Chapter 5. The Sensorimotor System

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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

By Denise Grady Year after year for two decades, Nancy Wexler led medical teams into remote villages in Venezuela, where huge extended families lived in stilt houses on Lake Maracaibo and for generations, had suffered from a terrible hereditary disease that causes brain degeneration, disability and death. Neighbors shunned the sick, fearing they were contagious. “Doctors wouldn’t treat them,” Dr. Wexler said. “Priests wouldn’t touch them.” She began to think of the villagers as her family, and started a clinic to care for them. “They are so gracious, so kind, so loving,” she said. Over time, Dr. Wexler coaxed elite scientists to collaborate rather than compete to find the cause of the disorder, Huntington’s disease, and she raised millions of dollars for research. Her work led to the discovery in 1993 of the gene that causes Huntington’s, to the identification of other genes that may have moderating effects and, at long last, to experimental treatments that have begun to show promise. Now, at 74, Dr. Wexler is facing a painful and daunting task that she had long postponed. She has decided it’s time to acknowledge publicly that she has the disease she’s spent her life studying and that killed her mother, uncles and grandfather. “There is such stigma, and such ostracization,” Dr. Wexler, a professor of neuropsychology at the College of Physicians and Surgeons at Columbia University, said in a lengthy interview. “I think it’s important to destigmatize Huntington’s and make it not as scary. Of course it is scary. Having a fatal disease is scary and I don’t want to trivialize that. But if I can say, I’m not stopping my life, I’m going to work, we’re still trying to find a cure, that would help. If I can do anything to take the onus off having this thing, I want to do it.” Among her greatest concerns are the thousands of Venezuelans from the families full of the disease, whose willingness to donate blood and skin samples, and the brains of deceased relatives, made it possible to find the gene. But they live in an impoverished region, and, Dr. Wexler said, they are still outcasts. The clinic that she and her colleagues opened has been shut down by Venezuela’s government. © 2020 The New York Times Company

Keyword: Huntingtons; Genes & Behavior
Link ID: 27110 - Posted: 03.10.2020

By Karen Weintraub At age 16, German Aldana was riding in the back seat of a car driven by a friend when another car headed straight for them. To avoid a collision, his friend swerved and hit a concrete pole. The others weren’t seriously injured, but Aldana, unbuckled, was tossed around enough to snap his spine just below his neck. For the next five years, he could move only his neck, and his arms a little. Right after he turned 21 and met the criteria, Aldana signed up for a research project at the University of Miami Miller School of Medicine near his home. Researchers with the Miami Project to Cure Paralysis carefully opened Aldana's skull and, at the surface of the brain, implanted electrodes. Then, in the lab, they trained a computer to interpret the pattern of signals from those electrodes as he imagines opening and closing his hand. The computer then transfers the signal to a prosthetic on Aldana's forearm, which then stimulates the appropriate muscles to cause his hand to close. The entire process takes 400 milliseconds from thought to grasp. A year after his surgery, Aldana can grab simple objects, like a block. He can bring a spoon to his mouth, feeding himself for the first time in six years. He can grasp a pen and scratch out some legible letters. He has begun experimenting with a treadmill that moves his limbs, allowing him to take steps forward or stop as he thinks about clenching or unclenching the fingers of his right hand. But only in the lab. Researchers had permission to test it only in their facility, but they’re now applying for federal permission to extend their study. The hope is that by the end of this year, Aldana will be able to bring his device home — improving his ability to feed himself, open doors and restoring some measure of independence.

Keyword: Robotics
Link ID: 27107 - Posted: 03.09.2020

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 Building a beautiful robotic hand is one thing. Getting it to do your bidding is another. For all the hand-shaped prostheses designed to bend each intricate joint on cue, there’s still the problem of how to send that cue from the wearer’s brain. Now, by tapping into signals from nerves in the arm, researchers have enabled amputees to precisely control a robotic hand just by thinking about their intended finger movements. The interface, which relies on a set of tiny muscle grafts to amplify a user’s nerve signals, just passed its first test in people: It translated those signals into movements, and its accuracy stayed stable over time. “This is really quite a promising and lovely piece of work,” says Gregory Clark, a neural engineer at the University of Utah who was not involved in the research. It “opens up new opportunities for better control.” Most current robotic prostheses work by recording—from the surface of the skin—electrical signals from muscles left intact after an amputation. Some amputees can guide their artificial hand by contracting muscles remaining in the forearm that would have controlled their fingers. If those muscles are missing, people can learn to use less intuitive movements, such as flexing muscles in their upper arm. These setups can be finicky, however. The electrical signal changes when a person’s arm sweats, swells, or slips around in the socket of the prosthesis. As a result, the devices must be recalibrated over and over, and many people decide that wearing a heavy robotic arm all day just isn’t worth it, says Shriya Srinivasan, a biomedical engineer at the Massachusetts Institute of Technology. © 2020 American Association for the Advancement of Science

Keyword: Robotics
Link ID: 27095 - Posted: 03.05.2020

When the spinal cord is injured, the damaged nerve fibers — called axons — are normally incapable of regrowth, leading to permanent loss of function. Considerable research has been done to find ways to promote the regeneration of axons following injury. Results of a study performed in mice and published in Cell Metabolism suggests that increasing energy supply within these injured spinal cord nerves could help promote axon regrowth and restore some motor functions. The study was a collaboration between the National Institutes of Health and the Indiana University School of Medicine in Indianapolis. “We are the first to show that spinal cord injury results in an energy crisis that is intrinsically linked to the limited ability of damaged axons to regenerate,” said Zu-Hang Sheng, Ph.D., senior principal investigator at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and a co-senior author of the study. Like gasoline for a car engine, the cells of the body use a chemical compound called adenosine triphosphate (ATP) for fuel. Much of this ATP is made by cellular power plants called mitochondria. In spinal cord nerves, mitochondria can be found along the axons. When axons are injured, the nearby mitochondria are often damaged as well, impairing ATP production in injured nerves. “Nerve repair requires a significant amount of energy,” said Dr. Sheng. “Our hypothesis is that damage to mitochondria following injury severely limits the available ATP, and this energy crisis is what prevents the regrowth and repair of injured axons.” Adding to the problem is the fact that, in adult nerves, mitochondria are anchored in place within axons. This forces damaged mitochondria to remain in place while making it difficult to replace them, thus accelerating a local energy crisis in injured axons.

Keyword: Regeneration
Link ID: 27091 - Posted: 03.04.2020

By Abdul-Kareem Ahmed “I use a spoon instead of a fork, so I spill less,” the patient said. “I eat sandwiches and hamburgers so I can use both hands to hold my food.” He was 73 and had suffered from essential tremor for the past decade. His hands would shake uncontrollably, more on the right than on the left, which would worsen if he tried using them. “I could still do crowns, but giving injections became impossible,” he said. His disease, gradual and grasping, had forced the Baltimore-area dentist into early retirement. The patient, who is not being named to protect his privacy, was going to undergo surgery to treat his tremor, which I was curious to observe. I headed to the MRI exam suite to meet him. Wearing a hospital gown, he sat at the edge of his bed, talking to the attending neurosurgeon. He was tall, and balder today than he usually was. As was required, he had shaved his head. Essential tremor is a neurological disease that can affect the torso, arms, neck, head or even voice. Medications are used to attenuate symptoms, but for many patients, these fail or are difficult to tolerate. “I don’t want to take medications forever,” he said. A particularity to this disease is social visibility. Like our patient, people with essential tremor tend to withdraw from society, feeling self-conscious about their inability to perform simple tasks. Dropping food, drinks or other objects is quickly noticed by others.

Keyword: Movement Disorders
Link ID: 27087 - Posted: 03.03.2020

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

Merrit Kennedy As doctors in London performed surgery on Dagmar Turner's brain, the sound of a violin filled the operating room. The music came from the patient on the operating table. In a video from the surgery, the violinist moves her bow up and down as surgeons behind a plastic sheet work to remove her brain tumor. The King's College Hospital surgeons woke her up in the middle of the operation in order to ensure they did not compromise parts of the brain necessary for playing the violin, such as parts that control precise hand movements and coordination. "We knew how important the violin is to Dagmar, so it was vital that we preserved function in the delicate areas of her brain that allowed her to play," Keyoumars Ashkan, a neurosurgeon at King's College Hospital, said in a press release. Turner, 53, learned that she had a slow-growing tumor in 2013. Late last year, doctors found that it had become more aggressive and the violinist decided to have surgery to remove it. In an interview with ITV News, Turner recalled doctors telling her, "Your tumor is on the right-hand side, so it will not affect your right-hand side, it will affect your left-hand side." "And I'm just like, 'Oh, hang on, this is my most important part. My job these days is playing the violin,' " she said, making a motion of pushing down violin strings with her left hand. Ashkan, an accomplished pianist, and his colleagues came up with a plan to keep the hand's functions intact. © 2020 npr

Keyword: Epilepsy; Movement Disorders
Link ID: 27054 - Posted: 02.20.2020

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

Scott Grafton When people ask me about the “mind-body connection,” I typically suggest walking on an icy sidewalk. Skip the yoga, mindfulness, or meditation, and head to the corner on a cold, windy, snowy day. Every winter, much of North America becomes exceedingly slippery with ice. Emergency rooms across the continent see a sharp uptick in fractured limbs and hips as people confidently trudge outside in such conditions, unveiling a profound disconnection between what people believe and what they can actually do with their bodies. One might think that a person could call on experience from years past to adjust their movement or provide a little insight or caution. But the truth is that the body forgets what it takes to stay upright in these perilous conditions. Why is there so much forgetting and relearning on an annual basis? We remember how to ride a bike. Why can’t we remember how to walk on ice? I attempt to answer this and other questions concerning the connection (or lack thereof) between motion in the mind and motion by the body in my new book, Physical Intelligence: The Science of How the Body and the Mind Guide Each Other Through Life. Pantheon, January 2020 Falling on ice reveals a delicate tradeoff that the brain must reconcile as it pilots the body. On the one hand, it needs to build refined motor programs to execute skills such as walking, running, and throwing. On the other hand, those programs can’t be too specific. There is a constant need to tweak motor plans to account for dynamic conditions. When I throw a backpack on, my legs don’t walk in the same way as they do without the pack: my stance widens, my stride shortens. Often, the tweaking needs to happen in moments. As I pick the pack up, I need to lean in or I could tip myself over. Just as importantly, as soon as I put it down, I need to forget I ever held it in the first place. © 1986–2020 The Scientist

Keyword: Learning & Memory
Link ID: 27001 - Posted: 01.28.2020

By Megan Schmidt Scientists say they’ve figured out what causes essential tremor, a common neurological disorder characterized by involuntary, rhythmic trembling that typically occurs in the hands. In a paper published in Science Translational Medicine this week, researchers at National Taiwan University and Columbia University Irving Medical Center discovered that people with essential tremor have abnormal connections among the neurons in their cerebellum, a region in the back of the brain that’s involved in the coordination of voluntary movement. Researchers say people with these abnormalities tend to generate overactive brain waves, or too much electrical activity, in this region of the brain, which is what fuels the tremors. In addition to pinpointing the roots of the disorder, the researchers say their work uncovered some new approaches that could potentially treat and diagnose essential tremor more effectively. Essential tremor is often mistaken for Parkinson’s disease, but there are some key distinctions that set these movement disorders apart. Parkinson’s, which is less common than essential tremor, is caused by the progressive loss of dopamine neurons in the midbrain, a small region of the brain that plays an important role in motor function. Essential tremor, as this new research reveals, is linked to abnormalities in the hindbrain — specifically, the cerebellum. © 2020 Kalmbach Media Co.

Keyword: Movement Disorders
Link ID: 26994 - Posted: 01.25.2020

Abby Olena Understanding the array of neural signals that occur as an organism makes a decision is a challenge. To tackle it, the authors of a study published last week (January 16) in Cell imaged large swaths of the larval zebrafish brain as the animals decided which way to move their tails to avoid an undesirable situation. Finding patterns in the data, they were then able to use imaging to predict—10 seconds in advance—the timing and direction of the fish’s movement. “In a lot of other model systems it’s really difficult to actually . . . record something that’s happening throughout the whole brain with a high level of precision,” says Kristen Severi, a biologist at the New Jersey Institute of Technology who was not involved in the study. “When you have something like a larval zebrafish where you have access to the entire brain with single-cell resolution in a transparent vertebrate, it’s a great place to start to try to look for activity patterns that might be distributed and might be hard to connect.” Even if an animal has learned to do something, it doesn’t execute the exact same motor responses every time, says biophysicist Alipasha Vaziri of the Rockefeller University. He adds that common approaches to studying the neural basis of decision-making may not tell the whole story. For instance, monitoring a handful of neurons and then extrapolating from their activity what’s happening brain-wide means that researchers might miss the big picture. Likewise, recording across the whole brain and then averaging results across trials risks losing details essential to understanding how the brain encodes this behavior. © 1986–2020 The Scientist

Keyword: Brain imaging
Link ID: 26990 - Posted: 01.24.2020

By Karen Weintraub A small injury to a nerve outside the brain and spinal cord is relatively easy to repair just by stretching it, but a major gap in such a peripheral nerve poses problems. Usually, another nerve is taken from elsewhere in the body, and it causes an extra injury and returns only limited movement. Now researchers at the University of Pittsburgh have found an effective way to bridge such a gap—at least in mice and monkeys—by inserting a biodegradable tube that releases a protein called a growth factor for several months. In a study published Wednesday in Science Translational Medicine, the team showed that the tube works as a guide for the nerve to grow along the proper path, and the naturally occurring protein induces the nerve to grow faster. Kacey Marra, a professor at the university’s departments of plastic surgery and bioengineering, says she’s been working for a dozen years on the device, which she particularly hopes will help soldiers injured in combat. More than half of injured soldiers suffer nerve injuries, she says. And as the daughter and granddaughter of military men, she considers it her mission to help their successors. Combat gear does a good job of protecting a soldier’s chest and head, but arms and legs are often exposed, which is why peripheral nerve injuries are so common, Marra says. Car crashes and accidents involving machinery such as snowblowers can also damage nerves involved in hand, arm, leg and foot control. In the U.S., there are about 600,000 nerve injuries every year, she says, though she is unsure how many are severe enough to require the relocation of a second nerve because that information is not tracked yet. When the injuries are severe, the only current treatment is to take a nerve from somewhere else on the body, Marra says. But patients recover just about 50 to 60 percent of function in the damaged nerve. © 2020 Scientific American,

Keyword: Regeneration
Link ID: 26985 - Posted: 01.23.2020

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

By Jane E. Brody If you live with or work with someone who suffers from migraine, there’s something very important you should know: A migraine is not “just a headache,” as many seem to think. Nor is it something most sufferers can simply ignore and get on with their lives. And if you are a migraine sufferer, there’s something potentially life-changing that you should know: There are now a number of medications available that can either prevent or alleviate many attacks, as well as a newly marketed wearable nerve-stimulating device that can be activated by a smartphone to relieve the pain of migraine. Migraine is a neurological disorder characterized by recurrent attacks of severe, often incapacitating headache and dysfunction of the autonomic nervous system, which controls the body’s myriad automatic activities like digestion and breathing. The throbbing or pulsating pain of migraine is often accompanied by nausea and vomiting. Translation: Migraine is a headache, all right, but with body-wide effects because the brain converses with the rest of the body. It is often severe enough to exact a devastating toll on someone’s ability to work, interact with others, perform the tasks of daily life, or even be in a normal living environment. When in the throes of a migraine attack, sufferers may be unable to tolerate light, noise, smells or even touch. Dr. Stephen Silberstein, a neurologist at Thomas Jefferson University and director of the Jefferson Headache Center, told me “There are 47 million people in this country with migraine, and for six million, the condition is chronic, which means they have more than 15 headache days a month,” he said. “It’s time to destigmatize migraine and provide sufferers with effective treatment,” said Dr. David W. Dodick, neurologist at the Mayo Clinic in Scottsdale. “They’re not fakers, weak individuals who are trying to get out of work.” © 2020 The New York Times Company

Keyword: Pain & Touch
Link ID: 26936 - Posted: 01.07.2020