Vicki Hird Does a worm feel pain if it gets trodden on? Does a fly ache when its wings are pulled off? Is an ant happy when it finds a food source? If so, they may be sentient beings, which means they can “feel”, a bit or a lot, like we do. Invertebrate sentience is becoming an ever livelier topic of debate and with new science we are getting new insights. But Dr Andrew Crump at the Royal Veterinary College, who helped ensure that new UK laws recognising animal sentience were amended to include large cephalopod molluscs and decapod crustaceans – octopuses, lobsters, crabs to you and me – says this is not at all straightforward. Nervous systems are hugely complex, and identifying consciousness and sentience – and not just automatic pain reflexes – is hard. Are responses or reactions you see from an animal – be it a wolf or a wolf ant – feelings or just automatic reflexes? Crump and his colleagues found that bees, for example, were not simple stimulus-response robots, but reacted to stimuli in sophisticated, context-dependent ways. They were found to learn colour cues for their decisions on feeding – choosing painful overheated sugars they previously avoided when non-heated options had a low sugar concentration. So they made trade-offs by processing in the brain then modifying their behaviour. In fact, new research has shown that many responses in the larger invertebrates were complex, long-lasting, and pretty consistent with criteria for pain that had been produced initially for vertebrates such as rats. Octopuses, for example, can perform amazing feats of learning to avoid painful environments and choose painkilling environments. All this establishes and quantifies “feelings” in beings that are very different from us. The work of Crump and other scientists meant that the Animal Welfare (Sentience) Act 2022 recognised for the first time in UK law (vertebrate sentience was previously covered by EU regulation) that certain invertebrates can “feel”, requiring modifications to their treatment in areas such as farming and research. © 2025 Guardian News & Media Limited

Keyword: Pain & Touch; Evolution
Link ID: 29684 - Posted: 02.26.2025

By Fred Schwaller Andrea West remembers the first time she heard about a new class of migraine medication that could end her decades of pain. It was 2021 and she heard a scientist on the radio discussing the promise of gepants, a class of drug that for the first time seemed to prevent migraine attacks. West followed news about these drugs closely, and when she heard last year that atogepant was approved for use in the United Kingdom, she went straight to her physician. West had endured migraines for 70 years. Since she started taking the drug, she hasn’t had one. “It’s marvellous stuff. It’s genuinely changed my life,” she says. For ages, the perception of migraine has been one of suffering with little to no relief. In ancient Egypt, physicians strapped clay crocodiles to people’s heads and prayed for the best. And as late as the seventeenth century, surgeons bored holes into people’s skulls — some have suggested — to let the migraine out. The twentieth century brought much more effective treatments, but they did not work for a significant fraction of the roughly one billion people who experience migraine worldwide. Now there is a new sense of progress running through the field, brought about by developments on several fronts. Medical advances in the past few decades — including the approval of gepants and related treatments — have redefined migraine as “a treatable and manageable condition”, says Diana Krause, a neuropharmacologist at the University of California, Irvine. At the same time, research is leading to a better understanding about the condition — and pointing to directions for future work. Studies have shown, for example, that migraine is a broad phenomenon that originates in the brain and can manifest in many debilitating symptoms, including light sensitivities and aura, brain fog and fatigue. “I used to think that disability travels with pain, and it’s only when the pain gets severe that people are impaired. That’s not only false, but we have treatments to do something about it,” says Richard Lipton, a neurologist at the Albert Einstein College of Medicine in New York City. © 2025 Springer Nature Limited

Keyword: Pain & Touch
Link ID: 29681 - Posted: 02.22.2025

By Gina Kolata The Food and Drug Administration approved a new medication Thursday to treat pain from an injury or surgery. It is expensive, with a list price of $15.50 per pill. But unlike opioid pain medicines, it cannot become addictive. That is because the drug, suzetrigine, made by Vertex Pharmaceuticals and to be sold as Journavx, works only on nerves outside the brain, blocking pain signals. It cannot get into the brain. Researchers say they expect it to be the first of a new generation of more powerful nonaddictive drugs to relieve pain. To test the drug, Vertex, which is based in Boston, conducted two large clinical trials, each with approximately 1,000 patients who had pain from surgery. They were randomly assigned to get a placebo; to get the opioid sold as Vicodin, a widely used combination pain medicine of acetaminophen (Tylenol) and hydrocodone; or to get suzetrigine. In one trial, patients had an abdominoplasty, or tummy tuck. In the other, they had a bunionectomy. Side effects of suzetrigine reported by patients were similar to the ones reported by those taking the placebo. The company also submitted data from a 250-person study that assessed the drug’s safety and tolerability in patients with pain from surgery, trauma or accidents. Suzetrigine eased pain as much as the combination opioid. Both were better than the placebo at relieving pain. Suzetrigine’s price, though, is much higher than that of acetaminophen plus hydrocodone. Patients are expected to take two pills a day, for a total cost of $31 a day. The older drug, said Dr. John D. Loeser, an emeritus pain expert at the University of Washington, is “dirt cheap” at pennies per pill. But suzetrigine does not have opioids’ unpleasant side effects like nausea and drowsiness, and it is nonaddictive. © 2025 The New York Times Company

Keyword: Pain & Touch; Drug Abuse
Link ID: 29653 - Posted: 02.01.2025

By Laura Sanders Scratching an itch can bring a contradictory wave of pleasure and misery. A mouse study on scratching, reported in the Jan. 31 Science, fleshes out this head-scratching paradox and could point out ways to better curb pernicious itch in people. First, the bad news: Scratching itchy ears led to a round of inflammation. Itch-provoking substances, such as the oil in poison ivy, activate mast cells, immune sentries that release itch signals and kick off inflammation. But so does scratching, the new study suggests. “The act of scratching is actually triggering the inflammation by synergizing with mast cells to make them more effective,” says study coauthor Daniel Kaplan, a dermatologist and immunologist at the University of Pittsburgh. Mice that couldn’t scratch their itchy ears, thanks to tiny cones of shame, had less inflammation than mice that scratched. The same was true for mice that didn’t sense the itch, the researchers report. Kaplan relates the results to a mosquito bite. “Most of the time, it’ll go away in five, 10 minutes,” he says. “But if you start scratching it, now, you get a really big, inflamed, itchy lesion on your skin that can stick around for several days. It’s a lot worse. And I think this could be a mechanism that explains why.” Now onto the good news: Scratching lessened the amount of potentially harmful bacteria (Staphylococcus aureus) on mice’s skin, perhaps through the heightened immune reaction it prompts. “That was a clear demonstration that scratching can have a benefit in the context of an acute infection,” Kaplan says. But too much scratching can rip the skin and usher in more bacteria, he cautions. “In that sense, scratching, through a different mechanism, also makes things even worse.” © Society for Science & the Public 2000–2025.

Keyword: Pain & Touch
Link ID: 29648 - Posted: 02.01.2025

By Katherine Ellison “American Ninja Warrior” contestant Jimmy Choi was 27 when he was diagnosed with young-onset Parkinson’s disease after a routine medical exam. Today, Choi, 50, is an adviser to the Michael J. Fox Foundation for Parkinson’s Research who champions physical fitness and works to inspire others via public speaking and social media posts. More than 1 million Americans have Parkinson’s disease, a neurological illness that can cause tremors, loss of balance, confusion and depression. Choi spent the eight years after his diagnosis in denial as his symptoms grew worse. After a mortifying fall, however, his perspective changed, and he embraced exercise — in a big way. Since 2011, the Chicago-based former tech executive (he retired from full-time work in 2018, though he still works as a consultant) has run 16 marathons and earned three Guinness World records, the most recent in 2023 for consecutive double high five push-ups. He has also competed seven times on “American Ninja Warrior,” the reality-TV show in which contestants make their way past daunting obstacles, crossing unstable bridges, running up walls and leaping through the air, all while trying to avoid falling into a large pool of water. Last year Choi finished his seventh, and, he insists, last “Ninja” appearance. It’s set to air this spring. Q: What led to your diagnosis? A: It was a routine exam for health insurance, in 2003. A nurse noticed the way I was walking and said I should talk to my doctor. I had to see four neurologists before I got diagnosed, and for several years afterward, I lost my motivation. I started isolating from friends, gained a lot of weight and couldn’t walk without a cane.

Keyword: Parkinsons
Link ID: 29645 - Posted: 01.29.2025

By Angie Voyles Askham More than 150 years after the first known description of Huntington’s disease and 32 years after the causative gene, HTT, was identified, new evidence has emerged to explain how variants linked to the disease devastate the brain: The toxicity comes not from the initial variant itself but rather from its dynamic expansion past a set threshold in specific cells, according to a study published today in Cell. The results help explain why most people with Huntington’s disease don’t start to show symptoms—including muscle rigidity, irregular movements and severe psychological issues—until age 30 to 50, with the gradual loss of striatal projection neurons, also called medium spiny neurons, says co-lead researcher Steven McCarroll, professor of biomedical science and genetics at Harvard Medical School. “We hadn’t been thinking about mutations as dynamic things” that become toxic only later in life, he says. The HTT variants associated with Huntington’s disease all have extra repeats of the DNA triplet CAG. Typical people carry about 15 to 30 of these repeats, and those with the disease tend to have 40 or more. The disease-linked expansions, which are known to grow even larger over time, result in a gangly version of the Huntington’s protein that is thought to cause neurons to malfunction and degenerate. But the expansion does not appear to affect a cell’s biology until it exceeds 150 CAG copies, according to the new study. And the repeats accumulate quietly over the course of years, and at different rates for different cells. Striatal projection neurons with more than 150 repeats have severely dysregulated transcriptomes, McCarroll and his colleagues found by analyzing gene expression in postmortem tissue from people with Huntington’s disease. But other cell types in the striatum, including oligodendrocytes and interneurons, do not end up with as many repeats, nor do they undergo similar transcriptomic changes, the work shows. © 2025 Simons Foundation

Keyword: Huntingtons; Genes & Behavior
Link ID: 29636 - Posted: 01.22.2025

By Phie Jacobs For more than 30 years, scientists have known the genetic culprit behind Huntington disease, a devastating neurodegenerative disorder that causes cells deep in the brain to sicken and die. But they couldn’t account for why people who inherit the faulty gene variant take so long to develop symptoms, or why disease progression varies so widely from person to person. A study published today in Cell helps explain: In the brain cells that die off in Huntington, a repetitive stretch of a gene’s DNA gets longer and longer over a person’s life, and this accelerating expansion turns deadly to the cell—and ultimately to the person. The findings represent “a really remarkable insight,” says Leslie Thompson, a neuroscientist at the University of California, Irvine who wasn’t involved in the new research. “This study and some others are changing the way that we’re thinking about the disease.” People who develop Huntington inherit a flawed version of the HTT gene, which produces a protein called huntingtin. This gene contains an unusual stretch of DNA, where a sequence of three of its nucleotide bases—cytosine, adenine, and guanine, or CAG in genetic parlance—are repeated multiple times in a row. And although most people inherit versions of HTT with about 15 to 30 consecutive CAG repeats and never develop Huntington, those with 40 or more in the gene almost always have symptoms later in life, including psychological and cognitive problems and uncontrolled, jerking movements known as chorea. The genetic stutter produces an abnormally large, unstable version of the huntingtin protein, which forms clumps inside brain cells. The condition usually leads to early death, often from issues related to difficulty swallowing, injuries from falls, or suicide. The longer a person’s stretch of repeats, the earlier the disorder rears its head. Scientists originally thought the number of CAG repeats only increased as the HTT gene was passed down through generations; a child of a parent with Huntington might themselves develop the condition at an earlier age. But it turns out the length of this genetic “stutter” can change over a person’s life in at least some of their cells. A 2003 study analyzed brain samples donated by people who had died of Huntington and found shockingly large CAG expansions in a part of the brain known as the striatum.

Keyword: Huntingtons; Genes & Behavior
Link ID: 29634 - Posted: 01.18.2025

By Jennifer Kahn Here’s a strange story: One day two summers ago, I woke up because my arms — both of them — hurt. Not the way they do when you’ve slept in a funny position, but as if the tendons in my forearms and hands were moving through mud. What felt like sharp electric shocks kept sparking in my fingers and sometimes up the inside of my biceps and across my chest. Holding anything was excruciating: a cup, a toothbrush, my phone. Even doing nothing was miserable. It hurt when I sat with my hands in my lap, when I stood, when I lay flat on the bed or on my side. The slightest pressure — a bedsheet, a watch band, a bra strap — was intolerable. It was August, and every doctor seemed to be away on vacation. The ones I did manage to see were politely stumped. It wasn’t carpal tunnel, tennis elbow or any other injury they could identify. I did nothing unusual the day before: an hour of work on my laptop, followed by a visit with a friend. We sat in her backyard and talked. For the first few weeks, I could barely sleep. Over the following months, I lost weight — almost a pound a week. I couldn’t drive, or cook, or use my laptop for work, or even hold a book or a pen. I would have been bored, except the pain was so tiring that I could barely function. I spent the days shuffling around the house listening to audiobooks and doing voice-to-text searches for “nerve pain arms” with my phone flat on the table, then carefully, painfully, scrolling through the results. I think we’re past the point where I have to explain that chronic pain is not the result of imbalanced humors or a wandering uterus or possession by demons. But for more modern skeptics, this is where I should add that chronic pain also isn’t just “all in your head” or “not really that bad” — or any of the other ways in which people who suffer from it are still regularly gaslit and dismissed. Personally, I never had to contend with not being believed, almost certainly because I’m an otherwise healthy, reasonably well-off white woman with a clean medical history and no significant record of anxiety or depression. Instead, I was taken seriously. A whole gamut of tests was run. My wrists were X-rayed. I had an M.R.I. on my cervical spine. Each new doctor ordered new blood tests: some for vitamin deficiencies, others for autoimmune diseases like rheumatoid arthritis. © 2025 The New York Times Company

Keyword: Pain & Touch
Link ID: 29628 - Posted: 01.15.2025

By Terence Monmaney The road switches back and forth again and again as it climbs into Montchavin, perched in the French Alps at 4,100 feet above sea level. The once-sleepy mountainside village, developed into a ski resort in the 1970s, is dotted with wooden chalet-style condo buildings and situated in the midst of a vast downhill complex known as Paradiski, one of the world’s largest. Well known to skiers and alpinistes, Montchavin also has grabbed the attention of medical researchers as the site of a highly unusual cluster of a devastating neurological disease, amyotrophic lateral sclerosis. ALS, brought about by the progressive loss of nerve function in the brain, spinal cord and motor neurons in the limbs and chest, leading to paralysis and death, is both rare and rather evenly distributed across the globe: It afflicts two to three new people out of 100,000 per year. Though Montchavin is flooded with visitors in winter and summer, the year-round resident population is only a couple hundred, and neighboring villages aren’t much bigger, so the odds are strongly against finding more than just a few ALS patients in the immediate area. Yet physicians have reported 14. The first of the village patients to arouse suspicion in Emmeline Lagrange, the neurologist who has led the investigation into the problem, was a woman in her late thirties, a ski instructor and ski lift ticket-checker originally from Poland who worked in the offseason at the local tourism office. It was 2009. A physician in Montchavin had referred the woman to Lagrange, who practices at Grenoble University Hospital, 84 miles southwest of the village. Lagrange diagnosed ALS and recalls phoning the Montchavin physician to explain the consequences: “The first thing she said was, ‘I certainly know what it is. It’s the fourth case in the village. My neighbor died of ALS 20 years ago and two friends of hers are still victims of the disease.’”

Keyword: ALS-Lou Gehrig's Disease ; Neurotoxins
Link ID: 29606 - Posted: 12.21.2024

By Lisa Sanders, M.D. The 62-year-old woman shifted in her seat. The flight to Honolulu was full, the mood a little giddy. The unbroken ocean and sky filled the window. She and her daughter were four hours into the trip from Los Angeles to the wedding of a close family friend; it was going to be a great week. Then, she caught herself scratching lightly at a place on her forearm, just below the crease of her elbow. She lifted her arm to look at the spot. Nothing there. Immediately she was filled with dread. She reached over her head to touch the call button. She needed ice, lots of ice, and she needed it right away. The mild itch had already exploded into spasms of an intense sensation — it seemed wrong to call it an itch; surely there was a better word for it. The fierce intensity of the feeling shocked her. It was a feeling that insisted she scratch. Except scratching never helped. And she had the scars to prove it. She had suffered episodes of itching like this a few times in the past couple of years, though never quite as bad as it was on this flight. Her doctor back home had no idea what caused the crazy itch or what more she might do about it. These attacks came out of nowhere but immediately brought life to a standstill as she tried to ease the unbearable sensation. A bout could last for hours and almost always ended with her arm a bloody mess. When her daughter first saw her mother raking her nails over the invisible injury and the distress she felt fighting this unwinnable battle, she had offered her a Valium. And it helped. The itch was still there but the intensity somehow lessened. On the flight, the woman retrieved the pills she now carried with her all the time. The little bags of ice brought by the flight attendant melted slowly, numbing the hand that pressed them against her arm and easing the itch. She knew from experience that as soon as the ice was removed, the itch would roar back. The attendant brought an ice bucket. But within the hour, she needed more ice. More Valium. She was drenched with the condensation. Her clothes were dotted with blood. She didn’t care. She just had to get through it. © 2024 The New York Times Company

Keyword: Pain & Touch
Link ID: 29583 - Posted: 12.04.2024

Heather Margonari The opioid crisis remains a significant public health challenge in the United States. In 2022, over 2.5 million American adults had an opioid use disorder, and opioids accounted for nearly 76% of overdose deaths. Some patients are fearful of using opioids after surgery due to concerns about dependence and potential side effects, even when appropriately prescribed by a doctor to manage pain. Surgery is often the first time patients receive an opioid prescription, and their widespread use raises concerns about patients becoming long-term users. Leftover pills from a patient’s prescriptions may also be misused. Researchers like us are working to develop a personalized and comprehensive surgical experience that doesn’t use opioids. Our approach to opioid-free surgery addresses both physical and emotional well-being through effective anesthesia and complementary pain-management techniques. What is opioid-free anesthesia? Clinicians have used morphine and other opioids to manage pain for thousands of years. These drugs remain integral to anesthesia. Help us raise up the voices of experts. Most surgical procedures use a strategy called balanced anesthesia, which combines drugs that induce sleep and relax muscles with opioids to control pain. However, using opioids in anesthesia can lead to unwanted side effects, such as serious cardiac and respiratory problems, nausea and vomiting, and digestive issues. Concerns over these adverse effects and the opioid crisis have fueled the development of opioid-free anesthesia. This approach uses non-opioid drugs to relieve pain before, during and after surgery while minimizing the risk of side effects and dependency. Studies have shown that opioid-free anesthesia can provide similar levels of pain relief to traditional methods using opioids. Copyright © 2010–2024, The Conversation US, Inc.

Keyword: Pain & Touch
Link ID: 29575 - Posted: 11.27.2024

By Fred Schwaller Scott Imbrie still remembers the first time that physicians switched on the electrodes sitting on the surface of his brain. He felt a tingling, poking sensation in his hand, like “reaching into an evergreen bush”, he says. “It was like I was decorating a Christmas tree.” Back in 1985, a car crash shattered three of Imbrie’s vertebrae and severed 70% of his spinal cord, leaving him with very limited sensation or mobility in parts of his body. Now, thanks to an implanted brain–computer interface (BCI), Imbrie can operate a robotic arm, and receive sensory information related to what that arm is doing. Imbrie spends four days a week, three hours at a time, testing, refining and tuning the device with a team of researchers at the University of Chicago in Illinois. Scientists have been trying to restore mobility for people with missing or paralysed limbs for decades. The aim, historically, was to give people the ability to control prosthetics with commands from the nervous system. But this motor-first approach produced bionic limbs that were much less helpful than hoped: devices were cumbersome and provided only rudimentary control of a hand or leg. What’s more, they just didn’t feel like they were part of the body and required too much concentration to use. Scientists gradually began to realize that restoring full mobility meant restoring the ability to sense touch and temperature, says Robert Gaunt, a bioengineer at the University of Pittsburgh in Pennsylvania. Gaunt says that this realization has led to a revolution in the field. A landmark study1 came in 2016, when a team led by Gaunt restored tactile sensations in a person with upper-limb paralysis using a computer chip implanted in a region of the brain that controls the hand. Gaunt then teamed up with his Pittsburgh colleague, bioengineer Jennifer Collinger, to integrate a robotic arm with the BCI, allowing the individual to feel and manipulate objects. © 2024 Springer Nature Limited

Keyword: Robotics; Pain & Touch
Link ID: 29557 - Posted: 11.13.2024

Terry Gross We've all had bug bites, or dry scalp, or a sunburn that causes itch. But what if you felt itchy all the time — and there was no relief? Journalist Annie Lowrey suffers from primary biliary cholangitis (PBC), a degenerative liver disease in which the body mistakenly attacks cells lining the bile ducts, causing them to inflame. The result is a severe itch that doesn't respond to antihistamines or steroids. "It feels like being trapped inside your own body," Lowrey says of the disease. "I always describe it as being like a car alarm. Like, you can't stop thinking about it." PBC is impacts approximately 80,000 people in the U.S., the majority of whom are women. At its worst, Lowrey says, the itch caused her to dig holes in her skin and scalp. She's even fantasized about having limbs amputated to escape the itch. Lowrey writes about living with PBC in the Atlantic article, "Why People Itch and How to Stop It." She says a big part of her struggle is coming to terms with the fact that she may never feel fully at ease in her skin. "I talked to two folks who are a lot older than I was, just about like, how do you deal with it? How do you deal with the fact that you might itch and never stop itching? … And both of them were kind of like, 'You put up with it, stop worrying about it and get on with your life,'" she says. "I think I was mentally trapped ... and sometimes it's like, OK, ... go do something else. Life continues on. You have a body. It's OK." © 2024 npr

Keyword: Pain & Touch
Link ID: 29556 - Posted: 11.13.2024

By Erin Garcia de Jesús The first detailed structure of an infectious prion that causes chronic wasting disease, or CWD, reveals features that could help guide vaccine development or explain why the illness hasn’t yet made the leap to people, researchers report October 24 in Acta Neuropathologica. One such feature is a 180-degree twist between two sections of the prion. In versions engineered to infect rodents in order to study the disease, that twist doesn’t exist. Like the prion illness Creutzfeldt-Jakob disease in people, CWD prions in deer, elk and moose transform a healthy brain protein called PrP into misshapen versions that clump together and cause symptoms such as listlessness, drastic weight loss and lack of fear. While no person has contracted the disease and studies in mice and primates suggest that the risk to humans is extremely low, CWD’s spread among animals that people eat has raised concerns that it one day could jump to people (SN: 6/10/24). Understanding how deer prions misfold could help reveal why CWD doesn’t easily spread to humans. But “prions are messy,” says Byron Caughey, a biochemist at the National Institutes of Health’s Rocky Mountain Laboratories in Hamilton, Mont. Because the proteins “are very sticky and they tend to cling together,” researchers have a tough time getting a clear picture of what diseased prions look like. Previous studies looking at other prions, including rodent-adapted versions originally from sheep, showed that the proteins stack together like plates. Using hundreds of thousands of electron microscopy images, Caughey and colleagues found that a natural prion from the brain tissue of a white-tailed deer stacks in a similar way, but with some potentially key differences. © Society for Science & the Public 2000–2024.

Keyword: Prions
Link ID: 29552 - Posted: 11.13.2024

By Miryam Naddaf When a dog shakes water off its fur, the action is not just a random flurry of movements — nor a deliberate effort to drench anyone standing nearby. This instinctive reflex is shared by many furry mammals including mice, cats, squirrels, lions, tigers and bears. The move helps animals to remove water, insects or other irritants from hard-to-reach places. But underlying the shakes is a complex — and previously mysterious — neurological mechanism. Now, researchers have identified the neural circuit that triggers characteristic ‘wet dog’ shaking behaviour in mice — which involves a specific class of touch receptors, and neurons that connect the spinal cord to the brain. Their findings were published in Science on 7 November1. “The touch system is so complex and rich that [it] can distinguish a water droplet from a crawling insect from the gentle touch of a loved one,” says Kara Marshall, a neuroscientist at Baylor College of Medicine in Houston, Texas. “It’s really remarkable to be able to link a very specific subset of touch receptors to this familiar and understandable behaviour.” The hairy skin of mammals is packed with more than 12 types of sensory neuron, each with a unique function to detect and interpret various sensations. Study co-author Dawei Zhang, a neuroscientist then at Harvard Medical School in Boston, Massachusetts, and his colleagues focused on a type of ultra-sensitive touch detecting receptors called C-fibre low-threshold mechanoreceptors (C-LTMRs), which wrap around hair follicles. In humans, these receptors are associated with pleasant touch sensations, such as a soft hug or a soothing stroke. But in mice and other animals, they serve a protective role: alerting them to the presence of something on their skin, whether it’s water, dirt or a parasite. When these stimuli cause hairs on the skin to bend it activates the C-LTMRs, says Marshall, “extending the sensibility of the skin beyond just the surface”. © 2024 Springer Nature Limited

Keyword: Pain & Touch; Evolution
Link ID: 29551 - Posted: 11.09.2024

By Amber Dance For Cherise Irons, chocolate, red wine and aged cheeses are dangerous. So are certain sounds, perfumes and other strong scents, cold weather and thunderstorms. Stress and lack of sleep, too. She suspects all of these things can trigger her migraine attacks, which manifest in a variety of ways: pounding pain in the back of her head, exquisite sensitivity to the slightest sound, even blackouts and partial paralysis. Irons, 48, of Coral Springs, Florida, once worked as a school assistant principal. Now, she’s on disability due to her migraine. Irons has tried so many migraine medications she’s lost count — but none has helped for long. Even a few of the much-touted new drugs that have quelled episodes for many people with migraine have failed for Irons. Though not all are as impaired as Irons, migraine is a surprisingly common problem, affecting 14 percent to 15 percent of people. Yet scientists and physicians remain largely in the dark about how triggers like Irons’s lead to attacks. They have made progress nonetheless: The latest drugs, inhibitors of a body signaling molecule called CGRP, have been a blessing for many. For others, not so much. And it’s not clear why. The complexity of migraine probably has something to do with it. “It’s a very diverse condition,” says Debbie Hay, a pharmacologist at the University of Otago in Dunedin, New Zealand. “There’s still huge debate as to what the causes are, what the consequences are.”

Keyword: Pain & Touch
Link ID: 29519 - Posted: 10.16.2024

By Laura Sanders CHICAGO — Big news for fighting sisters: Scientists have found the sensors that signal the painful zing of a hair pull. And this pain message can rip along a nerve fiber at about 100 miles an hour, placing it among the fastest known pain signals. The discovery, presented October 8 at the annual meeting of the Society for Neuroscience, offers insight into the diverse ways our bodies sense and respond to different sorts of pain. Pain can come from many catastrophes — cuts, jabs, pinches, cramps, bites, slaps, stubbing a toe in the dark. And while our bodies can generally tell these insults apart thanks to a variety of biological pathways, they all hurt. “It’s not surprising that we have figured out many, many ways to make [pain] happen,” says neuroscientist Gregory Dussor of the University of Texas at Dallas. “Because when it doesn’t, we don’t live.” Laboratory tests showed a hair pull to be about 10 times as painful as a pinprick, neuroscientist Emma Kindström of Linköping University in Sweden and colleagues found. The pain of the pull relies on a large, propeller-shaped protein called PIEZO2, further tests showed. That sensor was known to detect mechanical forces, including light touches, but wasn’t thought to detect acute pain signals. People who lack this protein don’t feel hair-pull pain. A hair-pull signal moves along nerve fibers much faster than other sorts of pain, Kindström says, traveling in bursts along an insulated conduit called an Aβ nerve fiber. Other kinds of pain signals, such as a burn from a hot stove, travel more slowly along different kinds of fibers. © Society for Science & the Public 2000–2024.

Keyword: Pain & Touch
Link ID: 29512 - Posted: 10.12.2024

By Simon Makin The word “bionic” conjures sci-fi visions of humans enhanced to superhuman levels. It’s true that engineering advances such as better motors and batteries, together with modern computing, mean that the required mechanical and electronic systems are no longer a barrier to advanced prostheses. But the field has struggled to integrate these powerful machines with the human body. That’s starting to change. A recent trial tested one new integration technique, which involves surgically reconstructing muscle pairs that give recipients a sense of the position and movement of a bionic limb. Signals from those muscles control robotic joints, so the prosthesis is fully under control of the user’s brain. The system enabled people with below-knee amputations to walk more naturally and better navigate slopes, stairs and obstacles, researchers reported in the July Nature Medicine. Engineers have typically viewed biology as a fixed limitation to be engineered around, says bioengineer Tyler Clites, who helped develop the technique several years ago while at MIT. “But if we look at the body as part of the system to be engineered, in parallel with the machine, the two will be able to interact better.” That view is driving a wave of techniques that reengineer the body to better integrate with the machine. Clites, now at UCLA, calls such techniques “anatomics,” to distinguish them from traditional bionics. “The issue we were tackling wasn’t an engineering problem,” he says. “The way the body had been manipulated during the amputation wasn’t leaving it in a position to be able to control the limbs we were creating.” In an anatomics approach, bones are exploited to provide stable anchors; nerves are rerouted to create control signals for robotic limbs or transmit sensory feedback; muscles are co-opted as biological amplifiers or grafted into place to provide more signal sources. © Society for Science & the Public 2000–2024.

Keyword: Robotics
Link ID: 29507 - Posted: 10.05.2024

By Cassandra Willyard Megan Hodge’s first bout of intense pain arrived when she was in her mid-20s. Hodge and her husband were getting ready to visit family for Thanksgiving. Though Hodge had been dealing with a variety of chronic health issues, her workout had gone well that morning and she finally felt like she was getting a handle on her health. Hodge began packing. As she reached into her closet to grab a sweater, her back gave out. The pain was excruciating, so intense that she felt light-headed and thought she might vomit. As the years passed, Hodge had more frequent and more severe bouts of back pain. Any small movement could be a trigger — grabbing a towel from the linen closet, picking up a toy off the floor, sneezing. In 2021, Hodge experienced a particularly bad flare-up. None of the strategies she had previously used to help her manage seemed to be working. She was afraid to make any movement. She felt hopeless. “I just could not regain footing, metaphorically and physically,” she says. “I truly felt frozen in my chronic pain and chronic health journey.” Hodge is far from alone. In the United States, chronic pain affects tens of millions of people — about 1 in 5 adults and nearly 1 in 3 people ages 65 and older. “The amount of suffering from arthritis and aging that I’ve seen in my pain clinic, it’s overwhelming to me as a pain doctor,” says Antje Barreveld, an anesthesiologist at Mass General Brigham’s Newton-Wellesley Hospital in Massachusetts. What’s more, the mainstay therapy for severe acute and chronic pain — prescription opioids — has helped fuel an epidemic that kills tens of thousands of people each year. “We have to have some better alternatives,” she says. So researchers have doubled down in their quest to find new pain treatments that aren’t as addictive as opioids. “The pain field has really made very rapid and tremendous progress in the last decade,” says D.P. Mohapatra, a former pain scientist who now oversees research at the National Institute of Neurological Disorders and Stroke in Bethesda, Md. © Society for Science & the Public 2000–2024.

Keyword: Pain & Touch; Drug Abuse
Link ID: 29470 - Posted: 09.07.2024

By Pam Belluck When Shawn Connolly was diagnosed with Parkinson’s disease nine years ago, he was a 39-year-old daredevil on a skateboard, flipping and leaping from walls, benches and dumpsters through the streets of San Francisco. He appeared in videos and magazines, and had sponsorships from skateboard makers and shops. But gradually, he began to notice that “things weren’t really working right” with his body. He found that his right hand was cupping, and he began cradling his arm to hold it in place. His balance and alignment started to seem off. Over time, he developed a common Parkinson’s pattern, fluctuating between periods of rapid involuntary movements like “I’ve got ants in my pants” and periods of calcified slowness when, he said, “I could barely move.” A couple of years ago, Mr. Connolly volunteered for an experiment that summoned his daring and determination in a different way. He became a participant in a study exploring an innovative approach to deep brain stimulation. In the study, which was published Monday in the journal Nature Medicine, researchers transformed deep brain stimulation — an established treatment for Parkinson’s — into a personalized therapy that tailored the amount of electrical stimulation to each patient’s individual symptoms. The researchers found that for Mr. Connolly and the three other participants, the individualized approach, called adaptive deep brain stimulation, cut in half the time they experienced their most bothersome symptom. Mr. Connolly, now 48 and still skateboarding as much as his symptoms allow, said he noticed the difference “instantly.” He said the personalization gave him longer stretches of “feeling good and having that get-up-and-go.” © 2024 The New York Times Company

Keyword: Parkinsons
Link ID: 29447 - Posted: 08.21.2024