Chapter 5. The Sensorimotor System
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By ANDREW POLLACK In a confrontation between the hopes of desperate patients and clinical trial data, advisers to the Food and Drug Administration voted on Monday not to recommend approval of what would become the first drug for Duchenne muscular dystrophy. The negative votes came despite impassioned pleas from patients, parents and doctors who insisted that the drug, called eteplirsen, was prolonging the ability of boys with the disease to walk well beyond when they would normally be in wheelchairs. The problem was that the drug’s manufacturer, Sarepta Therapeutics, was trying to win approval based on a study involving only 12 patients without an adequate placebo control. The advisory panel voted 7 to 3, with three abstentions, that the clinical data did not meet the F.D.A. requirements for well controlled studies necessary for approval. However, some of the panel members had trouble reconciling the often compelling patient testimony with the F.D.A. legal requirements. “I was just basically torn between my mind and my heart,” said Richard P. Hoffmann, a pharmacist who was the consumer representative on the committee and who abstained. Dr. Bruce I. Ovbiagele, chairman of neurology at the Medical University of South Carolina, voted against approval but said, “Based on all I heard, the drug definitely works, but the question was framed differently.” On another question of whether the drug could qualify for so-called accelerated approval, a lower hurdle, the panel voted 7 to 6 against the drug. The F.D.A., which does not have to follow the advice of its advisory panels, is scheduled to decide whether to approve eteplirsen by May 26. © 2016 The New York Times Company
Medical research and new drugs to treat human illness usually start with studies on mice and rats. But that type of research has been traditionally sexist — using far more male than female rodents. Scientists warn that has already led to drugs and treatments that are potentially dangerous for women and say the approach slows down the development of treatments and drugs that are safe and effective for everyone. Cara Tannenbaum, scientific director of the Institute of Gender and Health at the Canadian Institutes of Health Research, cited a couple of examples on CBC's The Current of cases where drug side-effects turned out to be far more harmful in women: A stomach drug called cisapride that was sold in the 1990s under the name Prepulsid was withdrawn by Health Canada in 2000 because it sometimes caused irregular heartbeat and sudden death "in women only," Tannenbaum said. Among the victims was the 15-year-old daughter of former Ontario MP Terence Young. "It's not clear that the drug was ever tested in female animals or minors," Tannenbaum added. Health Canada has issued a warning about sleeping pills containing the drug zolpiclone, also known as Ambien, Tannenbaum said. Women are recommended to take half the dose that is prescribed to men. "It was recently discovered that the level of the drug was 45 per cent higher in women the next day, which can lead to car accidents," Tannenbaum said. Jeffrey Mogil, a neuroscientist and pain specialist at McGill University, said there are lots of reasons to suspect men and women respond differently to many different kinds of drugs, but very little actual data. "We actually don't know the scope of the problem," he told The Current. ©2016 CBC/Radio-Canada.
Melissa Davey Researchers have developed the world’s first blood test that can detect the abnormal metabolism of blood cells in people with Parkinson’s disease, which means the blood test could be used to diagnose the disorder. At present the only way to diagnose Parkinson’s disease, a degenerative neurological condition, is through ordering a range of tests and scans to rule out other disorders, combined with examining symptoms. Patients are often diagnosed only after they have developed symptoms and brain cells have already been destroyed. While there is no cure for Parkinson’s, early detection allows treatment with medication and physiotherapy to begin, which may slow the deterioration of motor functions in patients. Because diagnosing the disease is a process of elimination, and the symptoms mimic those of other neurological disorders, patients are also at risk being diagnosed and treated for the wrong disease. The group of Australian researchers from La Trobe University believe their blood test will enable doctors to detect Parkinson’s disease with unprecedented reliability and lead to earlier treatment. Their findings are under review by an international medical journal. © 2016 Guardian News and Media Limited
Link ID: 22120 - Posted: 04.20.2016
By BENEDICT CAREY Five years ago, a college freshman named Ian Burkhart dived into a wave at a beach off the Outer Banks in North Carolina and, in a freakish accident, broke his neck on the sandy floor, permanently losing the feeling in his hands and legs. On Wednesday, doctors reported that Mr. Burkhart, 24, had regained control over his right hand and fingers, using technology that transmits his thoughts directly to his hand muscles and bypasses his spinal injury. The doctors’ study, published by the journal Nature, is the first account of limb reanimation, as it is known, in a person with quadriplegia. Doctors implanted a chip in Mr. Burkhart’s brain two years ago. Seated in a lab with the implant connected through a computer to a sleeve on his arm, he was able to learn by repetition and arduous practice to focus his thoughts to make his hand pour from a bottle, and to pick up a straw and stir. He was even able to play a guitar video game. “It’s crazy because I had lost sensation in my hands, and I had to watch my hand to know whether I was squeezing or extending the fingers,” Mr. Burkhart, a business student who lives in Dublin, Ohio, said in an interview. His injury had left him paralyzed from the chest down; he still has some movement in his shoulders and biceps. The new technology is not a cure for paralysis. Mr. Burkhart could use his hand only when connected to computers in the lab, and the researchers said there was much work to do before the system could provide significant mobile independence. But the field of neural engineering is advancing quickly. Using brain implants, scientists can decode brain signals and match them to specific movements. Previously, people have learned to guide a cursor on a screen with their thoughts, monkeys have learned to skillfully use a robotic arm through neural signals and scientists have taught monkeys who were partly paralyzed to use an arm with a bypass system. This new study demonstrates that the bypass approach can restore critical skills to limbs no longer directly connected to the brain. © 2016 The New York Times Company
Link ID: 22106 - Posted: 04.14.2016
Dr. Perri Klass First of all, nobody takes a small child on an airplane for the fun of it. I have been there and I know. Don’t get me wrong, I’m no airplane saint; you won’t generally catch me offering to hold someone else’s kid, or making friends around the seatback. I don’t usually admit to being a pediatrician, for fear of hearing a medical saga. But I have put in my time on airplanes with my own infants and toddlers and small children, and I certainly know how it feels. Probably the best thing that can be said for traveling with young children is that it teaches you to appreciate traveling without them, however puzzling the inflight announcements, however long the delays, however tightly spaced the seats. I did enough economy-class traveling with children while my own were young that my reflexive reaction to all flight cancellations, turbulence or the moment when the person in front of me reclines the seat very suddenly, knocking my laptop closed, is now: At least I don’t have a small child with me – thank heavens. Babies do not cry on airplanes for the fun of it either. Nor do they cry, by and large, to let you know that their parents are neglectful or callous. They cry for infant versions of the same reasons that adults snap at one another about reclining seats, or elbow each other with quiet savagery over the armrest. They cry because their ears hurt and they’re being made to stay in a certain position when they don’t want to or the air smells strange and the noises are loud, or their stomachs feel upset or the day has been too long and they still aren’t there yet or they’re just plain cranky. As are we all. Crying is an evolutionary strategy to summon adult aid; over millennia, crying has probably evolved to be hard to ignore. I don’t know if it’s any comfort, but when you’re the parent with the crying baby, it doesn’t particularly help to be an expert. “I remember one flight where my daughter screamed the whole way and kept trying to get out of her seatbelt,” said my old friend, Dr. Elizabeth Barnett, a professor of pediatrics at Boston University and a travel medicine specialist. “As a parent, you feel two things — you’re in distress because you’re trying to comfort your child and not succeeding, so you feel bad for your child, and you also feel guilty because you know your child is disturbing everybody else.” © 2016 The New York Times Company
For decades, it was thought that scar-forming cells called astrocytes were responsible for blocking neuronal regrowth across the level of spinal cord injury, but recent findings challenge this idea. According to a new mouse study, astrocyte scars may actually be required for repair and regrowth following spinal cord injury. The research was funded by the National Institutes of Health, and published in Nature. “At first, we were completely surprised when our early studies revealed that blocking scar formation after injury resulted in worse outcomes. Once we began looking specifically at regrowth, though, we became convinced that scars may actually be beneficial,” said Michael V. Sofroniew, M.D., Ph.D., professor of neurobiology at the University of California, Los Angeles, and senior author of the study. “Our results suggest that scars may be a bridge and not a barrier towards developing better treatments for paralyzing spinal cord injuries.” Neurons communicate with one another by sending messages down long extensions called axons. When axons in the brain or spinal cord are severed, they do not grow back automatically. For example, damaged axons in the spinal cord can result in paralysis. When an injury occurs, astrocytes become activated and go to the injury site, along with cells from the immune system and form a scar. Scars have immediate benefits by decreasing inflammation at the injury site and preventing spread of tissue damage. However, long-term effects of the scars were thought to interfere with axon regrowth.
By JOANNA KLEIN Misconception: Migraines are psychological manifestations of women’s inability to manage stress and emotions Actually: Neurologists are very clear that migraines are a real, debilitating medical condition related to temporary abnormal brain activity. The fact that they may be more common for some women during “that time of the month” has nothing to do with emotions. For centuries, doctors explained migraines as a woman’s problem caused by emotional disturbances like hysteria, depression or stress. “Bizarrely, the recommended cure was marriage!” said Dr. Anne MacGregor, the lead author of the British Association for the Study of Headache’s guidelines for diagnosing and managing migraines. While that prescription may be far behind us, the misconception that migraines are fueled by a woman’s inability to cope persists. “It was considered psychological, or that I was a nervous overachiever, so I would never tell people that I have them,” said Lorie Novak, an artist in her sixties who has suffered from migraines since she was 8. After reading Joan Didion’s 1968 essay “In Bed,” about the writer’s struggle with migraines, Ms. Novak decided to tackle the representation of these debilitating headaches. Starting in 2009, Ms. Novak photographed herself every time she got a migraine. Under the hashtag #notjustaheadache, hundreds of others on Twitter and Instagram have demonstrated their own frustration with a widespread lack of understanding of the reality of migraines. © 2016 The New York Times Company
By Sandhya Somashekhar African Americans are routinely under-treated for their pain compared with whites, according to research. A study released Monday sheds some disturbing light on why that might be the case. Researchers at the University of Virginia quizzed white medical students and residents to see how many believed inaccurate and at times "fantastical" differences about the two races -- for example, that blacks have less sensitive nerve endings than whites or that black people's blood coagulates more quickly. They found that fully half thought at least one of the false statements presented was possibly, probably or definitely true. Moreover, those who held false beliefs often rated black patients' pain as lower than that of white patients and made less appropriate recommendations about how they should be treated. The study, published in the Proceedings of the National Academy of Sciences, could help illuminate one of the most vexing problems in pain treatment today: That whites are more likely than blacks to be prescribed strong pain medications for equivalent ailments. A 2000 study out of Emory University found that at a hospital emergency department in Atlanta, 74 percent of white patients with bone fractures received painkillers compared with 50 percent of black patients. Similarly, a paper last year found that black children with appendicitis were less likely to receive pain medication than their white counterparts. And a 2007 study found that physicians were more likely to underestimate the pain of black patients compared with other patients.
By C. CLAIBORNE RAY Q. Why do we become desensitized to a perfume we are wearing while others can still smell it? A. Ceasing to smell one’s perfume after continuous exposure while casual passers-by can still smell it is just one example of a phenomenon called olfactory adaptation or odor fatigue. After some time without exposure, sensitivity is usually restored. A similar weakening of odor signals with continued exposure also takes place in animals other than humans, and researchers often rely on animal studies to try to understand the cellular and molecular bases for the condition. It has been suggested that odor fatigue is useful because it enables animals to sort out the signals of a new odor from the background noise of continuous odors. It may also enable them to sense when an odor grows stronger. Studies published in the journal Science in 2002 pinpointed a chemical that seems to act as a gatekeeper for neurons involved in smell, opening and closing their electric signal channels. Genetically engineered mice that did not produce the substance, a protein called CNGA4, had profoundly impaired olfactory adaptation. A separate test-tube study found similar changes on a cellular level, with the signal channels remaining open when CNGA4 was absent. email@example.com © 2016 The New York Times Company
Keyword: Chemical Senses (Smell & Taste)
Link ID: 22042 - Posted: 03.29.2016
By Esther Hsieh Spinal implants have suffered similar problems as those in the brain—they tend to abrade tissue, causing inflammation and ultimately rejection by the body. Now an interdisciplinary research collaboration based in Switzerland has made a stretchable implant that appears to solve this problem. Like Lieber's new brain implant, it matches the physical qualities of the tissue where it is embedded. The “e-dura” implant is made from a silicone rubber that has the same elasticity as dura mater, the protective skin that surrounds the spinal cord and brain, explains Stéphanie Lacour, a professor at the school of engineering at the Swiss Federal Institute of Technology in Lausanne. This feature allows the implant to mimic the movement of the surrounding tissues. Embedded in the e-dura are electrodes for stimulation and microchannels for drug therapy. Ultrathin gold wires are made with microscopic cracks that allow them to stretch. Also, the electrodes are coated with a special platinum-silicone mixture that is stretchable. In an experiment that lasted two months, the scientists found that healthy rats with an e-dura spinal implant could walk across a ladder as well as a control group with no implant. Yet rats with a traditional plastic implant (which is flexible but not stretchable) started stumbling and missing rungs a few weeks after surgery. The researchers removed the implants and found that rats with a traditional implant had flattened, damaged spinal cords—but the e-dura implants had left spinal cords intact. Cellular testing also showed a strong immune response to the traditional implant, which was minimal in rats with the e-dura implant. © 2016 Scientific American
By Roni Caryn Rabin Sixty-five million Americans suffer from chronic lower back pain, and many feel they have tried it all: physical therapy, painkillers, shots. Now a new study reports many people may find relief with a form of meditation that harnesses the power of the mind to manage pain. The technique, called mindfulness-based stress reduction, involves a combination of meditation, body awareness and yoga, and focuses on increasing awareness and acceptance of one’s experiences, whether they involve physical discomfort or emotional pain. People with lower back pain who learned the meditation technique showed greater improvements in function compared to those who had cognitive behavioral therapy, which has been shown to help ease pain, or standard back care. Participants assigned to meditation or cognitive behavior therapy received eight weekly two-hour sessions of group training in the techniques. After six months, those learning meditation had an easier time doing things like getting up out of a chair, going up the stairs and putting on their socks, and were less irritable and less likely to stay at home or in bed because of pain. They were still doing better a year later. The findings come amid growing concerns about opioid painkillers and a surge of overdose deaths involving the drugs. At the beginning of the trial, 11 percent of the participants said they had used an opioid within the last week to treat their pain, and they were allowed to continue with their usual care throughout the trial. “This new study is exciting, because here’s a technique that doesn’t involve taking any pharmaceutical agents, and doesn’t involve the side effects of pharmaceutical agents,” said Dr. Madhav Goyal of Johns Hopkins University School of Medicine, who co-wrote an editorial accompanying the paper. © 2016 The New York Times Company
Results from a new study, funded in part by the National Center for Complementary and Integrative Health, demonstrate that mindfulness meditation works on a different pain pathway in the brain than opioid pain relievers. The researchers noted that because opioid and non-opioid mechanisms of pain relief interact synergistically, the results of this study suggest that combining mindfulness-based and pharmacologic/nonpharmacologic pain-relieving approaches that rely on opioid signaling may be particularly effective in treating pain. Previous research has shown that mindfulness meditation helps relieve pain, but researchers have been unclear about how the practice induces pain relief — specifically, if meditation is associated with the release of naturally occurring opiates. Researchers recorded pain reports in 78 healthy adults during meditation or a non-meditation control in response to painful heat stimuli and intravenous administration of the opioid antagonist naloxone (a drug that blocks the transmission of opioid activity) or placebo saline. Participants were randomized to one of four treatment groups: 1) meditation plus naloxone; 2) control plus naloxone; 3) meditation plus saline; or 4) control plus saline. People in the control groups were instructed to “close your eyes and relax until the end of the experiment.” The researchers found that participants who meditated during saline administration had significantly lower pain intensity and unpleasantness ratings compared to those who did not meditate while receiving saline. Importantly, data from the meditation plus naloxone group showed that naloxone did not block meditation’s pain-relieving effects. No significant differences in reductions of pain intensity or pain unpleasantness were seen between the meditation plus naloxone and the meditation plus saline groups. Participants who meditated during naloxone administration also had significantly greater reductions in pain intensity and unpleasantness than the control groups.
Keyword: Pain & Touch
Link ID: 22006 - Posted: 03.19.2016
BRAINS get data about the world through senses – sight, hearing, taste, smell and touch. In a lab in North Carolina, a group of rats is getting an extra one. Thanks to implants in their brains, they have learned to sense and react to infrared light. The rats show the brain’s ability to process unfamiliar data– an early step towards augmenting the human brain. Miguel Nicolelis of Duke University School of Medicine is leading the experiment. His team implanted four clusters of electrodes in the rats’ barrel cortex – the part of the brain that handles whisker sensation (doi.org/bdb6). Each cluster is connected to a sensor that converts infrared light into an electrical signal. Feeding stations placed at the four corners of the rats’ cage take turns emitting infrared signals that guide the rats to them, releasing a reward only when the rats press a button on the feeding station that is emiting the infrared signal. In an older, single sensor version of the experiment, it took the rats one month to adapt. With four sensors, it took them just three days. “This is a truly remarkable demonstration of the plasticity of the mammalian brain,” says Christopher James of the University of Warwick, UK. All the extra data that goes into making the rats’ new sense doesn’t appear to diminish their original senses. “The results show that nature has apparently designed the adult mammalian brain with the possibility of upgrades, and Nicolelis’ team is leading the way showing how to do it,” says Andrea Stocco of the University of Washington in Seattle. © Copyright Reed Business Information Ltd.
The CDC recommends non-opioid therapy, including exercise and over-the-counter pain medications, as the preferred treatment for chronic pain. It says opioids should only be prescribed — at the lowest effective dosage possible — when the benefits from pain reduction and bodily function outweigh the risks. In 2014, American doctors wrote nearly 200 million prescriptions for opioid painkillers, while deaths linked to the drugs climbed to roughly 19,000 — the highest number on record. The number of Canadians who die every year from opioids is not readily known — the Canadian Centre on Substance Abuse does not track the statistics — but Toronto physician Nav Persaud told CBC News in 2014 that more than 1,000 Canadians die from painkillers every year. A 2012 study says one in eight deaths among young adults age 25 to 34 in Ontario and one out of every 170 deaths in the province as a whole are opioid overdoses. One in four people who entered a withdrawal management program at St. Joseph's Healthcare in Hamilton, Ont., were opioid patients in 2012, up from one in ten in 2002. Other studies have cast doubt on the effectiveness of opioids on chronic pain, raising questions on whether its limited long-term effects are worth the harmful risks. "The science is clear," CDC director Tom Frieden said Tuesday. "For the vast majority of patients, the known and often fatal risks [of opioids] far outweigh the proven and transient benefits." ©2016 CBC/Radio-Canada.
By Sandra G. Boodman Kim Pace was afraid he was dying. In six months he had lost more than 30 pounds because a terrible stabbing sensation on the left side of his face made eating or drinking too painful. Brushing his teeth was out of the question and even the slightest touch triggered waves of agony and a shocklike pain he imagined was comparable to electrocution. Painkillers, even morphine, brought little relief. Unable to work and on medical leave from his job as a financial consultant for a bank, Pace, then 59, had spent the first half of 2012 bouncing among specialists in his home state of Pennsylvania, searching for help from doctors who disagreed about the nature of his illness. Some thought his searing pain might be the side effect of a drug he was taking. Others suspected migraines, a dental problem, mental illness, or an attempt to obtain painkillers. Even after a junior doctor made what turned out to be the correct diagnosis, there was disagreement among specialists about its accuracy or how to treat Pace. His wife, Carol, a nurse, said she suspects that the couple’s persistence and propensity to ask questions led her husband to be branded “a difficult case” — the kind of patient whom some doctors avoid. And on top of that, a serious but entirely unrelated disorder further muddied the diagnostic picture. So on July 17, 2012, when Pace told his wife he thought he was dying, she fired off an emotional plea for help to the office of a prominent specialist in Baltimore. “I looked at Kim and it hit me: He was going to die,” she said. “He was losing weight and his color was ashen” and doctors were “blowing him off. I thought, ‘Okay, that’s it,’ and the nurse in me took over.”
Sara Reardon Elite ski jumpers rely on extreme balance and power to descend the steep slopes that allow them to reach up to 100 kilometres per hour. But the US Ski and Snowboard Association (USSA) is seeking to give its elite athletes an edge by training a different muscle: the mind. Working with Halo Neuroscience in San Francisco, California, the sports group is testing whether stimulating the brain with electricity can improve the performance of ski jumpers by making it easier for them to hone their skills. Other research suggests that targeted brain stimulation can reduce an athlete’s ability to perceive fatigue1. Such technologies could aid recovery from injury or let athletes try 'brain doping' to gain a competitive advantage. Yet many scientists question whether brain stimulation is as effective as its proponents claim, pointing out that studies have looked at only small groups of people. “They’re cool findings, but who knows what they mean,” says cognitive psychologist Jared Horvath at the University of Melbourne in Australia. The USSA is working with Halo to judge the efficacy of a device that delivers electricity to the motor cortex, an area of the brain that controls physical skills. The company claims that the stimulation helps the brain build new connections as it learns a skill. It tested its device in an unpublished study of seven elite Nordic ski jumpers, including Olympic athletes. © 2016 Nature Publishing Group,
Keyword: Movement Disorders
Link ID: 21979 - Posted: 03.12.2016
By Amy Ellis Nutt Surgeons snaked the electrodes under the 65-year-old woman’s scalp. Thirty years of Parkinson’s disease had almost frozen her limbs. The wires, connected to a kind of pacemaker under the skin, were aimed at decreasing the woman’s rigidity and allowing for more fluid movement. But five seconds after the first electrical pulse was fired into her brain, something else happened. Although awake and fully alert, she seemed to plunge into sadness, bowing her head and sobbing. One of the doctors asked what was wrong. “I no longer wish to live, to see anything, to hear anything, feel anything,” she said. Was she in some kind of pain? “No, I’m fed up with life. I’ve had enough,” she replied. “Everything is useless.” The operating team turned off the current. Less than 90 seconds later, the woman was smiling and joking, even acting slightly manic. Another five minutes more, and her normal mood returned. The patient had no history of depression. Yet in those few minutes after the electrical pulse was fired, the despair she expressed met nine of the 11 criteria for severe major depressive disorder in the Diagnostic and Statistical Manual of Mental Disorders. Fascinated by the anomaly, the French physicians wrote up the episode for the New England Journal of Medicine. The year was 1999, and hers was one of the first documented cases of an electrically induced, instantaneous, yet reversible depression. © 1996-2016 The Washington Post
Laura Sanders For some adults, Zika virus is a rashy, flulike nuisance. But in a handful of people, the virus may trigger a severe neurological disease. About one in 4,000 people infected by Zika in French Polynesia in 2013 and 2014 got a rare autoimmune disease called Guillain-Barré syndrome, researchers estimate in a study published online February 29 in the Lancet. Of 42 people diagnosed with Guillain-Barré in that outbreak, all had antibodies that signaled a Zika infection. Most also had recent symptoms of the infection. In a control group of hospital patients who did not have Guillain-Barré, researchers saw signs of Zika less frequently: Just 54 out of 98 patients tested showed signs of the virus. The message from this earlier Zika outbreak is that countries in the throes of Zika today “need to be prepared to have adequate intensive care beds capacity to manage patients with Guillain-Barré syndrome,” writes study coauthor Arnaud Fontanet of the Pasteur Institute in Paris and colleagues, some of whom are from French Polynesia. The study, says public health researcher Ernesto Marques of the University of Pittsburgh, “tells us what I think a lot of people already thought: that Zika can cause Guillain-Barré syndrome.” As with Zika and the birth defect microcephaly (SN: 2/20/16, p. 16), though, more work needs to be done to definitively prove the link. Several countries currently hard-hit by Zika have reported upticks in Guillain-Barré syndrome. Colombia, for instance, usually sees about 220 cases of the syndrome a year. But in just five weeks between mid-December 2015 to late January 2016, doctors diagnosed 86 cases, the World Health Organization reports. Other Zika-affected countries, including Brazil, El Salvador and Venezuela, have also reported unusually high numbers of cases. © Society for Science & the Public 2000 - 2016. All rights reserved.
Cathleen O'Grady When we speak, listen, read, or write, almost all of the language processing that happens in our brains goes on below the level of conscious awareness. We might be aware of grasping for a particular forgotten word, but we don’t actively think about linguistic concepts like morphemes (the building blocks of words, like the past tense morpheme “-ed”). Psycholinguists try to delve under the surface to figure out what’s actually going on in the brain, and how well this matches up with our theoretical ideas of how languages fit together. For instance, linguists talk about morphemes like “-ed”, but do our brains actually work with morphemes when we’re producing or interpreting language? That is, do theoretical linguistic concepts have any psychological reality? An upcoming paper in the journal Cognition suggests an unusual way to investigate this: by testing synaesthetes. Synaesthesia comes in many forms. Some synaesthetes associate musical tones or notes with particular colours; others attach personalities to letters or numbers. A huge number of synaesthetes have associations that are in some way linguistic, and one of the most common forms of all is grapheme-colour (GC) synaesthesia, which is the association of colours with particular letters or numbers. For instance, a GC synaesthete might have a consistent perception of the letter “A” being red. This association often extends to a whole word, so “ant” might be red, too. © 2016 Guardian News and Media Limited
Link ID: 21937 - Posted: 02.27.2016
Mo Costandi People who are prone to falling and injuring and injuring themselves in middle age are at significantly increased risk of developing Parkinson’s Disease decades later, according to a new study by researchers in Sweden. The findings, published earlier this month in the open access journal PLoS Medicine, suggest that frailty – and especially an increased risk of falling and fracturing one’s hip – could be a marker for degenerative brain changes, which may occur decades before disease symptoms appear, and possibly aid in early diagnosis. Parkinson’s Disease is a progressive neurodegenerative disease characterised by the death of dopamine-producing neurons in a region of the midbrain called the substantia nigra. This causes the three main symptoms of tremor, muscle rigidity, and slow movements, which typically appear at around 60 years of age, and progress at varying rates. Although widely considered to be a movement disorder, Parkinson’s is also associated with cognitive impairments, which in severe cases can develop into full-blown dementia. Last year, Peter Nordström of Umeå University and his colleagues published the results of a large population study, in which they examined the medical records of all the approximately 1.35 million Swedish men conscripted at age 18 for compulsory military service between the years of 1969 and 1996. Looking specifically at measures of muscle strength, they found that those who scored lowest on handgrip and elbow flexion strength at the time of conscription were significantly more likely to develop Parkinson’s 30 years later. © 2016 Guardian News and Media Limited
Link ID: 21919 - Posted: 02.20.2016