Abstract

PurposeBecause a lowered intracranial pressure (ICP) is a possible mechanism of optic neuropathy, we wished to study the CSF dynamics in the optic nerve chamber by recording possible changes in the optic nerve subarachnoid space pressure (ONSP) and the impact on it when acutely lowering ICP. MethodsIn eight normal dogs pressure probes were implanted in the left brain ventricle, lumbar cistern, optic nerve subarachnoid space and in the anterior eye chamber. Following CSF shunting from the brain ventricle we monitored changes of ICP, lumbar cistern pressure (LCP), ONSP and intraocular pressure (IOP). ResultsAt baseline, the pressures were different with ICP>LCP>ONSP but correlated with each other (P<0.001). The “trans-lamina cribrosa pressure gradient” (TLPG) was highest for IOP–ONSP, lower for IOP–LCP, and lowest for IOP–ICP (P<0.001). During CSF shunting the ICP gradually decreased in a linear fashion together with the ONSP (“ICP-depended zone”). But when the ICP fell below a critical breakpoint, ICP and ONSP became uncoupled and ONSP remained constant despite further ICP decline (“ICP-independent zone”). ConclusionsBecause the parallel decline of ICP and ONSP breaks down when ICP decreases below a critical breakpoint, we interpret this as a sign of CSF communication arrest between the intracranial and optic nerve SAS. This may be caused by obstructions of either CSF inflow through the optic canal or outflow into the intra-orbital cavity. This CSF exchange arrest may be a contributing factor to optic nerve damage and the optic nerve chamber syndrome which may influence the loss of vision or its restoration.

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