الفهرس 
Effect of AgingOnly 14 pages are availabe for public view
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Abstract
There is a reciprocal relationship between the vitreous body and diabetic retinopathy. Diabetes mellitus as a metabolic disease process influences the biochemistry of the vitreous and vitreoretinal interface, this biochemical changes in their turn influence the aging changes in the vitreous and vitreoretinal interface. One expression of this is early posterior vitreous detachment. The presence of vitreous cortex material at the vitreoretinal interface probably plays a key role in transition phase of background retinopathy towards proliferative retinopathy.
Diabetic PVD follows a course different than that in age related PVD, diabetic PVD most frequently starts at the area surrounding the macula and the optic disc. These are naturally occurring areas where the vitreous is more firmly attached like: the vitreous base, along major retinal vessels and retinal tufts. Acquired areas of more firm vitreoretinal attachment include lattice degeneration, some post-inflammatory lesions, areas of degenerative remodeling and some vitreous base lesions. Additional pathological vitreoretinal adhesions consist of newly formed fibro-vascular tissue connecting the retinal with the posterior vitreous lamina and the vitreous cortex.
OCT provides essential information in assessing the vitreoretinal interface. It has revolutionized the manner in which entities such as vitreomacular traction syndrome, macular edema, epiretinal membrane, full thickness macular hole, pseudohole, lamellar hole, and macular schisis are diagnosed and managed.
Furthermore, OCT has given insight into the normal evolution of posterior vitreous detachment in healthy eyes as well as the tractional complications of its early (macular) stages. In addition, OCT of the vitreoretinal interface can often be helpful in planning surgical intervention and providing postoperative prognostic information, non-contact, non-invasive mode of imaging is essential in the complete assessment of these disorders that are difficult to characterize by biomicroscopy alone.
There is a significant correlation between the features of OCT and fluorescein angiography in diabetic macular edema. The analysis of clinically significant macular edema based on both OCT and fluorescein angiography can provide information that may be useful to disclose the pathogenesis of the edema and to optimize the treatment for each type.
A classification system, modified from the Otani scheme was developed for the OCT images of clinically significant diabetic macular edema. The OCT findings of the macular edema were categorized into four types: type 1, thickening of the fovea with homogenous optical reflectivity throughout the whole layer of the retina; type 2, thickening of the fovea with markedly decreased optical reflectivity in the outer retinal layer; type 3, thickening of the fovea with subfoveal fluid accumulation and distinct outer border of detached retina; and type 3A, without foveal traction, and type 3B, with apparent vitreofoveal traction. When two types coexisted in one eye, the case was categorized according to the predominant type.
Fluorescein angiography findings were categorized into three types: focal leakage type, which was predominantly well defined focal areas of leakage from microaneurysm or localized dilated capillaries; diffuse leakage type, predominantly widespread and ill-defined leakage involving the whole circumference of the fovea; and diffuse cystoid leakage type, predominantly diffuse leakage but with pooling of dye in the cystic spaces of the macula in the late phase.
OCT testing should be considered in eyes with PDME to evaluate the vitreomacular interface, particularly when FA discloses no significant leakage or ischemia. This study discloses a high prevalence of VMIA in eyes with PDME and documents the superiority of OCT in detecting such abnormalities. Our findings raise several pertinent issues:
5) Should patients be treated differently if VMIA are present?
6) Do these interface changes predict a poor response to laser?
7) Are eyes with VMIA and PDME after initial laser therapy at higher risk of failing further laser treatment and thus appropriate ones for which to consider an alternative intervention?
8) Are treatment methods that address the VMIAs warranted in such eyes?