The pathophysiology of cerebral ischemia in the borderzones between the large cerebral arteries has been the topic of considerable debate since this disease entity was defined in the first half of the twentieth century. Hemodynamic failure and microembolization were two seemingly mutually exclusive pathophysiological concepts that were proposed to explain the phenomenon of borderzone infarction in patients with arterial occlusive disease. Sufficient evidence has now accumulated, however, to indicate that borderzone infarcts are in fact caused by an interaction between hypoperfusion and microembolization. In this Review, we summarize the historical background of borderzone infarction and current knowledge regarding the various possible pathophysiological concepts. We present a representative survey of publications from the 1950s to the present day, starting with early autopsy-based studies, followed by later anatomical and in vitro studies, as well as CT-based and MRI-based investigations. The clinical symptoms of borderzone infarction and the possibility of a clinical distinction between borderzone and territorial infarcts are discussed. In addition, we consider techniques to localize hemodynamic risk zones in patients with arterial occlusive disease, such as perfusion-weighted MRI, and techniques to identify a hemodynamic component of stroke, such as investigation of the cerebrovascular reserve capacity with transcranial Doppler ultrasound.