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The explosion of fascia research

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This posting is a modified version of an article I have written for a British cranial osteopathic publication.

Because I am actively involved in the organizational aspects of next year’s Fascia Research Congress in Vancouver I have had only a limited amount of time to give to writing for the blog – hence this recycled – but I hope interesting – update on fascia.

When I was studying osteopathy in the late 1950s (BCNO – now BCOM) fascia entered into the lessons and lectures as a somewhat mysterious part of the economy of the body. It featured large in the historical aspects of osteopathy’s evolution, with early pioneers referring to its all-pervading nature – it was everywhere, and there were theories and assertions as to its relevance, but there was very little that was rooted in science. (Still 1902)

So, the question remained – what did fascia do?

Clues were to be found in American osteopathic writing. For example, decades ahead of his time Cathie (1974) described fascia’s potential for contractility as well as its rich neural supply – features that would not be validated by research until very recently. (Schleip 2006, Stecco 2008).

Osteopaths – and others – in the USA (Little 1969, Taylor 1958, Rolf 1962) made it clear that that fascia was not just a background material, with little function apart from its obvious supporting role, but rather a widespread, tenacious, connective tissue involved deeply in almost all of the fundamental processes of the body’s structure, function and metabolism.

In therapeutic terms it became clear there can be little logic in trying to consider muscles and joints as separate structures from fascia, because they are so intimately related. Remove connective tissue from the scene and any muscle left would be a jelly-like structure without form or functional ability, and joints would quite simply fall apart. (Cantu et al 1992)

We now know that there exists a state of structural and functional continuity between all of the body’s hard and soft tissues, with fascia being the ubiquitous elastic–plastic, gluey, component that invests, supports and separates, connects and divides, wraps and gives cohesion, to the rest of the body – the fascial, connective tissue network. (Ingber 2008, Myers 2009)

Any tendency to think of a local dysfunction, as existing in isolation needs to be discouraged as we try to visualize a complex, interrelated, symbiotically functioning assortment of tissues, comprising skin, muscles, ligaments, tendons and bone, as well as the neural structures, blood and lymph channels, and vessels that bisect and invest these tissues – all given shape, form and functional ability by the fascia. (Schleip 2006, Ingber 2008, Solomonow 2009)

Fascial function and dysfunction revealed

Fascia, when healthy, forms a gliding interface with underlying muscle [allowing] free excursion of the muscle under the relatively immobile skin. A plane of potential movement exists in the form of the areolar tissue layer, apparently lined with a lubricant, hyaluronic acid. (McCombe et al 2001)

This process of ‘sliding fascia’ can now be visualised, using real-time ultrasound and elastography – as was demonstrated recently by Langevin (2010b). Dramatic video images demonstrated the free movement of lumbodorsal fascia in pain free individuals, contrasted with that of individuals with low back pain.

Similar images were displayed of myofascial trigger points, during the same panel presentation, that I co-chaired (Shah 2010). Both elastography and ultrasound images show trigger points to be denser than surrounding, normal, tissue.

When fascia is excessively mechanically stressed, inflamed or immobile, collagen and matrix deposition becomes disorganized, resulting in fibrosis and adhesions, and fascial ‘thickening’ (Langevin et al 2009), also described as ‘densification’ (Stecco et al 2009). This process involves distortion of myofascial relationships, altering muscle balance and proprioception. Consequent binding among layers, that should stretch, glide and/or shift on each other, potentially impairs motor function (Fourie 2009), and leads to chronic tissue loading, which contributes to ‘global soft tissue holding patterns’ (Myers 2009).

Cramer et al (2010) in rat studies showed that “hypomobility results in time-dependent adhesion development within the zygapophyseal joints”. Such adhesion development may have relevance to spinal manipulation, which could theoretically break up Z joint intra-articular adhesions”

Some therapeutic implications

A review by Schleip (2003) has documented both myelinated and unmyelinated fibers in fascia, including sympathetic endings. Stecco et al. (2008) found that the outer layers of the deep fascia contained a rich vascular and nerve supply, with intrafascial nerve fibres seen throughout. Some of these were presumed to be stretch receptors.

Bialowski (2008) has hypothesised that mechanical force (soft tissue & manipulative) initiates neurophysiological responses – peripheral and central – possibly evoking and explaining the clinical outcomes of manual therapy. These hypotheses have been expanded on by Simmonds et al (2011) who suggest that HVLA manipulative therapies (i.e. rapid) stimulate fascial tissues (as in the Z-joint example described earlier), while myofascial therapies (such as myofascial release and muscle energy technique) deliberately stimulate fascial tissues

Langevin’s in vivo and in vitro studies have shown that loose connective tissue responds to light tissue stretch, which “may be key to the therapeutic mechanismof treatments using mechanical stimulationof connective tissue” (Langevin & Sherman 2006, Langevin 2010a)

Myers (2010) suggests that stretching can be applied not only to ‘length’ problems, but also to ‘stuck layer’ problems, using shear stress to allow the restoration of increased relative movement between the adjacent planes of fascia (Schwind 2004)

In Germany, Pohl (2010) has demonstrated, using real-time ultrasound imaging, changes in collagen density in various layers of skin before and after connective tissue massage (CTM) involving skin rolling

Mechanotransduction and strain transmission

What has now been established is the remarkable degree to which muscular effort depends on the multiple links that muscles have with connective tissue structures.

These connections mean that – for example – a hamstring stretch will produce 240% of the resulting strain in the Iliotibial tract – and 145% in the ipsilateral lumbar fascia – compared with the hamstrings.

The process of strain transmission that occurs during stretching, involves many other tissues beyond the muscle that is being targeted, largely due to fascial connections, making the use of the word ‘isolated’ – together with ‘stretching’ – difficult to justify. (Franklyn-Miller et al 2009)

A fascial hydraulic effect?

Klingler & Schleip (2004), at the University of Ulm, measured wet & dry “freshly harvested” human fascia and found that during an isometric stretch, water is extruded, refilling afterwards. As water extrudes temporary relaxation occurs in the longitudinal arrangement of the affected collagen fibres. If only moderate strain is involved there are no micro-injuries, and water soaks back into the tissue until it swells, becoming stiffer again. It therefore seems that some tissue responses to manual therapy may relate to this sponge-like squeezing and refilling in the semi-liquid ground-substance, with its water binding glycosaminoglycans and proteoglycans.

Fascia related therapeutic approaches

The range of methods and modalities that focus attention on fascial dysfunction are proliferating. A few of those where a degree of supporting validation exists are summarised below :

· Heat in the therapeutic range, relaxes many fascial contractures associated with myofascial dysfunction. External heat has been shown to be beneficial in low back pain (Klingler 2011)

· Graston Technique® (GT) is an instrument-assisted soft tissue assessment and mobilization method delivering load deformation via stainless steel instruments. Mechanical deformation influences the extracellular matrix (ECM,) modulating the synthesis of proteoglycans and collagen by fibroblasts, increasing collagen formation (Hammer 2007)

· Neurologically active scars can restrict back flexion, which the patient feels as low back pain. This can be relieved by treatment of scars on the abdomen and/or below the symphysis (Kobesová, 2007)

· Fryer & Fossum have suggested that apart from the influence of mechanoreceptors on pain (via both ascending and descending pathways), Muscle Energy Techniques induce in-vivo mechanical stretching of fibro-blasts that both alters interstitial osmotic pressure as well as increasing blood flow, so reducing concentrations of pro-inflammatory cytokines, reducing sensitization of peripheral nociceptors.

· Standley & Meltzer (2008) have demonstrated – on a cellular level – the beneficial effects, on fibroblasts, of both myofascial release and positional release (Strain/counterstrain) methods. ……strain direction, frequency and duration, impact important fibroblast physiological functions known to mediate pain, inflammation and ROM….”

· Borgini et al (2010) have demonstrated the influence of direct compressive force on dense fascial restrictions, using the Italian modality developed at the University of Padua, Fascial Manipulation®

· The benefits of Connective Tissue Massage have been demonstrated in a number of clinical trials – notably in relation to chronic pelvic pain (Fitzgerald 2009)

· The methods used in structural integration (Rolfing) are directed mainly at fascia and connective tissue, which are treated with fingers, open hands, clenched fists, and elbows, with pressure directed to release adhesions between what should be freely sliding structures. (Findley & Schleip 2007)

· Fernandez-de-las-Penas and Pilat (2010) have described the successful use of neuromuscular technique (NMT) in treatment of myofascial pain

Much more to learn

What has emerged from the first two Fascia research conferences – Boston 2007 and Amsterdam 2009 – suggests that there is far more yet to learn.

These conferences brought clinicians of all schools, together with scientific researchers, in the hope and expectation that this would lead to a cross-fertilization, in which the clinical needs, confusions and questions of practitioners and therapists would inform researchers, who in turn would help clinicians to better understand the real nature of fascial structure and function, in relation to their patient’s problems and their own therapeutic efforts. It was further hoped that researchers would be spurred to new directions of study fascia.

And this has happened, and continues, with studies emerging at a remarkable pace, that have further clarified the nature and multiple functions and roles of fascia in the body.

The theme of the 3rd Fascia Research Congress (Vancouver, Canada, March 28 – 30, 2012) will be: Fascia: What do we know? What do we feel? Continuing the Scientist/Clinician Dialogue.

As the organising committee have said : The 2012 Fascia Congress will centre on the latest and best research on human fasciae. Additionally—and recognizing the interests of clinicians in gaining insights that will bear on practical applications—the program will be designed to include more presentation time to relating the research findings to clinical issues, particularly the practical applications of fascial layers.

The conference proper will be preceded (March 23-27) by a Fascial Dissection Workshop, with a range of additional pre and post-conference workshops, on March 27th and March 31st .

At this early stage the planning for the Vancouver conference is already advanced.

For example, among the confirmed keynote speakers are:

· Cesar Fernandez de las Penas DO PhD : Muscular and fascial aspects of myofascial Pain

· Al Banes PhD : Mechanical Loading and Fascial Changes – Tendon Focus

· Karen Sherman PhD : Existing trials on fascia in the context of manual therapies

· Carla Stecco MD : Fascial Anatomy Overview

· Dr. Rolf K. Reed : Fluid Dynamics and fascia (lymph, circulation etc)

· Mary Francis Barbe : Changes in Fascia Related to Repetitive Motion Disorders

A number of panel sessions are also in the planning stage that will highlight the needs and interests of all clinicians – including exploration of modern imaging methods

· The conference website is http://www.fasciacongress.org/2012/

· A call for Abstracts will soon be displayed on that website

Proceeding books and DVDs from the 2007 and 2009 congresses can be purchased via this link

British Osteopathic representation in fascia research?

There has to date been little evidence of interest from British osteopaths in current fascial research or the Research Congresses. In contrast, senior members of the American osteopathic profession (including Brian Degenhardt, Michael Kuchera, Frank Willard) are active in research as well as promotion of this trend via participation in the organisation of the 3rd Congress (Vancouver 2012). For example Dr Kuchera is co-chair of the Scientific Committee, of which I am a member, as are several US based chiropractic researchers.

The possibilities for active involvement in the next congress, via submission of abstracts, is something I would encourage British DOs to consider. In my studies of cranial concepts, the intercranial structures (Tentorium cerebelli, Falx cerebri and others) were always central considerations. Has there been any cranial research that could stand scrutiny in the form of an abstract – and/or possible oral presentation? Are there perhaps a series of cases that could be described, written up, presented?

And if not now – when?

References

Bialosky J et al 2009 The mechanisms of manual therapy in the treatment of musculoskeletal pain Manual Therapy 14:531–538

Borgini E et al 2010 How much time is needed to modify fascial fibrosis? Jnl Bodywork & Movement Therapies 14(4):318-325

Cantu R Grodin A 1992 Myofascial Manipulation Gaithersburg Maryland; Aspen Publications

Cathie A 1974 Selected writings. Academy of Applied Osteopathy Yearbook 1974, Colorado Springs

Cramer G et al 2010 Zygapophyseal joint adhesions after induced hypomobility. Journal of Manipulative and Physiological Therapeutics 33:508-518

Fernandez-de-las-Penas C Pilat A 2010 IN: Chaitow L Lovegrove R (Eds.) Practical Physical Medicine Approaches to Chronic Pelvic Pain (CPP) & Dysfunction Elsevier IN PRESS

Findley T Schleip R 2007 Fascia Research. Basic Science and Implication for Conventional and Complementary Health Care vols. 2–3, Elsevier, Germany

FitzGerald, M.P. et al 2009 Randomized Multicenter Feasibility Trial of Myofascial Physical Therapy for the Treatment of Urological Chronic Pelvic Pain Syndromes. Journal of Urology 182(2):570-580

Fourie W 2009 IN: Fascial Research II: Basic Science and Implications for Conventional and Complementary Health Care Munich: Elsevier GmbH

Fryer G Fossum C 2009 Therapeutic Mechanisms Underlying Muscle Energy Approaches. In: Physical Therapy for tension type and cervicogenic headache: physical examination, muscle and joint management Fernández de las Peñas C Arendt-Nielsen L Gerwin R (eds): Jones & Bartlett, Boston

Hammer W 2007 Functional Soft-Tissue Examination & Treatment by Manual Methods 3rd ed. Sudbury, MA, Jones & Bartlett pp 33-161

Ingber D 2008Tensegrity and mechanotransduction, Jnl Bodywork and Movement Therapies 12(3):198–200, 2008.

Klingler W Schleip R Zorn A 2004 European Fascia Research Project Report. 5th World Congress Low Back and Pelvic Pain, Melbourne, November 2004

Klingler W 2011 IN: Chaitow L Lovegrove R (Eds.) Practical Physical Medicine Approaches to Chronic Pelvic Pain (CPP) & Dysfunction Elsevier IN PRESS

Kobesova A et al M 2007 Twenty-year-old pathogenic “active” postsurgical scar: a case study of a patient with persistent right lower quadrant pain. Journal of Manipulative and Physiological Therapeutics 30(3):234-238

Langevin H, Sherman K 2006 Pathophysiological model for chronic low back pain integrating connective tissue and nervous system mechanisms. Medical Hypotheses 68(1):74–80

Langevin H 2009 Fibroblast Cytoskeletal Remodeling Contributes to Viscoelastic Response of Areolar Connective Tissue Under Uniaxial Tension, as reported in Fascial Research II, Elsevier GmbH Munich

Langevin H et al 2010a Tissue stretch induces nuclear remodelling in connective tissue fibroblasts. Histochem. Cell Biol. 133(4):405-15

Langevin H 2010b Presentation: Ultrasound Imaging of Connective Tissue Pathology Associated with Chronic Low Back Pain. 7th Interdisciplinary Congress on Low Back & Pelvic Pain (Los Angeles, November 11 2010)

Little L 1969 Towards more effective manipulative management of chronic myofascial strain and stress syndromes. Jnl American Osteopathic Association 68:675-685

McCombe D et al 2001Jnl. Histochemical structureof the deep fascia and its structural response to surgery. Hand Surgery 26B:2: 89-97

Meltzer K et al 2009 In vitro modelling of repetitive motion injury and Myofascial Release. Jnl Bodywork & Movement Therapies 14:162-171

Myers T 2009 Anatomy Trains, 2nd edition Edinburgh: Churchill Livingstone

Myers T Fascial Stretching. IN: Schleip, Findley, Huijing & Chaitow. Fascia in Manual Therapy. Elsevier, Edinburgh IN PRESS

Pohl H 2010 Changes in structure of collagen distribution in the skin caused by a manual technique J. Bodywork Movement Th. 14(1):27-34

Rolf I 1962 Structural Dynamics. British Academy of Applied Osteopathy Yearbook 1962. BAAO London

Schleip R, Naylor I, Ursu D, et al 2006 Passive muscle stiffness may be influenced by active contractility of intramuscular connective tissue, Med Hypotheses 66(1):71

Schleip R 2003 Journal of Bodywork & Movement Therapies 7:104-116

Schwind P 2006 Fascia and Membrane Technique, Edinburgh: Churchill Livingstone

Shah J 2010 Ultrasound techniques reveal objective abnormalities of myofascial trigger points and surrounding connective tissue. 7th Interdisciplinary Congress on Low Back & Pelvic Pain (Los Angeles, November 11 2010)

Simmonds N et al 2011 A theoretical framework for the role of fascia in manual therapy. Jnl. Bodywork & Movement Therapies IN PRESS

Solomonow M 2009 Ligaments: A source of musculoskeletal disorders, Journal Bodywork and Movement Therapies 13(2):136-154

Standley PR, Meltzer KR 2008 In vitro modeling of repetitive motion strain and manual medicine treatments: potential roles for pro- and anti-inflammatory cytokines. Journal of Bodywork & Movement Therapies 12:201-203.

Stecco A et al 2009 Anatomical study of myofascial continuity, anterior upper limb. J Bodyw Mov Ther. 13: 53-62

Stecco C et al 2008 The expansions of the pectoral girdle muscles onto the brachial fascia: morphological aspects and spatial disposition. Cells Tissues Organs. 188: 320-9.

Still AT. 1902 Philosophy and mechanical principles of osteopathy. Kansas City, MO: Hudson-Kimberly Pub. Co.

Taylor R 1958 Bioenergetics of man. Academy of Applied Osteopathy Yearbook 1958. Carmel California

9 Comments

  1. I note you wrote the Paper for the British Cranial Association…why is no-one addressing papers which indicate cranial has no inter-operator reliability or sound scientific basis? See one paper below….

    http://chiromt.com/content/14/1/10

    Thanks

    • very little in manual therapy has sound reliability evidence…and some that does is disputed…

  2. Cranial mechanisms are, and for many years have been, debated with passion. My book Cranial Manipulation Theory and Practice 2nd edition (Elsevier) evaluates the different perspectives and models.
    I am comfortable that much cranial treatment has value, while absolutely accepting that mechanisms remain unexplained. Inter-operator reliability is a problem throughout manual medicine, not just cranial – but this does not negate the apparent value of such treatment

  3. Thanks for your response.

    Is it not time though for the osteopathic profession in the 21st century to come up with good quality evidence to support cranial? So far no study has shown any inter-operator reliability for cranial which has to a limited extent been found in other manual treatments. Are osteopaths suffering from a ‘condition’ as explained in the article ‘Why do ineffective treatments seem helpful?” http://chiromt.com/content/pdf/1746-1340-17-10.pdf . I do not think it is good enough in these times of EBM to just say it has value! Regards Gary

  4. Do you have any concept of the cost of mounting research such as you advocate?
    WHo would pay for it and why is it necessary?
    With surveys of mainstream medicine suggesting that barely 40% of methods used have obvious and provable benefit, I do think that there are better tasks for professions using methods where there is no evidence of harm, and a great deal of anecdotal and some research evidence of benefit.

    clinicalevidence.bmj.com/ceweb/about/knowledge.jsp (accessed 20/07/2010)

    El Dib RP, Atallah AN, Andriolo RB (August 2007). “Mapping the Cochrane evidence for decision making in health care”. J Eval Clin Pract 13 (4): 689–92

    Ioannidis JP. Why Most Published Research Findings Are False. PLoS Medicine 2005; 2 (4): e124

  5. Hi
    I refer you to the abstract in Hartman’s “Why do ineffective treatments seem helpful” referenced above. I think it answers “why is it necessary?” With regard to cost if there was a ‘will’ to test cranial money would be found by the profession!

    Cheers

    Gary

  6. You are entitled to your opinion Gary
    however I disagree
    Your comment about money being found if there is a will, is naive.
    There are far more important research issues awaiting funds that don’t exist.
    I cannot publish my opinion of Hartman’s analysis and perspectives – it would too close to slander
    My sense is that this conversation has reached a point where we need to acknowledge that we see things differently
    I will not respond to anything further that you post on this matter.

  7. Thanks for the elegant summary of recent research and the references.

  8. DOCTOR CHAITOW LO FELICTIO POR TODOS SUS LOGROS, SOLO QUISERA SABER SI USTED PODRIA REPARTIR CURSOS O CHARLAS EN PERU PORFAVOR, SOY FISIOTERAPEUTA MI NOMBRE ES RONALD GRACIAS DOCTOR.

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