OPIOID INVOLVEMENT IN ELECTROMYOGRAPHIC (EMG) RESPONSES INDUCED BY INJECTION OF INFLAMMATORY IRRITANT INTO DEEP NECK TISSUES

Previously, we have demonstrated (Hu et al., 1993) that injection of t he small-fiber excitant and inflammatory irritant mustard oil (MO) int o deep paraspinal tissues surrounding C-1-C-2 vertebrae can evoke a su stained and reversible increase of electromyographic (EMG) activity of neck and jaw muscles, and can also produce an acute inflammatory resp onse. This increased EMG activity lasts up to 20 min; within 30 min fo llowing MO injection, the activity returns to preinjection levels. The aim of our present study was to determine whether an opioid suppressi ve mechanism may be involved in limiting the increased EMG activity, d espite the presence of an ongoing inflammatory response. Three doses ( 0.6 mg/kg, 1.2 mg/kg, and 2.5 mg/kg) of the opioid antagonist naloxone , along with vehicle (saline), were administered intravenously to dete rmine whether naloxone is capable of inducing a significant recurrence (''rekindling'' effect) of EMG activity. A dose-dependent process in the naloxone-induced rekindling effect was demonstrated for the area u nder the curve of rectified and integrated EMG activity. At the highes t dose (2.5 mg/kg), the relative area of naloxone-evoked EMG activity increases reached 83% of the original MO-induced EMG activity level. T hese results suggest that a central opioid suppressive mechanism is ac tivated by the MO-induced small-afferent barrage, and that this may li mit the duration and magnitude of the evoked EMG changes.