Chapter 5. The Sensorimotor System
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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
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.
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.
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
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
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
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
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.
Link ID: 23423 - Posted: 03.29.2017
By Anil Ananthaswamy People who have chronic pain are more likely to experience mood disorders, but it’s not clear how this happens. Now a study in mice has found that chronic pain can induce genetic changes in brain regions that are linked to depression and anxiety, a finding that may lead to new treatments for pain. “At least 40 per cent of patients who suffer from severe forms of chronic pain also develop depression at some point, along with other cognitive problems,” says Venetia Zachariou of the Icahn School of Medicine at Mount Sinai in New York. To see if there might be a genetic link between these conditions, Zachariou and her team studied mice with damage to their peripheral nervous system. These mice show symptoms similar to chronic pain in people – they become hypersensitive to harmless touch, and avoid other situations that might also cause them pain. Until now, pain behaviour in mice had only been studied for at most a week at a time, says Zachariou, whose team monitored their mice for 10 weeks. “At the beginning, we saw only sensory deficits and pain-like symptoms. But several weeks later, the animals developed anxiety and depression-like behaviours.” The team then examined gene activity in three regions in the mouse brains we know are associated with depression and anxiety. Analysing the nucleus accumbens, medial prefrontal cortex, and periaqueductal gray, they found nearly 40 genes where activity was significantly higher or lower than in mice without the nervous system damage. © Copyright Reed Business Information Ltd.
By DENISE GRADY Dr. Lewis P. Rowland, a neurologist who made fundamental discoveries in nerve and muscle diseases and clashed with government investigators during the McCarthy era, died on March 16 in Manhattan. He was 91. The cause was a stroke, his son Steven said. Dr. Rowland, the chairman of Columbia University’s neurology department for 25 years, died at NewYork-Presbyterian/Columbia University Medical Center. Dr. Rowland was a prolific researcher and writer, with nearly 500 published scientific articles that focused on devastating neuromuscular diseases, including muscular dystrophy, myasthenia gravis and many rare syndromes. He took a special interest in amyotrophic lateral sclerosis, or A.L.S., also called Lou Gehrig’s disease, which causes degeneration of nerves in the brain and spinal cord, leading to weakness, paralysis and death. Dr. Rowland led research teams that delineated a number of uncommon diseases that had been poorly understood. They also found that in a subgroup of A.L.S. patients, the disease was linked to lymphoma, a cancer of the immune system. Other studies led to the discovery that a gene defect causes an unusual form of dementia in some patients with A.L.S. In myasthenia gravis, Dr. Rowland and his colleagues documented its high death rate and helped identify treatments that prolonged survival. In the 1970s, long before the tools existed to study DNA’s role in neurological diseases like A.L.S., Alzheimer’s and Parkinson’s, Dr. Rowland predicted correctly that genetics would be the key to understanding them. One of his accomplishments at Columbia was the expansion in 1982 of an intensive care unit that added beds for patients who were severely ill with neurological disorders. Before then, it was often difficult to find I.C.U. space for them. © 2017 The New York Times Company
by Laura Sanders Many babies born early spend extra time in the hospital, receiving the care of dedicated teams of doctors and nurses. For these babies, the hospital is their first home. And early experiences there, from lights to sounds to touches, may influence how babies develop. Touches early in life in the NICU, both pleasant and not, may shape how a baby’s brain responds to gentle touches later, a new study suggests. The results, published online March 16 in Current Biology, draw attention to the importance of touch, both in type and number. Young babies can’t see that well. But the sense of touch develops early, making it a prime way to get messages to fuzzy-eyed, pre-verbal babies. “We focused on touch because it really is some of the basis for communication between parents and child,” says study coauthor Nathalie Maitre, a neonatologist and neuroscientist at Nationwide Children’s Hospital in Columbus, Ohio. Maitre and her colleagues studied how babies’ brains responded to a light puff of air on the palms of their hands — a “very gentle and very weak touch,” she says. They measured these responses by putting adorable, tiny electroencephalogram, or EEG, caps on the babies. The researchers puffed babies’ hands shortly before they were sent home. Sixty-one of the babies were born early, from 24 to 36 weeks gestation. At the time of the puff experiment, they had already spent a median of 28 days in the hospital. Another group of 55 babies, born full-term, was tested in the three days after birth. |© Society for Science & the Public 2000 - 2017
A study in Neurology suggests that analyzing levels of the protein p75ECD in urine samples from people with amyotrophic lateral sclerosis (ALS) may help monitor disease progression as well as determine the effectiveness of therapies. The study was supported by National Institute of Neurological Disorders and Stroke (NINDS) and National Center for Advancing Translational Sciences (NCATS), both part of the National Institutes of Health. Mary-Louise Rogers, Ph.D., senior research fellow at Flinders University in Adelaide, Australia, and Michael Benatar, M.D., Ph.D, professor of neurology at the University of Miami, and their teams, discovered that levels of urinary p75 ECD increased gradually in patients with ALS as their disease progressed over a 2-year study period. “It was encouraging to see changes in p75ECD over the course of the study, because it suggests an objective new method for tracking the progression of this aggressive disease,” said Amelie Gubitz, Ph.D., program director at NINDS. “In addition, it indicates the possibility of assessing whether levels of that protein decrease while patients try future treatments, to tell us whether the therapies are having any beneficial effects.” Further analysis of the samples from 54 patients revealed that those who began the study with lower levels of urinary p75ECD survived longer than did patients who had higher levels of the protein initially, suggesting that it could be a prognostic marker of the disease and may inform patients about their illness. Dr. Benatar and his team noted that this may be useful in selecting participants for clinical trials and in improving study design.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 23396 - Posted: 03.23.2017
By Jia Naqvi A drug frequently prescribed for pain is no more effective than a placebo at controlling sciatica, a common source of pain in the lower back and leg, according to a study published Wednesday in the New England Journal of Medicine. The researchers at the George Institute for Global Health in Australia followed 209 sciatica patients in Sydney who were randomly assigned to receive either the drug pregabalin, more commonly known as Lyrica, or a placebo. The results showed no significant differences in leg pain intensity between the group on the placebo and that on Lyrica after eight weeks taking the drug or during the rest of the year on follow-up exams. Similarly, there were no differences for other outcomes such as back pain, quality of life and degree of disability. After Lyrica was approved in 2004, it has become the most commonly prescribed medicine for neuropathic pain, which is caused by damage to the nervous system. The drug was ranked as the 19th-highest-earning pharmaceutical in 2015, with worldwide sales rising annually at a rate of 9 percent and sale revenue of more than $3 billion in 2015 in the United States. “We have seen a huge rise in the amount of prescriptions being written each year for patients suffering from sciatica. It’s an incredibly painful and disabling condition, so it’s no wonder people are desperate for relief and medicines such as pregabalin have been widely prescribed,” Christine Lin, one of the authors of the study and an associate professor at the George Institute for Global Health, said in a news release. © 1996-2017 The Washington Post
Keyword: Pain & Touch
Link ID: 23395 - Posted: 03.23.2017
By THOMAS FULLER SANTA ROSA, Calif. — In the heart of Northern California’s wine country, a civil engineer turned marijuana entrepreneur is adding a new dimension to the art of matching fine wines with gourmet food: cannabis and wine pairing dinners. Sam Edwards, co-founder of the Sonoma Cannabis Company, charges diners $100 to $150 for a meal that experiments with everything from marijuana-leaf pesto sauce to sniffs of cannabis flowers paired with sips of a crisp Russian River chardonnay. “It accentuates the intensity of your palate,” Mr. Edwards, 30, said of the dinners, one of which was held recently at a winery with sweeping views of the Sonoma vineyards. “We are seeing what works and what flavors are coming out.” Sonoma County, known to the world for its wines, is these days a seedbed of cannabis experimentation. The approval of recreational cannabis use by California voters in November has spurred local officials here to embrace the pot industry and the tax income it may bring. “We’re making this happen,” said Julie Combs, a member of the Santa Rosa City Council, who is helping lead an effort to issue permits to cannabis companies. “This is an industry that can really help our region.” Of the many ways in which California is on a collision course with the Trump administration, from immigration to the environment, the state’s enthusiastic embrace of legalized and regulated marijuana may be one of the biggest tests of the federal government’s power. Attorney General Jeff Sessions has equated marijuana with heroin and, on Wednesday, mentioned cannabis in the context of the “scourge of drug abuse.” © 2017 The New York Times Compan
By Daniel Barron It was 4 P.M., and Andrew* had just bought 10 bags of heroin. In his kitchen, he tugged one credit-card-sized bag from the rubber-banded bundle and laid it on the counter with sacramental reverence. Pain shot through his body as he pulled a cutting board from the cabinet. Slowly, deliberately, he tapped the bag's white contents onto the board and crushed it with the flat edge of a butter knife, forming a line of fine white powder. He snorted it in one pass and shuffled back to his armchair. It was bitter, but snorting heroin was safer than injecting, and he was desperate: his prescription pain medication was gone. I met Andrew the next day in the emergency room, where he told me about the previous day's act of desperation. I admitted him to control his swelling legs and joint pain. He was also detoxing from opioids. Andrew looked older than his 69 years. His face was wrinkled with exhaustion. A frayed, tangled mop of grizzled hair fell to his shoulders. Andrew had been a satellite network engineer, first for the military, more recently for a major telecommunications company. An articulate, soft-spoken fellow, he summed up his (rather impressive) career modestly: “Well, I'd just find where a problem was and then find a way to fix it.” Yet there was one problem he couldn't fix. “Doctor, I'm always in the most terrible pain,” he said, with closed eyes. “I had no other options. I started using heroin, bought it from my neighbor to help with the pain. I'm scared stiff.” © 2017 Scientific American
By Jia Naqvi Sixty percent of the calls to poison control centers for help with prescription opioid exposure involved children younger than 5. (Rich Pedroncelli/Associated Press) The phone rings once approximately every 45 minutes — that is how often poison control centers in the United States receive calls about children being exposed to prescription opioids, according to a study published Monday. Over a span of 16 years, from January 2000 until December 2015, about 188,000 calls were placed to poison control centers regarding pediatric and teenage exposure to opioids, the study published in the journal Pediatrics found. Sixty percent of the children exposed to opioids were younger than 5, while teenagers accounted for 30 percent. Pediatric exposure to opioids increased by 86 percent from 2000 to 2009 but decreased overall for all ages under 20 from 2009 until 2015, the study found. Increasing awareness among people with prescription drugs, physicians putting more thought into prescribing opioids, and prescription drug monitoring programs implemented by many states and efforts by different organizations could have contributed to the decrease in exposure, said Marcel Casavant, study author, medical director of the Central Ohio Poison Center and chief toxicologist at Nationwide Children’s Hospital in Columbus. “We are not quite sure, and so it would be good to try to sort out of all the things that we are trying, which ones are the most effective and how can we spend more time doing that,” Casavant said. © 1996-2017 The Washington Post