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Related Experiment Video

Updated: Jul 16, 2026

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

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Published on: March 12, 2016

The Pathophysiological Association Between Obstructive Sleep Apnea and Glaucoma: A Current Update.

Wojciech Mazurek¹, Łukasz Mazurek², Barbara Rękas-Mazurek¹

¹Department of Ophthalmology, Military Institute of Medicine-National Research Institute, 04-141 Warsaw, Poland.

Journal of Clinical Medicine

|July 15, 2026

Summary

Obstructive sleep apnea (OSA) may contribute to glaucoma development through chronic hypoxia and reduced ocular pressure. This relationship is crucial for understanding normal-tension glaucoma and warrants multidisciplinary ophthalmic screening.

Keywords:

chronic intermittent hypoxia continuous positive airway pressure glaucoma lamina cribrosa normal-tension glaucoma obstructive sleep apnea ocular perfusion pressure

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Last Updated: Jul 16, 2026

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

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Published on: March 12, 2016

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Published on: February 15, 2022

Area of Science:

Ophthalmology
Neurology
Sleep Medicine

Background:

Glaucoma is a leading cause of irreversible blindness.
Elevated intraocular pressure (IOP) is a key risk factor, but not the sole cause.
Systemic conditions like obstructive sleep apnea (OSA) are implicated in glaucoma pathogenesis.

Purpose of the Study:

To review the pathophysiological links between OSA and glaucoma.
To explore the role of mechanical and vascular theories in this relationship.
To highlight the relevance for normal-tension glaucoma.

Main Methods:

Literature review of current theories on glaucoma pathophysiology.
Analysis of mechanisms connecting OSA and glaucoma.
Examination of clinical relevance and early markers.

Main Results:

Chronic intermittent hypoxia and reduced ocular perfusion pressure are principal connecting mechanisms.
These factors trigger optic nerve head hypoxia, oxidative stress, and lamina cribrosa remodeling.
A vicious cycle compromises optic nerve axon metabolic support, particularly in normal-tension glaucoma.

Conclusions:

OSA-related mechanisms are significant contributors to glaucoma, especially normal-tension glaucoma.
Retinal nerve fiber layer thinning is an early indicator of optic nerve damage.
A multidisciplinary approach with ophthalmic screening for subclinical damage is recommended.