Cerebral Hyperperfusion Syndrome After Angioplasty

Abstract

Cerebral hyperperfusion syndrome (CHS) was first described by Sundt et al. (1981) as a clinical syndrome following carotid endarterectomy (CEA) characterized by headache, neurological deficit, and epileptic seizures that is not caused by cerebral ischemia. This chapter deals with this uncommon but not exceptional complication of endovascular treatment of the arteries that supply the brain. We use the term carotid artery stenting (CAS) to refer to stenting of the internal carotid artery (ICA) because most publications are centered on this artery. Moreover, we include angioplasty without stent placement in the term CAS to facilitate reading comprehension because the relation between endovascular treatment and CHS is related to revascularization itself rather than to stent placement per se. Given the high rate of ischemic brain disease in relation to carotid stenosis and the high prevalence of asymptomatic carotid stenosis, numerous publications discuss CHS in relation to CEA: the incidence in these series ranges from 0.3% to 2.2%. However, CAS has continually evolved in recent years to the point where, after more than 40 years’ experience, it is considered an alternative to CEA. Furthermore, the development of new materials for stents, filters for distal protection, dual antiplatelet treatment, and the learning curve are minimizing the shortand long-term adverse effects of CAS. Documented complications of CAS include cerebral embolism, hemodynamic compromise, vessel dissection, and early restenosis and occlusion, as well as the hyperperfusion syndrome we deal with in this chapter. Moreover, the spectacular increase in endovascular treatment has revealed that hyperperfusion syndrome can also occur after revascularization of other arteries, such as the vertebral arteries, the subclavian arteries, or even those located within the brain, mainly the middle cerebral artery (MCA). In this chapter we will begin by discussing the pathophysiology, clinical presentation, and incidence of CHS in the different published series. We will then discuss the risk factors, diagnostic methods, and strategies for prevention and treatment. We will also discuss a