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A famous critique of the "trigger point phenomenon"

PainSci » bibliography » Quintner et al 2015
Tags: muscle pain, injections, trigger points doubts, classics, deep, bad news, muscle, pain problems, medicine, treatment

Eighteen articles on PainSci cite Quintner 2015: 1. When to Worry About Low Back Pain2. The Complete Guide to Trigger Points & Myofascial Pain3. Quite a Stretch4. The Complete Guide to Low Back Pain5. The Complete Guide to Chronic Tension Headaches6. The Complete Guide to Neck Pain & Cricks7. Tennis Ball Massage for Myofascial Trigger Points8. Basic Self-Massage Tips for Myofascial Trigger Points9. Review of The Trigger Point Therapy Workbook10. A Historical Perspective On Aches ‘n’ Pains11. Can Massage Therapy Cause Nerve Damage?12. Toxic Muscle Knots13. Therapy Babble14. Trigger Point Doubts15. The Trigger Point Identity Crisis16. Trigger Points on Trial17. The 3 Basic Types of Pain18. Neurodynamic Stretching

PainSci commentary on Quintner 2015: ?This page is one of thousands in the 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 wherever possible.

Quintner, Cohen, and Bove argue that the common picture of trigger points as lesions in muscle and soft tissue, spelled out most formally in Gerwin 2004, is “flawed both in reasoning and in science,” and that treatments (e.g. massage, needling) based on that idea produces results “indistinguishable from the placebo effect.” They believe that all of the biological evidence put forward over the years (like Shah 2008) is critically flawed in one way or another, while other evidence leads elsewhere, and so the old picture of trigger points “remains conjecture in the face of conflicting data.” They also point out that the theory is inappropriately treated like an established fact by a great many people.

Not even these fierce critics of trigger points deny that people have pain that seems to come from their muscles. But if it’s not coming from the muscle, where is it coming from? They briefly discuss two other ideas of their own: inflamed nerve fibres, and referred pain and tenderness from deeper structures. They do not thoroughly explore or defend either idea.

Neuritis is undoubtedly worth investigating, but it requires us to believe that nerve axons are routinely inflamed for no apparent reason, which doesn’t seem much different than the theory it is supposed to replace. The evidence cited to support it is just as limited as the evidence for trigger points, if not more so (just a few papers, all from the authors themselves, or their research colleagues).

The proposal of “referred pain and tenderness” from deeper tissues with unspecified troubles and/or “altered central nociceptive mechanisms” is imprecise. We know that these mechanisms probably exist, but there is not a jot of evidence that they have anything to do with the subjective experience of “muscle pain.” This is just a proposal to look somewhere other than the integrated hypothesis.

This paper is an abridged version of a much more detailed argument laid out in a chapter of an extremely expensive textbook: see Quintner.

~ Paul Ingraham

original abstract Abstracts 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.

The theory of myofascial pain syndrome (MPS) caused by trigger points (TrPs) seeks to explain the phenomena of muscle pain and tenderness in the absence of evidence for local nociception. Although it lacks external validity, many practitioners have uncritically accepted the diagnosis of MPS and its system of treatment. Furthermore, rheumatologists have implicated TrPs in the pathogenesis of chronic widespread pain (FM syndrome). We have critically examined the evidence for the existence of myofascial TrPs as putative pathological entities and for the vicious cycles that are said to maintain them. We find that both are inventions that have no scientific basis, whether from experimental approaches that interrogate the suspect tissue or empirical approaches that assess the outcome of treatments predicated on presumed pathology. Therefore, the theory of MPS caused by TrPs has been refuted. This is not to deny the existence of the clinical phenomena themselves, for which scientifically sound and logically plausible explanations based on known neurophysiological phenomena can be advanced.

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