Chapter 5. The Sensorimotor System
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David Cyranoski A Chinese neuroscientist has been sacked after reporting he had used magnetic fields to control neurons and muscle cells in nematode worms (pictured), using a protein that senses magnetism. Tsinghua University in Beijing has sacked a neuroscientist embroiled in a dispute over work on a long-sought protein that can sense magnetic fields. The university has not given a specific reason for its dismissal, however, and the scientist involved, Zhang Sheng-jia, says that he will contest their action. In September, Zhang reported in the journal Science Bulletin1 that he could manipulate neurons in worms by applying a magnetic field — a process that uses a magnetic-sensing protein. But a biophysicist at neighbouring Peking University, Xie Can, who claims to have discovered the protein’s magnetic-sensing capacity and to have a paper detailing his research under review, complained that Zhang should not have published his paper before Xie’s own work appeared. Xie said that by publishing, Zhang violated an agreement that the pair had reached — although the two scientists tell different versions about the terms of their agreement, and have different explanations of how Zhang came to be working with the protein. © 2015 Nature Publishing Group
Keyword: Animal Migration
Link ID: 21608 - Posted: 11.06.2015
By SINDYA N. BHANOO Some kinds of itching can be caused by the lightest of touches, a barely felt graze that rustles tiny hairs on the skin’s surface. This type of itch is created via a dedicated neural pathway, a new study suggests. The finding, which appears in the journal Science, could help researchers better understand chronic itchiness in conditions like eczema, diabetic neuropathy, multiple sclerosis and some cancers. The study also may help researchers determine why certain patients do not respond well to antihistamine drugs. “In the future, we may have some way to manipulate neuron activity to inhibit itching,” said Quifu Ma, a neurobiologist at Harvard University and one of the study’s authors. In the study, Dr. Ma and his colleagues inhibited neurons that express a neuropeptide known as Y or NPY in mice. When these neurons were suppressed and the mice were poked with a tiny filament, they fell into scratching fits. Normally, mice would not even respond to this sort of stimuli. “We start to see skin lesions — they don’t stop scratching,” Dr. Ma said. “It’s pretty traumatic.” The neurons only seem related to itches prompted by light touching, known as mechanically induced itches. Chemical itches, like those caused by a mosquito bite or an allergic reaction, are not transmitted by the same neurons. © 2015 The New York Times Company
Keyword: Pain & Touch
Link ID: 21593 - Posted: 11.03.2015
By Hanae Armitage Fake fingerprints might sound like just another ploy to fool the feds. But the world’s first artificial prints—reported today—have even cooler applications. The electronic material, which mimics the swirling designs imprinted on every finger, can sense pressure, temperature, and even sound. Though the technology has yet to be tested outside the lab, researchers say it could be key to adding sensation to artificial limbs or even enhancing the senses we already have. “It’s an interesting piece of work,” says John Rogers, materials scientist at the University of Illinois, Urbana-Champaign, who was not involved in the study. “It really adds to the toolbox of sensor types that can be integrated with the skin.” Electronic skins, known as e-skins, have been in development for years. There are several technologies used to mimic the sensations of real human skin, including sensors that can monitor health factors like pulse or temperature. But previous e-skins have been able to “feel” only two sensations: temperature and pressure. And there are additional challenges when it comes to replicating fingertips, especially when it comes to mimicking their ability to sense even miniscule changes in texture, says Hyunhyub Ko, a chemical engineer at Ulsan National Institute of Science and Technology in South Korea. So in the new study, Ko and colleagues started with a thin, flexible material with ridges and grooves much like natural fingerprints. This allowed them to create what they call a “microstructured ferroelectric skin” The e-skin’s perception of pressure, texture, and temperature all come from a highly sensitive structure called an interlocked microdome array—the tiny domes sandwiched in the bottom two layers of the e-skin, also shown in the figure below. © 2015 American Association for the Advancement of Science
Laura Sanders A fly tickling your arm hair can spark a maddening itch. Now, scientists have spotted nerve cells in mice that curb this light twiddling sensation. If humans possess similar itch-busters, the results, published in the Oct. 30 Science, could lead to treatments for the millions of people who suffer from intractable, chronic itch. For many of these people, there are currently no good options. “This is a major problem,” says clinician Gil Yosipovitch of Temple University School of Medicine in Philadelphia and director of the Temple Itch Center. The new study shows that mice handle an itch caused by a fluttery touch differently than other kinds of itch. This distinction “seems to have clinical applications that clearly open our field,” Yosipovitch says. In recent years, scientists have made progress teasing apart the pathways that carry itchy signals from skin to spinal cord to brain (SN: 11/22/2008, p. 16). But those itch signals often originate from chemicals, such as those delivered by mosquitoes. All that’s needed to spark a different sort of itch, called mechanical itch, is a light touch on the skin. The existence of this kind of itch is no surprise, Yosipovitch says. Mechanical itch may help explain why clothes or even dry, scaly skin can be itchy. The new finding came from itchy mice engineered to lack a type of nerve cell in their spinal cords. Without prompting, these mice scratched so often that they developed sore bald patches on their skin. © Society for Science & the Public 2000 - 2015
Keyword: Pain & Touch
Link ID: 21587 - Posted: 10.31.2015
Adam Cole Watch a scary movie and your skin crawls. Goose bumps have become so associated with fear that the word is synonymous with thrills and chills. But what on earth does scary have do to with chicken-skin bumps? For a long time, it wasn't well understood. Physiologically, it's fairly simple. Adrenaline stimulates tiny muscles to pull on the roots of our hairs, making them stand out from our skin. That distorts the skin, causing bumps to form. Call it horripilation, and you'll be right — bristling from cold or fear. Charles Darwin once investigated goose bumps by scaring zoo animals with a stuffed snake. He argued for the now accepted theory that goose bumps are a vestige of humanity's ancient past. Our ancestors were hairy. Goose bumps would have fluffed up their hair. When they were scared, that would have made them look bigger — and more intimidating to attackers. When they were cold, that would have trapped an insulating layer of air to keep them warm. We modern humans still get goose bumps when we're scared or cold, even though we've lost the advantage of looking scarier or staying warmer ourselves. And researchers have found that listening to classical music (or Phil Collins), seeing pictures of children or drinking a sour drink can also inspire goose bumps. There's clearly a link with emotion and reward, too. © 2015 npr
By Diana Kwon Six years before her husband was diagnosed with Parkinson’s disease, a progressive neurodegenerative disorder marked by tremors and movement difficulties, Joy Milne detected a change in his scent. She later linked the subtle, musky odor to the disease when she joined the charity Parkinson’s UK and met others with the same, distinct smell. Being one of the most common age-related disorders, Parkinson’s affects an estimated seven million to 10 million people worldwide. Although there is currently no definitive diagnostic test, researchers hope that this newly found olfactory signature will lead help create one. Milne, a super-smeller from Perth, Scotland, wanted to share her ability with researchers. So when Tilo Kunath, a neuroscientist at the University of Edinburgh, gave a talk during a Parkinson’s UK event in 2012, she raised her hand during the Q&A session and claimed she was able to smell the disease. “I didn’t take her seriously at first,” Kunath says. “I said, ‘No, I never heard of that, next question please.’” But months later Kunath shared this anecdote with a colleague and received a surprising response. “She told me that that lady wasn’t wrong and that I should find her,” Kunath says. Once the researchers found Milne, they tested her claim by having her sniff 12 T-shirts: six that belonged to people with Parkinson’s and six from healthy individuals. Milne correctly identified 11 out of 12, but miscategorized one of the non-Parkinson’s T-shirts in the disease category. It turned out, however, she was not wrong at all—that person would be diagnosed with Parkinson’s less than a year later. © 2015 Scientific American
By Diana Kwon | In the human form of mad cow disease, called Creutzfeldt-Jakob, a person's brain deteriorates—literally developing holes that cause rapidly progressing dementia. The condition is fatal within one year in 90 percent of cases. The culprits behind the disease are prions—misfolded proteins that can induce normal proteins around them to also misfold and accumulate. Scientists have known that these self-propagating, pathological proteins cause some rare brain disorders, such as kuru in Papua New Guinea. But growing evidence suggests that prions are at play in many, if not all, neurodegenerative disorders, including Alzheimer's, Huntington's and Parkinson's, also marked by aggregations of malformed proteins. Until recently, there was no evidence that the abnormal proteins found in people who suffer from these well-known diseases could be transmitted directly from person to person. The tenor of that discussion suddenly changed this September when newly published research in the journal Nature provided the first hint such human-to-human transmission may be possible. (Scientific American is part of Springer Nature.) For the study, John Collinge, a neurologist at University College London, and his colleagues conducted autopsies on eight patients who died between the ages of 36 and 51 from Creutzfeldt-Jakob. All the subjects had acquired the disease after treatment with growth hormone later found to be contaminated with prions. The surprise came when the researchers discovered that six of the brains also bore telltale signs of Alzheimer's—in the form of clumps of beta-amyloid proteins, diagnostic for the disease—even though the patients should have been too young to exhibit such symptoms. © 2015 Scientific American,
by Helen Thompson Five, six, seven, eight! All together now, let's spread those jazz hands and get moving, because synchronized dancing improves our tolerance of pain and helps us bond as humans, researchers suggest October 28 in Biology Letters. A team of psychologists at the University of Oxford taught high school students varied dance routines — each requiring different levels of exertion and synchronized movement — and then tested their pain tolerance with the sharp squeeze of a blood pressure cuff. Statistically, routines with more coordinated choreography and full body movement produced higher pain thresholds and sunny attitudes toward others in the group. Coordinated dancing with a group and exerting more energy may independently promote the release of pain-blocking endorphins as well as increase social bonding, the team writes. |© Society for Science & the Public 2000 - 2015
Keyword: Pain & Touch
Link ID: 21575 - Posted: 10.28.2015
By Hanae Armitage CHICAGO, ILLINOIS—Huntingtons disease, a neurological condition caused by brain-destroying mutant proteins, starts with mood swings and twitching and ends in dementia and death. The condition, which afflicts about 30,000 Americans, has no cure. But now, a new gene-editing method that many believe will lead to a Nobel Prize has been shown to effectively halt production of the defective proteins in mice, leading to hope that a potent therapy for Huntingtons is on the distant horizon. That new method is CRISPR, which uses RNA-guided enzymes to snip out or add segments of DNA to a cell. In the first time it has been applied to Huntingtons disease, CRISPR’s results are “remarkably encouraging,” says neuroscientist Nicole Déglon of the University of Lausanne in Switzerland, who led the mouse study, results of which she and her co-researcher Nicolas Merienne shared yesterday at the Society for Neuroscience Conference in Chicago, Illinois. As neurological diseases go, Huntingtons is an ideal candidate for CRISPR therapy, because the disease is determined by a single gene, Déglon notes. A mutation in the gene, which codes for a normally helpful brain protein called huntingtin, consists of different numbers of “tandem repeats,” repeating segments of DNA that cause the protein to fold into a shape that is toxic to the brain. Déglon and her team wondered whether CRISPR could halt production of this dangerous molecule. Using a virus as a delivery vehicle, the researchers infected two separate groups of healthy adult mice with a mutant huntingtin gene, but only one group received the therapy: a CRISPR “cassette,” which includes DNA for the gene-editing enzyme Cas9 and the RNA to target the huntingtin gene. © 2015 American Association for the Advancement of Science
Link ID: 21538 - Posted: 10.21.2015
Alan Hoffman says nilotinib has changed his life. Just weeks after he started taking the drug in a clinical trial, he began to feel himself recovering from his Parkinson’s disease. The retired professor of social science first started to show the signs of Parkinson’s in 1997. Over the years, his symptoms worsened. “I couldn’t get out of bed without my wife,” Hoffman says. Once a prolific reader, devouring four or five books a week, Hoffman found himself unable to keep his attention on even a short magazine article. His body became increasingly rigid, and he started to lose his sense of balance. “I fell a lot,” he says. And it affected his social life. The disorder was such a struggle, Hoffman says he considered taking his own life. He tried a range of medications, which eased his symptoms to varying degrees. In 2008, he had surgery to implant an electrode into his brain. The deep brain stimulation that followed helped with the rigidity, he says. But deep brain stimulation doesn’t offer a cure – the brain cells continue to die. So Hoffman agreed to join a six-month clinical trial of nilotinib – a drug typically used to treat leukaemia. Nilotinib blocks a protein that interferes with lysosomes – cell structures that destroy harmful proteins. Researchers behind the trial think that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. (For a full report on the effect of the drug see “People with Parkinson’s walk again after promising drug trial”.) © Copyright Reed Business Information Ltd.
Link ID: 21537 - Posted: 10.21.2015
Mr Tickle can’t bamboozle a baby. Unlike grown-ups, young infants don’t let the positioning of their bodies confuse their sense of touch. If adults who can see are touched on each hand in quick succession while their hands are crossed, they can find it hard to name which hand was touched first. Adults who have been blind from birth don’t have this difficulty, but people who become blind later in life have the same trouble as those who can still see. “That suggests that early on in life, something to do with visual experience is crucial in setting up a typical way of perceiving touch,” says Andrew Bremner at Goldsmiths, University of London. To investigate how this develops in infancy, Bremner and his colleagues compared how babies reacted to having one foot tickled. With their legs crossed over, babies aged 6 months moved the foot being tickled half of the time. But 4-month-olds did better, moving the tickled foot 70 per cent of the time – as often as they did with their legs uncrossed. The team concludes that at 4 months, babies haven’t yet learned to relate what they touch to the physical space that their body occupies. For many adults, the concept might be difficult to envision. “It’s like imagining that you feel a touch on your body, but not really knowing how that’s related to what you’re looking at,” says Bremner. “It’s almost like you have multiple sensory worlds: a visual world, an auditory world and a tactile world, which are separate and not combined in space.” © Copyright Reed Business Information Ltd.
An expensive cancer drug may reverse late-stage Parkinson’s disease, enabling participants in a small clinical trial to speak and walk again for the first time in years. While there are several treatments for the symptoms of Parkinson’s, if confirmed this would be the first time a drug has worked on the causes of the disease. “We’ve seen patients at end stages of the disease coming back to life,” says Charbel Moussa of Georgetown University Medical Center in Washington DC, who led the trial. The drug, called nilotinib, works by boosting the brain’s own “garbage disposal system” to clear proteins that accumulate in the brains of people with Parkinson’s disease, says Moussa. These proteins are thought to trigger the death of brain cells that make molecules like dopamine that are needed for movement and other functions. Nilotinib is already approved to treat cancer – it blocks a protein that drives chronic myeloid leukaemia. It also blocks another protein that interferes with lysosomes – cell structures that destroy harmful proteins. Moussa thinks that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. Tests in animals showed promise, so Moussa, his colleague Fernando Pagan and their team set up a small trial of 12 volunteers with Parkinson’s disease or a similar condition called dementia with Lewy bodies. The trial was designed to test only the safety of the oral drug, which was given as a daily dose for six months. © Copyright Reed Business Information Ltd.
Link ID: 21528 - Posted: 10.20.2015
Three teams of scientists supported by the National Institutes of Health showed that a genetic mutation linked to some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD) may destroy neurons by disrupting the movement of materials in and out of the cell’s nucleus, or command center where most of its DNA is stored. The results, published in the journals Nature and NatureNeuroscience, provide a possible strategy for treating the two diseases. “This research shines a spotlight on the role of nuclear transport in the health of neurons,” said Amelie Gubitz, Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “The results provide new insights into how this mutation derails an essential process in neurons and opens new avenues for therapy development.” Both ALS and FTD are caused by the death of specific neurons. In ALS, this leads to movement difficulties and eventually paralysis, while in FTD, patients experience problems with language and decision making. Past research has connected a specific mutation in the C9orf72 gene to 40 percent of inherited ALS cases and 25 percent of inherited FTD cases, as well as nearly 10 percent of non-inherited cases of each disorder. The recent experiments, conducted in yeast, fruit flies, and neurons from patients, found that the mutation prevents proteins and genetic material called RNA from moving between the nucleus and the cytoplasm that surrounds it. “At the end of the day, this culminates in a defect in the flow of genetic information, which leads to problems expressing genes in the right place at the right time,” said J. Paul Taylor, M.D., Ph.D., a researcher at St. Jude’s Children’s Research Hospital in Memphis, Tennessee, and the senior author of one of the papers.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 21524 - Posted: 10.17.2015
By Robert F. Service Prosthetic limbs may work wonders for restoring lost function in some amputees, but one thing they can’t do is restore an accurate sense of touch. Now, researchers report that one day in the not too distant future, those artificial arms and legs may have a sense of touch closely resembling the real thing. Using a two-ply of flexible, thin plastic, scientists have created novel electronic sensors that send signals to the brain tissue of mice that closely mimic the nerve messages of touch sensors in human skin. Multiple research teams have long worked on restoring touch to people with prosthetic limbs. 2 years ago, for example, a group at Case Western Reserve University in Cleveland, Ohio, reported giving people with prosthetic hands a sense of touch by wiring pressure sensors on the hands to peripheral nerves in their arms. Yet although these advances have restored a rudimentary sense of touch, the sensors and signals are very different from those sent by mechanoreceptors, natural touch sensors in the skin. For starters, natural mechanoreceptors put out what amounts to a digital signal. When they sense pressure, they fire a stream of nerve impulses; the more pressure, the higher the frequency of pulses. But previous tactile sensors have been analogue devices, where more pressure produces a stronger electrical signal, rather than a more frequent stream of pulses. The electrical signals must then be sent to another processing chip that converts the strength of the signals to a digital stream of pulses that is only then sent on to peripheral nerves or brain tissue. © 2015 American Association for the Advancement of Science.
By Nicholas Bakalar Physical therapy may provide little relief for recent-onset low back pain, a small randomized trial has found. The study, published in JAMA, included 207 men and women, average age 37, with a score of 20 or higher on a widely used 100-point scale that quantifies disability from low back pain. The study included people with recent-onset pain who were assigned to one of two groups. The first received four sessions of exercise and manipulation under the guidance of a trained physical therapist. Those in the other group were told that low back pain usually gets better, and were advised to be as active as possible. There were no significant differences at any time in pain intensity, quality of life or the number of visits to health care providers. Compared with the usual care group, the physical therapy group did show significant improvement on the disability scale after three months. But after one year, there was no difference between the two groups in this measure either. “Most treatments that are effective have only modest effects,” said the lead author, Julie M. Fritz, a professor in the department of physical therapy at the University of Utah. “The pattern of low back pain is one of recurrence and remission, and changing that pattern is a real challenge. There are no magic answers.” © 2015 The New York Times Company
Keyword: Pain & Touch
Link ID: 21513 - Posted: 10.15.2015
By Gretchen Reynolds Can a shot of salt water make you a faster runner? The answer appears to be a resounding yes, if you believe that the salt water contains something that should make you a faster runner, according to a new study of the power of placebos in athletic performance. Anyone who exercises knows from experience that our minds and mental attitudes affect physical performance. Who hasn’t faced a moment when, tiring at the end of a strenuous workout or race, we are about to quit before suddenly being passed on the path or shown up in the gym by someone we know we should outperform, and somehow we find an extra, unexploited gear and spurt on? This phenomenon is familiar to physiologists, many of whom believe that our brains, in order to protect our bodies, send out signals telling those bodies to quit before every single resource in our muscles and other tissues is exhausted. We think we are at the outer limits of our endurance or strength, when, in reality, we may still have a physical reserve available to us, if we can find a way to tap it. Past studies have shown that lying to people is one way to exploit that reserve. Telling athletes that they are moving slower than in fact they are, for instance, often results in their speeding up past the pace that they thought they could maintain. Or give them a sugar pill that they think contains caffeine or steroids and they will run more swiftly or lift more weight than before. But none of these studies tested the effects of placebos and deception in relatively real-world competitive situations, which have their own effects on mental responses. People are almost always faster during competitive races than in training, studies show, even when they are trying to replicate race pace. © 2015 The New York Times Company
Keyword: Pain & Touch
Link ID: 21509 - Posted: 10.14.2015
By Christopher Intagliata If you're lost, you need a map and a compass. The map pinpoints where you are, and the compass orients you in the right direction. Migratory birds, on the other hand, can traverse entire hemispheres and end up just a couple miles from where they bred last year, using their senses alone. Their compass is the Sun, the stars and the Earth's magnetic field. But their map is a little more mysterious. One theory goes that they use olfactory cues—how a place smells. Another is that they rely on their sense of magnetism. Researchers in Russia investigated the map issue in a past study by capturing Eurasian reed warblers on the Baltic Sea as they flew northeast towards their breeding grounds near Saint Petersburg. They moved the birds 600 miles east, near Moscow. And the birds just reoriented themselves to the northwest—correctly determining their new position. Now the same scientists have repeated that experiment—only this time, they didn't move the birds at all. They just put them in cages that simulated the magnetic field of Moscow, while still allowing the birds to experience the sun, stars and smells of the Baltic. Once again, the birds re-oriented themselves to the northwest—suggesting that the magnetic field alone—regardless of smells or other cues, is enough to alter the birds' mental map. The study is in the journal Current Biology. [Dmitry Kishkinev et al, Eurasian reed warblers compensate for virtual magnetic displacement] And if you're envious of that sixth sense—keep in mind that since the Earth's magnetic field fluctuates, the researchers say magnetic route-finding is best for crude navigation. Meaning for door-to-door directions—you’re still better off with your GPS. © 2015 Scientific American,
Keyword: Animal Migration
Link ID: 21508 - Posted: 10.14.2015
By Nancy Szokan Sensory deprivation is Sushma Subramanian’s topic in the October issue of Women’s Health magazine, and she offers a couple of extreme examples. Julie Malloy, 33, from York, Pa., describes living without the sense of touch: “I was born with a rare sensory illness that leaves me unable to feel pain, temperature, deep pressure, or vibrations in my arms, legs, and the majority of my chest and back. I use vision to compensate as much as I can. . . . “I always wash my face with cold water; I once burned myself without realizing it. . . . When I drive, I can’t really tell how hard I’m pushing on the pedals. I watch others really enjoy it when someone kisses their arm or get tingly when someone hugs them, but I can’t even feel anything during sex.” Erin Napoleone, 31, from Havre de Grace, Md., describes losing her sense of smell: “As a teen, I was in a car accident. A few days later, I watched my father make homemade tomato sauce — but I didn’t smell a thing. Then I couldn’t detect my mom’s familiar perfume. A head CT scan confirmed my sense of smell was gone for good.” The magazine points out that some senses naturally deteriorate with age and that taking care of your skin — say, by keeping it moisturized and protecting it from damage — can help preserve the sense of touch. But olfactory nerves facing “prolonged exposure to rank odors (think freeway fumes or curbside trash)” can be permanently damaged.
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
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