ACETYLSALICYLIC-ACID ACTIVATES ANTINOCICEPTIVE BRAIN-STEM REFLEX ACTIVITY IN HEADACHE PATIENTS AND IN HEALTHY-SUBJECTS

The exteroceptive suppression (ES) of electrical activity in the temporal muscle is an inhibitory antinociceptive brain-stem reflex. We investigated whether aspirin can significantly modulate latencies or durations of the early (ES1) and late (ES2) exteroceptive suppression periods of electrical activity in the temporal muscle. Participating in the randomized double-blind crossover study were 20 patients with migraine without aura, 20 patients with tension-type headache, and 20 healthy subjects. ES1 and ES2 elicited by an electrical stimulus of 20 mA lasting 0.2 msec were recorded during maximal voluntary contraction of the mastication muscles before and 30 min after medication. In a randomized and double-blind fashion half of the subjects were given 1200 mg of aspirin in the form of an effervescent solution and the other half were given an identically tasting solution without aspirin. One week later the experiment was repeated with the substances exchanged in crossover fashion. The administration of placebo as well as aspirin caused a highly significant increase in ES1 duration (P less-than-or-equal-to 0.001). While aspirin caused a highly significant increase in ES2 duration (P less-than-or-equal-to 0.001) the taking of placebo showed no significant effect on ES2 duration. In giving aspirin as opposed to the placebo, there was a significant interaction between groups and drug effect on the latency of ES1; whereas in migraine patients and in patients with tension-type headache the latency of ES1 was reduced by administration of aspirin, it was increased in healthy subjects (P less-than-or-equal-to 0.05). Neither aspirin nor placebo significantly varied the ES2 latency. The results indicate that aspirin and placebo influence antinociceptive functions of the brain-stem. Beyond the placebo effect aspirin is also able to activate complex pain control mechanisms as the polysynaptically mediated ES2. Finally in patients who suffer from migraine or tension-type headache, these pain control mechanisms appear to have partially other functional characteristics than in healthy individuals.