Chapter 8. General Principles of Sensory Processing, Touch, and Pain

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By Alejandra Manjarrez People wear gloves when making a snowman for a reason: Handling cold stuff can hurt. A new mouse study reveals what may be a key player in this response: a protein already known to enable sensory neurons in worms to detect cold. New evidence published this week in Nature Neuroscience confirms that this protein has the same function in mammals. “The paper is exciting,” says Theanne Griffith, a neuroscientist at the University of California, Davis who was not involved in the research. She notes that the protein, called GluK2, is found in the brain and has “traditionally been thought to play a major role in learning and memory.” The new work shows that elsewhere in the body, it has an unsuspected and “completely divergent role.” We perceive touch, pain, and temperature thanks to a system of nerves that extends throughout our bodies. Researchers have identified skin sensors that detect hot and warm stimuli. Cold sensors, though, have proved more challenging to find. Researchers have proposed various candidates but found limited and contradictory evidence for their function. An ion channel named TRPM8 is the exception. Famous for detecting the “cool” sensation of menthol, it also detects cold temperatures and helped earn its discoverers the Nobel Prize in Physiology or Medicine in 2021. “Nobody questions that TRPM8 is a cold sensor,” says sensory neurobiologist Félix Viana of the Institute for Neuroscience in Alicante, Spain. But it could not be the whole story. It works most efficiently at temperatures above roughly 10°C, and mice lacking the gene for TRPM8 can still detect very cold temperatures. A few years ago, University of Michigan neuroscientists Shawn Xu and Bo Duan and their colleagues found another candidate: a protein on certain sensory neurons in the tiny roundworm Caenorhabditis elegans that causes the animals to avoid temperatures between 17°C and 18°C, which are colder than their preferred temperatures. Preliminary data from that study hinted that the equivalent protein in mammals, GluK2, also allowed mice to sense cold.

Keyword: Pain & Touch
Link ID: 29190 - Posted: 03.16.2024

By Regina G. Barber, Anil Oza, Ailsa Chang, Rachel Carlson Neuroscientist Nathan Sawtell has spent a lot of time studying a funky looking electric fish characterized by its long nose. The Gnathonemus petersii, or elephantnose fish, can send and decipher weak electric signals, which Sawtell hopes will help neuroscientists better understand how the brain pieces together information about the outside world. But as Sawtell studied these electric critters, he noticed a pattern he couldn't explain: the fish tend to organize themselves in a particular orientation. "There would be a group of subordinates in a particular configuration at one end of the tank, and then a dominant fish at the other end. The dominant fish would swim in and break up the group, and they would scatter. A few seconds later, the group would coalesce and it would stay there for hours at a time in this stationary configuration," Sawtell, who runs a lab at Columbia University's Zuckerman Institute says. Initially Sawtell and his team couldn't put together why the fish were always hanging out in this configuration. "What could they really be talking to each other about all of this time?" A new study released this week in Nature by Sawtell and colleagues at Columbia University could have one potential answer: the fish are creating an electrical network that is larger than any field an individual fish can muster alone. In this collective field, the whole school of fish get instantaneous information on changes in the water around them, like approaching predators. Rather than being confused by the flurry of electric signals from other fish, "these fish were clever enough to exploit the pulses of group members to sense their environment," Sawtell says. © 2024 npr

Keyword: Pain & Touch
Link ID: 29187 - Posted: 03.09.2024

By Simon Makin A new device makes it possible for a person with an amputation to sense temperature with a prosthetic hand. The technology is a step toward prosthetic limbs that restore a full range of senses, improving both their usefulness and acceptance by those who wear them. A team of researchers in Italy and Switzerland attached the device, called ”MiniTouch,” to the prosthetic hand of a 57-year-old man named Fabrizio, who has an above-the-wrist amputation. In tests, the man could identify cold, cool and hot bottles of liquid with perfect accuracy; tell the difference between plastic, glass and copper significantly better than chance; and sort steel blocks by temperature with around 75 percent accuracy, researchers report February 9 in Med. Thank you for being a subscriber to Science News! Interested in more ways to support STEM? Consider making a gift to our nonprofit publisher, Society for Science, an organization dedicated to expanding scientific literacy and ensuring that every young person can strive to become an engineer or scientist. “It’s important to incorporate these technologies in a way that prosthesis users can actually use to perform functional tasks,” says neuroengineer Luke Osborn of Johns Hopkins University Applied Physics Laboratory in Laurel, Md., who was not involved in the study. “Introducing new sensory feedback modalities could help give users more functionality they weren’t able to achieve before.” The device also improved Fabrizio’s ability to tell whether he was touching an artificial or human arm. His accuracy was 80 percent with the device turned on, compared with 60 percent with it off. “It’s not quite as good as with the intact hand, probably because we’re not giving [information about] skin textures,” says neuroengineer Solaiman Shokur of EPFL, the Swiss Federal Institute of Technology in Lausanne. © Society for Science & the Public 2000–2024.

Keyword: Pain & Touch
Link ID: 29144 - Posted: 02.10.2024

By Holly Barker Sensory issues associated with autism may be caused by fluctuating neuronal noise — the background hum of electrical activity in the brain — according to a new mouse study. Up to 90 percent of autistic people report sensory problems, including heightened sensitivity to sounds or an aversion to certain smells. Yet others barely register sensory cues and may seek out sensations by making loud noises or rocking back and forth. But thinking in terms of hyper- or hyposensitivity may be an oversimplification, says Andreas Frick, lead investigator and research director at INSERM. “It’s becoming clear now that things are a lot more nuanced.” For instance, the brain’s response to visual patterns — measured using electroencephalography (EEG) recordings — varies more between viewings in autistic people than in those without the condition, one study found. And functional MRI has detected similar variability among autistic people, suggesting sensory problems may arise from inconsistent brain responses. In the new study, Frick and his colleagues found variability in the activity of individual neurons in a mouse model of fragile X syndrome, one of the leading causes of autism. That variability in neuronal response maps to fluctuations in the levels of noise in the brain, the study found. Noise within the brain isn’t necessarily a bad thing. In fact, an optimum amount is ideal: a little can give neurons the ‘push’ they might need to fire an action potential, while too much can make it difficult for the brain to distinguish between different stimuli. But in animals modeling fragile X syndrome, noise fluctuates such that they process sensory information less reliably, Frick says. © 2023 Simons Foundation.

Keyword: Autism
Link ID: 29105 - Posted: 01.18.2024

By Henkjan Honing In 2009, my research group found that newborns possess the ability to discern a regular pulse— the beat—in music. It’s a skill that might seem trivial to most of us but that’s fundamental to the creation and appreciation of music. The discovery sparked a profound curiosity in me, leading to an exploration of the biological underpinnings of our innate capacity for music, commonly referred to as “musicality.” In a nutshell, the experiment involved playing drum rhythms, occasionally omitting a beat, and observing the newborns’ responses. Astonishingly, these tiny participants displayed an anticipation of the missing beat, as their brains exhibited a distinct spike, signaling a violation of their expectations when a note was omitted. Yet, as with any discovery, skepticism emerged (as it should). Some colleagues challenged our interpretation of the results, suggesting alternate explanations rooted in the acoustic nature of the stimuli we employed. Others argued that the observed reactions were a result of statistical learning, questioning the validity of beat perception being a separate mechanism essential to our musical capacity. Infants actively engage in statistical learning as they acquire a new language, enabling them to grasp elements such as word order and common accent structures in their native language. Why would music perception be any different? To address these challenges, in 2015, our group decided to revisit and overhaul our earlier beat perception study, expanding its scope, method and scale, and, once more, decided to include, next to newborns, adults (musicians and non-musicians) and macaque monkeys. The results, recently published in Cognition, confirm that beat perception is a distinct mechanism, separate from statistical learning. The study provides converging evidence on newborns’ beat perception capabilities. In other words, the study was not simply a replication but utilized an alternative paradigm leading to the same conclusion. © 2023 NautilusNext Inc., All rights reserved.

Keyword: Hearing; Language
Link ID: 29067 - Posted: 12.27.2023

By Sandra G. Boodman His plane was coming in for a landing at Philadelphia International Airport when Allen M. Weiss, a marketing professor at the University of Southern California, felt a spasm of pain pierce his left cheek near his nose. “It was really weird,” recalled Weiss, then director of Mindful USC, a group of meditation-based programs at the Los Angeles university. “My face froze up.” Within minutes the pain disappeared and the final leg of Weiss’s December 2015 trip home to California was uneventful. But over the next few months the sensation recurred in the same spot. At first the unpredictable pain was fairly mild and merely bothersome; later it became an excruciating daily torment. Several years after the pain first occurred Weiss, who had consulted dentists, oral pain experts and an otolaryngologist, was given a diagnosis that ended up being correct. But his complicated medical history, a radiology report that failed to describe an important finding and a cryptic warning by one of his doctors delayed effective treatment for three more years. “It was completely confusing,” Weiss said. In June 2023 he underwent surgery that has significantly reduced his pain and improved the quality of his life. N. Nicole Moayeri, the Santa Barbara, Calif., neurosurgeon who operated on Weiss, said a protracted search for a diagnosis and treatment is not unusual for those suffering from Weiss’s uncommon malady. “I commonly see people who’ve had multiple dental procedures for years” when the problem was not in their mouths, Moayeri said. “It’s really shocking to me that so many people suffer” with this for so long. After three months of intermittent pain following the flight, Weiss consulted his internist. For reasons that are unclear, the doctor told Weiss the cause was probably psychological, not physical, and that it wasn’t serious. He sent Weiss to an ear, nose and throat specialist whom he saw in March 2016. She performed an exam and ordered a CT scan that revealed a deviated septum, a typically painless condition estimated to affect up to 80 percent of the population in which the bone or cartilage that divides the nostrils is off-center. A moderate or severe deviation can contribute to the development of sinus infections, headaches and breathing problems. But Weiss had none of these. And a deviated septum didn’t explain the spasms of pain.

Keyword: Pain & Touch
Link ID: 29054 - Posted: 12.19.2023

By Carolyn Wilke Newborn bottlenose dolphins sport a row of hairs along the tops of their jaws. But once the animals are weaned, the whiskers fall out. “Everybody thought these structures are vestigial — so without any function,” said Guido Dehnhardt, a marine mammal zoologist at the University of Rostock in Germany. But Dr. Dehnhardt and his colleagues have discovered that the pits left by those hairs can perceive electricity with enough sensitivity that they may help the dolphins snag fish or navigate the ocean. The team reported its findings Thursday in The Journal of Experimental Biology. Dr. Dehnhardt first studied the whisker pits of a different species, the Guiana dolphin. He expected to find the typical structures of hair follicles, but those were missing. Yet the pits were loaded with nerve endings. He and his colleagues realized that the hairless follicles looked like the electricity-sensing structures on sharks and found that one Guiana dolphin responded to electrical signals. They wondered whether other toothed cetaceans, including bottlenose dolphins, could also sense electricity. For the new study, the researchers trained two bottlenose dolphins to rest their jaws, or rostrums, on a platform and swim away anytime they experienced a sensory cue like a sound or a flash of light. If they didn’t detect one of these signals, the dolphins were to stay put. “It’s basically the same as when we go to the doctor’s and do a hearing test — we have to press a button as soon as we hear a sound,” said Tim Hüttner, a biologist at the Nuremberg Zoo in Germany and a study co-author. Once trained, the dolphins also received electrical signals. “The dolphins responded correctly on the first trial,” Dr. Hüttner said. The animals were able to transfer what they had learned, revealing that they could also detect electric fields. Further study showed that the dolphins’ sensitivity to electricity was similar to that of the platypus, which is thought to use its electrical sense for foraging. © 2023 The New York Times Company

Keyword: Hearing
Link ID: 29037 - Posted: 12.09.2023

Nell Greenfieldboyce If you've got itchy skin, it could be that a microbe making its home on your body has produced a little chemical that's directly acting on your skin's nerve cells and triggering the urge to scratch. That's the implication of some new research that shows how a certain bacteria, Staphylococcus aureus, can release an enzyme that generates an itchy feeling. What's more, a drug that interferes with this effect can stop the itch in laboratory mice, according to a new report in the journal Cell. "That's exciting because it's a drug that's already approved for another condition, but maybe it could be useful for treating itchy skin diseases like eczema," says Isaac Chiu, a scientist at Harvard Medical School who studies interactions between microbes and nerve cells. He notes that eczema or atopic dermatitis is actually pretty common, affecting about 20% of children and 10% of adults. In the past, says Chiu, research on itchy skin conditions has focused on the role of the immune response and inflammation in generating the itch sensation. People with eczema often take medications aimed at immune system molecules. But scientists have also long known that people with eczema frequently have skin that's colonized by Staphylococcus aureus, says Chiu, even though it's never been clear what role the bacteria might play in this condition. Chiu's previous lab work had made him realize that bacteria can directly act on nerve cells to cause pain. "So this made us ask: Could certain microbes like Staphylococcus aureus also particularly be in some way linked to itch?" says Chiu. "Is there a role for microbes in talking to itch neurons?" He and his colleagues first found that putting this bacteria on the skin of mice resulted in vigorous scratching by these animals, leading to damaged skin that spread beyond the original exposure site. © 2023 npr

Keyword: Pain & Touch
Link ID: 29022 - Posted: 11.26.2023

By Veronique Greenwood When someone brushes a hand across your skin, it’s like a breeze blowing through a forest of countless small hairs. Nerves that surround your hair follicles detect that contact, and very far away in your brain, other cells fire. Some of the neurons responding to light contact might make you shiver and give you goose bumps. Some might tell you to move away. Or they might tell you to move closer. Scientists who study the sense of touch have explored which cells bear these messages, and they have made an intriguing discovery: Follicle cells triggered by hair movements release the neurotransmitters histamine and serotonin, chemical messengers linked to biological phenomena as varied as inflammation, muscle contraction and mood changes. The observation, reported in October in the journal Science Advances, lays the groundwork for tracing how gentle touch makes us feel the way it does. Studying hair follicles is challenging, because they begin to decay soon after being removed from the body, said Claire Higgins, a bioengineering professor at Imperial College London and an author of the study. So she and her colleagues went to a hair transplant clinic. There, they were able to look at freshly harvested follicles, which they gently prodded with a very small rod to simulate touch. The scientists knew from work done by other groups that the neurons in the skin surrounding hair follicles are capable of sensing movement. “When you brush your hair, you feel it because the sensory neurons are directly being stimulated,” Dr. Higgins said. But they were curious whether the cells of the follicle itself — the tube from which a hair sprouts — could be contributing to some of the feelings associated with more gentle touch. Not all of the follicle cells had movement sensors, but some did. The researchers identified these and watched them carefully as the rod touched them. “We found that when we stimulated our hair follicle cells, they actually released mood-regulating neurotransmitters serotonin and histamine,” Dr. Higgins said. © 2023 The New York Times Company

Keyword: Pain & Touch; Emotions
Link ID: 28999 - Posted: 11.11.2023

Marlys Fassett Itching can be uncomfortable, but it’s a normal part of your skin’s immune response to external threats. When you’re itching from an encounter with poison ivy or mosquitoes, consider that your urge to scratch may have evolved to get you to swat away disease-carrying pests. However, for many people who suffer from chronic skin diseases like eczema, the sensation of itch can fuel a vicious cycle of scratching that interrupts sleep, reduces productivity and prevents them from enjoying daily life. This cycle is caused by sensory neurons and skin immune cells working together to promote itching and skin inflammation. But, paradoxically, some of the mechanisms behind this feedback loop also stop inflammation from getting worse. In our newly published research, my team of immunologists and neuroscientists and I discovered that a specific type of itch-sensing neuron can push back on the itch-scratch-inflammation cycle in the presence of a small protein. This protein, called interleukin-31, or IL-31, is typically involved in triggering itching. This negative feedback loop – like the vicious cycle – is only possible because the itch-sensing nerve endings in your skin are closely intertwined with the millions of cells that make up your skin’s immune system. The protein IL-31 is key to the connection between the nervous and immune systems. This molecule is produced by some immune cells, and like other members of this molecule family, it specializes in helping immune cells communicate with each other. © 2010–2023, The Conversation US, Inc.

Keyword: Pain & Touch; Neuroimmunology
Link ID: 28961 - Posted: 10.14.2023

Linda Geddes Science correspondent The former Premier League goalkeeper Brad Friedel once said that to be able to work well in the box, you have to be able to think outside the box. Now scientific data supports the idea that goalies’ brains really do perceive the world differently – their brains appear able to merge signals from the different senses more quickly, possibly underpinning their unique abilities on the football pitch. Goalkeeping is the most specialised position in football, with the primary objective of stopping the opposition from scoring. But while previous studies have highlighted differences in physiological and performance profiles between goalkeepers and other players, far less was known about whether they have different perceptual or cognitive abilities. “Unlike other football players, goalkeepers are required to make thousands of very fast decisions based on limited or incomplete sensory information,” said Michael Quinn, a former goalkeeper in the Irish Premiership, who is now studying for a master’s degree in behavioural neuroscience at University College Dublin. Suspecting that this ability might hinge on an enhanced capacity to combine information from different senses, Quinn and researchers at Dublin City University and University College Dublin recruited 60 professional goalkeepers, outfield players and age-matched non-players to do a series of tests, looking for differences in their ability to distinguish sounds and flashes as separate from one another. Doing so enabled them to estimate volunteers’ temporal binding windows – the timeframe in which different sensory signals are fused together in the brain. The study, published in Current Biology, found that goalkeepers had a narrower temporal binding window relative to outfielders and non-soccer players. © 2023 Guardian News & Media Limited

Keyword: Attention; Vision
Link ID: 28954 - Posted: 10.10.2023

Regina G. Barber Ever had an itch you can't scratch? Maybe it's out of reach, or your hands are full, or you don't want to damage your skin. It can be deeply frustrating. And even though the itch response, or what scientists refer to simply as "itch," has a purpose — it's one of our bodies' alert systems — it can also go very wrong. The importance of a regular itch Itch is evolution's way of drawing our attention to something on our skin that needs removing. This could be a stinging bug, a nesting parasite or an irritating plant (poison ivy, anyone?!). All these things urge us to scratch, which generally removes the threat and soothes the itch. "We know that itch can activate sensory neurons and the signal will be transmitted to the brain. When we scratch the skin, somehow other neural circuits will be activated. And these neural circuits will suppress the itch circuits and alleviate the itch sensation," says Qin Liu, a neuroscientist at the Washington University School of Medicine in St. Louis. Because the itch sensation has separate neural circuitry from temperature, pressure and pain, applying pressure or ice or scratching can relieve an itch. They're effective neural distractions. Oftentimes, when someone experiences hives or an insect bite, histamine is involved, a chemical released by our immune system that can contribute to itchiness. So relieving that itch only requires antihistamine medication. "But most other forms of itch, like atopic dermatitis, eczema, other conditions, they don't actually have a pathway for histamine as the itch mediator," says Kwatra. © 2023 npr

Keyword: Pain & Touch
Link ID: 28929 - Posted: 09.27.2023

By Claudia López Lloreda When someone loses a hand or leg, they don’t just lose the ability to grab objects or walk—they lose the ability to touch and sense their surroundings. Prosthetics can restore some motor control, but they typically can’t restore sensation. Now, a preliminary studyposted to the preprint server bioRxiv this month—shows that by mimicking the activity of nerves, a device implanted in the remaining part of the leg helps amputees “feel” as they walk, allowing them to move faster and with greater confidence. “It's a really elegant study,” says Jacob George, neuroengineer at the University of Utah who was not involved with the research. Because the experiments go from a computational model to an animal model and then, finally humans, he says, “This work is really impactful, because it's one of the first studies that's done in a holistic way.” Patients with prosthetics often have a hard time adapting. One big issue is that they can’t accurately control the device because they can’t feel the pressure that they’re exerting on an object. Hand and arm amputees, for example, are more prone to drop or break things. As a result, some amputees refuse to use such prosthetics. In the past few years, researchers have been working on prosthetic limbs that provide more natural sensory feedback both to help control the device better and give them back a sense of agency over their robotic limb. In a critical study in 2019, George and his team showed that so-called biomimetic feedback, sensory information that aims to resemble the natural signals that occur with touch, allowed a patient who’d lost his hand to more precisely grip fragile objects such as eggs and grapes. But such studies have been limited to single patients. They’ve also left many questions unanswered about how exactly this feedback helps with motor control and improves the use of the prosthetic. So in the new work, researchers used a computer model that re-creates how nerves in the foot respond to different inputs, such as feeling pressure. The goal was to create natural patterns of neural activity that might occur when sensing something with the foot or walking. © 2023 American Association for the Advancement of Science.

Keyword: Pain & Touch; Robotics
Link ID: 28863 - Posted: 08.02.2023

By Charlotte Stoddart Charlotte Stoddart: Can a sugar pill make you feel better? What about the rituals surrounding a visit to the doctor? Can the care of a doctor or your trust in them reduce the amount of pain you feel? I’m Charlotte Stoddart and this is Knowable. This episode is all about the placebo effect. We’re going to look in detail at one key paper to learn how the placebo effect has been used in medicine and how it’s been understood and misunderstood. The paper is called “The Powerful Placebo.” It was written by Henry Beecher and published in JAMA, the Journal of the American Medical Association, in 1955. I chose this paper because it’s often referred to as a classic, and it’s still one of the most frequently cited papers on the placebo effect. I’ve enlisted the help of Ted Kaptchuk, who knows the paper well. Ted Kaptchuk: I enjoyed rereading it, actually. It’s a remarkable paper. I’ve read it probably 15 times in my life. Charlotte Stoddart: Ted is director of the Program in Placebo Studies at the Beth Israel Deaconess Medical Center in Boston and a professor of medicine at Harvard Medical School, where Henry Beecher also held a professorship. Beecher also worked at Massachusetts General Hospital. Charlotte Stoddart: During the Second World War, Beecher served in the US Army, and there’s a story about how that experience got him interested in the placebo effect. It goes like this: Beecher was working at a military hospital. One day, a badly injured soldier needed surgery, but the hospital had run out of morphine. So Beecher injected the soldier with saline solution instead. The soldier relaxed and Beecher carried out the operation without any real anesthetic. This, so the story goes, is when Beecher realized the power of the mind over the body. There are several different versions of this story, but Ted says it’s likely some version of it is true. © 2023 Annual Reviews

Keyword: Pain & Touch; Attention
Link ID: 28832 - Posted: 06.28.2023

John Michael Streicher Opioid drugs such as morphine and fentanyl are like the two-faced Roman god Janus: The kindly face delivers pain relief to millions of sufferers, while the grim face drives an opioid abuse and overdose crisis that claimed nearly 70,000 lives in the U.S. in 2020 alone. Scientists like me who study pain and opioids have been seeking a way to separate these two seemingly inseparable faces of opioids. Researchers are trying to design drugs that deliver effective pain relief without the risk of side effects, including addiction and overdose. One possible path to achieving that goal lies in understanding the molecular pathways opioids use to carry out their effects in your body. How do opioids work? The opioid system in your body is a set of neurotransmitters your brain naturally produces that enable communication between neurons and activate protein receptors. These neurotransmitters include small proteinlike molecules like enkephalins and endorphins. These molecules regulate a tremendous number of functions in your body, including pain, pleasure, memory, the movements of your digestive system and more. Analysis of the world, from experts Opioid neurotransmitters activate receptors that are located in a lot of places in your body, including pain centers in your spinal cord and brain, reward and pleasure centers in your brain, and throughout the neurons in your gut. Normally, opioid neurotransmitters are released in only small quantities in these exact locations, so your body can use this system in a balanced way to regulate itself. The opioids your body produces and opioid drugs bind to the same receptors. The problem comes when you take an opioid drug like morphine or fentanyl, especially at high doses for a long time. These drugs travel through the bloodstream and can activate every opioid receptor in your body. You’ll get pain relief through the pain centers in your spinal cord and brain. But you’ll also get a euphoric high when those drugs hit your brain’s reward and pleasure centers, and that could lead to addiction with repeated use. When the drug hits your gut, you may develop constipation, along with other common opioid side effects. Targeting opioid signal transduction How can scientists design opioid drugs that won’t cause side effects? One approach my research team and I take is to understand how cells respond when they receive the message from an opioid neurotransmitter. Neuroscientists call this process opioid receptor signal transduction. Just as neurotransmitters are a communication network within your brain, each neuron also has a communication network that connects receptors to proteins within the neuron. When these connections are made, they trigger specific effects like pain relief. So, after a natural opioid neurotransmitter or a synthetic opioid drug activates an opioid receptor, it activates proteins within the cell that carry out the effects of the neurotransmitter or the drug. © 2010–2023, The Conversation US, Inc.

Keyword: Drug Abuse; Pain & Touch
Link ID: 28809 - Posted: 06.03.2023

By Laura Sanders Scientists can see chronic pain in the brain with new clarity. Over months, electrodes implanted in the brains of four people picked up specific signs of their persistent pain. This detailed view of chronic pain, described May 22 in Nature Neuroscience, suggests new ways to curtail the devastating condition. The approach “provides a way into the brain to track pain,” says Katherine Martucci, a neuroscientist who studies chronic pain at Duke University School of Medicine. Chronic pain is incredibly common. In the United States from 2019 to 2020, more adults were diagnosed with chronic pain than with diabetes, depression or high blood pressure, researchers reported May 16 in JAMA Network Open. Chronic pain is also incredibly complex, an amalgam influenced by the body, brain, context, emotions and expectations, Martucci says. That complexity makes chronic pain seemingly invisible to an outsider, and very difficult to treat. One treatment approach is to stimulate the brain with electricity. As part of a clinical trial, researchers at the University of California, San Francisco implanted four electrode wires into the brains of four volunteers with chronic pain. These electrodes can both monitor and stimulate nerve cells in two brain areas: the orbitofrontal cortex, or OFC, and the anterior cingulate cortex, or ACC. The OFC isn’t known to be a key pain influencer in the brain, but this region has lots of neural connections to pain-related areas, including the ACC, which is thought to be involved in how people experience pain. But before researchers stimulated the brain, they needed to know how chronic pain was affecting it. For about 3 to 6 months, the implanted electrodes monitored brain signals of these people as they went about their lives. During that time, the participants rated their pain on standard scales two to eight times a day. © Society for Science & the Public 2000–2023.

Keyword: Pain & Touch; Brain imaging
Link ID: 28795 - Posted: 05.23.2023

By Priyanka Runwal Researchers have for the first time recorded the brain’s firing patterns while a person is feeling chronic pain, paving the way for implanted devices to one day predict pain signals or even short-circuit them. Using a pacemaker-like device surgically placed inside the brain, scientists recorded from four patients who had felt unremitting nerve pain for more than a year. The devices recorded several times a day for up to six months, offering clues for where chronic pain resides in the brain. The study, published on Monday in the journal Nature Neuroscience, reported that the pain was associated with electrical fluctuations in the orbitofrontal cortex, an area involved in emotion regulation, self-evaluation and decision making. The research suggests that such patterns of brain activity could serve as biomarkers to guide diagnosis and treatment for millions of people with shooting or burning chronic pain linked to a damaged nervous system. “The study really advances a whole generation of research that has shown that the functioning of the brain is really important to processing and perceiving pain,” said Dr. Ajay Wasan, a pain medicine specialist at the University of Pittsburgh School of Medicine, who wasn’t involved in the study. About one in five American adults experience chronic pain, which is persistent or recurrent pain that lasts longer than three months. To measure pain, doctors typically rely on patients to rate their pain, using either a numerical scale or a visual one based on emojis. But self-reported pain measures are subjective and can vary throughout the day. And some patients, like children or people with disabilities, may struggle to accurately communicate or score their pain. “There’s a big movement in the pain field to develop more objective markers of pain that can be used alongside self-reports,” said Kenneth Weber, a neuroscientist at Stanford University, who was not involved in the study. In addition to advancing our understanding of what neural mechanisms underlie the pain, Dr. Weber added, such markers can help validate the pain experienced by some patients that is not fully appreciated — or is even outright ignored — by their doctors. © 2023 The New York Times Company

Keyword: Pain & Touch; Brain imaging
Link ID: 28794 - Posted: 05.23.2023

Katharine Sanderson Researchers have developed an electronic skin that can mimic the same process that causes a finger, toe or limb to move when poked or scalded. The technology could lead to the development of a covering for prosthetic limbs that would give their wearers a sense of touch, or help to restore sensation in people whose skin has been damaged. The ‘e-skin’ was developed in the laboratory of chemical engineer Zhenan Bao at Stanford University in California. Her team has long been trying to make a prosthetic skin that is soft and flexible, but that can also transmit electrical signals to the brain to allow the wearer to ‘feel’ pressure, strain or changes in temperature. The latest work, published on 18 May in Science1, describes a thin, flexible sensor that can transmit a signal to part of the motor cortex in a rat’s brain that causes the animal’s leg to twitch when the e-skin is pressed or squeezed. “This current e-skin really has all the attributes that we have been dreaming about,” says Bao. “We have been talking about it for a long time.” In healthy living skin, mechanical receptors sense information and convert it into electrical pulses that are transmitted through the nervous system to the brain. To replicate this, an electronic skin needs sensors and integrated circuits, which are usually made from rigid semiconductors. Flexible electronic systems are already available, but they typically work only at high voltages that would be unsafe for wearable devices. To make a fully soft e-skin, Bao’s team developed a flexible polymer for use as a dielectric — a thin layer in a semiconductor device that determines the strength of the signal and the voltage needed to run the device. The researchers then used the dielectric to make stretchy, flexible arrays of transistors, combined into a sensor that was thin and soft like skin. © 2023 Springer Nature Limited

Keyword: Pain & Touch; Robotics
Link ID: 28790 - Posted: 05.21.2023

By Lucy Odling-Smee Philip Kass spends 90% of his day lying on a twin bed in a sparsely decorated room that used to belong to his niece. He takes most meals with a plate balanced on his chest, and he usually watches television because reading is too stressful. “I’m barely living,” he told me on a warm night in June last year. Ever since a back injury 23 years ago, pain has been eating away at Kass’s life. It has cost him his career, his relationships, his mobility and his independence. Now 55, Kass lives with his sister and her family in San Francisco, California. He occasionally joins them for dinner, which means he’ll eat while standing. And once a day he tries to walk four or five blocks around the neighbourhood. But he worries that any activity, walking too briskly or sitting upright for more than a few minutes, will trigger a fresh round of torment that can take days or weeks to subside. Philip Kass has dealt with pain for more than two decades. Some of what Kass describes is familiar. I have been pinned to the floor by spinal pain several times in my life. In my twenties, I was immobilized for three months. In my thirties and forties, each episode of severe pain lasted more than a year. I spent at least another half decade standing or pacing through meetings, meals and movies — for fear that even a few minutes spent sitting would result in weeks of disabling pain. For years, I read anything I could find to better understand why my pain persisted.

Keyword: Pain & Touch
Link ID: 28723 - Posted: 03.29.2023

Miryam Naddaf It is thanks to proteins in the nose called odour receptors that we find the smell of roses pleasant and that of rotting food foul. But little is known about how these receptors detect molecules and translate them into scents. Now, for the first time, researchers have mapped the precise 3D structure of a human odour receptor, taking a step forwards in understanding the most enigmatic of our senses. The study, published in Nature on 15 March1, describes an olfactory receptor called OR51E2 and shows how it ‘recognizes’ the smell of cheese through specific molecular interactions that switch the receptor on. “It’s basically our first picture of any odour molecule interacting with one of our odour receptors,” says study co-author Aashish Manglik, a pharmaceutical chemist at the University of California, San Francisco. Smell mystery The human genome contains genes encoding 400 olfactory receptors that can detect many odours. Mammalian odour-receptor genes were first discovered in rats by molecular biologist Richard Axel and biologist Linda Buck in 19912. Researchers in the 1920s estimated that the human nose could discern around 10,000 smells3, but a 2014 study suggests that we can distinguish more than one trillion scents4. Each olfactory receptor can interact with only a subset of smelly molecules called odorants — and a single odorant can activate multiple receptors. It is “like hitting a chord on a piano”, says Manglik. “Instead of hitting a single note, it’s a combination of keys that are hit that gives rise to the perception of a distinct odour.” Beyond this, little is known about exactly how olfactory receptors recognize specific odorants and encode different smells in the brain. Technical challenges in producing mammalian olfactory-receptor proteins using standard laboratory methods have made it difficult to study how these receptors bind to odorants. © 2023 Springer Nature Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 28710 - Posted: 03.18.2023