have been reporting a remarkable phenomenon -- many patients treated with drugs to increase the activity of dopamine in the brain as a therapy for motor symptoms such as tremors and muscle rigidity are developing new creative talents, including painting, sculpting, writing, and more.
Prof. Rivka Inzelberg of Tel Aviv University's Sackler Faculty of Medicine first noticed the trend in her own Sheba Medical Center clinic when the usual holiday presents from patients -- typically chocolates or similar gifts -- took a surprising turn. "Instead, patients starting bringing us art they had made themselves," she says.
Inspired by the discovery, Prof. Inzelberg sought out evidence of this rise in creativity in current medical literature. Bringing together case studies from around the world, she examined the details of each patient to uncover a common underlying factor -- all were being treated with either synthetic precursors of dopamine or dopamine receptor agonists, which increase the amount of dopamine activity in the brain by stimulating receptors. Her report will be published in the journal Behavioral Neuroscience.
Giving in to artistic impulse Dopamine is involved in several neurological systems, explains Prof. Inzelberg. Its main purpose is to aid in the transmission of motor commands, which is why a lack of dopamine in Parkinson's patients is associated with tremors and a difficulty in coordinating their movements.
But it's also involved in the brain's "reward system" -- the satisfaction or happiness we experience from an accomplishment. This is the system which Prof. Inzelberg predicts is associated with increasing creativity. Dopamine and artistry have long been connected, she points out, citing the example of the Vincent Van Gogh, who suffered from psychosis. It's possible that his creativity was the result of this psychosis, thought to be caused by a spontaneous spiking of dopamine levels in the brain.
There are seemingly no limits to the types of artistic work for which patients develop talents, observes Prof. Inzelberg. Cases include an architect who began to draw and paint human figures after treatment, and a patient who, after treatment, became a prize-winning poet though he had never been involved in the arts before.
It's possible that these patients are expressing latent talents they never had the courage to demonstrate before, she suggests. Dopamine-inducing therapies are also connected to a loss of impulse control, and sometimes result in behaviors like excessive gambling or obsessional hobbies. An increase in artistic drive could be linked to this lowering of inhibitions, allowing patients to embrace their creativity. Some patients have even reported a connection between their artistic sensibilities and medication dose, noting that they feel they can create more freely when the dose is higher.
Therapeutic value Prof. Inzelberg believes that such artistic expressions have promising therapeutic potential, both psychologically and physiologically. Her patients report being happier when they are busy with their art, and have noted that motor handicaps can lessen significantly. One such patient is usually wheelchair-bound or dependent on a walker, but creates intricate wooden sculptures that have been displayed in galleries. External stimuli can sometimes bypass motor issues and foster normal movement, she explains. Similar types of art therapy are already used for dementia and stroke patients to help mitigate the loss of verbal communication skills, for example.
The next step is to try to characterize those patients who become more creative through treatment through comparing them to patients who do not experience a growth in artistic output. "We want to screen patients under treatment for creativity and impulsivity to see if we can identify what is unique in those who do become more creative," says Prof. Inzelberg. She also believes that such research could provide valuable insights into creativity in healthy populations, too.
Thursday, January 24, 2013
Friday, December 21, 2012
Better Stroke Care, Everywhere: Study Boosts Local Hospitals' Clotbuster Use
Dec. 20, 2012 — From the moment a stroke occurs, patients must race against the clock to get treatment that can prevent lasting damage. Now, a new study shows the promise -- and the challenges -- of getting them state-of-the-art treatment safely at their local hospital, saving precious minutes.
The results come from an effort that tested methods to improve delivery of a time-sensitive, clot-busting drug in stroke patients at 24 community hospitals across Michigan. To date, clot-busting treatment has been mostly used at larger hospitals.
The research effort was coordinated by members of the University of Michigan Health System's Department of Emergency Medicine, Department of Neurology and Stroke Program, which offered half the hospitals education and round-the-clock treatment assistance by phone. The study was funded by the National Institute of Neurological Disorders and Stroke at the National Institutes of Health.
By the end of the study, the community hospitals across Michigan that had the U-M experts as the "sixth man" on their teams did better at delivering the drug called tPA to eligible patients than those that didn't.
The findings of the randomized controlled trial are published in Lancet-Neurology. They show that community hospitals can indeed improve patients' chances of getting tPA in the first few hours of a stroke, without increased risk of dangerous bleeding.
Data from 22 of the hospitals show that tPA use more than doubled in the 11 hospitals that were randomly chosen to get the extra help, versus a smaller increase in the 11 that didn't. Some hospitals even surpassed national targets for tPA use that large stroke centers don't always reach -- a true game-changing performance.
Across the U.S., less than 2 percent of stroke patients receive tPA -- when more than 11 percent could -- largely because of the time limits on its use and delays in getting patients to a hospital. That's why it's important for community hospitals to offer it.
The investigation, called INSTINCT for INcreasing Stroke Treatment through INterventional Change Tactics, demonstrates that tPA can be used safely and appropriately in the community hospital setting -- and that more work needs to be done to expand public access to the only treatment approved by the U.S. Food and Drug Administration to reverse the effects of stroke. While improvement at the target community hospitals that got the education was statistically significant, it was not as large as hoped for. But the findings suggest that relatively low-cost and low-tech interventions can improve local stroke care.
Lead author Phillip Scott, M.D., a U-M emergency physician and principal investigator of the trial, likens the results to the performance of teams from smaller athletic conferences that beat larger, more celebrated teams, to reach the final stages of the annual NCAA college basketball tournament.
"This study suggests that community hospitals can evaluate and treat enough emergency stroke patients to keep their teams' treatment skills sharp, but are of a size that creates rapid lines of communication and stable physican and nurse teams. This may facilitate rapid, safe stroke diagnosis and care," says Scott, an associate professor of emergency medicine at the U-M Medical School. "Four of the hospitals that received the educational intervention achieved tPA use rates of 5 to 8 percent of all stroke patients, compared to only one of the control hospitals. That's a rate many large medical centers strive to reach."
"This study, while finding only modest improvements, provides encouraging evidence that intensive professional education at community hospitals has the potential to improve the use of tPA in acute stroke care," said Scott Janis, Ph.D., program director at the NINDS. "Importantly, it also lays the groundwork for future strategies that should be explored to develop evidence-based interventions that would improve patient access to this proven therapy following stroke."
How it was done, and more about the results:
The study started by collecting baseline data on stroke treatment from 2005 and 2006 at all the hospitals. After the sites were randomized, the U-M team offered continuing medical education classes at the hospitals, workshops at U-M, and other support, including 24-hour phone consultation availability, to the hospitals chosen to receive the intervention.
All the hospitals were in the lower peninsula of Michigan, and were chosen at random from among hospitals with at least 100 stroke discharges per year. All hospitals that participated stayed in the trial until data collection ended in 2010. Hospitals could hold primary stroke center designation, as granted by the Joint Commission, but could not be tertiary academic comprehensive stroke centers.
In all, 188 tPA treatments occurred among 15,065 stroke patients during the baseline period, and 557 treatments occurred among 25,758 stroke patients from 2007 to 2010. The authors note that tPA use at hospitals nationwide rose somewhat during the study period, due to factors such as insurance reimbursement and new data on tPA's effectiveness at preventing disability.
The INSTINCT study findings were complicated by the fact that one of the hospitals enrolled in the trial became an academic stroke center after starting the study. When it and its matched hospital are excluded from the analysis, the remaining hospitals showed enough of an impact from the educational effort to be statistically significant -- a 105 percent increased use of tPA over baseline.
"We essentially saw a doubling of tPA usage, using standard technologies for education and support. Importantly, the increase was achieved safely," Scott says. "This shows we can translate the knowledge of effective stroke treatment into a community setting." The size of the study, with 557 stroke patients treated after intervention began, makes it one of the largest tPA studies in the world.
More about stroke treatment:
The use of tPA in ischemic stroke has grown around the world in the last decade, but many patients who could get the drug still do not. The "treatment window" for tPA has been seen as three hours from the onset of stroke symptoms, though recent studies suggest patients can see benefit even four and a half hours out. The importance of early treatment, however, cannot be overstated, as patients treated earlier have greater benefits and the drug is not currently FDA-approved for use beyond three hours.
Considering that most stroke sufferers wait more than an hour after symptoms start before they seek help, and that travel time to a tPA-providing hospital is around 30 minutes, that leaves hospitals about an hour to do medical imaging, make a firm diagnosis and initiate tPA treatment.
Patients must then be monitored to check for brain bleeding, and to assess the impact of their stroke. To reliably accomplish this, a system for the care of acute stroke patients must already be in place when a patient arrives at the emergency department.
Patients who don't reach a location where they can received standard tPA treatment in time can still potentially be treated with advanced catheter-based clot removal treatment at a major referral hospital such as U-M. These advanced therapies have a longer time window for treatment, but have not been proven more effective than early standard treatment. The Stroke Program at U-M is participating in multiple trials to improve advanced stroke treatment.
Additional authors: William Meurer, M.D., Shirley Frederiksen, M.S., and Robert Silbergleit, M.D. of U-M Emergency Medicine; John Kalbfleisch, Ph.D., Zhenzhen Xu, Ph.D. and Mary Haan, DrPH of the U-M School of Public Health; and Lewis B Morgenstern, M.D., of U-M Neurology. Morgenstern directs, and Scott, Meurer, Frederiksen and Silbergleit are members of, the U-M Stroke Program.
Funding source: NINDS R01-NS-050372
Wednesday, November 14, 2012
Alzheimer's Plaques in PET Brain Scans Identify Future Cognitive Decline
Among patients with mild or no cognitive impairment, brain scans using a new radioactive dye can detect early evidence of Alzheimer's disease that may predict future decline, according to a multi-center study led by researchers at Duke University Medical Center.
The finding is published online July 11, 2012, in the journal Neurology, the medical journal of the American Academy of Neurology. It expands on smaller studies demonstrating that early detection of tell-tale plaques could be a predictive tool to help guide care and treatment decisions for patients with Alzheimer's disease.
"Even at a short follow-up of 18 months we can see how the presence of amyloid plaques affects cognitive function," said P. Murali Doraiswamy, M.D., professor of psychiatry at Duke who co-led the study with R. Edward Coleman, M.D., professor of radiology at Duke . "Most people who come to the doctor with mild impairment really want to know the short-term prognosis and potential long-term effect."
Doraiswamy said such knowledge also has some pitfalls. There is no cure for Alzheimer's disease, which afflicts 5.4 million people in the United States and is the sixth-leading cause of death among U.S. adults. But he said numerous drugs are being investigated, and identifying earlier disease would improve research into their potential benefits and speed new discoveries, while also enhancing care and treatment of current patients.
In the Neurology study, 151 people who had enrolled in a multi-center test of a new radioactive dye called florbetapir (Amyvid) were recruited to participate in a 36-month analysis. Of those participants, 69 had normal cognitive function at the start of the study, 51 had been diagnosed with mild impairment, and 31 had Alzheimer's dementia.
All completed cognitive tests and underwent a brain scan using Positron Emission Tomography, or PET imaging. The technology uses radioactive tracers designed to highlight specific tissue to create a three-dimensional picture of an organ or a biological function.
The dye used in the study, florbetapir, was recently approved by the U.S. Food and Drug Administration for PET imaging of the brain to estimate beta-amyloid plaque density in patients who are being evaluated for cognitive impairment. It binds to the amyloid plaques that characterize Alzheimer's disease, providing a window into the brain to see if the plaques have formed, and how extensively.
Patients in the study were reassessed with additional cognitive exams at 18 months and 36 months. At the 18-month point, patients with mild cognitive impairment who had PET evidence of plaque at the trial's start worsened to a great degree on cognitive tests than patients who had no evidence of plaque at the trial's start. Twenty-nine percent of the plaque-positive patients in this group developed Alzheimer's dementia, compared to 10 percent who started with no plaque.
Cognitively normal patients with a plaque-positive PET scan at the start of the study also showed more mental decline at 18 months compared to those who were negative for plaque.
The study additionally found that people with negative scans reversed from minimally impaired to normal more often than people with positive PET scan, suggesting test anxiety or concentration problems could have affected their initial performance.
"For the most part we have been blind about who would progress and who wouldn't, so this approach is a step toward having a biomarker that predicts risk of decline in people who are experiencing cognitive impairment," Doraiswamy said.
He said the study's results provide initial data that needs to be verified by additional research. Final, 36-month data from the study has been completed and will be presented at the Alzheimer's Association International Conference this week in Vancouver, Canada. Doraiswamy also cautioned that florbetapir is currently not approved to predict the development of dementia or other neurologic conditions and stressed that it should not be used as a screening tool in otherwise normal or minimally impaired people. Likewise, a positive scan is not necessarily diagnostic for Alzheimer's by itself.
In addition to Doraiswamy and Coleman (who died in June), study authors included; Reisa A. Sperling and Keith A. Johnson of Massachusetts General Hospital, Boston Medical School; Eric M. Reiman of Banner Alzheimer's Institute; Mat D. Davis of the University of Pennsylvania; Michael Grundman of Global R&D Partners and the University of California, San Diego; Marwan N. Sabbagh of Banner-Sun Health Research Institute; Carl H. Sadowsky of Nova SE University; Adam S. Fleisher of Banner Alzheimer's Institute and UCSD; and Alan Carpenter, Christopher M. Clark (deceased), Abhinay D. Joshi, Mark A. Mintun, Daniel M. Skovronsky, and Michael J. Pontecorvo of Avid Radiopharmaceuticals.
The study was funded by Eli Lilly/Avid Radiopharmaceuticals, which markets florbetapir and conducted by Avid and the AV45-A11 study group, a consortium of Alzheimer's clinical research centers. Doraiswamy receives advisory and speaker fees from Lilly/Avid, as well as other companies, and owns shares in Sonexa and Clarimedix.
The finding is published online July 11, 2012, in the journal Neurology, the medical journal of the American Academy of Neurology. It expands on smaller studies demonstrating that early detection of tell-tale plaques could be a predictive tool to help guide care and treatment decisions for patients with Alzheimer's disease.
"Even at a short follow-up of 18 months we can see how the presence of amyloid plaques affects cognitive function," said P. Murali Doraiswamy, M.D., professor of psychiatry at Duke who co-led the study with R. Edward Coleman, M.D., professor of radiology at Duke . "Most people who come to the doctor with mild impairment really want to know the short-term prognosis and potential long-term effect."
Doraiswamy said such knowledge also has some pitfalls. There is no cure for Alzheimer's disease, which afflicts 5.4 million people in the United States and is the sixth-leading cause of death among U.S. adults. But he said numerous drugs are being investigated, and identifying earlier disease would improve research into their potential benefits and speed new discoveries, while also enhancing care and treatment of current patients.
In the Neurology study, 151 people who had enrolled in a multi-center test of a new radioactive dye called florbetapir (Amyvid) were recruited to participate in a 36-month analysis. Of those participants, 69 had normal cognitive function at the start of the study, 51 had been diagnosed with mild impairment, and 31 had Alzheimer's dementia.
All completed cognitive tests and underwent a brain scan using Positron Emission Tomography, or PET imaging. The technology uses radioactive tracers designed to highlight specific tissue to create a three-dimensional picture of an organ or a biological function.
The dye used in the study, florbetapir, was recently approved by the U.S. Food and Drug Administration for PET imaging of the brain to estimate beta-amyloid plaque density in patients who are being evaluated for cognitive impairment. It binds to the amyloid plaques that characterize Alzheimer's disease, providing a window into the brain to see if the plaques have formed, and how extensively.
Patients in the study were reassessed with additional cognitive exams at 18 months and 36 months. At the 18-month point, patients with mild cognitive impairment who had PET evidence of plaque at the trial's start worsened to a great degree on cognitive tests than patients who had no evidence of plaque at the trial's start. Twenty-nine percent of the plaque-positive patients in this group developed Alzheimer's dementia, compared to 10 percent who started with no plaque.
Cognitively normal patients with a plaque-positive PET scan at the start of the study also showed more mental decline at 18 months compared to those who were negative for plaque.
The study additionally found that people with negative scans reversed from minimally impaired to normal more often than people with positive PET scan, suggesting test anxiety or concentration problems could have affected their initial performance.
"For the most part we have been blind about who would progress and who wouldn't, so this approach is a step toward having a biomarker that predicts risk of decline in people who are experiencing cognitive impairment," Doraiswamy said.
He said the study's results provide initial data that needs to be verified by additional research. Final, 36-month data from the study has been completed and will be presented at the Alzheimer's Association International Conference this week in Vancouver, Canada. Doraiswamy also cautioned that florbetapir is currently not approved to predict the development of dementia or other neurologic conditions and stressed that it should not be used as a screening tool in otherwise normal or minimally impaired people. Likewise, a positive scan is not necessarily diagnostic for Alzheimer's by itself.
In addition to Doraiswamy and Coleman (who died in June), study authors included; Reisa A. Sperling and Keith A. Johnson of Massachusetts General Hospital, Boston Medical School; Eric M. Reiman of Banner Alzheimer's Institute; Mat D. Davis of the University of Pennsylvania; Michael Grundman of Global R&D Partners and the University of California, San Diego; Marwan N. Sabbagh of Banner-Sun Health Research Institute; Carl H. Sadowsky of Nova SE University; Adam S. Fleisher of Banner Alzheimer's Institute and UCSD; and Alan Carpenter, Christopher M. Clark (deceased), Abhinay D. Joshi, Mark A. Mintun, Daniel M. Skovronsky, and Michael J. Pontecorvo of Avid Radiopharmaceuticals.
The study was funded by Eli Lilly/Avid Radiopharmaceuticals, which markets florbetapir and conducted by Avid and the AV45-A11 study group, a consortium of Alzheimer's clinical research centers. Doraiswamy receives advisory and speaker fees from Lilly/Avid, as well as other companies, and owns shares in Sonexa and Clarimedix.
Wednesday, October 17, 2012
CONCERNED ABOUT MEMORY PROBLEMS?
TAKE ACTION…GET FREE, CONFIDENTIAL MEMORY SCREENINGS
TUESDAY, NOVEMBER 13, 2012
A. Why is memory screening so important?
Ø As the body ages, so does the brain, especially the ability to remember declines. There are many reasons that cause memory loss; stress, depression, vitamin deficiency, thyroid problems, medical illnesses, Alzheimer’s disease, or just normal aging memory decline.
Ø Memory screenings are the first step toward finding out if the person has early stages of Alzheimer’s dementia vs another condition vs normal aging memory decline.
Ø It is very important to identify the disease or problem that is causing memory loss. Early detection leads to early treatment, which in turn, leads to improved quality of life
Ø Memory screenings can also let the person know that everything is ok. The screenings could turn out normal and put the mind at ease.
Ø Normal scores on a memory screenings provides a valuable opportunity to establish a baseline score for future comparison
Ø A memory screening is not used to diagnose any particular illness & does not replace consultation with a qualified physician or health care provider
B. What is the process of memory screenings?
Ø A screening consists of a series of questions and tasks that are designed to test memory and thinking ability. These tools are non-invasive, safe, and reliable instruments that are sensitive to even mild brain dysfunction
Ø Feedback will be provided immediately following screenings.
Ø While health plans do not typically cover screenings, if additional testing is recommended, most health plans will cover the cost based on individual medical benefits. If necessary, referrals will be provided to seek further examination.
FOR ADDITIONAL INFORMATION, PLEASE CONTACT OUR OFFICE 949-481-8414
TAKE ACTION…GET FREE, CONFIDENTIAL MEMORY SCREENINGS
TUESDAY, NOVEMBER 13, 2012
A. Why is memory screening so important?
Ø As the body ages, so does the brain, especially the ability to remember declines. There are many reasons that cause memory loss; stress, depression, vitamin deficiency, thyroid problems, medical illnesses, Alzheimer’s disease, or just normal aging memory decline.
Ø Memory screenings are the first step toward finding out if the person has early stages of Alzheimer’s dementia vs another condition vs normal aging memory decline.
Ø It is very important to identify the disease or problem that is causing memory loss. Early detection leads to early treatment, which in turn, leads to improved quality of life
Ø Memory screenings can also let the person know that everything is ok. The screenings could turn out normal and put the mind at ease.
Ø Normal scores on a memory screenings provides a valuable opportunity to establish a baseline score for future comparison
Ø A memory screening is not used to diagnose any particular illness & does not replace consultation with a qualified physician or health care provider
B. What is the process of memory screenings?
Ø A screening consists of a series of questions and tasks that are designed to test memory and thinking ability. These tools are non-invasive, safe, and reliable instruments that are sensitive to even mild brain dysfunction
Ø Feedback will be provided immediately following screenings.
Ø While health plans do not typically cover screenings, if additional testing is recommended, most health plans will cover the cost based on individual medical benefits. If necessary, referrals will be provided to seek further examination.
FOR ADDITIONAL INFORMATION, PLEASE CONTACT OUR OFFICE 949-481-8414
Thursday, July 19, 2012
New Biomarker In The Blood May Help Predict Alzheimer's Disease
ScienceDaily (July 18, 2012) — Higher levels of a certain fat in the blood called ceramides may increase a person's risk of developing Alzheimer's disease, according to a study published in the July 18, 2012, online issue of Neurology®, the medical journal of the American Academy of Neurology.
"Our study identifies this biomarker as a potential new target for treating or preventing Alzheimer's disease," said study author Michelle M. Mielke, PhD, an epidemiologist with the Mayo Clinic in Rochester, Minn. Mielke was with Johns Hopkins University at the time of the research.
For the study, 99 women between the ages of 70 and 79 and free of dementia in the Women's Health and Aging Study II had their blood tested for levels of serum ceramides, a fatty compound found throughout the body that is associated with inflammation and cell death. The participants were placed into three groups: high, middle and low levels of ceramides. They were then followed for up to nine years. Of the 99 participants, 27 developed dementia and 18 of those were diagnosed with probable Alzheimer's disease.
The study found that women who had the highest levels of the biomarker were 10 times more likely to develop Alzheimer's disease than women with the lowest levels. Those with middle levels of the biomarker were nearly eight times more likely to develop the disease than those with the lowest levels.
"These findings are important because identifying an accurate biomarker for early Alzheimer's that requires little cost and inconvenience to a patient could help change our focus from treating the disease to preventing or delaying it," said Valory Pavlik, PhD, with the Alzheimer's Disease and Memory Disorders Center of Baylor College of Medicine in Houston and a member of the American Academy of Neurology, in an accompanying editorial.
According to Pavlik, "While a larger, more diverse study is needed to confirm these findings, projections that the global prevalence of Alzheimer's disease will double every 20 years for the foreseeable future have certainly increased the sense of urgency among researchers and health care agencies to identify more effective screening, prevention and treatment strategies."
The study was supported by the National Institute on Aging, the National Institute of Neurological Disorders and Stroke and the Johns Hopkins Older Americans Independence Center.
"Our study identifies this biomarker as a potential new target for treating or preventing Alzheimer's disease," said study author Michelle M. Mielke, PhD, an epidemiologist with the Mayo Clinic in Rochester, Minn. Mielke was with Johns Hopkins University at the time of the research.
For the study, 99 women between the ages of 70 and 79 and free of dementia in the Women's Health and Aging Study II had their blood tested for levels of serum ceramides, a fatty compound found throughout the body that is associated with inflammation and cell death. The participants were placed into three groups: high, middle and low levels of ceramides. They were then followed for up to nine years. Of the 99 participants, 27 developed dementia and 18 of those were diagnosed with probable Alzheimer's disease.
The study found that women who had the highest levels of the biomarker were 10 times more likely to develop Alzheimer's disease than women with the lowest levels. Those with middle levels of the biomarker were nearly eight times more likely to develop the disease than those with the lowest levels.
"These findings are important because identifying an accurate biomarker for early Alzheimer's that requires little cost and inconvenience to a patient could help change our focus from treating the disease to preventing or delaying it," said Valory Pavlik, PhD, with the Alzheimer's Disease and Memory Disorders Center of Baylor College of Medicine in Houston and a member of the American Academy of Neurology, in an accompanying editorial.
According to Pavlik, "While a larger, more diverse study is needed to confirm these findings, projections that the global prevalence of Alzheimer's disease will double every 20 years for the foreseeable future have certainly increased the sense of urgency among researchers and health care agencies to identify more effective screening, prevention and treatment strategies."
The study was supported by the National Institute on Aging, the National Institute of Neurological Disorders and Stroke and the Johns Hopkins Older Americans Independence Center.
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