Chapter 8. General Principles of Sensory Processing, Touch, and Pain
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
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
By Sarah C. P. Williams Looking at photos of starving refugees or earthquake victims can trigger a visceral sense of empathy. But how, exactly, do we feel others’ agony as our own? A new study suggests that seeing others in pain engages some of the same neural pathways as when we ourselves are in pain. Moreover, both pain and empathy can be reduced by a placebo effect that acts on the same pathways as opioid painkillers, the researchers found. “This study provides one of the most direct demonstrations to date that first-hand pain and pain empathy are functionally related,” says neurobiologist Bernadette Fitzgibbon of Monash University in Melbourne, Australia, who was not involved in the new research. “It’s very exciting.” Previous studies have used functional magnetic resonance imaging (fMRI) scans to show that similar areas of the brain are activated when someone is in pain and when they see another person in pain. But overlaps on a brain scan don’t necessarily mean the two function through identical pathways—the shared brain areas could relate to attention or emotional arousal, among other things, rather than pain itself. Social neuroscientist Claus Lamm and colleagues at the University of Vienna took a different approach to test whether pain and empathy are driven by the same pathways. The researchers first divided about 100 people into control or placebo groups. They gave the placebo group a pill they claimed to be an expensive, over-the-counter painkiller, when in fact it was inactive. This well-established placebo protocol is known to function similarly to opioid painkillers, while avoiding the drugs’ side effects. © 2015 American Association for the Advancement of Science.
By Jane E. Brody Mark Hammel’s hearing was damaged in his 20s by machine gun fire when he served in the Israeli Army. But not until decades later, at 57, did he receive his first hearing aids. “It was very joyful, but also very sad, when I contemplated how much I had missed all those years,” Dr. Hammel, a psychologist in Kingston, N.Y., said in an interview. “I could hear well enough sitting face to face with someone in a quiet room, but in public, with background noise, I knew people were talking, but I had no idea what they were saying. I just stood there nodding my head and smiling. “Eventually, I stopped going to social gatherings. Even driving, I couldn’t hear what my daughter was saying in the back seat. I live in the country, and I couldn’t hear the birds singing. “People with hearing loss often don’t realize what they’re missing,” he said. “So much of what makes us human is social contact, interaction with other human beings. When that’s cut off, it comes with a very high cost.” And the price people pay is much more than social. As Dr. Hammel now realizes, “the capacity to hear is so essential to overall health.” Hearing loss is one of the most common conditions affecting adults, and the most common among older adults. An estimated 30 million to 48 million Americans have hearing loss that significantly diminishes the quality of their lives — academically, professionally and medically as well as socially. One person in three older than 60 has life-diminishing hearing loss, but most older adults wait five to 15 years before they seek help, according to a 2012 report in Healthy Hearing magazine. And the longer the delay, the more one misses of life and the harder it can be to adjust to hearing aids. © 2015 The New York Times Company
By Simon Makin Most people associate the term “subliminal conditioning” with dystopian sci-fi tales, but a recent study has used the technique to alter responses to pain. The findings suggest that information that does not register consciously teaches our brain more than scientists previously suspected. The results also offer a novel way to think about the placebo effect. Our perception of pain can depend on expectations, which explains placebo pain relief—and placebo's evil twin, the nocebo effect (if we think something will really hurt, it can hurt more than it should). Researchers have studied these expectation effects using conditioning techniques: they train people to associate specific stimuli, such as certain images, with different levels of pain. The subjects' perception of pain can then be reduced or increased by seeing the images during something painful. Most researchers assumed these pain-modifying effects required conscious expectations, but the new study, from a team at Harvard Medical School and the Karolinska Institute in Stockholm, led by Karin Jensen, shows that even subliminal input can modify pain—a more cognitively complex process than most that have previously been discovered to be susceptible to subliminal effects (timeline below). The scientists conditioned 47 people to associate two faces with either high or low pain levels from heat applied to their forearm. Some participants saw the faces normally, whereas others were exposed subliminally—the images were flashed so briefly, the participants were not aware of seeing them, as verified by recognition tests. © 2015 Scientific American
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
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
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
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.
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
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
Mo Costandi When we say that we are “in pain”, we usually mean that an injured body part is hurting us. But the phenomenon we call pain consists of more than just physical sensations, and often has mental and emotional aspects, too. Pain signals entering the black box of the brain can be subjected further processing, and these hidden thought processes can alter the way we perceive them. We still know very little about these non-physical aspects of pain, or about the brain processes responsible for them. We do know, however, that learning and mental imagery can both diminish and enhance the experience of felt pain. Two new studies now extend these findings – one shows that subliminal learning can also alter pain responses, and the other explains how mental imagery can do so. It’s well known that simple associative learning procedures can alter responses to pain. For example, newborn babies who have diabetic mothers and are repeatedly exposed to heel pricks in the first few days of life exhibit larger pain responses during subsequent blood tests than healthy infants. Learning also appears to explain the placebo effect, and why it is often so variable. Several years ago, Karin Jensen, who is now at Harvard Medical School, and her colleagues showed that subliminal cues can reactivate consciously-learned associations to either enhance or diminish pain responses. In their latest study, the researchers set out to determine the extent to which this type of learning can occur non-consciously. © 2015 Guardian News and Media Limited
Victoria E Brings & Mark J Zylka A study finds that pain hypersensitivity in male and female mice is differentially dependent on microglia and T cells, and describes a sex-specific response to microglia-targeted pain treatments. This sex difference will be important to consider when developing treatments for pain and other neurological disorders involving microglia and immune cells. Animal studies1, 2 have spawned great interest in using microglial inhibitors such as minocycline to treat pain in humans. However, these studies were conducted largely on male rodents. Now, Sorge et al.3 have evaluated several microglial inhibitors in nerve-injured mice of both sexes. The study—led by Jeffrey Mogil, who has championed the testing of males and females in pain studies4—found that microglial inhibitors did reduce allodynia, a form of pain hypersensitivity to touch, in males. Surprisingly, however, these inhibitors were ineffective in female mice, despite a robust activation of spinal microglia (Fig. 1). The authors instead found that cells of the adaptive immune system promote pain hypersensitivity in females. Although focused on pain, these findings could have implications for other neurological disorders that disproportionately affect one sex, such as autism and neurodegeneration, and in which microglia and immune cells are implicated5, 6. Figure 1: Pain mechanisms differ in male and female mice. Pain mechanisms differ in male and female mice. Nerve injury activates microglial cells in the spinal cord of male and female mice, but microglial inhibitors only block allodynia in males. P2RX4 is upregulated in males only. Female mice have about twice as many T cells as males. Testosterone increases PPARα and decreases PPARγ gene expression in T cells. Compounds that activate PPARα inhibit mechanical pain hypersensitivity (allodynia) in males, whereas those that activate PPARγ inhibit allodynia in females. © 2015 Macmillan Publishers Limited
By Annick Laurent Can you tell a pygmy blue whale from an Antarctic blue whale? If not, you aren’t alone. Marine biologists have had trouble distinguishing these enormous mammals with mottled skin patterns ever since they began studying them—and that has complicated efforts to figure out where they breed and how to best protect them. Now, researchers have caught a break thanks to a pygmy whale named Isabela. Researchers first photographed the whale and collected her DNA in 1998 in the waters off the Galapagos Islands. Then, in 2006, another team photographed and collected samples from a similar looking whale off Chile (both photos above). Now, in a study published online before print in Marine Mammal Science, scientists compared those samples and photographs, and discovered that they both belonged to the same whale. That means Isabela (named after the lead author’s daughter to represent hope for future preservation efforts) migrated a minimum of 5200 km, the longest recorded latitudinal migration made by any Southern Hemisphere blue whale on record. The findings suggest Chile's and the Galapagos’ blue whale aggregations are connected, meaning those feeding in the Gulf of Corcovado off Chile may be breeding in the Tropical Eastern Pacific. Knowing where this species migrates—including its feeding and breeding grounds—can help conservationists and governments better establish marine protected areas, the team says. © 2015 American Association for the Advancement of Science
Keyword: Animal Migration
Link ID: 21213 - Posted: 07.25.2015
By Sarah Schwartz Scientists think they have a new understanding of a potential long-lasting, targeted treatment for chronic pain. When injected into the spinal cord of a mouse with nerve damage, cells extracted from mouse bone marrow flock to injured cells and produce a pain-relieving protein, researchers report July 13 in the Journal of Clinical Investigation. The results may lead to better chronic pain treatments in humans. The specialized cells honed in on their ultimate destination by following chemical signals released by the injured nerve cells. There, the injected cells produced an anti-inflammatory protein, called transforming growth factor beta 1 (TGFB1), which provided long-term pain relief. Researchers had known that the marrow cells relieved pain, but didn’t know how, says study coauthor Ru-Rong Ji, a neurobiologist at Duke University Medical Center. “These cells make drugs at sites of injury,” says biologist Arnold Caplan of Case Western Reserve University in Cleveland. “They’re drugstores.” Ji and colleagues found that they could relieve chronic nerve pain in mice by injecting 250,000 cells or fewer into the narrow space under the spinal cord membrane. This site is protected by the blood-brain barrier, preventing immune attacks on the injected cells and allowing these cells to live longer, Ji says. Some clinical trials inject cells like these into the bloodstream, Caplan says, requiring the use of many more cells, many of which get stuck in the lungs and liver. © Society for Science & the Public 2000 - 2015
Keyword: Pain & Touch
Link ID: 21167 - Posted: 07.14.2015
By Esther Hsieh Strap on a headset, immerse yourself in an alternate reality and cure your pain—that's the idea of a recent study in Psychological Science. Most people think of pain as something that happens in the body—I twist my head too far, and my neck sends a “pain signal” to the brain to indicate that the twisting hurts. In reality, pain is simply the brain telling us we are in danger. Although certain nerve endings throughout the body can indeed detect bodily harm, their signals are only one factor that the brain uses to determine if we should experience pain. Many cases of chronic pain are thought to be the result of obsolete brain associations between movement and pain. To explore the mind's influence over pain, Daniel Harvie, a Ph.D. candidate at the University of South Australia, and his colleagues asked 24 participants who suffer from chronic neck pain to sit in a chair while wearing virtual-reality glasses and turn their head. The displays were manipulated to make the participants think that they were turning their head more or less than they actually were. Subjects could swivel their head 6 percent more than usual if the virtual reality made them think they were turning less, and they could rotate 7 percent less than usual when they thought they were turning more. The findings suggest that virtual-reality therapy has the potential to retrain the brain to understand that once painful movements are now safe, extinguishing the association with danger. © 2015 Scientific American
Keyword: Pain & Touch
Link ID: 21155 - Posted: 07.11.2015