Chapter 11. Motor Control and Plasticity
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In a global study of myasthenia gravis, an autoimmune disease that causes muscle weakness and fatigue, researchers found that surgical removal of an organ called the thymus reduced patients’ weakness, and their need for immunosuppressive drugs. The study, published in the New England Journal of Medicine, was partially funded by the National Institutes of Health. “Our results support the idea that thymectomy is a valid treatment option for a major form of myasthenia gravis,” said Gil Wolfe, M.D., Professor and Irvin and Rosemary Smith Chair of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, New York, and a leader of the study. The Thymectomy Trial in Non-Thymomatous Myasthenia Gravis Patients Receiving Prednisone (MGTX) was a randomized, controlled study conducted on 126 patients aged 18-65 between 2006 and 2012. The researchers compared the combination of surgery and immunosuppression with the drug prednisone with prednisone treatment alone. They performed extended transternal thymectomies on 57 patients. This major surgical procedure aims to remove most of the thymus, which requires opening of a patient’s chest. On average the researchers found that the combination of surgery and prednisone treatment reduced overall muscle weakness more than prednisone treatment alone. After 36 months of prednisone treatment, both groups of patients had better QMG scores, a measure of muscle strength. Scores for the patients who had thymectomies and prednisone were 2.84 points better than patients who were on prednisone alone.
Meghan Rosen Exercise may not erase old memories, as some studies in animals have previously suggested. Running on an exercise wheel doesn’t make rats forgetprevious trips through an underwater maze, Ashok Shetty and colleagues report August 2 in the Journal of Neuroscience. Exercise or not, four weeks after learning how to find a hidden platform, rats seem to remember the location just fine, the team found. The results conflict with two earlier papers that show that running triggers memory loss in some rodents by boosting the birth of new brain cells. Making new brain cells rejiggers memory circuits, and that can make it hard for animals to remember what they’ve learned, says Paul Frankland, a neuroscientist at the Hospital for Sick Children in Toronto. He has reported this phenomenon in mice, guinea pigs and degus (SN: 6/14/14, p. 7). Maybe rats are the exception, he says, “but I’m not convinced.” In 2014, Frankland and colleagues reported that brain cell genesis clears out fearful memories in three different kinds of rodents. Two years later, Frankland’s team found similar results with spatial memories. After exercising, mice had trouble remembering the location of a hidden platform in a water maze, the team reported in February in Nature Communications. Again, Frankland and colleagues pinned the memory wipeout on brain cell creation — like a chalkboard eraser that brushes away old information. The wipe seemed to clear the way for new memories to form. Shetty, a neuroscientist at Texas A&M Health Science Center in Temple, wondered if the results held true in rats, too. “Rats are quite different from mice,” he says. “Their biology is similar to humans.” |© Society for Science & the Public 2000 - 2016. All rights reserved.
Keyword: Learning & Memory
Link ID: 22510 - Posted: 08.03.2016
By Libby Copeland Don’t get him wrong: Dean Burnett loves the brain as much as the next neuroscientist. But if he’s being honest, it’s “really quite rubbish in a lot of ways,” he says. In his new book, Idiot Brain, Burnett aims to take our most prized organ down a peg or two. Burnett is most fascinated by the brain’s tendency to trip us up when it’s just trying to help. His book explores many of these quirks: How we edit our own memories to make ourselves look better without knowing it; how anger persuades us we can take on a bully twice our size; and what may cause us to feel like we’re falling and jerk awake just as we’re falling asleep. (It could have something to do with our ancestors sleeping in trees.) We caught up with Burnett, who is also a science blogger for The Guardian and a stand-up comic, to ask him some of our everyday questions and frustrations with neuroscience. Why is it that we get motion sickness when we’re traveling in a plane or a car? We haven’t evolved, obviously, to ride in vehicles; that’s a very new thing in evolutionary terms. So the main theory as to why we get motion sickness is that it’s essentially a conflict in the senses that are being relayed to the subcortical part of the brain where the senses are integrated together. The body and the muscles are saying we are still. Your eyes are saying the environment is still. The balance sense in the ears are detecting movement. The brain is getting conflicting messages from the fundamental senses, and in evolutionary terms there’s only one thing that can cause that, which is a neurotoxin. And as a result the brain thinks it’s been poisoned and what do you do when you’ve been poisoned? Throw up.
Link ID: 22508 - Posted: 08.03.2016
Nisha Gaind Most people in the United States are more worried than enthusiastic about the prospect of scientific advances such as gene editing and brain-chip implants, a survey of thousands suggests. The Pew Research Center in Washington DC asked 4,726 US people about the potential uses of three biomedical technologies that it classified as ‘potential human enhancement’: gene editing to reduce disease risk in babies; brain implants to enhance concentration and brain processes, and transfusions of synthetic blood to improve strength and stamina. (None of these procedures are a reality, but the underlying technologies are being researched.) Those who took the survey were overwhelmingly wary about all of the ideas. In each case, more than 60% said that they would be worried about the technologies, and fewer than half expressed enthusiasm about them — with the prospect of brain implants prompting the most concern and least excitement. More than 70% thought that the procedures would become available before they were well understood or officially deemed safe. Around one-third thought the technologies were morally unacceptable, and about 70% were concerned that such enhancements would widen social divides — for instance, because initially only wealthy people would be able to afford them. © 2016 Macmillan Publishers Limited
Link ID: 22505 - Posted: 08.02.2016
Ian Sample and Nicky Woolf When Bill Gates pulled on a red and white-striped cord to upturn a bucket of iced water positioned delicately over his head, the most immediate thought for many was not, perhaps, of motor neurone disease. But the ice bucket challenge, the charity campaign that went viral in the summer of 2014 and left scores of notable persons from Gates and Mark Zuckerberg to George W. Bush and Anna Wintour shivering and drenched, has paid off in the most spectacular way. Dismissed by some at the time as “slacktivism” - an exercise that appears to do good while achieving very little - the ice bucket challenge raised more than $115m (£88m) for motor neurone disease in a single month. Now, scientists funded with the proceeds have discovered a gene variant associated with the condition. In the near term the NEK1 gene variant, described in the journal Nature Genetics this week, will help scientists understand how the incurable disorder, known also as Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig’s disease, takes hold. Once the mechanisms are more clearly elucidated, it may steer researchers on a path towards much-needed treatments. The work may never have happened were it not for the curious appeal of the frozen water drenchings. The research grants that scientists are awarded do not get close to the €4m the study required. Instead, Project MinE, which aims to unravel the genetic basis of the disease and ultimately find a cure, was funded by the ALS Association through ice bucket challenge donations. © 2016 Guardian News and Media Limited
By Gretchen Reynolds Learning requires more than the acquisition of unfamiliar knowledge; that new information or know-how, if it’s to be more than ephemeral, must be consolidated and securely stored in long-term memory. Mental repetition is one way to do that, of course. But mounting scientific evidence suggests that what we do physically also plays an important role in this process. Sleep, for instance, reinforces memory. And recent experiments show that when mice and rats jog on running wheels after acquiring a new skill, they learn much better than sedentary rodents do. Exercise seems to increase the production of biochemicals in the body and brain related to mental function. Researchers at the Donders Institute for Brain, Cognition and Behavior at Radboud University in the Netherlands and the University of Edinburgh have begun to explore this connection. For a study published this month in Current Biology, 72 healthy adult men and women spent about 40 minutes undergoing a standard test of visual and spatial learning. They observed pictures on a computer screen and then were asked to remember their locations. Afterward, the subjects all watched nature documentaries. Two-thirds of them also exercised: Half were first put through interval training on exercise bicycles for 35 minutes immediately after completing the test; the others did the same workout four hours after the test. Two days later, everyone returned to the lab and repeated the original computerized test while an M.R.I. machine scanned their brain activity. Those who exercised four hours after the test recognized and recreated the picture locations most accurately. Their brain activity was subtly different, too, showing a more consistent pattern of neural activity. The study’s authors suggest that their brains might have been functioning more efficiently because they had learned the patterns so fully. But why delaying exercise for four hours was more effective than an immediate workout remains mysterious. By contrast, rodents do better in many experiments if they work out right after learning. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22486 - Posted: 07.28.2016
By Sara Chodosh There has long been debate about a link between serious blows to the head and the development of neurodegenerative diseases later in life. Research has made cases for and against a relationship between traumatic brain injuries and neurological ailments such as Alzheimer’s, Parkinson’s and general dementia. Now the question is drawing ever more scrutiny as the alarming extent of these injuries becomes better known—and new research is finally casting some light on this murky and often quietly terrifying topic. A large-scale analysis of three separate studies published this week in JAMA Neurology found no association between unconsciousness-causing traumatic brain injuries (TBI) and Alzheimer’s disease or general dementia—but it did find a strong association between TBI and Parkinson’s disease. “I can’t decide if the positive or negative findings are more surprising,” says one of the study’s investigators, physician and Alzheimer’s researcher Paul Crane at the University of Washington. The positive association his team found between Parkinson’s and TBI was not entirely novel, but Crane says the magnitude of the link was unexpected. The researchers found the risk of Parkinson’s rose threefold for people whose head injuries had caused them to go unconscious for more than an hour. The more contentious finding is the lack of an association between TBI and Alzheimer’s. Prior research has been divided on whether there is a link, but many of the previous studies have been smaller in scale and conducted less-comprehensive analyses. “Although early studies suggested a clear link between TBI and an increased risk for Alzheimer’s disease, this has not been replicated,” explains Frances Corrigan at the University of Adelaide, who studies how TBI influences neurodegeneration. © 2016 Scientific American,
By Gretchen Reynolds To strengthen your mind, you may first want to exert your leg muscles, according to a sophisticated new experiment involving people, mice and monkeys. The study’s results suggest that long-term endurance exercise such as running can alter muscles in ways that then jump-start changes in the brain, helping to fortify learning and memory. I often have written about the benefits of exercise for the brain and, in particular, how, when lab rodents or other animals exercise, they create extra neurons in their brains, a process known as neurogenesis. These new cells then cluster in portions of the brain critical for thinking and recollection. Even more telling, other experiments have found that animals living in cages enlivened with colored toys, flavored varieties of water and other enrichments wind up showing greater neurogenesis than animals in drab, standard cages. But animals given access to running wheels, even if they don’t also have all of the toys and other party-cage extras, develop the most new brain cells of all. These experiments strongly suggest that while mental stimulation is important for brain health, physical stimulation is even more potent. But so far scientists have not teased out precisely how physical movement remakes the brain, although all agree that the process is bogglingly complex. Fascinated by that complexity, researchers at the National Institutes of Health recently began to wonder whether some of the necessary steps might be taking place far from the brain itself, and specifically, in the muscles, which are the body part most affected by exercise. Working muscles contract, burn fuel and pump out a wide variety of proteins and other substances. The N.I.H. researchers suspected that some of those substances migrated from the muscles into the bloodstream and then to the brain, where they most likely contributed to brain health. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22429 - Posted: 07.13.2016
By Aviva Rutkin At first glance, she was elderly and delicate – a woman in her 90s with a declining memory. But then she sat down at the piano to play. “Everybody in the room was totally startled,” says Eleanor Selfridge-Field, who researches music and symbols at Stanford University. “She looked so frail. Once she sat down at the piano, she just wasn’t frail at all. She was full of verve.” Selfridge-Field met this woman, referred to as ME to preserve her privacy, at a Christmas party around eight years ago. ME, who is now aged 101, has vascular dementia: she rarely knows where she is, and doesn’t recognise people she has met in the last few decades. But she can play nearly 400 songs by ear – a trick that depends on tapping into a memory of previously stored musical imprints – and continues to learn new songs just by listening to them. She has even composed an original piece of her own. ME’s musical talent, despite her cognitive impairments, inspired Selfridge-Field to spend the last six years observing her, and she presented her observations today at the International Conference on Music Perception and Cognition in San Francisco, California. ME experienced a stroke-like attack when she was in her 80s, and a few years later was diagnosed with vascular dementia. She struggles most to remember events and encounters that are recent, and her memory is selective, focusing on specific periods – such as her childhood between the ages of 3 and 8. She can recognise people that she met before the age of about 75 to 80. She is never quite sure of her surroundings. © Copyright Reed Business Information Ltd.
Link ID: 22420 - Posted: 07.11.2016
Beatrice Alexandra Golomb, Statins can indeed produce neurological effects. These drugs are typically prescribed to lower cholesterol and thereby reduce the risk of heart attack and stroke. Between 2003 and 2012 roughly one in four Americans aged 40 and older were taking a cholesterol-lowering medication, according to the Centers for Disease Control and Prevention. But studies show that statins can influence our sleep and behavior—and perhaps even change the course of neurodegenerative conditions, including dementia. The most common adverse effects include muscle symptoms, fatigue and cognitive problems. A smaller proportion of patients report peripheral neuropathy—burning, numbness or tingling in their extremities—poor sleep, and greater irritability and aggression. Interestingly, statins can produce very different outcomes in different patients, depending on an individual's medical history, the statin and the dose. Studies show, for instance, that statins generally reduce the risk of ischemic strokes—which arise when a blocked artery or blood clot cuts off oxygen to a brain region—but can also increase the risk of hemorrhagic strokes, or bleeding into the brain. Statins also appear to increase or decrease aggression. In 2015 my colleagues and I observed that women taking statins, on average, showed increased aggression; men typically showed less, possibly because of reduced testosterone levels. Some men in our study did experience a marked increase in aggression, which was correlated with worsening sleep. © 2016 Scientific American
Andrew Orlowski Special Report If the fMRI brain-scanning fad is well and truly over, then many fashionable intellectual ideas look like collateral damage, too. What might generously be called the “British intelligentsia” – our chattering classes – fell particularly hard for the promise that “new discoveries in brain science” had revealed a new understanding of human behaviour, which shed new light on emotions, personality and decision making. But all they were looking at was statistical quirks. There was no science to speak of, the results of the experiments were effectively meaningless, and couldn’t support the (often contradictory) conclusions being touted. The fMRI machine was a very expensive way of legitimising an anecdote. This is an academic scandal that’s been waiting to explode for years, for plenty of warning signs were there. In 2005, Ed Vul, now a psychology professor at UCSD, and Hal Pashler – then and now at UCSD – were puzzled by a claim being made in a talk by a neuroscience researcher. He was explaining study that purported to report a high correlation between a test subject’s brain activity and the speed with which they left the room after the study. “It seemed unbelievable to us that activity in this specific brain area could account for so much of the variance in walking speed,” explained Vul. “Especially so, because the fMRI activity was measured some two hours before the walking happened. So either activity in this area directly controlled motor action with a delay of two hours — something we found hard to believe — or there was something fishy going on.” IT © 1998–2016
Keyword: Brain imaging
Link ID: 22410 - Posted: 07.08.2016
Jon Hamilton Researchers have identified a substance in muscles that helps explain the connection between a fit body and a sharp mind. When muscles work, they release a protein that appears to generate new cells and connections in a part of the brain that is critical to memory, a team reports Thursday in the journal Cell Metabolism. The finding "provides another piece to the puzzle," says Henriette van Praag, an author of the study and an investigator in brain science at the National Institute on Aging. Previous research, she says, had revealed factors in the brain itself that responded to exercise. The discovery came after van Praag and a team of researchers decided to "cast a wide net" in searching for factors that could explain the well-known link between fitness and memory. They began by looking for substances produced by muscle cells in response to exercise. That search turned up cathepsin B, a protein best known for its association with cell death and some diseases. Experiments showed that blood levels of cathepsin B rose in mice that spent a lot of time on their exercise wheels. What's more, as levels of the protein rose, the mice did better on a memory test in which they had to swim to a platform hidden just beneath the surface of a small pool. The team also found evidence that, in mice, cathepsin B was causing the growth of new cells and connections in the hippocampus, an area of the brain that is central to memory. But the researchers needed to know whether the substance worked the same way in other species. So they tested monkeys, and found that exercise did, indeed, raise circulating levels of cathepsin in the blood. © 2016 npr
Megan Scudellari Shinya Yamanaka looked up in surprise at the postdoc who had spoken. “We have colonies,” Kazutoshi Takahashi said again. Yamanaka jumped from his desk and followed Takahashi to their tissue-culture room, at Kyoto University in Japan. Under a microscope, they saw tiny clusters of cells — the culmination of five years of work and an achievement that Yamanaka hadn't even been sure was possible. Two weeks earlier, Takahashi had taken skin cells from adult mice and infected them with a virus designed to introduce 24 carefully chosen genes. Now, the cells had been transformed. They looked and behaved like embryonic stem (ES) cells — 'pluripotent' cells, with the ability to develop into skin, nerve, muscle or practically any other cell type. Yamanaka gazed at the cellular alchemy before him. “At that moment, I thought, 'This must be some kind of mistake',” he recalls. He asked Takahashi to perform the experiment again — and again. Each time, it worked. Over the next two months, Takahashi narrowed down the genes to just four that were needed to wind back the developmental clock. In June 2006, Yamanaka presented the results to a stunned room of scientists at the annual meeting of the International Society for Stem Cell Research in Toronto, Canada. He called the cells 'ES-like cells', but would later refer to them as induced pluripotent stem cells, or iPS cells. “Many people just didn't believe it,” says Rudolf Jaenisch, a biologist at the Massachusetts Institute of Technology in Cambridge, who was in the room. But Jaenisch knew and trusted Yamanaka's work, and thought it was “ingenious”. © 2016 Macmillan Publishers Limited,
By ALAN COWELL LONDON — When Muhammad Ali died last week, the memories spooled back inevitably to the glory days of the man who called himself the Greatest, a champion whose life intertwined with America’s traumas of race, faith and war. It was a chronicle of valor asserted in the most public of arenas scrutinized by an audience that spanned the globe. But there was another narrative, just as striking to some admirers, of a private courage beyond his klieg-lit renown. For the minority afflicted by Parkinson’s disease, Ali’s 30-year struggle with the same illness magnified the broader status he built from his boxing prowess as a black man who embraced radical Islam, refused to fight in Vietnam, earned the opprobrium of the establishment and yet emerged as an icon. “It was his longest bout, and one that ultimately he could not win,” the reporter Patrick Sawer wrote in The Telegraph, referring to Ali’s illness. Yet the affliction “only served to increase the worldwide admiration he had gained before the disease robbed him of his powers.” As a global superstar, Ali touched many lands, and Britain felt a particular bond. Boxing fans recalled his far-flung bouts — the “Rumble in the Jungle” against George Foreman in Zaire, as the Democratic Republic of Congo was then called, in 1974; “The Thrilla in Manila” in the Philippines against Joe Frazier a year later. But in Britain, his two defeats in the 1960s of Henry Cooper, a much-loved British heavyweight who died in 2011, and his feisty appearances in prime-time television interviews left an indelible mark. © 2016 The New York Times Company
Link ID: 22308 - Posted: 06.11.2016
By Esther Landhuis About 100 times rarer than Parkinson’s, and often mistaken for it, progressive supranuclear palsy afflicts fewer than 20,000 people in the U.S.—and two thirds do not even know they have it. Yet this little-known brain disorder that killed comic actor Dudley Moore in 2002 is quietly becoming a gateway for research that could lead to powerful therapies for a range of intractable neurodegenerative conditions including Alzheimer’s and chronic traumatic encephalopathy, a disorder linked to concussions and head trauma. All these diseases share a common feature: abnormal buildup of a protein called tau in the brains of patients. Progressive supranuclear palsy has no cure and is hard to diagnose. Although doctors may have heard of the disease, many know little about it. It was not described in medical literature until 1964 but some experts believe one of the earliest accounts of the debilitating illness appeared in an 1857 short story by Charles Dickens and his friend Wilke Collins: “A cadaverous man of measured speech. A man who seemed as unable to wink, as if his eyelids had been nailed to his forehead. A man whose eyes—two spots of fire—had no more motion than if they had been connected with the back of his skull by screws driven through them, and riveted and bolted outside among his gray hair. He had come in and shut the door, and he now sat down. He did not bend himself to sit as other people do, but seemed to sink bolt upright, as if in water, until the chair stopped him.” © 2016 Scientific American
By DENISE GRADY Muhammad Ali, who died on Friday after a long struggle with Parkinson’s disease, was given the diagnosis in 1984 when he was 42. The world witnessed his gradual decline over the decades as tremors and stiffness set in, replacing his athletic stride with a shuffle, silencing his exuberant voice and freezing his face into an expressionless mask. What is Parkinson’s disease? It is a progressive, incurable deterioration of the part of the brain that produces a chemical needed to carry signals to the regions that control movement. How common is Parkinson’s? About one million people in the United States, and between seven million and 10 million worldwide, are thought to have Parkinson’s, according to the Parkinson’s Disease Foundation. What causes it? Was boxing a factor for Ali? The exact cause is not known. As with many disorders, experts suspect a combination of genes and environment, meaning that people with a particular genetic makeup may be predisposed to the disease if they are exposed to certain environmental factors. Head injuries, such as those sustained repeatedly in boxing, are among the possible risk factors listed by the National Parkinson Foundation. So is exposure to certain pesticides. These factors have both been suggested as possible contributors in Muhammad Ali’s case. Can Parkinson’s disease be treated? Medication can ease the symptoms for a time, but the disease continues to progress. In some cases, implanted devices called deep-brain stimulators can also help with symptoms. But Parkinson’s is not curable. © 2016 The New York Times Company
Link ID: 22284 - Posted: 06.06.2016
By Gretchen Reynolds A weekly routine of yoga and meditation may strengthen thinking skills and help to stave off aging-related mental decline, according to a new study of older adults with early signs of memory problems. Most of us past the age of 40 are aware that our minds and, in particular, memories begin to sputter as the years pass. Familiar names and words no longer spring readily to mind, and car keys acquire the power to teleport into jacket pockets where we could not possibly have left them. Some weakening in mental function appears to be inevitable as we age. But emerging science suggests that we might be able to slow and mitigate the decline by how we live and, in particular, whether and how we move our bodies. Past studies have found that people who run, weight train, dance, practice tai chi, or regularly garden have a lower risk of developing dementia than people who are not physically active at all. There also is growing evidence that combining physical activity with meditation might intensify the benefits of both pursuits. In an interesting study that I wrote about recently, for example, people with depression who meditated before they went for a run showed greater improvements in their mood than people who did either of those activities alone. But many people do not have the physical capacity or taste for running or other similarly vigorous activities. So for the new study, which was published in April in the Journal of Alzheimer’s Disease, researchers at the University of California, Los Angeles, and other institutions decided to test whether yoga, a relatively mild, meditative activity, could alter people’s brains and fortify their ability to think. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22270 - Posted: 06.01.2016
by Bruce Bower For a landmark 1977 paper, psychologist Andrew Meltzoff stuck his tongue out at 2- to 3-week-old babies. Someone had to do it. After watching Meltzoff razz them for 15 seconds, babies often stuck out their own tongues within the next 2½ minutes. Newborns also tended to respond in kind when the young researcher opened his mouth wide, pushed out his lips like a duck and opened and closed the fingers of one hand. Meltzoff, now at the University of Washington in Seattle, and a colleague were the first to report that babies copy adults’ simple physical deeds within weeks of birth. Until then, most scientists assumed that imitation began at around 9 months of age. Newborns don’t care that imitation is the sincerest form of flattery. For them, it may be a key to interacting with (and figuring out) those large, smiley people who come to be known as mommy and daddy. And that’s job number one for tykes hoping to learn how to talk and hang out with a circle of friends. Meltzoff suspected that babies enter the world able to compare their own movements — even those they can feel but not see, such as a projecting tongue — to corresponding adult actions. Meltzoff’s report has inspired dozens of papers on infant imitation. Some have supported his results, some haven’t. A new report, published May 5 in Current Biology, falls in the latter group. The study of 106 Australian babies tracked from 1 to 9 weeks of age concludes that infants don’t imitate anyone. © Society for Science & the Public 2000 - 201
Keyword: Development of the Brain
Link ID: 22246 - Posted: 05.25.2016
By Ian Randall As if you needed another reason to hate the gym, it now turns out that exercise can exhaust not only your muscles, but also your eyes. Fear not, however, for coffee can perk them right up again. During strenuous exercise, our muscles tire as they run out of fuel and build up waste products. Muscle performance can also be affected by a phenomenon called “central fatigue,” in which an imbalance in the body’s chemical messengers prevents the central nervous system from directing muscle movements effectively. It was not known, however, whether central fatigue might also affect motor systems not directly involved in the exercise itself—such as those that move the eyes. To find out, researchers gave 11 volunteers a carbohydrate solution either with a moderate dose of caffeine—which is known to stimulate the central nervous system—or as a placebo without, during 3 hours of vigorous cycling. After exercising, the scientists tested the cyclists with eye-tracking cameras to see how well their brains could still control their visual system. The team found that exercise reduced the speed of rapid eye movements by about 8%, impeding their ability to capture new visual information. The caffeine—the equivalent of two strong cups of coffee—was sufficient to counteract this effect, with some cyclists even displaying increased eye movement speeds, the team reports today in Scientific Reports. So it might be a good idea to get someone else to drive you home after that marathon. © 2016 American Association for the Advancement of Science.
Link ID: 22243 - Posted: 05.25.2016
By D. T. Max When a spinal cord is damaged, location is destiny: the higher the injury, the more severe the effects. The spine has thirty-three vertebrae, which are divided into five regions—the coccygeal, the sacral, the lumbar, the thoracic, and the cervical. The nerve-rich cord traverses nearly the entire length of the spine. The nerves at the bottom of the cord are well buried, and sometimes you can walk away from damage to these areas. In between are insults to the long middle region of the spine, which begins at the shoulders and ends at the midriff. These are the thoracic injuries. Although they don’t affect the upper body, they can still take away the ability to walk or feel below the waist, including autonomic function (bowel, bladder, and sexual control). Injuries to the cord in the cervical area—what is called “breaking your neck”—can be lethal or leave you paralyzed and unable to breathe without a ventilator. Doctors who treat spinal-cord-injury patients use a letter-and-number combination to identify the site of the damage. They talk of C3s (the cord as it passes through the third cervical vertebra) or T8s (the eighth thoracic vertebra). These morbid bingo-like codes help doctors instantly gauge the severity of a patient’s injury. Darek Fidyka, who is forty-one years old, is a T9. He was born and raised in Pradzew, a small farming town in central Poland, not far from Lodz. ... Several of the wounds punctured his lungs, and one nearly cut his spinal cord in half. As Fidyka lay on the ground, he felt his body change. “I can remember very vividly losing feeling in my legs, bit by bit,” he says. “It started in the upper part of the spine and was moving down slowly while I lay waiting for the ambulance to arrive.”
Link ID: 22230 - Posted: 05.19.2016