Both after death and in vivo, microplasmin induces a dose-dependent cleavage between the vitreous cortex and the ILM without morphologic alterations of the retina. In the feline eye, there is no cellular response of retinal glial cells or neurons.

Aims: To investigate the ultrastructure of the vitreoretinal interface in patients with vitreomacular traction syndrome. Methods: 14 patients with vitreomacular traction syndrome underwent standard pars plana vitrectomy. After induction of posterior vitreous detachment, epiretinal tissue and the inner limiting membrane (ILM) of the retina were removed, and processed for transmission electron microscopy. Results: Ultrastructural analysis revealed two basic patterns of vitreoretinal pathology in eyes with vitreomacular traction syndrome. Seven specimens showed mostly single cells or a cellular monolayer covering closely the vitreal side of the ILM, not resulting in a biomicroscopically detectable epiretinal fibrocellular proliferation. The other seven specimens revealed premacular fibrocellular tissue which was separated from the ILM by a layer of native collagen, resembling the clinical features of idiopathic epiretinal membranes. In both groups of eyes, the myofibroblast was the predominant cell type. Fibrous astrocytes and fibrocytes were less frequent. Retinal pigment epithelial cells and macrophages were absent. Deposits of newly formed collagen were present only adjacent to fibrocellular multilayers. Conclusions: There are two distinct clinicopathological features of vitreomacular traction syndrome which suggest different forms of epiretinal fibrocellular proliferation: (1) epiretinal membranes interposed in native vitreous collagen and (2) single cells or a cellular monolayer proliferating directly on the ILM. The presence of remnants of the cortical vitreous which remain attached to the ILM following posterior vitreous separation may determine the clinicopathological feature of the disease. The predominance of myofibroblasts may help to explain the high prevalence of cystoid macular oedema and progressive vitreomacular traction characteristic for this disorder.T he 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][3][4][5][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 fib...

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