Migraine pain has traditionally been ascribed to dilatation of primarily extracranial arteries. Such dilatation has, however, not been demonstrated so far. Studies of microcirculation reveal no major hyperperfusion or ischemia in the temporal muscle or the subcutaneous tissue in the temporal region during attacks of migraine. However, a reduction in the orthostatic reactivity of the subcutaneous arterioles was observed on the side of the headache. Increased tenderness of the pericranial myofascial tissues is observed during migraine attacks, particularly on the side of the headache. Increased tension of pericranial muscles on the other hand is not a constant finding and migraine attacks are not induced by experimentally increased tension of the temporal and masseter muscles. Extracranial pain and tenderness may, however, be induced experimentally by intramuscular injections of hypertonic saline and potassium chloride as well as of endogenous substances like bradykinin with 5-hydroxytryptamine and bradykinin with substance P. The extracranial arteries and myofascial structures are both supplied by unmyelinated trigeminal sensory nerve fibers containing a variety of neuropeptides which are released during migraine attacks. Axonal reflexes between extracranial arteries and neighbouring myofascial tissues as well as referred pain mechanisms may account for the observed tenderness during migraine attacks.