What is visceral manipulation?

Over the last three decades, French osteopath Jean-Pierre Barral has pioneered the practice of “visceral manipulation” as a distinct branch of osteopathy.

According to Barral’s estimates: “In a single day, your internal organs move 30,000 times” and “Your liver alone travels 600 meters. But when one organ cannot move in harmony with its viscera due to abnormal tone, adhesions or displacement, it works against the body’s other organ’s and muscular, membranous, fascial and osseous structures” [Skari, 2001].

His key insight was that each internal bodily organ has a capacity to cause spinal pain, whereas conventional osteopathic thinking had assumed the opposite:

“At the time nobody was talking about manipulating organs but I kept seeing patients with aches and pains that I could relieve simply by kneading their organs” [Skari, 2001].

In the March 2013 issue of Osteopathy Today, Barral outlined his approach to diagnosis:

“I use a lot of listening which means you put your hands on the body and your hand is attracted to the tissues which have a density or express a tension and then it is up to your medical knowledge to know what kind of tissue you have found. It is to let the body express itself.”

As to the question of diagnosis, Barral claimed to be able to locate areas of “stress” in the body by palpating the associated (thermal) energy.

The therapeutic approach is then to coax “traumatised” or malfunctioning organs (e.g. kidneys, liver, stomach and other soft tissues) back to their natural movement by applying soft pressure to the respective abdominal, thoracic and urogenital areas:

“The goal is to help the body’s normal forces remove abnormal effects, whatever their sources. Those effects can be global, encompassing many areas of bodily function. These gentle manipulations can potentially improve the functioning of individual organs, the systems the organs function within, and the structural integrity of the entire body.”

In relation to fibromyalgia, visceral manipulation is included in the list of manual therapy techniques that are said to possess the extraordinary capacity to “help to calm down the autonomic nervous system, decrease inflammation in soft tissue, release adhesions of the organs, and calm down irritation of the spinal cord.”

Historical antecedents

There are at least three threads in the history of Medicine that can be teased out to uncover the origins of some of the remarkable ideas behind visceral manipulation.

1. Glénard’s disease

The idea that a wandering uterus could cause health problems is an ancient one, and is allied to that of mischief being caused by other “wandering organs” [Desvoeux, 1752].

During the 19th century there was a body of authoritative surgical opinion that excessively movable abdominal organs could be held responsible for abdominal pain and for even more widespread symptoms [Treves, 1896; Daly, 1996].

Some thought that descent of the stomach could result in neurasthenia, the 19th century counterpart of fibromyalgia and chronic fatigue syndrome. Gastropexy (fixation of the stomach) was deemed to be an effective and safe procedure [Daly, 1996].

Colenard, a French physician practicing in Lyons, was the first to describe, in a paper published in 1885, the condition of enteroptosis, or falling of the viscera, due to relaxation of their supporting ligaments [Lund, 1897].

Frantz Glénard (1848-1920), a French physician who for health reasons left Paris to live at Vichy, wrote a number of papers on the subject of visceroptosis (“sinking of abdominal viscera”) [Glénard, 1899].

He devised a simple test wherein the examiner, standing behind the patient, places his arms around the patient so that his hands meet in front of the patient’s abdomen; he squeezes and raises the viscera and then allows them to fall suddenly. If the patient feels relieved by the raising pressure and experiences distress upon release, the condition is probably one of visceroptosis.

2. The Irish stroker

Valentine Greatrakes [1628-1666] was a soldier who served as a lieutenant in the ranks of Cromwell’s army. By harnessing the popular belief in the efficacy of “the king’s touch” – the belief that illness could be cured by the touch of a divinely inspired leader – he is said to have practiced a lay form of psychotherapy [Alexander & Selesnick, 1967].

Greatrakes became known as the “Irish stroker” when, after the beheading of Charles I in 1649, it was widely believed that the healing power of the king’s touch had been passed on to him and that through this method he could cast out evil spirits causing disease. Thousands of patients came to be touched by him, and “his barns and outhouses were crammed with innumerable specimens of suffering humanity [Laurence, 1910].”

3. Mesmerism

Franz Anton Mesmer [1734-1815], who had studied medicine in Vienna, claimed that he too could cure, initially by using a horseshoe magnet and later on by simply touching his patient with his bare hand.

Mesmer and his followers believed that obstacles to the free flow of this fluid caused illness, and that skilled healers or “sensitives” could remove these obstructions by making passes over the patient’s body with their hands.

Mesmer thought he had discovered a specific magnetic force in humans and that this force could be transferred through the laying on of hands [Lanska & Lanska, 2007].

Like many other therapists of all times, Mesmer was unable to appreciate that his successes were due, not to his non-existent magnetic force, but to powerful suggestion [Ackerknecht, 1968].


When assessing the place of visceral manipulation as a form of therapy, perhaps the words of Ecclesiastes 1:9 still ring true:

“What has been will be again, what has been done will be done again, there is nothing new under the sun.”


Ackerknecht EH. A Short History of Medicine. New York: The Ronald Press Company, 1968: 208-209.

Alexander FG, Selesnick ST. The History of Psychiatry. London: George Allen and Unwin Ltd., 1967: 71-88.

Daly A. Fantasy Surgery 1880-1930: with special reference to Sir William Arbuthnot Lane. Clio Medica 38/The Wellcome Institute Series in the History of Medicine. Amsterdam: Editions Rodopi B.V 1996.

Desvoeux V. The Compendious Library: or, Literary Journal Revived. For November and December, 1751. Dublin: S. Powell, 1752.

Glénard F. Les Ptoses Viscérales: Diagnostic et Nosographie.  Paris: Ancienne Libraire Gemmer Balliere & Co., 1899.

Lanska DJ, Lanska JT. Franz Anton Mesmer and the rise and fall of animal magnetism: dramatic cures, controversy and ultimately a triumph for the Scientific Medicine. In: Whitaker H, Smith CUM, Finger S. Brain, Mind and Medicine. New York: Springer Science, 2007: 301-320.

Laurence RM. Primitive Psychotherapy and Quackery. Boston: Houghton Mifflin, 1910: 255.

Lund FB. Enteroptosis. Boston Med Surg J 1897; 1(8): 7-11.

Skari T. Has your liver been liberated? Time 2001; 157 (15): 64.

Treves F. The treatment of Glenard’s disease by abdominal section. Brit Med J 1896; i: 1-4.

Fibromyalgia Meets Craniosacral Therapy

The current criteria for making the diagnosis of fibromyalgia are based upon the scoring obtained from two subjective measures, the Widespread Pain Index and the Symptom Severity Scale, the results of which are then combined [Wolfe et al, 2010]. Fibromyalgia is therefore neither a distinct syndrome nor a specific disease, which is now being understood as an indication of polysymptomatic distress [Wolfe et al. 2013].

Complementary and Alternative Medicine
Practitioners who operate under the umbrella of Complementary and Alternative Medicine (CAM) have exploited this diagnostic uncertainty, as evidenced by a recent systematic overview of such therapies, which are utilized by many patients with fibromyalgia [Lauche et al., 2015].

Although some of the interventions appeared to be beneficial, in others the outcomes were either inconsistent or inconclusive. The investigators remarked upon the “methodological flaws limiting definite conclusions about their efficacy and safety” [Lauche et al., 2015].

Somewhat surprisingly, craniosacral therapy (CST) was not included in the systematic overview. However, this form of therapy is being confidently offered around the world to patients with fibromyalgia. [For example, see:]

The origins of craniosacral Therapy (CST)
CST is an approach that appears to have been modeled upon the remarkable theories of 18th century Swedish philosopher and scientist, Emanuel Swedenborg [Tubbs et al. 2011]. Because of his many prescient insights about the brain and nervous system, Swedenborg has been recognized as a neuroscientist who was well ahead of his time [Gross, 2009], and has been accorded a prominent place in the history of neurology [McHenry, 1969].

He gave an accurate account of the importance of the cerebral cortex as the seat of the higher psychical functions and was the first to suggest somatotopic organization of the motor cortex, as well as the importance and function of the pituitary gland (which he termed the “arch gland”).

Swedenborg was aware of the phenomenon of pulsation of the brain [Maier, 1994] and believed that it imparted a motion to the cerebrospinal fluid [Squires, 1940]. The movements of the brain and the central nervous system were said to be reciprocal to those of the lungs i.e., when the lungs expand, the brain contracts, and vice versa. During the expansile motion of the brain cerebrospinal fluid is expressed from the IVth ventricle into the subarachnoid space.

The pumping action of the brain forced “nervous fluid” through the nerves. The spinal ganglia were thought to help propel the fluid, which was eventually returned to the spinal cord and brain by way of the meninges [McHenry, 1969].

Swedenborg attempted to explain mental events in terms of minute vibrations or “tremulations”. These, and his other important contributions to neuroscience, were only recognized when his manuscripts were discovered, translated, and published in the late 1800s.

Swedenborg’s influence
Swedenborg’s ideas seem to have influenced William Garner Sutherland (1873-1954), an American osteopathic physician, who proceeded to elaborate upon them [Scarr, 2013].

Sutherland described five components of what he called The Primary Respiratory Mechanism, an intrinsic motion that expressed itself through the entire body and was held to be a “fundamental expression of life itself.”

Agreeing with Swedenborg, Sutherland observed that the brain and spinal cord undulate rhythmically, as does the cerebrospinal fluid. Moreover, this fluid was able to move throughout the body by passing along the spinal nerve sheaths and through extra-cranial lymphatics, thereby fulfilling a nutritive function. The movements of the brain and cerebrospinal fluid also became evident in the spinal membranes as a “dynamic shifting of tension” within them.

Sutherland believed that the dura mater was held under constant tension and could transmit external forces along its length. Because of its attachment to the cranial bones, this tissue was responsible for maintaining the structural integrity of the cranium.

Thus, excessive forces applied by the dura mater to the cranium could lead to distortion of its components, which although they grew to approximate each other, remained in constant motion. The cranial sutures were thus kept open by tiny movements, estimated to be of the order of 100ths of an inch.

Sutherland’s views were at odds with the conventional thinking of anatomists, which held that the bones of the skull fused in early life. But Sutherland interpreted the fusion of certain cranial sutures to be indicative of a pathological condition, said to follow cranial traumata.

The importance given to the sacrum is due to its role in anchoring the dura mater. Motility at the level of the occiput is transmitted to the sacrum. Any trauma to the sacrum could also have an effect on the cranium (e.g. be a cause of headache).

Sutherland also believed that the body’s connective tissues are subject to a cyclic change in tension and a small amount of motion, typically 2-14 times a minute [Scarr, 2103].

In summary, the “craniosacral system” comprises the bones of the skull, the cerebrospinal fluid flowing within the spinal meninges, and the anchoring sacrum.

Upledger’s contribution
The idea of cranial bone movement and a “dural pulse” were further developed in the 1970’s through research performed by osteopath John E. Upledger (1932-2012) and his associates at the University of Michigan.

A key part of the ‘cranial’ concept is that bones of the skull remain distinct throughout life and have a rhythmic motion that is palpable as the ‘cranial rhythmic impulse’ [Scarr, 2012].

This mobility allows the CST practitioner to palpate the pulse and at the same time to gently move the cranial bones in such a way as to remove any restrictions, in order to restore bodily balance, and relieve tension in fascial tissues throughout the body. Headaches, muscles spasm, and chronic pain are said to then be able to rapidly dissipate.

In contrast to Sutherland’s Primary Respiratory Mechanism Model, Upledger suggested that the cerebrospinal fluid pressure rhythmically fluctuates according to its cycle of production and resorption. It is this “pressurestat” mechanism that drives the ventricular system of the brain to dilate and contract rhythmically—rather than “some intrinsic contractile power of the brain tissue itself” [Upledger & Vredevoogd, 1983].

Upledger’s model centered upon the presumed existence of sensory nerves and receptors positioned within human sagittal sutures that are responsive to compression and stretch, acting as a signaling system between the respective suture and the choroid plexus.

When a suture expanded, stretch receptors were activated and the production of cerebrospinal fluid (CSF) decreased. As fluid was reabsorbed into the venous system, volume and pressure of CSF reduced, activating compression receptors within the suture and signaling the choroid plexus to resume production of CSF. According to Upledger [1995]:

“The brain, in turn, rhythmically tones and relaxes the myofascial system via the motor division of the nervous system. This effect is delicate and easily inhibited by connective tissue that is restricted and not able to respond to this gentle urging of the craniosacral system via the motor system. Hence, these restrictions are easily found by the skilled therapist practicing craniosacral therapy.”

Alaquel et al. [2006] reviewed the evidence that cranial sutures do respond to mechanical loads and believed that they function as a cushion between adjacent bones. The sutures can indeed be subject to compressive stress, tensile stress, and shear stress as the underlying brain expands during development and as forces are transmitted from the masticatory muscles.

But these forces are technically difficult to measure with accuracy. Alaquel et al. [2006] considered that additional research is needed to elucidate the mechanotransduction events by which cranial sutures respond to the application of mechanical force.

Inter-rater reliability of CST
When Wirth-Pattullo and Hayes [1994] tested the claim that craniosacral therapists are able to palpate changes in cyclical movements of the cranium, they found that inter-rater reliability was unacceptable for clinical decision-making and treatment. They also wondered about the very existence of craniosacral motion and whether the evaluators in their study might have imagined such motion.

In a lengthy response, Upledger [1995] affirmed the usefulness of his “pressurestat” model and argued that other factors needed to be considered besides an assessment of the rate, amplitude, symmetry, and quality of the craniosacral rhythmical activity, as palpated using the “vault hold” on the head.

Upledger [1995] argued: “we should not allow strict adherence to the rules of experimental design to fetter human intelligence, nor should we allow it to stifle our creativity.”

He then defended his position by calling upon therapists to factor in the “wisdom of the body,” or in other words, to harness the placebo response:

“Implicit in craniosacral therapy is the concept that the patient’s own body and craniosacral system know how best to correct the problem. Our goal as therapists is to tune into that inherent wisdom and assist and facilitate its self-corrective processes.”

Controlled trials of CST in fibromyalgia
In a randomized controlled trial of a 20-week programme using a CST protocol in patients with fibromyalgia, symptoms did improve but there was no comparable control group (i.e. patients receiving another form of manual therapy) [Cástro-Sanchez et al. 2011]. The same serious design fault was evident in another study performed by the same group of researchers [Mataran-Peñarrocha et al. 2011]. The control group in each of these studies had received disconnected magnetotherapy.

The complex treatment protocol administered by the researchers was aimed at “removing the restrictive obstacle and returning the system to its natural state.” But it is noteworthy that they failed to record the nature and site of any such obstacles they encountered in members of either group.

From the available scientific evidence, one can only agree with the conclusion of Rogers and Witt [1997] that the opinions or beliefs of practitioners of CST do not provide sufficient reasons to support its use as an effective treatment. At the very least this appears to be the case for those with fibromyalgia.


Alaquel SM, Hinton RJ, Oppenehim LA. Cellular response to force application at craniofacial sutures. Orthod Craniofacial Res 2006; 9: 111-122.

Castro-Sánchez AM, Mataran-Peñarrocha GA, Sánchez-Labraca N, et al. A randomized controlled trial investigating the effects of craniosacral therapy on pain and heart rate variability in fibromyalgia patients. Clin Rehabil 2011; 26: 25-36.

Gross CG. Three before their time: neuroscientists whose ideas were ignored by their contemporaries. Exp Brain Res 2009; 192: 321-334.

Lauche R, Cramer H, Häuser W, et al. A systematic overview of reviews for complementary and alternative therapies in the treatment of the fibromyalgia syndrome. Evid Based Complement Alternat Med 2015, Article ID 610615, 13 pages.

Maier SE, Hardy CJ, Jolesz FA. Brain and cerebrospinal fluid motion: real time quantification with M-mode MR imaging. Radiology 1994; 193: 477-483.

Mataran-Peñarrocha GA, Castro-Sánchez AM, Garcia GC, et al. Influence of Craniosacral Therapy on Anxiety, Depression and
McHenry L, Jr. Garrison’s History of Neurology, revised and enlarged. Springfield: Charles C Thomas, Publisher, 1969: 107-108.

McHenry L, Jr. Garrison’s History of Neurology, revised and enlarged. Springfield: Charles C Thomas, Publisher, 1969: 107-108.

Rogers JS, Witt PL. The controversy of cranial bone motion. JOSPT 1997; 26: 95-103.

Scarr G. Palpatory phenomena in the limbs: a proposed mechanism. Int J Osteopath Med 2013; 16; 114-120.

Squires AW. Emanuel Swedenborg and the cerebrospinbal fluid. Ann Hist Med 1940; 2: 52-53.

Tubbs RS, Riech S, Verma K, et al. Emanuel Swedenborg (1688-1772): pioneer of neuroanatomy. Childs Nerv Syst 2011; 27: 1353-1355.

Upledger JE, Vredevoogd JD. Craniosacral Therapy. Seattle: Eastland Press, 1983.

Upledger JE [Letter]. Craniosacral therapy. Phys Ther 1995; 75: 328-329.

Wirth-Pattullo V, Hayes KW. Interrater reliability of craniosacral rate measurements and their relationship with subjects’ and examiners’ heart and respiratory rate measurements. Phys Ther 1994; 74: 908-916.

Wolfe F, Clauw DJ, Fitzcharles M-A, et al. The American College of Rheumatology preliminary diagnostic criteria for fibromyalgia and measurement of symptom severity. Arthritis Care Res 2010; 62: 600-610.

Wolfe F, Brähler E, Hinz A, Häuser W. Fibromyalgia prevalence, somatic symptom reporting, and the dimensionality of polysymptomatic distress: results from a survey of the general population. Arthritis Care Res 2013; 65: 777-785.

Could Fibrositis be Making a Comeback?


As I perused the abstracts for the upcoming 4th International Fascial Research Congress (September 2015), I came upon one that made me stop and think. It related to a half-day post-conference workshop by Kirstie Segarra – Managing Fascial Health for Individuals in Fibromyalgia:

To demonstrate clearly that managing widespread pain must include treatment of the fascia as we are structured determined systems, and to decrease pain is to invite change in the structure through the fascial matrix in order to have a correlating change in the central nervous system. In this way we restore homeostasis in the client.

Could pathology within fascia have been overlooked in the search for a peripheral source of nociception in this condition? Well, it appears that this is no longer the case.

Pathophysiological considerations

Liptan [1] hypothesized that fibromyalgia could be seen as a “bodywide fasciitis,” comparable to situations characterised by more focal fasciitis (e.g. plantar fasciitis).

The culprit appears to be chronic tension within the fascia responsible for causing micro-injuries (i.e. tears) in those with a “dysfunctional” healing response. Such a response is said to result from insufficient growth hormone release consequent upon inadequate deep sleep.

In summary, Liptan argued that: “Fascial dysfunction and inflammation may lead to widespread pain and central sensitization seen in fibromyalgia.”

She explained the tender points as possibly reflecting “areas that suffer the greatest microtrauma and mechanical stress from daily activities, and thus have higher levels of fascial inflammation.”

The main evidence put forward in support of her hypothesis derived from “recent biopsy studies [which] have found increased levels of collagen and inflammatory mediators in the fascia of fibromyalgia patients.”

But is this a novel hypothesis? In the Background section of her paper, Liptan harks back to the early 1900s when the aetiology of “muscular rheumatism” was indeed a hot topic.

Muscular rheumatism

In speculating upon the pathophysiology of low back pain, the great British neurologist, William Gowers [1904] coined the term “fibrositis” and thus championed the central role of the fascia in this condition:

In all parts it seems it seems the most susceptible to the influence we call “rheumatism” … The relation of lumbago to rheumatism would alone, make us expect to find it an affection of the fibrous tissue of the muscles, the tissue in which the spindles are situated, rather than of these alone … important proof that the malady is an affection of fibrous tissue; it may spread, and it spreads by continuity of this tissue.

Gowers postulated both focal and generalised forms of “fibrositis”:

We are thus compelled to regard lumbago in particular, and muscular rheumatism in general, as a form of inflammation of the fibrous tissue of the muscles.

The pathological findings

Ralph Stockman [1913], a Scottish pathologist, soon announced:

The essential lesion is a chronic inflammatory hyperplasia of white fibrous tissue in patches and as fibrous tissue is spread throughout the body the lesions may also be widely spread or may affect only a single limited area.

But after other researchers had repeatedly failed to find biopsy evidence of fibrous tissue inflammation, the “fibrositis” construct was eventually superseded by that of “fibromyalgia” [Hench, 1976] and classified in the nebulous category of non-articular rheumatism [Atkinson, 1981].


As did Gowers, Liptan [2010] ascribed a limited role to anti-inflammatory drugs (NSAIDs and corticosteroids), which should be used only during the initial phase of injury repair.

According to Liptan [2010] “only slow and sustained pressure will effect changes in the fascial tissue” and she recommended manual therapy techniques that “don’t cause further injury and inflammation, but rather gently break apart existing fascial restrictions and adhesions to promote tissue healing.”

She wondered whether techniques said to target the fascia, which included “Rolfing” (a technique of deep tissue manipulation) and “myofascial release,” could “help define the role of fascia in producing fibromyalgia pain.”

Based upon Liptan’s hypothesis, a pilot trial was undertaken comparing Swedish massage with myofascial release therapy (MFR), each administered over 90 minutes a week for 4 consecutive weeks [Liptan et al. 2013]. The former technique utilized moderate pressure stroking of the neck, back, arms and legs, whereas MFR consisted of “prolonged assisted stretching of painful areas of soft tissue” in the same regions.

The rationale given for MFR manoeuvres is that they are designed to “break up fascial adhesions” presumed to be the consequence of tissue injuries occurring in the fascia of patients with fibromyalgia [Liptan et al. 2013]. That for Swedish massage is to increase circulation and promote general relaxation.

Although numbers were small, both forms of treatment were found to be “safe, tolerable and acceptable” with MFR producing better symptom reduction.

By contrast, the mainstay of treatment recommended by Gowers was complete rest:

Not even passive movement should be employed until it causes no pain, and then it should be most gentle. The avoidance of pain should be made the standard for all local measures.

Gowers observed that counter-irritation (cautery being the most effective form) sometimes lessens the pain, as does deep hypodermic injection of cocaine, repeated daily for 2-3 weeks.

Other treatment strategies worth trying included a Turkish bath, mild aperients and, in the most acute cases, medicinal agents such as salicylates, nitrous ether, colchicum and perchloride of mercury.

Looking ahead

Gowers conceded: “we are without any direct evidence of the real nature of these affections” but he did hope that opportunities for pathological research would be seized upon:

We cannot wonder at our ignorance, still less complain of it, for it is only quite recently that the minute structure of the sensory elements of muscle and tendon has been clearly perceived, and much of the normal structure remains obscure.

But over a century later, direct histological evidence to support the related concepts of “fibrositis” and “fascial adhesions” is still lacking.

Nonetheless, Liptan [2010] calls for the use of existing methods of in vivo microdialysis to investigate the chemical composition of fascial interstitial fluid for evidence of inflammation, as well as for evidence of activation of fibroblasts removed from fascial tissues. He did not canvass the possibility that any such inflammation might in fact be “neurogenic” [Julius & Basbaum, 2001].

As for the role of manual therapy, Liptan et al. [2013] hope that various measurement tools being developed “may provide insight into which symptom of function domains are most malleable to various types of massage intervention.”


To date, the search for underlying peripheral musculoskeletal pathology in fibromyalgia has not been fruitful.  Yet, a recently published book – Fascial Dysfunction: Manual Therapy Approaches (2014) – is being advertised to manual therapists with this rather astounding claim appearing in the blurb:

Fascial dysfunction is now recognized as one of the main underlying causes of musculoskeletal pain leading to impaired and reduced mobility.  [Link:]

Could Gowers have been right after all? Should we now discard the term fibromyalgia and revert to his “fibrositis” model? It seems a most unlikely possibility but a critical review is urgently needed to once and for all resolve this important question.


Atkinson MH. Nonarticular rheumatism. Can Fam Physician 1981; 27: 254-258.

Gowers WR. A lecture on lumbago: its lessons and analogues. Brit Med J 1904; i: 117-121.

Hench PK. Nonarticular rheumatism, 22nd rheumatism review: review of the American and English literature for the years 1973 and 1974. Arthritis Rheum 1976; 19(suppl): 1081–1089.

Julius D, Basbaum AI. Molecular mechanisms of nociception. Nature 2001; 413: 203–210.

Liptan GL. Fascia: a missing link in our understanding of the pathology of fibromyalgia. J Bodywork Mov Ther 2010; 14: 3-12.

Liptan G, Mist S, Wright C, Arzt A, Jones KD. A pilot study of myofascial release therapy compared to Swedish massage in Fibromyalgia. J Bodywork Mov Ther 2013; 17: 365-370.

Stockman R.  Discussion on fibrositis. Proc R Soc med 1913; 6: 36-39.



Fibromyalgia was officially recognised in 1990 when a Multicenter Criteria Committee of the American College of Rheumatology recommended the term be used as a means of classifying patients presenting with chronic widespread pain and tenderness [1].

Pain was considered to be “widespread” when it was experienced in all four quadrants of the body (i.e. on both the left and right sides and above and below the waist).

Tenderness was assessed over 18 specifically chosen tender points. When patients with widespread pain were judged by their clinician to be hypersensitive at 11 or more of these points, the diagnosis of Fibromyalgia could be applied.

Some 20 years later, the criteria for diagnosis were broadened by the introduction of a symptom severity scale score to replace the tender point count. Widespread pain remained a diagnostic criterion [2].

The clinical problem of “RSI” (repetitive strain injury)

In Australia the term “RSI” (repetitive strain injury) came to be broadly applied to all conditions characterised by neck and/or upper limb pain presenting in an occupational context.

“RSI” embraced localised conditions, such as carpal tunnel syndrome, dorsal wrist tenosynovitis, lateral epicondylitis and rotator cuff “tendonitis”, along with poorly understood conditions characterised by diffuse pain felt in the neck, pectoral girdle and arms, often accompanied by positive sensory symptoms, cramp, loss of muscle strength, and vasomotor abnormalities [3,4].

A vigorous medical debate had taken place during the 1980s over the categorization of the sub-group of patients with diffuse pain. On the one side were those who espoused the theory of muscle overuse injury, whilst on the other side were those who argued that those with these conditions were reflecting psychological distress that was manifest as somatic symptoms [5].

However, the homogeneity of presentation of these patients implied not only a common pathophysiology but also one that could be attributed to dysfunction of the nociceptive system itself, consistent with what was then the current definition of “neuropathic” pain. This explanatory model was proposed on the basis of careful clinical observation integrated with current knowledge of mechanisms of nociception [3,6].

Fibromyalgia becomes a regional condition

The 1980s brought the dreaded “RSI” (repetition strain injury) with interaction between Fibromyalgia Syndrome and the medico-legal system [7].

One of the key proponents in Australia of fibromyalgia, Geoffrey Littlejohn, was keen to extend the construct to subsume these syndromes of less diffuse pain, which were then being called “RSI”. He and his colleagues argued that these conditions were in fact a “subset” of fibromyalgia. 

They conjectured: Mechanisms similar to those in generalised fibromyalgia are likely to operate, although to a lesser extent, in patients with primary chronic localised pain or localized fibromyalgia [8].

This reconceptualisation of “primary chronic localised pain” as “regional fibromyalgia” presumed the validity of a parent syndrome.

However this exercise was an example of the logical fallacy known as “begging the question,” and was particularly problematic when the diagnostic credibility of both conditions was being hotly contested.

In the absence of knowledge or theory regarding the pathogenesis of fibromyalgia, these authors nonetheless took a bold step to explain the pathogenesis of local pain that became regional.

To accomplish this, Littlejohn invented the concept of “simple injury to the muscle-tendon unit” but neglected to provide any pathological evidence to support the existence of such an entity:

The majority of patients with the “RSI problem” have a chronic pain syndrome, which, although it may be triggered by a simple injury to the muscle-tendon unit, is not due to persisting tissue damage of injury. Extensive investigations seeking out tissue damage will only show age-related changes which do not explain the diffuse symptoms” [9].

Thus, in summary, “RSI” is seen as a complex pathophysiological pain problem where clinical features may be approached using the paradigm of localised fibromyalgia syndrome” [9].

This step needs to be dissected in order to understand the transmutation of fibromyalgia.  A diffuse pain syndrome of unknown pathogenesis was invoked to explain “regional” or “local” apparently similar conditions of allegedly known pathogenesis.  There was never a “paradigm” of “localized fibromyalgia syndrome”; it was never proposed that (diffuse) fibromyalgia syndrome could be “triggered by a simple injury to the muscle-tendon unit”.

These assertions were and are entirely conjectural.

Medico-legal implications

Littlejohn’s next contribution was to downplay the nexus between “localised fibromyalgia syndrome” and work-related factors. This strategy was to have important implications for those with the condition who might be seeking workers’ compensation payments, particularly so in New Zealand [10].

Fibromyalgia can also occur as a syndrome of localised or regionalized pain and a low pain threshold. This situation is common after otherwise short-lived “soft tissue” injuries involving spinal areas, particularly in the context of compensation” [11].

Littlejohn defined “low pain threshold” in terms of sensitivity at the arbitrarily chosen “tender points” in fibromyalgia, which he claimed to be “characteristic regions used clinically to define pain threshold” – a circular argument – and that “sensitivity at these points is increased in pain-free subjects, but to an even greater extent in patients with fibromyalgia syndrome.”

But defining “sensitivity” in terms of the stimulus being applied is highly subjective and influenced by contextual effects and, as Littlejohn noted, this diagnostic criterion (along with widespread pain) has not been validated for medicolegal or disability purposes.

Furthermore, he did not produce evidence to support his claim that “low pain thresholds were common” after short-lived “soft tissue injuries” involving spinal areas. Yet again, conjecture was being passed off as established knowledge.

Littlejohn [12] then raised the spectre of psychogenesis:

The regional features seem to relate to local biomechanical factors around the spine, either postural or secondary to simple strains. When central sensitisation occurs it is likely that central neurophysiological factors, including psychological influences, allow for the amplification of otherwise subclinical spinal reflexes. These in turn cause regional pain, tenderness, muscle tightness and dermatographia.

The concept of “otherwise subclinical spinal reflexes” is yet another of Littlejohn’s conjectures. Furthermore, he failed to explain the mechanism(s) by which “central neurophysiological factors” could be responsible not only for their amplification but also for the various clinical phenomena.

Finally, Littlejohn [13] announced “operational” criteria for a diagnosis of localised fibromyalgia. But in fact they were Littlejohn’s own non-validated criteria [12]:

Regional pain syndromes are also referred to as localised fibromyalgia. Although no validated classification or diagnostic criteria exist for these condition, operational or clinically useful criteria have been proposed: regional pain and regional lowering of pain threshold, and the presence of sleep disturbance, fatigue, muscular stiffness and emotional distress in the absence of a primary nociceptive cause for pain.

“Using this model, regional pain syndrome appears to be on a spectrum between the simple self-limited aches and pains of everyday life and persistent musculoskeletal syndromes such as fibromyalgia.”

Littlejohn’s pronouncements are tautological: if regional pain syndrome is in fact localized fibromyalgia syndrome, then it follows that fibromyalgia is generalised regional pain syndrome.

What was achieved?

Where has this transmutation of fibromyalgia taken us? Has any light been shed on diffuse or regional pain syndromes?

Littlejohn attempted to fill gaps in our understanding of  “RSI” by interpolating his personal views on Fibromyalgia into the debate.  However all he achieved was to introduce circular arguments based on conjecture.   How did the guardians of the literature allow that to happen?

John Quintner (Physician in pain medicine and rheumatology)

Milton Cohen (Specialist pain medicine physician and rheumatologist)


1. Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombadier C, Goldenberg DL, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Arth Rheum 1990; 33: 160-172.

2. Wolfe F, Clauw DJ, Fitzcharles MA, Goldenberg DL, Katz RS, Mease P, et al. The American College of Rheumatology preliminary diagnostic criteria fibromyalgia and measurement of symptom severity. Arthritis Care Res 2010; 62-600-610.

3. Cohen ML, Arroyo JF, Champion CD, Browne CD. In search of the pathogenesis of refractory cervicobrachial pain syndrome. Med J Aust 1992 ; 156: 432-436.

4. Cohen ML, Arroyo JF, Champion GD. The relevance of concepts of hyperalgesia to “RSI”. In: Bammer G, ed. Working Paper No. 31. Canberra: Australian National University, 1992.

5. Quintner JL. The Australian RSI debate: stereotyping and medicine. Disabil Rehab 1995; 17(5): 256-262.

6. Quintner JL, Elvey RL. The neurogenic hypothesis of RSI. In: Bammer G, ed. Working Paper No. 24. Canberra: Australian National University, 1991.

7. Reilly P, Littlejohn GO. Fibrositis/fibromyalgia syndrome: the key to the puzzle of chronic pain. Med J Aust 1990; 226-228.

8. Granges G, Littlejohn GO. Pressure pain thresholds in pain free subjects, in patients with chronic regional pain syndrome, and in fibromyalgia syndrome. Arthritis Rheum 1993; 36: 642-646.

9. Littlejohn GO. Key issues in repetitive strain injury. J Musculoskel Pain 1995; 3(2): 25-33.

10. Rankin DB. Viewpoint: the fibromyalgia syndrome: a consensus report. NZ Med J 1999; 112: 18-19.

11. Littlejohn GO. Med J Aust 1996; 165: 387-391.

12. Littlejohn GO. Clinical update on other pain syndromes. J Musculoskeletal Pain 1996: 163-179.

13. Littlejohn GO. Fibromyalgia syndrome and disability: the neurogenic model. Med J Aust 1998; 168(8): 398-401.




The following announcement has just appeared on Myopain Seminars, one of the websites run by proponents of “dry needling”: The Federation of State Boards of Physical Therapy is working on developing a list of competencies needed for physical therapists to perform dry needling, and we would greatly appreciate your help! The Federation has developed a survey based on the Physical Therapy Practice Analysis, developed by the Federation in 2011. The survey contains a list of knowledge, skills, and activities that physical therapist have and undergo. Based on this list, the survey asks if each item is necessary to competently perform dry needling. This survey is the preliminary stage of determining the list of dry needling competencies. Although this is one of the first steps, it is critical. Please follow the link below to complete the survey. Additionally, the Federation asks that you share the survey with any colleagues or practitioners who may be performing dry needling. Please complete the survey no later than April 5, 2015. We truly appreciate your help in this endeavor! If you have any questions, please feel free to contact the Federation at any time.


Before such a survey is undertaken, the really important question that needs to be asked and urgently addressed by the Federation is whether the currently available scientific evidence supports a continuation of the popular practice by its constituency of “dry needling” muscles and other deep tissues. Clearly, this form of treatment is irrational and therefore the answer must be an unequivocal NO!

A couple of points on fibromyalgia

“Name Witheld” has a website entitled She is not a fan of the fibromyalgia idea and has been writing asking  me to post a link to her web site – something I haven’t done until now. But she has come up with a good question and I thought I’d offer a reply. “How,” she writes, “is someone with rheumatoid arthritis and fibromyalgia different than someone who just has rheumatoid arthritis?” One of the things prompting the question is a rumble that a second clinical trial of the fibromyalgia “blood test” is in the works. Something the blood test developers apparently want to do (in addition to cashing in big) is to distinguish fibromyalgia from rheumatoid arthritis (RA).

As a clinician, I know that persons with RA have swollen joints and tenderness in their affected joints. Often they have certain positive blood tests and often evidence of joint damage that is seen on X-range examination. If you ask people with RA where it hurts, they most often report problems in their affected joints. People with RA and fibromyalgia have all of the these features. But they also have pain in different, but characteristic regions–in the upper and lower back, the hips and shoulders. They are also more tender when examined in specific tender point spots. It’s not hard, and actually it is very simple and easy to identify fibromyalgia in people with RA. All you have to do is to stop and listen. As a sop to Dr. Quintner, I admit flat out that there are a lot of intellectual and logical problems with the fibromyalgia idea that he and I both acknowledge. But for now, lets suspend some disbelief. Dr. Lampman has been very correctly criticizing the nature of fibromyalgia studies. He couldn’t be more correct. People who fit the fibromyalgia diagnostic criteria have severe problems in hundreds of areas. They are always different from those without fibromyalgia. In the absence of a Gold Standard for fibromyalgia, it is hard to see how an expensive blood test could approach the current diagnostic criteria in the ability to accurately diagnose fibromyalgia, nor is it clear exactly what is being measured with the blood test.

The fibromyalgia idea is not so bad if you don’t take it too seriously.


We are back

Sometime last year I stopped posting to this blog and kind of let things go. We hadn’t been able to attract some the fibromyalgia leaders to participate, and I wondered if it was all worth the effort. I am going to try again, now. Still, we had many participants and a wide variety of comments. There are several reasons I decided to go on. First, Dr. John Quintner, who has been an inveterate source of comments, comforts and articles, suggested I should. His recent post on Trigger Points is an example of his very high quality work. It starts a discussion that has been long needed. Second, I have many comments and ideas about fibromyalgia that are very hard to express with the current system of journals and reviews. I want to publish these thoughts here. More about that to come.

The blog was designed for professionals, with the idea that professional would have a good idea of the scientific method (whatever that is) and could respond based on data and scientific analysis. Some of you might say this was a dubious belief, but at least the standard should be known to this group. Later, we opened the blog to non-professionals, including patients, provided they met certain rules. We blocked post from those who did not follow the rules; and we blocked some health professional, too. But some of the best comments we have had have come from non-professionals. See the series of important posts from “Nancy.”

So if you want to post, we welcome your comments. But pay attention to the rules. I repeat them here. From the “About” section:

This blog is designed to facilitate open, vigorous discussion about fibromyalgia and fibromyalgia-related issues. Say here what you think. We want to open up frank discussions of the full spectrum of fibromyalgia-related ideas and consequences. But do keep in mind Niels Bohr’s admonition, ‘It is not enough to be wrong, one must also be polite.’

Rules about posting and articles:

About comments. We want this blog to be about research and discussions concerning fibromyalgia. To post to this blog you should be a published author, have other academic credentials, or would be welcomed as a discussant in an academic journal. We make these somewhat arbitrary rules to try to exclude the general, non-scientific public. We welcome comments by all scientists and social scientists, not just those who are physicians. This blog is moderated, meaning that the editors decide what will appear. In general, we will not censor on-topic scientific posts provided authors meet the above guidelines. If you don’t fit our guidelines and think you have something to contribute, send the editors an email at [As a modification, we will accept post from non-profesionals provided they meet certain criteria.]

About articles. We welcome submissions of articles. By articles we mean new subject posts of varying length. They can be long. In fact, we might even publish short academic articles. If you want to submit a new-subject post, write and discuss this with the editors first at

From some previous posts: “We will not publish insulting or crude comments. They just won’t appear. If you have something to say, try to think about it in a scientific way. Provide evidence. Think about why you might be wrong. We’ll give it a try.

I (we) can’t and won’t answer personal problems. We won’t give medical advice. People with fibromyalgia know a lot. You can help us with thoughtful comments.”

Non-Professional authors who are uncertain if we will publish their comments are welcome to write to me with questions.





Below we publish Quintner, Bove and Cohen’s Response to Dommerholt and Gerwin: Did we miss the point? The  Dommerholt and Gerwin article is a reply to Quintner, Bove and Cohen’s important refutation of the trigger point concept. If you haven’t seen it, you should read it. It is a landmark in the trigger point debate. We publish this additional commentary here in the spirit of encouraging discussion, as it is hard to bring debate and discussion to convention medical journals. Similarly, we offer space to Dommerholt and Gerwin. – Fred Wolfe, MD


It should by now be obvious to those who have read our paper (Quintner et al. 2015) that we do not share the same beliefs as do Dommerholt and Gerwin (2015), who mounted a spirited defense of their preferred theory of myofascial pain arising from trigger points (MTrP).

This is a most important academic debate. Both Robert Gerwin and Jan Dommerholt claim to have studied and worked with the founders of MTrP theory, Drs Janet Travell and David Simons. They lecture and teach around the world under the banner of Myopain Seminars. “Dry needling” of MTrPs is their favoured treatment modality for pain that is deeply felt within muscles.

The position taken by Dommerholt and Gerwin

In summary, Dommerholt and Gerwin (2015) have made their position quite clear:

Based on our understanding of the literature, Quintner et al. have not presented any convincing evidence to believe that the Integrated TrP hypothesis should be laid to rest” and that “insufficient evidence is to be taken that further studies are needed …” and that “Quintner et al have not succeeded in providing sufficient evidence that the current TrP hypotheses should be rejected.”

Dommerholt and Gerwin have raised a number of important issues and made accusations that impugn our scientific credibility. They have very publicly thrown down the gauntlet.

In this article I do not intend to address each and every accusation raised in their “rebuttal”, but will examine those that seem to be most relevant. Our shorter and more focused response is currently available as an article “in press” and we understand that it will be published in the July issue of the Journal of Bodywork and Movement Therapy.

Preconceived bias?

Dommerholt and Gerwin appear to have interpreted as bias our seizing upon the lack of epistemological discipline shown by the original proponents of MTrP theory (Travell & Rinzler, 1952; Travell and Simons 1983).  We first exposed the major flaws in this theory in 1994 (Quintner & Cohen, 1994). To date, these flaws have not been acknowledged, let alone addressed by proponents of the theory. It was this lack of response that prompted our second paper on the subject (Quintner et al. 2015).

Biased review of the literature?

“Quintner et al’s paper is a biased review of the literature replete with unsupported opinions and accusations.”

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. But when arguing from a false premise (i.e. 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.

Discrediting MTrP research?

“In doing so, they specifically discredit much of the research on myofascial TrPs that has been published as unreliable, without providing any alternative studies specifically done on the pain phenomena that is attributed to TrPs.”

Dommerholt and Gerwin concede that several aspects of “myofascial pain” remain elusive and are not well understood, and that “a distinct mechanistic understanding of this disorder does not exist.” Therefore, as they appear to agree with us, there is no need to resile from the first proposition.

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.

Our use of “theory” and “hypothesis”

Dommerholt and Gerwin are critical of our use of “theory” and “hypothesis” and claim that we have used them in a non-scientific manner.

“Scientific inquiry commonly starts with observations, followed by the development of hypotheses, which through experiments are confirmed, modified, or refuted. Through repeated experimental testing of the hypothesis it is continually refined until a theoretical basis can be constructed that addresses different aspects of the hypothesis.”

A theory is a generally accepted explanation for an observed set of phenomena. Hypotheses can be deduced from theory. Refutation of (the claims made by) a hypothesis should lead to modification of the theory. Repeated refutations of hypotheses generated by modified theory should lead to refutation of the theory.  In this way, even cherished theories such as MTrP can be contested.

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.

Diagnosis of trigger point

We acknowledge that there has not been a study to demonstrate the minimum essential features of the TrP needed to identify it for diagnosis and treatment purposes.”

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.

The nature and validity of latent TrPs

“The differentiation between normal muscle tissue, active and latent TrPs reflects the degree of contraction, as confirmed objectively by vibration elastography. Their mechanical attributes are, however, not directly correlated with pain pressure threshold scores (Ballyns et al 2012), which Quintner et al interpreted as another nail in the coffin of the TrP hypothesis.

… Ballyns et al. clearly were able to distinguish and visualize contractured nodules on muscle that were only painful when stimulated (Ballyns et al. 2012).

Ballyns et al. (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. Some of the smaller regions of stiffness were said to represent “latent” trigger points. One may well ask on what grounds were they able to make these inferences?

In the section dealing with patient selection, Ballyns et al. 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!

Sonographic evidence

Sonography is not only used for research and possible diagnostic purposes, but can also be applied to guide trigger point needling (Botwin et al. 2008, Bubnov 2010, Suh et al. 2014) and to objectively measure the outcome of TrP interventions such as dry needling. (Maher et al, 2013)

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.

Pathogenesis of the trigger point

Apparently, they believe that TrPs are some kind of anatomical entity, although there has never been a credible anatomic pathology associated with myofascial TrPs.”

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”.

Quintner et al. refer to “fibrositic nodules” which have nothing in common with TrPs and their relevancy escapes us.”

But they go on to assert that TrPs are “palpable as hard nodules within a band of contractured fibres …”

They would appear to have contradicted themselves!

Use of animal studies

The majority of the studies of electrical activity of the TrP were carried out on animals and were based on palpation of locally contracted muscles.”

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.

Tissue biochemistry

Quintner et al. criticize the findings of Shah et al (2003, 2005, 2008), who have reported higher concentrations of neurotransmitters and cytokines in the extracellular fluid in the immediate vicinity of TrPs as being non-specific.”

In fact we made no such criticism but did offer two possible neuroscientific explanations for these findings, the most likely one being “neurogenic inflammation”.

Muscle pain versus myofascial pain

Perhaps Quintner et al. would consider our reasoning an example of conjecture, but the facts are that a low pH is common at active TrPs, and can cause muscle pain and hyperalgesia.”

We suggest that Dommerholt and Gerwin have fallen into the trap of conflating all pain felt in muscles with pain in muscles said to arise from supposed “myofascial TrPs”.

Twitch response

Quintner et al. … suggest that a local twitch response, which is an entirely different feature of the taut band, is nothing more than a myotatic stretch reflex.”

According to Audette et al. (2004) the literature does indeed differentiate the “localised twitch response” from a myotatic stretch reflex.

In a discussion by Simons (1976), “two features suggest a hyperirritable spinal reflex phenomenon: the increased motor unit response with increasingly vigorous palpation and the simultaneous activation of adjacent palpable bands.”

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).

Central sensitization induced by TrPs

 Some of the phenomena that seem to trouble Quintner et al. result from the fact that TrPs induce central sensitization and referred pain. Muscles do have nociceptors and activation of those nociceptors can initiate and perpetuate central sensitization.”

We are indeed troubled by the first proposition. It has yet to be shown that MTrPs are capable of activating nociceptors. But we have no argument with the second proposition.

It is true that Mense (2008) did accept (albeit with some reservation) the notion of MTrPs as potential peripheral generators of nociceptive activity. But following his brief summary of the hypothesis proposed by Simons (2004), he commented “this supposed mechanism leaves many questions unanswered but is currently the only comprehensive hypothesis on the origin of MTrPs.”

 We agree with Mense that there are still unanswered questions.

Low–level isometric contractions and TrP formation

 In 2006 and 2011, two complementary studies … explored whether the Cinderella Hypothesis could apply to the formation of TrPs.” Both studies provided evidence that low-level exertions can lead to the formation of TrPs (Treaster et al. 2006, Hoyle et al. 2011)

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.

Based on our assessment of these rather unusually designed studies, we cannot agree with Dommerholt and Gerwin that they “provided evidence that low-level exertions can lead to the formation of TrPs.”

 New evidence provided by Dommerholt and Gerwin

“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)”.

Our problem with the approach of Jafri (2014) is that in his introductory remarks he begged the question that is at the heart of this debate:

While myofascial pain syndrome is complex in its presentation, the onset and persistence of myofascial pain syndrome are known to be caused by myofascial trigger points.”

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.

Moseley confirmed that especially myofascial TrPs and joints are widely held to be common contributors to somatic referred pain.”

We acknowledge, as does Moseley (2012), that such an opinion is widely held amongst physical therapists. 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.

When discussing somatic referred pain Moseley suggested that “disrupted transmission” happens within the central nervous system and he viewed “somatic referred pain from TrPs and joints as the brain’s efforts to localize the pain in response to ambiguous input.”

We are not aware of evidence for such “disrupted transmission” or for “ambiguous input” associated with referred pain phenomena.

But we can agree with Moseley’s concluding remarks: “This is a field where clinical practice may change as new evidence emerges, or new evidence may underscore the validity of current clinical practice.

 Hypotheses of Quintner et al.

Dommerholt and Gerwin dealt mainly with one of the two explanatory models we advanced in our paper – that based upon the “neuritis” model. They accepted the model of “referred pain and tenderness” but asserted that its maintenance “is dependent on ongoing nociceptive input from the site of primary muscle pain.”

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.


Arendt-Nielsen L, Svensson P. Referred muscle pain: basic and clinical findings. Clin J Pain 2001; 17: 11-19.

Audette JF, Wang F, Smith H. Bilateral activation of motor unit potentials with unilateral needle stimulation of active myofascial trigger points. Am J Phys Med Rehabil 2004; 83: 368-374.

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.

Botwin K, Sharma K, Saliba R, Patel BC. Ultrasound-guided trigger point injections in the cervicothoracic musculature: a new and unreported technique. Pain Physician 2008; 11: 885-889.

Bubnov RV. The use of trigger point “dry” needling under ultrasound guidance for the treatment of myofascial pain (technological innovation and literature review). Lik Sprava 2010: 56-64.

Gerwin, RD, Dommerholt, J & Shah, JP. An expansion of Simons’ integrated hypothesis of trigger point formation. Curr Pain Headache Rep 2004; 8: 468-475.

Hall TM, Quintner JL. Responses to mechanical stimulation of the upper limb in painful cervical radiculopathy.  Aust J Physio 1996; 42: 277-285.

Hoyle JA, Marras WS, Sheedy JE, Hart DE.  Effects of postural and visual stressors on myofascial trigger point development and motor unit rotation during computer work. J Electromyogr Kinesiol 2011; 21: 41-48

Jafri MS. Mechanisms of myofascial pain. International Scholarly Research Notices Volume 2014 (2014): Article ID 523924, 16 pages.

Maher RM, Hayes DM, Shinohara M. Quantification of dry needling and posture effects on myofascial trigger points using ultrasound shear-wave elastography. Arch Phys Med Rehabil 2013; 94; 2146-2150.

Mense S. Muscle pain mechanisms and clinical significance. Dtsch Arztebl Int 2008; 105: 214-219.

Moseley GL. 2012. Pain: why and how does it hurt? In: Brukner P, Khan K, eds. Clinical Sports Medicine, 4th ed. Sydney: McGraw-Hill Aust Pty Ltd. 2012: 41-53.

Quintner JL, Cohen ML. Referred pain of peripheral neural origin: an alternative to the “Myofascial Pain” construct. Clin J Pain 1994; 10: 243-251.

Quintner JL, Bove GM, Cohen ML. A critical evaluation of the “trigger point” phenomenon. Rheumatology 2015; 54: 392-399

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. Novel applications of ultrasound technology to visualize and characterize myofascial trigger points and surrounding soft tissue. 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.

Simons DG. Review of enigmatic MTrPs as a common cause of enigmatic musculoskeletal pain and dysfunction.  J Electromyogr Kinesiol 2004; 14: 95–107.

Travell J, Rinzler SH.  The myofascial genesis of pain. Postgrad Med 1952: 11: 425-434.

Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Baltimore: Williams and Wilkins, 1983.

Treaster D, Marras WS, Burr D, Sheedy JE, Hart D.Myofascial trigger point development from visual and postural stressors during computer work. J Electromyogr Kinesiol 2006; 16: 115-124.


A sharp critique of the fibromyalgia idea and the research that surrounds it

Dr. James Lampman has sent along a set of slides about fibromyalgia and his view about limitations of the fibromyalgia idea and research. It is well worth looking at, He writes

“While I developed my findings as early as 2006, this year I did a more in-depth review of the claims of the FM research community.  I concluded that the published experimental studies had serious flaws and that actually none had addressed a principal research question: to determine if the pain-processing and neurochemistry of patients labeled as fibromyalgics is anything other than the normal way manifested in all patients with common kinds of enduring pain.

As an illustration, I analyzed several iconic studies in the fibromyalgia literature, finding reason to believe that the peer review system largely failed in its role to limit authors’ conclusions to those which can reasonably be substantiated by the evidence in each publication.  Part II of my lecture is devoted to a brief analysis of 8 studies.
I found it helpful to start with a recognition that the concept of fibromyalgia can be presented as a hypothesis with several components, each one of which should be subjected to scrutiny and testing.
While I personally feel that fibromyalgia is in fact a “failed hypothesis,” no doubt many readers would be dismissive of my conclusion. Nevertheless, I hope the currently prevailing belief system will not prevent you or your readers from at least sampling and judging my ideas.” Click on the link below.


 The human understanding when it has once adopted an opinion draws all things else to support and agree with it. And though there be a greater number and weight of instances to be found on the other side, yet these it either neglects or despises, or else – by some distinction sets aside and rejects, in order that by this great and pernicious determination the authority of its former conclusion may remain inviolate. [Francis Bacon (1620) from Novum Organum, Book 1, Aphorism XLVI.]

Introduction.The latest fads from the shadowy world of pseudo-science have always been quick to take off. For those who are keen on approaching pain sufferers with their sharp needles, the invention of Neural Prolotherapy by Dr John Lyftogt, of Christchurch in New Zealand, must have come as a godsend. A quick search on the Internet reveals that this invention is being taken seriously by a number of health practitioners who one might have expected to have known better than to accept it so uncritically.

The claims for Neural Prolotherapy “Prolo-” is short for proliferation and derives from the Latin “to regenerate or rebuild”. Prolotherapy with injectable substances that are being acclaimed as growth factors is now the subject of intensive research. But Dr Lyftogt favours hypertonic sugar injections.

Here are some remarkable extracts from his website (

“After the success of Neural Prolotherapy with Achilles tendonitis other persistent painful conditions of the neck, back, shoulders, elbows, wrists, knees, ankles and feet have been effectively treated by targeting the local inflamed superficial nerves with micro-injections of low dose Glucose.”

Comment: there have been no properly conducted clinical trials of Neural Prolotherapy.

“More recently Dr Lyftogt has developed effective neural prolotherapy treatment protocols for Migraine. ‘Fibromyalgia,’ CRPS, compartment syndrome and other difficult to treat persistent painful conditions.”

Comment: Again, no clinical trials have been conducted. The evidence is purely anecdotal and subject to all forms of bias.

“Neural prolotherapy is an effective novel and evolving treatment for non-malignant persistent pain, based on sound neuroscientific principles.”

“Subcutaneous prolotherapy with a series of percutaneous near nerve injections has been shown to be an effective treatment for a variety of recalcitrant painful conditions caused by prolonged neurogenic inflammation.”

Comment: This is the logical fallacy called circular argument: the conclusion is assumed before the evidence is presented. Dr Lyftogt offers no evidence that these conditions are associated with “prolonged neurogenic inflammation”.

The “sound neuroscientific principles”

Dr Lyftogt targets the “guilty” superficial nerves by injecting 5% Mannitol or 5% dextrose and thereby claims to modulate the neurogenic inflammation that he believes is responsible for “neuropathic pain”. He refers to the work of a highly regarded authority:

“Quintessential to the working hypothesis that subcutaneous prolotherapy treats prolonged pathological neurogenic inflammation is the work by Douglas W Zochodne from the Neuroscientific Research Unit at Calgary University.” [1]

When contacted by the author, Professor Zochodne replied: “I can indicate that I have no interest in it, have not endorsed it or plan to endorse it and am disappointed our work would be quoted for something without evidence.”

But there is more!

“The author hypothesizes that subcutaneous prolotherapy injections of hypertonic glucose and 0.1% lignocaine induce apoptosis of proliferating peptidergic noceffectors (i.e. SP and CGRP) and neovessels by reducing VEGF (vascular endothelial growth factor) levels and restoring “effective repair processes” with reduction of pain.” [2]

Comment: In this author’s opinion, this is pure speculation.

On his website and in a recent email to Associate-Professor Geoff Bove, a world leader in experimental studies of nervi nervorum (“the nerves of the nerves”), Dr Lyftogt claims that his injections target specific receptors (TRPV1) present on the nervi nervorum.

“The very small nerve fibers, innervating the nerve trunk, identified as unmyelinated C-fibers or ‘Nervi Nervorum’ are responsible for pain and swelling of the protective sheath of the nerve trunk. This was already demonstrated 125 years ago by Professor John Marshall from London and called neuralgia. It is now called ‘neurogenic inflammation’.”

Comment: Dr Marshall was in fact advocating “nerve stretching” in his Bradshaw Lecture given in London. Fortunately, this form of treatment has long been abandoned as being both ineffective and potentially dangerous.

Dr Bove made the following personal response to Dr Lyftogt in relation to his facile incrimination of the nervi nervorum:

“Dextrose does not do anything to TRPV1 receptors, and it is certainly not selective for abnormal ones (and there is no knowledge that those exist). You are not targeting nervi nervorum other than in your mind; they are few and far between on the small peripheral nerves, and maybe nonexistent. Regardless, you have nothing to offer regarding the injected dextrose reducing their function and thus reducing neurogenic inflammation, or reducing neurogenic inflammation at all.

The bottom line

According to Dr Lyftogt: “The growing scientific evidence supporting the view that neuropathic pain syndromes are caused by unremitting peripheral neurogenic inflammation involving the autonomic and sensory nerves may lead to renewed interest in prolotherapy and neural therapy as these treatments are effective and seem to target the PNS.” [3]

However, Dr Lyftogt has yet to demonstrate the presence of the unremitting (enhanced) neurogenic inflammation that he claims to have identified and treated with his sugar injectates.


The question as to the efficacy of Neural Prolotherapy, as practiced and taught around the world by Dr Lyftogt, is outside the scope of this article. There are no published trials upon which to base any firm conclusions.

Anecdotally, there may be face validity for this treatment but to date there has been no discussion of placebo effect, observer bias, expectation bias, reversion to the mean of the conditions being treated etc.

But what is abundantly clear is that published animal experimental research by leading neurobiologists Professor Douglas Zochodne and Associate-Professor Geoffrey Bove does NOT in any way support Dr Lyftogt’s hypothesis. This should be the end of the story but I suspect that the aphorism by Francis Bacon is as true today as it was over 400 years ago. All we can do is hope that good science will triumph over its rival.

Author: Dr John Quintner, Physician in Rheumatology and Pain Medicine

Dr Quintner accepts full responsibility for the content and opinions expressed in this article.


1. Lyftogt J. Subcutaneous prolotherapy treatment of refractory knee, shoulder and lateral elbow pain. Australasian Musculoskeletal Medicine November, 2007: 83-85.

2. Lyftogt J. Prolotherapy for recalcitrant lumbago. Australasian Musculoskeletal Medicine May 2008: 18-20.

3. Lyftogt J. Pain conundrums: which hypothesis? Australasian Musculoskeletal Medicine November 2008: 72-7