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  • December 1, 2016

[75]        Her symptoms are not likely to improve. It covers so many aspects of symptoms, diagnosis, the systemic aspects of these diseases (immune function, sleep), treatments, lifestyle, and more, that you will delve into it time and again. This is a most important academic debate. When the complex system of bones, joints, tendons, nerves and muscles in your head and jaw do not work in unison or they become imbalanced the result can be painful. After a diagnosis of Myofascial Pain Syndrome (MPS) or Chronic Myofascial Pain (CMP) you may have many questions. The pain in TMJ disorders is usually Myofascial Pain. Palpation of a hypersensitive bundle or nodule of muscle fiber of harder than normal consistency is the physical finding typically associated with a trigger point.

The condition is chronic, meaning that the sufferer will experience pain in the affected area for some time. The cause of myofascial pain is over-stimulation of the nerve connected to the muscle. He understandably was frustrated because he was not able to pinpoint what activities were exacerbating his problem. (tinnitus), and dizziness may be symptoms of trigger points in the muscles around the jaw, face, head and neck. (Full record) 2. You have a few treatment options to help treat this syndrome. Limitations of space in Rheumatology meant that the many studies that have been undertaken based upon the premise that TrPs were potential sources of nociception resulting from localised muscle damage could not be included.

As such, they tend to causes continual pain, a reduction in muscle elasticity and muscle weakness. in this case an unwarranted assumption regarding the properties of TrPs), no amount of evidence can ever rectify such a fundamental fallacy of logical reasoning. These muscles will often respond by developing TPs. As for the second proposition, it was not our brief to provide “alternative studies specifically done on the pain phenomenon.”  But at the very least our paper calls for such studies to be undertaken as a matter of priority. Furthermore, in our paper we have pointed a way towards achieving this objective. A theory is a generally accepted explanation for an observed set of phenomena. Hypotheses can be deduced from theory.

Although these theories are related more to risk factors than to actual causes, they are still helpful in understanding everything better. Tender points, by comparison, are associated with pain at the site of palpation only, are not associated with referred pain, and occur in the insertion zone of muscles, not in taut bands in the muscle belly.8 Patients with fibromyalgia have tender points by definition. 2:  Anatomy of a trigger point complex. We did mention the face validity of the generally accepted explanation for the phenomena associated with the MTrP, but in our paper we went on to argue strongly against it on the grounds that its proponents were lacking in epistemological discipline. Although Dommerholt and Gerwin agree with the absence of agreement about the pathognomonic feature of their explanatory model, despite 50 years of investigation, they still argue that more studies are needed. But we fail to see how such studies would avoid the twin errors of confirmation bias and circular argument. They definitely cannot be stretched out in the traditional way we think of stretching.

(2012) were indeed able to provide an objective assessment of relatively superficial soft tissue, but did not make a comment as to whether the reported abnormalities in painful muscle were consistent with “contractured nodules”. They did find regions that were “stiffer” than surrounding muscle tissue and equated them with “active” trigger points. For instance, muscle pain is probably more common than repetitive strain injuries (RSIs), because many so-called RSIs may actually be muscle pain. Eventually these muscle contractions cause trigger points to form in addition to the tender points of fibromyalgia. This therapy is designed to reduce any muscle spasms and/or referred pain that patients may be experiencing. did not explain how they were able to exclude from the study those patients whose pain and tenderness was likely to have been referred into the muscle(s) being studied. Sikdar et al (2009) claimed to have excluded those with “neck and shoulder conditions” including cervical radiculopathy.

But did they really exclude patients whose pain may have been referred into these muscles from, for example, cervical zygapophyseal joints? We think not! In a preliminary study Maher et al. (2013) found that the shear modulus of the upper trapezius muscle with MTrPs was significantly reduced after dry needling of the most painful TrP and also when the subjects assumed the prone position from supine lying. These changes were accompanied by palpable reductions in stiffness. The authors did not address the important questions as to whether these reductions were transient and whether pain relief accompanied them. Yet, in the studies we reviewed, and in the various other studies cited by Dommerholt and Gerwin, the authors assumed that an anatomical lesion actually existed.

This logical fallacy is known as “begging the question”. Our difficulty in accepting data derived from findings in muscles from normal animals is covered in our paper. Moreover as Dommerholt and Gerwin acknowledge “there has not been a study to demonstrate the minimum essential features needed to identify it for diagnosis and treatment purposes.” If this issue has yet to be resolved in humans, we fail to see how it has been resolved in animals. It should be noted that mechanical irritation of a hypersensitive peripheral nerve appears to generate a motor efferent response with activation of at least a subset of the motor neuron pool (Hall and Quintner, 1996). We are indeed troubled by the first proposition. It has yet to be shown that MTrPs are capable of activating nociceptors. It is believed that MPS is caused by the body’s inability to interpret pain correctly, a drop in levels may actually be the main cause to the condition.

This conjecture concerns low threshold motor units, termed “Cinderella” fibers, which are being continually recruited and overloaded during low-level static exertions. It is not made clear how could one ever know this? Presumably damage to such fibers provides the basis for nociceptive input in these situations. This conjecture forms the central plank of the Integrated Hypothesis (Gerwin et al 2004). In the second study, the authors concede that their findings were solely dependent on the expertise of a clinician not only to palpate the upper division of the trapezius muscle to locate and diagnose a taut band as a MTrP but also to rate its “sensitivity”. Readers are then asked to accept the dubious proposition that once the examiners had located a TrP, “all detected trigger points in the trapezius and surrounding muscles were released by a combination of percussion, stretch and relaxation techniques” immediately prior to the commencement of the experimental task (approximately 60 minutes of computer typing). Following task completion, the subjects were then re-examined by the same clinicians to detect recurrence of any MTrPs, which were again duly “released”.

Surface EMG was recorded from a grid overlying the identified MTrPs. The authors speculated that MTrPs may be one causal pathway for pain during low-level static exertions and both postural and visual demands may play a role in muscle activation patterns, perhaps contributing to MTrP development and related discomfort. “Rather than ignoring the worldwide developments in this field, we prefer the approach by Jafri, who critically reviewed the current thinking and contributed to a more in-depth understanding of possible underlying mechanisms (Jafri 2014)”. Jafri accepts without reservation the opinion of David Simons (2004), one of the main proponents of MTrP theory. Unfortunately the remainder of his paper fails to rise above the level of conjecture. The roller has its benefits; so does a ball, or a therapy cane. However, Moseley then asserts: “trigger points are present in all patients with musculoskeletal pain …” Drawing an analogy here with the universal generalization that “all swans are white” seems inescapable.

The observation of one black swan (or of one patient without a trigger point) falsifies the argument. Physical therapists and chiropractors are often preoccupied to a fault with joint function, biomechanics, and exercise therapy. Some of their concerns about the “neuritis” model can easily be resolved when one accepts the readily available evidence that pain of peripheral nerve origin may not necessarily be accompanied by changes in cutaneous sensation, by objective signs of motor deficit or by changes detected on conventional electrodiagnostic examination (Quintner and Cohen, 1994). Dommerholt and Gerwin prefer to rely upon evidence from the experimental studies of Arendt-Nielsen and Svensson (2001) and Rubin et al. (2009) to support the importance of “ongoing nociceptive input from the site of primary muscle pain in maintaining the phenomenon of referred pain.” But no such experiment has been shown to mimic the clinical situation. We do not doubt that nociceptor fibres innervate muscles and that they can be activated by a variety of noxious stimuli. We agree that central mechanisms are important in explaining the phenomena of referred pain.

However, it has yet to be demonstrated that a hypothetical “painful lesion” residing in “myofascial” tissues can be responsible for initiating and maintaining a state of central hypersensitivity. As we have shown, Dommerholt and Gerwin (and others) have been arguing from the false premise of an unwarranted assumption – that MTrPs are primary sources of nociception. No amount of evidence they can adduce will rectify this logical error. But if, as we believe, MTrP theory has been well and truly refuted, the scientific credibility of those who offer courses in “dry needling” to physical therapists can legitimately be called into question. Prepared by John Quintner, Physician in Rheumatology and Pain Medicine, first author of “A critical evaluation of the trigger point phenomenon (2015).” He writes here on behalf of his co-authors. Ballyns JJ, Turo D, Otto P, Shah JP, Hammond J, Gebreab T, Gerber LH, Sikdar, S. Office-based elastographic technique for quantifying mechanical properties of skeletal muscle.

J Ultrasound Med 2012; 31: 1209-1219. Rubin TK, Henderson LA, Macefield VG. Changes in the spatiotemporal expression of local and referred pain following repeated intramuscular injections of hypertonic saline: a longitudinal study. J Pain 2010; 11: 737-745. Sikdar S, Shah JP, Gebreab T, Yen RH, et al. Besides, physical therapists also help to correct the poor postures which may be the cause of the pain. Arch Phys Med Rehabil 2009; 90: 1829-1838.

Simons DG. Electrogenic nature of palpable bands and “jump sign” associated with myofascial trigger points. In: Bonica JJ, Albe-Fessard D, eds. Adv Pain Res Ther (vol.1). New York: Raven Press, 1976: 913-926. Suh MR, Chang WH, Choi HS, Lee, SC. Ultrasound-guided myofascial trigger point injection into brachialis muscle for rotator cuff disease patients with upper arm pain: a pilot study.

Ann Rehabil Med 2014; 38: 673-681.

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