The role of optic nerve blood flow in the pathogenesis of glaucoma.

Many theories have surfaced regarding the exact mechanisms behind glaucomatous damage, but the complex nature of the disease and the inaccessibility of the internal structures of the human eye have limited current knowledge. Increased intraocular pressure is the risk factor most often associated with glaucomatous optic neuropathy; ischemic insult to the optic nerve has also been suggested as a possible cause of cellular damage. The aim of this review is to cover the possible role of optic nerve head hemodynamics in the pathogenesis of glaucoma.

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

PURPOSE: To compare cerebral blood flow velocities between open-angle glaucoma (OAG) patients and controls, at baseline and during hyperoxia. DESIGN: Observational cohort study. METHODS: A prospective study was conducted in a single institution. Sixteen OAG patients and 15 normal subjects, matched for age, were enrolled. Patients and controls were studied at baseline, while breathing room air, and during 100% oxygen breathing. The eye with the more severe visual field defect was chosen in glaucoma patients, while in controls, the study eye was chosen randomly. Subjects with history of diabetes, cardiovascular, or respiratory disease were excluded. Measurements included brachial arterial pressure, heart rate, intraocular pressure and transcranial Doppler (TCD). Mean and peak velocity and pulsatility index of the ipsilateral middle cerebral artery (MCA) were measured by TCD. RESULTS: At baseline, MCA mean and peak systolic blood flow velocities were significantly lower in glaucoma patients compared with controls velocities were significantly lower in glaucoma patients compared with controls (mean velocity: 50.2 vs 65.3 cm/s, P <.05; peak velocity: 74.2 vs 96.8 cm/s, P <.05). Additionally, while hyperoxia significantly decreased both mean and peak systolic velocities in MCA of controls (mean velocity: 65.3 vs 57.7 cm/s, P <.05; peak velocity 96.8 vs 87.9 cm/s, P <.05), it did not cause any significant change in OAG patients. CONCLUSIONS: Glaucoma patients were found to have lower MCA blood flow velocities and an absence of vasoreactivity to hyperoxia, compared with controls. The relationship of these cerebral hemodynamic abnormalities to glaucoma pathogenesis and progression remains to be explored.