Vitreomacular Adhesion and the Normal Vitreoretinal Interface
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
FIGURE 30.1 Enhanced vitreous imaging spectral-domain optical coherence tomography (SD-OCT) of a patient with vitreomacular adhesion (VMA) with significantly increased visualization of the vitreous interface and anatomy.