OBJECTIVE: To investigate the effect of increased sympathetic outflow to muscle (by means of elevated intrathoracic pressure) on painful-area electrical activity. DESIGN: In six subjects with myofascial painful areas in trapezius muscles during normal respiration and during elevated intrathoracic pressure, electromyographic epochs were recorded from a monopolar needle electrode inserted over the painful area and advanced until action potentials were detected, a second needle electrode inserted to the same depth over a nontender control area, and surface electrodes placed nearby. RESULTS: The painful-area electromyographic activity increased (P < 0.05) from 49 +/- 53 microV during normal respiration to 121 +/- 80 microV during elevated intrathoracic pressure. The control-area electromyographic activity and the surface-electrode electromyographic activity did not increase significantly. CONCLUSION: The significant electromyographic increase from painful areas and no significant increase from control channels are consistent with the view that sympathetic neural outflow increases painful-area electrical activity.
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Chung et al. (2004) studied this question.
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