Case Report Serendipitous Recanalization of Basilar Artery Occlusion Jeffrey A. Switzer, DO, MCTS,* Scott E. Forseen, MD,† Askiel Bruno, MD,* and David C. Hess, MD* Objective: To describe a case of recanalization of a basilar artery occlusion with intravenous (IV) tenecteplase. Case: A 74-year-old man with a history of cardiomyopathy presented to an outside hospital with acute vertigo, dysarthria, gaze deviation, and ataxia. Computerized tomography arteriography demonstrated occlusion of the proximal basilar artery. IV tissue plasminogen activator was ordered; however, the patient received a cardiac dose of IV tenecteplase. The patient was transferred to our facility, whereby symptoms resolved, and repeat computerized tomography arteriography displayed recanalization of the basilar artery. Conclusions: Tenecteplase has enhanced biochemical and pharmacokinetic properties that may be ideal for treatment of basilar artery occlusion and should be further investigated in a randomized clinical trial. Key Words: Basilar artery occlusion—thrombolytic therapy—acute stroke—tenecteplase. Ó 2013 by National Stroke Association Outcome from basilar artery occlusion (BAO) is often poor and the optimal strategy to achieve reperfusion is uncertain.1-3 Intravenous (IV) tissue plasminogen activator (tPA) may be ineffective, particularly in proximal-tomid-BAO,4 and endovascular revascularization strategies are frequently attempted.5 Tenecteplase is a genetically modified tPA with longer half-life, increased fibrin specificity, and plasminogen activator inhibitor-1 resistance.6 Compared with tPA, tenecteplase may increase recanalization and improve outcome in selected middle cerebral artery territory occlusions.7 A From the *Department of Neurology, Georgia Regents University, Augusta, GA; and †Department of Radiology, Georgia Regents University, Augusta, GA. Received March 1, 2013; revision received May 17, 2013; accepted June 8, 2013. Disclosures: None. Sources of funding: None. Address correspondence to Jeffrey A. Switzer, DO, MCTS, Department of Neurology, 1122, 15th St, Augusta, GA 30912. E-mail: jswitzer@gru.edu. 1052-3057/$ - see front matter Ó 2013 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2013.06.019 phase IIB trial of tenecteplase in unselected patients was terminated prematurely because of slow enrollment,8 and tPA remains the only approved fibrinolytic for acute stroke. We present a patient with BAO who mistakenly received IV tenecteplase with recanalization and resolution of neurologic deficits. Case Report A 74-year-old man with a history of dilated cardiomyopathy developed sudden onset of vertigo, nausea, vomiting, and dysarthria. He was taken to a local emergency department where his symptoms progressed to include bilateral hearing loss. Examination revealed left gaze paresis and dysmetria on finger-to-nose and heel–knee–shin bilaterally. Computed tomography angiography showed proximal thrombosis of the BA (Fig 1). IV tPA was ordered 5 hours after symptom onset; however, as a result of an apparent pharmacy error, a high dose of tenecteplase (50 mg, .53 mg/kg) was administered. The patient was transferred to our hospital for consideration of endovascular revascularization. The error in drug delivery was not noted until arrival at our hospital and after the infusion was complete. Journal of Stroke and Cerebrovascular Diseases, Vol. 22, No. 8 (November), 2013: pp e671-e673 e671 J.A. SWITZER ET AL. e672 Figure 1. Three-dimensional reconstruction of computed tomography arteriogram displaying lack of blood flow in distal vertebral arteries and proximal basilar artery (A) and complete recanalization post-tenecteplase (B). On arrival, the patient was significantly improved and neurologic examination revealed only mild dysarthria that resolved over several hours. A repeat computed tomography angiography demonstrated complete recanalization (TIMI 3) of the BA without brain infarction or hemorrhage (Fig 1). Discussion We describe the first case of IV tenecteplase for BAO that we are aware of with resulting recanalization and favorable outcome. Although functional outcome from BAO is quite variable, IV tPA is often ineffective for proximal or large clot burdens.4 Although bridging strategies, intra-arterial fibrinolysis, or mechanical thrombectomy may potentially be more effective, none have been tested in randomized clinical trials of BAO. Furthermore, these strategies are restricted to tertiary centers with endovascular capabilities. Fibrinolytic agents that could be administered IV and achieve rapid recanalization more effectively than IV tPA are, therefore, appealing. Tenecteplase was engineered to enhance the safety and efficacy of tPA. In a dose-escalation trial of IV tenecteplase for acute myocardial infarction, doses of 30-50 mg achieved complete reperfusion in 57%-64% of patients.9 Whether IV tenecteplase improves clinical outcome compared with IV tPA in stroke is undetermined8; however, patients with large artery occlusion involving the MCA and an associated perfusion mismatch had higher recanalization rates and better functional outcomes compared with IV tPA.7 A dose-escalation trial of IV tenecteplase in acute stroke demonstrated an increase rate of symptomatic intracranial hemorrhage at doses of .5 mg/kg.10 However, the risk of symptomatic intracranial hemorrhage may be lower in patients with posterior circulation strokes11,12 potentially permitting the safe administration of higher fibrinolytic doses. Our patient received a standard cardiac dose of 50 mg (.53 mg/kg). Considering the potentially grave prognosis of persistent BAO, such a dose of tenecteplase may be warranted. 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