Links for Keyword: Parkinsons
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By Anne Pycha Future doctors may ask us to say more than “Ahhh.” Several groups of neuroscientists, psychiatrists and computer scientists are now investigating the extent to which patients' language use can provide diagnostic clues—before a single laboratory test is run. Increased computing power and new methods to measure the relation between behavior and brain activity have advanced such efforts. And although tests based on the spoken word may not be as accurate as gene sequencing or MRI scans, for diseases lacking clear biological indicators, language mining could help fill the gap. Psychiatrists at Columbia University interviewed 34 young adults at risk for psychosis, a common sign of schizophrenia that includes delusions and hallucinations. Two and a half years later five of the subjects had developed psychosis, and the remaining 29 remained free of the disorder. A specially designed algorithm combed the initial interviews collectively to look for language features that distinguished the two groups and found that psychosis correlated with shorter sentences, loss of flow in meaning from one sentence to the next and less frequent use of the words “that,” “what” and “which.” When later tested on each individual interview, the computer program predicted who did and who did not develop psychosis with 100 percent accuracy. The results were recently published in Schizophrenia, and a second round of testing with another group of at-risk subjects is now under way. Parkinson's Disease Twenty-seven subjects in a study at Favaloro University in Argentina listened to recorded sentences containing verbs associated with specific hand shapes (such as “applaud” or “punch”). As soon as they understood the sentence, participants pressed a button while keeping both hands in either a flat or clenched-fist position. © 2016 Scientific American
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 21818 - Posted: 01.25.2016
Videos just discovered show the first people ever to be treated for the symptoms of Parkinson’s disease. The footage, hidden for half a century, shows Chilean miners with severe movement problems improving on daily doses of L-dopa. The videos were filmed by George Cotzias at Brookhaven National Laboratory in Upton, New York. In 1963, while studying the toxic effects of manganese in human tissues, Cotzias learned of four workers in the Corral del Quemado mine in Andacollo, Chile, who had developed a syndrome called manganism – which resembled Parkinson’s – through inhaling manganese dust. Cotzias travelled to Chile to include the miners in a trial of leva-dopa, a chemical building block that the body converts into dopamine, low levels of which cause uncontrolled movements in people with Parkinson’s. L-dopa was being tested in Parkinson’s patients around the same time but with little success – even small amounts caused adverse side-effects that prevented a high enough dose reaching the brain. The footage clearly shows the severe problems with walking and turning miners had before treatment. After several months of receiving a daily dose of L-dopa, they were able to feed themselves, shave, tie their shoelaces, and run. “It’s a very important part of the history of neurology,” says Marcelo Miranda, a researcher at Clinica Las Condes in Santiago, Chile, who found the footage, some of which was shown at a conference in the 1960s, but hasn’t been seen since. “It’s the only available document of that period that shows the first patients with Parkinson’s symptoms treated with L-dopa and their extraordinary response.” © Copyright Reed Business Information Ltd.
By Diana Kwon Six years before her husband was diagnosed with Parkinson’s disease, a progressive neurodegenerative disorder marked by tremors and movement difficulties, Joy Milne detected a change in his scent. She later linked the subtle, musky odor to the disease when she joined the charity Parkinson’s UK and met others with the same, distinct smell. Being one of the most common age-related disorders, Parkinson’s affects an estimated seven million to 10 million people worldwide. Although there is currently no definitive diagnostic test, researchers hope that this newly found olfactory signature will lead help create one. Milne, a super-smeller from Perth, Scotland, wanted to share her ability with researchers. So when Tilo Kunath, a neuroscientist at the University of Edinburgh, gave a talk during a Parkinson’s UK event in 2012, she raised her hand during the Q&A session and claimed she was able to smell the disease. “I didn’t take her seriously at first,” Kunath says. “I said, ‘No, I never heard of that, next question please.’” But months later Kunath shared this anecdote with a colleague and received a surprising response. “She told me that that lady wasn’t wrong and that I should find her,” Kunath says. Once the researchers found Milne, they tested her claim by having her sniff 12 T-shirts: six that belonged to people with Parkinson’s and six from healthy individuals. Milne correctly identified 11 out of 12, but miscategorized one of the non-Parkinson’s T-shirts in the disease category. It turned out, however, she was not wrong at all—that person would be diagnosed with Parkinson’s less than a year later. © 2015 Scientific American
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 21582 - Posted: 10.31.2015
Alan Hoffman says nilotinib has changed his life. Just weeks after he started taking the drug in a clinical trial, he began to feel himself recovering from his Parkinson’s disease. The retired professor of social science first started to show the signs of Parkinson’s in 1997. Over the years, his symptoms worsened. “I couldn’t get out of bed without my wife,” Hoffman says. Once a prolific reader, devouring four or five books a week, Hoffman found himself unable to keep his attention on even a short magazine article. His body became increasingly rigid, and he started to lose his sense of balance. “I fell a lot,” he says. And it affected his social life. The disorder was such a struggle, Hoffman says he considered taking his own life. He tried a range of medications, which eased his symptoms to varying degrees. In 2008, he had surgery to implant an electrode into his brain. The deep brain stimulation that followed helped with the rigidity, he says. But deep brain stimulation doesn’t offer a cure – the brain cells continue to die. So Hoffman agreed to join a six-month clinical trial of nilotinib – a drug typically used to treat leukaemia. Nilotinib blocks a protein that interferes with lysosomes – cell structures that destroy harmful proteins. Researchers behind the trial think that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. (For a full report on the effect of the drug see “People with Parkinson’s walk again after promising drug trial”.) © Copyright Reed Business Information Ltd.
An expensive cancer drug may reverse late-stage Parkinson’s disease, enabling participants in a small clinical trial to speak and walk again for the first time in years. While there are several treatments for the symptoms of Parkinson’s, if confirmed this would be the first time a drug has worked on the causes of the disease. “We’ve seen patients at end stages of the disease coming back to life,” says Charbel Moussa of Georgetown University Medical Center in Washington DC, who led the trial. The drug, called nilotinib, works by boosting the brain’s own “garbage disposal system” to clear proteins that accumulate in the brains of people with Parkinson’s disease, says Moussa. These proteins are thought to trigger the death of brain cells that make molecules like dopamine that are needed for movement and other functions. Nilotinib is already approved to treat cancer – it blocks a protein that drives chronic myeloid leukaemia. It also blocks another protein that interferes with lysosomes – cell structures that destroy harmful proteins. Moussa thinks that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. Tests in animals showed promise, so Moussa, his colleague Fernando Pagan and their team set up a small trial of 12 volunteers with Parkinson’s disease or a similar condition called dementia with Lewy bodies. The trial was designed to test only the safety of the oral drug, which was given as a daily dose for six months. © Copyright Reed Business Information Ltd.
By Kristin Ozelli Four years ago writer and producer Jon Palfreman was diagnosed with Parkinson’s disease. He has chronicled his experience and that of many other “Parkies,” as patients sometimes call themselves, in two books, the latest of which is Brain Storms: The Race to Unlock the Mysteries of Parkinson’s Disease, published this year by Scientific American / Farrar, Straus and Giroux, which traces some of the recent progress of medical researchers in treating this disease. He shared with Scientific American MIND senior editor Kristin Ozelli some of the insights he gleaned while working on this book. You wrote an earlier book about Parkinson’s and produced a prize-winning documentary, The Case of the Frozen Addicts, and have experienced the disease personally. While you were researching Brain Storms, was there anything new you learned about the disease that really surprised you? What is truly surprising is just how long biomedical research takes to deliver life-changing therapies. The promising therapies around when I wrote my first book 20 years ago, like neural grafting and growth factors—therapies designed to replace, revive or protect dopamine neurons—well they haven’t panned out. On the other hand, since my first involvement with Parkinson’s, there have been some extraordinary advances in basic science. In a sense, the disease has been rebranded from a movement disorder (resulting from damage to a very small part of the brain) to a systemic condition involving not only tremor and rigidity but also a whole host of symptoms—from depression to sleep disorders, from constipation to dementia. Indeed, there’s an entirely new theory of the disease that sees it as being driven by a protein alpha-synuclein that goes rogue and, prionlike, jumps from neuron to neuron creating havoc. © 2015 Scientific American
A choir of Canadians with Parkinson's disease is helping researchers test how well the performers regain facial movement to express emotions. Tremors and difficulty walking are often the most noticeable symptoms of Parkinson's disease, which affects about one in 500 people in Canada. Those with the disease may also have limited facial movement, which hampers the ability to express themselves. For people with Parkinson's who have "masked face syndrome," it can be difficult for others to decipher how they're feeling. That's because we unknowingly mimic or mirror each other during interaction to connect. "Within a hundred milliseconds of seeing someone else smile or frown, we are smiling or frowning," said Frank Russo, a psychology professor at Ryerson University in Toronto. "We're mirroring what the other person is doing. And that's one of the things that is absent in Parkinson's. It's the absence of mirroring that is leading to some of the deficit in understanding other people's emotions." Having a static face can leave people with Parkinson's seem cold and aloof as they also show deficits in understanding other people's emotions. The patient can then become emotionally disconnected from others. Studying the 28 members of the Parkinson's choir has bolstered Russo's thinking that singing, facial expressions and social communications are interconnected. So far Russo has found that mirroring effect or mimicry was restored among choir participants who sang for 13 weeks. ©2015 CBC/Radio-Canada.
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21410 - Posted: 09.15.2015
By Diana Kwon Each year doctors diagnose approximately 60,000 Americans with Parkinson’s disease, an incurable neurodegenerative condition for which the number-one risk factor is age. Worldwide an estimated seven to 10 million people currently live with the malady. As U.S. and global populations grow older, it is becoming increasingly urgent to understand its causes. So far, researchers know that Parkinson’s involves cell death in a few restricted areas of the brain including the substantia nigra (SNc), one of two big cell clusters in the midbrain that house a large population of dopamine neurons. These cells release dopamine and are involved in a variety of functions including reward processing and voluntary movement. Their death leads to the motor control and balance issues that are core symptoms of the disease. New research shows that these brain cells, most at risk in Parkinson’s disease, require unusually high amounts of energy to carry out their tasks because of their highly branched structures. Like a massive car with an overheating engine, these neurons are susceptible to burnout and early death. This discovery emerged from a comparison of energy use in nigral dopamine neurons and in similar neurons found in the nearby ventral tegmental area (VTA), also in the midbrain. “We were trying to understand why dopamine neurons of the substantia nigra die in Parkinson’s disease patients while there are so many other brain cells that have no problem at all,” says Louis-Eric Trudeau, a neuroscientist at the University of Montreal and senior author of the study published in the August 27 Current Biology. © 2015 Scientific American,
Sarah Schwartz In 2011, science journalist Jon Palfreman saw a doctor about a tremor in his left hand. The doctor diagnosed Palfreman, then 60, with Parkinson’s disease. The disorder, which is newly diagnosed in 60,000 Americans each year, promised a crippling future of tremors, loss of mobility, dementia and more. Palfreman decided to use his reporting expertise to investigate how Parkinson’s disease affects the body and learn about efforts to find a cure. With Brain Storms, Palfreman follows Parkinson’s history from the careful observations of 19th century physicians to today’s cutting-edge research. Palfreman relates complex research studies as gripping medical mysteries. He describes how scientists connected Parkinson’s with the dramatic loss of the brain chemical dopamine and with tenacious protein knots called Lewy bodies that are a hallmark of the disease. Palfreman also explores treatments past and present, including the widely used drug levodopa that restores motion (sometimes uncontrollably), gene therapies, brain surgeries and promising experimental antibody treatments that attack and dissolve misfolded Parkinson’s-related proteins. Ultimately, Brain Storms is about more than Parkinson’s disease; it’s about the people living with the disorder. Palfreman describes patients who must teach themselves to walk without falling over or who freeze in place. He writes about a researcher driven to search for a cure after the disease affects his own father. © Society for Science & the Public 2000 - 2015
By Smitha Mundasad Health reporter A type of diabetes drug may offer a glimmer of hope in the fight against Parkinson's disease, research in the journal Plos Medicine suggests. Scientists found people taking glitazone pills were less likely to develop Parkinson's than patients on other diabetes drugs. But they caution the drugs can have serious side-effects and should not be given to healthy people. Instead, they suggest the findings should prompt further research. 'Unintended benefits' There are an estimated 127,000 people in the UK with Parkinson's disease, which can lead to tremor, slow movement and stiff muscles. And charities say with no drugs yet proven to treat the condition, much more work is needed in this area. The latest study focuses solely on people with diabetes who did not have Parkinson's disease at the beginning of the project. Researchers scoured UK electronic health records to compare 44,597 people prescribed glitazone pills with 120,373 people using other anti-diabetic treatment. They matched participants to ensure their age and stage of diabetes treatment were similar. Scientists found fewer people developed Parkinson's in the glitazone group - but the drug did not have a long-lasting benefit. Any potential protection disappeared once patients switched to another type of pill. Dr Ian Douglas, lead researcher at the London School of Hygiene and Tropical Medicine, said: "We often hear about negative side-effects associated with medications, but sometimes there can also be unintended beneficial effects. "Our findings provide unique evidence that we hope will drive further investigation into potential drug treatments for Parkinson's disease." © 2015 BBC
by Andy Coghlan A man in his mid-50s with Parkinson's disease had fetal brain cells injected into his brain last week. He is the first person in nearly 20 years to be treated this way – and could recover full control of his movements in roughly five years. "It seemed to go fine," says Roger Barker of the University of Cambridge, who is leading the international team that is reviving the procedure. The treatment was pioneered 28 years ago in Sweden, but two trials in the US reported no significant benefit within the first two years following the injections, and the procedure was abandoned in favour of deep brain stimulation treatments. What these trials overlooked is that it takes several years for fetal cells to "bed in" and connect properly to the recipient's brain. Many Swedish and North American recipients improved dramatically, around three years or more after the implants – long after the trials had finished. "In the best cases, patients who had the treatment pretty much went back to normal," says Barker. After the fetal cells were wired up properly in their brains, they started producing the brain signalling chemical dopamine – low levels of this cause the classic Parkinson's symptom of uncontrolled movements. In fact, the cells produced so much dopamine that many patients could stop taking their Parkinson's drugs. "The prospect of not having to take medications for Parkinson's is fantastic," says James Beck of the Parkinson's Disease Foundation in the US. © Copyright Reed Business Information Ltd
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 20989 - Posted: 05.27.2015
Patricia Neighmond Terri Bradford has suffered debilitating headache pain all her life. Some days the pain is so bad, she says, "By 11 o'clock in the morning, I'm on the couch in a darkened room with my head packed in ice." Over the years, Bradford, who is 50 years old and lives in Bedford, Mass., has searched desperately for pain relief. She's been to the doctor countless times for countless tests. "Everything I've had, I've had twice," she says. "I've had two spinal taps; I've had so many nerve blocks I've lost count." Bradford is not alone. It's estimated that every year 12 million Americans go to the doctor seeking help for headaches. Nearly one quarter of the population suffers from recurrent severe tension headaches or migraines. People who go to the doctor for headache pain are more likely to be sent for advanced testing and treatment, a study finds. That testing is expensive, it may not be necessary and could even be harmful, says lead researcher Dr. John Mafi of Beth Israel Deaconess Medical Center in Boston. Mafi looked at the rates of advanced imaging like CT scans and MRIs in people with headaches, as well as referrals to other doctors, presumably specialists. He found that from 1999 to 2010, the number of diagnostic tests rose from 6.7 percent of all doctor visits to 13.9 percent. At the same time, referrals to other doctors increased from 6.9 percent to 13.2 percent. So almost double what it was a decade ago. Mafi says this isn't because more people are suffering headaches. The headache rate has remained virtually the same over the past decade. But what has changed is supply and demand. Today there are a lot more advanced diagnostic machines than there were a decade ago, and more patients are asking to be tested. © 2015 NPR
Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 20906 - Posted: 05.11.2015
Roger Dobson Tapping your fingers on the table is usually a sign of boredom or irritation. But not all tappers are equal, it seems. Men drum their digits slightly faster than women and people in their twenties tap substantially faster than people twice their age. The results of the first study into finger-tapping speeds also found that smokers tap a little faster than non-smokers and fit people tap faster than those who avoid exercise. The research, carried out by scientists at two universities in Istanbul – Bogazici University and Fatih University – examined the tapping rates and “finger load capacities” of 148 people aged between 18 and 85. Each participant was asked to perform a one-minute tapping exercise on a keyboard at “maximum volitional tempo”. Researchers found that the index finger on the right hand of both men and women was the fastest digit, achieving a tapping rate of up to five beats a second among those in their twenties. The middle finger was almost as nifty as the index finger, but the little finger – the slowest digit in the bunch – was capable only of a sluggish 3.8 taps a second among people in the same age group. At first glance, the study might appear to be rather frivolous. But a deeper understanding of finger tapping could aid the design of computer keyboards and musical instruments. It may also aid researchers who use finger-tapping tests for medical assessment of neurological conditions such as Parkinson’s disease, schizophrenia and Alzheimer’s.
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 20887 - Posted: 05.05.2015
Scientists have raised hopes that they may be able to create a vaccine to block the progress of Parkinson’s disease. They believe new research provides evidence that an abnormal protein may trigger the condition. If the theory is correct, researchers say it might be possible to prime a person’s immune system – using a special vaccine – so it is ready to attack the rogue protein as it passes through the body. In this way, the protein would be prevented from destroying a person’s dopamine-manufacturing cells, where the disease inflicts its greatest damage. This new vision of Parkinson’s has been arousing excitement among researchers. “It has transformed the way we see Parkinson’s,” said Roger Barker, professor of clinical neurosciences at Cambridge University. Parkinson’s does not usually affect people until they are over 50. However, researchers have uncovered recent evidence that suggests it may be caused by an event occurring 10 to 20 years before its main symptoms – tremors, rigidity and slowness of movement – manifest themselves. “If you ask Parkinson’s patients if, in the past, they have experienced loss of sense of smell or suffer from disturbed sleep or have problems with their bowels, very often they reply they have,” said Barker, whose work is backed by the charity Parkinson’s UK, whose Parkinson Awareness week ends on Sunday. “Frequently these patients manifest symptoms several years before it becomes apparent they have the disease. We now believe there is a link.” © 2015 Guardian News and Media Limited
Carl Zimmer In 1998, Dr. Philip A. Starr started putting electrodes in people’s brains. A neurosurgeon at the University of California, San Francisco, Dr. Starr was treating people with Parkinson’s disease, which slowly destroys essential bits of brain tissue, robbing people of control of their bodies. At first, drugs had given his patients some relief, but now they needed more help. After the surgery, Dr. Starr closed up his patients’ skulls and switched on the electrodes, releasing a steady buzz of electric pulses in their brains. For many patients, the effect was immediate. “We have people who, when they’re not taking their meds, can be frozen,” said Dr. Starr. “When we turn on the stimulator, they start walking.” First developed in the early 1990s, deep brain stimulation, or D.B.S., was approved by the Food and Drug Administration for treating Parkinson’s disease in 2002. Since its invention, about 100,000 people have received implants. While D.B.S. doesn’t halt Parkinson’s, it can turn back the clock a few years for many patients. Yet despite its clear effectiveness, scientists like Dr. Starr have struggled to understand what D.B.S. actually does to the brain. “We do D.B.S. because it works,” said Dr. Starr, “but we don’t really know how.” In a recent experiment, Dr. Starr and his colleagues believe they found a clue. D.B.S. may counter Parkinson’s disease by liberating the brain from a devastating electrical lock-step. The new research, published on Monday in Nature Neuroscience, may help scientists develop better treatments for Parkinson’s disease. It may also help researchers adapt D.B.S. for treatment of such brain disorders as depression and obsessive compulsive disorder. © 2015 The New York Times Company
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 20817 - Posted: 04.18.2015
Jane Brody The Holy Grail in any progressive disease is to find it early enough to start effective treatment before irreversible damage has occurred. For Parkinson’s disease, which afflicts 1.5 million Americans and growing, a new study has brought this goal a little closer. The study, conducted among more than 54,000 British men and women, identified a slew of symptoms that were more likely to be present in people who years later were diagnosed with Parkinson’s. The findings underscore the prevailing view among neurologists that the damage caused by this disease begins long before classic symptoms like tremors, rigidity and an unsteady gait develop and a definite diagnosis can be made. The study, by Dr. Anette Schrag and fellow neurologists at the University College London, was published in The Lancet in January. As many as five years before a diagnosis of Parkinson’s, those who developed it were more likely to have experienced tremor, balance problems, constipation, low blood pressure, dizziness, erectile and urinary dysfunction, fatigue, depression and anxiety. In addition, Dr. Claire Henchcliffe, director of the Parkinson’s Disease and Movement Disorders Institute at Weill Cornell Medical Center, said that REM sleep behavior disorder, characterized by a tendency to act out one’s dreams while asleep, is one of the strongest prediagnostic symptoms, along with a lost sense of smell and subtle changes in cognition. Dr. Melissa J. Nirenberg, a Parkinson’s disease specialist at New York University Medical Center, said, “Up to 80 percent of people with the sleep disorder get Parkinson’s or a similar neurodegenerative disease.” © 2015 The New York Times Company
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 10: Biological Rhythms and Sleep
Link ID: 20698 - Posted: 03.19.2015
By JON PALFREMAN EUGENE, Ore. — FOUR years ago, I was told I had Parkinson’s disease, a condition that affects about one million Americans. The disease is relentlessly progressive; often starting with a tremor in one limb on one side of the body, it spreads. The patient’s muscles become more rigid, frequently leading to a stooped posture, and movements slow down and get smaller and less fluid. As the disease advances — usually over a number of years — the patient becomes more and more disabled, experiencing symptoms from constipation to sleep disorders to cognitive impairment. Can Parkinson’s be slowed, stopped or even reversed? Can the disease be prevented before it starts, like polio and smallpox? More than at any time in history, success seems possible. Having sequenced the human genome, biomedical researchers have now set their sights on the ultimate frontier — the human brain. The formidable puzzle is to figure out how a three-pound lump of mostly fatty matter enables us to perform a seemingly endless number of tasks, like walking, seeing, hearing, smelling, tasting, touching, thinking, loving, hating, speaking and writing ... and why those awesome abilities break down with neurological disease. Many scientists view Parkinson’s as a so-called pathfinder. If they can figure out what causes Parkinson’s, it may open the door to understanding a host of other neurodegenerative diseases — and to making sense of an organ of incredible complexity. In Parkinson’s, the circuitry in a tiny region of the brain called the basal ganglia becomes dysfunctional. Along with the cerebellum, the basal ganglia normally acts as a kind of adviser that helps people learn adaptive skills by classic conditioning — rewarding good results with dopamine bursts and punishing errors by withholding the chemical. Babies rely on the basal ganglia to learn how to deploy their muscles to reach, grab, babble and crawl, and later to accomplish many complex tasks without thinking. For example, when a tennis player practices a stroke over and over again, the basal ganglia circuitry both rewards and “learns” the correct sequence of activities to produce, say, a good backhand drive automatically. © 2015 The New York Times Company
By Lenny Bernstein Parkinson's Disease patients secretly treated with a placebo instead of their regular medication performed better when told they were receiving a more expensive version of the "drug," researchers reported Wednesday in an unprecedented study that involved real patients. The research shows that the well-documented "placebo effect" -- actual symptom relief brought about by a sham treatment or medication -- can be enhanced by adding information about cost, according to the lead author of the study. It is the first time that concept has been demonstrated using people with a real illness, in this case Parkinson's, a progressive neurological disease that has no cure, according to an expert not involved in the study. "The potentially large benefit of placebo, with or without price manipulations, is waiting to be untapped for patients with [Parkinson's Disease], as well as those with other neurologic and medical diseases," the authors wrote in a study published online Wednesday in the journal Neurology. But deceiving actual patients in a research study raised ethical questions about violating the trust involved in a doctor-patient relationship. Most studies in which researchers conceal their true aims or other information from subjects are conducted with healthy volunteers. This one was subjected to a lengthy review before it was allowed to proceed, and, in an editorial that accompanied the article, two other physicians wrote that "the authors do not mention whether there was any possible effect (reduction) on trust in doctors or on willingness to engage in future clinical research."
Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 5: The Sensorimotor System
Link ID: 20542 - Posted: 02.02.2015
By SAM ROBERTS When he was just 5 years old, Thomas Graboys declared that he intended to become a doctor. As a young physician, he visited a nephew serving in the Peace Corps in Mauritania and remained for two months, treating dozens of patients a day. He skied and played tennis and joined fellow cardiologists as the drummer in a rock band called the Dysrhythmics. In Boston, he was famous as a member of the team that diagnosed the Celtics star Reggie Lewis’s heart defect before he died abruptly on a basketball court. In short, “he was a medical version of one of Tom Wolfe’s masters of the universe,” one reviewer concluded after Dr. Graboys (pronounced GRAY-boys) published his autobiography. But barely 60, after experiencing horrific nightmares, frequently flailing in bed, losing his memory, suffering tremors and finally collapsing on his wedding day, he acknowledged that he was suffering from Parkinson’s disease and the onset of dementia. He informed his patients that he had no choice but to close his practice. “My face is often expressionless, though I still look younger than my 63 years,” he recalled in the autobiography, “Life in the Balance: A Physician’s Memoir of Life, Love, and Loss With Parkinson’s Disease and Dementia,” which was published in 2008. “I am stooped,” he continued. “I shuffle when I walk, and my body trembles. My train of thought regularly runs off the rails. There is no sugarcoating Parkinson’s. There is no silver lining here. There is anger, pain, and frustration at being victimized by a disease that can to some extent be managed but cannot be cured.” After managing for more than a decade, Dr. Graboys died on Jan. 5 at his home in Chestnut Hill, Mass., his daughter, Penelope Graboys Blair, said. The cause was complications of Lewy Body Dementia, which was diagnosed after his Parkinson’s. He was 70. © 2015 The New York Times Company
Stem cells can be used to heal the damage in the brain caused by Parkinson's disease, according to scientists in Sweden. They said their study on rats heralded a "huge breakthrough" towards developing effective treatments. There is no cure for the disease, but medication and brain stimulation can alleviate symptoms. Parkinson's UK said there were many questions still to be answered before human trials could proceed. The disease is caused by the loss of nerve cells in the brain that produce the chemical dopamine ,which helps to control mood and movement. To simulate Parkinson's, Lund University researchers killed dopamine-producing neurons on one side of the rats' brains. They then converted human embryonic stem cells into neurons that produced dopamine. Parkinson's Disease Parkinson's is one of the commonest neurodegenerative diseases These were injected into the rats' brains, and the researchers found evidence that the damage was reversed. There have been no human clinical trials of stem-cell-derived neurons, but the researchers said they could be ready for testing by 2017. Malin Parmar, associate professor of developmental and regenerative neurobiology, said: "It's a huge breakthrough in the field [and] a stepping stone towards clinical trials." A similar method has been tried in a limited number of patients. It involved taking brain tissue from multiple aborted foetuses to heal the brain. Clinical trials were abandoned after mixed results, but about a third of the patients had foetal brain cells that functioned for 25 years. BBC © 2014