Objective Objectivation of functional shifts in nervous system through sensory evoked potentials at chronic nociceptive afferentation induced by pathological neuronic autorhythmicity. Methods Pre-and post-treatment assessment of component parameters of evoked potentials with muscular pain and myofascial trigger points with different pain severity. Active pre-treatment autorhythmicity was treated as amplitude increase and any component latency reduction. Autorhythmicity regression was treated as amplitude decay and latency increase. Results Pain relief correlated with myofascial trigger points transformation into latent. Comparing to milder pain, pronounced pain syndrome revealed more significant functional changes (generators of autorhythmicity) at higher levels of nervous system. However, in milder pain, plenty low activity generators were detected revealing subnormal antinociceptive system activity. After treatment, number of pathologically enhanced excitation generators decreased significantly with migration to caudal nerve system regions. Changes may serve a neurophysiological basis for myofascial pain exacerbations. Conclusions There’s correlation between number of active myofascial trigger points and availability of active generators of autorhythmicity at different levels of nervous system. After treatment, latent generator migrates to caudal region of pre-existing initial pain syndrome generator. Key message Changes may serve a neurophysiological basis for myofascial pain exacerbations.