Fluorescein angiography has been utilized to study the microvascular supply of the prelaminar optic disc and the peripapillary choroid. Observation of hypofluorescence of these structures both in patients with anterior ischemic optic neuropathy (AION) and with chronic open-angle glaucoma (COAG) has led to speculation as to the pathogenetic mechanism in each disorder. In AION, studies consistently show defective filling of the disc without atrophy, suggesting hypoperfusion as a primary mechanism. In COAG, defective filling is common, but typically occurs in regions of atrophy or increased cupping, which may show hypofluorescence as a nonspecific sequela of disc tissue loss. The hypofluorescence seen in some ocular hypertensive patients supports but does not confirm a primary vascular role in the pathogenesis of COAG. Peripapillary choroidal filling delay outside the range of normal is consistently seen in arteritic AION, but not in either nonarteritic AION or COAG. This finding suggests that any vasculopathy present in these disorders is distal within the branches of the posterior ciliary artery system.