eye disorders
Overview of Glaucoma
Pathophysiology of Glaucoma
Axons of retinal ganglion cells travel through the optic nerve carrying visual information from the eye to the brain. Damage to these axons causes ganglion cell death with resultant optic nerve atrophy and patchy vision loss. Elevated intraocular pressure (IOP) plays a role in axonal damage, either by direct nerve compression or diminution of blood flow. However, the relationship between externally measured pressure and nerve damage is complicated. Normal IOP ranges (ie, within 2 standard deviations of the mean) from 11 to 21 mm Hg. Of people with IOP>21 mm Hg (ie, ocular hypertension), only about 1 to 2% a year (about 10% over 5 years) develop glaucoma. Additionally, about one third of patients with glaucoma do not have IOP>21 mm Hg (known as low-tension glaucoma or normal-tension glaucoma). One factor may be that externally measured IOP does not always reflect true IOP; the cornea may be thinner than average, which leads to a higher IOP measurement, or thicker than average, which leads to a lower IOP measurement, inside the eye than externally measured IOP. Another factor may be that a vascular disorder compromises blood flow to the optic nerve. Also, it is likely that there are factors within the optic nerve that affect susceptibility to damage. IOP is determined by the balance of aqueous secretion and drainage. Elevated IOP is caused by inhibited or obstructed outflow, not oversecretion; a combination of factors in the trabecular meshwork (eg, dysregulation of extracellular matrix, cytoskeletal abnormalities) appear to be involved. In Primary Open-Angle Glaucoma , IOP is elevated because outflow is inadequate despite an angle that appears macroscopically unobstructed. In 