Chapter 11. Motor Control and Plasticity
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Charles Q. Choi Prions, the infectious agents best known for causing degenerative brain disorders such as ‘mad cow’ disease, may have been spotted in bacteria. A section of a protein in Clostridium botulinum, the microbe that causes botulism, can behave like a prion when it is inserted into yeast and Escherichia coli bacteria, researchers report in the 13 January issue of Science1. Prions are formed by proteins that can fold in a number of structurally distinct ways. A prion version of a protein can perpetuate itself in an infectious manner by converting normal forms of that protein into the prion version. Scientists first discovered prions in the 1980s as the agents behind fatal brain disorders known as transmissible spongiform encephalopathies. Since then, researchers have found the misfolded proteins in mammals, insects, worms, plants and fungi2, and learned that not all prions harm their hosts. But until now, prions were only seen in the cells of eukaryotic organisms, a group that includes animals, plants and fungi. In the latest study, researchers analysed roughly 60,000 bacterial genomes using software trained to recognize prion-forming proteins in yeast. They focused on a section of the bacterial protein Rho. In many bacteria, such as C. botulinum and E. coli, Rho is a global regulator of gene expression, meaning that it can control the activity of many genes. © 2017 Macmillan Publishers Limited,
Link ID: 23104 - Posted: 01.14.2017
Parkinson’s disease, a chronic, progressive movement disorder characterized by tremors and stiffness, is not considered a fatal disease in and of itself, though it may reduce life expectancy by a modest amount. It is often said that people die “with” Parkinson’s rather than “of” the disease. “People who are healthy when diagnosed will generally live about as long as other people in their age cohort,” said James Beck, the vice president for scientific affairs at the Parkinson’s Disease Foundation, which is involved in research, education and advocacy. “It is not a death sentence.” Since Parkinson’s generally affects people later in life — patients are typically given a diagnosis in their 60s — patients often die of unrelated age-related diseases like cancer, heart disease or stroke. But the most common cause of death in those with Parkinson’s is pneumonia, because the disease impairs patients’ ability to swallow, putting them at risk for inhaling or aspirating food or liquids into their lungs, leading to aspiration pneumonia. Since Parkinson’s also impairs mobility and balance, those with the disease are also at high risk for falls and accidents, which can trigger a cascade of medical problems, including being bedridden and developing pneumonia, Dr. Beck said. In its advanced stages, the disease can make walking and talking difficult and cause other problems not related to movement, including cognitive impairment. Patients often cannot care for themselves and need assistance carrying out simple activities of daily living. One long-term study followed a group of 142 Parkinson’s patients after they were given their diagnosis; their mean age at diagnosis was around 70. The researchers found that 23 percent were generally doing well 10 years later, meaning they could maintain their balance and did not have dementia. But over half of the patients in the original group had died, with the most common cause related to Parkinson’s being pneumonia. © 2017 The New York Times Company
Link ID: 23094 - Posted: 01.13.2017
Valerie Piro The alarm goes off at 4:30 a.m. Groggy, I turn on the lamp on my night stand and try to sit up. I put my right hand on the wall next to my bed to steady myself, and push my left into the bed. Right away, my abs and back seize up and my legs spasm and kick out straight, forcing me back down onto the bed. Clearly my body thinks it is too early to get up, but I don’t have time to argue with it. I have to get physical therapy out of the way so I can be on time for my medieval history class. After I sit up, I place my hands under my right knee and clasp them together as I bring my knee up and closer to my chest. I reach out to my right foot and cross its heel over my left thigh so that I can plant my heel on the bed. I hug my right leg against my torso and chest and feel a stretch in my lower back and butt. I repeat this on my other side and then proceed to stretch each ankle. Paralysis requires maintenance. I then hop toward the foot of my bed, where my commode chair sits. I set both feet on the footrests as best I can, grab the armrest on the far side of the chair with my left hand, and, using my right hand to drive down into my bed, lift myself onto the commode wheelchair, and wheel to the bathroom. I emerge at 5:35 a.m. I transfer now into a wheelchair whose dimensions are friendly toward my Functional Electrical Stimulation (F.E.S.) cycle — something like a gym exercise bike, without the seat. I pull some milk out of the mini-fridge and pour it over a bowl of cereal. I eat while checking and answering email. At 6:30 it’s time to start cycling. I put two small rectangular electrodes on my left shin muscles, and then two on my right, connect them to the cycle, then strap in my legs and feet. Then two more electrodes then two more, and so on, until most of my lower body is tapped and wired. After I turn on the tablet that’s attached to the cycle, I choose from one of several preset programs to start my workout. Within a couple of minutes, electrical shocks are pulsing into my legs, causing them to contract into pedaling. Imagine pedaling a bicycle uphill for an hour; this is my workout. © 2017 The New York Times Company
Keyword: Movement Disorders
Link ID: 23081 - Posted: 01.11.2017
By Anna Azvolinsky Hummingbirds are efficient hoverers, suspending their bodies midair using rapid forward and backward strokes. Aside from their unique ability to hover, the tiny avians are also the only known birds that can fly in any direction, including sideways. Hummingbird brains appear to be adapted for this flying ability, researchers have now shown. According to a study published today (January 5) in Current Biology, a highly conserved area of the brain—the lentiformis mesencephali (LM), which receives panoramic visual motion information directly from the retina—processes the movement of objects from all directions. In contrast, the LMs of other bird species and all other four-limbed vertebrates studied to date predominantly sense back-to-front motion. While the authors had predicted the neurons of this hummingbird brain region would be tuned to slow motion, they in fact found the opposite: LM neurons were sensitive to quick visual motion, most likely because hummingbirds must process and respond to their environments quickly to avoid collisions, both during hovering and in other modes of flight. “This ancient part of the brain the authors studied has one job: to detect the motion of the image in front of the eyes,” explained Michael Ibbotson, a neuroscientist at the University of Melbourne who penned an accompanying editorial but was not involved in the research. The results of this study suggest that “hummingbirds evolved this area of the brain to have fine motor control to be able to hover and push in every direction possible,” Ibbotson said. © 1986-2017 The Scientist
Link ID: 23064 - Posted: 01.07.2017
By KATIE THOMAS The Food and Drug Administration has approved the first drug to treat patients with spinal muscular atrophy, a savage disease that, in its most severe form, kills infants before they turn 2. “This is a miracle — seriously,” Dr. Mary K. Schroth, a lung specialist in Madison, Wis., who treats children who have the disease, said of the approval, which was made last week. “This is a life-changing event, and this will change the course of this disease.” Dr. Schroth has previously worked as a paid consultant to Biogen, which is selling the drug. The drug, called Spinraza, will not come cheap — and, by some estimates, will be among the most expensive drugs in the world. Biogen, which is licensing Spinraza from Ionis Pharmaceuticals, said this week that one dose will have a list price of $125,000. That means the drug will cost $625,000 to $750,000 to cover the five or six doses needed in the first year, and about $375,000 annually after that, to cover the necessary three doses a year. Patients will presumably take Spinraza for the rest of their lives. The pricing could put the drug in the cross hairs of lawmakers and other critics of high drug prices, and perhaps discourage insurers from covering it. High drug prices have attracted intense scrutiny in the last year, and President-elect Donald J. Trump has singled them out as an important issue. “We believe the Spinraza pricing decision is likely to invite a storm of criticism, up to and including presidential tweets,” Geoffrey C. Porges, an analyst for Leerink Partners, said in a note to investors on Thursday. Mr. Porges said the price could lead some insurers to balk or to limit the drug to patients who are the most severely affected, such as infants, even though the F.D.A. has approved Spinraza for all patients with the condition. © 2016 The New York Times Company
Ian Sample Science editor The first subtle hints of cognitive decline may reveal themselves in an artist’s brush strokes many years before dementia is diagnosed, researchers believe. The controversial claim is made by psychologists who studied renowned artists, from the founder of French impressionism, Claude Monet, to the abstract expressionist Willem de Kooning. While Monet aged without obvious mental decline, de Kooning was diagnosed with Alzheimer’s disease more than a decade before his death in 1997. Strobe lighting provides a flicker of hope in the fight against Alzheimer’s Alex Forsythe at the University of Liverpool analysed more than 2,000 paintings from seven famous artists and found what she believes are progressive changes in the works of those who went on to develop Alzheimer’s. The changes became noticeable when the artists were in their 40s. Though intriguing, the small number of artists involved in the study means the findings are highly tentative. While Forsythe said the work does not point to an early test for dementia, she hopes it may open up fresh avenues for investigating the disease. The research provoked mixed reactions from other scientists. Richard Taylor, a physicist at the University of Oregon, described the work as a “magnificent demonstration of art and science coming together”. But Kate Brown, a physicist at Hamilton College in New York, was less enthusiastic and dismissed the research as “complete and utter nonsense”. © 2016 Guardian News and Media Limited
Link ID: 23033 - Posted: 12.29.2016
By DANNY HAKIM LONDON — Syngenta, the Swiss pesticide giant, claims on its website that data from an influential 2011 study shows that farmers who use the weed killer paraquat are less likely to develop Parkinson’s disease than the general population. However, Syngenta’s claim is at odds with the actual findings of the study, according to two of its authors. The 2011 study, carried out by the National Institutes of Health and researchers from other institutions around the world, found that people who used paraquat or another pesticide, called rotenone, were roughly two and a half times more likely to develop Parkinson’s. The work is known as the Farming and Movement Evaluation, or FAME, study. It drew on a sweeping United States government project called the Agricultural Heath Study, which tracked more than 80,000 farmers and their spouses, as well as other people who applied pesticides, in Iowa and North Carolina. The FAME researchers identified 115 people from the Agricultural Health Study who developed Parkinson’s, and studied 110 of them who provided information on the pesticides they used. The study was influential even among some people who had been skeptics of a connection between the chemicals and the disease. Gary W. Miller, a professor of environmental health at Emory University, referred to a link between Parkinson’s and paraquat as a “red herring” in a 2007 publication. But while Dr. Miller said in a recent email exchange that he had concerns about some previous research making the connection, “the FAME data are strong and should be considered.” He said the study “appears to show a connection between paraquat exposure and Parkinson’s disease.” Because of the prominence of the FAME study, Syngenta addresses it on one of its websites, paraquat.com. Syngenta claims that the study shows that only 115 people had Parkinson’s out of the more than 80,000 people in the broader Agricultural Health Study. Therefore, “the incidence of Parkinson’s disease” in the study “appears to be lower than in the general U.S. population,” Syngenta says. © 2016 The New York Times Company
By Kelly Servick The “mad cow disease” epidemic that killed more than 200 people in Europe peaked more than a decade ago, but the threat it poses is still real. Eating meat contaminated with bovine spongiform encephalopathy and its hallmark misshapen proteins, called prions, can cause a fatal and untreatable brain disorder, variant Creutzfeldt-Jakob disease (vCJD). Thousands of Europeans are thought to be asymptomatic carriers, and they can spread prions through blood donations. So for years, researchers have sought a test to safeguard blood supplies. This week, two teams bring that goal closer. They describe methods for detecting prions in blood that proved highly accurate in small numbers of samples from infected people and controls. “There is new technology to go forward, and it looks promising,” says Jonathan Wadsworth, a biochemist who studies prion disease at University College London. “These are definitely very welcome papers.” Analyses of discarded appendix and tonsil samples suggest that as many as one in 2000 people in the United Kingdom carries abnormal prions—misfolded variations of a naturally abundant protein, which prompt surrounding healthy proteins to fold and clump abnormally. No one knows how many of these carriers will ever develop vCJD; incubation periods as long as 50 years have been reported. Once symptoms occur—first depression and hallucinations, and eventually dementia and loss of motor control—patients survive about a year. Four people are known to have contracted vCJD through a blood transfusion from an infected donor. © 2016 American Association for the Advancement of Science.
Link ID: 23007 - Posted: 12.22.2016
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