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Vitreous Detachment

About: Vitreous Detachment is a research topic. Over the lifetime, 239 publications have been published within this topic receiving 6605 citations.


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Journal ArticleDOI
TL;DR: Unifying the spectrum of vitreo-retinal diseases into the conceptual framework of APVD underscores that to more effectively treat, and ultimately prevent, these disorders it is necessary to replicate the two components of an innocuous PVD, i.e., gel liquefaction and vitreoschisis.
Abstract: Posterior vitreous detachment (PVD) is the consequence of changes in the macromolecular structure of gel vitreous that result in liquefaction, concurrent with alterations in the extracellular matrix at the vitreo-retinal interface that allow the posterior vitreous cortex to detach from the internal limiting lamina of the retina. Gel liquefaction that exceeds the degree of vitreo-retinal dehiscence results in anomalous PVD (APVD). APVD varies in its clinical manifestations depending upon where in the fundus vitreo-retinal adhesion is strongest. At the periphery, APVD results in retinal tears and detachments. In the macula, APVD causes vitreo-macular traction syndrome, results in vitreoschisis with macular pucker or macular holes, or contributes to some cases of diabetic macular edema. At the optic disc and retina, APVD causes vitreo-papillary traction and promotes retinal and optic disc neovascularization. Unifying the spectrum of vitreo-retinal diseases into the conceptual framework of APVD underscores that to more effectively treat, and ultimately prevent, these disorders it is necessary to replicate the two components of an innocuous PVD, i.e., gel liquefaction and vitreo-retinal dehiscence. Pharmacologic vitreolysis is designed to mitigate against APVD by chemically breaking down vitreous macromolecules and weakening vitreo-retinal adhesion to safely detach the posterior vitreous cortex. This would not only facilitate surgery, but if performed early in the natural history of disease, it should prevent progressive disease.

422 citations

Journal ArticleDOI
TL;DR: In this article, the authors reviewed 158 eyes with evolving or completed idiopathic macular holes and found that prefoveal vitreous cortex contraction is probably the cause of macular hole development.

385 citations

Journal ArticleDOI
TL;DR: Characterization of the molecular events underlying changes will elucidate the mechanisms of the phenomena of synchisis, syneresis, and detachment, and may provide methods with which to prevent or induce vitreous detachment prophylactically.
Abstract: Changes in vitreous structure that occur with aging are important in the pathogenesis of vitreous liquefaction (synchisis senilis), vitreous detachment, and retinal disease. Vitreous morphology was studied in 59 human eyes post-mortem using dark-field horizontal slit illumination of the entire dissected vitreous. In many individuals younger than 30 years, the vitreous was homogeneous in structure. Middle-aged individuals had macroscopic fibers in the central vitreous, which coursed anteroposteriorly and inserted into the vitreous base and the vitreous cortex, posteriorly. During senescence, the vitreous volume was reduced, the vitreous body was collapsed (syneresis), and the fibers were thickened, tortuous, and surrounded by liquid vitreous. This sequence of age-related changes probably results from a progressive reorganization of the hyaluronic acid and collagen molecular networks. Characterization of the molecular events underlying these changes will elucidate the mechanisms of the phenomena of synchisis, syneresis, and detachment, and may provide methods with which to prevent or induce vitreous detachment prophylactically.

262 citations

Journal ArticleDOI
TL;DR: 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.
Abstract: PURPOSE. To demonstrate the efficacy of microplasmin in inducing posterior vitreous detachment (PVD) and to evaluate the human and the feline retina after treatment. METHODS. Thirteen human donor eyes were injected with 62.5, 125, or 188 g microplasmin. The 13 fellow eyes received balanced salt solution. Four of the microplasmin-treated eyes received an additional intravitreal gas injection. After incubation at 37°C for 30 minutes, all globes were placed in 4% paraformaldehyde. Retinal specimens were processed for scanning (SEM) and transmission (TEM) electron microscopy. Five feline eyes were injected with 14.5- or 25-g microplasmin. Animals were killed after 1 day, 3 days, or 3 weeks, and retinal specimens were evaluated by electron and confocal microscopy. RESULTS. In all control eyes, SEM demonstrated the cortical vitreous covering the inner limiting membrane (ILM). Intravitreal injection of 125 or 188 g microplasmin resulted in complete PVD. After treatment with 62.5 g microplasmin, SEM revealed collagen fibrils covering the ILM. Additional gas injection did not change the dose necessary for PVD. In vivo in cats, 25 g microplasmin resulted in complete PVD after 3 days. After 3 weeks, there was complete PVD with both doses of microplasmin. The retina and the ILM were well preserved in all eyes. CONCLUSIONS. 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. (Invest Ophthalmol Vis Sci. 2004;45:641‐ 647)

185 citations

Journal ArticleDOI
TL;DR: The important parts that vitreous shrinkage and detachment play in the course of proliferative diabetic retinopathy apparently have not been widely recognized.
Abstract: Introduction Although an extensive literature on various aspects of diabetic retinopathy has accumulated over the years, few studies of the natural course of the proliferative stage have been reported An excellent summary of previous work is to be found in Larsen's 1960 monograph 1 More recently, Dobree 2 has emphasized the characteristic cycle of growth and regression of new vessels in proliferative diabetic retinopathy, and Beetham 3 has provided valuable long-term statistics on the rate of progression and degree of visual impairment found in these cases The important parts that vitreous shrinkage and detachment play in the course of proliferative diabetic retinopathy apparently have not been widely recognized Larsen 1 states that he found no discussion of vitreous detachment in his extensive review of the literature on diabetic retinopathy, except for one case described by Hruby 4 Larsen describes one characteristic picture of vitreous detachment, that in which fresh hemorrhage

176 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20216
20206
20197
20189
20176
201613