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

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By Lisa Sanders, M.D. The pain woke the 52-year-old physician from a dead sleep. It was as if all the muscles in his right leg, from those in the buttock down his thigh to the very bottom of his calf, were on fire. He shifted slightly to see if he could find a more comfortable position. There was a jag of pain, and he almost cried out. He glanced at the clock: 4 a.m. In just three hours he would have to get up. He had a full day of patients to see. Massage didn’t help. He couldn’t get comfortable lying flat, so finally he moved to the living room, to a recliner. Only then, and only by lying completely still, did he manage to get the pain to abate. He drifted off, but never for long. The searing pain in his leg and buttock slowly eased, and by the time his alarm went off, he could stand and walk — though his muscles still ached and he had to baby his right leg, causing a limp. Between patients, he arranged to see his own doctor. He’d had pain off and on in his buttocks, one side or the other, for more than a year. The pain was in the middle of each cheek and was worse when he was sitting and at the end of the day. Walking to and from his car on the way home was brutal. And then, as mysteriously as it came, it would disappear — only to come back a week or two later. When he first told his doctor about his pain, the exam didn’t show much. He was a little tender at the bottom of the bones you sit on, called the ischia. His doctor thought it was ischial bursitis. Between the tips of the ischia and the largest muscles of the buttocks, there are little pads called bursae. Sometimes these pads become inflamed. The man’s doctor recommended stretching exercises for the muscles around the bursae. He did them regularly, though he wasn’t sure they helped. The pain he had that night, though, was different, and a whole lot worse. Again, his doctor couldn’t find much. Maybe it was a kind of nerve pain, like sciatica, the patient suggested. The doctor agreed and ordered an M.R.I. to look for a pinched nerve. The result was normal. © 2020 The New York Times Company

Keyword: Pain & Touch; Neuroimmunology
Link ID: 27474 - Posted: 09.16.2020

By Amanda Loudin Last summer while out on a bike ride, 35-year-old Andrew Bernstein of Boulder, Colo., was hit by a van that knocked him off the road and kept on going. A passing driver spotted Bernstein lying, unmoving, in a ditch and called 911. Bernstein’s injuries were life threatening. After multiple surgeries, 10 weeks recovering in the hospital and more than three weeks in inpatient rehab, Bernstein has spent the better part of every week since then working with a number of practitioners to help him progress to where he is today — in a wheelchair and walking with the assistance of a full-length leg brace and crutches. But almost all of that effort came to a complete halt when the coronavirus pandemic hit in March and all of his physical therapy facilities either closed or dramatically reduced their patient contact. “I typically worked with a variety of therapists nine or 10 times a week at four different facilities,” Andrew Bernstein says. He was given a home-based plan but “the disruptions to my therapies was challenging. It was frustrating to do without supervision, because my condition changes from one week to the next, something my therapists might notice even if I don’t.”“I typically worked with a variety of therapists nine or 10 times a week at four different facilities,” Andrew Bernstein says. He was given a home-based plan but “the disruptions to my therapies was challenging. It was frustrating to do without supervision, because my condition changes from one week to the next, something my therapists might notice even if I don’t.”

Keyword: Pain & Touch
Link ID: 27460 - Posted: 09.09.2020

Abby Carney Shortly after relocating to Texas from California three years ago, Cheryl Webster started hosting a game night at her home as a way of meeting new people. They stopped meeting due to Covid-19, and Webster has only heard from one person in the group in the months since they were able to play. Eventually, she decided to pick up the phone herself – but nobody called back. “I think that’s the hardest part about loneliness,” she said. “Is it my fault? Am I not a very nice person? Or is there something wrong with me?” End of the office: the quiet, grinding loneliness of working from home Read more Webster, 65, is a proactive doer who volunteers regularly and has even helped finance the education of several friends’ children. She sits on the board of the Austin housing authority and the chamber of commerce, and is sure the Christian business leaders’ group she meets with monthly would say flattering things about her. Though divorced and childless, Webster is not a Havisham spinster – putting herself “out there” comes naturally. And so she supposes many people in her life would be surprised to learn that she’s lonely. Despite following the advice of experts to ward off the feeling, her heart still aches. Advertisement Webster is not alone. A growing number of people share her affliction – so much so that some governments are incorporating loneliness into their health public policy. To help people like her, a number of scientists are researching medical solutions, such as pills and nasal sprays. But will treating loneliness like a disease, rather than an existential question, work to ease their pain? © 2020 Guardian News & Media Limited

Keyword: Pain & Touch; Hormones & Behavior
Link ID: 27405 - Posted: 08.06.2020

By Abdul-Kareem Ahmed “He doesn’t look like himself,” his wife said. It was midnight, and I was consulting on a patient in the emergency room. He was 48 years old and complaining of a headache. Ten years ago my attending had partially removed a benign tumor growing in his cerebellum, part of the hindbrain that controls movement, coordination and speech. Our team had also placed a shunt in his brain. The brain is buoyed and bathed by cerebrospinal fluid. This clear fluid is made in large cavities, called ventricles, and is eventually absorbed by veins. The tumor’s inoperable remnant had blocked the fluid’s natural escape, causing it to build up, a condition known as hydrocephalus. A shunt is a thin rubber tube that is placed in the ventricles of the brain and tunneled under the skin, into the abdomen. It can have a programmable pressure valve, a gauge that sits under the scalp. His shunt had been siphoning excess fluid to his abdomen for years where it was absorbed, preventing life-threatening high pressure in the brain. Today, however, something was wrong, and I thought it was revealed on his new head CT. His ventricles were very large, suggesting high pressure. “I get a bad headache when I sit up,” he mumbled. “Sometimes I vomit. I feel better when I lie flat.” His wife, a strong and kindhearted woman, corroborated his complaint. “He’s also having memory problems, and he’s losing his balance when he walks,” she added. His symptoms were the opposite of what I expected. He was describing a low-pressure headache. He was relieved by lying down but worsened when sitting up.

Keyword: Pain & Touch
Link ID: 27397 - Posted: 08.03.2020

Ewen Callaway Despite their rough and tumble existence, Neanderthals had a biological predisposition to a heightened sense of pain, finds a first-of-its kind genome study published in Current Biology on 23 July1. Evolutionary geneticists found that the ancient human relatives carried three mutations in a gene encoding the protein NaV1.7, which conveys painful sensations to the spinal cord and brain. They also showed that in a sample of British people, those who had inherited the Neanderthal version of NaV1.7 tend to experience more pain than others. “It’s a first example, to me, about how we begin to perhaps get an idea about Neanderthal physiology by using present-day people as transgenic models,” says Svante Pääbo at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, who led the work with Hugo Zeberg at the Karolinska Institute in Stockholm. Pain-sensing protein Researchers have access to only a few Neanderthal genomes, and most of those have been sequenced at a low resolution. This has made it hard to identify mutations that evolved after their lineage split from that of humans some 500,000–750,000 years ago. But in the past few years, Pääbo and his team have generated three high-quality Neanderthal genomes from DNA found in caves in Croatia and Russia. This allows them to confidently identify mutations that were probably common in Neanderthals, yet very rare in humans. Mutations in a gene called SCN9A — which encodes the NaV1.7 protein — stood out because all of the Neanderthals had three mutations that alter the shape of the protein. The mutated version of the gene was found on both sets of chromosomes in all three Neanderthals, hinting that it was common across their populations. © 2020 Springer Nature Limited

Keyword: Pain & Touch; Evolution
Link ID: 27382 - Posted: 07.25.2020

By Erik Stokstad Dogs are renowned for their world-class noses, but a new study suggests they may have an additional—albeit hidden—sensory talent: a magnetic compass. The sense appears to allow them to use Earth’s magnetic field to calculate shortcuts in unfamiliar terrain. The finding is a first in dogs, says Catherine Lohmann, a biologist at the University of North Carolina, Chapel Hill, who studies “magnetoreception” and navigation in turtles. She notes that dogs’ navigational abilities have been studied much less compared with migratory animals such as birds. “It’s an insight into how [dogs] build up their picture of space,” adds Richard Holland, a biologist at Bangor University who studies bird navigation. There were already hints that dogs—like many animals, and maybe even humans—can perceive Earth’s magnetic field. In 2013, Hynek Burda, a sensory ecologist at the Czech University of Life Sciences Prague who has worked on magnetic reception for 3 decades, and colleagues showed dogs tend to orient themselves north-south while urinating or defecating. Because this behavior is involved in marking and recognizing territory, Burda reasoned the alignment helps dogs figure out the location relative to other spots. But stationary alignment isn’t the same thing as navigation. In the new study, Burda’s graduate student, Kateřina Benediktová, initially put video cameras and GPS trackers on four dogs and took them on trips into the forest. The dogs would scamper off to chase the scent of an animal for 400 meters on average. The GPS tracks showed two types of behavior during their return trips to their owner (see map, below). In one, dubbed tracking, a dog would retrace its original route, presumably following the same scent. In the other behavior, called scouting, the dog would return along a completely new route, bushwhacking without any backtracking. Benediktová et al., eLife (2020) 10.7554 (CC BY) © 2020 American Association for the Advancement of Science.

Keyword: Animal Migration
Link ID: 27374 - Posted: 07.18.2020

by Angie Voyles Askham Toddlers with autism have unusually strong connections between sensory areas of the brain, according to a new study1. And the stronger the connections, the more pronounced a child’s autism traits tend to be. Overconnectivity in sensory areas may get in the way of an autistic child’s brain development, says lead investigator Inna Fishman, associate research professor at San Diego State University in California. “Their brain is busy with things it shouldn’t be busy with.” The findings add to a complicated field of research on brain connectivity and autism, which has shown weakened connectivity between some brain areas, strengthened connectivity between others, or no difference in connectivity at all. Previous brain-imaging studies have found that babies and toddlers with autism have altered connectivity in various brain areas and networks, including sensory areas. But most of these data come from ‘baby sibs’ — the younger siblings of autistic children, who are about 20 times more likely to have autism than the general population. “A lot of our early knowledge is from these high-risk samples of infant siblings,” says Benjamin Yerys, assistant professor of psychology in psychiatry at the University of Pennsylvania, who was not involved with the study. “If their behaviors and genetics are different, then all of this early brain work may also be different.” By contrast, the new work focused on autistic children who were newly diagnosed. “There are very, very few studies focused on this age, right around the time the diagnosis can be made,” says Christine Wu Nordahl, associate professor at the University of California, Davis MIND Institute. “I think that is the major strength of the study.” © 2020 Simons Foundation

Keyword: Autism
Link ID: 27345 - Posted: 07.06.2020

By William Schwalbe More than three years ago, I came down with a mysterious illness I thought might be a flu, but turned out to be something entirely different. My blizzard of symptoms began innocuously in November 2016 with terribly cold feet. So cold that even when I got under the covers with a hot water bottle between them, and they were warm to the touch, they still felt like painful ice-blocks. At other times, I had the equally unpleasant sensation that my feet and shins were burning or already burnt. A few weeks later, I started to experience intense throbbing pain in all my toes, as if someone had seconds before stomped on them with heavy boots, which made walking or standing difficult. Often my legs were so heavy that I could barely move them. Occasionally, my feet turned bright red. And every few hours came shooting pains, electric shocks that traveled up my legs. In my 55 years on earth, I’d never felt pain like that — except when a dentist drilled without Novocain. All the symptoms increased at night, so sleep became elusive. I wound up sticking my feet outside the covers because even a sheet brushing against them proved too painful to bear. Before long, the same panoply of pains had moved to my hands and then arms — and occasionally my face and stomach. Heat made the symptoms worse; cold and damp made them much worse. But often these pains flared for no discernible reason. Totally unrelated, or so I thought, were other things that began to go wrong with me over the next few months: I often found myself pouring with sweat from my forehead, but became unable to sweat on my legs and arms; I lost all the hair on my lower legs; I was increasingly faint and dizzy, with my heart racing whenever I changed position or had a shower; and I was experiencing a fatigue and bone-pain so profound that every few hours I needed to stop whatever I was doing and lie down on the floor. © 1996-2020 The Washington Post

Keyword: Pain & Touch
Link ID: 27334 - Posted: 06.29.2020

by Tessa van Leeuwen, Rob van Lier Have you ever considered what your favorite piece of music tastes like? Or the color of Tuesday? If the answer is yes, you might be a synesthete. For people with synesthesia, ordinary sensory events, such as listening to music or reading text, elicit experiences involving other senses, such as perceiving a taste or seeing a color. Synesthesia is not to be confused with common metaphors — such as saying someone ‘sees red’ to describe anger. Instead, synesthetic associations are perceptual, highly specific and idiosyncratic, and typically stable beginning in childhood. And many types exist: A taste can have a shape, a word can have a color, the months of the year may be experienced as an array around the body. In the general population, the phenomenon is relatively rare: Only 2 to 4 percent of people have it. But as much as 20 percent of people with autism experience synesthesia1,2. Why would two relatively rare conditions occur together so often? Over the past few years, researchers have found that people with synesthesia or autism share many characteristics. Synesthetes often have sensory sensitivities and attention differences, as well as other autism traits3,4. The two conditions also share brain connectivity patterns and possibly genes, suggesting they have common biological underpinnings. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27304 - Posted: 06.17.2020

Ashley Yeager It had been seven weeks since I’d touched another human being. Arms outstretched, I walked quickly toward my dad, craving his embrace. In the instant before we touched, we paused, our minds probably running quick, last-minute calculations on the risk of physical contact. But, after turning our faces away from each other and awkwardly shuffling closer, we finally connected. Wrapped in my dad’s bear hug, I momentarily forgot we were in the midst of the worst global crisis I have ever experienced. “Touch is the most powerful safety signal of togetherness,” says Steve Cole, a psychiatrist and biobehavioral scientist at the University of California, Los Angeles. Like more than 35 million other Americans, I live alone, and with the guidelines of physical distancing set by the Centers for Disease Control and Prevention, I hadn’t been getting close to anyone to avoid being infected with (or potentially spreading) SARS-CoV-2, the virus that causes COVID-19. I’d been working, thankfully, at home and staying connected with friends and family through Zoom and Skype, but those virtual interactions were no replacement for being with loved ones in person. “When we get lonely and isolated our brainstem recognizes that suddenly we are in insecure territory and flips on a bunch of fight-or-flight stress responses without us even knowing it,” Cole says. “There’s all sorts of things in our social world that lead us to calculate that we are either safe or unsafe. You can think of physical touch, supportive and affectionate touch, as the most fundamental signal that you’re with somebody who cares about you . . . a fundamental signal of safety and well-being.” © 1986–2020 The Scientist.

Keyword: Pain & Touch; Stress
Link ID: 27259 - Posted: 05.21.2020

Sirin Kale Alice,* a 31-year-old director from London, has been breaking the coronavirus lockdown rules. “I almost don’t want to tell you this,” she says, lowering her voice. Her violation? Once a week, Alice, who lives alone, walks to the end of her garden to meet her best friend Lucy.* There, with the furtiveness of a street drug deal, Lucy hugs her tightly. Alice struggles to let her go. “You just get that rush of feeling better,” Alice says. “Like it’s all OK.” Aside from Lucy’s hugs, Alice hasn’t been touched by another person since March 15, which is when she went into a self-imposed lockdown, a week before the official government advice to self-isolate. “I’ve found it really hard,” she says. “I am a huggy person. You start to notice it after a while. I miss it.” She feels guilty about her surreptitious hugs. “I feel like I can’t tell my other friends about it,” Alice says. “There’s a lot of shaming going on. I know we aren’t meant to. But I am so grateful to her for checking in on me. It gives me such a lift.” Alice is experiencing the neurological phenomenon of "skin hunger," supercharged by the coronavirus pandemic. Skin hunger is the biological need for human touch. It’s why babies in neonatal intensive care units are placed on their parent’s naked chests. It’s the reason prisoners in solitary confinement often report craving human contact as ferociously as they desire their liberty. © 2020 Condé Nast.

Keyword: Emotions; Pain & Touch
Link ID: 27240 - Posted: 05.08.2020

Emiliano Rodríguez Mega On a cold Friday night in February 1995, addiction researcher Nora Volkow and her husband got into their car after a long day at Brookhaven National Laboratory in Upton, New York. Ice had covered the trees and the roads, making them sparkle. But as the couple drove down a slope, the tyres lost their grip. The vehicle spun out of control. Volkow curled up to shield herself as an oncoming car crashed into her door. Metal bit into her flesh. The pain was unrelenting. Finally, the fire service arrived to break her free and an ambulance rushed her to the nearest emergency department, where a doctor gave her Demerol, a powerful and highly addictive opioid painkiller also known as pethidine, which is similar to morphine. Volkow had spent countless hours talking to people with addiction and had read hundreds of papers on the mechanisms of drug abuse. Neither prepared her for what happened next. “It was extraordinary, those impressive sensations,” she says. A moment of ecstasy, one she describes as comparable only to long-lasting sexual pleasure, eclipsed all other feelings. She stayed on the medication for another few days and was sent home with more. But she decided not to take it. She was afraid — she knew many of her patients could not stop once they started. She would get through the pain without the help of drugs. © 2020 Springer Nature Limited

Keyword: Drug Abuse; Pain & Touch
Link ID: 27162 - Posted: 04.02.2020

by Laura Dattaro / Mice missing an autism gene called SHANK3 respond to much lighter touches than typical mice do, according to a new study1. And this hypersensitivity seems to result from the underactivity of neurons that normally dampen sensory responses. The study is the first to examine sensory sensitivity in mice missing SHANK3. Mice with mutations in other genes tied to autism, including MECP2 and GABRB3, have also been shown to be hypersensitive to puffs of air blown onto their backs. Up to 90 percent of autistic people have sensory problems, including hypersensitivity to sensations such as sound or touch. These disruptions may underlie many of the difficulties autistic people face in navigating the world, says lead investigator Guoping Feng, professor of neuroscience at the Massachusetts Institute of Technology. “Sensory overload is one of the reasons that autistic people cover their ears, [hide] in corners, want to be quiet,” Feng says. “It’s important to understand mechanisms.” Up to 2 percent of people with autism have a mutation in SHANK3, which encodes a protein needed for neurons to communicate with one another2. Autism is also common in people with Phelan-McDermid syndrome, a condition caused by deletions of the chromosomal region in which SHANK3 is located. Other experts also say the study underscores the importance of studying sensory problems in autistic people. “Hyperreactivity to sensory input might be connected with autism in a really deep way,” says Sam Wang, professor of neuroscience at Princeton University, who was not involved in the work. “If sensory experience in the first few years of life is necessary for setting up a model of the world, an understanding of the world, then sensory processing would be a gateway to all kinds of other difficulties.” © 2020 Simons Foundation

Keyword: Autism; Attention
Link ID: 27151 - Posted: 03.30.2020

Katarina Zimmer Long believed to be simple, pathogen-eating immune cells, macrophages have a far more extensive list of job duties. They appear to have specialized functions across body tissues, help repair damaged tissue, play a key role in regulating inflammation and pain, and participate in other roles scientists are just beginning to reveal. Now, a group of researchers in the Netherlands has identified a mechanism by which macrophages may help resolve inflammatory pain in mice. In a study recently posted as a preprint to bioRxiv, they report that the immune cells shuttle mitochondria to sensory neurons that innervate inflamed tissue, and that this helps resolve pain. The researchers speculate that the mechanism could replenish functional mitochondria in neurons during chronic inflammatory conditions, which is associated with dysfunctional mitochondria. “I think the transfer of mitochondria is quite convincing,” Jan Van den Bossche, an immunologist at Amsterdam University Medical Center who wasn’t involved in the research, writes to The Scientist in an email. If the findings can be replicated, “this could have [implications for] many diseases with chronic inflammation and pain,” he adds. The research is the result of a five-year project that began when Niels Eijkelkamp, a neuroimmunologist at the University Medical Center Utrecht, and his colleagues started investigating how inflammatory pain resolves, “so we could understand what causes chronic pain,” he says. © 1986–2020 The Scientist

Keyword: Glia; Pain & Touch
Link ID: 27097 - Posted: 03.06.2020

By Kelly Servick The dark side of opioids’ ability to deaden pain is the risk that they might kill their user. The same brain receptors that blunt pain when drugs such as morphine or oxycodone bind to them can also signal breathing to slow down. It’s this respiratory suppression that causes most overdose deaths. So scientists have hoped to design opioids that are “biased” toward activating painkilling signals while leaving respiratory signaling alone. Several companies have cropped up to develop and test biased opioids. But two new studies in mice contest a key hypothesis underlying these efforts—that a signaling protein called beta-arrestin2 is fundamental to opioids’ effect on breathing. “It seems like the premise was wrong,” says Gaspard Montandon, a neuroscientist and respiratory physiologist at the University of Toronto. He and others doubt that the good and bad effects of opioids can be disentangled. Hopes first arose in the late 1990s and early 2000s, as neuroscientist Laura Bohn, biochemist Robert Lefkowitz, and colleagues at Duke University explored the cascades of signals triggered when a drug binds to muopioid receptors on a neuron. This binding changes the receptor’s structure and its interactions with two types of proteins inside the cell—signaling molecules known as G-proteins, and beta-arrestins, which, among other effects, inhibit G-protein signaling. It’s still not clear how the resulting signal cascades influence cells or brain circuits. But the researchers reported in 1999 that mice engineered to lack the gene for beta-arrestin2 got stronger and longer lasting pain relief from morphine. And in 2005, Bohn and her colleagues at Ohio State University found that two morphine-induced side effects, constipation and slowed breathing, were dramatically reduced in these “knockout” mice. The findings suggested that a drug able to nudge the mu-opioid receptors toward G-protein signaling and away from beta-arrestin2 signaling would prompt more pain relief with fewer risks. © 2020 American Association for the Advancement of Science

Keyword: Pain & Touch; Drug Abuse
Link ID: 27083 - Posted: 02.28.2020

By Virginia Morell Dogs’ noses just got a bit more amazing. Not only are they up to 100 million times more sensitive than ours, they can sense weak thermal radiation—the body heat of mammalian prey, a new study reveals. The find helps explain how canines with impaired sight, hearing, or smell can still hunt successfully. “It’s a fascinating discovery,” says Marc Bekoff, an ethologist, expert on canine sniffing, and professor emeritus at the University of Colorado, Boulder, who was not involved in the study. “[It] provides yet another window into the sensory worlds of dogs' highly evolved cold noses.” The ability to sense weak, radiating heat is known in only a handful of animals: Black fire beetles, certain snakes, and one species of mammal, the common vampire bat, all of which use it to hunt prey. Most mammals have naked, smooth skin on the tip of their noses around the nostrils, an area called the rhinarium. But dogs’ rhinaria are moist, colder than the ambient temperature, and richly endowed with nerves—all of which suggests an ability to detect not just smell, but heat. To test the idea, researchers at Lund University in Sweden and Eotvos Lorand University in Hungary trained three pet dogs to choose between a warm (31 C degrees) and an ambient-temperature object, each placed 1.6 meters away. The dogs weren’t able to see or smell the difference between these objects. (Scientists could only detect the difference by touching the surfaces.) After training, the dogs were tested on their skill in double-blind experiments; all three successfully detected the objects emitting weak thermal radiation, the scientists reveal today in Scientific Reports. © 2020 American Association for the Advancement of Science

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27081 - Posted: 02.28.2020

By Joshua Sokol As an astronomer at Chicago’s Adler Planetarium, Lucianne Walkowicz usually has to stretch to connect the peculiarities of space physics with things that people experience on Earth. Then came the email about whales. Sönke Johnsen, a biologist at Duke University, told Dr. Walkowicz that his team had stumbled upon a bizarre correlation: When the surface of the sun was pocked with dark sunspots, an indicator of solar storms, gray whales and other cetacean species seemed more likely to strand themselves on beaches. The team just needed an astronomer’s help wrangling the data. “This was like a dream request,” Dr. Walkowicz said. “And I finally got to do something in marine biology, even though I didn’t study it.” With that assistance, there is some evidence of this peculiar correlation, the researchers said in a paper published Monday in Current Biology. “The study convinced me there is a relationship between solar activity and whale strandings,” said Kenneth Lohmann, a biologist at the University of North Carolina who did not participate in the research. This coincidence across 93 million miles of space is more plausible than it might seem. Sunspots are a harbinger of heightened solar weather, marking times when the tangled plasma of the sun’s atmosphere coughs out more photons and charged particles than usual. These disturbances sail outward and smash into our planet’s magnetic field, creating colorful light shows like the aurora borealis and sometimes disrupting communications. Biologists have already demonstrated that many animals can navigate by somehow sensing Earth’s magnetic field lines. Gray whales, which migrate over 10,000 miles a year through a featureless expanse of blue, might be relying on a similar hidden sense. But unlike a migrating bird, a whale is not easily placed in a magnetized box for controlled experiments. Instead, Jesse Granger, a Duke graduate student, looked at whale strandings, which previous studies had suggested seemed to track with sunspot activity. She narrowed a list of gray whale strandings kept by the National Oceanic and Atmospheric Administration, to highlight the percentage of whales that were stranded alive, as well as whales that were released back to sea and seemed to recover. In theory, those cases were examples of healthy whales that had merely taken a wrong turn. © 2020 The New York Times Company

Keyword: Animal Migration
Link ID: 27076 - Posted: 02.27.2020

Elena Renken The sting of a paper cut or the throb of a dog bite is perceived through the skin, where cells react to mechanical forces and send an electrical message to the brain. These signals were believed to originate in the naked endings of neurons that extend into the skin. But a few months ago, scientists came to the surprising realization that some of the cells essential for sensing this type of pain aren’t neurons at all. It’s a previously overlooked type of specialized glial cell that intertwines with nerve endings to form a mesh in the outer layers of the skin. The information the glial cells send to neurons is what initiates the “ouch”: When researchers stimulated only the glial cells, mice pulled back their paws or guarded them while licking or shaking — responses specific to pain. This discovery is only one of many recent findings showing that glia, the motley collection of cells in the nervous system that aren’t neurons, are far more important than researchers expected. Glia were long presumed to be housekeepers that only nourished, protected and swept up after the neurons, whose more obvious role of channeling electric signals through the brain and body kept them in the spotlight for centuries. But over the last couple of decades, research into glia has increased dramatically. “In the human brain, glial cells are as abundant as neurons are. Yet we know orders of magnitude less about what they do than we know about the neurons,” said Shai Shaham, a professor of cell biology at the Rockefeller University who focuses on glia. As more scientists turn their attention to glia, findings have been piling up to reveal a family of diverse cells that are unexpectedly crucial to vital processes. All Rights Reserved © 2020

Keyword: Glia; Pain & Touch
Link ID: 27002 - Posted: 01.28.2020

By Benedict Carey Soldiers with deep wounds sometimes feel no pain at all for hours, while people without any detectable injury live in chronic physical anguish. How to explain that? Over drinks in a Boston-area bar, Ronald Melzack, a psychologist, and Dr. Patrick Wall, a physiologist, sketched out a diagram on a cocktail napkin that might help explain this and other puzzles of pain perception. The result, once their idea was fully formed, was an electrifying theory that would become the founding document for the field of modern pain studies and establish the career of Dr. Melzack, whose subsequent work deepened medicine’s understanding of pain and how it is best measured and treated. Dr. Melzack died on Dec. 22 in a hospital near his home in Montreal, where he lived, his daughter, Lauren Melzack, said. He was 90, and had spent most of his professional life as a professor of psychology at McGill University. When Dr. Melzack and Dr. Wall, then at the Massachusetts Institute of Technology, met that day in 1959 or 1960 (accounts of their encounter vary), pain perception was thought to work something like a voltmeter, in which nerves send signals up to the brain that reflect the severity of the injury. But that model failed to explain not only battlefield experience but also a host of clinical findings and everyday salves. Most notably, rubbing a wound lessens its sting — and accounting for just that common sensation proved central to the new theory. Doctors knew that massaging the skin activated so-called large nerve fibers, which are specialized to detect subtle variations of touch; and that deeper, small fibers sounded the alarm of tissue damage. The two researchers reasoned that all these sensations must pass through a “gate” in the spinal cord, which adds up their combined signals before sending a message to the brain. In effect, activating the large fibers blocks signals from the smaller ones, by closing the gate. © 2020 The New York Times Company

Keyword: Pain & Touch
Link ID: 26950 - Posted: 01.13.2020

Amber Dance The girl tried hard to hold her arms and hands steady, but her fingers wriggled and writhed. If she closed her eyes, the squirming got worse. It wasn’t that she lacked the strength to keep her limbs still — she just didn’t seem to have control over them. Carsten Bönnemann remembers examining the teenager at a hospital in Calgary, Canada, in 2013. As a paediatric neurologist with the US National Institute of Neurological Disorders and Stroke in Bethesda, Maryland, he often travelled to weigh in on puzzling cases. But he had never seen anything like this. If she wasn’t looking at her limbs, the girl didn’t seem to have any clue where they were. She lacked the sense of her body’s position in space, a crucial ability known as proprioception. “This is something that just doesn’t occur,” says Bönnemann. His team sequenced the girl’s genes, and those of another girl with similar symptoms1, and found mutations in a gene called PIEZO2. Their timing was fortunate: just a few years earlier, researchers looking for the mechanisms that cells use to sense touch had found that the gene encoded a pressure-sensitive protein2. The discovery of Piezo2 and a related protein, Piezo1, was a high point in a decades-long search for the mechanisms that control the sense of touch. The Piezos are ion channels — gates in the cell membrane that allow ions to pass through — that are sensitive to tension. “We’ve learned a lot about how cells communicate, and it’s almost always been about chemical signalling,” says Ardem Patapoutian, a molecular neurobiologist at Scripps Research in La Jolla, California, whose group identified the Piezos. “What we’re realizing now is that mechanical sensation, this physical force, is also a signalling mechanism, and very little is known about it.” © 2020 Springer Nature Limited

Keyword: Pain & Touch
Link ID: 26944 - Posted: 01.09.2020