SHORT COMMUNICATION Thrombotic occlusion of the common carotid artery (CCA) in acute ischemic stroke treated with intravenous tissue plasminogen activator (TPA) V. K. Sharma, G. Tsivgoulis, A. Y. Lao, M. Flaster, J. L. Frey, M. D. Malkoff and A. V. Alexandrov Department of Neurology, Barrow Neurological Institute, Phoenix, AZ, USA Keywords: Acute common carotid occlusion, cardioembolic, tandem lesions, thrombo- lysis Received 10 August 2006 Accepted 15 September 2006 Although common carotid artery (CCA) occlusions are rare, acute clinical presenta- tions vary from mild to devastating strokes primarily due to tandem occlusions in the intracranial arteries. Three patients with acute CCA occlusions were treated with systemic tissue plasminogen activator (TPA). Blood pressures were kept at the upper limits allowed with TPA therapy with fluid balance and the Ôhead-downÕ position. Recanalization occurred in intracranial vessels only. Marked early neurological improvement occurred in two of three patients. CCA occlusions should not be considered contra-indication to systemic thrombolysis. Introduction The common carotid artery (CCA) occlusion is a rare finding seen in no >2% of patients evaluated for cerebrovascular diseases [1]. A wide range of presenta- tions can be seen from completely asymptomatic to a devastating stroke [2,3]. Chronic arterial occlusions are frequently attributed to atherosclerosis, whilst other less frequent causes include Takayasu arteritis, post- radiation arteriopathy, cardiac embolism, syphilis, trauma and homocystinuria, etc. [3–5]. In acute is- chemic stroke, the nature and extent of mostly throm- boembolic acute internal carotid artery (ICA) occlusions have been described; however, acute CCA thrombosis has rarely, if ever, been reported in detail in patients with acute cerebral ischemia. At our tertiary care hospital, acute stroke patients first undergo an emergency non-contrast enhanced brain CT and thrombolytic therapy with intravenous tissue plasminogen activator (TPA) is initiated in eli- gible patients. Suitable patients are further subjected to rapid CT angiography (CTA) and bedside ultrasound studies [transcranial Doppler (TCD) and cervical du- plex] in the emergency room with no delay in the ini- tiation of thrombolysis. Here, we describe clinical, neuroimaging and outcome findings in patients with acute CCA occlusions and ischemic strokes eligible for standard systemic TPA therapy. Case presentations From September 2005 to May 2006, 47 ischemic stroke patients received IV-TPA therapy within 3 h of symp- tom onset at our hospital. All patients underwent either CTA of head and neck or transcranial/cervical ultra- sound before TPA bolus. Our ultrasound scanning and interpretation protocols include assessment of intra- cranial and extracranial vessels including CCA patency in all patients. A total of three patients (6%) were found to have CCA occlusions before TPA bolus. Times elapsed between symptom onset and TPA bolus were 145 min (case 1), 115 min (case 2) and 160 min (case 3). Carotid duplex studies demonstrated CCA occlusions extending into the ICA and external carotid artery (ECA) with mobile thrombi in all three patients (Fig. 1). CCA occlusions were also seen on CTA of neck (n ¼ 3) and conventional digital subtraction ang- iography (DSA) (n ¼ 1) performed after the initiation of systemic thrombolysis. All patients received 0.9 mg/ kg of IV-TPA treatment and no additional intra- arterial rescue was performed. Clinical, imaging and short-term outcomes of the three patients are summarized in the Table 1. Computer tomography angiography and DSA of intracranial arteries revealed occlusion in the C1 and C2 ICA segments in all three cases. Additionally, ÔTÕ type occlusion of the terminal ICA, involving M1 segment of middle cerebral artery (MCA) and A1 segment of anterior cerebral artery (ACA) segments in case 2 was noted. TCD also showed anterior cross-filling via the anterior communicating artery with ACA reversal and delayed systolic acceleration in the MCA on the affected sides in cases 1 and 3. All three patients had a history of atrial fibrillation (AF) and hypertension, and two had markedly elevated blood pressures before TPA treatment. Blood pressure was lowered with nicardipine and maintained in the systolic range of 160–180 mmHg range during the IV- TPA infusion and immediately thereafter. Fluids were given to maintain euvolemia. All the patients were kept in the Ôhead-downÕ (flat) position. At 2 h after IV-TPA bolus, TCD showed complete proximal MCA recanal- ization in cases 1 and 3 despite persistence of the Correspondence: Dr Vijay Sharma, Department of Neurology, Bar- row Neurological Institute, Phoenix, AZ 85013, USA (tel.: 602 406 6016; fax: 602 406 6261; e-mail: drvijay@singnet.com.sg). Ó 2007 EFNS 237 European Journal of Neurology 2007, 14: 237–240 doi:10.1111/j.1468-1331.2006.01654.x