Atrophic age-related macular degeneration (AMD) represents the late stage of “dry” AMD. It is characterized by the development of atrophic patches, which may initially occur in the parafoveal area (1, 2, 3, 4). These atrophic areas appear funduscopically as sharply demarcated areas of depigmentation through which deep choroidal vessels can be seen. During the natural course of the disease, the areas of atrophy slowly enlarge over time. In atrophic AMD, characteristically, the fovea remains uninvolved until the advanced stages of the disease, a phenomenon referred to as “foveal sparing.” A widely established term used to refer to this advanced form of dry AMD is “geographic atrophy” (GA). By contrast, the term “areolar choroidal atrophy” is usually used to refer to findings that are similar but caused by monogenetic retinal macular dystrophies, which may manifest earlier in life.

Severe visual loss secondary to GA occurs in about 20% of all patients with AMD (5, 6, 7, 8). Hence, GA is, after choroidal neovascularization (CNV), the second most common cause of legal blindness due to AMD. Patients with primary GA tend to be older than those with neovascular forms of AMD at the time of initial presentation, and it has been speculated that GA occurs in eyes in which a neovascular angiogenic event has not developed. As opposed to the recent breakthrough with anti-VEGF (vascular endothelial growth factor) therapy for active neovascular AMD, there is to date no treatment available for patients with GA, other than visual aids and visual rehabilitation. Therefore, a better understanding of the pathogenesis of GA appears to be mandatory. Sensitive diagnostic tools and prognostic markers to evaluate disease stage and future progression in the individual patient are needed.

It is clinically well established that GA atrophy can affect one or both eyes (9,10). The fellow eye can be affected by any other AMD manifestation and development, including CNV or disciform scarring. It has been reported that eyes demonstrating typical early features of GA can also develop CNV; in these patients, severe and sudden visual loss occurs (11). When CNV develops in an eye with previously diagnosed pure GA, it usually has an evanescent appearance and it is often difficult to outline its borders and differentiate between hyperfluorescence resulting from the CNV and that caused by atrophic areas. In this context, careful slit-lamp biomicroscopy may allow the identification of subretinal fluid or hemorrhage, which would indicate the presence of a CNV. Optical coherence tomography (OCT) may also be helpful in identifying a CNV in these cases.