The role of the villain in high-pressure glaucoma is played by ocular hypertension. Alterations of lamina cribosa, other mechanical alterations, and a possible loss of optic nerve head capillaries are all accountable, and from a therapeutic standpoint most clinicians readily perceive that lowering ocular pressure is the single most important management goal and are satisfied with such results. Yet, when confronted with normal intraocular pressure, other perturbing factors or at least other accomplices must be studied; in this case, an ischemic origin becomes the primary suspect, potentially engendering therapeutic consequences of a different nature.