Conclusion: In patients with cervical artery dissection (CAD), stroke is most frequently associated with direct and indirect signs of artery-to-artery embolization. Summary: In young adults, extracranial CAD accounts for 20% of strokes (Leys D et al, Neurology 2002;59:26-33). It is somewhat controversial whether artery-to-artery embolization is the main mechanism of stroke in CAD or that stroke results from reduced flow from the primary cervical lesion. Should stroke result from reduced flow from the primary cervical lesion, one could argue for open or endovascular revascularization, whereas if artery-to-artery embolization is the primary event, anticoagulation or antiplatelet regimens would seem to be most advantageous to prevent secondary embolic events. Imaging studies can potentially distinguish hemodynamic from thromboembolic infarcts. For example, acute thromboembolism can be demonstrated directly on brain magnetic resonance (MR) imaging using the T2 sequence where intraluminal acute thrombus appears as signal loss along the course of an occluded symptomatic cerebral artery (Flacke S et al, Radiology 2000;215:476-82). Presumed embolic mechanism of stroke can also be evoked indirectly on diffusion-weighted imaging (DWI). DWIs demonstrating a pial or perforating territory stroke pattern are more likely reflective of an embolic mechanism of stroke; however, DWIs indicating junctional or watershed infarcts more likely indicate stroke of hemodynamic origin. The authors used imaging studies to identify the most likely mechanism of stroke in patients with CAD. They retrospectively evaluated cervical ultrasound studies, cervical MR angiography, and stroke brain MR imaging in consecutive patients with CAD. An embolic mechanism was considered as the mechanism stroke in cases of direct visualization of intracranial embolism as a susceptibility vessel sign on T2 imaging or in the case of pial artery territory infarction with DWI. A hemodynamic mechanism was infarction was implicated in the case of watershed infarction and pial artery territory infarction where two or more of the following were present: severe stenotic or occlusive CAD, reduced intracranial velocity on ultrasound or signal on MR angiography, or hyperintense vessel sign on fluid-attenuated inversion recovery. The remaining patients were considered to have a mixed mechanism of stroke after CAD. Of 172 consecutive patients with CAD, 100 (58%) had evidence of acute stroke on DWI imaging. Of these 100 patients, stroke was attributed to a thromboembolic mechanism in 85, to a hemodynamic mechanism in 12, and a mixed mechanism was felt to be present in only three. Comment: The data in this study apply to patients with spontaneous CAD. Patients with CAD secondary to a traumatic mechanism do not appear to have been entered into the study. Nonetheless, the data do suggest that thromboembolism rather than hemodynamic infarction is the most frequent cause of stroke when a cervical artery dissects. Prevention of artery-to-artery embolization would therefore appear to be the major priority in the large majority of patients with CAD, certainly those with spontaneous CAD. The relative efficacy of antiplatelet therapy vs vitamin K antagonists in preventing artery-to-artery embolization in CAD is not definitely known. Randomized controlled trials are needed to obtain Level 1 evidence of the role of heparin or antiplatelet therapy and operative or endovascular therapies in the management of CAD.