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Management of Dissections of the Carotid and Vertebral Arteries
Introduction
Cervicocerebral arterial dissection is an important cause of stroke; however, the majority of dissections are asymptomatic and do not warrant invasive therapy. The treatment of carotid and vertebral artery dissections has evolved significantly since the early diagnosis and management descriptions by Fisher and colleagues in the 1970s. As surgical technology and our understanding of the natural histories of these entities have evolved, radical surgical interventions have increasingly been replaced by minimally invasive endovascular procedures and nonsurgical interventions. However, this is a double-edged sword because the development of endovascular techniques has also led to heightened awareness and prevalence of iatrogenic dissections. In this chapter, we will review the pathophysiology, clinical presentation, treatment, and outcomes associated with cervical and intracranial dissections of the carotid and vertebral arteries.
Pathophysiology and Histopathology
Symptomatic cervical carotid and vertebral artery dissections present with signs and symptoms of central nervous system ischemia. This is in contradistinction to intracranial dissections, which tend to present with intracranial hemorrhage, especially subarachnoid hemorrhage. The observed differences in presenting symptoms result from differences in the histopathology of dissected vessels in the neck compared with the intracranial compartment. All cervicocerebral artery dissections (CADs) arise from a tear in one or more of the three layers of the vessel wall. Depending upon the extent of the tear, associated hemodynamic forces, and strength of the various arterial layers, a dissection may result in stenosis or aneurysmal dilatation of the artery. Subintimal dissections tend to cause stenosis of the parent artery through elevation of an occlusive intimal flap, whereas subadventitial dissections tend to result in pseudoaneurysm formation through loss of the relatively constraining muscularis layer. Compared with extracranial arteries, intradural arteries have a thinner tunica media and adventitia with a relative paucity of elastic fibers, making them more susceptible to subadventitial dissection resulting in pseudoaneurysm formation. The transmural pressure—the driving force behind all ruptured aneurysms—across the wall of an intracranial pseudoaneurysm is defined by the difference between the intracranial pressure and the arterial blood pressure. In the neck, transmural pressure is defined not by cerebrospinal fluid pressure but rather the tissue pressure of the neck, where relatively large muscles and either the fibrous carotid sheath or the bony transverse foramina externally bolster the cervical carotid or vertebral arteries, respectively. This difference explains the relative incidences of pseudoaneurysm hemorrhage in the two compartments. Extradural arteries are more likely to have subintimal dissections presenting with arterial stenosis or occlusion, and resultant thromboembolic complications. ,
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