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Abstract
In owl monkeys, elevation of intracranial pressure to 500 mm. saline for 4 to 7 hours failed to cause an accumulation at the optic nerve head of protein carried by rapid axonal transport. This suggests that the block of rapid transport observed by others during papilledema may be the result of axon swelling, not its cause. Alternatively, more than 8 hours may be required for intracranial pressure to show an effect, only the slow transport may be affected initially, or other factors than simple hydrostatic pressure may be operative in papilledema. In addition, the elevated intracranial pressure did not prevent the block of axonal transport at the lamina cribrosa produced by elevated intraocular pressure, even though the elevated intracranial pressure reduced the pressure gradient to which the axon is subjected as it crosses the lamina cribrosa. Perhaps the block produced by intraocular pressure is not due to a simple mechanical or hydrostatic mechanism.