Hayreh S S
Arch Ophthalmol. 1977 Sep;95(9):1553-65. doi: 10.1001/archopht.1977.04450090075006.
The pathogenesis of optic disc edema (ODE) in raised intracranial pressure is discussed in the light of recent observations on the subject. The findings indicate that ODE is a mechanical phenomenon. The raised cerebrospinal fluid pressure (CSFP) in the sheath of the optic nerve produces axoplasmic flow stasis in the optic nerve head. This results in swelling of the axons, which manifests as early ODE and secondarily produces the well-known optic disc and retinal vascular changes associated with ODE. The pathogenesis of ODE seen in different conditions without raised CSFP cannot be explained by any single mechanism in spite of the occurrence of axoplasmic flow stasis in most cases, because the stasis in different situations has different mechanisms.
根据最近关于该主题的观察结果，讨论了颅内压升高时视盘水肿（ODE）的发病机制。研究结果表明，ODE是一种机械现象。视神经鞘内脑脊液压力（CSFP）升高会导致视神经乳头处轴浆流淤滞。这会导致轴突肿胀，表现为早期ODE，并继发产生与ODE相关的众所周知的视盘和视网膜血管变化。尽管在大多数情况下会发生轴浆流淤滞，但在没有CSFP升高的不同情况下出现的ODE发病机制不能用任何单一机制来解释，因为不同情况下的淤滞有不同的机制。
