Objective: One of the important characteristics of myofascial trigger point [MTrP] is spontaneous electrical activity [SEA]. Spontaneous electrical activity is recorded from an active locus [a basic unit] of MTrP and has been considered as an abnormal endplate potential, which might be due to excessive acetylcholine release in neuromuscular junction. This study is designed to test the hypothesis that active loci in MTrPs are related to neuromuscular transmission disorder. Methods: Twenty-one adult New Zealand rabbits were anesthetized and their biceps femoris were exposed to localize myofascial trigger spot [MTrS, equivalent to MTrP in human]. A monopolar needle electrode was first used for searching SEA in an MTrS region. Then, a single fiber electromyography [SFEMG] electrode was used to collect the neuromuscular jitter at the site where SEA was recorded. The same procedure was performed at the normal muscle site [no SEA recorded] in contralateral limb to collect the neuromuscular jitter as a control. Mean value of consecutive differences [MCD] of 100 successive inter-potential intervals was calculated to express the neuromuscular jitter. Results: There was no statistically significant difference [P > 0.05] in MCD of MTrS between the active loci and control sites. Conclusion: It appears that the neuromuscular transmission of end-plate in MTrS in rabbits is not impaired based on this SFEMG study using jitter as the sole criteria. Spontaneous electrical activity is not related to neuromuscular transmission abnormality. Further studies are required to clarify the mechanism of dysfunctional endplates in relation to MTrP.
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