Glaucoma can be divided roughly into two main categories, "open angle" or chronic glaucoma and "closed angle" or acute glaucoma. Angle closure, acute glaucoma appears suddenly and often with painful side effects and so is usually diagnosed quickly, although damage and loss of vision can also occur very suddenly. Open angle, chronic glaucoma tends to progress more slowly and so the patient may not notice it until the disease has progressed quite significantly.

Glaucoma has been nicknamed the "sneak thief of sight" because the loss of visual field often occurs gradually over a long time and may only be recognized when it is already quite advanced. Once lost, this damaged visual field can never be recovered. Worldwide, it is the second leading cause of blindness. Glaucoma affects one in two hundred people aged fifty and younger, and one in ten over the age of eighty. If the condition is detected early enough it is possible to arrest the development or slow the progression with medical and surgical means.

Symptoms

To begin with there may be no symptoms, so it is important to have regular eye checks to diagnose the disease. Patchy peripheral vision is sometimes noticed as the nerve cell layer is affected and there is often a loss of contrast sensitivity. A contrast sensitivity test should be performed along with a field test to measure visual loss. A field test has to be performed by an ophthalmologist or optometrist, but a contrast sensitivity test can be performed regularly at home. If any loss of contrast sensitivity is detected an eye specialist consultation is recommended. Symptoms may include pain in or behind the eye ball, headache and sensitivity to pressure.

Pathophysiology

The major risk factor for most glaucomas and focus of modeling and treatment is increased intraocular pressure. Intraocular pressure is a function of production of liquid aqueous humor by the ciliary body of the eye and its drainage through the trabecular meshwork. Aqueous humor flows from the ciliary bodies into the posterior chamber, bounded posteriorly by the lens and the zonule of Zinn and anteriorly by the iris. It then flows through the pupil of the iris into the anterior chamber, bounded posteriorly by the iris and anteriorly by the cornea. From here the trabecular meshwork drains aqueous humor via Schlemm's canal into scleral plexuses and general blood circulation. In open angle glaucoma there is reduced flow through the trabecular meshwork ; in angle closure glaucoma, the iris is pushed forward against the trabecular meshwork, blocking fluid from escaping.

The inconsistent relationship of glaucomatous optic neuropathy with ocular hypertension has provoked hypotheses and studies on anatomic structure, eye development, nerve compression trauma, optic nerve blood flow, excitatory neurotransmitter, trophic factor, retinal ganglion cell/axon degeneration, glial support cell, immune, and aging mechanisms of neuron loss.