Approximately 20–25% of ischemic strokes occur in the posterior circulation. Symptomatic vertebrobasilar disease carries a high annual recurrent stroke risk, averaging 10–15% per year. Vertebrobasilar insufficiency (VBI) is a condition characterized by poor blood flow through the posterior circulation of the brain, which supplies the brainstem, thalamus, hippocampus, cerebellum, occipital lobes, and medial temporal lobes. Narrowing or occlusion of the vertebral arteries may be caused by atherosclerosis, dissection, thrombosis, compression, and fibromuscular dysplasia; in addition, an unusual entity, called Bowhunter’s syndrome, manifests as posterior circulation ischemia due to transient, positional compromise of the vertebral artery (VA), usually the dominant VA and rarely both. However, VBI more often refers to the chronic steno-occlusive process associated with atherosclerotic disease. Vertebral artery disease can result in a range of neurological symptoms, including dizziness, imbalance, and dysarthria. The literature highlights hemodynamic compromise as an important source of stroke and VBI in vertebrobasilar disease [1], [2], [3], [4], [5], [6], [7], [8], such that stenosis of 80% or more produces the most significant reduction in cerebral blood flow [7]. However, posterior circulation strokes can also originate from atherosclerotic plaques that rupture and form emboli.

Collateral circulation often compensates for a flow deficit produced by VA stenosis, but many patients have inadequate intracranial anastomoses due to an incomplete circle of Willis or diffuse atherosclerotic disease. An incomplete circle of Willis can be present in 48–58% of the population [8]. Other anatomical variants may also contribute to a poor collateral network. A posterior cerebral artery (PCA) branching directly from the internal carotid artery with an absent or hypoplastic P1 defines the fetal posterior cerebral artery (fPCA), and patients with bilateral fPCA often have a small basilar artery (BA). Although it is unclear whether the presence of fPCA inherently increases the risk of stroke [9], [10], [11], [12], diffuse intracranial atherosclerotic disease may potentially place a patient with small caliber posterior circulation at higher risk of VBI.

If symptomatic patients fail medical management, revascularization of the VA should be considered. Endovascular options have grown in the past few decades, and procedures to restore blood flow may involve transluminal balloon angioplasty or stent placement or both. Despite the technological advances in endovascular techniques, some cases may still require surgery. Several factors must be considered when determining the appropriate revascularization strategy: location and severity of the blockage, history of prior intervention, and patient comorbidities. Surgical revascularization of the VA requires understanding and careful consideration of skull base and neck anatomy. This review article will focus on bypass of the VA in the setting of ischemic pathology, describing the technique, anatomical nuances, steps involved in preoperative planning, and postoperative management.