Previous studies have attributed changes in the retinal surface over or adjacent to large superficial retinal vessels to a variety of conditions, the most common being 'anomalous vitreoretinal attachments.' The fundamental nature of the lesions and their pathogenesis, however, has remained controversial. The present study was undertaken to categorize the ultrastructural alterations of the vitreoretinal juncture over retinal vessels in the posterior fundus of man, and to clarify the relationship of these fundamental changes to clinically significant lesions in this region. Results show no difference in vitreoretinal, or more specifically vitreolaminar attachments over vessels when compared with adjacent regions. The cause of the more significant anomalies, notably surface breaks and their sequelae, is apparently multifactorial and related to a sequence of events. Initially three events predispose to or cause small surface breaks: developmental thinning of the inner limiting lamina; subsurface retinal degeneration; and transmigrating macrophages. These small surface breaks, when complicated by vitreous incarceration or by simple epiretinal membrane formation, can during posterior vitreous detachment cause peeling of the retinal surface, and the resulting large surface breaks may in turn provoke more complex proliferative lesions of the vitreoretinal juncture.