The term “blindness” is relative because governments—not doctors—decide who qualifies as “blind.” In many cases, being labeled “blind” doesn’t mean a total lack of vision; it merely signifies a range of visual abilities that differ from typical sighted experience.

10 Fascinating Things: A Quick Overview

10 Nothing

“What do you see?” is perhaps the most over‑asked question by sighted folks. The honest answer from many blind individuals is simply “nothing.” Not black, not a shade of gray—absolute nothingness. Trying to explain this void to someone with full vision is as futile as describing the taste of a color to a person who has never seen it.

Imagine attempting to convey color to someone who has been blind since birth; it’s impossible. In the same way, someone who has never experienced visual input cannot truly describe the sensation of seeing nothing. The concept remains elusive on both sides of the visual divide.

There is, however, a practical way to simulate that emptiness. Close one eye, focus intently on something with the other, and keep your concentration. While the closed eye remains shut, it registers absolutely no visual information—not even the darkness that appears when both eyes are covered. That void is the closest approximation to what totally blind people experience.

9 Light

Back in 1923, Harvard student Clyde Keeler made a surprising discovery: blind mice’s pupils contracted when exposed to illumination. At the time, scientists believed that only the two classic retinal photoreceptors handled light detection, and those should have been inactive in blind animals.

Keeler’s observations led to the identification of a third type of photoreceptor—intrinsically photosensitive retinal ganglion cells (ipRGCs). Unlike the classic photoreceptors that feed visual images to the brain’s image‑processing centers, ipRGCs relay light information to other brain regions without forming pictures, allowing blind individuals to sense light without “seeing.”

More recently, researchers at the University of Montreal placed three blind participants in a controlled room, toggling the lights on and off while asking them to indicate the change. Most participants correctly identified the lighting state, provided their brains were actively engaged at the moment—a clear demonstration that light perception can persist without conventional vision.

8 Facial Expressions

Humans are wired for emotional contagion: we instinctively mirror the facial cues of those around us—smiling when we see a smile, yawning when someone else does. Blind individuals share this uncanny ability, even without visual access to the faces that spark these reactions.

Neuroscientist Marco Tamietto from Tilburg University investigated this phenomenon with two participants who lost vision in one eye due to visual‑cortex damage. By presenting pictures of smiling and frowning faces to the eye linked to the damaged cortex versus the healthy eye, Tamietto found that the participants responded more rapidly to images processed by the impaired side.

The takeaway? Even without sight, the brain can pick up on facial expressions, leading blind people to instinctively mimic a smile when you smile at them—a subtle yet powerful reminder of shared humanity.

7 Death Experiences)

Near‑death experiences (NDEs) often involve vivid visual narratives: tunnels of light, encounters with familiar faces, or out‑of‑body observations. Surprisingly, some blind individuals report comparable phenomena, claiming that they “see” during these moments despite lifelong visual deprivation.

Psychologist Kenneth Ring at the University of Connecticut examined 21 blind case studies from the 1990s. Fifteen participants described regaining sight during their NDE, reporting clear visual detail. Three reported seeing nothing, while the remaining three were uncertain about any visual component.

One striking account describes a man who found himself in a library brimming with billions of books, each crystal‑clear. Another, Vicki Umipeg, recounted watching herself and surgeons operate on her after her soul left her body, then traveling through a tunnel to meet luminous beings. These narratives suggest that, under extreme physiological stress, the brain may generate visual experiences even in those who have never seen before.

6 Nightmares

Nightmares stem from the emotional and stress‑laden moments we experience while awake. A study by Denmark’s Center for Sleep Medicine revealed that people born blind are four times more likely to endure nightmares than sighted individuals, likely due to heightened emotional processing.

The researchers compared 50 participants—25 blind and 25 sighted. Among the blind group, 11 were congenitally blind, while 14 lost vision later in life. Results showed that those born blind reported nightmares in 25 % of their sleep cycles, compared with only 7 % for those who became blind later and 6 % for sighted controls.

Dream content also diverged. Blind participants, regardless of when they lost sight, frequently dreamed of awkward social scenarios and vehicular accidents. However, those born blind never described visual imagery; their dreams centered on sounds, textures, tastes, and smells. In contrast, sighted dreamers reported vivid visual scenes, while those who became blind still retained some visual dreaming, which gradually faded over time.

5 Up Ads

You’re reading this article on the web, and like every other net‑user, you’ve encountered online advertisements. Among the many formats, pop‑up ads are the most intrusive—suddenly leaping onto the screen and wrecking an otherwise smooth browsing experience.

Ethan Zuckerman wrote the original pop‑up code over two decades ago, later dubbing it the Internet’s “original sin.” Whether blind users can forgive him is uncertain, as these ads have become a unique nightmare for them.

For a screen‑reader user, a pop‑up appears as an unexpected burst of spoken text. If the ad lacks a clear “close” command, the user may wander through the ad for minutes before realizing something’s amiss, disrupting the flow of the original page.

This problem intensifies because many pop‑ups are not properly labeled for assistive technology, forcing the screen reader to restart from the top of the page after the user finally dismisses the ad, replaying the entire article.

Ad‑blocking extensions could eliminate this annoyance, but some sites block such tools to preserve ad revenue. Moreover, developers have devised ways to bypass blockers, ensuring that pop‑ups continue to intrude on blind users’ browsing experiences.

4 Movement

When Milena Channing suffered a massive stroke at 29, she assumed her vision was gone forever—until she noticed moving water while bathing her daughter. Her doctor dismissed it as hallucination, insisting, “You’re blind, and that’s it!”

Undeterred, Milena observed that she could perceive falling rain, steam rising from a hot mug, and the sway of her daughter’s ponytail, yet she could not see static objects. Doctors later identified her experience as Riddoch’s phenomenon, a condition where only moving stimuli are consciously perceived.

The stroke spared the brain region responsible for processing motion, allowing her to “see” anything that moved. Realizing that motion enhanced her perception, Milena even acquired a rocking chair to keep herself in gentle motion, thereby improving her limited visual experience.

3 Visual Hallucinations

Charles Bonnet syndrome (CBS) describes vivid visual hallucinations that occur in people who have recently lost their sight. Those affected recognize that the images are not real, yet the hallucinations can be strikingly detailed and last from a few weeks up to a year and a half, sometimes even five years.

One 69‑year‑old man reported seeing bizarre shapes, people, and animals—including a spider he tried to swat—six months after becoming blind. He also claimed to see acquaintances sitting beside him, despite knowing they were not physically present.

Researchers suspect CBS results from the brain’s attempt to compensate for missing visual input. Supporting this theory, an experiment blindfolded 13 participants for five days; ten of them experienced visual hallucinations after just a single day of sensory deprivation.

2 Color

While those born blind may never experience visual color, individuals who lose sight after having seen can sometimes retain vivid chromatic sensations. BBC journalist Damon Rose, who became blind following a childhood surgery, now perceives an overwhelming cascade of colors that flash like lights, constantly shifting in shape and intensity.

Rose describes the colors as so abundant that they become a distraction. They can appear as solitary hues or layered, with one color overlaying another. Intriguingly, the one thing he never perceives is darkness—a void he deeply misses despite his colorful internal world.

1 Everything

Some blind people have mastered echolocation, a technique where they emit a sound and interpret the returning echo to gauge the size, shape, and location of surrounding objects—much like bats and dolphins navigate their environments.

Unlike those animals, which can detect tiny insects, humans need larger obstacles—roughly the size of a drinking glass—to generate a discernible echo. Nevertheless, with practice, echolocation can become a powerful substitute for sight.

Daniel Kish, who lost both eyes as an infant due to bilateral retinoblastomas, learned to “see” using echolocation. He now navigates complex spaces, rides a bicycle, and performs daily tasks relying solely on sound reflections.

Similarly, Ben Underwood, who also lost his eyes to retinoblastoma at age two, independently honed echolocation skills. He could walk, skateboard, and play without a guide dog or cane, effectively operating as if he weren’t blind. Sadly, he passed away in 2009 after his cancer returned.

When I turned 23, my eyesight started to wobble, and the medical team was left scratching their heads. This is the top 10 terrifying roster of conditions that can steal your sight, illustrated by my own two‑year odyssey through endless referrals and baffling test results.

10 Brain Tumor

top 10 terrifying Brain Tumor Details

“Mass lesion.” Those two ominous words, scribbled in a hurried hand on a medical pad, felt like a death sentence. I caught a glimpse of the note while the optometrist stepped out, and my mind instantly raced to funeral plans. The eye chart I’d just struggled with confirmed something was off, and right beneath the alarming headline lay the results of my visual‑field test, which revealed massive scotomas—blind spots—in both eyes.

The scotomas showed a striking symmetry: the left eye suffered a major defect in its upper‑left quadrant, while the right eye’s problem sat in the upper‑right quadrant. The optometrist theorized that a tumor might be pressing on my optic chiasm—the crossroads where the optic nerves intersect at the base of the brain. Such pressure could explain the bilateral field loss I was experiencing.

The visual‑field exam was ordered after it became clear I couldn’t read the 20/20 line even with my corrected glasses—a red flag usually reserved for older adults, not a 23‑year‑old. This discrepancy set off alarm bells and pushed the investigation toward a possible intracranial mass.

Of course, the optometrist couldn’t confirm a diagnosis on the spot, so “mass lesion” was a referral cue, not a final verdict. He promptly arranged an MRI to see if a tumor was the culprit stealing my sight.

After what felt like an eternity—four days that stretched into an agonizing marathon—the MRI finally arrived. The scan was clean: no tumor, no sinister growth. I was spared a fatal diagnosis, yet the mystery of my disappearing vision remained unsolved. The remaining entries on this list represent the other possibilities my doctors considered, and one that ultimately turned out to be the truth.

9 Retinitis Pigmentosa

Commonly abbreviated as RP, retinitis pigmentosa is exactly as frightening as its name suggests. Picture your peripheral vision slowly eroding, turning your wide‑angle view into a narrowing tunnel that eventually collapses, leaving you in total darkness.

The condition earns its name because it causes the breakdown and loss of retinal cells—the light‑sensing tissue lining the back of the eye. Over 50 genes are implicated, each essential for the health of photoreceptors, the rods and cones that detect light and color. Though rare, RP isn’t unheard of; roughly one in every 4,000 people worldwide wrestles with it.

Early RP typically manifests as night blindness and a gradual shrinkage of the visual field. Progression rates differ, but most sufferers eventually lose most of their sight, making everyday tasks—reading, driving, navigating, recognizing faces—extremely challenging. Fun, right?

One diagnostic tool for RP is the electroretinogram (ERG), which measures electrical responses of the photoreceptors. A diminished response points to fewer functional cells, confirming RP. In my case, the ERG returned normal results, ruling this disease out.

8 Macular Degeneration

Macular degeneration stands as the leading cause of vision loss in the United States, affecting over 10 million people—more than cataracts and glaucoma combined. Unlike cataracts, which are surgically removable, or glaucoma, which can be managed with medication, macular degeneration is essentially incurable and largely unstoppable.

The disease attacks the macula, the central portion of the retina responsible for sharp, detailed vision. We rely on the macula for reading, driving, distinguishing colors, and recognizing faces. When it deteriorates, central vision blurs or disappears.

Prognoses vary wildly. Some patients experience no noticeable loss, while others see wavy or blurred vision that progresses to complete central vision loss, leaving only peripheral sight—a reversal of the tunnel‑vision effect seen in RP.

Two main forms exist: “dry” macular degeneration, which accounts for roughly 85‑90 % of cases and involves the buildup of yellow deposits called drusen beneath the macula, and “wet” macular degeneration, where abnormal blood vessels grow and leak fluid, causing rapid, severe vision loss.

Wet macular degeneration’s leaky vessels can cause sudden, dramatic deterioration, whereas dry forms tend to progress more slowly, often preserving a functional visual acuity around 20/40.

Age‑related macular degeneration typically appears later in life, but a rarer form called Stargardt disease can strike younger individuals. My macula, however, was perfectly healthy, eliminating this condition from my differential.

7 River Blindness

When doctors encounter an unexplained vision loss, they often ask seemingly obscure questions—like whether you’ve recently visited Africa or any tropical region. This line of inquiry aims to rule out the infamous “River Blindness,” formally known as onchocerciasis.

Onchocerciasis is transmitted by the bite of a blackfly that breeds near fast‑flowing rivers, hence the nickname. The tiny worm released by the fly multiplies into countless microfilariae that wander into the skin and eyes. When these larvae die, they release toxic substances that cause intense itching and eye lesions, eventually leading to irreversible blindness and disfiguring skin disease.

In some West African villages, up to 50 % of men over 40 have been blinded by this parasite. Fortunately, I had never set foot in Africa, Latin America, or any region where the disease is endemic, so this diagnosis was swiftly dismissed.

6 Lead Poisoning

“Have you ever been exposed to old paint, rusty pipes, or water that didn’t taste fresh?” That blunt question is the medical equivalent of asking if you’ve been eating paint chips.

Lead poisoning isn’t just a brain‑affecting issue; it can also wreak havoc on the optic nerve, the conduit that carries visual information to the brain. Damage to this nerve can manifest as difficulty seeing in low light, blurriness, chronic irritation, and an increased risk of cataract formation—though cataracts are unlikely in someone in their early twenties.

The doctors needed to rule out lead exposure, especially after the Flint, Michigan water crisis reminded everyone how pervasive and preventable lead toxicity can be. Historically, lead has been embedded in gasoline, paint, crafts, and plumbing, making exposure a real concern.

Fortunately, widespread lead exposure in developed nations is now rare, and my tests came back clean, eliminating this as a cause of my visual decline.

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5 Nonarteritic Anterior Ischemic Optic Neuropathy

… is a mouthful for what doctors call an “ocular stroke.” In this condition, the optic nerve suddenly suffers a drop in blood flow, depriving it of oxygen and nutrients. The event can be isolated to the eye or part of a larger cerebrovascular incident.

Like any stroke, the severity ranges widely. Approximately one in 10,000 people experience this, including notable New York Times columnist Frank Bruni, who penned a poignant piece titled “Am I Going Blind?” describing his own brush with the disorder.

Bruni’s narrative captures the terror: “They say death comes like a thief in the night; lesser vandals have the same M.O. The affliction that stole my vision, or at least a big chunk of it, did so as I slept. I went to bed seeing the world one way. I woke up seeing it another.” He likened the visual loss to a “thick, dappled fog” that clouded half of his visual field, leaving him feeling “drunk without being drunk.”

Patients who survive an ocular stroke often live with lingering vision loss and the constant dread that another event could strike the remaining eye. Bruni estimated a 20 % chance of a repeat episode over five years, essentially a one‑in‑five risk of functional blindness.

My own visual pattern didn’t fit the classic picture of an ocular stroke, so while NAION remained a “maybe,” it never became the leading suspect.

4 Devic’s Disease

One of the disorders that most closely mirrored my symptoms was Devic’s Disease, also known as neuromyelitis optica. Think of it as multiple sclerosis on steroids: both attack the nervous system, but Devic’s tends to be far more aggressive.

While classic MS often presents with optic neuritis affecting a single eye, Devic’s typically produces sizable scotomas—blind spots—in both eyes. My examinations confirmed bilateral vision loss, and a neuro‑ophthalmologist noted that my optic nerves were thinner than average, suggesting the cables (nerve fibers) were frayed even though the cameras (eyes) themselves were intact.

Devic’s is brutally unforgiving. Like its cousin MS, it involves immune‑mediated attacks on the optic nerves and spinal cord, but its relapses are often more severe, causing abrupt, profound loss of sight and mobility. Symptoms can range from blindness in one or both eyes to weakness, painful spasms, loss of sensation, uncontrollable vomiting, and bladder or bowel dysfunction.

An MRI of my spine returned inconclusive, prompting a spinal tap—an invasive procedure that extracts cerebrospinal fluid for analysis. The fluid showed no definitive signs of Devic’s or MS, leaving the mystery alive.

Although the tap was normal, the search for the true cause persisted, and Devic’s remained on the differential list for a while.

3 Coloboma of the Eye

Derived from the Greek word meaning “curtailed,” coloboma refers to a group of congenital anomalies where normal eye tissue is missing. This can involve the macula, lens, uvea, optic nerve, or even the eyelids. The visual impact ranges from negligible to severe, depending on the structures involved.

If my case had been confirmed, it would have been a moderate optic‑nerve coloboma—a hollowed‑out segment of the optic passage. Since colobomas are present from birth, they often go unnoticed until adolescence or early adulthood when routine eye exams reveal subtle deficits.

My mother suffered from preeclampsia during pregnancy, a condition that can restrict oxygen flow to the fetus and potentially cause birth defects. This connection offered a plausible explanation for a congenital eye anomaly, especially given the tragic loss of my mother during a later pregnancy.

However, most colobomas are genetic, and there was no family history of the condition. With no definitive test to confirm its presence, coloboma remained a “maybe”—a hopeful possibility, as colobomas rarely worsen over time.

2 Leber’s Syndrome

Officially termed Leber Hereditary Optic Neuropathy (LHON), Leber’s Syndrome is a mitochondrial disease that attacks retinal ganglion cells and their axons, the nerve fibers that funnel visual signals to the brain. Although it predominantly affects young men, the mutation is passed down exclusively from mothers, since mitochondria are inherited maternally.

LHON typically presents with a sudden onset of visual loss, first affecting one eye and then the other within weeks. In about a quarter of cases, both eyes go dark simultaneously. The disease swiftly leads to optic atrophy and a permanent drop in visual acuity.

During the acute phase, affected eyes display a fluid‑filled appearance of the nerve fiber layer and enlarged or damaged peripapillary vessels. A relative pupillary defect may also be evident, reflecting the eye’s struggle to gather light.

Two hallmark signs of LHON aligned with my symptoms: impaired color vision and cecocentral scotomas—blind spots that originate at the natural blind spot where the optic nerve exits the eye and then expand outward. These features would have signaled LHON, but my diagnostic work‑up did not support it.

Had I been afflicted with Leber’s, I would likely be nearly blind today. Fortunately, the condition was ruled out.

1 Dominant Optic Atrophy

After nearly two years of diagnostic limbo, the doctors arrived at a conclusion by process of elimination: Dominant Optic Atrophy (DOA). This unsettlingly named disorder is loosely defined but revolves around the gradual degeneration of the optic nerves.

Also known by its acronym DOA, the condition is hereditary—hence the “dominant” label. My father’s history of mild optic neuritis offered a genetic clue, suggesting a familial pattern.

DOA typically emerges in the first decade of life, with affected individuals experiencing moderate visual loss and color‑vision deficits. The severity is highly variable: some retain near‑normal vision, while others slip into legal blindness (20/200 corrected).

The disease remains a medical enigma; mutations in several genes have been implicated, and some responsible genes are still unidentified. At present, there is no cure or preventive measure for DOA.

Adding a twist of fate, DOA carries a “Sword of Damocles” quality—it can pause for years, then suddenly restart without warning. Thankfully, it’s been over 15 years since I’ve noticed any measurable decline, but the specter of further loss lingers in my mind.

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About The Author: Christopher Dale (@ChrisDaleWriter) writes on politics, society and sobriety issues. His work has appeared in Daily Beast, NY Daily News, NY Post and Parents.com, among other outlets.