Chapter 5. The Sensorimotor System

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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 Mark MacNamara The notion of boxing as the “sweet science” is often thought to have been coined in 1956 by the great New Yorker writer A.J. Liebling. He used the term as the title of his definitive book on the sport, but he took it—with much appreciation—from a British sportswriter, Pierce Egan. In 1813, Egan wrote about the “sweet science of bruising” in his master work, Boxiana. The book is a collection of magazine pieces set in a bloody, bare-knuckled world opposite Jane Austen’s. As for the “sweet science,” no one ever really defines it. A carefully thrown knockout punch to a sweet spot on the chin is one possible derivation. There’s also the play on a science with so little apparent sweetness. But that’s not it. The sweet science Liebling and Egan describe had more to do with British principles of “stoic virtues,” “generosity,” and “true courage”—altogether, life in a contradictory place. It’s a square ring, after all, where sometimes hope transcends the specter of an awful inevitability. Or so I’ve come to think, on a journey I’ve begun in the past year, exploring how the sweet science can be used as a treatment for Parkinson’s disease—that increasingly common degenerative disorder of the nervous system, tied to a loss of the brain chemical dopamine, which is involved in movement, memory, motivation, and cognition. Someone told her she moved like a wavy wind sock outside a used car lot. “Exactly how I feel,” she said. In October 2022, a longtime tennis partner noticed something “strange” in my stride, along with a noisy shuffle. “Fatigue,” I replied with pique. The truth is I’m 75 and had known something might not be right for years, particularly the ominous hand tremors, as well as the night-of-the-living-dead gait and a facial expression to match. Add severe anxiety in public places and bizarre nightmares, some quite disturbing. © 2023 NautilusNext Inc.,

Keyword: Parkinsons
Link ID: 29055 - Posted: 12.19.2023

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

By Esther Landhuis Dropping an ice crystal into a bottle of near-frozen water produces a dramatic effect: very quickly, the liquid crystallizes into a block of ice. At the molecular level, an ice crystal has a distinct shape—a lattice structure. As incoming water molecules reshape to join the lattice, the crystal grows. Some researchers think an analogous process underlies Alzheimer’s disease, Parkinson’s disease and other neurodegenerative illnesses. According to this theory, these diseases begin when a particular protein misfolds, or fails to assume the proper shape for its intended role. That misshapen molecule ensnares normal versions of the protein, causing them to similarly misfold, and over time, these rogue proteins clump into toxic clusters that spread through the brain. In mad cow disease—a brain disorder in cattle that can spread to people who eat meat from ill animals —the toxic proteins, called prions, ravage the mind quickly, leading to dementia and death within months. Prion diseases are rare. About 350 cases of the most common type, Creutzfeldt-Jakob disease, are reported each year in the U.S. By comparison, each year, nearly 500,000 people in the U.S. are diagnosed with Alzheimer’s, which develops more gradually. Plaques made up of abnormal beta-amyloid proteins can accumulate in the brain for years or even decades before a person notices signs of mental decline. While the time lines for toxicity differ, “the mechanism of misfolding is the same,” says Mathias Jucker, a neuroscientist at the Hertie Institute for Clinical Brain Research at the University of Tübingen in Germany. Just as all of the water in a bottle freezes after a “‘misfolded’ water molecule” slips into the vessel, if “you have one misfolded protein, all the other ones will take the same shape.” The idea that many diseases could arise from a common prionlike process raises an intriguing and troubling question: Under certain circumstances, could neurodegenerative disorders be transmitted from person to person? © 2023 SCIENTIFIC AMERICAN,

Keyword: Alzheimers; Prions
Link ID: 29032 - Posted: 12.06.2023

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 Sandra G. Boodman The first sign of trouble was difficulty reading. In late 2014 Cathy A. Haft, a New York real estate broker who divides her time between Brooklyn and Long Island, thought she needed new glasses. But an eye exam found that her prescription was largely unchanged. Bladder problems came next, followed by impaired balance, intermittent dizziness and unexplained falls. By 2018 Haft, unable to show properties because she was too unsteady on her feet, was forced to retire. For the next four years specialists evaluated her for neuromuscular and balance-related ear problems in an attempt to explain her worsening condition, which came to include cognitive changes her husband feared was Alzheimer’s disease. In August 2022 Haft, by then dependent on a walker, consulted a Manhattan neurosurgeon. After observing her gait and reviewing images from a recent brain scan, he sent her to a colleague. Less than eight weeks later Haft underwent brain surgery for a condition that is frequently unrecognized or misdiagnosed. The operation succeeded in restoring skills that had gradually slipped away, stunting Haft’s life. “It’s pretty astonishing that this disorder is not that uncommon and no one put the pieces together,” she said. In her case a confluence of confounding symptoms, a complex medical history and the possible failure to take a holistic approach may have led doctors to overlook a condition that can sometimes be reversed — with dramatic results.

Keyword: Movement Disorders; Alzheimers
Link ID: 29020 - Posted: 11.26.2023

By Tina Hesman Saey WASHINGTON — Scientists have uncovered a clue about why it takes so long for Huntington’s disease to develop. And they may have a lead on how to stop the fatal brain disease. Huntington’s is caused by a mistakenly repeated bit of a gene called HTT. Until recently, researchers thought the number of repeats a person is born with doesn’t change, though repeats may expand when passed to future generations. But in some brain cells, the repeats can grow over time to hundreds of copies, geneticist Bob Handsaker reported November 2 at the annual meeting of the American Society of Human Genetics. Once the number of repeats passes a certain point, the activity of thousands of other genes in the brain cells changes drastically, leading the cells to die. These findings suggest that adding repeats to the HTT gene in vulnerable brain cells is what is driving Huntington’s disease, says Handsaker, of the Broad Institute of MIT and Harvard in Cambridge, Mass. The research also suggests that preventing the repeats from growing may stop the development of the disease. The new work gives “serious insight into the disease mechanism,” says Russell Snell, a geneticist at the University of Auckland in New Zealand who was not involved in the work. About 41,000 people in the United States have symptomatic Huntington’s disease, and another 200,000 are at risk of developing it. Inheriting just one copy of a repeat-riddled HTT gene produces symptoms. Even though individuals are born with the disease-causing gene, symptoms don’t usually appear until people are in their 30s to 50s. Those symptoms include depression, mood swings, forgetfulness, balance problems, involuntary movements and slurred speech. Eventually, a person with the disease may be paralyzed and can die from complications such as pneumonia or heart failure. © Society for Science & the Public 2000–2023.

Keyword: Huntingtons
Link ID: 29008 - Posted: 11.15.2023

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

Liam Drew In a laboratory in San Francisco, California, a woman named Ann sits in front of a huge screen. On it is an avatar created to look like her. Thanks to a brain–computer interface (BCI), when Ann thinks of talking, the avatar speaks for her — and in her own voice, too. In 2005, a brainstem stroke left Ann almost completely paralysed and unable to speak. Last year, neurosurgeon Edward Chang, at the University of California, San Francisco, placed a grid of more than 250 electrodes on the surface of Ann’s brain, on top of the regions that once controlled her body, face and larynx. As Ann imagined speaking certain words, researchers recorded her neural activity. Then, using machine learning, they established the activity patterns corresponding to each word and to the facial movements Ann would, if she could, use to vocalize them. The system can convert speech to text at 78 words per minute: a huge improvement on previous BCI efforts and now approaching the 150 words per minute considered average for regular speech1. Compared with two years ago, Chang says, “it’s like night and day”. In an added feat, the team programmed the avatar to speak aloud in Ann’s voice, basing the output on a recording of a speech she made at her wedding. “It was extremely emotional for Ann because it was the first time that she really felt that she was speaking for almost 20 years,” says Chang. This work was one of several studies in 2023 that boosted excitement about implantable BCIs. Another study2 also translated neural activity into text at unprecedented speed. And in May, scientists reported that they had created a digital bridge between the brain and spinal cord of a man paralysed in a cycling accident3. A BCI decoded his intentions to move and directed a spinal implant to stimulate the nerves of his legs, allowing him to walk. © 2023 Springer Nature Limited

Keyword: Brain imaging; Language
Link ID: 28997 - Posted: 11.11.2023

Emily Waltz A highly experimental implant that delivers electrical stimulation to the spinal cord has substantially improved mobility for one man with advanced Parkinson’s disease, according to a report published today in Nature Medicine1. Stimulating spinal cord helps paralysed people to walk again The technology, developed by researchers at the Swiss Federal Institute of Technology in Lausanne (EPFL), enables the man to walk fluidly and to navigate terrain without falling — something he couldn’t do before the treatment. Parkinson’s causes uncontrollable movements and difficulty with coordination that worsens over time. The effects of the treatment have lasted for two years. “There are no therapies to address the severe gait problems that occur at a later stage of Parkinson’s, so it’s impressive to see him walking,” says Jocelyne Bloch, a neurosurgeon at the EPFL and a lead author of the paper. But with only one individual tested, it remains unclear whether the approach will work for other people with the disease. The next step “would be to do a randomized, controlled trial”, says Susan Harkema, a neuroscientist at the University of Louisville in Kentucky who works on stimulation therapy in people with spinal cord injuries. Spinal cord stimulation involves surgically implanting a neuroprosthetic device that delivers pulses of electricity to specific regions of the spinal cord in an effort to activate dysfunctional neural circuits. The technique has been used experimentally to enable people paralysed by spinal cord injury to stand on their own, and even to walk short distances. © 2023 Springer Nature Limited

Keyword: Parkinsons; Robotics
Link ID: 28994 - Posted: 11.08.2023

By Laura Sanders Like tiny, hairy Yodas raising X-wings from a swamp, rats can lift digital cubes and drop them near a target. But these rats aren’t using the Force. Instead, they are using their imagination. This telekinetic trick, described in the Nov. 3 Science, provides hints about how brains imagine new scenarios and remember past ones. “This is fantastic research,” says Mayank Mehta, a neurophysicist at UCLA. “It opens up a lot of exciting possibilities.” A deeper scientific understanding of the brain area involved in the feat could, for instance, help researchers diagnose and treat memory disorders, he says. Neuroscientist Albert Lee and his colleagues study how brains can go back in time by revisiting memories and jump ahead to imagine future scenarios. Those processes, sometimes called “mental time travel,” are “part of what makes our inner mental lives quite rich and interesting,” says Lee, who did the new study while at Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Va. To dip into these complex questions, the researchers began with a simpler one: “Can you be in one place and think about another place?” says Lee, who is now an HHMI investigator at Beth Israel Deaconess Medical Center in Boston. “The rat isn’t doing anything fancier than that. We’re not asking them to recall their summer vacation.” Neuroscientist and engineer Chongxi Lai, also now at Beth Israel Deaconess, Lee and colleagues trained rats to move on a spherical treadmill in the midst of a 3-D virtual world projected onto a surrounding screen. While the rats poked around their virtual world, electrodes recorded signals from nerve cells in the rats’ hippocampi, brain structures known to hold complex spatial information, among other things (SN: 10/6/14). In this way, researchers matched patterns of brain activity with spots in the virtual world. © Society for Science & the Public 2000–2023.

Keyword: Attention
Link ID: 28988 - Posted: 11.04.2023

By Matt Richtel An Oxford University researcher and her team showed that digital wearable devices can track the progression of Parkinson’s disease in an individual more effectively than human clinical observation can, according to a newly published paper. By tracking more than 100 metrics picked up by the devices, researchers were able to discern subtle changes in the movements of subjects with Parkinson’s, a neurodegenerative disease that afflicts 10 million people worldwide. The lead researcher emphasized that the latest findings were not a treatment for Parkinson’s. Rather, they are a means of helping scientists gauge whether novel drugs and other therapies for Parkinson’s are slowing the progression of the disease. Quotable Quotes The sensors — six per subject, worn on the chest, at the base of the spine and one on each wrist and foot — tracked 122 physiological metrics. Several dozen metrics stood out as closely indicating the disease’s progression, including the direction a toe moved during a step and the length and regularity of strides. “We have the biomarker,” said Chrystalina Antoniades, a neuroscientist at the University of Oxford and the lead researcher on the paper, which was published earlier this month in the journal npj Parkinson’s Disease. “It’s super exciting. Now we hope to be able to tell you: Is a drug working?” Until now, Dr. Antoniades said, drug trials for Parkinson’s had relied on clinical assessment of whether a treatment was slowing the progression of the disease. But clinical observation can miss changes that happen day to day or that might not show up clearly in periodic visits to a doctor, she added. In the paper, the study’s authors concluded that the sensors proved more effective at tracking the disease progression “than the conventionally used clinical rating scales.” © 2023 The New York Times Company

Keyword: Parkinsons
Link ID: 28965 - Posted: 10.17.2023

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 Jocelyn Kaiser Parkinson’s disease, a brain disorder that gradually leads to difficulty moving, tremors, and usually dementia by the end, is often difficult to diagnose early in its yearslong progression. That makes testing experimental treatments challenging and slows people from getting existing drugs, which can’t stop the ongoing death of brain cells but temporarily improve many of the resulting symptoms. Now, a study using rodents and tissue from diagnosed Parkinson’s patients suggests DNA damage spotted in blood samples offers a simple way to diagnose the disease early. Although the potential test needs to be validated in clinical studies, the detected DNA damage joins a “flurry” of other biomarkers recently identified for Parkinson’s and “adds to our ability to state confidently that an individual has Parkinson’s disease or not,” says neurodegeneration researcher Mark Cookson of the National Institute on Aging, whose grantmaking arm helped fund the new work, published today in Science Translational Medicine. A blood test based on the findings could also help patients go on existing treatments earlier and boost clinical trials evaluating new therapies, the study’s authors say. “It’s really exciting because it’s something [physicians] could use to detect [Parkinson’s] before the clinical symptoms emerge,” says neuroscientist Malú Tansey of the University of Florida, who also was not involved with the research. Parkinson’s occurs when the death of certain neurons in the brain causes levels of the neurotransmitter dopamine to drop, leading to muscle stiffness, balance problems, speech and cognitive problems, and other symptoms over time. The disorder, tied to both environmental and genetic factors, afflicts up to 1 million people in the United States.

Keyword: Parkinsons
Link ID: 28897 - Posted: 09.07.2023

By R. Douglas Fields One day, while threading a needle to sew a button, I noticed that my tongue was sticking out. The same thing happened later, as I carefully cut out a photograph. Then another day, as I perched precariously on a ladder painting the window frame of my house, there it was again! What’s going on here? I’m not deliberately protruding my tongue when I do these things, so why does it keep making appearances? After all, it’s not as if that versatile lingual muscle has anything to do with controlling my hands. Right? Yet as I would learn, our tongue and hand movements are intimately interrelated at an unconscious level. This peculiar interaction’s deep evolutionary roots even help explain how our brain can function without conscious effort. A common explanation for why we stick out our tongue when we perform precision hand movements is something called motor overflow. In theory, it can take so much cognitive effort to thread a needle (or perform other demanding fine motor skills) that our brain circuits get swamped and impinge on adjacent circuits, activating them inappropriately. It’s certainly true that motor overflow can happen after neural injury or in early childhood when we are learning to control our bodies. But I have too much respect for our brains to buy that “limited brain bandwidth” explanation. How, then, does this peculiar hand-mouth cross-talk really occur? Tracing the neural anatomy of tongue and hand control to pinpoint where a short circuit might happen, we find first of all that the two are controlled by completely different nerves. This makes sense: A person who suffers a spinal cord injury that paralyzes their hands does not lose their ability to speak. That’s because the tongue is controlled by a cranial nerve, but the hands are controlled by spinal nerves. Simons Foundation

Keyword: Language; Emotions
Link ID: 28894 - Posted: 08.30.2023

By Simon Makin Rats are extremely playful creatures. They love playing chase, and they literally jump for joy when tickled. Central to this playfulness, a new study finds, are cells in a specific region of rats’ brains. Neurons in the periaqueductal gray, or PAG, are active in rats during different kinds of play, scientists report July 28 in Neuron. And blocking the activity of those neurons makes the rodents much less playful. The results give insight into a poorly understood behavior, particularly in terms of how play is controlled in the brain. “There are prejudices that it’s childish and not important, but play is an underrated behavior,” says Michael Brecht, a neuroscientist at Humboldt University in Berlin. Scientists think play helps animals develop resilience. Some even relate it to optimal functioning. “When you’re playing, you’re being your most creative, thoughtful, interactive self,” says Jeffrey Burgdorf, a neuroscientist at Northwestern University in Evanston, Ill., who was not involved in the new study. This is the opposite of depressive states, and Burgdorf’s own research aims to turn understanding the neuroscience of play into new therapies for mood disorders. For the new study, Brecht and colleagues got rats used to lab life and being tickled and played with in a game of chase-the-hand. When rats play, they squeal with glee at a frequency of 50 kilohertz, which humans can’t hear. The researchers recorded these ultrasonic giggles as a way of measuring when the rats were having fun. To explore how a specific brain region in rats might relate to their well-documented play behavior, researchers tickled rats on their bellies and backs and played chase-the-hand. Rats also played together, chasing and play-fighting. Ultrasonic giggles, processed to make them audible to humans, coordinate social play and show that the rats are having fun. © Society for Science & the Public 2000–2023.

Keyword: Emotions; Evolution
Link ID: 28864 - Posted: 08.02.2023

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