EXTEROCEPTIVE SUPPRESSION OF TEMPORALIS MUSCLE-ACTIVITY DURING MIGRAINE ATTACK AND MIGRAINE INTERVAL BEFORE AND AFTER TREATMENT WITH SUMATRIPTAN

We compared the early (ES1) and late (ES2) exteroceptive suppression ( ES) periods of temporalis muscle activity in 18 migraine patients duri ng both the migraine interval and migraine attack and investigated the effect of sumatriptan and placebo on ES parameters. The measurements were performed in a balanced sequence at four different times on each patient, twice during the migraine interval and once in each of two mi graine attacks. First ES1 and ES2 were measured (stimulus intensity 20 mA, stimulus duration 0.2 ms, stimulation frequency 2 Hz, averaging o f 10 responses), then the medication was given on a double-blind. basi s with an autoinjector using either 6 mg sumatriptan or a placebo solu tion. Thirty minutes after application the measurements were repeated. No significant differences were found in early and late exteroceptive suppression latencies and durations between baseline measurements. Tr eatment did not affect the latencies of ES1 and ES2. While sumatriptan caused a significant increase in ES1 duration (p less-than-or-equal-t o 0.05) both during the migraine interval and during the migraine atta ck, placebo showed no significant effect on ES1 duration. Treatment wi th sumatriptan during the migraine attack was accompanied by a signifi cant increase in the duration of ES2 (p less-than-or-equal-to 0.05), b ut no significant changes in the durations of the late suppression per iods were observed under any other conditions. The results do not supp ort the assumption that under the experimental conditions chosen migra ine attacks are accompanied by a paroxysmal change in the brain-stem m echanisms involved in the modulation of the ES parameters. Since sumat riptan during the migraine interval selectively lengthens ES1 but not ES2, it can be assumed that the substance has a primary effect on brai n-stem mechanisms in migraine patients that cannot be explained in ter ms of secondary pain-induced mechanisms.