Each vertebral artery (VA) begins in the root of the neck as a branch of the first part of the subclavian artery. The anatomic course has been divided into four segments, designated as V1 to V4 (Fig. 32-1). V1, the first segment, originates from the subclavian artery and ascends vertically until entering the transverse foramina at C6 or C5. Its origin generally arises just proximal to the internal thoracic artery from a somewhat posterior position on the subclavian. The V2 segment, the intraosseous portion, continues cephalad through a protective bony canal formed by the transverse foramina of the vertebrae from C6 to C2. The distal extracranial vertebral artery, V3, inclines laterally in the transverse foramen of C2, ascends vertically into the transverse foramen of C1, and then bends posteriorly at right angles to wind around the superior part of the lateral mass of the atlas where the artery pierces the posterior atlanto-occipital membrane, the dura mater, and the arachnoid to become intracranial. The artery enters the subarachnoid space of the cerebromedullary cistern at the level of the foramen magnum. The fourth segment is intracranial, originating at the piercing of the dura and extending to the formation of the basilar artery, and runs anteriorly on the anterolateral surface of the medulla to unite with the contralateral artery at the caudal border of the pons and form the basilar artery. Branches from the V4 segment include the posterior inferior cerebellar arteries and the anterior spinal arteries, which join in the midline to form the anterior spinal artery.

There are numerous anatomical variations in the origin and course of the vertebral artery. The most common anomalous origin is a VA arising directly from the aortic arch on the left side (5%), and entering the bony canal at C5 rather than C6 in this variation. Other variations include an aortic origin distal to the left subclavian, or rarely the VA may arise from the left common carotid or the left external carotid arteries. Origin of the right VA from the innominate or right common carotid is very rare and is present in patients with a retroesophageal right subclavian artery. In up to 15% of the healthy population, one VA is atretic (<2 mm diameter) and supplies little to the basilar artery flow. The left vertebral is dominant in approximately 50%, the right in 25%, and in the remaining cases the arteries are of similar caliber. The variations have little or no clinical significance unless there is associated VA origin or proximal subclavian artery stenosis. The VA enters the vertebral column most commonly at C6 for both left and right arteries. The entrance, however, may be low at C7 or higher at C5 or C4. The point of entrance of V1 is symmetrical in 85% of cases and asymmetrical in 15%, with the right VA entering at a lower level. Abnormally high entry into the spine is associated with prevertebral segment duplication. The V3 segment may be duplicated or may pierce the dura more caudally at C1 or between C1 and C2, instead of at the atlanto-occipital membrane. Due to the narrower subarachnoid space in the spine, this course may cause compression symptoms.

The anatomy of the vertebral artery has several important clinical applications (Table 32-1). First, the technical challenges provided by exposure of the intraosseous (V2) and intracranial (V4) portions of the VA preclude, or at least complicate, a direct surgical approach—the majority of the surgical approaches are oriented to the V1 and V3 segments. Second, the V1 segment is the most prone to atherosclerotic change, particularly at its origin. Third, an abnormally low entry at the level of C7 instead of C6 is associated with a short V1 segment and could prove an inadequate length for transposition to the common carotid artery. Fourth, an abnormally high level of entry into the spine, at C4 or C5, forms a sharp angulation to the artery that is then in jeopardy from extrinsic compression by surrounding musculotendinous structures. Next, the incarcerated course of V2 through the intraosseous canal provides for possible extrinsic compression by oseophytes or the longus colli tendon. In addition, the tortuous nature of the V3 segment has been referred to as the “safety loop,” because the redundancy allows for adequate mobility of the atlanto-occipital and atlanto-axial joints during neck movements. The most common problems at this level are arterial dissection, arteriovenous fistulae, and arteriovenous aneurysms. Furthermore, as the VA penetrates the dura, the vessel becomes thinner and loses the external elastica; this allows dissections at this level to rupture into the extravascular space and cause subarachnoid hemorrhage. Lastly, a rich source of collaterals, including the occipital branch of the external carotid artery, may become hypertrophied in the presence of proximal VA stenosis or occlusion and maintain the patency of the distal (segments V3 and V4) vertebral and basilar arteries. The collaterals also provide retrograde flow and negate the need for shunts during surgical repair.

Pathology affecting the VAs includes atherosclerosis, dissection, Takayasu arteritis, giant cell arteritis, fibromuscular dysplasia, compressive mechanisms, and blunt and penetrating trauma. The vertebrobasilar system is the source of blood supply to 10 of the 12 cranial nerves; the auditory, visual,
and vestibular systems; parts of the cerebral hemispheres; and all of the ascending and descending nerve tracts of the spinal cord. Vertebrobasilar ischemia (VBI) is caused by embolic mechanisms and hemodynamic (atherosclerotic stenosis, dissection, external compression, and trauma) mechanisms. The most common causes of VBI are listed in Table 32-2.

VBI may be caused by microembolization or flow limitation, if bilateral disease is present. Embolic sources include the heart and the arteries supplying the basilar artery (innominate, proximal subclavian, and vertebral arteries). Embolization presents as a transient ischemic attack (TIA) or infarction in the basilar artery territory. The hemodynamic, flow-limiting mechanism of VBI is more common than the embolic, although patients present similarly. In the hemodynamic mechanism, most commonly a result of atherosclerosis, the patients have ischemia due to stenosis or occlusion of the VA and inadequate compensation from the contralateral vertebral artery and/or the arteries through the circle of Willis.

Atherosclerosis is the most common cause of VBI, and up to 25% of ischemic strokes involve the posterior or vertebrobasilar circulation. VA stenosis may occur in the extra- or intracranial portions, and it accounts for up to 20% of posterior circulation ischemic strokes. The most common location of plaque is the VA origin from the subclavian artery, followed by lesions in V2 as the artery navigates the bony cervical canal. For white males, the most common site of disease is the VA origin, followed by the proximal subclavian artery, the intracranial VA, and the basilar artery. The V3 segment is rarely involved. Premenopausal women, African Americans, and Asians are prone to disease involving the intracranial VA and the basilar arteries, but they have limited involvement of the vertebral origin. Occlusion of one artery with normal contralateral flow does not result in impaired posterior circulation because the VA are paired. However, vertebral lesions causing distal emboli with or without contralateral VA occlusion can produce TIA or infarction. Because of the VA paired anatomy and rich collateral blood supply that reconstitutes the distal artery after proximal occlusion, hemodynamic stroke occurs less commonly. Embolism from cardiac sources and extracranial VA stenosis are the most common causes of proximal posterior circulation stroke (medullary and PICA cerebellar territory stroke). In severe symptomatic intracranial VA occlusive disease, the primary site of disease is distal to the origin of the PICA. Concomitant basilar artery disease and distal posterior circulation strokes have the poorest outcome. The most frequent sites of infarction are in the cerebellum and occipital lobes.

Dissection of the extracranial cervical arteries (vertebral and carotid) is a major cause of nonatherosclerotic cerebral infarction in younger (30 to 50 years) adults. One out of five strokes in younger adults is caused by dissection, and the annual incidence is 2.6 per 100,000 persons with a mean age of 45 years. Cervical arterial dissections are caused by hemorrhage within the medial layer of the arterial wall, with the source either an intimal tear with blood dissecting into media or primary hemorrhage of the vasa vasorum of the media. Dissections close to the intima will result in narrowing of the lumen that may progress to a complete occlusion. VA dissections usually involve the distal extracranial segment, and they usually occur in the setting of extreme neck rotation. Dissections may extend into the intracranial VA, where a subarachnoid hemorrhage can result due to the thinning of the artery after dural penetration. Both subintimal and subadventitial tears expose basement membrane that leads to platelet aggregation and thrombus formation. Three pathophysiologic mechanisms of arterial dissection have been reported: blunt, penetrating, or iatrogenic trauma; spontaneous (including trivial trauma) events; and in association with underlying disease, such as fibromuscular dysplasia, cystic medial necrosis, Marfan syndrome, and type IV Ehlers-Danlos syndrome (EDS). Dissections of the VA are associated with neck manipulation, torsion, or minor trauma in up to 80% of cases, with chiropractic manipulation,

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