Chapter 5. The Sensorimotor System
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By Kristin Ozelli Four years ago writer and producer Jon Palfreman was diagnosed with Parkinson’s disease. He has chronicled his experience and that of many other “Parkies,” as patients sometimes call themselves, in two books, the latest of which is Brain Storms: The Race to Unlock the Mysteries of Parkinson’s Disease, published this year by Scientific American / Farrar, Straus and Giroux, which traces some of the recent progress of medical researchers in treating this disease. He shared with Scientific American MIND senior editor Kristin Ozelli some of the insights he gleaned while working on this book. You wrote an earlier book about Parkinson’s and produced a prize-winning documentary, The Case of the Frozen Addicts, and have experienced the disease personally. While you were researching Brain Storms, was there anything new you learned about the disease that really surprised you? What is truly surprising is just how long biomedical research takes to deliver life-changing therapies. The promising therapies around when I wrote my first book 20 years ago, like neural grafting and growth factors—therapies designed to replace, revive or protect dopamine neurons—well they haven’t panned out. On the other hand, since my first involvement with Parkinson’s, there have been some extraordinary advances in basic science. In a sense, the disease has been rebranded from a movement disorder (resulting from damage to a very small part of the brain) to a systemic condition involving not only tremor and rigidity but also a whole host of symptoms—from depression to sleep disorders, from constipation to dementia. Indeed, there’s an entirely new theory of the disease that sees it as being driven by a protein alpha-synuclein that goes rogue and, prionlike, jumps from neuron to neuron creating havoc. © 2015 Scientific American
Link ID: 21435 - Posted: 09.23.2015
David Cyranoski A dispute has broken out at two of China’s most prestigious universities over a potentially groundbreaking discovery: the identification of a protein that may allow organisms to sense magnetic fields. On 14 September, Zhang Sheng-jia, a neuroscientist at Tsinghua University in Beijing, and his colleagues published a paper1 in Science Bulletin claiming to use magnetic fields to remotely control neurons and muscle cells in worms, by employing a particular magnetism-sensing protein. But Xie Can, a biophysicist at neighbouring Peking University, says that Zhang’s publication draws on a discovery made in his laboratory, currently under review for publication, and violates a collaboration agreement the two had reached. Administrators at Tsinghua and Peking universities, siding with Xie, have jointly requested that the journal retract Zhang’s paper, and Tsinghua has launched an investigation into Zhang’s actions. The dispute revolves around an answer to the mystery of how organisms as diverse as worms, butterflies, sea turtles and wolves are capable of sensing Earth’s magnetic field to help them navigate. Researchers have postulated that structures in biological cells must be responsible, and dubbed these structures magnetoreceptors. But they have never been found. In research starting in 2009, Xie says that he used a painstaking whole-genome screen to identify a protein containing iron and sulfur that seems, according to his experiments, to have the properties of a magnetoreceptor. He called it MagR, to note its purported properties, and has since been examining its function and structure to determine how it senses magnetic fields. © 2015 Nature Publishing Group,
Keyword: Animal Migration
Link ID: 21431 - Posted: 09.22.2015
Nathan Seppa For a historically mistrusted drink, coffee is proving to be a healthy addiction. Scientific findings in support of coffee’s nutritional attributes have been arriving at a steady drip since the 1980s, when Norwegian researchers reported that coffee seemed to fend off liver disease. Since then, the dark brown beverage has shown value against liver cancer, too, as well as type 2 diabetes, heart disease and stroke. Coffee even appears to protect against depression, Parkinson’s and Alzheimer’s diseases. Taken as a whole, these results might explain the most astonishing finding of all. People who drink two or more cups of coffee a day live longer than those who don’t, after accounting for behavioral differences, U.S. researchers reported in 2012. Studies in Japan, Scotland and Finland agree. Talk about a twofer. Coffee not only picks you up, it might put off the day they lower you down. Yet coffee has had trouble shaking its bad-for-you reputation. It may be one of the most widely consumed drinks in the world, but people have long assumed that, at least in its energizing caffeinated version, coffee comes with a catch. “People notice the caffeine,” says cardiologist Arthur Klatsky, who has researched coffee for decades at the Kaiser Permanente Northern California Division of Research in Oakland. “And there is this general feeling that anything that has some effect on the nervous system has to have something bad about it.” It doesn’t help that caffeine is mildly addictive.
By Larry Greenemeier Advanced prosthetics have for the past few years begun tapping into brain signals to provide amputees with impressive new levels of control. Patients think, and a limb moves. But getting a robotic arm or hand to sense what it’s touching, and send that feeling back to the brain, has been a harder task. The U.S. Defense Department’s research division last week claimed a breakthrough in this area, issuing a press release touting a 28-year-old paralyzed person’s ability to “feel” physical sensations through a prosthetic hand. Researchers have directly connected the artificial appendage to his brain, giving him the ability to even identify which mechanical finger is being gently touched, according to the Defense Advanced Research Projects Agency (DARPA). In 2013, other scientists at Case Western Reserve University also gave touch to amputees, giving patients precise-enough feeling of pressure in their fingertips to allow them to twist the stems off cherries. The government isn’t providing much detail at this time about its achievement other than to say that researchers ran wires from arrays connected to the volunteer’s sensory and motor cortices—which identify tactile sensations and control body movements, respectively—to a mechanical hand developed by the Applied Physics Laboratory (APL) at Johns Hopkins University. The APL hand’s torque sensors can convert pressure applied to any of its fingers into electrical signals routed back to the volunteer’s brain. © 2015 Scientific American
A choir of Canadians with Parkinson's disease is helping researchers test how well the performers regain facial movement to express emotions. Tremors and difficulty walking are often the most noticeable symptoms of Parkinson's disease, which affects about one in 500 people in Canada. Those with the disease may also have limited facial movement, which hampers the ability to express themselves. For people with Parkinson's who have "masked face syndrome," it can be difficult for others to decipher how they're feeling. That's because we unknowingly mimic or mirror each other during interaction to connect. "Within a hundred milliseconds of seeing someone else smile or frown, we are smiling or frowning," said Frank Russo, a psychology professor at Ryerson University in Toronto. "We're mirroring what the other person is doing. And that's one of the things that is absent in Parkinson's. It's the absence of mirroring that is leading to some of the deficit in understanding other people's emotions." Having a static face can leave people with Parkinson's seem cold and aloof as they also show deficits in understanding other people's emotions. The patient can then become emotionally disconnected from others. Studying the 28 members of the Parkinson's choir has bolstered Russo's thinking that singing, facial expressions and social communications are interconnected. So far Russo has found that mirroring effect or mimicry was restored among choir participants who sang for 13 weeks. ©2015 CBC/Radio-Canada.
Ever waited for a bus rather than take the short walk to work? Headed for the escalator instead of the stairs? Humans clearly harbour a deep love of lethargy – and now we know how far people will go to expend less energy. We will change our walking style on the fly when our normal gait becomes even a little more difficult. The finding could have implications for the rehabilitation offered to people with spinal injuries. Jessica Selinger and her colleagues at Simon Fraser University in Burnaby, British Columbia, Canada, strapped volunteers into a lightweight robotic exoskeleton and put them on a treadmill. Initially, the team let the volunteers find their preferred walking rhythm – which turned out to be 1.8 steps per second, on average. Then the researchers switched on the exoskeleton, programming it to make it more difficult for the volunteers to walk at their preferred pace by preventing the knee from bending – and leg swinging – as freely. The exoskeleton didn’t interfere with the human guinea pigs’ ability to walk faster or slower than they preferred. Within minutes the volunteers had found a walking style that the exoskeleton would allow without offering resistance. Remarkably, though, they did so despite the fact that the exoskeleton only ever offered minimal resistance. By using breathing masks to analyse the volunteers’ metabolic activity, Selinger’s team found that subjects would shift to an awkward new gait even if the energy saving was only 5 per cent. “People are able to adapt and fine-tune in order to move in the most energetically optimal way,” says Selinger. “People will change really fundamental characteristics of their gait.” © Copyright Reed Business Information Ltd.
Keyword: Movement Disorders
Link ID: 21398 - Posted: 09.11.2015
By Olivia Campbell Leave it to childbirth to cause a woman who’s never felt pain in her life to now experience persistent discomfort. When a 37-year-old woman with a condition known as congenital insensitivity to pain gave birth, her labor was as painless as expected. But during the delivery, she sustained pelvic fractures and an epidural hematoma that impinged on a nerve in her lower spine. Since then, she has added an unfortunate variety of words to her vocabulary: Her hips “hurt” and “ache;” she feels a “continuous buzzing in both legs and a vice-like squeezing in the pelvis.” When resting, she is left with “tingling” and “electric shocks.” She now has headaches, backaches, period pains, and stomach cramps; and even describes “the sting” of a graze and “the sharpness” of an exposed gum. According to doctors who treated her, the woman's sensitivity to pain -- tested on the tops of her feet -- is 10 times higher than it was before she gave birth. Congenital insensitivity to pain is an incredibly rare genetic disorder — there are only 20 recorded cases — that causes individuals to be totally unaware of pain. Co-author of the paper Michael Lee explained how pain pathways start with specialized nerves, called nociceptors, that sense damaging temperatures or pressure and then fire off signals to the brain. Those signals make us feel pain to prevent further damage. In people with CIP, a defective gene prevents these signals from going through. But pain can also arise when nociceptors or nerves are damaged, as was the case when this woman’s lumbar nerve was pinched during childbirth.
Keyword: Pain & Touch
Link ID: 21379 - Posted: 09.03.2015
By Jennifer Couzin-Frankel Some rare diseases pull researchers in and don’t let them go, and the unusual bone condition called fibrodysplasia ossificans progressiva (FOP) has long had its hooks in Aris Economides. “The minute you experience it it’s impossible to step back and forget it,” says the functional geneticist who runs the skeletal disease program at Regeneron Pharmaceuticals in Tarrytown, New York. “It’s devastating in the most profound way.” The few thousand or so people with FOP worldwide live with grueling uncertainty: Some of their muscles or other soft tissues periodically, and abruptly, transform into new bone that permanently immobilizes parts of their bodies. Joints such as elbows or ankles may become frozen in place; jaw motion can be impeded and the rib cage fixed, making eating or even breathing difficult. Twenty years after he first stumbled on FOP, Economides and his colleagues report today that the gene mutation shared by 97% of people with the disease can trigger its symptoms in a manner different than had been assumed—through a single molecule not previously eyed as a suspect. And by sheer chance, Regeneron had a treatment for this particular target in its freezers. The company tested that potential therapy, a type of protein known as a monoclonal antibody, on mice with their own form of FOP and lo and behold, they stopped growing unwelcome new bone. © 2015 American Association for the Advancement of Science.
By Simon Makin Scientists claim to have discovered the first new human prion in almost 50 years. Prions are misfolded proteins that make copies of themselves by inducing others to misfold. By so doing, they multiply and cause disease. The resulting illness in this case is multiple system atrophy (MSA), a neurodegenerative disease similar to Parkinson's. The study, published August 31 in Proceedings of the National Academy of Sciences, adds weight to the idea that many neurodegenerative diseases are caused by prions. In the 1960s researchers led by Carleton Gajdusek at the National Institutes of Health transmitted kuru, a rare neurodegenerative disease found in Papua New Guinea, and Creutzfeldt–Jakob disease (CJD), a rare human dementia, to chimpanzees by injecting samples from victims' brains directly into those of chimps. It wasn't until 1982, however, that Stanley Prusiner coined the term prion (for “proteinaceous infectious particle”) to describe the self-propagating protein responsible. Prusiner and colleagues at the University of California, San Francisco, showed this process caused a whole class of diseases, called spongiform encephalopathies (for the spongelike appearance of affected brains), including the bovine form known as “mad cow” disease. The same protein, PrP, is also responsible for kuru, which was spread by cannibalism; variant-CJD, which over 200 people developed after eating beef infected with the bovine variety; and others. The idea that a protein could transmit disease was radical at the time but the work eventually earned Prusiner the 1997 Nobel Prize in Physiology or Medicine. He has long argued prions may underlie other neurodegenerative diseases but the idea has been slow to gain acceptance. © 2015 Scientific American
Boer Deng Palaeontologist Stephen Gatesy wants to bring extinct creatures to life — virtually speaking. When he pores over the fossilized skeletons of dinosaurs and other long-dead beasts, he tries to imagine how they walked, ran or flew, and how those movements evolved into the gaits of their modern descendents. “I'm a very visual guy,” he says. But fossils are lifeless and static, and can only tell Gatesy so much. So instead, he relies on XROMM, a software package that he developed with his colleagues at Brown University in Providence, Rhode Island. XROMM (X-ray Reconstruction of Moving Morphology) borrows from the technology of motion capture, in which multiple cameras film a moving object from different angles, and markers on the object are rendered into 3D by a computer program. The difference is that XROMM uses not cameras, but X-ray machines that make videos of bones and joints moving inside live creatures such as pigs, ducks and fish. Understanding how the movements relate to the animals' bone structure can help palaeontologists to determine what movements would have been possible for fossilized creatures. “It's a completely different approach” to studying evolution, says Gatesy. XROMM, released to the public in 2008 as an open-source package, is one of a number of software tools that are expanding what researchers know about how animals and humans walk, crawl and, in some cases, fly (see ‘Movement from inside and out’). That has given the centuries-old science of animal motion relevance to a wide range of fields, from studying biodiversity to designing leg braces, prostheses and other assistive medical devices.“We're in an intense period of using camera-based and computer-based approaches to expand the questions we can ask about motion,” says Michael Dickinson, a neuroscientist at the California Institute of Technology in Pasadena. © 2015 Nature Publishing Group
Keyword: Movement Disorders
Link ID: 21370 - Posted: 09.01.2015
By Diana Kwon Each year doctors diagnose approximately 60,000 Americans with Parkinson’s disease, an incurable neurodegenerative condition for which the number-one risk factor is age. Worldwide an estimated seven to 10 million people currently live with the malady. As U.S. and global populations grow older, it is becoming increasingly urgent to understand its causes. So far, researchers know that Parkinson’s involves cell death in a few restricted areas of the brain including the substantia nigra (SNc), one of two big cell clusters in the midbrain that house a large population of dopamine neurons. These cells release dopamine and are involved in a variety of functions including reward processing and voluntary movement. Their death leads to the motor control and balance issues that are core symptoms of the disease. New research shows that these brain cells, most at risk in Parkinson’s disease, require unusually high amounts of energy to carry out their tasks because of their highly branched structures. Like a massive car with an overheating engine, these neurons are susceptible to burnout and early death. This discovery emerged from a comparison of energy use in nigral dopamine neurons and in similar neurons found in the nearby ventral tegmental area (VTA), also in the midbrain. “We were trying to understand why dopamine neurons of the substantia nigra die in Parkinson’s disease patients while there are so many other brain cells that have no problem at all,” says Louis-Eric Trudeau, a neuroscientist at the University of Montreal and senior author of the study published in the August 27 Current Biology. © 2015 Scientific American,
Link ID: 21353 - Posted: 08.28.2015
By Emily Underwood It is famous for robbing Lou Gehrig of his life and Stephen Hawking of his mobility and voice, but just how amyotrophic lateral sclerosis (ALS) destroys motor neurons in the brain and spinal cord remains a mystery. Now, scientists are converging on an explanation, at least for a fraction of the ALS cases caused by a specific mutation. In cells with the mutation, the new work shows, pores in the membrane separating the nucleus and cytoplasm become clogged, preventing vital molecules from passing through and creating a fatal cellular traffic jam. For now, the work applies only to the mutation dubbed C9orf72—a DNA stutter in which a short nucleotide sequence, GGGGCC, is repeated hundreds to thousands of times in a gene on chromosome 9. Nor do the multiple labs reporting results this week agree on exactly what plugs those nuclear pores and how the cells die. Still, the work is “a major breakthrough” in ALS research, says Amelie Gubitz, program director of the neurodegeneration division at the National Institute of Neurological Disorders in Bethesda, Maryland. The groups worked independently, starting with different hypotheses and experimental designs, yet reached similar conclusions, making the finding more convincing. And it suggests that boosting traffic through nuclear pores could be a new strategy for treating some cases of ALS and frontotemporal dementia (FTD), another neurodegenerative condition C9orf72 can cause. Based on past work by their own and other groups, neuroscientists Jeff Rothstein and Tom Lloyd at Johns Hopkins University in Baltimore, Maryland, suspected that the long strands of excess RNA produced by C9orf72 cause neurodegeneration by binding to, and thus sequestering, key cellular proteins. The team tested the idea in fruit flies with the mutation, which display damage in the nerve cells of their eyes and in motor neurons. © 2015 American Association for the Advancement of Science
A placebo can make you feel a little better – and now we know how to boost the effect. Drugs based on hormones that make us more cooperative seem to enhance the placebo effect. The finding could lead to changes in the way some trials are performed. Sometimes a sugar pill can be all you need, even when you know it doesn’t contain any medicine. We’re still not entirely sure why. The brain’s natural painkillers, such as dopamine and opioids, seem to be involved, but other factors may be at work too. Evidence that a compassionate, trustworthy carer can speed recovery suggests that there is also a social dimension to the placebo effect. “This interaction between the patient and care provider seems to be based on a more complex system,” says Luana Colloca at the University of Maryland in Baltimore. Hormones that modulate our social behaviour might play a role. Last year, a team led by Ulrike Bingel of the University Duisburg-Essen in Germany, found that oxytocin – the so-called “cuddle chemical” that is thought to help us trust, bond and form relationships – seems to boost the placebo effect, at least in men. In the study, Bingel’s team applied an inert ointment to the arms of male volunteers. Half of them were told that the cream would reduce the degree of pain caused by the painfully hot stimulus subsequently applied. Men who were told that they were receiving pain relief said that the heat was less painful than those who knew that the cream was inert. When oxytocin was squirted up volunteers’ noses, the men reported being in even less pain. The team didn’t test oxytocin in women. © Copyright Reed Business Information Ltd.
By Robert F. Service Move over, poppies. In one of the most elaborate feats of synthetic biology to date, a research team has engineered yeast with a medley of plant, bacterial, and rodent genes to turn sugar into thebaine, the key opiate precursor to morphine and other powerful painkilling drugs that have been harvested for thousands of years from poppy plants. The team also showed that with further tweaks, the yeast could make hydrocodone, a widely used painkiller that is now made chemically from thebaine. “This is a major milestone,” says Jens Nielsen, a synthetic biologist at Chalmers University of Technology in Göteborg, Sweden. The work, he adds, demonstrates synthetic biology’s increasing sophistication at transferring complex metabolic pathways into microbes. By tweaking the yeast pathways, medicinal chemists may be able to produce more effective, less addictive versions of opiate painkillers. But some biopolicy experts worry that morphinemaking yeast strains could also allow illicit drugmakers to brew heroin as easily as beer enthusiasts home brew today—the drug is a simple chemical conversion from morphine. That concern is one reason the research team, led by Christina Smolke, a synthetic biologist at Stanford University in Palo Alto, California, stopped short of making a yeast strain with the complete morphine pathway; medicinal drug makers also primarily use thebaine to make new compounds. Synthetic biologists had previously engineered yeast to produce artemisinin, an antimalarial compound, but that required inserting just a handful of plant genes. To get yeast to make thebaine, © 2015 American Association for the Advancement of Science.
A healthy motor neuron needs to transport its damaged components from the nerve-muscle connection all the way back to the cell body in the spinal cord. If it cannot, the defective components pile up and the cell becomes sick and dies. Researchers at the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS) have learned how a mutation in the gene for superoxide dismutase 1 (SOD1), which causes ALS, leads cells to accumulate damaged materials. The study, published in the journal Neuron, suggests a potential target for treating this familial form of ALS. More than 12,000 Americans have ALS, also known as Lou Gehrig’s disease, and roughly 5-10 percent of them inherited a genetic mutation from a parent. These cases of familial ALS are often caused by mutations in the gene that codes for SOD1, an important enzyme located in the neuron’s mitochondria, the cell’s energy-producing structures. This mutation causes the death of motor neurons that control the patient’s muscles, resulting in progressive paralysis. “About 90 percent of the energy in the brain is generated by mitochondria,” said Zu-Hang Sheng, Ph.D., an NINDS scientist and the study’s senior author. “If the mitochondria aren’t healthy, they produce energy less efficiently; they can also release harmful chemicals called reactive oxygen species that cause cell death. As a consequence, mitochondrial damage can cause neurodegeneration.” In healthy neurons, storage containers called late endosomes collect damaged mitochondria and various destructive chemicals. A motor protein called dynein then transports the endosomes to structures called lysosomes, which use the chemicals to break down the endosomes. Dr. Sheng’s team discovered that this crucial process is faulty in nerve cells with SOD1 mutations because mutant SOD1 interferes with a critical molecule called snapin that hooks the endosome to the dynein motor protein.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 21294 - Posted: 08.13.2015
Richard Harris Hospitals have a free and powerful tool that they could use more often to help reduce the pain that surgery patients experience: music. Scores of studies over the years have looked at the power of music to ease this kind of pain; an analysis published Wednesday in The Lancet that pulls all those findings together builds a strong case. When researchers in London started combing the medical literature for studies about music's soothing power, they found hundreds of small studies suggesting some benefit. The idea goes back to the days of Florence Nightingale, and music was used to ease surgical pain as early as 1914. (My colleague Patricia Neighmond reported on one of these studies just a few months ago). Dr. Catherine Meads at Brunel University focused her attention on 73 rigorous, randomized clinical trials about the role of music among surgery patients. "As they studies themselves were small, they really didn't find all that much," Meads says. "But once we put them all together, we had much more power to find whether music worked or not." She and her colleagues now report that, yes indeed, surgery patients who listened to music, either before, during or after surgery, were better off — in terms of reduced pain, less anxiety and more patient satisfaction. © 2015 NPR
Keyword: Pain & Touch
Link ID: 21293 - Posted: 08.13.2015
Sarah Schwartz In 2011, science journalist Jon Palfreman saw a doctor about a tremor in his left hand. The doctor diagnosed Palfreman, then 60, with Parkinson’s disease. The disorder, which is newly diagnosed in 60,000 Americans each year, promised a crippling future of tremors, loss of mobility, dementia and more. Palfreman decided to use his reporting expertise to investigate how Parkinson’s disease affects the body and learn about efforts to find a cure. With Brain Storms, Palfreman follows Parkinson’s history from the careful observations of 19th century physicians to today’s cutting-edge research. Palfreman relates complex research studies as gripping medical mysteries. He describes how scientists connected Parkinson’s with the dramatic loss of the brain chemical dopamine and with tenacious protein knots called Lewy bodies that are a hallmark of the disease. Palfreman also explores treatments past and present, including the widely used drug levodopa that restores motion (sometimes uncontrollably), gene therapies, brain surgeries and promising experimental antibody treatments that attack and dissolve misfolded Parkinson’s-related proteins. Ultimately, Brain Storms is about more than Parkinson’s disease; it’s about the people living with the disorder. Palfreman describes patients who must teach themselves to walk without falling over or who freeze in place. He writes about a researcher driven to search for a cure after the disease affects his own father. © Society for Science & the Public 2000 - 2015
Link ID: 21284 - Posted: 08.12.2015
Joe Palca The sea snail Conus magus looks harmless enough, but it packs a venomous punch that lets it paralyze and eat fish. A peptide modeled on the venom is a powerful painkiller, though sneaking it past the blood-brain barrier has proved hard. The sea snail Conus magus looks harmless enough, but it packs a venomous punch that lets it paralyze and eat fish. A peptide modeled on the venom is a powerful painkiller, though sneaking it past the blood-brain barrier has proved hard. Courtesy of Jeanette Johnson and Scott Johnson Researchers are increasingly turning to nature for inspiration for new drugs. One example is Prialt. It's an incredibly powerful painkiller that people sometimes use when morphine no longer works. Prialt is based on a component in the venom of a marine snail. Prialt hasn't become a widely used drug because it's hard to administer. Mandë Holford is hoping to change that. She and colleagues explain how in their study published online Monday in the journal Scientific Reports. Holford is an associate professor of chemical biology at Hunter College in New York and on the scientific staff of the American Museum of Natural History. As is so often the case in science, her path to working on Prialt wasn't exactly a direct one. She's a chemist, and her first passion was peptides — short strings of amino acids that do things inside cells. "I started out with this love for peptides," Holford says, then laughs. "Love! Sounds weird to say you love peptides out loud." © 2015 NPR
Keyword: Pain & Touch
Link ID: 21255 - Posted: 08.04.2015
RACHEL MARTIN, HOST: Every day, according to the Centers for Disease Control, 44 Americans die because they have overdosed on prescription painkillers. The CDC calls it an epidemic, and drug companies are responding by trying to develop versions of the most addictive painkillers, opioids, that will diminish a user's physical craving for the medicine. Now, to do this, to create these less addictive drugs, pharmaceutical companies are recruiting thousands of self-identified drug users to test their products. David Crow is a reporter for the Financial Times. He's just published a big report on this, and he joins me now to talk more about it. Thanks so much for being with us. Opioids, as we mentioned, are the worst in terms of their addictive quality. These companies are trying to come up with drugs that will achieve the same painkilling effect without the addictiveness. So this is actually possible? CROW: What they're trying to do is develop a new generation of opioid painkillers that have features that make them harder to abuse. Some of the strategies that have been pursued include hard shells that make it harder to crush up the pill so that you can snort it or gumming agents that make it harder to put into a syringe so that you can inject it. And some companies are experimenting with putting different chemicals in the center of the pill that will remain dormant. But if it's tampered with, that chemical would be released, and it would counteract the effect of the opioid. They're testing these drugs on recreational drug users. And the participants go through a screening process where they have to wash out, where they don't have any opioid in their system, and also where they're given a drug called naloxone, which cuts off the effects of opioids. And at that point, if you were addicted or physically dependent, your body would show signs of withdrawal. And that is the screening process. © 2015 NPR
By David Noonan Leaping through the air with ease and spinning in place like tops, ballet dancers are visions of the human body in action at its most spectacular and controlled. Their brains, too, appear to be special, able to evade the dizziness that normally would result from rapid pirouettes. When compared with ordinary people's brains, researchers found in a study published early this year, parts of dancers' brains involved in the perception of spinning seem less sensitive, which may help them resist vertigo. For millions of other people, it is their whole world, not themselves, that suddenly starts to whirl. Even the simplest task, like walking across the room, may become impossible when vertigo strikes, and the condition can last for months or years. Thirty-five percent of adults older than 39 in the U.S.—69 million people—experience vertigo at one time or another, often because of damage to parts of the inner ear that sense the body's position or to the nerve that transmits that information to the brain. Whereas drugs and physical therapy can help many, tens of thousands of people do not benefit from existing treatments. “Our patients with severe loss of balance have been told over and over again that there's nothing we can do for you,” says Charles Della Santina, an otolaryngologist who studies inner ear disorders and directs the Johns Hopkins Vestibular NeuroEngineering Laboratory. Steve Bach's nightmare started in November 2013. The construction manager was at home in Parsippany, N.J. “All of a sudden the room was whipping around like a 78 record,” says Bach, now age 57. He was curled up on the living room floor in a fetal position when his daughter found him and called 911. He spent the next five days in the hospital. © 2015 Scientific American
Keyword: Movement Disorders
Link ID: 21248 - Posted: 08.01.2015