Variants of neovascular age-related macular degeneration: type 3 neovascularization (intraretinal neovascularization or retinal angiomatous proliferation)

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.