Abstract
It is widely suspected that tissue ischemia initiates or participates in optic disk damage in glaucoma. The details are not well delineated. Particularly puzzling is the clear separation of the clinical appearances of glaucoma and anterior ischemic optic neuropathy, which is also a presumed ischemic disease. When venous pressure at the exit point from the eye is elevated by intraocular pressure (IOP), the arteriovenous pressure difference is reduced. Nutrition is maintained only because of blood flow autoregulation. Intraocular pressure–induced ischemia can result if autoregulation is impaired in an individual, either because of an innate deficiency or, perhaps, as a result of vasospastic disease. Autoregulation can also be impaired if another disease (e.g., an atheroma) has caused much of the autoregulatory capacity to be already utilized, so that little or none is left to respond to the additional challenge of IOP. Ischemia might also result from microvascular occlusion with platelet or clotting abnormalities, perhaps inducing glaucomatous optic neuropathy that is not dependent on IOP. A better understanding of the pathogenic mechanism (and how it may be different in various cases) is needed to predict more successfully an individual’s risk of glaucomatous damage, to make decisions about the aggressiveness of treatment, and, one day, to direct therapy at the type of vascular abnormality present, in addition to or instead of lowering IOP.
