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Glaucoma: Overview

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...

Open Angle Glaucoma: Treatment

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...

Angle Closure Glaucoma: Treatment

Angle Closure Glaucoma: Treatment

Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...

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Related Experiment Video

Updated: Mar 1, 2026

Characterizing the Relationship Between Eye Movement Parameters and Cognitive Functions in Non-demented Parkinson's Disease Patients with Eye Tracking

Characterizing the Relationship Between Eye Movement Parameters and Cognitive Functions in Non-demented Parkinson's Disease Patients with Eye Tracking

Published on: September 26, 2019

Delayed saccadic eye movements in glaucoma.

Raageen Kanjee¹, Yeni H Yücel^1,2, Martin J Steinbach^3,4

¹Ophthalmology and Vision Sciences, Laboratory Medicine and Pathobiology, St Michael's Hospital, University of Toronto.

|May 26, 2017

Summary

This summary is machine-generated.

Glaucoma patients exhibit delayed saccadic eye movements, specifically in reaction time and express saccade frequency. These findings suggest saccade testing could offer a new method for assessing visual function in glaucoma.

Keywords:

brain latency quality of life superior colliculus visual dysfunction visual field

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Area of Science:

Ophthalmology
Neuroscience
Visual Science

Background:

Glaucoma is a progressive optic neuropathy characterized by visual field loss.
Saccadic eye movements are rapid, ballistic movements crucial for visual exploration.
Altered saccadic function may indicate underlying neurological or visual pathway dysfunction.

Purpose of the Study:

To investigate potential alterations in saccadic eye movements among patients diagnosed with glaucoma.
To compare saccadic parameters between glaucoma patients and age-matched healthy controls.

Main Methods:

Prospective study involving 16 glaucoma patients and 21 controls.
Utilized a pro-saccade step task with infrared oculometry for saccade recording.
Analyzed saccade reaction time, duration, amplitude, peak velocity, express saccade frequency, and direction errors.

Main Results:

Glaucoma patients showed significantly prolonged saccade reaction times (p=0.036).
A significant decrease in the frequency of express saccades was observed in glaucoma patients (p=0.007).
No significant differences were found in saccade duration, amplitude, or peak velocity; no correlation with visual field loss.

Conclusions:

Saccadic eye movements are significantly delayed in glaucoma patients across disease stages.
Median saccade reaction time may serve as a novel functional test for quantifying visual function.
Further research is required to elucidate the pathological basis and functional impact of saccadic delays.