Foos R Y
Albrecht Von Graefes Arch Klin Exp Ophthalmol. 1977 Dec 31;204(4):223-34. doi: 10.1007/BF00415316.
Previous studies have attributed changes in the retinal surface over or adjacent to large superficial retinal vessels to a variety of conditions, the most common being 'anomalous vitreoretinal attachments.' The fundamental nature of the lesions and their pathogenesis, however, has remained controversial. The present study was undertaken to categorize the ultrastructural alterations of the vitreoretinal juncture over retinal vessels in the posterior fundus of man, and to clarify the relationship of these fundamental changes to clinically significant lesions in this region. Results show no difference in vitreoretinal, or more specifically vitreolaminar attachments over vessels when compared with adjacent regions. The cause of the more significant anomalies, notably surface breaks and their sequelae, is apparently multifactorial and related to a sequence of events. Initially three events predispose to or cause small surface breaks: developmental thinning of the inner limiting lamina; subsurface retinal degeneration; and transmigrating macrophages. These small surface breaks, when complicated by vitreous incarceration or by simple epiretinal membrane formation, can during posterior vitreous detachment cause peeling of the retinal surface, and the resulting large surface breaks may in turn provoke more complex proliferative lesions of the vitreoretinal juncture.
以往的研究将视网膜大表层血管上方或附近视网膜表面的变化归因于多种情况,最常见的是“异常玻璃体视网膜附着”。然而,这些病变的基本性质及其发病机制一直存在争议。本研究旨在对人眼底后部视网膜血管上方玻璃体视网膜连接处的超微结构改变进行分类,并阐明这些基本变化与该区域临床显著病变的关系。结果显示,与相邻区域相比,血管上方的玻璃体视网膜,或更具体地说是玻璃体板层附着并无差异。更显著异常(尤其是表面破裂及其后遗症)的原因显然是多因素的,且与一系列事件有关。最初,有三个事件易引发或导致小的表面破裂:内界膜的发育性变薄;视网膜下变性;以及游走的巨噬细胞。这些小的表面破裂,当因玻璃体嵌顿或单纯视网膜前膜形成而变得复杂时,在后玻璃体脱离过程中可导致视网膜表面剥离,而由此产生的大的表面破裂反过来可能引发玻璃体视网膜连接处更复杂的增殖性病变。