Clinical Application of Neuromuscular Techniques The Upper Body Volume 1

30 CL I N I CA L A P PL I CATI O N OF N E U RO M U S C U LAR T EC H NIQU ES: T H E U P P E R B ODY Box 2.2 (continued) the head and neck and right side of the thorax and empties in a coursing th rough these 'precollector' vessels which empty into lymph similar manner to that of the l eft side. col lectors. Stimulation of Iymphangions (and therefore lymph movement) The collectors have valves every 6-20 mm that occur directly occurs as a result of automotoricity of the Iymphangions (electrical between two to th ree layers of spira l muscles, the unit being potentials from the autonomic nervous system) (Kurz 1 986). As the ca l l ed a Iymphangian (Fig. 2.7). The alternation of valves and spiral muscles of the vessels contract, they force the lymph through muscles gives a characteristic 'moniliform' shape to these vessels, the flap valve, which prevents its return. Additionally, stretching of the like pearls on a string. The Iymphangions contract in a peristaltic muscle fibers of the next Iymphangion (by increased fluid volume of man ner that assists in pressing the fluids through the va lved system. the segment) leads to reflex muscle contraction (internally stimulated), When stimulated, the muscles can substantially increase (up to thereby producing peristaltic waves along the lymphatic vessel. There 20-30 ti mes) the capacity of the whole lymphatic system (Chikly 200 1 ) . are a lso external stretch receptors that may be activated by manual methods of lymph drainage which create a similar peristalsis. The la rgest of the lymphatic vessels is the thoracic duct, wh ich begins at the cisterna chyli, a large sac-like structure withi n the Lymph movement is also augmented by respiration as the altering abdominal cavity located at approximately the level of the 2nd intrathoracic pressure produces a suction on the thoracic duct and lumbar vertebra. The thoracic duct, containing lymph fluids from cisterna chyli and thereby increases lymph movement in the duct both of the lower extremities and a l l abdominal viscera except part and presses it toward the venous arch (Kurz 1 986, 1 987). Skeletal of the liver, runs posterior to the stomach a n d intestines. Lymph muscle contractions, movement of limbs, peristalsis of smooth fluids from the left upper extremity, left thorax and the left side of muscles, the speed of blood movement in the veins into which the cranium and neck may join it just before it empties into the left subclavian vein or may empty nearby into the internal jugular vein, ducts empty and the pulsing of nearby arteries a l l contribute to brachiocepha l ic junction or directly into the subclavian vein. The lymph movement (Wittl inger & Wittl inger 1 982). Exposure to cold, right lymphatic duct d rains the right upper extrem ity, right side of tight cloth ing, lack of exercise and excess protein consumption can hinder lymphatic flow (Kurz 1 986, Wittlinger & Wittlinger 1 982). White pulp Spleen Afferent lymphatic vessels via Lymphatic efferent drainage lymphatic vessels marrow tissue: including: connective tissue, epithelia, non-encapsulated lymphoid tissue of gut, elc. Figure 2.7 Lymph pathway (a Iymphangion is shown in insert). box continues

2 M uscles 31 Box 2.2 (continued) significantly increases lymph movement by crosswise and lengthwise stretching of the anchoring filaments that open the lymph Contraction ofneighboring muscles compresses lymph vessels, mov­ capillaries, thus allowing the i n terstitial fluid to enter the lymphatic system. However, shearing forces (like those created by deep ing lymph in the directions determined by their valves; extremely little pressure gliding techniques) can lead to temporary i n hibition of lymph flow by inducing spasms of lymphatic muscles (Kurz 1 986). lymph flows in an immobilized limb, whereas flow is increased by Unless the vessels are d amaged, lymphatic movement can then be reactivated by use of manual tech niques that sti mulate the either active or passive movements. This fact has been used clinically Iym phan g i o n s . to diminish dissemination of toxins from infected tissues by immobi­ While each case has to be considered individual ly, numerous conditions, ranging from postoperative edema to premenstrual fluid lization of the relevant regions. Conversely, massage aids the flow of retention, may benefit from lymphatic d rainage. There are, however, conditions for which lymphatic d rainage would be contrai ndicated or lymph from oedematous regions. (Gray's Anatomy 1995) precautions exercised. Some of the more serious of these conditions i n c l ud e : By recovering up to 20% of the interstitial fluids, the lymphatic system rel ieves the venous system (and therefore the heart) of the • acute infections and acute inflammation (generalized and local) responsibility of transporting the large molecules of protein and • thrombosis debris back to the general circulation. Additional ly, the lymphocytes • circulatory problems remove particulate matter by means of phagocytosis, that is, the • cardiac conditions process of ingestion and digestion by cel ls of solid substances (other • hemorrhage cells, bacteria, bits of necrosed tissue, foreign particles). By the time • malignant cancers the fluid has been returned to the veins, it is ultrafiltered, condensed • thyroid problems and hig hly concentrated. • acute phlebitis. In effect, ifthe lymphatic system did not regain the 2-20% ofthe Conditions that might benefit from lymphatic d rainage but for which precautions are indicated include: protein-rich liquid that escaped in the interstitium (a large part of • certain edemas, depending upon their cause, such as cardiac which the venous system cannot recover), the body would probably insufficiency develop major edemas and autointoxication and die within 24-48 • carotid stenosis hours. (Chikly 2001, Guyton 1986) • bronchial asthma • burns, scars, bruises, moles Conversely, when applying lymph d rainage techniques, care must be • abdom i nal surgery, radiation or undetermined bleeding or pain taken to avoid excessive increases in the volume of lymph flow in • removed spleen people who have heart conditions as the venous system must • major kidney problems or insufficiency accom modate the load once the fluid has been delivered to the • menstruation (drain prior to menses) subclavian veins. Significantly increasing the load could place • gynecological infections, fibromas or cysts excessive strain on the heart. • some pregnancies (especially in the first 3 months) • chronic infections or inflammation Lymphatic circulation is separated i n to two layers. The superficial • low blood pressure. circulation, which constitutes approxi mately 70% of all lymph flow (Chikly 2001 1. is located just under the dermoepidermic junction. The deep muscular and visceral circulation, below the fascia, is activated by muscular contraction; however, the superficial circulation is not directly sti mulated by exercise. Additional ly, lymph capi l l aries (Iacteals) in the jejunum and i l eum of the digestive tract absorb fat and fat-soluble nutrients that ultimately reach the liver through the blood ci rculation (Braem 1 994). Manual or mechanical lymphatic d rainage tech niques are effective ways to increase lymph removal from stag nant or edemic tissue. The manual techn iques use extremely light pressure, which MOTOR CONTROL AND RESPIRATORY below), which interferes with the first tvvo of those three ele­ ALKALOSIS ments - the CNS as well as muscle function. Motor control is a key component in injury prevention. Loss People who 'overbreathe', or who have marked upper of motor control involves failure to con trol joints, com­ chest breathing patterns ('brea thing pattern disorders' or monly because of incoordination of agonist-antagonist BPD), automatically exhale more carbon dioxide (C02) than muscle coactivation. According to Panjabi (1992), three sub­ is appropriate for their current metabolic needs. Exhaled systems work together to maintain joint and spinal stability: CO2 derives from carbonic acid in the bloodstream, and an excessive reduction of this leads to a situation known as res­ 1. The central nervous subsystem (control) piratory alkalosis, where the pH of the blood becomes more 2. The muscle subsystem (active) alkaline than its normal of ::'::7.4 (Lum 1987, Pryor & Prasad 3. The osteoligamentous subsystem (passive). 2002). Anything that interferes with any aspect of these features of There are a number of major consequences of increased normal motor control may contribute to dysfunction and alkalinity, one of which is a contrac tion of smooth muscle pain. This includes a condition in which the bloodstream cells (SMC) . This reduces the diameter of all struc tures sur­ increases in alkalinity because of overbreathing (for exam­ rounded by smooth muscles, such as the blood vessels and ple hyperventilation, the extreme of overbreathing, see intestinal structures. Reduced diameter of blood vessels limits blood supply to the tissues and the brain, thereby

32 C L I N I CA L A P P L I CATI O N OF N E U RO M USCULAR TEC H N IQU ES: TH E U P PER B ODY resulting in a variety of symptoms (see below), one of which motor discharges, muscular tension and spasm, speeding of is increased fatigability. It is postulated that SMC contrac­ spinal reflexes, heightened perception (pain, photophobia, tion may also influence fascial tone (Schleip et aI 2004). (See hyperacusis) and other sensory disturbances. ' Muscles Chapter 1 for information regarding smooth muscle cells affected in this way inevitably become prone to fatigue, and their location and behavior in connective tissues.) altered function, cramp and trigger point evolution (George et al 1964, Levitzky 1995, Macefield & Burke 1991). TWO KEY DEFINITIONS CORE STABILITY, TRANSVERSUS ABDOMINIS, • Hypocapnia: Deficiency of CO2 in the blood, possibly resul ting from hyperventilation, leading to respiratory THE DIAPHRAGM AND BPD alkalosis. It is well established that the tone of both the diaphragm • Hypoxia: Reduction of O2 supply to tissue, below physio­ and transversus abdominis hold the key to maintenance of logical levels despite adequate perfusion of the tissue by core stability (Panjabi 1992) . blood. McGill et al (1995) have observed a reduction in spinal Lum (1987) reports that research indica tes that not less than support if there is both a load challenge to the low back, 10% of patients attending general internal medicine practice combined with a demand for increased breathing (imagine in the US have such breathing pattern disorders as their pri­ shoveling snow!). 'Modulation of muscle activity needed to mary diagnosis. Newton (2001) agrees with this assessment. facilitate breathing may compromise the margin of safety of tissues that depend on constant muscle activity for support.' The authors of this text suggest that there exists a large patient population with BPDs who do not meet the criteria Hodges & Gandevia (2000) reported that after approxi­ for hyperventilation, but whose breathing patterns may mately 60 seconds of overbreathing, the postural (tonic) and contribute markedly to their symptom picture, and whose phasic functions of both the diaphragm and transversus mo tor control is likely to be negatively affected as a result abdominis are reduced or absent. (Chaitow 2004). SUMMARY • Breathing pattern disorders are female dominated, rang­ ing from a ratio of 2:1 to 7:1 (Lum 1994). • BPDs alter blood pH, thereby creating respiratory alkalosis. • Women are more at risk, possibly because progesterone is a respiratory accelerator (Damas-Mora et aI 1980). • This induces increased sympathetic arousal, which affects neuronal function (including motor control). • Progesterone is known to cause hyperventilation and hypercapnia in the luteal phase of a normal menstrual • There will be an increased sense of apprehension and cycle (Brown 1998, Rajesh et al 2000, Stahl et aI 1985). anxiety. As a result, the person's balance may be compro­ mised (Winters & Crago 2000). • During post ovulation phase, CO2 levels drop ::+::25% (Lum 1994). • Depletion of Ca and Mg ions enhances neural sensitiza­ tion, encouraging spasm and reducing pain thresholds. • Additional stress then, 'increases ventilation when CO2 levels are already low' (Lum 1994). • As pH rises, smooth muscle cells constrict, leading to vasoconstriction that reduces blood supply to the brain THE BOHR EFFECT (Fried 1987, Pryor Et and tissues (particularly the muscles) and possibly alters Prasad 2002) fascial tone. The Bohr effect states that a rise in alkalinity (due to a • Reduced oxygen release to cells, tissues and brain (Bohr decrease in CO2) increases the affinity of hemoglobin (Hb) effect) leads to ischemia, fatigue and pain, and the evolu­ for oxygen (02). This means that when tissues, and the tion of myofascial trigger points. bloodstream, increase in alkalinity the Hb molecule binds more firmly to the oxygen it is carrying, releasing it less effi­ • If the individual is deconditioned, not involved in aero­ ciently, which leads to hypoxia. Increased OrHb affinity bic activity, this sequence will trigger release of acid also leads to changes in serum calcium and red cell phos­ wastes when tissues a ttempt to produce ATP in a rela­ phate levels which both reduce. tively anaerobic environment (as discussed earlier in this chapter). Additionally, there is a loss of intracellular Mg2+ as part of the renal compensation mechanism for correcting alkalo­ • Biomechanical overuse stresses emerge along with com- sis. The function of motor and sensory axons will be signif­ promised core stability and postural decay. icantly affected by lower levels of calcium ions and these sensi tive neural structures will tend toward hyperirritabil­ What this (overbreathing) scenario illustrates is that when ity, negatively affecting motor control (Seyal et a11998). pain and dysfunction involving neuromuscular imbalance are evident in a patient, any therapeutic intervention that Lum (1994) explains: 'Loss of CO2 ions from neurons fails to pay attention to breathing patterns is less likely to be stimulates neuronal activity, causing increased sensory and successful than if this receives appropriate clinical evalua­ tion and rehabilitation, if necessary (see Chapter 4).

2 M uscles 33 MAJOR TYPES OF VOLUNTARY CONTRACTION Epimysium w-;_-- Perimysium Muscle contractions can be: • isometric (with no movement resulting) • isotonic concentric (where shortening of the muscle pro­ duces approximation of its attachments and the struc­ tures to which the muscle attaches) or • isotonic eccentric (in which the muscle lengthens during its contraction, therefore the attachments separate during contraction of the muscle). TERMINOLOGY Basement • The terms origin and insertion are somewhat inaccurate, Thin filament with attachments being more appropriate. Attachments Thick filament Crossbridge can be further classified as proximal or distal (in the extremities) or by location, such as sternal, clavicular, Cross-sections show costal or humeral attachments of pectoralis major. relationships of • In many instances, muscular attachments can adaptively myofilaments within reverse their roles, depending on what action is involved myofibril at levels and therefore which attachment is fixed. As an example, psoas can flex the hip when its lumbar attachment is 'the indicated origin' (fixed point) or it can flex the spine when the femoral attachment becomes 'the origin', i.e. the pOint �H � toward which motion is taking place. ,,\"'V\"IO Q) MUSCLE TONE AND CONTRACTION A E -, Muscles display excitability - the ability to respond to stimuli 0 and, by means of a stimulus, to be able to actively contract, extend (lengthen) or to elastically recoil from a distended posi­ u tion, as well as to be able to passively relax when stimulus ceases. ro Lederman (1997) suggests that muscle tone in a resting (/) muscle relates to biomechanical elements - a mix of fascial and connective tissue tension together with intramuscular /z ----- - - - fluid pressure, with no neurological input (therefore, not 11\\.I/1\\1'LV!1� 1 _Myofilaments measurable by EMG). If a muscle has altered morphologi­ cally, due to chronic shortening, for example, or to compart­ Figure 2.8 Organization of skeletal muscle. Redrawn after Hansen ment syndrome, then muscle tone, even at rest, will be & Koeppen (2002). altered and palpable. A motor nerve fiber will always activate more than one He differentiates this from motor tone, which is measura­ muscle fiber and the collection of fibers it innervates i s ble by means of EMG and which is present in a resting mus­ called a motor unit. The greater the degree o f fine control a cle only under abnormal circumstances - for example, muscle is required to produce, the fewer muscle fibers a when psychological stress or protective activity is involved. nerve fiber will innervate in that muscle. This can range from 10 muscle fibers being innervated by a single motor Motor tone is either phasic or tonic, depending upon the neuron in the extrinsic eye muscles to one motor neuron nature of the activity being demanded of the muscle - to innervating several hundred fibers in major limb muscles move something (phasic) or to stabilize it (tonic). In normal (Gray's Anatomy 2005, p. 121). muscles, both activities vanish when gravitational and activity demands are absent. Because there is a diffuse spread of influence from a sin­ gle motor neuron throughout a muscle (i.e. neural influence Contraction occurs in response to a motor nerve impulse does not necessarily correspond to fascicular divisions) acting on muscle fibers. only a few need to be active to influence the entire muscle. The functional contractile unit of a muscle fiber is its sar­ comere, which contains filaments of actin and myosin. These myofilaments (actin and myosin) interact in order to shorten the muscle fiber. Gray's Anatomy (2005) describes the process as follows: At higher power, sarcomeres are seen to consist oftwo types of filament, thick and thin, organized into regular arrays.

34 CLI N I CAL A P PL I CAT I O N OF N E U RO M U S C U LA R TEC H N I Q U E S : T H E U P P E R B O DY The thick filaments, which are c. 15 nm in diameter, are There are also several phasiC (type II) fiber forms, notably: composed mainly of myosin. The thin filaments, which are 8 nm in diameter, are composed mainly of actin. The arrays • type IIa (fast-twitch fibers) which contract more speedily of thick and thin filaments form a partially overlapping than type I and are moderately resistant to fatigue with structure . . . The A-band consists of the thick filaments, relatively high concentrations of mitochondria and myo­ together with links of thinfilaments that interdigitate with, globulin and thus overlap, the thick filaments at either end . . . The I-band consists of the adjacent portions of two neighbouring • type IIb (fast-twitch glycolytic fibers) which are less sarcomeres in which the thin filaments are not overlapped fatigue resistant and depend more on glycolytic sources of by thickfilaments. It is bisected by the Z-disc, into which the energy, with low levels of mitochondria and myoglobulin thin filaments of the adjacent sarcomeres are anchored. In addition to the thick and thin filaments, there is a third type • type lIm (superfast fibers) which depend upon a unique of filament composed of the elastic protein, titin . . . The myosin structure that, along with a high glycogen con­ banded appearance of the individual myofibrils is thus tent, differentia tes them from the other type II fibers attributable to the regular alteration of the thick and thin fil­ (Rowlerson 1981). These are found mainly in the jaw aments arrays. muscles. VULNERABLE AREAS As mentioned above, long-term stress involving type I mus­ cle fibers leads to them shortening, whereas type II fibers, • In order to transfer force to its attachment site, contractile undergOing similar stress, will weaken without shortening units merge with the collagen fibers of the tendon which over their whole length (they may, however, develop local­ attaches the muscle to bone. ized areas of sarcomere contracture, for example where trig­ ger points evolve without shortening the muscle overall). • At the transition area, between muscle and tendon, these structures virtually 'fold' together, increasing strength Shortness/ tightness of a postural muscle does not neces­ while reducing the elastic quality. sarily imply strength. Such muscles may test as strong or weak. However, a weak phasic muscle will not shorten • This increased ability to handle shear forces is achieved overall and will always test as weak. at the expense of the tissue's capacity to handle tensile forces. Fiber type is not totally fixed, in that evidence exists as to the potential for adaptability of muscles, so that committed • The chance of injury increases at those locations where muscle fibers can be transformed from slow twitch to fast elastic muscle tissue transitions to less elastic tendon and twitch, and vice versa (Lin 1994). finally to non-elastic bone - the attachment sites of the body. An example of this potential, which has profound clinical significance, involves the scalene muscles. Lewit (1985) con­ MUSCLE TYPES firms that they can be classified as either a postural or a pha­ sic muscle. The scalenes, which are largely phasic (type II) Muscle fibers exist in various motor unit types - basically and dedicated to movement, can have postural functions type I slow red tonic and type II fast white phasic (see thrust upon them, as with forward head postures, or when below). Type I are fatigue resistant while type II are more chronically contracted to maintain a virtually permanently easily fatigued. elevated status of the upper chest, as in asthma. If these pos­ tural demands are prolonged, more postural (type I) fibers All muscles have a mixture of fiber types (both I and II), may develop to meet the situation. If overuse continues (as although in most there is a predominance of one or the in upper chest breathing involving the upper ribs being reg­ other, depending on the primary tasks of the muscle (pos­ ularly elevated during inhalation), these now postural mus­ tural stabilizer or phasic mover). cles will shorten, as would any type I muscle when chronically stressed (Janda 1982, Liebenson 2006). Those which contract slowly (slow-twitch fibers) are clas­ sified as type I (Engel 1986, Woo 1987) . These have very low The following findings, relating to the scalene muscles, stores of energy-supplying glycogen, but carry high con­ were reported in a study that evaluated the link between centrations of myoglobulin and mitochondria. These fibers these and inappropriate breathing patterns, in this instance, fatigue slowly and a re mainly involved in postural and sta­ mainly asthma. bilizing tasks. The effect of overuse, misuse, abuse or disuse on postural muscles (see Chapters 4 and 5) is that, over The incidence of scalene muscle pathology was assessed in time, they will shorten. This tendency to shorten is a clini­ 46 consecutively hospitalized patients with bronchial cally important distinction between the response to 'stress' asthma and irritable cough diagnoses. Three tests described of type I and type II muscle fibers (see below). by Travell & Simons were used in patient evaluation, including palpation for scalene trigger points and the use of Adson's test. Breathing patterns were also evaluated in all patients for the presence of paradoxical breathing patterns. Scalene muscle pathologtj [dysfunction] was identified in 20 of the 38 bronchial asthma patients (52%), and in 5 of the

2 M uscles 35 Sternocleidomastoid ---e\\. l'+-- Upper trapezius Pectoralis major -----+... Levator scapula --.\"-� --- Deltoid Sacrospinalis --1-+tI -\\-- Latissimus dorsi External oblique --h- B.\".:++-+-Quadratus lumborum ..�\\--- \\- Quadratus lumborum Flexors --J-r. +--+ Iliopsoas Piriformis ---\"f�j+ Tensor fascia lata ---I;'HJf lY--\\l*iAdductor longus Rectus femoris ---\\H: Adductor magnus ---It_ :+-/'-- Biceps femoris Semimembranosus ----1 jIJF-<-J -1+- I�ft--- --- Semitendinosus A.Jf-- Gastrocnemius 11:..f.-/Tibialis posterior AB Figure 2. 9 Major postural muscles. A : Anter ior. B : Posterior. Reproduced with permission from Chaitow ( 1 996). 8 irritable cough syndrome patients (62%). Postisometric abdominal (or lower) aspects of pectoralis major, middle relaxation technique [muscle energJj] was used in those with and lower aspects of trapezius, the rhomboids, serratus scalene dysfunction. Self-administered stretching tech­ anterior, rectus abdominis, gluteals, the peroneal muscles, niquesfor home use were also taught. One patient with par­ vasti and the extensors of the arms. adoxical breathing pattern was taught an alternative breathing pattern. The authors are of the opinion that Some muscle groups, such as the scalenii, are equivocal. bronchial asthma and irritable cough syndrome patients Although commonly listed as phasic muscles, this is how should be examined and evaluated by Rehabilitation they start life but they can end up as postural ones if suffi­ Medicine Department stafffor functional pathology of the cient demands are made on them (see above). scalene muscles. They are also of the opinion that examina­ tion, treatment and self-administered stretching techniques COOPERATIVE MUSCLE ACTIVITY should be a par t ofroutine management ofbronchial asthma patients. (Pleidelova et al 2002) Few, if any, muscles work in isolation, with most move­ ments involving the combined effort of two or more, with Among the more important postural muscles that become one or more acting as the 'prime mover ' or agonist. hypertonic in response to dysfunction are: Almost every skeletal muscle has an antagonist that per­ • trapezius (upper), sternocleidomastoid, levator scapula forms the opposite action, with one of the most obvious and upper aspects of pectoralis major in the upper trunk examples being the elbow flexors (biceps brachii) and and the flexors of the arms extensors (triceps brachii). • quadratus lumborum, erector spinae, oblique abdomi­ Prime movers usually have synergistic muscles that nals and iliopsoas in the lower trunk assist them and which contract at almost the same time. An example of these roles would be hip abduction, in which • tensor fascia latae, rectus femoris, biceps femoris, add uc­ gluteus medius is the prime mover, with tensor fascia latae tors (longus, brevis and magnus), piriformis, semimem­ and gluteus minimus acting synergistically and the hip branosus and semitendinosus in the pelvic and lower adductors acting as antagonists, being reciprocally inhibited extremity region. (RI) by the action of the agonists if movement is to occur. RI is the physiological phenomenon in which there is an auto­ Phasic muscles, which weaken in response to dysfunction matic inhibition of a muscle when its antagonist contracts, (i.e. are inhibited), include the paravertebral muscles (not also known as Sherrington's law II. erector spinae), scalenii and deep neck flexors, deltoid, the

36 CL I N I CA L A P PL I CATION OF N E U RO M USCULAR TECH N I Q U E S : T H E U P P E R BODY Box 2.3 Alternative cat�ton of musc:l� result in postural adaptations. Treatment would aim to nor­ ma lize the tissues and lengthen the fibers. It is general ly accepted that muscles respond to overuse, misuse or disuse by either shortening or weaken ing (and possibly lengtheni ng). Many of these categories interface - for instance, overused tight As Kolar has explained (in Liebenson 2006, p. 533) : 'There is clinical muscles tend to create joint pressure leading to interneuron and experimental evidence that some muscles are inclined to responses. Psychological stress might result in muscle tightening and inh ibition (hypotonus, weakness, inactivity), while other muscle trigger point formation. Al though the body has a number of response groups are likely to be hyperactive with a tendency to become short: choices that it can make to cope with the load to which it is It was Janda (1 969, 1 983a) who first showed that these cha nges adapting (biochemical, biomechan ical and psychosocial), the fol lowed certa in rules, and who named them as phasic (those practitioner also has a wide range of choices in the way of tending to inhibition) and postural (those tending to shortening). A i nterventions. Chapters 9 a nd 10 carry a ful l discussion of some of plethora of different descriptors have been used to l abel these two those options. muscle groups, including stabil izer, mobil iz er; global, local ; superficial, deep, etc. (Norris 1 995a,b), adding a sense o f potential In sum mary, whatever the causes, there are two main responses disagreement and confusion to the understa nding of what is in by muscles when chronically stressed : essence relatively simple: some muscles fol low one pathway toward dysfunction, while others fol low a different pathway - whatever 1 . They are inh ibited and show evidence of hypotonus and weakness names they are ascribed. In the interest of simpl icity, the authors of (phasic). or this text have continued to designate these different muscle types as posturaI a nd phasic. 2. They develop hypertonus, and possibly spasm and rigidity (postural). Liebenson (2006, p. 4 1 1 ) d iscusses Janda's classification of tense and tight muscles and further separates muscle dysfunction into a These cha nges appear to involve mainly the contractile elements of va riety of different treatment-specific categories that are either muscles. However, i n some i nstances, connective tissue may a lso be neuromuscular or connective tissue related. involved, resulting in contracture (Ja nda 1 99 1 ) . These classifications are as fol lows: There is quite natura l ly n o t only a functional but a lso a structural aspect to these differences, and these have been identified by • Neuromuscular: physiologists. As Kolar expla ins (Liebenson 2006, p. 533) : 1. Reflex spasm: As a response to n ociception, this often acts as a spl inting mechan ism. Treatment would aim toward removal Differences are found in the nervous structure in control of these [dif­ of the cause of pa in, such an infla med appendix. 2. Interneuron: This del icate part of the reflex arc can become ferent] muscles, for it is the type of neurons that determines the type involved when afferent information is sent from spinal or of muscle fibre. It is therefore better to speak of tonic and phasic peripheral joints. Treatment would a i m to normalize the motor units. Tonic motorneurons, i.e. small alpha motor cells, inner­ involved joints. vate red muscle fibres, whereas phasic motorneurons (large alpha 3. Trigger point: This is thought to be associated with loca l ized congestion within the muscle stemming from short muscle cells) innervate white muscle fibres. In humans, both types of motor fibers. A variety of treatments are offered in this book to nor­ units are present in every muscle, in different proportions. malize myofascial tissue. 4. Limbic: This is associated with psychological stress. It can be Examples of patterns of imbalance which emerge as som e muscles treated with counseling, stress management and a variety of weaken and lengthen and their synergists become overworked, while relaxation methods including yoga and meditation. their antagonists shorten, ca n be summarized as follows. • Connective tissue: 1 . Overuse muscle tightness: This stems from muscle imba la nces, overuse, faulty movement patterns and other stresses that Len gthened or underactive stabi l izer Overactive synergist Shortened a ntagonist 1 . Gluteus medius TFL, QL, piriformis Thigh adductors 2. Gluteus maximus Iliocostalis lumborum Et hamstrin gs Iliopsoas, rectus femoris 3. Transversus abdominis Rectus abdom i n is Il iocostalis lumborum 4. Lower trapezius Levator scapulae/Upper trapezius Pectora lis major 5. Deep neck flexors SCM Suboccipita ls 6. Serratus anterior Pectora lis major/minor Rhomboids 7. Diaphragm Scalenes, pectoralis major/minor Observation muscle l ength tests, movement patterns and inner holding Observation can often provide evidence of a n imbalan.ce involving endurance times. Posture is valuable because it provides a quick screen. cross patterns of weakness/lengtheni n g and shortness. A number of tests can be used to assess muscle i mbalance: postural i n spection, box continues

2 M u scles 37 M uscle i n h i bition/weakness/lengthening . Transversus abdominis Serratus anterior Observable sign Lower trapezius Protru d i ng umbi licus Deep neck flexors Winged scapula Gluteus medius Elevated shoulder gi rd le ('gothic' shoulders) Gluteus maximus Chin 'poking' Un level pelvis o n one-legged standing Sagging buttock Inner range endurance tests • Gluteus maximus: Patient is prone. Practitioner lifts one leg i n to 'I nner holding isometric endura nce' tests can be performed for extension at the hip (knee flexed to 90') and the patient is asked muscles that have a tendency to lengthen, in order to assess their to hold this position. ability to maintain joint alignment in a neutral zone. Usually a lengthened muscle will demonstrate a loss of endura nce, when • Posterior fibers ofgluteus medius: Patient is sidelying with lower tested in a shortened position. This ca n be tested by the practitioner leg straight and uppermost leg flexed at hip and knee so that the passively prepositioning the muscle in a shortened position and m edial aspect of both the knee and foot are resting on the assessing the d u ration of time that the patient can hold the muscle floor/surface. Practitioner places the flexed leg into a position of in this position. There a re various methods used, including 10 maximal unforced externa l rotation at the hip, so that sole of repetitions of the holding position for 10 seconds at a time. foot is in contact with the floor su rface, and the patient is asked Alternatively, a single 30-second hold can be requested. If the to maintain this position. patient ca nnot hold the position actively from the moment of passive prepositioning, this is a sign of ina ppropriate antagon ist Norris states: muscle shortening. Optimal endurance is indicated when the full inner range position can Norris (1 999) describes an exa mple of inner range holding tests. be held for 10 to 20 seconds. Muscle lengthening is present if the limb • Iliopsoas: Patient is seated. Practitioner lifts one leg i nto greater hip flexion so that foot is well clear of floor and the patient is falls away from the inner range position immediately. asked to hold this position. Movement can only take place normally if there is coor­ even within the same muscle, changes dependent upon the dination of all the interacting muscular elements. With desired effect. many habitual complex movements, such as how to rise from a sitting position, a great number of involuntary, The ways in which skeletal muscles produce or deny largely unconscious reflex activities are involved. In many movement in the body, or in part of it, can be classified as: cases, patterns of dysfunction, including muscle substitu­ tion and changes in firing sequence, develop and often add • postural, where stability is induced. If this relates to undesirable consequences. Altering such patterns has to standing still, it is worth noting that the maintenance of involve a relearning or repatterning process (see Chapters 4 the body's center of gravity over its base of support and 5). requires constant fine tuning of a multitude of muscles, with continuous tiny shifts back and forth and from side The most important action of an antagonist occurs at the to side outset of a movement, where its function is to facilita te a smooth, controlled initiation of movement by the agonist • ballistic, in which the momentum of an action carries on and its synergists, those muscles that share in and support beyond the activation produced by muscular activity the movement. When agonist and antagonist muscles con­ (the act of throwing, for example) tract simultaneously they act in a stabilizing fixator role, which results in virtually no movement. • tension movement, where fine control requires constant muscular activity (playing a musical instrument, such as Sometimes a muscle has the ability to have one part act­ the violin, for example, or giving a massage). ing as an antagonist to other parts of the same muscle, a phenomenon seen in the deltoid, where its anterior fibers MUSCLE SPASM, TENSION, ATROPHY are antagonistic to its posterior fibers during internal and (Liebenson 1996, Walsh 1 992) external rotation of the humerus. Interestingly, these same fibers become synergists in the movement of lateral abduc­ Muscles are often said to be short, tight, tense or in spasm; tion of the humerus. Hence the role that various fibers play, however, these terms are often used very loosely.

38 C L I N I C A L A P P LI CATI O N O F N E U R O M U S C U LA R TEC H N I Q U E S : T H E U P PER B O DY Muscles experience either neuromuscular, viscoelastic or • Muscle fibers housing trigger points have been shown to connective tissue alterations or combinations of these. A have different levels of EMG activity within the same tight muscle could have either increased neuromuscular functional muscle unit. tension or connective tissue modification (for example, fibrosis) that results in it palpating as tight. • Hyperexcitability, as shown by EMG readings, has been demonstrated in the nidus of the trigger point, which is It is worthwhile differentiating between three commonly situated in a taut band (that shows no increased EMG used terms: contraction, spasm and contracture. With activity) and has a characteristic pattern of reproducible regards to skeletal muscles, each of these produces a short­ referred pain (Hubbard & Berkoff 1993, Simons et aI 1999). ening or increase in tension of a muscle. However, they are unique in many ways. • When pressure is applied to an active trigger point, EMG activity is found to increase in the muscles to which sen­ CONTRACTION (TENSION WITH EMG E LEVATION , sations are being referred ('target area') (Simons 1994). VOLUN TARY) • A contracture differs from a contraction in that it is invol­ untary and that activation of the myofibrils is prolonged • Muscle tension, usually with shortening, that denotes the in the absence of ac tion potential activity (MacIntosh et al normal function of a muscle. 2006, Simons et aI 1999). • Electromyographic (EMG) activity is increased in these • These types of 'physiologic' contractures are differenti­ cases. a ted from the 'pathologic' contractures associated with permanent shortening of muscles produced by excessive • Contraction is voluntary, not obligatory, i.e. one can vol­ growth of fibrous tissue, such as seen in Duchenne mus­ untarily relax a contraction if desired. cular dystrophy (MacIntosh et aI 2006). • While contraction usually produces movement of the INCREASED STR E TCH SENSITIVITY joint(s) on which the muscle acts, it can also contract to produce stability in a moving joint, as a result of anxiety • Increased sensitivity to stretch can lead to increased mus­ or for postural purposes. cle tension. SPASM (TENSION WITH E MG ELEVATION, • This can occur under conditions of local ischemia, which have also been demonstrated in the nidus of trigger INVOLUN TARY) points, as part of the 'energy crisis' \"vhich, it is hypothe­ sized, produces them (Mense 1993, Mense et al 2001, • Muscle spasm is a neuromuscular phenomenon relating Simons 1994) (see Chapter 6) . either to an upper motor neuron disease or an acute reac­ tion to pain or tissue injury. • Many free nerve endings in group III (smallest myeli­ nated) and IV (non-myelinated) afferent fibers are sensi­ • Electromyographic (EMG) activity is increased in these tive to pressure or stretch (MacIntosh et al 2006) and cases. would likely be affected by the degree of ischemia within the muscle. • Spasm is involuntary, i.e. one cannot voluntarily relax a spasm. • These same afferents also become sensitized in response to a build-up of metabolites (MacIntosh et al 2006) when • Examples include spinal cord injury, reflex spasm (such as sustained mild contractions occur, such as occurs in pro­ in a case of appendicitis) or acute Iwnbar antalgia with longed slumped sitting (Johansson 1991). loss of flexion relaxation response (Triano & Schultz 1987). • Mense (1993) and Mense et al (2001) suggest that a range • Long-lasting noxious (pain) stimulation has been shown of dysfunctional events emerge from the production of to activate the flexion withdrawal reflex (Dahl et aI 1992). local ischemia that can occur as a result of venous con­ gestion, local contracture and tonic activation of muscles • Using electromyographic evidence Simons (1994) has by descending motor pathways. shown that myofascial trigger points can 'cause reflex spasm and reflex inhibition in other muscles, and can • Sensitization (which, in all but name, is the same phenom­ cause motor incoordination in the muscle with the trig­ enon as facilitation, as discussed more fully in Chapter 6) ger point'. involves a change in the stimulus-response profile of neu­ rons (Mense et aI 2001), leading to a decreased threshold as CONTRACTUR E (TENSION OF MUSCLES well as increased spontaneous activity of types III and IV primary afferents. WITHOUT EMG E LE VATION , INVOLUN TARY) • Schiable & Grubb (1993) have implicated reflex dis­ • Increased muscle tension can occur without a consis­ charges from (dysfunctional) joints in the production of tently elevated EMG. such neuromuscular tension. Liebenson (2006) notes that 'joint inflammation or pathology initiates a complex neu­ • Contracture is involuntary, i.e. one cannot voluntarily romuscular response in the dorsal horn of the spinal cord, relax a contracture. resulting in flexor facilitation and extensor inhibition'. • An example is trigger points, in which muscle fibers fail to relax properly.

2 Muscles 39 • According to Janda (199 1 ), and agreed to by Liebenson • Type I (postural or aerobic) fibers hypertrophy on the (2006), neuromuscular tension can also be increased by symptomatic side and type II (phasic or anaerobic) fibers central influences due to limbic dysfunction. atrophy bilaterally in chronic back pain patients (Fitzmaurice et aI 1992). VISCOELASTI C INFLU ENCE WHAT IS WEA KNESS? • Muscle stiffness is a viscoelastic phenomenon that has to do with fluid mechanics and viscosity (so-called sol or True muscle weakness is a result of lower motor neuron dis­ gel) of tissue (Liebenson 2006, Walsh 1992), which is ease (e.g. nerve root compression or myofascial entrap­ explained more fully in Chapter 1 . ment) or disuse atrophy. In chronic back pain patients, generalized atrophy has been demonstra ted. This atrophy • Fibrosis occurs gradually in muscle or fascia and is typi­ is selective in the type II (phasic) muscle fibers bila terally. cally related to post trauma adhesion formation (see notes on fibrotic change in Chapter 1, p. 16) . Muscle weakness is another term tha t is used loosely. A muscle may simply be inhibited, meaning that it has not • Fibroblasts proliferate i n inj ured tissue during the suffered disuse atrophy but is weak due to a reflex phe­ inflammatory phase (Lehto et aI 1986). nomenon. Inhibited muscles are capable of spontaneous strengthening when the inhibitory reflex is identified and • If the inflammatory phase is prolonged then a connective remedied (commonly achieved through soft tissue or joint tissue scar will form as the fibrosis is not absorbed. manipulation). A typical example is reflex inhibition from an antagonist muscle due to Sherrington's law of reciprocal .AT RO PHY AND CHRONIC BACK PAIN inhibition, which declares that a muscle will be inhibited when its antagonist contracts. • In chronic back pain patients, generalized atrophy has been observed and to a greater extent on the symp to­ • Reflex inhibition of the vastus medialis oblique (VMO) matic side (Stokes et aI 1992). muscle after knee inflammation/injury has been repeat­ edly demonstrated (DeAndrade et al 1965, Spencer et al Box 2.4 Muscle strength testing 1984). For efficient m uscle strength testing it is necessa ry to ensure • Hides et al (1994) found unilateral, segmental wasting of that: the multifidus in acute back pain patients. This occurred rapidly and thus was not considered to be disuse atrophy. • the patient builds force slowly after engaging the barrier of resista nce offered by the practitioner • In 1994, Hallgren et al found tha t some individuals with chronic neck pain exhibited fatty degeneration and atro­ • the patient uses maximum control led effort to move in the phy of the rectus capitis posterior major and minor muscles prescribed direction as visualized by MR!. Atrophy of these small suboccipital muscles oblitera tes their important proprioceptive output, • the practitioner ensures that the point of m uscle origin is effi­ which may destabilize postural balance (McPartland et al ciently stabilized 1997) (see Chapter 3 for more detail on these muscles). • care is taken to avoid use by the patient of 'tricks' in which Various pathological situa tions have been listed that can synergists are recruited. affect either the flexibility or the strength of muscles. The result is muscular imbalance involving increased tension or • Muscle strength is most usua l ly graded as follows. tigh tness in postural muscles, coincidental with inhibition • G rade 5 is normal, demonstrating a complete ( 1 00%) ra nge of or weakness of phasic muscles. movement against gravi ty, with firm resistance offered by the TRICK PATTERNS practitioner. • Grade 4 is 75% efficiency in achieving ra nge of motion against g ravity with slight resistance. • Grade 3 is 50% efficiency in achievi ng ra nge of motion against gravity without resistance. • Grade 2 is 25% efficiency in achieving range of motion with gravity eliminated. • Grade 1 shows slight contractility without joint motion. • G rade 0 shows no evidence of contractility. Box 2.5 Two-joint muscle testing Al tered muscular movement pa tterns were first recognized clinically by Janda (1982) when it was noticed that classic As a rule when testing a two-joint muscle good fixation is muscle-testing methods did not differentiate between nor­ essentia l. The same applies to a l l m uscles in children and in mal recruitment of muscles and 'trick' patterns of substitu­ adults whose cooperation is poor and whose movements a re tion during an action. So-called trick movements (see u ncoord inated and weak. The better the extremity is stead ied, the below) are uneconomical and place unusual strain on joints. less the stabilizers are activated and the better and more They involve muscles that function in uncoordinated ways accu rate are the results of the muscle function test. (Janda and are related to both altered motor control and poor 1 983b) endurance.

40 C L I N I CA L A P P L I CATI O N OF N EU R O M U S C U LA R TEC H N I Q U E S : T H E U P P E R B O DY In a traditional test of prone hip extension it is difficult to This was in contrast to subjects without low back pain identify overactivity of the lumbar erector spinae or ham­ who showed that contraction of transversus abdominis strings as substitutes for an inhibited gluteus maximus. precedes contraction of the muscles involved in limb Tests developed by Janda are far more sensitive and allow movement (Hodges & Richardson 1996). us to iden tify muscle imbalances, faulty (trick) movement • The upper and deep cervical flexor muscles (type II, pha­ patterns and joint overstrain by observing or palpating sic) have been shown to lose their endurance capacity in abnormal substitution during muscle-testing protocols. For subjects with neck pain and headache (Watson & Trott example, in a prone position, hip extension should be initi­ 1993). ated by gluteus maxim us. If the hamstrings undertake the • When testing for activity in these deep flexor muscles, it role of prime mover and gluteus maximus is inhibited, this has been found that patients w i th neck pain tend to sub­ is easily noted by palpating activity wi thin each of them as stitute with the superficial flexor muscles (sternocleido­ movement is initiated. mastoid and scalenes) to achieve the desired position of the neck (Ju1l 2000). Similar imbalances can be palpated and observed in the • The posterior suboccipital muscles, which control the shoulder region where the upper fixators dominate the position of the head, have been shown to atrophy in lower fixa tors by inhibiting them, which results in major patients with chronic neck pain (McPartland et al 1997). neck and shoulder stress. These patterns have major reper­ The synergistic function of these muscles may be lost so cussions, as will become clear when crossed syndromes, that other muscles, such as upper trapezius and levator and Janda's functional assessment methods, are outlined in scapulae, substitute for the suboccipital muscles during Chapter 5 (Janda 1978). functional movements. This is confirmed by studies that have reported increased activity in these muscles in As Sterling et al (2001) explain: people with neck pain (Bansevicius & Sjaastad 1996) . Musculoskeletal pain potentially produces many changes in These examples offer insights into the adaptive capacity of motor activity. Some of these changes can be explained by the musculoskeletal system when faced with problems of peripheral mechanisms in the muscles themselves and by pain, overuse and disuse. There is clear evidence that some mechanisms within the central nervous system. Certainly, muscles respond by becoming inhibited and/or by losing pain has a potent effect on motor activity and control. stamina, while others shorten. The dysfunction that occurs in the neuromuscular sys­ JOINT IM PLICATIONS tem in the presence of pain is extremely complex. In addition to the more obvious changes, such as increased muscle activ­ When a movement pattern is altered, the activation ity in some muscle groups, and inhibition of others, more sequence, or firing order of different muscles involved in a subtle anomalous patterns of neuromuscular activation specific movement, is disturbed. The prime mover may be seem to occur . . . Loss of selective activation and inhibition slow to activate while synergists or stabilizers substitute of certain muscles that perform key synergistic functions, and become overactive. When this is the case, new joint leading to altered patterns of neuromuscular activation, and stresses will be encountered. Sometimes the timing the ensuing loss ofjoint stability and control, are initiated sequence is normal yet the overall range may be limited due with acute pain and tissue injury. However, these phenom­ to joint stiffness or antagonist muscle shortening. Pain may ena persist into the period of chronicity and could be one well be a feature of such dysfunctional patterns. reasonfor ongoing symptoms. WHEN SHOUL D PAIN AND DYSFUNCTION Exa mples BE LEFT ALONE? • Pain may lead to inhibition or delayed activation of spe­ Splinting (spasm) can occur as a defensive, protective, cific muscles or muscle groups involved in key synergis­ involuntary phenomenon associated with trauma (fracture) tic functions. This seems to most commonly occur in the or pathology (osteoporosis, secondary bone tumors, neuro­ deep local muscles that perform a synergistic function to genic influences, etc.). Splinting-type spasm commonly dif­ control joint stability (Cholewicki et aI 1997). fers from more common forms of contraction and hypertonicity because it often releases when the tissues that • EMG has been used to detect selective fatigue of lumbar it is protecting, or immobilizing, are placed at rest. multifidus, as opposed to other erector spinae muscles (Roy et aI 1989). When splinting remains long term, secondary problems may arise in associated joints (e.g. contractures) and bone • U1trasonography was used by Hides et al (1994) to identify (e.g. osteoporosis) . Travell & Simons (1983) note that, a marked atrophy of lumbar multifidus ipsilateral to the 'Muscle-splinting pain is usually part of a complex process. patients' symptoms. These changes remained even after Hemiplegic and brain-injured patients do identify pain that the patients had ceased to report pain (Hides et aI 1996). • A delay of contraction of transversus abdominis was noted in subjects with low back pain when they per­ formed limb movements (Hodges & Richardson 1999) .

2 M uscles 41 depends on muscle spasm'. They also note 'a degree of mas­ it is tight and consider that, in some circums tances, it is seteric spasm which may develop to relieve strain in trigger points in its parallel muscle, the temporalis'. offering beneficial support to the 51} or that it is reducing Travell & Simons (1983) note a similar phenomenon in low back stress (Simons 2002, Thompson 2001). It is possible the lower back: to conceive similar supportive responses in a variety of set­ tings, including the shoulder joint when lower scapular fix­ In patients with low back pain and with tenderness to pal­ a tors have weakened, thus throwing the load onto other pation ofthe paraspinal muscles, the superficial layer tended muscles (see discussion of upper crossed syndrome in to show less than a normal amount of EMC activity until Chap ter 5). the test movement became painful. Then these muscles showed increased motor unit activity or 'splinting' . . . This SOMATIZATION - MIND AND MUSCLES observation fits the concept ofnormal muscles 'taking over' (protective spasm) to unload and protect a parallel muscle It is entirely possible for musculoskeletal symptoms to that is the site ofsignificant trigger point activity. represent an unconscious attempt by the patient to entomb their emotional distress. As most cogently expressed by Recognition of this degree of spasm in soft tissues is a mat­ Philip Latey (1996), pain and dysfunction may have psy­ ter of training and intuition. Whether attempts should be chological distress as their root cause. The patient may be made to release, or relieve, what appears to be protective somatizing the distress and presenting with apparently spasm depends on understanding the reasons for its exis­ somatic problems (see Chapter 4). tence. If splinting is the result of a cooperative a ttempt to unload a painful but not pathologically compromised struc­ BUT HOW IS ONE TO KNOW? ture, in an injured knee or shoulder for example, then treat­ ment is obviously appropriate to ease the cause of the Karel Lewit (1992) suggests that, 'In doubtful cases, the original need to protect and support. If, on the other hand, physical and psychological components will be distin­ spasm or splinting is indeed protecting the structure it sur­ guished during the treatment, when repeated comparison rounds (or supports) from movement and further (possibly) of (changing) physical signs and the patient's own assess­ serious damage, as in a case of advanced osteoporosis for ment of them will provide objective criteria'. In the main, he example, then it should clearly be left alone. suggests, if the patient is able to give a fairly p recise description and localization of his pain, we should be reluc­ BENEFICIALLY OVERACTIVE MUSC L E S tant to regard it as 'merely psychological'. Van Wingerden et al (1997) report that both intrinsic and In masked depression, Lewit suggests, the reported symptoms may well be of vertebral pain, particularly extrinsic support for the sacroiliac joint (51]) derives, in part, involving the cervical region, with associated muscle ten­ sion and 'cramped' posture. As well as being alerted by from hamstring (biceps femoris) status. Intrinsically, the abnormal responses during the course of treatment to the fact that there may be something other than biomechanical influence is via the close anatomic and physiological rela­ causes of the problem, the history should provide clues. If the masked depression is treated appropriately, the verte­ tionship between biceps femoris and the sacrotuberous lig­ brogenic pain will clear up rapidly, he states. ament (they frequently attach via a strong tendinous link). In particular, Lewit notes, 'The most important symp tom is disturbed sleep. Characteristically, the patient falls asleep They state: 'Force from the biceps femoris muscle can lead normally but wakes within a few hours and cannot get back to sleep'. Pain and dysfunction can be masking major psy­ to increased tension of the sacrotuberous ligament in vari­ chological distress and awareness of it, how and when to cross-refer should be part of the responsible practitioner's ous ways. Since increased tension of the sacrotuberous liga­ skills base. ment diminishes the range of sacroiliac joint tmheotSiIo}n, ,(Vthane Muscles cannot be separated, in reality or intellectually, biceps femoris can play a role in stabilization of from the fascia that envelops and supports them. Whenever it appears we have done so in this book, it is meant to high­ Wingerden et al 1997; see also Vleeming 1 989). light and reinforce particular characteristics of each. When it comes to clinical applications, these structures have to be Van Wingerden et al (1997) also note that in low back considered as integrated units. As muscular dysfunction is being modified and corrected it is almost impossible to con­ pain patients forward flexion is often painful as the load on ceive that fascial structures are not also being remodeled. Some of the quite amazingly varied functions of fascia are the spine increases. This happens whether flexion occurs in the spine or via the hip joints (tilting of the pelvis). If the hamstrings are tight and short, they effectively prevent pelvic tilting. 'In this respect, an increase in hamstring ten­ sion might well be part of a defensive arthrokinematic reflex mechanism of the body to diminish spinal load.' If such a state of affairs is long standing, the hamstrings (biceps femoris) will shorten (see discussion of the effects of stress on postural muscles, p. 25), possibly influencing sacroiliac and lumbar spine dysfunction. The decision to treat a tight hamstring should therefore take account of why

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44 CLI N I CA L A P PL I CATI O N O F N E U R O M U S C U LAR TEC H N I Q U E S : T H E U P P ER B O DY Walsh E G 1992 Muscles, masses and motion. The physiology of Wittlinger H, Wittlinger G 1982 Textbook of Dr. Vodder's manual normality, hypotonicity, spasticity, and rigidity. MacKeith Press, lymph drainage, vol l: basic course, 3rd edn. Karl F Haug, Blackwell Scientific, Oxford Heidelberg Watson 0, Trott P 1993 Cervical headache: an investigation of natu­ Woo S L-Y 1987 Injury and repair of musculoskeletal soft tissues. ral head posture and upper cervical flexor muscle performance. American Academy of Orthopedic Surgeons Symposium, Cephalalgia 13:272-284 Savannah, GA Winters J, Crago P (eds) 2000 Biomechanics and neural control of posture and movement. Springer, New York

45 Chapter 3 Reporting stations and the brain CHAPTER CONTENTS Irwin Korr (1970), osteopathy's premier researcher into the Proprioception 45 physiology of the musculoskeletal system, has described it Fascia and proprioception 46 as 'the primary machinery of life'. Reflex mechanisms 47 The musculoskeletal system (not our digestive or our Local reflexes 50 immune system) is the largest energy consumer in the body. Central influences 50 It allows us to perform tasks, play games and musical instru­ ments, make love, give treatment, paint and, in a multitude Neuro muscular dysfunction following injury 51 of other ways, engage in life. Korr stated that the parts of the Mechanisms that alter proprioception 52 body act together 'to transmit and modify force and motion An example of proprioceptive dysfunction 52 through which man acts out his life'. This coordinated inte­ gration takes place under the control of the central nervous Rectus capitis posterior minor (RCPMin) research system as it responds to a huge amount of sensory input evidence 52 from both the internal and the external environment. Neural influences 53 Our journey through the structures that make up these Effect of contradictory proprioceptive information 53 communication pathways includes an overview of the Neural overload, entrapment and crosstalk 57 ways in which information, most notably from the soft tis­ Manipulating the reporting stations 58 sues, reaches the higher centers. The neural reporting sta­ tions represent 'the first line of contact between the Therapeutic rehabilitation using reflex systems 59 Conclusion 60 environment and the human system' (Boucher 1996). PROPR I O CEPTIO N Information that is fed into the central control systems of the body relating to the external environment flows from extero­ ceptors (mainly involving data relating to things we see, hear and smell). A wide variety of internal reporting stations also transmit data on everything from the tone of muscles to the pOSition and movement of every part of the body. The vol­ ume of information entering the central nervous system for processing almost defies comprehension and it is little won­ der that, at times, the mechanisms providing the information, or the way it is transmitted, or received, or the way it is processed and responded to, become dysfunctional. Proprioception can be described as the process of deliv­ ering information to the central nervous system as to the position and motion of the body relative to other neighbor­ ing parts of the body. In contrast to six exteroception human senses that advise us of the outside world (sight, smell,

46 CLI N I CA L A PPLICA TI O N O F N EU R O MU S C U LAR TEC HN IQUES: THE U PPER B O DY taste, hearing, touch and balance), proprioception provides Butler and Moseley (2003) seek to clarify the concept of information solely on the status of the internal body. The nociceptors (pain sensors) when they say: information is derived from neural reporting stations (affer­ ent receptors) in the muscles, the skin, other soft tissues and We don't actually have 'pain receptors', or 'pain pathways' joints, independent of vision, and is combined with input or 'pain centers'. However, there are some neurons that from the vestibular apparatus. The term 'proprioception' respond to all manner of stimuli, if those stimuli are suffi­ was first used by Sherrington in 1907 to describe the sense cient to be dangerous to the tissue. Activation of these spe­ of position, posture and movement. Janda (1996) states that cial neurons sends a prioritized alarm signal to [the] spinal it is now used ('not quite correctly') in a broader way, 'to cord, which may send it towards the brain. describe the function of the entire afferent system'. Whether a message sent by a nociceptor is actually per­ Schafer (1987) describes proprioception as 'kinesthetic ceived as pain depends on many factors, perhaps the most awareness' relating to 'body posture, position, movement, important being the interpretation given to the message by weight, pressure, tension, changes in equilibrium, resistance the brain. This is discussed further in Chapter 7 where we of external objects, and associated stereotyped response pat­ examine the phenomenon of pain. tems'. In addition to the unconscious data being transmitted from the proprioceptors, Schafer lists the sensory receptors as: Lewit has shown that altered function can produce increased pain perception, and that this is a far more com­ • Mechanoreceptors, which detect deformation of adjacent mon occurrence than pain resulting from direct compres­ tissues. These are excited by mechanical pressures or dis­ sion of neural structures, such as that which produces tortions and so would respond to touch or to muscular radicular pain when the sciatic nerve is compressed. movement. Mechanoreceptors can become sensitized fol­ lowing what is termed a 'nociceptive barrage' so that they Lewit (1985) suggests that there is seldom a need to explain start to behave as though they are pain receptors. This pain by actual mechanicalirritation of nervous structures, as in would lead to pain being sensed (reported) centrally in the root-compression model. It would be a peculiar conception response to what would normally have been reported as of the nervous system (a system dealing with information) movement or touch (Schaible & Grubb 1993, Willis 1993). that would have it reacting, as a rule, not to stimulation of its receptors but to mechanical damage to its own structures. • chemoreceptors, which report on obvious information such as taste (gustation) and smell (olfaction), as well as Lewit offers as examples of the reflex nature of much pain local biochemical changes such as CO2 and O2 levels. perception: referred pain from deeper structures (organs or Taste buds and olfactory epithelium, rich with receptor ligaments) which produce radiating pain, altered skin sensi­ cells, allow distinction among a wide range of chemical tivity (hyperalgesia) and sometimes muscle spasm. These stimuli. Information obtained is transmitted to the limbic reflex referrals are discussed later in this chapter in the con­ system, a portion of the brain that can respond to emo­ text of somatosomatic and viscerosomatic reflexes. Even true tion and thought (Butler & Moseley 2003). radicular pain (for example, resulting from disc prolapse) usually involves stimulation of nociceptors that are present • thermoreceptors, which detect modifications in tempera­ in profusion in the dural sheaths and the dura rather than ture, such as when something hot or cold is applied to the direct compression that would produce paresis and anesthe­ skin, as well as changes in the immediate climate. These sia (loss of motor power and numbness) but not pain. are also used in palpation of tissue temperature varia­ tions and are most dense on the hands and forearms (and Pain derives from irritation of pain receptors, and where the tongue). this results from functional changes (such as inappropriate degrees of maintained tension in muscles), Lewit suggests • electromagnetic receptors, which respond to light entering the most appropriate descriptive term would be 'functional the retina. pathology of the motor system'. • nociceptors, which register pain. The word nociception FASCIA AND PROPRIOCEPTION actually means 'danger reception'. These receptors can become sensitized when chronically stimulated, leading Bonica (1990) suggests that fascia is critically involved in to a drop in their threshold (see notes on facilitation, proprioception and that, after joint and muscle spindle Chapter 6, p. 105). This is thought by some to be a process input is taken into account, the majority of remaining pro­ associated with trigger point evolution (Korr 1976). prioception occurs in fascial sheaths (Earl 1965, Wilson 1966). Staubesand (1996) confirms this and has demon­ • polymodal receptor (PMR), a type of nociceptor responsive strated that myelinated sensory neural structures exist in to mechanical (e.g. acup uncture), thermal (moxibustion) fascia, relating to both proprioception and pain reception. and chemical stimuli. Its sensory terminals are free nerve endings and exist in various tissues throughout the body. The various neural reporting organs in the body provide a Research suggests that these pain receptors may play a constant source of information feedback to the central nerv­ significant part in the evolution of trigger points, and are ous system, and higher centers, as to the current state of also capable of being used to modify pain (Kawakita et al tone, tension, movement, etc. of the tissues housing them 2002). PMR is discussed further in Chapter 6. (Travell & Simons 1983, 1992, Wall & Melzack 1991). It is

3 Reporting stations and the brain 47 Box 3.1 Neurotrophic influences t\"vo-way traffic along neural pathways, is arguably at least as important as the passage of impulses with which we usually I rvin Korr (Korr 1 967, 1 986) spent half a century investigating the associate nerve function. scientific backg round to osteopathic methodology and theory. Some of his most im portant work related to the role of neu ral REFLEX MECHAN ISMS structures in the delivery of trophic substances. The various patterns of stress that are covered in the next chapter are As Schafer (1987) points out, 'The human body exhibits an capable of d rastically affecting this axoplasmic transportation. astonishingly complex array of neural circuitry'. Among these are receptors, reflex arcs and mechanisms that com­ Korr states: municate from outside the muscular system. These 'trophic' proteins are thought to exert long-term influences A receptor (proprioceptor, mechanoreceptor, etc.) resides on the cell surface or within the cytoplasm and is composed of on the developmental, morphologic, metabolic and functional structural protein molecules. It binds to a specific factor, such qualities of the tissues - even on their viability. Biomechanical as a neurotransmitter, by which it is stimulated as follows. abnormalities in the musculoskele tal system can cause trophic • An afferent impulse travels, via the central nervous system, to a part of the brain that we can call an integrative center. disturbances in ot least two ways: (7) by mechanical deformation • This integrative center evaluates the message and, with (compression, stretching, angUla tion, torsion) of the nerves, which influences from higher centers, sends an efferent response. impedes axonal transport; and (2) by sustained hyperactivity of • This travels to an effector unit, perhaps a motor endplate, and a response occurs. neurons in facilitated segments of the spinal cord [see discussion Additionally, the basic reflex arcs, which control much of of this phenomenon in Chap ter 6J which slows axonal transport the body's 'immediate reaction' responses, can be summa­ rized as follows (Sato 1992). and which, because of metabolic changes, may affect protein • A sensory receptor (or proprioceptor, mechanoreceptor, synthesis by the neurons. It appears that manipula tive treatment etc.) is stimulated. would alleviate such impairments of neurotrophic function. • An afferent impulse travels via a sensory neuron to the spinal cord. The manufactu ring process of macromolecules for transportation takes place in nerve cells, is packaged by the Golgi apparatus and • The sensory neuron synapses with an interneuron, which, transported along the neural axon to the target neurons (Ochs Et in turn, synapses with the motor neuron to send an effer­ Ranish 1 969). The speed of transportation along axons is ent response, without any intervention by the brain. sometimes remarkably swift at the rate of up to half a meter per day (although much slower than the 1 20 meters per second of • This travels to an effector unit, perhaps a motor endplate, actual neural transmission) (Ochs 1 975). and a response occurs (see Box 3.2). Once the macromolecu les reach their destination, where they Reflex mechanisms extend beyond the musculoskeletal sys­ influence the development and maintenance of the tissues being tem. It is possible to further characterize the reflex mecha­ supplied, a return transportation of materials for reprocessing nisms that operate as part of involuntary nervous system com mences. When there is interference in axonal flow (because function as follows. of com pression, etc.) the tissues not receivin g the trophic material degenerate and a build-up of axoplasm occu rs, forming • Somatosomatic reflexes, which may involve stimuli from a swelling (Schwartz 1 980). sensory receptors in the skin, subcutaneous tissue, fascia, Korr ( 1 98 1 ) has shown that w h en a m uscle is denervated by striated muscle, tendon, ligament or joints, producing injury and atrophies, it is the interruption of trophic substances reflex responses in segmentally related somatic struc­ which causes this rather than loss of neural impulses (see tures - for example, from one such site on the body to notes on rectus capitis posterior minor denervation following another segmentally related site on the body. Such whiplash, p. 294). reflexes are commonly triggered by manual therapy tech­ niques (during application of compression, vibration, Research has shown that when the neural supply to a postural massage, manipulation, application of heat or cold, etc.). (predominantly red fiber) m uscle is su rgically altered, so that it receives neurotrophic material originally destined for a phasic • Somatovisceral reflexes, which involve a localized somatic (white fiber) muscle, there is a transformation in which the postural muscle can become a phasic m u scle (and vice versa) stimulation (from cutaneous, subcutaneous or muscu­ based on the trophic material it receives. This suggests that loskeletal sites) producing a reflex response in a segmen­ genetic expression can be neurally mediated. The axoplasm tells tally related visceral structure (internal organ or gland) the muscle what its function is going to be (Guth 1 968). (Simons et aI1999). Such reflexes are also commonly trig­ gered by manual therapy techniques (during application important to realize that the traffic between the center and the of compression, vibration, massage, manipulation, appli­ periphery in this dynamic mechanism operates in both direc­ cation of heat or cold, etc.). tions along efferent (away from the CNS and brain) and affer­ ent (toward the CNS and brain) pathways. Any alteration in normal function at the periphery (such as a proprioceptive source of information) leads to adaptive mechanisms being initiated in the central nervous system, and vice versa (Freeman 1967). It is also important to reahze that it is not only neural impulses that are transmitted along nerve pathways, in both directions, but also a host of important trophic substances. This process of the transmission of trophic substances, in a

48 CLI N ICAL A PPLI CATIO N O F N EU RO M U S C U LA R TEC H N IQ U ES : TH E U PPER B O DY . .. @y. ... Lacrimal gland Eye Gray rami ... .. communicantes Parotid gland - . . .. . . . ,. . .. .C1 . . . ... . 1......... ... . ... .. . Submandibular gland . . . . . . .. . .... .. . Sublingual gland . Larynx ... ... Trachea . .. Bronchi Lungs --T1 Heart Innervation to arrector •-.::.�::.::::.:::.::.: :�: -o>;r-_- _-_::-G_ :;re: ;a-t;er th�oraC/.c $pl. . ..�. fI7 ����.. . ... Sl�'h pili muscles,vascular ..·.:.: :tb.. .··:.. ·U· .·· smooth musde and ---- ��..q-. \"�f]lc 9c.)\":;-I sweat glands of skin Iadder Gray ramus communicans Bile ducts While ramus communicans Pancreas � ....:....\"t�.::'�..:·).!/. ,S1-- .� . . .Aortiroreoal Kidneys . Intestines -.:.:�:. ===v, --.;;:=����---+- --<.,....�. � Descending colon Sigmoid colon �����. ; ... .. . -../, Rectum mesenlenc �:7.;': 9i \"dd\" S::: �.� �� --- Preganglionic fibres InlenerP9'\"�::,:'b...,� ..................... Posiganglionic fibres \": : :1UJ�:::hy nc Extemal genitalia plexus A F ig u re 3.1 A EtB : Co rd level of organ i n n ervation via (A ) sympathetic nervous system an d (B) parasympathetic nervous system. Drawn after N etter (2006). • Viscerosomatic reflexes, in which a localized visceral (inter­ the intensity of the visceral stimulus. Obvious examples of this include right shoulder pain in gallbladder disease and nal organ or gland) stimulus produces a reflex response in cardiac ischemia producing the typical angina distribution a segmentally related somatic structure (cutaneous, subcu­ of left arm and thoracic pain. Giamberardino (2005) notes taneous or musculoskeletal) (Fig. 3.1). It has been sug­ that visceral pain can affect the somatic tissues in the area gested that such reflexes, feeding into the superficial of referral for months or even years, and long after the vis­ structures of the body, can give rise to trigger points ceral problem has been resolved. and/or dysfunction in the somatic tissues (De Sterno 1977, Giamberardino 2005, Simons et al 1999). Balduc (1983) • Viscerocutaneous reflex, in which organ dysfunction stim­ reports that these reflexes are intensity oriented, which is to say that the degree of reflex response relates directly to uli produce superficial effects involving the skin (includ­ ing pain, tenderness, heightened sensitivity to heat,

3 R eporting stations and the brain 49 Medulla :: (::. . .� Lacrimal gland oblongala -'- . .. ::: ' / ... . . Eye . Parotid gland • Inferior Submandibular gland T1 -- • hypogastric Sublingual gland Larynx • Trachea • Bronchi • Lungs • Pulmonary plexus • • Heart • • Stomach • • Liver • Gallbladder L1 -- • Bile ducts • Pancreas • • Kidneys • Intestines 1S1 -_ • Descending colon Sigmoid colon S2 Rectum --- Preganglionic fibres S3 Urinary bladder ..................... Postganglionic fibres Prostate M�-�- External genitalia • Pelvic splanchnic nerves B Fig u re 3.1 (Continued) touch or pinprick, etc.). Examples of this include itch pat­ coronary heart disease plus gallbladder calculosis, for terns and heightened skin sensitivity associated with the instance, may experience more frequent attacks of angina and biliary colic than patients with a single condition, referral pattern of an organ. based upon the partially overlapping (T5) afferent path­ • Viscerovisceral reflex in which a stimulus in an internal organ ways from the heart and gallbladder. Women with both or gland produces a reflex response in another segmentally dysmenorrhea and irritable bowel syndrome (IBS) tend to complain of more intense menstrual pain, intestinal pain related internal organ or gland. Giamberardino (2005) and referred abdominal/pelvic hyperalgesia than do women with only one of these conditions. She suggests places particular importance on 'visceroviscero hyperalge­ that treatment of one visceral condition may improve sia, an augmentation of pain symptoms due to the sensory interaction between two different internal organs that share at least part of the afferent circuitry. Patients with

50 CLINICAL A PP LICATIO N OF N EU RO MU S C U LAR TEC H N IQ U ES : THE U PPER B O DY symptoms from another. It should be noted, however, that • Afferent messages are received centrally from somatic, such pathologies, layered one over the other, often present vestibular (ears) and visual sources, all reporting new a complex symptomatology and are difficult to diagnosis­ data and providing feedback for requested information. a clear cause for each symptom may never be proven. To compound the situation, prolonged visceral afferent bar­ • If all or any of this information is excessive, noxious or rage into the CNS may produce long-term sensitization inappropriately prolonged, sensitization (see notes on that results in hyperalgesia, trophic changes and somatic facilitation, Chapter 6, p. 108) can occur in aspects of the pain that is deceptive, and may delay appropriate treat­ central control mechanisms, which results in dysfunc­ ment, unless the viscera are fully considered. tional and inappropriate output (Mense et al 2001, Russell 2001). Whether such reflexes have bidirectional potential is debated. Some research suggests that a visceral problem • The limbic system of the brain can also become dysfunc­ can exhjbit in a specific dermatomal segment via a viscero­ tional and inappropriately process incoming data, leading cutaneous reflex (Giamberardino 2005) and that stimulation to complex problems, such as fibromyalgia (Goldstein of the skin could have a distinct effect on related visceral 1996) (see Box 3.4). areas via a cutaneovisceral reflex. • The entire suprasegmental motor system, including the Schafer (1987) makes the very important observation cortex, basal ganglia, cerebellum, etc., responds to the that, 'The difference between somatovisceral and visceroso­ afferent data input with efferent motor instructions to matic reflexes appears to be only quantitative and to be the body parts, with skeletal activity receiving its input accounted for by the lesser density of nociceptive receptors from alpha and gamma motor neurons, as well as the in the viscera'. This can best be understood by means of motor aspects of cranial nerves. Head's law, which states that when a painful stimulus is applied to a body part of low sensitivity (such as an organ) • As noted in Chapter 2, any alteration in pH, for example that is in close central connection (the same segmental sup­ when respiratory alkalosis follows overbreathing, modi­ ply) with an area of higher sensitivity (such as a part of the fies neural function, which can include speeding reflexes, soma), pain will be felt at the point of higher sensitivity reducing thresholds (such as pain) and allowing sensiti­ rather than where the stimulus was applied. zation to occur more easily (Chaitow et aI2002). LOCAL RE FLEXES Schafer (1987) sums up the process: A number of mechanisms exist in which reflexes are stimu­ Whether a person is awake or asleep, the brain is constantly lated by sensory impulses from a muscle leading to a bombarded by input from all skin and internal receptors. response being transmitted to the same muscle. Examples This barrage of incoming messages is examined, valued, and include the stretch reflexes, myotatic reflexes and the deep translated relative to a framework composed of instincts, tendon reflexes. experiences and psychic conditioning. In some yet to be dis­ covered manner, an appropriate decision is arrived at that is The stretch reflex is a protective mechanism in which a transmitted to all pertinent muscles necessary for the contraction is triggered when the annulospiral receptors in response desired. By means of varying synaptic facilitation a muscle spindle are rapidly elongated. Concurrently there and restraints within the appropriate circuits, an almost are inhibitory messages transmitted to the motor neurons of limitless variety of neural integrntion and signal transmis­ the antagonist muscles inducing reciprocal inhibition, with sion is possible. simultaneous facilitating impulses to the synergists. The sum of proprioceptive information results in specific If enough fibers are involved the threshold of the Golgi responses. tendon organs will be breached, leading to the muscle 'giv­ ing way'. This is a reflex process known as autogenic inhibi­ • Motor activity is refined and reflex corrections of move­ tion (Ng 1980). ment patterns occur almost instantly. CENTRAL INFLUENCES • A conscious awareness occurs of the position of the body and the part in space. Sensory information received by the central nervous system can be modulated and modified both by the influence of the • This body awareness in the brain relates to the presence mind and changes in blood chemistry, to which the sympa­ there of a 'virtual body', a homunculus ('little man'), a thetic nervous system is sensitive (see notes on carbon dioxide 'sensory map' of the brain, that is aware of the spatial influences on neural sensitivity, Chapter 4, p. 77). Whatever location of the parts, and that responds to messages of local biochemical influences may be operating, the ultimate distress (danger) that may be interpreted as pain (Butler overriding control on the response to any neural input & Moseley 2003). derives from the brain itself. • The more neurons a particular part of the body has to represent it in the brain, the more attention the message receives, with the hands, face, tongue and genitals being highly represented, compared, for example, with the rest of the head or the chest. This is discussed in more detail in Chapter 7, particularly in relation to phantom pain.

3 Reporting stations and the brai n 51 • Over time, lperaorpnreidocperpotcievseseisnfcoarnmbaetimonodaifnieddninewresmpoonvsee­ to altered ment patterns can be learned and stored. • It is this latter aspect, the possibility of learning new pat­ terns of use, that makes proprioceptive influence so important in rehabilitation. Fig u re 3.2 The h o m u nc u l u s represents the a m o u n t of cerebral N E U R OMUSCULAR DYSFU N CTIO N cortex designated to p rocess 'touch receptors'. Rep rod uced with permission from BrainCo n nection. FOLLOWI N G INJU RY (Ryan 1994) • Functional instability may result from altered proprio­ ception following trauma, e.g. the ankle 'gives way' (functional instability) during walking when no appar­ ent structural reason exists (Lederman 1997). • Proprioceptive loss following injury has been demon­ strated in spine, knee, ankle and TMJ (following trauma, surgery, etc.) (Spencer 1984). • These changes contribute to progressive degenerative joint disease and muscular atrophy (Fitzmaurice 1992). • The motor system will have lost feedback information for refinement of movement, leading to abnormal mechanical stresses of muscles/joints. Such effects of proprioceptive deficit may not be evident for many months after trauma. Box 3.2 Reporting stations -j.• . Some important structures involved in this i nternal information The pacinian corpuscle. This is fou n d in periarticu lar connective highway, which may under given circumstances be involved in the tissue and adapts rapidly. It triggers discharges, and then ceases production or maintenance of pain (LaMotte 1992), are listed below. reporting in a very short space of time. These messages occur successively, d u ring motion, and the CNS can, therefore, be aware of Ruffini end-organs. Fou n d within the joint capsu le, around the the rate of acceleration of movement taking place in the area. It is joints, so that each is responsible for describing what is happening sometimes called an acceleration receptor. over an angle of approximately 15' with a deg ree of overlap between it and the adjacent end-organ. These organs are not easily Skin receptors are responsive to touch, pressure and pain and are fatigued and are progressively recruited as the joint moves, so that involved in primitive responses such as withdrawal and g rasp movement is smooth and not jerky. The prime concern of Ruffini reflexes. end-organs is a steady position. They are also to some extent concerned with reporting the direction of movement. Cervical receptors, especially relative to the suboccipital m usculature (see notes on rectus capitis posterior minor, p. 292), Golgi end-organs. These, too, adapt slowly and continue to in teract with the labyrinthine (ear) receptors to maintain balance discharge over a lengthy period. They are fou nd in the ligaments and an appropriate positioning of the head in space. associated with the joint. Unlike the Ruffin i end-organs, which respond to muscular contraction that alters tension in the joint capsule, Golgi There are other end-organs, but those described above can be seen end-organs can deliver information independently of the state of to provide information on the present status, position, direction and muscular contraction. This helps the body to know just where the joint rate of movement of any muscle or joint and of the body as a whole. is at any given moment, irrespective of muscular activity. Muscle spindle. This receptor is sensitive and complex (Macintosh Slow-adapting joint receptors (above) have a powerful et al 2006). modu lating influence on reflex responses (for example, in the sacroiliac joint) and seem to have the ability to produce long-lasting • It detects, evaluates, reports and adjusts the length of the muscle influences, either in maintaining dysfunction or in helping in its in which it lies, setting its tone. resolution (if pressure/stress on them can be normalized). Direct joint manipulation (Lefebvre et al 1993) can have just such an effect or, as • Acting with the Golgi tendon organ, most of the information as Lewit has shown, so can normalization ofjoint function by less to m uscle tone and movement is reported. direct means. Lewit (1985) emphasizes this by saying : • Spindles lie paral lel to the m uscle fibers and are attached to The basic [soft tissue] techniques . . . are very gentle and are also very either skeletal m uscle or the tendinous portion of the m uscle. effective for mobilization, using muscular facilitation and inhibition, i.e. the inherent forces of the patient. It is most unfortunate that in • Inside the spind le are fibers that may be one of two types. One is the minds of most people, physicians and laymen alike, manipula tion described as a 'nuclear bag' fiber and the other as a chain fiber. is tantamount to thrusting techniques - techniques that should rather be the exception. • In different muscles, the ratio of these internal spindle fibers differs. • In the center of the spindle is a receptor called the annu lospiral receptor (or primary ending) and on each side of this lies a 'flower spray receptor' (secondary ending). • The primary ending discharges rapid ly and this occurs in response to even small changes in muscle length. box continues

52 C L I N ICAL A P P L I CAT I ON OF N EU R OM U SCULA R TEC H N I QUES: TH E UPPER B ODY Box 3.2 (continued) • The activities of the spindle appear to provide information as to length, velocity of contraction and changes in velocity (Gray's • The secondary ending compensates for this, because it fires Anatomy 2005). How long is the m uscle, how quickly is it changing messages only when l a rger changes in m uscle length have length and what is happening to this rate of change of length? occurred. Go/gi tendon receptors. These structures indicate how hard the • The spind le is a 'length comparator' (a lso called a 'stretch recep­ m uscle is working (whether contracting or stretching) since they tor') and it may discharge for long periods at a time. reflect the tension of the m uscle, rather than its length. If the tendon organ detects excessive overload it may cause cessation of • Within the spind l e there a re fine, intrafusal fibers which a lter the fu nction of the m uscle to prevent damage. This produces relaxation. sensitivity of the spind le. These can be a l tered without any actual change taking place in the length of the m uscl e itself, via a n independent gamma efferent supply to the intrafusal fibers. This has im plications in a variety of acute and ch ronic problems. MECHANISMS THAT ALTER PROPRIOCEPTION head translation, this space nearly vanishes (Penning 1989). (Lederman 1997) • Hack et al (1995) noted that a fascial bridge between the RCPMin and the dura is oriented perpendicularly, resist­ • Ischemic or inflammatory events at receptor sites may pro­ ing movement of the dura toward the spinal cord with duce diminished proprioceptive sensitivity due to the head translation. build-up of metabolic by-products that stimulate group III • The attachment of the ligamentum nuchae into the dura and IV, mainly pain afferents (this also occurs in muscle between the atlas and axis serves a complementary func­ fatigue). tion with the RCPMins (Mitchell et aI1998). • Through the ligamentum nuchae, other posterior mus­ • Physical trauma can directly affect receptor axons (artic­ cles may also be acting indirectly with the RCPMin to ular receptors, muscle spindles and their innervations). coordinate dural position with head movement. 1. In direct trauma to muscle, spindle damage can lead • EMG studies suggest RCPMin does not fire during exten­ to denervation (e.g. following whiplash) (Hallgren sion, but rather does so when the head translates for­ et aI1993). wards (Greenman 1997, personal communication). 2. Structural changes in parent tissue lead to atrophy • The high density of muscle spindles found in the RCPMs and loss of sensitivity in detecting movement, as well suggests the value of these muscles lie not in their motor as altered firing rate (e.g. during stretching). function but in their role as 'proprioceptive monitors' of the cervical spine and head. • Loss of muscle force (and possibly wasting) may result • Observations linking the suboccipital and cervical mus­ when a reduced afferent pattern leads to central reflexo­ cles with equilibrium are not new (Longet 1845). genic inhibition of motor neurons supplying the affected • In 1955, the importance of proprioceptors in this region muscle. was recognized and the term 'cervical vertigo' was coined (Ryan & Cope 1955). • Psychomotor influences (e.g. feeling of insecurity) can • Cervical proprioception currently is recognized as an alter patterns of muscle recruitment at local level and essential component in maintaining balance. This is par­ may result in disuse and muscle weakness. ticularly true in the elderly, in whom there is a shift in emphasis from vestibular reflexes to cervical reflexes in • The combination of muscular inhibition, joint restriction maintaining balance (Wyke 1985). and trigger point activity is, according to Liebenson (1996), 'the key peripheral component of the functional pathology of the motor system'. AN EXAMPLE OF PROPRIOCEPTIVE DYSFUNCTION In order to appreciate some of the profound influences that Proprioception and pain proprioceptive function offers and the devastating effect disturbance of this function can produce in terms of pos­ • Proprioceptive signals from these suboccipital mus­ tural stability and pain, a particular example is summarized cles may also serve as a 'gate' that blocks nocicep­ below involving rectus capitis posterior minor. tor (pain fiber) transmission into the spinal cord and higher centers of the central nervous system (Wall RECTUS CAPITIS POSTERIOR MINOR (RCPMin) 1989). RESEARCH EVIDENCE • According to the gate theory of pain, large-diameter • In head extension, the posterior atlas arch maintains a (A-beta) fibers from proprioceptors and mechanorecep­ mid-position between the occiput and the axis. In forward tors enter the spinal cord and synapse on interneurons in the dorsal horn of the spinal cord.

3 R eporting stations and th e brain 53 Occipital bone RCPMin ev�luation and treatment Dura • McPartland (1997) palpated individuals with RCPMin atrophy and found they had twice as many areas of cer­ Rectus capitis posterior minor muscle vical somatic dysfunctions as control subjects. '--r.:onnprli'vp tissues • Somatic dysfunctions were identified by tenderness of paraspinal muscles, asymmetry of joints, restriction in First cervicat vertebra ROM and tissue texture abnormalities. First cervical nerve root • Janda (1978) screened for proprioceptive dysfunction by testing standing balance with eyes closed. Bohannon et al Fig u re 3.3 Lateral view of the upper cervical joint complex. (1984) suggest that between the ages of 20 and 49 a main­ Redrawn with permission from the Journol ofMonipulative and tained balance time of between approximately 25 and 29 Physiological Therapeutics 1999; 22(8):534-539. seconds is normal. Between ages 49 and 59, 21 seconds is normal, while between 60 and 69 just over 10 seconds is • Interneurons inhibit nociceptor transmission, specifically acceptable. After 70 years of age 4 seconds is normal. nociceptors that synapse in lamina V of the dorsal Anything less than this is regarded as indicating degrees horn. of proprioceptive dysfunction. Patients with propriocep­ tive dysfunction are treated with 'sensory motor retrain­ • Chronic postural stress (slouching or 'chin poking') or ing' - balance retraining with the eyes closed. (See trauma may lead to hypertonic suboccipital muscles. Volume 2, Chapter 2 for more on balance retraining.) • Hallgren et al (1994) found that some individuals with • In Chapter 2 of this text there is a description of respiratory chronic neck pain exhibited fatty degeneration and atro­ alkalosis resulting from common overbreathing patterns. phy of the RCPMin and RCPMaj, as visualized by MRl. It is worth noting that a common feature of respiratory alkalosis is a disturbance in the individual's ability to • Atrophy of the RCPMin reduces its proprioceptive output maintain balance, suggesting that in any attempt to restore and this may destabilize poshual balance (McPartland normal balance, breathing retraining should form a part of 1997). the protocol (Balaban & Theyer 2001). • Subjects with chronic neck pain (and RCPMin atrophy as N E U RAL I N FLUEN CES seen by MRl) showed a decrease in standing balance when compared to control subjects. EFFECT OF CONTRAD ICTORY PROPRIOCEPTIVE II\\IFORMATIOI\\I • Reduced proprioceptive input facilitates the transmis­ sion of impulses from a wide dynamic range of nocicep­ Korr (1976) reminds us: tors, which can develop into a chronic pain syndrome. The spinal cord is the keyboard on which the brain plays • When muscle pain increases in intensity referral of the when it calls for activity or for change in activity. But each pain sensation to remote sites occurs, such as to other 'key' in the console sounds, not an individual 'tone', such as muscles, fascia, tendons, joints and ligaments (Mense & the contraction of a particular group of muscle fibers, but a Skeppar 1991). whole 'melody' of activity, even a 'symphony' of motion, In other words, built into the cord is a large repertoire of pat­ • Noxious stimulation of the rectus capitus posterior terns of activity, each involving the complex, harmonious, muscles causes reflex EMG activity in distal muscles, delicately balanced orchestration of the contractions and including the trapezius and the masseter muscles (Hu relaxations of many muscles. The brain 'thinks' in terms of et aI1993). Hu and colleagues (1995) showed that irrita­ whole motions, not individual muscles. It calls selectively, tion of the dural vasculature in the upper cervical spine for the preprogrammed patterns in the cord and brain stem, leads to reflexive EMG activity of the neck and jaw modifying them in countless ways and combining them in muscles. an infinite variety of still more complex patterns. Each activity is also subject to further modulation, refinement, • Injury or dysfunction of the RCPMin may irritate the C1 and adjustment by the afferent feedback continually stream­ nerve, which, if chronic, may lead to facilitation of sym­ ing infrom the participating muscles, tendons, and joints, pathetic fibers associated with Ct resulting in a chronic pain syndrome. This means that the pattern of information fed back to the CNS and brain reflects, at any given time, the steady state of joints, • Alternatively, chronic C1 irritation may refer pain to the the direction as well as speed of alteration in position of joints, neck and face, via C1's connections with C2 and cranial together with data on the length of muscle fibers, the degree of nerve V. load that is being borne and the tension this involves. It is a • Conclusion: RCPMin dysfunction (atrophy) leads to increased pain perception and reduced proprioceptive input, reflexively affecting, for example, other cervical and jaw muscles (Hack et aI1995).

54 C LI NICA L A PP LI C AT I O N OF N E U R O M U SC U LA R TECH N I Q U E S : T H E U P P E R B O DY Box 3.3 Co-contraction and strain A The work of Laurence Jones DO ( 1 995) in developing his treatment B method of strain and cou nterstrain (see Chapter 9) led him to research the mechanisms that might occur u nder conditions of acute t strain. His concept is based on the predictable physiological responses of m uscles in given situations. c BC A Jones describes how in a ba lanced state the proprioceptive functions of the va rious muscles su pporting a joint will be feeding a Brachialis flow of information derived from the neural receptors in those III! I J!JI!! 1 Triceps m uscles and their tendons. For exa mple, the Golgi tendon organs will I\":'t': '\" :\",1,\"\"':\":''':::':IIII!!II ! l! be reporting on tone, while the various receptors in the spind les wil l Fi g u re 3.4 A: Arm flexor (brach i al is) and extensor ( triceps brachii) b e firing a consta nt stream o f information (slowly or rapidly, in e asy normal rel ationsh i p i n dicated by rate of firing on the scale depending u pon the demands being placed on the tissues) regarding for each muscle. B: When sudden force is appl ied, the flexors are their resting length and any cha nges which mig ht be occurring in that length (Korr 1 947, 1 974, Mathews 1981). stretche d an d the extensors protect the joi n t by rapidly shortening. Jones (1964) first observed the phenomenon of spontaneous C: Stretch receptors i n the flexors continue to fi re as though release when he 'accidental ly' placed a patient who was in considerable pain and some degree of compensatory distortion into a stretch conti n u es. Firing of both flexors and extensors con ti n ues at position of comfort (ease) on a treatment table. Despite no other treatment being given, after just 20 minutes resting in a position of i n appropri ately h i g h rates, producing the effect noted in a strai ned relative ease the patient was able to stan d upright and was free of pain. The pain-free position of ease into which Jones had hel ped the joint where restriction exists w i th i n the join t's physiolog i cal range patient was one that exaggerated the deg ree of distortion in which his body was being held. He had taken the patient into the of motion. Reproduced w i th permission from Chaitow (2007). direction of ease (rather than toward tension or 'bind') since any attempt to correct or straighten the body wou ld have been some of which ensures that the relaxed flexor muscles remain even met by both resista nce and pain. In contrast, moving the body more relaxed due to inhibitory activity. further into distortion was acceptable and easy and seemed to al low operation of the physiological processes involved in resolution The central nervous system wou ld at this time have minimal of spasm. information as to the status of the relaxed flexors and, at the moment when the crisis demand for stabilization occurred, these The events that occur at the moment of strain provide the key to understa nding the mecha nisms of neurological ly induced positional box continues release. For exam ple, consider an a l l too common exa mple of someone bending forwa rd. At this time the tru nk flexors would be short of their resting length and their muscle spindles wou ld be firing slowly, indicating little or no activity and no change of length taking place. At the sa me time the spinal erector g roup wou ld be stretched, or stretching, and firing rapidly. Any stretch affecting a m uscle (and therefore its spindles) will increase the rate of reporting, which will reflexively induce further contraction (myotatic stretch reflex) and an increase in tone in that muscle. This prod uces a n insta nt reciprocal inhibition o f t h e function a l a ntagonists to it (flexors), reducing even further the a l ready limited deg ree of reporting from their muscle spindles. This feedback link with the central nervous system is the primary muscle spindle afferent response, modulated by an additional muscle spindle function, the gamma efferent system, which is controlled from higher (brain) centers. In simple terms, the gamma efferent system influences the primary afferent system, for example when a muscle is in a quiescent state. When it is relaxed and short with little information coming from the primary receptors, the gamma efferent system might fine-tune and increase ('turn up') the sensitivity of the primary afferents to ensure a continued information flow (Mathews 1 98 1 ). /! Crisis Now imagine an emergency situation in which im mediate demands for stabilization a re made on both sets of muscles (the short, relatively 'quiet' flexors and the stretched, relatively actively firing extensors) even though they a re in q uite different states of prepared ness for action. The flexors would be 'unloaded', relaxed and providing minimal feedback to the control centers, while the spinal exte�sors would be at stretch, providing a rapid outflow of spind le-derived information,

3 Reporting stations and the brain 55 Box 3.3 (tonti'W��:. function. One would be shorter and one longer than its normal resting length. shortened and relaxed flexors would be obliged to stretch quickly to a length which would balance the a l ready stretched extensors - At this time any attempt to extend the a rea/joint(s) would be which would be contracting rapidly to stabilize the a rea. strongly resisted by the tonically shortened flexor group. The individual wou l d be locked into a forward-bending distortion. i n this As this ha ppened the annulospiral receptors in the short (flexor) example. The joints involved would not have been taken beyond their muscles would respond to the sudden stretch demand by contracting normal physiological range and yet the normal range would be even more. as the stretch reflex was triggered. The neural reporting u navailable due to the shortened status of the flexor group (in this stations in these shortened muscles would be firing impulses as if particular exa mple). Going further into flexion. however. would the m uscles were being stretched - even when the muscle remained present no problems or pain. well short of its normal resting length. At the same time the extensor muscles. which had been at stretch and which in the alarm situation Walther ( 1 988) summarizes the situation as fol l ows. were obliged to rapidly shorten. wou ld remain l onger than their normal resting length as they were attempting to stabilize the When proprioceptors send conflicting information there may be situation. simul taneous contraction of the antagonists . . . without an tagonis t Korr has described what happens in the abdomina l m uscles (flexors) in such a situation. He says that. because of their relaxed muscle inhibition joint and o ther strain results . . . a reflex pa ttern status short of their resting length. a silencing of the spindles occurs. However. due to the sudden demand for information by the develops which causes muscle or o ther tissue to main tain this contin­ higher centers. gamma gain is increased so that. as the muscle contracts rapidly to stabilize the situation and demands for uing strain. It [strain dysfunction] often rela tes to the inappropriate information are received from the central nervous system. the muscle reports back that it is being stretched when it is actually short of its signaling from muscle proprioceptors that have been strained from normal resting length. This results in co-contraction of both sets of muscles. agonists and antagonists. In effect. the muscles wou ld rapid change that does not allow proper adaptation. have adopted a restricted position as a result of ina ppropriate proprioceptive reporting (Korr 1 976). The two opposing sets of muscles This situation wou ld be u nlikely to resolve itself spontaneously and is become locked into positions of imbalance in relation to their normal the 'strain' position in Jones' strain/counterstrain method. We can recognize it in an acute setting in torticol lis as wel l as in acute 'Iumbago: It is a lso recognizable as a feature of many types of chronic somatic dysfu nction in which joints remain restricted due to muscular imba lances of this type. This is a time of intense neurological and proprioceptive confusion. This is the moment of 'strain: Box 3.4 Biochemistry. the mind and neurosom atic disorders Goldstein ( 1 996) has described many chronic health conditions. 3. Genetica lly predetermined susceptibility to viral infection affecting the neurons and g lia. 'Persistent CNS viral infections including chronic fatigue and fibromyalgia syndromes (CFS. FMS). as cou ld a lter production of transmitters as well as cel l ular m ec h a n i sms: neurosomatic disorders. q uoting Yu nus ( 1 994) who says they are ·. . .the 4. Increased susceptibility to environmental stressors due to reduction commonest grou p of il l nesses for which patients consult physicians: in neural plasticity (resulting from all or any of the causes listed in 1 -3 above). This might include deficiency in glutamate or nitric Neurosomatic disorders are ill nesses which Goldstein suggests are oxide (NO) secretions, which results in encoding new memory. 'Neural plasticity' capacity may be easily overtaxed in such individu­ caused by 'a complex interaction of genetic. developmental and als which. Goldstein suggests, is why neurosomatic patients often develop their problems after a degree of increased exposure to envi­ environmenta l factors'. often involving the possibility of early ronmental stressors such as acute infection. sustained attention. exercise. immunization. emergence from anesthesia. trauma. etc. physical. sexual or psychological abuse (Fry 1 993). Symptoms emerge Goldstein (1 996) describes the limbic system and its dysreg ulation as a result of 'impaired sensory information processing' by the neural thus. network (including the bra i n). Examples given a re of light touch 1 . The limbic system acts as a regu lator (integrative processing) i n t h e b ra i n with effects on fatigue, pain. sleep. memory. attention. being painful. mild odors producing nausea. walking a short distance weight. appetite. libido, respiration. temperatu re, blood pressure. mood. immune and endocrine function. being exhausting. climbing stairs being like going up a mou ntain. 2. Limbic function dysreg u lation influences a l l or any of these fu nc­ reading something lig ht ca using cog nitive impairment - all of which tions and systems. examples a re true for many people with CFS/FMS. 3. Regulation of autonomic control of respiration derives from the limbic system and major abnormalities (hyperventilation tenden­ Goldstein is critical of psychological approaches to treatment of cies. irregu l a rity in tida l volu me, etc.) in breathing function a re noted in people with chronic fatigue syndrome. along with abnor­ ssuucghgecsotsn d. .i.t. imo nasy. apart from cog nitive behaviour therapy. which he mal responses to exercise (including failure to find expected lev­ be more appropriate. since coping with the els of cortisol increase. catecholamines. g rowth hormone, somatostatin. increased core temperatu re, etc.) (Gerra 1 993, vicissitudes of these ill nesses. which wax and wane u n predictably. is Goldstein Et Daly 1 993. G riep 1 993, M u nschauer 1 99 1 ) . a major problem for most of those afflicted'. He claims that most box continues major medical journals concerned with psychosomatic medicine rarely discuss neurobiology and 'apply the concept of somatization to virtually every topic between their covers' (Hudson 1 992. Yunus 1 994). The four basic influences on neurosomatic i l lness are. he believes. as follows. 1 . Genetic susceptibility, which can be strong or weak. If only a weak tendency exists. other factors a re needed to influence the trait. 2. If a child feels unsafe between birth and puberty. hypervigila nce may develop and interpretation of sensory input will a lter.

56 C LI N I CA L A P P L I CATI O N O F N E U R O M U SC U LA R TECH N I QU E S : T H E U P PE R B O DY Box 3.4 � 4. Dysfu nction of the l i m bic system ca n resu l t from centra l or Early intense peripheral i nfl uences ('stress'). psychosocial stress (abuse, 5. Sensory gating (the weight given to sensory inputs) has been etc . ) shown to be less effectively i n h ibited i n women than in men (Swerdlow 1 993). Additional multiple 6. Many biochemical i m balances are i nvolved i n l imbic dysfunction environmental and no attempt will be made in this summary to deta i l them all. stressors 7. The trigeminal nerve, states Goldstein, modulates l imbic regula­ Allostasis = modified homeostasis (genetically or via early experience) tion. 'The trigeminal nerve may produce expansion of the recep­ which produces exaggerated or insufficient responses, for example: tive field zones of wide dynamic-ra nge neurons and nociceptive-specific neurons under certai n cond itions, perhaps • stress-hormone elevation involving increased secretion of substance P, so that a greater • behavioral and neuroimmunoendocrine disorders n u m ber of neurons w i l l be activated by sti m u lation of a receptive • physiological regulation of abnormal states (out of balance) zone, causi ng innocuous sti m u l i to be perceived as painful' • glucocorticoid elevation (Dubner 1 992). • various key sites in the brain produce neurohumoral changes 8. Goldstein reports that nitrous oxide, which is a primary vasod ila­ potentially influencing almost any part of the body or its tor i n the brain, has profound infl u ences on glutamate secretion functions. and the neurotransm itters which infl uence short-term memory (Sandman 1 993), anxiety (Jones 1 994), dopamine release Figure 3.5 Schematic representation of a l l ostasis. Reprodu ce d (Hanbauer 1 992) (so affecting fatigue), descending pain inh ibi­ with permission from Chaitow (2003a). tion processes, sleep induction and even m enstrual problems. ' Female patients with CFS/FMS usually have premenstru a l exacer­ bations of their symptoms. Most of the symptoms of late luteal phase dysphoric diso rder [premenstrual syndrome) a re sim ilar to those of CFS, and it is likely that this d isorder has a l imbic etiol­ ogy sim ilar to CFS/FMS' (Iadecola 1 993). Allostasis is a major feature of Goldstein's model. He reports the fol lowing. • Approximately 40% of CFS/FMS patients screened have been shown to have been physical ly, psychologica l ly or sexua l ly abused • Allostatic load, in contrast to homeostatic mechan isms which in childhood. By testing for brain electricity imbalances, using stabilize deviations in normal variables, is 'the price the body pays brain electricity activity mapping (BEAM) techniques, Goldstein for containing the effects of a rousing stimuli and the expectation has been able to demonstrate abnorm a l ities in the left tempora l of negative consequences' (Schul kin 1 994). area, a feature of people who have been physica l ly, psychologi­ • Chronic negative expectations and subsequent a rousal seem to cally or sexually abused in childhood (as compared with non­ increase allostatic load. This is cha racterized by a nxiety and abused controls) (Teicher 1 993). anticipation of adversity leading to elevated stress hormone levels • Major childhood stress, he reports, i ncreases cortisol levels (Sterling Et Eyer 1 98 1 ) . which can affect hi ppocampal function and structure • Goldstein attempts t o explain t h e imme nsely complex biochemi­ (McEwan 1 994, Sa polsky 1 990). It seems that early experience cal and neural i nteractions which are involved i n this scenario, and environmental stimuli interacting with undeveloped biologi­ embracin g a reas of the brain such a s the a mygdala, the pre­ c a l systems l e a d t o altered homeostatic responses: 'For frontal cortex, the lower brainstem and other sites, as well as exam ple, exaggerated or i nsufficient H PA axis responses to myriad secretions including hormones (including g lucocorticoids), defend a homeostatic state i n a stressful situation cou ld resu lt in neurotransmitters, substance P, dopamine a nd nitric oxide. behavioural and neuroi m munoendocrine diso rders i n adulthood, • Final ly, he states, prefrontal cortex function can be alte red by particularly if stimuli that should be non-stressful were n u m erou s triggering agents in the predisposed individual (possibly evaluated ... ina ppropriately by the prefrontal cortex .. .' (Meaney i nvolving genetic featu res or early trau ma) includ ing: 1 994). • Sa polsky ( 1 990) has studied this area of 'a l l ostasis' (regu lation of 1 . viral infections that alter neuronal function internal m i l ieu through dynam ic change in a number of hormonal 2. immunizations that deplete biogenic amines (Gardier 1 994) and physical variables that a re not i n a steady-state condition) 3. orga nophosphate or hydrocarbon exposure a nd identifies as a primary feature a sense of lack of control. 4. head i nj u ry Sapolsky a l so identifies a sense of lack of predictability and vari­ 5. childbirth ous other stressors which infl u ence the H PA axis and which are 6. electromag netic fields less balanced in i ndividuals with CFS/FMS; all these stressors 7. sleep deprivation involve 'ma rked absence of control, predictabil ity, or outlets for 8. general a nesthesia frust ra t i o n '. 9. 'stress', e.g. physica l, such a s marathon running , or mental or • In studies of this topic CFS/FMS patients are found to predomi­ emotional. nantly attribute their symptoms to external factors (virus, etc.) while control subjects (depressives) usually experience i nward What Goldstein is reporting is a n a l tered neurohumoral response in attribution (Powell 1 990). individuals whose defense and repair systems a re predisposed to this - - - - - - - - - - - - - -- - - - - - - - - - - - - - - - ----------- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -- - - -- ------------------ box continues

3 Reporting stations and the brain 57 Box 3.4 (continued) . happening, either because of i nherited tendencies or because of nutritional approaches. Goldstein h a s offered us insights and his own early developmental (physical or psychological) insul t(s), to which solutions. Not everyone w i l l necessarily accept these sol u tions but additional multiple stressors have been added. His sol ution is a the illu mination of the highly com plicated mechanisms involved, biochemical (drug) modification of the i m balances he iden tifies as which he offers, is to be commended. key features of this situation. It is also worth reflecting on the possible effects, on predisposed Alternative approaches might attempt to modify behavior or to mechanisms, of whiplash-type i nj u ries, as d iscussed in this cha pter. a lter other aspects of the complex d isturbances, possibly using totality of information that is received, rather than individual papers offering glimpses of what may be going on in the pieces of information from particular reporting stations. apparently never-ending pain states. • Dommerholt (2004a,b) has examined one such syndrome­ Should any of this mass of information be contradictory and CRPS (chronic regional pain syndrome, previously known actually conflict with other information being received, what as reflex sympathetic dystrophy). He notes that, 'It is then? If conflicting reports reach the cord from a variety of likely that CRPS is a disease of the central nervous sys­ sources simultaneously, no discernible pattern may be recog­ tem, but at the same time there are numerous indications nized by the CNS (see Korr 's discussion below and Box 3.3). In that point to peripheral inflammatory processes, abnor­ such a case no adequate response would be forthcoming and mal sympathetic-afferent coupling, and adrenoreceptor it is probable that activity would be stopped and a protective pathology. It is plausible that there are multiple simulta­ co-contraction ('freezing', splinting) spasm could be the result. neous processes that contribute to the development of CRPS' (Dommerholt 2004a). Sensitization • Dommerholt (2004b) acknowledges that when attempt­ ing to treat such conditions, while physical (manual) • W hen pain persists past the time that an injury should therapy may be useful, there is no research evidence to have healed, a process of central sensitization may have validate its efficacy. There is certainly no general prescrip­ occurred. tion as to what will help most in any of the widespread pain conditions listed above. However, Dommerholt sug­ • Similarly, if pain, instead of reducing in the area involved gests that (and the authors of this text agree) : 'Therapy [of over time, gradually spreads, sensitization is a probable CRPS] should include at least general range of motion cause. exercises, inactivation of myofascial trigger points, desen­ sitization interventions, aquatic physical therapy, posture • Sensitization is also the likely mechanism if pain inten­ training and movement retraining.' sity increases for no apparent reason. In later chapters all of these options will be explored, along • The process of sensitization involves the dorsal horn of with nutrition, stress management and emotional well­ the spinal cord and/or the brain becoming increasingly being, all of which can also be influential to these conditions. easily irritated, with its threshold reduced. NEURAL OVERLOAD , ENTRAPMENT AND • A process known as wind-up, and another known as long­ CROSSTAL K term potentiation (see Box 3 .5) may result in a degree of sensitization and chronic pain, such as allodynia, where Korr (1976) discusses a variety of insults that may result in even a light stimulus provokes extreme pain (Kandel increased neural excitability, including the triggering of a et al 2000, Van Griensven 2005). barrage of supernumerary impulses to and from the cord that can result in 'crosstalk', in which axons may overload • Commonly, when central sensitization occurs, move­ and pass impulses to one another directly. Muscle contrac­ ments become limited because of the pain and a degree tion disturbances, vasomotion, pain impulses, reflex mech­ of anxiety and 'pain behavior' starts, in which activities anisms and disturbances in sympathetic activity may aU are reduced to avoid an increase in pain. result from such behavior, due to what might be relatively slight tissue changes (in the intervertebral foramina, for • The sorts of conditions that might have these characteris­ example), possibly involving neural compression or actual tic may carry labels such as fibromyalgia, chronic fatigue entrapment. syndrome, somatoform pain disorder, myofascial pain syndrome, non-specific neuropathic pain . . . and many In addition, Korr states that normal patterned transmis­ others, depending on who made the diagnosis, who sion from the periphery can be jammed when any tissue is offered the 'label' . disturbed, whether bone, joint, ligament or muscle. These • Aspects of the mechanisms described i n Box 3.4, a s well as in Box 3.5, may be involved in central sensitization, with altered biochemistry as a feature, possibly relating to early childhood stresses (biochemical and/or psychological). • The fact is that complex chronic pain syndromes appear to have multiple possible causes, and the processes involved remain unclear - despite mountains of research

58 C LI N I CA L APPLICATI O N OF N E U R OM USCU LA R TECH N IQUES: T H E U PP E R B O DY factors, combined with any mechanical alterations in the tis­ debated. Some take a pOSition that this is a minimal effect sues, are the background to much somatic dysfunction. (Lederman 1997), while others suggest a strong, if tempo­ rary, influence that allows for an easier stretch of previ­ Korr summarizes the picture as follows: ously shortened structures (Lewit 1985). In Chapter 9 new These are the somatic insults, the sources of incoherent and research evidence is described that helps to explain just meaningless feedback, that cause the spinal cord to halt nor­ what does happen following an isometric contraction as mal operations and tofreeze the status quo in the offending used in MET and other soft tissue manipulation tech­ and offended tissues. It is these phenomena that are niques such as 'hold-relax' and 'contract-relax-antagonist detectable at the body surface and are reflected in disorders contract'. of muscle tension, tissue texture, visceral and circulatory • Positional release techniques (PRT) - muscle spindles are function, and even secretory junction; the elements that are influenced by methods which take them into an 'ease' so much a part of osteopathic diagnosis. state and which theoretically allow them an opportunity Goldstein (1996) offers a more complex scenario in which the to 'reset' and reduce hypertonic status. Jones' (1995) 'strain brain itself (or at least part of it) becomes hyperreactive and and counterstrain' and other positional release methods starts to miSinterpret incoming information (see Box 3.4). use the slow and controlled return of distressed tissues to the position of strain as a means of offering spindles a MANIPULATING THE REPORTING STATIONS chance to reset and so normalize function. This is particu­ There exist various ways of 'manipulating' the neural larly effective if they have inappropriately held an area in reporting stations to produce physiological modifications in just such protective splinting. soft tissues. • Direct inf luences can be achieved, for example, by means of pressure applied to the spindles or Golgi tendon • Muscle energy technique (MET) - isometric contractions uti­ organs (sometimes termed 'ischemic compression' or lized in MET affect the Golgi tendon organs, although the 'inhibitory pressure', equivalent to acupressure method­ degree of subsequent inh ibition of muscle tone is strongly ology) (Stiles 1984). • Proprioceptive manipulation (applied kinesiology) is possi­ STRENGTHEN ble (Walther 1988). For example, kinesiological muscle tone correction utilizes two key receptors in muscles to �c� achieve its effects. A muscle in spasm may be helped to WEAKEN relax by the application of direct pressure (using approx­ imately 2 1bs or 0.5 kilos of pressure) away from the belly A = Golgi tendon organs B = belly of muscle C = muscle spindle of the muscle, in the area of the Golgi tendon organs, and/or by the application of the same amount of pres­ F ig u re 3.6 Proprioceptive m a n i pu l a t i o n of m u scles as described i n sure toward the belly of the muscle, in the area of the muscle spindle cells (Fig. 3.6). the text. Reproduced with permission from Ch aitow (2003b). • The precise opposite effect (i.e. temporary toning or strengthening of the muscle) is achieved by applying pressure away from the belly, in the muscle spindle region, or toward the belly of the muscle in the tendon organ region. • The mechanoreceptors in the skin are very responSive to stretching or pressure and are, therefore , easily influenced Box 3:5 It is in teresting to note that wind-up develops whether a person is conscious or not. A person undergoing surgery may develop long Van Griensven (2005, p . 64) explains t h e processes th at occur lasting sensitization of the dorsal horns supplying the operation site with sensory nerves, even though they are under general in the dorsal horn that can lead to central sensitization and extreme anaesthetic. pain : Long-term potentiation is thought to be the result of wind-up and Wind-up is a phenamenon that has been observed in laboratory other forms of persistent nociceptive stimulation. The bombardment settings. When a C fibre is stimulated repeatedly at a relatively high of the secondary neuron with glutamate opens more ion channels in frequency. it continues to depolarize even when stimulation has its membrane than when stimulation is of shorter duration and lower ceased. The spontaneous firing can take a lang time to fizzle out and intensity. The result is an ever-increasing calcium influx into the sec­ it can be main tained by successive stimulatian. In ather wards, ondary cell, which makes it even more exitable. although it takes in tense and high frequency stimula tion for a C fibre to go in to a state of wind up, it requires much less to main tain . . . box continues

Box 3.5 (continued) 3 R eporting stations and t h e brain 59 A Dorsal Presynaptic horn Tissue B Presynaptic receptors Dorsal opened horn Postsynaptic Tissue Figure 3.7 The role of N M DA channels. A: Nociceptive F i g u re 3.8 State dependent processing. A : Control state. sti m u l ation leads to the release of g l utamate, w h i c h opens A M PA Mech a n ical sti m u l i affect low t h reshold affe rents and noxious channels. The N M DA c h a n n e l s rema i n b l ocked by m a g nesi u m sti m u l i affect high thresho ld affe rents. The signals a re passed (Mg2+). B : Pe rsistent sti m u lation causes the ej ection o f M g 2 + , o n u n c h a nged. B : Sensitized state. Sti m u l i a re a m p l ified . I n put creati ng a n infl ux o f ca l c i u m (Ca2 + ) . As long as the channels remain un blocked, a small amount of glutamate has a greater from high t h reshold a fferents generates hyperalgesia. I n p u t effect than when only the AM PA c h a n n e l s a re opened. I n creased levels of i ntracel l u la r calci u m trigger processes i nside the from low th reshold afferents i s felt a s i ntense (hyperaesthesia) postsyna ptic ce l l , leading to a greater response. They a lso trigger the release of retrog rade messengers that fac i l itate the release of or even painfu l (a l lodynia). C: Suppressed state. All i n put is g l utamate from the presy n a ptic mem bra ne. Reproduced with reduced in intensi ty. 'Re pro du c ed w ith permission from van permission from van Griensven (2005). Griensven (2005). NMDA, N-methyl d-aspartate;AMPA, alpha-amina-3-hydroxy-5-methyl-4-isaxazo/e propionic acid Note: It may be useful to refer to the discussion of facititation in Chapter 6 to compare the similarities and d i fferences between t h i s phenomenon a n d centra l faci l itation. by methods which rub them (e.g. massage), apply pres­ reprogramming proprioceptive information (Chaitow & sure to them (NMT, reflexology, acupressure, shiatsu, DeLany 2002, Liebenson 2006). etc.), stretch them or 'ease' them (as in osteopathic func­ tional technique, see Chapter 9). THERAPEUTI C REHABI LITATI O N U SING • The mechanoreceptors in the joints, tendons and liga­ REFLEX SYSTEMS ments are influenced to varying degrees by active or pas­ sive movement including articulation, mobilization, V ladimir Janda has researched and developed ways in which adjustment and exercise (Lederman 1997). reeducation of dysfunctional patterns of use can best be • Sensory motor stimulation, using a variety of tools (see achieved, using our knowledge of neural reporting stations - a below), may activate afferent pathways as a means of

60 C L I N I C A L A P P L I CAT I O N OF N E U R O M U SC U LA R TECH N I QU E S : T H E U P P E R B O DY 'sensory motor' approach Ganda 1996). There are, he states, trampolines and many others, including balance exercises, two stages to the process of learning new motor skills or such as Tai Chi (see Volume 2, Chapter 2) . The principles of relearning old ones. this approach are based on the work of Bobath & Bobath (1964) who developed motor education programs for chjJ­ 1. The first is characterized by the learning of new ways of dren w i th cerebral pa lsy. A program of reeducation of sen­ performing particular functions. This involves the cortex sory motor function can apparently double the speed of of the brain in conscious participation in the process of muscle contraction, significantly improving general and skill acquisition. As this process proceeds, Janda says, 'the postural function (Bullock-Saxton et aI 1993) . brain tries to minimize the pathways and to simplify the regulatory circuits', speeding up this relatively slow C O N C LU S I O N means of rehabiJita tion. However, he warns, 'If such a motor program has become fixed once, i t is difficult, if not A n appreciation o f the roles o f the neural reporting stations impossible, to change it. This calls for other approaches'. helps us in our understanding of the ways in which dys­ functional adaptive responses progress, as they evolve out 2. The speedier approach to motor learning involves bal­ of patterns of overuse, misuse, abuse and disuse. ance exercises tha t a ttempt to assist the proprioceptive Compensatory changes that emerge over time or as a result system and associated pa thways relating to posture and of adaptation to a single trauma tic event are seen to have a equilibrium. Janda (1996) informs us that, 'From the logical progression. We will focus on these pa tterns in the pOint of view of afference, recep tors in the sole of the next chapter. There we will take both a broad and a local foot, from the neck muscles, and in the sacroiliac area view of compensations and adaptations to the normal have the main proprioceptive influence' (Abrahams (gravity) and abnormal (use patterns or trauma) stresses of 1977, Freeman et a1 1965, Hinoki & Ushio 1975). life and how these impact our remarkably resilient bodies. Aids to stimulating the proprioceptors in these areas include wobble boards, rocker boards, balance shoes, mini Refe rences Dommerhol t J 2004a Complex regional pain syndrome - 1: history, diagnostic criteria and etiology. Journal of Bodywork and Abrahams V 1977 Physiology o f neck muscles: their role in head Movement Therapies 8:] 67-177 movement and main tenance of posture. 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Chapter 4 63 Causes of musculoskeletal dysfunction :::oJ CHAPTER CONTENTS The struggle with gravity is a lifelong battle, often compli­ cated by the sheer range of adaptive stresses to which we Adaptation - GAS and LAS 63 subject our bodies throughout life. Adaptation and com­ Posture, respiratory function and the adaptation pensation are the processes by which our functions �re phenomenon 64 An example of 'slow' adaptation 66 gradually compromised as we respond to an endless senes What of adaptation to trauma? 67 of demands, ranging from postural repositioning in our What of adaptation to habits of use? 67 work and leisure activities to habitual patterns (such as how Making sense of the picture 67 we choose to sit, walk, stand or breathe). There are local Example 68 tissue changes as well as whole body compensations to Postural and emotional influences on musculoskeletal short- and long-term insults imposed on the body. A sum­ dysfunction 69 mary discussion of the adaptive mechanisms involved, PosturaI interpretations 69 together with a deeper examination of key features m the Contraction patterns 69 evolution of musculoskeletal dysfunction, will support an Emotional contractions 69 understanding of how the body adapts, how it may be 'Middle fist' functions 70 assisted and when it might be appropriate to leave the 'Upper fist' functions 70 adaptation alone. Behavior and personality issues 71 Cautions and questions 72 ADAPTATION - GAS AND LAS Postural imbalance and the diaphragm 73 Balance 74 When we examine musculoskeletal function and dysfunc­ Respiratory influences 75 tion we become aware of a system that can become compro­ Effects of respiratory alkalosis in a deconditioned mised as a result of adaptive demands exceeding its capacity to absorb the load, while attempting to maintain something individual 75 Respiratory entrainment and core stability issues 75 � :approaching normal function. Elastic limits ay at tim � be Summary of effects of hyperventilation 76 Neural repercussions 77 exceeded, resulting in structural and functlOnal modlfIca­ Tetany 77 tions. Assessing these dysfunctional patterns - making sense Biomechanical changes in response to upper chest of what can be observed, palpated, demonstrated - allows for detection of causes and guidance toward remedial breathing 77 action. Additional emotional factors and musculoskeletal The demands that lead to dysfunction can either be violent, dysfunction 78 forceful, single events or they can be the cumulative influence Selective motor unit involvement 78 of numerous minor events (microtrauma). Each such event is Conclusion 79 a form of stress and provides its own load demand on the local area as well as the body as a whole. To better understand these processes it is useful to refer back to the principal researcher of this phenomenon, Hans Selye. Selye (1956) called stress the 'non-specific element' in disease production. He described the general adaptatzon

64 C L I N I CA L A P P LICAT I O N O F N E U R O M U S C U LA R T E C H N I Q U E S : TH E U P P E R B O DY ADAPTING TO STRESS Alarm phase Aching muscles Postural changes, shoulders slumped, head pushed forwards Different activities Changes Strengthening muscles in dominant arm place the body under Increased heart strength Possible changes to eyesight as eye muscles different kinds of Adaptation adapt to long periods focused on screen stress. It is how we phase adapt to the stresses Regular movement Lack of awareness that determines how Recovery or and postural of changes we are affected by breakdown them. These two Improvement of Injury or strain, No long-term Repetitive strain examples show the strength and e.g. tennis elbow damage injury two paths taken during coordination the adaptation phase - the planned adaptation No injury or tissue path leads to recovery damage without injury or damage; unplanned adaptation leads to breakdown and the development of particular problems. Figure 4.1 Examples of appropriate and inapp ropriate responses to stress. Redrawn after Peters (2005). syndrome (GAS) as being composed of three distinct changes that occur when particular load is applied to, or par­ stages: ticular demands are made of, body areas (Norris 2000a,b). • the alarm reaction when initial defense responses occur Selye demonstrated that stress results in a pattern of adap­ ('fight or flight') tation, individual to each organism. He also showed that when an individual is acutely alarmed, stressed or aroused, • the resistance (adaptation) phase (which can last for homeostatic (self-normalizing) mechanisms are activated. many years, as long as homeostatic - self-regulating - However, if the alarm status is prolonged or if adaptive mechanisms can maintain function) demands are excessive, long-term, chronic changes occur and these are almost always at the expense of optimal functional • the exhaustion phase (when adaptation fails) where integrity. frank disease emerges. When assessing or palpating a patient or a dysfunctional GAS affects the organism as a whole, while the local adaptation area, neuromusculoskeletal changes can often be seen to syndrome (LAS) goes through the same stages but affects represent a record of the body's attempts to adapt and adjust localized areas of the body. For example, imagine the tissue to the multiple and varied stresses that have been imposed response to digging the garden, chopping wood or playing upon it over time. The results of repeated postural and trau­ tennis after a period of relative inactivity - an 'acute adap­ matic insults over a lifetime, combined with the somatic tive response' would result with accompanying stiffness and effects of emotional and psychological origin, will often aching, followed by resolution of the stress effects after a few present a confusing pattern of tense, shortened, bunched, days. Imagine the same activity repeated over and over fatigued and, ultimately, fibrous tissue (Chaitow 1989). again, in which adaptive ('training') responses would result, leading to chronic tissue responses involving hypertrophy, POSTURE, RESPIRATORY FUNCTION AND possible shortening, strengthening and so on. Anyone who THE ADAPTATION PHENOMENON regularly trains by running or lifting weights will recognize this seguence. The body, or part of the body, responds to Some of the many forms of soft tissue stress responses that the repetitive stress (running, lifting, etc.) by adapting to the affect the body include the following (Barlow 1959, needs imposed on it. It gets stronger or fitter, unless the Basmajian 1974, Dvorak & Dvorak 1984, Janda 1982, 1983, adaptive demands are excessive, in which case it would Korr 1978, Lewit 1985, Simons et a11999, Travell & Simons ultimately break down or become dysfunctional (see 1992). Fig. 4.1). The acronym SAID (specific adaptation to imposed demand) has been coined to illustrate this process of the

4 Causes of musculoskeletal dysfunction 65 ] Immobilization Adaptation Shrinking of • Ischemia itself has not been considered to be a producer of to non-use capsular tissues pain; however, an ischemic muscle that contracts rapidly does produce pain (Lewis 1942, Liebenson 1996, Mense Trauma or Inflammation et al 2001). repeated microtrauma • However, it is now hypothesized (Ost et al 2006) that local hypoxia/ischemia creates pain via venous congestion Pain Degeneration Elevated or temporized arterial perfusion. For example, pelvic compression of venous microvascular dysfunction and congestion has articular cartilage been speculated to be a contributing factor in women with chronic pelvic pain (Foong et al 2002). In addition, Figure 4.2 Changes in biochemistry associated with reduced hypoxia may increase the rate of muscle fatigue and dis­ physical activity. Redrawn with permission after Liebenson (2006). comfort. On a cellular level, alterations in oxygen supply may alter the regulation of cellular respiration, affecting 1. Congenital and inborn factors, such as short or long leg, the onset of impaired Ca2+ handling associated with small hemipelvis, fascial influences (e.g. cranial distor­ such fatigue (Hepple 2002). tions involving the reciprocal tension membranes due to birthing difficulties, such as forceps delivery), or tendency • Increased tone might also lead to a degree of edema. to hypermobility (see Chapter 1). • An environment of ischemia results in local energy crisis, 2. Overuse, misuse and abuse factors, such as injury or which is associated with trigger point formation (Simons inappropriate or repetitive patterns of use involved in et aI1999). work, sport or regular activities. • These factors (retention of wastes/ischemia/edema/trig­ ger point formation) can all contribute to discomfort 3. Immobilization, disuse (can result in loss of muscles or pain. strength at the rate of 10% per week) (Liebenson 2006) • Discomfort or pain reinforces hypertonicity. (see Chapter 7). • Inflammation or, at least, chronic irritation may result. • Neurological reporting stations in these distressed hyper­ 4. Postural stress patterns (see below). tonic tissues \\·vill bombard the CNS with information 5. Inappropriate breathing patterns (see below). regarding their status, leading, in time, to a degree of sensi­ 6. Chronic negative emotional states such as depression, tization of neural structures and the evolution of facilita­ tion and its accompanying hyperreactivity. anxiety, etc. (see below). • Macrophages are activated, as is increased vascularity 7. Reflexive influences (trigger points, facilitated spinal and fibroblastic activity (see Chapter 6). • Connective tissue production increases with cross­ regions) (see Chapter 6). linkage, leading to shortened fascia. • Chronic muscular stress (a combination of the load/'stress As a result of these influences, which affect each and every and strain' involved, and the number of repetitions or the one of us to some degree, acute and painful adaptive changes degree of sustained influence) results in the gradual can occur, thereby producing the dysfunctional patterns and development of hysteresis, in which collagen fibers and events on which neuromuscular therapies focus. proteoglycans are rearranged to produce an altered structural pattern (see Chapter 1). When the musculoskeletal system is 'stressed', by these • This results in tissues that are far more easily fatigued or other means, a sequence of events occurs as follows. and prone to frank damage, if strained. • Since all fascia and other connective tissue is continuous • 'Something' (see list above) occurs that leads to increased throughout the body, any distortions or contractions that muscular tone. develop in one region can potentially create fascial defor­ mations elsewhere, resulting in negative influences on • If this increased tone is anything but short term, retention structures that are supported by or attached to the fascia, of metabolic wastes may occur, particularly in a decondi­ including nerves, muscles, lymph structures and blood tioned person who is not aerobically fit (Nixon & vessels (Myers 2001). Andrews 1996). • Hypertonicity in a normal muscle will usually produce inhibition of its antagonist(s) and aberrant behavior in its • Increased tone simultaneously leads to a degree of synergist(s). hypoxia, localized oxygen deficiency (relative to the tis­ • Chain reactions evolve in which some muscles sue needs), and the development of ischemia. (postural - type I) shorten while others (phasic - type II) weaken. • Because of sustained increased muscle tension, ischemia in tendinous structures occurs, as it does in localized

6 6 C L I N I CA L A P P L I CATI O N O F N EU R O M U S C U LA R TEC H N I Q U ES : T H E U P PER B O DY areas of muscles, leading to tendon and attaclunent inflam­ The chronic adaptive changes that develop in such a sce­ mation and the development of periosteal pain. nario lead to the increased likelihood of future acute exacer­ • Compensatory adaptations evolve, leading to habituaL bations as the increasingly chronic, less supple and less 'built-in' patterns of use emerging, as the CNS learns to resilient biomechanical structures attempt to cope with compensate for modifications in muscle strength, length additional stress factors resulting from the normal demands and functional behavior. of modern living. • Abnormal biomechanics result, involving malcoordination of movement (with antagonistic muscle groups being For example, Bakker et al (2003) have reported that not either hypertonic or weak - for example, erector spinae tightens while rectus abdorninis is inhibited and weakens). only do musculoskeletal tissues weaken from overuse or • The normal firing sequence of muscles involved in par­ disuse, but also that the actual shape of the vertebrae and ticular movements alters, resulting in muscle substitu­ the intervertebral discs, as well as the ligaments, adapt and adjust to the type of load imposed. This is clearly an exam­ tion and additional strain (Janda 1982, 1983). ple of a specific adaptation to imposed demand (Conroy & • Joint biomechanics are directly influenced by the accu­ Earle 2000) and is supported by Wolff's law (see Chapter 1). mulated influences of such soft tissue changes and can themselves become significant sources of referred and The degree of physiological musculoskeletal adaptation - local pain, reinforcing soft tissue dysfunctional patterns that causes changes to both function and structure - is largely determined by the magnitude of the load, as well as the use, (DeFranca 2006, Schaible & Grubb 1993). or misuse, to which the spine is put. • Deconditioning of the soft tissues becomes progressive as a Wallden (2000) has described such adaptation sequences result of the combination of simultaneous events involved in slightly different terms, identifying both the rate of tissue in soft tissue pain, 'spasm' (hypertonic guarding), jOint damage (micro trauma) and the rate of tissue repair as key fea­ stiffness, antagonist weakness, overactive synergists, etc. tures in the rate of advance toward adaptation exhaustion: • Progressive evolution of localized areas of hyperreactivity Across the life-span of an organism, or ofa tissue, the rate of of neural structures occurs (facilitated areas) in paraspinal repair slowly declines, whilst the rate of cumulative micro­ regions or within muscles (myofascial trigger points) (see trauma to the organism/tissue increases. The point at which the rate of trauma exceeds the rate of repair is the point at Chapter 6). which the organism/tissue fails. If repair mechanisms are optimal, the organism or tissue should realize its genetic • In the region of these trigger points (see discussion of potential. If repair mechanisms are impaired or overloaded, potential is not realized, and adaptation will fail. myofascial triggers, p. 97) a great deal of increased neu­ This observation highlights a need to focus on both reduction rological activity occurs (for which there is EMG evi­ of microtrauma as well as enhancement of repair potentials dence) that is capable of adversely influencing distant (nutrition, etc.). tissues (Hubbard 1993, Simons 1993, Simons et aI1999). AN EXAMPLE OF 'SLOW' ADAPTATION • Energy wastage, due to unnecessarily sustained hyper­ Consider the cumulative effects of a leg-length imbalance. tonicity and excessively active musculature, leads to gen­ Using data on leg-length inequality, obtained by accurate eralized fatigue as well as to a local 'energy crisis' in the and reliable x-ray methods, Knutson (2005) fOlmd the preva­ local tissues (see trigger point discussion, p. 97). lence of anatomic leg length inequality to be 90%. The evi­ • More widespread functional changes develop - for exam­ dence suggested that, for most people, anatomic leg-length ple, affecting respiratory function and body posture - with inequality does not appear to be clinically significant until the repercussions on the total economy of the body. magnitude reaches approximately 20mm (74\"). • Induction of muscle hypertonicity is part of the alarm Janda (1988) has described the sequence of adaptive reaction of the flight/fight alarm response. In the pres­ ence of a constant neurological feedback of impulses to changes, resulting from the presence of a significant degree of the CNS/brain from neural reporting stations indicating leg shortness, that culminate in back, head, neck and facial heightened arousaL there will be increased levels of psy­ chological arousal and a reduction in the ability of the pain. This is summarized in Chapter 5 (p. 84). individual, or the local hypertonic tissues, to relax effec­ tively. This will consequently result in reinforcement of Over time, adaptational modifications may progress from hypertonicity. the production of soft tissue changes to evidence of dysfunc­ tion (e.g. low back pain) and the evolution of actual patho­ • Functional patterns of use of a biologically unsustainable nature will emerge, probably involving chronic muscu­ logical changes. For example, Gofton & Trueman (1971) loskeletal problems and pain. found a strong association between leg length and unilat­ At this stage, restoration of normal function requires thera­ eral osteoarthritis (OA) on the side of the anatomically long peutic input which addresses both the multiple changes leg. They noted that all subjects with this type of OA 'had that have occurred, and the need for a reeducation of the led healthy active lives prior to the onset of hip pain' and individual as to how to use his body, to breathe and to carry few subjects were aware of any difference in leg length. himself in more sustainable ways.

4 Causes of musculoskeletal dysfunction 67 They also point out that this form of OA has its onset picture of health. From the shoes we wear to the seats we sit around the age of 53, but acknowledge that many people upon, to the awkward positions we assume in the work with precisely this anatomic asymmetry failed to develop environment, daily activities have perhaps the most pro­ an arthritic hip, suggesting that factors other than the leg found impact. Further discussion of the myriad of static and length disparity are also important. dynamic influences is found in Volume 2 of this text. This underscores the importance of the context in which MAKING SENSE OF THE PIC TURE these mechanical adaptations are being processed by the tis­ sues under stress - with some joints becoming arthritic and Motor control is a key component in injury prevention and others not. loss of motor control involves failure to control joints, com­ monly due to incoordination of the agonist/antagonist mus­ It may be useful to ask what the other variables were that cle coactivation (McGill 1998). allowed some people with significant leg length discrepan­ cies to avoid arthritic changes and others to develop According to Panjabi (1992), three subsystems work them: Nutritional? Genetic? Gender? Weight? Occupation? together to maintain spinal stability: Other? • the central nervous subsystem (control). This subsystem is WHAT OF ADAPTATION TO TRAUMA? capable of becoming dysfunctional due to anything that interferes with nerve function, and can be enhanced by Slow adaptation to overuse, misuse and factors such as an exercises that focus on improving proprioception (Norris anatomic short leg can be contrasted with the adaptations 2000b). that occur in response to injury. • the osteoligamentous subsystem (passive). The efficiency Lederman (1997) points out that following actual trau­ of this subsystem can be reduced by injury (or by matically induced structural damage, tissue repair may lead hypermobility). to compensating patterns of use, with reduction in muscle force and possible wasting, often observed in backache • the muscle subsystem (active). This subsystem can be patients. If uncorrected, such altered patterns of use inevitably impaired by deconditioning and inhibition (for example, by lead to the development of habitual motor patterns and even­ overactive antagonists, or the presence of trigger points), tually to structural modifications. and can be enhanced by strength training. The possible adaptational sequelae to trauma may include: Anything that interferes with any aspect of these features of normal motor control may contribute to dysfunction • modified proprioceptive function due to alteration in and pain. mechanoreceptor behavior In the discussion below, attention will be given to various • inhibition of joint afferents influencing local muscle func­ core elements of the evolution of musculoskeletal dysfunc­ tion, possibly involving the build-up of metabolic tion - including musculoskeletal stress resulting from pos­ by-products, if joint damage has occurred tural, emotional and respiratory causes. These three factors interface with each other and reinforce any resulting dys­ • altered motor patterns resulting from higher center res­ functions. As will become clear in these descriptions, there ponses to injury, possibly involving a sense of insecurity is a constant merging and mixing of fundamental influences and the development of protective behavior patterns, on health and ill health. In trying to make sense of a resulting in actual structural modification, such as mus­ patient's problems, it is frequently clinically valuable to cle wasting cluster etiological factors. One model that the authors find useful divides negative influences into: • associated non-painful reflexogenic responses to pain, and also to injury (Hurley 1991). • biomechanical (congenital, overuse, misuse, trauma, dis­ use, etc.) WHAT OF ADAPTATION TO HABITS OF USE? • biochemical (toxicity, endocrine imbalance, nutritional Habits of use, as well as the close environment that comes in deficiency, ischemia, inflammation, hydration) intimate contact with the body, can have profound effects on tissue tone, flexibility and behavior. Prolonged periods of • psychosocial (anxiety, depression, unresolved emotional distorted or strained positioning that is often involved in states, somatization, etc.). professional or leisure activities may produce shortened and/or weakened, fibrotic, indurated or, in some other way, Obviously some of these features are inborn, while others are dysfunctional tissues. Stresses being loaded onto these acquired. Some are easily modified and some are extremely already compromised tissues that would not have been difficult to change. harmful to normal tissue may result in injury. Part of the practitioner/therapist'S role is to help to identify Everything that comes in contact with the body, or to what can be most easily modified by treatment or altered which the body must conform, is important in the overall

68 CLI N I CAL APPLICATI O N OF N E U R O M U S C U LA R TEC H N I QU ES: THE U P P E R B O DY behavior - say inhibited or overtight muscles - and the rea­ result of the CO2 imbalance caused by this breathing sons for these changes, as well as helping to improve func­ pattern, or might possibly be breathing in this way because tion so that the stress load can be better handled (postural of a predisposing anxiety (Chaitow et al 2002, Timmons and breathing rehabilitation, balance training, etc.). 1994). The usefulness of this approach is that it allows a focus to • Interventions that reduce anxiety will help all associated be brought to factors that are amenable to change via (for symptoms and these could involve biochemical modifi­ example): cation (herbs, drugs), stress coping approaches (includ­ ing breathing rehabilitation) or psychotherapy. • manual methods, rehabilitation, reeducation and exer­ cise, all of which influence biomechanical factors • Interventions that improve breathing function, probably involving easing of soft tissue distress (including deacti­ • nutritional or pharmaceutical tactics, which modify bio­ vation of trigger points) and/or joint restrictions, as well chemical influences, and as breathing retraining, should significantly help to reduce symptoms associated with musculoskeletal dys­ • psychological approaches, which deal with psychOSOCial function. influences. The most appropriate approach will be the one that most In truth, the overlap between these causative categories is closely deals with causes rather than effects and which so great that in many cases interventions can be randomly allows for long-term changes that will reduce the likelihood selected since, if effective, all will (to some degree) modify of recurrence. Biochemistry, biomechanics and the mind are the adaptation demands, or will enhance self-regulatory seen in this example to be inextricably melded to each other. functions sufficiently for benefit to be noted. In other examples, etiological influences may not always be as clearly defined; however, they will almost always impact EXAMPLE on each other. Consider someone who is habitually breathing in an upper The theme of respiratory influence on musculoskeletal chest mode, the stress of which will place adaptive dysfunction is explored further, later in this chapter. Before demands on the accessory breathing muscles, with conse­ that, a summary of postural and emotional influences will quent stiffness, pain, trigger point activity (particularly in prepare us for a more comprehensive understanding of one the scalenes) and joint involvement. This individual will of the most important body processes - respiration. probably display evidence of anxiety (see below) as a direct Psychosocial influences - including I- -iI depression, anxiety traits, poor stress coping abilities, loneliness, fear, M ... consequences of childhood abuse, etc. ------ M U N E Biochemical influences - including acquired or self-generated S toxicity, nutrient deficiencies, infectious, r-:-'l�=i7 y endocrine, allergic and other factors S Biomechanical influences - including T structural (congenital, e.g. short leg or E hypermobility features, postural or M traumatically induced characteristics) ..-. :-7- ------i- or functionally induced changes The interacting influences of a biochemical, biomechanical and psychosocial nature (overuse, misuse, e.g. hyperventilation do not produce single changes. For example: stresses on respiratory mechanisms and structures) a negative emotional state (e.g. depression) produces specific biochemical changes, impairs immune function and leads to altered muscle tone. hyperventilalion modifies blood pH, alters neural reporting (initially hyper and then hypo), creates feelings of anxiety/apprehension and directly impacts on the structural components of the thoracic and cervical region - muscles and joints. altered chemistry affects mood; altered mood changes blood chemistry; altered structure (posture for example) modifies function and therefore impacts on chemistry (e.g. liver function) and potentially on mood. Within these categories - biochemical, biomechanical and psych9social- are to be found most major influences on health. Figure 4-3 Biochemical, biomechanical and psychosocial influences on health. Reproduced with permission from Chaitow (2003).

4 Causes of musculoskeletal dysfunction 69 POSTURAL AND EMOTIONA L INFLUENCES ON which to accompany more mechanistic interpretations of MUSCULOSKELETA L DYSFUNCTION what may be happening in any given dysfunctional pattern. Below is a brief discussion of his work insofar as this relates An insightful Charlie Brown cartoon depicts him standing to the main theme of this book. in a pronounced stooping posture, while he philosophizes to Lucy that it is only possible to get the most out of being POSTURAL INTERPRETATIONS depressed if you stand this way. Standing up straight, he asserts, removes all sense of being depressed. Latey describes the patient entering the consulting room as displaying an image posture, which is the impression the Once again, as in the breathing dysfunction example patient subconsciously wishes you to see. above, we can see how emotions and biomechanics are closely linked. Anything that relieved the depressed state If the patient is requested to relax as far as possible, the would almost certainly result in a change of body language next image noted is that of slump pasture, in which gravity and, if Charlie is correct, standing tall should impact (to acts on the body as it responds according to its unique some extent at least) on his state of mind. attributes, tensions and weakness. Here it is common to observe overactive muscle groups coming into operation - Australian-based British osteopath Philip Latey (1996) hands, feet, jaw and facial muscle may writhe and clench or has found a useful metaphor to describe observable and twitch. palpable patterns of distortion that coincide with particular clinical problems. He uses the analogy of 'clenched fists' Finally, when the patient lies down and relaxes we come because, he says, the unclenching of a fist correlates with to the deeper image, the residual posture. Here are to be physiological relaxation, while the clenched fist indicates found the tensions the patient cannot release. These are pal­ fixity. rigidity, overcontracted muscles, emotional turmoil, pable and, says Latey, leaving aside sweat, skin and circula­ withdrawal from communication and so on. tion, represent the deepest 'layer of the onion' available to examination. Latey states: CONTRACTION PATTERNS The 'lower fist' is centered entirely on pelvicfunction. When I describe the 'upper fist' I will include the head, neck, shoul­ What is seen varies from person to person according to their ders and arms with the upper chest, throat and jaw. The state of mind and wellbeing. Apparent is a record or psy­ 'middle fist' will be focused mainly on the lower chest and chophysical pattern of the patient's responses, actions, upper abdomen. transactions and interactions with their environment. The patterns of contraction that are observed and palpated often We find Latey's manner of describing the emotional back­ have a direct relationship with the patient's unconscious ground to physical responses a meaningful vehicle with and provide a reliable avenue for discovery and treatment. One of Latey's concepts involves a mechanism that leads to muscular contraction as a means of disguising a sensory barrage resulting from an emotional state. Thus Latey describes: • a sensation which might arise from the pit of the stomach being hidden, masked, by contraction of the muscles attached to the lower ribs, upper abdomen and the junc­ tion between the chest and lower spine • genital and anal sensations which might be drowned out by contraction of hip, leg and low back musculature • throat sensations which might be concealed with con­ traction of the shoulder girdle, neck, arms and hands. Figure 4.4 Cartoon showing Latey's 'middle fist' concept. EMOTIONAL CONTRACTIONS Reproduced with permission from the Journal ofBodywork and Movement Therapies 1996; 1(1):50. A restrained expression of emotion itself results in suppres­ sion of activity and, ultimately, chronic contraction of the muscles which would be used were these emotions to be expressed (such as rage, fear, angel� joy, frustration, sorrow or anything else). Latey points out that all areas of the body producing sensations that arouse emotional excitement may have their blood supply reduced by muscular contraction.

70 CLI N I CAL A P PLI CATI O N OF N E U R O M U SCULA R T E C H N I Q U ES : THE U P P E R B O DY Also sphincters and hollow organs can be held tight until whereas, in vomiting, it remains in total contraction through­ numb. He gives as examples the muscles that surround the out each eliminative wave. Between waves of vomiting the genitals and anus as well as the mouth, nose, throat, lungs, breathing remains in the inspiratory phase, with upper chest stomach and bowel. panting. Transversus is slack in this phase. Latey suggests that often it is only muscle fatigue that breaks cycles of When considering the 'middle fist', Latey concentrates laughter/weeping/vomiting. his attention on respiratory and diaphragm function and the many emotional inputs which affect this region. He dis­ The clinical problems associated with 'middle fist' dys­ counts as a popular misconception the idea that breathing is function relate to distortions of blood vessels, internal organs, produced by contraction of the diaphragm and the muscles autonomic nervous system involvement and alteration in that raise the rib cage, with exhalation being simply a relax­ the neuroendocrine balance. Diarrhea, constipation and colitis ation of these muscles. He states, 'The even flow of easy may be involved, but more direct results relate to lung and breathing should be produced by dynamic interaction of ... stomach problems. Thus, bronchial asthma is an obvious two sets of muscles'. example of 'middle fist' fixation. The active exhalation phase of breathing is instigated, he There is a typical associated posture with the shoulder suggests, by the following muscles. girdle raised and expanded as if any letting go would pre­ cipitate a crisis. Compensatory changes usually include very 1. Transversus thoracis which lies inside the front of the taut, deep neck and shoulder muscles (see Janda's upper chest and attaches to the back of the sternum, \\·vhile fan­ ning out inside the rib cage and then continuing to the crossed syndrome description, discussed in Chapter 5) lower ribs where the fibers separate. This forms an inverted (Janda 1983). 'V' below the chest. This muscle, Latey says, has direct intrinsic abilities to generate all manner of uniquely pow­ In treating such a problem, Latey starts by encouraging erful sensations, with even light contact sometimes pro­ function of the 'middle fist' itself, then extending into the ducing reflex contractions of the whole body or of the neck and shoulder muscles, while encouraging them to relax abdomen or chest. Feelings of nausea and choking and and drop. He then goes back to the 'middle fist'. Dramatic all types of anxiety, fear, anger, laughter, sadness, weep­ expressions of alarm, unease and panic may be seen. The ing and other emotions may be displayed. He discounts patient, on discussing what they feel, might report sensa­ the idea that the muscle's sensitivity is related to the tions of being smothered, drowned, choked, engulfed or 'solar plexus', suggesting that its closeness to the internal crushed. thoracic artery is probably more significant since, when it is contracted, it can exert direct pressure on the artery. He 'UPPER FIST' FUN CTION S believes that physiological breathing has, as its central event, a rhythmical relaxation and contraction of this The 'upper fist' involves muscles which extend from the thorax to the back of the head, where the skull and spine muscle. Rigidity is often seen in the patient with 'middle join, and extends sideways to include the muscles of the shoulder girdle. These muscles therefore set the relative fist' problems, where 'control' dampens the emotions positions of the head, neck, jaw, shoulders and upper chest that relate to it. and, to a large extent, the rest of the body follows this lead (it 2. The other main exhalation muscle is serratus posterior was F.M. Alexander (1932) who showed that the head-neck inferior, which runs from the lower thoracic and upper relationship is the primary postural control mechanism). This lumbar spine and fans upwards and outwards over the lower ribs, which it grasps from behind to pull them region, says Latey, is 'the center, par excellence, of anxieties, ten­ down and inwards on exhalation. These two muscles mirror each other and work together. Latey states that it sions and other amorphous expressions of unease'. is common to find a static overcontracture of serratus In chronic states of disturbed 'upper fist' function, he posterior inferior, with the underlying back muscles in a state of fibrous shortening and degeneration, reflecting asserts, the main physical impression is one of a restrained, 'the fixity of the transversus, and the extent of the emo­ overcontrolled, damped down expression. The feeling of the tional blockage'. muscles is that they are controlling an 'explosion of affect'. Those experiences that are not allowed free play on the face 'MIDDLE FIST' FUN CTIONS are expressed in the muscles of the skull and the base of the skull. This is, he believes, of central importance in problems of Latey reports that laughing, weeping and vomiting are three emotional 'safety valve' functions of 'middle fist' function, headache, especially migraine. Says Latey, 'I have never seen used by the body to help resolve internal imbalance. Anything stored internally that cannot be contained emerges explo­ a migraine sufferer who has not lost complete ranges of facial sively via this route. In laughing and weeping, there is a expression, at least temporarily'. definite rhythm of contraction/relaxation of transversus Effects of 'upper fist' patterns The mechanical consequences of 'upper fist' fixations are many and varied, ranging from stiff neck to compression fac­ tors leading to disc degeneration and facet wear. Swallowing

4 Causes of musculoskeletal dysfunction 71 and speech difficulties are common, as are shoulder dys­ the scope of this text. However, it is important to consider functions including brachial neuritis, Reynaud's syndrome emotional influences, particularly those that are most and carpal tunnel problems. impacting. Latey states: What are the backgrounds to feelings that Latey conjures up in his 'clenched fist' model of physical contraction and The medical significance of 'upper fist' contracture is mainly congestion - of being stressed, pressured, tense, anxious? circulatory. Just as 'lower fist' contraction contributes to Without doubt, there are probably as many different back­ circulatory stasis in the legs, pelvis, perineum and lower grounds as there are people affected. However, some common abdomen, so may 'upper fist' contracture have an even more elements seem likely, and most of these have become familiar profound effect. The blood supply to the head, face, special to us through the popular media - with 'life events' and senses, the mucosa of the nose, mouth, upper respiratory 'type A personality' being among the most obvious. tract, the heart itself and the main blood vessels are con­ trolled by the sympathetic nervous system and its main Life events 'junction boxes' (ganglia) lie just to the front of the verte­ brae at the base of the neck. Holmes & Rahe (1967) studied some 5000 people who had recently been ill, inquiring into the 'events' that had taken Thus, headaches, eye pain, ear problems, nose and throat as place over the previous 12 months. Using questionnaires that well as many cardiovascular troubles may contain strong listed both major events, such as 'death of a spouse' (100 mechanical elements relating to 'upper fist' muscle contrac­ points or 'life crisis units'), 'divorce' (60 points), as well as tions. Latey reminds us that it is not uncommon for cardio­ minor ones such as 'moving house' (15 points) and 'taking a vascular problems to manifest at the same time as chronic minor loan' (10 points), they were able to demonsh'ate a muscular shoulder pain (such as avascular necrosis of the cumulative effect. rotator cuff tendons) and that the longus colli muscles are often centrally involved in such states. If the 'score' resulting from the 50 or so questions totaled 250 or more, an 80% risk of serious illness within 2 years He looks to the nose, mouth, lips, tongue, teeth, jaws and was suggested. Different scores carried with them varying throat for evidence of functional change related to 'upper percentages of risk, although it was recognized that people fist' dysfunction, with relatively simple psychosomatic had different degrees of stress susceptibility, meaning that disturbances underlying these. Sniffing, sucking, biting, for some people a far lower score than 250 might suggest cheWing, tearing, swallowing, gulping, spitting, dribbling, significant risk. burping, vomiting, sound making and so on are all signifi­ cant functions which might be disturbed acutely or chroni­ The attractiveness of the model constructed by Rahe & cally. These patterns of use can all be approached via Holmes was that it illustrated the cumulative effect of a breathing function. number of minor stresses as having the same potential to cause harm (if not adequately adapted to) as major events. When all the components of the 'upper fist' are relaxed, the This is a concept that Selye (1956) had identified in his act of expiration produces a noticeable rhythmical move­ model of the general adaptation syndrome. It also allowed ment. The neck lengthens, the jaw rises slightly (rocking the a rough and ready picture of vulnerability. However, a whole head), the face fills out, the upper chest drops. When number of provisos need to be made in relation to the accu­ the patient is in difficulty [ may try to encourage these racy of the 'life event' model. movements by manual work on the muscles and gentle direction to assist relaxed expiration. Again, by asking the 1. Correlation does not prove cause. In other words, because patient to let go and let feelings happen, I encourage resolu­ many people had become ill within a certain time of a tion. Specific elements often emerge quite readily, especially major, or a number of minor, stress events, this did not those mentioned with the 'middle fist', the need to vomit, prove that the stresses caused the illness, only that there cry, scream, etc. was a probable link. Note: More detail of Latey's perspective regarding 'lower 2. The way the scale was created did not allow for individ­ fist' function is presented in Volume 2 of this book, which ual variations in the way people respond to the stresses deals with the lower body. affecting them. BEHAVIOR AN D PERSON ALITY ISSUES 3. Nevertheless the questionnaire and scale offers a relatively simple way of scoring the amount of stress people are In this segment, focus will be on the everyday contributory suffering, suggesting their current risk of becoming ill. states ('anxiety', 'tension' and 'stress') that add to muscu­ loskeletal distress, arising from a background of what may Type-A personality be termed exaggerated emotional states. The authors have deliberately avoided discussion of the potential biomechani­ Within the framework of behavior and personality, as it cal influences of true psychological illness as they lie beyond relates to how stress is handled, the now (in)famous Type-A personality is a major feature.

72 C L I N I CAL A P P L I CATI O N OF N E U R O M USCU LAR TECHN I Q U ES : THE U P P E R B O DY Alarm reaction is perceived as challenging rather than threatening, then he/ she is more likely to cope successfully with stress. The Minor stress events - person without hardiness characteristics tends to have poor individually incapable of self-image and commitment; feels vulnerable to the vicissi­ triggering alarm reaction tudes of life, as though at the mercy of fate; and feels threat­ ened rather than challenged. A combination of minor stresses, each incapable of triggering an alarm reaction in the general adaptation The hardy individual recognizes that while we cannot syndrome can, when combined or sustained, produce always control events in our external world, we have the sufficient adaptive demand to initiate that alarm. ability to control how we view these events and the emo­ In fibromyalgia a combination of major and minor tional response we choose to have to them. biochemical, biomechanical and psychosocial stressors commonly seem to be simutaneously active. Among the main features of hardiness are: Figure 4.5 Schematic representation of multiple minor stressors • an internal sense of control producing similar effect to sing le major stress event. • action orientation (not passive) Reproduced with permission from Chaitow (2003). • high levels of self-esteem • having a life plan with established priorities. The important aspect of knowledge of hardiness is that it can be acquired. It is possible, by a process of awareness and adoption of new ways of viewing and dealing with life events, that a vulnerable individual can begin to 'stress­ proof him/herself and can become 'hardy' (Wooten 1996). The importance of these simple concepts is as important in the context of musculoskeletal dysfunction as it is in rela­ tion to general health concerns. Type A has been defined as a person with an 'action­ CAUTIONS AN D QUESTION S emotion complex' with a 'tendency to aggressively struggle to achieve more and more in less and less time' (Booth­ -- Kewley & Friedman 1987). This is the 'workaholic' individual, feverishly working to deadlines, often - as Norman Cousins There is (justifiably) intense debate regarding the question (1979) showed - with a tendency to cardiac disease (Booth­ of the intentional induction of 'emotional release' in clinical Kewley & Friedman 1987). settings in which the therapist is relatively untrained in psychotherapy. There is unlikely to be an easy ability to relax, and if exer­ cise is taken it is also likely to be with great intensity. A car­ • If the most appropriate response an individual can cur­ toon of a patient speaking to his doctor sums up the nature rently make to the turmoil of their life is the 'locking of the true Type-A individual: 'I am learning to relax doctor, away' of the resulting emotions into their musculoskele­ but I want to relax better and faster ... in fact I want to be at tal system, what is the advisability of unlocking the emo­ the cutting edge of relaxation as quickly as possible.' tions that the tensions and contractions hold, especially when the practitioner has no training and the patient has The bodyworker attempting t o relax the muscles o f a no skills with which to handle those emotions? Type-A patient is fighting an uphill battle, unless an internal awareness of the problem is achieved, accompanied by • If there exists no current ability to mentally process the behavior modification. pain that these somatic areas are holding, are they not best left where they are until counseling or psychother­ Hard iness apy or self-awareness leads to the individual's ability to reflect, handle, deal with and eventually work through But there are healthy Type-As, just as there are people who the issues and memories? cope adequately and actually seem to suffer little ill-effect physically or mentally, even though they endure severe • What are the advantages of triggering a release of emo­ overload of 'life events'. This appears to be because they tions, manifested by crying, laughing, vomiting or what­ carry the attributes of what has been termed 'hardiness' ever - as described by Latey and others - if neither the (Kobassa 1983, Maddi & Kobassa 1984). individual nor the therapist can then take the process to a healthier position? The key 'hardiness factors' that increase a person's resilience to stress and prevent burnout are commitment, In the experience of one of the authors (LC) there are indeed control and challenge. If an individual has a strong commit­ patients whose musculoskeletal and other symptoms are ment to him/ herself; and believes that he /she is in control patently linked to devastating life events (torture, abuse, of the choices in life (internal locus of control); and if change witness to genocide, refugee status and so on) to the extent that extreme caution is called for in addressing obvious symptoms for the reasons suggested above.

4 Causes of musculoskeletal dysfu nction 73 What would emerge from a 'release'? How would the stress can hav� on associated tissues, starting with diaphrag­ person handle it? The truth is that there are many examples matic weakness. in modern times of people whose symptoms represent the end result of appalling social conditions and life experiences. The main factors which determine the maintenance of the Healing may require a changed life (often impossible to envis­ abdominal viscera in position are the diaphragm and the age) or many years of work with psychological rehabilitation, abdominal m uscles, both of which are relaxed and cease to and not interventions that address apparent symptoms, support in faulty posture. The disturbances of circulation which may be the merest tips of large icebergs. resultingfrom a low diaphragm and ptosis may give rise to chronic passive congestion in one or all of the organs of the The contradictory perspective to these questions suggests abdomen and pelvis, since the local as well as general that there would not be a 'spontaneous' release of 'emotional venous drainage may be impeded by the failure of the baggage' unless the person was able to intellectually and diaphragmatic pump to do its full work in the drooped body. emotionally handle whatever emerged from the process. Furthermore, the drag of these congested organs on their This is indeed a debate without obvious resolution. The nerve supply, as well as the pressure on the sympathetic authors feel it worthy of exposure in this context but cannot ganglia and plexuses, probably causes many irregularities offer definitive answers. These questions are intended to be in their function, varying from partial paralysis to over­ thought-provoking. It is suggested that each patient and stimulation. All these organs receive fibers from both the each therapist/practitioner should reflect on these issues vagus and sympathetic systems, either one of which may be before removing (however gently and however temporarily) disturbed. It is probable that one or all of these factors are the defensive armoring that life may have obliged vulnera­ active at various times in both the stocky and the slender ble individuals (almost all of us at one time or another) to anatomic types, and are responsible for many functional erect and maintain. It may be that, in some circumstances, an digestive disturbances. These disturbances, if continued individual's 'physical tensions' may be all that are prevent­ long enough, may lead to diseases later in life. Faulty body ing him/her from fragmenting emotionally. mechanics in early life, then, becomes a vital factor in the production of the vicious cycle of chronic diseases and pres­ It is important to differentiate between the skill to pro­ ents a chief point of attack in its prevention . . . In this voke an emotional release and the skill to adequately u pright position, as one becomes older, the tendency is for process the resulting emotional instability. Many trainings the abdomen to relax and sag more and more, allowing a teach the skills to provoke emotional release, but few offer ptosic condition of the abdominal and pelvic organs unless any training whatsoever in appropriate steps to resolution. the supporting lower abdominal muscles are taught to con­ Practitioners who practice 'emotional release' techniques tract properly. As the abdomen relaxes, there is a great ten­ are responsible for also acquiring training, skills and proper dency towards a drooped chest, with narrow rib angle, licensure to ensure safe handling of the patient's emotional forward shoulders, prominent shoulder blades, a forward state, regardless of whether the emotional release courses position of the head, and probably pronated feet. When provided those skills as part of the training. the human machine is out of balance, physiological func­ tion cannot be perfect; muscles and ligaments are in an At the very least we should all learn skills that allow the abnormal state of tension and strain. A well-poised body safe handling of 'emotional releases' that may occur with­ means a machine working perfectly, with the least amount out deliberate efforts to induce them. And we should have a of muscular effort, and therefore better health and strength referral process in place to direct the person for further pro­ for daily life. fessional help. Note how closely Goldthwaite mirrors the picture Janda As a first-aid approach, should such an event occur dur­ paints in his upper and lower crossed syndrome and 'pos­ ing or following treatment, emphasis should be on initiat­ ture and facial pain' descriptions (see Chapter 5, p. 84). ing calm, and this may best be achieved through slow breathing, focusing on the outbreath. The patient should be Also note the descriptions of faulty body mechanics, a.nd allowed to talk if he/she wishes but, unless adequately try to imagine that same individual standing in a balanced h'ained, the practitioner should avoid any attempt to advise manner while breathing in a slow, deep, relaxed way. The or to try to 'sort out' the patient's problems. The focus should idea of normal postural or respiratory (or almost any other be on helping the patient through the crisis to a state of calm physiologic) function emerging from an unbalanced and before offering an appropriate referral. crowded, anatomically compromised structure, is far-fetched at best. POSTURAL IM B A LANC E AND THE Goldthwaite, in his description above, speaks of 'the fail­ DIAPHRAGM (Goldthwa ite 1 945) ure of the diaphragmatic pump' being able to do its work in a 'drooped body'. This highlights one of the key elements Goldthwaite, in his classic 1930s discussion of posture, links required to normalize posture and breathing pattern disor­ a wide array of health problems to the absence of balanced ders. There is a need not only to encourage (and teach if posture. Clearly, some of what he hypothesized remains possible) better breathing and postural habits, but also to conjecture but we can see j ust how much impact postural

74 C L I N I CA L A P P L I CAT I O N O F N E U R O M U S C U LA R TE C H N I Q U E S : T H E U P P E R B O DY focus attention on the drooped and crowded structures that upon neural circuits that are shared by pathways that medi­ will, over time, have become compromised - and which will, ate autonomic control, vestibuloautonomic interactions and unless appropriately treated (loosened, stretched, mobilized, anxiety: etc.), be virtually unable to improve their function. The core of this circuitry is a parabrachial nucleus network, A key measure of good posture is optimal balance. consisting of the parabrachial nucleus . . . a site of conver­ gence of vestibular information processing, and somatic and BALAN CE visceral sensory information processing, in pathways that appear to be involved in avoidance conditioning, anxiety, Maintaining body balance and equilibrium is a primary role and conditioned fear. of functionally coordinated muscles, acting in task-specific patterns, and this is primarily dependent on normal motor At its simplest, balance depends on optimal motor control, control (Winters & Crago 2000). and motor control depends on coordinated neurological direction. Feelings of anxiety - such as can be triggered by Without doubt, balance largely depends on adequate breathing pattern disorders - or imbalances such as those proprioceptive input, as discussed in Volume 2, Chapter 2. described above (also see notes on deconditioning below), Without a steady flow of proprioceptive information (deriv­ result in poor motor control, unbalanced body function, and ing from the eyes, inner ear, muscles and joints of the entire the likelihood of malcoordinated use patterns. Resultant body) reaching the higher centers, balance is going to be adaptations lead to shortening of postural muscles, inhibi­ compromised. tion of phasic muscles and the evolution of trigger points. Balaban & Theyer (2001) have examined the neurological basis for links between balance control and anxiety, based Body goes on alert (the 'fight or flight' response) Psychological effects: Symptoms Rapid pulse, Upper body tiredness, sensory are frightening sweating, tension; breathing disturbance, dizziness Aching shoulders, butterflies in the becomes more Physical effects: exhaustion, head and stomach, rapid tingling, cramps, weakness, neck pain etc. Nociceptors tense muscles, more sensitive 'twitchiness' - increases pain perception Low calcium Increased dioxide lost causes nerves and swallowing rate through muscles to and bloating overbreathing function poorly Calcium Blood pH lost in urine becomes more alkaline as carbonic acid is mobilized Smooth muscles constrict, reducing arterial blood supply to the brain and tissues, leading to fatigue and 'brain fog' Figure 4.6 Negative health infl uences of a dysfunctional breathing pattern such as hyperventilation. Reproduced with permission from Peters et aI (2002).

4 Causes of musculoskeletal dysfunction 75 These thoughts offer an example of the meeting poin t of The products of this process, which is more extreme in mind and body - where biochemistry, biomechanics and deconditioned individuals, include the b uild-up of acids, the mind interact seamlessly. Here we can see emotions such as lactic and pyruvic acids (Fried 1987) . As lactate (anxiety, for example) influencing function (brea thing), aCCLUTIulates in muscle cells and the bloodstream, pH reduces while at the same time being aware tha t the reverse is also and this triggers a homeostatic retention of bicarbonate true, that an habitual breathing pa ttern can trigger anxiety. (part of renal function) in an attempt to balance the increasing Whichever way round this cause-and-effect cycle goes, the acidity. This, in turn, stimula tes the brea thing rate, causing end result is - a series of disturbed neurological and func­ CO2 levels to drop again, resulting in symp toms of brea th­ tional patterns, operating in a biochemically compromised lessness (dyspnea) and fatigue. And the fluctua ting cycle system, where pH is unbalanced and calcium and magne­ continues to repeat i tself (Lum 198 1 ) . sium reserves are seriously affected. Out of this environment emerges the likelihood (virtual certainty) of disturbed bal­ According t o Nixon & Andrews ( 1996) the outcomes of ance, increased sympa thetic arousal, sensitized neurons, these events in a decondi tioned individual include: muscular distress, trigger point activity, fatigue and pain (Chaitow et al 2002). • loss of muscle mass (due partly to poor protein synthesis) • decreased ability to use energy substra tes efficiently These complications from respiratory influences are wor­ • decreased neuromuscular transmission thy of the following deeper investigation. • decreased efficiency in m uscle fiber recrui tment, with RESPIRATORY IN F LUENCES indications of disruption of normal motor control being apparent (Wittink & Michel 2002). Breathing dysfunction is seen to be at least an associated factor in most chronically fatigued and anxious people, and Nixon & Andrews (1996) summa rized the emerging symp­ almost aU people subject to panic a ttacks and phobic behavior, toms tha t result from overbrea thing in a decondi tioned many of whom also display multiple musculoskeletal symp­ individual as follows: toms. In modern inner cities in particular and early 21st­ century existence in general, there exists a vast expression • Muscular aching at low levels of effort of respiratory imbalance, as seen in paradoxical brea thing, • Restlessness and heightened sympathetic activity upper chest breathing and chronic hyperventilation (Aust & • Increased neuronal sensitivity Fischer 1997, Cholewicki & McGill 1996, Hodges et aI 200 1 ) . • Constriction of smooth muscle tubes (e.g. vascular, respi­ A s a tendency toward upper chest brea thing becomes ratory and gastrointestinal) tha t can accompany the basic more pronounced, biochemical imbalances occur when symptom of inability to make and sustain normal levels excessive amounts of carbon dioxide (C02) are exhaled, of effort. leading to relative alkalosis, which automatically produces a sense of apprehension and anxiety. This condition of res­ In practice this means that patients who are not aerobically piratory alkalosis frequently leads to panic attacks and pho­ fi t are the most likely individuals whose motor con trol will bic behavior, from which recovery is possible only when be impaired, and who will be most vulnerable to muscle breathing is normalized (King 1988, Lum 1981). and joint - particularly the spine - dysfunction (Panjabi 1992). Since carbon dioxide is one of the major regulators of cerebral vascular tone, any reduction due to hyperventilation RESP I RATORY EN TRAIN MEN T AN D CORE patterns leads to vasoconstriction and cerebral oxygen defi­ ciency. Whatever oxygen there is in the bloodstream then STABILITY ISSU ES has a tendency to become more tightly bound to its hemo­ globin carrier molecule, leading to decreased oxygenation Diaphragm and transversus abdominis tone are well estab­ of tissues. All this is accompanied by a decreased threshold lished as key features in the provision of core stability (Panjabi of peripheral nerve firing. 1992). There is evidence tha t increased intraabdominal pres­ sure (lAP), even with limited participa tion of the abdominal E F FECTS OF RESPIRATORY AL KALOSIS IN A or back muscles, augments the stability of the spine (Hodges et al 2001, 2005). DECON DITION ED IN DIVIDUAL Recent data confirm that the activity of the diaphragm Oxygen is a necessary ingredient of ATP (energy) production occurs in association with tasks tha t challenge the stabi lity in normal tissues. However, when respiratory alkalosis occurs, of the spine (Hodges & Gandevia 2000a,b, Hodges et al the activation of anaerobic energy pathways starts (anaero­ 1997). When, however, a challenge occurs that ma kes pos­ bic glycolysis - the p roduction of energy in the relative tural/stabilizing demands on the diaphragm at the same absence of oxygen), leading to an accumulation of incom­ time that respiratory demands are occurring, it is the stability pletely oxidized products of metabolism (Fried 1987). element that s uffers. Using a 1 0% CO2 gas mixture to elevate breathing, McGill et al (1995) demonstrated that reduction in the support offered to the spine by the muscles of the torso may occur if there is a load challenge to the low back combined with a breathing

76 C L I N I CA L A P P L I CAT I O N O F N E U R O M U S C U LA R TE C H N I Q U E S : TH E U P P E R B O DY challenge (shovelling snow is given as an easily understood Box 4. 1 Partial pressure symbols example in real-life rather than under research conditions). 'Modulation of muscle activity needed to facilitate breath­ Partial pressure was formerly symbolized by p, followed by the ing may compromise the margin of safety of tissues that chemical symbol in capital letters (e.g. pC02, p02)' Curre ntly, in depend on constant muscle activity for support: respiratory physiology, P, followed by subscripts, denotes location and/or chem ical species (e.g. PC02, P02, PaC02). McGill et al offer the dramatic example of an individual shovelling snow, placing enormous torsional and shear PC02 = partial p ressure of carbon d ioxide forces onto the spine, while breathing rapidly. Other exam­ P02 = p a rtial pressure of oxygen ples come to mind in both work and leisure settings, but PaC02 = arterial carbon dioxide tension (where a = arterial) wha tever the particular scenario, spinal stress, combined with rapid brea thing, presents the control mechanisms of Box 4.2 Hyperventilation in context the body with choices, and survival (i.e. breathing) clearly takes precedence over stability in that contest. The sim plest d efinition of hyperve ntilation is that it represents a pattern of (over)breathing which is in excess of metabolic requ ire­ To amplify McGill's message, Hodges et al (2001) noted ments. It is normal to hyperventilate ('puffing and panting') in tha t after approximately 60 seconds of overbreathing, both association w ith physical exertion, such as running, or if there the postural (tonic) and phasic functions of the diaphragm exists a heig htened degree of acid in the bloodstream (acidosis), and transversus abdominis are reduced or absent. 'The possibly a result of kidney or liver d isease. I n these examples the present data suggest tha t increased central respira tory d rive rapid breathing p attern produces a reduction i n acid ity v i a may a ttenuate the postural commands reaching motoneu­ exh a l ation o f CO2 and i s therefore seen to b e help ing to resto re rons. This attenuation can affect the key inspiratory and normal acid- a l k a l ine balance (pH 7.4). expira tory muscles, and is likely to be co-ordinated at a pre­ motoneuronal site.' It is when a p attern of overbre ath ing occurs without an associated acidosis that problems arise, as this leads to alkalosis Hodges et al further hypothesize: and all the sym ptoms w h ich flow from t h at state (see m a in text for details). Although investigation of spinal mechanics is required to There are m a ny ind ividuals whose blood g as profile would not confirm the extent to which spinal control is compromised by categorize them as h aving reached a state of true hyperventila­ tion, but who are clearly prog ressing toward that state. It is such increases in respiratory demand, it is hypothesised that such a individu als who often display many of the e a rly signs of chronic unwellness, ranging from fatigue to chronic muscular pains and compromise may lead to increased potential for injury to loss of concentration. These individuals may well benefit from a combination of stress m a n agement, musculoskeletal norm aliza­ spinal structures and reduced postural control. During stren­ tion and breathing retraining approaches. llOUS exercise, when the physical stresses to the spine are individual performing regular arm or leg movement in work or leisure activity, is obvious. greater, the physiological vulnerability of the spine to injury is Leaving aside all other considerations outlined in this likely to be increased. chapter, the influence of upper chest (non-diaphragmatic) overbreathing alone can be seen to be capable of compro­ Clearly other spinal support is required to take over when mising spinal stability. this sort of reduction occurs in primary stabilizing muscles; however, whether the additional stability is in fact available SUMMARY OF EFFECTS OF HYPERVEN TILAT I ON will depend on the overall level of fitness and tone. • Reduction in PC02 (tension or partial pressure of carbon Studies by O'Su llivan et al (2002) have also indica ted that dioxide) causes respiratory alkalosis via reduction in arte­ people with sacroiliac pain have impaired recruitment of rial carbonic acid, which leads to abnormally decreased the diaphragm and pelvic floor. arterial carbon dioxide tension (hypocapnia) and major systemic repercussions (see Figs 4.6 and 4.7,. Hodges et al (2001) also investiga ted respiratory and pos­ tural diaphragm function during repetitive upper limb • The first and most direct response to hyperventilation is movement and showed a virtual entrainment between limb cerebral vascular constriction, reducing oxygen availability movement and respiratory rate. 'Results indicate tha t activ­ by about 50%. ity of human phrenic motoneurones is organised such that it contributes to both posture and respiration during a task • Of aU body tissues, the cerebral cortex is the most vulnera­ which repetitively challenges trunk posture.' ble to hypoxia, which depresses cortical activity and causes dizziness, vasomotor instability, blurred consciousness Peper (2004) has recorded the effect on breathing rate (as ('foggy brain') and visual disturbances. well as on the EMG activity of the scalenes and forearm extensors) of an individual sitting with hands on Jap, mov­ • Loss of cortical inhibition results in emotional lability. ing the hands to the keyboard, and then starting to type. The breathing rate goes from a slow rhythm to rapid as the EMG activity increases during the stages mentioned, and reverses as the person stops typing with hands still on the keyboard, and then returns to the initial calm state when hands return to the lap. The implications, relative to the respi­ ratory rate and all that th.is means relative to the health of an

4 Causes of musculoskeletal dysfunction 77 Breathing in Reduced PC02 1 . Upper fixator overactivity excess of = respiratory alkalosis metabolic shor tening of accessory requirements I breathing muscles 2. Painful nodules in nape of • neck, anterior chest and 'Tetany, muscle spasm, 'Sympathetic dominance - dilated 'Increased neuronal activity shoulder girdle paresthesia pupils, dry mouth, sweaty palms, gut speeding spinal reflexes as well 3. Temporal headaches Increased neuronal irritability and digestive dysfunction, abdominal (initially) as heightened pain 4. Painful legs Reduced blood flow to brain, bloating, tachycardia perception + photophobia, 5. Whole body expresses limbs and heart + hyperacusis tension - cannot relax in any position t ... • Dizziness, lightheadedness, 'foggy brain' 'all these symptoms are increased during progesterone phase of menstrual cycle • Cold extremities � Increased circulating histamines • Chest pain make allergic reaction more • Anxiety, apprehension (sense violent and possibly more likely of mild panic) • Depressed cortical activity • Vasomotor instability, blurring of consciousness and vision • Loss of cortical inhibition results in emotional lability Figure 4.7 Negative health infl uences of a dysfunctional breathing pattern such as hyperventilation. N EURAL REPERCUSSI ON S most likely to be affected and these are also common sites for active myofascial trigger points (Timmons 1994). Loss of CO2 ions from neurons during moderate hyperven­ tilation stimulates neuronal activity, while producing mus­ • Painful muscular contractions (,nodules') develop and cular tension and spasm, speeding spinal reflexes as well as are easily felt in the nape of the neck, anterior chest and producing heightened perception (pain, photophobia, hyper­ shoulder girdle. acusis) - all of which are of major importance in chronic pain conditions. \\A/hen hypocapnia is more severe or prolonged • Temporal headaches centered on painful nodules in the it depresses neural activity until the nerve cell becomes parietal region are common. inert. • Sympathetic dominance is evident by virtue of dilated What seems to occur in advanced or extreme hyperventi­ pupils, dry mouth, sweaty palms, gut and digestive dys­ lation is a change in neuronal metabolism; anaerobic glycol­ function, abdominal bloating and tachycardia. ysis produces lactic acid in nerve cells, while lowering pH. Neuronal activity is then diminished so that in extreme • Allergies and food intolerances are common due to hypocapnia (reduced levels of CO2), neurons become inert. increased circulating histamines. Thus, in the extremes of this clinical condition, initial hyper­ activity gives way to exhaustion, stupor and coma (Lum BIOMECHAN ICAL CHAN GES IN RESPONSE TO 1 98 1 ) . UPPER CHEST BREATHI N G TETANY \\\"ihereas Goldthwaite (1945), Janda ( 1 982) and others point According to Stedman's Medical Dictionary (2004) tetany is to the collapse of normal posture leading inevitably to characterized by muscle twitches, cramps and cramping of changes which preclude normal breathing function, Garland the hands and feet and, if severe, may include laryngospasm (1994) presents the picture in reverse, suggesting that it is the and seizures. These findings reflect irritability of the central functional change of inappropriate breathing (e.g. hyper­ and peripheral nervous systems, which may result from ventilation or upper chest patterns of breathing) that ulti­ low serum levels of ionized calcium or, rarely, magnesium. mately modifies structure. It was Garland who coined the A reduced degree of CO2 resulting in excessive alkalinity memorable phrase 'where psychology overwhelms physi­ can also produce this effect. ology' to describe the changes which occur. In tetany that is secondary to alkalosis (excessive alkalin­ Garland describes the somatic changes that follow from a ity), muscles which maintain 'attack-defense' mode (hunched pattern of hyperventilation and upper chest breathing: shoulders, jutting head, clenched teeth, scowling) are those • A degree of visceral stasis and pelvic floor weakness will develop, as will an imbalance between increasingly weak abdominal muscles and increasingly tight erector spinae muscles.

78 C L I N I C A L A P P L I CAT I O N OF N E U R O M U S C U LA R T E C H N I Q U E S : T H E U P P E R B O DY • Fascial restriction from the central tendon of the Remember that thefunctional status of the diaphragm is prob­ diaphragm via the pericardial fascia, all the way up to the ably the most powerful mechanism of the whole body. It not basiocciput, will be noted. only mechanically engages the tissues of the pharynx to the perineum, several times per minute, but is physiologically • The upper ribs will be elevated and there will be sensi­ indispensable to the activity of every cell in the body. A work­ tive costal cartilage tension. ing knowledge of the crura, tendon, and the extensive ramifi­ cation of the diaphragmatic tissues, graphically depicts the • The thoracic spine will be disturbed by virtue of the lack significance of structural continuity andfunctional unity. The of normal motion of the articulation with the ribs and wealth of soft tissue work centering in the powerful mecha­ sympa thetic outflow from this area may be affected. nism is beyond compute, and clinically it is very practical. • Accessory muscle hypertonia, notably affecting the scale­ ADDITIONAL EMOTIONAL FACTORS AND nes, upper trapezius and levator scapulae, will be palpa­ MUSCULOSKELETA L DYS FUNCTION ble and observable. • Use of electromyographic techniques has shown a statis­ • Fibrosis will develop in these muscles as will myofascial tical correlation between unconscious hostility and arm trigger points (see pp. 65-66). The cen1ical spine will tension as well as leg muscle tension and sexual distur­ become progressively more rigid, with a fixed lordosis bances (Shagass & Malmo 1954). being a common feature in the lower cervical spine. • Wolff (1948) proved that the majority of patients with • A reduction in the mobility of the 2nd cervical segment headache showed 'marked contraction in the muscles of and disturbance of vagal ou tflow from this region is the neck . . . most commonly due to sustained contrac­ likely. tions associa ted with emotional strain, dissatisfaction, apprehension and anxiety'. Although not noted in Garland's list of dysfunctions, the other changes which Janda has listed in his upper crossed • Barlow (1959) sums up the emotion/muscle connection syndrome (see p. 82) are likely consequences, including the thus: potentially devastating effects on shoulder function of the altered position of the scapulae and glenoid fossae as this Muscle is not only the vehicle of speech and expressive gesture, pattern evolves. but has at least afinger in a number of other emotional pies - for example, breathing regulation, control of excretion, sexual Also worth noting in relation to breathing function and functioning and, above all, an influence on the body schema dysfunction are the likely effects on two important muscles, through proprioception. Not only are emotional attitudes, say, not included in Garland's description of the dysfunctions of fear and aggression, mirrored immediately in the muscle, resulting from inappropriate breathing patterns, quadratus but also such moods as depression, excitement and evasion lumborum and iliopsoas, both of which merge fibers with have their characteristic muscular patterns and postures. the diaphragm. • A comprehensive review by Linton (2000) of over 900 Since these are both postural muscles, with a propensity studies involving back and neck pain concluded that to shortening when stressed, the impact of such shortening, psychological factors play a significant role, not only in uni- or bilaterally, can be seen to have major implications chronic but also in the etiology of acute pain - particu­ for respiratory function, whether the primary feature of larly in the process of transition to chronicity. 'Stress, dis­ such a dysfunction lies in diaphragmatic or muscular tress or anxiety as well as mood and emotions, cognitive d istress. functioning, and pain behavior, all were found to be significant in the analysis of 913 potentially relevant Among possible stress factors that will result in shorten­ articles . ' ing of postural muscles is disuse. When upper chest breath­ ing has replaced diaphragmatic breathing as the norm, We must not ignore the influence of emotion on muscu­ reduced diaphragmatic excursion results and consequent loskeletal dysfunction at our (and our patients') peril. reduction in activity for those aspects of quadratus lumbo­ rum and psoas which are integral with it. Shortening (of SELECTIVE MOTOR UNIT INVOLVEMENT any of these) would likely be a result of this disuse pattern. (Waersted et a l 1 992, 1 993) Garland concludes his listing of somatic changes associ­ ated with hyperventilation: 'Physically and physiologically The effect of psychogenic influences on muscles may be [all of] this runs against a biologically sustainable pattern, more complex than a simplistic 'whole' muscle or regional and in a vicious cycle, abnormal function (use) alters nor­ involvemen t. Researchers at the Na tional Institute of mal structure, which disallows return to normal function.' Occupational Health in Oslo, Norway, have demonstrated Garland also suggests that counseling (for associated anxiety or depression, perhaps) and breathing retraining are far more likely to be successfully initiated if the biome­ chanical component(s), as outlined, are appropriately treated. Pioneer osteopathic physician Carl McConnell (1962) reminds us of wider implications of respiratory dysfunction.

4 Causes of musculoskeletal dysfu nction 79 J that a small number of motor units, particularly muscles, The researchers report tha t similar observa tions have been may display almost constant, or repeated, activity when noted in a pilot study (Waersted et aI 1992). influenced psychogenical ly. In their study normal individu­ als performing reaction time tasks were evaluated, creating The implications of this information are profound since a 'time pressure' anxiety. Using the trapezius muscle as the they suggest tha t emotional stress can selectively involve focus of attention, the researchers were able to demonstrate postural fibers of muscles, which shorten over time when low-amplitude levels of activity (using surface EMC) even stressed (Janda 1983). The possible 'metabolic crisis' sug­ when the muscle was not being employed. They explain gested by this research has strong parallels with the evolu­ this phenomenon as follows. tion of myofascial trigger pOints as suggested by Wolfe & Simons (1992), a topic which will be discussed in greater In spite oflow total activity level ofthe muscle, a small pool of detail in later chapters. low-threshold motor units may be under considerable loadfor prolonged periods of time. Such a recruitment pattern would CONC LUSION be in agreement with the 'size principle' first proposed by Henneman (1957), saying that motor units are recruited We have observed in this cha pter evidence of the negative according to their size. Motor units with type I [postural] influence on the biomechanical components of the body, the fibers are predominant among the small, low-threshold units. muscles, joints, etc., of overuse, misuse, abuse and disuse, If tension-provoking factors [anxiety, for example] are fre­ whether of a mechanical (posture) or psychological (depres­ quently present and the subject, as a result, repeatedly sion, anxiety, etc.) na ture. We have also seen the interaction recruits the same motor units, the hypothesized overload may of biomechanics and biochemistry in such processes, with follow. This can possibly result in a metabolic crisis and the breathing dysfunction as a key example of this. In the next appearance of type I fibers with abnormally large diameters, chapter we will explore some of the patterns which emerge as dysfunction progresses. or 'ragged-red'fibers, which are interpreted as a sign of mito­ chondrial overload. 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