Cerebral and extracranial circulatory disturbances in migraine: pathophysiological implications.

Abstract

Studies of regional cerebral blood flow (rCBF) are rapidly increasing our understanding of migraine mechanisms. In the early phase of an attack, migraine with aura (previously classic migraine) is associated with posterior focal hypoperfusion in one hemisphere. This spreads forward, usually to involve the posterior one-third to one-half of a hemisphere. Hypoperfusion persists into the headache phase and is associated with partial or complete vasoparalysis. From patient to patient, it varies in severity, ranging from almost normal to well below the usual ischemic threshold. After 1 h to several hours, the formerly hypoperfused areas becomes hyperperfused. The headache begins while rCBF is decreased and relates topographically to the area affected by rCBF changes. There is no association with hyperperfusion, which usually begins long after headache onset and often outlasts headache. In migraine without aura, there are no focal rCBF abnormalities but a dispute as to whether flow is globally increased. For a number of reasons, pain mechanisms, however, are likely to be the same as in migraine with aura, just initiated by something else. Extracranial blood flow is unchanged during migraine attacks but the superficial temporal artery on the side of the headache is dilated and recent transcranial Doppler studies have been interesting although difficult to interpret. These results will stimulate further studies of large arteries. The migrainous aura is probably the clinical manifestation of a cortical spreading depression. The resulting ionic and neurotransmitter changes are by way of local irritation of pial perivascular nerves, the most likely mechanism of migraine headache.