Among older adults, age-related macular degeneration (AMD) is a prevalent disabling condition that begins as subtle visual disturbances and can progress to permanent loss of central vision. In its late neovascular form, AMD is treatable with inhibitors of vascular endothelial growth factor, the key driver of exudative disease. In the atrophic form, treatment remains elusive. This review addresses the natural history of AMD – through early, intermediate, and advanced disease stages – and concentrates on diagnosis and risk stratification, deficiencies of current treatments, and the promising findings of emerging therapies.

It is estimated that 16.4 million adults are affected by RVO worldwide, corresponding to 13.9 million with BRVO and 2.5 million with CRVO (1). The classification of RVO into BRVO and CRVO is based on the anatomical site of the vascular occlusion. Although the pathogenesis of RVO is not yet fully understood, an increased secretion of the vascular endothelial growth factor (VEGF) is observed, and therefore the use of anti-VEGF agents by intravitreal injections has become common (2). Many treatment regimens have been suggested with anti-VEGF agents, such as monthly injections or injections pro re nata (PRN), but the ideal regimen has not been defined (2) and management in the long-term of RVO-related complications and visual loss has not been established (1).

Nonarteritic anterior ischemic optic neuropathy (NA-AION) is the most common nonglaucomatous optic neuropathy in adults over 50 years of age. It is usually related to cardiovascular risk factors. The primary objective of this study was to evaluate choroidal thickness in patients with chronic NA-AION, and the secondary objective was to evaluate macular thickness in these patients. This cross-sectional study compared two groups: group 1 included 20 eyes of 20 patients with chronic NA-AION, and group 2 included 31 eyes of 31 healthy controls. In both groups, the choroidal thickness was measured using the enhanced depth imaging program of Heidelberg Spectralis Õ optical coherence tomography (Heidelberg Engineering, Heidelberg, Germany). The macular thickness was also measured using the automatic software of the same device. The mean follow-up time after NA-AION in group 1 was 57.17 ± 26.92 months. The mean choroidal thickness of the posterior pole was 244.38 ± 61.03 mm in group 1 and 214.18 ± 65.97 mm in group 2 (p = 0.004). The mean macular thickness was higher in group 2. Macular thickness is reduced in eyes that had an episode of NA-AION, whereas choroidal thickness is generally higher in these eyes when compared with normal eyes. The increase in choroidal thickness may be due to a local dysfunction in vascular autoregulatory mechanisms, which may predispose to ischemic phenomena.