Glaucoma is a disease that affects over 1 million people in the United States, and is one of the three leading causes of blindness nationwide. Loss of vision from glaucoma is believed to be the result of damage to the axons of the retina ganglion cells as they pass through the lamina cribrosa, which spans the opening in the back of the eye wall called the scleral canal. It is known that elevations of intraocular pressure (IOP) are associated with this damage, but the exact mechanisms by which the level of IOP causes these changes are unknown and controversial.
The objective of this work is to investigate how the load-bearing connective tissues within and around the optic nerve head (ONH) respond to changes in intraocular pressure, and how these responses are altered when the tissues are damaged early in glaucoma. The connective tissues of the ONH provide support for the retinal ganglion cell axons as they pass through the wall of the eye, and are crucial in maintaining axonal health at the ONH. Since the ONH is the principal site o f glaucomatous damage, understanding how these connective tissues respond to different loading conditions provide insight into the pathophysiology of the retinal axons in this disease.
Histologic measurements made in 4 fxm serial sagittal sections show that acute increases in IOP can deform the load-bearing connective tissues of the ONH. This is true both when the IOP increase is from 0 to 10 mm Hg, and when the increase is from 10 to 30 or 45 mm Hg. Additionally, these measurements show that in eyes that have been given early experimental glaucoma, the magnitude of the deformations caused by a given IOP increase is larger than in normal eyes, and that these larger deformations have both a plastic and hyperelastic component. Using digitized three-dimensional reconstructions, these profound deformations can visualized. Finally, using finite element modeling that incorporates these digital reconstructions, a better understanding was gained of how regional stresses and strains are related to these deformations, and how all of these factors are associated with the onset and progression of glaucoma.