"Trigger points" and pain

[Diane]

Here is a fresh link to an old friend, a paper that deconstructs the poor construct validity of "myofascial pain" and connecting them to trigger points.
I'm copying and pasting the whole thing, because I never ever want to lose this paper from a dead link again. Unfortunately, the tables do not copy well.

Myofascial Pain Management

Evaluated material for both the health care provider and consumer.

REFERRED PAIN OF PERIPHERAL NERVE ORIGIN:
AN ALTERNATIVE TO THE "MYOFASCIAL PAIN" CONSTRUCT

John L. Quintner and *Milton L. Cohen

Wyllie Arthritis Centre, Perth, Western Australia, and *St. Vincent's Hospital, Sydney, and University of New South Wales, Sydney, New South Wales, Australia

Although painful conditions of varying degrees of severity involving the soft tissues (i.e., muscles, tendons, ligaments, and peripheral nerves) occur frequently, their underlying pathogenesis is poorly understood. During the 19th century, these conditions were called muscular rheumatism or fibrositis to distinguish them from conditions such as articular rheumatism, which primarily involve joints (1). Chronic forms of muscular rheumatism were attributed to inflammation of a "peculiar" kind affecting the fibrous tissues around joints; this inflammation was found in tendons, bursae, ligaments, fascia, nerve sheaths, muscles, and periosteum (2). Others only used the term rheumatism when they wished to denote the presence of non-specific inflammation involving voluntary muscle fibres (1,3).

In the early part of this century, the English neurologist Gowers (4) championed the concept of "fibrositis" as a painful inflammatory disorder of the fibrous structure of muscle spindles (at that time the only known sensory structures in muscle). He taught that "fibrositic" inflammation could spread by direct fascial extension to involve nearby ten- dons, joints, and nerve sheaths (interstitial neuritis), thus unifying the two conceptual models of the 19th century. By the 1930s his views had gained general acceptance. The committee on "arthritis and allied conditions" appointed by the British Medical Association in 1933 recognized the following subgroups of fibrositis: intramuscular and facial; periarticular; bursal and tenosynovial; subcutaneous (panniculitis); and perineuritic (5). The clinical sequelae attributed to "perineuritis" included radiating pain, paresthesiae, cutaneous hyperesthesia, tenderness in muscles and joints in the sensory area served by the nerves involved, and tenderness over the site of the nerve itself, which was attributed to the involvement of the nervi nervorum. Motor and sensory impairments were uncommon (5).

Over the next 50 years, clinicians attempting to unravel the complex nature of muscular rheumatism focused their attention on palpatory findings in and around voluntary muscles, almost to the exclusion of a possible contribution to pain from peripheral nerves or other tissues. The concept of the "fibrositic nodule," described as "an area in the substance of a muscle or its tendinous sheath which gives rise to pain either in the same locality or referred to a distance when stimulated" (6), was discarded when it became clear that it lacked pathological support (7). In addition, as knowledge of spinal disc pathology increased, it was argued that so-called fibrositic lesions in muscles could be explained as secondary or referred phenomena (8).

However, those who still adhered to the belief that many localized or regional chronic pain syndromes are attributable to more subtle pathological changes occurring solely within voluntary muscle put forward the construct of the myofascial pain syndrome (9). More recently, another, competing, construct has been redefined to account for chronic and widespread musculoskeletal pain, namely fibromyalgia syndrome (10). The main diagnostic criterion for this syndrome is the presence of a defined number of "tender points" at predetermined anatomical sites. We have argued elsewhere that this construct conveys no pathophysiological insights, having been derived by a process of circular argument (11). Moreover, some authors have recognized that there may be considerable clinical overlap between the two syndromes (12,13). In view of the controversial and complex nature of these pain syndromes, a critical analysis of the prevailing hypotheses is justified to clarify the situation.

In this article, the hypothesis that pain arising from trigger areas within muscles is of primary myofascial origin is critically examined. It will be shown on epistemological, clinical, and pathophysiological grounds that the myofascial pain syndrome (MPS) construct is invalid and that the phenomena it purports to explain are better understood as secondary hyperalgesia of peripheral neural origin.

THE "MYOFASCIAL PAIN" CONSTRUCT

The major sources for the synthesis provided herein are the principal writings of the proponents of MPS (9,14-19). Definition and basic phenomenology

Myofascial pain has been described as "the most common cause of chronic pain" (17). Introduced in 1952 after a decade of research, and developed since by Travell and her co-workers (9,15), MPS has been defined as a regional pain syndrome with two major components: (a) the trigger point, a localized area of deep muscle tenderness or hyperirritability; and (b) a predictable, discrete reference zone of deep aching pain, which may be located in the immediate region of or remote from the trigger point (TrP), may be quite extensive, and is worsened by palpation of the TrP.

Trigger points have been described in skin, joint capsules, ligaments, and periosteum as well as in muscles and their fasciae. Myofascial TrPs are said to be located within palpable taut bands, purported to represent shortened muscle fibres. On "snapping" palpation or needling of a myofascial TrP, a local twitch response can be elicited. This clinical sign is accompanied by an irritable electromyographic response. A muscle containing a TrP exhibits antalgic inhibition when tested for strength and is also intolerant to stretch. In a seeming contradiction, muscle stretching is recommended as being efficacious treatment for myofascial pain. Relief of pain requires "inactivation" of the relevant trigger area, by physical (needling or stretch) or chemical (local anaesthetic) means.

Travell and Simons (15) insist that the "specific muscle or muscle group that causes the symptoms should be identified." More recently, Simons (19) has defined MPS as "primarily a dysfunction of one or more specific muscles" (emphasis added). The constancy of distribution of pain referred from individual muscles is said to enable the clinician to "work backward" and thus locate the TrP(s) responsible for particular pain patterns.

One of our main criticisms of the construct of myofascial pain is that its major proponents have incorporated their preferred hypothesis of causation within the definition. As will be shown elsewhere in this article, this error in reasoning has limited the discussion of other explanations for the various clinical phenomena observed in these syndromes. Metaphysics of trigger points

The TrP is said to "cause" (16) or have "the propensity to cause" (18) or "the responsibility for causing" (17) local and referred pain. It has even been suggested that TrPs may at times "refer" hypoaesthesia or anaesthesia instead of pain (19). Trigger points may be "active," "latent," "satellite," or "secondary." Active TrPs are more likely to be found in musculature of the neck, shoulder, and pelvic girdles and in the muscles of mastication. They can occur in multiple locations in any one muscle; their site(s) can vary from person to person and their irritability is said to vary from hour to hour and from day to day.

A TrP is considered latent or dormant if it is not causing" referred pain. Latent TrPs can be found in asymptomatic subjects, in whom the TrPs are nonetheless said to restrict movement and cause weakness in the affected muscle (20). Latent TrPs are said to accumulate with advancing age (14).

Satellite TrPs are those that can be found in muscles within the pain reference zone of another TrP. Secondary TrPs develop in muscles that are either synergists or antagonists of the muscle that contains the primary TrP. Synergists are said to be overloaded when they substitute for the affected muscle and antagonists are said to be overloaded when they counter its tautness.

Initiation

It was originally proposed that myofascial TrPs may be initiated by "direct trauma to muscle or joint, chronic muscular strain, chilling of fatigued muscle, acute myositis, arthritis, nerve root injury, visceral ischemia or dykinesia, and hysteria" (9). These same factors, plus resumption of normal activity after periods of immobility, are also said to be capable of activating latent TrPs. A latent TrP may even be activated during therapy: as one set of muscles is being stretched, their antagonists, which presumably contain the latent TrP, are shortening.

Myofascial pain is now mainly ascribed to an initial insult to muscle fibers, either from macrotrauma or repetitive microtrauma (16). The consequences of such an insult may include release of such substances as histamine, serotonin, kinins, and prostandins which may then activate nociceptors and cause reflex muscle contraction.

However, this proposition of muscle injury lacks empirical support. Muscle pain and damage following eccentric contractions have been extensively studied (21). In normal subjects, complete recovery is the rule and no long lasting effects have been noted. Unless muscle strains are severe (e.g.., complete tears) or associated with deep haematoma formation, recovery is complete. Sever distraction or contusion injuries are common in sport but no evidence has been presented that such well-defined acute injuries are antecedents of MPS. Furthermore, electromyography of painful muscles (22) and thermographic studies of the tissues overlying them (23) have not demonstrated abnormalities in TrPs. Muscle biopsy studies of TrPs have also been largely unrewarding in terms of muscle inflammation or damage.

Perpetuation

The chronicity of pain that follows the activation of a myofascial TrP has been explained by a feedback cycle maintained by bombardment of the central nervous system (CNS) by impulses from TrPs themselves: that is, they become self-perpetuating. However, remote lesions in joints or chronic visceral disease and dysfunction may also provide noxious input into this cycle, as may emotional stimuli, chronic infection, various metabolic disturbances, and even dietary deficiencies (14).

As the painful muscles in MPS are electrically silent, the presence of muscle spasm that may reflect ectopic impulse formation seems most unlikely (22). Furthermore, the efferent arm of the proposed vicious cycle has been tested. Mense (24) found that gamma-motoneuron activity was diminished rather than increased in muscles with carrageenan-induced injury and concluded that the proposed vicious-circle models "have to be considered as working hypotheses rather than explanations of known mechanisms.

Spread

Spread of pain is attributed to latent TrPs being activated or to active myofascial TrPs "metastasizing" to sites within or outside of the pain-reference zone of the original TrP(s) (18). Travell (14) postulated a chain reaction whereby an ever-increasing number of satellite TrPs come into being, causing complex overlapping patterns of pain.

Reliability of TrP phenomena

When blinded as to diagnosis, those expert in the field of MPS were able to detect active TrPs in only 18% of examinations of subjects with a MPS diagnosis (25). In the same study, expert assessments for taut bands and muscle twitch responses were also found to be unreliable. These findings call into question the internal validity of the construct.

Treatment

Inactivation of the TrP by physical and chemical means would be predicted if the TrP is indeed a site of primary hyperalgesia. However, reports of the efficacy of this approach are only anecdotal; inactivation has not been subjected to formal trial. Furthermore, the persistence of using the recommended approach in the face of clinical inefficacy, along with the continuing failure over time to reveal a reasonable anatomical or pathophysiological basis for so doing, is not only irrational but also fails to acknowledge powerful placebo effects (26) and the wider psychosocial context of chronic pain (27). Objections to MPS construct

The definition of MPS incorporates a preferred hypothesis of causation. This logical error has resulted in a system of diagnosis and treatment that has become popular but remains entirely anecdotal. Moreover, the proposition that myofascial pain and TrPs are intimately related constitutes circular reasoning: that is, by virtue of its form this proposition must always be true (Table 1).

In their efforts to preserve the centrality of the myofascial TrP, myofascial pain theorists have al- lowed the number and nature of predisposing, precipitating, and perpetuating factors to be open-ended and to encompass the full spectrum of aetiology, including the untestable psychogenic level. (16,17). This serves only to perpetuate the circularity of the reasoning.

Perhaps in an attempt to provide external validity, researchers have said that TrPs arise from muscle damage, despite electrical silence and the lack of histological or biochemical evidence. Furthermore, there is neither support from an animal experimental model (24) nor from studies of human muscle injury (21). Trigger points are nonetheless said to be maintained via the CNS, not only by their own activity but also by a legion of processes associated with afferent neural input. Spread of pain is attributed to the activation of latent TrPs or to the metastasis of TrPs. This teleological argument is physiologically unsound.

Taken together, the tenets of the MPS construct arise out of circular reasoning, which should condemn MPS as epistemologically unacceptable."MYOFASCIAL PAIN" VERSUS PERIPHERAL NEURAL PAIN

The argument that follows explores a putative relationship between "myofascial pain" and pain of peripheral neural origin. We show that the explanation for peripheral neural involvement in MPS, which depends on nerve compression by "taut bands," is speculative and unconvincing. Application of current concepts of the physiology of nociception can lead to an alternate construct. Differential diagnosis of MPS

The differential diagnosis of myofascial pain, as proposed (14,16), includes a variety of painful and somewhat loosely defined neurological conditions such as thoracic outlet syndrome (28), radiculopathies, and polyneuropathies. Their differentiation from myofascial pain is said to be facilitated by the presence of accompanying neurological deficits (particularly those matching a peripheral nerve or root distribution) and electrodiagnostic abnormalities (15). Although a fundamental distinction has been made between TrP pain (deep and aching) and pain of peripheral neural origin (prickling, tingling, and numbing), Dalton and Jull (29) were not able to distinguish between somatogenic and neurogenic cervicobrachial pain when they relied solely on the characteristics of pain. Moreover, peripheral neural pain can occur without neurological deficit (30) and without conventional electrodiagnostic abnormality (31).

By contrast, when neurological deficit (often accompanied by electrodiagnostic abnormality) accompanies MPS, it has been ascribed to peripheral nerve entrapment by the taut band containing the TrP (16,19). The taut band is said to cause an overall shortening of the involved muscle, which then, in turn, can lead to a "secondary" nerve entrapment syndrome (32). The dual propositions that neurogenic mechanisms can activate myofascial TrPs and that myofascial TrPs can cause neurogenic pain add up to a circular argument. Furthermore, the neurological literature does not include the TrP taut band as a recognized anatomical cause of entrapment neuropathy (33,34).

However, on clinical grounds alone, there appears to be an intimate relationship between MPS and defined neuropathology. This relationship is worth exploring in terms of current understanding of nociceptive mechanisms. Characteristics of myofascial pain

The pain attributed to myofascial TrPs is described as deep, dull, and aching, varying in intensity from mild to severe and occurring either at rest or only on motion (Table 2). These are the characteristics of deep somatic pain. By the 1930s, it had been long known that pain arising in deeply situated joints was often referred to anatomically distant structures. The seminal clinical experiments carried out by Lewis (35) and Keligren (36) convincingly demonstrated the same phenomenon for pain arising in other deep musculoskeletal tissues, such as muscles, ligaments, and periosteum.

According to Kellgren (36), "The diffuse pain from a given muscle is always distributed within certain regions, though the distribution within these limits varies from individual to individual, and according to the part of the muscle stimulated" and "pain from muscle may be confused with pain arising from other deep structures such as joints and testis."

Some caution is therefore necessary before a mechanically provoked pain response is attributed to a particular structure or structures. Afferents from muscles that are the sites of referred pain and tenderness are the very ones that converge centrally onto spinal neurones that could be involved in processing information from a region of deep damage, thus leading to central summation effects (37).

Vasoconstriction, hypoesthesia, dermographia, and hyperhidrosis have been observed in the skin overlying a region of deep pain. These phenomena appear to be reflexly induced concomitants of somatic referred pain (38). Peripheral neural pain

The connective tissues of human peripheral nerves are well-innervated. They derive their nerve supply from axons within the nerve and from fibres accompanying the extrinsic vessels that provide its nutrition (39). As well as regulating intraneural microcirculation, this intrinsic nerve system, the nervi nervorum, is thought to have a nociceptive function (40).

Two types of pain, present singly or in combination, have been described in patients with peripheral neuropathy: "nerve trunk pain" and "dysesthetic pain" (41). The former pain has been described as aching, knifelike, or tender, whereas the latter has been described as burning, tingling, searing, crawling, drawing, or electric. Nerve trunk pain is therefore indistinguishable from pain described as myofascial (see Table 2). Nerve trunk pain has been attributed to increased activity in mechanically or chemically sensitized nociceptors within the nerve sheath, while dysesthetic pain has been attributed to damaged nociceptive afferent axons themselves.

Nerve trunk pain characteristically follows the course of the involved nerve, which is found to be tender, whereas dysesthetic pain is felt in its peripheral sensory distribution (41). However, when pain of nerve origin is severe, it can be felt in regions outside the sensory distribution of the particular nerve (33,34).

Peripheral neural pain may be associated with neurological deficit, but it can be accompanied by a hyperaesthetic syndrome, which includes both allodynia (pain due to a normally non-painful stimulus) and hyperalgesia (an increased response to a normally painful stimulus) (42-44). The term peripheral neuropathic pain has recently been suggested to embrace the combination of positive and negative symptoms in patients in whom pain is due to pathological changes or dysfunction in peripheral nerves or nerve roots (45).

Pain with the characteristics of "nerve trunk pain" has been described by patients with irritative cervical (46) and lumbar (47) radicular lesions, with brachial neuropathy (40), and following peripheral nerve injury (48).

Most nerve pain syndromes commence with symptoms more in keeping with an irritative than a destructive process (49,50). Local tenderness is commonly found over nerve trunks at sites of entrapment or metabolic insult; this tenderness has been attributed to sensitization of free nerve endings within neural connective tissue (nervi nervorum) (40). Such specific tender points over peripheral nerves, palpation of which could cause distant pain, was reported over a century ago (51). It has recently been suggested that radiating pain and other sensory phenomena could originate from ectopic neural pacemaker nodules formed at a site of entrapment (52). Tenderness has also been noted over motor bands (zone of innervation) and muscles in association with cervical and lumbar radicular pain without gross physical signs of denervation (53). Neuropathic pain states are frequently accompanied by abnormalities in functioning of the sympathetic nervous system (54). Referred neural pain

lntraneural stimulation of muscle fascicles within the median and ulnar nerve trunks of normal volunteers has been shown to refer pain both distally to muscles within the innervation territories of each nerve, and proximally to deep structures (muscle and bone) in segmentally related regions outside the innervation territory of each nerve (55,56).

Recounting his personal and clinical experience, Ochoa (57) described both local elbow pain and referral of pain into the ipsilateral scapular region following mechanical stimulation of an entrapped ul-nar nerve at the elbow. In his own and the other cases, none of the distal symptomatology typical of ulnar neuropathy was present.

Thus, peripheral neural tissue is a rich source of local and potential referred pain. Anatomical concordance of myofascial TrPs and peripheral nerves

Some TrPs said to be myofascial could be situated in an adjacent hyperaigesic nerve trunk. For example, the discrete upper-limb pain syndromes attributed to TrPs in the middle finger extensor, the extensor carpi radialis, and the supinator muscles can equally be attributed to TrPs in the radial or posterior interosseous nerve trunks. The TrP said to be situated in the pronator teres muscle coincides with the median nerve, and the pain projected therefrom into the thenar muscles follows the course of the median nerve in the forearm. TrPs in the flexores digitorum referring pain into the hand may represent a tender compressed median nerve in the proximal forearm. MPSs in the shoulder girdle region may represent entrapment of the suprascapular nerve, the long thoracic nerve, the axillary nerve, and the dorsal scapular nerve, as the pain- reference zone of the TrPs follow the course of these nerves. In the lower limb, MPSs have been attributed to TrPs close to the sciatic, tibial, and superficial and deep peroneal nerves. ALTERNATIVE EXPLANATIONS FOR MPS PHENOMENA

Alternative explanations for MPS phenomena are summarized in Table 3.TrPs as sites of secondary hyperalgesia

The weight of evidence does not support myofascial TrPs as the anatomical sites of pain origin. By contrast, the presence of hyperalgesia in muscles that are structurally and electrically normal suggests that it must be secondary (referred) hyperalgesia (58). This hyperalgesia could be due to peripheral mechanisms such as antidromic activation or sensitization of nociceptive afferents (59) or, more likely, to a state of central sensitization, including spontaneous firing and expansion of the receptive fields of nociceptive dorsal horn neurones (60). Spread of pain

Latent, metastasising, and secondary TrPs lack supporting evidence, as does nerve entrapment by taut bands. The spread of pain is more likely to be the consequence of altered central nociceptive processes and enlarged receptive fields in response to ongoing nociception or ectopic impulse generation (60). Intolerance of muscle to stretch

The taut bands described in muscles containing TrPs may represent reflex spasm secondary to nociception in structures innervated by the same spinal segment (8). The intolerance to stretch could also be explained as a reflex response to the stretching of adjacent hyperalgesic neural tissue. Chronicity of pain

MPS theorists attribute chronicity of pain to the self-perpetuating propensity of TrPs, usually in the presence of an assortment of other factors such as a short leg, poor posture, somatoform pain disorder, chronic infection, and secondary gain-all of which are teleological arguments. Alternatively, it has been shown that the altered central processing held responsible for secondary hyperalgesia may be maintained by nociception elsewhere possibly including, of course, peripheral neural structures (61). Hypoesthesia

There are two explanations for hypoesthesia in MPS theory: compressive neuropathy by a taut band or a referred phenomenon reflecting the down- ward modulation of receptive fields in the pain reference zone of the TrP (19). Irrespective of the particular entrapping mechanism, it is accepted that hypoesthesia results from the loss of sensory afferents due to nerve compression at the site of an entrapment (33). However, hypoaesthesia has also been attributed to a functional block occurring at spinal or higher levels associated with a peripheral neural pain state (43). Vasomotor and sudomotor disturbances

Disturbances of sympathetic efferent function that have been described in association with MPS have also been recognised as reflexly induced accompaniments of neuropathic pain states.

CONCLUSION

The construct of MPS, as proposed to explain chronic, deep, aching, poorly localized pain, not only lacks internal and external validity but also is epistemologically unsound. The emphasis on the primacy of the TrP phenomenon has directed attention away from other possible explanations. By contrast, there are anatomical and physiological grounds to suggest that the phenomenon of the TrP, on which depends the theory of MPS, is better understood as a region of secondary hyperalgesia of peripheral nerve origin. This proposition is testable to achieve external validity for the described clinical phenomena.


TABLE 2. Comparison of peripheral neural pain with myofascial pain
TABLE 3. Pathophysiological explanation for the phenomena of myofascial pain syndrome
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60. Dubner R. Neuronal plasticity in the spinal and medullary dorsal horns: a possible role in central pain mechanisms. In: Casey KL, ed. Pain and central nervous system disease: the central pain syndromes. New York: Raven Press, 1991; 143- 55.

61. Gracely RH, Lynch SA, Bennett GJ. Painful neuropathy: altered central processing maintained dynamically by peripheral input. Pain 1992;51:175-94.

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[Jason Silvernail]

Diane-
This is great. Treating trigger points has never made sense to me.

This is from the Clinical Journal of Pain, 1994, the pubmed link is here.

I'd love to see an update that addresses some of the recent research published addressing the TrP issue.

[Diane]

I'd love to see an update on this too. Quintner has several articles on sore spots.
I've always treated them, but was glad to leave mesodermalism behind thanks in part to this article, just treat them as spots where the nervous system isn't working well.

[Luke Rickards]

I made a point of bringing up this paper in the last paragraph of my review. It's a shame they haven't published any more on this topic since '94

[Diane]

I found another Quintner article.
THE DERAILMENT OF RAILWAY SPINE: A TIMELY LESSON FOR POST-TRAUMATIC FIBROMYALGIA SYNDROME . The more time goes by the more things stay the same?

[Mariette]

"These syndromes are in no way different from other chronic pain syndromes in that their presentation is coloured by cognitive, affective, and behavioural factors. To postulate an initial pertubation of nociception which sets in train both physiological and psychological processes provides a unifying model which avoids the fallacies of dualistic thinking".

I've spent the past weekend at a course where I was often wondering what I was doing there. Of the 13 hours spent on peripheral neural dysfunction 22min....yes I actually timed it, were spent on what the patient may or may not think, descending inhibition, cognition and pain.
Sorry to say it is "not catching up" as fast as I would have wanted it.

[ginger]

Thanks Dianne, good to have further science putting paid to the old and very tired notion that muscles and other distal soft tissues are somehow 'bad' or pathological. Rather than taking part in a pattern of tone , behaviour and pain events directed by central neural directions. The physiology of these central mechanisms are , according to the daily examples I witness in my work , ideally explained by irritation related to inflammatory events. These inflammatory events also well explained by the likely and common themes of facet joint behaviour, as would be expected when protective tone increases limit spinal joint movement. By reducing hypertonicity of parazygoapophyseal muscle and restoring normal facet movement behaviour , immediate reductions in these distal muscle "trigger point" indicators are seen. No point jabbing away at the muscles when control and normal behaviour can be better asserted by restoring an irritation free condition by direct attention to central structures. These central structures are easily accessed, found and palpated. Also easily moved , sensed in their movement responses and considered by therapists hands ( thumbs to be precise).
Continuous mobilisation as a method of choice has a lot going for it. Not the least of which is its immediate and lasting effect on the very muscle behaviour this study maintains is centrally mediated .

[nari]

Milton Cohen is regarded as a figure of note in and around the traps.

I think this group of specialists should move their specialty's name away from the ancient word rheum.. It perpetuates the idea that muscle and bone are to blame for almost everything, though that is not their intention.

Nari

[Keats Snideman]

So are you guys basically saying that trigger points don't exist (at least in the context by which they are commonly explained)? What about the common referall paterns that can be elicited in a majority of subjects?

Are trigger points really just issues with the central and peripheral nervous system; some sort of "neural lesions?"

[Diane]

Hi Keats
What do you think, having read the paper?

[ginger]

Keats, trigger points do exist , that is , there are certainly points in muscle bellies that with digital and other pressures applied to those points, observations of tone decreases ( and sometimes the reproduction and reduction in referred pain ) to those muscles can often be made. These situations give massage therapists of various levels, hours of fun and games in their treatment lives, by offering what appears to be useful therapeutic change. What I refer to in my post above is an attempt to answer the question, "why is it so " ( I'm always tempted to say this with a Julius Sumner Miller voice ).
It is clear to those whose interests and experience includes the restoration of normal spinal joint/nerve function, that in the process of undoing, as it were, the results of what I term protective responses, leading to joint hypomobility and irritation of nerves, that trigger points are firmly linked phenomena.
In plainer speak , when I fix the spine, the trigger points go away, along with the kind of altered behaviour , sensation and other observations pertinant to the complained of limb problem. It seems then, that going hard directly at the muscle, by and large, is a time wasting effort , where therapists attention is directed at the effect , rather than the cause.
Alternate views do exist on the nature of that "central" irritation, some expressed on these pages. What is common to a "central first "theme however , is that neurology is the common denominator That when adressed , is often found to have been the origin of pain/dysfunction and indeed the only theme worth attention.

[nari]

It seems that all sorts of treatment are aimed at resolving this 'muscle problem'; the origin of this pain is not considered. Total lack of evidence that it is due to some microtrauma, as pointed out in the above paper, should convince TP enthusiasts to consider the origin of any pain, not just some supposed local problem.

One of the classic signs of referred pain is around the deltoid, often near the MT junction, and mobilisation of the cervical spine often resolves this rapidly. (Ginger, I know you will say almost always).
Diane's DNM techniques also resolves those pesky pain spots.
Instinctive movement as described by Barrett and others does the same. Neurodynamically-focused movements ditto. Ginger's CM techniques ditto.

Perhaps one way of looking at these options is to think about the simplest method, based on pain physiology as it is known at present, which will resolve the problem/s.
The issue with local attention to the painful spots with the assumption that they are muscle-based is that temporary pain relief is quite possible but surely our aim is to provide more than that. By that statement, I mean the person who keeps going back ad infinitum to a practitioner who simply offers muscle-based temporary pain relief, is not being appropriately managed.

Keats, the phrase "neural lesion" suggests a pathology exists, which is not accurate. Think instead, of heightened sensitivity of the nerve/s. Keep reading this forum Persistent Pain Problems, and some of the posts earlier on (it started in 2004) if you are not sure what sensitivity really means in a physiological sense.

Nari

[emad]

I think that Nervous System is the key element within the techiques Nari mentioned above . I think that the Trigger point is a Sensitive within the nervous system not the muscle ( however I do not negate the muscle completely , I do not consider it passive completely ) .When we mobilize the Cervical ,we actually mobilizing the nervous system .However , I think David Buttler mentioned Trigger points in his book as If it real exist . Trigger Points are fired because of stress physically and psychologically ,just a matter of Nervous System reaction .

cheers
Emad

[boneill]

Having studied with Dr David Simons and being somewhat of a myofascist myself, I thought I should rise to the defense of the myofascial community. Below is a link to a relatively recent update on Simon's trigger point hypothesis. Certainly, the academic and clinical myofascial community (small though it may be) is interested in all aspects of pain physiology. Jay SHah at the NIH has shown in trigger points, through a micropipette analysis technique, the presence of an acid Ph, and elevated levels of multiple nociceptive sensitizing chemicals including histamine, bradykinin, IL3, IL6 and others. Of course, this may be the end result of nervous system dysfunction and not the result of local muscle dysfunction. Clearly they are linked. I personally have found elimination of of trigger points and correction of biomechanical issues very effective. I believe through successive treatment, I am desensitizing an upregulated nervous system. Until, I learn a more effective way to do that, I will continue. I am hopeful that some of you may have those more effective ways and can point me in the right direction to obtain some of those skills. Enjoy the article.
Bryan


http://www.painpoints.com/profession...gerwdomm04.pdf

[Luke Rickards]

Hi Bryan,

I am familiar with the paper you refer to and have included it in my review of MTrPs last year. The full text is available here for members with access to the SoS.

Although the paper was a very big step in strengthening the MPS hypothesis I agree that we cannot yet rule out the presence of these inflammatory mediators as a result of peripheral nerve sensitisation.

If you read the review you will see that evidence supporting the effectiveness of treatments for the MTrP entity itself is somewhat ambiguous.

[boneill]

Apparently, I dont have access to SoS. Can someone tell he how to obtain that?
Bryan

[Jon Newman]

Hi Bryan,

There are two methods that I know of. One is post more (10 posts total and 30 days on the board after registration is normally required.) The other is to ask Bernard. He does SoS rehab and can get people there faster than they would otherwise do on their own.

[bernard]

Boneill
Just read the subject and follow the instructions.

Join the SomaSimplers' Group!

[boneill]

Thanks Bernard. I was able to access the article.
I am still finding my way around this incredible web site. It is packed with information.
Bryan

[Karie]

I was reading in David Butler's Book, The Sensitive Nervous System when I remembered Emad had suggested that David made reference to trigger points in his book and he does. Here's the quote that I happened upon, "Many trigger points may be small AIGS in cutaneous nerves struggling with their relationship to fascia and muscle and postural demands." He then refers to his section on "notalgia paraesthetica," in Chapter 15.

Just a FYI to add to the topic.

Karie

[emad]

Thanks Karie ;

That is correct ,however I did not read the Book ,but seems I picked it from the Book contents , I can not remember well from where I picked that .
notalgia paraesthetica ? can you please clear his view regarding that ?

cheers
Emad

[boneill]

Karie
What is an AIGS?
I have ordered Butler's book and am anxiously awaiting its arrival.
Bryan

[Diane]

Bryan, an AIGS is an abnormal impulse generating site. Nerve axons that are stressed (physically, either mechanically or chemically) develop too many receptor sites, sensitive to substances (sensitization from DRG out). These take three days to settle completely (physiologically clear, normalize) upon successful treatment.

[EricM]

AIGS is the acronym for an Abnormal Impulse Generating Site. Here's a few threads on the topic.

Pulling the Trigger
Bits and Bites on AIGS

[anoopbal]

Foam rollers are almost manadatory for any athletic training facilty to iron out trigger points.

I know its a nervous sytem phemonenon. Is there any effective way to target the nervous sytem or the cause in this case?

Anoop

[nari]

Foam rollers? Ironing out TrPs sounds helpful, as long as it is realised what the rollers are actually doing. Sounds very ectodermal to me.

We all have trigger points, and if anyone pokes somebody's arm, back, neck or leg there will be some degree of tenderness at certain spots. To do that the ectoderm is being poked at.
They become a problem when the nervous system is sensitised - ie they become AIGS, which can be very uncomfortable. Axons are not meant to develop receptor sites, but act as messengers.
What is pertinent is the fact these sites do not have to be treated locally for good effect.
If someone has painful sites around the neck or traps, for instance, mobilising the relevant nerve half a metre away can alter that sensation.
DNM, without localising the site, can do the same.
Dry needling (I have no reason to doubt its effectiveness) is probably an invasive alternative, if this is so desired.
Patients have reported good pain relief from their 'sore spots' after they exprience ideomotion.

If one has a cranky nail/AIGS or two, they don't need to be hit with hammers.

Nari

[boneill]

I just thought I would post these recent articles from Archives of PM&R. This is Jay Shah's follow up paper and David Simons' response. I agree with Luke's earlier comments that finding abnormalities in the periphery in the area of Trps does not prove the etiology is not central or simply sensitization in the periphery.

[Luke Rickards]

Interesting. Thanks for these Bryan.

I might have more to say when I've read them.

[Diane]

I gave the articles a quick read. What struck me most was the insistance the authors all have in making the assumption that they are feeling or testing muscle tissue. I have a few thoughts:

1. They seem to not realize that there could be neural structures inside some of those "taut bands" they are looking to study.

2. They talk about the substances seeping through tissue and bothering it, but they fail to mention that these 11 substances are secreted by peripheral afferent nerves, not just registered by them.

3. They don't hook in the plausible hypothesis that the accumulation of these substances to a critical level bringing on nociception, might be due to a deficiency of venous drainage carrying them off in a timely manner. This could be due to mechanical reasons, or local neural dysfunction (local neural autonomic dysregulation in a small zone).

4. They fail to mention or perhaps have never considered that the neural tissue weaving through muscle as well as through everything else, and the nervi nervorum of the nerves themselves, is likely the most "sensitive" and most likely to send a warning signal or produce a "tender" spot.

I should think these are all possible confounding factors to their "theory" of trigger points and would have to be ruled out first, but it seems to me they haven't done so.

They are still thinking structure, not function. Furthermore they are thinking of the nervous system but only to justify operating from a mesodermal mindset, not as a sensitive structure in its own right. Their mindset appears to be that the neural tissue is there to serve muscle "sensation", not the other way round.

[Baecker]

Ginger you wrote here: By reducing hypertonicity of parazygoapophyseal muscle and restoring normal facet movement behaviour , immediate reductions in these distal muscle "trigger point" indicators are seen.

First you say that the muscles are not to be blamed and then on the other hand the parazygoapophyseal muscle is the culprit. Kind of odd it sounds to me.

I can say also vice versa if I treat the Trp of a certain muscle I found hypertonic paraspinal muscles go soft as well. The Body is not a one way street. I am going for the option that the nerves are cranky.

[Diane]

Another point:
The Chen study that proposes a method of visualizing soft tissue dysfunction (taut bands) with chevron patterns, etc., to objectify their existence, make them visible to those who can't "feel" them, looks good. I don't deny the existence of taut bands. I presume imaging will pick up whatever it picks up. My issue is with the suggestion that taut bands, or the visualized patterns bouncing off them, are of or from "muscle", as implied by this statement:

The goal of this study was to investigate the potential of MRE imaging in the quantification of muscular pathophysiology.

Why did they use the word "muscular" as if muscular was the only type of "pathophysiology" that could possibly exist?

There is a lot of other contractile stuff in the body besides striated "muscle". Smooth muscle comprises a lot of the tubing that reaches all through striated muscle. It is driven by neurochemical stimulation, and/or sympathetic innervation. The author leaves the reader to think that no other kind of soft tissue but muscle exists, or might exhibit contractility. I should think that a vascular (small, local) autonomic dysregulation could set up quite a distress signal that could manifest as hardened or taut bands that are palpable. Especially along nerve trunks/tunnels.

I would have no objection to the substitution of the word "contractile" for the word "muscular".

[BB]

Or even the term "pathophysiology." In my mind there is nothing pathological in general about the protective mechanism that generates the phenomenon of TrP's.

Although, I guess this normal response could eventually generate a pathological state of the local tissue, given enough time and local change.

[Diane]

In my mind there is nothing pathological in general about the protective mechanism that generates the phenomenon of TrP's.

Good point Cory.

[ginger]

Baecker, muscles involved in the protective ( increased ) tone around facet joints are not culprits so much as participants in a series of events. Those events I maintain are ideally rationalised , in my view, as providing a usefull ,if potentially painfull service. The conduct then of muscles near to these joiunts , when altered and tone reduced , reduces and ultimately eliminates , irritants to nerves. The mechanism of change , using Cm , is via the joint and its complex of nerves. I rationalise that changes seen to distal behaviour of muscles ( and other structures ) is due to a reduction in nerve irritation local to the facet joints . More complex feedback ( "loops " ) within the nerves themselves may certainly play a role. Either way muscles do not behave according to their own private program , they do whatever they do at the effect of nerves and nerve related behaviour.
cheers

[boneill]

Diane and others,
Your comments are most appropriate. I have forwarded some of the ideas to Jay Shah at NIH, and again invited him to join SS and perhaps consider that online interview regarding myofascial trigger point theory. As both his invitro micropipette analysis and the MRE technique are validated, they may prove useful in documenting and studying somewhat objectively tissue/neuro changes with other manual techniques. Let's hope he responds.
Bryan

[Jon Newman]

Hi Ginger,

You may be interested in the podcast debate between Tim Flynn and Chris Maher. After the introduction, the podcast opens with a Tim Flynn soundbite

If you're going to manipulate, manipulate. Don't shake the joint around.

I know you have a different opinion on that particular point. The use of low velocity techniques versus high velocity techniques is currently being discussed at EIM and you can read along or comment as you wish.

I linked to the conversation here

[Luke Rickards]

Some comments from Nic.

The biochemical analysis study claims that pH etc is higher in a muscle with active TrP in comparison to a muscle with latent or no TrP. However, all this hinges on their ability to identify 'active', 'latent', and 'no TrP. Since latent trigger points occur in asymptomatic people, the results are more correctly interpreted at present as pH etc is lower in symptomatic subjects compared to asymptomatic subjects.

The imaging study doesn't seem to be clinically correlated. With only n=2 it lacks applicability. Also, while MRE might identify something different with the muscle in terms of 'muscle tone', they have made the assumption that this is also the 'taut band'. What they really need is a validity study, showing that an examiner can locate the same site as the MRE.

[ginger]

Hi Jon, often it seems the lives of researchers and academics are set towards seemingly endless debate on topics where the outcome is merely to confirm the obvious. It seems to be this way with the manip vs low velocity joint treatments debate.
The difference in outcomes would be obvious to anyone whose skills included a variety of joint related treatments, both high and low velocity. For myself there is no doubt , that from a clinical perspective, manips have short term shallow effect, CM has long term deeper effects. Were I to choose a technique on the basis of ensuring I had more work and business to do, I would choose manipulation. I very rarely use this method however as CM provides what the patient invariably seeks, a return to pain free normal movement and function.

[MaxG]

I know I'm late to the party, but reading through the Quintner and Cohen article, I stumbled over the following:

However, when pain of nerve origin is severe, it can be felt in regions outside the sensory distribution of the particular nerve (33,34).

By what mechanism does this occur?

Is this discussed in the referenced papers as I was not able to locate the full length texts?


33. Stewart JD, Aguayo AJ. In: Dyck PJ, Thomas PK, Lambert EH, eds. Peripheral neuropathy. 2nd ed. Vol 2. Philadelphia: Saunders, 1984:1435-57.

34. Lundborg G, Dahlin LB. The pathophysiology of nerve compression. Hand Clin 1992;8:215-27.

[Diane]

It depends where along which nerve we're talking. In the dorsal horn, segments can talk to each other. That means a lot of other branches of other entire nerve roots can become involved. Out somewhere in a single branch of the neural tree of a single nerve root, other twigs on the same branch can become interested/affected, just by regular sensitization at just one segment in the dorsal horn.

[Barrett Dorko]

The mechanisms aren't difficult to understand, and in a system like this location doesn't mean much.

Of much greater import is the origin of the pain.

[MaxG]

Just to be clear, my comment wasn't intended to question the premise of the article, just a matter of understanding.

Thank you for the replies, they were both helpfull.

[Diane]

Here is Paul Ingraham's "coming out" essay - coming out as a trigger point skeptic: Trigger point doubts • Why I feel the need to challenge the clinical concept of trigger points

The pain is real! But are “trigger points”? The more I learn, the more I wonder.

Trigger point Koolaid (one of the most pernicious kinds of Koolaid in existence) is slowly but surely being eliminated from his brain, by his brain, thanks to his deployment of Occam's Razor and Occam's Koolaid Eliminator on himself.

[zimney3pt]

Wow, that is simply a great article that Paul wrote on so many levels.

For someone to step down from his "bread and butter" and risk the negative fallout from it because of his commitment to science is unfortunately almost unheard of in this day in age. I've always enjoyed and respected Paul's stuff (had some trouble with the TrP stuff), but my respect for him just increased 10 fold.

Paul, I know you read here every now and then, just wanted to let you know how impressed I am with your commitment to science and not personal gains. It needs to be applauded and shouted out from the roof tops to get more to do the same.

[amacs]

Originally Posted by zimney3pt

Wow, that is simply a great article that Paul wrote on so many levels.

For someone to step down from his "bread and butter" and risk the negative fallout from it because of his commitment to science is unfortunately almost unheard of in this day in age. I've always enjoyed and respected Paul's stuff (had some trouble with the TrP stuff), but my respect for him just increased 10 fold.

Paul, I know you read here every now and then, just wanted to let you know how impressed I am with your commitment to science and not personal gains. It needs to be applauded and shouted out from the roof tops to get more to do the same.

amen to that!

ANdy

[AdamB]

Wanted to bump this great article and Paul's blogpost.

Quintner is by the way commenting on Lorimers blogpost about catastrophizing at the moment.