Abstract
The concept that migraine results from an initial vasoconstriction due to increased release of noradrenaline from the sympathetic nerves to cranial blood vessels has been reappraised in the light of recently acquired knowledge of the mechanisms of action of drugs used in the treatment of migraine, physiological and pharmacological evidence implicating noradrenaline, and the observations by others that several migraine variants may be associated with some degree of sympathetic overactivity. If the theory is correct, it suggests that both prophylaxis and management of the acute condition should be possible by means of selective alpha-adrenoceptor antagonism. The use of drugs with potentially dangerous vasoconstrictor properties appears to be unnecessary. The suggestion is made that the increased adrenergic activity might result from changes within the hypothalamus.