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The relative risk of having primary open-angle glaucoma is increased about two- to four-fold for people who have a sibling with glaucoma. [28] Glaucoma, particularly primary open-angle glaucoma, is associated with mutations in several genes, including MYOC, ASB10, WDR36, NTF4, TBK1, [29] and RPGRIP1. [30]
Primary congenital glaucomas most commonly occur sporadically. [4] Juvenile open-angle glaucoma is typically an autosomal dominant, inherited condition. [6] [15] A primary cause is myocilin protein dysfunction. [16] Myocilin gene mutations are identified in approximately 10% of patients affected by juvenile glaucoma. [citation needed]
Over many years, glaucoma has been defined by an intraocular pressure of more than 20 mm Hg. Incompatible with this (now obsolete) definition of glaucoma was the ever larger number 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 ...
The crystalline lens inside the human eye has been implicated as a causative factor in many forms of glaucoma. Lens induced glaucomas or Lens related glaucomas are either open-angle or closed-angle glaucomas that can occur due to a neglected advanced cataract (cloudiness of the lens) or a dislocated lens. It is a type of secondary glaucoma.
Glaucoma 1 is a form of primary open-angle glaucoma (POAG), which is characterized based on a specific pattern of defects in the optic nerve, thus causing visual defects. [5] [21] The disease causes an angle in the anterior chamber of the eye to be left open, which in turn causes the intraocular pressure to be increased.
Field defects are seen mainly in primary open angle glaucoma. Because of the unique anatomy of the RNFL, many noticeable patterns are seen in the visual field. Most of the early glaucomatous changes are seen within the central visual field, mainly in Bjerrum's area, 10°-20° from fixation.
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