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Updated: Jun 28, 2026

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation
Published on: March 12, 2016
The treatment of normal-tension glaucoma
Priya V Desai1, Joseph Caprioli
1Jules Stein Eye Institute, UCLA, 100 Stein Plaza, Suite 2-118, Los Angeles, CA 90095, USA. Desai@jsei.ucla.edu
Abstract:
Normal-tension glaucoma (NTG) is generally defined as visual field loss and optic nerve defects consistent with glaucoma and an intraocular pressure (IOP) that does not exceed 21 mmHg (Allingham, R.R., Damji, K., Freedman, S., Moroi, S., Shafranov, G., Shields, M.B. (2005). In: Pine J. and Murphy J. (Eds.), Shields' Textbook of Glaucoma, 5th edn., Lippincott Williams & Wilkins, Philadelphia, PA, pp. 197-207, Chapter 11). If a patient has an atypical presentation (unilateral disease, decreased central visual acuity or visual field loss not consistent with optic disk appearance) then the clinician should rule out medical or neurologic etiologies. IOP-dependent and IOP-independent mechanisms play a role in NTG nerve damage. The exact mechanisms of IOP-independent damage are not currently known. Research has shown that vascular etiologies, such as vascular insufficiency and vasospasm, may be possible mechanisms for IOP-independent damage. The mainstay of glaucoma treatment remains robust IOP reduction. The chief goal of ongoing glaucoma research is to more clearly identify IOP-independent mechanisms of damage and to find neuroprotective treatment strategies to prevent retinal ganglion cell death and consequent visual loss.
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