Abstract
The pathophysiology of both classical and common migraine is still not understood, and there is controversy as to whether the origin is vascular, neuronal, or both. Although the mechanism for the prophylactic effect of β-blockers in migraine has not been elucidated yet, the therapeutic action of β1-blockers and non-selective β-blockers devoid of intrinsic activity is well established by many controlled trials. Mainly on the basis of data from animal experiments, the possible role of central β-adrenoceptor-mediated mechanisms involved in the control of the activity of noradrenergic neurons will be discussed with reference to migraine.
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