The musculoskeletal system – sometimes referred to as the locomotor system – is the means whereby we act out and express our human existence – ‘The primary machinery of life’ is what one of osteopathy’s greatest researchers, Irwin Korr (1970), 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 biomechanical structure through which we live and function. It is by means of our musculoskeletal system (not our kidneys or livers) 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 one another and the planet.

The musculoskeletal system – comprising mainly bones, muscle and connective tissue structures, such as ligaments, gives shape and stability, and allows movement, to the human body, while also protecting the vital organs (Mooar 2007).

The musculoskeletal system is also by far the greatest energy user in the body, as well as being one of our primary sources of pain, discomfort and disability, whether localized or general, referred or reflex, acute or chronic.

The term ‘somatic dysfunction’ offers an accurate and a comprehensive term to describe all lesions of the musculoskeletal system – osseous and soft tissue (Licciardone 2005).

Somatic dysfunction can be defined as any impairment, or altered function, of related components of the somatic system (body framework), i.e. skeletal, arthrodial and myofascial structures, as well as related vascular, lymphatic and neural elements. This general expression (somatic dysfunction) obviously requires specific definition in any given situation, which should include identification of the particular structure, tissue or area involved.

Sometimes somatic dysfunction is the primary cause of pain, however sometimes it generates reflexive symptoms, or may act as a perpetuating feature. Palpation may provide clues to the true nature of an injury (Stanton 1996). A process of assessment and examinations may help to identify structural factors associated with pain and dysfunction, often associated with repeated injury or cumulative microtrauma involving postural, habitual or occupational ergonomic stresses.

Identifying sources of pain

Different dysfunctional tissues produce different qualities of symptoms (Kuchera 2005). For example: sclerotomal tissues (skeletal, arthrodial, and ligamentous generators) typically relate to dull, aching pain – which may be experienced some distance from the actual source; myotomal (muscle) pain is also poorly localized, possibly also at a distance from the generating site. Trigger point activity in hypertonic tissues might be involved. The pain is typically described as involving stiffness, aching and sometimes having a cramp-like quality. Note: Examples of sclerotomes and myotomes are illustrated in Chapter 5, while the palpatory characteristics (such as tissue texture changes) of dysfunctional tissues that generate pain locally, or at a distance, are to be found in Chapter 3.

The objectives, if not the methods we are discussing, are not new. Carl McConnell, a major force in early 20th century osteopathy, discussed the soft tissues as follows (McConnell 1962):

A pathological point of prime importance, for example, is that osseous malalignment is sustained by ligamentous rigidity. This rigidity is incepted by way of muscular fascial and tendinous tensions and stresses. Every case portrays a uniqueness in accordance with location, architectural plan and laws, tissue texture, regional and strength ratios, resident properties, environmental settings, resolution of forces etc. Remember I am speaking of the solid biological background of individual pathogenesis, the veritable soil of prediseased conditions. The lack of either sufficient, or efficient, soft-tissue work, is one reason for mediocre technique and recurrence of lesions. The same is evident in the correction of postural defects.

The causes and the results of local and general somatic dysfunction, whether traumatic, functional, postural, pathological or psychological in origin, require a brief overview as we explore different aspects of the issues and the tissues involved, so that some of their possible solutions might become clearer.

Coherent and incoherent patterns

In Chapter 3 we will examine one of the major causes of somatic pain and dysfunction, myofascial trigger points, and the causes of this widespread phenomenon. It will then become clear that, while many forms of (referred) pain follow predictable and neurologically coherent pathways, there also exist patterns of pain and dysfunction that do not.

In this chapter our task is to evaluate a variety of influences on the evolution of soft tissue dysfunction, which follow a chronological sequence – the ways in which what is happening in an acute setting differs from what is taking place in a chronic situation, where an initial alarm state progressively gives way to a degree of organization, adaptation, compensation and (if not prevented) decompensation and dysfunction. It will also be explained just why not all muscles respond to stressors in quite the same way.

Reporting stations

The reporting mechanisms in the soft tissues and joints (Travell & Simons 1983, 1992, Wall & Melzack 1991) may be thought of as providing answers to a number of basic questions that the central nervous system (CNS) requires answering.

These questions were expressed by Keith Buzzell (1970) as follows: ‘What is happening in the peripheral machinery with respect to three questions? What is the present position? If there is motion, where is it taking us? And, third, how fast is it taking us there?’

The various neural reporting organs provide a constant information feedback to the CNS and higher centres as to the current state of tone, tension, movement, etc. of the tissues housing them. Such sensory information can be modulated and modified both by the influence of the mind, and by changes in blood chemistry, to which the sympathetic nervous system is sensitive. A variety of inputs of information will give the answers to these important questions so that the body can provide appropriate responses to the demands and adaptations constantly called for by varying situations. Some important structures involved in this internal information highway are summarized in Box 1.1.

Box 1.1 Reporting stations

Ruffini end-organs

These are found within the joint capsule, around the joint, so that each is responsible for describing what is happening over an angle of approximately 15°, with a degree of overlap between it and the adjacent end-organ. These organs are not easily fatigued, and are recruited progressively as the joint moves, so that movement is smooth and not jerky. The prime concern of Ruffini end-organs is to maintain a steady position. They are also, to some extent, concerned with reporting the direction of movement.

Golgi end-organs

These, too, adapt slowly, and continue to discharge over a lengthy period. They are found in the ligaments associated with the joint. Unlike the Ruffini end-organs, which respond to muscular contraction that alters tension in the joint capsule, Golgi end-organs are not thus affected, and can deliver information independently of the state of muscular contraction. This helps the body to know just where the joint is at any given moment, irrespective of muscular activity.

Pacinian corpuscle

This is found in periarticular connective tissue, and adapts rapidly. It triggers discharges, and then ceases reporting in a very short space of time. These messages occur successively, during motion, and the CNS can therefore be aware of the rate of acceleration of movement taking place in the area. It is sometimes called an acceleration receptor.

There are other end-organs, but these three can be seen to provide information regarding the present position, direction and rate of movement of any joint.

Muscle spindle

This receptor is sensitive and complex. It detects, evaluates, reports and adjusts the length of the muscle in which it lies, setting its tone. Acting with the Golgi tendon organ, most of the information as to muscle tone and movement is reported. The spindles lie parallel to the muscle fibres, and are attached either to skeletal muscle or to the tendinous portion of the muscle. Inside the spindle are fibres that may be one of two types. One is described as a ‘nuclear bag’ fibre, and the other as a chain fibre. In different muscles the ratios of these internal spindle fibres differ. In the centre of the spindle is a receptor called the annulospiral receptor (or primary ending), and on each side of this lies a ‘flower spray receptor’ (secondary ending). The primary ending discharges rapidly, and this occurs in response to even small changes in muscle length. The secondary ending compensates for this, because it fires messages only when larger changes in muscle length have occurred.

The spindle is a ‘length comparator’, and may discharge for long periods at a time. Within the spindle there are fine, intrafusal fibres that alter the sensitivity of the spindle. These can be altered without any actual change taking place in the length of the muscle itself, via an independent γ-efferent supply to the intrafusal fibres. This has implications in a variety of acute and chronic problems.

The proprioceptive role of muscles of the suboccipital region is directly related to the number of spindles per gram of muscle. There are an average of 36 spindles per gram in some of the suboccipital muscles, such as rectus capitis posterior minor, and 30.5 spindles per gram in rectus capitis posterior major, compared, for example, with 7.6 spindles per gram in splenius capitis and just 0.8 spindles per gram in gluteus maximus (Peck et al 1984). McPartland & Brodeur (1999) suggest that ‘The high density of muscle spindles found in the RCPM muscles suggests a value … [which] lies not in their motor function, but in their role as “proprioceptive monitors” of the cervical spine and head.’

Buzzell (1970) describes the neural connections with the CNS thus:

The central connections of the spindle receptors are important. The annulospiral fibre has the only known monosynaptic relationship in the body. As the fibre passes to the cord, and through the dorsal horn, it goes without synapse, directly to the anterior horn cells that serve the muscle fibres in the vicinity of the spindle. This is the basis of the so called ‘tendon reflex’, which actually is not a tendon reflex, but simply a spindle response to a sudden elongation of the muscle.

In contrast, the secondary fibres have various synapses in their central connection which can be traced to higher cortical centres. Conscious activity may, therefore, provide a modifying influence, via these structures, on muscle tone. The activities of the spindle appear to provide information regarding length, velocity of contraction and changes in velocity. How long is the muscle? How quickly is it changing length? And what is happening to this rate of change of length? (Gray 1977).

Golgi tendon receptors

These structures indicate how hard the muscle is working, they reflect the tension of the muscle, rather than its length, as does the spindle. If the tendon organ detects excessive overload it may cause cessation of function of the muscle, to prevent damage. This produces relaxation.

There are various ways of ‘manipulating’ the neural reporting stations to produce physiological modifications in soft tissues – notably of the Golgi tendon organ in muscle energy techniques (METs) and of the spindle in various positional release (PR) techniques, such as strain/counterstrain (SCS) (Jones 1980, Stiles 1984).

Effect of contradictory information

Korr’s words regarding the nature of the information that these, and other, reporting stations are providing to the CNS are worth recording (Korr 1976). He 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.

This means that the pattern of information fed back to the CNS and brain from neural reporting stations (proprioceptors, mechanoreceptors, nociceptors, etc.) reflects, at any given time, the steady state of joints, the direction as well as speed of alteration in position of joints, together with data on the length of muscle fibres, the degree of load that is being borne, along with the tension this involves. This total input is what occurs, rather than individual pieces of information, as outlined above, from particular reporting stations.

Contradictory gibberish?

But what if any of the mass of information being constantly received should be contradictory, and actually conflict with the other information being received?

Buzzell puts it this way:

It is possible, for example, for the excessive force exerted by external trauma to induce such hyperactivity of the joint and muscle receptors that the reports from that area become gibberish.

Should conflicting reports reach the cord from a variety of sources simultaneously, no discernible pattern may be recognized by the CNS. In such a case no adequate response would be forthcoming, and it is probable that activity would be stopped. Spasm, or splinting, could therefore result.

When somatosensory, vestibular or visual afferent systems provide conflicting information, a variety of symptoms may result. Somatosensory afferent systems depend on coherent input, from the soles of the feet, the neck and lumbar spine (Gagey 1986).

Neural ‘cross-talk’

Korr (1976) discussed a variety of insults that could result in increased neural excitability: the triggering of a barrage of supernumerary 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, for example in the intervertebral foramina.

In addition, Korr reported that when any tissue is disturbed, whether bone, joint, ligament or muscle, the local stresses feed constant information to the cord, and effectively jam normal patterned transmission from the periphery. These factors, combined with any mechanical alterations in the tissues, are the background to much somatic dysfunction.

He summarized thus (Korr 1976):

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. 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; the elements that are so much a part of osteopathic diagnosis.

These are the palpable changes that we will be evaluating in later chapters that can allow us the opportunity to ‘read’ dysfunction, and to potentially choose therapeutic measures – such as neuromuscular technique – to assist in restoration of normal function.

Mechanisms that alter proprioception

(Lederman 1997)

• Ischaemic or inflammatory events at the receptor site may produce diminished proprioceptive sensitivity due to metabolic byproduct build-up stimulating groups III and IV, mainly pain afferents (this also occurs in muscle fatigue).

• Physical trauma can directly affect receptor axons (articular receptors, muscle spindles and their innervations).

• In direct trauma to muscle, spindle damage can lead to denervation and atrophy (e.g. following whiplash) (Hallgren et al 1993).

• Structural changes in parent tissue lead to atrophy and loss of sensitivity in detecting movement, plus altered firing rate (e.g. during stretching).

• Loss of muscle force (and possibly wasting) may result when a reduced afferent pattern leads to central reflexogenic inhibition of motor neurons supplying affected muscle.

• Psychomotor influences (e.g. feeling of insecurity) can alter patterns of muscle recruitment at the local level, and may result in disuse muscle weakness.

Trophic neural influences

Setting aside for the moment the obviously important feature of nerves, and their message-carrying functions, we need to consider the less understood role they play in transporting substances – proteins, phospholipids, glycoproteins, neurotransmitters, enzymes, mitochondria and more (Canals et al 2004).

Transportation takes place, at a rate of anything from 1 mm/24 h to several hundred millimetres per 24 h, depending on what is being transported and the presence, or absence, of interfering factors. Movement occurs in both directions along nerves, with retrograde (returning from the target tissues towards the CNS) transportation seemingly ‘a fundamental means of communication between neurons and between neurons and non-neuronal cells’ which strongly influences the ‘plasticity of the nervous system’, according to Korr’s research (Korr 1981).

Patterson & Wurster (1997) note that substances known as nerve growth factors (NGFs) are supplied to the neural structures by the target (end) organ to which neurotrophic substances are being transported. ‘If the end organ does not supply the NGF, the synaptic contact is lost.’ They continue: ‘Complete withdrawal of NGF or of the material delivered by the nerve to its end organ may result in loss of function … The occurrence of the tissue tensions and fluid flow disturbances often associated with somatic dysfunctions can be factors in altering axoplasmic flows.’

Butler (1991) reports that there are two speeds of delivery of trophic substances via the nerves:

The fast transport moves at approximately 400 mm per day and the substances carried, such as neurotransmitters and transmitter vesicles, are for use in transmission of impulses at the synapse. This transport depends on an uninterrupted supply of energy from the blood. Various toxic substances and deprivation of blood will slow or block the transport.

In the slow antegrade (delivery) transport (1–6 mm per day), cytoskeletal material is carried. The return transportation (retrograde) along the nerve carries recycled transmitter vesicles and extracellular material. Butler suggests that ‘It also seems likely that the retrograde flow carries “trophic messages” about the status of the axon, the synapse and the general environment around the synapse including the target tissues.’

Very significantly, Butler states: ‘If the retrograde flow is altered by physical constriction, or from loss of blood flow, nerve cell body reactions are induced.’

Korr (1981) demonstrated that red (postural) and white (phasic) muscle fibres, which differ morphologically, functionally, chemically and, as we will discover later in this chapter, in their response to stress, can have all of their characteristic differences reversed if their innervation is ‘crossed’, so that red muscles receive white muscle innervation and vice versa. ‘This means, in effect, that the nerve instructs the muscle what kind of muscle to be, and is an expression of a neurally mediated genetic influence’, according to Korr (1981).

Neural influences on gene expression

Korr’s research (1981) therefore suggests that it is the nervous system that largely determines which genes in a muscle will be suppressed, and which expressed, and this information is carried in the material being transported along the axons. (See Box 1.2 for additional influences on gene expression.)

Box 1.2 Gene expression

Korr (1981) demonstrated that obstruction of axonal transport modifies gene expression. Additional modulation of gene expression is now known to derive from biomechanical influences, specifically the status of minute structures – integrins – that penetrate the cell surface, acting as a communicating mechanism between the extracellular and intracellular environment.

‘Integrin molecules carry tension from the extracellular matrix, across the cell surface to the cytoskeleton which behaves as a tensegrity matrix’ (Wang et al 1993).

‘Of particular interest are the roles of the integrins in the migration of cells that defend the body against disease and repair injuries’ (Horwitz 1997, Hynes 1992).

The precise effects of tense, distorted, contracted, fibrosed or otherwise dysfunctional tissues on the integrins of the cells in these tissues, and subsequent gene expression, are topics for research, as are the potentially beneficial influences of appropriate bodywork designed to normalize such tissues (Oschman 2000).

Moving beyond neural and mechanical influences on gene expression, Martin (2001) interviewed functional medicine expert Jeffrey Bland, who observed:

Functional genomics derived out of the human genome project, in which it was thought that by dissecting the code of life in our 23 pairs of chromosomes, people would be able to understand how they were going to die. They would see locked in their genes heart disease, cancer, diabetes, arthritis, whatever it might be, and they would tell from these genetic imperfections what day, and what disease, they would finally fall prey to … Mendelian determinism … said that locked into our genes, when the sperm met the egg, were these strengths and weaknesses that we call the recessive and dominant characteristics of inheritance, … [and that] basically if we had the genes for cancer we would die of cancer, [and] if we had the genes for heart disease we would die of heart disease. It turns out that the human genome project has discovered that the genes that we thought were hard-wired to produce these diseases, are not hard-wired at all. Within our genes are multiple messages, and the message that is expressed at any moment – that’s in our phenotype – is a consequence of the environmental messages including diet, lifestyle, environment, that wash over our genes to give rise to different expression paths of the genes … some may be healthy, some may be unhealthy … what we’re really seeing is that the major determinants for the expression of genetic patterns, over decades of living, are the decisions that we make, either consciously or subconsciously, every day. How we exercise, how we work, what our stress patterns are.

A picture emerges that suggests structural features, neural function, stress and emotion, as well as environmental factors including diet, all determine the way in which genetic predispositions are either modified, modulated, contained or expressed.

When a muscle loses contact with its nerve (as in anterior poliomyelitis, for example) atrophy occurs, not as a result of disuse but because of loss of the integrity of the connection between nerve cells and muscle cells at the myoneural junction, where nutrient exchange occurs irrespective of whether or not impulses are being transmitted.

Korr (1981) also describes just how vulnerable these highways of nutrition are:

Any factor which causes derangement of transport mechanisms in the axon, or that chronically alters the quality or quantity of the axonally transported substances, could cause the trophic influences to become detrimental. This alteration in turn would produce aberrations of structure, function and metabolism, thereby contributing to dysfunction and disease.

What could cause such neurotrophic interference?

Korr specifies: ‘Deformations of nerves and roots, such as compression, stretching, angulation and torsion’, especially, he tells us, ‘in their passage over highly mobile joints, through bony canals, intervertebral foramina, fascial layers and tonically contracted muscles’.

Mention by Korr, Butler and others of the changes that can have a negative influence on neurotrophic flow include altered circulatory status as well as hypertonicity. Trigger point activity, as we will see in later chapters, should be capable of directly producing just such changes. Normalization of trigger point activity, and the aetiological factors that produced them, utilizing NMT for example, should therefore be at least one way of assisting more normal neurotrophic function.

More general normalization of somatic dysfunctions, which include not just trigger points but the entire range of shortened, fibrotic, hypertonic, oedematous, inflamed, restricted or otherwise compromised soft and osseous structures, can therefore be seen to offer benefit in restoration of neurotrophic function, and therefore of body functions generally.

Maitland and Butler: ‘abnormal neural movement’

Butler & Gifford (1989), building on the original work of Maitland (1986), have shown how what they term ‘adverse tension’ in the nervous system can impair its mobility and elasticity, and how many painful problems can result from this. Butler and Gifford’s detailed analysis of the diagnosis and treatment of such restrictions and tensions is highly recommended to manual therapists. The tissues that surround neural structures are known as the mechanical interface (MI). These adjacent tissues are those that can move independently of the nervous system; for example, supinator muscle is the MI to the radial nerve, as it passes through the radial tunnel.

There is no general agreement as to the terminology that should be used in describing such biomechanical changes in the neural environment. Maitland et al (2001), for example, suggest that ‘abnormal neural movement’ is a more accurate description than ‘neural tension’.

Whatever we term the dysfunctional pattern, Butler and Gifford’s focus on those ‘adverse mechanical’ changes that negatively influence neural function, and that cause a multitude of symptoms, including pain, has been an important contribution to our understanding of some aspects of pain and dysfunction.

Any pathology in the MI can produce abnormalities in nerve movement, resulting in tension on the neural structure with unpredictable ramifications. Examples of MI pathology include nerve impingement by disc protrusion, or osteophyte contact, and carpal tunnel constriction. These problems would be regarded as mechanical in origin as far as the nerve restriction is concerned. Any symptoms resulting from mechanical impingement on neural structures will be more readily provoked in tests that involve movement rather than pure (passive) tension (Alshami & Hodges 2006).

Chemical or inflammatory causes of neural tension can also occur, resulting in ‘interneural fibrosis’, which leads to reduced elasticity and increased ‘tension’, and would become obvious with tension testing of these structures.

Pathophysiological changes resulting from inflammation, or from chemical damage (i.e. toxicity), are noted by Butler & Gifford (1989) as commonly leading on to internal mechanical restrictions of neural structures in a different manner to mechanical causes such as those, for example, imposed by a disc lesion.

Korr (1970) states:

To appreciate the vulnerability of the segmental nervous system to somatic insults it must be understood that much of the pathway taken by nerves as they emerge from the cord is actually through skeletal muscle. The great contractile forces of skeletal muscles with the accompanying chemical changes exert profound influences on the metabolism and excitability of neurons. In this environment the neurons are subject to quite considerable mechanical and chemical influences of various kinds, compression and torsion and many others … slight mechanical stresses may, over a period of time, produce adhesions, constrictions and angulations imposed by protective layers.

Adverse mechanical tension changes do not necessarily affect nerve conduction, according to Butler and Gifford; however, Korr’s research indicates that axonal transport may be affected.

From the perspective of the manual therapist, this knowledge is extremely important.

The dysfunctional tissues and patients being treated by massage therapists, neuromuscular therapists, physiotherapists, Rolfers, Heller Workers, osteopathic and chiropractic practitioners, and those using movement therapies (Pilates, Feldenkrais, etc.), all have the potential to involve the mechanically interfacing structures in which neural tissues lie, and where normal mobility should be present (and often is not).

The role of neuromuscular techniques in management of adaptive overload

This book has, as a primary focus, the use of neuromuscular techniques (NMTs) in assessing and treating somatic dysfunction. The objectives of neuromuscular technique (NMT as practised in Europe) and neuromuscular therapy (NMT as practised in the USA) are summarized in Box 1.3.

Box 1.3 NMT: European (Lief’s) neuromuscular technique and American neuromuscular therapy (Chaitow & Delaney 2000)

Neuromuscular technique, as the term is used in this book, refers to the manual application of specialized (usually) digital pressure and strokes, most commonly applied by finger or thumb contact. These digital contacts can have either a diagnostic (assessment) or therapeutic objective, and the degree of pressure employed varies considerably between these two modes of application. There are subtle differences between the European and American versions of NMT. Detailed descriptions of Lief’s NMT will be found in Chapter 6, while the American NMT version is outlined by Judith DeLany in Chapter 10.

Additional complementary manual methods to NMT (both versions) include massage, muscle energy technique (MET), positional release technique (PRT), myofascial release technique (MRT) and variations of these soft tissue manipulation approaches.

Aims of NMT

Therapeutically, NMT aims to produce modifications in dysfunctional tissue, encouraging a restoration of functional normality, with a particular focus of deactivating focal points of reflexogenic activity, such as myofascial trigger points.

An alternative objective of NMT application is toward normalizing imbalances in hypertonic and/or fibrotic tissues, either as an end in itself or as a precursor to joint mobilization or manipulation.

NMT attempts to:

• offer reflex benefits

• deactivate myofascial trigger points

• prepare for other therapeutic methods such as exercise or manipulation

• relax and normalize tense, fibrotic muscular tissue

• enhance lymphatic and general circulation and drainage

• simultaneously offer the practitioner diagnostic information.

Neuromuscular therapy (USA) utilizes similar manual methods, as well as re-education, rehabilitation and home-care approaches, to those utilized in European methodology.

NMT attempts to address a number of features that are all commonly involved in causing or intensifying pain and dysfunction (Chaitow & DeLany 2000) including, among others:

• biochemical features – nutritional imbalances and deficiencies, toxicity (exogenous and endogenous), endocrine imbalances (e.g. thyroid deficiency), ischaemia, inflammation

• pyschosocial factors – stress, anxiety, depression, etc.

• biomechanical factors – posture, including patterns of use, hyperventilation tendencies, as well as locally dysfunctional states such as hypertonia, trigger points, neural compression or entrapment.

NMT sees its role as attempting to normalize or modulate whichever of these (or additional) influences on musculoskeletal pain and dysfunction can be identified in order to remove or modify as many aetiological and perpetuating influences as possible (Simons et al 1999), without creating further distress or requirement for excessive adaptation.

To understand the context for application of such approaches, we need to appreciate time-related influences on the evolution of dysfunction: how, over time, a progression occurs that alters acute responses, as the tissues locally, or the body as a whole, modify, accommodate, compensate and adapt to the demands, stresses and insults of daily life.

General adaptation syndrome (GAS) and local adaptation syndrome (LAS), and connective tissue

Selye (1976) 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 fails), which affects the organism as a whole – and the local adaptation syndrome (LAS), which affects a specific stressed area of the body, Selye also emphasized the importance of connective tissue. He demonstrated that stress results in a pattern of adaptation, individual to each organism. He further showed that, when an individual is acutely alarmed, stressed or aroused, homeostatic (self-normalizing) mechanisms are activated – this is the alarm reaction of Selye’s general (and local) adaptation syndromes.

If the alarm status is prolonged or repetitive, defensive adaptation processes commence and produce long-term – chronic – changes. In assessing (palpating) the patient, these neuromusculoskeletal 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 repeated postural and traumatic insults of a lifetime, combined with changes of emotional and psychological origin, will often present a confusing pattern of tense, contracted, bunched, fatigued and ultimately fibrous tissue (Chaitow 1989).

The minutiae of the process are not, for the moment, at issue. What is important is the realization that, due to prolonged stress of a postural, psychic 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 nature (Wall & Melzack 1991) (e.g. a single injury or repetitive postural strain) or purely psychic in nature (Latey 1983) (e.g. chronically repressed anger). An example of localized emotional stress influences on muscle tissue is given in Box 1.4. Wider biomechanical responses to emotional stress are discussed later in this chapter.

Box 1.4 Selective motor unit involvement

The effect of psychological influences on muscles seems to be more complex than a simplistic ‘whole’ muscle or regional involvement. It has been demonstrated that a small number of motor units in particular muscles may display almost constant, or repeated, activity when influenced psychogenically (Waersted et al 1993). The reaction time taken to perform tasks was evaluated in normal individuals, so creating a ‘time pressure’ anxiety. Researchers were able to demonstrate low-amplitude levels of activity (using surface EMG in trapezius muscles) even when the muscle was not being employed. It seems that, in spite of low total activity level of the muscle, a small pool of low-threshold motor units may be under considerable load for prolonged periods of time.

Such a recruitment pattern would be in agreement with the ‘size principle’ first proposed by Henneman (1957), which states that motor units are recruited according to their size. Motor units with type I (postural) fibres are predominant among the small, low-threshold units. If tension-provoking factors (e.g. anxiety) are frequently present, and the subject repeatedly recruits the same motor units, overload may follow, possibly resulting in a metabolic crisis and the appearance of type I fibres with an abnormally large diameter, or ‘ragged-red’ fibres, which are interpreted as a sign of mitochondrial overload (Edwards 1988, Larsson et al 1990). The implications of this information are profound, because they suggest that emotional stress can selectively involve postural muscle fibres that have a tendency to shorten over time when stressed (Janda 1983).

The possible ‘metabolic crisis’ suggested by this research has strong parallels with the evolution of myofascial trigger points as suggested by Simons, a topic that is discussed in greater detail in later chapters (Wolfe & Simons 1992).

More often than not a combination of emotional and physical stresses will so alter neuromusculoskeletal 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.

As described in this and later chapters, predictable chain reactions of compensating changes will evolve in the soft tissues in most instances of chronic adaptation to biomechanical and psychogenic stress (Lewit 1992). Such adaptation is almost always at the expense of optimal function, as well as being an ongoing source of further physiological embarrassment.