摘要筛板一直被认为是青光眼视网膜神经节细胞和轴突发生损伤的初始部位,观察筛板的形态学改变有助于认识青光眼的病理机制.以往研究结果显示局灶性筛板缺损与青光眼进展相关,但两者的因果关系和作用机制并不清楚.本文指出相干光层析成像术发展,首次揭示了青光眼局灶性筛板缺损可以平衡跨筛板压力梯度,从而起到延缓或终止青光眼视神经损伤进展的作用,该发现为跨筛板压力梯度学说在青光眼发病机制中的作用提供了直接的临床依据,深化了临床对局灶性筛板缺损与青光眼进展的认识,从另一角度阐述了原发性开角型青光眼的发病机制,为该疾病的治疗和预后判断提供了新的思路.

abstractsLamina cribrosa (LC) is considered as the original site of glaucomatous damage of axons of retinal ganglion cells,and therefore understanding the morphological changes in the LC will help to uncover the pathogenesis of glaucoma.Previous studies have indicated that the progress of glaucomatous optic neuropathy may be associated with the LC defects.Based on imaging by swept source optical coherence tomography B-Scan of the optic discs of patients with glaucoma,for the first time the spontaneous local LC defects have been found to balance the gradient between intraocular and cerebrospinal fluid pressures,which in turn can slow down the progress of glaucomatous optic neuropathy.This article provides the direct evidence supporting the role of intraocular and cerebrospinal fluid pressure gradient in the pathogenesis of glaucoma.This finding will increase our understanding of the mechanisms underlying glaucoma and help to develop novel strategies for its treatment and prognosis analysis.