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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.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
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

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27382 - Posted: 07.25.2020

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

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 27334 - Posted: 06.29.2020

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.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 5: The Sensorimotor System
Link ID: 27259 - Posted: 05.21.2020

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

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27083 - Posted: 02.28.2020

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

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
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

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
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

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26936 - Posted: 01.07.2020

By Debbie Jackson BBC Scotland "Fluffing your son's hair, really hugging him, holding his hand." For someone who has been through what she has in the space of a year, Corinne Hutton doesn't need much to make her happy. Last January she got the double hand transplant she had been waiting more than five years for, and feared would never happen. This January, she will celebrate her "handiversary", a year since a surgeon handed her back her independence. Being able to do the simplest things for 11-year-old son Rory means the world to Finding Your Feet charity founder Cor. "From an emotional point of view to be able to do things for him - make the packed lunches or the washing, or do the ironing is great," she said. "But on top of that, being able to hold his hand, fluff his hair, little things that might not be hugely exciting to him - but they matter a lot to me. "People don't appreciate what it means to have lost them," she said. Cor became the first Scot to undergo a double hand transplant when, in a 12-hour procedure, Prof Simon Kay attached two donor hands to her arms at Leeds general Infirmary. The 48-year-old lost her hands and feet in 2013 after suffering acute pneumonia and sepsis, which almost killed her. After more than a dozen false alarms over the years, a match for her own blood group, skin tone and hand size had been found. Much celebration and wonder was made of the news that the transplant had finally happened, but the aftermath was far from easy. © 2019 BBC.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26922 - Posted: 12.30.2019

By Richard Sima Luke Miller, a cognitive neuroscientist, was toying with a curtain rod in his apartment when he was struck by a strange realization. When he hit an object with the rod, even without looking, he could tell where it was making contact like it was a sensory extension of his body. “That’s kind of weird,” Miller recalls thinking to himself. “So I went [to the lab], and we played around with it in the lab.” Sensing touch through tools is not a new concept, though it has not been extensively investigated. In the 17th century, philosopher René Descartes discussed the ability of blind people to sense their surroundings through their walking cane. While scientists have researched tool use extensively, they typically focused on how people move the tools. “They, for the most part, neglected the sensory aspect of tool use,” Miller says. In a 2018 Nature study, Miller and his colleagues at Claude Bernard Lyon 1 University in France reported that humans are actually quite good at pinpointing where an object comes into contact with a handheld tool using touch alone, as if the object were touching their own skin. A tool is not innervated like our skin, so how does our brain know when and where it is touched? Results in a follow-up study, published in December in Current Biology, reveal that the brain regions involved with sensing touch on the body similarly processes it on the tool. “The tool is being treated like a sensory extension of your body,” Miller says. In the initial experiment, the researchers asked 16 right-handed subjects to determine where they felt touches on a one-meter-long wooden rod. In a total of 400 trials, each subject compared the locations of two touches made on the rod: If they were felt in different locations, participants did not respond. If they were in the same location, the people in the study tapped a foot pedal to indicate whether the touches were close or far from their hand. Even without any experience with the rod or feedback on their performance, the participants were, on average, 96 percent accurate. © 2019 Scientific American,

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26914 - Posted: 12.26.2019

By Austin Frakt Some days I’m grumpy; other times, my head hurts or my feet or my arms do. Yet when I play the trumpet, my mood improves and the pain disappears. Why? Alternative medicine — including music therapy — is full of pain-relief claims. Although some are simply too good to be true, the oddities of pain can explain why others hold up, as well as why my trumpet playing helps. One thing we tend to believe about pain, but is wrong, is that it always stems from a single, fixable source. Another is that pain is communicated from that source to our brains by “pain nerves.” That’s so wrong it’s called “the naïve view” by neuroscientists. In truth, pain is in our brain. Or as the author and University of California, San Diego, neuroscientist V. S. Ramachandran put it, “Pain is an opinion.” We feel it because of how our brain interprets input transmitted to it from all our senses, not necessarily because of the inherent properties of the input itself. There are no nerves dedicated to sensing and transmitting pain. Anyone who has willed themselves to not feel a tickle as ticklish can appreciate the difference between stimulation and our perception of it. Pain can be experienced and relieved in phantom limbs. Discomfort and swelling increase when people believe a painful hand or knee is larger. They decrease when it seems smaller, for example in a distorted image or based on virtual reality technology. Injections are less painful when we don’t watch them. Using our brains, we can exert some control over it. © 2019 The New York Times Company

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26865 - Posted: 12.02.2019

Ruth Williams Throughout the animal kingdom, there are numerous examples of neurons that respond to multiple stimuli and faithfully transmit information about those various inputs. In the mouse, for example, there are certain neurons that respond to both temperature and potentially damaging touch. In the fruit fly, there are neurons that sense light, temperature, pain, and proprioceptive stimuli—those arising as a result of body position and movement. And in C. elegans, two sensory neurons, known as PVD neurons, that run the length of the body on either side are thought to regulate proprioception as well as responses to harsh touch and cold temperature. Scientists have now figured out how a single PVD neuron can relay two different stimuli: while harsh touch results in typical firing of the neuron—an impulse that travels the length of the cell—proprioception causes a localized response in one part of the cell with no apparent involvement of the rest. The findings are reported today (November 14) in Developmental Cell. “[The] paper illustrates that different parts of the neuron do different things,” says neuroscientist Scott Emmons of Albert Einstein College of Medicine who did not participate in the research, “and that just makes the whole system much more complex to interpret,” he says. To examine how a single neuron interprets distinct inputs and drives corresponding behaviors, neuroscientist Kang Shen of Stanford University and colleagues focused on PVD neuron–regulated escape behavior when a worm is poked with a wire and the worm’s normal wiggling motion as it responds to proprioceptive stimuli. © 1986–2019 The Scientist

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: Development of the Brain
Link ID: 26823 - Posted: 11.16.2019

Kas Roussy · CBC News · At the Toronto Rehabilitation Institute, Dr. Andrea Furlan, a pain specialist, is holding a regular meeting with some of her colleagues. Sitting around the table are physiotherapists, pharmacists, doctors and nurses. Other health-care professionals have joined in via teleconferencing. The discussion focuses on chronic pain and the role opioids have in treating the condition at a time when current prescribing guidelines in Canada advises doctors to put the prescription pad down. On a monitor, someone asks Furlan how she should start tapering her patient who is prescribed opioids. "Each patient is different," Furlan said. "I don't have a recipe for everyone. The patients are afraid of the pain getting worse. They are afraid of the withdrawal symptoms. You need to provide a lot of education." She also suggests exercise and physiotherapy — even diet and sleep can have an impact on chronic pain. One in five Canadians suffers from chronic pain (i.e., pain that is ongoing and lasts longer than six months like low back pain, nerve damage or arthritis). For these pain sufferers, opioids are a lifesaver. But access to the pain medication is getting harder because of doctors' concerns about addiction and abuse. More than 12,800 apparent opioid-related deaths occurred from January 2016 to March 2019, according to the Public Health Agency of Canada, the vast majority from illicit fentanyl use. "I have had patients referred to us because their doctors cut them from opioids," said Furlan. "That's ridiculous because they were not addicted. They were not having any complications. They were not on a high dose." ©2019 CBC/Radio-Canada

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 26786 - Posted: 11.04.2019

By Aimee Cunningham At age 37, Hope Hartman developed a painful, burning rash in her right ear, in the part “you would clean with a Q-tip,” the Denver resident says. The pain got so bad she went to a local emergency room, where the staff was flummoxed. Hartman was admitted to the hospital, where she started to lose sensation on the right side of her face. During that 2013 health crisis, Hartman’s husband, Mike, sent a picture of the ear to his mom, a nurse. She said it looked like zoster, better known as shingles, which is caused by the varicella zoster virus. She “diagnosed it from an iPhone photo,” Hartman recalls. Antiviral treatment didn’t fully clear the infection. For about two weeks after her release from the hospital, Hartman coped with severe pain, hearing loss and difficulty eating. Her right eye wouldn’t fully open or close. Following an appointment with neurologist Maria Nagel of the University of Colorado School of Medicine in Aurora, Hartman was admitted to the university’s hospital to get another antiviral drug intravenously. The pain subsided, and Hartman regained her hearing and the feeling in her face. To spare others the same trauma of a delayed diagnosis, Hartman arranged for Nagel to give a talk on the virus at the local hospital where staff missed the signs of the illness, known as Ramsay Hunt syndrome. That’s the name for a shingles infection that strikes the facial nerve important to facial movement. As Hartman experienced, varicella zoster virus can cause a grab bag of symptoms that go beyond the typical torso rash. Hartman’s young age didn’t help with the diagnosis. Shingles is more common in people 50 and older. But no one is risk-free. Varicella zoster virus lives in about 95 percent of the U.S. adult population, thanks to the virus’s first line of attack: chicken pox. The body eventually clears the itchy, red pox from the skin, but the virus remains, dormant in nerve cells. The rash kept scores of U.S. children home from school until about 1995 (when a vaccine became available). © Society for Science & the Public 2000–2019.

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26773 - Posted: 10.31.2019

People with long-term health problems such as arthritis are more likely to feel pain on humid days, a study has suggested. Folklore suggests the cold makes pain worse - but there is actually little research into the weather's effects. And this University of Manchester study of 2,500 people, which collected data via smartphones, found symptoms were actually worse on warmer, damper days. Researchers hope the findings will steer future research into why that is. Hearing someone say their knee is playing up because of the weather is pretty common - usually because of the cold, Some say they can even predict the weather based on how their joints feel. But carrying out scientific research into how different types of weather affect pain has been difficult. Previous studies have been small, or short-term. In this research, called Cloudy with a Chance of Pain, scientists recruited 2,500 people with arthritis, fibromyalgia, migraine and neuropathic pain from across the UK. They recorded pain symptoms each day, for between one and 15 months, while their phones recorded the weather where they were. Damp and windy days with low pressure increased the chances of experiencing more pain than normal by about 20%. So if someone's chances of a painful day with average weather were five in 100, they would increase to six in 100 on a damp and windy day. Cold, damp days also made pain worse. But there was no association with temperature alone, or rainfall. 'Pain forecast' Prof Will Dixon, of the Centre for Epidemiology Versus Arthritis, at the University of Manchester, who led the study said: "Weather has been thought to affect symptoms in patients with arthritis since [ancient Greek physician] Hippocrates. © 2019 BBC

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26746 - Posted: 10.24.2019

Will Stone & Allison Aubrey There's no doubt that opioids have been massively overprescribed in U.S. In the haste to address the epidemic, there's been pressure on doctors to reduce prescriptions of these drugs — and in fact prescriptions are declining. But along the way, some chronic pain patients have been forced to rapidly taper or discontinue the drugs altogether. Now, the U.S. Department of Health and Human Services has a new message for doctors: Abrupt changes to a patient's opioid prescription could harm them. On Thursday, the agency issued new guidelines for physicians on how best to manage opioid prescriptions. They recommend a deliberate approach to lowering doses for chronic pain patients who have been on long-term opioid therapy. "It must be done slowly and carefully," says Adm. Brett P. Giroir, MD, assistant secretary for health for HHS. "If opioids are going to be reduced in a chronic patient it really needs to be done in a patient-centered, compassionate, guided way." This is a course correction of sorts. In 2016, the Centers for Disease Control and Prevention issued prescribing guidelines. Those highlighted the risks of addiction and overdose and encouraged providers to lower doses when possible. In response, many doctors began to limit their pain pill prescriptions, and in some cases cut patients off. These guidelines led to rigid rules in some cases. Giroir says it's concerning that some clinicians, policymakers, and health systems are "interpreting guidelines as mandates." © 2019 npr

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26691 - Posted: 10.11.2019

By Jane E. Brody My grandson Stefan was about 8 years old when he began to get migraine headaches. As soon as he could after getting home from school, he would lie down and go to sleep, awakening an hour or two later, usually with the headache gone. But before the pain abated, he sometimes vomited, prompting him and his relatives to keep barf bags handy at all times. Then as Stefan approached puberty, these debilitating headaches stopped as mysteriously as they had begun. Though Stefan’s headaches were disruptive and disabling, he was luckier than his grandma. My migraine attacks (misdiagnosed as sinus headaches) began around puberty, usually occurred three times a month, each lasting for three days, and didn’t end until menopause. Even though sleep can often terminate a migraine attack, nothing I tried brought relief, and there were no prescription medications at the time to treat or prevent them. Attention parents, teachers, coaches, doctors and anyone else who interacts with children and teens: Too often, adults tell them to “suck it up, it’s just a headache.” A migraine is not “just a headache,” nor is it something they can ignore. A migraine makes you feel sick all over, often acutely sensitive to light and noise, nauseated and unable to concentrate on anything but the desire for relief. Very young children with migraine may be spared the head pain and instead get only gastrointestinal symptoms like vomiting and stomach pain. Migraine is a disease with a genetic component and often runs in families. The pounding, nauseating headache is a symptom of that disease. Before puberty, the disorder affects boys and girls equally, but after puberty, when testosterone kicks in to suppress migraine attacks in boys, the incidence among girls becomes very much higher. © 2019 The New York Times Company

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 26674 - Posted: 10.07.2019

Katarina Zimmer Several recent studies in high-profile journals reported to have genetically engineered neurons to become responsive to magnetic fields. In doing so, the authors could remotely control the activity of particular neurons in the brain, and even animal behavior—promising huge advances in neuroscientific research and speculation for applications even in medicine. “We envision a new age of magnetogenetics is coming,” one 2015 study read. But now, two independent teams of scientists bring those results into question. In studies recently posted as preprints to bioRxiv, the researchers couldn’t replicate those earlier findings. “Both studies . . . appear quite meticulously executed from a biological standpoint—multiple tests were performed across multiple biological testbeds,” writes Polina Anikeeva, a materials and cognitive scientist at MIT, to The Scientist in an email. “I applaud the authors for investing their valuable time and resources into trying to reproduce the results of their colleagues.” The promise of magnetogenetics Being able to use small-scale magnetic fields to control cells or entire organisms would have enormous potential for research and medical therapies. It would be a less invasive method than optogenetics, which requires the insertion of optical fibers to transmit light pulses to specific groups of neurons, and would provide a more rapid means of inducing neural activity than chemogenetics, which sparks biochemical reactions that can take several seconds to stimulate neurons. © 1986–2019 The Scientist

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 26642 - Posted: 09.24.2019

Alex Smith Lori Pinkley, a 50-year-old from Kansas City, Mo., has struggled with puzzling chronic pain since she was 15. She's had endless disappointing visits with doctors. Some said they couldn't help her. Others diagnosed her with everything from fibromyalgia to lipedema to the rare Ehlers-Danlos syndrome. Pinkley has taken opioids a few times after surgeries but says they never helped her underlying pain. "I hate opioids with a passion," Pinkley says. "An absolute passion." Recently, she joined a growing group of patients using an outside-the-box remedy: naltrexone. It is usually used to treat addiction, in a pill form for alcohol and as a pill or a monthly shot for opioids. As the medical establishment tries to do a huge U-turn after two disastrous decades of pushing long-term opioid use for chronic pain, scientists have been struggling to develop safe, effective alternatives. When naltrexone is used to treat addiction in pill form, it's prescribed at 50 mg, but chronic-pain patients say it helps their pain at doses of less than a tenth of that. Low-dose naltrexone has lurked for years on the fringes of medicine, but its zealous advocates worry that it may be stuck there. Naltrexone, which can be produced generically, is not even manufactured at the low doses that seem to be best for pain patients. Instead, patients go to compounding pharmacies or resort to DIY methods — YouTube videos and online support groups show people how to turn 50 mg pills into a low liquid dose. Some doctors prescribe it off-label even though it's not FDA-approved for pain. © 2019 npr

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26641 - Posted: 09.24.2019

Patti Neighmond For people who live with chronic pain, getting up, out and moving can seem daunting. Some fear that physical activity will make their pain worse. But in fact, researchers find the opposite is true: The right kind of exercise can help reduce pain. Today, Emma Dehne agrees. Dehne is 44, lives in Chapel Hill, N.C., and works as a business officer in the office of the executive vice chancellor at the University of North Carolina. She says her commitment to exercise is relatively recent. Just a year and a half ago, Dehne pretty much avoided any physical movement she didn't have to make. Just climbing stairs was painful — "sometimes to the point where I would have to hold on to the banister to help myself up," she says, "and I couldn't even extend my leg." At times, it felt as though the ligaments in her knees "were tearing." Dehne was diagnosed around age 40 with osteoarthritis in both knees, a painful swelling and deterioration of the cushioning cartilage in those joints that reduces their range of motion. Luckily for her, she says, she worked at the Thurston Arthritis Research Center at the University of North Carolina. The woman working in the cubicle next to hers ran a program that encouraged people with osteoarthritis to start walking to help reduce their pain. Dehne was skeptical but felt she was just too young to be burdened by this disease; she agreed to give brisk walks a try. In the beginning she felt stiff, tired and out of breath. That changed quickly. © 2019 npr

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 5: The Sensorimotor System
Link ID: 26635 - Posted: 09.23.2019