ABSTRACT
INTRODUCTION According to the Gass classifi cation of choroidal neovascularization (CNV), neovascular proliferation may occur in two distinct forms (1). In the fi rst, coined “type 1 neovascularization,” the neovascular tissue is confi ned to the sub-retinal pigment epithelial (sub-RPE) space and is usually visible on fl uorescein angiography (FA) as “poorly defi ned” or “occult” leakage. This is the most common form of CNV in age-related macular degeneration (AMD) (2). In contrast, “type 2 neovascularization” refers to neovascular tissue originating in the choroid that gains access to the subretinal space via a breach in the Bruch’s membrane/RPE complex. This is usually associated with “well defi ned” or “classic” leakage on FA. Type 2 neovascularization often occurs in the setting of pathological myopia, choroidal rupture, angioid streaks, and infl ammation (3). The existence of intraretinal neovascularization has been described. In a logical progression from the anatomical classifi cation system proposed by Gass, Freund et al. (4) have described this as “type 3 neovascularization.” This form of neovascularization has distinct demographic, funduscopic, and prognostic features that set it apart from type 1 and type 2 neovascularization.
