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 block of axonal transport in papilledema, it is likely that in eyes with papilledema there does not exist a complete block 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.
|Original language||English (US)|
|Number of pages||11|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Jan 1 1980|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience