Pseudo-occlusion of the extracranial carotid artery caused by intracranial carotid artery stenosis

Abstract

A 70-year-old female with hypertension and diabetes presented to the emergency room with sudden-onset drowsy mentation and disorientation. Her blood pressure was 130/80 mmHg, pulse rate was 70 beats per minute, respiratory rate was 18 breaths per minute, and body temperature was 36.7 C. Neurologic examination indicated confusion and generalized myoclonic jerks. Blood chemistry tests revealed an elevation of blood urea nitrogen and creatinine (83 and 3.5 mg/dl, respectively). Small deep infarcts on the right basal ganglia and corona radiata were visible on brain MRI (Fig. 1a), but a high signal intensity was not evident on the diffusion weighted image. In addition, her right proximal internal carotid artery (ICA) was invisible on contrast-enhanced magnetic resonance angiography (CE-MRA) (Fig. 1b). MRI was performed with a Signa Excite XI Twin Speed 1.5T system (GE Healthcare, Milwaukee, WI, USA). Her neurological symptoms resolved upon reduction of her blood urea nitrogen and creatinine levels, therefore, the patient was tentatively diagnosed with uremic encephalopathy. After improvement of her symptoms, we performed carotid duplex ultrasonography (CDUS, GE LOGIQ 7 PRO US machine, 12 MHz linear array transducer) to evaluate the right ICA on hospital day 6. There was no sonographic evidence of blood flow from the right carotid bifurcation to the proximal ICA (Fig. 1c). Transcranial Doppler could not be performed because she had a poor temporal window. Since MRI and CE-MRA showed multiple silent infarcts mainly in the right anterior circulation and string sign around the lacerum segment of the ipsilateral distal ICA, we planned further investigation including digital subtraction angiography (DSA) to assess her cerebral vascular reserve and vasculature and to determine how to prevent a stroke. DSA, performed on hospital day 8, revealed that the lacerum segment of the right ICA was severely stenotic, but the bulbous segment was not. Proximal to distal blood flow in the right ICA was significantly slower compared to the external carotid artery blood flow (Fig. 1d). The right anterior cerebral artery was filled by the left anterior cerebral and communicating arteries, but the right middle cerebral artery was only supplied by the ipsilateral ICA and was not visualized on vertebral or contralateral cerebral angiography. On hospital day 12, we decided to perform percutaneous transluminal balloon angioplasty (Fig. 2a). Since the diameters of the proximal and distal parent vessels adjacent to the stenotic lesion were 2.03 and 1.89 mm, respectively, we did not deploy a stent. On hospital day 14, follow-up CDUS showed normal configuration of the ICA and normal blood flow velocity (peak systolic velocity: 69.8 cm/s, end diastolic velocity: 33.2 cm/s; Fig. 2b). Since then she has been healthy and asymptomatic, and the blood flow velocity of the right proximal ICA (peak systolic: 69.1 cm/s, end diastolic: 34.8 cm/s; image not shown) was not reduced on 2-year follow-up CDUS. Pseudo-occlusion of the ICA was defined in previous studies as a collapsed distal ICA due to the reduced flow velocity caused by a severe stenotic lesion of the proximal ICA [1]. In this case, contrary to the classical definition of a D. Lee S. H. Heo D.-I. Chang (&) Departments of Neurology, College of Medicine, Kyung Hee University Hospital, Kyung Hee University, #1 Hoegi-dong, Dongdaemun-gu, Seoul 130-702, Korea e-mail: dichang@khmc.or.kr