The primary management strategies for BCVI include observation, surgical repair, antithrombotic drugs, and endovascular therapy. In determining the treatment for an individual, the location and grade of the injury (Table 1) as well as symptomatology must all be considered.³² Given the high morbidity and mortality rates historically associated with untreated BCVI, observation should not be chosen unless there are contraindications to alternative strategies. Currently, surgical therapy for BCVI is limited. Grade I injuries are associated with a low enough stroke risk that surgical repair is not justified. Repair is warranted in higher-grade injuries, but surgical access is often precluded by involvement of the carotid artery at the base of the skull.¹¹ Consequently, nonsurgical management is the first-line treatment of BCVI. There are no published prospective randomized studies comparing treatment strategies; management recommendations are made based on retrospective analyses of patients managed per institutional protocols. Early reports recommended systemic anticoagulation with heparin (no bolus; 10 U/kg/h to target partial thromboplastin time 40–50 s), demonstrating improved neurologic outcomes among symptomatic patients and stroke prevention among asymptomatic patients.^5,11,12 A few retrospective, uncontrolled case series,^33–35 as well as more recent large reports from Memphis¹⁹ and Denver³⁶ suggest that systemic heparinization and antiplatelet therapy (clopidogrel 75 mg daily or aspirin 325 mg daily) are equally efficacious in stroke prevention. In the absence of controlled data, systemic heparin may be preferred among patients with neurologic symptoms and in those who have no contraindications. The Memphis data⁵ demonstrate systemic heparinization’s clear efficacy in improving neurologic outcomes among symptomatic patients. Furthermore, although statistical significance was not achieved, the large series in Denver¹¹ suggests that heparin may be superior to antiplatelet therapy in stroke prevention (p = 0.07) and in neurologic improvement after ischemic insult (p = 0.15).