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Clinical Trial Summary

The mechanism by which vision loss in glaucoma occurs is still unknown, but it is clear that increased Intraocular Pressure (IOP) is a major risk factor. It is also thought that the lamina cribrosa (LC) is a site of primary damage during the pathogenesis of the disease. The changes caused by intraocular pressure (IOP) modulation at the level of the optic nerve head and LC will be evaluated in the present study. Subjects with keratoconus exhibit abnormal collagen properties that can impair their LC behavior. By evaluating their lamina biomechanical response we can advance our understanding on the role of the lamina in glaucoma pathogenesis. A better understanding of the process will ultimately lead to improved detection and management of glaucoma. It is hypothesized that subjects with keratoconus have an abnormal biomechanical response of the lamina cribrosa in response to IOP modulation.


Clinical Trial Description

n/a


Study Design


Related Conditions & MeSH terms


NCT number NCT03560609
Study type Interventional
Source NYU Langone Health
Contact Jamika Singleton-Garvin
Phone 929-455-5522
Email Jamika.Singleton-Garvin@nyulangone.org
Status Recruiting
Phase N/A
Start date November 15, 2018
Completion date July 31, 2024

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