Radius R L
Department of Ophthalmology, Medical College of Wisconsin, Milwaukee.
Surv Ophthalmol. 1987 Jul-Aug;32(1):35-44. doi: 10.1016/0039-6257(87)90072-5.
The mechanism of axon damage in eyes with glaucomatous optic neuropathy remains undefined. Interestingly, it has been observed that, although the entire nerve cross-section may be involved by the nerve damage, in many instances, the superior and inferior axon bundles are preferentially affected by the pressure insult. Thus, recent studies by many investigators have stressed a re-examination of the optic nerve head anatomy, including the nerve head microcirculation, the glial and connective tissue elements within the nerve head, and the morphology of the axons themselves. Any correlation between regional differences in this anatomy and the preferential involvement by specific axon bundles within the nerve head by the pressure insult may suggest some further insight into the mechanisms underlying the pressure-induced axon loss in glaucomatous eyes.
青光眼性视神经病变患者眼部轴突损伤的机制仍不明确。有趣的是，人们观察到，尽管整个神经横断面可能都受到神经损伤的影响，但在许多情况下，上下轴突束优先受到压力损伤的影响。因此，许多研究者最近的研究都强调要重新审视视神经乳头的解剖结构，包括神经乳头微循环、神经乳头内的神经胶质和结缔组织成分以及轴突本身的形态。这种解剖结构的区域差异与神经乳头内特定轴突束优先受到压力损伤之间的任何关联，可能会为青光眼性眼内压力诱导轴突丢失的潜在机制提供一些进一步的见解。
