Age-related macular degeneration (AMD) is the leading cause of blindness in the western world among individuals older than 50 years of age. It is a bilateral condition that has three stages. Early AMD is characterized by the presence of small or a few medium-sized drusen (yellow spots due to accumulation of material in one layer of the retina) and has a very low risk (<2% chance) of progressing to advanced AMD within 5 years. Intermediate AMD is characterized by the presence of at least one large-sized drusen (greatest linear dimension at least 125 microns,µ) or many (approximately 20 or more) medium-sized drusen (greatest linear dimension at least 63 µ but less than 125µ) or non-foveal geographic atrophy. Patients with bilateral intermediate AMD have a 25% risk of progressing to advanced AMD within 5 years in one eye, while intermediate AMD with focal hyperpigmentation of the retinal pigment epithelium (RPE) within 1500 microns of the foveal center in one eye with advanced neovascular AMD in the other eye carries a high risk (43% chance) of progressing to advanced AMD within 5 years.1-4 There are two forms of advanced AMD, an atrophic form, termed geographic atrophy (GA) and a neovascular form, termed choroidal neovascularization (CNV). At least two-thirds of the cases that progress from the intermediate to the advanced stage develop the neovascular form of advanced AMD.5-7
Unfortunately, it is impossible to identify which ones among the AMD patients will eventually progress to CNV and when this progression will occur. It is clear, however, that the lesion will grow rapidly once the neovascular process begins. The pathology initially appears at an extra-foveal area and advances to the optic disc area at an average rate of 18 microns per day8-10. Without treatment at this stage, visual acuity may deteriorate dramatically within weeks, when the lesion reaches the sub-foveal areas. One of the factors that delays diagnosis is the fact that the patient is asymptomatic at the early stages of CNV and is utterly unaware of the neovascular process due to effective brain compensation mechanisms.
The three most common symptoms of CNV secondary to AMD reported are: metamorphoses, blurred vision, and scotoma11. These symptoms are the result of anatomical changes in the sub-retinal space and in the sub-RPE space, with subsequent functional deterioration of the photoreceptors in the macular area.
The use of daily oral vitamin supplementation with specific doses of vitamins C and E, beta-carotene, zinc oxide, and cupric oxide can reduce the risk of developing advanced AMD by about 25%. 12
Lucentis (Ranibizumab) has been recently shown to stabilize visual acuity (VA) in patients who developed neovascular AMD, but only 35-40% had improvement in their vision since most of the patients presented with VA already deteriorated to the point of precluding normal daily functions.10, 13
Detection of the condition while good vision functions are still preserved will lead to better treatment outcomes and subsequently reduce the burden of blindness from AMD.
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