Abstract
Quintner and Cohen have challenged the existence of myofascial trigger points ⇓. However, there is strong evidence that myofascial trigger points (MTPs) are a peripheral source of nociception, and act as ongoing nociceptive stimuli contributing to pain propagation and widespread pain ⇓. Pressure pain thresholds (PPTs) measurement applied to different locations over the muscles shows that the sites with the lowest PPT corresponding to the locations of MTPs, indicating that muscle nociceptors are sensitized. The sensitized nociceptors lead to an increased neuronal firing. In addition to the nociceptor sensitization, non-nociceptors (mainly the large diameter muscle afferents) may also via central neuronal reorganisation and sensitization contribute to pain perception generated from MTPs. Thus, local pain and tenderness at MTPs are largely due to nociceptor sensitization most likely with a lesser contribution from non-nociceptor activation ⇓. The study by Freeman et al. ⇓, found that anesthetizing of painful trigger points, provokes a remarkably rapid change in central sensitization symptoms (measuring PPTs in a site far away from the areas that had been infiltrated) due to the reduced nociceptive drive needed for maintaining central sensitization. Why such focal pain generators persist and remain active after a reasonable healing period for soft tissue remains unclear. The …
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