Acute and chronic experimental optic neuritis. Alteration in the blood-optic nerve barrier.

Horseradish peroxidase (HRP) tracer studies in experimental allergic optic neuritis showed alterations in the blood-optic nerve barrier. Light and electron microscopic examination of the optic disc disclosed intense leakage of HRP at the lamina scleralis, with extracellular staining of both axonal and glial columns, despite the lack of inflammation at this region. The intraorbital optic nerve showed leakage of HRP at the sites of both acute and chronic demyelination. Ultrastructurally, leakage of HRP was confined to the perivascular and extracellular spaces. The mechanism of leakage seems to be by diffusion through the endothelial cell junctions or vesicular transport across the endothelial cells. The high predilection for involvement of the optic nerve in chronic demyelinating disorders may be due to the inherent weakness of the blood-brain barrier at the optic nerve head.