Chapter 11. Motor Control and Plasticity

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Allison Aubrey The condition strikes young children. It can start with run-of-the-mill virus symptoms, like fever or sniffles. But, then the kids lose control of their limbs, may have trouble swallowing or breathing, or even end up paralyzed. This terrifying experience happened to more than 570 families since 2014, whose children were struck with an illness called acute flaccid myelitis, or AFM. "It was really scary," says Susan Coyne, the mother of a son, Evan Mazanec, who developed AFM back in 2014 when he was 7 years old. "When this first started, no one really knew what it was," she says. It came on quickly, starting with a fever and an ear infection. Coyne says the limb weakness and paralysis began several days later — just as Evan was getting over the fever. He lost control of his arms and legs. "He couldn't move them, he couldn't lift them, he couldn't walk," Coyne says. He spent a year and a half in intensive rehab. He had to learn to walk and move his arms again. "It set him back years," Coyne says. Scientists have struggled to understand what causes this rare childhood disease. Now, one theory is gaining ground. A paper published Monday in the journal Pediatrics finds the condition may be triggered by a virus. The disease follows a pattern: Scientists have documented outbreaks every other year, beginning in 2014, and again in 2016 and 2018. Last year, there were 233 cases in the U.S. It strikes young kids, average age of 6. And, it can lead to long-term paralysis. © 2019 npr

Keyword: Movement Disorders; Development of the Brain
Link ID: 26684 - Posted: 10.09.2019

By Jason Gutierrez MANILA — President Rodrigo Duterte of the Philippines has revealed that he has a neuromuscular disease that has led to a slew of medical problems, including making his eye droop. Mr. Duterte, who was in Russia for a state visit, told the Filipino community there on Saturday night that he has myasthenia gravis, a chronic autoimmune disease that leads to skeletal muscle weakness. He said the disease ran in his family. The revelation came amid continued public speculation about his health. There have been periods when the famously bombastic president has been out of the public eye for days, prompting headlines guessing about his whereabouts, and even rumors of his death. But his communications officers have said that Mr. Duterte, 74, like any other older person, needs his own personal time. The president revealed the ailment after he apparently made a joke about not being able to look straight at a woman with whom he had danced a duet during the event in Moscow. “I have a talent,” Mr. Duterte said, according to official transcripts provided by his office afterward. “When I look at you, my other eye droops. Do you see? The other eye is smaller. It goes where it wants.” He added: “Actually, that’s myasthenia gravis. It’s a nerve malfunction.” Mr. Duterte said his grandfather had also had the disease, adding, “So I believe, really, in genetics.” The disease often affects the muscles that control the eyes, facial expression, speaking and swallowing, according to the Philippine Medical Association. Mr. Duterte came to power in 2016 vowing to rid the country of drug dealers and to wipe out other crimes. Since then, the Philippines’ war on drugs has led to thousands of killings allegedly by the police and vigilantes, which rights groups have denounced as an atrocity. © 2019 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 26676 - Posted: 10.07.2019

By James Gallagher Health and science correspondent A man has been able to move all four of his paralysed limbs with a mind-controlled exoskeleton suit, French researchers report. Thibault, 30, said taking his first steps in the suit felt like being the "first man on the Moon". His movements, particularly walking, are far from perfect and the robo-suit is being used only in the lab. But researchers say the approach could one day improve patients' quality of life. And he can control each of the arms, manoeuvring them in three-dimensional space How easy was it to use? Thibault, who does not want his surname revealed, was an optician before he fell 15m in an incident at a night club four years ago. The injury to his spinal cord left him paralysed and he spent the next two years in hospital. But in 2017, he took part in the exoskeleton trial with Clinatec and the University of Grenoble. Initially he practised using the brain implants to control a virtual character, or avatar, in a computer game, then he moved on to walking in the suit. "It was like [being the] first man on the Moon. I didn't walk for two years. I forgot what it is to stand, I forgot I was taller than a lot of people in the room," he said. It took a lot longer to learn how to control the arms. © 2019 BBC.

Keyword: Robotics
Link ID: 26670 - Posted: 10.04.2019

Ashley Yeager During her time as a postdoc at the University of Basel in Switzerland, Sarah Shahmoradian decided to study the abnormal aggregates of protein that develop inside nerve cells and contribute to Parkinson’s disease. The protein clumps develop over time in the brains of Parkinson’s patients, leading some scientists to think they wreak havoc on nerve cells, causing severe damage and hastening their death. A fresh look at the clumps, called Lewy bodies, with cutting-edge microscopy tools could reveal insights that might lead to new treatments for Parkinson’s, Shahmoradian recalls thinking. “The original goal was to really find out what the building blocks of Lewy bodies are, what they are made of, and what they actually look like.” The clumps were first identified in the early 1900s, appearing as abnormal material in nerve cells viewed under a microscope. Additional studies using antibodies that bound to various proteins revealed that the clumps contained a protein called α-synuclein, and after more work probing Lewy bodies, scientists developed a rough sketch of their structure—essentially, a dense mass surrounded by a halo of twisted filaments of α-synuclein. It’s these filaments, known as fibrils, that Shahmoradian and her colleagues were most interested to analyze in postmortem human brains. Fibrils had been repeatedly produced in cultured cells and in animal models, but no one had ever gotten a clear view of them in human brain tissue. “We were originally looking for fibrils,” Shahmoradian says, “but unexpectedly, we found an abundance of . . . mitochondria, other organelles, and lipid membranes [in the Lewy bodies].” The researchers also found evidence of lysosomes, organelles that facilitate cellular waste removal. They did see α-synuclein in the Lewy bodies, as well, but the cores of the structures weren’t composed of twisted and tangled fibrils as researchers had thought. Instead, the protein was intermingled with other cellular material. © 1986–2019 The Scientist

Keyword: Parkinsons
Link ID: 26669 - Posted: 10.03.2019

By Gretchen Reynolds Physically fit young adults have healthier white matter in their brains and better thinking skills than young people who are out of shape, according to a large-scale new study of the links between aerobic fitness and brain health. The findings suggest that even when people are youthful and presumably at the peak of their mental prowess, fitness — or the lack of it — may influence how well their brains and minds work. We already have plenty of tantalizing evidence that aerobic fitness can beneficently shape our brains and cognition. In animal experiments, mice and rats that run on wheels or treadmills produce far more new neurons in their brains than sedentary animals and perform better on tests of rodent intelligence and memory. Similarly, studies involving people show strong relationships between being physically active or fit and having greater brain volume and stronger thinking abilities than people with low fitness or who rarely exercise. But most of these past studies focused on middle-aged or older adults, whose brains often are starting to sputter and contract with age. For them, fitness and exercise are believed to help slow any decline, keeping brain tissue and function relatively youthful. Much less has been known about whether fitness likewise might be related to the structure and function of healthy, younger people’s brains. So, for the new study, which was published last month in Scientific Reports, scientists at the University of Münster in Germany decided to look inside the skulls of a large group of young adults. They began by turning to a hefty trove of data gathered as part of the Human Connectome Project, an international collaborative effort that aims to help map much of the human brain and tease out how it works. © 2019 The New York Times Company

Keyword: Development of the Brain
Link ID: 26662 - Posted: 10.02.2019

By Dean McLaughlin BBC News NI A Londonderry man who was diagnosed with Parkinson's at the age of 30 says more young people need to be aware of the disease. Ronan Coyle first noticed the symptoms at 24 but only found out what the problem was six years later. "People think I'm drunk when I walk down the street," he told BBC Radio Foyle. Now 37, Ronan plays golf and squash and likes to swim to take his mind off the disease. A spokesperson for Parkinson's UK said playing sport "helps ease the mind". Parkinson's is thought to be linked to a chemical called dopamine, which is lacking in the brains of people with the condition. There are more than 40 symptoms and these can include vomiting as the body struggles to process food in the gut. Parkinson's can also affect people's mood. Often a person will feel they have got to grips with their condition and then a new symptom will emerge. It was while studying for his Irish history and politics degree that Ronan first noticed the symptoms. "I was writing notes for an essay and I couldn't write properly," he said. "Come exam time, I was under a lot of stress. It got really bad. "Then I noticed my walking was funny. I went to a couple of neurologists and they more or less said you have a tremor and that it was nothing to worry about." When Ronan turned 30 he was referred to a neurologist in Belfast. After a number of scans it was confirmed that he had the disease. © 2019 BBC

Keyword: Parkinsons
Link ID: 26658 - Posted: 10.01.2019

Jon Hamilton Too much physical exertion appears to make the brain tired. That's the conclusion of a study of triathletes published Thursday in the journal Current Biology. Researchers found that after several weeks of overtraining, athletes became more likely to choose immediate gratification over long-term rewards. At the same time, brain scans showed the athletes had decreased activity in an area of the brain involved in decision-making. The finding could explain why some elite athletes see their performance decline when they work out too much — a phenomenon known as overtraining syndrome. The distance runner Alberto Salazar, for example, experienced a mysterious decline after winning the New York Marathon three times and the Boston Marathon once in the early 1980s. Salazar's times fell off even though he was still in his mid-20s and training more than ever. "Probably [it was] something linked to his brain and his cognitive capacities," says Bastien Blain, an author of the study and a postdoctoral fellow at University College London. (Salazar didn't respond to an interview request for this story.) Blain was part of a team that studied 37 male triathletes who volunteered to take part in a special training program. "They were strongly motivated to be part of this program, at least at the beginning," Blain says. Half of the triathletes were instructed to continue their usual workouts. The rest were told to increase their weekly training by 40%. The result was a training program so intense that these athletes began to perform worse on tests of maximal output. After three weeks, all the participants were put in a brain scanner and asked a series of questions designed to reveal whether a person is more inclined to choose immediate gratification or a long-term reward. "For example, we ask, 'Do you prefer $10 now or $60 in six months,' " Blain says. © 2019 npr

Keyword: Attention
Link ID: 26656 - Posted: 09.28.2019

By Laura Sanders Survey any office, and you’ll see pens tapping, heels bouncing and hair being twiddled. But jittery humans aren’t alone. Mice also fidget while they work. What’s more, this seemingly useless motion has a profound and widespread effect on mice’s brain activity, neuroscientist Anne Churchland of Cold Spring Harbor Laboratory in New York and colleagues report September 24 in Nature Neuroscience. Scientists don’t yet know what this brain activity means, but one possibility is that body motion may actually shape thinking. Researchers trained some mice to lick a spout corresponding to an area where a click or a flash of light originated. To start their task, mice grabbed a handle and waited for the signal. As the mice focused on their jobs, researchers used several different methods to eavesdrop on nerve cell behavior in the animals’ brains. All the while, video cameras and a sensor embedded on a platform under the mice picked up every move the rodents made — and there were a lot. Mice wiggled their noses, flicked their whiskers and fiddled their hind paws while concentrating on finding the sound or light, the team found. Those fidgets showed up in nerve cell activity. When a whisker moved, for instance, nerve cells involved in moving and sensing sprang into action. Fidgets predicted a big chunk of neural behavior, mathematical models suggested. Mice’s fidgets even had stronger effects on brain activity than did the task at hand, the researchers report. © Society for Science & the Public 2000–2019

Keyword: Brain imaging
Link ID: 26653 - Posted: 09.28.2019

Patti Neighmond For people who live with chronic pain, getting up, out and moving can seem daunting. Some fear that physical activity will make their pain worse. But in fact, researchers find the opposite is true: The right kind of exercise can help reduce pain. Today, Emma Dehne agrees. Dehne is 44, lives in Chapel Hill, N.C., and works as a business officer in the office of the executive vice chancellor at the University of North Carolina. She says her commitment to exercise is relatively recent. Just a year and a half ago, Dehne pretty much avoided any physical movement she didn't have to make. Just climbing stairs was painful — "sometimes to the point where I would have to hold on to the banister to help myself up," she says, "and I couldn't even extend my leg." At times, it felt as though the ligaments in her knees "were tearing." Dehne was diagnosed around age 40 with osteoarthritis in both knees, a painful swelling and deterioration of the cushioning cartilage in those joints that reduces their range of motion. Luckily for her, she says, she worked at the Thurston Arthritis Research Center at the University of North Carolina. The woman working in the cubicle next to hers ran a program that encouraged people with osteoarthritis to start walking to help reduce their pain. Dehne was skeptical but felt she was just too young to be burdened by this disease; she agreed to give brisk walks a try. In the beginning she felt stiff, tired and out of breath. That changed quickly. © 2019 npr

Keyword: Pain & Touch
Link ID: 26635 - Posted: 09.23.2019

By Michelle Roberts Health editor, BBC News online A drug used to treat enlarged prostates may be a powerful medicine against Parkinson's disease, according to an international team of scientists. Terazosin helps ease benign prostatic hyperplasia (BPH) by relaxing the muscles of the bladder and prostate. But researchers believe it has another beneficial action, on brain cells damaged by Parkinson's. They say the drug might slow Parkinson's progression - something that is not possible currently. Cell death They studied thousands of patients with both BPH and Parkinson's. Their findings, published in the Journal of Clinical Investigation, suggest the alpha-blocker drug protects brain cells from destruction. Parkinson's is a progressive condition affecting the brain, for which there is currently no cure. Existing Parkinson's treatments can help with some of the symptoms but can't slow or reverse the loss of neurons that occurs with the disease. Terazosin may help by activating an enzyme called PGK1 to prevent this brain cell death, the researchers, from the University of Iowa, in the US and the Beijing Institute for Brain Disorders, China, say. When they tested the drug in rodents it appeared to slow or stop the loss of nerve cells. To begin assessing if the drug might have the same effect in people, they searched the medical records of millions of US patients to identify men with BPH and Parkinson's. They studied 2,880 Parkinson's patients taking terazosin or similar drugs that target PGK1 and a comparison group of 15,409 Parkinson's patients taking a different treatment for BPH that had no action on PGK1. Patients on the drugs targeting PGK1 appeared to fare better in terms of Parkinson's disease symptoms and progression, which the researchers say warrants more study in clinical trials, which they plan to begin this year. Lead researcher Dr Michael Welsh says while it is premature to talk about a cure, the findings have the potential to change the lives of people with Parkinson's. © 2019 BBC

Keyword: Parkinsons
Link ID: 26619 - Posted: 09.17.2019

Three years ago, Ady Barkan, a longtime activist and a leader of the Fed Up campaign pushing for policies that would encourage full employment and higher wages, was diagnosed with amyotrophic lateral sclerosis (ALS). The neurodegenerative disease, which paralyzes the body and has an average survival rate of three years, has put Barkan, now 35, in a wheelchair. He can no longer speak on his own. But he remains an organizer for the Center for Popular Democracy, now focusing on health care after co-founding the Be A Hero Project, and in April came to Washington from his home in California to testify for the Democrats’ Medicare-for-all bill. He spoke assisted by a computer. Barkan’s memoir, “Eyes to the Wind,” is being published Tuesday. He was interviewed recently by Lucy Kalanithi, host of a forthcoming podcast about hardship. She is an internist on the faculty at the Stanford University School of Medicine and widow of neurosurgeon Paul Kalanithi, who wrote the memoir “When Breath Becomes Air.” Here is an excerpt from their conversation, edited for clarity and length: LK: You have built this whole career defined around resistance and resisting injustice, and then you suddenly become a person for whom acceptance is this big priority, and the resistance part has to recede. How did you get there? AB: There were, perhaps, two different components to my acceptance. The first was intellectual: acknowledging that the disease is no joke and no bad dream, that it will almost certainly kill me and that the long future we had planned for was not going to happen. That intellectual acceptance happened very quickly. It was informed by my awareness of my tremendous privilege compared to most of the world’s 7 billion people and the others who came before us. Knowing what others have gone through made me feel less disbelieving that this could happen to me. But I think when we talk about acceptance, we mean something deeper, like finding peace in the new reality. © 1996-2019 The Washington Post

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26589 - Posted: 09.09.2019

By Joanna Broder It had been two agonizing years of not knowing what was wrong with their baby who, since birth, had frequent spells of eye flickering, uncontrollable muscle contractions, pain and temporary paralysis. Simon and Nina Frost had spared no expense, taking Annabel to all the best neurologists around the country. Finally a potential diagnosis emerged: alternating hemiplegia of childhood, an ultrarare genetic disorder. The Frosts’ initial excitement at having answers quickly waned, however. They learned that, for many of the 900 or so children in the world affected by AHC, mutations in one of the genes that code for a subunit of the body’s critical sodium potassium pump interferes with the body’s ability to repeatedly fire nerve cells. In addition to Annabel’s other symptoms, difficulty breathing, choking and falling are common. They also learned that there is no effective treatment or cure, that any one of Annabel’s episodes has the potential to lead to permanent brain damage or death, and that it is hard to get information about the disease. Foundations dedicated to AHC informally recommend only four physicians in the United States as knowledgeable enough about the disorder to see patients. Of those who are closest to the Frosts, who live in Northwest D.C., one was too busy to see Annabel. There was a two-month wait to see the other one. The foundations themselves didn’t have many answers to the Frosts’ initial questions about life expectancy or what course Annabel’s disease might take. The Frosts discovered that relatively few scientists and clinicians study AHC, and their focus seemed to be basic research and not developing a therapy. © 1996-2019 The Washington Post

Keyword: Movement Disorders
Link ID: 26565 - Posted: 09.03.2019

Sarah Horn, M.D., and Howard Hurtig, M.D. While people usually regard Parkinson’s disease (PD) as a disorder characterized by abnormalities of the brain’s motorfunctions (movement), such as tremor, stiffness, and difficulties with balance and walking, there is less public awareness that non-motor features, such as cognitive impairment, are equally important. At some point during the long course of this progressive disorder, most patients will be confronted with one or more non-motor symptoms, some of which develop during the premotor or prodromalstage of the illness, when a loss of neurons is accumulating throughout the nervous system before the onset of the classic motor symptoms. Understanding the full range of motor and non-motor features of PD can alert people to recognize the earliest phases of PD and thereby proactively begin a partnership with a health care provider (usually a neurologist) to develop a comprehensive plan of management. In 1817, the British neurologist James Parkinson, in his essay The Shaking Palsy, accurately described through casual observation the same motor signs and symptoms of PD that we see today. He would never learn about the disease’s non-motor abnormalities, nor would he believe that intellect was affected. Much has changed in 200 years, but only in the last two decades has it become clear that non-motor features are an integral to the pathophysiology of PD. Such features have in fact become defining markers of the disease process, particularly during the prodromal stage of the disease. The recognition of PD as a common neurological disorder—caused by a lack of the chemical dopamine in the brain—has been bolstered by its prevalence among celebrities, including Muhammad Ali, Michael J. Fox, Linda Ronstadt, Pope John Paul II, and more recently Jesse Jackson and Alan Alda. The average age at diagnosis is 62.5 years, and an estimated 10 percent of patients are diagnosed at age 50 or younger .

Keyword: Parkinsons
Link ID: 26545 - Posted: 08.27.2019

By Bret Stetka Among the human body’s many maladies, few have stumped medical researchers like those that decimate the brain. After decades of effort, effectively treating—let alone curing—neurodegenerative disorders such as Huntington’s and Alzheimer's disease has been a source of frustration for many, as old theories are questioned and clinical trials fail. Basic scientists have achieved some progress. Over the past few decades, they have made serious headway in identifying single inherited genes responsible for genetic forms of various neurodegenerative diseases such as Alzheimer’s—and also the molecular and neural mechanisms behind nongenetic, or sporadic, forms of brain maladies. Yet translating these findings into working therapies has proved challenging. With genetic engineering technologies, such as CRISPR, that literally rewrite our DNA still a ways away from routine use, a number of clinical researchers have turned to a more immediate genome-based approach to treat disorders of the brain: manipulating RNA to modify levels of proteins associated with disease. DNA provides our genetic code, with its sister molecule RNA translating that code into the proteins that run our brains and myriad bodily functions. Scientists can now use molecules called antisense oligonucleotides (ASOs) to modify this process by binding to RNA and altering translation. ASOs are DNA-like molecules that greatly resemble the DNA that produced the RNA they correspond to in the first place. Depending on where they are designed to bind, these antisense molecules can prevent an RNA from being translated into a protein, which reduces levels of that protein in the body or brain. Alternatively, these same DNA-like molecules can be crafted to interfere with RNA machinery that normally inhibits or slows translation. In this case, more protein is made. © 2019 Scientific American

Keyword: Alzheimers; ALS-Lou Gehrig's Disease
Link ID: 26504 - Posted: 08.15.2019

Anna Moore On a lazy Sunday morning in May last year, Isobel Lloyd was at her boyfriend’s house, having coffee with his mum. The conversation had worked around to Lloyd’s grandma – her mother’s mother – who’d died in her 50s, when Lloyd was very young. Lloyd’s only memories of her had been hospice visits where her grandma lay bedbound, unable to talk or swallow, with no control over how her body moved. Lloyd had forgotten the name of her grandma’s disease, hadn’t thought about it in years. Like most 20-year-olds, she was future-focused – a student from Yorkshire, keen on her studies, in love with her boyfriend of four years. Sitting in his family kitchen, they began reeling off degenerative diseases. Motor neurone. Multiple sclerosis. Parkinson’s. Alzheimer’s. Then finally Huntington’s disease (HD). In a flash of recognition, Lloyd knew that was the one her grandma had. “It just clicked,” she says. “I Googled it on my phone – and that’s when I read that it was genetic. My mum had a 50% risk of getting it – and if she did, I had a 50% risk, too.” She didn’t tell her boyfriend’s mother what she’d just learned, “But I felt the colour rush out of my face,” says Lloyd, an only child. “I thought, ‘No way, that can’t be true.’ I was 20 years old and no one had told me?” In fact, that’s not so unusual. Secrecy, evasion and lies are frequent features for families grappling with genetic disease. Whether it’s HD, a breast cancer gene, inheritable bowel cancer, early-onset Alzheimer’s, it’s not uncommon for younger generations to stumble upon their inheritance by noticing patterns, asking questions. By then, they’re faced not just with their frightening at-risk status, but also anger at all those years in the dark. © 2019 Guardian News & Media Limited

Keyword: Huntingtons; Genes & Behavior
Link ID: 26498 - Posted: 08.15.2019

A new study analyzing samples from patients with and without acute flaccid myelitis (AFM) provides additional evidence for an association between the rare but often serious condition that causes muscle weakness and paralysis, and infection with non-polio enteroviruses. The National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, funded the research, which was conducted by investigators at Columbia University’s Center for Infection and Immunity and investigators from the Centers for Disease Control and Prevention. The findings are reported in the online journal mBio. There have been 570 confirmed cases since CDC began tracking AFM in August 2014. AFM outbreaks were reported to the CDC in 2014, 2016 and 2018. AFM affects the spinal cord and is characterized by the sudden onset of muscle weakness in one or more limbs. Spikes in AFM cases, primarily in children, have coincided in time and location with outbreaks of EV-D68 and a related enterovirus, EV-A71. Both of these viruses typically cause mild respiratory illness from which most people recover fully. Despite the epidemiological link between enterovirus circulation and AFM cases, evidence of direct causality has not been found. The researchers first looked for direct evidence of enterovirus infection in the cerebrospinal fluid (CSF) of 13 children and one adult diagnosed with AFM in 2018. They also examined five CSF samples taken from people with other central nervous system diseases. The team used a new tool they developed called VirCapSeq-VERT, which can detect any viral genetic material that is at least 60% like that of any known vertebrate virus. They found enteroviral genetic material (EV-A71) in only the one adult AFM case and genetic material from another enterovirus (echovirus 25) in one of the non-AFM cases.

Keyword: Movement Disorders; Neuroimmunology
Link ID: 26493 - Posted: 08.13.2019

Cassandra Willyard Rob Summers was flat on his back at a rehabilitation institute in Kentucky when he realized he could wiggle his big toe. Up, down, up, down. This was new — something he hadn’t been able to do since a hit-and-run driver left him paralysed from the chest down. When that happened four years earlier, doctors had told him that he would never move his lower body again. Now he was part of a pioneering experiment to test the power of electrical stimulation in people with spinal-cord injuries. “Susie, look, I can wiggle my toe,” Summers said. Susan Harkema, a neurophysiologist at the University of Louisville in Kentucky, sat nearby, absorbed in the data on her computer. She was incredulous. Summers’s toe might be moving, but he was not in control. Of that she was sure. Still, she decided to humour him. She asked him to close his eyes and move his right toe up, then down, and then up. She moved on to the left toe. He performed perfectly. “Holy shit,” Harkema said. She was paying attention now. “How is that happening?” he asked. “I have no idea,” she replied. Summers had been a university baseball player with major-league ambitions before the vehicle that struck him snapped all the ligaments and tendons in his neck, allowing one of his vertebra to pound the delicate nerve tissue it was meant to protect. Doctors classified the injury as complete; the motor connections to his legs had been wiped out. When Harkema and her colleagues implanted a strip of tiny electrodes in his spine in 2009, they weren’t trying to restore Summers’s ability to move on his own. Instead, the researchers were hoping to demonstrate that the spine contains all the circuitry necessary for the body to stand and to step. They reasoned that such an approach might allow people with spinal-cord injuries to stand and walk, using electrical stimulation to replace the signals that once came from the brain.

Keyword: Robotics
Link ID: 26471 - Posted: 07.31.2019

By Dom Vukovic Robotic skeletons may sound like something out of a science fiction movie but they are now being used to help people with severe spinal cord injuries take their first steps. The device known as a Rex bionic exoskeleton is one of only a few in the country and researchers in a trial have named their protype HELLEN. In a joint initiative between the University of Newcastle and the Australian Institute of Neuro-Rehabilitation, the robot is being used as a therapy device to see if it can help improve health and mobility outcomes in people with conditions including stroke, multiple sclerosis and now quadriplegia. Chief investigator Jodie Marquez said the trial was one of the first in the world to capture data about physiological and neurological changes that might occur in patients who undergo therapy while wearing the robotic suit. "We're seeing whether exercising in the exoskeleton device can improve both real measures of strength and spasticity, but also bigger measures such as mood and quality of life and function," Dr Marquez said. "I have no doubt that robotics will become a part of rehabilitation and a part of our lives in the future, I think that's unquestionable." Lifesaver Jess Collins is the first person with severe spinal injuries to participate in the trial. She had a near fatal surfing accident while on holidays with friends in May last year leaving her paralysed from the chest down. "I've hit the board and then the sandbank and then instantly I didn't have any movement or feeling and I wasn't sure where I was placed in the water … I was face down, which was horrific and I was conscious the entire time," she said. © 2019 ABC

Keyword: Robotics
Link ID: 26460 - Posted: 07.29.2019

Anna Ploszajski A man who lost his hand 17 years ago has been given the sense of touch through a brain-controlled robotic prosthetic. Keven Walgamott, whose arm was amputated below the elbow after an accident, can now feel 119 different touch sensations through the prosthetic as if it were his own limb. He is able to distinguish between large, small, soft and hard objects when blindfolded, and handle delicate objects such as grapes and eggs. Everyday tasks such as putting on his wedding ring, peeling a banana or holding a mobile phone are now possible. “The most amazing thing for me is what the team was able to do,” said Walgamott. “[They] take a bunch of mechanical pieces and provide, through a computer, not only the ability to move all fingers and grasp things but be able to feel again.” The prosthetic hand and wrist has been in development for 15 years. Electrodes were implanted in the remaining part of his arm, allowing communication between the prosthetic hand and his brain. The hand can move in six directions and is equipped with 19 sensors that detect touch and positioning. The arrays interpret the signals Walgamott’s brain sends to his arm nerves, and a computer outside the body translates these into digital information, which then instructs the prosthetic to move as the wearer intends. They also provide Walgamott’s nerves with computer-generated touch signals from the prosthesis, which are then interpreted by his brain. © 2019 Guardian News & Media Limited

Keyword: Pain & Touch; Robotics
Link ID: 26449 - Posted: 07.25.2019

Tina Hesman Saey A friendly gut bacterium can help lessen ALS symptoms, a study of mice suggests. Mice that develop a degenerative nerve disease similar to amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, fared better when bacteria making vitamin B3 were living in their intestines, researchers report July 22 in Nature. Those results suggest that gut microbes may make molecules that can slow progression of the deadly disease. The researchers uncovered clues that the mouse results may also be important for people with ALS. But the results are too preliminary to inform any changes in treating the disease, which at any given time affects about two out of every 100,000 people, or about 16,000 people in the United States, says Eran Elinav, a microbiome researcher at the Weizmann Institute of Science in Rehovot, Israel. “With respect to ALS, the jury is still out,” says Elinav, also of the German Cancer Research Center in Heidelberg. “We have to prove that what we found in mice is reproducibly found in humans.” Elinav and his colleagues examined the gut microbiomes — bacteria, archaea and other microbes that live in the colon, or large intestine — of mice that produce large amounts of a mutated form of the SOD1 protein. In the mice, as in human ALS patients, faulty SOD1 proteins clump together and lead to the death of nerve cells. |© Society for Science & the Public 2000 - 2019

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26439 - Posted: 07.23.2019