Bodywork Masterclass Series-6:Understanding the Soft Tissues

The musculoskeletal system is the means whereby we act out and express our human existence – ‘the primary machinery of life’ is what osteopathy’s greatest researcher Irwin Korr¹ called it. While medically speaking the musculoskeletal system may lack the glamour and fascination of vital organs and systems the fact is that the cardiovascular and neuroendocrine and digestive (and other) systems and organs exist only to service this great machine through which we live and function.

It is by means of our musculoskeletal system that we perform tasks, play games, make love, impart treatment, perform on musical instruments, paint and, in these and a multitude of other ways, interact with each other and the planet.

The musculoskeletal system is also the greatest energy user in the body as well as being one of our primary sources of pain, discomfort and disability and it is vastly complex with a host of interacting and interdependent elements.

Korr’s words² reminds us:

“The spinal cord is the keyboard on which the brain plays when it calls for activity or for change in 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 ‘melody’ of activity, even a ‘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 relaxations 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 of still more complex patterns. Each activity is also subject to further modulation, refinement, and adjustment by the afferent feedback continually streaming in from the participating muscles, tendons, and joints.”

The information fed back to the CNS and brain, reflects the steady state of joints, the direction and speed of alteration in position of joints, together with data as to the length of muscle fibres, the degree of load being borne, along with the tension this involves.

Korr³ discusses a variety of insults which may result in increased neural excitability; the triggering of a barrage of supernumery impulses, to and from the cord, and also what he terms ‘cross-talk’, in which axons may overload and pass impulses to one another directly; muscle contraction disturbances, vasomotion, pain impulses, reflex mechanisms, disturbances in sympathetic activity, all may result from such activity, due to what might be relatively slight tissue changes.

He summarises thus, ‘These are the somatic insults, the sources of incoherent, and meaningless feedback, that causes the spinal cord to halt normal operations and to freeze the status quo in the offending and offended tissues (causing spasm for example). It is these phenomena that are detectable at the body surface, and are reflected in disorders of muscle tension, tissue texture, visceral and circulatory function, and even secretory function.’

Selye⁴ called stress the non-specific element in disease production. In describing the relationship between the General Adaptation Syndrome (GAS) i.e. alarm reaction, resistance (adaptation) phase followed by the exhaustion phase (when adaptation finally breaks down) which affects the organism as a whole – and the Local Adaptation Syndrome (LAS) which affects a specific stressed area or the body. He demonstrated that stress results in a pattern of adaptation, individual to each organism and also showed that when an individual is acutely alarmed, stressed, aroused – homeostatic (self-normalising) mechanisms are activated. This is the alarm element of Selye’s general and local adaptation syndromes.

If the alarm status is prolonged or repetitive defensive adaptation processes commence, chronic changes are produced. In assessing and palpating the patient these neuro-musculo-skeletal changes represent a record of the attempts on the part of the body to adapt and adjust to the stresses imposed upon it as time passes.

The results of the repeated postural and traumatic insults of a lifetime, combined with the tensions of emotional and psychological origin, will often present a confusing pattern of tense, contracted, bunched, fatigued and ultimately fibrous tissue.⁵

The minutiae of the process are not for the moment at issue. What is important is the realisation that, due to prolonged stress of a postural, emotional or mechanical type, discrete areas of the body become so altered by the efforts to compensate and adapt, that structural and, eventually, pathological changes become apparent. Researchers have shown that the type of stress involved can be entirely physical in nature⁶ (e.g. a single injury or repetitive postural strain) or purely psychic in nature⁷ (e.g. chronically repressed anger). More often than not though a combination of emotional and physical stresses will so alter neuro-musculo-skeletal structures as to create a series of identifiable physical changes, which will themselves generate further stress, such as pain, joint restriction, general discomfort and fatigue. Predictable chain-reactions of compensating changes will evolve in the soft tissues in most instances of chronic adaptation to biomechanical and psychogenic stress⁸. Such adaptation will almost always be at the expense of optimum function as well as also being an on-going source of further physiological embarrassment.

It is on these patterns of dysfunction and the consequent chain reactions they involve that this series of articles will at first focus – how to ‘read’ the signs and symptoms of the body and how to begin to normalise what is dysfunctional.

If successful treatment is to be applied it is important to realise that quite different approaches are needed to release tense muscle which is under neurological control and tense tight muscle which has become fibrotic and which requires a more ‘mechanical’ approach to normalisation.These variables will be considered in a subsequent article.

Stress Response Sequence^{9,10,11,12,13,14,15}

When the musculoskeletal system is ‘stressed’ a sequence of events, starting with increased muscular tone, occurs as a result of:

• Congenital factors (for example short or long leg, small hemipelvis, fascial, cranial and other distortions)
  

  
  

• Overuse, misuse and abuse (and disuse) factors (such as injury or inappropriate patterns involved in work, sport or regular activities)
  

  
  

• Postural stresses
  

  
  

• Chronic negative emotional states (anxiety etc)
  

  
  

• Reflexive factors (trigger points, facilitated spinal regions – which will be discussed in more detail in a future article)
  

As a result of which –

• Chronically increased muscle tone develops which leads to a retention of metabolic wastes.
  

  
  

• Prolonged increased tone also leads to localised arterial embarrassment – (relative to the efforts being demanded of the tissues) – resulting in oxygen deficiency in the tissues – ischemia
  

  
  

• Increased tone might also lead to a degree of oedema.
  

  
  

• These factors (retention of wastes/ischemia/oedema) result in discomfort and pain.
  

  
  

• Discomfort and pain lead to increased or maintained hypertonicity, a self-perpetuating cycle has started.
  

  
  

• Inflammation or at least chronic irritation may be a result.
  

  
  

• Macrophages are activated as is increased vascularity and fibroblastic activity.
  

  
  

• Connective tissue production increases with cross linkage leading to shortened fascia.
  

  
  

• Since all fascia/connective tissue is continuous throughout the body any distortions which develop in one region can potentially create distortions elsewhere, so negatively influencing structures which are supported, invested or divided by, or which attach to, the fascia, including nerves, muscles, lymph structures and blood vessels.
  

  
  

• The chronic changes which result in the elastic (muscle) tissues lead to chronic hypertonicity and ultimately to fibrotic changes if inflammation has been part of the process.
  

  
  

• Hypertonicity in any muscle will produce inhibition of its antagonist muscles.
  

  
  

• Chain reactions evolve in which some muscles (postural – Type 1) shorten while others (phasic, active moving – Type ll) progressively weaken.
  

  
  

• Because of sustained increased muscle tension ischemia in tendonous structures occurs, as it does in localised areas of muscles and because of tendon strain periosteal pain areas develop.
  

  
  

• Abnormal biomechanics develop involving malcoordination of movement with antagonist muscle groups being either hypertonic (for example erector spinae) – or weak (for example weak rectus abdominis group)
  

  
  

• Joint restrictions and/or imbalances as well as fascial shortenings evolve.
  

  
  

• Neurological reporting stations in hypertonic tissues will bombard the CNS with information regarding their status, leading to a degree of sensitisation of neural structures and the evolution of facilitation – hyper-reactivity of the local nerves – in paraspinal regions or within muscles (trigger points).
  

  
  

• The degree of energy wastage due to unnecessarily maintained hypertonicity leads to generalised fatigue.
  

  
  

• More widespread functional changes develop – for example affecting respiratory function – with repercussions on the total economy of the body.
  

  
  

• In the presence of a constant neurological feedback of impulses to the CNS/brain from neural reporting stations indicating heightened arousal in muscles and other soft tissues there will be increased levels of psychological arousal and an inability to relax adequately with consequent exacerbation of hypertonicity.
  

  
  

• Functional patterns of use of a physiologically unsustainable nature will emerge, involving chronic musculoskeletal problems and pain.
  

  
  

• At this stage restoration of normal function requires therapeutic input which addresses both the multiple changes which have occurred as well as the need for a reeducation of the individual as to how to use their body, to breathe, carry and use themselves in less stressful ways.
  

  
  

• The chronic adaptive changes which develop in such a scenario lead to the increased likelihood of future acute episodes as the chronically tense and fibrotic biomechanical structures attempt to cope with new stress factors resulting from the normal demands of modern living.
  

This then is the ground on which bodywork operates. Dysfunction which is widespread, and which influences the total economy of the body – its circulation, nervous system, energy status, immune system, drainage and elimination functions, mechanical efficiency and most certainly its emotions. There is no ‘quick fix’ option if long lasting improvement is the objective. A comprehensive understanding of what is happening and a logical plan of action is called for.
In order to make sense of such patterns as they enter our practices we need sound palpation and assessment tools as well as a repertoire of skills with which to help to restore normal function.

Palpatory Diagnosis^16,17,18,19

One of the most successful initial methods of palpatory diagnosis is to run the pads of a finger or several fingers extremely lightly over the area being checked, assessing changes in the skin and thereby the tissues below it. After localising any changes in this way, deeper periaxial structures can be evaluated by means of the application of greater pressure. There are a number of specific changes to be sought in light palpatory examination which apply to both acute and chronic dysfunction. Among these are:

1. Skin changes.²⁰ The skin overlying reflexively active areas such as trigger points (or active acupuncture points) tends to produce a sensation of ‘drag’ as it is lightly stroked – due to increased sympathetic activity and hydrosis. The skin will lose some elastic quality, so that on light stretching (taking an area of skin to its easy resistance barrier on stretching) it will test as less elastic than neighbouring skin. The skin above reflexively active structures will be more adherent to the underlying fascia, evident in any attempt to glide or roll it.
   

   
   

2. Induration. A slight increase in diagnostic pressure will ascertain whether or not the superficial musculature has an increased indurated feeling, a tension and immobility indicating chronic fibrotic changes within and below these structures.
   

   
   

3. Temperature changes. In acute dysfunction a localised increase in temperature may be evident. In chronic conditions there may, because of relative ischaemia, be a reduced temperature of the tissues.
   

   
   

4. Oedema. An impression of swelling, fullness and congestion can often be palpated in the overlying tissues in acute dysfunction. In chronic dysfunction this is usually absent having been replaced by fibrotic changes.
   

The questions which need to be asked include:

• ‘What am I feeling?’
  

  
  

• ‘What significance does it have in relation to the patient’s condition/symptoms?’
  

  
  

• ‘How does this relate to any other areas of dysfunction I have noted?’
  

  
  

• ‘Is this a local problem or part of a larger pattern of dysfunction?’
  

  
  

• ‘What does this mean?’
  

In deep palpation the pressure of the palpating fingers or thumb needs to increase sufficiently to make contact with deeper structures such as the periaxial (paravertebral) musculature without provoking a defensive response. Amongst the changes which might be noted may be immobility, tenderness, oedema, deep muscle tension, fibrotic and interosseous changes. Apart from the fibrotic changes, which are indicative of chronic dysfunctions, all these changes can be found in either acute or chronic problems.

In the next article a variety of palpation and evaluation skills, as well as exercises to practice these will be outlined.

References

1. Korr I The physiological basis of osteopathic medicine. Postgraduate Institute of Osteopathic Medicine and Surgery New York 1970

2. Korr I Spinal cord as organiser of disease process. Academy of Applied Osteopathy Yearbook 1976

3. Korr I op cit

4. Selye, H., The Stress of Life, (McGraw Hill, 1956).

5. Chaitow L Soft Tissue manipulation Thorsons London 1989

6. Wall P Melzack R Textbook of Pain Churchill Livingstone London 1989

7. Latey P D.O. Muscular Manifesto Self-published London 1983

8. Lewit K Manipulation in rehabilitation of the locomotor system Butterworths 1992

9. Janda V Introduction to functional pathology of the motor system. Proceedings Vll Commonwealth and international conference on Sport. Physiotherapy in Sport 3:39 198

10. Travell J Simon G Myofascial pain an dysfunction – The trigger point manual. Williams and Wilkins Baltimore 1983/1991

11. Basmajian J Muscles Alive Williams and Wilkins Baltimore 1974

12. Janda V Muscle Function Testing Butterworths London 1983

13. Lewit K Manipulation in rehabilitation of the locomotor system Butterworths London 1985

14. Korr I Neurologic mechanisms in Manipulative Therapy Plenum Press New York 1978 (p27)

15. Dvorak J and Dvorak V Manual Medicine – Diagnostics Georg Thiem Verlag Thieme-Stratton Stuttgart 1984

16. Baldry P Acupuncture Trigger points and musculoskeletal pain Churchill Livingstone London 1993

17. DiGiovanna E (ed) An osteopathic approach to diagnosis and treatment Lippincott Philadelphia 1991

19. Beal M Palpatory Testing of somatic dysfunction in patients with cardiovascular disease Jn American Osteopathic Association July 1983

20. Travell J Simons D Myofascial Pain and Dysfunction (vol 1 & 2) Williams and Wilkins 1986 and 1993