特发性黄斑裂孔发病机制探讨

The investigation of the pathogenesis of idiopathic macular hole

目的根据OCT图像，探讨特发性黄斑裂孔的发病机制。方法观察特发性黄斑裂孔59例65只眼的OCT图像。Ⅰ期裂孔6例6只眼；II期裂孔22例24只眼，其中Ⅱ期裂孔的早期10例10只眼，Ⅱ期裂孔的晚期12例14只眼；Ⅲ期裂孔21例25只眼；Ⅳ期裂孔10例10只眼。结果Ⅰ期裂孔中有4／6可观察到黄斑前双凸型玻璃体后脱离对中心凹的牵拉。Ⅱ期裂孔的早期中有9／10可观察到黄斑前双凸型玻璃体后脱离对中心凹的牵拉；Ⅱ期的晚期中有10／14可观察到裂孔盖膜，这些盖膜中有8／10可观察到含有部分撕脱下来的视网膜神经组织。Ⅲ期裂孔中有16／25及Ⅳ期裂孔中有7／10可观察到内界膜增厚，反光增强，部分患眼还可观察到合并有视网膜前膜的形成。结论特发性黄斑裂孔Ⅰ期和Ⅱ期的主要发病机制是中心凹玻璃体前后方向的牵拉，而Ⅲ期和Ⅳ期的主要发病机制是内界膜的收缩。

Objective To investigate the pathogenesis of IMH,according to the image of OCT. Patients and. Methods 59 eases （65 eyes） oflMH were examined by OCT. Stage Ⅰ ：6 cases （6 eyes）. Stage Ⅱ ： 22 cases （24 eyes）, early stage Ⅱ ： 10 cases （ 10 eyes）, late stage Ⅱ： 12 cases （ 14 eyes）. Stage Ⅲ ： 21 cases （25 eyes）. Stage Ⅳ ： 10 eases （ 10 eyes）. Results In stage Ⅰ , 4/6 was found the traction of biconvex posterior vitreous detachment at fovea. In early stage Ⅱ, 9/10 was found the traction of biconvex posterior vitreous detachment at fovea. In late stage Ⅱ, 10/14 was found the opereulum, and among the opercula, 8/10 was found some evulsed retinal tissue. In stage Ⅲ and Ⅳ, 16/25 and 7/10 were found that the thickness and glisten of internal limiting membrane （ILM） were increased, and epretina membrane could be found in some cases. Conelusion In stageⅠ and Ⅱ ,the pathogenesis of IMH is the fore-and-aft traction of vitreous at the fovea. In stage Ⅲ and Ⅳ,the pathogenesis of IMH is the contraction of ILM.