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The Trigger Point Identity Crisis

The biological evidence that a trigger point is a lesion in muscle tissue

Paul Ingraham and Brian James, MD • • 15m read

The idea of the “trigger point” — a tender nodule in muscle tissue, often also called a “muscle knot” — has been criticized by some experts.1 Skeptics have pointed to the lack of evidence that trigger point therapy works,2 the lack of a reliable physical exam to identify trigger points in the first place, inadequate evidence that there is even anything to find, and all of this even after several decades of research — an ontological crisis.3 Since a gold standard for diagnosing trigger points by feel (palpation) has never been established,4 and may not be possible even in principle, we must turn to other methods of detection.

Is there evidence of a lesion in muscle? Does it fit with the most popular explanation for them, the “tiny spasm” theory of trigger points?5 This is an overview of the biological evidence of the existence of such a muscle lesion.

A subtle lesion

There is no disease without a lesion.6 For trigger points to “exist,” there has to be some kind of lesion somewhere, a sign in the tissues. The existence of symptoms is not the issue — everyone agrees that people have sore spots associated with pain. This is a pathophysiological identity crisis: what is a trigger point? What causes the symptom?

Specifically, is it what it seems? Is it a lesion in muscle? If so, obviously it’s not an obvious lesion, which is hardly unusual. Many lesions now mastered by medical science were never obvious, many more remain difficult to detect and understand, and there are undoubtedly still some completely unknown lesions — which are probably the relatively minor ones, the transient and tiny, the faint and blurry, the pathological needles in the haystack of biology.

If trigger points are a lesion, they must be a subtle one, mysterious and unconfirmed even after decades of research. If those lesions exist, it’s hardly a surprise that it’s taking so long to figure out something so tricky (but also relatively unimportant in the medical big picture).

The body is a cell state in which every cell is a citizen. Disease is merely the conflict of the citizens of the state brought about by the action of external forces.

Rudolf Virchow, Die Cellularpathologie, 1858

Clinical diagnosis of trigger points is irrelevant

Many clinicians believe they “know” trigger points: they are sure that they can feel them, patients seem to get better when they are treated, and therefore trigger points must exist. Problem solved? Not even close. Those clinical experiences are no more explanatory than the pain that patients experience: a phenomenon to be explained, not the explanation. What professionals think they are doing with patients’ trigger points doesn’t have much to do with the formal identity crisis.

Clinical diagnosis — from physical exam and presumptive treatment — is not how we confirm the presence any pathological phenomenon. Too much pathology is well beyond the reach of inspection and palpation, even well-known pathology. Looking for subtle lesions with a physical exam is fraught with problems.8 The lack of reliability is unsurprising even if there is something there to find — it’s not a deal-breaker.9

Even with a valid and reliable physical exam for trigger points, clinical assessment wouldn’t be the diagnostic bottom line — no more than with many uncontroversial diagnoses.

Even more valuable to the clinician is “presumptive treatment,” based on educated diagnostic gambling: It might be a trigger point, so let’s treat it like one and see what happens. Presumptive treatment goes on constantly in the real world, and it was made famous by House, MD — a show that was almost entirely based on the inherent drama of experimenting on people and making life-or-death bets about what’s really wrong. But, importantly, treatment success does not confirm what the problem was.10

In clinical settings, rigorous confirmation of lesions often never actually happens, even in the case of some dramatic and “obvious” pathologies.11 Trigger points should not be held to a higher standard than other diagnoses.

The sketchy reliability of physical exam and the unclear results of presumptive treatments are just sideshows to the real challenge, relevant but not deal-breakers. They can’t tell us if a pathology exists and how it works. There are just too many ways they can fail and mislead. The existence and nature of a pathology can only be nailed down by histologic study and imaging12 — by direct evidence of a lesion.

For a subtle lesion, it’s a long road to confirmation and characterization. Ultimately, you have to have a critical mass of biological evidence.

The biological evidence for tiny painful spasms

There are four categories of histologic and imaging evidence that provide direct support for a muscle lesion associated with the clinical phenomenon of a trigger point. Although that evidence is imperfect and incomplete, much of it is good quality, and all of it is consistent with the integrated hypothesis of trigger points.

  1. Biopsies and photomicrographs of trigger points.
  2. Scans of trigger points using new imaging technologies, especially elastography.
  3. Measurements the abnormal electrical signature of trigger points (“endplate noise”).
  4. Samples of the acidic, “toxic” tissue chemistry of trigger points.

That’s quite a bit of pathophysiological smoke.

“Photographic” evidence of trigger points

Only a single biopsy study of trigger points in humans has even been done,13 but it’s an important piece of evidence. That single study found “enlarged and darkly-staining muscle fibers compared to elsewhere in the muscle.” The difference is obvious even to the untrained eye.

Tissue stiffness: scans of trigger points using two kinds of elastography

Since the mid-2000s, two key imaging technologies have been used to reveal taut bands of muscle tissue containing focal nodules that previously could only be (unreliably) identified by feel. Vibration sonoelastography (VSE, a rather exotic type of ultrasound) and magnetic resonance elastography (MRE) both detect tissue stiffness (“elasto”!) in different ways. MRE is a well-understood and validated technology.14 It was used by Chen et al in 2007 and 2008 to hunt for trigger points.1516 Sikdar et al did the same with VSE in 2009.17

All of these studies produced good evidence of stiff (“tight”) tissue at the location of suspected trigger points. Dr. David Simons believed these technologies “may open a whole new chapter in the centuries-old search for a convincing demonstration of the cause of MTP symptoms.”18

Endplate noise: the electrical signature of trigger points

The electrical signature of a trigger point is called endplate noise or spontaneous electrical activity (SEA). End plate potentials (EPPs) are the waves of electrical activity that spread out from the point where motor neurons attach to muscles (which have a distinctive saucer-like appearance). EPPs can be measured with electrodes on the skin, or a probe inserted into the muscles. This is electromyography (EMG). The only direct EMG evidence of this phenomenon to date is from Simons et al way back in 2002,19 and then replication from Kuan et al in 2007,20 two small but straightforward studies, both clearly finding EPPs at putative trigger points.

Electromyography isn’t exactly straightforward: it can be tricksy, and there is room for error in both technique and interpretation. However, these were quite simple EMG studies, and it’s promising that two research groups found the same thing.

Other researchers have done experiments based on the assumption that EPPs are associated with trigger points, producing indirect but somewhat supporting evidence.2122

Tissue chemistry of trigger points

Two studies by Shah et al, one in 2005 and then a bit more convincingly in 2008,2324 claim to have shown that the tissue fluid in and around a trigger point is painfully “poisonous” — full of molecules associated with metabolic exhaustion and pain … which is what we’d expect to find if the main theory of how trigger points work is correct. In 2011, Hsieh et al found the same and dug a little deeper.25 Unfortunately, there have been no more attempts to replicate this evidence, which is a good example of how the science of trigger points is exasperatingly half-baked. Although these two papers are a great start, we could really use more and better data.

Some of it may be wrong or misleading, but probably not all of it. And although it’s not enough (or the right kind) of evidence to prove that “trigger points are real” or how they work, it is more than enough to justify clinical interest and continued debate and more research. It’s enough to say that trigger points probably do “exist,” that something goes wrong with muscle tissue.

Are trigger points hot? Probably not, but thermography has been tried

Small thermograph of a trigger point hot spot on the back of a man’s shoulder.

Not an actual thermograph from the study — just an example of what it might look like.

Infrared thermography has been used to look for a “heat signature” of trigger points on the skin, but this evidence is much less of a slam dunk than the two elastographies, MRE/VSE. Dibai-Filho et al found that there is so far “no agreement on skin temperature patterns in the presence of MTrPs” in a few existing studies.26 On the other hand, they think their own method could do the trick (promising if you’re an optimist, and a bit fishy if you’re not).27

Not much of a identity crisis after all

The above evidence is good enough for a moderate degree of confidence that:

  1. the general hypothesis that the clinical phenomenon known as “trigger points” is indeed associated with some kind of muscle lesion
  2. the lesion has characteristics that are consistent with the more specific “integrated hypothesis” that it’s essentially a small contracture

High confidence is not justifed by the evidence available so far. But the evidence is good enough to justify conservative presumptive treatment, with informed consent. No patient should be treated for trigger points without being informed that their nature is speculative and treatment is experimental. No one has any real idea if these lesions can be effectively treated.

The evidence so far is also enough to justify further research, which is by no means a given (many ideas are not worthy of more research, such as chiropractic Spinal Subluxation). To clinch the case, further validation studies should be directed at developing normative values with VSE. It could become a new gold standard of trigger point diagnosis, which could then lend further validity to studies done with other modalities such as EMG.

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About Paul Ingraham

Headshot of Paul Ingraham, short hair, neat beard, suit jacket.

I am a science writer in Vancouver, Canada. I was a Registered Massage Therapist for a decade and the assistant editor of for several years. I’ve had many injuries as a runner and ultimate player, and I’ve been a chronic pain patient myself since 2015. Full bio. See you on Facebook or Twitter., or subscribe:

What’s new in this article?

Four updates have been logged for this article since publication (2016). All updates are logged to show a long term commitment to quality, accuracy, and currency. more Like good footnotes, update logging sets apart from most other health websites and blogs. It’s fine print, but important fine print, in the same spirit of transparency as the editing history available for Wikipedia pages.

I log any change to articles that might be of interest to a keen reader. Complete update logging started in 2016. Prior to that, I only logged major updates for the most popular and controversial articles.

See the What’s New? page for updates to all recent site updates.

2016 — Added some detail about electromyography and the results of a studies of endplate noise.

2016 — Added Dr. James’ bio, miscellaneous minor corrections and editing.

2016 — Editing and integration with other related articles.

2016 — Important clarifications about presumptive treatment, and a more precise definition of “spasm” and the difference from non-neurologically mediated contracture. Miscellaneous editing.

2016 — Publication.


  1. Quintner JL, Bove GM, Cohen ML. A critical evaluation of the trigger point phenomenon. Rheumatology (Oxford). 2015 Mar;54(3):392–9. PubMed 25477053 ❐ Quintner, Cohen, and Bove think the most popular theory about the nature of trigger points (muscle tissue lesions) is “flawed both in reasoning and in science,” and that treatment based on that idea gets results “indistinguishable from the placebo effect.” They argue that all biological evidence put forward over the years is critically flawed, while other evidence leads elsewhere, and take the position that the debate should be ended. (They also point out that the theory is treated like an established fact by a great many people, which is definitely problematic.)

    Importantly, there are no other noteworthy examples of criticism of the trigger point construct published in peer-reviewed journals. This and some blogging is the extent of it. This is notably different from other prominent, controversial treatment ideas like chiropractic subluxations, acupuncture, homeopathy, and reiki, which have been thoroughly excoriated by skeptics both formally and informally for a long time (decades in some cases).

  2. Trigger point massage 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 of the less-bad studies 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.
  3. Ontology deals with questions concerning what entities exist or may be said to exist, and how such entities may be grouped, related within a hierarchy, and subdivided according to similarities and differences.
  4. A diagnostic gold standard requires a test with both validity and inter-rater reliability: confirmation that it measures what it is supposed to measure, and that different clinicians can all detect the same thing with some consistency.
  5. The “expanded integrated hypothesis” was presented by Dommerholt, Gerwin, and Shah in 2004. It’s detailed and technical! When abridged and oversimplified, it closely resembles the integrated hypothesis (“a possible explanation”) put forward by Travell and Simons in the first edition of their famous textbook in 1981. The expanded integrated hypothesis 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, but also causes a section of the muscle to tighten up — a micro cramp — 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.

  6. This was the insight of Rudolph Virchow, father of medical pathology, and which became one of the pillars of scientific medicine: if we are sick, it’s because some cells, somewhere, are damaged or misbehaving somehow.
  7. That doesn’t mean nerves aren’t involved — never bet against the involvement of nerves! — just that the contraction probably was not called for by the central nervous system. That kind of (neurologically mediated) contraction has many features that are not consistent with the clinical phemomenon of trigger points, like contraction of entire motor units.
  8. The wide range of training and experience in musculoskeletal evaluation, the subjectivity of palpation, the cognitive distortion of pareidolia (perceiving patterns or findings where none exist) and sampling bias inherent in palpation; and signal detection theory, false positives and negatives plague most diagnostic challenges. Even well-trained practitioners should be expected to fail: they are the most likely to be contaminated by confirmation bias, due to a strong a priori belief in what they are looking for.
  9. In any case the lack of inter-rater reliability in trigger point assessment has been overstated by critics: it’s just unknown, not proven to be unreliable.
  10. Pathologies overlap. Problems get better on their own, or remit and then relapse. Every episode of House featured treatment “successes” that quickly proved to be frightening illusions. In real life, the comeuppance is rarely so conveniently quick and clear.
  11. The patient’s history, physical exam results, test results, and the apparent outcome of presumptive treatment all contribute to a confidence level about a diagnosis, which tentatively assumes the existence. If a pathology is well understood and has obvious signs, this can be quite straightforward: “You have cancer.” And there are times when a more definitive diagnosis is necessary to guide treatment (e.g. cancer, emergent surgical issues). But the point is that a diagnosis is usually “just a theory,” which gets tested by treatment, rather than confirmed by unambiguous identification of a lesion. Actually understanding and formally characterizing pathologies in the first place is not a clinician’s job.
  12. Histologic study is needed to identify deviations from normalized physiological parameters at the microscopic scale, and imaging to identify tissue changes on a macroscopic level.
  13. Reitinger A, Radner H, Tilscher H, et al. [Morphologic study of trigger points]. Manualle Medizin. 1996;34:256–252.
  14. Mariappan YK, Glaser KJ, Ehman RL. Magnetic resonance elastography: a review. Clin Anat. 2010 Jul;23(5):497–511. PubMed 20544947 ❐ PainSci Bibliography 54049 ❐
  15. Chen Q, Bensamoun S, Basford JR, Thompson JM, An KN. Identification and quantification of myofascial taut bands with magnetic resonance elastography. Arch Phys Med Rehabil. 2007 Dec;88(12):1658–1661. PubMed 18047882 ❐
  16. Chen Q, Basford J, An KN. Ability of magnetic resonance elastography to assess taut bands. Clin Biomech (Bristol, Avon). 2008 Jun;23(5):623–9. PubMed 18206282 ❐ PainSci Bibliography 54057 ❐
  17. Sikdar S, Shah JP, Gebreab T, et al. Novel applications of ultrasound technology to visualize and characterize myofascial trigger points and surrounding soft tissue. Arch Phys Med Rehabil. 2009 Nov;90(11):1829–38. PubMed 19887205 ❐ PainSci Bibliography 54058 ❐
  18. Simons DG. New Views of Myofascial Trigger Points: Etiology and Diagnosis. Archives of Physical Medicine & Rehabilitation. 2008 Jan;89(1):157–159. PubMed 18164347 ❐
  19. Simons DG, Hong CZ, Simons LS. Endplate potentials are common to midfiber myofacial trigger points. Am J Phys Med Rehabil. 2002 Mar;81(3):212–22. PubMed 11989519 ❐ Simons, Hong, and Simons looked for three kinds of EPPs at trigger points, in the taut bands of muscle found with them, and endplate zones (the neuromuscular junction). They examined one test site and two control sites in eleven muscles in ten subjects. They found endplate noise at all the trigger points, in four muscles at endplate zones away from TrPs, and nowhere else. The closer they were to a TrP, the more endplate noise they found. They concluded that “endplate noise seems to be characteristic of, but is not restricted to, the region of a myofascial trigger point.”
  20. Kuan TS, Hsieh YL, Chen SM, et al. The myofascial trigger point region: correlation between the degree of irritability and the prevalence of endplate noise. Am J Phys Med Rehabil. 2007 Mar;86(3):183–9. PubMed 17314703 ❐ In 32 patients with presumed trapezius trigger points, Kuan et al. found endplate noise at the location of the putative trigger points, but not in adjacent muscle, concluding that “The irritability of an MTrP is highly correlated with the prevalence of endplate noise in the MTrP region of the upper trapezius muscle.”
  21. Hsieh YL, Chou LW, Joe YS, Hong CZ. Spinal cord mechanism involving the remote effects of dry needling on the irritability of myofascial trigger spots in rabbit skeletal muscle. Arch Phys Med Rehabil. 2011 Jul;92(7):1098–105. PubMed 21529778 ❐
  22. Ge HY, Fernández-de-Las-Peñas C, Yue SW. Myofascial trigger points: spontaneous electrical activity and its consequences for pain induction and propagation. Chin Med. 2011;6:13. PubMed 21439050 ❐ PainSci Bibliography 54060 ❐
  23. Shah JP, Phillips TM, Danoff JV, Gerber LH. An in vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle. J Appl Physiol. 2005;99(5):1977–1984. PainSci Bibliography 56247 ❐
  24. Shah JP, Danoff JV, Desai MJ, et al. Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points. Arch Phys Med Rehabil. 2008;89(1):16–23. PubMed 18164325 ❐
  25. Hsieh YL, Chou LW, Joe YS, Hong CZ. Spinal cord mechanism involving the remote effects of dry needling on the irritability of myofascial trigger spots in rabbit skeletal muscle. Arch Phys Med Rehabil. 2011 Jul;92(7):1098–105. PubMed 21529778 ❐
  26. Dibai-Filho AV, Guirro ECO, Ferreira VTK, et al. Reliability of different methodologies of infrared image analysis of myofascial trigger points in the upper trapezius muscle. Braz J Phys Ther. 2015;19(2):122–8. PubMed 25993626 ❐ PainSci Bibliography 54063 ❐
  27. Dibai-Filho AV, Guirro RRd. Evaluation of myofascial trigger points using infrared thermography: a critical review of the literature. J Manipulative Physiol Ther. 2015 Jan;38(1):86–92. PubMed 25467609 ❐


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