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The hallmark of vitreomacular traction syndrome is a persistent attachment of the vitreous to the macula in eyes with an incomplete posterior vitreous detachment. The most common morphological configuration is a vitreous separation peripheral to a zone where the cortical vitreous remains attached to the retina at the macula and the optic nerve head. Traction on the macula causes decreased vision, metamorphopsia, photopsia, and micropsia. 1 Pars plana vitrectomy has been shown to relieve macular traction and result in visual improvement in most cases. 2- 6
There are remarkable variations concerning the vitreoretinal morphology in eyes with vitreomacular traction syndrome. This syndrome comprises a broad spectrum of frequently unrecognised clinical findings, ranging from peripheral vitreous separation with residual foveal attachment to multiple areas of traction retinal detachment caused by persistent, focal posterior and peripheral vitreous attachment. 2, 7- 9 Clinically and histopathologically, the disorder shares similarities with idiopathic epiretinal membranes in eyes with complete posterior vitreous detachment, such as the presence of fibrocellular tissue at the macula as reported previously. 4, 10, 11 However, there are also distinct differences, such as the clinical course of the disease and ultrastructural findings. 2, 3, 11 Clinical and surgical experience has disclosed either a visible epiretinal membrane, or a layer of cortical vitreous, or both over the posterior pole. 11 Ultrastructural evaluation of epiretinal tissue removed during vitrectomy for vitreomacular traction syndrome revealed fibrocellular membranes composed of fibrous astrocytes, fibrocytes, myofibroblasts, collagen, and fragments of the inner limiting membrane (ILM). 11 However, material chosen for analysis has been epiretinal tissue rather than detached posterior hyaloid, and the pathology of the vitreous, the fibrocellular tissue, and the ILM of the retina, leading to persistent vitreomacular traction and fibrocellular proliferation has not yet been clarified. Whether anteroposterior traction alone causes macular pathology or whether tangential traction induced by fibrocellular proliferation is relevant to the pathogenesis of vitreomacular traction syndrome, is still a matter of debate. Moreover, the clinicopathological correlation in eyes with different clinical features of vitreomacular traction syndrome has not been addressed and determined as yet. Therefore, we describe the ultrastructure of the vitreomacular interface in 14 eyes with vitreomacular traction syndrome with special regard to the clinical variation of the disease. We are aware that our approach...