“
“Several recent studies have shown that in migraine patients, the prevalence of an incomplete Circle of Willis is higher than in controls.1-3 This might suggest that such an anatomic anomaly is a risk factor for developing migraine. As an explanation, it has been commonly proposed that an incomplete Circle of Willis could prevent regional cerebral KU-57788 molecular weight blood flow adaptation in the face of increased metabolic demand. A resulting local ischemia could then, in hyperexcitable persons,

lead to a cortical spreading depression that is by many investigators believed to be the cause of migraine attacks.[3] Unfortunately, these studies did not measure regional cerebral blood flow during increased brain activity or, eg, a one-sided carotid artery occlusion. We doubt whether in subjects with an incomplete see more Circle of Willis such conditions will importantly diminish cerebral perfusion. In this paper, we argue that an incomplete Circle of Willis might increase the risk for migraine by elevated wall shear stress in small-diameter anastomotic vessels. Aberrations in the Circle of Willis do not automatically cause a dramatic reduction of anastomotic flow to the brain. Only a simultaneous absence of both the anterior communicating artery (or an A1 segment) and

a posterior communicating artery (or P1 segment) would definitely prohibit flow compensation via the Circle of Willis (see Figure). The presence of this combination seems, however, rare because it was not observed in a study on 360 normal fixed brains.[4] Furthermore, even a moderate decrease of cerebral blood flow (from 47 to 37 mL/100 g/min) is sufficient to attenuate attention and motor reactions.[5] It is hard to believe that in half of the population, having similar morphologic variants, such signs of diminished brain function, will be elicited by increased brain activity or by head rotation. Indeed, occlusion of a carotid artery in patients with incomplete Circle of Willis, anesthetized for open arch surgery or kept conscious for carotid endarterectomy, did not elicit signs of transient cerebral

ischemia, even not in the presence of severe bilateral carotid artery stenosis.[6, 7] In addition, secondary collateral pathways are formed by the external carotid artery via the ophthalmic selleck artery and via leptomeningeal anastomoses at the brain surface.[8] An imminent shortage of regional cerebral blood supply will obviously be corrected by a rise of blood flow velocity in the patent portions of the circuit, as a result of an increased pressure gradient. An example of this is observed in a study with carotid occlusion in healthy volunteers, showing increased flow velocity, as measured by transcranial color-coded duplex sonography, in a posterior communicating artery.[9] An increased flow velocity may enhance wall shear stress.