Chapter 7. Vision: From Eye to Brain
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Beau Lotto When you open your eyes, do you see the world as it really is? Do we see reality? Humans have been asking themselves this question for thousands of years. From the shadows on the wall of Plato’s cave in “The Republic” to Morpheus offering Neo the red pill or the blue bill in “The Matrix,” the notion that what we see might not be what is truly there has troubled and tantalized us. In the eighteenth century, the philosopher Immanuel Kant argued that we can never have access to the Ding an sich, the unfiltered “thing-in-itself ” of objective reality. Great minds of history have taken up this perplexing question again and again. They all had theories, but now neuroscience has an answer. The answer is that we don’t see reality. The world exists. It’s just that we don’t see it. We do not experience the world as it is because our brain didn’t evolve to do so. It’s a paradox of sorts: Your brain gives you the impression that your perceptions are objectively real, yet the sensory processes that make perception possible actually separate you from ever accessing that reality directly. Our five senses are like a keyboard to a computer — they provide the means for information from the world to get in, but they have very little to do with what is then experienced in perception. They are in essence just mechanical media, and so play only a limited role in what we perceive. In fact, in terms of the sheer number of neural connections, just 10 percent of the information our brains use to see comes from our eyes. The rest comes from other parts of our brains, and this other 90 percent is in large part what this book is about. Perception derives not just from our five senses but from our brain’s seemingly infinitely sophisticated network that makes sense of all the incoming information. © 2017 The Associated Press.
Link ID: 23529 - Posted: 04.25.2017
Jonathan Rée Beau Lotto is a gung-ho neuroscientist. “[The] great minds of history,” he says, “had theories, but now neuroscience has an answer.” The latest research has, it seems, established that everything you experience “takes place in the brain” and that “you never, ever see reality!” (Lotto loves his italics and exclamation marks.) Your brain may be beautiful, but “what makes it beautiful is that it is delusional” and you should therefore get shot of your inhibitions and summon the courage to “deviate!” Perhaps we should back up a little. Early in the book, Lotto mentions a French scientist called Michel Chevreul who started working at the Gobelins textile factory in Paris in the 1820s. Chevreul had to deal with complaints about coloured yarns that seemed to fade after being woven into tapestries, and his patient chemical analyses did not get him anywhere. But then he shifted his attention from the science of dyestuffs to the psychology of perception, and he was on the way to a solution: colours, he discovered, change their appearance when looked at side by side. I needed respite from Lotto’s exclamation marks so I spent an afternoon in the British Library looking through a gorgeous old volume in which Chevreul expounded his “law of the simultaneous contrast of colours”. Chevreul began by showing how a black line has drastic effects on the appearance of adjacent colours, and how a red patch makes its surroundings look green. He then discussed the difference between colours in an object and colours in a painting, and offered suggestions about the design of picture frames and the use of colour in theatre; and he finished with wonderful planting plans for beds of multicoloured crocuses and dahlias. The book is itself an exuberant work of art, with tinted pages and fold-out arrays of coloured dots looking like prototypes of the spot paintings of Damien Hirst.
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By Pascal Wallisch One of psychologist Robert Zajonc’s lasting contributions to science is the “mere exposure effect,” or the observation that people tend to like things if they are exposed to them more often. Much of advertising is based on this notion. But it was sorely tested in late February 2015, when “the dress” broke the internet. Within days, most people were utterly sick of seeing or talking about it. I can only assume that now, two years later, you have very limited interest in being here. (Thank you for being here.) But the phenomenon continues to be utterly fascinating to vision scientists like me, and for good reason. The very existence of “the dress” challenged our entire understanding of color vision. Up until early 2015, a close reading of the literature could suggest that the entire field had gone somewhat stale—we thought we basically knew how color vision worked, more or less. The dress upended that idea. No one had any idea why some people see “the dress” differently than others—we arguably still don’t fully understand it. It was like discovering a new continent. Plus, the stimulus first arose in the wild (in England, no less), making it all the more impressive. (Most other stimuli used by vision science are generally created in labs.) Even outside of vision scientists, most people just assume everyone sees the world in the same way. Which is why it’s awkward when disagreements arise—it suggests one party either is ignorant, is malicious, has an agenda, or is crazy. We believe what we see with our own eyes more than almost anything else, which may explain the feuds that occurred when “the dress” first struck and science lacked a clear explanation for what was happening.
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Nicola Davis Sitting in a padded car seat, a small black and white bullseye stuck to his cheek, four-month-old Teo Bosten-Lam gazes at a computer. The screen is a mottled grey, like the snow on a old-fashioned television, but in the top right-hand corner is a deep blue circle. Teo has spotted it. He glances at the circle and, as he does so, it morphs into a smiley face and a triumphant jingle fills the darkened room. Buoyed by the reaction, he looks around. Suddenly a black and white spinning disc appears on the screen, issuing a sound that can only be described as “boing”. “Babies can’t resist the black and white swirl things,” says researcher Alice Skelton. “When they look away we play it and it brings them back to the screen.” A PhD student in the baby lab at the University of Sussex, Skelton is attempting to unpick a conundrum that has fascinated parents and scientists alike: when it comes to colour, exactly what can babies can see? It’s a mission that takes technology: Teo’s ability to pick up on colour is being probed with an eye-tracking system. The sticker on his cheek directs the camera to his face, while his corneal reflections and the position of his pupils are automatically detected. “What we are looking to see is, do you have to have a more saturated blue for a baby to see it than you would for a red, for example,” says Skelton. If Teo can see a colour, the novelty will attract his attention, triggering the smiley face and jingle. And this isn’t the only ingenious idea. At the first sound that indicates our participant is becoming fed up with this science lark, the screen flashes to a clip from the 1980s cartoon Dogtanian. Teo, once again, is transfixed.
By Eric Boodman, MEDFORD, Mass. — They look like little more than grayish-black grains of couscous floating in water. But they are actually African clawed frogs-to-be, replete with minuscule blobs that will become eyes. “These little beans here are what I do the surgery on,” said Douglas Blackiston, a postdoctoral fellow at Tufts University’s Allen Discovery Center, holding out a Petri dish. On Thursday, Blackiston published the results of a few years’ worth of those microscopic surgeries, and the finding is bizarre: If you transplant an eye onto what will become the tadpole’s tail, that organ — misplaced though it may be — can allow the animal to see. Admittedly, it’s impossible for humans to look through a clawed frog’s eyes, and in this case, Blackiston and the director of his lab, Michael Levin, were mainly testing whether the tadpoles could perceive movement and colored light. But they say their research doesn’t just have implications for scientists’ ability to restore vision; it also sheds light on how to connect implants and grafts to the body’s own wiring. “You implant these organs, but you want them to be functionally integrated with the host nervous system otherwise they aren’t going to work,” said Levin, the lead author of a paper published Thursday in Nature Regenerative Medicine. Do you have to “connect up every neuron,” he wondered, or can you make use of the natural ability of the nervous system to adapt and rewire itself? © 2017 Scientific American
By Erin Blakemore It’s scientific canard so old it’s practically cliché: When people lose their sight, other senses heighten to compensate. But are there really differences between the senses of blind and sighted people? It’s been hard to prove, until now. As George Dvorsky reports for Gizmodo, new research shows that blind people’s brains are structurally different than those of sighted people. In a new study published in the journal PLOS One, researchers reveal that the brains of people who are born blind or went blind in early childhood are wired differently than people born with their sight. The study is the first to look at both structural and functional differences between blind and sighted people. Researchers used MRI scanners to peer at the brains of 12 people born with “early profound blindness”—that is, people who were either born without sight or lost it by age three, reports Dvorsky. Then they compared the MRI images to images of the brains of 16 people who were born with sight and who had normal vision (either alone or with corrective help from glasses). The comparisons showed marked differences between the brains of those born with sight and those born without. Essentially, the brains of blind people appeared to be wired differently when it came to things like structure and connectivity. The researchers noticed enhanced connections between some areas of the brain, too—particularly the occipital and frontal cortex areas, which control working memory. There was decreased connectivity between some areas of the brain, as well.
Austin Frakt By middle age, the lenses in your eyes harden, becoming less flexible. Your eye muscles increasingly struggle to bend them to focus on this print. But a new form of training — brain retraining, really — may delay the inevitable age-related loss of close-range visual focus so that you won’t need reading glasses. Various studies say it works, though no treatment of any kind works for everybody. The increasing difficulty of reading small print that begins in middle age is called presbyopia, from the Greek words for “old man” and “eye.” It’s exceedingly common, and despite the Greek etymology, women experience it, too. Every five years, the average adult over 30 loses the ability to see another line on the eye reading charts used in eye doctors’ offices. By 45, presbyopia affects an estimated 83 percent of adults in North America. Over age 50, it’s nearly universal. It’s why my middle-aged friends are getting fitted for bifocals or graduated lenses. There are holdouts, of course, who view their cellphones and newspapers at arm’s length to make out the words. The decline in vision is inconvenient, but it’s also dangerous, causing falls and auto accidents. Bifocals or graduated lenses can help those with presbyopia read, but they also contribute to falls and accidents because they can impair contrast sensitivity (the ability to distinguish between shades of gray) and depth perception. I’m 45. I don’t need to correct my vision for presbyopia yet, but I can tell it’s coming. I can still read the The New York Times print edition with ease, but to read text in somewhat smaller fonts, I have to strain. Any year now, I figured my eye doctor would tell me it was time to talk about bifocals. Or so I thought. Then I undertook a monthslong, strenuous regimen designed to train my brain to correct for what my eye muscles no longer can manage. © 2017 The New York Times Company
Link ID: 23407 - Posted: 03.27.2017
By Jason G. Goldman In the summer of 2015 University of Oxford zoologists Antone Martinho III and Alex Kacelnik began quite the cute experiment—one involving ducklings and blindfolds. They wanted to see how the baby birds imprinted on their mothers depending on which eye was available. Why? Because birds lack a part of the brain humans take for granted. Suspended between the left and right hemispheres of our brains sits the corpus callosum, a thick bundle of nerves. It acts as an information bridge, allowing the left and right sides to rapidly communicate and act as a coherent whole. Although the hemispheres of a bird's brain are not entirely separated, the animals do not enjoy the benefits of this pathway. This quirk of avian neuroanatomy sets up a natural experiment. “I was in St. James's Park in London, and I saw some ducklings with their parents in the lake,” Martinho says. “It occurred to me that we could look at the instantaneous transfer of information through imprinting.” The researchers covered one eye of each of 64 ducklings and then presented a fake red or blue adult duck. This colored duck became “Mom,” and the ducklings followed it around. But when some of the ducklings' blindfolds were swapped so they could see out of only the other eye, they did not seem to recognize their “parent” anymore. Instead the ducklings in this situation showed equal affinity for both the red and blue ducks. It took three hours before any preferences began to emerge. Meanwhile ducklings with eyes that were each imprinted to a different duck did not show any parental preferences when allowed to use both eyes at once. The study was recently published in the journal Animal Behaviour. © 2017 Scientific American
By Chris Baraniuk It’s sometimes practically impossible to tell similar colours apart. Even side by side, they look the same. A special pair of spectacles gives us new power to see more distinct colours, and could one day help to spot counterfeit banknotes or counteract camouflage. The glasses, devised by a team at the University of Wisconsin-Madison, basically enhance the user’s colour vision, allowing them to see metamers – colours that look the same but give off different wavelengths of light – as recognisably distinct hues. Human colour vision relies on three types of cone cells that react to short (blue), medium (green) and long (red) wavelengths. While brushing up on his knowledge of the eye before teaching a photonics class, physicist Mikhail Kats had a brainwave. Could the eye be tricked into effectively having another type of cone cell? In theory, this could take our vision from being trichromatic, which uses three colour channels, to tetrachromatic. Some animals see in four (or more) channels. Goldfish, for example, have cells for red, blue, green and ultraviolet light. Some researchers suggest that a very small number of humans may be tetrachromats too. Read more: Human eye proteins detect red beyond red To make their glasses, Kats and his colleagues designed two colour filters, one for each eye that strip out specific parts of the blue light spectrum. With each eye receiving slightly different spectral information about blue things, the team hypothesised that any subtle differences in colour would be more pronounced. And they were right. © Copyright Reed Business Information Ltd
Link ID: 23381 - Posted: 03.21.2017
By DENISE GRADY Three women suffered severe, permanent eye damage after stem cells were injected into their eyes, in an unproven treatment at a loosely regulated clinic in Florida, doctors reported in an article published Wednesday in The New England Journal of Medicine. One, 72, went completely blind from the injections, and the others, 78 and 88, lost much of their eyesight. Before the procedure, all had some visual impairment but could see well enough to drive. The cases expose gaps in the ability of government health agencies to protect consumers from unproven treatments offered by entrepreneurs who promote the supposed healing power of stem cells. The women had macular degeneration, an eye disease that causes vision loss, and they paid $5,000 each to receive stem-cell injections in 2015 at a private clinic in Sunrise, Fla. The clinic was part of a company then called Bioheart, now called U.S. Stem Cell. Staff members there used liposuction to suck fat out of the women’s bellies, and then extracted stem cells from the fat to inject into the women’s eyes. The disastrous results were described in detail in the journal article, by doctors who were not connected to U.S. Stem Cell and treated the patients within days of the injections. An accompanying article by scientists from the Food and Drug Administration warned that stem cells from fat “are being used in practice on the basis of minimal clinical evidence of safety or efficacy, sometimes with the claims that they constitute revolutionary treatments for various conditions.” © 2017 The New York Times Company
By Anna Azvolinsky Delivering a CRISPR/Cas9–based therapy directly to the eye via a viral vector can prevent retinal degeneration in a mouse model of retinitis pigmentosa, a team led by researchers at the National Eye Institute reported in Nature Communications today (March 14). Retinitis pigmentosa, which affects around one in 4,000 people, causes retinal degeneration that eventually leads to blindness. The inherited disorder has been mapped to more than 60 genes (and more than 3,000 mutations), presenting a challenge for researchers working toward a gene therapy. The results of this latest study suggest that a broader, gene-editing–based therapeutic approach could be used to target many of the genetic defects underlying retinitis pigmentosa. “Given the lack of effective therapies for retinal degeneration, particularly the lack of therapies applicable to a broad range of different genetic varieties of this disease, this study represents a very exciting and important advance in our field,” Joseph Corbo, a neuropathologist at the Washington University School of Medicine in St. Louis who was not involved in the work, wrote in an email to The Scientist. This combination of “CRISPR technology with an adeno-associated virus vector, a system tried and true for delivering genetic information to the retina, may represent the first step in a global treatment approach for rod-mediated degenerative disease,” Shannon Boye, whose University of Florida lab develops gene replacement strategies for eye disorders, wrote in an email to The Scientist. © 1986-2017 The Scientist
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By Andy Coghlan A woman in her 80s has become the first person to be successfully treated with induced pluripotent stem (iPS) cells. A slither of laboratory-made retinal cells has protected her eyesight, fighting her age-related macular degeneration – a common form of progressive blindness. Such stem cells can be coaxed to form many other types of cell. Unlike other types of stem cell, such as those found in an embryo, induced pluripotent ones can be made from adult non-stem cells – a discovery that earned a Nobel prize in 2012. Now, more than a decade after they were created, these stem cells have helped someone. Masayo Takahashi at the RIKEN Laboratory for Retinal Regeneration in Kobe, Japan, and her team took skin cells from the woman and turned them into iPS cells. They then encouraged these to form retinal pigment epithelial cells, which are important for supporting and nourishing the retina cells that capture light for vision. The researchers made a slither of cells measuring just 1 by 3 millimetres. Before transplanting this into the woman’s eye in 2014, they first removed diseased tissue on her retina that was gradually destroying her sight. They then inserted the small patch of cells they had created, hoping they would become a part of her eye and stop her eyesight from degenerating. © Copyright Reed Business Information Ltd.
By STEPH YIN Despite being just the size of a rice grain, robber flies, which live all over the world, are champion predators. In field experiments, they can detect targets the size of sand grains from nearly two feet away — 100 times the fly’s body length — and intercept them in under half a second. What’s more, they never miss their mark. A team led by scientists at the University of Cambridge has started to unveil the secrets to the robber fly’s prowess. In a study published Thursday in Current Biology, the team outlined the mechanics of the fly’s pursuit, from its impressive eye anatomy to how it makes a successful catch every time. Notably, the researchers observed a behavior never before described in a flying animal: About 30 centimeters from its prey, the insect slows, turns slightly and brings itself in for a close catch. “This ‘lock-on’ phase and change in behavior during a flight is quite remarkable,” said Sam Fabian, a graduate student at Cambridge and an author of the study. “We would actually expect them to do something very simple — just accelerate and hit the target.” The scientists surveyed robber flies in the field using a “fly teaser,” which consisted of beads on a rapidly moving fishing line controlled by a motor. As the flies charged at the bait, the researchers captured their movements using high-speed cameras. At the start of the robber fly’s conquest, it sits on a perch and scans the sky for passing prey. When it glimpses a potential meal, it takes flight, maintaining a steady angle between itself and its target. This proactive strategy, using a “constant bearing angle,” is also employed by fish, bats and sailors, Mr. Fabian said. © 2017 The New York Times Company
Link ID: 23346 - Posted: 03.11.2017
By JESS BIDGOOD SALEM, Mass. — A few years ago, Bevil Conway, then a neuroscientist at Wellesley College, got an interesting request: Could he give a lecture to the curators and other staff at the Peabody Essex Museum, the art and culture museum here? So Mr. Conway gathered his slides and started from the beginning, teaching the basics of neuroscience — “How neurons work, how neurons talk to each other, issues of evolutionary biology,” Mr. Conway said — to people who run an institution best known for its venerable collections of maritime and Asian art. It was an early step in what has become a galvanizing mission for the museum’s director, Dan L. Monroe: harnessing the lessons of brain science to make the museum more engaging as attendance is falling around the country. “If one’s committed to creating more meaningful and impactful art experiences, it seems a good idea to have a better idea about how our brains work,” he said. “That was the original line of thinking that started us down this path.” The museum, known as P.E.M., has been looking at neuroscience to incorporate its lessons into exhibitions ever since. In an effort to build shows that engage the brain, it has tried breaking up exhibition spaces into smaller pieces; posting questions and quotes on the wall, instead of relying only on explanatory wall text; and experimenting with elements like smell and sound in visual exhibitions. And those efforts are about to increase. The museum recently received a $130,000 grant from the Barr Foundation, a Boston-based philanthropic organization, to bring a neuroscience researcher on staff, add three neuroscientists to the museum as advisers and publish a guide that will help other museums incorporate neuroscience into their exhibition planning. “A lot of what we’re seeing in museums right now is the interpretation of pieces, or artwork,” said E. San San Wong, a senior program officer with the foundation. “What this is looking at is: How do we more actively engage people with art, in multiple senses?” © 2017 The New York Times Company
Researchers at Vanderbilt University in Nashville, Tennessee, have discovered that in zebrafish, decreased levels of the neurotransmitter gamma-aminobutyric acid (GABA) cue the retina, the light-sensing tissue in the back of the eye, to produce stem cells. The finding sheds light on how the zebrafish regenerates its retina after injury and informs efforts to restore vision in people who are blind. The research was funded by the National Eye Institute (NEI) and appears online today in Stem Cell Reports. NEI is part of the National Institutes of Health. “This work opens up new ideas for therapies for blinding diseases and has implications for the broader field of regenerative medicine,” said Tom Greenwell, Ph.D., NEI program officer for retinal neuroscience. For years, vision scientists have studied zebrafish to understand their retinal regenerative capacity. Zebrafish easily recover from retinal injuries that would permanently blind a person. Early studies in zebrafish led to the idea that dying retinal cells release signals that trigger support cells in the retinal called Muller glia to dedifferentiate — return to a stem-like state — and proliferate. However, recent studies in the mouse brain and pancreas suggest GABA, a well-characterized neurotransmitter, might also play an important role in regeneration distinct from its role in communicating local signals from one neuron to the next. Scientists studying a part of the brain called the hippocampus found that GABA levels regulate the activity of neural stem cells. When GABA levels are high, the stem cells stay quiet, and if GABA levels decrease, then the stem cells start to divide, explained James Patton, Ph.D., Stevenson Professor of Biological Sciences at Vanderbilt and senior author of the new study in zebrafish retina. A similar phenomenon was reported in mouse pancreas.
By JANE E. BRODY In letters to The Times, blind readers reacted with heartfelt reassurance and practical guidance to Edward Hoagland’s essay, “Feeling My Way Into Blindness,” published in November. Stanley F. Wainapel, clinical director of physical medicine and rehabilitation at Montefiore Medical Center in the Bronx, admitted that “adapting to vision loss is a major challenge.” But he disputed Mr. Hoagland’s allusion to “enforced passivity,” pointing out that many advances in technology — from screen-reading software for computers to portable devices that read menus or printed letters “with a delay of only seconds” — can keep productivity, creativity and pleasure very much alive for people who can no longer see. Rabbi Michael Levy, president of Yad HaChazakah, the Jewish Disability Empowerment Center, also acknowledged that “transition to a world without sight is far from easy.” But he insisted, “Blindness does not cut me off from the world.” He cited skillful use of a cane, travel devices that tell him where he is and what is around him and periodicals available in real time by telephone among myriad other gadgets that “see” for him. Annika Ariel, a blind student double-majoring in English and political science at Amherst College, wrote that her problems are not with her blindness but rather from people’s attitudes that depict the blind as helpless and dependent. She said she travels independently, uses assistive technologies to complete her work as efficiently as others who can see, and excels academically and socially. Equally inspiring was the response of Mark Riccobono, president of the National Federation of the Blind, who became legally blind at age 5 and lost all useful vision to glaucoma at 14. © 2017 The New York Times Company
Link ID: 23284 - Posted: 02.27.2017
By JANE E. BRODY “Feeling My Way Into Blindness,” an essay published in The New York Times in November by Edward Hoagland, an 84-year-old nature and travel writer and novelist, expressed common fears about the effects of vision loss on quality of life. Mr. Hoagland, who became blind about four years ago, projected deep-seated sadness in describing the challenges he faces of pouring coffee, not missing the toilet, locating a phone number, finding the food on his plate, and knowing to whom he is speaking, not to mention shopping and traveling, when he often must depend on the kindness of strangers. And, of course, he sorely misses nature’s inspiring vistas and inhabitants that fueled his writing, though he can still hear birds chatter in the trees, leaves rustle in the wind and waves crash on the shore. Mr. Hoagland is hardly alone in his distress. According to Action for Blind People, a British support organization, those who have lost some or all sight “struggle with a range of emotions — from shock, anger, sadness and frustration to depression and grief.” When eyesight fails, some people become socially disengaged, leading to isolation and loneliness. Anxiety about a host of issues — falls, medication errors, loss of employment, social blunders — is common. A recent study from researchers at the Wilmer Eye Institute at Johns Hopkins University School of Medicine found that most Americans regard loss of eyesight as the worst ailment that could happen to them, surpassing such conditions as loss of limb, memory, hearing or speech, or having H.I.V./AIDS. Indeed, low vision ranks behind arthritis and heart disease as the third most common chronic cause of impaired functioning in people over 70, Dr. Eric A. Rosenberg of Weill Cornell Medical College and Laura C. Sperazza, a New York optometrist, wrote in American Family Physician. © 2017 The New York Times Company
By Michael Price BOSTON--Among mammals, primates are unique in that certain species have three different types of light-sensitive cone cells in their eyes rather than two. This allows humans and their close relatives to see what we think of as the standard spectrum of color. (Humans with red-green color blindness, of course, see a different spectrum.) The standard explanation for why primates developed trichromacy, as this kind of vision is called, is that it allowed our early ancestors to see colorful ripe fruit more easily against a background of mostly green forest. A particular Old World monkey, the rhesus macaque (pictured), has a genetic distinction that offers a convenient natural test of this hypothesis: a common genetic variation makes some females have three types of cone cells and others have two. Studies with captive macaques has shown that trichromatic females are faster than their dichromatic peers at finding fruit, but attempts to see whether that’s true for wild monkeys has been complicated by the fact that macaques are hard to find, and age and rank also play big roles in determining who eats when. A vision researcher reported today at the annual meeting of AAAS, which publishes Science, that after making more than 20,000 individual observations of 80 different macaques feeding from 30 species of trees on Cayo Santiago, Puerto Rico, she can say with confidence that wild trichromatic female monkeys do indeed appear to locate and eat fruit more quickly than dichromatic ones, lending strong support to the idea that this advantage helped drive the evolution of trichromacy in humans and our relatives. © 2017 American Association for the Advancement of Science.
By LISA SANDERS, M.D. The 3-year-old girl was having a very bad day — a bad week, really. She’d been angry and irritable, screaming and kicking at her mother over nothing. Her mother was embarrassed by this unusual behavior, because her husband’s sister, Amber Bard, was visiting. Bard, a third-year medical student at Michigan State, was staying in the guest room while working with a local medical practice in Grand Rapids so that she could spend a little time with her niece. The behavior was strange, but the mother was more concerned about her child’s left eye. A few days earlier it was red and bloodshot. It no longer was, but now the girl had little bumps near the eye. The mother asked Bard whether she could look at the eye. “I’m a third-year medical student,” Bard told her. “I know approximately nothing.” But Bard was happy to try. She turned to the girl, who immediately averted her face. “Can you show me your eye?” she asked. The girl shouted: “No! No, no, no!” Eventually Bard was able to coax her into allowing her a quick look at the eye. She saw a couple of tiny pimples along the lower lid, near the lashes, and a couple more just next to the eye. The eye itself wasn’t red; the lid wasn’t swollen. She couldn’t see any discharge. Once the child was in bed, Bard opened her laptop and turned to a database she’d been using for the past week when she started to see patients. Called VisualDx, it’s one of a dozen or so programs known as decision-support software, designed to help doctors make a diagnosis. This one focuses mostly on skin findings.
Link ID: 23242 - Posted: 02.17.2017
By Amitha Kalaichandran, When pain researcher Diane Gromala recounts how she started in the field of virtual reality, she seems reflective. She had been researching virtual reality for pain since the early 1990s, but her shift to focusing on how virtual reality could be used for chronic pain management began in 1999, when her own chronic pain became worse. Prior to that, her focus was on VR as entertainment. Gromala, 56, was diagnosed with chronic pain in 1984, but the left-sided pain that extended from her lower stomach to her left leg worsened over the next 15 years. "Taking care of my chronic pain became a full-time job. So at some point I had to make a choice — either stop working or charge full force ahead by making it a motivation for my research. You can guess what I chose," she said. Diane Gromala Pain researcher Diane Gromala found that taking care of her own chronic pain became 'a full-time job.' (Pain studies lab at Simon Fraser University) Now she's finding that immersive VR technology may offer another option for chronic pain, which affects at least one in five Canadians, according to a 2011 University of Alberta study. "We know that there is some evidence supporting immersive VR for acute pain, so it's reasonable to look into how it could help patients that suffer from chronic pain." Gromala has a PhD in human computer interaction and holds the Canada Research Chair in Computational Technologies for Transforming Pain. She also directs the pain studies lab and the Chronic Pain Research Institute at Simon Fraser University in Burnaby, B.C. ©2017 CBC/Radio-Canada.