The eclipse of 21 August 2017 was, in the specific sense that matters to astronomers, an ordinary eclipse. It was total across a narrow band of the continental United States, from Oregon to South Carolina, and partial across the rest of the country. The public interest in it was, however, extraordinary. Tens of millions of people bought or borrowed protective eyewear. Millions more stepped outside and looked up at the sun anyway.

Among the people who stepped outside that afternoon was a 26-year-old woman in Staten Island, New York, named Nia Payne. She did not have protective eyewear. What she did have was the same set of instincts most human beings carry about looking at the sun, which is that you can glance at it for a fraction of a second without harm, and that the moment it becomes uncomfortable you look away. Her city was inside the zone of partial coverage. Approximately seventy per cent of the sun’s disc was hidden behind the moon.

She glanced up for about six seconds.

Then, uneasy, she borrowed what looked to her like a pair of eclipse glasses from someone nearby. They were not, on the subsequent assessment of the ophthalmologists who would examine her, the ISO-12312-2 certified filters the American Astronomical Society had spent months warning viewers to use. She then looked at the sun for another fifteen to twenty seconds through the inadequate glasses. By the time she went inside, her left eye already had a blurred area in the centre of her visual field. Over the next two days, the blurred area resolved into a specific and unmistakable shape. A crescent, positioned exactly where the moon had been when she had glanced at it, sitting in the middle of everything she tried to look at.

What was happening at the back of her eye

According to the peer-reviewed case report published in JAMA Ophthalmology in December 2017 by Chris Y. Wu, Michael E. Jansen, Jorge Andrade, Toco Y.P. Chui, Anna T. Do, Richard B. Rosen and Avnish Deobhakta at the New York Eye and Ear Infirmary of Mount Sinai and the Icahn School of Medicine at Mount Sinai, titled “Acute Solar Retinopathy Imaged With Adaptive Optics, Optical Coherence Tomography Angiography, and En Face Optical Coherence Tomography”, Payne presented at Mount Sinai several days after the eclipse. Her visual acuity was 20/20 in her right eye and 20/25 in her left, which by clinical standards was relatively mild degradation. What her subjective experience described, however, was much worse. In the centre of her vision, the crescent-shaped scotoma sat over anything she tried to read, focus on, or recognise.

What the ophthalmologists were looking for, and what they found, was damage to the photoreceptor layer at the back of her retina. The retina is the thin sheet of specialised neural tissue lining the inside of the eyeball. Its outer layer consists of the photoreceptors, meaning the individual cells that respond to light. Rods handle low-light and peripheral vision. Cones handle colour and fine detail, and are concentrated most densely in a small central region called the fovea, which is the specific patch of tissue you use every time you look directly at something.

Solar retinopathy is what happens when photoreceptors are exposed to concentrated sunlight for long enough to be damaged by two overlapping mechanisms. The first is straightforward thermal injury. The lens of the eye focuses incoming light onto the retina, and when the incoming light is sunlight, the focused point is bright enough to raise the temperature of the tissue at that point above the level cells can tolerate. The second, and typically the more damaging one, is a photochemical process. Ultraviolet and short-wavelength visible light contain enough energy per photon to break specific molecular bonds inside the light-sensitive proteins of the photoreceptor cells, producing free radicals that damage surrounding structures even at temperatures below the thermal threshold. Photoreceptors, once destroyed, do not regenerate. The tissue does not grow back.

To learn more about what happens to us during a solar eclipse, watch this video we recently made:

The drawing and the imaging that matched it

What the Mount Sinai team asked Payne to do, when she first arrived at their clinic, was to draw what she was seeing. Not describe. Draw. On a piece of paper, using ordinary pen and pencil, she reproduced the shape of the blind area sitting in the centre of her vision. What she drew, on the surviving contemporary record, was a crescent. Specifically, a crescent oriented the way the partial eclipse had been oriented when she had glanced at the sun on 21 August. The concave curve of the moon’s disc, imprinted on the visual field of a person who was no longer looking at the sun, staring back out at her from the middle of everything she tried to look at.

The next step, on the primary-source record of the case report, was to look inside her eye and see whether the damage there matched the shape she had drawn. The clinicians used a technique called adaptive optics scanning light ophthalmoscopy, which is a high-resolution imaging method that corrects for the small imperfections in the shape of a person’s own cornea and lens in real time, allowing the retina to be photographed at cellular resolution. The technology was originally developed for astronomy, to correct for atmospheric turbulence when photographing distant stars. Adapted for medical imaging, it lets clinicians see individual photoreceptor cells inside a living human eye.

What the imaging revealed, on the JAMA Ophthalmology figures accompanying the case report, was a region of destroyed photoreceptors in the central retina of Payne’s left eye, and a milder version of the same pattern in her right. The destroyed region, in both eyes, was crescent-shaped. Its orientation matched, within the small tolerances of biological variation, the specific orientation of the drawing Payne had produced. The imaging matched the sketch, and the sketch matched the eclipse.

According to the Mount Sinai Hospital’s own official statement on the case, released alongside the JAMA publication in December 2017, Dr Avnish Deobhakta, the study’s senior author, described the correspondence between the drawing and the imaging as unusually direct. What was visible in the adaptive optics scan was the specific imprint of a physical process the eye’s own optics had performed on itself. The lens had focused the crescent of visible sun onto the specific area of retina where the crescent had landed, and the light had destroyed the cells at that specific location, and the pattern of destruction had appeared in Payne’s vision as the same crescent she had originally been looking at, only inverted, sitting between her and everything she now tried to see.

Payne’s condition, on the peer-reviewed literature covering the years since, has neither materially worsened nor improved. Solar retinopathy has no treatment. Photoreceptors do not regenerate. She has, over the years since the eclipse, retrained herself to use her right eye as dominant. Reading remains difficult. Screens require close proximity. And in the centre of her vision, on any bright surface she looks at, the small pale crescent she drew for the doctors at Mount Sinai in the autumn of 2017 continues to sit exactly where it always was, doing exactly what the case report predicted it would keep doing, quietly, for the rest of her life.

Kiran Athar is not an ophthalmologist or a medical researcher. She writes about science, medicine, and the ordinary corners of modern life where the two intersect, drawing on peer-reviewed research and primary-source scholarship.