Chapter 11. Motor Control and Plasticity
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By Meredith Wadman There have been few happy endings when it comes to spinal muscular atrophy (SMA), the most common genetic cause of death in childhood. The disease inexorably destroys the motor neurons of the spinal cord and brainstem that control movement, including swallowing and breathing. In its most severe form, SMA kills those afflicted at about age 2, most commonly by suffocating them. There are no Food and Drug Administration (FDA)–approved drugs for the disease. That is almost certainly about to change. An innovative drug that helps cells bypass the genetic flaw responsible for SMA may be approved as soon as this month, on the heels of strongly positive results from late-stage clinical trials. On 7 November, a trial of the drug, nusinersen, in wheelchair-bound children aged 2 to 12, was stopped on the grounds that it was unethical to deny the drug to children in the control arm, given the positive results in the treated children. In August, a similar trial in infants was stopped for the same reason, allowing the untreated infants in a control arm to begin receiving the drug. And today, a paper appearing in The Lancet provides compelling biological evidence that nusinersen is having its desired effect in the cells of the brain and spinal cord. “These [infant-onset] SMA kids are going to die. And not only are they now not dying, you are essentially on the path to a true cure of a degenerative [neurological] disease, which is unheard of,” says Jeffrey Rothstein, a neurologist at the Johns Hopkins School of Medicine in Baltimore, Maryland, who was not affiliated with the trials of the drug and is not connected with either of the two companies involved in its development: Ionis of Carlsbad, California, and Biogen of Cambridge, Massachusetts. © 2016 American Association for the Advancement of Science
Sometimes the biggest gifts arrive in the most surprising ways. A couple in Singapore, Tianqiao Chen and Chrissy Luo, were watching the news and saw a Caltech scientist help a quadriplegic use his thoughts to control a robotic arm so that — for the first time in more than 10 years — he could sip a drink unaided. Inspired, Chen and Luo flew to Pasadena to meet the scientist, Richard Andersen, in person. Now they’ve given Caltech $115 million to shake up the way scientists study the brain in a new research complex. Construction of the Tianqiao and Chrissy Chen Institute for Neuroscience at Caltech will begin as early as 2018 and bring together biology, engineering, chemistry, physics, computer science and the social sciences to tackle brain function in an integrated, comprehensive way, university officials announced Tuesday. The goal of connecting these traditionally separate departments is to make “transformational advances” that will lead to new scientific tools and medical treatments, the university said. Research in shared labs will include looking more deeply into fundamentals of the brain and exploring the complexities of sensation, perception, cognition and human behavior. Neuroscience research has advanced greatly in recent years, Caltech President Thomas Rosenbaum said. The field now has the tools to look at individual neurons, for example, as well as the computer power to analyze massive data sets and an entire system of neurons. Collaborating across traditional academic boundaries takes it to the next level, he said. “The tools are at a time and place where we think that the field is ready for that sort of combination.”
Link ID: 22960 - Posted: 12.07.2016
Scientists have developed a mind-controlled robotic hand that allows people with certain types of spinal injuries to perform everyday tasks such as using a fork or drinking from a cup. The low-cost device was tested in Spain on six people with quadriplegia affecting their ability to grasp or manipulate objects. By wearing a cap that measures electric brain activity and eye movement the users were able to send signals to a tablet computer that controlled the glove-like device attached to their hand. Participants in the small-scale study were able to perform daily activities better with the robotic hand than without, according to results published Tuesday in the journal Science Robotics. The principle of using brain-controlled robotic aids to assist people with quadriplegia isn't new. But many existing systems require implants, which can cause health problems, or use wet gel to transmit signals from the scalp to the electrodes. The gel needs to be washed out of the user's hair afterward, making it impractical in daily life. "The participants, who had previously expressed difficulty in performing everyday tasks without assistance, rated the system as reliable and practical, and did not indicate any discomfort during or after use," the researchers said. It took participants just 10 minutes to learn how to use the system before they were able to carry out tasks such as picking up potato chips or signing a document. ©2016 CBC/Radio-Canada.
Link ID: 22959 - Posted: 12.07.2016
Emily Conover A bird in laser goggles has helped scientists discover a new phenomenon in the physics of flight. Swirling vortices appear in the flow of air that follows a bird’s wingbeat. But for slowly flying birds, these vortices were unexpectedly short-lived, researchers from Stanford University report December 6 in Bioinspiration and Biomimetics. The results could help scientists better understand how animals fly, and could be important for designing flying robots (SN: 2/7/15, p. 18). To study the complex air currents produced by birds’ flapping wings, the researchers trained a Pacific parrotlet, a small species of parrot, to fly through laser light — with the appropriate eye protection, of course. Study coauthor Eric Gutierrez, who recently graduated from Stanford, built tiny, 3-D‒printed laser goggles for the bird, named Obi. Gutierrez and colleagues tracked the air currents left in Obi’s wake by spraying a fine liquid mist in the air, and illuminating it with a laser spread out into a two-dimensional sheet. High-speed cameras recorded the action at 1,000 frames per second. The vortex produced by the bird “explosively breaks up,” says mechanical engineer David Lentink, a coauthor of the study. “The flow becomes very complex, much more turbulent.” Comparing three standard methods for calculating the lift produced by flapping wings showed that predictions didn’t match reality, thanks to the unexpected vortex breakup. |© Society for Science & the Public 2000 - 20
Link ID: 22952 - Posted: 12.06.2016
By Israel Robledo As has often been said, with great power comes great responsibility. As we saw in the recent election, social media is a great example of a powerful medium that can change minds and change lives but can also give credibility to false or misguiding information. As someone diagnosed with Parkinson’s disease (PD) nine years ago, I’ve thrilled at seeing social media’s growing power as an agent for good. As our advocacy community has grown, social media has allowed for more information to be circulated in the PD community than ever before, and has become a vital link through which we share experiences, raise awareness about quality of life issues, point people to clinical trials, spread knowledge about cutting-edge research—and importantly, raise critical dollars to fund it. Connecting our community more tightly together has underscored the important role each of us can play in finding an eventual cure. A downside to the awesome power of this platform comes from not knowing or perhaps not caring about the source of information shared on social media. Just as “fake news” has flourished in an environment where speed, rather than accuracy, is what counts, patients—who are understandably vulnerable to hopeful reports about their disease—must recognize that not everything they read is equally credible. In my years of advocating for PD-related causes, hundreds of so-called “miracles” have been announced, all of which have proven to have disappointing results. © 2016 Scientific American
Link ID: 22950 - Posted: 12.05.2016
By Clare Wilson WE HAVE been thinking about Parkinson’s disease all wrong. The condition may arise from damage to the gut, not the brain. If the idea is correct, it opens the door to new ways of treating the disease before symptoms occur. “That would be game-changing,” says David Burn at Newcastle University, UK. “There are lots of different mechanisms that could potentially stop the spread.” Parkinson’s disease involves the death of neurons deep within the brain, causing tremors, stiffness and difficulty moving. While there are drugs that ease these symptoms, they become less effective as the disease progresses. One of the hallmarks of the condition is deposits of insoluble fibres of a substance called synuclein. Normally found as small soluble molecules in healthy nerve cells, in people with Parkinson’s, something causes the synuclein molecules to warp into a different shape, making them clump together as fibres. The first clue that this transition may start outside the brain came about a decade ago, when pathologists reported seeing the distinctive synuclein fibres in nerves of the gut during autopsies – both in people with Parkinson’s and in those without symptoms but who had the fibres in their brain. They suggested the trigger was some unknown microbe or toxin. © Copyright Reed Business Information Ltd.
Link ID: 22938 - Posted: 12.01.2016
Sara Reardon A new technique might allow researchers and clinicians to stimulate deep regions of the brain, such as those involved in memory and emotion, without opening up a patient’s skull. Brain-stimulation techniques that apply electrodes to a person’s scalp seem to be safe, and proponents say that the method can improve some brain functions, including enhancing intelligence and relieving depression. Some of these claims are much better supported by research than others. But such techniques are limited because they cannot reach deep regions of the brain. By contrast, implants used in deep brain stimulation (DBS) are much more successful at altering the inner brain. The devices can be risky, however, because they involve surgery, and the implants cannot be repaired easily if they malfunction. At the annual Society for Neuroscience conference, held in San Diego, California, last week, neuroengineer Nir Grossman of the Massachusetts Institute of Technology in Cambridge and his colleagues presented their experimental method that adapts transcranial stimulation (TCS) for the deep brain. Their approach involves sending electrical signals through the brain from electrodes placed on the scalp and manipulating the electrical currents in a way that negates the need for surgery. The team used a stimulation device to apply two electric currents to the mouse's skull behind its ears and tuned them to slightly different high frequencies. They angled these two independent currents so that they intersected with each other at the hippocampus. © 2016 Macmillan Publishers Limited,
By R. Douglas Fields SAN DIEGO—A wireless device that decodes brain waves has enabled a woman paralyzed by locked-in syndrome to communicate from the comfort of her home, researchers announced this week at the annual meeting of the Society for Neuroscience. The 59-year-old patient, who prefers to remain anonymous but goes by the initials HB, is “trapped” inside her own body, with full mental acuity but completely paralyzed by a disease that struck in 2008 and attacked the neurons that make her muscles move. Unable to breathe on her own, a tube in her neck pumps air into her lungs and she requires round-the-clock assistance from caretakers. Thanks to the latest advance in brain–computer interfaces, however, HB has at least regained some ability to communicate. The new wireless device enables her to select letters on a computer screen using her mind alone, spelling out words at a rate of one letter every 56 seconds, to share her thoughts. “This is a significant achievement. Other attempts on such an advanced case have failed,” says neuroscientist Andrew Schwartz of the University of Pittsburgh, who was not involved in the study, published in The New England Journal of Medicine. HB’s mind is intact and the part of her brain that controls her bodily movements operates perfectly, but the signals from her brain no longer reach her muscles because the motor neurons that relay them have been damaged by amyotrophic lateral sclerosis (ALS), says neuroscientist Erick Aarnoutse, who designed the new device and was responsible for the technical aspects of the research. He is part of a team of physicians and scientists led by neuroscientist Nick Ramsey at Utrecht University in the Netherlands. Previously, the only way HB could communicate was via a system that uses an infrared camera to track her eye movements. But the device is awkward to set up and use for someone who cannot move, and it does not function well in many situations, such as in bright sunlight. © 2016 Scientific American,
Laura Sanders SAN DIEGO — Over the course of months, clumps of a protein implicated in Parkinson’s disease can travel from the gut into the brains of mice, scientists have found. The results, reported November 14 at the annual meeting of the Society for Neuroscience, suggest that in some cases, Parkinson’s may get its start in the gut. That’s an intriguing concept, says neuroscientist John Cryan of the University College Cork in Ireland. The new study “shows how important gut health can be for brain health and behavior.” Collin Challis of Caltech and colleagues injected clumps of synthetic alpha-synuclein, a protein known to accumulate in the brains of people with Parkinson’s, into mice’s stomachs and intestines. The researchers then tracked alpha-synuclein with a technique called CLARITY, which makes parts of the mice’s bodies transparent. Seven days after the injections, researchers saw alpha-synuclein clumps in the gut. Levels there peaked 21 days after the injections. These weren’t the same alpha-synuclein aggregates that were injected, though. These were new clumps, formed from naturally occurring alpha-synuclein, that researchers believe were coaxed into forming by the synthetic versions in their midst. Also 21 days after the injections, alpha-synuclein clumps seemed to have spread to a part of the brain stem containing nerve cells that make up the vagus nerve, a neural highway that connects the gut to the brain. Sixty days after the injections, alpha-synuclein had accumulated in the midbrain, a region packed with nerve cells that make the chemical messenger dopamine. These are the nerve cells that die in people with Parkinson’s, a progressive brain disorder that affects movement. © Society for Science & the Public 2000 - 2016
Link ID: 22881 - Posted: 11.17.2016
Amir Kheradmand, When we spin—on an amusement park ride or the dance floor—we often become disoriented, even dizzy. So how do professional athletes, particularly figure skaters who spin at incredible speeds, avoid losing their balance? The short answer is training, but to really grasp why figure skaters can twirl without getting dizzy requires an understanding of the vestibular system, the apparatus in our inner ear that helps to keep us upright. This system contains special sensory nerve cells that can detect the speed and direction at which our head moves. These sensors are tightly coupled with our eye movements and with our perception of our body's position and motion through space. For instance, if we rotate our head to the right while our eyes remain focused on an object straight ahead, our eyes naturally move to the left at the same speed. This involuntary response allows us to stay focused on a stationary object. Spinning is more complicated. When we move our head during a spin, our eyes start to move in the opposite direction but reach their limit before our head completes a full 360-degree turn. So our eyes flick back to a new starting position midspin, and the motion repeats as we rotate. When our head rotation triggers this automatic, repetitive eye movement, called nystagmus, we get dizzy. © 2016 Scientific American
Link ID: 22878 - Posted: 11.17.2016
By Jessica Hamzelou HB, who is paralysed by amyotrophic lateral sclerosis (ALS), has become the first woman to use a brain implant at home and in her daily life. She told New Scientist about her experiences using an eye-tracking device that takes about a minute to spell a word. What is your life like? All muscles are paralysed. I can only move my eyes. Why did you decide to try the implant? I want to contribute to possible improvements for people like me. What was the surgery like? The first surgery was no problem, but the second had a negative impact for my condition. Can you feel the implant at all? No. How easy is it to use? The hardware is easy to use. The software has been improved enormously by the UNP (Utrecht NeuroProsthesis) team. My part isn’t difficult anymore after these improvements. The most difficult part is timing the clicks. How has the implant changed your life? Now I can communicate outdoors when my eye track computer doesn’t work. I’m more confident and independent now outside. What are the best and worst things about it? The best is to go outside and be able to communicate. The worst were the false-positive clicks. But thanks to the UNP team that is fixed. Now that the study has been completed, would you like to keep the implant, or remove it? Of course I keep it. How do you feel about being the first person to have this implant? It’s special to be the first. Thinking ahead to the future, what else would you like to be able to do with the implant? I would like to change the television channel and my dream is to be able to drive my wheelchair. © Copyright Reed Business Information Ltd.
By STEPH YIN Researchers have designed a system that lets a patient with late-stage Lou Gehrig’s disease type words using brain signals alone. The patient, Hanneke De Bruijne, a doctor of internal medicine from the Netherlands, received a diagnosis of amyotrophic lateral sclerosis, also known as A.L.S. or Lou Gehrig’s disease, in 2008. The neurons controlling her voluntary muscles were dying, and eventually she developed a condition called locked-in syndrome. In this state, she is cognitively aware, but nearly all of her voluntary muscles, except for her eyes, are paralyzed, and she has lost the ability to speak. In 2015, a group of researchers offered an option to help her communicate. Their idea was to surgically implant a brain-computer interface, a system that picks up electrical signals in her brain and relays them to software she can use to type out words. “It’s like a remote control in the brain,” said Nick Ramsey, a professor of cognitive neuroscience at the University Medical Center Utrecht in the Netherlands and one of the researchers leading the study. On Saturday, the research team reported in The New England Journal of Medicine that Ms. De Bruijne independently controlled the computer typing program seven months after surgery. Using the system, she is able to spell two or three words a minute. “This is the world’s first totally implanted brain-computer interface system that someone has used in her daily life with some success,” said Dr. Jonathan R. Wolpaw, the director of the National Center for Adaptive Neurotechnologies in Albany. © 2016 The New York Times Company
David Cyranoski For more than a decade, neuroscientist Grégoire Courtine has been flying every few months from his lab at the Swiss Federal Institute of Technology in Lausanne to another lab in Beijing, China, where he conducts research on monkeys with the aim of treating spinal-cord injuries. The commute is exhausting — on occasion he has even flown to Beijing, done experiments, and returned the same night. But it is worth it, says Courtine, because working with monkeys in China is less burdened by regulation than it is in Europe and the United States. And this week, he and his team report1 the results of experiments in Beijing, in which a wireless brain implant — that stimulates electrodes in the leg by recreating signals recorded from the brain — has enabled monkeys with spinal-cord injuries to walk. “They have demonstrated that the animals can regain not only coordinated but also weight-bearing function, which is important for locomotion. This is great work,” says Gaurav Sharma, a neuroscientist who has worked on restoring arm movement in paralysed patients, at the non-profit research organization Battelle Memorial Institute in Columbus, Ohio. The treatment is a potential boon for immobile patients: Courtine has already started a trial in Switzerland, using a pared-down version of the technology in two people with spinal-cord injury. © 2016 Macmillan Publishers Limited
Ian Sample Science editor Partially-paralysed monkeys have learned to walk again with a brain implant that uses wireless signals to bypass broken nerves in the spinal cord and reanimate the useless limbs. The implant is the first to restore walking ability in paralysed primates and raises the prospect of radical new therapies for people with devastating spinal injuries. Scientists hope the technology will help people who have lost the use of their legs, by sending movement signals from their brains to electrodes in the spine that activate the leg muscles. One rhesus macaque that was fitted with the new implant regained the ability to walk only six days after it was partially paralysed in a surgical procedure that severed some of the nerves that controlled its right hind leg. “It was a big surprise for us,” said Grégoire Courtine, a neuroscientist who led the research at the Swiss Federal Institute of Technology. “The gait was not perfect, but it was almost like normal walking. The foot was not dragging and it was fully weight bearing.” A second animal in the study that received more serious damage to the nerves controlling its right hind leg recovered the ability to walk two weeks after having the device fitted, according to a report published in the journal, Nature. Both monkeys regained full mobility in three months. The “brain-spine interface” is the latest breakthrough to come from the rapidly-advancing area of neuroprosthetics. Scientists in the field aim to read intentions in the brain’s activity and use it to control computers, robotic arms and even paralysed limbs. © 2016 Guardian News and Media Limited
By Neuroskeptic A new paper could prompt a rethink of a basic tenet of neuroscience. It is widely believed that the motor cortex, a region of the cerebral cortex, is responsible for producing movements, by sending instructions to other brain regions and ultimately to the spinal cord. But according to neuroscientists Christian Laut Ebbesen and colleagues, the truth may be the opposite: the motor cortex may equally well suppress movements. Ebbesen et al. studied the vibrissa motor cortex (VMC) of the rat, an area which is known to be involved in the movement of the whiskers. First, they determined that neurons within the VMC are more active during periods when the rat’s whiskers are resting: for instance, like this: whiskerThe existence of cells whose firing negatively correlates with movement is interesting, but by itself it doesn’t prove that much. Maybe those cells are just doing something else than controlling movement? However, Ebbesen et al. went on to show that electrical stimulation of the VMC caused whiskers to stop moving, while applying a drug (lidocaine) to suppress VMC activity caused the rat’s whiskers to whisk harder. Ebbesen et al. go on to say that the inhibitory role of VMC may extend to other regions of the rat motor cortex, and to other movements beyond the whiskers: Rats can perform long sequences of skilled, learned motor behaviors after motor cortex ablation, but motor cortex is required for them to learn a task of behavioral inhibition (they must learn to postpone lever presses)35. When swimming, intact rats hold their forelimbs still and swim with only their hindlimbs. After forelimb motor cortex lesions, however, rats swim with their forelimbs also36.
Keyword: Movement Disorders
Link ID: 22837 - Posted: 11.07.2016
Laura Sanders A protein that can switch shapes and accumulate inside brain cells helps fruit flies form and retrieve memories, a new study finds. Such shape-shifting is the hallmark move of prions — proteins that can alternate between two forms and aggregate under certain conditions. In fruit flies’ brain cells, clumps of the prionlike protein called Orb2 stores long-lasting memories, report scientists from the Stowers Institute for Medical Research in Kansas City, Mo. Figuring out how the brain forms and calls up memories may ultimately help scientists devise ways to restore that process in people with diseases such as Alzheimer’s. The new finding, described online November 3 in Current Biology, is “absolutely superb,” says neuroscientist Eric Kandel of Columbia University. “It fills in a lot of missing pieces.” People possess a version of the Orb2 protein called CPEB, a commonality that suggests memory might work in a similar way in people, Kandel says. It’s not yet known whether people rely on the prion to store long-term memories. “We can’t be sure, but it’s very suggestive,” Kandel says. When neuroscientist Kausik Si and colleagues used a genetic trick to inactivate Orb2 protein, male flies were worse at remembering rejection. These lovesick males continued to woo a nonreceptive female long past when they should have learned that courtship was futile. In different tests, these flies also had trouble remembering that a certain odor was tied to food. |© Society for Science & the Public 2000 - 2016. All rights reserved.
By Dan Hurley The Centers for Disease Control and Prevention has confirmed 89 cases of the paralyzing disease in the United States through September. A 6-year-old boy suspected of having AFM died in Seattle on Sunday, the first death believed to be caused by the disease. One of the drugs in development, pocapavir, was used briefly on a few patients during a 2014 outbreak of AFM under a compassionate-use exception that allows extremely sick patients to be given unapproved drugs without the usual kinds of placebo-controlled trials required by the Food and Drug Administration. “There were a couple of kids who got pocapavir in the Colorado outbreaks,” said Benjamin Greenberg, a neurologist who has treated children with AFM at the University of Texas Southwestern in Dallas. “It had relatively weak but measurable impact on viral replication. A larger study would definitely be warranted. We'll take anything we can get.” Although the CDC says no cause has been conclusively linked to AFM, many researchers suspect a family of viruses known as enteroviruses. “I have been studying enteroviruses for 40 years now,” said John Modlin, deputy director of the polio eradication program at the Bill and Melinda Gates Foundation. “If I had a child with acute flaccid myelitis, I would be on the phone in a second to the companies making these drugs.” © 1996-2016 The Washington Post
Keyword: Movement Disorders
Link ID: 22830 - Posted: 11.04.2016
By Helen Thomson IN THE 2009 Bruce Willis movie Surrogates, people live their lives by embodying themselves as robots. They meet people, go to work, even fall in love, all without leaving the comfort of their own home. Now, for the first time, three people with severe spinal injuries have taken the first steps towards that vision by controlling a robot thousands of kilometres away, using thought alone. The idea is that people with spinal injuries will be able to use robot bodies to interact with the world. It is part of the European Union-backed VERE project, which aims to dissolve the boundary between the human body and a surrogate, giving people the illusion that their surrogate is in fact their own body. In 2012, an international team went some way to achieving this by taking fMRI scans of the brains of volunteers while they thought about moving their hands or legs. The scanner measured changes in blood flow to the brain area responsible for such thoughts. An algorithm then passed these on as instructions to a robot. “The feeling of embodying the robot was good, although the sensation varied over time“ The volunteers could see what the robot was looking at via a head-mounted display. When they thought about moving their left or right hand, the robot moved 30 degrees to the left or right. Imagining moving their legs made the robot walk forward. © Copyright Reed Business Information Ltd.
Link ID: 22795 - Posted: 10.27.2016
Richard Harris Researchers have launched an innovative medical experiment that's designed to provide quick answers while meeting the needs of patients, rather than drug companies. Traditional studies can cost hundreds of millions of dollars, and can take many years. But patients with amyotrophic lateral sclerosis, or Lou Gehrig's disease don't have the time to wait. This progressive muscle-wasting disease is usually fatal within a few years. Scientists in an active online patient community identified a potential treatment and have started to gather data from the participants virtually rather than requiring many in-person doctor's visits. How is that possible? In this case, doctors and patients alike got interested in an extraordinary ALS patient whose symptoms actually got better, which rarely occurs. He'd been taking a dietary supplement called lunasin, "and lo and behold six months later, [his] speech [was] back to normal, swallowing back to normal, doesn't use his feeding tube, [and he was] significantly stronger as measured by his therapists," said Richard Bedlack, a neurologist who runs the ALS clinic at Duke University. Of course, it could just be a coincidence that the man who got better happened to be taking these supplements. To find out, Bedlack teamed up to run a study with Paul Wicks, a neuropsychologist and vice president for innovation at a web-based patient organization called PatientsLikeMe. © 2016 npr
Keyword: ALS-Lou Gehrig's Disease
Link ID: 22788 - Posted: 10.26.2016
Ian Sample Science editor Experiments with a fake body part have revealed how the brain becomes confused during a party trick known as the rubber hand illusion. Researchers in Italy performed the trick on a group of volunteers to explore how the mind combines information from the senses to create a feeling of body ownership. Under the illusion, people feel that a rubber hand placed on the table before them is their own, a bizarre but convincing shift in perception that is accompanied by a sense of disowning their real hand. The scientists launched the study after noticing that some stroke patients in their care experienced similar sensations, at times becoming certain that a paralysed limb was not their own, and even claiming ownership over other people’s appendages. “It is a very strong belief,” said Francesca Garbarini at the University of Turin. “We know that the feeling of body ownership can be dramatically altered after brain damage.” For the study, healthy volunteers sat with their forearms resting on a table and their right hand hidden inside a box. A lifelike rubber hand was then placed in front of them and lined up with their right shoulder. A cloth covered the stump of the hand, but the fingers remained visible. To induce the illusion, one of the researchers stroked the middle finger of the participant’s real hand while simultaneously stroking the same finger on the rubber hand. © 2016 Guardian News and Media Limited
Keyword: Pain & Touch
Link ID: 22780 - Posted: 10.24.2016