The role of intracranial pressure in glaucoma and therapeutic implications

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Abstract
Despite glaucoma being the second leading cause of blindness globally, its pathogenesis remains incompletely understood. Although intraocular pressure (IOP) contributes to glaucoma, and reducing IOP slows progress of the disease, some patients progress despite normal IOP (NTG). Glaucomatous damage causes characteristic cupping of the optic nerve where it passes through the lamina cribrosa. There is evidence that cerebrospinal fluid (CSF) within the optic nerve sheath has a different composition from CSF surrounding the brain. Furthermore, fluctuations in CSF flow into the optic nerve sheath may be reduced by trabeculae within the sheath, and on standing intracranial pressure (ICP) within the sheath is stabilised at around 3 mmHg due to orbital pressure. Blood pressure has been linked both to glaucoma and ICP. These facts have led some to conclude that ICP does not play a role in glaucoma. However, according to stress formulae and Laplace’s Law, stress within the lamina cribrosa is dependent on the forces on either side of it, (IOP and ICP), and its thickness. On lying flat at night, ICP between the brain and optic nerve sheath should equalise. Most evidence suggests ICP is lower in glaucoma than in control groups, and that the lamina cribrosa is thinner and more posteriorly displaced in glaucoma. Subjects who have had ICP reduced have developed signs of glaucoma. This review finds most evidence supports a role for low ICP in the pathogenesis of glaucoma. Caffeine, theophylline and vitamin A may increase ICP, and could be new candidates for an oral treatment.

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