Chapter 5. The Sensorimotor System

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Carl Zimmer When you drive toward an intersection, the sight of the light turning red will (or should) make you step on the brake. This action happens thanks to a chain of events inside your head. Your eyes relay signals to the visual centers in the back of your brain. After those signals get processed, they travel along a pathway to another region, the premotor cortex, where the brain plans movements. Now, imagine that you had a device implanted in your brain that could shortcut the pathway and “inject” information straight into your premotor cortex. That may sound like an outtake from “The Matrix.” But now two neuroscientists at the University of Rochester say they have managed to introduce information directly into the premotor cortex of monkeys. The researchers published the results of the experiment on Thursday in the journal Neuron. Although the research is preliminary, carried out in just two monkeys, the researchers speculated that further research might lead to brain implants for people with strokes. “You could potentially bypass the damaged areas and deliver stimulation to the premotor cortex,” said Kevin A. Mazurek, a co-author of the study. “That could be a way to bridge parts of the brain that can no longer communicate.” In order to study the premotor cortex, Dr. Mazurek and his co-author, Dr. Marc H. Schieber, trained two rhesus monkeys to play a game. The monkeys sat in front of a panel equipped with a button, a sphere-shaped knob, a cylindrical knob, and a T-shaped handle. Each object was ringed by LED lights. If the lights around an object switched on, the monkeys had to reach out their hand to it to get a reward — in this case, a refreshing squirt of water. © 2017 The New York Times Company

Keyword: Learning & Memory; Movement Disorders
Link ID: 24408 - Posted: 12.08.2017

Aimee Cunningham To halt the misuse of opioids, it may help to slash the number of pills prescribed, a new study suggests. Five months after the implementation of new opioid prescription guidelines at a University of Michigan hospital, roughly 7,000 fewer pills went home with patients — a drop that might reduce the risk of accessible pills leading to substance abuse. But the opioid reduction didn’t leave patients who had undergone a routine surgery with more pain, the team reports online December 6 in JAMA Surgery. “The decline in opioid volume after the intervention was dramatic,” says physician Mark Bicket of Johns Hopkins University School of Medicine, who was not involved in the study. Around 50 percent of people who misuse opioids get the drugs from a friend or relative for free, while 22 percent obtain them from a doctor, according to the U.S. Department of Health and Human Services. Michael Englesbe, a surgeon at the University of Michigan in Ann Arbor, says that part of doing a better job of managing patients’ pain “will be preventing chronic opioid use after surgical care and making sure fewer pills get into the community.” Englesbe and colleagues looked at 170 people who had a minimally invasive surgery to remove their gall bladders at the University of Michigan hospital from 2015 to 2016. All had received a prescription for opioids. Of those patients, 100 completed a survey detailing how much of the prescription they took, whether they also used a common painkiller such as ibuprofen or acetaminophen, and how they rated their pain during the first week after surgery. © Society for Science & the Public 2000 - 2017.

Keyword: Drug Abuse; Pain & Touch
Link ID: 24400 - Posted: 12.07.2017

Allison Aubrey Nobody likes the feeling of being left out, and when it happens, we tend to describe these experiences with the same words we use to talk about the physical pain of, say, a toothache. "People say, 'Oh, that hurts,' " says Nathan DeWall, a professor of psychology at the University of Kentucky. DeWall and his colleagues were curious about the crossover between physical pain and emotional pain, so they began a series of experiments several years back. In one study, they found that acetaminophen (the active ingredient in Tylenol) seemed to reduce the sting of rejection that people experienced after they were excluded from a virtual ball-tossing game. The pain pills seemed to dim activity in regions of the brain involved in processing social pain, according to brain imaging. "People knew they were getting left out [of the game], it just didn't bother them as much," DeWall explains. As part of the study, participants were given either acetaminophen or a placebo for three weeks. None of the participants knew which one they were given. Each evening, participants completed a Hurt Feelings Scale, designed as a standardized measure of emotional pain. They were asked to rank themselves on statements such as: "Today, being teased hurt my feelings." It turned out that the pain medicine reduced reports of social pain. The emotional dampening documented in these experiments is not huge, but it appears significant enough to nudge people into a less-sensitive emotional state. © 2017 npr

Keyword: Pain & Touch; Emotions
Link ID: 24391 - Posted: 12.05.2017

By RONI CARYN RABIN A. Bell’s palsy is a temporary partial facial paralysis that occurs when the nerve controlling the facial muscles is inflamed. But identifying the underlying cause of the inflammation “is a question for the ages,” said Dr. Joseph Safdieh, a neurologist at Weill Cornell Medicine and a fellow of the American Academy of Neurology. The current prevailing theory is that Bell’s palsy develops after a viral infection activates the immune system, Dr. Safdieh said, adding that “once the immune system is activated, it goes and attacks a nerve.” The condition usually affects only one side of the face, causing asymmetry or drooping on one side (the reason for that is not known either). Some experts believe Bell’s palsy is related to the herpes simplex or common cold sore virus. But several large randomized controlled trials that compared treatment with antiviral agents and prednisolone, an oral steroid that suppresses the immune system, found the steroid to be most effective. The results reinforce the idea that the condition is caused by an immune system reaction rather than the virus itself, Dr. Safdieh said. The condition has also been associated with recent vaccinations and upper respiratory infections, “but many people are vaccinated and have upper respiratory infections and don’t develop Bell’s palsy,” Dr. Safdieh said. “The ultimate answer is ‘we don’t know,’ but that many things that activate the immune system can trigger it.” One specific cause that should be ruled out is Lyme disease, especially if Bell’s palsy develops in the summer or early fall or in children, in whom it is less common, Dr. Safdieh said. Treatment will differ if the patient has Lyme disease. © 2017 The New York Times Company

Keyword: Movement Disorders
Link ID: 24385 - Posted: 12.04.2017

By Lydia Denworth A macaque monkey sat in front of a computer. A yellow square—the target—appeared in the periphery on the left side of the screen. After a few seconds delay, a second target appeared on the right. The question was: Which target would the monkey look at first? So far so routine as neuroscience experiments go, but the next step was unusual. By non-invasively directing bursts of inaudible acoustic energy at a specific visual area of the brain, a team of scientists steered the animal’s responses. If they focused on the left side of the brain, the monkey looked to the right more often. If they focused on the right side, the monkey looked to the left more often. The results of the experiment, which were presented last week at the annual Society for Neuroscience meeting, marked the first time that focused ultrasound was safely and effectively used in a nonhuman primate to alter brain activity rather than destroy tissue. A second study, in sheep, had similar results. “The finding paves the way to noninvasive stimulation of specific brain regions in humans,” says Jan Kubanek, a neural engineer at Stanford University School of Medicine and lead author of the macaque study. The technology might ultimately be used to diagnose or treat neurological diseases and disorders like Parkinson’s disease, epilepsy, addiction and depression. Other scientists are optimistic. “The idea that, with a very carefully designed dose, you could actually deliver [focused ultrasound] and stimulate the brain in the place you want and modulate a circuit rather than damage it, is a really important proof of principle,” said Helen Mayberg, MD, of Emory University School of Medicine, who was not involved with the study. © 2017 Scientific American

Keyword: Parkinsons; Depression
Link ID: 24384 - Posted: 12.01.2017

A new migraine drug that can halve the length of attacks has been hailed as “the start of real change” in how the condition is treated. Erenumab, a laboratory-made antibody that blocks a neural brain pathway called CGRP, is the first drug in 20 years proven to prevent migraine attacks. Phase three trial data on nearly 1,000 patients showed that it typically cut between three and four “migraine days” per month. In half the patients treated, migraine duration was reduced at least by half. Migraines are characterised by an intense, throbbing headache, sensitivity to light and noise, nausea, vomiting, low energy, and visual disturbances. Attacks can last anything from four to 72 hours. Each year more than 8.5 million people in the UK are thought to experience migraine – more than the number affected by asthma, diabetes and epilepsy combined. The condition is linked to depression and sick days caused by migraine are estimated to cost the UK economy more than £2bn per year. The trial, called Strive, compared patients taking erenumab for six months with others given a non-active placebo dummy drug. The research revealed that by months four to six, at least a 50% reduction in mean migraine days per month was achieved for just over 43% of patients injected under the skin with 70-mg of erenumab each month, while half of patients injected with the higher dose of 140-mg had such results. However, those given a placebo also saw benefits, with 26.6% of participants in this group experiencing such a reduction. © 2017 Guardian News and Media Limited

Keyword: Pain & Touch
Link ID: 24381 - Posted: 11.30.2017

By DENISE GRADY Scientists have found prions — abnormal proteins widely believed to cause a rare, brain-destroying disease — in the skin of 23 patients who had died from it, according to a study published on Wednesday. The discovery suggests that skin samples might be used to improve detection of the disorder, Creutzfeldt-Jakob disease, which now is usually diagnosed with much more difficult procedures, like brain biopsies or autopsies. But the presence of prions in the skin also raises unsettling questions about whether medical instruments could become contaminated even during surgery that does not involve the brain and then spread the disease to other patients. The prions stick to stainless steel and are notoriously hard to destroy. Creutzfeldt-Jakob disease affects one person in a million worldwide, with about 300 cases a year in the United States, according to the National Institutes of Health. People are typically about age 60 when it starts. It is cruel and rapidly fatal: Most patients die within a year of becoming ill. They deteriorate mentally, weaken, move uncontrollably, and may become blind and unable to speak. The disease belongs to the same class of brain disorders as mad-cow disease. The findings do not mean that Creutzfeldt-Jakob disease can be transmitted by touch or casual contact, said the senior author of the study, Dr. Wen-Quan Zou, at Case Western University School of Medicine. Patients are not dangerous, he emphasized. The researchers also said that although the disease had been transmitted decades ago by corneal transplants and certain neurosurgical procedures, there was no definitive evidence that other types of surgery had ever spread it. And the levels found in skin are far lower than those in the brain. Despite the new findings, there is no reason to change the medical care given to patients with the disease or to people known to have genetic mutations that may predispose them to Creutzfeldt-Jakob or related illnesses, the researchers said. © 2017 The New York Times Company

Keyword: Prions
Link ID: 24356 - Posted: 11.24.2017

(Reuters) - Cytokinetics Inc will stop developing one of its treatments for ALS, which afflicts Stephen Hawking, after the drug failed in a late-stage trial, the company said on Tuesday, sending its shares tumbling about 35 percent. The drugmaker said two of the three doses it was testing failed to show a statistically significant difference compared to a placebo when measured by their ability to lower the lungs’ ‘slow vital capacity’, a measure of respiratory function. Amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, is a fatal neuro-degenerative condition that affects nerve cells in the brain and the spinal cord. Deaths and disability in ALS patients are strongly related to respiratory failure, according to Cytokinetics. More than 6,000 people are diagnosed with the disease in the United States every year, according to the ALS Association. ALS garnered international attention in 2014 with the “Ice Bucket Challenge”, which involved people pouring ice-cold water on themselves, posting a video on social media, and donating funds for research on the disease. After the failure of its drug tirasemtiv, Cytokinetics said it will focus on its other ALS treatment, CK-2127107, that it is developing in collaboration with Japan’s Astellas Pharma Inc. Cytokinetics’ chief executive, Robert Blum, said he believes that the limitations of tirasemtiv will be addressed in the development of CK-2127107. © 2017 Business Insider Inc.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 24345 - Posted: 11.22.2017

By NIRAJ CHOKSHI The Rev. Jesse L. Jackson, the longtime civil rights leader and former Democratic presidential candidate, said Friday he has Parkinson’s disease. In a letter posted on Twitter on Friday afternoon, Mr. Jackson, 76, shared the news and his struggle to accept it. “Recognition of the effects of this disease on me has been painful, and I have been slow to grasp the gravity of it,” he wrote. “For me, a Parkinson’s diagnosis is not a stop sign but rather a signal that I must make lifestyle changes and dedicate myself to physical therapy in hopes of slowing the disease’s progression.” Parkinson’s is a movement disorder. Its symptoms include muscle tremors and stiffness and poor balance and coordination. It typically begins after age 50 and can cause difficulty sleeping, chewing, swallowing or speaking. Mr. Jackson has been a civil rights advocate for 50 years and sought the Democratic presidential nominations in 1984 and 1988. He was also a close associate of the Rev. Dr. Martin Luther King Jr. Mr. Jackson wrote that he and his family about three years ago began to notice he was having increasing difficulty performing routine tasks and was initially reluctant to see doctors. He said he saw the diagnosis as “an opportunity” to use his platform to advocate a cure and said that he would not let it disrupt his other advocacy. “I will continue to try to instill hope in the hopeless, expand our democracy to the disenfranchised and free innocent prisoners around the world,” he wrote. © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 24338 - Posted: 11.20.2017

By Meredith Wadman When people die from overdoses of opioids, whether prescription pain medications or street drugs, it is the suppression of breathing that almost always kills them. The drugs act on neuronal receptors to dull pain, but those in the brain stem also control breathing. When activated, they can signal respiration to slow, and then stop. The results are well-known: an epidemic of deaths—about 64,000 people in the United States alone last year. Countering this lethal side effect without losing opioids' potent pain relief is a challenge that has enticed drug developers for years. Now, for the first time, the U.S. Food and Drug Administration (FDA) in Silver Spring, Maryland, is considering whether to approve an opioid that is as effective as morphine at relieving pain and poses less risk of depressing breathing. Trevena, a firm based in Chesterbrook, Pennsylvania, announced on 2 November that it has submitted oliceridine, an intravenous opioid meant for use in hospitalized patients, to FDA for marketing approval. The drug, which would be marketed under the name Olinvo, is the most advanced of what scientists predict will be a growing crop of pain-relieving "biased agonists"—so called because, in binding a key opioid receptor in the central nervous system, they nudge it into a conformation that promotes a signaling cascade that kills pain over one that suppresses breathing. And in a paper out this week in Cell, a veteran opioid researcher and her colleagues unveil new biased opioid agonists that could surpass oliceridine, though they haven't been tested in people yet. "There are many groups creating [such] biased agonists. And one of them is going to get it right," says Bryan Roth, a molecular pharmacologist at the University of North Carolina in Chapel Hill. "To have a drug you can't die of an overdose with would be a huge lifesaver for tens of thousands of people every year." © 2017 American Association for the Advancement of Science.

Keyword: Drug Abuse; Pain & Touch
Link ID: 24337 - Posted: 11.17.2017

By RONI CARYN RABIN A. Parkinsonism refers to a group of movement abnormalities — such as stiffness, slowness, shuffling of the feet and often tremor — that are classic features of Parkinson’s disease but that can also be caused by medications and other disorders with overlapping symptoms, said Dr. Michael S. Okun, a neurologist and the national medical director of the Parkinson’s Foundation. He said that he makes no assumptions about the cause of parkinsonism “until I see the patient and pinpoint the diagnosis.” Determining the cause of parkinsonism involves asking a series of questions, starting with, “Do we think this is regular Parkinson’s disease?” said Dr. Okun, who is also co-director of the Center for Movement Disorders and Neurorestoration at the University of Florida College of Medicine in Gainesville. Though a diagnosis of Parkinson’s disease strikes fear in patients, Dr. Okun said that the illness, a neurodegenerative brain disorder caused by the loss of dopamine-containing neurons and other cells, progresses slowly in many people and generally responds well to drugs that replenish dopamine in the brain. Some patients whose parkinsonism is not caused by Parkinson’s disease also respond to these drugs, but the medications are most effective for people with Parkinson’s disease, Dr. Okun said. It’s important to rule out other potential causes of parkinsonism, he said. The condition can be triggered by antipsychotic medications that affect dopamine levels in the brain, as well as by other drugs, including stimulants like amphetamines and cocaine. Discontinuing the drugs may stop the symptoms over time, though not always. Parkinsonism may also be caused by repeated injuries to the head, exposure to various toxins or brain lesions. Once doctors rule out Parkinson’s disease, they must consider several other serious neurological disorders. The three most common ones are multiple system atrophy, a degenerative disorder also referred to as Shy-Drager syndrome, which may or may not respond well to Parkinson’s medications; progressive supranuclear palsy, or PSP, which also may respond to high doses of drugs that replace dopamine in the brain; and corticobasal degeneration (CBD). Patients with a form of dementia called Lewy body dementia may also exhibit symptoms of parkinsonism, which may or may not respond to dopamine. Various other movement disorders, called ataxias or dystonias, also may display features of parkinsonism. © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 24335 - Posted: 11.17.2017

Jon Hamilton The goal is simple: a drug that can relieve chronic pain without causing addiction. But achieving that goal has proved difficult, says Edward Bilsky, a pharmacologist who serves as the provost and chief academic officer at Pacific Northwest University of Health Sciences in Yakima, Wash. "We know a lot more about pain and addiction than we used to," says Bilsky, "But it's been hard to get a practical drug." Bilsky is moderating a panel on pain, addiction and opioid abuse at the Society for Neuroscience meeting in Washington, D.C., this week. Brain scientists have become increasingly interested in pain and addiction as opioid use has increased. About 2 million people in the U.S. now abuse opioids, according to the Centers for Disease Control and Prevention. But at least 25 million people suffer from chronic pain, according to an analysis by the National Institutes of Health. That means they have experienced daily pain for more than three months. The question is how to cut opioid abuse without hurting people who live with pain. And brain scientists think they are getting closer to an answer. One approach is to find drugs that decrease pain without engaging the brain's pleasure and reward circuits the way opioids do, Bilsky says. So far, these drugs have been hampered by dangerous side effects or proved less effective than opioids at reducing pain. But substances related to snail venom look promising, Bilsky says. © 2017 npr

Keyword: Pain & Touch
Link ID: 24321 - Posted: 11.13.2017

By Roni Dengler The bills of even newly hatched ducks might be as sensitive as our hands, as touch sensors in their beaks are as abundant as those in our fingertips and palms. That’s the take-away of new research published today in the Proceedings of the National Academy of Sciences that describes the origins of touchiness in the common duck’s quacker. Researchers knew that duck bills can sense light touch but have muted responsiveness to temperature. This comes in handy (or bill-y) since the birds forage for food in cold, murky bottom waters. Now, researchers find the sensors duck bills use to perceive touch work even before hatching. That likely helps young ducklings scavenge for food alongside adults soon after birth. In keeping with the need to feel for food, the ducks have more nerve cells to relay touch signals than chickens, which rely on eyesight to find sustenance, they report. That means different developmental programs are at work in ducks and chickens, which could help scientists uncover how touch evolved. Because the duck’s touch sensors are similar to mammals’ and their bills aren’t covered in fur, the authors suggest embryonic duck bills might be a better model than standard laboratory rodents to study touch sensation as it applies to us relatively hairless humans. © 2017 American Association for the Advancement of Science

Keyword: Pain & Touch; Development of the Brain
Link ID: 24298 - Posted: 11.07.2017

By Jocelyn Kaiser CENTREVILLE, VIRGINIA—Nothing unusual jumps out upon meeting Evelyn, a bubbly almost-3-year-old with red curls—except that she should not be here, chatting with a visitor in her family’s living room, twirling in her tights to the Pharrell Williams song “Happy.” Evelyn’s older sister Josephine had spinal muscular atrophy type 1 (SMA1), a genetic disease that gradually paralyzes babies. She died at 15 months. Evelyn was an unexpected pregnancy, but her parents decided to have the baby despite one-in-four odds of a second tragedy. Soon after Evelyn was born in December 2014, they were devastated to learn from genetic testing that she, too, had SMA1. “We knew what we were dealing with: We’ll love her for as long as we can,” says her father, Milan Villarreal. But that same night, frantically searching the internet, they learned about a clinical trial in Ohio and sent an email. At 8 weeks old, Evelyn received a gene therapy treatment that gave her body a crucial missing protein. And now here she is, not so different from any healthy toddler. Although she has weak thighs and can’t run normally or jump, she can walk quickly, dance, trace letters, toss foam blocks, carry a small chair, and climb onto her mother Elena’s lap. After the heartbreak of losing their first baby, the Villarreals have watched in amazement as Evelyn has crawled, walked, and talked. “It was just a miracle. Every milestone was like a celebration. We opened a bottle of wine for every little thing she did,” Milan says. © 2017 American Association for the Advancement of Science.

Keyword: Movement Disorders; Genes & Behavior
Link ID: 24280 - Posted: 11.02.2017

By Jessica Hamzelou Can you catch Alzheimer’s disease? Fear has been growing that the illness might be capable of spreading via blood transfusions and surgical equipment, but it has been hard to find any evidence of this happening. Now a study has found that an Alzheimer’s protein can spread between mice that share a blood supply, causing brain degeneration, and suggesting that the disease may transmissible in a similar way to Creutzfeldt-Jacob Disease (CJD). We already know from CJD that misfolded proteins can spread brain diseases. Variant CJD can spread through meat products or blood transfusions infected with so-called prion proteins, for example. Like CJD, Alzheimer’s also involves a misfolded protein called beta-amyloid. Plaques of this protein accumulate in the brains of people with the illness, although we still don’t know if the plaques cause the condition, or are merely a symptom. There has been evidence that beta-amyloid may spread like prions. Around 50 years ago, many people with a growth disorder were treated with growth hormone taken from cadavers. Many of the recipients went on to develop CJD, as these cadavers turned out to be carrying prions. But decades later, it emerged in postmortems that some of these people had also developed Alzheimer’s plaques, despite being 51 or younger at the time. The team behind this work suggested investigating whether beta-amyloid was spreading via blood products or surgical instruments, just as they can spread prions. © Copyright New Scientist Ltd

Keyword: Alzheimers; Prions
Link ID: 24266 - Posted: 10.31.2017

By JANE E. BRODY After two hourlong sessions focused first on body awareness and then on movement retraining at the Feldenkrais Institute of New York, I understood what it meant to experience an incredible lightness of being. Having, temporarily at least, released the muscle tension that aggravates my back and hip pain, I felt like I was walking on air. I had long refrained from writing about this method of countering pain because I thought it was some sort of New Age gobbledygook with no scientific basis. Boy, was I wrong! The Feldenkrais method is one of several increasingly popular movement techniques, similar to the Alexander technique, that attempt to better integrate the connections between mind and body. By becoming aware of how one’s body interacts with its surroundings and learning how to behave in less stressful ways, it becomes possible to relinquish habitual movement patterns that cause or contribute to chronic pain. The method was developed by Moshe Feldenkrais, an Israeli physicist, mechanical engineer and expert in martial arts, after a knee injury threatened to leave him unable to walk. Relying on his expert knowledge of gravity and the mechanics of motion, he developed exercises to help teach the body easier, more efficient ways to move. I went to the institute at the urging of Cathryn Jakobson Ramin, author of the recently published book “Crooked” that details the nature and results of virtually every current approach to treating back pain, a problem that has plagued me on and off (now mostly on) for decades. Having benefited from Feldenkrais lessons herself, Ms. Ramin had good reason to believe they would help me.

Keyword: Pain & Touch; Attention
Link ID: 24259 - Posted: 10.30.2017

A new study published in the journal Neuron sheds light on the normal function of LRRK2, the most common genetic cause for late-onset Parkinson’s disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For more than 10 years, scientists have known that mutations in the LRRK2 gene can lead to Parkinson’s disease, yet both its role in the disease and its normal function in the brain remain unclear. In a study in mice, researchers have now found that LRRK is necessary for the survival of dopamine-containing neurons in the brain, the cells most affected by Parkinson’s. Importantly, this finding could alter the design of treatments against the disease. “Since its discovery, researchers have been trying to define LRRK2 function and how mutations may lead to Parkinson’s disease,” said Beth-Anne Sieber, Ph.D., program director at NINDS. “The findings in this paper emphasize the importance of understanding the normal role for genes associated with neurodegenerative disorders.” LRRK2 is found along with a closely related protein, LRRK1, in the brain. A mutation in LRRK2 alone can eventually produce Parkinson’s disease symptoms and brain pathology in humans as they age. In mice, however, LRRK2 loss or mutation does not lead to the death of dopamine-producing neurons, possibly because LRRK1 plays a complementary or compensatory role during the relatively short, two-year mouse lifespan.

Keyword: Parkinsons
Link ID: 24254 - Posted: 10.28.2017

Bill Chappell It has the power to save lives by targeting opioid overdoses — something that kills more than 140 Americans every day. And now Narcan, the nasal spray that can pull a drug user back from an overdose, is being carried by all of Walgreens' more than 8,000 pharmacies. "By stocking Narcan in all our pharmacies, we are making it easier for families and caregivers to help their loved ones by having it on hand in case it is needed," said Walgreens vice president Rick Gates. The pharmacy chain is making the move as America struggles to respond to an opioid epidemic that President Trump is declaring a national emergency on Thursday, hoping to fight the opioid crisis that has struck families and communities from rural areas to cities. Calling the Walgreens move "an important milestone," Seamus Mulligan, CEO of Narcan maker Adapt Pharma, said that letting people get the medicine "without an individual prescription in 45 states is critical in combating this crisis." In recent years, both Walgreens, the nation's No. 2 pharmacy chain, and CVS, the No. 1 chain, have moved to widen access to Narcan and other products that contain naloxone, a fast-acting overdose antidote. As of last month, CVS reportedly offered prescription-free naloxone in 43 states. The chain has said that its pharmacies "in most communities have naloxone on hand and can dispense it the same day or ordered for the next business day." © 2017 npr

Keyword: Drug Abuse
Link ID: 24249 - Posted: 10.27.2017

As a ballet dancer in a former life, countless rehearsal hours in pointe shoes once landed me in a podiatrist’s office with a particularly inflamed ingrown toenail. To my surprise – and the doctor’s – a typical injection of local anesthesia did nothing to numb the searing pain as his knife dug into my big toe. It was not until a second full injection made my toe the size of a golf ball that I became blissfully unaware of the pain. Was my hair color to blame? It is, after all, a rumor every redhead has heard: we feel more pain and need more painkillers. A look at the published research suggests that the genes that determine my hair color may play a role, but the science itself is murky. What makes a redhead? Our luster-filled locks derive from a pair of mutated genes. For most people, hair color is determined by the melanocortin-1 receptor, or MC1R gene that leads to the production of a brown-black melanin pigment called eumelanin. The more eumelanin created by this gene, the darker and blacker the hair. Most redheads have a recessive version of the MC1R gene caused by the pairing of three possible mutant alleles. The resulting gene expression shuts off eumelanin production, shifting the dominant pigment to the reddish-toned pheomelanin. McGill University behavioral neuroscientist Jeffrey Mogil examined the gene as part of his research on the perception and inhibition of pain. “The purpose of this MC1R gene is to produce dark pigments. If it works, it does, and if it doesn’t, it produces pigment that isn’t dark like it’s supposed to be. So, it really is a dysfunction,” he said.

Keyword: Pain & Touch; Genes & Behavior
Link ID: 24248 - Posted: 10.27.2017

By GRETCHEN REYNOLDS Do brains trump brawn? A remarkable new study of how the human body prioritizes its inner workings found that if you intensely think at the same time as you intensely exercise, your performance in both thinking and moving can worsen. But your muscles’ performance will decline much more than your brain’s will, the study found. The results raise interesting questions about the roles that our body’s wide-ranging abilities may have played in the evolution of humans and also whether a hard workout is the ideal time to be cogitating. Compared to almost all other animals, we humans have disproportionately large brains for our size. Our supersized cranial contents probably provided an advantage during our evolution as a species. Smart creatures presumably could have outwitted predators and outmaneuvered prey, keeping themselves fed, uneaten and winners in the biological sweepstakes to pass on their genes. But most other species eschewed developing similarly outsized brains during evolution, because large brains carry a hefty metabolic cost. Brains are extraordinarily hungry organs, requiring, ounce for ounce, more calories to sustain their operations than almost any other tissue, and these caloric demands rise when the brain is hard at work. Thinking demands considerable bodily fuel. In order to feed and maintain these large brains, early humans’ bodies had to make certain trade-offs, most evolutionary biologists agree. Our digestive systems shrank during evolution, for one thing, since food processing is also metabolically ravenous. But whether a similar trade-off occurred with our muscles has remained in doubt. Muscles potentially provided another route to survival during our species’ early days. With sufficient brawn, animals, including people, could physically overpower prey and sprint from danger. © 2017 The New York Times Company

Keyword: Attention
Link ID: 24243 - Posted: 10.26.2017