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By PAULA SPAN DEDHAM, Mass. — Jerome Medalie keeps his advance directive hanging in a plastic sleeve in his front hall closet, as his retirement community recommends. That’s where the paramedics will look if someone calls 911. Like many such documents, it declares that if he is terminally ill, he declines cardiopulmonary resuscitation, a ventilator and a feeding tube. But Mr. Medalie’s directive also specifies something more unusual: If he develops Alzheimer’s disease or another form of dementia, he refuses “ordinary means of nutrition and hydration.” A retired lawyer with a proclivity for precision, he has listed 10 triggering conditions, including “I cannot recognize my loved ones” and “I cannot articulate coherent thoughts and sentences.” If any three such disabilities persist for several weeks, he wants his health care proxy — his wife, Beth Lowd — to ensure that nobody tries to keep him alive by spoon-feeding or offering him liquids. VSED, short for “voluntarily stopping eating and drinking,” is not unheard-of as an end-of-life strategy, typically used by older adults who hope to hasten their decline from terminal conditions. But now ethicists, lawyers and older adults themselves have begun a quiet debate about whether people who develop dementia can use VSED to end their lives by including such instructions in an advance directive. Experts know of just a handful of people with directives like Mr. Medalie’s. But dementia rates and numbers have begun a steep ascent, already afflicting an estimated 30 percent of those older than 85. Baby boomers are receiving a firsthand view of the disease’s devastation and burdens as they care for aging parents. They may well prove receptive to the idea that they shouldn’t be kept alive if they develop dementia themselves, predicted Alan Meisel, the director of the University of Pittsburgh’s Center for Bioethics and Health Law. © 2015 The New York Times Company
Link ID: 20495 - Posted: 01.20.2015
By Consumer Reports The headlines about coffee’s impact on your health seem to change as quickly as the time it takes to drink a cup. Should you savor every drop or try to cut down? Here’s what we know right now: It may lengthen your life. True, coffee drinkers are more likely than nondrinkers to smoke, eat red meat, skimp on exercise and have other life-shortening habits, according to a large 2012 study published in the New England Journal of Medicine. But even after adjusting for such factors, they found that people age 50 to 71 who drank at least one cup of coffee per day had a lower risk than nondrinkers of dying from diabetes, heart disease or other health problems when followed for more than a decade. That may be due to beneficial compounds in coffee such as antioxidants — which might ward off disease — and not caffeine. Decaf drinkers had the same results. It may make you happier. Coffee is not just a pick-me-up; it also has been linked to a lower risk of depression. In a study led by the Harvard School of Public Health that tracked 50,000 women for 10 years, those who drank four or more cups of caffeinated coffee per day were 20 percent less likely to develop depression than nondrinkers. Another study found that adults who drank two to four cups of caffeinated coffee were about half as likely to attempt suicide as decaf drinkers or abstainers. The researchers speculated that long-term coffee drinking may boost the production of “feel good” hormones such as dopamine. It contains many good-for-you chemicals.
Closing your eyes when trying to recall events increases the chances of accuracy, researchers at the University of Surrey suggest. Scientists tested people's ability to remember details of films showing fake crime scenes. They hope the studies will help witnesses recall details more accurately when questioned by police. They say establishing a rapport with the person asking the questions can also help boost memory. Writing in the journal Legal and Criminological Psychology, scientists tested 178 participants in two separate experiments. In the first, they asked volunteers to watch a film showing an electrician entering a property, carrying out work and then stealing a number of items. Volunteers were then questioned in one of four groups. People were either asked questions with their eyes open or closed, and after a sense of rapport had been built with the interviewer or no attempt had been made to create a friendly introduction. People who had some rapport with their interviewer and had their eyes shut throughout questioning answered three-quarters of the 17 questions correctly. But those who did not have a friendly introduction with the interviewer and had their eyes open answered 41% correctly. The analysis showed that eye closing had the strongest impact on remembering details correctly ,but that feeling comfortable during the interview also helped. In the second experiment, people were asked to remember details of what they had heard during a mock crime scene. © 2015 BBC
By Melissa Healy A pill may help those whose out-of-control eating is a cause of extreme distress An ADHD drug may offer hope for a different psychiatric disorder Binge eating disorder, a newly recognized condition in which bouts of voracious eating lead to guilt, shame and often obesity, may yield to lisdexamfetamine (marketed as Vyvanse), a medication that has been used for several years to treat attention deficit and hyperactivity disorder in children and adults. In an 11-week clinical trial that tested a range of Vyvanse dosages, researchers found that, compared to those taking a placebo pill, subjects diagnosed with binge eating disorder who took a daily 50 or 70 mg dose of the ADHD drug had fewer binge eating episodes, were more likely to cease binge eating for a four-week period, reported greater improvement in their functioning, and lost substantially more weight. The findings, published online early in the journal JAMA Psychiatry on Wednesday, offer early evidence that patients whose consumption patterns are punctuated by episodes of out-of-control eating may be helped by some medication. The disorder, which has in recent years won wider recognition by the psychiatric establishment, has traditionally been treated with psychotherapy. It has proved a difficult condition to treat. Among those getting lisdexamfetamine, side effects were similar to those experienced by adults who take the medication to treat symptoms of ADHD, including dry mouth, difficulty falling asleep, increased heart rate and headaches. Adverse events prompted six of 196 subjects in the active arm of treatment to withdraw from the study.
Keyword: Anorexia & Bulimia
Link ID: 20492 - Posted: 01.17.2015
By Tia Ghose Being around strangers can cause people stress and, in turn, make them less able to feel others' pain, new research suggests. But giving people a drug that blocks the body's stress response can restore that sense of empathy, scientists said. What's more, the same effect shows up in both humans and mice. "In some sense, we've figured out what to do about increasing empathy as a practical matter," said Jeffrey Mogil, a neuroscientist at McGill University in Montreal. "We've figured out what stops it from happening and, therefore, the solution to make it happen more between strangers." Decreasing stress by doing a shared activity could be a simple way to increase empathy between people who don't know each other, the findings suggest. Past studies had found that mice seemed to feel the pain of familiar mice but were less responsive to foreign mice. Other studies found that, in both humans and mice, stress levels tended to rise around strangers. To see how stress and empathy are connected, Mogil and his colleagues placed two mice together in a cage, then inflicted a painful stimulus on one of them. When the mice were cage mates, the unaffected mouse showed more signs of pain than when they were strangers. But when the team gave the mice a drug called metyrapone, which blocks the formation of the stress hormone cortisol, the mice responded equally to the strangers' pain.
Link ID: 20491 - Posted: 01.17.2015
By Viviane Callier In the deep sea, where light is dim and blue, animals with bigger eyes see better—but bigger eyes are more conspicuous to predators. In response, the small (10 mm to 17 mm), transparent crustacean Paraphronima gracilis has evolved a unique eye structure. Researchers collected the animals from 200- to 500-meter deep waters in California’s Monterey Bay using a remote-operated vehicle. They then characterized the pair of compound eyes, discovering that each one was composed of a single row of 12 distinct red retinas. Reporting online on 15 January in Current Biology, the researchers hypothesize that each retina captures an image that is transmitted to the crustacean’s brain, which integrates the 12 images to increase brightness and contrast sensitivity, adapting to changing light levels. Future work will focus on how images are processed by the neural connections between the retinas and the brain. © 2015 American Association for the Advancement of Science.
by Bethany Brookshire Drugs that treat anxiety can be real downers. While they may help you feel less anxious, drugs such as Valium and Xanax can leave you drowsy and unfocused. Long-term use of these compounds, a class of drugs called the benzodiazepines, can lead to dependence and tolerance. And patients often need higher and higher doses to calm their anxiety. Getting off the drugs requires careful weaning to avoid insomnia, tremors and other nasty withdrawal effects. But Subhashis Banerjee and colleagues at the Scripps Research Institute in Jupiter, Fla., have identified a potential new target for anti-anxiety drugs that avoids the drowsiness and other side effects that come with the standard treatments. The target is an integral part of the body’s internal clock, and in tests in mice, compounds aimed at it reduced measures of anxiety while keeping the mice awake. The possibilities show how basic science questions, such as how the body produces sleep and internal rhythms, could have clinical applications. But it’s important to remember that it’s a long way between mice and people. The proteins REV-ERB alpha and REV-ERB beta are found in cell nuclei throughout the body. These proteins are receptors that sense levels of heme, subsections of chemicals in the body containing iron atoms. Levels of heme rise and fall based on a cell’s activity. REV-ERB responds to these heme level changes by controlling the activation of genes within the cell’s nucleus that govern the cell’s 24-hour internal clock. This circadian rhythm plays an important role in controlling our sleep. © Society for Science & the Public 2000 - 2015.
By Brady Dennis The Food and Drug Administration on Wednesday approved a device aimed at helping obese people shed weight in a novel way – by targeting the nerve pathway between the brain and the stomach that controls feelings of hunger and fullness. The Maestro Rechargeable System, as it is known, consists of an electrical charge generator, wire leads and electrodes that are implanted surgically into a patient’s abdomen. It sends electrical pulses designed to interfere with the vagus nerve, which signals to the brain when the stomach is full or empty. Though researchers don't know exactly how such electrical stimulation leads to weight loss, the approach seems promising. In a year-long clinical trial involving 233 patients with a body-mass index, or BMI, of 35 or greater, those who received a working Maestro device lost 8.5 percent more weight than those without it. About half those in the experimental group lost at least 20 percent of their excess weight, and more than a third lost more than 25 percent of their excess weight. The overall figure was below the original goal of the trial, which was to show weight loss of 10 percent more excess weight in the control group than in those using the new device. Nevertheless, an FDA advisory group said the data showed sustained weight loss among participants and argued that the benefits of the device outweigh its risks for certain patients. In the clinical trial, some patients experienced nausea, vomiting, surgical complications and other side effects. The FDA is requiring the device's manufacturer, EnteroMedics, to conduct a five-year, post-approval study to gather additional data about its safety and effectiveness.
Link ID: 20488 - Posted: 01.15.2015
by Jessica Hamzelou YOU'RE not imagining the pain. But your brain might be behind it, nonetheless. For the first time, it is possible to distinguish between brain activity associated with pain from a physical cause, such as an injury, and that associated with pain linked to your state of mind. A fifth of the world's population is thought to experience some kind of chronic pain – that which has lasted longer than three months. If the pain has no clear cause, people can find themselves fobbed off by doctors who they feel don't believe them, or given ineffective or addictive painkillers. But a study led by Tor Wager at the University of Colorado, Boulder, now reveals that there are two patterns of brain activity related to pain. One day, brain scans could be used to work out your relative components of each, helping to guide treatment. "Pain has always been a bit of a puzzle," says Ben Seymour, a neuroscientist at the University of Cambridge. Hearing or vision, for example, can be traced from sensory organs to distinct brain regions, but pain is more complex, and incorporates thoughts and emotions. For example, studies have linked depression and anxiety to the development of pain conditions, and volunteers put in bad moods have a lower tolerance for pain. So does this mean we can think our way into or out of pain? To find out, Wager and his colleagues used fMRI to look at the brain activity of 33 healthy adults while they were feeling pain. First, the team watched the changing activity as they applied increasing heat to the volunteers' arms. As the heat became painful, a range of brain structures lit up. The pattern was common to all the volunteers, so Wager's team called it the neurologic pain signature. © Copyright Reed Business Information Ltd.
by Ashley Yeager The brain's got its own set of pipes for flushing waste. The plumbing is delicate, however — a finding that may complicate scientists' attempts to create a blood test to diagnose traumatic brain injuries. Bumps to the head can knock proteins out of brain cells. The brain's plumbing system is supposed to wash these proteins away from the damaged area and eventually into the blood. But new research in mice shows that slight alterations to the brain's self-cleaning system, even from treating head injuries, can change the levels of proteins flushed into the blood. As a result, the proteins are unreliable markers of injury, researchers report January 14 in the Journal of Neuroscience. © Society for Science & the Public 2000 - 2015.
By SAM ROBERTS When he was just 5 years old, Thomas Graboys declared that he intended to become a doctor. As a young physician, he visited a nephew serving in the Peace Corps in Mauritania and remained for two months, treating dozens of patients a day. He skied and played tennis and joined fellow cardiologists as the drummer in a rock band called the Dysrhythmics. In Boston, he was famous as a member of the team that diagnosed the Celtics star Reggie Lewis’s heart defect before he died abruptly on a basketball court. In short, “he was a medical version of one of Tom Wolfe’s masters of the universe,” one reviewer concluded after Dr. Graboys (pronounced GRAY-boys) published his autobiography. But barely 60, after experiencing horrific nightmares, frequently flailing in bed, losing his memory, suffering tremors and finally collapsing on his wedding day, he acknowledged that he was suffering from Parkinson’s disease and the onset of dementia. He informed his patients that he had no choice but to close his practice. “My face is often expressionless, though I still look younger than my 63 years,” he recalled in the autobiography, “Life in the Balance: A Physician’s Memoir of Life, Love, and Loss With Parkinson’s Disease and Dementia,” which was published in 2008. “I am stooped,” he continued. “I shuffle when I walk, and my body trembles. My train of thought regularly runs off the rails. There is no sugarcoating Parkinson’s. There is no silver lining here. There is anger, pain, and frustration at being victimized by a disease that can to some extent be managed but cannot be cured.” After managing for more than a decade, Dr. Graboys died on Jan. 5 at his home in Chestnut Hill, Mass., his daughter, Penelope Graboys Blair, said. The cause was complications of Lewy Body Dementia, which was diagnosed after his Parkinson’s. He was 70. © 2015 The New York Times Company
Link ID: 20485 - Posted: 01.15.2015
By Peter Holley "Lynchian," according to David Foster Wallace, "refers to a particular kind of irony where the very macabre and the very mundane combine in such a way as to reveal the former's perpetual containment within the latter." Perhaps no other word better describes the onetime fate of Martin Pistorius, a South African man who spent more than a decade trapped inside his own body involuntarily watching "Barney" reruns day after day. "I cannot even express to you how much I hated Barney," Martin told NPR during the first episode of a new program on human behavior, "Invisibilia." The rest of the world thought Pistorius was a vegetable, according to NPR. Doctors had told his family as much after he'd fallen into a mysterious coma as a healthy 12-year-old before emerging several years later completely paralyzed, unable to communicate with the outside world. The nightmarish condition, which can be caused by stroke or an overdose of medication, is known as "total locked-in syndrome," and it has no cure, according to the National Institute of Neurological Disorders and Stroke. In a first-person account for the Daily Mail, Pistorius described the period after he slipped into a coma: I was completely unresponsive. I was in a virtual coma but the doctors couldn’t diagnose what had caused it. When he finally did awaken in the early 1990s, around the age of 14 or 15, Pistorius emerged in a dreary fog as his mind gradually rebooted itself.
By Will Boggs MD NEW YORK (Reuters Health) - Patients with chronic pain show signs of glial activation in brain centers that modulate pain, according to results from a PET-MRI study. "Glia appears to be involved in the pathophysiology of chronic pain, and therefore we should consider developing therapeutic approaches targeting glia," Dr. Marco L. Loggia from Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, told Reuters Health by email. "Glial activation is accompanied by many cellular responses, which include the production and release of substances (such as so-called 'pro-inflammatory cytokines') that can sensitize the pain pathways in the central nervous system," he explained. "Thus, glial activation is not a mere reaction to a pain state but actively contributes to the establishment and/or maintenance of persistent pain." To test their hypothesis that patients with chronic pain demonstrate in vivo activation of brain glia, Dr. Loggia's team imaged the brains of 19 individuals diagnosed with chronic low back pain as well as 25 pain-free healthy volunteers using 11C-PBR28, a PET radioligand that binds to the translocator protein (TSPO), a protein upregulated in activated microglia and reactive astrocytes in animal models of pain. Each patient exhibited higher 11C-PBR28 uptakes than his/her age-, sex-, and TSPO genotype-matched control in the thalamus, and there were no brain regions for which the healthy controls showed statistically higher uptakes than the patients with chronic low back pain. © 2015 Scientific American
By Michael Balter If there’s one thing that distinguishes humans from other animals, it’s our ability to use language. But when and why did this trait evolve? A new study concludes that the art of conversation may have arisen early in human evolution, because it made it easier for our ancestors to teach each other how to make stone tools—a skill that was crucial for the spectacular success of our lineage. Researchers have long debated when humans starting talking to each other. Estimates range wildly, from as late as 50,000 years ago to as early as the beginning of the human genus more than 2 million years ago. But words leave no traces in the archaeological record. So researchers have used proxy indicators for symbolic abilities, such as early art or sophisticated toolmaking skills. Yet these indirect approaches have failed to resolve arguments about language origins. Now, a team led by Thomas Morgan, a psychologist at the University of California, Berkeley, has attacked the problem in a very different way. Rather than considering toolmaking as a proxy for language ability, he and his colleagues explored the way that language may helps modern humans learn to make such tools. The researchers recruited 184 students from the University of St. Andrews in the United Kingdom, where some members of the team were based, and organized them into five groups. The first person in each group was taught by archaeologists how to make artifacts called Oldowan tools, which include fairly simple stone flakes that were manufactured by early humans beginning about 2.5 million years ago. This technology, named after the famous Olduvai Gorge in Tanzania where archaeologists Louis and Mary Leakey discovered the implements in the 1930s, consists of hitting a stone “core” with a stone “hammer” in such a way that a flake sharp enough to butcher an animal is struck off. Producing a useful flake requires hitting the core at just the right place and angle. © 2015 American Association for the Advancement of Science.
|By Gareth Cook What is flavor? Beginning with this simple question, the Pulitzer prize-winning journalist John McQuaid weaves a fascinating story with a beginning some half a billion years ago. In his new book, Tasty, McQuaid argues that the sense of taste has played a central role in the evolution of humans. McQuaid’s tale is about science, but also about culture, history and, one senses, our future. What made you decide to write a book about taste? I have two kids, a boy and a girl born two years apart – now teens – and a few years ago, I became fascinated with how their tastes and preferences in food differed. My son liked extremes, especially super-hot chili peppers and whole lemons and limes. My daughter hated that stuff. She preferred bland comfort foods such as mashed potatoes, pasta, cheese and rice. White foods. Both kids were also picky eaters. They liked what they liked, and it didn’t overlap (except for pizza). Speaking as a parent, this was maddening. So I wondered where these differences came from. Were they genetic? The kids had mostly the same genes. Environment? They lived in the same place. And yet clearly both genes and environment were in play somehow. So I began to look into the question, and a whole world opened up. And the basic answer to my original question is: kids are, biologically speaking, weird creatures. Pickiness seems to be programmed by evolution: it would have protected small children from eating strange, possibly poisonous items. Certain preferences, meanwhile, can develop arbitrarily and become very strong, then suddenly fade – every kid goes through phases as the brain matures and the neural networks that shape perception and behavior grow. Each person’s sense of flavor is like a snowflake or a fingerprint, in this way, shaped by partly by genes, but largely by experience. And always changing as more meals are eaten. © 2015 Scientific American
By Susan Svrluga Edwin Chapman’s secretary handed him a pile of prescription slips, and the doctor’s pen moved quickly across them: “Buprenorphine/naloxone.” “Buprenorphine/naloxone.” “Buprenorphine/naloxone.” His waiting room was full of heroin-addicted patients there to refill their generic prescriptions for Suboxone, a drug that helps keep their relentless cravings at bay and now outpaces methadone as a treatment. Chapman is an internist, a cardiologist. This drug has transformed his D.C. medical practice — now more than half of his patients are there to seek it, addicts edging out elderly ladies with arthritis and diabetes. And the drug, he believes, has transformed lives. He wishes more people could get it. Yet even as heroin use surges in the United States, destroying neighborhoods and families — drug overdoses kill more people than any other kind of accident — both addicts and doctors say there are barriers that keep some from the treatment they desperately need. “In the past we’ve kind of run away from these patients, put them in methadone clinics, places no one can see them,” said Chapman, who estimates that two-thirds of his heroin-addicted patients tested positive for hepatitis C and more than one in 10 for HIV. “We need to reverse that. Put them in primary care. We need to be taking care of sick folks, not running away from them.
Keyword: Drug Abuse
Link ID: 20480 - Posted: 01.14.2015
By Neuroskeptic A new study offers two reasons to be cautious about some of the claims made for the role of the hormone oxytocin in human behavior. The paper’s out now in PLoS ONE from researchers James C. Christensen and colleagues, who are based at the US Air Force Research Laboratory in Ohio. That the military are interested in oxytocin at all is perhaps a testament to the huge amount of interest that this molecule has attracted in recent years. Oxytocin has been called the “hug hormone”, and is said to be involved in such nice things as love and trust. But according to Christensen et al., quite a lot of previous oxytocin research may be flawed. Their paper is in two parts. Christensen et al. first show that the only accurate way to measure oxytocin levels in blood is by performing plasma extraction before chemical analysis. Using unextracted plasma, they find, leads to seriously distorted measures. The differences between extracted and unextracted plasma estimates of oxytocin have been noted before, but Christensen et al. show directly that unextracted plasma interferes with oxytocin measurement. They found that oxytocin test kits were unable to detect a ‘spike’ of pure oxytocin added to some unextracted plasma samples, whereas the spike was reliably detected when added to an extracted sample. This was true using either the ELISA or RIA method for quantification of oxytocin. With ELISA, unextracted oxytocin measures were also very noisy and unrealistically high:
Keyword: Hormones & Behavior
Link ID: 20479 - Posted: 01.14.2015
Vernon Mountcastle, one of Johns Hopkins Medicine's giants of the 20th century, died peacefully at his North Baltimore home on Sunday, with Nancy, his wife of seven decades, and family at his bedside. He was 96. Mountcastle was universally acknowledged as the "father of neuroscience" and served Johns Hopkins with extraordinary dedication for nearly 65 years. A 1942 graduate of the School of Medicine and a member of the faculty since 1948, Mountcastle served as director of the Department of Physiology and head of the Philip Bard Laboratories of Neurophysiology at Johns Hopkins from 1964 to 1980. He later became one of the founding members of Johns Hopkins' Zanvyl Krieger Mind/Brain Institute, where he continued to work until his retirement at 87. Colleagues remember his dedication to the professional development of neuroscientists, fiercely focused work ethic, and devotion to collaborative research. Also see: Mind/Brain's Mountcastle wins NAS award for lifetime of groundbreaking work (Gazette, April 1998) Mountcastle once was dubbed the "Jacques Cousteau of the cortex" for his revolutionary research delving into the unknown depths of the brain and establishing the basis for modern neuroscience. In 1957, he made the breakthrough discovery that revolutionized the concept of how the brain is built. He found that the cells of the cerebral cortex are organized in vertical columns, extending from the surface of the brain down through six layers of the cortex, each column processing a specific kind of information.
Keyword: Brain imaging
Link ID: 20478 - Posted: 01.14.2015
By CATHERINE SAINT LOUIS A nationwide outbreak of a respiratory virus last fall sent droves of children to emergency departments. The infections have now subsided, as researchers knew they would, but they have left behind a frightening mystery. Since August, 103 children in 34 states have had an unexplained, poliolike paralysis of an arm or leg. Each week, roughly three new cases of so-called acute flaccid myelitis are still reported to the Centers for Disease Control and Prevention. Is the virus, called enterovirus 68, really the culprit? Experts aren’t certain: Unexplained cases of paralysis in children happen every year, but they are usually scattered and unrelated. After unusual clusters of A.F.M. appeared this fall, enterovirus 68 became the leading suspect, and now teams of researchers are racing to figure out how it could have led to such damage. “It’s unsatisfying to have an illness and not know what caused it,” said Dr. Samuel Dominguez, an epidemiologist and an infectious disease specialist at Children’s Hospital Colorado, which has had the largest cluster of patients. For many families, the onset of persistent limb paralysis has been a bewildering experience. Roughly two thirds of the children with A.F.M. have reported some improvement, according to the C.D.C. About a third show none. Only one child has fully recovered. In August, Jack Wernick, a first grader in Kingsport, Tenn., developed a “crummy little cold,” said his father, Dan Wernick, who works for a paper company. It seemed ordinary, until Jack complained that his right arm was heavy, his face began drooping and pain started shooting down his right leg. © 2015 The New York Times Company
Keyword: Movement Disorders
Link ID: 20477 - Posted: 01.13.2015
|By Matthew H. Schneps Many of the etchings by artist M. C. Escher appeal because they depict scenes that defy logic. His famous “Waterfall” shows a waterwheel powered by a cascade pouring down from a brick flume. Water turns the wheel and is redirected uphill back to the mouth of the flume, where it can once again pour over the wheel in an endless cycle. The drawing shows us an impossible situation that violates nearly every law of physics. In 2003 a team of psychologists led by Catya von Károlyi of the University of Wisconsin–Eau Claire made a discovery using such images. When the researchers asked people to pick out impossible figures from similarly drawn illustrations, they found that participants with dyslexia were among the fastest at this task. Dyslexia is often called a learning disability. And it can indeed present learning challenges. Although its effects vary widely, some children with dyslexia read so slowly that it would typically take them months to read the same number of words that their peers read in a day. Therefore, the fact that people with this difficulty were so adept at rapidly picking out the impossible figures puzzled von Károlyi. The researchers had stumbled on a potential upside to dyslexia, one that investigators have just begun to understand. Scientists had long suspected dyslexia might be linked to creativity, but laboratory evidence for this was rare. In the years to follow, sociologist Julie Logan of Cass Business School in London showed that there is a higher incidence of dyslexia among entrepreneurs than in the general population. Meanwhile cognitive scientist Gadi Geiger of the Massachusetts Institute of Technology found that people with dyslexia could attend to multiple auditory inputs at once. © 2015 Scientific American