Animal Models of Myofascial Trigger Points

ABSTRACT

Objective: One of the typical symptoms of myofascial pain syndrome is trigger points [TrPs] in a taut band. It has been reported that hyperalgesic muscle [delayed onset muscle soreness or DOMS] after lengthening contraction [LC] has similarities with clinical TrPs, such as mechanically sensitive spots in hardening of the muscle, and electromyographic activities. Using this model we studied the mechanism by which DOMS is generated and maintained.

Findings: We found that bradykinin released during exercise triggers nerve growth factor [NGF] upregulation in the muscle through the activation of B2 bradykinin receptors. NGF upregulation started 12 hours after LC, and lasted for one to two days, a compatible time course for muscle mechanical hyperalgesia. Injection of anti-NGF antibody into the exercised muscle two days after LC reversed the mechanical hyperalgesia. NGF sensitized muscle thin-fiber receptors recorded in vitro to mechanical stimulation after a short latency of 10 to 20 minutes.

Conclusions: The sensitization of muscle nociceptors to mechanical stimulation by NGF upregulated in the muscle after LC is considered to be a mechanism for mechanical hyperalgesia after exercise. Determining whether there is any difference in expression of NGF or sensitivity of muscle nociceptors in the TrP and in other areas will be an important key for clarifying the mechanism of TrPs.

KEYWORDS :

• Delayed onset muscle soreness
• mechanical hyperalgesia
• nerve growth factor