Abstract
An increase in the spontaneous release of acetylcholine (ACh) at the motor endplate is directly related to the generation of myofascial trigger points (MTrPs). In this study, percutaneous electric fields were applied to an animal model of MTrPs with high levels of spontaneous ACh release. All experiments were performed on Swiss mice and Sprague Dawley rats. For evaluating the spontaneous neurotransmission, intracellular recordings were performed, and the frequency of miniature endplate potentials was evaluated. Electromyographic recordings were also conducted to evaluate the endplate noise. Finally, the number and strength of local twitch responses (LTR) were evaluated using ultrasound recordings. The protocols used for the electric currents were 0.4 mA for five seconds and four repetitions (protocol 1), 1.5 mA for five seconds and three repetitions (protocol 2), and 3 mA for three seconds and three repetitions (protocol 3). After a subcutaneous injection of neostigmine (NTG), a great increase was observed in the frequency of mEPPs, together with an elevated endplate noise. Protocols 2 and 3 were the most effective. Protocol 3 could completely reverse the action of NTG at both three hours and 24 hours, respectively. The application of percutaneous currents produced both an increase in the number (144%) and in the speed (230% faster) of LTR compared with dry needling. In conclusion, higher doses of electrical current are more effective for decreasing MTrPs findings in an animal model.
Highlights
Myofascial trigger points (MTrPs) can generate a characteristic type of muscle pain called myofascial pain syndrome (MPS), encompassing sensory, motor, and autonomic symptoms [1, 2]
Higher doses of electrical current are more effective for decreasing myofascial trigger points (MTrPs) findings in an animal model
A model of myofascial trigger points (MTrPs) is obtained when neostigmine is injected in mice
Summary
Myofascial trigger points (MTrPs) can generate a characteristic type of muscle pain called myofascial pain syndrome (MPS), encompassing sensory, motor, and autonomic symptoms [1, 2]. An increase in ACh released spontaneously at the level of the motor endplate is directly related to the generation of myofascial trigger points (MTrPs) [1, 4]. One of the possible benefits is the destruction of the dysfunctional neuromuscular junctions that cause the MTrPs [1] and, the replacement of these synapses by nerve regeneration [9]. This local muscle destruction involves an inflammatory reaction [9] that can remove the GAGs, together with trapped substances. Some authors suggest that DN is more effective if an LTR is obtained during the procedure
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