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By Catherine Offord Neurobiologist John Wood has long been interested in how animals feel pain. His research at University College London (UCL) typically involved knocking out various ion channels important in sensory neuronal function from mouse models and observing the effects. But in the mid-2000s, a peculiar story about a boy in Pakistan opened up a new, and particularly human-centric, research path. The story was relayed by Geoff Woods, a University of Cambridge geneticist. “Geoff had been wandering round Pakistan looking for consanguineous families that had genes contributing to microcephaly,” Wood recalls. During his time there, “somebody came to see him and said that there was a child in the marketplace who was damaging himself for the tourists—and was apparently pain-free.” The boy would regularly stick knives through his arms and walk across burning coals, the stories went. Wood’s group at UCL had just published a paper describing a similarly pain-insensitive phenotype in mice genetically engineered to lack the voltage-gated sodium channel NaV1.7 in pain-sensing neurons, or nociceptors. NaV1.7 controls the passage of sodium ions into the cell—a key step in membrane depolarization and, therefore, a neuron’s capacity to propagate an action potential. Wood’s postdoc, Mohammed Nassar, had shown that mice lacking functional NaV1.7 in their nociceptors exhibited higher-than-normal pain thresholds; they were slower to withdraw a paw from painful stimuli and spent less time licking or biting it after being hurt.1 Having read the study, Cambridge’s Woods reached out to the group in London to discuss whether this same channel could help explain the bizarre behavior of the boy he’d heard about in Pakistan. © 1986-2018 The Scientist

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24503 - Posted: 01.09.2018

By Catherine Offord Graduate student Anne Murphy had run out of rats. Or rather, she’d run out of male rats, the animals she was using to study brain regions involved in pain modulation for her PhD at the University of Cincinnati in the early 1990s. At a time when neuroscientists almost exclusively used male animals for research, what Murphy did next was unusual: she used a female rat instead. “I had the hardest time to get the female to go under the anesthesia; she wasn’t acting right,” Murphy says. Her advisor’s explanation? “‘Well, you know those females, they have hormones, and those hormones are always fluctuating and they’re so variable,’” Murphy recalls. The comments struck a nerve. “It really got to me,” she says. “I’m a female. I have hormones that fluctuate. . . . It made me determined to investigate the differences between males and females in terms of pain processing and alleviation.” Her decision was timely. Since the ’90s, evidence has been accumulating to suggest that not only do women experience a higher incidence of chronic pain syndromes than men do—fibromyalgia and interstitial cystitis, for example—females also generally report higher pain intensities. Additionally, Murphy notes, a handful of clinical studies has suggested that women require higher doses of opioid pain medications such as morphine for comparable analgesia; plus, they experience worse side effects and a higher risk of addiction. © 1986-2018 The Scientist

Related chapters from BN8e: 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: 24486 - Posted: 01.04.2018

Beyond the usual suspects of snakes, spiders, and scorpions, the animal kingdom is filled with noxious critters: snails, frogs, fish, anemones, and more make toxins for defense or predation. The noxious chemicals these animals produce are potent, and they often strike where it hurts: pain pathways. These compounds have long captivated researchers hoping to understand their effects and use that knowledge to develop drugs that suppress pain in a wide variety of ailments affecting humans. Paradoxically, some of these toxins are themselves analgesic, and researchers have worked to develop synthetic derivatives that can be tested as painkillers. Such is the case for the only toxin-derived analgesic to be approved by the US Food and Drug Administration (FDA): ziconotide (Prialt), a compound 1,000 times more potent than morphine that was inspired by a component of the venom of the cone snail Conus magus. Other toxins elicit pain, and researchers have used these compounds to identify inhibitors of ion channels on the pain-sensing neurons they target. Despite more than half a century of research in this field, however, scientists have had a frustrating time developing effective analgesics. Challenges include ensuring that the drugs are highly specific to their targets—each family of ion channels involved in pain sensing in humans contains several conserved proteins—and getting them to those targets, which often lie beyond the blood-brain barrier in the central nervous system. Nevertheless, several toxin-derived candidates are beginning to prove their worth in preclinical experiments and a handful of clinical trials, and bioprospectors continue to mine the animal kingdom’s vast library of venoms and poisons for more leads. The next big thing in painkillers could soon be slithering, creeping, hopping, or swimming into the pipeline. © 1986-2018 The Scientist

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24485 - Posted: 01.04.2018

By Mark R. Hutchinson When someone is asked to think about pain, he or she will typically envision a graphic wound or a limb bent at an unnatural angle. However, chronic pain, more technically known as persistent pain, is a different beast altogether. In fact, some would say that the only thing that acute and persistent pain have in common is the word “pain.” The biological mechanisms that create and sustain the two conditions are very different. Pain is typically thought of as the behavioral and emotional results of the transmission of a neuronal signal, and indeed, acute pain, or nociception, results from the activation of peripheral neurons and the transmission of this signal along a connected series of so-called somatosensory neurons up the spinal cord and into the brain. But persistent pain, which is characterized by the overactivation of such pain pathways to cause chronic burning, deep aching, and skin-crawling and electric shock–like sensations, commonly involves another cell type altogether: glia.1 Long considered to be little more than cellular glue holding the brain together, glia, which outnumber neurons 10 to 1, are now appreciated as critical contributors to the health of the central nervous system, with recognized roles in the formation of synapses, neuronal plasticity, and protection against neurodegeneration. And over the past 15 to 20 years, pain researchers have also begun to appreciate the importance of these cells. Research has demonstrated that glia seem to respond and adapt to the cumulative danger signals that can result from disparate kinds of injury and illness, and that they appear to prime neural pathways for the overactivation that causes persistent pain. In fact, glial biology may hold important clues to some of the mysteries that have perplexed the pain research field, such as why the prevalence of persistent pain differs between the sexes and why some analgesic medications fail to work. © 1986-2018 The Scientist

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 24482 - Posted: 01.03.2018

By Catherine Offord As a physiotherapist at University Hospital Zurich in the mid-2000s, Annina Schmid often encountered people with chronic pain. “My interest in research got sparked while I was seeing my patients,” she says. “It was very difficult to treat them, or to understand why pain persists in some people, while it doesn’t even occur in others.” Schmid, who grew up in Switzerland, had earned her master’s degree in clinical physiotherapy in 2005 at Curtin University in Perth, Australia, and she was keen to return down under. In 2008, she secured an Endeavour Europe Scholarship from the Australian Government and moved to the University of Queensland in Brisbane for a PhD in neuroscience. “She’s very motivated,” says Schmid’s colleague and collaborator Brigitte Tampin, a musculoskeletal physiotherapist at Curtin University and at Osnabrück University of Applied Sciences in Germany. Tampin adds that Schmid’s physiotherapy background was an asset for her PhD work and beyond. “She can think as a clinician and as a researcher.” For her PhD, Schmid focused on animal models of mild nerve compression, also called entrapment neuropathy, in which pressure on nerve fibers—from bone, for example—can cause pain and loss of motor function. Using a tube to compress the sciatic nerves of rats, Schmid was able to replicate not only local symptoms seen in humans, but also inflammation at distant sites, a possible explanation for why patients often report pain in other parts of the body.1 © 1986-2018 The Scientist

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24477 - Posted: 01.02.2018

By Daniel Barron Earlier this year, I wrote about my patient, Andrew, an engineer who developed a heroin habit. An unfortunate series of joint replacements had left Andrew with terrible pain and, when his medication ran out, he turned to heroin. Months after his surgeries—after his tissue and scars had healed—Andrew remained disabled by a deep, biting pain. I recall puzzling over his pain, how it had spread throughout his body and how previous clinical teams had prescribed progressively higher doses of opioids to tame it. Andrew had transitioned from acute pain (i.e., pain from his surgical wounds) to chronic pain (i.e., pain in the absence of an obvious cause), but it was unclear to me whether this reflected a drug tolerance or a different pain process. The difference between drug tolerance and chronic pain is a difficult concept to get hold of. In the hospital workroom one morning, I realized how confused I was by the topic and paged the hospital’s on-call pain specialist. Fortune smiled and Donna-Ann M Thomas, Yale University’s Pain Medicine Division Chief, picked up the phone and patiently explained how tolerance and chronic pain are quite different. Andrew became tolerant to opioids when his body required progressively larger doses to have the same effect. Opioids activate the Mu opioid receptor, which blocks pain signals in the spinal cord. To find a way around the opioid blockade, Andrew’s body had made more Mu receptors to compensate for the drug, meaning more drug had to be present to stifle the pain signal, hence the escalating doses. © 2017 Scientific American,

Related chapters from BN8e: 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: 24471 - Posted: 12.30.2017

John Daley Seven years ago, Robert Kerley, who makes his living as a truck driver, was loading drywall onto his trailer when a gust of wind knocked him off. He fell 14 feet and hurt his back. For pain, a series of doctors prescribed him a variety of opioids: Vicodin, Percocet and Oxycontin. In less than a year, the 45-year-old from Federal Heights, Colo., says he was hooked. "I spent most of my time high, laying on the couch, not doing nothing, sleeping, dozing off, falling asleep everywhere," he says. Kerley lost weight. He lost his job. His relationships with his wife and kids suffered. He remembers when he hit rock bottom. One night hanging out in a friend's basement, he drank three beers and the alcohol reacted with an opioid in his system. "I was taking so much morphine that I respiratory arrested because of it," Kerley says. "I stopped breathing." An ambulance arrived, and EMTs administered the overdose reversal drug naloxone. Kerley was later hospitalized. As the father of a 12-year-old son, he knew he needed to turn things around. That's when he signed up for Kaiser Permanente's Integrated Pain Service. "After seven years of being on narcotics and in a spiral downhill, the only thing that pulled me out of it was going to this class," he says. "The only thing that pulled me out of it was doing and working the program that they ask you to work." © 2017 npr

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24465 - Posted: 12.29.2017

By JOANNA KLEIN Most rodents are just rodents. And the ones with exceptional abilities are usually cartoon rats or mice. But here in the real world of flesh, bones, brains and nerves that we mammals use each second to survive, some woodland rodents really do have a superpower that helps them tolerate cold and endure harsh winters. In grasslands from central Canada to Texas, a species known as thirteen-lined ground squirrels can adjust their body temperature to match the air around them. This is especially important during hibernation: They don’t have to fatten up like bears or find warm hide-outs like conventional mice and rats. They slumber, surviving in bodies just above freezing. Another species, the Syrian hamster, does it too. “They combine warm and cold blooded animals in one,” said Elena Gracheva, a neurophysiologist at Yale University. This uncanny ability to withstand prolonged cold (and even hypothermia) results in part from an adaptation these rodents have developed in molecules they share with other mammals, including us, Dr. Gracheva and her colleagues found in a study published last week in the journal Cell Reports. Unique properties of TRPM8, a cold-sensing protein found in their peripheral nervous systems, shields these rodents from harsh weather. It’s really important because if they’re too cold, they can’t hibernate — just like if you’re too cold, you might have trouble sleeping. The new research brings scientists closer to understanding enigmas of hibernation and solving a mystery of how this molecular sensor works. The work also may lead to therapies for allodynia, a nerve condition that causes some people to misperceive something normally not-so-cold as painful. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: The Sensorimotor System
Link ID: 24464 - Posted: 12.28.2017

A promising approach to post-operative incision-site pain control uses a naturally occurring plant molecule called resiniferatoxin (RTX). RTX is found in Euphorbia resinifera, a cactus-like plant native to Morocco, which is 500 times more potent than the chemical that produces heat in hot peppers, and may help limit the use of opioid medication while in the hospital and during home recovery. In a paper published online in Anesthesiology, the peer-reviewed medical journal of the American Society of Anesthesiologists, researchers found that RTX could be used to block postoperative incisional pain in an animal model. Many medical providers turn to opioids, such as morphine or fentanyl, for moderate to severe post-operative pain relief, but these often come with side effects that can interfere with recovery, including respiratory depression, inhibition of gut motility and constipation, nausea and vomiting. Prolonged use of opioids can produce tolerance and introduces the risk of misuse. RTX is not an opioid and does not act in the brain but rather on the nerve endings in the skin. Scientists found that it can be used to block pain from the surgical incision selectively for approximately 10 days. In the study, researchers pre-treated the skin incision site with RTX to render the nerve endings in the skin and subcutaneous tissue along the incision path selectively insensitive to pain. Unlike local anesthetics, which block all nerve activity including motor axons, RTX allows many sensations, like touch and vibration, as well as muscle function, to be preserved. Long after the surgery, and towards the end of healing of an incision wound, the nerve endings eventually grow back. Thus, pain from the skin incision is reduced during the recovery period.

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24451 - Posted: 12.22.2017

By Jessica Hamzelou An Italian family that is barely able to sense pain has had the genetic root of their shared disorder uncovered. Understanding this gene may lead to new painkiller drugs. The affected family members include a 78-year-old woman, her two middle-aged daughters, and their three children. All of them fail to sense pain in the way most of us do, and don’t notice when they are being injured. When they were assessed, the family members were found to have bone fractures in their arms and legs that they hadn’t realised were there. “Sometimes they feel pain in the initial break but it goes away very quickly,” says James Cox, of University College London. “For example, Letizia broke her shoulder while skiing, but then kept skiing for the rest of the day and drove home. She didn’t get it checked out until the next day.” To find the cause of their lack of pain sensitivity, Cox and his colleagues performed a series of tests on the family members. The team found that all six individuals had normal numbers of nerves in their skin, but that they all had a mutation in a gene called ZFHX2. When the team deleted this gene entirely in mice, they found that the animals were not as good at sensing when painful pressure was applied to their tails, but they were hypersensitive to heat sensations. This suggests the gene may play a role in controlling whether stimuli are painful or not. © Copyright New Scientist Ltd.

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24422 - Posted: 12.14.2017

Allison Aubrey Nobody likes the feeling of being left out, and when it happens, we tend to describe these experiences with the same words we use to talk about the physical pain of, say, a toothache. "People say, 'Oh, that hurts,' " says Nathan DeWall, a professor of psychology at the University of Kentucky. DeWall and his colleagues were curious about the crossover between physical pain and emotional pain, so they began a series of experiments several years back. In one study, they found that acetaminophen (the active ingredient in Tylenol) seemed to reduce the sting of rejection that people experienced after they were excluded from a virtual ball-tossing game. The pain pills seemed to dim activity in regions of the brain involved in processing social pain, according to brain imaging. "People knew they were getting left out [of the game], it just didn't bother them as much," DeWall explains. As part of the study, participants were given either acetaminophen or a placebo for three weeks. None of the participants knew which one they were given. Each evening, participants completed a Hurt Feelings Scale, designed as a standardized measure of emotional pain. They were asked to rank themselves on statements such as: "Today, being teased hurt my feelings." It turned out that the pain medicine reduced reports of social pain. The emotional dampening documented in these experiments is not huge, but it appears significant enough to nudge people into a less-sensitive emotional state. © 2017 npr

Related chapters from BN8e: 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: 24391 - Posted: 12.05.2017

A new migraine drug that can halve the length of attacks has been hailed as “the start of real change” in how the condition is treated. Erenumab, a laboratory-made antibody that blocks a neural brain pathway called CGRP, is the first drug in 20 years proven to prevent migraine attacks. Phase three trial data on nearly 1,000 patients showed that it typically cut between three and four “migraine days” per month. In half the patients treated, migraine duration was reduced at least by half. Migraines are characterised by an intense, throbbing headache, sensitivity to light and noise, nausea, vomiting, low energy, and visual disturbances. Attacks can last anything from four to 72 hours. Each year more than 8.5 million people in the UK are thought to experience migraine – more than the number affected by asthma, diabetes and epilepsy combined. The condition is linked to depression and sick days caused by migraine are estimated to cost the UK economy more than £2bn per year. The trial, called Strive, compared patients taking erenumab for six months with others given a non-active placebo dummy drug. The research revealed that by months four to six, at least a 50% reduction in mean migraine days per month was achieved for just over 43% of patients injected under the skin with 70-mg of erenumab each month, while half of patients injected with the higher dose of 140-mg had such results. However, those given a placebo also saw benefits, with 26.6% of participants in this group experiencing such a reduction. © 2017 Guardian News and Media Limited

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24381 - Posted: 11.30.2017

Jon Hamilton The goal is simple: a drug that can relieve chronic pain without causing addiction. But achieving that goal has proved difficult, says Edward Bilsky, a pharmacologist who serves as the provost and chief academic officer at Pacific Northwest University of Health Sciences in Yakima, Wash. "We know a lot more about pain and addiction than we used to," says Bilsky, "But it's been hard to get a practical drug." Bilsky is moderating a panel on pain, addiction and opioid abuse at the Society for Neuroscience meeting in Washington, D.C., this week. Brain scientists have become increasingly interested in pain and addiction as opioid use has increased. About 2 million people in the U.S. now abuse opioids, according to the Centers for Disease Control and Prevention. But at least 25 million people suffer from chronic pain, according to an analysis by the National Institutes of Health. That means they have experienced daily pain for more than three months. The question is how to cut opioid abuse without hurting people who live with pain. And brain scientists think they are getting closer to an answer. One approach is to find drugs that decrease pain without engaging the brain's pleasure and reward circuits the way opioids do, Bilsky says. So far, these drugs have been hampered by dangerous side effects or proved less effective than opioids at reducing pain. But substances related to snail venom look promising, Bilsky says. © 2017 npr

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24321 - Posted: 11.13.2017

Paula Span Medical researchers and government health policymakers, a cautious lot, normally take pains to keep expectations modest when they’re discussing some new finding or treatment. They warn about studies’ limitations. They point out what isn’t known. They emphasize that correlation doesn’t mean causation. So it’s startling to hear prominent experts sound positively excited about a new shingles vaccine that an advisory committee to the Centers for Disease Control and Prevention approved last month. “This really is a sea change,” said Dr. Rafael Harpaz, a veteran shingles researcher at the C.D.C. Dr. William Schaffner, preventive disease specialist at the Vanderbilt University School of Medicine, said, “This vaccine has spectacular initial protection rates in every age group. The immune system of a 70- or 80-year-old responds as if the person were only 25 or 30.” “This really looks to be a breakthrough in vaccinating older adults,” agreed Dr. Jeffrey Cohen, a physician and researcher at the National Institutes of Health. What’s causing the enthusiasm: Shingrix, which the pharmaceutical firm GlaxoSmithKline intends to begin shipping this month. Large international trials have shown that the vaccine prevents more than 90 percent of shingles cases, even at older ages. The currently available shingles vaccine, called Zostavax, only prevents about half of shingles cases in those over age 60 and has demonstrated far less effectiveness among elderly patients. Yet those are the people most at risk for this blistering disease, with its often intense pain, its threat to vision and the associated nerve pain that sometimes last months, even years, after the initial rash fades. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 24316 - Posted: 11.11.2017

By Roni Dengler The bills of even newly hatched ducks might be as sensitive as our hands, as touch sensors in their beaks are as abundant as those in our fingertips and palms. That’s the take-away of new research published today in the Proceedings of the National Academy of Sciences that describes the origins of touchiness in the common duck’s quacker. Researchers knew that duck bills can sense light touch but have muted responsiveness to temperature. This comes in handy (or bill-y) since the birds forage for food in cold, murky bottom waters. Now, researchers find the sensors duck bills use to perceive touch work even before hatching. That likely helps young ducklings scavenge for food alongside adults soon after birth. In keeping with the need to feel for food, the ducks have more nerve cells to relay touch signals than chickens, which rely on eyesight to find sustenance, they report. That means different developmental programs are at work in ducks and chickens, which could help scientists uncover how touch evolved. Because the duck’s touch sensors are similar to mammals’ and their bills aren’t covered in fur, the authors suggest embryonic duck bills might be a better model than standard laboratory rodents to study touch sensation as it applies to us relatively hairless humans. © 2017 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 24298 - Posted: 11.07.2017

By JANE E. BRODY After two hourlong sessions focused first on body awareness and then on movement retraining at the Feldenkrais Institute of New York, I understood what it meant to experience an incredible lightness of being. Having, temporarily at least, released the muscle tension that aggravates my back and hip pain, I felt like I was walking on air. I had long refrained from writing about this method of countering pain because I thought it was some sort of New Age gobbledygook with no scientific basis. Boy, was I wrong! The Feldenkrais method is one of several increasingly popular movement techniques, similar to the Alexander technique, that attempt to better integrate the connections between mind and body. By becoming aware of how one’s body interacts with its surroundings and learning how to behave in less stressful ways, it becomes possible to relinquish habitual movement patterns that cause or contribute to chronic pain. The method was developed by Moshe Feldenkrais, an Israeli physicist, mechanical engineer and expert in martial arts, after a knee injury threatened to leave him unable to walk. Relying on his expert knowledge of gravity and the mechanics of motion, he developed exercises to help teach the body easier, more efficient ways to move. I went to the institute at the urging of Cathryn Jakobson Ramin, author of the recently published book “Crooked” that details the nature and results of virtually every current approach to treating back pain, a problem that has plagued me on and off (now mostly on) for decades. Having benefited from Feldenkrais lessons herself, Ms. Ramin had good reason to believe they would help me.

Related chapters from BN8e: 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: 24259 - Posted: 10.30.2017

As a ballet dancer in a former life, countless rehearsal hours in pointe shoes once landed me in a podiatrist’s office with a particularly inflamed ingrown toenail. To my surprise – and the doctor’s – a typical injection of local anesthesia did nothing to numb the searing pain as his knife dug into my big toe. It was not until a second full injection made my toe the size of a golf ball that I became blissfully unaware of the pain. Was my hair color to blame? It is, after all, a rumor every redhead has heard: we feel more pain and need more painkillers. A look at the published research suggests that the genes that determine my hair color may play a role, but the science itself is murky. What makes a redhead? Our luster-filled locks derive from a pair of mutated genes. For most people, hair color is determined by the melanocortin-1 receptor, or MC1R gene that leads to the production of a brown-black melanin pigment called eumelanin. The more eumelanin created by this gene, the darker and blacker the hair. Most redheads have a recessive version of the MC1R gene caused by the pairing of three possible mutant alleles. The resulting gene expression shuts off eumelanin production, shifting the dominant pigment to the reddish-toned pheomelanin. McGill University behavioral neuroscientist Jeffrey Mogil examined the gene as part of his research on the perception and inhibition of pain. “The purpose of this MC1R gene is to produce dark pigments. If it works, it does, and if it doesn’t, it produces pigment that isn’t dark like it’s supposed to be. So, it really is a dysfunction,” he said.

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24248 - Posted: 10.27.2017

By Amina Zafar, CBC News The soothing power of touch eases both physical pain and the sting of hurt feelings, say researchers — a finding that may be increasingly important in our social-media-driven world. When someone hurts an arm, they may brace and rub it to make it feel better. In the past 20 years, scientists have discovered that our hairy skin has cells that respond to a stroking touch. It's a trait we share with other mammals. Now psychologists in England say their work shows, for the first time, that a gentle touch can be a buffer against social rejection, too. In an experiment described in this week's issue of Scientific Reports, researchers recruited 84 healthy women and told them they were going to play a game of Cyberball, an online ball-tossing game. What the women didn't know was that their "opponents" were computer-generated avatars. Participants were told they could throw to anyone they wished, and they believed everyone would play fairly. When participants reported feeling excluded by the other "players," receiving a slow-paced stroke reduced hurt feelings from the perceived rudeness compared with a faster stroke. The study builds on previous ones showing that receiving touch from loved ones after a physical injury is supportive. "In our lab, it's tiny in effect, but the fact that it is significantly, systematically so across many participants is important," said the study's senior author, Katerina Fotopoulou, an associate professor of psychology at University College London ©2017 CBC/Radio-Canada.

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24222 - Posted: 10.20.2017

Expensive medicines can seem to create worse side-effects than cheaper alternatives, suggests a new study that looked at the "nocebo" effect of drugs. The opposite of the placebo effect — perceived improvement when no active medicine is given — nocebo is the perception of negative side-effects from a benign "medication" in a blind trial. These findings about nocebo effects could help improve the design of clinical trials that test new medications, said Dr. Luana Colloca, who wrote a journal commentary about the study. "The main information for patients is that they should be aware that sometimes our brain … reacts as a result of our beliefs and expectations," said Colloca, a pain researcher at University of Maryland School of Nursing. fMRI Researchers used a functional MRI scanner to identify areas along the spinal cord that became activated during the nocebo effect. (Alexandra Tinnermann and Tim Dretzler/University Medical Center Hamburg-Eppendorf) The study, published recently in the journal Science, focused on the pain perceptions of patients who were treated with creams they believed had anti-itch properties but actually contained no active ingredients. Researchers in Germany studied 49 people, randomly assigning some to receive a "cheap" cream and others to receive an "expensive" cream. Those in the expensive group received cream packaged in a colourful box labelled Solestan Creme. The others received cream packaged in a drab box labelled with the more generic sounding name Imotadil-LeniPharma Creme. ©2017 CBC/Radio-Canada.

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24218 - Posted: 10.19.2017

Laura Sanders Hydrogen peroxide, a molecule produced by cells under duress, may be a common danger signal, helping to alert animals to potential harm and send them scurrying. New details from planarian flatworms of how this process works may deepen scientists’ understanding of how people detect pain, and may ultimately point to better ways to curb it. “Being able to get a big-picture view of how these systems are built and what they’re cuing in on is always really helpful,” says biologist Paul Garrity of Brandeis University in Waltham, Mass. And by finding cellular similarities among planarians, fruit flies and people, the new study, published online October 16 in Nature Neuroscience, provides hints about how this threat-detecting system might have operated hundreds of millions of years ago. The results center on a protein called TRPA1, a well-known pain detector in people. Embedded in the outside of cells, TRPA1 helps many different animals detect (and ultimately escape) harmful chemicals, physical injuries and extreme temperatures. In humans, mutations in the TRPA1 gene can cause syndromes marked by intense pain. But scientists have puzzled over TRPA1’s seemingly inconsistent behavior in different animals. In Caenorhabditis elegans worms, for instance, the protein is activated by cold. But in other animals such as mosquitoes, TRPA1 is activated by heat. “The more people started looking at activation of TRPA1 in different species, the more the puzzle became complicated,” says study coauthor Marco Gallio of Northwestern University in Evanston, Ill. © Society for Science & the Public 2000 - 2017.

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 24211 - Posted: 10.18.2017