Stories about: Ophthalmology

Can virtual reality headsets save vision in people with lazy eye?

Luminopia amblyopia virtual reality
IDHA’s Matt Murphy tries out Luminopia’s VR headset with Dean Travers (photo: Greb Weintraub)

Three to five percent of the population has amblyopia, a.k.a. lazy eye, in which a healthy eye never “learns” to see because isn’t used. This usually happens because of a focusing problem or subtle misalignment of that eye. The brain learns to ignore input from that eye, and unless this is noticed early, it weakens and can slowly go blind.

“When I can diagnose amblyopia early enough, I can treat it with an eye patch or eye drops to block the ‘good’ eye,” says David Hunter, MD, PhD, chief of ophthalmology at Boston Children’s Hospital. “This gives the eye with amblyopia time to catch up.”

Unfortunately, eye patching doesn’t work well at older ages, and kids hate the socially stigmatizing patches, which often need to be worn for more than a year. As Dean Travers, cofounder of Luminopia, put it at Boston Children’s Hospital’s Innovators’ Showcase last week, “Being a pirate isn’t cool for very long.”

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StrabisPIX: Assessing strabismus from patients’ smartphone photos

strabismus smartphone
(Lapina/Shutterstock)

New smartphone-based diagnostic tools are enabling consumers to take their temperatures, diagnose simple skin conditions and much more. As advanced smartphone imaging puts more and more capabilities in patients’ hands, it’s no surprise that clinicians and numerous digital health startups are leveraging them.

As a case in point, the Department of Ophthalmology and the Innovation & Digital Health Accelerator (IDHA) at Boston Children’s Hospital have co-developed a smartphone application for patients with strabismus, or misalignment of the eyes, to securely capture and transmit photos of their eyes to their providers.

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Age-related macular disease: Is energy starvation a cause?

age-related macular degneration
Hunger distress signal: Energy-starved photoreceptor cones in the retina (colored blue) call for nourishment by releasing a cloud of vascular endothelial growth factor (VEGF; in yellow). The VEGF draws poor-quality, leakage-prone blood vessels (in red), branching from a nearby blood supply. (Image: Jean-Sebastien Joyal)

New insights could potentially change the treatment of two diseases causing blindness: “Wet” age-related macular degeneration (AMD), the leading cause of severe vision loss in Americans over 60, and a less common condition called macular telangiectasia (MacTel) that occurs in middle age.

Both diseases are caused by abnormal growth of misshapen, leaky blood vessels in the eye that damages the macula, the central part of the retina needed to for straight-ahead vision.

The trigger for this pathologic process had been widely thought to be oxygen deprivation. However, findings published today by Nature Medicine suggest another cause: dysfunctional energy metabolism in the eye that starves the retina’s photoreceptors of fuel.

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Blocking bad vessels: A new target for retinopathy, macular degeneration

blood vessels retinopathy

The development of blood vessels is a part of normal growth in almost all tissues. But it can also be pathological: Many eye conditions leading to blindness involve abnormal blood vessel formation, including retinopathy of prematurity in infants, diabetic retinopathy and wet, age-related macular degeneration (AMD).

Blood vessels produced under stress conditions such as inflammation or low oxygen, especially in the retina, are apt to be poorly constructed and leaky. Vascular endothelial growth factor, or VEGF, has been shown to contribute to pathologic vessel growth, and anti-VEGF treatments are now widely used to control the overproliferation of blood vessels, such as Lucentis for wet macular degeneration.

Unfortunately, VEGF-binding antibodies can block not just excess VEGF but the baseline normal amount needed for vessels and neighboring neurons to survive, with potentially serious side effects.

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Telemedicine brings expert blindness screenings to preemies

ROP screening in the NICU
Gretchen Hamn (L) and Margie Young screen a premature infant for retinopathy of prematurity. (Photos: Katherine C. Cohen)

We’re in the Neonatal Intensive Care Unit at South Shore Hospital. Six tiny, swaddled preemies are ready to be examined, their eyes numbed and their pupils dilated with special drops.

Gretchen Hamn, NNP, and medical assistant Margie Young go from isolette to isolette. Young tends to the first baby and gently positions him for his exam. Hamn pulls over a cart and extends a kind of hose with a camera at the tip. This she places directly on each of the baby’s eyes, taking a digital video of his retinas.

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First light: Vision restored in blind mice

Regenerating nerve fibers from the retina (shown in red) are seen coming into the dorsal lateral geniculate nucleus, a principal visual relay area of the brain.

Some kinds of vision loss are reversible: Lucentis and Avastin can restore some visual acuity in macular degeneration, and gene therapy in the eye has had success in genetic forms of blindness like Leber’s hereditary neuropathy, affecting light receptors in the retina. But when the optic nerve is damaged – from a traumatic injury or from glaucoma — all bets are off. The eyes may take in visual information, but it can’t get to the brain. It’s the end of the road.

Larry Benowitz, PhD, and other neurobiologists at Boston Children’s Hospital and elsewhere have tried for years to rebuild that road. Regeneration of the optic nerve, and in the central nervous system in general, was once thought impossible. But through patient tinkering to coax natural growth signals and silence growth-inhibiting signals, neurons in the retina – known as retinal ganglion cells — began to grow a bit into the optic nerve. Then a bit more.

In a 2010 paper, Benowitz’s team combined their top three interventions, and showed a synergistic effect – the greatest growth of optic nerve fibers (axons) to date. But no one had been able to demonstrate recovery of vision after severe optic nerve damage – until now.

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The neurology resident that could

Eye muscles, the nerves that control them, and where things go wrong (click to enlarge)

Elizabeth Engle used to wait in peoples’ driveways until midnight, hoping to enroll them in her genetic studies of eye-movement disorders. She landed there by chance: during her neurology residency, she saw a little boy whose eyes were frozen in a downward gaze. Wanting to find a solution to a disorder that others had written off, she talked her way into the muscular dystrophy genetics lab of Alan Beggs and Lou Kunkel at Children’s.

Why muscular dystrophy? That tragic muscle-weakening disease somehow spares the eye muscles. Engle thought if Beggs and Kunkel took her on, she could answer two questions at once – what was protecting the eye muscles in muscular dystrophy, and what had caused the little boy’s fixed gaze and droopy eyelids. Plus, she needed laboratory training to study the samples she’d started gathering. “I didn’t have a PhD and was never officially trained in the lab,” she once said. “I didn’t even know how to make chemical solutions.”

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A simple screening test that could save children’s vision

Hunter hopes to make amblyopia screening routine for all preschoolers.

Children with “lazy eye,” or amblyopia, have structurally intact eyes that may appear normal. But one eye isn’t used, generally because of a subtle misalignment. Unless someone notices this early enough, the “lazy” eye can slowly go blind, simply because the brain hasn’t received proper stimulation from it. It’s learned to ignore input from that eye.

“While amblyopia is easy to treat if you get to the kids early, it’s hard for us as ophthalmologists to get to the kids early because often the condition isn’t detected in the pediatric office,” says David Hunter, chief of ophthalmology at Children’s Hospital Boston.

Treatment consists of patching the sound eye, forcing the child to use the weaker eye. Ideally, this should be started before age 5, when the brain is still able to relearn; once a child reaches 8 to 10 years it’s often too late to restore his vision.

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Alzheimer’s drugs for “lazy eye”?

When my parents told me I should walk around with my right eye patched like a pirate—on regular days, not just Halloween—I wondered if they were joking. They weren’t: those really were the doctor’s orders.

As a child, I had amblyopia, or “lazy eye”: my left eye had much poorer vision than my right eye. The eye itself was fine, but my brain wasn’t processing information coming from it. The plan was, by patching the “good” eye, to force my brain to use inputs from the amblyopic eye.

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