Glaucoma is caused by damage to the optic nerve, the cable of nerve fibers that carries visual information from your eye to your brain. In most cases, this damage is driven by fluid pressure building up inside the eye, though the exact trigger varies by type. Normal eye pressure falls between 10 and 20 mmHg, and when the eye’s internal drainage system can’t keep up with fluid production, that pressure rises and gradually destroys nerve fibers responsible for vision.
How Fluid Pressure Builds Inside the Eye
Your eye constantly produces a clear fluid called aqueous humor. The ciliary body, a small ring of tissue behind the iris, filters components from your blood and actively secretes this fluid into the space behind your iris. From there, the fluid flows forward through the pupil, nourishes the lens and cornea, and drains out through a spongy, triangular tissue called the trabecular meshwork near the base of the iris.
Once through the meshwork, fluid enters a ring-shaped channel called Schlemm’s canal, then passes through tiny collector channels into the surrounding veins. It’s a continuous loop: fluid in, fluid out. When everything works, the rate of production and drainage stay balanced, and pressure remains stable. Glaucoma develops when something disrupts the drainage side of that equation.
Open-Angle Glaucoma: The Most Common Form
About 90% of glaucoma cases are “open-angle,” meaning the drainage angle where the iris meets the cornea looks physically open, yet fluid still can’t get out efficiently. The problem lies in microscopic changes deep within the trabecular meshwork, specifically in the layer closest to Schlemm’s canal called the juxtacanalicular region.
In this region, the tissue gradually accumulates extra material in the spaces between cells. Researchers have identified a buildup of fibrous deposits embedded in proteins, sometimes called “plaque material,” that thickens the sheaths around elastic fibers in the tissue. This extra material clogs the drainage pathway the way sediment slowly clogs a filter. The blockage increases resistance to fluid outflow, pressure rises, and the optic nerve begins to suffer. The process is painless and typically takes years, which is why open-angle glaucoma often goes undetected until significant vision loss has occurred.
Angle-Closure Glaucoma: A Structural Problem
In angle-closure glaucoma, the drainage pathway is physically blocked rather than microscopically clogged. This happens through two main mechanisms.
The first is called pupillary block. The iris rests against the lens, and in some eyes the contact is tight enough to prevent fluid from flowing freely from behind the iris to the front chamber. Fluid trapped behind the iris pushes it forward into a bowed shape, pressing it against the trabecular meshwork and sealing off drainage. This is most likely to happen when the pupil is partially dilated, because that’s when iris-lens contact is greatest. An acute episode can cause a sudden, painful spike in eye pressure.
The second mechanism involves an unusual anatomy called plateau iris, where the ciliary body sits farther forward than normal, pushing the base of the iris up against the drainage angle. In these eyes, the central part of the front chamber may appear relatively deep, but the periphery is dangerously narrow. When the pupil dilates, the bunched-up iris tissue at the edges can block outflow even without the bowing pattern seen in pupillary block.
How High Pressure Damages the Optic Nerve
The optic nerve exits the back of the eye through a mesh-like structure called the lamina cribrosa, a sieve of connective tissue with tiny pores that nerve fibers pass through. This is the most vulnerable point. When pressure inside the eye rises, it places mechanical strain on this structure, compressing and distorting the pores.
That strain disrupts the supporting glial cells that normally supply energy and structural support to nerve fibers. When glial cells lose function, the nerve fibers can no longer maintain energy-dependent processes like transporting nutrients along their length. Starved of support, the retinal ganglion cells (the nerve cells whose fibers make up the optic nerve) begin to die. Each one that dies takes a small piece of your visual field with it, typically starting with peripheral vision and progressing inward.
Normal-Tension Glaucoma: Damage Without High Pressure
Some people develop the same pattern of optic nerve damage even though their eye pressure never exceeds the normal range. This is called normal-tension glaucoma, and it points to causes beyond pressure alone.
The leading theory centers on poor blood flow to the optic nerve. If the tiny blood vessels supplying the nerve head don’t deliver enough oxygen, nerve fibers become vulnerable even at pressures that wouldn’t normally cause harm. Research supports this: people with conditions that impair circulation are significantly more likely to develop normal-tension glaucoma. A large case-control study found that migraines increased the odds roughly 7.5 times, angina (chest pain from reduced heart blood flow) increased odds more than 11 times, and peripheral vascular disease nearly doubled the risk. Conditions like Raynaud’s syndrome, sleep apnea, and diabetes also showed elevated prevalence among patients with normal-tension glaucoma, all of which share a common thread of vascular dysfunction.
Genetic Factors
Glaucoma has a strong hereditary component. Having a first-degree relative with glaucoma substantially raises your own risk, and researchers have identified specific genes responsible for a portion of cases. Mutations in a gene called MYOC account for 3% to 4% of open-angle glaucoma cases that involve elevated pressure. Mutations in OPTN or TBK1 are linked to 1% to 3% of normal-tension cases. A separate group of six gene mutations can cause glaucoma in children or young adults, a rare but serious form that appears much earlier in life.
Most glaucoma cases, however, don’t trace to a single gene. They likely result from the combined influence of many genetic variants, each contributing a small amount of risk, interacting with age and environmental factors.
Secondary Causes: Medications, Injury, and Inflammation
Glaucoma can also be triggered by external factors rather than the eye’s own aging process.
- Corticosteroid use. Steroid medications, whether taken as pills, nasal sprays, inhalers, or eye drops, can raise eye pressure at high enough doses in nearly everyone. A particular concern is combination eye drops prescribed by non-eye specialists that contain both an antibiotic and a steroid. Patients may not realize prolonged use of these drops can lead to vision loss.
- Eye trauma. A blunt injury to the eye can damage the trabecular meshwork directly, or blood and debris inside the eye can physically block drainage. Traumatic glaucoma can appear immediately after injury or develop years later.
- Inflammation. Conditions that cause inflammation inside the eye, including certain forms of arthritis, lymphoma, and HIV, can obstruct fluid outflow. Sometimes the inflammation has no identifiable cause. In all these cases, the inflammatory material clogs the drainage system and drives pressure up.
Who Is Most at Risk
Age is the single strongest risk factor. CDC prevalence data from 2022 shows the pattern clearly: about 2% of Americans aged 60 to 64 have glaucoma, rising to roughly 6% by ages 75 to 79, and exceeding 10% by age 95. The increase is steady and steep.
Race plays a significant role as well. Black Americans have the highest prevalence at nearly 2%, more than double the rate among white Americans (about 0.9%). They also experience vision-threatening glaucoma at higher rates. Hispanic Americans fall between these groups. The reasons are complex and likely involve both genetic susceptibility and differences in access to early detection.
Other risk factors include high myopia (nearsightedness), which stretches and thins the structures at the back of the eye, and a family history of glaucoma. Having naturally thin corneas was long thought to increase risk, but recent genetic analysis has complicated this picture, suggesting that thinner corneas may simply cause pressure readings to appear lower than they actually are, leading to delayed diagnosis rather than a true biological increase in vulnerability.