Links for Keyword: Pain & Touch

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.

Links 1 - 20 of 1053

Dr. Sanjay Gupta explains what we do — and still don't — know about pain

Marielle Segarra When neurosurgeon and journalist Dr. Sanjay Gupta set out to write a book about pain, it wasn't because he felt like he had all the answers. It was because he was still so often mystified by it. "Most of my patients come to me for pain. Head pain, back pain, neck pain, whatever it might be," he says. "If that's what the majority of your professional life is, you should understand it as best you can." His 2025 book, It Doesn't Have to Hurt: Your Smart Guide to a Pain-Free Life, gathers the latest developments in pain science, based on his own experience with patients and conversations with researchers and doctors. What he found may challenge your own understanding of pain and even give you the tools to help you feel better. There's evidence, for example, that just learning about pain and how it works "seems to be pain relieving" for those with chronic pain conditions, he says. Gupta, who also serves as the chief medical correspondent for CNN, explains what we still don't know about pain and shares a few effective new treatments. This interview has been edited for length and clarity. In your book, you say that one of the most significant developments emerging in pain treatment is the fact that the brain is at the center of any pain experience. Can you tell us more about why that matters? What I think has become clear — and I'm not the first person to say this — is the idea that if the brain doesn't decide you have pain, then you don't have pain. © 2026 npr

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 14: Attention and Higher Cognition
Link ID: 30189 - Posted: 04.04.2026

Two neurobiologists win 2026 Brain Prize for discovering mechanics of touch

By Helena Kudiabor Two neurobiologists who helped decipher how the somatosensory system detects touch and pain have won this year’s Brain Prize, the world’s largest award in neuroscience. Patrik Ernfors, professor of tissue biology at the Karolinska Institutet, and David Ginty, professor of neurobiology at Harvard University, will share the 10 million Danish kroner (about $1.6 million) prize. The award was announced today by the Lundbeck Foundation, which founded the Brain Prize in 2011. The honorees will be officially awarded at a ceremony in Copenhagen in May. Research by Ernfors and Ginty has “created a blueprint for understanding normal touch and for pinpointing where things go wrong in disorders such as chronic pain,” said Andreas Meyer-Lindenberg, chair of the Brain Prize selection committee, in a press release announcing the winners. Ernfors was honored for his contributions to classifying the neurons that make up the sensory nervous system in mice. Historically, neuroscientists differentiated among different somatosensory neurons based on a handful of functional features, such as conduction velocity, individual markers and cell morphology, Ernfors says. He and his colleagues have instead classified different types of neurons based on the constellation of genes they express. For example, in one of his most-cited analyses, Ernfors and his colleagues distinguished 622 mouse sensory neurons based on their gene expression patterns. “Now that we know what kinds of neurons there are, we can establish where they project peripherally, centrally, how they connect to each other and what makes them active or inactive,” Ernfors explains. © 2026 Simons 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: 30149 - Posted: 03.07.2026

Susan Leeman, 95, Dies; Explored How the Brain Influences the Body

By Delthia Ricks Susan E. Leeman, who helped reshape scientific understanding of how the brain sends chemical signals throughout the body, did not hesitate to leave the laboratory when her research demanded it — even if it meant visiting slaughterhouses. In the late 1960s, while running a small lab at Brandeis University, she was trying to isolate a stress hormone and needed large quantities of the bovine hypothalamus, a cow’s version of the structure found deep in all mammalian brains. When supplies ran short at a local meatpacker in Boston, Dr. Leeman traveled to Chicago, home at the time to the sprawling Union Stock Yards, to secure fresh tissue. What ultimately emerged was not the hormone that she sought but an elusive chemical called Substance P. Discovered decades earlier but never fully understood, it was finally identified by Dr. Leeman in 1970 as a neuropeptide, released by cells in the brain or spinal cord in response to pain. Three years later, she identified another neuropeptide. The two discoveries established her as a leading figure in neuroendocrinology. Dr. Leeman died on Jan. 20 in Manhattan, at the home of her daughter Eve Leeman, where she had been living. She was 95. Her death was confirmed by another daughter, Jennifer Leeman. Although Substance P was identified in 1931 by Ulf von Euler and John Gaddum, researchers working in London, it was Dr. Leeman who discovered that it was a neuropeptide — a tiny, protein-like molecule released by neurons, or nerve cells in the brain and spinal cord, that transmits signals to target tissues. It was the first neuropeptide discovered in what would become a large class known as tachykinins. Dr. Leeman found that Substance P relays pain signals and amplifies the sensation of pain by triggering inflammation. It has since been linked to chronic pain syndromes, arthritis pain and migraines. © 2026 The New York Times Company

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: 30135 - Posted: 02.25.2026

An Elephant Is Blind Without Its Whiskers

By Alexa Robles-Gil Every elephant has about 1,000 whiskers on its trunk. They play a crucial role for the animals, which have thick skin and poor eyesight. Elephants cannot regrow these hairs, meaning a lost one creates a permanent sensory blind spot on a trunk, which they use for almost everything in daily life. And as such an important feature, they are also unique among mammalian facial hairs. “Elephant whiskers are aliens,” said Andrew Schulz, a mechanical engineer at the Max Planck Institute for Intelligent Systems in Germany. In a study published Thursday in the journal Science, Dr. Schulz and his colleagues identified the structural features that give elephant whiskers a kind of “built-in” intelligence, providing the sensitivity that the largest mammals on land need to navigate their world. While other animals like rats can move their whiskers around, a behavior known as “whisking,” elephants lack the necessary muscles. That leaves their whiskers essentially stationary, even if they protrude from the flexible trunk. This puzzled Dr. Schulz, who had previously studied the movement of their trunks. “If elephant trunk whiskers can’t move, there’s probably something built into them that allows them to” function in a way similar to mammals that whisk, Dr. Schulz said. To find out, Dr. Schulz gathered scientists from many fields. Engineers, neuroscientists, biologists and material scientists were among the few who studied whiskers from baby and adult Asian elephants. (All elephant whiskers came from animals that had died naturally, and were donated by a zoo veterinarian; “We did not go up and pluck whiskers from elephants,” Dr. Schulz said.) © 2026 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: 30123 - Posted: 02.14.2026

PIEZO channels are opening the study of mechanosensation in unexpected places

By Calli McMurray In 2010, Ardem Patapoutian unmasked a piece of cellular machinery that had long evaded identification: PIEZO channels, pores wrenched open by changes in a cell’s membrane tension to allow ions to flow through, thereby converting mechanical force into electrical activity. The discovery marked a turning point for the field of mechanosensation—a process that can be unwieldy to study, says Arthur Beyder, associate professor of physiology and medicine at the Mayo Clinic, because “it reaches its fingers into everything.” The field needed “something to grab onto,” he says, to untangle these processes from other sensory ones—and PIEZO channels provided the first handhold. The PIEZO discovery garnered much attention, and since then, a flurry of studies have outlined how the channels contribute to touch, itch and proprioception. In 2021, Patapoutian shared the Nobel Prize in Physiology or Medicine for his contributions to this work. Now, a growing cadre of researchers is using these receptors as a tool to explore interoception, or the brain’s sense of what the internal organs are doing. “We’re seeing a resurgence and an expansion of research in this area,” says Miriam Goodman, professor of molecular and cellular physiology at Stanford University. The field, she adds, is in the middle of a “PIEZO-driven renaissance.” Even a body at rest is in constant motion: The heart pumps blood, the lungs expand and contract, the gut squeezes food, and the bladder stretches with urine. Biologists had intuited that mechanical force was a key part of these processes—and also part of how organs communicate with the brain—but for decades they did not have a way to dive into the molecular mechanisms behind them. © 2026 Simons Foundation

This newfound cascade of events may explain some female gut pain

By Bethany Brookshir Women of reproductive age are more likely than other people to report gut problems like irritable bowel syndrome (IBS), and can feel dismissed by doctors, as clinicians often put the pain down to diet, stress or hormones. It was never just “in their heads.” A complex interplay between an important hormone, chemical signals, rare populations of gut cells and the output of gut bacteria could explain why, researchers report December 18 in Science. While the findings are in mice, they suggest new opportunities for treatment. Gut pain is a visceral experience — literally, pain in the viscera, from nerves that spread throughout the torso and abdomen. “It can be bloating, it can be a sharp pain or it can be just sort of a constant, dull pain,” says David Julius, a neurophysiologist at University of California, San Francisco. About 10 percent of the global population — mostly women —suffers symptoms of IBS, which can occur with diarrhea, constipation or a mix between the two. “What makes this so bad is that these women are feeling this pain, they go into the physician … and they were just ignored,” says Holly Ingraham, a physiologist also at the University of California, San Francisco. Ingraham and Julius knew that the hormone estrogen played a role in this type of pain, which can fluctuate with the menstrual cycle and pregnancy. In a 2023 paper, they showed that female mice are more sensitive to this visceral pain than males. Without estrogen, that extra sensitivity disappeared. The researchers immediately went looking for cells that might sense estrogen in the gut. To affect a given organ, its cells must have proteins called receptors that recognize estrogen and set off signals in response. © Society for Science & the Public 2000–2025

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: 30056 - Posted: 12.20.2025

Can adding light sensors to nerve cells switch off pain, epilepsy, and other disorders?

By Kelly Servick In the past 20 years, mice with glowing cables sprouting from their heads have become a staple of neuroscience. They reflect the rise of optogenetics, in which neurons are engineered to contain light-sensitive proteins called opsins, allowing pulses of light to turn them on or off. The method has powered thousands of basic experiments into the brain circuits that drive behavior and underlie disease. As this research tool matured, hopes arose for using it as a treatment, too. Compared with the electrical or magnetic brain stimulation approaches already in use, optogenetics offers a way to more precisely target and manipulate the exact cell types underlying brain disorders. So far only one optogenetic application—addressing certain kinds of vision loss by introducing opsins into cells in the eye—has made it into human trials. But its promising early results, along with the discovery of more sensitive and sophisticated opsins, are inspiring researchers to look beyond the eye, developing treatments that would act on peripheral nerves or deep in the brain. Initial tests of these strategies in animal models of epilepsy, amyotrophic lateral sclerosis (ALS), and other neurological disorders have been encouraging, researchers reported last month at the annual meeting of the Society for Neuroscience (SfN) in San Diego. One company is hoping to launch a human trial for an optogenetic pain treatment by 2027. “We definitely don’t want to oversell the idea of using optogenetics [on human brains] any time soon, but we also are firmly convinced that this is now the right moment to be thinking about this seriously,” University of Geneva neurologist and neuroscientist Christian Lüscher told an SfN session he chaired, in which participants presented a newly published road map for bringing optogenetics to the clinic. Still, the presenters acknowledged major remaining challenges, including possible risks of inserting genes for opsins—many of which are derived from algae or other microbes—into a person’s nerves or brain cells. © 2025 American Association for the Advancement of Science.

A diet low in glutamate may ease migraines

By Laura Sanders SAN DIEGO — A diet low in the amino acid glutamate may ease migraines, a small study suggests. A month of staying away from high-glutamate foods led to fewer migraines in a group of 25 people with Gulf War Illness. The specifics of these veterans’ migraines, part of a collection of symptoms resulting from the Gulf War, may differ from those of other people who suffer from migraines. But if the underlying relationship between glutamate and migraines is similar, the diet could help the estimated 1 billion people worldwide who have migraines. Current drugs for treating migraines, including a new class of compounds that block a chemical messenger called CGRP, can help. But existing drugs don’t work for everyone, says neuroscientist Ian Meng of the University of New England in Biddeford, Maine. A dietary change could be a low-risk and accessible way to bring relief. Glutamate is both a signal that excites nerve signals in the brain and an amino acid found in tomatoes, processed meats, aged cheese, mushrooms and, of course, monosodium glutamate, or MSG. For a month, 25 veterans of the Gulf War ate a low-glutamate diet full of whole fruits and veggies and avoided high-glutamate foods including soy sauce, mushrooms and ultraprocessed foods. Before this diet, 64 percent of these people reported having a migraine in the previous week. After a month of a low-glutamate diet, that number dropped to about 12 percent, neuroscientist Ashley VanMeter said November 16 in a news briefing at the annual meeting of the Society for Neuroscience. After the one-month diet ended, 88 percent of the people in the study chose to remain on the diet. “They feel that [the diet] is definitely benefiting them,” said VanMeter, of Georgetown University in Washington, D.C. © Society for Science & the Public 2000–2025.

Adult human cortex does not reorganize after amputation

By Angie Voyles Askham The adult cortex can rewire itself after injury, according to a series of classic experiments. When a monkey loses sensory input from a finger, for example, the region of the somatosensory cortex dedicated to that finger becomes overrun by inputs from the animal’s nearby fingers or face; the cortical map for the unused finger fades, and nearby maps of other body parts expand. “This is what I read in my textbook. This is what the lecturers told me in my lectures in university,” says Tamar Makin, professor of cognitive neuroscience at the University of Cambridge. But—contrary to those classic findings—such large-scale cortical reorganization did not happen in three people who lost an arm, according to a new functional imaging study Makin and her colleagues published today in Nature Neuroscience. Instead, the somatosensory map of each person’s hands, feet and lips, generated when they moved or attempted to move that body part, remained stable in the years before and after their hand was removed. “The representation of the hand persists,” says Makin, who led the study. The work is the first longitudinal look at whether amputation changes that cortical mapping. The results confirm what previous cross-sectional studies have hinted at, and they should put an end to the debate about how readily the adult cortex can shift its function, Makin says. But not everyone agrees. The study is an important contribution to the field, and it shows that maps of somatosensation driven by motor input remain stable after amputation, says Ben Godde, professor of neuroscience at Constructor University, who was not involved in the new work or the classic experiments. But that does not mean that other cortical maps are not shifting as a result of changing inputs, he says. “It’s not evidence that there’s no plasticity.” © 2025 Simons Foundation

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: 29900 - Posted: 08.23.2025

Treating Chronic Pain Is Hard. An Experimental Approach Shows Promise.

By Pam Belluck Sometimes the pain felt like lightning bolts. Or snakes biting. Or needles. “Just imagine the worst burn you’ve ever had, all over your body, never going away,” said Ed Mowery, 55, describing his life with chronic pain. “I would wake up in the middle of night, screaming at the top of my lungs.” Beginning with a severe knee injury he got playing soccer at 15, he underwent about 30 major surgeries for various injuries over the decades, including procedures on his knees, spine and ankles. Doctors put in a spinal cord stimulator, which delivers electrical pulses to relieve pain, and prescribed morphine, oxycodone and other medications, 17 a day at one point. Nothing helped. Unable to walk or sit for more than 10 minutes, Mr. Mowery, of Rio Rancho, N.M., had to stop working at his job selling electronics to engineering companies and stop playing guitar with his death metal band. Out of options four years ago, Mr. Mowery signed up for a cutting-edge experiment: a clinical trial involving personalized deep brain stimulation to try to ease chronic pain. The study, published on Wednesday, outlines a new approach for the most devastating cases of chronic pain, and could also provide insights to help drive invention of less invasive therapies, pain experts said. “It’s highly innovative work, using the experience and technology they have developed and applying it to an underserved area of medicine,” said Dr. Andre Machado, chief of the Neurological Institute at Cleveland Clinic, who was not involved in the study. Chronic pain, defined as lasting at least three months, afflicts about 20 percent of adults in the United States, an estimated 50 million people, according to the Centers for Disease Control and Prevention. In about a third of cases, the pain substantially limits daily activities, the C.D.C. reported. © 2025 The New York Times Company

New Implant Offers Hope for Easing Rheumatoid Arthritis

By Roni Caryn Rabin The Food and Drug Administration on Wednesday approved a medical device that offers new hope to patients incapacitated by rheumatoid arthritis, a chronic condition that afflicts 1.5 million Americans and is often resistant to treatment. The condition is usually managed with medications. The device represents a radical departure from standard care, tapping the power of the brain and nervous system to tamp down the uncontrolled inflammation that leads to the debilitating autoimmune disease. The SetPoint System is an inch-long device that is surgically implanted into the neck, where it sits in a pod wrapped around the vagus nerve, which some scientists believe is the longest nerve in the body. The device electrically stimulates the nerve for one minute each day. The stimulation can turn off crippling inflammation and “reset” the immune system, research has shown. Most drugs used to treat rheumatoid arthritis suppress the immune system, leaving patients vulnerable to serious infections. On a recent episode of the American College of Rheumatology podcast, the SetPoint implant was described as representing a “true paradigm shift” in treatment of the disease, which until now has relied almost entirely on an evolving set of pharmaceutical interventions, from gold salts to powerful agents called biologics. The F.D.A. designated the implant as a breakthrough last year in order to expedite its development and approval. It represents an early test of the promise of so-called bioelectronic medicine to modulate inflammation, which plays a key role in diseases including diabetes, heart disease and cancer. Clinical trials are already underway testing vagus nerve stimulation to manage inflammatory bowel disease in children, lupus and other conditions. Trials for patients with multiple sclerosis and Crohn’s disease are also planned. In a yearlong randomized controlled trial of 242 patients that included a sham-treatment arm, over half of the participants using the SetPoint implant alone achieved remission or saw their disease recede. Measures of joint pain and swelling fell by 60 percent and 63 percent, respectively. © 2025 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: 29873 - Posted: 08.02.2025

Why Do Headaches Feel So Different From Other Kinds of Pain?

By Tom Zeller Jr. During the week between two experimental infusions at the Danish Headache Center, where I had agreed to be a test subject, I rented a small flat in central Copenhagen, near Assistens Cemetery. This is where many notable Danes have been laid to rest, and I took some time that September to visit the monuments, which were shrouded in manicured stands of mature poplars and willows. The accompanying article is adapted from “The Headache: The Science of a Most Confounding Affliction — and a Search for Relief,” by Tom Zeller Jr. (Mariner Books, 310 pages). Copyright © 2025. Reprinted by permission. The grave of Niels Bohr, one of the 20th century’s leading figures in theoretical physics, is marked by a gray stone pillar with an owl perched on top. Hans Christian Andersen, the author who gave us “The Little Mermaid” and “The Ugly Duckling,” among other treasured stories, resides here too. But it felt most appropriate to my mission that Danish philosopher Søren Kierkegaard, who thought suffering was where life’s meaning is forged, occupied his own leafy corner of the park. In the Kierkegaardian tradition, suffering is redemptive — the feedstock of enlightenment — and rather than wallow in its insults and pains, the sufferer should embrace its power to transform. “Even the heaviest suffering cannot be heavier than a mountain,” he once wrote. “And thus, if the sufferer believes that his suffering is beneficial to him — yes, then he moves mountains. In order to move a mountain, you must get under it.” I was thinking of Kierkegaard when I first presented my arm to Lanfranco Pellesi, then a researcher at the Danish Headache Center, for my initial infusion. Pellesi had an early interest in studying near-death experiences, before turning his attention to pain, and then from pain to headaches. It struck me as such an obvious trajectory — one that followed an almost inevitable path — and I asked him how he made sense of that progression. “I think probably it links to the problem of conscience — where it is, where it’s not.”

The fascinating science of pain – and why everyone feels it differently

By Celina Ribeiro Some say it was John Sattler’s own fault. The lead-up to the 1970 rugby league grand final had been tense; the team he led, the South Sydney Rabbitohs, had lost the 1969 final. Here was an opportunity for redemption. The Rabbitohs were not about to let glory slip through their fingers again. Soon after the starting whistle, Sattler went in for a tackle. As he untangled – in a move not uncommon in the sport at the time – he gave the Manly Sea Eagles’ John Bucknall a clip on the ear. Seconds later – just three minutes into the game – the towering second rower returned favour with force: Bucknall’s mighty right arm bore down on Sattler, breaking his jaw in three places and tearing his skin; he would later need eight stitches. When his teammate Bob McCarthy turned to check on him, he saw his captain spurting blood, his jaw hanging low. Forty years later Sattler would recall that moment. One thought raged in his shattered head: “I have never felt pain like this in my life.” But he played on. Tackling heaving muscular players as they advanced. Being tackled in turn, around the head, as he pushed forward. All the while he could feel his jaw in pieces. At half-time the Rabbitohs were leading. In the locker room, Sattler warned his teammates, “Don’t play me out of this grand final.” McCarthy told him, “Mate, you’ve got to go off.” He refused. “I’m staying.” Sattler played the whole game. The remaining 77 minutes. At the end, he gave a speech and ran a lap of honour. The Rabbitohs had won. The back page of the next day’s Sunday Mirror screamed “BROKEN JAW HERO”. © 2025 Guardian News & Media Limited

Why a new opioid alternative is out of reach for some pain patients

Sydney Lupkin Jerry Abrams, a 64-year-old marketing strategist in Minneapolis, used to run marathons. But two decades of degenerative spine disease have left him unable to run — and he's grieving. For Abrams, losing running felt like "the loss of a loved one – that friend who's been with you every day you needed him. "You know, having that taken away from you because of pain is the hardest thing of all," he says. The constant pain in his lower back makes running impossible. Sometimes, when the pain isn't under control, he can't get out of bed. Abrams has tried taking opioids. They help, but he feels he has to be careful because they're potentially addictive. He's also worried about building up a tolerance to them "I don't ever want to be in a situation where I need surgery and need to recover and opioid medication no longer does what it needs to do," he explains. The Food and Drug Administration approved a new non-opioid drug earlier this year called Journavx. It's a pill for severe acute pain that works by blocking plain signals from where someone hurts. It's offered hope for the 1 in 5 Americans who suffer from chronic pain, but it's also just out of reach. Journavx is the first new kind of painkiller in more than 20 years, and the medical community is cautiously optimistic that Journavx doesn't have the same addictive potential as opioids do. But the new pills are expensive, and not everyone has been able to access them, thanks to a narrowly-focused FDA approval and limited insurance coverage Abrams' doctor wanted him to be able to try Journavx. But the FDA only approved the medication for short-term use for acute pain, which is usually defined as lasting less than three months, such as right after surgery. Because Abrahm's pain is chronic, his insurance wouldn't cover it. A single Journavx pill costs around $15 without insurance, according to Vertex Pharmaceuticals, the drug's manufacturer. © 2025 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: 29849 - Posted: 07.12.2025

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

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

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

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

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

Links By Chapter:

Links for Keyword: Pain & Touch