Vertebrobasilar insufficiency is a well-known syndrome, but no corresponding hemodynamic deficit has yet been established. We propose to define nuclear hemodynamic vertebrobasilar insufficiency on the basis of an oligemia lower than 35 mL/100 g per minute in the brain stem-cerebellar region with use of the xenon Xe 133 inhalation method. Fifteen patients fulfilling this criterion underwent four-vessel angiography, computed tomography, and a standardized neurologic examination. An acetazolamide test showed poor reactivity in more than half of the patients, sometimes specifically in the vertebrobasilar area. With use of single-photon emission computed tomography and intravenous technetium Tc 99m-labeled hexamethylpropyleneamineoxime in two cases, the considerable decrease of regional cerebral blood flow in the brain stem-cerebellar region was confirmed. An excellent correlation was observed between the existence of nuclear hemodynamic vertebrobasilar insufficiency and angiographically proved arterial occlusions. The dominant nuclear oligemic zone was regularly on the side of the anatomic arterial chief lesion. Clinical manifestations included rare transient ischemic attacks (in one of 15 patients), intermittent basilar symptoms (in 15 of 15 patients), and a subacute vertebrobasilar "threatening" syndrome. Thus, imaging of a nuclear hemodynamic vertebrobasilar deficit provides an objective basis to the diagnosis of vertebrobasilar insufficiency and useful objective data for revascularization surgery.