UCLA

Ocular rotation can cause mechanical deformation of the optic nerve head and surrounding tissues. During extreme angles of gaze, the optic nerve can become stretched and impose strain on other ocular tissues. Over a lifetime, the ill effects of repetitive mechanical injury from large adduction can compound, resulting in progressive optic neuropathy in some glaucoma patients.

We investigated the etiology of this form of glaucoma through a series of papers focusing on anatomical analysis of the human optic nerve from donated tissue and clinical studies utilizing optical coherence tomography (OCT) and confocal scanning laser ophthalmoscopy (cSLO). The optic nerve is surrounded and protected by a bi-layered dural sheath that bears the bulk of exerted mechanical force. Elastin fibers embedded within the sheath and peripapillary tissues around the nerve head form a three-dimensional meshwork that reinforces the tissue against mechanical strain. While the tissue at the globe optic nerve junction is heavily fortified with organized layers of collagen and elastin fibers, irregularities in the elastin fiber arrangement resulting in large dense elastin deposits were observed to correlate with older age. These elastin deposits could be a pathologic byproduct of optic nerve injury from mechanical strain, or serve as a protective mechanism to further reinforce the ocular tissues.

In OCT studies, adduction of angles beyond 26� caused marked deformation of the peripapillary tissues around the optic nerve head, and choroidal volume change. cSLO imaging showed similar deformations of the retina surface during large angle adduction. Ocular tissue of younger subjects appears more compliant, while those of glaucoma patients were stiffer and thus experienced less deformation.

We explored possible therapies for optic nerve traction during eye movement. Using collagen crosslinking to fortify ocular tissue, we observed that exposure to riboflavin and UV light can stiffen scleral tissue. In addition, we investigated whether prostaglandin agonists could be used to reduce ocular fat and found that topical administration of these agonists had insignificant effects on the retrobulbar fat.