Ocular hypertension (increased pressure within the eye) is the most important risk factor for<unk> , but only about 50% of people with primary open-angle<unk>  actually have elevated ocular pressure. Ocular hypertension—an intraocular pressure above the traditional threshold of or even above —is not necessarily a pathological condition, but it increases the risk of developing<unk> . One study found a conversion rate of 18% within five years, meaning fewer than one in five people with elevated intraocular pressure will develop<unk> tous visual field loss over that period of time. It is a matter of debate whether every person with an elevated intraocular pressure should receive<unk>  therapy; currently, most ophthalmologists favor treatment of those with additional risk factors. Open-angle<unk>  accounts for 90% of<unk>  cases in the United States. Closed-angle<unk>  accounts for fewer than 10% of<unk>  cases in the United States, but as many as half of<unk>  cases in other nations (particularly East Asian countries). Dietary No clear evidence indicates that vitamin deficiencies cause<unk>  in humans. As such, oral vitamin supplementation is not a recommended treatment. Caffeine increases intraocular pressure in those with<unk> , but does not appear to affect normal individuals. Ethnicity Many people of East Asian descent are prone to developing angle closure<unk>  because of shallower anterior chamber depths, with the majority of cases of<unk>  in this population consisting of some form of angle closure. Higher rates of<unk>  have also been reported for Inuit populations, compared to White populations, in Canada and Greenland. Genetics Positive family history is a risk factor for<unk> . The relative risk of having primary open-angle<unk>  (POAG) is increased about two- to four-fold for people who have a sibling with<unk> .<unk> , particularly primary open-angle<unk> , is associated with mutations in several genes, including MYOC, ASB10, WDR36, NTF4, TBK1, and RPGRIP1, although most cases of<unk>  do not involve these genetic mutations. Normal-tension<unk> , which comprises one-third of POAG, is also associated with genetic mutations (including OPA1 and OPTN genes). Various rare congenital/genetic eye malformations are associated with<unk> . 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<unk> tous optic neuropathy may also occur with these anomalies and has been modelled in mice. Other Other factors can cause<unk> , known as "secondary<unk> ", including prolonged use of steroids (steroid-induced<unk> ; conditions that severely restrict blood flow to the eye, such as severe diabetic retinopathy and central retinal vein occlusion (neovascular<unk> ; ocular trauma (angle-recession<unk> ; and inflammation of the middle layer of the pigmented vascular eye structure (uveitis), known as uveitic<unk> . Laser Doppler imaging reveals arterial blood flow reversal in neovascular<unk> . The color change of the Doppler image in the central retinal artery during the cardiac cycle indicates arterial flow reversal.
Glaucoma
Keratitis
Normal tension glaucoma
Conjunctivitis
Cat eye syndrome
Uveitis
Phacolytic glaucoma
Ocular hypertension