Links for Keyword: Pain & Touch

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Pete Etchells Autonomous Sensory Meridian Response, or ASMR, is a curious phenomenon. Those who experience it often characterise it as a tingling sensation in the back of the head or neck, or another part of the body, in response to some sort of sensory stimulus. That stimulus could be anything, but over the past few years, a subculture has developed around YouTube videos, and their growing popularity was the focus of a video posted on the Guardian this last week. It’s well worth a watch, but I couldn’t help but feel it would have been a bit more interesting if there had been some scientific background in it. The trouble is, there isn’t actually much research on ASMR out there. To date, only one research paper has been published on the phenomenon. In March last year, Emma Barratt, a graduate student at Swansea University, and Dr Nick Davis, then a lecturer at the same institution, published the results of a survey of some 500 ASMR enthusiasts. “ASMR is interesting to me as a psychologist because it’s a bit ‘weird’” says Davis, now at Manchester Metropolitan University. “The sensations people describe are quite hard to describe, and that’s odd because people are usually quite good at describing bodily sensation. So we wanted to know if everybody’s ASMR experience is the same, and of people tend to be triggered by the same sorts of things.” The study asked a range of questions about where, when and why people watch ASMR videos, whether there was any consistency in ASMR-triggering content, as well as whether individuals felt it had any effect on their mood. There was a remarkable consistency across participants in terms of triggering content – whispering worked for the majority of people, followed by videos involving some sort of personal attention, crisp sounds, and slow movements. For the most part, participants reported that they watched ASMR videos for relaxation purposes, or to help them sleep or deal with stress. © 2016 Guardian News and Media Limited

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: 21767 - Posted: 01.09.2016

By Emily Underwood As long as she can remember, 53-year-old Rosa Sundquist has tallied the number of days per month when her head explodes with pain. The migraines started in childhood and have gotten worse as she’s grown older. Since 2008, they have incapacitated her at least 15 days per month, year-round. Head-splitting pain isn’t the worst of Sundquist’s symptoms. Nausea, vomiting, and an intense sensitivity to light, sound, and smell make it impossible for her to work—she used to be an office manager—or often even to leave her light-proofed home in Dumfries, Virginia. On the rare occasions when she does go out to dinner or a movie with her husband and two college-aged children, she wears sunglasses and noise-canceling headphones. A short trip to the grocery store can turn into a full-blown attack “on a dime,” she says. Every 10 weeks, Sundquist gets 32 bee sting–like injections of the nerve-numbing botulism toxin into her face and neck. She also visits a neurologist in Philadelphia, Pennsylvania, who gives her a continuous intravenous infusion of the anesthetic lidocaine over 7 days. The lidocaine makes Sundquist hallucinate, but it can reduce her attacks, she says—she recently counted 20 migraine days per month instead of 30. Sundquist can also sometimes ward off an attack with triptans, the only drugs specifically designed to interrupt migraines after they start. Millions of others similarly dread the onset of a migraine, although many are not afflicted as severely as Sundquist. Worldwide, migraines strike roughly 12% of people at least once per year, with women roughly three times as likely as men to have an attack. © 2016 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: 21764 - Posted: 01.08.2016

By Stephani Sutherland A technique called optogenetics has transformed neuroscience during the past 10 years by allowing researchers to turn specific neurons on and off in experimental animals. By flipping these neural switches, it has provided clues about which brain pathways are involved in diseases like depression and obsessive-compulsive disorder. “Optogenetics is not just a flash in the pan,” says neuroscientist Robert Gereau of Washington University in Saint Louis. “It allows us to do experiments that were not doable before. This is a true game changer like few other techniques in science.” Since the first papers were published on optogenetics in the mid-aughts some researchers have mused about one day using optogenetics in patients, imagining the possibility of an off-switch for depression, for instance. The technique, however, would require that a patient submit to a set of highly invasive medical procedures: genetic engineering of neurons to insert molecular switches to activate or switch off cells, along with threading of an optical fiber into the brain to flip those switches. Spurred on by a set of technical advances, optogenetics pioneer Karl Deisseroth, together with other Stanford University researchers, has formed a company to pursue optogenetics trials in patients within the next several years—one of several start-ups that are now contemplating clinical trials of the technique. Circuit Therapeutics, founded in 2010, is moving forward with specific plans to treat neurological diseases. (It also partners with pharmaceutical companies to help them use optogenetics in animal research to develop novel drug targets for human diseases.) © 2016 Scientific America

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 5: The Sensorimotor System
Link ID: 21758 - Posted: 01.07.2016

A woman born incapable of feeling pain has been hurt for the first time – thanks to a drug normally prescribed for opioid overdoses. She was burned with a laser, and quite liked the experience. The breakthrough may lead to powerful new ways to treat painful conditions such as arthritis. Only a handful people around the world are born unable to feel pain. These individuals can often suffer a range of injuries when they are young. Babies with the condition tend to chew their fingers, toes and lips until they bleed, and toddlers can suffer an increased range of knocks, tumbles and encounters with sharp or hot objects. The disorder is caused by a rare genetic mutation that results in a lack of ion channels that transport sodium across sensory nerves. Without these channels, known as Nav1.7 channels, nerve cells are unable to communicate pain. Researchers quickly sought to make compounds that blocked Nav1.7 channels, thinking they might be able to block pain in people without the disorder. “It looked like a fantastic drug target,” says John Wood at University College London. “Pharma companies went bananas and made lots of drugs.” But while a few compounds saw some success, none brought about the total pain loss seen in people who lack the channel naturally. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 21677 - Posted: 12.05.2015

By David Noonan The 63-year-old chief executive couldn't do his job. He had been crippled by migraine headaches throughout his adult life and was in the middle of a new string of attacks. “I have but a little moment in the morning in which I can either read, write or think,” he wrote to a friend. After that, he had to shut himself up in a dark room until night. So President Thomas Jefferson, in the early spring of 1807, during his second term in office, was incapacitated every afternoon by the most common neurological disability in the world. The co-author of the Declaration of Independence never vanquished what he called his “periodical head-ach,” although his attacks appear to have lessened after 1808. Two centuries later 36 million American migraine sufferers grapple with the pain the president felt. Like Jefferson, who often treated himself with a concoction brewed from tree bark that contained quinine, they try different therapies, ranging from heart drugs to yoga to herbal remedies. Their quest goes on because modern medicine, repeatedly baffled in attempts to find the cause of migraine, has struggled to provide reliable relief. Now a new chapter in the long and often curious history of migraine is being written. Neurologists believe they have identified a hypersensitive nerve system that triggers the pain and are in the final stages of testing medicines that soothe its overly active cells. These are the first ever drugs specifically designed to prevent the crippling headaches before they start, and they could be approved by the U.S. Food and Drug Administration next year. If they deliver on the promise they have shown in studies conducted so far, which have involved around 1,300 patients, millions of headaches may never happen. © 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: 21662 - Posted: 11.28.2015

By Virginia Morell Plunge a live crab into a pot of boiling water, and it’s likely to try to scramble out. Is the crab’s behavior simply a reflex, or is it a sign of pain? Many scientists doubt that any invertebrate (or fish) feels pain because they lack the areas in the brain associated with human pain. Others argue this is an unfair comparison, noting that despite the major differences between vertebrate and invertebrate brains, their functions (such as seeing) are much the same. To get around this problem, researchers in 2014 argued that an animal could be classified as experiencing pain if, among other things, it changes its behavior in a way that indicates it’s trying to prevent further injury, such as through increased wariness, and if it shows a physiological change, such as elevated stress hormones. To find out whether crabs meet these criteria, scientists collected 40 European shore crabs (Carcinus maenas), shown in the photo above, in Northern Ireland. They placed the animals into individual tanks, and gave half 200-millisecond electrical shocks every 10 seconds for 2 minutes in their right and left legs. The other 20 crabs served as controls. Sixteen of the shocked crabs began walking in their tanks, and four tried to climb out. None of the control crabs attempted to clamber up the walls, but 14 walked, whereas six didn’t move at all. There was, however, one big physiological difference between the 16 shocked, walking crabs and the 14 control walkers, the scientists report in today’s issue of Biology Letters: Those that received electrical jolts had almost three times the amount of lactic acid in their haemolymph, a fluid that’s analogous to the blood of vertebrates—a clear sign of stress. Thus, crabs pass the bar scientists set for showing that an animal feels pain. © 2015 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 21623 - Posted: 11.11.2015

By Arlene Karidis Several years ago, Peggy Chenoweth began having excruciating cramping in her ankle. It felt severely sprained and as if her toe were twisting to the point where it was being ripped off her foot. “The pain is right here,” she told an orthopedic surgeon, “in my ankle and foot.” But the 41-year-old Gainesville, Va., resident no longer had that ankle and foot. Her leg had been amputated below the knee after a large piece of computer equipment fell off a cart, crushed her foot and caused nerve damage. Further, she insisted that since the amputation, she could feel her missing toes move. Chenoweth’s surgeon knew exactly what was going on: phantom pain. Lynn Webster, an anesthesiologist and past president of the American Academy of Pain Medicine, explains the phenomenon: “With ‘phantom pain,’ nerves that transmitted information from the brain to the now-missing body part continue to send impulses, which relay the message of pain.” It feels as if the removed part is still there and hurting, but pain is actually in the brain. The sensation ranges from annoying itching to red-hot burning. Physicians wrote about phantom pain as early as the 1860s, but U.S. research on this condition has increased recently, spurred by the surge of amputees returning from warfare in Iraq and Afghanistan and by increasing rates of diabetes. (Since 2003, nearly 1,650 service members have lost limbs, according to the Congressional Research Service. In 2010, about 73,000 amputations were performed on diabetics in the United States, according to the Centers for Disease Control and Prevention.)

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: 21620 - Posted: 11.10.2015

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

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: 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

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: 21588 - Posted: 10.31.2015

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

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: 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

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 5: The Sensorimotor System
Link ID: 21586 - Posted: 10.31.2015

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

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: 21575 - Posted: 10.28.2015

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.

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 21530 - Posted: 10.20.2015

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.

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: 21519 - Posted: 10.16.2015

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