Glaucoma: a vascular dysregulation Increased cupping of the optic nerve head, a result of progressive loss of the retinal nerve fibres and remodelling of the supporting connective tissue in and around the lamina cribrosa, characterises glaucomatous optic neuropathy. Although reducing intraocular pressure represents a relevant approach in the treatment of glaucoma, many details of the pathway leading to this clinical picture remain unclear, and various additional contributors to the damage, such as altered ocular blood flow, have also been postulated to play a part.1 In this issue of the journal, Plange et al 2 present a study on the correlation of retinal blood flow with the size of the rim of the optic disc. Such a result is in line with recent histological findings showing a decrease in density of optic nerve capillary vessels in patients with primary open-angle glaucoma, whereas damage due to a secondary increase in intraocular pressure, such as in pseudoexfoliation, is devoid of such peculiarities.3 Further, the finding of hypoxia-inducible factor 1α expression in the glia of the optic nerve head and the retina of glaucomatous donor eyes,4 as well as earlier studies suggesting that ocular blood flow is reduced in eyes before actual damage occurs, lend credence to the hypothesis of a pathophysiological role of ocular perfusion in glaucoma.5–7 Although the haemodynamic theory of glaucomatous damage is nearly as old as the mechanical postulate, proponents of the haemodynamic theory have been less successful in implementing their thoughts into daily practice, principally owing to methodological difficulties. Whenever blood flow …