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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

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
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

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 5: The Sensorimotor System
Link ID: 21509 - 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.

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 21504 - Posted: 10.13.2015

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.

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
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,

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
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.

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21458 - Posted: 09.29.2015

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

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 14: Attention and Consciousness
Link ID: 21438 - Posted: 09.24.2015

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

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 5: The Sensorimotor System
Link ID: 21411 - Posted: 09.15.2015

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.

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
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.

Related chapters from BP7e: Chapter 5: Hormones and the Brain; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 5: The Sensorimotor System
Link ID: 21336 - Posted: 08.25.2015

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

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
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

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 21255 - Posted: 08.04.2015

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

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21247 - Posted: 08.01.2015

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

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 8: Hormones and Sex
Link ID: 21229 - Posted: 07.29.2015

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

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
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

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 21155 - Posted: 07.11.2015

Moheb Costandi Different immune cells regulate pain sensitization in male and female mice, according to research published on 29 June in Nature Neuroscience1. The surprising biological divide may explain why some clinical trials of pain drugs have failed, and highlights shortcomings in the way that many researchers design their experiments. The immune system has important roles in chronic pain, with cells called microglia being key players. Microglia express a protein called brain-derived neurotrophic factor (BDNF) to signal to spinal-cord neurons. When injury or inflammation occurs, this signal sensitizes the body to pain, so that even light touch hurts. Robert Sorge, a psychologist at the University of Alabama in Birmingham, and his colleagues induced persistent pain and inflammation in healthy male and female mice by severing two of the three sciatic nerve branches in their hind paws. Seven days later, they injected the animals with one of three drugs that inhibit microglial function. They found that all three drugs reversed pain sensitization in the male animals, as had been previously reported. But the treatments had no effect on the females, even though the animals had displayed equivalent levels of pain. The researchers also genetically engineered mice in which the BDNF gene could be deleted in microglia at any time during the animals' lives. At first, these animals exhibited normal responses to a nerve injury. Killing the microglia one week later extinguished that hypersensitivity in the male animals, but not in the females. This confirmed that in males, hypersensitivity to pain depends on BDNF signals from microglia, but that in females it is mediated by some other mechanism. © 2015 Nature Publishing Group,

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 8: Hormones and Sex
Link ID: 21113 - Posted: 06.30.2015

Patricia Neighmond We all know that listening to music can soothe emotional pain, but Taylor Swift, Jay-Z and Alicia Keys can also ease physical pain, according to a study of children and teenagers who had major surgery. The analgesic effects of music are well known, but most of the studies have been done with adults and most of the music has been classical. Now a recent study finds that children who choose their own music or audiobook to listen to after major surgery experience less pain. The catalyst for the research was a very personal experience. Sunitha Suresh was a college student when her grandmother had major surgery and was put in intensive care with three other patients. This meant her family couldn't always be with her. So they decided to put her favorite south Indian classical Carnatic music on an iPod, so she could listen around the clock. It was very calming, Sunitha says. "She knew that someone who loved her had left that music for her and she was in a familiar place." This may be the most efficient way to get in shape, but it may also be the least fun. Suresh could see the music relaxed her grandmother and made her feel less anxious, but she wondered if she also felt less pain. That would make sense, because anxiety can make people more vulnerable to pain. At the time Suresh was majoring in biomedical engineering with a minor in music cognition at Northwestern University where her father, Santhanam Suresh, is a professor of anesthesiology and pediatrics. © 2015 NPR

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 21080 - Posted: 06.22.2015

Bill Chappell In what researchers say is a first, they've discovered the neuron in worms that detects Earth's magnetic field. Animals have been known to sense the magnetic field; a new study identifies the microscopic, antenna-shaped sensor that helps worms orient themselves underground. The sensory neuron that the worm C. elegans uses to migrate up or down through the soil could be similar to what many other animals use, according to the team of scientists and engineers at The University of Texas at Austin. The team's work was published Wednesday by eLife. In contrast to previous breakthroughs — such as a 2012 study on how pigeons' brains use information about magnetic fields, and another from the same year on olfactory cells in trout — the new work identifies the sensory neuron that detects magnetic fields. "We also found the first hint at a novel sensory mechanism for detecting the magnetic field," says Jon Pierce-Shimomura, an assistant professor of neuroscience who worked on the study. "Now researchers can check to see if this is used in other animals too." The list of animals that could be studied for their use of magnetic fields is long — and it seems to grow each year. In early 2014, for instance, a study found that dogs who need to relieve themselves of waste prefer to align themselves on a north-south axis when the magnetic conditions are right. Pierce-Shimomura says his team was surprised to make a new breakthrough in magnetism by looking at worms, which aren't known for their sophisticated migrations. © 2015 NPR

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 21072 - Posted: 06.18.2015

By Andrea Alfano There are many types of touch. A cold splash of water, the tug of a strong breeze or the heat and heft of your coffee mug will each play on your skin in a different way. Within your skin is an array of touch sensors, each associated with nerve fibers that connect to the central nervous system. These sensors comprise specialized nerve endings and skin cells. Along with the fibers, they translate our physical interactions with the world into electrical signals that our brain can process. They help to bridge the gap between the physical act of touching and the cognitive awareness of tactile sensation. Even a simple stroke across the forearm engages several distinct nerve fibers. Three types—A-beta, A-delta and C fibers—have subtypes that are specialized for sensing particular types of touch; other subtypes carry information related to pain. The integration of information from these fibers is what allows us to gain such rich sensory experiences through our skin, but it has also made it more challenging for researchers to understand the fibers’ individual roles. Although these fibers do not act in isolation, the examples that follow highlight the primary nerve fibers engaged by different types of touch. © 2015 Scientific American

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 21066 - Posted: 06.18.2015