Radius R L, Anderson D R
Invest Ophthalmol Vis Sci. 1980 Feb;19(2):158-68.
Previous work has documented impairment of slow axonal transport in papilledema, but the abnormalities in rapid transport were less certain. Therefore fast axonal transport was studied in 19 primate eyes subjected to ocular hypotony for 6 to 72 hr following surgical fistulization of the anterior chamber. Mild, irregular alterations in fast axonal transport were detected only after nerve head swelling was apparent. These changes in fast transport mechanisms in cases of nerve head edema occur after, and may be secondary to, impaired slow axoplasmic flow and the resultant axonal swelling. Furthermore, since prolonged complete interruption of axonal transport is theoretically inconsistent with the continued normal neuron function characteristic of papilledema and, moreover, since previous data shows a "slowdown" rather than complete blockade of axonal transport in papilledema, it is likely that in eyes with papilledema there does not exist a complete flock of axonal transport. Therefore we hypothesize that the swelling results when slow axoplasmic flow is locally slowed down but not totally stopped, with the axon distention producing secondary mild, irregular changes in fast axonal transport.
以往的研究记录了视乳头水肿中轴突慢速运输的受损情况，但快速运输的异常情况尚不确定。因此，对19只灵长类动物的眼睛进行了研究，这些眼睛在前房手术造瘘后经历了6至72小时的低眼压。仅在视乳头明显肿胀后才检测到快速轴突运输出现轻微、不规则的改变。在视乳头水肿病例中，快速运输机制的这些变化发生在轴浆慢速流动受损及由此导致的轴突肿胀之后，且可能是其继发结果。此外，由于从理论上讲，轴突运输的长期完全中断与视乳头水肿所特有的神经元持续正常功能不一致，而且，由于先前的数据显示视乳头水肿时轴突运输是“减慢”而非完全阻断，所以视乳头水肿的眼睛中很可能不存在完全的轴突运输停滞。因此我们推测，当轴浆慢速流动局部减慢但未完全停止时就会导致肿胀，轴突扩张会在快速轴突运输中产生继发的轻微、不规则变化。
