Anthony J. Bellezza

TL;DR: Modeling the ONH as a biomechanical structure generates a group of testable hypotheses regarding the central mechanisms of glaucomatous damage and provides a logic for classifying the principal components of the susceptibility of an individual ONH to a given level of IOP.

TL;DR: Findings suggest that damage to the ONH connective tissues occurs early in the monkey model of experimental glaucoma, and both plastic (permanent) and hypercompliant deformation of the lamina cribrosa and anterior scleral canal wall are present in young adult monkey eyes with early experimental glAUcoma.

TL;DR: Initial finite element models show that IOP-related stress within the load-bearing connective tissues of the optic nerve head is substantial even at low levels of IOP.

TL;DR: Profound fixed posterior deformation and thickening of the lamina are accompanied by mild posterior deformed and thinning of the scleral flange and peripapillary sclera at the onset of confocal scanning laser tomography (CSLT)-detected ONH surface change in young adult monkey eyes with early experimental glaucoma.

TL;DR: The long-term viscoelastic material properties of monkey peripapillary sclera are altered by exposure to moderate, short-term, chronic IOP elevations and these alterations are present at the onset of CSLT-detected glaucomatous damage to the ONH.