Chapter 11. Motor Control and Plasticity
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Helen Shen Automated assistance may soon be available to neuroscientists tackling the brain’s complex circuitry, according to research presented last week at the Aspen Brain Forum in Colorado. Robots that can find and simultaneously record the activity of dozens of neurons in live animals could help researchers to reveal how connected cells interpret signals from one another and transmit information across brain areas — a task that would be impossible using single-neuron studies. The robots are designed to perform whole-cell patch-clamping, a difficult but powerful method that allows neuroscientists to access neurons' internal electrical workings, says Edward Boyden of the Massachusetts Institute of Technology in Cambridge, who is leading the work. Manually performing the method on live animals requires extensive training to perfect and, as a result, only a handful of neurophysiologists use the technique, says Boyden, who presented at the conference. He is developing the automated tool with Craig Forest at the Georgia Institute of Technology in Atlanta and others. “We think that it helps democratize procedures that require a lot of skill,” he says. In May, the group described how a basic version of the robot can record electrical currents in single neurons in the brains of anaesthetized mice1. The robot finds its target on the basis of characteristic changes in the electrical environment near neurons. Then, the device nicks the cell’s membrane and seals itself around the tiny hole to access the neuron's contents. On 24 August, Boyden presented results showing that a more advanced version of the robot could be used to identify and probe four neurons at once — and he says he wants to push the design further, perhaps to tap as many as 100 neurons at a time. © 2012 Nature Publishing Group
Link ID: 17215 - Posted: 08.29.2012
by Jessica Hamzelou When something goes wrong in your brain, you'd think it would be a good idea to get rid of the problem. Turns out, sometimes it's best to keep hold of it. By preventing faulty proteins from being destroyed, researchers have delayed the symptoms of a degenerative brain disorder. SNAP25 is one of three proteins that together make up a complex called SNARE, which plays a vital role in allowing neurons to communicate with each other. In order to work properly, all the proteins must be folded in a specific way. CSP alpha is one of the key proteins that ensures SNAP25 is correctly folded. Cells have a backup system to deal with any misfolded proteins – they are destroyed by a bell-shaped enzyme called a proteasome, which pulls the proteins inside itself and breaks them down. People with a genetic mutation that affects the CSP alpha protein – and its ability to correctly fold SNAP25 – can develop a rare brain disorder called neuronal ceroid lipofuscinosis (NCL). The disorder causes significant damage to neurons – people affected gradually lose their cognitive abilities and struggle to move normally. To find out what role proteasomes might play in NCL, Manu Sharma and his colleagues at Stanford University in California blocked the enzyme in mice that were bred to lack CSP alpha. "We weren't sure what would happen," says Sharma. Either the misfolded SNAP25 would accumulate and harm the cells, or some of the misfolded proteins may work well enough to retain some of their function. © Copyright Reed Business Information Ltd.
By Kathleen Raven A compound already sitting on the shelves of biomedical laboratories and emergency room supply closets seems to interrupt the formation of neurodegenerative protein clumps found in Huntington’s disease, according to a preliminary animal study published August 7 in the Journal of Neuroscience. This versatile agent, called methylene blue, gets a mention in medical literature as early as 1897 and was used to treat, at one time or another, ailments ranging from malaria to cyanide poisoning. The U.S. Food and Drug Administration has never formally approved it as a therapy for any illnesses. But that fact hasn’t stopped biomedical researchers from tinkering with the agent’s apparent ability to improve cognitive function. And although the new paper out today relies on a Huntington’s disease model in flies and mice, scientists are hopeful. "Because of existing knowledge of methylene blue and the fact that it’s not harmful to humans, I would hope that progress toward clinical trials could go relatively quickly," says Leslie Thompson, a neurobiologist at University of California–Irvine and lead author on the new study. Huntington’s disease occurs when the C-A-G sequence of DNA base pairs repeat too often on the HTT gene, resulting in an abnormally long version of the huntingtin protein, that therefore folds incorrectly and forms clumps in the brain. The illness usually begins to affect people in their 30s and 40s, causing movement problems and early death. No drug is currently available to stop the disease from progressing. © 2012 Scientific American
Link ID: 17168 - Posted: 08.15.2012
By KATIE HAFNER SEATTLE — Dr. Richard Wesley has amyotrophic lateral sclerosis, the incurable disease that lays waste to muscles while leaving the mind intact. He lives with the knowledge that an untimely death is chasing him down, but takes solace in knowing that he can decide exactly when, where and how he will die. Under Washington State’s Death With Dignity Act, his physician has given him a prescription for a lethal dose of barbiturates. He would prefer to die naturally, but if dying becomes protracted and difficult, he plans to take the drugs and die peacefully within minutes. “It’s like the definition of pornography,” Dr. Wesley, 67, said at his home here in Seattle, with Mount Rainier in the distance. “I’ll know it’s time to go when I see it.” Washington followed Oregon in allowing terminally ill patients to get a prescription for drugs that will hasten death. Critics of such laws feared that poor people would be pressured to kill themselves because they or their families could not afford end-of-life care. But the demographics of patients who have gotten the prescriptions are surprisingly different than expected, according to data collected by Oregon and Washington through 2011. Dr. Wesley is emblematic of those who have taken advantage of the law. They are overwhelmingly white, well educated and financially comfortable. And they are making the choice not because they are in pain but because they want to have the same control over their deaths that they have had over their lives. © 2012 The New York Times Company
Keyword: ALS-Lou Gehrig's Disease
Link ID: 17153 - Posted: 08.13.2012
by Anil Ananthaswamy Advocates of free will can rest easy, for now. A 30-year-old classic experiment that is often used to argue against free will might have been misinterpreted. In the early 1980s, Benjamin Libet, a neuroscientist at the University of California in San Francisco, used electroencephalography (EEG) to record the brain activity of volunteers who had been told to make a spontaneous movement. With the help of a precise timer that the volunteers were asked to read at the moment they became aware of the urge to act, Libet found there was a 200 millisecond delay, on average, between this urge and the movement itself. But the EEG recordings also revealed a signal that appeared in the brain even earlier, 550 milliseconds, on average, before the action. Called the readiness potential, this has been interpreted as a blow to free will, as it suggests that the brain prepares to act well before we are conscious of the urge to move. This conclusion assumes that the readiness potential is the signature of the brain planning and preparing to move. "Even people who have been critical of Libet's work, by and large, haven't challenged that assumption," says Aaron Schurger of the National Institute of Health and Medical Research in Saclay, France. One attempt to do so came in 2009. Judy Trevena and Jeff Miller of the University of Otago in Dunedin, New Zealand, asked volunteers to decide, after hearing a tone, whether or not to tap on a keyboard. The readiness potential was present regardless of their decision, suggesting that it did not represent the brain preparing to move. Exactly what it did mean, though, still wasn't clear. © Copyright Reed Business Information Ltd.
COFFEE can give you the shakes, but caffeine seems to have the opposite effect in people with Parkinson's disease, helping to relieve tremors and get them back on the move. In the past, caffeine has been shown to reduce the risk of Parkinson's, but its effects have never been tested in people who already have the disease. Ronald Postuma of McGill University in Montreal, Canada, and colleagues gave 61 people with Parkinson's a 6-week course of pills containing the caffeine equivalent of about three cups of coffee every day, or a placebo. Only people in the caffeine group showed a significant improvement in tests for motor problems, such as the severity of their tremors, and general mobility (Neurology, DOI: 10.1212/WNL.0b013e318263570d). Motor problems associated with Parkinson's are caused by a lack of dopamine in areas of the brain where dopamine-producing cells are destroyed. Adenosine receptors normally inhibit the production of dopamine. Caffeine blocks adenosine receptors and so acts to boost available dopamine. Drugs that target adenosine receptors are already in clinical trials but caffeine could provide a cheaper alternative. © Copyright Reed Business Information Ltd.
Link ID: 17123 - Posted: 08.04.2012
By Sandra Upson All elite athletes train hard, possess great skills and stay mentally sharp during competition. But what separates a gold medalist from an equally dedicated athlete who comes in 10th place? A small structure deep in the brain may give winners an extra edge. Recent studies indicate that the brain's insular cortex may help a sprinter drive his body forward just a little more efficiently than his competitors. This region may prepare a boxer to better fend off a punch his opponent is beginning to throw as well as assist a diver as she calculates her spinning body's position so she hits the water with barely a splash. The insula, as it is commonly called, may help a marksman retain a sharp focus on the bull's-eye as his finger pulls back on the trigger and help a basketball player at the free-throw line block out the distracting screams and arm-waving of fans seated behind the backboard. The insula does all this by anticipating an athlete's future feelings, according to a new theory. Researchers at the OptiBrain Center, a consortium based at the University of California, San Diego, and the Naval Health Research Center, suggest that an athlete possesses a hyper-attuned insula that can generate strikingly accurate predictions of how the body will feel in the next moment. That model of the body's future condition instructs other brain areas to initiate actions that are more tailored to coming demands than those of also-rans and couch potatoes. This heightened awareness could allow Olympians to activate their muscles more resourcefully to swim faster, run farther and leap higher than mere mortals. In experiments published in 2012, brain scans of elite athletes appeared to differ most dramatically from ordinary subjects in the functioning of their insulas. © 2012 Scientific American
Keyword: Brain imaging
Link ID: 17088 - Posted: 07.25.2012
By Janice Lynch Schuster, It was early May, a hot and humid Friday night for the under-11 boys soccer game. My 10-year-old son collapsed on the field, unable to breathe. The coach grabbed another child’s inhaler and administered it to Ian, who, after six puffs (instead of the usual two) was able to catch his breath and stand. I wasn’t at the game, so I heard about the incident from my husband, who is unruffled at even the most dramatic moments. “Oh, yeah,” he said that night as we were headed to bed. “Ian had an asthma attack during the game, but he was fine.” It was only later that I heard the full, scary story from the coach. A few years earlier, on the heels of an upper-respiratory infection, Ian had been given a diagnosis of asthma. For a few months, he occasionally used an inhaler, but then the attacks stopped and we eventually stopped carrying it with us. Now, we were afraid, we were back to the asthma diagnosis. On Saturday morning, we took him to the nurse practitioner at the pediatrician’s office. She diagnosed a sports-induced bronchiospasm and sent Ian on his way with an inhaler (two puffs before every practice and game) along with antihistamines to counter any allergies he might be experiencing. She didn’t think it was anything serious — it seemed like a situation that millions of children and adults live with each day. © 1996-2012 The Washington Post
by Nicola Guttridge Whether a tree branch or a computer mouse is the target, reaching for objects is fundamental primate behaviour. Neurons in the brain prepare for such movements, and this neural activity can now be deciphered, allowing researchers to predict what movements will occur. This discovery could help us develop prosthetic limbs that can be controlled by thought alone. To find out what goes on in the brain when we reach for things, biomedical engineers Daniel Moran and Thomas Pearce at Washington University in St Louis, Missouri, trained two rhesus macaques to participate in a series of exercises. When the monkeys reached for items, electrodes measured the activity of neurons in their dorsal premotor cortex, a region of the brain that is involved in the perception of movement. The monkeys were trained to reach for a virtual object on a screen to receive a reward. In some tasks the monkeys had to reach directly for an object, in others they had to reach around an obstacle to get to the target. Impulsive grab Moran and Pearce managed to identify the neural activity corresponding with several aspects of the planned movement, such as angle of reach, hand position and the final target location. The findings could one day allow the design of prosthetic limbs that can be controlled with thought alone, which is "one of the reasons we did the study", says Moran. © Copyright Reed Business Information Ltd.
Keyword: Movement Disorders
Link ID: 17073 - Posted: 07.21.2012
A simple insole could help people who've survived a stroke to regain their balance. When someone suffers a stroke, one side of the body can be weakened, which raises the possibility of unstable walking and debilitating falls. Physiotherapists try to help patients learn to shift their body weight slightly to the weaker side that's been affected by the stroke to regain their balance, but it doesn't always work well. When the lower extremities and muscles are weakened after a stroke, people often learn how not to use that side of the body, even after they've recovered a bit, said Alexander Aruin, a physical therapy professor at the University of Illinois at Chicago. Aruin, who has a background in engineering, invented an insole that when fitted into a patient's shoe slightly lifts and tilts the body toward the stroke-affected side to restore balance. Physical therapy for stroke aims to help patients learn to shift their body weight slightly to the weaker side.Physical therapy for stroke aims to help patients learn to shift their body weight slightly to the weaker side. (Kim Kyung Hoon/Reuters) The device is used in conjunction with physical therapy to help people learn to bear weight equally through both legs and improve their strength and maintain balance. In a study, Aruin's team gave the insoles to individuals with stroke for six weeks and compared them to a control group who did not receive the insoles but did do physiotherapy. © CBC 2012
Link ID: 17071 - Posted: 07.21.2012
Researchers have linked newly discovered gene mutations to some cases of the progressive fatal neurological disease amyotrophic lateral sclerosis — ALS, also known as Lou Gehrig’s disease. Shedding light on how ALS destroys the cells and leads to paralysis, the researchers found that mutations in this gene affect the structure and growth of nerve cells. ALS attacks motor neurons, the nerve cells responsible for controlling muscles. People with ALS experience such early symptoms as limb weakness or swallowing difficulties. In most people, the disease leads to death three to five years after symptoms develop, usually as a result of respiratory failure. Scientists at the University of Massachusetts Medical School, Worcester, collaborated with international ALS researchers to search for gene mutations in two large families with an inherited form of ALS. The researchers used a technique to decode only the protein-encoding portions of DNA, known as the exome, allowing an efficient yet thorough search of the DNA regions most likely to contain disease-causing mutations. This deep sequencing of the exome led to the identification of several different mutations in the gene for profilin (PFN1) which were present only in the family members that developed ALS. Further investigations of 272 other familial ALS cases across the world showed that profilin mutations were also found in a small subset (about 1 to 2 percent) of the familial ALS cases studied. The protein profilin is a key part of the creation and remodeling of a nerve cell's scaffolding or cytoskeleton. In fly models, disrupting profilin stunts the growth of axons — the long cell projections used to relay signals from one neuron to the next or from motor neurons to muscle cells. After identifying the PFN1 mutations in ALS patients, the researchers demonstrated that these mutations inhibited axon growth in laboratory-grown motor neurons as well. They also found that mutant profilin accumulated in clumps in neural cells, as has been seen for other abnormal proteins associated with ALS, Parkinson's and Alzheimer's.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 17061 - Posted: 07.18.2012
By Scicurious Think about what happens when you walk. Really THINK about it. What does it take to walk? Well, your feet and legs have to move (far more complicated than they look), which means your muscles have to move, which means your nerves have to control your muscles, which means your brain has to send the signals in the first place. All of this is based on further information, knowing where you are in space and where you’re going, how fast you need to get there. And then there’s even more! How do you know where you are? How do you know how fast you’re going? How do you know which direction you’re headed? And behind all of this are thousands and millions of neurons firing, together and separately. And underlying THAT are thousands of biochemical processes which allow the neurons to fire… …now take that walking speed, and make it a run. The sheer number of neurobiological processes and number of things that need to happen to make you walk into your workplace every morning is the kind of thing that makes neuroscientists stop in their tracks with wonder. And today, we’re going to talk about a paper that may have worked out a tiny piece of how the brain might deal with things like increased speed. How does your brain keep up with your feet? By running a little faster. To understand how this works. We need to talk about two major things: place neurons, and oscillatory networks. © 2012 Scientific American
Keyword: Movement Disorders
Link ID: 17059 - Posted: 07.18.2012
By PAM BELLUCK The way people walk appears to speak volumes about the way they think, so much so that changes in an older person’s gait appear to be an early indicator of cognitive impairment, including Alzheimer’s disease. Five studies presented at the Alzheimer’s Association International Conference in Vancouver this month provide striking evidence that when a person’s walk gets slower or becomes more variable or less controlled, his cognitive function is also suffering. Thinking skills like memory, planning activities or processing information decline almost in parallel with the ability to walk fluidly, these studies show. In other words, the more trouble people have walking, the more trouble they have thinking. “Changes in walking may predate actually observable cognitive changes in people who are on their way to developing dementia,” said Molly Wagster, chief of the National Institute on Aging’s behavioral and systems neuroscience branch. Experts said the studies could lead to developing a relatively simple tool that doctors could use to forecast, if not diagnose, possible Alzheimer’s disease. “You can probably just watch them walk down the hall in your office and look for people who are starting to show deterioration in their gait and have no other explanation for it,” said William Thies, the chief medical and scientific officer for the Alzheimer’s Association. “If gait begins to deteriorate, we begin to have a conversation about how is your memory.” © 2012 The New York Times Company
Link ID: 17053 - Posted: 07.17.2012
By KATE YANDELL When Nancy Mulhearn learned she had Parkinson’s disease seven years ago, she kept the diagnosis mostly to herself, hiding it from friends, colleagues — even, at first, her mother, sister and teenage children. After seven months, she decided she had to tell her family, and they settled into an unspoken agreement not to talk about the disease. She also realized her colleagues already suspected the truth: One asked why she had trouble applying her lipstick. She sometimes could not control her shaking hands. Still, it was years before Ms. Mulhearn, now 51, of Bethlehem Township, N.J., felt she could talk freely about her condition. Ms. Mulhearn, a school secretary, regrets having waited so long. “I didn’t want anybody to feel sorry for me,” she said. “To have people look at you and start crying — that’s not what anyone wants.” In that, Ms. Mulhearn is hardly alone. Doctors and researchers say it’s not uncommon for people with Parkinson’s to conceal their diagnoses, often for years. But the secrecy is not just stressful to maintain; experts fear that it also may be slowing down the research needed to find new treatments. Parkinson’s disease progresses over many years as brain cells that produce dopamine, a neurotransmitter, slowly waste away. Without dopamine, nerves have trouble sending messages; muscle movement becomes erratic and difficult to control. Some patients, though not all, experience memory problems, altered speech, cognitive difficulty, insomnia and depression. Copyright 2012 The New York Times Company
Link ID: 17019 - Posted: 07.10.2012
by Liz Else THOUSANDS of people may soon be making a very important three-minute phone call - to a computer. It could tell them whether or not they have Parkinson's disease. Technology has long promised a revolution in "smart medicine", allowing painful pokes and prods to be replaced with faster, more accurate and non-invasive ways of diagnosing a range of diseases. That vision took a big step forward last week, when Max Little of the Massachusetts Institute of Technology's Media Lab appealed for people worldwide to test a voice-based system he helped develop for diagnosing Parkinson's. The software uses a speech-processing algorithm to identify telltale changes in the voice of a person with the disease. Parkinson's affects some 6 million people worldwide. Although surgery and drugs can hold back its progression, there is no cure. Diagnosing it and tracking its course usually relies on an assessment of someone's symptoms using the Unified Parkinson's Disease Rating Scale, which involves tests of motor skills, for example. The process is time-consuming, expensive and requires people to attend a clinic for the tests to be carried out. It is partly because of this that it is thought that around a fifth of cases of Parkinson's are never diagnosed. But the disease often manifests early on in the voice, as it affects the ability to control the vocal cords and soft palate. Common signs include a quaver in the voice, softer speech and breathiness or hoarseness, though they can be subtle at first. This makes Parkinson's a perfect candidate for diagnosis over the phone. © Copyright Reed Business Information Ltd.
Link ID: 17018 - Posted: 07.10.2012
By Jane Wakefield Technology reporter, Parkinson's is a devastating disease for those living with the condition and currently there is no cure. Diagnosis can also be slow as there are no blood tests to detect it. But now mathematician Max Little has come up with a non-invasive, cheap test which he hopes will offer a quick new way to identify the disease. He will be kicking off the TEDGlobal conference in Edinburgh calling for volunteers to contribute to a huge voice database. Mr Little has discovered that Parkinson's symptoms can be detected by computer algorithms that analyse voice recordings. In a blind test of voices, the system was able to spot those with Parkinson's with an accuracy of 86%. Mr Little was recently made a TED Fellow. The non-profit organisation behind the TED (Technology, Entertainment and Design) conference creates 40 such fellowships each year. The programme aims to target innovators under the age of 40 and offers them free entry to conferences and other events. Mr Little became interested in understanding voice from a mathematical perspective while he was studying for a PhD at Oxford University in 2003. BBC © 2012
Link ID: 16976 - Posted: 06.27.2012
By Scicurious A colleague handed me this paper, not just as an interesting aspect of Parkinson’s, but as somewhat supportive paper for the role of serotonin in depression. I have said before that I think the serotonin theory of depression (as depicted in Zoloft commercials) is probably wrong, but my views are actually a bit more nuanced than that. The serotonin theory is probably wrong, but not because it is wrong, rather, it is oversimplified. I think that low serotonin levels on their own probably don’t cause depression, but it looks like there may still be a role for serotonin in depressive symptoms, and this paper seems to agree. Science, it’s always more complicated than you think at first. Parkinson’s is something that no one wants to get. It’s a degenerative disorder of the nervous system, which results in a wide variety of symptoms. Most people think of Parkinson’s and picture a shuffling gait, severe hand tremor, slowness of movement and rigidity. But there are other symptoms as well, include depression, hallucinations, fatigue, sleep disturbances, and cognitive deficits as the disease progresses. And when most people think of potential causes for Parkinson’s, they think of a deficit in dopamine, the neurotransmitter that I usually think of with regard to reward and reinforcement, but which is extremely important in motor systems as well. In Parkinson’s patients, you see a striking loss of dopamine neurons in motor areas like the substantia nigra (it’s easy to see because the melanin in the substantia nigra, which is latin for “black substance” dyes the cells black, and when those cells die, the stubstantia nigra becomes a lot less substantia and nigra). But again, it’s not just dopamine in the substantia nigra, there are other systems involved and differences in signaling that also play a role as the disease progresses. © 2012 Scientific American,
Jeannine Stamatakis, There is no denying the high you feel after a run in the park or a swim at the beach. Exercise not only boosts your physical health--as one can easily see by watching a marathon or a boxing match--but it also improves mental health. According to a recent study, every little bit helps. People who engaged in even a small amount of exercise reported better mental health than others who did none. Another study, from the American College of Sports Medicine, indicated that six weeks of bicycle riding or weight training eased stress and irritability in women who had received an anxiety disorder diagnosis. To see how much exercise is required to relieve stress, researchers at the National Institute of Mental Health observed how prior exercise changed the interactions between aggressive and reserved mice. When placed in the same cage, stronger mice tend to bully the meeker ones. In this study, the small mice that did not have access to running wheels and other exercise equipment before cohabitating with the aggressive mice were extremely stressed and nervous, cowering in dark corners or freezing when placed in an unfamiliar territory. Yet meek rodents that had a chance to exercise before encountering their bullies exhibited resistance to stress. They were submissive while living with the aggressive mice but bounced back when they were alone. The researchers concluded that even a small amount of exercise gave the meeker mice emotional resilience. The scientists looked at the brain cells of these so-called stress-resistant mice and found that the rodents exhibited more activity in their medial prefrontal cortex and their amygdala, both of which are involved in processing emotions. The mice that did not exercise before moving in with the aggressive mice showed less activity in these parts of the brain. © 2012 Scientific American,
By Hilda Bastian What do you believe about the effects of exercise and depression – and why do you believe it? Are you personally unenthusiastic about exercising, or are you closer to religious fervor about it? These are critical questions. Because it doesn’t matter how much you believe in the importance of science. If you have a very strong prior existing belief, chances are it’s going to exert a strong bias on how you select and react to evidence on the subject. In the ideal rational world with loads of expertise and time on your hands, that wouldn’t matter when you came across research. If you were interested in the issue, you would carefully assess the biases and strengths of new research, with an equally careful assessment of the existing body of research. You wouldn’t make up your mind about the current state of knowledge till after this systematic assessment was done. But that’s not what it’s like, is it? In the real world, what we already believe often determines whether we even read something at all. And if it reinforces our belief – “Ha! See? I knew it! More proof!” – we might whizz off an email or a tweet without more than a brief skim of the abstract (or even less). But if research challenges beliefs we hold dear, we might tear the challenging article to pieces. We tend to look for methodological weaknesses in a way that we don’t do if we agree with conclusions. © 2012 Scientific American
Link ID: 16910 - Posted: 06.14.2012
By Branwen Jeffreys Health correspondent, BBC News Combining exercise with conventional treatments for depression does not improve recovery, research suggests. In the NHS-funded study - published in the British Medical Journal - some patients were given help to boost their activity levels in addition to receiving therapy or anti-depressants. After a year all 361 patients had fewer signs of depression, but there was no difference between the two groups. Current guidelines suggest sufferers do up to three exercise sessions a week. The National Institute for Health and Clinical Excellence (Nice) drew up that advice in 2004. At the time it said that on the basis of the research available, increased physical activity could help those with mild depression. The latest study, carried out by teams from the Universities of Bristol and Exeter, looked at how that might actually work in a real clinical setting. All 361 people taking part were given conventional treatments appropriate to their level of depression. But for eight months some in a randomly allocated group were also given up advice on up to 13 separate occasions on how to increase their level of activity. BBC © 2012
Link ID: 16877 - Posted: 06.06.2012