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 the small-fiber excitant and inflammatory irritant mustard oil (MO) into deep paraspinal tissues surrounding C1-C2 vertebrae can evoke a sustained and reversible increase of electromyographic (EMG) activity of neck and jaw muscles, and can also produce an acute inflammatory response. This increased EMG activity lasts up to 20 min; within 30 min following MO injection, the activity returns to preinjection levels. The aim of our present study was to determine whether an opioid suppressive mechanism may be involved in limiting the increased EMG activity, despite 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 determine 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 under the curve of rectified and integrated EMG activity. At the highest dose (2.5 mg/kg), the relative area of naloxone-evoked EMG activity increases reached 83% of the original MO-induced EMG activity level. These results suggest that a central opioid suppressive mechanism is activated by the MO-induced small-afferent barrage, and that this may limit the duration and magnitude of the evoked EMG changes.