In general, ischemic mechanisms in vertebrobasilar insufficiency can be categorized as hemodynamic or embolic. Symptoms of vertebrobasilar insufficiency include dizziness, vertigo, drop attacks, diplopia, perioral numbness, alternating paresthesia, tinnitus, dysphasia, dysarthria, and ataxia. When two or more of these symptoms are present, vertebrobasilar ischemia is more likely to be the inciting cause. Unlike other regions of the brain, strokes in the posterior circulation territory occur due to large artery occlusive diseases.

Patients with “hemodynamic” ischemia experience transient vertebrobasilar symptoms due to inadequate vertebral artery inflow or collateral circulation. Symptoms are typically short lived, repetitive, somewhat predictable, and rarely result in stroke. Postural hypotension may precipitate serious traumatic injury, however, when patients lose their balance with standing.

Embolic events may also precipitate vertebrobasilar ischemia as well as cerebellar and brainstem infarction. Microemboli from the heart, aortic arch, or any arteries leading directly to the basilar artery may arise from atherosclerotic lesions, intimal defects, repetitive trauma, fibromuscular dysplasia lesions, aneurysms, or dissections. Although much less common than hemodynamic vertebrobasilar insufficiency, when present, microemboli are much more likely to cause fatal events or debilitating infarcts.^{2, 3, 4}

Timing of the onset of symptoms following positional changes may help differentiate vertebrobasilar insufficiency from labyrinthine disorders. In the latter circumstance, rapid head movement invokes immediate symptoms. In the case of vertebrobasilar insufficiency, however, a short delay usually precedes the onset of symptoms, including nystagmus.

Magnetic resonance imaging (MRI) provides safe, noninvasive, and detailed evaluation of the aortic arch and great vessels, the extracranial and intracranial arterial vasculature, as well as the presence of mass lesions, fluid collections, or parenchymal defects in the posterior fossa. Contrastenhanced magnetic resonance angiography (MRA), with three-dimensional reconstruction and maximum image intensity techniques, provides excellent image quality in high resolution (FIG 1). As in other applications, however, in low-flow circumstances, excessive signal dropout may result in overestimation of lesion severity based on signal intensity alone.

In contrast to computed tomographic (CT) imaging, transaxial MRI readily diagnoses both acute and chronic brain infarctions in the posterior fossa. Brainstem infarctions are typically small and as such may be overlooked with noncontrast CT imaging. Brain MRI is performed in symptomatic patients prior to vertebral artery intervention to identify infarctions when they are present and provide baseline images for future comparison.

Evaluation of vertebral anatomy via catheter-based, contrast arteriography requires acquisition of images in multiple projections to fully evaluate the entire extent of both vertebral arteries. Evaluation begins with the aortic arch to determine the origin of the bilateral vertebral arteries. Anomalous origin of the left vertebral artery, arising directly from the aorta proximal to the left subclavian, is present in 6% of patients. Much less frequently, the right vertebral artery originates from the innominate or right common carotid artery. This anomaly often accompanies an aberrant right subclavian artery, which itself may precipitate symptoms of dysphagia lusoria.