Chapter 5. The Sensorimotor System

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 3047

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

Keyword: Pain & Touch; Development of the Brain
Link ID: 26823 - Posted: 11.16.2019

Catherine Offord A clinical trial of a gene therapy for Duchenne muscular dystrophy has been halted after a patient suffered serious side effects following treatment, Reuters reports today (November 12). After receiving Solid Biosciences’s experimental therapy, SGT-001, the patient experienced kidney injury and drops in red blood cell count, leading the US Food and Drug Administration (FDA) to place the study on hold. “We are encouraged that this patient is recovering,” Ilan Ganot, Solid Biosciences’s CEO, president, and cofounder, says in a statement. “In the coming weeks, we anticipate that we will have a better understanding of the biological activity and potential benefit of SGT-001. We look forward to sharing this additional data and working with the FDA to resolve the clinical hold and determining next steps for the program.” SGT-001 has been administered to six people so far, and involves the transfer of an engineered version of the dystrophin gene DMD, which is dysfunctional in people with Duchenne muscular dystrophy, using an adeno-associated virus (AAV) as a vector. Sarepta Therapeutics, Pfizer, and other biopharmaceutical companies are investigating similar approaches to treat the condition, although the choice of AAV varies. See “Positive Trial Results for Experimental DMD Gene Therapy” This isn’t the first time Solid Biosciences’s trial of SGT-001 has been put on hold. Early last year, the FDA halted the same study after a patient receiving a low dose of the therapy experienced a drop in red blood cell count and had to be hospitalized. The company was allowed to resume the trial last June after making changes to the study design. © 1986–2019 The Scientist

Keyword: Movement Disorders; Muscles
Link ID: 26816 - Posted: 11.14.2019

Nicole Ireland · Recent video from Thailand showing paralyzed Humboldt Broncos hockey player Ryan Straschnitzki moving his legs after an electrical stimulation device was surgically implanted in his spine has sparked excitement — as well as questions — about therapies available to Canadians with spinal injuries. The procedure Straschnitzki, 20, had is called epidural stimulation, and although promising, it's still highly experimental, experts in both Canada and the U.S. say. It's in early stages of clinical trials in the U.S. and Europe to evaluate the safety and effectiveness of restoring physical abilities — from bowel and bladder function to moving arms and legs — to people who desperately want to get some normalcy back after spinal injury. Barry Munro understands all too well why people's immediate reaction is to ask why they can't try the procedure here in Canada. He's been hoping for — and working toward — finding a cure for spinal cord injury ever since he dove into a lake in his 20s and was left quadriplegic. Now 55, Munro is chief development officer for the Canadian Spinal Research Organization and works with the North American Spinal Injury Consortium. For more than 30 years, he's seen the headlines come and go, inciting hope that a cure is on the horizon. "I've been down this road before," Munro told CBC News. "I really, really believe in finding a cure and believe it will happen and I have that hope. But — there's a big but — we have to be careful." Milos Popovich, director of the KITE Research Institute at the University Health Network's Toronto Rehabilitation Institute, echoes that need to proceed with caution. He said that epidural stimulation must proceed through many more stages of scientifically sound clinical trials to prove it works before it could be made available as a therapy in Canada. ©2019 CBC/Radio-Canada.

Keyword: Regeneration; Movement Disorders
Link ID: 26810 - Posted: 11.11.2019

By Tina Hesman Saey A newly discovered type of mitochondrial self-destruction may make some brain cells vulnerable to ALS, also known as Lou Gehrig’s disease. In mice genetically engineered to develop some forms of a degenerative nerve disease similar to amyotrophic lateral sclerosis, energy-generating organelles called mitochondria appear to dismantle themselves without help from usual cell demolition crews. This type of power plant self-destruction was spotted in upper motor neurons, brain nerve cells that help initiate and control movements, but not in neighboring cells, researchers report November 7 in Frontiers in Cellular Neuroscience. Death of those upper motor neurons is a hallmark of ALS, and the self-destructing mitochondria may be an early step that sets those cells up to die later. Pembe Hande Özdinler, a cellular neuroscientist at Northwestern University Feinberg School of Medicine in Chicago, and her colleagues have dubbed the mitochondrial dissolution “mitoautophagy.” It is a distinct process from mitophagy, the usual way that cellular structures called autophagosomes and lysosomes remove damaged mitochondria from the cell, Özdinler says. Usually, clearing out old or damaged mitochondria is important for cells to stay healthy. When mitochondria sustain too much damage, they may trigger the programmed death of the entire cell, known as apoptosis (SN: 8/9/18). Özdinler’s team spotted what she describes as “awkward” mitochondria in electron microscope images of upper motor neurons from 15-day-old mice. These unweaned mice are equivalent to human teenagers, Özdinler says. ALS typically doesn’t strike until people are 40 to 70 years old. But by the time symptoms appear, motor neurons are already damaged, so Özdinler’s group looked at the young mice to capture the earliest signs of the disease. © Society for Science & the Public 2000–2019

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26804 - Posted: 11.08.2019

Maheen Mausoof Adamson, Ph.D. The 1982 science fiction film classic Blade Runner is a gritty detective story set in the dystopian future that raises questions about what it means to be human. In the film, Harrison Ford plays Rick Deckard, a police officer turned bounty hunter searching the streets of Los Angeles for a replicant (human-like androids) rebellion leader Roy Batty. Batty is presented as a technologically perfected being fitted with a human-template brain completely rewired to create an enemy to be deathly feared. Fear of the perfect altered brain is prominent in science fiction—and may be particularly prevalent today, amid growing concerns about genetic editing and artificial intelligence. The prospect of a fully artificial human brain remains very distant. However, we are in the midst of a neuromodulation revolution that will increase our ability to treat disease and optimize human performance. We must, however, carefully consider the benefits and risks of these techniques in fully evaluating their potential for society as well as the individual. A large number of patients suffering from neurological or psychiatric disorders—depression, pain, and post-traumatic stress disorder among them—are resistant to or can develop resistance to standard medication and psychotherapy, suggesting the need for new approaches. Neuromodulation may possibly be such an approach. The term (aka neurostimulation) refers to direct stimulation and modification of the nervous system through the use of electrical, chemical, or mechanical signals. Neuromodulation therapy is already used to treat many brain disorders, most commonly movement disorders, chronic pain, and depression. © 2019 The Dana Foundation.

Keyword: Parkinsons; Depression
Link ID: 26797 - Posted: 11.07.2019

By Gretchen Reynolds Being physically fit may sharpen the memory and lower our risk of dementia, even if we do not start exercising until we are middle-aged or older, according to two stirring new studies of the interplay between exercise, aging, aerobic fitness and forgetting. But both studies, while underscoring the importance of activity for brain health, also suggest that some types of exercise may be better than others at safeguarding and even enhancing our memory. The scientific evidence linking exercise, fitness and brain health is already hefty and growing. Multiple studies have found that people with relatively high levels of endurance, whatever their age, tend to perform better on tests of thinking and memory than people who are out of shape. Other studies associate better fitness with less risk for developing Alzheimer’s disease. But many of these studies have been one-time snapshots of people’s lives and did not delve into whether and how changing fitness over time might alter people’s memory skills or dementia risk. They did not, in other words, tell us whether, by midlife or retirement age, it might be too late to improve our brain health with exercise. So, for the first of the new studies, which was published this month in The Lancet Public Health, researchers at the Norwegian University of Science and Technology in Trondheim, Norway, helpfully decided to look into that very issue, taking advantage of the reams of health data available on average Norwegians. They began by turning to records from a large-scale health study that had enrolled almost every adult resident in the region around Trondheim beginning in the 1980s. The participants completed health and medical testing twice, about 10 years apart, that included estimates of their aerobic fitness. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26794 - Posted: 11.06.2019

Darian Woods Recently, Purdue Pharma filed for bankruptcy as part of a tentative multi-billion dollar settlement with state and local governments over lawsuits alleging that the company misled doctors and the public about the addictive nature of their well-known painkiller, Oxycontin. But Purdue Pharma's story is part of a pattern that has repeated itself throughout the history of the opium trade. It's a pattern documented by the book Opium: How An Ancient Flower Shaped And Poisoned Our World by Dr. John H. Halpern and David Blistein. The cycle begins when an opium product proves devastating to users. Innovators come along, promising a safer alternative, and virtually every time, they downplay the risks of addiction. Addiction ensues. Then come new innovators, promising something better and less addictive, and the cycle continues. This cycle, Halpern and Blistein recount, goes all the way back to Ancient Greece. Aulus Cornelius Celsus was a doctor famous for writing one of the world's first medical encyclopedias, which included a recipe for opium pills. He recommended it for insomnia, bad headaches, and joint pain. It didn't turn out so well. Opium addiction spread, and its victims included Roman emperor Marcus Aurelius. Around 1000 AD, Persian physician Avicenna developed standard opium doses the size of chickpeas. Dose standardization helped prevent overdoses but opium addiction rose in Persia over the following centuries. Avicenna himself died of an opium overdose. © 2019 npr

Keyword: Drug Abuse; Pain & Touch
Link ID: 26791 - Posted: 11.05.2019

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

Keyword: Pain & Touch; Drug Abuse
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.

Keyword: Pain & Touch
Link ID: 26773 - Posted: 10.31.2019

By Gretchen Reynolds Taking more steps during the day may be related to better sleep at night, according to an encouraging new study of lifestyle and sleep patterns. The study, which delved into the links between walking and snoozing, suggests that being active can influence how well we sleep, whether we actually exercise or not. Sleep and exercise scientists have long been intrigued and befuddled by the ties between physical activity and somnolence. To most of us, it might seem as if that relationship should be uncomplicated, advantageous and one-way. You work out, grow tired and sleep better that night. But a variety of past studies indicate that the effects of exercise on sleep are more scrambled than that. In some studies, when people work out strenuously, they sleep relatively poorly, suggesting that intense exercise might disrupt slumber. Other experiments have found that the impacts of exertion and sleep work both ways; after a night of ragged sleep, people often report finding their normal workout extra wearing. Past research also has produced conflicting results about whether and how the timing of exercise matters, and if afternoon workouts aid or impair that night’s sleep. Most of these past studies have focused on planned exercise, though, not more incidental, everyday physical activity, and much of the research has involved people with clinical sleep problems, such as insomnia. Little has been known about whether simply moving around more during the day, absent formal exercise, might influence sleep, particularly in people who already tend to sleep fairly well. © 2019 The New York Times Company

Keyword: Sleep
Link ID: 26771 - Posted: 10.30.2019

By Robert Martone We humans have evolved a rich repertoire of communication, from gesture to sophisticated languages. All of these forms of communication link otherwise separate individuals in such a way that they can share and express their singular experiences and work together collaboratively. In a new study, technology replaces language as a means of communicating by directly linking the activity of human brains. Electrical activity from the brains of a pair of human subjects was transmitted to the brain of a third individual in the form of magnetic signals, which conveyed an instruction to perform a task in a particular manner. This study opens the door to extraordinary new means of human collaboration while, at the same time, blurring fundamental notions about individual identity and autonomy in disconcerting ways. Direct brain-to-brain communication has been a subject of intense interest for many years, driven by motives as diverse as futurist enthusiasm and military exigency. In his book Beyond Boundaries one of the leaders in the field, Miguel Nicolelis, described the merging of human brain activity as the future of humanity, the next stage in our species’ evolution. (Nicolelis serves on Scientific American’s board of advisers.) He has already conducted a study in which he linked together the brains of several rats using complex implanted electrodes known as brain-to-brain interfaces. Nicolelis and his co-authors described this achievement as the first “organic computer” with living brains tethered together as if they were so many microprocessors. The animals in this network learned to synchronize the electrical activity of their nerve cells to the same extent as those in a single brain. The networked brains were tested for things such as their ability to discriminate between two different patterns of electrical stimuli, and they routinely outperformed individual animals. © 2019 Scientific American

Keyword: Robotics; Language
Link ID: 26770 - Posted: 10.30.2019

By Maya Vijayaraghavan On Jan. 1, my husband asked me whether he would die that year. I said no. It happened to be my birthday, and I wanted to feel jubilant despite the tragic turn of events in our life. I thought Rahul might have another year, that he might beat the odds of dying this year. In other words, his hazard ratio was favorable compared with someone else in his situation. He liked talking about something related, hazard scores — a composite score of one’s genetic risk for a particular outcome such as diagnosis of a disease. It was his thing as a neuroscientist-physician. He developed one for Alzheimer’s disease, and was on his way to developing one for amyotrophic lateral sclerosis (ALS), the disease he had been studying even before he got sick with it. In reality, he had declined significantly since his diagnosis of ALS two years prior. First, he lost his speech, then his mobility, and very quickly breathing became a struggle. But any talk of decline came with an acceptance that his life was imminently finite, and neither of us were willing to accept that outcome. But Rahul did die, six months after that conversation. I remember some of our last conversations, when things were very difficult. His forewarning that this existence with him teetering at the brink of life and death was much easier than the life I would lead as a widow, raising two young children. I think neither of us really understood that the emptiness I’d feel would be soul-crushing. That I would cry all the time. That I would miss him so much. That I would become a ghost of my former self. That this thing they call complicated grief, in which healing doesn’t occur as it’s supposed to, and which supposedly happens only after a year, is something that I feel now. That I would think constantly about the time when my husband was first diagnosed and he got into a fight with our then-3-year-old (now 5) about how he could not carry him because he did not have the strength to and not because he did not want to.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26761 - Posted: 10.28.2019

By Owain Clarke BBC Wales health correspondent World-leading research is helping scientists find new ways of trying to help younger people who have had a stroke get back to work. The study led by Manchester Metropolitan University found the speed a patient can walk is a major factor in determining how likely they are able to return to the workplace. Researchers have been working with physiotherapists and patients in Wales. It includes moving rehabilitation outdoors, including the Brecon Beacons. It is hoped it could lead to new rehabilitation methods being developed to target younger stroke patients. The average age to have a stroke in the UK is 72 for men and 78 for women. But there has been a 40% worldwide rise in people under 65 who have strokes in the last decade, according to the researchers. Image copyright Manchester Metropolitan University Image caption Researchers are studying the skeletons of stroke patients to see how joints perform when they walk What does the science say? It looked at 46 patients across Wales who had a stroke when younger than 65 years old and only 23% were able to return to work It found walking speed was a key predictor of whether a younger adult who has had a stroke could return to work They calculated a walking speed threshold of 0.93m/s (3ft a second) was a good benchmark for the likelihood of returning to work - and as a result this could be a goal set during rehabilitation As well as looking at the best environment for younger patients to recover in, it is now looking at using CGI technology to study joints to find out how stroke patients walk Nikki Tomkinson had a stroke at 53. "The world started shifting" while she was out driving in Cardiff. © 2019 BBC

Keyword: Stroke
Link ID: 26759 - Posted: 10.28.2019

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

Keyword: Pain & Touch
Link ID: 26746 - Posted: 10.24.2019

By Kelly Servick CHICAGO, ILLINOIS—By harnessing the power of imagination, researchers have nearly doubled the speed at which completely paralyzed patients may be able to communicate with the outside world. People who are “locked in”—fully paralyzed by stroke or neurological disease—have trouble trying to communicate even a single sentence. Electrodes implanted in a part of the brain involved in motion have allowed some paralyzed patients to move a cursor and select onscreen letters with their thoughts. Users have typed up to 39 characters per minute, but that’s still about three times slower than natural handwriting. In the new experiments, a volunteer paralyzed from the neck down instead imagined moving his arm to write each letter of the alphabet. That brain activity helped train a computer model known as a neural network to interpret the commands, tracing the intended trajectory of his imagined pen tip to create letters (above). Eventually, the computer could read out the volunteer’s imagined sentences with roughly 95% accuracy at a speed of about 66 characters per minute, the team reported here this week at the annual meeting of the Society for Neuroscience. The researchers expect the speed to increase with more practice. As they refine the technology, they will also use their neural recordings to better understand how the brain plans and orchestrates fine motor movements. © 2019 American Association for the Advancement of Science.

Keyword: Robotics; Brain imaging
Link ID: 26745 - Posted: 10.24.2019

Anna Azvolinsky Nearly 30 years ago, Kamran Khodakhah, now a neuroscientist at Albert Einstein College of Medicine, signed up for a TV repair course that met several times a week at night at a local community college in London. While many of the other students were attending with the obvious goal of repairing TVs and other appliances, Khodakhah had a different aim. He reasoned that if he could understand how a television worked, he could design new tools to study the rat brain slices he had collected. Khodakhah was working as a PhD student in the lab of neuroscientist David Ogden at the National Institute for Medical Research, trying to determine whether a particular signaling pathway—the inositol trisphosphate (InsP3)/calcium signaling pathway—could be activated in nerve cells called Purkinje neurons. They are found in the cerebellum and have a high density of InsP3 receptors. By taking the TV repair class, Khodakhah wanted to learn to build an electronic circuit to enhance his camera images in order to better visualize the Purkinje cells within slices of the cerebellum and to study the InsP3/calcium ion signaling pathway. He used the new imaging setup, combined with existing lab tools such as flash photolysis, to introduce inert precursor molecules of InsP3—called caged InsP3—into Purkinje neurons in cerebellar slices prepared from rat brains. When stimulated with light, a caged InsP3 molecule is rapidly converted into an active form that binds to InsP3 receptors. Khodakhah then used a fluorescent calcium indicator and recorded the calcium channel activity to see if the binding of InsP3 receptors caused release of calcium from internal stores. At the time, researchers knew that in liver and other non-neuronal cells, InsP3 molecules act as messengers, stimulating the release of calcium ions, which then activates internal cellular pathways. Whether something similar happened in Purkinje neurons wasn’t clear, but if it did, the process might reveal something about how the cerebellum coordinates movement, Khodakhah thought. © 1986–2019 The Scientist.

Keyword: Movement Disorders
Link ID: 26736 - Posted: 10.23.2019

By Pam Belluck About 10 days after what seemed like a garden-variety cold, Luca Waugh, a healthy 4-year-old, developed troubling symptoms. Suddenly, his neck became so weak that he fell backward. Then his right arm couldn’t move. Within days, recalled his mother, Dr. Riley Bove, he developed “head-to-toe paralysis, where he could kind of move his eyes a little bit and one side of his face.” Doctors diagnosed Luca with acute flaccid myelitis or A.F.M., a mysterious neurological condition that can cause limb weakness and polio-like paralysis, mostly in young children. A.F.M. is rare, but in 2014, when Luca became afflicted, health authorities identified a burst of 120 cases. Since then, A.F.M. has made headlines as cases have spiked every two years, and nearly 600 have been confirmed across the country since 2014. What exactly causes A.F.M. has eluded experts, frustrating attempts to prevent or treat it. Now, a study by a team that includes Luca’s mother, Dr. Bove, who happens to be a neurologist, provides strong evidence of a likely cause. It involved dozens of children with A.F.M., including Luca, whose paralysis improved after weeks of hospitalization but who remains disabled five years later. The research, published Monday in the journal Nature Medicine, points to a long-suspected culprit: enteroviruses, a group of common viruses that usually produce mild effects, but can sometimes cause neurological symptoms. Using sophisticated laboratory techniques, researchers found antibodies to enteroviruses in the cerebrospinal fluid of nearly 70 percent of the children with A.F.M., a sign their bodies had mobilized to defend against enterovirus infection. © 2019 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 26734 - Posted: 10.22.2019

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

Keyword: Pain & Touch; Drug Abuse
Link ID: 26691 - Posted: 10.11.2019

Allison Aubrey The condition strikes young children. It can start with run-of-the-mill virus symptoms, like fever or sniffles. But, then the kids lose control of their limbs, may have trouble swallowing or breathing, or even end up paralyzed. This terrifying experience happened to more than 570 families since 2014, whose children were struck with an illness called acute flaccid myelitis, or AFM. "It was really scary," says Susan Coyne, the mother of a son, Evan Mazanec, who developed AFM back in 2014 when he was 7 years old. "When this first started, no one really knew what it was," she says. It came on quickly, starting with a fever and an ear infection. Coyne says the limb weakness and paralysis began several days later — just as Evan was getting over the fever. He lost control of his arms and legs. "He couldn't move them, he couldn't lift them, he couldn't walk," Coyne says. He spent a year and a half in intensive rehab. He had to learn to walk and move his arms again. "It set him back years," Coyne says. Scientists have struggled to understand what causes this rare childhood disease. Now, one theory is gaining ground. A paper published Monday in the journal Pediatrics finds the condition may be triggered by a virus. The disease follows a pattern: Scientists have documented outbreaks every other year, beginning in 2014, and again in 2016 and 2018. Last year, there were 233 cases in the U.S. It strikes young kids, average age of 6. And, it can lead to long-term paralysis. © 2019 npr

Keyword: Movement Disorders; Development of the Brain
Link ID: 26684 - Posted: 10.09.2019

By Jason Gutierrez MANILA — President Rodrigo Duterte of the Philippines has revealed that he has a neuromuscular disease that has led to a slew of medical problems, including making his eye droop. Mr. Duterte, who was in Russia for a state visit, told the Filipino community there on Saturday night that he has myasthenia gravis, a chronic autoimmune disease that leads to skeletal muscle weakness. He said the disease ran in his family. The revelation came amid continued public speculation about his health. There have been periods when the famously bombastic president has been out of the public eye for days, prompting headlines guessing about his whereabouts, and even rumors of his death. But his communications officers have said that Mr. Duterte, 74, like any other older person, needs his own personal time. The president revealed the ailment after he apparently made a joke about not being able to look straight at a woman with whom he had danced a duet during the event in Moscow. “I have a talent,” Mr. Duterte said, according to official transcripts provided by his office afterward. “When I look at you, my other eye droops. Do you see? The other eye is smaller. It goes where it wants.” He added: “Actually, that’s myasthenia gravis. It’s a nerve malfunction.” Mr. Duterte said his grandfather had also had the disease, adding, “So I believe, really, in genetics.” The disease often affects the muscles that control the eyes, facial expression, speaking and swallowing, according to the Philippine Medical Association. Mr. Duterte came to power in 2016 vowing to rid the country of drug dealers and to wipe out other crimes. Since then, the Philippines’ war on drugs has led to thousands of killings allegedly by the police and vigilantes, which rights groups have denounced as an atrocity. © 2019 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 26676 - Posted: 10.07.2019