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Travell trigger points--molecular and osteopathic perspectives.

John M McPartland¹

¹Faculty of Health & Environmental Science, Unitec Institute of Technology, Auckland, New Zealand. jmcpartland@unitec.ac.nz

The Journal of the American Osteopathic Association

|July 6, 2004

Summary

Travell trigger points (TrPs) stem from abnormal motor end plate depolarization. New treatments focus on acetylcholine pathways and novel therapies like capsaicin.

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Area of Science:

Neurology
Pain Management
Osteopathic Medicine

Background:

The understanding of Travell trigger points (TrPs) etiology is evolving.
Recent research implicates abnormal motor end plate depolarization in TrP formation.

Purpose of the Study:

To review revised concepts on TrP etiology.
To describe new treatment approaches for TrPs based on updated understanding.

Main Methods:

Exploration of presynaptic, synaptic, and postsynaptic mechanisms of abnormal depolarization.
Review of new therapeutic agents including capsaicin and acetylcholine antagonists.
Examination of osteopathic manipulative techniques applied to TrP treatment.

Main Results:

Abnormal depolarization involves excessive acetylcholine release, acetylcholinesterase defects, or nicotinic acetylcholine-receptor upregulation.
Traditional treatments like ischemic compression are being replaced by techniques such as muscle-energy and myofascial release.
Emerging therapies utilize capsaicin and various acetylcholine antagonists.

Conclusions:

The revised etiology of TrPs necessitates a shift in treatment strategies.
New therapeutic avenues offer promising alternatives for managing TrPs.
Further research into these novel approaches is warranted.

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