ABSTRACT
We use the term ischemia as opposed to insufficiency, which is more traditionally attached to vertebrobasilar symptoms, because in approximately a third of cases the symptoms are secondary to thromboembolic disease rather than to hypoperfusion secondary to stenosis or occlusion. The proximal subclavian artery (SA) is discussed within the context of vertebrobasilar ischemia (VBI) because disease of this segment of the SA may result in vertebrobasilar ischemia and operations on this artery are part of the surgical correction of the VBI syndrome. The same applies to lesions of the innominate artery, which are described elsewhere in the book.
The concept of VBI secondary to disease of the vertebral artery (VA) or proximal SA has traditionally been considered a hemodynamic problem resulting in hypoperfusion of the vertebrobasilar territory.[1] Available evidence suggests that about 30% of patients presenting with symptoms of VBI suffer thromboembolization from either the SA, VA, or basilar artery.[2-4] Rancurel et al.[5] defined two types of VBI: hypoperfusion and thromboembolic. The hypoperfusion syndrome may be due to a blockage in the SA or VA, causing a drop in perfusion pressure in the basilar artery by reducing blood flow into it and, occasionally, by diverting flow from the basilar artery, as in the reversal of VA flow, the so-called subclavian steal syndrome. The symptoms of VBI arise from the territory supplied by the vertebrobasilar arteries, including the brainstem, the cerebellum, and-in patients where the basilar artery gives rise to the posterior cerebral arteries-the occipital lobes and posterior portion of the temporal lobes.
