الفهرس 
Pathogenesis of Glaucomatous Optic NeuropathyOnly 14 pages are availabe for public view
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Abstract
Glaucoma, a leading cause of blindness worldwide , is a multifactorial progressive disease which is characterized by structural damage to the optic nerve head and slow progressive loss of retinal ganglion cells (RGCs) and their axons resulting in visual field defects and optic atrophy. So it is a neurodegenerative disease of the optic nerve.
Several mechanisms have been hypothesized to explain the pathogenesis of glaucomatous neuropathy. They include the vascular mechanism (ischemia/hypoxia), mechanical stress (increased IOP), glutamate-induced excitotoxicity associated with increased intracellular calcium and free radicals generation, excessive nitric oxide production and depletion of neurotrophic factors.
Recent studies have revealed that the mode of cell death most often associated with glaucomatous loss is apoptosis which is a form of programmed cell death involving several factors and genes.
As for the vulnerability of the optic nerve to damage in glaucomatous patients, this is determined by several factors other than IOP. Local ocular factors include central corneal thickness, corneal hysteresis, myopia, parapapillary changes, disk hemorrhages , presence of nerve fiber layer defects, systemic risk factors including vasospastic diseases, diabetes, hypertension, endothelial dysfunction, obstructive sleep apnea syndrome and smoking ,that’s why Some patients continue to experience disease progression despite lowering IOP.
Neuroprotection is aimed at blocking primary destructive events or enhancing survival mechanisms of the retinal ganglion cells or optic nerve fibers. Current potential neuroprotective approaches include, ocular hypotensive agents, blood flow enhancers (as calcium channel blockers and vasodilators), sodium channel blockers, glutamate inhibitors, nitric oxide inhibitors, supplying neurotrophic factors and heat shock proteins. Thus, an ideal glaucoma drug would reduce IOP, increase ocular blood flow, and prevent apoptosis and loss of RGCs.