ABSTRACT
INTRODUCTION Neovascular (formerly termed exudative) age-related macular degeneration (AMD) was fi rst described and illustrated in the literature in 1875 by Pagenstecher (1), who termed this condition “chorioidioretinitis in regione maculae luteae.” In 1905, Oeller fi rst used the term disciform degeneration (degeneratio maculae luteae disciformis) (2). Later, Julius and Kuhnt in 1926 further elaborated on this condition and established it as a disease (3). Further work by clinicians and pathologists over the next several decades led to the revelation that choroidal neovascularization (CNV) was responsible for the manifestations of neovascular AMD. The histopathological association of CNV with disciform scars was discovered in 1928 by Holloway and Verhoeff who described eight eyes with “disc like” degeneration of the retina (4). In 1937, Verhoeff and Grossman similarly demonstrated CNV in their cases of macular degeneration and emphasized that blood vessels erupted through Bruch’s membrane (5). It was not until 1951 that clinicopathologic correlations by Ashton and Sorsby demonstrated that CNV with breaks in Bruch’s membrane results in subretinal fl uid (6). Finally, in 1967 Gass implicated CNV as having a primary role in what was then called “senile disciform macular degeneration” (7,8). In 1971, Blair and Aaberg showed the clinical and fl uorescein angiographic characteristics of CNV in these eyes with “senile macular degeneration” (9). In 1976, Small published a clinicopathologic correlation of the evolution of a lesion which was comprised of CNV and a serous pigment epithelial detachment (PED) to a disciform scar (10). In 1977, Green and Key (11) studied the histopathologic features of 176 eyes from 115 patients with AMD. Their work supported the view that drusen predispose to development of CNV. Since then, numerous studies have given us ample histopathologic data on CNV.
