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Article
January 1973

Intracranial Pressure and Ocular Hemodynamics

Author Affiliations

Miami
From the Bascom Palmer Eye Institute, Department of Ophthalmology, University of Miami School of Medicine, and the Department of Neurology, Veterans Administration Hospital, Miami. Dr. Anderson holds an RPB Eye Research Professorship from Research to Prevent Blindness, Inc.

Arch Ophthalmol. 1973;89(1):52-58. doi:10.1001/archopht.1973.01000040054013
Abstract

In owl monkeys, controlled elevation of subarachnoid pressure was produced either intracranially, in the optic nerve sheath, or in both. When intracranial pressure was elevated, orbital venous pressure became elevated, but it did not keep pace with intracranial pressure elevation, because orbital veins have anastomoses to facial veins and need not depend entirely on cavernous sinus for drainage. The central retinal vein pressure is additionally affected by pressure in optic nerve sheaths, and keeps pace with vaginal sheath pressure elevation, because anastomotic connections at the optic disc between central retinal vein and vortex vein were not sufficient to relieve fully pressure in the central retinal vein. Intraocular blood flow was slowed in regions drained by central retinal vein (retina and disc). The choroidal flow, which drains via vortex veins into orbital veins, was affected less.

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