Structural and functional changes after macular hole surgery: A review

摘要

Macular hole (MH) is characterized by full-thickness anatomic defect at the fovea leading to loss of central vision. The majority (~85%) of MHs were once thought to be idiopathic with a smaller proportion being secondary to trauma, inflammation, or high myopia.1 However, recent optical coherence tomography (OCT) imaging suggests that early MHs originate from an intraretinal split of the macula that evolves into intraretinal cysts (Fig. 1). It has been hypothesized that MHs develop from tangential traction from prefoveal vitreous cortex and/or epiretinal membranes and anteroposterior traction at the vitreoretinal interface resulting in vitreomacular traction syndrome.2