Case Report
Detection of Cerebral Hyperperfusion Syndrome after Carotid
Endarterectomy with CT Perfusion
Karl Schoknecht, Szendro Gabi, MD, Gal Ifergane, MD, Alon Friedman, MD, PhD, Ilan Shelef, MD
From the Department of Neuroradiology, Soroka University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel (KS, IS); Department of Vascular Surgery,
Soroka University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel (SG); Department of Neurology, Soroka University Medical Center, Ben-Gurion
University of the Negev, Beer-Sheva, Israel (GI); Department of Physiology, Zlotowski Center for Neuroscience, Faculty of Health Sciences, Ben-Gurion University of the Negev,
Beer-Sheva, Israel (AF); and Institute of Neurophysiology, Charité Universitätsmedizin Berlin, Berlin, Germany (KS).

ABSTRACT
We present the case of a 60-year-old female patient, who developed symptomatic internal
carotid artery stenosis and subsequently underwent carotid endarterectomy. Four days
after an uneventful surgery the patient developed confusion, seizures, and was admitted to
the ICU. CT perfusion revealed reduced ispilateral time-to-peak and mean-transient-time
and increased cerebral blood volume and cerebral blood flow, confirming the diagnosis of
cerebral hyperperfusion syndrome. We thus propose CT perfusion as a diagnostic means
for cerebral hyperperfusion syndrome, a syndrome that remains underdiagnosed.

Keywords: Cerebral hyperperfusion syndrome, CT perfusion, cerebrovascular
autoregulation.
Acceptance: Received February 23,
2012, and in revised form July 23,
2012. Accepted for publication August 27,
2012.
Conflicts of Interest: None
Correspondence: Address correspondence to Ilan Shelef, MD, Department
of Diagnostic Imaging Faculty of Health
Sciences, Ben-Gurion University of the
Negev Beer-Sheva, 84105 Israel. E-mail:
shelef@bgu.ac.il.
J Neuroimaging 2014;24:295-297.
DOI: 10.1111/j.1552-6569.2012.00773.x

Clinical Case
A 60-year-old female patient with a history of systemic lupus erythematosus, hypothyroidism, 30 pack years, and mild
chronic hypertension developed symptomatic internal carotid
artery (ICA) stenosis indicated by recurrent transient ischemic
attacks (TIAs). Carotid duplex sonography revealed narrowing
of 80% at the left and 50% at the right carotid bifurcation. The
patient subsequently underwent left side carotid endarterectomy (CEA), which was uneventful. There were no signs of
significant pre-/intra- or acute postsurgical changes in blood
pressure and 100 mg of acetylsalicylic acid were given daily for
anticoagulation. Four days after surgery the patient developed
confusion and seizures and was admitted to the ICU with a
hypertensive blood pressure of 200/120 mmHg. Noncontrast
CT showed diffuse left hemispheric edema with sulcal effacement (Fig 1A). CT angiography demonstrated patent lumen at
the CEA site. Diffuse hemispheric vessel congestion was noted
without any evidence of small vessel occlusion (Fig 1B). On CT
perfusion, increased ipsilateral cerebral blood volume (CBV)
was noted (Fig 1C, increase of 81% in region 1 + 3 vs. 2 + 4). In
these regions time-to-peak (TTP) (Fig 1D) and mean-transienttime (MTT) (Fig 1E) were shortened by 13% and 48% indicating
increased ipsilateral cerebral blood flow (CBF). Elevated CBF

(by a factor of 3.5 in the selected regions of interest) was further
supported by the computed CBF map (Fig 1F), confirming the
diagnosis of cerebral hyperperfusion syndrome (CHS). Thereafter the blood pressure was lowered to 134/75 mmHg using
β-blockers and kept under close control. Seizures were treated
with valproic acid. The clinical signs of CHS resolved within 2
days and a follow-up noncontrast CT on day 4 after the onset
of CHS confirmed regressive cerebral edema with no signs of
infarction. One week postadmission, the patient was discharged
home with unremarkable neurological status.

Discussion
CHS is a clinically under-recognized complication observed in
1-3% of the patients after both CEA and carotid angioplasty
with stenting. Its clinical symptoms can arise within hours and
up to 1 month after surgery and include headache, seizures, focal neurological deficits, and cognitive impairment.1-4 Failure
of autoregulation of CBF has been identified as an important
factor initiating CHS and may result in severe brain edema and
intracranial hemorrhage.5 In CHS brain vessels lack the ability
to physiologically dilate or constrict in response to changes in
blood pressure-dependant tissue perfusion.1,6 Visualizing this
impaired autoregulation in CHS is challenging, yet crucial for

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Fig 1. Noncontrast CT and CT perfusion in a patient suffering from cerebral hyperperfusion syndrome. Noncontrast CT reveals diffuse edema
and sulcal effacement (A, arrow marks affected hemisphere). CT angiography confirms ipsilateral vascular congestion (B). CT perfusion 4 days
post carotid endarterectomy shows increased cerebral blood volume (CBV), reduced time-to-peak (TTP), and reduced mean-transient time
(MTT) in the ipsilateral territory of internal carotid artery blood supply (C–E), indicating increased cerebral blood flow (CBF) (F). The absolute
values for TTP, MTT, CBV, and CBF of two ipsi- and two contralateral regions of interest are listed at the bottom left of each image (D–F).

the syndrome’s diagnosis and early treatment before the onset of its devastating complications. Multiple functional diagnostics and imaging approaches have been used to identify
CHS, including single-photon emission computed tomography
(SPECT), which helped to identify presurgically reduced blood
flow reserve as a risk factor for the development of CHS.7-9
However, for clinical routine use, there is no unitary view about
the adequate diagnostic modality. SPECT is suitable to diagnose CHS, yet not practical because of its high cost and limited
availability. Transcranial Doppler sonography is a cost-effective
noninvasive method to diagnose CHS, however its accuracy
strongly depends on the examiner and fails in about 10% of the
cases due to limited access to a bone window that allows ultrasound transmission.1,6 Electroencephalography may reveal
altered neuronal activity (eg, epileptiform activity), however
these findings are nonspecific and do not allow the diagnosis
of CHS.1,10 In this case study, we demonstrate failure of autoregulation using CT perfusion,11 a technique that provides a
rapid diagnosis of CHS (also see Refs. 12, 13) and is sufficient
to rule out important post-CEA differential diagnosis, mainly
thromboembolic events and hemorrhagic stroke.14 In addition,
CT perfusion may help to identify patients at risk of developing CHS following CEA or carotid stenting, consequently
suggesting closer monitoring and earlier treatment to prevent

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malignant outcome of CHS. CT perfusion is suitable to assess reduced CBF reserve—a risk factor for CHS (also see
SPECT above)—indicative for chronic maximal vasodilation as
a compensatory mechanism to malperfusion distal to a stenotic
carotid artery.15 A presurgical difference in MTT >3 seconds
(ipsi- vs. contralateral) and presurgically increased relative TTP
and CBV (ipsi- vs. contralateral) have been associated with CHS
following carotid angioplasty with stenting (CAS).16,17 Furthermore, after surgical intervention contrast-enhanced imaging
methods provide information about blood-brain barrier dysfunction, which may cause the symptoms (eg, seizures and
headache) of CHS.10 Perfusion MRI is not universally accessible (see OECD statistics18 on medical technologies) and thus
less suitable. Hence, we propose CT perfusion as a rapid, largely
user-independent, and quantifiable diagnostic means for CHS
and highlight its role for presurgical assessment of patients at
risk for CHS.

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