Abstract
While the pathophysiology of glaucoma remains elusive, a growing body of evidence suggests that intracranial pressure may play a significant role. This review aims to highlight recent findings on the role of intracranial pressure in the development of glaucomatous optic neuropathy. The translaminar pressure gradient is defined as intraocular pressure (IOP) minus intracranial pressure (ICP) divided by the thickness of the lamina cribrosa. Prior research has demonstrated the effect of elevated IOP of ganglion cell apoptosis, but newer research shows that ganglion cell death may occur with normal IOP but reduced ICP. Additionally, patients with normal tension glaucoma have lower ICPs than controls. Stresses and strains on the lamina cribrosa may be responsible for some of the development of glaucomatous optic neuropathy. The pathophysiology of glaucomatous optic neuropathy may include a delicate balance of the translaminar pressure differential involving intraocular pressure, intracranial pressure, and lamina cribrosa biomechanics.
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