By NICHOLAS BAKALAR Having migraine headaches increases the risk for cardiovascular diseases, a new study has found. Using the Danish National Patient Registry, researchers matched 51,032 people with migraines, 71 percent of them women, with 510,320 people in the general population without migraines. The subjects were, on average, age 35 at the start of the study, and researchers followed them for 19 years. The absolute risk for cardiovascular disease was small, unsurprising in a group this young. Nevertheless, after adjustment for other variables, over the course of the study people with migraines had a 49 percent increased chance of heart attack, and roughly double the risk of stroke. They also had a 59 percent increased risk of a blood clot in their veins. These risks were even higher in the first year after a migraine diagnosis. The observational study, in BMJ, found no association of migraine with peripheral artery disease or heart failure. “We now have accumulating evidence that migraine is a risk factor for cardiovascular disease. It’s important to take it into consideration,” said the lead author, Dr. Kasper Adelborg, a postdoctoral researcher at Aarhus University. “And it’s important to find out if the agents that prevent migraine could also reduce the burden of cardiovascular disease.” © 2018 The New York Times Company

Keyword: Stroke; Pain & Touch
Link ID: 24597 - Posted: 02.01.2018

By Shawna Williams When the late organic chemist John Daly was on the hunt for poisonous frogs, he employed an unadvisable method: “It involved touching the frog, then sampling it on the tongue. If you got a burning sensation, then you knew this was a frog you ought to collect,” he once told a National Institutes of Health (NIH) newsletter writer. Daly survived to gather frogs from South America, Madagascar, Australia, and Thailand, and he extracted more than 500 compounds from their skin (many of which the frogs in turn had harvested from their insect diets). One of these compounds, the toxin epibatidine, turned out to have an analgesic effect 200 times more potent than morphine in rodents, Daly and his colleagues reported in 1992 (J Am Chem Soc, 114:3475-78, 1992); and rather than working through opioid receptors, epibatidine bound to nicotinic receptors. “To have a drug that works as well [as opioids] but is actually targeting a completely independent receptor system is really one of those holy grails of the drug industry,” says Daniel McGehee, who studies nicotinic receptors at the University of Chicago. But an epibatidine-related compound tested by Abbott Labs as an analgesic in the late 2000s caused uncontrollable vomiting, McGehee says. Although research on nicotinic receptors continues, he’s not aware of any epibatidine analogs currently in the drug development pipeline. But frogs may yet hold clues to killing pain. At least one frog does deploy an opioid: the waxy monkey tree frog (Phyllomedusa sauvagii), whose skin is laced with the peptide dermorphin. Although the compound does not appear to be a toxin that wards off predators, dermorphin has about 40 times the potency of morphine in a guinea-pig ileum assay, but it doesn’t effectively cross the blood-brain barrier, says pharmacologist Tony Yaksh of the University of California, San Diego. Dermorphin also boasts an unusual chemical property: the inclusion of a D-amino acid in its sequence. Almost all amino acids found in natural compounds are L-isomers, and dermorphin’s stereochemistry makes it resistant to metabolism and “certainly renders it more potent,” Yaksh writes in an email to The Scientist. © 1986-2018 The Scientist

Keyword: Pain & Touch; Drug Abuse
Link ID: 24577 - Posted: 01.27.2018

By Katarina Zimmer | Cellular senescence, the process by which cells cease to divide in response to stress, may be a double-edged sword. In addition to being an important anti-cancer mechanism, recent studies show it may also contribute to age-related tissue damage and inflammation. A study published in Cell Reports yesterday (January 23) suggests that cellular senescence could be a factor underlying neurodegeneration in sporadic forms of Parkinson’s disease. “I think the proposition that cellular senescence drives neurodegeneration in Parkinson’s disease and other ageing-related neurodegenerative diseases . . . has a great deal of merit,” writes D James Surmeier, a physiologist at Northwestern University, to The Scientist in an email. “To my knowledge, [this study] is the first strong piece of evidence for this model.” Cellular senescence may be the basis by which the herbicide and neurotoxin paraquat, which has been previously linked to Parkinson’s disease, can contribute to the disease, the researchers propose. The vast majority of Parkinson’s disease cases are sporadic, rather than inherited, and caused by a combination of environmental and genetic factors. Julie Andersen, a neuroscientist at the Buck Institute for Research on Aging, says her laboratory decided to focus on paraquat based on epidemiological evidence linking it to the condition in humans and on lab work showing that mice treated with the chemical suffer a loss of dopaminergic neurons in the same region that is affected in humans. It is an acutely toxic chemical—capable of causing death—and was banned in the E.U. in 2007 over safety concerns, but is still used extensively by American farmworkers. © 1986-2018 The Scientist

Keyword: Parkinsons; Glia
Link ID: 24574 - Posted: 01.26.2018

Ian Sample Science editor In work that could open a new front in the war on Parkinson’s disease, and even ageing itself, scientists have shown that they can stave off some of the effects of the neurodegenerative disease by flushing “zombie cells” from the brain. The research in mice raises hopes for a fresh approach to treating the most common forms of Parkinson’s disease, which typically arise through a complex interplay of genetics, lifestyle and potentially toxic substances in the environment. But the approach may have benefits far beyond Parkinson’s, with other neurodegenerative diseases – and the ageing process more broadly – all being linked to the ill effects of these “senescent” cells, which linger in tissues after entering a state of suspended animation in the body. “It’s a completely new way of looking at neurodegenerative disease and finding potential drugs,” said Marco Demaria, a molecular biologist on the team at the University of Groningen in the Netherlands. “For most of these conditions, we don’t have any way to counteract them.” Parkinson’s disease affects about 10 million people worldwide, and usually takes hold when certain types of neurons in the brain become impaired or die off completely. The neurons in question produce a substance called dopamine, which is crucial for enabling the brain to produce smooth and coordinated physical movements. © 2018 Guardian News and Media Limited

Keyword: Parkinsons
Link ID: 24562 - Posted: 01.24.2018

By Abby Olena Studying scorpions comes with its share of danger, as biologist Bryan Fry of the University of Queensland knows all too well. On a 2009 trip to the Brazilian Amazon, Fry was stung while trying to collect the lethal Brazilian yellow scorpion (Tityus serrulatus), and for eight hours he says it felt as though his finger was in a candle flame. Meanwhile, his heart flipped between racing and stopping for up to five seconds at a time. “At least the insane levels of pain helped keep my mind off my failing heart,” Fry writes in an email to The Scientist. His symptoms were caused by an arsenal of toxins in the animal’s sting, which contribute to one of the most painful attacks in the animal kingdom. But at least one mammal—the southern grasshopper mouse (Onychomys torridus)—regularly chows down on Arizona bark scorpions (Centruroides sculpturatus) and doesn’t seem to experience pain, despite receiving plenty of stings. In 2013, Ashlee Rowe, now of Michigan State University, and colleagues showed that bark scorpion venom interacts with the NaV1.8 voltage-gated sodium channel in grasshopper mice, in addition to activating the NaV1.7 channel as it does in other mammals (Science, 342:441-46). Rowe’s team showed that grasshopper mice have evolved amino acid changes in NaV1.8 that allow it to bind scorpion venom components, and in turn prevent the channel’s activation. Because NaV1.8 is responsible for transmitting pain signals to the central nervous system following NaV1.7 binding, blocking its activation prevents the sensation of pain. In other mammals, scorpion venom has no effect on NaV1.8. © 1986-2018 The Scientist

Keyword: Pain & Touch; Neurotoxins
Link ID: 24557 - Posted: 01.24.2018

By Jenny Rood Opioid drugs are well-established double-edged swords. Extremely effective at analgesia, they cause an array of harmful side effects throughout the body, including itching, constipation, and respiratory depression—the slowed breathing that ultimately causes death in overdose cases. What’s more, the body’s interaction with opioids is dynamic: our receptors for these compounds become desensitized to the drugs’ activity over time, requiring ever larger doses to suppress pain and eventually provoking severe dependence and protracted withdrawal. In the past few years, these side effects have plagued growing numbers of US citizens, plunging the country into the throes of a devastating opioid crisis in which nearly 100 people die from overdoses every day. Even so, opioids are still among the most effective pain-relief options available. “Over hundreds of years, [opioid receptors] have remained a target,” says Laura Bohn, a biochemist at the Scripps Research Institute in Jupiter, Florida. “Therapeutically, it works.” Since the early 2000s, intriguing evidence has emerged suggesting that opioids’ useful properties could be separated from their harmful attributes. (See “Pain and Progress,” The Scientist, February 2014.) In 2005, Bohn, then at the Ohio State University College of Medicine, and colleagues showed that shutting down one of the signaling pathways downstream of the opioid receptor targeted by morphine not only amped up the drug’s painkilling effects in mice, but also reduced constipation and respiratory depression (J Pharmacol Exp Ther, 314:1195-201). © 1986-2018 The Scientist

Keyword: Pain & Touch; Drug Abuse
Link ID: 24550 - Posted: 01.22.2018

By Kate Baggaley The pain came without warning. It was February of last year, and the man was eating dinner. He’d just reached for a glass of wine. “It really burned my mouth when I started to drink,” says Greg (the healthcare worker in Toronto asked for his name to be changed). The odd and disquieting sensation had no apparent cause—no burns or cuts or other injuries. Yet the burning and tingling Greg felt on his tongue and the roof of his mouth persisted. “It was very intense during the middle of the day and then subsided at nighttime,” he says. Perhaps, he was told when finally visiting the family doctor months later, the pain was related to a yeast infection on the tongue. But the prescribed anti-fungal medication made no difference. Next Greg saw a dentist, who found no abnormalities in his mouth and recommended he get a blood test to rule out an autoimmune disorder. Eventually, though, one of Greg’s doctors referred him to Miriam Grushka, an oral medicine specialist in Toronto. Grushka has spent decades studying and treating Greg's condition, which is called burning mouth syndrome. “People say they feel like they burnt their tongue on a cup of coffee, but the burning never went away,” says Grushka. “In the vast majority of cases it’s benign, but it’s very uncomfortable.” Each week, she sees around 15 patients who have burning mouth syndrome or similar conditions. These hallucinations, or phantoms, are characterized by a taste or feeling in the mouth that will not go away. Oral phantoms are often treatable, and are rooted not in the mouth but the brain. But much else about these phantom feelings is still a mystery. Grushka and other researchers are still unraveling why they happen and how to banish them. © 2018 Popular Science.

Keyword: Pain & Touch; Chemical Senses (Smell & Taste)
Link ID: 24548 - Posted: 01.22.2018

By Anna Azvolinsky David Julius entered the biochemistry graduate program at the University of California, Berkeley, in 1977. “It was all one foot in front of the other. I wasn’t trying to figure out what I would be doing in 10 years,” says the University of California, San Francisco (UCSF) professor of physiology. “When I arrived, I thought, ‘Classes are pretty much over. This is like a real job, and I can just go in the lab and do my thing.’” Julius joined the UC Berkeley lab of Jeremy Thorner, who was studying hormonal signaling and trying to understand how budding yeast cells switch mating type. Randy Schekman, a Berkeley researcher who worked on protein secretion and vesicular transport, served as Julius’s coadvisor. “What was great about Jeremy and Randy was that they were both trained as biochemists and then had decided to take advantage of the yeast genetic system to understand the biochemistry of cellular signaling.” Haploid yeast cells can be either “type a” or “type α,” and mate with cells of the opposite type. Julius worked on the synthesis of alpha factor, one of two mating hormones produced and secreted by yeast. His graduate studies produced three Cell papers. The first, published in 1983, reported that a class of enzymes, the dipeptidyl aminopeptidases, is necessary to cleave a longer precursor of alpha factor into the final 13-amino-acid peptide. To identify the specific dipeptidyl aminopeptidase and elucidate its role, Julius took advantage of yeast mutants, including one called ste13 (for sterile 13), which cannot produce normal alpha factor. It was the first time anyone had characterized the biochemical functioning of one of the yeast sterile mutants. © 1986-2018 The Scientist

Keyword: Pain & Touch
Link ID: 24543 - Posted: 01.20.2018

By Esther Landhuis As the sun went down on a recent Friday, the hospital clinic buzzed with activity. “Loads of patients turned up without appointments,” says Sarah Tabrizi, a neurologist at University College London. It wasn’t just the typical post-holiday rush. Many rushed in, Tabrizi suspects, after hearing news last month about a potential new therapy for Huntington’s disease, a brain disorder that cripples the body and blurs speech and thinking, sometimes not too long after a person’s 30th birthday. Like other neurodegenerative disorders such as Lou Gehrig’s, Parkinson’s and Alzheimer’s, Huntington’s has no cure. Over decades biotech companies have poured billions of dollars into developing and testing pharmaceuticals for these devastating conditions, only to unleash storms of disappointment. Yet in December a ray of something approximating hope poked through when a California company released preliminary findings from its small Huntington’s study. Results from this early-stage clinical trial have not yet been published or reported at medical meetings. But some researchers have growing confidence that the drug should work for Huntington’s and perhaps other diseases with clear genetic roots. The initial data showed enough promise to convince Roche to license the drug from California-based Ionis Pharmaceuticals, which sponsored the recent Huntington’s trial. The pharma giant paid Ionis $45 million for the right to conduct further studies and work with regulatory agencies to bring the experimental therapy to market. © 2018 Scientific American

Keyword: Huntingtons
Link ID: 24536 - Posted: 01.17.2018

Richard Harris The results of an IQ test can depend on the gender of the person who's conducting the test. Likewise, studies of pain medication can be completely thrown off by the gender of the experimenter. This underappreciated problem is one reason that some scientific findings don't stand the test of time. Colin Chapman found out about this problem the hard way. He had traveled to Sweden on a Fulbright scholarship to launch his career in neuroscience. And he decided to study whether a nasal spray containing a hormone called oxytocin would help control obesity. The hormone influences appetite and impulsive behavior in obese men. "I was really excited about this project, from what I understood about how the brain works, I thought it was kind of a slam dunk," he says. Chapman set up the experiment and then left for a few years to attend Harvard Law School. When he returned, the findings were not at all what he expected, "and I was really disappointed because this was my baby, it was my big project going into neuroscience." But Chapman, who is now a graduate student at the University of Uppsala, says his idea turned out to be right after all. "There was another research group that around the same time came up with the same idea," he says. "And they ran basically the same project and they got exactly the results I was expecting to get." © 2018 npr

Keyword: Sexual Behavior; Pain & Touch
Link ID: 24517 - Posted: 01.11.2018

By Dina Fine Maron One evening this past fall a patient stumbled into the emergency room at Brigham and Women’s Hospital in Boston. “I don’t feel so…” she muttered, before losing consciousness. Her breathing was shallow and her pupils were pinpoints, typical symptoms of an opioid overdose. Her care team sprang into action. They injected her with 0.4 milligram of naloxone, an overdose antidote—but she remained unresponsive. They next tried one milligram, then two, then four. In total they used 12 milligrams in just five minutes, says Edward Boyer, the physician overseeing her care that night. Yet the patient still had trouble breathing. They put a tube down her throat and hooked her to a ventilator. Twenty minutes later she woke up—angry and in drug withdrawal, but alive. The patient, whose identifying details may have been altered to protect patient confidentiality, had apparently injected herself with a synthetic opioid such as fentanyl right outside of the hospital building. That gave her just enough time to seek help. But many users of synthetic opioids are not so lucky. These drugs, which bear little chemical resemblance to any opioid derived from the opium poppy, are much more powerful than poppy-based heroin and semisynthetic opioids such as oxycodone or hydrocodone. Thus, the standard dose of naloxone employed by first responders (and sold in bystander overdose kits) is often not potent enough to save a synthetic opioid user’s life. © 2018 Scientific American

Keyword: Drug Abuse; Pain & Touch
Link ID: 24505 - Posted: 01.09.2018

By Catherine Offord Neurobiologist John Wood has long been interested in how animals feel pain. His research at University College London (UCL) typically involved knocking out various ion channels important in sensory neuronal function from mouse models and observing the effects. But in the mid-2000s, a peculiar story about a boy in Pakistan opened up a new, and particularly human-centric, research path. The story was relayed by Geoff Woods, a University of Cambridge geneticist. “Geoff had been wandering round Pakistan looking for consanguineous families that had genes contributing to microcephaly,” Wood recalls. During his time there, “somebody came to see him and said that there was a child in the marketplace who was damaging himself for the tourists—and was apparently pain-free.” The boy would regularly stick knives through his arms and walk across burning coals, the stories went. Wood’s group at UCL had just published a paper describing a similarly pain-insensitive phenotype in mice genetically engineered to lack the voltage-gated sodium channel NaV1.7 in pain-sensing neurons, or nociceptors. NaV1.7 controls the passage of sodium ions into the cell—a key step in membrane depolarization and, therefore, a neuron’s capacity to propagate an action potential. Wood’s postdoc, Mohammed Nassar, had shown that mice lacking functional NaV1.7 in their nociceptors exhibited higher-than-normal pain thresholds; they were slower to withdraw a paw from painful stimuli and spent less time licking or biting it after being hurt.1 Having read the study, Cambridge’s Woods reached out to the group in London to discuss whether this same channel could help explain the bizarre behavior of the boy he’d heard about in Pakistan. © 1986-2018 The Scientist

Keyword: Pain & Touch
Link ID: 24503 - Posted: 01.09.2018

Nicola Davis The prospect of a non-addictive alternatives to morphine and other opioids has moved a step closer as scientists say they have cracked a key challenge in developing safe and effective substitute painkillers. Overuse of highly addictive opioids has led to a health crisis across the world, especially in the US where more than 60,000 people died after overdoses in 2016 alone; president Donald Trump has declared the epidemic a public health emergency. Researchers looking for alternatives examined a receptor protein that interacts with opioids in the brain, and have now revealed its structure as it binds to a molecule related to morphine. While the structure of the receptor had previously been reported, this is the first time scientists have unveiled its structure as it interacts with a drug. The development, they say, could prove pivotal. The protein, known as the kappa opioid receptor, is one of four that interacts with opioids, but – crucially – while it can trigger pain-killing effects, it is not linked to problems including constipation, addiction risk and death as a result of overdose. “Tens of thousands of people are dying every year in the US because of opioid overdoses; in the last year more than 50,000 people died. That is as many as died in the Vietnam war in the US. It is a terrible, terrible crisis,” said Bryan Roth, co-author of the research from the University of North Carolina at Chapel Hill. © 2018 Guardian News and Media Limited

Keyword: Drug Abuse; Pain & Touch
Link ID: 24497 - Posted: 01.06.2018

By Catherine Offord Graduate student Anne Murphy had run out of rats. Or rather, she’d run out of male rats, the animals she was using to study brain regions involved in pain modulation for her PhD at the University of Cincinnati in the early 1990s. At a time when neuroscientists almost exclusively used male animals for research, what Murphy did next was unusual: she used a female rat instead. “I had the hardest time to get the female to go under the anesthesia; she wasn’t acting right,” Murphy says. Her advisor’s explanation? “‘Well, you know those females, they have hormones, and those hormones are always fluctuating and they’re so variable,’” Murphy recalls. The comments struck a nerve. “It really got to me,” she says. “I’m a female. I have hormones that fluctuate. . . . It made me determined to investigate the differences between males and females in terms of pain processing and alleviation.” Her decision was timely. Since the ’90s, evidence has been accumulating to suggest that not only do women experience a higher incidence of chronic pain syndromes than men do—fibromyalgia and interstitial cystitis, for example—females also generally report higher pain intensities. Additionally, Murphy notes, a handful of clinical studies has suggested that women require higher doses of opioid pain medications such as morphine for comparable analgesia; plus, they experience worse side effects and a higher risk of addiction. © 1986-2018 The Scientist

Keyword: Pain & Touch; Sexual Behavior
Link ID: 24486 - Posted: 01.04.2018

Beyond the usual suspects of snakes, spiders, and scorpions, the animal kingdom is filled with noxious critters: snails, frogs, fish, anemones, and more make toxins for defense or predation. The noxious chemicals these animals produce are potent, and they often strike where it hurts: pain pathways. These compounds have long captivated researchers hoping to understand their effects and use that knowledge to develop drugs that suppress pain in a wide variety of ailments affecting humans. Paradoxically, some of these toxins are themselves analgesic, and researchers have worked to develop synthetic derivatives that can be tested as painkillers. Such is the case for the only toxin-derived analgesic to be approved by the US Food and Drug Administration (FDA): ziconotide (Prialt), a compound 1,000 times more potent than morphine that was inspired by a component of the venom of the cone snail Conus magus. Other toxins elicit pain, and researchers have used these compounds to identify inhibitors of ion channels on the pain-sensing neurons they target. Despite more than half a century of research in this field, however, scientists have had a frustrating time developing effective analgesics. Challenges include ensuring that the drugs are highly specific to their targets—each family of ion channels involved in pain sensing in humans contains several conserved proteins—and getting them to those targets, which often lie beyond the blood-brain barrier in the central nervous system. Nevertheless, several toxin-derived candidates are beginning to prove their worth in preclinical experiments and a handful of clinical trials, and bioprospectors continue to mine the animal kingdom’s vast library of venoms and poisons for more leads. The next big thing in painkillers could soon be slithering, creeping, hopping, or swimming into the pipeline. © 1986-2018 The Scientist

Keyword: Pain & Touch; Neurotoxins
Link ID: 24485 - Posted: 01.04.2018

By Mark R. Hutchinson When someone is asked to think about pain, he or she will typically envision a graphic wound or a limb bent at an unnatural angle. However, chronic pain, more technically known as persistent pain, is a different beast altogether. In fact, some would say that the only thing that acute and persistent pain have in common is the word “pain.” The biological mechanisms that create and sustain the two conditions are very different. Pain is typically thought of as the behavioral and emotional results of the transmission of a neuronal signal, and indeed, acute pain, or nociception, results from the activation of peripheral neurons and the transmission of this signal along a connected series of so-called somatosensory neurons up the spinal cord and into the brain. But persistent pain, which is characterized by the overactivation of such pain pathways to cause chronic burning, deep aching, and skin-crawling and electric shock–like sensations, commonly involves another cell type altogether: glia.1 Long considered to be little more than cellular glue holding the brain together, glia, which outnumber neurons 10 to 1, are now appreciated as critical contributors to the health of the central nervous system, with recognized roles in the formation of synapses, neuronal plasticity, and protection against neurodegeneration. And over the past 15 to 20 years, pain researchers have also begun to appreciate the importance of these cells. Research has demonstrated that glia seem to respond and adapt to the cumulative danger signals that can result from disparate kinds of injury and illness, and that they appear to prime neural pathways for the overactivation that causes persistent pain. In fact, glial biology may hold important clues to some of the mysteries that have perplexed the pain research field, such as why the prevalence of persistent pain differs between the sexes and why some analgesic medications fail to work. © 1986-2018 The Scientist

Keyword: Pain & Touch; Glia
Link ID: 24482 - Posted: 01.03.2018

By Catherine Offord As a physiotherapist at University Hospital Zurich in the mid-2000s, Annina Schmid often encountered people with chronic pain. “My interest in research got sparked while I was seeing my patients,” she says. “It was very difficult to treat them, or to understand why pain persists in some people, while it doesn’t even occur in others.” Schmid, who grew up in Switzerland, had earned her master’s degree in clinical physiotherapy in 2005 at Curtin University in Perth, Australia, and she was keen to return down under. In 2008, she secured an Endeavour Europe Scholarship from the Australian Government and moved to the University of Queensland in Brisbane for a PhD in neuroscience. “She’s very motivated,” says Schmid’s colleague and collaborator Brigitte Tampin, a musculoskeletal physiotherapist at Curtin University and at Osnabrück University of Applied Sciences in Germany. Tampin adds that Schmid’s physiotherapy background was an asset for her PhD work and beyond. “She can think as a clinician and as a researcher.” For her PhD, Schmid focused on animal models of mild nerve compression, also called entrapment neuropathy, in which pressure on nerve fibers—from bone, for example—can cause pain and loss of motor function. Using a tube to compress the sciatic nerves of rats, Schmid was able to replicate not only local symptoms seen in humans, but also inflammation at distant sites, a possible explanation for why patients often report pain in other parts of the body.1 © 1986-2018 The Scientist

Keyword: Pain & Touch
Link ID: 24477 - Posted: 01.02.2018

Just 10 minutes of aerobic exercise can improve executive function by priming parts of the brain used to laser focus on the task at hand, according to a new study. This paper, “Executive-Related Oculomotor Control Is Improved Following a 10-minute Single-Bout of Aerobic Exercise: Evidence from the Antisaccade Task,” was published in the January 2018 issue of Neuropsychologia. This research was conducted by Matthew Heath, who is a kinesiology professor and supervisor in the Graduate Program in Neuroscience at the University of Western Ontario, along with UWO master’s student Ashna Samani. For this study, Samani and Heath asked a cohort of healthy young adults to either sit quietly and read magazines or perform 10 minutes of moderate-to-vigorous physical activity (MVPA) on a stationary bicycle. (MVPA aerobic intensity is hard enough that you might break a sweat but easy enough that you can carry on a conversation.) Immediately after the 10-minute reading task or time spent doing aerobic exercise, the researchers used eye-tracking equipment to gauge antisaccades, which is a way to measure varying degrees of executive control. As the authors explain in the study abstract, “Antisaccades are an executive task requiring a goal-directed eye movement (i.e., a saccade) mirror-symmetrical to a visual stimulus. The hands- and language-free nature of antisaccades coupled with the temporal precision of eye-tracking technology make it an ideal tool for identifying executive performance changes.” © 1991-2018 Sussex Publishers, LLC

Keyword: Attention
Link ID: 24476 - Posted: 01.02.2018

By Daniel Barron Earlier this year, I wrote about my patient, Andrew, an engineer who developed a heroin habit. An unfortunate series of joint replacements had left Andrew with terrible pain and, when his medication ran out, he turned to heroin. Months after his surgeries—after his tissue and scars had healed—Andrew remained disabled by a deep, biting pain. I recall puzzling over his pain, how it had spread throughout his body and how previous clinical teams had prescribed progressively higher doses of opioids to tame it. Andrew had transitioned from acute pain (i.e., pain from his surgical wounds) to chronic pain (i.e., pain in the absence of an obvious cause), but it was unclear to me whether this reflected a drug tolerance or a different pain process. The difference between drug tolerance and chronic pain is a difficult concept to get hold of. In the hospital workroom one morning, I realized how confused I was by the topic and paged the hospital’s on-call pain specialist. Fortune smiled and Donna-Ann M Thomas, Yale University’s Pain Medicine Division Chief, picked up the phone and patiently explained how tolerance and chronic pain are quite different. Andrew became tolerant to opioids when his body required progressively larger doses to have the same effect. Opioids activate the Mu opioid receptor, which blocks pain signals in the spinal cord. To find a way around the opioid blockade, Andrew’s body had made more Mu receptors to compensate for the drug, meaning more drug had to be present to stifle the pain signal, hence the escalating doses. © 2017 Scientific American,

Keyword: Pain & Touch; Attention
Link ID: 24471 - Posted: 12.30.2017

By Keith Doucette, In what her mother calls a "Christmas miracle," a Nova Scotia woman who suffered a catastrophic brain injury in a 1996 car accident communicated one-on-one with her mother for the first time in 21 years. Louise Misner said her 37-year-old daughter Joellan Huntley used eye-motion cameras and software on an iPad to respond to a comment from Misner about her clothes. Huntley has been severely disabled since she was 15, unable to walk or talk and is fed through a tube. She has always responded to family members' presence by making sounds, but was unable to communicate any thoughts. The breakthrough occurred during a Christmas Day visit at the Kings Regional Rehabilitation Centre in Waterville, N.S. "I said, 'Joellan, I like your new Christmas outfit you got on,"' Misner said in a telephone interview on Friday. Misner said her daughter then used the technology to find an icon for a short-sleeved shirt. "And then she said no, and went to a long-sleeve shirt because she was trying to tell me what she had on." Misner said her reaction to the long-hoped-for communication was immediate. "Christmas miracle," she said. "It was God's way of telling me that she's finally achieved what she needed to since the accident." Settlement helped buy technology Huntley was thrown from a car that had swerved to avoid a dog running loose along a road in Centreville, N.S., on April 18, 1996. The accident claimed the life of her boyfriend and a young girl who was the sister of the driver. ©2017 CBC/Radio-Canada.

Keyword: Movement Disorders; Robotics
Link ID: 24469 - Posted: 12.30.2017