Nerve tissues, once damaged, do not regenerate
In the quiet routine of a cashier's daily life, a curtain of darkness descended over one eye — and what seemed like a need for new glasses revealed itself as a rare autoimmune assault on the nervous system itself. Tan Lee Chern, a 58-year-old Singaporean woman, was diagnosed with neuromyelitis optica spectrum disorder, a condition in which the body turns against its own central nervous system, threatening blindness and paralysis with urgent speed. Her story sits at the intersection of medical fragility and human resilience, illuminating how a single timely referral, a recently approved drug, and a family's quiet sacrifice can determine whether darkness becomes permanent. It is also a reminder that rare does not mean impossible, and that speed, in the face of nerve damage, is everything.
- A dark curtain across her vision sent a convenience store cashier to the emergency room, where doctors raced to identify an attack on her own nervous system before irreversible blindness could set in.
- NMOSD is a rare but aggressive condition — affecting roughly one in 120,000 globally yet striking East Asian populations at significantly higher rates — and it can destroy optic nerves and spinal cord tissue with alarming speed.
- The window for intervention is brutally narrow: nerve damage does not heal, making early antibody testing, high-dose steroids, and plasma exchange not merely helpful but potentially the difference between sight and permanent blindness.
- Singapore's March 2025 approval of Ravulizumab offered Madam Tan a new line of defense, but the drug carries a staggering annual cost of $300,000, placing the financial weight squarely on her family even with partial insurance coverage.
- She has returned to work, but the disease has left its mark — her depth perception and peripheral vision compromised enough that she can no longer safely walk while looking at her phone, a small but daily reminder of what was lost and what was saved.
Tan Lee Chern first noticed something wrong in November — her left eye had gone cloudy, as though a dark curtain had been drawn halfway across her sight. The 58-year-old cashier assumed she needed new glasses, but the optician she visited heard her description and sent her straight to the emergency department, warning that what she was experiencing could be a stroke.
At Woodlands Hospital, doctors ruled out stroke and referred her to specialists at Tan Tock Seng Hospital, where she was diagnosed with neuromyelitis optica spectrum disorder — NMOSD — a rare chronic autoimmune condition in which the immune system attacks the optic nerves and spinal cord. In her case, antibodies were targeting aquaporin-4, a protein that forms water channels in nerve cell membranes. The inflammation that followed threatened to take her sight entirely.
NMOSD affects roughly one in 120,000 people globally, but the rate climbs significantly in East Asia — in Singapore, it affects nearly four in 100,000, and higher still among ethnic Chinese residents. For decades the condition was misclassified under multiple sclerosis; only the 2004–2005 discovery of the AQP4 antibody gave doctors the tools to diagnose and treat it properly.
Treatment is a race against time. Nerve tissue does not regenerate, so speed is everything — early antibody testing, steroids, and plasma exchange to strip harmful antibodies from the bloodstream. Madam Tan was started on Ravulizumab, a targeted antibody drug approved in Singapore in March 2025, administered intravenously at a cost of $300,000 per year. Her insurance covered much of it, with her family absorbing the remainder.
She has returned to her job as a cashier, but recovery is partial. Her depth perception and peripheral awareness remain compromised — she can no longer safely walk while looking at her phone. The disease has left its mark. Yet swift detection and intervention kept the worst at bay, and in a condition where the margin between sight and blindness can be measured in hours, that is no small thing.
Tan Lee Chern noticed something wrong with her left eye in November. The vision had gone cloudy, as though a dark curtain had been drawn halfway across her field of sight, leaving only a thin opening through which to see. She tilted her head backward just to look out. A 58-year-old convenience store cashier, she assumed she needed new glasses. When she visited an optician and described the sensation—that black shade pulled partway down—the optician did not write her a prescription. Instead, the optician told her to go to the emergency department immediately. What she was describing, the optician said, could be a stroke.
At Woodlands Hospital, near her home, doctors ran tests and scans. They ruled out stroke and other conditions, then settled on a possibility: an immune system disorder. She was referred to specialists at Tan Tock Seng Hospital, where an ophthalmologist confirmed the diagnosis. Madam Tan had neuromyelitis optica spectrum disorder, or NMOSD—a rare, chronic autoimmune condition in which the body's own immune system attacks the central nervous system, targeting primarily the eyes and spine. The fear was immediate and justified. Without urgent treatment, she was told, blindness would come quickly.
NMOSD works through a specific mechanism. The immune system, in a healthy body, has a process for destroying cells that mistakenly recognize the body's own tissues as invaders. In NMOSD, this deletion process fails. Antibodies slip through and cross into the brain, spinal cord, and optic nerves, attacking them. In Madam Tan's case, the antibodies were targeting a protein called aquaporin-4, which forms water channels in nerve cell membranes and helps regulate fluid flow in the central nervous system. When these antibodies attack the optic nerve, inflammation follows—and vision can be lost with startling speed. The optic nerve, as one specialist explained, is essentially the wire connecting the brain to the eyes, which is why it becomes a target. The condition can also strike the spinal cord, causing weakness, numbness, loss of bladder control, or back pain. In some patients, the antibodies attack the brain's vomiting center, causing intractable hiccups and vomiting—symptoms so disconnected from neurology that patients are often sent for extensive stomach and intestinal scans before the true diagnosis emerges.
Globally, NMOSD affects roughly one in 120,000 people, but the rate is significantly higher in East Asia. In Singapore, studies show a prevalence of nearly four in 100,000, rising to about five in 100,000 among ethnic Chinese residents. There appears to be a genetic component; certain genetic risk factors are more common in East Asian populations. Multiple sclerosis, a closely related disease, by contrast, is far more prevalent among Caucasians. For decades, NMOSD was simply grouped under the umbrella of multiple sclerosis, called optical spinal MS. The turning point came in 2004 and 2005, when researchers identified the antibody targeting aquaporin-4. That discovery transformed how doctors could diagnose and treat the disease.
There is no cure for NMOSD, but treatment options exist for acute attacks, relapse prevention, and symptom management. The critical factor is speed. Nerve tissue, once damaged, does not regenerate. Early detection through antibody testing is therefore essential—it allows doctors to begin steroids and plasma exchange quickly if needed. Plasma exchange is a mechanical process: blood is separated from plasma using a specialized machine, removing the harmful antibodies and immune factors circulating in the bloodstream. Drugs can also prevent future relapses. Madam Tan was started on Ravulizumab, an antibody medication approved in Singapore in March 2025, given intravenously. She has received four treatments. The drug costs $300,000 per year.
The financial burden fell on her family. Her son, a 29-year-old radiography student, checked with her insurance company and found that the treatment was covered, though with a co-payment. The family is helping to cover the remainder, though he declined to specify the amount. With regular treatment, Madam Tan has returned to work as a cashier. But recovery is incomplete. Her vision has not fully returned. She can no longer walk while looking at her phone; her depth perception and peripheral awareness have been compromised enough that she cannot safely judge what lies ahead of her. The disease has left its mark. Still, early detection and swift intervention saved her from the blindness that was bearing down on her. The race against time, in her case, was won—though not without cost.
Notable Quotes
I was also told I needed to go for immediate treatment, otherwise I would be blind quite quickly.— Madam Tan Lee Chern, on her diagnosis
Nerve tissues, once damaged, do not regenerate, so time is of the essence when it comes to treating the condition.— Assistant Professor Kelvin Li, consultant ophthalmologist at Tan Tock Seng Hospital
The Hearth Conversation Another angle on the story
Why did the optician immediately send her to the emergency department instead of just writing a prescription?
Because the specific way she described the vision loss—that black shade pulled halfway down—is a recognized warning sign of stroke. An optician knows the difference between a refractive error and a neurological event. That description triggered alarm.
So the immune system is attacking her own nerve tissue. How does the body not catch that and stop it?
Normally it does. There's a process that deletes immune cells that would attack the body's own tissues. In NMOSD, that deletion process breaks down. The antibodies slip through and cross the blood-brain barrier, which usually protects the nervous system. Once they're in, they find their target—in her case, a protein in nerve cell membranes—and attack.
The hiccups and vomiting you mentioned—that seems almost cruel, that the disease would attack the vomiting center.
It is. And it's why so many NMOSD patients are misdiagnosed for months. A doctor sees intractable hiccups and vomiting and thinks stomach, thinks gastroenterology. They order endoscopies. They find nothing. It's only when the disease hits the eyes or spine hard enough that someone thinks to look at the nervous system.
Why is it so much more common in East Asians?
There's a genetic component. Certain genetic risk factors that make someone susceptible to NMOSD are more common in East Asian populations. It's similar to how multiple sclerosis is far more prevalent in Caucasians. The disease follows genetic geography.
The drug costs $300,000 a year. How many people in Singapore can actually afford that?
That's the real question. She was fortunate—her insurance covered most of it. But not everyone has that coverage. The drug was only approved in Singapore in March 2025, so we're still in the early days of understanding access and affordability. For now, it's a lifeline for those who can reach it.
Even with treatment, her vision didn't fully come back.
No. That's the hard truth about nerve damage. Once it's done, it's done. The goal of treatment is to stop the attack, to prevent further damage, to prevent blindness. Recovery of what's already been lost is limited. She got her life back, but not her vision.