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.
|Title of host publication||Age-related macular degeneration|
|Editors||Jennifer I. Lim|
|Place of Publication||Boca Raton, FL|
|Publisher||CRC Press, Taylor & Francis Group|
|Number of pages||15|
|Publication status||Published - 2013|