Behold the Mighty Trigger Point

Some clinicians are still endeavoring to prove that myofascial pain is a distinct localised clinical entity attributable to “trigger points” (TrPs) within muscles if not also other soft tissues.

There are others who continue to propose that the pain of FMS (fibromyalgia syndrome) “is largely composed of pain arising, at least partially, from TrPs” [Fernández-de-Las-Penãs & Arendt-Nielsen 2016].

It might seem therefore that MPS and FMS are two sides of the TrP coin, the label used depending on which side the coin lands. If only those TrPs could be treated!

Recently Kumbhare et al. [2017] reviewed the very limited literature that in their opinion justifies the use of ultrasound-guided injection techniques in the treatment of patients in whom “trigger points” are thought to be the cause of their pain. Have they found the ultimate solution?

The significant problems that bedevil this article quickly become evident from an analysis of the opening sentences:

Myofascial pain syndrome (MPS) is a common regional musculoskeletal pain syndrome that can cause local or referred pain.   In other words, a pain syndrome is said to cause itself, which is of course a logical impossibility!

The authors then appear to accept the existence of pathophysiological entities for which there is no evidence: It [MPS] is characterized by myofascial trigger points (MTrPs), which are hard, palpable discrete localized nodules located within taut bands of skeletal muscle and can be painful on compression. However, such nodules have never been objectively demonstrated – histologically, ultrastructurally, biochemically or electrically. So how can it be known that they are the primary cause of musculoskeletal pain?

To be fair, the authors do point out that diagnosis is difficult, not least because palpation is unreliable and there are no accepted standardized clinical criteria for the diagnosis of MTrPs. Yet Khumbare et al. [2017] advise clinicians to rely on palpation to detect taut bands in muscle prior to applying the ultrasound probe to these regions. To find what? Some studies report finding hypoechoic regions, whereas others report the regions of interest to be hyperechoic. Elsewhere in the article the authors favour the former possibility but provide no reason for this choice.

So, what is the “gold standard” for the identification of a phantom? And if, as the authors concede, there are no data on inter-rater reliability when using ultrasonography and no consensus within the literature on what can be identified, how can they logically – let alone ethically – recommend injection therapy?

The only valid conclusion that can be drawn from this article is that the authors are locked into a bogus construct about which they are hopelessly confused [Quintner & Cohen 2015; Quintner et al. 2015].

 

John Quintner, Milton Cohen, Asaf Weisman.

 

References:

Fernández-de-Las-Penãs C, Arendt-Nielsen L. Myofascial pain and fibromyalgia: two different but overlapping disorders. Pain Manag 2016; 6: 401-408.

Kumbhare D, Singh D, Rathbone A, et al. Ultrasound-guided interventional procedures: myofascial trigger points with structured literature review. Reg Anesth Pain Med 2017; 42: 407-412.

Quintner JL, Cohen ML. Myofascial pain: a bogus construct. In: Hutson M, Ward A, eds. Oxford Textbook of Musculoskeletal Medicine, 2nd ed. 2015: 132-142.

Quintner J, Bove G, Cohen M. A critical evaluation of the “trigger point” phenomenon. Rheumatology 2015; 54: 392-399.

 

 

 

 

9 Comments

  1. I am keen on participating on discussions on this forum. I have read through a few of the posts and comments. I am 52 years old, FM symptom onset was at 25 and diagnosis at 29. I have a lot of experience, most of which was bad up until 4 years ago. I have done a lot of reading and formed some potential hypotheses to explain the condition and my own improvement upon the adoption of the “right” mix of strategies.

    I am someone who was a competitive athlete (cycling) with strong belief in my own capabilities, at the time of symptom onset, of which the earliest manifestation was failure to recover from post-exercise pain, and loss of stamina – I got “left behind” more and more but continued a rigorous training regime, in a state of refusal to accept that I had new limitations. I categorically reject any hypothesis that FM is a problem of “in the mind” attitude. I would say that I spent two decades falsely believing in “mind over matter” and now regard this as a obstacle to coping with FM and achieving rehabilitation. I call what I have done, rehabilitation, not a cure.

    I think that the hypotheses about myofascia dysfunction and pain are “on the right track” but the focus on “trigger points” and the associated approaches are a blind alley. However, I disagree completely that “hard, palpable discrete localized nodules located within taut bands of skeletal muscle (that) can be painful on compression” can be dismissed with a wave of the hand. If “objective science” has “failed to prove their existence” then sorry, I regard that as a failure of all “objective science” research approaches so far, not as a clear verdict that these things are irrelevant.

    I have decades of experience with massage therapists of all kinds, and every single one of them was clear that I (and others with FM) have these all over the body, and normal healthy people do not. They are to be found as specific “injuries” at specific locations in normal healthy people, and often resolve with the right hands-on treatment. This is what massage therapy is mostly all about. However, people with FM have these abnormalities body–wide and they do not resolve with hands-on therapies that work for most specific “injuries” in normal healthy people. Most hands-on therapy is merely painful and useless for people in the full grip of FM.

    I have a lot more to say, obviously, but that is my introductory comment.

  2. Phil, thank you for your comments, which do touch upon a number of important and highly controversial issues.

    Let me respond to your comment:

    ‘However, I disagree completely that “hard, palpable discrete localized nodules located within taut bands of skeletal muscle (that) can be painful on compression” can be dismissed with a wave of the hand. If “objective science” has “failed to prove their existence” then sorry, I regard that as a failure of all “objective science” research approaches so far, not as a clear verdict that these things are irrelevant.’

    I agree that the findings you mention should not be dismissed with “a wave of the hand”. They demand a scientific explanation.

    The authors of the study [Kumbhare et al. 2017] believe that they are “myofascial trigger points” and as such are the primary source of muscle pain. They (and others) have been going to great lengths to provide scientific evidence to support their belief. To date they have been unsuccessful.

    They have diligently applied the methods of “objective science” and have come up with nothing of substance. Science has not failed them. Perhaps they have been looking in the wrong place!

    Nevertheless, they are fully committed to the destruction and/or inactivation of these hypothetical lesions. Their “weapon of mass destruction” is the stainless steel needle.

    Another problem they have not been able to overcome is to agree upon the exact location of their target(s). Kumbhare et al. [2017] do indeed highlight this problem.

    You assert that in one context these nodules are sites of injury at specific locations yet deny this possibility when they are found to be ubiquitous in those with the label fibromyalgia (chronic widespread pain).

    Let me leave you with our comment above: “It might seem therefore that MPS and FMS are two sides of the TrP coin, the label used depending on which side the coin lands. If only those TrPs could be treated!”

  3. Thank you, John. We are agreed that these spots are “palpable”, whatever they are? It is “what” they are, that is “hypothetical”, is it not? Also, that they are painful is not hypothetical, but the nature of that pain is – and the hypotheses are numerous and often controversial.

    I think that every “WMD” so far for the resolution of these palpable “lumps” in people with FM, is a failure on its own, whether needles, injections, “myofascial release”, direct pressure (like acupressure or “trigger point therapy” but I hate that term), etc. But so is virtually every treatment from every branch of medicine, whether directed at these palpable lumps or not. I believe (and I am not alone in this) that there is an underlying pathology that causes the formation of these lumps, so that any therapy that succeeds in resolving a lump is short-lived; it returns. But I never experienced any therapy that did so once I had FM. Massage therapy, earlier in my life, applied to exertion/injury-related lumps at a specific location, was successful.

    Numerous therapies have good track records of resolving individual post-injury lumpy spots that were causing pain and limitation long after the original injury (eg a sprain, a broken bone, a major impact wound, etc) is expected to have “healed”. I do not know what the state of the “science” is on these post-injury problem spots, only that it is common knowledge that they exist and are often finally resolved permanently when the sufferer tried out the “right” therapy (sometimes acupressure, sometimes myofascial release, sometimes other things). But the ubiquitous spots in FM do not resolve with any treatment.

    I am interested that you imply that ubiquitous spots of pain in FM might be injury-related just like these spots are when they are at a specific location following an injury that otherwise should have healed. The only reason I might have been “excluding” this hypothesis is because my understanding of “injury” might be too limited. Please tell me more about how something ubiquitous yet not subsequent to a calamitous “ubiquitous” impact or strain or breakage, can fall into the category of “injury”.

    I am interested in your use of the term “lesion” because it includes more than lumps – maybe there are more than lumps in this problem. Maybe there are lesions of multiple kinds involved here as well as lumps.

    It has long been a mystery to me why researchers using high-tech diagnostic tools have been “unable to confirm the existence of palpable lumps”. Are researchers deliberately not looking in the right place? What are the potential motivations for a reluctance to “find” something palpable? How do they find anything? How do they find an organ, or find cancer? If a cancer is “tissue cells growing out of control” but otherwise indistinguishable from tissue not growing out of control, how do they “find” the cancer? Oh, there is something lumpy here but it looks like normal tissue, therefore it is irrelevant.

    Excuse my frustration at the state of FM research. I suggest that the focus of research and the funding of it, on CNS dysfunction as the ORIGIN of the problem, just because “objective science” can’t “see the lumps”, is worse than wrong, it is illogical and immoral. Some therapies have been known to temporarily resolve these palpable lumps (eg cortisone injections) but they always return. Is CNS dysfunction making them return? How many other hypotheses might more usefully be explored? How about the possibility that the CNS is rendered dysfunctional in the first place BECAUSE of chronic pain from ubiquitous “injuries”?

    Robert Schleip and colleagues hypothesise that the fascia is implicated in the “lumps” that remain long after an original injury to a specific muscle, and that the successful therapies release “adhesions” or similar, in myofascial surfaces. They do not seem to have considered FM as yet, which is a pity, because their explanation could well be the right one in the case of a ubiquitous “injury” that does not resolve – and the reason it does not resolve, or always recurs, is “the cause of FM”. And I think “the CNS” is one of the weakest potential hypotheses for this.

    I also learned recently that the Chinese hospital system has long included highly trained massage therapists on their staff, whose job is to pre-empt the formation of chronic post-injury, or post-surgery, lumpiness in muscle tissue. Schleip argues that the discipline of surgery needs to know a lot more about the fascia and how to avoid long-term complications for patients. It is not just cling-wrap around the muscles and bundles of muscle fibres!

  4. “How about the possibility that the CNS is rendered dysfunctional in the first place BECAUSE of chronic pain from ubiquitous “injuries”?”

    Some fibromyalgia theorists have promoted this view, but the scientific evidence is rather thin on the ground (and that is being very kind to them). The discussion on this link is relevant: http://www.fmperplex.com/2016/08/23/why-centralized-is-unacceptable-as-a-descriptor-for-the-pain-of-fibromyalgia/

    The “fascia” story has also been trotted out in relation to fibromyalgia by Dr Ginevra Liptan. Her speculative views hark back to the “fibrositis” construct, which was in my view properly discarded in the first half of the 20th century:. See: http://www.fmperplex.com/2015/07/14/could-fibrositis-be-making-a-comeback/

    In my opinion, the only scientifically credible and testable published hypothesis for fibromyalgia (aka Chronic Widespread Pain) is that which I co-authored..

    Here is a summary:

    Evolution, Stress and Fibromyalgia

    Adapted from: Lyon P, Cohen M, Quintner J. An evolutionary stress-response hypothesis for Chronic Widespread Pain (Fibromyalgia Syndrome). Pain Med 2011; 12: 1167-1178.

    Despite affecting huge numbers worldwide and being researched extensively over 25 years, fibromyalgia syndrome (FMS) remains a problematic construct, for clinicians and patients alike.

    Characterised by persistent widespread pain and tenderness disproportionate to demonstrable tissue damage, of which there may be none, the syndrome often includes sleep disturbance, fatigue, ‘irritable bowel,’ cognitive and affective changes, and, less frequently, skin disorders. Without a cogent model of pathogenesis for this complex syndrome, effective treatment remains elusive.

    An evolutionary approach provides insight.

    Several clinical features of FMS accord with “sickness behavior,” found widely in the animal kingdom, which is the observable manifestation of physiological processes working to restore proper functioning. Sickness behavior is part of the organism’s response to some sort of stressor (threat, disturbance), which may be perceived via innate immunity or cognitively. The building blocks of the human stress response (i.e., cytokines, neurotransmitters, hormones) are evolutionarily ancient.

    The systems that underlie the human stress response (SR) are multiple, co-modulatory and co-regulatory. Almost from the moment a SR is activated, countervailing processes also activate, to ensure that the dramatic molecular events marshaled to save the animal don’t damage the animal. This is because many molecular actors involved in SRs are double-edged,’ and can have negative as well as positive effects on organism functioning. The response to stress thus is designed to engage, repair, and stop (resolve).

    When an SR is prolonged in any organism, for whatever reason, profound changes occur in functioning and behaviour. Chronic SR activation in humans is associated with some of the most medically important diseases in the developed world, including cardiovascular disease, type 2 diabetes, and metabolic syndrome.

    One of the ‘double-edged’ molecules involved in vertebrate SRs and associated with a
    wide variety of chronic human diseases is substance p (SP), a deeply conserved neuropeptide also found in insects and molluscs.

    In humans, SP operates in both the central and peripheral nervous systems. With its preferred receptor neurokinin-l (NK1R), SP is involved in a staggering range of defensive mechanisms, including cytokine release, cell manufacture and migration to sites of injury, mast cell granulation, edema, vomiting, gut contraction, cell death, and aversive reinforcement learning.

    Its importance to human functioning is reflected in ontogeny: SP is one of the first neurotransmitters to appear in foetal development, before other SR actors, including corticotropin-releasing hormone, adrenaline, noradrenaline, dopamine, and serotonin.
    The relevance of SP for understanding FMS is three-fold.

    First, elevated SP in cerebral spinal fluid is the most reliable biomarker of FMS. Patients typically have SP levels 2-3 times those of healthy controls.

    Second, SP is highly correlated with the common co-morbidities of FMS, including depression, sleep disturbance, irritable bowel and psoriatic skin disorders.

    Third, recent research shows that SP is necessary for the development of central sensitization in the spinal cord’s dorsal horn. Central sensitization is widely thought to be the most promising explanation of how chronic pain is induced.

    From this perspective, FMS can be seen as a clinical outcome of prolonged activation, or dysregulation of a complex, evolutionarily conserved system designed to defend the organism against threat.

    There are several explanatory benefits to such a view.

    First, this perspective explains why a chronically activated or unresolved SR might manifest as labile widespread pain in association with other co-morbidities.

    Second, it explains the clinical overlap of FMS with post-traumatic stress disorder, which is also associated with elevated CSF-SP.

    Third, because SR systems are among the most genetically and phenotypically variable systems in biology, this perspective may help to explain the great differences between individuals in clinical presentation. SR systems in mammals are highly susceptible to modification in early development, producing different stress reactivity profiles, so childhood exposures to stressors, including serious disease or injury, may be relevant to clinical presentation.

    The SP/SR hypothesis may help to explain why SP and NK1R antagonists did not fulfill their promise as treatments for FMS. SP/NK1R participates in many defensive systems important to whole-organism functioning, not just chronic pain, and they work in combination with many other molecules.
    Finally, the hypothesis might also help to explain why certain holistic, nonpharmacologic therapies (e.g., patient education, cognitive-behavioural therapy, mindfulness/relaxation) appear to help a substantial proportion of patients, particularly when combined with exercise. It takes a system to treat a system.

    Pamela Lyon, Visiting Research Fellow, Social Epidemiology and Evaluation Research Group, University of South Australia; Milton Cohen, Specialist Pain Medicine Physician and Rheumatologist, St Vincent’s Campus, NSW; John Quintner, Consultant Physician in Rheumatology and Pain Medicine, Pain Medicine Unit, Fremantle Hospital.

    P.S. The trigger point debate is now over: https://bodyinmind.org/evaluating-trigger-point/

  5. Phil, those who are promoting “fascia” as a key player in persistent pain conditions are in the same leaky boat as those who incriminate “trigger points” in muscle. They have yet to come up with the evidence. I am not holding my breath until they do so.

    In the context of chronic widespread pain, the internationally acclaimed expert Professor Dan Clauw [2014] believes that fibromyalgia is best thought of as a disease of the central nervous system.

    But he suggested that the term he favoured as the third pain descriptor – “centralised” – also implies “peripheral nociceptive input might be responsible for some of a patient’s pain but central nervous system factors likely amplify the pain.”

    Thus, in Clauw’s opinion, peripheral nociceptive input (e.g. from “fibrositic nodules” etc.) is not a necessary contributor to a patient’s pain. But should it happen to be the case, Clauw proposed that the patient feels “more pain than would normally be expected based on the degree of nociceptive input.” But he does not disclose how a clinician/observer is able to make such a determination with any degree of confidence! It sounds to me like a lot of guesswork is involved.

    When discussing amplification of pain, Clauw uses the analogy of an electronic device, i.e. the amplifier. Apparently, the levels of neurotransmitters that can either facilitate or reduce “pain transmission” determine where the dial is set for a particular patient.

    Of course, the belief that pain is “transmitted” along “pain pathways” (as claimed by Clauw) is flawed and outdated. Nerves transmit electrical impulses rather than a “thing” called pain.

    Furthermore, given that the brain produces the lived experience that we call “pain,” it seems impossible to conceive of a brain being able to amplify an experience for which it is primarily responsible.

    According to Clauw (2014), “Fibromyalgia and other centralized pain states are much better understood now than ever before.”

    But he gave the game away when he suggested that on the one hand fibromyalgia can be considered as a “discrete diagnosis” whilst on the other hand it can be considered as “a constellation of symptoms characterized by central nervous system pain amplification with concomitant fatigue, memory problems, and sleep and mood disturbances.” According to his formulation, clinicians are permitted to choose either possibility.

    Far from there being a “better understanding” of fibromyalgia, it seems to me that an appreciable element of diagnostic confusion and circularity still exists.

    Reference: Clauw DJ. Fibromyalgia: a clinical review. JAMA 2014; 311(15): 1547-1555.

  6. Phil, for the record, I do not adhere to the “CNS first” explanation of the clinical features of “fibromyalgia”.

    Please read the summary of our “stress response hypothesis” very carefully and you will find that we can offer an explanation for the clinical features of fibromyalgia, which we see as manifestations of undampened activation of evolutionarily conserved stress or sickness responses.

  7. Phil, time did not allow me to respond to your hypothesis, as you stated it:

    My “biological” hypothesis is simply that chronically inappropriately tensed muscles as a result of stress or nervous trauma, renders one more susceptible to fascia “adhering” when there are other factors that render the fascia more “adhesive”. In the absence of these other factors, the adhesions do not occur. The muscle tensions themselves will probably cause pain, and appropriate release techniques and relaxation techniques will resolve the problem if CNS commands to “relax because of the pain” do not do it first. However if the fascia is “adhesive”, permanent lumps will form and no therapy or techniques will resolve them until some other treatment or strategy starts to flush out whatever is causing the adhesiveness. This explains why cortisone injections resolve these lumps temporarily – the cause of fascia adhesiveness is still present and eventually re-forms the lumps.

    Your hypothesis bears a similarity to that advanced by Dr Liptan. I have already discussed it in relation to Dr Liptan’s article, as mentioned above. Link: http://www.fmperplex.com/2015/07/14/could-fibrositis-be-making-a-comeback/

    The “fibrositis” hypothesis is interesting from an historical viewpoint but, as presented, lacks biological plausibility. Yet, innumerable manual therapists make their living by attempting to “treat” these phantom lesions in muscles and fascia. Alas, all to no avail!

  8. Phil, I suspect that we will keep going around in circles until the epigenetic mechanisms that usually tightly regulate our stress response systems are better understood. Then and only then will we be in a position to know how to switch off the stress-response genes that are maintaining the “rage”.

    Of course, we may be looking in the wrong direction but when you look closely, there is a remarkable similarity of human stress/sickness responses to those of other members of the animal kingdom.

  9. The “mighty trigger point” has crossed the Atlantic Ocean to take up residence in Harley Street, London. Trigger point therapy has also crossed disciplines, moving from physical therapy into pain medicine..

    For those who are interested in cost, it appears that “wet needling” is much more expensive than its “dry” alternative.

    It has been said that “we are in the era of the musculoskeletal magicians who conjure up constructs that only their potions can fix!”

    I am not so sure that this is true. We could well be going back to the future.

    As Rudyard Kipling [1865-1936] wrote in the 19th century:

    Wonderful little, when all is said,
    Wonderful little our fathers knew,
    Half of their remedies cured you dead,
    Most of their teaching was quite untrue.

    Yet when the sickness was sore in the land,
    And neither planet nor herbs assuaged,
    They took their lives in the lancet hand,
    And Oh, what a wonderful war they waged!

    And here is the evidence: https://www.londonpainclinic.com/our-services/fibromyalgia/

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