Glaucoma agonists work by opening uveoscleral passageways. Beta-blockers, such as timolol, work by decreasing aqueous formation. Carbonic anhydrase inhibitors decrease bicarbonate formation from ciliary processes in the eye, thus decreasing the formation of Aqueous humor. Parasympathetic analogs are drugs that work on the trabecular outflow by opening up the passageway and constricting the pupil. Alpha 2 agonists (brimonidine, apraclonidine) both decrease fluid production (via. inhibition of AC) and increase drainage. Developmental glaucoma (Q15.0) Secondary glaucoma (H40.3-H40.6) Neovascular glaucoma, an uncommon type of glaucoma, is difficult or nearly impossible to treat, and is often caused by proliferative diabetic retinopathy (PDR) or central
Normal tension glaucoma of cases that have been reported in medical literature in the 1980s and 1990s who had the typical signs of glaucomatous damage, like optic nerve head excavation and thinning of the retinal nerve fiber layer, while these patients had an IOP that would generally have been regarded as "normal". It is now widely estimated that a larger percentage of patients with primary open-angle glaucoma (POAG) are suffering from normal tension glaucoma: probably half of all POAG patients in Europe and the majority of POAG patients in East Asia. Among Americans of Japanese descent, for instance, the prevalence of NTG is