The presence of CNV is the defining characteristic of the neovascular form of AMD. Degenerative changes in Bruch membrane (eg, the accumulation of drusen and progressive thickening of the membrane that characterize nonneovascular AMD) provide a proangiogenic environment that can stimulate neovascularization to develop in the choriocapillaris and perforate the membrane. These new vessels, which are accompanied by fibroblasts, may leak and bleed, disrupting the normal architecture of the RPE–photoreceptor complex with a degenerate fibrovascular complex that ultimately produces a hypertrophic fibrotic disciform scar.