Chapter 10. Vision: From Eye to Brain

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By Lisa Mulcahy If you’ve ever had your vision “white out” (or “gray out”), you’ve probably felt a little unnerved by the experience. “You’ll see a bright light, and your vision will go pale,” says Teri K. Geist, an optometrist and trustee of the American Optometry Association. As disconcerting as they are, vision whiteouts are usually benign. Making sure, though, means talking with a physician or optometrist. Before you do, here are some things to consider. If you have recurrent whiteouts, counting their duration in real time can help get you the correct diagnosis. Note any specific details the whiteouts appear to have in common. Do they happen right after you stand up from a chair, for example? Most often, whiteouts occur when a person is ready to pass out because of a sudden drop in blood pressure. About 1 in 3 people will faint at some point in their lives. “Fainting can be benign when it’s related to a sudden stress,” says Sarah Thornton, a neuro-ophthalmologist at Wills Eye Hospital in Philadelphia. “Standing up too fast, overexerting, becoming dehydrated or taking certain medications can also lead to hypotension — low blood pressure — and potentially, a whiteout.” A less common risk: “Whiteouts can occur with changes in G force,” says Geist, for instance, in a car accident or on a roller coaster. A whiteout caused by physical stress or exertion will clear within just a few minutes. Although fainting is usually benign, always tell your doctor if you’ve fainted — occasionally, whiteouts and fainting are tied to something serious. “An underlying heart condition, such as aortic stenosis, could cause fainting symptoms, including whiteout,” says Dean M. Cestari, a neuro-ophthalmologist at Mass General Brigham Mass Eye and Ear in Boston and associate professor of ophthalmology at Harvard Medical School. Other such conditions can include arrhythmias, heart failure and atrial fibrillation.

Keyword: Vision
Link ID: 28568 - Posted: 11.30.2022

By Nicola Jones What color is a tree, or the sky, or a sunset? At first glance, the answers seem obvious. But it turns out there is plenty of variation in how people see the world — both between individuals and between different cultural groups. A lot of factors feed into how people perceive and talk about color, from the biology of our eyes to how our brains process that information, to the words our languages use to talk about color categories. There’s plenty of room for differences, all along the way. For example, most people have three types of cones — light receptors in the eye that are optimized to detect different wavelengths or colors of light. But sometimes, a genetic variation can cause one type of cone to be different, or absent altogether, leading to altered color vision. Some people are color-blind. Others may have color superpowers. Our sex can also play a role in how we perceive color, as well as our age and even the color of our irises. Our perception can change depending on where we live, when we were born and what season it is. To learn more about individual differences in color vision, Knowable Magazine spoke with visual neuroscientist Jenny Bosten of the University of Sussex in England, who wrote about the topic in the 2022 Annual Review of Vision Science. This conversation has been edited for length and clarity. How many colors are there in the rainbow? Physically, the rainbow is a continuous spectrum. The wavelengths of light vary smoothly between two ends within the visible range. There are no lines, no sharp discontinuities. The human eye can discriminate far more than seven colors within that range. But in our culture, we would say that we see seven color categories in the rainbow: red, orange, yellow, green, blue, indigo and violet. That’s historical and cultural. © 2022 Annual Reviews

Keyword: Vision
Link ID: 28531 - Posted: 10.28.2022

Yuta Senzai Massimo Scanziani Does rapid eye movement during sleep reveal where you’re looking at in the scenery of dreams, or are they simply the result of random jerks of our eye muscles? Since the discovery of REM sleep in the early 1950s, the significance of these rapid eye movements has intrigued and fascinated scores of scientists, psychologists and philosophers. REM sleep, as the name implies, is a period of sleep when your eyes move under your closed eyelids. It’s also the period when you experience vivid dreams. We are researchers who study how the brain processes sensory information during wakefulness and sleep. In our recently published study, we found that the eye movements you make while you sleep may reflect where you’re looking in your dreams. Past studies have attempted to address this question by monitoring the eye movements of people as they slept and waking them up to ask what they were dreaming. The goal was to find a possible connection between the content of a dream just before waking up (say, a car coming in from the left) and the direction the eyes moved at that moment. Unfortunately, these studies have led to contradictory results. It could be that some participants inaccurately reported dreams, and it’s technically difficult to match a given eye movement to a specific moment in a self-reported dream. We decided to bypass the problem of dream self-reporting. Instead, we used a more objective way to measure dreams: the electrical activity of a sleeping mouse brain. Mice, like humans and many other animals, also experience REM sleep. Additionally, they have a sort of internal compass in their brains that gives them a sense of head direction. When the mouse is awake and running around, the electrical activity of this internal compass precisely reports its head direction, or “heading,” as it moves in its environment. © 2010–2022, The Conversation US, Inc.

Keyword: Sleep; Vision
Link ID: 28453 - Posted: 08.27.2022

By Betsy Mason 08.05.2022 What is special about humans that sets us apart from other animals? Less than some of us would like to believe. As scientists peer more deeply into the lives of other animals, they’re finding that our fellow creatures are far more emotionally, socially, and cognitively complex than we typically give them credit for. A deluge of innovative research is revealing that behavior we would call intelligent if humans did it can be found in virtually every corner of the animal kingdom. Already this year scientists have shown that Goffin’s cockatoos can use multiple tools at once to solve a problem, Australian Magpies will cooperate to remove tracking devices harnessed to them by scientists, and a small brown songbird can sometimes keep time better than the average professional musician — and that’s just among birds. This pileup of fascinating findings may be at least partly responsible for an increase in people’s interest in the lives of other animals — a trend that’s reflected in an apparent uptick in books and television shows on the topic, as well as in legislation concerning other species. Public sentiment in part pushed the National Institutes of Health to stop supporting biomedical research on chimpanzees in 2015. In Canada, an outcry led to a ban in 2019 on keeping cetaceans like dolphins and orcas in captivity. And earlier this year, the United Kingdom passed an animal welfare bill that officially recognizes that many animals are sentient beings capable of suffering, including invertebrates like octopuses and lobsters. Many of these efforts are motivated by human empathy for animals we’ve come to see as intelligent, feeling beings like us, such as chimpanzees and dolphins. But how can we extend that concern to the millions of other species that share the planet with us?

Keyword: Vision; Hearing
Link ID: 28447 - Posted: 08.27.2022

By Fionna M. D. Samuels, Liz Tormes Experiencing art, whether through melody or oil paint, elicits in us a range of emotions. This speaks to the innate entanglement of art and the brain: Mirror neurons can make people feel like they are physically experiencing a painting. And listening to music can change their brain chemistry. For the past 11 years, the Netherlands Institute for Neuroscience in Amsterdam has hosted the annual Art of Neuroscience Competition and explored this intersection. This year’s competition received more than 100 submissions, some created by artists inspired by neuroscience and others by neuroscientists inspired by art. The top picks explore a breadth of ideas—from the experience of losing consciousness to the importance of animal models in research—but all of them tie back to our uniquely human brain. In the moment between wakefulness and sleep, we may feel like we are losing ourself to the void of unconsciousness. This is the moment Daniela de Paulis explores with her interdisciplinary project Mare Incognito. “I always had a fascination for the moment of falling asleep,” she says. “Since I was a very small child, I always found this moment as quite transformative, also quite frightening in a way.” The winning Art of Neuroscience submission is the culmination of her project: a film that recorded de Paulis falling asleep among the silver, treelike antennas of the Square Kilometer Array at the Mullard Radio Observatory in Cambridge, England, while her brain activity was converted into radio waves and transmitted directly into space. “We combined the scientific interest with my poetic fascination in this idea of losing consciousness,” she says. In the clip above, Tristan Bekinschtein, a neuroscientist at the University of Cambridge, explains the massive change humans and their brain experience when they drift from consciousness into sleep. As someone falls asleep, their brain activity slows down in stages until they are fully out. Then bursts of activity light up their gray matter as their brain switches over to rapid eye movement (REM) sleep, and they begin to dream. © 2022 Scientific American,

Keyword: Vision; Brain imaging
Link ID: 28446 - Posted: 08.27.2022

By Diana Kwon During an embryo's development, a piece of the still-growing brain branches off to form the retina, a sliver of tissue in the back of the eye. This makes the retina, which is composed of several layers of neurons, a piece of the central nervous system. As evidence builds that changes in the brain can manifest in this region, scientists are turning to retinas as a potential screening target for early signs of Alzheimer's, an incurable neurodegenerative disease that affects an estimated six million people in the U.S. alone. Initially clinicians could diagnose Alzheimer's only through brain autopsies after patients died. Since the early 2000s, however, research advances have made it possible to pinpoint signs of the disease—and to begin to investigate treatment—years before symptoms first appear. Today positron emission tomography (PET) brain imaging and tests of cerebrospinal fluid (CSF), the clear liquid surrounding the brain and spinal cord, aid Alzheimer's diagnosis at its early stages. “There have been tremendous improvements in our ability to detect early disease,” says Peter J. Snyder, a neuropsychologist and neuroscientist at the University of Rhode Island. But these diagnostic methods are not always readily available, and they can be expensive and invasive. PET imaging requires injecting a radioactive tracer molecule into the bloodstream, and spinal fluid must be extracted with a needle inserted between vertebrae in the back. “We need ways of funneling the right high-risk individuals into the diagnostic process with low-cost screening tools that are noninvasive and simple to administer,” Snyder says. The retina is a particularly attractive target, he adds, because it is closely related to brain tissue and can be examined noninvasively through the pupil, including with methods routinely used to check for eye diseases. © 2022 Scientific American,

Keyword: Alzheimers; Vision
Link ID: 28442 - Posted: 08.24.2022

By Betsy Mason What is special about humans that sets us apart from other animals? Less than some of us would like to believe. As scientists peer more deeply into the lives of other animals, they’re finding that our fellow creatures are far more emotionally, socially, and cognitively complex than we typically give them credit for. A deluge of innovative research is revealing that behavior we would call intelligent if humans did it can be found in virtually every corner of the animal kingdom. Already this year scientists have shown that Goffin’s cockatoos can use multiple tools at once to solve a problem, Australian Magpies will cooperate to remove tracking devices harnessed to them by scientists, and a small brown songbird can sometimes keep time better than the average professional musician — and that’s just among birds. This pileup of fascinating findings may be at least partly responsible for an increase in people’s interest in the lives of other animals — a trend that’s reflected in an apparent uptick in books and television shows on the topic, as well as in legislation concerning other species. Public sentiment in part pushed the National Institutes of Health to stop supporting biomedical research on chimpanzees in 2015. In Canada, an outcry led to a ban in 2019 on keeping cetaceans like dolphins and orcas in captivity. And earlier this year, the United Kingdom passed an animal welfare bill that officially recognizes that many animals are sentient beings capable of suffering, including invertebrates like octopuses and lobsters. Many of these efforts are motivated by human empathy for animals we’ve come to see as intelligent, feeling beings like us, such as chimpanzees and dolphins. But how can we extend that concern to the millions of other species that share the planet with us?

Keyword: Vision; Hearing
Link ID: 28420 - Posted: 08.06.2022

By Paula Span Dementia cases are climbing along with an aging world population, and yet another much-anticipated Alzheimer’s medication, crenezumab, has proved ineffective in clinical trials — the latest of many disappointments. Public health experts and researchers argue that it is past time to turn our attention to a different approach — focusing on eliminating a dozen or so already known risk factors, like untreated high blood pressure, hearing loss and smoking, rather than on an exorbitantly priced, whiz-bang new drug. “It would be great if we had drugs that worked,” said Dr. Gill Livingston, a psychiatrist at University College London and chair of the Lancet Commission on Dementia Prevention, Intervention and Care. “But they’re not the only way forward.” Emphasizing modifiable risks — things we know how to change — represents “a drastic change in concept,” said Dr. Julio Rojas, a neurologist at the University of California, San Francisco. By focusing on behaviors and interventions that are already widely available and for which there is strong evidence, “we are changing how we understand the way dementia develops,” he said. The latest modifiable risk factor was identified in a study of vision impairment in the United States that was published recently in JAMA Neurology. Using data from the Health and Retirement Study, the researchers estimated that about 62 percent of current dementia cases could have been prevented across risk factors and that 1.8 percent — about 100,000 cases — could have been prevented through healthy vision. Though that’s a fairly small percentage, it represents a comparatively easy fix, said Dr. Joshua Ehrlich, an ophthalmologist and population health researcher at the University of Michigan and the study’s lead author. © 2022 The New York Times Company

Keyword: Alzheimers; Vision
Link ID: 28388 - Posted: 07.05.2022

Killian Fox Born in Aldershot in 1959, Russell Foster is a professor of circadian neuroscience at Oxford and the director of the Nuffield Laboratory of Ophthalmology. For his discovery of non-rod, non-cone ocular photoreceptors he received numerous awards including the Zoological Society scientific medal. His latest book – the first he has written without a co-author – is Life Time: The New Science of the Body Clock, and How It Can Revolutionize Your Sleep and Health. What is circadian neuroscience? It’s the fundamental understanding of how our biology ticks on a 24-hour basis. But also it’s bigger than that – it’s an understanding of how different structures interact within the brain and how different genes and their protein products generate a complex behaviour. And that is then embedded throughout our entire biology. Is it an exciting field? What’s happened over the past 25 years has been a move into understanding how these internal 24-hour oscillations are generated and I think it’s one of the amazing success stories in biomedicine. One of the great aims of neuroscience is identifying different bits of the brain with different functions and here we’ve got one: the suprachiasmatic nucleus (SCN), with 50,000 cells, is the master circadian pacemaker. If you don’t have that, then all of our 24-hour rhythms just disappear. How did you first get interested in circadian research? It was largely through photoreceptors. During my second year as an undergraduate – I did zoology at Bristol – I was reading the extraordinary The Life of Vertebrates by JZ Young and I came across a bit about lampreys. They have a parietal third eye, which mammals don’t have; we only have ocular photoreceptors, whereas fish, reptiles, birds, all have multiple photoreceptors. And I just thought: wow, this is so cool. For my PhD, I was trying to understand how light is detected and measured to regulate the seasonal biology of birds. Then I started to address what seemed a simple question: how are the clocks of mammals regulated? We don’t have weird photoreceptors, we have visual cells that grab light in a fraction of a second and then forget it. So how can that light sensory system also be used to gather light information over long periods of time – dawn-dusk detectors? Way back in the early 1990s, we suggested that there was [an undiscovered photoreceptor] in the eye and there was a huge outcry. © 2022 Guardian News & Media Limited

Keyword: Biological Rhythms; Sleep
Link ID: 28379 - Posted: 06.25.2022

Allison Whitten When our phones and computers run out of power, their glowing screens go dark and they die a sort of digital death. But switch them to low-power mode to conserve energy, and they cut expendable operations to keep basic processes humming along until their batteries can be recharged. Our energy-intensive brain needs to keep its lights on too. Brain cells depend primarily on steady deliveries of the sugar glucose, which they convert to adenosine triphosphate (ATP) to fuel their information processing. When we’re a little hungry, our brain usually doesn’t change its energy consumption much. But given that humans and other animals have historically faced the threat of long periods of starvation, sometimes seasonally, scientists have wondered whether brains might have their own kind of low-power mode for emergencies. Now, in a paper published in Neuron in January, neuroscientists in Nathalie Rochefort’s lab at the University of Edinburgh have revealed an energy-saving strategy in the visual systems of mice. They found that when mice were deprived of sufficient food for weeks at a time — long enough for them to lose 15%-20% of their typical healthy weight — neurons in the visual cortex reduced the amount of ATP used at their synapses by a sizable 29%. But the new mode of processing came with a cost to perception: It impaired how the mice saw details of the world. Because the neurons in low-power mode processed visual signals less precisely, the food-restricted mice performed worse on a challenging visual task. “What you’re getting in this low-power mode is more of a low-resolution image of the world,” said Zahid Padamsey, the first author of the new study. All Rights Reserved © 2022

Keyword: Vision
Link ID: 28376 - Posted: 06.15.2022

Researchers from the National Eye Institute (NEI) have identified a new disease that affects the macula, a small part of the light-sensing retina needed for sharp, central vision. Scientists report their findings on the novel macular dystrophy, which is yet to be named, in JAMA Ophthalmology. NEI is part of the National Institutes of Health. Macular dystrophies are disorders that usually cause central visual loss because of mutations in several genes, including ABCA4, BEST1, PRPH2, and TIMP3. For example, patients with Sorsby Fundus Dystrophy, a genetic eye disease specifically linked to TIMP3 variants, usually develop symptoms in adulthood. They often have sudden changes in visual acuity due to choroidal neovascularization– new, abnormal blood vessels that grow under the retina, leaking fluid and affecting vision. TIMP3 is a protein that helps regulate retinal blood flow and is secreted from the retinal pigment epithelium (RPE), a layer of tissue that nourishes and supports the retina’s light-sensing photoreceptors. All TIMP3 gene mutations reported are in the mature protein after it has been “cut” from RPE cells in a process called cleavage. “We found it surprising that two patients had TIMP3 variants not in the mature protein, but in the short signal sequence the gene uses to ‘cut’ the protein from the cells. We showed these variants prevent cleavage, causing the protein to be stuck in the cell, likely leading to retinal pigment epithelium toxicity,” said Bin Guan, Ph.D., lead author. The research team followed these findings with clinical evaluations and genetic testing of family members to verify that the two new TIMP3 variants are connected to this atypical maculopathy.

Keyword: Vision
Link ID: 28364 - Posted: 06.11.2022

Smriti Mallapaty Live-cell imaging of the eye’s transparent cornea has revealed a surprising resident — specialized immune cells that circle the tissue, ready to attack pathogens. “We thought that the central cornea was devoid of any immune cells,” says Esen Akpek, a clinician-scientist who works on immunological diseases of the cornea at Johns Hopkins University in Baltimore, Maryland. The study, published in Cell Reports1 on 24 May, could help researchers to better understand diseases that affect the eye and to develop therapies that target infections on the eye’s surface, says Tanima Bose, an immunologist at the pharmaceutical company Novartis in Kundl, Austria. Immune response The cornea has a dampened response to infection, in part because aggressive immune cells could damage the clear layer of tissue and obstruct vision, says co-author Scott Mueller, an immunologist at the University of Melbourne, Australia. For this reason, the immune cells that mount a quick but crude response to an infection, such as dendritic cells and macrophages, largely reside in the outer sections of the cornea and emerge only when needed. But in almost every tissue in the body are long-lived immune cells, known as T cells, that swiftly attack pathogens they have previously encountered — a process called ‘immune memory’. Mueller and his colleagues wondered whether such cells lived in the cornea. Using a powerful multiphoton microscope for studying living tissue, the researchers examined the corneas of mice whose eyes had been infected with herpes simplex virus. They saw that cytotoxic T cells and T-helper cells — precursors for immune memory — had infiltrated the cornea and persisted for up to a month after the infection. Further investigations, including more intrusive microscopy techniques, revealed that the cytotoxic T cells had developed into long-lived memory cells that resided in the cornea. © 2022 Springer Nature Limited

Keyword: Vision; Neuroimmunology
Link ID: 28357 - Posted: 06.07.2022

By Colleen DeGuzman Jessica Oberoi, 13, cannot remember when her eyesight started getting blurry. All she knows is that she had to squint to see the whiteboard at school. It wasn’t until last fall when her eighth-grade class in Bloomington, Ind., got vision screenings that Jessica’s extreme nearsightedness and amblyopia, or lazy eye, were discovered. She has been going through intense treatment since then, and her optometrist, Katie Connolly, said Jessica has made great improvements — but her lazy eye, which causes depth perception problems, may never go away. The chances of it being completely corrected would have been much higher if her condition had been caught earlier, said Connolly, chief of pediatric and binocular vision service at Indiana University’s School of Optometry. Jessica is one of the countless students falling through the cracks of the nation’s fractured efforts to catch and treat vision problems among children. A mobile clinic is helping low-income students to see clearly — one pair of glasses at a time The Centers for Disease Control and Prevention estimates that more than 600,000 children and teens are blind or have a vision disorder. A recent opinion article published on JAMA Network notes that a large number of these children could be helped simply with glasses, but because of high costs and lack of insurance coverage, many are not getting them. Yet the National Survey of Children’s Health, funded by the U.S. Health Resources and Services Administration, found that in 2016-2017 a quarter of children were not regularly screened for vision problems. And a large majority of those vision impairments could be treated or cured if caught early, Connolly said. “Screenings are important for kids because kids don’t realize what’s abnormal,” Connolly said. “They don’t know what their peers around them — or even their parents — are seeing to realize their experience is different.” © 1996-2022 The Washington Post

Keyword: Vision
Link ID: 28355 - Posted: 06.07.2022

The Age-Related Eye Disease Studies (AREDS and AREDS2) established that dietary supplements can slow progression of age-related macular degeneration (AMD), the most common cause of blindness in older Americans. In a new report, scientists analyzed 10 years of AREDS2 data. They show that the AREDS2 formula, which substituted antioxidants lutein and zeaxanthin for beta-carotene, not only reduces risk of lung cancer due to beta-carotene, but is also more effective at reducing risk of AMD progression, compared to the original formula. A report on the study, funded by the National Institutes of Health, published in JAMA Ophthalmology. “Because beta-carotene increased the risk of lung cancer for current smokers in two NIH-supported studies, our goal with AREDS2 was to create an equally effective supplement formula that could be used by anyone, whether or not they smoke,” said Emily Chew, M.D., director of the Division of Epidemiology and Clinical Application at the National Eye Institute (NEI), and lead author of the study report. “This 10-year data confirms that not only is the new formula safer, it’s actually better at slowing AMD progression.” AMD is a degenerative disease of the retina, the light-sensitive tissue at the back of the eye. Progressive death of retinal cells in the macula, the part of the retina that provides clear central vision, eventually leads to blindness. Treatment can slow or reverse vision loss; however, no cure for AMD exists. The original AREDS study, launched in 1996, showed that a dietary supplement formulation (500 mg vitamin C, 400 international units vitamin E, 2 mg copper, 80 mg zinc, and 15 mg beta-carotene) could significantly slow the progression of AMD from moderate to late disease. However, two concurrent studies also revealed that people who smoked and took beta-carotene had a significantly higher risk of lung cancer than expected.

Keyword: Vision
Link ID: 28348 - Posted: 06.04.2022

Researchers have identified distinct differences among the cells comprising a tissue in the retina that is vital to human visual perception. The scientists from the National Eye Institute (NEI) discovered five subpopulations of retinal pigment epithelium (RPE)—a layer of tissue that nourishes and supports the retina’s light-sensing photoreceptors. Using artificial intelligence, the researchers analyzed images of RPE at single-cell resolution to create a reference map that locates each subpopulation within the eye. A report on the research published in Proceedings of the National Academy of Sciences. “These results provide a first-of-its-kind framework for understanding different RPE cell subpopulations and their vulnerability to retinal diseases, and for developing targeted therapies to treat them,” said Michael F. Chiang, M.D., director of the NEI, part of the National Institutes of Health. “The findings will help us develop more precise cell and gene therapies for specific degenerative eye diseases,” said the study’s lead investigator, Kapil Bharti, Ph.D., who directs the NEI Ocular and Stem Cell Translational Research Section. Vision begins when light hits the rod and cone photoreceptors that line the retina in the back of the eye. Once activated, photoreceptors send signals through a complex network of other retinal neurons that converge at the optic nerve before traveling to various centers in the brain. The RPE sits beneath the photoreceptors as a monolayer, one cell deep. Age and disease can cause metabolic changes in RPE cells that can lead to photoreceptor degeneration. The impact on vision from these RPE changes varies dramatically by severity and where the RPE cells reside within the retina. For example, late-onset retinal degeneration (L-ORD) affects mostly peripheral retina and, therefore, peripheral vision. Age-related macular degeneration (AMD), a leading cause of vision loss, primarily affects RPE cells in the macula, which is crucial for central vision.

Keyword: Vision
Link ID: 28318 - Posted: 05.07.2022

By Helen Ouyang After an hour-and-a-half bus ride last November, Julia Monterroso arrived at a white Art Deco building in West Hollywood, just opposite a Chanel store and the Ivy, a restaurant famous for its celebrity sightings. Monterroso was there to see Brennan Spiegel, a gastroenterologist and researcher at Cedars-Sinai who runs one of the largest academic medical initiatives studying virtual reality as a health therapy. He started the program in 2015 after the hospital received a million-dollar donation from an investment banker on its board. Spiegel saw Monterroso in his clinic the week before and thought he might be able to help alleviate her symptoms. Monterroso is 55 and petite, with youthful bangs and hair clipped back by tiny jeweled barrettes. Eighteen months earlier, pain seized her lower abdomen and never went away. After undergoing back surgery in September to treat a herniated disc — and after the constant ache in her abdomen worsened — she had to stop working as a housecleaner. Eventually, following a series of tests that failed to reveal any clear cause, she landed in Spiegel’s office. She rated her pain an 8 on a 10-point scale, with 10 being the most severe. Chronic pain is generally defined as pain that has lasted three months or longer. It is one of the leading causes of long-term disability in the world. By some measures, 50 million Americans live with chronic pain, in part because the power of medicine to relieve pain remains woefully inadequate. As Daniel Clauw, who runs the Chronic Pain and Fatigue Research Center at the University of Michigan, put it in a 2019 lecture, there isn’t “any drug in any chronic-pain state that works in better than one out of three people.” He went on to say that nonpharmacological therapy should instead be “front and center in managing chronic pain — rather than opioids, or for that matter, any of our drugs.” Virtual reality is emerging as an unlikely tool for solving this intractable problem. The V.R. segment in health care alone, which according to some estimates is already valued at billions of dollars, is expected to grow by multiples of that in the next few years, with researchers seeing potential for it to help with everything from anxiety and depression to rehabilitation after strokes to surgeons strategizing where they will cut and stitch. In November, the Food and Drug Administration gave authorization for the first V.R. product to be marketed for the treatment of chronic pain. © 2022 The New York Times Company

Keyword: Pain & Touch; Vision
Link ID: 28304 - Posted: 04.27.2022

Yasemin Saplakoglu A mosquito watches you through a lattice of microscopic lenses. You stare back, fly swatter in hand, closely tracking the bloodsucker with your humble single-lens eyes. But it turns out that the way you see each other — and the world — may have more in common than you might think. A study published last month in Science Advances found that inside mammalian eyes, mitochondria, the organelles that power cells, may serve a second role as microscopic lenses, helping to focus light on the photoreceptor pigments that convert the light into neural signals for the brain to interpret. The findings, which draw a striking parallel between mammalian eyes and the compound eyes of insects and other arthropods, suggest that our own eyes have hidden levels of optical complexity, and that evolution has found new uses for very old parts of our cellular anatomy. Abstractions navigates promising ideas in science and mathematics. Journey with us and join the conversation. The lens at the very front of the eye focuses light from the environment onto a thin layer of tissue called the retina in the back. There, photoreceptor cells — cones that paint our world in color and rods that help us navigate in low light — absorb the light and translate it into nerve signals that propagate into the brain. But light-sensitive pigments sit at the very ends of photoreceptors, right behind a thick bundle of mitochondria. The odd placement of this bundle turns the mitochondria into seemingly unnecessary, light-scattering obstacles. The mitochondria are the “final hurdle” for the light particles, said Wei Li, a senior investigator at the National Eye Institute and senior author on the paper. For years, vision scientists couldn’t make sense of this odd placement of these organelles — after all, most cells have their mitochondria hugging their center organelle, the nucleus. All Rights Reserved © 2022

Keyword: Vision
Link ID: 28272 - Posted: 04.06.2022

Minuscule involuntary eye movements, known as microsaccades, can occur even while one is carefully staring at a fixed point in space. When paying attention to something in the peripheral vision (called covert attention), these microsaccades sometimes align towards the object of interest. New research by National Eye Institute (NEI) investigators shows that while these microsaccades seem to boost or diminish the strength of the brain signals underlying attention, the eye movements are not drivers of those brain signals. The findings will help researchers interpret studies about covert attention and may open new areas for research into attention disorders and behavior. NEI is part of the National Institutes of Health. Scientists working on the neuroscience of attention have recently become concerned that because both attention and eye movements, like microsaccades, involve the same groups of neurons in the brain, that microsaccades might be required for shifting attention. “If microsaccades were driving attention, that would bring into question a lot of previous research in the field.” said Richard Krauzlis, Ph.D., chief of the NEI Section on Eye Movements and Visual Selection, and senior author of a study report on the research. “This work shows that while microsaccades and attention do share some mechanisms, covert attention is not driven by eye movements.” Krauzlis’ previous research has shown that covert attention causes a modulation of certain neuronal signals in an evolutionarily ancient area of the brain called the superior colliculus, which is involved in the detection of events. When attention is being paid to a particular area – for example, the right-hand side of one’s peripheral vision – signals in the superior colliculus relating to events that occur in that area will receive an extra boost, while signals relating to events occurring somewhere else, like on the left-hand side, will be depressed.

Keyword: Attention; Vision
Link ID: 28254 - Posted: 03.26.2022

Terry Gross One morning in 2017, New York Times columnist Frank Bruni woke up to find that everything looked blurry and smeared. "There was a fog, a dappled fog over the right side of my field of vision," Bruni says. "And I thought for hours that there must be some gunk in my eye, or maybe I'd had too much to drink the night before. Then I thought, Oh, no, it's my eyeglasses. I just have to clean them. And on and on, until deep into the day, I realized there was something wrong beyond all of that." Bruni, then 52, soon learned that he'd experienced a rare kind of stroke that had irreparably damaged his optic nerve. The prognosis: His vision in that eye would never return. What's more, there was a 20 to 40% chance that another stroke would impact his good eye. The news was devastating. "I had some emotional, psychological and really spiritual work to do to accept this and figure out how to go on in the most productive and constructive fashion," he says. But after going through a period of shock and terror, Bruni saw himself at a decision point: He could fixate on what had been lost, or he could focus on what remained. He chose to do the latter. "I feel like once you've recognized what's happened, ... it is so important and so constructive and so right to focus instead on all the things you can still do, all the blessings that remain," he says. "I ended up determined — determined to show myself that I could adapt to whatever was going to happen." In the memoir, The Beauty of Dusk, Bruni chronicles the changes to his vision and the adaptations he's had to make in his work, personal life and attitude. The book also profiles a number of other people who've survived and thrived in ways that Bruni says are profoundly instructive. © 2022 npr

Keyword: Vision; Stroke
Link ID: 28248 - Posted: 03.23.2022

By Lisa Sanders, M.D. “You can’t see the ceiling, can you?” the man asked his 31-year-old wife. She grimaced, then shook her head. She was lying in bed looking toward the familiar shadows and shapes cast by the wintry morning sun. But she couldn’t see them. It was as if a dense white fog lay between her and those daily shifting patterns. Squinting didn’t help. Opening her eyes as wide as she could didn’t, either. All her life she had perfect vision. It was a secret source of pride. She’d never even seen an eye doctor. But that morning changed everything. She first noticed the trouble in her eyes six months earlier. She is a professional violinist and a teacher and that summer took her students to Italy to experience the sacred music and art. As she gazed up at the frescos decorating the ceiling of a favorite cathedral, a shimmering shape with jagged, irregular edges appeared out of nowhere. The points seemed to twinkle as the starlike image slowly enlarged. Inside the glittering outline, the colors were jumbled, like the crystals in a kaleidoscope. It was beautiful and terrifying. She dropped her head, closed her eyes and rubbed her aching neck. When she opened her eyes, the star burst, with its glimmering edges, was still there, distorting all that lay beyond it. It grew so large that it was almost all she could see. Then slowly it began to fade; after nearly a half-hour, the world started to resume its familiar look and shape. There had been similar, if less severe, experiences: Every now and then, when she would get up quickly after sitting or lying down, she would feel an intense pressure inside her head, and when it released, everything briefly looked faded and pale before returning to normal hues. These spells only lasted a few seconds and happened only a handful of times over the past few years. She wrote it off to fatigue or stress. After that day in Italy, those glistening star bursts appeared weekly, then daily. Stranger still, straight lines developed weird lumps and bumps when she looked at them out of the corner of her eye. Doorways, curbs and table edges seemed to waver, growing bulges and divots. When she looked at the object full on, it would obediently straighten out but resumed its aberration once it was on the sidelines again. © 2022 The New York Times Company

Keyword: Vision
Link ID: 28242 - Posted: 03.19.2022