Abstract
Cerebral hyperperfusion is a relatively rare syndrome with significant and potentially preventable clinical consequences. The pathophysiology of cerebral hyperperfusion syndrome (CHS) may involve dysregulation of the cerebral vascular system and hypertension, in the setting of increase in cerebral blood flow. The early recognition of CHS is important to prevent complications such as intracerebral hemorrhage. This review will focus on CHS following carotid endarterectomy and carotid artery stenting. We will discuss the typical clinical features of CHS, risk factors, pathophysiology, diagnostic modalities for detection, identification of patients at risk, and prevention and treatment. Although currently there are no specific guidelines for the management of CHS, identification of patients at risk for CHS and aggressive treatment of hypertension are recommended.
Highlights
Cerebral hyperperfusion syndrome (CHS) is a relatively rare condition after carotid endarterectomy (CEA) or carotid artery stenting (CAS) but is potentially preventable
Bouri et al suggest the following four criteria to define post-CEA CHS [1]: (1) Occurrence within 30 days post-CEA; (2) Clinic features such as new onset headache, seizure, hemiparesis, and glasgow coma scale (GCS)
Moulakakis and colleagues in a retrospective review of 4689 patients undergoing CEA and 4446 patients undergoing CAS reported the incidence of CHS and ICH following CAS as 1.16 and 0.74 %, respectively, whereas following CEA the incidence of CHS and ICH was 1.9 and 0.37 % [3]
Summary
Cerebral hyperperfusion syndrome (CHS) is a relatively rare condition after carotid endarterectomy (CEA) or carotid artery stenting (CAS) but is potentially preventable. Microangiopathy and blood brain barrier damage In general, patients with severe carotid artery stenosis often have underlying systemic hypertension and undergo CEA to reduce the risk of stroke in a vascular bed that may be subject to chronic cerebral ischemia.
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