Mechanistic Insights into the Pathogenesis of Proliferative and Nonproliferative Vitreomacular Traction

To describe the vitreoretinal interface in vitreomacular traction (VMT) by using novel optical coherence tomography (OCT) methods; wide-angle montage, and pseudomotion OCT imaging systems.

Observational case series.

Wide-angle montage OCT images of horizontal and vertical scans through the fovea were acquired in 50 eyes of 46 consecutive patients with VMT. Baseline fundus scans were obtained. These were followed by scans acquired with an eye-tracking system performed immediately after vertical and horizontal eye movements. Three scans were then superimposed to compare changes in the contour and position of the posterior vitreous.

The subjects were classified as VMT with ("proliferative"; 48.0%) and without ("nonproliferative"; 52.0%) thickened posterior vitreous. Epiretinal membrane was observed in 26.9% of nonproliferative and 95.8% of proliferative VMT eyes (P = 3.6 × 10^-7). No eye of proliferative and 57.7% of nonproliferative VMT eyes had wavy contoured posterior vitreous (P = 4.0 × 10^-6). None with proliferative VMT, but 91.7% of nonproliferative VMT eyes, showed motion induced changes of posterior vitreous following eye movement (P = 2.0 × 10^-8). The posterior vitreous detachment extended beyond the scanned area in 34.6% of nonproliferative and 8.3% of proliferative VMT eyes (P = .040).

By dynamically evaluating the vitreoretinal interface of patients with VMT, the static contraction forces of a thickened posterior vitreous at the macula are implicated in proliferative VMT. This contractile force is not strongly implicated in the majority of VMT eyes with nontaut and more mobile vitreous (nonproliferative VMT). VMT and its associated complications are determined by at least 2 different pathophysiological mechanisms.