Chapter 11. Motor Control and Plasticity

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/ By Venkat Srinivasan It started as a tremor in his left hand and arm. It seemed harmless, but it surprised him. He was a gardener in his 50s and had no history of rheumatism or seizures or any other significant pain. He brushed it off at first, chalking it up to the exhausting daily work. But it wouldn’t go away. Writing and reading became difficult. He could not direct his fork to his mouth, and had to be fed. “It’s like a Russian doll. Within each molecule, there are so many functions.” It was the early 1800s, and a surgeon in London had started to collect notes — not just on the gardener but on a number of patients with similar symptoms. Their hands simply failed “to answer with exactness to the dictates of the will.” The years dragged on; the disease spread to the gardener’s legs, and his trunk started to bow significantly. People couldn’t understand him when he spoke. He passed urine without knowing. The tremors became more and more violent, waking him at night. Nobody understood what he was suffering from. Finally, in 1817, Dr. James Parkinson published an essay on this shaking palsy. He apologized for his speculative approach, writing that “analogy is the substitute for anatomical examination, the only sure foundation for pathological knowledge.” Two centuries later, the disease named for Parkinson is still a puzzle. It is now known that the telltale external symptoms — rigidity, slow movement, a resting tremor — result from a loss of dopamine-rich neurons in a region of the brain called the substantia nigra. But the complete network of steps leading to this cell death is still vague, and the underlying causes remain one of medicine’s great mysteries. Copyright 2018 Undark

Keyword: Parkinsons
Link ID: 24763 - Posted: 03.16.2018

By Frankie Schembri When you go to catch a Frisbee, you don’t need to stare at your hand until it makes contact. You have an intuitive sense of where your arm is—and where it’s going—based on how your muscles and joints feel. This sense of body position, known as kinesthesia, has proved tricky to build into prosthetic arms. Now, researchers have recreated the feeling of kinesthesia in six arm amputees by sending finely tuned vibrations into the skin of their upper arms and shoulders. The approach improved their ability to feel and control their prosthetic arms when performing actions such as gripping and pinching, the team reports today in Science Translational Medicine. The amputees in the study had previously undergone surgery to rewire the nerves in their upper bodies to act as messengers for the specific electric signals associated with arm and hand movement. Three also completed tests where they were asked to close their hand as if gripping a cylinder, while not being able to see their prosthetic arm. When the subjects performed the task again while receiving kinesthesia vibrations simulating the feeling of the motion, they more instinctively moved their prosthetics into the grip and were faster in correcting their mistakes, such as when some of their fingers had not closed into the grip. The subjects also indicated in surveys that they felt greater control over their prosthetic arms when receiving the kinesthesia vibrations. The authors of the study say that more experiments need to be run in order to determine the effectiveness of the vibrations in helping with everyday activities such as picking up objects, and on a test group larger than six people. © 2018 American Association for the Advancement of Science

Keyword: Pain & Touch; Robotics
Link ID: 24751 - Posted: 03.15.2018

NIH-funded researchers at Stanford University used the gene editing tool CRISPR-Cas9 to rapidly identify genes in the human genome that might modify the severity of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) caused by mutations in a gene called C9orf72. The results of the search, published in Nature Genetics, uncovered a new set of genes that may hasten neuron death during the disease. Accounting for nearly 40 percent of inherited cases of ALS and 25 percent of inherited FTD cases, disease-causing mutations in C9orf72 insert extra sequences of DNA, called hexanucleotide repeats, into the gene. These repeats produce potentially toxic RNA and protein molecules that kill neurons resulting in problems with movement and eventually paralysis for ALS patients and language and decision-making problems for FTD patients. Led by Aaron D. Gitler, Ph.D., and Michael C. Bassik, Ph.D., the researchers used CRISPR to disable each gene, one-by-one, in a line of human leukemia cells and then tested whether the cells would survive exposure to toxic proteins derived from the hexanucleotide repeats, called DPRs. Any disabled genes that caused cells to live longer or die faster than normal were considered suspects in DPR toxicity. They confirmed that genes that control the movement of molecules in and out of a cell’s nucleus may be partners. They also identified several new players, including genes that modify chromosomes and that help cells assemble proteins passing through a maze-like structure called the endoplasmic reticulum (ER). A second CRISPR search conducted on mouse brain cells confirmed the initial results. Disabling the top 200 genes identified in the leukemia cells helped neurons survive DPR exposure.

Keyword: ALS-Lou Gehrig's Disease ; Alzheimers
Link ID: 24745 - Posted: 03.13.2018

Researchers say they may have worked out why there is a natural loss of muscle in the legs as people age - and that it is due to a loss of nerves. In tests on 168 men, they found that nerves controlling the legs decreased by around 30% by the age of 75. This made muscles waste away, but in older fitter athletes there was a better chance of them being 'rescued' by nerves re-connecting. The scientists published their research in the Journal of Physiology. As people get older, their leg muscles become smaller and weaker, leading to problems with everyday movements such as walking up stairs or getting out of a chair. It is something that affects everyone eventually, but why it happens is not fully understood. Prof Jamie McPhee, from Manchester Metropolitan University, said young adults usually had 60-70,000 nerves controlling movement in the legs from the lumbar spine. But his research showed this changed significantly in old age. "There was a dramatic loss of nerves controlling the muscles - a 30-60% loss - which means they waste away," he said. "The muscles need to receive a proper signal from the nervous system to tell them to contract, so we can move around." The research team from Manchester Metropolitan University worked with researchers from the University of Waterloo, Ontario, and the University of Manchester. They looked at muscle tissue in detail using magnetic resonance imaging (MRI) and they recorded the electrical activity passing through the muscle to estimate the numbers and the size of surviving nerves. The good news is that healthy muscles have a form of protection: surviving nerves can send out new branches to rescue muscles and stop them wasting away. This is more likely to happen in fit people with large, healthy muscles, Prof McPhee said. © 2018 BBC.

Keyword: Movement Disorders; Development of the Brain
Link ID: 24737 - Posted: 03.12.2018

By Ashley Yeager | Human neural stem cells transplanted into the injured spines of monkeys matured into nerve cells, spurring neuronal connections and giving the animals an improved ability to grasp an orange, researchers report today (February 26) in Nature Medicine. “This type of cellular therapy, though still in its infancy, may eventually be a reasonable approach to treating central nervous system injury and possibly even neurodegenerative disease in humans,” Jonathan Glass, a neurologist at Emory University School of Medicine, tells The Scientist by email. Glass, who was not involved in the study, notes that the differentiation of stem cells over time is “impressive,” as is their ability to make connections in the monkeys’ central nervous systems, but more work needs to be done to show if the cells can grow extremely long axons to connect motor and sensory neurons after spinal injury in humans. Up to this point, most of the work on transplanting neural stem cells had been done in rats. This is the first study to show the treatment can be successfully scaled up to primates. “We definitely have more confidence to do this type of treatment in humans,” study coauthor Mark Tuszynski, a neuroscientist at the University of California, San Diego, School of Medicine, tells The Scientist. In the study, Tuszynski and his colleagues cut into a section of the spinal cord of rhesus monkeys and then two weeks later inserted a graft of human neural progenitor cells into the injury site. In the first four monkeys, the grafts did not stay in position, a finding that forced the researchers to add to the transplants more fibrinogen–thrombin, a protein-enzyme mixture the makes the graft adhere more quickly to site. The team also had to tilt the operating table to drain cerebral spinal fluid, which would wash the graft away. © 1986-2018 The Scientist

Keyword: Regeneration; Stem Cells
Link ID: 24705 - Posted: 02.27.2018

By GRETCHEN REYNOLDS Exercise may help the brain to build durable memories, through good times and bad. Stress and adversity weaken the brain’s ability to learn and retain information, earlier research has found. But according to a remarkable new neurological study in mice, regular exercise can counteract those effects by bolstering communication between brain cells. Memory has long been considered a biological enigma, a medley of mental ephemera that has some basis in material existence. Memories are coded into brain cells in the hippocampus, the brain’s memory center. If our memories were not written into those cells, they would not be available for later, long-term recall, and every brain would be like that of Dory, the memory-challenged fish in “Finding Nemo.” But representations of experience are extremely complex, and aspects of most memories must be spread across multiple brain cells, neuroscientists have determined. These cells must be able to connect with one another, so that the memory, as a whole, stays intact. The connections between neurons, known as synapses, are composed of electrical and chemical signals that move from cell to cell, like notes passed in class. The signals can be relatively weak and sporadic or flow with vigor and frequency. In general, the stronger the messages between neurons, the sturdier and more permanent the memories they hold. Neuroscientists have known for some time that the potency of our synapses depends to some degree on how we live our lives. Lack of sleep, alcohol, diet and other aspects of our lifestyles, especially stress, may dampen the flow of messages between brain cells, while practice fortifies it. Repeat an action and the signals between the cells maintaining the memory of that action can strengthen. That is learning. © 2018 The New York Times Company

Keyword: Learning & Memory
Link ID: 24683 - Posted: 02.21.2018

by Sandra G. Boodman “What are you doing ?” Laura Hsiung’s friends asked as she slowly loped across a Maryland handball court, her ankle off-kilter so that she was walking on the outside of her left foot. Hsiung recalls wondering the same thing. One minute she was walking normally, and then all of a sudden, she wasn’t. “I couldn’t figure it out,” Hsiung said. “I hadn’t rolled my ankle. But my left foot just would not function normally.” For the next two years, Hsiung consulted specialist after specialist — orthopedists, a podiatrist and a neurologist — each of whom was unable to explain what was causing her weird walk. She underwent surgery which didn’t help and felt increasingly desperate about the problem, which did not affect her right foot. “Doctors would literally say, ‘I don’t know what’s wrong with you,’ ” said Hsiung, who lives in Montgomery County. Nor, she said, did most of them seem interested in unearthing a probable cause. After nearly two years of frustration and anxiety, a consultation with a physical therapist ultimately led to a diagnosis, followed by treatment that has helped alleviate Hsiung’s unusual disorder. Although they met only twice, the impact of her encounters with that physical therapist had a galvanizing effect on another aspect of Hsiung’s life, pushing her to make a midlife career change she had been contemplating. © 1996-2018 The Washington Post

Keyword: Movement Disorders
Link ID: 24677 - Posted: 02.19.2018

Dan Garisto If you’ve ever felt the urge to tap along to music, this research may strike a chord. Recognizing rhythms doesn’t involve just parts of the brain that process sound — it also relies on a brain region involved with movement, researchers report online January 18 in the Journal of Cognitive Neuroscience. When an area of the brain that plans movement was disabled temporarily, people struggled to detect changes in rhythms. The study is the first to connect humans’ ability to detect rhythms to the posterior parietal cortex, a brain region associated with planning body movements as well as higher-level functions such as paying attention and perceiving three dimensions. “When you’re listening to a rhythm, you’re making predictions about how long the time interval is between the beats and where those sounds will fall,” says coauthor Jessica Ross, a neuroscience graduate student at the University of California, Merced. These predictions are part of a system scientists call relative timing, which helps the brain process repetitive sounds, like a musical rhythm. “Music is basically sounds that have a structure in time,” says Sundeep Teki, a neuroscientist at the University of Oxford who was not involved with the study. Studies like this, which investigate where relative timing takes place in the brain, could be crucial to understanding how the brain deciphers music, he says. |© Society for Science & the Public 2000 - 2018.

Keyword: Hearing
Link ID: 24675 - Posted: 02.17.2018

By Andy Coghlan Surgical instruments may need to be cleaned more thoroughly after brain operations, following the news that they might be spreading proteins linked to Alzheimer’s disease. There’s no evidence yet that spreading these proteins from one person to another can cause Alzheimer’s disease itself. But a study of eight people suggests that unclean instruments may sometimes lead to a rare and potentially fatal kind of brain bleeding disorder. People who have Alzheimer’s disease typically have plaques of sticky amyloid proteins in their brains, although it remains unclear whether these are a cause or a consequence of the condition. But when amyloid builds up in blood vessels in the brain, it can sometimes make them so brittle that they leak or burst. This condition, called cerebral amyloid angiopathy (CAA), usually doesn’t develop until people reach their sixties or older. But Sebastian Brandner, at University College London, and his team have been investigating the cases of eight people who developed CAA under the age of 60. Scouring their medical records, the team found that all eight of these people had undergone brain surgery during childhood or their teenage years for a variety of reasons. Of the eight people, at least three have already died from strokes, which can be caused by CAA. They died between the ages of 37 and 57. © Copyright New Scientist Ltd.

Keyword: Alzheimers; Prions
Link ID: 24665 - Posted: 02.15.2018

National Institutes of Health scientists developing a rapid, practical test for the early diagnosis of prion diseases have modified the assay to offer the possibility of improving early diagnosis of Parkinson’s disease and dementia with Lewy bodies. The group, led by NIH’s National Institute of Allergy and Infectious Diseases (NIAID), tested 60 cerebral spinal fluid samples, including 12 from people with Parkinson’s disease, 17 from people with dementia with Lewy bodies, and 31 controls, including 16 of whom had Alzheimer’s disease. The test correctly excluded all the 31 controls and diagnosed both Parkinson’s disease and dementia with Lewy bodies with 93 percent accuracy. Importantly, test results were available within two days, compared to related assays that require up to 13 days. The group conducted the tests using Real-Time Quaking-Induced Conversion (RT-QuIC), an assay developed and refined over the past decade at NIAID’s Rocky Mountain Laboratories. Scientists from the University of California San Diego, University of Verona in Italy, Indiana University School of Medicine, Indianapolis, and the Case Western Reserve University School of Medicine, Cleveland, collaborated on the project. The research findings were published in Acta Neuropathologica Communications. Multiple neurological disorders, including Parkinson’s disease and dementia with Lewy bodies, involve the abnormal clumping of a protein called alpha-synuclein into brain deposits called Lewy bodies. The pathological processes in these diseases resembles prion diseases in mammal brains. Like prion diseases, Parkinson’s disease and dementia with Lewy bodies result in progressive deterioration of brain functions and, ultimately, death. Parkinson’s disease is about 1,000 times more common than prion diseases, affecting up to 1 million people in the United States, with 60,000 new cases diagnosed each year. Lewy body dementia affects an estimated 1.4 million people in the United States, according to the Lewy Body Dementia Association.

Keyword: Movement Disorders; Parkinsons
Link ID: 24641 - Posted: 02.10.2018

By Kimberly Hickok Your webcam may know your face, but your keyboard knows your gender. Computer models can predict with 95.6% accuracy whether a man or woman is typing, according to a new study. To conduct the research, computer engineers installed keystroke-logging software onto the personal computers of 75 volunteers—36 men, 39 women—which monitored their daily computer use for 10 months. The researchers then used a program they created, called “ISqueezeU” to calculate the relative helpfulness of different typing features for determining gender—things like the time between two specific keystrokes, or the amount of time a key is pressed down during a single keystroke. A few features stood out as being more useful than others. For example, the average time between pressing the “N” key to pressing the “O” key was the most helpful, followed by the average time between pressing the “M” and “O” keys. The program isn’t capable of specifying whether a man or woman types those keys faster or more often—only that there is a difference. The researchers then tested the program’s findings using five machine learning models, which are computer programs that build models based on what they “learn” from existing data. All five models were able to predict gender accurately more than 78% of the time, with the most successful model being more than 95% accurate, the engineers report this week in Digital Investigation. The team proposes the use of keystroke dynamics as a cost-efficient and nonintrusive way to identify the gender of unknown computer users in criminal investigations, such as in cases of cyberstalking or identity theft. The researchers plan to expand their data collection with more volunteers, and see whether incorporating other variables such as handedness or education level can increase accuracy. © 2018 American Association for the Advancement of Science

Keyword: Sexual Behavior
Link ID: 24639 - Posted: 02.10.2018

By LISA SANDERS, M.D. “Something’s wrong,” the woman told the young doctor, her face lined with worry. “This is not my husband.” The 68-year-old man lay unmoving in the hospital bed, his eyes dull, his face expressionless. His wife stood by him, as she had for nearly four decades of marriage. You don’t know him, she said, but if you did, you’d know that something is not right. George Goshua, a doctor in his first year of residency, looked at the distressed woman and then back at the man in the bed. He had spent nearly an hour reviewing the man’s hospital chart before coming to see him, and he knew the patient had been dangerously ill in the intensive-care unit for the last week. It all began about two weeks before, the wife explained. They were preparing for their son’s wedding, and her husband, normally a workhorse, was not feeling well. He was a tough guy — he worked as an estimator for a local builder and constructed his own house pretty much single-handedly. But now he said he was exhausted. At one point, just two days before the wedding, he said, “I think I might die.” At the time, she was irritated, because she thought he was just trying to get out of the work. Now she knew otherwise. They made it through the wedding, but the next day he was a wreck. His neck was stiff, as if there were a crick on both sides. He went to the local urgent-care center. They thought it was probably just a sore muscle and gave him something for the pain. The day after that, he had a fever. And the following day he was so weak he couldn’t walk. When his wife realized he was too sick to see his own doctor, she called an ambulance. As she struggled to get him out of his pajamas and into his clothes, he slid off the couch onto the floor. He just lay there, unable to even sit up. She couldn’t lift him. When the E.M.T.s arrived, they loaded him into an ambulance, and she followed them to Yale New Haven Hospital, in New Haven, Conn. © 2018 The New York Times Company

Keyword: Movement Disorders
Link ID: 24621 - Posted: 02.06.2018

By Katarina Zimmer | Cellular senescence, the process by which cells cease to divide in response to stress, may be a double-edged sword. In addition to being an important anti-cancer mechanism, recent studies show it may also contribute to age-related tissue damage and inflammation. A study published in Cell Reports yesterday (January 23) suggests that cellular senescence could be a factor underlying neurodegeneration in sporadic forms of Parkinson’s disease. “I think the proposition that cellular senescence drives neurodegeneration in Parkinson’s disease and other ageing-related neurodegenerative diseases . . . has a great deal of merit,” writes D James Surmeier, a physiologist at Northwestern University, to The Scientist in an email. “To my knowledge, [this study] is the first strong piece of evidence for this model.” Cellular senescence may be the basis by which the herbicide and neurotoxin paraquat, which has been previously linked to Parkinson’s disease, can contribute to the disease, the researchers propose. The vast majority of Parkinson’s disease cases are sporadic, rather than inherited, and caused by a combination of environmental and genetic factors. Julie Andersen, a neuroscientist at the Buck Institute for Research on Aging, says her laboratory decided to focus on paraquat based on epidemiological evidence linking it to the condition in humans and on lab work showing that mice treated with the chemical suffer a loss of dopaminergic neurons in the same region that is affected in humans. It is an acutely toxic chemical—capable of causing death—and was banned in the E.U. in 2007 over safety concerns, but is still used extensively by American farmworkers. © 1986-2018 The Scientist

Keyword: Parkinsons; Glia
Link ID: 24574 - Posted: 01.26.2018

Ian Sample Science editor In work that could open a new front in the war on Parkinson’s disease, and even ageing itself, scientists have shown that they can stave off some of the effects of the neurodegenerative disease by flushing “zombie cells” from the brain. The research in mice raises hopes for a fresh approach to treating the most common forms of Parkinson’s disease, which typically arise through a complex interplay of genetics, lifestyle and potentially toxic substances in the environment. But the approach may have benefits far beyond Parkinson’s, with other neurodegenerative diseases – and the ageing process more broadly – all being linked to the ill effects of these “senescent” cells, which linger in tissues after entering a state of suspended animation in the body. “It’s a completely new way of looking at neurodegenerative disease and finding potential drugs,” said Marco Demaria, a molecular biologist on the team at the University of Groningen in the Netherlands. “For most of these conditions, we don’t have any way to counteract them.” Parkinson’s disease affects about 10 million people worldwide, and usually takes hold when certain types of neurons in the brain become impaired or die off completely. The neurons in question produce a substance called dopamine, which is crucial for enabling the brain to produce smooth and coordinated physical movements. © 2018 Guardian News and Media Limited

Keyword: Parkinsons
Link ID: 24562 - Posted: 01.24.2018

By Esther Landhuis As the sun went down on a recent Friday, the hospital clinic buzzed with activity. “Loads of patients turned up without appointments,” says Sarah Tabrizi, a neurologist at University College London. It wasn’t just the typical post-holiday rush. Many rushed in, Tabrizi suspects, after hearing news last month about a potential new therapy for Huntington’s disease, a brain disorder that cripples the body and blurs speech and thinking, sometimes not too long after a person’s 30th birthday. Like other neurodegenerative disorders such as Lou Gehrig’s, Parkinson’s and Alzheimer’s, Huntington’s has no cure. Over decades biotech companies have poured billions of dollars into developing and testing pharmaceuticals for these devastating conditions, only to unleash storms of disappointment. Yet in December a ray of something approximating hope poked through when a California company released preliminary findings from its small Huntington’s study. Results from this early-stage clinical trial have not yet been published or reported at medical meetings. But some researchers have growing confidence that the drug should work for Huntington’s and perhaps other diseases with clear genetic roots. The initial data showed enough promise to convince Roche to license the drug from California-based Ionis Pharmaceuticals, which sponsored the recent Huntington’s trial. The pharma giant paid Ionis $45 million for the right to conduct further studies and work with regulatory agencies to bring the experimental therapy to market. © 2018 Scientific American

Keyword: Huntingtons
Link ID: 24536 - Posted: 01.17.2018

Just 10 minutes of aerobic exercise can improve executive function by priming parts of the brain used to laser focus on the task at hand, according to a new study. This paper, “Executive-Related Oculomotor Control Is Improved Following a 10-minute Single-Bout of Aerobic Exercise: Evidence from the Antisaccade Task,” was published in the January 2018 issue of Neuropsychologia. This research was conducted by Matthew Heath, who is a kinesiology professor and supervisor in the Graduate Program in Neuroscience at the University of Western Ontario, along with UWO master’s student Ashna Samani. For this study, Samani and Heath asked a cohort of healthy young adults to either sit quietly and read magazines or perform 10 minutes of moderate-to-vigorous physical activity (MVPA) on a stationary bicycle. (MVPA aerobic intensity is hard enough that you might break a sweat but easy enough that you can carry on a conversation.) Immediately after the 10-minute reading task or time spent doing aerobic exercise, the researchers used eye-tracking equipment to gauge antisaccades, which is a way to measure varying degrees of executive control. As the authors explain in the study abstract, “Antisaccades are an executive task requiring a goal-directed eye movement (i.e., a saccade) mirror-symmetrical to a visual stimulus. The hands- and language-free nature of antisaccades coupled with the temporal precision of eye-tracking technology make it an ideal tool for identifying executive performance changes.” © 1991-2018 Sussex Publishers, LLC

Keyword: Attention
Link ID: 24476 - Posted: 01.02.2018

By Keith Doucette, In what her mother calls a "Christmas miracle," a Nova Scotia woman who suffered a catastrophic brain injury in a 1996 car accident communicated one-on-one with her mother for the first time in 21 years. Louise Misner said her 37-year-old daughter Joellan Huntley used eye-motion cameras and software on an iPad to respond to a comment from Misner about her clothes. Huntley has been severely disabled since she was 15, unable to walk or talk and is fed through a tube. She has always responded to family members' presence by making sounds, but was unable to communicate any thoughts. The breakthrough occurred during a Christmas Day visit at the Kings Regional Rehabilitation Centre in Waterville, N.S. "I said, 'Joellan, I like your new Christmas outfit you got on,"' Misner said in a telephone interview on Friday. Misner said her daughter then used the technology to find an icon for a short-sleeved shirt. "And then she said no, and went to a long-sleeve shirt because she was trying to tell me what she had on." Misner said her reaction to the long-hoped-for communication was immediate. "Christmas miracle," she said. "It was God's way of telling me that she's finally achieved what she needed to since the accident." Settlement helped buy technology Huntley was thrown from a car that had swerved to avoid a dog running loose along a road in Centreville, N.S., on April 18, 1996. The accident claimed the life of her boyfriend and a young girl who was the sister of the driver. ©2017 CBC/Radio-Canada.

Keyword: Movement Disorders; Robotics
Link ID: 24469 - Posted: 12.30.2017

By Sharon Begley Technologies to detect brain activity — fine, we’ll come right out and call it mind reading — as well as to change it are moving along so quickly that “a bit of a gold rush is happening, both on the academic side and the corporate side,” Michel Maharbiz of the University of California, Berkeley, told a recent conference at the Massachusetts Institute of Technology. Here are three fast-moving areas of neuroscience we’ll be watching in 2018: Neural dust/neurograins Whatever you call these electronics, they’re really, really tiny. We’re eagerly awaiting results from DARPA’s $65 million neural engineering program, which aims to develop a brain implant that can communicate digitally with the outside world. The first step is detecting neurons’ electrochemical signaling (DARPA, the Pentagon’s Defense Advanced Research Projects Agency, says 1 million neurons at a time would be nice). To do that, scientists at Brown University are developing salt-grain-sized “neurograins” containing an electrode to detect neural firing as well as to zap neurons to fire, all via a radio frequency antenna. Advertisement Maharbiz’s “neural dust” is already able to do the first part. The tiny wireless devices can detect what neurons are doing, he and his colleagues reported in a 2016 rat study. (The study’s lead scientist recently moved to Elon Musk’s startup Neuralink, one of a growing number of brain-tech companies.) Now Maharbiz and team are also working on making neural dust receive outside signals and cause neurons to fire in certain ways. Such “stimdust” would be “the smallest [nerve] stimulator ever built,” Maharbiz said. Eventually, scientists hope, they’ll know the neural code for, say, walking, letting them transmit the precise code needed to let a paralyzed patient walk. They’re also deciphering the neural code for understanding spoken language, which raises the specter of outside signals making people hear voices — raising ethical issues that, experts said, neurotech will generate in abundance. © 2017 Scientific American

Keyword: Brain imaging; Robotics
Link ID: 24468 - Posted: 12.29.2017

By Helen Shen Brain-controlled prosthetic devices have the potential to dramatically improve the lives of people with limited mobility resulting from injury or disease. To drive such brain-computer interfaces, neuroscientists have developed a variety of algorithms to decode movement-related thoughts with increasing accuracy and precision. Now researchers are expanding their tool chest by borrowing from the world of cryptography to decode neural signals into movements. During World War II, codebreakers cracked the German Enigma cipher by exploiting known language patterns in the encrypted messages. These included the typical frequencies and distributions of certain letters and words. Knowing something about what they expected to read helped British computer scientist Alan Turing and his colleagues find the key to translate gibberish into plain language. Many human movements, such as walking or reaching, follow predictable patterns, too. Limb position, speed and several other movement features tend to play out in an orderly way. With this regularity in mind, Eva Dyer, a neuroscientist at the Georgia Institute of Technology, decided to try a cryptography-inspired strategy for neural decoding. She and her colleagues published their results in a recent study in Nature Biomedical Engineering. “I’ve heard of this approach before, but this is one of the first studies that’s come out and been published,” says Nicholas Hatsopoulos, a neuroscientist at the University of Chicago, who was not involved in the work. “It’s pretty novel.” © 2017 Scientific American,

Keyword: Movement Disorders; Robotics
Link ID: 24462 - Posted: 12.28.2017

By Sally Abrahams BBC News For years, Mary Rose struggled to get off to sleep or to stay asleep, because she felt like she was being attacked by insects. "Imagine having a swarm of bees buzzing inside the skin of your legs, biting you," she says, describing the sensation that overwhelmed her. "It's really very, very painful." Now in her 80s, the art historian has a condition called restless legs syndrome (RLS), which tortures her at night. "It makes you want to scratch your legs and get up and walk about - it was just impossible to lie down and sleep because one's legs were twitching in this uncontrollable way," she explained. The symptoms were so severe, she didn't want to go to bed at night. 'No sleep at all' Mary Rose can't remember when the problem began, but the condition went undiagnosed for years. "People would say 'oh you've got cramp; you must take quinine or sleep with corks in your bed'. And I did all these things." Of course, they had no effect. She also tried rubbing ointment into her legs to ease the stinging sensation, but that never lasted long enough to let her sleep through the night. Visits to her GP also failed to bring relief. Eventually, she was referred to the sleep clinic at Guy's and St Thomas's hospitals in London, where she's now being treated by neurologist Dr Guy Leschziner. "Restless legs syndrome is a common neurological disorder that causes an irresistible urge to move, particularly at night, and is often linked with unpleasant sensations in the legs," Dr Leschziner explains. "It affects up to one in 20 adults," he continues, "and can cause severe sleep deprivation." At its worst, Mary Rose was surviving on only a few hours' sleep at night, sometimes even less. "I have had complete nights without any sleep at all," she says. © 2017 BBC

Keyword: Sleep; Movement Disorders
Link ID: 24457 - Posted: 12.26.2017