Myofascial Pain Syndrome has been defined as a muscular pain disorder involving regional pain referred by trigger points within the myofascial structures to sites local or distant from the pain. Spontaneous electrical activity from putative trigger points has been reported in several studies but the origin of the activity is poorly understood. One hypothesis is that this activity arises from abnormal release of acetylcholine at the neuromuscular junction. This hypothesis predicts no relation to activity at the motor neurons. Objectives: Our specific aim was to test this hypothesis by inhibiting or disfacilitating the motor neurons with an electrical shock to a peripheral nerve. Methods: Trigger points in the trapezius muscles of 9 subjects were located by palpation of taut bands and nodules, and reports of referred pain; then confirmed by lower pressure pain thresholds than control sites. Electromyographic (EMG) activity was recorded with monopolar needles at the site. Results: Spontaneous activity was observed over a narrow range of depths with the subject instructed to relax as much as possible. Accessory nerve (XI) stimulation above the threshold for a muscle twitch showed inhibition of the spontaneous EMG activity in all subjects. Conclusions: We interpret the EMG activity as arising from the putative trigger point and, based on its inhibition by the shock, suggest that the existence of the EMG activity in trigger points arises at least in part from neural activity of the motor neurons and not solely from abnormal release of acetylcholine at the neuromuscular junction.

Back to the Neuroscience / TMJ Program
Back to the IADR/AADR/CADR 82nd General Session (March 10-13, 2004)

Top Level Search