Critique of:

Quintner, J. L., Bove, G. M., & Cohen, M. L. (2014). A critical evaluation of the trigger point phenomenon. Rheumatology54(3), 392-399.

by Brent Brookbush DPT, PT, COMT, MS, PES, CES, H/FS, HMS

Author's Note:

I generally feel that publicly critiquing other credentialed professionals adds to the culture of "trolling", and with that in mind I try to refrain. However, there are certain claims being made in the industry, which are supported by little more than opinion, fallacies and the misrepresentation/interpretation of research. This paper falls into that category. The paper is full of biased language, false accusations, logical missteps, and academic dishonesty in the form of egregious errors in citation. This paper should not have been published, should be retracted, marks a poor job by the editorial staff of Rheumatology. As you read my critiques, please keep in mind, they were not originally compiled with the intent of criticizing the authors. I was reviewing the article and its bibliography for continued work on my article/course on Muscle Fiber Dysfunction and Trigger Points (as well as other associated courses). Rather than the Quintner et al. paper adding wonderful alternative views, theories and citations, it proved to be a good example of how bias can destroy objectivity, and how poor citation can destroy trust in the authors and potentially the journal. Further, I attempted to contact Rheumatology with my notes in attempt to have the paper retracted (without making these notes public). They did not respond. I have done my best to only report "objective" errors, and minimize my subjective complaints (opinions) about this article.

Big thank you to Paul Ingraham and his blog, Painscience.com, it was his articles on this topic that made me aware of the debate. He has been kind enough to mention this critique - Trigger Point Doubts.

Summary of Issues:

  • Biased wording throughout, demonstrating a lack of objectivity.
  • Based on the number of available studies on this subject matter, there are relatively few citations.
  • The number of reviews, editorials and articles cited (not original studies) make this a tertiary resource.
  • Egregious mis-citation - 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.
  • There are many logical errors (fallacies and missteps)

    • Implying that a lack of evidence is evidence of absence
    • Claiming statements of correlation are proof of circular logic
    • A few points in the paper use gaps in the body of research as a whole, or an inherent weakness of a a study type, as an argument against the trigger point hypothesis. These arguments should not be viewed as trigger point specific critique (e.g., inherent weaknesses of cadaver studies or animal studies).
    • Creating "strawman arguments" by refuting claims that were never made by the authors being "critically evaluated".

  • Cherry-picking; certain points of the paper seem to have purposefully omitted studies.
  • This paper offers an alternative hypothesis that is so poorly supported it is hard to compare it to current hypotheses.
  • This paper does not offer alternative treatment options, suggesting the authors wish to replace research-supported techniques with no intervention at all, or replace research-supported techniques with interventions that are not well-supported.

Upper Body Trigger points: Posterior Deltoid, Upper Trapezius and Levator Scapulae Upper Body Trigger points: Posterior Deltoid, Upper Trapezius and Levator Scapulae

Critique:

Italicized text is quoted from Quintner et al. (2014)

  • Bullets are commentary

Evolution of MPS theory

It has long been believed that muscle pain might originate from focal lesions within connective tissues . The initial description put forward by Stockman was of fibrositic nodules, which were suggested to harbour low-grade inflammation that activated sensory fibres innervating muscle spindles and the interstitial tissues between muscle fibres. However, Stockman’s claim that ‘the essential lesion is a chronic inflammatory hyperplasia of white fibrous tissue in patches’ has never been confirmed .

  • Keep in mind, Quintner et al. are criticizing studies published between 1903 - 1941 for the inability to see microscopic lesions in living tissue. The issue here is actually insufficient technology, which is still an issue today. This isn't a critique of trigger point research, as much as a critique on available technology in all research. Ironically the inability to see microscopic lesions in living tissue also creates the same issues in the author's alternative "neuroscientific explanation".
  • Further, this paragraph implies a lack of evidence is evidence of absence. This is a logical fallacy, a lack of evidence means there is no support for the claim, either for or against.

Travell and Simons composed anatomical charts of TrPs and their characteristic pain referral patterns. However, it appears that their diagrams had ‘sometimes been chosen arbitrarily, there being no accepted standard’ .

  • This is actually a paraphrased statement of a paraphrased statement of a text that summarizes available research at the time of publication, and the paraphrase here misrepresents the intent of the statement being alluded to. That is, this is Quintner et al. referring to Lewitt referring to a textbook by Travell and Simons. Although some of the methods used by Travell and Simons would not be publishable as “formal studies”, the trigger point maps were constructed from injection and diagramming of all muscles over years of practice. This would be the equivalent of a systematic "pilot study". This was a monumental project unto itself that has lead to volumes of research.

Speculation took a new turn when Travell and Rinzler [ 5 ] conceptualized that pain felt in voluntary muscles is myofascial in origin. Their claim, that ‘trigger areas in myofascial structures can maintain pain cycles indefinitely’ [ 5 ], was reminiscent of the vicious circle hypothesis.

  • Quintner et al. continue to use biased language throughout the article; however, their replacement of words like hypothesis generation, inquiry and theory, with words like speculate, conjecture and "make up" should have been red flags to the editors that this paper lacks objectivity.  Hypothesis generation and theory are a key part of the discovery process inherent in the development of any research project. Further, papers published in scientific journals are supposed to be scientific, that is, rely on the scientific method, which in large part attempts to replace bias with objectivity.  If Rheumatology wants to be respected as a scientific journal, some attempt to reduce bias in publications should be made.
  • Note, the vicious cycle hypothesis refers to a hypothesized "positive feedback". Positive feedback loops are fairly common in the human body (for example, the inflammatory cascade). The author's of this paper try to claim that this is evidence of circular logic, which is a false accusation.

However, it appears that their diagrams had ‘sometimes been chosen arbitrarily, there being no accepted standard’ .

  • Frightening level of mis-citation: The citation here makes it appear as if the statement is supported by original work; however, it actually took a significant effort to find the quote buried in an editorial (opinion) section of a paper by Lewitt. Again, this amounts to paraphrasing someone else's opinion of a textbook, and altering it enough with biased language to mislead.

To explain the puzzling onset of pain in ostensibly lesion-free tissues, Travell and Simons [ 14 ] found it necessary to invent the latent TrP, a site of potential tenderness within a muscle unassociated with spontaneous pain but having the potential to be activated by a myriad of factors, within or outside the body. In an attempt to extend the theory to explain more widespread pain, they claimed that TrPs could self-propagate to become secondary TrPs in other muscles and even to metastasize throughout the bodily musculature.

  • "Found it necessary to invent" are obviously judgmental words that imply bias on the part of Quintner et al. Latent trigger points were found (and confirmed in prevalence studies following the referenced publication) by Travell and Simons, and ideas about their origin and influence on movement were discussed in various publications. However, Travell and Simons were far more conservative with their implications, and clearly communicated the difference between their objective findings and their interpretation of those findings.
  • Note, there is no citation in the second half of this paragraph. It is essentially the authors biased interpretation of the work cited. It is incredibly important that you the reader, understand that not a single resource could be found that made the bolded statement in the second half of the paragraph.

The recent conjecture that peripheral pain generators can reside within muscles (i.e. myofascial tissues), and be responsible not only for spontaneous pain but also for the initiation and maintenance of profound changes within the CNS (known as central sensitization) rests upon these dubious premises [ 17 , 18 ]. Similarly, prominent rheumatologists are among those who maintain that TrPs are responsible for the initiation and maintenance of the syndrome of chronic widespread pain (FM) [ 17–23 ].

  • Conjecture and dubious are obviously judgmental words that imply bias on the part of Quintner et al.
  • Further, these citations have almost nothing to do with the statement being made. 17, 18, 22 and 23 are articles by respected experts in the field discussing the prevalence of trigger points in those with fibromyalgia and myofascial pain syndrome. 19 is an RCT demonstrating that sensitization can be maintained by muscle afferents. 20 is a study that demonstrates mapping the pain and referral patterns of stimulated active trigger points, mimics the pain pattern described by fibromyalgia patients. Although 17, 18, 22 and 23 we may be able see past, as these are secondary sources susceptible to author bias (although still strangely not related to the claims made by Quintner et al). 19 and 20 are high quality studies that refute the statement made in this paragraph.

An extensive review identified at least 19 different sets of diagnostic criteria used for the MPS/TrP syndrome, and concluded there was a lack of consistency and consensus on case definition [ 26 ]. The authors suggested that until reliable diagnostic criteria had been established, ‘there is a need for greater transparency in research papers on how a case of MTrP pain syndrome is defined, and claims for effective interventions in treating the condition should be viewed with caution’ [ 26 ]. A similar study found that the diagnosis of MPS from putative TrPs was based on a clinical test of unknown reliability and validity with no accepted reference standard [ 27 ].

  • This is not wrong, but likely hyperbole. Certain criteria are consistent, for example the presence of taut bands, palpable nodules, trigger points, referral pain and additional contributing factors such as posture, mental or emotional stress are consistently used criteria. Further, the lack of reliability studies does not imply that that testing is not reliable (again, the absence of evidence is not evidence of absence). More research is certainly needed, but the lack of support in either direction does not support the stance of Quintner et al.

Beliefs in TrP theory and the associated concept of MPS continue to be strongly held [ 24 ], despite the fact that such beliefs exemplify circular reasoning: TrPs cause myofascial pain because painful muscles contain them [ 25 ].

  • This statement is biased and odd. I could not find a single study that circular logic, although there are numerous correlation studies. Note, correlation and circular logic are not the same thing. Observation of a relationship, does not imply that the relationship itself exists because of the relationship.
  • The way this sentence alone is cited should cast major doubts on the credibility of the authors: The first citation is a text book by Mense, Simons and Russel. Essentially, supporting the fact that significant evidence exists to support a correlation between trigger points and MPS. Citation "25" is Quintner himself. So, the damning part of this statement is supported by the guy making the statement. If you are not paying attention you would think this statement has the unbiased support of an objective resource... nope... just a a guy, supporting himself, to make himself look supported.  Now who is using circular logic?

Clinical diagnosis

.......

In studies of inter-examiner reliability, examiners were given the muscle to palpate with or without an accompanying diagnosis [ 28–31 ]. In one study, extensive training coupled with the use of an algometer resulted in examiner agreement that the phenomenon could be localized [ 29 ]. Another study reported that the assessments of an individual examiner were consistent from one test to another [ 31 ], and that more experience in assessment leads to better inter-examiner agreement [ 30 ]. These studies suggest that when shown where a problem may exist, examiners may agree. However, when blinded as to diagnosis, those who claimed expertise in the field were unable to detect putative TrPs in the majority of subjects with a MPS diagnosis [32 ]. In this study, there was virtually no inter-examiner reliability for either putative TrPs or taut bands. This finding questions the reliability of the diagnostic criteria used by these experts. More recent studies [ 33 , 34 ] have also reported poor inter-examiner diagnostic reliability and poor methodological quality [ 35 ].

.....

  • The paragraphs in this section were fairly well written. Note how this paragraph differs from others, citing specific details from each study. It does point to an issue regarding the reliability of palpation and assessment... two areas that research has not been kind to.  More sensitive assessment protocols, and better, more consistent instruction for palpating structures is needed.
  • Interesting that the strongest case against the trigger point hypothesis was treated well in this paper, and the rest of the paper is of questionable quality.
  • Citation 32 is misrepresented. The mistake here is fairly nuanced. Quintner et al. uses a study showing that trigger point evaluation in Fibromyalgia (FS) patients is not very reliable to diagnose FS, to imply that the palpation of trigger points was not reliable.

Pathology

The first histological analysis of fibrositic nodules reported diffuse inflammatory changes [ 9 ]. These findings were not confirmed, although tender muscles contained increased extracellular fluid [ 36 ]. The authors suggested that the resulting turgor might explain the observed finding of mechanical tenderness.

The term myogelosis describes a change in muscle structure analogous to TrPs [ 37 ]. Samples taken from unfixed cadavers following detection of such areas showed altered histology [ 37 ], but the clinical relevance to the findings on palpation is unknown.

  • This statement is very misleading. The end of this sentence implies that the observations made with cadaver samples are not applicable, when in actuality descriptive cadaver studies are a common starting point for practical research. In essence, this is a critique on all cadaver research, and not trigger point research specifically.
  • Further theses statements seem to be in opposition to the statement made at the beginning of the paper - "However, Stockman’s claim that ‘the essential lesion is a chronic inflammatory hyperplasia of white fibrous tissue in patches’ has never been confirmed ."

Tissue biochemistry

Shah et al. [ 38 , 39 ] employed microdialysis to sample tissue fluid within and near to a palpated trigger zone in trapezius muscles in patients with a diagnosis of TrPs and also in normal pain-free subjects. Samples were taken from the following regions: normal (no pain, no TrP), active (pain and TrP detected) and latent (no pain, TrP detected). Samples were also taken from asymptomatic gastrocnemius muscles. Elevated levels of calcitonin gene-related peptide (CGRP), substance P (SP), norepinephrine, TNF-α, IL-1, IL-6 and low pH were reported in fluid from all sampled regions of symptomatic patients. However, elevated levels were also found in uninvolved, control muscle areas.

These reported alterations in biochemical milieu are consistent with inflammation due either to tissue damage or to altered peripheral nerve function, in contrast to pathology necessarily being in the tissue sampled [ 40 , 41 ].

  • Again, this is egregious misrepresentation of research findings to support a biased view:
  • From 38 and 39:

    • 38 - "Concentrations of protons, bradykinin, calcitonin gene-related peptide, substance P, tumor necrosis factor-α, interleukin-1β, serotonin, and norepinephrine were found to be significantly higher in the active group than either of the other two groups (P < 0.01). pH was significantly lower in the active group than the other two groups (P < 0.03)."
    • 39 - "Subjects with active MTPs in the trapezius muscle have a biochemical milieu of selected inflammatory mediatorsneuropeptides, cytokines, and catecholamines different from subjects with latent or absent MTPs in their trapezius. These concentrations also differ quantitatively from a remote, uninvolved site in the gastrocnemius muscle. The milieu of the gastrocnemius in subjects with active MTPs in the trapezius differs from subjects without active MTPs."

  • Although chemical markers were higher at all points in symptomatic individuals, they were significantly higher at active trigger point sites. That is why comparisons were made between active, latent and remote sites... to address this potential confounding variable. The well designed comparison studies, make the additional studies (40, 41) non-consequential for the point being made.  (Essentially, these studies show the presence of inflammatory chemicals in symptomatic individuals.)
  • Additional notes: Many more microdialysis studies like this have become available over the last decade (See Muscle Fiber Dysfunction and Trigger Points). Overall, there seems to be an increase in inflammatory chemicals in symptomatic individuals; however, there are differences in the chemical environment of both latent and active trigger points when compared to remote sites, and further differences between active and latent trigger points that may aid in explaining why active trigger points are painful.

EMG studies

In one study, EMG examination of TrPs failed to provide evidence of ongoing denervation or focal muscle spasm [ 42 ]. But another study did report spontaneous electrical activity (i.e. endplate noise and spikes) in regions considered to be TrPs in patients with chronic tension headache and pericranial muscle tenderness [ 43 ].

Simons et al. [ 44 ] addressed the question of whether endplate noise and spikes arise from normal endplates by performing EMG on 25 patients who met the ACR 1990 criteria for FM and 8 pain-free subjects in whom latent TrPs had been identified by manual palpation of taut bands and characteristic referral of pain [ 45 , 46 ]. Unfortunately, the researchers conflated the TrPs of MPS and the tender points of FM, another issue yet to be resolved [ 47 ]. They concluded that endplate noise is characteristic of but not restricted to TrPs, and that the finding could not be considered a reliable diagnostic criterion [ 45 , 46 ].

An alternative interpretation of these EMG findings is that insertional and spontaneous activity (i.e. endplate noise) from single muscle fibres generated by the activation of i.m. nerve termini irritated by the needle was being recorded [ 48 ]. Nonetheless, it is still asserted that spontaneous electrical activity is one of the characteristics of myofascial TrPs [ 49 ].

  • Cherry-picking and twisting the truth:
  • A quick summary from my article Muscle Fiber Dysfunction and Trigger Points (please feel free to visit the article and check my citations)

    • "Hubbard et al. (1993), first demonstrated spontaneous discharges in the order of 10-50 µV and intermittent high-amplitude discharges (up to 500 µV) in painful trigger points that were absent in non-trigger points (214). Since that study, several studies comparing trigger points and normal muscle fibers have demonstrated trigger points exhibit more high amplitude discharges, more instances of spontaneous electric activity, more instances of twitch response and significantly higher root mean square activity (214 - 221)."

  • The mid 90s was pretty pivotal for research on EMG activity and trigger points. At this point in history, research focuses less on whether spontaneous discharges are strictly a trigger point phenomenon and starts comparing overall activity (the number of spontaneous discharges, root mean square activity, etc.).
  • Quintner et al.'s use of citations 42, 43 and 44 is suspect as they are early studies from 1991 - 1993 when the evidence was not focusing on "amount of activity". Further, 44 is not Simon's et al. it's Wolfe et al.
  • Citation 46, Simons et al. stats that EMG is not a reliable diagnostic tool for trigger points, but Quintner et al. implies that Simons stated it is a reliable diagnostic tool, and then argues against him.
  • 45 showed an increase in end plate potentials from trigger points which opposes the statement it cites.
  • 46 is an article not an original study, judgement is passed on citation 47 without discussing the findings, 48 has nothing to do with trigger points, and 49 is being used as a prop to show that someone, somewhere is making the claim that EMG activity differs at trigger points.  This whole paragraph seems purposefully built to mislead; cherry-picked studies, misrepresented research, and the misuse of citations to fake objective support.

Imaging studies

Seven patients with a 3-year history of myofascial pain associated with the presence of a taut band in the upper trapezius muscle were examined using magnetic resonance elastography [ 50 ]. A signature chevron-like pattern was reported, with its leading edge coincident with the physician-identified taut band. The authors did not offer diagnostic criteria nor make any comment on the relationship of a taut band to a TrP. A subsequent study of eight subjects, four of whom were said to have MPS and four of whom did not, is open to the same criticism [ 51 ].

  • Same author for both studies:

    • From 50 - "It is also supportive that the location of the taut band as identified by the physician in his examination was the same as that identified in the MRE images."
    • From 51 - "Subjects with myofascial pain were examined by a physician experienced in the diagnosis and treatment of condition who palpated and traced the locations of their taut bands before undergoing MRE examination."

  • Although the description in the methodology section of this paper is not ideal, it does not necessarily refute the findings of the study, and it certainly does not support Quintner et al.'s premise that the trigger point hypothesis is questionable.
  • The fact that the assessment was done by a physician experienced in assessing trigger point/taut bands, and that the assessed trigger points match the trigger points found on MRI is actually evidence of validity of the assessment. In fact, one can imagine that a validity study, investigating whether trigger points could be reliably palpated, would look similar to this study.

Attempts were made to visualize TrPs using diagnostic US of the anterior abdominal wall of 10 patients [ 52 ]. The points in question appeared as a mixed echoic area in the rectus abdominis muscle that became prominent on injection of local anaesthetic solution [ 52 ]. They conceded that the findings could have been coincidental. Also, the image presented is consistent with the normal sonographic appearance of abdominal muscles53 ].

  • Again, this is blatant misrepresentation of study findings. 53 was not a bad study, and you have to really look for this conceit… almost as if Quintner et al. was looking for the worst possible quote to pull from this publication. The quote can be found in the discussion, where the author is discussing possible weaknesses. Researchers discussing weaknesses in their study is great professional practice and should never be used against the researcher... the idea is to promote better research methods in future studies.  Can you imagine if everyone started pulling "potential weaknesses" as cited quotes for every study? Note, there were statistically significant findings in this study the Quintner et al. did not mention.

In another study, 44 patients with acute cervical pain and at least one putative TrP identified by palpation in the upper trapezius were evaluated using sonoelastography and Doppler imaging [ 54 ]. The authors claimed to have measured TrP size and to have distinguished normal muscle from active and latent TrPs. Although the data on which these assertions were made were not presented, the authors found no correlation between claimed TrP area and pain pressure threshold. The absence of pain-free control subjects is yet another flaw. These methodological concerns do not lend credibility to the findings.

  • From the study (54):

    • "The results presented in this study show that myofascial trigger points may be classified by area using sonoelastography."
    • "Active and latent sites had significantly lower pain pressure thresholds than normal sites (P < .05) and active sites had lower pain pressure thresholds than latent sites (P < .05; Figure 3). Receiver operating characteristic curves were generated to evaluate the binary classification strength of pain pressure threshold scores to be able to delineate normal sites from active or latent sites and active from latent sites (Figure 4)."

  • What is there to say? Did Quintner et al. just hope that nobody would read the study?

Animal models

Animal models are often informative about pathophysiology in ways that are impossible to demonstrate in humans. To be considered relevant, models must have symptomatic and/or pathological similarities to the condition being studied. For TrP research, no such model exists.

  • Note that there are no citations in this paragraph. This is conjecture, that is, the opinion of Quintner et al. Other experts in the field would strongly disagree with these statements.

Simons and Stolov [ 55 ] biopsied ostensibly normal canine muscles, seeking to correlate palpated taut bands with morphological and histological changes. The findings were negative, given that there was no indication of pain or a pathological condition present prior to these studies. The researchers observed ‘rubbing palpation produced a transient contraction which could be primarily responsible for the sensation of a hardness palpated in the dog muscles’ [ 55 ]. This is the myotatic reflex, which correlates with the twitch response also evocable on palpation of normal human muscle [ 56 ].

  • 55 - again this is horrific misrepresentation of research and a lapse in logic by Quintner et al. At the beginning of the paper Quintner et al. claimed that consistent criteria for trigger points was not available, and now this study is refuted because pain was not included in the assessment.  The study itself mentions that structural and histological differences were investigated in "taut bands" that were assessed by rubbing palpation. That is all... there is no mention of evaluation of myofascial pain syndrome or trigger points.
  • 56 - is a textbook that has nothing to do with trigger points, but this citation is being used as if it were a comparison study between myotatic reflex and the twitch response in active trigger points.

Based upon the conjecture that ‘… latent TrPs can be identified in almost all skeletal muscles of normal adults’ [ 14 ], a rabbit model of TrPs was proposed [ 57 , 58 ]. Rabbit leg muscles were palpated until they exhibited a myotatic reflex. Such muscles were considered to contain taut bands and, by assumption, TrPs. A number of papers have since been published using this model [ 58–65 ], but have not offered evidence of clinical relevance.

  • This paragraph reminds me of those movies were a serial killer writes their victim a note by cutting out the letters of various magazines and posting them on one page.  Look at the first sentence. 3 citations, having little to do with one another, are mashed together. Quotation of the first half of the sentence is used to make it look like its a legitimate statement, and then a massive leap logic happens and 2 more citations. Quintner et al. created the leap in logic by taking phrases out of context and piecing a sentence together from 3 relatively unrelated studies. Any one of those citations does a better job at explaining the use of animal models. This is pretty egregious professional misconduct, in this case demonstrating significant effort and planning with the intent to mislead.
  • None of the citations in this paragraph mention myotatic reflex. Quintner et al. make a huge assumption that a twitch response and myotatic reflex are one in the same.  Of course, the intent here is to make the reader believe that a twitch response from a trigger point was not found, and instead just a normal response of stretch reflex to stretching a muscle fiber.  This is conjecture on the part of Quintner et al.
  • Last, the statement about "clinical relevance" is the biased opinion of Quintner et al.

Delayed onset muscle soreness

Studies of delayed onset muscle soreness (DOMS) have been undertaken using eccentric exercise to cause symptoms, in both humans and animals. Although DOMS has been related to TrPs in only one study [ 66 ], this model was proposed for MPS [ 67 ]. The relevant experiment was performed in humans and used eccentric exercise of the extensor digitorum of the middle finger [ 66 ]. Following the development of DOMS, the muscle was palpated, revealing a tender band judged to be taut. However, since the muscle itself is a band, relating the description to TrPs seems meaningless. It should be noted that DOMS is self-limiting, whereas whatever phenomenon is occurring with chronic muscle-related pain is not. The relevance of DOMS to TrPs remains unclear.

  • The first statement is not true. There is more than one study (see below) demonstrating a relationship between eccentric exercise and trigger points (an additional study is listed below). Further, the chemical environments of muscle cells with trigger points and muscle cells damaged post eccentric exercise are very similar (too many citations to add here, but please refer to Muscle Fiber Dysfunction and Trigger Points.)
  • In the second half of the paragraph Quintner et al. assume that there was no methodology to differentiate taut bands, claiming that the muscle is a band, when in fact the extensor mass is an ample muscle with width and breadth (I think he was thinking of the tendon).
  • Quintner et al.'s conclusion relies on a relationship that is not being implied by trigger point researchers. Investigations into DOMS as part of the muscle fiber dysfunction/trigger point model is an attempt to understand the process of muscle fiber damage. The only correlation is trying to understand how a muscle fiber goes from healthy to not healthy… an analogous scientific pursuit would be understanding the inflammatory cycle by investigating the inflammatory cascade in tissues damaged from various injuries.

    • Itoh, K., Okada, K., & Kawakita, K. (2004). A proposed experimental model of myofascial trigger points in human muscle after slow eccentric exercise. Acupuncture in medicine22(1), 2-2.
    • Huang, Q. M., Lv, J. J., Ruanshi, Q. M., & Liu, L. (2015). Spontaneous electrical activities at myofascial trigger points at different stages of recovery from injury in a rat model. Acupuncture in Medicine33(4), 319-324.
    • Dozens of studies exist demonstrating similarities between chemical environments of trigger points and eccentrically damaged muscle cells.

Integrated hypothesis

Dommerholt et al. [ 68 , 69 ] postulated that low-level isometric muscle contraction or eccentric or submaximal concentric contractions could result in muscle dysfunction or damage, and that the formation of TrPs would follow. According to Gerwin et al. [ 70 ], excessive release of acetylcholine from dysfunctional neuromuscular endplates might be responsible for the taut band phenomenon (i.e. focal muscle contraction modulated by muscle spindle afferents) and that these bands could in turn produce muscle ischaemia, apparently by compressing adjacent capillaries supplying the muscle. This physiological process could precipitate an energy crisis in the relevant working muscle, which would respond by releasing proinflammatory molecules, thereby activating nociceptive neurons. Although there is no experimental evidence in support of this hypothesis, others [ 71 , 72 ] have accepted the motor endplate and the energy crisis theories of tonic muscle hyperactivity and TrP formation.

  • There is many issues with this paragraph.
  • First, Citations 68 and 69 are reference to reviews by Dommerholt et al., which are updates of models proposed by Travell and Simons. Further, several models support the same idea of "constant low load activity" resulting in muscle fiber dysfunction.
  • Second, these models are built from characteristics correlated with myalgia/trigger points and a reliance on a small number of motor units, aspects of motor control and tissue architecture that explain why a small number of motor units would be relied upon, reduced blood flow during contraction (especially isometric contractions) and evidence of hypoxia at the muscle cell, the development of myalgia with constant low load activity, the development of trigger points with continuous low load activity, the prevelance of trigger point development in postural muscles and muscle used in repetitive tasks, etc.... all of which can be supported by dozens of original research studies (too many to cite here).

    • Please see "Constant low-load activity" in Muscle Fiber Dysfunction and Trigger Points for a review of this research. Again, I recommend checking the citations in my article, which are well organized in the bibliography. I am not expecting you to take my word for it.

  • The jump to the study by Gerwin (70) is odd. First because the citation is a review and not the original study implicating excessive ACh in the development of taut bands, and second because excessive ACh and taut bands is not a necessary component of "Constant low-load activity" models.

    • Original citation that provides more direct evidence of the relationship between ACh and the development of taut bands:

      • Mense, S., Simons, D. G., Hoheisel, U., & Quenzer, B. (2003). Lesions of rat skeletal muscle after local block of acetylcholinesterase and neuromuscular stimulation. Journal of applied physiology94(6), 2494-2501.

  • The bolded statement is a lie. As mentioned above, there are dozens of studies that resulted in the development of these models. Further, citation 71 and 72 do not support this statement, nor do they have anything to do with claims being made by Quintner et al. Again this is mis-citation to fain at support from published studies.

Recent studies of induced muscle pain in humans has not provided evidence for a reflex increase in fusimotor drive and spindle discharge [ 7374 ]. In fact, persistent musculoskeletal pain is associated with decreased agonist muscle tone [ 75 ]; in other words, digital pressure or other stimuli that evoke pain will decrease the tone of the muscle stimulated. The validity of the paradigm that correlates endplate activity or noise with pain arising from the TrP became further suspect when it was reported that injection of botulinum toxin A in the region of a TrP had no effect on pain intensity or mechanical pain thresholds, but did significantly reduce motor endplate activity and the EMG interference pattern [ 76 ]. Finally, the vicious circle hypothesis has now been laid to rest by microneurographic recordings in humans performed during sustained muscle pain [ 73 , 74 ]. The integrated hypothesis remains conjecture in the face of conflicting data.

  • This paragraph is poorly written overall. Their conclusion has little to due with the topic sentence, and the supports are so poorly explained it’s hard to understand what point was trying to be made.
  • Citation 73 induces pain on the skin not in muscles
  • Citation 74 induces pain by injection of tonic solution into the muscle.  Note, in all studies that tonic solution is injected into muscles to induce pain, there is decrease in muscle activity. This may imply that injection itself is the cause of the decrease in activity, and results should not be generalized to other painful stimuli.
  • Citation 75 is a review and not an original study, and the review is not specific to trigger points.
  • "in other words, digital pressure or other stimuli that evoke pain will decrease the tone of the muscle stimulated" - This statement is made up. None of the citations mention digital pressure, although it should be mentioned that Quintner et al. contradict themselves by implying that manual release (ischemic compression) may be effective for reducing trigger point activity.
  • Citation 76 is well represented here, but there is an error in logic made by Quintner et al. The research on trigger points implies that both motor endplate dysfunction and sensitization by the nervous system are involved. It seems likely that botulinum toxin A reduces motor end plate activity by affecting the nueromuscular junction, but does not effect receptors that may result nociception and pain.
  • 73 and 74 do not support this statement (in fact, I am not sure they mention the vicious cycle hypothesis) - "the vicious circle hypothesis has now been laid to rest by microneurographic recordings in humans performed during sustained muscle pain".
  • Note, no conflicting evidence was cited to support this opinion of Quintner et al. -  "The integrated hypothesis remains conjecture in the face of conflicting data." The statement itself is conjecture.

Treatment

Non-invasive interventions that have been advocated include compression of the TrP, spray and stretch, transcutaneous electrical stimulation and, more recently, high-intensity focused US [ 77 ]. Invasive treatments have included injection of local anaesthetic agents, injection of CSs, injection of botulinum toxin, needle acupuncture and dry needling [ 78 ].

  • These statements are fair, although the citations used are strange. There are review of treatment techniques available, the two citations used are not treatment technique reviews:

    • 77. Unalan, H., Majlesi, J., Aydin, F. Y., & Palamar, D. (2011). Comparison of high-power pain threshold ultrasound therapy with local injection in the treatment of active myofascial trigger points of the upper trapezius muscle. Archives of physical medicine and rehabilitation92(4), 657-662.
    • 78. Lavelle, E. D., Lavelle, W., & Smith, H. S. (2007). Myofascial trigger points. Anesthesiology clinics25(4), 841-851.

In their systematic review, Cummings and White [ 79 ] were unable to find evidence that needling therapies have any specific effect. Their later review of 1517 studies found only seven that were of high enough quality for meaningful analysis [ 80 ]. Rickards [ 81 ] also found limited strength of evidence for any treatment of TrPs.

  • Again, misrepresentation of a citation: Citation 79 states, in the conservative language of a good researcher, that there seems to be evidence that needling (likely without the need for saline or drug) is effective for triggerpoints; however, controlled trials testing the efficacy of treatment against placebo are needed. Conclusion from 79 below:

    • Quoted from Citation 79: "Conclusions: Direct needling of myofascial trigger points appears to be an effective treatment, but the hypothesis that needling therapies have efficacy beyond placebo is neither supported nor refuted by the evidence from clinical trials. Any effect of these therapies is likely because of the needle or placebo rather than the injection of either saline or active drug. Controlled trials are needed to investigate whether needling has an effect beyond placebo on myofascial trigger point pain."

  • Misrepresentation (Again) and Attributing Weaknesses in Research to Trigger Points: Quoted from Citation 80: "However, the limited sample size and poor quality of these studies highlights and supports the need for large scale, good quality placebo controlled trials in this area."

    • The problem with Quintner et al.'s statement alludes to a problem regarding nearly all research in rehabilitation, strength, manual therapy, etc. A new research quality standard has been set by some, resulting in a very small set of recent publications meeting the criteria. It is both a fallacious argument to consider large RCTs the best research type for every question, just as it is fallacious to disregard all research that does not meet the new standard. This is a large philosophical issue that could fill a text book, but in essence, data is data, and the quality and quantity of evidence is relative. Quintner et al. makes this point, citing that of 1517 studies, the meta-anlaysis is only going to look at 8 studies. Although those 8 studies may be weighed more heavily, if they contradict 1509 studies, there is likely a more nuanced explanation that is not being given credit.  The truth is, those 8 studies more or less agree with the 1509 studies that were not included.  However, when you try to do a meta-analysis using so few studies, it results in regression to the mean; which essentially is a wash-out of any effect size. If you have read a few meta-analyses in the field, you might have noticed they almost always result in "limited evidence to support....". Regression to the mean needs to be given more attention before we mistakenly think that nothing we do is particularly effective.

  • How is this congruent with Quintner et al.'s statiement "Rickards [ 81 ] also found limited strength of evidence for any treatment of TrPs."?

    • Quoted from Citation 81  - "According to the results of this review there is a significant evidence that laser therapy may be effective as a short-term intervention for reducing pain intensity in myofascial trigger point pain of the neck and upper back. Further research is necessary to determine the long-term effectiveness, the most effective type of laser, and the optimum dosage, duration and frequency of treatment. TENS appears to have an immediate effect in decreasing pain intensity in myofascial trigger point pain of the neck and upper back. However, there are insufficient data to provide the evidence of effectiveness for TENS beyond immediately after treatment. There is limited evidence for the use of FREMS, HVGS, EMS and IFC for myofascial trigger point pain. Moderate evidence derived from one high quality and two lower quality studies indicates that conventional ultrasound is no more effective than placebo or no treatment for myofascial trigger point pain in the neck and upper back. Preliminary evidence suggests that magnet therapy may be effective, however, further studies are needed to support the findings. Due to the heterogeneity of trials examining physical and manual therapies the current evidence did not exceed the moderate level. Trials examining manual techniques suggest that such approaches may be effective, however, no conclusions can be drawn regarding medium to long-term effectiveness or effect beyond placebo. Evidence for many of the commonly used treatments for myofascial trigger point pain is lacking."

Another review remarked upon the heterogeneity of the populations being treated, and the lack of widely accepted standard diagnostic criteria for MPS [ 82 ]. This review also concluded that there was insufficient evidence to support the use of most interventions.

  • Regarding 82, see the notes above regarding citation 80
  • Quintner et al.'s view -  "This review also concluded that there was insufficient evidence to support the use of most interventions." 
  • Alternative  view - "There is insufficient evidence to contradict professional experience, and current protocols driven by outcome based practice. Further research is needed to recommend altering current treatment protocols."

    • These two views allude to an ethical dilemma of sorts. Is Quintner et al. suggesting that professionals should stop treating with all current modalities until research of pristine quality has been published of something that does work? Are they really suggesting that no one should even try to help individuals in pain if they are diagnosed with trigger points, MPS, fibromyalgia, etc.?
    • Keep in mind, if the same criteria is used to critique the treatment recommendations of Quintner et al., their recommendations would also have insufficient evidence.

A systematic review of botulinum toxin A for TrP treatment located 21 randomized controlled trials, with 12 eligible for consideration but only five suitable for inclusion, and concluded that the current evidence does not support any therapeutic value [ 83 ]. Again, these authors reported that the data were limited and that the patient populations were heterogeneous.

These studies provide little evidence that dry needling of TrPs is associated with a treatment effect compared with standard care [ 3 ]. They are based on small sample sizes, uncertainty as to whether TrPs were the sole cause of pain, as well as neglect of technical issues such as the variability in the location of TrPs and the depth of needle insertion.

  • Again, this is implying that a lack of evidence is evidence of absence. However, citation 3 does a better job of critical evaluation of trigger points than Quintner et al.

With these results in mind, why do many clinicians insist that their treatments work? One explanation is that the treatments are rarely performed in an isolated fashion; that is, treatment is accompanied by manual therapy, home exercises and stretching.

  • Or.... clinicians are using other assessment parameters including subjective pain, range of motion, special tests outcomes measure questionnaires, etc. Quintner et al. creates a straw-man argument by insinuating that clinicians "insist their treatment" works without clinical evidence.

Contextual effects could explain the plethora of anecdotal responses to treatment [ 84 , 85 ]. This is not unexpected when a medical treatment with high face validity is based solely on practical experience rather than reflecting a rational approach based on pathogenesis. Apparent effectiveness of any treatment may be attributed to the natural history of the particular problem being treated, regression to the mean, and the expectation of something being done to the area in question. This can lead to the fallacy known as post hoc ergo propter hoc (after this, therefore because of this), when the treatment offered in fact had nothing to do with the pathogenesis of the condition towards which it was directed. A recent study comparing dry needling with manual compression, in which there was no control group, exemplifies this critical methodological issue [ 86 ].

  • Note: 84 and 85 have nothing to do with trigger points, and are instead papers discussing potential sources of bias. This is not inappropriate for this paragraph, but the connection between these citations and how they specifically relate to trigger point research is unclear... and not made any more clear throughout the paragraph.
  • The bolded statement is a lie. In fact, if there was an argument to be made about trigger points it would be that despite strong research regarding their pathogenesis, there is a small number of high quality studies on assessment and treatment.
  • Regarding citation 86 - this is a well done randomized trial comparing dry needling to ischemic compression, with pre and post assessment of a specific parameter (pain pressure threshold). I'm not sure how that relates to post hoc ergo propter hoc, when the study itself was based on prior studies including those with control groups, and the pre-assessmeent/screen is clearly stated in the methodology.

One common factor shared by most therapies is that they elicit pain at the site of their application; that is, they are noxious stimuli. If they do work, this similarity suggests a common mechanism of action. One possible mechanism is counterirritation, or application of a competing noxious stimulus [ 87 , 88 ]. It is not surprising that a noxious stimulus applied in the region where pain is experienced, whether or not there is local pathology present at that site, would elicit a transient reduction in pain intensity by recruiting those higher order brain regions responsible for anti-nociception [ 89 , 90 ]. In conclusion, the vast majority of studies and meta-analyses do not support the prediction from MPS theory that focal treatment of TrPs is effective.

  • The citations are specific to the counter-irritant phenomenon, but the methods used in these studies have no resemblance to any documented treatment for trigger points or myofascial pain. Quintner et al. makes a huge leap in logic to suggest that this phenomenon is somehow responsible for the reduction in pain noted during trigger point treatment. This leap of logic is especially large in regard to the direct treatment of trigger points (e.g. dry needling or compression), as the studies on the counter-irritant phenomenon are demonstrated via methods like ice bath on left foot reduces perception of pain on the right foot.

An impasse

In 1976, Simons hoped that: ‘It would now appear possible to resolve much of the conflicting data of the past by carefully distinguishing trigger from reference zones, and acute from chronic lesions using modern electrodiagnostic, biochemical, histochemical, and ultramicroscopic techniques’ [ 1 ]. Some three decades later, he conceded that acceptance of the concept of TrPs had been hampered by two outstanding considerations: the lack of a diagnostic gold standard and the lack of generally recognized pathogenesis [ 91 ].

  • The citation 91 (2003) predates the majority of the Microdialysis studies. Note, Quintner makes almost no mention of this research. At the very least, much has been learned about the biochemical and histochemical changes associated with trigger points. Further, some ultramicroscopic images are alluding to the causes of palpable phenomenon (again, too many citations to cite here, please refer to "Chemical Changes involved in Trigger Points" in the article Muscle Fiber Dysfunction and Trigger Points.

We propose that sufficient research has been performed to allow TrP theories to be discarded. The scientific literature shows not only that diagnosis of the pathognomonic feature of MPS (the TrP) is unreliable, but also that treatment directed to the putative TrP elicits a response that is indistinguishable from the placebo effect. As these conclusions refute MPS, formulating a plausible scientific explanation for pain perceived by patients as coming from their muscles remains a challenge.

  • The first statement is conjecture, and further, if that opinion was based on the citations referenced in this article I can understand why that conclusion was made. However, there are literally 100s of citations missing from this review. This is not just citations that were published following the publication of this work, but 100s of studies that were published before the publication date of this article.
  • This bolded statement is a misstatement. Returning to the quoted text from citation 80 of this article ""However, the limited sample size and poor quality of these studies highlights and supports the need for large scale, good quality placebo controlled trials in this area." Trigger points treatment has not been found to be indistinguishable from the placebo effect; rather, there is simply not enough placebo control studies on trigger point treatment.  Again, this is a lack of evidence, not evidence of absence. 

Towards explaining the clinical phenomena

In our opinion, current neuroscientific hypotheses can form the basis for collaborative scientific investigation to explain the clinical phenomena. We offer two for consideration, neither of which relies on local pathophysiology.

  • Why disregard the research on pathophysiology? Isn't the goal of scientific discovery to integrate information?

Neuritis model

Nerve inflammation as a source of pain was discussed in the 19th century [ 92–97 ], but focused research on nerve inflammation as a primary disease aetiology has been limited.

  • Note: These citations date between 1828 to 1877... that is not a typo. These references are 150 - 200 years old.

Quintner and Cohen [ 25 ] hypothesized that the TrP was an area of what was then called secondary hyperalgesia occurring in muscles that are structurally and physiologically unimpaired. Noting the remarkable proximity of TrPs to known peripheral nerves, these authors argued that sensitization of the axons within the nerves, possibly by inflammation, may inform the underlying mechanism. Subsequent research has emerged in support of this hypothesis.

  • Note: If we were to use the language of Quintner et al. to describe the claim made in this paragraph we could word it as follows: "Quintner and Cohen (25) decided to make-up the term secondary hyperalgesia to account for the trigger point phenomenon, and then arbitrarily attribute symptoms to peripheral nerves in proximity. Further, Quintner et al. claim that there is evidence to support this claim, but then fail to provide citations."
  • The key point: 25 is paper by Quintner et al. and not 3rd party objective data. Further, there is no support for the claims made in this paragraph.

Focal inflammation of peripheral nerves leads to ectopic axonal mechanical sensitivity and spontaneous discharge of some but not all of the nociceptors within the inflamed nerve [ 98–101 ]. These changes can be expected to lead to focal areas of neurogenic inflammation and possibly to sensitization in the muscle innervated. If confirmed, they can inform further investigation that might be highly relevant to explaining the phenomenon of chronic muscle pain.

  • 98 is an interesting study, and may aid in explaining some of the painful phenomena associated with trigger points; however, there is no evidence to suggest that this does not occur in conjunction with the integrated trigger point hypothesis.
  • 99 is a study discussing the impact of stretch and pressure on sensitized nerves
  • 100 is a study on rat sciatic nerves and the association between the research findings and trigger points is indirect at best
  • 101 is a study on the development of chronic regional pain syndrome (note this syndrome has some characteristics that differentiate it significantly from the trigger point phenomenon.

    • Again these citations have nothing to do with trigger points. Quintner et al. seems to be implying that evidence that nerves can be sensitized and spontaneously discharge, disproves that nerves can also stimulated by neurotransmitters related to trigger points. This is the fallacy of “false zero-sum game”. Quintner et .al seems to think that anything that proves them correct, proves trigger points wrong, but it is obvious that these studies and studies regarding how trigger points may contribute to nociception could co-exist.
    • Using indirect research to generate a hypothesis is common practice in scientific inquiry, but it is not good practice to make strong claims with indirect evidence alone. Note the bolded text implies the reader should take Quintner et al.'s word for it; that these indirect studies are the real reason why we "feel trigger points", and are a suitable replacement for all the references discussed previously in this paper.
    • "If confirmed, they can inform ......" A question for Quintner et al. might be.... "Why should we refute the trigger point phenomenon based on enough time and study to confirm or reject the hypothesis, but a hypothesis that was generated 100 years earlier should be given more time? (As if there was a time limit on scientific inquiry... how long did it take to go from elemental make up, to elements, to atoms, to subatomic particles?)

Referred pain and tenderness (allodynia)

Kellgren [ 102–104 ] reported the critical observation that, in addition to referred pain, referred tenderness could be induced by targeted injections of hypertonic saline into tissues such as interspinous ligaments, periosteum, cancellous bone, or voluntary muscle. His studies and those of others [ 105 , 106 ] showed that nociception in deep tissues can induce the phenomena of remote localized pain and tenderness. This relegates the TrP to being a site of secondary allodynia reflecting altered central nociceptive mechanisms [ 107 ].

  • Kellgren (102 - 104) Written in 1938, 1938 and 1977, these are not experimental studies. They are editorials, about clinical observations. Although this is interesting work and may be viewed as a "pilot study" of sorts (similar to much of Travell and Simons early work on referral pain patterns), Quintner et al. make the mistake of holding the trigger point hypothesis to a standard that includes the careful execution of randomized comparative studies with control, and then does not apply the same standard to their own alternative hypothesis and supporting citations.

    • Note: For all students, researchers and clinicians. It is good practice to turn your critical evaluations on your own hypotheses. We are often more "creative" or "innovative" when critiquing others, and it is great practice to think skeptically, but... once you have realized the presence of certain biases or weaknesses in an argument, test your own arguments for the same.

  • The second sentence of this paragraph regarding referral pain is true, when viewed in isolation from the rest of the paragraph. In fact, better citations and supports could have been found.

    • 105 from 1956 on referral pain
    • 106 from 2001 on referral pain.

  • 107 is a paper on centralization, but it does not support the claim made that trigger points can be relegated to secondary allodynia that result from CNS adaptations. A positive finding in one study does not relegate other findings to secondary status. No attempt was made in these studies to find a primary and secondary source of pain, or to create a hierarchy of stimuli. This conclusion is stranger still when consider that most studies describing the etiology of trigger points were published using more sophisticated methodologies between 15 after 30 years after these studies (102 – 107) were published.

    • Note, again there is 100s of references correlating physical phenomenon within the muscle cell to trigger points.  What can be said is that trigger point associated pain may be related to, or cause CNS adaptations, and that centralization is a piece of the integrated explanation of the trigger point phenomenon. (See "Muscle Fiber Dysfunction, Pain and the Nervous System" in Muscle Fiber Dysfunction and Trigger Points)

Conclusion

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. In contrast, evolving insights into the neurobiology of nociception and pain suggest plausible hypotheses that form a basis for advancing knowledge and therapeutics in this challenging area.

  • What is the difference between conjecture, hypothesis and a model? Obviously conjecture as meant as an insult, but the model Quintner et al. are rejecting is better defined, supported, and refined then their alternative hypothesis. I would argue that MPS caused by TrPs is not conjecture; but rather, a growing model, being refined by research, that still suffers from the gaps that many models in our field suffer. The second sentence (in bold) in this paragraph is so hideously biased, irresponsible and hyperbolic, it should have raised red flags with editors. It's a lie that all hypotheses have been refuted; in fact, most of the research and hypotheses on trigger points were not even addressed in this paper. His last statement is based on 30 - 40-year-old studies, that have nothing to do with trigger points.  How these concluding statements could be printed is beyond reason, and certainly not academically responsible.

End Note from Brookbush:

Although good papers are published and bad papers are published, it is fairly rare that I see such an egregious attempt to mislead. In my humble opinion, the false accusations, mis-citations, and erroneous claims in this paper warrant punishment - retraction of the paper with a request for a public statement of apology, an X-year ban from future publication in the journal, and potentially dismissal of the editor at Rheumatology who allowed the paper to be published as is. This paper is one of the worst pieces I have read. I only make that point to emphasize that the majority of peer-reviewed publications are trustworthy, most journals do not ignore such obvious bias, and most academics have every intent to help via objective observation and scientific inquiry. I apologize for referencing my own work throughout the article (Muscle Fiber Dysfunction and Trigger Points); I only did so to prevent this critique from becoming a long, drawn-out annotated bibliography. I expect that you will apply the same level of critique to my work, as I have to this paper by Quintner et al. I have tried to organize Muscle Fiber Dysfunction and Trigger Points, both the article and bibliography, in a way that would make critique as easy as possible. I hope that you found that both this critique, and Muscle Fiber Dysfunction and Trigger Points were as accurate as possible, informative and enjoyable.

Again, Big thank you to Paul Ingraham of Painscience.com, and thanks for the dialogue and articles (Trigger Point Doubts).

Keep reading and learning; everyday if possible.

Sincerely,

Dr. B2

© 2019 Brent Brookbush

Questions, comments and criticisms welcome and encouraged -