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, Charit´ e Universit¨ atsmedizin Berlin, Berlin, Germany (KS). Keywords: Cerebral hyperperfusion syn- drome, 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 correspon- dence 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 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. Clinical Case A 60-year-old female patient with a history of systemic lu- pus 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 endarterec- tomy (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 efface- ment (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-transient- time (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). There- after 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, fo- cal 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 Copyright ◦ C 2012 by the American Society of Neuroimaging 295