Age-related macular degeneration (AMD) is an insidious progressive loss of visual function that occurs with aging, and is the leading cause of visual loss in the Western Hemisphere in the elderly.1,2 Although common, the pathways mediating its onset and progression are complex and multifactorial. While many studies have looked at the pathogenesis and physiological changes that occur at the outer retina during AMD, research on inner retinal changes is less common. More specifically, when AMD is compounded by degenerative tractional changes at the vitreomacular interface and inner retina, the problem becomes greater than the sum of its parts. In this article, we address the different etiologies of vitreomacular interface pathologies found in association with both dry and exudative AMD, their pathogenesis, and how their pharmacological and surgical treatment responses differ from the presentation and treatment of either condition alone.
Vitreomacular adhesion (VMA) defines a condition in which the vitreous gel and posterior hyaloid are abnormally adherent to the retina. When a posterior vitreous detachment (PVD) is incomplete and does not undergo a normal synchronous sequence of synchisis and syneresis, a taut anterior/posterior traction on the underlying macula can be created.3,4 This leads to vitreomacular traction (VMT) and subsequent visual degradation, now identifiable and characterizable on a more regular basis through advances in time- and spectral-domain optical coherence tomography (OCT) imaging.5,6 More commonly, traction can lead to a spectrum of retinal architectural distortions, ranging fromcystoid macular edema, epiretinal membrane (ERM), and macular holes up to macular and retinal pigment epithelium (RPE) detachments.7
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