Fechtner R D, Weinreb R N
Department of Ophthalmology and Visual Sciences, University of Louisville, Kentucky.
Surv Ophthalmol. 1994 Jul-Aug;39(1):23-42. doi: 10.1016/s0039-6257(05)80042-6.
Several mechanisms have been postulated to explain the optic nerve damage that occurs in primary open angle glaucoma (POAG). No single mechanism can adequately explain the great variations in susceptibility to damage and the patterns of damage seen in this syndrome. The etiology of POAG is likely to be multifactorial. Mechanical, vascular and other factors may influence individual susceptibility to optic nerve damage. An enhanced understanding of the nature of the optic nerve damage in POAG and improved methods of study may result in earlier diagnosis or may allow us to distinguish among different pathological processes all currently grouped under the diagnosis of POAG. As we gain a better understanding of the neuropharmacology and cellular biology of injury and repair of the visual system we will undoubtedly refine the concepts of glaucomatous optic neuropathy.
已经提出了几种机制来解释原发性开角型青光眼（POAG）中发生的视神经损伤。没有单一机制能够充分解释该综合征中损伤易感性的巨大差异以及所观察到的损伤模式。POAG的病因可能是多因素的。机械、血管和其他因素可能影响个体对视神经损伤的易感性。对POAG中视神经损伤本质的深入理解以及改进的研究方法可能会带来更早的诊断，或者使我们能够区分目前都归类于POAG诊断之下的不同病理过程。随着我们对视觉系统损伤和修复的神经药理学及细胞生物学有更好的理解，我们无疑将完善青光眼性视神经病变的概念。
