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Article
August 1977

Optic Disc Edema in Raised Intracranial PressureIV. Axoplasmic Transport in Experimental Papilledema

Author Affiliations

From the Georgiana Theobald Ophthalmic Pathology Laboratory, University of Illinois Eye and Ear Infirmary, Chicago and the Armed Forces Institute of Pathology, Washington, DC (Dr Tso), and the Department of Ophthalmology, University of Iowa, Iowa City (Dr Hayreh). This study was conducted in part while Dr Tso was at the Armed Forces Institute of Pathology, Washington, DC. Dr Tso is a Research to Prevent Blindness-William Friedkin Scholar, 1976-1977.

Arch Ophthalmol. 1977;95(8):1458-1462. doi:10.1001/archopht.1977.04450080168023
Abstract

• 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.

(Arch Ophthalmol 95:1458-1462, 1977)

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