By Sydney Wyatt The red nucleus—a pale pink brainstem structure that coordinates limb movements in quadruped animals—also projects to brain areas that shape reward-motivated and action-based movements in people, according to a new functional imaging study. The finding suggests the region, like the cerebral cortex, took on a more complex role over the course of evolution. Many researchers had assumed that brainstem structures remained stuck in evolutionarily ancient roles, says Joan Baizer, professor of physiology and biophysics at the University at Buffalo. Activity in the red nucleus, a structure that emerged once animals began to use limbs for walking, coordinates the speed and accuracy of those movements in rats and helps to control posture in monkeys, previous electrophysiological recordings have shown. And in nonhuman primates, neurons in the red nucleus project to the motor cortex and spinal cord, anatomical studies have demonstrated, seemingly confirming the area’s role in motor function. By contrast, the human red nucleus primarily connects to cortical and subcortical regions involved in action control, reward and motivated behavior, the new work reveals. “If this is such a motor structure, why isn’t it projecting to the spinal cord? That doesn’t really fit with our notion of what this structure is supposed to be doing,” says study investigator Samuel Krimmel, a postdoctoral fellow in Nico Dosenbach’s lab. The new imaging suggests that, at least in people, the neural underpinnings of motivated movement—previously considered to be the role of higher-order brain areas—reach “all the way down into the brainstem,” says Dosenbach, professor of neurology at Washington University School of Medicine, who led the work. The findings were published last month in Nature Communications. © 2025 Simons Foundation

Keyword: Learning & Memory; Evolution
Link ID: 29790 - Posted: 05.17.2025

Bobbi-Jean MacKinnon A new scientific study has found no evidence of a mystery brain disease in New Brunswick, says a report published Wednesday in the Journal of the American Medical Association, known as JAMA. Instead, an independent reassessment of 25 of 222 patients diagnosed by Moncton neurologist Alier Marrero as having a "neurological syndrome of unknown cause" concluded that all of the cases were attributable to well-known conditions. These include common neurodegenerative diseases, such as Alzheimer's and Parkinson's, functional neurological disorder, traumatic brain injury, and metastatic cancer, says the report. Despite the small sample size, "when we did the statistics … the chances of any of those other individuals having a mystery disease was less than one in a million," said Dr. Anthony Lang, a senior neurologist and neuroscientist in Toronto, and one of the 13 co-authors. The researchers, affiliated with the University of Toronto, New Brunswick's Horizon Health Network and other Canadian institutions, do not believe exposure to something in the environment, such as the herbicide glyphosate or heavy metals, made the patients ill either, said Lang, director of the Edmund J Safra Program in Parkinson's Disease at the University Health Network. "The neurological problems varied a great deal. Some had neurodegenerative diseases, but others had other neurological problems and therefore a single environmental toxin … could never have explained this broad variety of neurological abnormalities." Lang, who got involved in the study because he started hearing about a mystery disease but wasn't seeing any publications in medical literature, is not surprised by the results. ©2025 CBC/Radio-Canada.

Keyword: Movement Disorders; Alzheimers
Link ID: 29779 - Posted: 05.10.2025

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

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

Keyword: Pain & Touch; Obesity
Link ID: 29760 - Posted: 04.26.2025

Smriti Mallapaty Two hotly anticipated clinical trials using stem cells to treat people with Parkinson’s disease have published encouraging results. The early-stage trials demonstrate that injecting stem-cell-derived neurons into the brain is safe1,2. They also show hints of benefit: the transplanted cells can replace the dopamine-producing cells that die off in people with the disease, and survive long enough to produce the crucial hormone. Some participants experienced visible reductions in tremors. The studies, published by two groups in Nature today, are “a big leap in the field”, says Malin Parmar, a stem-cell biologist at Lund University, Sweden. “These cell products are safe and show signs of cell survival.” Japan’s big bet on stem-cell therapies might soon pay off with breakthrough therapies The trials were mainly designed to test safety and were small, involving 19 individuals in total, which is not enough to indicate whether the intervention is effective, says Parmar. “Some people got slightly better and others didn’t get worse,” says Jeanne Loring, a stem-cell researcher at Scripps Research in La Jolla, California. This could be due to the relatively small number of cells transplanted in these first early-stage trials. Parkinson’s is a progressive neurological condition driven by the loss of dopamine-producing neurons, which causes tremors, stiffness and slowness in movement. There is currently no cure for the condition, which is projected to affect 25 million people globally by 2050. Cell therapies are designed to replace damaged neurons, but previous trials using fetal tissue transplants have had mixed results. The latest findings are the first among a handful of global trials testing more-advanced cell therapies. © 2025 Springer Nature Limited

Keyword: Parkinsons; Stem Cells
Link ID: 29751 - Posted: 04.19.2025

Dyani Lewis Human brain cells engineered to evade detection by the immune system have successfully restored muscle control in a rat model of Parkinson’s disease1. The study is a step towards the development of a ‘universal’ cell line that can be transplanted into anyone, to cure a raft of diseases without the need for anti-rejection drugs. “It’s a one-cell-fits-all proposal,” says Clare Parish, a stem-cell biologist at the Florey Institute of Neuroscience and Mental Health in Melbourne, Australia, and a co-author of the study. The work, published today in Cell Stem Cell, builds on earlier efforts to ‘cloak’ cells from the immune system. Cloaking is a key goal for cell-replacement therapies being tested for conditions ranging from type 2 diabetes and Parkinson’s disease to heart failure and blindness. It would eliminate the need for immunosuppressant drugs, which increase the risk of infection and cancer, and cause tissue damage that ultimately shortens the life of a recipient. To help cells to evade the immune system, the researchers created a cell line with eight genes altered to increase their activity so they acted as an immune invisibility cloak. All of the genes have been shown to assist the placenta and cancer cells in naturally evading immune surveillance. For example, mouse embryonic stem cells engineered with the same set of genes were able to evade detection when transplanted into mice2. Instead of mouse embryonic cells, Parish and her team used human pluripotent stem cells, which can develop into most types of cell found in the body. After being engineered with the cloaking genes, the cells differentiated into nerve cells suitable for treating Parkinson’s disease. The researchers injected the neurons into mice whose immune systems had been replaced with human immune cells, and the neurons were not rejected, suggesting that they were able to evade detection. © 2025 Springer Nature Limited

Keyword: Parkinsons
Link ID: 29742 - Posted: 04.12.2025

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

Keyword: Pain & Touch; Development of the Brain
Link ID: 29739 - Posted: 04.12.2025

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.

Keyword: Pain & Touch; Glia
Link ID: 29729 - Posted: 04.05.2025

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

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

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

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

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

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

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

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

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

Keyword: Parkinsons
Link ID: 29645 - Posted: 01.29.2025

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

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

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

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

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

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

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

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

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

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

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

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

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

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