Pocket-sized retina camera, no dilating required

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Posted on 2nd May 2017 by Pacific ClearVision Institute in General |Retina

It’s the part of the eye exam everyone hates: the pupil-dilating eye drops. The drops work by opening the pupil and preventing the iris from constricting in response to light and are often used for routine examination and photography of the back of the eye. The drops sting, can take up to 30 minutes to work, and cause blurry vision for several hours afterwards, often making them inconvenient for both patient and doctor.

Now, researchers at the University of Illinois at Chicago College of Medicine and Massachusetts Eye and Ear/Harvard Medical School have developed a cheap, portable camera that can photograph the retina without the need for pupil-dilating eye drops. Made out of simple parts mostly available online, the camera’s total cost is about $185.

“As residents seeing patients in the hospital, there are often times when we are not allowed to dilate patients — neurosurgery patients for example,” said Dr. Bailey Shen, a second-year ophthalmology resident at the UIC College of Medicine. “Also, there are times when we find something abnormal in the back of the eye, but it is not practical to wheel the patient all the way over to the outpatient eye clinic just for a photograph.”

The prototype camera can be carried in your pocket, Shen said, and can take pictures of the back of the eye without eye drops. The pictures can be shared with other doctors, or attached to the patient’s medical record.

The camera is based on the Raspberry Pi 2 computer, a low-cost, single-board computer designed to teach children how to build and program computers. The board hooks up to a small, cheap infrared camera, and a dual infrared- and white-light-emitting diode. A handful of other components — a lens, a small display screen and several cables — make up the rest of the camera.

The camera works by first emitting infrared light, which the iris — the muscle that controls the opening of the pupil — does not react to. Most retina cameras use white light, which is why pupil-dilating eye drops are needed.

The infrared light is used to focus the camera on the retina, which can take a few seconds. Once focused, a quick flash of white light is delivered as the picture is taken. Cameras exist that use this same infrared/white light technique, but they are bulky and often cost thousands of dollars.

Shen’s camera photos show the retina and its blood supply as well as the portion of the optic nerve that leads into the retina. It can reveal health issues that include diabetes, glaucoma and elevated pressure around the brain.

Shen and his co-author, Dr. Shizuo Mukai, associate professor of ophthalmology at Harvard Medical School and a retina surgeon at Massachusetts Eye and Ear, describe their camera and provide a shopping list of parts, instructions for assembly, and the code needed to program the camera in the Journal of Ophthalmology.

“This is an open-source device that is cheap and easy to build,” said Mukai. “We expect that others who build our camera will add their own improvements and innovations.”

“The device is currently just a prototype, but it shows that it is possible to build a cheap camera capable of taking quality pictures of the retina without dilating eye drops, ” Shen said. “It would be cool someday if this device or something similar was carried around in the white-coat pockets of every ophthalmology resident and used by physicians outside of ophthalmology as well.”

Myopia cell discovered in retina: Dysfunction of cell may be linked to amount of time a child spends indoors

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Posted on 2nd May 2017 by Pacific ClearVision Institute in General |Retina

Northwestern Medicine scientists have discovered a cell in the retina that may cause myopia when it dysfunctions. The dysfunction may be linked to the amount of time a child spends indoors and away from natural light.

“This discovery could lead to a new therapeutic target to control myopia,” said Greg Schwartz, lead investigator and assistant professor of ophthalmology at Northwestern University Feinberg School of Medicine.

More than a billion people in the world have myopia, whose incidence is rising and is linked to how much time people spend indoors as children.

The newly discovered retinal cell — which is highly sensitive to light — controls how the eye grows and develops. If the cell instructs the eye to grow too long, images fail to be focused on the retina, causing nearsighted vision and a lifetime of corrective glasses or contact lenses.

“The eye needs to stop growing at precisely the right time during childhood,” Schwartz said.

It has long been long known the retina contains a signal to focus the image in the eye, and this signal is important for properly regulating eye growth during childhood.

“But for years no one knew what cell carried the signal,” Schwartz said. “We potentially found the key missing link, which is the cell that actually does that task and the neural circuit that enables this important visual function.”

Schwartz named the cell, “ON Delayed,” in reference to its slow responses to lights becoming brighter. The cell was unique among many other cell types tested in its exquisite sensitivity to whether an image was in focus.

He described the neural circuit as the diagram that reveals how this cell is wired to other cells in the retina to acquire this unique sensitivity.

How too much time indoors may trigger myopia

The indoor light spectrum has high red/green contrast, which activates these clusters of photoreceptors in the human eye, creating the equivalent of an artificial contrast image on the retina. It’s likely the human version of the ON Delayed retinal ganglion cell would be overstimulated by such patterns, causing aberrant over-growth of the eye, leading to myopia, Schwartz said.

The study will appear in the Feb. 20 print issue of Current Biology. It was published online Jan. 26.

To conduct the study, Schwartz and co-author Adam Mani, a postdoctoral fellow in ophthalmology at Feinberg, used microscopic glass electrodes to record electrical signals from cells in a mouse retina while presenting patterns of light on a digital projector.

The next goal is to find a gene specific to this cell. Then scientists can turn its activity up or down in a genetic mouse model to try to induce or cure myopia.

The study is part of Schwartz’s larger body of research to reverse engineer the retina by identifying new retinal cell types in mice. The retina has about 50 types of retinal ganglion cells, which together convey all the information we use to perceive the visual world. Each of these cells provides different visual information — such as color or motion — about any point in space.

Schwartz, who is funded by the National Institutes of Health (NIH), wants to identify the new cells by their specific function, analyze their genetic signatures and understand how the cells are interconnected within the retina and to their targets in the brain. His research could lead to gene therapy to treat blindness and to improve the function of artificial retinal prosthetics.

The article is titled “Circuit Mechanisms of a Retinal Ganglion Cell with Stimulus-Dependent Response Latency and Activation Beyond Its Dendrites.”

Fish oil component helps damaged brain, retina cells survive, shows research

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Posted on 2nd May 2017 by Pacific ClearVision Institute in General |Retina

A team of researchers led by Nicolas Bazan, MD, PhD, Boyd Professor and Director of the Neuroscience Center of Excellence at LSU Health New Orleans School of Medicine, has shown for the first time that NDP1, a signaling molecule made from DHA, can trigger the production of a protective protein against toxic free radicals and injury in the brain and retina. The research, conducted in an experimental model of ischemic stroke and human retinal pigment epithelial (RPE) cells, is available in Advance Publication Online in Nature Research’s Cell Death and Differentiation.

Neuroprotectin D1 (NPD1) is a lipid messenger made from the omega-3 fatty acid docosahexaenoic acid (DHA) made on demand when cell survival is compromised. NPD1 was discovered and named in 2004 by Dr. Bazan and colleagues. Oxidative stress, resulting from the constant production of damaging free radicals, lays the groundwork for cell death. Cell death is accelerated by catastrophic events, like ischemic stroke, as well as neurodegenerative and blinding-eye diseases. The research team found that when systematically administered one hour after two hours of experimental stroke, NPD1 increased the production and availability of ring finger protein 146, which has been named Iduna. Iduna facilitates DNA repair and protects against a form of programmed cell death in stroke known as parthanatos by suppressing the production of a destructive protein called PARP. Their findings also include that NDP1 enhanced the production of Iduna and protection in two types of human RPE cells (ARPE-19 and primary RPE) undergoing uncompensated oxidative stress. The researchers found that the effect of NDP1 on Iduna activity peaked at six hours after the onset of the oxidative stress, A dose-dependent curve showed an increase of Iduna activity starting as 25 nM NPD1 in both types of human RPE cells. These results suggest that NDP1 selectively induces Iduna activity when uncompensated oxidative stress triggers the formation of NPD1 that in turn activates Iduna.

“These findings are significant because they show how NPD1, a lipid mediator made ‘on demand,’ modulates the abundance of a critically important protein (Iduna) toward cell survival,” notes Nicolas Bazan, MD, PhD, Boyd Professor and Director of the Neuroscience Center of Excellence at LSU Health New Orleans School of Medicine. “This protein, relatively little studied, turns out to be key for cell functional re-programing and subsistence.” DHA, found in fish oil, is an essential omega-3 fatty acid and is vital for proper brain function. It is also necessary for the development of the nervous system, including vision. A study from the Bazan laboratory published in 2011 found that DHA triggered the production of Neuroprotectin D1, a naturally occurring neuroprotective molecule in the brain derived from DHA. NDP1 bioactivity governs key gene interactions decisive in cell survival when threatened by disease or injury.

“The further unraveling of the molecular details of DHA-NPD1-Iduna expression signaling may contribute to possible therapeutic interventions for retinal degenerations and ischemic stroke.” says Bazan.

Research on retinal pigment epithelial cells promises new future treatment for glaucoma patients

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Posted on 2nd May 2017 by Pacific ClearVision Institute in General |Retina

Scientific research builds its own momentum as one discovery triggers another, building an ongoing wave of unexpected possibilities. In the world of glaucoma, such a surge began when advances in stem cell research opened doors experts had never imagined.

With this new perspective, they began to consider innovative ways to use specialized cells in the eye, like retinal pigment epithelial cells and ganglion cells. Today researchers continue to follow that path, knowing that each small step they take may lead to future glaucoma treatments.

What Are Retinal Pigment Epithelium (RPE) Cells?

Most people know at least a little about the retina. The retina is a thin tissue that’s about an inch in diameter, yet it contains all the photoreceptor cells responsible for beginning vision and their circuits that produce signals that become vision.

If you could look beneath the retina, you’d find a sheet of black cells called the retinal pigment epithelium, (RPE). The easiest way to describe the RPE is to say it supports the retina, but that doesn’t begin describe its value. These cells help by renewing the light-absorbing pigments contained in the rod and cone photoreceptors on a daily basis. They also enhance vision by absorbing scattered light. They ensure survival of photoreceptor cells by delivering nutrients, while also serving as a barrier that blocks damaging substances from getting into the retina. The RPE also stops free radicals before they can damage the retina.

The retinal pigment epithelial cells are shaped like a six-sided hexagon, so they fit together as tight as a puzzle. Tiny projections extend from RPE cells, reach out to cover photoreceptor cells and carry nutrients into the cells. When RPE cells are damaged, photoreceptor cells die, ultimately leading to blindness.

What do RPE Cells Have to do Glaucoma?

Glaucoma doesn’t typically damage RPE cells, but thanks to advances in stem cell research, it looks like RPE cells may play a crucial role in finding a cure to the degenerative disease. Experts have been studying stem cells for the last seven decades, but their time and effort is beginning to pay off.

Researchers discovered that mature stem cells from various places in the body can be removed and injected with a combination of genes that reprogram the adult cells back into their fresh embryonic state. These cells are called induced pluripotent stem cells. This has been put into practice in the lab, where adult stem cells taken from bone marrow were reprogrammed to grow into various eye cells.

When certain induced pluripotent stem cells are grown together with RPE cells, they can be reprogrammed to turn into photoreceptor cells and other retinal cells. It may even be possible to develop a group of protective nerve cells in the retina — retinal ganglion cells — that are damaged by glaucoma. While these amazing discoveries have yet to take shape as a viable treatment option for glaucoma, they certainly make it possible to believe that research using RPE cells may one day lead to a novel stem cell-based treatment that could stop or even reverse the progression of glaucoma.

A closer look at the eye: New retinal imaging technique

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Posted on 2nd May 2017 by Pacific ClearVision Institute in General |Retina

Researchers at the University of Rochester Medical Center have developed a new imaging technique that could revolutionize how eye health and disease are assessed. The group is first to be able to make out individual cells at the back of the eye that are implicated in vision loss in diseases like glaucoma. They hope their new technique could prevent vision loss via earlier diagnosis and treatment for these diseases.

In a study highlighted in the Proceedings of the National Academy of Sciences, Ethan A. Rossi, Ph.D., assistant professor of Ophthalmology at the University of Pittsburgh School of Medicine, describes a new method to non-invasively image the human retina, a layer of cells at the back of the eye that are essential for vision. The group, led by David Williams, Ph.D., Dean for Research in Arts, Sciences, and Engineering and the William G. Allyn Chair for Medical Optics at the University of Rochester, was able to distinguish individual retinal ganglion cells (RGCs), which bear most of the responsibility of relaying visual information to the brain.

There has been a longstanding interest in imaging RGCs because their death causes vision loss in glaucoma, the second leading cause of acquired blindness worldwide. Despite great efforts, no one has successfully captured images of individual RGCs, in part because they are nearly perfectly transparent.

Instead of imaging RGCs directly, glaucoma is currently diagnosed by assessing the thickness of the nerve fibers projecting from the RGCs to the brain. However, by the time retinal nerve fiber thickness has changed detectably, a patient may have lost 100,000 RGCs or more.

“You only have 1.2 million RGCs in the whole eye, so a loss of 100,000 is significant,” said Williams. “The sooner we can catch the loss, the better our chances of halting disease and preventing vision loss.”

Rossi and his colleagues were able to see RGCs by modifying an existing technology — confocal adaptive optics scanning light ophthalmoscopy (AOSLO). They collected multiple images, varying the size and location of the detector they used to gather light scattered out of the retina for each image, and then combined those images. The technique, called multi-offset detection, was performed at the University of Rochester Medical Center in animals as well as volunteers with normal vision and patients with age-related macular degeneration.

Not only did this technique allow the group to visualize individual RGCs, but structures within the cells, like nuclei, could also be distinguished in animals. If Rossi can achieve that level of resolution in humans, he hopes to be able to assess glaucoma before the retinal nerve fiber thins — and even before any RGCs die — by detecting size and structure changes in RGC cell bodies.

While RGCs were the main focus of Rossi’s investigations, they are just one type of cell that can be imaged using this new technique. In age-related macular degeneration, cone photoreceptors that detect color and are important for central vision are the first to die. AOSLO has been used to image cones before, but these cells were difficult to see in areas near Drusen, fatty deposits that are the most common early sign of the disease. Using their multi-offset technique in age-related macular degeneration patients, Rossi was able to assess the health of cones near Drusen and in areas where the retina had been damaged.

“This technique offers the opportunity to evaluate many cell classes that have previously remained inaccessible to imaging in the living eye,” said Rossi. “Not only RGCs, but potentially other translucent cell classes and cellular structures.”

Rossi and his colleagues warn that their study included a small number of volunteers and an even smaller number of age-related macular degeneration patients. More studies will be needed to improve the robustness of the technique and ensure their results are reproducible before it can be widely used in the clinic. Rossi is now setting up his own laboratory at the University of Pittsburgh and plans to continue working with Williams’ group in studying this technique and its ability to detect changes in retinal cells over the course of retinal diseases.

Brain diseases manifest in the retina of the eye

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Posted on 5th December 2016 by Pacific ClearVision Institute in General |Retina

Diseases of the central nervous system (CNS) may manifest as pathological changes in the retina of the eye. Research from the University of Eastern Finland (UEF) shows that retinal changes may be detected earlier than brain changes. Findings from mouse models suggest that eye examination could be used as a noninvasive screening tool for human brain diseases.

Retina, the light sensing tissue on the bottom of the eye, can be considered an integral part of the central nervous system (CNS). During fetal development, it matures from part of the brain and its innervation closely resembles that of the brain. Retinal structure and function can be readily examined with noninvasive or minimally invasive methods, whereas direct brain research has numerous limitations. If the health status of the brain could be indirectly assessed through the eyes, diagnostic screening of brain diseases could become more efficient.

In his Ph.D. project, Dr. Henri Leinonen investigated functional abnormalities of the retina using mouse models of human central nervous system diseases. Electroretinography (ERG) and visual evoked potentials (VEP) were chosen as research techniques, since similar methodology can be applied in both laboratory animals and humans. ERG can precisely track the function of retina using corneal or skin electrodes, whereas VEP measures the function of visual cortex. These methods were used to test different attributes of vision in three distinct genetically engineered mouse models of human CNS diseases. Furthermore, basic life science methods were used to test the correlation between functional abnormalities and the anatomical status of the retina.

Day and color vision associated retinal dysfunction was found in a mouse model of Huntington´s disease (HD), while the mouse was presymptomatic. Retinal structure remained relatively normal, even in an advanced disease state, although aggregation of toxic mutated huntingtin-protein was widespread in the diseased mouse retina. Although the retinopathy in mice is exaggerated compared to human HD patients, the finding is partly in line with patient data showing impaired color vision but no clear-cut anatomical retinopathy.

In a mouse model of Alzheimer´s disease (AD), researchers observed abnormality in night vision associated retinal function. Specifically, rod-mediated inner retinal responses to dim light flashes were faster in diseased mice than in their wild-type controls. The observation may be explained by impaired cholinergic neurotransmission that is also partly causative for the deterioration of memory in AD.

In a mouse model of late infantile neuronal ceroid lipofuscinosis (NCL), a pediatric neurological disease, the researchers described retinal degenerative changes that mimic the characteristic pathology of age-related macular degeneration (AMD). These included impaired function of retinal pigment epithelium and subsequent blindness due to photoreceptor atrophy and death. It has been postulated that the retinal degeneration in human patients progresses similarly.

The results add to the growing body of evidence that show pathological changes in the retina in addition to the brain in CNS diseases. Functional changes of the retina were found in three mouse models of human CNS diseases whose phenotype, age of onset and pathological mechanism clearly differ from each other. Visual impairment was the fastest progressive symptom in two models tested. The findings support the idea of eye examinations as potential screening tools for CNS diseases. Development of efficient, safe and economic screening tools for CNS diseases is imperative, since the diagnosis of these diseases is often obtained only in the advanced disease state when as such satisfactory remedies are poorly effective. Since eye and vision research can be conducted noninvasively, advancement of trials from the preclinical to the clinical phase could be relatively fast.

The findings were originally published in PLoS One, Journal of Alzheimer’s Disease, and Human Molecular Genetics.

Alzheimer’s disease proteins could be at fault for leading cause of vision loss among older people

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Posted on 5th December 2016 by Pacific ClearVision Institute in General |Retina

Research from the University of Southampton gives new insight into possible causes of Age-related Macular Degeneration (AMD), a leading cause of vision loss among people aged 50 and older.

The study, published in the journal Experimental Eye Research, discovered that a group of proteins, which are linked to Alzheimer’s disease, are able to accumulate in the retina and damage it.

The researchers hope that the discovery could lead to better treatments for patients.

AMD is a progressive disease that causes the death of the retinal photoreceptors, the light-sensitive cells at the back of the eye. The most severe damage occurs in the macula, a small area of the retina that is needed for sharp, central vision necessary for reading, driving and other daily tasks.

There are two different types of AMD — ‘wet’ and ‘dry’. In wet AMD, the growth of leaky blood vessels which damage the retina can be stopped.. However, this does not work for everyone, and is a way to manage rather than cure wet AMD. By contrast, dry AMD has no approved treatment as yet.

Dr Arjuna Ratnayaka, a Lecturer in Vision Sciences at the University of Southampton, who led the study, said: “We know that AMD is caused by a combination of genetic, environmental and lifestyle risk factors, but this novel discovery could open up new possibilities to understand how the aging retina becomes damaged. Such advances are important if we are to develop better AMD treatments in the future.

“AMD currently affects more than 600,000 people in the UK and 50 million individuals worldwide. This figure is expected rise significantly as our society grows older. We urgently need new treatments to stop people spending their twilight years in blindness.”

The study, which used both cell cultures and mouse models, analysed how quickly Amyloid beta proteins, which are thought to be a likely cause of Alzheimer’s disease, entered the retina and how they damaged it.

The team found that the Amyloid beta proteins entered the cells of the retina within 24 hours of exposure and then began to break the cell’s scaffold structure.

Dr Ratnayaka added: “The speed in which these proteins entered the retinal cells was unexpected. These findings have given some insights into how a normal healthy retina can switch to a diseased AMD retina. We hope that this could lead to designing better treatments for patients in the future.”

The research team’s next step will be to evaluate how the Amyloid beta proteins get into retinal cells and study more closely how damage occurs, with a view of establishing preventative measures or treatment options.

Woman who lost vision to diabetes shares experience to raise awareness

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Posted on 5th December 2016 by Pacific ClearVision Institute in General |Retina

It was Labor Day 2015 when Rosetta Ivey-Foster, a 76-year-old retired bank clerk, learned first-hand how quickly diabetes can deteriorate vision. Swift action restored most of her eyesight.

Diagnosed with type 1 diabetes more than 25 years ago, Ivey-Foster had carefully managed her disease. That included getting regular comprehensive dilated eye exams to detect early signs of diabetic eye disease, a group of conditions that includes diabetic retinopathy, cataract, and glaucoma. The National Eye Institute recommends that people with diabetes get a dilated eye exam at least once a year to detect early signs of diabetic eye disease.

A few days before Labor Day, Ivey-Foster noticed the sudden appearance of a floater in her right eye. “It looked like a blob or a water bubble,” she said, noting that she’d had floaters before, but they’d always disappeared after a couple of days. This one persisted. As she sat on her balcony to watch a local Labor Day air show with a neighbor, she realized something was terribly wrong with her vision. “I couldn’t see the planes!” she said.

Diabetes, a growing threat to vision

More than 25 million Americans have diabetes, and that number may double or triple by 2050. All people with diabetes are at risk for diabetic eye disease. African Americans, American Indians/Alaska Natives, and Hispanics/Latinos are at higher risk for losing vision or going blind from diabetic eye disease. Diabetic retinopathy poses the greatest risk to vision. It is the most common cause of vision loss among people with diabetes and the most common cause of blindness among working-age Americans. Over time, high blood sugar levels from diabetes affect the tiny blood vessels in the tissue in the back of the eye called the retina.

Timely treatment saved her vision

Ivey-Foster saw her eye doctor at once. Suber Huang, M.D., founder of the Retina Center of Ohio in Cleveland, discovered that Ivey-Foster could read none of the letters on the eye chart with her right eye. She had developed proliferative diabetic retinopathy, an advanced stage of the disease. New, abnormal blood vessels were growing on the surface of her retina and leaking blood — the cause of her floaters.

Huang treated Ivey-Foster’s right eye with a laser to burn and shrink abnormal blood vessels in the retina. He also removed the bloody gel-like fluid in her eye and replaced it with a clear saline solution, a procedure called vitrectomy.

“I was so relieved when he took the bandages off of my eye and I could see again,” Ivey-Foster exclaimed. By Labor Day 2016, Ivey-Foster had regained enough vision to again see the planes in the air show.

Studies stress controlling diabetes

“Well-controlled glycemia, or blood sugar level, has a positive, measurable, and lasting effect on eye health,” said Emily Chew, M.D., deputy director of the NEI Division of Epidemiology and Clinical Applications. In a recent study, she and colleagues found less diabetic retinopathy progression among people with type 2 diabetes who intensively controlled their blood sugar levels. “This study sends a powerful message to people with type 2 diabetes,” she said. The message also applies to people with type 1 diabetes.

For people who have diabetes, the NEI’s National Eye Health Education Program recommends these important steps to keep their health on TRACK:

• Take your medications as prescribed by your doctor.
• Reach and maintain a healthy weight.
• Add physical activity to your daily routine.
• Control your ABC’s — A1C, blood pressure, and cholesterol levels.
• Kick the smoking habit.

Ivey-Foster emphasized, “I would say to anyone that has diabetes, make sure you get regular eye exams.” In addition to early detection, her experience highlights the importance of timely treatment.

Research reveals new treatment options

Today, people like Ivey-Foster have an alternative to laser therapy. In 2015, the NEI-funded Diabetic Retinopathy Clinical Research Network showed that eye injections of the anti-VEGF drug Lucentis (ranibizumab) are highly effective in treating proliferative diabetic retinopathy. VEGF is what stimulates abnormal blood vessel growth and leakage in the retina. The finding was the first major treatment advance for proliferative diabetic retinopathy in 40 years.

In 2016, the DRCR.net reported results of a clinical trial that compared three anti-VEGF drugs for diabetic macular edema, a complication of diabetic retinopathy that causes the build-up of fluid in a region of the retina called the macula. The study found that Lucentis, Avastin (bevacizumab), and Eylea (aflibercept) were similarly effective when patients’ vision loss was mild. Eylea outperformed Avastin and Lucentis among patients who started treatment with moderate (20/50) or worse vision.

Zika and glaucoma linked for first time in new study

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Posted on 5th December 2016 by Pacific ClearVision Institute in General |Retina

A team of researchers in Brazil and at the Yale School of Public Health has published the first report demonstrating that the Zika virus can cause glaucoma in infants who were exposed to the virus during gestation.

Exposure to the Zika virus during pregnancy causes birth defects of the central nervous system, including microcephaly. Brazilian and Yale School of Public Health researchers had reported early during the microcephaly epidemic that the virus also causes severe lesions in the retina, the posterior portion of the eye. However, until now, there has been no evidence that Zika causes glaucoma, a condition that can result in permanent damage to the optic nerve and blindness.

“We identified the first case where Zika virus appears to have affected the development of the anterior chamber or front portion of the eye during gestation and caused glaucoma after birth,” said Dr. Albert Icksang Ko, professor at the Yale School of Public Health and co-author of the study published in the journal Ophthalmology. Ko has longstanding research collaborations in Brazil and has worked with local scientists since Zika first appeared in the Americas to better understand the birth defects that are caused by the virus and the risk factors for Zika Congenital Syndrome.

While conducting their investigations of the microcephaly epidemic in Salvador in Northeast Brazil, the researchers identified a three-month-old boy who was exposed to Zika virus during gestation. While no signs of glaucoma were present at the time of birth, the infant developed swelling, pain, and tearing in the right eye. The research team diagnosed glaucoma as the cause of symptoms and together with local ophthalmologists, performed a trabeculectomy, an operation that successfully alleviated the pressure within the eye.

While this is the first known incidence of glaucoma in an infant with the Zika virus, clinicians treating patients with Zika should be aware that glaucoma is another serious symptom of the disease that should be monitored, said the investigators. Additional research is needed to determine if glaucoma in infants with Zika is caused by indirect or direct exposure to the virus, either during gestation or postpartum.

The Zika virus, which is primarily transmitted through infected mosquitoes, has reached epidemic levels in several areas worldwide, and is of particular concern in Brazil, where the Pan American Health Organization reports more than 200,000 suspected cases and 109,000 confirmed cases of the disease. Since the outbreak began in 2015, Zika has now reached the United States, with more than 4,000 travel-related cases reported, and 139 locally acquired mosquito-borne cases confirmed, according to the CDC. There is currently no vaccine for the Zika virus.

Brain training video games help low-vision kids see better

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Posted on 5th December 2016 by Pacific ClearVision Institute in General |Retina

A new study by vision scientists at the University of Rochester and Vanderbilt University found that children with poor vision see vast improvement in their peripheral vision after only eight hours of training via kid-friendly video games. Most surprising to the scientists was the range of visual gains the children made, and that the gains were quickly acquired and stable when tested a year later.

“Children who have profound visual deficits often expend a disproportionate amount of effort trying to see straight ahead, and as a consequence they neglect their peripheral vision,” said Duje Tadin, associate professor of brain and cognitive sciences at Rochester. “This is problematic because visual periphery — which plays a critical role in mobility and other key visual functions — is often less affected by visual impairments.”

“We know that action video games (AVG) can improve visual perception, so we isolated the AVG components that we thought would have the strongest effect on perception and devised a kid-friendly game that compels players to pay attention to the entire visual field, not just where their vision is most impaired,” said Tadin, who is also a professor in the Center for Visual Science. “As a result, we’ve seen up to 50 percent improvement in visual perception tasks.”

Successful AVG players distribute and switch their attention across a wide area, while at the same time they remain vigilant for unexpected moving targets to appear, all while ignoring irrelevant stimuli.

The researchers created a training game with these specific task characteristics while eliminating other components of AVGs, such as the demand for speeded hand-eye coordination, and any violent or other non-child-friendly material.

Game Training

Twenty-four low-vision youths from the Tennessee and Oklahoma Schools For The Blind participated in the training experiment that appears in Scientific Reports. Pre-training screening showed that while most children had central visual acuity worse than the 20/200 legal blindness limit, they also underutilized their peripheral vision.

According to the study’s lead author, Jeffrey Nyquist, founder and CEO of NeuroTrainer, the students’ issues with the periphery were in part attentional.

Nyquist and the team hypothesized that training the students to pay more attention to their peripheral visual field could have quick results.

“We didn’t improve the kids’ hardware — these children have profound physical problems with their optics, muscles, and retina, and we can’t fix that,” said Nyquist. “But we could improve their software by training their brain to reallocate attentional resources to make better use of their periphery vision.”

The students were divided into 3 groups: a control group that played a Tetris-like game; a group that played a kid-friendly commercially-available AVG, Ratchet & Clank; and a group that used the training game devised by the researchers. All games were played on a large projection screen to better involve visual periphery.

The game the researchers developed has a dual-task component. Students tracked multiple moving objects simultaneously while being on the lookout for another object that briefly appears and requires a response from the player.

“The goal is to pay attention to a number of objects over a large area, and to be prepared to react to unexpected events in the even further periphery,” explained Tadin. “It forces the low-vision students to expand their visual field — to shift their attention to the neglected areas of the visual field.”

After a total of eight hours of training, groups who trained with the commercially-available AVG and the custom dual-task game showed significant visual improvements.

Improvements were seen in a range of visual tasks. The students were able to better perceive moving objects (motion perception) in the far periphery, they were able to better attend to visual crowding, such as identifying a specific letter within a field of other letters, and they were much faster at finding objects in cluttered scenes (visual search), like finding a stapler on a messy desk.

“We were surprised by the range of improvements, and we were even more surprised when we tested a few of the students a year later and found that the gains they made were stable,” said Nyquist. “Within just a few hours of training, they were able to expand their usable visual field and visual search ability.”

Nyquist notes that when the researchers began their work with the students, it was to assess how they maneuver around their environments. “But we quickly went from assessing to thinking ‘maybe we have something that can train them and improve their real-life abilities,’” he said. “When we realized that the students achieved up to 50 percent improvement in visual tasks, we were blown away.”