Migraine is a common disease which expresses itself by paroxysmal headache, commonly accompanied by transient neurological symptoms. There are at the moment two important theories concerning the cerebral mechanisms of migraine: The vascular theory which attributes migraine to spasm of a cerebral artery causing local hypoxia and transient focal symptoms followed by neurogenically mediated extra- and/or intracranial vasodilation causing headache, i.e. migraine is understood in terms of a primary perturbation of blood vessel function. Another, but neglected viewpoint relates migraine to a paroxysmal, transient depolarization of primarily cortical neurones causing transient focal symptoms and headache, i.e. migraine is understood in terms of a primary perturbance of neuronal function. This review summarizes clinical and experimental studies concerning these two theories with special emphasis on classic migraine, i.e. paroxysmal headache accompanied by focal symptoms of short duration. At begin of the classic migraine attack regional cerebral blood flow (rCBF) declines in the posterior part of the brain. Subsequently the hypoperfused region expands anteriorly, independent of the territories of supply of the large cerebral arteries. This observation speaks clearly against reduced perfusion as consequence of arterial spasm. The rate of spread of the reduced perfusion is about 2 mm/min and the changes of perfusion appear to follow the cortex corresponding to the convexities. Tests of regulation of rCBF show normal blood pressure autoregulation, but reduced responsiveness to change of arterial carbon dioxide tension and in response to mental activation. These observations are consistent with arteriolar vasoconstriction as cause of reduced perfusion. Vascular tone at the arteriolar level is, however, mainly determined by local factors, and change of local neuronal function could therefore be the basis of increased arteriolar tone and reduced rCBF. Analysis of the time course of perfusion reduction and symptoms reveals that perfusion frequently declines before the patient experiences any focal symptoms. The focal symptoms frequently start after spread of the hypoperfusion has begun, but usually ceases altogether within another 30 minutes, while the reduced perfusion persists for a couple of hours, when the patient suffers from headache. This temporal relationship between symptoms and rCBF changes precludes that the focal symptoms are secondary to reduced rCBF. Furthermore, migraine headache is not related to increased rCBF. On this background the acute migraine attack can hardly be explained by a primary arterial vasospasm.(ABSTRACT TRUNCATED AT 400 WORDS)