Chapter 16. None
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It can start with flashing lights, a tingling sensation and a feeling of unease, followed by excruciating pain. Migraines can be triggered by lack of food or too much stress but their underlying cause has remained a mystery. Now researchers have found that a migraine may be triggered by a protein deep in the brain that stimulates the neurons controlling facial sensations. The discovery creates a potential new target for safer migraine medicines and adds weight to the theory that neurons, not blood vessels, are responsible for migraine attacks. “Where a migraine starts is a key question,” says Debbie Hay at the University of Auckland in New Zealand. “There has been a great deal of debate around the mechanisms of migraine. If we can pin this down, we may have better chances of preventing it.” To investigate, Simon Akerman at New York University and Peter Goadsby at Kings College London, UK, studied two neuropeptides released by neurons thought to play a role in the pain associated with migraine. These protein-like molecules, called VIP and PACAP, first raised suspicion after they were found to be elevated in blood drained from the brains of people having a migraine attack. When researchers administered these peptides to volunteers, they found that they could cause a headache or migraine about two hours later. Both peptides widen blood vessels, which was thought to be significant in migraine. In fact, the only drugs specifically developed for migraine that are in use today – triptans – were designed to shrink blood vessels in the brain. As a result, they cannot be used by people with cardiovascular disorders. © Copyright Reed Business Information Ltd.
Keyword: Pain & Touch
Link ID: 21489 - Posted: 10.08.2015
By Gretchen Reynolds We’ve probably all heard someone exclaim, “Ah, my endorphins are kicking in!” at the end of a good run. Endorphins are famous for supposedly producing “runner’s high,” that fleeting sense of calm and euphoria that engulfs many of us after a satisfying workout. But in fact, endorphins may be unfairly hogging the credit for making workouts enjoyable, according to an enlightening new experiment with animals. The findings suggest that endorphins have little to do with runner’s high. Instead, that euphoric feeling may be the product of a completely different but oddly familiar substance — the body’s own endocannabinoids, the chemicals that, like the cannabinoids in marijuana, lighten mood. Endorphins first became a household word in the 1980s, when researchers found that blood levels increased after prolonged exercise. This finding made sense. Exercise can cause discomfort or pain, and endorphins are the body’s self-produced opiates, with pain-relieving properties much like morphine. From that discovery, it was a short step to believing that endorphins must also produce the pleasurable mental sensations that many people feel after exercise. But there is a substantial problem with that idea, and it involves the substantial-ness of endorphins. They are large molecules, too big to pass through the blood-brain barrier. They might staunch pain in the muscles, but they wouldn’t have effects directly inside the brain, where any high would originate. So for the past decade or so, scientists have been looking for other substances that might be involved in making exercisers feel high, which led them, perhaps unsurprisingly, to endocannabinoids. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 21488 - Posted: 10.08.2015
Jo Marchant Most new painkiller drugs fail in clinical trials — but a growing placebo response may be to blame. Drug companies have a problem: they are finding it ever harder to get painkillers through clinical trials. But this isn't necessarily because the drugs are getting worse. An extensive analysis of trial data1 has found that responses to sham treatments have become stronger over time, making it harder to prove a drug’s advantage over placebo. The change in reponse to placebo treatments for pain, discovered by researchers in Canada, holds true only for US clinical trials. “We were absolutely floored when we found out,” says Jeffrey Mogil, who directs the pain-genetics lab at McGill University in Montreal and led the analysis. Simply being in a US trial and receiving sham treatment now seems to relieve pain almost as effectively as many promising new drugs. Mogil thinks that as US trials get longer, larger and more expensive, they may be enhancing participants’ expectations of their effectiveness. Stronger placebo responses have already been reported for trials of antidepressants and antipsychotics2, 3, triggering debate over whether growing placebo effects are seen in pain trials too. To find out, Mogil and his colleagues examined 84 clinical trials of drugs for the treatment of chronic neuropathic pain (pain which affects the nervous system) published between 1990 and 2013. © 2015 Nature Publishing Group,
Keyword: Pain & Touch
Link ID: 21484 - Posted: 10.07.2015
Laura Sanders Scribes usually have pretty good handwriting. That’s not the case for one prolific 13th century writer known to scholars only as the Tremulous Hand of Worcester. Now scientists suggest the writer suffered from a neurological condition called essential tremor. Neurologist Jane Alty and historical handwriting researcher Deborah Thorpe, both of the University of York in England, made the retrospective diagnosis August 31 in Brain after studying the spidery wiggles that pervade the scribe’s writing. Essential tremor can cause shaking of the hands, head and voice and is distinct from other tremor-causing conditions such as Parkinson’s disease. Here, the anonymous writer’s peculiar script is evident (lighter portion of text) in an early Middle English version of the Nicene Creed, a summary of the Christian faith. Buried in the manuscript are clues that helped the researchers conclude that essential tremor plagued the Tremulous Hand. The Tremulous Hand of Worcester’s writing appeared in more than 20 books, including the Nicene Creed, a summary of the Christian faith. The writer’s distinctive script is the lighter portion of the text, about a third of the way down the page. Several clues led researchers to diagnose the scribe with essential tremor (see following images). © Society for Science & the Public 2000 - 2015.
Keyword: Movement Disorders
Link ID: 21482 - Posted: 10.07.2015
By Virginia Morell How homing pigeons find their way home has long mystified scientists. Experiments have shown they rely on smells to create a mental map of their route and on the sun or Earth’s magnetic fields to navigate. But they also use vision, memorizing roads, railway lines, and rivers. To understand just how important pigeons’ visual memories are for homing, scientists trained 12 birds to fly to their home lofts while wearing patches covering one eye (as in the photo above). Each bird wore a GPS logging device and made 18 flights with the left or right eye blocked, followed by another 18 trips with the opposite eye covered. Unlike mammals, birds lack a key neural structure—the corpus callosum—that allows both hemispheres of the brain to access what an animal sees. The experiments revealed that this missing neural structure affects the pigeons’ homing abilities, the scientists report in today’s the Proceedings of the Royal Society B. Pigeons that learned their way home with a blocked left eye couldn’t repeat the same journey when they wore a patch over their right eye, and vice versa. Instead, they flew slightly off course, following more of a curve than a straight line. The new work proves that vision, too, plays a key role in how pigeons find their way home. © 2015 American Association for the Advancement of Science.
By Miriam E. Tucker Before he got sick, Whitney Dafoe was an award-winning photographer and a world traveler. He’d helped build a nunnery in India, ridden a motorcycle in the Himalayas and visited all 50 American states. He also worked on Barack Obama’s 2008 presidential campaign, and although he was already ill by January 2009, pushed himself to travel to Washington from his California home to photograph the inauguration. But now, at 31, Whitney lies in bed in a darkened room in his parents’ home, unable to talk, walk or eat. He is fed intravenously and is barely able to tolerate light, sounds or being touched. His parents and the medical personnel who see him wear plain clothing when they enter his room because bright colors, shapes or any kind of print make him feel even worse, as does any movement that he’s not expecting. “It’s hard to explain how fragile he is,” says his mother, Janet Dafoe. This isn’t the picture that people imagine when they hear “chronic fatigue syndrome,” which is often viewed by the public and the health-care community as a trivial or primarily psychological complaint. In a February report, the Institute of Medicine gave the illness a new name — systemic exertion intolerance disease. Many patients have long criticized the name “chronic fatigue syndrome” for not reflecting the seriousness of the illness. The new name, some say, is not much of an improvement. Some patients call it by an older name, “myalgic encephalomyelitis.” Most official documents refer to it with a compromise term, “myalgic encephalomyelitis/chronic fatigue syndrome,” or ME/CFS.
Link ID: 21479 - Posted: 10.06.2015
By ANDREW POLLACK What could become the first gene therapy to win approval in the United States moved closer to market on Monday, when its developer announced that the medicine had succeeded in a late-stage clinical trial in treating an inherited eye disease that can cause blindness. The developer, Spark Therapeutics, said the treatment had allowed people with certain so-called inherited retinal dystrophies to more easily maneuver in dimmer light than they could before. The company said it planned to apply to the Food and Drug Administration next year for approval to sell the product. “We saw substantial restoration of vision in patients who were progressing toward complete blindness,” Dr. Albert M. Maguire, a professor of ophthalmology at the University of Pennsylvania and a lead researcher in the study, said in a news release being issued by Spark. Dr. Katherine High, Spark’s president and chief scientific officer, said this was the first successful randomized, controlled trial for any gene therapy aimed at an inherited disease. “I’ve been working in gene therapy for most of my career,” she said. “It’s been a long time coming, and I’m delighted.” Besides encouraging the once beleaguered field of gene therapy, the results — if interpreted positively by investors — could help lift biotechnology stocks, which have been battered recently by concerns over a backlash against high drug prices. Still, much remains unknown. Spark did not provide the actual trial data, saying only that the treatment achieved the main goal of the study as well as two out of three of its secondary goals. It is also unclear what the F.D.A. will deem sufficient for approval of the product. Spark’s stock had slumped in the last two months as it changed how it would measure the results of the trial. © 2015 The New York Times Company
Link ID: 21475 - Posted: 10.05.2015
Gareth Cook talks to Douwe Draaisma Much has been written on the wonders of human memory: its astounding feats of recall, the way memories shape our identities and are shaped by them, memory as a literary theme and a historical one. But what of forgetting? This is the topic of a new book by Douwe Draaisma, author of The Nostalgia Factory: Memory, Time and Ageing (Yale University Press, 2013; 176 pages) and a professor of the history of psychology at the University of Groningen in the Netherlands. In Forgetting: Myths, Perils and Compensations (Yale University Press, 2015; 288 pages), Draaisma considers dreaming, amnesia, dementia and all the ways in which our minds—and lives—are shaped by memory’s opposite. He answered questions from contributing editor Gareth Cook. What is your earliest memory, and why, do you suppose, have you not forgotten it? Quite a few early memories in the Netherlands involve bicycles; mine is no exception. I was two and a half years old when my aunts walked my mother to the train station. They had taken a bike to transport her bags. I was sitting on the back of the bike. Suddenly the whole procession came to a halt when my foot got caught between the spokes of a wheel. I am pretty sure this memory is accurate because I had to see a doctor, and there is a dated medical record. It is a brief, snapshotlike memory, black-and-white. I do not remember any pain, but I do remember the consternation among my mom and her sisters. Looking back on this memory from a professional perspective, I would say that it has the flashlike character typical for first memories from before age three; “later” first memories are usually a bit longer and more elaborate. © 2015 Scientific American
Keyword: Learning & Memory
Link ID: 21474 - Posted: 10.05.2015
Carl Zimmer In recent years, a peculiar sort of public performance has taken place periodically on the sidewalks of Seattle. It begins with a woman named Kaeli N. Swift sprinkling peanuts and cheese puffs on the ground. Crows swoop in to feed on the snacks. While Ms. Swift observes the birds from a distance, notebook in hand, another person walks up to the birds, wearing a latex mask and a sign that reads “UW CROW STUDY.” In the accomplice’s hands is a taxidermied crow, presented like a tray of hors d’oeuvres. This performance is not surreal street theater, but an experiment designed to explore a deep biological question: What do crows understand about death? Ms. Swift has been running this experiment as part of her doctoral research at the University of Washington, under the guidance of John M. Marzluff, a biologist. Dr. Marzluff and other experts on crow behavior have long been intrigued by the way the birds seem to congregate noisily around dead comrades. Dr. Marzluff has witnessed these gatherings many times himself, and has heard similar stories from other people. “Whenever I give a talk about crows, there’s always someone who says, ‘Well, what about this?’ ” he said. Dr. Marzluff and Ms. Swift decided to bring some scientific rigor to these stories. They wanted to determine whether a dead crow really does trigger a distinctive response from living crows and, if so, what the purpose of the large, noisy gatherings might be. To run the experiment, Ms. Swift began by delivering food to a particular spot each day, so that the crows learned to congregate there to eat. Then one of her volunteers would approach the feast with a dead crow, and Ms. Swift observed how the birds reacted. © 2015 The New York Times Company
By Margaret M. McCarthy “We have raised our children in a gender-neutral household since the day they were born, and we never allowed any sort of weapons, not even a water pistol,” a young mother told me emphatically from the microphone in the lecture hall where I’d just given a talk on the differences between male and female brains. “But the other day my seven-year-old son bit his peanut butter and jelly sandwich into the shape of a gun and started shooting his little sister with it!” The audience laughed appreciatively; everyone had a similar story. “What did we do wrong?” she pleaded. This story is a common refrain I hear when discussing my research on sex differences in the brain. There is no single correct answer when it comes to human behavior. Some researchers would insist that there is nothing parents can do to suppress the innate tendencies of boys to gravitate to guns and trucks while girls prefer dolls and tea sets. Others would disagree, arguing that there is no inherent biological difference between the brains of boys and girls. Rather, it is the parents’ own implicit biases and those of society at large that influence their children to behave in gender-typical ways. In the end, my response is that sex differences in the brain are more than some would like and less than others believe. Just how large those differences are, however, is the crux of an ongoing debate in science. And how much a brain’s function can be attributed to biology versus cultural expectations is a challenging question to answer. Confounding the issue is the concept of gender, a purely human construct that can itself influence brain development. Gender refers to both personal and societal perceptions of one’s sex, and embodies all the complexities of cultural expectations, inherent biases, and predetermined norms of behavior, each of which differs for boys and girls and can affect the young brain. © 1986-2015 The Scientist
Keyword: Sexual Behavior
Link ID: 21472 - Posted: 10.03.2015
By Emily Underwood WASHINGTON, D.C.—As part of President Barack Obama’s high-profile initiative to study the brain, the Kavli Foundation and several university partners today announced $100 million in new funding for neuroscience research, including three new institutes at universities in Maryland, New York, and California. Each of the institutes will receive a $20 million endowment, provided equally by their universities and the foundation, along with start-up funding to pursue projects in areas such as brain plasticity and tool development. The new funding, geared at providing stable support for high-risk, interdisciplinary research, exceeds the original commitment of $40 million that the Kavli Foundation made to the national Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, when it was first launched by President Obama in 2013. The funds are also unrestricted, allowing each institute to determine which projects to pursue. “That’s the most precious money any scientist can have,” Robert Conn, president and CEO of The Kavli Foundation, noted at a meeting today on Capitol Hill. Neuroscientist Loren Frank, who will serve as co-director at the new institute at the University of California, San Francisco, says the funds will allow his lab to explore fundamental questions such as how the brain can maintain its function despite constant change, and to form interdisciplinary partnerships with labs such as the Lawrence Livermore National Laboratory. The other two sites creating new institutes are Johns Hopkins University in Baltimore, Maryland, and Rockefeller University in New York City. In addition, Kavli announced a $40 million boost for four of its existing neuroscience institutes, located at Yale University, UC San Diego, Columbia University, and the Norwegian University of Science and Technology. © 2015 American Association for the Advancement of Science.
Keyword: Brain imaging
Link ID: 21471 - Posted: 10.03.2015
By Steve Mirsky Harvard neuroscientist Beth Stevens, talking about glia cells, which make up more than half the human brain. This week Stevens got a MacArthur Fellowship, the so-called genius grant, for her studies of glia. “These cells are incredibly responsive to damage or injury. They can protect our brain by, for example, clearing bacteria or debris in the brain in the case of injury and disease… “Until about 10 years ago, almost all of the research devoted to these cells was in these contexts. We discovered that there was another role for these cells in the normal healthy brain, in particular during development… “So a synapse is the junction of communication between two neurons, it’s how neurons talk to each other…we’re actually born with an excess of synaptic connections…and through this normal developmental process called pruning, a large number of these extra synapses get permanently removed or eliminated while others get strengthened and maintained. These microglial cells were in fact engulfing or eating these extra synapses. So these cells are necessary to do this and now of course we’re trying to better understand how it is that they know which synapse to prune and which synapse to leave alone. “A hallmark of many neurodegenerative diseases, including Alzheimer’s disease, is the early loss of synaptic connections or synapses…And what’s most striking about this is, it’s thought that the synapse loss happens years before you see signs of cognitive impairment or pathology. © 2015 Scientific American
By Lisa Sanders, M.d. On Thursday we challenged Well readers to solve the case of a 27-year-old woman who had vomiting, weakness and confusion months after having weight loss surgery. More than 200 readers offered their perspective on the case. Most of you recognized it as a nutritional deficiency, and nearly half of you totally nailed it. The diagnosis is: Wernicke’s encephalopathy due to thiamine (vitamin B1) deficiency. The very first reader to post a comment, Dr. Adrian Budhram, figured it out. His answer landed on our doorstep just five minutes after the case went up. Dr. Budhram is a second year neurology resident at Western University in London, Ontario. He says that Wernicke’s is on the list of diseases he thinks about every time someone is brought to the hospital because they are confused. Thiamine, or vitamin B1, is a nutrient essential for the body to break down and use sugars and proteins. It is found in many foods, including beans, brown rice, pork and cereals. Although the body only stores enough of the vitamin to last three to four weeks, deficiencies are rare when a full and varied diet is available. Diseases caused by a thiamine deficiency were described in Chinese medicine as early as 2600 B.C. – well before the vitamin was identified chemically. Western medicine came to know the disease as beriberi – a Sinhalese term meaning weak (apparently from the phrase “I can’t, I can’t”) characterized by either numbness and weakness in the legs (dry beriberi) or a weakened heart leading to hugely swollen legs (wet beriberi). © 2015 The New York Times Company
Keyword: Learning & Memory
Link ID: 21469 - Posted: 10.03.2015
Joe Palca Mothers have been warned for years that sleeping with their newborn infant is a bad idea because it increases the risk the baby might die unexpectedly during the night. But now Israeli researchers are reporting that even sleeping in the same room can have negative consequences: not for the child, but for the mother. Researchers at Ben-Gurion University of the Negev wanted to see whether sleeping in the same room as their newborn affected mothers' or babies' sleep. The short answer: It did, and the effect wasn't good for moms. The researchers recruited 153 married couples expecting their first child to participate in the study. The new parents weren't told where or how to sleep. They were simply asked to record whether they slept in the same room as their newborn, the same bed and same room, or if the child slept in another room. To measure sleep patterns, both mom and baby wore wristbands designed to measure movement during the night, a measurement that gives a pretty accurate indication of sleep patterns for both mother and child. The researchers measured sleep patterns before the babies were born, at 3 months and at 6 months. Mothers who slept in the same room as their infants, whether in the same bed or just the same room, had poorer sleep than mothers whose babies slept elsewhere in the house: They woke up more frequently (approximately three times per night versus two), were awake approximately 20 minutes longer per night, and had shorter periods of uninterrupted sleep (approximately 136 minutes versus 166 minutes). These results held true even taking into account that many of the women in the study were breast-feeding their babies. © 2015 NPR
Link ID: 21468 - Posted: 10.03.2015
By Jon Cohen A virus that long ago spliced itself into the human genome may play a role in amyotrophic lateral sclerosis (ALS), the deadly muscle degenerative disease that crippled baseball great Lou Gehrig and ultimately took his life. That’s the controversial conclusion of a new study, which finds elevated levels of human endogenous retrovirus K (HERV-K) in the brains of 11 people who died from the disease. “This certainly is interesting and provocative work,” says Raymond Roos, a neurologist at the University of Chicago in Illinois who treats and studies ALS but who was not involved with the finding. Still, even the scientists behind the work caution that more research is needed to confirm the link. “I’m very careful to say HERV-K doesn’t cause the disease but may play a role in the pathophysiology,” says study leader Avindra Nath, a neuroimmunologist at the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland. “The darn thing is in the chromosomes to begin with. It’s going to be very hard to prove causation.” It was another retrovirus, HIV, that led Nath to first suspect a connection between viruses and ALS. In 2006, he was helping a patient control his HIV infection with antiretroviral drugs when he noticed that the man’s ALS also improved. “That intrigued me, and I looked in the ALS literature and saw that people had reported they could see reverse transcriptase in the blood.” Reverse transcriptase, an enzyme that converts RNA to DNA, is a hallmark of retroviruses, which use it to insert copies of their genes into chromosomes of their hosts. © 2015 American Association for the Advancement of Science
By BENEDICT CAREY Medical literature has overstated the benefits of talk therapy for depression, in part because studies with poor results have rarely made it into journals, researchers reported Wednesday. Their analysis is the first effort to account for unpublished tests of such therapies. Treatments like cognitive behavior therapy and interpersonal therapy are indeed effective, the analysis found, but about 25 percent less so than previously thought. Doctors have long known that journal articles exaggerate the benefits of antidepressant drugs by about the same amount, and partly for the same reason — a publication bias in favor of encouraging findings. The new review, in the journal PLOS One, should give doctors and patients a better sense of what to expect from various forms of talk therapy, experts said, if not settle long-running debates in psychiatry about the relative merits of one treatment over another. Five million to six million Americans receive psychotherapy for depression each year, and many of them also take antidepressant drugs, surveys find. Most people find some relief by simply consulting a doctor regularly about the problem, experts said. Engaging in a course of well-tested psychotherapy, according to the new analysis, gives them an added 20 percent chance of achieving an even more satisfying improvement, or lasting recovery. Before accounting for the unpublished research, that figure was closer to 30 percent, a difference that suggests that hundreds of thousands of patients are less likely to benefit. The new paper is the latest chapter in a broad retrenchment across science in which researchers are scrutinizing past results to weed out publication bias and other, more deliberate statistical manipulations. © 2015 The New York Times Company
Link ID: 21464 - Posted: 10.01.2015
Are you good at picking someone out of a crowd? Most of us are better at recognising faces than distinguishing between other similar objects, so it’s long been suspected there’s something mysterious about the way the brain processes a face. Now further evidence has emerged that this is a special, highly evolved skill. A study of twins suggests there are genes influencing face recognition abilities that are distinct from the ones affecting intelligence – so it’s not that people who are good with faces just have a better memory, for instance. “The idea is that telling friend from foe was so important to survival that there was very strong pressure to improve that trait,” says Nicholas Shakeshaft of King’s College London. Previous studies using brain scanning have suggested there is a part of the brain dedicated to recognising faces, called the fusiform face area. But others have suggested this region may in fact just be used for discriminating between any familiar objects. Wondering if genetics could shed any light, Shakeshaft’s team tested more than 900 sets of UK twins – including both identical and non-identical pairs – on their face recognition skills. The ability turned out to be highly heritable, with identical twins having more similar abilities than fraternal ones. The same went for intelligence, which had earlier been tested as part of a long-running study. © Copyright Reed Business Information Ltd.
By Puneet Kollipara The list of health problems that scientists can confidently link to exposure to hormone-disrupting chemicals has grown to include diabetes, cardiovascular disease, and obesity, a new scientific statement suggests. The statement, released today by the Endocrine Society, also adds support to the somewhat controversial idea that even minute doses of these chemicals can interfere with the activity of natural hormones, which play a major role in regulating physiology and behavior. But the report—which updates a similar statement released in 2009—is drawing sharp criticism from the chemical industry. An executive summary of the new statement, which synthesizes 1300 studies on endocrine disrupters, posits that scientists are more confident than ever before in linking these substances to a host of known health issues, including reproductive and developmental problems, thyroid impairment, certain reproductive cancers, and neurodevelopmental problems such as decreased IQ. But studies suggest those links can now be extended to heart and weight problems, and diabetes, says the executive summary's first author, Andrea C. Gore, a professor of pharmacology and toxicology at the University of Texas, Austin. Six years ago, scientists couldn’t make such a strong case for those links, Gore says, because there weren’t enough good studies. “But this has really been an emerging field where there is much stronger evidence now,” Gore told reporters today on a conference call. Still, some toxicologists and industry groups have long disputed the assertion that endocrine disrupters can trigger effects at minimal doses; this idea can be tough to test in lab animals, which are usually exposed to high doses in toxicology studies. © 2015 American Association for the Advancement of Science
Neuroscientist Dr. Charles Tator has asked the family of former NHL enforcer Todd Ewen to donate Ewen's brain so he can study it. This week, Ewan's death was ruled a suicide and Tator wants to examine his brain to determine whether it has signs of degeneration. In particular, he's interested in what Ewen's brain may have in common with the other brains of athletes he's studying as part of the Canadian Sports Concussion Project. Brent Bambury speaks with Dr. Tator about how concussions can affect athletes and what big unanswered questions remain when it comes to the links between concussions, brain injury and self-harm. This conversation has been edited for clarity and length. Brent Bambury: You and your team already have examined the brains of eighteen former professional athletes. What do you hope to learn by looking at Todd Ewen's brain? Dr. Charles Tator: Well we want to know if he had C.T.E. In other words, was this the cause of his decline in terms of depression, for example. BB: What is C.T.E. ? CT: Well C.T.E. is chronic traumatic encephalopathy which is a specific type of brain degeneration that occurs after repetitive trauma like multiple concussions. BB: Is that something that you can only determine by examining the brain from a cadaver? CT: Unfortunately, even though we are getting clues about it from other tests like M.R.I., at this point in 2015, you have to do an autopsy to be sure that it's C.T.E. So with the Todd Ewen donation, if we're fortunate enough to have that opportunity to examine his brain, we would want to see if there were any manifestations of these previous concussions that he had in his career. ©2015 CBC/Radio-Canada
Keyword: Brain Injury/Concussion
Link ID: 21450 - Posted: 09.28.2015
A 26-year-old man who is paralysed in both legs has walked for the first time in five years – just by thinking about it. He is the first person to have his brain activity recorded and used to control a muscle-stimulating device in his legs. Every year, 250,000 to 500,000 people worldwide suffer spinal cord injuries, which can leave them partially or completely paralysed below the site of damage. Many rehabilitation clinics already offer functional electric stimulation (FES) devices, which activate the nerves that innervate leg muscles at the push of a button. But people with upper-body paralysis are not always able to operate the FES in this way. The new system bypasses the button and returns control to the brain. “We want to re-establish the connection between the brain and the leg muscles, to bring back the function that was once present,” says Zoran Nenadic at the University of California Irvine. To do that, Nenadic and his colleagues combined an FES system with a brain-computer interface. The team developed an electrode cap that picks up the brainwaves created when a person thinks specifically about walking or standing still. They tailored the device to pick up brain signals from their volunteer – a man who has had little sensation below his shoulder blades for five years. © Copyright Reed Business Information Ltd.
Link ID: 21437 - Posted: 09.24.2015