2006). In chronic occlusive disease (e. g., chronic ICA oc­clusion) this border might further be shifted, resulting in a smaller MCA territory. In this constellation, an external BZI may appear morphologically as a cortical territorial infarc­tion. But even in infarctions that are clearly localized within the border zone, it may still be debatable whether the underlying cause is hemodynamic or embolic or a combination of both (Caplan and Hennerici 1998). A hy­pothesis for combined pathogenesis is that emboli are more likely to develop and are at the same time less likely to subsequently disintegrate in low-flow regions, such as the border zones, afterwards leading to embolic infarcts within the borders. A recent diffusion-weighted MR study supports the above hypothesis of embolic mechanisms, at least for external BZIs. The authors compared 45 patients with internal BZIs and 75 patients with external BZIs. The latter patients had more small cortical infarct patterns and fewer stenoocclusive altered vessels. In people with inter­nal BZIs, a rosarylike infarct pattern was found and more underlying ICA or MCA stenoocclusive pathology was present. Occlusion or marked stenosis (≥ 50 %) were found in 91.1 % of patients with internal BZIs, but only in 73.3 % of patients with external BZIs. The authors concluded that embolism maytherefore have a greater role in external BZI and that acute hypotensive events may be of more rele­vance in internal BZI (Yong et al. 2006). To further analyze the underlying pathomechanisms and toquestion or prove the embolic hypothesis several studies have been initiated combining the assessment of large vessel status, ultra­sound embolus detection and diffusion-weighted MRI. In MCA stenosis, microembolic signals were more frequently observed in patients with multiple lesions on diffusion­weighted MR images, especially along the border zones, whichwereconsideredtobecausedbyimpaireddisrup­tion and clearance of emboli (Wong et al. 2002).