The interaction between intracranial pressure, intraocular pressure and lamina cribrosal compression in glaucoma.

This review examines some of the biomechanical consequences associated with the opposing intraocular and intracranial forces. These forces compress the lamina cribrosa and are a potential source of glaucomatous pathology. A difference between them creates a displacement force on the lamina cribrosa. Increasing intraocular pressure and/or decreasing intracranial pressure will increase the trans-lamina cribrosa pressure difference and the risk of its posterior displacement, canal expansion and the formation of pathological cupping. Both intraocular pressure and intracranial pressure can be elevated during a Valsalva manoeuvre with associated increases in both anterior and posterior lamina cribrosa loading as well as its compression. Any resulting thinning of or damage to the lamina cribrosa and/or retinal ganglion cell axons and/or astrocyte and glial cells attached to the matrix of the lamina cribrosa and/or reduction in blood flow to the lamina cribrosa may contribute to glaucomatous neuropathy. Thinning of the lamina cribrosa reduces its stiffness and increases the risk of its posterior displacement. Optic nerve head posterior displacement warrants medical or surgical lowering of intraocular pressure; however, compared to intraocular pressure, the trans-lamina cribrosa pressure difference may be more important in pressure-related pathology of the optic nerve head region. Similarly important could be increased compression loading of the lamina cribrosa. Reducing participation in activities which elevate intraocular and intracranial pressure will decrease lamina cribrosa compression exposure and may contribute to glaucoma management and may have prognostic significance for glaucoma suspects.