Optic disc edema in raised intracranial pressure. IV. Axoplasmic transport in experimental papilledema
M. O. Tso and S. S. Hayreh
Tritiated leucine was injected intravitreously into the eyes of rhesus
monkeys that had developed papilledema secondary to implantation of
intracranial balloons. Autoradiographic studies of the optic nerve head
showed that six hours after intravitreous injection of the isotope the fast
component of axoplasmic transport accumulated in the regions of the lamina
choroidalis and lamina scleralis. The slow component arrived at the optic
nerve head two to four days after injection, and the swollen axons of the
entire optic nerve head were filled with radioactive isotopes. Twelve days
after injection of isotope, the axons in the optic nerve head were still
diffusely labeled. Disturbance of axoplasmic transport was one of the
primary events resulting in swelling of axons in papilledema. The pattern
of axoplasmic disturbances in papilledema secondary to raised intracranial
pressure was similar to that observed in papilledema secondary to ocular
hypotony or increased intraocular pressure. Ocular hypotony, raised
intracranial pressure, and increased intraocular pressure appear to share a
final common pathway. All these conditions apparently converge into this
final common pathway of disturbance of axoplasmic transport to give rise to
papilledema.
