Exteroceptive Suppression of Temporalis Muscle Activity During Migraine Attack and Migraine Interval Before and After Treatment with Sumatriptan
- 1 April 1994
- journal article
- clinical trial
- Published by SAGE Publications in Cephalalgia
- Vol. 14 (2) , 143-148
- https://doi.org/10.1046/j.1468-2982.1994.1402143.x
Abstract
We compared the early (ES1) and late (ES2) exteroceptive suppression (ES) periods of temporalis muscle activity in 18 migraine patients during 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 migraine attacks. First ES1 and ES2 were measured (stimulus intensity 20 mA, stimulus duration 0.2 ms, stimulation frequency 2 Hz, averaging of 10 responses), then the medication was given on a double-blind basis with an autoinjector using either 6 mg sumatriptan or a placebo solution. 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. Treatment did not affect the latencies of ES1 and ES2. While sumatriptan caused a significant increase in ES1 duration (p ≤ 0.05) both during the migraine interval and during the migraine attack, placebo showed no significant effect on ES1 duration. Treatment with sumatriptan during the migraine attack was accompanied by a significant increase in the duration of ES2 (p ≤ 0.05), but no significant changes in the durations of the late suppression periods were observed under any other conditions. The results do not support the assumption that under the experimental conditions chosen migraine attacks are accompanied by a paroxysmal change in the brain-stem mechanisms involved in the modulation of the ES parameters. Since sumatriptan during the migraine interval selectively lengthens ES1 but not ES2, it can be assumed that the substance has a primary effect on brain-stem mechanisms in migraine patients that cannot be explained in terms of secondary pain-induced mechanisms.Keywords
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