Kishi S, Yokozuka K, Kamei Y
Department of Ophthalmology, Gunma University School of Medicine, Maebashi, Japan.
Nippon Ganka Gakkai Zasshi. 1991 Jul;95(7):678-85.
We examined the vitreous of 37 eyes of 31 patients with macular holes of various stages. There was no posterior vitreous detachment (PVD) in 18 of 18 impending and 19 of 20 newly formed macular holes. In newly formed macular holes, the operculum was located either at the level of or immediately anterior to the retinal surface. The gel component of the vitreous was always separated from the posterior fundus by intervening liquefied lacuna, simulating PVD. However, the cortical vitreous was located posterior to the liquefied lacuna and remained attached to the retina. PVD failed to develop in all of 15 eyes during the follow-up period of 3 months after formation of a macular hole. The incidence of PVD increased in the eyes with macular holes lasting for 1 year or longer. In our present series, PVD in its classical sense did not contribute to the pathogenesis of macular holes as it developed after formation of the latter. Instead, a subtle anterior displacement of vitreous cortex strictly confined to the area of the fovea seemed to trigger the development of idiopathic macular holes.
我们检查了31例不同阶段黄斑裂孔患者的37只眼的玻璃体。18只急性黄斑裂孔和20只新形成的黄斑裂孔中有18只未发生玻璃体后脱离（PVD）。在新形成的黄斑裂孔中，盖片位于视网膜表面或紧邻视网膜表面的前方。玻璃体的凝胶成分总是被中间的液化腔隙与眼底后部分隔开，模拟玻璃体后脱离。然而，皮质玻璃体位于液化腔隙后方并仍附着于视网膜。在黄斑裂孔形成后的3个月随访期内，15只眼中均未发生玻璃体后脱离。黄斑裂孔持续1年或更长时间的眼中玻璃体后脱离的发生率增加。在我们目前的系列研究中，经典意义上的玻璃体后脱离在黄斑裂孔形成后才发生，因此对黄斑裂孔的发病机制没有影响。相反，严格局限于中央凹区域的玻璃体皮质的轻微前移似乎触发了特发性黄斑裂孔的形成。
