Over the past 15 years I have been privileged to teach soft tissue methods in the UK and at chiropractic, osteopathic and massage schools throughout the USA, Scandinavia and Israel. More recently my teaching has formed a module in the new MA in Therapeutic Bodywork at the University of Westminster. Where chiropractors are concerned the vexed, sometimes highly charged question which forms the title of this article is never far from the lips of those attending, many of whom seem to have made up their minds in advance of asking the question.
I believe it is vital that all those treating musculoskeletal dysfunction have available a range of skills which can address both joint (intra-articular) restrictions and those of a soft tissue nature, or results will never be as good as they might be.
The Evolution of Musculoskeletal Dysfunction.
The normal response of muscle to any form of stress is to increase its tone.
Stress affecting musculoskeletal soft tissues produces hypertonicity, irritation and pain, and can include:
- Acquired postural imbalances
- ‘Pattern of use’ stress (occupational, recreational etc)
- Inborn imbalance (short leg, small hemipelvis, fascial distortion via birth injury etc)
- The effects of hyper or hypomobile joints, including arthritic changes
- Repetitive strain from hobby, recreation, sport etc (overuse)
- Emotional stress factors
- Trauma (abuse), inflammation and subsequent fibrosis
- Disuse, immobilisation
- Reflexogenic influences (viscerosomatic, myofascial and other reflex inputs)
- Climatic stress such as chilling
- Nutritional imbalances (vitamin C deficiency reduces collagen efficiency for example)
A chain-reaction of events may evolve as any combination of these or other stress factors demand increased muscular tone in those tissues obliged to compensate for, or adapt to them.
- Muscles antagonistic to the hypertonic muscles become weaker (inhibited) – as may the hypertonic muscles themselves.
- Stressed muscles develop localised areas of relative ischemia while simultaneously there will be a reduction in the efficiency of metabolic waste removal.
- The combined effect of toxic build-up (largely the by-products of the tissues themselves) and oxygen deprivation leads to irritation, sensitivity and pain, which creates more hypertonicity and pain. This often becomes self-perpetuating.
- Oedema may be part of the soft tissue response to stress.
- If inflammation is part of the process fibrotic changes in connective tissue may follow.
- Neural structures in the area may become facilitated, and so hyper-reactive to stimuli, often evolving into active ‘trigger points’, adding to imbalance and dysfunction.
- Initially when stressed the soft tissues will show a reflex resistance to stretch and after some weeks a degree of fibrous infiltration may appear as the tissues under greatest stress adapt to the situation.
- The tendons and insertions of the hypertonic muscles become stressed and pain and localised changes will manifest in these regions. Tendon and periosteal pain and discomfort start.
- If any of the hypertonic structures cross joints, and many do, these become crowded and some degree of imbalance will manifest, as abnormal movement patterns evolve (with antagonistic and synergistically related muscles being excessively hypertonic and/or hypotonic) leading ultimately to joint dysfunction.
- Localised reflexively active structures (myofascial trigger points) will emerge in the highly stressed,ischaemic, tissues, and these become responsible for the development of new dysfunction at distant target sites, typically inhibiting antagonist muscles.
- Because of excessive hypertonic activity there will be energy wastage and a tendency to fatigue – both locally and generally.
- Functional imbalances will occur, for example involving respiratory function, when chain reactions of hypertonicity and weakness impact this. ,
- Muscles become involved in ‘chain-reactions’ of dysfunction as some muscles are used inappropriately as they compensate for other structures which are weak or restricted, leading to a loss loss of their ability to act synergistically or normally.
- Over time the central nervous system accepts altered use patterns, as normal, complicating recovery since rehabilitation then requires a relearning process as well as more obvious structural and functional muscle and joint corrections.
In order to make sense of patterns of soft tissue change it is necessary to conceptualise muscular function and dysfunction as being something other than a local event.
Irwin Korr stated the position elegantly and eloquently:
‘The spinal cord is the keyboard on which the brain plays when it calls for activity. But each ‘key’ in the console sounds not an individual ‘tone’ such as the contraction of a particular group of muscle fibres, but a whole ‘symphony’ of motion. In other words, built into the cord is a large repertoire of patterns of activity, each involving the complex, harmonious, delicately balanced orchestration of the contractions and relaxation of many muscles.The brain thinks in terms of whole motions, not individual muscles. It calls,selectively, for the preprogrammed patterns in the cord and brain stem, modifying them in countless ways and combining them in an infinite variety is still more complex patterns. Each activity is subject to further modulation refinement, and adjustment by the feedback continually streaming in from the participating muscles, tendons and joints.’
We must never forget the complex interrelationships between the soft tissues, the muscles, fascia and tendons and their armies of neural reporting stations, as we attempt to understand the nature of dysfunction and of what is required to achieve normalisation.
Postural Muscles – a factor to keep in mind
Research by Lewit, Korr, Janda, Basmajian, and others shows that muscles which have predominantly stabilising functions will shorten when stressed while others which have more active ‘moving’ or phasic functions will not shorten but will become weak (inhibited).
The muscles which shorten are those which have a primarily postural rather than phasic (active, moving) role and it is possible to learn to conduct, in a short space of time (ten minutes or so) an assessment sequence in which the majority of these can be identified as being either short or normal.
Janda informs us that postural muscles have a tendency to shorten, not only under pathological conditions but often under normal circumstances. He has noted, using electromyographic instrumentation, that 85 per cent of the walking cycle is spent on one leg or the other, and that this is the most common postural position for man. Those muscles which enable this position to be satisfactorily adopted (one-legged standing) are genetically older; they have different physiological, and probably biochemical, qualities compared with phasic muscles which normally weaken and exhibit signs of inhibition in response to stress or pathology.
Those muscles which respond to stress by shortening comprise the following:
Gastrocnemius, soleus, medial hamstrings, short adductors of the thigh, hamstrings,psoas, piriformis, tensor fascia lata, quadratus lumborum, erector spinae muscles, latissimus dorsi, upper trapezius, sternomastoid, levator scapulae, pectoralis major and the flexors of the arms.
Janda has also shown that before any attempt is made to strengthen weak muscles any hypertonicity in their antagonists should be addressed by appropriate treatment which relaxes them, for example by stretching using MET. Relaxation of hypertonic muscles leads to an automatic regaining of strength of their antagonists. Should the hypertonic muscle also be weak it commonly regains strength following stretch/relaxation.
Commenting on this phenomenon, chiropractic rehabilitation expert, Dr.Craig Liebenson states:
‘Once joint movement is free, hypertonic muscles relaxed, and connective tissue lengthened, a muscle-strengthening and movement coordination program can begin. It is important not to commence strengthening too soon because tight, overactive muscles reflexively inhibit their antagonists, thereby altering basic movement patterns. It is inappropriate to initiate muscle strengthening programs while movement performance is disturbed, since the patient will achieve strength gains by use of ‘trick’ movements’.
Where Do Joints Fit Into the Picture?
Janda has an answer to the emotive question when he says that it is not known whether dysfunction of muscles causes joint dysfunction or vice versa.
He points out however that since clinical evidence abounds that joint mobilisation (thrust or gentle mobilisation) influences the muscles which are in anatomic or functional relationships with the joint, it may well be that normalisation of the muscles’ excessive tone in this way is what is providing the benefit, and that by implication normalisation of the muscle tone by other means (e.g. Muscle Energy Technique – MET) provides an equally useful basis for joint normalisation. Since reduction in muscle spasm/contraction commonly results in a reduction in joint pain, the answer to many such problems would seem to lie in appropriate soft tissue attention.
Liebenson not unnaturally has a chiropractic bias, ‘The chief abnormalities of (musculoskeletal) function include muscular hypertonicity and joint blockage. Since these abnormalities are functional rather than structural they are reversible in nature….Once a particular joint has lost its normal range of motion, the muscles around that joint will attempt to minimise stress at the involved segment.’
After describing the processes of progressive compensation as some muscles become hypertonic while inhibiting their antagonists, he continues, ‘What may begin as a simple restriction of movement in a joint can lead to the development of muscular imbalances and postural change. This chain of events is an example of what we try to prevent through adjustments of subluxations.’
We are left then with one view which has it that muscle release will frequently normalise joint restrictions, as well as a view which holds the opposite, that joint normalisation sorts out soft tissue problems, leaving direct work on muscles for rehabilitation settings and for attention if joint mobilisation fails to deal with long-term changes (fibrosis etc).
It is possible that both are to some extent correct, however it is worth restating that once soft tissues have shortened and become fibrotic the degree of shortening they display is no longer under neurological control,a structural modification has occurred in the tissues and no amount of joint manipulation can ever restore normality. Some additional approach is vital.
What emphasis each practitioner gives to their prime focus – be it joint or be it soft tissues – the certainty is that what is required is anything but a purely local view, as Janda helps us to understand.
Before treating dysfunction there are many pertinent questions which need answering such as:
- Which muscle groups have shortened and contracted?
- Is the evident restriction in a specific soft tissue structure or joint related to neuromuscular influence (which could be recorded on an EMG reading of the muscle) or tightness due to connective tissue fibrosis (which would not show on an EMG reading). or both?
- Which muscles have become significantly weaker, and is this through inhibition or through atrophy?
- What ‘chain reactions’ of functional imbalance have occurred as one muscle group (because of its excessive hypertonicity) has inhibited and weakened its antagonists?
- What joint restrictions are associated with these soft tissue changes – either as a result or as a cause of these?
- Is a restriction primarily of soft issue or of joint origin, or a mixture of both?
- How does the obvious dysfunction relate to the nervous system and the rest of the musculoskeletal system of this patient?
- What patterns of compensating postural stress have such changes produced (or have produced them) and how is this further stressing the body as a whole, affecting its energy levels and function?
- Within particular muscle areas which are stressed what local soft tissue changes (fascia etc) have occurred leading, for example, to myofascial trigger point development?
- What symptoms, whether of pain or other forms of dysfunction, are the result of reflexogenic activity such as trigger points ?
In other words what palpable, measurable, identifiable evidence is there which connects what we can observe, test and palpate to the symptoms (pain, restriction, fatigue etc) of this patient?
- And what, if anything, can be done to remedy or modify the situation, safely and effectively?
- Is this a self-limiting condition which treatment can make more tolerable as it normalises?
- Is this a condition which can be helped towards normalisation by therapeutic intervention?
- Is this a condition which can not normalise but which can be modified to some extent, so making function easier or reducing pain?
- What mobilisation, relaxation and/or strengthening strategies are most likely to be of assistance, and how can this patient learn to use themselves less stressfully following this?
- To what degree can the patient participate in the process of recovery, normalisation, rehabilitation?
Fortunately, as a part of such therapeutic intervention well structured assessment protocols exist as do a vast range of Muscle Energy Techniques (MET), Positional Release methods (Strain/counterstrain – SCS) and Neuromuscular techniques (NMT) exist as means of achieving normality.