The vitreous includes an outer cortex of primarily type 2 collagen (ie, the posterior hyaloid) that attaches the posterior vitreous body to the internal limiting membrane (ILM).¹

Macromolecular attachment complexes at this interface, composed of fibronectin, laminin, and other components, form a gluelike matrix that plays a role in vitreoretinal adhesion.²

This connection persists from birth through young adulthood and constitutes the normal vitreoretinal interface. With age, the vitreous gel liquifies (synchysis), collapses (syneresis), and the cortex separates from the ILM (a process known as posterior vitreous detachment [PVD]).

Perifoveal PVD that occurs with persistent attachment at the fovea with maintenance of a normal foveal morphology is called a vitreomacular adhesion (VMA).

VMAs are nonpathologic and asymptomatic, but persistent adhesion may lead to secondary tractional disease such as vitreomacular traction (VMT) or macular hole.

Transition to VMT can aggravate underlying retinal conditions like diabetic macular edema or age-related macular degeneration.³

Optical coherence tomography (OCT) has enabled better understanding of the vitreoretinal interface and is critical to evaluate potential abnormalities.⁴