Intraocular Pressure Matters

Abstract

To date, evidence from multiple randomized controlled trials has shown that effective intraocular pressure (IOP)-lowering therapy significantly reduces the risk of glaucomatous progression across all stages of the disease. Changes in IOP have a substantial impact on the load-bearing connective tissues of the optic nerve head (ONH), as well as the overlying neurovascular tissues of the ONH and retina. An initial treatment goal of reducing IOP by 25% to 35%-and possibly more in advanced cases-can help prevent progression. Additionally, maintaining stable IOP by minimizing both diurnal and long-term fluctuations may further enhance disease control and reduce the risk of worsening. FINANCIAL DISCLOSURE(S): Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

Keywords: Fluctuation; Glaucoma; Intraocular pressure.

Figure 1.. Mechanobiolology of the Optic Nerve and Retina:

Increased Intraocular pressure (IOP) is counterbalanced by optic nerve sheath pressure (ONSP) resulting in tissue strain in the optic nerve head (ONH). This can damage axons directly, reduce focal perfusion, and activate cellular mechanotransduction that drives remodeling of the ONH. This remodeling alters ONH morphology and stiffness creating a negative feed back loop (−) that increases the vulnerability of the retinal ganglion cell (RGC) axons to further glaucomatous injury. Additionally, RGC somal injury can occur when IOP elevation reduces ocular perfusion pressure, which occurs most often with acute IOP elevation a function of IOP and blood pressure (BP), beyond the capacity for retinal autoregulation.