Abstract
Glaucoma comprises a heterogeneous group of disorders, the final common pathways of which result in the death of retinal ganglion cells (RGC) and subsequent characteristic patterns of visual field loss and excavation of the optic nerve head. Those glaucomas in which elevated intraocular pressure (IOP) predominate are characterized by dysfunction of the trabecular meshwork, resulting in increased resistance to aqueous outflow. Non-pressure-dependent mechanisms remain poorly delineated and may consist of cardiovascular and local ischemic conditions, autoimmune and connective tissue disorders, and genetic predisposition to retinal ganglion cell death.
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