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bibliography * The PainScience Bibliography contains plain language summaries of thousands of scientific papers and others sources, like a specialized blog. This page is about a single scientific paper in the bibliography, Gerwin 2004.

An expansion of Simons' integrated hypothesis of trigger point formation

updated
Gerwin RD, Dommerholt J, Shah JP. An expansion of Simons' integrated hypothesis of trigger point formation. Curr Pain Headache Rep. 2004 Dec;8(6):468–75. PubMed #15509461.
Tags: muscle pain, classics, muscle, pain problems

PainSci summary of Gerwin 2004?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided at the bottom of the page, as often as possible. ★★★★☆?4-star ratings are for bigger/better studies and reviews published in more prestigious journals, with only quibbles. Ratings are a highly subjective opinion, and subject to revision at any time. If you think this paper has been incorrectly rated, please let me know.

Until further notice, the most popular provisional explanation for the trigger point phenomenon is the “expanded integrated hypothesis.” It was first presented in this 2004 paper by Drs. Robert Gerwin, Jan Dommerholt, and Jay Shaw. It’s harrowingly detailed and technical. (Read it just below, if you dare!) When abridged and oversimplified, the “expanded” part is largely lost — it was mostly just filling in some details missing from the original integrated hypothesis (“a possible explanation”), which was put forward by Travell and Simons in the second edition of the Big Red Books in 1999, which was in turn an elaboration on the energy crisis hypothesis that debuted in the first edition in 1981. This has been a work-in-progress for quite a while.

Here’s a careful translation of the expanded integrated hypothesis:

Under some circumstances, muscular stresses can cause patches of poor circulation, which results in the pooling of noxious metabolic wastes and high acidity in small areas of the muscle. This is both directly uncomfortable, but also causes a section of the muscle to tighten up and perpetuate a vicious cycle. This predicament is often called an “energy crisis.” It constitutes a subtle lesion. TrPs research has largely been concerned with looking for evidence of a lesion like this.

And here’s the integrated hypothesis fully spelled out. Brace yourself!

It can be hypothesized that the activating event in the development of the TrP is the performance of unaccustomed eccentric exercise, eccentric exercise in unconditioned muscle, or maximal or submaximal concentric exercise that leads to muscle fiber damage and to segmental hypercontraction within the muscle fiber. Adding to the physical stress of such exercise is hypoperfusion of the muscle caused by capillary constriction, which results from muscle contraction. Capillary constriction is increased by sympathetic nervous system adrenergic activity. The resultant ischemia and hypoxia adds to the development of tissue injury and produces a local acidic pH with an excess of protons. Acidic pH results in inhibition of acetylcholinesterase activity, increased release of CGRP, and activation of ASIC on muscle nociceptors. Acidic pH alone (in the absence of muscle damage) is sufficient to cause widespread changes in the pain matrix. However, the breakdown of muscle fibers results in the release of several proinflammatory mediators such as SP, CGRP, K+, 5-HT, cytokines, and BK that profoundly alter the activity of the motor endplate and activity/sensitivity of muscle nociceptors and wide dynamic-range neurons. Motor endplate activity is increased because of an apparent increase in the activity of ACh. This apparent increase in effectiveness is caused by several factors that include an increase in the release of ACh that is mediated by CGRP, presynaptic motor terminal adrenergic receptor activity, and by AChE inhibition caused by CGRPand acidic pH. AChRs are up-regulated through the action of CGRP, creating more docking sites for ACh, thereby increasing the efficiency of binding to the receptor. The taut band results from the increase in ACh activity. Miniature endplate potential frequency is increased as a result of greater ACh effect. Release of BK, K+, H+, and cytokines from injured muscle activates the muscle nociceptor receptors, thereby causing tenderness and pain. The presence of CGRP drives the system to become chronic, potentiating the motor endplate response and potentiating, with SP, activation of muscle nociceptors. The combination of acidic pH and proinflammatory mediators at the active TrP contributes to segmental spread of nociceptive input into the dorsal horn of the spinal cord and leads to the activation of multiple receptive fields. Neuroplastic changes in dorsal horn neurons occur in response to continuous nociceptive barrage, causing further activation of neighboring and regional dorsal horn neurons that now have lower thresholds. This results in the observed phenomena of hypersensitivity, allodynia, and referred pain that is characteristic of the active myofascial TrP.

~ Paul Ingraham

original abstractAbstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Simons' integrated hypothesis proposed a model of trigger point (TrP) activation to explain known TrP phenomena, particularly endplate noise. We propose an expansion of this hypothesis to account for new experimental data and established muscle pathophysiology.

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These five articles on PainScience.com cite Gerwin 2004 as a source:


This page is part of the PainScience BIBLIOGRAPHY, which contains plain language summaries of thousands of scientific papers & others sources. It’s like a highly specialized blog. A few highlights: