• Cerebral Hyperperfusion (reperfusion) Syndrome (CHS) can occur within hours to days after a revascularization procedure (most commonly carotid endarterectomy)
    • the peak incidence of CHS and hemorrhage after carotid endarterectomy (CEA) is  5-7 days, while it is 12-48 hours after carotid artery stenting (CAS)   [Ogasawara, 2007]
    • a longer delay (days to weeks) has also been reported
    • CHS after aortic stenosis surgery may lead to bilateral lesions
  • diagnostic criteria include new-onset symptoms (headache, neurological deficit, and seizure) + evidence of hyperperfusion measured by TCD, MRI or SPECT
  • incidence 1-14% (usually ∼ 7%)
  • the cornerstone of prevention is strict perioperative blood pressure (BP) control (for at least 14-21 days)
  • TCD should be available to identify patients with hyperperfusion

Is hyperperfusion always present in symptomatic patients?

  • hyperperfusion is seen in most cases of CHS, but symptoms can also occur in patients with only moderate increases in CBF (30–50% above baseline) following CEA (these cases should referred to as reperfusion injury)
  • the risk of developing CHS is 10 times higher in patients with hyperperfusion than in those without

Procedures associated with CHS

  • carotid endarterectomy
  • carotid and vertebral artery stenting
  • carotid and vertebral angioplasties
  • extra-cranial intracranial bypass
  • clipping of internal carotid artery aneurysm
  • subclavian angioplasty
  • revascularization in moyamoya syndrome
  • repair of severe aortic valve stenosis


  • the terms hyperperfusion (excessive flow/hyperemia) and reperfusion (flow normalization) are often used synonymously because both can cause cerebral injury with similar clinical presentation
  • CHS results from a failure of cerebral blood flow autoregulation, leading to hyperemia
    • long-term hypoperfusion, seen in conditions like high-grade stenosis, is compensated by maximal peripheral vasodilation
    • the autoregulatory capacity is thus exhausted, and the blood vessels are unable to respond immediately with vasoconstriction when the perfusion pressure suddenly increases after successful CEA/CAS → tissue is therefore exposed to hyperemia
  • hyperemia is usually defined as an increase in cerebral blood flow (CBF) >100% compared to the baseline   → Cerebral blood flow regulation
    • preoperative CBF value is usually unknown; the interhemispheric difference may be used (except in patients with contralateral stenosis)
    • the risk of CHS can also be estimated using TCCD/TCD – a 1.5- or 2-fold postoperative increase in mean MCA flow velocity compared to baseline may predict the occurrence of CHS   (Fujimoto, 2004)
    • symptomatic CHS was also reported with a CBF increase of < 50%; in such cases, the term reperfusion syndrome should be preferred (Karapanayiotides, 2004)
  • reperfusion injury (typically after acute stroke therapy) is usually caused by rapid normalization of flow within the infarcted tissue
    • these patients have normal or only mildly increased CBF (20–44% above baseline)
    • however, true hyperperfusion syndrome may also develop in acute stroke patients   (Kneihsl, 2021)
  • TCCD studies indicate that blood flow normalizes within one month after surgery; autoregulation is restored within approx. 6 weeks [Megee, 1992]

Hyperperfusion syndrome

clinical signs and symptoms + markedly increased CBF

Reperfusion syndrome

clinical signs and symptoms + normal or only mildly increased CBF

  • reperfusion symptoms are increasingly recognized in many other organs following revascularization procedures, such as:
    • reperfusion arrhythmias
    • gastrointestinal injury after reperfusion, leading to decreased intestinal barrier function 
    • marked polyuria after angioplasty in patients with renovascular disease
CHS risk factors
  • patients with severely reduced intracranial flow (usually in the MCA, ACA) on the side of a high-grade stenosis
  • patients with impaired preoperative cerebrovascular (vasomotor) reactivity (CVR) on TCD/TCCD
  • surge in velocity or pulsatility index by over 100% after the intervention
  • larger ischemia from a previous stroke
  • decompensated hypertension
  • coagulopathy/thrombocytopathy
  • perioperative ischemic stroke
  • recent contralateral CEA
  • contralateral carotid occlusion

Changes in the brain tissue resemble hypertonic encephalopathy:

  • cerebral edema
  • intracerebral hemorrhage (ICH) /hemorrhagic transformation of ischemia
  • intraventricular hemorrhage (IVH)
  • subarachnoid hemnorrhage (SAH)

Clinical presentation

  • severe headache
    • worsening in the prone position
    • ipsilateral to the lesion side or diffuse
  • impaired consciousness
  • epileptic seizures (often focal)
  • focal neurologic deficit (usually with ICH)

Diagnostic evaluation

Parenchymal Imaging (CT/MRI)

  • CT depicts edema/ICH/SAH in the territory of the recanalized artery
    • edema is typically found in white matter (vasogenic), with or without mass effect
    • bleeding can be petechial or even large parenchymal
  • MRI findings may resemble those of PRES
    • T2/FLAIR – diffuse hyperintense lesions
    • T1C+ – possible leptomeningeal enhancement, not parenchymal
      • hyperintense acute reperfusion marker (HARM) – delayed gadolinium enhancement of the cerebrospinal fluid space on FLAIR   Cerebral hyperperfusion syndrome - delayed enhancement on FLAIR  (Cho, 2014)
    • DWI shows no lesions (typically, there is no cytotoxic edema)
    • hemorrhage signal is age-dependent → MRI in hemorrhage diagnosis

Vascular imaging (CTA/neurosonology)

  • CT angiography excludes thrombotic complications in the carotid artery and/or distal embolization
  • TCD/TCCD shows an increased flow (↑PSV) and decreased resistance (↓PI and RI) in the MCA of >100% compared to the pre-intervention values

Perfusion imaging

  • typical ipsilateral findings on CTP: ↑CBF, ↑CBV, ↓MTT
Cerebral hyperperfusion syndrome manifested by subarachnoid hemorrhage
Cerebral hyperfusion syndrome - hemorrhagic transformation of ischemia after endarterectomy
Post-CEA reperfusion injury with parenchymal and subarachnoid hemorrhages


  • timing of the procedure
    • benefit of CEA is greatest in the first 2 weeks following an ischemic event
    • in the case of large ischemia, however, some delay is advisable
  • perioperative TCD/TCCD monitoring
    • enables early detection of hyperperfusion and the need for even more strict BP control
  • strict blood pressure control
    • blood pressure reduction should be considered even in normotensive patients with hyperperfusion on TCD, as some may develop delayed hypertension.
    • the exact target value is unknown, and an individualized approach is advised (age, comorbidities, etc.)
    • blood pressure should preferably be lowered with drugs that do not increase CBF, such as labetalol and clonidine  (avoid ACE-I, CCB, and especially vasodilators)
  • use of free-radical scavengers – further trials are needed


  • rigorous blood pressure correction (ideally <120/80 mmHg) – it also serves as a preventive measure
  • in the case of seizure activity, administer Anti Seizure Medication (ASM) – PHE, VPA, LEV → acute symptomatic seizures
  • start antiedema therapy

Management of patients with hemorrhagic transformation/SAH/ICH

  • discontinue antiplatelet therapy and consider platelet concentrate infusion
  • administer METHYLPREDNISOLON (Solumedrol)  25-125 mg IV (to neutralize the effect of clopidogrel or other thienopyridines) [Qureshi, 2008]
    • this approach is not standardized and is based on limited evidence
  • if the CT scan indicates no progression in 24h, patients with stent should get aspirin; delay clopidogrel therapy for 5-7 days


  • depends on timely recognition of hyperperfusion and adequate treatment of hypertension before cerebral edema or ICH develops
  • the prognosis after ICH is poor (mortality of 36–63%, significant morbidity in the survivors)
  • the prognosis of CHS in patients without ICH is much better, with low mortality


What is Cerebral Hyperperfusion Syndrome (CHS)?
  • A rare but serious condition with an increase in blood flow to a previously hypoperfused brain region. This can lead to complications like cerebral edema and hemorrhage

What causes CHS?
  • CHS often occurs after procedures like carotid endarterectomy or carotid artery stenting, especially in patients with a significant reduction in cerebral blood flow before the procedure

What are the symptoms of CHS?
  • common symptoms include severe headaches, seizures, focal neurological deficits, and altered consciousness
How is CHS diagnosed?
  • the diagnosis is typically clinical, supported by imaging studies like CT or MRI. Transcranial Doppler (TCD) may also provide valuable information about cerebral blood flow patterns

How is CHS treated?
  • treatment involves managing symptoms, rigorous blood pressure control, and sometimes the use of corticosteroids to reduce cerebral edema

What precautions should be taken post-surgery to prevent CHS?
  • regular monitoring of cerebral blood flow, maintaining optimal blood pressure, and close clinical observation for any neurological changes are essential

How long does CHS last?
  • the duration of CHS can vary; some patients recover within a few days, while others may experience symptoms for several weeks

What is the prognosis for CHS?
  • early detection and appropriate management improve the prognosis
  • if left untreated, CHS can lead to ICH with permanent neurological damage or even death

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Cerebral hyperperfusion syndrome
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