In approximately one-quarter of all cases of ischemic stroke, there is involvement of the posterior or vertebrobasilar circulation. Stenoses of the vertebral artery are the cause of up to 20% of all cases of ischemic stroke in the posterior flow region. Proximal stenoses of the vertebral artery are the second most frequent cause of ischemic stroke after stenoses of the internal carotid artery. As in the pathogenesis of internal carotid artery stenoses, stroke in the posterior flow region most often results from emboli from arteriosclerotic plaques. Hemodynamic compromise must be regarded as comparatively rare in the posterior flow region, as the basilar artery is supplied by two vertebral arteries. In contrast to the internal carotid artery, the vertebral artery also has many collateral vessels that are able to compensate cerebral perfusion when there is proximal constriction of a vertebral artery.
Good familiarity with the extracranial and intracranial anatomy is decisive for treatment of the relevant vascular occlusion processes. The left common carotid artery arises from the aortic arch, and the right one from the bifurcation of the brachiocephalic trunk. The common carotid artery does not have any side branches. At the level of the upper edge of the thyroid cartilage, it divides into the internal and external carotid arteries. The external carotid artery supplies the temporomandibular joint, the face, the neck, and the meninges. It has two terminal branches—the superficial temporal artery and the maxillary artery. These two branches may also serve, along with the occipital artery, as collaterals if there is occlusion of the internal carotid artery or vertebral artery. The internal carotid artery ascends laterally behind the hypopharynx, where it can be palpated. It branches into the anterior and medial cerebral arteries. It has no visible side branches in its extracranial course up to the branching point. The first major intracranial branch is the ophthalmic artery. The vertebral artery arises from the subclavian artery and travels to the sixth cervical vertebra, where it passes through the transverse foramen in the transverse process of the sixth vertebra and courses in a sharply cranial direction in the same way through the corresponding foramina of cervical vertebrae C5 to C1. In this segment, the vertebral artery courses more or less parallel to the carotid artery. At C1, the vertebral artery turns posteriorly and arches around the posterior part of the vertebral arch. It then passes through the foramen magnum into the cranial cavity. At the lower margin of the pons, the left and right vertebral arteries unite to form the basilar artery, which in turn flows into the circle of Willis. Although generally the vertebral arteries make only a minor contribution to the overall cerebral circulation, they can be of significant importance when occlusion or stenosis of the internal carotid artery develops. The circle of Willis is the most important intracranial collateral pathway. Via the anterior and posterior communicating arteries, the anterior, middle, and posterior cerebral arteries are connected in a circuit. In situations in which a proximal atherosclerotic process progresses slowly, the circle of Willis is able to compensate for vascular occlusions. However, the circle is not fully developed in all individuals. In patients with an incomplete circle of Willis, even brief occlusion of a vessel can lead to a stroke.
1.1.3 Clinical findings
The clinical symptoms of stenosis of the internal carotid artery or vertebral artery are characterized by ischemia in the corresponding region of cerebral flow. Symptomatic stenosis of the internal carotid artery is defined by syndromes in the ipsilateral hemisphere during the previous 6 months:
Symptomatic stenosis of the vertebral artery can become manifest in the form of:
1.1.4 Differential diagnosis
Etiological differential diagnosis of ischemic stroke:
– Atherosclerotic
– Non-atherosclerotic (dissection, fibromuscular dysplasia, giant cell arteritis, Takayasu syndrome, bacterial or viral vasculitides)
– Atherosclerotic
– Non-atherosclerotic (vasculitides)
– Atrial fibrillation, atrial myxoma, atrioseptal aneurysm, acute myocardial infarction, endocarditis, status post-cardiac valve replacement, dilated cardiomyopathy
– Atrial septal defect, persistent oval foramen, in deep vein thrombosis in the lower extremity or pelvis, thrombophilia
– Genetic—e.g., in antithrombin III deficiency, protein S/protein C deficiency, activated protein C (APC) resistance, factor V Leiden mutation
– Acquired in disseminated intravascular coagulation—e.g., in multiple trauma, sepsis
– e.g., polycythemia, hemoglobinopathies, iron-deficiency anemia, leukemia, thrombocythemia
Differential diagnosis of acute focal neurological deficit:
In cases of suspected stenosis of the vertebral artery with no evidence of cerebral ischemia in the posterior region of flow, all of the differential