Skepticism about trigger points (TrPs) and myofascial pain syndrome surged with the publication of an important opinion paper in late 2014. But this started more than 20 years before that …
- In 1994, Drs. John Quintner and Milton Cohen published a paper in The Clinical Journal of Pain1 making the case against the popular notion that myofascial pain syndrome (MPS) is caused by little muscle malfunctions known as “trigger points.” This was back when the idea was starting to get entrenched as conventional wisdom.
- Two decades later, they revisited the topic armed with another couple decades of inconclusive trigger point science. They published the same arguments in Rheumatology (Oxford)2 — a bit of a step up in impact factor.
- And it had some impact. A long rebuttal was soon published in Journal of Bodywork & Movement Therapies, by Drs. Dommerholt and Gerwin: “A Critical Evaluation of Quintner et al: Missing the Point.”3 (Other credible critics have written much more strongly worded responses.4)
- And that was soon followed by a longish letter in response: “Did we miss the point?”5 (Spoiler alert: they didn’t think they missed the point.)
- Team Quintner also published some thoughts on Body In Mind,6 and then also on Dr. Fred Wolfe’s FMPerplex.org,7 both widely shared and cited.
- Since then, several well-known bloggers and skeptics have piled on with “me too” editorializing, mainly supporting and summarizing the arguments already laid out by Quintner et al.
- In late 2015, an unabridged version of Quintner et al. was published as “Myofascial pain: a bogus construct,” a chapter in a new textbook.8
So, it’s a scholarly pissing match! A polarizing poopstorm! To an almost alarming degree, it seems that everyone is now on one team or the other. I have biases that pull me in both directions.9 Lucky for me, I don’t actually have to choose a team to root for: I’m just reporting on the key features of the public debate, for readers who are wondering what all the fuss is about.
The controversy is not about whether trigger points are “real”
Because of this argument/debate, many professional now assert that trigger points are not “real.” They often do this without making a critical distinction between the clinical phenomenon (which no one disputes) and the explanation for it (desputed by many).
Literally everyone, including Quintner et al., agrees that people do often suffer from many aching spots in their soft tissues. There’s even broad agreement about some their clinical characteristics (they are sensitive when poked, for instance).
The argument is about almost everything else — what they are, how they work, whether they can be felt, and so on. It’s mainly an inside baseball argument about the explanation for the problem commonly known as “trigger points.”
If you are skeptical about the nature of trigger points, please beware of suggesting to patients that they aren’t “real.”
What idea exactly is on trial?
The “expanded integrated hypothesis” is on trial. It is the “official” explanation for those sore spots, insofar as it is the only one that is widely known and accepted. In a nutshell, the hypothesis says that a trigger point is a kind of tiny cramp in muscle tissue. It has been exhaustively described in many texts, books, papers, articles, and this website. It was presented by Dommerholt, Gerwin, and Shah in 2004. It’s detailed and technical!10 (Go ahead, read that footnote, I double dare ya.) When abridged and oversimplified, it still closely resembles the integrated hypothesis (“a possible explanation”) put forward by Travell and Simons in 1981. It basically says this:
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 and 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.
Quintner et al. believe that what seems to be muscle pain is not caused by any problem with muscle tissue itself. They think the integrated hypothesis is “flawed both in reasoning and in science” and “an invention without a scientific basis.” They think it’s therapy babble.
They could be right. They could also be wrong. Their objections are as uncertain as the hypothesis itself.
Agree or disagree, the critical evaluation is important
Even today, trigger points remain an idea on the fringes of health care, despite their alleged importance. There is a conventional wisdom about them, but it’s certainly not mainstream, and the scientific argument about it is even more obscure. This topic is not in any spotlight.
Although medical history is peppered with competing theories and debate about the nature of sore spots, MPS, and TrPs, direct criticism of the modern conventional wisdom is rare. Almost everyone not only uncritically accepts the conventional wisdom, but treats patients as though it were an established fact and a firm foundation for expensive therapy. Treating trigger points as if the conventional wisdom is correct is a big business. It may be dwarfed by the scale of most health care, but it is still a large slice of the musculoskeletal medicine pie.
In other words, TrPs do need critical analysis. Right or wrong, what Quintner et al. have done is valuable and important. We need to hear from anyone who believes the Emperor has no clothes.
Three main problems, according to Team Quintner
Quintner et al. make three main arguments against MPS/TrPs:
- Treatment based on these ideas produces results “indistinguishable from the placebo effect.”
- The biological evidence of muscle pathology is unconvincing, while some other evidence leads elsewhere, and so the old picture of trigger points “remains conjecture in the face of conflicting data.”
- They argue that the validity of MPS is based on a major logical error that “exemplifies circular reasoning: TrPs cause myofascial pain because painful muscles contain them.”
They also present “testable hypotheses are identified that point the way to neuroscientific explanations for the observed clinical phenomena.” These ideas can’t show that the IH is wrong any more than belief in one god can disprove another, but their plausibility is relevant.
More common ground than you’d think
Despite the appearance of a strong disagreement, I see a lot of common ground. On the one hand, Quintner et al. concede that people experience pain and sensitivity that seems to be in muscle tissue. The pain is real, and the need for an explanation and effective treatment is real:
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.
Meanwhile, Team Dommerholt concedes that we still don’t really know what’s going on:
A distinct mechanistic understanding of this disorder does not yet exist.
… there has never been a credible anatomic pathology associated with myofascial TrPs.
There are several more concessional statements like this in their rebuttal (which Quintner et al. gleefully quote back at them).11 Dommerholt et al. don’t seem to mind the uncertainty. They know they’re working with “just a theory.”
We did not present new data as dogma, but followed the scientific process of re-evaluating the Integrated TrP Hypothesis as new data became available.
So Quintner et al. do not deny that there is a painful phenomenon, and propose an alternative explanation that is strikingly similar: just one sort of irritated tissue (nerve) instead of another (muscle). And just as unvalidated. Just a theory. And Dommerholt et al. obviously concede that the science is half-baked and we don’t know for sure how this kind of pain works — we just have circumstantial evidence.
With all this common ground, what’s the argument about?!
Quittin’ time: the price of absolutism
Quintner et al. take a notably extreme view. They aren't merely critical of the integrated hypothesis, they think it has no value whatsoever. They argue that the idea of trigger points is completely bankrupt.
The construct of MPS caused by TrPs remains conjecture. All working hypotheses derived from this conjecture have been refuted and therefore the theory can be discarded.
MTrP theory has been well and truly refuted
It is time to shine the light of critical inquiry elsewhere in pursuit of explanations for these clinical phenomena.
This is such a dramatic conclusion I think it’s fair to say that it is unwisely absolutist: they are not just saying that the conventional wisdom has problems, they are declaring it dead.
To convinct the integrated hypothesis of fraud and send it to the electric chair, its “guilt” must be established “beyond a reasonable doubt.” To remain viable as an unproven hypothesis, the defense only has to establish that the idea still has some merit and further investigation is worthwhile. Which is not a high bar to clear, particularly when everyone agrees there’s a painful problem that needs explaining. I think Dommerholt et al. step over that low bar fairly easily. They present many evidence-informed counter-arguments, which constitute “reasonable doubts,” and conclude:
Quintner et al. have not succeeded in providing sufficient evidence that the current TrP hypotheses should be rejected.
They aren’t saying it should be accepted uncritically — just that it’s not entirely washed up. That’s a more moderate position, and a much easier one to defend.
I’ll just be sitting on this fence over here
I endorse the spirit of what Quintner et al. are trying to do. Their criticisms are valuable, and I am moved by some of their arguments — but I am not moved off the fence. I think there are reasonable doubts about the “guilt” of the integrated hypothesis. I cannot in good conscience convict it of fraud.
For instance, Quintner et al. have argued that the treatment of trigger points produces results “indistinguishable from the placebo effect.” This is clearly debatable, and I think there is a strong case to be made that the evidence is inadequate and inconclusive — an absence of evidence, not evidence of absence.12 (I get into much more detail on this point in my main “trigger point doubts” article.)
Quinter et al. represent an small expert minority of skeptics on this topic. There are no other noteworthy peer-reviewed papers expressing similar views. There is no body of research supporting their own competing hypothesis — indeed, “the three included references do not provide any support for their assumption.”13 There are no books that you can recommend to someone who has trigger point doubts. None of this means that they are wrong, but it’s relevant context.
Compare and contrast this with other ideas that have been declared dead, where there is an avalanche of objections in the medical literature: vaccines causing autism, homeopathy, chiropractic subluxation theory, acupuncture, and so on. Those are dead horses (or, at the very least, the controversies about them are heavily skewed in favour of the skeptics).
In contrast, the hypothesis of an ubiquitous uncomfortable metabolic crisis in muscle seems merely wounded. Unilaterally declaring its death seems premature and overconfident to me. This a legitimate scientific controversy, and debate and study should continue.
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About Paul Ingraham
I am a science writer, former massage therapist, and I was the assistant editor at ScienceBasedMedicine.org for several years. I have had my share of injuries and pain challenges as a runner and ultimate player. My wife and I live in downtown Vancouver, Canada. See my full bio and qualifications, or my blog, Writerly. You might run into me on Facebook or Twitter.
What’s new in this article?
2019 — Added citation to another rebuttal to Quintner et al: see Critique of Quintner et al. 2015.
- Quintner JL, Cohen ML. Referred pain of peripheral nerve origin: an alternative to the "myofascial pain" construct. Clin J Pain. 1994 Sep;10(3):243–51. PubMed #7833584 ❐ PainSci #54775 ❐
- Quintner JL, Bove GM, Cohen ML. A critical evaluation of the trigger point phenomenon. Rheumatology (Oxford). 2015 Mar;54(3):392–9. PubMed #25477053 ❐
- Dommerholt J, Gerwin RD. A Critical Evaluation of Quintner et al: Missing the Point. J Bodyw Mov Ther. 2015 Apr;19(2):193–204. PubMed #25892372 ❐
- Brentbrookbush.com [Internet]. Brookbush B. Critique of Quintner et al. 2015; 2019 February 6 [cited 19 Feb 19]. This is a fierce critique of Quintner et al, more pointed and strongly worded than Dommerholt et al’s more formal rebuttal. It will be warmly received by the choir, but dismissed as crankery and ax grinding by anyone on “Team Quintner.” I’m happy to see it added to the debate.
I agree with most of the key points made by Brookbush. In particular, I believe he is especially correct to point out that “the authors consistently misuse and misrepresent citations. If you do not look at each individual citation you would assume this paper is well supported. It is not.” And that “most of the research and hypotheses on trigger points were not even addressed in this paper.” And finally, I also particularly agree that Quintner et al. attack “claims that were never made.”
- Quintner et al. Letter to Journal of Bodywork & Movement Therapies. Response to Dommerholt and Gerwin: Did we miss the point? 2015.
- BodyInMind.org [Internet]. Moseley L, Quintner JL. A critical evaluation of the trigger point phenomenon; 2015 Mar 4 [cited 15 Mar 5].
- FMperplex.com [Internet]. Quintner JL, Bove GM, Cohen ML. The Decline and Fall of the Trigger Point Empire; 2015 Mar 5 [cited 15 Nov 21].
- Quintner JL, Cohen ML. Oxford Textbook of Musculoskeletal Medicine. 2nd ed. Oxford University Press; 2015. Chapter 14: Myofascial pain: a bogus construct; p. 134–42.
- I have several relevant conflicts of interest, but they pull me in different directions. I profit substantially from a popular book about trigger points, and yet I also have my own well-known doubts about them, as do many of my mentors and betters, and I have a strong reputation as a skeptic that is part of my “brand.” It would definitely be awkward if I had to “pick a team.”
- 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 CGRP￼and 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.
- I particularly had to chuckle at their tortuous phrasing when addressing the lack of evidence that dry needling is an effective therapy: “We agree with Quintner et al that studies of the efficacy of TrP interventions have shown such marked statistical heterogeneity that it can be difficult to evaluate outcomes.” In other words: “After much research, we still haven’t really got the answer we’d like to see.”
- Trigger point masssage has never been subjected to even one sufficiently rigorous clinical trial. There are only about a dozen studies worth knowing about, and all have serious flaws and were conducted by researchers with a high risk of bias. Most report only minor benefits, and a couple are blatantly negative despite positive-sounding conclusions (if you look at the actual data). Only one (Aguilera 2009) reports a more robust effect; three other of the less-bad studies papers are Hodgson 2006, Gemmell 2008, and Morikawa 2017. I’ve reviewed all the evidence thoroughly in my main trigger points tutorial, but the bottom line is clear: the evidence is promising if you’re a trigger point therapist, but damningly faint praise if you’re a skeptic, and just inconclusive if you don’t have a dog in the fight.
- They continue: “While we appreciate the paper by Bove et al. about increased ectopic mechanical sensitivity in the axons of nocicepters, this paper does not provide any explanation of myofascial pain or even of the formation of TrPs (Bove et al., 2003). The other two references by Dilley et al. are valuable contributions to the scientific literature about mechanosensitivity of peripheral nerves, but the connection to myofascial pain remains unclear (Dilley and Bove, 2008; Dilley et al., 2005). Even a more recent publication by Bove and Dilley about ongoing or spontaneous nociceptive activity does not add anything to a better understanding of the underlying mechanisms of myofascial pain and TrPs (Bove and Dilley, 2010).”