Cerebral aneurysms (CA) are acquired lesions, affecting 5–10% of the population, being about three times more common in women than in men. The absolute majority of CA is asymptomatic. However, in symptomatic cases, cerebral aneurysms present without about 80% of cases with severe intracranial hemorrhage, with mortality up to 50% and severe morbidity of up to 80%. At this point, the carotid siphon is particularly important because it is the blood gateway to the anterior cerebral circulation, being the most sinuous portion of the internal carotid artery, and because it houses about 30% of the intracranial aneurysm. The constant interactions of blood flow with carotid siphon curvatures are apparently intrinsically related to the epidemiology of these lesions in the various locations of the intracranial circulation and their presentation form. It is well established that a greater anterior knee angle has a significant independent relation with intracranial aneurysms located after carotid siphon, larger aneurysms, and greater risk of rupture. These findings may be associated with the hemodynamic interactions of blood flow and the curvature of carotid siphon. Little is known about the anatomical changes in carotid siphon and, consequently, the repercussions of the hemodynamic changes that the neurosurgical interventions mechanisms could entail. Devices such as intracranial stents, detachable coils, and even clips of aneurysms can modify the morphology of carotid siphon, and the knowledge of these consequences could be used to obtain better therapeutic results. In the last 10 years, a new device for the treatment of intracranial aneurysms has been presenting promising results, flow diverters stents (FDS), and its use to treat aneurysms in carotid siphon appears to cause morphological changes characterized by increased anterior and posterior angles. Specifically, the anterior angle increase was associated with better angiographic results. Aneurysms of the extracranial carotid artery (ECAA) are rare and little is known about its natural history. The etiology is diverse and most ECAA are asymptomatic, but they may progress to a pulsatile mass, cranial nerve compression, or cause a stroke. ECAA treatment is still controversial and a better insight into natural history and risk of complications of the different treatments is needed in order to get the consensus.
Part of the book: Carotid Artery