Glaucoma is one of the world’s leading causes of irreversible blindness — and at the same time one of the diseases where early detection and consistent treatment change the picture almost completely. It is not a single disease but a group of conditions sharing progressive damage to the optic nerve, usually on a background of raised intraocular pressure. This page explains what glaucoma is, how it is diagnosed, and how it is treated. For the separate matter of disability percentages, see glaucoma and disability percentages.
What happens in the eye
The eye continually produces a clear fluid — aqueous humour — that nourishes the front of the eye and drains out through a fine meshwork in the angle between the iris and the cornea. When that drainage becomes less efficient, fluid accumulates and the intraocular pressure rises. The raised pressure gradually damages the fibres of the optic nerve — the data cable that carries the image from the eye to the brain — and that damage is what is called glaucoma.
The injury characteristically begins in the peripheral fibres, so the first gaps in vision are at the edges rather than in the centre. This is a critical point: intraocular pressure is the only factor that can be changed by treatment. The optic nerve cannot be strengthened or rejuvenated, but the pressure harming it can be lowered — and that is exactly what every treatment does.
The main types
Open-angle glaucoma is the most common form. The angle through which the fluid drains looks open, but drainage through the meshwork gradually becomes less efficient. The pressure rises slowly, the disease develops over years without pain or symptoms, and this is why it is called the “silent thief of sight”.
Angle-closure glaucoma occurs when the iris physically blocks the angle and the drainage. In an acute attack the pressure surges within hours, with severe pain, redness, blurred vision, halos around lights and sometimes nausea — this is a medical emergency requiring immediate treatment.
Normal-tension glaucoma is a state in which the optic nerve is damaged even though the intraocular pressure measures within the normal range, probably because of an especially vulnerable nerve or poor blood supply. Secondary glaucoma stems from another cause — pseudoexfoliation, pigment, prolonged steroid use, trauma, or diseases that produce new blood vessels in the angle. And there is also congenital glaucoma, rare, appearing in infancy.
Who is at risk
The risk rises with age, especially from 60. Other significant factors are a family history of glaucoma, high intraocular pressure, a thin central cornea, African or Asian ancestry, diabetes, high myopia and prolonged steroid use. Someone with more than one factor — and especially a family history — is at increased risk of developing the disease earlier and more severely, and is advised to begin monitoring sooner.
How it is diagnosed
Because the damage is irreversible and the disease is silent, early diagnosis rests on a combination of tests, not on symptoms:
- Intraocular pressure measurement (tonometry) — the central parameter, but not on its own.
- Optic nerve examination — assessing the cup-to-disc ratio, directly and by OCT imaging of the nerve fibre layer, which detects thinning even before a visual field defect appears.
- Visual field testing (perimetry) — mapping the peripheral gaps and allowing progression to be tracked.
- Gonioscopy — examining the angle, distinguishing an open from a closed angle and determining the type of glaucoma and its treatment.
- Corneal thickness measurement (pachymetry) — a thin cornea raises the risk and affects the interpretation of the pressure reading.
The value of monitoring lies not only in the initial diagnosis but in the sequence over time: change between examinations is what shows whether the disease is stable or progressing.
The treatment ladder
Every treatment has one aim — lowering the intraocular pressure to a level at which the optic nerve stops being harmed.
Laser (SLT). Selective laser treatment of the meshwork improves fluid drainage and lowers the pressure. Following large trials in recent years it is now regarded as a legitimate first-line option, alongside drops and sometimes ahead of them, allowing some patients pressure control without drops. Its effect wanes over the years but it can be repeated.
Eye drops. Several families exist, usually starting with one and adding as needed: prostaglandin analogues (a common first line, one drop a day), beta-blockers, alpha agonists, carbonic anhydrase inhibitors and the newer rho-kinase inhibitors. Adherence — taking them regularly — is among the most important factors in the treatment’s success.
Minimally invasive surgery (MIGS). Implants and gentle procedures that improve drainage, suited to mild-to-moderate glaucoma and often combined with cataract surgery in the same setting.
Filtration surgery (trabeculectomy) or drainage implants are reserved for advanced cases or where the pressure is not controlled by other means. In angle-closure glaucoma, laser to open an opening in the iris (iridotomy) reopens the drainage and prevents attacks.
Living with glaucoma
Glaucoma is a chronic disease managed over years, not cured at a stroke. But proper management — treatment that lowers the pressure, regular use, and consistent follow-up with visual fields and OCT — allows most patients to preserve their vision for life. Vision already lost will not return, but progression can be halted, and that is the whole picture: keeping what there is.
Anyone seeking to understand how the disease affects disability percentages — an entirely separate matter from medical treatment — will find a full explanation in glaucoma and disability percentages, and on the field damage in visual field loss. For an overview of other eye diseases, see eye diseases.
Bottom line
Glaucoma strikes silently and painlessly, begins at the margins of the visual field, and causes damage that cannot be reversed. But it is also one of the diseases where early detection and consistent treatment make the greatest difference. Lowering the intraocular pressure — by laser, drops or surgery — halts the progression and preserves the vision. The most important thing anyone can do is simply to be examined in time, especially those with a family history or other risk factors.
The information on this page is general and not a substitute for a personal examination and medical advice. Anyone experiencing symptoms or at risk is welcome to be examined by an ophthalmologist.
Frequently asked questions
What causes glaucoma?
Glaucoma is progressive damage to the optic nerve, in most cases linked to raised intraocular pressure. The eye produces a fluid (aqueous humour) that should drain through the meshwork in the angle of the eye; when drainage becomes impaired, pressure rises and presses on the optic nerve fibres. It is important to know that intraocular pressure is the only factor that can be changed by treatment — which is why all treatments aim to lower it. There is also a form that develops at normal pressure, in which the optic nerve is especially vulnerable.
Why is glaucoma called the 'silent thief of sight'?
Because in its common form it develops without pain and without noticeable signs. The damage begins in the peripheral field, and central vision — the vision used for reading and recognition — is preserved until a late stage. The brain also 'fills in' the missing areas, so a person can lose a substantial part of the visual field without noticing. This is why periodic eye examinations are the main way to catch the disease in time.
Can vision lost to glaucoma be restored?
No. The damage to the optic nerve is irreversible, and vision already lost cannot be brought back. But further deterioration can certainly be stopped or slowed by lowering the intraocular pressure. The goal of every treatment is therefore to preserve what remains — and early detection, before much is lost, is the single most significant factor in the long-term outcome.
Acute glaucoma — when is it an emergency?
Angle-closure glaucoma in an acute attack is a medical emergency. It is accompanied by severe pain in the eye and head, redness, blurred vision, halos around lights and sometimes nausea and vomiting. The intraocular pressure surges rapidly and can cause damage within hours, so immediate care is needed. This is entirely different from the common form, which develops slowly and without symptoms.
