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Macular degeneration is a major cause of gradual, painless, central vision loss in the elderly.(1) It occurs as a result of geographic atrophy, serous detachment of the retinal pigment epithelium, and/or choroidal neovascularization. There are two forms that occur. One is a nonexudative or dry form, which begins with the accumulation of extracellular deposits, called drusen, underneath the retinal pigment epithelium. When examined ophthalmoscopically, they appear as discrete, small, yellow lesions, clustered in the macula. As the process continues, they become larger, more numerous, and confluent. Generally, they cluster in the posterior pole, but may occur anywhere in the fundus. Drusen in an extramacular location are of no visual consequence. The drusen alone do not cause visual loss, although mild metamorphopsia (distortion), loss of reading speed, and impaired contrast sensitivity may occur. They do represent a significant risk factor for subsequent geographic atrophy and choroidal neovascularization. Vision becomes impaired when the retinal pigment epithelium becomes focally detached and atrophic, interfering with photoreceptors.
In the exudative, or wet form, which actually occurs much less frequently, neovascular vessels from the choroids grow through a defect in Bruch's membrane into the potential space beneath the retinal pigment epithelium. Blurring of vision and distortion occurs as leakage from these vessels produces elevation of the retina and retinal pigment epithelium. Although it is widely accepted that the primary loci of the disease are the choriocapillaris, Bruch's membrane, and the retinal pigment epithelium, the visual loss in age-related macular degeneration results from dysfunction and death of the overlying photoreceptors.(2) The onset of symptom is usually gradual, however, acute vision loss may occur if bleeding from subretinal choroidal neovascular membranes occurs. Neovascular membranes are not easily seen on fundus examination because they are behind the retina, so flurorscein angiography is extremely useful for their detection. Occasionally, laser oblation may be performed to halt the exudative process, however, the process is usually a recurring one requiring vigilance and often repeated photocoagulation. Major or repeated hemorrhage from neovascular membranes results in fibrosis, development of a disciform macular scar and permanent loss of central vision.
The disease is one found primarily in the elderly, as implied by the name. Previously known as "senile macular degeneration," the name has been changed to age-related macular degeneration, (ARMD), due to the unflattering reference to advanced age.
The average age at onset of visual loss is about 75 years. After the age of 50 years, the incidence steadily increases; over one-third of people in their ninth decade of life are affected.(3) The actual incidence of the disease depends upon how it is defined.
The Framingham Eye Study revealed that ARMD affects about 2% of Americans aged 52-64 years: 11% aged 65-74 years; and 28% aged 75 years and older.(4)
Despite its prevalence and extensive ocular morbidity, the pathogenesis of the disease remains unclear. Arteriosclerosis, oxidative damage, photic damage, inflammation, diet, vitamin and rare element deficiencies, and genetics have been implicated by various researchers. Genetic factors become very hard to quantify due to the fact that parents and siblings may not be alive, and children may be too young to manifest clinical findings. It has been determined that systemic arterial hypertension and cigarette smoking are associated with an increased risk of neovascular ARMD. Other suggested risk factors include hyperopia and increased horizontal cup-to-disc ratio, and risk factors associated with cardiovascular disease. Another relationship to ARMD was suggested in an evaluation of 51 older patients with recent-onset bil
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