Nicoară S
Clinica Oftalmologică, Cluj Napoca.
Oftalmologia. 2000;51(2):9-13.
The reduction of the visual performances in glaucoma may be explained by several theories. The most admitted theory, for the present, considers glaucoma as a progressive primitive optic neuropathy, having the origin at the retinal ganglion cells, associated with a disease of the sclero-corneal trabeculum, whose porosity is diminishing. The most important pathogenic hypothesis in glaucoma are: the vascular, the mechanical and the collagenic hypothesis. The vascular theory considers that the prolonged ischemia is a responsible for the neuronal alteration. In this process are participating a lot of factors: the intraocular pressure, the blood pressure and some other factors governing the vascular tone of the optic nerve (myogenic factors, metabolic factors, vasoactive factors, circulating hormones and endothelial factors). From therapeutical point of vue, these modern concepts are reflected in the new therapeutic perspectives, with a special attention for the axonal outflow and trabecular cell disfunction and also for the dysregulation of the cellular oxidoreduction.
青光眼患者视觉功能下降可由多种理论来解释。目前，最被认可的理论认为青光眼是一种进行性原发性视神经病变，起源于视网膜神经节细胞，与巩膜 - 角膜小梁疾病相关，其孔隙率正在降低。青光眼最重要的致病假说是：血管假说、机械假说和胶原假说。血管理论认为长期缺血是神经元改变的原因。在这个过程中，许多因素都发挥了作用：眼压、血压以及其他一些控制视神经血管张力的因素（肌源性因素、代谢因素、血管活性因素、循环激素和内皮因素）。从治疗角度来看，这些现代概念反映在新的治疗前景中，特别关注轴突流出和小梁细胞功能障碍以及细胞氧化还原调节异常。
