Glaucoma happens when nerve fibers at the back of your eye are gradually destroyed, most often because fluid pressure inside the eye builds up too high. Your eye constantly produces a clear fluid that nourishes its internal structures and maintains its shape. When that fluid can’t drain out fast enough, pressure rises and damages the optic nerve, the cable that carries visual information to your brain. The damage is permanent, and because it typically starts with peripheral vision, most people don’t notice it until significant sight has already been lost.
How Fluid Builds Up Inside the Eye
Your eye produces a small amount of clear fluid called aqueous humor around the clock. At the same time, an equal amount is supposed to flow out through a tiny drainage system near the front of the eye. Normal eye pressure sits between 10 and 20 millimeters of mercury (mmHg). When production and drainage stay in balance, pressure holds steady in that range.
In principle, pressure could rise because the eye makes too much fluid or because the drainage system isn’t working well enough. In practice, the problem is almost always insufficient drainage. Fluid backs up, pressure climbs, and the optic nerve starts taking damage.
The Eye’s Two Drainage Routes
Fluid leaves the eye through two pathways, both located in a narrow angle where the iris meets the cornea. The primary route passes through a lattice-like filter called the trabecular meshwork. Think of it as a biological sieve: fluid seeps through layers of tiny collagen beams lined with specialized cells, then enters a ring-shaped channel that connects to the bloodstream through a network of small collector vessels. Most of the fluid exits this way.
The secondary route is simpler. Fluid drains through the muscle tissue behind the iris and eventually passes through the white outer wall of the eye. This pathway handles a smaller share of the total outflow, but it matters. When either route becomes partially blocked or starts resisting flow, pressure creeps upward.
Open-Angle Glaucoma: The Most Common Form
About 90% of glaucoma cases are open-angle, meaning the drainage angle between the iris and cornea looks physically open but the meshwork filter itself has become resistant to fluid flow. The exact reason varies, but the filter’s microscopic structure gradually becomes less permeable over time. Pressure rises slowly, often over years, with no pain or obvious symptoms. By the time you notice vision changes, a substantial number of nerve fibers may already be gone.
This slow, silent progression is what makes open-angle glaucoma so dangerous. Eye pressure can sit in the low-to-mid 20s for a long time, doing cumulative damage without triggering any warning signs.
Angle-Closure Glaucoma: A Structural Problem
In angle-closure glaucoma, the drainage angle is physically narrow or gets blocked by the iris itself. Some people are born with a shallower-than-normal space between the iris and cornea. Under certain conditions, particularly when the pupil dilates in dim lighting, the peripheral iris can bow forward and press against the meshwork filter, cutting off drainage entirely.
When the iris makes prolonged or repeated contact with the meshwork, scar-like adhesions can form, creating a permanent blockage. This is the mechanism behind acute angle-closure attacks, which cause sudden, severe eye pain, headache, nausea, and blurred vision. Unlike open-angle glaucoma, this version announces itself dramatically and requires urgent treatment to prevent rapid vision loss.
People with naturally thicker peripheral iris tissue or unusually shallow front chambers are more susceptible. The condition is more common in people of Asian descent and in those who are farsighted, since farsighted eyes tend to have smaller front chambers.
How Pressure Damages the Optic Nerve
The optic nerve exits the eye through a sieve-like structure at the back called the lamina cribrosa, a thin plate of connective tissue with tiny holes that nerve fibers pass through. When pressure in the eye rises, it compresses these fibers against that plate. Over time, the sustained mechanical stress disrupts the nerve cells’ internal energy factories, their mitochondria, triggering a cascade of damage that kills the cells.
As nerve fibers die, the center of the optic disc (the circular area where the nerve exits) becomes hollowed out. Eye doctors measure this as the “cup-to-disc ratio.” In a healthy eye, the cup takes up less than half the disc’s diameter. As glaucoma progresses, the cup grows larger, reflecting the loss of nerve tissue.
Once those nerve fibers are gone, they don’t regenerate. Each lost fiber represents a tiny piece of your visual field that won’t come back, which is why early detection matters so much.
Normal-Tension Glaucoma: Damage Without High Pressure
Some people develop the same pattern of optic nerve damage even though their eye pressure stays within the normal range. This is called normal-tension glaucoma, and it challenges the idea that pressure alone explains the disease.
The leading explanation involves blood flow. The optic nerve needs a steady supply of oxygen, and that supply depends on the balance between blood pressure pushing blood into the eye and eye pressure pushing back. In people with normal-tension glaucoma, blood flow to the optic nerve appears to be disrupted. Several factors contribute. Naturally low blood pressure, especially overnight dips greater than 10% of daytime levels, can starve the nerve of oxygen during sleep. People with a pattern of exaggerated blood vessel spasms (sometimes linked to migraines or cold hands and feet) appear to be at higher risk. Sleep apnea, which causes repeated drops in blood oxygen overnight, can also damage the blood vessel lining and impair the nerve’s blood supply.
Interestingly, when researchers monitor eye pressure continuously with sensors rather than checking it at a single office visit, many normal-tension patients show significant pressure spikes at night that go undetected during daytime appointments. So in some cases, pressure may still play a larger role than a single reading suggests.
Secondary Glaucoma: External Triggers
Glaucoma can also develop as a consequence of another event or condition. The common thread is always the same: something obstructs the drainage of fluid from the eye.
- Eye injuries. A blow to the eye can directly damage the trabecular meshwork or cause bleeding inside the eye. Blood and debris physically block the drain.
- Inflammation. Infections or autoimmune conditions that inflame the inside of the eye produce inflammatory debris that clogs the outflow system.
- Steroid medications. Corticosteroids, whether taken as eye drops, pills, inhalers, or injections, can raise eye pressure in nearly anyone if the dose is high enough. The effect is usually reversible when the medication is stopped, but prolonged use can cause lasting damage.
Who Is Most at Risk
Glaucoma can affect anyone, but certain groups face significantly higher odds. African Americans are six to eight times more likely to develop glaucoma than white people and tend to develop it about a decade earlier than other groups. Hispanic and Asian populations also carry elevated risk, with Asian populations particularly susceptible to angle-closure forms.
Age is a major factor across all groups. Risk rises substantially after 40 for African Americans and after 60 for the general population. Having a parent or sibling with glaucoma increases your risk, as does having diabetes. The genetic component is strong enough that family history alone is considered a reason to start screening earlier and more frequently.
Because the most common form of glaucoma produces no symptoms until vision is already lost, routine eye exams that include pressure measurement and optic nerve evaluation are the only reliable way to catch it early. The damage can’t be reversed, but when detected early, treatment to lower eye pressure can slow or stop further nerve loss in most people.