Summary

This study seeks to understand the physical defects that occur in glaucomatous eyes prior to nerve injury and investigate whether these defects are reversible.

Project Details

Glaucoma is typically associated with elevated intraocular pressure (IOP) caused by increased aqueous outflow resistance. In previous studies of bovine eyes, we found that the area available for outflow increases when IOP and outflow resistance decreases, suggesting a relationship between available area for outflow and outflow resistance. The morphological correlation of reduction in the area available to outflow, with increasing IOP, seems to be related to a progressive collapse of the Schlemm's canal and a previously unrecognized, progressive herniation of the inner wall and the JCT into the collector channel ostia. A similar herniation of the inner wall into the collector channel ostia was also seen when the eyes were fixed even at 0 mmHg raising the prospect that initially reversible herniations can become irreversible. We hypothesize that the herniations we have documented will be found to be reversible in eyes without glaucoma but can become irreversible, leading to increased outflow resistance and IOP. The results of this study will help us to better understand glaucoma pathophysiology and will also better direct us to the anatomical sites where the pathological resistance resides.