Bilateral atherosclerotic internal carotid artery occlusion causing acute bihemispheric infarctions

Abstract

Multiple acute brain infarctions in both cerebral hemispheres involving the anterior circulation are uncommon (affecting less 1.0–6.0 % of acute stroke patients) and usually suggest an embolic mechanism, particularly one of aortic or cardiac origin [1–4]. Unilateral internal carotid artery (ICA) atherosclerotic lesions may rarely cause acute bihemispheric infarctions through crossflow in the anterior communicating artery with the contralateral anterior cerebral artery (ACA) territory being invariably involved in all described cases [4]. To the best of our knowledge there has been no report of bilateral extracranial atherothrombotic ICA occlusion causing acute bihemispheric infarctions involving both middle cerebral artery territories. A 73-year-old man with a history of hypertension, hypercholesterolemia and smoking presented with an acute right upper arm weakness that he noticed on awakening. Admission brain CT and electrocardiogram were normal. Neurological examination disclosed a mild left hemipareris and left-side visual neglect with an NIH Stroke Scale score (NIHSS-score) of 5 points. The patient underwent emergent carotid duplex evaluation showing multiple hyperechoic plaques in both common carotid arteries (CCA) and acute bilateral ICA occlusion (Fig. 1a, b). Transcranial Doppler examination showed (1) acute bilateral middle cerebral artery (MCA) occlusion with minimal flow (thrombolysis in brain ischemia grade I) in right and blunted flow (thrombolysis in brain ischemia grade II) in left MCA, (2) present collateral flow through reversed ophthalmic artery (OA) bilaterally and (3) absent collateral flow through posterior communicating arteries. The patient also underwent 30-min bilateral transcranial doppler monitoring that documented the presence of microembolic signals in both MCAs (Fig. 2). Acute reperfusion therapies including intravenous or intra-arterial thrombolysis as well as mechanical thrombectomy were withheld because of unknown time of stroke onset. Emergent echocardiography excluded the presence of cardiac thrombus and other source of cardiogenic embolism (including aortic arch dissection). He was treated with aspirin (325 mg) and enoxeparin (40 mg). Fourteen hours later, he became quadriplegic and lethargic (NIHSS-score 26 points). Repeat brain CT (performed after 12 h from the baseline CT) showed bilateral cortical infarctions (Fig. 1c, d) in both MCA territories (arrowheads). The patient expired the following day. Simultaneous occurrence of multiple infarcts in different arterial territories is a characteristic feature of cardioembolic stroke according to the findings of recent studies G. Tsivgoulis (&) I. Heliopoulos K. Vadikolias M. Flamouridou S. Tsakaldimi C. Piperidou Department of Neurology, University Hospital of Alexandroupolis, Democritus University of Thrace, Kapodistriou 3, Nea Xili, Alexandroupolis 68100, Greece e-mail: tsivgoulisgiorg@yahoo.gr