Perifoveal vitreous detachment is the primary pathogenic event in idiopathic macular hole formation

To evaluate the relationship between the posterior vitreous cortex and the posterior retina in eyes with early stages of idiopathic macular hole formation.

Twenty-six eyes of 26 consecutive patients with stage 1 or stage 2 idiopathic macular hole underwent complete ophthalmologic examination, contact lens biomicroscopy, and B-scan ultrasonography or vitreoretinal surgery or both. In eyes that were operated on, the posterior cortical vitreous layer was meticulously examined with a silicone-tipped cannula prior to inducing a posterior vitreous detachment.

In 25 (96%) of 26 eyes, one or more examination techniques revealed a shallow, localized detachment of the perifoveal vitreous, typically extending to the level of the vascular arcades. Among these 25 eyes, the posterior hyaloid membrane separation was detectable biomicroscopically in 4 (16%) of 25 eyes, ultrasonographically in 17 (74%) of 23 eyes, and intraoperatively in 23 (100%) of 23 eyes. Persistent vitreous adherence to the foveola was evident in 6 (100%) of 6 eyes with a stage 1 hole and in 12 (92%) of 13 eyes with a stage 2 hole but no operculum.

These findings suggest that localized perifoveal vitreous detachment (an early stage of age-related posterior vitreous detachment) is the primary pathogenic event in idiopathic macular hole formation. We postulate that detachment of the posterior hyaloid from the pericentral retina leads to foveal dehiscence by exerting anterior traction on the foveola and by localizing into the foveola the dynamic vitreous traction associated with ocular rotations.