This paper is a survey of the literature in an attempt to provide the basis for our current understanding of the disciform process. Particular emphasis is placed on its pathogenesis and the role of subretinal neovascularization. No two lesions appear exactly alike because of the many stages and combinations possible. Gass (1967) has delineated the broad spectrum with the many different clinical manifestations of this disease process. Verhoeff and Grossman (1937) provided the histopathologic basis for our understanding of the disciform process. The histologic correlation of the clinical "predisciform" state would seem to offer the most promising information for understanding the pathogenesis of the disciform process (Frank et al. 1973; Green and Key 1977; Kornweig 1967; Sarks 1973 and 1976; Small et al. 1976; Zauberman 1970). It is hoped that this literature review has sufficiently emphasized the inherent deficiencies of strictly clinical studies and the need for an appropriate experimental animal model (Ryan 1979).

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Mechanical and enzymatic disruption of Bruch's membrane and induction of subretinal neovascularization in an experimental primate model have produced limited success. The methods and results are reported here to identify some problems encountered in methodology and to detail the results of this approach to subretinal neovascularization.