Chapter 5. The Sensorimotor System

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By LISA SANDERS, M.D. The woman woke to the sound of her 57-year-old husband sobbing. They’d been married for 30 years, and she had never heard him cry before. “I hurt so much,” he wailed. “I have to go back to the hospital.” The symptoms started two weeks earlier. One afternoon, coming home from his job as a carpenter, he felt hot and tired. He shook with shivers even though the day was warm. He drank a cup of tea and went to bed. The next day he felt fine, until the end of the day, when he felt overwhelmed by the heat and chills again. The day after that was the same. When he woke one morning and saw that his body was covered with pale pink dots — his arms, his face, his chest and thighs — he started to worry. His wife took him to the Griffin Hospital emergency room in Derby, Conn. The first doctor who saw him thought he probably had Lyme disease. Summer had just started, and he’d already seen a lot of cases. He sent the patient home with an antibiotic and steroid pills for the rash. The man took the medications but didn’t get any better. Soon everything started to hurt. His muscles, his joints and his back felt as if he’d been beaten. He dragged himself back to the E.R. He was given pain pills. A few days later, he went to the E.R. a third time and was given more pain meds. After waking up crying, he went yet again, and this time, the doctors admitted him. By then the patient had had several blood tests, which showed no sign of Lyme or other tick-borne diseases. A CT scan was equally uninformative. The next day, the man was walking to the bathroom when his legs gave out and he fell down. The doctor in charge of his care came and examined him once again. The man looked fit and healthy, despite the now-bright-red rash, but his legs were extremely weak. If the doctor applied even light pressure to the raised leg, it sagged back down to the bed. And his feet felt numb. He had a sensation of tingling in his hands, as if they had gone to sleep. That was how the weakness and numbness in his legs started, he told the doctor. And the next day, his hands were so weak he had to use both just to drink a cup of water. © 2017 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 23644 - Posted: 05.22.2017

Laura Beil Even though a sprained ankle rarely needs an opioid, a new study of emergency room patients found that about 7 percent of patients got sent home with a prescription for the potentially addictive painkiller anyway. And the more pills prescribed, the greater the chance the prescription would be refilled, raising concerns about continued use. The research adds to evidence that it’s hard for some people to stop taking the pills even after a brief use. State officials in New Jersey recently enacted a law limiting first-time prescriptions to a five-day supply, and other states should consider similar restrictions, says Kit Delgado, an assistant professor of Emergency Medicine and Epidemiology at the University of Pennsylvania. “The bottom line is that we need to do our best not to expose people to opioids,” Delgado says. “And if we do, start with the smallest quantity possible.” The research was presented May 17 at the Society for Academic Emergency Medicine’s annual meeting in Orlando. Previous research has found that the more opioids such as hydrocodone and oxycodone are prescribed, the more likely patients are to keep taking them. But previous studies have been too broad to account for differences in diagnoses — for instance, whether people who received refills kept taking the drug simply because they still were in pain, Delgado says. He and colleagues limited their study to prescriptions written after ankle sprains to people who had not used an opioid in the previous six months. Usually, those injuries aren’t serious and don’t require opioids. |© Society for Science & the Public 2000 - 2017

Keyword: Drug Abuse; Pain & Touch
Link ID: 23638 - Posted: 05.20.2017

By: Ted Dinan, M.D., Ph.D, and John F. Cryan, Ph.D. O ver the past few years, the gut microbiota has been implicated in developmental disorders such as schizophrenia and autism, neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease, mood disorders such as depression, and even addiction disorders. It now seems strange that for so many decades we viewed the gut microbiota as bacteria that did us no harm but were of little benefit. This erroneous view has been radically transformed into the belief that the gut microbiota is, in effect, a virtual organ of immense importance. What we’ve learned is that what is commonly referred to as “the brain-gut-microbiota axis” is a bidirectional system that enables gut microbes to communicate with the brain and the brain to communicate back to the gut. It may be hard to believe that the microbes in the gut collectively weigh around three pounds—the approximate weight of the adult human brain—and contain ten times the number of cells in our bodies and over 100 times as many genes as our genome. 1 If the essential microbial genes were to be incorporated into our genomes, it is likely that our cells would not be large enough for the extra DNA. Many of those genes in our microbiota are important for brain development and function; they enable gut bacteria to synthesize numerous neurotransmitters and neuromodulators such as γ-aminobutyric acid (GABA), serotonin, dopamine, and short-chain fatty acids. While some of these compounds act locally in the gut, many products of the microbiota are transported widely and are necessary for the proper functioning of diverse organs. This is a two-way interaction: gut microbes are dependent on us for their nourishment. Any pathological process that reduces or increases food intake has implications for our microbes. © 2017 The Dana Foundation. All Rights Reserved.

Keyword: Parkinsons
Link ID: 23636 - Posted: 05.19.2017

By Roman Liepelt and Jack Brooks An amputee struggles to use his new prosthetic limb. A patient with a frontal-lobe brain lesion insists that her left hand has a mind of its own. The alleged criminal claims in court that he did not fire the gun, even though several eyewitnesses watched him do it. Each of these individuals is grappling with two elements of the mind-body connection: ownership, or an ability to separate ourselves from the physical and social environments, and agency, a conviction that we have control over our limbs. We are quick to investigate a sticker placed on our forehead when looking in a mirror, recognizing the foreign object as abnormal. The human brain typically handles these phenomena by comparing neural signals encoding the intended action with those signals carrying sensory feedback. When we are born, we make erratic reaching and kicking movements to map our body and to calibrate our sensorimotor system. During infancy, these movements solidify our self-awareness, and around the time we first walk, we are quick to investigate a sticker placed on our forehead when looking in a mirror, recognizing the foreign object as abnormal. By the age of four, our brains are proficient at distinguishing self and other. In the amputee, the brain lesion patient, and the defendant on trial, the sense of self is disrupted due to discordance between sensory feedback from the limb and the brain’s expectations of how a movement should feel. © 1986-2017 The Scientist

Keyword: Pain & Touch
Link ID: 23625 - Posted: 05.17.2017

By DENISE GRADY A new drug for amyotrophic lateral sclerosis, or Lou Gehrig’s disease, was approved on Friday by the Food and Drug Administration. The drug, called Radicava or edaravone, slowed the progression of the degenerative disease in a six-month study in Japan. It must be given by intravenous infusion and will cost $145,524 a year, according to its manufacturer, MT Pharma America, a subsidiary of the Japanese company Mitsubishi Tanabe Pharma Corporation. Radicava is only the second drug ever approved to treat A.L.S. The first, riluzole, was approved by the F.D.A. more than 20 years ago. Riluzole can increase survival by two or three months. There is no information yet about whether Radicava has any effect on survival. In the study in Japan, 137 patients were picked at random to receive either Radicava or a placebo. At the end of six months, the condition of those taking the drug declined less than those receiving placebos. Dr. Neil A. Shneider, director of the Eleanor and Lou Gehrig ALS Center at Columbia University Medical Center, said, “The effect is modest but significant.” He added, “I’m very happy, frankly, that there is a second drug approved for A.L.S.” The disease kills nerve cells that control voluntary muscles, so patients gradually weaken and become paralyzed. Most die within three to five years, usually from respiratory failure. About 12,000 to 15,000 people in the United States have A.L.S., according to the Centers for Disease Control and Prevention. Dr. Shneider predicted that patients would be eager to try the new drug. He said several of his patients were already receiving it because they had obtained it themselves from Japan. If more want it, he will prescribe it, he said. “It’s very safe,” he said. But he was uncertain about whether he would actually recommend it, because the method of administration is difficult. Patients have to have an intravenous line inserted and left in place indefinitely, which poses an infection risk. The first round of treatment requires a one-hour infusion every day for 14 days, followed by 14 days off. After that, the infusions are given daily for 10 out of 14 days, with 14 days off. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease ; Trophic Factors
Link ID: 23585 - Posted: 05.06.2017

By Moheb Costandi Pain in infants is heartbreaking for new parents, and extremely difficult to treat effectively—if at all. Every year an estimated 15 million babies are born prematurely, most of whom will then undergo numerous lifesaving but painful procedures, such as heel pricking or insertion of a thin tube known as a cannula to deliver fluids or medicine. Preterm babies in the intensive care unit are subjected to an average of 11 such “skin-breaking” procedures per day, but analgesia is only used just over one third of the time. We know that repetitive, painful procedures in early infancy can impact brain development negatively—so why is pain in infants so undertreated? One reason is the lack of standard guidelines for administering the drugs. Some analgesics given to adults are unsuitable for infants, and those that can be used often have different effects in children, making dosing a problem. What is more, newborn babies are incapable of telling us how they feel, making it impossible to determine how effective any painkiller might be. Researchers at the University of Oxford may now have overcome this latter challenge, however. They report May 3 in Science Translational Medicine having identified a pain-related brain wave signal that responds to analgesics, and could be used to measure the drugs’ efficacy. Until as recently as the 1980s, it was assumed that newborn babies do not feel pain, and that giving them analgesics would do more harm than good. Although these misconceptions have been cleared up, we still have very little understanding of infant pain, and so treating it is a huge challenge for clinicians. © 2017 Scientific American

Keyword: Pain & Touch
Link ID: 23576 - Posted: 05.05.2017

Douglas Fox Six times a day, Katrin pauses whatever she's doing, removes a small magnet from her pocket and touches it to a raised patch of skin just below her collar bone. For 60 seconds, she feels a soft vibration in her throat. Her voice quavers if she talks. Then, the sensation subsides. The magnet switches on an implanted device that emits a series of electrical pulses — each about a milliamp, similar to the current drawn by a typical hearing aid. These pulses stimulate her vagus nerve, a tract of fibres that runs down the neck from the brainstem to several major organs, including the heart and gut. The technique, called vagus-nerve stimulation, has been used since the 1990s to treat epilepsy, and since the early 2000s to treat depression. But Katrin, a 70-year-old fitness instructor in Amsterdam, who asked that her name be changed for this story, uses it to control rheumatoid arthritis, an autoimmune disorder that results in the destruction of cartilage around joints and other tissues. A clinical trial in which she enrolled five years ago is the first of its kind in humans, and it represents the culmination of two decades of research looking into the connection between the nervous and immune systems. For Kevin Tracey, a neurosurgeon at the Feinstein Institute for Medical Research in Manhasset, New York, the vagus nerve is a major component of that connection, and he says that electrical stimulation could represent a better way to treat autoimmune diseases, such as lupus, Crohn's disease and more. Several pharmaceutical companies are investing in 'electroceuticals' — devices that can modulate nerves — to treat cardiovascular and metabolic diseases. But Tracey's goal of controlling inflammation with such a device would represent a major leap forward, if it succeeds. © 2017 Macmillan Publishers Limited

Keyword: Neuroimmunology; Pain & Touch
Link ID: 23573 - Posted: 05.04.2017

Laura Sanders An electrode on top of a newborn’s scalp, near the soft spot, can measure when the baby feels pain. The method, described online May 3 in Science Translational Medicine, isn’t foolproof, but it brings scientists closer to being able to tell when infants are in distress. Pain assessment in babies is both difficult and extremely important for the same reason: Babies don’t talk. That makes it hard to tell when they are in pain, and it also means that their pain can be more easily overlooked, says Carlo Bellieni, a pediatric pain researcher at the University Hospital Siena in Italy. Doctors rely on a combination of clues such as crying, wiggling and facial grimacing to guess whether a baby is hurting. But these clues can mislead. “Similar behaviors occur when infants are not in pain, for example if they are hungry or want a cuddle,” says study coauthor Rebeccah Slater of the University of Oxford. By relying on brain activity, the new method promises to be a more objective measurement. Slater and colleagues measured brain activity in 18 newborns between 2 and 5 days old. Electroencephalography (EEG) recordings from electrodes on the scalp picked up collective nerve cell activity as babies received a heel lance to draw blood or a low-intensity bop on the foot, a touch that’s a bit like being gently poked with a blunt pencil. One electrode in particular, called the Cz electrode and perched on the top of the head, detected a telltale neural spike between 400 and 700 milliseconds after the painful event. This brain response wasn’t observed when these same babies received a sham heel lance or an innocuous touch on the heel. |© Society for Science & the Public 2000 - 2017

Keyword: Pain & Touch; Development of the Brain
Link ID: 23566 - Posted: 05.04.2017

Amber Dance Biologist Leo Smith held an unusual job while an undergraduate student in San Diego. Twice a year, he tagged along on a chartered boat with elderly passengers. The group needed him to identify two particular species of rockfish, the chilipepper rockfish and the California shortspine thornyhead. Once he’d found the red-orange creatures, the passengers would stab themselves in the arms with the fishes’ spines. Doing so, the seniors believed, would relieve their aching arthritic joints. Smith, now at the University of Kansas in Lawrence, didn’t think much of the practice at the time, but now he wonders if those passengers were on to something. Though there’s no evidence that anything in rockfish venom can alleviate pain — most fish stings are, in fact, quite painful themselves — some scientists suspect fish venom is worth a look. Studying the way venom molecules from diverse fishes inflict pain might help researchers understand how nerve cells sense pain and lead to novel ways to dull the sensation. Smith is one of a handful of scientists who are studying fish venoms, and there’s plenty to investigate. An estimated 7 to 9 percent of fishes, close to 3,000 species, are venomous, Smith’s work suggests. Venomous fishes are found in freshwater and saltwater, including some stingrays, catfishes and stonefishes. Some, such as certain fang blennies, are favorites in home aquariums. Yet stinging fishes haven’t gotten the same attention from scientists as snakes and other venomous creatures. |© Society for Science & the Public 2000 - 2017

Keyword: Pain & Touch; Neurotoxins
Link ID: 23515 - Posted: 04.20.2017

Laurel Hamers Earth’s magnetic field helps eels go with the flow. The Gulf Stream fast-tracks young European eels from their birthplace in the Sargasso Sea to the European rivers where they grow up. Eels can sense changes in Earth’s magnetic field to find those highways in a featureless expanse of ocean — even if it means swimming away from their ultimate destination at first, researchers report in the April 13 Current Biology. European eels (Anguilla anguilla) mate and lay eggs in the salty waters of the Sargasso Sea, a seaweed-rich region in the North Atlantic Ocean. But the fish spend most of their adult lives living in freshwater rivers and estuaries in Europe and North Africa. Exactly how eels make their journey from seawater to freshwater has baffled scientists for more than a century, says Nathan Putman, a biologist with the National Oceanic and Atmospheric Administration in Miami. The critters are hard to track. “They’re elusive,” says study coauthor Lewis Naisbett-Jones, a biologist now at the University of North Carolina at Chapel Hill. “They migrate at night and at depth. The only reason we know they spawn in the Sargasso Sea is because that’s where the smallest larvae have been collected.” |© Society for Science & the Public 2000 - 2017.

Keyword: Animal Migration
Link ID: 23492 - Posted: 04.14.2017

By Andy Coghlan Using a virus to reprogram cells in the brain could be a radical way to treat Parkinson’s disease. People with Parkinson’s have difficulty controlling their movements due to the death of neurons that make dopamine, a brain signalling chemical. Transplants of fetal cells have shown promise for replacing these dead neurons in people with the disease, and a trial is currently under way. But the transplant tissue comes from aborted pregnancies, meaning it is in short supply, and some people may find this ethically difficult. Recipients of these cells have to take immunosuppressant drugs too. Ernest Arenas, at the Karolinska Institute in Stockholm, Sweden, and his team have found a new way to replace lost dopamine-making neurons. They injected a virus into the brains of mice whose dopamine neurons had been destroyed. This virus had been engineered to carry four genes for reprogramming astrocytes – the brain’s support cells – into dopamine neurons. Five weeks later, the team saw improvements in how the mice moved. “They walked better and their gait showed less asymmetry than controls,” says Arenas. This is the first study to show that reprogramming cells in the living brain can lead to such improvements, he says. © Copyright Reed Business Information Ltd.

Keyword: Parkinsons
Link ID: 23488 - Posted: 04.14.2017

In two studies of mice, researchers showed that a drug, engineered to combat the gene that causes spinocerebellar ataxia type 2 (SCA2), might also be used to treat amyotrophic lateral sclerosis (ALS). Both studies were published in the journal Nature with funding from National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “Our results provide hope that we may one day be able to treat these devastating disorders,” said Stefan M. Pulst, M.D., Dr. Med., University of Utah, professor and chair of neurology and a senior author of one the studies. In 1996, Dr. Pulst and other researchers discovered that mutations in the ataxin 2 gene cause spinocerebellar ataxia type 2, a fatal inherited disorder that primarily damages a part of the brain called the cerebellum, causing patients to have problems with balance, coordination, walking and eye movements. For this study his team found that they could reduce problems associated with SCA2 by injecting mouse brains with a drug programmed to silence the ataxin 2 gene. In the accompanying study, researchers showed that injections of the same type of drug into the brains of mice prevented early death and neurological problems associated with ALS, a paralyzing and often fatal disorder. “Surprisingly, the ataxin 2 gene may act as a master key to unlocking treatments for ALS and other neurological disorders,” said Aaron Gitler, Ph.D., Stanford University, associate professor and senior author of the second study. In 2010, Dr. Gitler and colleagues discovered a link between ataxin 2 mutations and ALS.

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 23486 - Posted: 04.13.2017

By Knvul Sheikh For the past five decades pharmaceutical drugs like levodopa have been the gold standard for treating Parkinson’s disease. These medications alleviate motor symptoms of the disease, but none of them can cure it. Patients with Parkinson’s continue to lose dopamine neurons critical to the motor control centers of the brain. Eventually the drugs become ineffective and patients’ tremors get worse. They experience a loss of balance and a debilitating stiffness takes over their legs. To replace the lost dopamine neurons, scientists have begun investigating stem cell therapy as a potential treatment or even a cure. But embryonic cells and adult stem cells have proved difficult to harness and transplant into the brain. Now a study from the Karolinska Institute in Stockholm shows it is possible to coax the brain’s own astrocytes—cells that typically support and nurture neurons—into producing a new generation of dopamine neurons. The reprogrammed cells display several of the properties and functions of native dopamine neurons and could alter the course of Parkinson’s, according to the researchers. “You can directly reprogram a cell that is already inside the brain and change the function in such a way that you can improve neurological symptoms,” says senior author Ernest Arenas, a professor of medical biochemistry at Karolinska. Previously, scientists had to nudge specialized cells like neurons into becoming pluripotent cells before they could develop a different kind of specialized cell, he says. It was like having to erase all the written instructions for how a cell should develop and what job it should do and then rewriting them all over again. But Arenas and his team found a way to convert the instructions into a different set of commands without erasing them. © 2017 Scientific American

Keyword: Parkinsons; Glia
Link ID: 23475 - Posted: 04.11.2017

By Paul Taylor One of the bummers of getting older, as most baby boomers can attest, is that the list of stuff you don’t do as well as you once did keeps getting longer. Bennett Beach, 67, can measure his decline with a stopwatch. Three hours, 27 minutes, 56 seconds: That’s the difference between his best time in the Boston Marathon (2:27:26) and his worst (5:55:22). On April 17, he’ll be running the famous race once again. If he completes the course in less than six hours, he will have officially finished his 50th consecutive Boston Marathon. No one has ever done that. Nor, as far as he knows, will any of his 32,000 fellow racers be coping, as he is, with the rare and debilitating neurological movement disorder known as task-specific dystonia. Whenever he strides, Beach’s left leg gets hijacked by erratic signals from his brain. His walk is nearly normal, but for the past 15 years he has been running with a severe limp. His pursuit of the milestone has been fueled in roughly equal measure by antithetical parts — an Ahab-grade obsession mixed with an older-but-wiser acceptance of his body’s limits. “If someone had told me 30 years ago I’d be struggling to finish this race in six hours, I’d have said, ‘Spare me.’ Now I’m grateful.” Beach is a marathoner by demeanor: quiet, unassuming, self-effacing, iron-willed. And by body type: 5-foot-7, 125 pounds. He played all sports as a kid, distinguishing himself at none: “I just didn’t have the size or strength.” As a senior in prep school, he happened upon a radio broadcast of the Boston Marathon. “It was 30 degrees, it was sleeting, and these guys were out there running 26 miles,” he remembers. “Just the sort of bizarre, crazy thing I was drawn to. I already knew I’d be in Boston the next year, so I decided I’d give it a shot.” © 1996-2017 The Washington Post

Keyword: Movement Disorders
Link ID: 23471 - Posted: 04.10.2017

David Cyranoski For decades, scientists have wondered how animals can navigate huge distances using the weak signals of Earth’s magnetic field. So, interest was piqued in 2015 when two teams released papers in quick succession describing the functions of a protein found in animals that seemed to sense magnetic fields. But the claims have proved controversial, and questions have been piling up. The basic science behind the discovery was reported by Xie Can, a biophysicist at Peking University in Beijing, and his colleagues. In a paper in Nature Materials1, they claimed that a protein in animal cells forms a structure that responds to magnetic fields, and so might help in navigation. In the same year, a group led by Zhang Sheng-jia, then at Tsinghua University in Beijing, had published a paper in Science Bulletin2 reporting that the same protein could offer a powerful means of controlling brain cells. An academic battle has long raged between Xie and Zhang, but mounting evidence has cast doubt on both of their discoveries. Several researchers have challenged Xie’s claims that the protein reacts to magnetic fields. And last month, Xie co-authored a paper in Frontiers in Neural Circuits3 disputing Zhang’s work on the protein’s potential to magnetically control cells. This has all given rise to serious questions about the role of the molecule at the centre of the dispute. In their 2015 paper1, Xie and his colleagues reported that a protein called IscA1 forms a complex with another protein, Cry4, that explains how organisms pick up magnetic cues. The study found that this complex incorporates iron atoms, which gives it magnetic properties, and has a rod-like shape that aligns with an applied magnetic field. © 2017 Macmillan Publishers Limited

Keyword: Animal Migration
Link ID: 23452 - Posted: 04.05.2017

By Erik Stokstad A year after a deadly and highly contagious wildlife disease surfaced in Norway, the country is taking action. Chronic wasting disease (CWD), caused by misfolded proteins called prions, has already ravaged deer and elk in North America, costing rural economies millions in lost revenue from hunting. Its presence in Norway’s reindeer and moose—the first cases in Europe—is “a very serious situation for the environment and for our culture and traditions,” says Bjørnar Ytrehus, a veterinary researcher at the Norwegian Institute for Nature Research in Trondheim. Last week, Norway’s minister of agriculture and food gave the green light for hunters to kill off the entire herd in which three infected individuals were found, about 2000 reindeer, or nearly 6% of the country’s wild population. “We have to take action now,” says Karen Johanne Baalsrud, director of plant and animal health at the Norwegian Food Safety Authority in Oslo. The deer’s habitat will be quarantined for at least 5 years to prevent reinfection. The odds of a successful eradication, experts say, will depend largely on how long CWD has been present in Norway. CWD, discovered in 1967, has been found in 24 U.S. states and two Canadian provinces, and it has been spread in part by shipments of infected animals. Many species of cervids are susceptible, including elk, moose, and several kinds of deer. Infected animals typically begin showing symptoms such as weight loss, lethargy, and drooling 2 to 3 years after infection and then die within months. In Wyoming, where CWD has been endemic for decades, up to 40% of some herds are infected, and white-tailed deer populations are declining by 10% a year. © 2017 American Association for the Advancement of Science

Keyword: Prions
Link ID: 23443 - Posted: 04.04.2017

By STEPH YIN It’s a small fish, only a couple of inches long, and its bright colors make it pop in the Pacific coral reefs it calls home. The first thing that makes this fish peculiar is the striking pair of large lower canines it sports. But when attacked by a predator, this fish, part of a group called fang blennies,does something even more strange. A predator that puts this fang blenny in its mouth would experience a “violent quivering of the head,” according to George Losey, a zoologist who observed this species up close in a series of feeding experiments in the 1970s. Then the predator would open its jaws and gills. The little blenny would swim away, unscathed. A study published on Thursday in Current Biology now lays bare the details of the fish’s unusual defense mechanism: Unlike most venomous fish, which inject toxins through their fins, fang blennies deliver venom through their bite. Furthermore, fang blenny venom does not appear to produce potent pain, at least in mice. Instead, it causes a sudden drop in blood pressure, which might temporarily stupefy predators. “This is one of the most in-depth studies of how venom functions in any particular group of fish,” said Matthew Davis, an assistant professor of biology at St. Cloud State University in Minnesota, who did not participate in the research. A CT scan of Meiacanthus grammistes, a venomous fang blenny species. Anthony Romilio The authors of the study took a multipronged approach to studying venomous fang blennies. First, they imaged the jaws of fang blennies collected from around the Pacific and Indian Oceans to confirm what scientists long suspected: Not all fang blennies have venom glands at the base of their teeth. © 2017 The New York Times Company

Keyword: Pain & Touch; Neurotoxins
Link ID: 23432 - Posted: 03.31.2017

By NICHOLAS BAKALAR Hepatitis infection may increase the risk for Parkinson’s disease, though the reasons for the link remain unknown. British investigators used records of 100,390 patients hospitalized with various forms of hepatitis or H.I.V. from 1999 to 2011. They compared Parkinson’s incidence in these patients with incidence in more than six million people admitted for medical or surgical conditions like cataracts, knee replacement or varicose veins. The study, in Neurology, found that people with hepatitis B had a 76 percent higher risk of having Parkinson’s, and people with hepatitis C a 51 percent higher risk, than the control group. Those with other forms of hepatitis or H.I.V. had no increased risk. The study was restricted to hospitalized patients, and the authors did not have detailed information about the severity and treatment of the diseases. “We can’t be sure what is underlying this association,” said the lead author, Dr. Julia Pakpoor, a researcher at the University of Oxford. “It could be the treatment for the hepatitis, or it could be that Parkinson’s and hepatitis have common risk factors we haven’t identified.” A different kind of study would be needed, she said, to determine possible mechanisms that might be involved. © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 23430 - Posted: 03.31.2017

Workplace exposure to electromagentic fields is linked to a higher risk of developing the most common form of motor neurone disease. Amyotrophic lateral sclerosis (ALS) is a disease that ravages the body’s nerve cells, leaving people unable to control their bodies. People can die as soon as two years after first experiencing symptoms. “Several previous studies have found that electrical workers are at increased risk of ALS,” says Neil Pearce, at the London School of Hygiene and Tropical Medicine. “We don’t know why the risk is higher, but the two most likely explanations involve either electrical shocks, or ongoing exposure to extremely low frequency magnetic fields.” Now an analysis of data from more than 58,000 men and 6,500 women suggests it is the latter. Roel Vermeulen, at Utrecht University in the Netherlands, and his team found that people whose jobs exposed them to high levels of very low frequency magnetic fields were twice as likely to develop ALS as people who have never had this kind of occupational exposure. Jobs with relatively highe extremely low frequency electromagnetic fields levels include electric line installers, welders, sewing-machine operators, and aircraft pilots, says Vermuelen. “These are essentially jobs where workers are placed in close proximity to appliances that use a lot of electricity.” © Copyright Reed Business Information Ltd.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 23424 - Posted: 03.30.2017

Sarah Boseley Health editor A man who was paralysed from below the neck after crashing his bike into a truck can once again drink a cup of coffee and eat mashed potato with a fork, after a world-first procedure to allow him to control his hand with the power of thought. Bill Kochevar, 53, has had electrical implants in the motor cortex of his brain and sensors inserted in his forearm, which allow the muscles of his arm and hand to be stimulated in response to signals from his brain, decoded by computer. After eight years, he is able to drink and feed himself without assistance. “I think about what I want to do and the system does it for me,” Kochevar told the Guardian. “It’s not a lot of thinking about it. When I want to do something, my brain does what it does.” The experimental technology, pioneered by the Case Western Reserve University in Cleveland, Ohio, is the first in the world to restore brain-controlled reaching and grasping in a person with complete paralysis. For now, the process is relatively slow, but the scientists behind the breakthrough say this is proof of concept and that they hope to streamline the technology until it becomes a routine treatment for people with paralysis. In the future, they say, it will also be wireless and the electrical arrays and sensors will all be implanted under the skin and invisible.

Keyword: Robotics
Link ID: 23423 - Posted: 03.29.2017