Symptomatic Vitreomacular Adhesion (VMA)
Symptomatic VMA is an increasingly recognized sight-threatening disease of the vitreoretinal interface.1 VMA may lead to symptoms such as metamorphopsia, decreased visual acuity, and central visual field defect.2-4 VMA can cause traction resulting in anatomical damage, which may lead to severe visual consequences, including macular hole (Figure 1).
Figure 1. VMA can cause traction resulting in anatomical damage, which may lead to severe visual consequences.
The vitreous cavity is filled with a gel-type substance consisting mostly of water, with macromolecules such as hyaluronic acid, proteins, and collagens comprising the remainder.7 The posterior vitreous cortex attaches to the internal limiting membrane (ILM) via a matrix that includes collagen fibrils, fibronectin, and laminin.7,8 The anatomic junction of the vitreous and retina is referred to as the vitreoretinal interface (VRI; Figure 2).
Figure 2. Components of the VRI include the vitreous cortex and the internal limiting membrane (ILM), which separates the retina from the vitreous, and is composed of a matrix that includes collagen fibrils, laminin, and fibronectin.
The natural aging process of the vitreous results in its liquefaction and separation from the retina in many eyes.9-11 In some eyes, the adhesion between the vitreous and the macula does not weaken sufficiently to allow for separation of vitreous, resulting in a condition known as VMA (Figure 3). This persistent adhesion can lead to symptoms (ie, symptomatic VMA), including metamorphopsia (distorted vision), decreased visual acuity and central visual field defect.2-4 These symptoms are due to the traction caused by the persistent VMA at the vitreoretinal interface, often referred to as vitreomacular traction (VMT). VMT can lead to the formation of a macular hole (Figure 3).5,12
Figure 3. VMA occurs when the vitreous fails to completely separate from the retina during normal liquefaction and weakening of the normal adhesions between the posterior vitreous cortex and the ILM.
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* Eye Clinic, Department of Clinical Science “Luigi Sacco”, Sacco Hospital, University of Milan, Milan, Italy.
