PURPOSE OF REVIEW

Cerebral hyperperfusion syndrome (CHS) is a rare but significant complication after carotid revascularization and is increasingly recognized after acute stroke treatments. In this review, we discuss the epidemiology and pathophysiology of CHS, clinical presentation including ipsilateral headache, seizures, and focal neurological deficits, and radiographic presentation. We propose preventive therapies with emphasis on acute stroke post-thrombectomy hyperperfusion.

RECENT FINDINGS

CHS was first described after carotid revascularization but is now also reported in patients with acute ischemic stroke. Proposed criteria involve a combination of new clinical symptoms, radiographic evidence of hyperperfusion, and/or presence of intracerebral hemorrhage occurring within 30 days after the carotid or intracranial vessel manipulation. Strongest risk factors include reduced cerebral vasoreactivity, contralateral stenosis of ≥ 70%, post-procedure hypertension, and recent ipsilateral stroke. Pathophysiology is incompletely understood but is likely due to increase in cerebral blood flow and impaired cerebral autoregulation, particularly in the areas of disrupted blood-brain barrier, as well as baroreceptor dysfunction during carotid surgery. Strict blood pressure control pre-, during, and post-procedure is recommended, depending on the recanalization status of the vessel. However, there is no randomized data regarding the goal blood pressure to prevent cerebral hyperperfusion syndrome. With technical advances, carotid or intracranial vessel manipulation is increasingly common. CHS is a likely under-recognized and serious complication of carotid revascularization and intracranial thrombectomy. Awareness of and surveillance for CHS is important to reduce morbidity and mortality. Future research should focus on validation of proposed diagnostic criteria and determining optimal post-procedure hemodynamic management to prevent CHS.