Halpern D Lynn, Grosskreutz Cynthia L
Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, 243 Charles Street, Boston, MA 02114, USA.
Ophthalmol Clin North Am. 2002 Mar;15(1):61-8. doi: 10.1016/s0896-1549(01)00012-8.
The optic neuropathy of glaucoma appears to be multifactorial in etiology. Both mechanical and vasogenic theories remain viable explanations for the observed nerve damage and the destructive effect of trophic withdrawal could be espoused by either theory. Each theory feeds into the final common pathway of cell death; even the immune system may kill cells in glaucoma by apoptosis. This knowledge has led to the hope that glaucomatous nerve damage can be curtailed or even prevented with the use of neuroprotective agents. Indeed, there are many intriguing new therapeutic possibilities on the horizon. Until evidence from clinical trials demonstrates the effectiveness of these agents however, control of IOP will remain the mainstay of treatment for glaucoma.
青光眼性视神经病变的病因似乎是多因素的。机械学说和血管源性学说对于所观察到的神经损伤而言仍是可行的解释，并且营养物质缺乏的破坏作用在这两种学说中都可能成立。每种学说都指向细胞死亡的最终共同途径；甚至免疫系统也可能通过凋亡在青光眼中杀死细胞。这一认识带来了一种希望，即使用神经保护剂可以减少甚至预防青光眼性神经损伤。确实，有许多引人入胜的新治疗可能性即将出现。然而，在来自临床试验的证据证明这些药物的有效性之前，控制眼压仍将是青光眼治疗的主要手段。
