A second edition of this book has become necessary because of the emergence over the past few years of extremely important research evidence.
This evidence does not negate or nullify information contained in the first edition, but rather builds on, and provides greater understanding of aspects of fascial function – offering insights into ways of providing support to inherent self-regulating features. For example, studies on a cellular level, by Dittmore and colleagues (2016), as well as Humphrey et al. (2014), have yielded a greater understanding of the ways in which the primary protein in fascia, collagen, repairs itself.
What emerges is that collagen health depends on a mixture of balanced external and internal (e.g. osmotic pressure) tension (Masic et al. 2015). When this tissue tension is deficient (or excessive) spontaneous local events occur that lead to local collagen fibrils degrading, and being rebuilt. This feature of ‘balanced tension’ involves cells – using integrins and their cytoskeletons – being able to sense and respond to the immediate mechanical status of their local environment (e.g. the extracellular matrix).
Dysfunction emerges when these processes are unable to maintain tissue wellbeing, or when responses become excessive.
The most basic interpretation of this newly emerging knowledge is that balanced tension and adequate hydration lead to more efficient homeostatic behavior. Hardly earth-shattering, perhaps – but a useful reminder that old-fashioned balanced stability, on a macro-scale, is most likely to result in health at all levels. As Susilo et al. (2016) put it: ‘
Mechanical loading induces stabilizing changes, internal to the fibrils themselves, or in the fibril–fibril interactions.
’ This fascinating research is outlined in
Chapter 1
.
Another emerging area of exciting research relates to a remarkable type of connective-tissue cell – the telocyte (TC) – which is attracting a great deal of research into its huge range of maintenance, repair and communication features (Dawidowicz et al. 2015).
‘TCs [are found in] skeletal muscle interstitium…
[close to]
… capillaries, nerve fibres, satellite cells and myocytes, suggesting their potential roles in muscle regeneration. Electron microscopy showed that
[they]
extended to neighbouring cells, inter-connected by different kinds of junctions, suggesting TCs potentially form a 3D interstitial network in skeletal muscle tissue …
[with]
possible roles in mechanical sensing, mechanochemical conversion tasks and tissue remodelling/renewal’
(Bei et al. 2015).
There is much else that is new in this second edition, relative to the critical feature of dosage in application of manual and movement therapies in management of fascial dysfunction. When – for example – physical load (stretch, compression, etc.) is applied to soft tissues not only is the degree of load critical to therapeutic outcomes, but also the direction(s) and duration of that applied load (Zein-Hamoud et al. 2015); see
Chapter 5
in particular.
In
Section II
of the book, three new chapters that describe several exciting topics have been added, including Gua Sha (and cupping) (
Ch. 11
); Global Postural Re-education (
Ch. 17
); and scar remodeling (
Ch. 19
).
Debate: What’s in a name?
Chapter 3
of the book (
Global postural assessment
) is again by Tom Myers. He has raised a question that reflects on the book’s title. He observed (personal communication 2018): ‘
Despite this writer’s obvious support for this book’s intent, he doubts whether there is such a thing as ‘fascial dysfunction’. More accurate would be ‘fascia doing the best it can under less than optimal neuromuscular patterning
.’
Of course, fascia can be injured in traumatic encounters, or degraded in pathology, genetic anomaly, or due to poor nutrition. And, in truth, most chronic injuries
have an essential fascial/connective tissue component. But far more often fascia is simply responding, as best it can, to the imposition of a deeper neuromuscular pattern. The fascia is forced to adapt, and accommodate, to inner tensional habitual patterns and gravity, among other exogenous forces. Thus, it is not fascia’s ‘fault’ that it densifies, adheres, inflames, or becomes dehydrated, and clinicians would do well to recognize that they are facilitators of health, rather than mechanics out to ‘fix’ anything.
All therapists, of all disciplines, could benefit from recognizing such patterns, in order to focus attention on the pattern as a whole, rather than chasing symptoms, or trying to change or correct just one element in the adaptive pattern.
Retraining the neuromotor ‘set’ – through improved ergonomics, posture, functional exercise, etc. – should lead to positive changes in the fascial webbing over time, possibly reducing the need for direct manipulation of the fascia.
Manual therapists will additionally benefit from learning to recognize certain states within the fascial fabric – as discussed throughout this book. While hand-to-hand instruction is superior to the printed page in such matters, we have found that nearly all fascially oriented bodywork is less effective if the client remains still under your hands, and far more effective if the client is moving under your hands. Small movements are fine, but any movement has the advantage of reducing discomfort, keeping the client aware and engaged, and facilitating tissue hydration, the prevention of adhesions, and the re-establishment of enhanced proprio- and interoception.
If the power of one-handed manipulation is designated as
x
, then the coordinated use of two hands is
x
2
, and two hands plus coordinated movement on the part of the client, yields
x
3
.
My responses:
It is a truism to say that, with few exceptions – whether through overuse, misuse (poor posture, stressful patterns of use, disordered breathing patterns etc.), abuse (e.g. trauma) or disuse (as may occur due to aging) – most of the conditions discussed in this book (apart from frank pathology) are the result of adaptation in progress, or of failed adaptation, where the tissues and systems of the body have responded, as best they can, to biochemical, biomechanical or psychosocial load.
Whether such observed, symptom-producing changes are termed ‘dysfunction’, or ‘evidence of adaptation in action’, therefore becomes a matter of individual preference.
As editor of this text I have chosen to use the word dysfunction, as shorthand for what is observed by the clinician, and experienced by the individual, as symptoms such as pain or limitations of ranges of motion. Therefore, if a combination of adaptive demands, and the failure to adequately cope with these, lie at the heart of dysfunction, therapeutic choices can be reduced to identifying objectives that aim to:
•
modify or eliminate the adaptive demands being coped with, or
•
improve the ability of the tissues locally, or the body as a whole, to handle these demands, or
•
offer palliative, symptom-oriented approaches
•
…. or perhaps aspects of all of these objectives
Once dysfunction is identified, and therapeutic measures (of any sort – biomechanical, psychosocial, biochemical) have been introduced, adaptation is once more at the core of what then unfolds.
Whether a therapeutic intervention involves manual treatment, surgery, acupuncture, exercise prescription, stress-management, lifestyle changes, etc. – unless targeted solely at symptom reduction, the process is always one that involves modulating adaptive demands, or of inducing an adaptive, self-regulating response from the body.
All treatment therefore involves a search for more functional adaptation. The art and the science of successful ‘treatment’ – of any condition – requires the appropriate choice of therapeutic input, based on a judgment as to the ability of the individual’s homeostatic systems to respond beneficially.
Treatment of a given condition would clearly be different depending on the age, functionality, vitality, resilience, degree of susceptibility of the individual – as well as of the tissues, structures, organs being addressed – in acute, subacute or chronic situations.
Also – as discussed in
Chapter 1
– the application of therapeutic load, whether this involves compression, traction, stretch, shear force, vibration/friction – or any combination of such forces – needs to be tailored to the individual’s ability to respond. Too much load, or too little load, may evoke either negative, or negligible, responses. The type of therapeutic load (manual, mechanical, movement, etc.) – as well as the dosage as to degree, direction, duration (and other variables) – all deliver different mechanical (and therefore biochemical), or neurologically mediated messages to the tissues being addressed – and therefore will evoke different responses.
The clinical value of the appropriate selection and application of a wide range of treatment and rehabilitation methods directed at fascial dysfunction, or ‘fascia doing the best it can under less than optimal neuromuscular patterning’ – as Myers identifies what is being treated – are the themes explored throughout this book.
Leon Chaitow
Corfu
2018
References
Bei Y et al 2015 Telocytes in regenerative medicine. J Cell Mol Med 19(7):1441–1454
Dawidowicz J et al 2015 Electron microscopy of human fascia lata: focus on telocytes. J Cell Mol Med 19(10):2500–2506
Dittmore A et al 2016 Internal strain drives spontaneous periodic buckling in collagen and regulates remodeling. Proc Natl Acad Sci USA 113(30):8436–8441
Humphrey J et al 2014 Mechanotransduction and extracellular matrix homeostasis. Nat Rev Mol Cell Biol 15:803–812
Masic A et al 2015 Osmotic pressure induced tensile force in tendon collagen. Nat Commun 22:6
Susilo ME et al 2016 Collagen network strengthening following cyclic tensile loading. Interface Focus 6(1): 20150088
Zein-Hamoud M, Standley P 2015 Modeled osteopathic manipulative treatments. J Am Osteopath Assoc 115(8):490–502