We read with great interest the recent commentary by Stewart et al1 describing the evidence of the blood-flow disturbances in the pathogenesis of the glaucomatous damage. Although I agree with some of the findings of this excellent review, there are several important points that should be addressed:

1. After reading this article, one may think that there is not evidence that ocular blood-flow abnormalities are involved in the pathogenesis of the glaucomatous damage. Different studies, using different devices, point in the same general direction, indicating that on average, blood flow is decreased in some glaucoma patients, especially in primary open-angle glaucoma (POAG) patients and in patients who progress despite normalised intraocular pressure (IOP).2 Furthermore, this decrease in blood flow is not confined to the eye alone.3

2. Many different methods are being used to measure directly or calculate indirectly in vivo ocular blood flow. Although there is still not a single method that can provide all the relevant information in one reading, the development of newer techniques and their corrected use provides the potential for assessing blood flow in humans.

3. On the other hand, the Authors reveal the lack of evidence of a pathogenic link between glaucoma and impaired ocular blood flow. They asked for a long-term prospective study, which includes carefully selected patient groups, with similar baseline demographic and clinical characteristics, but with dissimilar baseline ocular haemodynamics. We published a paper that prospectively investigated the value of colour Doppler imaging of the ophthalmic artery and short posterior ciliary arteries in the prognosis of disease progression in patients with POAG.4 When baseline demographic and clinical characteristics were stratified according to whether the eyes progressed during the 3-year follow-up period, the only parameters to show significant differences were the resistivity index of the ophthalmic artery and the resistivity index of the short posterior ciliary arteries. Our study concluded that poor blood flow in the retrobulbar vessels is closely linked to visual-field deterioration in POAG patients.

In conclusion, we think that the understanding of the role of ocular blood flow disturbances in the pathogenesis of glaucoma has improved greatly. We have evidence that ocular blood flow is altered independently from IOP or level of damage in patients with progressive glaucoma, which could represent a primary risk factor for disease progression. In looking forward, we need long-term prospective multicentre studies to evaluate both the impact of ocular blood flow in glaucoma and the benefit of improving ocular blood flow.