Chapter 10. Vision: From Eye to Brain
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By PETER ANDREY SMITH In a cavernous basement laboratory at the University of Minnesota, Thomas Stoffregen thrusts another unwitting study subject — well, me — into the “moving room.” The chamber has a concrete floor and three walls covered in faux marble. As I stand in the middle, on a pressure sensitive sensor about the size of a bathroom scale, the walls lurch inward by about a foot, a motion so disturbing that I throw up my arms and stumble backward. Indeed, the demonstration usually throws adults completely off balance. I’m getting off lightly. Dr. Stoffregen, a professor of kinesiology, uses the apparatus to study motion sickness, and often subjects must stand and endure subtle computer-driven oscillations in the walls until they are dizzy and swaying. Dr. Stoffregen’s research has also taken him on cruises — cruise ships are to motion sickness what hospitals are to pneumonia. “No one’s ever vomited in our lab,” he said. “But our cruises are a different story.” For decades now, Dr. Stoffregen, 56, director of the university’s Affordance Perception-Action Laboratory, has been amassing evidence in support of a surprising theory about the causes of motion sickness. The problem does not arise in the inner ear, he believes, but rather in a disturbance in the body’s system for maintaining posture. The idea, once largely ignored, is beginning to gain grudging recognition. “Most theories say when you get motion sick, you lose your equilibrium,” said Robert Kennedy, a psychology professor at the University of Central Florida. “Stoffregen says because you lose your equilibrium, you get motion sick.” Motion sickness is probably a problem as old as passive transportation. The word “nausea” derives from the Greek for “boat,” but the well-known symptoms arise from a variety of stimuli: lurching on the back of a camel, say, or riding the Tilt-a-Whirl at a fair. “Pandemonium,” the perpetually seasick Charles Darwin called it. Copyright 2013 The New York Times Company
At Pimlico Race Course in Baltimore every May, the winning horse in the Preakness Stakes is draped with a blanket covered with what appear to be the Maryland state flower, the black-eyed Susan. But the flower doesn't bloom until later in the season. Those crafting the victory blanket must resort to using yellow Viking daisies — and painting the centers black. That might fool race fans, but bees can see through the ruse. With eyes equipped to detect ultraviolet light, a bee can pick out an additional band in the black-eyed Susan's bull's-eye. The insect's livelihood depends on it. At the center of the target is the flower's nutritional payload, nectar and pollen, which also glows in UV light. As with other members of the sunflower family, black-eyed Susan flower heads are composed of two kinds of florets. The dark center is made up of numerous disc florets, each of which contains male and female reproductive components. When a bee or other pollinator fertilizes a disc floret, it develops a single seed that ripens and falls from the flower head in the autumn. Seeds can remain viable for more than 30 years. Circling the disc florets are bright yellow ray florets, which flag down pollinators and act as landing strips. The inner portion of each ray floret contains several compounds that absorb UV rays. The outer portion reflects UV rays, contributing a visually energetic outer ring to the pattern — provided you're a bee. Black-eyed Susan, Rudbeckia hirta. © 1996-2013 The Washington Post
By Philip Yam The harvest moon is almost upon us—specifically, September 19. It’s the full moon closest to the autumnal equinox, and it has deep significance in our cultural histories. Namely, it enabled our ancestral farmers to toil longer in the fields. (Today, electricity enables us to toil longer in the office—thanks, Tom Edison.) One enduring belief is that the harvest moon is bigger and brighter than any other full moon. That myth is probably the result of the well-known illusion in which the moon looks bigger on the horizon than it does overhead. Back when I was taking psych 101, my professor explained that the moon illusion was simply a function of having reference objects on the horizon. But then I saw this TED-Ed video by Andrew Vanden Heuvel. It turns out that the explanation from my college days really isn’t sufficient to explain the illusion. In fact, scientists really aren’t sure, and there is much debate. Check it out and see what you think. © 2013 Scientific American
By Melissa Hogenboom Science reporter, BBC News Smaller animals tend to perceive time in slow-motion, a new study has shown. This means that they can observe movement on a finer timescale than bigger creatures, allowing them to escape from larger predators. Insects and small birds, for example, can see more information in one second than a larger animal such as an elephant. The work is published in the journal Animal Behaviour. "The ability to perceive time on very small scales may be the difference between life and death for fast-moving organisms such as predators and their prey," said lead author Kevin Healy, at Trinity College Dublin (TCD), Ireland. The reverse was found in bigger animals which may miss things that smaller creatures can rapidly spot. In humans, too, there is variation among individuals. Athletes, for example, can often process visual information more quickly. An experienced goalkeeper would therefore be quicker than others in observing where a ball comes from. The speed at which humans absorb visual information is also age-related, said Andrew Jackson, a co-author of the work at TCD. "Younger people can react more quickly than older people, and this ability falls off further with increasing age." The team looked at the variation of time perception across a variety of animals. They gathered datasets from other teams who had used a technique called critical flicker fusion frequency, which measures the speed at which the eye can process light. BBC © 2013
By Philip Yam If you’re a fan of optical illusions and perceptual tricks, check out this AsapSCIENCE video. As usual, producers Michael Moffitt and Gregory Brown do a great job distilling the essential ideas and presenting them in a fun, entertaining and informative way. Here, they show you how your brain judges brightness and color in context. Visit their YouTube channel to see more (including a frequency test for your ears). You can also check out our compilation of the 169 best illusions (ia sampling of them is on our site) as well as our Illusions Chasers blog, by Susana Martinez-Conde and Steven Macknik, which explore illusions each week. © 2013 Scientific American
Link ID: 18645 - Posted: 09.14.2013
By Sandra G. Boodman, Amy Epstein Gluck remembers how relieved she felt when it seemed that the vision of her youngest child, 9-month-old Sam, might turn out to be normal. Months earlier, doctors had worried that he was blind, possibly as the result of an inherited disorder or a brain tumor. But subsequent tests and consultations with pediatric specialists in Washington and Baltimore instead suggested a temporary developmental delay. Epstein Gluck and her husband, Ira Gluck, were so thrilled with Sam’s progress that they threw a big party to celebrate the end of an arduous year and, they hoped, their son’s frightening problem. But two months later, on Sam’s first birthday in February 2006, the pediatric ophthalmologist who had been treating him delivered news that made it clear a celebration had been premature. “It was such a blow,” Epstein Gluck recalled. On the way to Johns Hopkins, the couple had discussed finding a specialist closer to their Bethesda home, assuming they no longer needed a neuro-ophthalmologist. The ride home was somber: “I was so upset I couldn’t even recount the conversation,” she said. “I had thought we were done.” Instead, they were struggling with the implications of an unexpected finding that, more than a year later, would culminate in a new diagnosis. In March 2005, when Sam was about 5 weeks old, his mother noticed that his eyes would periodically oscillate back and forth. Epstein Gluck, whose other children were then 3 and 5, called her pediatrician. © 1996-2013 The Washington Post
By Neuroskeptic An intriguing new paper in the Journal of Neuroscience introduces a new optical illusion – and, potentially, a new way to see ones own brain activity. The article is called The Flickering Wheel Illusion: When α Rhythms Make a Static Wheel Flicker by Sokoliuk and VanRullen. Here’s the illusion: It’s a simple black and white “wheel” with 32 spokes. To see the illusion, get the wheel in your peripheral vision. Look around the edge of your screen and maybe a bit beyond – you should find a ‘sweet spot’ at which the center of the wheel starts to ‘flicker’ on and off like a strobe light. Remarkably, it even works as an afterimage. Find a ‘sweet spot’, stare at that spot for a minute, then look at a blank white wall. You should briefly see a (color-reversed) image of the wheel and it flickers like the real one (I can confirm it works for me). By itself, this is just a cool illusion. There are lots of those around. What makes it neuroscientifically interesting is that – according to Sokoliuk and VanRullen – that flickering reflects brain alpha waves. First some background. Alpha (α) waves are rhythmical electrical fields generated in the brain. They cycle with a frequency of about 10 Hz (ten times per second) and are strongest when you have your eyes closed, but are still present whenever you’re awake. When Hans Berger invented the electroencephalograph (EEG) and hooked it up to the first subjects in 1924, these waves were the first thing he noticed – hence, “alpha”. They’re noticable because they’re both strong and consistent. They’re buzzing through your brain right now. But this raises a mystery – why don’t we see them? Alpha waves are generated by rhythmical changes in neuronal activity, mainly centered on the occipital cortex. Occipital activity is what makes us see things. So why don’t we see something roughly 10 times every second?
Link ID: 18543 - Posted: 08.22.2013
By Ella Davies Reporter, BBC Nature An unusual caterpillar uses the sun to navigate as it jumps to safety, according to scientists. The larva of Calindoea trifascialis, a species of moth native to Vietnam, wraps itself in a leaf before dropping to the forest floor. It then spends three days searching for a suitable place to pupate, despite not being able to see out of its shelter. Experts found the insect used a piston-like motion to jump away from strong sunlight. "We believe the object of the jumping is to find shade - to avoid overheating and desiccation," explained Mr Kim Humphreys from the Royal Ontario Museum, Canada who conducted the research alongside Dr Christopher Darling. Their findings are published in the Royal Society journal Biology Letters. Although Mr Humphreys described the caterpillar as "non-descript" in appearance, he said its behaviour makes it unique in a number of ways. "Caterpillars or larvae that jump are rare in themselves," he said. "[This] caterpillar is remarkable for its jumping, which no other insect does in this way. It also makes its own vehicle [or] shelter to jump in." "It is also the only one I know of that jumps in an oriented way." BBC © 2013
The EnChroma Color Blindness Test measures the type and extent of color vision deficiency. The test takes between 2-5 minutes to complete. Your test results may be anonymously recorded on our server for quality assurance purposes. This test is not a medical diagnosis. Please consult an eye care professional for more information regarding color vision deficiency. Copyright 2013 EnChroma, Inc.
Link ID: 18525 - Posted: 08.19.2013
A few weeks back, I wrote about special lenses that were developed to give doctors “a clearer view of veins and vasculature, bruising, cyanosis, pallor, rashes, erythema, and other variations in blood O2 level, and concentration,” especially in bright light. But these lenses turned out to have an unintended side effect: they “may cure red-green colorblindness.” I’m severely red-green colorblind, so I was eager to try these $300 lenses. Turns out they didn’t help me; the company said that my colorblindness is too severe. They have helped many others, though (their Amazon reviews makes that clear). After my column appeared, I heard from another company that makes color-enhancing glasses — this time, specifically for red-green colorblind folks. The company’s called EnChroma, and the EnChroma Cx sunglasses are a heartbeat-skipping $600 a pair. “Our lenses are specifically designed to address color blindness,” the company wrote to me, “and utilize a 100+ layer dielectric coating we engineered for this precise purpose by keeping the physiology of the eyes of colorblind people in mind.” I asked to try out a pair. (You can, too: there’s a 30-day money-back guarantee.) To begin, you figure out which kind of colorblindness you have — Protan or Deutan — by taking the test at enchroma.com. Turns out I have something called Strong Protan. (“Protanomaly is a type of red-green color vision deficiency related to a genetic anomaly of the L-cone (i.e. the red cone).”) I’d never heard of it, but whatever. © 2013 The New York Times Company
Link ID: 18524 - Posted: 08.19.2013
By Melinda Wenner Moyer Our world is determined by the limits of our five senses. We can't hear pitches that are too high or low, nor can we see ultraviolet or infrared light—even though these phenomena are not fundamentally different from the sounds and sights that our ears and eyes can detect. But what if it were possible to widen our sensory boundaries beyond the physical limitations of our anatomy? In a study published recently in Nature Communications, scientists used brain implants to teach rats to “see” infrared light, which they usually find invisible. The implications are tremendous: if the brain is so flexible it can learn to process novel sensory signals, people could one day feel touch through prosthetic limbs, see heat via infrared light or even develop a sixth sense for magnetic north. Miguel Nicolelis, a neurobiologist at Duke University, and his colleagues trained six rats to poke their nose inside a port when the LED light above it lit up. Then the researchers surgically attached infrared cameras to the rats' head and wired the cameras to electrodes they implanted into the rats' primary somatosensory cortex, a brain region responsible for sensory processing. When the camera detected infrared light, it stimulated the animals' whisker neurons. The stimulation became stronger the closer the rats got to the infrared light or the more they turned their head toward it, just as brain activation responds to light seen by the eyes. Then the scientists let the animals loose in their chambers, this time using infrared light instead of LEDs to signal the ports the rats should visit. At first, none of the rats used the infrared signals. But after about 26 days of practice, all six had learned how to use the once invisible light to find the right ports. © 2013 Scientific American
Here's what the Swedish artist Oscar Reutersvard did. In 1934, he got himself a pen and paper and drew cubes, like this. He called this final version "Impossible Triangle of Opus 1 No. 293aa." I don't know what the "293aa" is about, but he was right about "impossible." An arrangement like this cannot take place in the physical universe as we know it. You follow the bottom row along with your eyes, then add another row, but when the third row pops in, where are you? Nowhere you have ever been before. At some step in the process you've been tricked, but it's very, very hard to say where the trick is, because what's happening is your brain wants to see all these boxes as units of a single triangle and while the parts simply won't gel, your brain insists on seeing them as a whole. It's YOU who's playing the trick, and you can't un-be you. So you are your own prisoner. At first, this feels like a neurological trap, like a lie you can't not believe. But when you think about for a bit, it's the opposite, it's a release. Twenty years later, the mathematician/physicist Roger Penrose (and his dad, psychologist Lionel Penrose) did it again. They hadn't seen Reutersvard's triangle. Theirs was drawn in perspective, which makes it even more challenging. Here's my version of their Penrose Triangle. What's cool about this? I'm going to paraphrase science writer John D. Barrow, in several places: We know that these drawings can't exist in the physical world. Even as we look at them, particularly when we look at them, we know they are impossible. And yet, we can imagine them anyway. Our brains, it turns out, are not prisoners of the world we live in; we can fly free! We can, any time we like, create the impossible. ©2013 NPR
Richard Johnston Scientists have mapped the dense interconnections and neuronal activity of mouse and fruitfly visual networks. The research teams, whose work is published in three separate studies today in Nature1–3, also created three-dimensional (3D) reconstructions, shown in the video above. All three studies interrogate parts of the central nervous system located in the eyes. In one, Moritz Helmstaedter, a neurobiologist at the Max Planck Institute of Neurobiology in Martinsried, Germany, and his collaborators created a complete 3D map of a 950-cell section of a mouse retina, including the interconnections among those neuronal cells. To do so, the team tapped into the help of more than 200 students, who collectively spent more than 20,000 hours processing the images1. The two other studies investigated how the retinas of the fruitfly (Drosophila melanogaster) detect motion. Shin-ya Takemura, a neuroscientist at the Howard Hughes Medical Institute in Ashburn, Virginia, and his collaborators mapped four neuronal circuits associated with motion perception and found that each is wired for detecting motion in a particular direction — up, down, left or right2. In the third study, Matthew Maisak, a computational biologist at the Max Planck Institute of Neurobiology, and his colleagues mapped the same four cellular networks and tagged the cells of each with protein markers that fluoresce in red, green, blue or yellow in response to stimulation with light3. © 2013 Nature Publishing Group,
Link ID: 18479 - Posted: 08.08.2013
Researchers have achieved dynamic, atomic-scale views of a protein needed to maintain the transparency of the lens in the human eye. The work, funded in part by the National Institutes of Health, could lead to new insights and drugs for treating cataract and a variety of other health conditions. Aquaporin proteins form water channels between cells and are found in many tissues, but aquaporin zero (AQP0) is found only in the mammalian lens, which focuses light onto the retina, at the back of the eye. The lens is primarily made up of unique cells called lens fibers that contain little else besides water and proteins called crystallins. Tight packing of these fibers and of the crystallin proteins within them helps create a uniform medium that allows light to pass through the lens, almost as if it were glass. Abnormal development or age-related changes in the lens can lead to cataract — a clouding of the lens that causes vision loss. Besides age, other risk factors for cataract include smoking, diabetes, and genetic factors. Mutations in the AQP0 gene can cause congenital cataract and may increase the risk of age-related cataract. “The AQP0 channel is believed to play a vital role in maintaining the transparency of the lens and in regulating water volume in the lens fibers, so understanding the molecular details of how water flows through the channel could lead to a better understanding of cataract,” said Dr. Houmam Araj, who oversees programs on lens, cataract and oculomotor systems at NIH’s National Eye Institute (NEI), which helped fund the research.
Link ID: 18465 - Posted: 08.06.2013
By Meeri Kim, Dizziness, vertigo and nausea are common symptoms of an inner-ear infection. But they can also be signs of a stroke. For doctors, especially those working in emergency rooms, quickly and accurately making the distinction is vital. But basic diagnostic tools, including the otoscope and simple eye-movement tests, are far from definitive. As a result, many doctors resort to a pricey imaging test such as a CT scan or an MRI. Nearly half of the 4 million people who visit U.S. emergency rooms each year with dizziness are given an MRI or CT scan, according to a study issued last month. Only about 3 percent of those 4 million people are actually having strokes. Why did the physical therapist’s staff push him to make more visits? Hefty insurance payments, perhaps. For the 25 percent of strokes that restrict blood flow to the back portions of the brain, CT scans are a poor diagnostic tool, according to the study’s leader, David Newman-Toker, an associate professor of neurology and otolaryngology at the Johns Hopkins University School of Medicine. “CT scans are so bad at detecting [these strokes] that they miss about 85 percent of them” in the first day after symptoms begin, he said. “That’s pretty close to useless.” Even MRIs miss almost 20 percent of strokes if the test is done within the first 24 hours. A new device offers a promising option for rooting out the cause of dizziness: eye-tracking goggles. © 1996-2013 The Washington Post
By Susana Martinez-Conde and Stephen L. Macknik According to a legend that one of us (Martinez-Conde) heard growing up in Spain, anybody can see the Devil's face. All you need to do is to stare at your own face in the mirror at the stroke of midnight, call the Devil's name and the Prince of Darkness will look back at you. Needless to say, I was both fascinated and terrified by the possibility. And I knew this was an experiment I must try. I waited a day or two to gather my courage, then stayed awake until midnight, got up from my bed, and into the bathroom I went. I closed the door behind me so that my family would not hear me calling out loud for Satan, faced my wide-eyed reflection, made my invocation, and ... nothing happened. I was disenchanted (literally) but also quite relieved. Now, three decades later, a paper entitled “Strange-Face-in-the-Mirror Illusion,” by vision scientist Giovanni B. Caputo of the University of Urbino in Italy, may explain my lack of results. Caputo asked 50 subjects to gaze at their reflected faces in a mirror for a 10-minute session. After less than a minute, most observers began to perceive the “strange-face illusion.” The participants' descriptions included huge deformations of their own faces; seeing the faces of alive or deceased parents; archetypal faces such as an old woman, child or the portrait of an ancestor; animal faces such as a cat, pig or lion; and even fantastical and monstrous beings. All 50 participants reported feelings of “otherness” when confronted with a face that seemed suddenly unfamiliar. Some felt powerful emotions. After reading Caputo's article, I had to give “Satan” another try. I suspected that my failure to see anything other than my petrified self in the mirror 30 years ago had to do with suboptimal lighting conditions for the strange-face illusion to take place. © 2013 Scientific American
Link ID: 18441 - Posted: 08.01.2013
If you look directly at the "spinning" ball in this illusion by Arthur Shapiro, it appears to fall straight down. But if you look to one side, the ball appears to curve to one side. The ball appears to swerve because our peripheral vision system cannot process all of its features independently. Instead, our brains combine the downward motion of the ball and its leftward spin to create the impression of a curve. Line-of-sight (or foveal) vision, on the other hand, can extract all the information from the ball's movement, which is why the curve disappears when you view the ball dead-on.
Link ID: 18419 - Posted: 07.29.2013
Sleepless night, the moon is bright. People sleep less soundly when there's a full moon, researchers discovered when they analyzed data from a past sleep study. If you were tossing and turning and howling at your pillow this week, you’re not necessarily a lunatic, at least in the strictest sense of the word. The recent full moon might be to blame for your poor sleep. In the days close to a full moon, people take longer to doze off, sleep less deeply, and sleep for a shorter time, even if the moon isn’t shining in their window, a new study has found. “A lot of people are going to say, ‘Yeah, I knew this already. I never sleep well during a full moon.’ But this is the first data that really confirms it,” says biologist Christian Cajochen of the University of Basel in Switzerland, lead author of the new work. “There had been numerous studies before, but many were very inconclusive.” Anecdotal evidence has long suggested that people’s sleep patterns, moods, and even aggression is linked to moon cycles. But past studies of potential lunar effects have been tainted by statistical weaknesses, biases, or inconsistent methods, Cajochen says. Between 2000 and 2003, he and his colleagues had collected detailed data on the sleep patterns of 33 healthy volunteers for an unrelated study on the effects of aging on sleep. Using electroencephalograms (EEG) that measure brain activity, they recorded how deep and how long each participant’s nightly sleep was in a controlled, laboratory setting. Years after the initial experiment, the scientists were drinking in a pub—during a full moon—and came up with the idea of going back to the data to test for correlations with moon cycles. © 2012 American Association for the Advancement of Science.
By Susan Milius When a peacock fans out the iridescent splendor of his train, more than half the time the peahen he’s displaying for isn’t even looking at him. That’s the finding of the first eye-tracking study of birds. In more than 200 short clips recorded by eye-tracking cameras, four peahens spent less than one-third of the time actually looking directly at a displaying peacock, says evolutionary biologist Jessica Yorzinski of Purdue University in West Lafayette, Ind. When peahens did bother to watch the shimmering male, they mostly looked at the lower zone of his train feathers. The feathers’ upper zone of ornaments may intrigue human observers, but big eyespots there garnered less than 5 percent of the female’s time, Yorzinski and her colleagues report July 24 in the Journal of Experimental Biology. These data come from a system that coauthor Jason Babcock of Positive Science, an eye-tracking company in New York City, engineered to fit peahens. Small plastic helmets hold two cameras that send information to a backpack of equipment, which wirelessly transmits information to a computer. One infrared head camera focuses on an eye, tracking pupil movements. A second camera points ahead, giving the broad bird’s-eye view. The rig weighs about 25 grams and takes some getting used to. If a peahen with no experience of helmets gets the full rig, Yorzinski says, “she just droops her head to the ground.” Adding bits of technology gradually, however, let Yorzinski accustom peahens to walking around, and even mating, while cameraed up. © Society for Science & the Public 2000 - 2013
Steve Connor Author Biography The prospect of restoring the sight of blind people with stem-cell transplants has come a step closer with a study showing that it is possible to grow the light-sensitive cells of the eye in a dish with the help of an artificial retina, scientists said. For the first time, researchers have not only grown the photoreceptors of the eye in the laboratory from stem cells but transplanted them into eyes of blind mice where the cells have become fully integrated into the complex retinal tissue. So far the scientists have been unable to show any improvement in the vision of the blind mice – but they are confident that this will soon be possible in further experiments, which should enable them to move to the first clinical trials on patients within five years. Professor Robin Ali of University College London, who led the research at the Institute of Ophthalmology and Moorfields Eye Hospital, said that the technique could lead to stem cell transplants for improving the vision of thousands of people with degenerative eye disorders caused by the progressive loss of photosensitive cells. “The breakthrough here is that we’ve demonstrated we can transplant photoreceptors derived from embryonic stem cells into adult mice. It paves the way to a human clinical trial because now we have a clear route map of how to do it,” Professor Ali said. The loss of photosensitive cells, the rods and cones of the retina, is a leading cause of sight loss in a number of degenerative eye diseases, such as age-related macular degeneration, retinitis pigmentosa and diabetes-related blindness. © independent.co.uk