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Aspirin Activates Antinociceptive Inhibitory Reflex Activity in the Brain Stem

AIM OF INVESTIGATION: The effector mechanism of so-called peripherally effective analgesics in headache and other kinds of pain has not yet been clearly understood. It is increasing controversial whether the inhibition of prostaglandin synthesis can be viewed as the general analgesic, antipyretic, and anti-inflammatory effector principle of the salicylates and other non-steroid anti-rheumatic drugs. New studies may indicate a central analgesic effectiveness of Aspirin. The exact effector site of Aspirin in the central nervous system, however, is unknown. The exteroceptive suppression (ES) of electrical activity in the temporal muscle is an inhibitory antinociceptive brain stem reflex; its early (ESt) and late (ES2) suppression periods are influenced in particular by presynaptic and post-synaptic inhibitions in the reticular nuclei, the spinal trigeminal nuclei and the peri-aquaductal grey matter including the rapheal nucleus. A change in the parameters of this inhibitory brain stem reflex by administration of Aspirin could provide quantitative information about the possible effect of Aspirin on the anti-nociceptive systems of the brain stem. For this reason we investigated whether Aspirin can significantly modulate latencies or durations of the suppression phases.