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

Keyword: Pain & Touch; Attention
Link ID: 30189 - Posted: 04.04.2026

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

Keyword: Pain & Touch
Link ID: 30149 - Posted: 03.07.2026

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

Keyword: Pain & Touch
Link ID: 30135 - Posted: 02.25.2026

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

Keyword: Pain & Touch; Evolution
Link ID: 30123 - Posted: 02.14.2026

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

Keyword: Pain & Touch
Link ID: 30101 - Posted: 01.31.2026

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

Keyword: Pain & Touch; Sexual Behavior
Link ID: 30056 - Posted: 12.20.2025

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.

Keyword: Pain & Touch; Epilepsy
Link ID: 30046 - Posted: 12.13.2025

By Carl Zimmer Last year, Ardem Patapoutian got a tattoo. An artist drew a tangled ribbon on his right arm, the diagram of a protein called Piezo. Dr. Patapoutian, a neuroscientist at Scripps Research in San Diego discovered Piezo in 2010, and in 2021 he won a Nobel Prize for the work. Three years later, he decided to memorialize the protein in ink. Piezo, Dr. Patapoutian had found, allows nerve endings in the skin to sense pressure, helping to create the sense of touch. “It was surreal to feel the needle as it was etching the Piezo protein that I was using to feel it,” he recalled. Dr. Patapoutian is no longer studying how Piezo informs us about the outside world. Instead, he has turned inward, to examine the flow of signals that travel from within the body to the brain. His research is part of a major new effort to map this sixth, internal sense, which is known as interoception. Scientists are discovering that interoception supplies the brain with a remarkably rich picture of what is happening throughout the body — a picture that is mostly hidden from our consciousness. This inner sense shapes our emotions, our behavior, our decisions, and even the way we feel sick with a cold. And a growing amount of research suggests that many psychiatric conditions, ranging from anxiety disorders to depression, might be caused in part by errors in our perception of our internal environment. Someday it may become possible to treat those conditions by retuning a person’s internal sense. But first, Dr. Patapoutian said, scientists need a firm understanding of how interoception works. “We’ve taken our body for granted,” he said. Everyone has a basic awareness of interoception, whether it’s a feeling of your heart racing, your bladder filling or a flock of butterflies fluttering in your stomach. And neuroscientists have long recognized interoception as one function of the nervous system. Dr. Charles Sherrington, a Nobel Prize-winning neuroscientist, first proposed the existence of “intero-ceptors,” in 1906. © 2025 The New York Times Company

Keyword: Obesity; Stress
Link ID: 30030 - Posted: 11.26.2025

Davide Castelvecchi Pigeons can sense Earth’s magnetic field by detecting tiny electrical currents in their inner ears, researchers suggest. Such an inner compass could help to explain how certain animals can achieve astonishing feats of long-distance navigation. The team performed advanced brain mapping as well single-cell RNA sequencing of pigeon inner-ear cells. Both lines of evidence point to the inner ear as the birds’ ‘magnetoreception’ organ. The results appeared in the Science on 20 November 1. “This is probably the clearest demonstration of the neural pathways responsible for magnetic processing in any animal,” says Eric Warrant, a sensory biology researcher at the University of Lund in Sweden. Studies have suggested that various animals, including turtles, trout and robins, can sense the direction and strength of magnetic fields, although the evidence has sometimes been contested — and the mechanisms have remained controversial. Bird-brained navigation Two leading hypotheses have led the research into how birds sense magnetic fields. One is a quantum-physics effect in retina cells where birds ‘see’ magnetic fields. Another is that microscopic iron oxide particles in the beak could act as tiny compass needles. However, it’s largely unknown where magnetic information is sensed in animals’ brains and how sensory neurons confer sensitivity to electromagnetic changes. In 2011, researchers found hints that magnetic fields triggered pigeons’ vestibular system, the organ that enables vertebrates to sense accelerations (including gravity) and helps them to stay balanced2. The structure is made of three fluid-filled loops which are mutually perpendicular, so they can communicate to the brain the direction of an acceleration by breaking it down into three ‘x, y, z’ components. © 2025 Springer Nature Limited

Keyword: Animal Migration; Hearing
Link ID: 30024 - Posted: 11.22.2025

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.

Keyword: Pain & Touch
Link ID: 30021 - Posted: 11.22.2025

By Siddhant Pusdekar Taste and smell are so intimately connected that a whiff of well-loved foods evokes their taste without any conscious effort. Now, brain scans and machine learning have for the first time pinpointed the region responsible for this sensory overlap in humans, a region called the insula, researchers report September 12 in Nature Communications. The findings could explain why people crave certain foods or are turned away from them, says Ivan de Araujo, a neuroscientist at Max Planck Institute for Biological Cybernetics in Tübingen, Germany. Smell and taste become associated from the moment we bite into something, says Putu Agus Khorisantono, a neuroscientist at Karolinska Institutet in Stockholm. Some food chemicals activate sweet, salty, sour, bitter or umami taste receptors on the tongue. Others travel through the roof of the mouth, activating odor receptors in the back of the nose. These “retronasal odors” are what distinguish mangoes from peaches, for example. Both taste mostly sour, Khorisantono says, “but it’s really the aroma that differentiates them.” The brain combines these signals to create our sense of flavor, but scientists have struggled to identify where this happens in the brain. In the new study, Khorisantono and colleagues gave 25 people drops of beverages designed to activate only their taste or retronasal receptors, while scanning brain activity over multiple sessions. Previously, the participants had learned to associate the combination of smells and tastes with particular flavors. © Society for Science & the Public 2000–2025.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29967 - Posted: 10.11.2025

By Jennie Erin Smith The marine whiff of ambergris. The citrusy tang of grapefruit. The must of “corked” wine. The human nose can detect a virtually infinite palette of odors, some at vanishingly low concentrations. But puzzlingly, our bodies only use about 400 receptor proteins to interpret them. Now, fragrance researchers in Switzerland have landed on a new way to study the proteins in the laboratory—and their results, they say, challenge a foundational theory of how smell works. For decades, scientists have struggled to get cells commonly used in laboratory settings to express the genes that encode olfactory receptors (ORs), proteins primarily found on neurons in our nasal cavities. Using a process they describe today in Current Biology, researchers at the Swiss fragrance and flavorings company Givaudan say they have tweaked lab-friendly cells into readily expressing ORs. The result was an in vitro system for identifying specific ORs, including those that strongly respond to molecules in ambergris, grapefruit, and corked wine. The Swiss group’s discovery, other olfaction researchers say, stands to make ORs much easier to study. But more controversially, the group also claims to have observed patterns of receptor activity that call into question combinatorial coding, a long-standing hypothesis of olfaction that helped Linda Buck and Richard Axel win a Nobel Prize in 2004. Combinatorial coding holds that multiple ORs act in concert to pick up different parts of an odorant molecule, creating patterns or codes that are recognized by the brain. Beyond that, says neuroscientist Joel Mainland of the Monell Chemical Senses Center, the model is “pretty vague on the details.” It has been hard to test, because olfactory neurons can’t be cultured in the lab. Determining which OR detects which odorant required extensive tests in rodents, and it’s not ideal “to have to sacrifice an animal each time you want to do an experiment,” says Claire de March, a chemist at CNRS, the French national research agency. As a result, investigators were left with many so-called orphan receptors whose ligands, or binding molecules, are unknown. © 2025 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Development of the Brain
Link ID: 29966 - Posted: 10.11.2025

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

Keyword: Pain & Touch; Development of the Brain
Link ID: 29900 - Posted: 08.23.2025

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

Keyword: Pain & Touch
Link ID: 29889 - Posted: 08.16.2025

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

Keyword: Pain & Touch; Neuroimmunology
Link ID: 29873 - Posted: 08.02.2025

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.”

Keyword: Pain & Touch
Link ID: 29861 - Posted: 07.19.2025

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

Keyword: Pain & Touch
Link ID: 29857 - Posted: 07.16.2025

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

Keyword: Pain & Touch; Drug Abuse
Link ID: 29849 - Posted: 07.12.2025

By Laura Sanders GLP-1 drugs may possess a new power: Easing migraines. In a small, preliminary study, a GLP-1 drug nearly halved the number of days people spent with a migraine in a given month. The results, presented June 21 at the European Academy of Neurology Congress in Helsinki, Finland, expand the possible benefits of the powerful new class of obesity and diabetes drugs. These pernicious, debilitating headaches are estimated to affect one billion people worldwide. Earlier studies have shown that GLP-1 agonists can reduce the pressure inside the skull, a squeeze that’s been implicated in migraines. Neurologist Simone Braca of the University of Naples Federico II in Italy and his colleagues explored whether liraglutide, an older relative of Ozempic and Wegovy, might help migraine sufferers. Thirty-one adults, 26 of them women, got daily injections of liraglutide for 12 weeks. These adults all had obesity and continued to take their current migraine medicines too. At the start of the experiment, participants had headaches on about 20 days out of a month. After 12 weeks of liraglutide, the average number dropped to about 11 days. “Basically, we observed that patients saw their days with headache halved, which is huge,” Braca says. Participants’ weight stayed about the same during the trial, suggesting that headache reductions weren’t tied to weight loss. If the results hold up in larger studies, they may point to treatments for migraine sufferers who aren’t helped by existing drugs. The results may also lead to a deeper understanding of the role of pressure inside the head in migraines, Braca says. © Society for Science & the Public 2000–2025.

Keyword: Obesity; Pain & Touch
Link ID: 29846 - Posted: 07.02.2025

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

Keyword: Pain & Touch
Link ID: 29761 - Posted: 04.26.2025