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.

The present study will briefly increase the pressure in eyes of living subjects and examine the effect of elevated intraocular pressure on optic nerve topography and position during pressure elevation using optical coherence tomography imaging of the posterior eye. Outcome measures will include measurements in microns based on these images quantifying the deformation of the lamina cribrosa.

Inclusion Criteria:

Healthy volunteers

• 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.

Glaucoma suspects

• Normal visual field as defined above.
• Either IOP between 25 to 30 mmHg with central corneal thickness < 550µm, or a difference ≥ 0.2 in cup to disc ratio between eyes.

Glaucoma

• Glaucomatous ONH abnormality: rim thinning, notching, undermining (excavation) or diffuse or localized RNFL defects that are characteristic of glaucoma.
• Two consecutive abnormal SITA standard perimetry tests with GHT outside normal limits.

Exclusion Criteria:

• 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).
• Neurological and non-glaucomatous causes for visual field damage.
• Any intraocular non-glaucomatous ocular disorders.