The V1 segment is the first segment of the vertebral artery. The V1 segment typically arises from the subclavian artery, courses posteriorly and superiorly in the superior mediastinum, and then enters the C6 transverse foramen to become the V2 segment.

The V2 segment courses superiorly through the C3–C6 transverse foramina, turns superolaterally through the “inverted L-shaped” C2 transverse foramen, and then exits superiorly through the C2 transverse foramen to become the V3 segment. The V2 segment resides inside the vertebral column (Fig. 13) and is vulnerable to vertebral fractures, especially fractures which violate the transverse foramina.

The V3 segment courses posteriorly and medially around the atlantooccipital joint (forming a groove along the posterior ring of the atlas) and then sharply turns anteriorly and superiorly to pierce the dura to become the V4 segment. The V3 segment resides outside the vertebral column and is vulnerable to rotational forces which can injure the artery at its dural insertion.

The V4 segment courses superiorly, anteriorly, and medially through the foramen magnum and then superomedially behind the clivus. The V4 segments unite to form the basilar artery near the pontomedullary junction.

Along its course, the vertebral artery gives rise to numerous arterial branches: cervical branches, meningeal branches, and intracranial branches. These arteries are described below.

The cervical branches originate from the extracranial vertebral artery as it courses up the neck. The cervical branches are categorized into the spinal branches (which supply the spinal cord and vertebral bodies) and the muscular branches (which supply the deep cervical musculature). The muscular branches provide an important collateral pathway in the vertebrobasilar circulation, communicating with the occipital branch of the external carotid artery.

The meningeal branches originate from the distal extracranial vertebral artery. The meningeal branches are categorized into the anterior meningeal artery and the posterior meningeal artery. The anterior meningeal artery arises from V2 and supplies the dura around the foramen magnum. The posterior meningeal artery arises from V3 and supplies the falx cerebellum.

The intracranial branches originate from the intracranial vertebral artery (i.e., the V4 segment). The intracranial branches are categorized into the anterior spinal arteries, the posterior spinal arteries, the posterior inferior cerebellar arteries, and the perforating arteries. The anterior spinal arteries unite in 50 % of cases and course inferiorly in the anteromedian sulcus of the spinal cord to supply the anterior spinal cord. The posterior spinal arteries course inferiorly along the posterolateral spinal cord to supply the posterior spinal cord. The posterior inferior cerebellar arteries course around the medullary tonsils to supply portions of the medulla, inferior cerebellum, and choroid plexus of the fourth ventricle. The perforating arteries arise off the intracranial vertebral artery to supply portions of the medulla, inferior cerebellar peduncles, and olivary bodies.

Variant anatomy of the posterior inferior cerebellar artery is common. Anomalous origin of the posterior inferior cerebellar arteries from V3 occurs in up to 10 % of cases. Duplication of the posterior inferior cerebellar arteries is less common, occurring in approximately 2 % of cases [4]. Occasionally, the posterior inferior cerebellar arteries arise from a single common trunk. Occasionally, the vertebral artery terminates in the posterior inferior cerebellar artery; in this situation, the contralateral vertebral artery supplies the majority of the posterior circulation blood flow [4]. Familiarity with these common variants helps avoid confusion when interpreting the intracranial branches of the vertebral arteries.

The cerebellum is predominantly supplied by three paired arteries: the superior cerebellar arteries, the posterior inferior cerebellar arteries, and the anterior inferior cerebellar arteries. The superior cerebellar arteries supply the superior surface of the cerebellum and the upper vermis. The posterior inferior cerebellar arteries supply the posterior and inferior surfaces of the cerebellum and inferior vermis. The anterior inferior cerebellar arteries supply the petrosal surface of the cerebellum. The central portions of the vermis and cerebellar hemispheres represent a watershed area with variable contributions from all three vessels.

The brainstem is predominantly supplied by the basilar artery and its perforating branches. However, the superior cerebellar arteries supply portions of the superior pons while the distal vertebral arteries and the posterior inferior cerebellar arteries supply portions of the medulla. Occlusion of one of the posterior inferior cerebellar arteries can cause infarction of the lateral medulla, resulting in Wallenberg syndrome. This syndrome is clinically characterized by contralateral sensory deficits affecting the body and extremities, as well as ipsilateral sensory deficits affecting the face.

The most common nontraumatic condition affecting the extracranial vertebral arteries is atherosclerotic disease [6]. Atherosclerosis is a systemic arterial disease, prevalent in industrialized nations. It is responsible for the majority of ischemic strokes, resulting in healthcare-associated costs over $30 billion each year [7]. There are multiple well-known risk factors for atherosclerosis, both modifiable and nonmodifiable. Common nonmodifiable risk factors include family history, age, and male gender. Common modifiable risk factors include age, hypertension, hyperlipidemia, diabetes, smoking, and renal failure (Table 1) [8].

There is a strong association between vertebral artery atherosclerosis and carotid artery atherosclerosis; however, the vertebral arteries tend to be less severely and less diffusely affected than the carotid arteries [6].

Most patients with vertebral artery atherosclerosis are asymptomatic; however, if the degree of vertebral artery stenosis is significant, patients can present with vertebrobasilar insufficiency which can manifest as vertigo, ataxia, imbalance, syncope, and cranial nerve deficits [8]. Patients can also present with a myriad of non-neurologic symptoms related to systemic atherosclerosis, including angina from coronary artery disease and claudication from peripheral vascular disease.

Atherosclerosis is a complex pathologic process with endothelial injury playing a central role in its pathogenesis [8, 9]. Endothelial injury results in increased permeability of the arterial wall to lipids, which deposit in the intima resulting in the fibrofatty plaque. Microscopically, the fibrofatty plaque is composed of lipids, foam cells, and connective tissue. A fibrotic cap, composed of smooth muscle and collagen, forms over the surface of the fibrofatty plaque. Disruption of the fibrotic cap results in exposure of the thrombogenic fibrofatty plaque to the bloodstream, which can result in acute thrombosis and/or thromboembolus [9]. In addition, as the fibrofatty plaque enlarges, it progressively narrows the arterial lumen. In general, a 50 % decrease in luminal diameter is required before hemodynamic consequences occur, as compensatory physiologic vasodilation mitigates the effects of mild atherosclerotic disease [9]. It should be noted that tandem stenoses can be additive in their hemodynamic effects, much like serial resistances in a circuit [8]. Ultimately, clinical symptoms occur when the arterial demand outstrips the arterial supply, resulting in a demand-supply mismatch and end-organ ischemia. If the mismatch is transient and infarction has not occurred, then the clinical manifestations are transient and the episode is referred to as a transient ischemic attack. However, if the mismatch is prolonged and infarction has occurred, then the clinical manifestations are prolonged and the episode is referred to as a cerebrovascular accident or stroke. Patients with prior transient ischemic attacks have a ten times increased risk of stroke [9].

Vertebral artery stenosis severity is categorized per the North American Symptomatic Carotid Endarterectomy Trial (NASCET) method [10]. The NASCET method defines the percent stenosis as the ratio of the difference between the normal and diseased luminal diameter to the normal luminal diameter (i.e., percent stenosis = (normal lumen − minimal diseased lumen) / (normal lumen) × 100%). Flow-limiting atherosclerotic disease is graded by the percent stenosis, with mild narrowing <50 %, moderate narrowing 50–70 %, and severe narrowing >70 % (Table 2). Irregular atheromatous plaques are at an increased risk of thromboembolism and are considered an independent risk factor for stroke [4].

Ultrasound with pulsed Doppler has a very limited role in evaluating vertebral artery atherosclerosis, largely due to its inability to visualize the vertebral artery in its entirety. As with other blood vessels, arterial stenosis is characterized on ultrasound by increased velocities, turbulence, high-resistance waveforms, and elevated resistive indices [6, 8, 11]. The post-stenotic segment is characterized by decreased velocities, loss of pulsatility, “parvus-tardus” waveforms, and decreased resistive indices. Severe stenosis in one vertebral artery can result in overestimation in stenosis of the contralateral vertebral artery due to compensatory increased blood flow [9].

CTA or MRA is often the initial diagnostic examination for vertebral artery atherosclerosis, with >90 % sensitivity and >90 % specificity [5, 8, 9]. Both imaging modalities offer complete visualization of the vertebral arteries and allow for routine NASCET characterization of atherosclerotic disease. In general, atherosclerosis is characterized by smooth or irregular plaques resulting in luminal narrowing, often with concomitant arterial wall calcification [8]. Atherosclerotic disease is typically most severe at the ostia of the vertebral arteries (Fig. 14). Multiplanar reformats and/or 3D vessel analysis can be useful in accurately quantifying the degree of arterial stenosis, especially in vessel segments which do not run orthogonal to the axial plane.

Advanced atherosclerotic disease can manifest as near-occlusion or occlusion of the vertebral artery (Figs. 15 and 16 respectively). However, if the clinical suspicion for significant atherosclerosis is low (e.g., young patient without atherosclerotic risk factors), other causes of vertebral artery stenosis should be considered, such as vertebral artery dissection, radiation arteritis, fibromuscular dysplasia, or vasculitis [8]. In these cases, MRA may provide additional information by directly visualizing fibrofatty atherosclerotic plaque and excluding other causes of luminal narrowing (Fig. 17). Lastly, the role of DSA in evaluating atherosclerotic disease is generally reserved for planning for endovascular interventions (Fig. 18).

The management of vertebral artery atherosclerotic disease has historically been with medical therapy targeting atherosclerotic risk factors such as hypertension or hypercholesterolemia. Surgery, while frequently performed for carotid artery atherosclerosis, is rarely performed for vertebral artery atherosclerosis [12]. With the advent of minimally invasive endovascular techniques, angioplasty and stenting now have a role in patients who fail maximum medical therapy. Endovascular treatment involves aggressive procedural anticoagulation and deployment of a self-expanding stent across the stenotic lesion. The angiographic success rate of endovascular techniques has been reported to be up to 95 %, with a stroke rate of <2 % [9]. However, endovascular stenting suffers from restenosis and neointimal hyperplasia which often occurs at the margin of previously placed stents (Fig. 19) [5]. Drug-eluting stents and other methods of reducing restenosis and neointimal hyperplasia are currently being developed and studied.

Vertebral artery dissection has an annual incidence of 1 per 100,000 patients and is one of the most common causes of stroke in young adult patients [4]. Vertebral artery dissection constitutes approximately 27 % of all craniocervical arterial dissections and causes up to 40 % of all posterior fossa ischemic strokes [4, 13]. The mean age at presentation is approximately 45 years; there is a slight male predominance [4, 14, 15]. Patients can present with dizziness/vertigo, headache, neck pain, ataxia, visual symptoms, nausea/vomiting, nystagmus, Horner syndrome, sensory deficits, cranial nerve palsies, dysphagia, and tinnitus (Table 3) [13, 16]. In a meta-analysis of nearly 2,000 patients, Gottesman et al. found that the most common symptom was dizziness/vertigo (58 %), followed by headache (51 %) and neck pain (48 %) [16]. However, it should be noted that nearly one in four patients with proven vertebral artery dissection have no headache or neck pain at the time of diagnosis; thus, the absence of these symptoms do not exclude the diagnosis.