Chapter 5. The Sensorimotor System
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By Emily Underwood As long as she can remember, 53-year-old Rosa Sundquist has tallied the number of days per month when her head explodes with pain. The migraines started in childhood and have gotten worse as she’s grown older. Since 2008, they have incapacitated her at least 15 days per month, year-round. Head-splitting pain isn’t the worst of Sundquist’s symptoms. Nausea, vomiting, and an intense sensitivity to light, sound, and smell make it impossible for her to work—she used to be an office manager—or often even to leave her light-proofed home in Dumfries, Virginia. On the rare occasions when she does go out to dinner or a movie with her husband and two college-aged children, she wears sunglasses and noise-canceling headphones. A short trip to the grocery store can turn into a full-blown attack “on a dime,” she says. Every 10 weeks, Sundquist gets 32 bee sting–like injections of the nerve-numbing botulism toxin into her face and neck. She also visits a neurologist in Philadelphia, Pennsylvania, who gives her a continuous intravenous infusion of the anesthetic lidocaine over 7 days. The lidocaine makes Sundquist hallucinate, but it can reduce her attacks, she says—she recently counted 20 migraine days per month instead of 30. Sundquist can also sometimes ward off an attack with triptans, the only drugs specifically designed to interrupt migraines after they start. Millions of others similarly dread the onset of a migraine, although many are not afflicted as severely as Sundquist. Worldwide, migraines strike roughly 12% of people at least once per year, with women roughly three times as likely as men to have an attack. © 2016 American Association for the Advancement of Science.
By Stephani Sutherland A technique called optogenetics has transformed neuroscience during the past 10 years by allowing researchers to turn specific neurons on and off in experimental animals. By flipping these neural switches, it has provided clues about which brain pathways are involved in diseases like depression and obsessive-compulsive disorder. “Optogenetics is not just a flash in the pan,” says neuroscientist Robert Gereau of Washington University in Saint Louis. “It allows us to do experiments that were not doable before. This is a true game changer like few other techniques in science.” Since the first papers were published on optogenetics in the mid-aughts some researchers have mused about one day using optogenetics in patients, imagining the possibility of an off-switch for depression, for instance. The technique, however, would require that a patient submit to a set of highly invasive medical procedures: genetic engineering of neurons to insert molecular switches to activate or switch off cells, along with threading of an optical fiber into the brain to flip those switches. Spurred on by a set of technical advances, optogenetics pioneer Karl Deisseroth, together with other Stanford University researchers, has formed a company to pursue optogenetics trials in patients within the next several years—one of several start-ups that are now contemplating clinical trials of the technique. Circuit Therapeutics, founded in 2010, is moving forward with specific plans to treat neurological diseases. (It also partners with pharmaceutical companies to help them use optogenetics in animal research to develop novel drug targets for human diseases.) © 2016 Scientific America
Keyword: Pain & Touch
Link ID: 21758 - Posted: 01.07.2016
By NICHOLAS WADE After decades of disappointingly slow progress, researchers have taken a substantial step toward a possible treatment for Duchenne muscular dystrophy with the help of a powerful new gene-editing technique. Duchenne muscular dystrophy is a progressive muscle-wasting disease that affects boys, putting them in wheelchairs by age 10, followed by an early death from heart failure or breathing difficulties. The disease is caused by defects in a gene that encodes a protein called dystrophin, which is essential for proper muscle function. Because the disease is devastating and incurable, and common for a hereditary illness, it has long been a target for gene therapy, though without success. An alternative treatment, drugs based on chemicals known as antisense oligonucleotides, is in clinical trials. But gene therapy — the idea of curing a genetic disease by inserting the correct gene into damaged cells — is making a comeback. A new technique, known as Crispr-Cas9, lets researchers cut the DNA of chromosomes at selected sites to remove or insert segments. Three research groups, working independently of one another, reported in the journal Science on Thursday that they had used the Crispr-Cas9 technique to treat mice with a defective dystrophin gene. Each group loaded the DNA-cutting system onto a virus that infected the mice’s muscle cells, and excised from the gene a defective stretch of DNA known as an exon. Without the defective exon, the muscle cells made a shortened dystrophin protein that was nonetheless functional, giving all of the mice more strength. The teams were led by Charles A. Gersbach of Duke University, Eric N. Olson of the University of Texas Southwestern Medical Center and Amy J. Wagers of Harvard University. © 2016 The New York Times Company
Tina Hesman Saey SAN DIEGO — Friendly ghosts help muscles heal after injury. Connective tissue sheaths that bundle muscle cells together leave behind hollow fibers when muscles are injured, Micah Webster of the Carnegie Institution for Science in Baltimore and colleagues discovered. Muscle-repairing stem cells build new tissue from inside those empty tunnels, known as ghost fibers, Webster reported December 13 at the annual meeting of the American Society for Cell Biology. Researchers previously knew that stem cells can heal muscle, but how stem cells integrate new cells into muscle fibers has been a mystery. Webster and colleagues used a special microscopy technique to watch stem cells in live mice as the cells fixed muscles damaged by snake venom. Stem cells from undamaged parts of the muscle fiber crawled back and forth through the ghostly part of the fibers and spaced themselves out evenly. Stem cells replicated themselves to reconstruct each muscle fiber inside its ghostly shell the researchers found. Stem cells didn’t move from one ghost fiber to another. The finding suggests that researchers will need to create artificial ghost fibers to repair injuries in which chunks of muscles are lost, such as in soldiers hit by explosives, Webster said. The researchers also reported the results online December 10 in Cell Stem Cell. M.T. Webster et al. Intravital imaging reveals ghost fibers as architectural units guiding muscle progenitors. Annual meeting of the American Society for Cell Biology, San Diego, December 13, 2015. M.T. Webster et al. Intravital imaging reveals ghost fibers as architectural units guiding myogenic progenitors during regeneration. Cell Stem Cell. Published online December 10, 2015. doi: 10.1016/j.stem.2015.11.005 © Society for Science & the Public 2000 - 2015
Link ID: 21704 - Posted: 12.16.2015
The clock is ticking for Ronald Cohn. He wants to use CRISPR gene editing to correct the genes of his friend’s 13-year-old son. The boy, Gavriel, has Duchenne muscular dystrophy, a genetic disease in which muscles degenerate. Breathing and heart problems often start by the time people with the condition are in their early twenties. Life expectancy is about 25 years. By the standards of science, the field of CRISPR gene editing is moving at a lightning fast pace. Although the technique was only invented a few years ago, it is already being used for research by thousands of labs worldwide to make extremely precise changes to DNA. A handful of people have already been treated using therapies enabled by the technology, and last week an international summit effectively endorsed the idea of gene editing embryos. It is too soon to try the technique out, but the summit concluded that basic research on embryos should be permitted, alongside a debate on how we should use the technology. But for people like Cohn, progress can’t come fast enough. Gavriel was diagnosed at age 4. He has already lost the use of his legs but still has some movement in his upper body, and uses a manual wheelchair. Cohn, a clinician at the Hospital for Sick Children in Toronto, estimates that he has three years to develop and test a CRISPR-based treatment if he is to help Gavriel. Muscular dystrophy is caused by a faulty gene for the protein dystrophin, which holds our muscles together. Gavriel has a duplicated version of the gene. This week, Cohn’s team published a paper describing how they grew Gavriel’s cells in a dish and used CRISPR gene-editing techniques to snip out the duplication. With the duplication removed, his cells produced normal dystrophin protein. © Copyright Reed Business Information Ltd.
By Gretchen Reynolds Physical fitness may be critical for maintaining a relatively youthful and nimble brain as we age, according to a new study of brain activation patterns in older people. For most of us, our bodies begin to lose flexibility and efficiency as we enter our 40s. Running and other movements slow down and become more awkward, and something similar seems to occur within our heads. As middle age encroaches, our thinking becomes less efficient. We don’t toggle between mental tasks as nimbly as we once did or process new information with the same aplomb and clarity. Recently, neuroscientists have begun to quantify how those cognitive changes play out in our brains, to disquieting effect. In studies comparing brain activation in young people with that of people past 40, they have found notable differences, especially during mental tasks that require attention, problem solving, decision-making and other types of high-level thinking. Such thinking primarily involves activation of the brain’s prefrontal cortex. In young people, activation in the cortex during these cognitive tasks tends to be highly localized. Depending on the type of thinking, young people’s brains light up almost exclusively in either the right or left portion of the prefrontal cortex. But in older people, studies show, brain activity during the same mental tasks requires far more brainpower. They typically display activity in both hemispheres of their prefrontal cortex. In effect, they require more of their brains’ resources to complete the same tasks that young people do with less cognitive effort. Neuroscientists coined an acronym for this phenomenon: Harold, for hemispheric asymmetry reduction in older adults. Most agree that it represents a general reorganization and weakening of the brain’s function with age. © 2015 The New York Times Company
by Chris Samoray Every fall, blackpoll warblers fly from North America to South America in what’s the longest migration route of any warbler in the Western Hemisphere. But some of the tiny songbirds take a detour before making their epic transoceanic leap. Over 40 years of data from 22,295 birds show that blackpoll warblers (Setophaga striata) living in western North America head east for a pit stop to put on weight, giving the birds the energy stores they need to cross the Atlantic Ocean, researchers report December 9 in the Auk: Ornithological Advances. For birds that breed farther west in places like Alaska, the eastern stopover means a migration distance that’s nearly twice that of their eastern U.S. counterparts, the scientists find. © Society for Science & the Public 2000 - 2015.
Keyword: Animal Migration
Link ID: 21687 - Posted: 12.10.2015
By SINDYA N. BHANOO Moderate levels of exercise may increase the brain’s flexibility and improve learning, a new study suggests. The visual cortex, the part of the brain that processes visual information, loses the ability to “rewire” itself with age, making it more difficult for adults to recover from injuries and illness, said Claudia Lunghi, a neuroscientist at the University of Pisa and one of the study’s authors. In a study in the journal Current Biology, she and her colleagues asked 20 adults to watch a movie with one eye patched while relaxing in a chair. Later, the participants exercised on a stationary bike for 10-minute intervals while watching a movie. When one eye is patched, the visual cortex compensates for the limited input by increasing its activity level. Dr. Lunghi and her colleagues tested the imbalance in strength between the participants’ eyes after the movie — a measure of changeability in the visual cortex. © 2015 The New York Times Company
Link ID: 21681 - Posted: 12.08.2015
A woman born incapable of feeling pain has been hurt for the first time – thanks to a drug normally prescribed for opioid overdoses. She was burned with a laser, and quite liked the experience. The breakthrough may lead to powerful new ways to treat painful conditions such as arthritis. Only a handful people around the world are born unable to feel pain. These individuals can often suffer a range of injuries when they are young. Babies with the condition tend to chew their fingers, toes and lips until they bleed, and toddlers can suffer an increased range of knocks, tumbles and encounters with sharp or hot objects. The disorder is caused by a rare genetic mutation that results in a lack of ion channels that transport sodium across sensory nerves. Without these channels, known as Nav1.7 channels, nerve cells are unable to communicate pain. Researchers quickly sought to make compounds that blocked Nav1.7 channels, thinking they might be able to block pain in people without the disorder. “It looked like a fantastic drug target,” says John Wood at University College London. “Pharma companies went bananas and made lots of drugs.” But while a few compounds saw some success, none brought about the total pain loss seen in people who lack the channel naturally. © Copyright Reed Business Information Ltd.
By David Noonan The 63-year-old chief executive couldn't do his job. He had been crippled by migraine headaches throughout his adult life and was in the middle of a new string of attacks. “I have but a little moment in the morning in which I can either read, write or think,” he wrote to a friend. After that, he had to shut himself up in a dark room until night. So President Thomas Jefferson, in the early spring of 1807, during his second term in office, was incapacitated every afternoon by the most common neurological disability in the world. The co-author of the Declaration of Independence never vanquished what he called his “periodical head-ach,” although his attacks appear to have lessened after 1808. Two centuries later 36 million American migraine sufferers grapple with the pain the president felt. Like Jefferson, who often treated himself with a concoction brewed from tree bark that contained quinine, they try different therapies, ranging from heart drugs to yoga to herbal remedies. Their quest goes on because modern medicine, repeatedly baffled in attempts to find the cause of migraine, has struggled to provide reliable relief. Now a new chapter in the long and often curious history of migraine is being written. Neurologists believe they have identified a hypersensitive nerve system that triggers the pain and are in the final stages of testing medicines that soothe its overly active cells. These are the first ever drugs specifically designed to prevent the crippling headaches before they start, and they could be approved by the U.S. Food and Drug Administration next year. If they deliver on the promise they have shown in studies conducted so far, which have involved around 1,300 patients, millions of headaches may never happen. © 2015 Scientific American
Keyword: Pain & Touch
Link ID: 21662 - Posted: 11.28.2015
By Nala Rogers If you travel with a group of friends, you might delegate navigation to the person with the best sense of direction. But among homing pigeons, the leader is whoever flies the fastest—even if that pigeon has to pick up navigation skills on the job, according to a new study. To find out how the skills of individual pigeons influence flock direction, researchers tested four flocks on journeys from three different locations, each about 5 kilometers from their home loft near Oxford, U.K. At each site, the researchers tracked the pigeons during solo flights before releasing them together for several group journeys. The fastest birds surged to the front during group flights and determined when the flock turned, despite the fact that these leaders were often poor navigators during their initial solo expeditions. But on a final set of solo flights—made after the group journeys—these same leaders chose straighter routes than followers, the researchers report today in Current Biology. Apparently, being responsible for group decisions helped pigeons learn the route, say scientists, raising questions about the two-way interplay between skills and leadership. © 2015 American Association for the Advancement of Science
By Karen Weintraub Essential tremor is involuntary shaking – usually of the hands, but sometimes also of the neck, jaw, voice or legs. “Any fine tasks with the hands can be very difficult when the tremor is pronounced,” said Dr. Albert Hung, center director of the Massachusetts General Hospital National Parkinson Foundation Center of Excellence. Essential tremor can affect balance, walking, hearing and cognition, and can get worse over time, said Dr. Elan Louis, chief of the division of movement disorders at Yale School of Medicine. People with essential tremor run almost twice the risk of developing Alzheimer’s as the general population. Essential tremor appears with movement; if people let their hands sit still, they don’t tremble. That is the big difference between an essential tremor and the tremor of Parkinson’s disease, which can occur while at rest, Dr. Louis said. Essential tremor also tends to strike both hands while Parkinson’s is more one-sided at first, said Dr. Hung. The cause of essential tremor remains a mystery, though it seems to run in families. People of any age or sex can have the condition, though it is more common as people grow older. Roughly 4 percent of 40-year-olds have essential tremor, compared with about 20 percent of 90-year-olds, Dr. Louis said. Available treatments “aren’t great,” Dr. Louis said. Two medications – the beta blocker propranolol and the epilepsy drug primidone, sold under the brand name Mysoline – can reduce tremors by 10 to 30 percent, he said, but they work only in about half of patients. Deep brain stimulation – implanting electrodes into the brain to override faulty electrical signals – has been shown to markedly reduce hand tremor severity, he said. But the treatment can worsen cognitive and balance problems and “doesn’t cure the underlying disease. It merely and temporarily lessons a single symptom, which is the tremor.” © 2015 The New York Times Company
Keyword: Movement Disorders
Link ID: 21653 - Posted: 11.24.2015
By Gretchen Reynolds Sturdy legs could mean healthy brains, according to a new study of British twins. As I frequently have written in this column, exercise may cause robust improvements in brain health and slow age-related declines in memory and thinking. Study after study has shown correlations between physical activity, muscular health and mental acuity, even among people who are quite old. But these studies have limitations and one of them is that some people may be luckier than others. They may have been born to have a more robust brain than someone else. Their genes and early home environment might have influenced their brain health as much as or more than their exercise habits. Their genes and early home environment also might have influenced those exercise habits, as well as how their bodies and brains responded to exercise. In other words, genes and environment can seriously confound experimental results. That problem makes twins so valuable for scientific purposes. (Full disclosure, I am a twin, although not an identical one.) Twins typically share the same early home environment and many of the same genes, and if they are identical, all their genes are the same. So if one twin’s body, brain and thinking abilities begin to differ substantially over the years from their twin’s, the cause is less likely to be solely genetic or the early environment, and more likely to be attributable to lifestyle, including exercise habits. It was that possibility that recently prompted Claire Steves, a senior lecturer in twin research at King’s College London, to consider twins and their thighs. © 2015 The New York Times Company
Link ID: 21641 - Posted: 11.18.2015
Ian Sample Science editor Tiny biological compasses made from clumps of protein may help scores of animals, and potentially even humans, to find their way around, researchers say. Scientists discovered the minuscule magnetic field sensors in fruit flies, but found that the same protein structures appeared in retinal cells in pigeons’ eyes. They can also form in butterfly, rat, whale and human cells. The rod-like compasses align themselves with Earth’s geomagnetic field lines, leading researchers to propose that when they move, they act on neighbouring cell structures that feed information into the nervous system to create a broader direction-sensing system. Professor Can Xie, who led the work at Peking University, said the compass might serve as a “universal mechanism for animal magnetoreception,” referring to the ability of a range of animals from butterflies and lobsters to bats and birds, to navigate with help from Earth’s magnetic field. Whether the compasses have any bearing on human navigation is unknown, but the Peking team is investigating the possibility. “Human sense of direction is complicated,” said Xie. “However, I believe that magnetic sense plays a key role in explaining why some people have a good sense of direction.” The idea that animals could sense Earth’s magnetic field was once widely dismissed, but the ability is now well established, at least among some species. The greatest mystery that remains is how the sensing is done. © 2015 Guardian News and Media Limited
Keyword: Animal Migration
Link ID: 21638 - Posted: 11.17.2015
Ewen Callaway Ringo, a golden retriever born in 2003 in a Brazilian kennel, was never expected to live long. Researchers bred him and his littermates to inherit a gene mutation that causes severe muscular dystrophy. They hoped that the puppies would provide insight into Duchenne muscular dystrophy (DMD), an untreatable and ultimately fatal human disease caused by inactivation of the same gene. But Ringo’s muscles didn't waste away like his littermates', and researchers have now determined why: he was born with another mutation that seems to have protected him from the disease, according to a paper published in Cell1. Scientists hope that by studying Ringo’s mutation — which has never before been linked to muscular dystrophy — they can find new treatments for the disease. As many as 1 in 3,500 boys inherit mutations that produce a broken version of a protein called dystrophin, causing DMD. (The disease appears in boys because the dystrophin gene sits on the X chromosome, so girls must inherit two copies of the mutated gene to develop DMD.) The protein helps to hold muscle fibres together, and its absence disrupts the regenerative cycle that rebuilds muscle tissue. Eventually, fat and connective tissue replace muscle, and people with DMD often become reliant on a wheelchair before their teens. Few survive past their thirties. Some golden retriever females carry dystrophin mutations that cause a similar disease when passed onto male puppies. Dog breeders can prevent this through genetic screening. But Mayana Zatz, a geneticist at the University of São Paulo in Brazil, and her colleagues set out to breed puppies with the mutation to model the human disease. © 2015 Nature Publishing Group,
By Emily Underwood Researchers have found a way to increase how fast, and for how long, four paralyzed people can type using just their thoughts. The advance has to do with brain-machine interfaces (BCI), which are implanted in brain tissue and record hundreds of neurons firing as people imagine moving a computer cursor. The devices then use a computer algorithm to decode those signals and direct a real cursor toward words and letters on a computer screen. One of the biggest problems with BCIs is the brain itself: When the soft, squishy organ shifts in the skull, as it frequently does, it can displace the electrode implants. As a result, the movement signal extracted from neuronal firing is constantly being distorted, making it impossible for a patient to keep the cursor from drifting off course without a researcher recalibrating the instrument every 10 minutes or so. In the new study, part of a clinical trial of BCIs called BrainGate, researchers performed several software tweaks that allow the devices to self-correct in real time by calculating the writer’s intention based on the words they’ve already written. The devices can now also correct for neuronal background noise whenever a person stops typing. These improvements, demonstrated in the video above, allow BCI users to type faster and for longer periods of time, up to hours or days, the team reports today in Science Translational Medicine. Though the technology still needs to be miniaturized and wireless before it can be used outside of the lab, the new work is a big step towards BCIs that paralyzed people can use on their own at home, the scientists say. © 2015 American Association for the Advancement of Science
Link ID: 21626 - Posted: 11.12.2015
By Virginia Morell Plunge a live crab into a pot of boiling water, and it’s likely to try to scramble out. Is the crab’s behavior simply a reflex, or is it a sign of pain? Many scientists doubt that any invertebrate (or fish) feels pain because they lack the areas in the brain associated with human pain. Others argue this is an unfair comparison, noting that despite the major differences between vertebrate and invertebrate brains, their functions (such as seeing) are much the same. To get around this problem, researchers in 2014 argued that an animal could be classified as experiencing pain if, among other things, it changes its behavior in a way that indicates it’s trying to prevent further injury, such as through increased wariness, and if it shows a physiological change, such as elevated stress hormones. To find out whether crabs meet these criteria, scientists collected 40 European shore crabs (Carcinus maenas), shown in the photo above, in Northern Ireland. They placed the animals into individual tanks, and gave half 200-millisecond electrical shocks every 10 seconds for 2 minutes in their right and left legs. The other 20 crabs served as controls. Sixteen of the shocked crabs began walking in their tanks, and four tried to climb out. None of the control crabs attempted to clamber up the walls, but 14 walked, whereas six didn’t move at all. There was, however, one big physiological difference between the 16 shocked, walking crabs and the 14 control walkers, the scientists report in today’s issue of Biology Letters: Those that received electrical jolts had almost three times the amount of lactic acid in their haemolymph, a fluid that’s analogous to the blood of vertebrates—a clear sign of stress. Thus, crabs pass the bar scientists set for showing that an animal feels pain. © 2015 American Association for the Advancement of Science.
By Arlene Karidis Several years ago, Peggy Chenoweth began having excruciating cramping in her ankle. It felt severely sprained and as if her toe were twisting to the point where it was being ripped off her foot. “The pain is right here,” she told an orthopedic surgeon, “in my ankle and foot.” But the 41-year-old Gainesville, Va., resident no longer had that ankle and foot. Her leg had been amputated below the knee after a large piece of computer equipment fell off a cart, crushed her foot and caused nerve damage. Further, she insisted that since the amputation, she could feel her missing toes move. Chenoweth’s surgeon knew exactly what was going on: phantom pain. Lynn Webster, an anesthesiologist and past president of the American Academy of Pain Medicine, explains the phenomenon: “With ‘phantom pain,’ nerves that transmitted information from the brain to the now-missing body part continue to send impulses, which relay the message of pain.” It feels as if the removed part is still there and hurting, but pain is actually in the brain. The sensation ranges from annoying itching to red-hot burning. Physicians wrote about phantom pain as early as the 1860s, but U.S. research on this condition has increased recently, spurred by the surge of amputees returning from warfare in Iraq and Afghanistan and by increasing rates of diabetes. (Since 2003, nearly 1,650 service members have lost limbs, according to the Congressional Research Service. In 2010, about 73,000 amputations were performed on diabetics in the United States, according to the Centers for Disease Control and Prevention.)
Keyword: Pain & Touch
Link ID: 21620 - Posted: 11.10.2015
By Jason G. Goldman When a monkey has the sniffles or a headache, it doesn't have the luxury of popping a few painkillers from the medicine cabinet. So how does it deal with the common colds and coughs of the wildlife world? University of Georgia ecologist Ria R. Ghai and her colleagues observed a troop of more than 100 red colobus monkeys in Uganda's Kibale National Park for four years to figure out whether the rain forest provides a Tylenol equivalent. Monkeys infected with a whipworm parasite were found to spend more time resting and less time moving, grooming and having sex. The infected monkeys also ate twice as much tree bark as their healthy counterparts even though they kept the same feeding schedules. The findings were published in September in the journal Proceedings of the Royal Society B. The fibrous snack could help literally sweep the intestinal intruder out of the simians' gastrointestinal tracts, but Ghai suspects a more convincing reason. Seven of the nine species of trees and shrubs preferred by sick monkeys have known pharmacological properties, such as antisepsis and analgesia. Thus, the monkeys could have been self-medicating, although she cannot rule out other possibilities. The sick individuals were, however, using the very same plants that local people use to treat illnesses, including infection by whipworm parasites. And that “just doesn't seem like a coincidence,” Ghai says. © 2015 Scientific American,
by Laura Sanders Babies’ minds are mysterious. Thoughts might be totally different in a brain that lacks words, and sensations might feel alien in a body so new. Are babies’ perceptions like ours, or are they completely different? Even if babies could talk, words would surely fail to convey what it’s like to experience, oh, every single thing for the first time. A recent paper offers a sliver of insight into young babies’ inner lives. The study, published October 19 in Current Biology, finds an example in which 4-month-old babies are happily oblivious to the external world. The research focuses on a perceptual trick that suckers adults and 6-month-old babies alike. When the hands are crossed, people often mistake which hand feels a touch. Let’s say your left hand (now crossed over to the right side of your body) gets a tickle. Your eyes would see a hand on the right side of your body get touched — a place usually claimed by your right hand, but now occupied by your left. Those mismatches between sight, touch and expectation can thwart you from quickly and correctly saying which hand was touched. Here’s the twist: 4-month-old babies don’t fall for this trick, Andrew Bremner of Goldsmiths, University of London and his colleagues found. In the experiment, a researcher would hold infants’ legs in either a crossed position or straight, while one of two remote-controlled buzzers taped to their feet tickled one foot. The researchers then watched which foot or leg wiggled as a result. If the buzzed foot moved, that meant that the baby got it right. © Society for Science & the Public 2000 - 2015.