Experimental injury of the optic nerve with optic disc swelling.
An ultrastructural study utilizing horseradish peroxidase was performed to determine the mechanism and consequences of leakage of vascular protein following injury of the optic nerve. Unilateral optic nerve injuries were produced in four rhesus monkeys by making a cautery lesion on the retrobulbar portion of the optic nerve. Optic disc changes were followed with stereo fundus photography and fluorescein angiography. Three to 14 days after injury horseradish peroxidase was given intravenously and the tissue was prepared for electron microscopy, including serial sections of selected tissue blocks. Fundus photography and fluorescein angiography showed edema of the optic disc in two animals. There was leakage of horseradish peroxidase into the optic nerve head from the optic nerve lesion and the peripapillary choriocapillaris. Although the pathway of horseradish peroxidase leakage in the injured optic nerve was not entirely clear, serial sections indicated intraendothelial channels as one possible route. Alterations of the optic nerve head were confined to the axon segments anterior to the injury, and included aggregation of mitochondria, disruption of neurotubules, and swelling. These findings suggest that optic nerve injury produces damming of axoplasmic flow and that swelling of the optic nerve head is the result of axon enlargement.
D000818:Animals; D005110:Extracellular Space / Q000201:enzymology; D005451:Fluorescein Angiography; D000882:Haplorhini; D006735:Horseradish Peroxidase / Q000032:analysis; D009887:Ophthalmoscopy; D009900:Optic Nerve / Q000473:pathology; D020221:Optic Nerve Injuries; D010211:Papilledema / Q000209:etiology*
D006735:Horseradish Peroxidase