The neurovascular theory of migraine integrates the phenomena of head pain (due to vascular inflammation and dilation) and aura (cortical neuronal spreading depression), which precedes or accompanies headache in a sizable minority. The trigeminal nerves play a prominent role, emanating from the brainstem and innervating the vasculature, although the exact nature of the coupling of pain and aura remains elusive. In addition to the central role in headache, the vasculature also plays an important role in migraine-related stroke, a phenomenon of increasing interest. Among a variety of putative stroke mechanisms, intracerebral large vessel spasm, microcirculatory vasoconstriction (causing oligemia), and craniocervical arterial dissection involve the vasculature supplying the brain. In this issue of Neurology , Vanmolkot et al.1 present evidence for another role of the vasculature in vascular headache and its sequelae, namely endothelial dysfunction. Endothelial dysfunction, a product of oxidative stress, results in decreased vascular reactivity, as well as in hypercoagulability and inflammation. Earlier studies of cerebral arteries, utilizing transcranial Doppler, …