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.
The major types of glaucoma are discussed below.
Ocular hypertension (increased pressure within the eye) is the largest risk factor in most glaucomas, but in some populations only 50% of patients with primary open angle glaucoma actually have elevated ocular pressure.
Those of African descent are three times more likely to develop primary open angle glaucoma. People who are older, have thinner corneal thickness, and myopia also are at higher risk for primary open angle glaucoma. People with a family history of glaucoma have about a six percent chance of developing glaucoma. Many Asian groups, such as Mongolian, Chinese, Japanese, and Vietnamese, are prone to developing angle closure glaucoma due to their shallower anterior chamber depth, with the majority of cases of glaucoma in this population consisting of some form of angle closure.
Inuit also have a twenty to forty times higher risk than Caucasians of developing primary angle closure glaucoma. Women are three times more likely than men to develop acute angle-closure glaucoma due to their shallower anterior chambers. Other factors can cause glaucoma, known as "secondary glaucomas," including prolonged use of steroids (steroid-induced glaucoma); conditions that severely restrict blood flow to the eye, such as severe diabetic retinopathy and central retinal vein occlusion (neovascular glaucoma); ocular trauma (angle recession glaucoma); and uveitis (uveitic glaucoma).
Primary open angle glaucoma (POAG) has been found to be associated with mutations in genes at several loci. Normal tension glaucoma, which comprises one third of POAG, is associated with genetic mutations. There is increasing evidence that ocular blood flow is involved in the pathogenesis of glaucoma. Current data indicate that fluctuations in blood flow are more harmful in glaucomatous optic neuropathy than steady reductions. Unstable blood pressure and dips are linked to optic nerve head damage and correlate with visual field deterioration.
A number of studies also suggest that there is a correlation, not necessarily causal, between glaucoma and systemic hypertension (i.e. high blood pressure). In normal tension glaucoma, nocturnal hypotension may play a significant role. There is no clear evidence that vitamin deficiencies cause glaucoma in humans, nor that oral vitamin supplementation is useful in glaucoma treatment Various rare congenital/genetic eye malformations are associated with glaucoma.
Occasionally, failure of the normal third trimester gestational atrophy of the hyaloid canal and the tunica vasculosa lentis is associated with other anomalies. Angle closure induced ocular hypertension and glaucomatous optic neuropathy may also occur with these anomalies. and modelled in mice . Those at risk for glaucoma are advised to have a dilated eye examination at least once a year. |
