Migraine is a common and frequently disabling
neurological disorder, but the initiating
migraine mechanisms are still poorly understood.
Potassium channel opening may cause
migraine, and we therefore examined the
migraine-inducing effect of
MaxiPost, a large (big)-conductance
calcium-activated
potassium (BKCa) channel opener, on
migraine induction and cephalic vasodilation in individuals with
migraine. Twenty-six patients with
migraine without aura were randomly allocated to receive an infusion of
MaxiPost or placebo on 2 study days separated by at least 1 week. The primary endpoint was the difference in incidence of
migraine attacks after
MaxiPost compared with placebo. The secondary endpoints were the difference in incidence of
headaches and the difference in area under the curve for
headache intensity scores (0-12 hours), for middle cerebral artery blood flow velocity (VMCA) (0-2 hours), and for superficial temporal artery and radial artery diameter. Twenty-two patients completed the study. Twenty-one of 22 (95%) developed
migraine attacks after
MaxiPost compared with none after placebo (P < 0.0001); the difference of incidence is 95% (95% confidence interval 86%-100%). The incidence of
headache over the 12-hour observation period was higher after
MaxiPost day (n = 22) than after placebo (n = 7) (P < 0.0001). We found a significant increase of VMCA and superficial temporal and radial arteries' diameter. Because BKCa channel opening initiates
migraine attacks, we suggest that BKCa channel blockers could be potential candidates for novel antimigraine drugs.