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Cluster headaches are ‘the most painful condition on the planet’

Sammie Seamon Peter was working late, watching two roulette tables in play at a London casino, when he felt something stir behind his right eye. It was just a shadow of sensation, a horribly familiar tickle. But on that summer night in 2018, as chips hit the tables and gamblers’ conversation swelled, panic set in. He knew he only had a few minutes. Peter found his boss, muttered that he had to leave, now, and ran outside. By then, the tickle had escalated; it felt like a red-hot poker was being shoved through his right pupil. Tears flowed from that eye, which was nearly swollen shut, and mucus from his right nostril. Half-blinded, gripping at his face, he stumbled along the street, eventually escaping into a company car that whisked him home, where he blacked out. Every day that followed, Peter, then in his early 40s, would experience the same attack at 10am, 2pm and 6pm, like perfect clockwork. “Oh God, here it comes,” he’d think to himself, before fireworks exploded in his temple and the poker stabbed into the very roots of his teeth, making him scream and sometimes vomit. “It just grows, and it thumps, and it thumps, and it thumps with my heartbeat,” said Peter, recalling the pain. Peter had experienced these inexplicable episodes since he was a kid, always in the summer. An attack left him shaking and exhausted, and waiting on the next bout was a kind of psychological torture – within the short respites, he dreaded the next. Once, when Peter felt one starting, he threw on his shoes and sprinted through the streets of south London. He didn’t care which turns he took. Maybe if he ran fast enough, his lungs full of air, he could outrun the thing. His heart pumped in his chest, more from fear than the exercise itself. When the pain escalated to an unbearable pitch, he slowed to a stop, dry heaving, and sat down to press on his eye. He was three miles away from home. © 2025 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: 29761 - Posted: 04.26.2025

Baffling chronic pain eases after doses of gut microbes

Humberto Basilio What Rina Green calls her “living hell” began with an innocuous backache. By late 2022, two years later, pain flooded her entire body daily and could be so intense that she couldn’t get out of bed. Painkillers and physical therapy offered little relief. She began using a wheelchair. Green has fibromyalgia, a mysterious condition with symptoms of widespread and chronic muscle pain and fatigue. No one knows why people get fibromyalgia, and it is difficult to treat. But eight months ago, Green received an experimental therapy: pills containing living microorganisms of the kind that populate the healthy human gut. Her pain decreased substantially, and Green, who lives in Haifa, Israel, and is now 38, can go on walks — something she hadn’t done since her fibromyalgia diagnosis. Green was one of 14 participants in a trial of microbial supplements for the condition. All but two reported an improvement in their symptoms. The trial is so small that “we should take the results with a grain of salt”, says co-organizer Amir Minerbi, a pain scientist at the Technion — Israel Institute of Technology in Haifa. “But it is encouraging [enough] to move forward.” The trial results and data from other experiments linking fibromyalgia to gut microbes are published today in Neuron1. Fibromyalgia affects up to 4% of the global population and occurs in the absence of tissue damage. In 2019, Minerbi and his colleagues discovered that the gut microbiomes — the collection of microbes living in the intestines — of women with fibromyalgia differed significantly from those of healthy women2. This led the scientists to wonder whether a dose of microbes from healthy people would ease the pain and fatigue caused by the condition. After all, previous research3 had shown that gut microbes might indirectly influence an array of chemical signals tied to pain perception. The team transplanted minuscule samples of microbe-laden faeces from both women with fibromyalgia and healthy women into mice without any microbes in their bodies. The researchers found that mice that received microbes from women with fibromyalgia showed signs of greater sensitivity to pain in response to pressure, heat and cold than did mice that got microbes from healthy women. The first group also showed more evidence of spontaneous pain. © 2025 Springer Nature Limited

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 29760 - Posted: 04.26.2025

Pain pathway in a dish could aid search for new analgesic drugs

Jon Hamilton Researchers created an assembloid by integrating four organoids that represent the four components of the human sensory pathway, along which pain stimuli signals are conveyed to the brain. Stimulation of the sensory organoid (top) by pain-inducing substances, such as capsaicin, triggers neuronal activity in that organoid which is then transmitted to the adjacent spinal-cord organoid, the thalamic organoid and, finally, to the cortical organoid (bottom) Researchers integrated four organoids that represent the four components of the human sensory pathway, along which pain signals are conveyed to the brain. Stimulation of the sensory organoid (top) by substances, such as capsaicin, triggers neuronal activity that is then transmitted throughout the rest of the organoids. Pasca lab/Stanford Medicine Scientists have re-created a pain pathway in the brain by growing four key clusters of human nerve cells in a dish. This laboratory model could be used to help explain certain pain syndromes, and offer a new way to test potential analgesic drugs, a Stanford team reports in the journal Nature. "It's exciting," says Dr. Stephen Waxman, a professor at Yale School of Medicine who was not involved in the research. © 2025 npr

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory and Learning
Link ID: 29739 - Posted: 04.12.2025

Immune cells have unexpected role in fighting pain

By Mitch Leslie Unlike the combative immune cells that protect us from pathogens, regulatory T cells (Tregs) are nurturers. They salve inflammation, promote healing of injured tissue, and rein in immune attacks to curb self-inflicted damage. Now, a study of mice reported today in Science suggests some Tregs also act on nerve cells to quell a specific type of pain—but only in females. Why only female rodents seem to benefit remains unclear, but researchers hope they might someday enlist these Tregs to address pain conditions, many of which disproportionately affect women. “It’s a very impressive paper,” says neuroscientist Gila Moalem-Taylor of the University of New South Wales Sydney, who wasn’t connected to the research. The study “uses elegant, sophisticated methods to conclusively demonstrate the mechanisms” by which the cells reduce one kind of sensitivity to pain, she says. Tregs, a type of white blood cell, are best known for their role in keeping the immune system in balance and preventing autoimmunity. But researchers have recently found that they also help control pain. For example, a 2021 study by neuroscientist Allan Basbaum of the University of California San Francisco (UCSF) and colleagues showed that Tregs reduce mice’s sensitivity to pain triggered by other immune cells that reside in the brain and spinal cord. That research and additional work suggested Tregs influence pain by targeting various immune cells and tamping down inflammation. But these studies left open the possibility that Tregs might also directly affect pain-sensing nerve cells. Basbaum, his postdoc Élora Midavaine, UCSF dermatologist Sakeen Kashem, and their colleagues launched the new study to nail down how the regulatory cells curb pain. They focused on Tregs that dwell in the meninges—the membranes that sheathe the brain and spinal cord—and in similar nearby membranes. The cells are much more abundant in these structures than elsewhere in the nervous system. To find out whether the cells affect pain perception, the scientists used genetically engineered mice whose Tregs are vulnerable to a toxin produced by the bacteria that cause diphtheria. Injecting this toxin into the meninges in the lower back killed about 90% of the Tregs in the membranes without harming Tregs in the rest of the body.

Do worms feel pain and are ants happy? Why the science on invertebrate feelings is evolving

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

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: 29684 - Posted: 02.26.2025

Migraine is more than a headache — a radical rethink offers hope to one billion people

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

F.D.A. Approves Drug to Treat Pain Without Opioid Effects

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

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: 29653 - Posted: 02.01.2025

Scratching an itch is so good, and so bad

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.

Chronic Pain Is a Hidden Epidemic. It’s Time for a Revolution.

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

She Was Scratching Her Arms Raw. Would Anything Stop This Itch?

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

Opioid-free surgery treats pain at every physical and emotional level

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.

Chronic itch is miserable. Scientists are just scratching the surface

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

Why do wet dogs shake themselves dry? Neuroscience has an answer

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

Studies of migraine’s many triggers offer paths to new therapies

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.”

Hair pulling prompts one of the fastest known pain signals

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.

A next-gen pain drug shows promise, but chronic sufferers need more options

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.

New Pain Medication Suzetrigine Prevents Pain Signals from Reaching Brain

By Marla Broadfoot When doctors ask Sara Gehrig to describe her pain, she often says it is indescribable. Stabbing, burning, aching—those words frequently fail to depict sensations that have persisted for so long they are now a part of her, like her bones and skin. “My pain is like an extra limb that comes along with me every day.” Gehrig, a former yoga instructor and personal trainer who lives in Wisconsin, is 44 years old. At the age of 17 she discovered she had spinal stenosis, a narrowing of the spinal cord that puts pressure on the nerves there. She experienced bursts of excruciating pain in her back and buttocks and running down her legs. That pain has spread over the years, despite attempts to fend it off with physical therapy, anti-inflammatory injections and multiple surgeries. Over-the-counter medications such as ibuprofen (Advil) provide little relief. And she is allergic to the most potent painkillers—prescription opioids—which can induce violent vomiting. Today her agony typically hovers at a 7 out of 10 on the standard numerical scale used to rate pain, where 0 is no pain and 10 is the most severe imaginable. Occasionally her pain flares to a 9 or 10. At one point, before her doctor convinced her to take antidepressants, Gehrig struggled with thoughts of suicide. “For many with chronic pain, it’s always in their back pocket,” she says. “It’s not that we want to die. We want the pain to go away.” Gehrig says she would be willing to try another type of painkiller, but only if she knew it was safe. She keeps up with the latest research, so she was interested to hear earlier this year that Vertex Pharmaceuticals was testing a new drug that works differently than opioids and other pain medications. That drug, a pill called VX-548, blocks pain signals before they can reach the brain. It gums up sodium channels in peripheral nerve cells, and obstructed channels make it hard for those cells to transmit pain sensations. Because the drug acts only on the peripheral nerves, it does not carry the potential for addiction associated with opioids—oxycodone (OxyContin) and similar drugs exert their effects on the brain and spinal cord and thus can trigger the brain’s reward centers and an addiction cycle.

The Painkiller Used for Just About Anything

By Paula Span Mary Peart, 67, a retired nurse in Manchester-by-the-Sea, Mass., began taking gabapentin a year and a half ago to reduce the pain and fatigue of fibromyalgia. The drug helps her climb stairs, walk her dog and take art lessons, she said. With it, “I have a life,” she said. “If I forget to take a dose, my pain comes right back.” Jane Dausch has a neurological condition called transverse myelitis and uses gabapentin as needed when her legs and feet ache. “It seems to be effective at calming down nerve pain,” said Ms. Dausch, 67, a retired physical therapist in North Kingstown, R.I. Amy Thomas, who owns three bookstores in the San Francisco Bay Area, takes gabapentin for rheumatoid arthritis. Along with yoga and physical therapy, “it’s probably contributing to it being easier for me to move around,” Ms. Thomas, 67, said. All three are taking the non-opioid pain drug for off-label uses. The only conditions for which gabapentin has been approved for adult use by the Food and Drug Administration are epileptic seizures, in 1993, and postherpetic neuralgia, the nerve pain that can linger after a bout of shingles, in 2002. But that has not stopped patients and health care providers from turning to gabapentin (whose brand names include Neurontin) for a startling array of other conditions, including sciatica, neuropathy from diabetes, lower back pain and post-surgery pain. Also: Agitation from dementia. Insomnia. Migraines. Itching. Bipolar disorder. Alcohol dependence. Evidence of effectiveness for these conditions is all over the map. The drug appears to provide relief for some patients with diabetic neuropathy but not with some other kinds of neuropathic pain. Several small studies indicate that gabapentin can reduce the itching associated with kidney failure. But the data for its effectiveness against low back pain or a number of psychiatric disorders are limited and show no meaningful impact. “It’s crazy how many indications it’s used for,” said Dr. Michael Steinman, a geriatrician at the University of California, San Francisco, and a co-director of the U.S. Deprescribing Research Network. “It’s become a we-don’t-know-what-else-to-do drug.” © 2024 The New York Times Company

What causes migraines? Study of ‘brain blackout’ offers clues

By Miryam Naddaf About one-third of people who suffer from migraines experience a phenomenon known as aura before the headache.Credit: Tunatura/Getty For one billion people worldwide, the symptoms can be debilitating: throbbing head pain, nausea, blurred vision and fatigue that can last for days. But how brain activity triggers these severest of headaches — migraines — has long puzzled scientists. A study1 in mice, published in Science on 4 July, now offers clues about the neurological events that spark migraines. It suggests that a brief brain ‘blackout’ — when neuronal activity shuts down — temporarily changes the content of the cerebrospinal fluid, the clear liquid that surrounds the brain and spinal cord. This altered fluid, researchers suggest, travels through a previously unknown gap in anatomy to nerves in the skull where it activates pain and inflammatory receptors, causing headaches. “This work is a shift in how we think the headaches originate,” says Gregory Dussor, a neuroscientist at the University of Texas at Dallas in Richardson. “A headache might just be a general warning sign for lots of things happening inside the brain that aren’t normal.” “Migraine is actually protective in that way. The pain is protective because it’s telling the person to rest and recover and sleep,” says study co-author Maiken Nedergaard, a neuroscientist at the University of Copenhagen. The brain itself has no pain receptors; the sensation of headaches comes from areas outside the brain that are in the peripheral nervous system. But how the brain, which is not directly linked to the peripheral nervous system, triggers nerves to cause headaches is poorly understood, making them difficult to treat. © 2024 Springer Nature Limited

How does a migraine aura trigger a headache?

By Rodrigo Pérez Ortega It starts with blind spots, flashing lights, and blurry vision—a warning of what’s to come. About an hour later, the dreadful headache kicks in. This pairing, a shining visual experience called an aura and then a headache, happens in about one-third of people who live with migraine. But researchers haven’t been able to figure out exactly how the two are linked at the molecular level. Now, a new study in mice, published today in Science, establishes a direct mechanism: molecules traveling in the fluid that bathes the brain. The finding could lead to new targets for much-needed migraine treatments. “It’s exciting,” says Rami Burstein, a translational neuroscientist at Harvard Medical School who was not involved in the new study. “It takes a very large step into understanding how something that happened in the brain can alter sensation or perception,” he says. It may also explain why the pain of migraine is experienced only in the head, he adds. Migraine, a debilitating neurological disorder, affects about 148 million people worldwide. Recently developed medications can help reduce headaches but are not effective for everyone. Although exact causes remain elusive, research has shown migraines most likely start with a pathological burst of neural activity. During an aura before a migraine, researchers have observed a seizurelike phenomenon called cortical spreading depression (CSD), in which a wave of abnormal neural firing slowly travels throughout the brain’s outer layer, or cortex. But because the brain itself contains no pain-sensing neurons, signals from the brain would have to somehow reach the peripheral nervous system—the nerves that communicate between the body parts and the brain—to cause a headache. In particular, they’d have to get to the two lumps of neurons below the brain called the trigeminal ganglia, which innervate the two sides of our face and head. Scientists knew that pain fibers from the trigeminal ganglion were nested in the meninges—the thin, delicate membranes that envelop and protect the brain.

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