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Chloe Tenn On October 4, physiologist David Julius and neurobiologist Arden Patapoutian were awarded the Nobel Prize in Physiology or Medicine for their work on temperature, pain, and touch perception. Julius researched the burning sensation people experience from chilies, and identified an ion channel, TRPV1 that is activated by heat. Julius and Patapoutian then separately reported on the TRPM8 ion channel that senses menthol’s cold in 2002. Patapoutian’s group went on to discover the PIEZO1 and PIEZO2 ion channels that are involved in sensing mechanical pressure. The Nobel Committee wrote that the pair’s work inspired further research into understanding how the nervous system senses temperature and mechanical stimuli and that the laureates “identified critical missing links in our understanding of the complex interplay between our senses and the environment.” This year saw innovations in augmenting the brain’s capabilities by plugging it in to advanced computing technology. For example, a biology teacher who lost her vision 16 years ago was able to distinguish shapes and letters with the help of special glasses that interfaced with electrodes implanted in her brain. Along a similar vein, a computer connected to a brain-implant system discerned brain signals for handwriting in a paralyzed man, enabling him to type up to 90 characters per minute with an accuracy above 90 percent. Such studies are a step forward for technologies that marry cutting-edge neuroscience and computational innovation in an attempt to improve people’s lives. © 1986–2021 The Scientist.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 15: Language and Lateralization
Link ID: 28134 - Posted: 12.31.2021

By Cara Giaimo Sign up for Science Times Get stories that capture the wonders of nature, the cosmos and the human body. Get it sent to your inbox. It’s tough out there for a mouse. Outdoors, its enemies lurk on all sides: owls above, snakes below, weasels around the bend. Indoors, a mouse may find itself targeted by broom-wielding humans or bored cats. Mice compensate with sharp senses of sight, hearing and smell. But they may have another set of tools we’ve overlooked. A paper published last week in Royal Society Open Science details striking similarities between the internal structures of certain small mammal and marsupial hairs and those of man-made optical instruments. In this paper as well as other unpublished experiments, the author, Ian Baker, a physicist who works in private industry, posits that these hairs may act as heat-sensing “infrared antennae” — further cluing the animals into the presence of warm-blooded predators. Although much more work is necessary to connect the structure of these hairs to this potential function, the study paints an “intriguing picture,” said Tim Caro, a professor of evolutionary ecology at the University of Bristol in England who was not involved. Dr. Baker has spent decades working with thermal imaging cameras, which visualize infrared radiation produced by heat. For his employer, the British defense company Leonardo UK Ltd., he researches and designs infrared sensors. But in his spare time he often takes the cameras to fields and forests near his home in Southampton, England, to film wildlife. Over the years, he has developed an appreciation for “how comfortable animals are in complete darkness,” he said. That led him to wonder about the extent of their sensory powers. © 2021 The New York Times Company

Related chapters from BN: 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: 28120 - Posted: 12.18.2021

Jon Hamilton Scientists may have learned why opioids depress breathing while relieving pain. The finding could lead to pain drugs that don't cause respiratory failure, the usual cause of death in opioid overdoses. When people feel pain, they tend to breathe faster. When they take an opioid to kill that pain, their breathing slows down. Now scientists think they know how pain and respiration are connected in the brain. NPR's Jon Hamilton reports that the discovery could eventually lead to safer pain drugs. JON HAMILTON, BYLINE: Sung Han has been studying the link between pain and breathing in his lab at the Salk Institute in San Diego. But he got a real-world demonstration recently while taking a shower. SUNG HAN: I forgot to change the temperature, and the cold water just suddenly came out and covered my entire body. And then I just - I was breathing really fast. HAMILTON: A typical reaction to what Han calls aversive sensory information - and he thinks he knows the cause. Han's lab has identified a brain circuit in mice that appears to link the emotional experience of pain to breathing rhythm. Han says the circuit involves two populations of brain cells both found in the same small area of the brain stem. HAN: One population regulate pain and the other population regulate breathing, and that's the reason why pain and breathing are interacting each other. HAMILTON: They're linked together. If that's also true in people, it would help explain the mysterious connection between breathing and emotion, which has puzzled scientists for centuries. And the finding, which appears in the journal Neuron, could also have practical applications. That's because both groups of brain cells - the ones for breathing and the ones for pain - respond to opioids. Han says this is why an overdose can be fatal. © 2021 npr

Related chapters from BN: 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: Development of the Brain
Link ID: 28117 - Posted: 12.18.2021

By Lisa Sanders, M.D. The 66-year-old man had just started his third lap at the community swimming pool outside Poughkeepsie, N.Y., when it struck. As he was turning his head to take a breath, an octopus of pain wrapped around the right side of his skull, starting at the joint where the jaw connects and slamming across his face and head with tentacles of squeezing agony. For a moment he was paralyzed — first with pain, then with fear. He couldn’t breathe; he could barely move. He struggled to the side of the pool and hung on, his breath ragged through involuntarily clenched teeth. His wife hurried over. He was a good swimmer; what was wrong? She saw his lips move and leaned closer. His jaw was clenched. “I can’t speak,” he mumbled. She helped him out of the pool. “We’re going to go to urgent care,” she said as she handed him a towel. These strange pains had been tormenting the man for nearly three weeks. It started as a headache that woke him from a dead sleep, a squeezing pressure deep inside his brain. He got up and took some acetaminophen. When he awoke the next morning, the headache was gone, but the regions around his head and face where the pressure had been strongest felt strangely tender. He couldn’t even brush his hair on the right side of his head. Bizarre as this was, he most likely would have soon forgotten about it except that it happened again the next night — and just about every night since. The pain in his jaw started a couple of days later. Opening and closing his mouth, and especially chewing, made his jaw throb. Eating anything more solid than mashed potatoes triggered excruciating pain. He went to his dentist, who poked and prodded. The only tenderness was in the joint where the jaw attached to the skull. It’s most likely TMJ, the dentist concluded — temporomandibular joint pain. That joint and the many attached muscles make speech and facial expressions possible. Lots of people have pain there, the dentist added. Bad habits like jaw-clenching and tooth-grinding aggravate the joint. The treatment is behavior modification to unlearn these habits, and sometimes a bite block, a custom-made piece of acrylic worn at night to protect teeth from injury. © 2021 The New York Times Company

Related chapters from BN: 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: 28113 - Posted: 12.15.2021

By David Dobbs Chronic pain is both one of the world’s most costly medical problems, affecting one in every five people, and one of the most mysterious. In the past two decades, however, discoveries about the crucial role played by glia — a set of nervous system cells once thought to be mere supports for neurons — have rewritten chronic pain science. These findings have given patients and doctors a hard-science explanation that chronic pain previously lacked. By doing so, this emerging science of chronic pain is beginning to influence care — not by creating new treatments, but by legitimizing chronic pain so that doctors take it more seriously. Although glia are scattered throughout the nervous system and take up almost half its space, they long received far less scientific attention than neurons, which do the majority of signaling in the brain and body. Some types of glia resemble neurons, with roughly starfish-like bodies, while others look like structures built with Erector sets, their long, straight structural parts joined at nodes. When first discovered in the mid-1800s, glia — from the Greek word for glue — were thought to be just connective tissue holding neurons together. Later they were rebranded as the nervous system’s janitorial staff, as they were found to feed neurons, clean up their waste and take out their dead. In the 1990s they were likened to secretarial staff when it was discovered they also help neurons communicate. Research over the past 20 years, however, has shown that glia don’t just support and respond to neuronal activity like pain signals — they often direct it, with enormous consequences for chronic pain. If you’re hearing this for the first time and you’re one of the billion-plus people on Earth who suffer from chronic pain (meaning pain lasting beyond three to six months that has no apparent cause or has become independent of the injury or illness that caused it), you might be tempted to say that your glia are botching their pain-management job. © 2021 The New York Times Company

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 28075 - Posted: 11.13.2021

By James Gallagher An innovative type of medicine - called gene silencing - is set to be used on the NHS for people who live in crippling pain. The drug treats acute intermittent porphyria, which runs in families and can leave people unable to work or have a normal life. Clinical trials have shown severe symptoms were cut by 74% with the drug. While porphyria is rare, experts say the field of gene silencing has the potential to revolutionise medicine. Sisters Liz Gill and Sue Burrell have both had their lives turned around by gene silencing. Before treatment, Liz, from County Durham, remembers the trauma of living in "total pain" and, at its worst, she spent two years paralysed in hospital. Younger sister Sue says she "lost it all overnight" when she was suddenly in and out of hospital, made redundant and did know whether her partner would stick with her (he did). "It was scary," she tells me. Both became used to taking potent opioid painkillers on a daily basis. But even morphine could not block the pain during a severe attack that needed hospital treatment. Gene silencing gets to the root-cause of the sisters' disease rather than just managing their symptoms. Their porphyria leads to a build-up of toxic proteins in the body, that cause the physical pain. Gene silencing "mutes" a set of genetic instructions to block that protein production. Both had been taking the therapy as part of a clinical trial and are still getting monthly injections. © 2021 BBC.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28046 - Posted: 10.23.2021

Brenda Patoine Science likes to package its successes in neat stories that show a clear progression from this to that. The “bench-to-bedside” story—when biological insights yield targeted treatments—is a long-time favorite. Reality, however, doesn’t always cooperate, and history is littered with basic-science discoveries that seemed important but failed to yield viable treatments. When they do succeed, it’s cause for celebration—and awards. Migraine research is an example. Although it is the second most disabling condition in the world, affecting one billion people, migraine had long been relegated to the backwaters of scientific research. Only recently has research bloomed—scientific papers sharply increased from the 1990s onward, with discoveries in basic science driving a new class of drugs that some in the field are calling game changers. This year, the recognition of four migraine researchers with a major neuroscience award has pushed the field into the limelight of science. The 2021 Brain Prize recognizes science that embodies the so-called bench-to-bedside research described above. That’s a jargony term scientists seem to love that denotes the rare and wonderful occurrence when laboratory research aimed at illuminating fundamental mechanisms (the “bench”) yields insights that lead to drugs that ultimately help millions of sick people (the “bedside”). In the case of migraine research, the leading character is a neuropeptide called calcitonin gene-related peptide (CGRP). © 2021 The Dana Foundation.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28040 - Posted: 10.16.2021

Jordana Cepelewicz We often appreciate the world around us in terms of its glorious sights, stirring sounds and evocative smells, all of which mark important stimuli and changes in our environment. But senses that are no less crucial to our survival are often taken for granted, including our abilities to register heat, cold and touch, a form of perception called somatosensation. Because of them, we can feel the warmth of the sun or the gentle caress of a breeze against our skin, as well as the positions and movement of our own bodies. In fact, the somatosensory neurons that make all these sensations possible constitute the largest sensory system in mammals. Scientists knew that for somatosensation to occur, there must be molecular receptors on some cells that could detect temperature and touch, and could convert those stimuli into electrical and chemical signals for the nervous system to process. For the discovery of some of those receptors David Julius, a physiologist at the University of California, San Francisco, and Ardem Patapoutian, a molecular biologist and neuroscientist at Scripps Research in La Jolla, have now been awarded the 2021 Nobel Prize in Physiology or Medicine. Julius and his colleagues started with questions about receptors for heat and pain. To find answers, they turned to capsaicin, the compound that causes us to experience a burning and sometimes painful sensation when we eat chili peppers or other spicy food. Based on our physiological response to the chemical, which includes sweating, capsaicin seemed to be inducing the nervous system to register a change in body temperature. To figure out how, Julius and his team screened millions of DNA fragments for a gene that could induce a response to the compound in cells that typically don’t react to it at all. After an arduous search, and what the Nobel Prize committee called “a high-risk project,” the researchers identified a gene that allowed cells to sense capsaicin. It encoded a novel ion channel protein, later called TRPV1, that Julius and his team discovered could be activated by hot temperatures perceived as painful. All Rights Reserved © 2021

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 28025 - Posted: 10.06.2021

Nicola Davis Premature babies appear to feel less pain during medical procedures when they are spoken to by their mothers, researchers have found. Babies that are born very early often have to spend time in neonatal intensive care units, and may need several painful clinical procedures. The situation can also mean lengthy separation from parents. Now researchers say they have found the sound of a mother’s voice seems to decrease the pain experienced by their baby during medical procedures. Dr Manuela Filippa, of the University of Geneva and first author of the study, said the research might not only help parents, by highlighting that they can play an important role while their baby is in intensive care, but also benefit the infants. Advertisement Last man out: the haunting image of America’s final moments in Afghanistan “We are trying to find non-pharmacological ways to lower the pain in these babies,” she said, adding that there was a growing body of evidence that parental contact with preterm babies could be important for a number of reasons, including attachment. Filippa said the team focused on voice because it was not always possible for parents to hold their babies in intensive care, while voice could be a powerful tool to share emotion. Mothers’ voices were studied in particular because infants would already have heard it in the womb. But Filippa said that did not mean a father’s voice could not become as familiar over time. “We are [also] running studies on fathers’ vocal contacts,” she said. Writing in the journal Scientific Reports, Filippa and colleagues at the University of Geneva, Parini hospital in Italy and the University of Valle d’Aosta, report how they examined the pain responses of 20 premature babies in neonatal intensive care to a routine procedure in which the foot is pricked and a few drops of blood collected. © 2021 Guardian News & Media Limited

Related chapters from BN: 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: 27973 - Posted: 09.01.2021

By Sabrina Imbler In a way, nausea is our trusty personal bodyguard. Feeling nauseated is widely accepted to be an evolutionary defense measure that protects people from pathogens and parasites. The urge to gag or vomit is “well-suited” to defend ourselves against things we swallow that might contain pathogens, according to Tom Kupfer, a psychological scientist at Nottingham Trent University in England. But vomiting is somewhat futile against a tick, an ectoparasite that latches on to skin, not stomachs. In an experiment that produced both stomach churning and skin crawling sensations — I can confirm these and some other physiological responses firsthand — Dr. Kupfer and Daniel Fessler, an evolutionary anthropologist from the University of California, Los Angeles, argue in a paper published on Wednesday in the journal Proceedings of the Royal Society B that humans have evolved to defend themselves against ectoparasites through a skin response that elicits scratching. Although some outside experts say more research is needed, the findings align with some understandings of the evolution of disgust. “It makes sense to have developed adaptive defensive strategies against the ‘nasty’ ones,” Cécile Sarabian, a cognitive ecologist studying animal disgust at the Kyoto University Primate Research Institute in Japan, wrote in an email. The disgusting investigation began in 2017 on the grounds of Chicheley Hall in Buckinghamshire, England. Here, Dr. Kupfer was presenting findings to colleagues on trypophobia, the aversion to clustered holes experienced by some people. His data showed that participants with trypophobia often reacted to holey images with the urge to itch or scratch, sometimes to the point of bleeding. Dr. Kupfer suggested that trypophobia might not represent fear, but rather a disgust reaction to signs of parasites or infectious diseases, which can both result in clusters of lesions or pustules.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27926 - Posted: 07.28.2021

By Tom Zeller Jr. I have headaches. Not the low-grade, annoying, “I’ve got a headache” sort of headaches. I get those, too. Most everyone does, and they are a drag. No, when I say that I get headaches, I mean that at intervals that are largely unpredictable, a knot of pain rises deep inside my head, invariably sensed behind my right eyeball. It then swiftly clicks up through the intensity scale, racing past that dull ache you might get from staring at the screen too long, leapfrogging over that doozy you had the morning after your brother’s wedding, skipping past the agonizing-but-fleeting stab of an ice-cream headache, and arriving, within a matter of minutes, at a pain so piercing and sustained that I can only grip something sturdy, rock back and forth, and grunt until it subsides. Mine are what doctors call one of the “primary headaches” — recurring and often excruciating disorders that are not byproducts of another condition (or self-inflicted by last night’s cocktails), but relentless, and in many ways still poorly understood disorders unto themselves. We know them by common names like migraine, which affects tens of millions of Americans, disproportionately women. I suffer from another flavor known as cluster headaches (technically “trigeminal autonomic cephalalgias”). And there are others, with myriad and imperfectly drawn lines distinguishing them. If you experience migraines or cluster headaches — and research suggests that more than a billion people worldwide do — you probably know something about shuttling from doctor to doctor looking for someone who “gets it.” You know what it’s like to gladly gobble up pills that don’t really work and that leave you miserable in other ways. And you might even know the same sort of incredulous exasperation that has driven me to wonder, from my fetal position on the bathroom floor: “How is it possible that science can’t fix a damn headache?” © 2021 The New York Times Company

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27924 - Posted: 07.24.2021

By Jackie Rocheleau Placebos can make us feel better. Mild electric zaps to the brain can make that effect even stronger, scientists report online May 3 in Proceedings of the National Academy of Sciences. The finding raises the possibility of enhancing the power of expectations to improve treatments. This is the first study to boost placebo and blunt pain-inducing nocebo effects by altering brain activity, says Jian Kong, a pain researcher at Massachusetts General Hospital in Charlestown. The placebo effect arises when someone feels better after taking an inactive substance, like a sugar pill, because they expect the substance to help. The nocebo effect is the placebo’s evil twin: A person feels worse after taking an inactive substance that they expect to have unpleasant effects. To play with people’s expectations, Kong’s team primed 81 participants for painful heat. The heat was delivered by a thermal stimulator to the forearm while participants lay in a functional MRI scanner. Each person received three creams, each to a different spot on their arms. One cream, participants were told, was a numbing lidocaine cream, one was a regular cream and one was a pain-increasing capsaicin cream. But in fact, all the creams were the same inert lotion, dyed different colors. © Society for Science & the Public 2000–2021

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27810 - Posted: 05.08.2021

By Kathiann Kowalski On most mornings, Jeremy D. Brown eats an avocado. But first, he gives it a little squeeze. A ripe avocado will yield to that pressure, but not too much. Brown also gauges the fruit’s weight in his hand and feels the waxy skin, with its bumps and ridges. “I can’t imagine not having the sense of touch to be able to do something as simple as judging the ripeness of that avocado,” says Brown, a mechanical engineer who studies haptic feedback — how information is gained or transmitted through touch — at Johns Hopkins University. Many of us have thought about touch more than usual during the COVID-19 pandemic. Hugs and high fives rarely happen outside of the immediate household these days. A surge in online shopping has meant fewer chances to touch things before buying. And many people have skipped travel, such as visits to the beach where they might sift sand through their fingers. A lot goes into each of those actions. “Anytime we touch anything, our perceptual experience is the product of the activity of thousands of nerve fibers and millions of neurons in the brain,” says neuroscientist Sliman Bensmaia of the University of Chicago. The body’s natural sense of touch is remarkably complex. Nerve receptors detect cues about pressure, shape, motion, texture, temperature and more. Those cues cause patterns of neural activity, which the central nervous system interprets so we can tell if something is smooth or rough, wet or dry, moving or still. © Society for Science & the Public 2000–2021.

Related chapters from BN: 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: 27787 - Posted: 04.24.2021

By Lisa Sanders, M.D. It was dark by the time the 41-year-old woman was able to start the long drive from her father’s apartment in Washington, D.C., to her home in Westchester County, N.Y. She was eager to get back to her husband and three children. Somewhere after she crossed the border into Maryland, the woman suddenly developed a terrible itch all over her body. She’d been a little itchy for the past couple of weeks but attributed that to dry skin from her now-faded summertime tan. This seemed very different: much stronger, much deeper. And absolutely everywhere, all at the same time. The sensation was so intense it was hard for the woman to pay attention to the road. She found herself driving with one hand on the steering wheel and the other working to respond to her skin’s new need. There was no rash — or at least nothing she could feel — just the terrible itch, so deep inside her skin that she felt as if she couldn’t scratch hard enough to really get to it. By the light of the Baltimore Harbor Tunnel she saw that her nails and fingers were dark with blood. That scared her, and she tried to stop scratching, but she couldn’t. It felt as if a million ants were crawling all over her body. Not on her skin, but somehow under it. The woman had gone to Washington to help her elderly father move. His place was a mess. Many of his belongings hadn’t been touched in years. She figured that she was having a reaction to all the dust and dirt and who knows what else she encountered while cleaning. As soon as she got home, she took a long shower; the cool water soothed her excoriated skin. She lathered herself with moisturizer and sank gratefully into her bed. But the reprieve didn’t last, and from that night on she was tormented by an itch that no scratching could satisfy. © 2021 The New York Times Company

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 8: Hormones and Sex
Link ID: 27775 - Posted: 04.17.2021

By Veronique Greenwood There’s nothing quite like the peculiar, bone-jarring reaction of a damaged tooth exposed to something cold: a bite of ice cream, or a cold drink, and suddenly, that sharp, searing feeling, like a needle piercing a nerve. Researchers have known for years that this phenomenon results from damage to the tooth’s protective outer layer. But just how the message goes from the outside of your tooth to the nerves within it has been difficult to uncover. On Friday, biologists reported in the journal Science Advances that they have identified an unexpected player in this painful sensation: a protein embedded in the surface of cells inside the teeth. The discovery provides a glimpse of the connection between the outer world and the interior of a tooth, and could one day help guide the development of treatments for tooth pain. More than a decade ago, Dr. Katharina Zimmerman, now a professor at Friedrich-Alexander University in Germany, discovered that cells producing a protein called TRPC5 were sensitive to cold. When things got chilly, TRPC5 popped open to form a channel, allowing ions to flow across the cell’s membrane. Ion channels like TRPC5 are sprinkled throughout our bodies, Dr. Zimmerman said, and they are behind some surprisingly familiar sensations. For instance, if your eyes start to feel cold and dry in chilly air, it’s a result of an ion channel being activated in the cornea. She wondered which other parts of the body might make use of a cold receptor such as TRPC5. And it occurred to her that “the most sensitive tissue in the human body can be teeth” when it comes to cold sensations. © 2021 The New York Times Company

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27748 - Posted: 03.27.2021

By Karen J. Bannan Hayley Gudgin of Sammamish, Wash., got her first migraine in 1991 when she was a 19-year-old nursing student. “I was convinced I was having a brain hemorrhage,” she says. “There was no way anything could be that painful and not be really serious.” She retreated to her bed and woke up feeling better the next day. But it wasn’t long until another migraine hit. And another. Taking a pill that combines caffeine with the pain relievers acetaminophen and codeine made life manageable until she got pregnant and had to stop taking her medication. After her son was born, the migraines came back. She started taking the drugs again, but they didn’t work and actually made her attacks worse. By the time Gudgin gave birth to her second son in 1997, she was having about 15 attacks a month. Her symptoms worsened over time and included severe pain, nausea, sensitivity to light, swollen hands, difficulty speaking, vomiting and diarrhea so intense she often wound up dehydrated in the emergency room. “It hit me [that] I had to do something when I was vomiting in the toilet, and my 3-year-old came and pulled my hair back,” she says. “It was no way to live — and not just because of the pain. You go to sleep every night not knowing how you’re going to wake up. You make plans knowing you might have to cancel them.” A headache specialist prescribed several preventive medicines, but each caused side effects for Gudgin, including weight gain and kidney stones. Then, in 2018, Gudgin read about a new type of treatment for frequent migraine sufferers. Her neurologist agreed it was worth a try. After much wrangling with her insurance company — the drug is costly, and she had to prove that two other drugs had failed to help her — she got approval to take it. © Society for Science & the Public 2000–2021.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27743 - Posted: 03.23.2021

Ariana Remmel A gene-silencing technique based on CRISPR can relieve pain in mice, according to a study1. Although the therapy is still a long way from being used in humans, scientists say it is a promising approach for squelching chronic pain that lasts for months or years. Chronic pain is typically treated with opioids such as morphine, which can lead to addiction. “It’s a real challenge that the best drugs we have to treat pain give us another disease,” says Margarita Calvo, a pain physician at the Pontifical Catholic University of Chile, in Santiago, who wasn’t involved in the research. That’s why the CRISPR-based technique is exciting, she says. Scientists are already evaluating CRISPR therapies that edit a person’s genome as treatments for blood diseases and some forms of hereditary blindness. The new version of CRISPR doesn’t edit genes directly — it stops them from being expressed — and so shouldn’t cause permanent changes, although it’s unclear how long its effects last for. Some studies estimate that a large proportion of the population in Europe and the United States — as high as 50% — experiences chronic pain2,3. This pain can become debilitating over time by limiting a person’s activity and having a negative effect on their mental health. Despite the prevalence of the condition, few options exist for providing long-term relief without side effects. Even so, doctors have been moving away from prescribing opioids owing to addiction risk, and that has pared down their options even further.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27728 - Posted: 03.13.2021

By Kelly Servick Swallowing an oxycodone pill might quiet nerves and blunt pain, but the drug makes other unwanted visits in the brain—to centers that can drive addiction and suppress breathing. Now, a study in mice shows certain types of pain can be prevented or reversed without apparent side effects by silencing a gene involved in pain signaling. If the approach weathers further testing, it could give chronic pain patients a safer and longer lasting option than opioids. “It’s a beautiful piece of work,” says Rajesh Khanna, a neuroscientist who studies pain mechanisms and potential treatments at the University of Arizona. Despite successes of gene therapy against rare and life-threatening disorders, few teams have explored genetic approaches to treating pain, he says. That’s in part because of reluctance to permanently change the genome to address conditions that, although disabling, aren’t always permanent or fatal. But the new approach doesn’t alter the DNA sequence itself and is theoretically reversible, Khanna notes. “I think this study is going to be our benchmark.” A prick of the finger or a punch in the gut causes pain because nerves branching through our bodies reach into the spinal cord to relay messages to the brain. Those messages can persist even after the initial injury has healed, causing chronic pain. To fire their electrical signals, pain-sensing nerves rely on the flow of ions across protein channels in their membranes. One such channel, called Nav1.7, stands out for the remarkable pain disorders that arise when it malfunctions. People with genetic mutations that make Nav1.7 overactive are prone to attacks of burning pain. Those with mutations that deactivate Nav1.7 feel no pain at all. © 2021 American Association for the Advancement of Science.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27726 - Posted: 03.11.2021

By Erin Garcia de Jesus A whiff of catnip can make mosquitoes buzz off, and now researchers know why. The active component of catnip (Nepeta cataria) repels insects by triggering a chemical receptor that spurs sensations such as pain or itch, researchers report March 4 in Current Biology. The sensor, dubbed TRPA1, is common in animals — from flatworms to people — and responds to environmental irritants such as cold, heat, wasabi and tear gas. When irritants come into contact with TRPA1, the reaction can make people cough or an insect flee. Catnip’s repellent effect on insects — and its euphoric effect on felines — has been documented for millennia. Studies have shown that catnip may be as effective as the widely used synthetic repellent diethyl-m-toluamide, or DEET (SN: 9/5/01). But it was unknown how the plant repelled insects. So researchers exposed mosquitoes and fruit flies to catnip and monitored the insects’ behavior. Fruit flies were less likely to lay eggs on the side of a petri dish that was treated with catnip or its active component, nepetalactone. Mosquitoes were also less likely to take blood from a human hand coated with catnip. Insects that had been genetically modified to lack TRPA1, however, had no aversion to the plant. That behavior — coupled with experiments in lab-grown cells that show catnip activates TRPA1 — suggests that insect TRPA1 senses catnip as an irritant. Puzzling out how the plant deters insects could help researchers design potent repellents that may be easier to obtain in developing countries hit hard by mosquito-borne diseases. “Oil extracted from the plant or the plant itself could be a great starting point,” says study coauthor Marco Gallio, a neuroscientist at Northwestern University in Evanston, Ill. © Society for Science & the Public 2000–2021

Related chapters from BN: 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: 27719 - Posted: 03.06.2021

Linda Geddes Four scientists who discovered a key mechanism that causes migraines, paving the way for new preventive treatments, have won the largest prize for neuroscience in the world, sharing £1.1m. The Lundbeck Foundation in Denmark announced on Thursday that the British researcher Peter Goadsby, Michael Moskowitz of the US, Lars Edvinsson of Sweden and Jes Olesen of Denmark had won the Brain prize. Speaking at a press briefing ahead of the announcement, Goadsby, a professor of neurology at King’s College London, said: “I’m excited that migraine research is getting this award and that migraine – this disabling problem that is a brain disorder – is being recognised in an appropriate way.” Formally known as the Grete Lundbeck European brain research prize, the annual award recognises highly original and influential advances in any area of brain research. The award ceremony will take place in Copenhagen on 25 October, where the prize will be presented by Crown Prince Frederik of Denmark. The prize-winning research revolves around unpicking the neural basis of migraine, a crippling neurological condition characterised by episodes of throbbing head pain, as well as nausea, vomiting, dizziness, extreme sensitivity to sound, light, touch and smell. It affects about one in seven people globally and is about three times more common in women than men. In the UK, it is estimated that migraines result in the loss of 25m work or school days each year at an economic cost of £2.3bn. © 2021 Guardian News & Media Limited

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27717 - Posted: 03.06.2021