About this trial
The purpose of this study is to improve understanding of the pathophysiologic process that leads to the development of glaucamotous damage. 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 LC is a site of primary damage during pathogenesis of the disease. This prospective study with determine the in-vivo mechanical response to IOP modulation at the level of the ONH and LC.
Eligibility criteria
Qualifiers
No family history (first degree relative) of glaucoma.
No history of IOP >22 mmHg.
Normal appearing optic discs and RNFL on dilated fundus examination.
Normal Swedish interactive thresholding algorithm (SITA) standard perimetry tests as defined by glaucoma hemifield test (GHT) within normal limits.
Disqualifiers
Media opacity (e.g. lens, vitreous, cornea).
Strabismus, nystagmus or a condition that would prevent fixation.
Diabetes with evidence of retinopathy.
Previous intraocular surgery or ocular trauma (with the exception of laser procedures and subjects that have undergone uneventful cataract surgery more than 6 months from enrollment date).
Trial design
Treatments tested in this trial
- Increasing of intraocular pressure (IC)
Treatment groups
Sponsors and collaborators
NYU Langone Health
Lead sponsor
National Eye Institute (NEI)
Collaborator