Travell trigger points--molecular and osteopathic perspectives

J Am Osteopath Assoc. 2004 Jun;104(6):244-9.


The proposed etiology of Travell trigger points (TrPs) has undergone a fundamental revision in recent years. New research results suggest that TrPs are evoked by the abnormal depolarization of motor end plates. This article expands the proposed etiology to include presynaptic, synaptic, and postsynaptic mechanisms of abnormal depolarization (ie, excessive release of acetycholine [ACh], defects of acetylcholinesterase, and upregulation of nicotinic ACh-receptor activity, respectively). This working hypothesis regarding the etiology of TrPs has changed the approach to treating TrPs. As an example, Travell and Simons abandoned the application of ischemic compression to TrPs; instead the authors adopted several techniques associated with osteopathic medicine (ie, muscle-energy, myofascial, counterstrain; high-velocity, low-amplitude). Scientists are now proposing and reporting the results of new approaches using capsaicin, a vanilloid-receptor agonist, and ACh antagonists (eg, dimethisoquin hydrochloride, botulinum toxin, quinidine, linalool). The purpose of this article is to review these new concepts and describe new resulting approaches to the treatment of TrPs.

Publication types

  • Review

MeSH terms

  • Biomechanical Phenomena
  • Humans
  • Motor Endplate / physiopathology
  • Muscle, Skeletal / physiopathology
  • Myofascial Pain Syndromes / etiology*
  • Myofascial Pain Syndromes / physiopathology*
  • Myofascial Pain Syndromes / therapy
  • Osteopathic Medicine