| pubmed-article:2678144 | pubmed:abstractText | CME is the final common pathway of many intraocular and systemic diseases. It involves the retinal vasculature and often has a choroidal and vitreal component. Obviously, at some level of this complex pathophysiological process, mediators must be involved. The question is whether the characteristic distribution of vascular leakage and retinal edema is best explained by the diffusion of mediators released by from a remote site, as proposed by Miyake (see Miyake et al., 1989), or whether it reflects the distribution of pre-existing anatomical structures causing the local release of mediators by exerting mechanical stress. The fact that vitreous adhesions are present at the lens and vitreous base anteriorly and at the major vessels, optic disc, and macula posteriorly support the mechanical concept. The anatomic sites of vitreo-retinal attachments have in common the thinness of their basal lamina and firmness of their fibrous vitreal attachments to the Muller cells. Although adhesion at two opposite sites is the precondition for the development of traction, it will only be generated through intrinsic or extrinsic pathologic changes in the vitreous. In a normal anatomical situation, many vitreous fibers distribute tractional forces evenly to numerous Muller cell attachments. In partial PVDs, fewer fibers and Muller cells endure most of the traction. This may lead to chronic Muller cell irritation and local release of a variety of mediators which, in turn, may facilitate vascular leakage. Vitreous shrinkage and possibly chronic Muller cell irritation may, therefore, facilitate abnormal leakage at all sites of attachment. A typical example is pars planitis, with leakage at the peripheral retina and around major blood vessels, the disc and macula. This pattern of leakage suggests that vitreous traction may be a co-factor in many cases. Most traction develops slowly, passing through stages of partial PVD. The occurrence of a traumatic macular hole and vitreous base avulsion as a result of trauma is the exception. While the pattern of PVD in vivo has not been investigated in detail, PVD with normal adhesions is frequently found in age-related liquefaction and collapse of the vitreous. PVD with abnormal adhesions and shrinkage is found in association with diabetes, proliferative vitreoretinopathy, and inflammation. As to the macula itself, two types of attachment are suggested, a firm central foveolar attachment and a larger, weaker perifoveal attachment, corresponding to the nuclear and cortical vitreous and to two types of pathologic traction; anteroposterior and tangential.(ABSTRACT TRUNCATED AT 400 WORDS) | lld:pubmed |
