Brubaker R F
Department of Ophthalmology, Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA.
Am J Ophthalmol. 1996 May;121(5):473-83. doi: 10.1016/s0002-9394(14)75421-2.
This study is a systematic exploration of why some patients with glaucoma continue to lose visual field long after therapeutic normalization of their increased intraocular pressures.
Three cases of glaucoma are described that had increased intraocular pressures and good initial visual fields.
The following four hypotheses are offered to explain delayed functional loss in these patients: (1) A process independent of intraocular pressure is killing ganglion cells. (2) Unmeasured increases of pressure are killing ganglion cells. (3) The ganglion cells have a genetically determined hypersensitivity to intraocular pressure. (4) The ganglion cells have been rendered hypersensitive to intraocular pressure by irreversible damaging effects of previously increased intraocular pressures
The current state of knowledge does not permit the elimination of any of the four hypotheses. An additional hypothesis is that the final stage of ganglion cell death is mediated by apoptosis. If so, a potential new treatment for glaucoma would be to inhibit the apoptotic pathway.
本研究旨在系统探究为何部分青光眼患者在眼压升高经治疗恢复正常后很长时间仍持续出现视野缺损。
描述了3例眼压升高且初始视野良好的青光眼病例。
提出以下四种假说来解释这些患者出现延迟性功能丧失的原因:(1)一个与眼压无关的过程正在杀死神经节细胞。(2)未检测到的眼压升高正在杀死神经节细胞。(3)神经节细胞对眼压具有基因决定的超敏性。(4)先前眼压升高产生的不可逆损伤作用使神经节细胞对眼压变得超敏。
目前的知识水平尚无法排除这四种假说中的任何一种。另一种假说是神经节细胞死亡的最后阶段由细胞凋亡介导。如果是这样,青光眼潜在的新治疗方法可能是抑制细胞凋亡途径。