Issuu

LETTER TO READERS

THE GHOST IN

THE CHART Dear Readers, Welcome to our spooky (and brilliantly insightful) Halloween issue of COOKIE Magazine for Clinical Optometry—where we ask a haunting question: What exactly are we seeing when we “see”? This month, we celebrate the fact that vision is as much a brain story as an eye story, stitched together from sensation, interpretation, attention and prediction. When any part of that system falters, the results can be astonishing: eerie, confusing and sometimes clinically deceptive. In our cover story, we explore how patients may pass every eye chart with perfect acuity, yet still struggle to recognize faces or everyday objects, or even realize their own blindness. The eye may deliver the signal, but the brain decides what that signal means. Optical clarity on a chart does not always equal visual ability in real life… and that distinction matters at the chairside. This theme—Spooky Eyes & Optical Illusions—threads through our other articles, each designed to sharpen your diagnostic instincts while keeping a little wonder in the room. We take a guided tour through:

The optics behind classic “optical” illusions and why they work on the visual system the way they do. The ongoing quest to understand low-vision outcomes through our profile of Dr. Alex Bowers. We also look at modern tools and their limits: what VR can and can’t do for amblyopia, and where evidence should guide enthusiasm. Then we move from “tricks” to clinical realities with features on Charles Bonnet syndrome, transient vision loss and the critical optometrist’s role in traumatic brain injury—when visual symptoms can reflect something more than eye disease. So yes—this month has optical tricks, visual puzzles and moments that make you blink twice. But behind the Halloween atmosphere is a serious clinical message: don’t stop at the chart, and don’t assume that a “normal” visual acuity automatically means normal vision. Keep your differential broad, your questions open-ended and your exam eyes—wide awake.

The evolutionary design of different pupil shapes in the animal kingdom and what those forms can teach us about function. Entoptic phenomena: what’s normal, what’s expected and when “floating lights” should prompt further evaluation. Diagnosing true diplopia versus illusory doubling (because not all double vision is created equal).

Best, Dr. Carmen Abesamis-Dichoso OD, MAT, FPCO, FIACLE, FBCLA, FAAO

ISSUE

In this

COVER STORY

COOL OPTOMETRY

The Eye That Doesn’t Lie Perfect vision meets a deceived brain

6 The Sinister Slit

What pupil shape reveals about how predators and prey see

That Go Bump 8 Things in the Vitreous Entoptic phenomena and when to worry

OPTICS

KUDOS

Double, Double, Toil and Trouble Diagnosing true diplopia vs. illusory doubling

Anatomy of an Illusion The optics behind the classics

20 Seeing What Isn’t There What lurks in the peripheral vision

INNOVATION

ENLIGHTENMENT

Ghosts, 27 Seeing Saying Nothing When vision loss conjures apparitions, faces and phantom scenes

23 Masked Vision

What VR can and can’t do for amblyopia

First Stop, Not Last Why optometry needs a central role in traumatic brain injury care

NOVEMBER 2026

30 Trick or TIA?

When transient vision loss wears a costume

ADVISORY BOARD MEMBERS

DR. CARMEN ABESAMIS-DICHOSO Abesamis Eye Care & Contact Lens Center Manila, Philippines carmen.dichoso@gmail.com

Matt Young CEO & Publisher Gloria D. Gamat Chief Editor

DR. PURVI THOMSON OCL Vision London, United Kingdom purvi@oclvision.com

DR. KRISTIE NGUYEN Dr. Feenstra and Associates Dr. Kristie Nguyen PLLC, Floria, USA kristie817@gmail.com

DR. LI LIAN FOO Singapore National Eye Centre (SNEC) Singapore drfoolilian@gmail.com

DR. MONICA CHAUDHRY Learn Beyond Vision New Delhi, India monica.rchaudhry@gmail.com

DR. MARIA SAMPALIS Sampalis Eyecare Cranston, Rhode Island, USA

Diana Truong Managing Editor Andrés Pacheco Art Director Chris McBride Editorial Creative Lead Nhat Vo Olivia Gunawan Yura Yu Graphic Designers Artwork credits to: Andrés Pacheco, Chris McBride, Lieu Truong, Nhat Vo, Olivia Gunawan, Thoi Le, Yura Yu Writers Chow Ee-Tan Hazlin Hassan Kendra Bruning Marhiel Garrote Michaela Perez Sam McCommon Tan Sher Lynn Ruchi Ranga Societies Relationships & Conference Manager

Society Friends

msampalis@hotmail.com

International Business Development Brandon Winkeler Robert Anderson Sven Mehlitz

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COOL OPTOMETRY

WHAT PUPIL SHAPE REVEALS ABOUT HOW PREDATORS AND PREY SEE Why does a cat need a slit while a goat needs a band? The answer lies in the visual challenges posed by stalking prey, spotting predators and navigating life at ground level. By Marhiel Garrote

There is something unsettling about a cat staring back at you through a narrow vertical slit. In bright light, when the pupils collapse into little more than a black line, the eye looks almost engineered for a Halloween poster. But the slit isn’t there for theatrical effect. Across the animal kingdom, pupils come in strikingly different shapes: vertical slits in many ambush predators, horizontal bands in grazing animals and the familiar circle in humans. Research led by Prof. Martin Banks (United States) of the University of California, Berkeley, suggests these differences are closely tied to the visual problems each animal needs to solve.* That makes the pupil more than an aperture regulating how much light reaches the retina. Its shape can influence depth of field, the pattern of blur and even how useful certain visual cues become. So the next time a black cat crosses your path and fixes you with that eerie slit, consider what problem that shape evolved to solve. Sometimes a very small opening offers a surprisingly wide view of how vision works. LYING IN WAIT The easiest way to understand a slit pupil is to borrow a lesson from photography. “The bigger the pupil, the shorter…the depth of field,” Prof. Banks explained. With a large pupil, objects at one distance may be sharp while nearer and farther objects blur. Make the pupil smaller, and the range that stays relatively sharp increases. A vertical slit is narrow horizontally but tall vertically, so its optical effects depend on orientation. Prof. Banks and his team proposed that this design is particularly useful for ambush predators, animals that wait motionless before striking rather than chasing their prey down.* The catch is movement. “They can’t move much because the prey will see them and run away,” Prof. Banks said. “So they have to sit there and decide how far away the prey is, and they have to know that pretty accurately to make an accurate strike.”

Their hypothesis combines two sources of distance information. The first is stereopsis, in which the brain estimates depth from differences between the images reaching the two eyes. Because the eyes are separated horizontally, vertical contours are particularly useful for detecting that horizontal disparity. The second is blur. “We think they use blur to estimate the distance of horizontal contours and they use stereopsis to measure the distance of vertical contours,” he said. “That pupil design is ideal for that.” The vertical slit, in other words, may help an animal answer one crucial question: Can I make that jump? Height matters too. According to Prof. Banks, vertical pupils are more useful in shorter predators, whose eyes sit closer to the ground. “The taller you are, the more you look down on the scene, and this blur effect becomes less and less useful,” he explained. EYES IN THE BACK OF THE HEAD Now flip the problem. An ambush predator needs to know exactly where its next meal is. A grazing animal needs to make sure it doesn’t become one. In sheep and goats, the eyes sit on the sides of the head and the pupils stretch horizontally. Rather than optimizing for a close-range strike, their visual system favors surveillance across the ground.* “We think it’s really important for those animals to see all around them because they’re worried about predators approaching them from any angle,” Prof. Banks said. The horizontal pupil helps maintain useful vision in front of and behind the animal, particularly along the ground, where an approaching predator is most likely to appear.* Then things get stranger. When a goat lowers its head to graze, its pupils do not tilt with its skull. The eyes rotate to keep the pupils aligned with the ground.

“If the eye went with the head—doesn’t rotate—then the horizontal pupil would become vertical relative to the ground,” Prof. Banks explained. “So the usefulness would go away.” This, he noted, is the finding people tend to find most surprising. “These animals are rotating their eyes by 40°,” he said. “It’s a huge amount.” Humans, by comparison, can produce only small movements of this kind. What makes it all the more remarkable is how ordinary these animals are. Sheep, goats, horses and cattle have been hiding this in plain sight all along, subtly performing an eye movement most of us never notice. COMING FULL CIRCLE Which brings us back to our own eyes. Next to the vertical slit of a cat or the horizontal band of a goat, the human pupil looks remarkably plain. Plain, however, is not the same as inferior.

“The circular pupil is good for general purpose,” he said, “and not specifically designed for one particular niche.” There is no single ideal shape. The vertical slit, the horizontal band and the human circle solve different optical problems because their owners lead very different visual lives.* So the next time a black cat crosses your path and fixes you with that eerie slit, the interesting question isn’t why its pupil looks different from ours. It’s what problem that shape evolved to solve. *Banks MS, Sprague WW, Schmoll J, Parnell JAQ, Love GD. Why do animal eyes have pupils of different shapes? Sci Adv. 2015;1(7):e1500391.

CONTRIBUTOR

“A circular pupil makes you equally able to see sharp images for verticals and horizontals,” Prof. Banks explained. Humans are also too tall to make use of the ground-based blur cue available to shorter predators.

Prof. Martin Banks Professor of Optometry and Vision Science at the University of California, Berkeley. martybanks@berkeley.edu

This content is intended exclusively for healthcare professionals. It is not intended for the general public. Products or therapies discussed may not be registered or approved in all jurisdictions, including Singapore.

NOVEMBER 2026

COOL OPTOMETRY

THINGS THAT

GO BUMP IN THE VITREOUS

ENTOPTIC PHENOMENA AND WHEN TO WORRY Patients swear they’ve seen worms, webs and lightning. Most are vitreous debris in costume, but a few are retinal detachments in disguise. By Hazlin Hassan

A black worm wriggles across the vision field. A spider web drifts wherever the eye moves. Tiny sparkling dots dance against a blue sky. A streak of blue-white lightning flashes at the edge of vision in a darkened room.

THE MOST FREQUENT VISITOR The classic entoptic phenomenon is the floater. With age, the vitreous gradually liquefies, and the opacities that form within it become the drifting shapes patients describe.

It sounds like the opening scene of a horror film, and to some patients, it feels like one.

“Floaters, or muscae volitantes in Latin, are caused by shadows cast on the retina by opacities in the vitreous gel in front of it, usually comprising vitreous fibril condensations or cells,” said Prof. Dr. Mae-Lynn Catherine Bastion of the National University of Malaysia.

To the ophthalmologist, the explanation is usually far more earthly. These are entoptic phenomena, visual effects generated by structures within the eye itself. The vitreous gel, the retinal vasculature and even mechanical stimulation of the retina can all produce images with no external object behind them. Most are harmless. Occasionally, though, a familiar-looking phenomenon is the first clue to sight-threatening disease.

The Latin translates, rather aptly, as “flying flies.”

LIGHT SHOWS, NO LIGHT REQUIRED A phosphene is the perception of light without light entering the eye. Firm pressure on closed eyelids, for instance, produces shimmering patterns or bursts of color through mechanical

stimulation of the retina. Other forms of stimulation can have the same effect. Its clinically more important cousin is photopsia: flashes or streaks of light with no external source. These can occur when vitreous movement exerts traction on the retina, particularly during posterior vitreous detachment (PVD).

A GLIMPSE OF THE EYE’S OWN PLUMBING The Purkinje tree is an entoptic image of the viewer’s own retinal vasculature, “the shadow of one’s own blood vessels, visible when light is shone at a certain angle through the closed or open eye,” said Prof. Bastion. The blue-field entoptic phenomenon, meanwhile, produces tiny bright dots darting across a blue background. Research indicates these correspond to white blood cells traveling through the retinal capillaries. In other words, that vmysterious swarm of lights is nothing more exotic than the body’s own circulation. So if these structures are always present, why aren’t they obvious to everyone all the time? “This is difficult to explain,” said Prof. Bastion, “Some patients are aware whilst others have learned to ignore them after a long period of time.”

WHEN THE GHOST IS A WARNING The key clinical question is not only what the patient sees, but when it started and what came with it. Prof Bastion’s advice is in line with the American Academy of Ophthalmology guidance1: “New f lashes and sudden increase in f loaters, including red floaters, should have an urgent ophthalmologist check-up. A visual field defect accompanying these may mean an emergency because the retinal detachment can quickly involve the central vision (macula).” History matters too. Myopia, ocular trauma and previous intraocular surgery all raise suspicion of PVD and retinal detachment. Red f loaters preceded by f lashes, with an accompanying field defect, may indicate rhegmatogenous retinal detachment. Pain, redness, discharge or reduced vision can point towards serious disease such as posterior uveitis. On examination, Prof. Bastion advised, assess the vitreous for blood, white blood cells or abnormal cells, and examine the retina from the posterior pole to the periphery, noting any macular swelling or retinal vascular involvement. If a detachment is present, document whether the macula is involved, locate the causative break and exclude other types of detachment.

“I use an eye model to explain the cause of the floaters, namely that the gel has undergone degeneration resulting in vitreous opacities that cast a shadow on the retina,” she shared. She also asks patients to draw what they see and, where possible, uses imaging of the posterior hyaloid to show how a Weiss ring or other opacity matches their description. That conversation can turn an apparently supernatural experience into understandable anatomy. For patients whose persistent floaters affect their quality of life, options include observation, YAG laser vitreolysis in selected cases, and pars plana vitrectomy. The evidence for YAG vitreolysis is encouraging, with a randomized trial in symptomatic Weiss-ring floaters finding greater subjective improvement with YAG than with sham treatment.2 “The biggest misconception is that a patient has to put up with disturbing floaters and must get used to them. On the contrary, we have effective and relatively safe treatment options available for them,” said Prof. Bastion.

THE GHOST THAT FADES “A long-standing floater that is not disturbing and present for a long time usually does not have a sinister cause,” she cautioned. “Floaters that are more recent should be checked by an ophthalmologist.” Most of the ghosts patients report are just passing through. The skill lies in spotting the one that means it’s time to turn on the lights, and dilate.

REFERENCES 1.

Gudgel D. Flashes of Light. AAO; EyeSmart. April 5, 2024. Accessed on September 30, 2026. 2. Shah CP, Heier JS. YAG laser vitreolysis vs sham YAG vitreolysis for symptomatic vitreous floaters: a randomized clinical trial. JAMA Ophthalmol. 2017;135(9):918-923. CONTRIBUTOR

UNMASKING THE GHOST Prof. Bastion has developed a practical approach after seeing a patient who feared their symptoms were paranormal visions or hallucinations.

Prof. Dr. Mae-Lynn Catherine Bastion Professor at the Department of Ophthalmology, National University of Malaysia (UKM). mae-lynn@ppukm.ukm.edu.my

NOVEMBER 2026

OPTICS

Double, Double, Toil and Trouble DIAGNOSING TRUE DIPLOPIA VS. ILLUSORY DOUBLING Most double vision is harmless. Some are an aneurysm or a stroke in disguise. Here’s how to unmask the dangerous few before they slip out your door. By Michaela Perez

Diplopia is, quite literally, a problem that comes in pairs. The patient sees two of everything. Now you have to decide, quickly and correctly, whether you’re looking at a refractive nuisance you can fix in the chair or a vascular emergency that needs to leave your office ASAP. That call matters more than you might think. In the United States, diplopia is the chief complaint in 850,000 medical consultations a year, and in one study, 16% of those patients had a potentially life-threatening underlying condition.1 The good news? The whole work-up starts with one simple question. ONE QUESTION TO SPLIT THE DOUBLE Cover one eye. Does the double vision go away? If it does, the diplopia is binocular, and the visual axes are out of alignment. 2,3 If the ghost image sticks around, the

diplopia is monocular, and the cause is almost always inside the eye itself.1-3 That single answer sets your entire path and tells you how worried to be. Monocular diplopia is annoying, but it isn’t dangerous. Binocular diplopia, on the other hand, can be.1 THE MONOCULAR BRANCH When the doubling won’t go away with one eye covered, start your search close to home. Uncorrected astigmatism and cataract are the most common culprits.1,3 Dry eye can cause doubling that comes and goes, usually getting worse as the day wears on. Corneal irregularities such as keratoconus, post-surgical changes and scarring create more persistent aberrations. Poorly fitted contact lenses, iris abnormalities, vitreous opacities and macular disorders round out the list.3

The pinhole test makes a handy first filter. If the image improves through a pinhole, you’re dealing with an optical cause, either refractive error or a media irregularity. Many of these are yours to treat with glasses, contact lenses or artificial tears. When cataract is the culprit, refer for surgical evaluation. If the pinhole doesn’t help, look for a non-optical cause inside the eye, and refer when what you find calls for a specialist.3 THE BINOCULAR BRANCH If covering one eye makes the double disappear, you’re looking at a misalignment problem. This is where things can get scary, because the causes run all the way from a harmless decompensated phoria to a posterior circulation stroke. Decompensated latent strabismus and cranial nerve palsies account for about 70% of cases. Orbital, brainstem and cerebellar diseases make up much of the rest.1 Your best tool here is a good history. When did it start? Sudden diplopia, especially on waking, leans vascular. Gradual onset or a shifting pattern points toward something compressive.2,3 Which way are the images split? Horizontal doubling implicates the horizontal recti or cranial nerve VI. Vertical or oblique doubling points to cranial nerve IV, the vertical recti or thyroid eye disease. Torsional doubling suggests cranial nerve IV palsy or lateral medullary syndrome.3 When is it worst? If the doubling creeps in through the afternoon and eases with rest, think myasthenia gravis. If it’s worst first thing in the morning, think thyroid eye disease.3

Decompensated phoria is the most common cause of all. It typically shows up as horizontal, intermittent diplopia, brought on by fatigue or illness. Ask about a longstanding squint, then pull out the alternating cover test to reveal the latent deviation.1 WHEN THE BRAIN CONJURES THE DOUBLE Before you write off a strange presentation as functional, consider whether the doubling is coming from the brain. Lesions of the primary or secondary visual cortex can produce multiple images. These lesions are most often caused by occipital infarction, tumor or migraine, and the images may appear in one eye or across the entire visual field.3 They can tile, shimmer or even linger with the eyes closed, and they often travel with a hemianopia or other posterior circulation signs. These are the true phantoms of diplopia, conjured by the brain rather than the eye. So when a patient describes visual disturbance that is bilateral, bizarre or doesn’t clear up neatly with occlusion, think posterior circulation and refer promptly. RED FLAGS THAT CAN’T WAIT Refer urgently for neuroimaging1-3 , typically through the emergency department, for: • • • • • •

Acute binocular diplopia with headache A third nerve palsy with pupil involvement New diplopia with any neurological sign Diplopia with papilledema Rapidly progressive diplopia without a clear benign cause Any new diplopia in a child

And if your patient mentions headache, a droopy lid, facial numbness or limb weakness, stop and act fast.

THE LAST WORD

THE MASQUERADERS Some conditions show up in costume, imitating something else entirely.

Start there, and the rest of the mystery unravels, no crystal ball required.

Myasthenia gravis is the master of disguise. It can pass for almost any cranial nerve palsy, with fatigable, variable diplopia and, frequently, ptosis. The giveaway is that the pupils are always normal.3

Cover one eye. Does it go away?

REFERENCES 1.

The ice test, which is highly sensitive and specific, is a quick way to unmask it in the chair. Hold ice on the droopy eyelid for five minutes. If the ptosis improves by more than 2 mm, the test is positive.3 Thyroid eye disease usually targets the inferior rectus, which causes vertical diplopia and a chin-up head posture.3 Here’s the trick: thyroid function tests are often normal. Autoimmune markers, including TSI and thyroid peroxidase antibody, are more informative, so mention them when you refer to the patient.3

Lagrèze WA, Lischka T, Eckstein A, Oeverhaus M, Dieterich M, Strupp M. The differential diagnosis of diplopia. Dtsch Arztebl Int. 2026;123:367-374. 2. Jalilov N, Ismoilova SD. Binocular and monocular diplopia: differential diagnosis. Int J Artif Intell. 2026;6(2):962-969. 3. Iliescu DA, Timaru CM, Alexe N, et al. Management of diplopia. Rom J Ophthalmol. 2017;61(3):166-170.

NOVEMBER 2026

OPTICS

ANATOMY OF AN

ILLUSION THE OPTICS BEHIND THE CLASSICS

Grey spots that aren’t there, straight lines that lean, and two equal lines that refuse to measure up. Vision scientists explain what classic illusions reveal about the processing between retina and cortex, and why it matters for the patient in your chair. By Tan Sher Lynn

Look at a Hermann grid and ghostly grey spots appear where none exist. Stare at a Café Wall pattern and perfectly parallel lines start to lean. Add arrowheads to two identical lines in the Müller-Lyer illusion and one suddenly looks longer than the other. We know these perceptions are wrong. Our visual system, evidently, didn’t get the memo. Even the term “optical illusion” doesn’t quite hold up, according to vision scientist Prof. Michael Bach (Germany). “‘Optical illusions’ are a misnomer—that would only apply to the rainbow and to floaters.,” he said. “‘Perceptual illusion’ would be better, and I frequently prefer ‘visual phenomenon’ because there is no error in perception.” What we perceive, he explained, is far more than what actually reaches the brain via the eyes. “Much is actually ‘invented’ by the visual system, allowing for rapid assessment in typical situations,” he explained. “But this inventiveness runs astray in atypical ones, which leads to what we call ‘optical illusions’.” NOT SO RETINAL AFTER V The Hermann grid has long been held up as the classic demonstration of retinal processing. Black squares are separated by white corridors, and in peripheral vision, grey spots appear at the intersections. Those spots vanish the moment you look directly at one.

For decades, the standard explanation centered on lateral inhibition and the center-surround receptive fields of retinal ganglion cells. These cells respond to the difference between the center of their receptive field and its surrounding, rather than to absolute luminance. That organization enhances local contrast and helps the visual system find boundaries. “Center-surround organization is a dominant way to organize visual information because it intrinsically highlights anything that is different from the background,” explained cognitive neuroscientist Prof. Hinze Hogendoorn (Australia). Combining signals from these cells also allows neurons further along the visual pathway to respond to increasingly complex features, including orientation. Applied to the Hermann grid, the logic seems straightforward. A receptive field centered on an intersection has more white in its inhibitory surround than one centered on a corridor. It should, therefore, be more inhibited, producing a darker spot. Elegant? Yes, but incomplete. “For a while, the Hermann grid was thought to result from retinal processes alone, but slight modifications to the image that should not have affected the putative retinal causes were found to eliminate the illusion,” said Prof. Hogendoom.

“The modern interpretation is due to the extraction of more complex features in the cortex,” he added. “It seems to be that the brain is detecting overlapping bars, but is somehow making incorrect assumptions about how those bars behave at their intersections, causing the strange scintillating dots at the intersections when viewed peripherally.” Wavy lines, for example, can abolish the effect. Vision scientist Prof. Juno Kim (Australia) noted that even rotating the grid can modify it. Such findings are hard to reconcile with a purely retinal center-surround account. OFF THE STRAIGHT AND NARROW Now consider a brick wall. In the Café Wall illusion, rows of alternating dark and light tiles are offset horizontally from one another and separated by thin “mortar” lines. The mortar lines are perfectly parallel, yet they appear to converge, diverge or tilt. Here, there isn’t even a tempting retinal explanation. Prof. Bach noted that retinal receptive fields are broadly circular, whereas cortical receptive fields can be elongated and orientation-selective. He attributes the Café Wall illusion primarily to cortical processing. The key ingredients are contrast boundaries, orientation and the spatial arrangement of neighboring elements. Computational models suggest that interactions among orientation-sensitive receptive fields can produce neural response patterns that match the perceived tilt.¹

relative to the direction of the tiles. When the pattern then zigzags the other way, the perceived orientation changes. “This depends on local and global processing of orientation information in the brain,” he said. In other words, the visual system doesn’t analyze each line in isolation. Neurons respond to edges, orientations and spatial relationships, and these local signals are integrated into a global percept. Prof. Hogendoorn groups the Café Wall with other geometric illusions, in which the orientation and context of contrast edges bias perceived geometry. The mortar hasn’t changed. Its neighbors have. THE VISUAL SYSTEM ADDS A DIMENSION The Müller-Lyer illusion takes things a step further. Two lines of identical length are capped with fins pointing either inward or outward, and one reliably appears longer. Retinal center-surround processing can’t account for this, and neither can simple edge detection. Both Prof. Bach and Prof. Kim favor an explanation based on perspective and higher-level visual processing. In a 2005 paper, vision scientist Richard Gregory argued that the effect reflects the visual system’s interpretation of three-dimensional space.² Prof. Bach still prefers that account to the so-called “cultural byproduct” explanation. Prof. Kim agreed that the effect “really depends on 3D perspective,” drawing on the same processes used to recover shape and magnitude from a visual scene.

Prof. Kim explained that when consecutive rows of dark tiles are displaced in the same direction, the mortar appears to tilt

NOVEMBER 2026

OPTICS

That points to a problem the visual system must solve every waking moment: the world is three-dimensional, but the retinal images from which we reconstruct it are not.

Bonnet syndrome is a striking demonstration that when visual input becomes incomplete, the perceptual system can generate experiences that go beyond what the eyes are delivering.

“We only understand 3D world properties from 2D image structure that reaches our eye,” said Prof. Kim. Low-level processes extract features. Higher-level processes must then work out what those features are likely to represent in the real world.

Prof. Hogendoorn is more cautious about using illusions as models of pathology. He sees them primarily as “non-invasive (and fun) ways to investigate and gain insight in healthy vision,” because they expose the shortcuts a normally functioning visual system takes to solve difficult perceptual problems. Understanding those shortcuts may be where their real clinical value lies.

Because those retinal signals are inherently incomplete, Prof. Hogendoorn added, the brain has to make assumptions about the most likely cause of any given pattern. Most of the time, those assumptions work spectacularly well. The Müller-Lyer figure simply supplies contextual cues that push the calculation towards an answer that disagrees with the ruler. RETINA, CORTEX AND EVERYTHING IN BETWEEN It’s tempting to file each illusion neatly under one anatomical level: the Hermann grid under retina, the Café Wall under V1, MüllerLyer under higher cognition. As the Hermann grid has already shown, reality is less tidy. Prof. Kim suggests a more useful framework: think of perception as involving low-level retinal, mid-level cortical and higher-level cognitive processing. Information is already being transformed within the retina before it travels via the optic nerve and thalamus to the primary visual cortex. Cortical neurons then extract and combine increasingly complex features. Later stages interpret those features according to context, prior knowledge and likely real-world causes.

Seeing, in short, is anything but passive. Before we’re consciously aware of anything, the visual system has enhanced contrast, found boundaries, extracted orientation, integrated context and inferred three-dimensional structure. Illusions are simply the moments we catch it in the act. As Prof. Bach put it, they’re “not an error in perception.” Instead, they offer a window onto the unconscious processing that lets us act quickly, and usually correctly, on incomplete information. REFERENCES 1.

Todorović D. Extension of a computational model of a class of orientation illusions. Vision Res. 2024;223:108459. 2. Gregory RL. The Medawar Lecture 2001 knowledge for vision: vision for knowledge. Philos Trans R Soc Lond B Biol Sci. 2005;360(1458):1231-1251.

CONTRIBUTORS

Nor should the retina be dismissed as a mere camera sensor. Cognitive neuroscientists may underestimate how much computation happens there, Prof. Hogendoorn cautioned, particularly for evolutionarily fundamental properties such as position and motion. WHY CLINICIANS SHOULD CARE For optometrists, all of this matters well beyond visual curiosities on a screen. Patients don’t experience retinal or neurological disease as optical coherence tomography scans, visual-field plots or contrastsensitivity curves. They experience changes in perception: missing areas, distortion, altered contrast, movement or visual phenomena that are hard to put into words. What a patient sees is the product of processing throughout the visual system, not simply an image projected onto an intact retina. Prof. Bach pointed to negative scotomata and Charles Bonnet syndrome as particularly interesting clinical examples. Charles

Prof. Michael Bach Vision scientist at the Eye Center, University Medical Center in Freiburg, Germany. bach@uni-freiburg.de

Prof. Hinze Hogendoorn Professor of cognitive neuroscience at Queensland University of Technology in Australia. hinze.hogendoorn@qut.edu.au

Prof. Juno Kim Vision scientist at the School of Optometry and Vision Science, University of New South Wales, Australia. juno.kim@unsw.edu.au

COVER STORY

PERFECT VISION MEETS A DECEIVED BRAIN When the ocular exam can’t explain the complaint, the trail leads into a brain haunted by its own faulty account of the world. In some patients, intensive retraining may revive visual functions once thought permanently lost. By Kendra Bruning

An 80-year-old man’s wife noticed he could no longer read the clock on the wall. He insisted nothing had changed. Seven years earlier, he’d received a kidney transplant. His doctors later proposed that sirolimus-induced thrombotic microangiopathy, a rare complication of the anti-rejection drug, had led to bilateral occipital infarction.1 On examination, his vision measured barely enough to detect a moving hand at close range in either eye, with preserved pupillary reflexes and unremarkable fundoscopy. Nothing in the exam explained the profound loss.1

A clinician asked him to point out the person in the room wearing a striped shirt. Nobody was wearing stripes. Without hesitation, he pointed at someone in a plain shirt with complete certainty.1 He wasn’t lying, and he wasn’t guessing. Brain imaging later showed bilateral occipital strokes, the region containing the brain’s primary visual cortex.1 His diagnosis was Anton syndrome, in which profound visual loss comes paired with a genuine, brain-based inability to recognize that anything is wrong.

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COVER STORY

Anton syndrome is the most dramatic example of a pattern that runs through cerebral visual disorders. The eye passes inspection, while vision, recognition or awareness fails further along the pathway. BEYOND THE EYEBALL “This may sound strange, but vision is more about the brain than the eyes,” said Prof. Jason Barton (Canada), a professor of neurology and ophthalmology at the University of British Columbia. “The eyes provide information about what wavelengths of light are striking different parts of the retina at different times, but it is up to the brain to organize this information and make sense of it, to make inferences about what is happening in the visual world, and to relate what it ‘sees’ to what the person has experienced in the past.” Prof. Barton organizes cerebral visual disorders into three tiers. 2 • • •

Low-level vision covers acuity and field loss. Intermediate-level vision covers color, form and motion. High-level vision covers recognition of objects, faces, scenes and words.

“The beauty of the visual system,” Prof. Huxlin said, “is that there are…at the very least 13 or more different visual cortical processing centers in the brain.” The brain can operate opportunistically, recruiting whatever surviving routes remain. Her lab trains patients to exploit that residual capacity by discriminating motion or orientation at mapped locations inside the blind field. Sessions run 300 trials at least twice a day, five days a week, often for months. •

The tiers can be mistaken for one another. A blind person can’t read or recognize faces, but that doesn’t mean they also have alexia or prosopagnosia. Anatomy adds to the confusion. The optic radiations run beneath cortical regions responsible for higher-level processing, so a stroke may produce a higher-level deficit alongside partial field loss. 2 Damage at the first cortical station also doesn’t necessarily silence every visual route. SECONDARY ROUTES THROUGH A DARK FIELD Clinicians reserve the term cortical blindness for bilateral damage to the brain’s primary visual cortex that causes profound, near-total loss, as in the opening case. Unilateral damage more often produces a homonymous field defect, such as quadrantanopia or hemianopia.2 Prof. Krystel Huxlin (United States), a professor of ophthalmology at the University of Rochester, avoids the word blindness for many patients. “I prefer the term visual impairment,” she said. “I think that is more accurate.” The distinction applies to cortical loss that leaves measurable capacity behind. True bilateral cortical blindness is just as profound under either name. Standard perimetry, Prof. Huxlin noted, largely tests whether a patient can detect a small point of light. It says little about motion or other qualities a damaged field may still register.

That gap helps explain blindsight, in which a patient reports no conscious perception of a stimulus yet responds to it above chance under controlled testing.3 Destroyed V1 tissue does not regrow, but surviving extrastriate and subcortical pathways can still carry sparse visual information, which splits what the visual system registers from what the patient can report.3

•

Measurable gains. A study of 17 trained patients and five untrained controls used eye tracking to rule out compensatory gaze shifts. Training produced real gains in both the trained discriminations and perimetry.4 Timing matters. Recovery was faster and fuller when training began in the subacute period, within three months of a stroke, than when it was delayed by years.5 Durability varies. In a follow-up, seven of 11 participants who improved kept their gains three months later. Four did not.6

The gains are neither guaranteed nor interchangeable. In a small pilot study, motion-discrimination training altered visual-cortex activity without improving task performance.7 Altered brain activity, better lab performance, a wider perimetric field and confident navigation of daily life are four different outcomes. Evidence for one does not establish the others. Because discrimination training remains confined to research protocols, routine management relies on compensation. Peripheral prism glasses shift information from the blind side into the seeing field8, while scanning therapy trains deliberate eye and head movements toward the missing side.2 Prof. Huxlin’s team is developing a more portable, virtual reality–based version of its training, though it is not yet available to patients. DRAINED OF COLOR, FROZEN IN TIME Unlike congenital color vision deficiency, cerebral achromatopsia stems from damage to color-processing regions in the ventral occipitotemporal cortex. Patients often describe the world as washed out, gray or dirty. Some lose the ability to judge a surface’s true color as lighting changes, a subtler failure than missing a

color-vision plate. The deficit can appear alongside field loss and other cerebral disorders.9 Severe acquired akinetopsia, the loss of motion perception, is exc eptionally rare and has no standardized clinical test.9 The most extensively studied case is LM, a German patient who lost the perception of continuous motion after bilateral posterior brain injury associated with cerebral venous thrombosis.10 She described fluids as appearing “frozen, like a glacier,” which made it hard to judge when to stop pouring.10 Crossing the street was worse. A car could appear far away one instant and dangerously close the next, with no sense of its approach.11 LM remains the field’s reference case because she was studied so thoroughly, but her experience is not a template for every patient. Her deficit was relatively pure and severe, and it was unchanged when researchers reexamined her eight years later.12 WHO GOES THERE? Visual object agnosia is impaired recognition that poor acuity, field loss, language trouble or general cognitive decline cannot explain. Some patients cannot identify it by sight, even though they may recognize it by touch. The failure is often selective, so a patient might identify tools but not animals.9 Other higher visual disorders separate recognition from action. In optic ataxia, a patient may identify an object yet reach for it inaccurately. The brain’s system for guiding a reach has failed independently of its system for recognition.2 Prosopagnosia is often described as an inability to see faces, which overstates the deficit. “Most of them know ‘face-ness,’” Prof. Barton said. “They can find faces in scenes. They know if the features of a face are correctly arranged.” What fails is recognition of facial identity, while perception of expression, age or gender may be preserved. Testing that accounts for prior expertise tells a more mixed story. Some patients with prosopagnosia struggle to recognize individual examples of nonface categories they know well, such as cars. A smaller number show a much sharper face-specific gap.13 Simultanagnosia breaks the usual shorthand that a patient sees the trees but not the forest. Prof. Barton describes something less tidy, a restricted visual-attentional window in which local detail and the overall scene compete for awareness.14

In patients tested with Giuseppe Arcimboldo’s composite portraits, paintings built entirely from fruit and vegetables arranged into a face, the face can capture attention so completely that the fruit disappears from awareness. With other images, a local element won and the overall shape disappeared. Which side collapses depends on the patient and the image.14 THE CASE OF THE VANISHING WORDS An 84-year-old woman with known dry age-related macular degeneration and 20/20 acuity in each eye. She could write, though she could not read back what she had just written. Examinations revealed a right homonymous hemianopia, and imaging showed a left occipital stroke extending into the splenium, the fiber bundle connecting the brain’s two hemispheres.15 Her macular disease was no phantom, but it could not explain an abrupt, category-specific loss. Only the field test and the scan identified the true culprit.15 “Most know that they are looking at a written word, but cannot work out what it says without employing laborious strategies to identify each individual letter,” said Prof. Randi Starrfelt (Denmark), a professor of neuropsychology at the University of Copenhagen. A practiced reader processes several letters in parallel, so word length barely affects reading speed. In letter-by-letter reading, each additional letter adds measurable time, because letters must be identified in sequence before meaning emerges. Prof. Starrfelt has described the resulting alexia as patients seeing too little, too late, for fluent reading.16 A single-letter acuity chart may miss this disorder entirely, because it never asks a patient to read at speed. Timed reading aloud, compared across word lengths, can reveal it. Prof. Starrfelt noted that moving text into an intact part of the field can help separate a field-driven reading problem from true pure alexia. Some patients relearn with children’s books and deliberate practice. Others turn to text-to-speech software or a phone camera that reads signs aloud. PHANTOMS IN THE BLIND FIELD The case of the striped shirt blends three phenomena that are easily confused. Dr. Isaiah Kletenik (United States), a neurologist at Brigham and Women’s Hospital, describes Anton syndrome more precisely as “vision loss with unawareness.” • •

Cortical blindness is the visual loss itself. Visual anosognosia is the failure to recognize that loss. It can accompany a partial field defect as well as complete blindness.17

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COVER STORY

•

Confabulation fills the resulting void with a plausible but inaccurate account. It is a fabricated narrative, not a sensory experience like a hallucination.

A lesion network mapping study linked visual anosognosia to lesions functionally connected to the visual association cortex and posterior cingulate.18 Across visual and motor anosognosia, the shared network centered on memory-related regions.18 The pattern suggests that recognizing one’s own impairment may require the brain to compare incoming evidence against memory and its internal model of the self. Two earlier reports from a single cohort of 32 patients revealed different fractures in visual awareness. Twenty did not recognize their homonymous field loss. Thirteen experienced positive visual phenomena within the blind field, including photopsias, hallucinations and palinopsia.17,19 Anosognosia conceals the loss from the patient. Positive phenomena haunt the blind field with flashes, images or repetitions. These are perceptual experiences, not confabulations. The category is broader than Charles Bonnet syndrome, which describes visual hallucinations arising with visual loss or visual-pathway disease, often with insight preserved.20 Dr. Kletenik, who led the study, said the findings may align with a cognitive-awareness model in which “sensory or motor inputs must be compared to prior expectations stored in memory to recognize a new deficit.”

The striped shirt, then, was not evidence of sight. It was a plausible detail painted over the blank left by missing visual evidence. UNMASKING THE CULPRIT When a complaint doesn’t match the ocular exam, the patient deserves a second look.

Sensory or motor inputs must be compared to prior expectations stored in memory to recognize a new deficit. - Dr. Isaiah Kletenik

Is the problem present whichever eye is tested? Does it respect the same side of visual space in both eyes? Is it selective for motion, color, faces, objects or words? Careful perimetry, timed reading and recognition tasks spanning several visual categories can expose what a standard exam misses. Sudden cerebral visual symptoms warrant urgent neurological evaluation, since a genuine chronic eye condition can mask an acute stroke.2,15 Prisms, scanning and text-to-speech help patients work around what has vanished from the field. Restoration research ventures

Photopsias, palinopsia and other positive phenomena do not qualify simply because they occur in a blind field.

into stranger territory, coaxing surviving visual circuits to make better use of the signals still flickering through them, though it remains investigational.2,3,7 Prof. Huxlin put the principle for residual vision plainly. “If you ignore it, you are not going to make any sense of it. If you pay attention to it and actually try to use it, that is when you will be able to keep it functioning, build upon it and learn to interpret it,” she noted. “Even though it may look a little bit degraded—a little bit off color, strange or distorted—the more you use it, the less you lose it.”

REFERENCES 1.

Mankoo D. Anton syndrome with bilateral occipital infarct: a case report. Radiol Case Rep. 2023;18(12):4461-64. 2. Barton JJS. Cerebral visual loss. Ann Indian Acad Neurol. 2022;25(Suppl 2):S106-12. 3. Cavanaugh MR, Fahrenthold BK, Huxlin KR. What V1 damage can teach us about visual perception and learning. Annu Rev Vis Sci. 2025;11(1):217-41. 4. Cavanaugh MR, Huxlin KR. Visual discrimination training improves Humphrey perimetry in chronic cortically induced blindness. Neurology. 2017;88(19):1856-64. 5. Saionz EL, Tadin D, Melnick MD, Huxlin KR. Functional preservation and enhanced capacity for visual restoration in subacute occipital stroke. Brain. 2020;143(6):1857-72. 6. Willis HE, Fahrenthold B, Millington-Truby RS, et al. Persistence of training-induced visual improvements after occipital stroke. Prog Brain Res. 2025;292:113-42. 7. Larcombe SJ, Kulyomina Y, Antonova N, et al. Visual training in hemianopia alters neural activity in the absence of behavioural improvement: a pilot study. Ophthalmic Physiol Opt. 2018;38(5):538-49. 8. Giorgi RG, Woods RL, Peli E. Clinical and laboratory evaluation of peripheral prism glasses for hemianopia. Optom Vis Sci. 2009;86(5):492-502. 9. Haque S, Vaphiades MS, Lueck CJ. The visual agnosias and related disorders. J Neuroophthalmol. 2018;38(3):379-92. 10. Zihl J, von Cramon D, Mai N. Selective disturbance of movement vision after bilateral brain damage. Brain. 1983;106(Pt 2):313-40. 11. Zihl J, Heywood CA. The contribution of LM to the neuroscience of movement vision. Front Integr Neurosci. 2015;9:6. 12. Zihl J, von Cramon D, Mai N, Schmid C. Disturbance of movement vision after bilateral posterior brain damage: further evidence and followup observations. Brain. 1991;114(Pt 5):2235-52.

13. Barton JJS, Albonico A, Susilo T, et al. Object recognition in acquired and developmental prosopagnosia. Cogn Neuropsychol. 2019; 36(1-2):54-84. 14. Dalrymple KA, Kingstone A, Barton JJS. Seeing trees OR seeing forests in simultanagnosia: attentional capture can be local or global. Neuropsychologia. 2007;45(4):871-5. 15. Foster Z, Kini A, Al Othman B, et al. Seeing is not believing. Surv Ophthalmol. 2020;65(3):386-90. 16. Starrfelt R, Habekost T, Leff AP. Too little, too late: reduced visual span and speed characterize pure alexia. Cereb Cortex. 2009;19(12):2880-90. 17. Celesia GG, Brigell MG, Vaphiades MS. Hemianopic anosognosia. Neurology. 1997;49(1):88-97. 18. Kletenik I, Gaudet K, Prasad S, et al. Network localization of awareness in visual and motor anosognosia. Ann Neurol. 2023;94(3):434-41. 19. Vaphiades MS, Celesia GG, Brigell MG. Positive spontaneous visual phenomena limited to the hemianopic field in lesions of central visual pathways. Neurology. 1996;47(2):408-17. 20. O’Brien J, Taylor JP, Ballard C, et al. Visual hallucinations in neurological and ophthalmological disease: pathophysiology and management. J Neurol Neurosurg Psychiatry. 2020;91(5):512-19.

CONTRIBUTORS Dr. Jason Barton Professor in neurology, ophthalmology and visual sciences, and psychology, at the University of British Columbia. jasonbarton@shaw.ca

Prof. Krystel Huxlin The James V. Aquavella Professor of Ophthalmology at the Flaum Eye Institute, University of Rochester. khuxlin@ur.rochester.edu

Prof. Randi Starrfelt Professor of neuropsychology in the Department of Psychology, University of Copenhagen. randi.starrfelt@psy.ku.dk

NOVEMBER 2026

KUDOS | WOMEN IN OPTOMETRY

WHAT LURKS IN THE PERIPHERAL VISION Dr. Alex Bowers has built a career exploring the curious territory between eyesight and perception, helping people with vision loss navigate a world they cannot always see. By Chow Ee-Tan

Half a person’s visual world can vanish, but what’s missing may not always be obvious to the person experiencing it. This is the intriguing territory Dr. Alex Bowers (United States) has spent much of her career investigating. For people with homonymous hemianopia—loss of the same half of the visual field in both eyes following damage to the brain— pedestrians, obstacles and other hazards on the affected side may simply go unseen. The consequences can be serious when crossing a street, walking through a crowded space or getting behind the wheel.1 Dr. Bowers is a clinician scientist at the Schepens Eye Research Institute of Mass Eye and Ear and associate professor of ophthalmology at Harvard Medical School. An optometrist by training, she completed a PhD in vision rehabilitation research at Glasgow Caledonian University in 1998 before joining Schepens.

Her research focuses on functional vision; less on what a patient can read off an eye chart and more on how they use their remaining vision in everyday life. THE VANISHING ACT Much of Dr. Bowers’ research has involved driving simulators, where potentially dangerous situations can be recreated without putting anyone at risk. “There is an underlying assumption that if someone has visual field loss they will automatically learn to compensate for that by moving their head and eyes,” she told the U.S. National Eye Institute (NEI). 2 But her data tell a messier story. When her team tested 12 drivers with similar hemianopias, performance diverged sharply. “Some scanned the environment very well and detected as many pedestrians on the blind side as the seeing side. Others hardly scanned at all,” Dr. Bowers told the NEI. 2

In other words, two people can have similar visual-field loss on paper, yet function very differently in the real world.

and still failed to register them, a phenomenon researchers call “looked-but-failed-to-see.”4

Her earlier simulator studies illustrate the potential consequences. When drivers with hemianopia were asked to detect pedestrians appearing along simulated roads and at intersections, performance on the blind side varied widely between individuals.3

Then there is change blindness, where a person misses a major visual change in their environment. Dr. Bowers’ team found that people with homonymous visual-field loss experienced more often overall than normally sighted participants, though individual variation was substantial.5

The findings raise an important clinical question: can a visualfield test alone tell us how safely or effectively someone functions outside the examination room? Her research suggests that the answer is not always straightforward. LOOKING, NOT SEEING In one driving-simulator study, Dr. Bowers and colleagues examined why drivers with hemianopia failed to detect pedestrians. Insufficient scanning towards the blind side accounted for many misses. But eye- and head-tracking data also captured something stranger: instances where participants looked towards a pedestrian

Seeing, in other words, involves more than functioning eyes. Attention, memory and how the brain processes visual information all shape what we actually perceive. AN EARLY WARNING SYSTEM So can optics compensate for what’s missing? One approach is peripheral prism glasses, developed by Dr. Bowers’ Schepens colleague Dr. Eli Peli. The prism segments shift visual information from the blind side into the seeing field. They do not restore the missing vision, but may alert the wearer to something

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KUDOS | WOMEN IN OPTOMETRY

that would otherwise go unnoticed. As Dr. Bowers put it, “They work like an early warning system.”2 An earlier sham-controlled trial found that significantly more participants preferred real peripheral prisms to sham glasses after trying both. Six months on, 41% were still wearing the real prisms, particularly for navigating crowded or unfamiliar places.6 More recently, Dr. Bowers and colleagues compared two peripheral prism designs in a multicenter randomized crossover trial published in June 2026. Participants navigated a virtual, busy shopping mall while attempting to detect pedestrians on a possible collision course. Of 38 eligible participants, 63% improved their detection of pedestrians approaching from the blind side with at least one of the two prism designs.7 The underlying principle holds regardless of design: shift where the visual information appears, and a hazard once outside the usable field of vision may become detectable. ARE YOU LOOKING AT ME? Dr. Bowers’ interest in perception extends beyond roads and obstacles into something more social: how we know when someone is looking at us. Eye contact is an important form of non-verbal communication, yet judging another person’s gaze depends on subtle visual cues. In one study, participants viewed a life-sized virtual head and adjusted its eyes to indicate whether the face appeared to be looking directly at them.8 People with bilateral central scotomas were more variable in judging gaze direction than normally sighted participants, though their overall ability to perceive mutual gaze remained relatively robust.8

The gap between what’s physically present and what a person actually perceives isn’t a party trick. For someone with visual-field loss, it can shape mobility, driving and social interaction. So, two patients with similar field loss may adapt in very different ways. Someone can look at a hazard and still fail to detect it. And a relatively simple optical device can help bring something previously unseen into view. To Dr. Bowers, understanding how a patient experiences and navigates the world requires looking beyond the test result. Because sometimes, what we see only tells half the story.

REFERENCES 1.

5. A later study involving people with hemianopia found that those with left-sided field loss, particularly participants with a history of visual neglect, had greater difficulty judging another person’s gaze.9 Sight, it turns out, does more than help us dodge obstacles and traffic; it helps us read faces and navigate a social world. BEYOND THE EYE CHART Dr. Bowers’ body of research has earned her considerable recognition. In 2023, she received the American Academy of Optometry’s Glenn A. Fry Award; two years later, the Academy’s William Feinbloom Award for distinguished and significant contributions to clinical excellence and the advancement of visual and optometric care.

9. Her work has also extended beyond hemianopia, into driving and mobility across a range of visual impairments, along with assistive technologies and rehabilitation strategies designed to help patients make the most of their remaining vision.

Bowers AR. Driving with homonymous visual field loss: a review of the literature. Clin Exp Optom. 2016;99(5):402-418. National Eye Institute. Low vision research shifts into overdrive. February 20, 2018. Accessed on September 18, 2026. Bowers AR, Mandel AJ, Goldstein RB, Peli E. Driving with hemianopia, I: Detection performance in a driving simulator. Invest Ophthalmol Vis Sci. 2009;50(11):5137–5147. Bowers AR, Alberti J, Hwang A, Goldstein R, Peli E. Pilot Study of Gaze Scanning and Intersection Detection Failures by Drivers with Hemianopia. Driving Assessment Conference. 2015(8);240–246. Accessed on September 18, 2026. Swan G, Xu J, Baliutaviciute V, Bowers AR. Change blindness in simulated driving in individuals with homonymous visual field loss. Cogn Res Princ Implic. 2022;7(1):44. Massachusetts Eye and Ear. Peripheral prism glasses help hemianopia patients get around. Press release. November 7, 2013. Accessed on September 18, 2026. Bowers AR, Manda S, Shekar S, Hwang AD, Jung JH, Peli E. A randomized crossover clinical trial of multi-periscopic and Fresnel peripheral prism glasses for hemianopia. Optom Vis Sci. 2026;103(6):e70072. Sheldon S, Quint J, Hecht H, Bowers AR. The Effect of Central Vision Loss on Perception of Mutual Gaze. Optom Vis Sci. 2014;91(8):1000–1011. Bowers AR, Sheldon S, Hecht H. The Effects of Hemianopia on Perception of Mutual Gaze. Optom Vis Sci. 2019;96(11):860–865.

INNOVATION

WHAT VR CAN AND CAN’T DO FOR AMBLYOPIA Every October, kids beg for an eye patch. The rest of the year, they rip it off. Dichoptic VR promises a friendlier deal, but the trials tell a messier story, and the headset’s best trick may not be treatment at all. By Sam McCommon

For a long time, the workhorse of amblyopia care was a simple patch. Cover the strong eye, and hope the child leaves it on.

even when Snellen lags, because it’s training the brain to use both eyes, not practicing the letter chart.

However, the previous decade has offered a potentially different bargain. Instead of just shutting one eye, show each eye a different picture at the same time and force the brain to combine them. That, in a nutshell, is dichoptic stimulation: contrast rebalanced, pieces of a scene withheld from the fellow eye, with detail delivered to the amblyopic eye.

The hardware lineage is messy, and for a reason. Early interactive binocular treatment like the I-BiT used shutter glasses and a clinic screen—a common background to both eyes, with the interesting foreground to the amblyopic eye.

Virtual reality (VR) didn’t invent the idea, but a headset made it easy. After all, it already has two displays. The public story has been about treatment: games and children’s TV as a friendlier occlusion. The other story is diagnosis: imbalance, suppression, and stereo, measured in the same headset. TWO PICTURES, ONE TASK Normal seeing is dioptic: both eyes get the same world from slightly different angles. Dichoptic presentation is a deliberate mismatch. The fellow eye sees a dimmer or incomplete image. The amblyopic eye sees the missing parts. The only way to play the game, or to see the full show, is to use both eyes. That is a different theory of the disease. If amblyopia is a binocular suppression problem as well as a letter-chart problem, punishing the good eye may be the wrong first move. Stereoacuity can move

Commercial VR later put that split into a consumer headset. Luminopia (Luminopia; Massachusetts, United States) streams children’s television with contrast cut in the fellow eye and complementary masks, so the full frame exists only if both eyes contribute. THE EVIDENCE DOESN’T LINE UP It’s tempting to write that VR replaced the patch. Unfortunately, the papers won’t allow it. I-BiT is the cautionary tale. A 2013 pilot in ten children, half an hour a week for six weeks, reported a mean acuity gain of about 0.18 logMAR and no obvious harm.1 The 2016 randomized trial was larger and…well, colder. Seventyfive children aged 4 to 8—most residual amblyopes, most with strabismus—were assigned to I-BiT games, I-BiT video or non I-BiT binocular games. At six weeks the amblyopic eye had improved by roughly 0.07 logMAR in every arm of the study. 2

NOVEMBER 2026

INNOVATION There was no advantage to the active dichoptic condition. The authors pointed at a short dose, a previously treated population and a case mix that’s hard on binocular therapy. That’s a lot of real patients.

the novelty wears off, the strap hurts or the kid takes it off. Age and fit matter, and so does fusion. Trials routinely exclude people who can’t put the two images together—large-angle strabismus isn’t the sweet spot for this treatment.

Other programs look different, in other patients, at other doses. A review of 48 VR papers through early 2023 found the field split between phone-in-a-headset viewers and standalone commercial headsets, almost all built on vision-therapy or dichoptic software.3 The conclusion? The hardware is still too mixed to be clinic-ready.

WHERE IT STANDS Tomorrow’s protocol isn’t going to be “headset first, always.” That sci-fi dream is still in the future, if at all. The plausible lanes, rather, are after refractive adaptation—as an add-on or a rescue when a patch won’t stay on, and as a diagnostic add-on for suppression and imbalance.

A Boston Children’s trial of a VR prototype in older children and adults who had already failed conventional treatment found no meaningful acuity gain.4 Stereoacuity improved statistically, but the authors called the change clinically minute. A Spanish pilot in older children who had refused or failed patching—nine hours of an immersive binocular game over a month—reported gains in near acuity, a binocular-function score and distance negative fusional vergence.5 It was a single-arm study in a rescue population, and there wasn’t a control group.

Eye tracking inside the display is the hardware that might matter more than a prettier game. A headset can’t take the place of a human with a prism bar. But it can present two different worlds at once and tell you how the brain combines them. That’s worth having. It’s not, by itself, a diagnosis or a cure. What clinicians do with that split—and whether the chart, the stereo test or the child’s week actually changes—is still an evidence problem.

So, for now, the honest takeaway is not “stereo works, acuity doesn’t” or vice versa. Dichoptic care is biologically plausible, but clinically uneven. Results shift depending on variables involved, and whether the endpoint is reading a chart or a stereo book. We can’t claim that a headset restores 20/20, that games have beaten occlusion in every child or that patches are obsolete.

REFERENCES

WHAT THE HEADSET CAN MEASURE Treatment can make the headlines, but measurement may be the real story of progress.

Binocular imbalance is the clearest example. A dichoptic letter chart in a commercial VR headset can ask how much contrast the fellow eye needs before it dominates. In mixed clinical samples, that kind of test has been doable across a wide age range, stable on retest, and correlated with interocular acuity difference and stereoacuity.6 It also has a job when stereo is unmeasurable, which is often. Worth 4-Dot (Optics Trainer; California, United States) is categorical, and an imbalance score is something you can follow. Alignment is earlier. Headset-camera systems can flag pediatric strabismus with some agreement on presence and type. Measuring the exact angle can still be tricky. That’s an adjunct for a cover test, not a replacement. For now, a headset is a controlled way to split and score the two eyes. But it doesn’t examine the fundus.

WHO ACTUALLY WEARS IT Patching fails as often from psychology as from brain function. A show in a headset is an easier sell than a pirate patch. That is, until

Herbison N, Cobb S, Gregson R, et al. Interactive binocular treatment (I-BiT) for amblyopia: results of a pilot study of 3D shutter glasses system. Eye. 2013; 27:1077–1083. Herbison N, MacKeith D, Vivian A, et al. Randomised controlled trial of video clips and interactive games to improve vision in children with amblyopia using the I-BiT system. Br J Ophthalmol. 2016;100(11):1511-1516. Chan HS, Tang YM, Do CW, Ho Yin Wong H, Chan LY, To S. Design and assessment of amblyopia, strabismus, and myopia treatment and vision training using virtual reality. Digit Health. 2023;9:20552076231176638. Elhusseiny A, Bishop K, Staffa S, Zurakowski D, Hunter DG, Mantagos IS. Virtual reality prototype for binocular therapy in older children and adults with amblyopia. J JAAPOS. 2021;25(4): 217.e1-217.e6. Leal-Vega L, Coco-Martín MªB, Molina-Martín A, et al. NEIVATECH pilot study: immersive virtual reality training in older amblyopic children with noncompliance or non-response to patching. Sci Rep. 2024 Nov 14;14(1):28062. Martín S, Portela JA, Ding J, Ibarrondo O, Levi DM. Evaluation of a Virtual Reality implementation of a binocular imbalance test. PLoS One. 2020;15(8): e0238047.

ENLIGHTENMENT

WHY OPTOMETRY NEEDS A CENTRAL ROLE IN TRAUMATIC BRAIN INJURY CARE TBI often leaves vision problems in its wake, yet optometry is usually patients’ last stop, not their first. Dr. Don Lyon wants to change that. By Michaela Perez

Dr. Lyon (United States) frames his role in a way that cuts straight through the clinical complexity. “I do not diagnose a concussion or TBI [traumatic brain injury],” he said, because that’s been done already. Instead, “I’m going to handle the direct vision-related incidents and symptoms and signs that I see.” It sounds like a boundary. In fact, it’s an invitation to every optometrist to step into a patient population that is larger, more underserved and more consequential than the profession has fully recognized. THE SCALE OF THE PROBLEM More than 50 million people worldwide sustain a TBI each year, at an estimated global cost of $400 billion annually.* Many experience visual problems, such as diplopia, photosensitivity, eye strain, track ing dif ficulties, c onve r g e nc e i n s u f f ic ie nc y a nd accommodative dysfunction.

Because the visual system is distributed widely across the brain, Dr. Lyon explained, an injury can expose deficiencies that were already there. “Concussions are really good at showing us our weakness,” he said. “If your weakness is your tear film, your weakness is your accommodation or your vergence, the concussion is going to show that because your brain can’t handle that anymore.” Yet referral is often slow. Dr. Lyon has seen patients with double vision or light sensitivit y who weren’t referred to optometry until six months or more after their injury. UNMASKING OPTOMETRY’S ROLE ON THE TEAM Dr. Lyon is director of the Concussion Care Service and a clinical professor at the Indiana University School of Optometry, where he works alongside physiatrists, NOVEMBER 2026

physical therapists, occupational therapists and neurologists. “When I first started out, I would let the sports med docs and the physiatrists lead on vision,” he recalled. “What I found out relatively quickly was, no—they want me to take the lead.” Once colleagues understood the scope of optometric care, referrals followed. Patients who had spent weeks in occupational therapy without progress were redirected for vision assessment and began to improve. “When you’ve seen one, you’ve seen one,” Dr. Lyon says of TBI patients. Presentations vary, but the core examination does not. “As an optometrist, you know how to do each and every one of these exam elements,” he said. “You have the skills. You have the training.”

ENLIGHTENMENT WHAT LURKS BEHIND THE SYMPTOMS Many patients reach Dr. Lyon’s clinic with concussion symptoms that have lingered for months or even years. Complaints can include double or blurred vision, eye strain, dry eye, headaches, light sensitivity, dizziness and eye pain. Moderate and severe injuries may also involve peripheral field loss. He begins with the Brain Injury Vision Symptom Survey (BIVSS), since other standard concussion surveys include only one or two questions about vision. The history should cover not just the mechanism of injury but also what other care the patient is receiving.

Early in his career, some of his referrals fell through the cracks, and patients returned months later without having received the recommended care. Now, he lays out the plan for every patient, including who will receive the referral, what to expect and when to call if they haven’t heard anything. Optometrists without a TBI service can apply the same principle. A referral should start a coordinated process, not simply end an examination.

Testing may include: • Visual acuity • The m-VOMS (modified Vestibular/ Ocular Motor Screening) • Near point of convergence (NPC) • Accommodative and vergence testing • Fundus examination

GROWING THE COMFORT ZONE Not every optometrist will establish a concussion clinic, but Dr. Lyon’s message applies to anyone who sees a patient with a history of head trauma and is unsure how to proceed.

The goal is to identify vision-related diagnoses while recognizing symptoms that may have other causes.

“If you’re not comfortable with something,” he said, “it needs to be referred out.”

“If I think that there are other things— like lack of sleep or cognitive issues—that may be indirectly affecting the eyes,” Dr. Lyon said, “it is my job to make sure those patients get the care they need.” CHASING GHOSTS WITHOUT A BASELINE Many patients who arrive after a TBI haven’t had an eye exam in years, a gap that is widest for those in remote areas or lower socioeconomic circumstances. “If they don’t have baseline data where they were before, they really don’t know the impact,” he said. “The doctors don’t know the impact either, and that doesn’t help anybody.” This is where the World Council of Optometry’s (WCO) public health mandate meets TBI care. Routine eye exams establish the baseline that makes post-injury changes easier to recognize.

DON’T GHOST THE REFERRAL Identifying a problem is only half the job. “That patient is still yours,” Dr. Lyon said. “You refer that patient out, [but] they’re still your responsibility.”

Following up with the receiving provider builds confidence for the next case. That matters most where specialist services are scarce and the general optometrist may be the only vision professional a patient ever sees. “Don’t be afraid to see these patients, ”Dr. Lyon said. “They’re out there, and they need our help.”

“[Optometrists] need to be considered an integral part of the medical team,” he said. Earning that recognition means communicating what optometry offers beyond refraction and dispensing, and building stronger referral networks with clinical colleagues. For WCO, TBI care reflects a broader public health priority: identifying vision problems, ensuring access to care and making sure referrals lead to meaningful follow-up, from uncorrected refractive error to diabetic retinopathy. For individual optometrists, the work starts with knowing what they can manage and when to refer, and making sure no patient vanishes between providers. Brain injury may be invisible. Optometry’s role in treating it shouldn’t be. *Maas AIR, Menon DK, Adelson PD, et al; InTBIR Participants and Investigators. Traumatic brain injury: integrated approaches to improve prevention, clinical care, and research. Lancet Neurol. 2017;16(12):987-1048.

Editor’s Note This article is published in collaboration with the World Council of Optometry (WCO).

CONTRIBUTOR

One post-concussion patient told him his team had given her hope, a comment he carries with him. “I want [optometrists] to give…patients hope,” he said. “Hope that their visual system will improve. Hope that it’s not in their head. Hope that the symptoms can be mitigated and decreased with proper management and therapy.”

Dr. Don Lyon Director of Concussion Care Service and clinical professor at Indiana University School of Optometry. dwlyon@iu.edu

FROM AFTERTHOUGHT TO ESSENTIAL TBI is Dr. Lyon’s clinical focus, but his argument extends across healthcare.

ENLIGHTENMENT

SEEING GHOSTS, SAYING NOTHING WHEN VISION LOSS CONJURES APPARITIONS, FACES AND PHANTOM SCENES

Insects on dinner plates. Strangers in empty chairs. Charles Bonnet syndrome is common in your clinic and rarely mentioned in it. Here’s how to break the silence. By Michaela Perez

NOVEMBER 2026

ENLIGHTENMENT

She knew the insects on her plate weren’t real. She could see them anyway, vivid and persistent, appearing every time she sat down to eat. She understood, intellectually, that they weren’t there. But the experience was so overwhelming, she eventually stopped eating altogether. Her health deteriorated, and she died. “That story made me realize very early on that CBS [Charles Bonnet Syndrome] should not be dismissed as simply an interesting or unusual consequence of sight loss,” said Dr. Lee Jones (United Kingdom), research fellow at UCL Institute of Ophthalmology. “For some people, what they see can profoundly affect their behavior, wellbeing and quality of life.” CBS consists of vivid, silent visual hallucinations in people with significant vision loss who remain fully aware that what they’re seeing is not real. It’s not a psychiatric illness. It’s not dementia. It’s not a sign that someone is losing their mind.¹ Yet far too many patients never find that out. SEEING THINGS The range of what patients see is extraordinary. “At one end, people may see relatively simple things such as colored blobs, grids or vivid geometric patterns,” Dr. Jones said. “At the other, hallucinations can be remarkably detailed, featuring people, animals, buildings, landscapes or entire scenes unfolding in front of them.” Unfamiliar faces. Edwardian children. Exotic animals. Figures sitting in empty chairs. One useful way to frame it is that when the brain receives less visual information from the eyes, the visual system starts generating imagery of its own and fills the silence with its own programming. The numbers are far from trivial. A systematic review and metaanalysis of 49 studies involving more than 20,000 patients put overall CBS prevalence in ophthalmic populations at 10.2%. It rose to 24.5% among vision rehabilitation patients and to roughly one in six among those with retinal disease, low vision or glaucoma.² A prospective cross-sectional study of Danish patients with geographic atrophy found a rate of 20.8%, or one in five.³ In other words, CBS is almost certainly sitting in your waiting room this week. It just isn’t saying anything. THE CONVERSATION NOBODY STARTS In the Danish study, 52% of patients with confirmed CBS had never been told the condition existed. Of those who knew they had it, 40% had never told anyone.³ Not a family member, a friend or a doctor.

“People may worry that…they are developing dementia, experiencing a psychiatric illness or losing their mind,” Dr. Jones said. “That fear can prevent them from telling anyone, including their doctor.” That fear is also well documented. A scoping review of 89 studies identified patients’ reluctance to disclose as one of the main barriers to diagnosis, alongside clinicians’ unfamiliarity with the condition. As a result, CBS is frequently missed altogether.⁴ “I have met people who experienced hallucinations for years without telling anybody,” Dr. Jones said. “They may become anxious, lose sleep, withdraw from activities or spend years questioning what is happening to them.” His research has also found that about a third of patients with CBS are not confident their own doctor recognizes the condition. “People with sight loss interact with optometrists, GPs, nurses, neurologists, psychiatrists, geriatricians and many other services,” he said. “We need sufficient awareness across all of these settings.” JUST ASK The fix, at its simplest, is a single question: Do you ever see things that aren’t really there, or that other people cannot see? “Every patient experiencing sight loss should have an opportunity to be asked something along those lines,” Dr. Jones said. For a more structured approach, validated screening tools are available. The North-East Visual Hallucination Interview

(NEVHI) and the self-administered QR-SCB questionnaire have both shown clinical utility in practice.⁴

the language to describe experiences many previously felt unable to voice.

But also, how the clinician responds matters just as much as asking.

“Awareness should be the beginning rather than the end point,” Dr. Jones noted. “Somebody with sight loss should not have to be fortunate enough to encounter a clinician who happens to know about CBS. Recognition, explanation and support should be a routine part of eye care.”

“If the clinician appears shocked or dismissive, the person may never mention it again,” Dr. Jones noted. “The response needs to communicate that we have heard of experiences like this before, that they can occur with sight loss, and that the person is not alone.” Ideally, that conversation takes place before the first hallucination does. As he puts it, “Forewarned really can be forearmed in this case.” MANAGING THE UNREAL Education and reassurance remain the cornerstones of care. “For somebody who has spent months believing their hallucinations mean they are developing dementia, being told what CBS is and why it happens can be enormously powerful,” Dr. Jones said. Beyond that, support needs to be tailored to the individual. Some patients benefit from changes to their lighting. Others interrupt a hallucination with behavioral techniques such as rapid eye movements, changing position or shifting their attention.⁵ Pharmacological options remain limited. Antipsychotics, anticonvulsants and SSRIs appear in case reports, but no medication is definitively recommended.⁵ “The aim should not simply be to tell somebody that their hallucinations are harmless and send them away,” Dr. Jones said. “We need to understand whether they are distressed, how CBS is affecting their life, and what support would actually help them.” THE SCIENCE COMES INTO FOCUS CBS research is gathering pace. The condition’s inclusion in ICD11 has raised its clinical profile.⁴ A major new research collection in Therapeutic Advances in Ophthalmology, co-edited by Dr. Jones, covers its prevalence, mechanisms, psychosocial impact and management.⁶ The neurobiology is still coming into focus. A neuroimaging study using magnetic resonance spectroscopy and functional MRI found no significant difference in GABA levels between people with CBS and matched controls, which gives no support to the excitation/ inhibition imbalance hypothesis. Meaningful neurochemical differences may emerge only during active hallucinations, which are notoriously difficult to catch in a scanner.⁷

For a condition defined by seeing what isn’t there, CBS is remarkably good at going unseen. Changing that costs one question and a few minutes of listening.

REFERENCES 1.

Mars JA, Rojas LC, Gurnani B. Charles Bonnet syndrome. Updated December 13, 2025. In: StatPearls [Internet]. Accessed on September 25, 2026. Christoph SEG, Boden KT, Siegel R, Seitz B, Szurman P, Schulz A. The prevalence of Charles Bonnet syndrome in ophthalmic patients: a systematic review and meta-analysis. Brain Res Bull. 2025;223:111282. Eriksen NS, Mousavi N, Subhi Y, Nielsen MK, Sørensen TL. Charles Bonnet syndrome in patients with geographic atrophy secondary to age-related macular degeneration: a cross-sectional study. Ther Adv Ophthalmol. 2025;17:1-7. Borsellino PJ, Schauer S, Rivas A, Aharonian K, Vida TA. Filling in the blind spot: integrating Charles Bonnet syndrome screening in ophthalmology. Clin Ophthalmol. 2025;19:3619-3657. Jones L, Jolly JK, Potts J, et al. From research to action: recommendations for Charles Bonnet syndrome care and policy. BMJ Open Ophthalmol. 2025;10:e002009. Jones L, Moosajee M. Charles Bonnet syndrome: taking another look at visual hallucinations in sight loss. Ther Adv Ophthalmol. 2025;17:1-3. Bridge H, Wyllie A, Kay A, et al. Neurochemistry and functional connectivity in the brain of people with Charles Bonnet syndrome. Ther Adv Ophthalmol. 2024;16:1-18.

CONTRIBUTOR

Much of the field’s progress has been driven by patients and advocates. Chief among them is Esme’s Umbrella (www.esme.org.uk), the UK charity that has given people

Dr. Lee Jones Research fellow at the University College London, Institute of Ophthalmology. lee-jones@ucl.ac.uk

NOVEMBER 2026

ENLIGHTENMENT

TRICORK

? A I T

WHEN TRANSIENT VISION LOSS WEARS A COSTUME

Transient vision loss is a master of disguise. The real cause can hide under more than one costume, so how do you tell what’s underneath? By Sam McCommon

Imagine this scenario. A patient says their vision went out for a minute. The eyes look quiet, and the chart is unremarkable. That’s the trap: everything looks fine…until it doesn’t. Transient visual loss (TVL) and transient visual disturbances are a family of spells that sound alike in a busy clinic but call for very different next steps. You might reassure the patient and send them home, direct them to a stroke center, or arrange a same-day referral for high-dose steroids before any labs come back. The three “costumes” that should be on your watch? Migraine aura, amaurosis fugax—a type of transient ischemic attack (TIA)— and giant cell arteritis (GCA). Miss the first, and you may overinvestigate a known migraineur. Miss the second, and a retinal TIA can become a hemispheric stroke. Miss the third in an older adult, and the second eye can go dark within days. “In transient monocular vision loss [TMVL], the eye exam is usually normal and the history is the most important part of the initial evaluation,” said neuro-ophthalmologist Dr. Andrew Lee (United States). Age, vascular risk and migraine history are only starting points. The clues that separate one costume from another are what the vision did, which eye was tested and what else hurt that week. PEEKING UNDER THE MASK At first glance, TVL presentations look alike. The differences lie in the company they keep. Dr. Lee sorts these clues into five categories:

Demographics, onset and pace. Migraine aura builds gradually over five to 20 minutes, is often followed by headache, and is most common in younger patients with a migraine history. Amaurosis fugax is sudden and often painless, and it occurs in older vasculopathic patients. GCA onset is also often sudden. In elderly patients, though, it’s typically preceded by systemic symptoms such as headache, jaw pain or scalp pain. Duration. Migraine aura typically lasts 20 to 60 minutes, and amaurosis fugax lasts one to 15 minutes. GCA varies, from brief episodes to permanent vision loss. Visual character. Aura is a positive phenomenon: flashing lights, jagged fortification lines, zigzags and scintillating scotomas that expand across the field. amaurosis fugax is negative: dimming, blur or blackness in one eye. It is often altitudinal, like a curtain coming down or up. GCA can produce dimming, blur or altitudinal loss, and that loss can be diffuse and severe, down to no light perception. Laterality. Aura is typically homonymous, affecting the same half of space in both eyes. A truly monocular spell can still be migraine or retinal vasospasm, but that story raises the concern for ischemia. Amaurosis fugax is strictly monocular, while cortical ischemia can be homonymous. Bilateral dimming, especially on standing, points to hypoperfusion rather than a single-eye embolus. GCA is often monocular, but both eyes can be affected at once or in rapid succession. Associated signs. Aura may be followed by headache, though not always. Amaurosis fugax can come with focal neurologic deficits, such as weakness or aphasia, if the TIA is cortical. GCA

If labs are available, markedly elevated ESR, CRP or platelets also qualify. Steroids are typically started before biopsy confirmation to protect the fellow eye, so the referral can’t wait for a routine appointment. HIGH-STAKES PATIENT PHRASES Dr. Lee listens for five patient phrases that point the way. Opticians often hear these first, at the dispensing table or on the phone, and any of the first two or the last one warrants getting the patient to an optometrist or emergency care the same day. 1. “It was like a shade or curtain pulled down over one eye.” Refer immediately to a stroke center or emergency department. 2. “My jaw hurts or gets tired when I chew food.” Arrange a same-day referral for urgent inflammatory markers and empiric high-dose steroids. Dr. Lee notes that jaw claudication is the most specific clinical symptom of GCA.

can present with jaw claudication, scalp tenderness, proximal joint pain, fever and weight loss. Two clues are less reliable than they seem. First, headache doesn’t discriminate much. Aura can occur without one, and TIA or GCA can occur with one. Second, a patient’s report of “one eye” visual loss can’t be taken at face value, because patients often mistake a homonymous hemianopia for a monocular problem. Ask whether they covered each eye in turn during the episode. TRIAGE WORKFLOW Dr. Lee sorts TMVL patients into three lanes: home, emergency stroke referral or same-day GCA referral. Who goes home. These are patients with a textbook aura, meaning gradually expanding scintillating scotomas lasting under an hour. They also have a known migraine history, normal neuro and eye exams, normal visual fields and normal blood pressure. Who gets emergency stroke referral. In a vasculopathic patient, abrupt monocular loss lasting seconds to minutes is a TIA until proven otherwise. The eye exam is still essential, but its job here is to rule out non-TIA causes of TMVL, such as dry eye, angle closure or papilledema. Once those are excluded, Dr. Lee’s rule is blunt: “A stroke of the eye is a stroke, and needs a stroke workup by the stroke doctor at the stroke center.”

3. “I saw bright, shimmering zig-zag lines in both eyes that got bigger over 15 minutes and then my typical migraine followed.” This is most likely migraine, provided the rest of the history and exam agree. 4. “Everything went blurry when I stood up quickly.” Check orthostatic blood pressure. This story suggests systemic hypotension or hypoperfusion rather than thromboembolism or arteritis, so coordinate with the patient’s primary care provider. 5. “The vision went completely black for 10 minutes.” In an elderly patient, severe loss is a red flag for GCA and warrants emergency referral. Severe here means hand motion, light perception or no light perception. THE PEARL IN THE CANDY BAG “Time is brain, and time is eye,” said Dr. Lee. Look for an ocular cause first. If none turns up, treat the spell as a TIA until proven otherwise…unless it’s the textbook aura patient you’ve already sent home. Not every mask hides a monster. But in TMVL, assume one might until the history proves otherwise. CONTRIBUTOR

Who gets same-day GCA referral. This lane is for any patient over 50 with transient visual loss and GCA symptoms, such as jaw claudication, new temporal headache or marked scalp tenderness.

Dr. Andrew Lee Neuro-ophthalmologist and Chair of Ophthalmology at the Blanton Eye Institute, Houston Methodist Hospital. aglee@houstonmethodist.org

NOVEMBER 2026