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, that damage results from a buildup of fluid pressure inside the eye. Your eye constantly produces a clear fluid that nourishes its internal structures, and when that fluid can’t drain properly, pressure rises and gradually destroys nerve fibers. But pressure isn’t the whole story. Some people develop glaucoma even with normal eye pressure, pointing to other causes like poor blood flow to the optic nerve.
How Eye Pressure Builds Up
To understand what goes wrong, it helps to know how your eye manages fluid. A structure called the ciliary body, located behind the iris, continuously produces a clear liquid called aqueous humor. This fluid flows through the pupil into the front chamber of the eye, where it nourishes the lens and cornea. It then drains out through a ring-shaped mesh of tissue near the base of the iris and enters tiny channels that feed into the bloodstream.
Healthy eyes maintain a balance: fluid is produced and drained at roughly the same rate, keeping internal pressure between 10 and 20 mmHg. When the drainage tissue becomes clogged or blocked, fluid backs up, pressure climbs, and the optic nerve at the back of the eye bears the force. The nerve fibers most vulnerable sit at the rim of the optic disc, and as they die off, blind spots develop in your peripheral vision, often without you noticing.
Open-Angle Glaucoma: The Most Common Type
About 85% of all glaucoma cases are open-angle glaucoma, where the drainage angle between the iris and cornea looks physically open but the microscopic mesh tissue within it resists fluid flow. Over time, the cells lining this meshwork decrease in number, the spaces between them shrink, and the surrounding structural material stiffens. These changes slow drainage enough to raise pressure gradually, sometimes over years.
What’s striking is that these same changes happen to some degree in every aging eye. The drainage tissue naturally becomes less permeable with age, which is one reason glaucoma risk rises sharply after 40. In glaucomatous eyes, the process is simply accelerated or more severe than in age-matched healthy eyes. The pressure increase is painless and slow, which is why open-angle glaucoma is often called the “silent thief of sight.” Most people have no symptoms until significant peripheral vision is already gone.
Angle-Closure Glaucoma: A Sudden Blockage
Angle-closure glaucoma works differently. Instead of a slow clogging of the drainage tissue, the iris itself physically blocks the drainage pathway. This happens when the lens presses against the back of the iris, trapping fluid behind it. That trapped fluid pushes the iris forward like a sail catching wind, and the outer edge of the iris seals against the cornea, completely cutting off drainage.
Because the blockage can happen suddenly, pressure can spike from normal levels to dangerously high in hours. An acute attack causes intense eye pain, headache, nausea, blurred vision, and halos around lights. This is a medical emergency. Without rapid treatment to relieve the pressure, permanent vision loss can occur within a day. People with naturally smaller eyes or shallower front chambers are more prone to this type because the iris sits closer to the drainage angle to begin with.
When Normal Pressure Still Causes Damage
Normal-tension glaucoma challenges the assumption that high pressure is always the culprit. In these cases, the optic nerve sustains the same pattern of damage seen in high-pressure glaucoma, but intraocular pressure stays within the normal range. Researchers have proposed several explanations, and the reality is likely a combination of factors.
The leading theory involves blood supply. The optic nerve requires constant, well-regulated blood flow. If that flow is disrupted, whether by low blood pressure, vasospasm (the kind of blood vessel constriction seen in Raynaud’s phenomenon), or sleep apnea, nerve tissue can starve and die. Another theory focuses on structural weakness: some people may have a thinner or more fragile supporting plate (the lamina cribrosa) at the back of the eye, making their optic nerve less able to withstand even normal pressure levels.
A third line of thinking points to the fluid that bathes the brain and spinal cord. This fluid also surrounds the optic nerve from behind, providing a kind of counterpressure against the eye’s internal pressure. If that counterpressure drops too low, the pressure difference across the optic nerve increases, potentially causing damage even when eye pressure itself is unremarkable. More recently, researchers have also proposed that a failure in the nerve’s waste-clearance system may allow toxic metabolic byproducts to accumulate, gradually killing nerve cells.
Secondary Causes of Glaucoma
Glaucoma can also develop as a consequence of other eye conditions, injuries, or medications. Eye trauma, previous surgeries, severe eye infections, and inflammatory conditions can all scar or damage the drainage system. Tumors inside the eye or abnormal blood vessel growth, as sometimes occurs in advanced diabetes, can physically obstruct fluid outflow.
Corticosteroid medications are a well-known trigger. Steroid eye drops, and to a lesser extent oral or inhaled steroids, can cause changes in the drainage tissue’s cells that reduce its permeability. Not everyone is equally susceptible. People who already have glaucoma or a family history of it are more likely to experience steroid-related pressure spikes. The effect is usually reversible once the medication is stopped, but prolonged use can cause lasting damage.
Genetics and Family History
Glaucoma runs in families, though no single gene accounts for all cases. Multiple genes appear to be involved, each contributing a piece of risk that interacts with environmental and age-related factors. The hereditary component is substantial: in population studies, relatives of glaucoma patients had a lifetime risk of developing glaucoma of about 22%, compared to roughly 2% for relatives of people without the condition. That translates to a risk roughly nine times higher than average.
Siblings of glaucoma patients carry the highest risk. In one large study, 10.4% of siblings of glaucoma patients had the disease themselves, compared to 0.7% of siblings in a control group. The inheritance pattern doesn’t follow a simple dominant or recessive model. Instead, different families likely carry different combinations of risk genes, which helps explain why glaucoma severity and age of onset vary so widely even among relatives.
Who Is Most at Risk
Age is the single biggest risk factor. The global prevalence of open-angle glaucoma in people over 40 is currently around 2.8%, but that figure is projected to rise as populations age. An estimated 80.5 million people worldwide had the condition in 2024, a number expected to more than double to nearly 187 million by 2060.
Race and ethnicity play a significant role. Black individuals are about 2.4 times more likely to develop glaucoma than white individuals, and they tend to develop it earlier and with more aggressive progression. People of East Asian descent have higher rates of angle-closure glaucoma, partly because of anatomical differences in eye structure. Hispanic and Latino populations also face elevated risk compared to white populations.
Other risk factors include severe nearsightedness, which changes the shape and structural support of the eye, diabetes, and conditions that affect blood flow like chronic low blood pressure or sleep apnea. Having a thinner cornea is also associated with higher risk, possibly because it reflects broader structural characteristics of the eye’s connective tissue. High eye pressure alone, without any nerve damage, is classified as ocular hypertension rather than glaucoma, but it remains the strongest individual predictor of future glaucoma development and the only risk factor that can currently be treated.