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 out a lack of reliable physical exam and inadequate evidence that there is even anything to find, even after several decades of research — an ontological crisis.2 Since a gold standard for diagnosing trigger points by feel (palpation) has never been established,3 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?4 This is an overview of the biological evidence of the existence of such a muscle lesion.
There is no disease without a lesion.5 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
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 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.7 The lack of reliability is unsurprising even if there is something there to find — it’s not a deal-breaker.8
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.9
In clinical settings, rigorous confirmation of lesions often never actually happens, even in the case of some dramatic and “obvious” pathologies.10 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 imaging11 — 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.
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.
That’s quite a bit of pathophysiological smoke.
Only a single biopsy study of trigger points in humans has even been done,12 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.
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) and magnetic resonance elastography (MRE) both detect tissue stiffness (“elasto”!) in different ways. MRE is a well-understood and validated technology.13 It was used by Chen et al in 2007 and 2008 to hunt for trigger points.1415 Sikdar et al did the same with VSE in 2009.16
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.”17
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 2002,18 and then replication from Kuan et al in 2007,19 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.
Two studies by Shah et al, one in 2005 and then a bit more convincingly in 2008,2223 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.24 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” — something wrong with muscle tissue.
Ideally, we need to firm up vibration sonoelastography
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.25 On th other hand, they think their own method could do the trick (promising if you’re an optimist, and bit fishy if you’re not).26
We believe that the above evidence is good enough for a moderate degree of confidence that:
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.
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.
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— Added some detail about electromyography and the results of a studies of endplate noise.
— Added Dr. James’ bio, miscellaneous minor corrections and editing.
— Editing and integration with other related articles.
— Important clarifications about presumptive treatment, and a more precise definition of “spasm” and the difference from non-neurologically mediated contracture. Miscellaneous editing.
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).BACK TO TEXT
The “expanded integrated hypothesis” was presented out 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:
BACK TO TEXT
Under some circumstances, muscular stresses can causes 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.