Factors other than intraocular pressure (IOP) elevation must be involved in
initiation and progression of glaucoma. An additional element in disease c
ausation may be ischemia in the retina and optic nerve head. Ischemic damag
e to neurons in the CNS is similar mechanistically and histopathologically
to changes seen in glaucoma. Further, glaucoma patients with normal IOP sho
w clear evidence for cerebral and ocular ischemia. Aging and atherosclerosi
s reduce the ability of the eye to autoregulate blood flow when ocular perf
usion pressure changes: the dependence of blood flow on perfusion pressure
links ischemia to IOP. Consequently, neuroprotective treatments for glaucom
a should be designed to both reduce IOP and improve ocular nutrient deliver
y.