Premise and prediction-how optic nerve head biomechanics underlies the susceptibility and clinical behavior of the aged optic nerve head.
We propose that age-related alterations in optic nerve head (ONH) biomechanics underlie the clinical behavior and increased susceptibility of the aged ONH to glaucomatous damage. The literature which suggests that the aged ONH is more susceptible to glaucomatous damage at all levels of intraocular pressure is reviewed. The relevant biomechanics of the aged ONH are discussed and a biomechanical explanation for why, on average, the stiffened peripapillary scleral and lamina cribrosa connective tissues of the aged eye should lead to a shallow (senile sclerotic) form of cupping is proposed. A logic for why age-related axon loss and the optic neuropathy of glaucoma in the aged eye may overlap is discussed. Finally, we argue for a need to characterize all forms of clinical cupping into prelaminar and laminar components so as to add precision to the discussion of clinical cupping which does not currently exist. Such characterization may lead to the early detection of ONH axonal and connective tissue pathology in ocular hypertension and eventually aid in the assessment of etiology in all forms of optic neuropathy including those that may be purely age-related.
Optic Nerve Head Research Laboratories, Devers Eye Institute, Portland, OR 97232, USA. cfburgoyne@deverseye.org
Claude F
CF
Burgoyne
J Crawford
JC
Downs
D000375:Aging / Q000502:physiology*; D001369:Axons / Q000502:physiology; D001696:Biomechanical Phenomena; D005901:Glaucoma / Q000503:physiopathology*; D006801:Humans; D009898:Optic Disk / Q000503:physiopathology*; D009900:Optic Nerve / Q000502:physiology; D009901:Optic Nerve Diseases / Q000503:physiopathology*