Gass J D
Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami School of Medicine, FL 33101.
Arch Ophthalmol. 1988 May;106(5):629-39. doi: 10.1001/archopht.1988.01060130683026.
Evidence is presented that idiopathic senile macular hole is caused by focal shrinkage of the vitreous cortex in the foveal area. The most reliable biomicroscopic signs of impending hole formation (stage 1) are the development of a yellow spot or ring in the center of the fovea, loss of the foveal depression, and no evidence of separation of the vitreous from the foveal retina. Although in a majority of eyes with stage 1 changes there is a progression to hole formation, spontaneous separation of the vitreous without hole formation may occur in some cases (44%) and cause characteristic biomicroscopic changes, including foveal reattachment, disappearance of the yellow spot or ring, and, in some cases, a pseudo-operculum, with one or more lamellar holes or facets. A prospective collaborative study is recommended to confirm these findings and to test the clinical value of surgical peeling of the vitreous cortex in eyes with stage 1 changes as a means of preventing hole formation.
有证据表明,特发性老年性黄斑裂孔是由黄斑区玻璃体皮质的局部收缩引起的。即将形成裂孔(1期)最可靠的生物显微镜体征是黄斑中心出现黄斑或黄环、黄斑凹陷消失,以及没有玻璃体与黄斑视网膜分离的迹象。尽管在大多数有1期改变的眼中会进展为裂孔形成,但在某些情况下(44%)可能会发生玻璃体自发分离而不形成裂孔,并引起特征性的生物显微镜改变,包括黄斑复位、黄斑或黄环消失,以及在某些情况下出现假盖膜,伴有一个或多个板层裂孔或小平面。建议进行一项前瞻性合作研究以证实这些发现,并测试在有1期改变的眼中手术剥除玻璃体皮质作为预防裂孔形成手段的临床价值。