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):

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.

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:

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:

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 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

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:

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.)

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:

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:

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.

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.

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.

A biomechanical stress response sequence

When the musculoskeletal system is ‘stressed’, a sequence of events occurs which can be summarized as follows:

Unsustainable without consequences

In the presence of a constant neurological feedback of impulses to the CNS/brain from neural reporting stations indicating heightened arousal (a hypertonic muscle status is the alarm reaction of the flight/fight alarm response), there will be increased levels of psychological arousal and an inability to relax adequately with consequent increase in hypertonicity. Functional patterns of use, of a biologically unsustainable nature, will emerge, commonly involving chronic musculoskeletal problems and pain.

At this stage, restoration of normal function requires therapeutic input which addresses the multiple changes that have occurred as well as the need to re-educate the individual as to how to use their body – to breathe, to carry and to use themselves – in less stressful ways.

The chronic adaptive changes that develop in such a scenario lead to the increased likelihood of future acute exacerbations, as the progressively chronic, less supple and resilient, biomechanical structures attempt to cope with new stress factors resulting from the normal demands of modern living.

Some major soft tissue stress categories

Other models of pain genesis

Stoddard’s osteopathic perspective

Stoddard (1969), in discussing contracted musculature, describes its ‘stringy’ feel, resulting from the continuous contraction of some muscle fibres, and ascribes the cause to the underlying joint dysfunction. The resulting ache and pain, he believes, is usually a result of circulatory embarrassment as metabolic wastes build up due to sustained muscular contraction. Muscular guarding is always seen to indicate deeper pathological changes (e.g. tuberculosis of the spine, osteomyelitis, disc herniation).

Stoddard sees the metabolic wastes, which may result from a degree of stasis, as causing a vicious cycle in perpetuating muscular contraction, leading eventually to fibrous changes. There is no indication that Stoddard considers such changes to be of primary importance in his treatment programme. He does stress the importance of exercises (to strengthen muscle groups) and of correct posture, but does not indicate any great interest in treatment of the soft tissues themselves.

While release of muscular restrictions and shortening could be considered a desirable step in the restoration of normality, it is worth emphasizing that once adaptive fibrotic changes have taken place in the soft tissues (whether in response to emotional stress or anything else) these changes are no longer under purely neurological control and therefore cannot simply be ‘released’ (by exercises or anything else): they require a physical input that alters, stretches and effectively breaks down concretions such as fibrotic tissue.

Modern pain concepts

The complexity of muscular pain mechanisms becomes clearer as the diligent research and reporting of Mense & Simons (2001) is examined. Interestingly, many of the ideas promoted half a century ago, by Barlow and others, are confirmed by modern research, although far more detail is now available with regard to pain mechanisms.

A brief summary of the key elements described by Mense and Simons is offered below; however, this captures no more than a superficial glimpse of the material in their book.

Common subgroups of muscular pain are identified:

Mense and Simons consider that most other terms used to describe muscular pain can be subsumed into these three terms.

Sensitization

Sensitization of nociceptors by vasoneuroreactive substances (such as bradykinin and prostaglandins) leads to long-lasting tenderness of trigger points (Fig. 1.1). This is discussed further in Chapter 3.

Figure 1.1 Schematic diagram showing hypothesized mechanism for sustained tenderness in trigger points. (SP = substance P)

Redrawn from Mense S & Simons D, Muscle pain, Williams & Wilkins, 2001, with permission.

The process of sensitization involves local oedema, release of neuropeptides such as substance P, subsequent compression of venous vessels, venous congestion (which reduces blood supply) and therefore local ischaemia. Ischaemic conditions lead to the release of more bradykinin, ensuring a vicious cycle, which engenders sensitization of pain receptors.

In skeletal muscle, ischaemia results in interference with normal energy (ATP) production, which leads to disturbance of normal calcium pump activity, preventing actin and myosin filaments from releasing their contractured state. This is the hypothesized cause of ‘taut bands’, which are a key feature of myofascial trigger points (see Ch. 3).

Mense & Simons (2001) suggest that when inflammation occurs in muscle for a period as short as 12 days, the concentration of thin nerve fibres containing neuropeptides increases markedly, leading to a greater reporting of pain sensations (Reinert & Mense 1993).

The widely held belief that a pain–spasm–pain cycle exists is questioned by Mense & Simons (2001). Their arguments are too complex to summarize without losing accuracy, but the following remarks offer a glimpse:

Mense and Simons argue that although excitation of dorsal horn neurons by muscle nociceptors is established there is no proof that homonymous [alpha]-motor neurons are similarly activated: ‘An acute noxious stimulus to a muscle is likely to inhibit rather than excite homonymous motor neurons if the muscle is an extensor.’

They believe that because flexor muscle motor neurons display only short-lasting excitation (if any), and painful muscles frequently show little or no electrical activity when at rest, ‘the postulated [pain–spasm–pain] reflex is not functional in every muscle and cannot explain long-lasting spasm.’

Apart from the idea that spasm results via reflex arcs, as outlined above, a variety of other working hypotheses exists to explain the phenomenon of spasm, none of which is proven. These include the possibility that joint nociceptors act as initiators resulting in reflex stabilization via chronic muscle spasm.

Mense and Simons reject this, saying it cannot be universally valid, because ‘in many cases of painful joint lesions…neighbouring muscles are reflexly inhibited.’

Neuroplastic sensitization involves a process in which nociceptive input to the cord or brainstem leads to synaptic sensitization in the dorsal horn neurons. ‘Following such an input, the neurons are thought to increase their excitability and exhibit enhanced responses to both pathologic and normal afferent inflow.’

Central sensitization is then thought to perpetuate nociceptive activity.

This is a concept close to facilitation mechanisms, as hypothesized by osteopathic medicine, and discussed in Chapter 3.

There may be a malfunctioning of the descending antinociceptive system, in which central damping down of pain messages fails to be effective. Mense and Simons state: ‘It is conceivable that a malfunction of the descending antinociceptive system, which might occur spontaneously, or following a central or peripheral lesion, leads to chronic pain sensations from deep tissues, even in the absence of a peripheral lesion.’

Fibromyalgic pain may result from such a process.

Psychological factors modulate pain perception; however, controversially, Mense & Simons (2001) contend that whilst ‘psychological stress can be a potent aggravating factor … as we learn more about the pathophysiology concerning the origin of muscle pain, the less psychogenic and more somatic it becomes.’

A variety of mechanical (e.g. poor posture, asymmetry) and systemic (e.g. anaemia, low thyroid function, vitamin B deficiency) factors may interact to aggravate and perpetuate painful conditions.

Mense and Simons insist that it is essential to be aware of, and able to distinguish between, pain and tenderness that is local, projected (caused by peripheral nerve irritation), referred and of central origin – and of overlaps between these.

Additional insights from Mense and Simons will be introduced in later chapters.

At this stage it is useful to observe that pain is complex, confusing and demanding. The task of uncovering the mechanisms involved in any given patient’s painful muscular condition calls for the ability to evaluate muscular and articular status, and neurological features, as well as identification of myofascial trigger points and fibromyalgia characteristics.

One requirement for such a process is the ability to distinguish between different muscular responses to stress: overuse, misuse, disuse and abuse.

Different responses in postural and phasic muscles

It is not within the scope of this book to provide detailed physiological analysis; however, it is vital that the ways in which different muscle fibre types respond to stress are understood. To be sure there are several models in which different muscle groups are designated according to their main functions and characteristics, and an attempt is made in Box 1.5 to summarize these.

In this book the categorizations ‘postural’ and ‘phasic’ (Janda 1982, 1996, Lewit 1992, Liebenson 2006) are used, as these have been found by the principal author to be the most useful in clinical practice. What has been demonstrated is that, when stressed (overuse, misuse, abuse, disuse, etc.), postural muscles have a propensity to shorten, whereas phasic muscles undergoing similar ‘stress’ are inhibited, become weaker, and possibly lengthen (although localized contractures may be present).

Fetal position influences

Kolar (1999) reports that the muscles that tend to hypertonicity and shortening (i.e. ‘postural’ muscles) include most muscles shortened in the fetal position. These include finger, hand and wrist flexors; shoulder internal rotators and adductors; shoulder girdle elevators, as well as ankle plantar flexors and inverters; hip flexors, internal rotators and adductors.

The antagonists to these tend to become reciprocally inhibited (i.e. ‘phasic’ muscles). Janda (1996) suggests that these are the muscles whose neurodevelopment brings about the upright posture.

Role of the muscles in low back problems

If we examine the role of the muscular component of musculoskeletal structures, we find strong evidence for its involvement in many acute and chronic conditions.

Jokl (1984) tells us that disuse muscular atrophy, following back injury, is a major factor in the progression from an acute back problem to a chronic one. Changes take place that are observable, histologically and biochemically, in the muscle fibres, and that are translated into functional changes. The effects of these changes involve decreased endurance and weakened muscles, as well as spasm. We should remind ourselves of the basic anatomy of the low back, which includes the division of the musculature into:

Muscle types (see Box 1.5)

Any, or all, of these muscles can have a major influence on the onset of low back problems and pain. The division of muscles with regard to their different postural and phasic (volitional movement) types is worthy of re-emphasis. As mentioned earlier, muscle fibres may be differentiated into types by virtue of their role, as well as their main energy source.

The muscles that support the spine are mainly type I, endurance and stamina muscles. Their activities are in the main related to static, antigravity efforts, which require prolonged contraction, and these muscles are far more susceptible to disuse atrophy and shortening. The strength of such muscles may not indicate much change, even after a period of disuse, but the endurance factor could be greatly affected. This necessitates a certain degree of caution when interpreting muscle strength tests involving the paravertebral musculature.

Jokl (1984) points out that electromyographic (EMG) studies indicate that paraspinal muscles show marked fatigue in individuals with low back pain. This fatigue factor may play a major part in worsening, or accentuating, an already demonstrable degree of dysfunction in this region. When such a situation exists (pain and easy fatigue of supporting musculature), it may be assumed that an increasing number of muscle fibres has been recruited in order to maintain spinal stability, which in turn results in increased muscular pressure. Jokl tells us that normal muscle can work for long periods without any EMG evidence of fatigue. As muscles become weaker, they work at an increased percentage of their maximum voluntary contraction. Ultimately this leads to muscle spasm, which allows ischaemia to develop, and pain to result.

The cycle of increased effort, local spasm and ischaemia, leading to pain, may ultimately result in paraspinal spasm and splinting.

Therapeutic choices

The use of both neuromuscular technique (NMT) and muscle energy technique (MET), are indicated in such a situation, as a means of disrupting the cycle and, initially, relaxing the contracted muscles. NMT methods have a combined effect, both relaxing the tissues as well as increasing the vascularity and mobility of these structures. They become more ‘extensible’, to use Grieve’s phrase (Grieve 1985). He enlarges on this aspect thus:

The explanations of Jokl, Korr, Patterson and Grieve, as discussed above, help us to gain a clearer picture of the structural changes that take place as stress factors, operating over a period of time, impact on the soft tissues.

Postural and phasic muscle lists

Type I postural muscles are prone to loss of endurance capabilities when disused or subject to pathological influences and become shortened or tighter, whereas type II phasic muscles, when abused or disused, become weak (Janda 1982, Lewit 1992, Liebenson 2006).

Postural muscles that become hypertonic and shorten in response to dysfunction include (Fig. 1.2):

Figure 1.2A Major postural muscles of the anterior aspects of the body.

Figure 1.2B Major postural muscles of the posterior aspects of the body.

Phasic muscles, which weaken (i.e. are inhibited), and may lengthen, in response to dysfunction, include:

Muscle groups such as the scaleni are equivocal: they start out as phasic muscles but can end up as postural.

Note: Lewit (1999) does not subscribe to the theory that phasic and postural muscles can be differentiated by virtue of their fibre type, as do Grieve and Jokl, but certainly subscribes to their differences in all other regards.

Fibrositis changes its name to fibromyalgia

In Chapter 3, in which the phenomenon of local soft tissue dysfunction, most notably myofascial trigger point activity, is analysed in detail, the evolution of thinking regarding ‘fibrositis’ is also examined. Fibromyalgia (the new incarnation of fibrositis), with its causes, associated conditions and diagnostic criteria, requires discussion in that context because of the confusion that currently exists regarding the overlap between fibromyalgia syndrome (FMS), myofascial pain syndrome (MPS) and chronic fatigue syndrome (CFS). The fascia of the body has profound influence, and it is to this focus that we now turn.

Functional fascial continuities

Myers (2001) has created a model in which myofascial linkages are described in terms of railway junctions and tracks, which he has termed ‘myofascial meridians’. While the interconnectedness of fascia throughout the body has long been understood, Myers’ descriptions highlight specific linkages. The myofascial chains, which he describes as ‘long functional continuities’, are of important clinical value when attempting to identify functional connections between anatomically distant structures, for example the plantar fascia and fascia of the scalp, attaching to the brow ridge, as described in his superficial back line (Fig. 1.3), or the anterior compartment of the periosteum of the tibia and the sternocleidomastoid attachment to the temporal bone, as described in his superficial front line (Fig. 1.4). These fascial bridges are also of potential clinical importance in application of the progressive inhibition of neuromuscular structures (PINS) method, described by Dennis Dowling in Chapter 11 of this book.

Figure 1.3 Myers’ superficial back line.

Redrawn from Journal of Bodywork and Movement Therapies 1997; 1(2):95, with permission.

Figure 1.4 Myers’ superficial front line.

Redrawn from Journal of Bodywork and Movement Therapies 1997; 1(2):97, with permission.

Soft tissue changes – energy and fascial considerations

Taylor (1958) has postulated that tissue changes, apparent to the trained palpating hand, often result from changes in thermodynamic equilibrium. He states that the body is a thermodynamic system and, as such, alterations in the extracellular fluids, viscosity, pH, electrophoretic changes, colloidal osmotic pressure, etc., are subject to thermodynamic laws. One of these laws states that the total energy of such a system and its surroundings must remain constant, although the energy may be changed from one form to another as a result of alterations of the stresses imposed.

For example, through postural stress and gravitational effects, particular changes in the fascia involved would result in energy loss and therefore stasis and stagnation. One of the characteristics of thermodynamics is that of thixotropy, in which gels become more solid with energy loss and more fluid with energy input. Such changes are certainly palpable in soft tissues, before and after neuromuscular and other forms of manual treatment (Mikova et al 2008).

Over and above the important factors of posture, functional ability and pain, the musculoskeletal component of the body plays a vital role in the conservation – wastage – of energy and in the attainment, or otherwise, of a truly relaxed mind. Whilst the origins of musculoskeletal dysfunction can be either psychic or physical, the constant interaction of the soma with the mind ensures a degree of psychic stress occurring as a feedback from physically caused chronic muscular tensions.

Rolf (1962) suggests that the human organism, as an energy mass, is subject to gravitational law. As a plastic medium, capable of change, Rolfing attempts to reorganize and balance the body in relation to gravitational forces. This is done by using pressure and stretch techniques on the fascial tissues in a precise sequence of body areas. The beneficial effects are claimed to be physical, emotional, postural and behavioural.

Rolf (1962) states:

Osteopaths have observed and recorded the extent to which all degenerative change in the body – whether muscular, nervous, circulatory or organic – reflects in the superficial fascia. Any degree of degeneration, however minor, changes the bulk of the fascia, modifies its thickness and draws it into ridges in areas overlying deeper tensions and rigidities. Conversely, as this elastic envelope is stretched, manipulative mechanical energy is added to it, and the fascial colloid becomes more ‘sol’ and less ‘gel’ (Greenman 1989). Without minimizing the clinical importance of the structural and biomechanical aspects of the connective tissues, Oschman (2000) has examined and evaluated research, which suggests that far more may be taking place during manual treatment than current understanding can fully explain. See Box 1.7 for a brief summary of aspects of these concepts.

Fascial stress responses and therapeutic opportunities

Changes in the fascia can result from passive congestion, which results in fibrous infiltration and a more ‘sol’-like consistency than is the norm. Under healthy conditions a ‘gel’-like ground substance follows the laws of fluid mechanics. Clearly, the more resistive drag there is in a colloidal substance, the greater will be the difficulty in normalizing this.

Scariati (1991) points out that colloids are not rigid: they conform to the shape of their container, and respond to pressure even though they are not compressible. The amount of resistance they offer increases proportionally to the velocity of motion applied to them, which makes a gentle touch a fundamental requirement if viscous drag and resistance are to be avoided when attempting to produce a release.

When stressful forces (undesirable or therapeutic) are applied to fascia, there is a first reaction in which a degree of slack is allowed to be taken up, followed by what is colloquially referred to as ‘creep’ – a variable degree of resistance (depending on the state of the tissues).

Creep is an honest term that accurately describes the slow, delayed yet continuous, stretch that occurs in response to a continuously applied load, as long as this is gentle enough to not provoke the resistance of colloidal ‘drag’.

As the fascia comprises a single structure, the implications for body-wide repercussions of distortions in that structure are clear (Fig. 1.6). An example of one possible negative influence of this sort is to be found in the fascial divisions within the cranium, the tentorium cerebelli and falx cerebri, which are commonly warped during birthing difficulties (too long or too short a time in the birth canal, forceps delivery, etc.) and which are noted in craniosacral therapy as affecting total body mechanics via their influence on fascia (and therefore the musculature) throughout the body (Brookes 1984).

Figure 1.6 Balanced posture (A) compared with two patterns of musculoskeletal imbalance that involve fascial, and general, tissue and joint adaptations.

Cantu & Grodin (1992) describe what they see as the ‘unique’ feature of connective tissue as its ‘deformation characteristics’. This refers to a combined viscous (permanent) deformation characteristic as well as an elastic (temporary) deformation characteristic. This leads to the clinically important manner in which connective tissue responds to applied mechanical force by first changing in length, followed by some of this change being lost while some remains. The implications of this phenomenon can be seen in the application of stretching techniques to such tissues, as well as in the way they respond to postural and other repetitive insults.

Such changes are not, however, permanent, because collagen (the raw material of fascia/connective tissue) has a limited (300–500 days) half-life and, just as bone adapts to stresses imposed upon it, so does fascia. Therefore, if negative stresses (posture, use, etc.) are modified for the better and/or positive ‘stresses’ are imposed (e.g. manipulation and/or exercise), dysfunctional connective tissue can usually be improved over time (Neuberger et al 1953).

Cantu & Grodin (1992), in their evaluation of the myofascial complex, concluded that therapeutic approaches that sequence their treatment protocols to involve the superficial tissues (involving autonomic responses) as well as deeper tissues (influencing the mechanical components of the musculoskeletal system), and which also address the factor of mobility (movement), are in tune with the requirements of the body when dysfunctional. NMT, as it will be presented here, does take this comprehensive approach, and much that it offers seems to be similar to the myofascial release methods currently receiving so much attention in the USA.

Cathie (1974) maintains that the contractile phase of fascial activity supersedes all its other qualities. The attachments of fascia, he states, have a tendency to shorten after periods of marked activity that are followed by periods of inactivity, and the ligaments become tighter and thicker with advancing age. The properties of fascia (connective tissue) that he regards as being important to therapeutic consideration are:

Greenman (1989) describes how fascia responds to loads and stress in both a plastic and an elastic manner, its response depending upon the type, duration and amount of the load. The responses to either acute injury or repetitive microtrauma (e.g. resulting from a short leg imbalance) are, according to Greenman, likely to follow a sequence of inflammation which subsequently leads to absorption of inflammatory fluids into the superficial fascia, as well as into tight compartmentalized areas in the deep fascia – with this latter event being both palpable and detrimental.

Another variable (apart from the nature of the stress load) that influences the way in which fascia responds to stress, and what the individual feels of the process, relates to the number of collagen and elastic fibres contained in any given region.

Neural receptors within the fascia report to the CNS as part of any adaptation process, with the Pacinian corpuscles being particularly important in terms of their involvement in reflex responses.

Ligaments and muscle tone

Other neural input into the pool of activity, and responses to biomechanical stress, involve specialized fascial structures such as tendons and ligaments that contain highly specialized and sensitive mechanoreceptors and proprioceptive reporting stations.

Solomonow (2009) summarizes the role of ligaments as follows:

Solomonow adds some important information regarding the link between muscle behaviour and ligamentous function:

A strong clue relative to the potential therapeutic use of ligament behaviour, in for example positional release methodology (see Ch. 8), can be gained from Solomonow’s (2009) observation that:

Having briefly scanned the influences of stress, both short and long term, on the musculoskeletal system, and of the varying ways in which the soft tissues respond – acutely, chronically and with variations based on their structure – and before looking more closely at reflex phenomena a brief introduction to neuromuscular technique (see Ch. 2) will provide an indication of its potential for dealing with soft tissue distress.