Reduced cerebrovascular blood flow velocities and vasoreactivity in open-angle glaucoma

Abstract

I read with special interest the article by Dr. Harris and coworkers (Am J Ophthalmol 2003;135:144–147) in which they concluded that glaucoma patients have lower middle cerebral artery blood flow velocities and absence of vasoreactivity to hyperoxia. It is a thought-provoking issue. The internationally accepted definition of glaucoma suggests that it is a form of optic neuropathy. It has also been suggested that there are programmed cell death or apoptosis causing magnocellular ganglion cell loss in glaucoma earlier than parvocellular ganglion cells. Elevated intraocular pressure and decreased optic nerve blood supply are thought to trigger apoptotic ganglion cell death. Glaucoma patients have been found to have compromised blood supply to the optic nerve head, retina, and the choroids. 1 Michelson G. Langhans M.J. Harazny J. Dichtl A. Visual field defect and perfusion of the juxtapapillary retina and the neuroretinal rim area in primary open angle glaucoma. Graefes Arch Clin Exp Ophthalmol. 1998; 236: 80-85 Crossref PubMed Scopus (88) Google Scholar Ischemic damage to the optic nerve is already regarded as a well-recognized cause for the glaucomatous damage seen in glaucoma. 2 Nickells R.W. Retinal ganglion cell death in glaucoma The how, the why, and the maybe. J Glaucoma. 1996; 5: 345-356 Crossref PubMed Google Scholar Therefore, it is a very relevant and important study. It reconfirms the issue of relative optic nerve ischemia as a consistent and contributory cause for glaucomatous optic neuropathy.