The main cause of glaucoma is a buildup of fluid pressure inside the eye, which damages the optic nerve over time. This happens when the eye’s natural drainage system fails to move fluid out efficiently, causing intraocular pressure (IOP) to rise above the normal range of roughly 10 to 21 mmHg. That said, pressure alone doesn’t explain every case, and the full picture involves drainage anatomy, genetics, blood flow, and individual nerve sensitivity.
How Eye Pressure Builds Up
Your eye constantly produces a clear fluid called aqueous humor, which nourishes the front of the eye and maintains its shape. This fluid is made by a structure behind the iris called the ciliary body, primarily through active secretion. Once produced, the fluid flows from behind the iris into the front chamber of the eye, then drains out through two exit routes.
The primary route, handling most of the outflow, is a ring of spongy tissue called the trabecular meshwork. Fluid passes through this meshwork into a tiny channel (Schlemm’s canal), then into small veins that carry it back into the bloodstream. A secondary route runs through the muscle tissue behind the iris. In a healthy eye, fluid production and drainage stay balanced, keeping pressure stable. When drainage slows down but production continues at the same rate, pressure climbs.
About 75% of the resistance to fluid leaving the eye is concentrated in the trabecular meshwork. This is why problems in this one structure are responsible for most glaucoma cases.
Open-Angle Glaucoma: The Most Common Type
Open-angle glaucoma accounts for the majority of cases worldwide, and it develops gradually over years. The drainage angle between the iris and cornea stays physically open, but the trabecular meshwork itself becomes increasingly resistant to fluid flow. Think of it like a coffee filter that slowly clogs: the pathway looks clear, but the filter material won’t let liquid through efficiently.
Research has revealed something striking about what goes wrong at the cellular level. In glaucomatous eyes, the trabecular meshwork tissue is roughly 20 times stiffer than in healthy eyes. The cells lining the drainage canal also become stiffer, measuring about 1.24 kilopascals compared to 0.79 in normal eyes. This stiffening involves a buildup of structural proteins in the tissue, increased cellular contraction, and remodeling of the scaffolding between cells. The result is a meshwork that physically resists the passage of fluid, causing pressure to rise slowly enough that most people don’t notice until significant nerve damage has already occurred.
Angle-Closure Glaucoma: A Structural Problem
Angle-closure glaucoma has a different mechanism. Instead of the meshwork slowly clogging, the iris physically blocks the drainage angle. The major predisposing factor is the structural anatomy of the front of the eye: a shallower than normal space between the iris and cornea, a larger or more forward-positioned lens, or a narrow entrance to the drainage angle.
The most common trigger is something called pupillary block. In eyes with these anatomical features, the iris sits very close to the lens, impeding fluid flow from the back chamber to the front. Pressure builds behind the iris, causing it to bow forward like a sail catching wind. This pushes the outer edge of the iris against the trabecular meshwork, sealing off the drain entirely. The acute form causes a sudden, dramatic spike in eye pressure with severe pain, blurred vision, and halos around lights. Other, less common mechanisms include plateau iris syndrome (where the iris root is abnormally positioned) and a lens that shifts forward with age.
How Pressure Damages the Optic Nerve
Elevated pressure ultimately causes glaucoma by killing retinal ganglion cells, the neurons whose long fibers bundle together to form the optic nerve. The dominant theory is that high pressure physically compresses nerve fibers where they exit the eye through a sieve-like structure called the lamina cribrosa. This compression blocks the transport of growth-sustaining molecules that travel along the nerve fibers back to the cell bodies, starving the cells.
There’s also a chemical dimension. Elevated pressure triggers retinal ganglion cells to release enzymes that break down the supportive scaffolding around them. As this scaffolding degrades, cells lose the survival signals they normally receive from their surroundings and undergo programmed cell death. Excess glutamate, a neurotransmitter that becomes toxic at high levels, may amplify this destructive cascade. The damage is irreversible: once these nerve cells die, they don’t regenerate, and the corresponding areas of vision are permanently lost.
When Pressure Isn’t Elevated
One of the more puzzling aspects of glaucoma is that it can develop even when eye pressure falls within the normal range. This is called normal-tension glaucoma, and it suggests the optic nerve in some people is unusually vulnerable to damage at pressures that most eyes tolerate without issue.
Several pressure-independent factors appear to play a role. Disrupted blood flow to the optic nerve is one leading candidate. Ocular perfusion pressure, the difference between blood pressure pushing blood into the eye and the intraocular pressure resisting it, influences how well the optic nerve is nourished. Population studies have found strong relationships between low ocular perfusion pressure and both the development and progression of open-angle glaucoma. A person with relatively low blood pressure combined with even a modest IOP may have inadequate blood flow to the nerve.
Structural abnormalities in the optic nerve itself also contribute. A recent study found that 86% of optic nerves in normal-tension glaucoma patients showed abnormal kinking, compared to just 18% in controls. Impaired circulation of cerebrospinal fluid around the optic nerve may allow neurotoxic substances to accumulate locally, adding another layer of damage independent of eye pressure. These findings help explain why lowering IOP, while effective, doesn’t always stop the disease from progressing.
Genetics and Family History
Glaucoma has a strong hereditary component. Having a first-degree relative with glaucoma significantly increases your risk, and researchers have identified several genes involved. Mutations in the myocilin gene cause about 2 to 4% of open-angle glaucoma cases. This gene produces a protein found in the trabecular meshwork, and when it’s defective, drainage function suffers. Mutations in the optineurin gene are linked specifically to normal-tension glaucoma, while mutations in the CYP1B1 gene appear across multiple forms of the disease.
Still, identified gene mutations account for only a small fraction of all cases. Most glaucoma likely results from the combined influence of many common genetic variants, each contributing a small amount of risk, interacting with age, anatomy, and environmental factors.
Who Faces the Highest Risk
Age is the single strongest demographic risk factor. The trabecular meshwork stiffens and becomes less efficient with age in everyone, but the process accelerates in some people more than others. Ethnicity also plays a meaningful role. A large multicenter study found glaucoma prevalence of 5.8% in Black populations compared to 2.4% in White populations. After adjusting for age, Black individuals had 2.75 times the prevalence of White individuals, while mixed-race individuals had 1.85 times the rate.
Other well-established risk factors include high myopia (nearsightedness), which stretches and thins the structures of the eye, a thinner than average cornea, and diabetes. Family history compounds all of these: if you carry genetic susceptibility and also have anatomical or vascular risk factors, the combined effect is greater than any single factor alone.
Steroid Use as a Secondary Cause
Corticosteroids, whether taken as eye drops, oral medication, or injections, can trigger a form of secondary glaucoma. Steroids cause multiple changes in the trabecular meshwork: they promote the buildup of structural proteins and water-absorbing molecules that swell the tissue, inhibit the self-cleaning function of meshwork cells, and reduce the production of molecules that normally help regulate fluid outflow. The net effect is increased resistance to drainage and rising eye pressure.
In steroid-responsive individuals, pressure typically rises within the first few weeks of use, though it can happen within hours or after years of chronic use. Intravitreal steroid injections are particularly potent, raising pressure in about 50% of patients within two to four weeks. The good news is that steroid-induced pressure elevation usually reverses within one to four weeks after stopping the medication, though prolonged exposure can cause permanent damage that mirrors primary glaucoma.